ACUTE CARE HANDBOOK

FOR PHYSICAL THERAPISTS

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 ACUTE CARE HANDBOOK
FOR PHYSICAL THERAPISTS
THIRD EDITION

Jaime C. Paz, PT, DPT, MS

Clinical Associate Professor
Division of Physical Therapy
Walsh University
North Canton, Ohio;
Associate Clinical Professor
Department of Physical Therapy
Bouvé College of Health Sciences
Northeastern University
Boston, Massachusetts

Michele P. West, MS, PT

Supervisor
Inpatient Physical Therapy Rehabilitation Services
St. Joseph Hospital
Nashua, New Hampshire
11830 Westline Industrial Drive
St. Louis, Missouri 63146

Acute Care Handbook for Physical Therapists,Third Edition ISBN: 978-1-4160-4899-2

Copyright ! 2009 by Saunders, an imprint of Elsevier Inc.

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Notice
Knowledge and best practice in this field are constantly changing. As new research and experience broaden
our knowledge, changes in practice, treatment, and drug therapy may become necessary or appropriate.
Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the
manufacturer of each product to be administered to verify the recommended dose or formula, the method
and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on
his or her own experience and knowledge of the patient, to make diagnoses, to determine dosages and the
best treatment for each individual patient, and to take all appropriate safety precautions.To the fullest extent
of the law, neither the publisher nor the author assumes any liability for any injury and/or damage to persons
or property arising out of or related to any use of the material contained in this book.
The Publisher

Previous editions copyrighted 1997, 2002

Library of Congress Cataloging-in-Publication Data

Paz, Jaime C., 1966^

Acute care handbook for physical therapists/Jaime C. Paz, Michele P.West. ^ 3rd ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4160-4899-2 (pbk.: alk. paper)
1. Medicine ^Handbooks, manuals, etc. 2. Hospital care ^Handbooks, manuals, etc. 3. Physical
therapists^Handbooks, manuals, etc.
I.West, Michele P., 1969^ II. Title.
[DNLM: 1. Acute Disease ^therapy^Handbooks. 2. Intensive Care ^Handbooks. 3. Physical Therapy
(Specialty)^Handbooks.WB 39 P348a 2009]
RC55. P375 2009
616^dc22 2008036877

Vice President and Publisher: Linda Duncan

Executive Editor: Kathy Falk
Developmental Editor: Megan Fennell
Publishing Services Manager: CatherineJackson
Senior Project Manager: David Stein
Design Direction:Teresa McBryan

Printed in the United States

Last digit is the print number: 9 8 7 6 5 4 3 2 1

 Contributors
Sean M. Collins, PT, ScD, CCS
Chairperson and Associate Professor
Department of Physical Therapy
School of Health and Environment
University of MassachusettsçLowell
Lowell, Massachusetts
Konrad J. Dias, PT, DPT, CCS
Assistant Professor
Physical Therapy Program
Maryville University of St. Louis
St. Louis, Missouri
Margarita V. DiVall, PharmD, BCPS
Associate Clinical Professor
Department of Pharmacy Practice
Northeastern University
Boston, Massachusetts
James J. Gaydos, MS, PT
Senior Physical Therapist
Department of Inpatient Acute Care
New England Baptist Hospital
Boston, Massachusetts
Marka Gehrig, MPT
Department of Rehabilitation Medicine
The Cleveland Clinic Foundation
Cleveland, Ohio;
Therapy Partners
Cleveland, Ohio
Jennifer Lee Hunt, MS, PT
Physical Therapist
Rehabilitation Services
Lahey Clinic
Burlington, Massachusetts
Marie Jarell-Gracious, PT
Owner
Specialty Care
Mokena, Illinois
Kimberly Knowlton, PT
Clinical Lead Physical Therapist
Rehabilitation Services
University of Massachusetts Memorial Medical Center
Worcester, Massachusetts
Eileen F. Lang, PT
Senior Physical Therapist
Rehabilitation Services
Lahey Clinic
Burlington, Massachusetts
V. Nicole Lombard, MS, PT
Staff Physical Therapist
Department of Physical Therapy
New England Baptist Hospital
Boston, Massachusetts
Rachael Maiocco, MSPT
Physical Therapist
Brigham and Women’s Hospital
Boston, Massachusetts
Leah Moinzadeh, PT
Physical Therapist
Inpatient Rehabilitation
Rehabilitation Services
Lahey Clinic
Burlington, Massachusetts
v
vi CONTRIBUTORS

Jackie A. Mulgrew, PT, CCS Jason D. Rand, PT

Clinical Specialist Physical Therapist
Physical Therapy Services Inpatient Physical Therapy Services
Massachusetts General Hospital Winthrop University Hospital
Boston, Massachusetts Mineola, NewYork

David Nicoloro, PT, MS Hillary A. Reinhold, DPT

In-Patient Physical Therapy Coordinator
Department of Rehabilitation Services
Newton-Wellesley Hospital
Newton, Massachusetts;
Clinical Instructor
Northeastern University
Department of Physical Therapy
Boston, Massachusetts
Kara O’Leary, MS, PT, CCS
Senior Physical Therapist
Inpatient Physical Therapy and Outpatient
Pulmonary Rehabilitation
Rehabilitation Services
Lahey Clinic
Burlington, Massachusetts
Inpatient Physical Therapy
Rehabilitation Services
Lahey Clinic
Burlington, Massachusetts
Jennifer A. Silva, MS, PT
Physical Therapist
Outpatient Rehabilitation Center
South Shore Hospital
SouthWeymouth, Massachusetts
Falguni Vashi, PT, DPT
Staff Physical Therapist
Lahey Clinic
Burlington, Massachusetts

Susan Polich, PT, MA (ASCP), MEd

Assistant Clinical Specialist
Department of Physical Therapy
Northeastern University
Boston, Massachusetts;
Adjunct Instructor
Physical TherapyAssistant Program
Community College of Rhode Island
Newport, Rhode Island
ToTallie,Will and Henry: my love, my joy, my future.
I am truly blessed.

To Nay and Tay, as always, my eternal gratitude.

J.C.P.

For my wonderful daughters, Isabelle and Genevieve,

May you each find a profession that you love.
To my parents, for everything.
M.P.W.
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 Preface
Acute Care Handbook for Physical Therapists was originally
developed to provide clinicians with a handy reference
for patient care in the hospital setting. It was created
primarily for physical therapy students and clinicians
unfamiliar with acute care. Because of the positive
comments and feedback for the first two editions, the
third edition was written to serve the same purpose
and includes:
 A revision of all chapters with additional figures
and illustrations to improve understanding of the
material and key concepts.
 Updated literature in all chapters and appendices
to assist with developing evidence-based practice
in this setting.
 Pertinent practice patterns from the Guide to Physical
Therapist Practice, Second Edition, in each chapter to facil-
itate the development of safe and efficient plans of
care.
 Information on new surgical and invasive pro-
cedures such as minimally invasive orthopedic
surgery and bariatric procedures, as well as a fully
revised and comprehensive description of circula-
tory assist devices.
 A fully revised pharmacology appendix written by
a pharmacology expert that includes more pharma-
cological implications for physical therapists con-
cerning medication side effects and the use of
combination drugs.
 An expanded neurological chapter with new infor-
mation on the vestibular system, including tests and
measures for vestibular dysfunction, a discussion
of dementia, and the latest in stroke evaluation and
management.
 Revised appendices that:
* Discuss the latest concepts of patient safety,
documentation, and confidentiality related to
theJoint Commission standards.
* Present an array of new information relevant
to the acute care setting, including anesthesia
and patient positioning in the operating room,
alcohol withdrawal syndrome, intensive care
unit psychosis, and palliative care.
* Provide additional guidelines, based on litera-
ture, for implementing functional tests in certain
patient populations.
 A slimmer, larger format that allows the book to
lie open for easier reading.
 An improved design that highlights clinical tips
and other key features, allowing you to locate
important information quickly in a busy clinical
setting.
Additionally, the talents of more new contributors
have given this edition a much broader perspective on
clinical practice in the acute care setting.
As a member of the health care team, the physical
therapist is often expected to understand hospital pro-
tocol, safety, medical-surgical ‘‘lingo,’’ and the many
aspects of patient care from the emergency room
setting to the intensive care unit to the general ward.
This handbook is therefore intended to be a resource
to aid in the interpretation and understanding of the
medical-surgical aspects of acute care.
Each chapter in this edition of Acute Care Handbook
for Physical Therapists discusses a major body system.
The chapters include:
 A review of basic structure and function
 An overview of the medical-surgical evaluation of
a patient admitted to the hospital, including diagnos-
tic procedures and laboratory tests
 A review of pathophysiology that emphasizes signs
and symptoms of specific diseases and disorders
 Guidelines for physical therapy intervention
Clinical Tips appear throughout each chapter.These
helpful hints are intended to maximize safety, quality,
and efficiency of care.These clinical tips are suggestions
from the editors and contributors that, from clinical
experience, have proved to be valuable in acclimating
therapists to the acute care setting. Appendices provide
information to complement topics presented in the
chapters.
It is important to remember that all the information
presented in this book is intended to serve as a guide
to stimulate independent critical thinking within the
spectrum of medical-surgical techniques and trends.
ix
x PREFACE

Developing and maintaining a rapport with the information while reviewing charts, preparing for
medical-surgical team are highly recommended therapy intervention, and making clinical decisions in
because the open exchange of information among the acute care setting.
professionals is invaluable. We believe this new
edition of Acute Care Handbook for Physical Therapists can J.C.P.
enhance the clinical experience by providing valuable M.P.W.
 Acknowledgments
We offer sincere gratitude to the following
people:
Kathy Falk and Elsevier for their confidence in
creating a third edition of this book.
Megan Fennell for all of her patience, guidance, and
resourcefulness during the editorial process.
David Stein for his production assistance.
The contributorsçboth old and newçwe sincerely
appreciate your expertise and the time taken out of
your lives to work on this project.
The many patients and students, who have challenged
yet enriched our lives, both professionally and
personally.
Personal thanks from Jaime to the following:
Personal thanks from Michele to the following:
My husband, Jim, for bearing with me through
another edition of this book…I owe you one.
My family and friends, who offered encouragement
throughout the publishing process.
MissJess, Miss Nikki, and Miss Danielle for spending
many fun hours in our playroom with the girls.
The former Lahey Clinic Inpatient PT’s for providing
me with an opportunity to develop my orientation
and mentoring skills.
My new St. Joe’s colleagues, especially the Inpatient
PT/OTs, for your support and encouragement
through the completion of this manuscript.
My co-workers and patients, who inspire me to
become a better clinician.

The Physical Therapy Community in Bostonçover

the many years you have given me a wonderful
foundation to continue building upon.
Jessica Capurso, Ciara Kelliher, and Latanya Lemon
for your suggestions and contributions in developing
the practice patterns for each of the chapters.
Melanie Parker and Kimberly Nadeau for your expert
clinical reviews of Chapter 7.
The DPTclass of 2009 at NUPTçI will wear my Red
Sox jacket proudly and forever cherish myT-shirt.
The Physical Therapy Faculty at Northeastern
Universityçwhat a journey it’s been.
The Physical Therapy Faculty at Walsh Universityç
thanks for your warm welcome.

xi
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xii
 Contents
1 Cardiac System, 1 8 Gastrointestinal System, 297
Sean M. Collins, Konrad J. Dias Jaime C. Paz, David Nicoloro

1-A Description of ECG Characteristics and Associated

Causes, 38
1-B Common Rhythm Disturbances, 42
9 Genitourinary System, 327
Jaime C. Paz

2 Respiratory System, 47
Michele P. West, Jaime C. Paz, Kara O’Leary
10 Infectious Diseases, 353
Jaime C. Paz, V. Nicole Lombard, Rachael Maiocco

3 Musculoskeletal System, 87 10-A Disorders of Altered Immunity, 374

Michele P. West, James J. Gaydos, Marka Gehrig

3-A Management and Physical Therapy Interventions

11 Endocrine System, 377
for Fractures, 138 Jaime C. Paz
Michele P. West

4 Nervous System, 151

12 Organ Transplantation, 401
Jennifer Lee Hunt, Leah Moinzadeh
Michele P. West, Hillary A. Reinhold

APPENDICES
5 Oncology, 199
I-A The Medical Record, 427
Susan Polich, Jaime C. Paz
Michele P. West

6 Vascular System
I-B Acute Care Setting, 430
and Hematology, 219
Michele P. West
Michele P. West, Jaime C. Paz, Falguni Vashi

II Fluid and Electrolyte

7 Burns and Wounds, 263
Michele P. West, Kimberly Knowlton,
Imbalances, 437
Marie Jarell-Gracious, Jaime C. Paz Susan Polich, Jaime C. Paz

xiii
xiv CONTENTS

III-A Medical-Surgical Equipment VI Pain Management, 535

in the Acute Care Setting, 441 Jaime C. Paz
Eileen F. Lang, Michele P. West
VII Amputation, 543
III-B Mechanical Ventilation, 463 Jason D. Rand, Jaime C. Paz
Sean M. Collins, Jaime C. Paz
VIII Postural Drainage, 551
III-C Circulatory Assist Devices, 473 Michele P. West
Jackie A. Mulgrew
IX Functional Tests, 555
IV Pharmacologic Agents, 485 Jaime C. Paz, Jennifer A. Silva

Margarita V. DiVall
X Physical Therapy
V Anesthesia: Perioperative Considerations for Patients
and Postoperative Who Complain of Chest
Considerations, 531 Pain, 569
Michele P. West Michele P. West
 1 Cardiac System

Sean M. Collins INTRODUCTION

Konrad J. Dias Physical therapists in acute care facilities commonly encounter patients
with cardiac system dysfunction as either a primary morbidity or comor-
bidity. Recent estimates conclude that while the death rate associated
with cardiovascular disease has declined in recent years, the overall
burden of the disease remains high.1 Based on current estimates,
80,700,000 (one in three) Americans have one or more types of cardiovas-
cular disease (CVD).1 In 2005, CVD ranked first among all disease cate-
gories and accounted for 6,159,000 hospital discharges.1 In the acute care
setting, the role of the physical therapist with this diverse group of
patients remains founded in examination, evaluation, intervention, and
discharge planning, for the purpose of improving functional capacity
and minimizing disability. The physical therapist must be prepared
to safely accommodate for the effects of dynamic (pathologic,
physiologic, medical, and surgical intervention) changes into his or
her evaluation and plan of care.
The normal cardiovascular system provides the necessary pumping
force to circulate blood through the coronary, pulmonary, cerebral, and
systemic circulation. To perform work, such as during functional tasks,
energy demands of the body increase, therefore increasing the oxygen
demands of the heart. A variety of pathologic states can create impair-
ments in the cardiac system’s ability to successfully meet these demands,
ultimately leading to functional limitations. To fully address these func-
tional limitations, the physical therapist must understand normal
and abnormal cardiac function, clinical tests, and medical and surgical
management of the cardiovascular system.
The objectives of this chapter are to provide the following:
1. A brief overview of the structure and function of the cardiovascular
system
2. An overview of cardiac evaluation, including physical examination and
diagnostic testing
3. A description of cardiac diseases and disorders, including clinical find-
ings and medical and surgical management
4. A framework on which to base physical therapy evaluation and inter-
vention in patients with CVD
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:
 6A: Primary Prevention/Risk Reduction for Cardiovascular/Pulmonary
Disorders

1
2 CHAPTER 1 Cardiac System
 6B: Impaired Aerobic Capacity/Endurance
Associated with Deconditioning
 6D: Impaired Aerobic Capacity/Endurance
Associated with Cardiovascular Pump Dysfunction
or Failure
Please refer to the back cover of this book for a com-
plete list of preferred practice patterns, as individual
patient conditions are highly variable and other practice
patterns may be applicable.
STRUCTURE
The heart and the roots of the great vessels (Figure 1-1)
occupy the pericardium, which is located in
FIGURE 1-1
Anatomy of the right coronary artery and left coronary artery,
including left main, left anterior descending, and left
circumflex coronary arteries. (From Becker RC: Chest Pain:
The Most Common Complaints Series. Boston:
Butterworth-Heinemann, 2000.)
the mediastinum. The sternum, the costal cartilages,
and the medial ends of the third to fifth ribs on the
left side of the thorax create the anterior border of
the mediastinum. It is bordered inferiorly by the dia-
phragm, posteriorly by the vertebral column and ribs,
and laterally by the pleural cavity (which contains the
lungs). Specific cardiac structures and vessels and their
respective functions are outlined inTables 1-1 and 1-2.
Note: The mediastinum and the heart can be dis-
placed from their normal positions with changes in
the lungs secondary to various disorders. For example,
a tension pneumothorax will shift the mediastinum
away from the side of dysfunction (see Chapter 2 for
a further description of pneumothorax).
FUNCTION
The cardiovascular system must adjust the amount of
nutrient- and oxygen-rich blood pumped out of the
heart (cardiac output [CO]) to meet the wide spectrum
of daily energy (metabolic) demands of the body.
The heart’s ability to pump blood depends on the
following characteristics2:
 Automaticity:The ability to initiate its own electrical
impulse
 Excitability: The ability to respond to electrical
stimulus
 Conductivity: The ability to transmit electrical
impulse from cell to cell within the heart
 Contractility: The ability to stretch as a single unit
and then passively recoil while actively contracting
 Rhythmicity: The ability to repeat the cycle in
synchrony with regularity
Cardiac Cycle
Blood flow throughout the cardiac cycle depends on cir-
culatory and cardiac pressure gradients. The right side
of the heart is a low-pressure system with little vascular
resistance in the pulmonary arteries, whereas the left
side of the heart is a high-pressure system with high vas-
cular resistance from the systemic circulation. The car-
diac cycle is the period from the beginning of one
contraction, starting with sinoatrial (SA) node depolari-
zation, to the beginning of the next contraction.
Systole is the period of contraction, whereas diastole is
the period of relaxation. Systole and diastole can also be
categorized into atrial and ventricular components:
1. Atrial diastole is the period of atrial filling.The flow
of blood is directed by the higher pressure in the
venous circulatory system.
 Cardiac System CHAPTER 1 3

Table 1-1 PRIMARY STRUCTURES OF THE HEART

Structure Description Function
Pericardium Double-walled sac of elastic connective tissue, Protects against infection and trauma
a fibrous outer layer, and a serous inner layer
Epicardium Outermost layer of cardiac wall, covers surface Protects against infection and trauma
of heart and great vessels
Myocardium Central layer of thick muscular tissue Provides major pumping force of the ventricles
Endocardium Thin layer of endothelium and connective tissue Lines the inner surface of the heart, valves,
chordae tendineae, and papillary muscles
Right atrium Heart chamber Receives blood from the venous system and
is a primer pump for the right ventricle
Tricuspid valve Atrioventricular valve between right atrium Prevents backflow of blood from the right
and ventricle ventricle to the atrium during ventricular
systole
Right ventricle Heart chamber Pumps blood to the pulmonary circulation
Pulmonic valve Semilunar valve between right ventricle Prevents backflow of blood from the pulmonary
and pulmonary artery artery to the right ventricle during diastole
Left atrium Heart chamber Acts as a reservoir for blood and a primer pump
for the left ventricle
Mitral valve Atrioventricular valve between left atrium Prevents backflow of blood from the left
and ventricle ventricle to the atrium during ventricular
systole
Left ventricle Heart chamber Pumps blood to the systemic circulation
Aortic valve Semilunar valve between left ventricle and aorta Prevents backflow of blood from the aorta to
the left ventricle during ventricular diastole
Chordae Tendinous attachment of atrioventricular valve Prevents valves from everting into the atria
tendineae cusps to papillary muscles during ventricular systole
Papillary muscle Muscle that connects chordae tendineae to Constricts and pulls on chordae tendineae
floor of ventricle wall to prevent eversion of valve cusps during
ventricular systole

Table 1-2 GREAT VESSELS OF THE HEART AND THEIR FUNCTION

Structure Description Function
Aorta Primary artery from the left ventricle that Ascending aorta delivers blood to neck, head,
ascends and then descends after exiting and arms
the heart Descending aorta delivers blood to visceral
and lower body tissues
Superior vena cava Primary vein that drains into the right atrium Drains venous blood from head, neck, and
upper body
Inferior vena cava Primary vein that drains into the right atrium Drains venous blood from viscera and lower
body
Pulmonary artery Primary artery from the right ventricle Carries blood to lungs
4 CHAPTER 1 Cardiac System
2. Atrial systole is the period of atrial emptying and
contraction. Initial emptying of approximately 70%
of blood occurs as a result of the initial pressure gra-
dient between the atria and the ventricles. Atrial
contraction then follows, squeezing out the remain-
ing 30%.3 This is commonly referred to as the
atrial kick.
3. Ventricular diastole is the period of ventricular filling.
It initially occurs with ease; then, as the ventricle is
filled, atrial contraction is necessary to squeeze the
remaining blood volume into the ventricle. The
amount of stretch placed on the ventricular walls dur-
ing diastole, referred to as left ventricular end diastolic
pressure (LVEDP), influences the force of contrac-
tion during systole. (Refer to the Factors Affecting
Cardiac Output section for a description of preload.)
4. Ventricular systole is the period of ventricular con-
traction. The initial contraction is isovolumic
(meaning it does not eject blood), which generates
the pressure necessary to serve as the catalyst for
rapid ejection of ventricular blood.The left ventric-
ular ejection fraction (EF) represents the percent of
end diastolic volume ejected during systole and is
normally approximately 60%.2
Cardiac Output
Cardiac output (CO) is the quantity of blood pumped by
the heart in 1 minute. Regional demands for tissue per-
fusion (based on local metabolic needs) compete for
systemic circulation, and total CO adjusts to meet
these demands. Adjustment to CO occurs with changes
in heart rate (HRçchronotropic) or stroke volume
(SVçinotropic).3 Normal resting CO is approximately
4 to 8 liters per minute; with a resting HR of 70 beats
per minute [bpm], resting SV is approximately 71 ml/
beat).2 The maximum value of CO represents the func-
tional capacity of the circulatory system to meet the
demands of physical activity.
CO ðliters per minuteÞ ¼ HR ðbpmÞ  SV ðlitersÞ
CO can also be described relative to body mass as the
cardiac index (CI), the amount of blood pumped per
minute per square meter of body mass. Normal CI is
between 2.5 and 4.2 liters/min/m2. This wide normal
range makes it possible for cardiac output to decline
by almost 40% and still remain within the normal
limits. While there are several factors that interrupt a
direct correlation between CI and functional aerobic
capacity, a CI below 2.5 liters/min/m2 represents a
marked disturbance in cardiovascular performance
and is always clinically relevant.4
FACTORS AFFECTING CARDIAC OUTPUT
PRELOAD. Preload is the amount of tension on the
ventricular wall before it contracts. It is related to
venous return and affects SV by increasing left ventric-
ular end diastolic volume as well as pressure and there-
fore contraction.2 This relationship is explained by the
Frank-Starling mechanism and is demonstrated in
Figure 1-2.
FRANK-STARLING MECHANISM. The Frank-Starling
mechanism defines the normal relationship between the
length and tension of the myocardium.5 The greater
the stretch on the myocardium before systole (preload),
the stronger the ventricular contraction. The length-
tension relationship in skeletal muscle is based on the
response of individual muscle fibers; however, relation-
ships between cardiac muscle length and tension consist
of the whole heart. Therefore, length is considered in
terms of volume; tension is considered in terms of pres-
sure. A greater volume of blood returning to the heart
during diastole equates to greater pressures generated
initially by the heart’s contractile elements. Ultimately
facilitated by elastic recoil, a greater volume of blood
is ejected during systole. The effectiveness of this
mechanism can be reduced in pathologic situations.3
Afterload
Afterload is the force against which a muscle must con-
tract to initiate shortening.5 Within the ventricular
wall, this is equal to the tension developed across its
wall during systole. The most prominent force contri-
buting to afterload in the heart is blood pressure (BP),
specifically vascular compliance and resistance. BP
affects aortic valve opening and is the most obvious
load encountered by the ejecting ventricle. An example
of afterload is the amount of pressure in the aorta at
the time of ventricular systole.2
Cardiac Conduction System
A schematic of the cardiac conduction system and a
normal electrocardiogram (ECG) are presented in
Figure 1-3. Normal conduction begins in the SA node
and travels throughout the atrial myocardium (atrial
depolarization) via intranodal pathways to the atrioven-
tricular (AV) node, where it is delayed momentarily.
It then travels to the bundle of His, to the bundle
branches, to the Purkinje fibers, and finally to the
myocardium, resulting in ventricular contraction.6
Disturbances in conduction can decrease CO (refer to
the Pathophysiology section for a discussion of
rhythm and conduction disturbances).7

FIGURE 1-2
Factors affecting left ventricular function. (Adapted from Braunwal E, RossJ, Sonnenblick E, et al.
Mechanisms of Contraction of the Normal and Failing Heart [2nd ed]. Boston: Little, Brown, 1976.)
FIGURE 1-3
Schematic representation of the sequence of excitation in the
heart. (From Walsh M, Crumbie A, Reveley S. Nurse
Practitioners: Clinical Skills and Professional Issues.
Boston: Butterworth-Heinemann, 1999.)
Cardiac System CHAPTER 1 5
Neural Input
The SA node has its own inherent rate. Neural input can,
however, influence HR, heart rate variability (HRV), and
contractility through the autonomic nervous system.2,8
Parasympathetic system (vagal) neural input gener-
ally decelerates cardiac function, thus decreasing HR
and contractility. Parasympathetic input travels through
the vagus nerves. The right vagus nerve primarily sti-
mulates the SA node and affects rate, whereas the left
vagus nerve primarily stimulates the AV node and
affects AVconduction.2,8
Sympathetic system neural input is through the
thoracolumbar sympathetic system and serves to
increase HR and augment ventricular contractility,
thus accelerating cardiac function.2
Endocrine Input
In response to physical activity or stress, a release in
catecholamines increases HR, contractility, and periph-
eral vascular resistance for a net effect of increased car-
diac function.2 Refer toTable 1-3 for the cardiac effects
of hormones.
6 CHAPTER 1 Cardiac System

Table 1-3 CARDIAC EFFECTS OF HORMONES

Hormone Primary Site Stimulus Cardiac Effect
Norepinephrine Adrenal medulla Stress/exercise Vasoconstriction
Epinephrine Adrenal medulla Stress/exercise Coronary artery vasodilation
Angiotensin Kidney Decreased arterial pressure Vasoconstriction, increased
blood volume
Vasopressin Posterior pituitary Decreased arterial pressure Potent vasoconstrictor
Bradykinin Formed by polypeptides in Tissue damage/inflammation Vasodilation, increased
blood when activated capillary permeability
Histamine Throughout tissues of body Tissue damage Vasodilation, increased
capillary permeability
Atrial natriuretic Atria of heart Increased atrial stretch Decreased blood volume
peptides
Aldosterone Adrenal cortex Angiotensin II (stimulated) Increased blood volume,
by hypovolemia or kidneys excrete more
decreased renal perfusion potassium
Data from Guyton AC, HallJE.Textbook of Medical Physiology (9th ed). Philadelphia: Saunders, 1996.

Local Input
Tissue pH, concentration of carbon dioxide (CO2), con-
centration of oxygen (O2), and metabolic products
(e.g., lactic acid) can affect vascular tone.2 During exer-
cise, increased levels of CO2, decreased levels of O2,
decreased pH, and increased levels of lactic acid at the
tissue level dilate local blood vessels and therefore
increase CO distribution to that area.
Cardiac Reflexes
Cardiac reflexes influence HR and contractility and can
be divided into three general categories: baroreflex
(pressure), Bainbridge reflex (stretch), and chemoreflex
(chemical reflex).
Baroreflexes are activated through a group of
mechanoreceptors located in the heart, great vessels,
and intrathoracic and cervical blood vessels. These
mechanoreceptors are most plentiful in the walls of
the internal carotid arteries.2 Mechanoreceptors are
sensory receptors that are sensitive to mechanical
changes, such as pressure and stretch. Activation of the
mechanoreceptors by high pressures results in an inhi-
bition of the vasomotor center of the medulla that
increases vagal stimulation. This chain of events is
known as the baroreflex and results in vasodilation,
decreased HR, and decreased contractility.
Mechanoreceptors located in the right atrial myo-
cardium respond to stretch. With an increased volume
in the right atrium, there is an increase in pressure on
the atrial wall. This reflex, known as the Bainbridge
reflex, stimulates the vasomotor center of the medulla,
which in turn increases sympathetic input and
increases HR and contractility.2 Respiratory sinus
arrhythmia, an increased HR during inspiration and
decreased HR during expiration, may be facilitated
by changes in venous return and SVcaused by changes
in thoracic pressure induced by the respiratory cycle.
At the beginning of inspiration, when thoracic
pressure is decreased, venous return is greater, and
therefore there is a greater stretch on the atrial wall.9
Chemoreceptors located on the carotid and aortic
bodies have a primary effect on increasing rate and
depth of ventilation in response to CO2 levels, but they
also have a cardiac effect. Changes in CO2 during the
respiratory cycle may also result in sinus arrhythmia.2
Coronary Perfusion
For a review of the major coronary arteries, refer to
Figure 1-1. Blood is pumped to the large superficial cor-
onary arteries during ventricular systole. At this time,
myocardial contraction limits the flow of blood to the
myocardium; therefore, myocardial tissue is perfused
during diastole.
Systemic Circulation
For a review of the distribution of systemic circulation,
refer to Figure 1-4. Systemic circulation is affected
by total peripheral resistance (TPR), which is the
 Cardiac System CHAPTER 1 7

Systemic CO2 O2
capillaries
Circulation to
tissues of head
and upper body

Lung
Lung

CO2
CO2
O2
O2

Pulmonary
capillaries

Pulmonary circulation

CO2 O2

Circulation to
tissues of
lower body

Systemic circulation
FIGURE 1-4
Schematic of systemic circulation. (FromThibodeau GA: Structure & Function of the Body [13th ed].
St Louis: Mosby, 2007.)

resistance to blood flow by the force created by the
aorta and arterial system.Two factors that contribute to
resistance are (1) vasomotor tone, in which vessels
dilate and constrict, and (2) blood viscosity, in which
greater pressure is required to propel thicker blood.
Also called systemic vascular resistance, TPR and CO
influence BP.2 This relationship is illustrated in the
following equation:
BP ¼ CO  TPR
CARDIAC EVALUATION
Cardiac evaluation consists of patient history, physical
examination (which consists of observation, palpation,
BP measurement, and heart sound auscultation),
laboratory tests, and diagnostic procedures.
Patient History
In addition to the general chart review presented in
Appendix I-A, the following pertinent information
about patients with cardiac dysfunction should be
obtained before physical examination3,10-12:
 Presence of chest pain (see Appendix X for an
expanded description of characteristics and etiology
of chest pain)
 Location and radiation
 Character and quality (crushing, burning, numb-
ing, hot), and frequency
 Angina equivalents (what the patient feels
as angina [e.g., jaw pain, shortness of
breath, dizziness, lightheadedness, diaph-
oresis, burping, nausea, or any combination of
these])
 Aggravating and alleviating factors
 Precipitating factors
 Medical treatment sought and its outcome
 Presence of palpitations
 Presence of cardiac risk factors (Table 1-4)
 Family history of cardiac disease
 History of dizziness or syncope
 Previous myocardial infarction (MI), cardiac studies,
or procedures
8 CHAPTER 1 Cardiac System

Table 1-4 CARDIAC RISK FACTORS — PRIMARY AND SECONDARY PREVENTION

Major Independent Risk Factors Predisposing Risk Factors Conditional Risk Factors
Smoking Physical inactivity Elevated triglycerides
Hypertension Obesity Small LDL particles
Elevated serum cholesterol, Body mass index >30 kg/m2 Elevated homocysteine
total (and LDL) Abdominal obesity (waist-hip ratio) Elevated lipoprotein (a)
Decreased high-density Men > 40 in. Elevated inflammatory markers
lipoprotein cholesterol Women > 35 in. C-reactive protein
Diabetes mellitus Family history of premature heart disease Fibrinogen
Advancing age Psychosocial factors
Job strain
Ethnic characteristics
LDL, Low-density lipoprotein.
Data from Grundy SM, Pasternak R, Greenland P, et al. Assessment of Cardiovascular Risk by Use of Multiple-Risk-Factor Assessment
Equations: A Statement for Healthcare Professionals from the American Heart Association and the American College of Cardiology.
Circulation 1999;100:1481-1492; and Belkic KL, Landsbergis PA, et al. IsJob Strain a Major Source of Cardiovascular Disease Risk?
Scand J Work Environ Health 2004;30(2):85-128.

above the sternum. Pulsations higher than this

CLINICAL TIP
 When discussing angina with a patient, use the patient’s
terminology. If the patient describes the angina as
‘‘crushing’’ pain, ask the patient if he or she experiences
the crushing feeling during treatment as opposed to
asking the patient if he or she has chest pain.
 The common medical record abbreviation for chest pain
is CP.
Physical Examination
OBSERVATION
Key components of the observation portion of the
physical examination include3,7:
1. Facial color, skin color and tone, or the presence of
diaphoresis
2. Obvious signs of edema in the extremities
3. Respiratory rate
4. Signs of trauma (e.g., paddle burns or ecchymosis
from cardiopulmonary resuscitation)
5. Presence of jugular venous distention, which results
from the backup of fluid into the venous system
from right-sided congestive heart failure (CHF)
(Figure 1-5)
a. Make sure the patient is in a semirecumbent posi-
tion (45 degrees).
b. Have the patient turn his or her head away from
the side being evaluated.
c. Observe pulsations in the internal jugular neck
region. Pulsations are normally seen 3 to 5 cm
or absent pulsations indicate jugular venous
distention.
PALPATION
Palpation is the second component of the physical
examination and is used to evaluate and identify the
following:
 Pulses for circulation quality, HR, and rhythm
(Table 1-5, Figure 1-6)
 Extremities for pitting edema bilaterally (Table 1-6)
CLINICAL TIP
 When palpating HR, counting pulses for 15 seconds
and multiplying by 4 is sufficient with normal rates
and rhythms. If rates are faster than 100 bpm
or slower than 60 bpm, palpate the pulse for
60 seconds. If the rhythm is irregularly irregular
(e.g., during atrial fibrillation) or regularly irregular
(e.g., premature ventricular contractions [PVCs]),
perform auscultation of heart sounds to identify the
apical HR for a full minute.
 In these cases, palpation of pulse cannot substitute for
ECG analysis to monitor the patient’s rhythm, but it may
alert the therapist to the onset of these abnormalities.
 Use caution in palpating pulses, as manual pressure
on the carotid sinus may cause reflexive drops
in HR, BP, or both.
 Cardiac System CHAPTER 1 9

FIGURE 1-5
Measurement of jugular venous distention (JVP).TheJVP reading is the maximum height, in
centimeters, above the sternal angle at which venous pulsations are visible. (Modified fromThompsonJM,
McFarland GK, HirschJE, et al. Mosby’s Clinical Nursing [5th ed]. St. Louis: Mosby, 2002.)

BLOOD PRESSURE
BP measurement with a sphygmomanometer (cuff) and
auscultation is an indirect, noninvasive measurement
of the force exerted against the arterial walls during
ventricular systole (systolic blood pressure [SBP]) and
during ventricular diastole (diastolic blood pressure).
BP is affected by peripheral vascular resistance
(blood volume and elasticity of arterial walls) and CO.
Table 1-7 lists normal BP ranges. Occasionally, BP
measurements can only be performed on certain limbs
secondary to the presence of conditions such as a

Table 1-5 PULSE AMPLITUDE CLASSIFICATION AND PULSE ABNORMALITIES

Pulse Amplitude Classification
Scale Degree Description
0 Absent pulse No pulseçno circulation
1+ Diminished pulse Reduced stroke volume and ejection fraction,
increased vascular resistance
2+ Normal pulse Normal resting conditions, no pathologies
3+ Moderately increased Slightly increased stroke volume and ejection
fraction
4+ Markedly increased (bounding)* Increased stroke volume and ejection fraction, can
be diminished with vasoconstriction

Pulse Abnormalities
Abnormality Palpation Description
Pulsus alternans Regular rhythm with strong pulse waves Indicates left ventricular failure when present
alternating with weak pulse waves at normal heart rates
Bigeminal pulses Every other pulse is weak and early Due to preventricular contractions (bigeminy)
Pulsus paradoxus Reduction in strength of the pulse with May be caused by chronic obstructive lung disease,
an abnormal decline in blood pressure pericarditis, pulmonary emboli, restrictive
during inspiration cardiomyopathy, and cardiogenic shock
*Corrigan’s pulse is a bounding pulse visible in the carotid artery that occurs with aortic regurgitation.
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S (eds). Cardiac Nursing (4th ed). Philadelphia: Lippincott, 2000.
10 CHAPTER 1 Cardiac System

Table 1-7 NORMAL BLOOD PRESSURE RANGES

Temporal
pulse Systolic Diastolic
Carotid pulse Age 8 years 85-114 mm Hg 52-85 mm Hg
Age 12 years 95-135 mm Hg 58-88 mm Hg
Apical Adult <120 mm Hg <80 mm Hg
pulse Prehypertension 120-139 mm Hg 80-89 mm Hg
Hypertension
Brachial Stage 1 140-159 mm Hg 90-99 mm Hg
pulse Stage 2 160 mm Hg 100 mm Hg
Normal exercise Increases 5-12 10 mm Hg
Radial
mm Hg per MET
pulse increase in
workload
Data from Chobanian AV, Bakris GL, et al. Seventh Report of the
Femoral Joint National Committee on Prevention, Detection, Evaluation,
pulse and Treatment of High Blood Pressure. Hypertension
2003;42(6):1206-1252; and American College of Sports Medicine,
Popliteal Armstrong LE, et al. ACSM’s Guidelines for ExerciseTesting and
pulse Prescription, Philadelphia: Lippincott Williams & Wilkins, 2005.

Posterior
tibial pulse
percutaneous inserted central catheter, arteriovenous
Pedal pulse fistula for hemodialysis, blood clots, scarring from
(dorsalis pulse)
brachial artery cutdowns, or lymphedema (e.g., status
FIGURE 1-6
post mastectomy). BP of the upper extremity should
Arterial pulses. (From Pierson FM: Principles & Techniques
of Patient Care [4th ed]. St Louis: Saunders, 2007.) be measured in the following manner:
1. Check for posted signs, if any, at the bedside that
indicate which arm should be used in taking BP.
BP variations of 5 to 10 mm Hg between the right
and left upper extremity are considered normal.
Patients with arterial compression or obstruction
may have differences of more than 10 to 15 mm Hg.12
2. Use a properly fitting cuff. The inflatable bladder
should have a width of approximately 40%, and
length of approximately 80% of the upper arm
Table 1-6 PITTING EDEMA SCALE circumference.13
Scale Degree Description
3. Position the cuff 2.5 cm above the antecubital crease.
4. Rest the arm at the level of the heart.
1+ Trace Slight Barely perceptible 5. To determine how high to inflate the cuff, palpate
depression
2+ Mild 0-0.6 cm Easily identified
the radial pulse, inflate until no longer palpable,
depression (EID) and note the cuff inflation value. Deflate the cuff.
(skin rebounds Note:With a patient who is in circulatory shock, aus-
in <15 sec) cultation may be too difficult. In these cases, this
3+ Moderate 0.6-1.3 cm EID (rebound 15-30 sec) method can be used to measure the SBP and is
4+ Severe 1.3-2.5 cm EID (rebound > 30 sec) recorded as systolic BP/P (i.e.,‘‘BP is 90 over palp’’).13
6. Place the bell of the stethoscope gently over the
Data from Woods SL, Sivarajian Froelicher ES, Underhill-Motzer S
(eds). Cardiac Nursing (4th ed). Philadelphia: Lippincott, 2000; and
brachial artery.
Hillegass EA, Sadowsky HS (eds). Essentials of Cardiopulmonary 7. Reinflate the cuff to 30 to 40 mm Hg greater than the
Physical Therapy (2nd ed). Philadelphia: Saunders, 2001. value in step 5. Then slowly deflate the cuff. Cuff

deflation should occur at approximately 2 to 3 mm
Hg per second.13
8. Listen for the onset of tapping sounds, which repre-
sents blood flow returning to the brachial artery.
This is the systolic pressure.
9. As the pressure approaches diastolic pressure, the
sounds will become muffled and in 5 to 10 mm Hg
will be completely absent.These sounds are referred
to as Korotkoffsounds (Table 1-8).12,13
CLINICAL TIP
 Recording preexertion, paraexertion, and postexertion
BP is important in identifying BP responses to
activity. During recovery from exercise, blood vessels
dilate to allow for greater blood flow to muscles.
In cardiac-compromised or very deconditioned
individuals, total CO may be unable to support this
increased flow to the muscles and may lead to
decreased output to vital areas, such as the brain.
 If unable to obtain BP on the arm, the thigh
is an appropriate alternative, with auscultation
at the popliteal artery.
 Falsely high readings will occur if the cuff is too
small or applied loosely, or if the brachial artery
is lower than the heart level.
 Evaluation of BP and HR in different postures can
be used to monitor orthostatic hypotension with
repeat measurements on the same arm 1 to
5 minutes after position changes. The symbols
that represent patient position are shown in
Figure 1-7.
Cardiac System CHAPTER 1 11
 The same extremity should be used when serial
BP recordings will be compared for an evaluation of
hemodynamic response.
 A BP record is kept on the patient’s vital sign flow
sheet. This is a good place to check for BP trends
throughout the day and, depending on your
hospital’s policy, to document BP changes during
the therapy session.
 An auscultatory gap is the disappearance of sounds
between phase 1 and phase 2 and is common
in patients with high BP, venous distention,
and severe aortic stenosis. Its presence can create
falsely low systolic pressures if the cuff is not
inflated high enough (which can be prevented by
palpating for the disappearance of the pulse prior to
measurement), or falsely high diastolic pressures if
the therapist stops measurement during the gap
(prevented by listening for the phase 3 to phase
5 transitions).13
AUSCULTATION
Evaluation of heart sounds can yield information
about the patient’s condition and tolerance to medical
treatment and physical therapy through the evaluation
of valvular function, rate, rhythm, valvular compli-
ance, and ventricular compliance.3 To listen to heart
sounds, a stethoscope with both a bell and a diaphragm
is necessary. For a review of normal and abnormal
heart sounds, refer to Table 1-9. The examination
should follow a systematic pattern using both the bell

Table 1-8 KOROTKOFF SOUNDS

Phase Sound Indicates

1 First sound heard, faint tapping Systolic pressure (blood starts to flow through compressed artery).
sound with increasing intensity
2 Start swishing sound Because of the compressed artery, blood flow continues to be heard while
the sounds change due to the changing compression on the artery.
3 Sounds increase in intensity with Blood flow is increasing as artery compression is decreasing.
a distinct tapping
4 Sounds become muffled Diastolic pressure in children < 13 years of age and in adults who are
exercising, pregnant, or hyperthyroid (see phase 5).
5 Disappearance Diastolic pressure in adultsçoccurs 5-10 mm Hg below phase 4 in normal
adults. In states of increased rate of blood flow, it may be > 10 mm Hg
below phase 4. In these cases, the phase 4 sound should be used as
diastolic pressure in adults.
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer, S (eds). Cardiac Nursing (4th ed). Philadelphia: Lippincott, 2000; and
Bickley LS, Szilagyi PG. Bates’ Guide to Physical Examination and History Taking. Philadelphia: Lippincott Williams & Wilkins, 2003.
12 CHAPTER 1 Cardiac System

 Avoid auscultation of heart sounds over clothing

FIGURE 1-7
Orthostatic blood pressure symbols.
(for low-pitched sounds) and diaphragm (for high-
pitched sounds) and should cover all auscultatory
areas, as illustrated in Figure 1-8. Abnormal sounds
should be noted with a description of the conditions
in which they were heard (e.g., after exercise or during
exercise).
CLINICAL TIP
 Always ensure proper function of a stethoscope
by tapping the diaphragm before applying
the stethoscope to the patient.
 Avoid rubbing the stethoscope on extraneous objects
because it can add noise and detract from true
examination.
because it muffles the intensity of both normal and
abnormal sounds.
 If the patient has an irregular cardiac
rhythm, determine HR through auscultation
(apical HR). To save time, this can be done
during a routine auscultatory examination
with the stethoscope’s bell or diaphragm in
any location.
 Heart sounds can be heard online at
the Auscultation Assistant, available at:
http://www.med.ucla.edu/wilkes/intro.html.
Diagnostic and Laboratory Measures
The diagnostic and laboratory measures discussed in
this section provide information that is used to deter-
mine medical diagnosis, guide interventions, and
assist with determining prognosis. The clinical rele-
vance of each test in serving this purpose varies
according to the pathology. This section is organized
across a spectrum of least invasive to most invasive
measures. When appropriate, the test results most
pertinent to the physical therapist are highlighted.
Information that bears a direct impact on physical
therapy clinical decision making usually includes that
which helps the therapist identify indications for

Table 1-9 NORMAL AND ABNORMAL HEART SOUNDS

Sound Location Description
S1 (normal) All areas First heart sound; signifies closure of atrioventricular valves and corresponds
to onset of ventricular systole.
S2 (normal) All areas Second heart sound; signifies closure of semilunar valves and corresponds
with onset of ventricular diastole.
S3 (abnormal) Best appreciated Immediately following S2; occurs early in diastole and represents filling of the
at apex ventricle. In young healthy individuals, it is considered normal and called
a physiologic third sound. In the presence of heart disease, it results from
decreased ventricular compliance (a classic sign of congestive heart failure).
S4 (abnormal) Best appreciated Immediately preceding S1; occurs late in ventricular diastole; associated with
at apex increased resistance to ventricular filling; common in patients with
hypertensive heart disease, coronary heart disease, pulmonary disease,
or myocardial infarction, or following coronary artery bypass grafts.
Murmur Over respective Indicates regurgitation of blood through valves; can also be classified as
(abnormal) valves systolic or diastolic murmurs. Common pathologies resulting in murmurs
include mitral regurgitation and aortic stenosis.
Pericardial Third or fourth Sign of pericardial inflammation (pericarditis), associated with each beat
friction rub intercostal space, of the heart; sounds like a creak or leather being rubbed together.
(abnormal) anterior axillary line
Data from Bickley LS, Szilagyi PG. Bates’Guide to Physical Examination and HistoryTaking. Philadelphia: LippincottWilliams & Wilkins, 2003.

FIGURE 1-8
Areas for heart sound auscultation. (Courtesy Barbara Cocanour, Ph.D., University of Massachusetts,
Lowell, Department of Physical Therapy.)
intervention, relative or absolute contraindications for
intervention, possible complications during activity
progression, and indicators of performance.
OXIMETRY
Oximetry (SaO2) is used to indirectly evaluate the
oxygenation of a patient and can be used to titrate
supplemental oxygen. Refer to Chapter 2 for a further
description of oximetry.
ELECTROCARDIOGRAM
An ECG provides a graphic analysis of the heart’s elec-
trical activity. The ECG is commonly used to detect
arrhythmias, heart blocks, and myocardial perfusion.
It can also detect atrial or ventricular enlargement.
An ECG used for continuous monitoring of patients
in the hospital typically involves a 3- to 5-lead system.
A lead represents a particular portion or ‘‘view’’ of the
heart. The patient’s rhythm is usually displayed in his
or her room, in the hall, and at the nurses’ station.
Diagnostic ECG involves a 12-lead analysis, the
description of which is beyond the scope of this book.
For a review of basic ECG rate and rhythm analysis,
refer toTable 1-10 and Figure 1-3.
HOLTER MONITORING. Holter monitoring is 24-
or 48-hour ECG analysis. This is performed to detect
cardiac arrhythmias and corresponding symptoms
during a patient’s daily activity.12 Holter monitoring
is different from telemetric monitoring because the
Cardiac System CHAPTER 1 13
ECG signal is recorded on a tape, and the subsequent
analysis follows from the recording.
Indications for Holter monitoring include the
evaluation of syncope, dizziness, shortness of breath
with no other obvious cause, palpitations, antiarrhyth-
mia therapy, pacemaker functioning, activity-induced
silent ischemia, and risk of cardiac complications with
the use of HRV.
HEART RATE VARIABILITY. The most common
measure of HRV is the standard deviation of all HR
intervals during a 24-hour period (SDNN).8 Evidence
continues to grow regarding the clinical utility of
HRV for cardiology.14 HRVand subsequently SDNN is
generally measured with a Holter monitor and has
been used in clinical studies to test a variety of health
outcomes.8,15,16 In healthy populations, low HRV has
been shown to be a risk factor for all causes of cardiac
mortality,17-19 as well as new onset of hypertension.20
Low HRV is also a risk for mortality in patients who
have had an MI,21-23 have coronary artery disease,24 or
have CHF.25 A classic study performed by Kleiger and
colleagues26 demonstrated a fivefold risk of reinfarction
in post MI patients with an SDNN (in milliseconds)
of less than 50, when compared to patients with an
SDNN of greater than 100.26
TELEMETRIC ELECTROCARDIOGRAM MONITORING.
Telemetric ECG monitoring provides real-time ECG
visualization via radiofrequency transmission of the
ECG signal to a monitor. Telemetry has the benefit of
14 CHAPTER 1 Cardiac System

Table 1-10 ELECTROCARDIOGRAPH INTERPRETATION

Duration
Wave/Segment (seconds) Amplitude (mm) Indicates
P wave < 0.10 1-3 Atrial depolarization
PR interval 0.12-0.20 Isoelectric line Elapsed time between atrial depolarization and
ventricular depolarization
QRS complex 0.06-0.10 25-30 Ventricular depolarization and atrial repolarization
(maximum)
ST segment 0.12 —1=2 to +1 Elapsed time between end of ventricular
depolarization and beginning of repolarization
QT interval 0.42-0.47 Varies Elapsed time between beginning of ventricular
(QTc) repolarization and end of repolarization
(QTc is corrected for heart rate)
T wave 0.16 5-10 Ventricular repolarization
Data from RS Meyers (ed). Saunders Manual of Physical Therapy Practice. Philadelphia: Saunders, 1995; Aehlert B (ed). ACLS Quick Review
Study Guide. St. Louis: Mosby, 1994; and Davis D (ed). How to Quickly and Accurately Master ECG Interpretation (2nd ed). Philadelphia:
Lippincott Williams & Wilkins, 1992.

Holter monitoring (because there is no hardwire con-
nection of the patient to the visual display unit) as well
as the benefit of the standard ECG monitor attachment,
because there is a real-time graphic display of the ECG
signal.
CLINICAL TIP
 Some hospitals use an activity log with Holter
monitoring. If so, be sure to document physical
therapy intervention on the log. If there is no log
available, be sure to document time of day and
intervention during physical therapy in the medical
record.
COMPLETE BLOOD CELL COUNT
Relevant values from the complete blood cell count are
hematocrit, hemoglobin, and white blood cell counts.
Hematocrit refers to the number of red blood cells per
100 ml of blood and therefore fluctuates with changes
not only in the total red blood cell count (hemoglobin)
but also with blood volume. Elevated levels of hemato-
crit (which may be related to dehydration) indicate
increased viscosity of blood that can potentially
impede blood flow to tissues.12 Hemoglobin is essential
for the adequate oxygen-carrying capacity of the
blood. A decrease in hemoglobin and hematocrit
levels (10% below normal is called anemia) may
decrease activity tolerance or make patients more
susceptible to ischemia secondary to decreased
oxygen-carrying capacity.11,27 Slight decreases in hemat-
ocrit due to adaptations to exercise (with no change in
hemoglobin) are related to increases in blood volume.
The concomitant exercise-related decreases in blood
viscosity may be beneficial to post MI patients.28
Elevated white blood cell counts can indicate that
the body is fighting infection, or they can occur with
inflammation caused by cell death, such as in MI.
Erythrocyte sedimentation rate (ESR), another hema-
tologic test, is a nonspecific index of inflammation
and is commonly elevated for 2 to 3 weeks after MI.27
Refer to Chapter 6 for more information about these
values.
COAGULATION PROFILES
Coagulation profiles provide information about the
clotting time of blood. Patients who undergo treatment
with thrombolytic therapy after the initial stages of MI
or who are receiving anticoagulant therapy owing to
various cardiac arrhythmias require coagulation pro-
files to monitor anticoagulation in an attempt to pre-
vent complications, such as bleeding. The physician
determines the patient’s therapeutic range of anti-
coagulation by using the prothrombin time (PT),
partial thromboplastin time, and international normal-
ized ratio.27 Refer to Chapter 6 for details regarding
these values and their significance to treatment.
Patients with low PT and partial thromboplastin
time are at higher risk of thrombosis, especially if they

have arrhythmias (e.g., atrial fibrillation) or valvular
conditions (mitral regurgitation) that produce stasis of
the blood. Patients with a PTgreater than 2.5 times the
reference range should not undergo physical therapy
because of the potential for spontaneous bleeding.
Likewise, an international normalized ratio of more
than 3 warrants asking the physician if treatment
should be withheld.27
BLOOD LIPIDS
Elevated total cholesterol levels in the blood are a sig-
nificant risk factor for atherosclerosis and therefore
ischemic heart disease.29 Measuring blood cholesterol
level is necessary to determine the risk for development
of atherosclerosis and to assist in patient education,
dietary modification, and medical management.
Normal values can be adjusted for age; however, levels
of more than 240 mg/dl are generally considered
high, and levels of less than 200 mg/dl are considered
normal.
A blood lipid analysis categorizes cholesterol into
high-density lipoproteins (HDLs) and low-density
lipoproteins (LDLs) and provides an analysis of
triglycerides.
HDLs are formed by the liver and are considered
beneficial because they are readily transportable and
do not adhere to the intimal walls of the vascular
system. People with higher amounts of HDLs are at
lower risk for coronary artery disease.27,29 HDL levels
of less than 33 mg/dl carry an elevated risk of heart dis-
ease, and a more important risk for heart disease is an
elevated ratio of total cholesterol to HDL. Normal
total cholesterol to HDL ratios range from 3 to 5.12
LDLs are formed by a diet excessive in fat and are
related to a higher incidence of coronary artery disease.
Low-density lipoproteins are not as readily transporta-
ble, because they adhere to intimal walls in the vascular
system.27 Normal LDLs are below 100 mg/dl.12
Triglycerides are fat cells that are free floating in the
blood. When not in use, they are stored in adipose
tissue.Their levels increase after eating foods high in fat
and decrease with exercise. High levels of triglycerides
are associated with a risk of coronary heart disease.27
CLINICAL TIP
 Cholesterol levels may be falsely elevated after an
acute MI; therefore, preinfarction levels (if known)
are used to guide risk factor modification. Values
will not return to normal until at least 6 weeks
post MI.
Cardiac System CHAPTER 1 15
C-REACTIVE PROTEIN
C-reactive protein is a test that measures the amount
of a protein in the blood that signals acute inflam-
mation. To determine a person’s risk for heart disease,
a more sensitive CRP test called a high-sensitivity C-reactive
protein (hs-CRP) assay is available. A growing number
of studies have determined that high levels of hs-CRP
consistently predict recurrent coronary events in
patients with unstable angina and acute myocardial
infarction. In addition, elevated hs-CRP levels are
associated with lower survival rates in these patients
with cardiovascular disease.30-32
 hs-CRP lower than 1.0 mg/L indicates a low risk
of developing cardiovascular disease.
 hs-CRP between 1.0 and 3.0 mg/L indicates an
average risk of developing cardiovascular disease.
 hs-CRP higher than 3.0 mg/L indicates a high risk
of developing cardiovascular disease.
BIOCHEMICAL MARKERS
After an initial myocardial insult, the presence of tissue
necrosis can be determined by increased levels of bio-
chemical markers. Levels of biochemical markers, such
as serum enzymes (creatine kinase [CK]) and proteins
(Troponin I and T), can also be used to determine the
extent of myocardial death and the effectiveness of
reperfusion therapy. In patients presenting with specific
anginal symptoms and diagnostic ECG, these bio-
chemical markers assist with confirmation of the diag-
nosis of an MI (Table 1-11). Enzymes play a more
essential role in medical assessment of many patients
with nonspecific or vague symptoms and inconclusive
ECG changes.33 Such analysis also includes evaluation
of isoenzyme levels.34 Isoenzymes are differentchemical
forms of the same enzyme that are tissue specific and
allow differentiation of damaged tissue (e.g., skeletal
muscle vs. cardiac muscle).
CK (formally called creatine phosphokinase) is released
after cell injury or cell death. CK has 3 isoenzymes.
The CK-MB isoenzyme is related to cardiac muscle
cell injury or death. The most widely used value is the
relative index (100% [CK-MB/Total CK]).33 Temporal
measurements of the CK-MB relative index help physi-
cians diagnose MI, estimate the size of infarction, eval-
uate the occurrence of reperfusion, as well as possible
infarct extension. An early CK-MB peak with rapid
clearance is a good indication of reperfusion.12 Values
may increase from skeletal muscle trauma, cardiopul-
monary resuscitation, defibrillation, and open-heart
surgery. Postoperative coronary artery bypass surgery
16 CHAPTER 1 Cardiac System
Table 1-11 BIOCHEMICAL MARKERS
Normal
Enzyme or Marker Isoenzyme Value
Creatine kinase (CK) 55-71 IU
CK-MB 0-3%
TroponinT (cTnT) ç < 0.2 pg/liter
Troponin I (cTnI) ç < 3.1 pg/liter
Data from Christenson RH, Azzazy HME. Biochemical Markers of the Acute Coronary Syndromes. Clin Chem 1998;44:1855-1864; and Kratz
AK, Leqand-Rowski KB. Normal reference laboratory values. N EnglJ Med 1998;339:1063-1072.
tends to elevate CK-MB levels secondary to cross-clamp
time. Early postoperative peaks and rapid clearance
seem to indicate reversible damage, whereas later
peaks and longer clearance times with peak values
exceeding 50 U/liter may indicate an MI.12 Treatment
with thrombolytic therapy, such as streptokinase or a
tissue plasminogen activator (tPa), has been shown to
falsely elevate the values and may create a second peak
of CK-MB, which strongly suggests successful
reperfusion.12,33
Troponins are essential contractile proteins found in
both skeletal and cardiac muscle. Troponin I is an iso-
type found exclusively in the myocardium and is there-
fore 100% cardiac specific. Troponin T is another
isotype, and although it is sensitive to cardiac damage,
it also rises with muscle and renal failure.33 These mar-
kers have emerged as sensitive and cardiac-specific
clinical indicators for diagnosis of MI and for risk
stratification.
CLINICAL TIP
 Physical therapy geared toward testing functional
capacity or increasing the patient’s activity should be
withheld until cardiac enzymes levels have peaked
and begun to fall.
 It is best to await the final diagnosis of location,
size, and type of MI before active physical therapy
treatment. This allows for rest and time for the
control of possible post MI complications.
NATRIURETIC PEPTIDES
Three natriuretic peptides have been identified in
humans. These include atrial natriuretic peptide (ANP),
brain natriuretic peptide (BNP), and C-natriuretic pep-
tide(CNP).4 ANPisstored intherightatriumandreleased
in response to increased atrial pressures. BNP is stored
Onset of Rise Time of Peak Return to
(hours) Rise Normal
3-6 12-24 hours 24-48 hours
4-8 18-24 hours 72 hours
2-4 24-36 hours 10-14 days
2-4 24-36 hours 10-14 days
in the ventricles and released in response to increased
ventricular distending pressures. ANP and BNP cause
vasodilatation and natriuresis and counteract the water-
retaining effects of the adrenergic and renin angiotensin
system. CNP is located primarily in the vasculature.
The physiologic role of CNP is not yet clarified.
Circulating levels of ANP and BNP are elevated in
the plasma in patients with heart failure. In normal
human hearts, ANP predominated in the atria, with a
low level expression of BNP and CNP. Patients with
heart failure demonstrate an unchanged content of
ANP in the atrial with a marked increase in the concen-
trations of BNP.There is no level of BNP that perfectly
separates patients with and without heart failure.
Normal levels include BNP < 100 pg per milliliter.
Values above 500 are generally considered to be positive.
There is a diagnostic gray area between 100 and 500.4,35
ARTERIAL BLOOD GAS MEASUREMENTS
Arterial blood gas measurement may be used to evalu-
ate the oxygenation (PaO2), ventilation (PaCO2), and pH
in patients during acute MI and exacerbations of CHF
in certain situations (i.e., obvious tachypnea, low
SaO2). These evaluations can help determine the need
for supplemental oxygen therapy and mechanical venti-
latory support in these patients. Oxygen is the first
drug provided during a suspected MI. Refer to
Chapter 2 and Appendix III-A for further description
of arterial blood gas interpretation and supplemental
oxygen, respectively.
CHEST RADIOGRAPHY
Chest x-ray can be ordered for patients to assist in the
diagnosis of CHF or cardiomegaly (enlarged heart).
Patients in CHF have an increased density in pulmo-
nary vasculature markings, giving the appearance
of congestion in the vessels.3,7 Refer to Chapter 2 for
further description of chest x-rays.

ECHOCARDIOGRAPHY
Transthoracic echocardiography or ‘‘cardiac echo’’ is a
noninvasive procedure that uses ultrasound to evaluate
the function of the heart. Evaluation includes the size
of the ventricular cavity, the thickness and integrity of
the septum, valve integrity, and the motion of individ-
ual segments of the ventricular wall. Volumes of the
ventricles are quantified, and EF can be estimated.3
Transesophageal echocardiography (TEE) is a
newer technique that provides a better view of the
mediastinum in cases of pulmonary disease, chest wall
abnormality, and obesity, which make standard echo-
cardiography difficult.12,36 For this test, the oropharynx
is anesthetized and the patient is given enough sedation
to be relaxed but still awake since he or she needs to
cooperate by swallowing the catheter. The catheter,
a piezoelectric crystal mounted on an endoscope, is
passed into the esophagus. Specific indications for
transesophageal echocardiography include bacterial
endocarditis, aortic dissection, regurgitation through
or around a prosthetic mitral or tricuspid valve, left
atrial thrombus, intracardiac source of an embolus,
and interarterial septal defect. Patients usually fast for
at least 4 hours prior to the procedure.36
Principal indications for echocardiography are to
assist in the diagnosis of pericardial effusion, cardiac
tamponade, idiopathic or hypertrophic cardiomyopa-
thy, a variety of valvular diseases, intracardiac masses,
ischemic cardiac muscle, left ventricular aneurysm,
ventricular thrombi, and a variety of congenital heart
diseases.12
Transthoracic echocardiography (TTE) can also be
performed during or immediately following bicycle or
treadmill exercise to identify ischemia-induced wall
motion abnormalities or during a pharmacologically
induced exercise stress test (e.g., a dobutamine stress
echocardiograph [DSE]). This stress echocardiograph
adds to the information obtained from standard stress
tests (ECGs) and may be used as an alternative to
nuclear scanning procedures. Transient depression of
wall motion during or after stress suggests ischemia.37
CONTRAST ECHOCARDIOGRAPH. The ability of the
echocardiograph to diagnose perfusion abnormalities
and myocardial chambers is improved by using an intra-
venously injected contrast agent. The contrast allows
greater visualization of wall motion and wall thickness,
and calculation of EF.38
DOBUTAMINE STRESS ECHOCARDIOGRAPH.
Dobutamine is a potent alpha-1 (a1) agonist and a
beta-receptor agonist with prominent inotropic and
Cardiac System CHAPTER 1 17
less-prominent chronotropic effects on the myocardi-
um. Dobutamine (which, unlike Persantine, increases
contractility, HR, and BP in a manner similar to exercise)
is injected in high doses into subjects as an alternative
to exercise.37 Dobutamine infusion is increased in a step-
wise fashion similar to an exercise protocol.The initial
infusion is 0.01 mg/kg and is increased 0.01 mg/kg every
3 minutes until a maximum infusion of 0.04 mg/kg is
reached. Typically, the echocardiograph image of wall
motion is obtained during the final minute(s) of infu-
sion. This image can then be compared to baseline
recordings.37 If needed, atropine is occasionally added
to facilitate a greater HR response for the test.37 Low-
dose DSE has the capacity to evaluate the contractile
response of the impaired myocardium. Bellardinelli
and colleagues39 have demonstrated that improvements
in functional capacity after exercise can be predicted by
low-dose DSE. Patients with a positive contractile
response
. to dobutamine were more likely to increase
theirVO2max after a 10-week exercise program. Having a
positive contractile response on the low-dose DSE had
a positive predictive value of 84% and a negative
predictive value of 59%.39 With research such as this
study beginning to demonstrate the prognostic value
of certain medical tests for determining functional
prognosis, physical therapists will need to be prepared
to critically assess this area of literature in order to
assist the medical team in determining the level of reha-
bilitative care for a patient during his or her recovery.
EXERCISE TESTING
Exercise testing, or stress testing, is a noninvasive
method of assessing cardiovascular responses to
increased activity.The use of exercise testing in cardiac
patients can serve multiple purposes, which are not
mutually exclusive.The most widespread use of exercise
testing is as a diagnostic tool for the presence of coro-
nary artery disease. Other uses include determining
prognosis and severity of disease, evaluating the effec-
tiveness of treatment, early detection of labile hyperten-
sion, evaluation of CHF, evaluation of arrhythmias,
and evaluation of functional capacity.37 Exercise testing
involves the systematic and progressive increase in
intensity of activity (e.g., treadmill walking, bicycling,
stair climbing, arm ergometry). These tests are accom-
panied by simultaneous ECG analysis, BP measure-
ments, and subjective reports, commonly using Borg’s
Rating of Perceived Exertion (RPE).40,41 Occasionally,
the use of expired gas analysis can provide useful infor-
mation about pulmonary function and maximal
oxygen consumption.37 Submaximal tests, such as the
18 CHAPTER 1 Cardiac System

12- and 6-minute walk tests, can be performed to assess
a patient’s function. For further discussion of the
6-minute walk test, refer to Appendix IX.
Submaximal tests differ from maximal tests because
the patient is not pushed to his or her maximum HR;
instead, the test is terminated at a predetermined end
point, usually at 75% of the patient’s predicted maxi-
mum HR.42 For a comparison of two widely used exer-
cise test protocols and functional activities, refer to
Table 1-12. For a more thorough description of submax-
imal exercise testing, the reader is referred to Noonan
and Dean.42
Contraindications to exercise testing include43:
 Recent MI (less than 48 hours earlier)
 Acute pericarditis
 Unstable angina
 Ventricular or rapid arrhythmias
 Untreated second- or third-degree heart block
 Decompensated CHF
 Acute illness
Exercise test results can be used for the design of an
exercise prescription. Based on the results, the patient’s
actual or extrapolated maximum HR can be used to
determine the patient’s target HR range and safe activity
intensity. RPE with symptoms during the exercise test
can also be used to gauge exercise or activity intensity,
especially in subjects on beta-blockers. (Refer to the
Physical Therapy Intervention section for a discussion
on the use of RPE.)
Any walk test that includes measurement of distance
and time can be utilized to estimate metabolic equivalents
(METs) aswell as oxygen consumptionwith the equations:
V_ o2 ml=kg=min ¼ ðmphÞð26:83 m=minÞ
ð:1 ml=kg=minÞ þ 3:5 ml=kg=min
METs ¼ V_ o2 ml=kg=min  3:5
MPH ¼ ðpace ½feet=min  60Þ  5280 ðfeet=mileÞ
There is a direct relationship between pace on a level
surface and METs (oxygen consumption). A therapist
can utilize walking pace to estimate oxygen consump-
tion and endurance for other functional tasks that
fall within a patient’s oxygen consumption (aerobic
functional capacity).

Table 1-12 COMPARISON OF EXERCISE TEST PROTOCOLS AND FUNCTIONAL TASKS—ENERGY

DEMANDS
Oxygen Metabolic Treadmill: Bruce Bike Ergometer: for
Requirements Equivalents Protocol 3-minute 70 kg of Body
(ml O2/kg/min) (METS) Functional Tasks Stages (mph/elevation) Weight (kg/min)
52.5 15
49.5 14
45.5 13 4.2/16.0 1,500
42.0 12 1,350
38.5 11 1,200
35.0 10 Jogging 3.4/14.0 1,050
31.5 9 900
28.0 8 750
24.5 7 2.5/12.0
21.0 6 Stair climbing 600
17.5 5 1.7/10.0 450
14.0 4 Walking (level surface) 300
10.5 3 150
7.0 2 Bed exercise (arm exercises in
supine or sitting)
Data from American Heart Association, Committee on Exercise. ExerciseTesting and Training of Apparently Healthy Individuals:
A Handbook for Physicians. Dallas, 1972; and Brooks GA, FaheyTD,WhiteTP (eds). Exercise Physiology: Human Bioenergetics and Its
Applications (2nd ed). MountainView, CA: Mayfield Publishing, 1996.

6.00
5.00
4.00
METs
3.00
2.00
Sitting – Light activity
1.00
METs = 0.0087 (Feet/Minute) + 1
0.00
0.00 100.00
FIGURE 1-9
Relationship between walking pace, METs, and oxygen consumption on level surfaces. (Data from
Fletcher GF, Balady GJ, Amsterdam EA, et al. Exercise standards for testing and training: a statement for
healthcare professionals from the American Heart Association. Circulation 2001;104:1694-1740.)
Figure 1-9 depicts the relationship between pace
(feet/min) and METs for level surface ambulation.
Bruce Protocol Stage 1 (due to its incline when at 1.7
mph) is similar to ambulation at 400 feet/min on a
level surface. If a patient cannot sustain a particular
pace for at least 10 minutes, it can be concluded
that this pace exceeds the patient’s anaerobic threshold;
if the patient cannot sustain a pace for at least
1 minute, it can be concluded that the pace is close to
the patient’s maximal MET (oxygen consumption).
Therefore, continuous aerobic exercise programs
should be at a walking pace below anaerobic
threshold. For interval aerobic training, work periods
at walking paces that can be sustained for1to10 minutes
would be appropriate with an equal period of rest.
If a patient is routinely required to exceed maximal
oxygen consumption during daily tasks, he or she is
much more likely to experience signs of fatigue
and exhaustion over time when considering capacity
for repeated bouts of activity during a day.
CLINICAL TIP
 Synonyms for exercise tests include
exercise tolerance test (ETT) and graded exercise
test (GXT).
THALLIUM STRESS TESTING. Thallium stress testing
is a stress test that involves the injection of a radio-
active nuclear marker for the detection of myocardial
Cardiac System CHAPTER 1 19
Bruce Protocol - Stage 1
Stair climbing
Raking lawn / Gardening
Household tasks
Standing – Light activity
200.00 300.00 400.00 500.00 600.00
Feet per Minute
perfusion. The injection is typically given (via an intra-
venous line) during peak exercise or when symptoms
are reported during the stress test. After the test, the
subject is passed under a nuclear scanner to be evalua-
ted for myocardial perfusion by assessment of the
distribution of thallium uptake. The subject then
returns 3 to 4 hours later to be reevaluated for myocar-
dial reperfusion. This test appears to be more sensitive
than stress tests without thallium for identifying
patients with coronary artery disease.12
PERSANTINE THALLIUM STRESS TESTING. Persantine
thallium stress testing is the use of dipyridamole
(Persantine) to dilate coronary arteries. Coronary
arteries with atherosclerosis do not dilate; therefore,
dipyridamole shunts blood away from these areas. It is
typically used in patients who are very unstable, decon-
ditioned, or unable to ambulate or cycle for exercise-
based stress testing.37 Patients are asked to avoid all
food and drugs containing methylxanthines (e.g.,
coffee, tea, chocolate, cola drinks) for at least 6 hours
prior to the test as well as phosphodiesterase drugs,
such as aminophylline, for 24 hours. While the patient
is supine, an infusion of dipyridamole (0.56 ml/kg
diluted in saline) is given intravenously over 4 minutes
(a large-vein intracatheter is used). Four minutes after
the infusion is completed, the perfusion marker (thal-
lium) is injected, and the patient is passed under a
nuclear scanner to be evaluated for myocardial perfu-
sion by assessment of the distribution of thallium
uptake.37
20 CHAPTER 1 Cardiac System

CARDIAC CATHETERIZATION pressure to reduce the risk of vascular

complications.12
Cardiac catheterization, classified as either right or left,
 Some hospitals may use a knee immobilizer to assist
is an invasive procedure that involves passing a flexible,
with immobilizing the lower extremity.
radiopaque catheter into the heart to visualize cham-
 Physical therapy intervention should be deferred
bers, valves, coronary arteries, great vessels, cardiac
or limited to bedside treatment within the
pressures, and volumes to evaluate cardiac function
limitations of these precautions.
(estimate EF, CO).
 During the precautionary period, physical therapy
The procedure is also used in the following
intervention, such as bronchopulmonary hygiene
diagnostic and therapeutic techniques12:
or education, may be necessary. Bronchopulmonary
 Angiography
hygiene is indicated if there are pulmonary
 Percutaneous transluminal coronary angioplasty
complications or if risk of these complications exists.
(PTCA)
Education is warranted when the patient is anxious
 Electrophysiologic studies (EPSs)
and needs to have questions answered regarding his
 Cardiac muscle biopsy
or her functional mobility.
Right-sided catheterization involves entry through a
 After the precautionary period, normal mobility
sheath that is inserted into a vein (commonly subcla-
can progress to the limit of the patient’s
vian) for evaluation of right heart pressures; calculation
cardiopulmonary impairments; however, the
of CO; and angiography of the right atrium, right ven-
catheterization results should be incorporated
tricle, tricuspid valve, pulmonic valve, and pulmonary
into the physical therapy treatment plan.
artery.12 It is also used for continuous hemodynamic
monitoring in patients with present or very recent
heart failure to monitor cardiac pressures (see
Appendix III-A). Indications for right heart catheteriza- ANGIOGRAPHY
tion include an intracardiac shunt (blood flow between Angiography involves the injection of radiopaque con-
right and left atria or right and left ventricles), myocar- trast material through a catheter to visualize vessels or
dial dysfunction, pericardial constriction, pulmonary chambers.
vascular disease, valvular heart disease, and status post Different techniques are used for different
heart transplant. assessments12:
Left-sided catheterization involves entry through a Aortography Aorta and aortic valve
sheath that is inserted into an artery (commonly Coronary arteriography Coronary arteries
femoral) to evaluate the aorta, left atrium, and left ven- Pulmonary Pulmonary circulation
tricle; left ventricular function; mitral and aortic valve angiography
function; and angiography of coronary arteries.
Indications for left heart catheterization include aortic Ventriculography Right or left ventricle and
dissection, atypical angina, cardiomyopathy, congenital AV valves
heart disease, coronary artery disease, status post MI,
valvular heart disease, and status post heart transplant. ELECTROPHYSIOLOGIC STUDIES
EPSs are performed to evaluate the electrical conduc-
tion system of the heart.12 An electrode catheter is
CLINICAL TIP inserted through the femoral vein into the right ventri-
 After catheterization, the patient is on bed rest for
cle apex. Continuous ECG monitoring is performed
approximately 4 to 6 hours when venous access is
both internally and externally.The electrode can deliver
performed, or for 6 to 8 hours when arterial access
programmed electrical stimulation to evaluate conduc-
is performed.12
tion pathways, formation of arrhythmias, and the auto-
 The sheaths are typically removed from the vessel 4 to
maticity and refractoriness of cardiac muscle cells.
6 hours after the procedure, and pressure is applied
EPSs evaluate the effectiveness of antiarrhythmic med-
constantly for 20 minutes following sheath removal.12
ication and can provide specific information about
 The extremity should remain immobile with a
each segment of the conduction system.12 In many hos-
sandbag over the access site to provide constant
pitals, these studies may be combined with a therapeu-
tic procedure, such as an ablation procedure (discussed

in the Management section). Indications for EPSs
include12:
 Sinus node disorders
 AVor intraventricular block
 Previous cardiac arrest
 Tachycardia at greater than 200 bpm
 Unexplained syncope
CLINICAL TIP
 Patients undergoing EPS should remain on bed rest
for 4 to 6 hours after the test.
PATHOPHYSIOLOGY
When disease and degenerative changes impair the
heart’s capacity to perform work, a reduction in CO
occurs. If cardiac, renal, or central nervous system per-
fusion is reduced, a vicious cycle resulting in heart fail-
ure can ensue. A variety of pathologic processes can
impair the heart’s capacity to perform work. These
pathologic processes can be divided into four major
categories: (1) acute coronary syndrome, (2) rhythm
and conduction disturbance, (3) valvular heart disease,
and (4) myocardial and pericardial heart disease. CHF
occurs when this failure to pump blood results in an
increase in the fluid in the lungs, liver, subcutaneous
tissues, and serous cavities.5
Acute Coronary Syndrome
When myocardial oxygen demand is higher than
supply, the myocardium must use anaerobic metabo-
lism to meet energy demands.This system can be main-
tained for only a short period of time before tissue
ischemia will occur, which typically results in angina
(chest pain). If the supply and demand are not balanced
by rest, medical management, surgical intervention, or
any combination of these, injury of the myocardial
tissue will ensue, followed by infarction (cell death).
This balance of supply and demand is achieved in
individuals with normal coronary circulation; how-
ever, it is compromised in individuals with impaired
coronary blood flow. The following pathologies can
result in myocardial ischemia:
 Coronary arterial spasm is a disorder of transient
spasm of coronary vessels that impairs blood flow
to the myocardium. It can occur with or without
the presence of atherosclerotic coronary disease. It
results in variant angina (Prinzmetal’s angina).12
Cardiac System CHAPTER 1 21
 Coronary atherosclerotic disease (CAD) is a multi-
step process of the deposition of fatty streaks or pla-
ques on artery walls (atherosis). The presence of
these deposits eventually leads to arterial wall
damage and platelet and macrophage aggregation
that then leads to thrombus formation and hardening
of the arterial walls (sclerosis).The net effect is a nar-
rowing of coronary walls. It can result in stable
angina or unstable angina (USA), or MI.3,5,12
Clinical syndromes caused by these pathologies are
as follows7,12:
 Stable (exertional) angina occurs with increased
myocardial demand, such as during exercise, is
relieved by reducing exercise intensity or terminating
exercise, and responds well to nitroglycerin.
 Variant angina (Prinzmetal’s angina) is a less-
common form of angina caused by coronary artery
spasm. This form of angina tends to be prolonged,
severe, and not readily relieved by nitroglycerin.
 USA is considered intermediate in severity between
stable angina and MI. It usually has a sudden onset,
occurs at rest or with activity below the patient’s
usual ischemic baseline, and may be different from
the patient’s usual anginal pattern. It is not induced
by activity or increased myocardial demand that
cannot be met. It can be induced at rest, when
supply is cut down with no change in demand.
A common cause of USA is believed to be a rupture
of an atherosclerotic plaque.
 MI occurs with prolonged or unmanaged ischemia.
It is important to realize that there is an evolution
from ischemia to infarction. Ischemia is the first
phase of tissue response when the myocardium is
deprived of oxygen. It is reversible if sufficient
oxygen is provided in time. However, if oxygen dep-
rivation continues, myocardial cells will become
injured and eventually will die (infarct).The location
and extent of cell death are determined by the coro-
nary artery that is compromised and the amount of
time that the cells are deprived. Refer to Table 1-13
for common types of MI and their complications.
Figure 1-10 provides a schematic of possible clinical
courses for patients admitted with chest pain.
CLINICAL TIP
 (ST) depression on a patient’s ECG of approximately
1 to 2 mm is generally indicative of ischemia.
 ST elevation is generally indicative of myocardial
injury or infarction.
22 CHAPTER 1 Cardiac System

Table 1-13 MYOCARDIAL INFARCTIONS (MIs)

MI/Wall Affected
Anterior MI/anterior left ventricle
Inferior MI/inferior left ventricle
Anterolateral MI/anterolateral left
ventricle
Anteroseptal MI/septal
regionçbetween left and right
ventricles
Posterior MI/posterior heart
Right ventricular MI
Transmural MI (Q-wave MI)
Subendocardial MI (non—Q-wave MI)
AV, Atrioventricular; CHF, congestive heart failure; LAD, left anterior descending; RCA, right coronary artery; LCA, left coronary artery.
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S (eds). Cardiac Nursing (4th ed). Philadelphia: Lippincott, 2000.
Possible Occluded
Coronary Artery Possible Complications
LCA Left-sided CHF, pulmonary edema, bundle branch
block, AV block, and ventricular aneurysm
(which can lead to CHF, dysrhythmias, and
embolism)
RCA AV blocks (which can result in bradycardia) and
papillary muscle dysfunction (which can result
in valvular insufficiency and eventually CHF)
LAD, circumflex Brady or tachyarrhythmias, acute ventricular septal
defect
LAD Brady or tachyarrhythmias, ventricular aneurysm
RCA, circumflex Bradycardia, heart blocks
RCA Right ventricular failure (can lead to left ventricular
failure and therefore cardiogenic shock), heart
blocks, hepatomegaly, peripheral edema
Any artery Full wall thickness MI, as above
Any artery Partial wall thickness MI, as above, potential
to extend to transmural MI

Rhythm and Conduction Disturbance Valvular Heart Disease

Rhythm and conduction disturbances can range from
minor alterations with no hemodynamic effects to
life-threatening episodes with rapid hemodynamic
compromise.3,5,7 Refer to Chapter Appendix 1-A for a
description ofatrial, ventricular, and junctional rhythms
and AV blocks. Refer to Chapter Appendix 1-B for
examples of common rhythm disturbances. Physical
therapists need to be able to identify abnormalities in
the ECG to determine patient tolerance to activity.
In particular, physical therapists should understand
progressions of common ECG abnormalities so they
can identify, early on, when the patient is not
tolerating an intervention. (Refer to the Physical
Therapy Intervention section for a discussion on ECG.)
A common form of rhythm disturbance is a PVC,
which also can be referred to as a ventricular premature
beat. These abnormalities originate from depolariza-
tion of a cluster of cells in the ventricle (an ectopic
foci), which results in ventricular depolarization.
From the term ectopic foci, PVCs may be referred to as
ventricular ectopy.
Valvular heart disease encompasses valvular diso-
rders of one or more of the four valves of the heart.
The following three disorders can occur3,5:
1. Stenosis involves the narrowing of the valve.
2. Regurgitation, the back flow of blood through the
valve, occurs with incomplete valve closure.
3. Prolapse involves enlarged valve cusps. The cusps
can become floppy and bulge backward.This condi-
tion may progress to regurgitation.
Over time, these disorders can lead to pumping
dysfunction and, ultimately, heart failure.
Refer to Table 1-14 for common valvular
heart diseases and a description of their signs and
symptoms.
Myocardial and Pericardial Heart Disease
Myocardial heart disease affects the myocardial muscle
tissue and can also be referred to as cardiomyopathy;
pericardial heart diseases affect the pericardium.
Refer to Tables 1-15 and 1-16 for common myocardial
and pericardial diseases.
 Cardiac System CHAPTER 1 23

FIGURE 1-10
Possible clinical course of patients admitted with chest pain. CABG, Coronary artery bypass graft; CHF,
congestive heart failure; CC, coronary care unit; d/c, discharge; ECG, electrocardiogram; h/o, history of; MI,
myocardial infarction; PAP, pulmonary arterial pressure; PTCA, percutaneous transluminal coronary
angioplasty; ST Elevation, electrocardiogram that shows elevation of the STsegment. (Data from American
College of Cardiology/American Heart Association. 1999 Update: ACC/AHA Guidelines for the
Management of Patients with Acute Myocardial Infarction: Executive Summary and Recommendations;
Circulation 1999;100:1016-1030; American College of Cardiology/American Heart Association. ACC/AHA
Guidelines for the Management of Patients with Acute Myocardial Infarction. J Am Coll Cardiol
1996;28:1328-1428; American College of Cardiology/American Heart Association. ACC/AHA Guidelines
for the Management of Patients with Unstable Angina and Non-ST Segment Elevation Myocardial
Infarction. J Am Coll Cardiol 2000;36:971-1048.)

Heart Failure Right-sided failure refers to failure of the right side of

Heart failure, a decrease of CO, can be caused by a vari-
ety of cardiac pathologies. Because CO is not main-
tained, life cannot be sustained if heart failure
continues without treatment. Heart failure results in
the congestion of the pulmonary circulation and, in cer-
tain cases, even the systemic circulation. Therefore, it
is commonly referred to as CHF. The most common
pathologic etiology of CHF is some type of cardiomy-
opathy (seeTable 1-15).
The following terms are used to classify the types of
cardiac impairment in CHF44:
Left-sided heart failure refers to failure of the left
ventricle, resulting in back flow into the lungs.
the heart, resulting in back flow into the systemic
venous system.
High-output failure refers to heart failure that is sec-
ondary to renal system failure to filter off excess
fluid. The renal system failure places a higher load
on the heart that cannot be maintained.
Low-output failure refers to the condition in which the
heart is not able to pump the minimal amount of
blood to support circulation.
Systolic dysfunction refers to a problem with systole or
the actual strength of myocardial contraction.
Diastolic dysfunction refers to a problem during dias-
tole or the ability of the ventricle to allow the filling
of blood.
 Table 1-14 SIGNS AND SYMPTOMS OF VALVULAR HEART DISEASES

Disease Symptoms Signs

Aortic stenosis Angina, syncope or near syncope, signs of left Elevated left ventricular wall pressure, decreased
ventricle failure (dyspnea, orthopnea, cough). subendocardial blood flow, systolic murmur,
ventricular hypertrophy
Chronic aortic Angina, symptoms of left ventricular failure. Dilated aortic root, dilated left ventricle, diastolic
regurgitation murmur, left ventricular hypertrophy
Acute aortic Rapid progression of symptoms of left ventricular Sinus tachycardia to compensate for decreased
regurgitation failure, pulmonary edema, angina. stroke volume, loud S3, diastolic murmur, signs
of ventricular failure
Mitral stenosis Symptoms of pulmonary vascular congestion Left atrial hypertrophy, pulmonary hypertension,
(dyspnea, orthopnea). If patient develops atrial fibrillation, can have embolus formation
pulmonary hypertension (which can cause (especially if in atrial fibrillation), long diastolic
hypoxia, hypotension), he or she may have murmur
angina, syncope.
Chronic mitral Symptoms of pulmonary vascular congestion, Left atrial enlargement, atrial fibrillation,
regurgitation angina, syncope, fatigue. elevated left atrial pressure
Acute mitral Rapid progression of symptoms of pulmonary Sinus tachycardia, presence of S3 or S4,
regurgitation vascular congestion. pulmonary edema
Mitral valve Most commonly asymptomatic, fatigue, Systolic click, may have tachyarrhythmia syncope
prolapse palpitation.
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S (eds). Cardiac Nursing (4th ed). Philadelphia: Lippincott, 2000; and
Cheitlin MD, Sokolow M, McIlroy MB. Clinical Cardiology (6th ed). Norwalk, CT: Appleton & Lange, 1993.

Table 1-15 MYOCARDIAL DISEASES—CARDIOMYOPATHIES

Functional Classification
Cardiomyopathy Dysfunction Description
Dilated Systolic Ventricle is dilated, and there is marked contractile dysfunction of myocardium
Hypertrophic Diastolic Thickened ventricular myocardium, less compliant to filling, and therefore
decreased filling during diastole
Restrictive Systolic and Endocardial scarring of ventricles, decreased compliance during diastole, and
diastolic decreased contractile force during systole

Etiologic Classification
Etiology Examples
Inflammatory Viral infarction, bacterial infarction
Metabolic Selenium deficiency, diabetes mellitus,
Fibroplastic Carcinoid fibrosis, endomyocardial fibrosis
Hypersensitivity Cardiac transplant rejection, methyldopa,
Genetic Hypertrophic cardiomyopathy, Duchenne’s muscular dystrophy
Idiopathic Idiopathic hypertrophic cardiomyopathy
Infiltrative Sarcoidosis, neoplastic
Hematologic Sickle cell anemia
Toxic Alcohol, bleomycin
Physical agents Heat stroke, hypothermia, radiation
Miscellaneous acquired Postpartum cardiomyopathy, obesity
Data from Cahalin L. Cardiac Muscle Dysfunction. In EA Hillegass, HS Sadowsky (eds). Essentials of Cardiopulmonary Physical Therapy
(2nd ed). Philadelphia: Saunders, 2001; HareJM:The Dilated, Restrictive, and Infiltrative Cardiomyopathies. In P Libby, RO Bonow, DL
Mann, et al: Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, (8th ed). Philadelphia: Saunders, 2008.
 Cardiac System CHAPTER 1 25

Table 1-16 SIGNS AND SYMPTOMS OF PERICARDIAL HEART DISEASES

Disease Symptoms
Acute pericarditis Retrosternal chest pain (worsened by supine
and/or deep inspiration), dyspnea, cough,
hoarseness, dysphagia, fever, chills, and
weakness may occur.
Constrictive pericarditis Abdominal swelling, peripheral edema,
fatigue, dyspnea, dizziness and/or syncope,
signs of pulmonary venous congestion,
vague nonspecific retrosternal chest pain.
Chronic pericardial May have vague fullness in anterior chest,
effusion (without cough, hoarseness, dysphagia.
tamponade)
Pericardial tamponade Symptoms of low cardiac output (dyspnea,
fatigue, dizziness, syncope); may have
retrosternal chest pain; may have cough,
hiccoughs, hoarseness.
ECG, Electrocardiogram
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S (eds). Cardiac Nursing (4th ed). Philadelphia: Lippincott, 2000; and
Cheitlin MD, Sokolow M, McIlroy MB. Clinical Cardiology (6th ed). Norwalk, CT: Appleton & Lange, 1993.
Signs
Pericardial friction rub; diffuse STsegment
elevation; decreased QRS voltage in all ECG
leads if pericardial effusion also present
Jugular venous distention; QRS voltage
diminished on ECG; occasionally atrial
fibrillation
Muffled heart sounds; may have pericardial
friction rub; QRS voltage diminished on
ECG; chest x-ray with cardiomegaly without
pulmonary congestion
Jugular venous distention, cardiomegaly,
diminished QRS voltage on ECG; becomes
tamponade from effusion when right heart
catheterization shows equal pressures in right
atrium, ventricle, and capillary wedge
(signifies left atria pressure), and left heart
catheterization shows equal pressure on left
side of heart to right side

Possible signs and symptoms of CHF are described

in Box 1-1. The American Heart Association revised BOX 1-1 SIGNS AND SYMPTOMS OF
the New York Heart Association (NYHA) Functional
Classification of Heart Disease, and this new classifica-
CONGESTIVE HEART FAILURE
tion is described in Table 1-17.While the NYHA classi-
Signs Symptoms
fication provides a good description of the patient’s
condition, it does not include management strategies  Cold, pale possibly cyanotic  Dyspnea
based on patient severity. Therefore another classifica- extremities  Tachypnea
tion system has been devised based on four stages  Weight gain  Paroxysmal
(A to D):45  Peripheral edema nocturnal
 Hepatomegaly dyspnea
Stage A: Patients who are at high risk for developing  Jugular venous distention  Orthopnea
left ventricular dysfunction.Treatment intervention  Crackles (rales)  Cough
is focused on risk factor modification.  Tubular breath sounds and  Fatigue
Stage B: Patients who have left ventricular dysfunction consolidation S3 heart sound
but are asymptomatic. Treatment intervention is  Sinus tachycardia
focused on prevention of symptoms with risk  Decreased exercise tolerance
factor modification. and physical work capacity
Stage C: Patients who have left ventricular dysfunction
are symptomatic.Treatment intervention is centered Adapted from Cahalin L: Cardiac Muscle Dysfunction.
around alleviating symptoms and slowing the In EA Hillegass, HS Sadowsky: Essentials of Cardiopulmonary
progression of the disease. Physical Therapy (2nd ed). Philadelphia: Saunders, 2001.
26 CHAPTER 1 Cardiac System

Table 1-17 AMERICAN HEART ASSOCIATION’S FUNCTIONAL CAPACITY AND OBJECTIVE ASSESSMENT
OF PATIENTS WITH DISEASES OF THE HEART

Class and Functional Capacity* Objective Assessment{

Class I Patients with cardiac disease but without resulting limitations of physical No objective evidence of
activity. Ordinary physical activity does not cause undue fatigue, cardiovascular disease
palpitation, dyspnea, or anginal pain.
Class II Patients with cardiac disease that results in a slight limitation of physical Objective evidence
activity. Patients are comfortable at rest, but ordinary physical activity of minimal
results in fatigue, palpitations, dyspnea, or anginal pain. cardiovascular disease
Class III Patients with cardiac disease that results in a marked limitation Objective evidence of
of physical activity. Patients are comfortable at rest, but less-than- moderately severe
ordinary activity causes fatigue, palpitations, dyspnea, or anginal pain. cardiovascular disease
Class IV Patients with cardiac disease that results in an inability to carry on any Objective evidence of
physical activity without discomfort. Fatigue, palpitations, dyspnea, severe cardiovascular
or anginal pain may be present even at rest. If any physical activity is disease
undertaken, symptoms increase.

Functional capacity refers to subjective symptoms of the patient.This aspect of the classification is identical to the NewYork Heart
Association’s Classification.
{
Objective assessment was added to the classification system by the American Heart Association in 1994.
It refers to measurements such as electrocardiograms, stress tests, echocardiograms, and radiologic images.43
FromThe Criteria Committee of the NewYork Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of the Heart and
Great Vessels, (9th ed). Boston, Mass: Little, Brown & Co;1994:253-256.

Stage D: Patients who have advanced stage refractory

heart failure.Treatment is based on specialized phar-
macologic and surgical interventions such as ven-
tricular assist devices (Appendix III-C) and possible
transplantation (Chapter 12).
Activity progression for patients hospitalized
with CHF is based on the ability of medical treatments
(e.g., diuresis, inotropes) to keep the patient out
of heart failure.When a patient with CHF is medically
stabilized, the heart is thought to be ‘‘compensated.’’
Conversely, when the patient is unable to maintain
adequate circulation, the heart would be ‘‘decompen-
sated.’’ Clinical examination findings allow the thera-
pist to continuously evaluate the patient’s tolerance
to the activity progression. Although metabolic
equivalent (MET) tables are not commonly used
clinically, they do provide a method of progres-
sively increasing a patient’s activity level. As greater
MET levels are achieved with an appropriate
hemodynamic response, the next level of activity
can be attempted. Table 1-12 provides MET levels
for common activities that can be performed with
patients.
MANAGEMENT
The following section discusses surgical and nonsurgi-
cal procedures, pharmacologic interventions, and phys-
ical therapy interventions for patients with cardiac
dysfunction.
Revascularization and Reperfusion of the
Myocardium
THROMBOLYTIC THERAPY
Thrombolytic therapy has been established as an
acute management strategy for patients experiencing
an MI because of the high prevalence of coronary
artery thrombosis during acute MI. Thrombolytic
agents, characterized as fibrin-selective and nonselec-
tive agents, are administered to appropriate candidates
via intravenous access. The most common agents
include: streptokinase (nonselective), anisylated plas-
minogenstreptokinase activatorcomplex (nonselective),
and tissue plasminogen activator (t-PA) (fibrin-selec-
tive).12 Fibrin-selective agents have a high velocity of
clot lysis, whereas the nonselective agents have a slower
clot lysis and more prolonged systemic lytic state.

The indication for thrombolytic therapy includes
chest pain that is suggestive of myocardial ischemia
and is associated with acute STsegment elevation on a
12-lead ECG or a presumed new left ventricular
bundle branch block. Hospital protocol regarding the
time period to perform thrombolytic therapy usually
varies, as clinical trials have led to some controversy.12
Some studies show benefits only if treatment is con-
ducted within 6 hours of symptoms, whereas others
have demonstrated improvement with treatment up to
24 hours after onset of symptoms.12
The contraindications to thrombolytic therapy gen-
erally include patients who are at risk for excessive
bleeding. Because of the variability that can occur
among patients, many contraindications are considered
relative cautions, and the potential benefits of therapy
are weighed against the potential risks. Thrombolytic
therapy is used in conjunction with other medical treat-
ments such as aspirin, intravenous heparin, intravenous
nitroglycerin, lidocaine, atropine, and a beta blocker.
As previously discussed, early peaking of CK-MB is
associated with reperfusion.12
PERCUTANEOUS REVASCULARIZATION
PROCEDURES
Percutaneous revascularization procedures are used to
return blood flow through coronary arteries that have
become occlusive secondary to atherosclerotic plaques.
The following list briefly describes three percutaneous
revascularization procedures12:
1. Percutaneous transluminal coronary angioplasty
(PTCA) is performed on small atherosclerotic lesions
that do not completely occlude the vessel. PTCA can
be performed at the time of an initial diagnostic
catheterization, electively at some time after a cathe-
terization, or urgently in the setting of an acute MI.
A sheath is inserted into the femoral, radial, or
brachial artery, and a catheter is guided through the
sheath into the coronary artery. A balloon system is
then passed through the catheter to the lesion site.
Inflations of variable pressure and duration may be
attempted to reduce the lesion by at least 20% diam-
eter with a residual narrowing of less than 50% in
the vessel lumen.12 Owing to some mild ischemia
that can occur during the procedure, patients occa-
sionally require temporary transvenous pacing,
intraaortic balloon counterpulsation, or femoro-
femoral cardiopulmonary bypass circulatory sup-
port during PTCA.
The use of endoluminal stents prevents the major
limitations of PTCA, which include abrupt closure
Cardiac System CHAPTER 1 27
(in up to 7.3% of patients), restenosis, anatomically
unsuitable lesions, chronic total occlusions, and
unsatisfactory results in patients with prior
coronary artery bypass graft (CABG) surgery.46
2. Coronary laser angioplasty uses laser energy to
create precise ablation of plaques without thermal
injury to the vessel. The laser treatment results in a
more pliable lesion that responds better to balloon
expansion. The use of laser angioplasty is limited
owing to the expense of the equipment and a high
restenosis rate (> 40%).47
3. Directional coronary atherectomy can be performed
by inserting a catheter with a cutter housed at the
distal end on one side of the catheter and a balloon
on the other side.12 The balloon inflates and presses
the cutter against the atheroma (plaque). The cutter
can then cut the atheroma and remove it from the
arterial wall. This can also be performed with a
laser on the tip of the catheter. Rotational ablation
uses a high-speed rotating bur coated with diamond
chips, creating an abrasive surface. This selectively
removes atheroma due to its inelastic properties as
opposed to the normal elastic tissue.12 The debris
emitted from this procedure is passed into the coro-
nary circulation and is small enough to pass through
the capillary beds. Commonly, PTCA is used as an
adjunct to this procedure to increase final coronary
diameter or to allow for stent placement.
4. Endoluminal stents are tiny spring-like tubes that
can be placed permanently into the coronary artery
to increase the intraluminal diameter. Stents are
occasionally necessary when initial attempts at
revascularization (e.g., angioplasty) have failed.12
Refer to the Diagnostic and Laboratory Measures
section for a discussion on precautions after a catheter-
ization procedure.
TRANSMYOCARDIAL REVASCULARIZATION
In transmyocardial revascularization, a catheter with a
laser tip creates transmural channels from patent coro-
nary arteries into an area of the myocardium that is
thought to be ischemic. It is intended for patients with
chronic angina who, due to medical reasons, cannot
have angioplasty or CABG. Theoretically, ischemia is
reduced by increasing the amount of oxygenated
blood in ischemic tissue. Angiogenesis (the growth of
new blood vessels) has also been proposed as a mecha-
nism of improvement after this procedure. Although
therapists should expect improvements in functional
capacity with decreased angina, the patient’s risk status
related to CAD or left ventricular dysfunction
28 CHAPTER 1 Cardiac System
does not change.48 Postcatheterization procedure pre-
cautions, as previously described, will apply after this
procedure.
CORONARY ARTERY BYPASS GRAFT
A CABG is performed when the coronary artery has
become completely occluded or when it cannot be cor-
rected by PTCA, coronary arthrectomy, or stenting. A
vascular graft is used to revascularize the myocardium.
The saphenous vein and the left internal mammary
artery (LIMA) are commonly used as vascular grafts.
CABG can be performed either through a median ster-
notomy, which extends caudally from just inferior to
the suprasternal notch to below the xiphoid process
and splits the sternum longitudinally, or through a
variety of minimally invasive incisions.12
A minimally invasive technique that is being used
for CABG includes a CABG with a median sternotomy
but without coronary bypass (off-pump CABG). This
procedure eliminates the need for cross-clamping the
aorta and is desirable in patients with left ventricular
dysfunction or with severe atherosclerosis.12
If a median sternotomy is performed instead of the
minimally invasive incisions, then patients are placed
on sternal precautions for at least 8 weeks for the pur-
pose of preventing wound dehiscence and to preserve
the integrity of sternal wiring. In general, sternal pre-
cautions include restrictions for upper extremity lifting
greater than 10 lbs, pushing or pulling, resistive exer-
cise, and minimal use of the arms for supine-to-sit and
sit-to-stand transfers.49 Recent research indicates that
bilateral (simultaneous) shoulder flexion and abduction
produce greater sternal skin stress than do other
planes of motion of the shoulder.50
CLINICAL TIP
 To help patients understand this concept,
inform them that a gallon of milk weighs
approximately 8.5 lb.
 Because of the altered chest wall mechanics and the
pain associated with a sternotomy, patients are at
risk of developing pulmonary complications after a
CABG. The physical therapist should be aware
of postoperative complication risk factors as well
as postoperative indicators of poor pulmonary
function. Refer to Chapter 2 and Appendix V
for further description of postoperative pulmonary
complications.
Secondary Prevention Following
Revascularization
Improved medical and surgical interventions have
reduced mortality due to cardiovascular disease,
however incidence and prevalence are still high.1
Following revascularization procedures, there is a
need to educate patients regarding cardiovascular dis-
ease risk factors as a mechanism to ensure continued
success of the procedures via secondary prevention
of primary disease processes (refer toTable 1-4).
ABLATION PROCEDURE
Catheter ablation procedures are indicated for supraven-
tricular tachycardia, AVnodal reentrant pathways, atrial
fibrillation, atrial flutter, and certain types of
ventricular tachycardia.12 The procedure attempts to
remove or isolate ectopic foci in an attempt to reduce
the resultant rhythm disturbance. Radiofrequency abla-
tion uses low-power, high-frequency AC current to
destroy cardiac tissue and is the most effective technique
forablation.12 After the ectopic foci are locatedunder flu-
oroscopic guidance, the ablating catheter is positioned
at the site to deliver a current for10 to 60 seconds.
Surgical ablation of atrial fibrillation is accom-
plished by the Maze procedure, which consists of surgi-
cally incising and resewing areas of ectopic foci in the
atria in order to help direct the electrical conduction
properly to the AV node and the ventricles. The result
of the surgical incisions often resembles a children’s
maze and hence the procedure was named for this
outcome. It is currently the standard for nonphar-
macologic treatment of atrial fibrillation and has been
the basis for ongoing refinement as currently there are
the cox-Maze, Maze III, and Maze IV procedures.51,52
CLINICAL TIP
 After an ablation procedure, the leg used for access
(venous puncture site) must remain straight and
immobile for 3 to 4 hours. If an artery was used,
this time generally increases to 4 to 6 hours.
(The exact time will depend on hospital policy.)
 Patients are sedated during the procedure and may
require time after the procedure to recover.
 Most of the postintervention care is geared toward
monitoring for complications. Possible complications
include bleeding from the access site, cardiac
tamponade from perforation, and arrhythmias.
 After a successful ablation procedure (and the initial
immobility to prevent vascular complications at the
access site), there are usually no activity restrictions.
 Cardiac System CHAPTER 1 29

CARDIAC PACEMAKER IMPLANTATION AND
AUTOMATIC IMPLANTABLE CARDIAC DEFIBRILLATOR
Cardiac pacemaker implantation involves the place-
ment of a unipolar or bipolar electrode on the myocardi-
um. This electrode is used to create an action potential
in the management of certain arrhythmias. Indications
for cardiac pacemaker implantation include the
following12,53,54:
 Sinus node disorders (bradyarrhythmias [HR lower
than 60 bpm])
 Atrioventricular disorders (complete heart block,
Mobitz type II block)
 Tachyarrhythmias (supraventricular tachycardia,
frequent ectopy)
 Improving atrioventricular and/or biventricular
synchrony
Temporary pacing may be performed after an acute
MI to help control transient arrhythmias and after a
CABG.Table 1-18 classifies the various pacemakers.
One of the most critical aspects of pacer function
for a physical therapist to understand is rate modula-
tion. Rate modulation refers to the pacer’s ability to
modulate HR based on activity or physiologic
demands. Not all pacers are equipped with rate modu-
lation; therefore, some patients have HRs that may
not change with activity. In pacers with rate modula-
tion, a variety of sensors are available to allow
adjustment of HR. The type of sensor used may
impact the ability of the pacer to respond to various
exercise modalities. For more detail, refer to the
review by Collins.54
CLINICAL TIP
 If the pacemaker does not have rate modulation,
low-level activity with small increases in metabolic
demand is preferred. Assessment of RPE, BP, and
symptoms should be used to monitor tolerance.
 If the pacemaker does have rate modulation,
then the type of rate modulation used should be
considered.
 With activity sensors, HR may respond sluggishly to
activities that are smooth—such as on the bicycle
ergometer.
 For motion sensors, treadmill protocols should include
increases in both speed and grade, as changes in grade
alone may not trigger an increase in HR.
 QT sensors and ventilatory driven sensors may
require longer warm-up periods owing to delayed
responses to activity.
 Medication changes and electrolyte imbalance may
impact responsiveness of HR with QT interval
sensors.
 The upper limit of the rate modulation should be
known. When HR is at the upper limit of rate

Table 1-18 PACEMAKER CLASSIFICATION

Position Three
Position One Position Two Response to a Position Four Position Five
Chamber(s) Paced Chamber(s) Sensed Sensed Event Rate Modulation Multisite Pacing
O = None O = None O = None O = None O = None
A = Atrium A = Atrium T = Triggered R = Rate modulation A = Atrium
in response to
sensor technology
V = Ventricle V = Ventricle I = Inhibited V = Ventricle
D = Dual D = Dual (atria D = Dual (inhibited D = Dual (atrium
and ventricles) and triggered) and ventricle)
S = Manufacturer’s S = Manufacturer’s
designation for single designation for single
(atrium or ventricle) (atrium or ventricle)
Inhibited, Pending stimulus is inhibited when a spontaneous stimulation is detected
Triggered, Detection of stimulus produces an immediate stimulus in the same chamber
Rate modulation, Can adjust rate automatically based on one or more physiologic variables
Adapted from Bernstein, A., et al.: ‘‘The Revised NASPE/BPG Generic Code for Antibradycardic, Adaptive-Rate, and Multisite Pacing.
North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group,’’Pacing and Clinical Electrophysiology.
25(2):260-264, February 2002.
30 CHAPTER 1 Cardiac System
modulation, BP needs to be monitored to be sure it
is maintained.
 In individuals who do not have rate-modulated
pacers, BP response can be used to gauge intensity,
as shown in the following equation
Training SBP ¼ ðSBP max  SBP restÞ
ðintensity usually 60%  80%Þ þ SBP rest
 For example,
Training SBP ¼ ð180  120Þð½0:6 for lower limit
½0:8 for upper limitÞ þ 120
Training SBP ¼ 156-168 mm Hg
An automatic implantable cardiac defibrillator
(AICD) is used to manage uncontrollable, life-
threatening ventricular arrhythmias by sensing the
heart rhythm and defibrillating the myocardium as
necessary to return the heart to a normal rhythm.
Indications for AICD include ventricular tachycardia
and ventricular fibrillation.54
VALVE REPLACEMENT
Valve replacement is an acceptable method for treat-
ment of valvular disease. Patients with mitral and
aortic stenosis, regurgitation, or both are the primary
candidates for this surgery. Like the CABG, a median
sternotomy is the route of access to the heart.
Common valve replacements include mitral valve repla-
cements (MVR) and aortic valve replacements (AVR).
Prosthetic valves can be classified as mechanical
(bi-leaflet and tilting disc valves are commonly used)
as well as biologic valves (derived from cadavers,
porcine, or bovine tissue).
Mechanical valves are preferred if the patient is
younger than 65 years of age and is already on anticoag-
ulation therapy (commonly due to history of atrial
fibrillation or embolic cerebral vascular accident). The
benefit of mechanical valves is their durability and
long life.12 Mechanical valves also tend to be thrombo-
genic and, therefore, require lifelong adherence to
anticoagulation. For this reason, they may be contrain-
dicated in patients who have a history of previous bleed-
ing-related problems, wish to become pregnant, or
have a history of poor medication compliance. These
patients may benefit from biologic valves since there is
no need for anticoagulation therapy. Biologic valves
may also be preferred in patients older than 65 years of
age.12 Postoperative procedures and recovery from
mitral valve replacement and aortic valve replacement
surgeries are very similar to CABG.12
CARDIAC TRANSPLANTATION
Cardiac transplantation is an acceptable intervention
for the treatment of end-stage heart disease. A growing
number of facilities are performing heart transplanta-
tion, and a greater number of physical therapists are
involved in the rehabilitation of pretransplant and post-
transplant recipients. Physical therapy intervention is
vital for the success of heart transplantation, as recipi-
ents have often survived a long period of convalescence
both before and after surgery, rendering them decondi-
tioned. In general, heart transplant patients are immu-
nosuppressed and are without neurologic input to
their heart. These patients rely first on the Frank-
Starling mechanism to augment SV and then on the
catecholamine response to augment both HR and
SV. Refer to Chapter 12 for information on heart
and heart-lung transplantation.
CARDIAC MEDICATIONS
Cardiac medications are classified according to func-
tional indications, drug classes, and mechanism of
action. Cardiac drug classes are occasionally indicated
for more than one clinical diagnosis. Appendix IV
lists the functional indications, mechanisms of action,
side effects, and the generic (trade names) of these
cardiac medications:
Table IV-1 Antiarrhythmic agents
Table IV-2 Anticoagulants
Table IV-3 Antihypertensives
Table IV-3a Combination drugs for hypertension
Table IV-4 Antiplatelet agents
Table IV-5 Lipid lowering agents
Table IV-6 Positive inotropes (pressors)
Table IV-7 Thrombolytics (also known as
fibrinolytics)
Table 1-19 summarizes the presentation of digitalis
toxicity.
Physical Therapy Intervention
In the acute care setting, physical therapy intervention
is indicated for patients with cardiac impairments
that result from ACS, CHF, or status post CABG.
However, a great majority of patients who receive
physical therapy present with one or many other car-
diac impairments or diagnoses. Given the high prev-
alence of cardiac disease in the elderly population and

Table 1-19 SIGNS AND SYMPTOMS OF
DIGITALIS TOXICITY
System Affected Effects
Central nervous Drowsiness, fatigue, confusion,
system visual disturbances
Cardiac system Premature atrial and/or ventricular
contractions, paroxysmal
supraventricular tachycardia,
ventricular tachycardia, high
degrees of atrioventricular
block, ventricular fibrillation
Gastrointestinal Nausea, vomiting, diarrhea
system
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S
(eds). Cardiac Nursing (4th ed). Philadelphia: Lippincott, 2000.
the hospital admissions for the elderly, the likeli-
hood of working with a patient who has cardiac
impairment is very high. This section discusses basic
treatment guidelines for physical therapists working
with patients who have present or past cardiac
impairments.
Goals
The primary goals in treating patients with primary or
secondary cardiac pathology are55:
 Assess hemodynamic response in conjunction with
medical or surgical management during self-care
activities and functional mobility.
 Maximize activity tolerance.
 Provide patient and family education regarding
behavior modification and risk factor reduction
(especially in patients with CAD, status post MI,
PTCA, CABG, or cardiac transplant).
Basic Concepts for the Treatment of Patients
with Cardiac Dysfunction
The patient’s medical or surgical status must be consid-
ered in intervention planning, because it is inappro-
priate to treat a hemodynamically unstable patient.
A hemodynamically unstable patient is a patient who
clearly requires medical intervention to stabilize a life-
threatening condition. A patient’s status may fluctuate
on a daily or hourly basis. Box 1-2 provides general
guidelines of when to withhold physical therapy
(i.e., instances in which further medical care should
precede physical therapy).56 These are provided as
Cardiac System CHAPTER 1 31
absolute and relative indications of instability. Relative
indications of instability should be considered on a
case-by-case basis.
Once it is determined that a patient is stable at rest,
the physical therapist is able to proceed with activity
or an exercise program, or both. Figure 1-11 provides a
general guide to determining whether a patient’s
response to activity is stable or unstable.
Everything the physical therapist asks a patient to do
is an activity that requires energy and therefore needs
to be supported by the cardiac system. Although an
activity can be thought of in terms of absolute energy
requirements (i.e., metabolic equivalentsçrefer to
Table 1-12), an individual’s response to that activity is
relative to that individual’s capacity. Therefore,
although MET levels can be used to help guide the
progression of activity, the physical therapist must be
aware that even the lowest MET levels may represent
near-maximal exertion for a patient or may result in an
unstable physiologic response.
Unstable responses provide some indication that the
patient is not able to meet physiologic demands owing
to the pathologic process for the level of work that the
patient is performing. In this situation, the physical
therapist needs to consider the patient’s response to
other activities and determine whether these activities
create a stable response. If it is stable, can the patient
function independently doing that level of work?
For example, some patients may be stable walking
10 feet to the bathroom at one time, yet this activity
may require maximal exertion for the patient and there-
fore should be considered too much for the patient to
continue to do independently throughout the day.
If the patient’s response is not stable, then the thera-
pist should try to discern why it is not stable, along with
finding out if anything can be done to make the patient
stable (i.e., medical treatment may stabilize this
response). Additionally, the therapist should find the
level of function that a patient could perform with a
stable response. However, at times, patients will not be
able to be stabilized to perform activity. In these cases,
physical therapists need to determine whether a condi-
tioning program would allow the patient to meet the
necessary energy demands without becoming unstable.
Proceeding with therapy at a lower level of activity is
based on the premise that conditioning will improve
the patient’s response. The cardiac system supports
the body in its attempt to provide enough energy to per-
form work. Often, becoming strongerçincreased
peripheral muscle strength and enduranceçwill
32 CHAPTER 1 Cardiac System
BOX 1-2 INDICATIONS OF PATIENT INSTABILITY
Absolute Indications That Patient Is Unstable
and Treatment Should Be Withheld
 Decompensated congestive heart failure
 Second-degree heart block coupled with
premature ventricular contractions (PVCs) of
ventricular tachycardia at rest
 Third-degree heart block
 More than 10 PVCs per minute at rest
 Multifocal PVCs, unstable angina pectoris with
recent changes in symptoms (less than 24 hrs),
and electrocardiographic changes associated
with ischemia/injury
 Dissecting aortic aneurysm
 New onset (less than 24 hours) of atrial
fibrillation with rapid ventricular response at
rest (HR > 100 bpm)
 Chest pain with new STsegment changes on ECG
BP, Blood pressure; ECG, electrocardiogram; HR, heart rate
Data from Cahalin LP. Heart Failure. PhysTher 1996;76:520; Ellestad MH. StressTesting: Principles and Practice (4th ed)
Philadelphia: FA Davis, 1996; and Wegener NK. Rehabilitation of the Patient with Coronary Heart Disease. In RC Schlant,
RWAlexander (eds), Hurst’s the Heart (8th ed). NewYork: McGraw-Hill, 1994, p 1227.
reduce the demands on the heart at a certain absolute
activity (work) level. Figure 1-12 provides a general
guide to advancing a patient’s activity while considering
his or her response to activity.
Physical therapy intervention should include a
warm-up phase to prepare the patient for activity.
This is usually performed at a level of activity that is
lower than the expected exercise program. For example,
it may consist of supine, seated, or standing exercises.
A conditioning phase follows the warm-up period.
Very often in the acute care hospital, this conditioning
phase is part of the patient’s functional mobility
training. With patients who are independent with
functional mobility, an aerobic-based conditioning
program of walking or stationary cycling may be used
for conditioning. Finally, a cool-down or relaxation
phase of deep breathing and stretching ends the
physical therapy session.
Listed below are various ways to monitor the
patient’s activity tolerance.
Relative Indications That Patient Is Unstable and
Treatment Should Be Modified or Withheld
 Resting heart rate > 100 bpm
 Hypertensive resting BP (systolic > 160 mm Hg,
diastolic > 90 mm Hg)
 Hypotensive resting BP (systolic < 80 mm Hg)
 Myocardial infarction or extension of infarction
within the previous 2 days
 Ventricular ectopy at rest
 Atrial fibrillation with rapid ventricular
response at rest (HR > 100 bpm)
 Uncontrolled metabolic diseases
 Psychosis or other unstable psychologic
condition
1. HR: HR is the primary means of determining the
exercise intensity level for patients who are not
takingbeta-blockers or whohave non—rate-responsive
pacemakers.
 There is a linear relationship between HR and
work.
 In general, a 20- to 30-beat increase from the rest-
ing value during activity is a safe intensity level
in which a patient can exercise.
 If a patient has undergone an exercise stress test
during the hospital stay, a percentage (e.g., 60%
to 80%) of the maximum HR achieved during
the test can be calculated to determine the exercise
intensity.57
 An example of a disproportionate HR response to
low-level activity (bed or seated exercises or
ambulation in room) is an HR of more than
120 bpm or less than 50 bpm.57
 HR recovery (HRR), which provides an indica-
tion of reduced parasympathetic activity and

FIGURE 1-11
Determination of stable vs. unstable responses to activity/exercise. BP, Blood pressure; CHF, congestive
heart failure; HR, heart rate; PVC, premature ventricular contraction; RPE, rating of perceived exertion;
Rx, treatment.
is an indicator of all-cause mortality, can be
utilized to document improvement of toler-
ance to functional demands.58 HRR is the
absolute difference between peak HR achie-
ved with exercise minus the HR at 60
seconds following the completion of exercise
(HRR60sec).59 An abnormal HRR at 1 minute,
after a treadmill test, is reported to be a decrease
of 12 bpm or less with a cool-down period
and less than 18 bpm without a cool-down
period.60
 When prescribing activity intensity for a patient
taking beta-blockers, the HR should not exceed
20 beats above resting HR.
 If prescribing activity intensity using HR for
patients with an AICD, the exercise target HR
Cardiac System CHAPTER 1 33
should be 20 to 30 beats below the threshold rate
on the defibrillator.57
 HR cannot be used to prescribe exercise status
post heart transplant secondary to denervation
of the heart during transplantation.
 Baseline HR and recent changes in medications
should always be considered before beginning
an exercise session.
2. BP: Refer to the Cardiac Evaluation section
regarding BP measurements and Table 1-7 for BP
ranges. Examples of a disproportionate response
to exercise are a systolic pressure decrease of
10 mm Hg below the resting value, a hypertensive
systolic response of more than 180 mm Hg, or a
hypertensive diastolic response of more than
110 mm Hg.57
34 CHAPTER 1 Cardiac System
FIGURE 1-12
Physical therapy activity examination algorithm. AROM, Active range of motion; LE, lower extremity;
PROM, passive range of motion; UE, upper extremity.
 If the patient is on a pacemaker that does not have
rate modulation, BP response can be used to gauge
intensity. Refer to the Cardiac Pacemaker Implan-
tation and Automatic Implantable Cardiac Defib-
rillator section for a discussion on pacemakers.
3. The Borg RPE Scale (6-20), the Borg CR10 Scale, and
the Borg CR100 (centiMax) Scale:
 The Borg RPE Scale (6-20) is used mainly for
overall ratings (R) of perceived (P) exertion (E)
during physical training and rehabilitation and
has evolved to be the classic means of objectively
documenting subjective feelings of exercise
intensity. This scale can also be used for breath-
lessness and muscle fatigue. 61,62
 The Borg CR10 Scale and the Borg CR100
(centiMax) Scale are general scales for measuring
intensities of most kinds of perceptions, experi-
ences, and feelings.62
 The Borg CR10 Scale is also used to measure rat-
ings of perceived exertion (RPE).
 The Borg CR100 (centiMax) Scale was developed
because a more finely graded scale became neces-
sary in certain situations.62
 These scales can be easily used to monitor exercise
intensity for the purpose of exercise prescription
in a variety of patient populations and it is the pre-
ferred method of prescribing exercise intensity
for a patient taking beta blockers.

 A general guideline for everyone is to exercise to a
point no greater than 5 on the 10-point scale and
no greater than 13 on the 6-20 scale.57
 In order for the scales tobe utilized inthe most safe,
reliable, and valid manner, complete instructions
about the scale and its usages must be provided to
the patient before its implementation. These
instructions are included with the scales and
should be followed exactly and not be modified.61
These scales are available at borgperception@
telia.com or at http://www.borgproducts.com.
4. Rate pressure product (RPP) is HR  SBP and is an
indication of myocardial oxygen demand.
 If a patient undergoes maximal exercise testing
and has myocardial ischemia, RPP can be calcu-
lated at the point when ischemia is occurring to
establish the patient’s ischemic threshold.
 This RPP value can then be used during exercise
to provide a safe guideline of exercise intensity.
5. Heart sounds: Refer to the section on Auscultation
and Table 1-9 for normal and abnormal heart
sounds.
 The onset of murmurs, S3 heart sounds, or S4
heart sounds during treatment may be detected
and could indicate a decline in cardiac function
during activity. This finding should be brought
to the attention of the nurse and physician.
6. Breath sounds: Refer to Chapter 2 for a discussion of
lung auscultation and the interpretation of breath
sounds.
 The presence of or increase in bibasilar crackles
during activity may be indicative of acute CHF.
Activity should be terminated and the nurse and
physician notified.
7. ECG rhythm: Refer to the Electrocardiogram sec-
tion and the Rhythm and Conduction Disturbance
section.
 When treating patients who are being
continuously monitoredbyan ECG, itis important
to know their baseline rhythm, the most recently
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 Description of
ECG Characteristics
Appendix 1-A and Associated Causes

Table 1-A.1 ELECTROCARDIOGRAPHIC (ECG) CHARACTERISTICS AND CAUSES OF ATRIAL RHYTHMS

Name ECG Characteristics
Supraventricular tachycardia Regular rhythm; rate of 160-
250 bpm; may originate
from any location above
atrioventricular node; can
be paroxysmal (comes and
goes without reason).
Atrial flutter Regular or irregular rhythm;
atrial rate of 250-350;
ventricular rate is variable
and depends on the
conduction ratio
(atrial:ventricular, e.g.,
atrial rate = 250,
ventricular rate = 125; 2:1
classic saw tooth P waves.)
Atrial fibrillation (AF) Irregular rhythm; atrial has
no rate (just quivers);
ventricular rate varies.
Premature atrial Irregular rhythm (can be
contractions regularly irregular, i.e.,
skip every third beat);
rate normal 60-100.
AF, Atrial fibrillation; CAD, coronary artery disease; CHF, congestive heart failure; RHD, rheumatoid heart disease.
Data from Aehlert B. ACLS Quick Review Study Guide. St. Louis: Mosby, 1993; and Chung EK. Manual of Cardiac Arrhythmias. Boston:
Butterworth-Heinemann, 1986.
Common Causes
Rheumatoid heart disease
(RHD), mitral valve
prolapse, cor pulmonale,
digitalis toxicity.
Mitral stenosis, CAD,
hypertension.
One of most commonly
encountered rhythms,
CHF, CAD, RHD,
hypertension, cor
pulmonale.
Normal people with caffeine,
smoking, emotional
disturbances; abnormal
with CAD, CHF,
electrolyte disturbances.
PT Consideration
May produce palpitations,
chest tightness, dizziness,
anxiety, apprehension,
weakness; PTwould not
treat if in supraventricular
tachycardia until
controlled.
Signs and symptoms
depend on presence or
absence of heart disease
but can lead to CHF,
palpitations, angina, and
syncope if cardiac output
decreases far enough to
reduce myocardial and
cerebral blood flow;
PT treatment would
depend on tolerance to
the rhythm.
Can produce CHF, syncope
secondary to no ‘‘atrial
kick’’; if new diagnosis,
hold PTuntil medical
treatment; if chronic and
not in CHF, would treat
with caution.
Usually asymptomatic but
needs to be considered
with other cardiac issues
at time of treatment; can
proceed with treatment
with close monitoring;
if they are consistent and
increasing, can progress
to AF.

38

Table 1-A.2 ELECTROCARDIOGRAPHIC (ECG) CHARACTERISTICS AND CAUSES OF VENTRICULAR
RHYTHMS
Name
Agonal rhythm
Ventricular tachycardia
(VT)
Multifocal VT (torsades
de pointes)
Premature ventricular
contractions (PVCs)
(focal = one ectopic foci
and all look the same;
multifocal = more than
one ectopic foci and will
have different wave
forms)
Ventricular fibrillation
Idioventricular rhythm
CAD, Coronary artery disease; CHF, congestive heart failure; CO, cardiac output; MI, myocardial infarction; MVP, mitral valve prolapse;VT,
ventricular tachycardia.
Data from Aehlert B. ACLS Quick Review Study Guide. St. Louis: Mosby, 1994; and Chung EK. Manual of Cardiac Arrhythmias. Boston:
Butterworth-Heinemann, 1986.
Description of ECG Characteristics and Associated Causes
ECG Characteristics Common Causes
Irregular rhythm, rate < 20, Near death
no P wave
Usually regular rhythm, rate CAD most common after
> 100, no P wave or with acute MI; may occur in
retrograde conduction and rheumatoid heart disease,
appears after the QRS cardiomyopathy,
complex hypertension
Irregular rhythm, rate > 150, Drug induced with
no P waves antiarrhythmic medicines
(quinidine, procainamide);
hypokalemia;
hypomagnesemia; MI;
hypothermia
Irregular rhythm, (can be In normal individuals,
regularly irregular, i.e., secondary to caffeine,
skipped beat every fourth smoking, emotional
beat); rate varies but is disturbances; CAD, MI,
usually normal 60-100; cardiomyopathy, MVP,
couplet is 2 in a row; digitalis toxicity
bigeminy is every other
beat; trigeminy is every
third beat
Chaotic Severe heart disease most
common after acute MI,
hyperkalemia or
hypokalemia, hypercalcemia,
electrocution
Essentially regular rhythm, Advanced heart disease; high CHF is common secondary
rate 20-40 degree of atrioventricular
block; usually a terminal
arrhythmia
APPENDIX 1-A 39
PT Considerations
Do not treat
Do not treat; patient needs
immediate medical
assistance; patient may
be stable (maintain CO)
for a short while but can
progress quickly to
unstable (no CO)ç called
pulseless VT.
Do not treat; patient needs
immediate medical
assistance.
Frequency will dictate effect
on CO; monitor
electrocardiograph with
treatment; can progress
toVT; more likely if
multifocal in nature or
if > 6 per minute; stop
treatment or rest if
change in frequency
or quality.
Do not treat; needs
immediate medical
assistance.
to slow rates; do not treat
unless rhythm well
tolerated.
40 APPENDIX 1-A Description of ECG Characteristics and Associated Causes

Table 1-A.3 ELECTROCARDIOGRAPHIC (ECG) CHARACTERISTICS AND CAUSES OF JUNCTIONAL

RHYTHMS

Name ECG Characteristics Common Causes PT Considerations

Junctional escape rhythm
Junctional tachycardia
AF, Atrial fibrillation; AV, atrioventricular; CHF, congestive heart failure.
Data from Aehlert B. ACLS Quick Review Study Guide. St. Louis: Mosby, 1994; and Chung EK. Manual of Cardiac Arrhythmias. Boston:
Butterworth-Heinemann, 1986.
Regular rhythm, rate 20-40;
inverted P wave before or
after QRS complex; starts
with ectopic foci in AV
junction tissue
Regular rhythm; rate 100-180;
P wave as above
Usual cause is physiologic to If occasional and
control the ventricles in AV
block, sinus bradycardia,
AF, sinoatrial block, drug
intoxication
Most common with chronic May produce or exacerbate
AF; also with coronary
artery disease, rheumatoid
heart disease, and
cardiomyopathy
intermittent during
bradycardia or chronic
AF, usually insignificant
and can treat (with close
watch of possible
worsening condition via
symptoms and vital
signs); if consistent and
present secondary to AV
block, acute myocardial
infarction, or drug
intoxication, can be
symptomatic with CHF.
(See Box 1-2.)
symptoms of CHF or
angina secondary to
decreased cardiac output;
PT treatment depends on
patient toleranceçif new,
onset should wait for
medical treatment.

Table 1-A.4 ELECTROCARDIOGRAPHIC CHARACTERISTICS AND CAUSES OF ATRIOVENTRICULAR
BLOCKS
Name
First-degree AV block
Second-degree AV block
type I (Wenkebach,
Mobitz I)
Second-degree AV block
type II (Mobitz II)
Third-degree AV block
(complete heart block)
AV, Atrioventricular; CHF, congestive heart failure; MI, myocardial infarction.
Data from Aehlert B. ACLS Quick Review Study Guide. St. Louis: Mosby, 1994; and Chung EK. Manual of Cardiac Arrhythmias. Boston:
Butterworth-Heinemann, 1986.
Description of ECG Characteristics and Associated Causes
ECG Characteristics
Regular rhythm, rate normal
60-100, prolonged PR
interval > 0.2 (constant).
Irregular rhythm, atrial rate
> ventricular rate, usually
both 60-100; PR interval
lengthens until P wave
appears without a QRS
complex.
Irregular rhythm, atrial rate
> ventricular rate, PR
interval may be normal or
prolonged but is constant
for each conducted QRS.
Regular rhythm, atrial rate
> ventricular rate.
Common Causes
Elderly with heart disease, If chronic, need to be more
acute myocarditis, acute MI
Acute infection, acute MI Symptoms are uncommon,
Anteroseptal MI
Anteroseptal MI, drug
intoxication, infections,
electrolyte imbalances,
coronary artery disease,
degenerative sclerotic
process of AVconduction
system
APPENDIX 1-A 41
PT Considerations
cautious of underlying
heart disease; if new
onset, monitor closely
for progression to higher
level block.
as above.
CHF is common; can have
dizziness, fainting,
complete
unconsciousness; may
need pacing and PT
treatment; should be held
for medical management.
Severe CHF; patient will
need medical
management; a pacer
(temporary or permanent,
depending on
reversibility of etiology)
is almost always
necessary.
 Common
Appendix 1-B Rhythm Disturbances

FIGURE 1-B.1
Paroxysmal supraventricular tachycardia. Note development from normal sinus rhythm. (From Walsh M,
Crumbie A, Reveley S. Nurse Practitioners: Clinical Skills and Professional Issues. Boston:
Butterworth-Heinemann, 1993.)

FIGURE 1-B.2
Atrial flutter. Note regular rhythm (P waves), but ventricular rhythm depends on conduction pattern.
(From Walsh M, Crumbie A, Reveley S: Nurse Practitioners: Clinical Skills and Professional Issues.
Boston: Butterworth-Heinemann, 1993.)

42
 Common Rhythm Disturbances APPENDIX 1-B 43

FIGURE 1-B.3
Atrial fibrillation. Note the irregular rhythm and absence of normal P waves. (From Walsh M, Crumbie A,
Reveley S: Nurse Practitioners: Clinical Skills and Professional Issues. Boston: Butterworth-Heinemann,
1993.)

FIGURE 1-B.4
Ventricular tachycardia. Rate 100-170 beats per minute. No P waves, broad electrocardiographic wave
complexes. (From Walsh M, Crumbie A, Reveley S: Nurse Practitioners: Clinical Skills and Professional
Issues. Boston: Butterworth-Heinemann, 1993.)

FIGURE 1-B.5
Ventricular ectopy with refractory period afterward. (From Walsh M, Crumbie A, Reveley S: Nurse
Practitioners: Clinical Skills and Professional Issues. Boston: Butterworth-Heinemann, 1993.)
44 APPENDIX 1-B Common Rhythm Disturbances

FIGURE 1-B.6
Sinus rhythm with premature ventricular contractions. (From Chung EK. Manual of Cardiac
Arrhythmias. Boston: Butterworth-Heinemann, 1986.)
 Common Rhythm Disturbances APPENDIX 1-B 45

FIGURE 1-B.7
Ventricular fibrillation. (From Walsh M, Crumbie A, Reveley S: Nurse Practitioners: Clinical Skills and
Professional Issues. Boston: Butterworth-Heinemann, 1993.)
46 APPENDIX 1-B Common Rhythm Disturbances

D
FIGURE 1-B.8
A to D, Degrees of heart block. (From Walsh M, Crumbie A, Reveley S: Nurse Practitioners: Clinical
Skills and Professional Issues. Boston: Butterworth-Heinemann, 1993.)
 2 Respiratory System

Michele P. West INTRODUCTION

Jaime C. Paz To safely and effectively provide exercise, bronchopulmonary hygiene
Kara O’Leary program(s), or both to patients with respiratory dysfunction, physical
therapists require an understanding of the respiratory system and of the
principles of gas exchange. The objectives of this chapter are to provide
the following:
1. A brief review of the structure and function of the respiratory
system
2. An overview of respiratory evaluation, including physical examination
and diagnostic testing
3. A description of respiratory diseases and disorders, including clinical
findings, medical-surgical management, and physical therapy
intervention

CLINICAL TIP
 Ventilation is defined as gas (oxygen [O2] and carbon dioxide [CO2])
transport into and out of lungs, and respiration is defined as gas
exchange across the alveolar-capillary and capillary-tissue interfaces. The
term pulmonary primarily refers to the lungs, their airways, and their
vascular system.1

The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:
 6B: Impaired Aerobic Capacity/Endurance Associated with
Deconditioning
 6C: Impaired Ventilation, Respiration/Gas Exchange, and Aerobic
Capacity/Endurance Associated with Airway Clearance Dysfunction
 6E: Impaired Ventilation and Respiration/Gas Exchange Associated
withVentilatory Pump Dysfunction or Failure
 6F: Impaired Ventilation and Respiration/Gas Exchange Associated
with Respiratory Failure
 6G: Impaired Ventilation, Respiration/Gas Exchange, and Aerobic
Capacity/Endurance Associated with Respiratory Failure in the
Neonate
Please refer to the back cover of this book for a complete list of the
preferred practice patterns, as individual patient conditions are highly
variable and other practice patterns may be applicable.

47
48 CHAPTER 2 Respiratory System

Table 2-1 STRUCTURE AND FUNCTION OF PRIMARY ORGANS OF THE RESPIRATORY SYSTEM
Structure Description Function
Nose Paired mucosal-lined nasal cavities supported by bone Conduit that filters, warms, and humidifies
and cartilage. air entering lungs.
Pharynx Passageway that connects nasal and oral cavities to larynx, Conduit for air and food.
and oral cavity to esophagus. Facilitates exposure of immune system to
Subdivisions naso-, oro-, and laryngopharynx. inhaled antigens.
Larynx Passageway that connects pharynx to trachea. Prevents food from entering the lower
Opening (glottis) is covered by vocal folds or respiratory tract.
by the epiglottis during swallowing. Voice production.
Trachea Flexible tube composed of C-shaped cartilaginous rings Cleans, warms, and moistens incoming air.
that are connected posteriorly to the trachealis muscle
Divides into the left and right main stem bronchi.
Bronchial Right and left main stem bronchi subdivide within Warms and moistens incoming air from
tree each lung into secondary bronchi, tertiary bronchi, trachea to alveoli.
and bronchioles, which contain smooth muscle. Smooth muscle constriction alters airflow.
Lungs Paired organs located within pleural cavities of the thorax. Contains air passageways distal to main stem
The right lung has three lobes, and the left lung has bronchi, alveoli, and respiratory
two lobes. membranes.
Alveoli Microscopic sacs at end of bronchial tree immediately Primary gas exchange site.
adjacent to pulmonary capillaries. Surfactant lines the alveoli to decrease surface
Functional unit of the lung. tension and prevent complete closure
during exhalation.
Pleurae Double-layered, continuous serous membrane Produces lubricating fluid that allows smooth
lining the inside of the thoracic cavity. gliding of lungs within the thorax.
Divided into parietal (outer) pleura and visceral Potential space between parietal and visceral
(inner) pleura. pleura.
Data from Marieb E: Human Anatomy and Physiology (3rd ed). Redwood City, CA: Benjamin-Cummings, 1995; MoldoverJR, SteinJ,
Krug PG: Cardiopulmonary Physiology. In EG Gonzalez, SJ Myers, JE Edelstein, et al: Downey & Darling’s Physiological Basis of
Rehabilitation Medicine (3rd ed) Philadelphia: Butterworth-Heinemann, 2001.
other controls voluntary respiration. Automatic respira-
STRUCTURE tion is controlled by the medullary respiratory center
in the brain stem, which is responsible for the rhythmic-
The primary organs and muscles of the respiratory ity of breathing. The pneumotaxic center located in
system are outlined in Tables 2-1 and 2-2, respectively. the pons controls respiratory rate and depth.Voluntary
A schematic of the pulmonary system within the respiration is mediated by the cerebral cortex, which
thorax is presented in Figure 2-1. sends impulses directly to the motor neurons of respira-
tory muscles.2,3
Chemical Control
FUNCTION
Arterial levels of CO2 (PCO2), hydrogen ions (H+), and
To accomplish ventilation and respiration, the respira- O2 (PO2) can modify the rate and depth of respiration.
tory system is regulated by many neural, chemical, and To maintain homeostasis in the body, specialized
nonchemical mechanisms, which are discussed in the chemoreceptors on the carotid arteries and aortic arch
sections that follow. (carotid and aortic bodies, respectively) will either
respond to a rise in PCO2 and H+ or to a fall in PO2.
Neural Control Stimulation of these chemoreceptors results in trans-
Respiration is regulated by two separate neural mech- mission of impulses to the respiratorycenters to increase
anisms: One controls automatic respiration, and the or decrease the rate or depth, or both, of respiration.

Table 2-2 PRIMARY AND ACCESSORY RESPIRATORY MUSCLES WITH ASSOCIATED INNERVATION
Respiratory Muscles
Primary inspiratory muscles Diaphragm
External intercostals
Internal intercostals
Accessory inspiratory muscles Trapezius
Sternocleidomastoid
Scalenes
Pectorals
Serratus anterior
Latissimus dorsi
Primary expiratory muscles Rectus abdominus
External obliques
Internal obliques
Accessory expiratory muscles Latissimus dorsi
Data from Kendall FP, McCreary EK (eds): Muscles:Testing and Function (3rd ed). Baltimore, Lippincott,Williams, and Wilkins, 1983;
RothsteinJM, Roy SH,Wolf SL:The Rehabilitation Specialist’s Handbook (2nd ed). Philadelphia, FA Davis, 1998.
For example, an increase in PCO2 would increase the
respiratory rate to help increase the amount of CO2
exhaled and ultimately lower the PCO2 levels in arterial
blood. Chemoreceptors are also found in the medulla
and will respond to a rise in PCO2 and H+ as well.4,5
Nonchemical Influences
Coughing, bronchoconstriction, and mucus secretion
occur in the lungs as protective reflexes to irritants
such as smoke or dust. Emotions, stressors, pain, and
visceral reflexes from lung tissue and other organ
systems can also influence respiratory rate and depth.
Respiratory Mechanics
After the respiratory muscles receive signals from the
respiratory centers, two motions (bucket and pump
handle) occur simultaneously with thoracic stabiliza-
tion to create pressure changes within the thorax.
Pressure changes result in the bulk flow of air (ventila-
tion) in and out of the lungs.When alveolar pressure is
less than atmospheric pressure, inspiration occurs;
when alveolar pressure is greater than atmospheric
pressure, expiration occurs. Changes in shape of the
thorax during inspiration and expiration result in
these pressure changes between the atmosphere and
the alveolar spaces. During inspiration, the diaphragm
lowers, and the rib cage elevates and expands in anterior
(pump handle) and lateral (bucket handle) directions
Respiratory System CHAPTER 2 49
Innervation
Phrenic nerve (C3-C5)
Spinal segmentsT1-T9
Spinal segmentsT1-T9
Cervical nerve (C1-C4), spinal part of cranial nerve XI
Spinal part of cranial nerve XI
Cervical/brachial plexus branches (C3-C8,T1)
Medial/lateral pectoral nerve (C5-C8,T1)
Long thoracic nerve (C5-C7)
Thoracodorsal nerve (C5-C8)
Spinal segmentsT5-T12
Spinal segmentsT7-T12
Spinal segmentsT8-T12
Thoracodorsal nerve (C5-C8)
to decrease the intrathoracic pressure. During expira-
tion, the diaphragm relaxes passively and elevates,
whereas the rib cage lowers to its resting position to
increase the intrathoracic pressure. These motions are
schematically outlined in Figure 2-2.6,7
Gas Exchange
Once air has reached the alveolar spaces, gas exchange
can occur at the alveolar-capillary membrane.
Diffusion of gases through the membrane is affected
by the following:
 A concentration gradient in which gases will diffuse
from areas of high concentration to areas of low
concentration (e.g., alveolar O2 = 100 mm Hg !
capillary O2 = 40 mm Hg)
 Surface area, or the total amount of alveolar-capillary
interface available for gas exchange (e.g., the break-
down of alveolar membranes that occurs in emphy-
sema will reduce the amount of surface area
available for gas exchange)
 The thickness of the barrier (membrane) between the
two areas involved (e.g., retained secretions in the
alveolar spaces will impede gas exchange through
the membrane)
Ventilation and Perfusion Ratio
Gas exchange is optimized when the ratio of air
flow (ventilation ½V_  ) to blood flow (perfusion ½Q_  )
50 CHAPTER 2 Respiratory System

approaches a 1:1 relationship. However, the actual V_ = Q_
ratio is 0.8, as alveolar ventilation is approxi-
mately equal to 4 liters per minute and pulmonary
blood flow is approximately equal to 5 liters per
minute.2,8,9
Gravity, body position, and cardiopulmonary dys-
function can influence this ratio. Ventilation is opti-
mized in areas of least resistance. For example, when a
person is in a sitting position, the upper lobes initially
receive more ventilation than the lower lobes; however,

B
FIGURE 2-1
A, Right lung positioned in the thorax. Bony landmarks assist in identifying normal right lung configuration.
B, Anterior view of the lungs in the thorax in conjunction with bony landmarks. Left upper lobe is divided
into apical and left lingula, which match the general position of the right upper and middle lobes.

C
FIGURE 2-1 Cont’d
C, Posterior view of the lungs in conjunction with bony landmarks. (From Ellis E, AlisonJ [eds].
Key Issues in Cardiorespiratory Physiotherapy. Oxford, UK: Butterworth-Heinemann, 1992;12.)
the lower lobes will have the largest net change in
ventilation.
Perfusion is greatest in gravity-dependent areas. For
example, when a person is in a sitting position, perfu-
sion is the greatest at the base of the lungs; when a
person is in a left side-lying position, the left lung
receives the most blood.
_
A V_ = Q mismatch (inequality in the relationship
between ventilation and perfusion) can occur in certain
situations. Two terms that are associated with V_ = Q_
mismatch are dead space and shunt. Dead space occurs
when ventilation is in excess of perfusion, as with a pul-
monary embolus. A shunt occurs when perfusion is
in excess of ventilation, as in alveolar collapse from
secretion retention. These conditions are shown in
Figure 2-3.
Gas Transport
O2 is transported away from the lungs to the tissues in
two forms: dissolved in plasma (PO2) or chemically
bound to hemoglobin on a red blood cell (oxyhemo-
globin). As a by-product of cellular metabolism, CO2
is transported away from the tissues to the lungs in
three forms: dissolved in plasma (PCO2), chemically
bound to hemoglobin (carboxyhemoglobin), and as
bicarbonate.
Respiratory System CHAPTER 2 51
Approximately 97% of O2 transported from the
lungs is carried in chemical combination with hemo-
globin. Ninety-three percent of CO2 transport occurs
in the combined forms of carbaminohemoglobin, and
bicarbonate. A smaller percentage, 3% of O2 and 7%
of CO2, is transported in dissolved forms.10 Dissolved
O2 and CO2 exert a partial pressure within the plasma
and can be measured by sampling arterial, venous, or
mixed venous blood.11 See the Arterial Blood Gas
Analysis section for further description of this process.
EVALUATION
Respiratory evaluation is composed of patient history,
physical examination, and interpretation of diagnostic
test results.
Patient History
In addition to the general chart review presented in
Appendix I-A, other relevant information regarding
respiratory dysfunction that should be ascertained
from the chart review or patient interview is listed
below.11-13
 History of smoking, including packs per day or pack
years (packs per day  number of years smoked)
52 CHAPTER 2 Respiratory System

FIGURE 2-2
Respiratory mechanics (bucket and pump handle motions). (From Snell RS [eds]. Clinical Anatomy for
Medical Students [5th ed]. Boston: Little, Brown, 1995;89.)

and the amount of time that smoking has been
discontinued (if applicable).
 Presence, history, and amount of O2 therapy at rest,
with activity, or both.
 Exposure to environmental or occupational toxins
(e.g., asbestos).
 Historyof pneumonia, thoracic procedures, or surgery.
 History of assisted ventilation or intubation with
mechanical ventilation.
 History or current reports of dyspnea either at rest
or with exertion. Dyspnea is the subjective com-
plaint of difficulty with respiration, also known as
 Respiratory System CHAPTER 2 53

Bronchiole

Alveoli

Capillary

A B C
FIGURE 2-3
Ventilation and perfusion mismatch. A, Normal alveolar ventilation. B, Capillary shunt. C, Alveolar dead
space. (Courtesy Michele West.)

shortness of breath. A visual analog scale or ratio Physical Examination

scale (Modified Borg scale) can be used to obtain a
The physical examination of the respiratory system
measurement of dyspnea. The American Thoracic
consists of inspection, auscultation, palpation, medi-
Society Dyspnea Scale can be found in Table 2-3.
ate percussion, and cough examination. Suggested
Note: The abbreviation DOE represents ‘‘dyspnea
guidelines for physical therapy intervention(s) that
on exertion.’’
are based on examination findings and diagnostic
 Level of activity before admittance.
test results are found at the end of this chapter.
 History of baseline sputum production.
 Sleeping position and number of pillows used. INSPECTION
A wealth of information can be gathered by simple
CLINICAL TIP observation of the patient at rest and with activity.
 Measurement of dyspnea at rest and with activity
Physical observation should proceed in a systematic
can be correlated with respiratory rate and used
fashion and include the following:
in goal writing (e.g., patient will ascend/descend 10
 General appearance and level of alertness.
stairs with one rail with reported dyspnea < 2/10).
 Ease of phonation.
 Another way of assessing dyspnea is to count the
 Skin color.
number of words a person can speak per breath. For
 Posture and chest shape.
example, a patient who is only able to speak one to
 Respiratory pattern (including assessment of rate
two words per breath will be noticeably more
[12 to 20 breaths per minute is normal], depth,
dyspneic than a person who can speak a full
ratio of inspiration to expiration [one to two is
sentence per breath.
normal], sequence of chest wall movement dur-
ing inspiration and expiration, comfort, presence

Table 2-3 AMERICAN THORACIC SOCIETY DYSPNEA SCALE

Grade Degree
0 None Not troubled with breathlessness except with strenuous exercise
1 Slight Troubled by shortness of breath when hurrying on the level or walking up a slight hill
2 Moderate Walks slower than people of the same age on the level because of breathlessness,
or has to stop for breath when walking at own pace on the level
3 Severe Stops for breath after walking about 100 yards or after a few minutes on the level
4 Very severe Too breathless to leave the house or breathless when dressing or undressing
From Brooks SM: Surveillance for respiratory hazards. ATS News 1982;8:12-16.
54 CHAPTER 2 Respiratory System

of accessory muscle use, and symmetry). Respir-

atory patterns vary among individuals and
may be influenced by (1) pain, (2) emotion, (3)
body temperature, (4) sleep, (5) body position,
(6) activity level, and (7) the presence of pulmonary,
cardiac, metabolic, or nervous system disease.
Table 2-4 provides a description of breathing
patterns.
 Presence of digital clubbing.
 Presence of supplemental O2 and other medical
equipment. (Refer to Appendix III-A.)
 Presence and location of surgical incisions.
CLINICAL TIP
 The optimal time, clinically, to examine a
patient’s breathing pattern is when he or she
is unaware of the inspection. Knowledge of
the physical examination can influence the
patient’s respiratory pattern. Therefore, compare
the patient’s respiratory pattern while he or she is
asleep with the patient’s respiratory pattern while
he or she is awake, or compare the patient’s
respiratory pattern during conversation at rest with
his or her respiratory pattern during activity.

Table 2-4 DESCRIPTION OF BREATHING PATTERNS AND THEIR ASSOCIATED CONDITIONS

Breathing Pattern Description Associated with

Apnea Lack of airflow to the lungs for Airway obstruction, cardiopulmonary arrest,
> 15 seconds. alterations of the respiratory center,
narcotic overdose
Biot’s respirations Constant increased rate and depth of Elevated intracranial pressure, meningitis
respiration followed by periods of
apnea of varying lengths.
Bradypnea Respiratory rate < 12 breaths per minute. Use of sedatives, narcotics, or alcohol;
neurologic or metabolic disorders;
excessive fatigue
Cheyne-Stokes Increasing depth of respiration followed Elevated intracranial pressure, CHF, narcotic
respirations by a period of apnea. overdose
Hyperpnea Increased depth of respiration. Activity, pulmonary infections, CHF
Hyperventilation Increased rate and depth of respiration Anxiety, nervousness, metabolic acidosis
resulting in decreased PCO2.
Hypoventilation Decreased rate and depth of respiration Sedation or somnolence, neurologic
resulting in increased PCO2. depression of respiratory centers,
overmedication, metabolic alkalosis
Kussmaul’s Increased regular rate and depth Diabetic ketoacidosis, renal failure
respirations of respiration.
Orthopnea Dyspnea that occurs in a flat supine Chronic lung disease, CHF
position. Relief occurs with more
upright sitting or standing.
Paradoxical Inward abdominal or chest wall movement Diaphragm paralysis, respiratory muscle
respirations with inspiration and outward movement fatigue, chest wall trauma
with expiration.
Sighing respirations The presence of a sigh > 2-3 times per minute. Angina, anxiety, dyspnea
Tachypnea Respiratory rate > 20 breaths per minute. Acute respiratory distress, fever, pain,
emotions, anemia
CHF, Congestive heart failure; PCO2 , partial pressure of carbon dioxide.
Data from Kersten LD: Comprehensive Respiratory Nursing: A Decision-Making Approach. Philadelphia, 1989, Saunders; DesJardinsT,
Burton GG: Clinical Manifestations and Assessment of Respiratory Disease (3rd ed.), St. Louis: Mosby, 1995.

 Objective observations of respiratory rate may
not always be consistent with a patient’s
subjective complaints of dyspnea. For example,
a patient may complain of shortness of breath
but have a respiratory rate within normal limits.
Therefore, the patient’s subjective complaints,
rather than the objective observations, may be a
more accurate measure of treatment intensity.
AUSCULTATION
Auscultation is the process of listening to the sounds
of air passing through the tracheobronchial tree and
alveolar spaces. The sounds of airflow normally dissi-
pate from proximal to distal airways, making the
sounds less audible in the periphery as compared with
the central airways. Alterations in airflow and respira-
tory effort result in distinctive sounds within the
thoracic cavity that may indicate pulmonary disease
or dysfunction.
Auscultation proceeds in a systematic, cephalocau-
dal fashion. Breath sounds on the left and right sides
are compared in the anterior, lateral, and posterior seg-
ments of the chest wall, as shown in Figure 2-4.The dia-
phragm (flat side) of the stethoscope should be used
for auscultation. The patient should be seated or lying
comfortably in a position that allows access to all lung
fields. Full inspirations and expirations are performed
by the patient through the mouth, as the clinician lis-
tens to the entire cycle of respiration before moving
the stethoscope to another lung segment.
There are normal and abnormal (adventitious)
breath sounds. Breath sounds should be documented
according to the location and the phase of respiration
A B
FIGURE 2-4
Landmarks for lung auscultation on (A) anterior, (B) posterior, and (C) lateral aspects of the chest wall.
(Courtesy Peter P.Wu.)
Respiratory System CHAPTER 2 55
(i.e., inspiration, expiration, or both) and in compari-
son with the opposite lung.
NORMAL BREATH SOUNDS
Tracheal, Bronchial, or Bronchovesicular Sounds.
Normal tracheal or bronchial breath sounds are loud
tubular sounds that are heard over the proximal air-
ways, such as the trachea and main stem bronchi. A
pause is heard between inspiration and expiration,
with the expiratory phase being longer than the inspira-
tory phase. Normal bronchovesicular sounds are very
similar to bronchial breath sounds; however, there is
no pause between inspiration and expiration.11,12
Vesicular Sounds. Vesicular sounds are soft rustling
sounds that are heard over the more distal airways and
lung parenchyma. Inspiration is longer and more pro-
nounced than expiration, as a decrease in airway
lumen during expiration limits transmission of airflow
sounds.11,12
Note: In most reference books, a distinction
between normal bronchial and bronchovesicular
sounds is made to help with standardization of termi-
nology. This distinction, however, is often not used
in the clinical setting.
CLINICAL TIP
 Clinically, tracheal or bronchial and vesicular breath
sounds are generally documented as ‘‘normal’’ or
‘‘clear’’ breath sounds; however, the use of tracheal
or vesicular breath sounds is more accurate. The
abbreviation CTA is also frequently used and stands
for ‘‘clear to auscultation.’’
ABNORMAL BREATH SOUNDS. Breath sounds are
abnormal if they are heard outside their usual location
C
56 CHAPTER 2 Respiratory System
in the chest or if they are qualitatively different from
normal breath sounds.14 Abnormal breath sounds with
possible sources are outlined in the following table:
Sound Possible Etiology
Bronchial (abnormal if Fluid or secretion
heard in areas where consolidation (airlessness)
vesicular sounds should that could occur with
be present) pneumonia
Decreased or Hypoventilation, severe
diminished (less audible) congestion, or emphysema
Absent Pneumothorax or lung
collapse
ADVENTITIOUS BREATH SOUNDS. Adventitious
breath sounds occur from alterations or turbulence in
airflow through the tracheobronchial tree and lung pa-
renchyma. These sounds can be divided into continu-
ous (wheezes and rhonchi) or discontinuous (crackles)
sounds.12,14
Continuous Sounds.
Wheeze. Wheezes occur most commonly with
airway obstruction from bronchoconstriction or
retained secretions and are commonly heard on expira-
tion. Wheezes may also be present during inspiration
if the obstruction is significant enough. Wheezes can
be high pitched (usually from bronchospasm or con-
striction, as in asthma) or low pitched (usually from
secretions, as in pneumonia).
Rhonchi. Low-pitched or ‘‘snoring’’ sounds that are
continuous characterize rhonchi. These sounds are
generally associated with large airway obstruction,
generally from secretions lining the airways.
CLINICAL TIP
 The American Thoracic Society and American
College of Chest Physicians have discouraged use
of the term rhonchi, recommending instead that
the term wheezes be used for all continuous
adventitious breath sounds.15 Many academic
institutions and hospitals continue to teach and
practice use of the term rhonchi, thus it is
mentioned here.
Stridor. Stridor is an extremely high-pitched wheeze
that occurs with significant upper airway obstruction
and is present during both inspiration and expiration.
The presence of stridor indicates a medical emergency.
Stridor is also audible without a stethoscope.
CLINICAL TIP
 Acute onset of stridor during an intervention session
warrants immediate notification of the nursing and
medical staff.
Discontinuous Sounds.
Crackles. Crackles are bubbling or popping sounds
that represent the presence of fluid or secretions, or
the sudden opening of closed airways. Crackles that
result from fluid (pulmonary edema) or secretions
(pneumonia) are described as‘‘wet’’or ‘‘coarse,’’ whereas
crackles that occur from the sudden opening of closed
airways (atelectasis) are referred to as ‘‘dry’’or ‘‘fine.’’
CLINICAL TIP
 Wet crackles can also be referred to as rales, but the
American Thoracic Society—American College of
Chest Physicians has moved to eliminate this
terminology for purposes of standardization.15
CLINICAL TIP
 Despite efforts to make the terminology of breath
sounds more consistent, terminology may still vary
from clinician to clinician and facility to facility.
Always clarify the intended meaning of the breath
sound description if your findings differ significantly
from what has been documented or reported.
EXTRAPULMONARY SOUNDS. These sounds are gen-
erated from dysfunction outside of the lung tissue. The
most common sound is the pleural friction rub. This
sound is heard as a loud grating sound, generally through-
outboth phases of respiration, and is almost always associ-
ated with pleuritis (inflamed pleurae rubbing on one
another).12,14
CLINICAL TIP
 Asking the patient to hold his or her breath can
help the clinician determine if the friction rub was
truly heard or possibly a sound artifact.
VOICE SOUNDS. Normal phonation is audible
during auscultation, with the intensity and clarity of
speech also dissipating from proximal to distal airways.
Voice sounds that are more or less pronounced in
distal lung regions, where vesicular breath sounds
should occur, may indicate areas of consolidation or

hyperinflation, respectively.The same areas of ausculta-
tion should be used when assessing voice sounds. The
following three types of voice sound tests can be used
to help confirm breath sound findings:
1. Whispered pectoriloquy. The patient whispers ‘‘one,
two, three.’’ The test is positive for consolidation if
phrases are clearly audible in distal lung fields. This
test is positive for hyperinflation if the phrases are
less audible in distal lung fields.
2. Bronchophony. The patient repeats the phrase
‘‘ninety-nine.’’ The results are similar to whispered
pectoriloquy.
3. Egophony. The patient repeats the letter e. If the
auscultation in the distal lung fields sound like a, then
fluid in the air spaces or lung parenchyma is suspected.
Respiratory System CHAPTER 2 57
PALPATION
The third component of the physical examination is
palpation of the chest wall, which is performed in a
cephalocaudal direction. Figure 2-5 demonstrates
hand placement for chest wall palpation of the upper,
middle, and lower lung fields. Palpation is performed
to examine the following:
 Presence of fremitus (a vibration caused by the pres-
ence of secretions or voice production, which is felt
through the chest wall) during respirations.11
 Presence, location, and reproducibility of pain,
tenderness, or both.
 Skin temperature.

CLINICAL TIP
To ensure accurate auscultation, do the following:
 Make sure stethoscope earpieces are pointing up
and inward before placing in the ears.
 Long stethoscope tubing may dampen sound
transmission. Length of tubing should
be approximately 30 cm (12 in.) to 55 cm A
(21 to 22 in.).12
 Always check proper function of the stethoscope
before auscultating by listening to finger tapping on
the diaphragm while the earpieces are in place.
 Apply the stethoscope diaphragm firmly against the
skin so that it lays flat.
 Observe chest wall expansion and breathing pattern
while auscultating to help confirm palpatory findings
of breathing pattern (e.g., sequence and symmetry).
For example, decreased chest wall motion that was
palpated earlier in the left lower lung field may B
present with decreased breath sounds in that same
area.
To minimize false-positive adventitious breath sound
findings, do the following:
 Ensure full, deep inspirations (decreased effort can
be misinterpreted as decreased breath sounds).
 Be aware of the stethoscope tubing’s touching other
objects (especially ventilator tubing) or chest hair.
 Periodically lift the stethoscope off the chest wall to
help differentiate extraneous sounds (e.g., chest or
nasogastric tubes, patient snoring) that may appear
to originate from the thorax. C
 To maximize patient comfort, allow periodic rest
periods between deep respirations to prevent FIGURE 2-5
Palpation of (A) upper, (B) middle, and (C) lower chest wall
hyperventilation and dizziness.
motion. (Courtesy Peter P.Wu.)
58 CHAPTER 2 Respiratory System
 Presence of bony abnormalities, rib fractures, or
both.
 Chest expansion and symmetry.
 Presence of subcutaneous emphysema (palpated as
bubbles popping under the skin from the presence
of air in the subcutaneous tissue; this finding is
abnormal, as it represents air that has escaped or is
escaping from the lungs. Subcutaneous emphysema
can occur from a pneumothorax [PTX], a complica-
tion from central line placement, or after thoracic
surgery).1
CLINICAL TIP
 To decrease patient fatigue while palpating each of
the chest wall segments for motion, all of the other
items listed above can also be examined
simultaneously.
MEDIATE PERCUSSION
Mediate percussion can evaluate tissue densities within
the thoracic cage, as well as indirectly measure dia-
phragmatic excursion during respirations. Mediate per-
cussion can also be used to confirm other findings in
the physical examination. The procedure is shown in
Figure 2-6 and is performed by placing the palmar
FIGURE 2-6
Demonstration of mediate percussion technique. (From
Hillegass EA, Sadowsky HS: Essentials of Cardiopulmonary
Physical Therapy [2nd ed]. Philadelphia: Saunders, 2001.)
surface of the index finger, middle finger, or both of
one hand flatly against the surface of the chest wall
within the intercostal spaces. The tips of the other
index finger, middle finger, or both then strike the
distal third of the fingers that are resting against the
chest wall. The clinician proceeds from side to side in
a cephalocaudal fashion, within the intercostal spaces,
for both anterior and posterior aspects of the chest
wall. Sounds produced from mediate percussion can
be characterized as one of the following:
 Resonant (over normal lung tissue)
 Hyperresonant (over emphysematous lungs or PTX)
 Tympanic (over gas bubbles in abdomen)
 Dull (from increased tissue density or lungs with
decreased air)
 Flat (extreme dullness over very dense tissues, such as
the thigh muscles)12
To evaluate diaphragmatic excursion with mediate
percussion, the clinician first delineates the resting
position of the diaphragm by percussing down the pos-
terior aspect of one side of the chest wall until a
change from resonant to dull (flat) sounds occurs. The
clinician then asks the patient to inspire deeply and
repeats the process, noting the difference in landmarks
when sound changes occur. The difference is the
amount of diaphragmatic excursion. The other side is
also examined, and a comparison can then be made of
the hemidiaphragms.
CLINICAL TIP
 Mediate percussion is a difficult skill and
is performed most proficiently by experienced
therapists or physicians. Mediate percussion
can also be performed over the abdominal cavity
to assess tissue densities, which is described
further in Chapter 8. Also, do not confuse
this examination technique with the intervention
technique of percussion, which is used
to help mobilize bronchopulmonary secretions
in patients.
COUGH EXAMINATION
An essential component of bronchopulmonary hy-
giene is cough effectiveness. The cough mechanism
can be divided into four phases: (1) full inspiration, (2)
closure of the glottis with an increase of intrathoracic
pressure, (3) abdominal contraction, and (4) rapid
expulsion of air. The inability to perform one or
more portions of the cough mechanism can lead to
 Respiratory System CHAPTER 2 59
decreased pulmonary secretion clearance. Cough
examination includes the following components11,12:
 Effectiveness (ability to clear secretions)
 Control (ability to start and stop coughs)
 Quality (wet, dry, bronchospastic)
 Frequency (how often during the day and night
cough occurs)
 Sputum production (color, quantity, odor, and
consistency)
The effectiveness of a patient’s cough can be exam-
ined directly by simply asking the patient to cough or
indirectly by observing the above components when
the patient coughs spontaneously.

CLINICAL TIP FIGURE 2-7

 Hemoptysis, the expectoration of blood during The oxyhemoglobin dissociation curve. (Courtesy Marybeth
coughing, may occur for many reasons. Hemoptysis is Cuaycong.)
usually benign postoperatively if it is not sustained
with successive coughs. The therapist should note
whether the blood is dark red or brownish in color
(old blood) or bright red (new or frank blood).
The presence of new blood in sputum should be
documented and the nurse or physician notified. Table 2-5 RELATIONSHIP BETWEEN OXYGEN
SATURATION, THE PARTIAL PRESSURE
OF OXYGEN, AND THE SIGNS AND
Diagnostic Testing SYMPTOMS OF HYPOXEMIA
OXIMETRY Oxyhemoglobin Oxygen Partial Signs and
Pulse oximetry (SpO2) is a noninvasive method of deter- Saturation Pressure (PaO2) Symptoms
(SaO2) (%) (mm Hg) of Hypoxemia
mining arterial oxyhemoglobin saturation (SaO2). It
also indirectly examines the partial pressure of O2. 97-99 90-100 None
Finger or ear sensors are generally applied to a patient 95 80 Tachypnea
on a continuous or intermittent basis. Oxyhemoglobin Tachycardia
saturation is an indication of pulmonary reserve and is 90 60 As above
dependent on the PO2 level in the blood. Figure 2-7 Restlessness
demonstrates the direct relationship of oxyhemoglobin Malaise
saturation and partial pressures of O2. As shown on Impaired judgment
the steep portion of the curve, small changes in PO2 Incoordination
levels below 60 mm Hg will result in large changes in Vertigo
oxygen saturation, which is considered moderately Nausea
hypoxic.11 The relationship between oxygen saturation 85 50 As above
and PO2 levels is further summarized in Table 2-5. The Labored respiration
affinity or binding of O2 to hemoglobin is affected by Cardiac
dysrhythmia
changes in pH, PCO2, temperature, and 2,3-diphospho- Confusion
glycerate (a by-product of red blood cell metabolism)
levels. Note that pulse oximetry can only measure 80 45 As above
changes in oxygenation (PO2) indirectly and cannot 75 40 As above
measure changes in ventilation (PCO2). Changes in From Frownfelter DL, Dean E: Principles and Practice
ventilation need to be measured by arterial blood gas of Cardiopulmonary Physical Therapy (4th ed), St. Louis:
(ABG) analysis.16 Mosby, 2006.
60 CHAPTER 2 Respiratory System

pH Degree of acidity or alkalinity

CLINICAL TIP in blood
 To ensure accurate O2 saturation readings, (1) check HCO3 Level of bicarbonate in the blood
for proper waveform or pulsations, which indicate Percentage A percentage of the amount
proper signal reception, and (2) compare pulse of SaO2 (O2 of hemoglobin sites filled
readings on an O2 saturation monitor with the saturation) (saturated) with O2 molecules
patient’s peripheral pulses or electrocardiograph (PaO2 and SaO2 are intimately
readings (if available). related but are not synonymous)
 O2 saturation readings can be affected by poor
circulation (cool digits), movement of sensor cord, NORMAL VALUES. The normal ranges for ABGs are
cleanliness of the sensors, nail polish, intense light, in- as follows19:
creased levels of carboxyhemoglobin (HbCO2), jaundice,
skin pigmentation, shock states, and severe hypoxia.17,18
PaO2 Greater than 80 mm Hg
PaCO2 35 to 45 mm Hg
pH 7.35 to 7.45
HCO3 22 to 26 mEq/liter
ARTERIAL BLOOD GAS ANALYSIS
ABG analysis examines acid-base balance (pH), ventil- ABGs are generally reported in the following
ation (CO2 levels), and oxygenation (O2 levels), as well format: pH/PaCO2/PaO2/HCO3 (e.g., 7.38/42/90/26).
as guiding respiratory interventions, such as mechani- ARTERIAL BLOOD GAS INTERPRETATION.
cal ventilation settings.11 For proper cellular metabo- Interpretation of ABGs includes the ability to deter-
lism to occur, acid-base balance must be maintained. mine any deviation from normal values and hypothe-
Disturbances in acid-base balance can be caused by size a cause (or causes) for the acid-base disturbance in
respiratory or metabolic dysfunction. Normally, the relation to the patient’s clinical history.
respiratory and metabolic systems work in synergy to The following terms are associated with ABG
help maintain acid-base balance. interpretation20:
The ability to interpret ABGs provides the physical  Acidemia occurs when the pH is less than 7.4.
therapist with valuable information regarding the cur-  Acidosis is the process that causes acidemia.
rent medical status of the patient, the appropriateness  Alkalemia occurs when the pH is greater than 7.4.
for bronchopulmonary hygiene or exercise treatments,  Alkalosis is the process that causes alkalemia.
and the outcomes of medical and physical therapy  Hypoxia occurs when Po2 is less than 80 mm Hg.
intervention.  Hypercarbia occurs when Pco2 is greater than
ABG measurements are usually performed on a rou- 50 mm Hg.
tine basis, which is specified according to need in the The following are the primary concepts of ABG
critical care setting. For the critically ill patient, ABG interpretation:
sampling may occur every 1 to 3 hours. In contrast, 1. Respiratory or metabolic disorders can cause states
ABGs may be sampled one or two times a day in a of acidemia or alkalemia.
patient whose pulmonary or metabolic status has stabi- 2. If respiratory or metabolic disorders cause acid-
lized. Unless specified, arterial blood is sampled from base imbalances, then they are called the primary
an indwelling arterial line. Other sites of sampling process.
include arterial puncture, venous blood from a periph- 3. Acid-base imbalances can be compensated for
eral venous puncture or catheter, and mixed venous (pH is close to 7.35 to 7.45) by the nonprimary
blood from a pulmonary artery catheter. Appendix system. For example, a primary respiratory
III-Adescribes vascular monitoring lines in more detail. acidosis can be compensated for by the metabolic
TERMINOLOGY. The following terms are frequently system.
used in ABG analysis: 4. If the nonprimary system fails to compensate
PaO2 (PO2) Partial pressure of dissolved for the primary system, the disorder is referred
O2 in plasma to as uncompensated (pH is higher or lower than
7.35 to 7.45).
PaCO2 (PCO2) Partial pressure of dissolved
5. Acid-base imbalances also can be corrected
CO2 in plasma
by addressing the primary process involved.
 Respiratory System CHAPTER 2 61
For example, a primary metabolic alkalosis
from renal system dysfunction can be corrected BOX 2-1 CAUSES OF ACID-BASE
by administering medical therapy to the renal IMBALANCES
system.
Knowledge of uncompensated, compensated, or Respiratory Acidosis Metabolic Acidosis
corrected acid-base disturbances provides insight Chronic obstructive Lactic acidosis
into the patient’s current medical status. The fol- pulmonary disease
lowing outline provides basic guidelines for ABG Sedation Ketoacidosis:
interpretation: Head trauma Diabetes
1. Examine the patient’s pH level to determine Drug overdose Starvation
acid-base balance. Pneumothorax Alcoholism
a. If the patient’s pH = 7.4, acid-base balance is Central nervous system Diarrhea
normal. disorders Parenteral nutrition
b. If the patient’s pH < 7.4, the patient is acidotic. Pulmonary edema
c. If the patient’s pH > 7.4, the patient is alkalotic. Sleep apnea
2. To determine if the patient’s pH change is due Chest wall trauma
to a primary respiratory process, examine the Respiratory Alkalosis Metabolic Alkalosis
PCO2. For every 10-point change in PCO2, there
is a 0.08-point change in pH in the opposite Pulmonary embolism Vomiting
direction. Pregnancy Nasogastric suction
a. A low pH and a high PCO2 indicate uncompen- Anxiety/fear Diuretics
sated respiratory acidosis. Hypoxia Steroids
b. A high pH and a low PCO2 indicate uncompen- Pain Hypokalemia
sated respiratory alkalosis. Fever Excessive ingestion of
3. To determine if the patient’s pH change is due Sepsis antacids
to a primary metabolic process, examine the Congestive heart failure Administration of
HCO3. For every 10-point change in HCO3, Pulmonary edema HCO3
there is a 0.15-point change in pH in the same Asthma Banked blood
direction. Acute respiratory transfusions
a. A low pH and a low HCO3 indicate uncompen- distress syndrome Cushing’s syndrome
sated metabolic acidosis.
b. A high pH and a high HCO3 indicate uncompen- From George-Gay B, Chernecky CC (eds). Clinical Medical-
sated metabolic alkalosis. Surgical Nursing: A Decision-Making Reference. Philadelphia:
4. To determine if the patient’s primary respiratory pro- WB Saunders, 2002;Table 5-1-9.
cess has been compensated for by the renal system,
examine HCO3.
a. A high HCO3 in respiratory acidosis indicates CLINICAL TIP
compensated respiratory acidosis.  Acid-base balance or pH is the most important ABG
b. A low HCO3 in respiratory alkalosis indicates value to be within normal limits. It is important
compensated respiratory alkalosis. to relate ABG values with medical history and clinical
5. To determine if the patient’s primary metabolic pro- course. ABG values and vital signs are generally
cess has been compensated for by the respiratory documented on a daily flow sheet, an invaluable source
system, examine the PCO2. of information. Changes in ABG values over time are
a. A low PCO2 in metabolic acidosis indicates com- more informative than a single ABG reading. Single
pensated metabolic acidosis. ABG readings should be correlated with previous ABG
b. A high PCO2 in metabolic alkalosis indicates readings, medical status, supplemental O2 or ventilator
compensated metabolic alkalosis. changes, and medical procedures.
The possible causes for these disorders are summar-  Be sure to note if an ABG sample is drawn from mixed
ized in Box 2-1. Decreased levels of alertness may venous blood, as the normal O2 value is lower. PO2 of
result from retained CO2. A list of signs and symptoms mixed venous blood is 35 to 40 mm Hg.
of CO2 retention is shown in Box 2-2.
62 CHAPTER 2 Respiratory System

BOX 2-2 CLINICAL PRESENTATION OF

CARBON DIOXIDE RETENTION
AND NARCOSIS
 Altered mental status
 Lethargy
 Drowsiness
 Coma
 Headache
 Tachycardia
 Hypertension
 Diaphoresis
 Tremor
 Redness of skin, sclera, or conjunctiva

From Kersten LD. Comprehensive Respiratory Nursing:

A Decision-Making Approach. Philadelphia: Saunders,
1989;351.
A

CLINICAL TIP
 Acid-base disturbances that occur clinically can
arise from both respiratory and metabolic
disorders; therefore, interpretation of the ABG
results may not prove to be as straightforward
as the example given above. Hence, the clinician
must use this information as part of a complete
examination process to gain full understanding
of the patient’s current medical status.

CHEST X-RAYS
Radiographic information of the thoracic cavity in
combination with a clinical history provides critical
assistance in the differential diagnosis of pulmonary
conditions. Figure 2-8 outlines the film markers of
anatomic structures that are used for chest x-ray
B
(CXR) interpretation.
FIGURE 2-8
Indications for CXRs are as follows21,22:
A, Normal chest radiograph (posteroanterior view). B, Same
 To assist in the clinical diagnosis and monitor radiograph as in A with normal anatomic structures labeled or
the progression or regression of the following: numbered. (1, trachea; 2, right main stem bronchus; 3, left main
 Airspace consolidation (pulmonary edema, stem bronchus; 4, left pulmonary artery; 5, pulmonary vein to
pneumonia, adult respiratory distress syndrome the right upper lobe; 6, right interlobar artery; 7, vein to right
[ARDS], pulmonaryhemorrhage, and infarctions) middle and lower lobes; 8, aortic knob; 9, superior vena cava;
 Large intrapulmonary air spaces and presence 10, ascending aorta.) (From Fraser RG, Peter Pare¤ JA, Pare¤ PD,
of mediastinal or subcutaneous air, as well et al. [eds]. Diagnosis of Diseases of the Chest,Vol. 1 [3rd ed].
as PTX Philadelphia: Saunders, 1988;287.)
 Lobar atelectasis

 Other pulmonary lesions, such as lung nodules
and abscesses
 Rib fractures
 To determine proper placement of endotracheal
tubes, central lines, chest tubes, or nasogastric
tubes
 To evaluate structural features, such as cardiac or
mediastinal size and diaphragmatic shape and
position
CXRs are classified according to the direction of
radiographic beam projection.The first word describes
where the beam enters the body, and the second word
describes the exit.
Common types of CXRs include the following:
Posterior-anterior Taken while the patient is
(P-A) upright sitting or standing
Anterior- Taken while the patient is
posterior (A-P) upright sitting or standing,
semireclined, or supine
Lateral Taken while the patient is
upright sitting or standing,
or decubitus (lying on the side)
Upright positions are preferred to allow full expan-
sion of lungs without hindrance of the abdominal
viscera and to visualize gravity-dependent fluid collec-
tions. Lateral films aid in three-dimensional, segmental
localization of lesions and fluid collections not visible
in P-A or A-P views.
The appearance of various chest structures on CXR
depends on the density of the structure. For example,
bone appears white on CXR because of absorption of
the x-ray beams, while air appears black. Moderately
dense structures such as the heart, aorta, and pulmo-
nary vessels appear gray, as do fluids such as pulmonary
edema and blood.2
A systematic approach should be used when per-
forming a basic CXR interpretation. First, assess the
densities of the various structures to identify air,
bone, tissue, and fluid. Next, determine if the findings
are normal or abnormal, and if they are consistent on
both sides of the lungs. Common CXR findings with
various pulmonary diagnoses are found in Tables 2-9
through 2-11.2
CLINICAL TIP
 Diagnosis cannot be made by CXR alone. The
therapist should use CXR reports as a guide for
decision making and not as an absolute parameter for
Respiratory System CHAPTER 2 63
bronchopulmonary hygiene evaluation and treatment.
CXRs sometimes lag behind significant clinical
presentation (e.g., symptoms of pulmonary infection
may resolve clinically, whereas CXR findings remain
positive for infection). CXR can also be a helpful
tool prechest and postchest physical therapy
sessions, to determine the effectiveness of the
treatment. This is more commonly done in the
ICU setting.
SPUTUM ANALYSIS
Analysis of sputum includes culture and Gram stain to
isolate and identify organisms that may be present in
the lower respiratory tract. Refer to Chapter 10 for
more details on culture and Gram stain. After the
organisms are identified, appropriate antibiotic therapy
can be instituted. Sputum specimens are collected
when there is a rise in the patient’s temperature or a
change in the color or consistency of sputum occurs.
They can also be used to evaluate the efficacy of antibi-
otic therapy. Sputum analysis can be inaccurate if a ster-
ile technique is not maintained during sputum
collection or if the specimen is contaminated with too
much saliva, as noted microscopically by the presence
of many squamous epithelial cells.
CLINICAL TIP
 Therapists involved in bronchopulmonary hygiene
and collecting sputum samples should have sterile
sputum collection containers and equipment on
hand before beginning the treatment session to
ensure successful sputum collection.
 Patients who present with a sputum analysis that is
negative for active infection may still have retained
secretions that could hinder gas exchange and
tolerance to activity; therefore, therapists will need
to clinically evaluate the need for secretion clearance
techniques.
FLEXIBLE BRONCHOSCOPY
A flexible, fiberoptic tube is used as a diagnostic and
interventional tool to directly visualize and aspirate
(suction) the bronchopulmonary tree. If a patient is
mechanically ventilated, the bronchoscope is inserted
through the endotracheal or tracheal tube. Refer to
Appendix III-B for more information on mechanical
ventilation and endotracheal and tracheal tubes. If the
64 CHAPTER 2 Respiratory System
BOX 2-3 DIAGNOSTIC AND THERAPEUTIC INDICATIONS FOR FLEXIBLE BRONCHOSCOPY
Diagnostic Indications
 Evaluation of neoplasms (benign or malignant)
in air spaces and mediastinum, tissue biopsy
 Evaluation of the patient before and after lung
transplantation
 Endotracheal intubation
 Infection, unexplained chronic cough, or
hemoptysis
 Tracheobronchial stricture and stenosis
 Hoarseness or vocal cord paralysis
 Fistula or unexplained pleural effusion
 Localized wheezing or stridor
 Chest trauma or persistent pneumothorax
 Postoperative assessment of tracheal,
tracheobronchial, bronchial, or stump
anastomosis
Data from Hetzed MR: Minimally InvasiveTechniques inThoracic Medicine and Surgery. London: Chapman & Hall,1995; RippeJM,
Irwin RS, Fink MP, et al.: Procedures andTechniques in Intensive Care Medicine. Boston,1994, Little, Brown; and Malarkey LM,
McMorrow ME: Nurse’s Manual of LaboratoryTests and Diagnostic Procedures (2nd ed), Philadelphia: Saunders, 2000.
patient is spontaneously breathing, a local anesthetic is
applied, and the bronchoscope is inserted through
one of the patient’s nares. Box 2-3 summarizes the diag-
nostic and therapeutic indications of bronchoscopy.
CLINICAL TIP
 Bronchoscopy can also be performed with a rigid
bronchoscope. This is primarily an operative
procedure.22-24
VENTILATION-PERFUSION SCAN
The V_ = Q_ scan is used to rule out the presence of pul-
monary embolism (PE) and other acute abnormalities
of oxygenation and gas exchange and as preoperative
and postoperative evaluation of lung transplantation.
During a ventilation scan, inert radioactive gases
or aerosols are inhaled, and three subsequent projec-
tions (i.e., after first breath, at equilibrium, and during
washout) of airflow are recorded.
During a perfusion lung scan, a radioisotope is
injected intravenously into a peripheral vessel, and six
projections are taken (i.e., anterior, posterior, both lat-
erals, and both posterior obliques). The scan is very
Therapeutic Indications
 Removal of retained secretions, foreign bodies,
and/or obstructive endotracheal tissue
 Intubation or stent placement
 Bronchoalveolar lavage
 Aspiration of cysts or drainage of abscesses
 Pneumothorax or lobar collapse
 Thoracic trauma
 Airway maintenance (tamponade for bleeding)
sensitive to diminished or absent blood flow, and
lesions of 2 cm or greater are detected.
Perfusion defects can occur with pulmonary embo-
lus, asthma, emphysema, and virtually all alveolar fill-
ing, destructive or space-occupying lesions in lung,
and hypoventilation. A CXR a few hours after the
perfusion scan helps the differential diagnosis.
Ventilationscans are performed first,followedby per-
fusion scan.The two scans are then compared to deter-
mine extent of V_ = Q_ matching. As described earlier, in
the Ventilation and Perfusion Ratio section, average
_
reference V_ = Q ratio is approximately equal to 0.8.23,25
COMPUTERIZED TOMOGRAPHIC PULMONARY
ANGIOGRAPHY
Computerized Tomographic Pulmonary Angiography
(CT-PA) is a minimally invasive test that allows direct
visualization of the pulmonary artery and subsequently
facilitates rapid detection of a thrombus. CT-PA is most
useful for detecting a clot in the main or segmental
vasculature. In recent years, CT-PA has become the
preferred method to diagnose acute PE, rather than
V_ = Q
_
scanning.26,27 Benefits of CT-PA include its wide
availability for testing, high sensitivity, and rapid
reporting. The test is also useful in determining other
pulmonary abnormalities that may be contributing to a

FIGURE 2-9
Lung volumes. (FromYentis SM, Hirsch NP, Smith GB [eds]. Anaesthesia and Intensive Care A-Z:
An Encyclopedia of Principles and Practice (2nd ed). Oxford, UK: Butterworth-Heinemann, 2000;340.)
patient’s symptoms. Both the American and European
Thoracic societies have incorporated CT-PA into
their algorithms for diagnosing PE.28,29 Prospective
Investigation of Pulmonary Embolism Diagnosis
(PIOPED II) investigators also recommend CT-PA as a
first-line imaging test in diagnosing PE.30
PULMONARY FUNCTION TESTS
Pulmonary function tests (PFTs) consist of measuring a
patient’s lung volumes and capacities, as well as inspira-
tory and expiratory flow rates. Lung capacities are com-
posed of two or more lung volumes. Quantification of
these parameters helps in distinguishing obstructive
from restrictive respiratory patterns, as well as deter-
mining how the respiratory system contributes to phys-
ical activity limitations. The respiratory system’s
volumes and capacities are shown in Figure 2-9.
Alterations in volumes and capacities will occur with
obstructive and restrictive diseases, and these changes
are shown in Figure 2-10.Volume, flow, and gas dilution
spirometers and body plethysmography are the mea-
surement tools used for PFTs. A flow-volume loop is
Respiratory System CHAPTER 2 65
also included as part of the patient’s PFTs and is
shown in Figure 2-11. A comprehensive assessment
of PFT results includes comparisons with normal
values and prior test results. PFT results may be
skewed according to a patient’s effort.Table 2-6 outlines
the measurements performed during PFTs.
The normal range of values for PFTs is variable and
is based on a person’s age, gender, height, ethnic
origin, and weight (body surface area). Normal pre-
dicted values can be extrapolated from a nomogram or
calculated from regression (prediction) equations
obtained from statistical analysis.
For example, based on a nomogram, the following
predicted values for forced vital capacity (FVC) and
forced expiratory volume in 1 second (FEV1) would be
approximately31:
 FVC = 4.1 liters, FEV1 = 3 liters for a man who is
55 years old and 66 in. tall
 FVC = 2.95 liters, FEV1 = 2.2 liters for a woman who
is 55 years old and 62 in. tall
Because there can be variability from person to
person, it is most useful to compare a person’s PFT
 A

B
FIGURE 2-10
A, How obstructive lung disorders alter lung volumes and capacities. B, How restrictive lung disorders
alter lung volumes and capacities. ERV, Expiratory reserve volume; FRC, functional residual capacity;
IC, inspiratory capacity; IRV, inspiratory reserve volume; RV, residual volume;TLC, total lung capacity;
VC, vital capacity;VT, tidal volume. (From DesJardinsT, Burton GC [eds]. Clinical Manifestations and
Assessment of Respiratory Disease [3rd ed]. St. Louis: Mosby, 1995;40,49.)
 Respiratory System CHAPTER 2 67

A B

C D
FIGURE 2-11
Characteristic flow-volume loops: (A) normal, (B) obstructive lung disease, (C) restrictive lung disease,
(D) tracheal/laryngeal obstruction. RV, Residual volume;TLC, total lung capacity. (FromYentis SM,
Hirsch NP, Smith GB [eds]. Anaesthesia and Intensive Care A-Z: An Encyclopedia of Principles and
Practice [2nd ed]. Oxford, UK: Butterworth-Heinemann, 2000.)

results from his or her previous tests. Indications for

PFTs are as follows31-33: represent the degree of airway patency during
 Detection and quantification of respiratory expiration, which affects airflow in and out of the
disease lung.
 Evaluation of pulmonary involvement in systemic  Predicted normal values for a person’s given age,
diseases gender, and height will be provided in the PFT report
 Assessment of disease progression for reference to the person’s actual PFT result.
 Evaluation of impairment, functional limitation, or
disability
 Assessment for bronchodilator therapy or surgical
intervention, or both, along with subsequent PATHOPHYSIOLOGY
response to the respective intervention
 Preoperative evaluation (high-risk patient Respiratory disorders can be classified as obstructive
identification) or restrictive. A patient may present with single or
multiple obstructive and restrictive processes, or with
a combination of both as a result of environmental,
CLINICAL TIP traumatic, orthopedic, neuromuscular, nutritional, or
 FEV1, FVC, and the FEV1/FVC ratio are the most drug-induced factors. These disorders may be infec-
commonly interpreted PFT values. These measures tious, neoplastic, or vascular in nature or involve the
connective tissue of the thorax.11
68 CHAPTER 2 Respiratory System
Table 2-6 DESCRIPTION AND CLINICAL SIGNIFICANCE OF PULMONARY FUNCTION TESTS
Test Description
Lung VolumeTests
Tidal volume (VT) The volume of air inhaled or exhaled during
a single breath in a resting state.
Inspiratory reserve volume The maximum amount of air that can be
(IRV) inspired following a normal inspiration.
Expiratory reserve volume The maximum amount of air that can be
(ERV) exhaled following a normal exhalation.
Residual volume (RV) The volume of air remaining in the lungs at
the end of maximal expiration that cannot
be forcibly expelled.
Total lung capacity (TLC) The volume of air contained in the lung
at the end of maximal inspiration.
(TLC = VT + IRV + ERV + RV)
Vital capacity (VC) The maximum amount of air that can
be expired slowly and completely
following a maximal inspiration.
(VC = VT + IRV + ERV)
Functional residual capacity The volume of air remaining in the lungs
(FRC) at the end of a normal expiration.
Calculated from body plethysmography.
(FRC = ERV + RV)
Inspiratory capacity (IC) The largest volume of air that can be inspired
in one breath from the resting expiratory
level. (IC = VT + IRV)
Residual volume to total The percentage of air that cannot be expired
lung capacity ratio in relation to the total amount of air that
(RV:TLC  100) can be brought into the lungs.
VentilationTests
Minute volume (VE) or The total volume of air inspired or expired
minute ventilation in 1 minute. (VE = VT respiratory rate)
Respiratory dead The volume of air in the lungs that
space (VD) is ventilated but not perfused in
conducting airways and nonfunctioning
alveoli.
Significance
Decreased tidal volume could be indicative
of atelectasis, fatigue, restrictive lung
disorders, and tumors.
Decreased IRVcould be indicative
of obstructive pulmonary disease.
ERV is necessary to calculate residual
volume and FRC. Decreased values could
be indicative of ascites, pleural effusion,
or pneumothorax.
RV helps to differentiate between
obstructive and restrictive disorders.
An increased RV indicates an obstructive
disorder, and a decreased RV indicates a
restrictive disorder.
TLC helps to differentiate between
obstructive and restrictive disorders.
An increased TLC indicates an obstructive
disorder; a decreased TLC indicates a
restrictive disorder.
A decreased VC can result from a decrease
in lung tissue distensibility or depression
of the respiratory centers in the brain.
FRC values help differentiate between
obstructive and restrictive respiratory
patterns.
An increased FRC indicates an obstructive
respiratory pattern, and a decreased
FRC indicates a restrictive respiratory
pattern.
Changes in IC usually parallel changes inVC.
Decreased values could be indicative of
restrictive disorders.
Values > 35% are indicative of obstructive
disorders.
VE is most commonly used in exercise or
stress testing.
VE can increase with hypoxia, hypercapnia,
acidosis, and exercise.
VD provides information about available
surface area for gas exchange.
Increased dead space = decreased gas
exchange.
 Respiratory System CHAPTER 2 69

Table 2-6 DESCRIPTION AND CLINICAL SIGNIFICANCE OF PULMONARY FUNCTION TESTS—cont’d

Test Description Significance

Alveolar ventilation (VA) The volume of air that participates in gas
exchange.
Estimated by subtracting dead space from
tidal volume. (VA = VT — VD)
Pulmonary SpirometryTests
Forced vital capacity (FVC) The volume of air that can be expired
forcefully and rapidly after a maximal
inspiration.
Forced expiratory volume The volume of air expired over a time interval
timed (FEVt) during the performance of an FVC
maneuver.
The interval is usually 1 second (FEV1).
After 3 seconds, FEV should equal FVC.
FEV% (usually FEV1/FVC The percent of FVC that can be expired
 100) over a given time interval, usually 1 second.
Forced expiratory flow The average flow of air during the middle
25-75% (FEF25-75%) 50% of an FEVmaneuver.
Used in comparison withVC.
Represents peripheral airway resistance.
Peak expiratory flow rate The maximum flow rate attainable at any time PEFR can assist with diagnosing obstructive
(PEFR) during an FEV.
Maximum voluntary The largest volume of air that can be breathed MVVmeasures status of respiratory muscles,
ventilation (MVV) per minute by maximal voluntary effort.
Test lasts 10 or 15 seconds and is multiplied
by 6 to 4, respectively, to determine
the amount of air that can be breathed
in a minute (liters/min).
Flow-volume loop A graphic analysis of the maximum forced
(F-V loop) expiratory flow volume followed by
a maximum inspiratory flow volume
Gas Exchange
Diffusing capacity of A known mixture of carbon monoxide and
carbon monoxide helium gas is inhaled and then exhaled after pulmonary capillary bed in contact with
(DLCO) 10 seconds, and the amount of gases are
remeasured.
VA measures the amount of oxygen available
to tissue, but it should be confirmed by
arterial blood gas measurements.
FVC is normally equal toVC, but FVC can
be decreased in obstructive disorders.
A decrease in FEV1 can indicate either
obstructive or restrictive airway disease.
With obstructive disease, a decreased FEV1
results from increased resistance to
exhalation.
With restrictive disease, a subsequent decrease
in FEV1 results from a decreased ability to
initially inhale an adequate volume of air.
FEV% is a better discriminator of
obstructive and restrictive disorders
than FEVt.
An increase in FEV1/FVC indicates a
restrictive disorder, and a decrease in FEV1/
FVC indicates an obstructive disorder.
A decrease in (FEF25-75%) generally indicates
obstruction in the medium-sized airways.
disorders such as asthma.
the resistance offered by airways and
tissues, and the compliance of the lung
and thorax.
The distinctive curves of the F-V loop are
created according to the presence or
absence of disease.
Restrictive disease demonstrates an equal
reduction in flow and volume, resulting
in a vertical oval-shaped loop. Obstructive
disease demonstrates a greater reduction
in flow compared with volume, resulting
in a horizontal tear-shaped loop.
DLCO assesses the amount of functioning
functioning alveoli (gas exchange area).
70 CHAPTER 2 Respiratory System
Common terminology that is often used when
describing respiratory dysfunction is listed below:
Air trapping: Retention of gas in the lung as a result
of partial or complete airway obstruction
Bronchospasm: Smooth muscle contraction of the bronchi
and bronchiole walls resulting in a narrowing of
the airway lumen
Consolidation: Transudate, exudate, or tissue replacing
alveolar air
Hyperinflation: Overinflation of the lungs at resting
volume due to air trapping
Hypoxemia: A low level of oxygen in the blood, usually
a PaO2 less than 60 to 80 mm Hg
Hypoxia: A low level of oxygen in the tissues available
for cell metabolism
Respiratory distress: The acute or insidious onset of dys-
pnea, respiratory muscle fatigue, abnormal respira-
tory pattern and rate, anxiety, and cyanosis related
to inadequate gas exchange; the clinical presentation
that usually precedes respiratory failure
Respiratory failure:The inability of the pulmonary system
to maintain an adequate exchange of oxygen and
carbon dioxide (see Appendix III-B)
Obstructive Pulmonary Conditions
Obstructive lungdiseases orconditions maybe described
by onset (acute versus chronic), severity (mild, mode-
rate, or severe), and location (upper or lower airway).
Obstructive pulmonary patterns are characterized
by decreased air flow out of the lungs as a result of narr-
owing of the airway lumen. This causes increased
dead space and decreased surface area for gas exchange.
Chronic obstructive pulmonary disease (COPD)
describes airflow limitation that is not fully reversible.
The Global Initiative for Obstructive Lung Disease
(GOLD) states that the airflow limitation in COPD is
usually progressive and associated with an abnor-
mal inflammatory response to noxious particles or
gases.34 The diagnosis of COPD is confirmed with
spirometric testing. Patients with COPD typically
have a combination of chronic bronchitis, emphysema,
and small airway obstruction.35 Table 2-7 outlines
obstructive disorders, their general physical and
diagnostic findings, and their general clinical
management.
ASTHMA
Asthma is an immunologic response that can result
from allergens (e.g., dust, pollen, smoke, pollutants),
food additives, bacterial infection, gastroesophageal
reflux, stress, cold air, and exercise.8 The asthmatic
exacerbation may be immediate or delayed, resulting in
air entrapment and alveolar hyperinflation during the
episode with symptoms disappearing between attacks.
The primary characteristics of an asthma exacerbation
are as follows:
 Bronchial smooth muscle constriction
 Mucus production (without infection) due to the
increased presence of leukocytes, such as eosinophils
 Bronchial mucosa inflammation and thickening due
to cellular and fluid infiltration36
Admission to a hospital occurs if signs and
symptoms of an asthma exacerbation do not improve
after several hours of medical therapy, especially if
FEV1 is less than 50% of normal.37 Status asthmaticus is
a severe, life-threatening airway obstruction with the
potential for cardiopulmonary complications, such as
arrhythmia, heart failure, and cardiac arrest. Status asth-
maticus is not responsive to basic medical therapies
and is characterized by severe hypoxemia and hyper-
carbia that require assisted or mechanical ventilation.38
CHRONIC BRONCHITIS
Chronic bronchitis is the presence of cough and pul-
monary secretion expectoration for at least 3 months,
2 years in a row.19,39 Chronic bronchitis is usually
linked to cigarette smoking or, less likely, to air pollu-
tion or infection. It begins with the following8:
 Narrowing of large, then small, airways due to
inflammation of bronchial mucosa
 Bronchial mucous gland hyperplasia and bronchial
smooth muscle cell hypertrophy
 Decreased mucociliary function
These changes result in air trapping, hyperinflated
alveoli, bronchospasm, and excess secretion retention.
The definition of an acute exacerbation of chronic
bronchitis is vague.40 The patient often describes
(1) worsened dyspnea at rest or with activity, with a
notable inability to ambulate, eat, or sleep; (2) fatigue;
and (3) abnormal sputum production or inability to
clear sputum. On clinical examination, the patient
may have hypoxemia, hypercarbia, pneumonia, cor pul-
monale, or worsening of comorbidities. Hospital
admission is determined by the degree of respira-
tory failure, hemodynamic stability, the number of
recent physician visits, home oxygen use, and doses of
pulmonary medications.40
EMPHYSEMA
Emphysema may be genetic (a1-antitrypsin protein
deficiency) in origin, in which the lack of proteolytic
inhibitors allows the alveolar interstitium to be
Table 2-7 CHARACTERISTICS AND GENERAL MANAGEMENT OF OBSTRUCTIVE DISORDERS

Disorder Observation Palpation Auscultation Cough Chest X-Ray Management

Asthma Tachypnea Tachycardia with Polyphonic Tight, usually During exacerbation: Removal of causative
(exacerbation) Fatigue weak pulse on wheezing on nonproductive, translucent lung agent
Anxiety inspiration expiration > then slightly fields, flattened Bronchodilators
Pursed lip Increased A-P inspiration productive of diaphragms, Corticosteroids
breathing chest diameter Diminished benign sputum increased Supplemental O2
Active expiration Decreased tactile breath A-P diameter IV fluid administration
Cyanosis, if severe and vocal sounds of chest, more
Accessory muscle fremitus horizontal ribs.
use Hyper-resonant Chest x-ray is normal
percussion between asthma
Pulsus paradoxus exacerbations.
(systolic blood
pressure
decreases on
inspiration),
if severe
Chronic ‘‘Blue bloater’’ Tachycardia Rhonchi Spasmodic cough Translucent lung fields. Smoking cessation
bronchitis with stocky Hypertension Diminished Sputum ranges Flattened diaphragms. Bronchodilator
build and Decreased breath sounds from clear to  Cardiomegaly Steroids
dependent tactile and Crackles purulent with increased Expectorants

Respiratory System
edema vocal fremitus Often most bronchovascular Antibiotics if infection
Tachypnea with Hyper-resonant productive markings. exists
prolonged percussion in the morning Diuretics if cor
expiratory Increased A-P chest pulmonale present
phase diameter Supplemental O2
Pursed lip Bronchopulmonary
breathing hygiene
Accessory muscle Assisted or mechanical
use, often with ventilation, if severe
fixed upper

CHAPTER 2
extremities
Elevated shoulders
Barrel chest
Fatigue
Anxiety
Continued

71
 72
Table 2-7 CHARACTERISTICS AND GENERAL MANAGEMENT OF OBSTRUCTIVE DISORDERS—cont’d

CHAPTER 2
Disorder Observation Palpation Auscultation Cough Chest X-Ray Management
Emphysema ‘‘Pink puffer’’ See Chronic Very diminished Usually absent and Translucent lung fields. Bronchodilators
with cachexia bronchitis, breath sounds nonproductive Flattened diaphragms. Supplemental O2
Otherwise, see above Wheeze Bullae. Nutritional support
Chronic Crackles  Small heart with
bronchitis, above decreased vascular
markings.

Respiratory System
Cystic fibrosis Tachypnea See Chronic Crackles Cough likely Translucent lung fields. Antibiotics
Fatigue bronchitis, Diminished tight, either Flattened diaphragms. Bronchodilators
Accessory above breath sounds controlled or Fibrosis Mucolytics
muscle use Rhonchi spasmodic Atelectasis Supplemental O2
Barrel chest Usually very Enlarged Bronchopulmonary
Cachexia viscous, greenish right ventricle. hygiene
Clubbing sputum  blood Linear opacities Nutritional support
streaks Psychosocial support
Lung transplantation
Bronchiectasis See Cystic fibrosis, See Chronic See Cystic fibrosis, Purulent, Patchy infiltrates. Antibiotics
above bronchitis, above odorous  Atelectasis. Bronchodilators
above sputum + Honeycombing, if Corticosteroids
 Hemoptysis advanced. Supplemental O2
Increased vascular IV fluid administration
markings. Nutritional support
Crowded bronchial Bronchopulmonary
markings. hygiene
 Pain control for
pleuritic pain
Lung transplantation
,With or without; A-P, anterior-posterior.

destroyed, or it may be caused by cigarette smoking, air
pollutants, or infection. Three types of emphysema
occur: centrilobular (centriacinar), panlobular (pana-
cinar), and paraseptal. Centrilobular emphysema affects
the respiratory bronchioles and the proximal acinus,
mostly within the upper lobes. Panlobular emphysema
affects the respiratory bronchioles, alveolar ducts
and sacs, and alveoli. Paraseptal emphysema affects
the distal acinus and can be associated with bullae
formation and pneumothorax.41
Emphysema leads to progressive destruction of
alveolar walls and adjacent capillaries secondary to the
following8:
 Decreased pulmonary elasticity
 Premature airway collapse
 Bullae formation (A bulla is a pocket of air sur-
rounded by walls of compressed lung parenchyma.)
These changes result in decreased lung elasticity, air
trapping, and hyperinflation.42 Reasons for hospital
admission are similar to those of a patient with chronic
bronchitis, except cor pulmonale does not develop
until the late stages of emphysema. A spontaneous
PTX is a sequela of emphysema in which a bleb
(a pocket of air between the two layers of visceral
pleura) ruptures to connect with the pleural space.
CYSTIC FIBROSIS
Cystic fibrosis (CF) is a lethal, autosomal-recessive trait
(chromosome 7) that affects exocrine glands of the
entire body, particularly of the respiratory, gastrointes-
tinal, and reproductive systems. Soon after birth, an
initial pulmonary infection occurs that leads to the
following changes throughout life8:
 Bronchial and bronchiolar walls become inflamed.
 Bronchial gland and goblet cells hypertrophy to
create tenacious pulmonary secretions.
 Mucociliary clearance is decreased.
These changes result in bronchospasm, atelec-
tasis, V_ = Q_ mismatch, increased airway resistance,
hypoxemia, and recurrent pulmonary infections.42
Hospitalization may be indicated if there is increased
sputum production or cough for longer than 2 weeks;
worsened dyspnea or pulmonary function; weight
loss; or the development of hemoptysis, PTX, or cor
pulmonale.43
BRONCHIECTASIS
Bronchiectasis is an obstructive, restrictive disorder
characterized by the following8:
 Destruction of the elastic and muscular bronchiole
walls
Respiratory System CHAPTER 2 73
 Destruction of the mucociliary escalator (in which
normal epithelium is replaced by nonciliated
mucus-producing cells)
 Bronchial dilatation
 Bronchial artery enlargement
It is defined as the permanent dilatation of airways
that have a normal diameter of greater than 2 mm.44
Bronchiectasis results in fibrosis and ulceration of
bronchioles, chronically retained pulmonary secre-
tions, atelectasis, and infection. The etiology of bron-
chiectasis includes previous bacterial respiratory
infection, CF, tuberculosis, and immobile cilia syn-
dromes.44 In order of frequency, bronchiectatic changes
occur in the left lower lobe, right middle lobe, lingula,
entire left lung, right lower lobe, and entire right
lung.44 Hospitalization usually occurs when complica-
tions of bronchiectasis arise, including hemoptysis,
pneumonia, PTX, empyema, or cor pulmonale.
Restrictive Pulmonary Conditions
Restrictive lung diseases or conditions may be
described by onset (acute versus chronic) or location
(i.e., pulmonary or extrapulmonary). Restrictive pat-
terns are characterized by low lung volumes that result
from decreased lung compliance and distensibility and
increased lung recoil. The end result is increased work
of breathing. Table 2-8 outlines restrictive disorders,
their general physical and diagnostic findings, and
their general clinical management.
ATELECTASIS
Atelectasis involves the partial or total collapse of
alveoli, lung segments(s), or lobe(s). It most commonly
results from hypoventilation or ineffective pulmonary
secretion clearance.The following conditions may also
contribute to atelectasis:
 Inactivity
 Upper abdominal or thoracic incisional pain
 Compression of lung parenchyma
 Diaphragmatic restriction from weakness or
paralysis
 Postobstructive pneumonia
 Presence of a foreign body
The result is hypoxemia from V_ = Q_ mismatch, trans-
pulmonary shunting, and pulmonary vasoconstriction
of variable severity depending on the amount of atelec-
tasis.8 General risks for the development of atelectasis
include cigarette smoking or pulmonary disease, obe-
sity, and increased age. Perioperative or postoperative
risk factors include altered surfactant function from
anesthesia, emergent or extended operative time,
 74
CHAPTER 2
Respiratory System
Table 2-8 CHARACTERISTICS AND GENERAL MANAGEMENT OF RESTRICTIVE DISORDERS
Disorder Observation Palpation Auscultation Cough Chest X-Ray Management
Atelectasis  Tachypnea  Tachycardia Crackles at Dry or wet Linear opacity of Incentive
 Fever Decreased tactile involved site Sputum ranges in involved area spirometry
 Shallow fremitus and Diminished color, depending If lobar collapse exists, Supplemental O2
respirations vocal resonance breath sounds on reason for white triangular- Functional
If lobar collapse atelectasis. shaped density mobilization
exists, absent or Fissure and Bronchopulmonary
bronchial breath diaphragmatic hygiene
sounds displacement
Pneumonia See Atelectasis See Atelectasis Crackles Initially dry to Well-defined density at Antibiotics
Fatigue Decreased chest Rhonchi more productive. the involved lobe(s) Supplemental O2
 Accessory wall expansion at Bronchial breath Sputum may be  Air bronchogram IV fluid
muscle use involved site sounds over area yellow, tan,  Pleural effusion administration
Dull percussion of consolidation green, or rusty. Functional
mobilization
Bronchopulmonary
hygiene
Pulmonary edema Tachypnea Increased tactile Symmetric wet Sputum may be Increased hilar Diuretics
Orthopnea and vocal crackles, thin, frothy, vascular markings Other medications,
Anxiety fremitus especially at clear, white, Kerley’s B lines (short, dependent on
Accessory bases or pink. horizontal lines at etiology
muscle use  Wheeze lung field periphery) Supplemental O2
 Pleural effusion Hemodynamic
Left ventricular monitoring
hypertrophy
Cardiac silhouette
Fluffy opacities
 Adult respiratory Labored breathing Hypotension Diminished breath Generally without Pulmonary edema Mechanical
distress and altered Tachycardia or sounds sputum, with diffuse bilateral ventilation
syndrome mental status at bradycardia Crackles although sputum patchy opacities Hemodynamic
(ARDS) onset Decreased bilateral Wheeze may be present if ‘‘Ground glass’’ monitoring
Tachypnea chest wall Rhonchi (rare) infection exists appearance IV fluid
Increased PA expansion or from the administration
pressure Dull percussion presence of an Prone positioning
endotracheal Nitrous oxide
tube. therapy
Pulmonary Rapid onset of Hypotension Diminished or Usually absent. Nondiagnostic for PE. Anticoagulation
embolism tachypnea Tachycardia absent breath May show density at Hemodynamic
(PE)  Chest pain Decreased chest sounds distal infarct site with stabilization
Anxiety wall expansion to PE lucency distal to Supplemental O2
Dysrhythmia at involved site Wheeze the infarct or mechanical
Lightheadedness Crackles Decreased lung ventilation
volume Inferior vena cava
Dilated PA with filter placement
increased vascular Thrombolysis
markings Embolectomy
 Atelectasis
Lung contusion Tachypnea Hypotension Wet crackles Weak cough if pain Patchy, irregular Pain management
Chest wall Tachycardia Diminished or present, dry or opacities localized Supplemental O2
ecchymosis Crepitus due to absent breath wet. to a segment or lobe Mechanical
Cyanosis, rib fracture sounds at Sputum may be  Consolidation ventilation
if severe involved site clear, white, or IV fluid
blood-tinged. administration

Respiratory System
,With or without; PA, pulmonary artery.
Data fromJM Thompson, GK McFarland, JE Hirsch, et al (eds): Clinical Nursing Practice. St Louis: Mosby, 1993; LM Malarkey, ME McMorrow (eds): Nurse’s Manual of
Laboratory Tests and Diagnostic Procedures (2nd ed). Philadelphia: Saunders, 2000.

CHAPTER 2
75
76 CHAPTER 2 Respiratory System
altered consciousness or prolonged narcotic use,
hypotension, and sepsis.
PNEUMONIA
Pneumonia is the multistaged inflammatory reaction of
the distal airways from the inhalation of bacteria,
viruses, microorganisms, foreign substances, gastric
contents, dusts, or chemicals, or as a complication of
radiation therapy.8 Pneumonia is often described
as community or hospital (nosocomial) acquired.
Nosocomial pneumonia is defined as pneumonia
occurring after 48 hours within a hospital stay and is
associated with ventilator use, contaminated equip-
ment, or poor hand washing.45,46 The consequences
of pneumonia are V_ = Q_ mismatch and hypoxemia.
The phases of pneumonia are the following44:
1. Alveolar edema with exudate formation (0 to 3 days)
2. Alveolar infiltration with bacterial colonization, red
and white blood cells, and macrophages (2 to 4 days)
3. Alveolar infiltration and consolidation with dead
bacteria, white blood cells, and fibrin (4-8 days)
4. Resolution with expectoration or enzymatic
digestion of infiltrative cells (after 8 days)
5. Pneumonia may be located in single or multiple
lobes either unilaterally or bilaterally. The complete
clearance of pneumonia can take up to 6 weeks.45
Resolution of pneumonia is slower with increased
age, previous pneumonia, positive smoking history,
poor nutritional status, or with coexisting illness.
PULMONARY EDEMA
The etiology of pulmonary edema can be categorized as
either cardiogenic or noncardiogenic. Cardiogenic pul-
monary edema is an imbalance of hydrostatic and on-
cotic pressures within the pulmonary vasculature that
results from backflow of blood from the heart.8
This backflow increases the movement of fluid from
the pulmonary capillaries to the alveolar spaces.
Initially, the fluid fills the interstitium and then pro-
gresses to the alveolar spaces, bronchioles, and, ulti-
mately, the bronchi. A simultaneous decrease in the
lymphatic drainage of the lung may occur, exacerbating
the problem. Cardiogenic pulmonary edema can occur
rapidly (flash pulmonary edema) or insidiously in asso-
ciation with left ventricular hypertrophy, mitral
regurgitation, or aortic stenosis. Cardiogenic pulmo-
nary edema results in atelectasis, V_ = Q_ mismatch, and
hypoxemia.8
Noncardiogenic pulmonary edema can result from
alterations in capillary permeability (as in Adult
Respiratory Distress Syndrome [ARDS] or
pneumonia), intrapleural pressure from airway obstr-
uction(s), or lymph vessel obstruction. The results are
similar to those of cardiogenic pulmonary edema.
CLINICAL TIP
 Beware of a flat position in bed or other positions
that worsen dyspnea during physical therapy
intervention in patients with pulmonary edema.
ADULT RESPIRATORY DISTRESS SYNDROME
ARDS is an acute inflammation of the lung that is
generally associated with aspiration, drug toxicity,
inhalation injury, pulmonary trauma, shock, systemic
infections, and multisystem organ failure.47 It is consid-
ered a critical illness and has a lengthy recovery and a
high mortality rate. Characteristics of ARDS include
the following:
1. An exudative phase (hours to days) characterized by
increased capillary permeability, interstitial and alve-
olar edema, hemorrhage, and alveolar consolidation
with leukocytes and macrophages
2. A proliferative stage (days to weeks) characterized
by hyaline formation on alveolar walls and intr-
aalveolar fibrosis resulting in atelectasis, V_ = Q_
mismatch, severe hypoxemia, and pulmonary
hypertension
Latent pulmonary sequelae of ARDS are vari-
able and range from no impairments to mild exe-
rtional dyspnea to mixed obstructive-restrictive
abnormalities.48
CLINICAL TIP
 Prone positioning can be used in the ICU setting as
a treatment strategy in patients with ARDS. Prone
positioning facilitates improved aeration to dorsal
lung segments, improved V_ = Q_ matching, and
improved secretion drainage.49,50 Prone
positioning should only be performed by
experienced clinicians and with proper equipment
(specialty frames or beds).
PULMONARY EMBOLISM
PE is the partial or full occlusion of the pulmonary vas-
culature by one large or multiple small emboli from
one or more of the following possible sources: throm-
boembolism originating from the lower extremity
(more than 90% of the time),51 air entering the venous

system through catheterization or needle place-
ment, fat droplets from traumatic origin, or tumor
fragments. A PE results in52
 Decreased blood flow to the lungs distal to the
occlusion
 Atelectasis and focal edema
 Bronchospasm from the release of humeral agents
 Possible parenchymal infarction
Emboli size and location determine the extent of
V_ = Q_ mismatch, pulmonary shunt, and thus the
degree of hypoxemia and hemodynamic instability.51
The onset of PE is usually extremely acute and may be
a life-threatening emergency, especially if a larger
artery is obstructed.
CLINICAL TIP
 PT intervention should be discontinued if the signs
and symptoms of PE arise during treatment (see
Table 2-7). Seat or lay the patient down, and call for
help immediately.
 If you are evaluating the patient for the first time
since a PE, make sure the patient has received a
therapeutic level of anticoagulation medicine or that
other medical treatment has been completed. Refer
to Chapter 6 for more information on
anticoagulation.
INTERSTITIAL LUNG DISEASE
Interstitial lung disease (ILD) is a general term for the
destruction of the respiratory membranes in multiple
lung regions that occurs after an inflammatory phase
in which the alveoli become infiltrated with macro-
phages and mononuclear cells, followed by a fibrosis
phase in which the alveoli become scarred with colla-
gen.44 Fibrotic changes may extend proximally toward
the bronchioles.There are more than 100 suspected pre-
disposing factors for ILD, such as infectious agents,
environmental and occupational inhalants, and drugs;
however, no definite etiology is known.8,53 Clinically,
the patient presents with exertional dyspnea and bilat-
eral diffuse chest radiograph changes, and without pul-
monary infection or neoplasm.54 ILD has a wide
variety of clinical features and patterns beyond the
scope of this text; however, the general sequela of ILD
is a restrictive pattern with V_ = Q_ mismatch.
LUNG CONTUSION
Lung contusion is the result of a sudden compres-
sion and decompression of lung tissue against the
Respiratory System CHAPTER 2 77
chest wall from a direct blunt (e.g., fall) or blast
(e.g., air explosion) trauma. The compressive force
causes shearing of the alveolar-capillary membrane
and results in microhemorrhage, whereas the
decompressive force causes a rebound stretching of
the parenchyma.55 There is a diffuse accumulation of
blood and fluid in the alveoli and interstitium
that causes alveolar shunting, decreased lung compli-
ance, and increased pulmonary vascular resistance.56
The resultant degree of hypoxemia is dependent on
the size of contused tissue. Lung contusion is usually
located below rib fracture(s) and is associated with
PTX and flail chest.
Restrictive Extrapulmonary Conditions
Disorders or trauma occurring outside of the visceral
pleura may also affect pulmonary function. Table 2-9
outlines restrictive extrapleural disorders, their gen-
eral physical findings, and their general medical
management.
PLEURAL EFFUSION
A pleural effusion is the presence of transudative or
exudative fluid in the pleural space. Transudative fluid
results from a change in the hydrostatic/oncotic
pressure gradient of the pleural capillaries, which is
associated with congestive heart failure, cirrhosis,
PE, and pericardial disease.57 Exudative fluid (con-
taining cellular debris) occurs with pleural or paren-
chymal inflammation or altered lymphatic drainage,
which is associated with neoplasm, tuberculosis
(TB), pneumonia, pancreatitis, rheumatoid arthritis,
and systemic lupus erythematosus.57,58 Pleural effusions
may be unilateral or bilateral, depending on the cause
of the effusion, and may result in compressive
atelectasis.
PNEUMOTHORAX
PTX is the presence of air in the pleural space that can
occur from (1) visceral pleura perforation with move-
ment of air from within the lung (spontaneous pneu-
mothorax), (2) chest wall and parietal pleura
perforation with movement of air from the atmosphere
(traumatic or iatrogenic pneumothorax), or (3) forma-
tion of gas by microorganisms associated with empye-
ma. Spontaneous PTX can be a complication of
chronic obstructive pulmonary disease or TB, or it
can occur idiopathically in tall persons secondary to
elevated intrathoracic pressures in the upper lung
zones.8 Traumatic PTX results from rib fracture,
chest wounds, or other penetrating chest trauma.
 78
Table 2-9 CHARACTERISTICS AND GENERAL MANAGEMENT OF EXTRAPLEURAL DISORDERS

Disorder Observation Palpation Auscultation Cough Chest X-Ray Management

Pleural effusion Tachypnea  Tachycardia Normal to Usually absent Homogenous If effusion is small and
 Discomfort Decreased tactile decreased breath density in respiratory status is

CHAPTER 2
from pleuritis fremitus sounds or dependent lung stable, monitor only
Decreased chest Dull percussion bronchial breath Fluid obscures Supplemental O2
expansion on sounds at the diaphragm and Chest tube placement
involved side level of the fills costophrenic for moderate or
effusion angle large effusion
Fluid shifts with Thoracocentesis if

Respiratory System
change in patient persistent
position Pleurodesis
Mediastinal shift to Diuretics
opposite side, Workup to determine
if severe cause if unknown
Pain management if
pleuritic pain present
Pneumothorax See Pleural See Pleural Diminished breath Usually absent Translucent area If PTX is small and
(PTX) effusion, effusion, sounds near usually at apex respiratory status is
above above involved site of lung stable, monitor only
Absent if tension  Associated If PTX is moderate-
PTX depressed size or large, chest
diaphragm, tube placement
atelectasis, lung Supplemental O2
collapse, Pain management if
mediastinal shift, pleuritic pain present
if severe
Visceral pleura can
be seen as thin
white line
Hemothorax See Pneumothorax, See Pleural See Pneumothorax, Usually absent, See Pleural Supplemental O2
above effusion, above unless associated effusion, above Chest tube placement
above with significant Pain management if
lung contusion pleuritic pain present
in which Monitor and treat for
hemoptysis may shock
occur Blood transfusion,
as needed
,With or without.

Complications of mechanical ventilation and central
line placement are two examples of iatrogenic PTX.
Pneumothoraces also may be described as follows:
 Closed: Without air movement into the pleural
space during inspiration and expiration (chest wall
intact)
 Open: With air moving in and out of the pleural
space during inspiration and expiration (pleural
space in contact with the atmosphere)
 Tension: With air moving into the pleural space only
during inspiration
PTX is usually unilateral. Complications of PTX
include atelectasis and V_ = Q_ mismatch. If a large or
tension PTX exists, there can be lung collapse, medias-
tinal shift (displacement of the mediastinum) to the
contralateral side, and cardiac tamponade (altered
cardiac function secondary to decreased venous return
to the heart from compression).8
HEMOTHORAX
Hemothorax is characterized by the presence of
blood in the pleural space from damage to the pleu-
ra and great or smaller vessels (e.g., interstitial
arteries). Causes of hemothorax are penetrating
or blunt chest wall injury, draining aortic aneur-
ysms, pulmonary arteriovenous malformations, and
extreme coagulation therapy. Blood and air together
in the pleural space, common after trauma, is a
hemopneumothorax.
FLAIL CHEST
Flail chest is caused by the double fracture of three or
more adjacent ribs, resulting from a crushing chest
injury or vigorous cardiopulmonary resuscitation.
The sequelae of this injury are8:
 A paradoxical breathing pattern, with the discontin-
uous ribs moving inward on inspiration and outward
on expiration as a result of alterations in atmospheric
and intrapleural pressure gradients
 Contused lung parenchyma under the flail portion
In severe cases, mediastinal shift to the contralateral
side occurs as air from the involved side is shifted and
rebreathed (pendelluft).
EMPYEMA
Empyema is the presence of anaerobic bacterial pus in
the pleural space, resulting from underlying infection
(e.g., pneumonia, lung abscess) that crosses the visceral
pleura or chest wall and parietal pleura penetration
from trauma, surgery, or chest tube placement.
Empyema formation involves pleural swelling and
Respiratory System CHAPTER 2 79
exudate formation, continued bacterial accumulation,
fibrin deposition on pleura, and chronic fibroblast
formation.
Chest Wall Restrictions
A restrictive respiratory pattern may be caused by
abnormal chest wall movement not directly related to
pulmonary pathology. Musculoskeletal changes of
the thoracic cage can occur with diseases such as anky-
losing spondylitis, rheumatoid arthritis, and kyphos-
coliosis, or with conditions such as pregnancy
and obesity. Neurologic diagnoses, such as cervical/
thoracic spinal cord injury, or Guillain-Barre¤ syn-
drome can also create restrictive breathing patterns
depending on the level of respiratory muscle weakness
or paralysis. Refer to Chapter 4 for more informa-
tion on neurologic disorders. Kyphoscoliosis and
obesity are discussed in further detail because of
their frequency in the clinical setting. Kyphoscoliosis
can result in atelectasis from decreased thoracic cage
mobility, respiratory muscle insufficiency, and paren-
chymal compression. Other consequences of kypho-
scoliosis are progressive alveolar hypoventilation,
increased dead space, hypoxemia with eventual pul-
monary artery hypertension, cor pulmonale, or
mediastinal shift (in very severe cases) toward the
direction of the lateral curve of the spine.8
Obesity (defined as body weight 20% to 30% above
age-predicted and gender-predicted weight) can
cause an abnormally elevated diaphragm position
secondary to the upward displacement of abdominal
contents, inefficient respiratory muscle use, and a
noncompliant chest wall. These factors result in early
airway closure (especially in dependent lung areas),
tachypnea, altered respiratory pattern, V_ = Q_ mis-
match, and secretion retention. Refer to Chapter 8
for more information on obesity management with
bariatric procedures.
MANAGEMENT
Pharmacologic Agents
The pharmacologic agents commonly used for the
management of respiratory dysfunction include adre-
nocortical steroids (glucocorticoids) (Appendix Table
IV-8), antihistamines (Appendix Table IV-9), broncho-
dilators (Appendix Table IV-10), leukotriene modifiers
(Appendix Table IV-11), and mast cell stabilizers
(AppendixTable IV-12).
80 CHAPTER 2 Respiratory System

Procedure Definition Indications

Pneumonectomy Removal of entire Malignant lesions
lung with or without
resection of the Unilateral tuberculosis
mediastinal lymph Extensive unilateral
nodes bronchiectasis
Multiple lung abscesses
Massive hemoptysis
Bronchopleural fistula
Lobectomy Resection of one or Lesions confined to a
more lobes of lung single lobe
Pulmonary tuberculosis
Bronchiectasis
Lung abscesses or cysts
Trauma
Segmental resection Resection of Small peripheral lesions
bronchovascular
segment of lung lobe Bronchiectasis
Congenital cysts or blebs
Wedge resection Removal of small Small peripheral lesions
wedge-shaped section (without lymph node
of lung tissue involvement)
Thoracic Procedures
The most common thoracic operative and nonopera-
tive procedures for respiratory disorders are described
below in alphabetical order.2,59,60 Lung transplanta-
tion is described separately in Chapter 12, along
with other transplant procedures. Illustrations of
many of the procedures described below are shown
in Figure 2-12.
Bronchoplasty: Also called a sleeve resection. Resection and
reanastomosis (reconnection) of a bronchus; most
commonly performed for bronchial carcinoma
(a concurrent pulmonary resection may be
performed as well).
Laryngectomy: The partial or total removal of one or
more vocal cords; most commonly performed for
laryngeal cancer.
Laryngoscopy: Direct visual examination of the larynx
with a fiberoptic scope; most commonly performed
to assist with differential diagnosis of thoracic
pathology or to assess the vocal cords.
Lobectomy: Resection of one or more lobes of the lung;

Peripheral granulomas
most commonly performed for isolated lesions.
Pulmonary blebs
Lung volume reduction: The unilateral or bilateral removal
of one or more portions of emphysematous lung
parenchyma, resulting in increased alveolar surface
Bronchoplastic reconstruction Resection of lung Small lesions involving the
area.
(also called sleeve resection) tissue and bronchus carina or major bronchus Mediastinoscopy: Endoscopic examination of the medias-
with end-to-end without evidence of
reanastomosis of metastasis tinum; most commonly performed for precise local-
bronchus
May be combined with ization and biopsy of a mediastinal mass or for the
lobectomy
removal of lymph nodes.
Pleurodesis: The obliteration of the pleural space; most
commonly performed for persistent pleural effu-
FIGURE 2-12 sions or pneumothoraces. A chemical agent is intro-
Images of thoracic surgeries: pneumonectomy, lobectomy, duced into the pleural space via thoracostomy
segmental resection, wedge resection, bronchoplastic resection (chest) tube or with a thoracoscope.
(AKA sleeve). (From Urden L, Stacy K, Lough M [eds]. Pneumonectomy: Removal of an entire lung; most com-
Thelan’s Critical Care Nursing: Diagnosis and Management monly performed as a result of bronchial carcinoma,
[5th ed]. St. Louis: Mosby, 2006;Table 23-6.) emphysema, multiple lung abscesses, bronchiectasis,
or TB.
Ribresection: Removal of a portion of one or more ribs for
CLINICAL TIP accessing underlying pulmonary structures as a
treatment for thoracic outlet syndrome or for bone
 Be aware of respiratory medication changes,
grafting.
especially the addition or removal of medications
Segmentectomy: Removal of a segment of a lung; most
from the regimen.
commonly performed for a peripheral bronchial or
 Generally, nebulized medications are optimally active
parenchymal lesion.
15 to 20 minutes after administration.
Thoracentesis: Therapeutic or diagnostic removal of
 If a patient has an inhaler, it may be beneficial for
pleural fluid via percutaneous needle aspiration.
the patient to bring it to physical therapy sessions in
Thoracoscopy (video-assisted thoracoscopic surgery):
case of activity-induced bronchospasm.
Examination, through the chest wall with a

thoracoscope, of the pleura or lung parenchyma for
pleural fluid biopsy or pulmonary resection.
Tracheal resection and reconstruction: Resection and reanasto-
mosis (reconnection) of the trachea, main stem
bronchi, or both; most commonly performed
for tracheal carcinoma, trauma, stricture, or
tracheomalacia.
Tracheostomy: Incision of the second or third tracheal
rings or the creation of a stoma or opening for a tra-
cheostomy tube; preferred for airway protection
and prolonged ventilatory support or after laryn-
gectomy, tracheal resection, or other head and neck
surgery.
Wedge resection: Removal of lung parenchyma without
regard to segment divisions (a portion of more
than one segment but not a full lobe); most
commonly performed for peripheral parenchymal
carcinoma.
Physical Therapy Intervention
GOALS
The primary physical therapy goals in the treatment of
patients with primary lung pathology include promot-
ing independence in functional mobility; maximizing
gas exchange (by improving ventilation and airway
clearance); and increasing aerobic capacity, respiratory
muscle endurance, and the patient’s knowledge of his
or her condition. General treatment techniques to
accomplish these goals are breathing retraining exer-
cises, secretion clearance techniques, positioning, func-
tional activity and exercise with vital sign monitoring,
and patient education.
A physiologically based treatment hierarchy for
patients with impaired oxygen transport, developed
by Elizabeth Dean, is a helpful tool in treating patients
with cardiopulmonary impairments. The hierarchy is
based on the principle that physiologic function is
best when an individual is upright and moving.42
Dean’s hierarchy is shown inTable 2-10.
BASIC CONCEPTS FOR THE TREATMENT OF
PATIENTS WITH RESPIRATORY IMPAIRMENTS
BRONCHOPULMONARY HYGIENE. The following
are basic concepts for implementing a bronchopulmo-
nary hygiene program for patients with respiratory
dysfunction:
 A basic understanding of respiratory pathophysiolo-
gy is necessary because bronchopulmonary hygiene
is not indicated for certain conditions, such as a
pleural effusion or pulmonary edema.
Respiratory System CHAPTER 2 81
 To develop a proper plan of care, the physical thera-
pist must also understand whether the respiratory
pathology is acute or chronic, reversible or irreversi-
ble, or stable or progressive, as well as the potential
for alterations in other body systems.
 The bronchopulmonary hygiene treatment plan will
vary in direct correlation to the patient’s respiratory
or medical status. The physical therapist must be
cognizant of the potential for rapid decline in
patient status and modify treatment accordingly.
 Bronchopulmonary hygiene requires constant reas-
sessment before, during, and after physical therapy
intervention as well as on a daily basis.
 Bronchopulmonary hygiene may be enhanced by the
use of supplemental O2 and medication such as
bronchodilators. Both O2 and bronchodilators are
medications that require a physician’s order.
 Tolerance to bronchopulmonary hygiene can be
monitored by pulse oximetry and can help determine
the need for supplemental O2 during therapy
sessions.
 Cough effectiveness can be enhanced with pain
medication before therapy, splinting (if there is an
incision or a rib fracture), positioning, and proper
hydration.
 Patients with an ineffective cough for secretion
removal may require nasotracheal suctioning. This
technique should only be performed by well-trained
therapists.
 Devices that provide oscillatory positive expiratory
pressure, such as the Flutter device, can be a good
adjunct to manual vibration/shaking in patients
with large amounts of secretions (e.g., CF,
bronchiectasis).16,61,62
 Patients with chronic respiratory diseases, such as CF
or bronchiectasis, usually have an established routine
for their bronchopulmonary hygiene. Although this
routine may require modification in the hospital,
maintaining this routine as much as possible will
optimize the continuity of care. Be aware of the
usual order of postural drainage positions and
whether certain positions are uncomfortable.
 Document baseline sputum production, including
certain times of the day when the patient is most
productive.
 Patients with an obstructive pulmonary disorder
generally do well with slow, prolonged exhalations,
such as in pursed lip breathing. A patient may
do this maneuver naturally. Frequent rest breaks
between coughs are also helpful to prevent air
trapping and improve secretion clearance.
82 CHAPTER 2 Respiratory System

Table 2-10 DEAN’S HIERARCHY FOR TREATMENT OF PATIENTS WITH IMPAIRED OXYGEN TRANSPORT
PREMISE:The Position of Optimal Physiologic Function Is Being Upright and Moving

I. Mobilization and exercise
II. Body positioning
III. Breathing control
maneuvers
IV. Coughing maneuvers
V. Relaxation and energy-
conservation
interventions
VI. ROM exercises
(cardiopulmonary
indications)
VII. Postural drainage
positioning
VIII. Manual techniques
IX. Suctioning
From Frownfelter D, Dean E: Cardiovascular and Pulmonary Physical Therapy: Evidence and Practice (4th ed.), St Louis: Mosby, 2006.
Goal:To elicit an exercise stimulus that
addresses one of the three effects on
the various steps in the oxygen
transport pathway, or some
combination thereof
Goal:To elicit a gravitational stimulus
that simulates being upright and
moving as much as possible: active,
active-assisted, or passive
Goal:To augment alveolar ventilation,
to facilitate mucociliary transport,
and to stimulate coughing
Goal:To facilitate mucociliary clearance
with the least effect on dynamic
airway compression and the fewest
adverse cardiovascular effects
Goal:To minimize the work of
breathing and of the heart and to
minimize undue oxygen demand
Goal:To stimulate alveolar ventilation
and alter its distribution
Goal:To facilitate airway clearance
using gravitational effects
Goal:To facilitate airway clearance
in conjunction with specific body
positioning
Goal:To facilitate the removal of airway
secretions collected centrally
A. Acute effects
B. Long-term effect
C. Preventive effects
A. Hemodynamic effects related to fluid shifts
B. Cardiopulmonary effects on ventilation and its
distribution, perfusion, ventilation, and
perfusion matching and gas exchange
A. Coordinated breathing with activity and
exercise
B. Spontaneous eucapnic hyperventilation
C. Maximal tidal breaths and movement in three
dimensions
D. Sustained maximal inspiration
E. Pursed-lip breathing to end-tidal expiration
F. Incentive spirometry
A. Active and spontaneous cough with closed
glottis
B. Active-assisted (self-supported or supported
by other)
C. Modified coughing interventions with open
glottis (e.g., forced expiratory technique, huff)
A. Relaxation procedures at rest and during
activity
B. Energy conservation, (i.e., balance of activity
and rest, performing activities in an energy-
efficient manner, improved movement
economy during activity)
C. Pain-control interventions
A. Active
B. Assisted-active
C. Passive
A. Bronchopulmonary segmental drainage
positions
A. Autogenic drainage
B. Manual percussion
C. Shaking and vibration
D. Deep breathing and coughing
A. Open suction system
B. Closed suction system
C. Tracheal tickle
D. Instillation with saline
E. Use of manual hyperinflation bag (bagging)

Table 2-11 RESPIRATORY EVALUATION FINDINGS AND SUGGESTED PHYSICAL THERAPY
INTERVENTIONS
Evaluation Finding
Inspection Dyspnea or tachypnea at rest or with
exertion
Asymmetric respiratory pattern
Abnormal sitting or standing posture
Palpation Asymmetric respiratory pattern
Palpable fremitus as a result of retained
pulmonary secretions
Percussion Increased dullness as a result of retained
pulmonary secretions
Auscultation Diminished or adventitious breath sounds as
a result of retained pulmonary secretions
Cough Ineffective cough
effectiveness
 Patients with a restrictive pulmonary disorder gener-
ally do well with therapeutic activities to improve
inspiration, such as diaphragmatic breathing and
chest wall stretching.
 Many hospitals (especially in the ICU setting) have
incorporated rotational beds to facilitate frequent
changes in patient positioning. Some beds also have
modules for percussion/vibration. While the use
of these beds has shown positive outcomes,63 they
should not replace standard bronchopulmo-
nary hygiene by physical therapists; they should
supplement it.
ACTIVITY PROGRESSION. The following are basic
concepts of activity progression for patients with respi-
ratory dysfunction:
 Rating of perceived exertion or the Dyspnea scale
(see Table 2-3) are better indicators of exercise in-
Respiratory System CHAPTER 2 83
Suggested PT Intervention
Repositioning for comfort or more upright posture.
Relaxation techniques.
Energy conservation techniques. Diaphragmatic or
lateral costal expansion exercise.
Incentive spirometry.
Postural exercises.
Stretching of trunk and shoulder musculature.
Administer or request supplemental O2
Diaphragmatic or lateral costal expansion exercise.
Incentive spirometry.
Coughing exercises.
Upper extremity exercise.
Functional activity.
Manual techniques.
Postural drainage positions (See Appendix VIII).
Flutter valve, if applicable.
See Palpation, above.
See Palpation, above.
Positioning for comfort or to maximize expiratory
force.
Incisional splinting, if applicable.
Huffing and coughing techniques. Functional activity
or exercise.
External tracheal stimulation (tracheal tickle).
Naso/endotracheal suctioning.
Requesting bronchodilator or mucolytic treatment.
tensity than heart rate because a patient’s respiratory
limitations, such as dyspnea, generally supersede
cardiac limitations. Monitoring O2 saturation can
also assist in determining the intensity of the activity.
 Shorter, more frequent sessions of activity are often
better tolerated than are longer treatment sessions.
Patient education regarding energy conservation
and paced breathing contributes to increased activity
tolerance.
 A treatment session may need to be scheduled
according to the patient’s other hospital activities to
ensure that the patient is not over-fatigued for
therapy.
 Document the need and duration of seated or stand-
ing rest periods during a treatment session to help
measure functional activity progression or
regression.
84 CHAPTER 2 Respiratory System
 Although O2 may not be needed at rest, supple-
mental O2 with exercise may decrease dyspnea and
prolong exercise duration and intensity.
 Bronchopulmonary hygiene before an exercise
session may optimize activity tolerance.
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 3 Musculoskeletal System

Michele P. West INTRODUCTION

James J. Gaydos An understanding of musculoskeletal pathology and medical-surgical
Marka Gehrig intervention is often the basis of physical therapy evaluation and treat-
ment planning for patients with acute orthopedic impairments. The
primary goal of the physical therapist working with a patient in the
acute care setting is to initiate rehabilitative techniques that foster
early restoration of maximum functional mobility and reduce the risk
of secondary complications. The objectives of this chapter are to pro-
vide the following:
1. A brief description of the structure and function of the musculoskeletal
system
2. An overview of musculoskeletal evaluation, including physical exami-
nation and diagnostic tests
3. A description of fractures, including etiology, medical-surgical man-
agement, clinical findings, and physical therapy intervention
4. A description of joint arthroplasty and common surgeries of the
spine, including surgical management and physical therapy
intervention
5. An overview of common soft-tissue injuries, including surgical man-
agement and physical therapy intervention
6. A brief overview of equipment commonly used in the acute care set-
ting, including casts, braces, external fixators, and traction devices
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:
Pathology Practice Pattern
Fractures 4G
Dislocations 4D
Arthroplasty, Joint Resurfacing 4H
Limb Salvage Surgery 4J
Hip Disarticulation
Hemipelvectomy
Osteotomy 4I
Surgeries of the Spine
Soft-Tissue Surgeries

Please refer to the back cover of this book for a complete list of the pre-
ferred practice patterns, as individual patient conditions are highly vari-
able and other practice patterns may be applicable.

87
88 CHAPTER 3 Musculoskeletal System
STRUCTURE AND FUNCTION OF THE
MUSCULOSKELETAL SYSTEM
The musculoskeletal system is made up of the bony skel-
eton and contractile and noncontractile soft tissues,
including muscles, tendons, ligaments, joint capsules,
articular cartilage, and nonarticular cartilage. This
matrix of soft tissue and bone provides the dynamic
ability of movement, giving individuals the ability to
move through space, absorb shock, convert reactive
forces, generate kinetic energy, and perform fine-
motor tasks. The musculoskeletal system also provides
housing and protection for vital organs and the central
nervous system. As a result of its location and function,
the musculoskeletal system commonly sustains trau-
matic injuries and degenerative changes. The impair-
ments that develop from injury or disease can
significantly affect an individual’s ability to remain
functional without further pathologic compromise.
MUSCULOSKELETAL EXAMINATION
The initial evaluation of a patient with orthopedic dys-
function is invaluable to clinical management in the
acute care setting. Physical therapy intervention for
the patient with orthopedic impairments typically
occurs postoperatively or after an injury is managed by
the medical-surgical team.
Patient History
In addition to a standard medical review (see
Appendix I-A), information pertaining to the patient’s
musculoskeletal history should include the following:
 Cause and mechanism of injury at present
 Previous musculoskeletal, rheumatologic, or neuro-
logic disease, injury, or surgery
 Functional level before admission
 Previous use of assistive device(s)
 Recreation or exercise level and frequency
 Need for adaptive equipment or footwear on a regu-
lar basis (e.g., a shoe lift)
 History of falls
 History of chronic pain
An understanding of the current medical-surgical
management of musculoskeletal disease or injury
should include:
 Physician-dictated precautions or contraindications
to treatment, such as weight-bearing status or activ-
ity level, or for the positioning of extremities
 The need for a splint, brace, or other equipment at
rest or with activity
 Most recent lab values (e.g., hematocrit)
 Type and last dose of pain medication
 Whether or not the patient has been out of bed since
admission to the hospital
Pain
Musculoskeletal pain quality and location should be
determined subjectively and objectively. Use a pain
scale appropriate for the patient’s age, mental status,
and vision. Note if pain is constant or variable, and if
movement or position increases or decreases the pain.
Refer to Appendix VI for more detailed information
on pain assessment and management.
Observation
A wealth of information can be gathered by simple
observation of the patient.This includes:
 General appearance
 Level of alertness, anxiety, or stress
 Willingness to move or muscle guarding
 Presence of external orthopedic devices or
equipment
 Muscle substitutions on active movement
More specifically, the physical therapist should
observe posture, limb position, and skin integrity.
POSTURE
Observe the patient’s resting posture in supine, sitting,
and standing positions.This includes inspection of the
head, trunk, and extremities for alignment, symmetry,
deformity, or atrophy.
LIMB POSITION
Observe the resting limb position of the involved
extremity. Compare to both normal anatomic position
and to the contralateral side. Note if the limb is in
position naturally or if it is supported with a pillow,
roll, or wedge.
CLINICAL TIP
 A limb in a dependent position is at risk for edema
formation, even if it is dependent for only a short
period of time.
 Maintain joints in a neutral resting position
to preserve motion and maintain soft-tissue length.
 Musculoskeletal System CHAPTER 3 89

SKIN INTEGRITY Upper- and Lower-Quarter Screens

The patient’s skin integrity should be inspected in gen-
eral for edema, discoloration, bruising, or scars. If
there is traumatic injury, carefully inspect the skin at
the level of and distal to the injury. Note any lacerations
or abrasions. If the patient has recently had surgery,
observe the location, direction, and quality of inci-
sion(s). Note any pressure sores or potential for such.
Refer to Chapter 7 for further discussion of skin integ-
rity evaluation.
CLINICAL TIP
 Pressure sores from prolonged or increased bed rest
after trauma or orthopedic surgery can develop in
anyone, regardless of age or previous functional
abilities. Inspect the uninvolved extremity for skin
breakdown too.
Palpation
Palpate skin temperature to touch, capillary refill, and
peripheral pulses at the level of or distal to injury or
the surgical site. Refer to Chapter 6 for further discus-
sion of vascular examination. A discussion of special
tests is beyond the scope of this text; however, the ther-
apist should perform special testing if results of the
interview or screening process warrant further
investigation.
Upper- and lower-quarter screening is the brief evalu-
ation of bilateral range of motion (ROM), muscle
strength, sensation, and deep tendon reflexes. It is a
very efficient examination of gross neuromuscular
status that guides the therapist to perform more
specific testing.1 The therapist should perform both
an upper- and lower-quarter screen, regardless of
the extremity involved. For example, for a patient
with lower-extremity involvement who will require
the use of an assistive device for functional mobility,
both functional range and strength of the upper
extremities must be assessed. Tables 3-1 and 3-2
describe a modified version of an upper- and lower-
quarter screen. Table 3-3 outlines normal ROM.
Peripheral nerve innervations for the upper and
lower extremities are listed in Chapter 4, Tables 4-7
and 4-8, respectively. Dermatomal innervation is
shown in Figure 4-6.
The sequencing of the upper- and lower-quarter
screen is as follows2:
1. Observe active ROM and test myotomes progress-
ing from proximal to distal and beginning at the
spinal level and moving distally to the extremities.
Remember that it is imperative to assess these
below the level of injury, as neurologic impairments
may exist.
2. Screen the patient’s sensation to light touch, proxi-
mally to distally, as above.

Table 3-1 UPPER-QUARTER SCREEN

Nerve Root Myotome Dermatome Deep Tendon Reflex

C1 Cervical rotation No innervation None
C2 Shoulder shrug Posterior head None
C3 Shoulder shrug Posterior neck None
C4 Shoulder shrug Acromioclavicular joint None
C5 Shoulder abduction Lateral arm Biceps
C5,6 Elbow flexion ç None
C6 Wrist extension Lateral forearm and palmar tip of thumb Brachioradialis
C7 Elbow extension and wrist flexion Palmar distal phalanx of middle finger Triceps
C8 Thumb extension and finger Palmar distal aspect of little finger None
flexion
Tl Finger abduction Medial forearm None
Data from Palmer ML, Epler ME (eds). Clinical Assessment Procedures in Physical Therapy. Philadelphia: Lippincott, 1990; Hoppenfeld S.
Physical Examination of the Spine and Extremities. East Norwalk, CT: Appleton & Lange, 1976.
90 CHAPTER 3 Musculoskeletal System

Table 3-2 LOWER-QUARTER SCREEN

Nerve Root Myotome Dermatome Deep Tendon Reflex
L1 Hip flexion Antero-superior thigh just below None
the inguinal ligament
L2 Hip flexion Anterior medial thigh 2.5 in. below the None
anterior superior iliac spine
L3 Knee extension with L4 Middle third of anterior thigh None
L4 Knee extension with L3 and L5 Patella and medial malleolus Patellar tendon
L4,5 Ankle dorsiflexion ç None
L5 Great toe extension Fibular head and dorsum of foot Posterior tibialis
S1 Ankle plantar flexion Lateral malleolus and plantar surface of foot Achilles tendon
Data from Palmer ML, Epler ME (eds). Clinical Assessment Procedures in Physical Therapy. Philadelphia: Lippincott, 1990; Hoppenfeld S.
Physical Examination of the Spine and Extremities. Norwalk, CT: Appleton & Lange, 1976.

3. If weakness is found, assess strength using manual sensation further. Assess deep tendon reflexes if
muscle testing. Break testing may also be performed appropriate. Refer toTable 4-16 for the reflex grading
as a modified way to assess isometric capacity of and interpretation system.
motor performance. If altered sensation to light
touch is found, assess deep touch or other types of
CLINICAL TIP
 Start the examination or screening process with
Table 3-3 NORMAL RANGE OF MOTION VALUES
the uninvolved side to minimize patient anxiety
MOST APPLICABLE IN THE ACUTE
and pain response.
CARE SETTING
 If manual muscle testing is not possible secondary
Normal Range of to conditions such as altered mental status, describe
Joint Motion (Degrees) strength in terms of quality or movement through
an ROM (e.g., active hip flexion is one-third range
Shoulder Flexion 0-180
in supine).
Extension 0-60
Abduction 0-180  Sensory testing is especially important over
Internal rotation 0-70 moderately or severely edematous areas, especially
External rotation 0-90 the distal extremities. The patient may not be
aware of subtle changes in sensation.
Elbow Flexion 0-150
 Girth measurements may be taken if edema of an
Forearm Pronation 0-80 extremity subjectively appears to increase.
Supination 0-80
Wrist Flexion 0-80
Extension 0-70
Hip Flexion 0-120 Functional Mobility and Safety
Extension 0-30 Functional mobility, including bed mobility,
Abduction 0-45
Internal rotation 0-45
transfers, and ambulation on level surfaces and stairs,
External rotation 0-45 should be evaluated according to activity level,
Knee Flexion 0-135 medical-surgical stability, and prior functional level.
Safety is a key component of function. Evaluate
Ankle Dorsiflexion/ 0-20 the patient’s willingness to follow precautions
plantar flexion
Plantar flexion 0-45 with consistency. Observe for the patient’s ability to
maintain weight bearing or comply with equipment

use. Monitor the patient’s self-awareness of risk for falls,
speed of movement, onset of fatigue, and body
mechanics.
CLINICAL TIP
 Safety awareness, or lack thereof, can be difficult to
document. Try to describe a patient’s level of safety
awareness as objectively as possible (e.g., patient
leaned on rolling tray table, unaware that it
could move).
 Nearly all patients will fear movement out of bed
for the first time to some degree, especially if a
fall or traumatic event led to the hospital
admission. This is particularly true with elders.
Before mobilization, use strategies to decrease
fear. These include an explanation of the treatment
before mobilizing the patient and of the sensations
the patient may feel (e.g., ‘‘Your foot will throb a
little when you lower it to the floor.’’).
Because orthopedic injuries can often be the final
result of other medical problems (e.g., balance disorders
or visual or sensory impairments), it is important that
the therapist take a thorough history, perform a muscu-
loskeletal screen, and critically observe the patient’s
functional mobility. Medical problems may be subtle
in presentation but may dramatically influence the
patient’s capabilities, especially with new variables,
such as pain or the presence of a cast. Collectively,
these factors lead to a decreased functional level.
CLINICAL TIP
 It may be the physical therapist who first
appreciates an additional fracture, neurologic
deficit, or pertinent piece of medical or social
history. Any and all abnormal findings should
be reported to the nurse or physician.
Diagnostic Tests
The most commonly used diagnostic tests for the
musculoskeletal system are listed in the following
sections. These tests may be repeated during or
after a hospital stay to assess bone and soft-tissue heal-
ing and disease progression, or whether there is a
sudden change in vascular or neurologic status
postoperatively.
Musculoskeletal System CHAPTER 3 91
RADIOGRAPHY
More commonly known as x-rays or plain films, radio-
graphic photographs are the mainstay in the detection
of fracture, dislocation, bone loss, or foreign bodies
or air in tissue. Sequential x-rays are standard intra-
operatively or postoperatively to evaluate component
position with joint arthroplasty, placement of orthope-
dic hardware, or fracture reduction. X-rays may also
detect soft-tissue injuries, such as joint effusion,
tendon calcification, or the presence of ectopic bone.2
COMPUTED TOMOGRAPHY
Computed tomography (CT) is the diagnostic test of
choice for the evaluation of cortical bone in certain
circumstances. For fracture and dislocations, CT can
provide three-dimensional views for the spatial rela-
tionship of fracture fragments or to further evaluate
fracture in anatomically complex joints, such as the
pelvis, sacrum, spine, or shoulder.3 CT is commonly
used to define and localize spinal stenosis, disc protru-
sion or herniation, nerve entrapment, bone tumor,
and osseous or articular bone infection or abscess.4
MAGNETIC RESONANCE IMAGING
Magnetic resonance imaging (MRI) is superior to x-ray
or CT for the evaluation of soft tissue. MRI detects par-
tial or complete tendon, ligament, or meniscal tears.
MRI is also used to (1) detect patellar tracking abnorm-
alities, rotator cuff tears, and arthritis; (2) detect and
localize soft-tissue masses, such as hematoma, cyst,
abscess, or lipoma; and (3) evaluate bone marrow.
Finally, the high resolution of MRI reveals stress frac-
tures and bone bruises that could be unobserved on
x-ray.3
BONE SCAN
A bone scan is the radiographic picture of the uptake in
bone of a radionuclide tracer. Scans of a portion of or
the whole body may be taken at the instant the tracer is
injected or 5 to 10 minutes or 2 to 4 hours postinjection.
Bone scan reflects the metabolic status of the skeleton
at the time of the scan and is extremely helpful in detect-
ing metabolic abnormalities of bone before the appear-
ance of structural changes on x-ray.5 It is therefore
used to detect skeletal metastases, especially in the
base of the skull, sternum, scapula, and anterior ribs.5
Other uses of bone scan include the diagnosis of stress
fractures and other nondisplaced fractures, early osteo-
myelitis, inflammatory or degenerative arthritis, avas-
cular necrosis (AVN), and myositis ossificans.
92 CHAPTER 3 Musculoskeletal System
ARTHROGRAPHY
An arthrogram is a radiograph of a joint with air or dye
contrast. Performed primarily on the knee, shoulder,
and hip, arthrography allows examination for internal
joint derangements or soft-tissue disruption.
Arthrograms may diagnose meniscal and cruciate liga-
ment tears or articular cartilage abnormalities of the
knee, adhesive capsulitis or rotator cuff tears of the
shoulder, and arthritis or intraarticular neoplasm of
the hip.6
MYELOGRAPHY
A myelogram is a radiograph or CTof the spinal cord,
nerve root, and dura mater with dye contrast. A myelo-
gram can demonstrate spinal stenosis, cord compres-
sion, intervertebral disc rupture, or nerve root injury.7
CLINICAL TIP
 X-rays may be ordered after any new event, such as
an in-hospital fall, abnormal angulation of an
extremity, possible loss of fixation or reduction, or
for a dramatic increase in pain. Regardless of the
situation, defer physical therapy intervention until
results are reported or the situation is managed.
 Physical therapy intervention is typically deferred for
the patient post myelography secondary to specific
postprocedure positioning and bed rest restrictions.
(Refer to the Myelography section in Chapter 4.)
 As with any test that includes contrast media,
contrast-related reactions post arthrogram or
myelogram may occur. Check with the nurse or
physician before physical therapy intervention.
FRACTURE MANAGEMENT
Types of Fracture
The analysis and classification of fracture reveal the
amount of energy impacted on bone and the potential
for secondary injury, and direct fracture management.
Fractures can be described according to the following8:
1. The maintenance of skin integrity
a. A closed fracture is a bony fracture without dis-
ruption of the skin.
b. An open fracture is a bony fracture with open lac-
eration of the skin or protrusion of the bone
through the skin.
FIGURE 3-1
Orientation of a fracture pattern.1,Transverse; 2, oblique;
3, segmental; 4, comminuted (With permission from A Unwin,
KJones [eds]. Emergency Orthopaedics and Trauma. Boston:
Butterworth-Heinemann, 1995;22.)
2. The site of the fracture
a. At the proximal third, distal third, or at the shaft
of long bones.
b. An intraarticular fracture involves the articular
surface. Intraarticular fractures are further
described as linear, comminuted, impacted, or
with bone loss. An extraarticular fracture does
not involve the articular surface.
c. An epiphyseal fracture involves the growth
plate.
3. The configuration of the fracture (Figure 3-1)
a. A linear fracture can be transverse (perpendi-
cular to the long axis of the bone), oblique
(on a diagonal to the long axis of the bone),
or spiral (similar to oblique with a greater sur-
face area of shaft involvement secondary to a
circular pattern).
b. A comminuted fracture has two or more frag-
ments. A butterfly (wedge-shaped) fragment
may or may not be present.
c. A segmental fracture has two or more fracture
lines at different levels of the bone.
4. The extent of the fracture
a. An incomplete fracture, in which one portion of
the cortex is interrupted.
b. A complete fracture, in which all cortices of
bone are interrupted.
5. The relative position of the fragments
a. A nondisplaced fracture is characterized by
anatomic alignment of fracture fragments.
b. A displaced fracture is characterized by abnor-
mal anatomic alignment of fracture fragments.
 Musculoskeletal System CHAPTER 3 93

A B C D E
FIGURE 3-2
Techniques of internal fixation. A, Plate and six screws for transverse or short oblique fracture. B, Screws
for long oblique or spiral fracture. C, Screws for long butterfly fragment. D, Plate and screws for short
butterfly fragment. E, Medullary nail for segmental fracture. (With permission from PG Beare, JL Myers
[eds]. Adult Health Nursing [3rd ed]. St. Louis: Mosby, 1998;1243.)

fixation devices (Figure 3-2), commonly referred to

Clinical Goal of Fracture Management
The goal of fracture management is bony union of
the fracture without further bone or soft-tissue
damage that enables early restoration of maximal
function.9 Early restoration of function minimizes
cardiopulmonary compromise, muscle atrophy, and
the loss of functional ROM. It also minimizes impair-
ments associated with limited skeletal weight bearing
(e.g., osteoporosis).
Fractures are managed either nonoperatively or
operatively on an elective, urgent, or emergent basis
depending on the location and type of fracture, pres-
ence of secondary injuries, and hemodynamic
stability. Elective or nonurgent management (days
to weeks) applies to stable fractures with an intact
neurovascular system or fracture previously managed
with conservative measures that have failed. Urgent
management (24 to 72 hours) applies to closed, unstable
fractures, dislocations, or long bone stabilization
with an intact neurovascular system. Emergent man-
agement applies to open fractures, fractures/disloca-
tions with an impaired neurovascular system or
compartment syndrome, and spinal injuries with
deteriorating neurologic deficits.9
Fracture reduction is the process of aligning and
approximating fracture fragments. Reduction may be
achieved by either closed or open methods. Closed
reduction is noninvasive and is achieved by manual
manipulation or traction. Open reduction internal
fixation (ORIF) techniques require surgery and
as hardware. ORIF is the treatment of choice when
closed methods cannot maintain adequate fixation
throughout the healing phase. Immobilization of
the fracture is required to maintain reduction and
viability of the fracture site. Immobilization is
accomplished through noninvasive (casts or splints)
or invasive (screws, plates, rods, pins, and external
fixators) techniques. Regardless of the method of
immobilization, the goal is to promote bone healing.
Bone healing occurs in four stages: (1) hematoma
formation within 72 hours, (2) fibrocartilage formation
in 3 days to 2 weeks, (3) pro-callus formation in 3 to
10 days, and (4) remodeling or permanent callus
formation in 3 to 10 weeks.8,10 Table 3-4 lists the
multitude of factors that contribute to the proper or
improper healing of bone and affect the time frames
for healing.
Complications of Fracture
Complications of fracture may be immediate (within
days), delayed (weeks to months), or late (months
to years). The immediate or early medical-surgical
complications of special interest in the acute care set-
ting include10:
 Loss of fixation or reduction
 Deep vein thrombosis, pulmonary or fat emboli
 Nerve damage, such as paresthesia or paralysis
 Arterial damage, such as blood vessel laceration
 Compartment syndrome
 Incisional infection
94 CHAPTER 3 Musculoskeletal System

sacrum, sacroiliac joints, and symphysis pubis.

Table 3-4 CONTRIBUTING FACTORS OF BONE Unstable pelvic fractures or dislocations occur in
HEALING the anterior or posterior column of the pelvis owing
Favorable Unfavorable to high-impact lateral or anteroposterior compression,
or vertical shearing forces.3 There is a disruption
Early mobilization Presence of disease, such as of the ring in two or more places, as shown in
Early weight bearing diabetes, anemia, Figure 3-3.
Maintenance of neuropathy, or malignancy
Stable pelvic fractures, due to low-impact direct
fracture reduction Vitamin deficiency
Younger age Osteoporosis blows or falls, do not involve or minimally involve
Good nutrition Infection the displacement of the pelvic ring.3 Stable pelvic
Distal or proximal Irradiated bone fractures include localized iliac wing, pubic rami,
shaft fracture Severe soft-tissue damage or sacral fractures. Avulsion fractures of anterior
Minimal soft-tissue Distraction of fracture fragments superior iliac spine, anterior inferior iliac spine, or
damage Severe comminution ischial tuberosity from strong contraction of muscle
Patient compliance Bone loss (typically seen in younger athletes) are considered
Presence of growth Multiple fracture fragments stable pelvic fractures.7 When a pelvic fracture is
hormone Disruption of vascular supply described as stable, it is inherent that further bony
to bone
displacement will not occur on physiologic loading
Avascular necrosis
Corticosteroid use and that invasive procedures are not needed before
mobilization.11
Data from: Christian CA. General Principles of FractureTreatment. Chapter AppendixTable 3-A.1 describes the fracture
In Canale ST (ed), Campbell’s Operative Orthopaedics,Vol. 3 classification and management of pelvic fractures.
(9th ed). St. Louis: Mosby, 1998;1999; JM Black. Nursing Care of
Clients with Musculoskeletal Trauma or Overuse. InJM Black,
External fixation is used for stable fractures only and
E Matassarian-Jacobs (eds), Medical-Surgical Nursing Clinical can decrease posttraumatic hemorrhage. It is a good
Management for Continuity of Care (5th ed). Philadelphia: choice if abdominal injuries are present. External
Saunders, 1997;2134; and LN McKinnis. Fundamentals of fixation will not stabilize vertical displacement.11
Orthopedic Radiology. Philadelphia: FA Davis, 1997. ORIF techniques are the optimal choice of treatment
for anterior and posterior pelvic displacement. Risks
 Orthostatic hypotension are high and should be taken only when benefits of
 Shock anatomic reduction and rigid fixation outweigh
Delayed and late complications are as follows10: problems of hemorrhage and infection.11
 Loss of fixation or reduction ACETABULAR FRACTURE. Acetabular fracture
 Delayed union (fracture fails to unite in a normal occurs when a high-impact blunt force is transmitted
time frame in the presence of unfavorable healing at one of four main points: the greater trochanter, a
factors) flexed knee, the foot (with the knee extended), or the
 Nonunion (failure of fracture to unite) posterior pelvis.12 The exact location and severity of
 Malunion (fracture healed with an angular or the fracture (Figure 3-4), with or without dislocation,
rotary deformity) can depend on the degree of hip flexion and extension,
 Pseudarthrosis (formation of a false joint at the abduction and adduction, or internal and external rota-
fracture site) tion at the time of injury.12 Acetabular fractures are
 Posttraumatic arthritis highly associated with multiple injuries and shock.
 Osteomyelitis Common immediate and early complications associat-
 Myositis ossificans (heterotropic bone in muscle) ed with acetabular fracture include retroperitoneal
 AVN hematoma, gastrointestinal or urologic injury, deglov-
ing injury, deep venous thrombosis (DVT), pulmonary
Fracture Management According to Body Region embolism, infection, and sciatic and superior gluteal
nerve injury.13 Common late complications include
PELVIS AND LOWER EXTREMITY AVN of the femoral head or acetabular segment, hyper-
PELVIC RING FRACTURE. Pelvic fracture stability is trophic ossification, and posttraumatic arthritis.14
defined by the degree of pelvic ring disruption. The Chapter Appendix Table 3-A.2 describes the classi-
pelvic ring is formed by the paired coxal bones, fication and management of acetabular fractures.
 Musculoskeletal System CHAPTER 3 95

A B C

D E F
FIGURE 3-3
Examples of unstable pelvic fractures include (A, B, and C) vertical shear (Malgaigne) fractures involving
ischiopubic rami and disruption of an ipsilateral sacroiliac joint, be they (A) throughout the joint itself,
(B) through a fracture of the sacral wing, or (C) through a fracture on the iliac bone. D, Straddle
fractures, involving all four ischiopubic rami. E, Bucket-handle fractures, involving an ischiopubic ramus
and contralateral sacroiliac joint. F, Dislocations involving one or both sacroiliac joints and the symphysis
pubis. (With permission from LN McKinnis [eds]. Fundamentals of Orthopedic Radiology. Philadelphia:
FA Davis, 1997;225.)

Acetabular fractures are by nature intraarticular; hence,
the management revolves around the restoration of a
functional weight-bearing joint while avoiding osteoar-
thritis.13 An acetabular fracture is a complex injury.
Determinants of outcome include fracture pattern,
degree of injury to the vascular status of the femoral
head, the presence of neurologic injury, and the accu-
racy of reduction of the roof of the acetabulum.15
HIP DISLOCATION. Hip dislocation is the result of a
high-velocity impact force and can occur in isolation
or with a femoral or acetabular fracture. The majority
of hip dislocations occur in a posterior direction, and
anterior dislocations are rare.16 A patient with a poster-
iorly dislocated hip has a limb that is shortened, inter-
nally rotated, and adducted in slight flexion.17 An
anteriorly dislocated hip appears adducted and exter-
nally rotated.16
Management of hip dislocation without fracture
includes closed reduction under conscious sedation
and muscle relaxation followed by traction or open
reduction if closed reduction fails. Functional mobility
(typically partial weight-bearing or weight-bearing as
tolerated), exercise, and positioning are per physician
order based on hip joint stability and associated

A B C D
FIGURE 3-4
Classification of acetabular fractures. A, Anterior column. B, Posterior column. C,Transverse, involving
both columns. D, Complex or T-shaped, involving both columns. (From LN McKinnis [ed].
Fundamentals of Orthopedic Radiology. Philadelphia: FA Davis, 1997.)
96 CHAPTER 3 Musculoskeletal System
FIGURE 3-5
Garden classification of sub capital fractures.1, 2, Nondisplaced; 3,4, displaced. (With permission from
A Unwin, KJones [eds]. Emergency Orthopaedics and Trauma. Boston: Butterworth-Heinemann,
1995;193.)
neurovascular injury. Hip dislocation with fracture typ-
ically warrants surgical repair.
CLINICAL TIP
 Posterior hip dislocation precautions typically exist
after hip dislocation reduction. This limits hip
flexion to 80 to 90 degrees, internal rotation to 0
degrees, and adduction to 0 degrees.
 Indirect restriction of hip movement after posterior
dislocation during rest or functional activity can be
achieved with the use of a knee immobilizer or hip
abduction brace. This may be beneficial if the
patient is confused or noncompliant.
FEMORAL HEAD AND NECK FRACTURES. Femoral
head and neck fractures are often referred to as hip frac-
tures. They can be classified as intracapsular or extra-
capsular. Femoral head and neck fractures occur from
a direct blow to the greater trochanter, from a force
with the hip externally rotated, or from a force along
the femoral shaft.18 In the elderly, a femoral neck frac-
ture can occur with surprisingly little force owing to
osteoporosis of the proximal femur. Femoral neck
fractures in younger adults are almost always the result
of high-impact forces, such as motor vehicle accidents.
Intracapsular fractures are located within the hip cap-
sule and are also called subcapital fractures. The four-stage
Garden scale (Chapter Appendix Table 3-A.3) is used
to classify femoral neck fractures and is based on the
amount of displacement and the degree of angulation
(Figure 3-5). Clinically, Garden III and IV fractures
are complicated by a disruption of the blood supply to
the femoral head as a result of extensive capsular
trauma. Poor blood supply from the circumflex femoral
artery can lead to AVN of the femoral head, fracture
nonunion, or both.7
Extracapsular fractures occur outside of the hip
capsule. They can be further classified as intertrochan-
teric or subtrochanteric. Intertrochanteric fractures
occur between the greater and lesser trochanters.
Subtrochanteric fractures occur in the proximal one-
third of the femoral diaphysis and can occur with inter-
trochanteric or shaft fractures.18 Intertrochanteric and
subtrochanteric fractures are summarized in Chapter
AppendixTable 3-A.4 and are shown in Figure 3-6.
FEMORAL SHAFT FRACTURE. Femoral shaft fractures
result from high-energy trauma and are often associat-
ed with major abdominal or pelvic injuries. Femoral
shaft fractures can be accompanied by life-threatening
systemic complications, such as hypovolemia, shock,
or fat emboli. Often, there is significant bleeding into
the thigh with hematoma formation. Hip dislocation
and patellar fracture frequently accompany femoral
shaft fractures.19 Chapter Appendix Table 3-A.5 lists
femoral shaft fracture management.
CLINICAL TIP
 The uninvolved leg or a single crutch can be used to
assist the involved lower leg in and out of bed.
 The patient should avoid rotation of and pivoting on
the lower extremity after intramedullary rod
placement, as microrotation of the intramedullary
rod can occur and place stress on the fixation
device.
DISTAL FEMORAL FRACTURES. Fractures of the
distal femur are supracondylar (involving the distal
femur shaft only), unicondylar (involving one femoral
condyle), intercondylar (involving both condyles), or a
combination of these. Involvement of the articular sur-
face of the knee joint complicates the fracture.
Typically, this type of fracture is caused by high-energy

FIGURE 3-6
Fractures of the proximal femur. (1, Subcapital; 2, transcervical;
3, basocervical; 4, intertrochanteric; 5, subtrochanteric.) (With
permission from A Unwin, KJones [eds]. Emergency
Orthopaedics and Trauma. Boston: Butterworth-Heinemann,
1995;190.)
trauma to the femur or a direct force that drives
the tibia cranially into the intercondylar fossa.
Distal femur fractures are often accompanied by
injury to localized skin, muscle, and joint ligaments
and cartilage with great potential for decreased knee
joint mechanics.20
The management of distal femur fractures is
summarized in Chapter Appendix Table 3-A.6.
Complications of femur fracture include malunion,
nonunion, infection, knee pain, and decreased knee
ROM.21
PATELLAR FRACTURE. A patellar fracture results
from direct trauma to the patella from a fall, blow, or
motor vehicle accidents (e.g., dashboard injury).
The knee is often flexed during injury, as the patella
fractures against the femur. Patellar fracture may also
occur from sudden forceful quadriceps contraction,
as in sports or from a stumbling fall.7 Patellar frac-
tures are associated with ipsilateral distal femoral or
shaft fractures, proximal tibial condyle fractures, and
posterior dislocation of the hip.22 Late complications
Musculoskeletal System CHAPTER 3 97
include patellofemoral or hardware pain, osteoarthritis,
and decreased terminal extension from abnormal
patellar mechanics, quadriceps weakness, or adhesions.
Chapter Appendix Table 3-A.7 describes the manage-
ment of patellar fractures. Most orthopedic surgeons
perform partial or total patellectomy as a last resort
because of the high incidence of an impaired quadri-
ceps mechanism months later.21
TIBIAL PLATEAU FRACTURE. Tibial plateau fractures
result from direct force on the proximal tibia (e.g.,
when a pedestrian is hit by an automobile), as shown
by the Schatzker classification in Figure 3-7. This
high-force injury often presents with open wounds,
soft-tissue injuries, ligamentous disruption, and
dislocation. Contralateral collateral ligament injuries
occur from varus or valgus force of injury.7
Ligamentous injuries are most common in nondis-
placed, compressed, and split compression fractures.21
The complexity of tibial plateau fractures cannot
be overstated. Chapter Appendix Table 3-A.8 lists the
management of tibial plateau fractures. Immediate or
early complications of tibial plateau fractures include
popliteal or peroneal nerve compression, compartment
syndrome, infection, and DVT. Late complications
include abnormal patellofemoral mechanics, lack of
ROM or stability, and posttraumatic arthritis of the
articular surface.
TIBIAL SHAFT AND FIBULA FRACTURES. Tibial
shaft and fibula fractures result from high-energy
trauma (e.g., motor vehicle accidents, crush injuries,
skiing accidents) via direct blow, twisting of the ankle,
or varus stress on the knee.7 The higher the energy on
impact, the more soft-tissue and bone damage occurs.
Tibial shaft fracture management (Chapter Appendix
Table 3-A.9) is very complicated because of associated
injuries similar to those of tibial plateau fractures.
Immediate or early complications include anterior
tibial artery damage, interosseous membrane rupture,
peroneal nerve injury, or degloving injuries. Delayed
or late complications include malunion, nonunion,
osteomyelitis, secondary amputation, or reflex sympa-
thetic dystrophy. The distal lower extremity must be
thoroughly evaluated for concomitant ankle trauma
(e.g., trimalleolar fracture, syndesmotic disruption, or
talar dome fracture).
DISTAL TIBIAL AND ANKLE FRACTURES. Fractures of
the distal tibia, distal fibula, and talus are described
together because of their frequent simultaneous
injury. Distal tibial fractures (i.e., pilon fractures) are
the result of high vertical loading forces, such as with
parachuting accidents, falls from heights, sporting
98 CHAPTER 3 Musculoskeletal System

FIGURE 3-7
Classification of tibial plateau fractures (Schatzker).Type 1 wedge fracture of the lateral tibial plateau.
Type 2 wedge fracture of the lateral plateau with depression of the adjacent plateau.Type 3 central
depression of the articular surface of the lateral plateau without a wedge fragment.Type 4 fracture of
the medial tibial plateau.Type 5 bicondylar fracture.Type 6 tibial plateau fracture with separation of
metaphysis from diaphysis. (With permission from A Unwin, KJones [eds]. Emergency Orthopaedics and
Trauma. Boston: Butterworth-Heinemann, 1995;226.)

injuries, and motor vehicle accidents.23 Often, long axis
compression throughout the proximal lower extremity
can cause associated tibial plateau fracture, hip disloca-
tion, or acetabular fracture.
Ankle fractures commonly result from torque
caused by abnormal loading of the talocrural joint
with body weight. Fractures may be simple, involving
avulsion of a portion of the distal fibula, or complex,
involving the entire mortise (trimalleolar fracture)
with disruption of the syndesmosis. Fracture severity
depends on the degree of foot inversion or eversion
in relation to the subtalar joint at the time of
injury.23 Stability of the ankle depends on joint con-
gruity and ligamentous integrity. Complications
associated with ankle fractures are malunion, delayed
union, traumatic arthritis, and osteomyelitis.23
Chapter Appendix Table 3-A.10 lists distal tibial and
ankle fracture management.
CALCANEAL AND FOREFOOT FRACTURES. The most
commonly fractured bone of the foot is the calcaneus,
with fractures caused by a direct blow, such as a fall
from a height or as an avulsion injury from a strong
contraction of the triceps surae. Calcaneal fractures,
usually bilateral, are associated with additional proxi-
mal leg injury or spinal fracture (e.g., burst fracture).24
Latent complications of complex calcaneal fracture
include joint pain, peroneal tendonitis, and heel spur
from malunion.24
Forefoot fracture or metatarsal fracture occurs as
a crush injury when a heavy object lands on the foot,
as a twisting injury, as a stress fracture, or as an avulsion
fracture at the base of the fifth metatarsal from force-
ful peroneus brevis contraction.7 Chapter Appendix
Table 3-A.11 lists the general types and management
of calcaneal and forefoot fractures.
SPINE
In order of frequency, fractures of the spine are caused
by automobile or motorcycle accidents, falls, sports
accidents, and violence as a result of flexion, extension,
rotation, and vertical compression forces.25 Spinal
fracture at any level is discussed in terms of location
(anterior or posterior column) or stability (mechanical
or neurologic). Anatomically, the anterior column
refers to the vertebral bodies and intervertebral discs
including the anterior and posterior longitudinal

FIGURE 3-8
Odontoid peg fractures.Type I fractures of the upper third of
the peg.Type II fractures at the junction of the peg with the
body of C2.Type III fractures essentially of the body of C2 at
the base of the peg. (With permission from A Unwin, KJones
[eds]. Emergency Orthopaedics and Trauma. Boston:
Butterworth-Heinemann, 1995;85.)
ligaments.25 The posterior column refers to the trans-
verse and spinous processes, pedicles, laminae, and
facets, including the interspinous, infraspinous,
supraspinous, and nuchal ligaments.25
A fracture may be considered stable if there is dis-
ruption of either the anterior or posterior column or
an injury without neurologic compromise. An unstable
fracture occurs if both the anterior and posterior col-
umns are disrupted or if there is a potential for neuro-
logic compromise. Potential neurologic injury can
occur from progressive swelling at the site of the
Musculoskeletal System CHAPTER 3 99
FIGURE 3-9
Burst fracture. (With permission from A Unwin, KJones (eds).
Emergency Orthopaedics and Trauma. Boston: Butterworth-
Heinemann, 1995;85.)
injury, hematoma formation, and associated interverte-
bral disc herniation or dislocation. Spinal fracture may
occur with or without spinal cord injury (refer to the
Spinal Cord Injury section in Chapter 4). Figures 3-8
and 3-9 are examples of high cervical (odontoid) and
lumbar burst fractures.
Basic cervical and thoracolumbar fracture descrip-
tion and management are described in Chapter
Appendix Tables 3-A.12 and 3-A.13, respectively. If sur-
gical management is required, it is performed as soon
as the patient is medically stable. Secondary manage-
ment of spinal fracture may also include the following:
 Examination and treatment of associated extremity
fracture, or head or internal injuries
 Very frequent (every 15 to 30 minutes) neurovascular
assessment by nursing
 Close monitoring of airway and breathing with cer-
vical spine fractures
CLINICAL TIP
 Until the cervical, thoracic, and lumbar spines have
been ruled out or ‘‘cleared’’ for fracture, do not
remove temporary immobilization devices (e.g.,
cervical collar) until ordered to do so by the
physician.
 Logroll precautions may exist before spinal fracture
clearance. This typically includes bed rest (with the
head of the bed at a 30-degree angle or less) and
100 CHAPTER 3 Musculoskeletal System
turning the patient via logroll (with the head and
torso as a unit).
 Refer to the Physical Therapy Intervention after
Spinal Surgery section for additional tips on
mobilizing a patient with back pain or after spinal
stabilization.
UPPER EXTREMITY
SHOULDER GIRDLE FRACTURES. Fracture of the
scapula is rare and often requires little treatment
(other than pain management), because the surround-
ing musculature serves to protect and immobilize the
fracture. Scapular fractures occur most commonly in
35- to 45-year-old adults as a result of axial loading on
an outstretched arm or a direct blow or force from
a fall onto the back or top of the shoulder.26 Injuries
associated with scapular fracture include rib fracture,
pulmonary contusion, pneumothorax, and spinal
fracture.
Fractures of the distal, middle, or medial third of
the clavicle result from direct impact, such as falls
or blows on the point of the shoulder. Management is
conservative (sling immobilization for comfort) for
nondisplaced fractures without ligamentous injury.
ORIF is required acutely if the clavicle fracture is
associated with neurovascular compromise, coracocla-
vicular ligament tear, floating shoulder (fracture of
both the clavicle and surgical neck of the scapula), or
for separation of fracture fragments by the deltoid
or trapezius muscle.27 Short-term immobilization is
typical after ORIF.
Fractures involving the articulation of the gleno-
humeral joint or coracoid process are more compli-
cated than scapular body and clavicular fractures.
Intraarticular glenoid fractures may involve the spine
of the scapula and are associated with shoulder dis-
location or acromioclavicular injury.28 Coracoid frac-
tures occur at either the tip or base and may also
involve the spine of the scapula.28 Management for
stable nondisplaced fractures is conservative (sling
immobilization) or ORIF for displaced fractures.
The vast majority of glenohumeral dislocation
occurs anteriorly as a result of forceful external rota-
tion and extension while the arm is abducted.7
Glenohumeral dislocation should be treated with
immediate closed reduction to minimize injury to the
neurovascular structures surrounding the joint. The
need for strict dislocation precautions for the patient
without risk factors for further dislocation is unlikely.29
PROXIMAL HUMERAL AND HUMERAL SHAFT
FRACTURES. Proximal humeral fractures occur when
the humerus is subjected to direct or indirect trauma
and can be associated with glenohumeral dislocation,
rotator cuff injuries, and brachial plexus or peripheral
nerve damage. Fracture of the humeral head, anatomic
neck, and lesser tuberosity are rare; however, fracture
of the greater tuberosity is common.7 The majority of
these fractures are nondisplaced or minimally dis-
placed.30 Complications of proximal humeral fractures
include nonunion, AVN of the humeral head, abnor-
mal posture, and abnormal scapulothoracic rhythm.
Humeral shaft fractures are also the result of direct
or indirect trauma, usually a fall on an outstretched
hand, motor vehicle accident, or direct load on the
arm.31 Humeral shaft fractures may be associated with
radial nerve or brachial plexus injury. Chapter
Appendix Table 3-A.14 summarizes proximal humeral
and humeral shaft fracture management.
CLINICAL TIP
 When the patient is lying supine, placing a thin
pillow or folded sheet under the upper arm will help
maintain neutral alignment and reduce pain.
 Getting in and out of bed on the opposite side of an
upper arm fracture is usually more comfortable for
the patient.
DISTAL HUMERAL, OLECRANON, AND RADIAL HEAD
FRACTURES. Distal humeral fractures are rare but com-
plex fractures to manage because of the bony configu-
ration of the elbow joint, adjacent neurovascular
structures (Figure 3-10), and minimal soft tissue sur-
rounding the joint.32 The most common distal
humerus fracture in the elderly is transcondylar (across
the condyles of the olecranon fossa) as the result of
a fall.7 An intercondylar fracture (i.e., T- or Y-shaped
condylar fracture) is the most common distal humeral
fracture in adults. A direct impact of the ulna against
the trochlea forces the condyles apart.32 This is
common after a motor vehicle accident or a high-
impact fall. Treatment consists of (1) immobilization,
followed by early ROM for a stable fracture; or (2)
ORIF or total elbow arthroplasty (TEA) for severely
comminuted intraarticular fractures. Late complica-
tions include hypomobility, nonunion, malunion,
ulnar neuropathy, and heterotrophic ossification.
Olecranon fractures (Figure 3-11) result from direct
trauma to a flexed elbow or a fall on an outstretched
hand. Severe comminution of the olecranon is
 Musculoskeletal System CHAPTER 3 101

FIGURE 3-11
Fracture of the olecranon. (With permission from A Unwin,
KJones [eds]. Emergency Orthopaedics and Trauma. Boston:
Butterworth-Heinemann, 1995;130.)

associated with humeral fracture and elbow disloca-

A tion. Late complications include loss of terminal
elbow extension, painful hardware, and posttraumatic
arthritis.32
A fall onto an outstretched hand with a pronated
forearm can cause a radial head or neck fracture
(Figure 3-12). Associated injuries include elbow dislo-
cation and disruption of the interosseous membrane,
medial collateral ligament, or wrist fibrocartilage.32
Complications of stable radial head fracture include
residual pain and hypomobility, whereas unstable
radial head fractures are associated with loss of fixation,

B
FIGURE 3-10
A, Fracture of the medial epicondyle. Note the ulnar nerve
runs immediately posterior to the fracture. B,The brachial
artery is at risk in supracondylar fractures. (With permission
from A Unwin, KJones (eds). Emergency Orthopaedics and
Trauma. Boston: Butterworth-Heinemann, 1995;126, 128.)

A B
FIGURE 3-12
Fractures of the radial neck. A, Displaced. B, Displaced and
angulated. (With permission from A Unwin, KJones [eds].
Emergency Orthopaedics and Trauma. Boston: Butterworth-
Heinemann, 1995;130.)
102 CHAPTER 3 Musculoskeletal System
nonunion, and painful hardware.32 Olecranon and
radial head fracture management is presented in
Chapter AppendixTable 3-A.15.
FOREARM FRACTURES. Fractures of the shaft or
distal portion of the radius or ulna occur from a wide
variety of direct trauma including falls, sports injuries,
or motor vehicle accidents. Owing to the high-energy
impact, the fracture is usually displaced, affects an adja-
cent articulation, and involves a wrist or distal humeral
fracture.7 Management for forearm fracture is summar-
ized in Chapter Appendix Table 3-A.16. Complications
of forearm fracture include compartment syndrome,
reflex sympathetic dystrophy, nonunion, malunion,
radial nerve injury, posttraumatic arthritis, and hypo-
mobility of the elbow, forearm, and wrist.7,29
CARPAL FRACTURES. Carpal fractures and associat-
ed ligamentous injury or dislocation are typically
due to compressive or hyperextension mechanisms of
injury.33 Management for the fracture of any carpal
bone is similar. Nondisplaced fractures are treated
with short arm cast immobilization with the wrist
positioned in neutral flexion-extension with slight
ulnar deviation.33 Displaced fractures are treated with
closed reduction and casting or ORIF with a postoper-
ative splint or cast. Patients with isolated carpal fracture
are usually treated in the ambulatory care setting.
CLINICAL TIP
 For patients who have concurrent lower- and upper-
extremity injuries and require the use of a walker or
crutches, a platform attachment placed on the
assistive device will allow weight bearing to occur
through the upper extremity proximal to the wrist.
METACARPAL AND PHALANGEAL FRACTURES.
Metacarpal fractures result from direct trauma, such
as a crush injury, or by long-axis loading, as with
punching injuries. The fracture may be accompanied
by severe soft tissue injuries that can result in a treat-
ment delay of 3 to 5 days to allow for a decrease in
edema. Definitive treatment depends on the location
of the fractureçeither the articular surface (ORIF),
neck (closed reduction, percutaneous pinning, immo-
bilization, or a combination of these), shaft (ORIF,
percutaneous pinning, immobilization, or a combina-
tion of these), or base (percutaneous pinning and
immobilization) of the metacarpal.
Phalangeal fractures result from crush forces and
consequently are usually compounded by skin,
tendon, and ligament damage. Management of
nondisplaced phalangeal fracture is reduction and
splinting. Management of displaced or intraarticular
fracture is ORIF with splinting. Patients with isolated
metacarpal and phalangeal fracture are usually treated
in the ambulatory care setting.
JOINT ARTHROPLASTY
Joint arthroplasty, the surgical reconstruction of articu-
lar surfaces with prosthetic components, is indicated
to restore function and motion to a joint that is affec-
ted by degenerative arthritic changes.34 Total joint
arthroplasty is reserved for the individual with pain
that is no longer responsive to conservative measures,
such as antiinflammatory medication, restriction or
modification of activity, exercise, weight loss, or the
use of an assistive device. This surgery is elective in
nature and can be unilateral or bilateral. The incidence
of bilateral total joint arthroplasties, simultaneous or
staged, being performed in the acute care setting has
increased in recent years. Bilateral joint arthroplasty
has been established to be a safe procedure that
reduces total rehabilitation time and hospital length
of stay, thus decreasing medical costs and length of
debilitation of the patient.35
Joint arthroplasty provides patients and caregivers
with a predictable postoperative course in the acute
orthopedic care setting. For this reason, there are high
expectations for these patients to achieve specific
short- and long-term functional outcomes.The follow-
ing sections provide basic surgical information and
clinical techniques and suggestions for the acute care
physical therapist.
Hip Arthroplasty
Hip arthroplasty involves the replacement of the
femoral head, the acetabulum, or both with prosthetic
components. A hip arthroplasty is most commonly
performed on patients with severe hip arthritis
(degenerative or rheumatoid), AVN, hip infection, or
congenital disorders. Refer to Box 3-1 for a complete
list of hip disorders that may require hip arthroplasty.
The most common type of hip arthroplasty, a total
hip arthroplasty (THA), is the replacement of both
the femoral head and the acetabulum with a combina-
tion of metal (titanium or cobalt alloys) and poly-
ethylene components (Figure 3-13). Technology and
research have introduced new materials for the weight-
bearing components, such as ultra-high-molecular-
weight polyethylene and ceramic-on-ceramic and

BOX 3-1 HIP DISORDERS THAT MAY
REQUIRE TOTAL HIP
ARTHROPLASTY
 Degenerative arthritis (hypertrophic or
osteoarthritis)
 Rheumatoid arthritis
 Atraumatic avascular necrosis
 Intrapelvic protrusio acetabuli*
 Congenital subluxation or dislocation
 Posttraumatic disorders (femoral neck,
trochanteric, or acetabular fractures)
 Failed reconstructive procedures (femoral
osteotomy, arthrodesis, or resurfacing)
 Metabolic disorders (Paget’s disease, Gaucher’s
disease, or sickle cell anemia)
 Fused hip or ankylosing spondylitis
 Infectious disorders (tuberculosis and pyogenic
arthritis)
 Bone tumors
 Neurologic disorders (cerebral palsy and
Parkinson’s disease)
*Chronic progression of the femoral head into the acetabulum
and pelvis.
Data from HarkessJW. Arthroplasty of the Hip. In ST Canale
(ed): Campbell’s Operative Orthopaedics (11th ed). St. Louis:
Mosby, 2007.
FIGURE 3-13
Bilateral total hip arthroplasty.
Musculoskeletal System CHAPTER 3 103
metal-on-metal implants; however, long-term sur-
vival of such components is not yet known.36
The acetabular and femoral components may be
uncemented or cemented. Uncemented components
are commonly used in the younger, active patient, as
well as in a patient with a revision THA involving a
failed cemented prosthesis. The uncemented compo-
nents have areas of porous coated metal on the surface
that may be treated with a biochemical agent, hydroxya-
patite, to promote bony ingrowth for improved fixa-
tion.37 Press-fit prostheses are also being used and
have heavily textured surfaces that achieve fixation
through interference or interlocking of bone and
metal surfaces.34 Use of uncemented components has
the advantage of biological fixation, reducing the inci-
dence of aseptic loosening (the loosening caused by
wear debris from the components). With uncemented
components, weight bearing can be limited by surgeon
protocol, but weight bearing should not be discour-
aged.38 Weight bearing promotes bony ingrowth with
the uncemented prosthetic components by allowing
physiologic strain in the bone, thus increasing the activ-
ity of remodeling.With uncemented THA, the empha-
sis for the patient should be the prevention of torque
or twisting on the operated leg while weight bearing.
The use of a cemented prosthesis (usually the femo-
ral component) is reserved for an individual with a
decreased ability to regenerate bone, such as a patient
with osteopenia or osteoporosis.39 A cemented prosthe-
sis allows for full weight bearing early in the recovery
phase.
A bipolar prosthesis consists of a metallic acetabular
cup and polyethylene liner with a snap-fit socket
placed over a femoral prosthesis, as shown in Figure
3-14.40 A bipolar prosthesis is a type of hip arthroplasty
used for revision when there is instability caused by os-
seous or muscular insufficiency that makes a patient’s
hip more likely to dislocate.
Surgical approaches and movement precautions for
THA are presented in Table 3-5.41,42 A good under-
standing of the surgical approach taken to expose the
hip joint is necessary to determine movement precau-
tions that prevent dislocation postoperatively. In the
acute care setting, the risk of dislocation is significant
because of the incision made in the muscle mass and
joint capsule for exposure of the hip during surgery.
Consequently, the hip remains at risk for dislocation
until these structures are well healed, edema is reduced,
and the surrounding musculature is strengthened.
Signs of dislocation include excessive pain with
motion, abnormal internal or external rotation of the
104 CHAPTER 3 Musculoskeletal System

hip with limited active and passive motion, and short-

ening of the limb.40
Medical complications that may occur after THA
include nerve injury, vascular damage and throm-
boembolism that can cause pulmonary embolism,
myocardial infarction, and cerebral vascular accident.
Complications pertaining to the implant can include
fracture, aseptic loosening, osteolysis, heterotopic
ossification, and infection.43
PHYSICAL THERAPY INTERVENTION AFTER HIP
ARTHROPLASTY
Early physical therapy intervention is focused on func-
tional mobility, patient education about movement
precautions during activities of daily living (ADLs),
ROM, and strengthening of hip musculature. Physical
FIGURE 3-14 therapy may assist in preventing complications, such
Modified bipolar cup. Polyethylene cup is placed over head, as atelectasis, blockage of the intestines because of
and then the metal cup is pressed over it, polyethylene liner is decreased peristalsis secondary to anesthesia (posto-
locked in metallic cup, and head is locked in socket of perative ileus), and DVT. Early mobilization improves
polyethylene liner. Entire cup moves with femoral head as one respiration, digestion, and venous return from the lower
unit, so cup cannot assume valgus or varus fixed position. extremities. Patients should be educated about these
Metal head can rotate in plastic socket in axis of neck. Cup
risks to assist in prevention of secondary complications.
must be used with the femoral prosthesis designed to fit
properly into plastic liner. (With permission fromJW Harkess.
 The priority of treatment is to achieve safe func-
Arthroplasty of Hip. In AH Crenshaw [eds], Campbell’s tional mobility (i.e., bed mobility, transfers, and
Operative Orthopaedics,Vol. 1 [8th ed]. St. Louis: Mosby, 1998.) ambulation with assistive devices) to maximize
independence and functional outcome. Patient
education is an important aspect of physical therapy.
The physical therapist should educate the patient
about movement precautions while encouraging
use of the operated limb with functional activities.
Verbal and tactile cueing may assist a patient in
Table 3-5 SURGICAL APPROACHES AND precaution maintenance; failure to do so may result
PRECAUTIONS FOR TOTAL HIP in hip dislocation. The therapist should educate
ARTHROPLASTY* the patient that movement of the operated hip can
decrease postoperative pain and stiffness.
Surgical Approach Precautions  ROM (passive and active assisted) should be main-
Posterolateral No hip flexion beyond tained within the parameters of the hip movement
(most common) 90 degrees precautions. An overhead frame with a sling can
No excessive internal rotation promote active-assisted exercise.
No hip adduction past neutral  Isometric exercises for the quadriceps and gluteal
Lateral No combined hip flexion muscles can be initiated immediately postopera-
beyond 90 degrees with
adduction, internal rotation,
tively, progressing to active-assisted exercises as
or both tolerated. Muscle spasm often occurs in the mus-
Anterolateral Hip extension and external culature surrounding the hip postoperatively.
rotation are to be avoided Instructing the patient in exercises to gain control
of the musculature involved in the surgery can
*Hip surgery performed in conjunction with a trochanteric help to reduce muscle spasms. Patients should be
osteotomy (removal and reattachment of the greater trochanter)
will require an additional movement restriction of no active encouraged to perform all exercises independently.
abduction or passive adduction.Weight bearing of the surgical limb  To assist in the prevention of DVT and reduce
may be limited further. postoperative edema, the patient should be

instructed to perform ankle-pumping exercises.
This can be combined with external compression
devices and antiembolic stockings to reduce the
risk of a thromboembolic event. Before use of
these modalities, ensure that the patient does not
have cardiovascular insufficiency that may be
exacerbated by their use.
 The patient should be instructed in additional anti-
embolic exercises to facilitate venous circulation
and isometric strengthening.These exercises include
quadriceps sets and gluteus sets. The patient should
perform 10 to 15 repetitions an hour (when awake)
for optimal benefits.These exercises, if not contrain-
dicated, are beneficial for many different types of sur-
geries and diagnoses.
 Before establishing an advanced strengthening pro-
gram consisting of progressive resistive exercises or
weight training, consult the surgeon, because exces-
sive strain can hinder healing of surgically involved
structures.
CLINICAL TIP
 All peripheral innervations, dermatomal and
myotomal, should be assessed on initial
examination, with emphasis on the femoral nerve
that innervates the quadriceps and the sciatic nerve
that innervates the peroneals.43 Neuropraxia of the
femoral nerve can occur secondary to compression
from surgical instrumentation and edema. A knee
immobilizer may be necessary to provide stability if
the quadricep lacks adequate strength and stability
for ambulation. If the peroneals are affected,
resulting in a footdrop on the affected side, a
custom-fit ankle-foot orthosis may be indicated for
the patient to optimize gait.
 The use of a knee immobilizer reduces hip flexion by
maintaining knee extension. This can be helpful in
preventing dislocation in patients who are unable to
maintain posterior hip precautions independently.
 Instruct the patient to avoid pivoting on the
operated extremity when ambulating. Instead, the
patient should turn by taking small steps and flexing
the knee of the operated leg to clear the toes. To
maintain movement precautions, encourage the
patient to turn away from the operated limb.
 Emphasize to the patient that combining any of the
restricted movements will increase the likelihood of
dislocation. Provide the patient and family with
written and illustrated educational materials on all
movement precautions.
Musculoskeletal System CHAPTER 3 105
 Elevation of the height of the bed can facilitate
sit-to-stand transfers by reducing the degree of hip
flexion and the work of the hip abductors and
extensors. This is especially helpful for patients with
bilateral THA. Also, instruct the patient to place the
operated leg forward when performing a stand-to-sit
transfer to decrease hip flexion.
 If available, a hip chair (or other elevated seating
surface) and commode chair should be used to
facilitate transfers while maintaining hip
precautions. Preoperative and postoperative
education in the use of furniture of the appropriate
height in the home should be initiated by the
physical therapist.
 As the initial healing stages begin, the patient may
feel as though one leg is longer while ambulating.
This is referred to as ‘‘apparent leg length
discrepancy’’ and is associated with the newly
restored joint space that was preoperatively lessened
by cartilage wearing. Patients are usually concerned
because it is a sudden noticeable increase in height,
whereas the progressive decrease in joint space
preoperatively was over time and less noticeable. It
is important to educate the patient on this subject
and assure him or her that this discrepancy most
typically resolves in 4 to 6 weeks. In the interim,
instructing the patient to wear a shoe on the
nonoperative leg and a slipper on the operative leg
may help to facilitate a more ‘‘even’’ sensation
during ambulation.
 Instruct the patient to lie flat in bed periodically
throughout the day as it will facilitate stretching of
the anterior hip musculature. Most patients are
typically in a reclined position or sitting in a chair
postoperatively, which allows for hip flexor
tightness. Lying flat in bed will allow the hip joint
and surrounding areas to adjust more comfortably
to a neutral position.
Joint Resurfacing
Joint resurfacing has evolved over time as a more con-
servative alternative to a total hip arthroplasty for
patients with osteonecrosis of the femoral head.
Depending on the severity of osteonecrosis, there are
two different types of joint resurfacing performed:
hemiresurfacing arthroplasty and total resurfacing
arthroplasty. Hemiresurfacing arthroplasty conserves
the majority of the bone and consists of the implanta-
tion of an adjusted cup to facilitate joint articulation.44
106 CHAPTER 3 Musculoskeletal System
Total joint resurfacing consists of resurfacing both the
femoral head and the acetabulum using a double
cup.45 These procedures are most favorable if per-
formed in the early stages of osteonecrosis with a
lesion smaller than 25% to 50%, as there is significant
risk for joint dislocation, loosening, and hardware
failure. Although this procedure is a conservative
intervention to address necrosis, the long-term suc-
cess is limited and often converted to a total hip
arthroplasty.46
PHYSICAL THERAPY AFTER JOINT RESURFACING
Specific precautions and therapeutic exercise restric-
tions should be confirmed with the surgeon depending
on the procedure performed. Physical therapy should
primarily be focused on bed mobility, transfer training,
and gait training reflecting specific weight-bearing
restrictions.The functional outcomes should be consis-
tent with those of a THA with emphasis on increased
joint integrity, strength, and increased functional
mobility and ambulation.
The patient should be instructed to follow total hip
precautions during exercise and mobility. These may
include no bending past 90 degrees at the hip, no cross-
ing of the legs, or no twisting or turning while weight
bearing (per THA protocol).
The exercise protocol is generally very similar to that
of the THA. Hip ROM and quadriceps strengthening
in the form of short and long arch quads should be
initiated as tolerated with careful consideration taken
to avoid any unnecessary stress on the joint.
Typically weight bearing is limited to partial
(approximately 70%) for the initial 4 to 6 weeks. This
is due to the increased risk of femoral neck fracture
postoperatively. Therefore the physical therapist needs
to select the most appropriate assistive device for the
patient to use in order to maintain this precaution.
Knee Arthroplasty
Knee arthroplasty is indicated for patients with
end-stage osteoarthritis, rheumatoid arthritis, trau-
matic arthritis, or nonseptic arthropathy. Pain reduc-
tion, gaining intrinsic joint stability, and restoration of
function are the primary goals associated with knee
arthroplasty and should only be considered when con-
servative measures have failed. The extent of damage
within the joint determines the type of prosthesis
implanted: unicompartmental or tricompartmental.
A unicompartmental (unicondylar) or partial knee
arthroplasty is the replacement of the worn femoral
and tibial articulating surfaces in either the medial or
FIGURE 3-15
Unicompartmental knee arthroplasty of the right medial
compartment.
lateral compartment of the joint (Figure 3-15). This
surgery is indicated for individuals who have osteo-
arthritis or osteonecrosis confined to one compart-
ment. Proponents of the unicompartmental knee
arthroplasty believe that it is a conservative measure to
promote a more functional knee.47 In unicompartmen-
tal knee arthroplasty (UKA), the goal is to maximize
the preservation of the articular cartilage of the heal-
thier compartment and spare bone that may in turn
delay a total knee arthroplasty. More of the joint is
preserved, including the cruciate ligaments, the oppo-
site tibiofemoral compartment, and the patellofemo-
ral joint. Preservation of the joint helps to maintain
the normal kinematics of the knee joint allowing
for a quicker rehabilitation process as the patient can
typically tolerate more aggressive mobility training
in the immediate postoperative stage. Revision
from a unicompartmental to a tricompartmental
knee arthroplasty is often warranted at a later time
because of continued degeneration; however, newer
unicompartmental prosthetic designs may show
improved results.48 Associated valgus deformities may
also be corrected by a tibial osteotomy and release of
soft tissue during the partial knee replacement.
The tricompartmental or total knee arthroplasty
(TKA) is the replacement of the femoral condyles, the
tibial articulating surface, and the dorsal surface of
the patella. This type of knee arthroplasty involves
 Musculoskeletal System CHAPTER 3 107
The methods of fixation inTKA are similar to those
of hip replacement. Cementing techniques can be
used to fix the components, or the prosthetic design
can allow for either porous ingrowth or press-fit. A
press-fit prosthesis has surface modifications or
grooves and bioactive hydroxyapatite to provide
macrointerlock with the bone.40 Many surgeons tend
to use a hybrid technique by using a cemented tibial
component with porous coated femoral and patellar
prostheses. Partial weight bearing or weight bearing
as tolerated often is allowed after TKA and is encour-
aged to promote use of the limb and promote bone
remodeling.49
Patients who undergo either type of knee arthro-
plasty may have associated preoperative soft-tissue con-
tractures. A lateral retinacular release can be
A performed to centralize patellar tracking. If performed,
there may be an increased risk of patellar subluxation
with flexion. Special procedures that are performed in
either type of knee arthroplasty should be taken into
consideration by the physical therapist, because the sur-
geon may impose restrictions to ROM and weight bear-
ing. Any additional procedure may prolong healing
time secondary to increased edema and pain, which
limits the patient’s functional mobility and tolerance
to exercise.
General medical complications after TKA are
similar to those described with THA. Box 3-2 lists
common complications specific to TKA.

B BOX 3-2 COMPLICATIONS AFTER TOTAL

FIGURE 3-16 KNEE ARTHROPLASTY
A, Anterior view of a right total knee arthroplasty. B, Lateral
view of a right total knee arthroplasty.  Thrombosis and thromboembolism
 Poor wound healing
 Infection
replacing the medial and lateral compartments of the  Joint instability
joint, as well as resurfacing the patellofemoral articula-  Fractures
tion with prosthetic components (Figure 3-16, A).  Patellar tendon rupture
These components are made of materials similar to  Patellofemoral instability, component failure, or
those of the THA. The femoral condyles are replaced loosening
with a metal-bearing surface that articulates with a  Peroneal nerve injury
polyethylene tray implanted on the proximal tibia.  Component loosening or breakage
The dorsal aspect of the patella is often resurfaced if  Wear and deformation
excessive erosion of the cartilage has occurred; how-
ever, some surgeons refrain from the patellar implant Data from GuytonJL. Arthroplasty of the Knee. In ST Canale
if the articular cartilage of the patella seems reasonably (ed): Campbell’s Operative Orthopaedics (11th ed). St. Louis:
intact, as shown in Figure 3-16, B.49 Mosby, 2007.
108 CHAPTER 3 Musculoskeletal System
PHYSICAL THERAPY INTERVENTION AFTER
KNEE ARTHROPLASTY
Physical therapy intervention after knee arthroplasty
is focused on increasing functional independence.
The patient must also perform ROM and strengthening
exercises and be educated in positioning techniques
to help reduce swelling. Restrictions on weight bear-
ing and precautions are also taught to the patient.
 Evaluation and treatment of functional mobility to
promote independence should begin immediately
postoperatively. To maximize functional outcomes
and safety, the patient should be instructed in bed
mobility, transfer training, and gait training on level
surfaces and stairs with appropriate assistive devices.
 The patient should be instructed in antiembolic
exercises to facilitate venous circulation and iso-
metric strengthening. These exercises include ankle
pumps, quadriceps sets, and gluteus sets. These
should be performed 10 to 15 repetitions per hour
(when awake) for optimal benefits. These exercises,
if not contraindicated, are beneficial for many differ-
ent types of surgeries and diagnoses.
 Strengthening exercises may begin immediately
postoperatively, emphasizing quadriceps exercises.
Quadriceps retraining may be accomplished with
overflow from the uninvolved limb or distal limb.
Active-assisted quadriceps exercises should be per-
formed to increase stability around the operated
knee. The patient should be encouraged to perform
exercises independently, within the limits of
comfort.
 Knee immobilizers are often prescribed to protect
the knee from twisting and buckling secondary to
decreased quadriceps strength.With a lateral release,
there may be increased pain and edema that may
hinder quadriceps functioning; therefore, a knee
immobilizer or brace may be required for a longer
period of time.
 ROM exercises should begin immediately after
TKA. ROM must be gained early in the rehabilita-
tion of a TKA and is accomplished by passive or
active-assisted exercises. If available, a continuous
passive motion (CPM) machine may be used imme-
diately postoperatively. The limitations to ROM are
often attributed to pain, swelling, muscle guarding,
and apprehension, all of which can be addressed
through physical therapy interventions and patient
education.
 Positioning and edema control should be initiated
immediately to help reduce pain and increase ROM.
The patient should be educated to elevate the oper-
ated extremity with pillows or towel rolls under the
calf to promote edema reduction and knee exten-
sion. Ice should be applied after exercise or when-
ever needed for patient comfort.
CLINICAL TIP
 Educate the patient to elevate the operated limb
without putting pillows or towel rolls under the
knee. This type of positioning keeps the knee flexed
and will increase the risk of flexion contractures and
edema.
 The therapist may place a towel roll or
blanket along the lateral aspect of the femur, near
the greater trochanter, to maintain the operated
extremity in a neutral position. Any external rotation
at the hip can result in slight flexion at the knee.
 The therapist should place a pillow or towel roll
under the knee in the degree of available ROM
while performing isometric exercises. This will
produce a stronger quadriceps contraction by
reducing passive stretch on joint receptors and pain
receptors. This will also provide posterior support to
the knee, providing increased tactile feedback for the
patient.
 ROM for the majority of TKA is at least 90 degrees
in the operating room. Consult the surgeon for the
maximum amount of flexion obtained. This will
provide the therapist with an idea of how much
pain, muscle guarding, and edema are limiting
patient performance.
 When performing active-assistive ROM, the use of
hold/relax techniques to the hamstrings assists to
decrease muscle guarding and increases knee flexion
through reciprocal inhibition of the quadriceps
muscle. This technique also provides a dorsal glide
to the tibia, preparing the posterior capsule for
flexion. Gentle massage of the quadriceps
mechanism over the muscle belly or throughout the
peripatellar region will improve ROM and reduce
muscle guarding.
 With patients who have excessive edema with
exercise, therapy sessions should be limited in
duration and should concentrate on functional
mobility. The use of a CPM in submaximal ranges in
conjunction with ice will maintain knee ROM while
assisting in edema reduction.
 If a brace or knee immobilizer is being used, the
therapist should always check that it is applied
properly. If the brace is not appropriately fitted to
 Musculoskeletal System CHAPTER 3 109

the patient or applied properly, it may keep the

knee flexed. The therapist should adjust the brace or
immobilizer to be certain that knee extension is
maintained when worn by the patient. Nursing staff
may need to be educated to different types of braces
and the proper donning and doffing of the brace.
 Treatment sessions should be coordinated with
administration of pain medication to increase
patient comfort and compliance with ROM exercises.

Minimally Invasive Hip and Knee Arthroplasty

Frequent practice of a minimally invasive approach
to total knee and hip arthroplasty is vastly becoming B
integrated into orthopedic surgery. Minimally invasive
surgery (MIS) can be performed arthroscopically or
open, with the open approach being the most com-
monly used in total joint replacements (Figure 3-17).
The indications for MIS are very similar to those
of a traditional arthroplasty; however this technique is
not commonly used for complex joints replacements
or joint revisions.
The many benefits to a MIS knee arthroplasty
include50:
 Decreased skin incision (6 to 11 cm)
 Quadriceps sparing to minimize muscle
compromise FIGURE 3-17
 Allowance for inferior and superior patellar A, Minimally invasive knee: Intraoperative measurement of
capsular releases incision line during MIS-TKA. B, Minimally invasive hip: A
 Lack of patella eversion typical length mini-incision. (A From Bonutti PM: Minimally
 Rare incidence of joint dislocation invasive total knee arthroplasty: a 10-feature evolutionary
approach. Orthop Clin North Am. 2004;35(2):217-226; B From
The MIS hip arthroplasty shares many of the same
SculcoTP, Jordan LC,Walter WL: Minimally invasive total hip
benefits as the knee, with the greatest advantage being arthroplasty: the Hospital for Special Surgery experience.
that this approach can be used for either an anterior- Orthop Clin North Am. 2004;35(2):137-142.)
lateral or posterior approach to the hip joint. The
difference in surgical intervention as compared to the
traditional arthroplasty is that MIS hip arthroplasty
contributes to decreased morbidity, reduced hospital
length of stay, less soft tissue and muscle compromise, Hip Arthroplasty sections for specific exercise guide-
less risk of infection, faster healing time, and increased lines. Also incorporated should be functional training
functional mobility postoperatively. (transfer, balance, and gait) and patient education on
precautions, use of assistive device, and home exercise
PHYSICAL THERAPY INTERVENTION AFTER programs. Total joint precautions regarding func-
MINIMALLY INVASIVE TOTAL JOINT ARTHROPLASTY tional mobility are not significantly different from
The most essential aspect of rehabilitation following those of the traditional total joint. Typically patients
an MIS joint arthroplasty is increased functional are allowed to weight bear as tolerated immediately
mobility. Physical therapy intervention should consist after surgery. For both MIS knee and hip arthroplasty,
of increasing joint mobility and integrity through the patient should be encouraged to avoid twisting
aggressive ROM and quadriceps/hamstring strength- or turning while weight bearing. Refer toTable 3-5 for
ening exercises. Refer to the Knee Arthroplasty and specificTHA precautions.51
110 CHAPTER 3 Musculoskeletal System

type that relies on soft-tissue integrity of the rotator

Rapid Recovery Program for Total Joint cuff and deltoid muscles. If these structures are insuffi-
Arthroplasty cient or damaged, repair may take place during
A rapid recovery approach to rehabilitation following shoulder arthroplasty surgery and may prolong rehabil-
an MIS or traditional total joint arthroplasty involves itation. The success of all TSA involves accurate surgi-
mobility and ambulation as early as 3 to 6 hours cal placement of the prosthesis and the ability of the
after surgery.52,53 Mobility may consist of sitting EOB surgeon to reconstruct the anatomic congruency of
or ambulation up to 100 feet depending on the patients the joint. Proper orientation of the prosthetic compo-
post operative medical status and activity tolerance. nents and preservation of structural length and mus-
This rapid recovery program is usually performed in cular integrity are key aspects of the surgery that
the recovery room with adequate monitoring and predispose favorable outcomes. The technical skill of
close observation of vitals and activity tolerance. the surgeon and advances in prosthetic components
In conjunction with increased functional mobility, have improved outcomes with TSA. With appropriate
performing therapeutic exercises immediately after patient selection and a properly functioning rotator
surgery is pivotal in significantly increasing ROM cuff, a patient with a TSA can be rehabilitated to
and quadriceps strength. In addition to an accelerated improve ROM and strength equal to that of the unaf-
physical therapy protocol, surgical/medical adjust- fected side.54
ments are involved in the success of early mobilization, A proximal humeral hemiarthroplasty (Figure 3-18)
including short-acting spinal analgesics resulting in can be performed when arthritic changes have affected
decreased effects of anesthesia, which allow for earlier only the humeral head. The humeral head is replaced
participation in therapy. Suggested benefits of this with a prosthetic component through a similar tech-
program include decreased length of hospital stay, nique as in TSA. Results are dependent on the integ-
decreased postanesthesia symptoms (e.g., nausea/ rity of the rotator cuff and deltoid, the precision of the
vomiting, orthostatic hypotension, and dizziness), surgeon, and the willingness of the patient to commit
improved joint ROM and quadriceps strength, and to a continual rehabilitation program. Rehabilitation
early functional mobility and ambulation.52,53 of the shoulder hemiarthroplasty is similar to that
of aTSA.
Shoulder Arthroplasty
Total shoulder arthroplasty (TSA) is indicated for
patients with severe pain and limited ROM caused
by osteoarthritis, rheumatoid arthritis, fracture, AVN,
or traumatic arthritis. Conservative treatment should
attempt to alleviate pain while increasing function.
Only when these measures have failed should TSA be
considered. If only the humeral head shows signifi-
cant degeneration, a shoulder hemiarthroplasty may
be considered. Prosthetic wear after TSA or shoulder
hemiarthroplasty is of less concern than after THA or
TKA, because the shoulder is not a weight-bearing
structure.54 The goals for surgery are to relieve pain
and regain lost function.
TSA involves the replacement of the glenoid articu-
lating surface and the humeral head with prosthetic
components. A polyethylene glenoid unit with metal
backing and keel articulates with a humeral prosthesis.
Fixation of these components is either cemented or
press-fit, processes similar to those in the other joint
replacement surgeries.55
There are three types of TSA prostheses available:
unconstrained, semiconstrained, and constrained. The FIGURE 3-18
most commonly used prosthesis is the unconstrained Proximal hemiarthroplasty of the right shoulder.

PHYSICAL THERAPY INTERVENTION AFTER
SHOULDER ARTHROPLASTY
The rehabilitation after TSA or shoulder hemiarthro-
plasty should emphasize functional independence and
patient education on therapeutic exercise. The physical
therapist should confirm the presence of any precau-
tions with the surgeon and educate the patient in pas-
sive and active-assisted ROM exercises to prevent the
formation of adhesions. The stability of the shoulder is
dependent on the rotator cuff and deltoid muscles,
and the rehabilitation program may be dictated by
their integrity. Maximum results from a TSA occur
approximately 18 to 24 months after the surgery and a
dedicated program of physical therapy.54
 Edema can be controlled with hand, wrist, and
elbow ROM exercises and ice packs used in conjunc-
tion with elevation. Having the patient squeeze a
ball or sponge will help maintain or strengthen
gripping.
 A sling may be used for patient comfort but should
be discontinued as soon as possible, following sur-
geon protocol, to increase ROM and strength.
 If there was extensive repair to the rotator cuff or
deltoid, patients may be required to wear an abduc-
tion or ‘‘scoi’’ brace for increased shoulder stability
and prevention of shoulder abduction. Instruction
should be given to patient and family/care providers
on donning and doffing the brace as it is difficult
for patients to do themselves. Typically patients are
allowed to remove the brace for exercise, dressing,
and hygiene.
 The patient should be instructed in pendulum exer-
cises. All four planes of motion (clockwise, counter-
clockwise, forward/backward, and side to side)
should be practiced. If the patient has difficulty
standing to perform this exercise, it may be per-
formed in sitting.
 With most TSAs, gentle passive or active assisted
ROM exercises specific to the surgeon’s protocol
should be initiated.
 Forward elevation and external rotation are typically
initiated after surgery. Forward elevation in the scap-
ular plane is typically allowed to patient tolerance,
however external rotation may be limited to a maxi-
mum of 20 to 30 degrees.
 These exercises maybe performed with a
wand to facilitate patient-controlled active-assisted
ROM.
 Initially active abduction and flexion should be lim-
ited according to surgeon protocol.
Musculoskeletal System CHAPTER 3 111
 Consult your surgeon for specific protocols, as these
may vary depending on surgical procedure.
Outpatient physical therapy should begin shortly
after the follow-up visit with the surgeon.
Instructing the patient in necessary precautions is
essential immediately after surgery.These may include:
 No weight bearing on the surgical extremity.
 No lifting anything heavier than a coffee cup.
 No rolling or lying on the surgical extremity.
 Not allowing the extremity to extend past mid-line
when lying in supine. (A towel or small pillow may
be needed to facilitate neutral positioning.)
These precautions should be followed for the first 4
to 6 weeks, depending on the specific surgical protocol.
Following this timeframe, lifetime precautions or lim-
itations may apply in some cases including not lifting
anything heavier than 20 lbs overhead. Please discuss
specific protocols with the surgeon.
CLINICAL TIP
 A shoulder CPM can be ordered by the surgeon and
applied postoperatively or for home use to assist
with ROM and to prevent formation of adhesions.
 The physical therapist should initiate a consult for
occupational therapy to instruct the patient on
ADLs, especially if the patient’s dominant arm is
affected.
Shoulder Surface Replacement Arthroplasty
Glenoid fixations and designs for total shoulder arthro-
plasty (TSA) vary depending on the pathology of the
joint. Most are cemented, which in turn leads to glenoid
looseningçthe most common indication for a revi-
sion.55-57 As traditional stemmed implants have been
the intervention of choice in the past, surface replace-
ment arthroplasty has proven to be a successful alterna-
tive as it allows for restoration of glenohumeral
anatomy and minimal bone loss.58-60 Surface replace-
ment arthroplasty of the shoulder is much like that of
the hip in that there is no cemented stem implant com-
promising bone integrity. Although resurfacing has
proven favorable outcomes, there are some instances
of failure that warrant a total shoulder revision.
Because the initial procedure is less invasive in that
there is no stem or cement placement, a revision is
much more easily performed.48 Physical therapy pre-
cautions and interventions after a surface replacement
arthroplasty are very similar to that of a total shoulder
arthroplasty as described above.
112 CHAPTER 3 Musculoskeletal System

results after TEA are those who are severely affected

Reverse Total Arthroplasty by rheumatoid arthritis.69 Posttraumatic arthritis is
A reverse total arthroplasty is very similar to a TSA also an indication for elbow arthroplasty; however,
in that it is essentially the same procedure but with patient satisfaction and outcomes are inferior com-
a different surgical approach into the joint. This tech- pared to those with rheumatoid arthritis.70 The goal of
nique can be used for a primary joint replacement or TEA is the restoration of function through decreasing
a revision and is best indicated for the following61-64: pain and increasing joint ROM and stability.
 Irreparable rotator cuff deficiency or failed rotator Early results of TEA with a fully constrained pros-
cuff repairs thesis have shown aseptic loosening. Conversely, an
 Joint injury, including arthritis, fractures, or failed unlinked or less-constrained prosthesis demonstrates a
implant decreased rate of loosening but has showed increased
 Poor active elevation of the shoulder (less than rates of failure secondary to weak collateral ligaments,
60 degrees) anterior capsule, and reduced bone stock. Therefore, a
 Anterior superior instability semiconstrained prosthesis (Figure 3-19) is now favored
 Pain for TEA to dissipate stress to the muscular and liga-
This procedure, also referred to as the Delta III, has mentous structures surrounding the elbow, thus
proven very successful in instances of significant rota- decreasing the rate of prosthetic loosening.71
tor cuff deficiency because it relies heavily on the del- Unconstrained or resurfacing arthroplasties attempt
toid muscle for stability instead of the rotator cuff.65 to duplicate the anatomic surfaces within the joint
The success of this technique is primarily due to posi- and depend on intact ligaments and the anterior cap-
tioning the center of rotation of the shoulder more sule for stability. A semiconstrained prosthesis may
inferior and medial, which again causes shoulder sta- have a metal-to-polyethylene articulation that connects
bility and function to rely heavily on the deltoid with a locking pin or snap-fit device70 and is indicated
muscle.65 The great advantage to this semiconstrained for use if there is injury to the musculature and lig-
technique is that it is found to exhibit similar movement amentous structures of the elbow. Implants are con-
patterns to that of the normal shoulder.66 structed of materials similar to those of other total
joint arthroplasties, and fixation techniques vary with
PHYSICAL THERAPY INTERVENTION FOR REVERSE cemented, uncemented, and hybrid (a combination of
TOTAL ARTHROPLASTY
The physical therapy protocol and precautions for a
reverse total arthroplasty is similar to that of a TSA
as described above. However because of the signifi-
cance of the deltoid muscle resection in this procedure,
patients are typically immobilized in slight abduction
and neutral rotation. Gentle passive forward elevation
and external rotation is started immediately posto-
peratively (refer to TSA protocol for specifics in these
planes). At approximately 3 to 4 weeks postoperatively,
active-assisted motion is allowed, and at approximately
6 weeks the patient may begin active movement with-
out the immobilizer. Patients are expected to return to
activities as tolerated at approximately 3 to 4 months.67
It is important to consult the surgeon for specific post-
operative protocols, as this is only for the typical patient
and may vary.
Total Elbow Arthroplasty
The reliability of TEA has progressed to outcomes
comparable to those of other types of joint arthroplas-
ty.68 Indications for TEA are pain, instability, and FIGURE 3-19
elbow ankylosis. Patients who demonstrate optimal Left total elbow arthroplasty shown in flexion.

cemented and uncemented) fixation designs. Patient
selection, surgical proficiency, and improved prosthetic
design have improved outcomes and reduced compli-
cations after TEA.
Complications after a TEA include:
 Component loosening (usually the humeral
component).
 Joint instability, including dislocation or
subluxation.
 Ulnar nerve palsy; triceps weakness.
 Delayed wound healing; and infection.69
Immediate rehabilitation of the patient with a TEA
includes functional mobility training, ADL training,
edema control, and ROM exercises per surgeon proto-
col. If available, an elbow CPM may be used. Passive
elbow flexion and extension ROM may be allowed as
tolerated according to patient pain levels while
strengthening exercises are avoided.
Total Ankle Arthroplasty
Total ankle arthroplasty has had difficulty gaining
popularity due to increased failure rate with early
prosthetic designs. There has been increased incidence
of complications involving superficial and deep
wound infections, loosening of the prosthesis, and
associated subtalar and midtarsal degenerative joint
disease. Debilitating arthritic pain is the primary indi-
cation for total ankle arthroplasty. Currently, the total
ankle arthroplasty is optimal for an elderly patient
with low physical demands, normal vascular status,
good bone stock, and no immunosuppression.72
Progress has been made with newer prosthetic designs
and improved surgical techniques involving limited
periosteal stripping, meticulous attention to position-
ing, and limited rigid internal fixation.
There are two types of prosthetic designs that have
been developed to create a semiconstrained articula-
tion. A two-component design with syndesmosis of
the tibia and fibula consists of a tibial articular surface
that is wider than the talar component. Fibular motion
is eliminated, and a greater surface for fixation of the
tibial component is created.72 The second prosthetic
design involves three components: a flat metal tibial
plate, a metal talar component, and a mobile polyethyl-
ene bearing.72 This system allows for multiplanar
motion while maintaining congruency of the articulat-
ing surfaces. Both types of design consist of metal
alloy and polyethylene components and rely on bony
ingrowth for fixation. Technical skill and experience
in component alignment and advanced instrumenta-
tion for component fixation are important aspects to
Musculoskeletal System CHAPTER 3 113
be considered to improve postoperative outcomes.
Current short-term results have shown reasonable
increases in function, with little or no pain in appro-
priately selected patients.72
During the early postoperative period, care is taken
to prevent wound complications. A short leg splint
is used until sutures are removed, and the patient
remains non—weight bearing until bony ingrowth is
satisfactory (approximately 3 weeks with hydroxyapa-
tite-coated implants).72 Early postoperative physical
therapy treatment focuses on functional mobility and
the patient’s ability to maintain non—weight bearing.
The patient should be educated in edema reduction
and early non—weight-bearing exercises, including
ankle ROM and hip and knee strengthening if pre-
scribed by the surgeon.
Total Joint Arthroplasty Infection and Resection
The percentage of total joint arthroplasties that
become infected (septic) is relatively small. However,
a patient may present at any time after a joint arthro-
plasty with fever; wound drainage; persistent pain;
and increased white blood cell count, erythrocyte sedi-
mentation rate, or C-reactive protein.73 Infection is
often diagnosed by aspirating the joint, culturing joint
fluid specimens, and examining laboratory results
from the aspirate. Once the type of organism is identi-
fied, there are several different avenues to follow for
treatment of the infection. Treatment choices include
antibiotic treatment and suppression, debridement
with prosthesis retention or removal, primary exchange
arthroplasty, two-stage reimplantation, or, in life-
threatening instances, amputation.74
Within the early postoperative period, an infection
in soft tissue with well-fixed implants can be treated
with an irrigation and debridement procedure,
exchange of polyethylene components, and antibiotic
treatment. With an infection penetrating the joint
space to the cement-bone interface, it is necessary
to perform a total joint arthroplasty resection,
consisting of the removal of prosthetic components,
cement, and foreign material with debridement of sur-
rounding tissue. A 6-week course of intravenous anti-
biotics should be followed before reimplantation of
joint components.48 The most successful results of
deep periprosthetic infection have been obtained
with the two-stage reimplantation and antibiotic treat-
ment.48 With reimplantation of prosthetic compo-
nents, fixation depends on the quality of the bone,
need for bone grafting, and use of antibiotic-impreg-
nated bone cement.43
114 CHAPTER 3 Musculoskeletal System
FIGURE 3-20
Total hip arthroplasty resection (Girdlestone).
Resection arthroplasty of the hip or knee is com-
monly seen in the acute care orthopedic setting. A
two-stage reimplantation is commonly performed.
First the hip or knee prosthetic is resected, and a
cement spacer impregnated with antibiotics is placed
in the joint to maintain tissue length and allow for
increased weight bearing. Then the prosthesis is reim-
planted when the infection has cleared.48,74 If the
extent of the infection does not allow for reimplan-
tation of prosthetic components, a knee resection
arthroplasty or hip Girdlestone (removal of the femo-
ral head, as in Figure 3-20)74 may be the only option
for the patient. Often, instability can be associated
with these surgeries, leading to decreased function,
and the patient often requires an assistive device for
ambulation. Unlike a hip resection, a patient with a
knee resection may undergo a knee arthrodesis or
fusion with an intermedullary nail to provide a stable
and painless limb.
PHYSICAL THERAPY INTERVENTION AFTER
RESECTION ARTHROPLASTY
Physical therapy after a resection arthroplasty without
reimplantation or a two-staged reimplantation is
dependent on the extent of joint or bone destruction
caused by the infection and the removal of the pros-
thetic components, cement, and debridement of soft
tissue. Weight-bearing restrictions may depend on use
of cement spacers and vary from non—weight bearing
to weight bearing as tolerated, as established by the
surgeon. Physical therapy sessions focus on func-
tional mobility, safety, assistive device evaluation, and
maintenance of muscle strength and endurance in
anticipation for reimplantation of the joint.
 Patients who have an infection and joint resection
arthroplasty may be compromised by general mal-
aise and decreased endurance secondary to the
infection, and, possibly, from increased blood loss
during surgery. This may lead to decreased pain tol-
erance. The physical therapist should take these
factors into account when mobilizing the patient.
Functional mobility training should begin when the
patient is stable, and physical therapy sessions
should be modified for patient tolerance.
 THA precautions often do not pertain after removal
of the prosthesis. The physical therapist should
verify any other precautions, such as trochanteric
precautions (see Table 3-5) and weight-bearing
status, with the surgeon. Without movement pre-
cautions, most isometric, active, and active-assisted
exercise may be appropriate. Progress the patient as
tolerated to maximize function, strength, and endur-
ance in preparation for eventual reimplantation of
the prosthesis.
 For knee resection surgery, strengthening exercises
for the quadriceps muscle can be initiated as long
as the extensor mechanism is intact. Isometrics,
active-assisted, and active—straight-leg raises can be
initiated according to patient comfort as well as
active hip abduction and adduction.
 Edema should be controlled with ice and elevation.
Positioning of the limb is important to decrease dis-
comfort from muscle spasm and the potential for
deformities caused by muscle contractures around
the hip and knee.
CLINICAL TIP
 A hip Girdlestone procedure may leave a patient
with a significant leg-length discrepancy. A patient’s
shoes should be adapted with a lift to correct gait
and increase weight bearing on the affected
extremity. However, this intervention is not typically
advised until the healing stages are complete as the
significance of the discrepancy may change from the
acute to chronic stages of healing.
 With decreased leg length, the musculature
surrounding the hip shortens. External (e.g., Buck)
traction can be used to maintain muscle length and
may be used while the patient is in bed. Shortened
muscles may spasm. Isometric exercises should be
encouraged to gain control of these muscles to
reduce spasm.

 ROM should be minimal with knee resection
so as to maintain integrity of bone surfaces if
reimplantation is planned. A brace or knee
immobilizer should be worn during functional
activities to maintain knee extension but can be
removed in bed. The unaffected limb can assist
with lifting the affected limb with transfers out
of bed.
 With a patient that is non—weight bearing,
a shoe on the unaffected side and a slipper sock on
the affected side can assist with toe clearance when
advancing the affected leg during the swing phase
of gait. Conversely, with a patient who has a
significant leg-length discrepancy, a slipper sock
on the unaffected side and a shoe on the affected
side can assist with ambulation until a shoe lift
is obtained.
Limb Salvage Surgery
Depending on the diagnosis and the stage of a sarcoma,
nearly all tumors will require surgical management,
as tumor resection leads to the most favorable out-
comes.75 Limb salvage or limb-sparing techniques are
becoming more widely used for the management of
end-stage tumors as the majority of sarcomas are
found in the soft tissue and bone of the pelvis, buttock,
or extremity.75 These different types of interventions
typically allow for a more rapid rehabilitation, preven-
tion of severe psychological problems, and improving
quality of life.76 However, the prognosis and survival
rate is highly dependent on metastasis and the com-
bined intervention of surgery, chemotherapy, and/or
radiation.75 These types of intervention are typically
a final recommendation in surgical management of
a sarcoma or tumor.
Total Femur Replacement
A total femur replacement is a radical surgical proce-
dure, typically indicated for a high-grade malignant
sarcoma with extracompartmental involvement.76 This
type of procedure is a more advanced intervention
allowing the patient the long-term benefit of increased
mobility postoperatively. The complicated surgical
technique varies, but typically involves a disarticulation
of both the hip and knee joints.76 The femoral artery
and vein are dissected and ligated at their branches to
ensure restoration of these vessels.77 The entire femur
and surrounding musculature are resected after an
Musculoskeletal System CHAPTER 3 115
osteotomy of the greater and lesser trochanter is per-
formed to allow for reattachment of the glutei and
psoas muscles.76 The prosthetic femur component is
then secured distally in the medullary canal of the
tibia and fit proximally into the acetabulum. Thus,
essentially the entire prosthesis consists of a hip joint
arthroplasty, a femur component, and a knee joint ar-
throplasty (Figure 3-21). This complex structure allows
for ROM at the hip and at the knee. The trochanters
are then fixated in specific holes in the prosthetic by
wire, and the wound is closed.76 Complications of this
type of intervention may include poor anastomosis of
the graft, limited joint stability, decreased prosthetic
integrity, and poor wound healing.76
PHYSICAL THERAPY INTERVENTION AFTER
A TOTAL FEMUR REPLACEMENT
A total femur replacement is an extremely compli-
cated and patient-specific procedure. Therefore, you
should always consult the surgeon regarding appro-
priate ROM and strengthening exercises as the integ-
rity of the soft tissue and the prosthesis may vary.
Typically, rehabilitation is a conservative approach
immediately postoperatively as the patient is not
allowed to fully bear weight until the joint stability
and graft anastomosis occurs.76,78 The patient should
remain toe touch or non—weight bearing. Evaluation
and treatment should begin immediately postopera-
tively, as soon as the patient is hemodynamically
stable. Bed mobility, transfer training, gait and bal-
ance training, and overall functional strength and
endurance make up the primary goals of rehabilitation.
Depending on the patient’s tolerance, mobility, gait,
and balance training should begin as soon as possible.
Crutch and/or walker training are essential in the
patient obtaining functional independence. This
should include increasing distance gradually and
eventually incorporating stair training.
Maintaining bilateral upper-extremity strength
and the nonoperative lower extremity strength is
essential, especially the upper extremities as they
will become a great contributor to weight bearing.
The patient should be instructed to maintain
the following precautions for the first 8 weeks
postoperatively.78
 No active or passive abduction or adduction
 No straight-leg raises
 No internal or external rotation of the hip
 No hip extension past neutral
 The patient may log roll with a pillow securely place
between the legs to avoid adduction.
116 CHAPTER 3 Musculoskeletal System
A B
FIGURE 3-21
Total femur replacement. (From Cheng EY: Surgical management of sarcomas. Hematol Oncol Clin
North Am 2005;19(3):451-470.)
Hip Disarticulation and Hemipelvectomy
Malignant soft-tissue or bone tumors are treated in
multiple ways. When conservative measures fail, a hip
disarticulation or hemipelvectomy is an alternative
way of treatment. Although the pathologies are
often of the same nature, there are differences between
the two procedures involving the resection of a
tumor. A hemipelvectomy may be better indicated
when the tumor involves the hip joint or a large portion
of the ilium. In specific cases where the tumor
has not interrupted the neuromuscular system and
obtains only a small portion of the pelvis, an internal
hemipelvectomy (Figure 3-22) is a more favorable
option as the lower extremity is typically spared with
this procedure.79
A hip disarticulation is a complex procedure that
involves the release of key pelvic/hip musculature
originating on the ischium and AIIS, and/or
inserting on the greater trochanter and femur.
The final portion of this procedure involves disloca-
ting the hip joint, dividing the ligamentum teres,
and completing the amputation by removing the
remaining limb.79
A hemipelvectomy is very similar to that of a hip
disarticulation mentioned above. This procedure is
typically more extensive as the resection encompasses
more of the pelvis as it begins at the PSIS and extends
along the iliac crest to the pubic symphysis. In most
cases, the effort to save the gluteus maximus muscle
is great if the tumor has not caused disruption. The
final steps of the amputation consist of an osteotomy
through the sacroiliac joint after the soft-tissue
and neurovascular structures have been divided.79
This allows for the complete removal of the entire
lower extremity.

FIGURE 3-22
Internal hemipelvectomy. Anterior-posterior radiograph of
pelvis demonstrating reconstruction, after modified internal
hemipelvectomy, using hemipelvic allograft-prosthetic
composite and total hip arthroplasty. Compression plate
internal fixation of reconstructed sacroiliac joint and superior
pubic ramus. Cemented total hip arthroplasty with acetabular
metallic cage. (From Cheng EY: Surgical management of
sarcomas. Hematol Oncol Clin North Am. 2005;19(3):451-470.)
Both of these procedures are invasive and complex
alternatives to management of malignant tumors. It is
important to consider the entire patient in these situa-
tions as they typically have multiple medical complica-
tions evolving. Typically these patients are currently
in the process of chemotherapy and/or radiation.
Additionally the emotional and physiological compo-
nent involved with this type of amputation and the sig-
nificant functional disabilities cannot be disregarded.
There are many postoperative complications to con-
sider including infection, poor wound healing, blood
loss, orthostatic hypotension, and phantom pain being
the most influential. In regards to the expected blood
loss and anemia during surgery and postoperatively,
the patient will most likely have a drain placed to
obtain excess blood from the surgical site. These
drains should be left intact and careful consideration
taken when performing mobility. Notify the physician
immediately if removed as they are at increased risk of
infection and/or bleeding if the area is compromised.
PHYSICAL THERAPY INTERVENTION AFTER A HIP
DISARTICULATION OR HEMIPELVECTOMY
Physical therapy after a hip disarticulation or hemipel-
vectomy is focused on increasing functional indepen-
dence. Typically these patents have a more difficult
time initiating mobility when compared to a patient
status post joint arthroplasty as they develop more
Musculoskeletal System CHAPTER 3 117
medical complications and have a limited activity toler-
ance initially. Extensive rehabilitation typically results
in the patient ambulating independently with forearm
or Lofstrand crutches. As the amputation involves
such a large portion, many patients choose not to use
a prosthetic as they are awkward and cumbersome but
instead live an independent life on crutches.
Evaluation and treatment should begin immediately
postoperatively, as soon as the patient is hemodynami-
cally stable. Bed mobility, transfer training, gait and
balance training, and overall functional strength and
endurance make up the primary goals of rehabilitation.
As mobility is encouraged from day one, the patient
should begin to build sitting tolerance, as this is usually
the biggest challenge. Typically patients are unable to
tolerate increased sitting secondary to pain and ortho-
static hypotension. This progression must be gradual
and carefully monitored.
Depending on the patient’s tolerance, gait and
balance training should begin as soon as possible.
Crutch and/or walker training are essential in the
patient obtaining functional independence. This
should include increasing distance gradually and even-
tually incorporating stair training.
The patient should be educated in and perform
ROM and strengthening exercises on the nonoperative
extremities, especially the upper extremities, as they
will become a greater contributor to weight bearing.
CLINICAL TIP
 Sitting tolerance is the greatest challenge to a
patient’s status post hemipelvectomy. Educate the
patient on the importance of mobility, but also
stress the concept of gradual and slow progression.
It is not uncommon for it to take months before a
patient may tolerate prolonged sitting without pain.
 To alleviate pressure and pain during sitting, it is
helpful to transfer the patient into a reclining
wheelchair. When the patient is no longer able to sit
in an upright position, the wheelchair can be
reclined for comfort and pressure disbursement. This
is an easy way to allow the patient to quickly lie
down without having to transfer him or her back
to bed.
 Custom seating cushions are essential for these
patients to avoid any excess skin breakdown on the
incision and also for added comfort. This is most
effective is a seating consult is placed immediately in
the acute care setting.
118 CHAPTER 3 Musculoskeletal System
 Upper-body strengthening is favorable as the patient
will rely heavily on his or her upper extremities for
mobility.
 Educate the patient on proper scooting techniques
so he or she will avoid shearing or irritation to the
incision with bed mobility.
Internal Hemipelvectomy
The internal hemipelvectomy is similar to the hemi-
pelvectomy described above as a large portion of the
pelvis and soft tissue is resected. However, the critical
difference is the sparing of the extremity. This proce-
dure is selectively used in younger patients who dem-
onstrate a favorable prognosis.75 There are many
different approaches to this type of intervention that
may or may not involve internal fixation and/or
THA. It is possible for these patients to permanently
mobilize non—weight bearing with a device. However,
if warranted, the placement of hardware will allow
for increased weight bearing and functional mobility
without a device. The postoperative complications
and medical issues are comparable to those of a hemi-
pelvectomy as listed below.
PHYSICAL THERAPY INTERVENTION AFTER AN
INTERNAL HEMIPELVECTOMY
As this specific procedure is complicated and may or
may not consist of a variety of hardware, it is essential
that you consult the surgeon before beginning any
ROM or strengthening exercises. If physical therapy
is warranted immediately postoperatively, it should
be a conservative approach to maintain the balance
of immobilization and limited weight bearing to pro-
mote healing and the initiation of mobility and joint
motion to prevent contractures.75
Depending on the patient’s tolerance, gait and
balance training should begin as soon as possible.
Crutch and/or walker training are essential in the
patient obtaining functional independence. This
should include increasing distance gradually and even-
tually incorporating stair training.
The patient should also be educated in and
perform ROM and strengthening exercises on the
nonoperative extremities, especially the upper extre-
mities, as they will become a great contributor to
weight bearing.
Keep in mind that patients undergoing such com-
plicated, invasive procedures as those listed above
typically have decreased activity tolerance. A gradual
approach to increasing endurance as the patient toler-
ates is most favorable.
Osteotomy
TIBIAL OSTEOTOMY
A proximal tibial osteotomy is a valuable alternative
to a total knee arthroplasty when surgical manage-
ment of knee osteoarthritis is warranted, as this tech-
nique allows for joint preservation.80 When compared
to a TKA, this procedure is a more conservative way
of achieving pain relief and increased knee function.
This procedure is best indicated for active young
patients with primary degenerative arthritis in a sin-
gle compartment malaligned limb; however, there
are favorable results noted for motivated active older
adults with localized knee arthritis.80,81 Managing
medial unicompartmental arthritis in an older
patient when a varus deformity is a result of osteo-
arthritis is the most common indication for a tibial
osteotomy. This specific surgical procedure involves
an osteotomy (bone resection) of the proximal
tibia with a primary goal of correcting the joint
to 8 to 10 degrees of valgus, when excessive varus
is evident.82,83
PHYSICAL THERAPY INTERVENTION FOR TIBIAL
OSTEOTOMY. The primary focus of physical therapy at
this point should be restoring independent functional
mobility and ambulation. It is important to consult
the surgeon on appropriate therapeutic exercise and
weight bearing restrictions as the interventions sug-
gested below are only indicated for a patient status
post a ‘‘typical’’ tibial osteotomy.
Evaluation and treatment should begin immediately
postoperatively, as soon as the patient is hemodyna-
mically stable. Bed mobility, transfer training, gait
and balance training, and overall functional strength
and endurance make up the primary goals of
rehabilitation.
The patient is generally limited to toe touch weight
bearing for the first 1 to 2 weeks postoperatively.
After the acute stage of healing, the patient may then
begin partial weight bearing with progression to full
weight bearing as instructed by the surgeon.80
The patient should also be instructed in therapeu-
tic exercise to maintain general strength in the surgi-
cal extremity. These should include antiembolics
such as ankle pumps, quad sets, and gluteus sets.
ROM as tolerated is allowed with emphasis on
active knee flexion and extension as opposed to pas-
sive to avoid any undesired forced flexion of the knee.

General strengthening exercises are indicated for all
other nonsurgical extremities to maintain function
and promote increased mobility with weight-bearing
limitations.
Strengthening exercises for the surgical extremity
should progress as tolerated, beginning with a more
conservative open chain protocol including active-
assisted straight-leg raises, hip abduction/adduction,
gentle active heel slides, and short arc quads to initiate
the early stages of quad strengthening.
TROCHANTERIC OSTEOTOMY
A Trochanteric Osteotomy is a procedure most typi-
cally used with surgical fixation of a hip fracture or
a total hip replacement. It is a safe and effective
approach to dislocation of the femoral head as it
allows for better visualization of the femoral head
and the acetabulum to avoid complications.84 In this
procedure, the greater trochanter is excised from the
femur, leaving the vastus lateralis, gluteus medius,
and gluteus minimus attached to the osteotomized
bone. After the fixation is complete, the trochanter
is reattached to the femur with cortical screws.
PHYSICAL THERAPY INTERVENTION FOR A
TROCHANTERIC OSTEOTOMY. The primary focus of
physical therapy at this point should be restoring
independent functional mobility and ambulation.
It is important to consult the surgeon on appropriate
therapeutic exercise and weight-bearing restrictions
as procedure and limitations may vary.
Evaluation and treatment should begin immediately
postoperatively, as soon as the patient is hemodynami-
cally stable. Bed mobility, transfer training, gait and
balance training, and overall functional strength and
endurance make up the primary goals of rehabilitation.
Weight bearing is typically toe touch (TTWB) or
20 to 30 lbs for the first 6 to 8 weeks postoperatively
with progression to weight bearing as tolerated.
Therefore, gait and transfer training is essential for
this patient. Also, the patient should be instructed in
proper gait pattern using TTWB and in the use of an
assistive device (e.g., walker or axillary crutches).
Abductor precautions are essential after this type
of surgery. This precaution allows the joint to be
passively abducted for stretching of the adductors, how-
ever no active or active assistive abduction is allowed.
Patients should be educated in performing exercise
and mobility while maintaining these precautions.
ROM and gentle strengthening of the surgical hip
may be initiated postoperatively to maintain joint
mobility. These exercises should include antiembolics
Musculoskeletal System CHAPTER 3 119
such as ankle pumps, quad sets, and gluteus sets. Heel
slides and short and long arc quads also may be incor-
porated as tolerated or as instructed by the surgeon.
The patient should be educated in and perform
ROM and strengthening exercises on the nonoperative
extremities, especially the upper extremities, as they
will become a greater contributor to weight bearing.
CLINICAL TIP
 The patient can be instructed in using a leg lifter to
support the surgical extremity and assist with
positioning and getting the limb in and out of bed
to avoid active abduction of the hip.
 It is also helpful to instruct a family member in
passive adduction stretching in addition to the home
program to avoid any adductor contractions.
SPINAL PATHOLOGIES
The vertebral column forms the central axial support
of the body and consists of bony segments and fibro-
cartilaginous discs connected by ligamentous struc-
tures and supportive musculature. Degenerative,
traumatic, or congenital changes can cause compensa-
tion in the vertebral bodies, intervertebral discs,
facets, and intervertebral foramen. Any changes in
these structures can result in dysfunction that, in
turn, causes pain. Some common dysfunctions of the
spine and associated structures are ligamentous
sprain, muscle strain, herniated nucleus pulposus,
rupture of the intervertebral disc, spinal stenosis
with nerve root compression, spondylolisthesis, and
degenerative disease of the disc, vertebral body, or
facet joints. Any dysfunction can present itself in the
cervical, thoracic, and lumbar spine.
Back pain is the major indication for spinal surgery.
Pain can be disabling to a patient, limiting the ability
to work or complete ADLs. Any acute injury, such as
muscle spasm, herniated nucleus pulposus, and chronic
low back pain exacerbations, should be managed
conservatively before surgical treatment is recom-
mended. Many injuries will heal with treatments, such
as bed rest, antiinflammatory medication, lifestyle
modification, education in proper body mechanics,
and outpatient physical therapy.85 Surgery may be
indicated when these measures fail to relieve a patient’s
symptoms or if there is a decline in the neurologic
status of the patient.
120 CHAPTER 3 Musculoskeletal System

Table 3-6 COMMON SPINAL SURGERIES AND THEIR INDICATIONS*

Surgery Indication Procedure
Discectomy or Herniated nucleus pulposus (HNP) Removal of the herniation or entire
microdiscectomy intervertebral disc.
Laminectomy Spinal stenosis or nerve root compression Removal of bone at the interlaminar space.
Foraminotomy Spinal stenosis, HNP, or multiple nerve Removal of the spinous process and the entire
root compression laminae to the level of the pedicle. Usually
done in conjunction with a fusion to
maintain spinal stability.
Corpectomy Multilevel stenosis, spondylolisthesis with Removal of the vertebral body.The disc above
nerve root compression and below the segment is removed, and a
strut graft with instrumentation is used to
fuse the anterior column.
Spinal fusion Segmental instability, fractures, facet joint Fusion of the facet joints using hardware and
arthritis bone graft. May use fusion cages or pedicle
screws and rods to achieve fixation.
Approaches can vary, and a fusion can be
done in conjunction with other spinal
procedures to decompress nerve roots.
*These procedures may be performed in any area of the spine when indicated.The approach may be anterior, posterior, or
posterolateral.Data from GW Wood. Lower Back Pain and Disorders of Intervertebral Disc. In ST Canale (ed), Campbell’s Operative
Orthopaedics,Vol. 1 (9th ed). St. Louis: Mosby, 1998; ReganJJ. Endoscopic Spinal Surgery Anterior Approaches. InJW Frymoyer (ed),The
Adult Spine Principles and Practice (2nd ed). NewYork: Lippincott-Raven, 1997.

may be treated surgically with a spinal fusion.

Surgeries of the Spine
Advances have been made in all areas of spinal surgery;
however, there is still no cure for low back pain. Low
back pain and leg pain can arise from degenerative
disc disease and herniation or rupture of the interverte-
bral disc. Surgical procedures can be performed to
relieve the symptoms associated with degenerative
disc disease when conservative measures have failed.
Open disc surgery and microdiscectomy remove disc
fragments and herniated disc material that compress
the adjacent nerve root. Microdiscectomy is a mini-
mally invasive procedure that uses a microscope to
view the surgical area, allowing for decreased surgical
exposure.85 Most microdiscectomy surgery can be
done on an outpatient basis, and early return to activity
can be accomplished. Symptom relief is high both ini-
tially postoperatively and on a long-term basis.86
If additional exposure of the nerve root is needed,
associated procedures, such as a laminectomy or fora-
minotomy, may be performed in conjunction with
discectomy or spinal fusion. Refer to Table 3-6 for
descriptions and indications for these procedures.
Pain that arises from spinal instability caused by
degenerative disc disease or degenerative joint disease
Anterior or posterolateral spinal fusion with decom-
pression attempts to fuse unstable spinal segments.
This is achieved through implantation of various
types of instrumentation with bone grafting to create
a single motion segment and eliminate the source of
pain, the disc.87 The spinal segments are fixed using
different types of rods, plates, and pedicle screws.
The use of interbody fusion cages with instrumenta-
tion has become common practice for spinal fusion.
An anterior lumbar interbody fusion, posterior
lumbar interbody fusion (Figure 3-23), or combination
can be performed.85 Titanium alloy fusion cages are
placed within the vertebral spaces, replacing the degen-
erated disc. These cages are then packed with bone
graft harvested from the iliac crest (autograft) or from
a bone bank (allograft). This bone graft can be supple-
mented with osteoinductive growth factors to facilitate
fusion.88 A combination of an anterior and posterior
fusion can be successful when a single approach fails.
Experimental designs of the total disc replacement
have been developed to reconstruct the disc, maintain
disc height, and preserve segmental motion of the
spine.89 Developers of the artificial disc replacement
believe that restoring mobility will decrease
 Musculoskeletal System CHAPTER 3 121
patients status post decompression combined with a
fusion or any type of instrumentation should follow
specific precautions that include minimizing bending
and twisting with activity, lifting restrictions per the
surgeon, and use of braces or corsets if prescribed.
 Patients should be taught to logroll to get out of bed.
The body rolls as a unit, minimizing trunk rotation.
Functional mobility training should begin the first
postoperative day. Ambulation should be stressed
as the only formal exercise postoperatively for
spinal surgery to promote healing of all tissues.
 Symptoms, such as radiating pain and sensory
changes present before surgery, may persist for a
significant period postoperatively secondary to
edema surrounding the surgical site. Patients
should be educated to this fact and should be told
to notify the nurse, surgeon, or both immediately
if any significant increase in pain or change in
bladder and bowel function occurs.
FIGURE 3-23
Lateral view of a posterior interbody fusion with pedicle CLINICAL TIP
screws.  For surgical procedures with an anterior approach,
the patient should be given a splinting pillow and be
degeneration of spinal segments above and below educated in its use to promote deep breathing and
the affected segment.90 Artificial disc implantation coughing. A corset can be used to aid patient
has been occurring in Europe, and clinical trials are comfort with activity.
beginning in the United States. Many generations of  Rolling walkers are useful to promote a step-through
the total disc design have shown promise, and if gait pattern and decrease stress on the spine caused
clinical trials are favorable, the total disc replacement by lifting a standard walker. Patients should
may become a tool to combat back pain.90 progress to a cane or no assistive device to promote
Complications that can occur postoperatively from upright posture.
spinal surgery are neurologic injury, infection, cauda  If an iliac crest bone graft is harvested through a
equina syndrome, dural tear with cerebrospinal fluid second incision, a patient may complain of increased
leak, and nonunion, as well as general surgical compli- pain at the surgical site. Ice can decrease swelling at
cations noted in previous sections. the donor site. With this type of graft, a patient will
likely need an assistive device to increase safety with
PHYSICAL THERAPY INTERVENTION AFTER ambulation and decrease pain.
SPINAL SURGERY  If interbody fusion cages are used, the patient
In the acute care setting, physical therapy should should be encouraged to sit in a chair as soon as
emphasize early functional mobilization, education on possible to increase compression on the cage and
proper body mechanics, gait training, and assessment promote bone ingrowth. Sitting time can be
of assistive devices to increase patient safety. Patients unlimited according to patient comfort.85
should be educated on movement precautions if appli-  Patients who have undergone spinal fusion should
cable to their surgical procedure. Typically patients be educated about the adverse effect that cigarette
who are status post decompression procedure without smoking has on the success of fusion.91 The health-
fusion, including microdiscectomy or laminectomy, care team should emphasize smoking cessation, or
only need to follow a 10 lb lifting precaution recom- the patient should be given the appropriate
mended by the surgeon.The patient should be encour- resources to assist with this task.
aged to mobilize as tolerated and avoid any excessively  The physical therapist should always check
painful motions. Unlike a decompression alone, orders for braces used by the surgeon and any
122 CHAPTER 3 Musculoskeletal System
other restrictions on activity. Braces are
usually worn when the patient is out of bed.
If necessary, a surgeon may limit raising the
head of the bed. The reverse Trendelenburg
position (putting the whole bed at a
45-degree angle, with head up) can assist
with patient ADLs.
 Treatment should be coordinated with the
administration of pain medication. Patients
should be educated in relaxation techniques or
breathing exercises to help manage their pain.
The physical therapist should also be aware of
any psychosocial factors that can interfere with
patient recovery. If necessary, consult the psychiatric
or chaplain services to assist with a patient’s
coping skills.
MINIMALLY INVASIVE SPINE SURGERIES
Minimally invasive procedures have evolved as one of
the most favorable approaches to surgical intervention.
This technique is widely used to correct many joint
deformities and/or pathologies; however it is rapidly
expanding to spine intervention. As the dorsal muscles
of the low back are large and deep, spinal incisions
can often cause more discomfort than the ultimately
compromised vertebral column. Given the significant
muscle soreness postoperatively, it is most advanta-
geous to the patient to use a smaller incisionçhence,
the new percutaneous approach to thoracic and
lumbar discectomy and/or instrumentation. Previously
a similar approach was only used for microdiscec-
tomies. Now as experimental interventions are becom-
ing more successful resulting in less postoperative
pain and increased functional mobility, the proce-
dure is also favorable in performing percutaneous
instrumentation.92
These types of procedures are performed by using
a combination of cannulated screws or portal systems
to access the spinal canal and intraoperative imaging
to allow accurate placement of instruments and visu-
alization of landmarks and/or pathology.92 This pro-
cedure is far from perfected as it typically only
allows intervention to a single level. Multilevel inter-
vention is more challenging with this approach, as
it is often performed with a larger incision.92 As
this type of intervention to the spinal canal is very
similar to the traditional approach, the same precau-
tions and physical therapy intervention described
previously would apply.
KYPHOPLASTY AND VERTEBROPLASTY
Vertebral augmentation is becoming a more widely
used treatment for progressive osteoporotic verte-
bral compression fractures.93 These minimally invasive
procedures are most commonly referred to as vertebro-
plasty or kyphoplasty and are noticeably effective
in restoring function and relieving acute pain ass-
ociated with compression fractures.94-101 There are
two different types of compression fractures, the first
being of a traumatic nature in that a sudden onset of
pain and muscle spasm is experienced.102,103 The
second type of fracture leads to more of a deformity
and a decrease in vertebral height that occurs over
time at multiple levels. These fractures are typically
referred to as an anterior wedge compression fracture
and occurs with minimal symptoms.102,104 Only in
recent times have these types of fracture been treated
with surgical intervention, the previous common treat-
ment of choice was conservative medical management
unless a neurologic complication was evident.105-108
However, over time the initial onset of pain progresses
into more chronic symptoms causing a disturbance in
spinal stability and affecting ADLs warranting a more
effective treatment approach early on.109,110
These two percutaneous procedures vary in tech-
nique depending on the nature of the fracture. A ver-
tebroplasty is a procedure that consists of injecting
a polymethylmethacrylate (PMMA) cement into the
vertebral space to provide stabilization of the com-
pression fracture with the risk of an open surgery
(Figure 3-24, A).111 The cement is injected percuta-
neously in a fluid state with a goal that it will permeate
into the cancellous bone. There are several benefits
to this procedure, including stabilization of the
facture and immediate pain relief; however, the lack of
height restoration and deformity restoration may lead
to more chronic pathologies.93 A kyphoplasty is differ-
entiated as it facilitates vertebral end plate elevation
and creates a space by percutaneously inserting an
inflatable balloon to allow accurate placement of the
PMMA cement (Figure 3-24, B).112 There are several
advantages to this procedure when compared to a ver-
tebroplasty, including decreased risk of cement leakage
as the cement is placed in a more designated area and
restoration of vertebral height and deformities of the
spine.112 Both of these procedures are extremely suc-
cessful in the treatment of vertebral compression frac-
tures; however some contraindications may include
fractures consistent with neurologic injury or protru-
sion into the spinal canal, or fractures that are in
 Musculoskeletal System CHAPTER 3 123

A B
FIGURE 3-24
A,Vertebroplasty. At two levels, insertion via needle of radio-opaque cement (arrows) has been used to
arrest compression fractures. B, Kyphoplasty. Balloon kyphoplasty. (A From Mettler: Essentials of
Radiology, 2nd ed. Philadephia, 2005, Saunders; B Redrawn from Griffin S: What the experts say:
treatment options for VCF, including balloon kyphoplasty, http://kyphon.com, Kyphon, Inc, Daly City,
Calif. In Canale: Campbell’s Operative Orthopaedics, ed 11. St Louis, 2008 Mosby.)

chronic healing stages.112 In these instances, more
invasive surgical interventions may be warranted as
mentioned above.
PHYSICAL THERAPY AFTER A VERTEBROPLASTY OR
KYPHOPLASTY. Please note that these guidelines
are only applicable to the typical vertebroplasty or
kyphoplasty, as every surgery varies. Consultation with
the surgeon for additional precautions should occur
when needed. The primary goal of physical therapy
immediately postoperatively is to increase functional
mobility and ambulation. General upper and lower
extremity AROM and light strengthening activities
may be initiated to prevent muscle atrophy. However,
like most spinal protocols, ambulation is the primary
source of exercise. Given that these procedures are
performed with fast-acting cement that rapidly
hardens to stabilize the fracture, most patients have
only one spinal precaution postoperatively, which
involves lifting nothing over 10 lbs.93
Generally these patients should not begin any
aggressive resistive strength training in the acute
healing stages. General strengthening is best achieved
through performing functional mobility. For example,
stair training is a functional and effective approach to
lower extremity and quadriceps strengthening.
The patient should be encouraged and instructed to
use a log roll when getting in and out of bed to avoid
any additional pain or stress on the spinal regions.
Instructing the patient in good body mechanics
is essential in the acute and chronic rehabilitation
stages to help prevent any further injury.
SOFT-TISSUE SURGERIES
There is a wide variety of soft-tissue surgeries encoun-
tered in the acute care orthopedic setting. The major-
ity of these surgeries are aimed at improving joint
stability by repairing the functional length of muscles,
tendons, and ligaments. Common soft-tissue surgeries
include tendon transfers, muscle repairs, fasciotomies,
cartilage resections or repairs, and ligament reconstruc-
tions. Many of these surgeries have progressed to be
ambulatory surgery, but discharge may be delayed
124 CHAPTER 3 Musculoskeletal System
BOX 3-3 COMPLICATIONS OF
ARTHROSCOPY
 Intraoperative
 Damage to intraarticular structures leading to
chondromalacic changes and degenerative
arthritis
 Damage to extraarticular structures, such as
blood vessels, nerves, ligaments, and tendons
 Surgical instrument failure
 Fracture postoperative
 Hemarthrosis
 Thrombophlebitis
 Infection
 Reflex sympathetic dystrophy
Data from Phillips BB. General Principles of Arthroscopy.
In ST Canale (ed), Campbell’s Operative Orthopaedics,Vol. 2
(9th ed). Boston: Mosby, 1998.
until the day after surgery secondary to inadequate pain
control or adverse reactions to anesthesia.
Arthroscopic surgery has become common practice
in the repair of joint structures in the acute care setting.
Arthroscopy is indicated for a variety of joint problems
not only as a diagnostic tool, but also, with advances
in instrumentation, to repair joint structures injured
by trauma or degeneration. The benefits of arthro-
scopic surgery are a reduced postoperative morbidity;
decreased size of incision; decreased local inflamma-
tion; improved diagnosis; absence of secondary effects,
such as neuroma, scarring, and functional imbalance;
decreased hospital costs; and reduced complication
rates.113However, complications after arthroscopy can
still occur (Box 3-3).
Knee Arthroscopy
In the acute care setting, a patient may be admitted after
an arthroscopic procedure, such as an anterior cruciate
ligament (ACL) repair. An ACL repair performed
arthroscopically involves the replacement of the ACL
with an autograft or allograft from the extensor
mechanism, hamstring tendons, or Achilles tendon.
Fixation of grafts involves the use of interference
screws and washers, nonabsorbable sutures secured
with staples, or bone plugs attached with screws or
wires into tibial and femoral tunnels (Figure 3-25).
Associated meniscal and ligamentous repairs, such as
meniscal repairs or meniscectomy, may be performed
with an ACL reconstruction or independently. Refer
to Table 3-7 for a description of these procedures and
physical therapy interventions.
Shoulder Arthroscopy
Shoulder surgeries for soft-tissue dysfunctions are
common in the acute care setting and include subacro-
mial decompression, acromioplasty, anterior capsular
shift, and rotator cuff repair.These surgeries can be per-
formed arthroscopically depending on the extent of
damage. Rotator cuff repairs may require increased
exposure so an open repair or mini—open repair may
be performed with associated procedures, such as sub-
acromial decompression.114 Refer to Table 3-8 for a
description of these procedures and associated physical
therapy interventions. Functional training may be nec-
essary for the older patient or for the patient with an
existing functional limitation prior to admission.
CARTILAGE TRANSPLANTATION
The advent of autologous cartilage transplantation is
a recent advance in technology aimed at the repair of
chondral defects in the knee. The clinical outcomes
will, it is hoped, slow the progression of arthritic
changes that may lead to more extensive surgery. Short-
term results have shown promising results for repairing
osteochondritis dissecans lesions on the femoral con-
dyles.115 Articular cartilage is harvested by arthroscopy
from a non—weight-bearing surface in the affected
knee, and growth of these cartilage cells then takes
place in a laboratory. After the cells are cultured, another
surgical procedure is performed in which the cartilage
cells are injected onto a patch of periosteum covering
the articular defect in the involved joint, as demonst-
rated in Figure 3-26.116 Weight bearing is limited to
approximately 40 pounds of the involved extremity,
and ROM with a CPM is encouraged to promote nutri-
tion in the articular cartilage.115 Exercise and weight
bearing are dependent on the location of the defect,
and all precautions should be verified with the surgeon.
EQUIPMENT FOR FRACTURE AND
SOFT-TISSUE INJURY MANAGEMENT
Casts
A cast is a circumferential rigid dressing used to provide
the immobilization of joints proximal and distal to frac-
ture fragments necessary for bone healing. Casts can
 Musculoskeletal System CHAPTER 3 125

A B
FIGURE 3-25
Fixation of graphs with bone fragments. A. Patellar bone piece fixed in femoral tunnel by Kirschner
wire; tibial bone piece fixed in tibial tunnel by small fragment AO screw. B. Heavy, nonabsorbable
sutures are placed through two holes in bone and tied around screw. (With permission from RH Miller,
3rd. Knee Injuries. In ST Canale [ed], Campbell’s Operative Orthopaedics,Vol. 2 [9th ed]. Boston: Mosby,
1998.)

be made of plaster, fiberglass, or synthetic material and
can be used on almost any body part. The rigidity of
the cast allows for fracture stabilization, prevention of
deformity, pain management, and protection.10
Specific joint positioning is determined by the physi-
cian. Table 3-9 lists the common types of casts. Some
casts may be split into two pieces (bivalved cast) to
allow periodic visualization of the involved area or to
relieve pressure. A small piece of cast may be cut out
(i.e., window) to allow access for pulse monitoring,
wound or drain care, or to relieve intraabdominal pres-
sure in a body cast.117 Casts can also be used to provide
low-load, prolonged, passive stretch to soft tissue to
improve ROM. This is known as serial casting. A cast
brace is the combination of casting material with
orthotic components (e.g., hinge joints). It is commonly
used in the treatment of nondisplaced fractures of the
elbow or knee or as an adjunct to internal fixation.118
Complications associated with casts include the
following:
 Compartment syndrome is neurovascular com-
promise caused by microvascular and venous
congestion within a muscle compartment that can
lead to tissue hypoxia.119 This may be caused by exces-
sive swelling or the improper fit of a cast. The pres-
sure increases within a facial compartment(s) of an
extremity and, left untreated, can progress to tissue
necrosis. The most reliable signs and symptoms of
compartment syndrome are pain (out of proportion
to the injury, unrelieved by pain medicine, and
increased by passive ROM or touch) and paresthe-
sia.119 Other signs and symptoms include pallor,
weakness, decreased peripheral pulses, and dense
tissues.
 Nerve compression is compression of a peripheral
nerve over a bony prominence (e.g., peroneal nerve
on the fibular head) by the cast. This form of nerve
entrapment can result in transient or permanent
nerve damage depending on the duration of
compression.
 Skin breakdown can occur secondary to increased
pressure, moisture development in the cast (causing
blister formation), open skin lesions, or any combina-
tion of these.
126 CHAPTER 3 Musculoskeletal System

Table 3-7 SOFT-TISSUE REPAIR AND RECONSTRUCTION SURGERIES OF THE KNEE AND PHYSICAL
THERAPY INTERVENTION

Type of Repair and

Reconstruction Procedure
Meniscectomy Removal of all or part of the medial or
lateral meniscus secondary to an
irreparable tear
Meniscal repair Repair of a torn meniscus in the
vascular portion of the meniscus,
where the likelihood of healing is
greatest
Lateral retinacular Release of the synovium, capsular and
release retinacular structures lateral to the
patella, and proximal muscle fibers
of the vastus lateralis
Anterior cruciate Reconstruction of the insufficient
ligament (ACL) ligament using autograft or allograft
reconstruction of the patellar tendon or hamstring
tendon
Posterior cruciate Reconstruction of the insufficient
ligament (PCL) ligament with autograft or allograft
reconstruction using the central third of the patellar
tendon or Achilles tendon
Quadricepsplasty Separation of the quadriceps
mechanism, lengthening of the
quadriceps mechanism, or both
CPM, Continuous passive motion; ROM, range of motion.
Data from BB Phillips. Arthroscopy of Lower Extremity. In ST Canale (ed), Campbell’s Operative Orthopaedics,Vol. 2 (9th ed). St. Louis:
Mosby, 1998.
Physical Therapy Intervention
Edema management.
Proximal and distal ROM exercises.
Quadriceps and hamstring strengthening, as
permitted by surgeon protocol.
Functional training per weight-bearing
precautions.
As above.
Restrictions on ROM and weight bearing may be
imposed by the surgeon.
Hinged brace, if prescribed.
Gentle ROM exercises per surgeon protocol.
Edema management.
Isometric exercises and quadriceps strengthening
consisting of straight-leg raises (SLRs). Short-
arc quadriceps strengthening should be
avoided. Functional training per weight-
bearing precautions.
Edema management.
Use of a brace per surgeon protocol (education to
don/doff brace).
Active and passive knee ROM exercises. (A CPM
may be prescribed for home use.) Isometric
exercises (quadriceps and hamstring) and
quadriceps strengthening consisting of SLR
per surgeon protocol. Functional training per
weight-bearing precautions.
See anterior cruciate ligament, above.
Limitation of ROM to less-than-full flexion
using a hinged brace. Gentle ROM exercise
and CPM to maximum of 90 degrees.
Passive knee extension. Active and active-assisted
exercises for quadriceps and hamstrings.
Functional training per weight-bearing
precautions.
 Musculoskeletal System CHAPTER 3 127

Table 3-8 SOFT-TISSUE REPAIR AND RECONSTRUCTION SURGERIES OF THE SHOULDER AND PHYSICAL
THERAPY INTERVENTION

Type of Repair and

Reconstruction Procedure Physical Therapy Intervention
Subacromial decompression or Resection of the undersurface of Use of a sling as indicated.
acromioplasty the acromion Edema management.
Hand, wrist, and elbow ROM.
Pendulum exercises.
Active and active-assisted shoulder ROM
exercises.
Rotator cuff repair Can include repair of the biceps See Subacromial decompression or
(arthroscopic, open, or mini- tendon, supraspinatus tendon, acromioplasty, above.
open procedure) or avulsed rotator cuff Self-assisted ROM exercises per surgeon protocol
(can be limited by the extent of repair).
Anterior reconstruction Indicated for recurrent anterior Immobilization using a sling, as indicated.
(Bankart repair) instability Hand, wrist, and elbow ROM
Includes an anterior capsular Edema management.
shift, labral repair, or both Passive ROM within parameters, if indicated by
the surgeon.
ROM, Range of motion.
Data from BB Phillips. Arthroscopy of Upper Extremity. In ST Canale (ed), Campbell’s Operative Orthopaedics,Vol. 2 (9th ed). St. Louis:
Mosby, 1998.

CLINICAL TIP can be lost in the cast or displace the stockinet

beneath the cast and cause a wound or increase the
 Notify the nurse, physician, or both immediately for
risk of pressure sore formation. Because the cast
any signs and symptoms of compartment syndrome,
provides a moist and warm environment, bacterial
nerve compression, suspected skin breakdown, or
growth can develop at an accelerated rate and
new drainage from within the cast.
progress into a gangrenous lesion. To relieve itching
 The therapist should elevate all distal extremities 4
below the cast, gently tap the cast or blow cool air
to 5 in. above the heart to allow gravity to assist
into it.118
venous return. Elevation of more than 5 in. can
 Most casts are not rigid enough to withstand the
increase venous pressure, causing increased
forces of weight bearing. Weight-bearing parameters
cardiovascular workload, and may be contraindicated
must be clarified by the physician.
for patients with congestive heart failure.
 A nonslip cast boot should be provided for patients
 Casts, especially plaster casts, should not get wet.
who have casts encompassing the foot and are
The therapist should instruct the patient to wrap the
allowed to weight bear with transfers and
cast in a waterproof bag during bathing or
ambulation.
showering. Exposing casting materials to water
 It is important to reinforce that the patient move all
weakens the structure and traps moisture against the
joints proximal and distal to the cast to maintain
skin.
functional ROM.
 The therapist should instruct the patient to contact
the physician if the following develop: symptoms of
burning or warmth, numbness, or tingling;
movement of the limb within the cast; increased Braces and Splints
edema; a discolored and cool hand or foot; or a
Braces and splints are used in conjunction with medical
strong odor from within the cast.
and surgical intervention techniques for management
 The therapist should discourage patients from sliding
of musculoskeletal dysfunctions. Functional bracing is
objects in the cast to scratch itchy skin. Such objects
based on the concept that continued function during
128 CHAPTER 3 Musculoskeletal System
FIGURE 3-26
Autologous chondrocyte implantation procedure. (With
permission from the Orthopaedic and Sports Sections of
the American Physical TherapyAssociation. SD Gillogly,
M Voight,T Blackburn, Treatment of the Articular
Cartilage Defects of the Knee with Autologous
Chondrocyte Implantation. J Orthop Sports PhysTher
1998;28:245.)
healing promotes osteogenesis (bone growth) and
enhances soft-tissue healing while preventing joint
hypomobility and disuse atrophy. Bracing and splint-
ing can be used to maintain fracture alignment dur-
ing healing, joint stabilization, and anatomic joint
alignment, and to minimize weight-bearing forces.
Braces can be applied immediately at the time of
injury or used as part of a progressive treatment
course after conventional casting or traction. They
may be prefabricated or custom made. Table 3-10 lists
some of the most commonly used braces and splints,
including spinal orthoses. Complications with braces
and splints include improper fit, skin breakdown, and
improper use or poor compliance.
CLINICAL TIP
 Patient education is vital for any patient
receiving a brace, splint, or orthosis. The patient
or caregiver should have a good working
knowledge of the function and purpose of the
device, as well as the ability to don and doff
the device.
 Often, a manufacturer’s brand name is used to
identify its most popular brace or splint. Therefore,
it is important to clarify and understand the specific
function of the brace or splint, not just the style or
popular name.
External Fixators
An external fixator is a device consisting of alumi-
num or titanium percutaneous pins inserted at obli-
que or right angles to the long axis of a bone that
connect externally to a frame. The frame provides
the alignment forces to fracture fragments and main-
tains reduction while healing occurs.117 In pin fixa-
tion, the frame is rod shaped. In ring fixation, the
frame is circular and is placed around the extremity.
External fixation devices are often the treatment of
choice for severely comminuted or open fractures;
fractures with severe soft tissue, vascular, or burn
injures; or when infection is present.120 An addi-
tional use of external fixation is to compress or
lengthen a long bone.9 An advantage of external fix-
ation is the ability to manage associated injuries,
such as skin grafts and areas of debridement. It also
allows for early functional mobilization. External
fixators can be placed on the upper extremity, lower
extremity, and pelvis. Complications of external fixa-
tion devices include the following9:
 Pin site infection
 Nerve, blood vessel, muscle, or tendon impingement
or impalement damage secondary to pin placement
 Loss of fracture reduction or refracture
 Nonunion or malunion
 Compartment syndrome
 Musculoskeletal System CHAPTER 3 129

Table 3-9 COMMON TYPES OF CASTS

Type of Cast Description
Short leg cast (SLC) Extends from metatarsal heads to tibial tubercle.
For distal tibia/fibula, ankle, and foot fractures.
Immobilizes foot and ankle, usually 90 degrees neutral or slight dorsiflexion.
Plantar flexion immobilization for Achilles tendon rupture.
Patellar tendon-bearing Extends from metatarsal heads to mid- or suprapatella.
cast Used for weight-bearing activity.
A patellar tendon bar dissipates some limb loading force to the external cast shell.
Knee position is 90 degrees flexion, neutral ankle, or slight dorsiflexion.
Long leg cast (LLC), Extends from metatarsal heads to the proximal/mid femur (to stabilize the tibia) or to
cylinder cast the greater trochanter (to stabilize the distal femur).
For proximal tibia and distal femur fractures.
Knee immobilized in full extension or 5 degrees flexion.
A cylinder cast is essentially an LLC that does not enclose the foot.
Hip spica Extends from lower trunk/pelvis to the involved distal thigh (single hip spica) or to the
involved entire lower extremity and thigh of the uninvolved side (11=2 hip spica).
For proximal femur and hip joint fractures or hip dislocation.
Hip is immobilized approximately 30 degrees of hip flexion and abduction with 30
degrees knee flexion.
Used rarely in adults.
Short arm cast (SAC) Extends from MCP joint to proximal forearm.
For radius and ulna fractures.
Wrist immobilized in best position for fracture reduction or slight extension.
Allows elbow flexion/extension and thumb/finger movement.
Long arm cast (LAC) Extends from MCP joint to proximal upper arm, or to the axilla/shoulder to limit
abduction and external rotation.
For distal humerus, elbow, and forearm fractures.
Elbow flexion typically immobilized at 90 degrees.
Thumb spica Extends from tip of thumb to any point on the forearm.
For distal radius, wrist, or thumb fractures.
Wrist immobilized in neutral to slight extension with thumb under second and third
fingers.
Shoulder spica Essentially a two-piece cast composed of a long arm cast and modified body cast
connected by stabilizing bars.
The cast does not cover either shoulder.
For complex humerus fractures or shoulder dislocation.
Shoulder immobilized in best position for reduction, usually 30 degrees flexion,
abduction, and external rotation.
Body cast Extends from above the nipple line to the pubis, enclosing the chest and abdomen.
For stable spine injuries, such as burst fractures.
Immobilizes the thoracic and lumbar spine.
MCP, Metacarpophalangeal.
Data from Stills ML, Christensen K. Management of Extremity Fractures: Principles of Casting and Orthotics. In MM Lusardi, CC Nielsen,
Orthotics and Prosthetics in Rehabilitation. Boston: Butterworth-Heinemann, 2000.
130 CHAPTER 3 Musculoskeletal System

Table 3-10 BRACES, SPLINTS, AND ORTHOSES COMMONLY USED IN THE ACUTE CARE SETTING
Type of Orthosis Description
Spine/trunk soft cervical collar Foam cylinder with a cloth cover that secures posteriorly (more extended spine) or
anteriorly (more flexed spine).
For injuries that do not require rigid cervical fixation (e.g., whiplash injury).
Serves primarily as a kinesthetic reminder to limit neck movement.
Reinforced cervical collar Bivalved total-contact padding reinforced within a semirigid plastic frame that
(Philadelphia, secures withVelcro.
MiamiJ, Aspen) Enclosing the neck, the chin is supported anteriorly, the occiput posteriorly, and it
rests on the superior trunk.
An anterior opening can accommodate a tracheostomy tube.
For situations that require moderate limitations of neck movement (e.g., s/p fusion).
Sterno-occipito-mandibular T-shaped yoke worn over the shoulders and anterior chest connects to an occipital
immobilizer (SOMI) support via a U-shaped metal rod.
The distal yoke is anchored by a strap around the midtrunk, and a mandibular
support attaches to the yoke by a single metal post and to the occipital support
by straps.
For instability at or above C4.
Strictly controls flexion.
Metal supports can be adjusted to position the neck in neutral or slight flexion/
extension.
Halo vest Percutaneous pins to the skull connect at the level of the forehead to a
circumferential frame, which is attached via vertical rods to a vest lined with
sheepskin.
Used for strict immobilization of the cervical or high thoracic spine (e.g., s/p unstable
fracture).
Abdominal binder Wide elastic fabric secured by Velcro.
Placed around the abdomen, pelvis, or both.
Provides external abdominal support (e.g., used after abdominal surgery to support a
large incision) and a kinesthetic reminder to minimize lower thoracic or lumbar
movement.
Jewitt brace Anterolateral aluminum frame with pads at the sternum, lateral midline of the trunk,
pubis, and lumbar spine.
Used to limit flexion and encourage hyperextension (e.g., lower thoracic or lumbar
compression fracture).
Molded thoracolumbosacral Custom-fabricated, total-contact thermoplastic shell (single unit or bivalved) secured
orthosis (TLSO) withVelcro.
Used to limit trunk flexion/extension, side bending, and rotation (e.g., fracture or
deformity of the thoracic or upper lumbar spine).
Lower extremity post-op shoe Sandal-type shoe with open areas at the toe and dorsum of the foot.
Velcro connects the medial and lateral sides.
Used for an edematous foot, to accommodate a bulky dressing on the foot, or for
painful toe/foot conditions (e.g., s/p open-toe amputation, patient with congestive
heart failure).
Ankle stirrup (Air-cast) Stirrup shaped, molded, and plastic-lined with an air-filled compartment.
Medial and lateral sides connect withVelcro.Worn in a shoe.
Permits plantar- and dorsiflexion but limits inversion/eversion.
For moderate-severe ankle sprains.
 Musculoskeletal System CHAPTER 3 131

Table 3-10 BRACES, SPLINTS, AND ORTHOSES COMMONLY USED IN THE ACUTE CARE SETTING—cont’d
Type of Orthosis Description
Short leg walking boot Prefabricated, bivalved, hard, plastic outer shell with foam-filled air cells that
encloses the foot and lower leg below the knee.
The plantar aspect has a nonslip rubber grip.
Used for conditions that allow weight bearing but require intermittent immobilization
(stable ankle fracture) or cushioning (e.g., bruised calcaneus).
Solid ankle-foot orthosis Thermoplastic posterior shell extends from just below the knee to the plantar
(AFO) aspect of the foot.
Secured proximally by Velcro and worn inside a shoe. For mediolateral ankle stability,
footdrop prevention, control of knee hyperextension or flexion (e.g., hypertonicity,
peroneal nerve palsy).
Knee immobilizer Cylinder-shaped foam secured withVelcro with either posterior or medial/lateral
aluminum stays.
Extends from the upper thigh to the calf.
Promotes knee extension.
For knee injuries not requiring rigid immobilization (e.g., ligamentous injury).
Drop-lock brace (Bledsoe) Lateral and medial metal struts at the thigh and lower leg connect to a hinge
mechanism at the knee.
The hinge has a dial to select the desired degree of flexion or extension at the
knee.
The metal struts, which secure withVelcro, adhere to foam at the thigh and calf.
For knee injuries requiring intermittent rigid immobilization (e.g., s/p anterior
cruciate ligament repair or patellar fracture).
Hip abduction orthosis A padded pelvic band with a lateral extension toward the greater trochanter connects
to a thigh cuff by a metal upright, including an adjustable hip joint.
The thigh cuff extends medially across the knee joint. May be used with a spine
orthosis or AFO.
For injuries or conditions that require limitation of hip flexion/extension (e.g., s/p total
hip revision, hip dislocation, or spine and pelvis trauma).
Upper extremity Simple arm Fabric sling with a strap around the neck positions the elbow in approximately
sling 90-degree flexion across the chest with the shoulder internally rotated.
Used for comfort and gentle support of the shoulder and upper extremity
(e.g., s/p stable clavicle or humeral fracture).
Rowe sling As above, a simple arm sling with a second strap around the trunk to limit shoulder
abduction and external rotation.
For conditions requiring stricter intermittent immobilization (e.g., s/p open rotator
cuff repair).
Resting hand splint Thermoplastic splint placed on the dorsal aspect of the hand, wrist, and forearm.
Positions the distal upper extremity at mid pronation/supination, 20- to 30-degree
wrist extension, proximal interphalangeal flexion, distal interphalangeal extension,
and partial thumb opposition.
Used to support, protect, or maintain a functional position of the wrist and hand
(e.g., neuromuscular disorders).
s/p, Status post.
Data from Lusardi MM, Nielsen CC (eds). Orthotics and Prosthetics in Rehabilitation. Boston: Butterworth-Heinemann, 2000.
132 CHAPTER 3 Musculoskeletal System

Table 3-11 COMMON TYPES OF TRACTION

Type Description
Buck Prefabricated boot on lower leg exerts a straight pull to distract lower extremity.
The hip may be positioned in neutral or slight abduction.
Typically used for femoral head or shaft fractures, hip dislocations, hip arthritis, post Girdlestone
procedure, sciatica, or to decrease hip muscle spasm.
Russell Essentially Buck traction with a sling below the knee.
Used for femoral head or tibial plateau fractures, or various knee injuries.
Pelvic A belt is applied to the lumbar spine and pelvis, and the HOB is elevated 20-30 degrees with the
foot of the bed elevated 45 degrees, or a sling suspends the buttocks just off the bed.
Used for back pain or pubic symphysis fracture, respectively.
Overhead 90-90 An L-shaped frame over the entire arm and a sling at the forearm suspend the upper extremity at
90 degrees each of shoulder and elbow flexion with the arm across the chest (0-degree
abduction).
Used for fracture and dislocation of the shoulder and upper arm.
Side arm Traction setup and indications similar to Overhead 90-90, except arm position is 90 degrees of
abduction, 90 degrees of elbow flexion, with palm facing foot of bed.
Cervical Cervical halter with a chin strap exerts a straight pull on the cervical spine.
The HOB may be flat or slightly elevated.
Used for cervical spine fracture, ruptured disc, or severe ligamentous strain and sprain.
HOB, Head of bed.
Data from ZimmerTraction Handbook. Zimmer, Inc., 1996;WC Dubuisson. Nursing Management of Adults with Musculoskeletal Trauma.
In PG Beare, JL Meyers. Adult Health Nursing (3rd ed). St. Louis:
Mosby, 1998.
traction) or indirect (skin traction) means.10 Skeletal
CLINICAL TIP traction uses pins or wires placed through the bone to
 It is important to maintain full ROM of all joints provide a prolonged distractive force. It is maintained
proximal and distal to the external fixator. A
continuously; therefore, the patient is on strict bed
footplate can be attached to the lower leg fixator to rest. Skeletal traction is more effective as a distraction
maintain neutral ankle dorsiflexion. tool than skin traction. Skin traction uses boots,
 The external fixator is very sturdy and can be used slings, or belts applied directly to the skin that can
to assist in moving the involved limb, if permitted be removed for intermittent use of the involved extrem-
by the physician. ity per physician’s orders. Table 3-11 lists the different
 Take extra care in the prevention of inadvertent types of traction.
tapping or banging of the external fixator against Complications associated with traction include the
objects, such as a walker or footstool, as the force following117:
(vibration) is transferred to the bone and is painful.  Hypomobility of the involved joint and hyper-
 Clear drainage, as well as slight bleeding, redness, mobility at the joint closest to the skeletal pin site
and swelling, at the pin sites, is normal.  Generalized muscle atrophy of the immobilized
limb
 Deconditioning of the cardiovascular system and
the general side effects of prolonged bed rest
Traction (see Appendix I-B)
Traction involves the use of a distractive force on an  Skin breakdown or decubitus ulcer formation of
extremity to reduce fracture, immobilize a joint, or the immobilized limb over high-pressure areas
decrease muscle spasm.121 A system of weights and (Refer to the Pathophysiology of Wounds section
pulleys restores the alignment of bone and muscle. in Chapter 7)
The traction apparatus connects to the patient  Infection of traction pin sites or osteomyelitis
(positioned in supine) by either direct (skeletal  Compartment syndrome
 Musculoskeletal System CHAPTER 3 133

CLINICAL TIP
 Do not adjust, remove, or reapply traction unless there is a good working knowledge of the traction apparatus.
Physician orders must be received to remove or adjust the traction unit.
 The patient’s body alignment or the position of the bed is specifically selected for proper countertraction; therefore,
the therapist must not change the positioning of the head or foot of the bed or the placement of blanket rolls or
sandbags.
 Keep weights hanging free when the patient is in traction. Be careful not to lower the height of the bed so as to let
the weight inadvertently rest on the floor.
 Never hang a weight over a patient.
 Notify the nurse of any frayed traction rope, loose knots, or any other alteration of the traction apparatus.
 It is important to monitor the patient’s skin integrity, pain report, and lower-extremity position when in traction,
because abnormal traction or extremity position can cause discomfort or nerve palsy (e.g., external hip rotation can
compress the peroneal nerve against a suspension device).
 Include isometric or active exercise of both the involved and uninvolved extremities as appropriate to minimize
strength loss, joint stiffness, and restlessness associated with prolonged bed rest, as well as to promote a positive
body image.

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 Management
and Physical Therapy
Appendix 3-A Interventions for Fractures

Michele P. West
This appendix was created as a guide for the physical
therapistçthese tables are not all-inclusive. Specific
fracture classification systems are used only if they are
universal or very commonly used; otherwise, fractures
are listed by general type such as nondisplaced or dis-
placed, closed or open, or stable or unstable. The
authors encourage the therapist to consult other
resources for specific fracture patterns or eponyms not
described here. The weight-bearing status is provided
as an estimate in the setting of a localized fracture;
therefore, be sure to follow physician-mandated orders
for weight-bearing, ROM, and exercise, especially if
there is a secondary fracture or associated soft-tissue
injury. Finally, it is inherent that patient/family educa-
tion is a part of each treatment session; thus it is not spe-
cifically listed in this appendix.
‘‘Gentle ROM’’ as it appears in this appendix, is
defined as active-assisted range of motion techniques
that are within the patient’s tolerance.Tolerance is deter-
mined in part by the subjective report of pain as well
as objective limitations of muscle guarding and pattern
of motion.

138
 Management and Physical Therapy Interventions for Fractures APPENDIX 3-A 139

Table 3-A.1 YOUNG CLASSIFICATION, MANAGEMENT, AND PHYSICAL THERAPY INTERVENTION FOR
PELVIC RING FRACTURES

Fracture Type Management Options Physical Therapy Intervention

APC, type Içdisruption of the pubic Symptomatic pain management Functional mobility PWB or
symphysis with < 2.5 cm of WBATas tolerated
diastasis; no significant posterior Hip and distal joint A/AAROM
pelvic injury
APC, type IIçdisruption of the External fixation Functional mobility NWB,
pubic symphysis of > 2.5 cm with Anterior ORIF TDWB, or PWB
tearing of the anterior sacroiliac, Hip and distal joint AA/AROM
sacrospinous, and sacrotuberous lower-extremity exercise
ligaments
APC, type IIIçcomplete disruption External fixation Functional mobility NWB or
of the pubic symphysis and Posterior percutaneous pinning TDWB (usually limited to
posterior ligament complexes, with Anterior and posterior ORIF transfer out of bed only) on
hemipelvic displacement the least-involved side
Distal lower-extremityA/
AAROM
LC, type Içposterior compression of Symptomatic pain management See APC, type I, above
the SIJ without ligament
disruption; oblique pubic ramus
fracture
LC, type IIçrupture of the posterior External fixation See APC, type III, above
sacroiliac ligament; pivotal internal Anterior and posterior ORIF
rotation of the hemipelvis on the
SIJ with a crush injury of the
sacrum and an oblique pubic ramus
fracture
LC, type IIIçfindings in type II with Anterior and posterior ORIF See APC, type III, above
evidence of an APC injury to the
contralateral pelvis
Vertical shearçcomplete ligament or Traction if not medically cleared for See APC, type III, above
bony disruption of a hemipelvis surgery Positioning, breathing exercise,
associated with hemipelvic Percutaneous fixation (SIJ) and uninvolved extremity
displacement External fixation exercise if on bed rest
Anterior and posterior ORIF
A/AAROM, Active/active-assistive range of motion; APC, anteroposterior compression; LC, lateral compression; PWB, partial weight
bearing; NWB, non—weight bearing; ORIF, open-reduction internal fixation; SIJ, sacroiliac joint;TDWB, touch-down weight bearing;
WBAT, weight bearing as tolerated.
Data from Cryer HG, Johnson E. Pelvic Fractures. In DV Feliciano, EE Moore, KL Mattox (eds),Trauma (3rd ed). Stamford, CT: Appleton
& Lange, 1996; AR Burgess, ALJones. Fractures of the Pelvic Ring. In CA Rockwood, DP Green, RW Bucholz, et al. (eds), Rockwood and
Green’s Fractures in Adults (4th ed). Philadelphia: Lippincott-Raven, 1996.
140 APPENDIX 3-A Management and Physical Therapy Interventions for Fractures

Table 3-A.2 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR ACETABULAR FRACTURES*
Fracture Type Management Options Physical Therapy Intervention
Stable (displacement of < 2-5 mm in Traction with bed rest Functional mobilityTDWB or PWB
the dome with an intact weight- Closed reduction Gentle ROM exercise
bearing surface) (e.g., distal anterior Positioning, breathing exercise, and
column, distal transverse, or both- uninvolved extremity exercise if on
column fracture without major bed rest
posterior column displacement)
Unstable (any fracture with a Percutaneous pinning Functional mobility PWB or weight
nonintact weight-bearing dome) Open reduction internal fixation (may bearing as tolerated
(e.g., large anterior, large posterior, involve trochanteric osteotomy if Gentle hip ROM
superior transverse, or T-shaped posterior wall fracture) Hip precautions per physician for total
fracture) Total hip arthroplasty hip arthroplasty
PWB, Partial weight bearing; ROM, range of motion;TDWB, touch-down weight bearing.
*The patient may have hip dislocation precautions if the acetabular fracture is associated with hip dislocation.
Data fromTG DiPasquale, RJ Nowinski.The Acute Care and Evaluation of Acetabular Fractures. In Bosse M, KellamJF, FisherTJ, et al (eds),
Orthopaedic Knowledge Update:Trauma (2nd ed). Rosemont, IL: American Academy of Orthopaedic Surgeons, 2000; M Tile. Fractures of
the Acetabulum. In CA Rockwood, DP Green, RW Bucholz, et al. (eds), Rockwood and Green’s Fractures in Adults (4th ed). Philadelphia:
Lippincott-Raven, 1996.

Table 3-A.3 GARDEN CLASSIFICATION, MANAGEMENT, AND PHYSICAL THERAPY INTERVENTION FOR
INTRACAPSULAR HIP FRACTURES
Fracture Type Management Options Physical Therapy Intervention
Garden I (impacted, incomplete Closed reduction and percutaneous Functional mobility PWB or NWB
fracture) pinning (spica)
Closed reduction and spica cast* A/AAROM exercises (limited by pain)
Lower-extremity strengthening
Garden II (complete fracture without Closed reduction, internal pin fixation Functional mobility PWB
displacement){ ORIF A/AAROM exercises (limited by pain)
Lower-extremity strengthening
Garden III (complete fracture with ORIF See Garden II, above
partial displacement, capsule
partially intact)
Garden IV (complete fracture with ORIF Functional mobility PWB or WBAT,
full displacement and capsule Unipolar or bipolar arthroplasty A/AAROM exercises and
disruption) strengthening, usually with
posterior hip precautions
A/AAROM, Active/active-assisted range of motion; NWB, non—weight bearing; ORIF, open-reduction internal fixation; PWB, partial
weight bearing, WBAT, weight bearing as tolerated.
*Rarely used secondary to risk of disimpaction of the fracture. Considered if the patient is agile and extremely compliant with NWB.
{
Garden II is considered unstable despite nondisplacement because of a lack of bone impaction of the femoral head.
Data from Guyton JL. Fractures of the Hip, Acetabulum, and Pelvis. In ST Canale (ed), Campbell’s Operative Orthopaedics,Vol. 3 (9th ed).
St. Louis: Mosby, 1998.
 Management and Physical Therapy Interventions for Fractures APPENDIX 3-A 141

Table 3-A.4 EVANS AND RUSSELL-TAYLOR CLASSIFICATION, MANAGEMENT, AND PHYSICAL THERAPY
INTERVENTION FOR INTERTROCHANTERIC AND SUBTROCHANTERIC FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Intertrochanteric, Evans type I Closed reduction internal fixation Functional mobility PWB
(fracture line extends upward and (CRIF) Gentle hip ROM exercise
outward from the lesser trochanter) ORIF Distal LE strengthening exercises
Intertrochanteric, Evans type II ORIF Functional mobilityTDWB
(fracture line extends down and  osteotomy and bone grafting Gentle hip ROM exercise
outward from lesser trochanter) Bipolar arthroplasty Distal LE strengthening exercise
Subtrochanteric, Russell-Taylor type ORIF See Intertrochanteric, Evans type I,
IA (single fracture line extends IMrod above
from below lesser trochanter to the
distal greater trochanter)
Subtrochanteric, Russell-Taylor type ORIF See Intertrochanteric, Evans type I,
IB (as in type IA with a second IMrod above
fracture line to the superior aspect
of the lesser trochanter)
Subtrochanteric, Russell-Taylor type ORIF/DHS See Intertrochanteric, Evans type I,
IIA (single fracture line extends IMrod above
from below the lesser trochanter
into the greater trochanter)
Subtrochanteric, Russell-Taylor type ORIF/DHS Functional mobility NWB orTDWB
IIB (as in type IIA, with a second Bone grafting Gentle hip ROM exercise
fracture line to the superior aspect Distal LE strengthening exercise
of the lesser trochanter)
,With or without; DHS, dynamic hip screw; IM, intramedullary; LE, lower extremity; NWB, non—weight bearing; ORIF, open-reduction
internal fixation; PWB, partial weight bearing; ROM, range of motion;TDWB, touch-down weight bearing.
Data from GuytonJL. Fractures of the Hip, Acetabulum, and Pelvis. In ST Canale (ed), Campbell’s Operative Orthopaedics,Vol. 3 (9th ed).
St. Louis: Mosby, 1998.

Table 3-A.5 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR FEMORAL SHAFT FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Closed; simple or nondisplaced IM rod Functional mobility NWB,TDWB, or
ORIF WBAT
Gentle ROM exercise
Closed; comminuted, Traction on bed rest Functional mobility NWB orTDWB
impacted, or both IM rod Lower extremity ROM exercise per physician
ORIF order
Positioning, breathing exercise, and
uninvolved extremity exercise if on bed rest
Open; comminuted and Irrigation and debridement with See Closed; comminuted, impacted, or both,
displaced immediate or delayed wound closure above
Short-term skeletal traction on bed rest
External fixation
IM rod
IM, Intramedullary; NWB, non—weight bearing; ORIF, open-reduction internal fixation; ROM, range of motion;TDWB, touch-down
weight bearing;WBAT, weight bearing as tolerated.
Data from GuytonJL. Fractures of the Hip, Acetabulum, and Pelvis. In ST Canale (ed), Campbell’s Operative Orthopaedics,Vol. 3 (9th ed).
St. Louis: Mosby, 1998.
142 APPENDIX 3-A Management and Physical Therapy Interventions for Fractures

Table 3-A.6 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR DISTAL FEMUR FRACTURES
Fracture Type Management Options Physical Therapy Intervention
Supracondylar; extraarticular, simple, Long leg cast Functional mobility NWB
nondisplaced Distal and proximal
A/AAROM exercise
Supracondylar; extraarticular, Traction on bed rest Functional mobility light PWB
displaced, or comminuted Closed reduction with percutaneous Distal and proximal A/AAROM
plate fixation exercise
Intramedullary nail Positioning, breathing exercise, and
ORIF uninvolved extremity exercise if on
Knee immobilizer or hinged knee brace bed rest
(stable fixation) or cast (less-stable
fixation)
Continuous passive motion
Unicondylar; intraarticular, Long leg cast with close monitoring for Functional mobility NWB orTDWB
nondisplaced loss of reduction Distal and proximal A/AAROM
exercise
Unicondylar; intraarticular, displaced Traction on bed rest Functional mobilityTDWB
Closed-reduction and percutaneous Gentle ROM exercise
fixation Continuous passive motion per
ORIF physician order or type of
Long leg splint or cast immobilization device
Intercondylar; intraarticular Long-term traction Functional mobilityTDWB or light
ORIF PWB
Cast brace if less-stable fixation Delayed gentle ROM and quadriceps
achieved exercise
Maintenance of functional ROM of hip
and ankle
A/AAROM, Active/active-assisted range of motion; NWB, non—weight bearing; ORIF, open-reduction internal fixation; PWB, partial
weight bearing; ROM, range of motion;TDWB, touch-down weight bearing.
Data from Whittle AP. Fractures of the Lower Extremity. In ST Canale (ed), Campbell’s Operative Orthopaedics,Vol. 3 (3rd ed). St. Louis:
Mosby, 1998.
 Management and Physical Therapy Interventions for Fractures APPENDIX 3-A 143

Table 3-A.7 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR PATELLAR FRACTURES
Fracture Type Management Options Physical Therapy Intervention
Nondisplaced Closed reduction Functional mobility PWB or WBAT
Long leg cast (or other immobilization Avoid strong straight leg raise and
brace) with full knee extension strong quadriceps contraction
because it can stress the fracture site
Displaced (simple vertical or ORIF with immobilization of the knee See Nondisplaced, above
transverse fracture) at full extension AAROM (per physician) after few days
Continuous passive motion of immobilization
Comminuted ORIF (with fragment removal, if Functional mobility NWB, PWB, or
applicable) WBAT
Partial patellectomy (when one large See Nondisplaced, above, in regard to
fragment remains) or total quadriceps
patellectomy (if no large fragments
remain) and quadriceps tendon
repair
Immobilization with long leg cast, long
leg brace, or posterior splint at full
knee extension or slight flexion
AAROM, Active-assisted range of motion; ORIF, open-reduction internal fixation; NWB, non—weight bearing; PWB, partial weight
bearing;WBAT, weight bearing as tolerated.
Data from Whittle AP. Fractures of the Lower Extremity. In ST Canale (ed.) Campbell’s Operative Orthopaedics,Vol. 3 (9th ed). St. Louis:
Mosby, 1998.

Table 3-A.8 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR TIBIAL PLATEAU FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Nondisplaced Closed reduction Functional mobilityTDWB or PWB
Cast-brace immobilization or AAROM exercise, continuous passive
postoperative knee brace motion to knee joint, or both
Ligament repair (if applicable)
Displaced; single condylar or split External fixation Functional mobility NWB,TDWB, or
compression fracture ORIF PWB
Cast-brace application or postoperative AAROM exercise, continuous passive
knee brace motion to knee joint, or both
Displaced; impacted, or severely Skeletal traction and bed rest ( 1 wk) Functional mobility NWB,TDWB, or
comminuted bicondylar fracture to allow for soft-tissue healing PWB
ORIF  bone graft Delayed knee A/AAROM
Simultaneous ligament or meniscal Positioning, breathing exercise, and
repair, if applicable uninvolved extremity exercise if on
Immobilization brace bed rest
A/AAROM, Active/active-assisted range of motion; AAROM, active-assisted range of motion; NWB, non—weight bearing; ORIF, open-
reduction internal fixation; PWB, partial weight bearing;TDWB, touch-down weight bearing.
Data from Whittle AP. Fractures of the Lower Extremity. In ST Canale (ed), Campbell’s Operative Orthopaedics,Vol. 3 (9th ed). St. Louis:
Mosby, 1998.
144 APPENDIX 3-A Management and Physical Therapy Interventions for Fractures

Table 3-A.9 MEDICAL-SURGICAL MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR TIBIAL
SHAFT FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Closed; minimally displaced Closed reduction Functional mobilityTDWB, PWB, or
Long leg cast WBAT
Quadriceps strengthening Edema
management
Closed; moderately displaced Open-reduction internal fixation Functional mobility NWB,TDWB
(ORIF) Knee ROM exercise
Short leg cast Quadriceps strengthening
Edema management
Closed; severely displaced, External fixation Functional mobility NWB
comminuted, or both Temporary calcaneal traction to allow Ankle  knee ROM exercises
for soft tissue healing Quadriceps strengthening
ORIF Edema management
Open External fixation See Closed; severely displaced,
comminuted, or both, above
,With or without; NWB, non—weight bearing; PWB, partial weight bearing; ROM, range of motion;TDWB, touch-down weight bearing;
WBAT, weight bearing as tolerated.
 Management and Physical Therapy Interventions for Fractures APPENDIX 3-A 145

Table 3-A.10 MEDICAL-SURGICAL MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR DISTAL
TIBIAL AND ANKLE FRACTURES

Fracture Type Medical-Surgical Options Physical Therapy Intervention

Distal tibial; closed, minimally Closed reduction Functional mobility NWB
displaced Short leg cast Knee ROM exercises
Proximal joint strengthening
Edema management
Distal tibial; closed, moderately ORIF See Distal tibial; closed, minimally
displaced Short leg cast displaced, above
Distal tibial; closed, severely displaced Temporary calcaneal traction Functional mobility NWB
External fixation Lower-extremity isometrics
ORIF Neutral ankle positioning
Edema management
Proximal joint strengthening
Edema management
Distal tibial; open External fixation Functional mobility NWB
Ankle ROM exercise
Neutral ankle positioning
Proximal joint strengthening
Edema management
Ankle; closed, nondisplaced Closed reduction Functional mobility NWB or PWB
Short leg cast or walking cast Edema management
Proximal lower-extremity
strengthening exercise
Ankle; closed, displaced, Closed reduction Functional mobility NWB
multifracture, or both ORIF Edema management
Cast application or other Proximal lower-extremity
immobilization method dependent strengthening exercise
on degree of edema Foot and ankle exercise as per physician
and type of immobilization device
Ankle; open Irrigation and debridement with See Ankle; closed, displaced,
immediate or delayed wound closure multifracture, or both, above
Traction
External fixation
ORIF
NWB, Non—weight bearing; ORIF, open-reduction internal fixation; PWB, partial weight bearing; ROM, range of motion.
Data from Geissler WB,Tsao AK, Hughes JL. Fractures and Injuries of the Ankle. In CA Rockwood, DP Green, RW Bucholz, et al. (eds),
Rockwood and Green’s Fractures in Adults (4th ed). Philadelphia: Lippincott-Raven, 1996.
146 APPENDIX 3-A Management and Physical Therapy Interventions for Fractures

Table 3-A.11 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR CALCANEAL AND FOREFOOT
FRACTURES*

Fracture Type Management Options Physical Therapy Intervention

Calcaneal; extraarticular, minimally Closed reduction Functional mobility NWB
displaced SLC Proximal lower-extremity strengthening
and ROM exercise
Edema management
Ankle/forefoot exercise as per physician
and type of immobilization device
Calcaneal; avulsion Closed reduction See Calcaneal; extraarticular,
ORIF minimally displaced, above
SLC
Calcaneal; intraarticular fracture Skeletal traction See Calcaneal; extraarticular,
involving the subtalar joint Immediate or delayed minimally displaced, above
SLC
Closed reduction and percutaneous
pinning
ORIF
Arthrodesis if fracture is very severe
Calcaneal; open Irrigation and debridement with See Calcaneal; extraarticular,
immediate or delayed wound closure minimally displaced, above
Skeletal traction
External fixation
Forefoot; minimally displaced Closed reduction Functional mobility NWB, PWB, or
Percutaneous pinning WBAT, dependent on exact
SLC or walking cast location and severity of fracture
Proximal lower-extremity strengthening
and ROM exercise
Edema management
Forefoot; moderate or severe ORIF See Forefoot; minimally displaced,
displacement, with fragmentation Percutaneous pinning above
or angulation SLC
Forefoot; open See Calcaneal; open, above See Forefoot; minimally displaced,
ORIF above
NWB, Non—weight bearing; ORIF, open-reduction internal fixation; PWB, partial weight bearing; ROM, range of motion; SLC, short leg
cast;WBAT, weight bearing as tolerated.
*For calcaneal fractures, cast application may not be in the neutral ankle position to protect the fracture site from strong ankle muscle
contractions.
Data from HeckmanJD. Fractures and Dislocations of the Foot. In CA Rockwood, DP Green, RW Bucholz, et al. (eds). Rockwood and
Green’s Fractures in Adults (4th ed). Philadelphia: Lippincott-Raven, 1996.
 Management and Physical Therapy Interventions for Fractures APPENDIX 3-A 147

Table 3-A.12 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR COMMON CERVICAL SPINE
FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Hangman’s fracture, or bilateral Cervical collar immobilization for Functional mobility with logroll
pedicle fracture of axis (C1) type I precautions
Type Içno angulation and < 3 mm Cervical traction/reduction followed by Posture and body mechanics training
displacement of C2 on C3 halo vest for type II and IIA (cervical Therapeutic exercise and active-
Type IIç> 3 mm displacement of collar for type II possible) assisted/passive range of motion
C2 on C3 Posterior open reduction and halo vest dependent on neurologic injury
Type IIAçminimal displacement or C1-3 fusion for type III Balance and scapular exercises for the
and significant angulation of C2 patient in a halo vest
Type IIIçfull unilateral or bilateral
facet dislocation
Odontoid process fracture Cervical collar immobilization for See Hangman’s fracture, or bilateral
Type Içoblique avulsion fracture type I pedicle fracture of axis (C1), above
of the tip of the odontoid Closed reduction or ORIF with halo
Type IIçfracture of the neck of the vest, anterior or posterior C1-2 fusion
odontoid  bone grafting with cervical collar
Type IIIçfracture extending to the for type II
C2 vertebral body Closed reduction or open-reduction
internal fixation with halo vest for
type III
Vertebral body (stable wedge) Cervical collar Functional mobility
fractureçbony impaction and Posture and body mechanics training
concavity of the vertebral body
Spinous process (stable, isolated) or Cervical collar SeeVertebral body (stable wedge)
laminal fracture fracture, above
,With or without; ORIF, open-reduction internal fixation.
Data from Sasso RC, ReillyTM. Odontoid and Hangman’s Fractures. Orthopaedic Knowledge Update:Trauma (2nd ed). Rosemont, IL:
American Academy of Orthopaedic Surgeons, 2000; Hockberger RS, Kirshenbaum KJ, Doris PE. Spinal Injuries. In P Rosen (ed),
Emergency Medicine Concepts and Clinical Practice (4th ed). St. Louis: Mosby, 1998.
148 APPENDIX 3-A Management and Physical Therapy Interventions for Fractures

Table 3-A.13 MANAGEMENT AND PHYSICAL THERAPY FOR COMMON THORACOLUMBAR SPINE
FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Spinous process, transverse process,
laminar, or facet fracture (stable,
isolated)
Vertebral body compression
(impacted anterior wedge)
fractureçstable
Vertebral body burst (axial
compression) fractureçunstable
Multidirectional fracture with disc
involvement and facet
dislocationçunstable
,With or without.
Data fromVaccaro AR, Singh K.Thoracolumbar Injuries: Nonsurgical Treatment; DC Kwok.Thoracolumbar Injuries:The Posterior
Approach. In Orthopaedic Knowledge Update:Trauma (2nd ed). Rosemont, IL: American Academy of Orthopaedic Surgeons, 2000.
Cervicothoracic or thoracolumbar
orthosis
Short-term bed rest
Vertebroplasty
Thoracolumbar or thoracolumbosacral
orthosis or hyperextension brace
Fusion (if severe)
Short-term bed rest
Thoracolumbosacral orthosis
Anterior/posterior decompression and
reconstruction  bone grafting
Anterior/posterior decompression and
fusion
Thoracolumbosacral orthosis
Functional mobility with logroll
precautions
Posture and body mechanics training
Therapeutic exercise and active-
assisted/passive range of motion
dependent on neurologic injury
See Spinous process, transverse
process, laminar, or facet fracture
(stable, isolated), above
See Spinous process, transverse
process, laminar, or facet fracture
(stable, isolated), above
See Spinous process, transverse
process, laminar, or facet fracture
(stable, isolated), above
 Management and Physical Therapy Interventions for Fractures APPENDIX 3-A 149

Table 3-A.14 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION OF PROXIMAL HUMERAL* AND
HUMERAL SHAFT FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Proximal humeral; displaced, Closed reduction Functional mobility NWB
one-part Sling immobilization Pendulum exercises and passive ROM
per physician
Elbow, wrist, and hand ROM exercises
Edema management
Proximal humeral; displaced, Closed reduction with percutaneous See Proximal humeral; displaced, one-
two-part pinning part, above
ORIF
Intramedullary rod
Sling immobilization
Proximal humeral; displaced, ORIF See Proximal humeral; displaced, one-
three-part Hemiarthroplasty part, above
See Physical Therapy Intervention after
Shoulder Arthroplasty section in
Chapter 3
Proximal humeral; displaced, Transcutaneous reduction with See Proximal humeral; displaced,
four-part fluoroscopy three-part, above
Percutaneous pinning
ORIF
Comminution of humeral head Hemiarthroplasty See Proximal humeral; displaced, one-
Sling immobilization part, above
Humeral shaft; closed, minimal Closed reduction Functional mobility NWB
displacement Sling, hanging arm cast, or functional Shoulder and elbow active/active-
brace assisted ROM exercises per physician
and type of immobilization
Isometric scapulothoracic exercise
Wrist and hand exercises
Edema management
Humeral shaft; closed, displaced ORIF See Humeral shaft; closed, minimal
with angulation Intramedullary displacement, above
Long arm splint
Humeral shaft; open Irrigation and debridement with See Humeral shaft; closed, minimal
immediate or delayed wound closure displacement, above
External fixation
ORIF
NWB, Non—weight bearing; ORIF, open-reduction internal fixation; ROM, range of motion.
*Proximal humeral fractures according to the Neer classification.
Data from Williams GR,Wong KL.Two-Part and Three-Part Fractures: Open Reduction and Internal FixationVersus Closed Reduction and
Percutaneous Pinning. Orthop Clin North Am 2000;31:1-21; ZuckmanJD, Koval KJ. Fractures of the Shaft of the Humerus.
In CA Rockwood, DP Green, RW Bucholz, et al. (eds), Rockwood and Green’s Fractures in Adults (4th ed). Philadelphia: Lippincott-Raven,
1996.
150 APPENDIX 3-A Management and Physical Therapy Interventions for Fractures

Table 3-A.15 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR OLECRANON AND RADIAL
HEAD FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Olecranon; closed, nondisplaced Long arm cast with elbow in Functional mobility NWB
midflexion Initiation of elbow active-assisted ROM in
pain-free range per physician
Distal and proximal joint active ROM
Edema management
Olecranon; closed, displaced ORIF See Olecranon; closed, nondisplaced, above
Olecranon; closed, comminuted ORIF See Olecranon; closed, nondisplaced, above
Immobilization
Radial head; closed, nondisplaced Closed reduction with early See Olecranon; closed, nondisplaced, above
or minimally displaced immobilization
Hematoma aspiration
Sling or short-term splint
Radial head; closed, displaced Closed reduction and short-term See Olecranon; closed, nondisplaced, above
splinting if ROM adequate, or
ORIF if ROM inadequate
Partial or total radial head excision
Radial head; closed, comminuted ORIF with immobilization See Olecranon; closed, nondisplaced, above
Radial head excision  radial head
prosthesis,  bone grafting
,With or without; NWB, non—weight bearing; ORIF, open-reduction internal fixation; ROM, range of motion.
Data from RN Hotchkiss. Fractures and Dislocations of the Elbow. In CA Rockwood, DP Green, RW Bucholz, et al. (eds), Rockwood and
Green’s Fractures in Adults (4th ed). Philadelphia: Lippincott-Raven, 1996.

Table 3-A.16 MANAGEMENT AND PHYSICAL THERAPY INTERVENTION FOR FOREARM FRACTURES

Fracture Type Management Options Physical Therapy Intervention

Shaft fracture of radius or ulna Closed reduction with casting, or casting Functional mobility NWB
alone if nondisplaced Distal and proximal ROM exercises
ORIF (if displaced) with functional brace Edema management
Distal radius; extraarticular Closed reduction and percutaneous See Shaft fracture, above
pinning
Sugar-tong splint or cast
ORIF  functional brace
Distal radius; intraarticular ORIF See Shaft fracture, above
Closed reduction with external fixation  Active and passive finger movement if
percutaneous pinning patient has an external fixator
Arthroscopic controlled internal fixation
Distal radius; intraarticular, Closed reduction with external fixation See Distal radius; intraarticular, above
comminuted ORIF
Bone grafting
Splint
,With or without; NWB, non—weight bearing; ORIF, open-reduction internal fixation; ROM, range of motion.
Adapted from Fernandez DL, Palmer AK. Fracture of the Distal Radius. In DP Green, RN Hotchkiss,WL Pederson (eds), Green’s Operative
Hand Surgery,Vol. 1 (4th ed). NewYork: Churchill Livingstone, 1998;950.
 4 Nervous System

Michele P. West INTRODUCTION

Hillary A. Reinhold The nervous system is linked to every system of the body and is respon-
sible for the integration and regulation of homeostasis. It is also
involved in the action, communication, and higher cortical function
of the body. A neurologic insult and its manifestations therefore have
the potential to affect multiple body systems. To safely and effectively
prevent or improve the neuromuscular, systemic, and functional sequelae
of altered neurologic status in the acute care setting, the physical thera-
pist requires an understanding of the neurologic system and the
principles of neuropathology. The objectives of this chapter are to pro-
vide the following:
1. A brief review of the structure and function of the nervous system
2. An overview of neurologic evaluation, including the physical exam-
ination and diagnostic tests
3. A description of common neurologic diseases and disorders, including
clinical findings, medical and surgical management, and physical ther-
apy interventions
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:

Diagnosis/Disease Possible Practice Patterns

Common Degenerative Central Nervous 5A, 5E, 5G, 6B, 6E, 7A
System Diseases:
Amyotrophic Lateral Sclerosis, Guillain-
Barre¤ Syndrome, Multiple Sclerosis,
Parkinson’s Disease, Huntington’s Disease
Vestibular Dysfunction: 5A
Bilateral Vestibular Hypofunction, Me¤ nie' re’s
Disease, AcuteVestibular Neuronitis, Benign
Positional Paroxysmal Vertigo,Vertigo,
Lightheadedness, Dysequilibrium
Neuroinfectious diseases: 4A, 5C, 5D, 5G, 5H, 6E,
Encephalitis, Meningitis, and Poliomyelitis 7A
(more info in Chapter 10)
Syncope 5A
Continued

151
152 CHAPTER 4 Nervous System

Diagnosis/Disease Possible Practice Patterns

Seizure: 5A, 5C, 5D, 5E
Status Epilepticus, Epilepsy, Simple Partial
Seizures, Complex Partial Seizures,
Tonic-Clonic Seizures
Ventricular Dysfunction: 5C, 5D
Cerebrospinal Fluid Leak and
Hydrocephalus
Spinal Cord Injury 5H, 7A, 7C
Traumatic Brain Injury 5C, 5D, 5I
Cerebrovascular Disease and 5C, 5D, 5I, 6E, 6F, 7A
Disorders:
Transient Ischemic Attack,
Cerebrovascular Accident, Dementia,
Subarachnoid Hemorrhage,
Arteriovenous Malformation and
Cerebral Aneurysm

Please refer to the back cover of this book for a com-
plete list of the preferred practice patterns as individual
patient conditions are highly variable and other practice
patterns may be applicable.
STRUCTURE AND FUNCTION OF THE
NERVOUS SYSTEM
The nervous system is divided as follows:
 The central nervous system (CNS), consisting of the
brain and spinal cord
 The peripheral nervous system, consisting of efferent
and afferent nerves outside the CNS.
The peripheral nervous system is divided into:
 The autonomic (involuntary) nervous system, con-
sisting of the sympathetic and parasympathetic sys-
tems innervating the viscera, smooth muscles, and
glands
 The somatic (voluntary) nervous system, consisting
of efferent and afferent nerves to all parts of the
body except the viscera, smooth muscles, and glands
Central Nervous System
BRAIN
The brain is anatomically divided into the cerebral
hemispheres, diencephalon, brain stem, and cerebel-
lum. A midsagittal view of the brain is shown in
Figure 4-1, A. Figure 4-1, B shows the basal ganglia
and the internal capsule. Although each portion of the
brain has its own function, it is linked to other
portions via tracts and rarely works in isolation.
When lesions occur, disruption of these functions
can be predicted. Tables 4-1 and 4-2 describe the
basic structure, function, and dysfunction of the
cerebral hemispheres, diencephalon, brain stem, and
cerebellum.
PROTECTIVE MECHANISMS. The brain is protected
by the cranium, meninges, ventricular system, and
blood-brain barrier.
Cranium. The cranium encloses the brain. It is
composed of eight cranial and 14 facial bones con-
nected by sutures and contains approximately 85 fora-
men for the passage of the spinal cord, cranial nerves
(CNs), and blood vessels.5 The cranium is divided
into the cranial vault, or calvaria (the superolateral
and posterior aspects), and the cranial floor, which is
composed of fossae (the anterior fossa supports the
frontal lobes; the middle fossa supports the temporal
lobes; and the posterior fossa supports the cerebellum,
pons, and medulla).6
Meninges. The meninges are three layers of connec-
tive tissue that cover the brain and spinal cord. The
dura mater, the outermost layer, lines the skull (perios-
teum) and has four major folds (Table 4-3). The ara-
chnoid, the middle layer, loosely encloses the brain.
The pia mater, the inner layer, covers the convolutions
of the brain and forms a portion of the choroid plexus
in the ventricular system. The three layers create very
important anatomic and potential spaces in the brain,
as shown in Figure 4-2 and described inTable 4-4.
 Nervous System CHAPTER 4 153

B
FIGURE 4-1
A, Medial (midsagittal) view of a hemisected brain. B, Horizontal section of the cerebrum showing the
basal ganglia. (A, From Gilman S, Newman SW [eds]. Manter and Gatz’s Essentials of Neuroanatomy and
Neurophysiology [7th ed]. NewYork: Oxford University Press, 1987;9. B, From Love RJ,Webb WG [eds].
Neurology for the Speech-Language Pathologist [4th ed]. Boston: Butterworth-Heinemann, 2001;38.)

Ventricular System. The ventricular system nourishes
the brain and acts as a cushion by increasing the buoy-
ancy of the brain. It consists of four ventricles and a
series of foramen, through which cerebrospinal fluid
(CSF) passes to surround the CNS. CSF is a colorless,
odorless solution produced by the choroid plexus of
all ventricles at a rate of 400 to 500 ml per day.6 CSF
circulates in a pulse-like fashion through the ventricles
and around the spinal cord with the beating of ependy-
mal cilia that line the ventricles and intracranial
blood volume changes that occur with breathing and
cardiac systole.7 The flow of CSF under normal condi-
tions, as shown in Figure 4-3, is as follows8:
 From the lateral ventricles via the interventricular
foramen to the third ventricle
 From the third ventricle to the fourth ventricle via
the cerebral aqueduct
 From the fourth ventricle to the cisterns, subarach-
noid space, and spinal cord via the median and lateral
apertures.
When ventricular pressure is greater than venous
pressure, CSF is absorbed into the venous system via
154 CHAPTER 4 Nervous System

Table 4-1 STRUCTURE, FUNCTION, AND DYSFUNCTION OF THE CEREBRAL HEMISPHERES

Lobe of Cerebrum Structure Function
Frontal lobe Precentral gyrus Voluntary motor cortex of
contralateral face, arm, trunk,
and leg
Supplementary Advanced motor planning
motor area Contralateral head and eye turning
(connections to cranial nerves III,
IV,VI, IX, X, and XII nuclei)
Prefrontal pole Personality center, including
abstract ideas, concern for others,
conscience, initiative, judgment,
persistence, and planning
Paracentral lobule Bladder and bowel inhibition
Broca’s area D: Motor speech center
ND: Appreciation of intonation
and gestures with vocalization
Parietal lobe Postcentral gyrus Somatosensory cortex of contralateral
pain; posture; proprioception;
and touch of arm, trunk, and leg
Parietal pole D: Ability to perform calculations
ND: Ability to construct shapes,
awareness of external
environment, and body image
Wernicke’s area D: Sensory speech (auditory and
written) comprehension center
ND: Appreciation of content
of emotional language
(e.g., tone of voice)
Optic radiation Visual tract
Gustatory cortex Perception of taste
Temporal lobe Superior temporal D: Appreciation of language
gyrus (auditory ND: Appreciation of music,
cortex) rhythm, and sound
Middle and inferior Learning and memory centers
temporal gyri
Limbic lobe and Affective and emotion center,
olfactory cortex including mood, primitive
behavior, self-preservation,
short-term memory, visceral
emotion processes, and
interpretation of smell
Wernicke’s area See Parietal lobe, above
Optic radiation Visual tract
Occipital lobe Striate and Perception of vision (visual cortex)
parastriate
cortices
D, Dominant, ND, nondominant.
Data from reference numbers 1-4, 11
Dysfunction
Contralateral mono- or
hemiparesis or hemiplegia
Contralateral head and eye
paralysis
Loss of inhibition and demonstration
of antisocial behaviors
Ataxia, primitive reflexes,
and hypertonicity
Urinary and bowel incontinence
Broca’s (expressive) aphasia
Contralateral sensation loss
D: Acalculia, agraphia, finger agnosia
ND: Constructional apraxia,
geographic agnosia, dressing
apraxia, anosognosia
Wernicke’s (receptive) aphasia
Lower homonymous quadrantanopia
Dysfunction is very uncommon
D: Decreased ability to hear
ND: Decreased ability to
appreciate music
Learning and memory deficits
Aggressive or antisocial behaviors
Inability to establish new memories
Wernicke’s (receptive) aphasia
Upper homonymous quadrantanopia
Homonymous hemianopsia with
or without macular involvement
 Nervous System CHAPTER 4 155

Table 4-2 STRUCTURE, FUNCTION, AND DYSFUNCTION OF THE DIENCEPHALON, BRAIN STEM,
AND CEREBELLUM

Brain Structure Substructure Function Dysfunction

Diencephalon
Thalamus Specific and Cortical arousal Altered consciousness
association nuclei Integrative relay station for all Signs and symptoms of increased
ascending and descending ICP
motor stimuli and all ascending Contralateral hemiplegia,
sensory stimuli except smell hemiparesis, or hemianesthesia
Memory Altered eye movement
Hypothalamus Mamillary bodies Autonomic center for sympathetic Altered autonomic function and
Optic chiasm and parasympathetic responses vital signs
Infundibulum (stalk) Visceral center for regulation of Headache
connects to the body temperature, food intake, Visual deficits
pituitary gland thirst, sleep and wake cycle, Vomiting with signs and symptoms
Forms inferolateral wall water balance of increased ICP
of third ventricle Produces ADH and oxytocin See Chapter 11 for more information
Regulates anterior pituitary gland on hormones and endocrine
Association with limbic system disorders
Epithalamus Pineal body Association with limbic system Dysfunction unknown
Posterior commissure,
striae medullares,
habenular nuclei and
commissure
Subthalamus Substantia nigra Association with thalamus for Dyskinesia and decreased motor
Red nuclei motor control control
Pituitary Anterior and posterior Production, storage, and secretion See Chapter 11 for more
lobes of reproductive hormones information on hormones
Secretion of ADH and oxytocin and endocrine disorders
Internal capsule Fiber tracts connecting Conduction pathway between Contralateral hemiparesis or
thalamus to the cortex the cortex and spinal cord hemiplegia and hemianesthesia
Brain Stem
Midbrain Superior cerebellar Conduction pathway between Contralateral hemiparesis or
peduncles higher and lower brain centers hemiplegia and hemianesthesia,
Superior and inferior Visual reflex altered consciousness and
colliculi Auditory reflex respiratory pattern, cranial
Medial and lateral nerve palsy
lemniscus
CNs III and IV nuclei
Reticular formation
Cerebral aqueduct
in its center
Pons Middle cerebellar Conduction pathway between See Midbrain, above
peduncles higher and lower brain centers
Respiratory center
CNs V-VIII nuclei
Forms anterior wall
of fourth ventricle
Continued
156 CHAPTER 4 Nervous System

Table 4-2 STRUCTURE, FUNCTION, AND DYSFUNCTION OF THE DIENCEPHALON, BRAIN STEM,
AND CEREBELLUM—cont’d

Brain Structure Substructure Function Dysfunction

Medulla Decussation of pyramidal Homeostatic center for cardiac, See Midbrain, above
tracts respiratory, vasomotor
Inferior cerebellar functions
peduncles
Inferior olivary nuclei
Nucleus cuneatus and
gracilis
CNs IX-XII nuclei
Cerebellum
Anterior lobe Medial portion Sensory and motor input of trunk Ipsilateral ataxia and
Lateral portion Sensory and motor input of discoordination or tremor
extremities for coordination of extremities
of gait
Posterior lobe Medial and lateral Sensory and motor input for Ipsilateral ataxia and
portions coordination of motor skills discoordination of the trunk
and postural tone
Flocculonodular Flocculus nodule Sensory input from ears Ipsilateral facial sensory loss and
Sensory and motor input from Horner’s syndrome, nystagmus,
eyes and head for coordination visual overshooting
of balance and eye and head Loss of balance
movement
ADH, Antidiuretic hormone; CN, cranial nerve; ICP, intracranial pressure.
Data from reference numbers 1-4, 11.

the arachnoid villi, capillary walls of the pia mater, and

Table 4-3 DURAL FOLDS
Falx cerebri Vertical fold that separates the two
cerebral hemispheres to prevent
horizontal displacement of these
structures
Falx cerebelli Vertical fold that separates the two
cerebellar hemispheres to prevent
horizontal displacement of these
structures
Tentorium Horizontal fold that separates
cerebelli occipital lobes from the cerebellum
to prevent vertical displacement
of these structures
Diaphragm Horizontal fold that separates that
sellae subarachnoid space from the sella
turcica and is perforated by the
stalk of the pituitary gland
Data from WilkinsonJL (ed). Neuroanatomy for Medical Students
(3rd ed). Oxford, UK: Butterworth-Heinemann, 1998.
lymphatics of the subarachnoid space near the optic
nerve.6
Blood-Brain Barrier. The blood-brain barrier is the
physiologic mechanism responsible for keeping
toxins, such as amino acids, hormones, ions, and urea,
from altering neuronal firing of the brain. It readily
allows water, oxygen, carbon dioxide, glucose, some
amino acids, and substances that are highly soluble
in fat (e.g., alcohol, nicotine, and anesthetic agents)
to pass across the barrier.9,10 The barrier consists of
fused endothelial cells on a basement membrane
that is surrounded by astrocytic foot extensions.10
Substances must therefore pass through, rather than
around, these cells. The blood-brain barrier is absent
near the hypothalamus, pineal region, anterior third
ventricle, and floor of the fourth ventricle.7
CENTRAL BRAIN SYSTEMS. The central brain systems
are the reticular activating system and the limbic
system. The reticular activating system (RAS) is com-
posed of an ascending tract and a descending tract.

FIGURE 4-2
Coronal section of cranial meninges showing a venous sinus and dural fold. (FromYoung PA,Young PH.
Basic Clinical Neuroanatomy. Philadelphia: Williams & Wilkins, 1997;8.)
The ascending RAS is responsible for human con-
sciousness level and integrates the functions of the
brain stem with cortical, cerebellar, thalamic, hypotha-
lamic, and sensory receptor functions.9 The descend-
ing RAS promotes spinal cord antigravity reflexes or
extensor tone needed to maintain standing.11
The limbic system is a complex interactive system,
with primary connections between the cortex, hypotha-
lamus, amygdala, and sensory receptors. The limbic
system plays a major role in memory, emotion, and vis-
ceral and motor responses involved in defense and
reproduction by mediating cortical autonomic func-
tion of internal and external stimuli.12,13
CIRCULATION. The brain receives blood from the
internal carotid and vertebral arteries, which are
linked together by the circle of Willis, as shown
Table 4-4 DURAL SPACES
Epidural Potential space between the skull and
(extradural) outer dura mater.
space
Subdural space Potential space between the dura and
the arachnoid mater; a split in the
dura contains the venous sinus.
Subarachnoid Anatomic space between the
space arachnoid and pia mater containing
cerebrospinal fluid and the vascular
supply of the cortex.
Nervous System CHAPTER 4 157
in Figure 4-4. Each vessel supplies blood to a certain
part of the brain (Table 4-5). The circulation of the
brain is discussed in terms of a single vessel or by
region (usually as the anterior or posterior circulation).
There are several anastomotic systems of the cerebral
vasculature that provide essential blood flow to the
brain. Blood is drained from the brain through a
series of venous sinuses. The superior sagittal sinus,
with its associated lacunae and villi, is the primary
drainage site. The superior sagittal sinus and sinuses
located in the dura and scalp then drain blood into the
internal jugular vein for return to the heart.
SPINAL CORD
The spinal cord lies within the spinal column and
extends from the foramen magnum to the first lumbar
vertebra, where it forms the conus medullaris and the
cauda equina and attaches to the coccyx via the filum
terminale. Divided into the cervical, thoracic, and
lumbar portions, it is protected by mechanisms similar
to those supporting the brain. The spinal cord is
composed of gray and white matter and provides the
pathway for the ascending and descending tracts, as
shown in cross-section in Figure 4-5 and outlined in
Table 4-6.
Peripheral Nervous System
The peripheral nervous system consists of the cranial
and spinal nerves and the reflex system. The primary
structures include peripheral nerves, associated
158 CHAPTER 4 Nervous System

FIGURE 4-3
The ventricular system of the brain. Arrows indicate the circulation of cerebrospinal fluid from the
site of formation in the choroid plexus to the site of absorption in the villi of the sagittal sinus. (From
BogousslavskyJ, Fisher M [eds].Textbook of Neurology. Boston: Butterworth-Heinemann, 1998;656.)

ganglia, and sensory receptors. There are 12 pairs of

FIGURE 4-4
Schematic representation of the arterial circle of Willis and
accompanying veins. Ant., anterior; Art., artery; Post.,
posterior. (From Gonzalez EG, Meyers SJ [eds]. Downey and
Darling’s Physiological Basis of Rehabilitation Medicine
[3rd ed]. Boston: Butterworth-Heinemann, 2001;22.)
CNs, each with a unique pathway and function (sensory,
motor, mixed, or autonomic). Thirty-one pairs of
spinal nerves (all mixed) exit the spinal cord to form
distinct plexuses (except T2 to T12). The peripheral
nerves of the upper and lower extremities and
thorax are listed in Tables 4-7 through 4-9, respect-
ively, and the dermatomal system is shown in Figure
4-6. The reflex system includes spinal, deep tendon,
stretch, and superficial reflexes and protective
responses.
Autonomic Nervous System
The portion of the peripheral nervous system that
innervates glands and cardiac and smooth muscle is
the autonomic nervous system. The parasympathetic
division is activated in time of rest, whereas the sympa-
thetic division is activated in times of work or ‘‘fight
or flight’’ situations. The two divisions work closely
together, with dual innervation of most organs, to
ensure homeostasis.
 Table 4-5 BLOOD SUPPLY OF THE MAJOR AREAS OF THE BRAIN

Artery Area of Perfusion

Anterior Circulation
Internal carotid artery (ICA) The dura, optic tract, basal ganglia, midbrain, uncus, lateral geniculate body,
pituitary gland, trigeminal ganglion, and tympanic cavity. Ophthalmic branch
supplies the eyes and orbits.
External carotid artery (ECA) All structures external to the skull, the larynx, and the thyroid.
Anterior cerebral artery (ACA) Medial and superior surface of frontal and parietal lobes. Medial striate branch
supplies anterior portion of the internal capsule, optic chiasm and nerve,
portions of the hypothalamus, and basal ganglia.
Middle cerebral artery (MCA) Lateral surface of the frontal, parietal, and occipital lobes, including the superior
and lateral surfaces of temporal lobes, posterior portion of the internal capsule,
and portions of the basal ganglia.
Posterior Circulation
Vertebral artery Medulla, dura of the posterior fossa, including the falx cerebri and tentorium
cerebelli.
Basilar artery Pons, and midbrain, internal ear, cerebellum.
Posterior inferior cerebellar artery Posterior and inferior surface of the cerebellum, and the choroid plexus
(PICA) of the fourth ventricle.
Anterior inferior cerebellar artery Anterior surface of the cerebellum, flocculus, and inferior vermis.
(AICA)
Superior cerebellar artery (SCA) Superior surface of the cerebellum and vermis.
Posterior cerebral artery (PCA) Occipital lobe and medial and lateral surfaces of the temporal lobes, thalamus,
lateral geniculate bodies, hippocampus, and choroid plexus of the third and
lateral ventricles.
Data from Rumbaugh CL,Wang A,Tsai FY (eds). Cerebrovascular Disease Imaging and Interventional Treatment Options. NewYork:
Igaku-Shoin Medical Publishers, 1995; Moore KI, DalleyAF (eds). Clinically Oriented Anatomy (4th ed). Baltimore: Lippincott Williams &
Wilkins, 1999; O’Sullivan SB, SchmitzTJ (eds). Physical Rehabilitation (5th ed). Philadelphia: FA Davis, 2007.

FIGURE 4-5
Cross-section of the spinal cord. Ant., Anterior; Lat., lateral; Post., posterior. (From Love RJ,Webb WG
[eds]. Neurology for the Speech-Language Pathologist [4th ed]. Boston: Butterworth-Heinemann,
2001;44.)
160 CHAPTER 4 Nervous System

Table 4-6 MAJOR ASCENDING AND DESCENDING WHITE MATTER TRACTS*

Tract Function
Fasciculus gracilis Sensory pathway for lower-extremity and lower-trunk joint proprioception,
vibration, two-point discrimination, graphesthesia, and double simultaneous
stimulation
Fasciculus cuneatus Sensory pathway for upper-extremity, upper-trunk, and neck joint
proprioception, vibration, two-point discrimination, graphesthesia, and
double simultaneous stimulation
Lateral spinothalamic Sensory pathway for pain, temperature, and light touch
Ventral spinocerebellar Sensory pathway for ipsilateral subconscious proprioception
Dorsal spinocerebellar Sensory pathway for ipsilateral and contralateral subconscious proprioception
Lateral corticospinal (pyramidal) Motor pathway for contralateral voluntary fine-muscle movement
Anterior corticospinal (pyramidal) Motor pathway for ipsilateral voluntary movement
Rubrospinal (extrapyramidal) Motor pathway for gross postural tone
Tectospinal (extrapyramidal) Motor pathway for contralateral gross postural muscle tone associated with
auditory and visual stimuli
Vestibulospinal (extrapyramidal) Motor pathway for ipsilateral gross postural adjustments associated with head
movements
*Sensory tracts ascend from the spinal cord; motor tracts descend from the brain to the spinal cord.
Data from Gilman S, Newman SW (eds). Manter and Gatz’s Essentials of Clinical Neuroanatomy and Neurophysiology (7th ed).
Philadelphia: FA Davis, 1989; Marieb EN (ed). Human Anatomy and Physiology (5th ed). San Francisco: Benjamin-Cummings, 2001.

Table 4-7 MAJOR PERIPHERAL NERVES OF THE UPPER EXTREMITY

Nerve Spinal Root Innervation

Dorsal scapular C5 Levator scapulae, rhomboid major and minor
Suprascapular C5 and C6 Supraspinatus, infraspinatus, and glenohumeral joint
Lower subscapular C5 and C6 Teres major and inferior portion of subscapularis
Upper subscapular C5 and C6 Superior portion of subscapularis
Axillary C5 and C6 Teres minor, deltoid, and glenohumeral joint
Radial C5, C6, C7, C8, and T1 Triceps, brachioradialis, anconeus, extensor carpi radialis longus and
brevis, supinator, extensor carpi ulnaris, extensor digitorum, extensor
digiti minimi, extensor indicis, extensor pollicis longus and brevis,
abductor pollicis brevis
Ulnar C8 and T1 Flexor digitorum profundus, flexor carpi ulnaris, palmaris brevis,
abductor digiti minimi, flexor digiti minimi brevis, opponens digiti
minimi, palmar and dorsal interossei, third and fourth lumbricals
Median C6, C7, C8, and T1 Pronator teres, flexor carpi radialis, palmaris longus, flexor digitorum
superficialis and profundus, flexor pollicis longus, pronator
quadratus, abductor pollicis brevis, opponens pollicis, flexor pollicis
brevis, first and second lumbricals
Musculocutaneous C5, C6, and C7 Coracobrachialis, brachialis, biceps
Data from Netter FH (ed). Atlas of Human Anatomy. Summit City, NJ: CIBAGEIGY Corporation, 1989; Moore KL and DalleyAF (eds).
Clinically Oriented Anatomy (4th ed), Baltimore: Lippincott Williams & Wilkins, 1999.
 Nervous System CHAPTER 4 161

Table 4-8 MAJOR PERIPHERAL NERVES OF THE Table 4-9 MAJOR PERIPHERAL NERVES OF THE
LOWER EXTREMITY TRUNK

Nerve Spinal Root Innervation Nerve Spinal Root Innervation

Femoral L2, L3, and L4 Iliacus Spinal accessory C3 and C4 Trapezius
Psoas major Phrenic C3, C4, and C5 Diaphragm
Sartorius
Pectinous Long thoracic C5, C6, and C7 Serratus anterior
Rectus femoris Medial pectoral C6, C7, and C8 Pectoralis minor
Vastus lateralis, and major
intermedius, and Lateral pectoral C7, C8, and T1 Pectoralis major
medialis
Thoracodorsal C7 and C8 Latissimus dorsi
Articularis genu
Intercostal Corresponds to External
Obturator L2, L3, and L4 Obturator externus
nerve root level intercostals
Adductor brevis, longus,
Internal
and magnus
intercostals
Gracilis
Levatores
Pectineus
costarum longi
Superior L4, L5, and S1 Gluteus medius and and brevis
gluteal minimus
Iliohypogastric L1 Transversus
Tensor fasciae latae
and abdominis
Inferior L5, S1, and S2 Gluteus maximus ilioinguinal Internal
gluteal abdominal
Sciatic L4, L5, S1, Biceps femoris oblique
S2, and S3 Adductor magnus
Semitendinosus
Semimembranosus
Tibial L4, L5, S1, S2, Gastrocnemius
and S3 Soleus
Flexor digitorum mental status examination; vital sign measurement;
longus vision, motor, sensory, and coordination testing; and
Tibialis posterior diagnostic testing.
Flexor hallucis longus
Common L4, L5, S1, Peroneus longus and
peroneal and S2 brevis Patient History
Tibialis anterior A detailed history, initially taken by the physician, is
Extensor digitorum
often the most helpful information used to delineate
longus
Extensor hallucis longus whether a patient presents with a true neurologic
Extensor hallucis brevis event or another process (usually cardiac or metabolic
Extensor digitorum in nature). The history may be presented by the patient
brevis or, more commonly, by a family member or person wit-
nessing the acute or progressive event(s) responsible
for hospital admission. One common framework for
organizing questions regarding each neurologic com-
plaint, sign, or symptom is as follows14,15:
NEUROLOGIC EXAMINATION  What is the patient feeling?
 When did the problem initially occur, and has it
The neurologic examination is initiated on hospital progressed?
admission or in the field and is reassessed contin-  What relieves or exacerbates the problem?
uously, hourly, or daily, as necessary. The neurologic  What are the onset, frequency, and duration of signs
examination consists of patient history; observation; or symptoms?
162 CHAPTER 4 Nervous System

FIGURE 4-6
Dermatome chart based on embryologic segments. (From Maitland GD [ed].Vertebral Manipulation
[5th ed]. Oxford, UK: Butterworth-Heinemann, 1986;46.)

In addition to the general medical record review

(see Appendix I-A), questions relevant to a complete
neurologic history include:
 Does the problem involve loss of consciousness?
 Did a fall precede or follow the problem?
 Is there headache, dizziness, or visual disturbance?
 What are the functional deficits associated with the
problem?
 Is there an alteration of speech?
 Does the patient demonstrate memory loss or
altered cognition?
 Does the patient have an altered sleep pattern?
 What is the handedness of the patient? (Handedness
is a predictor of brain [language] dominance.)
Observation
Data that can be gathered from close or distant obser-
vation of the patient include the following:
 Level of alertness, arousal, distress, or the need for
restraint
 Body position
 Head, trunk, and extremity posture, including
movement patterns
 Amount and quality of active movement
 Amount and quality of interaction with the environ-
ment or family members
 Degree of ease or difficulty with activities of daily
living

 Presence of involuntary movements, such as tremor
 Eye movement(s)
 Presence of hemibody or hemispace neglect
 Presence of muscle atrophy
 Respiratory rate and pattern
 Facial expression and symmetry
CLINICAL TIP
 The therapist should correlate these observations
with other information from the chart review and
other health care team members to determine (1) if
the diagnosis is consistent with the physical
presentation, (2) what types of commands or tone of
voice to use, (3) how much assistance is needed, and
(4) how to prioritize the portions of the physical
therapy evaluation.
Mental Status Examination
The mental status examination includes assessment of
level of consciousness, cognition, emotional state,
memory, and speech and language ability.
LEVEL OF CONSCIOUSNESS
Consciousness consists of arousal and the awareness of
self and environment, including the ability to interact
appropriately in response to any normal stimulus.16
Coma is often considered the opposite of conscious-
ness. Table 4-10 describes the different states of
consciousness. Evaluating a patient’s level of conscious-
ness is important because it serves as a baseline to
monitor stability, improvement, or decline in the
patient’s condition. It also helps to determine the
severity and prognosis of neurologic insult or disease
state, thus directing the medical plan of care.
CLINICAL TIP
 Level of consciousness is often vaguely described in
medical charts; therefore, be specific when
documenting a patient’s mental status. Describe the
intensity of stimulus needed to arouse the patient,
the patient’s best response, and the patient’s
response to the removal of the stimulus.16
 Changes in body position, especially the transition
from a recumbent position to sitting upright, often
stimulate increased alertness. Other stimuli to
increase alertness include daylight, radio or
television sound, or a cold cloth on the forehead.
Nervous System CHAPTER 4 163
 Use a progressive intensity of stimuli to arouse
a patient with decreased alertness or level of
consciousness. For example, call the patient’s name
in a normal tone of voice before using a loud tone
of voice, or tap the patient’s shoulder before
rubbing the shoulder.
 Time of day, fatigue, and side effects of medication
are factors that can cause variable levels of alertness
or participation in physical therapy. The
documentation of these factors is important for
communication among the health care team and
for the rehabilitation screening process.
 A & O  3 is a common abbreviation for alert and
oriented to person, place, and time. The number
may be modified to reflect the patient’s orientation
(e.g., A & O  1 [self]). A & O  4 may also be
used to identify the fact that the patient is oriented
to the situation.
GLASGOW COMA SCALE. The Glasgow Coma Scale
(GCS) is a widely accepted measure of level of
consciousness and responsiveness and is described in
Table 4-11. The GCS evaluates best eye opening (E),
motor response (M), and verbal response (V).
To determine a patient’s overall GCS, add each score
(i.e., E + M + V). Scores range from 3 to 15. A score of
8 or less signifies coma.17
CLINICAL TIP
 Calculation of the GCS usually occurs at regular
intervals. The GCS should be used to confirm the
type and amount of cueing needed to communicate
with a patient, determine what time of day a patient
is most capable of participating in physical therapy,
and delineate physical therapy goals.
COGNITION
Cognitive testing includes the assessment of attention,
orientation, memory, abstract thought, and the abil-
ity to perform calculations or construct figures.
General intelligence and vocabulary are estimated
with questions regarding history, geography, or cur-
rent events. Table 4-12 lists typical methods of test-
ing the components of cognition.
EMOTIONAL STATE
Emotional state assessment entails observation and
direct questioning to ascertain a patient’s mood,
164 CHAPTER 4 Nervous System
Table 4-10 NORMAL AND ABNORMAL STATES
OF CONSCIOUSNESS
Alert Completely awake.
Attentive to normal levels of
stimulation.
Able to interact meaningfully
with clinician.
Lethargic or Arousal with stimuli.
somnolent Falls asleep when not stimulated.
Decreased awareness.
Loss of train of thought.
Obtunded Difficult to arouse.
Requires constant stimulation to
maintain consciousness.
Confused when awake.
Interactions with clinicians may be
largely unproductive.
Stupor Arousal only with strong, generally
(semicoma) noxious stimuli and returns to
unconscious state when
stimulation is stopped.
Patient is unable to interact with
clinician.
Coma (deep Unarousable to any type of stimulus.
coma) Reflex motor responses may or may
not be seen.
Delirium State of disorientation marked by
irritability or agitation, suspicion
and fear, and misperception
of stimuli.
Patient demonstrates offensive, loud,
and talkative behaviors.
Dementia Alteration in mental processes
secondary to organic disease that
is not accompanied by a change
in arousal.
affect, perception, and thought process, as well as to
evaluate for behavioral changes. Evaluation of emotion
is not meant to be a full psychiatric examination;
however, it provides insight as to how a patient may
complete the cognitive portions of the mental status
examination.18
CLINICAL TIP
 It is important to note that a patient’s culture may
affect particular emotional responses.
 It is also important to be aware that patients who
recently have had a stroke or have a history of
Table 4-11 GLASGOW COMA SCALE
Response Score
Eye opening (E)
Spontaneous: eyes open without 4
stimulation
To speech: eyes open to voice 3
To pain: eyes open to noxious stimulus 2
Nil: eyes do not open despite variety of 1
stimuli
Motor response (M)
Obeys: follows commands 6
Localizes: purposeful attempts to move 5
limb to stimulus
Withdraws: flexor withdrawal without 4
localizing
Abnormal flexion: decorticate 3
posturing to stimulus
Extensor response: decerebrate 2
posturing to stimulus
Nil: no motor movement 1
Verbal response (V)
Oriented: normal conversation 5
Confused conversation: vocalizes in 4
sentences, incorrect context
Inappropriate words: vocalizes with 3
comprehensible words
Incomprehensible words: vocalizes with 2
sounds
Nil: no vocalization 1
Data fromJennett B,Teasdale G (eds). Management of Head
Injuries. Philadelphia: FA Davis, 1981.
stroke can be emotionally labile depending on the
site of the lesion. This can be quite stressful for
patients because they feel that they have little
control over their emotions.
 Be aware that chronic disease can result in
depression that may or may not be obvious to
the therapist.
SPEECH AND LANGUAGE ABILITY
The physician should perform a speech and language
assessment as soon as possible according to the patient’s

Table 4-12 TESTS OF COGNITIVE FUNCTION
Cognitive Function Definition
Attention Ability to attend to a specific stimulus
or task
Orientation Ability to orient to person, place,
and time
Memory Immediate recall
Short-term memory
Long-term memory
Calculation Ability to perform verbal or written
mathematical problems
Construction Ability to construct a two- or
three-dimensional figure or shape
Abstraction Ability to reason in an abstract rather
than a literal or concrete fashion
Judgment Ability to reason (according to age
and lifestyle)
Data from Bickley LS, Hoekelman RA (eds). Bate’s Guide to Physical Examination and HistoryTaking (7th ed). Philadelphia: Lippincott,1999.
level of consciousness. The main goals of this assess-
ment are to evaluate the patient’s ability to articulate
and produce voice and the presence, extent, and severity
of aphasia.19 These goals are achieved by testing
comprehension and repetition of spoken speech,
naming, quality and quantity of conversational speech,
and reading and writing abilities.19
A speech-language pathologist is often consulted
to perform a longer, more in-depth examination of
cognition, speech, and swallow using standardized
tests and skilled evaluation of articulation, phonation,
hearing, and orofacial muscle strength testing.
CLINICAL TIP
 The physical therapist should be aware of and use,
as appropriate, the speech-language pathologist’s
suggestions for types of commands, activity
modification, and positioning as related to risk of
aspiration.
 The physical therapist is often the first clinician to
notice the presence or extent of speech or language
dysfunction during activity, especially during higher-
level tasks or those activities that cause fatigue. The
physical therapist should report these findings to
other members of the health care team.
Nervous System CHAPTER 4 165
Task
Repetition of a series of numbers or letters
Spelling words forward and backward
Identify name, age, current date and season,
birth date, present location, town, etc.
Recount three words after a few seconds
Recount words (after a few minutes) or recent
events
Recount past events
Add, subtract, multiply, or divide whole
numbers
Draw a figure after a verbal command or
reproduce a figure from a picture
Interpret proverbs
Discuss how two objects are similar or different
Demonstrate common sense and safety
 Be sure to allow the patient ample time to respond
to a command or a question. Slowed response time
can be mistaken for aphasia.
Vital Signs
The brain is the homeostatic center of the body; there-
fore, vital signs are an indirect measure of neurologic
status and the body’s ability to perform basic functions,
such as respiration and temperature control.
Blood pressure, heart rate, respiratory rate and pat-
tern (see Table 2-3), temperature, and other vital signs
from invasive monitoring (see Appendix III-A) are
assessed continuously or hourly to determine neuro-
logic and hemodynamic stability.
CLINICAL TIP
 The therapist should be aware of blood pressure
parameters determined by the physician for the
patient with neurologic dysfunction. These
parameters may be set greater than normal to
maintain adequate perfusion to the brain or lower
than normal to prevent further injury to the brain.
166 CHAPTER 4 Nervous System
 It is important for the therapist to be aware of
vital sign trends (especially blood pressure) in the
neurologic patient over the course of the day(s).
An increase or decrease in blood pressure over time
may be intentional and related to medication
changes, or it may be unrelated to medication
changes. A change unrelated to medication (or
intravenous fluid administration) may be related to
neurologic decline due to increased intracranial
pressure. Trends in vital signs should be used by
the clinician to determine the safety of physical
therapy intervention.
Cranial Nerves
Cranial nerves (CN) testing provides information about
the general neurologic status of the patient and the
function of the special senses. The results assist in the
differential diagnosis of neurologic dysfunction and
may help in determining the location of a lesion. CNs
I through XII are tested on admission, daily in the hos-
pital, or when there is a suspected change in neurologic
function (Table 4-13).
Vision
Vision testing is an important portion of the neurologic
examination, because alterations in vision can indicate
neurologic lesions, as illustrated in Figure 4-7. In addi-
tion to the visual field, acuity, reflexive, and ophthal-
moscopic testing performed by the physician during
CN assessment, the pupils are further examined for
size and equality, shape, and reactivity.
 Size and equality. Pupil size is normally 2 to 4 mm or
4 to 8 mm in diameter in the light and dark, respec-
tively.20 The pupils should be of equal size, although
up to a 1-mm difference in diameter can normally
occur between the left and right pupils.21
 Shape. Pupils are normally round but may bec-
ome oval or irregularly shaped with neurologic
dysfunction.
 Reactivity. Pupils normally constrict in response to
light, as a consensual response to light shown in the
opposite eye or when fixed on a near object.
Conversely, pupils normally dilate in the dark.
Constriction and dilation occur briskly under
normal circumstances. A variety of deviations of
pupil characteristics can occur. Pupil reactivity can
be tested by shining a light directly into the patient’s
eye. Dilated, nonreactive (fixed), malpositioned,
or disconjugate pupils can signify very serious
neurologic conditions (especially oculomotor com-
pression, increased intracranial pressure [ICP], or
brain herniation).21
CLINICAL TIP
 Note any baseline pupil changes, such as those
associated with cataract repair (keyhole shape).
 If the patient’s vision or pupil size or shape changes
during physical therapy intervention, discontinue the
treatment and notify the nurse or physician
immediately.
 For a patient with diplopia (double vision), a cotton
or gauze eye patch can be worn temporarily over
one eye to improve participation during physical
therapy sessions.
 PERRLA is an acronym that describes pupil function:
pupils equal, round, and reactive to light and
accommodation.
The presence of nystagmus during the visual exam
should also be noted. Nystagmus is an involuntary
rhythmic movement of the eyes, which may be present
at rest or occur with eye or head movements.22
Nystagmus can be the result of vestibular dysfunction,
a cerebellar lesion, or an imbalance in the reflex activ-
ity coordinating the two. While observing nystagmus,
it is important to note the orientation (vertical versus
horizontal), direction (right versus left) and head
motions that increase the nystagmus. This will aid
the clinician in determining the cause. Nystagmus
involving the tracts/reflexes between the vestibular
system and cerebellum is usually horizontal in nature
and more pronounced when looking to the side of
the lesion.22 Vertical nystagmus is usually present
with lesions involving the anterior vermis of the cere-
bellum or medulla and indicates a poor prognosis for
recovery. Spontaneous (at rest) nystagmus is most
often observed after an acute unilateral insult to the
vestibular system.11
CLINICAL TIP
 One treatment technique to reduce nystagmus or
associated vertigo during mobility is to use gaze
stabilization. Direct the patient to look at a certain
point or object directly in front of him or her during
a transfer or during ambulation to avoid lateral
head movements.
 Nervous System CHAPTER 4 167

Table 4-13 ORIGIN, PURPOSE, AND TESTING OF THE CRANIAL NERVES

Nerve/Origin Purpose How to Test Signs/Symptoms of Impairment
Olfactory (CN I)/ Sense of smell Have the patient close one nostril, Anosmia.
cerebral cortex and ask the patient to sniff a mild-
smelling substance and identify it.
Optic (CN II)/ Central and peripheral Acuity: Have the patient cover one Blindness, myopia, presbyopia.
thalamus vision eye, and ask the patient to read
a visual chart.
Fields: Have the patient cover one eye, Homonymous hemianopsia.
and hold an object (e.g., pen cap) at
arm’s length from the patient in his
or her peripheral field. Hold the
patient’s head steady. Slowly move
the object centrally, and ask the
patient to state when he or she
first sees the object.
Repeat the process in all quadrants.
Oculomotor (CN Upward, inward, and CNs III, IV, and VI are tested together. Ophthalmoplegia with eye
III)/midbrain inferomedial eye Saccadic (patient is asked to look in deviation downward and
movement each direction) and pursuit (patient outward.
follows moving finger) eye Strabismus causing diplopia.
movements should both be tested.
Eyelid elevation Ask the patient to open eyes wide Ptosis
Pupil constriction Pupil reaction to light: Shine a Loss of ipsilateral pupillary
Visual focusing flashlight into one eye and observe light and accommodation
bilateral pupil reaction. reflexes.
Gaze: Hold object (e.g., pen) at arm’s
length from the patient, and hold the
patient’s head steady. Ask the patient
to follow the object with a full
horizontal, vertical, and diagonal
gaze.
Trochlear (CN Inferolateral eye See Oculomotor (CN III), above. Diplopia.
IV)/midbrain movement Head tilt to unaffected side.
Weakness in depression of
ipsilateral adducted eye.
Trigeminal (CN Sensation of face Conduct touch, pain, and temperature Loss of facial sensation.
V)/pons sensory testing over the patient’s face.
Mastication Observe for deviation of jaw. Ipsilateral deviation of opened
jaw.
Corneal reflex Wisp of cotton on the patient’s Loss of ipsilateral corneal
cornea. reflex.
Jaw jerk* Palpate masseter as the patient
clamps his or her jaw.
Abducens (CN Lateral eye movement and See Oculomotor (CN III), above. Diplopia.
VI)/pons proprioception Convergent strabismus.
Ipsilateral abductor paralysis.
*Rarely tested. Continued
Continued
168 CHAPTER 4 Nervous System

Table 4-13 ORIGIN, PURPOSE, AND TESTING OF THE CRANIAL NERVES—cont’d

Nerve/Origin Purpose How to Test Signs/Symptoms of Impairment
Facial (CN VII)/ Facial expression Ask the patient to smile, wrinkle brow, Paralysis of ipsilateral upper
pons purse lips, and close eyes tightly. and lower facial muscles,
Inspect closely for symmetry. resulting in inability to close
eye, facial droop, and/or
difficulty with speech
articulation.
Taste (anterior two-thirdsAsk patient to differentiate between Loss of taste on ipsilateral
of tongue) saline and sugar solutions applied two-thirds of tongue.
to the tongue with a cotton swab.
Autonomic innervation Introduce a stimulus to produce tears Loss of lacrimation, dry
of lacrimal and salivary such as exposing patient to a cut mouth.
glands onion.
Vestibulocochlear Vestibular branch: sense Oculocephalic reflex (Doll’s eyes): Vertigo, nystagmus,
(CN VIII)/ of equilibrium Rotate the patient’s head and watch dysequilibrium
pons Cochlear branch: sense for eye movement. (Normal: eyes will Deafness, impaired hearing,
of hearing move in the opposite direction of the tinnitus.
head prior to return to midline). Unilateral conductive loss: sound
Test balance: vestibulospinal function lateralized to impaired ear.
Test auditory acuity. Sensorineural loss: sound heard
Weber test:Vibrate a tuning fork, in good ear.
place it on the mid forehead, and Conductive loss: sound heard
ask the patient if sound is heard through bone is equal to or
louder in one ear. longer than air.
Rinne test:Vibrate a tuning fork on Sensorineural loss: sound heard
the mastoid bone, then close to ear through air is longer.
canal; sound heard longer through
air than bone.
Glossopharyngeal Gag reflex Test CNs IX and X together. Loss of gag reflex.
(CN IX)/ Motor and proprioception Induce gag with tongue depressor Dysphagia.
medulla of superior pharyngeal (one side at a time). Dry mouth.
muscle Patient phonates a prolonged vowel Loss of taste to ipsilateral
Autonomic innervation sound or talks for an extended one-third of tongue.
of salivary gland period of time. Impaired sensation to
Taste (posterior one-third Listen for voice quality and pitch. ipsilateral ear.
of tongue) Ask patient to differentiate between
Sensation from the saline and sugar solutions applied
external auditory to the tongue with a cotton swab.
meatus and skin Test sensation in posterior ear.
of posterior ear
Blood pressure regulation
Vagus (CN X)/ Swallowing See Glossopharyngeal (CN IX), above. Dysphagia.
medulla Palatal pharynx control Have patient say ‘‘ah’’; observe motion Soft palate paralysis,
Parasympathetic of soft palate (elevates) and position contralateral deviation of
innervation of heart, of uvula (remains midline). uvula, hoarseness.
lungs, and abdominal
viscera
Spinal accessory Motor control of the Ask patient to rotate the head or shrug LMN: weakness with head
(CN XI)/C1-C5 trapezius and the shoulders. Offer gentle resistance turning to contralateral side
sternocleidomastoid to movement. and ipsilateral shoulder
muscles shrug.
 Table 4-13 ORIGIN, PURPOSE, AND TESTING OF THE CRANIAL NERVES—cont’d

Nerve/Origin Purpose How to Test Signs/Symptoms of Impairment

UMN: weakness with head
turning to ipsilateral side and
contralateral shoulder shrug.
Hypoglossal (CN Movement and Ask the patient to stick out his or her Ipsilateral deviation of tongue
XII)/medulla proprioception of tongue, observe for midline, and ask during protrusion.
tongue for chewing patient to move side-to-side. Dysarthria.
and speech Listen for articulation problems.
CN, Cranial nerve.
Data from Lindsay KW, Bone I, Callander R (eds). Neurology and Neurosurgery Illustrated (2nd ed). Edinburgh, UK: Churchill
Livingstone, 1991; Marieb EN (ed). Human Anatomy and Physiology (5th ed). San Francisco: Benjamin-Cummings, 2001; McNeill ME (ed).
Neuroanatomy Primer. Baltimore: Lippincott Williams & Wilkins, 1997; O’Sullivan SB, SchmitzTJ (eds). Physical Rehabilitation (5th ed).
Philadelphia: FA Davis, 2007.

FIGURE 4-7
Visual pathway with lesion sites and resulting visual field defects.The occipital lobe has been cut away to
show the medial aspect and the calcarine sulci. (From Love RJ,Webb WG [eds]. Neurology for the
Speech-Language Pathologist [4th ed]. Boston: Butterworth-Heinemann, 2001;103.)
170 CHAPTER 4 Nervous System
Motor Function
The evaluation of motor function consists of strength,
tone, and reflex testing.
STRENGTH TESTING
Strength is the force output of a contracting muscle
directly related to the amount of tension that it can pro-
duce.23 Strength can be graded in the following ways
in the acute care setting:
 Graded 0-5/0-N (normal) with manual muscle
testing
 Graded as strong or weak with resisted isometrics
 Graded by the portion of a range of motion in
which movement occurs (e.g., hip flexion through
one-fourth of available range)
 Graded functionally
CLINICAL TIP
 The manner in which muscle strength is tested
depends on the patient’s ability to follow
commands, arousal, cooperation, and activity
tolerance, as well as on constraints on the patient,
such as positioning, sedation, and medical
equipment.
 If it is not possible to grade strength in any of the
described ways, then only the presence, frequency,
and location of spontaneous movements are noted
instead.
MUSCLE TONE
Muscle tone has been described in a multitude of ways;
however, neither a precise definition nor a quantitative
measure has been determined.24 It is beyond the scope
of this book to discuss the various definitions of tone,
including variants such as clonus and tremor. For
simplicity, muscle tone is discussed in terms of hyperto-
nicity, hypotonicity, or dystonia. Hypertonicity, an
increase in muscle contractility, includes spasticity
(velocity-dependent increase in resistance to passive
stretch) and rigidity (increased uniform resistance that
is present throughout the whole range of motion and
is independent of velocity) secondary to a neurologic
lesion of the CNS or upper motor neuron system.11
Hypotonicity, a decrease in muscle contractility,
includes flaccidity (diminished resistance to passive
stretching and tendon reflexes)25 from a neurologic
lesion of the lower motor neuron system (or as in the
early stage of spinal cord injury [SCI] known as spinal
shock). Dystonia, a hyperkinetic movement disorder,
is characterized by disordered tone and involuntary
movements involving large portions of the body result-
ing from a lesion in the basal ganglia (as in Parkinson’s
disease with excessive L-dopa therapy).11 Regardless of
the specific definition of muscle tone, clinicians agree
that muscle tone may change according to a variety of
factors, including stress, febrile state, pain, body posi-
tion, medical status, medication, CNS arousal, and
degree of volitional movement.11
Muscle tone can be evaluated qualitatively in the
following ways:
 Passively as mild (i.e., mild resistance to movement
with quick stretch), moderate (i.e., moderate resis-
tance to movement, even without quick stretch),
or severe (i.e., resistance great enough to prevent
movement of a joint)26
 Passively or actively as the ability or inability to
achieve full joint range of motion
 Actively as the ability to complete functional mobil-
ity and volitional movement
 As abnormal decorticate (flexion) or decerebrate
(extension) posturing. (Decortication is the result of
a hemispheric or internal capsule lesion that results
in a disruption of the corticospinal tract.21
Decerebration is the result of a brain stem lesion
and is thus considered a sign of deteriorating neuro-
logic status.21 A patient may demonstrate one or
both of these postures.)
 Numerically, using the Modified Ashworth Scale as
described in Table 4-14. This scale is considered
the ‘‘gold standard’’ because of its high interrater
(0.84) and intrarater (0.83) reliability.27
REFLEXES
A reflex is a motor response to a sensory stimulus and
is used to assess the integrity of the motor system in
the conscious or unconscious patient. The reflexes
most commonly tested are deep tendon reflexes
(DTRs). A DTR should elicit a muscle contraction of
the tendon stimulated. Table 4-15 describes DTRs
according to spinal level and expected response. DTR
testing should proceed in the following manner:
1. The patient should be sitting or supine and as relaxed
as possible.
2. The joint to be tested should be in midposition to
stretch the tendon.
3. The tendon is then directly tapped with a reflex
hammer. Both sides should be compared.
 Nervous System CHAPTER 4 171

Table 4-14 MODIFIED ASHWORTH SCALE FOR Table 4-16 DEEP TENDON REFLEX GRADES
GRADING ABNORMAL TONE AND INTERPRETATION

Grade Description Grade Response Interpretation

0 No increase in muscle tone. 0 No response Abnormal
1 Slight increase in muscle tone, manifested 1+ Diminished or Low normal
by a slight catch and release or by minimal sluggish response
resistance at the end of the range of motion 2+ Active response Normal
when the affected part(s) is moved in flexion 3+ Brisk response High normal
or extension. 4+ Very brisk response, Abnormal
1+ Slight increase in muscle tone, manifested by with or without
a catch, followed by minimal resistance clonus
throughout the remainder (less than half)
of the range of motion. Data from Bickley LS, Hoekelman RA. Bate’s Guide to Physical
Examination and HistoryTaking (7th ed). Philadelphia:
2 More marked increased in muscle tone through
Lippincott, 1999.
most of the range of motion, but affected
part(s) easily moved.
3 Considerable increase in muscle tone; passive
movement difficult.
4 Affected part(s) rigid in flexion and extension.
From: Bohannon RW, Smith MB. Interrater Reliability
of a Modified Ashworth Scale of Muscle Spasticity. PhysTher CLINICAL TIP
1987;67:206.  The numeric results of DTR testing may appear in a
stick figure drawing in the medical record. The DTR
grades are placed next to each of the main DTR
sites. An arrow may appear next to the stick figure
as well. Arrows pointing upward signify
Reflexes are typically graded as present (normal, hyperreflexia; conversely, arrows pointing downward
exaggerated, or depressed) or absent. Reflexes can signify hyporeflexia.
also be graded on a scale of 0 to 4, as described in
Table 4-16. Depressed reflexes signify lower motor A superficial reflex should elicit a muscle contraction
neuron disease or neuropathy. Exaggerated reflexes sig- from the cornea, mucous membrane, or area of the skin
nify upper motor neuron disease, or they may be due that is stimulated.The most frequently tested superficial
to hyperthyroidism, electrolyte imbalance, or other reflexes are the corneal (which involve CNs Vand VII),
metabolic abnormalities.28 gag and swallowing (which involve CNs IX and X), and
perianal reflexes (which involve S3-S5). These reflexes
are evaluated by physicians and are graded as present or
absent. Superficial reflexes may also be recurrent primi-
tive reflexes that are graded as present or absent. The
most commonly tested cutaneous reflex is the Babinski
Table 4-15 DEEP TENDON REFLEXES OF THE sign. A positive (abnormal) Babinski sign is great-toe
UPPER AND LOWER EXTREMITIES extension with splaying of the toes in response to
stroking the lateral plantar surface of the foot with the
Reflex Spinal Level Normal Response opposite end of a reflex hammer. It indicates corticospi-
Biceps C5 Elbow flexion nal tract damage. Other primitive reflexes that can be
Brachioradialis C6 Elbow flexion tested are flexor withdrawal and plantar or palmar
Triceps C7 Elbow extension grasp. These are all reflexes normally seen in infants
Patellar L4 Knee extension that become integrated at an early age. The presence
Posterior tibialis L5 Plantar flexion and of any of these three reflexes in an adult is abnormal
inversion and usually indicates significant UMN lesion or brain
Achilles S1 Plantar flexion
injury.
172 CHAPTER 4 Nervous System

the area being tested. Table 4-17 outlines the method

CLINICAL TIP
 A positive Babinski sign may be noted in a patient’s
chart as ‘‘upgoing toe(s) on the right (or left).’’
 Be aware when trying to determine if a patient is
able to follow commands; if the clinician asks a
patient to squeeze his or her hand, then the result is
not a primitive reflex (palmar grasp). If the patient
does squeeze the clinician’s hand, then ask him or
her to release it. This will be a better indicator if the
patient is truly following commands.
of sensation testing by stimulus.
CLINICAL TIP
 Before completing the sensory examination, the
physical therapist should be sure that the patient
can correctly identify stimuli (e.g., that a pinprick
feels like a pinprick).
 If more primitive sensation (such as light touch) is
not intact, then it may not be advisable to proceed
with the more complex sensation testing, such as
graphesthesia or two-point discrimination.

SENSATION
Sensation testing evaluates the ability to sense light
touch, proprioception, pressure, temperature, vibra-
tion sense, and pain. For each modality, the face, neck,
trunk, and extremities are tested bilaterally, proceeding
in a dermatomal pattern (see Figure 4-6). For more
reliable sensation testing results, the patient should
be asked to close his or her eyes or look away from
COORDINATION
Although each lobe of the cerebellum has its own
function, coordination tests cannot truly differentiate
among them. Coordination tests evaluate the presence
of ataxia (general incoordination), dysmetria (over-
shooting), and dysdiadochokinesia (inability to per-
form rapid alternating movements) with arm, leg, and

Table 4-17 SENSATION TESTING

Sensation Modality and Method

Pain Touch a pin or pen cap over the extremities or trunk. Ask the patient to distinguish
between dull (pen cap) or sharp (the pin) stimuli.
Pressure Using the therapist’s fingertip, apply pressure on the skin surface that is firm enough to
indent the skin and stimulate the deep receptors.The patient is asked to identify if there
is a stimulus present.
Light touch Apply light touch with the finger, a cotton ball, or washcloth over the extremities or trunk.
The patient is asked to identify if there is a stimulus present.
Proprioception Lightly grasp the distal interphalangeal joint of the patient’s finger or great toe, and move
the joint slowly up and down. Ask the patient to state in which direction the joint is
moved.Test distal to proximal (e.g., toe to ankle to knee).
Vibration Activate a tuning fork and place on a bony prominence. Ask the patient to state when the
vibration slows and stops. Proceed distal to proximal.
Temperature Place test tubes filled with warm or cold water on the area of the patient’s body to be tested.
Ask the patient to state the temperature. (Rarely done in the acute care setting.)
Stereognosis Place a familiar object in the patient’s hand and ask the patient to identify it.
Two-point discrimination Place two-point caliper or drafting compass on area to be tested. Ask the patient
to distinguish whether it has one or two points.
Graphesthesia Trace a letter or number in the patient’s open palm and ask the patient to state what was
drawn.
Double simultaneous Simultaneously touch two areas on the same side of the patient’s body. Ask patient to locate
stimulation and distinguish both points.
Data from Lindsay KW, Bone I, Callander R (eds). Neurology and Neurosurgery Illustrated (2nd ed). Edinburgh, UK: Churchill
Livingstone, 1991; Gilman S, Newman SW (eds). Manter and Gatz’s Essentials of Clinical Neuroanatomy and Neurophysiology (7th ed).
Philadelphia: FA Davis, 1989; HickeyJV (ed).The Clinical Practice of Neurological and Neurosurgical Nursing (4th ed). Philadelphia:
Lippincott, 1997.
 Nervous System CHAPTER 4 173

Table 4-18 COORDINATION TESTS

Test Method Impairment
Upper Extremity
Finger to nose Ask the patient to touch his or her nose.Then, ask patient Dysmetria
to touch his or her nose and then touch your finger Intention tremor
(which should be held an arm’s length away). Ask the
patient to repeat this rapidly.
Finger opposition Ask the patient to touch the thumb to each finger in sequence, Dysmetria
gradually increasing the speed. Intention tremor
Supination and Ask the patient to rapidly and alternately supinate and pronate Dysdiadochokinesia
pronation his or her forearms
Tapping Ask the patient to rapidly tap his or her hands on a surface Dysdiadochokinesia
simultaneously, alternately, or both.
Arm bounce Have the patient flex his or her shoulder to 90 degrees with Cerebellar
elbow fully extended and wrist in the neutral position; dysfunctionçimpaired
then apply a brief downward pressure on the arm. postural stability
(Excessive swinging of the arm indicates a positive test.)
Rebound Ask the patient to flex his or her elbow to approximately Cerebellar
phenomenon 45 degrees. Apply resistance to elbow flexion; then suddenly dysfunctionçimpaired
release the resistance. (Striking of the face indicates a postural stability
positive test.) Tricep weakness
Lower Extremity
Heel to shin Ask the patient to move his or her heel up and down the Dysmetria
opposite shin and repeat rapidly.
Tapping Ask the patient to rapidly tap his or her feet on the floor Dysdiadochokinesia
simultaneously, alternately, or both.
Romberg test Ask the patient to stand (heels together) with eyes open. Inability to maintain balance
Observe for swaying or loss of balance. Repeat with when the eyes are closed
eyes closed. is a positive test indicating
a loss of proprioception.
Gait Ask the patient to walk. Observe gait pattern, posture, Ataxia
and balance. Repeat with tandem walking to
exaggerate deficits.
Data from GilroyJ (ed). Basic Neurology (3rd ed). NewYork: McGraw-Hill, 2000; and O’Sullivan SB, SchmitzTJ (eds). Philadelphia: FA
Davis, 2007.

trunk movements, as well as with gait.15 The results of

each test (Table 4-18) are described in terms of the
patient’s ability to complete the test, accuracy, regularity
of rhythm, and presence of tremor.29
Another test is the pronator drift test, which is used
to qualify loss of position sense. While the patient is
sitting or standing, he or she flexes both shoulders
and extends the elbows with the palms upward. The
patient is then asked to close his or her eyes. The fore-
arm is observed for 10 to 20 seconds for (1) pronation
or downward drift, which suggests a contralateral
corticospinal lesion, or (2) an upward or sideward
drift, which suggests loss of position sense.30
DIAGNOSTIC PROCEDURES
A multitude of diagnostic tests and procedures is used
to evaluate, differentiate, and monitor neurologic dys-
function. Each has its own cost, accuracy, advantages,
and disadvantages. For the purposes of this text, only
the procedures most commonly used in the acute care
setting are described.
X-Ray
X-rays can provide anterior, posterior, lateral, and base
views of the skull that are used to assess the presence
174 CHAPTER 4 Nervous System
of calcification, bone erosion, or fracture, especially
after head or facial trauma or if a tumor is suspected.31
Anterior, lateral, posterior, and oblique views of the
cervical, thoracic, lumbar, and sacral spine are used to
assess the presence of bone erosion, fracture, disloca-
tion, spondylosis, spur, or stenosis, especially after
trauma or if there are motor or sensory deficits.21,32
X-rays are a quick way to screen for serious injury in
the trauma victim, but this method of imaging is
quickly being replaced by computed tomography
and/or magnetic resonance imaging.
Computed Tomography
Computed tomography (CT) is a series of successive
x-ray films put together and analyzed by a computer
to provide a three-dimensional view of the body
part being imaged. The CT image of the brain is
taken in the sagittal or coronal planes and is used
to identify such abnormalities as neoplasm, cortical
atrophy, cerebral aneurysm, intracranial hemorrhage,
arteriovenous malformation (AVM), cerebral infarc-
tion, and ventricular displacement or enlargement.33
Head CT is the preferred neuroimaging test for the
evaluation of acute cerebrovascular accident (CVA),
as it can readily distinguish a primary ischemic from
a primary hemorrhagic process and thus determine
the appropriate use of tissue plasminogen activator
(tPA) (see Appendix IV).11 CT of the spine and orbits
are also available to evaluate for fractures, neoplasm,
spinal cord compromise, or sinusitis. Xenon CT
can be used to evaluate cerebral blood flow (CBF).
The patient inhales xenon gas while in the CT
scanner. Xenon is diffused almost immediately into
the bloodstream and into the brain. The concentration
of the gas is calculated by the computer and converted
into CBF. Abnormalities identified using this scan
include cerebrovascular occlusive disease, increased
intracranial pressure, intracranial bleeding, and ‘‘brain
death’’ where CBF would equal zero.33
Magnetic Resonance Imaging and
Angiography
Views in any plane of the head, with or without
contrast, taken with magnetic resonance imaging
(MRI) are used to assess intracranial neoplasm,
degenerative disease, cerebral and spinal cord edema,
ischemia, hemorrhage, arteriovenous malformation
(AVM), cerebral atrophy, and congenital anomalies.21,32
MRI has several advantages over CT scans including
providing better contrast between normal and
pathologic tissues allowing for quicker identification
of areas of ischemia, improved visualization of blood
vessels, less obscuring bone artifact, and the ability
to image in any plane.33 Magnetic resonance angiog-
raphy (MRA) is a noninvasive method used to assess
the intracranial vasculature for CVA, transient ische-
mic attack (TIA), venous sinus thrombosis, AVM,
and vascular tumors or extracranially for carotid
bifurcation stenosis.34
Doppler Flowmetry
Doppler flowmetry is the use of ultrasound to assess
blood flow.
TRANSCRANIAL DOPPLER SONOGRAPHY
Transcranial Doppler sonography (TCD) involves
the passage of low-frequency ultrasound waves over
thin cranial bones (temporal) or over gaps in bones
to determine the velocity and direction of blood
flow in the anterior, middle, or posterior cerebral
and basilar arteries. It is used to assess arteriosclerotic
disease, collateral circulation, vasospasm, and brain
death, and to identify AVMs and their supply
arteries.21,32
CAROTID NONINVASIVE STUDIES
Carotid noninvasive studies use the passage of high-
frequency ultrasound waves over the common, inter-
nal, and external carotid arteries to determine the
velocity of blood flow in these vessels. It is used to
assess location, presence, and severity of carotid occlu-
sion and stenosis.21,32 Carotid ultrasound is now often
done in color and is referred to as a carotid duplex
ultrasound.
Digital-Subtraction Angiography
Digital-subtraction angiography (DSA) is the compu-
ter-assisted radiographic visualization of the carotids
and cerebral vessels with a minimal view of background
tissues. An image is taken before and after the injection
of a contrast medium. The first picture is ‘‘subtracted’’
from the second, a process that creates a highlight of
the vessels. Digital-subtraction angiography is used to
assess aneurysm, AVM, fistula, occlusion, or stenosis.
DSA is considered the ‘‘gold standard’’ in assessment
for carotid stenosis; however it is less cost efficient
and carries a small but significant risk of stroke or
death due to the invasive nature of the test compared
with MRA or carotid ultrasound.35 It is also used
in the operating room (i.e., television display) to
examine the integrity of anastomoses or cerebrovascu-
lar repairs.21,32

Cerebral Angiography
Cerebral angiography involves the radiographic visual-
ization (angiogram) of the displacement, patency, ste-
nosis, or vasospasm of intracranial or extracranial
arteries after the injection of a radiopaque contrast
medium via a catheter (usually femoral artery). It is
used to assess aneurysm, AVMs, occlusions, or stenosis
as a single procedure or in the operating room to exam-
ine blood flow after surgical procedures (e.g., after an
aneurysm clipping).21
CLINICAL TIP
 Patients are on bed rest with the involved hip and
knee immobilized for approximately 4 to 8 hours
(depending on the method of closure) to ensure
proper healing of the catheter insertion site.
Lumbar Puncture
A lumbar puncture (LP) is the collection of CSF from a
needle placed into the subarachnoid space below the
L1 vertebra, usually between L3 and L4. The patient is
placed in a side-lying position with the neck and hips
flexed as much as possible (to open the laminae for the
best access to the subarachnoid space). Multiple vials
of CSF are collected and tested for color, cytology,
chlorine, glucose, protein, and pH. The opening and
closing pressures are noted. LP is used to assist in the
diagnosis of primary or metastatic brain or spinal cord
neoplasm, cerebral hemorrhage, meningitis, encephali-
tis, degenerative brain disease, autoimmune diseases
involving the central nervous system, neurosyphilis,
and demyelinating disorders (such as multiple sclerosis
(MS) and acute demyelinating polyneuropathy). This
procedure may also be performed to inject therapeutic
or diagnostic agents, to administer spinal anesthetics,
or to reduce/drain the volume of CSF to a normal level
in normal pressure hydrocephalus or in patients with
pseudotumor cerebri.
CLINICAL TIP
 Headache is a common complaint after an LP
secondary to meningeal irritation or CSF leakage.
A patient may be placed on bed rest for one hour
after an LP to minimize upright positioning, which
increases headache.33 Other short-term
complications of LP include backache, bleeding at
the needle site, voiding difficulty, and fever.
Nervous System CHAPTER 4 175
Positron Emission Tomography
In positron emission tomography (PET), radioactive
chemicals that mimic the normal metabolic process of
the brain are administered to the patient (most com-
monly fluorodeoxyglucose or FDG). The positrons
emitted from the radioactive chemicals are sensed by a
series of detectors placed around the patient, and in
combination with computed tomography the emis-
sions are recorded into a high-resolution two- or
three-dimensional image.33 Areas in the brain that are
more metabolically active will take up more of the
FDG than normal areas of the brain, indicating pathol-
ogy such as cancer. Areas with less uptake would indi-
cate hypometabolism such as seen in Alzheimer’s
disease. PETscanning is most commonly used to assist
in the diagnosis of brain tumor, cerebrovascular disease
or trauma, dementia including Alzheimer’s disease, sei-
zure disorders, Parkinson’s disease, and psychiatric
disorders.36,37
Electroencephalography
Electroencephalography (EEG) is the recording of
electrical brain activity, using electrodes affixed to the
scalp at rest or sleep, after sleep deprivation, after
hyperventilation, or after photic stimulation.37 Brain
waves may show abnormalities of activity, amplitude,
pattern, or speed. Electroencephalography is used in
conjunction with other neurodiagnostic tests to
assess seizure focus, sleep and metabolic disorders,
dementia, and brain death. In epileptic states, seizure
activity is characterized by rapid, spiking waves on
the graph, whereas cerebral lesions such as tumors or
infarctions show abnormally slow EEG waves, depend-
ing on the size and location of the lesion. EEG
can also be used during surgery when a carotid vessel
is temporarily occluded to evaluate for tissue ischemia
in the brain indicating the need for temporary shunting
of blood to avoid CVA.33
Evoked Potentials
Evoked potentials (EPs) are electrical responses gener-
ated by the stimulation of a sensory organ. EP studies
allow clinicians to measure and assess the entire sen-
sory pathway from the peripheral sensory organ to the
brain cortex. Conduction delays indicate damage or
disease anywhere along the pathway to the cortex.33 A
visual evoked potential (VEP) or visual evoked
response (VER) is measured using electrodes that are
placed over the occipital lobe to record occipital
cortex activity after a patient is shown flashing lights
176 CHAPTER 4 Nervous System
or a checkerboard pattern.Visual evoked potentials are
used to assess optic neuropathies and optic nerve
lesions. Ninety percent of patients with MS show
abnormal latencies of VERs.33 A brain stem auditory
evoked response is measured using electrodes that are
placed over the cortex to record CN VIII, pons, and
midbrain activity after a patient listens to a series of
clicking noises through headphones. Brain stem audi-
tory evoked responses are used to assess acoustic
tumors, brain stem lesions in MS, or brain stem func-
tion (in comatose patients). A somatosensory evoked
potential is measured using electrodes over the contra-
lateral sensory cortex after the median or posterior
tibial nerve is electrically stimulated. Somatosensory
evoked potentials are used to assess SCI, cervical disc
disease, sensory dysfunction associated with MS, or
parietal cortex tumor.21,32
Electromyography and Nerve Conduction
Velocity Studies
Electromyography (EMG) is the recording of muscle
activity at rest, with voluntary movement, and with
electrical stimulation with needle electrodes. Nerve
conduction velocity studies are the measurement of
the conduction time and amplitude of an electrical
stimulus along a peripheral nerve(s). EMG and nerve
conduction velocity studies are used to assess and dif-
ferentiate myopathy and peripheral nerve injury,
respectively.21
Myelography
Myelography uses x-ray to show how a contrast medium
flows through the subarachnoid space and around the
vertebral column after the removal of a small amount
of CSF and the injection of dye via LP. It is used to
assess bone displacement, disc herniation, cord
compression, or tumor.21,32
CLINICAL TIP
 Depending on the type of dye used, a patient may
have positioning restrictions after a myelogram. If
water-based dye was used, the patient should remain
on bed rest with the head of the bed at 30 degrees
for approximately 8 to 24 hours, because the dye
may cause a seizure if it reaches the cranium. If an
oil-based dye was used, the patient may have to
remain in bed with the bed flat for 6 to 24 hours.
Additionally, the patient may experience headache,
back spasm, fever, nausea, or vomiting, regardless
of the type of dye used.32
Transesophageal Echocardiography
Transesophageal echocardiography (TEE) or the less
invasive transthoracic echocardiography (TTE) are
useful imaging techniques in patients who have had
or suspected to have had an ischemic stroke or
TIA.These images can help to identify cardiac sources
of arterial embolism and can guide treatments to
avoid a recurrence of CVA or TIA.33 Please refer to
Chapter 1 for more specific details of these tests.
PATHOPHYSIOLOGY
Traumatic Brain Injury
The medical-surgical treatment of traumatic brain
injury (TBI) is a complex and challenging task. Direct
or indirect trauma to the skull, brain, or both typically
results in altered consciousness and systemic homeosta-
sis. TBI can be described by location, extent, severity,
and mechanism of injury.38
1. Location: TBI may involve damage to the cra-
nium only, the cranium and brain structures, or
brain structures only. Frequently, head trauma is
categorized in the following manner:
Closed Protective mechanisms are maintained
Open Protective mechanisms are altered
Coup The lesion is deep to the site of impact
Contrecoup The lesion is opposite the site of
impact
Coup- A combination of coup and
contrecoup contrecoup
2. Extent:TBI maybe classified as primary (in reference
to the direct biomechanical changes in the brain) or
secondary (in reference to the latent intracranial or
systemic complications that exacerbate the original
injury). The terms focal and diffuse are often used to
describe a specific or gross lesion, respectively.
3. Severity: In addition to diagnostic tests,TBI may be
classified according to cognitive skill deficit and
GCS as mild (13 to 15), moderate (9 to 12), or severe
(3 to 8).
4. Mechanism of injury: The most common mechan-
isms responsible for primary TBI are acceleration-
deceleration, rotation forces, and direct impact.
These forces may be of low or high velocity and
result in the compression, traction, or shearing of
brain structures.
 Nervous System CHAPTER 4 177
Secondary brain injury occurs within minutes to Mechanism of
hours of the traumatic primary injury and is character- Injury Description
ized by inflammatory, vascular, and biomolecular
Hyperextension, causing protective structures
abnormalities. These changes include the release of
discontinuity of the remain intact
cytokines and a disruption of the blood-brain barrier,
anterior spinal
which causes the development of vasogenic (extracel-
ligaments, disc
lular) brain edema; impaired cerebral autoregulation
herniation, and
and ischemia in the setting of hypoxia and hypotension;
vertebral dislocation
tissue acidosis and an influx of electrolytes, which
or fracture
causes cytotoxic (intracellular) brain edema; and
Axial compression,
the loss of neurons, glial cells, and presynaptic term-
rotation, contusion,
inals from neurochemical and oxygen-free radical
laceration, or
reactions.39,40
transection

CLINICAL TIP Secondary SCI is a complex series of pathologic

vascular and inflammatory responses to primary SCI,
 The therapist should be aware of the most recent
which further compound the original injury over the
activity orders and blood pressure and heart rate
course of several days. A summary of secondary SCI
parameters to minimize secondary brain injury
includes (1) vasospasm of superficial spinal vessels,
during treatment.
intraparenchymal hemorrhage and disruption of the
blood-brain and spinal cord barrier, complicated by
Table 4-19 defines the most common types of TBI neurogenic shock and loss of autoregulation, and (2)
and describes the clinical findings. The management increased calcium levels, which stimulate free radical
of these conditions is discussed later in the General production to cause further ischemia, the release of
Management section and inTable 4-23. catecholamines and opioids, and the accumulation of
activated microglia and macrophages.41,42
Spinal Cord Injury
The severity of SCI is most commonly classified
Spinal cord injury (SCI) and the resultant paraplegia by the American Spinal Injury Association (ASIA)
or quadriplegia are typically due to trauma or, less fre- Impairment Scale.43 This scale classifies SCI according
quently, impingement of the spinal cord from abscess, to motor and sensory function44:
ankylosing spondylitis, or tumor. Primary SCI, the
direct trauma at the time of injury, can be described A Complete No sensory function or motor
according to location or mechanism of injury.41 function is preserved in S4-S5.
1. Location: SCI may involve the cervical, thoracic, or B Incomplete The preservation of sensory
lumbar spines. Table 4-20 identifies the loss of func- function without motor
tion that can be expected with the associated level function below the neurologic
of the spinal cord lesion. level and includes S4-S5.
2. Mechanism of injury: SCI may result from blunt or C Incomplete The preservation of motor
penetrating injuries. function below the neurologic
level. Muscle function of more
Mechanism of
than half of key muscles below
Injury Description
this level is less than 3/5.
Forward hyperflexion, Low velocity, in which D Incomplete The preservation of motor
causing the the spinal cord and function below the neurologic
discontinuity of the protective structures level. Muscle function of at
posterior spinal are injured directly least half of key muscles below
ligaments, disc High velocity, in which a this level is equal to or greater
herniation, and concussive force than 3/5.
vertebral dislocation injures the spinal
E Normal Motor function and sensory
or fracture cord, and the
function are intact.
Continued
178 CHAPTER 4 Nervous System

Table 4-19 CLINICAL FINDINGS AND GENERAL MANAGEMENT OF TRAUMATIC BRAIN INJURIES
Injury Definition Clinical Findings
Cerebral concussion Shaking of the brain secondary to acceleration- Brief loss of consciousness or ‘‘dazed’’
deceleration forces, usually as a result of presentation, headache, dizziness,
a fall or during sports activity. irritability, inappropriate laughter, nausea,
Can be classified as mild or classic. decreased concentration and memory,
Signs and symptoms of cerebral concussion retro- or ante-grade amnesia, altered gait
are reversible in most cases.
Postconcussive Clinical findings after a concussion that last Headache, nausea, dizziness, sensory
syndrome (PCS) for weeks to months. (Patients who initially sensitivity, memory or concentration
presented with headache, nausea, and difficulties, irritability, sleep disturbances,
dizziness are at higher risk for PCS.) and depression
Cerebral contusion Bruise (small hemorrhage) secondary to See Cerebral concussion, above. (Patients
acceleration-deceleration forces or beneath with a contusion are often delayed in their
a depressed skull fracture, most commonly clinical presentation.)
in the frontal or temporal areas.
Cerebral laceration Tear of the cortical surface secondary to S/S dependent on area involved, ICP, and
acceleration-deceleration forces, commonly degree of mass effect.
in occurrence with cerebral contusion over
the anterior and middle fossa where there
are sharp bony surfaces.
Diffuse axonal injury Occurs with widespread white matter shearing Coma, abnormal posturing (if severe), other
(DAI) secondary to high-speed acceleration- S/S dependent on area involved, ICP, and
deceleration forces, usually as a result of a degree or mass effect.
motor vehicle accident.
Can be classified as mild (6-24 hours of coma),
moderate (greater than 24 hours of coma),
or severe (days to weeks of coma).
Epidural hematoma Blood accumulation in the epidural space Headache, altered consciousness, abnormal
(EDH) secondary to tearing of meningeal arteries posture, contralateral hemiparesis, and
that compresses deep brain structures. other S/S dependent on specific location of
Associated with cranial fractures, particularly the lesion, ICP, and degree of mass effect.
the thin temporal bone and frontal and Can present with a ‘‘lucid’’ interval before loss
middle meningeal tears. of consciousness for a second time.
Subdural hematoma Blood accumulation in the subdural space that See Epidural hematoma, above.
(SDH) compresses brain structures as a result of
traumatic rupture or tear of cerebral veins,
increased intracranial hemorrhage, or
continued bleeding of a cerebral contusion.
The onset of symptoms may be acute Can present with a ‘‘lucid’’ interval before
(up to 24 hours), subacute (2 days to 3 weeks), loss of consciousness for a second time.
or chronic (3 weeks to 3-4 months).
Intracerebral hematoma Blood accumulation in the brain parenchyma See Epidural hematoma, above.
(ICH) secondary to acceleration-deceleration
forces, the shearing of cortical blood
vessels, or beneath a fracture.
May also arise as a complication of hypertension
or delayed bleeding with progression of blood
into the dural, arachnoid, or ventricular spaces.
ICP, Intracranial pressure, S/S, signs and symptoms.
Data from Marx JA (ed). Rosen’s Emergency Medicine: Concepts and Clinical Practice (6th ed). Philadelphia: Mosby, 2006.
 Nervous System CHAPTER 4 179
beyond the scope of this book to discuss in detail the
Table 4-20 SPINAL CORD INJURY WITH physiologic sequelae of SCI. However, other major
ASSOCIATED LOSS OF FUNCTION physiologic effects of SCI include autonomic dysre-
Level of Lesion Resulting Loss of Function flexia; orthostatic hypotension; impaired respiratory
function; bladder, bowel, and sexual dysfunction; mal-
C4 Spontaneous breathing nutrition; pressure ulcer; diabetes insipidus (DI); syn-
C5 Shrugging of shoulders
C6 Flexion at elbow
drome of inappropriate secretion of antidiuretic
C7 Extension at elbow hormone (SIADH); edema; and increased risk of deep
C8-T1 Flexion of fingers venous thrombosis.
T1-T12 Intercostal and abdominal muscles
L1-L2 Flexion at hip CLINICAL TIP
L3 Adduction at hip
L4 Abduction at hip  If, during physical therapy intervention, a patient
L5 Dorsiflexion of foot with SCI develops signs and symptoms associated
S1-S2 Plantar flexion of foot with autonomic dysreflexia, return the patient
S2-S4 Rectal sphincter tone to a reclined sitting position, and notify the nurse
or physician immediately. Signs and symptoms
From: MarxJA (ed). Rosen’s Emergency Medicine: Concepts and
Clinical Practice (6th ed). Philadelphia: Mosby, 2006. of autonomic dysreflexia include headache,
bradycardia, hypertension, and diaphoresis.45
 During the early mobilization of the patient with SCI
into the sitting position, consider using compression
The most common types of incomplete SCI syn- stockings or Ace wraps on the legs and an
dromes are described in Table 4-21. The immediate abdominal binder to prevent or minimize orthostatic
physiologic effect of SCI is spinal shock; the triad hypotension. Also, encourage the patient to sit with
of hypotension, bradycardia, and hypothermia is the head of the bed (HOB) elevated throughout the
secondary to altered sympathetic reflex activity.43 It is day to condition the body to an upright position.

Table 4-21 SPINAL CORD INJURY SYNDROMES

Syndrome Mechanism of Injury
Central cord Hyperextension injury, or as a result of
tumor, rheumatoid arthritis, or
syringo-myelia
Anterior cord Hyperflexion injury, acute large disc
herniation, or as a result of anterior
spinal artery injury
Brown-Se¤ quard Penetrating spinal trauma (e.g., stab
wound), epidural hematoma, spinal
arteriovenous malformation, cervical
spondylosis, or unilateral articular
process fracture or dislocation
Data from Buckley DA, Guanci MM. Spinal cord trauma. Nurs Clin North Am 1999;34(3); HickeyJV (ed).The Clinical Practice of
Neurological and Neurosurgical Nursing (4th ed). Philadelphia: Lippincott, 1997; MarxJA (ed). Rosen’s Emergency Medicine: Concepts and
Clinical Practice (6th ed). Philadelphia: Mosby, 2006.
Description
Lesion of the central cord exerts pressure on anterior
horn cells.Typically presents with bilateral motor
paralysis of upper extremities greater than lower
extremities, variable sensory deficits, and possible
bowel/bladder dysfunction.
Lesion of the anterior cord damages the anterolateral
spinothalamic tract, cortical spinal tract, and
anterior horn (gray matter).Typically presents with
bilateral loss of pain and temperature sensation and
motor function with retained light touch,
proprioception, and vibration sense.
Lesion of one-half of the spinal cord; typically
presents with contralateral loss of pain and
temperature sensation; ipsilateral loss of touch,
proprioception, and vibration sense; and ipsilateral
motor paresis or paralysis.Typically patients
maintain bowel and bladder function. Most become
ambulatory.
180 CHAPTER 4 Nervous System

The management of SCI typically includes medical

stabilization with ventilatory support (if indicated);
immobilization of the spine with a collar, orthosis, trac-
tion, halo vest, or surgical repair; methylprednisolone
or other pharmacologic therapies; treatment of sec-
ondary injures; pain management; and psychosocial
support.
Cerebrovascular Disease and Disorders
A patent cerebral vasculature is imperative for the deliv-
ery of oxygen to the brain. Alterations of the vascular
supply or vascular structures can cause neurologic
dysfunction from cerebral ischemia or infarction.
TRANSIENT ISCHEMIC ATTACK
A TIA is characterized by a brief episode of neurologic
dysfunction caused by a focal disturbance of brain or
retinal ischemia, with clinical symptoms typically last-
ing less than one hour, and without evidence of infarc-
tion.46 TIA is often a strong prognostic indicator of
stroke and is commonly caused by carotid or vertebro-
basilar disease. About 10% of patients with TIA will FIGURE 4-8
go on to have a major stroke within 90 days; 5% The most frequent sites of arterial and cardiac abnormalities
will have a major stroke within 2 days.47 The manage- causing ischemic stroke. (From Albers GW, Amarenco P,
ment of TIAs involves observation, treatment of caus- Easton JD, et al. Antithrombotic and ThrombolyticTherapy for
ative factor (if possible), anticoagulation, and carotid Ischemic Stroke:The Seventh ACCP Conference on
endarterectomy. Antithrombotic and ThrombolyticTherapy. Chest 2004;126(3
Suppl):483S-512S.)
CEREBROVASCULAR ACCIDENT
A CVA, otherwise known as a stroke or brain attack, is frequent sites of arterial and cardiac abnormalities
characterized by the sudden onset of focal neurologic causing ischemic stroke. The management of ische-
deficits of more than 24 hours’ duration or imaging of mic CVA involves blood pressure control (normal
an acute, clinically relevant lesion in patients with rap- to elevated range), treatment of causative factors
idly resolving symptoms secondary to insufficient (if possible), anticoagulation, recombinant tPA,50,51
oxygen delivery to the brain.48 cerebral edema control, prophylactic anticonvulsant
The most prominent risk factors for CVA include therapy, and carotid endarterectomy (if indicated).
older age, African-American race, hypertension, coro-
nary artery disease, hyperlipidemia, atrial fibrillation, CLINICAL TIP
hypercoagulable state, diabetes mellitus, obesity, smok-
ing, alcohol abuse, and physical inactivity.48,49 There  A patient who has received tPA is at risk for
are several types of cerebrovascular accident, including intracranial hemorrhage or bleeding from other sites
ischemic, hemorrhagic, and lacunar: and requires strict blood pressure control during the
1. Ischemic Cerebrovascular Accident: Ischemic CVA is first 24 hours of infusion.52 Physical therapy is
the result of cerebral hypoperfusion. An ischemic usually not initiated during this time frame.
CVA due to thrombotic disease, such as carotid
arterystenosis or arteriosclerotic intracranial arteries, 2. Hemorrhagic Cerebrovascular Accident: Hemorrha-
usually has a slow onset. Symptoms of an ischemic gic CVA involves cerebral hypoperfusion, which is
stroke caused by embolus from the heart in the setting abrupt in onset and is secondary to intraparenchy-
of atrial fibrillation, meningitis, prosthetic valves, mal hemorrhage associated with hypertension,
patent foramen ovale, or endocarditis will have a AVM, trauma, aneurysm rupture, or SAH. Patients
sudden onset. Refer to Figure 4-8 for the most usually present with sudden onset of headache,

vomiting, severely elevated blood pressure, and
focal neurologic deficits that progress over min-
utes.53 The management of hemorrhagic CVA
involves blood pressure control (low to normal
range), treatment of causative factors (if possible),
corticosteroids, anticoagulation (for reperfusion),
prophylactic anticonvulsant therapy, and surgical
hematoma evacuation (if appropriate). Patients
with hemorrhagic CVA have a poorer prognosis
than ischemic stroke, with a 30-day mortality rate
of 50%.53
3. Lacunar Cerebrovascular Accident: Lacunar or
small-vessel strokes are common in patients with
diabetes and hypertension and are caused by small-
vessel disease deep in cerebral white matter.
Infarctions range in size from a few millimeters to 2
centimeters and occur most commonly in the basal
ganglia, thalamus, pons, and internal capsule.53
Several syndromes have been identified dependent
on the site of infarcts, most commonly with pure
motor symptoms, pure sensory symptoms, or ataxic
hemiparesis. Lacunar strokes do not cause cognitive
impairment, aphasia, or visual deficits because the
higher cortical areas are preserved.11
Experimental treatment options for CVA include:
 Cytoprotective drugs such as antioxidants,
calcium channel blockers, and glutamate receptor
antagonists
 Catheter-based fibrinolysis, extending the current
therapeutic window beyond three hours54
 Mild to moderate hypothermia as a neuroprotec-
tive strategy
 A variety of mechanical clot retrieval devices53
The signs and symptoms of CVA depend on the
location (anterior versus posterior, and cortical versus
subcortical) and the extent of the cerebral ischemia or
infarction. General signs and symptoms include contra-
lateral motor and sensory loss, speech and perceptual
deficits, altered vision, abnormal muscle tone, head-
ache, nausea, vomiting, and altered affect. Refer to
Table 4-22 for presentation of symptoms dependent
on the specific area of infarction.
Other terms commonly used to describe CVA
include the following:
Completed stroke A CVA in which the neurologic
impairments have fully evolved
Stroke-in- A CVA in which the neurologic
evolution impairments continue to evolve
or fluctuate over hours or days55
Continued
Nervous System CHAPTER 4 181
Watershed stroke A cerebral infarct between the
terminal areas of perfusion of two
different arteries, typically
between the anterior and middle
cerebral arteries21
ARTERIOVENOUS MALFORMATION
Arteriovenous malformation (AVM) is a malformation
in which blood from the arterial system is shunted to
the venous system (thereby bypassing the capillaries)
through abnormally thin and dilated vessels, making
them prone to ruptures causing intracerebral hemor-
rhage. An AVM can occur in a variety of locations,
shapes, and sizes. The result of the bypass of blood is
degeneration of brain parenchyma around the site of
the AVM, which creates a chronic ischemic state.
Signs and symptoms of AVM include headache, dizzi-
ness, fainting, seizure, aphasia, bruit, and motor and
sensory deficits.56 Management of AVM includes cere-
bral angiogram to evaluate the precise location of the
AVM, followed by surgical AVM repair, embolization,
radiosurgery (stereotactic), photon beam therapy, or
medical management alone with close monitoring in
some cases.37
CEREBRAL ANEURYSM
Cerebral aneurysm is the dilation of a cerebral blood
vessel wall owing to a smooth muscle defect through
which the endothelial layer penetrates. Cerebral aneur-
ysms most commonly occur at arterial bifurcations
and in the larger vessels of the anterior circulation.
Signs and symptoms of unruptured cerebral aneurysm
are determined by size and location, detailed in Table
4-23. When an aneurysm ruptures, blood is released
under arterial pressure into the subarachnoid space
and quickly spreads through the cerebrospinal fluid
(CSF) around the brain and spinal cord.37 Signs and
symptoms of ruptured aneurysm include violent
headache, stiff neck, photophobia, vomiting, hemiple-
gia, aphasia, seizure, and CN (III, IV, VI) palsy.21
Management of cerebral aneurysm involves CT scan
or angiogram to closely evaluate the aneurysm,
followed by aneurysm clipping, embolization, coiling,
or balloon occlusion.
SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage (SAH), the accumulation
of blood in the subarachnoid space, is most commonly
the result of aneurysm rupture, or less commonly a
complication of AVM, tumor, infection, or trauma.
182 CHAPTER 4 Nervous System

Table 4-22 NEUROLOGIC SIGNS ASSOCIATED WITH CVA BY LOCATION

Artery Affected Neurologic Signs
Internal carotid artery supplies the cerebral Unilateral blindness
hemispheres and diencephalon by the ophthalmic Severe contralateral hemiplegia and hemianesthesia
and ipsilateral hemisphere arteries Profound aphasia
Middle cerebral artery supplies the frontal lobe, Alterations in communication, cognition, mobility and sensation
parietal lobe, and cortical surfaces of temporal Contralateral homonymous hemianopsia
lobe (affecting structures of higher cerebral Contralateral hemiplegia or hemiparesis, motor and sensory loss,
processes of communication; language greater in the face and arm than in the leg
interpretation; and perception and interpretation
of space, sensation, form, and voluntary movement).
Anterior cerebral artery supplies superior surfaces Emotional lability
of frontal and parietal lobes and medial surface Confusion, amnesia, personality changes
of cerebral hemispheres (includes motor and Urinary incontinence
somesthetic cortex serving the legs), basal ganglia, Contralateral hemiplegia or hemiparesis, greater in the leg
and corpus callosum. than in the arm
Posterior cerebral artery supplies medial and inferior Hemianesthesia
temporal lobes, medial occipital lobe, thalamus, Contralateral hemiplegia, greater in the face and arm than
posterior hypothalamus, and visual receptive area. in the leg
Cerebellar ataxia, tremor
Homonymous hemianopsia, cortical blindness
Receptive aphasia
Memory deficits
Vertebral or basilar arteries supply the brainstem
and cerebellum.
Incomplete occlusion Unilateral and bilateral weakness of extremities; upper motor
neuron weakness involving face, tongue, and throat; loss of
vibratory sense, two-point discrimination, and position sense
Diplopia, homonymous hemianopsia
Nausea, vertigo, tinnitus, and syncope
Dysphagia, dysarthria
Sometimes confusion and drowsiness
Anterior portion of the pons ‘‘Locked-in’’ Syndromeçno movement except eyelids; sensation
and consciousness preserved
Complete occlusion or hemorrhage Coma or death
Miotic pupils
Decerebrate rigidity
Respiratory and circulatory abnormalities
Posterior inferior cerebellar artery supplies Wallenberg syndrome
the lateral and posterior portion of the medulla. Dysphagia, dysphonia
Ipsilateral anesthesia of face and cornea for pain and temperature
(touch preserved)
Contralateral anesthesia of trunk and extremities for pain and
temperature
Ipsilateral Horner syndrome
Ipsilateral decompensation of movement
Anterior inferior and superior cerebellar arteries Difficulty with articulation, gross movements of limbsçataxia
supply the cerebellum. Nystagmus
From Seidel HM, BallJW, DainsJE, et al. (eds). Mosby’s Guide to Physical Examination (6th ed). Philadelphia: Mosby, 2006.

Table 4-23 FOCAL SIGNS IN PATIENTS WITH
ANEURYSMS AT VARIOUS SITES
Site of Aneurysms Clinical Findings
Internal carotid çpost Cranial nerve III palsy
communicating
Middle cerebral artery Contralateral face or hand
paresis
Aphasia (left side)
Contralateral visual neglect
(right side)
Anterior communicating Bilateral leg paresis
Bilateral Babinski’s sign
Basilar artery apex Vertical gaze paresis
Coma
Intracranial vertebral Vertigo
artery/posterior inferior Elements of lateral medullary
cerebellar artery syndrome
From Goetz CG (ed).Textbook of Clinical Neurology (2nd ed).
Philadelphia: Saunders, 2003.
It is graded from I toVaccording to the Hunt and Hess
scale21:
I. Asymptomatic
II. Moderate to severe headache, nuchal rigidity,
without neurologic deficit
III. Drowsiness, confusion, with mild focal neurolog-
ic deficit
IV. Stupor, moderate to severe focal deficits, such as
hemiplegia
V. Comatose, abnormal posturing
SAH is diagnosed by history, clinical examination,
noncontrast CT scan, LP, or angiogram. The manage-
ment of SAH depends on its severity and may include
surgical aneurysm repair with blood evacuation; ventri-
culostomy; and supportive measures to maximize neu-
rologic, cardiac, and respiratory status, rehydration,
and fluid-electrolyte balance.
Complications of SAH include rebleeding, hypona-
tremia, hydrocephalus, seizure, and vasospasm.
Vasospasm is the spasm (constriction) of one or more
cerebral arteries that occurs 4 to 12 days after SAH.57
The etiology is unknown and is diagnosed by either
transcranial Doppler, cerebral angiography, or CT.
Vasospasm results in cerebral ischemia distal to the
area of spasm if untreated. The signs and symptoms of
vasospasm are worsening level of consciousness, agita-
tion, decreased strength, altered speech, pupil changes,
headache, and vomiting, and they may wax and wane
with the degree of vasospasm. Vasospasm is treated
Nervous System CHAPTER 4 183
with induced hypertension, hypervolemia, and
hemodilution.57
Dementia
Dementia is a syndrome of acquired persistent dysfunc-
tion in several domains of intellectual function includ-
ing memory, language, visuospatial ability, and
cognition (abstraction, mathematics, judgment, and
problem solving).58 There are numerous conditions
that can cause or contribute to dementia including:
 Alzheimer’s disease
 AIDS
 Alcoholism
 Lewy body dementia
 Metabolic disorders
 Multi-infarct dementia
 Parkinson’s disease
 Vascular dementia
It is beyond the scope of this book to discuss each
type in depth. Below are some of the most common
dementias encountered in the acute care setting.
Alzheimer’s disease (AD) is the most common cause
of dementia.58 Patient’s with AD usually experience a
gradual onset of cognitive deficits caused by amyloid
plaques in the brain that replace healthy white matter.
There is no specific test for diagnosis. A detailed past
medical history, mini-mental exam, neurologic exam,
and MRI assist in diagnosing AD. In the acute care set-
ting, patients with AD are often admitted with a
sudden decline in function including decreased inter-
actions with caregivers, decrease in initiation, apraxia,
or combative behavior. Infection such as UTI can
cause the decline in function, and symptoms usually
improve with antibiotics.
Lewy body dementia (LBD) is characterized by
marked fluctuations in cognition, visual and auditory
hallucinations, clouding of consciousness, and mild
spontaneous extrapyramidal symptoms caused by a
pathologic accumulation of Lewy bodies in the brain
stem and cortex.58 These patients also display a pro-
nounced sensitivity to antipsychotics, with a tendency
to develop severe parkinsonism.59 The diagnosis is
made in a similar manner as Alzheimer’s disease and is
differentiated from AD by the day-to-day fluctuations
and the sensitivity to antipsychotics. The disease
process is progressive with an average mortality of
12 to 13 years after diagnosis.59
Vascular dementia is usually abrupt in onset and may
be a consequence of multiple cortical infarctions,
multiple subcortical infarctions (lacunar state), ischemic
injury to the deep hemispheric white matter, or a
184 CHAPTER 4 Nervous System
combination of these.58 Diagnosis is made through an
accurate history that may include atherosclerosis with
myocardial infarction, retinopathy, hypertension,
stroke; EEG; and MRI.The patient presents with rela-
tive preservation of personality with emotional lability,
depression, somatic preoccupation, and nocturnal
confusion.
The focus of physical therapy in the acute care set-
ting for all of these patients is to maximize function
while ensuring safety of the patient.
CLINICAL TIP
 Patients with dementia have an elevated fear of
falling interfering with mobility. It is helpful to
stand in front of the patient during transfers so that
the patient cannot see the floor.
 Keep instructions functional and simple, and repeat
them calmly if needed. For example: during a
transfer, instead of giving multistep instructions such
as ‘‘Move to the edge of the bed, place your hands
on the bed, and stand,’’ try ‘‘Stand up.’’
 Patients with dementia can easily become agitated
in unfamiliar settings and may ‘‘sundown,’’ or have
further cognitive decline associated with an increase
in agitation at the end of the day into the evening.
 Avoid distractions during treatment. Close the door
or pull the curtain to reduce stimuli if possible.
Ventricular Dysfunction
HYDROCEPHALUS
Hydrocephalus is the acute or gradual accumulation
of CSF, causing excessive ventricular dilation and
increased ICP. CSF permeates through the ventricular
walls into brain tissue secondary to a pressure gradient.
There are two types of hydrocephalus:
1. Noncommunicating (obstructive) hydrocephalus,
in which there is an obstruction of CSF flow within
the ventricular system. There may be thickening
of the arachnoid villi or an increased amount or
viscosity of CSF. This condition may be congenital
or acquired, often as the result of aqueduct stenosis,
tumor obstruction, abscess, or cyst, or as a complica-
tion of neurosurgery.8
2. Communicating hydrocephalus, in which there is an
obstruction in CSF flow as it interfaces with the
subarachnoid space. This condition can occur with
meningitis, after head injury, with SAH, or as a
complication of neurosurgery.6
Hydrocephalus may be of acute onset characterized
by headache, altered consciousness, decreased upward
gaze, and papilledema.15 Management includes treat-
ment of the causative factor if possible, or placement
of a ventriculoperitoneal (VP) or ventriculoatrial (VA)
shunt.
Normal-pressure hydrocephalus (NPH) is a type of
communicating hydrocephalus without an associated
rise in ICP and occurs primarily in the elderly.50
NPH is typically gradual and idiopathic but may be as-
sociated with previous meningitis, trauma, or SAH.50
The hallmark triad of NPH is altered mental status
(confusion), altered gait (usually wide-based and shuf-
fling with difficulty initiating ambulation), and uri-
nary incontinence. NPH is diagnosed by history, CT
scan, or MRI to document ventriculomegaly, and
lumbar puncture. LP is performed to remove excessive
CSF (usually 40 to 50 ml).50 The patient is often video-
taped before and after the lumbar puncture
to observe for improvements in gait and cognition.
If symptoms are significantly improved, the decision
may be made for VP shunt placement. Recent studies
have shown up to a 90% success rate in shunt place-
ment in patients who showed improvement after
lumbar puncture.60
CLINICAL TIP
 The clinician should be aware that patients with
NPH often present with a similar gait pattern
to patients with Parkinson’s disease.
CEREBROSPINAL FLUID LEAK
A CSF leak is the abnormal discharge of CSF from a
scalp wound, the nose (rhinorrhea), or the ear (otorrhea)
as a result of a meningeal tear. A CSF leak can occur
with anterior fossa or petrous skull fractures or, less
commonly, as a complication of neurosurgery. With a
CSF leak, the patient becomes at risk for meningitis
with the altered integrity of the dura. A CSF leak,
which usually resolves spontaneously in 7 to 10 days,21
is diagnosed by clinical history, CT cisternography,
and testing of fluid from the leak site. If the fluid is
CSF (and not another fluid, e.g., mucus), it will test
positive for glucose. The patient may also complain of
a salty taste in the mouth. Management of CSF
leak includes prophylactic antibiotics (controversial),
lumbar drainage for leaks persisting more than 4 days,
dural repair for leaks persisting more than 10 days, or
VP or VA shunt placement.56
 Nervous System CHAPTER 4 185

Classification Type Characteristics

CLINICAL TIP
Clonic Rhythmic jerking
 If it is known that a patient has a CSF leak, the muscle movements
therapist should be aware of vital sign or position without an initial
restrictions before physical therapy intervention. tonic phase
If a CSF leak increases or a new leak occurs during
physical therapy intervention, the therapist should Atonic Loss of muscle tone
stop the treatment, loosely cover the leaking area, Absence Very brief period
and notify the nurse immediately. (seconds) of
unresponsiveness
with blank staring
Seizure and the inability to
A seizure is defined as abnormal neurologic function- complete any
ing caused by abnormally excessive activation of neu- activity at the time
rons, either in the cerebral cortex or in the deep limbic of the seizure
system.53 The signs and symptoms of the seizure Myoclonic Local or gross rapid,
depend on the seizure locus on the cortex (e.g., visual nonrhythmic
hallucinations accompany an occipital cortex locus). jerking movements
Seizures can occur as a complication of CVA, head
trauma, meningitis, or surgery. Febrile state, hypoxia, Seizures are of acute onset, with or without any
hyper- or hypoglycemia, hyponatremia, severe uremic of the following: aura, tremor, paresthesia, sensation
or hepatic encephalopathy, drug overdose, and drug or of fear, gustatory hallucinations, lightheadedness,
alcohol withdrawal are also associated with seizures.61 and visual changes. Seizure activity can be irrefutably
Seizures are classified as partial (originating in a focal identified only by EEG. Synchronized EEG with
region of one hemisphere) or generalized (originating videotaping may be required to differentiate pseudo-
in both hemispheres or from a deep midline focus). seizures (also called psychogenic seizures) from seizures,
and both may coexist in the same patient.53 Medical
Classification Type Characteristics management of seizures involves the treatment of
causative factors (if possible) and antiepileptic drugs.
Partial Simple Partial seizures
Surgical management for seizure refractory to medi-
seizures61 partial without loss of
cal management may consist of the resection of the
consciousness
seizure focus or the implantation of a vagal nerve
Complex Brief loss of stimulator.62
partial consciousness Terms related to seizure include:21,61
marked by
motionless staring Prodrome The signs and symptoms (e.g., smells,
Partial with Progression to seizure auditory hallucinations, a sense of
secondary activity in both de¤ ja' vu) that precede a seizure by
generalization hemispheres hours
Generalized Tonic Sudden flexor or Aura The signs and symptoms (as above)
seizures61 extensor rigidity that precede a seizure by seconds
Tonic-clonic Sudden extensor or minutes
rigidity followed by Epilepsy or Refers to recurrent seizures
flexor jerking.This seizure
type of seizure may disorder
be accompanied by Status More than 30 minutes of continuous
incontinence or a epilepticus seizure activity or two or more
crying noise owing seizures without full recovery of
to rigidity of the consciousness between seizures.
truncal muscles. Generalized tonic-clonic status
Continued Continued
186 CHAPTER 4 Nervous System
epilepticus is a medical emergency
marked by the inability to sustain
spontaneous ventilation with
the potential for hypoxia
requiring pharmacologic and life
support. Often the result of tumor,
CNS infection, or drug abuse in
adults.
Postictal state The period of time immediately after
a seizure characterized by lethargy,
confusion, and, in some cases,
paralysis.This state can last minutes
to hours and even days
CLINICAL TIP
 Establish the seizure history, including prodrome or
aura (if any), for the patient with a recent seizure or
epilepsy by either chart review or interview to be as
prepared as possible to assist the patient if seizure
activity should occur.
Syncope
Syncope is the transient loss of consciousness and pos-
tural tone secondary to cerebral hypoperfusion, usually
accompanied by bradycardia and hypotension.62
Syncope can be any of the following63:
 Cardiogenic syncope, resulting from drug toxicity;
dysrhythmias, such as atrioventricular block or
supraventricular tachycardia; cardiac tamponade;
atrial stenosis; aortic aneurysm; pulmonary
hypertension; or pulmonary embolism
 Neurologic syncope, resulting from benign posi-
tional vertigo, cerebral atherosclerosis, seizure,
spinal cord lesions, or peripheral neuropathy associ-
ated with diabetes mellitus or with degenerative
diseases, such as Parkinson’s disease
 Reflexive syncope, resulting from carotid sinus
syndrome, pain, emotions, or a vasovagal response
after eating, coughing, or defecation
 Orthostatic syncope, resulting from the side
effects of drugs, volume depletion, or prolonged
bed rest
Syncope is diagnosed by clinical history, ECG,
Holter or continuous-loop event recorder, or tilt-table
testing. CT and MRI are only performed if new
neurologic deficits are found.63 The management of
syncope, dependent on the etiology and frequency
of the syncopal episode(s), may include treatment of
the causative factor; pharmacologic agents, such as
beta-adrenergic blockers; fluid repletion; or cardiac
pacemaker placement.
CLINICAL TIP
 Compression stockings and lower extremity exercises
at the edge of bed prior to standing can help to
reduce orthostatic hypotension.
Neuroinfectious Diseases
See Chapter 10 for a description of encephalitis, menin-
gitis, and poliomyelitis.
Vestibular Dysfunction
Dizziness is one of the leading complaints of patients
seeking medical attention. It is up to the clinician to
take a detailed history of the complaint to determine
the primary etiology. Patients use the term dizzy to
describe a multitude of symptoms:
 Vertigo: A sense that the environment is moving or
spinning (usually caused by vestibular dysfunction)
 Lightheadedness: A feeling of faintness (usually
caused by orthostatic hypotension, hypoglycemia,
or cardiac in origin; refer to Chapters 1 and 6 for
further details)
 Dysequilibrium: Sensation of being off balance
(usually associated with lower extremity weakness
or decreased proprioception caused by neuropathy)
Vertigo is the hallmark symptom of vestibular dys-
function. The vestibular system is complex and made
up of a peripheral system and a central system. The
peripheral system includes three semicircular canals
and two otolith organs in the inner ear. The central
system includes the pathways between the inner ear,
the vestibular nuclei in the brainstem, cerebellum, cere-
bral cortex, and the spinal cord. The vestibular system
functions to:
 Stabilize visual images on the retina during head
movement for clear vision
 Maintain postural stability during head movements
 Maintain spatial orientation
After the clinician has determined that there is a
vestibular system pathology (see Table 4-24 for tests
and measures), the next step is to determine if the
pathology is peripheral or central (Table 4-25).
Peripheral vestibular system pathology includes
benign positional paroxysmal vertigo, acute vestibular
neuronitis, Me¤ nie' re’s disease, and ototoxicity. These
conditions are discussed below. Central vestibular
pathology is caused by stroke affecting the cerebellar

blood supply and/or vertebral artery; TIA; traumatic
brain injury; migraine; tumor; and demyelinating
diseases such as MS that affect the eighth cranial
nerve.11,64,65 The underlying cause of the pathology
must be treated for optimal recovery. Physical therapy
focuses on the primary diagnosis and compensatory
strategies to help with nystagmus or unresolved vertigo.
BENIGN POSITIONAL PAROXYSMAL VERTIGO
Benign positional paroxysmal vertigo (BPPV), the
most common peripheral vestibular disorder,64 is char-
acterized by severe vertigo associated with specific
changes in head position with or without nausea and
vomiting. The impairments are directly caused by a
misplaced otoconia in the semicircular canal from
head trauma, whiplash injury, surgery, prolonged
inactivity, or aging.13 Typically, symptoms of vertigo
last less than 60 seconds11 and are precipitated by
specific head movements such as looking up to a
high shelf, rolling over in bed to one direction, or
lying on a specific side. The Hallpike-Dix test
(Figure 4-9) is the most common test for BPPV and
is performed in the following manner64: The patient
is positioned on an examination table such that
when he or she is placed supine, the head extends
over the edge. The patient is lowered with the head
supported and turned 45 degrees to one side or the
other. The eyes are carefully observed. If no abnormal
eye movements are seen, the patient is returned to
the upright position. The maneuver is repeated with
the head in the opposite direction and finally with
the head extended supine. The direction of the nystag-
mus is noted and is helpful in determining which
semicircular canal is involved. Once the canal has
been identified, the Epley maneuver (Figure 4-10) is
utilized to reposition the otoconia by sequentially
moving the head into four positions, staying in each
position for roughly 30 seconds. The recurrence rate
for BPPV after these maneuvers is about 30% at 1 year,
and in some instances a second treatment may be
necessary.66
CLINICAL TIP
 Contraindications for the Hallpike-Dix test and Epley
maneuver include vertebral artery stenosis, cervical
spine dysfunction, or osteoporosis.
 After the Epley maneuver, the patient should sleep
in a semirecumbent position (HOB at 45 degrees) for
the next night.67
Nervous System CHAPTER 4 187
ACUTE VESTIBULAR NEURONITIS
Acute vestibular neuronitis (vestibular neuritis) is an
inflammation of the vestibular nerve, usually caused
by viral infection.65 Symptoms include a dramatic,
sudden onset of vertigo lasting days, with gradual
improvement. Nystagmus may or may not be present
and hearing deficits are not noted.Treatment is usually
supportive, and symptoms should resolve with time.
Treatment with antivirals has not been shown to be
effective.68
MÉNIÈRE’S DISEASE
Me¤nie' re’s disease (idiopathic endolymphatic hydrops) is
a disorder of the inner ear associated with spontaneous,
episodic attacks of vertigo; sensorineural hearing loss
that usually fluctuates; tinnitus; and often a sensation
of aural fullness.64 This is likely caused by an increase
in endolymphatic fluid causing distention of the mem-
branous labyrinth.13 Me¤nie' re’s disease is usually treated
with a salt-restricted diet and the use of diuretics to con-
trol the fluid balance with the ear as well as vestibular
suppressing medications such as Meclizine. When
conservative treatment has failed, an endolymphatic
shunt can be placed; ablation of a portion of the
labyrinth can be attempted; or vestibular neurectomy
can be performed. Physical therapy focuses on patient
education and compensatory strategies such as gaze
and postural stabilization.
BILATERAL VESTIBULAR HYPOFUNCTION
Bilateral vestibular hypofunction (BVH) is most com-
monly caused by ototoxicity of aminoglycosides (genta-
micin, streptomycin). The bilateral loss of vestibular
function leads to oscillopsia (oscillating or swinging
vision) and unsteady gait to varying degrees.64
Impairments are usually permanent, although patients
can return to high levels of function by learning to use
visual and somatosensory information to make up for
the loss of vestibular function. Other, less common,
causes of BVH include meningitis, autoimmune disor-
ders, head trauma, tumors on each eighth cranial
nerve, TIA of vessels supplying the vestibular system,
and sequential unilateral vestibular neuronitis.11
Common Degenerative Central Nervous
System Diseases
AMYOTROPHIC LATERAL SCLEROSIS
Amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s
disease, is the progressive degeneration of upper and
188 CHAPTER 4 Nervous System
Table 4-24 TESTS AND MEASURES FOR VESTIBULAR DYSFUNCTION*
Test Test Procedure
Static ocular The eyes are examined for the presence
observation of nystagmus while the head is still. If nystagmus
is present, the clinician observes for any change
with gaze fixation.
Examination of Saccades are examined by asking the patient
saccades to alternately fixate (with the head still)
the examiner’s nose and then finger, held at
different locations at approximately 15 degrees
away from primary position.The velocity,
accuracy, and initiation time are observed.
Head thrust test The patient fixates on a close object (examiner’s
nose) while the head is manually rotated, by the
examiner, in an unpredictable direction using
a small amplitude, high acceleration angular
thrust.
Head- The patient closes his or her eyes while the
shaking—induced examiner flexes the head 308 and oscillates the
nystagmus head horizontally for 20 cycles at a frequency of
2 reps per second. Once the oscillations are
stopped, the patient opens his or her eyes and
the examiner observes for nystagmus.
Hallpike-Dix test The patient’s head is rotated 458 to one side in
sitting, and moved into a supine position with
the head extended 308 over the end of the
examination table with the head still rotated.
The examiner observes for the presence of
nystagmus.
Dynamic visual The patient attempts to read the lowest line of an
acuity (DVA) test eye chart while the clinician horizontally
oscillates the patient’s head at a frequency
of 2 reps per second.
Caloric testing Air or water is infused into the external auditory
canal.The change in temperature generates
nystagmus within the horizontal SCC in intact
vestibular systems.
Rotary chair test Patients are rotated in a chair in the dark.
Nystagmus is present in intact vestibular systems.
Rhomberg test Patient stands with the feet together with eyes
open and then with the eyes closed.
Sensory There are six parts to the test. 1.The patient stands
organization test on a fixed platform with eyes open. 2.The
patient stands on a fixed platform with the eyes
closed. 3.The patient stands on a fixed platform
with moving vision screen. In Conditions 1-3,
the patient is relying on somatosensory and
vestibular input.The test is repeated with a
Vestibular Pathology
Nystagmus is present when the head is still
and improves with gaze fixation indicative
of unilateral vestibular hypofunction.
Slowed saccades or the inability to complete
without also moving the head indicates
vestibular pathology.
The eyes will not move as quickly as the
head rotation, and the eyes move off
the target with a corrective saccade
to reposition the eyes on the target.
This is indicative of vestibular
hypofunction.
Horizontal nystagmus indicates a unilateral
peripheral vestibular lesion, with the slow
phase of nystagmus toward the side of the
lesion.
Vertical nystagmus suggests a central lesion.
The presence of nystagmus indicates BPPV.
A three or more line decrement in visual
acuity during the head movement
indicates vestibular hypofunction.
The absence of or slowed nystagmus
indicates pathology in the horizontal SCC.
The absence of or slowed nystagmus
indicates pathology in the horizontal SCC.
Increase in sway or loss of balance with the
eyes closed may indicate vestibular
dysfunction.
The patient will be unable to maintain
balance in condition six if vestibular
dysfunction is present and vision and
somatosensory input are intact.The
examiner has to be aware that patients
may also lose their balance in other
conditions due to impaired vision or
 Nervous System CHAPTER 4 189

Table 4-24 TESTS AND MEASURES FOR VESTIBULAR DYSFUNCTION*—cont’d

Test Test Procedure Vestibular Pathology
moving platform to distort somatosensory input sensation that is seen normally in the
and in the Condition 6 (moving platform and aging process.
moving vision screen, the patient is relying on
vestibular input alone). Sway is noted and
recorded as minimal, mild or moderate and fall.
*Before performing these tests, ensure that the patient’s cervical spine is intact and can tolerate neck/head rotation. Also ensure that the
vertebral arteries are not compromised.
SCC, Semicircular canal.
Data from reference numbers 11, 64.

lower motor neurons, primarily the motor cells of the
anterior horn and the corticospinal tract. The etiology
of ALS is unknown except for familial cases. Signs
and symptoms of ALS depend on the predominance
of upper or lower motor neuron involvement and may
include hyperreflexia, muscle atrophy, fasciculation,
and weakness, which result in dysarthria, dysphagia,
respiratory weakness, and immobility.69 If more upper
motor neurons are affected, the symptoms will be
primarily clumsiness, stiffness, and fatigue, whereas
lower motor neuron degeneration will present as weak-
ness or atrophy and occasionally fasciculations. Bulbar
symptoms include hoarseness, slurring of speech, chok-
ing on liquids, and difficulty initiating swallowing and
are more predominant in cases of familial ALS.37 ALS
is diagnosed by clinical presentation, EMG, nerve con-
duction velocity (NCV) studies, muscle and nerve biop-
sies, and neuroimaging studies to rule out other
diagnoses.11 Owing to the progressive nature of ALS,
management is typically supportive or palliative,
depending on the disease state, and may include
pharmacologic therapy (Rilutek [Riluzole]), spasticity
control, bronchopulmonary hygiene, and nutritional
and psychosocial support.56 Physical therapy and reha-
bilitation are important with patients with ALS to max-
imize compensatory strategies and to prescribe
appropriate adaptive equipment to maintain the
patient’s independence for as long as possible.
GUILLAIN-BARRÉ SYNDROME
Guillain-Barre¤ syndrome (GBS), or acute inflammatory
demyelinating polyradiculopathy, is caused by the
breakdown of Schwann cells by antibodies.56 There is
an onset of paresthesia, pain (especially of the lumbar
spine), symmetric weakness (commonly proximal fol-
lowed by distal, including the facial and respiratory
musculature), and autonomic dysfunction approxi-
mately 1 to 3 weeks after a viral infection. GBS is diag-
nosed by history, clinical presentation, CSF sampling
(increased protein level), and EMG studies (which
show decreased motor and sensory velocities).70 Once
diagnosed, the patient with GBS is hospitalized

Table 4-25 SYMPTOMS ASSOCIATED WITH PERIPHERAL VS. CENTRAL VESTIBULAR PATHOLOGY

Symptom Peripheral Central

Balance deficits Mild to moderate Severe, ataxia usually present
Hearing loss Accompanied with fullness of the ears Rare, if it does occur, often sudden
and tinnitus and permanent
Nystagmus Unidirectional in all gaze positions; Changes direction in different gaze
decreases with visual fixation positions; no change with visual fixation
Nausea Can be severe Variable, may be absent
Additional neurologic Usually not present Can include diplopia, altered consciousness,
impairment lateropulsion
Data from Cummings CW, Flint PW, et al. (eds). Otolaryngology: Head & Neck Surgery (4th ed). Philadelphia: Mosby, 2005; Schubert MC.
Vestibular Disorders. In O’Sullivan SB, SchmitzTJ (eds). Physical Rehabilitation (5th ed). Philadelphia: FA Davis, 2007;1013.
190 CHAPTER 4 Nervous System
FIGURE 4-9
Hallpike-Dix maneuver for eliciting nystagmus and vertigo due
to posterior canal BPPV.The patient’s head is first turned
45 degrees to the right.The patient’s neck and shoulders are
then brought into the supine position with the neck extended
below the level of the examination table.The patient is
observed for nystagmus or complaints of vertigo.The patient is
next returned to the upright position. (From Herdman [ed].
Vestibular Rehabilitation. Philadelphia: FA Davis, 1994.)
because of the potential for rapid respiratory muscle
paralysis.70 Functional recovery varies from full
independence to residual weakness that takes 12 to
24 months to resolve.56,70 GBS is fatal in 5% of cases.71
The management of GBS may consist of pharmacologic
therapy (immunosuppressive agents), plasma exchange,
intravenous immunoglobulin, respiratory support,
physical therapy, and the supportive treatment of asso-
ciated symptoms (e.g., pain management).
MULTIPLE SCLEROSIS
Multiple sclerosis (MS) is the demyelination of the
white matter of the CNS and of the optic nerve, presum-
ably an autoimmune reaction induced by a viral or
other infectious agent.11 Symptoms of MS are highly
variable from person to person and the specific type
of MS is categorized by the progression of symptoms
(see Box 4-1).11
MS typically occurs in 20 to 40 year olds and in
women more than men. It is diagnosed by history
(onset of symptoms must occur and resolve more than
once), clinical presentation, CSF sampling (increased
myelin protein and immunoglobulin G levels), evoked
potential recording, and MRI (which shows the pres-
ence of two or more plaques of the CNS).11,15 These
plaques are located at areas of demyelination where lym-
phocytic and plasma infiltration and gliosis have
occurred. Signs and symptoms of the early stages of
MS may include focal weakness, fatigue, diplopia,
blurred vision, equilibrium loss (vertigo), paresthesias,
and urinary incontinence. Additional signs and
symptoms of the later stages of MS may include ataxia,
paresthesias, spasticity, sensory deficits, hyperreflexia,
tremor, and nystagmus.69 The management of MS may
include pharmacologic therapy (corticosteroids; syn-
thetic interferons such as Avonex and Rebif; or immu-
nosuppressants such as Novantrone), skeletal muscle
relaxants (Baclofen), physical therapy, and the treatment
of associated disease manifestations (e.g., bladder
dysfunction).
CLINICAL TIP
 Patients with MS usually present with an adverse
reaction to heat, triggering an exacerbation marked
by decline in function and an increase in fatigue.
Heat stressors are anything that can raise body
temperature, including sun exposure, hot
environment, or a hot bath or pool. This
exacerbation usually resolves within 24 hours.
PARKINSON’S DISEASE
Parkinson’s disease (PD) is a neurodegenerative disor-
der caused by a loss of dopaminergic neurons in the
substantia nigra, as well as other dopaminergic and
nondopaminergic areas of the brain.72 PD is charac-
terized by progressive onset of bradykinesia, altered
posture and postural reflexes, resting tremor, and
cogwheel rigidity. Other signs and symptoms may
include shuffling gait characterized by the inability to
start or stop, blank facial expression, drooling,
decreased speech volume, an inability to perform fine-
motor tasks, and dementia.37,69 PD is diagnosed by his-
tory, clinical presentation, and MRI (which shows a
 Nervous System CHAPTER 4 191

FIGURE 4-10
The Epley maneuver. (From FurmanJM, Cass SP: Benign paroxysmal positional vertigo. N EnglJ Med
1999; 341:1590-1596. Copyright 1999 Massachusetts Medical Society. All rights reserved.)

light rather than dark substantia nigra).15 The manage- the effectiveness of fetal graft transplantation in
ment of PD mainly includes pharmacologic therapy humans,74 although multiple studies using rat models
with antiparkinsonian agents and physical therapy. have showed improvements.75,76
Levodopa is the most effective treatment for PD, but
chronic use can cause hallucinations, dyskinesias, and
motor fluctuations.37 There are also several surgical CLINICAL TIP
options that have emerged including the placement of
 The clinician should be aware that patients with
a deep brain stimulator (DBS) and, most recently, stem
PD have a higher incidence of orthostatic
cell implants. The DBS has showed the most promise
hypotension and have a tendency toward
with recent studies showing improvement in quality
retropulsion (pushing posteriorly in sitting and
of life rating73 and a decrease in tremors.74 To date
standing) with mobility.
there have been limited studies completed to support
192 CHAPTER 4 Nervous System

BOX 4-1 DEFINITIONS AND TERMINOLOGY

USED TO DESCRIBE CATEGORIES
OF MULTIPLE SCLEROSIS
Relapsing-remitting MS (RRMS): Characterized
by relapses with either full recovery or some
remaining neurologic signs/symptoms and
residual deficit upon recovery; the periods
between relapses are characterized by lack
of disease progression.
Primary-progressive MS (PPMS): Characterized
by disease progression from onset, without
plateaus or remissions or with occasional plateaus
A
and temporary minor improvements.
Secondary-progressive MS (SPMS):
Characterized by initial relapsing-remitting
course, followed by progression at a variable rate
that may also include occasional relapses and
minor remissions.
Progressive-relapsing MS (PRMS):
Characterized by progressive disease from onset
but without clear acute relapses that may or may
not have some recovery or remission; commonly
seen in patients who develop the disease after
40 years of age.
Benign MS: Characterized by mild disease
in which patients remain fully functional in all
neurologic systems 15 years after disease onset. B
Malignant MS (Marburg’s variant): FIGURE 4-11
Characterized by rapid progression leading Herniation syndromes depicted. Intracranial shifts from
to significant disability or death within a relatively supratentorial lesions. A, Normal location of structures.
short time after onset. B,Various herniation syndromes are demonstrated: 1. Cingulate
gyrus herniating under falx cerebri, 2.Temporal lobe herniating
downward through the tentorial notch, 3. Compression of
contralateral cerebral peduncle, 4. Downward displacement of
brain stem through tentorial notch showing central herniation
syndrome. (From Beare PG, MyersJL [eds]. Adult Health
GENERAL MANAGEMENT Nursing [3rd ed]. Philadelphia: Saunders, 1998;919.)

The three dynamic variables within the fixed skull

Intracranial and Cerebral Perfusion Pressure
The maintenance of normal ICPor the prompt recogni-
tion of elevated ICP is one of the primary goals of the
team caring for the postcraniosurgical patient or the
patient with cerebral trauma, neoplasm, or infection.
ICP is the pressure CSF exerts within the ventricles.
This pressure (normally 4 to 15 mm Hg) fluctuates
with any systemic condition, body position, or activity
that increases cerebral blood flow, blood pressure, or
intrathoracic or abdominal pressure; decreases venous
return; or increases cerebral metabolism.
are blood, CSF, and brain tissue. As ICP rises, these
variables change in an attempt to lower ICP via the
following mechanisms: cerebral vasoconstriction, com-
pression of venous sinuses, decreased CSF production,
or shift of CSF to the subarachnoid space.When these
compensations fail, compression of brain structures
occurs, and fatal brain herniation will develop
if untreated (Figure 4-11). The signs and symptoms of
increased ICP are listed in Table 4-26. The methods
of controlling ICP, based on clinical neurologic exami-
nation and diagnostic tests, are outlined in Table 4-27.

Table 4-26 EARLY AND LATE SIGNS OF INCREASED INTRACRANIAL PRESSURE
Observation Early
Level of consciousness Confusion, restlessness, lethargy
Pupil appearance Ipsilateral pupil sluggish to light, ovoid
in shape, with gradual dilatation
Vision Blurred vision, diplopia, and decreased
visual acuity
Motor Contralateral paresis
Vital signs Stable blood pressure and heart rate
Additional findings Headache, seizure, cranial nerve palsy
Data from HickeyJV.The Clinical Practice of Neurological and Neurosurgical Nursing (4th ed). Philadelphia: Lippincott, 1997.
Appendix Table III-A.5 describes the different types of
ICP monitoring systems.
Cerebral perfusion pressure (CPP), or cerebral blood
pressure, is mean arterial pressure minus ICP. It indi-
cates oxygen delivery to the brain. Normal CPP is
70 to 100 mm Hg. CPPs at or less than 60 mm Hg for a
prolonged length of time correlate with ischemia and
anoxic brain injury.77
The following are terms related to ICP:
Brain herniation The displacement of brain
parenchyma through an anatomic
opening; named according to the
location of the displaced
structure (e.g., transtentorial
herniation is the herniation of the
cerebral hemispheres,
diencephalon, or midbrain
beneath the tentorium cerebelli).
Mass effect The combination of midline shift,
third ventricle compression, and
hydrocephalus15
Midline shift The lateral displacement of the falx
cerebri secondary to a space-
occupying lesion
Space-occupying A mass lesion, such as a tumor or
lesion hematoma that displaces brain
parenchyma and may result in the
elevation of ICP and shifting of
the brain
Nervous System CHAPTER 4 193
Late
Coma
Papilledema, ipsilateral pupil dilated and
fixed, or bilateral pupils dilated and fixed
(if brain herniation has occurred)
Same as early signs but more exaggerated
Abnormal posturing, bilateral flaccidity
if herniation has occurred
Hypertension and bradycardia (Cushing’s
response), altered respiratory pattern,
increased temperature
Headache, vomiting, altered brain
stem reflexes
Another primary goal of the team is to prevent fur-
ther neurologic impairment. The main components of
management of the patient with neurologic dysfunc-
tion in the acute care setting include pharmacologic
therapy, surgical procedures, and physical therapy
intervention.
Pharmacologic Therapy
A multitude of pharmacologic agents can be prescribed
for the patient with neurologic dysfunction. These
include antianxiety medications (Appendix Table
IV-14), anticonvulsants (Appendix Table IV-15), anti-
depressants (Appendix Table IV-16), antipsychotics
(Appendix Table IV-17), mood stabilizers (Appendix
Table IV-18), Parkinson’s medications (Appendix
Table 1V-17), diuretics (Appendix Table IV-3), and
adrenocorticosteroids (AppendixTable IV-8).
Additional pharmacologic agents for medical
needs include antibiotics (e.g., for infection or after
neurosurgery), antihypertensives, thrombolytics,
anticoagulants, chemotherapy and radiation for CNS
neoplasm, stress ulcer prophylaxis (e.g., after SCI),
pain control, and neuromuscular blockade.
Neurosurgical Procedures
The most common surgical and nonsurgical neuro-
logic procedures are described below. Refer to Table
3-6 for a description of surgical spine procedures and
Appendix III-A.5 for a description of ICP monitoring
devices.
194 CHAPTER 4 Nervous System
Table 4-27 TREATMENT OPTIONS TO DECREASE
INTRACRANIAL PRESSURE (ICP)
Variable Treatment
Blood pressure Inotropic drugs to maintain mean
arterial pressure > 90 mm Hg
to aid in cerebral perfusion,
or antihypertensives
Osmotherapy Osmotic diuretic to minimize
cerebral edema
Mechanical Normocapnia* to maximize
ventilation cerebral oxygen delivery by
limiting cerebral ischemia from
the vasoconstrictive effects
of decreased PaCO2
Cerebrospinal Ventriculostomy to remove
fluid drainage cerebrospinal fluid
Sedation/paralysis Barbiturates to decrease cerebral
blood flow or other medication
to decrease the stress of noxious
activities
Positioning Head of the bed positioned at
30-45 degrees to increase
cerebral venous drainage
Promote neutral cervical spine
and head position
Environment Dim lights, decreased noise,
frequent rest periods to decrease
external stimulation
Seizure control Prophylactic anticonvulsant
medication
Temperature Normothermia or induced
control hypothermia to 32-358 C
(e.g., cooling blanket or
decreased room temperature)
to decrease cerebral metabolism
*Routine aggressive hyperventilation is no longer used for the
control of elevated ICP. Hyperventilation can contribute to
secondary brain injury because of a rebound increase in cerebral
blood flow and volume in response to a decreased cerebrospinal
fluid pH.
Data from Wong F. Prevention of Secondary Brain Injury. Crit Care
Nurs 2000;20:18-27.
Aneurysm The obliteration of an aneurysm with a
clipping surgical clip placed at the stem of
the aneurysm.
Burr hole A small hole made in the skull with a
drill for access to the brain for the
placement of ICP monitoring
systems, hematoma evacuation, or
stereotactic procedures; a series of
burr holes is made before
a craniotomy.
Craniectomy The removal of incised bone, usually
for brain (bone flap) tissue
decompression; the bone may be
permanently removed or placed in
the bone bank or temporarily placed
in the subcutaneous tissue of the
abdomen (to maintain blood
supply).
Cranioplasty The reconstruction of the skull with a
bone graft or acrylic material to
restore the protective properties of
the scalp and for cosmesis.
Craniotomy An incision through the skull for
access to the brain for extensive
intracranial neurosurgery, such as
aneurysm or AVM repair or tumor
removal; craniotomy is named
according to the area of the bone
affected (e.g., frontal, bifrontal,
frontotemporal [pterional],
temporal, occipital).
Embolization The use of arterial catheterization
(entrance usually at the femoral
artery) to place a material, such
as a detachable coil, balloon, or
sponge, to clot off an AVM or
aneurysm.
Evacuation The removal of an epidural, subdural,
or intraparenchymal hematoma via
burr hole or craniotomy.
Shunt The insertion of a shunt system that
placement connects the ventricular system with
the right atrium (VA shunt) or
peritoneal cavity (VP shunt) to allow
the drainage of CSF when ICP rises.
Stereotaxis The use of a stereotactic frame
(a frame that temporarily
attaches to the patient’s head)
in conjunction with head CT
results to specifically localize a
pretargeted site, as in tumor biopsy;
a burr hole is then made for access
to the brain.

CLINICAL TIP
 The physical therapist should be aware of
the location of a craniectomy, because
the patient should not have direct pressure
applied to that area. Look for signs posted at
the patient’s bedside that communicate positioning
restrictions.
 Pay close attention to head-of-bed positioning
restrictions for the patient who has recently
had neurosurgery. Often, the head of the bed
is at 30 degrees, or it may be flat for an initial
24 hours and then gradually elevated 15 to
30 degrees per day depending on the location
of surgery (supratentorial or infratentorial,
respectively).21
Physical Therapy Intervention
GOALS
The primary physical therapy goals in treating patients
with primary neurologic pathology in the acute care set-
ting include maximizing independence and promoting
safety with gross functional activity. Another main
goal is to assist in the prevention of the secondary man-
ifestations of neurologic dysfunction and immobility,
such as pressure sores, joint contracture, and the delete-
rious effects of bed rest (see Appendix I-B).
BASIC CONCEPTS FOR THE TREATMENT OF
PATIENTS WITH NEUROLOGIC DYSFUNCTION
 A basic understanding of neurologic pathophysiolo-
gy is necessary to create appropriate functional
goals for the patient. The therapist must appreciate
the difference between reversible and irreversible
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Postural Restriction inTreating Benign Paroxysmal
Positional Vertigo. Arch Otolaryngol Head Neck Surg
2006;132(5):501-505.
68. Strupp M, Zingler VC, Arbusow V. Methylprednisolone,
Valacyclovir, or the Combination for Vestibular Neuritis.
N EnglJ Med. 2004;351(4):354-361.
69. Fuller KS. Degenerative Diseases of the Central
Nervous System. In CC Goodman,WG Boissonnault
(eds). Pathology: Implications for the Physical Therapist.
Philadelphia: Saunders, 1998;723.
70. Newswanger DL,Warren CR. Guillain-Barre¤ Syndrome.
Am Fam Physician 2004;69(10):2405-2410.
71. WorshamTL. Easing the Course of Guillain-Barre¤
Syndrome. RN 2000;63(3):46-50.
72. Suchowersky O, Reich S, PerlmutterJ, et al. Practice
Parameters: Diagnosis and Prognosis of New Onset
Parkinson Disease (An Evidence-Based Review):
Report of the Quality Standards Subcommittee of the
American Academy of Neurology. Neurology
2006;66(7):976-982.
73. The Deep-Brain Stimulator for Parkinson’s Disease
Study Group. Deep-Brain Stimulation of the
Subthalamic Nucleus or Pars Interna of the Globus
Pallidus in Parkinson’s Disease. N EnglJ Med
2001;345:956-963.
74. Diamond A, ShahedJ, JankovicJ.The Effects of
Subthalamic Nucleus Deep Brain Stimulation on
ParkinsonianTremor. J Neurol Sci
2007;260(1-2):199-203.
75. Anderson L, Caldwell MA. Human Neural Progenitor
Cell Transplants into the Subthalamic Nucleus
Lead to Functional Recovery in a Rat Model of
Parkinson’s Disease. Neurobiol Dis 2007;27(2):133-140.
76. Wang XJ, Liu WG, Zhang YH, et al. Effect of
Transplantation of c17.2 CellsTransfected with
Interleukin-10 Gene on Intracerebral Immune Response
in Rat Model of Parkinson’s Disease. Neurosci Lett
2007;423(2):95-99.
77. King BS, Gupta R, Narayan RJ.The EarlyAssessment
and Intensive Care Unit Management of Patients with
SevereTraumatic Brain and Spinal Cord Injuries. Surg
Clin North Am 2000;80:855-870.
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 5 Oncology

Susan Polich INTRODUCTION

Jaime C. Paz Cancer is a term that applies to a group of diseases characterized by
the abnormal growth of cells. The physical therapist requires an under-
standing of underlying cancer pathology, as well as the side effects,
considerations, and precautions related to cancer care to enhance clini-
cal decision making to safely and effectively treat the patient with
cancer. This knowledge will also assist the physical therapist with the
early detection of previously undiagnosed cancer. The objectives for
this chapter are to provide the following:
1. An understanding of the medical assessment and diagnosis of a
patient with cancer, including staging and classification
2. An understanding of the various medical and surgical methods of
cancer management
3. A better understanding of a variety of the different body system
cancers, including common sites of metastases.
4. Examination, evaluation, and intervention considerations for the
physical therapist
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:
Diagnosis/Disease Possible Practice Patterns
Cancer: 4A, 4B, 4C, 5A, 6A, 6B,
Including but not limited to cancer of the 6E
breast, prostate, lung, colon, oral, uterine,
stomach
Skin Cancer 7C
Kaposi’s Sarcoma 6H, 7B, 7C, 7E
CNS Related Cancers 6E
ConnectiveTissue Related Cancers 7E
Please refer to the back cover of this book for a complete list of the
preferred practice patterns, as individual patient conditions are highly
variable and other practice patterns may be applicable.

DEFINITIONS
The terms neoplasm, tumor, and cancer are currently used interchangeably.
Neoplasm means ‘‘new growth’’ and applies to any abnormal mass of tissue

199
200 CHAPTER 5 Oncology
that exceeds the growth of normal tissue, grows at the
expense of its host, and persists even after the stimulus
to grow is removed. The term tumor originally applied
to the swelling caused by inflammation but now refers
only to a new growth. Cancer is the layperson’s term for
all malignant neoplasms.1-4
Normal cells change in size, shape, and type,
known collectively as dysplasia, if the proper stimu-
lus is provided. Hyperplasia refers to an increase
in cell number. Metaplasia is the change of one
cell type to canother. Hyperplasia and metaplasia
can be reversible and normalçor persistent and
abnormal.1,2,4
Neoplasms, or persistent abnormal dysplastic cell
growth, are classified by cell type, growth pattern,
anatomic location, degree of dysplasia, tissue of
origin, and their ability to spread or remain in the
original location. Two general classifications for
neoplasm are benign and malignant. Benign tumors
are usually considered harmless and slow growing and
have cells that closely resemble normal cells of
adjacent tissue. However, these benign tumors may
occasionally become large enough to encroach on
Table 5-1 CLASSIFICATION OF BENIGN AND MALIGNANT TUMORS
Tissue of Origin
Epithelium
Surface epithelium
Epithelial lining of gland or ducts
ConnectiveTissue and Muscle
Fibrous tissue
Cartilage
Bone
Smooth muscle
Striated muscle
NerveTissue
Glial
Meninges
Retina
Lymphoid Tissue
Bone Marrow
White blood cells
Plasma cells
From Baird S (ed). A Cancer Source Book for Nurses (6th ed). Atlanta: American Cancer Society, 1991;28.
surrounding tissues and impair their function.
Malignant neoplasms, or malignant tumors, grow
uncontrollably, invading normal tissues and causing
destruction to surrounding tissues and organs.
Malignant neoplasms may spread, or metastasize, to
other areas of the body through the cardiovascular or
lymphatic system.1-5
Tumors may also be classified as primary or
secondary. Primary tumors are the original tumors in
the original location. Secondary tumors are those
metastases that have moved from the primary site.4
NOMENCLATURE
Benign and malignant tumors are named by their cell of
origin (Table 5-1). Benign tumors are customarily
named by attaching -oma to the cell of origin.
Malignant tumors are usually named by adding
carcinoma to the cell of origin if they originate from
epithelium and sarcoma if they originate in mesen-
chymal tissue.1-3 Variations to this naming exist, such
as melanoma and leukemia.
Benign Malignant
Papilloma Carcinoma
Adenoma Adenocarcinoma
Fibroma Fibrosarcoma
Chondroma Chondrosarcoma
Osteoma Osteosarcoma
Leiomyoma Leiomyosarcoma
Rhabdomyoma Rhabdomyosarcoma
ç Glioma
Meningioma Meningeal sarcoma
ç Retinoblastoma
ç Lymphoma/lymphosarcoma
ç Leukemias
ç Multiple myeloma
 Oncology CHAPTER 5 201
Additional signs and symptoms that may indi-
ETIOLOGY AND RISK FACTORS cate cancer include fever, unexplained weight loss of
more than 10 pounds, undue fatigue, unexplained
The causes, or etiologies, of neoplasm are often divided pain, anorexia, anemia, and weakness.2
into two categories, external (or environmental) and Paraneoplastic syndromes are symptoms that can-
genetic. There are risk factors that are thought to not be related directly to the cancer’s growth and
predispose a person to cancer. Most cancers probably invasion of tissues.They are thought to be due to abnor-
develop from a combination of factors. The most mal hormonal secretions by the tumor. The syndro-
common etiologies can be found in Table 5-2. Risk mes are present in approximately 15% of persons
factors can be found inTable 5-3. diagnosed with cancer and often are the first sign
of malignancy. Clinical findings are similar to endo-
crinopathies (Cushing’s syndrome, hypoglycemia),
SIGNS AND SYMPTOMS nerve and muscle syndromes (myasthenia), derma-
tologic disorders (dermatomyositis), vascular and
Signs and symptoms of cancer are most often due hematologic disorders (venous thrombosis, anemia),
to the tumor’s growth and invasion of surrounding and others.1,7
tissues. The American Cancer Society has the
acronym CAUTION for several common signs of
cancer6: DIAGNOSIS
 C = Change in bowel or bladder habits
 A = A sore that does not heal After obtaining a medical history and performing a
 U = Unusual bleeding or discharge physical examination, the physician uses specific medi-
 T = Thickening or lump in the breast or elsewhere cal tests to diagnose cancer. These tests may include
 I = Indigestion or difficulty in swallowing medical imaging, blood tests for cancer markers,
 O = Obvious change in a wart or mole and several types of biopsy. Biopsy, or removal and
 N = Nagging cough or hoarseness examination of tissue, is the definitive test for cancer
identification. Advancements in the technology of
Positron Emission Tomography (PET) scans in recent
years have improved detection of cancer and subse-
Table 5-2 CANCER ETIOLOGIES quent management.9 Table 5-4 lists common medical
tests used to diagnose cancer.
Agent Etiology
Viruses Human papillomavirus
Epstein-Barr virus STAGING AND GRADING
Chemical agents Tar
Soot After the diagnosis of cancer is established, staging is
Dyes performed to describe the location and size of the
Polycyclic hydrocarbons primary site of the tumor, the extent of lymph node
Nickel involvement, and the presence or absence of metastasis.
Arsenic Staging helps to determine treatment options, predict
Excessive ethanol ingestion
Vinyl chloride
life expectancy, and determine prognosis for complete
Benzene resolution.
Physical agents Ionizing radiation The mostly commonly used method to stage cancer
Ultraviolet light is the TNM system. Tumors are classified according to
Asbestos the American Joint Committee on Cancer using this
Wood dust system based on the size of the primary tumor (T), pres-
Drugs Some chemotherapeutic agents ence or absence of tumor in local lymph nodes (N),
Hormones Estrogen and presence or absence of metastasis (M) (Table 5-5).1
Adapted fromTierney LM, McPhee SJ, Papadakis MA (eds). Certain types of cancers will have specific staging
Current Medical Diagnosis and Treatment. Stamford, CT: criteria, and these will be identified throughout this
Appleton & Lange, 1999. chapter for the respective cancers.
202 CHAPTER 5 Oncology

Table 5-3 RISK FACTORS FOR SELECTED CANCER SITES

Cancer Site High-Risk Factors
Lung Heavy smoker, older than age 40 yrs
Smoked one pack per day for 20 yrs
Started smoking at age 15 or before
Smoker working with or near asbestos
Breast Lump in breast
Nipple discharge
History of breast cancer
Family history of breast cancer
Benign breast disease
High-fat diet
Nulliparous or first child after age 30 yrs
Early menarche or menopause
Colon/rectum History of rectal polyps or colonic adenomatosis
Family history of rectal polyps
Ulcerative colitis or Crohn’s disease
Obesity
Increasing age
Uterus Unusual vaginal blood or discharge
History of menstrual irregularity
Late menopause
Nulliparity
Infertility through anovulation
Diabetes, hypertension, and obesity
Age 50-64 years
Skin Excessive exposure to the sun
Fair complexion that burns easily
Presence of congenital moles or history of dysplastic nevi or cutaneous melanoma
Family history of melanoma
Oral Heavy smoker and alcohol drinker
Poor oral hygiene
Long-term exposure to the sun, particularly to the lips
Ovary History of ovarian cancer among close relatives
Nulliparity or delayed age at first pregnancy
Age 50-59 years
Prostate Increasing age
Occupations relating to the use of cadmium
Family history
Stomach History of stomach cancer among close relatives
Diet heavy in smoked, pickled, or salted foods
From Baird S (ed). A Cancer Source Book for Nurses (6th ed). Atlanta: American Cancer Society, 1991;32.

Grading reports the degree of dysplasia, or diff-

erentiation, from the original cell type. The higher the
grade, the greater the differentiation, or appearance,
from the original cell. In some cases, tumor cells may
look so unlike any normal cell that no cell of origin
can be determined. Higher degree of differentiation is
linked to aggressive, fatal tumors (Table 5-6).1
MANAGEMENT
Not all cancers are curable. Physicians may therefore
focus treatment on quality of life with palliative thera-
pies rather than on curative therapies. Four major treat-
ment options include:
 Oncology CHAPTER 5 203

Table 5-4 DIAGNOSTIC TESTS FOR CANCER

Test Description
Biopsy Tissue is taken via incision, needle, aspiration procedures. A pathologist examines the
tissue to identify the presence or absence of cancer cells; if cancer is present, the
tumor is determined to be benign or malignant.The cell or tissue of origin, staging,
and grading are also performed.
Blood tests Blood can be assessed for the presence or absence of tumor markers:
Marker Cancer
Prostate surface antigen Prostate disease
Carcinoembryonic antigen Colon cancer
Prostatic-acid phosphatase Prostate cancer
Alpha-fetoprotein Liver cell cancer
CA125 Ovarian cancer
CA19-9 Colon cancer
CA15-3 Stool guaiac
Stool guaiac Detects small quantities of blood in stool.
Pap smear A type of biopsy in which cells from the cervix are removed and examined.
Sputum cytology A sputum specimen is inspected for cancerous cells.
Sigmoidoscopy The sigmoid colon is examined with a sigmoidoscope.
Colonoscopy The upper portion of the rectum is examined with a colonoscope.
Bronchoscopy A tissue or sputum sample can be taken by rigid or flexible bronchoscopy.
Mammography A radiographic method is used to look for a mass or calcification in breast tissue.
Radiography X-ray is used to detect a mass.
Magnetic resonance imaging These noninvasive imaging techniques are used to assess lesions suspected of being
and computerized axial cancerous.
tomography
Bone scan Radionuclide imaging used to detect the presence, amount of metastatic disease,
or both in bones.
Positron Emission An imaging technique that utilizes positively charged particles (positrons) injected into
Tomography (PET) scan the body, followed by imaging, to detect subtle changes in metabolic and chemical
activity within the body. Can be combined with CTscanning. Currently used to help
detect biopsy location, discern benign versus malignant conditions, stage disease,
and diagnose cancer recurrence.
CA, Carbohydrate antigen.

 Surgical removal of the tumor Surgery

 Radiation therapy
 Chemotherapy
 Biotherapy (including immunotherapy, hormonal
therapy, bone marrow transplantation, and mono-
clonal antibodies)
Additional treatments may include physical the-
rapy, nutritional support, acupuncture, chiropractic
treatment, alternative medicine, and hospice care.
Treatment protocols differ from physician to physi-
cian and from cancer to cancer. Standard treatment
includes some combination of surgery, radiation, and
chemotherapy.
Surgical intervention is determined by the size, loca-
tion, and type of cancer, as well as the patient’s age,
general health, and functional status. Successful local-
ization and resection of recurrent and/or metastatic
lesions found on PET positive scans may be optimized
with the intraoperative use of a hand-held PET probe.9
The following are the types of general surgical proce-
dures for resecting or excising a neoplasm:
 Exploratory surgery is the removal of regions of
the tumor to explore for staging or discover the
extent or invasion of the tumor.
 Excisionalsurgery is the removal of cancerous cells
and the surrounding margin of normal tissue.
204 CHAPTER 5 Oncology
Table 5-5 TNM SYSTEM
T: Primary TX: Primary tumor cannot be
tumor assessed.
T0: No evidence of primary tumor.
Tis: Carcinoma in situ (site of origin).
T1,T2,T3,T4: Progressive increase in
tumor size and local involvement.
N: Regional NX: Nodes cannot be assessed.
lymph node N0: No metastasis to local lymph
involvement nodes.
N1, N2, N3: Progressive involvement
of local lymph nodes.
M: Distant MX: Presence of distant metastasis
metastasis cannot be assessed.
M0: No distant metastasis.
M1: Presence of distant metastasis.
Tissue cells are sent to pathology to determine the
type of cancer cell and to determine whether the
entire growth was removed.
 Debulking is an incomplete resection used to
reduce the size of a large tumor to make the patient
more comfortable or prevent the tumor from
impinging vital tissue. This surgery is usually
used when the cancer is considered ‘‘incurable.’’
 Mohs’ surgery is a microscopically controlled
surgery in which layers of the tumor are removed
and inspected microscopically until all layers
have been removed.14
 Lymph node dissection involves the removal
or resection of malignant lymph nodes to help
control the spread of cancer.
 Skin grafting may be indicated in large resections
of tumors to replace areas of skin removed
during resection of a neoplasm with donor skin
(see Chapter 7).
 Reconstructive surgery is the surgical repair of
a region with a flap of skin, fascia, muscle,
and vessels. It aids in a more cosmetic and
Table 5-6 GRADING OF NEOPLASMS
Grade Characteristics
Grade I Tumor cells closely resemble original tissue.
Grades II Tumor cells are intermediate in appearance,
and III moderately differentiated.
Grade IV Tumor cells are so poorly differentiated
(anaplastic) that the cell of origin is
difficult or impossible to determine.
functional result of surgical repair and protects
the underlying resected area.
CLINICAL TIP
 Special care must be taken with skin grafts. Patients
usually remain on bed rest to allow the graft to begin
to adhere. (Length of bed rest is dependent on
physician’s protocol, ranging from 0 to 36 days.15-17
During bed rest, therapeutic exercise may be performed
with extremities not involving the skin graft site.
 Muscle contraction in newly constructed muscle
flaps should be minimized or avoided.
Radiation10
The primary objective in administering therapeutic
radiation is to destroy malignant tissue while minimiz-
ing damage to healthy tissue.This objective can further
be divided into six different indications based on the
disease presentation and practitioner’s intentions.
These indications are as follows:
1. Definitive treatment with the intent to cure
2. Neoadjuvant treatment to improve chances of
successful surgical resection
3. Adjuvant treatment to improve local control of
cancer growth after chemotherapy or surgery
4. Prophylaxis treatment to prevent growth of cancer in
asymptomatic, yet high risk areas
5. Control to limit growth of existing cancer cells
6. Palliation to relieve pain and suffering when cure is
not possible
Radiation therapy is delivered by three different mod-
alities: external beam radiation therapy (EBRT), bra-
chytherapy, or radioimmunotherapy. EBRT is the
primary modality utilized in most cases. Technological
advances have allowed EBRT to be further divided into
different modalities that allow better localization of
tumor margins along with gradation of radiation dose,
both of which can minimize damage to surrounding tis-
sues and maximize therapeutic effect. These different
forms of EBRT include intensity modulated radiation
therapy (IMRT), image-guided radiotherapy, stereotactic
radiosurgery, and image guided cyberknife radiosurgery.
Brachytherapy involves the placement (temporary or
permanent) of selected radioactive sources directly
into a body cavity (intracavitary), into tissue (intersti-
tial), into passageways (intraluminal), or onto tissue sur-
faces (plaque). The following malignancies can be
treated with brachytherapy: gynecologic, breast, lung,
esophageal, head and neck, brain and prostate tumors,

and certain types of melanoma. Brachytherapy can be
used alone or in combination with EBRT.
Another form of radiationtherapy is called intraoper-
ative radiation therapy (IORT) which consists of deliver-
ing a single, large fraction of radiation to an exposed
tumoror to a resected tumorbed duringa surgical proce-
dure. IORT is generally utilized in the management of
gastrointestinal, genitourinary, gynecologic, and breast
cancers.10
Common side effects of radiation therapy include skin
reactions, slow healing of wounds, limb edema, contrac-
tures, fibrosis, alopecia, neuropathy, headaches, cerebral
edema, seizures, visual disturbances, bone marrow
suppression, cough, pneumonitis, fibrosis, esophagitis,
nausea, vomiting, diarrhea, cystitis, and urinary fre-
quency.6,7 These side effects may occur immediately
after radiation therapy and/or reappear at a later time.
Additionally, radiation-induced malignancies may occur,
including skin carcinoma, leukemia, sarcoma, thyroid
cancer, lung cancer, and possibly breast cancer.10
CLINICAL TIP
 Physical therapy should be deferred while the
patient has implanted radioactive seeds.
 Massage and heating modalities should be withheld
for 1 year in an irradiated area.
 Radiation may lead to decreased skin distensibility
and resultant decreased range of motion. Therefore
promotion of active or passive range of motion may
help to prevent contracture.
 Patients undergoing irradiation by beam (EBRT)
will have blue markings where the radiation is being
delivered. Caution should be taken with the skin
and underlying tissues in that area because it will
be very fragile. Patients who have received the
maximum allowable radiation in an area will have
that area outlined in black. Special care should be
taken with the skin and other tissues in that area
because it will be very fragile.
 A patient may be prescribed antiemetics
(see Appendix IV, Table IV-20) after radiation
treatment to control nausea and vomiting. Notify
the physician if antiemetic therapy is insufficient
to control the patient’s nausea or vomiting during
physical therapy sessions.
Chemotherapy
The overall purpose of chemotherapy is to treat or pre-
vent metastatic disease and reduce the size of the
Oncology CHAPTER 5 205
tumor for surgical resection or palliative care. Patients
may receive single agents or a combination of agents.
Chemotherapy can be performed preoperatively and
postoperatively. Chemotherapy is usually delivered sys-
temically, via intravenous or central lines, but may be
directly injected in or near a tumor. Refer to Appendix
III-A, Table III-A.6 for information regarding totally
implantable intravascular catheters or tunneled central
venous catheter often used for chemotherapy. Patients
may receive a single or multiple rounds of chemother-
apy over time to treat their cancer and to possibly mini-
mize side effects. Side effects of chemotherapy include
nausea, vomiting, ‘‘cancer pain,’’ and loss of hair and
other fast-growing cells, including platelets, red blood
cells, and white blood cells.
Different types of chemotherapeutic agents have dif-
ferent mechanisms of action. Alkylating agents and
nitrosoureas inhibit cell growth and division by react-
ing with DNA. Antimetabolites prevent cell growth
by competing with metabolites in production of nucleic
acid. Plant alkaloids prevent cellular reproduction by
disrupting cell mitosis.25
Chemotherapeutic agents are listed in Appendix IV,
Table IV-21.
CLINICAL TIP
 Some chemotherapeutic agents are so toxic to
humans that patients may have to remain in their
rooms while the agents are being delivered to avoid
risk to other patients and health care workers.
Physical therapists should check with the patient’s
nurse or physician if unsure. Additionally, there may
be a hospital policy concerning this issue that the
therapist should become aware of.
 Nausea and vomiting after chemotherapy vary on a
patient-to-patient basis. The severity of these side effects
may be due to the disease stage, chemotherapeutic
dose, or number of rounds. Some side effects may be
so severe as to limit physical therapy, whereas others
can tolerate activity. Rehabilitation should be delayed
or modified until the side effects from chemotherapy
are minimized or alleviated.
 Patients may be taking antiemetics, which help to
control nausea and vomiting after chemotherapy.
The physical therapist should alert the physician
when nausea and vomiting limit the patient’s
ability to participate in physical therapy so that
the antiemetic regimen may be modified or
enhanced. Antiemetics are listed in Appendix IV,
Table IV-20.
206 CHAPTER 5 Oncology

changing hormone levels.6,7 Immunotherapy includes

 Chemotherapy agents affect the patient’s appetite
enhancing the patient’s immune system and changing
and ability to consume and absorb nutrients.
the immune system’s response to the cancer, most
This decline in nutritional status can inhibit the
commonly with recombinant growth factors, such as
patient’s progression in strength and conditioning
interferon-alpha or interleukin.
programs. Proper nutritional support should be
Hormonal therapy is most commonly used to treat
provided and directed by a nutritionist. Consulting
breast and prostate cancer. Some breast tumor cells con-
with the nutritionist may be beneficial when
tain estrogen in their cytoplasm (estrogen-receptor
planning the appropriate activity level that is based
positive). Use of antiestrogens, such as tamoxifen, may
on a patient’s caloric intake.
keep the tumor from enlarging or metastasizing. Elim-
 Patients should be aware of the possible side effects
ination of the source of androgens in prostate cancer
and understand the need for modification or delay
via orchiectomy may also reduce the cancer’s spread.
of rehabilitation efforts. Patients should be given
Colony-stimulating factors maybe used to sustain the
emotional support and encouragement when they
patient with low blood counts during cancer treatment.
are unable to achieve the goals that they have
Colony-stimulating factors, such as erythropoietin,
initially set. Intervention may be coordinated around
may be given to reduce anemia.7
the patient’s medication schedule.
Monoclonal antibodies are antibodies of a single
 Vital signs should always be monitored, especially
type produced by a single line of B lymphocytes.
when patients are taking the more toxic
The antibodies are produced specifically to
chemotherapy agents that affect the heart,
attach themselves to specific types of tumor cells.
lungs, and central nervous system.
These antibodies can be used alone to attack cancer
 Platelet, red blood cell, and white blood cell counts
cells or may have radioactive material bound to them.
should be monitored with a patient on
chemotherapy. The Bone Marrow Transplantation
section in Chapter 12 suggests therapeutic activities
with altered blood cell counts. CANCERS IN THE BODY SYSTEMS
 Patients receiving chemotherapy can become
Cancers can invade or affect any organ or tissue in the
neutropenic. They can be at risk for infections and
body. The following is an overview of various cancers
sepsis.7 (A neutrophil is a type of leukocyte or white
in each body system.
blood cell that is often the first immunologic cell at
the site of infection; neutropenia is an abnormally Pulmonary Cancers
low neutrophil count. Absolute neutrophil count
Cancer can affect any structure of the pulmonary
[ANC] will determine whether or not a patient is
system. There are two major categories of lung cancer,
neutropenic and subsequent precautions. Refer to
non—small-cell lung cancer (NSCLC) and small-cell
the Bone Marrow Transplantation section in
lung cancer (SCLC). Approximately 85% of lung can-
Chapter 12 for reference values of neutropenia.)
cers are NSCLC, which is composed of three subtypes:
Therefore, patients undergoing chemotherapy
squamous cell carcinoma, adenocarcinoma, and large-
may be on neutropenic precautions, such as being
cell undifferentiated carcinoma.6,7,11,25 Symptoms asso-
in isolation. Follow the institution’s guidelines
ciated with these include chronic cough, dyspnea,
for precautions when treating these patients to
adventitious breath sounds (e.g., wheezing, crackles),
help reduce the risk of infections. Examples of
chest pain, and hemoptysis.7 Common sites of metas-
these guidelines can be found in the Bone Marrow
tases, in order of occurrence, for lung cancer include
Transplantation section in Chapter 12.
the adrenal glands (50%), liver (30% to 50%), brain
(20%) and bone (20%).13
Nonsurgical techniques, such as x-ray, computerized
Biotherapy axial tomography, and positron emission tomography,
Hormonal therapy and immunotherapy also play an can be used to stage lung cancer.19 In addition to
important role in managing cancer. Hormonal therapy the TNM staging, NSCLC is further staged to help
includes medically or surgically eliminating the guide interventions and prognosis (Table 5-7). Table
hormonal source of cancer (e.g., orchiectomy, oopho- 5-8 describes pulmonary cancer sites and surgical
rectomy, or adrenalectomy) or pharmacologically procedures used in their management. Stages IA,
 Oncology CHAPTER 5 207

Table 5-7 STAGING OF NON—SMALL-CELL LUNG CANCER

Stage Tumor Node Metastasis
Grouping (TNM) Subsets Comments
Stage 0 Tis N0 M0 Tumor in situ
Stage IA T1 N0 M0 Tumor is 3 cm with no invasion of bronchus.
Stage IB T2 N0 M0 Tumor is > 3 cm, located in a main bronchus, with possible invasion
to visceral pleura.
Stage IIA T1 N1 M0 Tumor is 3 cm with no invasion of bronchus. Ipsilateral lymph node
involvement to hilum and peribronchial region.
Stage IIB T2 N1 M0 Tumor is either > 3 cm (T2), located in a main bronchus, with possible invasion
T3 N0 M0 to visceral pleura, or can be of any size (T3) with possible invasion to chest
wall, diaphragm, medistinal pleura, and parietal pericardium. Lymph node
involvement to ipsilateral hilum and peribronchial region (N1).
Stage IIIA T3 N1 M0 Any size tumor located in main bronchus with possible invasion to chest wall,
T(1-3) N2 M0 diaphragm, medistinal pleura, and parietal pericardium. Lymph node
involvement may range from ipsilateral hilum and peribronchial region
(N1) to the subcarinal region and ipsilateral mediastinum (N2).
Stage IIIB T4 Any N M0 Any size tumor with invasion to trachea, heart great vessels, esophagus,
AnyT N3 M0 vertebral body, and/or carina. Lymph node involvement for N3 includes
contralateral hilum and mediastinum, scalenes, and supraclavicular nodes.
Stage IV AnyT Any N M1 Presence of distant metastases.
Adapted from Lababede O, Meziane MA, Rice TW. TNM Staging of Lung Cancer: A Quick Reference Chart. Chest 1999;115:233-235.

IB, IIA, and IIB typically benefit from surgery,

whereas the more advanced stages do not.12 Recent
surgical advances include the use of video-assisted,
non—rib-spreading lobectomy to remove the tumor
and the use of an intraoperative ultrasound probe to
aid in tumor localization.20,21
(SaO2) should be monitored to ensure adequate
oxygenation, especially when increasing activity levels.
 Caution must be taken when positioning patients
after pneumonectomy. Placing patients with the
existing lung in the dependent position may adversely

CLINICAL TIP Table 5-8 SURGICAL INTERVENTIONS FOR

 Thoracic surgery may involve a large incision on the PULMONARY CANCERS
thoracic wall, the location of which generally results
in a very painful incision. Surgical incisions into the Area Involved Surgical Procedure Excision of
pleural space will cause deflation of the lung. Deep- Pleura Pleurectomy Portion of pleura
breathing exercises (along with mucus-clearance
Rib Rib resection Portion of rib
techniques with incisional splinting and range-
of-motion exercises of the upper extremity on the Trachea and Tracheal repair and Trachea
side of the incision) are important to prevent bronchi reconstruction
Sleeve resection Portion of main
postoperative pulmonary complications and restore
stem bronchus
shoulder and trunk mobility.
 Patients may have chest tubes in place immediately Lung Pneumonectomy Entire single lung
Lobectomy Single or multiple
after surgery (see Appendix III-A).
lobes of the lung
 Oxygen supplementation may be required in post- Wedge resection Wedge-shaped
thoracic surgical patients. Oxyhemoglobin saturation segment of lung
208 CHAPTER 5 Oncology

affect ventilation, perfusion, and, ultimately, BOX 5-1 PRIMARY TUMORS IN BONE
oxygenation. Positioning guidelines should be
clarified with the surgeon, if not already stated.22 Benign Malignant
 Review positioning guidelines for patients who are
Osteochondroma Myeloma
status post tracheal repair and resection as often
these patients need to maintain neck flexion Chondroma Malignant lymphoma
for 5 to 7 days postoperatively. Chondroblastoma Chondrosarcoma
Chondromyxoid Dedifferentiated
fibroma chondrosarcoma
Musculoskeletal Cancers Osteoid osteoma Mesenchymal
Tumors of bone are most commonly discovered after Osteoblastoma chondrosarcoma
an injury or fracture or during a medical workup for Giant cell tumor Osteosarcoma
pain. Some tumors in the bone or muscle may arise Fibrous histiocytoma Ewing tumor
from other primary sites. Common primary tumors Metaphyseal fibrous Giant cell tumor
that metastasize to bone include breast, lung, prostate, defect (fibroma) Adamantinoma
kidney, and thyroid tumors.23 Treatment of musculo- Hemangioma Malignant fibrous
skeletal tumors can include radiation, chemotherapy, Lipoma histiocytoma
amputation, arthroplasty (joint replacement), and Desmoplastic fibroma
reconstruction using an allograft (cadaver bone). Fibrosarcoma
Types of primary orthopedic cancers are described Chordoma
in Box 5-1. Hemangioendothelioma
Although not all metastases to bone cause patho- Hemangiopericytoma
logic fractures, surgical intervention can be used for a Liposarcoma
patient with a bone metastasis because of the risk of
pathologic fracture. These procedures may include the Data from Rosenberg AE. Bones, Joints, and Soft Tissue
use of intramedullary rods, plates, and prosthetic Tumors. InV Kumar, AK Abbas, N Fausto (eds). Robbins and
devices (e.g., total joint arthroplasty) and are described Cotran Pathologic Basis of Disease (7th ed). Philadelphia:
in Chapter 3 in the Fracture Management, Appendix, Saunders, 2005;1292.
andJoint Arthroplasty sections, respectively.

CLINICAL TIP
 A patient with bone metastases must receive
clearance from the physician before mobility, along
with clarifying the patient’s weight-bearing status.
 Patients commonly experience fractures owing
to metastatic disease in the vertebrae, proximal
humerus, and femur.18 Therefore, patients should
be instructed in safety management to avoid falls
or trauma to involved areas.
 Check the weight-bearing status of patients after
bone grafting, as weight bearing may be restricted.
Areas that are prone to metastases from breast cancer,
in order or occurrence, are the lungs, bones, liver, adre-
nal glands, brain, and meninges. Advancement in the
treatment of breast cancer includes inhibition of
growth factor receptors, stromal proteases, and angio-
genesis by pharmacologic agents or specific antibo-
dies.24 Common surgical procedures for the treatment
of breast cancer are listed in Table 5-10.

Breast Cancer CLINICAL TIP

 The physical therapist should check the physician’s
Breast cancer, although more prevalent in women, is orders regarding upper-extremity range-of-motion
also diagnosed in men to a lesser extent. It may be restrictions, especially with muscle transfers. The
discovered during routine breast examinations or mam- therapist must know what muscles were resected or
mography. Progression of breast cancer is staged ac- transferred during the procedure, the location of the
cording to growth and spread of the tumor (Table 5-9).
 Oncology CHAPTER 5 209

incision, and whether there was any nerve Table 5-9 STAGES OF BREAST CANCER
involvement before mobilization. Once this
information is clarified, the therapist should proceed Stage Characteristics
to assess the range of motion of the shoulder and Stage 0 Carcinoma in situ (either lobar or ductal
neck region, as it may be affected during surgical carcinoma)
interventions for breast cancer. Stage I Invasive carcinoma 2 cm or less in diameter
 Patients may exhibit postoperative pain, without nodal involvement or only
lymphedema, or nerve injury due to trauma or metastases that are < 0.02 cm in diameter
traction during the operative procedure. Stage II Invasive carcinoma 5 cm or less in diameter
with up to 3 axillary nodes involved or
 Postoperative drains may be in place immediately
invasive carcinoma > 5 cm without nodal
after surgery, and the physical therapist should take involvement
care to avoid manipulating these drains. Range- Stage III Invasive carcinoma 5 cm or less in diameter
of-motion exercises may cause the drain to be with 4 or more axillary nodes involved or
displaced. Invasive carcinoma > 5 cm with nodal
 Incisions resulting from muscle transfer flaps involvement or
involving the rectus abdominis, pectoralis, or Invasive carcinoma with 10 or more involved
latissimus dorsi should be supported when the axillary nodes or
patient coughs. Invasive carcinoma with involvement of
 The physical therapist should instruct the patient in ipsilateral internal mammary lymph nodes or
Invasive carcinoma with skin edema,
the log-roll technique, which is used to minimize
laceration, and chest wall fixation
contraction of the abdominal muscles while the Stage IV Any breast cancer with distant metastases
patient is getting out of bed. The therapist should
also instruct the patient to minimize contraction Data from Lester SC. The Breast. In V Kumar, Abbas AK,
of the shoulder musculature during transfers. Fausto N (eds). Robbins and Cotran Pathologic Basis of Disease
(7th ed). Philadelphia: Saunders, 2005;1147.
 Lymphedema may need to be controlled with
lymphedema massage, elevation, exercise while
wearing nonelastic wraps, elastic garments, or
compression pneumatic pumps, especially when Table 5-10 SURGICAL INTERVENTIONS FOR
surgery involves lymph nodes that are near the BREAST CANCER
extremities. These techniques have been shown
Surgical Intervention Tissues Involved
to be of value in decreasing lymphedema.26,28
Circumferential or water displacement measurements Radical mastectomy Removal of breast tissue, skin,
of the involved upper extremity may be taken pectoralis major and minor,
rib, and lymph nodes
to record girth changes and to compare with the
Modified radical Removal of breast, skin, and
noninvolved extremity. mastectomy sampling axillary lymph
 The physical therapist should consider the impact nodes
of reconstructive breast surgery on the patient’s Simple or total Removal of breast, then,
sexuality, body image, and psychological state.21 mastectomy in another procedure,
a sampling of the axillary
lymph nodes
Gastrointestinal and Genitourinary Cancers Partial mastectomy Removal of tumor and
surrounding wedge of tissue
Gastrointestinal (GI) cancers can involve the esopha- Lumpectomy or local Removal of tumor and axillary
gus, stomach, colon, and rectum with colorectal wide excision lymph nodes resection in
cancer being the most prevalent type of GI cancer. separate procedure
Common areas for metastases for colorectal cancer Reconstructionç Saline implanted surgically
include, in order of occurrence, regional lymph nodes, implants beneath the skin or muscle
liver, lungs, and bones.29 Cancers of the liver and pan- Reconstruction Muscle from stomach or back,
creas, although considered gastrointestinal, will be dis- çmuscle flap including layers of skin fat
transfer and fascia, transferred to
cussed separately. Surgical procedures used to treat
create a breast
gastrointestinal cancers are described inTable 5-11.
210 CHAPTER 5 Oncology

Table 5-11 SURGICAL INTERVENTIONS FOR stimulation may be necessary to restore control
GASTROINTESTINAL SYSTEM of urinary flow.31-33
CANCERS  Patients with gastrointestinal cancer may experience
bowel as well as urinary incontinence.
Surgical Intervention Excision  Both bowel and bladder incontinence can lead
Subtotal gastrectomy Portion of the stomach to areas of dampened skin, which are prone to
Near-total gastrectomy Body of the stomach breakdown.34 Therefore, physical therapists should
Total gastrectomy Entire stomach be careful to minimize shearing forces in these areas
Gastroduodenostomy Portion of the stomach and during mobility.
duodenum  Patients who are status post GI surgery may have
Gastrojejunostomy Portion of the stomach and resultant colostomy placements. Please refer to
jejunum
Chapter 8 for details and guidelines regarding this
Hemicolectomy Portion of the colon
Anterior or low-anterior Upper-third of the rectum procedure.
resection
Abdominal perineal Middle- and lower-third
resection of the rectum Hepatobiliary Cancers
Primary liver tumors can arise from hepatic cells, con-
nective tissue, blood vessels, or bile ducts. However
Genitourinary cancers can involve the uterus, ovar- metastatic cancer to the liver from breast, lung, and
ies, testicles, prostate, bladder, and kidney. Renal cell colon cancer are more common than primary hepatic
carcinoma tends to metastasize widely before symptoms cancer.35 If a primary malignant liver carcinoma is
are recognized, which generally leads to a later discov- present, it is almost always associated with cirrhosis.
ery of the disease. Additionally, renal cell carcinoma is Refer to Chapter 8 for a further description of cirrhosis.
usually discovered on unrelated imaging scans of the Benign liver tumors are associated with women taking
abdomen. Nephrectomy, total removal of a kidney, is oral contraceptives. Most benign liver tumors are
the choice of treatment; however, partial nephrectomy asymptomatic.
may be performed to help preserve some kidney func- Hepatic adenomas (benign hepatic cell tumors)
tion.30 Additional surgical procedures used to treat gen- are highly vascular, and patients carry the risk of hepa-
itourinary cancers are listed inTable 5-12. tic rupture. Hepatomas, or malignant hepatic paren-
chymal cell tumors, are closely associated with male
CLINICAL TIP gender, excessive ethanol use, hepatitis B, and hepati-
tis C. Treatment is usually with chemoembolization
 Patients with genitourinary cancer may experience or tumor resection. Patients with a small, nonmetasta-
urinary incontinence. Bladder control training, pelvic sizing hepatoma may be treated with liver trans-
floor exercises, and biofeedback or electrical plantation. Untreated hepatoma has a very poor

Table 5-12 SURGICAL INTERVENTIONS FOR GENITOURINARY SYSTEM CANCERS

Surgical Intervention Excision
Uterus Hysterectomy Uterus through abdominal wall or vagina
Total abdominal hysterectomy Body of uterus and cervix through abdominal
wall
Subtotal abdominal hysterectomy Uterus (cervix remains)
Ovary Oophorectomy One ovary
Ovaries and oviducts Bilateral salpingo-oophorectomy Both ovaries and oviducts
Prostate Radical prostatectomy Entire prostate
Testes Orchiectomy One or both testes

Table 5-13 SURGICAL INTERVENTIONS FOR
THE HEPATOBILIARY SYSTEM
Area Surgical
Involved Intervention Excision
Pancreas Whipple procedure Duodenum
(Refer to Chapter and proximal
8 for more details pancreas
on this procedure)
Liver Segmental resection Complete
segment of liver
Subsegmental Portion of a
resection segment of liver
prognosis. Five-year survival rates for treated tumors
are 15% to 45%.7
Cancer of the biliary tract is usually found during
surgery for another biliary disease or when metastasiz-
ing to other organs, particularly the liver. Treatment is
by surgery, but prognosis is poor.
In both hepatic cancer and biliary cancer, laboratory
values are used to diagnose, prognose, and monitor
the course of treatment. Liver function tests may
include bilirubin, aspartate aminotransferase (AST),
alanine aminotransferase (ALT), lactate dehydro-
genase (LDH), gamma-glutamyltransferase, alkaline
phosphatase, coagulation factors, and serum proteins.
Surgical interventions for the hepatobiliary system
are outlined inTable 5-13.
CLINICAL TIP
 Any patient with hepatic adenoma must be cautioned
to avoid lifting heavy objects or performing
maneuvers that increase intraabdominal pressure.
 Hepatic cancers can result in metabolic
complications, which may interfere with glucose
metabolism and subsequent energy production.
Pancreatic Cancer
The incidence of pancreatic cancer doubled in the late
twentieth century and has the highest mortality rates
of any cancer with a 5-year survival rate of 5%.36,37
Most pancreatic tumors arise from the pancreatic duct
and are found in the head of the pancreas. Pain and
jaundice are the most usual clinical manifestations;
these symptoms occur as the tumor invades sur-
rounding tissue, especially the liver and gallbladder.
Endoscopic ultrasonography and CTscan have proven
Oncology CHAPTER 5 211
to be valuable in diagnosis of pancreatic cancer.37
Treatment usually focuses on tumor resection, allevia-
tion of pain, and prevention of gastric outlet obstruc-
tion. Surgery, radiation, and chemotherapy are used as
treatment. Recent treatments include supravoltage radi-
ation plus chemotherapy.38 Patients with nonresectable
tumors have benefited from placement of a biliary
stent or gastric operative bypass.39 Even so, prognosis
is poor because the disease has usually metastasized by
the time it is diagnosed.3
Hematologic Cancers
Hematologic cancers can arise from any blood-forming
tissue. These malignancies include the leukemias, lym-
phomas, and multiple myeloma. The malignant cells
can occur in the bloodstream, bone marrow, spleen,
lymph nodes, and thymus, and, in some cases, they can
invade bone itself.
LEUKEMIA
The leukemias are malignancies of white blood cells,
most commonly granulocytes (neutrophils or polymor-
phonuclear leukocytes) and lymphocytes. These malig-
nant cells first occupy the bone marrow, replacing
normal cells, then spill into the bloodstream.
Because the malignant cells first occupy the bone
marrow, they can occlude the space occupied by
normal bone marrow cells. As a result, patients can
have anemia, thrombocytopenia, and leukopenia.
Often, the clinical manifestations of leukemia are fati-
gue, easy bruising, and infections. (Refer to Chapter 6
for hematologic information.)
Leukemia is classified as acute or chronic, depend-
ing on the maturity of the malignant cell. Acute leuke-
mia is from a more immature white blood cell; disease
progression tends to be rapid. Chronic leukemias are
from more mature cells; disease progression is usually
slower. Acute leukemias tend to occur in children and
young adults. Chronic leukemia tends to occur in
older adults. Types of leukemia, cells affected, and
common age ranges are listed inTable 5-14.
LYMPHOMAS
Lymphomas are malignancies of lymphocytic cells and
lymph tissues. Unlike leukemic cells that occupy bone
marrow and spill into the bloodstream, lymphomas
occupy lymph tissue (lymph nodes and spleen).
Occupation of the lymph nodes usually causes painless
enlargement, often the first sign of lymphoma.
The most common type of lymphoma is Hodgkin’s
lymphoma. The other most common types of
212 CHAPTER 5 Oncology

Table 5-14 TYPES OF LEUKEMIA Table 5-16 STAGES OF LYMPHOMA, ANN

ARBOR CLASSIFICATION
Age Range
Type Cells Involved (years) Stage Distribution of Disease
Acute lymphocytic Lymphocytes 3-7 I Single lymph node region or single
leukemia extralymphatic organ or site involved
Acute nonlymphocytic Stem cells 15-40 II Two or more lymph node regions on the
leukemia same side of the diaphragm involved
Chronic myelogenous Granulocytes 25-60 or involvement of limited continuous
leukemia extralymphatic organ
Chronic lymphocytic Lymphocytes 50+ III Lymph node regions on both sides
leukemia of the diaphragm, limited contiguous
extralymphatic organ involvement, or both
IV Multiple, disseminated involvement of one or
lymphoma are non-Hodgkin’s (malignant or lympho- more extralymphatic organs, with or without
sarcoma) and Burkitt’s lymphomas. Burkitt’s lymphoma lymphatic involvement
is a solid tumor of B-cell origin, endemic in Africa.1,7 Adapted from Carbone PP, Kaplan HS, Musshoff K, et al. Report
Characteristics of Hodgkin’s and non-Hodgkin’s of the Committee on Hodgkin’s Disease Staging Classification.
lymphomas can be found inTable 5-15. Cancer Res 1971;31(11):1860-1861.
For lymphoma, theTNM system has generally been
replaced by the Ann Arbor Classification.This classifi-
cation is based on the number and location of lymph chemotherapy, irradiation, or both. Some of the
nodes involved. The Ann Arbor Classification can be slower-growing leukemias are left untreated, especially
found inTable 5-16. if the patient is elderly.3 Bone marrow transplantation is
PROGNOSIS. If left untreated, all leukemias and lym- discussed in Chapter 12, and chemotherapy agents are
phomas are fatal. Malignant cells can infiltrate all described in Appendix IV,Table IV-21.
major blood vessels and organs, causing occlusion and
infarction. Infiltration into the musculoskeletal struc-
tures can result in joint hemorrhage, rheumatologic- CLINICAL TIP
type symptoms, and synovitis. Infiltration of neurolog-  Platelet counts and hematocrit should be assessed to
ic tissues can result in nerve palsies, encephalopathy, determine a safe level of activity or exercise. See the
headache, vomiting, blurred vision, and auditory pro- Bone Marrow Transplantation section in Chapter 12
blems.1 In addition, the decreased number of normal for specific guidelines.
immunologic cells leaves the patient highly susceptible  In patients with lymphoma, enlarged lymph nodes
to infection. may either be tender or painful. Therefore, it is
TREATMENT. Leukemias are treated with chemo- advisable to identify these regions prior to working
therapy, radiation, hormone therapy, and bone mar- with the patient in order take caution with manual
row transplantation. Lymphoma is treated with techniques and also to monitor any progression
of the disease.

Table 5-15 CHARACTERISTICS OF HODGKIN’S

AND NON-HODGKIN’S LYMPHOMAS
MULTIPLE MYELOMA
Hodgkin’s Non-Hodgkin’s Multiple myeloma is a malignancy of plasma cells,
Lymphoma Lymphoma which are derived from B-lymphocytes (B-cells), and
Nodal Usually involves Usually involves are responsible for creating antibodies. The disease
involvement single node site more than one is characterized by the tumor’s arising in the bone
site marrow of flat bones and the infiltration of the
Spread Usually orderly Nonorderly myeloma cells into the bone and, eventually, other
Extranodal Uncommon Common
involvement
organs. These malignant cells produce a single
type of antibody that may increase the viscosity of

Table 5-17 INTERNATIONAL STAGING SYSTEM
FOR MULTIPLE MYELOMA
Stage Criteria Median Survival
(months)
I Serum b2-microglobulin 62
< 3.5 mg/L
Serum albumin  3.5 g/dl
II Not stage I or III* 44
III Serum b2-microglobulin 29
 5.5 mg/L
*There are two categories for stage II: Serum b2-microglobulin
< 3.5 mg/L but serum albumin < 3.5 g/dl; or serum b2-
microglobulin 3.5 to < 5.5 mg/L irrespective of the serum
albumin level.
From Greipp PR et al., International Staging System for Multiple
Myeloma. J Clin Oncol 23(15)2005:3412-3420. Accessed from
http://jco.ascopubs.org/cgi/content/full/23/15/3412 on
December 10, 2007.
the blood. Classically, the disease produces bone
pain and decreased number of normal hematologic
cells (e.g., red blood cells, white blood cells, and plate-
lets). Staging of the disease has been updated from the
Durie-Salmon Classification to the International
Staging System, which is based on laboratory findings
of abnormal cells (Table 5-17).
The disease has a slow progression. Most persons
affected with multiple myeloma have an asymptomatic
period that can last up to 20 years.1 Bone pain, usually
the first symptom, occurs when the myeloma cells
have destroyed bone. Lesions created in the bone by
the malignant cells can cause pathologic fractures,
especially in the vertebral bodies. As further bone
is destroyed, calcium and phosphorus are released,
causing renal stones and renal failure.1,2,7
Amyloidosis may occur in patients with multiple
myeloma. Deposition of this glycoprotein in tissues
may cause them to become hard and waxy.
Myeloma is treated with chemotherapy, bioth-
erapy, radiation, and bone marrow transplantation.
No treatment is curative.
CLINICAL TIP
 Patients with advanced stages of multiple myeloma
may be dehydrated. Ensure proper hydration before
any type of intervention.
 Activity clearance should be obtained from the
physician before mobilizing anyone with bone
lesions.
Oncology CHAPTER 5 213
Head, Neck, and Facial Tumors
Head, neck, and facial cancers involve the paranasal
sinuses, nasal and oral cavities, salivary glands,
pharynx, and larynx. Environmental factors and
personal habits (e.g., tobacco use) are often closely
associated with the development of cancer in this
region.40
Physical therapy intervention may be indicated after
the treatment of head, neck, and facial tumors.
Surgical procedures include radical neck dissection, lar-
yngectomy, and reconstructive surgery. Radical neck
dissections (RND) may include removal or partial
removal of the larynx, tonsils, lip, tongue, thyroid
gland, parotid gland, cervical musculature (including
the sternocleidomastoid, platysma, omohyoid, and
floor of the mouth), internal and external jugular
veins, and lymph nodes.41 Reconstructive surgery may
include a skin flap, muscle flap, or both to cover
resected areas of the neck and face. The pectoralis or
trapezius muscle is used during muscle flap reconstruc-
tive procedures. A facial prosthesis is sometimes
used to help the patient attain adequate cosmesis
and speech.
CLINICAL TIP
 Postoperatively, impairment of the respiratory
system should be considered in patients with head,
neck, and facial tumors because of possible
obstruction of the airway or difficulty managing oral
secretions. A common associated factor in patients
with oral cancer is the use of tobacco (both chewing
and smoking); therefore, possible underlying
lung disease must also be considered. During
physical therapy assessment, the patient should
be assessed for adventitious breath sounds and
effectiveness of airway clearance. Oral secretions
should be cleared effectively before assessing
breath sounds.
 Proper positioning is important to prevent aspiration
and excessive edema that may occur after surgery
of the face, neck, and head. The surgeon will often
write orders to keep the patient’s head neutral.
HOB is almost always  30 degrees. Jackson-Pratt
drains are very common.
 Patients may also require a tracheostomy, artificial
airway, or both to manage the airway and
secretions. (Refer to Appendix III-B).
 After a surgical procedure, the physician should
determine activity and range-of-motion restrictions,
214 CHAPTER 5 Oncology
especially after skin and muscle flap
reconstructions. Physical therapy treatment
to restore posture and neck, shoulder,
scapulothoracic, and temporomandibular motion
is emphasized.
 When treating patients with head, neck, and facial
cancers, it is important to consider the potential
difficulties with speech, chewing, or swallowing and
loss of sensations, including smell, taste, hearing,
and sight.
 Because the patient may have difficulty with
communicating and swallowing, referring the
patient to a speech therapist and registered
dietitian may be necessary. If these disciplines
are already involved with the patient, be aware of
posted guidelines to facilitate communication,
including the use of an electronic larynx
(electropharynx).
Neurologic Cancers
Tumors of the nervous system can invade the brain,
spinal cord, and peripheral nerves. There are four
major classes of brain tumors: gliomas, neuronal
tumors, poorly differentiated neoplasms, and menin-
giomas.42 Primary brain tumors can occur in astrocytes
(astrocytoma), meninges (meningeal sarcoma), and
nerve cells (neuroblastoma), while secondary brain
tumors can be the result of another systemic cancer
that has metastasized to the brain.15 Symptoms related
to cancers of the nervous system depend on the size of
the tumor and the area of the nervous system involved.
Because of the compressive nature of central nervous
system tumors, clinical manifestations can occur with
either malignant or benign tumors.42 Neurologic
symptoms can persist after tumor excision, owing to
destruction of neurologic tissues. Changes in neuro-
logic status due to compression of tissues within the
nervous system can indicate further spread of the
tumor or may be related to edema of brain tissue.
Sequelae include cognitive deficits, skin changes,
bowel and bladder control problems, sexual dysfunc-
tion, and the need for assistive devices and positioning
devices. After resection of a brain tumor, patients
may demonstrate many other neurologic sequelae,
including hemiplegia and ataxia. Radiation therapy to
structures of the nervous system may also cause
transient neurologic symptoms. Refer to Chapter 4
for more details on neurologic examination and
intervention.
CLINICAL TIP
 The therapist should assess the patient’s need for
skin care, splinting, positioning, cognitive training,
gait training, balance, assistive devices, special
equipment, and assistance with activities of daily
living.
Skin Cancer
The physical therapist may identify suspicious lesions
during examination or treatment, and these should
be reported to the medical doctor. Suspicious lesions
are characterized by (1) irregular or asymmetric
borders, (2) uneven coloring, (3) nodules or ulceration,
(4) bleeding or crusting, and (5) change in color, size,
or thickness. Cancers of the skin include basal cell
cancer, squamous cell cancer, malignant melanoma,
and Kaposi’s sarcoma.1
Basal cell carcinoma is the most common skin
cancer.21 It is usually found in areas exposed to the
sun, including the face, ears, neck, scalp, shoulders,
and back. Risk factors include chronic exposure to
the sun, light eyes, and fair skin. Diagnosis is
made with a biopsy or a tissue sample. The following
are five warning signs of basal cell carcinoma the
physical therapist should look for when working
with patients43:
 Open sore that bleeds, oozes, or crusts and remains
open for 3 or more weeks
 Reddish patch or irritated area, which may crust, itch,
or hurt
 Smooth growth with an elevated, rolled border, and
an indentation in the center; tiny vessels may develop
on the surface
 Shiny bump or nodule that is pearly or translucent
and is often pink (can be tan, black, or brown in
dark-haired individuals)
 Scar-like area that is white, yellow, or waxy, with
poorly defined borders and shiny, taut skin
Squamous cell cancer usually occurs in areas
exposed to the sun or ultraviolet radiation. Lesions
may be elevated and appear scaly or keratotic (horny
growth).21 Squamous cell lesions can metastasize to
the lymph nodes, lungs, bone, and brain.
Malignant melanoma is a neoplasm that arises
from the melanocytes. Risk factors include previous
history or family history of melanoma, immunosup-
pression, and a history of blistering sunburns before
age 20. Malignant melanoma can metastasize to the
lymph nodes, lung, brain, liver, bone, and other

areas of the skin.21 Moles or pigmented spots exhibiting
the following signs (called the ABCD rule) may indicate
malignant melanoma21:
A = Asymmetry
B = Irregular border
C = Varied color
D = Diameter of more than 6 mm
CLINICAL TIP
 After resection of skin lesions, proper positioning
is important to prevent skin breakdown.
 The physical therapist should assess the need
for positioning and splinting devices.
 The physical therapist should determine the location
of the lesion and the need for range-of-motion
exercises to prevent contractures. If the lesion
involves an area that will be stressed (e.g., joints),
the physical therapist should check the physician’s
orders for precautions limiting motion.
GENERAL PHYSICAL THERAPY
GUIDELINES FOR PATIENTS WITH
CANCER
The following are general goals and guidelines for the
physical therapist working with the patient who has
cancer. These guidelines should be adapted to a
patient’s specific needs.
The primary goals of physical therapy in this patient
population are similar to those of other patients in the
acute care setting; however, because of the systemic
nature of cancer, the time frames for achieving
goals will most likely be longer. These goals are to
(1) optimize functional mobility, (2) minimize or
prevent cancer-related fatigue, (3) prevent joint
contracture and skin breakdown, (4) prevent or reduce
limb edema, and (5) prevent postoperative pulmonary
complications.
General guidelines include, but are not limited to,
the following:
 Knowing the stage and grade of cancer can help the
physical therapist modify a patient’s treatment para-
meters and establish realistic goals and intervention.
 Patients may be placed on bed rest while receiving
cancer treatment or postoperatively and will be at
risk for developing pulmonarycomplications, decon-
ditioning, and skin breakdown. Deep-breathing
Oncology CHAPTER 5 215
exercises, frequent position changes, and an exercise
program that can be performed in bed are beneficial
in counteracting these complications.
 Patients who have metastatic processes, especially to
bone, are at high risk for pathologic fracture.
Pulmonary hygiene is indicated for most patients
who undergo surgical procedures. Care should be
taken with patients who have metastatic processes
during the performance of manual chest physical
therapy techniques. Metastatic processes should
also be considered when prescribing resistive exer-
cises to patients, as the muscle action on the frail
bone may be enough to cause fracture.
In order to minimize the sequelae of cancer related
fatigue, the following guidelines are recommended44:
 Prior to prescribing an exercise program, evaluate
fatigue level and determine the need for more medi-
cal intervention. If the patient is cleared for exercise,
then utilize the following:
 Begin exercise program when patients start
cancer treatment, and continue until the end of
treatment.
 Prescribe intensity of exercise at moderate levels
(50% to 70% of heart rate maximum, or 11 to
13/20 on Borg’s Rating of Perceived Exertion
scale (6 to 20). (Refer to Chapter 1 for information
on Borg’s scale). Exercise should be predomi-
nantly aerobic in nature and progressive over
time, building duration of exercise.
 Emphasize the importance of an exercise log or
diary to help monitor progress and promote
adherence to the exercise program.
 Provide patient and family education regarding
safety management, energy conservation, postural
awareness, and body mechanics during activities
of daily living. An assessment of the appropriate
assistive devices, prosthetics, and required orthotics
should also be performed. Decreased sensation
requires special attention when prescribing and
fitting adaptive devices.
 If a patient is placed on isolation precautions, place
exercise equipment, such as stationary bicycles or
upper-extremity ergometers (after being thoroughly
cleaned with sterile solutions), in his or her room.
Assessment is necessary for the appropriateness
of this equipment, along with the safety of inde-
pendent use.
 When performing mobility or exercise treatments,
care should be taken to avoid bruising or bleeding
into joint spaces when patients have low platelet
counts.
216 CHAPTER 5 Oncology
 Emotional support for both the patient and family
is at times the most appreciated and effective
method in helping to accomplish the physical ther-
apy goals.
 Timely communication with the entire health care
team is essential for safe and effective care.
Communication should minimally include the
References
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the patient’s goals, and any factors that are interfering
with the patient’s progress.
 Laboratory values, especially hemoglobin/hemato-
crit, white blood cell count, platelet count, and
prothrombin time/international normalized ratio
(PT/INR) should be monitored daily.
17. Budny PG, LavelleJ, Regan PJ, et al. Pretibial Injuries in
the Elderly: A ProspectiveTrial of Early Mobilisation
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Surg 1993;46(7):594-598.
18. NorrisJ (ed). Professional Guide to Diseases (5th ed).
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19. Lewis RJ, Caccavale RJ, BocageJP, et al.Video-Assisted
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Simultaneously Stapled Lobectomy; A More
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20. Santambrogio R, Montorsi M, Bianchi P, et al.
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22. Burrell LO (ed). Adult Nursing in Hospital and
Community Settings. East Norwalk, CT: Appleton
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23. Baird S (ed). A Cancer Source Book for Nurses (6th ed).
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24. Lester SC.The Breast. InV Kumar, AK Abbas,
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26. Badger CM, PeacockJL, Mortimer PS. A Randomized,
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27. Berlin E, GjoresJE, Ivarsson C, et al. Postmastectomy
Lymphoedema.Treatment and a Five-Year Follow-Up
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28. Johansson K, Albertsson M, Ingvar C, et al. Effects of
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29. Liu C, CrawfordJM.The Gastrointestinal Tract.
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 6 Vascular System and
Hematology

Michele P. West INTRODUCTION

Jaime C. Paz Alterations in the integrity of the vascular and hematologic systems can
Falguni Vashi alter a patient’s activity tolerance. The physical therapist must be aware of
the potential impact that a change in blood composition or blood flow
has on a multitude of body functions, including cardiac output, hemosta-
sis, energy level, and healing.The objectives of this chapter are to provide
the following:
1. A review of the structure and function of blood and blood vessels
2. A review of vascular and hematologic evaluation, including physical
examination and diagnostic and laboratory tests
3. A description of vascular and hematologic diseases and disorders,
including clinical findings, medical and surgical management, and
physical therapy intervention
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:

Possible Practice
Disease/Pathology Patterns
Arterial Disorders: Atherosclerosis, Aneurysm, 4C, 4J, 6D, 7A
Aortic Dissection, Hypertension, Raynaud’s
Disease
Chronic Regional Pain Syndrome
Compartment Syndrome
Venous Disorders:VaricoseVeins,Venous 4C, 6D, 7A
Thrombosis, Pulmonary Embolism, Chronic
Venous Insufficiency
Combined Arterial and Venous Disorders: 4C, 6D, 7A
Arteriovenous Malformations
Hematologic Disorders: Erythrocytic Disorders 4C, 6D
(Anemia), Polycythemia
Thrombocytic Disorders
Lymphatic Disorders: Lymphedema 4C, 6D, 6H

Please refer to the back cover of this book for a complete list of the pre-
ferred practice patterns as individual patient conditions are highly variable
and other practice patterns may be applicable.

219
220 CHAPTER 6 Vascular System and Hematology

Table 6-2 CHARACTERISTICS OF BLOOD

STRUCTURE
The network of arteries, veins, and capillaries com-
poses the vascular system. Living blood cells and
plasma within the blood vessels are the structures that
compose the hematologic system. The lymphatic
system assists the vascular system by draining unab-
sorbed plasma from tissue spaces and returning this
fluid (lymph) to the heart via the thoracic duct, which
empties into the left jugular vein.The flow of lymph is
regulated by intrinsic contractions of the lymph vessels,
muscular contractions, respiratory movements, and
gravity.1
Vascular System Structure
All blood vessels are composed of three similar layers.
Table 6-1 describes the structural characteristics of the
three different blood vessel layers. Blood vessel dia-
meter, length, and wall thickness vary according to
location and function. Table 6-2 describes the unique
characteristics of arteries, veins, and capillaries. Figure
6-1 illustrates the structure of the artery and vein. In
addition, the arteries are divided into three types,
depending on their size and structural features.
Hematologic System Structure
Blood is composed of living cells in a nonliving plasma
solution and accounts for 8% of total body weight, or
4 to 5 liters in women and 5 to 6 liters in men. Table
6-3 describes the characteristics of the different blood
cells. Plasma is composed almost completely of water
and contains more than 100 dissolved substances. The
major solutes include albumin, fibrinogen, protein glo-
bules, nitrogenous substances, nutrients, electrolytes,
and respiratory gases.2
VESSELS
Vessel Description
Artery Large or elastic arteriesçaorta and its large
branches and pulmonary artery.
Medium or muscular arteriesçcomposing
other branches of aorta (i.e., coronary
arteries).
Small arteries and arterioles.
Thick tunica media layer allows arteries
to readily accommodate to pressure
changes from the heart.
Vein Small, medium, or large in diameter.
Thin tunica media and thick tunica
adventitia.
Valves prevent backflow of blood to
maintain venous return to the heart.
Capillary The interface of the arterial and venous
network systems where blood cells, fluids, and
gases are exchanged.
Capillary beds can be open or closed,
depending on the circulatory
requirements of the body.
Data from Marieb EN. Human Anatomy and Physiology (3rd ed).
Redwood City, CA: Benjamin-Cummings, 1995; Kumar V: Robbins
and Cotran Pathologic Basis of Disease (7th ed), 2005.
Lymphatic System Structure
The lymphatic system includes lymph vessels, lymph
fluid, and lymph tissues and organs (lymph nodes, ton-
sils, spleen, thymus, and the thoracic duct), and is paral-
lel to and works in concert with the venous system.

Table 6-1 BLOOD VESSEL LAYERS

Layer Description Function

Tunica intima Innermost layer: Endothelial layer over Provides a smooth surface for laminar blood
a basement membrane flow
Tunica media Middle layer: Smooth muscle cells and elastic Constricts and dilates for blood pressure
connective tissue with sympathetic innervation regulation
Tunica adventitia Outermost layer: Composed of collagen fibers, Protects and attaches blood vessels to nearby
lymph vessels, and the blood vessels that supply structures
nutrients to the blood vessel
Data from Marieb EN: Human Anatomy and Physiology (3rd ed). Redwood City, CA: Benjamin-Cummings, 1995.
 Vascular System and Hematology CHAPTER 6 221

Artery Vein

Endothelium
(tunica intima)

Valve

Elastic membrane
(thinner in veins)

Smooth muscle layer

(tunica media)
(thinner in veins)
Connective tissue
(tunica advenitia)

FIGURE 6-1
Structure of the arteries and veins. (From Lewis SL, Heitkepmer M, Dirksen S et al. Medical-Surgical
Nursing: Assessment and Management of Clinical Problems [7th ed]. St Louis: Mosby, 2007.)

Lymphatics are fragile and are more likely to collapse

Table 6-3 BLOOD CELL TYPES
Cell Description
Erythrocyte Contains hemoglobin molecules
(red blood responsible for oxygen transport
cell; RBC) to tissues.
Composed of four protein chains (two
alpha and two beta chains) bound
to four iron pigment complexes.
An oxygen molecule attaches to each
iron atom to become
oxyhemoglobin.
Leukocyte Five types of WBCs (neutrophils,
(white blood basophils, eosinophils, lymphocytes,
cell;WBC) and monocytes) are responsible
for launching immune defenses
and fighting infection.
WBCs leave the circulation to gain
access to a site of infection.
Thrombocyte Cell fragment responsible for clot
(platelet; Plt) formation.
Data from Marieb EN: Human Anatomy and Physiology (3rd ed).
Redwood City, CA: Benjamin-Cummings, 1995.
under pressure than the veins. Lymphatics are located
in all portions of the body except the central nervous
system and cornea. Lymph moves throughout the
body by a number of mechanisms, and the excess
lymph is transported to the thoracic duct and emptied
into the jugular vein trunks. Lymph fluid is first
absorbed at the capillary level, then channeled through
the small vessels and finally picked up by the larger
valved vessels.3
FUNCTION
The function of the blood vessels is to carry blood
throughout the body to and from the heart. Normal
alterations in the vessel diameter will occur, depending
on circulating blood volume and the metabolic needs
of the tissues.Table 6-4 describes the different functions
of the blood.
The function of the lymphatic system is to (1) protect
the body from infection and disease via the immune
response and (2) to facilitate movement of fluid back
and forth between the bloodstream and the interstitial
222 CHAPTER 6 Vascular System and Hematology

 Relevant social history that includes exercise and

Table 6-4 FUNCTIONS OF BLOOD dietary habits, as well as the use of tobacco or alcohol.
Function Method  History of recent prolonged bed rest and/or surgery
or a long flight.
Oxygen and carbon Binding to hemoglobin;  Pain in arms and legs. (Visceral pain and arthritis
dioxide transport dissolved in plasma pain may radiate to the extremities.)
Nutrient and metabolite Bound to plasma proteins;  Presence of intermittent claudication (pain, ache,
transport dissolved in plasma sense of fatigue, or other discomfort that occurs in
Hormone transport In plasma the affected muscle group with exercise, particularly
Transport of waste In plasma walking, and resolves with rest.) The speed, distance,
products to kidneys and the site of the pain, including what relieves the
and liver pain, should be noted.
Transport of cells and In plasma to site of  Buttock, hip, or thigh claudication typically
substances involved in infection or foreign body occurs in patients with obstruction of the aorta
immune reactions and iliac arteries. Calf claudication characterizes
Clotting at breaks in Hemostasis femoral and popliteal artery stenosis. The gastroc-
blood vessels nemius muscle consumes more oxygen during walk-
Maintenance of fluid Blood volume regulation ing than other muscle groups in the leg and hence
balance causes the most frequent symptom reported by
Body temperature Peripheral vasoconstriction patients.
regulation or dilation  Presence of nocturnal pain that can develop as the
Maintenance of acid- Acid-base regulation
vascular occlusion worsens. This type of pain
base balance occurs when the patient is in bed and is caused by a
combination of leg elevation and reduced cardiac
Data from Nettina S.The Lippincott Manual of Nursing Practice output.
(8th ed). Philadelphia: Lippincott Williams and Wilkins, 2005.  Presence of rest pain refers to pain that occurs in the
absence of activity and with legs in a dependent posi-
tion. Rest pain signals advanced occlusive disease,
typically > 90% occlusion.
fluid, removing excess fluid, blood waste, and protein  Presence or history of acute or chronic peripheral
molecules in the process of fluid exchange.3 edema. If chronic, what is the patient’s baseline
The vascular and hematologic systems are intimately level of edema?
linked, and the examination of these systems is often  Precautions, such as weight bearing or blood
similar. For the purpose of this chapter, however, the pressure parameters after vascular surgery.
evaluations of the vascular and hematologic systems
are discussed separately. CLINICAL TIP
 Intermittent claudication is often abbreviated in
the clinical setting as IC.
PHYSICAL EXAMINATION
INSPECTION
Vascular Evaluation
Observation of the following features can help delin-
HISTORY eate the location and severity of vascular disease
In addition to the general chart review (see Appendix and help determine whether these manifestations are
I-A), it is important to gather the following information arterial or venous in origin1,4,5,9:
during examination of the patient with a suspected  Skin color: Note the presence of any discoloration of
vascular disorder4-8: the distal extremities/nail bed, which is indicative
 Relevant medical history that includes diabetes of decreased blood flow (e.g., mottled skin).
mellitus, hypertension, hyperlipidemia, syncope or  Hair distribution: Patchy hair loss on the lower leg
vertigo, and nonhealing ulcers. may indicate arterial insufficiency.
 Vascular System and Hematology
 Venous pattern: Dilation or varicosities-dilated,
purplish, ropelike veins, particularly in the calf
 Edema or atrophy: Peripheral edema from right-
sided congestive heart failure occurs bilaterally in
dependent areas; edema from trauma, lymphatic
obstruction, or chronic venous insufficiency is gen-
erally unilateral. Refer to Table 1-6 for how to grade
pitting edema. Measurement of the extremities may
help to identify the edema or atrophy.With a flexible
tape, measure (1) the forefoot, (2) the smallest possi-
ble circumference above the ankle, (3) the largest cir-
cumference at the calf, (4) the midthigh, a measured
distance above the patella with the knee extended.
A difference of > 1 cm just above the ankle or 2 cm
at the calf is suggestive of edema.
 Presence of cellulitis.
 Presence of petechiae: Small, purplish, hemorrhagic
spots on the skin
 Skin lesions: Ulcers, blisters, or scars
 Digital clubbing: Could be indicative of poor arterial
oxygenation or circulation.
 Gait abnormalities.
PALPATION
During the palpation portion of the examination, the
physical therapist can assess the presence of pain and
tenderness, strength and rate of peripheral pulses, respi-
ratory rate, blood pressure, skin temperature, and limb
girth (if edematous). Changes in heart rate, blood pres-
sure, and respiratory rate may correspond to changes
in the fluid volume status of the patient. For example,
a decrease in fluid volume may result in a decreased
blood pressure that results in a compensatory increase
in heart and respiratory rates. The decreased fluid
volume and resultant increased heart rate in this
situation may then result in a decreased strength of
the peripheral pulses on palpation. In patients with
suspected or diagnosed peripheral vascular disease,
monitoring distal pulses is more important than
monitoring central pulses in the larger, more proximal
vessels.4
The following system/scale is used to grade periph-
eral pulses10:
0 Absent, not palpable
1 Diminished, barely
palpable
2 Brisk, expected
3 Full, increased
4 Bounding
CHAPTER 6 223
Peripheral pulses can be assessed in the following
arteries (see Figure 1-6):
 Temporal
 Carotid
 Brachial
 Ulnar
 Radial
 Femoral
 Popliteal
 Posterior tibial
 Dorsalis pedis
CLINICAL TIP
 Peripheral pulse grades are generally denoted in the
medical record by physicians in the following
manner: dorsalis pedis +1.
 A small percentage of the adult population may
normally have absent peripheral pulses—for
example, 10% to 17% lack dorsalis pedis pulses.1
 In patients who have disorders resulting in vascular
compromise (e.g., diabetes mellitus, peripheral
vascular disease, or hypertension), pulses should be
monitored before, during, and after activity not
only to determine any rate changes, but, more
important, to determine any changes in the
strength of the pulse.
 Notation should be made if the strength of pulses
is correlated to complaints of pain, numbness, or
tingling of the extremity.
 Compare the two extremities for color, temperature,
and swelling. Bilateral coldness is most often due
to cold environment and/or anxiety.5
 Carotid arteries should never be palpated
simultaneously, as excessive carotid sinus massage
can cause slowing of the pulse, cause a drop in
blood pressure, and compromise blood flow to the
brain. If the pulse is difficult to palpate, the
patient’s head should be rotated to the side being
examined to relax the sternocleidomastoid.10
AUSCULTATION
Systemic blood pressure and the presence of bruits
(whooshing sound indicative of turbulent blood flow
from obstructions) are assessed through auscultation.4
Bruits are often indicative of accelerated blood flow
velocity and flow disturbance at sites of stenosis.7
Bruits are typically assessed by physicians and nurses
(see Chapter 1 for further details on blood pressure
measurement).
224 CHAPTER 6 Vascular System and Hematology
VASCULAR TESTS
Various tests that can be performed clinically to evaluate
vascular flow and integrity are described in Table 6-5.
These tests can be performed easily at the patient’s
bedside without the use of diagnostic equipment.
DIAGNOSTIC STUDIES
NONINVASIVE LABORATORY STUDIES. Various non-
invasive procedures can examine vascular flow. The
phrases lower-extremity noninvasive studies and carotid noninva-
sive studies are general descriptions that are inclusive of
the noninvasive tests described inTable 6-6.
INVASIVE VASCULAR STUDIES. The most common
invasive vascular study is arteriography, typically
referred to as contrast angiography. This study is done
by injecting radiopaque dye into the femoral, lumbar,
brachial, or axillary arteries, followed by radiographic
viewing. Blood flow dynamics, abnormal blood vessels,
vascular anomalies, normal and abnormal vascular anat-
omy, and tumors are easily seen during the radiographic
viewing.With the use of digital subtraction angiography
(DSA), bony structures can be obliterated from the pic-
ture. DSA is useful when adjacent bone inhibits visual-
ization of the blood vessel to be evaluated.18 An
angiogram is a picture produced by angiography.
Angiography is generally performed before or during
therapeutic interventions, such as percutaneous angio-
plasty, thrombolytic therapy, or surgical bypass grafting.
Postangiogram care includes the following19:
 Bed rest for 4 to 8 hours.
 Pressure dressings to the injection site with assess-
ment for hematoma formation.
 Intravenous fluid administration to help with dye
excretion. Blood urea nitrogen (BUN) and creatinine
are monitored to ensure proper renal function
(refer to Chapter 9 for more information on BUN
and creatinine).
 Frequent vital sign monitoring with pulse
assessments.
 If a patient has been on heparin before angiography,
the drug is not resumed for a minimum of 4 hours.19
The complications of arteriography can be due to the
catheterization ordue to the contrast agentthat is injected.
Table 6-7 describes the complications of arteriography.
Hematologic Evaluation
The medical workup of the patient with a suspected
hematologic abnormality includes the patient’s medical
history and laboratory studies, in addition to the
patient’s clinical presentation.
HISTORY
In addition to the general chart review (see Appendix
I-A), the following questions are especially relevant
in the evaluation of the patient with a suspected hema-
tologic disorder20-22:
 What are the presenting symptoms?
 Was the onset of symptoms gradual, rapid, or associ-
ated with trauma or other disease?
 Is the patient unable to complete daily activities
secondary to fatigue?
 Is there a patient or family history of anemia or other
blood disorders, cancer, hemorrhage, or systemic
infection?
 Is there a history of blood transfusion?
 Is there a history of chemotherapy, radiation therapy,
or other drug therapy?
 Has there been an environmental or occupational
exposure to toxins?
 Have there been night sweats, chills, or fever?
 Is the patient easily bruised?
 Is wound healing delayed?
 Is there excessive bleeding or menses?
Other relevant data include the patient’s diet (for the
evaluation of vitamin- or mineral-deficiency anemia),
historyof weight loss (as awarningsignofcanceror altered
metabolism), whether the patient abuses alcohol (a cause
of anemia with chronic use), and race (some hematologic
conditions have a higher incidence in certain races).
INSPECTION
During the hematologic evaluation, the patient is
observed for the following20,23,24:
 General appearance (for lethargy, malaise, or apathy)
 Degree of pallor or flushing of the skin, mucous
membranes, nail beds, and palmar creases. Pallor
can be difficult to assess in dark-skinned individuals.
In these individuals, lips, tongue, mucosa, and nail
beds should be monitored.
 Presence of petechiae (purplish, round, pinpoint,
nonraised spots caused by intradermal or subcutane-
ous hemorrhage) or ecchymosis (bruising)
 Respiratory rate
PALPATION
The examination performed by the physician includes
palpation of lymph nodes, liver, and spleen as part of a
general physical examination. For specific complaints,
the patient may receive more in-depth examination of a
body system.Table 6-8 summarizes the abnormal hema-
tologic findingsbybodysystem on physical examination.
 Vascular System and Hematology
Table 6-5 VASCULAR TESTS
Test Indication Description
Capillary refill To assess vascular perfusion Nail beds of fingers or toes are
time* and indirectly assess squeezed until blanching
cardiac output (whitening) occurs, and then
they are released.
Elevation pallor To assess arterial perfusion A limb is elevated 30-40 degrees
for 15-60 seconds, and color
changes are observed over
60 seconds.
Normally color should not
change. A gray (dark-skinned
individuals) or pale/pallor
(fair-skinned individuals)
discoloration will result from
arterial insufficiency or
occlusion.
Trendelenburg’s To determine if superficial or To doTrendelenburg’s test, mark
test/Retrograde deep veins and their valves the distended veins with a pen
filling test are involved in causing while the patient stands.Then
varicosities have the patient lie on the
examination table and elevate
his or her leg for about a
minute to drain the veins.
Next, have the patient stand
while you measure venous
filling time.
If the veins fill in less than
30 seconds, have the patient
lie on the examination table
again, and elevate his or her
leg for 1 minute.Then apply a
tourniquet around his or her
upper thigh. Next, have the
patient stand.
Next, remove the tourniquet.
To pinpoint incompetent valve
location, repeat this procedure
by applying the tourniquet just
below the knee and then
around the upper calf.
Manual To detect competent valves Palpate the dilated veins with the
compression in the veins fingertips of one hand.With
test the other hand, firmly
compress the vein at a point at
least 8 inches (20.3 cm) higher.
Palpate the impulse under
your finger.
Allen’s test To assess the patency of the Flex the patient’s arm with the
radial and ulnar arteries, to hand above level of the elbow.
CHAPTER 6 225
Normal Results and Values
Blanching should resolve
(capillary refill) in less than
2 seconds.
Observe the amount of time it
takes for pallor to appear:
Pallor within 25 seconds
indicates severe occlusive
disease. Pallor within 25-40
seconds indicates moderate
occlusive disease.
Pallor within 40-60 seconds
indicates mild occlusive
disease.
Competent valves take at least
30 seconds to fill.
If leg veins still fill in less than
30 seconds, suspect
incompetent perforating vein
and deep vein valves
(functioning valves block
retrograde flow).
If the veins fill again in less
than 30 seconds, suspect
incompetent superficial vein
valves that allow backward
blood flow
With a competent valve, there
won’t be any detectable
impulse. A palpable impulse
indicates incompetent valves
in the vein segment between
the two hands.
When the patient opens the
hand the blanched area
Continued
226 CHAPTER 6 Vascular System and Hematology
Table 6-5 VASCULAR TESTS—cont’d
Test Indication
ensure the collateral
circulation of the hand.
Homans’sign{ To detect the presence of
deep vein thrombosis.
Ankle-Brachial To compare the perfusion
Index (ABI) pressures in the lower leg
with the upper extremity
using a blood pressure cuff
and Doppler probe.This
test is commonly used to
screen patients for
evidence of significant
arterial insufficiency.
*Variability is found in defining the time by different individuals, so Capillary Refill Time should not be considered an observation
with exquisite sensitivity and specificity and should be used more to confirm clinical judgment.
{
A 50% false-positive rate occurs with this test.Vascular laboratory studies are more sensitive.
{
An ABI of less than 0.95, is considered abnormal and is 95% sensitive for the angiographically verified peripheral arterial stenosis.
Data from reference numbers 1, 10-14, 30.
Description
Then compress the radial and
ulnar arteries at the level of
the wrist while the patient
clenches his or her fist.The
patient then opens his or her
hand and either the radial or
the ulnar artery is released.
The process is repeated for
the other artery.
The calf muscle is gently
squeezed, or the foot is
quickly dorsiflexed.
Place the patient in supine at
least 10 minutes before the
test. Obtain the brachial
pressure in each arm, and
record the highest pressure.
Place the cuff around the
lower leg 2.5 cm above the
malleolus. Apply acoustic gel
over the dorsalis pedis pulse
location. Hold the Doppler
probe lightly over the pedal
pulse. Inflate the cuff to a level
20-30 mm Hg above the point
that the pulse is no longer
audible. Slowly deflate the cuff
while monitoring for the
return of the pulse signal; the
point at which the arterial
signal returns is recorded as
the dorsal pedis pressure.
Repeat the procedure with
posterior tibial pulse location.
Calculate the ABI by dividing
the higher of the two ankle
pressures by the higher of the
brachial pressures.
Normal Results and Values
flushes within seconds if
collateral circulation is
adequate. If the area flushes
quickly, the test is positive.
The test is negative if the
blanched area does not flush
quickly. A negative test
means that collateral
circulation is inadequate to
support circulation to the
hand.
Pain that is elicited with either
squeezing or dorsiflexing
may indicate a deep vein
thrombosis.
The diagnosis of peripheral
arterial disease is based on the
limb symptoms or an ABI.
Interpretation of ABI
ABI  1.0-1.3: normal range.{
ABI  0.6-0.8: borderline
perfusion.
ABI 0.5: severe ischemia,
wound healing unlikely.
ABI 0.4: critical limb ischemia.
 Vascular System and Hematology CHAPTER 6 227

Table 6-6 NONINVASIVE VASCULAR STUDIES

Test Description
Doppler ultrasound High-frequency and low-intensity (1-10 MHz) sound waves are applied to the skin with
a Doppler probe (and acoustic gel) to detect the presence or absence of blood flow,
direction of flow, and flow character over arteries and veins with an audible signal.
Low-frequency waves generally indicate low-velocity blood flow.
Ultrasound examination has a sensitivity and specificity of approximately 95%.
Color duplex scanning Velocity patterns of blood flow along with visual images of vessel and plaque anatomy can
or imaging be obtained by combing ultrasound with a pulsed Doppler detector. Distinctive color
changes indicate blood flow through a stenotic area.
Plethysmography Plethysmography is a noninvasive test that provides measurement of changes in the volume
of the blood distal to the affected area indicating an occlusion and specifically for the
amount of time required for the veins to refill after being emptied.
Exercise testing Exercise testing is performed to assess the nature of claudication by measuring ankle
pressures and PVRs after exercise.
A drop in ankle pressures can occur with arterial disease.
This type of testing provides a controlled method to document onset, severity, and location
of claudication.
Screening for cardiorespiratory disease can also be performed, as patients with peripheral
vascular disease often have concurrent cardiac or pulmonary disorders (see Chapter 1).
Computed tomography CT is used to provide visualization of the arterial wall and its structures.
(CT) Indications for CT include diagnosis of abdominal aortic aneurysms and postoperative
complications of graft infections, occlusions, hemorrhage, and abscess.
Magnetic resonance MRI has multiple uses in evaluating the vascular system and is now more commonly used
imaging (MRI) to visualize the arterial system than arteriograms. Specific uses for MRI include detection
of deep venous thrombosis and evaluation of cerebral edema.
(Serial MRIs can also be used to help determine the optimal operative time for patients
with cerebrovascular accidents by monitoring their progression.)
Magnetic resonance MRA uses blood as a physiologic contrast medium to examine the structure and location
angiography (MRA) of major blood vessels and the flow of blood through these vessels.The direction and
rate of flow can also be quantified. MRA minimizes complications that may be associated
with contrast medium injection. Figure 6-2 illustrates the MRA of the aorta and lower
extremity.
Data from reference numbers 1, 8, 11, 15-17, 19, 31, 51, 113.

The physical therapist may specifically examine the LABORATORY STUDIES

following:
 The presence, location, and severity of bone or
joint pain using an appropriate pain scale (see
Appendix VI)
 Joint range of motion and integrity, including the
presence of effusion or bony abnormality
 Presence, location, and intensity of paresthesia
 Blood pressure and heart rate for signs of hypo-
volemia (see Palpation in the Vascular Evaluation
section for a description of vital sign changes with
hypovolemia)
In addition to the history and physical examination, the
clinical diagnosis of hematologic disorders is based
primarily on laboratory studies.
COMPLETE BLOOD CELL COUNT. The standard
complete blood cell (CBC) count consists of a red
blood cell (RBC) count, white blood cell (WBC)
count, WBC differential, hematocrit (Hct) measure-
ment, hemoglobin (Hgb) measurement, and platelet
(Plt) count. Table 6-9 summarizes the CBC. Figure 6-3
illustrates a common method used by the medical-
surgical team to document portions of the CBC in
228 CHAPTER 6 Vascular System and Hematology

daily progress notes. If a value is abnormal, it is usually

circled within this ‘‘sawhorse’’ figure.

CLINICAL TIP
 Hct is accurate in relation to fluid status; therefore,
Hct may be falsely high if the patient is dehydrated
and falsely low if the patient is fluid overloaded.
 Hct is approximately three times the Hgb value.
 A low Hct may cause the patient to experience
weakness, dyspnea, chills, or decreased activity
tolerance, or it may exacerbate angina.
 Patients with cancer such as leukemia or patients who
are receiving cancer treatment will most likely present
with lower Hct and Hgb values; therefore the therapist
should proceed with caution in these patients.
 The term pancytopenia refers to a significant
decrease in RBCs, all types of WBCs, and platelets.
 The term neutropenia refers to an abnormal
decrease in WBCs, particularly neutrophils.
 The term leukocytosis refers to an abnormal increase
in circulating WBCs.
 The term thrombocytopenia refers to a significant
decrease in platelets.
 The term thrombocytosis refers to an abnormal
increase in platelets.

FIGURE 6-2 ERYTHROCYTE INDICES. RBC, Hct, and Hgb values

Magnetic resonance angiography (MRA) of the aorta and lower are used to calculate three erythrocyte indices: (1)
extremity arterial circulation. (From Adam: Grainger &
mean corpuscular volume (MCV), (2) mean corpuscu-
Allison’s Diagnostic Radiology [5th ed]. London: Churchill
Livingstone, 2008.)
lar Hgb, and (3) mean corpuscular Hgb concentration.
At most institutions, these indices are included in the
CBC.Table 6-10 summarizes these indices.
Table 6-7 COMPLICATIONS OF CONTRAST ERYTHROCYTE SEDIMENTATION RATE. The eryth-
ARTERIOGRAPHY rocyte sedimentation rate (ESR) often referred to as the
sed rate, is a measurement of how fast RBCs fall in a
Puncture site or Hemorrhage/hematoma sample of anticoagulated blood. Normal values vary
catheter related Pseudoaneurysm widely according to laboratory method. According to
Arteriovenous fistula theWestergren method, the normal value for males is up
Atheroembolism to 15 mm per hour and the normal value for females is
Local thrombosis
up to 20 mm per hour.18 The sedimentation rate is a non-
Contrast agent Major (anaphylactoid) sensitivity
related reaction specific screening tool used to determine the presence
Minor sensitivity reactions or stage of inflammation, or the need for further medical
Vasodilation/hypotension testing, or it is used in correlation with the clinical
Nephrotoxicity course of such diseases as rheumatoid arthritis or
Hypervolemia temporal arteritis.25 It may be elevated in systemic
infection, collagen vascular disease, and human immu-
From Belkin M, Owens CD,Whittemore AD, et al: Peripheral
Arterial Occlusive Disease. In CM Townsend, RD Beauchamp,
nodeficiency virus. ESR is a fairly reliable indicator of
BM Evers, et al. Sabiston Textbook of Surgery:The Biological Basis the course of disease. In general, as the disease worsens,
of Modern Surgical Practice, 18th ed. Philadelphia: Saunders, 2007 the ESR increases; as the disease improves, the ESR
 Vascular System and Hematology CHAPTER 6 229

Table 6-8 SIGNS AND SYMPTOMS OF HEMATOLOGIC DISORDERS BY BODY SYSTEM

Body System Sign/Symptom Associated Condition
Cardiac Tachycardia Anemia, hypovolemia
Palpitations Anemia, hypovolemia
Murmur Anemia, hypovolemia
Angina Anemia, hypovolemia
Respiratory Dyspnea Anemia, hypovolemia
Orthopnea Anemia, hypovolemia
Musculoskeletal Back pain Hemolysis
Bone pain Leukemia
Joint pain Hemophilia
Sternal tenderness Leukemia, sickle-cell disease
Nervous Headache Severe anemia, polycythemia, metastatic
tumor
Syncope Severe anemia, polycythemia
Vertigo, tinnitus Severe anemia
Paresthesia Vitamin B12 anemia, malignancy
Confusion Severe anemia, malignancy, infection
Visual Visual disturbances Anemia, polycythemia
Blindness Thrombocytopenia, anemia
Gastrointestinal, urinary, Dysphagia Iron-deficiency anemia
and reproductive Abdominal pain Lymphoma, hemolysis, sickle-cell disease
Splenomegaly or Hemolytic anemia
hepatomegaly
Hematemesis, melena Thrombocytopenia and clotting disorders
Hematuria Hemolysis and clotting disorders
Menorrhagia Iron-deficiency anemia
Integumentary Petechiae Iron-deficiency anemia
Ecchymosis Hemolytic, pernicious anemia
Flushing Iron-deficiency anemia
Jaundice Hemolytic anemia
Pallor Conditions with low hemoglobin
Data from BlackJM, Matassarin-Jacobs E (eds). Medical-Surgical Nursing Clinical Management for Continuity of Care (5th ed).
Philadelphia: Saunders, 1997.

decreases.18 ESR may be decreased in the presence of
sickle-cell disease, polycythemia, or liver disease or
carcinoma.
PERIPHERAL BLOOD SMEAR. A blood sample may
be examined microscopically for alterations in size and
shape of the RBCs, WBCs, and platelets. RBCs are
examined for size, shape, and Hgb distribution.WBCs
are examined for proportion and the presence of
immature cells. Finally, platelets are examined for
number and shape.25 Peripheral blood smear results
are correlated with the other laboratory tests to diag-
nose hematologic disease.
COAGULATION PROFILE. Coagulation tests assess
the blood’s ability to clot. The tests used to determine
clotting are prothrombin time (PT) and partial throm-
boplastin time (PTT).
An adjunct to the measurement of PT is the
International Normalized Ratio (INR).The INRwas cre-
ated to ensure reliable and consistent measurement of
coagulation levels among all laboratories. The INR is
the ratio of the patient’s PT to the standard PT of the
laboratory, raised by an exponent (the sensitivity index
of the reagent) provided by the manufacturer.26 The
PT, PTT, and INR are used in clinical conditions in
which an increased risk of thrombosis is present, for
example, treatment of deep vein thrombosis (DVT),
thrombosis associated with prosthetic valves, and atrial
fibrillation.27 Table 6-11summarizes PT/INR and PTT.
230 CHAPTER 6 Vascular System and Hematology

Table 6-9 COMPLETE BLOOD CELL COUNT: VALUES AND INTERPRETATION*

Test Description Value Indication/Interpretation
Red blood cell Number of RBCs Female: 4.2-5.4 million/ml To assess blood loss, anemia, polycythemia.
(RBC) count per ml of blood Male: 4.7-6.1 million/ml Elevated RBC count may increase risk of
venous stasis or thrombi formation.
Increased: polycythemia vera, dehydration,
severe chronic obstructive pulmonary
disease, acute poisoning.
Decreased: anemia, leukemia, fluid overload,
recent hemorrhage.
White blood cell Number of WBCs 5-10  103 (5000-10,000) To assess the presence of infection,
(WBC) count per ml of blood inflammation, allergens, bone marrow
integrity.
Monitors response to radiation or
chemotherapy.
Increased: leukemia, infection, tissue necrosis.
Decreased: bone marrow suppression.
WBC differential Proportion (%) of Neutrophils 55%-70% To determine the presence of infectious states.
the different types Lymphocytes 20%-40% Detect and classify leukemia.
of WBCs (out of Monocytes 2%-8%
100 cells) Eosinophils 1%-4%
Basophils 0.5%-1%
Hematocrit (Hct) Percentage of RBCs Female: 37%-47% To assess blood loss and fluid balance.
in whole blood Male: 42%-52% Increased: polycythemia, dehydration.
Decreased: anemia, acute blood loss,
hemodilution.
Hemoglobin (Hgb) Amount of Female: 12-16 g/100 ml To assess anemia, blood loss, bone
hemoglobin in Male: 14-18 g/100 ml marrow suppression.
100 ml of blood Increased: polycythemia, dehydration.
Decreased: anemia, recent hemorrhage,
fluid overload.
Platelets (Plt) Number of platelets 150-450  109 To assess thrombocytopenia.
in ml of blood 150,000-450,000 ml Increased: polycythemia vera, splenectomy,
malignancy.
Decreased: anemia, hemolysis, DIC, ITP,
viral infections, AIDS, splenomegaly,
with radiation or chemotherapy.
*Lab values vary among laboratories. RBC, hemoglobin, and platelet values vary with age and gender.
AIDS, Acquired immunodeficiency syndrome; DIC, disseminated intravascular coagulopathy; ITP, idiopathic thrombocytopenic purpura.
Data from Elin RJ. Laboratory Reference Intervals and Values. In L Goldman, JC Bennett (eds), Cecil Textbook of Medicine,Vol. 2 (21st ed).
Philadelphia: Saunders, 2000;2305; E Matassarin-Jacobs. Assessment of Clients with Hematologic Disorders. InJM Black, E Matassarin-
Jacobs, Medical-Surgical Nursing Clinical Management for Continuity of Care (5th ed). Philadelphia: Saunders, 1997, 1465; Mosby’s
Diagnostic and LaboratoryTest Reference (8th ed), St. Louis: Mosby, 2007.

 When confirming an order for physical therapy in

CLINICAL TIP the physician’s orders, the therapist must be sure to
 As INR is more reliable and provides consistent differentiate between the order for physical therapy
measurement of coagulation levels, the INR value is and the blood test (i.e., the abbreviations for both
used more often than PT. physical therapy and prothrombin time are PT).
 Vascular System and Hematology CHAPTER 6 231
Edema/swelling should be evaluated at frequent time
intervals.

FIGURE 6-3
Illustration of portions of the complete blood cell count in
shorthand format. Hct, Hematocrit; Hgb, hemoglobin; Plt,
platelet;WBC, white blood cell.
D-DIMER. The D-dimer assay provides a highly spe-
cific measurement of the amount of fibrin degradation.
It is a simple and confirmatory test for disseminated
intravascular coagulation (DIC). Levels of D-dimer
can increase when a fibrin clot is lysed by thrombolytic
therapy. Thrombotic problems like DVT, PE, and
thrombosis of malignancy are associated with high
levels of D-dimer.The test accurately identifies patients
with DVT, and a negative test has a high predictability
that the patient does not have DVT.18
Lymphatic Evaluation3
Relevant history should include cancer and/or cancer
treatment, trauma, and surgery, and onset of swelling
at birth and/or puberty (primary lymphedema).
PATHOPHYSIOLOGY
This section is divided into a discussion of vascular and
hematologic disorders.
Vascular Disorders
Vascular disorders are classified as arterial, venous, or
combined arterial and venous disorders. Clinical find-
ings differ between arterial and venous disorders, as
described inTable 6-12.
ARTERIAL DISORDERS
ATHEROSCLEROSIS. Atherosclerosis is a diffuse and
slowly progressive process characterized by areas of
hemorrhage and the cellular proliferation of mono-
cytes, smooth muscle, connective tissue, and lipids.
The development of atherosclerosis begins early in life
with risk factors as described inTable 6-13.
In addition to these risk factors, a high level of an
inflammatory biomarker, C-reactive protein, has been
identified as a good predictive marker for early iden-
tification of atherosclerosis.28 Waist circumference

Table 6-10 ERYTHROCYTE INDICES: VALUES AND INTERPRETATION*

Test Description Value Interpretation
3
Mean corpuscular volume Mean size of a 80-100 mg Increased by macrocytic, folic acid, or vitamin
(MCV) (Hct  10/RBC) single RBC in B12 deficiency anemias; liver disease; and recent
a ml of blood alcohol use.
Decreased by microcytic, iron-deficiency,
and hypochromic anemias; thalassemia;
and lead poisoning.
Mean corpuscular Amount of Hgb 26-34 pg/cell Increased by macrocytic anemia.
hemoglobin (MCH) in one RBC Decreased by microcytic anemia.
(Hgb  10/RBC) Low mean corpuscular hemoglobin
indicates Hgb deficiency.
Mean corpuscular Proportion of each 31-37 g/dl Increased by spherocytosis (small round RBC).
hemoglobin RBC occupied Decreased by microcytic, hypochromic, and
concentration (MCHC) by Hgb iron-deficiency anemias and thalassemia.
(Hgb/Hct  100)
Hct, Hematocrit; Hgb, hemoglobin; RBC, red blood cell.
*Lab values vary among laboratories.
Data from Elin RJ. Laboratory Reference Intervals and Values. In L Goldman, JC Bennett (eds), Cecil Textbook of Medicine,Vol. 2 (21st ed).
Philadelphia: Saunders, 2000;2305; Matassarin-Jacobs, E. Assessment of Clients with Hematologic Disorders. InJM Black, E Matassarin-
Jacobs (eds), Medical-Surgical Nursing Clinical Management for Continuity of Care (5th ed). Philadelphia: Saunders, 1997;1466.
 Table 6-11 COAGULATION PROFILE

Test Description Value* (seconds) Indication/Interpretation

Prothrombin time/ Examines the extrinsic and PT 11-12.5 Used to assess the adequacy of warfarin
international common clotting factors (Coumadin) therapy or to screen for
normalized I, II,V,VII, and X bleeding disorders
ratio (PT/INR) Increased: Coumarin therapy, liver
diseases, bile duct obstruction, diarrhea,
salicylate intoxication, DIC, hereditary
factor deficiency, alcohol use, or drug
interaction
Decreased: Diet high in fat or leafy
vegetables, or drug interaction
Partial thromboplastin Examines the intrinsic and PTT 60-70 Used to assess the adequacy of heparin
time (PTT) common clotting factors APTT 30-40 therapy and to screen for bleeding
(activated PTT I, II,V,VIII, IX, X, XI disorders
[APTT] is a rapid Increased: Heparin or coumarin therapy,
version of PTT) liver disease, vitamin K or congenital
clotting factor deficiency, DIC
Decreased: Extensive cancer, early DIC
DIC, Disseminated intravascular coagulopathy.
*Values for PTand PTTvary between laboratories.
Data from Pagana KD, PaganaTJ. Blood Studies. Mosby’s Manual of Diagnostic and Laboratory Tests. St. Louis: Mosby, 1998; Mosby’s
Diagnostic and LaboratoryTest Reference (8th ed), St. Louis: Mosby, 2007.

Table 6-12 COMPARISON OF CLINICAL FINDINGS OF ARTERIAL AND VENOUS DISORDERS

Clinical Finding Arterial Disorders Venous Disorders

Edema May or may not be present Present
Worse at the end of the day
Improve with elevation
Muscle mass Reduced Unaffected
Pain Intermittent claudication Aching pain
Cramping Exercise improves pain
Worse with elevation Better with elevation
Cramping at night
Paresthesias, pruritus (severe itching)
Leg heaviness, especially at end of day
Commonly a positive Homans’sign
Pulses Decreased to absent Usually unaffected, but may be difficult to palpate
Possible systolic bruit if edema is present
Skin Absence of hair Broad, shallow, painless ulcers of the ankle and
Small, painful ulcers on pressure lower leg
points, especially lateral malleolus
Normal toenails
Tight, shiny skin
Thickened toenails
Color Pale Brown discoloration
Dependent cyanosis Dependent cyanosis
Temperature Cool May be warm in presence of thrombophlebitis
Sensation Decreased light touch Pruritus
Occasional itching, tingling, and
numbness
Data from BlackJM, Matassarin-Jacobs E (eds). Luckmann and Sorensen’s Medical-Surgical Nursing: A Psychophysiologic Approach
(4th ed). Philadelphia: Saunders, 1993;1261.
 Vascular System and Hematology
Table 6-13 RISK FACTORS FOR
ATHEROSCLEROSIS
Reversible Irreversible
Hypertension (controlled) Male gender
Diabetes (controlled) Strong family history
Hypercholesterolemia Genetic abnormalities
(controlled)
Cigarette smoking
Obesity
Sedentary lifestyle
Data from Bryant RA, Nix DP. Acute and Chronic Wounds
(3rd ed). St Louis: Mosby, 2007; Kumar V: Robbins and Cotran
Pathologic Basis of Disease (7th ed) St. Louis: Saunders, 2005.
and weight gain are the strongest predictors of early
atherosclerosis in healthy adults.29
Clinical manifestations of atherosclerosis result
from decreased blood flow through the stenotic areas.
Signs and symptoms vary according to the area, size,
and location of the lesion, along with the age and
physiologic status of the patient. As blood flows
through a stenotic area, turbulence will occur beyond
the stenosis, resulting in decreased blood perfusion
past the area of atherosclerosis. Generally, a 50% to
60% reduction in blood flow is necessary for patients
to present with symptoms (e.g., pain). Turbulence is
increased when there is an increase in blood flow to an
area of the body, such as the lower extremities during
exercise. A patient with no complaint of pain at rest
may therefore experience leg pain (intermittent
CHAPTER 6 233
claudication) during walking or exercise as a result
of decreased blood flow and the accumulation of
metabolic waste (e.g., lactic acid).4,30,31
The following are general signs and symptoms of
atherosclerosis32:
 Peripheral pulses that are slightly reduced to absent
 Presence of bruits on auscultation of major arteries
(i.e., carotid, abdominal aorta, iliac, and femoral)
 Coolness and pallor of skin, especially with elevation
 Presence of ulcerations, atrophic nails, and hair loss
 Increased blood pressure
 Subjective reports of continuous burning pain in
toes at rest that is aggravated with elevation (ischemic
pain) and relieved with walking. Pain at rest is usually
indicative of severe (80% to 90%) arterial occlusion.
 Subjective reports of calf or lower-extremity pain
induced by walking (intermittent claudication) and
relieved by rest
CLINICAL TIP
 Progression of ambulation distance in the patient
with intermittent claudication can be optimized if
ambulation is performed in short, frequent intervals
(i.e., before the onset of claudicating pain).
Symptoms similar to intermittent claudication may
have a neurologic origin from lumbar canal stenosis or
disk disease.These symptoms are referred to as pseudo-
claudication or neurologic claudication.Table 6-14 out-
lines the differences between true claudication and
pseudoclaudication.33 Medications that have been

Table 6-14 DIFFERENTIATING TRUE INTERMITTENT CLAUDICATION FROM PSEUDOCLAUDICATION

Characteristic of Discomfort Intermittent Claudication Pseudoclaudication

Activity-induced Yes Yes or no
Location Unilateral buttock, hip, thigh, calf and foot Back pain and bilateral leg pain
Nature Cramping Same as with intermittent claudication
Tightness or presence of tingling, weakness,
Tiredness and clumsiness
Occurs with standing No Yes
Onset Occurs at the same distance each time Occurs at variable distance each time
with walking on level surface with walking on level surfaces
Unchanged or decreased distance walking Increased distance when walking
uphill uphill
Unchanged or increased distance walking Decreased distance walking downhill
downhill
Relieved by Stopping activity Sitting
Data fromYoung JR, Graor RA, OlinJW, et al. (eds). Peripheral Vascular Diseases. St. Louis: Mosby, 1991;183; FritzJM. Spinal Stenosis.
InJD Placzek, DA Boyce (eds). Orthopaedic Physical Therapy Secrets. Philadelphia: Hanley & Belfus, 2001;344.
234 CHAPTER 6 Vascular System and Hematology
successful in managing intermittent claudication
include pentoxifylline and cilostazol.34
Treatment of atherosclerotic disease is based on
clinical presentation and can range from risk-factor
modifications (e.g., low-fat diet, increased exercise,
and smoking cessation) to pharmacologic therapy
(e.g., anticoagulation and thrombolytics) to surgical
resection and grafting. Modification of risk factors has
been shown to be the most effective method to lower
the risk of morbidity (heart attack or stroke) from
atherosclerosis.35,36
ANEURYSM. An aneurysm is a localized dilatation or
outpouchingof the vessel wall thatresults from degener-
ation and weakening of the supportive network of pro-
tein fibers with a concomitant loss of medial smooth
muscle cells. Aneurysms most commonly occur in the
abdominal aorta or iliac arteries, followed by the popli-
teal, femoral, and carotid vessels.30,35,37,38 The exact
mechanism of aneurysm formation is not fully under-
stood but includes a combination of the following:
 Genetic abnormality in collagen (e.g., with Marfan’s
syndrome)
 Aging and natural degeneration of elastin
 Increased proteolytic enzyme activity
 Atherosclerotic damage to elastin and collagen
A true aneurysm is defined as a 50% increase in the
normal diameter of the vessel38 and involves weakening
of all three layers of the arterial wall. True aneurysms
are also generally fusiform and circumferential in
nature. False and saccular aneurysms are the result of
trauma from dissection (weakness or separation of the
True aneurysm Normal vessel
FIGURE 6-4
True and false aneurysms. Center, Normal vessel. Left,True aneurysm.The wall bulges outward and may be attenuated but is intact.
Right, False aneurysm.The wall is ruptured, and there is a collection of blood (hematoma) that is bounded externally by adherent
extravascular tissues. (From Kumar V: Robbins and Cotran Pathologic Basis of Disease [7th ed], St Louis: Mosby, 2005.)
vascular layers) or clot formation.They primarily affect
the adventitial layer.37 Figure 6-4 demonstrates true
and false aneurysms, and Figure 6-5 illustrates an aortic
dissection.
Abdominal aneurysms may present with vague
abdominal pain but are relatively asymptomatic until
an emboli dislodges from the aneurysm or the aneu-
rysm ruptures.38 Approximately 80% of the aneurysms
are identified accidentally on abdominal ultrasound,
CTscan, MRI, or plain x-ray.39 Aneurysms will rupture
if the intraluminal pressure exceeds the tensile strength
of the arterial wall. The risk of rupture increases with
increased aneurysm size.40
CLINICAL TIP
 Abdominal aortic aneurysms are frequently referred
to as AAA or Triple A in the clinical setting.
The following are additional clinical manifestations
of aneurysms:
 Ischemic manifestations (described earlier in the
Atherosclerosis section), if the aneurysm impedes
blood flow.
 Cerebral aneurysms, commonly found in the circle of
Willis, present with increased intracranial pressure
and its sequelae (see the General Management sec-
tion in Chapter 4 for more information on intracrani-
al pressure).37
 Aneurysms that result in subarachnoid hemorrhage
are also discussed in Chapter 4.
Extravascular
connective
tissue
Extravasation
of
blood
Hematoma
False aneurysm
 Vascular System and Hematology
DeBakey I DeBakey II DeBakey III
Type A Type B
FIGURE 6-5
Classification of aortic dissections. A, Dissection of ascending
aorta (type A). B, Dissection of descending aorta (type B).
(From Kumar V: Robbins and Cotran Pathologic Basis of
Disease [7th ed], St Louis: Mosby, 2005.)
 Low back pain (aortic aneurysms can refer pain to the
low back).
 Dysphagia (difficulty swallowing) and dyspnea
(breathlessness) resulting from the enlarged vessel’s
compressing adjacent organs.
Surgical resection and graft replacement are gener-
ally the desired treatments for aneurysms.41 However,
endovascular repair of abdominal aneurysms is demon-
strating favorable results. Endovascular repair involves
threading an endoprosthesis through the femoral
artery to the site of the aneurysm. The endoprosthesis
is then attached to the aorta, proximal to the site of
the aneurysm, and distal, to the iliac arteries. This
effectively excludes the aneurysm from the circulation,
which minimizes the risk of rupture.38 Nonsurgical
candidates must have blood pressure and anticoagula-
tion management.41
AORTIC DISSECTION. Aortic dissection is caused by
intimal tear, which allows creation of a false lumen
between the media and adventitia. A history of
Marfan’s syndrome or hypertension is usually present.42
Figure 6-5 illustrates the classification of aortic dissec-
tions. Signs and symptoms generally reflect the type of
aortic dissection (whether Type A or Type B) and the
CHAPTER 6 235
extent of cardiovascular involvement.43 Signs and
symptoms of aortic dissection include43:
 Pain: Sudden and excruciating pain in the chest or
the upper back is the most common initial symptom.
Another important characteristic of the pain is its
tendency to migrate to the neck, abdomen, or
groin, generally following the path of dissection.
 Syncope.
 Reduced or absent pulses.
 Murmur of aortic regurgitation.
 Neurological manifestations (CVA and rarely altered
consciousness, coma).
 Electrocardiogram (EKG) findings in these patients
are nonspecific.7,42 Transesophageal echocardiogra-
phy (TEE) and CT scan are the primary diagnostic
tests used by most institutions to diagnose aortic
dissection.44
Management includes aggressive control of blood
pressure and pain control. Patients may be managed
medically or surgically, depending on the site of the
dissection and patient’s comorbidities.
ARTERIAL THROMBOSIS. Arterial thrombosis
occurs in areas of low or stagnant blood flow, such as
atherosclerotic or aneurysmal areas. The reduced or
turbulent blood flow in these areas leads to platelet
adhesion and aggregation, which then activates the
coagulation cycle to form a mature thrombus (clot).
Blood flow may then be impeded, potentially
leading to tissue ischemia with subsequent clinical
manifestations.37,41
ARTERIAL EMBOLI. Arterial emboli arise from areas
of stagnant or disturbed blood flow in the heart or
aorta.The most common sources of arterial emboli are
listed inTable 6-15.
Table 6-15 SOURCES OF PERIPHERAL EMBOLI
Source Percentage
Cardiac 80%
Atrial fibrillation 50%
Myocardial infarction 25%
5%
Other
Noncardiac 10%
Aneurysmal disease 6%
Proximal artery 3%
Paradoxical emboli 1%
Other or Idiopathic 10%
From Belkin M, Owens CD,Whittemore AD, et al: Peripheral
Arterial Occlusive Disease. In CM Townsend, RD Beauchamp, BM
Evers, et al: SabistonTextbook of Surgery:The Biological Basis of
Modern Surgical Practice, 18th ed) Philadelphia: Saunders, 2007.
236 CHAPTER 6 Vascular System and Hematology
Table 6-16 HYPERTENSION AS IT RELATES TO
DIFFERENT AGE GROUPS
Normal Blood Hypertensive Blood
Pressure (Systolic/ Pressure (Systolic/
Age Diastolic) Diastolic)
Infants 80/40 90/60
Children 100/60 120/80
Teenagers 115/70 130/80
(age 12-17
years)
Adults  18 <120/<80 (Prehypertension)
years 120-139/80-89
(Stage 1 hypertension)
140-159/90-99
(Stage 2 hypertension)
 160/ 100
Based on the average of two or more readings taken at each of two
or more visits after initial screening.
Data from Bullock B. Pathophysiology: Adaptations and
Alterations in Function (4th ed). Philadelphia: Lippincott-Raven,
1996;517; Chobanian A.The Seventh Report of the Joint National
Committee on Prevention, Detection, Evaluation and Treatment
of High Blood Pressure.TheJNC 7 Report. JAMA 2003: 289.
Areas in which arterial emboli tend to lodge and
interrupt blood flow are arterial bifurcations and areas
narrowed by atherosclerosis (especially in the cerebral,
mesenteric, renal, and coronary arteries). Signs and
symptoms of thrombi, emboli, or both depend on the
size of the occlusion, the organ distal to the clot, and
the collateral circulation available.37
Treatment of thrombi, emboli, or both includes
anticoagulation with or without surgical resection of
the atherosclerotic area that is predisposing the
formation of thrombi, emboli, or both. Acute arterial
embolus is a surgical emergency. The likelihood of
limb salvage decreases after 4 to 6 hours.44 Medical
management of arterial thrombosis can also include
antithrombotic drugs (e.g., tissue factor or factor Xa
inhibitors) or combined antithrombotic therapy with
aspirin, thienopyridine and warfarin, or both.45
HYPERTENSION. Hypertension is an elevated arterial
blood pressure, both systolic and diastolic, that is
abnormally sustained at rest. Table 6-16 outlines
normal and hypertensive blood pressures for a given
age group.
Signs and symptoms that can result from hyperten-
sion and its effects on target organs are described in
Table 6-17.
Two general forms of hypertension exist: essential
and secondary. Essential, or idiopathic, hypertension is an ele-
vation in blood pressure that results without a specific
medical cause but is related to the following risk
factors37,46:
 Genetic predisposition
 Smoking
 Sedentary lifestyle
 Type A personality
 Obesity
 Diabetes mellitus
 Diet high in fat, cholesterol, and sodium
 Atherosclerosis
 Imbalance of vasomediator production, nitric oxide
(vasodilator), and endothelin (potent vasoconstrictor)
Secondary hypertension results from a known medical
cause, such as renal disease and others listed in Table
6-18. If the causative factors are treated sufficiently,
systolic blood pressure may return to normal limits.37
A rise in diastolic blood pressure from a sitting to
standing position suggests essential hypertension,
whereas a fall in blood pressure from the sitting to
standing position indicates secondary hypertension.9
Management of hypertension consists of behavioral
(e.g., diet, smoking cessation, activity modification)
and pharmacologic intervention to maintain blood
pressure within acceptable parameters. Pharmacologic
treatment can likely be deferred in hypertensive
patients who regularly participate in aerobic exercise.
Exercise high in intensity and duration has a beneficial
effect in the management of hypertension, and the anti-
hypertensive effect of regular training can be main-
tained as long as 3 years.47 The primary medications
used are diuretics and angiotensin-converting enzyme
inhibitors along with beta blockers, calcium channel
blockers, and vasodilators.37,48-50 A summary of these
medications, their actions, and their side effects can be
found in AppendixTables IV-3 and IV-3a.
Hypertensive crisis is a medical emergency. It occurs
when the blood pressure is high enough to threaten
target organs acutely. Hypertensive emergency requires
admission to an intensive care unit and parenteral
therapy.51
CLINICAL TIP
 Knowledge of medication schedule may facilitate
activity tolerance by having optimal blood pressures
at rest and with activity.
 Review and clarify any strict blood pressure
parameters that the physician has designated for
 Vascular System and Hematology CHAPTER 6 237

Table 6-17 HYPERTENSIVE EFFECTS ON TARGET ORGANS

Organ Hypertensive Effect Clinical Manifestations
Brain Cerebrovascular accident Area of brain involved dictates presentation. May include severe occipital
headache, paralysis, speech and swallowing disturbances, or coma.
Encephalopathy Rapid development of confusion, agitation, convulsions, and death
Eyes Blurred or impaired vision Nicking (compression) of retinal arteries and veins, at the point of their
junction
Encephalopathy Hemorrhages and exudates on visual examination
Papilledema
Heart Myocardial infarction Electrocardiographic changes
Enzyme elevations
Congestive heart failure Decreased cardiac output.
Auscultation of S3 or gallop
Cardiomegaly on radiograph
Myocardial hypertrophy Increased angina frequency
ST- and T-wave changes on electrocardiogram
Dysrhythmias Ventricular or conduction defects.
Kidneys Renal insufficiency Nocturia.
Proteinuria
Elevated blood urea nitrogen and creatinine levels
Renal failure Fluid overload
Accumulation of metabolites
Metabolic acidosis
Data from Bullock B (ed). Pathophysiology: Adaptations and Alterations in Function (4th ed). Philadelphia: Lippincott-Raven, 1996;522.

the patient, as some patients need to have higher
or lower systolic pressures than expected normal
ranges.
 When the blood pressure measurement reveals an
elevated blood pressure, make sure the cuff size is
right for the patient’s arm, take the blood pressure
in the opposite extremity, and then notify the team.
 In certain patient populations (e.g., patients status
postmastectomy, patients with PICC line) there are
restrictions on taking blood pressure in the upper
extremities. In these cases, blood pressure can be
taken in the lower extremities.
 In patients receiving antihypertensive therapy, keep
in mind the signs and symptoms of low blood
pressure, such as dizziness, confusion, syncope,
restlessness, or drowsiness, especially in elderly
patients.
 Patients can present with an elevated blood pressure
when they are apprehensive, in pain, and in stress.
Keep this in mind, and try to calm the patient
(by applying a wet washcloth on the forehead and/
or neck and by distracting the patient through
talking). Repeat the measurement in a few minutes
for an accurate representation of blood pressure.
SYSTEMIC VASCULITIS. Systemic vasculitis is a gen-
eral term referring to the inflammation of arteries and
veins that progresses to necrosis, leading to a narrowing
of the vessels. Although the specific cause of many of
these disorders is not known, infectious organisms,
drugs, tumors and allergic reactions are some of the
defined triggers. Pathogenetic factors include immune
complex disease, antineutrophil cytoplasmic antibo-
dies, antiendothelial cell antibodies and cell-mediated
immunity.The major ischemic manifestations of vascu-
litis are defined by the type and size of blood vessels
involved and the tissue and organ damage caused by
the ischemia related to the vascular occlusion.52 The
secondary manifestations of vasculitis are numerous
and may include thrombosis, aneurysm formation,
238 CHAPTER 6 Vascular System and Hematology

frequently involved organs are the kidney, heart, liver,

Table 6-18 CAUSES OF SECONDARY and gastrointestinal tract, with symptoms representa-
HYPERTENSION tive of the dysfunction of the involved organ.
Origin Description Aneurysm formation with destruction of the medial
layer of the vessel is the hallmark characteristic of
Coarctation of Congenital constriction of the PAN. Pulmonary involvement can occur; however,
the aorta aorta at the level of the
ductus arteriosus, which
most cases of vasculitis in the respiratory tract are
results in increased pressure associated withWegener’s granulomatosis.
(proximal to the area) of Current management of PAN includes corticoster-
constriction and decreased oid therapy with or without concurrent cytotoxic
pressure (distal to the area) therapy with cyclophosphamide (Cytoxan). Antiviral
of constriction agents may also be used if there is an associated viral
Cushing’s disease See Pituitary Gland in infection. Elective surgical correction of PAN is not
or syndrome Chapter 11 feasible, given its diffuse nature. Patients diagnosed
Oral contraceptives May be related to an increased with PAN have a 5-year survival rate of 12% without
secretion of glucocorticoids medical treatment and 80% with treatment.40,53
from adrenal or pituitary
Wegener’s Granulomatosis. Wegener’s granulomato-
dysfunction
Pheochromocytoma Tumor of the adrenal medulla sis is a granulomatous necrotizing disease that affects
causing increased small- and medium-sized blood vessels throughout
catecholamine secretion the body, with primary manifestations in the upper
Primary Increased aldosterone secretion respiratory tract, lungs, and kidneys. The etiology
aldosteronism primarily as result of an is unknown; diagnosis and treatment are still in devel-
adrenal tumor opment. It occurs most commonly in the fourth and
Renin-secreting See Adrenal Gland in fifth decades of life and affects men and women with
tumors Chapter 11 equal frequency.42 Pulmonary signs and symptoms
Renovascular Parenchymal disease, such mimic those of pneumonia (i.e., fever, productive
disease as acute and chronic
glomerulonephritis
cough at times with negative sputum cultures, and
Narrowing stenosis of renal chest pain).48,53 The1-year mortality rate is 90% without
artery as a result of therapy, 50% with corticosteroid therapy, and 10%
atherosclerosis or congenital with combined corticosteroid and cytotoxic therapy.53
fibroplasia Treatment of Wegener’s granulomatosis may consist
of a combination of immunosuppressive agents and
Data from Bullock B (ed). Pathophysiology: Adaptations and
Alterations in Function (4th ed). Philadelphia: Lippincott-Raven,
corticosteroids (methotrexate and prednisone, respec-
1996;517. tively). Antiinfective agents may also be prescribed
if there is associated respiratory tract infection.33,36
Thromboangiitis Obliterans. Thromboangiitis oblit-
erans (Buerger’s disease) is a clinical syndrome that is
found mainly in young men ages 20 to 45 years and
hemorrhage, arterial occlusion, weight loss, fatigue, is directly correlated to a heavy smoking history.4,37,40
depression, fever, and generalized achiness that is If abstinence from tobacco is adhered to, the disease
worse in the morning. The recognized forms of vascu- takes a favorable course. If smoking is continued, the
litis are discussed in the following sections.31,40,53,54 disease progresses, leading to gangrene and small-
Polyarteritis Nodosa. Polyarteritis nodosa (PAN) is digit amputations.56 The disease is characterized by
an acute necrotizing vasculitis of medium-sized and segmental thrombotic occlusions of the small- and
small arteries.52 Most cases present with an unknown medium-sized arteries in the distal lower and upper
etiology; however, the hepatitis B virus has been extremities. The thrombotic occlusions consist of
evolving as one of the more common causative fac- microabscesses that are inflammatory in nature,
tors.53 PAN usually begins with nonspecific symptoms, suggesting a collagen or autoimmune origin, although
which may include malaise, fatigue, fever, myalgias, the exact etiology is still unknown.37,40 Rest pain is
and arthralgias. Skin lesions are common, and a major- common, along with intermittent claudication that
ity of patients have vasculitic neuropathy.55 The most occurs more in the feet than in the calf region.3
 Vascular System and Hematology
The diagnosis is made by invasive and noninvasive
methods. The noninvasive methods include physical
exam, Doppler ultrasound, plethysmography, and
ABI.The invasive methods include MRA, angiography,
and spiral CT.57
Treatment of Buerger’s disease can include smoking
cessation, corticosteroids, prostaglandin E1 infusion,
vasodilators, hemorheologic agents, antiplatelet agents,
and anticoagulants.37,40
Giant Cell Arteritis. Giant cell arteritis (GCA) is
another granulomatous inflammatory disorder of an
unknown etiology. It predominantly affects the large
arteries and is characterized by destruction of the
internal elastic lamina. Two clinical presentations of
GCA have been recognized: temporal arteritis and
Takayasu’s arteritis.37
Temporal arteritis is a more common and mild pre-
sentation of GCA that occurs after 50 years of age. The
primary signs and symptoms are persistent headache
(temporal and occipital areas), transient visual distur-
bances (amaurosis fugax and graying or blurring of
vision), and jaw and tongue pain. Polymyalgia rheuma-
tica, a clinical syndrome characterized by pain on
active motion and acute onset of proximal muscular
stiffness, is frequently associated with temporal arteri-
tis. The primary treatment for temporal arteritis is
prednisone.33,53
Takayasu’s arteritis generally affects young Asian
women but has been known to occur in both genders
of African Americans and Hispanics as well. It is a
form of generalized GCA that primarily involves
the upper extremities and the aorta and its
major branches. Lower-extremity involvement is less
common. Management of Takayasu’s arteritis may
consist of prednisone and cyclophosphamide, along
with surgical intervention if the disease progresses to
aneurysm, gangrene, or both.33
RAYNAUD’S DISEASE. Raynaud’s disease is an epi-
sodic vasospastic disorder characterized by digital
color change (white to blue to redçreflecting the vaso-
constriction, cyanosis, and vasodilation process,
respectively) with exposure to cold environment or
emotional stress. Numbness, tingling, and burning
pain may also accompany the color changes. However,
despite these vasoconstrictive episodes, peripheral
pulses remain palpable. If idiopathic, it is called
Raynaud’s disease. If associated with a possible precipita-
tion systemic or regional disorder (autoimmune
diseases, myeloproliferative disorders, multiple mye-
loma, cryoglobulinemia, myxedema, macroglo-
bulinemia, or arterial occlusive disease), it is called
CHAPTER 6 239
Raynaud’s phenomenon. In Raynaud’s disease, the disease
is symmetric by rule; in Raynaud’s phenomenon, the
changes may be most noticeable in one hand or even
in one or two fingers only. Infrequently, the feet and
toes are involved. Between attacks, the affected extremi-
ties may be entirely normal.The incidence of disease is
estimated to be as high as 10% in the general popula-
tion. An abnormality of the sympathetic nervous
system has long been implicated in the etiology of
Raynaud’s disease; recently, research has focused on
the theory of up-regulation of vascular smooth muscle
a2-adrenergic receptors. The distinction between
Raynaud’s disease and Raynaud’s phenomenon is
meant to reflect a difference in prognosis. Whereas
Raynaud’s disease is benign and often controllable,
Raynaud’s phenomenon may progress to atrophy of
the terminal fat pads and development of fingertip gan-
grene.Women 16 to 40 years of age are most commonly
affected, especially in cold climates or during the
winter season. Raynaud’s disease is usually benign,
causing mild discomfort on exposure to cold and pro-
gressing very slightly over the years. The prognosis of
Raynaud’s phenomenon is that of the associated dis-
ease.42 Areas generally affected are the fingertips, toes,
and the tip of the nose.4,33,48
Management of Raynaud’s disease and Raynaud’s
phenomenon may consist of any of the following:
conservative measures to ensure warmth and protection
of the body and extremities; regular exercise; diet
rich in fish oils and antioxidants (vitamins C and E);
pharmacologic intervention, including calcium chan-
nel blockers and sympatholytics; conditioning and bio-
feedback; acupuncture; and sympathectomy.33,42,58
COMPLEX REGIONAL PAIN SYNDROME. Complex
regional pain syndrome (CRPS) is a rare disorder of
the extremities characterized by autonomic and vaso-
motor instability. Use of the former name of this
entity, reflex sympathetic dystrophy (RSD), is now dis-
couraged because the precise role of the sympathetic
nervous system is unclear and dystrophy is not an inev-
itable sequela of the syndrome.
The presenting symptom is constant, extreme pain
that occurs after the healing phase of minor or major
trauma, fractures, surgery, or any combination of
these. Injured sensory nerve fibers may transmit con-
stant signals to the spinal cord that result in increased
sympathetic activity to the limbs. Affected areas
initially present as dry, swollen, and warm but then
progress to being cold, swollen, and pale or cyanotic.
It occurs in all age groups and equally in both sexes
and can involve either the arms or the legs.42
240 CHAPTER 6 Vascular System and Hematology
Three stages have been defined (Steinbrocker classi-
fication), although all patients may not have evolved
through the stages or proceed in a temporal fashion.52
Stage 1 (acute): Pain, tenderness, edema, and tempera-
ture changes predominate.
Stage 2 (dystrophic): Pain extends beyond the area
affected; loss of hair and dystrophic nails become
apparent. Muscle wasting, osteoporosis, and
decreased range of motion may occur.
Stage 3 (atrophic or chronic): Atrophy, demineraliza-
tion, functional impairment, and irreversible
damage are present.
Management of CRPS may consist of any of the
following33,59-62:
 Physical or occupational therapy, or both (corner-
stone therapy)
 Pharmacologic sympathetic blocks
 Surgical sympathectomy
 Spinal cord electrical stimulation
 Baclofen drug administration
 Prophylactic vitamin C administration after sustain-
ing fractures
 Bisphosphonate administration
The prognosis partly depends on the stage in which
the lesions are encountered and the extent and severity
of associated organic disease. Early treatment offers
the best prognosis for recovery.42
COMPARTMENT SYNDROME. Compartment syn-
drome is a condition in which the circulation within a
closed compartment is compromised by an increase in
pressure within the compartment, causing necrosis of
muscles and nerves and eventually of the skin because
of excessive swelling. Volkmann ischemic contracture
is a sequela of untreated or inadequately treated com-
partment syndrome in which necrotic muscle and
nerve tissue has been replaced with fibrous tissue.63
Compartment syndrome can occur after traumatic
injuries, which include fractures, crush injuries, hema-
tomas, penetrating injuries, circumferential burn
injury, electrical injuries, and status postrevasculariza-
tion procedures. External factors, such as casts and
circular dressings that are too constrictive, may also
lead to compartment syndrome.30,33,64 Compartment
syndrome can also occur as a chronic condition that
develops from overuse associated with strenuous
exercise. Diagnosis of compartment syndrome is
established by measuring compartment pressures.
Compartment pressures of 32 to 37 mm Hg can cause
compression of capillaries.64
A common symptom of compartment syndrome is
pain associated with tense, tender muscle groups that
worsens with palpation or passive movement of the
affected area. Numbness or paralysis may also be
accompanied by a gradual diminution of peripheral
pulses. Pallor, which indicates tissue ischemia, can
progress to tissue necrosis if appropriate management
is not performed.30,33,64
Management of compartment syndrome consists of
preventing prolonged external compression of the
involved limb, limb elevation, and, ultimately, fascioto-
my (incisional release of the fascia) if compartment
pressures exceed 37 to 52 mm Hg. Mannitol can also
be used to help reduce swelling.30,33,64
CLINICAL TIP
 Patient, staff, and family education on proper
positioning techniques can reduce the risk of
swelling and subsequent compartment syndrome.
 The physical therapist should delineate any range-
of-motion precautions that may be present after
fasciotomies that cross a joint line.
VENOUS DISORDERS
VARICOSE VEINS. Varicose veins are chronic dila-
tions of the veins that first result from a weakening in
the venous walls, which then lead to improper closure
of the valve cusps. Incompetence of the valves further
exacerbates the venous dilatation.Varicose veins can be
either primary or secondary. Primary varicose veins
originate in the superficial veinsçthe saphenous veins
and their branchesçwhereas secondary varicose
veins occur in the deep and perforating veins. Primary
varicose veins tend to run in families, affect both legs,
and are twice as common in females as in males.
Usually, secondary varicose veins only occur in one
leg. Both types are more common in middle adulthood.
Primary varicose veins can result from congenital
weakness of the valves or venous wall; from conditions
that produce prolonged venous stasis, such as preg-
nancy or wearing tight clothing; or from occupations
that necessitate standing for an extended period.
Secondary varicose veins result from disorders of the
venous system, such as deep vein thrombophlebitis,
trauma, and occlusion.9
Risk factors include female gender, pregnancy,
family history, prolonged standing, and history of
phlebitis.42
Patients generally complain of itchy, tired, heavy-
feeling legs after prolonged standing.30,65 Large vari-
cose veins are unsightly and may produce anxiety
 Vascular System and Hematology
and cause major lifestyle changes. Trauma to a varicose
vein may result in severe bleeding, particularly in
older adults, as their skin may be atrophic.66
Management of varicose veins may consist of any of
the following: behavioral modifications (e.g., avoiding
prolonged sittingor standing and constrictive clothing),
weight loss (if there is associated obesity), elevating the
feet for 10 to 15 minutes 3 or 4 times a day, gradual
exercise, applying well-fitting support stockings in the
morning, showering or bathing in the evening, sclero-
therapy (to close dilated veins), and surgical ligation
and stripping of incompetent veins.30,65
VENOUS THROMBOSIS. Venous thrombosis can
occur in the superficial or deep veins (DVT) and can
result from a combination of venous stasis, injury to
the endothelial layer of the vein, and hypercoagulabili-
ty. The primary complication of venous thrombosis is
pulmonary embolism (PE).30
The DVT proximal to the calf is associated with
higher risk of PE. Clinical studies indicate a strong
association between DVT and PE. As many as 50% of
patients who have a proximal DVT develop a PE, and
among those who have a clinically significant PE,
70% have evidence of DVT.67
The risk factors associated with DVT are listed in
Box 6-1.
BOX 6-1 RISK FACTORS FOR DVT
 Surgery and immobilization
 Obesity
 Hospital stay in a critical care area
 Pregnancy and postpartum period
 Heart failure or respiratory failure
 Tobacco use
 Central venous catheters, pacemakers, and
defibrillators
 Use of oral contraceptives or hormone
replacement therapy
 Cancer and chemotherapy
 Prolonged airline travel
 Diabetes
 Trauma
 Hypertension
 Varicose veins
 Stroke and spinal cord injury
 Increasing age
Data from Hill, KM. Careful Assessment and Diagnosis Can
Prevent Complications of DVT. Clinical Updates, May 2007.
CHAPTER 6 241
Signs and symptoms of venous thrombosis can
include the following33,68:
 Pain and swelling distal to the site of thrombus
 Redness and warmth in the area around the thrombus
 Dilated veins
 Low-grade fever
 A dull ache or tightness in the region of DVT
CLINICAL TIP
 Homans’ sign (pain in the upper calf with forced
ankle dorsiflexion) has been used as a screening tool
for venous thrombosis, but it is an insensitive and
nonspecific test (sensitivity and specificity are only
about 50%) that has a very high false-positive rate.43
 A positive Homans’ sign accompanied by swelling,
redness, and warmth may be more clinically
indicative of a DVT than a positive Homans’ sign
alone.
 Physical therapy intervention for patients with
suspected DVT should be withheld until cleared
by the medical-surgical team.
 Patients with DVT in a lower extremity may
complain of pain around the general area of the
thrombus with weight bearing.
 Physical therapists should be cautious for the signs
and symptoms of unusual bleeding in patients who
are on anticoagulation after the diagnosis of DVT.
The primary imaging study to identify patients with
DVT now is ultrasonography. It is relatively inexpen-
sive, noninvasive, and widely available. Ultrasound is
considered to be 90% to 95% sensitive for acute
thrombi above the knee. Other diagnostic methods
include venography and impedence plethysmography.
Magnetic resonance imaging (MRI) is developing a
growing role in the diagnosis of DVT, with a sensitivity
of 97% and specificity of 95%.43
Patients admitted to the hospital and/or undergoing
surgery are often on DVT prophylaxis, which includes
mechanical and pharmacological approaches67; lower-
extremity elevation or application of compression
stockings (elastic or sequential pneumatic), or both, if
bed rest is required; and anticoagulation medications
(intravenous heparin or oral warfarin [Coumadin]).
The initial treatment for DVT is anticoagulation
with heparin. Heparin blocks the extension of
thrombus and reduces the risk of further emboli.
It does not actively lyse a clot, but allows the body’s
own fibrinolytic mechanism to operate over a period
242 CHAPTER 6 Vascular System and Hematology
of several days to weeks. If a patient cannot be anticoa-
gulated, a device called an inferior vena cava (IVC) filter,
can prevent lower extremity thrombi from embolizing
to the lungs. The primary indications for IVC filter
placement include contraindications to anticoagula-
tion, recurrent embolism while on adequate therapy,
and significant bleeding complications during antico-
agulation. IVC filters are sometimes placed in the
setting of massive PE when it is believed that any
further emboli might be lethal. More recently, tempo-
rary filters have been used in patients in whom the risk
of bleeding appears to be short-term; such devices can
be removed up to 2 weeks later.55
Management of venous thrombosis may also consist
of thrombolytic therapy (streptokinase and urokinase),
or both, and surgical thrombectomy (limited uses).30
However, the use of thrombolytic therapy is not recom-
mended for an isolated DVT.43
Traditionally, all patients with the diagnosis were
required to be on bed rest for the first few days, because
of the fear of dislodging clots that may result in pulmo-
nary embolism. However, with the introduction of
low-molecular-weight heparin (LMWH), known by
the generic name of Lovenox, selected stable patients
are treated on an outpatient basis and are discharged
home on LMWH. Recent literature review shows that
bed rest has no influence on the risk of developing
PEs. Use of a compression stocking while ambulating
has an added advantage, and compression stockings
are reported to help with pain relief and leg
circumference.43,69-71
PULMONARY EMBOLISM. PE is the primary compli-
cation of venous thrombosis, with emboli commonly
originating in the lower extremities. Other sources are
the upper extremities and pelvic venous plexus.
Mechanical blockage of a pulmonary artery or capillary,
depending on clot size, results in an acute ventilation-
perfusion mismatch that leads to a decrease in
partial pressure of oxygen and oxyhemoglobin
saturation, which ultimately manifests as tissue hypox-
ia. Chronic physiologic sequelae from PE include
pulmonary hypertension, chronic hypoxemia, and
right congestive heart failure. Refer to the Laboratory
Studies section for details on the D-Dimer test.
Refer to Chapter 2 for more details on ventilation-
perfusion mismatches, as well as the respiratory seque-
lae (dyspnea, chest pain, hemoptysis, and tachypnea)
from PE.30,72
Management of PE consists of prevention of venous
thrombosis formation (see the VenousThrombosis sec-
tion), early detection, and thorough anticoagulation
therapy with standard or low—molecular-weight hepa-
rin.Thrombolytic therapy has also been used in patients
with PE. The placement of an inferior vena cava
filter is indicated when patients cannot be anticoagu-
lated or when there is recurrence of PE despite
anticoagulation.30,72
CLINICAL TIP
 Physical therapy intervention should be discontinued
immediately if the signs and symptoms of an
acute PE arise during an examination or treatment
session.
CHRONIC VENOUS INSUFFICIENCY AND
POSTPHLEBITIC SYNDROME. Chronic venous insuffi-
ciency and postphlebitic syndrome are similar disorders
that result from venous outflow obstruction, valvular
dysfunction from thrombotic destruction of veins, or
both.Valvular dysfunction is generally the most signif-
icant cause of either disorder. Figure 6-6 illustrates the
venous valves and the normal function of the valves.
Within 5 years of sustaining a DVT, approximately
50% of patients develop signs of these disorders. The
hallmark characteristics of both (chronic venous
insufficiency and postphlebitic syndrome) are the
following1,8,30,57,73:
 Chronic swollen limbs, which becomes worse while
the limbs are in a dependent position.
A B C
FIGURE 6-6
Venous valves. A, Open valves allow forward blood flow.
B, Closed valves prevent backflow. C, Incompetent valves
unable to fully close, causing blood to flow backward and
producing venous insufficiency. (From Bryant R, Nix D. Acute
and Chronic Wounds: Current Management Concepts [3rd ed].
St. Louis: Mosby, 2007.)
 Vascular System and Hematology
 Skin changes such as the following are common:
(1) hemosiderin staining or hemosiderosis, a classic indica-
tor of venous disease, is a discoloration of soft
tissue that results when extravasated RBCs break
down and release the pigment hemosiderin, result-
ing in a gray-brown pigmentation of the skin (also
called hyperpigmentation or tissue staining) and (2) lipoder-
matosis (fibrosis or hardening of the soft tissue in the
lower leg), which is indicative of long-standing
venous disease.
 Venous stasis ulceration
 Management of these disorders may consist of any
of the following: leg elevation above the level of
the heart 2 to 4 times daily for 10 to 15 minutes;
application of proper elastic supports (knee length
preferable); skin hygiene; avoidance of crossing
legs, poorly fitting chairs, garters, and sources of
pressure above the legs (e.g., tight girdles); elastic
compression stockings; pneumatic compression
stockings (if the patient needs to remain in bed);
exercise to aid muscular pumping of venous blood;
surgical ligation of veins; and wound care to venous
ulcers. Refer to Chapter 7 for more information on
wound care.1,30,73
CLINICAL TIP
 Caution should be taken in providing compressive
dressings and elevating the lower extremities of
patients who have arterial insufficiency, diabetes
mellitus, or congestive heart failure.
COMBINED ARTERIAL AND VENOUS DISORDERS
ARTERIOVENOUS MALFORMATIONS. Arteriovenous
malformations (AVMs) involve shunting of blood
directly from the artery to the vein, bypassing the capil-
lary bed. The presence of an arteriovenous fistula in
the AVM is usually the cause of the shunt.The majority
of AVMs occur in the trunk and extremities, with a cer-
tain number of cases also presenting in the cerebrovas-
cular region.40
Signs of AVMs may include the following40:
 Skin color changes (erythema or cyanosis)
 Venous varices
 Edema
 Limb deformity
 Skin ulceration
 Pulse deficit
 Bleeding
 Ischemic manifestations in involved organ systems
CHAPTER 6 243
Hematologic Disorders
ERYTHROCYTIC DISORDERS
Disorders of RBCs are generally categorized as a
decrease or an increase in the number of RBCs in the
circulating blood.
ANEMIA. Anemia is a decrease in the number of
RBCs. Anemia can be described according to etiology
as (1) a decrease in RBC production, (2) abnormal
RBC maturation, or (3) an increase in RBC destruc-
tion.20 Anemia can also be described according to mor-
phology based on RBC size or color.74 RBCs that are
of normal size are normocytic; RBCs that are smaller
than normal are microcytic; and RBCs that are larger
than normal are macrocytic. RBCs of normal color are
normochromic; RBCs of decreased color are micro-
chromic. Some of the most common anemias are
described in this section.
Posthemorrhagic Anemia. Posthemorrhagic anemia
can occur with rapid blood loss from traumatic artery
severance, aneurysm rupture, or arterial erosion from
malignant or ulcerative lesions, or as a result of surgery.
Blood loss results in a normocytic, normochromic
anemia.
The signs and symptoms of posthemorrhagic
anemia depend on the amount of blood loss and may
include the following75:
 With 20% to 30% blood volume lossçDizziness and
hypotension when not at rest in a recumbent posi-
tion; tachycardia with exertion.
 With 30% to 40% blood volume lossçThirst, dys-
pnea, diaphoresis, cold and clammy skin, hypoten-
sion and tachycardia, decreased urine output,
clouding or loss of consciousness when at rest in a
recumbent position.
 With 40% to 50% blood volume lossçA severe state
of shock with the potential for death ensues.
Management of posthemorrhagic anemia may con-
sist of any of the following: control of bleeding at the
source, intravenous and oral fluid administration,
blood and blood product transfusion, and supplemental
oxygen.21,74,76
Iron-Deficiency Anemia. Iron-deficiency anemia is
the most common cause of anemia, affecting at least
one-third of the world’s population.57,77 It occurs when
decreased iron storage in the bone marrow causes the
production of microcytic, microchromic RBCs.
The common causes of iron-deficiency anemia are
listed in Box 6-2.
The average American diet contains 10 to 15 mg of
iron per day, of which 10% is absorbed via the stomach,
244 CHAPTER 6 Vascular System and Hematology
BOX 6-2 CAUSES OF IRON DEFICIENCY
 Deficient diet
 Decreased absorption
 Increased requirements
 Pregnancy
 Lactation
 Blood loss
 Gastrointestinal
 Menstrual
 Blood donation
 Hemoglobinuria
 Iron sequestration
Adapted from McPhee SJ, Papadakis MA,Tierney LM. Current
Medical Diagnosis and Treatment. 46th ed. NewYork:
McGraw-Hill Medical, 2007.
duodenum, and upper jejunum. Menstrual blood loss
in women plays a major role in iron metabolism.
Women with heavy menstrual losses should absorb
3 to 4 mg of iron from the diet each day.42 Serum ferritin
is the preferred initial diagnostic test and is a good indi-
cator of the available iron stores in the body. A ferritin
level less than 10 mcg/L is diagnostic of iron-deficiency
anemia. Often, the iron-deficiency anemia is asympto-
matic if the onset is insidious.18,78,79
Signs and symptoms of iron-deficiency anemia
include the following66,77:
 Easy fatigability, tachycardia, palpitations, and
dyspnea on exertion.
 Dizziness, headache and irritability
 Dysphagia (Plummer-Vinson syndrome, a formation
of esophageal webs)
 Softening and spooning of nails; pale earlobes,
palms, and conjunctivae (severe anemia)
 Many iron-deficient patients develop pica, which
is the craving to eat unusual substances such as dirt
or ice.
Management of iron-deficiency anemia consist
of a medical workup to identify possible blood
loss site, iron supplementation, or nutritional counsel-
ing.21,74,76,80 Iron supplementation during pregnancy is
almost always required.42
Vitamin B12 Anemia. Decreased levels of vitamin B12
cause the production of macrocytic, normochromic
RBCs. Vitamin B12 deficiency is commonly caused by
poor absorption of vitamin B12 from enteritis or iliac
disease. It is less commonly associated with Crohn’s
disease and pancreatic insufficiency. Since Vitamin B12
is present in all foods of animal origin, dietary
Vitamin B12 insufficiency is extremely rare and is seen
only in vegans. The most common cause of Vitamin
B12 deficiency is associated with pernicious anemia.
Pernicious anemia is caused by the absence of intrinsic
factor available to bind to vitamin B12.42 In addition to
the general presentation of anemia, the signs and
symptoms of vitamin B12 deficiency may include the
following:
 Pale skin and mild icterus (a yellow discoloration of
the skin, mucous membranes, and sclerae of the
eyes, caused by greater than normal amounts of
bilirubin in the blood)81
 Anorexia and diarrhea
 Oral ulceration
Early neurologic symptoms include decreased vibra-
tory sensation, loss of proprioception, and ataxia.82
Later involvement results in spasticity, hyperactive
reflexes, and a positive Romberg’s sign.These neurolog-
ic symptoms result from the formation of a demyelinat-
ing lesion of the neurons of the spinal cord and
cerebral cortex.66
Vitamin B12 deficiency is diagnosed by clinical pre-
sentation, low serum vitamin B12 levels, elevated lactate
dehydrogenase and MCV values, and positive urine
sampling (Schilling test). Neurologic symptoms are
reversible if the onset is less than 6 months.54
Management of vitamin B12 anemia consists of lifelong
vitamin B12 supplementation and nutritional
counseling.21,74,76
CLINICAL TIP
 Patients who receive monthly vitamin B12 injections
may have improvements in their alertness and
activity tolerance for a few days after the injection.
Therefore, physical therapy intervention and goal
setting should accommodate these changes.
Folic Acid Anemia. Decreased folic acid (folate)
causes the production of macrocytic, normochromic
RBCs.The most common cause of folic acid deficiency
is inadequate dietary intake. Alcoholics, anorectic
patients, pregnant women, and patients who do not
eat fresh produce and those who overcook their food
are candidates for folate deficiency.80 The presentation
of folic acid anemia is similar to vitamin B12 deficiency
anemia, except there are no neurologic sequelae.
Folic acid anemia is diagnosed by clinical presentation,
a low serum folate level, and elevated lactate
 Vascular System and Hematology
dehydrogenase and MCVvalues.83 Management of folic
acid anemia consists of folic acid supplementation.80
Aplastic Anemia. Aplastic anemia is characterized by
a decreased RBC production secondary to bone
marrow damage. The bone marrow damage either
causes irreversible changes to the stem cell population,
rendering these cells unable to produce RBCs, or
alters the stem cell environment, which inhibits RBC
production. The exact mechanism of stem cell damage
is unknown; however, present theories include expo-
sure to radiation and chemotherapy or pharmacologic
agents, the presence of infection or malignancy, or as
an autoimmune response.84 RBCs are normochromic
and normocytic or macrocytic. WBC and platelet
counts are also decreased. The hallmark of aplastic
anemia is pancytopenia.42 Definitive diagnosis is by
bone marrow biopsy.
Signs and symptoms of aplastic anemia may include:
 Fatigue and dyspnea
 Petechiae, bleeding gums, hematuria, heavy
menstrual flow, or fecal blood
 Pallor is common and is observed on the mucosal
membranes and palmar surfaces
 Fever or infection
 Sore throat
Management of aplastic anemia may include any of
the following: investigation and removal of causative
agent; red blood cell and platelet transfusion; immuno-
suppression; bone marrow transplantation and periph-
eral stem cell transplantation; corticosteroids; and
antibiotics. Aplastic anemia can be fatal if untreated.*
Hemolytic Anemia. Hemolysis is the destruction or
removal of red blood cells from the circulation before
their normal life span of 120 days. Hemolysis can be a
lifelong process. It most often presents as anemia
when the formation of the RBCs cannot match the
pace of RBC destruction. The two types of hemolytic
anemia are extravascular and intravascular hemolytic
anemia. Extravascular hemolytic anemia involves the
destruction of RBCs outside of the circulation, usually
in the spleen and liver.86 This condition is usually the
result of an inherited defect of the RBC membrane or
structure, but it can be an autoimmune process in
which antibodies in the blood cause RBC destruction
through mononuclear phagocytosis.
Intravascular hemolytic anemia is the destruction of
RBC membrane within the circulation. It results in the
deposition of Hgb in plasma. This may occur because
*References 9,21,42,74,76,85.
CHAPTER 6 245
of a genetic enzyme deficit, the attack of oxidants on
RBCs, or infection. It may also occur traumatically
when RBCs are torn apart at sites of blood flow turbu-
lence, near a tumor, through prosthetic valves, or with
aortic stenosis.
Signs and symptoms of hemolytic anemia may
include:
 Fatigue and weakness
 Nausea and vomiting
 Fever and chills
 Decreased urine output
 Jaundice
 Abdominal or back pain and splenomegaly (intravas-
cular only)
Management of hemolytic anemia may include any
of the following: investigation and removal of the
causative factor, fluid replacement, blood transfusion,
corticosteroids, or splenectomy.21,74,76
Sickle Cell Anemia. Sickle cell anemia is an autoso-
mal homozygous (hemoglobin SS or HgSS) recessive
trait characterized by RBCs that become sickle (cres-
cent)-shaped when deoxygenated. Over time, cells
become rigid and occlude blood vessels, thus causing
tissue ischemia and infarction.The riskof cerebrovascu-
lar accident and infarction of other organs or muscles
is high. Symptoms and physical findings of sickle cell
anemia may include:
 Jaundice, nocturia, hematuria, pyelonephritis, renal
failure, splenohepatomegaly
 Retinopathy or blindness
 Chronic nonhealing ulcers of the lower extremity
 Systolic murmur and an enlarged heart
 Paresthesias
 Acute painful episodes that affect long bones and
joints, with the low back being the most frequent
site of pain. Other parts of the body affected are the
scalp, face, jaw, abdomen, and pelvis.The pain is usu-
ally nociceptive (secondary to tissue damage) and is
sharp and throbbing in nature.87
A complication of sickle cell anemia that may
require hospitalization is pain crisis, the intense pain
of any major organ or body area. This type of pain
crisis is usually treated with parenteral opioids.87 Pain
crisis, lasting from 4 to 6 days to weeks, can be precipi-
tated by infection, dehydration, hypoxia, sleep apnea,
exposure to cold, or menstruation, or it may be of
unknown etiology.88 Acute chest syndrome (ACS) is a
situation that requires hospital admission. The patient
presents with chest pain, dyspnea, hypoxemia, and
infiltrates on chest x-ray, perhaps with pleural effu-
sion.89 ACS may be caused by intrapulmonary sickling,
246 CHAPTER 6 Vascular System and Hematology
sickle cell emboli, or bone marrow or fat embolism, or
from infection.89 The ACS is currently defined as a
new infiltrate on chest radiograph associated with one
or more symptoms, such as fever, cough, sputum pro-
duction, tachypnea, dyspnea, or new-onset hypoxia.90
ACS is the leading cause of death in adolescents and
adults with sickle cell disease.23
Management of sickle cell anemia may include the
prevention or supportive treatment of symptoms with
rest; hydration; analgesia; supplemental oxygen; incen-
tive spirometry; use of corticosteroids or cytotoxic
agents, such as hydroxyurea 60; partial RBC exchange;
and psychosocial support.21,74,76,84,90 The average life
expectancy of a patient with sickle cell anemia is 40 to
50 years.80 Note that sickle cell anemia is differentiated
from sickle cell trait. A patient with sickle cell trait has
a heterozygous trait of Hgb that is asymptomatic for
the signs and symptoms of anemia, although RBCs
may sickle under the conditions of high altitude, stren-
uous exercise, or anesthesia.84 No treatment is usually
necessary; however, genetic counseling is a reasonable
strategy.42
CLINICAL TIP
 The use of oximetry can help the physical therapist
and patient monitor RBC oxygenation and gauge
exercise intensity.
Anemia of Chronic Diseases. The term anemia ofchronic
disease (ACD) designates an anemia syndrome typically
found in patients with chronic infections, inflamma-
tory disorders, or neoplastic disorders. ACD occurs in
approximately 50% of hospitalized patients, as identi-
fied by laboratory studies. ACD has also been observed
in acute trauma and critical care patients.
The clinical features are those of the causative condi-
tion. The diagnosis should be suspected in patients
with chronic diseases and is confirmed by low serum
level, low TIBC, and normal or increased serum
ferritin.
In most cases, no treatment is necessary. Purified
recombinant erythropoietin is effective for treatment
of anemia of renal failure or anemia related to cancer
and inflammatory conditions.77
POLYCYTHEMIA. Polycythemia is a chronic disorder
characterized by excessive production of RBCs, plate-
lets, and myelocytes. As these increase, blood volume,
blood viscosity, and Hgb concentration increases, caus-
ing excessive workload for the heart and congestion of
some organs.23 The three types of polycythemia are
primary polycythemia (polycythemia vera), secondary polycythemia,
and relativepolycythemia.
1. Primary polycythemia, or polycythemia vera, is an
acquired myeloproliferative disorder42 that causes
an increase in the number of RBCs,WBCs, and plate-
lets.92 The origin of this disease is unknown; how-
ever, there is an autonomous overproduction of
erythroid stem cells from bone marrow leading to
increased blood viscosity and expanded blood
volume.Thus, there is a risk for thrombus formation
and bleeding.80 Primary polycythemia may convert
to chronic myelogenous leukemia or myelofibrosis.
The hallmark of polycythemia vera is a hematocrit
above normal, at times greater than 60%.42
2. Secondary polycythemia is the overproduction of
RBCs owing to a high level of erythropoietin. The
increased erythropoietin level is a result of either
altered stem cells (which automatically produce
erythropoietin or erythropoietin-secreting tumors,
such as hepatoma or cerebellar hemangioblas-
toma)79 or chronic low oxygenation of tissues, in
which the body attempts to compensate for hypoxia.
The latter is common in individuals with chronic
obstructive pulmonary disease, cardiopulmonary
disease, or exposure to high altitudes.
3. Relative polycythemia is the temporary increase in
RBCs secondary to decreased fluid volume (dehy-
dration), as with excessive vomiting, diarrhea, or
excessive diuretic use, or after a burn injury.
Signs and symptoms of polycythemia may include44:
 Headache, dizziness, blurred vision, and vertigo, all a
result of hypervolemia
 Venous thrombosis, a result of hyperviscosity
 Bleeding from the nose, gastrointestinal bleeding,
and spontaneous bruising, all a result of platelet
dysfunction
 Fatigue
 Paresthesia in the hands and feet
 Splenomegaly (polycythemia vera only)
Management of polycythemia includes phlebotomy
as the main therapy. Blood is withdrawn from the
vein to decrease blood volume and decrease hematocrit
to 45%. Every 2 to 4 days, 250 to 500 ml of blood
is removed, depending on the age of the patient, with
a goal for the hematocrit to be below 42% for
females and 45% for males.23,55 Other treatments
used in polycythemia are myelosuppressive therapy
(hydroxyurea); interferon32; antiplatelet therapy
(aspirin); radiophosphorus (for primary polycythemia);
smoking cessation; and fluid resuscitation (for relative
polycythemia).
 Vascular System and Hematology
NEUTROPENIA
Neutropenia is defined as an absolute neutrophil count
(ANC) of less than 1,500/mL and is calculated from the
WBC differential: ANC = WBC (cells/mL)  percent
(PMNs + bands) divided by 100.93 A variety of bone
marrow disorders (e.g., leukemia) and nonmarrow con-
ditions (e.g., immunologic peripheral destruction,
sepsis, or hypersplenism) or chemotherapy may cause
neutropenia. Neutropenia is considered mild (ANC
between 1,000 and 1,500/mL), moderate (ANC between
500 and 1000/mL), or severe (ANC less than 500/mL).94
The risk of infection, typically bacterial, is related to
the severity of the neutropenia, with the risk of infec-
tion increasing at 1,000/mL.94 Usual signs of inflamma-
tory responses to infection may be absent in a
neutropenic patient; however, fever in a neutropenic
patient should always be assumed to be of infectious
origin. Refer to Chapter 12 for more information on
neutropenia.
Medical therapy consists of symptomatic manage-
ment of fever, discontinuation of causative drugs,
broad-spectrum antibiotics or antifungal agents to
treat infection, good dental hygiene, the administration
of myeloid growth factor, and hematopoietic cell
transplantation.42,94
THROMBOCYTIC DISORDERS
DISSEMINATED INTRAVASCULAR COAGULATION.
Disseminated intravascular coagulation (DIC) involves
the introduction of thromboplastic substances into the
circulation that initiate a massive clotting cascade
accompanied by fibrin, plasmin, and platelet activation.
It is a complex and paradoxic disorder characterized
by both hemorrhage and thrombus formation. First,
fibrin is deposited in the microcirculation, leading to
Table 6-19 COMMON SIGNS AND SYMPTOMS OF DISSEMINATED INTRAVASCULAR COAGULATION
System Related to Hemorrhage
Integumentary Bleeding from gums, venipunctures and old
surgical sites, epistaxis, ecchymoses
Cardiopulmonary Hemoptysis
Renal Hematuria
Gastrointestinal Abdominal distention, hemorrhage
Neurologic Subarachnoid hemorrhage
From Urden LD, Stacy KM, Lough ME:Thelan’s Critical Care Nursing: Diagnosis and Management, 5th ed). St. Louis: Mosby, 2006.
CHAPTER 6 247
organ ischemia and the destruction of RBCs as they
pass through these deposits. Second, platelets and clot-
ting factors are consumed and hemorrhage occurs.
Plasmin is activated to further decrease clotting factor,
and fibrin further inhibits platelet function, which fur-
ther increases bleeding.
DIC, either acute or chronic, is always a secondary
process mediated by inflammatory cytokines.95 DIC
may be mild and self-limiting or severe and is often
associated with critical illness.96 The onset of acute
DIC usually occurs in the presence of illness within
hours ordays of the initial injuryorevent.This condition
is associated with severe infection and Gram-negative
sepsis. Other causes of DIC include trauma, burn
injury, shock, tissue acidosis, antigen-antibody
complexes, or the entrance of amniotic fluid or placenta
into the maternal circulation.79 Organ failure is
common.6 Chronic DIC is associated with hemangio-
ma and other cancers (particularly pancreatic or
prostate cancer), systemic lupus erythematosus, or
missed abortion. DIC is a life-threatening condition
with high mortality and requires immediate medical
attention.6 Signs and symptoms of DIC are listed
inTable 6-19.
The diagnostic workup for DIC includes platelet
count (thrombocytopenia), PT and aPTT (prolonged),
INR (elevated), fibrinogen level (decreased), and pres-
ence of D-dimer.97 The D-dimer has high sensitivity
and specificity for diagnosing DIC.6
Management of DIC may include treatment of
the causative condition; hemodynamic and cardio-
vascular support, which includes fluid management,
oxygen supplementation, and invasive monitoring;
blood and blood product transfusion for active
bleeding; heparin therapy (this is controversial); and
recombinant protein factor therapy (experimental).23,95
Related to Thrombi
Peripheral cyanosis, gangrene
Dysrhythmias, chest pain, acute myocardial
infarction, pulmonary embolus, respiratory
failure
Oliguria, acute tubular necrosis, renal failure
Diarrhea, constipation, bowel infarct
Altered level of consciousness, cerebral vascular
accident
248 CHAPTER 6 Vascular System and Hematology
HEMOPHILIA. Hemophilia is a disease characterized
by excessive spontaneous hemorrhaging at mucous
membranes, into joint spaces (hemarthrosis) and mus-
cles, or intracranially. It is the result of a genetic defi-
ciency of a clotting factor.There are four basic types98:
1. Hemophilia A is characterized by the lack of factor
VIII and is inherited as an X-linked recessive trait.
2. Hemophilia B (Christmas disease) is characterized
by the lack of factor IX and is inherited as an
X-linked recessive trait.
3. Hemophilia C is characterized by the lack of factor
XI and is inherited as an autosomal recessive trait.
4. von Willebrand’s disease is characterized by the lack
of factor VIII and is inherited as an autosomal
dominant trait.
Patients with mild hemophilia experience bleeding
only with trauma or after surgical procedures, whereas
patients with severe hemophilia may bleed with minor
trauma or spontaneously.80
Hemophilia A, when severe, is characterized by
excessive bleeding into various organs of the body.
Soft-tissue hematomas and hemarthroses leading to
severe, crippling hemarthropathy are highly character-
istic of the disease. Bleeding into joints accounts for
approximately 75% of bleeding episodes in severely
affected patients with hemophilia A.99 In seriously
affected patients, major hemorrhages may dissect
through tissue planes, ultimately leading to compro-
mise of vital organs. However, bleeding episodes are
intermittent, and some patients do not hemorrhage
for weeks or months.100
Symptoms and physical findings of bleeding
episode from hemophilia may include:
 Petechiae, purpura, and ecchymosis
 Hematoma (Intramuscular hematomas are common
in hemophilia A, bleeding into the psoas muscle is
FIGURE 6-7
Acute hemarthrosis of the knee is a common complication of hemophilia. (From Forbes CD, Jackson WF.
Color Atlas and Text of Clinical Medicine [3rd ed]. London: Mosby, 2003.)
common, and femoral nerve involvement may be
partial or complete)101
 Disorientation
 Convulsions
 Tachycardia, tachypnea, and hypotension
 Intracranial bleeding is the major cause of death for
all age groups of hemophiliacs.6
 Pain
Patients with acute hemarthrosis have pain, with
objective findings of warmth, a tense effusion, tender-
ness, limitation of motion, and the joint is usually
held in flexion. Acute hemarthrosis of the knee is a
common complication of hemophilia. Figure 6-7 illus-
trates acute hemarthrosis of the knee. It may be con-
fused with acute infection unless the patient’s
coagulation disorder is known. Patients with subacute
or chronic arthritis (related to hemophilia) have chron-
ically swollen joints, which are usually painless and
slightly warm to touch.102 Repeated hemarthrosis
causes joint deformity and radiologic changes.
Management of hemophilia may include any of the
following: methods to stop active bleeding (e.g., direct
pressure), supportive therapy depending on the loca-
tion of the bleed (e.g., joint debridement), factor
replacement therapy, and pain management.84
CLINICAL TIP
 Watch for signs of joint effusion (warmth and
edema) in patients with hemophilia who are prone
to hemarthrosis, especially during weight-bearing
activities.
 Patients with psoas hematoma will present with
severe pain usually around the buttocks, and their
primary complaint is usually the inability to get
comfortable in any position.
 Vascular System and Hematology
THALASSEMIA Thalassemia is an autosomal-
recessive disease characterized by abnormal formation
of Hgb chains in RBCs, resulting in RBC membrane
damage and abnormal erythropoiesis and hemolysis.
Hgb is composed of two alpha and two beta chains.
a-Thalassemia is a defect in alpha-chain synthesis in
which one (alpha trait), two (a-thalassemia minor), or
three (Hgb H disease) genes are altered. Each type of
a-thalassemia varies in presentation from a lack of
symptoms (alpha trait and minor) to chronic severe
hemolytic anemia (Hgb H).79 b-Thalassemia minor is a
defect in beta-chain synthesis in one of two beta
chains and is usually asymptomatic. b-Thalassemia
major is a severe reduction or absence in beta-chain
production that results in severe anemia, growth
failure, bony deformities, hepatosplenomegaly, and
jaundice with a life expectancy of 20 to 30 years
from complications of heart failure, cirrhosis, and
endocrinopathy.80
Patientswith thalassemia are classified ashavingthal-
assemia minor, thalassemia intermedia, or thalassemia
major, depending on the severity of their anemia.
Patients with thalassemia minor generally have either
little or no hematologic disease. Patients with thalasse-
mia intermedia may require occasional transfusions.
Patients with thalassemia major require lifelong chronic
RBC transfusion to maintain adequate hemoglobin
levels.57
Management of the thalassemia may include folate
supplementation, blood transfusion, iron-chelating
agents, and splenectomy.80
THROMBOCYTOPENIA. Thrombocytopenia is an
acute or chronic decrease in the number of platelets
(less than 150,000/ml) in the circulation. It can result
from decreased platelet production (caused by infec-
tion, drug or immune responses, or blood vessel
damage), increased platelet destruction (caused by
malignancy, antiplatelet antibodies, or the use of
myelosuppressive drugs), or altered platelet distribu-
tion (caused by cardiac surgery—induced hypothermia,
portal hypertension, or splenomegaly).98
Signs and symptoms of thrombocytopenia may
include103:
 Bleeding of nose, gums, or puncture sites or blood
in emesis, urine, or stool
 Ecchymosis and petechiae
 Tachycardia and tachypnea
 Signs of increased intracranial pressure if a cranial
bleed is present
 Renal failure
 Splenomegaly
CHAPTER 6 249
Management of thrombocytopenia may include
treatment of the causative factor; immunosuppressive
therapy; anticoagulants in plasma transfusion or
plasma pheresis; corticosteroids; or splenectomy.98
HEPARIN-INDUCED THROMBOCYTOPENIA. Heparin-
induced thrombocytopenia (HIT) is the most
common type of drug-induced thrombocytopenia
and one of the most common causes of thrombocyto-
penia in hospitalized patients.42 Heparin can have a
dramatic thrombocytopenic effect, usually 5 to 10 days
after the initiation of heparin therapy. The clinical
presentation of HIT is distinct and may include104:
 Large, bilateral lower-extremity DVT
 Upper-extremity DVTat a venous catheter site
 Skin lesions at the injection site
 Aortic or ileofemoral thrombus with limb ischemia
 Pulmonary embolism
 An acute systemic reaction to heparin
HIT may be type I (the asymptomatic aggregation of
platelets) or type II (an immune response resulting in
platelet activation and venous or arterial thrombi).105
Type I is more common than type II, and type II is
associated with greater riskof life-threatening thrombo-
sis.106 HITis diagnosed byclinical presentation, a platelet
count less than 100  109/L, and a positive platelet
aggregation test. Heparin-PF 4 antibody testing is
recommended for patients suspected to have HIT.107
Management of HITstarts with the immediate disconti-
nuation of heparin and initiation of fast-acting,
non-heparin alternative anticoagulation. The direct
thrombin inhibitors argatroban, lepirudin, and bivaliru-
din are non-heparin anticoagulants that inhibit throm-
bin without interaction with heparin-PF4 antibodies.107
Management of HIT also includes plasmapheresis,
immunoglobulin therapy, in addition to supportive
therapies for alteration in skin integrity and pain.105
THROMBOTIC THROMBOCYTOPENIC PURPURA. Thro-
mbotic thrombocytopenic purpura (TTP) is the rapid
accumulation of thrombi in small blood vessels.TTP is
primarily seen in young adults 20 to 50 years of age.80
The etiology of TTP is unknown; however, it is associat-
ed with bacterial or viral infections, estrogen use, certain
drug use, pregnancy, and autoimmune disorders such as
acquired immunodeficiency syndrome.80 The diagnosis
of TTP is made by thrombocytopenia, anemia, and
elevated serum LDH.The coagulation tests are normal. 42
Signs and symptoms of TTP may include:
 Hemolytic anemia, thrombocytopenia
 Fatigue and weakness
 Fever
 Pallor, rash, petechiae
250 CHAPTER 6 Vascular System and Hematology
 Waxing and waning headache, confusion, altered
consciousness from lethargy to coma
 Hemiparesis and seizures
 Abdominal pain and tenderness due to pancreatitis
 Acute renal failure
Management of TTP may include emergent large-
volume plasmapheresis; plasma exchange; antiplatelet
agents; corticosteroids; immunosuppressive agents;
or splenectomy if not refractory to initial therapy or
if the condition recurs.80
CLINICAL TIP
 A physical therapist should exercise fall precautions
for the patient who is thrombocytopenic during all
physical therapy interventions.
 Patients with thrombocytopenia should be educated
about the fall risk precautions and the potential
for bleeding.
IDIOPATHIC THROMBOCYTOPENIC PURPURA.
Idiopathic thrombocytopenic purpura (ITP) is an auto-
immune disorder in which an IgG autoantibody is
formed that binds to the platelets. Platelets are not
destroyed by direct lysis, rather destruction takes place
in the spleen without subsequent enlargement (spleno-
megaly). An enlarged spleen should lead one to doubt
the diagnosis of ITP.
Patients are systemically well and usually not febrile.
The hallmark of the disease is thrombocytopenia.
The bone marrow will appear normal, and coagulation
studies will be entirely normal.
The common symptoms are of bleeding and include
epistaxis, oral bleeding, menorrhagia, purpura, and
petechiae. Most patients will require treatment, but
some patients will have spontaneous remissions.
Treatment is usually with corticosteroids, most com-
monly with prednisone and in some cases with immu-
noglobulins. Splenectomy is the most definitive
treatment for ITP, and most patients will ultimately
undergo splenectomy. Platelet transfusions are rarely
used in the treatment of ITP, since exogenous platelets
will survive no better than the patient’s own and will
usually survive less than a few hours.42
Lymphatic Disorders
LYMPHEDEMA. Lymphedema is a chronic disorder
characterized by an abnormal collection of lymph fluid
in the tissues of one or more body regions. The most
common cause for the accumulation of the fluid is a
mechanical insufficiency of the lymphatic system.
Lymphedema can be classified as primary or secondary.
Primary lymphedema is caused by a condition that is con-
genital or hereditary. In this case, the lymph node
or the lymph vessel formation is abnormal. Secondary
lymphedema is caused by injury to one or more compo-
nents of the lymphatic system in some other manner,
when some of the lymphatic system is blocked,
dissected, fibrosed, or damaged.
Signs and symptoms of lymphedema include:
 Swelling distal to or adjacent to the area where lymph
system function has been impaired.
 Symptoms usually not relieved by elevation.
 Pitting edema in early stages and non-pitting edema
in later stages, when fibrotic changes occur.
 Fatigue and heaviness, pressure, tightness, tingling,
and numbness in the affected region.
 Fibrotic changes in the skin.
 Loss of ROM.
Diagnosis of lymphedema can be made without the
use of special diagnostic tests. It is beyond the scope
of this text to discuss the diagnosis of lymphedema in
detail. Management includes manual lymphatic drain-
age and lymphedema bandaging. Early intervention is
of significance.The physical therapist should have spe-
cial training to treat this patient population. Manual
lymphatic drainage is a specialized manual therapy
technique that affects primarily superficial lymphatic
circulation. Manual lymphatic drainage improves
lymph transport capacity, redirects lymph flow toward
collateral vessels, and mobilizes excess lymph fluid.
Lymphedema bandaging is a highly specialized form
of bandaging that utilizes multiple layers of unique
padding materials and short stretch bandages to create
a supportive structure for edematous and lymphedema-
tous body segments. It is commonly used in between
the manual lymphatic drainage treatments.3
MANAGEMENT
The management of vascular disorders includes phar-
macologic therapy and vascular surgical procedures.
Hematologic disorders may be managed with pharma-
cologic therapy, as well as with nutritional therapy and
blood product transfusion.
Pharmacologic Therapy
Common drug classifications for the management of
vascular and hematologic disorders include:
 Anticoagulants (see AppendixTable IV-2)
 Antiplatelet agents (see AppendixTable IV-4)
 Vascular System and Hematology
 Thrombolytic agents (see AppendixTable IV-7)
 Colony stimulating factors (AppendixTable IV-22).
Anticoagulation Therapy
The standard INR goal for anticoagulation therapy
with warfarin (Coumadin) is 1.5 to 2.5 times a control
value and is categorized by condition or clinical state
according to the following55,108:
INR 2.0-3.0 Prophylaxis of venous thrombosis
(high-risk surgery)
Treatment of venous thrombosis and
pulmonary embolism
Prevention of systemic embolism
Tissue heart valves
Valvular heart disease
Atrial fibrillation
Recurrent systemic embolism
Cardiomyopathy
INR 2.5-3.5 Acute myocardial infarction
Mechanical prosthetic heart valve
replacement
The physical therapist should understand some basic
concepts of anticoagulation therapy to intervene safely
and estimate length of stay.
 The physician will determine the PT/INR and PTT
goal for each patient. This goal is documented in
the medical record.The patient remains in a hospital
setting until the goal is reached.
 The therapeutic effect of heparin is reached within
minutes or hours, whereas the effect of warfarin is
reached in 3 to 5 days; thus, heparin is usually pre-
scribed before warfarin. The dose of heparin is
increased or decreased depending on the PTT goal.
Both drugs are given simultaneously until the proper
PT/INR is achieved, then heparin is discontinued.
 The terms subtherapeutic and supertherapeutic imply a
coagulation level below or above the anticoagulation
goal, respectively.
 A subtherapeutic PT/INR or PTT indicates a risk for
thrombus formation, whereas a supertherapeutic
level indicates a risk for hemorrhage.
 Supertherapeutic anticoagulation is rapidly reversed
by vitamin K or fresh-frozen plasma.
 Anticoagulant agents are temporarily discontinued
before surgery to minimize bleeding intraoperatively
or postoperatively.
 The physical therapist should always monitor the
patient who is taking anticoagulants for signs and
CHAPTER 6 251
symptoms of bleeding, as bleeding can occur even
if the PT/INR is therapeutic.108
Blood Product Transfusion
Blood and blood products are transfused to replete
blood volume, maintain oxygen delivery to tissues,
or maintain proper coagulation.109 The need for
blood transfusion should be dependent on the patient’s
symptoms. It has been reported that refrigerated,
banked blood loses its ability to deliver oxygen in a
short period of time.110 Table 6-20 lists the most
common transfusion products and the rationale
for their use. Blood may be autologous (patient
donates own blood) or homologous (from a volunteer
donor).
Before transfusing blood or blood products, the
substance to be given must be typed and crossed.
This process ensures that the correct type of blood
is given to a patient to avoid adverse reactions. A
variety of transfusion reactions can occur during or
after the administration of blood products. Table 6-
21 lists the signs and symptoms of various types of
acute adverse transfusion reactions. These blood
transfusions are usually not fatal, but they can
extend a patient’s length of stay. Blood transfusions
are a form of liquid tissue transplant, and it can
cause significant immunosuppression. This effect is
known as TRIM (transfusion-related immunomodu-
lation), and it happens every time a patient receives
blood. Transfusion reactions can be nonimmuno-
logic and are caused by the physical and chemical
properties of the transfused blood.113 There is a
threat of transmitting infectious diseases via a
blood transfusion.110
In addition to these reactions, complications of
blood transfusion include air embolism (if the blood
is pumped into the patient) or circulatory overload
(from a rapid increase in volume). Circulatory overload
occurs when the rate of blood (fluid) transfusion
occurs faster than the circulation can accommodate.
Signs and symptoms include tachycardia, cough,
dyspnea, crackles, headache, hypertension, and
distended neck veins. To prevent circulatory overload
during a transfusion, intravenous fluids may be
stopped, or a diuretic (e.g., furosemide [Lasix]) may
be given. Delayed adverse transfusion reactions include
iron overload, graft-versus-host disease, hepatitis,
human immunodeficiency virus-1 infection, or
delayed hemolytic reaction (approximately 7 to 14 days
posttransfusion).114
252 CHAPTER 6 Vascular System and Hematology

Table 6-20 COMMON BLOOD PRODUCTS AND THEIR CLINICAL INDICATIONS AND OUTCOMES
Product Content Clinical Indications Outcome
Whole blood Blood cells and Acute major blood loss in setting Resolution of signs and
plasma of hypotension, tachycardia, symptoms of hypovolemic
tachypnea, pallor, and shock or anemia.
decreased Hct and Hgb. Hct should increase 3% in a
To treat oxygen-carrying nonbleeding adult (per unit
deficit (RBC) and volume transfused).
expansion (plasma).
When more than 10 units
of blood are required in
a 24-hour period.
Whole blood is rarely used.
Red blood cells RBCs only Acute or chronic blood loss. Resolution of signs and
(RBCs) To treat oxygen-carrying deficit symptoms of anemia.
in setting of tachycardia, Hct should increase 3% in a
tachypnea, pallor, fatigue, nonbleeding adult (per unit
and decreased Hct and Hgb. transfused).
Anemia without need for
volume expansion.
Platelets (Plts) Concentrated platelets To restore clotting function Resolution of
in plasma associated with or after thrombocytopenia.
blood loss. Prevention or resolution of
To increase platelet count in a bleeding.
bleeding patient with platelet Platelets should increase 5,000 in
<100,000, in advance of a a 70-kg adult (per unit).
procedure with platelet
<50,000, or prophylactically
with platelet <10,000.
Fresh-frozen All plasma To replace or increase Improved or adequate
plasma (FFP) components, namely coagulation factor levels. coagulation levels or factor
blood factors and Acute disseminated intravascular assays.
protein coagulopathy. One unit of FFP should increase
Thrombotic thrombocytopenic the level of any clotting factor
purpura. by 2% to 3%.
Factor XI deficiency.
Liver disease
Rapid reversal of warfarin
therapy.
Albumin Albumin cells with few Volume expansion in situations Acquire and maintain adequate
globulins and other when crystalloid (saline or blood pressure and volume
proteins Ringers lactate) is inadequate support.
such as shock, major
hemorrhage, or plasma
exchange.
Acute liver failure.
Burn injury.
Plasma protein Albumin, globulins, See Albumin, above. See Albumin, above.
fraction (PPF) and plasma proteins
 Table 6-20 COMMON BLOOD PRODUCTS AND THEIR CLINICAL INDICATIONS AND OUTCOMES—cont’d
Product Content
Cryoprecipitate Factors VIII and XIII,
von Willebrand’s
factor, and
fibrinogen in plasma
Hct, Hematocrit; Hgb, hemoglobin.
Data from National Blood Resource Education ProgramsTransfusionTherapy Guidelines for Nurses. US Department of Health and Human
Services, National Institutes of Health, September 1990;WH Churchill WH.TransfusionTherapy. NewYork: Scientific American Medicine,
2001;4; Current Medical Diagnosis and Treatment 2007; Avoiding bad blood. Key steps to safe transfusions, Nursing made incredibly easy!
2004;2(5).
Table 6-21 ACUTE ADVERSE BLOOD REACTIONS
Reaction Cause
Febrile reaction Patient’s blood (antileukocyte
antibodies) is sensitive to
transfused plasma protein,
platelets, or white blood
cells.
Allergic reaction Patient’s blood (IgE, IgG, or
both) is sensitive to
transfused plasma protein.
Septic reaction Transfused blood components
are contaminated with
bacteria.
Acute hemolytic Patient’s blood and transfused
reaction blood are not compatible,
resulting in red blood cell
destruction.
Anaphylactic Patient is deficient in IgA
reaction and develops IgA antibody
to transfused components.
Transfusion related Transfusion of antibodies in
acute lung injury donor plasma are reactive
with recipient granulocytes.
Ig, Immunoglobulin.
Data from reference numbers 80, 111, 112, 114.
Clinical Indications Outcome
Replacement of these factor Correction of these factor or
deficiencies. fibrinogen deficiencies.
Replacement of fibrinogen when Cessation of bleeding in uremic
an increase in volume would patients.
not be tolerated with FFP.
Bleeding associated with uremia.
Signs and Symptoms Onset
Chills followed by low-grade During transfusion or up to
fever, headache, nausea and 24 hours posttransfusion
vomiting, flushed skin, muscle
pain, anxiety (mild).
Hypotension, tachycardia,
tachypnea, cough (severe).
Hives, flushed or itchy skin, and Within minutes of starting
bronchial wheezing (mild). transfusion
Tachypnea, chest pain, cardiac
arrest (severe).
Rapid onset of high fever, Within minutes to 30 minutes
hypotension, chills, emesis, after transfusion
diarrhea, abdominal cramps,
renal failure, shock.
Fever with or without chills is Within minutes to hours after
the most common transfusion
manifestation.
Tachycardia, hypotension,
tachypnea, cyanosis, chest
pain, headache or backache,
acute renal failure, cardiac
arrest.
Hives (mild). Within a few seconds of
Wheezing or bronchospasm, starting transfusion
anxiety, cyanosis, nausea,
emesis, bloody diarrhea,
abdominal cramps, shock,
cardiac arrest (severe).
Chills, fever, chest pain, Within several hours after
hypotension, cyanosis, chest transfusion
radiograph shows florid
pulmonary edema.
254 CHAPTER 6 Vascular System and Hematology
CLINICAL TIP
 If the patient is receiving blood products, the
physical therapist should observe the patient for
signs or symptoms, or both, of transfusion reaction
before initiating physical therapy intervention.
 Depending on the medical status of the patient, the
therapist may defer out-of-bed or vigorous activities
until the transfusion is complete. On average, the
transfusion of a unit of blood takes 3 to 4 hours.
 Defer physical therapy intervention during the first
15 minutes of a blood transfusion as most blood
transfusion reactions occur within this time frame.
 During a blood transfusion, vital signs are usually
taken every 15 to 30 minutes by the nurse and
posted at the bedside.
 After a blood transfusion, it takes 12 to 24 hours
for the Hgb and Hct to increase.51
Vascular Surgical Procedures
Surgical management of coronary vascular disorders,
such as angioplasty, arthrectomy, and stent placement, is
described in Chapter 1 under Percutaneous Revascula-
rization Procedures.These same techniques are also used
in peripheral arteries rather than coronary arteries. This
section therefore concentrates on embolization therapy,
transcatheter thrombolysis/thrombectomy, endarterect-
omy, bypass grafting, and aneurysm repair and replace-
ment with synthetic grafts. Endovascular procedures are
becoming more and more common in patients with
peripheral arterial disease. The basic concept of most
endovascular procedures is to obtain percutaneous
access of a blood vessel and then to gain access across the
lesion (either stenosis or aneurysm) with a guide wire.115
EMBOLIZATION THERAPY
Embolization* therapy is the process of purposely
occluding a vessel with Gelfoam, coils, balloons, poly-
vinyl alcohol, and various glue-like agents, which are
injected as liquids and then solidify in the vessel.
Embolization therapy is performed with a specialized
intravascular catheter after angiographic evaluation
has outlined the area to be treated.
*The term embolization is general and can refer to a pathologic
occlusion of a vessel by fat, air, or a dislodged portion of a
thrombus, or to the therapeutic procedure described in this
section.The context in which embolization is discussed must be
considered to avoid confusion.
Indications for embolization therapy include disor-
ders characterized by inappropriate blood flow, such
as AVMs or, less commonly, persistent hemoptysis.
Complications of embolization therapy include tissue
necrosis, inadvertent embolization of normal tissues,
and passage of embolic materials through arteriovenous
communications.41
TRANSCATHETER THROMBOLYSIS AND/
THROMBECTOMY
Transcatheter thrombolysis is the process of directly
infusing thrombolytic agents such as urokinase and
tissue plasminogen activators (tPA) into occluded ves-
sels. The indications for this procedure include lysis of
clot in thrombosed bypass grafts, acute carotid occlu-
sions, and acute or chronic peripheral arterial ischemia.
Patients with an acute thrombotic arterial occlusion
are considered ideal candidates for lytic therapy.116
There is considerable debate about the indication of
thrombolysis in the setting of acute DVT. The tip of
the catheter is introduced into the center of the throm-
bus, and a low dose of thrombolytic agent is adminis-
tered. The catheter is left in place for extended periods
of time to allow for the clot to lyse properly.117 This pro-
cedure may also include angioplasty, if warranted, to
open a stenotic area. By injecting the thrombolytic
agent into the area of occlusion, transcatheter throm-
bolysis has less systemic complications of hemorrhage
compared to intravenous infusion of thrombolytic
agents.19 The major risk for thrombolytic therapy is
bleeding.55
Thrombectomy is a method to lyse or remove an
extensive thrombus in the lower extremity. This is an
immediate but invasive method of restoring perfusion.
Two main categories of the devices/catheters are used:
‘‘contact’’ and ‘‘noncontact’’ devices. The contact cathe-
ters come in direct contact with the vessel wall. The
noncontact catheters use a pressurized fluid to break
up the clot, which is then extracted by the catheter.116
PERIPHERAL VASCULAR BYPASS GRAFTING
To reperfuse an area that has been ischemic from
peripheral vascular disease, two general bypass grafting
procedures (with many specific variations of each type)
can be performed. The area of vascular occlusion can
be bypassed with an inverted portion of the saphenous
vein or with a synthetic material, such as Gore-Tex,
Dacron, or Lycra. (The synthetic graft is referred to as
a prosthetic graft.) Vascular surgeons generally describe
and illustrate in the medical record what type of proce-
dure was performed on the particular vascular anatomy.
 Vascular System and Hematology
The terminology used to describe each bypass graft
procedure indicates which vessels were involved. (For
example, a fem-pop bypass graft involves bypassing an
occlusion of the femoral artery with another conduit
to the popliteal artery distal to the area of occlusion.)
After a bypass procedure, patients require approxi-
mately 24 to 48 hours (depending on premorbid physio-
logic status and extent of surgery) to become
hemodynamically stable and are usually monitored in
an intensive care unit setting. Figures 6-8 and 6-9 illus-
trate two vascular bypass procedures.
Complications that can occur after bypass grafting
include the following30:
 Hemorrhage (at graft site or in gastrointestinal tract)
 Thrombosis
 Pseudoaneurysm formation at the anastomosis
 Infection
 Renal failure
 Sexual dysfunction
 Spinal cord ischemia
 Colon ischemia
ENDARTERECTOMY
Endarterectomy is a process in which the stenotic area
of an artery wall is excised and the noninvolved ends
of the artery are reanastomosed. It can be used to cor-
rect localized occlusive vascular disease, commonly in
the carotid arteries, eliminating the need for bypassing
the area.41
CLINICAL TIP
 The abbreviation CEA is often used to refer to a
carotid endarterectomy procedure.
ANEURYSM REPAIR AND RECONSTRUCTION
Aneurysm repair and reconstruction involve isolating
the aneurysm by clamping off the vessel proximal and
distal to the aneurysm, excising the aneurysm, and
replacing the aneurysmal area with a synthetic graft.
Performing the procedure before the aneurysm rup-
tures (elective surgery) is preferable to repairing a
ruptured aneurysm (emergency surgery), because a
ruptured aneurysm presents an extremely challenging
and difficult operative course owing to the hemody-
namic instability from hemorrhage. The cross-clamp
time of the vessels is also crucial, because organs distal
to the site of repair can become ischemic if the clamp
time is prolonged. Complications that may occur
after aneurysm repair are similar to those discussed in
CHAPTER 6 255
the Peripheral Vascular Bypass Grafting section.30
Figure 6-10 illustrates an aneurysm repair and
reconstruction.
CLINICAL TIP
 Incisions should be inspected before and after
physical therapy interventions to assess the patency
of the incision, as drainage or weeping may occur
during activity. If drainage or weeping occurs, stop
the current activity and inspect the amount of
drainage. Provide compression, if appropriate, and
notify the nurse promptly. Once the drainage is
stable or under the management of the nurse,
document the incidence of drainage accordingly
in the medical record.
 Abdominal incisions or other incisional pain can
limit a patient’s cough effectiveness and lead to
pulmonary infection. Diligent attention to position
changes, deep breathing, assisted coughing, and
manual techniques (e.g., percussion and vibration
techniques as needed) can help prevent pulmonary
infections.
 Grafts that cross the hip joint, such as aortobifemoral
grafts, require clarification by the surgeon regarding
the amount of flexion allowed at the hip.
 After a patient is cleared for out-of-bed activity,
specific orders from the physician should be
obtained regarding weight bearing on the involved
extremities, particularly those with recent bypass
grafts.
 Patients may also have systolic blood pressure
limitations postoperatively to maintain adequate
perfusion of the limb or to ensure the patency of
the graft area. Blood pressures that are below the
specified limit may decrease perfusion, whereas
pressures above the limit may lead to graft damage.
Thorough vital sign monitoring before, during, and
after activity is essential.20
 Patients who are status post bypass grafting
procedures should have improved peripheral
pulses; therefore, any reduction in the strength
of distal peripheral pulses that occurs after surgery
should be brought to the attention of the nurse and
physician.
Physical Therapy Interventions for Patients with
Vascular and Hematologic Disorders
The primary goal of physical therapy for patients with
vascular and hematologic disorders is the optimization
256 CHAPTER 6 Vascular System and Hematology

A B C

D E F
FIGURE 6-8
Peripheral arterial bypass procedures. A, Aortoiliac bypass. B, Aortobifemoral bypass. C, Axillobifemoral
bypass. D, Femorofemoral bypass. E, Femoropopliteal bypass. F, Femorotibial bypass. (From Urden LD.
Thelan’s Critical Care Nursing: Diagnosis and Management [5th ed], St Louis: Mosby, 2006.)
 Vascular System and Hematology CHAPTER 6 257

FIGURE 6-9
Aortofemoral graft. A, Schematic illustration of a preoperative aortogram. B, A segment of diseased aorta
is resected, and the distal aortic stump is oversewn. C, End-to-end proximal anastomosis. D, Completed
reconstruction. (From Rutherford RB (ed).Vascular Surgery [5th ed]. Philadelphia: Saunders, 2000.)

of functional mobility and activity tolerance. In
addition to these goals, patients with vascular
disorders require patient education to prevent
skin breakdown and DVT formation, manage
edema, and prevent joint contractures and muscle
shortening. Patients with hematologic disorders may
require patient education for activity modification,
pain management, or fall prevention (especially if
the patient is at risk of bleeding or on anticoagulant
therapy).
The following are guidelines for the physical
therapist working with the patient who has vascular or
hematologic dysfunction.
Patients with peripheral vascular disease commonly
have concurrent coronary artery disease and diabetes
mellitus; therefore, being watchful for signs and symp-
toms of angina in conjunction with monitoring vital
signs and blood glucose levels is essential.
Patients with peripheral vascular disease may also
have concurrent chronic obstructive pulmonary dis-
ease; therefore, activity tolerance may have pulmonary
limitations as well.
Patients with peripheral vascular disease may have
impaired sensation from arterial insufficiency,
comorbid diagnosis of diabetes mellitus, or peripheral
edema; therefore, sensation testing is an important
component of the physical therapy evaluation.
If sensory impairment is present, patient education
on frequent skin checks (lower extremities, buttocks)
should be part of the physical therapy intervention.
Peripheral edema can result from a variety of disor-
ders, including venous insufficiency, liver disease,
renal insufficiency or renal failure, and heart failure;
therefore, the physical therapist should perform a thor-
ough review of the patient’s medical history before per-
forming any edema management techniques. For
example, limb elevation may be helpful in chronic
venous insufficiency but may be detrimental in acute
congestive heart failure. Use of compression stocking
should be emphasized in all patients with a diagnosis
of DVT.
The physical therapist may need to modify or defer
physical therapy intervention when a patient is being
worked up for a diagnosis of aortic dissection. The
patient’s presentation and hemodynamic status should
be taken into consideration in the decision-making
process. Once the diagnosis is made, the option of treat-
ment (medical versus surgical) should be a guide to the
physical therapist’s decision. In either case, if the patient
is seen for physical therapy, the patient’s vital signs
should be monitored continuously, the patient’s pre-
senting symptoms should be kept in mind, and any
changes in the vital signs or in the patient’s symptoms
should be reported to the medical team.
258 CHAPTER 6 Vascular System and Hematology
A The physical therapist must determine the need to
C platelets and high INR) and should cautiously monitor
B INR who has a steady gait is a fall risk to a lesser
FIGURE 6-10
Surgical repair of an abdominal aortic aneurysm. A, Incising
the aneurysmal sac. B, Insertion of synthetic graft. C, Suturing
native aortic wall over synthetic graft. (From Lewis SM,
Heitkemper MM, Dirksen SR [eds]. Medical-Surgical Nursing,
Assessment and Management of Clinical Problems [5th ed].
St. Louis: Mosby, 2000.)
The physical therapist should monitor the patient’s
CBC and coagulation profile on a daily basis to deter-
mine the potential risk for bruising or bleeding, throm-
bus formation, and for altered oxygen-carrying
capacity with exertion.
To gain insight into the hemostatic condition of
the patient, determine (1) whether the abnormal
blood laboratory values are expected or consistent
with the patient’s medical-surgical status, (2) the
relative severity (mild, moderate, or severe) of the
abnormal laboratory values, (3) the patient’s presenta-
tion and clinical symptoms and (4) whether the patient
has a medical history or predisposing condition that
could be exacerbated by the abnormal laboratory
values.
modify or defer physical therapy intervention in the
setting of abnormal blood laboratory values, most
commonly alterations in Hct, platelet, and PT/INR.
Often, there is no specific numeric protocol for this
purpose; thus, the decision to modify or defer physical
therapy must be based on the clinical picture as well
as the quantitative data. For example, a patient may
have a low platelet count but is hemodynamically
stable without signs of active bleeding. The physical
therapist may therefore decide to continue to mobilize
the patient out of bed. Conversely, if a patient with a
low platelet count has new hemoptysis, the physical
therapist may then defer manual chest physical therapy
techniques, such as percussion. If the physical therapist
decides to mobilize the patient, the physical therapist
should be aware of the signs and symptoms of the
abnormal lab values (e.g., risk of bleeding with low
the patient for the same. The physical therapist
should consider the fall risk of mobilizing a patient
with an abnormal laboratory values (Hct, INR, Plt),
versus the benefit of mobilizing the patient. For exam-
ple, an elderly patient with high INR who has
unsteady gait is a fall risk; a young adult with high
extent. At the same time, the negative effects of bed
rest on the patient are significant. In this case, the
physical therapist needs to modify the physical therapy
intervention, based on the goals for that particular
patient (i.e., walking versus sitting out of bed in
a chair).
Exercise guidelines for patients with thrombocyto-
penia vary among hospitals. General rules regarding
exercises that should be performed are as follows: activ-
ities of daily living, active range of motion, and ambula-
tion with physician approval for platelet count of
< 20,000 mm3; active range of motion and walking as
tolerated for platelet count of 20,000 to 30,000 mm3;
active range of motion, ambulation, or stationary bicy-
cling for platelet count of 30,000 to 50,000 mm3;
and progressive resistive exercise, ambulation, or sta-
tionary bicycling for a platelet count of 50,000 to
150,000 mm3.4,118
For an INR greater than 3.5 (the standard highest
level for anticoagulation), consult with the nurse or phy-
sician before physical therapy intervention and modify
treatment accordingly. The risk of bleeding increases
as INR value reaches 4 and even more sharply when
the INR is higher than 5.48 There is no common proto-
col for activity guidelines for the patient with an INR
 Vascular System and Hematology
greater than 3.5; however, most patients continue
out-of-bed activities and activities of daily living with
caution or supervision with an INR slightly greater
than 3.5.
Mobilization of a patient who has an INRvalue more
than 4 should be dependent on the patient’s presenta-
tion, the medical intervention for the high INR, and
institutional guidelines and the risk/benefit of physical
therapy intervention. Physical therapy intervention
may need to be modified for certain patient populations
with high INR values.
Observe the patient for the signs and symptoms of
thrombus formation or bleeding during physical
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CHAPTER 6 259
therapy intervention. Immediately report any abnorm-
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The monitoring of blood pressure, heart rate,
oxygen saturation, and respiratory rate is recommended
at rest and with activity because the hemodynamic
sequelae of alterations in blood volume or viscosity
may be subtle or insidious in onset and first noticed in
response to exercise by the physical therapist.
Progression of activity tolerance in patients with
hematologic disorders does not occur at the same rate
as in patients with normal blood composition; there-
fore, the time frame for goal achievement may need to
be lengthened.
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 7 Burns and Wounds

Michele P. West INTRODUCTION

Kimberly Knowlton Treating a patient with a major burn injury or other skin wound is often a
Marie Jarell-Gracious specialized area of physical therapy.* Physical therapists should, however,
have a basic understanding of normal and abnormal skin integrity, includ-
Jaime C. Paz ing the etiology of skin breakdown and the factors that influence wound
healing. The main objectives of this chapter are therefore to provide a
fundamental review of the following:
1. The structure and function of the skin (integument)
2. The evaluation and physiologic sequelae of burn injury, including
medical-surgical management and physical therapy intervention
3. The etiology of different types of wounds and the process of wound
healing
4. The evaluation and management of wounds, including physical therapy
intervention
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:

Possible Practice
Diagnosis/Disease Patterns
Burns:Thermal, Electrical, Chemical, 6C, 6E, 7B, 7C, 7D, 7E
Ultraviolet, Ionizing, Radiation
Trauma Wounds 4H, 4J, 7C
Surgical Wounds 7A, 7C, 7D, 7E
Vascular Wounds: Arterial,Venous, 4J, 5G, 7A, 7B, 7C, 7D, 7E
Diabetic
Pressure Wounds 7B, 7C, 7D, 7E
Neuropathic or Neurotrophic Ulcers 7A, 7D, 7E

Please refer to the back cover of this book for a complete list of the
preferred practice patterns, as individual patient conditions are highly
variable and other practice patterns may be applicable.

*For the purpose of this chapter, an alteration in skin integrity secondary to a burn injury
is referred to as a burn. Alteration in skin integrity from any other etiology is referred to as
a wound.

263
264 CHAPTER 7 Burns and Wounds

STRUCTURE AND FUNCTION: NORMAL
INTEGUMENT
Structure
The integumentary system consists of the skin and its
appendages (hair and hair shafts, nails, and sebaceous
and sweat glands), which are located throughout the
skin, as shown in Figure 7-1. Skin is 0.5 to 4.0 mm
thick and is composed of two major layers: the epider-
mis and the dermis. These layers are supported by sub-
cutaneous tissue and fat that connect the skin to
muscle and bone.The thin, avascular epidermis is com-
posed mainly of cells containing keratin.The epidermal
cells are in different stages of growth and degeneration.
The thick, highly vascularized dermis is composed
mainly of connective tissue. Table 7-1 lists the major
contents of each skin layer.
The skin has a number of clinically significant varia-
tions: (1) Men have thicker skin than women; (2) the
young and elderly have thinner skin than adults1; and
(3) the skin on various parts of the body varies in thick-
ness, number of appendages, and blood flow.2 These
variations affect the severity of a burn injury or skin
breakdown, as well as the process of tissue healing.
Function
The integument has seven major functions3:
1. Temperature regulation. Body temperature is regu-
lated by increasing or decreasing sweat production,
superficial blood flow, or both.
2. Protection. The skin acts as a barrier to protect
the body from microorganism invasion, ultravi-
olet (UV) radiation, abrasion, chemicals, and
dehydration.
3. Sensation. Multiple sensory cells within the skin
detect pain, temperature, and touch.
4. Excretion. Heat, sweat, and water can be excreted
from the skin.
5. Immunity. Normal periodic loss of epidermal cells
removes microorganisms from the body surface,
and immune cells in the skin transport antigens
from outside the body to the antibody cells of the
immune system.
6. Blood reservoir. Large volumes of blood can be
shunted from the skin to central organs or muscles
as needed.
7. Vitamin D synthesis. Modified cholesterol molecules
are converted to vitamin D when exposed to UV
radiation.

PATHOPHYSIOLOGY OF BURNS
Skin and body tissue destruction occurs from the
absorption of heat energy and results in tissue coagula-
Stratum corneum tion. This coagulation is depicted in zones (Figure
Sweat duct EPIDERMIS 7-2). The zone of coagulation, located in the center
Capillary of the burn, is the area of greatest damage and contains
Sebaceous nonviable tissue referred to as eschar. Although eschar
gland covers the surface and may appear to take the place
Arrector pili
muscle of skin, it does not have any of the characteristics
DERMIS
Nerve or functions of normal skin. Instead, eschar is constric-
endings
Hair
tive, attracts microorganisms, and houses burn toxins
follicle that may circulate throughout the body.1 The zone of
Dermal stasis, which surrounds the zone of coagulation, con-
papilla
Sweat
tains marginally viable tissue. The zone of hyperemia,
gland SUBCUTANEOUS the outermost area, is the least damaged and heals
Fat TISSUE rapidly.
Blood vessels
Physiologic Sequelae of Burn Injury
FIGURE 7-1
Three-dimensional representation of the skin and A series of physiologic events occurs after a burn
subcutaneous connective tissue layer showing the arrangement (Figure 7-3). The physical therapist must appreciate the
of hair, glands, and blood vessels. (From BlackJM. Medical- multisystem effects of a burn injuryçnamely, that the
Surgical Nursing: Clinical Management for Positive Outcomes, metabolic demands of the body increase dramatically.
SingleVolume [7th ed]. St Louis: Saunders, 2004.) Tissue damage or organ dysfunction can be immediate
 Burns and Wounds CHAPTER 7 265

Table 7-1 NORMAL SKIN LAYERS: STRUCTURE AND FUNCTION

Layer Composition Function
Epidermis
Stratum corneum Dead keratinocytes Tough outer layer that protects deeper layers of epidermis
Pigment layer Melanocytes Produces melanin to prevent ultraviolet absorption
Stratum granulosum Mature keratinocytes Produces keratin to make the skin waterproof
Langerhans’cells Interacts with immune cells
Stratum spinosum Keratinocytes Undergoes mitosis to continue skin cell development but
to a lesser degree than basal
Stratum basale New keratinocytes The origin of skin cells, which undergoes mitosis, then
moves superficially
Merkel’s cells Detects touch
Dermis
Papillary layer Areolar connective tissue Binds epidermis and dermis together
Meissner’s corpuscles Detects light touch
Blood and lymph vessels Provides circulation and drainage
Free nerve endings Detects heat and pain
Reticular layer Collagen, elastin, and reticular fibers Provides strength and resilience
Hypodermis Subcutaneous fat Provides insulation and shock absorption
Pacinian cells Detects pressure
Free nerve endings Detects cold
Data from GA Thibodeau, KT Patton (eds). Structure and Function of the Body (11th ed). St Louis: Mosby, 2000.

or delayed, minor or severe, and local or systemic. Types of Burns

A summary of the most common complications of
burns is listed in Table 7-2. The amount of total body
surface area involved in burn injury and the presence
of inhalation injury are the primary risk factors for mor-
tality after burn injury.4
THERMAL BURNS
Thermal burns can be the result of conduction or
convection, as in contact with a hot object, hot liquid,
chemicals, flame, or steam. In order of frequency, the

A B C

Epidermis

Dermis

Subcutaneous
tissue

FIGURE 7-2
The zones of coagulation. A, Superficial burn. B, Partial-thickness burn. C, Full-thickness burn.
(Modified from Williams WG, Phillips LG. Pathophysiology of the Burn Wound. In DN Herndon [ed],
Total Burn Care. London: Saunders, 1996;65.)
266 CHAPTER 7 Burns and Wounds

FIGURE 7-3
The physiologic sequelae of major burn injury. BUN, blood urea nitrogen; Cl—, chlorine; Hct, hematocrit;
K+, potassium; Na+, sodium; O2, oxygen; RBC, red blood cell;WBC, white blood cell. (Modified from
MarvinJ.Thermal Injuries. InVD Caradona, PD Hurn, PJ Bastnagel Mason, et al. [eds],Trauma Nursing
from Resuscitation through Rehabilitation [2nd ed]. Philadelphia: Saunders, 1994;740; Demling RH,
LaLonde C. BurnTrauma. NewYork:Thieme, 1989;99.)

most common types of thermal burns are scalds, flame
burns, flash burns, and contact burns (Table 7-3).5 The
severity of burn depends on the location of the burn,
the temperature of the burn source, and the duration
of contact.6
ELECTRICAL BURNS
An electrical burn is caused by exposure to a low- or
high-voltage current and results in superficial burns,
as well as less-visible but massive damage of muscle,
nerves, and bone.Tissue necrosis of these deeper struc-
tures occurs from the high heat intensity of the current
and the electrical disruption of cell membranes.5
Tissue damage occurs along the path of the current,
with smaller distal areas of the body damaged most
severely. This pattern of tissue damage accounts for the
high incidence of amputation associated with electrical
injury.5,7 The severity of an electrical burn depends pri-
marily on the duration of contact with the source, as
well as the voltage of the source, the type and pathway

Table 7-2 SYSTEMIC COMPLICATIONS OF BURN
INJURY
Body System Complications
Respiratory Inhalation injury, restrictive
pulmonary pattern (which may
occur with a burn on the trunk),
atelectasis, pneumonia,
microthrombi, and adult
respiratory distress syndrome
Cardiovascular Hypovolemia/hypotension,
pulmonary hypertension,
subendocardial ischemia, anemia,
and disseminated intravascular
coagulopathy
Gastrointestinal/ Stress ulceration, hemorrhage, ileus,
genitourinary ischemic colitis, cholestasis, liver
failure, and urinary tract infection
Renal Edema, hemorrhage, acute tubular
necrosis, acute renal failure
Data from HA Linares.The Burn Problem: A Pathologist’s
Perspective. In DN Herdon (ed),Total Burn Care. London:
Saunders, 1996.
Table 7-3 THERMAL BURNS: TYPES AND CHARACTERISTICS
Burn Type Description
Scald burn Spill of or immersion in a hot
liquid, such as boiling water,
grease, or tar
Flame burn Flame exposure from fire or
flammable liquids, or ignition
of clothing
Flash burn Explosion of flammable liquid,
such as gasoline or propane
Contact burn Exposure to hot objects, such as
glass, plastic, metal, or coal
Data from GD Warden, DM Heimbach. Burns. In SI Schwartz (ed), Principles of Surgery,Vol. 1 (7th ed). NewYork: McGraw-Hill, 1999;
RF Edlich, JC Moghtader.Thermal Burns. In P Rosen (ed), Emergency Medicine Concepts and Clinical Practice,Vol. 1 (4th ed). St. Louis:
Mosby, 1998.
Burns and Wounds CHAPTER 7 267
of current, and the amperage and resistance through the
body tissues.7
Electrical burns are characterized by deep entrance
and exit wounds or arc wounds.The entrance wound is
usually an obvious necrotic and depressed area, whereas
the exit wound varies in presentation. The exit wound
can be a single wound or multiple wounds located
where the patient was grounded during injury.6 An arc
wound is caused by the passage of current directly
between joints in close opposition. For example, if the
elbow is fully flexed and an electrical current passes
through the arm, burns may be located at the volar
aspect of the wrist, antecubital space, and axilla.5
Complications specific to electrical injury include5,9:
 Cardiovascular: Cardiac arrest (ventricular fibrilla-
tion for electric current or asystolic for lightning),
arrhythmia (usually sinus tachycardia or nonspecific
STsegment changes) secondary to alterations in elec-
trical conductivity of the heart, myocardial contu-
sion or infarction, or heart wall or papillary muscle
rupture
 Neurologic: Headache, seizure, brief loss of con-
sciousness or coma, peripheral nerve injury (resulting
from ischemia), spinal cord paralysis (from demyeli-
nation), herniated nucleus pulposus, or decreased
attention and concentration
Characteristics
Often causes deep partial- or full-thickness burns.
Exposure to thicker liquids or immersion causes a deeper burn
from increased contact time.
Immersion burns commonly cover a larger total body surface area
than do spills.
Often causes superficial and deep partial-thickness burns.
Associated with carbon monoxide poisoning.
Often causes partial-thickness burns.
Burns may be distributed over all exposed skin.
Associated with upper airway thermal damage.
Most common in the summer and associated with the
consumption of alcohol.
Often causes deep partial- or full-thickness burns.
Associated with crushing injuries, such as motor vehicle accidents.
Most common cause of serious burns in the elderly.
268 CHAPTER 7 Burns and Wounds
 Orthopedic: Dislocations or fractures secondary to
sustained muscular contraction or from a fall
during the burn injury
 Other: Visceral perforation or necrosis, cataracts,
tympanic membrane rupture, anxiety, depression,
or posttraumatic stress disorder
Lightning
Lightning, considered a form of very high electrical
current, causes injury via four mechanisms10:
1. Direct strike, in which the person is the grounding
site
2. Flash discharge, in which an object deviates the
course of the lightning current before striking the
person
3. Ground current, in which lightning strikes the
ground and a person within the grounding area
creates a pathway for the current
4. Shock wave, in which lightning travels outside the
person and static electricity vaporizes moisture in
the skin
CHEMICAL BURNS
Chemical burns can be the result of reduction, oxida-
tion, corrosion, or desecration of body tissue with or
without an associated thermal injury.11 The severity of
burn depends on the type of chemical and its concen-
tration, duration of contact, and mechanism of action.
Unlike thermal burns, chemical burns significantly
alter systemic tissue pH and metabolism. These
changes can cause serious pulmonary complications
(e.g., airway obstruction from bronchospasm, edema,
or epithelial sloughing) and metabolic complications
(e.g., liver necrosis or renal dysfunction from pro-
longed chemical exposure).
ULTRAVIOLET AND IONIZING RADIATION BURNS
A sunburn is a superficial partial-thickness burn
from the overexposure of the skin to UV radiation.
Ionizing radiation burns with or without thermal
burn occur when electromagnetic or particulate radia-
tion energy is transferred to body tissues, resulting in
the formation of chemical free radicals.12 Ionizing radi-
ation burns usually occur in laboratory or industrial
settings. The severity of the ionizing radiation burn
depends on the dose, dose rate, and the tissue sensitiv-
ity of exposed cells. Often referred to as acute radiation
syndrome, complications of ionizing radiation burns
include12:
 Gastrointestinal: Cramps, nausea, vomiting,
diarrhea, and bowel ischemia
 Hematologic: Pancytopenia (decreased number of
red blood cells, white blood cells, and platelets),
granulocytopenia (decreased number of granular
leukocytes), thrombocytopenia (decreased number
of platelets), and hemorrhage
 Vascular: Endothelium destruction
BURN ASSESSMENT AND ACUTE CARE
MANAGEMENT OF BURN INJURY
Classification of a Burn
The extent and depth of the burn determine its severity
and dictate acute care treatment.
ASSESSING THE EXTENT OF A BURN
The accurate assessment of the extent of a burn is neces-
sary to calculate fluid volume therapy and is a predictor
of morbidity.13 The extent of a burn injury is referred to
as total body surface area (TBSA) and can be calculated
by the rule of nines or the Lund and Browder formula.
RULE OF NINES. The rule of nines divides the body
into sections, seven of which are assigned 9% of
TBSA. The anterior and posterior trunks are each
assigned 18%, and the genitalia is assigned 1% (Figure
7-4). This formula is quick and easy to use, especially
when a rapid initial estimation of TBSA is needed in
the field or the emergency room. To use the rule of
nines, the area of burn is filled in on the diagram, and
the percentages are added for a TBSA. Modifications
can be made if an entire body section is not burned.
For example, if only the posterior left arm is burned,
theTBSA is 4.5%.
LUND AND BROWDER FORMULA. Table 7-4
describes the Lund and Browder formula. The body is
divided into 19 sections, and each is assigned a different
percentage of TBSA. These percentages vary with age
from infant to adult to accommodate for relative
changes in TBSA with normal growth. The Lund and
Browder formula is a more accurate predictor of
TBSA than the rule of nines because of the inclusion
of a greater number of body divisions along with the
adjustments for age and normal growth.
ESTIMATING THE EXTENT OF IRREGULARLY SHAPED
BURNS. It is important to note that using the rule of
nines or the Lund and Browder formula may not be
accurate for irregularly shaped burns. To estimate
TBSA with irregularly shaped burns, the patient’s
palm is used to measure the shape of the burn. The
palm represents 1% TBSA.13

FIGURE 7-4
The rule of nines method of assessing the extent of a burn
injury. (From M Walsh [ed]. Nurse Practitioners: Clinical Skills
and Professional Issues. Oxford, UK: Butterworth-Heinemann,
1999;32.)
ASSESSING THE DEPTH OF A BURN
The depth of a burn can be described as superficial,
moderate partial thickness, deep partial thickness, or
full thickness (Figure 7-5). Each type has its own
appearance, sensation, healing time, and level of pain,
as described in Table 7-5. The assessment of burn
depth allows an estimation of the proper type of burn
care or surgery and the expected functional outcome
and cosmesis.14 Although clinical observation remains
the standard for burn depth estimation, there is often
error or underestimation. Experimental technologies
for more precise burn depth estimation include cell
biopsy, vital dyes, fluorescein fluorometry, laser
Burns and Wounds CHAPTER 7 269
Doppler flowmetry, thermography, ultrasound, and
nuclear magnetic resonance.5
A burn wound is considered to be a dynamic wound
in that it can normally change in appearance, especially
during the first few days. A partial-thickness burn can
convert to a full-thickness burn from infection, inade-
quate fluid resuscitation, or excessive pressure from
dressings or splints.15
Acute Care Management of Burn Injury
This section discusses the admission guidelines and
resuscitative and reparative phases of burn care.
ADMISSION GUIDELINES
In addition to the burn’s extent and depth, the presence
of associated pulmonary, orthopedic, or visual injuries
determines what level of care is optimal for the patient.
The American Burn Association recommends medical
care at a burn center if the patient has any of the
following16:
 Partial-thickness burns greater than 10% TBSA
 Burns that involve the face, hands, feet, genitalia,
perineum, or major joints
 Third-degree burns in any age group
 Electrical burns, including lightning injury
 Chemical burns
 Inhalation injury
 Burn injury in patients who have preexisting medi-
cal disorders that could complicate management,
prolong recovery, or affect mortality
 Burns and concomitant trauma (such as fractures) in
which the burn injury poses the greatest risk of mor-
bidity or mortality. In such cases, if the trauma
poses the greater immediate risk, patients may be
stabilized initially in a trauma center before being
transferred to a burn unit. Physician judgment is nec-
essary in such situations and should be in concert
with the regional medical control plan and triage
protocols.
 Burns in children who are in hospitals without qual-
ified personnel or equipment for the care of children
 Burn injury in patients who require special social,
emotional, or long-term rehabilitative intervention
RESUSCITATIVE PHASE
The objectives of emergency room management of
the patient who has a major burn injury include simul-
taneous general systemic stabilization and burn care.
The prioritization of care and precautions during
this initial time period have a great impact on survival
and illustrate some key concepts of burn care.
270 CHAPTER 7 Burns and Wounds

Table 7-4 LUND AND BROWDER METHOD OF ASSESSING THE EXTENT OF BURNS*
Birth 1-4 yrs 5-9 yrs 10-14 yrs 15 yrs Adult
Head and Trunk
Head 19 17 13 11 9 7
Neck 2 2 2 2 2 2
Anterior trunk 13 13 13 13 13 13
Posterior trunk 13 13 13 13 13 13
Right buttock 2.5 2.5 2.5 2.5 2.5 2.5
Left buttock 2.5 2.5 2.5 2.5 2.5 2.5
Genitalia 1 1 1 1 1 1
Upper Extremity
Right upper arm 4 4 4 4 4 4
Left upper arm 4 4 4 4 4 4
Right forearm 3 3 3 3 3 3
Left forearm 3 3 3 3 3 3
Right hand 2.5 2.5 2.5 2.5 2.5 2.5
Left hand 2.5 2.5 2.5 2.5 2.5 2.5
Lower Extremity
Right thigh 5.5 6.5 8 8.5 9 9.5
Left thigh 5.5 6.5 8 8.5 9 9.5
Right lower leg 5 5 5.5 6 6.5 7
Left lower leg 5 5 5.5 6 6.5 7
Right foot 3.5 3.5 3.5 3.5 3.5 3.5
Left foot 3.5 3.5 3.5 3.5 3.5 3.5
*Values represent percentage of total body surface area.
Adapted from WF McManus, BA Pruitt.Thermal Injuries. In DV Feliciano, EE Moore, KL Mattox (eds),Trauma. Stamford, CT: Appleton
& Lange, 1996;941; Lund CC, Browder NC.The Estimation of Areas of Burns. Surg Gynecol Obstet 1944;79:355.

General systemic stabilization involves (1) the assess-
ment of inhalation injury and carbon monoxide (CO)
poisoning and the maintenance of the airway and ven-
tilation with supplemental oxygen (see Appendix
III-A) or mechanical ventilation (see Appendix III-B),
(2) fluid resuscitation, (3) the use of analgesia (see
Appendix VI), and (4) the treatment of secondary
injuries.17
INHALATION INJURY AND CARBON MONOXIDE
POISONING. The inhalation of smoke, gases, or poi-
sons, which may be related to burn injuries, can cause
asphyxia, direct cellular injury, or both. Inhalation
injury significantly increases mortality and varies
depending on the inhalant and exposure time.There is
no strict definition of inhalation injury. Inhalation
injury is suspected if the patient was exposed to noxious
inhalants, especially in an enclosed space, or if the
patient has one or more of the following: (1) altered
mental status; (2) burns on the face, neck, or upper
chest; (3) singed eyebrows or nose hairs; (4) laryngeal
edema; (5) arterial blood gas levels consistent with
hypoxia; (6) abnormal breath sounds; (7) the presence
of soot in sputum; or (8) positive blood test results for
chemicals.
The oropharynx and tracheobronchial tree are usu-
ally damaged by thermal injury, whereas the lung paren-
chyma is damaged by the chemical effects of the
inhalant. Thermal airway injury is characterized by
immediate upper-airway mucosal edema, erythema,
hemorrhage, and ulceration.5 Elective endotracheal
intubation is indicated with this type of injury, as pro-
gressive edema can readily lead to airway obstruction.
The patient remains intubated until airway edema is
decreased, usually 2 to 4 days post injury.18
 A B

C D
FIGURE 7-5
The depth of burn injuries from (A) superficial to (D) full thickness. (With permission from M.Walsh
[ed]. Nurse Practitioners: Clinical Skills and Professional Issues. Oxford, UK: Butterworth-Heinemann,
1999;28.)

Table 7-5 BURN DEPTH CHARACTERISTICS

Depth
Superficial (first-degree):
Epidermis injured
Moderate partial-thickness
(second degree):
Superficial dermis injured
Deep partial-thickness
(second degree):
Deep dermis injured
with hair follicles and
sweat glands intact
Full-thickness:
Entire dermis injured
(third degree) or fat,
muscle, and bone
injured (fourth degree)
Data from P Wiebelhaus, SL Hansen. Burns: handle with care. RN 1999;62:52-75.
Appearance Healing Pain
Pink to red 3-5 days by Tenderness to
With or without edema epithelialization touch or
Dry appearance without blisters Skin appears intact painful
Blanches
Sensation intact
Skin intact when rubbed
Pink to mottled red or red with edema 5 days to 3 wks by Very painful
Moist appearance with blisters epithelialization
Blanches with slow capillary refill Pigmentation changes are
Sensation intact likely
Pink to pale ivory 3 weeks to months by Very painful
Dry appearance with blisters granulation tissue
May blanch with slow capillary refill formation and
Decreased sensation to pinprick epithelialization
Hair readily removed Scar formation likely
White, red, brown, or black Not able to regenerate No pain, perhaps
(charred if fourth degree) an ache
Dry appearance without blanching
May be blistered
Insensate to pinprick
Depressed wound
272 CHAPTER 7 Burns and Wounds
The pathophysiology of inhalation injury generally
occurs in three stages: (1) inhalation injury (0 to 36
hours after injury), (2) pulmonary edema (6 to 72 hours
after injury), and (3) bronchopneumonia (3 to 10 days
after injury). Pulmonary edema occurs from increased
lung capillary permeability, increased bronchial
blood flow, and impaired lymph function.19 There are
de-epithelialization and exudate formation throughout
the airways, as well as decreased alveolar surfactant.5
Decreased lung compliance (functional residual capac-
ityand vital capacity) and hypoxia are the primary effects
of inhalation injury, each of which is dependent on the
location and severity of the injury. Supplemental
oxygen, elective intubation, bronchodilators, and fluid
resuscitation are initiated to maximize gas exchange
and reverse hypoxia.20-22
The inhalation of carbon monoxide (CO), which is a
colorless, odorless, tasteless, combustible, nonirritating
gas produced by the incomplete combustion of organic
material, results in asphyxia. CO molecules displace
oxygen molecules from hemoglobin to form carboxyhe-
moglobin and shift the oxyhemoglobin curve to the
left, thereby decreasing the release of oxygen.
Additionally, CO molecules increase pulmonary secre-
tions and decrease the effectiveness of the mucociliary
elevator.23 Elevated carboxyhemoglobin levels cause
headache, disorientation, nausea, visual changes, or
coma, depending on the percentage. CO poisoning is
usually reversible with the use of 100% oxygen if the
patient has not lost consciousness.5
BURN CARE IN THE RESUSCITATIVE PHASE. During
the first 72 hours after a burn injury, medical manage-
ment consists of continued fluid resuscitation, infec-
tion control, body temperature maintenance, pain and
anxiety management, and initial burn care, which may
include escharotomy or fasciotomy.
Fluid Resuscitation. After a burn, fluid shifts from
vascular to interstitial and intracellular spaces because
of increased capillary pressure, increased capillary and
venular permeability, decreased interstitial hydrostatic
pressure, chemical inflammatory mediators, and
increased interstitial protein retention.24 This is com-
pounded by evaporative water loss from a disruption
of the skin.25 In burns of more than 20% TBSA, this
fluid shift becomes massive and requires immediate
fluid repletion.14 This fluid shift, referred to as burn
shock, is a life-threatening condition because of hypovo-
lemia and the potential for shock-induced renal failure
(see Figure 7-3). Plasma, sodium-rich solutions, and
other fluids are infused over a 48-hour period accord-
ing to a standard formula derived from individual
TBSA and body weight. The formula used varies
according to hospital preference.
During and after fluid administration, the patient is
monitored closely for adequacy of fluid resuscitation.
Heart rate, blood pressure, cardiac output, base deficit,
urine output, and bowel sounds provide valuable infor-
mation about the effectiveness of fluid resuscitation,
as do peripheral body temperature, capillary refill, and
mental status.24,26
Infection Control. Prevention of infection at the
burn site(s) is crucial in the resuscitative and reparative
phases of burn care. The patient with a major burn is
considered immunocompromised because of the loss
of skin and the inability to keep microorganisms from
entering the body. Infection control is achieved by the
following14:
 Observation of the patient for signs and symptoms of
sepsis (See the Sepsis section in Chapter 10)
 Minimization of the presence of microorganisms in
the patient’s internal and external environment
 Use of aseptic techniques in all interactions with the
patient
 Use of topical antimicrobial agents or antibiotics,
as needed
 Tetanus prophylaxis
CLINICAL TIP
 To minimize the risk of infection, the physical
therapist must use sterile techniques according to the
burn unit procedures when entering a patient’s room
or approaching the patient’s bedside. The physical
therapist should be familiar with the institution’s
policies regarding the use and disposal of protective
barriers, such as gloves, gowns, caps, and masks.
Body Temperature Maintenance. Thze patient with a
major burn injury is at risk for hypothermia from skin
loss and the inability to thermoregulate. Body heat is
lost through conduction to the surrounding atmo-
sphere and to the surface of the bed. Initially, dry dres-
sings may be placed on the patient to minimize heat
loss.The patient should be placed in a warm atmosphere
to maintain body temperature. The patient’s room,
burn unit, or both may have overhead radiant heat
panels and may be humidified in an effort to preserve
the patient’s body heat.
Pain Management. A patient with a burn injury can
experience pain as a result of any of the following:
 Free nerve ending exposure
 Edema

 Exudate accumulation
 Burn debridement and dressing changes
 Mobility
 Secondary injury, such as fracture
Patients may also experience fear from the injury and
burn treatment, which can exacerbate pain. Analgesia,
given intravenously, is therefore started as soon as pos-
sible. Opioids are the mainstays in pain management,
supplemented by nonsteroidal antiinflammatory drugs
(NSAIDs), mild analgesics, parenteral and inhaled
anesthetic agents and anxiolytics. Initial doses of
opioids may exceed the standard weight-based recom-
mendations in order to achieve adequate pain control.
No evidence exists for any increased risk of addiction
in this population as compared to others who require
opioids for pain management.27 Refer to Appendices
IV and VI for more information about pharmacologic
agents.
Initial Burn Care. To neutralize the burn source, the
patient’s clothing and jewelry are removed, and the
burn is rinsed or lavaged (for a chemical burn).
Initially, a burn is debrided, cleaned, and dressed with
the hospital’s or burn unit’s antimicrobial agent of
choice once the patient is stabilized from a cardiopul-
monary perspective. Topical antimicrobial agents
attempt to prevent or minimize bacterial growth in a
burn and expedite eschar separation. There is a vari-
ety of antimicrobial agents, each with its own
application, advantages, and disadvantages. Ideally, the
antimicrobial agent of choice should penetrate eschar,
work against a wide variety of microorganisms, have
minimal systemic absorption, and not impede heal-
ing.28 The physician determines whether to cover
the burn or leave it open and estimates the time
frame for burn repair, the need for surgical interven-
tion, or both.
Escharotomy and Fasciotomy. Circumferential burns
of the extremities or trunk can create neurovascular
complications. Inelastic eschar paired with edema can
cause increased tissue swelling in all directions with
the result of decreased blood flow, nerve compression,
and increased compartment pressures. Tissue ischemia
and loss of limb can ensue if these conditions are not
treated with escharotomy or fasciotomy. Escharotomy is
the surgical incision through eschar to decompress
tissue below the burn. Fasciotomy is the surgical incision
through fascia to decompress tissue within a fascial
compartment. Both procedures are typically performed
at the bedside. Clinical indications for escharotomy
or fasciotomy are decreased arterial blood flow, as
determined by loss of Doppler flowmetry signal,
Burns and Wounds CHAPTER 7 273
or increased compartment pressure measurements
( 30 mm Hg).28
BURN MANAGEMENT IN THE REPARATIVE PHASE
Tissue healing at burn sites occurs over weeks to
months according to the depth of the burn and is
described in the Process of Wound Healing section.
For a discussion of variables that can slow the process
of burn healing, see the Factors That Can Delay
Wound Healing section. After the healing process, a
scar forms. A burn scar may be normotrophic, with a
normal appearance from the dermal collagen fibers
that are arranged in an organized parallel formation,
or hypertrophic, with an abnormal appearance as a
result of the disorganized formation of dermal collagen
fibers.29 Another form of abnormal appearance or
pathologic scar is a keloid scar, which tends to extend
beyond the boundaries of the primary wound (whereas
a hypertrophic scar will stay within the boundaries of
the primary wound).30 A keloid scar is more prevalent
in people of color and presents as a prominent, raised
scar as a result of excessive collagen accummulation.31
Burn management can be divided into two major
categories: the surgical management of burns, and
burn cleaning and debridement. It is beyond the scope
of this book to discuss in detail the indications, advan-
tages, and disadvantages of specific surgical interven-
tions that facilitate burn closure. Instead, surgical
procedures related to burn care are defined below.
SURGICAL PROCEDURES. The cornerstone of pres-
ent surgical burn management is early burn excision
and grafting.32 Excision is the surgical removal of
eschar and exposure of viable tissue to minimize infec-
tion and promote burn closure. Grafting is the implan-
tation or transplantation of skin onto a prepared
wound bed.33 Early burn closure minimizes infection,
the incidence of multisystem organ failure, and morbid-
ity. Table 7-6 describes the different types of excision
and grafting. Table 7-7 describes the different artificial
and biological skin substitutes for use when there is a
lack of viable autograft sites.
Surgical excision and grafting are completed at any
site if patient survival will improve. If morbidity is
greater than 50%, the priority is for the excision and
grafting of large flat areas to rapidly reduce the burn
wound area.28 Grafting is otherwise performed to max-
imize functional outcome and cosmesis, with the
hands, arms, face, feet, and joint surfaces grafted
before other areas of the body.34 Permanent grafting is
ideal; however, grafting may be temporary. Temporary
grafting is indicated for small wounds expected to
274 CHAPTER 7 Burns and Wounds
Table 7-6 TYPES OF EXCISION AND GRAFTING
Procedure Description
Tangential excision Removal of eschar in successive
layers down to the dermis
Full-thickness Removal of eschar as a single
excision layer down to the
subcutaneous tissue
Autograft Surgical harvesting of a
patient’s own skin from
another part of the body
(donor site) and placing it
permanently on the burn
(recipient site)
Split-thickness skin Autograft consisting of
graft (STSG) epidermis and a portion
of dermis
Full-thickness skin Autograft consisting of
graft (FTSG) epidermis and the entire
dermis
Mesh graft Autograft placed through
a mesher (a machine that
expands the size of the graft
usually 3-4 times) before
being placed on the recipient
site
Sheet graft Autograft placed on the
recipient site as a single piece
without meshing
Cultured epidermal Autograft of unburned
autograft (CEA) epidermal cells cultured
in the laboratory
Composite skin graft Autograft of unburned
epidermal and dermal cells
cultured in the laboratory
Allogenic graft Autograft of unburned
epidermal cells and cadaver
skin cultured in the
laboratory
Homograft Temporary graft from cadaver
skin
Heterograft Temporary graft from another
(xenograft) animal species, typically
of porcine skin
Amnion graft Temporary graft from placental
membrane
Data from SF Miller, MJ Staley, RL Richard. Surgical Management
of the Burn Patient. In RL Richard, MJ Staley (eds), Burn Care
and Rehabilitation: Principles and Practice. Philadelphia:
FA Davis, 1994.
heal secondarily and for large wounds for which an
autograft would not last or if permanent coverage is
not available.35
Grafts, which typically adhere in 2 to 7 days, may not
adhere or ‘‘take’’ in the presence of any of the
following33,34:
 An incomplete eschar excision
 Movement of the graft on the recipient site
 A septic recipient site
 A hematoma at the graft site
 A recipient site with poor blood supply
 Poor nutritional status
CLINICAL TIP
 To promote grafting success, restrictions on weight
bearing and movement of a specific joint or entire
limb may be present postoperatively. The therapist
should become familiar with the surgeon’s
procedures and protocols and alter positioning,
range of motion (ROM), therapeutic exercise, and
functional mobility accordingly.
 The therapist should check with the physician to
determine whether the graft crosses a joint and how
close the graft borders the joint.
 If possible, observe the graft during dressing changes
to get a visual understanding of the exact location
of the graft.
 The autograft site or donor site is often more
painful than the burn itself.
 Donor sites are oriented longitudinally and are
commonly located on the thigh, low back, or outer
arm and may be reharvested in approximately 2 weeks.
NONSURGICAL PROCEDURES. Burn cleaning and
debridement may be performed many times a day to
minimize infection and promote tissue healing.32
These procedures, as described in the Wound
Cleaning and Debridement section, may be performed
by a physician, nurse, or physical therapist depending
on the hospital’s or burn unit’s protocol. Table 7-8 lists
the commonly used dressings for burn wounds, skin
grafts, and donor sites.
CLINICAL TIP
 The use of immersion hydrotherapy for wound
cleaning carries a risk of hypothermia in patients
with burn injury secondary to lack of
thermoregulation from loss of dermal tissue and
associated vascular components.
 Burns and Wounds CHAPTER 7 275

Table 7-7 TEMPORARY AND PERMANENT SKIN SUBSTITUTES FOR THE TREATMENT OF BURNS
Product Description Use
Biobrane (Bertex Temporary graft option. For small to medium superficial-
Pharmaceuticals, Two-layered graft composed of nylon mesh thickness burns or partial-thickness
Morgantown,WV) impregnated with porcine collagen and burns
silicone; the outer silicone layer is permeable Has had limited success on full-
to gases but not to fluid or bacteria. thickness burns because of infection
Applied within 24 hours. May also be used to protect a meshed
Spontaneously separates from a healed autograft
wound in 10-14 days.
Dermagraft TC Temporary graft option. For partial-thickness burns
(Advanced Tissue Two-layered material composed of biological
Sciences, LaJolla, CA) wound-healing factors (e.g., fibronectin, type I
collagen, tenascin) and growth factors
(e.g., factor b) on an external synthetic barrier.
TransCyte (Advanced Temporary graft option. Used for partial-thickness burns that
Tissue Sciences, Composed of a polymer membrane and newborn will require debridement and may
LaJolla, CA) human fibroblast cells cultured on a porcine heal without surgical intervention,
collagen-coated nylon mesh.The fibroblasts or on excised deep-partial or
secrete human dermal collagen, matrix full-thickness burns prior to
proteins, and growth factors. autografting
AlloDerm (Life Permanent graft option. For full-thickness burns
Cell Corp.,The Composed of chemically treated cadaver Also used in postburn reconstruction
Woodlands,TX) dermis with the epidermal antigenic after contracture release
cellular components removed so
that it is immunologically inert.
Applied to a debrided burn with an ultrathin
split thickness autograft immediately
applied over it.
Integra (Integra Permanent graft option. For life-threatening full-thickness
Life Sciences, Two-layered material composed of a disposable burns or deep partial-thickness
Plainsboro, NJ) outer layer of Silastic that acts as a barrier burns
to evaporative water loss and bacteria and an
inner layer of bovine collagen and chondroitin-
6-sulfate that becomes incorporated into the
burn to form a neodermis.When the
neodermis becomes vascularized, the
Silastic covering can be removed and
replaced with thin autografts.
Data from SL Hansen, DW Voigt, P Wiebelhaus, CN Paul. Using skin replacement products to treat burns and wounds. Adv Skin Wound
Care 2001;14:37-44; P Dziewulski, JP Barret. Assessment, Operative Planning, and Surgery for Burn Wound Closure. In SE Wolf,
DN Herndon (eds), Burn Care. Austin,TX: Landes Bioscience, 1999.

History
PHYSICAL THERAPY EXAMINATION
IN BURN CARE In addition to the general chart review (see Appendix
I-A), the following information is especially relevant in
Physical therapy intervention for the patient with a the evaluation, treatment planning, and understanding
burn injury is often initiated within 48 hours of hospital of the physiological status of a patient with a burn.
admission.  How, when, where, and why did the burn occur?
276 CHAPTER 7 Burns and Wounds

Table 7-8 COMMONLY USED DRESSINGS FOR BURN WOUNDS, SKIN GRAFTS, AND DONOR SITES
Dressings Category Examples Appropriate Indications
Nonbiologic Petrolatum Xeroform, Xeroflo, Adaptic, Partial-thickness burns, skin
Aquaphor gauze grafts, donor sites
Silver Acticoat, Acticoat-7, Partial-thickness burns, skin
Aquacel-Ag, Silvasorb grafts, donor sites
Polyurethane OpSite,Tegaderm Partial-thickness burns, donor
sites
Foam Lyofoam Partial-thickness burns
Silicone Mepitel Partial-thickness burns, skin
grafts, donor sites
Negative pressure therapy Wound VAC system Skin grafts
Biosynthetic and Oat Glucan II Partial-thickness burns, skin
biologic grafts, donor sites
Collagen and fibroblasts Transcyte, Apligraf Partial-thickness burns
Collagen, fibroblasts, and OrCel Partial-thickness burns
keratinocytes
Allograft (cadaver) Fresh or cryopreserved Partial-thickness burns
Xenograft Porcine skin, porcine Partial-thickness burns
intestinal submucosa
(Oasis)
From PhamTN, Gibran NS.Thermal and Electrical Injuries. Surg Clin N Am 2007;87(1):185-206.

 Did the patient get thrown (as in an explosion) or fall  Posture

during the burn incident?
 Is there an inhalation injury or CO poisoning?
 What are the secondary injuries?
 What are the extent, depth, and location of the burn?
 Does the patient have a condition(s) that might
impair tissue healing?
 Was the burn self-inflicted? If so, is there a history of
self-injury or suicide?
 Were friends or family members also injured?
Inspection and Palpation
To assist with treatment planning, pertinent data that
can be gathered from the direct observation of a patient
or palpation include the following:
 Level of consciousness
 Presence of agitation, pain, and stress
 Location of the burn or graft, including the
proximity of the burn to a joint
 Presence and location of dressings, splints, or
pressure garments
 Presence of lines, tubes, or other equipment
 Presence and location of edema
 Position of head, trunk, and extremities
 Heart rate and blood pressure, respiratory rate and
pattern, and oxygen saturation
CLINICAL TIP
 Avoid popping any blisters on the skin during
palpation or with manual contacts.
 Do not place a blood pressure cuff over a burn or
graft site or an area of edema.
Pain Assessment
Good pain control increases patient participation and
activity tolerance; therefore, pain assessment occurs
daily. For the conscious patient, the physical therapist
should note the presence, quality, and grade of (1) rest-
ing pain; (2) pain with passive, active-assisted, or
active ROM; (3) pain at the burn site versus the donor
site; and (4) pain before, during, and after physical
therapy intervention.

CLINICAL TIP
 The physical therapist should become familiar with
the patient’s pain medication schedule and arrange
for physical therapy treatment when pain medication
is most effective and when the patient is as
comfortable as possible.
 Restlessness and vital sign monitoring (i.e., heart
rate, blood pressure, and respiratory rate increases)
may be the best indicators of pain in sedated or
unconscious patients who cannot verbally report pain.
 Refer to Appendices Table VI-1 and VI-2 for
information on various pain assessment scales. The
Visual Analog Scale and the Faces Pain Rating Scale
are most commonly used by burn centers for pain
assessment.27
Range of Motion
ROM of the involved joints typically requires gonio-
metric measurements. Exact goniometric values can
be difficult to measure when the patient has bulky dres-
sings; therefore, some estimation of ROM may be nec-
essary. The uninvolved joints or extremities can be
grossly addressed actively or passively, depending on
the patient’s level of alertness or level of participation.
CLINICAL TIP
 The physical therapist should be aware of the
presence of tendon damage before ROM assessment.
ROM should not be performed on joints with
exposed tendons.
 The physical therapist should always have a good
view of the extremity during ROM exercise to
observe for banding or areas of tissue that appear
white when stretched.
 The physical therapist should pay attention to the
position of adjacent joints when measuring ROM
to account for any length-tension deficits of healing
skin or muscle.
 The physical therapist should appreciate the fact
that a major burn injury is usually characterized
by burns of different depths and types. The physical
therapist must be aware of the various qualities
of combination burns when performing ROM
or functional activities.
 ROM may be decreased by the presence of bulky
dressings. Try to evaluate or perform ROM when
the dressings are temporarily off or down.
Burns and Wounds CHAPTER 7 277
Strength
Strength on an uninvolved extremity is usually assessed
grossly by function. More formal strength testing,
such as resisted isometrics or manual muscle testing, is
indicated on either the involved or uninvolved side if
there is severe edema, electrical injury, or secondary
injury.36
Functional Mobility
Functional mobility may be limited depending on state
of illness, medication, need for warm or sterile environ-
ment, and pain. The physical therapist should evaluate
functional mobility as much as possible, according to
medical stability and precautions.
CLINICAL TIP
 The skin at grafted areas, as well as at donor site
areas, is more fragile than normal skin. These areas
should be ace wrapped figure-of-eight style to
provide support against venous pooling when the
patient is being mobilized out of bed. Without this
extra support, the skin is more prone to shearing at
graft sites and subcutaneous bleeding.
PHYSICAL THERAPY INTERVENTION
Goals
The primary goal of physical therapy intervention for
patients with burn injuries is to maximize function
with ROM exercise, stretching, positioning, strength-
ening, and functional activity. Significant improve-
ments in functional outcomes, as measured by the
cognitive and motor components of the functional
independence measure (FIM), have been demonstrated
following inpatient rehabilitation for patient’s status
post burn injury.37 General considerations for physi-
cal therapy intervention by impairment are listed in
Table 7-9.
Basic Concepts for the Treatment of Patients
with Burn Injury
 The patient with a burn can have multisystem organ
involvement and a hypermetabolic state; thus, the
physical therapist needs to be aware of cardiac,
respiratory, and neurologic status, as well as muscu-
loskeletal and integumentary issues.
278 CHAPTER 7 Burns and Wounds

Table 7-9 PHYSICAL THERAPY CONSIDERATIONS FOR BURN INJURY

Variable
Decreased ROM and
altered limb position
Decreased strength
Decreased endurance and
functional mobility
Risk for scar development
Patient/family knowledge
deficit related to burns
and physical therapy
ROM, Range of motion.
Data fromTrees DW, Ketelsen CA, HobbsJA. Use of a Modified Tilt Table for Preambulation StrengthTraining as an Adjunct to Burn
Rehabilitation: A Case Series. J Burn Care Rehabil, 2003;24(2):97-103;Ward RS. Burns. In MH Cameron, LG Monroe (eds). Physical
Rehabilitation: Evidence-Based Examination, Evaluation, and Intervention. St. Louis: Elsevier Saunders, 2007.
Considerations
Most patients have full ROM on admission but may readily begin to exhibit decreased ROM
due to edema, pain, and immobilization.
ROM of uninvolved joints may also be decreased secondary to the process of total body
edema.
Devices that can help to properly position the patient include splints, abduction pillows, arm
boards attached to the bed, pillows, and blanket rolls.
Incorporate the use of a modality (i.e., pulley) into stretching activities.
Active exercise is preferred unless sedation or the patient’s level of consciousness prevents it.
Active exercise (i.e., proprioceptive neuromuscular facilitation) provides muscle
conditioning, increased blood flow, edema reduction, and contraction prevention and
helps reduce hypertrophic scar formation.
Prolonged bed rest (see Appendix I-B) may be necessary for weeks or months secondary
to medical status or to accommodate grafting, especially of the lower extremity.
The use of a tilt table for progressive mobilization from bed rest may be necessary
if orthostatic hypotension or decreased lower-extremity ROM exists.
Assistive devices may need adaptations (i.e., platform walker) to accommodate for ROM and
strength deficits or weight-bearing restrictions.
Consider the use of active exercise (i.e., restorator) that addresses cardiovascular conditioning
while increasing ROM and strength.
Healing of deeper burns and skin-grafted burns is accompanied by some scarring.
Hypertrophic scarring can be decreased by the use of pressure garments, silicone gel sheets,
ROM, and massage.
Patient/family education emphasizes information about the role of physical therapy, exercise,
positioning, pain and edema control, and skin care.
Education before discharge is of the utmost importance to improve compliance, confidence,
and independence.

 Fluid resuscitation and pain medications can affect
blood pressure, heart rate, and respiratory pattern
and rate, as well as level of alertness. Monitoring
these variables will help the therapist gauge pain
level and determine how aggressively to intervene
during the therapy session.
 The patient with a burn requires more frequent
reevaluations than other patient populations,
because the patient’s status and therapy intervention
can change dramatically as swelling decreases,
wound debridement and closure occur, hemody-
namic and respiratory stability are achieved, and
mental status improves. The goals and plan of care
need to be updated throughout the patient’s admis-
sion, as activity may be temporarily restricted after
surgical grafting.
 A portion(s) of the plan of care is often held for 4 to
7 days after skin grafting to prevent shearing forces
on the newgraft. Shearing can disrupt the circulation
to the graft and cause it to fail. Grafts over joints or
areas with bony prominences, as well as grafts on
the posterior surfaces of the body, are at greater risk
for shear injury.
 Time frames for physical therapy goals vary widely
and are based heavily on TBSA, the location of the
burn, age, and preexisting functional status.
 The joints at risk for contracture formation need to
be properly positioned (Table 7-10). The positioning
needs to be consistently carried out by all caregivers
and documented in the patient care plan. Proper
positioning will decrease edema and prevent
contracture formation to facilitate the best recovery.
 Burns and Wounds CHAPTER 7 279

Table 7-10 PREFERRED POSITIONS FOR Types of Wounds

PATIENTS WITH BURN INJURY TRAUMA WOUNDS
Area of Body Position A trauma wound is an injury caused by an external force,
such as a laceration from broken glass, a cut from a
Neck Extension, no rotation knife, or penetration from a bullet.
Shoulder Abduction (908)
External rotation SURGICAL WOUNDS
Horizontal flexion (108) A surgical wound is the residual skin defect after a sur-
Elbow and forearm Extension with supination gical incision. For individuals who do not have pro-
Wrist Neutral or slight extension blems healing, these wounds are sutured or stapled,
Hand Functional position (dorsal burn) and they heal without special intervention. As the ben-
Finger and thumb extension efits of moist wound healing become more widely
(palmar burn) accepted, gels and ointments are now more frequently
Trunk Straight postural alignment applied to surgical wounds.When complications, such
as infection, arterial insufficiency, diabetes, or venous
Hip Neutral extension/flexion
Neutral rotation
insufficiency, are present, surgical wound healing can
Slight abduction be delayed and require additional care.
Knee Extension ARTERIAL INSUFFICIENCY WOUNDS
Ankle Neutral or slight dorsiflexion A wound resulting from arterial insufficiency occurs
No inversion secondary to ischemia of the tissue, frequently caused
Neutral toe extension/flexion
by atherosclerosis, which can cause irreversible
From Ward RS. Splinting, Orthotics, and Prosthetics in the damage. Arterial insufficiency wounds, described in
Management of Burns. In MM Lusardi, CC Nielson (eds), Table 7-11, occur most commonly in the distal lower
Orthotics and Prosthetics in Rehabilitation. Boston: Butterworth- leg because of a lack of collateral circulation to this
Heinemann, 2000;315.
area. Clinically, arterial ulcers frequently occur in the
pretibial areas and the dorsum of the toes and feet, but
they may be present proximally if the ulcers were ini-
tially caused by trauma.38-40 They show minimal signs
 The therapist should be creative in treating the of healing and are often gangrenous.
patient with a burn. Traditional exercise works well;
however, incorporating recreational activities and VENOUS INSUFFICIENCY WOUNDS
other modalities into the plan of care can often A wound resulting from venous insufficiency is caused
increase functional gains and compliance with less by the improper functioning of the venous system,
pain. which leads to poor nutrition to the tissues. This lack
 The plan of care must be comprehensive and address of nutrition causes tissue damage, and ultimately tissue
all areas with burns. For example, burns of the face, death, resulting in ulceration. The exact mechanism by
neck, and trunk require intervention specifically which this occurs has not been established, although
directed to these areas. some theories do exist. One theory is that venous
 The therapist should attend bedside rounds with hypertension is transmitted to the superficial veins in
the burn team to be involved in multidisciplinary the subcutaneous tissue and the overlying skin, which
planning and to inform the team of therapy causes widening of the capillary pores.41,42 Clinically,
progression. this would result in the first sign of venous disease,
which is the presence of a dilated long saphenous vein
on the medial aspect of the calf. This dilation allows
PATHOPHYSIOLOGY OF WOUNDS the escape of large macromolecules, including fibrino-
gen, into the interstitial space.This results in the devel-
The different types of wounds, their etiologies, and the opment of edema toward the end of the day because of
factors that contribute to or delay wound healing are the pooling of fluid in the dermis. In long-standing
discussed in the following sections. venous disease, fibrin accumulates in the dermis,
280 CHAPTER 7 Burns and Wounds
Table 7-11 CLINICAL INDICATORS OF
VASCULAR INSUFFICIENCY WOUNDS
AND DIABETIC ULCERS
Wound Etiology Clinical Indicators
Arterial Intermittent claudication
insufficiency Extreme pain, decreased with rest and
increased with elevation
Decreased or absent pedal pulses
Decreased temperature of the distal
limb
Distinct, well-defined wound edges
Deep wound bed
Cyanosis
Venous Localized limb pain, decreased with
insufficiency elevation and increased with
standing
Pain with deep pressure or palpation
Pedal pulses present
Increased temperature around the
wound
Indistinct, irregular edges
Edema around the wound
Shallow wound bed
Substantial drainage
Diabetic ulcer Painless ulcer; however, general lower-
(neuropathic) limb pain is present
Absent pedal pulses
Decreased temperature in the distal
limb
Deep wound bed frequently located at
pressure points (e.g., metatarsal
heads)
Shiny skin on distal limb
Data from reference numbers 39, 40, 41, 55, 56.
creating a fibrin cuff that presents as hard, nonpitting
edema, and the surface skin is rigid and fixed. The
theory states that this fibrin cuff forms a mechanical
barrier to the transfer of oxygen and other nutrients,
which progressively leads to cellular dysfunction, cell
death, and skin ulceration.41,42
Another hypothesis is called the whiteblood cell-trapping
hypothesis. This theory states that transient elevations in
venous pressures decrease capillary blood flow, result-
ing in trapping of white blood cells at the capillary
level, which in turn plugs capillary loops, resulting in
areas of localized ischemia.42 These white blood cells
may also become activated at this level, causing the
release of various proteolytic enzymes, superoxide free
radicals, and chemotactic substances, which can also
lead to direct tissue damage, death, and ulceration.42,43
Venous stasis ulcers, described in Table 7-11, are fre-
quently present on the medial malleolus, where the
long saphenous vein is most superficial and has its
greatest curvature. Venous ulcers may be present on
the foot or above the midcalf but are more likely to
have another primary etiology, such as trauma or infec-
tion.The leakage of red blood cells over time results in
the deposit of hemosiderin and stimulated melanin,
causing the characteristic hyperpigmentation around
the medial ankle. Other characteristics include a thin
skin surface with a loss of hair follicles and sweat
glands.41
PRESSURE WOUNDS
A pressure ulcer, sometimes referred to as a decubitus
ulcer, is caused by ischemia that develops as a result of
sustained pressure in excess of capillary pressure on
the tissue. The pressure usually originates from pro-
longed weight bearing on a bony prominence, causing
internal ischemia at the point of contact. This initial
point of pressure is where tissue death first occurs.
The tissue continues to necrotize externally until a
wound is created at the skin surface. By this time,
there is significant internal tissue damage. Superficial
tissue ulceration can be caused by the effect of mechan-
ical forces acting on localized areas of skin and subcuta-
neous tissue, whether the forces are of low intensity
over long periods or are higher forces applied intermit-
tently.44,45 The relationships between the amount of
force applied, the duration of force, and the direction
of the force contribute to the occurrence and severity
of a pressure ulcer. Not only can direct pressure create
tissue ischemia, but friction and shearing forces, along
with moisture contribute as well.44, 46-49 Refer to the
Wound Staging and Classification section for the
pressure ulcer grading system.
All bed- or chair-bound patients or any patients with
an impaired ability to reposition themselves or weight
shift are at risk of developing pressure ulcers. When a
patient is lying in supine position, common pressure
ulcer sites include the back of the head, scapular
spines, spinous processes, elbows, sacrum, and heels.
While side-lying, a patient may experience increased
pressure on the ear, acromion process, rib, iliac crest,
greater trochanter, medial and lateral condyles, and
the malleoli.46,50 A person’s body weight also plays a
role in pressure ulcer development. A person who is
too thin has more prominent bony prominences,
whereas a person who is overweight has increased
pressure on weight-bearing surfaces.47,48,50

NEUROPATHIC OR NEUROTROPIC ULCERS
A neuropathic or neurotropic ulcer (see Table 7-11) is a
secondary complication that occurs from a triad of dis-
orders, including peripheral vascular disease, periph-
eral neuropathy, and infection.51 Neuropathic ulcers
are most commonly associated with diabetes. The
development of ulcers and foot injuries are the leading
causes of lower-extremity amputation in people with
diabetes.52 Additionally, there is an increased incidence
of atherosclerosis, which appears earlier and progresses
more rapidly than in patients without diabetes.
However, many people with diabetes who develop
foot ulcers have palpable pulses and adequate periph-
eral blood flow.53
Individuals with diabetes may also have changes in
the mechanical properties of the skin. Insulin is essen-
tial for fibroblastic and collagen synthesis. A lack of
insulin in type 1 diabetes can lead to diminished colla-
gen synthesis that can cause stiffness and poor tensile
strength of tissue, both of which increase the suscepti-
bility of wound development and decrease healing
potential.54
The peripheral and central nervous systems can be
adversely affected in diabetes. Peripheral neuropathy is
common, and sensation and strength can be impaired.
Diminished light touch, proprioception, and tempera-
ture and pain perception decrease the ability of the
patient with diabetes to identify areas that are being sub-
jected to trauma, shearing forces, excessive pressure,
and warm temperatures, allof which can cause ulcers.53-57
Loss of protective sensation can be examined by
several methods including vibration testing with a 128
Hz tuning fork, vibration perception threshold testing,
and pressure assessment with Semmes-Weinstein
monofilaments.58
Structural deformities can occur as the result of the
neuropathies that may be present secondary to diabetes.
Any structural deformities, such as ‘‘hammer toes’’ or
excessive pronation or supination, can create pressure
points that lead to ischemia and a subsequent ulcer.55- 57
Excessive plantar callus formation may develop at
the sites of increased pressure and in itself can increase
pressure to the affected area.53 The minor repetitive
ischemia that occurs every time the patient bears
weight on the pressure points in the tissue underlying
the callus can eventually cause the tissue to fail, and
ulceration occurs.57
Peripheral motor neuropathy contributes to the
development of an equinus contracture at the ankle as
stronger plantarflexors overcome the weaker dorsiflex-
ors.Weakness of the small intrinsic muscles of the foot
Burns and Wounds CHAPTER 7 281
causes clawing of the toes. These foot deformities lead
to increased weight distribution through the forefoot
and increased pressure under the metatarsal heads.
The abnormal mechanical forces and intermittent
forces can stimulate callus formation.53
A neuropathy of the autonomic nervous system
is present in the majority of individuals with diabetes
and neuropathic ulcers.The autonomic nervous system
regulates skin perspiration and blood flow to the micro-
vascular system. Lack of sweat production contributes
to the development of a callus. Altered cross-linkage
between collagen and keratin results in predisposal to
hyperkeratosis and callus formation. Beneath the
callus, a cavity often forms as a response to the increased
pressure and shear forces and fills with serous fluid,
causing a seroma. If the deep skin fissure comes in con-
tact with an underlying seroma, it can become colonized
with bacteria and result in ulcer formation.53
The immune system is also affected by elevated glu-
cose levels and their resultant problems. Edematous tis-
sues and decreased vascularity, which contribute to
lack of blood flow, decrease the body’s ability to fight
infection because of its inability to deliver oxygen,
nutrients, and antibiotics to the area.59-65
Although neuropathic ulcers are most often associ-
ated with diabetes, they may also occur in individuals
with spina bifida, neurologic diseases, muscular degen-
erative disease, alcoholism, and tertiary syphilis because
of similar risk factors among these populations.40
CLINICAL TIP
 In patients with diabetes, evaluation of their
footwear, if available, is essential to help determine
appropriateness of use, wear pattern, and fit, all of
which can contribute to ulcer formation, particularly
in the presence of foot deformities.
PROCESS OF WOUND HEALING
Epidermal wounds heal by reepithelialization. Within
24 to 48 hours after an injury, new epithelial cells prolif-
erate and mature. Deeper wounds, which involve the
dermal tissues and even muscle, go through a rather
complex and lengthy sequence of (1) an inflammatory
response, (2) a fibroplastic phase, and (3) a remodeling
phase.45-49
In the inflammatory phase, platelets aggregate and
clots form. Leukocytes, followed by macrophages,
282 CHAPTER 7 Burns and Wounds
migrate to the area, and phagocytosis begins.
Macrophages also provide amino acids and sugars that
are needed for wound repair. In preparing the wound
for healing, they stimulate the fibroplastic phase.
During the fibroplastic phase, granulation begins.
Granulation is indicative of capillary buds growing
into the wound bed. Concurrently, fibrocytes and other
undifferentiated cells multiply and migrate to the area.
These cells network to transform into fibroblasts,
which begin to secrete strands of collagen, forming
immature pink scar tissue. In the remodeling phase,
scar tissue matures. New scar tissue is characterized by
its pink color, as it is composed of white collagen fibers
and a large number of capillaries. The amount of time
the entire healing process takes depends on the size and
type of wound. It may take from 3 days to several
months or more for complete closure to occur.59- 65
FACTORS THAT CAN DELAY WOUND
HEALING
In addition to the problems indigenous to the wound,
many other factors can delay wound healing. Age, life-
style, nutrition, cognitive and self-care ability, vascular
status, medical complications, and medications all can
affect wound healing.These factors may also be risk fac-
tors for the development of new wounds.These factors
should therefore be included in the physical therapy
assessment and considered when determining goals,
interventions, and time frames.
Age
Skin, just like other tissues and organs, changes with age.
Decreased cellular activity during the aging process
leads to decreased collagen production, which results in
less collagen organization in older individuals. Reduced
collagen organization results in decreased tensile
strength of the skin that could result in greater damage
after trauma in the older individual. Other examples of
skin changes with age include delayed wound contrac-
tion, decreased epithelialization, and delayed cellular
migration and proliferation.66 Other comorbidities that
delay wound healing, such as diabetes, peripheral neuro-
pathies, and related vascular problems, occur with
greater frequency in older individuals.
Lifestyle
A patient’s lifestyle can have a great impact on the prog-
nosis for healing, decision-making regarding wound
management, and preventive care. For example,
occupations and hobbies that require prolonged stand-
ing may predispose some individuals to varicosities
and other venous problems. Patients exposed to trau-
matic situations, such as construction workers, are also
more likely to reinjure healing wounds. Behaviors
such as cigarette smoking can impede wound healing
significantly because of the vasoconstriction that nico-
tine creates.
Nutrition
Good nutrition is necessary for the growth and mainte-
nance of all body tissues. Macronutrients (such as car-
bohydrates, fats, and proteins) and micronutrients
(such as vitamins) are necessary for cell metabolism,
division, and growth. Therefore, nutrition is closely
linked with all phases of healing.67 Generally, poor
nutrition decreases the body’s ability to heal.
Additionally, patients with burns, wounds, or infection
who are adequately nourished at the time of their
injury or the development of their wound may also
develop protein-calorie malnutrition.
There are major metabolic abnormalities associated
with injury that can deplete nutritional stores, includ-
ing increased output of catabolic hormones, decreased
output of anabolic hormones, a marked increase in met-
abolic rate, a sustained increase in body temperature, a
marked increase in glucose demands, rapid skeletal
muscle breakdown with amino acids used as an energy
source, lack of ketosis, and unresponsiveness to catabo-
lism to nutrient intake.68 Protein-calorie malnutrition
can delay wound healing and cause serious health con-
sequences in patients with wounds, especially if infec-
tion exists. Poor nutritional status, whether due to
decreased intake or the stress response, can set off a
series of metabolic events leading to weight loss, deteri-
oration of lean tissues, increased risk of infection,
edema, and breathing difficulty.68
These events can lead to severe debilitation and even
death. Inadequate diet control in patients with diabetes
exacerbates all symptoms of diabetes, including
impaired circulation, sensation, altered metabolic pro-
cesses, and delayed healing. A nutritional assessment
by a registered dietitian, nutritional supplements, and
careful monitoring of the patient’s nutritional status
and weight are important components of a comprehen-
sive assessment and treatment program for the patient
with a wound.
In addition, therapists should work with other
health care professionals to curb the systemic stress
response. Removing necrotic tissues, treating infec-
tions, and ensuring adequate hydration and blood

fluid volumes will help to limit physiologic stressors.
Premedication before painful procedures and avoiding
extreme temperatures help minimize stress. Exercise
serves as an anabolic stimulus for muscle, facilitating a
reduction of the catabolic state.68
Cognition and Self-Care Ability
There is an increased risk of infection and other wound
healing complications if neither the patient nor the
caregiver has the cognitive or physical ability, or both,
to properly care for a wound, including wound cleaning
and dressing removal and application. The patient’s or
caregiver’s abilities, or both, have a great influence in
the choice of dressing(s) and on discharge planning.
Certain dressings require more skill than others to
maintain. Complex wound care can justify a stay at a
rehabilitation hospital or skilled nursing facility.
Vascular Status
Any compromised vascular status may contribute to the
development of delayed wound healing owing to a
lack of oxygenation and nutrition to the tissues.
Medical Status
Generally, compromised health causes a decrease in the
body’s ability to progress through the healing process.
Preexisting infection or a history of cancer, chemother-
apy, radiation, acquired immunodeficiency syndrome,
or other immunodeficiency disorders can decrease the
patient’s ability to heal. Congestive heart failure, hyper-
tension, and renal dysfunction can also slow wound
healing.
Medications
Steroids, antihistamines, NSAIDs, and oral contracep-
tives may delay wound healing, as can chemotherapy
and radiation.These medications can decrease the ten-
sile strength of connective tissue, reduce blood
supply, inhibit collagen synthesis, and increase the
susceptibility to infection.69 Anticoagulants thin the
blood and decrease its ability to clot; therefore, the
healthcare provider needs to diligently monitor bleed-
ing during dressing removal and consider debridement
methods that will not cause bleeding. Antibiotics can
create hypersensitivity skin reactions as well as cause
diarrhea, which is a contributing factor to skin
ulceration.49
Chronic Wounds
In healthy patients without comorbidities, an acute
wound should heal within 3 to 6 weeks, with
Burns and Wounds CHAPTER 7 283
remodeling occurring over the next year. If a wound
remains in one of the stages of healing without pro-
gression, it becomes a chronic wound.70 Chronic
wounds are defined as wounds that have ‘‘failed to pro-
ceed through an orderly and timely process to produce
anatomic and functional integrity, or proceeded
through the repair process without establishing a sus-
tained anatomic and functional result.’’71 The acute
care therapist should be inclined to search for underly-
ing causes of delayed wound healing, especially when
treating a wound that has not healed in more than 6
weeks.
WOUND ASSESSMENT AND ACUTE CARE
MANAGEMENT OF WOUNDS
The evaluation of a patient with a skin wound includes
a general history (identification of factors that can
delay healing), a physical examination (of sensation,
pain, ROM, strength, and functional mobility), and a
specific examination of the wound itself.
History
In addition to the general chart and medical history
review (see Appendix I-A), the following information
is especially relevant for determining wound etiology
and risk factors, an intervention plan, and potential
outcomes.
WOUND HISTORY
 How and when did the wound occur?
 What diagnostic tests have been performed?
 What laboratory studies have been ordered?
 What interventions have been administered to the
wound thus far? What were the results?
 Is there a previous history of wounds? If so, what
were the etiology, intervention, and time frame of
healing?
CLINICAL TIP
 Measurement of Ankle-Brachial Index (see Chapter 6)
helps determine healing potential in patients with
diabetes or vascular disease.
 Measurement of blood glucose levels
(<110mg/dl fasting), serum albumin (3.2-4.5 gm/dl)
and prealbumin (15 to 35 mg/dl) help to
determine metabolic and nutritional status
of the patient.49
284 CHAPTER 7 Burns and Wounds
RISK FACTORS
 How old is the patient?
 Is the patient cognitively intact?
 Where and for how long is the patient weight bearing
on areas involving the wound site?
 What is the patient’s occupation or hobby? How
many hours does the patient spend on his or her
feet per day? In what positions and postures is the
patient throughout the day?
 Does the patient smoke?
 Is the patient generally well nourished? Is the patient
taking any supplements?
 Has the patient experienced any weight loss or gain
lately?
 If the patient has diabetes, is it well controlled?
 Does the patient have an immunodeficiency disorder
or a medical condition that increases his or her risk
of infection?
 Does the patient have a medical condition that causes
altered sensation?
 What medications (including anticoagulants) is the
patient taking? What are their effects on wound
healing?
PSYCHOSOCIAL FACTORS
 Does the patient have a good support system, includ-
ing physical assistance if necessary?
 What are the patient’s mobility needs?
A review of vascular tests, radiographic studies, and
tissue biopsy results also lends valuable information
about the integrity of the vascular and orthopedic
systems and the presence of underlying disease.
Physical Examination
SENSATION
Sensation to light touch, pressure, pinprick, tempera-
ture, and kinesthesia or proprioception (or both)
should be examined. Impaired or absent sensation
should be addressed through instruction in the appro-
priate prevention techniques, as well as modifications
to shoes, weight bearing, and water temperatures in
bathing.
PAIN
The evaluation of pain in the patient with a wound is
not unlike the evaluation of pain in any other type of
patient. The therapist should evaluate the nature of the
pain, including the location, onset, severity (using a
pain-rating scale), duration, aggravating and alleviating
factors, and the impact on activities of daily living.
Understanding the nature of the pain will ultimately
allow the physical therapist to provide or recommend
the appropriate intervention.
The pain experience associated with wounds has
been described as having one of three components: a
noncyclic acute component, a cyclic acute component,
or a chronic wound pain component.
Noncyclic acute wound pain is a single episode of
acute pain that is likely to occur with treatment (e.g.,
the pain felt during sharp debridement). Cyclic acute
pain is wound pain that recurs throughout the day
because of repeated treatments. For example, a patient
may experience pain after several days of dressing
changes, which creates repetitive trauma to the
wound. Chronic or consistent wound pain is persistent
wound pain that occurs intrinsically, not as a result of
external intervention (e.g., a patient with a neuropathic
ulcer who has a constant, dull ache in the foot).72
CLINICAL TIP
 The American Geriatric Society promotes the use of
‘‘persistent’’ pain rather than ‘‘chronic’’ pain to help
lessen negative connotations that accompany the
term chronic. Additionally, this society advocates
stating that patients ‘‘report pain,’’ rather than
‘‘complain of pain,’’ again to maximize the positive
interactions with patients.73
RANGE OF MOTION
Specific measurement of ROM may not be necessary in
a patient with a wound. However, specific goniometric
measurements are necessary if a wound crosses a joint
line, if edema is present at a joint, or if decreased
ROM inhibits mobility. Decreased ROM that inhibits
mobility or increases weight bearing, pressure, or both
may contribute to wound development. Therefore,
passive or active ROM exercise, or both, should be
included, as necessary, in the treatment plan.
STRENGTH
Strength should be evaluated for its impact on the
patient’s function. The therapist should keep in mind
that the patient may have different functional demands
secondary to the wound. For example, a patient who
needs to be non—weight bearing because of a wound
on his or her foot requires sufficient upper-extremity
strength to use an assistive device to maintain this
precaution while ambulating. If the patient does not

have adequate upper-extremity strength, then he or she
may be non-ambulatory until the weight-bearing
status is changed.
FUNCTIONAL MOBILITY
Functional mobility, including bed mobility, transfers,
and ambulation or wheelchair mobility, should be eval-
uated. The therapist should consider that the patient’s
function may have changed simply because of the con-
sequences of the presence of the wound. For example,
balance may be compromised if the patient requires
orthotics or shoe modifications because of a wound.
Gait training with an assistive device is often necessary
to decrease weight bearing on an affected lower
extremity.
EDEMA AND CIRCULATION
The evaluation of edema is important because it is
frequently an indicator of an underlying pathology.
Edema is also a critical factor in lowering tissue
perfusion of oxygen and increasing susceptibility to
infection. In fact, edema is almost equivalent to insuf-
ficient blood supply in lowering the oxygen tension in
the area of the wound. Ultimately, the presence of
edema must be addressed to heal the wound. Refer to
Table 1-6 for the scale on how to grade (pitting) edema.
Therapists should also consider that lymphedema
and chronic wounds can be closely linked.
Lymphedema is commonly associated in individuals
who are status post mastectomy; however, it can also
occur after other surgeries and traumas. Cellulitis may
actually be due to a compromised lymphatic system
that creates small, weeping blisters from fluids being lit-
erally pushed through the skin. In addition, edema sec-
ondary to chronic venous insufficiency frequently also
has a lymphatic component. Refer to Chapter 6 for a
description of lymphedema.
Circulation can be grossly evaluated and monitored
by examining skin temperature, distal limb color, and
the presence of pulses. Refer to theVascular Evaluation
section in Chapter 6 for more information on the eval-
uation of circulation. The therapist should notify the
physician when any significant changes in these indica-
tors occur.The therapist should be aware of any arterial
compromise before using compression bandages.
Wound Inspection and Evaluation
Wound observation and measurements create an objec-
tive record of the baseline status of a wound and can
help to determine the best intervention to facilitate
wound healing.
Burns and Wounds CHAPTER 7 285
CLINICAL TIP
 During any interaction with the patient, the clinician
should screen the wound for any overt changes as
well as determine the stability of the wound prior to
performing examination and intervention techniques.
LOCATION, ORIENTATION, SIZE, AND DEPTH
The location of the wound should be documented in
relation to anatomic landmarks. The orientation of a
wound; its length, width, and depth; the presence of
undermining (tunneling); or a combination of these
factors is essential measurements in wound assessment.
The orientation of the wound must be determined to
ensure consistent length and width measurements, par-
ticularly for a wound with an abstract shape or odd loca-
tion. One method of determining wound orientation
is to consider the wound in terms of a clock, with the
patient’s head being 12 o’clock (Figure 7-6).
When documenting length, the measurement is the
distance of the wound (measured in the direction
from the patient’s head to toe), and the width is the hor-
izontal measurement. There are a variety of methods
for measuring wounds. Tape measurements are one
method, but a calibrated grid on an acetate sheet on
which the wound can be traced is optimal, especially
for irregularly shaped wounds. Polaroid photographs
on grid film or digital photos can also be used.
11 12 1
10 2
9 3
8 4
7 5
6
FIGURE 7-6
Clockwise method of measuring pressure ulcer size. (From
Hamm RL.Tissue Healing and Pressure Ulcers. In MH
Cameron, LG Monroe [eds]. Physical Rehabilitation: Evidence-
Based Examination, Evaluation, and Intervention. St. Louis:
Saunders, 2007.)
286 CHAPTER 7 Burns and Wounds
CLINICAL TIP
 When taking a photograph of a wound, create or
follow a consistent procedure for taking
photographs, as changes in the distance of the
camera from the wound as well as the position of
the patient can affect the appearance of the wound.
 Also, to ensure consistency and accuracy in wound
assessments, use a consistent unit of measure among all
individuals measuring the wound. Centimeters, rather
than inches, are more universally used in the literature.
 Multiple wounds can be documented relative to each
other if the wounds are numbered—for example,
‘‘Wound #1: left lower extremity, 3 cm proximal to
the medial malleolus. Wound #2: 2 cm proximal to
wound #1.’’
Depth can be measured by placing a sterile cotton-
tip applicator perpendicular to the wound bed.
The applicator is then grasped or marked at the point
of the wound edge and measured. If the wound has
varying depths, this measurement is repeated.
Undermining or tunneling describes a continuation of
the wound underneath intact skin and is evaluated by
taking a sterile cotton-tip applicator and placing it
underneath the skin parallel to the wound bed and
grasping or marking the applicator at the point of the
wound edge. Assessment of undermining should be
done all around the wound. It can be documented
using the clock orientation (e.g., ‘‘Undermining: 2 cm
at 12 o’clock, 5 cm at 4 o’clock’’) (see Figure 7-6).
COLOR
The color of the wound should be documented because
it is an indicator of the general condition and vascularity
of the wound. Pink indicates recently epithelized tissue.
Red indicates healing, possibly granulating tissue.Yellow
indicates infection, necrotic material being sloughed
off from the wound, or both. Black indicates eschar.
It is important to document the percentage of each
color in the wound bed. An increase in the amount of
pink and red tissue, a decrease in the amount of yellow
and black tissue (or both) are indicative of progress.
An increase in the amount of black (necrotic) tissue is
indicative of regression.
DRAINAGE
Wound drainage is described by type, amount, and
odor. Drainage can be (1) serous (clear and thin; may
be present in a healthy, healing wound), (2)
serosanguineous (containing blood; may also be pres-
ent in a healthy, healing wound), (3) purulent (thick,
white, and pus-like; may be indicative of infection and
should be cultured), or (4) green (usually indicative of
Pseudomonas infection and should also be cultured).
The amount of drainage is generally documented as
absent, scant, minimal, moderate, large, or copious. (Note: there
is no consistent objective measurement that correlates
to these descriptions.) A large amount of drainage can
indicate infection, whereas a reduction in the amount
of drainage can indicate that an infection is resolving.
The presence and degree of odor can be documented
as absent, mild, or foul. Foul odors can be indicative of an
infection.
WOUND CULTURE
Awound culture is a sampling of microorganisms from
the wound bed that is subsequently grown in a nutrient
medium for the purpose of identifying the type and
number of organisms present. Caution must be taken
when measuring extent of undermining to avoid trau-
matic separation of tissues. A wound culture is indi-
cated if there are clinical signs of infection, such as
purulent drainage, large amounts of drainage, increased
local or systemic temperature, inflammation, abnormal
granulation tissue, local erythema, edema, cellulitis,
increased pain, foul odor, and delayed healing.74
Results of aerobic and nonaerobic cultures can deter-
mine whether antibiotic therapy is indicated.75
Methods of culturing include tissue biopsy, needle
aspiration, and swab cultures. Physical therapists may
administer swab cultures. Otherwise, wound cultures
are performed by the nurse or physician, depending
on the protocol of the institution.
All wounds are contaminated, which does not
necessarily mean they are infected. Contamination is
the presence of bacteria on the wound surface.
Colonization is the presence and multiplication of sur-
face microbes without infection. Infection is the inva-
sion and multiplication of microorganisms in body
tissues, resulting in local cellular injury.74,76
CLINICAL TIP
 Unless specifically prescribed otherwise, cultures
should be taken after debridement of thick eschar
and necrotic material and wound cleaning;
otherwise, the culture will reflect the growth of the
microorganisms of the external wound environment
rather than the internal environment.

SURROUNDING AREAS
The area surrounding the wound should also be evalu-
ated and compared to noninvolved areas. Skin color,
the absence of hair, shiny or flaky skin, the presence of
reddened or darkened areas, edema, or changes in nail
beds should all be examined and documented
accordingly.
CLINICAL TIP
 Increased localized temperature can indicate local
infection; decreased temperature can indicate
decreased blood supply.
Wound Staging and Classification
Superficial wounds involve only the epidermis. Partial-
thickness wounds further involve the superficial layers
of the dermis; full-thickness wounds continue through
to muscle and potentially to bone. This terminology
should be used to describe and classify wounds that
are not pressure ulcers. Pressure ulcers have their own
classification system because of their unique character-
istic of developing from the ‘‘inside out,’’ including
injury to the deeper subcutaneous tissues under intact
skin (Table 7-12). As pressure ulcers heal to a more shal-
low depth, lost muscle, subcutaneous fat, or dermis is
not replaced; rather granulation tissue fills in this
space. Therefore, avoid ‘‘reverse staging’’ when docu-
menting improvement in a pressure ulcer (e.g., a Stage
III ulcer does not improve to a Stage II ulcer). It is
more advisable to use descriptive terms to denote
improved wound characteristics or utilize available
tools such as the Pressure Ulcer Scale for Healing
(PUSH) tool, the Sussman Wound Healing Tool
(SWHT), or the Pressure Score StatusTool (PSST).49,77
Wound Cleaning and Debridement
It is beyond the scope of this book to discuss in detail
the methods of wound cleaning and debridement.
Instead, general descriptions and indications of each
are provided.Wound cleaning and debridement can be
performed by physical therapists, nurses, or physicians,
depending on the policy of an individual facility.
Physical therapists should also verify state practice acts
regarding their ability to perform sharp debridement.
Specific management considerations for physical thera-
pists who work with patients who have wounds are
described in the Physical Therapy Intervention section
at the end of this chapter.
Burns and Wounds CHAPTER 7 287
Table 7-12 PRESSURE ULCER STAGING
Stage Definition
Suspected deep Localized area of discoloration
tissue injury (purple or maroon) under intact
skin or blood-filled blister due
to damage of underlying soft tissue
from pressure and/or shear.
Stage I Usually over a bony prominence,
presents as intact, reddened skin
that does not blanch. Skin with
darker pigmentation may present as
a differing color from surrounding
areas.
Stage II A shallow open ulcer with a red pink
wound bed, denoting partial-
thickness loss of dermis, without
slough. Can present as an intact
or open/ruptured serum-filled
blister.
Stage III Subcutaneous fat may be visible
denoting full-thickness loss,
however muscle, tendon, or bone
are not exposed. May include
tunneling and undermining as well
as possible slough.
Stage IV Muscle, tendon, or bone are exposed
with this full-thickness loss. Often
includes tunneling and
undermining as well as slough or
eschar.
Unstageable Slough and/or eschar is covering
full-thickness loss in the
wound bed.
From Ayello EA, Baronski S, Lyder CH, et al. Pressure
Ulcersç2007 National Pressure Ulcer Advisory Panel Staging
Definitions. In S Baronski, EA Ayello.Wound Care Essentials:
Practice Principles. Philadelphia: Lippincott Williams & Wilkins,
2007:256-257.
WOUND CLEANING
Wound cleaning is not synonymous with wound debri-
dement or wound decontamination. The purpose of
cleaning a wound is to remove loosely attached cellular
debris and bacteria from the wound bed in order to
both prepare the wound bed for healing and help pre-
vent infection. In most cases, the use of sterile saline is
effective and safe for cleaning the wound surface.78,79
Many studies indicate that using unsterile tap water
does not increase the rate of infection and is
288 CHAPTER 7 Burns and Wounds
appropriate to use to cleanse wounds.78 There are many
commercial wound cleansers that contain surfactants.
Surfactants help to break the bonds between contami-
nants, debris, and the surface of the wound.78 The use
of antiseptics is appropriate in the early management
of acute traumatic wounds but is of little benefit in
chronic wounds.They may be cytotoxic to living tissues
and can delay healing.78,80,81 Wound cleaning can be
achieved by a variety of devices such as scrubbing
cloths, sponges, and brushes, as well as irrigation
devices.82
The most neutral solution that will meet the needs of
the patient should be used. Use aggressive agents only
when indicated. For example, a bleaching agent may
help to dry a heavily exudating wound.To avoid dama-
ging new tissue, discontinue cleansing when the major-
ity of a wound bed is granulating or when
reepithelialization is occurring.
CLINICAL TIP
 If the water source is known or suspected to be
contaminated, it should not be used for wound
cleaning.78 If the physical therapist is unsure, the
water can be cultured in the hospital laboratory.
 Sterile saline expires 24 hours after opening the
bottle and must be discarded. A saline solution can
be made by adding 2 tablespoons of salt to 1 quart
of boiling water.78,80 This recipe may be an
inexpensive alternative to purchasing saline for the
patient who will be cleaning wounds at home.
 It is best to use cleaning materials at body
temperature. The application of a cold solution
will reduce the temperature of the wound and
may affect blood flow.81
 Whirlpool, although commonly and perhaps
habitually used, does not cleanse the wound.
The use of whirlpool jets is actually mechanical
debridement and therefore should be used only
if mechanical debridement is indicated.
CLEAN VERSUS STERILE TECHNIQUE. Although
clean versus sterile technique remains somewhat con-
troversial, clean technique is sufficient for local wound
care to chronic wounds and is generally accepted in
the medical community. This is because the chronic
wound is already contaminated and far from sterile.
Sterile technique is typically reserved for surgical and
acute traumatic wounds.83
Sterile technique, which includes the use of sterile
instruments and sterile gloves, should always be used
when invading the bloodstream, as with sharp debride-
ment. Otherwise, the use of clean gloves is sufficient.
Additionally, originally sterile dressings, once opened,
can still be used as long as they are kept in a clean,
controlled area.83
WOUND DEBRIDEMENT
Debridement has three primary purposes.The first is to
remove necrotic tissue or foreign matter from the
wound bed, optimizing healing potential.The presence
of devitalized tissue prevents reepithelialization and
can splint the wound open, preventing contraction
and closure.The second purpose is to prevent infection.
The necrotic tissue itself can be the source of the patho-
genic organisms. The debridement of the slough and
eschar also increases the effectiveness of topical
agents. The third purpose is to correct abnormal
wound repair. Debridement is generally indicated for
any necrotic tissue present in a wound, although occa-
sionally it is advantageous to leave eschar in place. For
example, eschar on heel ulcers that is firmly adherent
to surrounding tissue (without inflammation of sur-
rounding tissue and without drainage and tenderness
on palpation) may not need to be removed.84
There are two types of debridement: selective and
nonselective. Selective debridement removes nonviable
tissue only and is indicated for wounds with necrotic
tissue adjacent to viable tissue. Methods of selective
debridement include sharp, autolytic, and enzymatic
debridement. Nonselective debridement removes
both viable and nonviable tissues. It is indicated in
necrotic wounds with minimal to no healthy tissue.
Mechanical debridement is a method of nonselective
debridement.84,85
SELECTIVE DEBRIDEMENT.
Sharp Debridement. Sharp debridement involves the
use of scalpels, scissors, forceps, hydrosurgery devices,
or lasers (only physicians are allowed to perform the
latter two methods) to remove necrotic tissue. It is a
highly skilled technique best performed by or under
the direct supervision of an experienced clinician.
(Note: Not all states and facilities allow physical thera-
pists to perform sharp debridement.) Because the true
selectivity of sharp debridement depends on the skill
of the clinician, sharp debridement can also result in
damage to healthy tissues that can cause bleeding and
a risk of infection. Sharp debridement is especially
expedient in the removal of large amounts of thick,

leathery eschar. Removal of eschar is important in the
patient who is immunocompromised, because the
underside of eschar can provide a medium for bacterial
growth. Sharp debridement has been shown to increase
the degree of wound healing when combined with the
use of a topical growth factor.86,87
Sharp debridement can be painful; it is therefore
recommended that pain medications or topical analge-
sics be administered before treatment.When debriding,
the clinician should spare as much tissue as possible
and be careful to have the technique remain selective
by not removing viable tissue. Because of the potential
for excessive bleeding, extra care should be taken with
patients who are taking anticoagulants.
Autolytic Debridement. Autolytic debridement is the
natural and most selective form of debridement. The
body uses its own enzymes to lyse necrotic tissue and
this is a normal process that occurs in any wound. It is
painless and does not harm healthy tissues. Applying a
moisture-retentive topical dressing, such as films,
hydrocolloids, hydrogels, and calcium alginates facili-
tates autolytic debridement in a pain free manner for
patients with adequate tissue perfusion.84,86,87 When
using autolytic debridement, it is important to cleanse
the wound to remove partially degraded tissue.86
Because it takes time for autolytic debridement to
occur, sharp debridement of eschar is recommended
before autolytic debridement to expedite the removal
of the necrotic tissue. Owing to the risk of infection,
autolytic debridement is contraindicated as the primary
method of debridement in patients who are immuno-
suppressed or otherwise require quick elimination of
necrotic material.
Enzymatic Debridement. Enzymatic debridement is
achieved through the topical application of enzymes
that lyse collagen, fibrin, and elastin. The type of
enzyme chosen depends on the type of necrotic tissue
in the wound. Enzymes are categorized as proteolytics,
fibrinolytics, and collagenases.84 Different enzymatic
debriding agents are effective with each of these tissues.
Wounds with heavy black eschar are best debrided by
proteinases and fibrinolytic enzymes. Collagenases are
used when necrotic collagen, which generally appears
yellowish, is present. Enzymatic debridement agents
are available only by prescription. Enzymatic debride-
ment is indicated for stage III and IV wounds with
yellow necrotic material but should be discontinued as
soon as the wound is clean. Sharp debridement of the
wound can be performed before the use of enzymes to
facilitate tissue healing.
Burns and Wounds CHAPTER 7 289
CLINICAL TIP
 When applying an enzymatic debriding agent
to eschar and it cannot be debrided, crosshatch
the eschar and pull in the edges to allow
the enzymes to penetrate the eschar.
 Certain metals, such as silver and zinc oxide, which
are present in certain cleansing agents, can
inactivate enzymes and interfere with enzymatic
debridement.86
NONSELECTIVE DEBRIDEMENT.
Mechanical Debridement. Mechanical debridement
removes dead tissue by agitating the necrotic tissue of
the wound or adhering it to a dressing and removing
it. Dry gauze dressings, whirlpool, and pulsed lavage
or irrigation (or both) are all examples of mechanical
debridement.
Wet-to-dry dressings mechanically debride the
wound by removing the dressing along with the necrot-
ic tissue embedded in it. If mechanical debridement is
indicated and gauze is used, the sponge or gauze with
the largest pores is the most effective for debridement.86
This technique involves applying a saline-moistened
gauze dressing to the wound, allowing it to dry, and
then removing the dressing. The dressing will also
adhere to any growing tissue in the wound bed and
may inadvertently remove it.84 The Centers for
Medicare and Medicaid Services (CMS) has stated that
the use of wet-to-dry dressings be limited in the man-
agement of pressure ulcers and should not be used on
clean, granulating wound beds.87
Whirlpool may be used to debride loosely adherent
tissue and exudate and deodorize the wound. It may
also help to prepare a wound for sharp debridement by
softening necrotic tissue and separating desiccated tis-
sues from the wound bed, or it can be used to soak off
adhered dressings. If the intention of the therapist is
to use a wet-to-dry technique for mechanical debride-
ment, the dressings should not be soaked off, as necrot-
ic tissue will not be removed.48,85,88
There are many precautions and contraindications
for the therapist to consider before using whirlpool.
For example, it may be inappropriate to place
the lower extremity of a patient with venous insuffi-
ciency in a dependent position with warm water, or per-
haps the treatment may need to be modified by
decreasing the temperature or length of a treatment.
290 CHAPTER 7 Burns and Wounds
Treatment duration can range between 10 and 20 min-
utes, and water temperature can range from tepid
(808 to 928 F [26.78 to 33.38 C]) to close to body temper-
ature (928 to 968 F [33.38 to 35.58 C]).87 As with wound
cleaning, the therapist should carefully weigh the bene-
fits of antibacterial agents that can be added to the
whirlpool versus their cytotoxic effects and use a solu-
tion that is most neutral and least damaging to viable
tissue. Infected wounds that have foul odors, copious
amounts of drainage, and a great deal of exudate and
necrotic tissue require more aggressive additives.
Whirlpool should be limited to stage III or IV
wounds with greater than 50% of necrotic tissue,
because, as with gauze debridement, granulating
tissue may be damaged.Whirlpool should be discontin-
ued once the objectives of the whirlpool have been
achieved.48,84,88
Pulsed lavage is now a viable treatment option for
wound management, and systems specifically designed
for wound care are currently available. Pulsed lavage
uses a pressurized, pulsed solution (usually saline) to
irrigate and debride wounds of necrotic tissue.
Suction may also be used to remove wound debris and
the irrigation solution.89 The pulsatile action is thought
to facilitate growth of granulation tissue because of its
effective debridement, and the negative pressure cre-
ated by the suction may also stimulate granulation.90
Pulsed lavage may be a more appropriate option than
whirlpool for patients who are incontinent, have
venous insufficiency, should not be in a dependent
position, have an intravenous line, or are mechanically
ventilated. Pulsed lavage may access narrow wound
tunnels that may not be reached with whirlpool as vari-
ous flexible tunneling tips are available from manufac-
turers. One must also consider risk of contamination
from aerolization of droplets during both pulsed
lavage and whirlpool treatments.
Dressings and Topical Agents
Wound dressings are identified as either primary or sec-
ondary. Primary dressings are applied directly to the
wound bed, while secondary dressings are utilized to
contain or anchor a primary dressing. Custom dres-
sings, which may contain more than one primary or
secondary dressing, may be indicated for a single
wound.49 When applying dressings, the therapist
should always follow universal precautions and use a
clean technique to prevent cross-contamination.When
choosing a dressing for a wound, four factors related
to the wound itself should be considered: (1) the color
of the wound, (2) the amount of drainage, (3) the
wound depth, and (4) the surrounding skin. Other sig-
nificant factors include the patient’s cognitive and phys-
ical ability to apply the dressing and the accessibility
of physical therapy or nursing services to the patient.
Cost is also a consideration.
A large number of wound care products are avail-
able, and it is virtually impossible to be aware of the pur-
pose and application instructions of every available
dressing. It is the responsibility of the therapist to read
the manufacturer’s instructions for application, to
know the purpose of the dressing, and to make edu-
cated decisions when choosing the appropriate dress-
ing for a given wound at each stage of the healing
process. Clinicians should not rely on manufacturer’s
claims of efficacy to justify a dressing’s effectiveness.
Although it is not possible to identify every dressing,
it is possible to catalog most dressings into some basic
categories: gauze, transparent film, hydrocolloids,
amorphous, hydrogels, foams, calcium alginates, colla-
gen matrix, topical dressings, and small intestine sub-
mucosa (SIS) dressings. Table 7-13 is a summary of the
indications, advantages, and disadvantages of different
dressings.56,90-92
Advanced Therapies
NEGATIVE PRESSURE WOUND THERAPY
The V.A.C. (Vacuum Assisted Closure) device (Kinetic
Concepts, Inc., San Antonio, Texas) assists in wound
closure by applying localized negative pressure to a spe-
cial porous dressing positioned in or over the wound.
The porous dressing distributes negative pressure to
the wound and helps remove interstitial fluids.The neg-
ative pressure applies noncompressive mechanical
forces to the wound site and draws the tissue inward,
subjecting it to subatmospheric pressure.The distortion
causes epithelial cells to multiply rapidly and form gran-
ulation tissue.The stretching also increases cell prolifer-
ation by activating ion channels within the cells and
releasing biochemical mediators from the plasma mem-
brane. It is also thought to stimulate the growth of
new blood vessels. The typical protocol consists of
using continuous negative pressure for the first 48
hours of treatment to decrease edema followed by inter-
mittent pressure to facilitate granulation of tissue.
Dressings for noninfected wounds can be changed
every 2-3 days or changed daily for infected wounds.
Indications for this therapy include wounds from all
etiologies. Exercise caution when utilizing the V.A.C
device for a patient who is on anticoagulants, and
note that wounds containing fistulas may require

Table 7-13 INDICATIONS AND USES OF BASIC TYPES OF DRESSINGS
Type of Dressing Indication(s)
Gauze May be used for any type of
wound if properly applied
and removed (although
other dressings may be
more effective)
Transparent film Autolytic debridement, to
reduce friction, superficial
wounds with minimal
drainage, secondary
dressing over foam or
gauze
Hydrocolloids Partial- or full-thickness
wounds with low to
moderate drainage,
including partially necrotic
wounds.
Provide a moist wound
environment and promote
autolysis
Amorphous Dry eschar wounds, clean
granulating wounds,
exposed tendon and bone
Hydrogels Partial-thickness wounds
with minimal drainage,
or as a secondary dressing
on full-thickness wounds
Foams Partial- or full-thickness
wounds with minimal
to moderate drainage
Calcium alginates Partial- and full-thickness
wounds with large
amounts of drainage,
infected or noninfected
wounds.
Provide a moist wound
environment and facilitate
autolysis
Collagen matrix Any recalcitrant wound to
facilitate migration of
collage
Burns and Wounds
Description
Highly porous.
Applied dry, wet-to-dry (i.e., the
dressing is put on wet but will
dry before removal), or wet-to-
wet (i.e., the dressing is put on
wet and removed when wet).
Polymer sheet with an adhesive
layer on one side
Dressings that contain absorptive
particles that interact with
moisture to form a gelatinous
mass.
Cause the pH of the wound
surface to decrease, thereby
inhibiting bacterial growth.
Polymers and water in a gel form
Gel composed of 96% water
or glycerin
Polyurethane foam with two
surfaces: a hydrophilic inner
surface and a hydrophobic
outer surface
Fibrous sheets and rope derived
from brown seaweed.
The main component, alginic
acid, is converted to calcium
and sodium salts, which in
turn convert to a viscous gel
after contact with wound
exudates.
Collagen derived from bovine
material, processed and
shaped into sheets, particles,
or gels
CHAPTER 7 291
Advantages
Readily available
Inexpensive
Conforms and adheres well
to surfaces, waterproof,
impermeable to bacteria,
cost-effective
Prevent secondary wound
infection.
Impermeable to water,
oxygen, and bacteria.
Available in many forms
(pastes, powders, and
sheets).
Changed infrequently
Maintains a moist
environment, assumes
shape of cavity wound,
promotes autolysis, non-
cytotoxic to granulation
tissue, cost-effective
Highly conformable.
Safe for fragile skin.
Available in many forms.
Nonadherent to skin surface.
Highly absorbable and
conformable.
Permeable to oxygen (reduce
risk of anaerobic infection).
Highly conformable
Conforms to wound bed,
promotes granulation and
epithelialization
Continued
292 CHAPTER 7 Burns and Wounds
Table 7-13 INDICATIONS AND USES OF BASIC TYPES OF DRESSINGS—cont’d
Type of Dressing Indication(s)
Topical dressings Wounds requiring topical
medications
Small intestine Full- or partial-thickness
submucosa (SIS) wounds, autograft donor
dressings sites, second-degree burns
Data from reference numbers 56, 50, 91, 92, 93, 94.
customized application of dressings and suction.
Contraindications include necrotic tissue or eschar
in 30% of the wound, untreated osteomyelitis,
malignancy in the wound, and exposed arteries or
veins.49,95,96
SKIN SUBSTITUTES AND BIOLOGICALS
Although these will not be a first line of defense, thera-
pists in the acute care setting should be aware of other
agents that may be used to treat the chronic, nonhealing
ulcer. Frequently a patient may have been receiving
treatment for a wound before hospitalization for an
acute medical condition and the therapist may be conti-
nuing or may need to recommend alternative healing
agents. Platelet-derived growth factor (PDGF) pro-
motes cellular migration of leukocytes and macro-
phages and stimulates fibroblasts to produce collagen.
An example of platelet-derived growth factor is
Regranex gel (becaplermin) and is available by prescrip-
tion for use in diabetic wounds. Another type of treat-
ment with growth factor is the use of autologous
platelet-derived concentrate, such as platelet-rich
plasma (PRP). This form of treatment is prepared at
the point of care for the patient, rather than at a manu-
facturer. Blood is taken from the patient and mixed
with a solution to create a gel that is applied to the
patient’s wound.97,98
Another possible solution is skin substitutes
(e.g., Dermagraft), which consist of fibroblasts from a
newborn foreskin donor, placed on a polygalactic acid
mesh. The fibroblasts multiply, attach to the mesh, and
release growth factors.96 Living skin equivalent
(e.g., graftskin [Apligraf]) consists of bovine type I
Description Advantages
Water- or petrolatum-based gels Allow local application of
and ointments (antimicrobials, antimicrobials bypassing
growth factors, silver, systemic administration.
enzymes, anesthetics) Maintain moist
environment.
Collagen tissue extracted from Promotes cell migration, no
porcine submucosa, processed rejection, minimizes
to remove cells and shaped scarring, reduces
into sheets frequency of dressing
changes, long shelf-life
collagen that is acid dissociated and added to a culture
system. Human fibroblasts are then added.98,99
These are typically fairly expensive treatments and
are reserved for nonhealing foot ulcers that have not
responded to other topical agents and treatments.
PHYSICAL THERAPY INTERVENTION IN
WOUND CARE
The responsibility and autonomy of the physical thera-
pist in the treatment of wounds vary greatly among
facilities. The physical therapist can and should play a
key role in the patient’s clinical course of preventing
a wound, initiating wound care (or both), as well as
recommending activity and footwear modifications,
and positioning aids. The physical therapist in the
acute care setting can also be make recommendations
about wound care on discharge from the hospital.
Unless the wound is superficial and caused by trauma,
wound closure is not likely to occur during the acute
care phase. Therefore, the ultimate long-term goal of
complete wound closure, which may occur over many
months, occurs at a different level of care, usually out-
patient or home care.
The following are the primary goals of physical ther-
apy for wound treatment in the acute care setting:
 To promote wound healing through wound assess-
ment, dressing choice and application, wound clean-
ing, and debridement
 To educate patients and families about wound care
and the prevention of further breakdown and future
wounds
 Burns and Wounds CHAPTER 7 293

Table 7-14 PHYSICAL THERAPY CONSIDERATIONS FOR WOUND CARE

Physical Therapy Intervention
Pain management
Range of motion, strength,
and functional mobility
Edema management
Prevention
Consideration
Coordinate physical therapy session with pain premedication to reduce acute cyclic
and noncyclic pain.
Consider the use of positioning, relaxation techniques, deep breathing, exercise,
or modalities to relieve pain.
Modify wound treatment techniques as able to eliminate the source of pain.
Adequate range of motion is necessary for proper positioning and minimizing
the risk of pressure ulcer formation.
Care should be taken with manual contacts with fragile skin, and care should be
taken not to disturb dressings during exercise.
Adequate strength is necessary for weight shifting and functional mobility with
the maintenance of weight-bearing precautions.
Depending on the etiology, exercise, compression therapy, lymphatic drainage,
limb elevation (used with caution in the patient with cardiac dysfunction),
or a combination of these can be used to manage edema.
Education (e.g., dressing application, infection control, wound inspection,
the etiology of wounds)
Positioning (e.g., splints, turning schedule)
Skin care and hygiene (e.g., dressing removal)
Pressure reduction surfaces (e.g., air mattress, wheelchair cushion)
Footwear adaptations (e.g., orthotics, inserts, extra-depth shoes)

 To maximize patient mobility and function while
accommodating needs for wound healing
(e.g., maintaining non—weight-bearing status)
 To minimize pain
 To provide recommendations for interdisciplinary
acute care
 To provide recommendations and referrals for
follow-up care
To fulfill these responsibilities, the therapist must
consider all information gathered during the evaluation
process and establish appropriate goals and time
frames. The etiology of the wound, risk factors, and
other data guide the therapist toward the proper inter-
vention. Objective, measurable, and functional goals
are as important in wound care as in any other aspect
of physical therapy.
Patients with wounds typically have many other
medical complications and needs that a physical
therapist cannot address alone. To provide optimal
care, the physical therapist should function as part
of an interdisciplinary team that may include a
physician, a nurse, a specialized skin and wound care
nurse (enterostomal therapist), a dietitian, and others.
The physical therapist should be aware of and
make proper recommendations to the appropriate
personnel for all of the patient’s needs for healing.
Specific considerations for physical therapy inter-
vention with a patient who has a wound include
pain management, ROM, strengthening, functional
mobility, edema management, and wound prevention.
Table 7-14 describes these considerations.

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 8 Gastrointestinal System

Jaime C. Paz INTRODUCTION

David Nicoloro Disorders of the gastrointestinal (GI) system can have numerous effects on
the body, such as decreased nutrition, anemia, and fluid imbalances.
These consequences may, in turn, affect the activity tolerance of a
patient, which will ultimately influence many physical therapy inter-
ventions. In addition, physical therapists must be aware of pain referral
patterns from the GI system that may mimic musculoskeletal
symptoms (Table 8-1). The objectives of this chapter are to provide the
following:
1. A basic understanding of the structure and function of the GI system
2. Information on the clinical evaluation of the GI system, including
physical examination and diagnostic studies
3. A basic understanding of the various diseases and disorders of the
GI system
4. Information on the management of GI disorders, including pharmaco-
logic therapy and surgical procedures
5. Guidelines for physical therapy intervention in patients with GI dis-
eases and disorders.
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:
 Pattern 4A: Primary Prevention/Risk Reduction for Skeletal
Demineralization
 Pattern 6B: Impaired Aerobic Capacity/Endurance Associated with
Deconditioning
 Pattern 7A: Primary Prevention/Risk Reduction for Integumentary
Disorders.
Please refer to the back cover of this book for a complete list of the
preferred practice patterns as individual patient conditions are highly
variable and other practice patterns may be applicable.

STRUCTURE AND FUNCTION

The basic structure of the GI system is shown in Figure 8-1, with the pri-
mary and accessory organs of digestion and their respective functions
described inTables 8-2 and 8-3.

297
298 CHAPTER 8 Gastrointestinal System

ascertained through patient interview, questionnaire

Table 8-1 GASTROINTESTINAL SYSTEM PAIN completion, or chart review. For a list of these items,
REFERRAL PATTERNS see Box 8-1. Appendix I-A also describes the general
Segmental Areas of Pain medical record review.
Structure Innervation Referral INSPECTION
Esophagus T4-T6 Substernal region Figure 8-2 demonstrates the abdominal regions associ-
Upper abdomen
ated with organ location. During inspection, the physi-
Stomach T6-T10 Upper abdomen cal therapist should note asymmetries in size and shape
Middle and lower in each quadrant, umbilicus appearance, and presence
thoracic spine
of abdominal scars indicative of previous abdominal
Small intestine T7-T10 Middle thoracic spine procedures or trauma. The physical therapist should
Pancreas T6-T10 Upper abdomen also note the presence of incisions, tubes, and drains
Upper and lower during inspection, because these may require particular
thoracic spine handling or placement during mobility exercises.1
Gallbladder T7-T9 Right upper abdomen
Right, middle, and
lower thoracic spine CLINICAL TIP
Liver T7-T9 Right, middle, and  The physical therapist should document any changes
lower thoracic spine in abdominal girth, especially enlargement.
Right cervical spine In addition, the nurses and physicians should be
Common bile T6-T10 Upper abdomen notified. Abdominal enlargement may hinder the
duct Middle lumbar spine patient’s respiratory and mobility status. Observe
for abdominal distention in postoperative patients
Large intestine T11—L1 Lower abdomen
Middle lumbar spine (especially orthopedic) taking narcotics (this can
be an early sign of paralytic ileus).
Sigmoid colon T11-T12 Upper sacral region
Suprapubic region
Left lower quadrant
of abdomen AUSCULTATION
From Boissonault WG, Bass C. Pathological Origins of Trunk
The abdomen is auscultated for the presence or absence
and Neck Pain: Part I. Pelvic and Abdominal Visceral Disorders. of bowel sounds and bruits (murmurs) to help evaluate
J Orthop Sports PhysTher 1990;12:194. gastric motility and vascular flow, respectively. Bowel
sounds can be altered postoperatively, as well as in
cases of diarrhea, intestinal obstruction, paralytic
CLINICAL EVALUATION ileus, and peritonitis. The presence of bruits may be
indicative of renal artery stenosis.1
Evaluation of the GI system involves combining infor-
mation gathered through physical examination and PERCUSSION
diagnostic studies. Mediate percussion is used to evaluate liver and spleen
size and borders, as well as to identify ascitic fluid,
Physical Examination solid- or fluid-filled masses, and air in the stomach
Physical examination of the abdomen consists of and bowel.1,2 The technique for mediate percussion is
inspection, auscultation, percussion, and palpation. described in the Physical Examination section of
Physicians and nurses usually perform this examination Chapter 2.
on a daily basis in the acute care setting; however, physi-
cal therapists can also perform this examination to help PALPATION
delineate between systemic and musculoskeletal pain. Light palpation and deep palpation are used to identify
abdominal tenderness, muscular resistance, and super-
HISTORY ficial organs and masses. The presence of rebound
Before performing the physical examination, the pres- tenderness (i.e., abdominal pain worsened by a quick
ence or absence of items related to GI pathology is release of palpatory pressure) is an indication of

FIGURE 8-1
Schematic representation of the gastrointestinal system. (Courtesy Peter Wu.)
peritoneal irritation from possible abdominal hem-
orrhage and requires immediate medical attention.
Muscle guarding during palpation may also indicate a
protective mechanism for underlying visceral
pathology.1,3
Diagnostic Studies
Discussion of the diagnostic evaluation for the GI
system will be divided into (1) the examination of the
GI tract and (2) the examination of the hepatic, biliary,
pancreatic, and splenic systems. Examination of the
GI tract includes the esophagus, stomach, and the intes-
tines (small and large).Table 8-4 summarizes the labora-
tory tests used to measure functional aspects of
secretion, digestion, absorption, and elimination
within the GI tract.4-11 Table 8-5 summarizes diagnostic
procedures used to visualize the GI tract.
Examination of the hepatic (liver), biliary (gall-
bladder and cystic ducts), pancreatic, and splenic sys-
tems involves numerous laboratory tests and
diagnostic procedures, which are often performed
Gastrointestinal System CHAPTER 8 299
concurrently to fully delineate the etiology of a patient’s
clinical presentation. Because of the common location
of these organs and shared access to the biliary tree, dis-
ease or dysfunction in one organ can often extend into
the other organs.12,13
CLINICAL TIP
 Laboratory tests used to examine the liver
are frequently referred to as liver function tests
or LFTs.
Hepatocellular injury results in cellular damage in
the liver, which causes increased levels of the following
enzymes: aspartate aminotransferase (AST; previously
called serum glutamic-oxaloacetic transaminase),
alanine aminotransferase (ALT; previously called
serum glutamate pyruvate transaminase), and lactate
dehydrogenase (LD).13,14
Hepatocellular dysfunction can be identified when
bilirubin levels are elevated or when clotting times are
300 CHAPTER 8 Gastrointestinal System
Table 8-2 STRUCTURE AND FUNCTION OF THE
PRIMARY ORGANS OF DIGESTION
Structure Function
Oral cavity Entrance to the
gastrointestinal system,
mechanical and chemical
digestion begins here
Pharynx Involved in swallowing and
mechanical movement of
food to esophagus
Esophagus Connects mouth to the
stomach, transports and
disperses food
Stomach (cardia, Mechanical functions: storage,
fundus, body, mixing, and grinding of
pylorus) food and regulation of
outflow to small intestine
Exocrinefunctions: secretion of
hydrochloric acid, intrinsic
factor, pepsinogen, and
mucus necessary for
digestion
Endocrinefunctions: secretion of
hormones that trigger the
release of digestive
enzymes from the pancreas,
liver, and gallbladder into
the duodenum
Small intestine Duodenum: neutralizes acid in
(duodenum, food transported from the
jejunum, ileum) stomach and mixes
pancreatic and biliary
secretions with food
Jejunum: absorbs nutrients,
water, and electrolytes
Ileum: absorbs bile acids and
intrinsic factors to be
recycled in the
bodyçnecessary to prevent
vitamin B12 deficiency
Large intestine Absorbs water and
(cecum; appendix; electrolytes
ascending, transverse, Stores and eliminates
descending, and indigestible material
sigmoid colon; as feces
rectum; anus)
Data from ScanlonJC, SandersT (eds). Essentials of Anatomy and
Physiology (2nd ed). Philadelphia: FA Davis, 1993;362; Guyton AC,
HallJE (eds).Textbook of Medical Physiology (9th ed).
Philadelphia: Saunders, 1996;803-844.
Table 8-3 Structure and Function of the
Accessory Organs of Digestion
Structure Function
Teeth Break down food to combine with
saliva.
Tongue Provides taste sensations by cranial
nerveVII (taste).
Keeps the food between the teeth
to maintain efficient chewing action
for food to mix with saliva.
Salivary glands Produce saliva, which is necessary
to dissolve food for tasting and
moisten food for swallowing.
Liver Regulates serum levels of fats, proteins,
and carbohydrates.
Bile is produced in the liver and is
necessary for the absorption of lipids
and lipid-soluble substances.
The liver also assists with drug
metabolism and red blood cell and
vitamin K production.
Gallbladder Stores and releases bile into the
duodenum via the hepatic duct
when food enters the stomach.
Pancreas Exocrine portion secretes bicarbonate
and digestive enzymes into
duodenum.
Endocrine portion secretes insulin,
glucagons, and numerous other
hormones into the bloodstream, all
of which are essential in regulating
blood glucose levels.
Spleen* Filters out foreign substances and
degenerates blood cells from the
bloodstream.
Also stores lymphocytes.
*The spleen is not part of the gastrointestinal system but is located
near other gastrointestinal components in the abdominal cavity.
Data from Scanlon JC, SandersT. Essentials of Anatomy and
Physiology (2nd ed). Philadelphia: FA Davis, 1993; and Guyton AC,
HallJE.Textbook of Medical Physiology (9th ed). Philadelphia:
Saunders, 1996;803-844.
increased (denoted by an increased prothrombin time
and the international normalized ratio [INR]). The
liver produces clotting factors and, therefore, an
increased prothrombin time or INR implicates
impaired production of coagulation factors. Refer
to Chapter 6 for more details on coagulation tests.
 Gastrointestinal System CHAPTER 8 301

BOX 8-1 ITEMS ASSOCIATED WITH GASTROINTESTINAL PATHOLOGY

Signs and Symptoms Stool and Urine Characteristics Associated Disorders
Nausea and vomiting Change in stool color History of hernia
Hemoptysis Change in urine color History of hepatitis
Constipation Hematochezia (bright red blood in stool) Drug and alcohol abuse
Diarrhea Melena (black, tarry stools) Fatty food intolerance
Jaundice
Heartburn
Abdominal pain

Data from Koopmeiners MB. Screening for Gastrointestinal System Disease. In WG Boisonnault (ed), Examination in Physical
Therapy Practice. NewYork: Churchill Livingstone, 1991;113; and Goodman CC.The Gastrointestinal System. In CC Goodman,
WG Boisonnault (eds), Pathology: Implications for the Physical Therapist. Philadelphia: Saunders, 1998;456-460.

Cholestasis is the impairment of bile flow from the
liver to the duodenum and results in elevations of the
following serum enzymes: alkaline phosphatase
(ALP), aspartate transaminase (previously known as
g-glutamine-oxaloacetic transaminase or g-glutamyl
transpeptidase), and 50 -nucleotidase.13,14
Table 8-6 summarizes the laboratory tests performed
to measure hepatic, biliary, and pancreatic function.
Table 8-7 summarizes the diagnostic procedures
performed to visualize these organs.
Additional diagnostic procedures used to evaluate
the GI system are laparoscopy, magnetic resonance
imaging (MRI), and positron emission tomography
(PET) scans. These methods are described in the
following sections.
LAPAROSCOPY
Laparoscopy is the insertion of a laparoscope (a fiberop-
tic tube) into the abdominal cavity through a small inci-
sion to the left of and above the umbilicus. To perform
this procedure, a local anesthetic is given, and gas
(i.e., nitric oxide or carbon dioxide) is infused into the
abdominal cavity to allow better visualization and
manipulation of the scope. Box 8-2 describes the
diagnostic and therapeutic interventions that may be
performed with a laparoscope.21,22

FIGURE 8-2
The four abdominal quadrants, showing the viscera found in each. (From Palastanga N, Field D,
Soames R. Anatomy and Human Movement: Structure and Function [2nd ed]. Oxford, UK:
Butterworth-Heinemann, 1989;783.)
302 CHAPTER 8 Gastrointestinal System

Table 8-4 Laboratory Tests for the Gastrointestinal System*

Test Description
Carcinoembryonic antigen (CEA) Purpose: tumor marker used to monitor recurrence of colorectal
Reference value: cancer.
Adult nonsmoker <2.5 ng/ml Venous blood is drawn periodically to monitor for increases above
Adult smoker: up to 5 ng/ml the reference range, indicating recurrence of colorectal cancer
and presence of metastases.
Gastric stimulation test (tube gastric analysis, Purpose: to evaluate the ability of the stomach to produce acid
pentagastrin stimulation test, gastric acid secretions in a resting state and after maximal stimulation.
stimulation test) Stomach acids are aspirated by a nasogastric tube during resting
Reference value: gastric pH 1.5-3.5 states (basal output) and after injection of pentagastrin to
Basal acid output: stimulate gastric acid stimulation (peak output).
Male, 0-10.5 mEq/hr; female, 0-5.6 mEq/hr Increased values can occur with duodenal ulcers and
Peak acid output: Zollinger-Ellison syndrome.
Male, 12-60 mEq/hr; female, 8-40 mEq/hr Decreased values can occur with gastric ulcers or cancer.
Gastrin (elevated) Hormone that stimulates the release of HCl in stomach
Reference value: 25-90 pg/ml Purpose: to confirm the diagnosis of Zollinger-Ellison syndrome.
Elevated levels of gastrin in venous blood occur with
Zollinger-Ellison syndrome.
Helicobacterpylori tests Purpose: to confirm the diagnosis of H. pylori infection, which is
the cause of most peptic ulcers and is a proven carcinogen for
gastric carcinoma.
Serologic test Purpose: to identify the presence of immunoglobulin G antibody
Reference value: immunoglobulin to H. pylori in the blood.
G negative
Urea breath test Purpose: to identify the presence of H. pylori in the stomach.
Reference value: negative
Tissue biopsy Purpose: to visualize H. pylori bacteria.
Reference value: negative for H. pylori A tissue biopsy is obtained during an endoscopy procedure and
microscopically examined.
5-Hydroxyindoleacetic acid (5-HIAA) Purpose: to diagnose a carcinoid tumor and provide ongoing
Reference value: 1-9 mg/24 hrs evaluation of tumor stability.
5-HIAA is a urinary metabolite of serotonin and is produced by
most carcinoid tumors.
Jejunal/duodenal biopsy Purpose: to assist in diagnosis of GI disorders such as irritable bowel
Reference value: negative for histological syndrome, Celiac disease, and malabsorption syndromes.
in sample tissue Biopsies of small bowel are taken and examined for histologic
changes that are consistent with above condition(s).
Lactose tolerance test (oral lactose Purpose: to identify lactose intolerance—lactase deficiency as a
tolerance test) cause of abdominal cramps and diarrhea, as well as to help identify
Reference value: the cause of malabsorption syndrome.
Blood glucose >30 mg/dl An oral dose of lactose is provided to a fasting patient, and serial
Urine lactose 12-40 mg/dl in 24 hours blood and urine samples are measured.
Minimal rise in blood glucose or urine lactose levels indicates
lactose intolerance—lactase deficiency.
Occult blood (fecal occult blood test, Purpose: a screening tool for early diagnosis of bowel cancer.
FOBT, FOB) Three stool specimens are collected and examined for the presence
Reference value: negative of occult (nonvisible) blood in the feces, which can be indicative
of adenocarcinoma and premalignant polyps in the colon.
 Table 8-4 Laboratory Tests for the Gastrointestinal System*—cont’d

Test Description
Serotonin (5-hydroxytryptamine) Purpose: to detect a carcinoid tumor.
Reference value: 50-200 ng/ml Venous blood levels of serotonin are measured, as carcinoid
tumors secrete excess amounts of serotonin.
*Text or abbreviations in parentheses signify synonyms to the test names.
Data from Malarkey LM, McMorrow ME (eds). Nures’s Manuel of LaboratoryTests and Diagnostic Procedures. Philadelphia: Saunders,
2001;412-431;Tornbolm H, Lindberg G, Nyberg B, et al. Full-thickness biopsy of the jejunum reveals inflammation and enteric neuropathy
in irritable bowel syndrome. Gastroenterology 2002;123(6):1972-1979

Table 8-5 DIAGNOSTIC PROCEDURES FOR THE GASTROINTESTINAL (GI) SYSTEM*

Test Description
Barium enema (BE) Purpose: to investigate and identify pathologic conditions that change the
Reference value: structure or function of the colon (large bowel).
No lesions, deficits, or The colon is emptied of feces, and contrast medium (barium) is instilled
abnormalities of the colon are rectally. Fluoroscopic and x-ray images are then taken to identify the
noted. presence of any structural anomalies.

Barium swallow (esophagography)
Reference value: No structural or
functional abnormalities are
visualized.
Colonoscopy (lower panendoscopy)
Reference value: No abnormalities
of structure or mucosal surface are
visualized in the colon or terminal
ileum.
Computed tomography of the GI tract
(CTscan, computerized axial
tomography [CAT])
Esophageal manometry
Reference value: Lower esophageal
sphincter (LES) pressure:
12-25 mm Hg.
Esophageal pH
Reference value: pH between
4 and 4.5%
Acid perfusion test (Bernstein test)
Reference value: Negative
Esophagogastroduodenoscopy
(EGD, upper gastrointestinal
endoscopy)
Purpose: to identify pathologic conditions that change the structure or function
of the esophagus.
The patient takes repeated swallows of barium liquid while x-ray and
fluoroscopic images are taken in vertical, semivertical, and horizontal
positions to examine the passage of contrast medium during swallowing and
peristaltic movement of the esophagus.
Purpose: to perform routine screening of the colon for the presence of polyps
or tumors and to investigate the cause of chronic diarrhea or other
undiagnosed GI complaints.
Patients are sedated, and an endoscope is inserted into the rectum and passed
through the various parts of the colon.Tissue biopsy may be performed
during this procedure.
Purpose: to detect intraabdominal abscesses, tumors, infarctions, perforation,
obstruction, inflammation, and diverticulitis. Metastases to the abdominal
cavity can also be detected. Intravenous or oral contrast may be used during
the procedure.
Purpose: to evaluate esophageal motor disorders that could be causing
dysphagia, placement of intraluminal devices, and preoperative evaluation of
patients who are being considered for antireflux surgery to rule out other
possible diagnoses.
LES pressures are measured with an endoscope that is inserted into the
esophagus either nasally or orally.
Purpose: to evaluate changes in esophageal pH levels via capsule that
is implanted into esophageal mucosa 5-6 cm above the gastroesophageal
junction. Monitoring takes place over 24- 48 hours.
Purpose: to determine that heartburn is of esophageal rather than
cardiac origin.
N. hydrochloric acid is instilled into the esophagus through the endoscope or
nasogastric tube. Complaints of heartburn with acid instillation confirm the
esophageal origin.
Purpose: to identify and biopsy tissue abnormality; to determine the location
and cause of upper GI bleeding; to evaluate the healing of gastric ulcers; to
evaluate the stomach and duodenum after gastric surgery; and to investigate
Continued
304 CHAPTER 8 Gastrointestinal System
Table 8-5 DIAGNOSTIC PROCEDURES FOR THE GASTROINTESTINAL (GI) SYSTEM*—cont’d
Test
Reference value: No abnormal
structures or functions are
observed in the esophagus,
stomach, or duodenum.
Gallium scan (gallium 67 imaging,
total body scan)
Reference value: No structural or
functional abnormalities are
visualized.
Gastric emptying scan
Reference value: No delay in gastric
emptying.
Gastrografin study
GI bleeding scan (GI scintigraphy)
Reference value: No evidence of
focal bleeding.
GI cytologic studies
Reference value: No evidence of
abnormal cells or infectious
organisms.
KUB (Kidneys, Ureters, Bladder)
X-Ray
Paracentesis and peritoneal fluid
analysis (abdominal paracentesis,
abdominal tap)
Reference value: Clear, odorless,
pale yellow.
Sigmoidoscopy and anoscopy
Reference value: No tissue
abnormalities are visualized in the
sigmoid colon, rectum, or anus.
Upper GI series and small bowel
series (small bowel follow-through)
Reference value: No structural or
functional abnormalities are found.
*Text or abbreviations in parentheses signify synonyms to the test names.
Data from Malarkey LM, McMorrow ME (eds). Nurse’s Manual of LaboratoryTests and Diagnostic Procedures. Philadelphia: Saunders,
2000;432-468.
Description
the cause of dysphagia, dyspepsia, gastric outlet obstruction, or
epigastric pain.
An endoscope is passed through the mouth into the esophagus to the stomach,
pylorus, and upper duodenum.Tissue biopsy can be performed during the
procedure.
Purpose: to locate malignancy, metastases, sites of inflammation, infection,
and abscess.A radionuclide is injected intravenously with images taken
in the following time frames:
4-6 hours later to identify infectious or inflammatory disease
24 hours later to identify tumors
72 hours later to identify infectious disease
Purpose: to investigate the cause of a rapid or slow rate of gastric emptying and
to evaluate the effects of treatment for abnormal gastric motility.
In a sitting position, the patient ingests a radionuclide mixed with food
substances, and images are taken of the stomach and duodenum for the
next 3 hours (15-minute intervals).The rate of gastric emptying is then
calculated from the images.
Purpose: to evaluate anatomical status of esophagus
Similar to barium swallow, except Gastrografin is used as an imaging agent.
Purpose: to evaluate the presence, source, or both, of GI bleeding.
Radionuclide-labeled red blood cells are injected intravenously, followed by
intermittent imaging studies of the abdomen and pelvis for up to 24 hours.
Purpose: to identify benign or malignant growth from tissue biopsy
of the GI tract.
Tissue specimens are obtained during an endoscopic examination.
Purpose: to provide x-ray image of abdomen.
Kidneys, ureters, bladder, small, and large intestines are visualized and resulting
images can be used in assisting with diagnosis of conditions to these organs.
Purpose:To help delineate the cause of ascites or suspected bowel per-foration
along with evaluating the effects of blunt abdominal trauma.
The peritoneal cavity is accessed with either a long thin needle or a trocar
and stylet with the patient under local anesthesia. Peritoneal fluid is collected
and examined.
Peritoneal tissue biopsy can also be performed during this procedure for
cytologic studies required for the differential diagnosis of tuberculosis,
fungal infection, and metastatic carcinoma.
Purpose: Sigmoidoscopy is used as a screening tool for colon cancer and to
investigate the cause of rectal bleeding or monitor inflammatory bowel
disease. Anoscopy is used to investigate bleeding, pain, discomfort, or
prolapse in the anus.
Purpose: to detect disorders of structure or function of the esophagus,
stomach and duodenum, and jejunum and ileum (the latter two are for
the small bowel series).
Imaging studies of all these areas are performed while the patient drinks a
barium solution. Passage of the barium through these structures can range
from 30 minutes to 6 hours.

Table 8-6 LABORATORY TESTS FOR THE HEPATIC, BILIARY, AND PANCREATIC SYSTEMS*
Test
Alanine aminotransferase (ALT, glutamic-
pyruvic transaminase [GPT], SGPT,
transaminase)
Reference value: 10-35 IU/L
Alkaline phosphatase (ALP, total alkaline
phosphatase [T-ALP])
Reference value: 4.5-13.0 King-Armstrong
units/dl
Alkaline phosphatase isoenzymes (I-ALP)
Reference value: liver isoenzymes
50%-70%
Alpha 1-fetoprotein (AFP1)
Reference value: <10 ng/ml
Ammonia (NH3)
Reference value: 15-45 pg/dl
Amylase, serum
Reference value: 27-131 U/L
Amylase, urine
Reference values:
2-19 U/hr (1-hr test)
4-37 U/2 hrs (2-hr test)
170-2,000 U/24 hrs (24-hr test)
Aspartate aminotransferase (AST, glutamate
oxaloacetate transaminase [GOT], SGOT,
transaminase)
Reference value: 8-20 U/L
Bilirubin
Reference values:
Total, 0.3-1.2 mg/dl
Direct (conjugated), 0-0.2 mg/dl
Indirect (unconjugated), <1.1 mg/dl
Carbohydrate antigen 19-9 (CA 19-9)
Reference value: <37 U/ml
Ceruloplasmin (stores copper and involved in
metabolism of iron)
Reference value: 18-45 mg/dl
Gastrointestinal System CHAPTER 8 305
Involved Systems Purpose
Hepatic To detect hepatocellular injury.
Very specific in detecting acute hepatitis from
viral, toxic, or drug-induced causes.
Hepatic, biliary Nonspecific indicator of liver disease, bone
disease, or hyperparathyroidism.
Nonspecific tumor marker for liver or bone
malignancy.
Hepatic, biliary Used to distinguish between liver and bone
pathology when total serum ALP is elevated.
There are ALP isoenzymes for both liver and
bone.
Hepatic, biliary A tumor marker for hepatocellular carcinoma in
nonpregnant adults.
AFP normally exists during pregnancy;
otherwise, levels are very low.
Hepatic To evaluate or monitor liver failure,
hepatoencephalopathy, and the effects of
impaired portal vein circulation.
Ammonia is a by-product of protein metabolism
and is converted to urea in the liver.
Pancreatic To assist in diagnosis of acute pancreatitis and
traumatic injury to the pancreas or as surgical
complication of the pancreas.
Pancreatic To confirm diagnosis of acute pancreatitis when
serum amylase levels are normal or borderline
elevated.
Hepatic Primarily indicates inflammation, injury, or
necrosis of the liver.
AST is highly concentrated in the liver, but it is
also minimally present in skeletal muscle,
kidney, brain, pancreas, spleen, and lungs.
Hepatic, biliary Used to evaluate liver function, diagnose
jaundice, and monitor progression of jaundice.
Total bilirubin is the sum of direct and indirect
bilirubin.
Elevation in direct (conjugated) bilirubin
indicates hepatic jaundice, whereas elevation in
indirect (unconjugated) bilirubin indicates
prehepatic jaundice.
Hepatic, A tumor marker used in the preoperative staging
pancreatic of pancreatic cancer.
Hepatic cirrhosis can falsely elevate this value in
the absence of pancreatic cancer.
Hepatic Used to evaluate chronic active hepatitis,
cirrhosis, and other liver diseases.
Continued
306 CHAPTER 8 Gastrointestinal System

Table 8-6 LABORATORY TESTS FOR THE HEPATIC, BILIARY, AND PANCREATIC SYSTEMS*—cont’d
Test Involved Systems Purpose
Fecal fat (fecal lipids, quantitative fat, Hepatic, biliary The definitive test to identify steatorrhea (high
72-hr stool collection, quantitative stool fat) levels of fat in the feces).This can be caused
Reference value: <7 g/24 hrs by hepatobiliary, pancreatic, and small
intestine disease.
Gamma-glutamyltransferase Hepatic, biliary, Used to detect hepatobiliary disease.
(g-glutamyl-transferase [GT], pancreatic Levels will rise with posthepatic jaundice and
g-glutamyl- transpeptidase other diseases of the liver and pancreas.
[GGT, GGTP, GTP])
Reference values:
Male, 22.1 U/liter
Female, 15.4 U/liter
Hepatitis virus tests Hepatic Distinguishes between the six types of viral
Reference value: negative (no presence hepatitis (HAV, HBV, HCV, HDV, HEV, HGV).
of antibodies) Presence of distinct antibodies for a specific virus
will help confirm the diagnosis and assist with
treatment planning.
Lipase Biliary, pancreatic Used to diagnose pancreatitis and pancreatic
Reference value: <200 U/L disease. Lipase is a digestive enzyme used to
digest fatty acids.
Elevated levels indicate onset of acute
pancreatitis
50 -Nucleotidase (50 N, 50 -NT) Hepatic, biliary, Works as a catalyzing enzyme
Reference value: 2-17 IU/L pancreatic Elevated levels help to identify extrahepatic or
intrahepatic biliary obstruction and cancer
of the liver.
Protein electrophoresis Hepatic Separates plasma proteins (albumin and
Reference value: albumin, 3.5-5.0 g/dl globulins) from the plasma to detect the
specific amounts of each protein type.
Decreased plasma protein levels are indicative
of hepatobiliary disease.
Serum proteins (albumin) Hepatic Provides general information about the
Reference value: 3.5-5.0 g/dl nutritional status, the oncotic pressure
of the blood, and the losses of protein
associated with liver, renal, skin, or
intestinal diseases.
Prothrombin time (PT, protime) Hepatic Elevated values are indicative of liver disease,
Reference value: 10-13 sec as the liver synthesizes clotting factors II,
VII, IX, and X.
Sweat test (sweat chloride, cystic fibrosis Pancreatic Gold Standard Test used to diagnose cystic
sweat test, iontophoresis sweat test) fibrosis in children, as these children have
Reference value: 5-40 mEq/L higher contents of sodium and chloride in
their sweat.
Urobilinogen, urine Hepatic, Used to screen for evidence of hemolytic
Reference value: biliary anemia or as an early indicator of liver cell
Male, 0.3-2.1 mg/2 hrs damage.
Female, 0.1-1.1 mg/2 hrs
*Text or abbreviation in parentheses signifies synonyms to the test names.
Data from reference numbers 4, 13, 15, 16.
 Gastrointestinal System CHAPTER 8 307

Table 8-7 DIAGNOSTIC PROCEDURES FOR THE HEPATIC, BILIARY, PANCREATIC, AND
SPLENIC SYSTEMS

Test Purpose
Computed tomography (CT) of Used to identify the presence of tumor, abscess, cyst, sites of bleeding, or
the liver, biliary tract, hematoma in these organs.
pancreas, and spleen Contrast medium may be used with CTscan of the liver and pancreas.
Endoscopic retrograde Used to investigate the cause of obstructive jaundice, persistent abdominal pain, or
cholangiopancreatography both.
and pancreatic cytology Generally identifies stones in the common bile duct as well as chronic pancreatitis
(ECRP)* and cancer.
HIDA (heptoiminodiacetic Purpose: to examine the gallbladder and the biliary ducts leading out of it.
acid) scan Radioactive material (HIDA) is injected into the patient, absorbed by the liver,
and excreted through biliary ducts; can diagnose obstructions in the ducts.
Liver biliary scan A radionuclide is injected intravenously, and imaging of the hepatobiliary system,
gallbladder, and biliary tree is performed to help diagnose acute or chronic
biliary tract disorder.
Liver biliary biopsy, To diagnose pathologic changes in the liver and monitor disease progression.
percutaneous
Liver-spleen scan A radionuclide is injected intravenously, and imaging of the liver and spleen is
performed.
Used to confirm and evaluate suspected hepatocellular disease and enlargement of
the liver or spleen.
Magnetic resonance Imaging test used to visualize gallbladder, biliary ducts, and pancreatic ducts. Can
cholangiopancreatography identify obstructions (stones) and other pathology in the gallbladder and ducts.
(MRCP)
Ultrasound of the liver, biliary Primary diagnostic tool for examining the liver, spleen, gallbladder, and pancreas.
tract, pancreas and spleen Cyst, abscess, hematoma, primary neoplasm, and metastatic disease can be detected
in the liver.
It is the best diagnostic tool to identify gallstones.
Pancreatic abscesses and tumors can also be identified.
*Text or abbreviation in parentheses signifies synonyms to the test names.
Data from reference numbers 4, 13, 15, 16.

MAGNETIC RESONANCE IMAGING Clinical uses of PET for the GI system include evalua-
The use of MRI of the GI system is primarily indicated tion of liver disease, pancreatic function, and GI
for imaging of the liver for hepatic tumors, iron over- cancer.23,30
load, and hepatic and portal venous occlusion.
Otherwise, computed tomography scans are preferred
for the visualization of other abdominal organs.23-25
Good success, however, has been reported recently in PATHOPHYSIOLOGY
using MRI for defining tissue borders for managing
and resecting colorectal tumors.26,27 MRI has also GI disorders can be classified regionally by the
been successful in helping to delineate the etiology of structure involved and may consist of the following:
cirrhosis between alcohol abuse and viral hepatitis.28,29  Motility disorders
 Inflammation or hemorrhage
POSITRON EMISSION TOMOGRAPHY  Enzymatic dysfunction
PET is the use of positively charged ions to cre-  Neoplasms
ate color images of organs and their functions.  Morbid obesity
308 CHAPTER 8 Gastrointestinal System
BOX 8-2 LAPAROSCOPIC UTILIZATION
Diagnostic
 Direct visualization
 Define and examine locations of
intraabdominal hemorrhage after blunt trauma
 Tissue biopsy
 Hepatic disease, staging of Hodgkin’s disease
and non-Hodgkin’s lymphoma, metastatic
disease, tuberculosis
 Fluid aspiration
 Determination of the etiology of ascites (free
fluid in the peritoneal cavity)
 Evaluation of patients with fever of unknown
origin
 Evaluation of patients with chronic or
intermittent abdominal pain
Therapeutic
 Aspiration of cysts and abscesses
 Lysis of adhesions
 Ligation of fallopian tubes
 Ablation of endometriosis or cancer by laser
 Cholecystectomy (gallbladder removal)
 Appendectomy
 Inguinal herniorrhaphy (hernia repair)
 Gastrectomy
 Colectomy
 Vagotomy
 Gastric bypass
Data from Eastwood GL, Avunduk C (eds). Manual of
Gastroenterology (2nd ed). Boston: Little Brown, 1994;27;
Malarkey LM, McMorrow ME (eds). Nurse’s Manual of
LaboratoryTests and Diagnostic Procedures. Philadelphia:
Saunders, 2000;537-540; Sheipe M. BreakingThrough Obesity
with Gastric Bypass Surgery. Nurse Pract 2006;31(10):12-21.
Esophageal Disorders
DYSPHAGIA
Dysphagia, or difficultyswallowing, can occur fromvar-
ious etiologies and is generallyclassified by the causative
factors ( Table 8-8). Dysphagia can also be classified by
its location as (1) proximal (cervical) or oropharyngeal
dysphagia or (2) distal or esophageal dysphagia.
Proximal dysphagia is difficulty swallowing in the
upper, or proximal, region of the esophagus and
generally results from neurologic or neuromuscular
etiologies, such as stroke, myasthenia gravis, or poly-
myositis.31-33
Table 8-8 Classification and Common Etiologies
of Dysphagia
Classification Common Etiologies
Obstructive Benign or malignant (squamous cell
carcinoma or adenoma) neoplasms,
cervical osteophyte, or bone spur.
Esophageal diverticula, rings, and
webs are anatomic abnormalities
that disrupt the normal cylindrical
shape of the esophagus.
Webs and diverticula tend to occur
proximally, whereas rings generally
occur distally at the
gastroesophageal junction.
Inflammatory Tonsillitis, pharyngitis, epiglottitis,
or infectious esophagitis, gastroesophageal reflux
disease.
Candida or herpes viruses (herpes
simplex, cytomegalovirus) are
causative agents in chronically
debilitated or
immunocompromised patients.
Neurologic Stroke, parkinsonism, amyotrophic
lateral sclerosis, multiple sclerosis,
myasthenia gravis.
Congenital Tracheoesophageal fistula, esophageal
compression by anomalous artery.
Data from Bailey BJ. Dysphagia: Uncovering the Cause WhenYour
Patient HasTrouble Swallowing. Consultant 1997;37(1):75; GageTP.
Esophageal Rings,Webs, and Diverticula. In MM van Ness, SJ
Chobanian (eds), Manual of Clinical Problems in Gastroenterology.
Boston: Little, Brown, 1994;32; Shay SS, van Ness MM. Infectious
Esophagitis. In MM van Ness, SJ Chobanian (eds), Manual of
Clinical Problems in Gastroenterology. Boston: Little, Brown,
1994;35.
Distal dysphagia is difficulty swallowing in the
lower, or distal, portion of the esophagus and is usu-
ally the result of mechanical obstruction to flow
from peptic strictures, mucosal rings, or malignant
neoplasms, such as squamous cell carcinoma and
adenocarcinoma of the esophagus.31-33
Dysphagia can also be characterized by whether or
not (1) it occurs with ingestion of solids, liquids, or
both; (2) it is accompanied by chest pain or heartburn;
(3) it is intermittent, constant, or progressive; and (4)
the patient complains of regurgitation or coughing
while eating. The location at which the food becomes
stuck should also be noted.31,32

MOTILITY DISORDERS AND ANGINA-LIKE
CHEST PAIN
Poor esophageal motility from smooth muscle spasms
or abnormal contraction patterns can present as anterior
chest pain and mimic anginal symptoms. Systematic
cardiac and GI workup should establish the differential
diagnosis. The following are common esophageal
motility disorders34:
Achalasia is a neuromuscular disorder of esopha-
geal motility characterized by esophageal dilation
and hypertrophy, along with failure of the lower
esophageal sphincter to relax after swallowing. A func-
tional obstruction then results from elevated sphinc-
ter pressure. A definitive etiology is currently
unknown. Suspected causes include autoimmune
dysfunction and genetic predisposition. Clinical
manifestations can include episodes of regurgitation,
chest pain while eating, and possible aspiration
pneumonia.32,35-37
Diffuse esophageal spasm is characterized by the
occurrence of normal peristalsis in the upper one-
third of the esophagus and intermittent nonperi-
staltic, simultaneous contractions of the body of the
esophagus. Clinical manifestations include intermit-
tent chest pain with or without eating. Patients will
also demonstrate a characteristic ‘‘cork-screw’’ pattern
on barium-swallow studies. The etiology is unknown,
and management is directed at smooth muscle
relaxation with pharmacologic agents.32,34,35,38
GASTROESOPHAGEAL REFLUX DISEASE
Gastroesophageal reflux disease (GERD) is character-
ized by gastric acid backflow into the esophagus as a
result of improper lower esophageal sphincter relax-
ation. Clinical manifestations include complaints of
heartburn (especially with sour or bitter regurgitation),
nausea, gagging, cough, or hoarseness. Although
the exact etiology of GERD is unknown, smoking,
along with the consumption of fats, alcohol, coffee,
or chocolate, has been associated with this inappro-
priate relaxation. Esophageal and gastric motility
disorders may also contribute to GERD. Gastroeso-
phageal reflux is a strong predisposing factor for
developing esophageal adenocarcinoma. Depending
on the severity of GERD, treatment can range
from either dietary modifications (avoid risk factors
and eat small frequent meals in an upright position),
antacids, antisecretory agents, or surgery. 32,39-41
Advancements in fundoplication have shown
Gastrointestinal System CHAPTER 8 309
good long-term outcomes in improving GERD
symptoms.42
BARRETT’S ESOPHAGUS
Barrett’s esophagus is a disorder in which columnar
epithelium replaces the normal stratified squamous
mucosa of the distal esophagus and is generally associat-
ed with chronic GERD. The mechanism of cellular
metaplasia is thought to occur from chronic inflam-
matory injury from acid and pepsin that refluxes from
the stomach into the distal esophagus.43,44 Barrett’s
esophagus is also a strong predisposing factor for devel-
oping esophageal adenocarcinoma, the incidence of
which has risen in the 1990s.44-46
Associated signs and symptoms include dysphagia,
esophagitis, ulceration, perforations, strictures, bleed-
ing, or adenocarcinoma.28,44,47 Treatment for Barrett’s
esophagus includes controlling symptoms of GERD
and promising new therapies that include endoscopic
ablation therapy combined with proton pump inhibi-
tion (for acid secretion control). Ablation therapy
includes such techniques as photodynamic therapy,
multipolar polar electrocautery, laser therapy, and,
most recently, argon plasma coagulation.43
ESOPHAGEAL VARICES
Varices are dilated blood vessels in the esophagus
caused by portal hypertension and may result in hemor-
rhage that necessitates immediate medical and, usually,
surgical management. Alcohol abuse is an associated
risk factor.48 Refer to the Cirrhosis section later in this
chapter for more information on portal hypertension
and alcoholic cirrhosis.
ESOPHAGEAL CANCER
A description of esophageal cancers with respect to
evaluation and management can be found in the
Cancers in the Body Systems section in Chapter 5.
CLINICAL TIP
 Patients who are s/p esophagectomy may likely have
chest tubes. Please refer to Appendix Table III-A.6
for chest tube management.
 Physical therapists should be aware of any
positioning precautions for patients with esophageal
disorders that may exacerbate their dysphagia or
GERD.
310 CHAPTER 8 Gastrointestinal System
Stomach Disorders
GASTROINTESTINAL HEMORRHAGE
Bleeding in the GI system can occur in either the upper
GI system (upper gastrointestinal bleed [UGIB]) or in
the lower GI system (lower gastrointestinal bleed
[LGIB]). A UGIB can result from one or more of
the following: (1) duodenal ulcers, (2) gastric erosion,
(3) gastric ulcers, (4) esophageal varices, and (5) use
of nonsteroidal antiinflammatory drugs (NSAIDs).
An LGIB can result from one or more of the following:
(1) inflammatory bowel disease (such as diverticulitis),
(2) neoplasms, and (3) anal and rectal lesions
(e.g., hemorrhoids).49-52
GI bleeds can be small and require minimal to no
intervention or very severe and constitute medical
emergencies because of hemodynamic instability that
can lead to shock. Hematemesis or dark brown
(‘‘coffee-ground’’) emesis (vomitus), hematochezia
(passage of blood from the rectum), and melena
(black, tarry stools) from acid degradation of hemoglo-
bin are the primary clinical manifestations of GI bleeds.
Patients are generally stabilized hemodynamically
with intravenous (IV) fluids, blood transfusions, or
both before the cause of bleeding can be fully deli-
neated. Nasogastric tubes (see Appendix Table III-A.6)
are typically used in the stabilization and management
of UGIB. Management is targeted at the causative
factors that resulted in either UGIB or LGIB.
Endoscopy, colonoscopy, or sigmoidoscopy can be
performed to help evaluate or treat the source of
upper or lower GI hemorrhage.49,50,52,53
GASTRITIS
Gastritis is the general term used to describe diffuse
inflammatory lesions in the mucosal layer of the
stomach. Gastritis can be classified as acute, chronic
nonerosive, or chronic erosive.
Etiology of acute gastritis includes associations with
smoking, alcohol abuse, aspirin, NSAIDs, and cortico-
steroid use, as well as physiologic stress and intense
emotional reactions. Clinical manifestations of acute
gastritis include nondescript complaints of burning or
discomfort in the stomach. Management of acute gas-
tritis involves removing the causative risk factors and
relieving the mucosal inflammation.35,54,55
The etiology of chronic nonerosive gastritis has been
definitively linked to Helicobacter pylori bacterial infec-
tion, which is thought to be transmitted by human-to-
human contact. 35,54,56,57 Patients with H. pylori gastritis
may be asymptomatic until the gastritis leads to gastric
ulceration, in which case there will be complaints of
dull, gnawing abdominal pain that typically occurs
when the stomach is empty.54 Management of H. pylori
gastritis includes triple or quadruple antibiotic thera-
pies, in combination with antacid medication, to eradi-
cate the bacterial infection. The primary antibiotics
used include metronidazole (Flagyl, Protostat) and
clarithromycin (Biaxin) and amoxicillin.58 Antacid
medication can include any one of the following:
omeprazole (Prilosec), lansoprazole (Prevacid), rabe-
prazole (Aciphex), pantoprazole (Protonix), and esome-
prazole (Nexium).54,56,57,59
The etiology of chronic erosive gastritis includes
NSAIDs and alcohol abuse. Clinical manifestations can
range from being asymptomatic to having anorexia ner-
vosa, gastric pain, nausea, and vomiting. Management of
chronic erosive gastritis involves removing the causative
risk factors and, possibly, antibiotic therapy similar to
that used for H.pylori gastritis.54
PEPTIC ULCER DISEASE
A peptic ulcer is a loss of the mucosal surface through
the muscularis mucosa of the esophagus, stomach, or
duodenum that is at least 5 mm in diameter.60 Peptic
ulcers can be classified as acute or chronic. Acute
peptic ulcers have lesions that involve the full thickness
of the mucosa, whereas chronic peptic ulcers have
lesions of varying depths. Peptic ulcers occur primarily
in the stomach or the first part of the duodenum, or
both.35
GASTRIC ULCER. Ulceration in the stomach is char-
acterized by a well-defined perforation in the gastric
mucosa that extends into the muscularis mucosa.61,62
Gastric ulcers are less common than duodenal ulcers;
however, patients with gastric ulcers have the highest
mortality rate among patients with peptic ulcer
disease. Patients with gastric ulcers apparently have
normal gastric acid secretion but have lowered
defense mechanisms in the mucosal lining to protect
against acid secretion. Other highly causative factors
for gastric ulcer include H. pylori infection and use of
NSAIDs.60,62 However, high levels of physiologic
and emotional stress cannot be ruled out as a contribut-
ing factor in the development of gastric ulcer
formation.63,64
Symptoms of a gastric ulcer may include abdominal
pain during or shortly after a meal, nausea with or with-
out vomiting, or both. Management of gastric ulcers
may consist of any or all of the following: modification
or elimination of causative agents, antacids, and
H. pylori therapies (see the Gastritis section).60,61

DUODENAL ULCER. Duodenal ulcers are more
common than gastric ulcers and are defined as a chronic
circumscribed break in the mucosa that extends
through the muscularis mucosa layer and leaves a resid-
ual scar with healing. Duodenal ulcers are also caused
by H. pylori and use of NSAIDs.65 Other risk factors
for developing duodenal ulcers include tobacco use,
chronic renal failure, alcoholic cirrhosis, renal trans-
plantation, hyperparathyroidism, and chronic obstruc-
tive pulmonary disease.
Clinical manifestations of duodenal ulcer disease
may include sharp, burning, or gnawing epigastric
pain that may be relieved with food or antacids.
Abdominal pain can also occur at night. Management
of duodenal ulcers is similar to that of gastric ulcers.60,61
ZOLLINGER-ELLISON SYNDROME
Zollinger-Ellison syndrome is a clinical triad that
includes gastric acid hypersecretion, recurrent peptic
ulcerations, and a non-beta islet cell tumor (gastrinoma)
in the pancreas. Symptoms mimic peptic ulcer disease,
but consequences are more severe if left untreated.
Patients with Zollinger-Ellison syndrome may also
present with diarrhea. Management is primarily
directed at surgical resection of the gastrinoma, along
with decreasing gastric acid hypersecretion.60,66-68
GASTRIC EMPTYING DISORDERS
Abnormal gastric emptying is described as either
decreased or increased emptying. Decreased gastric
emptying is also referred to as gastric retention or gastropa-
resis and may result from or be associated with (1) pyloric
stenosis as a consequence of duodenal ulcers, (2) hyper-
glycemia, (3) diabetic ketoacidosis, (4) electrolyte
imbalance, (5) autonomic neuropathy, (6) postoperative
stasis, and (7) pernicious anemia.69 Pharmacologic
intervention to promote gastric motility is indicated
for patients with decreased gastric emptying disorders.
Enhanced gastric emptying (also known as dumping
syndrome) is associated with an interruption of normal
digestive sequencing that results from vagotomy, gas-
trectomy, or gastric or duodenal ulcers. Gastric peristal-
sis, mixing, and grinding are disturbed, resulting in
rapid emptying of liquids, slow or increased emptying
of solids, and prolonged retention of indigestible
solids.69 With enhanced gastric emptying, blood glu-
cose levels are subsequently low and can result in signs
and symptoms of anxiety, sweating, intense hunger, diz-
ziness, weakness, and palpitations. Nutritional and
pharmacologic management are the usual treatment
choices.70
Gastrointestinal System CHAPTER 8 311
GASTRIC CANCER
The most common malignant neoplasms found in the
stomach are adenocarcinomas, which arise from
normal or mucosal cells. Benign tumors are rarely
found but include leiomyomas and polyps. For a more
detailed discussion of gastric oncology, see the
Cancers in the Body Systems section in Chapter 5.
Intestinal Disorders
APPENDICITIS
Inflammation of the appendix of the large intestine can
be classified as simple, gangrenous, or perforated.
Simple appendicitis involves an inflamed but intact
appendix. Gangrenous appendicitis is the presence of
focal or extensive necrosis accompanied by microscopic
perforations. Perforated appendicitis is a gross disrup-
tion of the appendix wall and can lead to serious
complications if it is not managed promptly.45 The
etiology of appendicitis includes a combination of
obstruction in the appendix lumen coupled with
infection.35,71
Signs and symptoms of appendicitis may include71-73:
 Right lower quadrant, epigastric, or periumbilical
abdominal pain that fluctuates in intensity
 Abdominal tenderness in the right lower quadrant
 Vomiting with presence of anorexia
 Constipation and failure to pass flatus
 Low-grade fever (no greater than 1028F or 398C)
Management of appendicitis involves timely and
accurate diagnosis of acute appendicitis to prevent per-
foration. Treatment choices include antiinfective
agents or surgical appendectomy.72-74
DIVERTICULAR DISEASE
Diverticulosis is the presence of diverticula, which is
an outpocketing, or herniation, of the mucosa of
the large colon through the muscle layers of the intes-
tinal wall. Diverticular disease occurs when the out-
pocketing becomes symptomatic. Diverticulitis is
the result of inflammation and localized perito-
nitis that occurs after the perforation of a single diver-
ticulum.35,71-73,75
Signs and symptoms of diverticular disease include
the following71:
 Achy, left lower quadrant pain and tenderness
(pain intensifies with acute diverticulitis)
 Pain referred to low back region
 Urinary frequency
 Distended and tympanic abdomen
312 CHAPTER 8 Gastrointestinal System
 Fever and elevated white blood cell count
(acute diverticulitis)
 Constipation, bloody stools, or both
 Nausea, vomiting, anorexia
Management of diverticular disease includes any
of the following71-73,76,77:
 Dietary modifications (e.g., increased fiber)
 Insertion of nasogastric tube in cases of severe
nausea, vomiting, abdominal distention, or any
combination of these
 IV fluids
 Pain medications
 Antiinfective agents
 Surgical repair of herniation, resection (colectomy),
or both with possible colostomy construction.
Video laparoscopic techniques are becoming a more
favored surgical approach for these procedures.75
HERNIA
ABDOMINAL HERNIA. An abdominal hernia is an ab-
normal protrusion of bowel that is generally classified by
the area where the protrusion occurs. These include the
following areas: (1) epigastric, (2) inguinal, (3) femoral,
(4) ventral or incisional, and (5) umbilical.78 Muscle weak-
ening from abdominal distention that occurs in obesity,
surgery, or ascites can lead to herniation through the
musclewall.Herniation mayalso develop congenitally.72,79
Signs and symptoms of abdominal herniation
include72,79:
 Abdominal distention, nausea, and vomiting
 Observable bulge with position changes, coughing,
or laughing
 Pain of increasing severity with fever, tachycardia,
and abdominal rigidity (if the herniated bowel is
strangulated)
Management of herniation includes any of the
following72,79,80:
 Wearing a binder or corset
 Herniorrhaphy (surgical repair, typically with a
laparoscope)
 Hernioplasty (surgical reinforcement of weakened
area with mesh, wire, or fascia)
 Temporary colostomy in cases of intestinal
obstruction
HIATAL HERNIA. A hiatal hernia is an abnormal pro-
trusion of the stomach upward through the esophageal
hiatus of the diaphragm. Causative risk factors for a
hiatal hernia are similar to those for abdominal
hernia. Clinical manifestations include heartburn-like
epigastric pain that usually occurs after eating and
with recumbent positioning.
Management of hiatal hernia can include behavior
modifications, such as avoiding reclining after meals,
eating spicyor acidic foods, drinking alcohol, and smok-
ing tobacco. Eating small, frequent, bland meals con-
taining high fiber content may also be beneficial.
Pharmacologic intervention typically includes acid-
reducing medications.79 In certain cases, when these
measures have proven ineffective, surgical management
of the hiatal hernia can be performed laparoscopically.81
CLINICAL TIP
 Positions associated with bronchopulmonary hygiene
or functional mobility may exacerbate pain in
patients who have a hernia, particularly a hiatal
hernia. Therefore, careful modification of these
interventions will be necessary for successful
completion of these activities.
INTESTINAL OBSTRUCTIONS
Failure of intestinal contents to propel forward can
occur by mechanical or functional obstructions.
MECHANICAL OBSTRUCTION. Blockage of the bowel
by adhesion, herniation, volvulus (twisting of bowel
on itself), tumor, inflammation, impacted feces, or in-
vagination of an adjacent bowel segment constitutes
mechanical obstructions.82
FUNCTIONAL OBSTRUCTIONS (PARALYTIC ILEUS).
Paralytic ileus is defined as ‘‘functional inhibition of
propulsive bowel activity.’’83 Obstructions may result
from abdominal surgery, intestinal distention, hypoka-
lemia, peritonitis, severe trauma, spinal fractures,
ureteral distention, or use of narcotics.72,73
CLINICAL TIP
 Paralytic ileus can be seen after major orthopedic
surgery (e.g., total joint arthroplasty) as a result of
frequent narcotic use for adequate pain control.
 Early mobilization with this (and all postoperative
surgical) populations can help to lessen the
likelihood of this complication.
 Abdominal distention will also have an impact
on other patient functions that may affect how
well they are able to progress with their physical
therapy treatment. The ability to take deep
breaths, reach for objects, and perform bed
mobility will be that much more difficult
secondary to the extra girth associated with
abdominal distention.

Signs and symptoms of intestinal obstructions
include the following72,73:
 Sudden onset of crampy abdominal pain that may
be intermittent in nature as peristalsis occurs
 Abdominal distension
 Vomiting
 Obstipation (inability to pass gas or stool)
 Localized tenderness
 High-pitched or absent bowel sounds (depending on
extent of obstruction)
 Tachycardia and hypotension in presence of dehydra-
tion or peritonitis
 Bloody stools
Management of intestinal obstructions includes any
of the following72,73,83-85:
 Insertion of a nasogastric tube in cases of severe
abdominal distention or intractable vomiting
 Supportive management of functional etiologies
(as able)
 Surgical resection (laparoscopic technique or open
laparotomy) of mechanical obstructions from adhe-
sions, necrosis, tumor, or unresolved inflammatory
lesions, particularly if the obstruction is in the large
intestine
 Colostomy placement and eventual colostomy
closure (Colostomy closure is also referred to as
colostomy takedown.)
INTESTINAL ISCHEMIA
Ischemia within the intestinal tract, also called ischemic
colitis, can be acute or chronic. It can result from many
factors, such as thrombosis or emboli to the superior
mesenteric artery; intestinal strangulation; chronic
vascular insufficiency; hypotension; oral contra-
ceptives (combined with history of thrombophilic
defects) 86; NSAIDs; and vasoconstrictors, such as vaso-
pressin and dihydroergotamine. Methamphetamine
and cocaine have vasoconstrictive properties that can
also lead to intestinal ischemia. Significant ischemia
that is not managed in a timely manner can lead to
intestinal necrosis or gangrene and prove to be a
life-threatening situation.72,73,87,88
Signs and symptoms of intestinal ischemia
include72,73:
 Abdominal pain ranging from colicky pain to a
steady severe ache, depending on the severity of
ischemia
 Nausea and vomiting
 Diarrhea or rectal bleeding
 Rebound tenderness, abdominal distention, and
rigidity (with necrosis)
Gastrointestinal System CHAPTER 8 313
 Tachycardia, hypotension, and fever (with necrosis)
Management of intestinal ischemia includes any of
the following72,87:
 Revascularization procedures, including balloon
angioplasty, bypass grafting, embolectomy, and
endarterectomy
 Resection of necrotic segments with temporary
colostomy or ileostomy placement and subsequent
reanastomosis of functional segments as indicated
 Antiinfective agents
 Vasodilators or vasopressors (blood perfusion
enhancement)
 Anticoagulation therapy
 IV fluid replacement
 Insertion of nasogastric tube
 Analgesic agents
IRRITABLE BOWEL SYNDROME
Irritable bowel syndrome (IBS), also referred to as
functional bowel disorder or spastic colon, is characterized by
inconsistent motility of the large bowel (i.e., constipa-
tion or diarrhea). Motility of the large bowel can be
affected by emotions; certain foods, such as milk pro-
ducts; neurohumoral agents; GI hormones; toxins;
prostaglandins; and colon distention.72,73,89 Recent
findings now suggest that patients with IBS may have
bacterial overgrowth in their small intestines and are
being successfully managed with antibiotic therapy.90
Signs and symptoms of IBS include72,73,89:
 Diffuse abdominal pain, reports of feeling bloated,
or both
 Constipation or diarrhea
 Correlation of GI symptoms with eating, high
emotional states, or stress
 No weight loss
 Tender sigmoid colon on palpation
Management of IBS includes any of the
following72,73,89,91:
 Laxatives or antidiarrheal (loperamide) agents
 Antispasmodic agents
 Dietary modifications, including a food diary to
determine causative risk factors
 Counseling or psychotherapy
 Antibiotic therapy
 Surgery (in rare cases)
MALABSORPTION SYNDROMES
Malabsorption syndrome is a general term for disorders
that are characterized by the small or large intestine’s
failure to absorb or digest carbohydrates, proteins,
fats, vitamins, and electrolytes. This syndrome is
314 CHAPTER 8 Gastrointestinal System
commonly associated with patients who have manifes-
tations of acquired immunodeficiency disease.The nu-
tritional deficits that result from malabsorption can
lead to other chronic disorders, such as anemia or
osteoporosis. Malabsorption syndromes can result
from any of the following72,92-94:
 Chronic pancreatitis
 Pancreatic carcinoma
 Crohn’s disease (see the Crohn’s Disease section)
 Celiac sprue (small intestine mucosal damage from
glutens [e.g., wheat, barley, rye, and oats])
 Amyloidosis (disorder of protein metabolism)
 Lactase deficiency
 Zollinger-Ellison syndrome (see the Zollinger-
Ellison Syndrome section)
 Whipple’s disease (infection of the small intestine by
Tropheryma whippelii bacteria)
Signs and symptoms of malabsorption syndromes
include95:
 Diarrhea, steatorrhea (excessive fat excretion), or both
 Anorexia and weight loss
 Abdominal bloating
 Bone pain
Management of malabsorption syndromes includes
any of the following72,93,95:
 Antibiotic therapy
 Dietary modifications and nutritional support
 Fluid, electrolyte, vitamin, and mineral support
PERITONITIS
Peritonitis is general or localized inflammation in
the peritoneal cavity as a result of bacterial or chemical
contamination. Etiologies can include bacterial infec-
tion, ascites, perforation of the GI tract, gangrene of
the bowel, trauma, and surgical irritants.3,72,73,96
Signs and symptoms of peritonitis include3:
 Fever
 Abdominal guarding with diffuse tenderness and
rigidity
 Abdominal distention
 Diminished or absent bowel sounds
 Nausea, vomiting, or both
 Pain with deep inspirations (therefore shallow
and rapid respirations)
 Tachycardia, hypotension
 Decreased urinary output
Management of peritonitis includes any of the
following3,72,96,97:
 Laparoscopic evaluation, with or without subse-
quent surgical correction of primary etiology
 Antibiotic therapy
 Fluid management with electrolytes and colloids
 Pain management
 Nasogastric suctioning
 Invasive monitoring of central hemodynamic
pressures
CROHN’S DISEASE
Crohn’s disease is a chronic, idiopathic, inflammatory
disorder occurring in any part of the GI system. The
small intestine, particularly the ileum and the proximal
portion of the colon, is most commonly involved,
whereas the esophagus and stomach are rarely affected.
Suspected causes of Crohn’s disease include genetic
predetermination, exaggerated immunologic mechan-
isms, infectious agents, psychological factors, dietary
factors, and environmental factors.72,98,99
Signs and symptoms of Crohn’s disease include the
following:
 Constant crampy abdominal pain, often in right
lower quadrant, not relieved by bowel movement
 Right lower quadrant abdominal mass
 Diarrhea
 Low-grade fever
 Fistula formation
Management of Crohn’s disease includes any of the
following72,98-101:
 Antiinflammatory medications (corticosteroids or
cytokines)
 Antibiotics
 IV fluids and dietary modification and support
(possible total parenteral nutrition use)
 Nasogastric suctioning
 Activity limitations (in acute phases)
 Surgical resection of involved area, either by open
laparotomy or video laparoscopy, with or without
need for ileostomy
Complications of Crohn’s disease can include72,98:
 Intestinal obstruction, possibly leading to fistula,
abscess, or perforations in the intestine
 Inflammation of the eyes, skin, and mucous
membranes
 Arthritis, ankylosing spondylitis
 Colon cancer
 Gallstones
 Vitamin B12 deficiency
 Obstructive hydronephrosis
ULCERATIVE COLITIS
Ulcerative colitis is a chronic inflammation of the intes-
tine limited to the mucosal layer of the colon and
rectum. The definitive etiology of ulcerative colitis is

unknown, but suspected causes are similar to those of
Crohn’s disease. Inflammation can be mild, moderate,
or severe.72,98,99,102
Signs and symptoms of ulcerative colitis
include72,98,102:
 Crampy lower abdominal pain that is relieved by a
bowel movement
 Small, frequent stools to profuse diarrhea (mild to
severe)
 Rectal bleeding
 Fever
 Fatigue with anorexia and weight loss
 Dehydration
 Tachycardia
Management of ulcerative colitis includes any of the
following72,98,101,102:
 Antiinflammatory medications, including steroids
and mesalamine suppositories
 Surgical resection of involved area with probable
ileostomy placement or, more recently, the develop-
ment of the double-stapled ileal reservoir and ileoa-
nal anastomosis, called the J pouch, has been very
effective and favored, as this repair keeps the entire
anal canal intact and avoids an external bag.
 Dietary modification and support (possible total
parenteral nutrition use)
 Activity limitations
 Iron supplements, blood replacement, or both
 Antidiarrheal agents
Related manifestations of ulcerative colitis may
include72,98:
 Arthritis, ankylosing spondylitis
 Inflammation of the eyes, skin, and mucous
membranes
 Hepatitis, bile duct carcinoma
 Colon cancer
POLYPS
GI polyps are usually adenomas that arise from the
epithelium above the mucosal surface of the colon
and rectum. Polyps are generally benign but have
the potential to proliferate into carcinoma of the
colon.72,103
Signs and symptoms of polyps include72,103:
 Rectal bleeding (occult or overt)
 Constipation or diarrhea
 Lower abdominal crampy pain
Management of polyps includes72,103:
 Modification of risk factors for colorectal cancer,
such as obesity, smoking, and excessive alcohol
consumption
Gastrointestinal System CHAPTER 8 315
 Colonoscopy, proctosigmoidoscopy, endoscopy, or
barium enema for detection of the polyp
 Tissue biopsy to determine its malignancy potential
 Polypectomy with electrocautery
 Surgical resection, if indicated, with or without
ileostomy
INTESTINAL TUMORS
Benign or metastatic neoplasms of the intestine include
colonic adenomas (polyps), villous or papillary adeno-
mas, lipomas, leiomyomas, and lymphoid hyperplasia.
Tumors affect motility and absorption functions in the
intestine (see the Cancers in the Body Systems section
in Chapter 5 for further details).
Anorectal Disorders
Disorders of the anus and rectum generally involve
inflammation, obstruction, discontinuity from colon,
perforations, or tumors. The most common disorders
are (1) hemorrhoids, (2) anorectal fistula, (3) anal fis-
sure, (4) imperforate anus, and (5) rectal prolapse.
Signs and symptoms include pain with defecation and
bloody stools. Management is supportive according to
the disorder, and surgical correction is performed as
necessary.
Morbid Obesity
Obesity is a complex disorder with many contributing
metabolic, psychological, and genetic factors.104 It is
defined as a chronic disease characterized by an
excess of body fat.105 The medical standard for
measuring obesity is body mass index (BMI).105 BMI
is determined by dividing the person’s weight in
kilograms by their height in meters squared.105 A
normal BMI is 18.5 to 24.9, overweight is 25 to 29.9,
and obese 30.106
Comorbidities such as diabetes, hypertension, dysli-
pidemia, obstructive sleep apnea, degenerative joint
disease, renal disease, cholelithiasis, and depression
have been linked to morbid obesity.107,108 Conservative
treatment involves weight loss measures such as diet
modifications and behavioral and lifestyle changes;
however, these measures have shown up to a 90%
relapse in weight gain.109 Therefore, surgical treatment
is recommended in these scenarios (assuming that the
patient is medically and psychologically appropriate
for the surgery).
Surgical options include104,109,110:
 Gastric Bypass: Roux-en-Y
 Vertical Gastric Banding
 Adjustable Gastric Banding
316 CHAPTER 8 Gastrointestinal System
CLINICAL TIP
 Following gastric bypass surgery, patients are very
mobile; however, advanced planning prior to
mobilization is essential in order to ensure both
safety of the patient and the treating clinicians,
given the body mass of these patients. It is essential
to have (1) sufficient assistance (in some cases more
than 1 clinician is required), (2) bariatric equipment
(gait/transfer belts, walkers, bed) designed to
accommodate more load, and (3) knowledge of
patient’s prior level of function.
Liver and Biliary Disorders
HEPATITIS
Hepatic inflammation and hepatic cell necrosis may be
acute or chronic and may result from viruses, toxins,
alcohol, leukemias, lymphomas, and Wilson’s disease
(a rare copper metabolism disorder). Viral hepatitis is
the most common type of hepatitis and can be classified
as hepatitis A, B, C, D, E, or G (i.e., HAV, HBV, HCV,
HDV, HEV, and HGV, respectively).
Hepatitis A, B, and C are the most common types of
viral hepatitis, whereas hepatitis G has recently been
discovered. Hepatitis A is transmitted via the fecal-
oral route, mostly from contaminated water sources.
Hepatitis B is more common than hepatitis C, but
both are transmitted through blood and body fluids.
Acute viral hepatitis generally resolves with appropriate
medical management, but in some cases, hepatitis
can become chronic and may ultimately require liver
transplantation.72,111-113
Signs and symptoms of hepatitis include72,111-113:
 Abrupt onset of malaise
 Fever
 Anorexia
 Nausea, abdominal discomfort, and pain
 Headache
 Jaundice
 Dark-colored urine
Management of hepatitis includes any of the
following72,111-113:
 Adequate periods of rest
 Vaccinations (only for HAV, HBV, HDV)
 Fluid and nutritional support
 Removal of precipitating irritants (e.g., alcohol and
toxins)
 Antiinflammatory agents
 Antiviral agents
CLINICAL TIP
 Health care workers who are exposed to blood
and body fluids during patient contact must ensure
that they are properly vaccinated against hepatitis
B and C. This includes receiving periodic
measurements of antibody titers to the viruses
and supplementation with booster shots as needed
to maintain appropriate immunity against these
infections.
 The liver is the only organ in the body with
regenerative properties; therefore, patients with
acute liver inflammation will heal well if given the
proper rest and medical treatment. Physical
therapists should aim not to overfatigue these
patients with functional activities to help promote
proper healing of the liver.
CIRRHOSIS
Cirrhosis is a chronic disease state that is characterized
by hepatic parenchymal cell destruction and necrosis,
and regeneration and scar tissue formation. The scar-
ring and fibrosis that occur in the liver reduce its
ability to synthesize plasma proteins (albumin), clotting
factors, and bilirubin. The primary complications that
can occur from cirrhosis include portal hypertension
(Figure 8-3), ascites, jaundice, and impaired clotting
ability.72,96,113,114
Cirrhosis may result from a variety of etiologies,
including72,113:
 Alcohol or drug abuse
 Viral hepatitis B, C, or D
 Hemochromatosis
 Wilson’s disease
 Alpha1-antitrypsin deficiency
 Biliary obstruction
 Venous outflow obstruction
 Cardiac failure
 Malnutrition
 Cystic fibrosis
 Congenital syphilis
Signs and symptoms of cirrhosis include72,96,113:
 Recent weight loss or gain
 Fatigability
 Jaundice
 Lower-extremity edema
 Anorexia, nausea, or vomiting
 Fever
 Decreased urine output (urine dark yellow or amber)
 Gastrointestinal System CHAPTER 8 317
HEART Signs and symptoms of hepatic encephalopathy that
may progress to coma include115:
Esophagus
 Altered states of consciousness (e.g., lethargy, stupor,
confusion, slowed responses)
Esophageal varices  Neuromuscular abnormalities (e.g., tremor, dyscoor-
LIVER dination, slurred speech, altered reflexes, ataxia,
(left lobe) rigidity, Babinski’s sign, and impaired handwriting)
Enlarged  Altered intellectual function (decreased attention
spleen span, amnesia, disorientation)
Collaterals
 Altered personality and behavioral changes
CIRRHOTIC (euphoria or depression, irritability, anxiety, para-
LIVER noia, rage)
(right lobe) Management of hepatic encephalopathy and coma
may consist of any of the following: 72,96,115
Portal
 Administering nonabsorbable disaccharides, such as
lactulose, is the mainstay of treatment
Splenic vein  Correction of fluid and electrolyte or acid-base
Gallbladder Dilated imbalances, or both
portal vein  Supplemental oxygen
Hepatic artery Blood from bowel  Removal of any precipitating substances
 Gastric lavage or enemas
Inferior vena cava Aorta
 Ammonia detoxicants
 Antiinfective agents
 Surgical correction of causal or contributing factors
FIGURE 8-3
(rare)
Portal hypertension. (From CC Goodman, KS Fuller,
WG Boissonnault [eds]. Pathology: Implications for the
Physical Therapist [3rd ed]. St Louis: Saunders, 2009.) CLINICAL TIP
 Hepatic encephalopathy may also be referred to
 Associated GI manifestations of esophageal varices, as portal systemic encephalopathy (PSE) because of
bowel habit changes, and GI bleeding the association between portal hypertension and
 Altered mental status cirrhosis in the development of encephalopathy.
Management of cirrhosis includes72,113:  Additionally, there is a numeric grading system
 Supportive care, including IV fluids, whole (I to IV) to denote severity of hepatic
blood and blood products, colloid (albumin), vita- encephalopathy.
min and electrolyte replacement, and dietary
and behavioral modifications (eliminate alcohol
consumption) CHOLECYSTITIS WITH CHOLELITHIASIS
 Medical or surgical correction (or both) of primary Cholecystitis is acute or chronic inflammation of the
etiology or secondary complications as indicated gallbladder. It is associated with obstruction by gall-
 Paracentesis stones in 90% of cases. Gallstone formation (chole-
 Supplemental oxygen lithiasis) is associated with three factors: gallbladder
 Liver transplantation (see Chapter 12) hypomobility, supersaturation of bile with cholesterol,
and crystal formation from an increased concentration
HEPATIC ENCEPHALOPATHY AND COMA of insoluble bilirubin in the bile. Cholelithiasis can
Acute and chronic liver diseases, particularly cirrhosis, lead to secondary bacterial infection that further
may lead to neuropsychiatric manifestations that exacerbates the cholecystitis.72,116,117
may progress from hepatic encephalopathy to precoma Signs and symptoms of cholecystitis
to coma. The majority of neuropsychiatric manifesta- include72,73,116,117:
tions are linked to ammonia intoxication from faulty  Severe abdominal pain in the right upper quadrant
liver metabolism.72, 96,115 with possible pain referral to interscapular region
318 CHAPTER 8 Gastrointestinal System

 Rebound tenderness and abdominal rigidity
 Jaundice
 Anorexia
 Nausea, vomiting, or both
 Fever
Management of cholecystitis includes any of the
following72,116,117:
 Laparoscopic cholecystectomy or cholecystostomy
(temporary drain placement in the gallbladder until
obstruction is relieved)
 Gallstone dilution therapy with chenodeoxycholic
and ursode-oxycholic acid
 Antiinfective agents
 Pain management
 IV fluids
 Insertion of nasogastric tube
Pancreatic Disorders
PANCREATITIS
Inflammation of the pancreas can be acute or chronic.
The incidence of acute pancreatitis is rising, and the
clinical sequelae are potentially fatal, including adult
respiratory distress syndrome (ARDS) and shock. This
section therefore focuses on acute pancreatitis. Acute
pancreatitis can be categorized as necrotizing or
interstitial. Pancreatitis involves an exaggerated release
and activity of pancreatic enzymes into the peritoneal
cavity, along with autodigestion of pancreatic paren-
chyma. The exact trigger to this process is unknown,
but the most common contributing factors are gall-
stones and alcohol and drug abuse.72,118,119 Other contri-
buting factors also include72,118,119:
 Trauma
 Endoscopic retrograde cholangiography (see
Table 8-7)
 Metabolic disorders
 Vasculitis
 Pancreatic obstruction
 Penetrating peptic ulcer
 Genetic predisposition
 Renal failure
 Hepatitis
 Medications
 Postoperative sequelae from abdominal or cardio-
thoracic surgery
Signs and symptoms of acute pancreatitis
include118-121:
 Steady, dull abdominal pain in the epigastrium, left
upper quadrant, or periumbilical area often radiating
to back, chest, and lower abdomen. Pain can be
exacerbated by food, alcohol, vomiting, and resting
in the supine position.
 Nausea, vomiting, and abdominal distention
 Fever, tachycardia, and hypotension (in acute cases)
 Jaundice
 Abdominal tenderness or rigidity
 Diminished or absent bowel sounds
 Associated pulmonary manifestations, such as pleu-
ral effusions and pneumonitis
 Decreased urine output
 Weight loss
Management of acute pancreatitis includes any of
the following118-121:
 Pain management, generally with narcotics, possi-
bly through patient-controlled analgesia (See
Appendix VI.)
 IV fluid and electrolyte replacement
 Elimination of oral food intake, and providing alter-
native nutritional support, such as total parenteral
nutrition
 Surgical correction or resection of obstructions
 Antacids
 Nasogastric suctioning
 Supplemental oxygen and mechanical ventilation
(as indicated)
 Invasive monitoring (in more severe cases)
MANAGEMENT
General management of GI disorders may consist of any
of the following: pharmacologic therapy, nutritional
support,dietary modifications, and surgical procedures.
Nutritional support and dietary modifications are
beyond the scope of this book.This section focuses on
pharmacologic therapy and surgical procedures. A dis-
cussion of physical therapy intervention is also included.
Pharmacologic Therapy
Medications used to treat GI disorders can be broadly
categorized as (1) those that control gastric acid secre-
tion and (2) those that normalize gastric motility.
Refer to Appendix VI for an overview of these medica-
tions (Table IV-23, Antacids;Table IV-24, Antidiarrheal
Medications; Table IV-25, Antispasmodic Medications;
Table IV-26, Cytoprotective Medications; Table IV-27,
Histamine-2 Receptor Antagonists (H2RAs); Table IV-
28 Laxatives; andTable IV-29, Proton Pump Inhibitors).
Other medications that do not fall into these catego-
ries are mentioned in specific sections under Pathophy-
siology, earlier in the chapter.

Surgical Procedures
Surgical intervention is indicated in GI disorders when
medical intervention is insufficient. The location and
extent of incisions depend on the exact procedure.
The decision to perform either an open laparotomy or
a laparoscopic repair will be dependent on physician
preference based on surgical difficulty. However, with
the progress of laparoscopic technology, many open
laparotomy procedures requiring large abdominal
incisions are being replaced with laparoscopic proce-
dures. Laparoscopic procedures have been shown to
reduce hospital length of stay, many postoperative
complications, or both.75,116,122,123 Postoperative com-
plications may include pulmonary infection, wound
infection, and bed rest deconditioning. Refer to
Appendix V for further descriptions of the effects of
anesthesia.
The following is a description of the more common
GI surgical procedures 72,75,116,122-126
Appendectomy Removal of the appendix.
Performed either through open
laparotomy or laparoscopically.
Cholecystectomy Removal of the gallbladder.
Generally performed
laparoscopically.
Colectomy Resection of a portion of the
colon.The name of the surgical
procedure generally includes the
section removed (e.g., transverse
colectomy is resection of the
transverse colon). A colectomy may
also have an associated colostomy
or ileostomy. Performed either
through open laparotomy or
laparoscopically.
Colostomy A procedure used to divert stool
from a portion of the diseased
colon.There are three general types
of colostomies: end, double-barrel,
and loop colostomy.
End Involves bringing the functioning
colostomy end of the intestine (the section of
bowel that remains connected to
the upper GI tract) out onto the
surface of the abdomen and
forming the stoma by cuffing the
intestine back on itself and suturing
the end to the skin.
Continued
Gastrointestinal System CHAPTER 8 319
Double-barrel Two separate stomas are formed on
colostomy the abdominal wall.The proximal
stoma is the functional end that is
connected to the upper GI tract and
will drain stool.The distal stoma,
also called a mucous fistula, is
connected to the rectum to drain
small amounts of mucus material.
This is most often a temporary
colostomy.
Loop Created by bringing a loop of
colostomy bowel through an incision in the
abdominal wall. An incision is
made in the bowel to allow the
passage of stool through the loop
colostomy. Also used as a
temporary colostomy.
Fundoplication Upper curve of stomach (fundus) is
wrapped around the esophagus at
its juncture with the stomach.
Helps to reinforce the esophageal
sphincter and prevent acid reflux.42
Gastric bypass Creation of a small gastric pouch to
limit oral intake in restrictive and
malabsorptive disorders.110
Roux-en-Y Creation of a gastric pouch with
20-30 ml capacity via stapling,
with stoma that is attached to
jejunum (distal stomach and
proximal small bowel bypassed).
Performed open and
laparoscopically (Figure 8-4).110
Vertical banded Creates a small gastric pouch via
gastroplasty permanent stapling, with an outlet
from the pouch that is restricted by
a band or ring that slows emptying
of food to the small intestine
(see Figure 8-4).109
Adjustable Creates a small pouch in the upper
gastric banding stomach using an adjustable silicone
band, with a resulting narrow
outlet to the small intestine
(see Figure 8-4).110
Gastrectomy Removal of a portion (partial) or all
(total) of the stomach. Partial
gastrectomy may either be a
Billroth I or Billroth II procedure.
Billroth I Resection of the pyloric portion
of the stomach.126
Continued
320 CHAPTER 8 Gastrointestinal System

COMMON BARIATRIC PROCEDURES

A B C

Vertical-banded Adjustable gastric Roux-en-Y gastric

gastroplasty banding bypass
FIGURE 8-4
Common bariatric procedures. (From Still CD, Jensen GL: Obesity. In RE Rakel, ET Bope [eds]: Conn’s
Current Therapy [60th ed]. Philadelphia: Saunders, 2008.)

Billroth II Resection of the distal portion of joining of the pancreatic duct to

the stomach and the duodenum.126
Ileostomy A procedure similar to a colostomy
and is performed in areas of the
ileum (distal portion of the small
intestine). A continent ileostomy is
another method of diverting stool
that, instead of draining into an
external pouch, drains either into
more distal and functioning
portions of the intestine or into an
internal pouch that is surgically
created from the small intestine.
Resection and The removal (resection) of a
reanastomosis nonfunctioning portion of the
GI tract and the reconnection
(reanastomosis) of proximal and
distal GI portions that are
functional.The name of the
procedure will then include the
sections that are resected or
reanastomosedçfor example, a
pancreaticojejunostomy is the
the jejunum after a dysfunctional
portion of the pancreas is
resected.120,121
Whipple Consists of en bloc removal of the
procedure duodenum, a variable portion
(pancreatico- of the distal stomach and the
duodenectomy) jejunum, gallbladder, common bile
duct, and regional lymph nodes.
This removal is followed by
pancreaticojejunostomy
and gastrojejunostomy.This
procedure is reserved for the
patient with severe or unremitting
chronic pancreatitis or pancreatic
cancer.120,121,127
New GI surgical Transplantation of various parts
procedures of the GI system, including the
stomach and intestines; is being
investigated as a possible
mechanism to alleviate GI
dysfunction in various patient
populations.

With all of the above colostomies, an external, plas-
tic pouch is placed over the stoma in which the
patient’s stool collects. Patients are instructed on
proper care and emptying of their colostomy pouch.
This procedure can be performed in the ascending,
transverse, and sigmoid portions of the colon, with
sigmoid colostomies being the most commonly
performed.
CLINICAL TIP
 Before any mobility treatment, the physical therapist
should ensure that the colostomy pouch is securely
closed and adhered to the patient. When possible,
coordinate with the nurse or the patient to empty
the colostomy bag before therapy to fully minimize
accidental spills.
 Patients who are experiencing abdominal pain from
recent surgical incisions may be more comfortable
in the side-lying position (if allowed) to help relieve
skin tension on the recent incision.
 Instructing the patient to bend his or her knees up
while the head of the bed is being lowered may
also decrease incisional discomfort.
Physical Therapy Intervention
The following are general goals and guidelines for the
physical therapist when working with the patient who
has GI dysfunction. These guidelines should be
adapted to a patient’s specific needs.
GOALS
The primary physical therapy goals for this patient
population are similar to those of other patients in
the acute care setting: (1) to optimize functional
mobility, (2) to maximize activity tolerance and end-
urance, and (3) to prevent postoperative pulmonary
complications.
GUIDELINES FOR PHYSICAL THERAPY
INTERVENTION
General guidelines include, but are not limited to, the
following:
1. Patients with GI dysfunction can have increased fati-
gue levels as a result of poor nutritional status from
malabsorption and anemia from inflammatory and
hemorrhagic conditions of the GI tract. Therefore,
consider the patient’s fatigue level with treatment
planning and setting of goals.
Gastrointestinal System CHAPTER 8 321
a. Consultation with the nutritionist is helpful
in gauging the appropriate activity prescrip-
tion, which is based on the patient’s caloric
intake. It is difficult to improve the patient’s
strength or endurance if his or her caloric intake
is insufficient for the energy requirements of
exercise.
b. Reviewing the patient’s laboratory values to
determine hematocrit and hemoglobin levels
before treatment may be helpful in planning the
patient’s activity level for that session. Refer to
Hematologic Evaluation in Chapter 6 for more
information on hematology.
c. Malabsorption syndromes can also lead to altered
metabolism of medications and, therefore, the
responses to medications will be less predictable
and can impact the treatment planning of the
therapist.23
2. Patients with GI dysfunction may have certain posi-
tioning precautions.
a. Dysphagia can be exacerbated in supine positions
and may also lead to aspiration pneumonia.128
b. Portal hypertension can be exacerbated in the
supine position because of gravitational effects
on venous flow.
c. If the patient has associated esophageal varices
from portal hypertension, then the risk of
variceal rupture may be increased in this position
as well.
d. Patients with portal hypertension and esophageal
varices should also avoid maneuvers that create a
Valsalva effect, such as coughing.
e. The increase in intraabdominal pressure from
Valsalva’s maneuvers can further exacerbate
the esophageal varices. (Huffing, instead of
coughing, may be more beneficial in these
situations.)
3. Nonpharmacologic pain management techniques
from the physical therapist may benefit patients
who have concurrent diagnoses of rheumatologic
disorders and GI dysfunction.
a. Because NSAIDs are a causative risk factor for
many inflammatory and hemorrhagic conditions
of the GI system, these medications typically are
withheld from the patient with any exacerbation
of these conditions.
b. Therefore, patients who were reliant on NSAIDs
for pain management before admission for their
rheumatologic conditions may have limitations
in functional mobility as a result of altered pain
management.
322 CHAPTER 8 Gastrointestinal System
4. Patients with ascites or large abdominal incisions are
at risk for pulmonary complications. Ascites and
surgical incisions create ventilatory restrictions for
the patient.
a. Additionally, these conditions can hinder cough
effectiveness and functional mobility, both of
which can further contribute to pulmonary
infection.
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 9 Genitourinary System

Jaime C. Paz INTRODUCTION

The regulation of fluid and electrolyte levels by the genitourinary system
is an essential component to cellular and cardiovascular function.
Imbalance of fluids, electrolytes, or both can lead to blood pressure
changes or impaired metabolism that can ultimately influence the patient’s
activity tolerance (see Appendix II). Genitourinary structures can also
cause pain that is referred to the abdomen and back.To help differentiate
neuromuscular and skeletal dysfunction from systemic dysfunction,
physical therapists need to be aware of pain referral patterns from these
structures (Table 9-1). The objectives for this chapter are to provide the
following:
1. A basic understanding of the structure and function of the genitouri-
nary system
2. Information about the clinical evaluation of the genitourinary system,
including physical examination and diagnostic studies
3. A basic understanding of the various diseases and disorders of the
genitourinary system
4. Information about the management of genitourinary disorders,
including dialysis therapy and surgical procedures
5. Guidelines for physical therapy intervention in patients with genitouri-
nary diseases and disorders
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:
 Pattern 4A: Primary Prevention/Risk Reduction for Skeletal
Demineralization
 Pattern 6B Impaired Aerobic Capacity/Endurance Associated with
Deconditioning
 Pattern 7A: Primary Prevention/Risk Reduction for Integumentary
Disorders.
Please refer to the back cover of this book for a complete list of the
preferred practice patterns as individual patient conditions are highly
variable and other practice patterns may be applicable.

STRUCTURE AND FUNCTION

The genitourinary system consists of two kidneys, two ureters, one uri-
nary bladder, and one urethra. The genitourinary system also includes
the reproductive organs: the prostate gland, testicles, and epididymis in
men, and the uterus, fallopian tubes, ovaries, vagina, external genitalia,

327
328 CHAPTER 9 Genitourinary System

 Acid-base balance regulation (H+ [acid] and HCO3

Table 9-1 SEGMENTAL INNERVATION AND PAIN [base] ions are reabsorbed or excreted to maintain
REFERRAL AREAS OF THE URINARY homeostasis.)
SYSTEM  Arterial blood pressure regulation (sodium excretion
Segmental Possible Pain and renin secretion to maintain homeostasis. Renin
Structure Innervation Referral Area is secreted from the kidneys during states of hypo-
tension, which results in formation of angiotensin.
Kidney T10-L1 Lumbar spine Angiotensin causes vasoconstriction to help increase
(ipsilateral flank)
blood pressure.)
Upper abdomen
 Erythropoietin secretion (necessary for stimulating
Ureter T11-L2, S2-S4 Groin red blood cell production)
Upper and lower  Gluconeogenesis (formation of glucose)
abdomen
Suprapubic region
The brain stem controls micturition through the
Scrotum autonomic nervous system. Parasympathetic fibers
Medial and proximal stimulate voiding, whereas sympathetic fibers inhibit
thigh it. The internal urethral sphincter of the bladder and
Thoracolumbar region the external urethral sphincter of the urethra control
Urinary T11-L2, S2-S4 Sacral apex flow of urine.2
bladder Suprapubic region
Thoracolumbar region
From Boissonault WG, Bass C. Pathological origins of trunk CLINICAL EVALUATION
and neck pain: part 1. Pelvic and abdominal visceral disorders.
J Orthop PhysTher 1990;12:194. Evaluation of the genitourinary system involves the
integration of physical findings with laboratory data.

and perineum in women. Of these reproductive organs,
only the prostate gland and uterus are discussed in this
chapter.
The anatomy of the genitourinary system is shown
in Figure 9-1. An expanded, frontal view of the kidney
is shown in Figure 9-2. The structural and functional
unit of the kidney is called the nephron. The nephron is
located in the renal cortex and the medulla and has
two parts: a renal corpuscle and a renal tubule. There
are approximately 1 million nephrons in each kidney.
Urine is formed in the nephron through a process con-
sisting of glomerular filtration, tubular reabsorption,
and tubular secretion.1
The following are the primary functions of the
genitourinary system1,2:
 Excretion of cellular waste products (e.g., urea, creat-
inine [Cr], and ammonia) through urine formation
and micturition (voiding)
 Regulation of blood volume by conserving or
excreting fluids
 Electrolyte regulation by conserving or excreting
minerals
Physical Examination
HISTORY
Patients with suspected genitourinary pathology often
present with characteristic complaints or subjective
reports. Therefore, a detailed history, thorough patient
interview, review of the patient’s medical record, or a
combination of these provides a good beginning to
the diagnostic process for possible genitourinary
system pathology. Renal and urinary pains can vary
according to their structural origins; however, they are
generally described as pain that is colicky, wave-like,
or burning, or occurring as dull aches in the abdomen,
back, or buttocks.3
Changes in voiding habits or a description of mictu-
rition patterns are also noted and are listed below2-4:
 Decreased force of urinary flow (can indicate
obstruction in the urethra or prostate enlargement)
 Increase in urinary frequency (can indicate obstruc-
tion from prostate enlargement or an acutely
inflamed bladder)
 Nocturia (urinary frequency at night, can indicate
congestive heart failure or diabetes mellitus)
 Polyuria (large volume of urine at one time, can indi-
cate diabetes mellitus, chronic renal failure [CRF],
or excessive fluid intake)

FIGURE 9-1
Schematic illustration of the genitourinary system, including trunk musculature. (Courtesy Marybeth
Cuaycong.)
 Oliguria (usually less than 400 ml of urine in a
24-hour period, can indicate acute renal failure
[ARF] or end-stage renal disease [ESRD])
 Anuria (less than 100 ml of urine in a 24-hour period,
can indicate severe dehydration, shock, transfusion
reaction, kidney disease, or ESRD)
 Dysuria (pain with voiding, can indicate a wide vari-
ety of disorders, including urinary tract infection)
 Hematuria (the presence of blood in urine, can indi-
cate serious pathology, e.g., cancer or traumatic
Foley catheterization). In either case, the physician
should be notified. (Refer to Appendix Table III-A.6
for a description of a Foley catheter.)
 Urinary urgency (can indicate bladder, urethral,
or prostate infection)
 Incontinence (an inability to control voiding, can
indicate sphincter and autonomic dysfunction)
Genitourinary System CHAPTER 9 329
CLINICAL TIP
 If the patient has a history of urinary incontinence,
a condom catheter (for men) or adult diapers (for
men and women) can be applied before mobility
treatment to aid in completion of the session.
 As a side effect of the medication phenazopyridine
(Pyridium), a patient’s urine may turn rust-colored and
be misinterpreted as hematuria. However, any new
onset of possible hematuria should always be alerted to
the medical team for proper delineation of the cause.
OBSERVATION
The presence of abdominal or pelvic distention,
peripheral edema, incisions, scars, tubes, drains, and
330 CHAPTER 9 Genitourinary System

FIGURE 9-2
Renal cross-section. (Courtesy Marybeth Cuaycong.)

catheters should be noted when performing patient

inspection, because these may reflect current pathology
and recent interventions. Patients with genitourinary
disorders may also present with skin changes, such as
pallor or rough, dry skin.4 The physical therapist must
handle external tubes and drains carefully during
positioning or functional mobility treatments.
CLINICAL TIP
 Securing tubes and drains with a pin or a clamp to
a patient’s gown during a mobility session can
help prevent accidental displacement (see Appendix
Table III-A.6).
 Moving tubes and drains out of the way during bed
mobility prevents the patient from possibly rolling
onto them (see Appendix Table III-A.6).
 Take caution in handling patients with skin changes
from dehydration to prevent any skin tears that can
lead to infection formation.
PALPATION
The kidneys and a distended bladder are the only
palpable structures of the genitourinary system.
Distention or inflammation of the kidneys results in
sharp or dull pain (depending on severity) with palpa-
tion. Kidney enlargement may be indicative of renal
carcinoma.2,4
PERCUSSION
Pain and tenderness that are present with fist percus-
sion of the kidneys can be indicative of kidney
infection or polycystic kidney disease. Fist percussion
is performed by the examiner’s striking the fist of
one hand against the dorsal surface of the other
hand, which is placed along the costovertebral angle
of the patient.4 Direct percussion with a closed fist
may also be performed over the costovertebral angles.
The patient should feel a ‘‘thud’’ but not pain or
tenderness.5
 Genitourinary System CHAPTER 9 331

AUSCULTATION Table 9-2 URINE ABNORMALITIES

Auscultation is performed to examine the blood flow to Abnormality Etiology
the kidneys from the abdominal aorta and the renal
arteries. The presence of bruits (murmurs) can indicate Glycosuria (presence Hyperglycemia and probable
impaired perfusion to the kidneys, which can lead to of glucose) diabetes mellitus.
renal dysfunction. Placement of the stethoscope is gen- Proteinuria (presence Proteins are usually too large to
erally in the area of the costovertebral angles and the of proteins) be filtered; therefore,
upper abdominal quadrants. Refer to Chapter 8, permeability has abnormally
increased.
Figure 8-2, for a diagram of the abdominal quadrants.4
Can occur with acute or chronic
renal failure, nephrotic
Diagnostic Tests* syndrome, high-protein diet,
URINALYSIS strenuous exercise,
dehydration, fever,
Urinalysis is a very common diagnostic tool used not or emotional stress.
only to examine the genitourinary system, but also to Hematuria (presence Possible urinary tract bleeding
help evaluate for the presence of other systemic dis- of blood and red or kidney diseases (calculi,
eases. Urine specimens can be collected by bladder cath- blood cells) cystitis, neoplasm,
eterization or suprapubic aspiration of bladder urine, glomerulonephritis,
or by having the patient void into a sterile specimen or miliary tuberculosis).
container. Urinalysis is performed to examine3,4,6: Bacteriuria (presence Generally indicates urinary tract
 Urine color, clarity, and odor of bacteria) infection.
 Specific gravity, osmolarity, or both (concentration Urine is generally cloudy in
of urine ranges from 300 [dilute] to 1,300 [concen- appearance, with the possible
trated] mOsm/kg) presence of white blood cells.
 pH (4.5 to 8.0) Ketonuria (presence Can result from diabetes,
 Presence of glucose, ketones, proteins, bilirubin, of ketones)* starvation, a high-protein
urobilinogen, occult blood, red blood cells, diet, dehydration, vomiting,
white blood cells, crystals, casts, bacteria or other or severe diarrhea.
microorganisms, enzymes, and electrolytes Bilirubinuria Usually an early indicator
 Urine abnormalities are summarized inTable 9-2. (presence of of liver disease and
bilirubin) hepatocellular jaundice.
Crystals (end Can occur with urolithiasis,
CLINICAL TIP products of food toxic damage to the kidneys,
 If the patient is having his or her urine collected metabolism) or chronic renal failure.
(to measure hormone and metabolite levels),
*Ketones are formed from protein and fat metabolism, and trace
the physical therapist should have the patient amounts in the urine are normal.
use the predesignated receptacle if the patient Data from reference numbers 1, 4, 5, 8.
needs to urinate during a physical therapy session.
This will ensure that the collection is not
interrupted.
 The predesignated receptacle can be a urinal estimate of the patient’s renal function.
for men or a collection ‘‘hat’’ placed on the toilet Measurements of the patient’s input and output
or commode for women. are often abbreviated I/Os.
 Urine may also be collected throughout the day
to measure the patient’s urine output relative to the
patient’s fluid intake (input). This provides a general CREATININE TESTS
Two measurements of Cr (end product of muscle
*The reference range of various laboratory values can vary among
metabolism) are performed: measurements of plasma
different facilities. Be sure to verify the reference values located in Cr and Cr clearance. Plasma Cr is measured by drawing
the laboratory test section of the medical record. a sample of venous blood. Increased levels are indicative
332 CHAPTER 9 Genitourinary System
of decreased renal function. The reference range of
plasma Cr is 0.5 to 1.5 mg/dl.
Cr clearance, also called a 24-hour urine test, specif-
ically measures glomerular filtration rate and is the
most practical and widely used clearance test.
Decreased clearance (indicated by elevated levels of
plasma creatinine relative to creatinine levels in the
urine) indicates decreased renal function. The normal
range of Cr clearance is 75 to 135 ml per minute.4,6-8
BLOOD UREA NITROGEN
As an end product of protein and amino acid met-
abolism, increased blood urea nitrogen (BUN) levels
can be indicative of any of the following: decreased
renal function or fluid intake, increased muscle
catabolism, increased protein intake, or acute infec-
tion. Levels of BUN need to be correlated with
plasma Cr levels to implicate renal dysfunction,
because BUN level can be affected by decreased
fluid intake, increased muscle catabolism, increased
protein intake, and acute infection. Alterations in
BUN and Cr level can also lead to an alteration in the
patient’s mental status. Normal BUN levels are 5 to
30 mg/dl.4,6-8
CLINICAL TIP
 Noting BUN and Cr levels on a daily basis for any
changes may help explain changes in the patient’s
mental status, participation in physical therapy
sessions, or both.
RADIOGRAPHIC EXAMINATION
KIDNEYS, URETERS, AND BLADDER X-RAY. An x-ray
of the kidneys, ureters, and bladder is generally per-
formed as an initial screening tool for genitourinary
disorders. The size, shape, and position of the renal,
ureteral, and bladder structures are delineated to help
identify renal calculi (kidney stones), tumor growth or
shrinkage (chronic pyelonephritis), and calcifications
in the bladder wall. An x-ray of the kidneys, ureters,
and bladder can also be performed when internal hem-
orrhage is suspected after major traumatic incidents.
Identification of any of these disorders requires further
evaluation.4,6,8
CLINICAL TIP
 This x-ray procedure is often abbreviated KUB.
PYELOGRAPHY. Radiopaque dyes are used to radio-
graphically examine the urinary system. Two types of
tests are performed: Intravenous pyelography (IVP)
and retrograde urography.
Intravenous pyelography consists of (1) taking a
baseline radiograph of the genitourinary system,
(2) intravenous injection of contrast dye, and (3)
sequential radiographs to evaluate the size, shape, and
location of urinary tract structures and to evaluate
renal excretory function. The location of urinary
obstruction or cause of nontraumatic hematuria may
be also be identified with this procedure.4,6,8
Retrograde urography consists of passing a catheter
or cystoscope into the bladder and then proximally
into the ureters before injecting the contrast dye.
This procedure is usually performed in conjunction
with a cystoscopic examination and is indicated when
urinary obstruction or trauma to the genitourinary
system is suspected. Evaluation of urethral stent or
catheter placement can also be performed with this
procedure.3,4,6,8
RENAL ARTERIOGRAPHY AND VENOGRAPHY. Renal
arteriography and venography consist of injecting
radiopaque dye into the renal artery (arteriography) or
vein (venography) through a catheter that is inserted
into the femoral or brachial artery or femoral vein.
Arterial and venous blood supply to and from the
kidneys can then be examined radiographically.
Indications for arteriography include suspected aneur-
ysm, renal artery stenosis, renovascular hypertension
and trauma, palpable renal masses, chronic pyelone-
phritis, renal abscesses, and determination of the
suitability of a (donor) kidney for renal transplantation.
Indications for venography include renovascular
hypertension, renal vein thrombosis, and renal cell
carcinoma.6,8,9
CLINICAL TIP
 Patients who are scheduled for procedures
involving contrast dye are generally restricted
from eating or drinking 8 hours before the
procedure. A patient who is scheduled for an
afternoon procedure may therefore be
fatigued earlier in the day and may want to
defer a scheduled therapy session. Modifying
the intended therapy session and respecting the
person’s wishes at this time are both suitable
alternatives.

BLADDER EXAMINATION: CYSTOSCOPY
AND PANENDOSCOPY
Cystoscopy consists of passing a flexible, fiberoptic
scope through the urethra into the bladder to exam-
ine the bladder neck, urothelial lining, and ureteral
orifices. The patient is generally placed under general
or local anesthesia during this procedure. Cystoscopy
is performed to examine the causes of hematuria
and dysuria, as well as for tumor or polyp removal.6,9
Panendoscopy is a similar procedure to cystos-
copy that is used to view the prostatitic urethra
(in men), external urinary sphincters, and anterior
urethra.6-9
CLINICAL TIP
 Patients may experience urinary frequency or dysuria
after cystoscopic procedures; therefore, the therapist
should be prepared for sudden interruptions during
a therapy session that is conducted the same day
after this diagnostic procedure.
URODYNAMIC STUDIES
CYSTOMETROGRAM. Cystometrogram is used to
evaluate bladder tone, sensations of filling, and bladder
stability in patients with incontinence or evidence of
neurologic bladder dysfunction. The procedure con-
sists of inserting a catheter into the bladder, followed
by saline instillation and pressure measurements of the
bladder wall.4,8
RADIOISOTOPE STUDIES
Diagnostic studies consisting of radioisotope injection
and subsequent imaging such as renography, renal
scan, and nuclear cystogram (radionuclide cystogram)
are not commonly performed and therefore will not
be described further.
ULTRASONOGRAPHY STUDIES
Ultrasound is used to (1) evaluate kidney size, shape,
and position; (2) determine the presence of kidney
stones, cysts, and prerenal collections of blood, pus,
lymph, urine, and solid masses; (3) identify the presence
of a dilated collecting system; and (4) help guide
needle placement for biopsy or drainage of a renal
abscess or for placement of a nephrostomy tube.6,9 It is
the test of choice to help rule out urinary tract
obstruction.8
Genitourinary System CHAPTER 9 333
COMPUTED TOMOGRAPHY SCAN
Indications for computed tomography of the genitouri-
nary system include defining renal parenchyma
abnormalities and differentiating solid mass densities
as cystic or hemorrhagic. Kidney size and shape, as
well as the presence of cysts, abscesses, tumors, calculi,
congenital abnormalities, infections, hematomas, and
collecting system dilation, can also be assessed with
computed tomography.3,6 CTscan is currently the gold
standard for renal stone diagnosis.8
MAGNETIC RESONANCE IMAGING
Multiple uses for magnetic resonance imaging include
imaging the renal vascular system without the potential
adverse effects of contrast dyes, staging of renal cell car-
cinoma, identifying bladder tumors and their local
metastases, and distinguishing between benign and
malignant prostate tumors.6 MRI is currently the gold
standard for diagnosing the presence of thrombus in
the renal veins.8
BIOPSIES
RENAL BIOPSY. A renal biopsy consists of examin-
ing a small portion of renal tissue that is obtained per-
cutaneously with a needle to determine the pathologic
state and diagnosis of a renal disorder, monitor kidney
disease progression, evaluate response to medical treat-
ment, and assess for rejection of a renal transplant.
A local anesthetic is provided during the procedure.4,6,8
BLADDER, PROSTATE, AND URETHRAL BIOPSIES.
Bladder, prostate, and urethral biopsies involve taking
tissue specimens from the bladder, prostate, and urethra
with a cystoscope, panendoscope, or needle aspiration
via the transrectal or transperineal approach. Biopsy
of the prostate can also be performed through an open
biopsy procedure, which involves incising the peri-
neal area and removing a wedge of prostate tissue.
Examinations of pain, hematuria, and suspected
neoplasm are indications for these biopsies.6,9
PATHOPHYSIOLOGY
Renal System Dysfunction
ACUTE RENAL FAILURE
Acute renal failure (or acute kidney failure [AKF]) can
result from a variety of causes and is defined as a
334 CHAPTER 9 Genitourinary System
sudden, rapid deterioration in renal function that
results in decreased urine output.10 There are three
types of ARF, categorized by their etiology: prerenal,
intrarenal, or postrenal.11
Prerenal ARF is caused by a decrease in renal blood
flow from dehydration, hemorrhage, shock, burns, or
trauma, and accounts for 55% to 70% of ARF.11
Intrarenal ARF involves primary damage to
kidneys and is caused by acute tubular necrosis
(ATN) glomerulonephritis, acute pyelonephritis,
renal artery or vein occlusion, bilateral renal cortical
necrosis, nephrotoxic substances (e.g., aminoglycoside
antibiotics or contrast dye), or blood transfusion
reactions.
Postrenal ARF involves obstruction distal to the
kidney and can be caused by urinary tract obstruction
by renal stones, obstructive tumors, or benign pros-
tatic hypertrophy.10,12-14 Postrenal failure accounts
for 5% of ARF cases.11
Despite advances in therapies, the mortality rate
from ARF is still relatively high, ranging from 25% to
90%.13-15
The following are four stages for all three types of
ARF10-12:
1. Onset is the time (hours to days) from the preci-
pitating event to the onset of decreased urine
output, or oliguria. Patient is generally asymp-
tomatic at this time.
2. The oliguric or anuric (no urine < 30 ml in 24 hours)
phase occurs when urine output is less than 400 ml
in 24 hours, which can last 1 to several weeks, with
prognosis worsening as the duration increases.
Nausea, vomiting, confusion, and ECG changes
with potential for congestive heart failure can
present during this phase.
3. The diuretic phase is marked by improvement in
renal function and urine output. This phase occurs
2 to 6 weeks after onset of the oliguric phase.
The patient’s mental status generally improves
during this phase, but postural hypotension with
tachycardia may be present as well.
4. The late or recovery period is the time (3 to12 months)
between falling to stabilizing (i.e., within normal
range) BUN levels. Patients will have decreased
energy levels during this phase.
Overall clinical manifestations of ARF include
the following10-14:
 Acid-base imbalance
 Hyperkalemia or hypokalemia
 Infection
 Hyperphosphatemia
 Hemodynamic instability, including hypovolemia
and hypertension
 Anemia
Management of ARF includes any of the fol-
lowing10,12-14:
 Treatment of the primary etiology, including antiin-
fective agents if applicable
 Hydration (intravenous fluids and osmotics [proteins])
 Diuretics in non—critically ill patients15
 Peritoneal dialysis, hemodialysis, continuous renal
replacement therapy (Refer to the Renal Replacement
Therapy section.)
 Transfusions and blood products
 Nutritional support
CHRONIC RENAL FAILURE
CRF is an irreversible reduction in renal function that
occurs as a slow, insidious process from the permanent
destruction of nephrons.The renal system has consider-
able functional reserve, and as many as 50% of the
nephrons can be destroyed before symptoms occur.
Progression of CRF to complete renal failure is
termed end stage renal disease (ESRD). At this point in
time only 10% of renal function remains, and dialysis
is required for patient survival.10-12,16
CRF can result from primary renal disease or
other systemic diseases. Primary renal diseases that
cause CRF are polycystic kidney disease, chronic
glomerulonephritis, chronic pyelonephritis, and chr-
onic urinary obstruction. The two primary sys-
temic diseases that cause CRF are type 2 diabetes and
hypertension.17 Other systemic diseases that can result
in CRF include gout, systemic lupus erythematosus,
amyloidosis, nephrocalcinosis, sickle cell anemia, scle-
roderma and human immunodeficiency virus.11
Complications of CRF are similar to those of ARF but
can also include decreased bone density as a result of
decreased activation of vitamin D, which impairs intes-
tinal absorption of calcium, resulting in low serum cal-
cium levels. Patients with CRF can also experience
episodes of ARF in situations when they are noncom-
pliant with their management, when their management
proves insufficient, or both.10,12,16,18,19
Management of CRF includes conservative man-
agement or renal replacement therapy.20
Conservative management includes the
following10,12,16,20:
 Nutritional support, dietary modifications
 Antacids, anticonvulsant, antihypertensive, antiin-
fective, and antiemetic agents for symptomatic
management of complications from CRF

Renal replacement therapy includes the
following10,12,16,20:
 Peritoneal dialysis or hemodialysis to maintain
fluid and electrolyte balance
 Renal transplantation (See Chapter 12.)
CLINICAL TIP
 Patients who are on bed rest or have yet to
begin consistently ambulating are likely to be
put on anticoagulants. For patients with chronic
renal disease, unfractionated heparin is the
preferred medication to use for venous
thromboembolism prophylaxis. Because most
medicines, including anticoagulants, are
eliminated through the kidneys, patients
with renal disease may have a higher
likelihood of bleeding if anticoagulant dosing
is not titrated closely.21 Therefore monitor
the patients’ clotting times prior to
moving them.
PYELONEPHRITIS
Pyelonephritis is an acute or chronic inflammatory
response in the kidney, particularly the renal pelvis,
from bacterial, fungal, or viral infection. It can be
classified as acute or chronic.
ACUTE PYELONEPHRITIS. Acute pyelonephritis
is frequently associated with concurrent cystitis
(bladder infection). The common causative agents
are bacterial, including Escherichia coli, Proteus,
Klebsiella, Enterobacter, and Pseudomonas. Predis-
posing factors for acute pyelonephritis include urine
reflux from the ureter to the kidney (vesicoureteral
reflux), kidney stones, pregnancy, neurogenic bladder,
catheter or endoscope insertion, and female sexual
trauma.Women are more prone to acute pyelonephritis
than men.12,20,22 Spontaneous resolution of acute
pyelonephritis may occur in some cases without
intervention.
Signs and symptoms of acute pyelonephritis include
any of the following12,20,22,23:
 Sudden onset of fever and chills
 Tenderness with deep palpatory pressure of one or
both costovertebral areas
 Flank or groin pain
 Urinary frequency
 Dysuria, hematuria, pyuria (presence of white blood
cells [leukocytes])
 Nausea, vomiting, and diarrhea24
Genitourinary System CHAPTER 9 335
Management of acute pyelonephritis includes any
of the following12,22-24:
 Antibiotic therapy commonly includes ciproflox-
acin (Cipro), ampicillin (Omnipen), trimethoprim/
sulfamethoxazole (Bactrim, Septra), or Ofloxacin.
A 7-day course of ciprofloxacin has been shown to
be the most effective treatment for women with
acute pyelonephritis thus far.25
 Ureteral reimplantation for children with chronic
vesicoureteral reflux.26
CHRONIC PYELONEPHRITIS. Chronic pyelonephritis
is recurrent or persistent inflammation and scarring of
one or both kidneys as a result of autoimmune infec-
tion. Chronic pyelonephritis can also result from kidney
stones or acute pyelonephritis and may lead to CRF.
Specific etiologies are difficult to diagnose.12,20,22,23,27
Signs and symptoms of chronic pyelonephritis
include any of the following12,22,23:
 Hypertension
 Mild and vague dysuria, urinary frequency, and
flank pain
 Renal insufficiency (decreased urine output), possi-
bly progressing to failure
 Pyuria (white blood cells in the urine), hematuria
(blood in urine)
Management of chronic pyelonephritis includes any
of the following12,22,23,27:
 Treatment of primary etiology (if diagnosed)
 Antiinfective agents similar to those mentioned with
ARF but for a prolonged treatment period ranging
from 3 to 6 months.24
GLOMERULONEPHRITIS
Glomerulonephritis is an inflammation of the glo-
merular portion of the kidney that can result from
immunologic abnormalities, drug or toxin effects,
vascular disorders, or systemic disorders. Definitive
etiology may be difficult to ascertain in some cases.
Glomerulonephritis can be classified according
to cause, pathologic lesions, disease progression, or
clinical presentation.
Cardinal signs and symptoms of acute glomerulone-
phritis include hematuria, dysmorphic red cells, red
cell casts, and mild proteinuria. Additionally, depen-
dent edema and hypertension are present. All of these
manifestations can either progress toward or be con-
current with acute renal failure.28 This section discu-
sses the common types of glomerulonephritis.12
IMMUNOGLOBULIN A NEPHROPATHY (BERGER’S
DISEASE). Immunoglobulin (Ig) A nephropathy is the
most common cause of glomerulonephritis, with
336 CHAPTER 9 Genitourinary System
25% to 40% of cases progressing to renal failure within
20 to 25 years of onset.29,30 IgA nephropathy is an
abnormality of immune system regulation that results
in deposition of IgA (antibody) complexes within the
glomeruli, ultimately resulting in a reduction of glo-
merular filtration. Hepatic cirrhosis, inflammatory
bowel disease, carcinomas, various infections, and
rheumatic disorders have been highly associated with
the development of IgA nephropathy.12,23,29,30
Signs and symptoms of IgA nephropathy include
any of the following12,23,29,30:
 Hematuria
 Proteinuria
 Oliguria
Management of IgA nephropathy includes the
administration of any of the following12,23,30:
 Antiinflammatory agents, such as oral glucocorti-
coids (prednisone)
 Angiotensin converting enzyme (ACE) inhibitors
 Cytotoxic agents
 Fish oils (effectiveness is controversial)30,31
POSTINFECTIOUS GLOMERULONEPHRITIS. As the
name states, postinfectious glomerulonephritis is
acute inflammation in the renal system that occurs
after infection. Group a- and b-hemolytic streptococci
are the common causative pathogens that lead to the
damage of surface proteins in the glomeruli.12,23,29,32
Other organisms that have been associated with this
form of acute glomerulonephritis include hepatitis
B virus, hepatitis C virus, and human immunodeficien-
cy virus; spirochetes, such as Treponema pallidum; proto-
zoa, such as Plasmodium malariae; and fungi, such as
Candida albicans.29 Prognosis is generally good once the
causative agent is identified and appropriate antiinfec-
tive and supportive therapies are provided.29,32
Signs and symptoms of poststreptococcal glomeru-
lonephritis include any of the following12,23,32:
 Acute onset of fluid retention, hypertension,
and peripheral edema
 Oliguria
 Hematuria
 Mild to moderate proteinuria
 Anemia
 Cola-colored urine with red blood cell casts
Management of poststreptococcal glomerulone-
phritis includes any of the following12,23,32:
 Antibiotics
 Antihypertensive agents
 Diuretics
 Fluid and electrolyte support (as needed)
 Hemodialysis (as needed)
RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS.
Rapidly progressive glomerulonephritis (RPGN) is
also known as subacute, crescentic, or extracapillary
glomerulonephritis. It involves glomerular inflamma-
tion that progresses to renal failure in a few days or
weeks.32 This disease primarily affects adults who are
in their fifties and sixties and has a relatively poor prog-
nosis. Early detection is critical to effective therapy
and patient survival.32,33 Causes of RPGN can include
acute or subacute infection from b-hemolytic strepto-
cocci or from other bacteria, viruses, or parasites. It
can also be caused by multisystem or autoimmune
disease.12,23,32
Signs and symptoms of RPGN include any of the
following12,23,32:
 Rapid, progressive reduction in renal function
 Severe oliguria
 Anuria, with irreversible renal failure
Management of RPGN includes any of the
following12,23,33:
 Antiinflammatory agents (e.g., prednisone)
 Plasmapheresis
 Anticoagulation treatment
 Hemodialysis
 Renal transplantation
CHRONIC GLOMERULONEPHRITIS. Chronic glomer-
ulonephritis is the culmination of diseases that can
affect the glomeruli leading to progressive renal failure
in 10 to 20 years. These diseases include those men-
tioned in the previous section, along with diabetes,
hepatitis, and systemic lupus erythematosus.34 Chronic
glomerulonephritis involves scarring and obliteration
of the glomeruli, along with vascular sclerosis of
arteries and arterioles.12,23
Signs and symptoms of chronic glomerulonephritis
include the following12,23:
 Uremia
 Proteinuria
 Hypertension
 Azotemia
Management of chronic glomerulonephritis
includes any of the following12,23:
 Treatment of primary disease or dysfunction
 Administration of steroidal antiinflammatory
agents
 Administration of antiinfective or cytotoxic agents,
or both
 Dialysis
 Renal transplantation
Other types of glomerulonephritis are minimal
change disease (lipoid nephrosis), focal segmental

glomerulonephritis membranous nephropathy, and
membranoproliferative glomerulonephritis (slowly
progressive glomerulonephritis).9 These are not dis-
cussed in this chapter, because they have similar clinical
manifestations as the types of glomerulonephritis
discussed previously.
NEPHROTIC SYNDROME
Nephrotic syndrome is a group of symptoms chara-
cterized by an increased permeability of the glomeru-
lar basement membrane that results in excessive
excretion of protein molecules, particularly albumin,
which ultimately leads to reduced osmotic pressures
that can result in peripheral edema. Many conditions
can lead to nephrotic syndrome, including10,12,28,33:
 Acute glomerulonephritis (IgA nephropathy)
 Diabetes mellitus
 Amyloidosis
 Systemic lupus erythematosus
 Infections (human immunodeficiency virus,
hepatitis B or C)
 Circulatory diseases
 Allergen or drug reactions (nonsteroidal antiin-
flammatory agents, penicillin, captopril, heroin)
 Pregnancy (preeclampsia)
 Chronic allograft rejection after renal
transplantation
Physical findings of nephrotic syndrome include
the following10,12,28,33:
 Hypoalbuminemia
 Generalized peripheral edema, which can progress
toward pleural effusions, ascites, and ultimately
dyspnea
 Hyperlipidemia
 Lipiduria (lipid casts or free fat droplets in urine)
 Vitamin D deficiency
Management of nephrotic syndrome includes any
of the following10,12,28,35,36:
 Treatment of underlying disease
 Administration of steroidal antiinflammatory agents
 Albumin and protein replacement
 Diuretics
 Anticoagulation therapy
 Dietary modifications (e.g., normal protein, low fat,
salt restrictions)
INTERSTITIAL NEPHRITIS
Infection, urinary tract obstruction, and reactions to
medications, particularly nonsteroidal antiinflammato-
ry agents, can result in inflammatory interstitial tissue
damage, which is referred to as interstitial nephritis.10,37,38
Genitourinary System CHAPTER 9 337
Scarring from the inflammatory process leads to
reduced kidney function that can progress to CRF.
Early detection is helpful in treating the inflammatory
response.10
Physical findings of interstitial nephritis include the
following10:
 Polyuria
 Nocturia
 Pyuria
 Mild hematuria
 Mild proteinuria
Management of interstitial nephritis includes any
of the following10,39:
 Fluid and nutritional support
 Antiinfective agents (as indicated)
 Dialysis (as indicated)
 Surgery to relieve obstructions (if present)
 Renal transplantation
NEPHROLITHIASIS
Nephrolithiasis is a condition that occurs more com-
monly in men and is characterized by renal calculi
(kidney stones) that form in the renal pelvis. There are
four primary types of kidney stones, which are categor-
ized according to the stone-forming substances: (1) cal-
cium oxalate, (2) struvite (composed of magnesium,
ammonium, and phosphate), (3) uric acid and (4) cys-
tine. Many factors contribute to stone formation and
include the following10,12,40,41:
 High urinary concentration of stone-forming
substances
 Presence of crystal growth facilitators
 Metabolic abnormalities
 Dietary factors (low fluid and high protein
intake)
 Infection may contribute to the formation of kidney
stones
 Urinary tract obstruction
 Medications (carbonic anhydrase inhibitors, triam-
terene, indinavir, and vitamin C)10,12,40
Signs and symptoms of kidney stones include the
following10,12,24:
 Pain in the flank or groin, depending on the stone
location (Pain increases greatly as the stone passes
through the ureters.)
 Hematuria
 Nausea and vomiting
 Fever
 Variable urine pH
 Variable levels of serum calcium, chloride, phos-
phate, carbon dioxide, uric acid, and Cr
338 CHAPTER 9 Genitourinary System
After identification of the stones by noncontrast CT
scan, management of kidney stones includes any of the
following10,12, 24,40,42:
 Analgesics
 Discontinuation of the aforementioned medications
 Antiinfective agents in conjunction with external
urinary drainage
 Reduction in dietary consumption of predisposing
factors, such as salt and protein
 Specific therapies aimed at reducing stone
formation, including thiazide diuretics, pyridoxine,
magnesium, orthophosphate, and potassium citrate
 Oral corticosteroids, alpha-blockers, and calcium
channel blockers may enhance passage of stones
 Ureteroscopic stone extraction or in situ extracorpo-
real shock wave lithotripsy (SWL) in cases where
stones do not pass spontaneously
DIABETIC NEPHROPATHY
Approximately 20% to 30% of people with type 1
or type 2 diabetes will develop diabetic nephro-
pathy,43 which is characterized by systemic vascular
changes in the kidneys that result in scarring (nephro-
sclerosis) of the glomeruli and, ultimately, in reduced
kidney function. Diabetic nephropathy is the most
common cause of ESRD in the United States.28
Pyelonephritis and necrosis of the renal papillae
are also associated with diabetic nephropathy.
Patients who demonstrate poor glycemic control
with resultant vascular disease and hypertension
are more likely to develop diabetic nephropathy.
Hypertension can lead to or result from diabetic
nephropathy.10,43,44
Signs and symptoms of diabetic nephropathy
include the following10,28,43,44:
 Microalbuminuria, oliguria, anuria. Microalbumi-
nuria is a critical screening tool for early detection
of nephropathy.
 Proteinuria
 Peripheral edema.
Management of diabetic nephropathy includes any
of the following10,43,44:
 Strict glycemic control (Refer to the Diabetes
Mellitus section in Chapter 11.)
 Antihypertensive agents (ACE inhibitors, calcium
channel blockers)
 Restriction of protein intake
 Hydration
 Diuretics
 Nutritional support
 Dialysis
 Simultaneous pancreas-kidney transplantation
(See Chapter 12.)
Renal Vascular Abnormalities
RENAL ARTERY STENOSIS OR OCCLUSION
Renal artery stenosis is a narrowing of the renal artery
lumen; renal artery occlusion is blockage of the renal
artery lumen. Renal artery stenosis or occlusion can
result from any or all of the following: atheroscle-
rotic disease, diabetes mellitus, subacute bacterial endo-
carditis, emboli from mitral valve stenosis, and mural
thrombi that develop after myocardial infarction.
Decreased renal perfusion results in renovascular hy-
pertension as a result of increased renin production.10,45
Signs and symptoms of renal artery stenosis or
occlusion include the following10,45:
 Hypertension
 Microscopic hematuria
 Flank or upper abdominal pain
 Abdominal aortic, renal artery bruits, or both
 Peripheral edema
 Acute renal failure after initiating ACE inhibitor
therapy28
Diagnosis can be established by Doppler ultrasono-
graphy, magnetic resonance angiography (MRA) and
renal angiography (which is the gold standard for
diagnosis).28
Management of renal artery stenosis or occlusion
includes any of the following10,45:
 Antihypertensive agents (ACE inhibitors)
 Anticoagulation agents
 Analgesics
 Dialysis
 Surgery: Angioplasty with possible stent placement
is the preferred invasive management, however
bypass grafting may still be performed.28
RENAL VEIN THROMBOSIS
Renal vein thrombosis is an uncommon disorder,
resulting in the accumulation of plaque in the renal
vein. Renal vein thrombosis can be caused by dehydra-
tion, sepsis, a hypercoagulable state, injury to the abdo-
men or back, renal tumors extending into the renal
vein, and nephrotic syndrome. Sudden occlusion of
the renal vein results in renal infarcts.10,46
Signs and symptoms of renal vein thrombosis
include the following9,10,46:
 Flank pain

 Gross hematuria
 Proteinuria
 Oliguria
Renal vein thrombosis can be managed with
anticoagulants or thrombolytic agents.9,10,46
Urinary Tract Dysfunction
CYSTITIS
Bacteria, viruses, fungi, chemical agents, radiation
exposure, and autoimmune dysfunction are all poten-
tial causative factors that can lead to cystitis, which is
an inflammation of the bladder wall. Cystitis and uri-
nary tract infections are not synonymous, as inflamma-
tion of the bladder can occur from noninfectious
causes. However, cystitis can occur with prostatitis or
pyelonephritis.23 Cystitis that occurs from noninfec-
tious causes is called interstitial cystitis and is relatively
uncommon.47,48 People who are sexually active or who
have an indwelling catheter, urinary tract obstructions,
diabetes mellitus, neurogenic bladder, or poor hygiene
are at greater risk of developing acute infectious
cystitis.23
Signs and symptoms of cystitis include the
following23,47,48:
 Urinary frequency and urgency
 Dysuria
 Hematuria (in more serious cases)
 Nocturia
 Suprapubic pain, low back pain, or both
Management of cystitis includes any of the
following23,24,47,48:
 Cephalexin, Ciprofloxacin, Nitrofurantoin (macro-
crystals), Norfloxacin, Ofloxacin, Trimethoprim-
sulfamethoxazole (although drug resistance is
developing with this agent).
 Increased fluid intake.
 Therapeutic hydrodistention with or without
intravesicular instillation. Therapeutic hydrodisten-
tion is performed under general anesthesia, and the
bladder is hydrodistended to help identify areas of
inflamed epithelium and promote healing of these
areas, as well as to help distend the bladder, which
may help with pain relief. Intravesicular instillation
is commonly performed with therapeutic
hydrodistention and involves infusion of agents
such as antiinflammatory analgesic agents into the
bladder.
 Surgical management with total or subtotal cystect-
omy, denervation of the bladder, or procedures that
Genitourinary System CHAPTER 9 339
increase bladder capacity (all of these are last-resort
measures).
URINARY CALCULI
Urinarycalculi are stones (urolithiasis) thatcan form any-
where in the urinary tract outside of the kidneys.
Formation of stones, symptoms, and management are
similar to that of kidney stones (see the Nephrolithiasis
section for further details on the formation and clinical
presentation of kidney stones).49 Management that may
be specific to urinary calculi includes extracorporeal
shock wave lithotripsy and ureteroscopy.28,50
NEUROGENIC BLADDER
A neurogenic bladder is characterized by bladder paral-
ysis that occurs with central nervous system disruption
(Parkinson’s disease, stroke, brain tumors, multiple
sclerosis, or trauma) at the cortical or spinal cord level,
resulting in urinary flow disturbances such as nocturia
and frequent leakage of small amounts of urine.51
Lesions above the sacral level of the spinal cord
result in loss of voluntary control of voiding; lesions
below the sacral level result in the loss of voluntary
and involuntary control of voiding. Neurogenic blad-
ders may lead to infection, especially when there is asso-
ciated bladder distention and urine retention, catheter
placement, or stone formation, which can be caused
by bone resorption from physical immobility.12,52
Symptoms of neurogenic bladders with infection are
difficult to assess, because altered sensation from neu-
rologic disturbance often masks pain or other symp-
toms. However, the patient may report a burning
sensation with voiding.12
Management consists of addressing the primary
neurologic disturbance (as able) and providing antiin-
fective agents for any associated infection.12 To assist
with a poorly contractile bladder, augment voiding
techniques such as suprapubic pressure and double
voiding may be employed. If these are unsuccessful,
then intermittent or indwelling catheterization is the
only management option.51 Anticholinergic agents
have also been helpful with this disorder.52 Table 9-3
provides a summary of the different types of urinary
incontinence.
Prostate Disorders
BENIGN PROSTATIC HYPERPLASIA
Benign prostatic hyperplasia (BPH) is a benign, pro-
gressive enlargement of the prostate gland and is the
340 CHAPTER 9 Genitourinary System
Table 9-3 TYPES OF URINARY INCONTINENCE
Type Description
Stress Loss of urine that occurs involuntarily
in situations associated with increased
intraabdominal pressure, such as with
laughing, coughing, or exercise
Urge Leakage of urine that occurs after a sensation
of bladder fullness is perceived
Overflow Leakage of urine from mechanical forces or
urinary retention from an overdistended
bladder
Functional The inability to void because of cognitive
or physical impairments, psychological
unwillingness, or environmental barriers
Adapted from Bullock BL. Disorders of Micturition and Obstruction of the GenitourinaryTract. In BL Bullock (ed), Pathophysiology:
Adaptations and Alterations in Function (4th ed). Philadelphia: Lippincott, 1996;648.
most common benign tumor in men, at times consid-
ered part of the normal aging process.53 There is a
20% incidence in men between the ages of 41 and 50
and a 50% incidence in men ages 51 to 60 years.24
Concern arises when enlargement interferes with
normal voiding patterns. Acute urinary retention and
urinary tract infection are the primary complications
of BPH.54 Signs and symptoms of BPH include the
following24,53,54:
 Palpable prostate gland lobes with digital rectal
examination
 Decreased force and caliber of urinary stream
 Straining to void
 Postvoid dribble
 Urinary frequency (less than 2 hours between voids)
with incomplete emptying
 Nocturia and dysuria
Management of BPH includes any of the
following24,53,54:
 Alpha1-adrenergic blocking agents (doxazosin
[Cardura], tamsulosin [Flomax], terazosin [Hytrin],
phenoxybenzamine, prazosin, alfuzosin) act to relax
the smooth muscle in the prostate and neck of the
bladder to facilitate voiding.
 5a-reductase enzyme inhibitor (finasteride
[Proscar]) inhibits male hormones to prostate
causing the gland to shrink over time.
 Antiinfective agents (if there is associated
infection).
Common Causes
Weakness in the bladder outlet region, urethral
sphincter, or pelvic floor muscles
Cystitis, urethritis, tumors, stones, outflow
obstructions, stroke, dementia, and parkinsonism
Obstruction by prostate, stricture or cystocele
A noncontractile bladder, as occurs in diabetes mellitus
or spinal cord injury
A neurogenic bladder, as occurs in multiple sclerosis or
other lesions above the sacral portion of the spinal
cord
Depression, anger, hostility, dementia, and other
neurologic disorders
 Intermittent self-catheterization.
 Phytotherapy with plant extracts such as palmetto
bark (interest in use is growing but not part of
standardized care)
 Surgical options include transurethral incision of
the prostate (TUIP), transurethral resection of the
prostate (TURP), suprapubic or retropubic prostatec-
tomy (open removal of the prostate), transurethral
laser-induced prostatectomy (TULIP), transure-
thral needle ablation of the prostate (TUNA),
transurethral electrovaporization of the prostate,
hyperthermia.
PROSTATITIS
Prostatitis is an inflammation of the prostate gland.
It can be divided into four categories: (1) acute
bacterial, (2) chronic bacterial, (3) nonbacterial, and
(4) prostatodynia (presence of prostatitis symptoms
without physical findings). Nonbacterial prostatitis
and prostatodynia occur more commonly than do
acute and chronic bacterial prostatitis. Causative
pathogens for acute and chronic bacterial prostati-
tis can include E. coli, Pseudomonas aeruginosa, and
Enteroccocus.24,53
Signs and symptoms of prostatitis include the
following49,53:
 Fever with rectal, perineal, or low back pain (acute
bacterial prostatitis)
 Increased urinary frequency or urgency to void

 Painful urination (dysuria)
 Bladder irritability
 Difficulty initiating a stream
 Nocturia
 Sexual dysfunction
Management of prostatitis includes any of the
following49,53:
 Dietary modifications as necessary (alcohol, chili
powder, and other hot spices can aggravate symptoms)
 Antiinfective agents (for bacterial prostatitis)
 Alpha1-adrenergic blocking agents (for prostatody-
nia, see the Benign Prostatic Hyperplasia section.)
 Antipyretics
 Surgery (open resection of the prostate orTURP)
Endometriosis
Endometriosis is the second most common cause of
dysmenorrhea and can be a confounding source of
musculoskeletal pain. Aberrant growth of endometrial
tissue occurs outside of the uterus, particularly in the
dependent parts of the pelvis and ovaries. The inci-
dence is greatest between the ages of 25 and 29 as well
as in infertile women.The exact nature of the pathogen-
esis and etiology are currently unknown; however, the
most well-accepted theory of endometrial implantation
is retrograde menstrual flow into the pelvic cavity
from the uterus. Differential diagnosis of endometrio-
sis includes pelvic inflammatory disease, ovarian neo-
plasms and uterine myomas, as well as possible bowel
neoplasms. Laparoscopic examination will confirm
the diagnosis of endometriosis.55,56
Signs and symptoms of endometriosis include the
following55,56:
 Pelvic pain (hypogastric and perineal regions) related
to the menstrual cycle
 Dysmenorrhea
 Dyspareunia (pain with intercourse)
 Pain in the low back and lower extremities
Management of endometriosis includes any of the
following55,56:
 Hormonal therapy aimed at reducing hormone levels
and cyclic stimulation of ectopic endometrial tissue.
Agents used include nafarelin nasal spray, Danazol,
oral or percutaneous contraceptives, and medroxy-
progesterone acetate.
 Laparoscopic ablation of endometrial implants
(ectopic tissue) with concurrent uterine nerve
ablation to significantly reduce pain.
 Total abdominal hysterectomy and bilateral
salpingo-oophorectomy (TAH-BSO) in women
who no longer wish to bear children.
Genitourinary System CHAPTER 9 341
MANAGEMENT
The specific management of various genitourinary
disorders is discussed earlier in the respective
pathophysiology sections. This section expands on
renal replacement therapy and surgical procedures.
Guidelines for physical therapy intervention for
patients who have genitourinary dysfunction are also
discussed.
Renal Replacement Therapy
The primary method of managing fluid and elec-
trolyte balance in patients with ARF or CRF is perito-
neal dialysis or intermittent hemodialysis. Both types
of dialysis use the principles of diffusion, osmosis,
and ultrafiltration to balance fluid and electrolyte
levels. Diffusion is the movement of solutes, such as
Cr, urea, or electrolytes, from an area of higher con-
centration to an area of lower concentration. Osmosis
is the movement of fluid from an area of lesser solute
concentration to an area of greater solute concentra-
tion. Ultrafiltration, the removal of water and fluid,
is accomplished by creating pressure gradients
between the arterial blood and the dialyzer membrane
or compartment.19
Another method to manage patients with ARF who
are critically ill is continuous renal replacement therapy
(CRRT).13,19
PERITONEAL DIALYSIS
Peritoneal dialysis (PD) involves using the peritoneal
cavity as a semipermeable membrane to exchange solu-
ble substances and water between the dialysate fluid
and the blood vessels in the abdominal cavity.10,13,19
Dialysate fluid is instilled into the peritoneal cavity
through an indwelling catheter that is either placed
surgically or nonsurgically. Surgical placement is prefer-
able, as direct visualization during the procedure facili-
tates better placement. After the dialysate is instilled
into the peritoneum, there is an equilibration period
when water and solutes pass through the semipermeable
membrane. Once equilibration is finished, then the
peritoneal cavity is drained of the excess fluid and
solutes that the failing kidneys cannot remove.
Instillation, equilibration, and drainage constitute one
exchange.19
The process of peritoneal dialysis can range from
45 minutes to 9 hours, depending on the method of
PD, and patients can have anywhere from 4 to
24 exchanges per day.19
342 CHAPTER 9 Genitourinary System
A dialyzer (artificial kidney). The dialysate fluid contains
B arteriovenous fistula is created by performing a
FIGURE 9-3
Schematic illustration of continuous ambulatory peritoneal
dialysis. A, Instillation of dialysate fluid. B, Drainage of excess
fluid and solutes. (Courtesy Peter Wu.)
There are two types of PD: automated PD and con-
tinuous ambulatory PD. Automated PD uses an auto-
matic cycling device to control the instillation,
equilibration, and drainage phases. Continuous ambu-
latory PD involves manually exchanging dialysate
fluids 4 times a day and is schematically represented in
Figure 9-3.19
The following are indications for peritoneal
dialysis7,10:
 Need for less rapid management of fluid and electro-
lyte imbalances
 Staff and equipment for hemodialysis unavailable
 Inadequate vascular access for hemodialysis
 Shock
 Status post cardiac surgery (e.g., coronary artery
bypass grafting)
 Severe cardiovascular disease
 Patient refusal of blood transfusions
The following are contraindications for peritoneal
dialysis:
 Peritonitis
 Abdominal adhesions
 Hernias
 Concurrent pulmonary complications, such as atelec-
tasis or pneumonia
 Recent abdominal surgery
INTERMITTENT HEMODIALYSIS
Kidney functions that are controlled by intermittent
hemodialysis include (1) fluid volume, (2) electrolyte
balance, (3) acid-base balance, and (4) filtration
of nitrogenous wastes. The patient’s arterial blood
is mechanically circulated through semipermeable
tubing that is surrounded by a dialysate solution in the
electrolytes similar to those in normal blood plasma
to permit diffusion of electrolytes into or out of
the patient’s blood.7,10 As the patient’s arterial blood
is being filtered through the dialyzer, ‘‘clean’’ blood
is returned to the patient’s venous circulation.
Figure 9-4 illustrates this process.
Vascular access is attained either through cannula
insertion (usually for temporary dialysis) or through
an internal arteriovenous fistula (for chronic dialysis
use), which is surgically created in the forearm. The
side-to-side, side-to-end, or end-to-end anastomosis
between the radial or ulnar artery and the cephalic
vein. If a native fistula cannot be created, then a syn-
thetic graft is surgically anastomosed between the arte-
rial and venous circulation.7,10,19 Figure 9-5 illustrates
these various types of vascular access.
Patients who require intermittent hemodialysis for
acute renal failure are generally required to replace
2 to 3 liters of fluid per dialysis session in order to
fully achieve clear waste products and achieve osmotic
balance. This large amount of fluid exchange can pro-
mote hypotension and possible ischemia of nephrons
in patients who are critically ill. Therefore in the more
unstable patient, continuous renal replacement therapy
may be more suitable.15
Patients who require chronic intermittent hemodial-
ysis usually have it administered three to four times
per week, with each exchange lasting approximately
3 to 4 hours. The overall intent of this process is to
extract up to 2 days’ worth of excess fluid and solutes
from the patient’s blood.13
Indications for hemodialysis include the
following7,10:
 Acute poisoning
 Acute and chronic renal failure
 Severe states of edema
 Hepatic coma
 Genitourinary System CHAPTER 9 343
Blood pump

Pressure
monitor Jugular
vein

Pressure
monitor Subclavian
Infusion pump vein

Superior
Temperature monitor vena
cava
Conductivity meter

Dialyzer

Purified Blood leak

water detector
Pressure
monitor

Air
Dialysate bubble
concentrate detector

Drain

Dialysate (negative)
pressure pump
FIGURE 9-4
Schematic representation of hemodialysis. (FromThompsonJM, McFarland GK, HirschJE, et al: Mosby’s
Clinical Nursing [3rd ed]. St. Louis: Mosby, 1993;938.)

 Metabolic acidosis  Associated major chronic illnesses

 Extensive burns with prerenal azotemia
 Transfusion reactions
 Postpartum renal insufficiency
 Crush syndrome (reduction in circulating plasma
volume, hypotension, and hemoconcentration after
crush injury)
Contraindications for hemodialysis include the
following10:
 No vascular access
 Hemorrhagic diathesis
 Extremes in age
 Poor compliance with treatment regimen
CONTINUOUS RENAL REPLACEMENT THERAPY
The purpose of continuous renal replacement therapy
(CRRT) is to provide a slow yet continuous mechanism
344 CHAPTER 9 Genitourinary System

C
FIGURE 9-5
Methods of vascular access for hemodialysis. A, Internal arteriovenous fistula. B, Looped graft in
forearm. C, External cannula or shunt. (From SM Lewis, MM Heitkemper, SR Dirsksen [eds]. Medical-
Surgical Nursing: Assessment and Management of Clinical Problems [5th ed]. St. Louis: Mosby,
2000;1325.)

to remove fluid and electrolytes as well as small and
medium solutes from the body in a manner that
mimics the natural function of the patient’s native
kidney. Because of the slow process involved with
CRRT, it is frequently used in the critical care setting
to stabilize and manage patients without the adverse
effects of hypotension that can occur with intermittent
hemodialysis. CRRT can be performed for as long as
30 to 40 days, with the hemofilter being changed
every 1 to 2 days. CRRT can also be performed as
an adjunct to intermittent hemodialysis. The several
types of CRRT are described in the following
paragraphs.13,15,19
Continuous arteriovenous hemofiltration (CAVH)
uses the femoral artery and vein as common sites for
vascular access. Pressure gradients between the arterial
and venous system along with oncotic pressures
help drive the hemofiltration process, which mimics
the urine formation process in the renal glomerulus.
Heparin is infused to help prevent clotting in the

FIGURE 9-6
Schematic representation of continuous arteriovenous hemofiltration. (Courtesy Peter Wu.)
hemofilter and tubing. Medications and nutrition
can also be administered through the circuit.10,13,19
Figure 9-6 illustrates CAVH. In critically ill patients
who experience frequent episodes of hypotension, the
pressure gradients are too weak to create a significant
driving pressure necessary to achieve adequate filtra-
tion rates. Therefore in this patient population, a
mechanical pump is necessary to help move the blood
at sufficient rates; this is achieved in continuous veno-
venous hemofiltration (CVVH), which is now the pre-
ferred mode of CRRT.15
Continuous venovenous hemofiltration uses the
venous system as access sites (internal jugular vein
or subclavian vein) along with a mechanical
pump and an external filter for blood exchange.
Replacement fluids are generally infused after the
blood has passed through the filter so that blood
that returns to the patient is more osmotically
balanced. CVVH can operate continuously 24 hours
a day for several days.15
Genitourinary System CHAPTER 9 345
Continuous venovenous hemodialysis (CVVHD) is
similar to CVVH except that a dialysate solution is
used to help waste products diffuse out of the blood-
stream. An advantage to this system is that filtration
rates can be set at a higher speed, allowing for more
efficient exchanges for patients who are appropriate
for this therapy.15
Continuous venovenous hemodiafiltration
(CVVHDF) utilizes convection, diffusion, and ultrafil-
tration to help clear both medium and small molecules
at an efficient rate. Slow continuous ultrafiltration
(SCUF) is a mechanism utilized to primarily remove
excess fluid without the need to balance electrolytes
and clear wastes.15
Indications for CRRT include the following:
 Cardiovascular instability
 Parenteral nutrition
 Cerebrovascular or coronary artery disease
 ARF with multiple organ failure
 Inability to tolerate hemodialysis
346 CHAPTER 9 Genitourinary System
 Azotemia
 Sepsis
Contraindications for CRRT include the following:
 Hypercatabolic state
 Hyperkalemia
 Poisoning
 Shock
 Low colloid oncotic pressure
 Congestive heart failure
 Severe arthrosclerosis
 Low blood flow (i.e., mean arterial pressure less than
60 mm Hg)
CLINICAL TIP
 Pulmonary hygiene treatments can be performed
during dialysis; however, this depends on the
hemodynamic stability of the patient and is at the
discretion of the nurse or physician. Extreme caution
should be taken with the access site to prevent
accidental disruption.
 The dialysis nurse is generally nearby to monitor the
procedure and is a valuable source of information
regarding the patient’s hemodynamic stability.
 Activity tolerance can be altered when fluid
and electrolyte levels are unbalanced. Patients will
demonstrate variable levels of fatigue; some are
more fatigued before a dialysis session, whereas
others are more fatigued after a dialysis session.
 Fluid and electrolyte imbalance can also alter the
hemodynamic responses to activity; therefore,
careful vital sign and symptom monitoring should
always be performed.
Surgical Interventions
Surgical interventions for genitourinary system disor-
ders can be categorized broadly as procedures that
remove diseased portions of the genitourinary tract or
procedures that restore urinary flow. These interven-
tions are briefly discussed in the following sections.
Refer to Appendix V for general postanesthesia
considerations.
NEPHRECTOMY
There are three types of nephrectomy. The primary
indications for removing a part or all of the kidney
include renal tumor, polycystic kidney disease, severe
traumatic injury to the kidney, and organ donation, as
well as removing a failing transplanted organ.57,58
Nephrectomy can be performed as an open or
laparoscopic procedure. Open nephrectomy is the con-
ventional method that requires an incision of approxi-
mately 7 in. Laparoscopic nephrectomy involves five
access sites, ranging from less than 0.5 in. to 3 in.
Laparoscopic nephrectomy is gaining acceptance as a
viable alternative to open nephrectomy, as there have
been fewer postoperative complications associated
with the procedure.57- 60 The types of nephrectomy
and their definitions follow:
Radical nephrectomyçremoval of the entire kidney, a sec-
tion of the ureter, the adrenal gland, and the fatty
tissue surrounding the kidney.
Simple nephrectomyçremoval of the entire kidney with a
section of the ureter. Generally performed when
harvesting donor organs for kidney transplantation.
Partialnephrectomyçonly the infected or diseased portion
of the kidney is removed.
OPEN PROSTATECTOMY
Open prostatectomy is the surgical removal of a pros-
tate gland with or without its capsule and is primarily
indicated for patients with prostate cancer. Five types
of surgical approaches can be used: (1) transcoccygeal,
(2) perineal, (3) retropubic, (4) transvesical, and (5)
suprapubic. This procedure is contraindicated if the
prostate is small and fibrous. The suprapubic and
retropubic approaches of this procedure are contra-
indicated in the presence of cancer.49
TRANSURETHRAL RESECTION
Transurethral resection refers to the surgical approach
performed when managing bladder tumors, bladder
neck fibrosis, and prostatic hyperplasia. The most
common type of transurethral resection is a TURP,
which this section focuses on. TURP is indicated for
obstructive BPH. Involved tissues are resected with a re-
sectoscope that is inserted through the urethra.
Excision and coagulation of tissue are accompanied
by continuous irrigation. Contraindications for TURP
include the presence of urinary tract infection and
a prostate gland weighing more than 40 g. TURP is
also contraindicated with conditions that interfere
with operative positioning for the procedure, such
as irreversible scrotal hernia or ankylosis of the hip.49
PERCUTANEOUS NEPHROSCOPIC STONE REMOVAL
Percutaneous nephroscopic stone removal involves the
removal of stones formed in the urinary tract with a per-
cutaneous nephrostomy tube that is placed under fluo-
roscopic monitoring. Depending on the size of the
stone, stones may need to be broken up, and then

removed with a basket. Small fragments can be flushed
through the system mechanically or physiologically.
Considerations for this procedure include controlling
septicemia before removal of the stones.49
OPEN UROLOGIC SURGERY
Open urologic surgery is a large category of surgical
procedures that is beyond the scope of this book but
includes the following49:
 Nephrolithotomy (renal incisions for kidney stone
removal)
 Pyelolithotomy (removal of the kidney stone from
the pelvis of the kidney)
 Ureterolithotomy (removal of a urinary stone from
the ureter)
 Cystectomy (bladder removal)
Radical cystectomy is the complete removal of the
bladder, and segmental resection is the partial removal
of the bladder.8
BLADDER NECK SUSPENSION
Bladder neck suspension is a procedure used in women
to help restore urinary continence by suturing the ure-
thra to the pubic bones, which increases urethral resis-
tance. It is indicated for women with stress
incontinence as a result of pelvic relaxation.This proce-
dure may also be called the Marshall-Marchetti-Krantz
procedure or retropubic suspension. Bladder neck sus-
pension is contraindicated in cases of urethral sphincter
damage leading to stress incontinence.49,61,62
URINARY DIVERSION
Obstructed urinary flow can be resolved by divert-
ing urine with any of these four procedures: (1) supra-
vesical diversion, (2) incontinent urinary diversion,
(3) continent urinary diversion, and (4) orthotopic
neobladder.8,49,57
SUPRAVESICAL DIVERSION. A supravesical diver-
sion is one in which the urine is diverted at the level of
the kidney by nephrostomy. Nephrostomy involves pla-
cing a catheter through the renal pelvis and into the
renal calyces to temporarily drain urine into an external
collection device (Figure 9-7). Complications, such as
stone formation, infection, hemorrhage, and hema-
turia, can be associated with long-term nephrostomy
tube placement.49,57
INCONTINENT URINARY DIVERSION. Incontinent
urinary diversion involves diverting urine flow to the
skin through a stoma, which then requires an external
appliance to collect urine. Segments of the ileum (ileal
conduit) or colon (colon conduit) are generally used as a
Genitourinary System CHAPTER 9 347
tube to bridge the gap from the ureter to the skin when
the bladder must be removed or bypassed (see Figure 9-
7). Once the diversion is complete, urine drains from
the stoma into the collecting device every few seconds.
These conduit segments of intestine become totally iso-
lated from the gastrointestinal tract.3,57 Bladder carci-
noma and severe neuropathic bladder dysfunction are
common indications for this procedure.8
CONTINENT URINARY DIVERSION. Continent uri-
nary diversions are internal urine reservoirs that are sur-
gically constructed from segments of the ileum,
ileocecal segment, or colon. The Kock continent ileal
reservoir is formed from loops of small intestine. The
ileocecal (Indiana) pouch is formed from the intestine
and ileum.8 These internal reservoirs eliminate the
need for external appliances and allow more control
for the patient. The internal reservoir is connected to
an abdominal stoma, which does not continually drain
urine, and patients perform intermittent self-catheteri-
zations through the stoma (see Figure 9-7).49,57
ORTHOTOPIC NEOBLADDER. Orthotopic neoblad-
der involves reshaping a portion of the distal ileum into
a neobladder and connecting the ureters and the urethra
to it.This procedure is indicated for patients with a func-
tional sphincter without cancer in the urethra, trigone,
or bladder neck. Connecting the urethra to the neoblad-
der allows for natural micturition without the need for
an external stoma. However, incontinence still may
occur occasionally with this procedure, and the patient
may also require intermittent catheterization.8,57
PHYSICAL THERAPY INTERVENTION
The following are general goals and guidelines for the
physical therapist when working with patients who
have genitourinary dysfunction. These guidelines
should be adapted to a patient’s specific needs.
The primary physical therapy goals in this patient
population are similar to those of other patients in the
acute care setting. These goals are to (1) optimize
safe functional mobility, (2) maximize activity toler-
ance and endurance, and (3) prevent postoperative
pulmonary complications.
General physical therapy management guidelines
and considerations revolve around the normal func-
tions of the genitourinary system that are disrupted by
the various disorders discussed earlier in this chapter.
These include, but are not limited to, the following:
1. Evaluating laboratory values before examination or
intervention can help the physical therapist decide
348 CHAPTER 9 Genitourinary System

A B

FIGURE 9-7
Methods of urinary diversion. A, Ureteroileosigmoidostomy. B, Ileal loop (or ileal conduit).
C, Ureterostomy (transcutaneous ureterostomy and bilateral cutaneous ureterostomies). D, Nephrostomy.
(From Lewis SM, Heitkemper MM, Dirsksen SR: Medical-Surgical Nursing: Assessment and
Management of Clinical Problems [5th ed]. St. Louis: Mosby, 2000;1292.)

which particular signs and symptoms to monitor as
well as determine the parameters of the session.
Refer to Appendix II for more information on fluid
and electrolyte imbalance.
2. The inability to regulate cellular waste products,
blood volume, and electrolyte levels can result in:
 Mental status changes from a buildup of ammo-
nia, BUN, Cr, or a combination of these. If this sit-
uation occurs, then the therapist may choose to
modify or defer physical therapy intervention,
particularly educational activities that require
concentration.
 Disruption of excitable tissues such as peripheral
nerves and skeletal, cardiac, and smooth muscle
from altered levels of electrolytes.63 If this situation
occurs, then the therapist may need to reduce exer-
cise intensity during muscle strengthening activ-
ities. Additionally, if peripheral neuropathy
results in sensory deficits, then the therapist needs
to take the appropriate precautions with the use
of modalities and educate the patient on protective
mechanisms to avoid skin breakdown.
 Peripheral or pulmonary edema from inability to
excrete excess body fluids.63 Pulmonary edema
can result in shortness of breath with activities
and recumbent positioning. Peripheral edema
can result in range-of-motion limitations and
skin breakdown. Refer to Table 1-6 for a descrip-
tion of pitting edema, and see Chapter 2 for a
description of pulmonary edema.
3. Blood pressure regulation can be altered by the
inability to excrete body fluids and activate the
renin-angiotensin system.63
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Function. In BL Bullock (ed), Pathophysiology:
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Genitourinary System CHAPTER 9 349
4. Activity tolerance can be reduced by the factors
mentioned in this list, as well as anemia that can
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from kidneys, which is necessary for stimulating
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5. Patients with CRF may present with concurrent clin-
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17. Boone CA. End-stage renal disease in African-
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19. Brunier B, Bartucci M. Acute and Chronic Renal
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20. Boissonault WG. UrinaryTract Disorders. In CC
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24. Stoller ML, Kane CJ, Meng MV. Urologic Disorders. In
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25. Talan DA, Stamm WE, Hooton TM, et al. Comparison
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26. Ellsworth PI, Cendron M, McCullough MF. Surgical
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28. Watnick S, Morrison G. Kidney Disease. InTierney LM,
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29. AmbrusJLJr, Sridhar NR. Immunologic aspects of
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33. Madaio MP, HarringtonJT.The diagnosis of glomerular
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35. Orth SR, Ritz E.The nephrotic syndrome. N EnglJ
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 10 Infectious Diseases

Jaime C. Paz INTRODUCTION

V. Nicole Lombard A patient may be admitted to the hospital setting with an infectious
Rachael Maiocco process acquired in the community or may develop one as a complication
from the hospital environment. An infectious disease process generally
has a primary site of origin; however, it may result in diffuse systemic
effects that may limit the patient’s functional mobility and activity
tolerance. Therefore, a basic understanding of these infectious disease
processes is useful in designing, implementing, and modifying physical
therapy treatment programs. The physical therapist may also provide
treatment for patients who have disorders resulting from altered immu-
nity. These disorders are mentioned in this chapter because immune
system reactions can be similar to those of infectious disease processes
(see Appendix 10-A for a discussion of four common disorders of altered
immunity: systemic lupus erythematosus, sarcoidosis, amyloidosis, and
rheumatoid arthritis).The objectives of this chapter are to provide a basic
understanding of the following:
1. Clinical evaluation of infectious diseases and altered immune disor-
ders, including physical examination and laboratory studies
2. Various infectious disease processes, including etiology, pathogenesis,
clinical presentation, and management
3. Commonly encountered altered immune disorders, including etiology,
clinical presentation, and management
4. Precautions and guidelines that a physical therapist should imple-
ment when treating a patient with an infectious process or altered
immunity
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:

Diagnosis/Disease Possible Practice Pattern

Nosocomial Infections: Escherichia 6B, 7A
coli, Staphylococcus aureus, Enterococcus
faecalis, Pseudomonas aeruginosa, Candida
albicans, and coagulase-negative
staphylococci
Antibiotic-Resistant Infections: 6B, 7A
Methicillin-resistant Staphylococcus
aureus,Vancomycin-Resistant
Enterococci
Continued

353
354 CHAPTER 10 Infectious Diseases

Diagnosis/Disease Possible Practice Pattern

Neurological Diseases: 4A, 5C, 5D, 5G, 6E,
Encephalitis, meningitis, 5H, 7A
poliomyelitis and postpoliomyelitis
syndrome
Upper RespiratoryTract Infections: 6B, 6F, 6G
Rhinitis, sinusitis, influenza,
pertussis
Lower RespiratoryTract Infections: 6B, 7C, 7D
Tuberculosis, Histoplasmosis
Cardiac Infections: Pericarditis, 6B, 6D
myocarditis, left-sided endocarditis,
acute rheumatic fever, Rheumatic
heart disease. See Chapters 1 and 10
Musculoskeletal Infections: 4G, 4H, 5H
Osteomyelitis and its variations
Skin Infections: Cellulitis, groups 4E, 6H, 7B, 7C, 7D, 7E
A and G streptococcus, and S.
aureus
Gastrointestinal Infections: Please refer to Chapter 8
Gastroenteritis, e. coli, clostridium
difficile, and salmonella
Immune System Infections: HIV, 4C, 6B
mononucleosis, cytomegalovirus
infection, and toxoplasmosis
Sepsis: Bacteremia, septicemia, and 5C, 6F, 6H
shock syndrome (or septic shock)

Please refer to the back cover of this book for a com- lead to the development of active infection. Patients in
plete list of the preferred practice patterns as individual the acute care setting often present with factors that
patient conditions are highly variable and other practice can create some or most of these defects, which can
patterns may be applicable. ultimately affect their immune system (Table 10-3).2

DEFINITION OF TERMS EVALUATION

To facilitate the understanding of infectious disease
processes, terminology that is commonly used when
referring to these processes is presented inTable 10-1.1-3
OVERVIEW OF THE IMMUNE SYSTEM
When an infectious process is suspected, a thorough
patient interview (history) and physical examination
are performed to serve as a screening tool for the
differential diagnosis and to help determine which lab-
oratory tests are further required to identify a specific
pathogen.4

A person’s immune system is composed of many com- History

plex, yet synergistic, components that defend against Potential contributing factors of the infection are
pathogens (Table 10-2).1 Any defect in this system may sought out, such as exposure to infectious individuals
 Infectious Diseases CHAPTER 10 355

Table 10-1 TERMINOLOGY ASSOCIATED WITH INFECTIOUS DISEASE PROCESSES

Antibody A highly specific protein that is manufactured in response to antigens and defends against
subsequent infection
Antigen (immunogen) An agent that is capable of producing antibodies when introduced into the body of a
susceptible person
Carrier A person who harbors an infectious agent that can cause a specific disease but who
demonstrates no evidence of the disease
Colonization The process of a group of organisms living together; the host can carry the microorganism
without being symptomatic
Communicable The ability of an infective organism to be transmitted from person to person, either directly
or indirectly
Disseminated host Distributed over a considerable area
The person whom the infectious agent invades and from whom it gathers its
nourishment
Immunocompromised An immune system that is incapable of responding to pathogenic organisms and
tissue damage
Immunodeficiency Decreased or compromised ability to respond to antigenic stimuli by appropriate cellular
immunity reaction
Immunosuppression The prevention of formation of an immune response
Nosocomial infection Infection that is acquired in the hospital setting
Opportunistic An infectious process that develops in immunosuppressed individuals
(Opportunistic infections normally do not develop in individuals with intact
immune systems.)
Pathogen An organism capable of producing a disease
Subclinical infection A disease or condition that does not produce clinical symptoms, or the time period
before the appearance of disease-specific symptoms

Table 10-2 COMPONENTS OF THE IMMUNE SYSTEM

Lines of Defense Components Description
First line of defense Skin, conjunctivae, mucous Physical barriers to pathogens.
membranes
Second line of defense Inflammatory response Inflammatory response acts to (1) contain pathogen and
(2) bring immune cells to antigen by releasing histamine,
kinins and prostaglandins that cause vasodilation and
vascular permeability.
Third line of defense Immune response Specific immune response to pathogens.
Humoral immunity B cells produce antibodies.
(B cells)*
Cellular immunity T cells: (1) Augment production of antibodies. (2) Directly
(Tcells)* kill antigens. (3) Turn off immune system.
*B cells and Tcells can also be referred to as B lymphocytes orT lymphocytes, respectively.
Data from NS Rote. Immunity. In SE Heuther, KL McCance (eds), Understanding Pathophysiology (2nd ed). St. Louis: Mosby, 2000;125-150;
Marieb EN (ed). Human Anatomy and Physiology (2nd ed). Redwood City, CA: Benjamin Cummins, 1992;690-723; Guyton AC, HallJE.
Textbook of Medical Physiology (9th ed). Philadelphia: Saunders, 1996;445-455.
356 CHAPTER 10 Infectious Diseases

be consistent with active infection. Lymphoid organs

Table 10-3 FACTORS AFFECTING THE IMMUNE (lymph nodes and spleen) can also be swollen and
SYSTEM tender with infection, as lymphocytes (processed in
these organs) are multiplying in response to the antigen.
Congenital Disruption in the development Inflammation and tenderness in these or other areas of
(rare) of lymphocytes
the body can further help to delineate the infectious
Acquired Pregnancy
Preexisting infections process.
Malignancies (Hodgkin’s disease, acute VITAL SIGNS
or chronic leukemia, nonlymphoid
malignancy, or myeloma) HEART RATE, BLOOD PRESSURE, AND RESPIRATORY
Stress (emotional or surgicalçanesthesia) RATE. Measurement of vital signs helps in determining
Malnutrition (insufficiency of calories, whether an infectious process is occurring. (Infections
protein, iron, and zinc) result in an increased metabolic rate, which presents
Age as an increased heart rate and respiratory rate.) Blood
Chronic diseases (diabetes, alcoholic pressure may also be elevated when metabolism is
cirrhosis, sickle cell anemia) increased, or blood pressure can be decreased second-
Lymph node dissection ary to vasodilation from inflammatory responses in
Immunosuppressive treatment
(corticosteroids, chemotherapy,
the body.
or radiation therapy) TEMPERATURE. Monitoring the patient’s tempera-
Indwelling lines and tubes ture over time (both throughout the day and daily) pro-
vides information regarding the progression (a rise in
Data from Rote NS, Heuther SE, McCance KL. Hypersensitivities, temperature) or a regression (a fall in temperature) of
Infection, and Immunodeficiencies. In SE Heuther, KL McCance
(eds), Understanding Pathophysiology (2nd ed). St. Louis: Mosby,
the infectious process.With an infectious process, some
2000;204-208. of the bacteria and extracts from normal leukocytes
are pyrogenic, causing the thermostat in the hypo-
thalamus to raise resulting in an elevated body tempera-
ture.5 A fall in body temperature from a relatively
elevated temperature may also signify a response to a
or recent travel to foreign countries. Also, a qualitative medication.
description of the symptomatology is discerned,
such as onset or nature of symptoms (e.g., a nonproduc-
tive versus productive cough over the past day or CLINICAL TIP
weeks).
 An afebrile status is not always indicative of the
absence of infection. If a patient is on antipyretics,
Physical Examination the fever symptoms may be controlled. Check the
OBSERVATION medication list and ask about the administration
Clinical presentation of infectious diseases is highly schedule. A patient must be afebrile for at least
variable according to the specific system that is involved. 24 hours before being discharged from an inpatient
However, common physical findings that occur with setting.
infection include sweating and inflammation, both of
which are related to the metabolic response of the
body to the antigen. The classic signs of inflammation AUSCULTATION
(redness and edema) in certain areas of the body can Heart and lung sounds determine whether infectious
help delineate the source, location(s), or both of infec- processes are a direct result from these areas or are
tion. Delineating the source of infection is crucial to indirectly affecting these areas.
the diagnostic process.
Laboratory Studies
PALPATION Most of the evaluation process for diagnosing an infec-
The presence of warmth and possible pain or tender- tious disease is based on laboratory studies. These
ness is another typical sign of inflammation that may studies are performed to (1) isolate the microorganisms

from various body fluids or sites; (2) directly examine
specimens by microscopic, immunologic, or genetic
techniques; or (3) assess specific antibody responses to
the pathogen.6 This diagnostic process is essential to
prescribing the most specific medical regimen possible
for the patient.
HEMATOLOGY
During hematologic studies, a sample of blood is taken
and analyzed to assist in determining the presence of
an infectious process or organism. Hematologic proce-
dures used to diagnose infection include leukocyte
count, differential white blood cell (WBC) count, and
antibody measurement.7
LEUKOCYTE COUNT. Leukocyte, or WBC, count
is measured to determine whether an infectious
process is present and should range between
5,000-10,000 cells/mm3.1 An increase in the number of
WBCs, termed leukocytosis, is required for phagocytosis
(cellular destruction of microorganisms) and can indi-
cate the presence of an acute infectious process.8
Leukocytosis can also be present with inflammation
and may occur after a surgery with postoperative
inflammation.5 A decreased WBC count from baseline,
termed leukopenia, can indicate altered immunity or the
presence of an infection that exhausts supplies of
certain WBCs.8 A decreased WBC count relative to a
previously high count (i.e., becoming more within
normal limits) may indicate the resolution of an infec-
tious process.8
DIFFERENTIAL WHITE BLOOD CELL COUNT. Five
types of WBCs exist: lymphocytes, monocytes, neutro-
phils, basophils, and eosinophils. Specific types of
infectious processes can trigger alterations in the
values of one or more of these cells. Detection of these
changes can assist in identification of the type of infec-
tion present. For example, an infection caused by bacte-
ria can result in a higher percentage of neutrophils,
which have a normal range of 2.0 to 7.5  109/liter.
In contrast, a parasitic infection will result in increased
eosinophils, which have a normal count of 0.0 to
0.45  109/liter.8
ANTIBODY MEASUREMENT. Antibodies develop in
response to the invasion of antigens from new infec-
tious agents. Identifying the presence and concentra-
tion of specific antibodies helps in determining past
and present exposure to infectious organisms.9
MICROBIOLOGY
In microbiology studies, specimens from suspected
sources of infection (e.g., sputum, urine, feces,
Infectious Diseases CHAPTER 10 357
wounds, and cerebrospinal fluid) are collected by
sterile technique and analyzed by staining, culture, or
sensitivity or resistance testing, or a combination of
all of these.
STAINING. Staining allows for morphologic exami-
nation of organisms under a microscope. Two types of
staining techniques are available: simple staining and
the more advanced differential staining. Many types of
each technique exist, but the differential Gram’s stain
is the most common.9
Gram’s stain is used to differentiate similar organisms
by categorizing them as Gram-positive or Gram-
negative. This separation assists in determining subse-
quent measures to be taken for eventual identification
of the organism. A specimen is placed on a microscope
slide, and a series of steps are performed.10 A red speci-
men atcompletion indicates a Gram-negative organism,
whereas a violet specimen indicates a Gram-positive
organism.10
CULTURE. The purpose of a culture is to identify and
produce isolated colonies of organisms found within a
collected specimen. Cells of the organism are isolated
and mixed with specific mediums that provide the
proper nourishment and environment (e.g., pH level,
oxygen content) needed for the organism to reproduce
into colonies. Once this has taken place, the resultant
infectious agent is observed for size, shape, elevation,
texture, marginal appearance, and color to assist with
identification.10
SENSITIVITY AND RESISTANCE. When an organism
has been isolated from a specimen, its sensitivity
(susceptibility) to antimicrobial agents or antibiotics
is tested. An infectious agent is sensitive to an
antibiotic when the organism’s growth is inhibited
under safe dose concentrations. Conversely, an agent
is resistant to an antibiotic when its growth is not
inhibited by safe dose concentrations. Because of a
number of factors, such as mutations, an organism’s
sensitivity, resistance, or both to antibiotics are
constantly changing.11
CYTOLOGY
Cytology is a complex method of studying cellular
structures, functions, origins, and formations.
Cytology assists in differentiating between an infectious
process and a malignancy and in determining the
type and severity of a present infectious process by
examining cellular characteristics.9,12 It is beyond the
scope of this book, however, to describe all of the
processes involved in studying cellular structure
dysfunction.
358 CHAPTER 10 Infectious Diseases
BODY FLUID EXAMINATION
PLEURAL TAP. A pleural tap, or thoracentesis, is the
process by which a needle is inserted through the chest
wall into the pleural cavity to collect pleural fluid for
examination of possible malignancy, infection, inflam-
mation, or any combination of these. A thoracentesis
may also be performed to drain excessive pleural fluid
in large pleural effusions.13
PERICARDIOCENTESIS. Pericardiocentesis is a proce-
dure that involves accessing the pericardial space
around the heart with a needle or cannula to aspirate
fluid for drainage, analysis, or both. It is primarily
used to assist in diagnosing infections, inflammation,
and malignancies and to relieve effusions built up by
these disorders.14
SYNOVIAL FLUID ANALYSIS. Synovial fluid analysis,
or arthrocentesis, involves aspirating synovial fluid
from a joint capsule. The fluid is then analyzed and
used to assist in diagnosing infections, rheumatic dis-
eases, and osteoarthritis, all of which can produce
increased fluid production within the joint.15
GASTRIC LAVAGE. A gastric lavage is the suctioning
of gastric contents through a nasogastric tube to
examine the contents for the presence of sputum
in patients suspected of having tuberculosis (TB).
The assumption is that patients swallow sputum
while they sleep. If sputum is found in the gastric
contents, the appropriate sputum analysis should
be performed to help confirm the diagnosis of TB.13,16
Gastric lavage is also used as a medical intervention to
prevent absorption of certain toxins that have been
ingested.17
PERITONEAL FLUID ANALYSIS. Peritoneal fluid
analysis, or paracentesis, is the aspiration of perito-
neal fluid with a needle. It is performed to (1) drain
excess fluid, or ascites, from the peritoneal cavity,
which can be caused by infectious diseases, such
as TB; (2) assist in the diagnosis of hepatic or sys-
temic malfunctions, diseases, infection such as
spontaneous bacterial peritonitis (SBP) or malignan-
cies; and (3) help detect the presence of abdominal
trauma.13,16,18
OTHER STUDIES
Imaging with plain x-rays, computed tomography
scans, positron emission tomography, and magnetic
resonance imaging scans can also help identify areas
with infectious lesions.19,20 In addition, the following
diagnostic studies can also be performed to help with
the differential diagnosis of the infectious process.
For a description of these studies, refer to the sections
and chapters indicated below:
 Sputum analysis (see DiagnosticTesting in Chapter 2)
 Cerebrospinal fluid (see Lumbar Puncture in
Chapter 4)
 Urinalysis (see Diagnostic Tests in Chapter 9)
 Wound cultures (see Wound Assessment and Acute
Care Management of Wounds in Chapter 7)
INFECTIOUS DISEASES
Various infectious disease processes, which are com-
monly encountered in the acute care setting, are
described in the following sections. Certain disease
processes that are not included in this section are
described in other chapters. Please consult the index
for assistance.
Nosocomial Infections
Nosocomialinfection is a general term that refers to an infec-
tion that is acquired in the hospital setting. Many patho-
gens can cause a nosocomial infection, but the most
commonly reported in the past years have been
Escherichia coli, Staphylococcus aureus, Enterococcus faecalis,
Pseudomonas aeruginosa, Candida albicans and coagulase-
negative staphyloccoci.21,22 Patients who are at risk
for developing nosocomial infections are those who
present with:23
1. Age: the very young or the very old
2. Immunodeficiency: chronic diseases (cancer, chronic
renal disease, chronic obstructive pulmonary
disease, diabetes, or acquired immunodeficiency
syndrome [AIDS])
3. Immunosuppression: chemotherapy, radiation ther-
apy, or corticosteroids
4. Misuse of antibiotics: overprescription of antibiotics
or use of broad-spectrum antibiotics, leading to the
elimination of a patient’s normal flora, which allows
for the colonization of pathogens and development
of drug-resistant organisms
5. Use of invasive diagnostic and therapeutic proce-
dures: indwelling urinary catheters, monitoring
devices, intravenous (IV) catheters, and mechanical
ventilation with intubation
6. Agitation: it can result in self-extubation and
removal of central venous catheter
7. Surgery: incisions provide access to pathogens
8. Burns: disrupt the first line of defense
9. Length of hospitalization: increases the exposure to
pathogens and medical intervention

The mode of transmission for pathogens that cause
nosocomial infections can vary from contact to air-
borne. Pathogens can also become opportunistic in
patients who are immunocompromised or immuno-
suppressed. Common sites for nosocomial infections
are in the urinary tract, surgical wounds, joints, and
the lower respiratory tract (e.g., pneumonia). Clinical
manifestations and management of nosocomial infec-
tions vary according to the type of pathogen and the
organ system involved. However, the primary manage-
ment strategy for nosocomial infections is prevention
by following the standard and specific precautions
outlined inTable 10-4.6,21,24,25
CLINICAL TIP
 Prevention or minimizing the risk of developing
a pneumonia in patients who have been on bed rest
and/or on mechanical intervention can be achieved
through chest PT and encouraged mobility. (Refer to
Table 2-11, Dean’s Hierarchy for Treatment of
Patients with Impaired Oxygen Transport).
ANTIBIOTIC-RESISTANT INFECTIONS
METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS
INFECTION. Methicillin-resistant S. aureus (MRSA) is a
strain of Staphylococcus that is resistant to methicillin
or similar agents, such as oxacillin and nafcillin.
Methicillin is a synthetic form of penicillin and was
developed because S. aureus developed resistance to
penicillin, which was originally the treatment choice
for S. aureus infection. However, since the early 1980s,
this particular strain of S. aureus has become increasingly
resistant to methicillin. The contributing factor that is
suggested to have a primary role in the increased inci-
dence of this nosocomial infection is the indiscriminate
use of antibiotic therapy.25,26
Additionally, patients who are at risk for developing
MRSA infection in the hospital are patients who26-28:
 Are debilitated, elderly, or both
 Are hospitalized for prolonged time periods
 Have multiple surgical or invasive procedures, an
indwelling cannula, or both
 Are taking multiple antibiotics, antimicrobial
treatments, or both
 Are undergoing treatment in critical care units
MRSA is generally transmitted by person-to-
person contact or person-to-object-to-person contact.
Infectious Diseases CHAPTER 10 359
Table 10-4 SUMMARY OF PRECAUTIONS TO
PREVENT INFECTION
Precaution Description
Standard Treat all patient situations as
potentially infectious.Wash hands
before and after each patient
contact.Wear a different set of
gloves with each patient. If
splashing of body fluids is likely,
wear a mask or face shield, or both,
and a gown.
Airborne* A mask is required in situations when
contagious pathogens can be
transmitted by airborne droplet
nuclei, as in the case of measles,
varicella (chickenpox), or
tuberculosis.
Droplet* A mask or face shield, or both, are
required when large-particle
droplet transmission (usually
3 ft or less) is likely.
Droplet transmission involves contact
of the conjunctivae or the mucous
membranes of the nose or mouth
with large-particle droplets
(larger than 5 mm in size) generated
from coughing, sneezing, talking,
and certain procedures, such as
suctioning and bronchoscopy.
Examples of pathogens requiring
droplet precautions are Haemophilus
influenzae, Neisseria meningitidis,
mycoplasmal pneumonia,
streptococcal pneumonia, mumps,
and rubella.
Contact* Gown and gloves are required when
pathogens are transmitted by direct
person-to-person contact or
person-to-object contact. Examples
of these pathogens include
Clostridium difficile, Escherichia coli,
herpes simplex virus, herpes zoster,
methicillin-resistant Staphylococcus
aureus, and vancomycin-resistant
Enterococcus.
*These precautions are in addition to practicing Standard
Precautions.
Data from Rice D, Eckstein EC. Inflammation and Infection.
In WJ Phipps, JK Sands, JF Marek (eds), Medical-Surgical
Nursing, Concepts and Clinical Practice (6th ed). St. Louis:
Mosby, 1999;237-245; Anderson KN (ed), Mosby’s Medical,
Nursing, and Allied Health Dictionary (5th ed). St. Louis:
Mosby, 1998;2BA5.
360 CHAPTER 10 Infectious Diseases
MRSA can survive for prolonged periods of time on
inanimate objects, such as telephones, bed rails, and
tray tables, unless such objects are properly sanitized.
Hospital personnel can be primary carriers of MRSA,
as the bacterium can be colonized in healthy adults.
MRSA infections can be diagnosed via nasal swabs.29
Management of MRSA is difficult and may consist
of combining local and systemic antibiotics, increasing
antibiotic dosages, and applying whole-body antiseptic
solutions. In recent years, vancomycin has become the
treatment of choice for MRSA; however, evidence has
shown that patients with this strain of S. aureus are also
developing resistance to vancomycin (vancomycin
intermediate S. aureusçVISA).25 Therefore, prevention
of MRSA infection is the primary treatment strategy
and includes the following21,26-28:
 Placing patients with MRSA infection on isolation
or contact precautions
 Strict hand-washing regulations before and after
patient care using proper disinfecting agent
 Use of gloves, gowns (if soiling is likely), or both
 Disinfection of all contaminated objects
VANCOMYCIN-RESISTANT ENTEROCOCCI INFECTION.
Vancomycin-resistant enterococci (VRE) infection is
another nosocomial infection that has become resistant
to vancomycin, aminoglycosides, and ampicillin. The
infection can develop as endogenous enterococci (nor-
mally found in the gastrointestinal or the female repro-
ductive tract) become opportunistic in patient
populations similar to those mentioned earlier with
MRSA.VRE infections can be diagnosed via rectal
swab.21,25,30,31
Transmission of the infection can also occur by
(1) direct patient-to-patient contact, (2) indirect contact
through asymptomatic hospital personnel who can
carry the opportunistic strain of the microorganism,
or (3) contact with contaminated equipment or
environmental surfaces.
Management of VRE infection is difficult, as the
enterococcus canwithstand harsh environments and sur-
vive well on the hands of health care workers and on hos-
pital objects. Treatment options are very limited for
patients with VRE, and the best intervention plan is to
prevent the spread of the infectious process.25 Strategies
for preventingVRE infections include the following30:
 The controlled use of vancomycin
 Timely communication between the microbiology
laboratory and appropriate personnel to initiate
contact precautions as soon as VRE is detected
 Implementation of screening procedures to detect
VRE infection in hospitals where VRE has not yet
been detected (i.e., randomly culturing potentially
infected items or patients)
 Preventing the transmission of VRE by placing
patients in isolation or grouping patients with VRE
together, wearing gown and gloves (which need to
be removed inside the patient’s room), and washing
hands immediately after working with an infected
patient
 Designating commonly used items, such as stetho-
scopes and rectal thermometers, to be used only
withVRE patients
 Disinfecting any item that has been in contact
with VRE patients with the hospital’s approved
cleaning agent
CLINICAL TIP
 Equipment used during physical therapy treatments
for patients with MRSA or VRE, such as assistive
devices, cuff weights, or goniometers, should be left
in the patient’s room and not be taken out until the
infection is resolved. If there is an equipment
shortage, thorough cleaning of the equipment is
necessary before using the equipment with other
patients. Linens, hospital curtains, and laboratory
coats also need to be properly cleaned to avoid
transmission of infection.
Respiratory Tract Infections
Infections of the respiratory tract can be categorized as
upper or lower respiratory tract infections. Upper respi-
ratory tract infections that are discussed in this section
consist of allergic and viral rhinitis, sinusitis, influenza,
and pertussis. Lower respiratory tract infections that
are discussed in this section consist of TB, histoplasmo-
sis, and legionellosis. Pneumonia is the most common
lower respiratory tract infection and is discussed in
Pathophysiology in Chapter 2.
UPPER RESPIRATORY TRACT INFECTIONS
RHINITIS. Rhinitis is the inflammation of the nasal
mucous membranes and can result from an allergic
reaction or viral infection. Allergic rhinitis is com-
monly a seasonal reaction from allergens, such as
pollen, or a perennial reaction from environmental
triggers, such as pet dander or smoke. Viral rhinitis,
sometimes referred to as the common cold, is caused
by a wide variety of viruses that can be transmitted by
airborne particles or by contact.

Clinical manifestations of allergic and viral rhinitis
include nasal congestion; sneezing; watery, itchy eyes
and nose; altered sense of smell; and thin, watery nasal
discharge. In addition to these, clinical manifestations
of viral rhinitis include fever, malaise, headache, and
thicker nasal discharge.
Management of allergic rhinitis includes antihista-
mines, decongestants, nasal corticosteroid sprays, and
allergen avoidance. Management of viral rhinitis
includes rest, fluids, antipyretics, and analgesics.32-34
SINUSITIS. Sinusitis is the inflammation or hyper-
trophy of the mucosal lining of any or all of the facial
sinuses (frontal, ethmoid, sphenoid, and maxillary).
This inflammation can result from bacterial, viral, or
fungal infection.
Clinical manifestations of sinusitis include pain over
the affected sinus, purulent nasal drainage, nasal
obstruction, congestion, fever, and malaise.
Management of sinusitis includes antibiotics
(as appropriate), decongestants or expectorants, and
nasal corticosteroids.33
CLINICAL TIP
 Despite the benign nature of rhinitis and sinusitis,
the manifestations (especially nasal drainage and
sinus pain) of these infections can be very disturbing
to the patient and therapist during the therapy
session and may lower the tolerance of the patient
for a given activity. The therapist should be
sympathetic to the patient’s symptoms and adjust
the activity accordingly.
INFLUENZA. Influenza (the flu) is caused by any of the
influenza viruses (A, B, or C and their mutagenic
strains) that are transmitted by aerosolized mucous
droplets. These viruses have the ability to change over
time and are the reason why a great number of patients
are at risk for developing this infection. Influenza B is
the most likely virus to cause an outbreak within a
community.
Clinical manifestations of influenza include (1) a
severe cough, (2) abrupt onset of fever and chills,
(3) headache, (4) backache, (5) myalgia, (6) prostration
(exhaustion), (7) coryza (nasal inflammation with pro-
fuse discharge), and (8) mild sore throat. Gastrointes-
tinal signs and symptoms of nausea, vomiting,
abdominal pain, and diarrhea can also present in
certain cases. The disease is usually self-limiting in
uncomplicated cases, with symptoms resolving in 7 to
10 days. A complication of influenza infection is
Infectious Diseases CHAPTER 10 361
pneumonia, especially in the elderly and chronically
diseased individuals.1,2,13,33
If management of influenza is necessary, it may
include the following1,2,13,33:
 Antiinfective agents
 Antipyretic agents
 Adrenergic agents
 Antitussive agents
 Active immunization by vaccines
 Supportive care with IV fluids and supplemental
oxygen, as needed
CLINICAL TIP
 Health care workers should be vaccinated against the
influenza virus to decrease the risk of transmission.
 A rapid flu nasal swab can diagnose influenza.
If results have not come back or they are positive,
wear a simple face mask to prevent transmission.
PERTUSSIS. Pertussis, or whooping cough, is an
acute bacterial infection of the mucous membranes of
the tracheobronchial tree. It occurs most commonly in
children younger than 1 year of age and in children
and adults of lower socioeconomic populations.
The defining characteristics are violent cough spasms
that end with an inspiratory ‘‘whoop,’’ followed by the
expulsion of clear tenacious secretions. Symptoms
may last 1 to 2 months. Pertussis is transmitted through
airborne particles and is highly contageous.35
Management of pertussis may include any of the
following13,35:
 Antiinfective and antiinflammatory medications
 Bronchopulmonary hygiene with endotracheal
suctioning, as needed
 Supplemental oxygen, assisted ventilation, or both
 Fluid and electrolyte replacement
 Active immunization by vaccines
 Respiratory isolation for 3 weeks after the onset of
coughing spasms or 7 days after antimicrobial therapy
LOWER RESPIRATORY TRACT INFECTIONS
TUBERCULOSIS. TB is a chronic pulmonary and
extrapulmonary infectious disease caused by the tuber-
cle bacillus. It is transmitted through airborne Mycobac-
terium tuberculosis particles, which are expelled into the
air when an individual with pulmonary or laryngeal
TB coughs or sneezes.36 When M. tuberculosis reaches
the alveolar surface of a new host, it is attacked by
macrophages, and one of two outcomes can result:
Macrophages kill the particles, terminating the
362 CHAPTER 10 Infectious Diseases
infection, or the particles multiply within the WBCs,
eventually causing them to burst. This cycle is then
repeated for a variable time frame between 2 and 12
weeks, after which time the individual is considered to
be infected withTB and will test positive on tuberculin
skin tests, such as the Mantoux test, which uses tubercu-
lin-purified protein derivative,* or the multiple punc-
ture test, which uses tuberculin. At this point, the
infection enters a latent period (most common) or
develops into activeTB.36,37
A six-category classification system has been devised
by the American Thoracic Society and the Centers for
Disease Control and Prevention (CDC) to describe the
TB status of an individual36,38:
1. NoTB exposure, not infected
2. TB exposure, no evidence of infection
3. Latent TB infection, no disease
4. TB, clinically active
5. TB, not clinically active
6. TB suspect (diagnosis pending)
Populations at high risk for acquiring TB include
(1) the elderly; (2) Native Americans, Eskimos, and
blacks (in particular if they are homeless or economi-
cally disadvantaged); (3) incarcerated individuals;
(4) immigrants from Southeast Asia, Ethiopia,
Mexico, and Latin America; (5) malnourished indivi-
duals; (6) infants and children younger than 5 years of
age; (7) those with decreased immunity (e.g., from
AIDS or leukemia, or after chemotherapy); (8) those
with diabetes mellitus, end-stage renal disease, or
both; (9) those with silicosis; and (10) those in close
contact with individuals with activeTB.3,36
Persons with normal immune function do not
normally develop active TB after acquisition and are,
therefore, not considered contagious. Risk factors for
the development of active TB after infection include
age (children younger than 8 years and adolescents are
at greatest risk), low weight, and immunosupression.39
When active TB does develop, its associated signs
and symptoms include (1) fever, (2) an initial nonpro-
ductive cough, (3) mucopurulent secretions that pre-
sent later, and (4) hemoptysis, dyspnea at rest or with
exertion, adventitious breath sounds at lung apices,
pleuritic chest pain, hoarseness, and dysphagia, all of
which may occur in the later stages. Chest films also
show abnormalities, such as atelectasis or cavitation
*A person who has been exposed to the tubercle bacillus will
demonstrate a raised and reddened area 2 to 3 days after being
injected with the protein derivative of the bacilli.
involving the apical and posterior segments of the
right upper lobe, the apical-posterior segment of the
left upper lobe, or both.36
ExtrapulmonaryTB occurs with less frequency than
pulmonary TB but affects up to 70% of human immu-
nodeficiency virus (HIV)-positive individuals diag-
nosed with TB.40 Organs affected include the
meninges, brain, blood vessels, kidneys, bones, joints,
larynx, skin, intestines, lymph nodes, peritoneum, and
eyes. When multiple organ systems are affected, the
term disseminated, or miliary,TB is used.40 Signs and symp-
toms that manifest are dependent on the particular
organ system or systems involved.
Because of the high prevalence of TB in HIV-positive
individuals (up to 60% in some states),40 it should be
noted that the areas of involvement and clinical features
of the disease in this population differ from those
normally seen, particularly in cases of advanced immu-
nosuppression. Brain abscesses, lymph node involve-
ment, lower lung involvement, pericarditis, gastricTB,
and scrotal TB are all more common in HIV-positive
individuals. HIV also increases the likelihood that TB
infection will progress to active TB by impairing the
body’s ability to suppress new and latent infections.40
Management of TB may include the following1,2,13:
 Antiinfective agents (see Appendix IV, Table IV-34,
Antitubercular Agents)
 Corticosteroids
 Surgical intervention to remove cavitary lesions
(rare) and areas of the lung with extensive disease or
to correct hemoptysis, spontaneous pneumothorax,
abscesses, intestinal obstruction, ureteral stricture,
or any combination of these
 Respiratory isolation until antimicrobial therapy is
initiated
 Blood and body fluid precautions if extrapulmonary
disease is present
 Skin testing (i.e., Mantoux test and multiple punc-
ture test)
 Vaccination for prevention
In recent years, new strains of M. tuberculosis that are
resistant to antitubercular drugs have emerged. These
multidrug-resistant TB strains are associated with
fatality rates as high as 89% and are common in
HIV-infected individuals. Treatment includes the use
of direct observational therapy (DOT) and direct
observational therapy, short-course (DOTS). These
programs designate health care workers to observe
individuals to ensure that they take their medications
for the entire treatment regimen or for a brief period,
respectively, in hopes of minimizing resistance.40

CLINICAL TIP
 Facilities often provide specialized masks to
wear around patients on respiratory precautions
for TB. The masks are impermeable to the
airborne mycobacterium. Always verify with
the nursing staff or physician before working
with these patients to determine which mask
to wear.
 Patients who are suspected of, but not diagnosed
with, TB are generally placed on ‘‘rule-out TB’’
protocol, in which case respiratory precautions
should be observed.
HISTOPLASMOSIS. Histoplasmosis is a pulmonary
and systemic infection that is caused by infective
spores (fungi), most commonly found in the soil of the
central and eastern United States. Histoplasmosis is
transmitted by inhalation of dust from the soil or bird
and bat feces. The spores form lesions within the lung
parenchyma that can be spread to other tissues. The
incidence of fungal infection is rising, particularly
in immunocompromised, immunosuppressed, and
chronically debilitated individuals who may also be
receiving corticosteroid, antineoplastic, and multiple
antibiotic therapy.41,42
Different clinical forms of histoplasmosis are
(1) acute, benign respiratory disease, which results in
flulike illness and pneumonia; (2) acute disseminated
disease, which can result in septic-type fever; (3) chronic
disseminated disease, which involves lesions in the
bone marrow, spleen, and lungs and can result in immu-
nodeficiency; and (4) chronic pulmonary disease,
which manifests as progressive emphysema.
Management of histoplasmosis may include the
following13,41,43,44:
 Antiinfective agents
 Corticosteroids
 Antihistamines
 Antifungal therapy (see Appendix IV, Table IV-33,
Antifungal Agents)
 Supportive care appropriate for affected areas in the
different forms of histoplasmosis
Cardiac Infections
Infections of the cardiac system can involve any layer of
the heart (endocardium, myocardium, and pericar-
dium) and generally result in acute or chronic depres-
sion of the patient’s cardiac output. Those infections
that result in chronic cardiomyopathy most likely
Infectious Diseases CHAPTER 10 363
require cardiac transplantation. Refer to Chapters 1
and 12 for a discussion of cardiomyopathy and cardiac
transplantation, respectively. This section focuses on
rheumatic fever and resultant rheumatic heart disease.
Acute rheumatic fever is a clinical sequela occurring
in up to 3% of patients with group A and b-streptococ-
cal infection of the upper respiratory tract. It occurs
primarily in children who are between the ages of
6 and 15 years. Rheumatic fever is characterized by
nonsuppurative inflammatory lesions occurring in any
or all of the connective tissues of the heart, joints,
subcutaneous tissues, and central nervous system. An
altered immune reaction to the infection is suspected
as the cause of resultant damage to these areas, but the
definitive etiology is unknown. Rheumatic heart disease is
the term used to describe the resultant damage to the
heart from the inflammatory process of rheumatic
fever.13,27,45,46
Cardiac manifestations can include pericarditis,
myocarditis, left-sided endocarditis, and valvular ste-
nosis and insufficiency with resultant organic heart
murmurs, as well as congestive heart failure. If not
managed properly, all of these conditions can lead to
significant morbidity or death.13,27,45
Management of rheumatic fever follows the treat-
ment for streptococcal infection. The secondary com-
plications mentioned previously are then managed
specifically. The general intervention scheme may
include the following13,27,45:
 Prevention of streptococcal infection
 Antiinfective agents
 Antipyretic agents
 Corticosteroids
 Bed rest
 IV fluids (as needed)
Neurologic Infections
POLIOMYELITIS
Poliomyelitis is an acute systemic viral disease that
affects the central nervous system. Polioviruses are a
type of enterovirus that multiply in the oropharynx
and intestinal tract.13,47
Poliomyelitis is usually transmitted directly by the
fecal-oral route from person to person but can also be
transmitted indirectly by consumption of contaminated
water sources.47
Clinical presentation can range from subclinical
infection, to afebrile illness (24 to 36 hours), to aseptic
meningitis, to paralysis (after 4 days), and, possibly, to
death. If paralysis does occur, it is generally associated
364 CHAPTER 10 Infectious Diseases
with fever and muscle pain. The paralysis is usually
asymmetric and involves muscles of respiration, swal-
lowing, and the lower extremities. Paralysis can resolve
completely, have residual deficits, or be fatal.13,47
Management of poliomyelitis primarily consists of
prevention with inactivated poliovirus vaccine (IPV)
given as four doses to children from the ages of 2 to
6 years of age.47 If a patient does develop active polio-
myelitis, then other management strategies may include
the following13:
 Analgesics and antipyretics
 Bronchopulmonary hygiene
 Bed rest with contracture prevention with position-
ing and range of motion
POSTPOLIOMYELITIS SYNDROME
Postpoliomyelitis syndrome, also known as postpolio
syndrome, occurs 30 to 40 years after an episode of
childhood paralytic poliomyelitis. The syndrome
results from overuse or premature aging of motor
units that were originally affected by the polio virus.
It results in muscle fatigue, pain, and decreased endur-
ance. Muscle atrophy and fasciculations may also be
present. Patients who are older or critically ill, who
have had a previous diagnosis of paralytic poliomy-
elitis, and who are female are at greater risk for devel-
opment of this syndrome.47-49
MENINGITIS
Meningitis is an inflammation of the meninges that
cover the brain and spinal cord, which results from
acute infection by bacteria, viruses, fungi, or parasitic
worms, or by chemical irritation.The route of transmis-
sion is primarily inhalation of infected airborne
mucous droplets released by infected individuals or
through the bloodstream via open wounds or invasive
procedures.50,51
The more common types of meningitis are
(1) meningococcal meningitis, which is bacterial in
origin and occurs in epidemic form; (2) Haemophilus
meningitis, which is the most common form of
bacterial meningitis; (3) pneumococcal meningitis,
which occurs as an extension of a primary bacterial
upper respiratory tract infection; and (4) viral (aseptic
or serous) meningitis, which is generally benign and
self-limiting.
Bacterial meningitis is more severe than viral menin-
gitis and affects the pia mater, arachnoid and subarach-
noid space, ventricular system, and the cerebrospinal
fluid.The primary complications of bacterial meningi-
tis include an increase in intracranial pressure, resulting
in hydrocephalus. This process frequently results in
severe headache and nuchal rigidity (resistance to neck
flexion). Other complications of meningitis include
arthritis, myocarditis, pericarditis, neuromotor and
intellectual deficits, and blindness and deafness from
cranial nerve (III, IV,VI,VII, orVIII) dysfunction.50,51
Management of any form of meningitis may include
the following13,50,52:
 Antimicrobial therapy, antiinfective agents, or im-
munologic agents
 Analgesics
 Mechanical ventilation (as needed)
 Blood pressure maintenance with IV fluids and
vasopressors (e.g., dopamine)
 Intracranial pressure control
ENCEPHALITIS
Encephalitis is an inflammation of the tissues of thebrain
and spinal cord, commonly resulting from viral or
amebic infection.Types ofencephalitis include infectious
viral encephalitis, mosquito-borne viral encephalitis,
and amebic meningoencephalitis.
Infectious viral encephalitis is transmitted by direct
contact of droplets from respiratory passages or other
infected excretions and is most commonly associated
with the herpes simplex type 1 virus.Viral encephalitis
can also occur as a complication of systemic viral infec-
tions, such as poliomyelitis, rabies, mononucleosis,
measles, mumps, rubella, and chickenpox. Manifesta-
tions of viral encephalitis can be mild to severe, with
herpes simplex virus encephalitis having the highest
mortality rate among all types of encephalitides.13,50,51
Mosquito-borne viral encephalitis is transmitted
by infectious mosquito bites and cannot be transmit-
ted from person to person. The incidence of this
type of encephalitis can be epidemic in nature and
typically varies according to geographic regions and
seasons.13,50,51
Amebic meningoencephalitis is transmitted in water
and can enter a person’s nasal passages while he or she
is swimming. Amebic meningoencephalitis cannot be
transmitted from person to person.
General clinical presentation of encephalitis may
include the following13,50,51:
 Fever
 Signs of meningeal irritation from increased intra-
cranial pressure (e.g., severe frontal headache,
nausea, vomiting, dizziness, nuchal rigidity)
 Altered level of consciousness, irritability, bizarre
behaviors (if the temporal lobe is involved)
 Seizures (mostly in infants)

 Aphasia
 Focal neurologic signs
 Weakness
 Altered deep tendon reflexes
 Ataxia, spasticity, tremors, or flaccidity
 Hyperthermia
 Alteration in antidiuretic hormone secretion
Management of encephalitis may include the
following13:
 Antiinfective agents
 Intracranial pressure management
 Mechanicalventilation, with or withouttracheostomy
(as indicated)
 Sedation
 Intravenous fluids and electrolyte replacement
 Nasogastric tube feedings
Musculoskeletal Infections
Osteomyelitis is an acute infection of the bone that can
occur from direct or indirect invasion by a pathogen.
Direct invasion is also referred to as exogenous or
acute contagious osteomyelitis and can occur any time
there is an open wound in the body. Indirect invasion
is also referred to as endogenous or acute hematoge-
nous osteomyelitis and usually occurs from the spread
of systemic infection. Both of these types can poten-
tially progress to subacute and chronic osteomyelitis.
Acute osteomyelitis typically refers to an infection
of less than 1 month’s duration, whereas chronic
osteomyelitis refers to infection that lasts longer than
4 weeks.53,54
Acute contagious osteomyelitis is an extension
of the concurrent infection in adjacent soft tissues
to the bony area. Trauma resulting in compound
fractures and tissue infections is a common example.
Prolonged orthopedic surgery, wound drainage, and
chronic illnesses, such as diabetes or alcoholism,
also predispose patients to acute contagious osteo-
myelitis.54, 55
Acute hematogenous osteomyelitis is a blood-borne
infection that generally results from S. aureus infection
(80%)1 and occurs mostly in infants; children (in the
metaphysis of growing long bones); or patients under-
going long-term IV therapy, hyperalimentation,
hemodialysis, or corticosteroid or antibiotic therapy.
Patients who are malnourished, obese, or diabetic, or
who have chronic joint disease, are also susceptible to
acute hematogenous osteomyelitis.53,54
Clinical presentation of both types of acute osteomy-
elitis includes (1) delayed onset of pain, (2) tenderness,
(3) swelling, and (4) warmth in the affected area.
Infectious Diseases CHAPTER 10 365
Fever is present with hematogenous osteomyelitis.
The general treatment course for acute osteomyelitis is
early and aggressive administration of the appropriate
antibiotics to prevent or limit bone destruction.1,43,53,54
Chronic osteomyelitis is an extension of the acute
cases discussed above. It results in marked bone
destruction, draining sinus tracts, pain, deformity, and
the potential of limb loss. Chronic osteomyelitis can
also result from infected surgical prostheses or infected
fractures. Debridement of dense formations (sequestra)
may be a necessary adjunct to the antibiotic therapy.
If the infection has spread to the surrounding soft
tissue and skin regions, then grafting, after debride-
ment, may be necessary. Good results have also been
shown with hyperbaric oxygen therapy for chronic
osteomyelitis.53,54
CLINICAL TIP
 Clarify weight-bearing orders with the physician
when performing gait training with patients
who have any form of osteomyelitis. Both
upper and lower extremities can be involved;
therefore, choosing the appropriate assistive
device is essential to preventing pathologic
fracture.
Skin Infections
Cellulitis, or erysipelas, is an infection of the dermis and
the subcutaneous tissue that can remain localized or
be disseminated into the bloodstream, resulting in bac-
teremia (rare). Cellulitis occurs most commonly on the
face, neck, and legs.
Groups A and G Streptococcus and S. aureus are the
usual causative agents for cellulitis and generally gain
entry into the skin layers when there are open wounds
(surgical or ulcers). Patients who are at most risk for
developing cellulitis include those who are postsurgical
and immunocompromised from chronic diseases or
medical treatment.
The primary manifestations of cellulitis are fever
with an abrupt onset of hot, stinging, and itchy skin
and painful, red, thickened lesions that have firm,
raised palpable borders in the affected areas.
Identifying the causative agent is often difficult
through blood cultures; therefore, localized cultures,
if possible in open wounds, may be more sensitive
in helping to delineate the appropriate antibiotic
treatment.55-57
366 CHAPTER 10 Infectious Diseases
Gastrointestinal Infections
Gastroenteritis is a global term used for the inflammation
of the digestive tract that is typically a result of
infection. The primary cause of gastroenteritis is
viral infection from rotavirus, adenovirus, astrovirus,
calicivirus, and small round-structured viruses.
Gastroenteritis can also occur from bacterial infection
from E. coli, Shigella (which causes bacterial dysentery),
Clostridium difficile, and Salmonella.
Transmission of these organisms is usually through
the ingestion of contaminated food, water, or both or
by direct and indirect fecal-oral transmission.
The primary manifestations of any form of gastroen-
teritis are crampy abdominal pain, nausea, and diar-
rhea, all of which vary in severity and duration
according to the type of infection. Gastroenteritis is
generally a self-limiting infection, with resolution
occurring in 3 to 4 days. However, patients in the hospi-
tal setting with reduced immunity can have longer per-
iods of recovery, with dehydration being a primary
concern.13,43,58
Management of acute gastroenteritis may include
the following13,43:
 Antiinfective agents
 IV fluid and electrolyte replacement
 Antiemetic agents (if nausea and vomiting occur)
CLINICAL TIP
 Strict contact and enteric precautions should be
observed with patients who have a diagnosis of
C. difficile infection.
Immune System Infections
HUMAN IMMUNODEFICIENCY VIRUS INFECTION
Two types of HIVexist: HIV-1 and HIV-2, with HIV-1
being the more prevalent and the one discussed here.
It is a retrovirus, occurring in pandemic proportions,
that primarily affects the function of the immune
system. Eventually, however, all systems of the body
become affected directly, such as the immune system,
or indirectly, as in the cardiac system, or through both
methods, as occurs in the nervous system. The virus is
transmitted in blood, semen, vaginal secretions, and
breast milk through sexual, perinatal, and blood or
blood product contact. Proteins on the surface of the
virus attach to CD4+ receptors, found primarily on
T4 lymphocytes.59 Other types of cells found to house
the virus include monocytes, macrophages, uterine
cervical cells, epithelial cells of the gastrointestinal
tract, and microglia cells.59
Upon entering the cell, the viral and cellular DNA
combine, making the virus a part of the cell.The exact
pathogenesis of cellular destruction caused by HIV is
not completely understood, and several methods of
destruction may be entailed. It is known that immedi-
ately after initial infection, HIV enters a latent period,
or asymptomatic stage, in which viral replication is
minimal, but CD4+ T cell counts begin to decline.59
Continued reduction results in decreasing immunity,
eventually leading to symptomatic HIV, in which
diseases associated with the virus begin to appear.59
This eventually leads to the onset of AIDS, which the
CDC defines as occurring when the CD4+ T-
lymphocyte count falls below 200 cells/ml (reference =
1,000 cells/ml) or below 14%, when 1 of 26 specific
AIDS defining disorders is contracted, most of which
are opportunistic infections, or a combination of
these factors.60,61
Six laboratory tests are available to detect HIV infec-
tion62-65:
1. Enzyme-linked immunosorbent assay or enzyme
immunoassay test.This procedure tests for the pres-
ence of antibodies to HIV proteins in the patient’s
serum. A sample of the patient’s blood is exposed
to HIVantigens in the test reagent. If HIVantibodies
are identified, it is inferred that the virus is present
within the patient.
2. Western blot test. This test detects the presence of
antibodies in the blood to two types of HIV viral
proteins and is, therefore, a more specific HIV test.
It is an expensive test to perform and is used as a
confirmatory tool for a positive enzyme-linked
immunosorbent assay test.
3. Immunofluorescence assay. In this test, the patient’s
blood is diluted and placed on a slide containing
HIV antigens. The slide is then treated with anti-
human globulin mixed with a fluorescent dye that
will bind to antigen-antibody complexes. If a fluo-
rescence is seen when the specimen is placed under
a microscope, then HIV antibodies are present in
the patient’s blood.
4. p24 Antigen assay. This test analyzes blood cells for
the presence of the p24 antigen located on HIV vir-
ions. It can be used to diagnose acute infection, to
screen blood for HIV antigens, to determine HIV
infection in difficult diagnostic cases, or to evaluate
the treatment effects of antiviral agents.
5. Polymerase chain reaction for HIVnucleic acid.This
highly specific and extremely sensitive test detects

the viral DNA molecule in lymphocyte nuclei by
amplifying the viral DNA. It is used to detect
HIV in neonates and when antibody tests are
inconclusive.
6. Rapid HIV testing.This highly sensitive and specific
test requires a sample of blood, serum, plasma or
oral fluid to detect HIV antibodies. This test can be
complete in 20 minutes.
CLINICAL TIP
 A false negative HIV test can occur if an individual
has not yet developed HIV antibodies. If an
individual has had exposure to HIV, he or she
should have a repeat HIV test to ensure a true
negative result.66
 Any clinician that sustains a finger stick injury when
working with a patient with a suspected HIV
infection should have an HIV test.
Once HIV has been detected, it can be classified in a
number of ways. The Walter Reed staging system has
six categories grouped according to the quantity of
helper T cells and characteristic signs, such as the
presence of an HIV antigen or antibody.67 However, a
more commonly used classification system was devised
by the CDC and was last updated in 1993. In this
system, infection is divided into three categories,
depending on CD4+ T-lymphocyte counts:
1. Category 1 consists of CD4+ T-lymphocyte counts
greater than or equal to 500 cells/ml.
2. Category 2 consists of counts ranging between
200 and 499 cells/ml.
3. Category 3 contains cell counts less than 200 cells/ml.
These groups are then subdivided into A, B, and C,
according to the presence of specific diseases.60
Advancement in the medical treatment of HIV,
in the form of antiretroviral therapy, has recently
been made. This therapy consists of four classes of
medications (see Appendix IV,Table IV-35)67:
1. Nucleoside analog reverse transcriptase inhibitors,
otherwise known as nucleoside analogs.
2. Protease inhibitors.
3. Non-nucleoside reverse transcriptase inhibitors.
4. Fusion inhibitor.
Each of these therapies assists in limiting HIV
progression by helping to prevent viral replication.
This prevention is further increased when the drugs
are used in combination in a treatment technique
termed highly active antiretroviral therapy or HAART.67
Infectious Diseases CHAPTER 10 367
There is a significant need for more effective and
cost-efficient preventions for HIV. Currently an HIV
vaccine is in the research and development stages with
multiple efficacy trials in place.68
As HIV progresses and immunity decreases, the risk
for and severity of infections not normally seen in
healthy immune systems increase. These opportunistic
infections, combined with disorders that result directly
from the virus, often result in multiple diagnoses and
medically complex patients. These manifestations of
HIV can affect every system of the body and present
with a wide array of signs and symptoms, many of
which are appropriate for physical therapy intervention.
Table 10-5 lists common manifestations and complica-
tions of HIV and AIDS and the medications generally
used in their management.
Disorders affecting the nervous system include HIV-
associated dementia complex, progressive multifocal
leukoencephalopathy, primary central nervous system
lymphoma, toxoplasmosis, and neuropathies. These
manifestations may cause paresis, decreased sensation,
ataxia, aphagia, spasticity, altered mental status, and
visual deficits.76 In the pulmonarysystem,TB, cytomega-
lovirus (CMV), and pneumonia can result in cough,
dyspnea, sputum production, and wheezing.77 In the
cardiac system, cardiomyopathy, arrhythmias, and con-
gestive heart failure can cause chest pain, dyspnea, tachy-
cardia, tachypnea, hypotension, fatigue, peripheral
edema, syncope, dizziness, and palpitations.78
Physical therapy intervention can assist in minimiz-
ing the effect of these deficits on functional ability,
therefore helping to maximize the independence and
quality of life of the individual. However, the course
of rehabilitation in HIV-affected individuals can often
be difficult owing to coinciding opportunistic infec-
tions, an often-rapid downhill disease course, low
energy states, and frequent hospitalizations.
MONONUCLEOSIS
Mononucleosis is an acute viral disease that has been
primarily linked to the Epstein-Barr virus and less com-
monly to CMV. Mononucleosis is transmitted generally
through saliva from symptomatic or asymptomatic
carriers (the Epstein-Barr virus can remain infective
for 18 months in the saliva).13,79
The disease is characterized by fever, lymphadenop-
athy (lymph node hyperplasia), and exudative pharyngi-
tis. Splenomegaly, hepatitis, pneumonitis, and central
nervous system involvement may occur as rare compli-
cations from mononucleosis.The infection is generally
self-limiting in healthy individuals, with resolution
368 CHAPTER 10 Infectious Diseases

Table 10-5 COMMON COMPLICATIONS FROM HUMAN IMMUNODEFICIENCY VIRUS (HIV) AND
ACQUIRED IMMUNODEFICIENCY SYNDROME AND ASSOCIATED MEDICAL TREATMENT

Complication Medication
Cardiomyopathy May be reversed with reduction or discontinuation of interleukin-2,
adriamycin, a2-interferon, ifosfamide, and foscarnet
Cerebral toxoplasmosis Trimethoprim-sulfamethoxazole
Coccidioidomycosis Amphotericin B, fluconazole, or itraconazole
Congestive heart failure Removal of all nonessential drugs followed by administration of
furosemide (Lasix); digoxin; angiotensin-converting enzyme inhibition
Cryptococcal meningitis Amphotericin B or fluconazole
Cytomegalovirus Ganciclovir, foscarnet, cidofovir
Distal symmetric polyneuropathy Pain management using tricyclic antidepressants, gabapentin, and narcotics
for severe cases
Herpes simplex Acyclovir, famciclovir, valacyclovir
Herpes zoster (shingles) Acyclovir, valacyclovir, famciclovir, foscarnet
HIV-associated dementia complex Antiretroviral therapy combining at least three drugs, two of which
penetrate the blood-brain barrier
Histoplasmosis Amphotericin B or itraconazole
Kaposi’s sarcoma Radiotherapy, cryotherapy with liquid nitrogen, daunorubicin
hydrochloride, or doxorubicin hydrochloride injections
Lymphomas Chemotherapy: cyclophosphamide, doxorubicin, vincristine, bleomycin,
methotrexate, leucovorin
Mycobacterium avium complex Clarithromycin, rifabutin, ciprofloxacin, ethambutol
Oral hairy leukoplakia Acyclovir if symptoms present
Pneumocystis carinii pneumonia Trimethoprim-sulfamethoxazole, dapsone, clindamycin, pentamidine
isethionate
Progressive multifocal Antiretroviral therapy, acyclovir, IVcytosine, adenosine-arabinoside,
leukoencephalopathy interferon-alphas
Pulmonary hypertension Low-flow O2 if hypoxia present, vasodilators, including nitroglycerin,
hydralazine, nifedipine, lisinopril, and prostaglandin E
Toxic neuronal neuropathy: neuropathy May be reversed with discontinuation or reduction in the following:
caused by certain medications zalcitabine, didanosine, and stavudine
Tuberculosis Four-drug regimen: isoniazid, rifampin, pyrazinamide, and ethambutol
Data from reference numbers 69-75

occurring in approximately 3 weeks without any CYTOMEGALOVIRUS INFECTION

specific treatment.13,79 CMV is a member of the herpesvirus group that can be
If management of mononucleosis is necessary, it may found in all body secretions, including saliva, blood,
include the following13,79,80: urine, feces, semen, cervical secretions, and breast
 Corticosteroids in cases of severe pharyngitis milk. CMV infection is a common viral infection that
 Adequate hydration is asymptomatic or symptomatic. CMV infection can
 Bed rest during the acute stage remain latent after the initial introduction into the
 Saline throat gargle body and can become opportunistic at a later point
 Aspirin or acetaminophen for sore throat and fever in time.

If CMV infection is symptomatic, clinical presenta-
tion may be a relatively benign mononucleosis in
adults, or in patients with HIV infection, manifesta-
tions such as pneumonia, hepatitis, encephalitis,
esophagitis, colitis, and retinitis can occur.
CMV is usually transmitted by prolonged contact
with infected body secretions, as well as congenitally
or perinatally.13,81
Management of CMV infection may include the
following13,81:
 Antiviral agents
 Corticosteroids
 Immune globulins
 Blood transfusions for anemia or thrombocytopenia
 Antipyretics
TOXOPLASMOSIS
Toxoplasmosis is a systemic protozoan infection caused
by the parasite Toxoplasma gondii, which is primarily
found in cat feces. Transmission can occur from three
mechanisms: (1) eating raw or inadequately cooked
infected meat or eating uncooked foods that have
come in contact with contaminated meat; (2) inadver-
tently ingesting oocysts that cats have passed in their
feces, either in a cat litter box or outdoors in soil
(e.g., soil from gardening or unwashed fruits or vegeta-
bles); and (3) transmission of the infection from a
woman to her unborn fetus. Fetal transmission of
T. gondii can result in mental retardation, blindness,
and epilepsy.82
Clinical manifestations can range from subclinical
infection to severe generalized infection, particularly
in immunocompromised individuals, to death.
The management trend of toxoplasmosis is through
prevention by safe eating habits (thoroughly cooking
meats, peeling and washing fruits and vegetables) and
minimizing the contact with cat feces when pregnant,
along with keeping the cat indoors to prevent
contamination.82
Sepsis
Sepsis is a general term that describes three progressive
infectious conditions: bacteremia, septicemia, and
shock syndrome (or septic shock).13
Bacteremia is a generally asymptomatic condition
that results from bacterial invasion of blood from con-
taminated needles, catheters, monitoring transducers,
or perfusion fluid. Bacteremia can also occur from a
preexisting infection from another body site.
Bacteremia can resolve spontaneously or progress to
septicemia.
Infectious Diseases CHAPTER 10 369
Septicemia is a symptomatic extension of bacteremia
throughout the body, with clinical presentations that
are representative of the infective pathogen and the
organ system(s) involved. Sites commonly affected are
the brain, endocardium, kidneys, bones, and joints.
Renal failure and endocarditis may also occur.
Shock syndrome is a critical condition of systemic
tissue hypoperfusion that results from microcirculatory
failure (i.e., decreased blood pressure or perfusion).
Bacterial damage of the peripheral vascular system is
the primary cause of the tissue hypoperfusion.
Management of sepsis may include any of the
following13:
 Removal of suspected infective sources (e.g., lines
or tubes)
 Antiinfective agents
 Blood pressure maintenance with adrenergic agents
and corticosteroids
 Intravenous fluids
 Blood transfusions
 Cardiac glycosides
 Supplemental oxygen, mechanical ventilation,
or both
 Anticoagulation
MANAGEMENT
Medical Intervention
Management of the various infectious diseases dis-
cussed in this chapter is described in the specific
sections of respective disorders. Appendix IV (Table
IV-32, Antibiotics; Table IV-33, Antifungal Agents;
Table IV-34, Antitubercular Agents; Table IV-35,
Antiretroviral Medications; and Table IV-36, Antiviral
Medications) also lists common antiinfective agents
used in treating infectious diseases.
Physical Therapy Intervention
The following are general physical therapy goals and
guidelines to be used when working with patients
who have infectious disease processes, as well as disor-
ders of altered immunity. These guidelines should be
adapted to a patient’s specific needs.
GOALS
The primary physical therapy goals in this patient pop-
ulation are similar to those of patient populations
in the acute care setting: (1) to optimize the patient’s
functional mobility, (2) to maximize the patient’s
370 CHAPTER 10 Infectious Diseases
activity tolerance and endurance, and (3) to maximize
ventilation and gas exchange in the patient who has
pulmonary involvement.
GUIDELINES FOR PHYSICAL THERAPY
INTERVENTION
General physical therapy guidelines include, but are not
limited to, the following:
1. The best modes of preventing the transmission of
infectious diseases are to adhere to the standard
precautions established by the CDC and to follow
proper hand-washing techniques.
 Facilities’ warning or labeling systems for bioha-
zards and infectious materials may vary slightly.
 Be sure to check the patient’s medical record or
signs posted on doors and doorways for indicated
precautions.
 Table 10-4 provides an outline of the types of
protective equipment that should be worn with
specific precautions.
2. Patients who have infectious processes have an ele-
vated metabolic rate, which will most likely manifest
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77. Rosen MJ. Overview of Pulmonary Complications.
Clin Chest Med 1996;17(4):621.

78. Yunis NA, StoneVE. Cardiac Manifestations of HIV/
AIDS. J Acquir Immune Defic Syndr Hum Retrovirol
1998;18:145.
79. Auwaerter PG. Infectious Mononucleosis in Middle
Age. (Grand Rounds at theJohns Hopkins Hospital).
JAMA 1999;281(5):454.
80. Ebell MH. Epstein-Barr Virus Infectious
Mononucleosis. Am Fam Physician 2004;70(7):1279-1287.
Infectious Diseases CHAPTER 10 373
81. Carson-De Witt RS. Cytomegalovirus Infection.
In K Boyden, D Olendorf (eds), Gale Encyclopedia of
Medicine. Farmington Hills, MI: Gale Group, 1999;892.
82. HughesJM, Colley DG. Preventing Congenital
Toxoplasmosis. Morb Mortal Wkly Rep
2000;49(RR02):57-75.
 Disorders of
Appendix 10-A Altered Immunity
SYSTEMIC LUPUS ERYTHEMATOSUS
Systemic lupus erythematosus (SLE) is a chronic, multi-
system autoimmune disease with strong genetic predis-
position. There is also evidence suggesting risk factors
that can trigger the onset of this disease, such as physical
or emotional stress, pregnancy, sulfa antibiotics, and
environmental factors, such as sun exposure. Women
who are black, Asian, and Native American, ages 20 to
40 years, are more susceptible than men in acquiring
this disease. SLE is characterized by a systemic, remit-
ting and relapsing clinical presentation.1-4
The primary laboratory test for diagnosis of SLE is
as antinuclear antibody titer.5 Diagnosis of SLE is con-
firmed if a patient has 4 of the following 11 manifesta-
tions of SLE: malar rash, discoid rash (individual
round lesions), photosensitivity, oral ulcers, arthritis,
serositis, renal disorder, neurologic disorder, hemato-
logic disorder, immunologic disorder, and the presence
of antinuclear antibodies.3
Prognosis for 10-year survival after diagnosis is 90%.
The most common cause of death in SLE is renal failure,
and the second most common is CNS dysfunction.1-3
Clinical presentation of SLE may include the
following1-4:
 Stiffness and pain in hands, feet, and large joints
 Red, warm, and tender joints
 Butterfly (malar) rash on face
 Fever, fatigue, anorexia, and weight loss
 Raynaud’s phenomenon
 Headache, seizures, organic brain syndrome
 Hemolytic anemia, thrombocytopenia, leukopenia
 Renal disease or failure
Management of SLE may consist of nonsteroidal
antiinflammatory drugs; hydroxychloroquine and
other antimalarial agents; glucocorticoids; immuno-
suppressive agents (cyclophosphamide); dialysis; and
renal transplantation in severe cases.1,2,4,6
SARCOIDOSIS
Sarcoidosis is a systemic granulomatous disorder that
primarily affects women and nonwhite adults in the
374
third decade of their life. The definitive etiology is
unknown, although an autoimmune process that is
environmentally triggered is the generally agreed-on
hypothesis. Sarcoidosis mayhave periods of progression
and remission.1, 6-9
The lungs are the primary organs affected by
sarcoidosis, with dyspnea, dry cough, and chest pain
being common symptoms. Pulmonary involvement
can be staged according to the following radiographic
evidence:7,8
 Stage 0: No radiographic abnormalities
 Stage I: Bilateral hilar lymphadenopathy
 Stage II: Bilateral hilar adenopathy and parenchymal
infiltration
 Stage III: Parenchymal infiltration without hilar
adenopathy
 Stage IV: Advanced fibrosis with evidence of
honeycombing, hilar retraction, bullae, cysts, and
emphysema
Other systems of the body can be affected as well,
including the following:
 Eye and skin lesions
 Fever, fatigue, and weight loss
 Hepatosplenomegaly
 Hypercalcemia, anemia, and leukopenia
 Arthralgia, arthritis
Management of sarcoidosis usually consists of
corticosteroid therapy, ranging from topical to oral
administration. Additionally, cytotoxic agents (metho-
trexate and azathioprine), antimalarial agents (chloro-
quine and hydroxychloroquine), and nonsteroidal
antiinflammatory drugs may be used. In severe cases
of pulmonary disease, single and double lung trans-
plantation may be performed.1,6-8
AMYLOIDOSIS
Amyloidosis is a very rare metabolic disorder character-
ized by deposition of amyloid (a type of protein) in var-
ious tissues and organs. Amyloidosis is classified
according to protein type and tissue distribution. The
etiology of amyloidosis is not fully understood;
 Disorders of Altered Immunity
however, relation to a disordered reticuloendothelial
system and abnormal immunoglobulin synthesis has
been shown.
Clinical signs and symptoms are representative of
the affected areas.The following areas may be affected:
 Tongue
 Heart
 Gastrointestinal tract
 Liver
 Spleen
 Kidney
 Peripheral nerves
 Pancreas
 Cerebral vessels
 Skin
In general, the deposition of protein in these areas
will result in firmer, less distensible tissues that com-
promise organ function.
Management of amyloidosis consists of controlling
any primarydisease processthat may promote deposition
of amyloid into the tissues.1,10
RHEUMATOID ARTHRITIS
Rheumatoid arthritis (RA) is an autoimmune disease
characterized by uncontrolled proliferation of synovial
tissue.11 It is a chronic disease involving systemic
inflammation, with periods of exacerbation and
remission.12 The etiology is not fully understood, but
it is believed there is a correlation between environ-
mental and genetic factors. Females have an increased
risk of developing RA as well as individuals with a
positive family history, silicate exposure, and smoking
history.11
There are two forms of RA; juvenile RA and adult
RA. Juvenile RA occurs most often during the toddler
and early adolescent developmental phases, while
adult RA has a peak onset in the third and forth decades
of life. Both forms of RA have a similar pathogenesis
and medical management.12
With RA, there is an increase of leukocytes from the
peripheral circulation into the synovial joint. Tumor
necrosis factor stimulates the release of more cytokines
resulting in an extreme inflammatory response.
Pannus can develop, a destructive granulation tissue
APPENDIX 10-A 375
that dissolves periarticular tissues, ultimately leading
to joint destruction.12
Clinical manifestations of RA can include articular
and extraarticular symptoms. Most body systems may
be involved including pulmonary, cardiovascular, neu-
rologic, and gastrointestinal.12 The joints most com-
monly affected by RA are those with the highest ratio
of synovium compared to articular cartilage including
the wrist, proximal interphalangeal, and metacarpo-
phalangeal joints.11 Common deformities associated
with RA are ulnar drift, swan-neck, and boutonniere
deformities.12 Other symptoms include anorexia, low-
grade fever, fatigue, and malaise.11 Osteoarthritis (OA),
also called degenerative joint disease, may result in joint
changes and deformation. Refer to Table 10-A.1 for a
comparison between OA and RA.12
Diagnosis of rheumatoid arthritis can be made
through the following seven criteria established by the
American Rheumatism Association:11
1. Morning stiffness
2. Arthritis of three or more joint areas
3. Hand joint involvement
4. Symmetric arthritis
5. Rheumatoid nodules
6. Serum rheumatoid factor positive
7. Radiographic changes of the wrist and hand joints
Laboratory diagnostic tests include a complete
blood cell count with differential, rheumatoid factor,
and erythrocyte sedimentation rate (ESR) or C-reactive
protein (CRP).11
Management of RA may include the following11:
 NSAIDs
 Glucocorticoids
 Disease-modifying antirheumatic drugs (DMARDs)
(Appendix IV,Table IV-13)
 Pain management
 Joint protection
 Control of systemic complications
CLINICAL TIP
 Modification of an assistive device may be necessary
based on the patient’s wrist and hand function. For
example, a platform walker may more appropriate
than a standard walker and loftstrand crutches may
be more appropriate than axillary crutches.
376 APPENDIX 10-A Disorders of Altered Immunity

Table 10-A.1 COMPARISON OF OSTEOARTHRITIS AND RHEUMATOID ARTHRITIS

OA RA
Onset Majority of adult age > 60 Adult: ages 25-50
Gradual onset Sudden onset
Incidence 2% U.S. adults 1%-2% U.S. adults
Gender Age < 45: predominantly males Female:male ratio 3:1
Age > 45: predominantly females
Etiology Inflammatory response Autoimmune process
Genetic, environmental factors
Manifestations Unilateral joint involvement Bilateral joint involvement
Affects: spine, hips, knees, feet, hands Affects any joint, predominantly upper-extremity
Inflammation present in 10% of cases joints
Brief morning stiffness Inflammation present in most cases
Prolonged morning stiffness
Systemic None Fatigue, malaise, weight loss, fever
symptoms
Lab values ESR: mildly-moderately increased ESR: markedly increased
Rheumatoid factor: absent Rheumatoid factor: present
Synovial fluid: low WBC and high Synovial fluid: highWBC and low viscosity
viscosity

References
1. Bullock BL. Pathophysiology: Adaptations and
Alterations in Function (4th ed). Philadelphia:
Lippincott, 1996.
2. Kimberly RP. Research Advances in Systemic Lupus
Erythematosus. JAMA 2001;285(5):650.
3. McConnell EA. About Systemic Lupus Erythematosus.
Nursing 1999;29(9):26.
4. Wallace DJ. Update on Managing Lupus Erythematosus.
J Musculoskeletal Med 1999;16(9):531.
5. GillJM, Quisel AM, Rocca PV, et al. Diagnosis
of Systemic Lupus Erythematosus. Am Fam Physician
2003;68(11):2179-2186.
6. Chandrasoma P,Taylor CR. Concise Pathology (2nd ed).
East Norwalk, CT: Appleton & Lange, 1995.
7. Morey SS. AmericanThoracic Society Issues Consensus
Statement on Sarcoidosis. Am Fam Physician
2000;61(2):553.
8. Johns CJ, MicheleTM.The Clinical Management
of Sarcoidosis. A 50-Year Experience at theJohns
Hopkins Hospital. Medicine 1999;78(2):65.
9. Judson MA,Thompson BW, Rabin DL, et al.
The Diagnostic Pathway to Sarcoidosis. Chest
2003;123(2):406-412.
10. Goodman CC, SnyderTEK. Differential Diagnosis
in Physical Therapy: Musculoskeletal and Systemic
Conditions. Philadelphia: Saunders, 1995.
11. RindfleischJA, Muller D. Diagnosis and Management
of Rheumatoid Arthritis. Am Fam Physician
2005;72(6):1037-1047.
12. Goodman CC, Boissonnault WG. Pathology:
Implications for the Physical Therapist. Philadelphia:
WB Saunders, 1998.
11 Endocrine System

Jaime C. Paz INTRODUCTION

The endocrine system consists of endocrine glands, which secrete
hormones into the bloodstream, and target cells for those
hormones. Target cells are the principal sites of action for the endo-
crine glands. Figure 11-1 displays the location of the primary endocrine
glands.
The endocrine system has direct effects on cellular function and
metabolism throughout the entire body, with symptoms of endocrine
dysfunction, metabolic dysfunction, or both, often mimicking those
of muscle fatigue. Also, the onset of clinical manifestations from
endocrine or metabolic dysfunction, or both, can often be insidious
and subtle in presentation. Therefore, it is important for the physical
therapist to carefully distinguish the source (endocrine versus muscu-
loskeletal) of these symptoms to optimally care for the patient. For
example, complaints of weakness and muscle cramps can result from
hypothyroidism or inappropriate exercise intensity. If the therapist is
aware of the patient’s current endocrine system status, then inquiring
about a recent medication adjustment may be more appropriate than
adjusting the patient’s exercise parameters.
The objectives of this chapter are to provide a basic understanding of:
1. Normal functions of the endocrine system, including the thyroid,
pituitary, adrenal, and parathyroid glands, as well as the pancreas
2. Clinical evaluation of these endocrine organs
3. Endocrine system dysfunction and subsequent medical management
4. Physical therapy guidelines for working with patients who have endo-
crine system dysfunction
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:
 Pattern 4A: Primary Prevention/Risk Reduction for Skeletal
Demineralization
 Pattern 6B Impaired Aerobic Capacity/Endurance Associated with
Deconditioning
 Pattern 7A: Primary Prevention/Risk Reduction for Integumentary
Disorders.
Please refer to the back cover of this book for a complete list of the pre-
ferred practice patterns as individual patient conditions are highly variable
and other practice patterns may be applicable.

377
378 CHAPTER 11 Endocrine System
FIGURE 11-1
Schematic representation of the primary endocrine glands in
women and men. (Courtesy Marybeth Cuaycong.)
SCREENING FOR METABOLIC AND
ENDOCRINE DYSFUNCTION
The following questions help to provide a basic method
to differentiate the patient’s symptoms and complaints
to a specific endocrine gland. These questions are not
comprehensive but may help with full integration of
the patient’s signs and symptoms. Ultimately, laboratory
data by the physician is necessary to accurately diagnose
the medical disorder. Physical therapists can use these
questions to help guide their evaluations and organize
inquiries for the medical team regarding treatment
parameters. For instance, if the questions lead the ther-
apist to suspect pituitary involvement, seeking clarifica-
tion from the physician regarding the appropriateness
of physical therapy intervention may be necessary.1
1. Pituitary
a. Are menses regular? (If they are irregular, hypo-
pituitarism may be suspected.)
b. Has there been a change in vision? (Large
pituitary tumors can result in vision loss.)
2. Adrenal
a. Is there skin darkening? (Chronic primary adre-
nal insufficiency results in hyperpigmentation.)
b. Is there weight loss, nausea, vomiting, or syn-
cope? (These are suggestive of adrenal insuffi-
ciency.)
c. Have there been episodes of tachycardia, head-
aches, and sweating? (These are suggestive of
pheochromocytoma.)
3. Thyroid
a. Is there a change in the patient’s neck size? (This
can indicate the presence of goiter or hyper-
thyroidism.)
b. What is the room-temperature preference of
the patient? (608 F suggests hyperthyroidism,
whereas 808 F suggests hypothyroidism.)
4. Parathyroid
a. Is there a history of thyroid surgery? (This is the
usual cause of hypoparathyroidism.)
b. Are kidney stones, polyuria, and constipation
present? (This could indicate hypercalcemia
from hypoparathyroidism.)
5. Pancreas
a. Is there nocturia or noctidipsia (urination or
drinking at night, respectively)? (Both of these
can suggest diabetes mellitus.)
b. Has there been a weight loss or gain and
increased appetite? (These also suggest diabetes.)
GENERAL EVALUATION OF
ENDOCRINE FUNCTION
Measurement of endocrine function can be performed
by examining (1) the endocrine gland itself, using
imaging techniques, or (2) levels of hormones or
hormone-related substances in the bloodstream or
urine. When reviewing the medical record, it is
important for the physical therapist to know that high
or low levels of endocrine substances can indicate endo-
crine dysfunction. A common method for assessing
levels of hormone is radioimmunoassay (RIA).2 RIA is
an immunologic technique for comparing levels of
radiolabeled hormone with unlabeled hormone,
which compete for binding sites on a given antibody.
Another method of evaluation, referred to as provoc-
ativetesting, can be classified into suppression or stimula-
tion tests. Stimulation tests are used for testing
endocrine hypofunction; suppression tests are useful
 Endocrine System CHAPTER 11 379
in evaluating endocrine hyperfunction.3 The most
commonly used endocrine tests are discussed in this Table 11-1 TARGET SITES AND ACTIONS OF
chapter. Clinicians should refer to their particular THYROID GLAND HORMONES
institution’s laboratory values (generally located in the Target
back of the clinical record) for normal ranges of hor- Hormone(s) Site(s) Actions
mone or hormone-related substances referenced in
Thyroxine (T4) and Systemic Increases metabolic
their setting. triiodothyronine rate; stimulates
(T3) growth, and
development of all
CLINICAL TIP cells, particularly of
the nervous system;
 An imbalance of hormone levels may affect and enhances the
the patient’s tolerance to activity. Familiarity effects of
with the endocrine tests and values can help the catecholamines
clinician gauge the intended treatment parameters Thyrocalcitonin Bone Inhibits bone resorption
(i.e., type, duration, frequency, and intensity) for the Lowers blood levels
next session(s). of calcium
Data from Fuller BF: Anatomy and Physiology of the Endocrine
System. In CM Hudak, BM Gallo (eds): Critical Care Nursing:
A Holistic Approach, ed 6. Philadelphia, Lippincott, 1994;75;
Hartog M (ed): Endocrinology. Oxford, Blackwell Scientific,
THYROID GLAND 1987;23; CorbettJV: LaboratoryTests and Diagnostic Procedures
with Nursing Diagnoses, ed 5. Upper Saddle River, NJ, Prentice
Hall Health, 2000;409.
Function
The thyroid gland secretes three hormones: thyroxine
(T4), triiodothyronine (T3), and calcitionin, with T4
and T3 commonly referred to as the thyroid hormones.
Thyroxine and triiodothyronine require the presence CLINICAL TIP
of adequate amounts of iodine to be properly synthe-
 Low levels of thyroid hormones T3 or T4 may result
sized. Therefore, dietary deficiencies of iodine can
in weakness, muscle aching, and stiffness. Based on
hinder thyroid hormone production. The production
this information, the physical therapist may decide
and secretion of thyroid hormones are regulated by thy-
to alter treatment parameters by decreasing the
rotropin (also called thyroid-stimulating hormone
treatment intensity to optimize activity tolerance,
[TSH]), which is secreted from the anterior pituitary
minimize patient discomfort, or both.
gland. TSH levels are directly influenced by T4 levels
 Patients may be on bed rest or precautions after
through a negative feedback loop. Thyrotropin is fur-
radionuclide studies. The physical therapist should
ther regulated by thyrotropin-releasing hormone,
refer to the physician’s orders after testing to
which is secreted from the hypothalamus.4-6 Table 11-1
clarify the patient’s mobility status.
summarizes the target sites and actions of the thyroid
gland hormones.
Thyroid Tests Thyroid Disorders
Thyroid hormones T4 and T3 circulate throughout the Disorders of the thyroid gland result from a variety of
bloodstream bound to proteins (approximately 99%) causes and can be classified as hyperthyroidism or
or unbound, in which case they are metabolically hypothyroidism.
active by themselves. Thyroxine-binding globulin
(TBG) is the major thyroid transport protein. Serum HYPERTHYROIDISM
levels of T4 and T3 are usually measured by RIA. Table Hyperthyroidism, or thyrotoxicosis, is primarily
11-2 describes the tests used to measure thyroid hor- characterized by excessive sympathomimetic and
mones, and Table 11-3 summarizes other tests used to catabolic activity resulting from overexposure of
measure thyroid function. tissues to thyroid hormones. However, recent literature
380 CHAPTER 11 Endocrine System

Table 11-2 THYROID HORMONE TESTS

Hormone Test Description Normal Value
Serum thyroxine Radioimmunoassay (RIA) 4-12 mg/dl
measurement.
Serum triiodothyronine RIA measurement. 40-204 ng/dl
Free thyroxine index Direct RIA measurement or indirect
calculated measurement. Direct: 0.8-2.7 ng/ml
Indirect: 4.6-11.2 ng/ml
Thyroid-stimulating hormone Radioisotope and chemical labeling 0.4-8.9 mU/ml
(TSH) measurement.
Thyrotropin-releasing hormone Intravenous administration of Normal rise in men and women is 6 mU/ml
(TRH) TRH to patients. above baselineTSH levels.
TRH augments the function The expected response is a rise Normal rise in men older than 40 years
of TSH in patients with inTSH levels. is 2 mU/ml above baseline.
hypothyroidism. Hypothyroidism is indicated by
Only performed in difficult increased response toTRH.
diagnostic cases. Hyperthyroidism is indicated by no
response toTRH.
Data from reference numbers 1, 4, 5, 6

demonstrates the likelihood that hyperthyroidism Management of hyperthyroidism primarily includes

results in both an increased sympathetic activity with
concurrent decreased vagal (parasympathetic tone).
Spectral analysis of heart rate variability has been
shown to detect these changes and is helpful in deter-
mining the severity of hyperthyroidism.7 Heart rate
variability is discussed further in Chapter 1. The most
common causes of hyperthyroidism are outlined in
Table 11-4.
Signs and symptoms of hyperthyroidism include the
following1,6:
 Nervousness, irritation, and emotional lability
 Fatigue, weakness, and weight loss despite normal or
increased appetite
 Palpitations, atrial fibrillation (common above the
age of 60 years), and tachycardia (heart rate of more
than 90 beats per minute at rest)
 Increased perspiration, moist and warm hands, and
smooth and velvety skin
 Heat intolerance
 Diarrhea
 Menstrual dysfunction
 Presence of goiter
 Tremor
 Lid lag, retraction, or both
 ‘‘Plumber’s nails’’ (onycholysis)
 Thyroid bruit
pharmacologic therapy, which is summarized in
Appendix IV, Table IV-39. Surgical management may
include the following:
Surgical subtotal-thyroidectomy (indicated for
patients who are pregnant, children who have adverse
reactions to antithyroid medications, patients with
excessively large goiters that are compressive, and
patients with thyroid carcinoma)
HYPOTHYROIDISM
Hypothyroidism is the insufficient exposure of
peripheral tissues to thyroid hormones. It affects
growth and development, as well as many cellular
processes. In the majority of cases, hypothyroidism
is caused by decreased thyroid hormone production
rather than the failure of tissues to respond to thy-
roid hormones. Primary hypothyroidism refers to thyroid
gland dysfunction, whereas secondary hypothyroidism
refers to pituitary disease resulting in reduced TSH
levels.
The following are the causes of primary and
secondary hypothyroidism8,9:
 Maldevelopment, hypoplasia, or aplasia of the
thyroid gland
 Inborn deficiencies of biosynthesis or action of
thyroid hormone

Table 11-3 THYROID FUNCTION TESTS
Test Description
Triiodothyronine RT3U indirectly measures the
resin uptake number of unoccupied protein-
(RT3U) binding sites for serum thyroxine
(T4) and serum triiodothyronine
(T3) by using radioisotopes.
RT3U qualifies levels of bound
versus unbound T4 and T3.
Thyroid hormone uptake is high
with hyperthyroidism and low
with hypothyroidism.
Thyroidal 24-hour Used to determine metabolic
radioactive activity of the thyroid gland.
iodine uptake Radioactive iodine is
administered, and the percentage
of total administered radioactive
iodine taken up by the thyroid in
24 hours is then calculated.
Normal radioactive iodine uptake
is 5% to 30%.
Hypothyroidism results in reduced
uptake.
Thyroid imaging Intravenous administration of
or scan radionuclides allows imaging or
scanning of particular areas of the
thyroid gland.
Increased or decreased uptake of the
radionuclide can help diagnose
dysfunction.
Ultrasound Nodules of the thyroid gland that
are palpable or suspected may
be delineated as cystic or solid
lesions by ultrasound.
Needle biopsy Fine-needle aspiration of thyroid
cells may help diagnose
a suspected neoplasm.
Data from BurchWM (ed). Endocrinology for the House Officer
(2nd ed). Baltimore: Williams & Wilkins, 1988;1; Hartog M (ed).
Endocrinology. Oxford, UK: Blackwell Scientific, 1987;25; and
Sacher RA, McPherson RA, CamposJM (eds).Widman’s Clinical
Interpretation of LaboratoryTests (11th ed). Philadelphia: FA Davis,
2000;786-793.
 Hashimoto’s thyroiditis (autoimmune inflammation)
 Lymphatic thyroiditis (autoimmune inflammation
that has hyperthyroid symptoms)
 Hypopituitarism or hypothalamic disease
 Severe iodine deficiency
Endocrine System CHAPTER 11 381
 Thyroid ablation from surgery, radiation of
cervical neoplasms, or radioiodine therapy for
hyperthyroidism
 Drug toxicity (from amiodarone, antithyroids, or
lithium)
General signs and symptoms of hypothyroidism
vary according to the degree of thyroid deficiency.
Signs and symptoms include the following1,6:
 Lethargy, somnolence, and slowness of thought
 Constipation and ileus (decreased motility)
 Rough, scaly, dry, and cool skin, and decreased
perspiration
 Slow relaxation time of deep tendon reflexes
 Marked cold intolerance
 Weakness, muscle cramps, and aching and stiffness
 Hoarseness and decreased hearing
 Paresthesia
 Pallid and yellow-tinted skin
 Nonpitting edema of eyelids, hands, and feet
 Bradycardia with elevated systolic and diastolic
blood pressure
 Cardiac failure
 Pericardial effusion
 Coma and respiratory failure in severe cases
Additional laboratory findings that are associated
with hypothyroidism include the following10:
 Low glucose and serum sodium levels
 Anemia
 Elevated levels of cholesterol, creatinine phosphoki-
nase (CK-MM), serum myoglobin, lactate dehydro-
genase, liver enzymes, homocysteine, and prolactin
 Proteinuria
Management of hypothyroidism typically includes
lifelong thyroid hormone replacement, primarily
consisting of generic and brand name variations of
levothyroxine. A complete list of medications is
provided in Appendix IV,Table IV-39.
CLINICAL TIP
 Properly managed hyperthyroidism or
hypothyroidism should not affect physical therapy
intervention or activity tolerance. If the signs
or symptoms mentioned above are present during
physical therapy evaluation, treatment, or both,
consultation with the medical team is indicated
to help differentiate the etiology of the physical
findings. See the Screening for Metabolic and
Endocrine Dysfunction section for more information
on screening.
382 CHAPTER 11 Endocrine System

Table 11-4 COMMON CAUSES OF HYPERTHYROIDISM

Cause Description
Graves’disease A familial, autoimmune disorder responsible for approximately 80% to 90%
of hyperthyroid cases. Occurs more commonly in women than men.
Distinguishing features include diffuse thyroid enlargement, ophthalmopathy (double
vision and sensitivity to light), exophthalmos (excessive prominence of the eyes),
pretibial myxedema (thickening, redness, and puckering of skin in the front of the
tibia), atrial fibrillation, fine hand tremors, and weakness of the quadriceps muscle.
Thyroiditis Inflammation of the thyroid gland can result from an acute bacterial infection,
a subacute viral infection, or chronic inflammation with unknown etiology.
Pain may or may not be present on palpation of the gland.
Toxic nodular and Areas of the enlarged thyroid gland (goiter) become autonomous and produce
multinodular goiter excessive amounts of thyroid hormones.
Thyroid adenoma Solitary, benign follicular adenomas that function autonomously result in
hyperthyroidism if the adenoma nodule is larger than 4 cm in diameter.
May present as a painless lump in the throat.
Thyroid carcinoma Four types of malignancies in the thyroid gland: papillary carcinoma (most common),
follicular carcinoma, anaplastic carcinoma, and medullary carcinoma.
Exogenous Ingestion of excessive amounts of thyroid hormone or iodine preparation.
hyperthyroidism Can be classified as iatrogenic hyperthyroidism, factitious hyperthyroidism,
or iodine-induced hyperthyroidism.
Ectopic thyroid hormone Thyroid hormone can be produced from the ovaries or from metastatic follicular
production thyroid carcinoma (rare occurrence).
Data from BurchWM (ed). Endocrinology for the House Officer (2nd ed). Baltimore: Williams & Wilkins, 1988;126;Woolf N (ed). Pathology,
Basic and Systemic. London: Saunders, 1998;863-873.

PITUITARY GLAND serum cortisol, and plasma adrenocorticotropic hor-

Function
Hormones secreted by the pituitary gland are responsi-
ble for a variety of functions that are summarized in
Table 11-5. Secretions of hormones from the pituitary
gland are closely regulated by the hypothalamus and
by negative feedback from the hormones that are
secreted from the pituitary gland.6
Pituitary Tests
Individual pituitary hormone levels can be measured (1)
by random blood samples; (2) by blood samples before
and after the administration of specific releasing sub-
stances, such as serum TSH, during a thyrotropin-
releasing hormone test (see Table 11-2); or (3) by blood
samples before and after the administration of specific
stimuli acting directly on the pituitary or via the
hypothalamus, such as serum growth hormone (GH),
mone (ACTH).
Table 11-6 describes common tests of pituitary func-
tion. Pituitary function can also be evaluated by (1) thy-
roid function tests, which are an indirect assessment
of TSH secretion from the pituitary, and (2) plain x-
rays or computed tomography with contrast to high-
light a pituitary tumor.11
Pituitary Disorders
Dysfunction of the pituitary-hypothalamic system gen-
erally results from hypersecretion or hyposecretion of
tropic hormones. Hypersecretion of pituitary hor-
mones (hyperpituitarism) is most commonly due to ad-
enoma in the anterior lobe (benign tumors).12
Hyposecretion of pituitary hormones (pituitary insuffi-
ciency) can result from pituitary disease, diseases affect-
ing the hypothalamus or surrounding structures, or
disturbance of blood flow around the hypothalamus
and pituitary.13,14
 Endocrine System CHAPTER 11 383

Table 11-5 TARGET SITES AND ACTIONS OF PITUITARY GLAND HORMONES

Hormone(s) Target Site(s) Action(s)
Anterior Lobe
Growth hormone Systemic Growth of bones, muscles, and other organs
Liver Formation of somatomedin
Thyrotropin Thyroid Growth and secretion activity of the thyroid gland
Adrenocorticotropin Adrenal cortex Growth and secretion activity of the adrenal cortex
Follicle-stimulating hormone Ovaries Development of follicles and secretion of estrogen
Testes Development of seminiferous tubules and spermatogenesis
Luteinizing or interstitial Ovaries Ovulation, formation of corpus luteum, and secretion
cell—stimulating hormone of progesterone
Testes Secretion of testosterone
Prolactin or lactogenic Mammary Secretion of milk
hormone glands
Melanocyte-stimulating Skin Pigmentation
hormone
Posterior Lobe
Antidiuretic hormone* Kidney Reabsorption of water
(also called vasopressin) Fluid and electrolyte balance
Oxytocin* Arterioles Blood pressure regulation
Uterus Contraction
Breast Expression of milk
*Actually produced in the hypothalamus but stored in the pituitary gland.
Data from Fuller BF. Anatomy and Physiology of the Endocrine System. In CM Hudak, BM Gallo (eds), Critical Care Nursing: A Holistic
Approach (6th ed). Philadelphia: Lippincott, 1994;875; Sacher RA, McPherson RA, CamposJM (eds).Widman’s Clinical Interpretation of
LaboratoryTests (11th ed). Philadelphia: FA Davis, 2000;744.

HYPERPITUITARISM
The overproduction of the pituitary hormones GH,
ACTH, and antidiuretic hormone (ADH) is discussed
below.
GROWTH HORMONE OVERPRODUCTION. The most
common presentation of excessive GH secretion is
acromegaly in adults or gigantism in children.
Excessive GH secretion has been linked primarily to
anterior pituitary adenomas and not necessarily to
excessive hypothalamic stimulation of the pituitary.14
Clinical manifestations for children with gigantism
are characterized by disproportionately long limbs.12
Signs and symptoms of adults with acromegaly
include the following1,14:
 Enlargement of hands and feet, coarse facial features
with furrowed brows
 Oligomenorrhea or amenorrhea in women
 Paresthesia of hands, carpal tunnel syndrome
 Sweating
 Headaches
 Impotence in men
 Diabetes mellitus
 Hypertension
 Joint pains, osteoarthritis
Management of acromegaly may include the follow-
ing: transphenoid surgical resection of anterior pitu-
itary adenoma (treatment of choice), GH suppression
with somatostatin and its analogs (octreotide), or with
dopamine agonists and external irradiation as a last
resort.15
CLINICAL TIP
 Given the multisystem effects in patients with
acromegaly, activity progression should proceed
cautiously, with a focus on energy conservation,
joint protection techniques, and fall-prevention
strategies.
384 CHAPTER 11 Endocrine System

Table 11-6 PITUITARY HORMONE TESTS

Hormone(s)
Growth hormone (GH)
Adrenocorticotropic
hormone (ACTH)
Antidiuretic hormone
(ADH or vasopressin)
Data from Malarkey LM, McMorrow ME (eds). Nurse’s Manual of LaboratoryTests and Diagnostic Procedures. Philadelphia: Saunders,
2000;580-584, 552-555, 613-614, 616-619.
Test Description
Serum level measurement by radioimmunoassay (RIA); normal values for men are
0 to 5 ng/ml; normal values for women are 0 to 10 ng/ml.
Growth hormone—stimulation test (arginine test or insulin tolerance test). Indicated for
children with retarded growth and if pituitary tumor is suspected. A baseline level
of GH is established, then arginine or insulin is administered to the patient, and
serial blood draws are performed to measure GH levels. GH should normally rise.
Decreased GH values, despite stimulation, could indicate pituitary dwarfism or
tumors.
Growth hormone suppression test (glucose load test). Indicated to confirm diagnoses of
gigantism in children and acromegaly in adults. A baseline level of GH is established,
followed by patient ingestion of a glucose solution. After 1 to 2 hours, levels of GH
are remeasured. Normally, glucose inhibits the secretion of GH. If GH levels remain
high despite the glucose load, then gigantism or acromegaly can be confirmed.
Plasma ACTH levels are measured by RIA. Normal values are 25 to 100 pg/ml in the
morning and 0—50 pg/ml in the evening.
ACTH-stimulation test (rapid ACTH testing, cosyntropin test, or Cortrosyn stimulating
test). Indicated for diagnosing primary and secondary adrenal insufficiency.
Cosyntropin (Cortrosyn) (synthetic form of ACTH) is administered to a patient after
a baseline level of cortisol is measured. ACTH acts to increase cortisol secretion
from the adrenal gland. Normal results show an increased plasma cortisol level to
> 20 pg/dl after 30 to 60 minutes.
Normal plasma levels of ADH are 2 to 12 pg/ml if serum osmolality is > 290 mOsm/kg
and < 2 if serum osmolality is < 290 mOsm/kg.
Waterdeprivation test (dehydration test or concentration test). Indicated for diagnosing
diabetes insipidus (DI). Normally, if water is withheld, ADH levels rise to help increase
water reabsorption in the kidneys. During the test, the patient is deprived of fluids, and
serial measurements of urine osmolality are taken. Normally, ADH secretion causes a
change in urine osmolality, but with DI, the osmolality remains unchanged.While the
patient is being deprived of water, vasopressin may be administered to help delineate
whether the DI is caused by pituitary or renal dysfunction.
Waterloading test. Indicated for diagnosing syndrome of inappropriate antidiuretic hormone
(SIADH). During the test, the patient ingests 20 to 25 ml/kg of fluid, with hourly
serum and urine osmolality levels being measured for 4 hours. Normally, with water
ingestion, the plasma and urine osmolality should decrease, and urine output should
increase.With SIADH, there is little or no change in these values.

ADRENOCORTICOTROPIC HORMONE OVERPRO-
DUCTION. An increase in ACTH production by the
pituitary gland results in increased levels of serum
cortisol, which is a glucocorticoid secreted by the
adrenal glands. Glucocorticoids are involved with car-
bohydrate, protein, and fat metabolism; therefore,
excess cortisol levels affect these cellular processes.
Any clinical syndrome that results in glucocorticoid
excess (hypercortisolism) is called Cushing’s syndrome.
Cushing’s disease, however, is specific to pituitary
lesions that cause bilateral adrenal hyperplasia and
is not discussed in this chapter.1 Pituitary hyper-
secretion of ACTH occurs in approximately 70% of
patients with Cushing’s syndrome. The hypersecretion
of ACTH is mainly from pituitary adenomas or
microadenomas.6
Signs and symptoms of Cushing’s syndrome include
the following6,11,14:
 Truncal obesity with thin extremities (loss of type II
muscle fibers)12

 Redness and rounding of the face (moon face)
 Easy bruising, thinning of the skin, and presence of
striae and darker pigmentation
 Hirsutism, oligomenorrhea, or amenorrhea
 Hypertension
 Osteoporosis (radiographically confirmed)
 Proximal muscle weakness
 Backache
 Glucose intolerance, glucosuria and polydipsia
Diagnosis of Cushing’s syndrome is established by
increased levels of urinary cortisol in a 24-hour
period.12 Management of Cushing’s syndrome may
include the following: surgical resection of pituitary
lesion, radiation or chemotherapy for the lesion, or
medical management with steroidogenic inhibitors
(ketoconazole, mitotane, etomidate, metyrapone, and
aminoglutethimide) or neuromodulators of ACTH
release (valproic acid, bromocriptine, and cyprohepta-
dine). Surgical resection of the adrenal glands is a
last-resort measure.15
CLINICAL TIP
 Management of weakness, myopathy, pain, edema,
and osteoporosis should be the focus of physical
therapy intervention and be complementary to the
medical management of the patient. Blood pressure
changes during activity should be monitored,
given the possibility of hypertension. Caution should
also be taken to avoid bruising during mobility.
Refer to Diabetes Mellitus for further activity
considerations.
ANTIDIURETIC HORMONE OVERPRODUCTION. The
syndrome of inappropriate ADH secretion (SIADH) is
a condition of fluid and electrolyte imbalance resulting
in hyponatremia (reduced sodium levels) from excessive
water reabsorption. In this condition, ADH is secreted
from the posterior pituitary gland when it should be
inhibited.
Numerous etiologies of SIADH exist, with the most
frequent cause being small cell or oat cell carcinomas
of the lung. Other etiologies include the following16,17:
 Bacterial pneumonias, chronic obstructive pulmo-
nary disease, tuberculosis, lung abscesses
 Malignancies of the pancreas, duodenum, colon,
lymphoid tissue, and thymus
 Medication side effects from antipsychotics, seda-
tive-hypnotics, diuretics, antihypertensives, analge-
sics, cardiac drugs, and antibiotics
 Head trauma, central nervous system neoplasms
Endocrine System CHAPTER 11 385
A mild condition of SIADH is usually asymptomatic.
More severe cases, however, can result in fluid and elec-
trolyte imbalances, resulting in interstitial edema from a
lack of serum sodium. Many systems will be affected by
this edema, with the nervous system being most severely
involved. Manifestations may include the following:
headaches, nausea, confusion, and cerebral edema that
leads to seizures and coma (in severe cases).12,16
Management of SIADH may include the following:
treatment of the underlying cause, fluid restriction,
intravenousadministration ofsodium chloride solution,
or administration of diuretics (furosemide).16
CLINICAL TIP
 The physical therapist should be aware of fluid
restriction guidelines for patients with SIADH,
especially because activity during physical therapy
may increase the patient’s thirst. These guidelines
are often posted at the patient’s bedside.
HYPOPITUITARISM
There are numerous causes for primary (pituitary
directly affected) or secondary (hypothalamus or
pituitary stalk affected) hypopituitarism. The most
common causes of primary hypopituitarism are pitu-
itary neoplasms, such as pituitary adenomas and cranio-
pharyngioma, and ischemic necrosis occurring during
the late stages of pregnancy (Sheehan’s syndrome).
Common causes of secondary hypopituitarism include
hypothalamic tumors, cranial trauma, sarcoidosis, sur-
gical destruction of the pituitary stalk, or a combination
of these.6,14,18,19
Symptoms, physical findings, and management
depend on the extent of the disorder and the specific
hormone (GH, TSH, or ACTH) and target cells
involved. Patients with complete pituitary hormone
deficiency (panhypopituitarism) present with the
following11,18:
 Hypogonadism
 Amenorrhea, regression of secondary sexual charac-
teristics, and infertility
 Dilutional hyponatremia
 Diabetes insipidus (DI)
 Short stature (in children)
 Hypothyroidism
 Glucocorticoid deficiency
Management of panhypopituitarism may include
the following: replacement therapy or pituitary
hormones, such as thyroxine, glucocorticoids, and
386 CHAPTER 11 Endocrine System

GH for children; desmopressin for DI; androgen ther-
apy for men; or estrogen therapy for women younger
than 50 years of age. Management of other clinical
sequelae of hypopituitarism is specific to the involved
areas.11,18
DIABETES INSIPIDUS
DI involves the excretion of a large volume (i.e., greater
than30ml/kg perday)ofdilute urine(hypotonicpolyuria).
DI may result from hypothalamic, posterior pituitary,
renal,or psychogenic disorders;however, most incidences
of DI are described as idiopathic.6,20 Pituitary DI involves
the failure to synthesize or release vasopressin (ADH).
Renal, or nephrogenic, DI is a deficiency of vasopressin
receptors in the renal collecting ducts. Failure to release
ADH from the pituitary gland is termed central DI as com-
pared to peripheral DI, which comes from renal dysfunc-
tion.12 Psychogenic or dipsogenic DI involves a large
intake of fluid that may suppress ADH secretion.8,11,17,20
Signs and symptoms of DI may be transient or
permanent, and include the following8,17,18,20:
 Polyuria, nocturia with resultant hypernatremia
(increased sodium)
 Thirst (especially for cold or iced drinks), polydipsia
 Dehydration
 Weight loss
 Dry skin with decreased turgor
 Central nervous system manifestations (e.g., irritabil-
ity, mental dullness, ataxia, hyperthermia, and
coma) if access to water is interrupted
Management of neurogenic (hypothalamic or pitu-
itary dysfunction) DI may include pharmacologic treat-
ment, such as the following: aqueous vasopressin or
deamino-8-D-arginine vasopressin (Desmopressin),
chlorpropamide (Diabinase), and clofibrate (Atromid-S).
Management of nephrogenic (renal) DI may include
diuretics such as hydrochlorothiazide (HydroDIURIL),
in combination with a sodium-restricted diet.8,17,21
ADRENAL GLAND
Function
The adrenal gland hastwo distinct areas, the outer cortex
and the inner medulla, that differ in their function and
embryologic origin.6 Table 11-7 summarizes the target
sites and actions of the adrenal gland hormones.
Adrenal and Metabolic Tests
ADRENAL TESTS
Evaluation of the adrenal cortical (glucocorticoids,
androgens, and mineralocorticoids) and medullary

Table 11-7 TARGET SITES AND ACTIONS OF ADRENAL GLAND HORMONES

Hormone(s) Target site(s) Action(s)
Cortex
Mineralocorticoids (aldosterone) Kidney Reabsorption of sodium and water
Elimination of potassium
Glucocorticoids (cortisol) Systemic Metabolism of carbohydrate, protein, and fat
Response to stress
Suppresses immune responses
Antiinflammation
Sex hormones (androgens, Systemic Preadolescent growth spurt, affects
progesterone, and estrogen) secondary sex characteristics
Medulla
Epinephrine Cardiac and smooth muscle, glands Emergency functions
Stimulates the action of the sympathetic
system
Norepinephrine Organs innervated by sympathetic Chemical transmitter substance
nervous system Increases peripheral resistance
Data from Fuller BF. Anatomy and Physiology of the Endocrine System. In CM Hudak, BM Gallo (eds), Critical Care Nursing: A Holistic
Approach (6th ed). Philadelphia: Lippincott, 1994;875; CorbettJV (ed). LaboratoryTests and Diagnostic Procedures with Nursing Diagnoses
(5th ed). Upper Saddle River, NJ: Prentice Hall Health, 2000;391.

(epinephrine and norepinephrine) hormones is des-
cribed below. Anatomic investigation of the adrenal
glands may also be performed to diagnose possible
adrenal dysfunction. Common methods to accomplish
this are computed tomography scan (to identify adrenal
tumors), radioisotope scan using seleno-cholesterol,
ultrasound, arteriogram, adrenal venogram (allows
measurements of hormone levels), and intravenous
pyelogram (see the Diagnostic Tests section in
Chapter 9).11,22
GLUCOCORTICOIDS. Glucocorticoids can be evalu-
ated by testing serum and urine cortisol levels,
24-hour urinary corticosteroids, or ACTH. Altered
glucocorticoid levels can affect protein and carbohy-
drate metabolism.
 Serum cortisol levels are measured by RIA, which is
indicated for diagnosing Cushing’s syndrome or
Addison’s disease. For accuracy, notation should be
made as to the time of day the serum was drawn,
because levels are highly dependent on the diurnal
rhythm of secretion. Normal serum levels are 5 to
23 mg/dl (8 to 10 AM) and 3 to 16 mg/dl (4 to 6 PM).22
 Twenty-four-hour urinary corticosteroids. Analysis
of urine over a 24-hour period to determine the uri-
nary levels of corticosteroids will provide a rough
outline of cortisol output. Also indicated for diag-
nosing Cushing’s syndrome or Addison’s disease.
Normal urine levels are 20 to 90 mg/dl for a 24-hour
period.22
 ACTH levels are usually examined concomitantly
with cortisol levels, as ACTH secretion from the
pituitary gland is necessary for cortisol secretion
from the adrenal glands. Refer toTable 11-6 for details
on ACTH measurement.
ANDROGENS. Individual androgen levels can be
measured by RIA in the serum or by metabolic products
(17-ketosteroids) in the urine.1,6 High concentrations
of androgens may result in the following changes in
women:
 Hirsutism, which is excessive hair growth in skin
zones considered male in distribution (i.e., upper
lip, sideburns, chin, neck, chest, and lower abdomen)
 Amenorrhea, which is the absence of menstruation in
women older than 16 years of age or the absence
of menses for longer than 6 months in women
of childbearing age who previously had been
menstruating
 Voice change
 Increased muscle mass
MINERALOCORTICOIDS. Mineralocorticoids can be
evaluated by testing serum electrolyte levels or plasma
Endocrine System CHAPTER 11 387
renin activity and aldosterone levels.11 Abnormalities
of serum electrolyte levels, such as an increased potassi-
um level, provide a valuable screening tool for miner-
alocorticoid secretion disorders. Aldosterone is the
primary mineralocorticoid and is controlled by the
renin-angiotensin system. A rise in serum potassium
and angiotensin II results in aldosterone secretion,
which helps to balance fluid and electrolyte levels.
Blood samples of aldosterone are usually taken first in
the early morning, while the patient is still recumbent,
and then again after 4 hours of being awake and active.
Normal serum levels of aldosterone range from 2 to
50 ng/dl, depending on whether blood was taken in
the supine or upright position.4,5,11
CATECHOLAMINES. Epinephrine and norepineph-
rine are commonly referred to as catecholamines, and
their levels are generally measured through 24-hour
urine samples. Dopamine, also a catecholamine, is the
precursor for epinephrine and norepinephrine and
therefore can also be measured to reflect the amount
of catecholamines circulating in the body. However,
the preferred screening tool is to measure the amount
of catecholamine metabolites in the urine.The primary
catecholamine metabolite is called vanillylmandelic
acid (VMA). Normal values for these substances are
as follows:4,5
 Dopamine: 65 to 100 mg per 24 hours
 Epinephrine: 1.7 to 22.4 mg per 24 hours
 Norepinephrine: 12.1 to 85.5 mg per 24 hours
 Vanillylmandelic acid: 1.4 to 6.5 mg per 24 hours
METABOLIC TESTS
Metabolic tests are described in this section, as gluco-
corticoids (cortisol) affect carbohydrate, protein, and
fat metabolism.
GLUCOSE TOLERANCE TEST. A glucose tolerance test
was primarily used to diagnose diabetes mellitus;
however, because of many confounding variables, it is
currently not relied on to establish diabetes mellitus,
but rather to help confirm the diagnosis in certain
cases. However, the glucose tolerance test is the primary
method of establishing the diagnosis of gestational
diabetes mellitus.4,6
To perform the test, a 75-g or 100-g glucose load is
given to the subject in the morning after a 10-hour fast.
Blood glucose levels are then measured at variable time
periods, ranging from every half hour to every hour for
the next 2 to 5 hours after the glucose administration.
The subject must remain inactive and refrain from smok-
ing throughout the duration of the test. Normally, the
blood glucose levels should fall back to baseline values
388 CHAPTER 11 Endocrine System
after a 2-hour period. Normal glucose value for a fasting
blood sugar (BS) is approximately 70 to110 mg/dl.1,4,6
Adrenal Disorders
ADRENAL HYPERFUNCTION
Increased secretion of glucocorticoids (hypercortiso-
lism) results in Cushing’s syndrome, which is discussed
in detail earlier in the chapter.
ADRENAL INSUFFICIENCY
Autoimmune dysfunction can lead to destruction of the
adrenal cortex (i.e., primary adrenal insufficiency or
Addison’s disease). Additionally, ACTH deficiency
from the pituitary gland can lead to atrophy of the adre-
nal cortex (secondary adrenal insufficiency). The net
result is an impaired adrenal system with decreased
levels of glucocorticoids (cortisols), mineralocorticoids
(aldosterone), and androgens. Given the systemic func-
tions of these hormones, Addison’s disease can have
severe consequences if left untreated. Fortunately, the
incidence of Addison’s disease is rare.
Cortisol deficiency results in decreased gluconeo-
genesis (glucose production), which in turn alters
cellular metabolism. Decreased gluconeogenesis also
results in hypoglycemia and decreased ability to
respond to stress. Aldosterone deficiency causes fluid
and electrolyte imbalance, primarily as a result of
increased water excretion that leads to dehydration.23,24
Symptoms and physical findings common to adrenal
insufficiency include the following1,6,25:
 Weakness, fatigue
 Weight loss, nausea, vomiting, vague abdominal
pain
 Muscle and joint pain
 Salt craving in fewer than 20% of patients
 Hyperpigmentation
 Hypotension
Management of adrenal insufficiency typically
includes pharmacologic interventionwith anyof the fol-
lowing steroids: hydrocortisone (Cortisol, Compound
F), hydrocortisone acetate, prednisone (Deltasone), dex-
amethasone (Decadron, Dexasone), or fludrocortisone
(Florinef).17,20 Caution must be taken, however, with
corticosteroid administration, as corticosteroids can
suppress the release of endogenous cortisol from the
adrenal gland.26
PHEOCHROMOCYTOMA
Pheochromocytoma is a rare adrenomedullary disorder
caused by a tumor of the chromaffin cells in the adrenal
medulla, which results in excess secretion of the
catecholamines, epinephrine, and norepinephrine.The
occurrence is equal between men and women during
their twenties and thirties. Given the rare occurrence
of this tumor, it often goes undiagnosed. However,
proper diagnosis is essential, as the sustained release of
catecholamines can be life threatening. Early diagnosis
generally has favorable results.6,25,27
Signs and symptoms of pheochromocytoma include
the following1,23,25,27:
 Hypertension (sustained or paroxysmal),palpitations,
tachycardia, and orthostatic hypotension
 Headache, palpitations, and diaphoresis
 Excessive perspiration
 Nervousness and emotional outbursts or instability
 Elevated blood glucose levels and glucosuria
Management of pheochromocytoma generally
includes surgical excision of the tumor with preop-
erative pharmacologic management with one of the
following medications: alpha-adrenergic blocking
agents (e.g., phenoxybenzamine [Dibenzyline], phen-
tolamine [Regitine]), beta-adrenergic blocking agents
(e.g., propranolol [Inderal]), or tyrosine inhibitors
(alphamethlyparatyrosine).17,27,30
Pancreatic Disorders
INSULIN RESISTANCE SYNDROME
Insulin resistance is emerging as an important link to
the development of metabolic syndrome, Type 2 dia-
betes, cardiovascular disease, and possibly some can-
cers. Patients who are either overweight or obese are
more likely to develop insulin resistance over time;
however, it is not necessary. Patients who have insulin
resistance also present with compensatory hyperinsuli-
nemia, and hyperglycemia. Furthermore, insulin resis-
tance in the absence of metabolic syndrome criteria
(see the next section) has also been shown to be inde-
pendently related to developing cardiovascular disease.
Insulin resistance has been detected 10 to 20 years
prior to developing diabetes in individuals who are
offspring of patients withType 2 diabetes. More investi-
gation into this topic is occurring on many levels to
help identify a potential critical link to a variety of
chronic diseases.29,30,31
METABOLIC SYNDROME
Metabolic syndrome is defined as the cluster of clinical
manifestations that are present just before the onset of
Type 2 diabetes.32 Patients with metabolic syndrome
have a high likelihood of having concurrent insulin

resistance. However, the difference between metabolic
syndrome and insulin resistance syndrome is that
metabolic syndrome focuses on establishing a diag-
nosis for patients who are at higher risk for Type 2
diabetes and cardiovascular disease and prescribing
timely intervention to offset the development of these
diseases and their complications. Currently, there is
no defined diagnostic criteria for insulin resistance
syndrome.29,33
The diagnosis of metabolic syndrome is established
when patients have at least 3 of the following criteria:
 Fasting glucose (mg/dl) > 110 (men and women)
 Blood pressure (mmHg) > 135/85 (men and women)
 Plasma triglycerides (mg/dl) > 150 (men and women)
 HDL cholesterol (mg/dl) < 45 (men), < 50 (women)
 Waist circumference (cm) > 102 (men), > 88 (women)
The cornerstone of management of this syndrome is
weight loss with a modest reduction in initial weight
of 7% to 10% demonstrating significant reduction in
the development of diabetes and cardiovascular dis-
ease.32 In addition to this therapeutic lifestyle change,
participation in an exercise program has been shown
to either delay or prevent the development of Type 2
diabetes as well as improve the cardiovascular risk
profile of patients by increasing HDL levels and
lowering blood pressure.33
CLINICAL TIP
 In the acute care setting, physical therapists
unfortunately will not have a significant role in
exercise prescription to create the long term changes
necessary to modify metabolic syndrome. However,
if therapists are working with patients who have
metabolic syndrome, then physical therapists should
ensure that patients can either continue with a
current exercise program or strongly recommend
follow-up services for the patients to begin an
exercise program.
DIABETES MELLITUS
Diabetes mellitus is a syndrome with metabolic, vascu-
lar, and neural components that originates from
glucose intolerance that in turn leads to hyperglycemic
states (increased plasma glucose levels). Hyperglycemia
can result from insufficient insulin production,
ineffective receptive cells for insulin, or both. Insulin
promotes storage of glucose as glycogen in muscle
tissue and the liver. Deficiency of insulin leads to
increased levels of plasma glucose.1,6,36
Endocrine System CHAPTER 11 389
The diagnosis of diabetes is based on the presence of
any one of the following three factors:6,35
1. Presence of polyuria, polydipsia, weight loss,
blurred vision, and random plasma glucose (regard-
less of last meal)  200 mg/dl
2. Fasting plasma glucose  126 mg/dl (no caloric
intake for at least 8 hours)
3. Two-hour postload glucose  200 mg/dl, using a
75-g oral glucose load dissolved in water
The diagnosis is confirmed when one of the above
factors is also found on a subsequent day.6,35
The two primary types of diabetes mellitus are type1
(insulin-dependent or juvenile-onset diabetes) and
type 2 (non—insulin-dependent or adult-onset dia-
betes). After much debate on the classification of
diabetes, the current terminology for diabetes uses
type 1 and type 2 diabetes to distinguish between the
two primary types.35,36 Other forms of glucose intoler-
ance disorders exist but are not discussed in this book.
TYPE 1 DIABETES. Type 1 diabetes is an autoim-
mune disorder with a genetic-environmental etiol-
ogy that leads to the selective destruction of beta
cells in the pancreas. This destruction results in
decreased or absent insulin secretion. Type 1 diabetes
represents 5% to 10% of the population with diabe-
tes and generally occurs in individuals under the age
of 40 years.34-38 Other etiologies for type 1 diabetes
exist but are not discussed in this book.
Classic signs and symptoms of type 1 diabetes are
described in the previous section with the diagnostic
criteria for diabetes.6,34
Management of type 1 diabetes may include the
following37-39:
 Close self- or medical monitoring of blood glucose
levels (Table 11-8).
 Insulin administration through oral medications,
intramuscular injection, or continuous subcutaneous
insulin infusion (CSII) pump. CSII therapy has
been shown to be as effective as multiple daily injec-
tions of insulin, while also providing the ability to
mimic a more natural glycemic response in fasting
and postprandial states (Table 11-9).
A medication summary is provided in Appendix IV,
Table IV-37.
 Diet modification based on caloric content, propor-
tion of basic nutrients and optimal sources, and
distribution of nutrients in daily meals.
 Meal planning.
 Exercise on a regular basis.
Research directed at curing type 1 diabetes is
aimed at specifically identifying the causative genes,
390 CHAPTER 11 Endocrine System

Table 11-8 TESTS TO MONITOR CONTROL OF DIABETES

Test Description
Self-monitoring
Blood glucose finger stick Monitors immediate control of diabetes.Very effective in establishing the correct
samples insulin dosages and preventing complications from diabetes.
Reference, 60-110 mg/dl Capillary blood is obtained by a needle stick of a finger or an earlobe and placed
on a reagent strip.The reagent strip is compared to a color chart or placed in a
portable electronic meter to read the glucose level.
Patients in the hospital can also have blood drawn from an indwelling arterial line,
for ease of use, without compromising accuracy of measurement.
Urine testing A reagent strip is dipped in the patient’s urine, and the strip is compared to a
color chart to measure glucose levels in the urine.
Provides satisfactory results only for patients who have stable diabetes; otherwise,
results can be insensitive for truly delineating hyperglycemia.
Medical monitoring
Glycosylated hemoglobin (GHB) Hyperglycemia results in saturation of hemoglobin molecules during the lifespan
of a red blood cell (approximately 120 days).
Reference, 7.5% to 11.4% of total Measuring the amount of GHB in the blood provides a weighted average of the
hemoglobin for a patient with glucose level over a period of time and is a good indicator of long-term control
controlled diabetes of diabetes, without confounding factors such as a recent meal or insulin
injection.
Measurements are performed every 3 to 6 months.
Fructosamine or glycated protein Similar to GHB test, hyperglycemia saturates serum proteins, particularly
albumin.
Reference, 300 mmol/liter The life span of albumin is approximately 40 days; therefore, this test is
= excellent diabetic control performed every 3 weeks to monitor short-term control of diabetes.
Data from CorbettJV (ed). LaboratoryTests and Diagnostic Procedures with Nursing Diagnoses (5th ed). Upper Saddle River, NJ: Prentice
Hall Health, 2000;192-197; Malarkey LM, McMorrow ME (eds). Nurse’s Manual of LaboratoryTests and Diagnostic Procedures. Philadelphia:
Saunders, 2000;577-580; Sacher RA, McPherson RA, CamposJM (eds).Widman’s Clinical Interpretation of LaboratoryTests (11th ed).
Philadelphia: FA Davis, 2000;817-818.

permanent replacement of lost beta-cell function
(which could involve islet cell transplantation), regener-
ation of beta cells, or development of an immortalized
insulin-secreting cell line.36
CLINICAL TIP
 Hypoglycemia may occur during exercise or up
to 24 hours after exercise because of an
inability to regulate insulin levels. To help
prevent this, the patient should consume extra
carbohydrates before and during exercise
(e.g., 10 g of carbohydrates per 30 minutes of
activity), and the nurse or patient may also
decrease the dose or rate of insulin infusion,
especially with CSII.
 The physical therapist should be aware of
catheter placement on the patient for CSII therapy
so the catheter will not be disrupted during
intervention.
 Circulation of insulin that is injected into an
exercising limb is enhanced as a result of
increased blood flow and temperature. The injection
into the exercising limb may, therefore, lead to
hypoglycemia. Insulin can be injected into the
abdomen to help prevent this process.
 Insulin is necessary to modulate lipolysis and
hepatic (liver) glucose production during
exercise. Performing exercise without
adequate insulin can lead to hyperglycemia
and ketogenesis.
 Endocrine System CHAPTER 11 391

Table 11-9 SUMMARY OF INSULIN PUMP THERAPY

Patient candidacy Demonstrated ability to self-monitor glucose and adjust insulin doses based on preprandial
blood glucose levels and anticipated future activity level.
Motivated to achieve and maintain improved glycemic control using intensive insulin therapy.
Pregnant patients with type 1 diabetes.
Patients unaware of hypoglycemic episodes with insulin therapy.
Patients who experience wide glycemic variations on a day-to-day basis.
Patients with a significant rise in hyperglycemia in the morning (‘‘dawn phenomenon’’).
Patients who need flexibility in their insulin regimen (e.g., erratic work schedules, travel
frequently).
Adolescents who experience frequent diabetic ketoacidosis.
Night-time use for children under 10 years of age who may not be able to adjust their own
insulin requirements.
Pump description Approximately the size of an electronic pager, weighing only 4 oz.
Patients are instructed on how to insert and change (every 2 to 3 days) infusion catheters into
the subcutaneous space of their abdomen.
The catheter can be detached from the insulin pump for bathing or intimate contact.
Two settings: basal rate and bolus doses, both adjustable by the patient depending on needs
(e.g., preprandial bolus or decreased basal rate with exercise).
Battery life is approximately 6 weeks.
Types of insulin Regular human buffered insulin (short acting).
Insulin analog (rapid acting).
Pump complications Hyperglycemia and diabetic ketoacidosis.
Hypoglycemia and hypoglycemic unawareness.
Skin infections.
Weight gain.
Data from UngerJ. A primary care approach to continuous subcutaneous insulin infusion. Clin Diabetes 1999;17(3):113; Continuous
subcutaneous insulin. Diabetes Care 2001;24(1):S98; Kaufman FR, Halvorson M, Kim C, et al. Use of insulin pump therapy at nighttime only
for children 7-10 years of age with type 1 diabetes. Diabetes Care 2000;123(5):579.

 The physical therapist should inquire about the

patient’s blood glucose levels before and after
exercise to assist in physical therapy planning.
 Coordinating physical therapy sessions with meals
and insulin injections may help optimize exercise
tolerance.
 Keeping graham crackers close by when working
with diabetic individuals is helpful in case
hypoglycemia does occur with activity.
TYPE 2 DIABETES. Type 2 diabetes is more common
in the United States than type 1 diabetes and generally
occurs after 40 years of age. Type 2 diabetes is
significantly linked to obesity, a sedentary lifestyle,
and aging. Genetic predisposition has also been
established.35,36,38
The mechanism of type 2 diabetes involves increasing
cellular resistance to insulin, which results in a
compensatory hypersecretion of insulin from the pan-
creaticbeta cellsthat ultimatelyleads to a failure in insulin
production.34-38 Other etiologies for type 2 diabetes
exist but are not discussed in this text.
Signs and symptoms of type 2 diabetes may be simi-
lar to those of type 1 diabetes but can also include the
following:
 Recurrent infections and prolonged wound healing
 Genital pruritus
 Visual changes
 Paresthesias
Management of type 2 diabetes is similar to that of
type 1 diabetes, with an emphasis on medical nutrition-
al therapy and exercise to control hyperglycemia. Oral
hypoglycemic agents and actual insulin administration
may also be used.37,39-41 CSII has been shown to be as
effective as multiple dose injections of insulin in
patients with type 2 diabetes.42 Clinical studies are also
392 CHAPTER 11 Endocrine System
investigating the use of inhaled insulin for these
patients, with preliminary results demonstrating
promising results.43,44
Appendix IV provides a summary of medications
used to manageType 2 Diabetes (Table IV-37)
Research direction for type 2 diabetes includes
identifying the gene(s) responsible for the predispo-
sition to type 2 diabetes and the mechanisms by which
environmental factors trigger this predisposition.
Also, identification of the cellular defects responsible
for insulin resistance and impaired insulin secretion in
type 2 diabetes will, it is hoped, lead to the development
of new medications that will be specific and relatively
free of unwanted adverse effects.36
CLINICAL TIP
 Glycemic control for patients with type 1 or
type 2 diabetes may be altered significantly with
the onset of new illnesses, such as systemic
infection, because these new processes require
added glucose metabolism. It is important for the
therapist to carefully monitor the patient’s blood
glucose levels during therapeutic interventions,
because the symptoms of diabetes may be
exacerbated in a patient with significant
comorbidities.
 Blood glucose levels are denoted in the medical
record as BS levels.
 Patients with diabetes present with a wide range
of their individual ‘‘normal’’ values. Therefore,
establishing the tolerable high or low value for each
patient during the initial evaluation is very
important in determining the parameters for
physical therapy intervention.
 Patients with poor glycemic control can have wide
fluctuations in the BS levels on a daily basis.
Therefore, be sure to always verify their BS level
before physical therapy intervention.
 Consult with the nurse or physician regarding
whether therapy should be deferred for patients
who were recently placed on intravenous insulin
to stabilize their glucose levels.
 Patients who were following a regular exercise
program for glycemic control before hospital
admission will require education about how
to modify their exercise parameters during the
hospitalization and on discharge. Modification
of exercise parameters will be dependent on the
nature of concurrent illnesses.
COMPLICATIONS OF DIABETES MELLITUS. Patients
with diabetes mellitus, despite management, can still
develop organ and organ system damage linked to
lesions of the small and large blood vessels. Complica-
tions can manifest 2 to 15 years after diagnosis. They
can be classified as (1) microangiopathy (microvascular
disease), which causes retinopathy (occurs in 60% to
80% of patients), nephropathy, and foot ischemia;
(2) macroangiopathy (macrovascular disease), which
accelerates widespread atherosclerosis; or (3) neuropa-
thy.31,37 Another complication from diabetes that is
not directly linked to vascular damage is diabetic
ketoacidosis (DKA).
Diabetic Ketoacidosis. Patients with Type 1 diabetes
have the potential to develop this complication as
a result of unusual metabolic stress (e.g., changes in
diet, infection) and can progress from mild to moderate
glucose intolerance, to fasting hyperglycemia, to keto-
sis, and, finally, to ketoacidosis. Most patients do not
progress to the ketotic state but have the potential to
do so if proper treatment is not administered.13
Patients who progress to DKA usually present with
a plasma glucose level between 500 and 700 mg/dl.31
DKA is the end result of ineffective levels of
circulating insulin, which lead to elevated levels of
ketone bodies in the tissues. This state of an elevated
level of ketone bodies is referred to as ketosis.
Decreased insulin levels lead to uncontrolled lipoly-
sis (fat breakdown), which increases the levels of
free fatty acids released from the liver and ultimately
leads to an overproduction of ketone bodies. Ketone
bodies are acids, and if they are not buffered properly
by bases, a state of ketoacidosis occurs. Ketoacidosis
almost always results from uncontrolled diabetes
mellitus; however, it may also result from alcohol
abuse.6,13,38
Signs and symptoms of DKA include the
following13:
 Polyuria, polydipsia, dehydration
 Weakness and lethargy
 Myalgia, hypotonia
 Headache
 Anorexia
 Nausea, vomiting, abdominal pain, acute abdomen
 Dyspnea, deep and sighing respirations (Kussmaul’s
respiration)
 Acetone-smelling (‘‘fruity’’) breath
 Hypothermia
 Stupor (coma), fixed, dilated pupils
 Uncoordinated movements
 Hyporeflexia

Management of DKA may include the following:
insulin administration, hydration, electrolyte (sodium,
potassium, and phosphorus) replacement, supplemen-
tal oxygen, and mechanical ventilation.6,34,38
Diabetic Dermopathy. Skin lesions in patients with
diabetes, particularly on their feet, are common and
multifactorial in nature. Lesions may result from any
combination of the following14,37,45:
 Loss of sensation from sensory neuropathy
 Skin atrophy from microangiopathy
 Decreased blood flow from macroangiopathy
 Sensory and autonomic neuropathy, resulting in
abnormal blood distribution that may cause bone
demineralization and Charcot’s joint (disruption of
the midfoot)46
Proper foot care in diabetic individuals helps pre-
vent complications, such as poor wound healing,
which can progress to tissue necrosis and ultimately
lead to amputation.45 Box 11-1 describes patient infor-
mation regarding foot care for patients with diabetes.
Refer to Chapter 7 for more details on diabetic ulcers.
BOX 11-1 FOOT CARE FOR PATIENTS WITH DIABETES
Don’t
Smoke
Wash feet in cold or hot water.The water
temperature should be lukewarm
(approximately 858 to 958F).
Use a heating pad, heating lamp, or hot
water bottles to warm the feet.
Use razor blades or scissors to cut corns
or calluses. Have a podiatrist perform
this procedure.
Use over-the-counter medications on corns
or calluses.
Cross legs when sitting.
Wear girdles or garters.
Walk barefoot.
Wear shoes without socks or stockings.
Wear sandals with thongs between the toes.
Wear socks or stocking with raised seams.
Place hands in shoes for inspection, if sensory
neuropathy is present in the hands. Instead
shake out the shoes for any objects.
Data from Burch WM (ed). Endocrinology for the House Officer (2nd ed). Baltimore: Williams & Wilkins, 1988;59; MayfieldJA,
Reiber GE, Sanders LJ. Preventive Foot Care in People with Diabetes. Diabetes Care 2001;24(1):S56.
Endocrine System CHAPTER 11 393
Infection. Individuals with diabetes are at a higher
risk for infection because of (1) decreased sensation
(vision and touch); (2) poor blood supply, which leads
to tissue hypoxia; (3) hyperglycemic states, which pro-
mote rapid proliferation of pathogens that enter the
body; (4) decreased immune response from reduced
circulation, which leaves white blood cells unable to
get to the affected area; (5) impaired white blood cell
function, which leads to abnormal phagocytosis; and
(6) chemotaxis.34,47
Diabetic Neuropathy. The exact link between neural
dysfunction and diabetes is unknown; however, the
vascular, metabolic, and immunologic changes that
occur with diabetes can promote destruction of
myelin sheaths and therefore interfere with normal
nerve conduction.48
Neuropathies can be manifested as (1) focal mono-
neuropathy and radiculopathy (disorder of single
nerve or nerve root); (2) symmetric sensorimotor neu-
ropathy, associated with disabling pain and depression;
or (3) autonomic neuropathy.
Do
Encourage the patient to have regular medical
or podiatric examinations to determine integrity
of his or her feet.
Inspect feet daily for abrasions, blisters, and cuts.
Use a mirror if soles cannot be seen. If vision
is poor, another person should check feet.
Wash feet daily with lukewarm water and soap.
Dry feet carefully, especially between the toes.
Apply hand cream or lanolin to feet (dry areas).
Be careful not to leave cream between the toes.
Wear clean socks or stockings daily.
Cut nails straight across and file down edges with
an emery board.
Wear comfortable shoes that fit and don’t rub.
Wear wide toe-box or custom-made shoes if foot
deformities exist.
Inspect the inside of shoes for any objects, tacks,
or torn linings before putting on the shoes.
394 CHAPTER 11 Endocrine System

The most common diabetic neuropathy is peripheral
symmetric polyneuropathy. Sensory deficits are greater
than motor deficits and occur in a glove-and-stocking
pattern, resulting in a loss of pinprick and light-touch sen-
sations in these areas. However, patients will commonly
present with a mixture of these three primary types of
neuropathies. Foot ulcers and footdrop are common
manifestations of diabetic neuropathies.11,34,37,38,48
Table 11-10 outlines the signs and symptoms of the
different types of diabetic neuropathy.
Management of diabetic neuropathy may include
the following48:
 Strict glycemic control (primary method)
 Pain relief with:
 Tricyclic antidepressants, such as amitriptyline,
nortriptyline, and desipramine
 Anticonvulsants, such as carbamazepine, pheny-
toin, gabapentin, and clonazepam
 Topical agents, such as capsaicin cream (0.025% to
0.075%) or lidocaine ointment
 Opioids (used as a last resort)
 Transcutaneous electrical nerve stimulation
 Aldose reductase inhibitors aimed at slowing the
progression of nerve damage
 Exogenous nerve growth factors
 Immunotherapy
 Pancreatic transplant
Additional complications from diabetes include
coronary artery disease, stroke, peripheral vascular
disease, and nephropathy. These are described in other
chapters as listed below.
Coronary Artery Disease. See Acute Coronary Syn-
drome in Chapter 1 for a discussion of coronary artery
disease.
Stroke. See the Cerebrovascular Accident section in
Chapter 4 for a discussion of stroke.

Table 11-10 SIGNS AND SYMPTOMS OF DIABETIC NEUROPATHY

Classification of Diabetic
Neuropathy Symptoms Signs
Symmetric Polyneuropathies
Peripheral sensory Paresthesias, numbness, coldness, tingling Absent ankle jerk
polyneuropathy pins and needles (mainly in feet) Impairment of vibration sense in feet
Pain, often disabling, worse at night Foot ulcers (often over metatarsal heads)
Peripheral motor Weakness Bilateral interosseous muscle atrophy,
neuropathy claw or hammer toes, decreased grip
strength, decreased manual muscle test
grades
Autonomic neuropathy Constipation or diarrhea, nausea or Incontinence, orthostatic hypotension,
vomiting, tremulousness, impotence, tachycardia, peripheral edema,
dysphagia gustatory sweating
Focal and Multifocal Neuropathies
Cranial neuropathy Pain behind or above the eye, headaches, Palpebral ptosis
facial or forehead pain Inward deviation of one eye
Trunk and limb Abrupt onset of cramping or lancinating Peripheral nerve-specific motor loss
mononeuropathy pain Abdominal wall weakness
Constricting band-like pain in trunk or
abdomen
Cutaneous hyperesthesia of the trunk
Proximal motor neuropathy Pain in lower back, hips, and thighs that Asymmetric proximal weakness
or diabetic amyotrophy is worse at night; loss of appetite, Atrophy in lower limbs
depression Absent or diminished knee jerk
Data from BoissonaultJS, Madlon-Kay D. Screening for Endocrine System Disease. In WG Boissonault (ed), Examination in Physical
Therapy: Screening for Medical Disease. NewYork: Churchill Livingstone, 1991;159; Melvin-Sater PA. Diabetic Neuropathy. Physician
Assistant 2000;24(7):63; Saudek CD. Diabetes Mellitus. InJD Stobo, DB Hellmann, PW Ladenson, et al. (eds),The Principles and Practice
of Medicine (23rd ed). Stamford CT: Appleton & Lange, 1996;330.

Peripheral Vascular Disease. See the Atherosclerosis
section in Chapter 6 for a discussion of peripheral
vascular disease.
Nephropathy. See the Immunoglobulin A
Nephropathy (Berger’s Disease) and Diabetic Neph-
ropathy sections in Chapter 9 for a discussion
on nephropathy.
HYPOGLYCEMIA (HYPERINSULINISM)
Hypoglycemia is a state of decreased BS levels
(< 50 mg/dl serum glucose). Excess serum insulin
results in decreased BS levels, which leads to symptoms
of hypoglycemia. Causes for this imbalance of insulin
and sugar levels can be grouped as (1) fasting, (2) post-
prandial, or (3) induced.
Fasting hypoglycemia occurs before eating and can
be caused by insulin-producing beta-cell tumors
(insulinomas), liver failure, chronic alcohol ingestion,
GH deficiency, extrapancreatic neoplasm, or leucine.
It can also occur in infants with mothers who have
diabetes.31
Postprandial hypoglycemia occurs after eating and
can be caused by reactive hypoglycemia (inappropriate
insulin release after a meal), early diabetes mellitus, or
rapid gastric emptying.
Hypoglycemia can also be induced by external
causes, such as exogenous insulin or oral hypoglycemic
overdose.6,17
Signs and symptoms of hypoglycemia may include:
 Tachycardia and hypertension
 Tremor, irritability, and sweating
 Hunger
 Weight changes
 Headache
 Mental dullness, confusion, and amnesia
 Seizures
 Paralysis and paresthesias
 Dizziness
 Visual disturbance
 Loss of consciousness
Management of hypoglycemia may include the
following: glucose administration (fruit juice or
honey); strict monitoring of insulin and oral hypogly-
cemic administration; dietary modifications; phar-
macologic agents, such as glucagon, which is the first
agent used in emergency cases of hypoglycemia;
diazoxide (Hyperstat) or streptozocin (Zanosar); sur-
gery (e.g., subtotal pancreatectomy, insulinoma resec-
tion); or a combination of these.17,49
Endocrine System CHAPTER 11 395
PARATHYROID GLAND
Function
Parathyroid hormone (PTH) is the primary hormone
secreted from the parathyroid gland. The target sites
are the kidneys, small intestine, and bone.The primary
function of PTH is to raise blood calcium levels by
mobilizing calcium that is stored in bone, increasing
calcium reabsorption from the kidneys, and increasing
calcium absorption from the small intestine.6,50
Parathyroid Tests
The primary measurements of parathryoid hormone
are summarized in Table 11-11. However, because PTH
exerts its effects on the intestines and kidneys, calcium
metabolism can also be evaluated by testing gastroin-
testinal and renal function. Refer to Chapters 8 and
9, respectively, for a summary of diagnostic tests for
the gastrointestinal and renal systems.
Table 11-11 PRIMARY TESTS USED TO
EVALUATE PARATHYROID
(PTH) FUNCTION
Test Description
Serum calcium Measurement of blood calcium levels
indirectly examines parathyroid
function. Normally, low calcium
levels stimulate parathyroid
hormone secretion, whereas high
calcium levels could be reflective
of high PTH levels.
Reference value for serum calcium
is 8.5 to 11.0 mg/dl in adults.
Calcium levels can also be measured
in the urine.
Reference value for urinary calcium
is 50 to 300 mg/dl.
Parathyroid Radioimmunoassays and urinalysis
hormone are used to measure parathyroid
hormone levels. Reference value
is 10 to 60 pg/ml.
Data from BurchWM (ed). Endocrinology for the House Officer
(2nd ed). Baltimore: Williams & Wilkins, 1988; JV Corbett (ed).
Laboratory Tests and Diagnostic Procedures with Nursing
Diagnoses (5th ed). Upper Saddle River, NJ: Prentice Hall Health,
2000;167-176; and Sacher RA, McPherson RA, CamposJM (eds).
Widman’s Clinical Interpretation of LaboratoryTests (11th ed).
Philadelphia: FA Davis, 2000;803-804.
396 CHAPTER 11 Endocrine System
Parathyroid Disorders
HYPERPARATHYROIDISM
Hyperparathyroidism is a disorder caused by overac-
tivity of one or more of the parathyroid glands that
leads to increased PTH levels, resulting in increased
blood calcium level, decreased bone mineralization,
and decreased kidney function. This disorder occurs
more frequently in women than in men. Radiation
therapy is also a risk factor for developing this
disorder.51
Hyperparathyroidism can be classified as primary,
secondary, or tertiary. Primary hyperparathyroidism
represents the most cases and usually results from
hyperplasia or an adenoma in the parathyroid
gland(s). Secondary hyperparathyroidism results from
another organ system disorder, such as renal failure,
osteogenesis imperfecta, Paget’s disease, multiple
myeloma, lymphoma, or bone metastases from pri-
mary breast, lung, or kidney tumors. Tertiary hyper-
parathyroidism occurs when PTH secretion is
autonomous despite normal or low serum calcium
levels.6,23,52
The primary clinical manifestations of hyper-
parathyroidism are hypercalcemia and hypercalciuria
(calcium in urine). Hypercalcemia may then result in
the following cascade of signs and symptoms:23,51,52
 Bone demineralization and resorption (which causes
skeletal changes, such as dorsal kyphosis)
 Backache, joint and bone pain, and pathologic
fractures
 Kidney stone formation, abdominal pain, and peptic
ulcer disease
 Nausea, thirst, anorexia, and constipation
 Hypertension and dysrhythmias
 Listlessness, seizure, depression, and paranoia
 Decreased neuromuscular excitability
Management of hyperparathyroidism may include
the following17 23,52:
 Parathyroidectomy (partial or total) is the preferred
treatment for patients with moderate to severe
hypercalcemia.51- 53 The use of intraoperative, rapid
PTH assay has been shown to be effective in fully
delineating the areas requiring resection, making
for a safer and more specific operative procedure.53
 Pharmacologic intervention is summarized in
Appendix IV,Table IV-38.
 Fluid replacement
 Dietary modification (a diet low in calcium and high
in vitamin D)
HYPOPARATHYROIDISM
Hypoparathyroidism is a disorder caused by underac-
tivity of one or more of the parathyroid glands that
leads to decreased PTH levels. Decreased levels of
PTH occur most commonly as a result of damage to
the parathyroid glands during thyroid or parathyroid
surgery. Less common causes may include radiation-
induced damage, infiltration by metastatic cells, and
autoimmune dysfunction.23, 52
Signs and symptoms of hypoparathyroidism include
the following23:
 Hypocalcemia
 Increased neuromuscular irritability (tetany); painful
muscle spasms
 Tingling of the fingers
 Laryngospasm
 Dysrhythmias
 Lethargy, personality changes
 Thin, patchy hair; brittle nails; dry, scaly skin
 Convulsions
 Cataracts
Management of hypoparathyroidism may include
the following17,23,52:
 Dietary modifications that promote a diet high in
calcium and low in phosphate
 Pharmacologic intervention with the following:
 PTH
 Vitamin D supplements: dihydrotachysterol (Hyta-
kerol), dihydroxycholecalciferol, or ergocalciferol
(Calciferol) (vitamin D2)
 Nutritional supplements: calcium gluconate, cal-
ciumglubionate,calcium lactate,orcalciumchloride
METABOLIC BONE DISORDERS
Osteoporosis
Osteoporosis is a multifactorial skeletal disorder that
leads to decreased bone density and organization, which
ultimately reduces bone strength.54 Bone strength is
often measured by bone mineral density studies, which
are used in the diagnosis of osteoporosis, as well as
monitoring tools for therapeutic improvements. Dual
Energy X-ray Absortiometry (DEXA) measurement
is currently the gold standard for determining bone
mineral density, which are reported as T- and Z-scores.
Investigations are ongoing regarding the use of bio-
chemical markers in blood and urine to help detect bone
loss and possibly to predict risk of fracture in patients.55

Osteoporosis can be classified as primary or sec-
ondary. Primary osteoporosis can occur in both
genders at all ages, but often follows menopause in
women and occurs later in life in men. Secondary
osteoporosis is a result of medications (e.g., glucocorti-
coids or anticonvulsants), alcoholism, other conditions
(e.g., hypogonadism or hypoestrogenism), or diseases
(e.g., hyperthyroidism).54
There is no clear etiology for osteoporosis. However,
many risk factors for women have been elucidated.
These risk factors include Caucasian or Asian race,
petite frame, inadequate dietary intake of calcium,
positive family history of osteoporosis, alcohol abuse,
cigarette smoking, high caffeine intake, sedentary
lifestyle, reduced bone mineral content (most predictive
factor), and early menopause or oophorectomy (ovary
removal).1,52,54
Signs and symptoms of osteoporosis may include the
following1,52:
 Back pain (aggravated by movement or weight
bearing, relieved by rest)
 Vertebral deformity (kyphosis and anterior wedging)
 Presence of vertebral compression fractures, Colles’
fracture, hip and pelvic fractures
Pulmonary embolism and pneumonia are complica-
tions that can occur secondary to these fractures.56
Management of osteoporosis may include the
following3,54,57,58:
 Daily supplementation with calcium and vitamin D
for all women with low bone mineral density
 Hormone replacement therapy with estrogen or
estrogen combined with progesterone (considered
only for women with significant osteoporosis risk)
 Selective Estrogen Receptor Modulation (SERM)
therapy with raloxifene
 Bisphosphonate supplementation (inhibits bone
resorption) with alendronate, ibandronate, and
risedronate
 Calcitonin supplementation (increases total body
calcium)
 Administration of PTH (teriparatide) in patients who
cannot tolerate estrogen therapy56
 Physical therapy for exercise prescription
 Fracture management (if indicated; refer to the
Fracture Management section in Chapter 3)
CLINICAL TIP
 Always consult with the physician to determine if
there are any weight-bearing precautions in patients
with osteoporosis.
Endocrine System CHAPTER 11 397
 An abdominal corset can provide additional support
for stable vertebral compression fracture(s).
 Also, using a rolling walker that is adjusted higher
than normal can promote a more upright posture.
Both of these techniques may also help to decrease
back pain in patients with osteoporosis.
 Gentle exercises to improve the strength of thoracic
extensors can also assist with posture and reduce
back pain.
 Caution with resistive exercises and manual contacts
should be taken during therapeutic activities to
avoid risk of microtrauma or fracture to osteoporotic
bones.
Osteomalacia
Osteomalacia, or rickets in children, is a disorder char-
acterized by decreased bone mineralization, reduced
calcium absorption from the gut, and compensatory
hyperparathyroidism. The etiology of osteomalacia
stems from any disorder that lowers serum levels of
phosphate, calcium, or vitamin D.11,52
Signs and symptoms of osteomalacia include the
following11,52:
 Bone pain and tenderness
 Softening of cranial vault (in children)
 Swelling of costochondral joints (in children)
 Predisposition to femoral neck fractures (in adults)
 Proximal myopathy
 Waddling gait
Medical management of osteomalacia may include
treating the underlying or predisposing condition or
supplementation with calcium and vitamin D.11,59
Paget’s Disease
Paget’s disease is a bone disease of unknown etiology
that usually presents after the age of 55 years. The
primary feature is thick, spongy bone that is unor-
ganized and brittle as a result of excessive osteoclastic
and subsequent osteoblastic activity. Some evidence
points to an inflammatory or viral origin. The axial
skeleton and femur are involved in 80% of the cases
with the tibia, ilium, skull, and humerus having less
involvement.56 Fractures and compression of the
cranial nerves (especially the eighth nerve) and
spinal cord are complications of Paget’s disease.52,60
Paget’s disease is generally asymptomatic; however,
the following clinical manifestations may present:52,60
 Bone pain that is unrelieved by rest and persists
at night
398 CHAPTER 11 Endocrine System
 Bone deformity (e.g., skull enlargement, bowing of
leg and thigh)
 Increased warmth of overlying skin of affected areas
 Headaches or hearing loss
Management of Paget’s disease primarily includes
bisphosphonate and calcitonin administration.
Bisphonates include etidronate, alendronate, risedro-
nate, pamidronate, and ibandronate.60,61
Other interventions may include the following52,60:
 Calcium supplementation (if necessary)
 Promotion of mobility
 Adequate hydration
 Symptomatic relief with nonsteroidal antiinflamma-
tory agents or acetaminophen
MANAGEMENT
Clinical management of endocrine dysfunction is
discussed earlier in specific endocrine gland and meta-
bolic disorders sections. This section focuses on goals
and guidelines for physical therapy intervention.
The following are general physical therapy goals and
guidelines for working with patients who have
endocrine or metabolic dysfunction. These guidelines
should be adapted to a patient’s specific needs.
Clinical tips are provided earlier to address specific
situations in which the tips may be most helpful.
Goals
The primary physical therapy goals in this patient
population are the following: (1) to optimize functional
References
1. BurchWM (ed). Endocrinology for the House Officer
(2nd ed). Baltimore: Williams & Wilkins, 1988.
2. Bullock BL (ed), Pathophysiology: Adaptations and
Alterations in Function (4th ed). Philadelphia:
Lippincott, 1996.
3. Diagnostic Procedures. In JM Thompson, GK
McFarland, JE Hirsch, et al. (eds), Mosby’s Manual
of Clinical Nursing Practice (2nd ed). St. Louis: Mosby,
1989;1594.
4. CorbettJV. LaboratoryTests and Diagnostic Procedures
with Nursing Diagnoses (5th ed). Upper Saddle River,
NJ: Prentice Hall Health, 2000.
5. Malarkey LM, McMorrow ME (eds). Nurse’s Manual
of LaboratoryTests and Diagnostic Procedures.
Philadelphia: Saunders, 2000;604-612.
mobility, (2) to maximize activity tolerance and endur-
ance, (3) to prevent skin breakdown in the patient
with altered sensation (e.g., diabetic neuropathy), (4) to
decrease pain (e.g., in patients with osteoporosis or
hyperparathyroidism), and (5) to maximize safety for
prevention of falls, especially in patients with altered
sensation or muscle function.
Guidelines
Patients with diabetes or osteoporosis represent the pri-
mary patient population with which the physical thera-
pist intervenes. Physical therapy considerations for
these patients are discussed in the form of clinical tips
in earlier sections (Diabetes Mellitus and Osteoporosis
sections, respectively).
For other patients with endocrine or metabolic
dysfunction, the primary physical therapy treatment
guidelines are the following:
1. To improve activity tolerance, it may be necessary to
decrease exercise intensity when the patient’s medica-
tion regimen is being adjusted. For example, a patient
with insufficient thyroid hormone replacement will
fatigue more quickly thanwill a patient with adequate
thyroid hormone replacement. In this example,
knowing the normal values of thyroid hormone and
reviewing the laboratory tests helps the therapist
gauge the appropriate treatment intensity.
2. Consult with the clinical nutritionist to help deter-
mine the appropriate activity level based on the
patient’s caloric intake, because caloric intake and
metabolic processes are affected by endocrine and
metabolic disorders.
6. Sacher RA, McPherson RA, CamposJM (eds),Widman’s
Clinical Interpretation of LaboratoryTests (11th ed).
Philadelphia: FA Davis, 2000;741-823.
7. ChenJL, Chiu HW,Tseng YJ, et al. Hyperthyroidism
is Characterized by Both Increased Sympathetic and
Decreased Vagal Modulation of Heart Rate: Evidence
from Spectral Analysis of Heart RateVariability.
Clin Endocrinol 2006;64(6):611-616.
8. Lavin N (ed), Manual of Endocrinology and
Metabolism (2nd ed). Boston: Little, Brown, 1994.
9. Elliot B. Diagnosing and Treating Hypothyroidism.
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18. Beers MH, Berkow R (eds), Merck Manual of
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 12 Organ Transplantation

Jennifer Lee Hunt INTRODUCTION

Leah Moinzadeh With advances in technology and immunology, organ and tissue transplan-
tation is becoming more common. There were 28,931 organ transplants
performed in the United States in 2006.1 As increasing numbers of hospi-
tals perform transplantations, physical therapists are involved more fre-
quently in the rehabilitation process for pretransplant and posttransplant
recipients.2 Owing to limited organ donor availability, physical therapists
often treat more potential recipients than posttransplant recipients.
Patients awaiting transplants often require admission to an acute care
hospital as a result of their end-stage organ disease. They may be very
deconditioned and may benefit from physical therapy during their stay.
The goal of physical therapy for transplant candidates is conditioning in
preparation for the transplant procedure and postoperative course and
increasing functional mobility and endurance in an attempt to return
patients to a safe functional level at home. Other transplant candidates
may be too acutely sick and may no longer qualify for transplantation
during that particular hospital admission. These patients are generally
unable to work and may need assistance at home from family members
or even require transfer to a rehabilitation facility.
Whether the patient is pretransplantation or posttransplantation, physical
therapists focus on conditioning patients to their maximum functional level
and should have a basic knowledge of the patient’s end-stage organ disease.
The objectives for this chapter are to provide information on the following:
1. The transplantation process, including criteria for transplantation,
organ donation, preoperative care, and postoperative care
2. Complications after organ transplantation, including rejection and
infection
3. The various types of organ transplantation procedures
4. Guidelines for physical therapy intervention with the transplant
recipient
The most relevant practice patterns for the diagnoses discussed in this
chapter, based on the American Physical Therapy Association’s Guide to
Physical Therapist Practice, ed. 2, are as follows:
 6B: Impaired Aerobic Capacity/Endurance Associated With
Deconditioning
 6D: Impaired Aerobic Capacity/Endurance Associated With
Cardiovascular Pump Dysfunction or Failure
 6E: Impaired Ventilation and Respiration/Gas Exchange Associated
WithVentilatory Pump Dysfunction or Failure.
 6F: Impaired Ventilation and Respiration/Gas Exchange Associated
With Respiratory Failure

401
402 CHAPTER 12 OrganTransplantation
Please refer to the back cover of this book for a com-
plete list of the preferred practice patterns as individual
patient conditions are highly variable and other practice
patterns may be applicable.
TYPES OF ORGAN TRANSPLANTS
The kidney, liver, pancreas, heart, lung, and intestine
are organs that are procured for transplantation. The
most frequent of those are the kidney, liver, and
heart.3 Double transplants, such as liver-kidney,
kidney-pancreas, and heart-lung, are performed if the
patient has multiorgan failure. Although bone marrow
is not an organ, bone marrow transplantation (BMT)
and peripheral blood stem cell transplant are common
types of tissue transplant that will be discussed.
Stem cell research has potential to provide an alter-
native to solid organ transplant with the hope of direct-
ing the cells to differentiate into specific cell types.
Embryonic stem cells can become any cell type, while
adult stem cells are limited to the tissue of origin.
Recent literature however suggests adult stem cells
may have plasticity allowing regeneration into cells
other than the original tissue type. Given the current
high demand and low supply of organs for transplanta-
tion, stem cells may provide an alternative treatment
for diseases such as rheumatoid arthritis, diabetes,
burns, cardiac disease, osteoarthritis, Parkinson’s dis-
ease, spinal cord injury, Alzheimer’s disease, and
stroke.4
CRITERIA FOR TRANSPLANTATION
Transplantation is offered to patients who have end-
stage organ disease for which alternative medical or sur-
gical management has failed. The patient typically has
a life expectancy of less than 1 to 3 years.5-7 Criteria for
organ recipients vary, depending on the type of organ
transplant needed and the transplant facility.
The basic criteria for transplantation include the
following8:
 The presence of end-stage disease in a transplantable
organ
 The failure of conventional therapy to treat the
condition successfully
 The absence of untreatable malignancy or irrevers-
ible infection
 The absence of disease that would attack the trans-
planted organ or tissue
In addition to these criteria, transplant candidates
must demonstrate emotional and psychological stabi-
lity, have an adequate support system, and be willing
to comply with lifelong immunosuppressive drug ther-
apy. Other criteria, such as age limits and absence of
drug or alcohol abuse, are specific to the transplant
facility. To determine whether transplantation is the
best treatment option for the individual, all transplant
candidates are evaluated by a team of health care profes-
sionals consisting of a transplant surgeon, transplant
nurse coordinator, infectious disease physician, psy-
chiatrist, social worker, and nutritionist. The patient
undergoes many laboratory and diagnostic studies
during the evaluation process. Acceptable candidates
for organ transplantation are placed on a waiting list.
Waiting times for an organ may range between 1 and
4 years.5,9 In the United States alone there are currently
more than 96,000 waiting list candidates, and less than
2,000 donors between January 2007 and April 2007.1
As a result, many patients die waiting for a suitable
organ to become available.
TRANSPLANT DONATION
Cadaveric Donors
Cadaveric donors are brain-dead individuals who have
had severe neurologic trauma, such as from head or
spinal cord injury, cerebral hemorrhage, or anoxia.10
Death must occur at a location where cardiopulmonary
support is immediately available to maintain the poten-
tial organ donor on mechanical ventilation, cardiopul-
monary bypass, or both; preserve organ viability; and
prevent ischemic damage to vital organs.10 The cadaver-
ic donor must have no evidence of malignancy, sepsis,
or communicable diseases, such as hepatitis B or
human immunodeficiency virus.8,11,12
Living Donors
Because there are not enough cadaveric organs donated
to meet the needs of all potential recipients, living
donor transplantation offers an alternative means of
organ donation. Living donors are always used for
bone marrow transplants, often used for kidney trans-
plants, and sometimes used for liver, lung, and pancreas
transplantation.They may be genetically or emotionally
related to the recipient that is, they are a blood relative
(e.g., sister) or non—genetically related individual (e.g.,
spouse or close friend). Living donors also are evaluated
by the transplant team to determine medical suitability.

The age of a potential donor can range from a term
newborn to 65 years, depending on the organ consid-
ered for donation and the recipient. Donors do not
have a history of drug or alcohol abuse, chronic disease,
malignancy, syphilis, tuberculosis, hepatitis B, or
human immunodeficiency virus infection. Ideally, the
donor’s height and weight approximate those of the
recipient for the best ‘‘fit.’’
Donor Matching
The matching of a cadaveric or living donor with a
recipient depends on the following factors:
 ABO blood typing
 Histocompatibility typing
 Size
The donor and recipient must be ABO blood type
identical or compatible.13 The process of finding com-
patible donors and recipients is called tissue typing or his-
tocompatibility typing. Histocompatibility typing attempts
to match the human leukocyte antigens (HLAs), which
are the antigens that cause graft rejection. It is per-
formed serologically by adding a standard panel of
typing antisera, complement, and tryphan blue stain
to purified lymphocytes and then observing the lym-
phocytotoxicity.14 The better the histocompatibility
match and degree of genetic similarity between the
donor and the recipient, the less severe is the rejection
response. In living related donors, an identical match
is ideal; however, a half match is acceptable.11 Also, a
white cell crossmatch is performed in which the lym-
phocytes from the donor are mixed with the serum
from the recipient and then observed for immune
responses. A negative crossmatch indicates no antibody
reaction and that the recipient’s antibodies are compat-
ible with the donor. A negative crossmatch is required
for successful kidney and kidney-pancreas transplants.9
Although pretransplant tissue typing is ideal, it is
not always performed. Sometimes, there is insufficient
time to perform HLA typing between donor and recip-
ient because of the short cold ischemic times for differ-
ent organs.14 Owing to the short ischemic time of less
than 6 hours for orthotopic cardiac transplants, ABO
blood type compatibility, body weight, and accrued
waiting time are used for allocation of the donor
heart.10,12 A lung transplant recipient is matched on
the basis of ABO blood type and size, because the ische-
mic time is less than 4 hours.8 A size match is based on
the donor’s height, weight, and thoracic dimensions as
determined by chest radiograph.15
IntheUnitedStates,organ procurement and distribu-
tion for transplantation are administered by the United
OrganTransplantation CHAPTER 12 403
Network for Organ Sharing (UNOS). UNOS sets the
standards for transplant centers, transplant physicians,
tissue typing laboratories, and organ procurement orga-
nizations. UNOS distributes organs based on the sever-
ity of the recipient’s illness, blood type, donor-recipient
weight match, and length of recipient waiting time.16
GENERAL POSTTRANSPLANTATION CARE
AND COMPLICATIONS
Postoperative Care for Living Donors
Postoperative care for living donors is similar to that of
any patient who has undergone major abdominal or car-
diothoracic surgery. These patients are taken off
mechanical ventilation in the recovery room and trans-
ferred to the general surgery or transplant ward. Vital
signs and blood counts are monitored closely for possi-
ble postoperative bleeding. Patients are usually out of
bed and ambulating on postoperative day 1. On average,
the duration of donor hospitalization may range from
2 days for a kidney donor to 8 days for a simultaneous
pancreas-kidney (SPK) donor.9,17 When minimally
invasive techniques are used, kidney donors may be
discharged from the hospital in 24 to 48 hours.
Postoperative Care for Transplant Recipients
Once an organ is transplanted, the postoperative care
focuses on the monitoring and treatment of the
following16:
 Allograft function
 Rejection
 Infection
 Adverse effects of immunosuppressive drugs
General postoperative care for transplant recipients
is also similar to the care patients receive after major
abdominal or cardiothoracic surgery. Except for
kidney transplant recipients, who are normally extu-
bated before leaving the operating room, most patients
are transferred from the operating room to the surgical
intensive care unit, where they are weaned from
mechanical ventilation within 24 to 48 hours.13,18,19
Once extubated and hemodynamically stable, recipi-
ents are transferred to specialized transplant floors.
Nursing staff monitors the recipient closely for signs
and symptoms of infection and rejection, which are
the leading causes of morbidity and mortality in the
first year after transplantation.
Complications from postoperative transplantation
may contribute to an increased length of hospital stay
404 CHAPTER 12 OrganTransplantation
or hospital readmissions. They can be grouped to
include the following types:
 Surgical
 Medical
 Rejection
 Infection
Surgical complications include vascular problems,
such as thrombosis, stenosis, leakage at anastomotic
sites, and postoperative bleeding. Medical complica-
tions may include fluid overload or dehydration,
electrolyte imbalance, or hypertension.
Rejection
The major problem in organ transplantation is not the
technical difficulties of surgery, but rather organ rejec-
tion, or the tendency of the recipient’s body to immedi-
ately reject anything that is ‘‘nonself.’’ Graft rejection is
actually a normal immune response to invasion of
foreign matter, the transplanted organ or tissue. Some
degree of rejection is normal; however, if the patient
is not treated with immunosuppressive drugs, the
donor organ would be completely rejected and cease
to be viable in 10 days.20 Transplant recipients must
receive immunosuppressive drugs for the rest of their
lives to suppress or minimize rejection of their trans-
planted organs. The pharmacologic agents most often
used to prevent organ rejection include a double or
triple drug therapy, consisting of a combination of
tacrolimus or cyclosporine with methylprednisolone,
and azathioprine or mycophenolate mofetil.21 See
Table 12-1 for common immunosuppressive medica-
tions used in organ transplantation.
These immunosuppressive drugs decrease the
body’s ability to fight infection. A delicate balance
must be reached between suppressing rejection and
avoiding infection. Insufficient immunosuppression
may result in rejection that threatens the allograft and
patient survival, whereas excessive immunosup-
pression increases the risk of infection and malig-
nancy.16 If detected early, rejection can be minimized
or reversed with an increase in daily doses of
immunosuppressive drugs.
Many different factors influence the combination of
drugs used posttransplant including the individual
patient’s condition, organ transplanted, and recent
literature. UNOS describes three different types of
posttransplant immunosuppression including:
 Induction immunosuppression: Encompasses high-
dose immunosuppressive medications given to
prevent acute rejection immediately after trans-
plantation. These medications can include
methylprednisolone, Atgam, Thymoglobulin,
OKT3, basiliximab, or daclizumab.
 Maintenance immunosuppression: Includes all
medications used for long-term immunosuppres-
sion. These medications can include prednisone,
cyclosporine, tacrolimus, mycophenolate mofetil,
azathioprine, or Rapamycin.
 Antirejection immunosuppression: Includes all im-
munosuppressive medications given for acute
rejection at any point posttransplantation. Medica-
tions in this group can include methylprednisolone,
Atgam, OKT3, Thymoglobulin, basiliximab, or
daclizumab.22
When treating postoperative transplant recipients, it
is important to monitor for adverse side effects of the
immunosuppressive drugs. Immunosuppression pro-
tocols now promote the rapid tapering of steroids post-
transplantation, which diminishes the harsh side
effects of the drugs.23
TYPES OF GRAFT REJECTION
There are three types of graft rejection: hyperacute,
acute, and chronic.
1. Hyperacute rejection is characterized by ischemia
and necrosis of the graft that occurs from the time
of transplant to 48 hours after transplant.8 It is
believed to be caused by ABO incompatibility and
by cytotoxic antibodies present in the recipient that
respond to tissue antigens on the donor organ. The
manifestations of hyperacute rejection include gen-
eral malaise and high fever. Rejection occurs before
vascularization of the graft takes place. Hyperacute
rejection is unresponsive to treatment, and removal
of the rejected organ is the only way to stop the reac-
tion. Therefore, the recipient will need immediate
retransplantation to survive.8,14,24
2. Acute rejection is a treatable and reversible form of
rejection that occurs within the first year after trans-
plantation. Almost every patient has some degree
of acute rejection after transplantation. T lympho-
cytes detect foreign antigens from the graft,
become sensitized, and set the immune response
into action. Phagocytes, which are attracted to the
graft site by the T lymphocytes, damage the inner
lining of small blood vessels in the organ. This
causes thrombosis of the vessels, resulting in tissue
ischemia and eventual death of the graft if left
untreated.11
The first signs of acute rejection may be detected
within 4 to 10 days postoperatively.8,9,11 The actual
manifestations of rejection vary with the affected

Table 12-1 IMMUNOSUPPRESSIVE DRUGS USED IN ORGAN TRANSPLANTATION
Immunosuppressive Drug Action
Corticosteroids Inhibit gene transcription for cytokines,
(methylprednisolone which affect all immune responses
[Solu-Medrol], Inhibit T-cell activation
prednisone) Used to reverse early rejection
Cyclosporine (Neoral, Inhibits immune responses by
Sandimmune) inhibitingT-cell lymphokine
production and cell-mediated
immunity by blocking transcription
of early activation genes
Used to prevent, rather than reverse,
acute rejection
Tacrolimus (FK506, InhibitsT-lymphocyte activation
Prograf) Used to prevent acute rejection
Azathioprine (Imuran) Inhibits lymphocyte proliferation
Inhibits DNA and RNA synthesis
Blocks antibody production
Suppresses entire immune system
Mycophenolate mofetil InhibitsT- and B-lymphocyte
(CellCept) proliferation
Suppresses antibody formation
Inhibits de novo pathway for purine
synthesis
Muromonab-CD3 InhibitsT-cell function and
(Orthoclone OKT3) proliferation
Used only for acute rejection that
is refractory to other agents
Sirolimus (Rapamune) InhibitsT lymphocyte activation and
proliferation that occurs in response
to antigenic and cytokine stimulation
Inhibits antibody production
Data from BlackJM, Matassarin-Jacobs E (eds). Medical-Surgical Nursing: Clinical Management for Continuity of Care (5th ed).
Philadelphia: Saunders, 1997;644-645; Bucher L, Melander S. Critical Care Nursing. Philadelphia: Saunders, 1999;343;Winkel E, DiSesaVJ,
Costanzo MR. Advances in Heart Transplantation. Dis Mon 1999;45(3):77-79; National PBM Drug Monograph. Available at:
www.pbm.va.gov/monograph/39857Sirolimusmonofinal0203.pdf. Accessed October 2007.
organ. General signs and symptoms of acute rejec-
tion include the following11:
 Sudden weight gain (6 lb in less than 3 days)
 Peripheral edema
 Fever, chills, sweating, malaise
 Dyspnea
 Decreased urine output, increased blood urea
nitrogen (BUN) and serum creatinine levels
OrganTransplantation CHAPTER 12 405
Possible Adverse Effects
Muscle loss and weakness, hypertension,
hyperglycemia, delayed wound healing,
osteoporosis, weight gain, peptic ulcers,
cataracts, hypokalemia, mood swings,
congestive heart failure
Hypertension, elevated cholesterol, renal
dysfunction, tremor, sodium retention,
hyperkalemia, hyperglycemia, paresthesias,
hepatic dysfunction, seizures, hirsutism, gum
hyperplasia, malignancy; long-term side
effects: diabetic neurotoxicity, decreased bone
density
Tremors, headache, hepatotoxicity,
hypertension, hyperglycemia, hyperkalemia,
constipation, diarrhea, nausea, vomiting,
renal dysfunction, mental status changes
Bone marrow suppression, hepatotoxicity,
leukopenia, pancreatitis, cholestasis
Nausea, vomiting, diarrhea, leukopenia,
neutropenia, sepsis, abdominal pain
Chest pain, fever, nausea, vomiting, diarrhea,
pulmonary edema, dyspnea, malignant
lymphoma, rigors, malaise, meningitis
Hyperlipidemia involving both
hypercholesterolemia and hypertriglyceridemia.
Bone marrow suppression, increased liver
function test, and thrombocytopenia in liver
transplant patients who have a preexisting
thrombocytopenia
 Electrolyte imbalances
 Increased blood pressure
 Swelling and tenderness at the graft site
Early intervention is the key to reversal of acute
rejection. Depending on the severity of rejection,
treatment varies from a new dose of intravenous ster-
oids, to a change in current immunosuppressive ther-
apy, to a 10-day course of the murine monoclonal
406 CHAPTER 12 OrganTransplantation
antibody muromonab-CD 3 (Orthoclone OKT3).21
Some immunosuppressant medications used to treat
acute rejection include corticosteroids (prednisone),
cyclosporine (Neoral), tacrolimus (Prograf), azathio-
prine (Imuran), muromonab-CD 3 (Orthoclone
OKT3), cyclophosphamide, antithymocyte globulin,
and antilymphocyte globulin.6
3. Chronic rejection of the graft occurs after the first
year of transplantation. It is believed to result from
immune complexes of immunoglobulin M and com-
plement that form in the blood vessels of the organ.
Deterioration of the graft is gradual and progressive.
Immunosuppressive drugs do not stop this type of
rejection.The more frequent and severe the rejection
episode, the poorer the prognosis. Increasing immu-
nosuppressive medications may slow the process,
and it may take years before the organ fails, but
eventually retransplantation is required.
Chronic rejection in patients with renal trans-
plants presents as a gradual increase in serum creati-
nine and BUN, electrolyte imbalance, weight gain,
new-onset hypertension, decrease in urine output,
and peripheral edema.8,11
In patients with liver transplants, chronic rejection is
seen as a gradual rise in serum bilirubin and elevation
of serum glutamic-oxaloacetic transaminase (aspartate
aminotransferase).21 Progressive thickening of the
hepatic arteries and narrowing of the bile ducts occur
and eventually lead to progressive liver failure.
In patientswith cardiac transplants, chronic rejection
manifests in the form of coronaryallograft vasculopathy,
inwhich there is acceleratedgraft atherosclerosis or myo-
cardial fibrosis and increasing blockage of the coronary
arteries, which leads to myocardial ischemia and
infarction.8
Chronic rejection in patients with lung transplants is
manifested as bronchiolitis obliterans with symptoms
of progressive dyspnea secondary to increasing airflow
obstruction and a progressive decline in the forced
expiratory volume in one second (FEV1).5,6
In patients with pancreas transplants, the pancre-
atic vessels thicken, leading to fibrosis, and there is
a decrease in insulin secretion with resultant
hyperglycemia.8
Infection
Suppression of the immune response prevents rejection
of the transplanted organ; however, the recipient is
more susceptible to infection. Infection may occur in
the lungs, liver, colon, and oral mucous membrane.
In addition to a surgical wound infection, the recipient
is at risk for bacterial, fungal, and viral infections.
Bacterial infections may occur in the urinary tract,
respiratory tree, and indwelling devices, such as a cen-
tral venous catheter.19 The highest risk for infection
is during the first 3 months after transplantation.25 If
infection is noted, fewer immunosuppressive drugs
are given, and antibiotic treatment is initiated.
Antibacterial, antiviral, and antifungal medications
are often given prophylactically. Bacterial infections
are treated using antibiotics. The use of trimethoprim/
sulfamethoxazole (Bactrim) in prophylactic doses has
been effective in preventing Pneumocystis carinii pneumo-
nia in cardiac transplant recipients. Fungal infection is
caused by yeast and can be treated with amphotericin.
Nystatin, an oral antifungal mouthwash, is used for
prevention of mucosal candidiasis that often occurs
due to immunosuppression. Viral infection, such as
cytomegalovirus (CMV), is very problematic. Cyto-
megalovirus causes different clinical syndromes,
including pneumonitis, hepatitis, nephritis, and gastro-
intestinal ulceration.19 If not detected and treated early
with ganciclovir, it can result in the loss of the graft.
While in the hospital, proper hand washing, before
and after direct contact with transplant recipients, is
the most important and effective way to prevent
infection.
General signs and symptoms of infection include
the following9:
 Temperature greater than 388 C (100.58 F)
 Fatigue
 Shaking chills
 Sweating
 Diarrhea lasting longer than 2 days
 Dyspnea
 Cough or sore throat
RENAL TRANSPLANTATION
Renal or kidney transplant is the most common organ
transplantprocedure.8 In 2006,therewere17,092 recorded
kidney transplants in the United States.1 Renal transplan-
tation is a means of restoring normal renal function to
patients with irreversible end-stage renal failure.
The most frequent causes of end-stage renal disease
requiring transplantation include the following10,14:
 Primary uncontrolled hypertension
 Glomerulonephritis
 Chronic pyelonephritis
 Diabetic nephropathy
 Polycystic kidney disease

Contraindications to renal transplantation include
the following14:
 Advanced cardiopulmonary disease
 Active vasculitis
 Morbid obesity
Cadaveric Versus Living Donor Renal
Transplantation
Kidney transplants may be cadaveric or living donor.
Cadaveric kidneys may be maintained for as long as
72 hours before transplantation and, as a result, are the
last organs to be harvested. Although less commonly
performed, living donor kidney transplants are pre-
ferred to cadaveric transplantation. Because the body
can function well with one kidney, the kidney donor
can lead a normal, active life after recovering from the
surgery. There is no increased risk of kidney disease,
hypertension, or diabetes, and life expectancy does
not change for the donor.9
The benefits for the recipient include a longer allo-
graft and patient survival from a living donor kidney
transplant.The recipients of living donor kidney trans-
plants have higher survival rates (11 to 15 years) than
the cadaveric transplant (7 to 8 years).9 The higher suc-
cess rate of the recipients of living donor transplants
can be attributed to the following9,26:
 The renal allograft from a living donor can be more
thoroughly evaluated before transplantation than
the cadaveric allograft. This results in closer genetic
matches between the donor and recipient.
 There is a lower chance of damage to the donor organ
during preservation and transport.
 The incidence of acute tubular necrosis (ATN) in
the postoperative period is 30% to 40% when a
cadaveric donor is used but is infrequent with a
living donor.
 Recipients of living donor transplants require less
immunosuppressive medications and may have less
risk of subsequent infection or malignancy.
 Living donor transplant recipients undergo trans-
plantation as an elective procedure and may be
healthier when they receive their transplant.
Renal Transplant Procedure
The renal allograft is not placed in the same location as
the native kidney. It is placed extraperitoneally in the
iliac fossa through an oblique lower abdominal inci-
sion.27, 28 The renal artery and vein of the donated
kidney are attached to the iliac artery and vein of the
recipient. The ureter of the donated kidney is sutured
to the bladder. The recipient’s native kidney is not
OrganTransplantation CHAPTER 12 407
removed unless it is a source of infection or uncon-
trolled hypertension. The residual function may be
helpful if the transplant fails and the recipient requires
hemodialysis.28,29
The advantages of renal allograft placement in the
iliac fossa versus placement in the correct anatomic
position include the following30:
 A decrease in the postoperative pain, because the
peritoneal cavity is not entered
 Easier access to the graft postoperatively for biopsy
or any reoperative procedure
 Ease of palpation and auscultation of the superficial
kidney to help diagnose postoperative complications
 The facilitation of vascular and ureteral anastomoses,
because it is close to blood vessels and the bladder.
Indication of Renal Function Posttransplant
Restoration of renal function is characterized by imme-
diate production of urine, massive diuresis, and declin-
ing levels of BUN and serum creatinine. Excellent renal
function is characterized by a urine output of 800 to
1,000 ml per hour.19 However, there is a 20% to 30%
chance that the kidney will not function immediately,
and dialysis will be required for the first few weeks.28
Dialysis is discontinued once urine output increases
and serum creatinine and BUN begin to normalize.
With time, normal kidney function is restored, and
the dependence on dialysis and the dietary restrictions
associated with diabetes are eliminated.28
Postoperative Care and Complications
Volume status is strictly assessed. Intake and output
records are precisely recorded. Daily weights should
be measured at the same time using the same scale.
When urine volumes are extremely high, intravenous
fluids may be titrated. Other volume assessment para-
meters include inspection of neck veins for distention,
skin turgor and mucous membranes for dehydration,
and extremities for edema. Auscultation of the chest is
performed to determine the presence of adventitious
breath sounds, such as crackles, which indicate the
presence of excess volume.14
The most common signs of rejection specific to the
kidney are an increase in BUN and serum creatinine,
decrease in urine output, increase in blood pressure,
weight gain greater than 1 kg in a 24-hour period, and
ankle edema.9,14,28 A percutaneous renal biopsy under
ultrasound guidance is the most definitive test for
acute rejection.31 Sometimes, ATN occurs posttrans-
plantation.Twenty percent to 30% of patients receiving
cadaveric kidneys preserved for longer than 24 hours
408 CHAPTER 12 OrganTransplantation
experience delayed graft function.28 This ischemic
damage from prolonged preservation results in ATN.
The delayed kidney function may last from a few days
to 3 weeks. Therefore, dialysis is required until the
kidney starts to function.9
Ureteral obstruction may occur owing to compres-
sion of the ureter by a fluid collection or by blockage
from a blood clot in the ureter. The obstruction can
cause hydronephrosis (dilation of the renal pelvis and
calyces with urine), which can be seen by ultrasound.28
The placement of a nephrostomy tube or surgery
may be required to repair the obstruction and prevent
irreversible damage to the allograft.28
Urine leaks may occur at the level of the bladder,
ureter, or renal calyx. They usually occur within the
first few days of transplantation.28 Renal ultrasounds
are performed to assess for fluid collections, and radio-
nucleotide scans view the perfusion of the kidney.
Other potential complications include posttransplant
diabetes, renal artery thrombosis or leakage at the ana-
stomosis; hypertension; hyperkalemia; renal abscess
or decreased renal function; and pulmonary
edema.8,15,28 Thrombosis most often occurs within the
first 2 to 3 days after transplantation.28 The most
common cause of decreased urine output in the imme-
diate postoperative period is occlusion of the urinary
catheter due to clot retention, in which case aseptic irri-
gation is required.14
CLINICAL TIP
 Physical therapists should closely monitor blood
pressure with exercise. To ensure adequate perfusion
of the newly grafted kidney, the systolic blood
pressure is maintained at greater than 110 mm Hg.
Kidney transplant recipients may be normotensive
at rest; however, they respond to exercise with
a higher-than-normal blood pressure.1
LIVER TRANSPLANTATION
The liver is the second most commonly recorded organ
transplanted in the United States with 6,650 patients
undergoing liver transplant surgery in 2006.1
Indications for liver or hepatic transplantation include
the following8,31:
 End-stage hepatic disease
 Primary biliary cirrhosis
 Chronic hepatitis B or C
 Fulminant hepatic failure (FHF) resulting from an
acute viral, toxic, anesthetic-induced, or medica-
tion-induced liver injury
 Congenital biliary abnormalities
 Sclerosing cholangitis
 Wilson’s disease
 Budd-Chiari syndrome
 Biliary atresia
 Confined hepatic malignancy (hepatocellular
carcinoma)
If the cause of liver failure is alcoholic cirrhosis, the
patient must be free from alcohol use for a period
determined by the transplant center, which is typically
6 months or more.
Contraindications to hepatic transplantation include
the following21,31:
 Uncontrolled extrahepatic bacterial or fungal
infections
 Extrahepatic malignancy
 Advanced cardiac disease
 Myocardial infarction within the previous 6 months
 Severe chronic obstructive pulmonary disease
 Active alcohol use or other substance abuse
Pretransplantation Care
Patients awaiting liver transplant are often decondi-
tioned and malnourished with resulting weakness and
muscle loss due to breakdown of muscle protein and
fat, which are utilized as alternative energy sources.32
Additionally, anasarca and/or ascites often lead to over-
all weight gain with associated balance impairments.
The goals of preoperative physical therapy include
aerobic conditioning, strength training, postural edu-
cation, and maximizing functional mobility with a
focus on education regarding postoperative follow-up,
fall prevention, home exercise program, and lifestyle
modification.
Table 12-2 provides some characteristics of liver
failure, their clinical effects, and their implications to
physical therapy.
Types of Liver Transplants
1. Orthotopic cadaveric liver transplantation. Orthotopic liver
transplantation involves removal of the diseased
liver and insertion of a cadaveric liver into the
normal anatomic position via a midline sternotomy
and continuous laparotomy.
2. Living adult donor liver transplant. A single lobe of the
liver from a living adult is transplanted into the
recipient. The removal of the lobe does not cause
any decrease in liver function to the living donor.9
 OrganTransplantation CHAPTER 12 409

Table 12-2 MEDICAL CHARACTERISTICS OF LIVER FAILURE, THEIR RELATED CLINICAL EFFECTS,
AND PHYSICAL THERAPY IMPLICATIONS

Medical Characteristics
of Liver Failure
" Bilirubin level
# Albumin synthesis
Altered clotting ability
Impaired glucose
production
Portal hypertension
Diminished phagocytic
activity
Failure to absorb vitamin D
", Elevated; #, decreased.
Data from KM Sigardson-Poor, LM Haggerty. Nursing Care of theTransplant Recipient. Philadelphia: Saunders, 1990;149—151;
RL Braddom (ed). Physical Medicine and Rehabilitation (2nd ed). Philadelphia: Saunders, 2000;1397.
Clinical Effects
Jaundice.
Dark, tea-colored urine.
May induce nausea and anorexia.
Accumulation of ascites fluid in the
peritoneal cavity causes abdominal
swelling and increased abdominal girth.
May promote protein loss and a negative
nitrogen balance.
May lead to anasarca (total body edema).
Increased prothrombin time and partial
thromboplastin time.
Low blood sugar.
Presence of esophageal varices.
May lead to hepatic encephalopathy.
Spontaneous bacterial peritonitis
or cholangitis.
Osteoporosis may result.
Physical Therapy Implications
None.
May cause pressure on the diaphragm, leading
to respiratory and nutritional difficulties.
Monitor for dyspnea with activity.
Patient may have an altered center of gravity
and decreased balance.
Prolonged bleeding time.
Patient bruises easily.
Monitor patient safety and prevention of falls.
Patient may have decreased energy.
Bleeding may occur spontaneously.
Patient may have altered mental status and
decreased safety awareness.
None.
May develop compression or pathologic
fractures.

Because of the unique ability of the liver to regener-
ate, the donor’s and recipient’s livers will grow back
to normal size within several months.9
3. Split liver transplant. Split liver transplants are some-
times used to expand the donor pool. Surgeons
divide an adult cadaveric liver in situ into two func-
tioning allografts.33 Usually, the smaller left lobe is
donated to a child, and the larger right lobe is given
to an adult.34
4. Dominoliver transplant. Domino liver transplant (DLT)
is a technique developed in Portugal in 1995. With
the current shortage of organs, transplant centers
across the globe are gradually utilizing this tech-
nique more frequently.35 Transplant centers in the
United States have gradually taken on this challen-
ging procedure, with UNOS reporting 51 DLTs per-
formed since 2000.1 This procedure involves
patients with familial amyloidotic polyneuropathy
(FAP). Patients with FAP have a metabolic defect
within the liver. The liver is structurally and func-
tionally normal, but it synthesizes an abnormal pro-
tein, transthyretin, that forms amyloid fibrils and
deposits them in the peripheral and autonomic
nerves, heart, kidney, and intestine. The domino
liver transplant involves three people: the donor,
the patient with FAP, and a patient listed on the
liver transplant waiting list. The patient with FAP
receives the donated liver. The removed liver (from
the patient with FAP) is then transplanted into the
other transplant recipient, hence the term domino
transplant. Liver transplantation for patients with
FAP leads to normal transthyretin protein produc-
tion. The recipient who received the FAP liver will
likely never experience any of the symptoms associ-
ated with FAP, because they take 40 to 60 years to
manifest.9
410 CHAPTER 12 OrganTransplantation
Indication of Liver Function Posttransplant
1. Once the graft is vascularized in the operating room,
the functioning liver starts to produce bile.14 Thus,
prompt outflow of bile through the biliary T tube,
which is inserted at the time of surgery, is an early
indicator of proper function of the transplanted
liver.11 Thick, dark-green bile drainage indicates
good liver function. A sudden drop in amount of
bile or change to a light yellow color indicates an
alteration in liver function.11
2. The most sensitive laboratory indices of liver func-
tion are the coagulation factors, prothrombin time
(PT), partial thromboplastin time (PTT), and inter-
national normalized ratio (INR). Alteration in liver
function is reflected very early by prolonged
coagulation times. A steady downward trend to
normalization of the PT and PTT should occur
postoperatively.14
3. The liver function tests (LFTs) should reveal a pro-
gressive decline after transplantation. The exact
values can vary from patient to patient. For example,
if the recipient required large amounts of blood
transfusion, the initial LFT levels may be low sec-
ondary to hemodilution. More accurate levels are
determined 6 to12 hours after surgery.14
4. In the immediate postoperative period, hypokale-
mia is another sign that the liver is functional.
Once the graft is vascularized, hepatocytes extract
potassium from the blood. On the other hand,
hyperkalemia often signifies cell death and that the
hepatocytes are nonfunctional.14
5. Hyperglycemia also indicates that the liver is able to
store glycogen and convert it to glucose.
Postoperative Care and Complications
Postoperatively, liver transplant recipients may emerge
with three Jackson-Pratt (JP) suction drains and a bili-
ary T tube. The JP drains lie over the superior surface
of the liver and drain blood-tinged fluid.Two of the JP
drains are removed within the first 48 hours of surgery.
The last JP drain is removed approximately 7 days
after surgery, in the absence of a biliary leak.9,19 The
T tube, which is placed in the bile duct, remains in
place for up to 12 weeks postoperatively. The amount,
color, and consistency of the bile are monitored. The
T tube is clamped once the bilirubin level falls
below 2.5 mg/dl (the reference range of total bilirubin
is 0.1 to 1.0 mg/dl).9,21
Primary graft failure is a sign of acute hepatic failure
that may be seen immediately postoperatively. It is
characterized by a markedly abnormal liver function;
prolonged PT, PTT, or both; oliguria; metabolic acido-
sis; hyperkalemia; hypoglycemia; and coma. In the
event of primary graft failure, retransplantation is
immediately required.
Potential medical complications include posttrans-
plant diabetes, abscess, atelectasis, and pneumonia sec-
ondary to ascites or peritonitis.8 Acute rejection
specific to a transplanted liver includes elevated LFTs
(especially an increase in bilirubin and prolonged PT,
PTT, or both); jaundice; right upper-quadrant pain;
clay-colored stools; tea-colored urine; decreased quan-
tity of bile; thin, watery, light-colored bile through
the T tube; and increased ascitic drainage. If rejection
is identified, immunosuppressive drug doses are
increased.
A liver biopsy is the definitive diagnostic test for
rejection and is performed at bedside. It can distin-
guish between early rejection and ischemic injury.
Mild rejection will result in elevated serum trans-
aminase or alkaline phosphatase (ALP), whereas an
elevated serum glutamicoxaloacetic transaminase
(SGOT) and serum glutamate-pyruvate transaminase
(SGPT) may indicate hepatocellular damage associated
with rejection.21
Surgical complications include hepatic artery
thrombosis, biliary leak, or stricture. These complica-
tions present with a rising bilirubin level and are identi-
cal in appearance to an acute rejection episode.21
Consequently, recipients undergo routine Doppler
ultrasound of the abdomen to check for fluid collec-
tions and patency of the hepatic artery and portal
vein.21 A cholangiogram, which examines the patency
of the biliary tree drainage system, may be performed
to rule out bile duct obstruction. Surgical intervention
is indicated if the biliary obstruction cannot be cor-
rected by a percutaneous transhepatic cholangiogram.
Portal vein thrombosis is evident if ascites persist or
variceal hemorrhage develops.15
Long-term evidence shows cardiovascular compli-
cations related to obesity, diabetes, and hyperlipidemia
in post—liver transplant patients. Corticosteroids used
to treat rejection are the primary risk factor for develop-
ment of these postoperative complications, however
recent studies indicate a significant decrease in these
complications when immunosuppressive therapy is
withdrawn 3 to 4 months posttransplant.36
Exercise and diet modification can play a role in pre-
venting posttransplant obesity and diabetes. Survival
rates for liver transplant recepients are improving with
90% one-year survival and 55% nine-year survival.37

CLINICAL TIP
 Postoperatively, many recipients still have ascites
from weeping of sodium-rich and albumin-rich fluid
from the liver’s surface.11 Along with ascites and
postsurgical fluid retention, liver transplant
recipients have an increased abdominal girth and
lower extremity edema that lead to a shift in the
patient’s center of gravity and impaired balance.
Often, patients have an increase in lumbar lordosis
and complain of low back pain.
 Deep breathing and physical activity are beneficial
during the early postoperative course. Liver
transplant recipients are susceptible to atelectasis
and pneumonia because of the long operative
procedure and large incision that hinders full chest
expansion and cough effectiveness.
 An individualized home exercise program with
follow-up home or outpatient physical therapy is
recommended due to the high incidence of obesity
and diabetes in post—liver transplant patients.
 Patients may have prolonged clotting time reflected
in the lab results (PT/INR). An INR of greater than
4.0 increases the risk of uncontrolled bleeding with
injury. Check the guidelines at your facility for
physical therapy intervention for the patient
with an elevated INR, and communicate with
the team.
PANCREAS TRANSPLANTATION
Indication for Pancreas Transplant
Pancreas transplant candidates have insulin-dependent,
type 1 diabetes mellitus and are preuremic (without
urea in the blood).These patients have severe brittle dia-
betes and metabolic imbalances, such as hypoglycemic
unawareness and subcutaneous insulin resistance.38,39
Pancreas transplantation attempts to stabilize or prevent
the devastating target organ complications of type 1
diabetes by returning the patient to normoglycemia
and improving the patient’s quality of life.40 Ideally,
pancreas transplantation should be performed before
secondary complications of diabetes (such as retino-
pathy, peripheral neuropathy, vasculopathy, and end-
stage renal disease) develop. Pancreas transplantation
has been demonstrated to inhibit the progression of
neuropathy and reverse diabetic nephropathic lesions
OrganTransplantation CHAPTER 12 411
in native kidneys after 5 to 10 years, but it has not been
shown to stop severe retinopathy or vascular disease.39
Because pancreas transplantation is not a life-saving
procedure, the patient’s condition is evaluated carefully
to determine whether the benefits outweigh the risks
of transplantation.
Contraindications to pancreas transplantation
include the following39:
 Severe cardiovascular disease
 Major amputation
 Complete blindness
 Morbid obesity
 Active smoking
Living donor pancreas transplantation, in which the
segment of the body and tail of the pancreas are used
from a living donor, may be performed; however,
whole-organ cadaveric pancreas transplantation is pre-
ferred. The donor pancreas is placed intraperitoneally
through an oblique lower-abdominal incision.15
Enteric Drainage Versus Bladder Drainage
The pancreas can be transplanted with a segment of the
duodenum to facilitate drainage of pancreatic exocrine
secretions.39 Enteric drainage involves anastomosis of
the donor duodenum to a loop of the recipient’s small
bowel.41 Bladder drainage is obtained by anastomosing
the donor duodenum with the recipient’s urinary
bladder.39 This permits exocrine secretions to be
expelled with the urine and allows monitoring of
urine amylase as a marker for rejection.39,41 The disad-
vantage of bladder drainage is that urologic and
metabolic complications are common. Large quantities
of sodium bicarbonate that are produced by the
pancreas and duodenum are lost, which can result in
metabolic acidosis.42 The pancreas also secretes 1 to
2 liters of fluid each day; thus, if the patient is not
adequately hydrated, the loss of this additional fluid
results in volume depletion or dehydration. Reflux of
the urine into the transplanted organ may cause
pancreatitis, and irritation of the bladder mucosa from
the digestive enzymes of the pancreas often results in
urinary tract infections and urethral stricture forma-
tion.42 Enteric conversion after transplantation may
be required if there are persistent poor bladder function
and recurrent urinary infections.39,41 Despite its disad-
vantages, the bladder drainage technique is more
common than the enteric drainage technique, because
it allows monitoring of urine amylase for detection of
rejection.38 Enteric drainage is more difficult to
monitor for acute rejection and has more episodes of
infection postprocedure. Ultimately, bladder, rather
412 CHAPTER 12 OrganTransplantation
than enteric, drainage is the choice of the transplant
surgeon.39
Indication of Pancreatic Function Posttransplant
Within 24 hours, the transplanted pancreas should be
producing insulin. Analysis of blood glucose response
and C-peptide levels is used to determine a successful
pancreatic transplant. Immediately after transplanta-
tion, blood sugar levels are monitored every hour,
because glucose levels typically drop 50 mg/dl each
hour, and dextrose infusion may be necessary.41 The
blood glucose level should range between 80 and 150
mg/dl within a few hours after the transplantation.15
C-peptide levels are elevated, and blood sugar level
returns to normal within 2 to 3 days postoperatively.8
After a diet is started, serum glucose is monitored
4 times a day. Recipients should return to normal or
near-normal fasting plasma glucose levels, glycosylated
hemoglobin levels (which represent the average blood
glucose level over the previous several weeks), and glu-
cose tolerance tests.38,43 The recipient weans from insu-
lin and becomes insulin independent with normal
carbohydrate metabolism for an indefinite period.15,43
The need for strict adherence to a diet and constant
blood sugar monitoring should diminish.8 Long-term
follow-up studies indicate the insulin independence
can be sustained for at least 5 years.43
Postoperative Care and Complications
The recipient is often placed on strict bed rest for a few
days postoperatively to prevent kinking of the vascular
allografts that may result from a position shift of the pan-
creas.15 A Foley catheter is left in place for at least the
first week to prevent distention of the bladder and leak-
age from the bladder anastomosis.15 During the first
postoperative day, a baseline radionuclide blood flow
study of the pancreas and a Doppler ultrasonography of
the allograft vasculature are performed. Repetition of
these studies and operative intervention are performed
urgently with any sign of pancreatic dysfunction.15
Acute rejection after pancreas transplantation is diffi-
cult to diagnose. Nonspecific clinical criteria, such as
fever, allograft tenderness, ileus, abdominal pain, hema-
turia, leukocytosis, and hyperglycemia, can be used in
combination to detect acute pancreas rejection.39,42
Hyperglycemia does not occur until 80% to 90% of
the graft has been destroyed.19 A decrease in bicarbo-
nate, urine pH, or urine amylase levels of more than
25% from baseline, an elevation of serum amylase,
or a combination of these factors also indicates acute
pancreas rejection in a bladder-drained pancreas trans-
plant recipient.14,15,17,42 Percutaneous ultrasound-
guided or cystoscopic biopsy of the transplanted pan-
creas is used as a sensitive histologic method to confirm
acute graft rejection.17,39
Complications related to the bladder drainage
procedure in pancreas transplantation include urinary
tract infections, dysuria, urethritis, duodenocys-
tostomy fistulas, duodenal-bladder anastomotic leak,
duodenal stump leak, chronic hematuria, allograft pan-
creatitis, metabolic acidosis, dehydration, and hyperka-
lemia.26,38 Severe dehydration and acidosis can occur
secondary to large losses of bicarbonate in the urine.15
Other potential complications include graft throm-
bosis, decreased pancreatic function, peritonitis,
pancreatic abscess, intraabdominal bleeding, and
infections.8,39
CLINICAL TIP
 Remind pancreas transplant recipients to drink
enough fluids to rehydrate themselves during and
after exercise. Hydration is critical in patients with
a bladder-drained pancreas. Recipients must take
in 3 to 4 liters of fluid per day.41
PANCREAS-KIDNEY TRANSPLANTATION
Types of Pancreas-Kidney Transplants
1. Simultaneous pancreas-kidney (SPK) transplants. Typically,
SPK transplants are offered to patients who have
type 1 diabetes mellitus with diabetic nephropathy
and renal insufficiency. SPK transplants are more
common than a non—life saving pancreas transplan-
tation alone, as physicians are reluctant to use
potent immunosuppressive drugs in patients with
diabetes before they need a concomitant renal trans-
plant.43 The benefits of a successful SPK transplant
include normoglycemia, elimination of dialysis,
and prevention of reoccurring diabetic nephropathy
in the kidney graft.38,43
SPK transplants may be cadaveric or from living
donors, in which case a segmental pancreas trans-
plant is performed. Using an abdominal midline
incision, the pancreatic graft is implanted first on
the right side, and then the kidney graft is implanted
on the left side.17

2. Pancreas after kidney (PAK) transplants. A pancreas
transplant is performed on a patient who has already
received a cadaveric or a living donor kidney
transplant.
Postoperative Care and Complications
In SPK transplants, pancreas rejection episodes fre-
quently occur concurrently with renal allograft rejec-
tion. Rejection of the donor pancreas is more difficult
to diagnose; therefore, acute rejection of both allografts
is recognized by a deterioration in kidney function
(i.e., an increase in serum creatinine).41,43 When rejec-
tion is clinically suspected, kidney biopsy specimens
are obtained.
The SPK transplant involves a more complex
surgical procedure, with more complications and
rehospitalizations and a higher incidence of rejection
and immunosuppression required than renal trans-
plant alone.41 The advantage of near-perfect glucose
metabolism and the prevention of further secondary
diabetic complications help to justify the increased
risk.41 However, graft survival after SKP transplant
is higher than graft survival after solitary pancreas
transplantation, because renal allograft rejection is
easier to detect.
CARDIAC TRANSPLANTATION
Candidates for heart transplantation have irreversible
end-stage cardiac disease, no other surgical or medical
options, and a poor prognosis for survival longer than
6 months.11 Patients typically present with low exercise
tolerance, cachexia, generalized weakness, decreased
muscle mass, marginal blood pressure, dyspnea, and
poor peripheral perfusion.44
Common indications for heart transplants include
the following7,11,24:
 Cardiomyopathy
 Severe left ventricular disease (ejection fraction less
than 20%)
 Ischemic heart disease
 Congenital heart disease
 Valvular disease
 Inoperable coronary artery disease, with angina
refractory to medical management
 Malignant ventricular dysrhythmias unresponsive to
medical or surgical therapy, or both
 Primary cardiac tumors with no evidence of spread
to other systems
OrganTransplantation CHAPTER 12 413
Contraindications to cardiac transplantation include
the following7,14,24,25:
 Fixed pulmonary hypertension
 Unresolved pulmonary infarction
 Active peptic ulcer disease
 Type 1 diabetes mellitus with secondary
complications
 Chronic obstructive pulmonary disease (COPD)
with an FEV1 of less than 50%
Pretransplantation Care
Despite an increase in the number of people with
heart failure over the last decade, the number of car-
diac transplants (approximately 2,000 annually) has
remained relatively unchanged. With demand for
hearts much higher than the supply, ventricular assist
devices (VAD) are often used as a bridge to cardiac
transplant.The use of VADs may lead to antibody pro-
duction and sensitivity, which can result in an increased
waiting time for a donor match.The literature indicates
bridge to transplant patients have an increased risk
for acute rejection, however long-term survival is not
affected.45
Physical therapists often treat patients with VADs
awaiting cardiac transplant. A thorough understanding
of not only the precautions and contraindications, but
the evidence related to physical therapy intervention
and outcomes is essential. Please refer to Appendix
III-C for information on pertinent physical therapy
implications when working with patients who have
VADs.
Orthotopic and Heterotopic Heart
Transplantation
Orthotopic and heterotopic transplantation are the two
types of heart transplant procedures. The more
common orthotopic procedure involves a median ster-
notomy with removal of the recipient’s heart (with the
exception of the posterior right atrium with sinoatrial
node, left atrium, aorta, and pulmonary artery) and the
insertion of the donor heart in the normal anatomic
position.7,12,46,47
In a heterotopic or ‘‘piggy-back’’ transplantation,
the diseased heart is left intact, and the donor heart
is placed in the right side of the thorax adjacent to
the native heart with anastomosis between the
two hearts. The purpose of the heterotopic transplant
is for the donor heart to assist the failing heart and
is often used for patients with pulmonary hyper-
tension. This procedure is rare with only a few
414 CHAPTER 12 OrganTransplantation
transplant centers in the United States currently utiliz-
ing this approach. Whether orthotopic or heterotopic
heart transplantation is performed, epicardial pacing
wires and mediastinal and pleural chest tubes are
inserted before closure of the chest wall (see
Appendix III-A).
Indication of Cardiac Function Posttransplant
Postoperatively, patients have a pulmonary artery
catheter (that indirectly assesses left ventricular func-
tion and cardiac output) and an arterial line (that
monitors peripheral arterial pressure) for hemody-
namic monitoring. Immediately after surgery, the
patient’s complete blood count, arterial blood gas,
serum electrolyte, metabolic functions, and cyclo-
sporine levels are monitored closely.7 In addition, an
echocardiogram is performed immediately postopera-
tively to evaluate heart function and left ventricular
ejection fraction. Pulmonary artery pressures and
fluid balance are monitored closely.7 Depending on
the hemodynamic values, lab values, and ejection
fraction, pharmacologic agents and mechanical sup-
port are initiated or weaned. Heart rate and rhythm
disturbances are treated pharmacologically or by use
of epicardial pacing wires.
The new heart takes a few days to achieve a stable
intrinsic rhythm.25 Isoproterenol hydrochloride is
typically used for its inotropic and chronotropic
effects. The inotropic effect of the drug decreases the
peripheral vascular resistance (PVR) and systemic
vascular resistance, thus assisting the recovery of
the donor heart.25 The chronotropic effect increases
the heart rate and is typically required for the first
3 postoperative days to increase preload and cardiac
output and maintain a heart rate of approximately
110 beats per minute.13,25 Systolic blood pressure
should be maintained at 90 to 110 mm Hg, with
afterload reduction agents, such as nitroglycerin, to
help reduce the PVR.7 Sometimes an intraaortic
balloon pump (IABP) must be used to decrease
afterload.7
Sinus node dysfunction, resulting from donor heart
ischemia, atrial stretch, or intraoperative trauma, may
cause a slow junctional rhythm. It is treated with
bipolar atrial pacing or with a chronotropic drug, such
as dobutamine.7 Ideally, the heart rate should be
maintained at 90 to 110 beats per minute to optimize
cardiac output.7 Cardiac function usually returns to
normal within 3 to 4 days, at which time intravenous
medications, mechanical support, and pacing mechan-
isms are weaned.7
Postoperative Care and Complications
Immediate postoperative care for cardiac transplant
recipients is similar to that of patients who have under-
gone cardiothoracic surgery. Chest tubes are typically
removed 2 days postoperatively once chest drainage is
less than 25 ml per hour, and pacing wires are removed
7 days after transplantation if there were no events of
bradycardia.7
During the early hours after the transplant, the
patient may manifest a variable global myocardial
depression.7 This may result from prolonged adminis-
tration of high levels of vasopressors, an elevated PVR
in the recipient, or a prolonged ischemic time.7
Ischemic time is the time from the cross-clamp of the
donor organ to the removal of the recipient’s new
heart from cardiopulmonary bypass.25 Ideally, the
ischemic time for a heart transplant should be less than
6 hours.10 With myocardial depression, the transplanted
heart may be affected temporarily by bradycardia,
decreased diastolic compliance, diminished systolic
function, and impaired contractility.7,15
Other potential complications after heart trans-
plant include mediastinal bleeding, cyclosporine-
induced hypertension, posttransplant diabetes,
thrombosis or leakage of anastomosis, right heart
failure, biventricular heart failure, pulmonary
hypertension, pericardial effusion, and renal dys-
function.7,12,16,25 Biventricular failure is a potential
complication that is seen in the first 24 to 48 hours
after transplantation. Most patients have some
degree of pulmonary hypertension because of native
left ventricular failure. Right heart failure is the most
common cause of cardiac dysfunction postopera-
tively.25 It may be caused by a preexisting elevated
PVR, donor size mismatch in which the donor heart
is too small for the recipient, long ischemic time of
more than 4 hours, and acute rejection.25 Clinical
evidence of right ventricular heart failure includes
hypotension, low cardiac output, an elevated central
venous pressure, and low urinary output.15 Right
atrial pressures, pulmonary artery pressure, PVR, car-
diac output, and signs of right-sided heart failure are
monitored closely.7 Medications, such as isoproterenol
hydrochloride or milrinone, are used to reduce
pulmonary pressures and make it easier for the right
heart to pump.25
Many cardiac transplant recipients have preexisting
renal insufficiency due to their low cardiac output, con-
gestive heart failure, and long-term diuretic use.7,25
After transplantation, cardiopulmonary bypass and

the use of cyclosporine, which is a nephrotoxic agent,
can cause renal failure in the transplant recipient.7
Dopamine is administered to improve renal blood
flow, and diuretics are used to maintain adequate urine
output.7 In addition, intravenous cyclosporine may be
held postoperatively, and, instead, less-nephrotoxic
agents may be administered.25
Heart transplant recipients have an increased risk
of excessive postoperative bleeding and cardiac tam-
ponade.15 Owing to chronic congestive heart failure,
patients usually have passive liver congestion, which
increases the risk of bleeding.25 Many patients also
receive anticoagulation therapy preoperatively to
prevent thrombus formation. However, inadequate
heparin reversal may occur and, depending on the
severity of anticoagulation, treatment includes transfu-
sion of platelets or fresh-frozen plasma.25
Objective characteristics of acute rejection specific
to cardiac transplant recipients include new cardiac
arrhythmias, hypotension, pericardial friction rub,
ventricular S3 gallop, decreased cardiac output,
peripheral edema, pulmonary crackles, and jugular
vein distention.12-14 Subjectively, recipients may
report vague symptoms of decreased exercise toler-
ance, fatigue, lethargy, or dyspnea. However, the
most reliable technique to diagnose rejection is by per-
forming periodic endomyocardial biopsy. The initial
biopsy is performed 5 to 10 days after transplantation.
Under local anesthesia, a bioptome catheter is
advanced through the right internal jugular vein into
the right ventricle under fluoroscopy. Because rejec-
tion usually occurs in small areas throughout the
heart, three to five tissue specimens are obtained
from different sites for histologic and immunologic
studies.13,25 The presence of lymphocytic infiltration,
polymorphonuclear leukocytes, interstitial hemor-
rhage, and myocytic necrosis is an indicator of cardiac
rejection, the latter being the most severe.14 The fre-
quency of surveillance endomyocardial biopsies
varies between transplant institutions. They are usually
performed weekly for the first month, biweekly for
the second and third months, monthly for the next
6 months, every 3 months up to the first 2 years,
and then annually.13,15 If rejection is identified,
immunosuppressive agents are intensified by admin-
istration of high-dose oral or intravenous cortico-
steroids, antilymphocyte antibodies, or both.16 If the
cardiac transplant recipient has frequent arrhythmias
(which often indicate ischemia), periodic coronary
angiography is performed to detect allograft coronary
disease.12,14
OrganTransplantation CHAPTER 12 415
CLINICAL TIP
 The patient is placed in a protective isolation
room. Positive-pressure flow rooms are
recommended to limit the transfer of airborne
pathogens. The use of a face mask and strict
hand washing are required.47
 In the initial postoperative period, mediastinal
drainage is promoted by elevating the head of the
bed to a 30-degree angle and turning the patient
every 1 to 2 hours.7
 Phase I cardiac rehabilitation usually begins 2 to
3 days postoperatively, once the patient is
hemodynamically stable. Exercise is progressive and
based on the patient’s activity tolerance. Exercise is
progressed from active supine exercises without
resistance to ambulation and stationary biking. Vital
signs are monitored before, during, and immediately
after exercise.
 The cardiac transplant recipient has a resting heart
rate that is higher than normal, owing to the absence
of parasympathetic nervous system or vagal tone that
would normally slow the heart rate.7 The rate is
usually between 90 and 110 beats per minute,
and it does not vary with the recipient’s respirations.
The transplanted heart is denervated because the
extrinsic nervous supply to the donor heart was
severed during the procurement surgery.13
Therefore, it no longer has autonomic nervous
system connection to the recipient’s body.
Consequently, it is unaffected by the recipient’s
sympathetic and parasympathetic nervous
system, which normally controls the rate
and contractility.7,11
 Patients should gradually increase and
decrease demands on the transplanted heart by
extending their warm-up and cool-down periods
to 5 to 10 minutes.11,13,47 In the absence of
neural regulation, heart rate increases during
exercise, but the increase at the onset of exercise
is delayed by 3 to 5 minutes.2,48 The denervated
heart depends on circulating catecholamines
to increase the rate and force of contractions.7
With exercise, heart rate and cardiac output
increase gradually over 3 to 5 minutes and
remain elevated for a longer period of time
at the completion of activity.2 As well, after
cessation of exercise, there is a slower-than-
normal return to preexercise heart rate
level.2,11-13
416 CHAPTER 12 OrganTransplantation

 The peak heart rate achieved during

maximal exercise is significantly lower in cardiac LUNG TRANSPLANTATION
transplant recipients than in age-matched
Major indications for lung transplantation include the
patients. As a result, exercise prescriptions
following5,6,18:
that are based on target heart rate are not
 COPD (with FEV1 of less than 20% of predicted
recommended.13 Instead, the Borg scale, which uses
value)
the rate of perceived exertion (RPE), is frequently
 Cystic fibrosis (with FEV1 of less than 30% of
used during exercise for self-monitoring. The
predicted value)
recipients exercise at an RPE between 11 and 13.13
 Emphysema
 Physical therapists should monitor blood pressure
 Bronchiectasis
before, during, and after activity. At rest, systolic
 Primary pulmonary hypertension
and diastolic blood pressures of heart transplant
 Pulmonary fibrosis
recipients are higher than normal.13,48 The systolic
 Eisenmenger’s syndrome (a congenital heart disease
blood pressure should be between 80 and 150 mm
in which there is a defect of the ventricular septum,
Hg, and the diastolic blood pressure should be less
a malpositioned aortic root that overrides the inter-
than 90 mm Hg.47
ventricular septum, and a dilated pulmonary artery)
 Orthostatic hypotension is common in the early
 Alpha1-antitrypsin deficiency
postoperative phase, owing to the absence of
Less-frequent indications include the following:
compensatory reflex tachycardia.7 Allow the patient
 Sarcoidosis (see Appendix 10-A)
time to change position slowly and adapt to the new
 Eosinophilic granuloma (growth in the bone or lung
position.49
characterized by eosinophils and histocytes)
 Because the transplanted heart is denervated, the
 Scleroderma
recipient does not experience anginal chest pain or
Contraindications to lung transplantation include
pressure. Myocardial ischemia is silent but can
the following18:
manifest as atrial or ventricular arrhythmias and
 Poor left ventricular cardiac function
with symptoms of dyspnea, lightheadedness, or an
 Significant coronary artery disease
increased RPE.50 While the patient exercises,
 Significant dysfunction of other vital organs
a cardiac nurse should closely monitor the
(e.g. liver, kidney, central nervous system)
telemetry for arrhythmias.12,14 Complaints of
 Active cigarette smoking
chest pain from the recipient may be due to the
There are three types of surgical procedures for lung
sternal incision and musculoskeletal manipulation
transplantation:
during surgery.51
1. Single-lung transplantation. This is the most common
 The electrocardiogram of a heart transplant recipient
surgical technique and is indicated for all types of
has two P waves, as both donor and recipient
end-stage lung disease, except cystic fibrosis and
sinoatrial nodes remain functional. The retained
bronchiectasis.5 It involves a single anterolateral or
atrium of the recipient generates a P wave; however,
posterolateral thoracotomy in which the right or
it does not cross the surgical suture line and
left cadaveric lung is transplanted into the
therefore does not produce a ventricular contraction.
recipient.18
Only the donor P wave can conduct an electrical
2. Double-lung or bilateral lung transplantation. With double-
response leading to a contraction of the heart
lung transplantation, the left and right lungs are
(i.e., the donor P wave is followed by a QRS
transplanted sequentially into one recipient, with
complex from the donor heart).25,27
the least functional lung resected and replaced
 Because fatigue is a sign of rejection or ischemia,
first.18 The incision used is a bilateral anterior thora-
it is important to monitor day-to-day changes in
cotomy in the fourth or fifth intercostal space.
a patient’s exercise tolerance and keep the patient’s
Some surgeons also may perform a transverse
nurse or physician notified of any significant
sternotomy to create a ‘‘clamshell’’ incision.18
changes.47
Patients with cystic fibrosis and bronchiectasis
 Patients should follow sternotomy precautions;
require double-lung transplantation to remove
they are not allowed to push, pull, or lift anything
both infected lungs. It is also the preferred proce-
heavier than 10 lb for 2 months after their surgery.
dure for patients with pulmonary hypertension.5,19

3. Living donor lobar transplantation. Transplantation of
lobes involves bilateral implantation of lower lobes
from two blood-group—compatible living donors.5
The donor’s lungs are larger than the recipient’s for
the donor lobes to fill each hemithorax.5 This proce-
dure is performed primarily for patients with cystic
fibrosis. In addition, patients with bronchopulmo-
nary dysplasia, primary pulmonary hypertension,
pulmonary fibrosis, and obliterative bronchiolitis
may benefit from a lobar transplantation.10,15
Preoperative Care
Patients awaiting lung transplant often present with
decreased work capacity in both respiratory and skeletal
muscles. Preoperative physical therapy should focus
on improving functional mobility and exercise capacity
with the goal of increasing quality of life and activity
tolerance postoperatively. The preoperative program
should include resistive training with focus on proxi-
mal muscles of the upper and lower extremities, core,
and respiratory muscles, as well as aerobic training.
The literature supports using tools, such as the
6-minute walk test (see Appendix IX), muscle endur-
ance test (using timed stair climbing), and shuttle test,
to assist in objectively demonstrating training effects.
Physical therapists also play a role in using airway
clearance techniques (see Chapter 2), as patients are
often admitted with pulmonary decompensation while
waiting for transplantation.52
Indication of Lung Function Posttransplant
For patients with pulmonary vascular disease, single-
lung and double-lung transplantation results in an
immediate and sustained normalization of pulmonary
vascular resistance and pulmonary arterial pressures.5
This is accompanied by an immediate increase in
cardiac output. Arterial oxygenation generally returns
to normal, and supplemental oxygen is no longer
required, usually by the time of hospital discharge.5
The maximum improvement in lung function and
exercise capacity is achieved within 3 to 6 months after
transplantation, once the limiting effects of postopera-
tive pain, altered chest wall mechanics, respiratory
muscle dysfunction, and acute lung injury have sub-
sided.5,6 After double-lung transplantation, normal pul-
monary function is usually achieved. However, in
single-lung transplantation, lung function improves
but does not normalize fully, owing to the disease
and residual impairment of the remaining nontrans-
planted lung. Lung volumes and flow rates improve to
two-thirds of normal in single-lung transplantation.6
OrganTransplantation CHAPTER 12 417
Most lung transplant recipients are therefore able
to resume an active lifestyle, free of supplemental
oxygen, with less dyspnea and improved exercise
tolerance.
Postoperative Care and Complications
Ineffective postoperative airway clearance occurs after
lung transplantation. Recipients present with an
impaired cough reflex, incisional pain, altered chest
wall musculoskeletal function, and diminished muco-
ciliary clearance. Coughing and deep breathing must be
relearned, because the lung is denervated.53 After extu-
bation, aggressive bronchopulmonary hygiene is per-
formed every 2 to 4 hours, while the patient is awake.14
Physical therapists, respiratory therapists, and nursing
staff provide this intensive pulmonary care. This
includes postural drainage, airway suctioning, vibra-
tion, gentle percussion, diaphragmatic breathing,
coughing exercises, and use of an incentive spirometer
and flutter valve device to maximize lung expansion
and prevent atelectasis and pneumonia.The large quan-
tity of secretions (20 to 60 ml per day) is generally thick
and blood tinged, and can lead to volume loss and con-
solidation in the transplanted lung if not suctioned or
expectorated.14 Bronchopulmonary hygiene is a crucial
part of the postoperative care, as it helps mobilize secre-
tions and prevent atelectasis and mucous plugging.
Postoperative complications that may develop in
the denervated transplanted lung include pulmonary
edema or effusion, acute respiratory distress syn-
drome, dehiscence of the bronchial anastomosis, and
anastomotic stenosis.5 Single-lung transplant recipi-
ents may experience complications of ventilation-per-
fusion mismatch and hyperinflation owing to the
markedly different respiratory mechanics in each
hemithorax.15 The rate of infection in lung transplant
recipients is higher than that of other organ transplant
recipients, because the graft is exposed to the external
environment through the recipient’s native airway.
The patient’s white blood cell (WBC) and absolute
neutrophil count are monitored closely.8 Bacterial
pneumonia and bronchial infections are very
common complications that usually occur in the first
30 days.5,15 Bronchoalveolar lavage is used to diagnose
opportunistic infections.19
Clinical manifestations of acute pulmonary rejec-
tion in lung transplant recipients include dyspnea,
nonproductive cough, leukocytosis, hypoxemia, pul-
monary infiltrates as seen on chest x-ray, sudden deteri-
oration of pulmonary function tests (PFTs), elevated
WBC count, need for ventilatory support, fever, and
418 CHAPTER 12 OrganTransplantation

fatigue.8,14,18 The rejection typically presents with a

 In the intensive care unit, during the first 24 hours
sudden deterioration of clinical status over 6 to
after surgery, patients with double-lung transplants
12 hours.19 Daily documentation of the oxygen satura-
should be turned side to side. Turning is initiated
tion and the FEV1 is used to monitor and detect early
gradually, beginning with 20- to 30-degree turns and
rejection, especially in bilateral lung transplant
assessing vital signs, and then increasing gradually
recipients, because a decline in oxygen saturation or
to 90 degrees each way, every 1 to 2 hours.
spirometry values in excess of 10% commonly accom-
Prolonged periods in supine position are avoided
pany episodes of rejection or infection.5,6,51
to minimize secretion retention.14
Bronchoscopic lung biopsy and bronchiolar lavages
 Patients with single-lung transplants should lie
are used to diagnose acute rejection. The presence of
on their nonoperative side to reduce postsurgical
perivascular lymphocytic infiltrates is the histologic
edema, assist with gravitational drainage of the
hallmark of acute rejection.5,19 Transbronchial biopsies
airway, and promote optimal inflation of the
often do not supply enough pulmonary parenchyma
new lung.14
for histologic testing.51 Instead, cytoimmunologic mon-
 Bronchopulmonary hygiene before exercise
itoring of the peripheral blood may be used as a specific
may enhance the recipient’s activity tolerance.
diagnostic test for acute pulmonary rejection.
 Schedule physical therapy visits after the patient
Bronchoscopy is performed routinely and whenever
receives his or her nebulizer treatment and after the
rejection is suspected to assess airway secretions,
patient is premedicated for pain control. Incisional
healing of the anastomosis, and the condition of the
pain can limit activity progression, deep breathing
bronchial mucous membrane.14 The first bronchoscopy
exercises, and coughing. Also, splinting the incision
is performed in the operating room to inspect the
with the use of a pillow can help reduce incisional
bronchial anastomosis.19 To prevent infection and
pain while coughing.
atelectasis, routine fiberoptic bronchoscopy with
 Lung transplant recipients follow strict thoracotomy
saline lavage and suctioning are used to reduce accumu-
precautions. They are not allowed to lift anything
lation of secretions that the recipient is unable to clear.15
heavier than 10 lb. They are restricted to partial
Recent studies indicate lower extremity skeletal
weight bearing of their upper extremities, which may
muscle dysfunction, rather than dyspnea, is the primary
limit the use of an assistive device.
limiting factor impairing exercise tolerance in patients
 Patients are on respiratory isolation precautions;
post lung transplant. Several factors may contribute to
exercise is performed in the recipient’s room.
impaired lower extremity function (specifically a
All staff must mask, gown, and glove on entering
reduced capacity for oxidative metabolism in the
the patient’s room for approximately 1 week.
quadriceps femoris muscle) such as skeletal muscle
However, the recipient may ambulate in the hallway,
changes seen pretransplant as a result of the disease
if a protective mask is worn.
process, corticosteroids and immunosuppressive drugs
 Always monitor the recipient’s oxygen saturation
given pretransplant and posttransplant, as well as inac-
before, during, and after exercise. If the patient
tivity.54 Further studies need to be conducted to deter-
is on room air at rest, supplemental oxygen may be
mine the best posttransplant exercise program to
beneficial during exercise to reduce dyspnea and
maximize functional outcomes in this population.
improve activity tolerance. The lung transplant
Current evidence suggests a program including lower
recipient should maintain an arterial
extremity strength and endurance training in addition
oxyhemoglobin saturation greater than 90%
to standard aerobic conditioning is beneficial.
with activity.49
 Multiple rest periods may be required during
CLINICAL TIP activity at the beginning of the postoperative
 If the recipient is intubated, suctioning may be period to limit the amount of dyspnea and muscle
performed with a premeasured catheter to prevent fatigue. Rest periods can be gradually decreased so
damage to the anastomosis. Suctioning removes that the patient advances toward periods of
secretions and helps maintain adequate oxygenation. continuous exercise as endurance improves.
 After lung transplantation, recipients should sleep in  Exercise programs should include lower extremity
reverse Trendelenburg position to aid in postural strength and endurance training to maximize peak
drainage, as long as they are hemodynamically stable. exercise capacity.

HEART-LUNG TRANSPLANTATION
Heart-lung transplantation is performed on patients
who have a coexistence of end-stage pulmonary
disease and advanced cardiac disease that produces
right-sided heart failure.14
Indications for heart-lung transplantation include
the following5,10,27:
 Primary pulmonary hypertension
 COPD
 Cystic fibrosis
 Pulmonary fibrosis
 Eisenmenger’s syndrome
 Irreparable cardiac defects or congenital heart
disease
 Advanced lung disease and coexisting left ventricular
dysfunction or extensive coronary artery disease
The heart and lung of the donor are removed en bloc
and placed in the recipient’s chest. The anastomosis to
join the donor organs is at the trachea, right atrium,
and aorta.10,15 Postoperative HLT care is similar to the
heart and lung posttransplant care previously discussed.
Rejection of the heart and lung allografts occurs inde-
pendent of each other.27 Bacterial pneumonia from
contamination in the donor tracheobronchial tree is
the most common cause of morbidity and mortality
after HLT.10
BONE MARROW TRANSPLANTATION AND
PERIPHERAL BLOOD STEM CELL
TRANSPLANTATION
Bone marrow transplantations are performed only
after conventional methods of treatment fail to replace
defective bone marrow. Bone marrow transplantation
recipients receive healthy marrow from a living
donor in an attempt to restore hematologic and immu-
nologic functions. The three types of bone marrow
transplantation are allogeneic, syngeneic, and autologous
transplants.
1. An allogeneic transplant is one in which bone marrow
is harvested from an HLA-matched donor and
immediately infused into the recipient after
cytoreduction therapy. The donor may be related
or unrelated. A move has been made toward
DNA-based tissue typing to improve HLA match-
ing, replacing the standard serological tissue
typing. Improved HLA matching has been shown
OrganTransplantation CHAPTER 12 419
to decrease time to engraftment, decrease incidence
of graft versus host disease, and improve overall
transplant survival.55
2. A syngeneic transplant is one in which bone marrow is
harvested from an identical twin.
3. An autologous transplant is one in which the donor and
recipient are the same. Bone marrow is harvested
from the patient when he or she is healthy or in com-
plete remission. The marrow is then frozen and
stored for future reinfusion.
Peripheral blood stem cells (PBSC) can be used in
either allogenic or autologous transplants. Stem cells
are primitive cells found in bone marrow or
circulating blood that evolve into mature blood cells
(white cells, red cells, and platelets). The patient’s
PBSCs are harvested by leukapheresis. During leuka-
pheresis, the patient’s blood is circulated through a
high-speed cell separator in which the peripheral
stem cells are frozen and stored, and the plasma cells
and erythrocytes are reinfused into the patient. The
patient may require three to seven harvests to achieve
an adequate number of stem cells.8 The PBSCs are
reinfused after the patient receives lethal doses of che-
motherapy, radiation, or both. Allogenic PBSC trans-
plant may be performed from a donor or by using
umbilical cord blood from a newborn.8 The hematolo-
gic recovery after PBSC transplant is 10 to 12 days,
which is approximately a week earlier than in
BMTs.50 This is because the stem cells procured from
the peripheral blood are more mature than those in
the bone marrow.
PBSC transplant is becoming more common
with faster immune recovery after allogenic trans-
plant and faster blood count recovery with autolo-
gous transplant when compared to bone marrow
transplantation. Some disadvantages include longer
process for donors and increased fluid to recipients
during transplantation with possible fluid overload to
the lungs.56
Indications for bone marrow transplantation
include the following11,50,53,57:
 Severe aplastic anemia
 Acute lymphocytic or myelogenous leukemia
 Chronic myelogenous leukemia
 Non-Hodgkin’s lymphoma
 Relapsed Hodgkin’s disease
 Multiple myeloma
 Neuroblastoma
 Testicular cancer
 Small cell lung cancer
 Breast cancer
420 CHAPTER 12 OrganTransplantation
Contraindications to bone marrow transplantation
include the following57:
 Inadequate cardiac function (left ventricular ejection
fraction less than 45%)
 Inadequate pulmonary function (forced expiratory
capacity and forced vital capacity less than 50%)
 Inadequate renal function (creatinine greater than
2 mg/dl)
 Inadequate hepatic function (bilirubin greater than
2 mg/dl)
Patient Preparation
Before the bone marrow transplantation, the recipient’s
body is deliberately immunosuppressed to gain the
greatest acceptance of the graft. The recipient under-
goes a 2- to 4-day cytoreduction protocol, consisting
of ablative chemotherapy, radiation, or both, designed
to destroy malignant cells and create space in the bone
marrow for the engraftment of new marrow.8,11,53
Harvesting Procedure and Indication of
Postprocedure Function
Bone marrow is harvested by multiple aspirations, most
commonly from the posterior and anterior iliac crests
of the donor or, less commonly, from the sternum.
Five hundred to 2,500 ml of aspirated marrow is fil-
tered, heparinized, mixed with peripheral blood,
frozen, and stored.11 One to three days after the last
dose of chemotherapy or radiation, the marrow is then
infused into the patient, much like a blood transfusion,
through a central venous access device or Hickman
right atrial catheter.8,58 The most common side effects
of reinfusion are fever, chills, nausea, headache, and
flushing. The stem cells from the marrow that were
infused migrate to the recipient’s marrow cavities,
mature, and begin to function 10 to 28 days posttrans-
plantation.53,58 A successful engraftment, which is indi-
cated by an increase in the platelet and WBC count, is
decided 10 to 20 days after transplantation.10,27,58
Postprocedure Care and Complications
All recipients undergoing bone marrow transplanta-
tion experience a period of bone marrow failure,
which generally begins within 10 days after the start of
chemotherapy or radiation and can last up to 3 weeks
after transplantation.53 During this time, recipients
may receive daily transfusions of platelets, lympho-
cytes, and granulocytes (preferably from the donor),
and antimicrobial therapy to counteract the side effects
of hemorrhage and infection.10,53 Daily bone marrow
aspirations and complete blood counts are performed
to monitor the progress of the grafts and to check for
recurrence of malignancy.
CLINICAL TIP
 Bone marrow transplantation recipients are very
susceptible to infection. When the patient’s
neutrophil count is less than 1,000/mm3, the patient
is placed on reverse protective isolation or
neutropenic precautions. Patients are placed in
reverse isolation in a private, sterile, laminar airflow
room. In the laminar airflow room, an air filtration
system preserves a sterile environment, and all items
entering the room must be sterile. Before entering
the patient’s room, physical therapists and other
hospital staff must thoroughly wash their hands and
wear a gown, and mask to maintain precautions.
Live plants and floral arrangements are not
permitted in the patient’s room, because they may
harbor bacteria and molds that may be harmful
to the patient during neutropenic episodes.
Any exercise equipment brought into the patient’s
room must be cleaned before entering the room.
 When the patient’s platelet count is 50,000/mm3
or less, the patient is placed on thrombocytopenic
precautions. Thrombocytopenic precautions are
observed (sometimes for months) until the platelet
count returns to normal. The physical therapist
should be aware of the recipient’s platelet count
before any treatment is initiated. Thrombocytopenia,
which occurs from chemotherapy, radiation, and the
underlying disease process, can cause spontaneous
bleeding. The most common bleeding sites include
the oral and nasal mucosa, the optic sclera, and the
epidermis (petechiae).53 Generally, patients with
platelet counts of 30,000/mm3 or greater are able to
tolerate moderate exercise if they are asymptomatic
and have no spontaneous hemorrhage.50 A patient
with platelet counts between 20,000/mm3 and
30,000/mm3 should only perform light exercise
consisting of active range of motion exercises and
ambulation as tolerated. Heavy resistance work
is contraindicated.50
 Caution should be used with patients who present
with temperature above 99.58 F.59
Bone marrow transplantation recipients are at risk
for fatal infection. Patients’ blood counts drop second-
ary to the cytoreduction therapy. Pancytopenia, which
is a marked reduction in red blood cells, WBCs, and
platelets, persists for at least 3 to 4 weeks after

transplantation. Normal immune function may not be
regained for 12 to 18 months, as it can take that long
for the transplanted immune system to mature and
develop normal function.11,58
Some major complications of BMT include infec-
tion, pneumonia, hemorrhage, marrow failure, veno-
occlusive disease of the liver, interstitial pneumonitis,
and graft versus host disease.8,11,19,46
Veno-occlusive disease is characterized by obstruc-
tion of the hepatic venules by deposits of collagen and
fibrin. Clinical manifestations of veno-occlusive
disease include sudden weight gain, increased LFTs,
hepatomegaly, right upper quadrant pain, ascites, and
jaundice.53 Veno-occlusive disease is related to the
amount of chemotherapy and radiation the patient
received before transplantation.Veno-occlusive disease
may occur 1 to 3 weeks after bone marrow transplanta-
tion and spontaneously resolves within 2 to 3 weeks in
approximately half of those affected.11
Graft versus host disease is a complication that
occurs in approximately 20% to 50% of allogeneic
transplant recipients.19 It does not occur in patients
with autologous bone marrow transplantation or
PBSC transplants.50 It is caused by the donor marrow’s
production of T lymphocytes that react immunologi-
cally to the host recipient. The peak onset is at 30 to
50 days after bone marrow transplantation. The major
organs affected by graft versus host disease are the
skin, liver, gastrointestinal tract, and lymphoid
system.8,53 Skin involvement manifests as an erythem-
atous rash that can progress to blistering and des-
quamation. Liver manifestations include increased
liver enzymes and bilirubin, right upper quadrant
pain, hepatomegaly, and jaundice. Gastrointestinal
tract manifestations include nausea, vomiting, diar-
rhea, malabsorption, ileus, sloughing of intestinal
mucosa, abdominal pain, cramping, and bloody
stools.8,53 Graft versus host disease is treated with
immunosuppressive medications, such as intravenous
methylprednisolone and oral prednisone.58
Physical Therapy for Bone Marrow
Transplantation Recipients
Physical therapy is beneficial to bone marrow trans-
plantation recipients during their long hospital stay.
Discharge from the hospital typically occurs 2 to
4 weeks posttransplantation. Prolonged bouts of
malaise, fever, diarrhea, nausea, and pain from inflam-
mation of mucous membranes of the mouth and
digestive tract that usually accompany bone mar-
row transplantation can be debilitating to patients.
OrganTransplantation CHAPTER 12 421
Initially, physical therapists provide a gentle exercise
program to prevent deconditioning and muscle atro-
phy from disuse and improve functional mobility as
patients slowly regain their strength. When patients
are confined to their rooms because of protective iso-
lation, they often use a stationary bicycle, treadmill,
or restorator (a portable device that a patient can
pedal seated at the bedside or in a chair) as part of
their exercise prescription. Recent evidence demon-
strates the benefits of a posttransplant exercise pro-
gram including possible decrease in fatique and time
in the hospital, as well as minimized WBC and platelet
drops frequently seen following transplantation.59
Bone marrow transplantation recipients typically
require 6 months to a year before they recover full
strength and return to a normal lifestyle.58
GENERAL PHYSICAL THERAPY
GUIDELINES FOR TRANSPLANT
RECIPIENTS
Physical therapists play an integral role in the rehabilita-
tion of transplant recipients. With the exception of
bone marrow transplantation recipients, the length of
stay in an acute care hospital, depending on the type
of organ transplantation and barring any complications,
ranges from 3 to 16 days: kidney, 3 to 7 days; liver,
heart, and lung, 10 to 14 days; pancreas, 5 to 12 days;
kidney-pancreas, 10 to 16 days.9,15,17,47 Given the short
length of stay for transplant recipients, physical thera-
pists are consulted in the early postoperative period to
provide treatment and assist the transplant team with a
safe discharge plan. If patients are medically stable but
need assistance for activities of daily living and ambula-
tion, they will require transfer to a rehabilitation facility
for further physical and occupational therapy before
discharge home.
Goals
In the acute care setting, the primary physical therapy
goals are similar to those of postoperative abdominal
or cardiothoracic surgical patients. They include maxi-
mizing functional mobility and endurance; improving
range of motion, strength, balance, and coordination;
and progressing the recipient to his or her maximum
independent functional level safely.
Many transplant recipients have experienced end-
stage organ disease for multiple years before receiving
their transplant and may present with other medical
422 CHAPTER 12 OrganTransplantation
comorbidities. As a result, they are usually physically
deconditioned and present with a marked reduction
in exercise capacity and skeletal muscle strength owing
to long-standing pretransplant physical inactivity. For
example, extreme fatigue and weakness are exhibited
in patients with chronic liver disease, reduced muscle
endurance is seen in patients with chronic heart failure,
and decreased oxygen uptake capacity is exhibited in
heart and lung disease.1 Generalized weakness results
from the disease process, fluid and electrolyte imbal-
ance, and poor nutrition. After their transplant, recipi-
ents generally require a longer time frame to regain
their strength and endurance and to achieve their goals.
Basic Concepts for the Treatment of
Transplant Recipients
 Coordinate the best time for physical therapy with
the patient’s nurse each day. The patient may be fati-
gued after nursing intervention or medically inap-
propriate for exercise owing to a decline in medical
status, especially in the intensive care unit or early
in the postoperative course.
 Analyze laboratory values daily, as they may change
dramatically from day to day. Many recipients have
very low platelet counts immediately posttransplan-
tation. Patients with low platelet counts or increased
PT/INR, PTT, or both are at risk for bleeding. It is
usually contraindicated to perform percussion on
patients with a platelet count less than 50,000/mm3.
Therefore, in this situation, bronchopulmonary
hygiene consists of coughing and performing deep-
breathing exercises, using the incentive spirometer,
and encouraging the patient to splint his or her inci-
sion to cough and mobilize to prevent pneumonia.
 Supine therapeutic exercise in the acute care setting is
implemented only if necessitated by the recipient’s
condition, such as high fever, chills, bed rest restric-
tion secondary to ventilator use, or low platelet
count. (A high temperature will result in elevated
respiratory and heart rates; therefore, it is important
to avoid strenuous cardiovascular and resisted exer-
cise during this time.)
 Generally, patients with an uncomplicated postoper-
ative course should be out of bed to chair and ambu-
lating in their rooms with assistance 24 to 48 hours
after surgery, with close monitoring of vital signs.
Early ambulation helps to decrease the risk of cardio-
vascular and pulmonary infection, increase blood
circulation, stimulate gastrointestinal function,
relieve gas pains, and maintain muscle tone.9,20
Many posttransplant patients retain fluid, especially
in the lower extremities.Weight bearing may be pain-
ful; however, ambulation for short periods of time
should still be encouraged. The recipient’s balance
may be altered secondary to increased fluid reten-
tion, and he or she may require the use of an assistive
device. The physical therapist will be required to
provide assistance or appropriate guarding to main-
tain maximum safety.
 Always monitor and document vital signs, oxygen
saturation, and RPE (for cardiac transplant recipi-
ents) before, during, and after physical therapy inter-
vention. Report any abnormal change in the
patient’s response to activity to the patient’s nurse.
An activity log or flow sheet may be used to docu-
ment daily progress or decline and vital sign
responses.
 Many patients experience some form of organ rejec-
tion. If approved by the transplant team, exercise
generally continues if their rejection episode is mild
to moderate.13,49
 The adverse effects of corticosteroids produce
delayed wound healing and can contribute to osteo-
porosis. Upper-extremity resistive training (for car-
diac and lung transplant recipients) should be
delayed until 6 weeks posttransplant, when wound
and tissue healing is complete.49 Patients should be
instructed in postural awareness, alignment, exer-
cise, and optimal body mechanics to combat the
effects of osteoporosis.44
 In addition to the recipient’s current medical status,
other preexisting impairments or medical condi-
tions, such as low back pain, peripheral neuropathy,
or arthritis, may affect the recipient’s activity toler-
ance. Thus, exercise should be modified according
to the patient’s ability.
Activity Progression
Activity is increased gradually, and treatment continues
until the patient is ambulating independently with suf-
ficient endurance to function safely at home. At first,
recipients will fatigue easily and require frequent rest
periods. Thus, shorter and more frequent treatment
sessions are beneficial to patients.
Ambulation is progressed in terms of frequency,
pace, and duration. Stair climbing is progressed with
the goal of achieving one to two flights of reciprocal
stair climbing as tolerated by each individual.
Patient Education
 Physical therapists assist in the education of transplant
recipients. Recipients must assume an active role in

their health care posttransplantation. Patients are edu-
cated about what to expect after transplantation.
Initially, the recipient is very weak and may have diffi-
culty learning during the early posttransplant rehabil-
itation phase. The physical therapist reinforces the
activity protocol with the patient. The transplant
teamusually providesthe recipientwith a comprehen-
sive guide that includes information on medications,
proper diet, exercise, and psychosocial changes. The
patient must adhere to the medication protocol post-
transplant and be able to monitor for signs and symp-
toms of infection, rejection, and toxicity to the
medications. Patients are instructed to monitor daily
their temperature and weight, inspect mouth and
gums, maintain proper oral hygiene, and report
fever or infectious symptoms.
 On discharge to home, transplant recipients
should participate in a daily home exercise routine.
The physical therapy department or the organ trans-
plant team may have preprinted exercise protocols.
Otherwise, the physical therapist should customize
an individual exercise program that consists of
stretching and strengthening exercises and a walking
or aerobic program that includes a warm-up and
References
1. OPTN. Latest Data. Available at: www.optn.org/
latestData. AccessedJuly 2007.
2. Kjaer M, Beyer N, Secher NH. Exercise and Organ
Transplantation. ScandJ Med Sci Sports 1999;9:1-14.
3. Doenges ME, Moorhouse MF, Geissler AC (eds),
Nursing Care Plans: Guidelines for
Individualizing Patient Care (4th ed). Philadelphia:
FA Davis, 1997;774.
4. NIH. Stem Cell Information: Stem Cell Basics.
Available at: http://stemcells.nih.gov/info/basics/
basics6.asp. AccessedJune 2008.
5. Arcasoy SE, Kotloff RM. LungTransplantation.
N EnglJ Med 1999;340(14):1081-1091.
6. Kesten S. Advances in LungTransplantation. Dis Mon
1999;45(3):101-114.
7. Becker C, Petlin A. Heart Transplantation: Minimizing
Mortality with Proper Management. AmJ Nurs
1999;(Suppl 5):8-14.
8. BlackJM, Matassarin-Jacobs E (eds). Medical-Surgical
Nursing: Clinical Management for Continuity of Care
(5th ed). Philadelphia: Saunders, 1997;584-585, 641-651,
1148, 1352-1353, 1898-1901, 1931.
OrganTransplantation CHAPTER 12 423
cool-down period. A gradual increase in ambulation
to at least 30 minutes a day is recommended. An
activity log may be used to document the patient’s
progress.
 Strenuous exercise and activities that stretch or put
pressure on the incision should be avoided until
approximately 2 months after discharge from the
hospital with clearance from the attending physician.
In addition, transplant recipients should avoid push-
ing, pulling, and lifting more than 10 lb until then.
Contact sports should be avoided for life after trans-
plantation to prevent trauma to the transplanted
organ.9
Organ transplantation provides a patient with end-
stage organ disease an opportunity to improve his or
her quality of life by receiving a donated organ, ‘‘the
gift of life.’’ With ongoing commitment and hard
work, transplant recipients can regain an independent,
healthy, and active lifestyle. The number and success
rate of organ transplantations will continue to grow
with continued advances in organ preservation, surgi-
cal techniques, tissue matching, immunosuppression
protocols, management and monitoring of rejection,
and antibiotic protocols.
9. Jenkins RL (ed), A Guide forTransplant Recipients.
Burlington, MA: Lahey Clinic, 2000.
10. Atkinson LJ, Howard, Fortunato N (eds),
Operating RoomTechnique (8th ed). Boston:
Mosby, 1996;897-912.
11. Monahan FD, Neighbors M. Medical-Surgical
Nursing (2nd ed). Philadelphia: Saunders,
1998;227-229, 480-483, 1196-1198, 1408-1411,
1448-1455, 1488-1491.
12. Winkel E, DiSesaVJ, Costanzo MR. Advances in
Heart Transplantation. Dis Mon 1999;45(3):62-87.
13. Sadowsky HS. CardiacTransplantation: A Review.
PhysTher 1996;76(5):498-515.
14. Smith SL.Tissue and OrganTransplantation. St. Louis:
Mosby, 1990;27-28, 179, 183, 202-203, 218, 220, 245, 257,
267, 287, 309.
15. Grenvik A, Ayres SM, et al. (eds).Textbook of
Critical Care (4th ed). Philadelphia: Saunders,
2000;1938-1985.
16. O’ConnellJB, Bourge RC, Costanzo-Nordin MR, et al.
CardiacTransplantation: Recipient Selection, Donor
Procurement, and Medical Follow-Up. Circulation
1992;86(3):1061-1075.
424 CHAPTER 12 OrganTransplantation
17. Gruessner RWG, Kendall DM, Drangstveit MB, et al.
Simultaneous Pancreas-KidneyTransplantation from
Live Donors. Ann Surg 1997;226(4):471-482.
18. Meyers BF, Patterson GA. LungTransplantation:
Current Status and Future Prospects.WorldJ Surg
1999;23:1156-1162.
19. HallJB, Schmidt GA,Wood LDH (eds), Principles of
Critical Care (2nd ed). NewYork: McGraw-Hill,
1998;1093-1094, 1325-1339.
20. LuckmannJ (ed). Medical-Surgical Nursing.
Philadelphia: Saunders, 1980;167, 1011.
21. Jenkins RL (ed), LiverTransplantation Protocol Manual.
Burlington, MA: Lahey Clinic, 1999;7, 8, 33, 37-41.
22. UNOS.Transplant Living: Organ Donation. Available
at: www.transplantliving.org//afterthetransplant/
medications/typesOfSuppressants. Accessed
October 2007.
23. Sheiner PA, MaglioccaJF, Bodian CA, et al. Long-Term
Medical Complications in Patients Surviving
 5 Years After LiverTransplant.Transplantation
2000;69(5):781-789.
24. Zavotsky KE, SapienzaJ,Wood D. Nursing
Implications for ED Care of Patients Who Have
Received Heart Transplants. J Emerg Nurs 2001;33-39.
25. Lynn-McHale D, Dorozinsky C. Cardiac Surgery and
Heart Transplantation. In L Bucher, S Melander (eds),
Critical Care Nursing. Philadelphia: Saunders,
1999;330-348.
26. Manske CL. Risks and Benefits of Kidney and Pancreas
Transplantation for Diabetic Patients. Diabetes Care
1999;22(Suppl 2):B114-B119.
27. Sigardson-Poor KM, Haggerty LM (eds), Nursing Care
of theTransplant Recipient. Philadelphia: Saunders,
1990;124, 149-151,187, 208, 210-211, 287.
28. Bartucci MR. KidneyTransplantation: State of the Art.
AACN Clin Issues 1999;10(2):153-163.
29. Pizer HF (ed), OrganTransplants: A Patient’s Guide.
Cambridge, MA: Harvard University Press, 1991;155.
30. Nolan MT, Augustine SM (ed),Transplantation
Nursing: Acute and Long-Term Management.
Stamford, CT: Appleton & Lange, 1995;201, 213-226.
31. Schluger LK, Klion FM.The Indications for and
Timing of LiverTransplantation. J Intensive Care Med
1999;14(3):109-116.
32. Cortazzo MH, Helkowski W, Pippin B, et al. Acute
Inpatient Rehabilitation of 55 Patients After Liver
Transplantation. AmJ Phys Med Rehabil
2005;84:880-884.
33. Busuttil RW, GossJA. Split LiverTransplantation.
Ann Surg 1999;229(3):313-321.
34. NeubergerJ. LiverTransplantation. QJM
1999;92:547-550.
35. Nunes F,Valente M, Pereira R, et al. Domino Liver
Transplant: Influence on the Number of Donors and
Transplant Coordination.Transplantation Proceedings
2004:36(4):916-917.
36. Wiesner RH, RakelaJ, Ishitani MB. Recent Advances
in LiverTransplantation. Mayo Clin Proc
2003;78(2):197-210.
37. CorreiaTD, Isabel M. Post-LiverTransplant Obesity and
Diabetes. Curr Opin Clin Nutr Metab Care
2003;6(4):457-460.
38. Shapira Z,Yussim A, Mor E. PancreasTransplantation.
J Pediatr Endocrinol Metab 1999;12(1):3-15.
39. Cicalese L, Giacomoni A, Rastellini C, et al. Pancreatic
Transplantation: A Review. Int Surg 1999;84:305-312.
40. Berkow R, Fletcher AJ. (eds),The Merck Manual
(16th ed). Rathway, NJ: Merck & Co, 1992;360-361.
41. Freise CE, Narumi S, Stock PG, et al. Simultaneous
Pancreas-KidneyTransplantation: An Overview of
Indications, Complications, and Outcomes.WestJ Med
1999;170(1):11-18.
42. McChesney LP. Advances in PancreasTransplantation for
theTreatment of Diabetes. Dis Mon1999;45(3):88-100.
43. Hricik DE. Combined Kidney-Pancreas
Transplantation. Kidney Int 1998;53:1091-1097.
44. Arthur EK. Rehabilitation of Potential and Cardiac
Transplant Recipients. Cardiopulmonary Rec APTA
Section 1986;1:11-13.
45. Fitzsimmons CL. Sensitivity,Ventricular Assist Devices,
and the Waiting Game in Heart Transplantation: What’s
New? Crit Care Nurs Q 2004;27(1):65-77.
46. Hillegass EA, Sadowsky HS (eds), Essentials of
Cardiopulmonary Physical Therapy. Philadelphia:
Saunders, 1994;165-166, 314-315.
47. Edinger KE, McKeen S, Bemis-DoughertyA, et al.
Physical Therapy Following Heart Transplant. PhysTher
Pract 1992;1(4):25-33.
48. Young MA, Stiens SA. Rehabilitation Aspects of Organ
Transplantation. In RL Braddom (ed), Physical
Medicine and Rehabilitation (2nd ed). Philadelphia:
Saunders, 2000;1385-1400.
49. Frownfelter D, Dean E (eds), Principles and Practice of
Cardiopulmonary Physical Therapy (3rd ed). St. Louis:
Mosby, 1996;703-719.
50. Goodman CC, Boissonnault WG (eds), Pathology:
Implications for the Physical Therapist. Philadelphia:
Saunders, 1998;120, 340-344, 363-366, 381,437-438.
51. Reichenspurner H, Dienemann H, Rihl M, et al.
Pulmonary Rejection Diagnosis After Lung and
Heart-LungTransplantation.Transplant Proc
1993;25(6):3299-3300.
52. Wells CL. LungTransplantation. Acute Care
Perspectives; Spring 2007:14-23.
53. James MC. Physical Therapy for Patients
After Bone MarrowTransplantation. PhysTher
1987;67(6):946-952.
54. Mathur S, Reid WD, Levy RD. Exercise Limitation
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2004;84(12):1178-1187.
55. Hurley CK, Baxter Lowe LA, Logan B, et al.
National Marrow Donor Program HLA-matching

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Biological Blood MarrowTransplant.
2003;9(10):610-615.
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1996;791-797.
OrganTransplantation CHAPTER 12 425
58. McGlave P. Hematopoietic Stem-Cell Transplantation
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2000;35(8):46, 49, 50.
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This page intentionally left blank.
 Appendix I-A The Medical Record
Michele P. West
INTRODUCTION
The medical record, whether paper or electronic, is a
legal document that chronicles a patient’s clinical
course during hospitalization and is the primary
means of communication between the various clini-
cians caring for a single patient. More specifically, the
medical record contains information about past or pres-
ent symptoms and disease(s), test and examination
results, interventions, and medical-surgical outcome.1
Additionally, the medical record may be used for qual-
ity improvement studies, conducting research, resol-
ving legal issues such as competency or disability, and
for education purposes.2
CONFIDENTIALITY
The medical record should be kept confidential, and all
health care providers should safeguard the availability
and integrity of health care information in oral, written,
or electronic forms.3 Specific topics, such as human im-
munodeficiency virus status, substance abuse, domestic
abuse, or psychiatric history, are privileged informa-
tion, and discussion of them is subject to additional eth-
ical and regulatory guidelines.4 The physical therapist
should comply with the Health Insurance Portability
and Accountability Act (HIPAA),5 the American
Physical Therapy Association’s Guide for Professional
Conduct and Code of Ethics,6 and any policies and pro-
cedures of the facility or state in regard to sharing med-
ical record information with the patient, family,
caretakers, visitors, or third parties.
CLINICAL TIP
 To ensure confidentiality of protected health
information (PHI) in the acute care setting, the
physical therapist should: log off the computer and
keep the written medical chart and flow books
closed when not in use, cover any paperwork kept
on clipboards when traveling in the facility, and
use discretion when discussing patient information
in shared rooms, hallways, and/or elevators.
DOCUMENTATION
The physical therapist should comply with the
documentation standards including, but not limited
to, the policies/procedures of the organization and
the state, the American Physical Therapy Associa-
tions Guidelines for Physical Therapy Documentation
of Patient/Client Management,7 and theJoint Commis-
sion (TJC) standards.8
In general, documentation must be:
 Dated and timed with an authenticated signature
 Complete and accurate
 Legible and in black ink (in a paper chart)
 Free of ambiguous or prohibitive abbreviations
 Entered in the medical record at the time
of intervention
COMPONENTS OF THE MEDICAL
RECORD
The organization of the medical record can vary from
institution to institution; however, the medical record
is typically composed of the following basic sections:
Orders
The order section is a log of all instructions of the plan
of care for the patient, including medications, diagnos-
tic or therapeutic tests and procedures, vital sign para-
meters, activity level, diet, the need for consultation
services, and resuscitation status. Orders may be written
by a physician, physician assistant, or nurse practitioner.
An order may be taken by a nurse or other health care
provider, including a physical therapist, according to
427
428 APPENDIX I-A The Medical Record
departmental, facility, and state policies. In the interest
of patient safety and error prevention, the process of
taking a verbal order has been minimized in many hos-
pitals.9 All (telephone) orders must be dated, timed,
and signed or cosigned by the appropriate personnel.
In addition, an order should be read back to the
person giving the order for the purpose of verification.9
CLINICAL TIP
 The order section of the patient’s medical record
should be reviewed prior to the initial and any
subsequent physical therapy intervention(s) for: the
actual order for physical therapy and the activity
level, vital sign parameters, and positioning
restrictions. Upon subsequent physical therapy
sessions, the review of the order section offers a
‘‘snapshot’’ of change(s) in a patient. Look for new
or discontinued medications, changes in PO status,
and new laboratory or diagnostic testing orders.
Admission Note Format
The following outline summarizes the basic format of
the initial admission note (often referred to as the
‘‘H&P’’or History and Physical, written by a physician,
physician’s assistant, or nurse practitioner in the medi-
cal record.10,11 The italicized items indicate the standard
information the physical therapist should review
before beginning an intervention.
I. History (subjective information)
A. Data that identify the patient, including the
source and degree of reliability of the
information.
B. History of present illness (HPI), including the chief
complaint and a chronologic list of the problems
associated with the chief complaint.
C. Medical or surgical history, risk factors for disease, and
allergies.
D. Family health history, including age and health or
age and cause ofdeath for immediate familymem-
bers as well as a relevant familial medical history.
E. Personal and social history, including occupation,
lifestyle, functional mobility status, the need for home or
outpatientservices, and architectural barriers at home.
F. Current medications, including level of compliance.
II. The physical examination (objective information).
Negative (normal) or positive (abnormal) findings are
described in detail according to the following outline:
A. General information, including vital signs,
laboratory findings, mental status, and appearance.
B. Head, eyes, ears, nose, throat (HEENT); and
neck
C. Chest
D. Heart (Cor)
E. Abdomen
F. Extremities
G. Neurologic system
III. Assessment. The assessment is a statement of the
condition and prognosis of the patient in regard
to the chief complaint and medical-surgical
status. If the etiology of the problem(s) is unclear,
then differential diagnoses are listed.
IV. Plan.The plan of care includes further observation,
tests, laboratory analysis, consultation with addi-
tional specialty services or providers, pharmaco-
logic therapies, other interventions, and discharge
planning.
Progress Notes
A progress note is a shortened version of the initial note
with an emphasis on any new physical findings, an
updated assessment, and plan. The progress note sec-
tion in a written record is typically multidisciplinary
with documentation from all caregivers in chronologic
order. Nursing documents its own admission assess-
ment, problem list, and care plan(s). Medication recon-
ciliation sheets, flow sheets, clinical pathways, consult
service notes from other physicians and allied health
professionals, and operative and procedural notes are
also included in this section.
Reports
Avariety of reports are filed chronologically in individ-
ual sections in the medical record (e.g., radiologic or
laboratory reports). Each report includes an interpreta-
tion or normal reference ranges, or both, for various
diagnostic or laboratory test results.

References
1. RoachWH, et al. Medical Record Entries. In Medical
Records and the Law. (4th ed). Boston: Jones and
Bartlett, 2006;51-61.
2. Monarch K. Documentation, Part 1: Principles for
Self-Protection. AJN 2007;107(7):58.
3. Protecting the Privacy of Patients’ Health Information.
U.S. Department of Health & Human Services.
Available at: http://www.hhs.gov/news/fcts/privacy.html.
Last accessed 10/16/2007.
4. Rutberg MP. Medical Records Confidentiality.
In MI Weintraub (ed), Neurologic Clinics:
Medical-Legal Issues Facing Neurologists. Neurol
Clin 1999;17:307-313.
5. Medical Privacy—National Standard to Protect the
Privacy of Personal Health Information. Office for
Civil Rights—HIPPA. Available at: http/www.hhs.gov/
ocr/hipaa/privacy.html. Last accessed
10/16/2007.
The Medical Record APPENDIX I-A 429
6. American Physical TherapyAssociation. Guide for
Professional Conduct and Code of Ethics. Available at:
http://www.apta.org. Last accessed 10/16/2007.
7. American Physical TherapyAssociation. Guidelines:
Physical Therapy Documentation of Patient/Client
Management BOD G03-05-16-41. Available at: http://
www.apta.org. Last accessed 10/16/2007.
8. TheJoint Commission. Official ‘‘Do Not Use’’ List.
Available at: http://www.jointcommission.org. Last
accessed 10/16/2007.
9. TheJoint Commission. Guidelines for Accepting and
TranscribingVerbal orTelephone Orders. Available at:
http://www.jcrinc.com. Last accessed 10/16/2007.
10. Swartz MH:The Clinical Record. In MH Swartz,
Textbook of Physical Diagnosis: History and
Examination. Philadelphia: WB Saunders, 1998;681-686.
11. Naumburg EH. Interviewing and the Health History.
Philadelphia: Lippincott, 1999;35-39.
 Appendix I-B Acute Care Setting
Michele P. West
INTRODUCTION
The physical therapist must have an appreciation for the
distinct aspects of inpatient acute care.The purpose of
this appendix is to briefly present information about
the acute care environment, including safety and the
use of physical restraints; the effects of prolonged bed
rest; end-of-life issues; and some of the unique circum-
stances, conditions, or patient responses encountered
in the hospital setting.
The acute care or hospital setting is a unique environ-
ment with protocols and standards of practice and safety
that may not be applicable to other areas of health care
delivery, such as an outpatient clinic or school system.
Hospitals are designed to accommodate a wide variety
of routine, urgent, or emergent patient care needs. The
staff and medical-surgical equipment (see Appendices
III-A to III-C) reflect these needs.The nature of the hos-
pital setting is to provide 24-hour care; thus, the patient,
family, and caregivers are faced with the physical, psycho-
logical, and emotional sequelae of illness and hospital-
ization. This can include the response(s) to a change in
daily routine; a lackof privacy and independence; or per-
haps a response to a potential lifestyle change, medical
crisis, critical illness, or long-term illness.
SAFE CAREGIVER AND PATIENT
ENVIRONMENT
Patient safety is a top priority. The physical therapist
should strive to keep the patient safe at all times,
comply with hospital initiatives that maximize patient
safety, and understand the Joint Commission’s (TJC)
annual National Patient Safety Goals. Basic guidelines
for providing a safe caregiver and patient environment
include the following:
 Always following Standard Precautions, including
thorough hand washing. Refer to Table 10-4 for a
summary of infection-prevention precautions,
including airborne, droplet, and contact precautions.
430
 Knowledge of the facility’s policy for accidental che-
mical, waste, or sharps exposure, as well as emer-
gency procedures for evacuation, fire, and natural
disaster. Know how to contact the employee health
service and hospital security.
 Confirm that you are with the correct patient prior to
initiating physical therapy intervention according to
the facilities policy. Most acute care hospitals require
two patient identifiers (by patient report or on an
identification bracelet) such as name and hospital
ID number. Notify the nurse if a patient is missing
an identification bracelet.
 Elevate the height of the bed as needed to ensure
proper body mechanics when performing a bedside
intervention (e.g., stretchingor bed mobility training).
 Leave the bed or chair (e.g., stretcher chair) in the
lowest position with wheels locked after physical
therapy intervention is complete. Leave the top bed
rails up for all patients.
 Only use equipment (e.g., assistive devices, recliner
chairs, wheelchairs) that is in good working condi-
tion. If equipment is unsafe, then label it as such
and contact the appropriate personnel to repair or
discard it.
 Keep the patient’s room as neat and clutter free as pos-
sible to minimize the risk of trips and falls. Pick up
objects that have fallen on the floor. Secure electrical
cords (e.g., for the bed or intravenous pumps) out of
the way. Keep small-sized equipment used for physi-
cal therapy intervention (e.g., cuff weights) in a
drawer or closet. Store assistive devices at the perime-
ter of the room when not in use. Do not block the
doorway or pathway to and from the patient’s bed.
 Provide enough light for the patient to move about
the room or read educational materials.
 Reorient a patient who is confused or disoriented.
In general, patients who are confused are assigned
rooms closer to the nursing station.
 Always leave the patient with the call bell or
other communication devices within close reach.
This includes eyeglasses and hearing aids.

 Make recommendations to nursing for the use of
bathroom equipment (e.g., tub bench or raised
toilet seat) if the patient has functional limitations
that may pose a safety risk.
 Dispose of linens, dressings, and garbage according
to the policies of the facility.
Latex Allergy
A latex allergy response is defined as ‘‘the state in which
an individual experiences an immunoglobulin E (IgE)-
mediated response to latex’’ from tactile, inhaled, or
ingested exposure to natural rubber latex.1 A latex reac-
tion may be immediate or delayed. Signs and symptoms
of an allergic reaction tolatex may include urticaria, con-
tact dermatitis, naso-rhinitis, upper respiratory tract
irritation, conjunctivitis, local angioedema, asthma,
hypotension, or even anaphylaxis.2
Natural rubber latex can be found in a multitude of
products and equipment found in the acute care setting.
These products most commonly used by the physical
therapist include gloves, stethoscopes, blood-pressure
cuffs, Ambu bags, adhesive tape, electrode pads, and
hand grips on assistive devices. If a patient has an
allergy or hypersensitivity to latex, then it is documen-
ted in the medical record, nursing cardex or report,
and at the patient’s bedside. Hospitals will provide a spe-
cial ‘‘latex-free kit,’’which consists of latex-free products
for use with the patient.
Recent research shows that health care providers
have an increase in sensitization and allergic symptoms
to natural rubber latex, in particular contact dermatitis,
rhinoconjunctivitis, and asthma.3 Health care providers
may be at risk for developing latex allergy from
increased exposure to latex in the work setting. If there
is a suspected latex hypersensitivity or allergy, then
seek assistance from the employee health office or a
primary care physician.
Use of Restraints
The use of a restraint may be indicated for the patient
who (1) is unconscious, (2) has altered mental status or
is at risk for wandering or pulling out lines and tubes,
(3) is unsafely mobile, (4) is physically aggressive, or
(5) is so active or agitated that essential medical-surgical
care cannot be completed.4 A restraint may be physical
or chemical. A physical restraint is defined as ‘‘any
manual method or physical or mechanical device, mate-
rial or equipment attached to or adjacent to a patient’s
body that he or she cannot easily remove, that restricts
freedom of movement or normal access to one’s
body.’’5 A chemical restraint is defined as ‘‘any
Acute Care Setting APPENDIX I-B 431
medication that is used for the specific purpose of
restricting the patients’ movement which is not a stan-
dard treatment for the patient medical or psychiatric
condition.’’5 The most common types of physical
restraints in the acute care setting are wrist or ankle
restraints, mitt restraints, or a vest restraint. The use of
restraint requires an order from a licensed independent
practitioner, which must be updated approximately
every 24 hours.6 A patient must be monitored on a fre-
quent basis, either continuously, hourly, or every 4 to
8 hours depending on the type of restraint used or
according to facility policy and procedure.6
General guidelines most applicable to the physical
therapist for the use of restraints include:
 Use a slipknot to secure a restraint rather than a
square knot. This ensures that the restraint can be
rapidly untied in an emergency.
 Do not secure the restraint to a moveable object
(e.g., the bed rail), to an object that the patient is not
lying or sitting on, or where the patient can easily
remove it.
 Ensure that the restraint is secure but not too tight.
Place two fingers between the restraint and the
patient to be sure circulation is not impaired.
 Always replace the restraint after a physical therapy
session.
 Be sure the patient does not trip on the ties or ‘‘tails’’
of the restraint during functional mobility training.
 Consult with the health care team to determine
whether a patient needs to have continued restraint
use, especially if you feel the patient’s behavior and
safety has improved.
The side effects of a chemical restraint may make a
patient drowsy or alter his or her mental status, thus
participation in a physicaltherapysession maybe limited.
EFFECTS OF PROLONGED BED REST
The effects of short-term (days to weeks) or long-term
(weeks to months) bed rest can be deleterious and
affect every organ system in the body. For the purposes
of this discussion, bed rest incorporates immobiliza-
tion, disuse, and recumbence with an end result of mul-
tisystem deconditioning. The physical therapist must
recognize that a patient in the acute care setting is
likely to have an alteration in physiology (i.e., a trau-
matic or medical-surgical disease or dysfunction) super-
imposed on bed rest, a second abnormal physiologic
state.7 The degree of impaired aerobic capacity is
directly related to the duration of bedrest.8
432 APPENDIX I-B Acute Care Setting
Most patients on bed rest have been in the intensive
care unit (ICU) for many weeks with multisystem
organ failure or hemodynamic instability requiring
sedation and mechanical ventilation. Other clinical
situations classically associated with long-term bed
rest include severe burns and multitrauma, spinal cord
injury, or grade IV nonhealing wounds of the lower
extremity or sacrum. It is beyond the scope of this
book to discuss in detail the effects of prolonged bed
rest; however, Table I-B.1 lists these major systematic
changes.
CLINICAL TIP
 Monitor vital signs carefully, especially during
mobilization out of bed for the first few times.
 Progressively raise the head of the bed before or
during a physical therapy session to allow blood
pressure to regulate.
 Use a tilt table if orthostatic hypotension persists
despite volume repletion, medication adjustments,
or therapeutic exercise.
 Time frames for physical therapy goals will likely be
longer for the patient who has been on prolonged
bed rest.
 Supplement formal physical therapy sessions with
independent or family-assisted therapeutic exercise
for a more timely recovery.
 Be aware of the psychosocial aspects of prolonged
bed rest. Sensory deprivation, boredom, depression,
and a sense of loss of control can occur.9 These
feelings may manifest as emotional lability or
irritability, and caregivers may incorrectly perceive
the patient to be uncooperative.
 As much as the patient wants to be off bed rest, the
patient will likely be fearful the first time out of
bed, especially if the patient has insight into his
or her muscular weakness and impaired aerobic
capacity.
 Leave the patient with necessities or commonly used
objects (e.g., the call bell, telephone, reading
material, beverages, tissues) within reach to
minimize the patient’s feelings of being confined
to bed.
END-OF-LIFE ISSUES
End-of-life issues are often complex moral, ethical, or
legal dilemmas, or a combination of these, regarding a
Table I-B.1 SYSTEMIC EFFECTS OF PROLONGED
BED REST
Body System Effects
Cardiac Increased heart rate at rest and with
submaximal exercise. Decreased
stroke volume and left ventricular
end-diastolic volume at rest.
:
Decreased cardiac output, VO 2 max
with submaximal and maximal
exercise.
Hematologic Decreased total blood volume, red
blood cell mass, and plasma
volume. Increased blood fibrinogen
and risk of venous thrombosis.
Respiratory Increased respiratory rate, forced vital
capacity, and total lung capacity
(slight). Increased risk of
pulmonary embolism and possible
ventilation-perfusion mismatch.
Gastrointestinal Decreased appetite, fluid intake, bowel
motility, and gastric secretion.
Genitourinary Increased mineral excretion, calculus
formation, difficulty voiding,
postvoid residuals, and overflow
incontinence. Decreased
glomerular filtration rate.
Endocrine Altered temperature and sweating
responses, circadian rhythm,
regulation of hormones, and
impaired glucose intolerance.
Musculoskeletal Muscle: increased muscle weakness
(especially in antigravity muscles),
atrophy, riskof contracture, weakened
myotendinous junction, and altered
muscle excitation. Bone: osteo-
porosis. Joints: degeneration of carti-
lage, synovial atrophy, and ankylosis.
Neurologic Sensory and sleep deprivation.
Decreased balance, coordination,
and visual acuity. Increased risk
of compression neuropathy.
Neurovascular Orthostatic hypotension.
Body Increased calcium, potassium,
composition phosphorus, sulfur, and nitrogen
loss; increased body fat and
decreased lean body mass.
:
V O 2 max, Maximum oxygen uptake.
Adapted from Buschbacher RM, Porter CD. Deconditioning,
Conditioning, and the Benefits of Exercise. In RL Braddom (ed),
Physical Medicine and Rehabilitation (2nd ed). Philadelphia: WB
Saunders, 2000;704.

patient’s vital physiologic functions, medical-surgical
prognosis, and quality of life as well as personal values
and beliefs.10 End-of-life issues facing patients, family,
and caregivers include the following:
Resuscitation Status
Do not resuscitate (DNR) is the predetermined deci-
sion to decline cardiopulmonary resuscitation, includ-
ing defibrillation and pharmacologic cardioversion in
case of cardiorespiratory arrest. Do not intubate
(DNI) is the predetermined decision to decline intuba-
tion for the purpose of subsequent mechanical ventila-
tion in case of respiratory arrest. DNR or DNI status is
officially documented in the medical record by the
attending physician. The acronym ‘‘DNAR’’ (Do not
attempt resuscitation) has been suggested for use
instead of DNR because DNR implies attempts to
resuscitate are inherently successful, which is not
always the case.11 The physical therapist must be aware
of each patient’s resuscitation or ‘‘code’’ status. DNR/
DNI orders do not directly affect the physical therapy
plan of care.
Withholding and Withdrawing Medical
Therapies
Withholding support is not initiating a therapy for the
patient, whereas withdrawing support is the disconti-
nuation of a therapy (usually after it has proven unbene-
ficial to the patient).12 Forgoing therapy is the
combination of withholding and withdrawing support
in which disease progression is allowed to take its
course.12 In the case of forgoing medical-surgical thera-
pies, an order for ‘‘comfort measures only’’ (CMO) is
written by the physician.The patient with comfort mea-
sures only status receives medications for pain control
or sedation, or to otherwise eliminate distress. The
patient on CMO status does not receive physical
therapy.
Palliative Care
Over the past few years, the concept of palliative care
has become an important component of acute care
with many hospitals creating palliative care teams.
Palliative care is defined as ‘‘an approach that improves
quality of life of patients and their families facing the
problems associated with life-threatening illness,
through the prevention and relief of suffering by
means of early identification and impeccable assess-
ment and treatment of pain and other problems, physi-
cal, psychosocial and spiritual.’’13 Palliative care is not
synonymous with hospice care in that the patient does
Acute Care Setting APPENDIX I-B 433
not have to forgo curative treatment and the prognosis
is not necessarily less than 6 months.14 Palliative care is
often interdisciplinary, including physical therapy,
with an emphasis on pain management or the relief of
other symptoms, functional training, or the use of
modalities/therapeutic exercise to improve the quality
of life. The role of physical therapy in hospital-based
palliative care may be consultative or ongoing.
Coma, Vegetative State, and Brain Death
The diagnosis of coma, vegetative state, or brain death
can be devastating.These conditions are very similar in
that there is unconsciousness and absent self-awareness,
but distinctions do exist in terms of neurologic function
and recovery. Coma is a sustained limited state of arousal
characterized by a lack of responsiveness to stimuli,
voluntary movement, and sleep-wake cycles.15
Characteristics of vegetative state (VS) include the pres-
ence of sleep-wake cycles and partial or complete hypo-
thalamic and autonomic brain stem functions but a lack
of cerebral cortical function for longer than 1 month
after acute traumatic or nontraumatic brain injury or
metabolic or degenerative disorders.15 The clinical crite-
ria for brain death include the absence of brain stem
reflexes, apnea, and hypothermia in the setting of a
known irreversible cause.16 Brain death is usually con-
firmed by cerebral angiography, evoked potential test-
ing, electroencephalography, or transcranial Doppler
sonography.17 Refer to Chapter 4 for more information
on these neurologic diagnostic tests.
The term minimallyconsciousstate has recently been used
in the literature to describe a low level of consciousness
in which there is evidence of self or environmental
awareness. The patient in a minimally conscious
state can follow simple commands, gesture, verbalize
and express yes/no, and demonstrate purposeful
behavior.15
INTENSIVE CARE UNIT SETTING
The ICU, as its name suggests, is a place of intensive
medical-surgical care for patients who require continu-
ous monitoring, usually in conjunction with therapies
such as vasoactive medications, sedation, circulatory
assist devices, and mechanical ventilation. ICUs may
be named according to the specialized care that they
provide, such as the coronary care unit (CCU) or surgi-
cal ICU (SICU). The patient in the ICU requires a
high acuity of care; thus, the nurse to patient ratio is
1:1 or 1:2.
434 APPENDIX I-B Acute Care Setting
Common Patient and Family Responses to
the Intensive Care Unit
 Behavioral changes or disturbances can occur in the
patient who is critically ill as a result of distress
caused by physically or psychologically invasive,
communication-impairing, or movement-restricting
procedures.18 When combined with the environ-
mental and psychological reactions to the ICU,
mental status and personality can be altered.
Environmental stresses can include crowding,
bright overhead lighting, strong odors, noise, and
touch associated with procedures or from those the
patient cannot see.18 Psychological stresses can
include diminished dignity and self-esteem, power-
lessness, vulnerability, fear, anxiety, isolation, and
spiritual distress.18
 An acute state of delirium, often termed ICUpsychosis,
encephalopathy, or acute confusional state, is a state of deliri-
um that can occur within hours or days of admission
to the ICU. Delirium is a ‘‘global disturbance in cog-
nitive function that is characterized by impaired
attention associated with changes in level of con-
sciousness, disorganized thinking’’ in a fluctuating
course of which arousal and awareness are retained.19
Delirium in the ICU, which is reversible, is associated
with many precipitating factors including infection,
hypoxia, substance withdrawal, mechanical ventila-
tion, opioid and benzodiazepine use, restraints,
sleep deprivation, and the ICU environment.19 Risk
factors associated with delirium in the ICU include
male gender, advanced age, malnutrition, poor func-
tional status, and a history of dementia.19 Treatment
for delirium consists of addressing precipitating fac-
tors, antipsychotic medications (e.g., haloperidol),
the discontinuation of nonessential medications,
proper oxygenation and hydration, and the company
of family or others.20
 The patient’s family is usually overwhelmed by the
ICU. Family members may experience fear, shock,
anxiety, helplessness, anger, hostility, guilt, withdra-
wal, or disruptive behaviors.18 Like the patient, the
family may be overwhelmed by the stimuli and tech-
nology of the ICU, as well as the stress of a loved
one’s facing a critical or life-threatening illness.
 The transfer of a patient from the ICU to a general
floor can also be a stress to the patient and family.
Referred to as transfer anxiety, the patient and family
may voice concerns of leaving staff that they have
come to recognize and know by name; they may
have to learn to trust new staff,18 or fear that the
level of care is inferior to that in the ICU.To minimize
this anxiety, the physical therapist may continue to
treat the patient (if staffing allows), slowly transition
care to another therapist, or reinforce with the
patient and family that the general goals of physical
therapy are unchanged.
Critical Illness Polyneuropathy
Critical illness polyneuropathy (CIP), otherwise known
as ICU neuropathy or the neuropathy of critical illness, is the
acute or subacute onset of widespread symmetric weak-
ness in the patient with critical illness, most commonly
with sepsis or multisystem organ failure, or both.21
The patient presents with distal extremity weakness,
wasting, and sensory loss, as well as parasthesia and
decreased or absent deep tendon reflexes.22 CIP is
often first discovered when the mechanically ventilated
patient fails to wean from the ventilator or when heavy
sedation is discontinued and the patient cannot move
his or her extremities.23 The clinical features that distin-
guish CIP from other neuromuscular disorders (e.g.,
Guillain-Barre¤ syndrome) are a lack of ophthalmople-
gia, dysautonomia, and cranial nerve involvement and
normal cerebrospinal fluid analysis.21,24 Nerve conduc-
tion studies show decreased motor and sensory action
potentials.24 The specific pathophysiology of critical ill-
ness polyneuropathy is unknown; however, it is
hypothesized to be related to drug, nutritional, meta-
bolic, and toxic factors, as well as prolonged ICU stay,
the number of invasive procedures, increased glucose
level, decreased albumin level, and the severity of multi-
system organ failure.24 There is no proven treatment
for CIP, however, an intensive insulin regimen has
been associated with a lower incidence of CIP.23
Critical Illness Myopathy
Critical illness myopathy (CIM), otherwise known as
acute quadriplegic myopathy or acute steroid myopathy, is the
acute or subacute onset of diffuse quadriparesis, respi-
ratory muscle weakness, and decreased deep tendon
reflexes24 in the setting of exposure to short-term or
long-term high-dose corticosteroids and simultaneous
neuromuscular blockade.25 It is postulated that neuro-
muscular blockade causes a functional denervation
that renders muscle fibers vulnerable to the catabolic
effects of steroids.25 Muscle weakness appears to affect
large proximal muscles, and sensation typically remains
intact.22 Diagnostic tests demonstrate elevated serum
creatine kinase levels at the onset of the myopathy. If
severe, myoglobinuria or renal failure, a myopathic pat-
tern with muscle fibrillation on electromyography, and

necrosis with dramatic loss of myosin (thick) filaments
on muscle biopsy can ensue.25
SLEEP PATTERN DISTURBANCE
The interruption or deprivation of the quality or hours
of sleep or rest can interfere with a patient’s energy
level, personality, and ability to heal and perform
tasks. The defining characteristics of sleep pattern dis-
turbance are difficulty falling or remaining asleep,
with or without fatigue on awakening, dozing during
the day, and mood alterations.26
In the acute care setting, sleep disturbance may be
relatedto frequentawakeningsrelatedtoa medicalproce-
dure or the need for nursing intervention (e.g., vital sign
monitoring); pain; an inability to assume normal sleep-
ing position; loss of routine or privacy; elevated noise
level; and excessive daytime sleeping related to medica-
tion side effects, stress, or environmental changes.27
Sleep pattern disturbance is often more prevalent in the
older adult population due to changes in circadian
rhythms, coexisting health conditions, and dementia.28
The physical therapist should be aware of the patient
who has altered sleep patterns or difficulty sleeping, as
lack of sleep can affect a patient’s ability to participate
during a therapy session. The patient may have trouble
concentrating and performing higher-level cognitive
tasks. The pain threshold may be decreased, and the
patient may also exhibit decreased emotional control.26
SUBSTANCE ABUSE AND WITHDRAWAL
The casual or habitual abuse of alcohol, drugs
(e.g., cocaine), or medications (e.g., opioids) is a known
contributor of acute and chronic illness, traumatic acci-
dents, drowning, burn injury, and suicide.29 The patient
in the acute care setting may present with acute intoxica-
tion or drug overdose or with a known (i.e., documented)
or unknown substance abuse problem.
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Acute Care Setting APPENDIX I-B 435
The physical therapist is not initially involved in the
care of the patient with acute intoxication or overdose
until the patient is medically stable. However, the phys-
ical therapist may become secondarily involved when
the patient presents with impaired strength, balance,
coordination, and functional mobility as a result of
chemical toxicity.
It is the patient with unknown substance abuse who
is hospitalized for days to weeks who is a challenge to
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For the purposes of this text, alcohol withdrawal will
be discussed because of its relatively high occurrence.
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 Fluid and
Appendix II Electrolyte Imbalances
Susan Polich and Jaime C. Paz
Many causes and factors can alter a patient’s fluid and
electrolytebalance.These imbalances can result in a mul-
titude of clinical manifestations, which in turn can
affect a patient’s functional mobility and activity toler-
ance. Recognizing the signs and symptoms of electrolyte
imbalance is, therefore, an important aspect of physical
therapy. Additionally, the physical therapist must be
aware of which patients are at risk for these imbalances,
as well as the concurrent pathogenesis, diagnosis, and
medical management of these imbalances.
Maintaining homeostasis between intracellular
fluid, extracellular fluid, and electrolytes is necessary
to allow proper cell function. Proper homeostasis
depends on the following factors:
 Concentration of intracellular and extracellular
fluids
 Type and concentration of electrolytes
 Permeability of cell membranes
 Kidney function
FLUID IMBALANCE
Fluid imbalance occurs when fluids are lost (either by
loss of body water or failure to intake) or gained (either
by fluid shift from the vasculature to the cell space or
excessive intake without proper elimination).1-3
Loss of bodily fluid (hypovolemia) can occur from
loss of blood (hemorrhage), loss of plasma (burns), or
loss of body water (vomiting, diarrhea). Hypovolemia
can also result from a fluid shift into the interstitial
spaces such as ascites caused by liver failure or pleural
effusion from heart failure. Any of these situations
can result in dehydration, hypovolemia, or shock
in extreme cases. Clinical manifestations include
decreased blood pressure, increased heart rate, changes
in mental status, thirst, dizziness, hypernatremia,
increased core body temperature, weakness, poor skin
turgor, altered respirations, and orthostatic hypoten-
sion.1-5 Clinical manifestations in children also include
poor capillary refill, absent tears, and dry mucous
membranes.5
Excessive bodily fluid (hypervolemia) can occur
when there is a shift of water from the vascular system
to the intracellular space, excessive sodium or fluid
intake, or sodium or fluid retention. Acute or chronic
renal failure can also result in hypervolemia. This can
result from excessive pressure in the vasculature (ventri-
cular failure), loss of serum albumin (liver failure), or
fluid overload (excessive rehydration during surgery).
Clinical manifestations of fluid overload include
weight gain, pulmonary edema, peripheral edema,
and bounding pulse. Clinical manifestations of this
fluid shift may also resemble those of dehydration
(e.g., tachycardia and hypotension), as there is a resul-
tant decrease in the intravascular fluid volume.1-3,5
Table II-1 provides an overview of hypovolemia and
hypervolemia.
CLINICAL TIP
 During casual conversation among physicians
and nurses, patients who are hypovolemic are
often referred to as being dry, whereas
patients who are hypervolemic are referred to
as being wet.
 Patients with interstitial edema may often be
referred to as third-spacing or auto-diuresing.
Both terms refer to the shift of fluid volume
from intravascular to extravascular spaces.
ELECTROLYTE IMBALANCE
Fluid imbalances are often accompanied by changes in
electrolytes. Loss or gain of body water is usually accom-
panied by a loss or gain of electrolytes. Similarly, a
change in electrolyte balance often affects fluid balance.
Cellular functions that are reliant on proper electrolyte
balance include neuromuscular excitability, secretory
activity, and membrane permeability.10 Clinical manifes-
tations will vary depending on the severity of the imbal-
ance and can include those noted in the Fluid
437
438 APPENDIX II Fluid and Electrolyte Imbalances
Table II-1 FLUID AND ELECTROLYTE IMBALANCES
Imbalance Definition Contributing Factors
Hypovolemia Fluid volume Vomiting, diarrhea,
deficit fever, blood loss,
uncontrolled
diabetes mellitus
Hypervolemia Fluid volume Renal failure, congestive heart Shortness of breath;
excess failure, blood transfusion,
prolonged corticosteroid
therapy
Hyponatremia Sodium deficit SIADH (refer to Chapter11);
(serum diuretic therapy; renal
sodium level disease; excessive
< 135 mEq/L) sweating; hyperglycemia;
NPO status; congestive
heart failure; side effects
from anticonvulsants,
antidiabetics,
antineoplastics,
antipsychotics, and sedatives
Hypernatremia Sodium Water deficit; diabetes
excess (serum insipidus; diarrhea;
sodium level hyperventilation;
> 145 mEq/L) excessive administration
of corticosteroid,
sodium bicarbonate,
or sodium chloride
Hypokalemia Potassium deficit Inadequate potassium intake, Fatigue; muscle weakness; STdepression or
(serum diarrhea, vomiting,
potassium chronic renal disease,
level of < 3.5 gastric suction, polyuria,
mEq/L) corticosteroid therapy,
digoxin therapy
Hyperkalemia Potassium excess Excessive potassium intake,
(serum renal failure, Addison’s
potassium disease, burns, use of
level of > 5 potassium-conserving
mEq/L) diuretics, ACE inhibitors,
NSAIDs, chronic heparin
therapy
BP, Blood pressure; BUN, blood urea nitrogen; ECG, electrocardiogram; NPO, nothing by mouth; SIADH, syndrome of inappropriate
antidiuretic hormone secretion; ACE, angiotensin converting enzyme; NSAIDs, nonsteroidal antiinflammatory drugs.
Data from references 6-10.
Clinical Manifestations Diagnostic Test Findings
Weak, rapid pulse; Decreased hemoglobin
decreased BP; dizziness; and hematocrit with
thirst; cool, pale skin whole blood loss;
over extremities; increased hematocrit
confusion; muscle with plasma fluid shift
cramps from intravascular to
interstitial spaces;
increased BUN,
serum sodium levels
Decreased hematocrit,
increased BP; bounding BUN; normal serum
pulse; presence of an sodium levels with
S3 heart sound and decreased potassium
cough if heart is failing; levels
dependent edema
Lethargy, nausea, Decreased urine and
apathy, muscle serum sodium levels;
cramps, muscular elevated hematocrit
twitching, confusion and plasma protein
(in severe states) levels
Elevated body Increased serum sodium
temperature; lethargy and decreased urine
or restlessness; thirst; sodium levels
dry, flushed skin;
weakness; irritability;
hyperreflexia; ataxia;
tremors; tachycardia;
hypertension or
hypotension; oliguria;
pulmonary edema
slow, weak pulse; prolonged PR interval
ventricular fibrillation; on ECG, increased
paresthesias; leg arterial pH and
cramps; constipation; bicarbonate levels,
decreased blood presure slightly elevated
glucose levels
Vague muscle weakness, STdepression; tall,
nausea, initial tented T waves; or
tachycardia followed by absent P waves on
bradycardia, ECG, decreased
dysrhythmia, flaccid arterial pH level
paralysis, paresthesia,
irritability, anxiety
 Fluid and Electrolyte Imbalances
FIGURE II-1
Schematic representation of electrolyte levels. BUN, Blood urea
nitrogen; BS, blood sugar; Cl, chloride; Cr, creatinine; HCO3,
bicarbonate; K, potassium; Na, sodium.
Imbalance section. In extreme cases, muscle tetany and
coma can also occur. Common electrolyte imbalances
are further summarized in Table II-1. Alterations in
arterial blood gas (ABG) levels are also considered
electrolyte imbalances.11 Note: electrolyte imbalances
can also occur from alterations in calcium (Ca++),
magnesium (Mg++), and phosphorus (phosphate), but
these are beyond the scope of this book.
CLINICAL TIP
 Electrolyte levels are generally represented
schematically in the medical record in a sawhorse
figure, as shown in Figure II-1. Electrolytes that are
out of reference range are either highlighted with a
circle or annotated with an arrow (" or #) to denote
its relationship to reference value.
Medical management includes diagnosing and
monitoring electrolyte imbalances via blood and urine
tests. These tests include measuring levels of sodium,
potassium, chloride, and calcium in blood and urine;
References
1. Rose BD (ed), Clinical Physiology of Acid-Base and
Electrolyte Disorders (2nd ed). NewYork: McGraw-Hill,
1984.
2. Cotran RS, Kumar V, Robbins S, et al. (eds), Robbins
Pathologic Basis of Disease. Philadelphia: Saunders,
1994.
3. KokkoJ,Tannen R (eds), Fluids and Electrolytes
(2nd ed). Philadelphia: Saunders, 1990.
4. McGee S, Abernethy WB III, Simel DL. Is this patient
hypovolemic? JAMA 1999;281(11):1022-1029.
APPENDIX II 439
arterial blood gases; and serum and urine osmolality.
Treatment involves managing the primary cause of the
imbalance(s), along with providing supportive care
with intravenous or oral fluids, electrolyte supplemen-
tation, and diet modifications.
CLINICAL TIP
 Review the medical record closely for any fluid
restrictions that may be ordered for a patient with
hypervolemia. These restrictions may also be posted
at the patient’s bedside.
 Conversely, ensure proper fluid intake before,
during, and after physical therapy intervention with
patients who are hypovolemic.
 Patients who are hypovolemic are at risk for
orthostatic hypotension, therefore monitor vital
signs carefully and proceed with upright activities
very gradually.
 Slight potassium imbalances can have significant
effects on cardiac rhythms; therefore, carefully
monitor the patient’s cardiac rhythm before,
during, and after physical therapy intervention.
If the patient is not on a cardiac monitor, then
consult with the nurse or physician regarding
the appropriateness of physical therapy
intervention with a patient who has potassium
imbalance.
 Refer to Chapter 1 for more information on
cardiac arrhythmias.
 Refer to Chapter 2 for more information on ABGs.
 Refer to Chapter 9 for more information on fluid
and electrolyte imbalances caused by renal
dysfunction.
 Refer to Chapter 11 for more information on fluid
and electrolyte imbalances caused by endocrine
dysfunction.
5. Springhouse. Portable Fluids & Electrolytes.
Philadelphia: Lippincott William & Wilkins, 2008.
6. Gorelick MH, Shaw KN, Murphy KO.Validity
and Reliability of Clinical Signs in the Diagnosis
of Dehydration in Children. Pediatrics 1997;99
(5):E6.
7. Mulvey M. Fluid and Electrolytes: Balance and
Disorders. In SC Smeltzer, BG Bare (eds), Brunner and
Suddarth’sTextbook of Medical-Surgical Nursing
(8th ed). Philadelphia: Lippincott, 1996.
440 APPENDIX II Fluid and Electrolyte Imbalances

8. Goodman CC, Kelly SnyderTE. Problems Affecting 11. Fukagawa M, Kurokawa K, Papadakis MA.
Multiple Systems. In CC Goodman,WG Boissonnault Fluid & Electrolyte Disorders. In LM Tierney,
(eds), Pathology: Implications for the Physical SJ McPhee, MA Papadakis (eds), Current Medical
Therapist. Philadelphia: Saunders, 1998. Diagnosis & Treatment. NewYork:
9. Fall PJ. Hyponatremia and Hypernatremia: A McGraw Hill, 2007.
Systematic Approach to Causes and Their Correction.
Postgrad Med 2000;107(5):75-82.
10. Marieb EN (ed), Human Anatomy and Physiology
(2nd ed). Redwood City, CA: Benjamin Cummings,
1992;911.
 Medical-Surgical Equipment
Appendix III-A in the Acute Care Setting
Eileen F. Lang and Michele P. West
INTRODUCTION
The purpose of this appendix is to (1) describe the var-
ious types of medical-surgical equipment commonly
used in the acute care setting, including oxygen (O2)
therapy and noninvasive and invasive monitoring and
management devices, and (2) provide a framework for
the safe use of such equipment during physical therapy
intervention.
Some equipment is used in all areas of the hospital,
whereas other types of equipment are used only in
specialty areas, such as the intensive care unit (ICU).
The ICU, otherwise known as the critical care unit, is
defined as ‘‘a place for the monitoring and care of
patients with potentially severe physiological instability
requiring technical and/or artificial life support.’’1 The
presence of certain types of equipment in a patient’s
room can provide the physical therapist with a prelimi-
nary idea of the patient’s general medical condition
and the appropriateness of therapeutic or prophylactic
physical therapy intervention, or both. The physical
therapist may initially be intimidated by the abundance
of medical-surgical equipment (especially in the ICU);
however, a proper orientation to such equipment
allows the physical therapist to appropriately intervene
with safety and confidence.
OXYGEN THERAPY
The general indication for O2 therapy is hypoxemia.
Hypoxemia is considered to be present when the arteri-
al oxyhemoglobin saturation (SaO2) is less than 90%,
corresponding to an arterial blood O2 partial pressure
(PaO2) of less than 60 mm Hg.2 Refer to Table 2-5 for
the relation between O2 saturation as measured by
pulse oximetry (SpO2) and PaO2 and to Figure 2-7 for
the oxyhemoglobin dissociation curve. The goal of O2
therapy is to treat and prevent hypoxemia, excessive
work of breathing, and excessive myocardial work by
increasing the PaO2.3
O2 moves across the alveolar-capillary membrane by
diffusion, the physiologic mechanism by which gas
moves across a membrane from a region of higher to
lower pressure and is driven by the partial pressure gra-
dient of O2 between alveolar air (PaO2) and pulmonary
capillary blood. To improve diffusion, a rise in PaO2
can be attained by increasing the fraction of inspired
O2 (FiO2) with supplemental O2.4
Supplemental O2 is delivered by variable perfor-
mance (Table III-A.1) or fixed performance (Table
III-A.2) systems. Each cannula or mask is designed to
provide a range of FiO2. A variable performance
system should not be used if a specific FiO2 is required.
Variable performance systems are not intended to
meet the total inspiratory requirements of the patient.
The actual FiO2 for a given flow rate in a variable
system is dependent on a patient’s tidal volume and
respiratory rate, and the type, fit, and placement of the
cannula or mask. If a specific FiO2 is required, then a
fixed performance system is indicated. Fixed perfor-
mance systems deliver a specific FiO2 despite the
patient’s respiratory rate and pattern.4
O2 deliverydevices with masks or reservoirs allow O2
to collect about the nose and mouth during exhalation,
which increases the availability of O2 during inhalation.
As the storage capacity of the mask or reservoir is
increased, the FiO2 for a given flow rate is also increased.4
The supplemental O2 requirements of a patient may
fluctuate with activity. Monitoring SaO2 with pulse ox-
imetry (identified as SpO2) and subsequent titration
(weaning) of O2 may be indicated during exercise. The
physician may order parameters for resting and exercise
SpO2 if a patient has a low activity tolerance or an abnor-
mally low SpO2 at baseline.
A patient with chronic obstructive pulmonary dis-
ease who has chronic carbon dioxide retention may
become desensitized to the respiratory stimulant effects
of carbon dioxide. In these patients, ventilation is
driven by means of a reflex ventilatory response to a
decrease in PaO2 originating in the aortic and carotid
bodies.5 In theory, providing supplemental O2 may
lead to a reduction in the hypoxic ventilatory drive.
441
442 APPENDIX III-A Medical-Surgical Equipment in the Acute Care Setting

Table III-A.1 VARIABLE PERFORMANCE OXYGEN DELIVERY FOR SPONTANEOUSLY BREATHING ADULTS*
Device/FiO2 Description
Nasal cannula Purpose:
RA
21% FiO2 Delivers supplemental O2 mixed with RA, usually 1-6 lpm.
1 lpm
24% FiO2 Consists of:
2 lpm
28% FiO2 Prongs, which are attached to an O2 source via small-bore plastic tubing and are
3 lpm
32% FiO2 positioned in the patient’s nose.The tubing is secured by placing it behind the patient’s
4 lpm
36% FiO2 ears and under the patient’s chin (Figure III-A.1, A).
5 lpm
40% FiO2 Clinical implications:
6 lpm
44% FiO2 The rule of thumb for the cannula system is that FiO2 is increased by 3-4% for each lpm
of O2.
Mouth breathing does not necessarily indicate that a patient is not receiving
supplemental O2.
If nasal passages are obstructed, O2 is able to collect in the oral and nasal cavities and is
drawn in on inspiration.
Flow rates of greater than 6 lpm are unlikely to increase delivered O2 further and may
prove uncomfortable and lead to mucosa irritation.
Provide mobile patients with adequate lengths of extension tubing or a portable O2 tank
to enable functional mobility. Patients should be instructed to avoid tripping over or
becoming tangled in the tubing.
Ensure that the cannula tubing is in place without kinks or external compression during
and after a physical therapy session.
The tubing may lead to irritation or skin breakdown behind the ears of some patients.
Soft gauze padding may be placed around the tubing to protect the patient’s skin.
Open face tent Purpose:
FiO2
30-55% Provides humidified, supplemental O2 mixed with RA.
Consists of:
A mask with straps under the chin, contacts the cheeks, and is open over the patient’s
nose. It is secured with an elastic strap around the patient’s head. It connects to a
humidified O2 source with large-bore tubing (Figure III-A.1, B).
Clinical implications:
A significant amount of mixing with RA occurs, although the capacity of the mask
allows O2 to collect about the nose and mouth.
May be more comfortable than a closed face mask for claustrophobic patients
or for patients with facial trauma.
Moisture may collect in the tubing and should be drained before moving the patient.
The aerosol system is more cumbersome and may make mobilization of the
patient more difficult than with nasal prongs. Collaborate with nursing to
determine whether nasal prongs or a closed face mask can be used when
mobilizing the patient.
Titrate O2 appropriately to maintain O2 saturation as indicated.
Closed face mask Purpose:
5-6 lpm
40% FiO2 Delivers supplemental O2 mixed with RA.The mask has a small capacity but does allow
6-7 lpm
50% FiO2 for the collection of O2 about the nose and mouth.
7-8 lpm
60% FiO2 Consists of:
A dome-shaped mask covering the nose and mouth with ventilation holes on either side.
An elastic strap around the patient’s head secures it in place. It is connected to an O2
source via small-bore tubing (Figure III-A.1, C).
Clinical implications:
The closed face mask interferes with coughing, talking, eating, and drinking and may be
very drying and uncomfortable. Patients often remove the mask for these reasons.
Educate the patient on the importance of keeping the mask in place.
 Medical-Surgical Equipment in the Acute Care Setting APPENDIX III-A 443

Table III-A.1 VARIABLE PERFORMANCE OXYGEN DELIVERY FOR SPONTANEOUSLY BREATHING

ADULTS*—cont’d

Device/FiO2 Description
Transtracheal catheter Purpose:
1 lpm
28% FiO2 Used for long-term O2 therapy. Provides continuous supplemental O2 mixed with RA.
2 lpm
36% FiO2 Consists of:
3 lpm
44% FiO2 A small-bore catheter, which is surgically inserted percutaneously between the second
4 lpm
52% FiO2 and third tracheal interspaces to provide O2. It is held in place by a narrow strap or
5 lpm
60% FiO2 chain around the patient’s neck. A low flow rate (approximately one-half with rest and
6 lpm
68% FiO2 two-thirds with exercise) is used instead of a nasal cannula system owing to the
continuous enrichment of the anatomic dead space with O2.
Clinical implications:
Patients with severe bronchospasm, uncompensated respiratory acidosis (pH <7.3),
or steroid use higher than 30 mg per day are excluded from the use of this device.
The use of this device for O2 delivery is delayed for 1 wk postoperatively to ensure that
a permanent tract is formed between the trachea and skin.
This device requires care and attention to hygienic maintenance.The most serious
complication is tracheal obstruction resulting from the accumulation of mucus on the
outside of the catheter, which can be avoided by routine secretion clearance multiple
times per day.
There is also a risk of infection around the catheter site and a risk of catheter
dislodgement.
Tracheostomy mask Purpose:
or collar Provides supplemental, humidified O2 or air at a tracheostomy site.
FiO2
28-100% Consists of:
A mask placed over a stoma or tracheostomy. It is held in place by an elastic strap
around the patient’s neck. Humidified O2 is delivered by large bore tubing
(Figure III-A.1, D).
Clinical implications:
Significant mixing with RA occurs.
Humidification is particularly important for a patient with a tracheostomy, as the
tracheostomy bypasses the natural humidification system.
Moisture may collect in the tubing and should be drained before moving the patient.
The mask can easily shift; reposition it over the site if necessary.
Gently pull the mask away from the patient to access the tracheostomy site for
bronchopulmonary secretion clearance.
Partial non-rebreather Purpose:
mask Provides a high FiO2 to the patient while conserving the O2 supply.
FiO2
40-60% Consists of:
A closed face mask covering the nose and mouth with ventilation holes on either side,
held in place with an elastic strap around the patient’s head. A reservoir bag is attached
at the base of the mask.The flow of O2 is regulated to permit the initial one-third of
the expired tidal volume (O2-rich anatomic dead space) to distend the reservoir
maximally, therefore allowing some rebreathing of air.The balance of expired air
does not enter the reservoir and is vented out the sides of the mask.
Clinical implications:
The partial non-rebreather mask is able to provide a similar FiO2 to the non-rebreather
mask at lower flow rates.
The closed face mask may interfere with talking, eating, and drinking.
High O2 concentration may be drying and uncomfortable; however, humidification
is not used with this method, because it interferes with O2 delivery.
The reservoir bag should remain at least 1=3 to 1=2 full on inspiration.
Continued
444 APPENDIX III-A Medical-Surgical Equipment in the Acute Care Setting

Table III-A.1 VARIABLE PERFORMANCE OXYGEN DELIVERY FOR SPONTANEOUSLY BREATHING

ADULTS*—cont’d

Device/FiO2 Description
Non-rebreather mask Purpose:
FiO2
60-80% Provides the patient with the highest concentration of supplemental O2 available via a face
mask in a variable performance system.
Consists of:
A closed face mask covering the nose and mouth. It is attached to a reservoir bag, which
collects 100% O2. A one-way valve between the mask and bag allows O2 to be inspired
from the bag through the mask. Additional one-way valves on the side of the mask
allow expired gases to exit the mask, thus preventing rebreathing of expired air (Figure
III-A.1, E).
Clinical implications:
See Partial non-rebreather mask, above.
Physical therapy intervention is usually deferred if a patient requires this type of device to
maintain oxygenation. However, bronchopulmonary hygiene may still be indicated.
FiO2, Fraction of inspired oxygen; lpm, liters per minute; O2, oxygen; RA, room air.
*Listed from least to most oxygen support.
Data fromJM Cairo. Administering Medical Gases: Regulators, Flowmeters, and Controlling Devices. InJM Cairo, SP Pilbeam (eds),
Mosby’s Respiratory Care Equipment (7th ed). St. Louis: Mosby, 2004; 59-85; L Arata, L Farris. Oxygen Delivery Devices. In B George-Gay,
CC Chernicky (eds). Clinical Medical Surgical Nursing. Philadelphia: Saunders, 2002;126-127.

A
FIGURE III-A.1
A, Nasal cannula with humidification. (A, From Hillegass E, Sadowsky HS: Essentials of
Cardiopulmonary Physical Therapy [2nd ed]. Philadelphia. Saunders, 2002. B to E, From Dewit SC:
Fundamental Concepts and Skills for Nursing [2nd ed]. St Louis: Saunders, 2004.)
 Medical-Surgical Equipment in the Acute Care Setting APPENDIX III-A 445

B C D

E
FIGURE III-A.1 Cont’d
B, Open face mask or tent. C, Closed face mask. D,Tracheostomy mask or collar. E, Non-rebreather mask.

Apnea may result if chronic hypoxemia is reversed with
higher flows of supplemental O2. Potential respiratory
depression should never contraindicate oxygen therapy
in severe hypoxemia, however. If hypoventilation is a
major problem, other support measures, including
mechanical ventilation, can be used.6
General Physical Therapy Considerations
with Oxygen Therapy
 Note that a green label designates the O2 supply on
hospital walls. A similar gauge supplies pressurized
air that is designated by a yellow label.
 Significant supplemental O2 requirements usually
indicate a respiratory compromise, which in turn
may indicate the need to modify or defer physical
therapy intervention.
 Observe the patient for clinical signs of hypoxemia:
shortness of breath, use of accessory muscles of
breathing, confusion, pallor, or cyanosis.
 The FiO2 for a given system is dependent on its
proper fit and application. Ensure that all connec-
tions are intact, that the O2 is flowing as indicated,
and that the cannula or mask is properly positioned.
 The O2 system may need added humidification, as
supplemental O2 may be drying to the nasal mucosa
 Table III-A.2 FIXED PERFORMANCE OXYGEN DELIVERY

Device/FiO2 Description
Air entrainment mask Purpose:
(Venti mask,Venturi Provides a specific concentration of supplemental O2.
mask) Consists of:
FiO2
24%-50% A high-flow system with a closed face mask over the nose and mouth and a jet mixing device
located at the base of the mask, which forces 100% O2 past an entrainment valve.The valve
can be adjusted to entrain a specific percentage of RA to mix with the O2, allowing precise
control of FiO2 (Figure III-A.2).
Clinical implications:
The closed face mask interferes with coughing, talking, eating, and drinking and may be very
drying and uncomfortable. Patients often remove the mask for these reasons.
Educate the patient on the importance of keeping the mask snug in place.
Humidification is not used when oxygen flow is < 4 lpm because humidification will interfere
with O2 delivery.
Useful for patients with COPD who requires a fixed precise FiO2.
BiPAP Purpose:
FiO2
21%-100% Provides positive inspiratory and positive end expiratory pressure to decrease the work of
breathing by reducing the airway pressure necessary to generate inspiration throughout
the respiratory cycle. May be used to avoid intubation and mechanical ventilation in cases of
acute respiratory failure. Often used in the hospital or home setting for the management
of obstructive sleep apnea.
Consists of:
A closed mask with a clear soft gasket around its border, placed over the nose to fit tightly
against the patient’s face. It is held firmly in place with straps around the top and back
of the head.
Clinical implications:
BiPAP may deliver supplemental O2 at a specific concentration, or it may deliver RA.
Patients may feel claustrophobic owing to the tight fit of the mask.
The equipment may be noisy; thus, the therapist may need to speak loudly to communicate
with the patient.
Abrasions on the bridge of the nose can occur and may be prevented with a dressing that
provides padding to the area without interfering with the tight fit of the mask.
Depending on the patient’s oxygen requirements, BiPAP may be turned off, and alternate
methods of O2 delivery may be used to allow the patient to participate in functional activities
or an exercise program.The unit may also be placed on a portable intravenous pole or cart for
this purpose.
T tube/piece Purpose:
FiO2
50%-80% Provides a specific concentration of supplemental O2 to an intubated, spontaneously breathing
patient while weaning from a ventilator.
Consists of:
A T-shaped tube attached directly to an endotracheal or tracheostomy tube. Humidified O2 is
delivered through one end of theT, and expired gas exits the other end.The tubing acts as a
reservoir for O2, allowing a specific concentration of O2 to be delivered.
Clinical implications:
Patients who are weaning from a ventilator can tire easily. Consult with the medical-surgical
team to determine whether the patient will tolerate ventilator weaning (i.e., the use of aT
piece) and physical therapy intervention simultaneously, or whether the patient would benefit
from bronchopulmonary hygiene to facilitate weaning.
BiPAP, Bi-level positive airway pressure; FiO2, fraction of inspired oxygen; lpm, liters per minute; O2, oxygen; RA, room air.
Data from Kirby RR,Taylor RW, CivettaJM (eds). Handbook of Critical Care (2nd ed). Philadelphia: Lippincott-Raven, 1997; RothsteinJM
(ed).The Rehabilitation Specialist’s Handbook (2nd ed). Philadelphia: FA Davis, 1998; Ryerson EF, Block AJ. Oxygen as a Drug: Clinical
Properties, Benefits, Modes and Hazards of Administration. In GG Burton, JE Hodgkin (eds), Respiratory Care: A Guide to Clinical
Practice (3rd ed). Philadelphia: Lippincott, 1991; CairoJM. Administering Medical Gases: Regulators, Flowmeters, and Controlling Devices.
InJM Cairo, SP Pilbeam (eds), Mosby’s Respiratory Care Equipment (7th ed). St. Louis: Mosby, 2004;59-85.
 Medical-Surgical Equipment in the Acute Care Setting
FIGURE III-A.2
Air entrainment mask or Venturi mask. (From Dewit SC:
Fundamental Concepts and Skills for Nursing [2nd ed].
St Louis: Saunders, 2004.)
and lead to nosebleeds (epistaxis); however, added
humidification is contraindicated in several systems,
as indicated inTable III-A.1 and Table III-A.2.
 Provide extra lengths of O2 extension tubing if func-
tional mobility will occur farther than 5 or 6 ft from
the bedside (i.e., the wall O2 source).
 Ensure that portable O2 tanks are turned on and have
sufficient levels of O2 before use. Have backup
tanks available.
 Observe masksfor the accumulation of mucusorclog-
ging. Clear or change the cannula or mask if needed.
 Monitor the patient’s skin for potential breakdown
due to pressure from the cannula or mask. Provide
appropriate padding without interfering with the
fit of the cannula or mask.
 Document the type and amount of supplemental O2
used during physical therapy intervention.
HEMODYNAMIC MONITORING
Monitoring hemodynamic events provides informa-
tion about the adequacy of a patient’s circulation,
APPENDIX III-A 447
perfusion, and oxygenation of the tissues and organ sys-
tems.The goal of hemodynamic monitoring is to main-
tain the balance between oxygen demand and oxygen
delivery with the measurements of cardiac and intravas-
cular pressures and volumes.7 Hemodynamic monitor-
ing can be accomplished using noninvasive (Table III-
A.3) or invasive (Table III-A.4) methods.
Noninvasive, or indirect, hemodynamic monitoring
provides physiologic information without the risks of
invasive monitoring and can be used in many settings.
Invasive, or direct, measurements are obtained by
penetration of the skin and insertion of a cannula or
catheter into a blood vessel, chamber of the heart, or
both. The cannula or catheter is attached to a monitor-
ing system, which consists of a transducer, amplifier,
and oscilloscope for the display of the vascular wave-
forms and pressure measurements.8 Direct monitoring
can provide continuous, accurate data; however,
thrombosis, infections, air embolisms, and trauma are
potential complications.8
During invasive hemodynamic monitoring, the
level of the right atrium is the standard zero reference
point and is identified by the phlebostatic axisçthe
intersection of the midaxillary line and the fourth inter-
costal space (Figure III-A.3).9 The nurse will ‘‘level’’
the system using a carpenters level or yardstick to align
the patient’s phlebostatic axis with the transducer.
Repositioning the patient may artificially alter wave-
forms by applying pressure to the catheter, shifting the
catheter or stopcock, or shifting the phlebostatic axis
relative to the transducer.9
General Physical Therapy Considerations
with Hemodynamic Monitoring
 Raising the level of the phlebostatic axis relative to
the transducer gives false high readings; lowering
the phlebostatic axis gives false low readings.9
 If a waveform changes during treatment, in the
absence of other clinical signs, reposition the patient
or limb (if an arterial line is in place) and reassess. If
the waveform does not return to baseline, notify the
nurse.
INTRACRANIAL PRESSURE MONITORING
Intracranial pressure (ICP) and cerebral perfusion pres-
sure may be measured in a variety of ways, depending
on how urgently ICP values are needed and the patient’s
neurologic or hemodynamic stability. The purpose of
ICP monitoring is the early identification of increased
448 APPENDIX III-A Medical-Surgical Equipment in the Acute Care Setting

Table III-A.3 NONINVASIVE MEDICAL MONITORING

Device Description
BP cuff (sphygmomanometer) Purpose:
Normal adult values: Indirectly measures arterial blood pressure.
Systolic
100-140 mm Hg Consists of:
Diastolic
60-90 mm Hg An inflatable cuff, usually placed 2.5 cm proximal to the antecubital space, attached to
a pressure monitoring device. Auscultate for Korotkoff’s sounds (refer toTable 1-8)
with a stethoscope over an artery, usually the brachial artery.
Clinical implications:
Do not use a BP cuff on an extremity with an arterial line, lymphedema, AV fistula or
graft, blood clot, or in an extremity ipsilateral to a mastectomy.Try to avoid
measuring BP in an extremity with a peripheral or central intravenous line. Look for
signs posted at the patient’s bedside stating whether the use of a BP cuff on a
particular extremity is contraindicated.
Use an appropriately sized cuff.The cuff bladder should be no less than 80% of limb
circumference. A cuff that is too small gives a falsely high reading, and a cuff that is
too big gives a falsely low reading.
The cuff may be placed on the upper extremity distal to the elbow with auscultation of
the radial artery.
Alternative sites for measurement in the lower extremity are proximal to the popliteal
space with auscultation of the popliteal artery or proximal to the ankle with
auscultation of the posterior tibial artery.
Avoid contact between stethoscope tubing and the cuff tubing to minimize extraneous
sounds.
ECG Purpose:
Continuous monitoring of heart rate and rhythm and respiratory rate (seeTable 1-10).
Consists of:
Three to five color-coded electrodes placed on the chest, either hardwired to a
monitor in a patient’s room or monitored at a distant site (telemetry).
Twelve electrodes are used for a formal ECG.
Clinical implications:
Notify the nurse before physical therapy intervention, as many activities may alter the
rate or rhythm or cause artifact (e.g., chest percussion).
If an electrode(s) becomes dislodged, reconnect it. One way to remember electrode
placement is ‘‘white is right’’ (white electrode is placed on the right side of the chest
superior and lateral to the right nipple),‘‘snow over grass’’ (green electrode is placed
below the white electrode on the anterolateral lower-right rib cage),‘‘smoke over
fire’’ (black electrode is placed on the upper-left rib cage superior and lateral to the
left nipple, and the red electrode is placed below the black one on the anterolateral
left rib cage).The brown electrode is usually placed more centrally.
Patients on telemetry should be instructed to stay in the area monitored by telemetry
antennas.
Collaborate with the nurse to determine whether or not patients who are ‘‘hardwired’’
to monitors in their room may be temporarily transferred to telemetry for
ambulation activities.
Telemetry boxes are usually equipped with a ‘‘record’’ button that when pressed will
print a rhythm strip of the ECG at the time of an ‘‘event’’ (i.e. when the patient is
symptomatic).
Pulse oximeter Purpose:
Normal SpO2 (at sea level) A noninvasive method of measuring the percentage of hemoglobin saturated with O2
 93%-94% in arterial blood.
 Medical-Surgical Equipment in the Acute Care Setting APPENDIX III-A 449

Table III-A.3 NONINVASIVE MEDICAL MONITORING—cont’d

Device Description
Pulse oximeter (cont’d) Consists of:
A probe with an electro-optical sensor placed on a finger, toe, earlobe, or nose.The
pulse oximeter emits two wavelengths of light to differentiate oxygenated from
deoxygenated hemoglobin.
Clinical implications:
SpO2 88% indicates the need for supplemental oxygen.
The waveform or pulse rate reading should match the ECG or palpated pulse.
Monitor changes in pulse oximetry during exercise and position changes.
Peripheral vascular disease, sunshine, or nail polish may lead to a false reading.
In low-perfusion states, such as hypothermia, hypotension, or vasoconstriction, pulse
oximetry may understate oxygen saturation.
Small changes in the percentage of hemoglobin sites chemically combined (saturated)
with oxygen (SaO2) can correspond to large changes in the partial pressure of
oxygen. Refer toTable 2-5 and Figure 2-7.
AV, Arteriovenous; BP, blood pressure; ECG, electrocardiography; SaO2, arterial oxyhemoglobin saturation; SpO2, measurement of SaO2 with
pulse oximetry.
Data from RR Kirby, RW Taylor, JM Civetta (eds). Handbook of Critical Care (2nd ed). Philadelphia: Lippincott-Raven, 1997; RothsteinJM
(ed).The Rehabilitation Specialist’s Handbook (2nd ed). Philadelphia: FA Davis, 1998; MR Kinney, Dunbar SB,Vitello-CicciuJM, et al. (eds).
AACN’s Clinical Reference for Critical Care Nursing (4th ed). St. Louis: Mosby, 1998.

Table III-A.4 INVASIVE MEDICAL MONITORING

Device/Normal Values Description

Arterial line (A-line) Purpose:
Normal values: To directly and continuously record systolic, diastolic, and mean arterial blood pressure; to
Systolic: obtain repeated arterial blood samples; or to deliver medications.
100-140 mm Hg Consists of:
Diastolic: A nontapered Teflon catheter. It is placed in the brachial, radial, or femoral artery.The
60-90 mm Hg catheter is usually connected to a transducer that converts a physiologic pressure into an
MAP: electrical signal that is visible on a monitor.
70-105 mm Hg Clinical implications:
If the A-line is displaced, the patient can lose a significant amount of blood at the insertion
site. If bleeding occurs from the line, immediately apply direct pressure to the site while
calling for assistance.
The normal A-line waveform is a biphasic sinusoidal curve with a sharp rise and a gradual
decline (Figure III-A.4, A). A dampened (flattened) waveform may indicate hypotension,
or it may be due to pressure on the line.
A patient with a femoral A-line is usually seen bedside. Hip flexion past 60-80 degrees is
avoided. After femoral A-line removal, the patient is usually on strict bed rest for
60-90 minutes, with a sandbag placed over the site.
Upper-extremity insertion sites are usually splinted with an arm board to stabilize the
catheter.
The patient with a radial or brachial A-line can usually be mobilized out of bed, although
the length of the line limits mobility to a few feet.The transducer may be taped to the
patient’s hospital gown at the level of the phlebostatic axis (see Figure III-A.3) during
mobilization.
Pacemaker Purpose:
(temporary) To provide temporary supportive or prophylactic cardiac pacing postoperatively, status post
myocardial infarction, for dysrhythmia or EPS diagnostic studies, or before permanent
pacemaker placement. Refer to the Management section in Chapter 1 for more
information on pacemakers.
Continued
450 APPENDIX III-A
Table III-A.4 INVASIVE MEDICAL MONITORING—cont’d
Device/Normal Values
Pacemaker (cont’d)
Pulmonary artery
catheterization
(PA line, Swan-Ganz)
Normal values:
PAP (mean): 10-20 mm
Hg
PAWP (mean): 4-12 mm
Hg
CVP: 2-6 cm H2O
RAP: 2-8 mm Hg
cor temperature: 98.28-
100.28F (36.88-37.98C)
CO: 4-8 lpm
CI (CO/body surface
area): 2.5-4 lpm/m2
A-line, Arterial line; CI, cardiac index; CO, cardiac output; CVP, central venous pressure; EPS, electrophysiology study; LAP, left atrial
pressure; lpm, liters per minute; MAP, mean arterial pressure; PAP, pulmonary artery pressure; PAWP, pulmonary artery wedge pressure;
RAP, right atrial pressure.
Data from BreitenbachJE. Putting an End to Perfusion Confusion. Nursing Made Incredibly Easy 2007;5(3). DirksJL. Cardiovascular
Therapeutic Management. In LD Urden, KM Stacy, ME Lough (eds),Thelan’s Critical Care Nursing: Diagnosis and Management (5th ed).
St. Louis: Mosby, 2006.
Medical-Surgical Equipment in the Acute Care Setting
Description
Consists of:
An external pulse generator connected to an insulated electrical lead and 1 to 3 electrodes.
There are three basic types.
Epicardial:The wires are placed after heart surgery on the epicardium and exit through a
mediastinal incision.
Transvenous:The wires are placed in the right atrium or ventricle via a subclavian or internal
jugular central line.
Transcutaneous: Large electrodes are placed on the skin over the anterior and posterior chest.
Clinical implications:
The presence of a temporary pacemaker does not, in and of itself, limit functional mobility.
However, the underlying indication for the pacemaker may limit the patient’s activity
level. Check for mobility restrictions.
Temporary pacing wires and electrodes should be kept dry.
Be aware of the location of the generator and wires at all times, especially during mobility
activities.
If a temporary pacemaker is placed after a coronary artery bypass graft (CABG), the wires
are usually removed 1 to 3 days after surgery.The patient is usually placed on bed rest for
1 hour after pacing wire removal, with vital sign monitoring every 15 minutes.
Patients with temporary pacemakers require continuous ECG monitoring to evaluate
pacemaker function.
Purpose:
To directly or indirectly measure PAP, PAWP, LAP, RAP, CVP, core body temperature, CI,
and CO in cases of hemodynamic instability, acute MI, heart failure, or shock states.
Provides access to mixed venous blood samples.
Consists of:
A radiopaque, multilumen balloon-tipped catheter inserted through an introducing sheath
into a large vein, usually the subclavian, or the brachial, femoral, or internal jugular vein
(Figure III-A.4, B).The catheter is directed by blood flow into various locations of the
heart and pulmonary artery, with proper placement confirmed by x-ray.
The catheter is connected to a transducer to allow for continuous monitoring.
The proximal lumen opens into the right atrium to measure RAP and CO, and for the
delivery of fluids or medications.
The distal lumen opens into the pulmonary artery to measure PAP and PAWP.
To obtain a PAWP measurement, a balloon at the end of the distal lumen is temporarily
inflated. It follows the blood flow from the right ventricle into the pulmonary artery to a
distal branch of the pulmonary artery, where it is ‘‘wedged’’ for a short time (up to
15 seconds).
Clinical implications:
The patient with a PA line is usually on bed rest.
Avoid head and neck (for subclavian access) or extremity movements that could disrupt the
PA line at the insertion site, including the line dressing.
PAWP is an indirect measure of LAP.
PAP is equal to right ventricle pressure.
RAP is equal to CVP.
CO equals stroke volume (SV)  heart rate (HR).
FIGURE III-A.3
The phlebostatic axis at the intersection of the fourth intercostal space (ICS) and the midpoint of the
anterior (A) and posterior (P) chest wall. (Courtesy Edwards Lifesciences LLC.)

B
FIGURE III-A.4
A, Arterial line tracing from different sites. B, Pulmonary artery (PA) catheter (four-lumen model) in a
branch of a PA with the balloon inflated; the pulmonary capillary wedge pressure (PCWP) reflects left
atrial pressure (LAP). LA, Left atrium; LV, left ventricle; RV, right ventricle. (A, FromYentis SM, Hirsh
NP, Smith GB [eds], Anaesthesia and Intensive Care A-Z. An Encyclopedia of Principles and Practice
[2nd ed]. Oxford, UK: Butterworth-Heinemann, 2000;45.) B, From LD Kersten [ed]. Comprehensive
Respiratory Nursing: A Decision-Making Approach. Philadelphia: Saunders, 1989;758.)
452 APPENDIX III-A Medical-Surgical Equipment in the Acute Care Setting

ICP prior to the occurrence of cerebral damage, to pro-
vide access for CSF sampling and/or drainage, and to
evaluate the effectiveness of medical-surgical treat-
ment.10 Refer to Intracranial and Cerebral Perfusion
Pressure in Chapter 4 for a description of these terms,
Table 4-26 for a description of the early and late signs
of increased ICP, and Table 4-27 for a list of treatment
options to decrease ICP.
Table III-A.5 describes the different types of ICP
monitors. For some ICP monitors, such as the intraven-
tricular catheter, the sensor and the transducer must be
level. Often, the zero point for the transducer is at the
tragus, or the top of the ear. A normal ICP waveform
has a triphasic sinusoidal waveform and should corre-
spond to heart rate.
New methods of monitoring for cerebral ischemia
and for the earlier prevention of secondary brain
injury include brain tissue oximetry, jugular venous oxi-
metry, brain temperature measurement, and cerebral
microdialysis.11
General Physical Therapy Considerations
with Intracranial Pressure Monitoring
 As with hemodynamic monitoring, be aware of the
ICP value and the corresponding waveform on the
monitor. The waveform may change shape (plateau
wave) if cerebral hypoxia or ischemia occurs.10
 Momentary elevations in ICP will normally occur. It
is a sustained elevation in ICP greater than 5 minutes
that is of concern10 and should be reported to the
nurse.
 Patients with elevated ICP are often positioned with
the head of the bed at 30 degrees, which maximizes
venous blood flow from the brain to help decrease
ICP.10 Therefore, be aware that lowering the head of
the bed may increase ICP. Other positions that
increase ICP are the Trendelenburg position, lateral
neck flexion, and extreme hip flexion.
 Additional conditions that increase ICP are the
Valsalva maneuver, noxious stimuli, coughing,
pain, stress, and frequent arousal from sleep.10
MEDICAL-SURGICAL MANAGEMENT
DEVICES
Different lines, tubes, catheters, and access devices
comprise the wide variety of medical-surgical equip-
ment used in the acute care setting. In general, these
devices may be peripheral or central, for short-term or
long-term use, and inserted or applied at the bedside
in a special procedure (e.g., under fluoroscopic gui-
dance) or in the operating room.Table III-A.6 describes
the medical-surgical management devices most com-
monly encountered in the acute care setting.
General Physical Therapy Considerations with
Medical-Surgical Management Devices
The following clinical tips apply to medical-surgical
equipment, as well as to the O2 therapy and noninva-
sive, invasive, and ICP monitoring equipment pre-
viously discussed.
CLINICAL TIP
 Before entering a patient’s room, review the medical
record, particularly new orders, recent progress
notes, and test results. Review graphic sheets for
vital signs, noting trends or variations from the
norms.
 Note whether any particular precautions protecting
the patient or the caregiver from specific pathogens
are in place (e.g., contact precautions). Refer to
Table 10-4 for a summary of infection prevention
precautions.
 Practice standard precautions. The likelihood of
encountering bodily fluids is increased in the acute
care setting, especially in the ICU.
 Discuss your planned intervention with the nurse.
Scheduled procedures may take precedence over this
intervention, or it may coordinate well with another
planned procedure.
 On entering the patient’s room, take inventory.
Observe the patient’s appearance and position.
Systematically observe the patient, and verify the
presence of all documented lines. Develop a
consistent method of surveying the room: left to
right, or top of bed to bottom of bed, to ensure that
all lines and equipment are observed and considered
in your treatment plan. Take note of all readings on
the monitors before intervention.
 Anticipate how your intervention may change
the patient’s vital signs and how this will likely
appear on the monitors. Be aware of which readings
may change artificially owing to relative position
change.
 Using appropriate precautions, gently trace each line
from the patient to its source. Ask for assistance, if
needed, to untangle any lines or to free any lines
that might be under the patient.
 Ensure that there is no tension on each line
before attempting to move the patient.
Continued on p. 461
 Medical-Surgical Equipment in the Acute Care Setting APPENDIX III-A 453

Table III-A.5 INTRACRANIAL PRESSURE (ICP) MONITORS

Device Description
Epidural sensor Purpose:
To monitor ICP.
Consists of:
A fiberoptic pneumatic flow sensor. It is placed in the epidural space (i.e., superficial to the
dura) and connects to a transducer and monitor.
Clinical implications:
The transducer does not need to be adjusted (releveled) with position changes.
Fair to good reliability.
Subarachnoid bolt Purpose:
To directly monitor ICP.
Consists of:
A hollow bolt or screw placed in the subarachnoid space through a burr hole.
Clinical implications:
The physician will determine the level to which the transducer should be positioned.
This is documented in the chart and posted at the bedside.
The transducer must be repositioned to the appropriate level with position changes.
Poor reliability and decreased accuracy at high ICP readings.
Complications include infection and blockage of the bolt by clot or brain tissue.
Intraventricular Purpose:
catheter To directly monitor ICP and provide access for the sampling and drainage of CSF.
(ventriculostomy) Occasionally used to administer medications or to instill air or contrast agent for
ventriculography.
Consists of:
A small catheter that is placed in the anterior horn of the lateral ventricle through a burr hole.
The catheter connects to a transducer and to a drainage bag, where CSF collects.
Clinical implications:
The nondominant hemisphere is the preferable insertion site.
There are two different types of drainage systems: intermittent and continuous.
The intermittent system allows the nurse to drain CSF for 30-120 seconds by momentarily
opening a stopcock when the ICP exceeds the parameters set by the physician.
A continuous system allows the drainage of CSF to occur against a pressure gradient when
the collection bag is positioned (leveled) above the foramen of Monro.This is usually
15 cm above the external auditory meatus (EAM).
The transducer must be repositioned to the appropriate level with position changes.
Very reliable.
Complications can include infection, meningitis, ventricular collapse, or catheter occlusion
by blood or brain tissue.
Fiberoptic transducer- Purpose:
tipped catheter To monitor ICP. Can also be used in conjunction with a CSF drainage device (if the catheter
is placed in the parenchyma).
Consists of:
A fiberoptic transducer-tipped catheter. It is placed in the ventricle, within the parenchyma,
in the subarachnoid or subdural space, or under a bone flap.
Clinical implications:
The transducer does not need to be adjusted (releveled) with position changes.
Very reliable.
CSF, Cerebrospinal fluid.
Data from Smeltzer SC, Bare BG, HinkleJL, et al. (eds). Management of Patients with Neurologic Dysfunction. In Brunner & Suddarth’s
Textbook of Medical-Surgical Nursing (11th ed). Philadelphia: Lippincott Williams & Wilkins, 2007.
Table III-A.6 MEDICAL-SURGICAL MANAGEMENT DEVICES*

Device Description
Arteriovenous (AV) Purpose:
graft or fistula Provides access for hemodialysis.
Consists of:
The graft is an artificial blood vessel, usually made of Gore-Tex or Dacron, used to
join an artery and vein when a patient’s own vessels are not viable for an AV fistula.
The fistula is the surgical joining of a peripheral artery and vein, allowing arterial
blood to flow directly to a vein. Usually located in the forearm.
Clinical implications:
Elevate and avoid weight bearing on the involved extremity for 24 hours after surgical
procedure.
Do not use blood pressure cuff on the involved extremity.
Avoid pressure or constriction over the site (as in sleeping on or bending accessed
limb for prolonged periods of time.)
Palpable turbulence is normal in the graft or fistula, which will have a raised, ropelike
appearance.
Complications can include thrombosis, infection, and vascular steal syndrome.
Central (venous) line Purpose:
Normal value, Provides vascular access for short-term or long-term use (days to months) forTPN,
CVP, 0-8 mm Hg repeated blood sampling, or administration of drugs or fluid. Particularly useful for
the administration of large/rapid fluid volumes. May measure CVP (see the
Pulmonary artery catheterization section inTable III-A.4).
Consists of:
A single-lumen or multiple-lumen intravenous line placed in the subclavian, basilic,
jugular, or femoral vein, terminating in the superior vena cava.
Clinical implications:
Do not use a blood pressure cuff on an extremity with a central line.
Greatly reduces the need for repeated venipuncture and reduces risk of vein irritation.
Chest tube Purpose:
Removes and prevents the reentry of air or fluid from the pleural space or mediastinal
space and provides negative intrapleural pressure. Used to treat pneumothorax,
hemothorax, pleural effusion, empyema, or chylothorax. May also be used for
chemical pleurodesis to treat recurrent pleural effusion or pneumothorax.
Consists of:
Tube(s) placed in the pleural or mediastinal space that exits the chest and is usually
connected to a drainage system (Figure III-A.5). The placement of the tube is
determined by indication. Mediastinal chest tubes, placed to drain the pericardium
after surgery, exit the chest directly below the sternum. Apical chest tubes drain air,
which typically collects in the apices of the pleural spaces. Fluid tends to collect near
the bases; in these cases, tubes are placed more inferiorly near the fluid collection.
Postoperatively, tubes often exit the chest through the surgical incision. If chest
tubes are placed in a nonsurgical situation, they are often placed along the
midaxillary line at the appropriate level.
Tubes usually connect to a drainage system with three compartments: the drainage
collection chamber, the water seal chamber with a one-way valve that prevents air or
fluid from reentering the drainage collection chamber, and the suction chamber,
which decreases excess pressure in the pleural space.
Tubes may be connected to a small one-way valve (Heimlich valve) that allows air
or fluid to escape from the pleural space while preventing reentry.
Clinical implications:
Chest tubes may cause discomfort, which may inhibit a cough, deep breath, mobility,
or lying on the involved side.
The patient may benefit from premedication for pain before treatment.
Chest tube is often abbreviated ‘‘CT.’’ If the chest tube has been removed from suction,
it is often referred to as ‘‘chest tube to water seal.’’
Table III-A.6 MEDICAL-SURGICAL MANAGEMENT DEVICES*—cont’d

Device Description
Chest tube (cont’d) The drainage system should be below the level of chest tube insertion.
Avoid tipping the collection reservoir.The reservoir may be hung from the side of the
bed or taped to the floor to prevent tipping.
If the reservoir is overturned, return the drainage container to the upright
position and notify the nurse.
If the chest tube itself becomes dislodged, stop activity and notify the nurse
immediately. If possible, place the patient in an upright sitting position, and
monitor the patient’s breath sounds, vital signs, and respiratory rate and pattern
for possible signs of tension pneumothorax.
The occlusive dressing, usually a petrolatum gauze dressing to prevent the influx
of air, should remain intact. Do not apply pressure over the insertion site.
Prevent kinks in the line.
The presence of a chest tube should not, in and of itself, limit activity. Position
changes and mobility can facilitate drainage.
Ask the nurse or doctor whether the chest tube may be temporarily disconnected from
suction during mobility activities. If the suction must remain connected, additional
lengths of tubing may be added, or a portable suction device may be used during
mobility activities.
Serial chest x-rays are often performed to determine chest tube placement and
effectiveness, and to assist the medical-surgical team in determining the chest tube
weaning process.
Esophagogastric balloon Purpose:
tamponade tube To compress hemorrhaging esophageal varices. Used temporarily while awaiting
(Sengstaken-Blakemore surgical intervention or if endoscopic therapy fails.
tube, Minnesota tube) The tube, which is passed by mouth through the esophagus into the stomach,
has a proximal (esophageal) cuff, which compresses esophageal varices,
and a distal (gastric) cuff, which compresses gastric varices. Channels allow
aspiration of gastric contents.The balloons typically remain in place
for up to 24-72 hours, as longer duration may cause tissue necrosis or
ulceration.
Clinical implications:
Patients with this device are typically very ill and unable to participate in physical
therapy.
Lumbar drain Purpose:
Drainage of CSF from the subarachnoid space in the lumbar spine. For the treatment
of CSF leaks/dural tears or shunt infections or to reduce intracranial pressure.
Consists of:
A spinal catheter inserted in L4-5 subarachnoid space, advanced to an appropriate
level, and connected to a sterile closed CSF collection system.
Clinical implications:
The position of the patient, the position of the transducer (if any), and the
position of the collection bag are determined by the rationale for the LDD
intervention.
Changes in the patient’s position, in the level of the collection bag, or in the
intrathecal pressure impact the amount and rate of drainage.
Patients are usually on bed rest while the drain is in place. Note any mobility and
positioning restrictions in the medical record or posted in the patient’s room.
Patients are often instructed to avoid coughing while practicing postoperative
deep-breathing exercises.
Over-drainage or under-drainage complications include tension pneumocranium,
central herniation of the brain, compression of the brain stem, and subdural
hematoma.
Continued
456 APPENDIX III-A Medical-Surgical Equipment in the Acute Care Setting

Table III-A.6 MEDICAL-SURGICAL MANAGEMENT DEVICES*—cont’d

Device Description
Lumbar drain (cont’d) Monitor the patient for any changes in neurologic status. Notify nursing immediately
if any changes are noted
Midline catheter Purpose:
Delivers IVmedications or fluids for up to 4-6 weeks. Cannot be used to draw blood.
Consists of:
A 3-inch to 8-inch peripheral catheter placed via the basilic, cephalic, or brachial veins
and terminating in the axillary vein.
Clinical implications:
Do not use blood pressure cuff on the involved extremity.
Nasoenteric feeding tube Purpose:
(Dobbhoff tube) Placed for enteral feedings when patients are unable to take in adequate nutrition by
mouth.
Consists of:
A radiopaque, small-diameter, tube inserted via the nostril, through the esophagus
into the stomach or duodenum, and held in place with tape across the nose. Can be
inserted at the bedside, by an Interventional Radiologist, or surgically. Surgically
placed tubes are inserted directly into the jejunum.
Clinical implications:
The position of the tube in the nostril and the back of the throat can be irritating to
the patient and may inhibit a cough.
The tube often hangs in front of the patient’s mouth and may also hinder airway
clearance.
The patient may be more comfortable if the tube is positioned away from his or her
mouth and taped to the forehead or cheek.
The tube can be dislodged easily. Check that the tape is secure.The tube may be
safety-pinned to the patient’s hospital gown for reinforcement. Notify the nurse
if the tube becomes dislodged.
Patient may be on aspiration precautions.
Place feedings on hold when the head of the bed is flat to minimize the risk of
regurgitation or aspiration.
This small-diameter tube can clog easily; some facilities require that feeding tubes be
flushed with water when placed on hold for > 15 minutes to minimize the risk of
clogging
Nasogastric tube (NGT) Purpose:
Keeps the stomach empty after surgery and rests the bowel by preventing gastric
contents from passing through the bowels. Also used for gastric decompression of
the upper GI tract. Some NGTs allow access to the stomach for medications or tube
feedings (see Nasoenteric feeding tube section).
Consists of:
A large bore tube inserted via the nostril, through the esophagus, and into the
stomach. Often attached to low-level suction pressure. Held in place with tape across
the nose.
Clinical implications:
See Nasoenteric feeding tube section for positioning tips.
Review the orders to determine if the patient’s NGT may be temporarily disconnected
from suction. Ask the nurse to disconnect or ‘‘clamp’’ the NGT from suction for
mobilization of the patient. If/when disconnected, monitor the patient for nausea or
abdominal distention.
When disconnected from suction, the open end should be capped. Monitor the NGT
to make sure it remains capped to prevent leaking
 Medical-Surgical Equipment in the Acute Care Setting APPENDIX III-A 457

Table III-A.6 MEDICAL-SURGICAL MANAGEMENT DEVICES*—cont’d

Device Description
Nebulizer Purpose:
Delivers inhaled medications, usually bronchodilators and mucolytics.
Consists of:
A hand-held chamber with a mouthpiece through which pressurized air aerosolizes
medications that are then inhaled. May deliver medications through ventilator or
tracheostomy tubing.
Clinical implications:
Treatment time is usually 10-20 minutes; however, the medications are usually effective
for 3-6 hours.
Patients may be better prepared for mobility activities or airway clearance after
nebulizer treatments.
These treatments are often referred to as ‘‘nebs.’’
Percutaneous endoscopically Purpose:
inserted gastrostomy/ Provides long-term access for nourishment to patients who are unable to tolerate food
jejunostomy tube by mouth. May be used to supplement nutrition taken by mouth.
(PEG/PEJ) tube Consists of:
A feeding tube placed by endoscopy into the stomach (PEG) or jejunum (PEJ)
through the abdominal wall.Tube is anchored with a balloon or disc inside the
stomach. May also be placed by a surgeon during an operative procedure.
Clinical implications:
Place tube feedings on hold when the head of the bed is flat to minimize the
risk of regurgitation/aspiration.
PEJ tube is considered postpyloric; therefore, the risk of aspiration from regurgitation
is minimized.
This small-diameter tube can clog easily; some facilities require that feeding tubes be
flushed with water when placed on hold for > 15 minutes to minimize the risk of
clogging
Percutaneous introducer Purpose:
sheath (Cordis) Cannulates a vein to provide a channel for the insertion of a pulmonary artery
(PA) catheter.
Consists of:
A Teflon sheath that often has a side port for IVaccess.
Clinical implications:
The patient may be mobilized with the sheath in place once the pulmonary catheter
has been removed.
A secure dressing should cover the sheath during any mobilization, as the large
bore opening of the sheath can allow air into the venous system if the sheath is
dislodged
Peripheral intravenous (IV) Purpose:
line Provides temporary access for delivery of medications, fluids, electrolytes, nutrients, or
blood product transfusions. Cannot be used to draw blood.
Consists of:
A short plastic catheter, 0.75 inches long, inserted into a small peripheral vein. Ideally
used in the cephalic or basilic veins on a noninvolved or nondominant upper
extremity. Covered with a transparent dressing and secured in place with tape. May
be secured further with a stretch net or armboard.
Clinical implications:
Avoid using blood pressure cuff on the involved extremity if possible.
Watch IV tubing for kinks or occlusions.
Position the patient to avoid occluding flow.
Continued
458 APPENDIX III-A
Table III-A.6 MEDICAL-SURGICAL MANAGEMENT DEVICES*—cont’d
Device
Peripheral intravenous (IV)
line (cont’d)
Peripherally inserted central
catheter (PICC line)
Rectal pouch/tube
Sequential compression
device (SCD) (pneumatic
compression boots)
Suprapubic catheter
Medical-Surgical Equipment in the Acute Care Setting
Description
Observe the patient for signs of infiltrated IVor phlebitis: localized pain, edema,
erythema, or tenderness. Notify the nurse if signs are present.
Notify the nurse if the IVdressing is not intact, appears infiltrated, or if the IV has
become dislodged. If the IV is accidentally removed, safely apply direct pressure to
the site with gloved hands.
The patient may experience pain at an IV site in the thumb or wrist area when weight
bearing or using an assistive device.
Purpose:
Provides IVaccess for long-term administration of TPN, medications, fluid, blood
products, or chemotherapy. Useful for the patient having head/neck surgery.
Consists of:
A single or double lumen catheter placed via the cephalic or basilic vein, terminating
in the superior (or inferior) vena cava.
Clinical implications:
Wait for x-ray results before mobilizing the patient to confirm proper placement
of the line as improper placement can break the line; cause a hematoma; pierce
the lung, causing a pneumothorax; or terminate in a vessel other than the vena
cava.
Do not use a blood pressure cuff on the involved extremity.
Encourage range of motion of the involved extremity.
Use of axillary crutches may be contraindicated especially if the PICC is inserted
in the basilic vein.
Purpose:
Temporarily collects and contains bowel drainage and protects fragile skin from
contact with feces. Also used for infection-control purposes.
Consists of:
An ostomy-type pouch placed externally and secured with an adhesive or a tube placed
internally in the rectum, connected to a drainage bag.
Clinical implications:
Both are easily dislodged.
Use a draw sheet when moving the patient in bed.
Keep the collection bag below the level of insertion.
Purpose:
Provides intermittent pressure to the lower extremities to promote venous return and
prevent deep vein thrombosis (DVT) secondary to prolonged or postoperative bed
rest.
Consists of:
Inflatable sleeves, applied to the lower legs, which intermittently inflate and deflate.
In some cases, the sleeve is applied to the leg from the ankle to mid-thigh.
Clinical implications:
Usually worn when the patient is in bed, but can be worn when sitting in a chair.
Reapply when patient returns to bed. Best fit occurs when sleeves are applied without
air in them.
Discontinued when the patient is ambulating on a regular basis.
Contraindicated in an extremity in which there is a known DVT.
Purpose:
Drains the bladder temporarily after some bladder or gynecologic surgeries, or
permanently in cases of blocked urethra due to a tumor, stricture, periurethral
abscess, or a severe voiding dysfunction.
 Medical-Surgical Equipment in the Acute Care Setting
Table III-A.6 MEDICAL-SURGICAL MANAGEMENT DEVICES*—cont’d
Device
Suprapubic catheter (cont’d)
Surgical drain
Texas catheter (Condom
catheter)
Vascular Access Port (VAP)
(Port-A-Cath,
MediPort,Pass-port, Infuse-A-
Port, S.E.A. Port)
APPENDIX III-A 459
Description
Consists of:
A catheter placed in the bladder through a surgical incision in the lower abdominal
wall (above the pubis) which is connected to a closed drainage system. Secured to
the abdominal wall with sutures or tape and covered with a sterile dressing.
Clinical implications:
Keep the collection bag below the level of the bladder.
The collection tubing may be taped to the patient’s thigh.
Avoid pressure over the insertion site.
May be removed after a successful voiding trial with the tube clamped.
Often more comfortable and allows greater mobility than a urethral catheter.
Purpose:
Removes excess blood or fluid from a surgical site that would otherwise collect
internally.
Surgical drains are of two basic types: passive (open) or active (closed). Passive
drainage is accomplished by gravity or capillary action. Drainage is further
facilitated by transient increases in intraabdominal pressure, as with coughing.
Passive surgical drains include Penrose, Foley, Malecot, and Word catheters. Active
drainage is accomplished by suction from a simple bulb device or with negative
pressure from a suction pump.These systems may be closed, like the Hemovac and
Jackson-Pratt (JP) drains.
Clinical implications:
Be aware of the location of the drain when moving the patient.
The drain or tubing may be taped or pinned to the patient’s skin or clothing to
prevent tugging.
Ask the nurse to temporarily disconnect a drain from suction, if necessary/appropriate.
Monitor any drains for leakage during a PTsession and report this to the nurse.
Purpose:
Noninvasively drains and collects urine from the penis.
Consists of:
A condom-like flexible sheath that fits over the penis to drain urine into a collection
bag.This noninvasive method of collecting urine has a much lower risk of infection
and irritation than does an indwelling catheter and is often the preferred method of
managing male urinary incontinence.
Clinical implications:
It is easily dislodged.
It may be held in place with aVelcro strap.
The drainage bag should always be below the level of the bladder to allow drainage by
gravity.
Keep the collection bag off the floor.
Secure the collection bag or catheter tubing to patient’s leg, clothing, or assistive
device to prevent the patient from tripping or becoming tangled in the tubing
during mobility activities.
Purpose:
For long-term (> 6 months) chemotherapy,TPN, or other intermittent infusion
therapy.
Consists of:
A completely indwelling surgically-implanted catheter, usually placed in the
subclavian or jugular vein, terminating in the superior vena cava. Access
to the catheter is obtained through a tunneled portion attached to a port that
is implanted in a subcutaneous pocket in the chest wall, usually below the clavicle.
May also be placed in the arm, abdomen, flank, or thigh.The subcutaneous
Continued
460 APPENDIX III-A
Table III-A.6 MEDICAL-SURGICAL MANAGEMENT DEVICES*—cont’d
Device
Vascular Access Port (VAP)
(cont’d)
Tunneled central venous
catheter (Hickman, Broviac,
Groshong, Silastic, and
Quinton catheters)
Urinary catheter
(Foley catheter)
Ventriculoperitoneal
shunt (VP);
Ventriculoatrial
shunt (VA)
Medical-Surgical Equipment in the Acute Care Setting
Description
titanium or plastic port has a reservoir with a self-sealing silicone
septum that is accessed by a special noncoring needle through intact skin.
The tunneled portion is anchored to a muscle or subcutaneous tissue with
sutures.
Clinical implications:
Once healed and cleared by MD, physical activity is not limited.
Patients can usually swim or bathe and exercise without limitation.
Appears as a slight protrusion under the skin.
Report signs/symptoms of infection or infiltration to the nurse.
Complications can include skin breakdown, site infection, extravasation,
or thrombosis
Purpose:
Surgically implanted single-lumen or multi-lumen silicone catheter used for
long-term chemotherapy,TPN, or other infusion therapy. May be used for
months to years.
Very similar to a vascular access port; however, access is obtained through
a ‘‘tailed’’ portion, which exits the skin from the anterior chest wall
superior to the nipple. A Dacron cuff surrounds the tunneled portion
just inside the exit site.The cuff causes a subcutaneous inflammatory
reaction to occur after insertion, which, when healed, provides
fixation and a barrier to venous infection within 7-10 days of
implantation.
Clinical implications:
The tailed portion should be taped down to prevent dislodging.
Do not perform manual techniques directly over the tail.
Patients are allowed to shower once the insertion site is healed; however, tub bathing
and swimming are usually limited.
Purpose:
Temporarily drains and collects urine from the bladder. Used for urinary
incontinence and retention, to assist with postoperative bladder drainage,
when accurate measurement of urine output is necessary, or to prevent leakage in
patients with Stage III to IV pressure ulcers.
Consists of:
A tube inserted through the urethra into the bladder that drains into a collection bag.
It is held in place internally by an inflated cuff.
Clinical implications:
Be aware of the position of the catheter.
The collection bag should always be below the level of the bladder to allow drainage
by gravity.
Secure the collection bag or tubing to the patient’s leg, clothing, or assistive device to
prevent the patient from tripping or becoming tangled in the tubing during
mobility activities.
The collection bag should be kept off the floor.
Purpose:
Drains excess CSF from the brain into the abdominal cavity/peritoneum (VP) or
right atrium of the heart (VA).
Consists of:
A shunt, tunneled under the skin, from the lateral ventricle of the brain to the
collection cavity.
Clinical implications:
The patient may be on bed rest for 24 hours after placement.
 Medical-Surgical Equipment in the Acute Care Setting APPENDIX III-A 461

Table III-A.6 MEDICAL-SURGICAL MANAGEMENT DEVICES*—cont’d

Device
Ventriculoperitoneal shunt
(VP); Ventriculoatrial shunt
(VA) (cont’d)
Yankauer suction
AV, Arteriovenous; CSF, cerebrospinal fluid; CVP, central venous pressure;TPN, total parenteral nutrition.
*Listed in alphabetical order.
Data from reference numbers 10, 12
Description
The shunt can often be palpated under the skin.
Avoid excess pressure over the shunt.
Monitor for signs of increased ICP.
Purpose:
Clears secretions from the oral cavity or the oropharynx.
Consists of:
A handheld clear rigid tube attached to wall suction via tubing.The suction pressure is
usually 120-150 mm Hg.
Clinical implications:
Some patients use this independently; if so, place within the patient’s reach.
Patients with a decreased cough reflex or dysphagia or on ventilator support may
collect secretions in the mouth or in the back of the throat. GentleYankauer
suctioning before rolling or other mobility may prevent aspiration of the collected
secretions.
Yankauer suctioning may stimulate a cough and help clear secretions in patients who
are unable to clear secretions independently.
If a patient bites down on theYankauer, do not attempt to pull on the device.Wait for
the patient to relax, and then gently slide theYankauer from the patient’s mouth.

 Never attempt to free a line that cannot be

completely visualized!
 Discuss with the nurse whether any lines can be
removed or temporarily disconnected from the
patient before your treatment.
 Ask for appropriate assistance when mobilizing
the patient.
 Most invasive monitoring systems have two alarm
controls: one to silence or discontinue the alarm
for a few minutes, and another to disable or
turn off the alarm. Do not silence an alarm
without permission from the nurse! It is not
recommended that the physical therapist disable
an alarm.
 If available and appropriate, use a portable
telemetry monitor when mobilizing a patient
(who has continuous ECG monitoring) away from
the bedside to maintain the continuity of the ECG.
 On completion of your treatment, ensure that all
appropriate alarms are turned on and that the
patient is positioned with the appropriate safety and
FIGURE III-A.5 communication measures in place. Notify the nurse
Tubing attachment to three-chamber collection unit. (From of any change in the patient’s status.
Phillips N. Berry and Kohn’s Operating RoomTechnique [11th
ed]. St. Louis: Mosby, 2008.)
462 APPENDIX III-A Medical-Surgical Equipment in the Acute Care Setting
References
1. Task Force of the American College of Critical Care
Medicine, Society of Critical Care Medicine:
Guidelines for Intensive Care Unit Admissions,
Discharge, and Triage. Crit Care Med
1999;27(3):633-638. Available at: www.sccm.org.
Last accessed March 5, 2008.
2. AARC Clinical Practice Guideline: OxygenTherapy for
Adults in the Acute Care Facilityç2002 Revision and
Update. Available at: www.aarc.org. Last accessed
March 1, 2008.
3. Kacmarek RM. OxygenTherapy. In RM Kacmarek,
CW Mack, S Dimas (eds),The Essentials of
Respiratory Care. (3rd ed). St. Louis: Mosby,
1990;408.
4. CairoJM. Administering Medical Gases:
Regulators, Flowmeters, and Controlling Devices.
InJM Cairo, SP Pilbeam (eds), Mosby’s
Respiratory Care Equipment. (7th ed). St. Louis:
Mosby, 2004;59-85.
5. Shapiro SD, Snider GL, Rennard SI. Chronic Bronchitis
and Emphysema. In Murray & Nadel’sTextbook of
Respiratory Medicine (4th ed). Philadelphia: Saunders,
2005;1152.
6. AmericanThoracic Society. COPD Guidelines: Setting
and Adjusting Oxygenation. Available at:
www.thoracic.org. Last accessed March 1, 2008.
7. BreitenbachJE. Putting an End to Perfusion
Confusion. Nursing Made Incredibly Easy
2007;5(3):50-60.
8. Lough ME. Cardiovascular Diagnostic Procedures.
In LD Urden, KM Stacy, ME Lough (eds):Thelan’s
Critical Care Nursing: Diagnosis and Management
(5th ed). St. Louis: Mosby, 2006.
9. Chernicky CC, Berger BJ (eds). In Chernicky & Berger:
LaboratoryTests and Diagnostic Procedures (5th ed).
Philadelphia: Saunders, 2008.
10. Smeltzer SC, Bare BG, HinkleJL, et al. (eds).
Management of Patients with Neurologic Dysfunction.
In Brunner & Suddarth’sTextbook of Medical-Surgical
Nursing (11th ed). Philadelphia: Lippincott Williams &
Wilkins, 2007;2171-2180.
11. Wartenberg KE, SchmidtJM, Mayer SA. Multimodality
Monitoring in Neurocritical Care. Crit Care Clin
2007;23(3):507-538.
12. I.V.Therapy Made Incredibly Easy! (3rd ed).
Philadelphia: Lippincott Williams & Wilkins, 2006.
13. Coughlin AM. Go with the Flow of Chest Tube
Therapy. Nursing, 2006;36(3):36-41.
14. Urden LD, KM Stacy, ME Lough (eds).Thelan’s Critical
Care Nursing: Diagnosis and Management. (5th ed).
St. Louis: Mosby, 2006.
15. George-Gay B, CC Chernicky (eds). Clinical Medical
Surgical Nursing. Philadelphia: Saunders, 2002.
16. Swearingen PL (ed). Manual of Medical-Surgical
Nursing Care (6th ed). St. Louis: Mosby, 2007.
17. Bryant RA, Nix DP (eds). Acute and Chronic Wounds:
Current Management Concepts (3rd ed). St. Louis:
Mosby, 2007.
 Appendix III-B Mechanical Ventilation
Sean M. Collins and Jaime C. Paz
Mechanical ventilatory support provides positive  Protection of airway from aspiration of gastric
pressure to inflate the lungs. Patients with acute illness, contents
serious trauma, exacerbation of chronic illness, or pro-  Reversal of respiratory muscle fatigue4
gression of chronic illness may require mechanical
ventilation.1
PROCESS OF MECHANICAL VENTILATION
Physiologic Objectives of Clinical Objectives of
Mechanical Ventilation2 Mechanical Ventilation2
Intubation
 Support or manipulate  Reverse hypoxemia
Intubation is the passage of an artificial airway (tube)
pulmonarygas and acute respiratory into the patient’s trachea (Figure III-B.1), generally
exchange acidosis
through the mouth (endotracheal tube intubation)
 Increase lung volume  Relieve respiratory
or occasionally through the nose (nasotracheal intuba-
 Reduce or manipulate distress
tion). Intubation is considered for the following
the work of breathing  Reverse ventilatory
reasons: (1) the presence of upper airway obstruc-
muscle fatigue
tion, (2) inability to protect the lower airways
 Permit sedation,
from aspiration, (3) inability to clear pulmonary secre-
neuromuscular
tions, (4) hypoxemia despite supplemental oxygen,
blockade, or both
(5) respiratory acidosis, (6) progressive general
 Decrease systemic or
fatigue including mental status deterioration, and
myocardial oxygen (7) the need for positive pressure ventilation.3,5 The
consumption and
process of removing the artificial airway is called
intracranial pressure
extubation.
 Stabilize the chest wall
When patients require ventilatory support for a pro-
 Provide access to
longed time period, a tracheostomy is considered.
tracheal-bronchial tree
According to one author, it is best to allow 1week of en-
for pulmonary hygiene
dotracheal intubation; then, if extubation seems unli-
 Provide access for
kely during the next week, tracheostomy should be
delivery of an anesthetic,
considered.1 Recent recommendations also state that,
analgesic, or sedative
depending on the patient’s condition, transfer out of
medication
the intensive care unit (ICU) can generally be consid-
ered at the same time tracheostomy is being consid-
The following are indications for mechanical ered.6 However, a patient can also be intubated for
ventilation2,3: many weeks without tracheostomy, depending on the
 Apnea clinical situation.
 Acute hypercapnia that is not quickly reversible with A tracheostomy tube is inserted directly into the
standard treatment anterior trachea below the vocal cords, generally per-
 Partial pressure of arterial oxygen of less than 50 mm formed in the operating room. Benefits of tracheosto-
Hg with supplemental oxygen my include (1) reduced laryngeal injury, (2) improved
 Respiratory rate of more than 30 breaths per minute oral comfort, (3) decreased airflow resistance, (4)
 Vital capacity less than 10 liters per minute increased effectiveness of airway care, and (5) feasibility
 Negative inspiratory force of less than 25 cm H2O of oral feeding and vocalization.5 If the patient is able

463
464 APPENDIX III-B Mechanical Ventilation
Depth
Standard 15 mm markings
connector
Pilot balloon
and valve
Murphy
eye
Tracheal
cuff
FIGURE III-B.1
A typical endotracheal tube. (From Durbin, CG. Airway
Management. InJM Cairo, SP Pilbeam [eds.]. Mosby’s
Respiratory Care Equipment [7th ed]. St. Louis: Mosby, 2004.)
to be weaned from ventilatory support, humidified
oxygen can be delivered through a tracheostomy mask
(see Appendix III-A,Table III-A.1).
Cuff
Approximately 0.5 in. from the end of an endotracheal
or tracheal tube is a cuff (balloon). The cuff is inflated
to (1) ensure that all of the supplemental oxygen being
delivered by the ventilator via the artificial airway
enters the lungs and (2) help hold the artificial airway
in place. Cuff inflation pressure should be adequate to
ensure that no air is leaking around the tube; however,
cuff pressures should not exceed 20 mm Hg. High cuff
pressures have been linked to tracheal damage and scar-
ring, which can cause tracheal stenosis.
CLINICAL TIP
 A cuff leak should be suspected if the patient is able
to phonate or audible sounds come from his or her
mouth.
 Cuff leaks can occur if the endotracheal tube is
shifted (positional leak) or if the pressure decreases
in the cuff.
 If a cuff leak is suspected, then the respiratory
therapist or nurse should be notified. (Physical
therapists who specialize in critical or
cardiopulmonary care may be able to add air to the
cuff according to the facility’s guidelines.)
Positive Pressure Ventilators
Positive pressure ventilators are classified based on the
method used to stop the inspiratory phase and allow
expiration (cycling method) to occur.5 There are three
basic cycling methods: (1) pressure cycled, (2) volume
cycled, and (3) time cycled.7
Pressure-cycled ventilators stop inspiration at a
preset pressure, volume-cycled ventilators stop inspira-
tion at a preset volume, and time-cycled ventilators
stop inspiration at a preset time interval. Although
these methods allow for increased control of certain
variables during inspiration, holding only one variable
constant for the termination of positive pressure inhala-
tion allows other factors to affect inspiration and poten-
tially cause barotrauma or reduced inspiratory
volumes. These factors include position changes and
manual techniques.
For example, with a volume-cycled ventilator, a
preset volume will be delivered regardless of the
patient’s position, and reductions in chest wall expan-
sion owing to a patient’s position (e.g., side lying)
may increase the pressure placed on the dependent
lung tissue and result in barotrauma. Conversely, in
the same scenario, if a patient is on a pressure-cycled
ventilator, then pressure will be delivered to the
predetermined level, but because the patient’s posi-
tion may hinder chest expansion, a resultant lower
volume of inspired air may be delivered, because
the preset pressure limit was reached. Many newer
ventilators provide the clinician with more than one
cycling option, and certain modes of ventilation
allow for more than one parameter to determine the
inspiratory phase (as discussed throughout this
appendix).

CLINICAL TIP
 Being aware of the cycling method, the therapist
can pay attention to changes in the pressure or
tidal volume (VT) associated with his or her
interventions.
 Wide bore plastic tubing is used to create the
mechanical ventilator’s circuit. The terminal end of
this circuit directly connects to an endotracheal or
tracheal tube or, less commonly, to a face mask.5
Some ventilator circuits have an extra port at their
terminal end for an ‘‘in-line’’ suction catheter, which
allows for suctioning without the removal of the
ventilator circuit from the patient.5
MODES OF VENTILATION
Modes of ventilation can range from providing total
support (no work performed by the patient) to minimal
support (near-total work performed by the patient).
Modes of ventilation are geared toward allowing the
patient to do as much of the work of breathing as is
Mechanical Ventilation APPENDIX III-B 465
physiologically possible, while meeting the intended
objectives of ventilatory support. Even short periods
(11 days) of complete dependence on positive pressure
ventilation can lead to respiratory muscle atrophy and
concomitant reductions in diaphragm strength (25%)
and endurance (36%).8 Figure III-B.2 provides a
schematic of the conventional modes of ventilation
based on the amount of support they provide.
Characteristics of conventional and alternative
modes of ventilation are presented in Tables III-B.1
and III-B.2, respectively.
VENTILATORY SETTINGS
Ventilatory settings are parameters established to
provide the necessary support to meet the patient’s
individual ventilatory and oxygenation needs.4,11
Establishment of the ventilatory settings is dependent
on the patient’s (1) arterial blood gas levels, (2) vital
signs, (3) airway pressures, (4) lung volumes, and (5)
pathophysiologic condition, including the patient’s
ability to spontaneously breathe.4,11 Ventilator settings,
subdivided into those that influence oxygenation
and those that influence ventilation, are presented in
Table III-B.3.

FIGURE III-B.2
Schematic of mechanical ventilator modes: the ability of patients to participate in the process of
ventilation and oxygenation in part determines the mode of ventilation. Parameters used to determine the
patient’s ventilatory effort include the presence of spontaneous breaths, the number of breaths per minute
he or she initiates (respiratory rate [RR]), the volume of those breaths per breath (tidal volume [VT]), and
the negative inspiratory force (NIF) generated with those breaths.The values indicated above are examples
of patient characteristics along the spectrum from complete ventilatory dependence to independence.The
effectiveness of the patient’s efforts needs to be assessed based not only on the above parameters, but on
‘‘outcome’’ variables, such as oxygenation (PaO2, oxygen saturation as measured by pulse oximetry),
ventilation (PaCO2), and overall status (hemodynamic stability, symptoms).
466 APPENDIX III-B Mechanical Ventilation

Table III-B.1 CONVENTIONAL MODES OF VENTILATION

Modes Characteristics
CV (CMV) Total control of the patient’s ventilation: preset rate; FiO2;VT; flow rate; I:E ratio.
Patients may be sedated or pharmacologically paralyzed.
No active respiratory muscle activity is necessary.
AV Patient controls respiratory pattern and rate; breath initiated by patient creates negative airway
pressure in circuit; once initiated, the volume is delivered with either a preset volume or
pressure and flow rate; respiratory muscles are still working.
Patient can trigger RRs that are too high, leading to respiratory alkalosis or auto PEEP
(refer to Complications of Mechanical Ventilation).
Assist/control Combination of CVand AV; delivers breath of predetermined tidal volume with the patient’s
ventilation inspiratory effort.1
If the patient does not initiate a breath within a specified time period, the ventilator will deliver
a breath to maintain preset RR.
IMV Delivers breaths intermittently at preset time intervals with a preset RR,VT, and flow rate.
Patient is allowed to breathe spontaneously through a separate circuit between machine-
delivered breaths.
Different from AV in that attempts to breathe by the patient are not assisted by the ventilator.
Patient may ‘‘fight’’ the ventilator if patient tries to exhale during the mechanical inspiratory
phase, leading to dyssynchrony; this mode has largely been abandonedçreplaced by SIMV.
SIMV Similar to IMV: Mandatory breaths are delivered with a preset RR,VT, and flow; however, like
AV, it will assist a patient-initiated breath.
Mandatory breaths are only delivered when the patient is not initiating enough breaths to allow
a preset minute ventilation.
Pressure-supported Patient-initiated breaths are augmented with a preset flow of gas from the ventilator to maintain
ventilation constant inspiratory pressure; when the inspiratory flow drops to a preset value, the flow of
gas terminates.
Patient controls RR, inspiratory time, and flow; patient and ventilator determineVT and minute
ventilation.
TheVT received from the machine is related not only to the patient’s effort but also to the
amount of pressure provided by the ventilator.
Continuous positive Intended to decrease work of breathing by reducing the airway pressure necessary to generate
airway pressure inspiration throughout the respiratory cycle while the patient is spontaneously breathing.
Positive pressure is constantly maintained above atmospheric pressure.
Most commonly used during weaning from the mechanical ventilator or in an attempt to
postpone intubation (can be delivered via an endotracheal tube or a specially designed face
mask, respectively).
Commonly used at night for the treatment of sleep apnea.
AV, Assisted ventilation; CV, controlled ventilation; CMV, continuous mechanical ventilation or continuous mandatory ventilation;
FiO2, fraction of inspired oxygen; I:E ratio, inspiratory time to expiratory time ratio; IMV, intermittent mandatory ventilation;
PEEP, positive end-expiratory pressure; RR, respiratory rate; SIMV, synchronous IMV;VT, tidal volume.
Data from reference numbers 1, 2, 4, 7.

capacity before the onset of the next inspiration. The

COMPLICATIONS OF MECHANICAL
VENTILATION
Auto Positive End-Expiratory Pressure
Auto positive end-expiratory pressure (PEEP) occurs
when lung volumes fail to return to functional residual
process leading to auto PEEP is referred to as dynamic
hyperinflation.2,4 The primary consequence of dynamic
hyperinflation is increased air trapping, which results
in physiologic dead space due to pulmonary shunting
(perfusion is delivered to alveolar units that are not
receiving fresh ventilation), which decreases gas
exchange. Ultimately, this leads to an increased work

Table III-B.2 ALTERNATIVE MODES OF VENTILATION
Mode
Pressure control ventilation
High-frequency oscillation
ventilation
Inverse ratio ventilation
Mandatory minute
ventilation
(minimum minute
ventilation or augmented
minute ventilation)
Noninvasive positive
pressure ventilators
(NPPV)
Negative pressure
ventilators
Airway pressure
release ventilation
(APRV)
Adaptive support
ventilation
Pressure-regulated volume
control
High-frequency jet
ventilation
Mechanical Ventilation APPENDIX III-B 467
Characteristics
Delivers a preset airway pressure for a predetermined inspiratory time interval.
Inspiratory time is usually prolonged, and patients are generally sedated because
of discomfort due to the prolonged mechanical inspiration.
VT is determined by lung compliance; useful in cases in which barotrauma is
thought to exacerbate the acute lung injury (ARDS); now also available in
ACVor SIMVmodes.
A technique of ventilation that is administered with frequencies of 100-3,000
breaths per minute and consequently small tidal volumes of 1-4 ml/kg.
Primary advantage is dramatic reduction of airway pressure and has shown
beneficial results in neonates and adults with ARDS, particularly those
adults who do not respond positively to conventional mechanical
ventilatory modes.
A rarely used technique involving the use of an inspiratory to expiratory
ratio of more than 1 to 1; can be delivered as a pressure-controlled or
volume-cycled mode.
The proposed benefit is the recruitment of a greater number of lung units
during the respiratory pause and longer inspiration.
Potential risk of generating auto PEEP and dynamic hyperinflation (refer to
Complications of Mechanical Ventilation).
Only set parameter is the minute ventilation; if spontaneous, unassisted breaths
do not meet that minute ventilation, the ventilator makes up the difference by
supplying mechanical breaths. Used primarily in weaning patients from a
ventilator.
Delivery of ACV, SIMV, and PSVmodes of ventilation via a nose mask or face
mask to reduce the need for intubation.
Bi-level positive airway pressure (BiPAP), also called bi-levelpressure assist, is a form of
NPPV that employs PSVand PEEP.
Shown to be useful in reducing in-hospital mortality in COPD patients and long-
term use in patients with neuromuscular diseases.
Exposes the chest wall to subatmospheric pressure during inspiration to reduce
intrapleural pressure, thereby allowing air to enter the lungs.
Efficacy has not been demonstrated in patients with COPD and is unproven for
acute respiratory failure.
Lungs are kept inflated with a preset airway pressure, and exhalation occurs during
cyclic reductions in pressure.
Advocated for protecting the lung from high-peak airway pressures, although no
benefit has been demonstrated over conventional methods.
A mode of ventilation that accommodates a patient’s breathing pattern by
changing the number of mandatory breaths and pressure support level until a
calculated tidal volume is reached.
Provides volume support to a patient while keeping peak inspiratory pressures
(PIP) at the lowest level by altering inspiratory time and peak flow. Useful in
patients with changing airway compliance or characteristics.
Uses a nozzle and injector to deliver jets of gas directly into the lung at high rates.
Indicated for the neonatal population who has pulmonary hypoplasia, restrictive
lung disease, and persistent pulmonary hypertension.Typically used in tandem
with a conventional ventilator.
Continued
468 APPENDIX III-B Mechanical Ventilation

Table III-B.2 ALTERNATIVE MODES OF VENTILATION—cont’d

Mode Characteristics
Partial liquid Uses perfluorocarbon liquids (does not mix with surfactant and has a high
ventilation solubility for O2 and CO2). Lungs are filled with the liquid to approximately
functional residual capacity, and then standard mechanical ventilation is
attempted.
Has not demonstrated benefits above conventional ventilator modes, and still
requires much research before being used routinely.

ACV, Assist/control ventilation; ARDS, adult respiratory distress syndrome; COPD, chronic obstructive pulmonary disease; I:E ratio,
inspiratory time to expiratory time ratio; PEEP, positive end-expiratory pressure; PSV, pressure supported ventilation; SIMV, synchronous
intermittent mandatory ventilation;VT, tidal volume.

of breathing owing to higher respiratory demand, as
well as altered length-tension relationships of the
inspiratory muscles. Auto PEEP and concomitant air
trapping can occur when the minute ventilation or
respiratory rate is too high; the inspiratory-expiratory
ratios are not large enough, or the endotracheal tube is
too narrow or kinked; there is excess water condensa-
tion in the tubing; or in patients with obstructive lung
disease. A combination of the aforementioned factors
can increase the likelihood of auto PEEP. In patients
with chronic obstructive pulmonary disease who are
on ventilator modes that allow them to initiate ventila-
tor-assisted breaths (assisted ventilation, assist/control
ventilation, synchronous intermittent mandatory venti-
lation [SIMV], pressure-supported ventilation [PSV]),
the therapist should realize that activity could increase
the patient-generated respiratory rate. Some modes
will then, given the initiation of a breath, provide a set
volume of air (assisted ventilation, assist/control
ventilation, SIMV) that could increase the likelihood
of hyperinflation owing to auto PEEP. This can also
happen in modes that do not deliver a set volume of
air (PSV), because inspiration is assisted with positive
pressure.
Barotrauma
Barotrauma refers to damage to the lungs caused by
excessive airway pressure. Many of the alternative
modes of ventilation are geared toward reducing this
complication (Table III-B.2). In the normal lung, spon-
taneous inhalation without ventilatory support takes
place because of negative pressure. The volume of
inhaled air is limited by the return of intrapulmonary
pressure back to atmospheric pressure in the lungs
during inhalation. Because mechanical ventilation is
predominantly delivered with positive inspiratory pres-
sure, these normal physiologic mechanisms for
preventing such trauma are bypassed, and pressures in
the lung exceed normal pressures. Another consider-
ation is that many of the lung conditions requiring
mechanical ventilation do not uniformly affect the
lungs (adult respiratory distress syndrome, pneumonia).
Inhalation volumes are delivered to those areas that
are still normal, which can overdistend (causing high
pressure) as a result. This can produce stress fractures
in the walls of the alveoli, thus exacerbating the acute
lung condition.12,13 Infants who are mechanically venti-
lated are five times more likely to develop bronchopul-
monary dysplasia than are infants who are not
mechanically ventilated.14 It is thought that barotrauma
exacerbates the acute lung injury associated with adult
respiratory distress syndrome.1 Other complications
associated with barotrauma include pneumothorax
and subcutaneous emphysema.4
Other possible complications of mechanical ventila-
tion are as follows2,4,11:
 Improper intubation can result in esophageal or
tracheal tears. If the artificial airway is mistakenly
placed in the esophagus and is not detected, gastric
distention can occur with the initiation of positive
pressure.
 Ventilator-associated pneumonia (VAP) — a form of
nosocomial infection that occurs in patients who
are mechanically ventilated longer than 48 hours.
VAP is highly problematic as it results in increased
length of stay for patients both in the ICU and in
the hospital. Mortality is also increased 27% to 48%
if a patient has VAP. Risk factors include immuno-
suppression, underlying lung conditions, body posi-
tion, level of consciousness, endotracheal tubing,
ventilator circuits, and hospital personnel not fol-
lowing standard precautions. Prevention consists of
good oral hygiene to the patient before intubation,
avoiding saline lavage during suctioning, changing
 Mechanical Ventilation APPENDIX III-B 469

Table III-B.3 VENTILATOR SETTINGS

Purpose Setting Characteristic
Oxygenation Fraction of inspired The percentage of inspired air that is oxygen; at normal respiratory rate (RR),
oxygen (FiO2) tidal volume (VT), and flow rates, an FiO2 of 21% (ambient air) yields a normal
oxygen partial pressure of 95-100 mm Hg; an increase in the percentage of
oxygen delivered to the alveoli results in a greater PaO2 and therefore a greater
driving force for the diffusion of oxygen into the blood.
FiO2 of 60% has been set as the threshold value to avoid toxicity with
prolonged use.
Positive end- The pressure maintained by the mechanical ventilator in the airways at the end
expiratory of expiration; normal physiologic PEEP (maintained by sufficient surfactant
pressure (PEEP) levels) is considered to be 5 cm H2O.
Settings are adjusted as needed to maintain functional residual capacity above
closing capacity to avoid closure of alveoli.
Closure of alveoli can result in shunting of blood past the alveoli without gas
exchange, which results in decreased oxygenation.
Ventilation RR Set according to the amount of spontaneous ventilatory efforts by the patient;
different ventilatory modes, described inTable III-B.1, are prescribed
according to the patient’s needs; patients who are unable to generate any
spontaneous breaths are fully ventilated at respiratory rates of 12-20 breaths
per minute.
This rate is decreased accordingly for those who are able to generate
spontaneous breaths.
The amount of volume delivered with each breath is adjusted with respiratory
rate to control partial pressure of arterial carbon dioxide (PaCO2).
VT Excessive volume leads to increased airway pressures, and therefore pressures
are routinely monitored to prevent barotrauma.
At times, hypercapnia is allowed to prevent high lung pressures due to the
delivered volume and noncompliance of lung tissue, termed permissive
hypercapnia.
Inspiratory Set to match the patient’s peak inspiratory demands; if this match is not correct,
flow rate it can cause the patient discomfort while breathing with the ventilator.
High flow rates deliver greater volume in less time and therefore allow longer
expiratory times (prevents hyperinflation); however, this also leads to greater
peak airway pressure and the possibility of barotrauma.
If the rate is too slow, the patient may attempt to continue to inhale against a
closed circuit, resulting in respiratory muscle fatigue.
Inspiratory-to- The inspiratory-to-expiratory ratio is set with the goal of allowing the ventilator
expiratory ratio to be as synchronous as possible with the patient’s respiratory ratio.
For patients who are not spontaneously breathing, this ratio is set according to
what is required to maintain adequate ventilation and oxygenation.
Sensitivity Pressure change is required in the airway to trigger an ACVor PSV breath;
typically —1 to —3 cm H2O.
If mechanical sensors respond poorly, then respiratory muscle fatigue can occur.
If the sensors are too sensitive, then hyperventilation can develop.
ACV, Assist/control ventilation; PaO2, oxygen saturation as measured by pulse oximetry; PSV, pressure-supported ventilation.
Data from Marino P.The ICU Book (2nd ed). Philadelphia: Lea & Febiger, 1998; SlutskyAS. Mechanical ventilation. American College of
Chest Physicians’ Consensus Conference. Chest 1993;104:1833; Howman SF. Mechanical Ventilation: A Review and Update for Clinicians.
Hospital Physician 1999;December:26-36.
470 APPENDIX III-B Mechanical Ventilation
positions frequently, and preventing aspiration by
keeping the head of the bed up 30 degrees.15
 Oxygen toxicity: Oxygen levels that are too high
and maintained for a prolonged time can result in
(1) substernal chest pain that is exacerbated by
deep breathing, (2) dry cough, (3) tracheal irritation,
(4) pleuritic pain with inspiration, (5) dyspnea,
(6) nasal stiffness and congestion, (7) sore throat,
and (8) eye and ear discomfort.
 Cardiovascular: High positive pressures can result in
decreased cardiac output from compression of great
vessels by overinflated lungs.
WEANING FROM MECHANICAL
VENTILATION
The process of decreasing or discontinuing mechanical
ventilation in a patient is referred to as the weaning pro-
cess.11 A contributing factor to a successful wean from
ventilatory support is the resolution or stability of the
condition that led to the need for ventilatory support.16
A spontaneous breathing trial (SBT) is typically per-
formed to evaluate a patient’s readiness to begin the
weaning process. The trial consists of the patient
breathing spontaneously for 15 to 30 minutes while
being closely monitored.7
The patient criteria for an attempt at weaning from
mechanical ventilation is as follows:
 Spontaneous breathing
 Fraction of inspired oxygen < 50% and PEEP < 5
cm H2O with oxygen saturation as measured by
pulse oximetry > 90%
 Maximal Inspiratory pressure > —30 cm H2O:
Pressures greater than —30 have been associated
with successful extubation, while pressures greater
than —15 are associated with an inability to maintain
spontaneous breathing17
 Respiratory rate < 35 breaths per minute
 Tidal volume > 325 ml17
 Respiratory rate/VT ratio of < 105 (A respiratory rate/
VT ratio > 105 indicates shallow and rapid breathing
and is a powerful predictor of an unsuccessful
wean.)17,18
Examples of weaning methods are as follows:
 IMV or SIMV: Decreasing the number of breaths
per minute that the ventilator provides requires
the patient to increase his or her spontaneous
breaths. This is commonly used after surgery,
while patients are waking up from anesthesia.
These patients typically have not been on support
for an extended period of time and do not usually
have a lung condition that required them to be intu-
bated in the first place. As soon as respiratory drive
and spontaneous breathing return, it is expected
that the patient can be removed from ventilatory
support.
 T-piece: Breathing off of the ventilator, while still
intubated, for increasing periods of time. This tech-
nique is sort of an all-or-none method. Patients
need to have the respiratory drive to breathe sponta-
neously and the capability to generate adequate VT
to attempt this weaning process. The process aims
to improve respiratory muscle strength and endur-
ance with prolonged time periods of independent
ventilation.
 PSV: The patient spends periods of time with
decreased pressure support to increase his or her
spontaneous ventilation.Two factors can be manipu-
lated with PSV: (1) to increase strength load on the
respiratory muscles, reduce the PSV, and (2) to
increase endurance requirement on the respiratory
muscles, increase the length of time that PSV is
reduced.
Currently it is the consensus that the T-piece and
PSV methods of weaning were superior to the IMV or
SIMVmethods.16,19
Additionally, two new techniques have been devel-
oped to possibly enhance the patient’s ability to wean
off the ventilator. These include automatic tube com-
pensation (ATC) and proportional-assist ventilation
(PAV). Both of these techniques are designed to lessen
the resistive load of the artificial airways and associated
ventilator tubing thus decreasing the work of breathing
of the patient and possibly increasing the tolerance of
the weaning process.16
Five major factors to consider during a patient’s
wean are as follows11:
1. Respiratory demand (the need for oxygen for meta-
bolic processes and the need to remove carbon diox-
ide produced during metabolic processes) and the
ability of the neuromuscular system to cope with
the demand
2. Oxygenation
3. Cardiovascular performance
4. Psychological factors
5. Adequate rest and nutrition
Signs of increased distress during a ventilator wean
are as follows4,11:
 Increased tachypnea (> 30 breaths per minute)
 Drop in pH to <7.25 to 7.30 associated with an
increasing PaCO2

 Paradoxical breathing pattern (refers to a discoordi-
nation in movements of the abdomen and thorax
during inhalation) (Refer to Chapter 2.)
 Oxygen saturation as measured by pulse oximetry
<90%
 Change in heart rate of > 20 beats per minute
 Change in blood pressure > 20 mm Hg
 Agitation, panic, diaphoresis, cyanosis, angina, or
arrhythmias
PHYSICAL THERAPY CONSIDERATIONS
A patient who is mechanically ventilated may require
ventilatory support for a prolonged period of time.
Patients who require prolonged ventilatory support are
at risk for developing pulmonary complications, skin
breakdown, joint contractures, and deconditioning
from bed rest. Physical therapy intervention, including
bronchopulmonary hygiene and functional mobility
training, can help prevent or reverse these complications
despite mechanical ventilation. Recently it was demon-
strated that patients whowere on mechanical ventilation
for greater than 4 days were able to safely participate in
activities such as sitting at the edge of the bed, sitting in
a chair, and ambulating distances up to 100 feet at time
of discharge from the ICU setting. These patients were
determined to be physiologically ready for activity
if (1) they were responsive to verbal stimulation,
(2) their FiO2 was 0.6, (3) their positive end-expiratory
pressure was 10 cm H2O, and (4) they had an absence
of orthostatic hypotension and catecholamine drips.20
Furthermore, early activity provided by a multi-
disciplinary team, including physical therapy, has
been shown to decrease length of hospital stay.21
Bronchopulmonary Hygiene
Patients on ventilatory support are frequently suc-
tioned as part of their routine care. Physical therapists
References
1. Marino P.The ICU Book (2nd ed). Philadelphia: Lea &
Febiger, 1998, 1998.
2. SlutskyAS. Mechanical ventilation. American College of
Chest Physicians’ Consensus Conference [see
comments]. Chest 1993;104:1833.
3. Chestnutt MS, MurrayJA, Prendergast TJ. Pulmonary
Disorders. In Current Medical Diagnosis & Treatment
(47th ed), LM Tierney, SJ McPhee, MA Papadakis (eds).
NewYork: McGraw Hill, 2008.
Mechanical Ventilation APPENDIX III-B 471
working with patients on their bronchopulmonary
hygiene and airway clearance should use suctioning as
the last attempt to remove secretions. Encouraging the
process of huffing and coughing during treatment
will improve or maintain cough effectiveness (huffing
is performed without glottis closure, which cannot be
achieved when intubated), owing to activation of the
expiratory muscles. If patients have difficulty with a
deep inspiration for an effective huff or cough, then
the use of manual techniques; postural changes; or
assistive devices, such as an adult manual breathing
unit (AMBU bag), can be used to facilitate depth of
inspiration.
Weaning from Ventilatory Support
During the weaning process, the physical therapist can
play a vital role on an interdisciplinary team responsible
for coordinating the wean. Physical therapists offer a
combined understanding of the respiratory difficulties
faced by the patient, the biomechanics of ventilation,
the principles of exercise (weaning is a form of exercise),
and the general energy requirements of functional
activities. Physical therapists can work with the multi-
disciplinary team to optimize the conditions under
which the patient attempts each wean (time of day, activ-
ities before and after the wean, position during the
wean) and parameters to be manipulated during the
wean (frequency, intensity, duration). Patients should
be placed in a position that facilitates the biomechanics
of their ventilation.22 For many patients, this is seated
and may also include the ability to sit forward with the
arms supported.
Biofeedback to increase VT and relaxation has been
shown to improve the effectiveness of weaning and
reduce time on the ventilator.23 Inspiratory muscle-
resistive training has also been shown to increase respi-
ratory muscle strength and endurance to facilitate the
weaning success.24
4. Howman SF. Mechanical Ventilation: A Review and
Update for Clinicians. Hospital Physician
1999;December:26-36..
5. Sadowsky HS.Thoracic Surgical Procedures,
Monitoring, and Support Equipment.
In EA Hillegass, HS Sadowsky (eds),
Essentials of Cardio-pulmonary Physical
Therapy (2nd ed). Philadelphia: Saunders,
2001;464-469.
472 APPENDIX III-B Mechanical Ventilation
6. Huntziner A. NAMDRC Recommendations for
Prolonged Mechanical Ventilation. Am Fam Physician
2006;73(7).
7. Pilbeam SP, CairoJM. Mechanical Ventilation:
Physiological and Clinical Applications (4th ed).
St. Louis: Mosby, 2006.
8. Anzueto A, PetersJI,Tobin MJ, et al. Effects of
Prolonged Mechanical Ventilation on Diaphragmatic
Function in HealthyAdult Baboons. Crit Care Med
1997;25:1187-1190.
9. Fan E, Stewart TE. New Modalities of Mechanical
Ventilation: High-frequency Oscillatory Ventilation and
Airway Pressure ReleaseVentilation. Clinics in Chest
Medicine 2006;27(4).
10. Chang DW. Clinical Application of Mechanical
Ventilation (3rd ed). NewYork:Thomson Delmar
Learning, 2006.
11. Gerold KB. Physical Therapists’ Guide to the Principles
of Mechanical Ventilation. Cardiopul PhysTher 1992;3:8.
12. Costello ML, Mathieu-Costello O,WestJB. Stress
Fracture of Alveolar Epithelial Cells Studied by
Scanning Electron Microscopy. Am Rev Respir Dis
1992;145:1446-1455.
13. Mathieu-Costello O,WestJB. Are Pulmonary Capillaries
Susceptible to Mechanical Stress? Chest
1994;105(Suppl):102S-107S.
14. Heimler R, Huffman RG, Starshak RJ. Chronic Lung
Disease in Premature Infants: A Retrospective
Evaluation of Underlying Factors. Crit Care Med
1988;16:1213-1217.
15. Augustyn B.Ventilator-Associated Pneumonia: Risk
Factors and Prevention. Crit Care Nurse 2007;27(4).
16. Eskandar N, Apostolakos MJ.Weaning from Mechanical
Ventilation. Crit Care Clin 2007;23(2).
17. Eskandar, SinerJM. Liberation from Mechanical
Ventilation: What Monitoring Matters? Crit Care Clin
2007;23(3):613-638.
18. Yang KL,Tobin MJ. A Prospective Study of Indexes
Predicting the Outcome of Trials of Weaning from
Mechanical Ventilation. N EnglJ Med
1991;324:1446-1495.
19. Dries DJ.Weaning from Mechanical Ventilation.
J Trauma 1997;43:372-384.
20. Baily P, et al. EarlyActivity Is Feasible and Safe in
Respiratory Failure Patients. Crit Care Med
2007;35(1):139-145.
21. Morris PE, Holbrook A,Thompson C, et al.
A Mobility Protocol for Acute Respiratory
Failure Patients Delivered by an ICU Mobility
Team Shortens Hospital Stay. Crit Care Med
2006;34(A20).
22. Shekleton ME. Respiratory Muscle Condition and
the Work of BreathingçA Critical Balance in the
Weaning Patient. AACN Clin Issues Crit Care
1991;2:405-414.
23. HollidayJE, HyersTM.The Reduction of WeanTime
from Mechanical Ventilation UsingTidal Volume and
Relaxation Biofeedback. Am Rev Respir Dis
1990;141:1214-1220.
24. AldrichTK, KarpelJP, Uhrlass RM, et al.Weaning from
Mechanical Ventilation: Adjunctive Use of Inspiratory
Muscle ResistiveTraining. Crit Care Med 1989;17:143-147.
 Appendix III-C Circulatory Assist Devices
Jackie A. Mulgrew
Circulatory assist devices are designed to support
patients in hemodynamic collapse, cardiogenic shock,
cardiopulmonary arrest, or prophylactically during
invasive procedures. Circulatory assist devices are
either percutaneous or surgically implanted.
There are four types of percutaneous devices:
1. Counterpulsation devices: Intraaortic balloon pump
(IABP), enhanced external counterpulsation
(EECP)
2. Cardiopulmonary assist devices: Cardiopulmonary
support (CPS)
3. Left ventricular assist devices: TandemHeart,
Impella
4. Extracorporeal membrane oxygenation (ECMO).
There is only one type of surgical device. It is the
ventricular assist device (VAD).These devices are man-
ufactured by companies such as Thoratec and
MicroMed.
The purpose of this appendix is to describe each of
these types of circulatory assist devices and to describe
the implications to physical therapy evaluation or
treatment.
PERCUTANEOUS DEVICES
Counterpulsation Devices
INTRAAORTIC BALLOON PUMP
The main function of the IABP is to lessen the work
(decreased myocardial oxygen demand) of the heart by
decreasing afterload in the proximal aorta through
a vacuum effect created by rapid balloon deflation.
The IABP also improves coronary artery perfusion
(increased myocardial oxygen supply) by increasing
diastolic pressure in the aorta and thereby displac-
ing blood proximally into the coronary arteries.1,2 The
IABP consists of a catheter with a sausage-shaped bal-
loon at the end of it, all of which is connected to an
external pump-controlling device. The catheter is
inserted percutaneously into the femoral artery and is
threaded antegrade until it reaches the proximal des-
cending thoracic aorta.
Figure III-C.1illustrates the balloon inflating during
ventricular filling (diastole) and deflating during ven-
tricular contraction (systole). The deflation of the bal-
loon just before the aortic valve opening decreases
afterload and therefore reduces resistance to the ejec-
tion of blood during systole. The blood in the aorta is
then propelled forward into the systemic circulation.
The inflation of the balloon during diastole assists
with the perfusion of the coronary and cerebral vessels.
This process is referred to as counterpulsation, because the
inflation and deflation of the balloon occur opposite
to the contraction and relaxation of the heart.1,2
Indications for IABP include the following3-7:
 Acute left ventricular failure
 Unstable angina
 Status post acute myocardial infarction
 Cardiogenic shock
 Papillary muscle dysfunction with resultant mitral
valve regurgitation
 Weaning patients from cardiopulmonary bypass
 Ventricular septal defect
 Refractory ventricular dysrhythmias
 Adjunctive therapy after thrombolysis in patients at
high risk for restenosis
 Adjunctive therapy in high risk or complicated
angioplasty
 Prophylaxis in patients with severe left main coro-
nary arterial stenosis or critical aortic stenosis in
whom surgery is pending
 Bridge to heart transplantation
The ratio of heartbeats to counterpulsations of the
IABP indicates the amount of circulatory support an
individual requires (e.g., 1 to 1 is one counterpulsation
to one heart beat; 1 to 4 is one counterpulsation to
every fourth heart beat; a ratio of 1 to 1 provides maxi-
mum circulatory support). Weaning from an IABP
involves gradually decreasing the number of counter-
pulsations to heartbeats, with the goal being 1 counter-
pulsation for every fourth heartbeat, as tolerated,
before discontinuing the IABP. Although weaning
473
474 APPENDIX III-C Circulatory Assist Devices

from the IABP is generally performed by decreasing the

number of counterpulsations, weaning also can be per-
formed by gradually decreasing the amount of inflation
pressure of the balloon in the aorta.1,2
Potential complications of IABP include the
following8-11:
 Ischemia of the involved limb secondary to occlu-
sion of the femoral artery from compression or
from thrombus formation
 Proximal slippage of the balloon resulting in occlu-
sion of subclavian, carotid, or brachiocephalic
arteries or distal slippage resulting in occlusion of
renal arteries
 Vascular laceration necessitating surgical repair
 Major hemorrhage
 Cholesterol embolization
 CVA
 Sepsis
 Balloon rupture
A
CLINICAL TIP
 During IABP, the lower extremity in which femoral
access is obtained cannot be flexed at the hip, and
the patient’s head cannot be raised higher than
30 degrees in bed in order to prevent the intraaortic
balloon catheter from migrating.12
 If the IABP becomes dislodged, allow 1 to 2 seconds
of bleeding to allow any clots to be removed before
applying firm pressure, and then call for the nurse
or doctor.12
 Once the IABP is removed, the patient should
be on bed rest for a minimum of 8 hours and
should avoid exercising the extremity to prevent
bleeding.12
 Depending on the amount of time spent on
the IABP, the patient is at risk for skin
breakdown due to limited mobility and
decreased perfusion to the affected extremity.
Therefore, patients benefit from pressure-reducing
or pressure-relieving mattresses; frequent
repositioning; and assessment of vascular, motor,
B and sensory function.12
 To prevent pulmonary complications while
FIGURE III-C.1
Mechanisms of action in intraaortic balloon pump. A, Diastolic on bed rest, patients benefit from frequent
balloon inflation augments coronary blood flow. B, Systolic repositioning and deep breathing and coughing
balloon deflation decreases afterload. (From Urden LD. exercises.
Thelan’s Critical Care Nursing: Diagnosis and Management  Patients may require range of motion or
[5th ed], St Louis: Mosby, 2006.) strengthening exercises for the hip and knee after
the IABP is removed. The ankle can be ranged
while the patient is on the IABP.12
 CirculatoryAssist Devices
ENHANCED EXTERNAL COUNTERPULSATION
Enhanced external counterpulsation is a noninvasive
technique that reduces angina and extends time to exer-
cise-induced myocardial ischemia in patients with
symptomatic coronary disease. This type of treatment
is primarily performed in outpatient clinics by EECP
technicians under the supervision of a cardiologist.
Information provided here is brief because it is not uti-
lized by the acute care physical therapist.
EECP uses the sequential inflation of three sets of
pneumatic cuffs wrapped around the lower extremities.
The cuffs are inflated sequentially from calf to thigh
to buttock at the onset of diastole, producing aor-
tic counterpulsation, diastolic augmentation, and
increased venous return, as illustrated in Figure III-C.2.
At the onset of systole, the external pressure in the
cuffs is released rapidly, producing a decrease in systolic
pressure.13 In contrast to IABP, EECP provides long-
lasting increase in coronary blood flow (12 months).14
A treatment procedure involves 1 to 2 hours per day
for a total of 35 hours of therapy. The patient lies
supine for the treatment. Upon completion of the 35
sessions, studies have shown that the time to exercise-
induced ischemia is delayed significantly and the
FIGURE III-C.2
Enhanced External Counterpulsation (EECP). (Courtesy
Vasomedical,Westbury, NY.)
APPENDIX III-C 475
frequency of angina is reduced significantly compared
with patients who did not receive EECP.14,15
Cardiopulmonary Assist Devices
CARDIOPULMONARY SUPPORT
Cardiopulmonary support provides full hemodynamic
support and oxygenation of venous blood. It is similar
to the support provided during coronary artery bypass
graft surgery and valve replacement surgery. CPS
involves placing large bore catheters in the central arte-
rial and venous circulation. Blood from the venous
catheter is removed from the patient and pumped
through an external heat exchanger and oxygenator; it
is then returned under pressure to the systemic arterial
circulation via the arterial cannula. The femoral artery
and the femoral vein are commonly a source of entry
into the body for CPS.16,17 CPS requires continuous,
highly technical support and is inserted in a cathe-
terization laboratory. CPS is in general not suitable for
long-term applications because of the large-bore
cannulas, resulting in significant pressure gradients
and eventually hemolysis.18 The mean duration for
CPS is 62 hours.19
Indications for CPS include the following17,18:
 Cardiogenic shock and cardiopulmonary arrest
 High-risk percutaneous transluminal coronary
angioplasty (PTCA)
 Pulmonary embolism
 Intractable ventricular arrhythmias
 Hypothermia
 Beating heart donor preservation for transplantation
CLINICAL TIP
 Due to the large cannulations required during this
procedure, assess the patient for local vascular or
neurologic changes after the cannulae are removed.
Left Ventricular Assist Devices
Percutaneous left ventricular assist devices (LVAD) pro-
vide short-term circulatory assist without the need for
cardiac surgery. Currently there are two types of percu-
taneous LVAD available:TandemHeart and Impella.
TANDEMHEART
The TandemHeart is an extracorporeal (external) con-
tinuous flow centrifugal assist device. Cannulas are
inserted percutaneously through the femoral vein and
are advanced across the interatrial septum into the
476 APPENDIX III-C Circulatory Assist Devices
left atrium. The pump withdraws oxygenated blood
from the left atrium back to the pump via the cannula
in the femoral vein before it is ejected into the left ven-
tricle.The blood returns via the cannula in the femoral
vein to the pump resting extracorporeally on the
upper thigh. The pump propels the blood by means of
a magnetically driven impeller through the outflow
port, and returns it to one or both femoral arteries via
arterial cannulas.20 Some of the blood in the femoral
arteries continues in a forward flow through the arterial
system to perfuse the lower extremities, and some
returns in a reverse flow back up to the aorta to provide
perfusion to the coronary arteries, the upper extremi-
ties, and the head. The reverse flow is possible because
there is no forward flow from the left ventricle to the
aorta. Through this pumping action, theTandemHeart
can provide a cardiac output of up to 4L/min.21,22
Figure III-C.3 illustrates theTandemHeart device.
By unloading the left ventricle, decreasing myocar-
dial oxygen consumption, and decreasing left atrial fill-
ing pressures, this percutaneous LVAD can provide
FIGURE III-C.3
TandemHeart percutaneous VAD. (Courtesy Cardiac Assist,
Pittsburgh, Pennsylvania.)
short-term support from a few hours to 14 days in the
intensive care unit. This gives time for the native heart
to recover.20
Indications for theTandemHeart include the follow-
ing20-22:
 High-risk percutaneous coronary interventions
 Bridge to emergency coronary bypass grafting
 Bridge to cardiac transplantation
 Bridge to surgically implanted left ventricular assist
device
 Postcardiotomy cardiogenic shock
Potential complications of theTandemHeart include
the following22,23:
 Bleeding
 Thromboembolism
 Transseptal cannula dislocation
 Arterial cannula dislocation
 Lower extremity ischemia
 Infection
CLINICAL TIP
 Avoid hip flexion > 20 degrees to prevent the
cannula from kinking or displacing.
 Use a knee immobilizer to prevent flexion of
the hip.
 Keep the head of the bed elevated < 20 degrees.
 Use the reverse Trendelenburg position
< 30 degrees.
 When the cannulae are removed, do not allow
hip flexion for at least 4 to 6 hours.
IMPELLA
The Impella is a minimally invasive percutaneous ven-
tricular unloading catheter that allows the heart to rest
and recover byactively unloading the ventricle and redu-
cing myocardial workload and oxygen consumption,
while increasing cardiac output, coronary perfusion,
and end organ perfusion.There are two types of percuta-
neous catheters: The Impella LP2.5 and the Impella
LP5.0. The Impella LP2.5 can provide up to 2.5 L/min
of cardiac output and can provide support for up to
5 days, whereas the Impella LP5.0 can provide up to
5 L/min of cardiac output and can provide support for
up to10 days. Figure III-C.4 illustrates an Impella LP 2.5.
Either catheter is inserted percutaneously in the car-
diac catheterization laboratory into the femoral artery,
however the Impella LP5.0 requires a small cut-down
of the femoral artery. The inflow cannula miniaturized
pump is inserted through the aortic valve under
 CirculatoryAssist Devices APPENDIX III-C 477

CLINICAL TIP
 There are currently no specific guidelines that
relate to hip ROM or mobility of the patient.
Typically these patients are critically ill, so
if you are consulted to evaluate a patient
with an Impella, follow your hospital’s
guidelines related to ROM and mobility
guidelines. Consider the risk of kinking or
displacing the femoral cannula in your clinical
decision making.

Extracorporeal Membrane Oxygenation

Extracorporeal membrane oxygenation involves the
use of a device external to the body for direct oxygena-
tion of blood, assistance with the removal of carbon
dioxide, or both. The primary indication for ECMO is
cardiac or respiratory failure that is not responding to
FIGURE III-C.4 maximal medical therapy and conventional mechanical
Illustration of the Impella LP 2.5. (CourtesyABIOMED, ventilation. The pediatric population with respiratory
Danvers, Massachusetts.) failure seems to benefit from this therapy the most;
however, the successful use of ECMO in the adult pop-
fluoroscopic guidance into the left ventricle to pump ulation is improving.24,25
blood from the left ventricle into the ascending aorta. Patient situations that may require ECMO include
An advantage of the Impella over the TandemHeart is the following:
that there is no need for a trans-septal puncture and  Neonatal respiratory distress syndrome
no extracorporeal blood.22  Congenital heart diseases
Indications for the Impella include the  Postcardiotomy cardiac or pulmonary support
following20,22:  Cardiac arrest
 Cardiogenic shock
Impella LP2.5  Primary respiratory failure
 High-risk percutaneous coronary interventions  Post lung or heart transplantation orVAD placement
 Post percutaneous coronary intervention support As illustrated in Figure III-C.5, the ECMO system
 Acute myocardial infarction with low cardiac output consists of a venous drainage cannula, a reservoir for
Impella LP5.0 blood, a pumping device that uses a centrifugal or a
 Postcardiotomy low cardiac output syndrome roller system, an oxygenator, and an arterial or a
 Post percutaneous coronary intervention support second venous return cannula.24,26
 Myocarditis The pumping device is used to help a failing ventri-
 Cardiogenic shock cle circulate blood, whereas the oxygenator device
 Acute heart failure assists the failing respiratory system to fully oxygenate
 Bridge to next decision the patient. Patients who have respiratory failure
require concurrent mechanical ventilation to prevent
Potential complications of the Impella include the atelectasis while on ECMO. However, less positive
following22: pressure is required to oxygenate blood when on
 Bleeding ECMO, resulting in a decreased incidence of
 Thromboembolism barotrauma.2,24
 Lower extremity ischemia The system that uses the venous drainage to arterial
 Pump displacement return cannula (V-A mode) is primarily performed on
 Infection patients who require cardiac or cardiorespiratory
478 APPENDIX III-C Circulatory Assist Devices
FIGURE III-C.5
Illustration of extracorporeal membrane oxygenation. (From Shanley CJ, Bartlett RH: Extracorporeal life
support:Techniques, indications, and results. In CameronJL [ed]: Current Surgical Therapy [4th ed].
St. Louis, Mosby-Year Book, 1992, pp 1062-1066.)
support. The V-A mode can be achieved in the follow-
ing three ways24:
1. Femoral vein to the ECMO system and back to the
femoral artery
2. Right atrium to the ECMO system and back to the
ascending aorta
3. Femoral vein to the ECMO system and back to the
ascending aorta
The system that uses the venous drainage to venous
return cannula (V-Vmode) is primarily used for patients
who only have respiratory failure. The V-V mode is the
preferred mode and can be achieved in the following
two ways24:
1. Internal jugular vein to the ECMO system and back
to the common femoral vein
2. Common femoral vein drainage to the ECMO
system and back to the contralateral common femo-
ral vein
Patients who are on V-A mode ECMO are typically
anticoagulated with heparin and may require the use
of IABP to further assist the ventricle. Patients on the
V-V mode may require sedation and/or medical paraly-
sis to help improve oxygenation to organs and tissues
by minimizing the metabolic demands of an awake
person.24
The following are potential complications of
ECMO26,27:
 Bleeding
 Lower limb ischemia
 Thrombocytopenia
 Thromboembolism
 Failure of the oxygenator device
CLINICAL TIP
 The physical therapist generally does not start direct
handling of a patient on ECMO until the ECMO
apparatus is disconnected due to the risk of
dislodgment in patients with severe medical
conditions.26
 CirculatoryAssist Devices
 However, if working with a patient with ECMO is
indicated, reducing the patient’s stress level
decreases the amount of energy expenditure while
on ECMO.26
 Rolling or turning the patient is not recommended
due to risk of dislodging the cannula.
 ROM should only be performed if the benefits
heavily outweigh the risks. If ROM is performed,
avoid ROM near the cannula insertion site.
 Many neonates require physical therapy once the
ECMO is removed to assess the patients for
neurological impairments such as cognitive changes,
developmental dysfunction, and hypotonia.28
SURGICAL DEVICES
Ventricular Assist Devices
A ventricular assist device is a mechanical pump that
provides prolonged (up to 7 years) circulatory assistance
in patients who have acute or chronic ventricular fail-
ure. Research has proven that VAD therapy is superior
to medical therapy in alleviating symptoms and
improving outcomes, including survival rates and qual-
ity of life in patients with Class IV heart failure.29 First
used over 30 years ago, multiple devices have been
designed and clinically tested, with ongoing clinical
trials developing the third generation of pumps.30
VADs are indicated in patients who are on optimal
maximal medical therapy, have a cardiac index of
< 1.8 liters per minute, a pulmonary capillary wedge
pressure > 25mm Hg, and a systolic blood pressure
< 90 mm Hg (all of which indicate left ventricular
failure). As well as restoring cardiac output and blood
pressure, the VAD provides a profound reduction in
left ventricular pressure and volume. This reduces the
pulmonary venous and arterial pressures and reduces
the pulmonary vascular resistance. The VAD also
improves perfusion to all body organs, which results
in improved autonomic function and normalization of
the neurohormonal and cytokine milieu that is present
in heart failure.31
Generally, the left ventricle is most commonly
assisted with a LVAD, but occasionally, the right ventri-
cle also needs assistance from a right ventricular assist
device (RVAD). In more severe situations, both ventri-
cles need to be assisted (BiVAD). In 20% to 30% of
cases where the LVAD provides pressure and volume
APPENDIX III-C 479
unloading of the left ventricle, the increase in venous
return to the right ventricle results in right ventricle
volume overload. This can be treated with inotropes
or pulmonary vasodilators, but in some instances a
RVAD is necessary.31
In general,VADs consist of a pump, a drive line pro-
viding electric or pneumatic energy, a system controller,
and a console.This is illustrated in Figure III-C.6.
The pumps generally fall into two main categories:
pulsatile pumps and axial flow pumps (nonpulsatile).
Pulsatile pumps tend to be larger than axial flow
pumps due to the number of components necessary to
engineer the pump. They are capable of producing a
stroke volume of 65 to 95 ml, generating a cardiac
output of 10 liters of blood flow per minute.
Axial flow pumps have fewer moving parts and
require less power to operate. Axial flow pumps are
capable of rotating at speeds of 7,000 to 12,500 revolu-
tions per minute to produce a cardiac output up to 10
liters per minute.32
CLINICAL TIP
 A peripheral pulse can typically be palpated in a
patient with a pulsatile pump, and a traditional
blood pressure can be measured.
 An axial flow pump provides continuous flow, so
there is no pulse due to no systole and no diastole.
An average blood pressure can be measured rather
than a traditional blood pressure.
 In the absence of a pulse and a blood pressure, the
therapist must rely on the patient’s symptoms, rate
of perceived exertion, and/or dyspnea on exertion.
The pumps are either temporary or permanent. If
the pump is temporary, it is referred to as a bridge to
heart transplantation (BTT) or a bridge to recovery (BTR). If
the pump is permanent, it is referred to as destination ther-
apy (DT). Weaning from a VAD that is designed for
BTR involves a gradual decrease in flow rates or pump
speed, which allows the patient’s ventricle to contribute
more to the total systemic circulation.
The mechanical pump can be intracorporeal
(internal) or extracorporeal (external) to the patient.
An intracorporeal VAD is designed to support the left
ventricle and consists of a pump that is surgically
placed in a preperitoneal or intraabdominal position
with the inflow conduit draining the left ventricle
through the apex of the heart and an outflow conduit
ejecting blood into the ascending aorta. The power
source line exits the abdomen and leads to an external
480 APPENDIX III-C Circulatory Assist Devices
FIGURE III-C.6
The HeartMate intracorporeal left ventricular assist device and system controller. (CourtesyThoratec
Corporation, Pleasanton, CA.)
control device. An extracorporeal VAD can be univen-
tricular or biventricular and consists of a pump(s) that
is completely external to the patient, but with inflow
and outflow conduits entering the abdomen, shunting
blood from the heart to the great vessels. This type of
VAD may be placed paracorporeally (lying on top of
the abdomen) and may be referred to as a‘‘paracorporeal
VAD.’’2,33 Figures III-C.6 and III-C.7 illustrate an
an implantable VAD and an extracorporeal VAD,
respectively.
The various types and general characteristics of in-
tracorporeal and extracorporeal VADs are described
briefly in Table III-C.1. The VADs described in this
table are either FDA-approved, investigational, or in
design stages. It is beyond the scope of this appendix
to describe in detail all aspects of each type of VAD;
however, physical therapists working with patients
who have a VAD need to be familiar with the type of
device that the patient is using, as well as the safety
features of theVAD.
CLINICAL TIP
 Every patient should wear an abdominal binder for
all activity to protect the exit site of the drive lines.
This allows scar tissue to form and reduces shearing
forces at the exit site, thereby decreasing the risk of
infection at the drive site. Abdominal binders may
need to be customized to fit the patient
appropriately and modified to provide an
attachment for the system controller.
 CirculatoryAssist Devices
FIGURE III-C.7
TheThoratec paracorporeal ventricular assist device. (Courtesy
Thoratec Corporation, Pleasanton, CA.)
 Each type of pump requires open heart surgery via a
sternotomy in order to place the inflow and outflow
conduits, therefore follow your hospital’s guidelines
for sternal precautions.
 Knowing if a VAD is implanted or extracorporeal will
influence your handling of the patient during
mobility. Extracorporeal pumps need to be
adequately supported during functional mobility.
EachVAD has an educational manual outlining the
relevant details of the components, operation, and
safety features. For example, the physical therapist
must know how to respond emergently in the event of
a pump failure. Pulsatile pumps can be hand pumped
if the pump fails. Physical therapists should be compe-
tent in hand pumping when treating patients in isola-
tion of the emergency response team.35 Axial flow
pumps cannot be hand pumped, so in the presence of
axial flow pump failure, follow your hospital’s emer-
gency code procedure.
Patients with VADs are still at risk for ventricular
arrhythmias. Patients with pulsatile pumps who require
defibrillation can be defibrillated after the pump is dis-
connected from power and hand pumping is started.
Patients with an axial flow pump can be shocked per
APPENDIX III-C 481
Advanced Cardiac Life Support (ACLS) guidelines
without disconnecting the pump from power. Other
complications of VAD include VAD malfunction,
thrombosis, bleeding, right heart failure, and infection
at or near the insertion sites of the access lines.
The combination of technological advancements
and a lack of donor organs have increased the use of
VADs in patients with heart failure.Therefore, physical
therapists are more likely to encounter this device in
the hospital. Research has demonstrated that patients
with aVAD can be mobilized safely in the hospital and
that their exercise tolerance (as demonstrated by peak
VO2, NYHA status, and subjective reports) can be
improved while awaiting transplantation or while
continuing with destination therapy.35-38 Currently,
case studies have demonstrated positive outcomes
with patients who participate in aerobic and resistance
training programs post VAD placement. Further VAD
research should include randomized controlled clinical
studies.38
PHYSICAL THERAPY CONSIDERATIONS
The following are general considerations for the physi-
cal therapist working with a patient with aVAD:
 Physical therapy can be initiated on postoperative
day one. In most cases, physical therapy is already
working with patients preoperatively.
 The patient’s native heart is still contracting
(albeit ineffectively), therefore the patient’s electro-
cardiogram will reflect the native heart’s electrical
activity. However, because the VAD is performing
a majority of the patient’s cardiac output, the
patient’s peripheral pulse is indicative of the rate
set on the VAD.35
 The rate or speed of aVAD can be fixed or automatic.
VADs that have automatic rates or speeds are able to
adjust their rate or speed according to the demands
of the patient. However, keeping the pump at a
fixed rate or fixed speed improves the pump’s longev-
ity, if the patient can tolerate it.32,35
 Postoperatively patients may have symptoms of pain
at the exit site of the access lines in the abdomen
and may need appropriate premedication with
analgesics before therapy.36
 Patients may also have symptoms of nausea due to the
position of the internal pump within the peritoneal
region of the trunk and may need antiemetic medica-
tion before therapy.
482 APPENDIX III-C Circulatory Assist Devices

Table III-C.1 VENTRICULAR ASSIST DEVICES

Device Duration Mechanism Position Purpose
Bio Medicus* Short Centrifugal Extracorporeal BTR, BTT
BVS 5000* Short Pneumatic Extracorporeal BTR, BTT
AB 5000* Short Pneumatic Extracorporeal BTR
HeartMate I* Long Pneumatic Intracorporeal BTR, BTT, DT
Thoratec IVAD* Long Pneumatic Intracorporeal BTR, BTT
Thoratec PVAD* Long Pneumatic Extracorporeal BTR, BTT
HeartMate II{ Long Axial flow Intracorporeal BTR, BTT, DT
HeartMate III{ Long Magnetically suspended centrifugal Intracorporeal BTR, BTT, DT
INCOR I{ Long Magnetically suspended axial flow Intracorporeal BTR, BTT, DT
Jarvik 2000{ Long Axial flow Intracorporeal BTR, BTT, DT
Levacor{ Long Magnetically suspended centrifugal Intracorporeal DT
Debakey{ Long Axial flow Intracorporeal BTT, DT
VentrAssist{ Long Centrifugal Intracorporeal BTR, BTT, DT
DuraHeart{ Long Magnetically suspended centrifugal Intracorporeal BTT, DT
BTR, Bridge to recovery; BTT, bridge to transplant; DT, destination therapy.
*FDA approved.
{
Investigational.
Data from reference numbers 24, 32-34.

 During mobility, someVADs can be powered by bat-
teries, making the patient independent to move
without the electric power source. Physical therapists
must be knowledgeable about the battery life. It is
important to always carry extra batteries and a
system controller when mobilizing the patient away
from the patient’s room. Most hospitals require
the patient and caregivers to be independent in
switching batteries before mobilizing away from
the unit.
 Patients withVADs still have heart failure, therefore,
a resistance exercise program is an important part
of their exercise prescription. Upper-extremity resis-
tance training is deferred until sternal precautions
are lifted.
 Indications to stop exercise in a patient with a VAD
are the same as when treating any patient with cardiac
disease (refer to Chapter 1 for more guidelines). In
addition, if a patient demonstrates a drop in the
pump flow or speed or rate, this may indicate pump
failure, occlusion of a tube, bleeding, and so on.
Therefore, stop exercise, investigate the cause, and
seek assistance as necessary.
 Patients should be educated to avoid strong static dis-
charges (e.g. television or computer screens), swim-
ming, and contact sports.
 Patients can shower provided they use a waterproof
shower kit that protects theVAD.
 Patients with electric pumps can be discharged to
home once they reach the appropriate level of inde-
pendence.This type of pump can be powered by bat-
teries, whereas patients with pneumatic pumps are
confined to the hospital.
 Patients need to manage mobilizing with the
VAD equipment. Physical therapists should target
the appropriate training to condition the patient in
preparation for this. For example, postural exercises
can assist in carrying the batteries in the battery
holster.
 Patients with VADs can benefit from outpatient
cardiac rehabilitation once discharged from the
hospital.
 CirculatoryAssist Devices
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 Appendix IV Pharmacologic Agents
Margarita V. DiVall
The purpose of this appendix is to provide an overview RESPIRATORY SYSTEM
of the pharmacologic agents that are commonly pre-
Table IV-8 Adrenocortical Steroids
scribed as an adjunct to the medical-surgical manage-
(Glucocorticoids)
ment of a wide variety of diseases and disorders. The
Table IV-9 Antihistamines
medications in this appendix are organized according
to systems (see the following index). Both generic and Table IV-10 Bronchodilators
common brand name(s) are listed for each agent. Table IV-11 Leukotriene Modifiers
Depending on the practice setting, you may see generic Table IV-12 Mast Cell Stabilizers
names being used all the time (acute, inpatient setting)
or brand names used (outpatient setting). Many drugs MUSCULOSKELETAL SYSTEM
are available as extended-release formulations. In that Table IV-13 Disease-Modifying Antirheumatic
case, several letters may be added to the generic/brand Drugs (DMARDs)
name of the drug. Common abbreviations include XL
(extended release), XT (extended release), SR (sustained CENTRAL NERVOUS SYSTEM
release), CR (controlled release), ER (extended release).
Pharmacy laws mandate the dispensing of a generic Table IV-14 Antianxiety Medications
medication if generic is available, even if the doctor Table IV-15 Anticonvulsants
writes a prescription using a brand name. A physician Table IV-16 Antidepressants
may indicate ‘‘No substitution’’ on the prescription if Table IV-17 Antipsychotics
he or she desires for only the brand name to be dis- Table IV-18 Mood Stabilizers
pensed. For each type of medication in this appendix,
Table IV-19 Parkinson’s Medications
a description of the indication(s), mechanism of
action, side effects, as well as important physical ther-
apy (PT) considerations are presented in tables.1,2 Note ONCOLOGY
that some pharmacologic agents are listed in another
Table IV-20 Antiemetic Medications
chapter or appendix.
The following is a list of tables in this appendix, Table IV-21 Chemotherapy
organized according to body system and drug classes.
VASCULAR SYSTEM AND HEMATOLOGY
Table IV-22 Colony-Stimulating Factors
CARDIOVASCULAR SYSTEM
GASTROINTESTINAL SYSTEM
Table IV-1 Antiarrhythmic Agents
Table IV-23 Antacids
Table IV-2 Anticoagulants
Table IV-24 Antidiarrheal Medications
Table IV-3 Antihypertensive Agents
Table IV-25 Antispasmodic Medications
Table IV-3a Combination Drugs for Hypertension
Table IV-26 Cytoprotective Medications
Table IV-4 Antiplatelet Agents
Table IV-27 Histamine-2 Receptor Antagonists
Table IV-5 Lipid-Lowering Agents
(H2RAs)
Table IV-6 Positive Inotropes (Pressors) Table IV-28 Laxatives
Table IV-7 Thrombolytics (Also Known as Table IV-29 Proton Pump Inhibitors (PPIs)
Fibrinolytics)

485
486 APPENDIX IV Pharmacologic Agents

GENITOURINARY SYSTEM ENDOCRINE SYSTEM

Table IV-30 Benign Prostatic Hypertrophy (BPH) Table IV-37 Hypoglycemic Agents
Therapy Table IV-38 Treatment of Hyperparathyroidism
Table IV-31 Oral Contraceptives Table IV-39 Treatment of Thyroid Disorders

INFECTIOUS DISEASE
Table IV-32 Antibiotics
Table IV-33 Antifungal Agents
Table IV-34 Antitubercular Agents
Table IV-35 Antiretroviral Medications
Table IV-36 Antiviral Medications

CARDIOVASCULAR SYSTEM

Table IV-1 ANTIARRHYTHMIC AGENTS

Indications:Treatment and prevention of arrhythmias.
Precautions: All antiarrhythmic drugs are proarrhythmic. Monitor vital signs, ECG, and side effects.

Class: Mechanism Generic Name (Common

of Action Brand Name[s]) Adverse Effects PT Considerations
Class I: Sodium Class common side Monitor for
channel blockersç effects: anticholinergic, orthostasis
slow the fast sodium nausea, vomiting,
channels, thereby dizziness, drowsiness,
controlling rate of fatigue
depolarization
Class Ia Disopyramide CHF
(Norpace)
Procainamide Lupus, fever, hematologic
(Pronestyl) toxicity
Quinidine (Biquin, Hypotension, diarrhea,
Cardioquin) tinnitus
Class Ib Lidocaine (Xylocaine), Disorientation, slurred
tocainide (Tonocard), speech, tinnitus,
mexiletine (Mexitil) seizures, tremor
Class Ic Flecainide Visual disturbances,
(Tambocor) dyspnea, tachycardia,
syncope
Propafenone Angina, CHF, AV block,
(Rythmol) ECG abnormalities,
syncope, constipation
Class II: Beta blockers SeeTable IV-3
 Pharmacologic Agents APPENDIX IV 487

Table IV-1 ANTIARRHYTHMIC AGENTS—cont’d

Class: Mechanism Generic Name (Common
of Action Brand Name[s]) Adverse Effects PT Considerations
Class III: Agents in this Amiodarone ECG abnormalities, This drug concentrates
class prolong the (Cordarone, bradycardia, hypotension in the tissues and
action potential and Pacerone) (IV form), pulmonary causes toxicities in
refractory period in fibrosis, hepatotoxicity, the heart, eyes,
myocardial tissue; thyroid dysfunction, thyroid, and lungs.
decrease AV corneal deposits, Any new symptoms
conduction and photosensitivity, should be reported.
sinus node constipation, This agent has
function blue-gray skin numerous
discoloration drug-drug
interactions
Dofetilide Arrhythmias dizziness, Requires initiation in
(Tikosyn) insomnia, headache, inpatient setting
GI side effects with constant
telemetry monitoring
due to high risk
of arrhythmias in
the first 3 days
Ibutilide (Corvert) Arrhythmias,
hypotension,
bradycardia,
headaches
Sotalol (Betapace, Bradycardia, chest pain, Has beta-blocking
Betapace AF) fatigue, dizziness, properties and
dyspnea, CHF, is associated
GI side effects with similar
side effects
Class IV: Non- SeeTable IV-3
dihydropyridine
calcium channel
blockers
Miscellaneous
Slows conduction Adenosine Facial flushing,
time through the (Adenocard, headache, dizziness,
AV node, interrupting Adenoscan) chest pressure,
the re-entry pathways dyspnea
through the
AV node
Direct suppression Digoxin Anorexia, lethargy,
of the AV node (Lanoxin) confusion, visual
conduction to disturbances, ECG
increase effective abnormalities,
refractory period and arrhythmias
decrease conduction
velocity
AV, Atrioventricular node; CHF, chronic heart failure; ECG, electrocardiogram; GI, gastrointestinal; IV, intravenous
488 APPENDIX IV Pharmacologic Agents

Table IV-2 ANTICOAGULANTS

Indications: Prevention and treatment of DVTand PE, prevention of ischemic stroke in patients at high risk (e.g. atrial
fibrillation patients), during ACS/MI.
Adverse Effects for all of these agents: Excessive bleeding.
PT Considerations for all of these agents: Do not perform deep-tissue massage; exercise fall precautions; monitor signs
and symptoms of bleeding: Hct, Hgb, bleeding from the nose, gums, or GI tract (blood in the stool or vomit); monitor
bruising, mental status changes (stroke).

Class: Mechanism Generic Name (Common

of Action
Coumarin derivatives:
Interfere with
synthesis of vitamin
K-dependent clotting
factors that decrease
prothrombin
Direct thrombin
inhibitors: Directly
inhibits thrombin, can
be used to treat
heparin-induced
thrombocytopenia
and as an alternative
to heparin in allergic
patients
Factor Xa inhibitor:
Selective inhibitor
of factor Xa
Heparin: Prolongs
clotting time by
inhibiting the
conversion of
prothrombin to
thrombin
Low-molecular-weight
heparins
ACS, Acute coronary syndrome; aPTT, activated partial thromboplastin time; DVT, deep vein thrombosis; Hct, hematocrit;
Hgb, hemoglobin; INR, international normalized ration; MI, myocardial infarction; OTC, over-the-counter; PE, pulmonary embolism.
Brand Name[s])
Warfarin (Coumadin)
Lepirudin (Refludan),
Argatroban
(Argatroban),
Bivalirudin (Angiomax)
Fondaparinux (Arixtra)
Heparin sodium
Dalteparin sodium
(Fragmin), Enoxaparin
sodium (Lovenox)
Adverse Effects
Systemic cholesterol
microembolism (purple toe
syndrome); rare
Anaphylaxis (with lepirudin)
Thrombocytopenia
Heparin-induced
thrombocytopeniaType 1
(small decline in platelet
count, self-resolving, more
common) and Type 2
(> 50% decrease in
platelets, an allergic
reaction, requires
immediate treatment;
rare)
Heparin-induced
thrombocytopenia
(see heparin); less common
than with heparin
PT Considerations
Monitor INR; goal INR is
2-3 for majority of
patients; lower INR
values are associated with
high risk of thrombotic
events; INR > 3
associated with increased
bleeding risk.Warfarin
has many drug-drug and
drug-food interactions
aPTT monitoring is
necessary with goal
values 1.5-2.5 times
control. Goal range
differs by institution
(typically 60-80 seconds);
high aPTTvalues are
associated with increased
bleeding risk; Argatroban
causes false-positive
elevations in INR
No special lab monitoring
required
aPTT monitoring is
necessary with goal
values 1.5-2.5 times
control. Goal range
differs by institution
(typically 60-80 seconds);
high aPTTvalues are
associated with increased
bleeding risk. Low doses
administered SC for
prophylaxis do not
require aPTT monitoring
No special lab monitoring
required
Table IV-3 ANTIHYPERTENSIVE AGENTS
Indications:Treatment of hypertension, heart failure, arrhythmias, ischemic heart disease.
Precautions: Monitor vital signs and the potential for orthostasis with most antihypertensive agents.

Generic Name (Common Brand

Class: Mechanism of Action
Adrenergic agonists: Stimulates
alpha2-adrenoceptors in the brain
stem, thus activating an inhibitory
neuron, resulting in reduced
sympathetic outflow from the CNS,
producing a decrease in peripheral
resistance, renal vascular resistance,
heart rate, and blood pressure
Adrenergic antagonists: competitively Doxazosin (Cardura), prazosin
inhibit postsynaptic alpha-
adrenergic receptors, which results
in vasodilation of veins and
arterioles and a decrease in total
peripheral resistance and blood
pressure
Angiotensin converting enzyme
(ACE) inhibitors: inhibit
conversion of angiotensin I to
angiotensin II and therefore act to
decrease excess water and sodium
retention while also preventing
vasoconstriction
Angiotensin II receptor blockers
(ARBs): Selectively antagonize
angiotensin II and therefore act to
decrease excess water and sodium
retention while also preventing
vasoconstriction
Name[s]) Adverse Effects PT Considerations
Clonidine (Catapres, Catapres Drowsiness, dizziness, dry mouth, Clonidine can also be used as an epidural
TTSçtransdermal patch) orthostasis, headache, lethargy, to control pain. It takes 2-3 days to see
weakness full efficacy after the first application
of the transdermal patch. Clonidine
levels will slowly decline over 2-3 days
after patch removal
Drowsiness, dizziness, first dose These agents should not be used for
(Minipress), tamsulosin syncope, palpitations, treatment of HTN due to increased
(Flomax), terazosin (Hytrin) orthostasis, weakness cardiovascular mortality (ALLHAT
trial) compared to other
antihypertensives.These are commonly
used to treat BPH.Tamsulosin is the
most selective for prostate and causes
the least amount of cardiovascular side
effects.Tamsulosin can also be used to
treat kidney stones (in both men and
women)
Captopril (Capoten), enalapril Common: Cough, hypotension, Report to other providers changes in
(Vasotec), fosinopril dizziness, hyperkalemia urine output, muscle cramps
(Monopril), lisinopril Serious: renal failure, angioedema, (indicative of hyperkalemia) and
(Prinivil, Zestril), perindapril anaphylaxis, neutropenia swelling or redness in the face and
(Aceon), quinapril (Accupril), neck area (indicative of angioedema)
ramipril (Altace), trandolapril
(Mavik), moexipril (Univasc)
Candesartan (Atacand), Common: hypotension, dizziness, Refer to ACE inhibitors above
eprosartan (Teveten), hyperkalemia
irbesartan (Avapro), losartan Serious: renal failure, angioedema,
(Cozaar), olmesartan anaphylaxis
(Benicar), valsartan (Diovan),
telmisartan (Micardis)
Continued

Table IV-3 ANTIHYPERTENSIVE AGENTS—cont’d
Class: Mechanism of Action
Beta-blockers: Decrease myocardial Beta-1 selective: Acebutolol
oxygen demand by decreasing
sympathetic input to myocardium,
therefore decreasing heart rate and
contractility
Calcium-channel blockers: Inhibit
calcium ion from entering the
‘‘slow channels’’or select voltage-
sensitive areas of vascular smooth
muscle and myocardium during
depolarization, producing a
relaxation of coronary vascular
smooth muscle and coronary
vasodilation; increases myocardial
oxygen delivery in patients with
vasospastic angina; Non-DHP CCB
also slow automaticity and
conduction of AV node
Diuretics
Thiazide diuretics: Inhibits sodium Chlorthalidone (Hygroton),
reabsorption in the distal tubules
causing increased excretion
of sodium and water as well as
potassium and hydrogen ions
Loop diuretics: Inhibits
reabsorption of sodium and
chloride in the ascending loop of
Henle, thus causing increased
excretion of water, sodium,
chloride, magnesium, phosphate,
and calcium
Generic Name (Common Brand
Name[s]) Adverse Effects
(Sectral), atenolol (Tenormin),
esmolol (Brevibloc),
metoprolol (Lopressor,Toprol
XL)
Non-selective beta 1 and 2:
Nadolol (Corgard), pindolol
(Visken), propranolol (Inderal)
Alpha and beta blockers:
Carvedilol (Coreg), Labetalol
(Normodyne)
Non-DHP: verapamil (Isoptin,
Calan,Verelan, Covera-HS),
diltiazem (Cardizem, Tiazac,
Cartia XT)
DHP: amlodipine (Norvasc),
felodipine (Plendil), nifedipine
(Procardia XL, Adalat CC),
isradipine (DynaCirc),
nicardipine (Cardene)
hydrochlorothiazide (Esidrix,
HydroDIURIL), metolazone
(Zaroxolyn)
Bumetanide (Bumex),
furosemide (Lasix), torsemide
(Demadex)
Common: smooth muscle spasm
(bronchospasm), exaggeration of
therapeutic cardiac actions
(bradycardia), fatigue, insomnia,
masking of hypoglycemic
symptoms in diabetics (except
diaphoresis), impaired glucose
tolerance, lipid abnormalities,
exercise intolerance
Serious: AV block
Bradycardia, hypotension,
AV block, CHF, constipation and
gingival hyperplasia (with
verapamil)
Hypotension, peripheral edema,
flushing, palpitations, headaches, peripheral vasculature vs. non-DHP
gingival hyperplasia (with
nifedipine)
Hypotension, orthostasis, volume
depletion, hypokalemia,
hyponatremia, photosensitivity,
hyperuricemia, hyperglycemia
Hyperglycemia, hyperuricemia,
hypokalemia, hypocalcemia,
hypomagnesemia, hypotension,
excessive urination,
dehydration, orthostasis
490
PT Considerations
APPENDIX IV
Negative inotropic effects prevent heart
rate to increase in response to exercise;
use Borg RPE scale to monitor
exertion rather than checking the
pulse; check blood sugar in diabetics
prior to exercise and administer a
carbohydrate snack with blood sugar
Pharmacologic Agents
100 mg/dl before exercise
Non-DHP CCB will decrease the heart
rate and prevent heart rate increase in
response to exercise similarly to
beta-blockers.
DHP-CCBs have more effects in the
CCBs, which have more central cardiac
effects.
All diuretics can cause volume depletion.
Monitor weight, urine output for
changes in renal function, orthostasis,
serum electrolytes (will decrease), signs
and symptoms of gout (due to increase
in uric acid)
 Potassium-sparing diuretics:
Interferes with potassium/sodium
exchange (active transport) in the
distal tubule, cortical collecting
tubule, and collecting duct;
spironolactone is an aldosterone
antagonist
Carbonic anhydrase inhibitors:
Inhibit carbonic anhydrase
enzyme resulting in reduction of
hydrogen ion secretion at renal
tubule and an increased renal
excretion of sodium, potassium,
bicarbonate, and water
Nitrates: Relaxes vascular smooth
muscle; decreased venous ratios
and arterial blood pressure;
reduces left ventricular work;
decreases myocardial O2
consumption. In addition to
hypertension indication, often
used in patients with ischemic
heart disease
Renin inhibitors: renin inhibitor,
resulting in blockade of the
conversion of angiotensinogen to
angiotensin I
Vasodilators: Direct vasodilation of
arterioles (with little effect on veins) minoxidil (Loniten)
with decreased systemic resistance
ACE, Angiotensin converting enzyme; ARB, angiotensin receptor blocker; BPH, benign prostatic hypertrophy; CCB, calcium channel blockers; CK, creatinine kinase;
CNS, central nervous system; DHP, dihydropyridine; HTN, hypertension; IV, intravenous; NTG, nitroglycerin; RPE, rating of perceived exertion.
Amiloride (Midamor),
Spironolactone,Triamterene
(Dyrenium)
Acetazolamide (Diamox),
dichlorphenamide (Daranide),
methazolamide (Neptazane)
Amyl nitrite (Aspirol,Vapor-ole; Hypotension, orthostasis, flushing, Patients with ischemic heart disease
inhalation), nitroglycerin
(NTG) (dosage forms:
sublingual, spray,
percutaneous ointment, oral,
sustained release, IV.) (Nitro-
Bid, Nitrostat; Nitro-Dur,
Transderm-Nitro, Nitrodisc;
transdermal patch), isosorbide
dinitrate (Isordil, Sorbitrate;
sublingual, oral, chewable),
isosorbide mononitrate
(ISMO)
Aliskiren (Tekturna)
Hydralazine (Apresoline),
Hyperkalemia, dizziness,
hypotension
With spironolactone: Gynecomastia,
breast pain hyperkalemia,
hyponatremia, dehydration,
hyperchloremic metabolic
acidosis in decompensated
hepatic cirrhosis, inability to
achieve or maintain an erection,
irregular menses, amenorrhea,
postmenopausal bleeding
Flushing, dizziness, drowsiness,
fatigue, allergic reactions,
hyperglycemia or hypoglycemia,
hypokalemia, hyponatremia,
metabolic acidosis, kidney stones,
hepatic insufficiency, myopia
tachycardia, headache, dizziness
Dizziness, rash, hyperkalemia,
increases in serum creatinine,
cough, increase in serum CK,
diarrhea
Headache, hypotension,
compensatory sympathetic reflex
causing increased heart rate, lupus caution.
with long-term hydralazine
Due to toxicities, these are not used as
diuretics, but can be used to treat
glaucoma, acute mountain sickness, or
metabolic alkalosis
should always carry rapid acting NTG
(sublingual or spray). In case of angina,
administer 1 tab or spray up to 3 times
every 5 minutes and call 911.
Sublingual NTG tabs have specific
storage requirements that should be
Pharmacologic Agents
followed (avoid heat, moisture, light).
If tablets no longer have their shape,
NTG is likely to be expired and may
not be effective. Monitor for
orthostasis.
New class of antihypertensive agents.
Monitor muscle cramps associated
with hyperkalemia. Monitor
urine output and weight for renal
APPENDIX IV
dysfunction
Monitor blood pressure and heart rate.
Patients at risk for orthostasis. Use
491
492 APPENDIX IV Pharmacologic Agents

Table IV-3a COMBINATION DRUGS FOR HYPERTENSION

Many patients require antihypertensive therapy with multiple agents. General principles of HTN management include
combining multiple agents with different mechanisms of action to achieve optimal blood pressure goals.This approach
allows for greater efficacy and lower toxicity rather than maximizing the dose of individual agents.To facilitate patient
adherence, there is a number of fixed-dose formulations that allow patients to take multiple medications in one pill. In
the majority of cases, these combinations are only available by brand name and are considerably more expensive than
individual components that may be available generically.The fixed-dose combinations may also be more difficult to
titrate at the start of therapy as opposed to individual components. PTs should consider the side effects and monitoring
of all individual components of the combination antihypertensives. (SeeTable IV-3.)

Combination Type Fixed-Dose Combination, mg* Trade Name

ACEIs and CCBs Amlodipine-benazepril hydrochloride (2.5/10, 5/10, 5/20, 10/20) Lotrel
Enalapril-felodipine (5/5) Lexxel
Trandolapril-verapamil (2/180, 1/240, 2/240, 4/240) Tarka
ACEIs and diuretics Benazepril-hydrochlorothiazide (5/6.25, 10/12.5, 20/12.5, 20/25) Lotensin HCT
Captopril-hydrochlorothiazide (25/15, 25/25, 50/15, 50/25) Capozide
Enalapril-hydrochlorothiazide (5/12.5, 10/25) Vaseretic
Fosinopril-hydrochlorothiazide (10/12.5, 20/12.5) Monopril/HCT
Lisinopril-hydrochlorothiazide (10/12.5, 20/12.5, 20/25) Prinzide,
Zestoretic
Moexipril-hydrochlorothiazide (7.5/12.5, 15/25) Uniretic
Quinapril-hydrochlorothiazide (10/12.5, 20/12.5, 20/25) Accuretic
ARBs and diuretics Candesartan-hydrochlorothiazide (16/12.5, 32/12.5) Atacand HCT
Eprosartan-hydrochlorothiazide (600/12.5, 600/25) Teveten-HCT
Irbesartan-hydrochlorothiazide (150/12.5, 300/12.5) Avalide
Losartan-hydrochlorothiazide (50/12.5, 100/25) Hyzaar
Olmesartan medoxomil-hydrochlorothiazide Benicar HCT
(20/12.5, 40/12.5, 40/25)
Telmisartan-hydrochlorothiazide (40/12.5, 80/12.5) Micardis-HCT
Valsartan-hydrochlorothiazide (80/12.5, 160/12.5, 160/25) Diovan-HCT
BBs and diuretics Atenolol-chlorthalidone (50/25, 100/25) Tenoretic
Bisoprolol-hydrochlorothiazide (2.5/6.25, 5/6.25, 10/6.25) Ziac
Metoprolol-hydrochlorothiazide (50/25, 100/25) Lopressor HCT
Nadolol-bendroflumethiazide (40/5, 80/5) Corzide
Propranolol LA-hydrochlorothiazide (40/25, 80/25) Inderide LA
Timolol-hydrochlorothiazide (10/25) Timolide
Centrally acting drug Methyldopa-hydrochlorothiazide (250/15, 250/25, 500/30, 500/50) Aldoril
and diuretic Reserpine-chlorthalidone (0.125/25, 0.25/50) Demi-Regroton,
Regroton
Reserpine-chlorothiazide (0.125/250, 0.25/500) Diupres
Reserpine-hydrochlorothiazide (0.125/25, 0.125/50) Hydropres
Diuretic and diuretic Amiloride-hydrochlorothiazide (5/50) Moduretic
Spironolactone-hydrochlorothiazide (25/25, 50/50) Aldactazide
Triamterene-hydrochlorothiazide (37.5/25, 75/50) Dyazide, Maxzide
HTN and lipid Amlodipine-atorvastatin (5/10, 5/20, 5/40, 5/80, 10/10, 10/20, Caduet
lowering 10/40, 10/80)
*Some drug combinations are available in multiple fixed doses. Each drug dose is reported in milligrams.
ACEIs, Angiotensin converting enzyme inhibitors; ARBs, angiotensin receptor blockers; BBs, Beta blockers; CCBs, calcium channel
blockers; HTN, hypertension.
 Pharmacologic Agents APPENDIX IV 493

Table IV-4 ANTIPLATELET AGENTS

Indications: Primary and secondary prevention of coronary heart disease, stroke; peripheral arterial disease; adjunct
therapy with anticoagulants during acute coronary syndrome; prevention of thrombosis after stent placement.
Precautions: Combination of these agents with other antiplatelet or anticoagulant drugs increases the risk of bleeding.

Generic Name (Common

Class: Mechanism of Action
Glycoprotein IIb/IIIa
inhibitors: block the
platelet glycoprotein
IIb/IIIa receptor, the
binding site for
fibrinogen, von
Willebrand factor,
and other ligands.
Inhibition of binding
at this final common
receptor blocks platelet
aggregation and prevents
thrombosis
Salicylates: inhibits
cyclooxygenase; blocks
prostaglandin synthetase
action, which prevents
formation of the platelet-
aggregating substance
thromboxane A2
Thienopyridine: Blocks
ADP receptors, which
prevent fibrinogen
binding at that site and
thereby reduce the
possibility of platelet
adhesion and aggregation
NSAIDs, Nonsteroidal antiinflammatory drugs.
Brand Name[s])
Abciximab (ReoPro)
Eptifibatide (Integrilin)
Tirofiban (Aggrastat)
Aspirin (many brand names,
available OTC)
Aspirin/Dipyridamole
(Aggrenox)
Clopidogrel (Plavix)
Adverse Effects
Produce potent antiplatelet
effect with high risk of
bleeding
Well tolerated at 81-325 mg
Common: dyspepsia, minor
bleeding
Serious: anaphylaxis,
bronchospasm, severe
bleeding
Common: dyspepsia,
gastritis, minor bleeding
Serious: bleeding
PT Considerations
Only used for short-term
therapy, typically, in
combination with
other antiplatelet and
anticoagulant agents;
high risk of bleeding
Many NSAIDs may
decrease the
antiplatelet effects of
aspirin; if used
concomitantly ^
patient should take
aspirin 2 hours prior
to NSAID

Table IV-5 LIPID-LOWERING AGENTS

Indications:Treatment of dyslipidemia.

Generic Name (Common

Class: Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Bile acid sequestrants: bind bile Cholestyramine Constipation, dyspepsia, These drugs cause
acids including glycocholic (Questran), colesevelam flatulence significant GI
acid in the intestine, impeding (WelChol), colestipol discomfort. Ask the
their reabsorption. Increases (Colestid) patient when his or her
the fecal loss of bile salt- symptoms are less severe
bound LDL-C to schedule your sessions
Continued
494 APPENDIX IV
Table IV-5 LIPID-LOWERING AGENTS—cont’d
Class: Mechanism of Action
Cholesterol absorption inhibitor:
Inhibits absorption of
cholesterol at the brush border
of the small intestine.This
leads to a decreased delivery of
cholesterol to the liver,
reduction of hepatic
cholesterol stores, and an
increased clearance of
cholesterol from the blood;
decreases total C, LDL-
cholesterol (LDL-C), ApoB,
and triglycerides (TG) while
increasing HDL-cholesterol
(HDL-C).
Fibric acid derivatives: fenofibric
acid is believed to increase
VLDL catabolism by
enhancing the synthesis of
lipoprotein lipase; as a result
of a decrease inVLDL levels,
total plasma triglycerides are
reduced by 30% to 60%;
modest increase in HDL
occurs in some
hypertriglyceridemic patients
Fish oil (Omega-3 fatty acids):
Mechanism has not been
completely defined. Possible
mechanisms include inhibition
of acetyl CoA:1,2
diacylglycerol acyltransferase,
increased hepatic beta-
oxidation, or a reduction in
the hepatic synthesis of
triglycerides.
HMG-CoA reductase inhibitors
(statins): Inhibit 3-hydroxy-
3-methylglutaryl coenzyme
A (HMG-CoA) reductase, the
rate-limiting enzyme in
cholesterol synthesis (reduces
the production of mevalonic
acid from HMG-CoA); results
in a compensatory increase in
the expression of LDL
receptors on hepatocyte
membranes and a stimulation
of LDL catabolism
Pharmacologic Agents
Generic Name (Common
Brand Name[s]) Adverse Effects PT Considerations
Ezetimibe (Zetia) Dizziness, headache, This medication is well
diarrhea tolerated. Often
combined with a statin
for additional LDL
reduction.
Benzafibrate (Bezalip), Constipation, LFT Monitor for hepatotoxicity:
fenofibrate (Antara, abnormalities yellow skin/sclera,
Lipofen,Tricor), abdominal pain.
gemfibrozil (Lopid) If combined with a statin,
higher potential for
hepatotoxicity and
muscle toxicity
Fish oil is available in Dyspepsia, fishy odor,
many formulations taster perversion
OTC. Due to concern
of impurities of OTC
formulations, there is
a product available by
prescription only
Trade name: Omacor
Atorvastatin (Lipitor), Headache, GI toxicity, LFTs must be monitored
fluvastatin (Lescol), hepatotoxicity, muscle routinely, monitor for
lovastatin (Mevacor), pain and weakness, hepatotoxicity. Patients
pravastatin (Pravachol), rhabdomyolysis (rare) with muscle pain not
rosuvastatin (Crestor), related to exercise should
simvastatin (Zocor) be referred to their
providers to check for
muscle breakdown
(CK levels are typically
checked)
 Pharmacologic Agents APPENDIX IV 495

Table IV-5 LIPID-LOWERING AGENTS—cont’d

Generic Name (Common
Class: Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Nicotinic acid: inhibits the Niacin (Niacor; Niaspan; Edema, flushing, Monitor blood pressure and
synthesis of very-low-density Slo-Niacin [OTC]). hypotension, heart rate and orthostasis,
lipoproteins orthostasis, signs and symptoms of
palpitations, hyperglycemia, and gout.
tachycardia, Monitor for
hyperglycemia, hepatotoxicity
hyperuricemia,
hepatotoxicity
Combinations: Advicor (lovastatin + niacin), Caduet (atorvastatin + amlodipine), Pravigard PAC (aspirin + pravastatin),Vytorin
(ezetimibe + simvastatin).
CK, Creatinine kinase; GI, gastrointestinal; HDL, high-density lipoprotein; HMG-CoA, hydroxy-3-methylglutaryl coenzyme A;
LDL, low-density lipoprotein; LFTs, liver function tests; OTC, over-the-counter;TG, triglycerides;VLDL, very-low-density lipoprotein.

Table IV-6 POSITIVE INOTROPES (PRESSORS)

Indications: Administered intravenously for hemodynamic support in patients with cardiovascular and/or respiratory
collapse, severe heart failure, severe sepsis with hemodynamic instability; some agents are used for resuscitation during
cardiovascular arrest.

Generic Name (Common

Mechanism of Action
Agents in this class
increase cardiac
output via stimulating
alpha, beta, and/or
dopaminergic
receptors.
Brand Name[s])
Dopamine, dobutamine,
epinephrine (Adrenalin,
EpiPen), norepinephrine
(Levophed), phenylephrine
(Neo-Synephrine),
vasopressin (Pitressin)
Adverse Effects
Increase BP and HR, chest
pain, ischemia, ACS,
arrhythmia
PT Considerations
These agents are used
acutely, typically in
unstable patients in the
ICU setting. Outpatient
intermittent infusions can
be used in severe heart
failure. Monitor vitals
and avoid exertion.

Table IV-7 THROMBOLYTICS (ALSO KNOWN AS FIBRINOLYTICS)

Indications: ACS, ischemic stroke, severe PE, clot lysis in IVcatheters (very small doses).

Generic Name (Common

Mechanism of Action Brand Name[s])
Initiate fibrinolysis by Alteplase (Activase,
binding to fibrin and Cathflo), reteplase
converting (Retavase), streptokinase
plasminogen to (Streptase), tenektaplase
plasmin (TNKase), urokinase
(Abbokinase)
ACS, Acute coronary syndrome; IV, intravenous; PE, pulmonary embolism; PT, physical therapy.
Adverse Effects
Bleeding at various sites,
including intracranial
hemorrhage
PT Considerations
These agents are used acutely,
typically in unstable patients.
Risk of bleeding is very high and
may outweigh the benefit of clot
lysis and restoration of blood
flow. PTwill probably not be
done in patients immediately
post thrombolysis.
496 APPENDIX IV Pharmacologic Agents
RESPIRATORY SYSTEM
Table IV-8 ADRENOCORTICAL STEROIDS (GLUCOCORTICOIDS)
Indications: Stabilize and limit the inflammatory response (bronchoconstriction) in the respiratory tract in patients with
asthma and COPD (inhaled and systemic); to decrease cerebral edema or inflammation in neoplastic or inflammatory
diseases, or both (systemic); relief of seasonal or perennial rhinitis (intranasal and inhaled).
Generic Name (Common
Mechanism of Action Brand Name[s])
Prevent the Systemic:
accumulation of Dexamethasone (Decadron),
inflammatory cells at fludrocortisone (Florinef),
the infection site, hydrocortisone (Cortef, Solu-
inhibit lysosomal Cortef), methylprednisolone
enzyme release and (Depo-Medrol, Medrol),
chemical mediators of prednisone (Deltasone,
inflammatory Sterapred, Sterapred DS),
response, reduce prednisolone (Orapred,
capillary dilatation Pediapred, Prelone),
and permeability triamcinolone (Aristocort)
Inhaled: Beclomethasone
(Beclovent,Vanceril),
budesonide (Pulmicort),
flunisolide (AeroBid),
fluticasone propionate
(Flovent, Advair (in
combination with salmeterol)),
triamcinolone acetonide
(Azmacort)
Intranasal: Beclomethasone
dipropionate (Beconase,
Vancenase), budesonide
(Rhinocort), fluticasone
propionate (Flonase),
mometasone furoate
monohydrate (Nasonex),
triamcinolone acetonide
(Nasacort)
COPD, Chronic obstructive pulmonary disease.
Adverse Effects
Common side effects:
Headache, vertigo,
diaphoresis, nausea,
vomiting. In susceptible
patients: euphoria,
insomnia, seizure,
muscle weakness,
cushingoid features
(chronic use), decreased
wound healing (chronic
use), ecchymosis, skin
atrophy (chronic use),
thromboembolism,
hypertension,
hyperglycemia,
hypokalemia
Serious reactions: adrenal
insufficiency, steroid
psychosis,
immunosuppression
(chronic use), peptic
ulcer, congestive heart
failure, osteoporosis
(chronic use)
Inhaled: oral thrush,
change of voice quality
Intranasal: local mucosal
irritation
PT Considerations
Systemic steroids:
Monitor blood
pressure (will increase)
and blood glucose
(will increase);
modalities that
increase the risk of
bruising or skin tears
should be avoided; be
aware of the risk of
osteoporosis with
chronic use ^ exercise
caution when
exercising and
prescribe weight-
bearing exercises that
promote bone health;
reinforce
complianceç abrupt
discontinuation leads
to adrenal
insufficiency crisis
Inhaled steroids:
emphasize compliance
to maintain disease
control, patients
should rinse mouth
after use to prevent
thrush; chronic use
and high doses
increases the risk of
systemic side effects,
especially osteoporosis
 Pharmacologic Agents APPENDIX IV 497

Table IV-9 ANTIHISTAMINES

Indications:To decrease inflammation and bronchoconstriction associated with hypersensitivity reactions, such as allergic
rhinitis.

Generic Name (Common Brand

Mechanism of Action Name[s])
Reduce or prevent the Azelastine (Astelin),
physiologic effects chlorpheniramine maleate
of histamine by (Chlor-Trimeton), cetirizine
competing for (Zyrtec), clemastine (Tavist),
histamine binding desloratadine (Clarinex),
sites diphenhydramine (Benadryl,
various), fexofenadine
(Allegra), loratadine (Alavert,
Claritin)
PT, Physical therapy.
Adverse Effects
Drowsiness, dizziness,
decreased coordination,
orthostatic hypotension,
hypotension, hypertension,
palpitations, bradycardia,
tachycardia, epigastric
distress, urinary frequency,
thickening of bronchial
secretions, dry mouth
PT Considerations
If patient experiences
drowsiness, avoid
scheduling PTsession
within a few hours of
administration with
short-acting
formulations. Many
are available in 12h
and 24h formulations,
so ask patient when
he or she feels the
most sedation.

Table IV-10 BRONCHODILATORS

Indications:To relieve bronchospasm associated with obstructive pulmonary disease, asthma, and exercise-induced
bronchospasm.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Anticholinergics: block the Ipratropium bromide Bronchitis, palpitations, Short-acting beta2 agonists are
action of acetylcholine at (Atrovent), tiotropium dizziness, dry mouth often referred to as‘‘rescue’’
parasympathetic sites in (Spiriva) inhalers. In patients with asthma
bronchial smooth muscle and COPD, maintenance therapy
causing bronchodilation. should minimize the use of
Also decrease mucous short-acting beta2 agonists.
secretion and play greater Observe if patients are using
role in the management their rescue inhalers too often,
of COPD and refer them to their health
Beta2 agonists: Relax Short-acting: Albuterol Common: tachycardia, care provider to titrate
bronchial smooth muscle (Proventil,Ventolin), palpitations maintenance therapy. Encourage
by action on beta2- arformoterol (Brovana), Rare: increased blood patients who have exertion- or
receptors with little effect epinephrine (various), pressure, angina, exercise-induced bronchospasm
on heart rate isoproterenol (Isubprel), hypokalemia to administer beta2 agonists10-
levalbuterol (Xopenex), 15 minutes before therapy
metaproterenol sessions.
(Alupent), pirbuterol Bronchodilator administration
(Maxair) can also facilitate chest PT
Long-acting: formoterol effectiveness
(Foradil), salmeterol
(Serevent)
Continued
498 APPENDIX IV Pharmacologic Agents

Table IV-10 BRONCHODILATORS—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Theophylline: Causes Theophylline Appropriate Monitor for signs and symptoms
bronchodilatation, (Elixophyllin, Quibron, therapeutic range of toxicity.Theophylline has
diuresis, CNS and cardiac Theo-24,TheoCap, is 5-20 mcg/ml. many drug interactions, and
stimulation, and gastric Theochron, Uniphyl) At therapeutic levels can rapidly change.
acid secretion by concentrations: Caffeine intake will exacerbate
blocking nervousness, insomnia, side effects
phosphodiesterase, which tachycardia, nausea and
increases tissue vomiting
concentrations of cyclic 15-25 mcg/ml: GI upset,
adenine monophosphate diarrhea, nausea/vomiting,
(cAMP) abdominal pain,
nervousness, headache,
insomnia, agitation,
dizziness, muscle cramp,
tremor
25-35 mcg/ml:Tachycardia,
occasional PVC
> 35 mcg/ml:Ventricular
tachycardia, frequent PVC,
seizure
Combination: Combivent (albuterol + ipratropium).
cAMP, Cyclin adenine monophosphate; CNS, central nervous system; COPD, chronic obstructive pulmonary disease.

Table IV-11 LEUKOTRIENE MODIFIERS

Indications: Long-term control of asthma and adults and children.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Leukotriene receptor Montelukast (Singulair), Montelukast and zafirlukast are Monitor for abdominal
antagonistçselective zafirlukast (Accolate), well tolerated with infrequent pain, yellow skin, and
competitive inhibitor zileuton (Zyflo) cough, dizziness, fatigue, sclera appearance with
of LTD4 and LTE4 dyspepsia. Zileuton can cause zileuton
receptors; hepatotoxicity
5-lipooxygenase
inhibitor
LTD4, Leukotriene D4; LTE4 , Leukotriene E4.
 Pharmacologic Agents APPENDIX IV 499

Table IV-12 MAST CELL STABILIZERS

Indications: Long-term control of asthma and adults and children, allergic rhinitis, exercise-induced asthma.

Generic Name (Common

Mechanism of Action
Decrease histamine release
from mast cells; block early
and late reaction to allergen;
inhibit acute response to
exercise, cold dry air, and
sulfur oxide
Brand Name[s])
Cromolyn (Intal),
nedocromil (Tilade)
Adverse Effects
Well tolerated; unpleasant
taste with nedocromil
PT Considerations
May take up to 2 weeks
to see complete
response. Effective to
prevent exercise-
induced asthma

MUSCULOSKELETAL SYSTEM

Table IV-13 DISEASE-MODIFYING ANTIRHEUMATIC DRUGS (DMARDs)

Indications:Treatment of rheumatoid arthritis (RA). Refer to Chapter Appendix 10-A.
Unlike the NSAIDs and acetaminophen, DMARDs can reduce and prevent joint damage and preserve joint integrity
and function. The American College of Rheumatology recommends initiation of DMARDs within the first 3 months
of diagnosis of RA in patients with ongoing joint pain despite adequate treatment with NSAIDs, significant morning
stiffness, active synovitis, persistent elevations in ESR and CRP levels, and/or radiographic evidence of joint damage.
Methotrexate is considered a first-line agent among DMARDs due to its long-term efficacy, low cost, and acceptable
toxicity profile. DMARDs lose efficacy over time, and patients are typically placed on combination regimens of
different DMARDs; with time, more expensive toxic agents may need to be tried. Many DMARDs do not begin to
work immediately; effect may not be seen for 3 to 6 months. DMARDs are potent antiinflammatory agents that can
lead to immunosuppression. PTs should exercise infection-control measures such as good hand hygiene, sanitizing of
the equipment, and avoiding contact with patients if feeling sick. DMARDs are listed in alphabetical order and not
in order of preference in the table below. Corticosteroids are frequently used as part of RA therapy, typically for short
courses (see Table IV-8).

Generic Name (Common

Mechanism Of Action Brand Name[s]) Adverse Effects PT Considerations
Selective costimulation Abatacept (Orencia) Headache, nausea, high Monitor blood pressure (may increase).
modulator; inhibits risk of infections (54% Monitor for and report any new
T-cell (T-lymphocyte) incidence), COPD symptoms associated with infections:
activation. Activated exacerbations, increase in WBC, fever, cough, skin
T lymphocytes are hypertension, dizziness, infections.
found in the synovium cough, back pain,
of rheumatoid arthritis infusion-related reactions
patients.
Blocks biologic activity Anakinra (Kineret) Injection site reactions are Monitor skin appearance for injection
of interleukin-1 very common. Also, site reactions. Exercise infection-
headache, nausea, control measures
diarrhea, sinusitis, flulike
symptoms, abdominal
pain, and infections
Bind and inhibit tumor Anti^tumor necrosis Rash, headache, nausea, Patients are at high risk for infection.
necrosis factor (TNF), factor therapy: cough Monitor for any signs and symptoms
Continued
500 APPENDIX IV Pharmacologic Agents

Table IV-13 DISEASE-MODIFYING ANTIRHEUMATIC DRUGS (DMARDs)—cont’d

Generic Name (Common
Mechanism Of Action Brand Name[s]) Adverse Effects PT Considerations
which produces potent Adalimumab (Humira), Serious: associated with including fever, productive
antiinflammatory effect etanarcept (Enbrel), infections, including cough, and increase inWBC.
infliximab (Remicade) serious mycobacterial, Exercise infection-control measures.
fungal, and opportunistic
complications.
Antagonizes purine Azathioprine (Imuran) Dose-related bone marrow Monitor WBC (will decrease; patients
metabolism and may suppression, stomatitis, will be at high risk for infection),
inhibit synthesis of diarrhea, rash, and liver hematocrit (will decrease; patient will
DNA, RNA, and failure complain of fatigue), platelets
proteins; may also (will decrease; the risk of bleeding
interfere with cellular will increase)
metabolism and
inhibits mitosis
Mechanism is unknown; Gold compounds With IM injections, Monitor skin appearance for rash.
appear to suppress the Gold sodium thiomalate patients can experience Avoid scheduling PTsessions
synovitis possibly (Myochrysine), injection reactions: immediately and soon after the IM
through stimulation aurothioglucose flushing, weakness, injection (injections are scheduled
of protective (Solganal), auranofin dizziness, sweating, every 2-3 weeks and then monthly).
interleukins 6 and 10 (Ridaura) syncope, hypotension Ensure that the injection site has no
Common: rash ranging adverse reaction prior to initiating
from simple erythema to therapy.
exfoliative dermatitis;
oral formulation causes
nausea, diarrhea, taste
disturbances
Rare: renal disease,
leukopenia,
thrombocytopenia
May inhibit interleukin 1 Hydroxychloroquine Rash, abdominal cramping, Monitor for muscle pain not associated
(IL-1) release by (Plaquenil) diarrhea, myopathy, skin with exercise. Monitor for tingling
monocytes, thereby pigment changes, and numbness of the extremities.
decreasing macrophage peripheral neuropathy Patients should be evaluated by
chemotaxis and Serious:retinaldamagethat ophthalmologist every 6-12 months.
phagocytosis. canleadtovisionloss Report any vision changes.
Inhibits dihydro-orotate Leflunomide (Arava) Diarrhea, alopecia, Monitor liver function (abdominal
dehydrogenase hypertension, rash, pain, yellow skin and sclera). Risk of
(an enzyme involved in hepatotoxicity hepatotoxicity is higher when used
the de novo pyrimidine in combination with methotrexate.
synthesis) and has
antiproliferative and
antiinflammatory effect
Inhibits dihydrofolate Methotrexate Nausea, vomiting, and Ask patients about GI side effects to
reductase and (Rheumatrex) stomatitis are common optimize scheduling PTsession.
interferes with DNA Serious: hepatotoxicity, Monitor WBC (will decrease; use
synthesis, repair, and bone marrow infection-control measures),
cellular replication. suppression, pulmonary hematocrit (will decrease; patient will
toxicity complain of fatigue), and platelets
(will decrease; patient will be at a
higher risk of bleeding)
Sulfasalazine is broken Sulfasalazine Headache, GI intolerance, Ask patient about GI side effects to
down by intestinal (Azulfidine) taste perception optimize scheduling of the session.
 Table IV-13 DISEASE-MODIFYING ANTIRHEUMATIC DRUGS (DMARDs)—cont’d
Generic Name (Common
Mechanism Of Action Brand Name[s]) Adverse Effects PT Considerations
flora into disturbances, rash, Use infection-control measures if
5-aminosalicylic acid leukopenia, WBC decreases (wash hands, sanitize
and sulfapyridine. thrombocytopenia equipment, avoid contact with
Sulfapyridine likely patient if sick). Use caution if platelet
inhibits endothelial cell count decreases (patient will be at
proliferation, reactive higher risk of bleeding)
oxygen species, and
cytokines
GI, Gastrointestinal; PT, physical therapy;WBC, white blood cells.

CENTRAL NERVOUS SYSTEM

Table IV-14 ANTIANXIETY MEDICATIONS

Indications:Treatment of generalized anxiety disorder, panic disorder, agoraphobia, obsessive-compulsive disorder, social
anxiety disorder, various phobias, posttraumatic stress disorder, anxiety, sleep problems.
Precautions:The acronym LOTcan be used to remember the three benzodiazepines with short half-lives that are preferred
in elderly patients: L (lorazepam), O (oxazepam), and T (temazepam).

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Benzodiazepines: Alprazolam (Xanax), Sedation, dizziness, Lorazepam, oxazepam,
potentiate the actions chlordiazepoxide (Librium), confusion, blurred temazepam have shorter
of GABA, an clonazepam (Klonopin), vision, diplopia, half-lives and no active
inhibitory diazepam (Valium), syncope, residual metabolites and are preferred
neurotransmitter estazolam (ProSom), daytime sedation, in elderly. Increased risk of
flurazepam (Dalmane), psychomotor and falls in this population. High
halazepam (Paxipam), cognitive impairment potential for abuse. Schedule
lorazepam (Ativan), session when the patient is
oxazepam (Serax), least sedated and provide
prazepam (Centrax), education about minimizing
quazepam (Doral), fall risk. Do not abruptly
temazepam (Restoril), discontinue BZD to avoid
triazolam (Halcion) withdrawal and seizures
Buspirone: poorly Buspirone (BuSpar) GI upset, headache, Onset of anxiolytic effect
understood; nervousness, less longer than with BZDs
stimulates presynaptic sedating (2-3 weeks)
5-HT1A receptors
Sedative-hypnotic Eszopiclone (Lunesta), Dizziness, somnolence, Shorter half-lives allow for less
agents: GABA ramelteon (Rozerem), confusion sedation in the morning.
receptor agonists; zaleplon (Sonata),
ramelteon affects zolpidem (Ambien)
melatonin receptors
BZD, Benzodiazepine; GABA, gamma-aminobutyric acid; GI, gastrointestinal; 5-HT, 5-hydroxytryptamine.
 Table IV-15 ANTICONVULSANTS

Indications:Treat and prevent seizures; many of the agents in this class can be used for other indications such as treatment
of the neuropathic pain and migraine prevention.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Multiple mechanisms Carbamazepine Rash, nausea, vomiting, drowsiness, Many drug interactions,
of actions: (Tegretol, dizziness, neutropenia, SIADH, complex pharmacokinetics,
enhancement of Carbatrol) osteomalacia, folic acid therapeutic drug level 4-12
sodium channel deficiency, hepatotoxicity, aplastic mcg/ml
inactivation, anemia Monitor for hepatotoxicity
reducing current Ethosuximide Aggressiveness, ataxia, disturbance Monitor changes in mood,
throughT-type (Zarontin) in sleep, dizziness, drowsiness, aggression, suicidal ideations
calcium channels, euphoria, fatigue, headache,
enhancement of hyperactivity, inability to
GABA activity, concentrate, irritability, lethargy,
antiglutamine mental depression (with cases of
activity overt suicidal intentions), night
terrors, paranoid psychosis
Fosphenytoin (Cerebyx), Nausea, vomiting, drowsiness, Many drug interactions;
phenytoin (Dilantin) dizziness, peripheral neuropathy, therapeutic drug levels
acne, hirsutism, gingival 10-20 mcg/ml
hyperplasia, folate deficiency,
hepatic failure, Steven-Johnson
syndrome
Felbamate Weight loss, hepatotoxicity, aplastic
(Felbatol) anemia
Gabapentin Well-tolerated, somnolence, ataxia, Popular for treatment of
(Neurontin), weight gain neuropathic pain
pregabalin (Lyrica)
Lamotrigine Rash, Steven-Johnson Refer to the prescriber if rash
(Lamictal) syndrome develops
Levetiracetam (Keppra) Behavioral symptoms (aggression,
hyperkinesias, irritability,
neurosis), somnolence, fatigue
Oxcarbazepine Dizziness, somnolence, headache,
(Trileptal), ataxia, fatigue, vertigo
tiagabine (Gabitril)
Phenobarbital (Barbital, Drowsiness, dizziness, High potential for abuse, very
Luminal, Solfoton) incoordination, sedating, therapeutic drug
decreased cognition, levels 15-40 mg/L
hepatic failure, Steven-Johnson
syndrome
Topiramate Drowsiness, dizziness, difficulty Make sure patient stays well
(Topamax), with concentration, loss of hydrated; patients who
zonisamide appetite, mood changes, develop oligohydrosis may
(Zonegran) metabolic acidosis, kidney stones, overheat easily and need to
weight loss, oligohydrosis stay well hydrated.
(inability to sweat)
Valproic acid Nausea and vomiting, significant Design an exercise regimen to
(Depakon, weight gain, alopecia, tremor, minimize weight gain;
Depakene, thrombocytopenia, fatal monitor abdominal pain for
Depakote) hepatotoxicity, fatal hemorrhagic liver and pancreatic toxicity
pancreatitis
GABA, Gamma-aminobutyric acid; Steven-Johnson syndrome, Severe and life-threatening hypersensitivity complex that affects the skin and the
mucous membranes.
Table IV-16 ANTIDEPRESSANTS
Indications:Treatment of depression and other psychologic disorders such as panic, obsessive compulsive disorder, etc.; some agents in this class can be
used to treat neuropathic pain (TCAs), prevent migraines (TCAs, SSRIs). It takes 4-6 weeks before full efficacy of drug therapy can be assessed.
Mechanism of Action
Monoamine oxidase (MAO)
inhibitors: increase the
synaptic concentrations
of NE, 5-HT, and DA by
inhibiting monoamine
oxidase (breakdown
enzyme)
Norepinephrine-dopamine
reuptake inhibitor
(NDRI): inhibits NE and
DA reuptake
Selective serotonin reuptake
inhibitors (SSRIs):
selectively inhibit 5-HT
reuptake
Serotonin-norepinephrine
reuptake inhibitors
(SNRI): inhibit reuptake
of NE and 5-HT
Tricyclic antidepressants
(TCAs): increase synaptic
concentration of 5-HT
and/or NE in the CNS
Generic Name (Common
Brand Name[s])
Phenelzine (Nardil),
tranylcypromine
(Parnate)
Bupropion
(Wellbutrin, Zyban)
Citalopram (Celexa),
escitalopram (Lexapro),
fluoxetine (Prozac,
Sarafem), fluvoxamine
(Luvox), paroxetine
(Paxil), sertraline
(Zoloft)
Duloxetine (Cymbalta),
venlafaxine (Effexor)
Amitriptyline (Elavil),
clomipramine
(Anafranil), desipramine
(Norpramin), doxepin
(Sinequan),
nortriptyline (Pamelor)
Adverse Effects
Orthostatic hypotension, weight gain,
sexual dysfunction, anticholinergic
effects, hypertensive crisis
GI upset, insomnia, anxiety, headache,
decreases seizure
threshold
GI complaints, nervousness, insomnia,
headache, fatigue, sexual
dysfunction. Safer in overdose.
SSRI withdrawal syndrome: flulike
symptoms, dizziness, nausea, tremor,
anxiety, and palpitations
GI upset, anxiety, headache, dose-
related hypertension
Orthostatic hypotension, tachycardia,
sedation, anticholinergic effects,
arrhythmias (prolongs QT), weight
gain, sexual dysfunction
PT Considerations
These agents are reserved for those
with depression refractory to
other treatments due to many
drug-drug interactions
(contraindicated with other drugs
that increase 5-HTand/or NE)
and dietary restrictions (avoid
tyramine containing foods).
Used for smoking cessation. Causes
less sexual dysfunction, but
monitor for seizures
These are considered first-line
treatment due to good tolerability
profile. Patients should not
abruptly discontinue SSRIs (taper
Pharmacologic Agents
over 2-4 weeks, with the
exception of fluoxetine)
Duloxetine has an indication for the
treatment of diabetic neuropathic
pain. Monitor blood pressure.
Establish the time of the day when
sedation is minimal to schedule
PTsessions.TCAs are deadly in
APPENDIX IV
overdose (they block sinoatrial
node). Drug serum levels can be
obtained to guide therapy.
Continued
503
 504
APPENDIX IV
Table IV-16 ANTIDEPRESSANTS—cont’d
Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations

Pharmacologic Agents
Mirtazapine: increases Mirtazapine (Remeron) Less GI side effects and anxiety; Sedation is more pronounced with
5-HTand NE in the sedation, increased appetite, weight this medication. Schedule PT
synapses; antagonizes 5- gain, constipation, elevation of LFTs sessions when patient is most
HT2A and 5-HT3 and TG alert. Design exercise program to
receptors minimize weight gain
Nefazadone: inhibits 5-HT Nefazadone (Serzone) GI upset, sedation, dry mouth, Monitor abdominal pain and yellow
and NE uptake and constipation, lightheadedness, appearance for hepatotoxicity
blocks 5-HT2A receptors minimal sexual dysfunction,
orthostasis, high incidence
of hepatotoxicity
Trazadone: inhibits 5-HT Trazadone Extremely sedating, orthostatic Commonly used for insomnia due
reuptake and blocks 5- (Desyrel) hypotension, priapism; no to sedating properties. Schedule
HT2A receptors anticholinergic and cardiovascular sessions later in the afternoon if
side effects sedation persists into the
morning
CNS, Central nervous system; GI, gastrointestinal; 5-HT, 5-hydroxytryptamine; LFTs, liver function tests; MAO, monoamine oxidase; NE, norepinephrine; PT, physical
therapy; SDRI, serotonin-dopamine reuptake inhibitor; SNRI, serotonin-norepinephrine reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor;TCA, tricyclic
antidepressant;TG, triglycerides.
 Pharmacologic Agents APPENDIX IV 505

Table IV-17 ANTIPSYCHOTICS

Indications:Treatment of various schizoaffective disorders, such as schizophrenia. Can be used to treat aggressive
behaviors associated with bipolar disorders and dementia.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Typical (conventional Chlorpromazine Sedation, orthostasis, Monitor for orthostasis and
antipsychotics): (Thorazine), weight gain, sedation. EPS can interfere with
Block postsynaptic fluphenazine (Prolixin), anticholinergic side therapy sessions.Tardive
dopamine-2 receptors. haloperidol (Haldol), effects (dry mouth, dyskinesia is irreversible. Report
Share anticholinergic, thioridazine (Mellaril) urinary retention, first signs of TD to health care
antihistamine, and constipation, confusion), providers. Symptom triad
alpha-blocking extrapyramidal side characteristic of TD:
properties (often (EPS) effects splayed writhing fingers;
producing undesirable (dystonia, akathisia, grimacing, bruxism, lip
side effects) pseudoparkinsonism, smacking; protrusion of tongue).
tardive dyskinesia (TD) Design exercise programs to
minimize weight gain
Atypical antipsychotics: Aripiprazole (Abilify), Sedation, orthostasis, weight Monitor for sedation, orthostasis,
weak dopamine and clozapine (Clozaril), gain, new onset diabetes, QT prolongations, signs and
dopamine-2 receptor olanzapine (Zyprexa), possible dose related symptoms of hyperglycemia
blockers that block risperidone (Risperdal), EPS with some agents (excessive thirst, urination).
serotonin and alpha- quetiapine (Seroquel), (incidence of EPS is Design programs to minimize
adrenergic, histamine, ziprasidone (Geodon) significantly less than weight gain.With clozapine,WBC
and muscarinic with conventional agents), count is monitored every 2 weeks;
receptors in the CNS QT prolongation; if patient becomes neutropenic,
hypersalivation and use precautions to
agranulocytosis with minimize exposure to viral and
clozapine bacterial illness.
EPS, Extrapyramidal side;TD, tardive dyskinesia;WBC, white blood cell.

Table IV-18 MOOD STABILIZERS

Indications: Bipolar disorders (acute treatment and prophylaxis of manic episodes).

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Lithium: unknown; facilitates Lithium (Lithobid, Tremor, polydipsia, Lithium has narrow
GABA and influences Eskalith CR, polyuria, nausea, therapeutic range.
reuptake of serotonin Cibalith-S) diarrhea, weight Therapeutic levels are 0.6-1.2
and norepinephrine gain, hypothyroidism, mEq/L (acute) and 0.8-1.0
mental dulling mEq/L (maintenance).
Monitor signs and symptoms
of lithium toxicity*
Divalproex sodium (Depakote and Carbamazepine (Tegretol) are anticonvulsant medications that can be used as mood stabilizers.
SeeTable IV-16.
*Mild lithium toxicity (1.5-2 mEq/L): GI upset, muscle weakness, fatigue, fine hand tremor, difficulty with concentration and memory;
moderate toxicity (2-2.5 mEq/L): ataxia, lethargy, nystagmus, worsening confusion, severe GI upset, coarse tremor, increased deep-tendon
reflexes; severe toxicity (> 3 mEq/L): severe impaired consciousness, coma, seizures, respiratory complications, death.
GABA, Gamma-aminobutyric acid.

Table IV-19 PARKINSON’S MEDICATIONS
Indications:Treat signs and symptoms associated with Parkinson’s disease.
Mechanism of Action
Amantadine: antiparkinsonian
activity may be due to its blocking
the reuptake of dopamine into
presynaptic neurons
or by increasing dopamine release
from presynaptic fibers
Anticholinergics: possess both
anticholinergic and antihistaminic
effects; may also inhibit the
reuptake and storage of dopamine,
thereby prolonging the action
of dopamine.
COMT inhibitors: Inhibit catechol-O-
methyltransferase (COMT).
Combined with levodopa resulting
in more sustained levodopa serum
levels, thereby providing for
increased CNS levels of dopamine,
the active metabolite of levodopa
Dopamine agonists: Centrally-active
dopamine agonists exert their
therapeutic effect by
directly stimulating
postsynaptic dopamine
receptors in the
nigrostriatal system.
Generic Name (Common
Brand Name[s])
Amantadine (Symmetrel)
Benztropine (Cogentin),
biperiden (Akineton)
procyclidine
(Kemadrin),
orphenadrine
(Disipal, Norflex),
trihexyphenidyl
hydrochloride (Artane,
Trihexy-5)
Entacapone (Comtan),
tolcapone (Tasmar)
Bromocriptine
mesylate (Parlodel),
pergolide mesylate
(Permax), pramipexole
(Mirapex), ropinirole
hydrochloride (Requip)
Adverse Effects
Orthostasis, peripheral edema,
anxiety, ataxia, dizziness,
hallucinations, insomnia,
somnolence, anorexia, GI
upset
Dry mouth, blurred vision,
constipation, nausea, urinary
retention, tachycardia,
somnolence, confusion
Nausea, dyskinesias, orthostasis,
dizziness, hallucinations,
diarrhea, brown-orange urine
discoloration. Hepatotoxicity
with tolcapone.
Nausea and vomiting, dizziness
or fainting; sudden,
unpredictable attacks of
sleepiness (these can be very
dangerous if they occur while
a person is driving);
orthostatic hypotension;
confusion or hallucinations;
depression; insomnia;
dyskinesias; irregular heart
rate and chest pain.
506
APPENDIX IV
PT Considerations
Rarely used; often combined with other
agents
Pharmacologic Agents
First line for tremor predominant
disease; can be used to treat motor
complications (dyskinesias) of
dopaminergic agents
These drugs are added to levodopa in
order to optimize motor function
and reduce motor complications.
Patients should be taking one of
these with each dose of levodopa.
These are first line in younger patients.
Compared to levodopa, the motor
complications are less common,
however, sleep attacks are more
common. Determine the pattern of
side effects before scheduling a
session. Pergolide has
been withdrawn from the market due
to heart valve damage (March 2007)
 Levodopa/Carbidopa: levodopa
converts into dopamine; carbidopa
is a peripheral decarboxylase
inhibitor that does not allow for
conversion of levodopa into
dopamine in the periphery.
Carbidopa does not penetrate the
blood-brain barrier and allows for
levodopa to convert to dopamine
in the brain at the site of dopamine
deficiency
Selegiline: potent irreversible
inhibitor of monoamine oxidase
with specificity for MAO-B at
commonly used doses. MAO-B
plays a major role in metabolism of
dopamine, so selegiline increases
dopamine concentrations in
the brain
Combination: Stalevo (levodopa + carbidopa + entacapone).
COMT, Catechol-O-methyltransferase; MAO, monoamine oxidase.
Levodopa Orthostasis, hypertension,
(Dopar, Larodopa), arrhythmias, dizziness,
carbidopa (Lodosyn) confusion, nightmares,
Levodopa/Carbidopa hallucinations, psychosis,
(Sinemet, Sinemet CR) gait abnormalities, increased
libido, GI upset, sialorrhea,
discoloration of urine and
sweat, hemolytic anemia,
pancytopenia, LFTelevations,
choreiform and involuntary
movements, paresthesia,
bone pain, shoulder pain,
muscle cramps,
weakness, hiccups,
dyskinesias
Selegiline (Eldepryl, Headache, insomnia,
Emsam, Zemplar) dizziness, nausea,
hypotension, orthostasis,
diarrhea, weight loss
Many side effects occur due to some
peripheral conversion to dopamine.
Onset of action is 30 minutes
for Sinemet and 60 minutes for
Sinemet CR.Timing your exercise
session during the peak activity of
Sinemet is best. Patients will require
increased dose and frequency as
the disease progresses. Motor
abnormalities and dyskinesias
are predominant side effects that
require management.
At doses higher than 20 mg per day
(recommended dose is 10 mg per
day), MAO-B specificity is lost and
patients can experience hypertensive
crisis with any other serotonergic,
sympathomimetic drugs and foods.
Pharmacologic Agents
APPENDIX IV
507
508 APPENDIX IV Pharmacologic Agents

ONCOLOGY

Table IV-20 ANTIEMETIC MEDICATIONS

Indications: Prevention and treatment of nausea and vomiting from any causes, including chemotherapy and radiation
induced and postoperative nausea and vomiting.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
5-HT3 receptor Dolasetron (Anzemet), Well tolerated; Nausea and vomiting is
antagonists: Selective granisetron (Kytril), headache, common for the first
5-HT3-receptor ondansetron (Zofran), constipation, 24 hours post
antagonists; block palonosetron (Aloxi) dizziness chemotherapy, but can
serotonin, both occur for up to 5 days.
peripherally on vagal Assess severity and
nerve terminals and frequency before
centrally in the scheduling therapy
chemoreceptor trigger
zone
Benzamides: Blocks Metoclopramide Drowsiness, fatigue, Monitor vitals and
dopamine receptors (Reglan) acute dystonic extrapyramidal
and (when given in reactions, akathisia, symptoms
higher doses) also confusion,
blocks serotonin neuroleptic
receptors in malignant syndrome
chemoreceptor trigger (rare), Parkinsonian-
zone of the CNS like symptoms,
diarrhea
Butyrophenones: Droperidol (Inapsine), QT prolongation, Monitor for QT
antiemetic effect is a haloperidol (Haldol) restlessness, anxiety, prolongation on ECG
result of blockade of extrapyramidal (high risk for
dopamine stimulation symptoms, seizure, torsades); schedule the
of the chemoreceptor altered central session when the
trigger zone temperature patient is least sedated
regulation, sedation,
drowsiness
Cannabinoids: Dronabinol Palpitations, Assess adverse side
Unknown, may (Marinol) vasodilation/facial effects before
inhibit endorphins in flushing, euphoria, scheduling the
the brain’s emetic dizziness, paranoia, session; can also be
center, suppress somnolence, used as an appetite
prostaglandin amnesia, anxiety, stimulant in cachexia.
synthesis, and/or ataxia,
inhibit medullary hallucinations
activity through an
unspecified cortical
action
CNS, Central nervous system; ECG, electrocardiogram; 5-HT, 5-hydroxytryptamine.
Table IV-21 CHEMOTHERAPY

Indications:Treat malignancy; some are used to treat autoimmune and inflammatory disorders such as Crohn’s disease and rheumatoid arthritis.
Chemotherapy has the greatest effect on rapidly dividing cells. Most of the potent agents work through damaging DNA. Therapeutic effects are seen
when cancer cells are killed, while adverse effects are seen when human cells that rapidly divide are damaged. These include hair follicles, lining of
the stomach and the rest of the GI tract, and bone marrow. Universal side effects: majority of the chemotherapeutic agents cause nausea and
vomiting, mucosal ulceration, myelosuppression (decreased white blood cells, red blood cells, and platelets), and alopecia. As the result of
myelosuppression, these patients are often immunocompromised and are at high risk for infection and are at increased risk of bleeding. Majority of
chemotherapeutic agents are also carcinogenic, teratogenic, and mutagenic. Majority of the chemotherapeutic agents cause sterility. These side
effects are not discussed with each class of agents. Only the most commonly used agents are listed as examples of each class.
In general, physical therapists should avoid working with patients when their blood counts are at nadir (lowest point) and right after chemotherapy
cycle administration (nausea and vomiting is most common in the first 24 hours but can occur for up to 5 days). However, a full evaluation of the
patient will ultimately determine if physical therapy intervention, depending on its nature, is appropriate. Always utilize infection-control measures
with cancer patients. Make sure that your hands are cleaned properly and any equipment is cleaned/sterilized. Avoid close contact with cancer
patients if you are sick. Special measures may be necessary with patients who are neutropenic (decreased white blood cell count), such as facial
masks and isolation from other patients.

Generic Name (Common

Mechanism Of Action Brand Name[s]) Adverse Effects PT Considerations
Alkylating agents: form Carmustine (BICNU), Pulmonary fibrosis (carmustine) and Monitor for signs of pulmonary toxicity,
covalent bonds with cyclophosphamide (Cytoxan, interstitial pneumonitis, hemorrhagic renal functionçurinary output, blood
nucleic acids and Neosar), dacarbazine cystitis (cyclophosphamide and in the urine. Mesna (an adjuvant
proteins resulting in (DTIC-Dome), ifosfamide ifosfamide), encephalopathy medication) and hydration are
cross-linking of DNA (Ifex), melphalan (Alkeran), (ifosfamide) administered with cyclophosphamide

stands and inhibition temozolomide (Temodar),
of DNA replication thiotepa (Thioplex)
Antimetabolites: act by Capecitabine (Xeloda),
falsely inserting cytarabine (Cytosar-U,
themselves in place of DepoCyt), fludarabine
a pyrimidine or (Fludara), fluorouracil (5-FU,
purine ring, causing Adrucil), gemcitabine
interference in nucleic (Gemzar), mercaptopurine
acid synthesis (Purinethol), methotrexate
(Rheumatrex)
Pharmacologic Agents
and ifosfamide to decrease the risk of
hemorrhagic cystitis
Hand-foot syndrome (redness, Monitor for tingling and swelling of the
tenderness, and possibly peeling of palms and soles, bruising, bleeding,
the palms and soles), severe diarrhea, diarrhea
fatigue, neurotoxicity (cytarabine,
fludarabine, methotrexate), rash and
fever, flulike symptoms
(gemcitabine), renal toxicity,
conjunctivitis (cytarabine), hemolytic

APPENDIX IV
uremic syndrome (gemcitabine),
tumor lysis syndrome, hepatotoxicity
(methotrexate, mercaptopurine)
Continued

509

Table IV-21 CHEMOTHERAPY—cont’d
Generic Name (Common
Mechanism Of Action Brand Name[s])
Antitumor antibiotics: Anthracyclines: doxorubicin
block DNA and/or (Adriamycin, Doxil),
RNA synthesis daunorubicin (Cerubidine,
through various Daunoxome), idarubicine
mechanisms (Idamycin), miloxantrone
(Novantrone)
Alkylating-like: mitomycin
(Mutamycin)
Chromomycin: dactinomycin
(Cosmegen)
Miscellaneous: bleomycin
(Blenoxane)
Biologic response Immunologic therapies:
modifiers and Aldesleukin (Proleukin),
monoclonal interferon-alpha 2b (Intron
antibodies: biologic A), levamisole (ergamisol)
response modifiers Monoclonal antibodies:
activate the body’s alemtuzumab (Campath),
immune-mediated bevacizumab (Avastin),
host defense cetuximab (Erbitux),
mechanisms to denileukin diftitox (Ontak),
cancerous cells. gemtuzumab (Mylotarg),
Monoclonal ibritumomab (Zevalin),
antibodies bind to rituximab (Rituxan),
specific antigens on tositumomab (Bexxar),
malignant cells and trastuzumab (Herceptin)
cause apoptosis,
an antibody-mediated
toxicity, or
complement mediated
lysis.
Hormones and Androgens: testosterone
antagonists: act on (Delatestryl),
hormone-dependent fluoxymesterone (Halotestin)
tumors by inhibiting Antiandrogens: flutamide
or decreasing the (Eulexin), bicalutamide
production of (Casodex), nilutamide
disease-causing (Nilandron)
hormone Antiestrogens: tamoxifen
(Nolvadex)
Adverse Effects
Severe nausea and vomiting, stomatitis,
and alopecia; acute and chronic heart
failure (anthracyclines); secondary
acute myelogenous leukemia;
pulmonary fibrosis and interstitial
pneumonitis with bleomycin; renal
toxicity with dactinomycin
Hypotension and hypersensitivity upon
infusion; cardiac, pulmonary, and
renal impairment; depression, fever,
chills, nausea, musculoskeletal pain;
tumor lysis (rituximab); bleeding,
hemorrhage, hypertension,
proteinuria, rash (bevacizumab);
cutaneous and infusion reactions,
interstitial lung disease (cetuximab);
hypothyroidism (tositumomab)
Edema, menstrual disorders,
hot flashes, transient bone
and muscle pain, thromboembolic
events, gynecomastia, elevated liver
enzymes, diarrhea, impotence,
decreased libido, endometrial cancer
(tamoxifen), bone loss (LHRH and
aromatase inhibitors); hypotension
and syncope (abarelix)
510
PT Considerations
All anthracyclines have limits on
cumulative lifetime dosing due to
APPENDIX IV
cardiotoxicity. Delayed nausea and
vomiting is common with
anthracyclines. Monitor vitals,
shortness of breath, fatigue, and
edema for signs of heart failure.
Pharmacologic Agents
Patients are typically premedicated with
Tylenol and Benadryl to decrease
infusion-related reactions. Monitor for
hypertension, fever, and organ toxicity
(lung: respiratory problems; heart:
blood pressure, pulse, exercise
tolerance; kidney: urine output,
weight, serum creatinine)
Note weight changes, abnormal vaginal
bleeding, body and bone pain.
Monitor for embolic disorders (DVT:
pain and swelling in the extremities;
PE: shortness of breath, chest pain)
 Aromatase inhibitors:
exemestane (Aromasin),
anastrozole (Arimidex),
letrozole (Femara)
Estrogens: ethinyl estradiol
(Estinyl)
GNRH agonists: abarelix
(Plenaxis)
LHRH agonists: goserelin
(Zoladex), leuprolide
(Leupron, Eligard),
triptorelin (Trelstar)
Progestins: megestrol (Megace),
medroxyprogesterone
(Provera)
Plant alkaloids: inhibit Camtothecins: irinotecan Edema (docetaxel), hypotension/ Monitor for peripheral neuropathy,
replication of (Camtosar), topotecan hypersensitivity upon administration blood pressure decrease. Acute and
cancerous cells (Hycamtin) (paclitaxel), neurotoxicity late onset diarrhea may interfere with
through various Epipodophyllotoxins: (vincristine), diarrhea, headache, therapy sessions
mechanisms etoposide (VePesid), secondary malignancies
Teniposide (Vumon) (epipodophyllotoxins), syndrome of
Taxanes: docetaxel (Taxotere), inappropriate antidiuretic hormone
paclitaxel (Taxol, Abraxane) secretion (vinca alkaloids)
Vinca alkaloids: vinoblastin

(Velban), vincristine
(Oncovin), vinorelbine
(Navelbine)
Platinum compounds: Carboplatin (Paraplatin),
alkylating-like, cause cisplatin (Platinol-AQ),
inhibition of DNA oxaliplatin (Eloxatin)
synthesis
Tyrosine kinase Dasatinib (Sprycel), erlotinib
inhibitors: inhibit (Tarceva), gefitinib (Iressa),
tyrosine kinase imatinib (Gleevec), Sutinib
Pharmacologic Agents
Nephrotoxicity, peripheral These agents are associated with severe
neurotoxicity, ototoxicity acute and delayed nausea and
vomiting
Hepatotoxicity, fluid retention, weight
gain, neutropenia, GI effects, muscle
cramps (imatinib); rash, interstitial

APPENDIX IV
(Sutent) lung disease (erlotinib); rash, acne
(gefitinib)
DNA, Deoxyribonucleic acid; GNRH, gonadotropin-releasing hormone, LHRH, luteinizing hormone-releasing hormone; RNA, ribonucleic acid.

511
512 APPENDIX IV Pharmacologic Agents

VASCULAR SYSTEM AND HEMATOLOGY

Table IV-22 COLONY-STIMULATING FACTORS

Indications: Stimulate formation of white and red blood cells.

Generic Name (Common

Mechanism of Action
Erythropoiesis-stimulating:
Induces erythropoiesis by
stimulating the division and
differentiation of committed
erythroid progenitor cells;
induces the release of
reticulocytes from the bone
marrow into the bloodstream,
where they mature to
erythrocytes
Granulocyte-stimulating:
Stimulates the production,
maturation, and activation of
neutrophils. Sargramostim also
stimulates the production,
maturation, and activation of
eosinophils, monocytes, and
macrophages
G-CSF, Granulocyte-colony stimulating factor; GI, gastrointestinal; GM-CSF, granulocyte-macrophage colony-stimulating factor;
GI, gastrointestinal; DVT, deep vein thrombosis.
Brand Name[s]) Adverse Effects PT Considerations
Darbepoetin alpha Hypertension, thrombotic and Monitor hemoglobin and
(Aranesp), Epoetin vascular events, edema, DVT, hematocrit; higher values
alpha (Epogen, fever, dizziness, insomnia, are associated with
Procrit) headache, pruritus, GI upset, thromboembolic
arthralgias, seizures (rare) complications; monitor
blood pressure
Filgrastim (Neupogen, Hypertension, edema, chest Monitor for musculoskeletal
G-CSF), pegfilgrastim pain, fever, headache, chills, pain; vital signs. G-CSF
(Neulasta, G-CSF), rash, pruritus, weakness, bone and GM-CSF is often
sargramostim pain, arthralgias, myalgias, GI used in severely
(Leukine, GM-CSF) upset; increase in serum neutropenic patients
creatinine, bilirubin, serum (high infectious
glucose, and cholesterol risk)çuse infection-
(sargamostim) control measures.

GASTROINTESTINAL SYSTEM

Table IV-23 ANTACIDS

Indications: Acid suppression for treatment of mild GERD and heartburn; adjunct therapy with more potent acid suppressive
therapy (PPIs and H2RAs) for breakthrough symptoms; can be used as phosphate binders in patients with renal disease.
There are a variety of antacids on the market. All are available over-the-counter. Antacids contain cations such as aluminum,
calcium, magnesium, or a combination. Sodium bicarbonate can also be used as an antacid. Only the most common
antacids are presented below. Calcium and magnesium^containing antacids have more ANC (acid neutralizing capacity)
per ml of suspension or tablet (i.e., they are more potent). Alginic acid acts as an absorbent and is sometimes added to
antacid formulations. Combination products are available with improved GI side-effect profile.

Generic Name (Common

Mechanism of Action
Antacids neutralize
gastric acid and
inhibit conversion of
pepsinogen to pepsin,
thus raising the pH of
gastric contents;
Brand Name[s])
Aluminum based:
aluminum carbonate
(Badaljel), aluminum
hydroxide (Amphojel,
ALternaGEL)
Adverse Effects
Constipation,
hypophosphatemia and
bone demineralization;
toxicity in patients with
renal diseaseçbone
abnormalities
PT Considerations
Constipation can interfere
with PT; monitor for
aluminum toxicity in
patients with reduced
renal function
 Pharmacologic Agents APPENDIX IV 513

Table IV-23 ANTACIDS—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
alginic acid reacts Calcium based: calcium Constipation Constipation can interfere
with sodium carbonate (TUMs) with PT
bicarbonate in saliva Magnesium based: Diarrhea; toxicity in patients Diarrhea can interfere with
to form sodium magnesium hydroxide with renal diseaseçdeep PT; monitor for signs
alginate viscous tendon reflex reduction, and symptoms of toxicity
solution, which floats muscle weakness, in patients with reduced
on the surface of arrhythmias renal function
gastric contents and Sodium bicarbonate Water retention, edema, Avoid in patients with
acts as a protective (Alka-Seltzer) exacerbation of cardiovascular disease
barrier hypertension and heart
failure
Combination therapy: aluminum hydroxide + magnesium hydroxide (Maalox), magaldrate (Riopan), alginic acid + aluminum hydroxide +
magnesium hydroxide (Gaviscon), calcium carbonate + magnesium hydroxide (Mylanta).

Table IV-24 ANTIDIARRHEAL MEDICATIONS

Indications:Treatment of diarrhea.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Inhibit/decrease Diphenoxylate/atropine Constipation; sedation, Assess for presence of CNS
GI motility (Lomotil), loperamide drowsiness, dizziness depression and timing of
(Imodium), opium (especially with opium diarrhea to optimize
tincture tincture) scheduling of the PTsession.
CNS, central nervous system; GI, gastrointestinal; PT, physical therapy.

Table IV-25 ANTISPASMODIC MEDICATIONS

Indications:Treatment of irritable bowel syndrome.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Selectively inhibit gastrointestinal Dicyclomine (Bentyl), Dizziness, lightheadedness, Monitor for dizziness
smooth muscle (via hyoscyamine (Hyosin, drowsiness, xerostomia, and blurred vision
anticholinergic properties) Levsin, Levbid) nausea, constipation,
and reduce stimulated colonic blurred vision
motor activity
514 APPENDIX IV Pharmacologic Agents

Table IV-26 CYTOPROTECTIVE MEDICATIONS

Indications: Protect GI mucosa from drug-induced or stress-related ulceration.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Sucralfate: forms a complex by Misoprostol (Cytotec), Diarrhea, abdominal GI side effects may interfere
binding with positively sucralfate (Carafate) pain (misoprostol); with PTsession.
charged proteins in exudates, constipation Sucralfate will bind other
forming a viscous pastelike, (sucralfate) drugs and reduce their
adhesive substance, which serves efficacy. Misoprostol is
as a protective coating that teratogenic and should
protects the lining against peptic not be used in women
acid, pepsin, and bile salts; who are pregnant or may
Misoprostol: synthetic become pregnant
prostaglandin E1 analog that
replaces the protective
prostaglandins consumed with
prostaglandin-inhibiting
therapies (e.g., NSAIDs)
Combination: misoprostol + dicolfenac (Arthrotec).
GI, Gastrointestinal, NSAID, nonsteroidal antiinflammatory drug; PT, physical therapy.

Table IV-27 HISTAMINE-2 RECEPTOR ANTAGONISTS (H2RAs)

Indications: Acid suppression for treatment of GERD, heartburn, peptic ulcer disease; treatment and prevention of
NSAID-induced ulcers; prevention of stress ulcers and drug-induced ulcers; treatment of H. pylori.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Suppress gastric acid Cimetidine (Tagamet), Very well tolerated; headache, Drug therapy should not
secretion by reversibly Famotidine (Pepcid), nausea, diarrhea, constipation influence PT; however
blocking histamine-2 Nizatidine (Axid), have been reported; confusion report any new signs
receptors on the Ranitidine (Zantac) can occur in elderly who take and symptoms of GI
surface of the gastric high doses; gynecomastia and upset or bleeding,
parietal cell impotence (cimetidine) which can occur in
case of therapy failure
Combination therapy: Ranitidine bismuth citrate (Tritec)çused specifically for the treatment of H. pylori; calcium carbonate + magnesium
hydroxide + famotidine (Pepcid Complete OTC).
GERD, gastroesophageal reflux disorder; GI, gastrointestinal; NSAID, nonsteroidal antiinflammatory drug; PT, physical therapy.
 Pharmacologic Agents APPENDIX IV 515

Table IV-28 LAXATIVES

Indications:Treatment of constipation.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Bulk-forming: Absorb water Methylcellulose (Citrucel), Impaction above Patients should ensure
in the intestine to form a viscous polycarbophil (Fiber-lax, strictures, fluid that they drink plenty
liquid that promotes peristalsis and FiberCon), psyllium overload, gas and of water to prevent
reduces transit time (Metamucil) bloating bowel obstruction
Emollients: reduce surface tension of Docusate (Colace), Mineral oil decreases Ask patients about
the oil-water interface of the stool mineral oil (Fleet absorption of vitamins bowel habits and
resulting in enhanced mineral oil enema, and many drugs adverse effects, such
incorporation of water and fat various) as nausea, cramping,
allowing for stool softening flatulence, in order to
Osmolar agents: produce an osmotic Glycerin (Fleet glycerin Nausea, bloating, identify the best time
effect in the colon with resultant suppositories), magnesium cramping, rectal for PTsession
distention promoting peristalsis citrate (Citroma), irritation; magnesium
magnesium sulfate toxicity in renally
(various), lactulose impaired patients
(Enulose, Generlac),
polyethylene glycol
(MiraLax)
Stimulants: stimulate Bisacodyl (Ducolax), senna Gastric irritation, fluid
peristalsis by directly irritating the (Senokot) and electrolyte
smooth muscle of the intestine abnormalities
Lubiprostone: Bicyclic fatty acid that Lubiprostone (Amitiza) Headache, nausea,
acts locally at the apical portion of diarrhea
the intestine as a chloride channel
activator, increasing intestinal water
secretion.

Combination: docusate + senna (PeriColace).

Table IV-29 PROTON PUMP INHIBITORS (PPIs)

Indications: Acid suppression for treatment of GERD, peptic ulcer disease; treatment and prevention of NSAID-induced
ulcers; treatment of acute GI bleed; prevention of stress ulcers and drug-induced ulcers; treatment of H. pylori.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Suppress gastric acid secretion Esomeprazole (Nexium), Very well tolerated; Drug therapy should not
specifically by inhibiting the omeprazole (Prilosec), headache, nausea, influence PT; however
H+- ATPase K+-ATPase lansoprazole (Prevacid diarrhea, report any new signs and
enzyme system of the SoluTab), pantoprazole constipation have symptoms of GI upset or
secretory surface of the (Protonix), rabeprazole been reported bleeding that can occur in
gastric parietal cell (Aciphex) case of therapy failure
Combination therapy: Lansoprazole + Amoxicillin + Clarithromycin (Prevpac)çThis combination is in terms of packaging only.
Medications are not combined into one pill, but rather packaged together for convenience to improve compliance with this commonly
utilized H. pylori regimen.
ATP, Adenosine 50 -triphosphate; GERD, gastroesophageal reflux disorder; GI, gastrointestinal; NSAID, nonsteroidal antiinflammatory
drug; PT, physical therapy.
516 APPENDIX IV Pharmacologic Agents

GENITOURINARY SYSTEM

Table IV-30 BENIGN PROSTATIC HYPERTROPHY (BPH) THERAPY

Indications:Treatment of symptomatic benign prostatic hypertrophy.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Alpha-1 blockers: competitively inhibits Alfuzosin (Uroxatral), Dizziness, palpitations, Monitor blood pressure
postsynaptic alpha1-adrenergic doxazosin (Cardura), orthostatic (hypotension).
receptors in prostatic stromal and prazosin (Minipress), hypotension, Patients will be at risk
bladder neck tissues.This reduces the tamsulosin (Flomax), syncope, headache, for orthostasis; use
sympathetic tone-induced urethral terazosin (Hytrin) drowsiness, urinary caution when
stricture causing BPH symptoms frequency exercising
5-Alpha-reductase inhibitors: Dutasteride (Avodart), Impotence, decreased Patients will be at risk
competitive inhibitor of both tissue finasteride (Proscar) libido, weakness, for orthostasis; use
and hepatic 5-alpha reductase.This postural caution when
results in inhibition of the conversion hypotension, edema, exercising.
of testosterone to dihydrotestosterone gynecomastia
and markedly suppresses serum
dihydrotestosterone levels

Table IV-31 ORAL CONTRACEPTIVES

There are a variety of formulations used for contraception, including injection, transdermal and intravaginal options. Oral
contraceptives typically combine an estrogen and a progestin.There are some progestin only contraceptives, including
oral pills and injections. For the purposes of this Appendix, numerous contraceptive formulations are not listed. PTs are
advised to recognize the active ingredients of the particular contraceptive preparation and refer to the table below for
drug information.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Estrogens: prevent Ethinyl estrogen (various), Nausea, vomiting, Most patients tolerate oral
development of mestranol (various) breakthrough bleeding, contraceptives well. PTs
dominant follicle by spotting, breast tenderness, should be monitoring for
suppression of FSH; do weight gain serious adverse effects.
not block ovulation Serious: venous thrombosis, Remember the mnemonic
pulmonary embolism, ACHES:
other thromboembolic abdominal pain,
disorders chest pain,
Progestins: block ovulation; Desogestrel, norgestrel, Depression, headache, headaches,
contributes to production levonorgestrel, irritability, acne eye problems,
of thick and impermeable ethynodiol diacetate, swelling and or aching in the
cervical mucus; norethindrone, legs and thighs
contributes to involution norethindrone acetate,
and atrophy of the norethynodrel (various)
endometrium
FSH, Follicle-stimulating hormone.
 Pharmacologic Agents APPENDIX IV 517

INFECTIOUS DISEASE

Table IV-32 ANTIBIOTICS

Indications:Treatment and prophylaxis of infections.

Mechanism Generic Name (Common

of Action Brand Name[s]) Adverse Effects PT Considerations
Aminoglycosides: Amikacin (Amikin), gentamicin Nephrotoxicity, Serum levels of aminoglycosides
inhibit bacterial (Garamycin), neomycin (Kantrex), ototoxicity require monitoring. High trough
protein synthesis streptomycin, tobramycin levels (at the end of the dosing
by binding to 30S (AKTob,TOBI,Tobrex) interval) are associated with renal
ribosomal subunit toxicity.Trough levels for
and inhibiting gentamicin and tobramycin should
bacterial RNA be < 2 mcg/ml. Monitor urine
synthesis output, serum creatinine for renal
function. Report any
changes in patient’s
hearing.
Carbapenems: Ertapenem (Invanz), imipenem- Nausea,vomiting, Monitor for GI side effects
inhibit cell wall cilastatin (Primaxin), meropenem diarrhea,leukopenia,
synthesis, thereby (Merrem) thrombocytopenia,
causing cell lysis seizures(imipenem-
and death cilastatinonly)
Cephalosporins: Firstgeneration:cefadroxil Allergic/ Monitor for rash, hives, swelling in
inhibit (Duricef),cefazolin(Ancef, hypersensitivity the face and neck for allergic
mucopeptide Kefzol),cephalexin(Keflex), reactions reactions. Ask patients about GI
synthesis in the cephapirin(Cefadryl),cephradine GI side effects with side effects to optimize the time of
bacterial cell wall, (Anspor) oral administration: therapy session. Monitor for
which leads to cell Second generation: cefaclor (Ceclor), nausea, vomiting, resolution of infection.
lysis and death cefonicid (Monocid), cefotetan diarrhea
(Cefotan), cefoxitin (Mefoxin), Serious: seizure,
cefprozil (Cefzil), cefuroxime nephrotoxicity
(Ceftin), loracarbef (Lorabid)
Third generation: cefixime (Suprax),
cefdinir (Omnicel), cefoperazone
(Cefobid), cefotaxime (Claforan),
cefpodoxime (Vantin),
ceftazidime (Fortaz), ceftibuten
(Cedax), ceftizoxime (Cefizox),
ceftriaxone (Rocephin)
Fourth generation: cefepime
(Maxipime)
Fluoroquinolones: Ciprofloxacin (Cipro), gatifloxacin Nausea, dyspepsia, Monitor blood sugar (may increase or
inhibit bacterial (Tequin), levofloxacin (Levaquin), headache, dizziness, decrease), especially in patients with
DNA lomefloxacin (Maxaquin), insomnia, diabetes. ECG should be checked for
topoisomerase and moxifloxacin (Avelox), ofloxacin hypoglycemia or QTprolongation, which predisposes
disrupts DNA (Floxin) hyperglycemia, patients to arrhythmias.Tendon
replication QT prolongation, rupture has been reported; avoid any
tendonitis, exercise that can increase that risk
photosensitivity, further. Use caution if utilizing UV
rash, urticaria light as part of therapy.
Continued
518 APPENDIX IV Pharmacologic Agents

Table IV-32 ANTIBIOTICS—cont’d

Mechanism Generic Name (Common
of Action Brand Name[s]) Adverse Effects PT Considerations
Macrolides and Macrolides: azithromycin GIupset:erythromycin Ask patients about GI side effects to
ketolides: bind to (Zithromax), clarithromycin canstimulateGI optimize the time of the therapy
50S RNA subunit, (Biaxin), erythromycin motilityandresultin session. Predisposes patients to
thereby inhibiting (Ery-tab, various) diarrhea; arrhythmias; monitor ECG for QT
RNA synthesis Ketolide: telithromycin (Ketek) clarithromycinhasthe prolongation.
leastGIsideeffects;
QTprolongation,
ototoxicity
Penicillins: bind to Natural penicillins: penicillin G Allergic/ Monitor for rash, hives, swelling in
penicillin-binding (Pfizerpen), penicillin G procaine hypersensitivity the face and neck for allergic
proteins and (Wycillin), penicillin G reactions in 3%-10% reactions. Ask patients about GI
inhibit cell wall benzathine (Bicillin LA), of patients side effects to optimize the time of
synthesis in the penicillinV (Pen-Vee K) GI side effects with therapy session. Monitor for
bacteria, causing Penicillinase-resistance penicillins: oral administration: resolution of infection
lysis and cell death oxacillin (Prostaphilin), Nafcillin nausea, vomiting,
(Nafcil, Unipen), Dicloxacillin diarrhea
(Dynapen, Dycill) Serious: seizure (rare),
Aminopenicillins: ampicillin hepatotoxicity
(Omnipen), amoxicillin (Amoxil, (oxacillin, nafcillin)
Trimox)
Carboxypenicillins: carbenicillin
(Geopen), ticarcillin (Ticar)
Ureidopenicillins: mezlocillin
(Mezlin), piperacillin (Pipracil)
Extended-spectrumpenicillinsplus
beta-lactamaseinhibitors:
amoxicillin-clavulanicacid
(Augmentin),ampicillin-sulbactam
(Unasyn),piperacillin-tazobactam
(Zosyn),ticarcillin-clavulanicacid
(Timentin)
Sulfonamides: Sulfadiazine, sulfamethizole Hypersensitivity Monitor for changes in skin
interfere with (Urobiotic), sulfamethoxazole/ reactions, appearance, utilize caution when
bacterial folic acid trimethoprim (Septra), dermatologic using UV light therapy
synthesis sulfisoxazole (Gantrisin) reactions: rash,
urticarial,
Stevens-Johnson
syndrome,
photosensitivity
Tetracyclines: inhibit Demeclocycline (Declomycin), Photosensitivity Use caution if using UV light therapy.
bacterial protein doxycycline (Vibramycin), reactions, Monitor for vestibular side effects
synthesis by minocycline (Minocin), hepatotoxicity, of minocycline therapy
binding to 30S tetracycline (Sumycin) diarrhea, nausea,
ribosomal subunit anorexia.
Minocycline use is
associated with
dizziness, ataxia,
vertigo, skin and
mucus membranes
pigmentation
 Pharmacologic Agents APPENDIX IV 519

Table IV-32 ANTIBIOTICS—cont’d

Mechanism Generic Name (Common
of Action Brand Name[s]) Adverse Effects PT Considerations
Miscellaneous
Inhibits 50S Clindamycin (Cleocin) Nausea, vomiting, Monitor for GI side effects. Diarrhea
subunit, thereby diarrhea, abdominal can be especially problematic with
inhibiting RNA pain, this drug, high incidence of C.
synthesis thrombophlebitis difficile colitis (do not recommend
over-the-counter antidiarrhea
medications)
Binds to Daptomycin (Cubicin) Diarrhea, nausea, CPK should be checked at baseline
components of vomiting, and monitored periodically
the cell membrane constipation,
of susceptible weakness,
organisms arthralgias, increase
and causes rapid in CPK
depolarization,
inhibiting
intracellular
synthesis of
DNA, RNA,
and protein
Binds to 23S Linezolid (Zyvox) Myelosuppression Monitor WBC (will decrease; use
ribosomal infection-control measures),
subunit of the hematocrit (will decrease; patient
50S RNA subunit, will complain of fatigue), and
which inhibits platelets (will decrease; patient will
bacterial be at a higher risk of bleeding)
translation
After diffusing Metronidazole (Flagyl) Nausea, vomiting, Monitor for GI adverse effects
into the organism, unusual/metallic
interacts with taste, dark urine,
DNA to cause a dizziness, headache
loss of helical
DNA structure
and strand
breakage resulting
in inhibition of
protein synthesis
and cell death in
susceptible
organisms
Quinupristin Quinupristin-dalfopristin Thrombophlebitis and Monitor bilirubin (will increase,
inhibits late-phase (Synercid) severe injection site patient’s skin and mucosal
protein synthesis; reactions, membranes will become more
dalfopristin hyperbilirubinemia, yellow, patient will complain of
inhibits arthralgias and itching). Arthralgias and myalgias
early-phase myalgias are common and can lead to drug
protein synthesis discontinuation
through binding
to 50S subunit
of bacterial RNA
Continued
520 APPENDIX IV Pharmacologic Agents

Table IV-32 ANTIBIOTICS—cont’d

Mechanism Generic Name (Common
of Action Brand Name[s]) Adverse Effects PT Considerations
Inhibits bacterial Vancomycin (Vancocin) Nephrotoxicity, Avoid scheduling sessions
cell wall synthesis; ototoxicity, immediately after vancomycin
may inhibit RNA thrombophlebitis, infusion due to possibility of
synthesis histamine-release ‘‘red-man syndrome.’’ Monitor
during or after urine output and serum creatinine
infusion (red-man for renal toxicity. Report any
syndrome): swelling changes in patient’s hearing
and redness in the
neck and face
CPK, Creatine phosphokinase; DNA, deoxyribonucleic acid; GI, gastrointestinal; RNA, ribonucleic acid;WBC, white blood cells.

Table IV-33 ANTIFUNGAL AGENTS

Indications:Treatment and prevention of fungal infections.

Generic Name (Common

Mechanism of Action
Binds to ergosterol in
the fungal cell wall,
leading to increased
permeability and cell
death
Azoles: inhibit fungal
cytochrome P450
14-alpha-demethylase,
thereby decreasing
ergosterol
concentrations
Inhibits synthesis of
b(1,3)-D-glucan, an
essential component
of the cell wall of
susceptible fungi.
LFTs, Liver function tests.
Brand Name[s])
Amphotericin B
(Fungizone),
amphotericin B lipid
complex (Abelcet),
amphotericin B
liposomal (AmBisome),
amphotericin B
cholesteryl sulfate
complex (Amphotec)
Fluconazole (Diflucan),
itraconazole (Sporanox),
ketoconazole (Nizoral),
voriconazole (Vfend)
Caspofungin (Cancidas)
Adverse Effects PT Considerations
Infusion reactions: fevers, Avoid scheduling PT
chills, hypotension, rigors, sessions immediately
pain, thrombophlebitis, after amphotericin
anaphylaxis infusion. Monitor
Nephrotoxicity (common and urine output and
dose-limiting); electrolyte serum creatinine for
disturbances: hypokalemia, renal toxicity; LFTs,
hypocalcemia, abdominal pain,
hypomagnesemia; anemia; yellow skin
increase LFTs and bilirubin appearance for hepatic
The incidence of renal and failure; electrolytes
infusion-related side effects (will decrease);
is lower with lipid hematocrit and
formulations hemoglobin (will
decrease)
Nausea, vomiting, abdominal Monitor for GI side
pain, diarrhea, increase in effects; abdominal
LFTs, rash, pruritus, pain, yellow skin
photosensitivity appearance for
(voriconazole only) hepatotoxicity
Increased LFTs, histamine- Avoid scheduling
release reactions, such as therapy sessions
rash, pruritus, anaphylaxis; immediately after
infusion reactions: fever, caspofungin infusion.
nausea, vomiting, myalgias Monitor for
hypersensitivity
reactions

Table IV-34 ANTITUBERCULAR AGENTS
Indications:Treatment and prevention of mycobacterial infections, including tuberculosis.
Mechanism of Action
Inhibits folic acid synthesis
Capreomycin is a cyclic
polypeptide antimicrobial.
Mechanism of action is
unknown.
Structurally similar to
d-alanine and inhibits
cell wall synthesis by
competing for
incorporation into the
bacterial cell wall
Inhibits bacterial cellular
metabolism
Inhibits peptide
synthesis
Unknown, but may include
the inhibition of myocolic
acid synthesis resulting in
disruption of the bacterial
cell wall
Converted to pyrazinoic acid Pyrazinamide (Tebrazid), Hepatotoxicity, gout
in susceptible strains of commonly abbreviated
Mycobacterium, which lowers as PZA
the pH of the
environment; exact
mechanism of action
unknown
Pharmacologic Agents APPENDIX IV 521
Generic Name (Common
Brand Name[s]) Adverse Effects PT Considerations
Aminosalicylic Nausea, vomiting, Monitor for GI side effects and
acid (Paser) abdominal pain, allergic reactions
diarrhea, hypersensitivity
reactions: fever,
joint pain, skin
eruptions
Capreomycin Nephrotoxicity and Monitor urine output and
(Capastat) ototoxicity in 30% serum creatinine. Report any
of patients; elevated changes in patient’s hearing
LFTs; hypersensitivity
reactions
Cycloserine Headache, vertigo, Assess CNS toxicity prior to
(Seromycin) confusion, psychosis, therapy
seizures
Ethambutol Optic neuritis with Report any changes in vision
(Myambutol) decrease visual
acuity, loss of red-
green color
discrimination
Ethionamide Hepatitis (rare) Monitor for hepatotoxicity
(Trecator) (abdominal pain, yellow
skin discoloration)
Isoniazid (Nydrazid), Peripheral neuropathy, Monitor for tingling and pain
commonly hepatotoxicity, in the extremities;
abbreviated as INH agranulocytosis, hepatotoxicity (abdominal
thrombocytopenia pain, yellow skin
discoloration); monitor
WBC (will decrease; use
infection-control measures),
hematocrit (will decrease;
patient will complain of
fatigue), and platelets (will
decrease; patient will be at
a higher risk of bleeding)
Monitor for hepatotoxicity
(abdominal pain, yellow skin
discoloration); monitor for
pain in joints (could indicate
gout)
Continued
522 APPENDIX IV Pharmacologic Agents

Table IV-34 ANTITUBERCULAR AGENTS—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Inhibits RNA synthesis Rifampin (Rifadin) Nausea, vomiting, diarrhea, Monitor for hepatotoxicity
abdominal pain, headache, (abdominal pain, yellow skin
dizziness, mental discoloration); monitor WBC
confusion, hepatotoxicity, (will decrease; use infection-
thrombocytopenia, control measures),
leukopenia, renal hematocrit (will decrease;
insufficiency patient will complain of
fatigue), and platelets (will
decrease; patient will be at a
higher risk of bleeding);
urine output and serum
creatinine for renal
insufficiency
Combinations: rifampin + isoniazid (IsonaRif; Rifamate), rifampin + isoniazid + pyrazinamide (Rifater).
LFTs, Liver function tests; RNA, ribonucleic acid; WBC, white blood cells.

Table IV-35 ANTIRETROVIRAL MEDICATIONS

Indications:Treatment of HIV/AIDS.
Treatment options for HIV/AIDS have expanded dramatically over the past decade.There are currently 4 classes of
antiretroviral drugs. Highly active antiretroviral therapy (HAART) typically consists of 3 to 5 agents from different drug
classes. Newer combination drugs allow patients to decrease the number of pills taken per day. Antiretroviral therapy is
associated with much toxicity. Class common toxicities: All nucleoside reverse transcriptase inhibitors (NRTIs) can cause
nausea, vomiting, and hepatic steatosis with lactic acidosis. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) are
associated with rash and hepatotoxicity (rash to one agent in this class does not predict rash to another agent in this
class). Protease inhibitors (PIs) can cause lipodystrophy (syndrome characterized by hyperglycemia, hyperlipidemia, fat
redistribution, buffalo hump, and truncal obesity), nausea, vomiting, diarrhea, and hepatotoxicity. Each individual agent
within these classes has other side effects that are listed in the table below. Physical therapists should utilize Universal
Precautions (avoid direct contact with infected body fluids). Resistance to antiretrovirals can develop fast in the setting of
insufficient viral suppression. It is very important for patients to take all of their medications as prescribed or to hold all
of their antiretroviral medications (as opposed to only one or two) in case of intolerable side effects. All members of the
health care team should provide support for patients with HIV/AIDS and reinforce the importance of adherence to
medication regiments. Antiretroviral drugs have many drug-drug and drug-food interactions. Patients should be referred
to a pharmacist/physician if any over-the-counter medications or supplements are recommended.

Generic Name (Common

Mechanism of Action
NRTIs: nucleotide
analogs that compete
with nucleotides for
incorporation into
replicating DNA,
thereby aborting viral
replication process
Brand Name[s]) Adverse Effects PT Considerations
Abacavir (Ziagen) Hypersensitivity reactions (can PTs should monitor for symptoms
present as combination of the of hypersensitivity. Patient
following symptoms: fever, should be referred to the
rash, nausea, vomiting, prescriber at once if
diarrhea, abdominal pain, hypersensitivity is detected due
dyspnea, cough, pharyngitis, to the potential for serious
malaise, fatigue anaphylactic reactions if therapy
is not discontinued
 Pharmacologic Agents APPENDIX IV 523

Table IV-35 ANTIRETROVIRAL MEDICATIONS—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Didanosine (Videx EC, Peripheral neuropathy, This medication must be taken on
commonly pancreatitis, diarrhea, nausea an empty stomach. Ask patients
abbreviated as ddI) about diarrhea to optimize
scheduling therapy sessions.
Monitor abdominal pain for
pancreatitis and tingling and
numbness in the extremities for
peripheral neuropathy
Emtricitabine (Emtriva), Well tolerated
lamivudine (Epivir,
commonly
abbreviated as 3TC)
Stavudine (Zerit, Peripheral neuropathy, Monitor abdominal pain for
commonly pancreatitis, lipoatrophy, pancreatitis and tingling and
abbreviated as (D4T) hyperlipidemia, rapidly numbness in the extremities for
ascending progressive peripheral neuropathy
neuromuscular weakness
Tenofovir (Viread) Diarrhea, flatulence, renal Monitor urine output and serum
insufficiency, asthenia, creatinine for renal failure
headache
Zidovudine (Retrovir, Headache, hyperpigmentation Monitor WBC (will decrease) and
commonly of skin and nails, anemia, hematocrit (will decrease;
abbreviated as AZT) neutropenia, myopathy patient will report fatigue).
Report any muscle pain/
weakness not associated with
exercise
NNRTIs: inhibit Efavirenz (Sustiva) Drowsiness, dizziness, Assess CNS side effects when
reverse transcriptase, insomnia, abnormal scheduling PTsessions.
an enzyme involved dreaming, agitation, Afternoon may be a preferred
in viral replication hallucinations time, since patients take this
medication at bedtime and may
still complain of side effects in
the morning
Nevirapine Severe rash and Report any indication of rash,
(Viramune) hepatotoxicity abdominal pain, yellow skin
appearance
Protease inhibitors: Atazanavir (Reyataz) Hyperbilirubinemia, prolonged Report yellow skin/sclera
inhibit protease, an PR interval on ECG, appearance. Monitor HR and
enzyme involved in asymptomatic first-degree ECG
viral replication heart block; does not have a
negative effect on lipids
Darunavir (Prezista) Rash, abdominal pain,
constipation
Fosamprenavir (Lexiva), Rash, nausea, diarrhea
tipranavir (Aptivus)
Indinavir (Crixivan) Nephrolithiasis (kidney stones), Remind patients to consume at
hyperbilirubinemia least 48 ounces of fluid per day
to prevent kidney stones
Lopinavir/ritonavir GI intolerance, asthenia Ask patients about GI side effects
(Kaletra) to optimize the time of the
therapy session
Continued
524 APPENDIX IV Pharmacologic Agents

Table IV-35 ANTIRETROVIRAL MEDICATIONS—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Nelfinavir (Viracept) Diarrhea Ask patients about GI side effects
to optimize the time of the
therapy session
Ritonavir (Norvir) Severe GI intolerance, taste Ritonavir is commonly used in
disturbances, asthenia, small doses to boost
paresthesias pharmacokinetics of another PI
and is better tolerated in lower
doses
Saquinavir (Invirase) GI intolerance Ask patients about GI side effects
to optimize the time of the
therapy session
Fusion inhibitor: Enfuvirtide (Fuzeon) Injection site reactions occur Monitor injection site reactions for
Inhibits the fusion of in all patients: itching, signs and symptoms of infection
HIV-1 virus with CD4 swelling, redness, pain (warm, swollen). Report any
cells by blocking the or tenderness, signs and symptoms associated
conformational induration, nodules and with hypersensitivity
change in gp41 cysts; hypersensitivity
required for reactions: rash, fever,
membrane fusion and nausea, vomiting, chills,
entry into CD4 cells rigors, hypotension,
elevated LFTs
Combinations: Lamivudine + zidovudine (Combivir), lamivudine + abacavir (Epzicom), lamivudine + abacavir + zidovudine (Trizivir),
tenofovir + emtricitabine (Truvada), efavirenz + tenofovir + emtricitabine (Atripla).
AIDS, Acquired immunodeficiency syndrome; CNS, central nervous system; DNA, deoxyribonucleic acid; EC, enteric coated;
ECG, electrocardiogram; GI, gastrointestinal; HAART, highly active antiretroviral therapy; HIV, human immunodeficiency virus; HR, heart
rate; LFTs, liver function tests; NRTI, nucleoside reverse transcriptase inhibitor; NNRTI, non-nucleoside reverse transcriptase inhibitor;
PI, protease inhibitor.

Table IV-36 ANTIVIRAL MEDICATIONS

Indications:Treatment and prevention of viral illnesses.

Generic Name (Common

Mechanism of Action
Inhibit DNA synthesis
and viral replication
by competing with
deoxyguanosine
triphosphate for viral
DNA polymerase and
being incorporated
into viral DNA.
Brand Name[s])
Acyclovir (Zovirax),
famciclovir
(Famvir), ganciclovir
(Cytovene,Vitrasert),
penciclovir (Denavir),
valganciclovir (Valcyte;
rapidly converts into
ganciclovir in the body)
Adverse Effects
Malaise, headache, nausea,
vomiting; topical
administration can produce
local redness and irritation;
acyclovir IVcan lead to
nephrotoxicity; ganciclovir
can cause neutropenia,
anemia,
thrombocytopenia.
PT Considerations
With IVacyclovir, monitor
urine output and serum
creatinine for renal
function; monitor blood
counts (will decrease)
 Pharmacologic Agents APPENDIX IV 525

Table IV-36 ANTIVIRAL MEDICATIONS—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Cidofovir diphosphate Cidofovir (Vistide) Chills, fever, pain, nausea, This drug is administered
suppresses CMV vomiting, diarrhea, every other week. Ask
replication by selective anemia, neutropenia, patients about toxicity
inhibition of viral weakness, renal failure to optimally schedule
DNA synthesis. therapy. Monitor urine
Incorporation of output and serum
cidofovir into growing creatinine for renal
viral DNA chain function. Monitor
results in reductions in WBC (will decrease)
the rate of viral DNA and hematocrit (will
synthesis. decrease, patient will
report fatigue).
Noncompetitive Foscarnet (Foscavir) Fever, headache, Monitor temperature (will
inhibitor of many hypokalemia, increase), electrolytes
viral RNA and DNA hypocalcemia, (will decrease), blood
polymerases as well as hypomagnesemia, counts (will decrease)
HIVreverse hypophosphatemia,
transcriptase nausea, diarrhea,
vomiting, anemia,
granulocytopenia, renal
toxicity
Inhibits influenza virus Oseltamivir (Tamiflu), Nausea, vomiting, abdominal Monitor for CNS toxicity
neuraminidase, with zanamivir (Relenza) pain, neuropsychiatric
the possibility of events (self-injury,
alteration of virus confusion, delirium)
particle aggregation
and release.
Inhibits replication of Ribavirin (Copegus; Fatigue, headache, This medication is very
RNA and DNA Rebetol) insomnia, nausea, toxic with high incidence
viruses; inhibits anorexia, anemia, fever, of side effects. Careful
influenza virus RNA depression, irritability, determination of
polymerase activity dizziness, alopecia, readiness for physical
and inhibits the pruritus, neutropenia, therapy should be
initiation and anemia, performed
elongation of RNA thrombocytopenia,
fragments resulting in myalgia, arthralgias,
inhibition of viral muscle pain, cough,
protein synthesis dyspnea, flulike
syndrome
CMV, cytomegalovirus; CNS, central nervous system; DNA, deoxyribonucleic acid; HIV, human immunodeficiency virus; IV, intravenous;
RNA, ribonucleic acid.
526 APPENDIX IV Pharmacologic Agents

muscle glucose uptake and inhibiting hepatic glucose

ENDOCRINE SYSTEM
Diabetes
PTs should be familiar with signs and symptoms of
hyperglycemia (polyuria, polydipsia, polyphagia, fati-
gue), hypoglycemia (shakiness, dizziness, sweating,
hunger, headache, pale skin color, sudden moodiness
or behavior changes, clumsy or jerky movements, sei-
zure, difficulty paying attention, confusion, tingling
sensations around the mouth), and ketoacidosis (short-
ness of breath, breath that smells fruity, nausea and
vomiting, very dry mouth, coma). Due to the effect of
exercise on blood glucose, physical therapists must pay
special attention to patients with diabetes.
Well-controlled insulin-treated diabetic patients
with adequate serum insulin concentrations will usually
have an exercise-induced fall in blood glucose concen-
trations that is much larger than that in normal subjects.
Several factors contribute to this response: (1) exoge-
nous insulin cannot be shut off, thereby maintaining
output; and (2) increased temperature and blood flow
associated with exercise may speed insulin absorption
from subcutaneous depots (storage/collection sites
where a drug remains before its release into the
bloodstream).
In contrast, exercise can cause a paradoxical eleva-
tion in blood glucose concentrations in diabetic
patients with poor metabolic control (blood glucose
concentration above 250 mg/dl, hypoinsulinemia, and
some ketonuria). In these patients, the lack of insulin
impairs glucose uptake by muscles and cannot prevent
an increase in hepatic glucose output that is medi-
ated by counterregulatory hormones. Blood glucose
should be managed before, during, and after exercise.
If the blood sugar (BS) is > 250 mg/dl, exercise
should be delayed until better control is achieved.
Alternatively, if the BS is close to or lower than
100 mg/dl, a carbohydrate snack should be consumed
before the exercise begins. Make sure that patients are
wearing proper footwear to reduce the chance of skin
ulcer formation.

Table IV-37 HYPOGLYCEMIC AGENTS

Indications:Treatment of hyperglycemia in patients with diabetes mellitus or drug-induced hyperglycemia

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Alpha-glucosidase Acarbose (Precose), Abdominal pain, diarrhea, GI side effects may interfere with PT
inhibitors: inhibit miglitol (Glyset) flatulence session; has an advantage of
pancreatic a-amylase and decreasing postprandial blood
intestinal brush border sugars; should be taken with each
alpha-glucosidases, meal (skip a meal, skip a dose). Do
resulting in delayed not cause hypoglycemia if used as
hydrolysis of ingested monotherapy (i.e., the only agent
complex carbohydrates used). Use only simple sugars (i.e.,
and disaccharides and glucose tabs) to treat hypoglycemic
absorption of glucose episodes, because these drugs delay
the breakdown of complex
carbohydrates
Amylin analog: Synthetic Pramlintide (Symlin) Nausea (50% of patients), Administered subcutaneously with
analog of human amylin hypoglycemia (in meals; can be used inType 1 and
co-secreted with insulin combination with Type 2 diabetes as adjunct therapy
by pancreatic beta cells; insulin) with insulin. Can cause weight
prolongs gastric loss
emptying time, reduces
postprandial glucagon
secretion, and reduces
caloric intake through
centrally-mediated
appetite suppression

Table IV-37 HYPOGLYCEMIC AGENTS—cont’d
Mechanism of Action
Biguanides: Decreases
hepatic glucose
production, decreasing
intestinal absorption of
glucose and improves
insulin sensitivity
(increases peripheral
glucose uptake and
utilization)
DPP-IV inhibitors: Inhibit
dipeptidyl peptidase
IV (DPP-IV) enzyme
resulting in prolonged
active incretin levels.
Incretin hormones
(e.g., glucagon-like
peptide-1 [GLP-1] and
glucose-dependent
insulinotropic polypeptide
[GIP]) regulate glucose
homeostasis by increasing
insulin synthesis and
release from pancreatic
beta cells and decreasing
glucagon secretion from
pancreatic alpha cells.
Incretin mimetic (GLP-1
analogs): An analog of
the hormone incretin
(glucagon-like peptide 1
or GLP-1) which
increases insulin
secretion, increases B-cell
growth/replication,
slows gastric emptying,
and may decrease food
intake
Insulin: Insulin acts via
specific membrane-
bound receptors on
target tissues to regulate
metabolism of
carbohydrate, protein,
and fats. Normally
secreted by the pancreas,
insulin products are
manufactured for
Pharmacologic Agents APPENDIX IV 527
Generic Name (Common
Brand Name[s]) Adverse Effects PT Considerations
Metformin Nausea, vomiting, No hypoglycemia and possible
(Glucophage) diarrhea, flatulence, weight loss are advantages of this
lactic acidosis agent; GI side effects may
interfere with PTsession; lactic
acidosis is rare, but fatal in 50%
of cases; risk factors for lactic
acidosis include age > 80,
reduced renal function,
liver disease, ischemic/acidotic
states, use of contrast dye for
imaging (hold metformin for at
least 48 hours postprocedure)
Sitagliptin Infrequent: headache, Oral therapy forType 2 DM; does
(Januvia) diarrhea not cause hypoglycemia when
used as monotherapy (i.e., the
only agent used)
Exenatide (Byetta) Hypoglycemia (when Administered subcutaneously with
combined with morning and evening meals to
sulfonylurea), nausea Type 2 DM patients; can cause
(45%) weight loss
Ultra-rapid acting: Aspart Atrophy or hypertrophy of Be aware of the time of onset and
(Novolin), glulisine subcutaneous fat tissue; peak effect, and duration to peak
(Apidra), insulin hypoglycemia, weight effect in order to determine when
inhalation (Exubera), gain; respiratory the hypoglycemia and
lispro (Humalog) infection, cough, hyperglycemia are most likely to
Rapid acting: Regular pharyngitis (with occur. Rapid-acting insulins:
(Humulin R, insulin inhalation; onset within 30 minutes, peak 1-2
Novolin R) contraindicated in hours, duration 3-5 hours.
smokers and patients Regular: onset 30 minutes, peak
with respiratory disease) 2-4 hours, duration 6-8 hours.
Continued
528 APPENDIX IV Pharmacologic Agents

Table IV-37 HYPOGLYCEMIC AGENTS—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Insulinçcont’d
pharmacologic use Intermediate: NPH NPH: onset 1-2 hours, peak 6-12
through recombinant (Humulin N, hours, duration 18-24 hours.
DNA technology and are Novolin N) Detemir: onset 3-4 hours,
categorized based on Intermediate to duration (dose-dependent): 6-23
promptness and duration long-acting: detemir hours. Glargine: onset 3-4 hours,
of effect. (Levemir) no peak, duration 24 hours
Long-acting: glargine
(Lantus)
Meglitinides (non- Nateglinide (Starlix), Hypoglycemia, weight These agents are short-acting and
sulfonylurea repaglinide (Prandin) gain are advantageous in controlling
secretagogues): stimulates postprandial blood glucose.They
insulin release from the should be taken with meals (skip a
pancreatic beta cells meal, skip the dose).
Sulfonylureas: Stimulates Glimeperide (Amaryl), Hypoglycemia, weight Monitor for hypoglycemia; design
insulin release from the glipizide (Glucotrol), gain, photosensitivity an exercise regimen to minimize
pancreatic beta cells; glyburide (Micronase, weight gain; use caution when
reduces glucose output Diabeta, Glynase) using ultraviolet light for therapy
from the liver; insulin
sensitivity is increased at
peripheral target sites
Thiazolidinediones: lower Pioglitazone (Actos), Edema, heart failure, These drugs do not cause
blood glucose by rosiglitazone (Avandia) weight gain; low risk hypoglycemia when used as
improving target cell of hepatotoxicityç monotherapy, however, when
response to insulin, requires periodic added to existing insulin therapy,
without increasing monitoring of LFTs the risk of hypoglycemia is very
pancreatic insulin high.These agents also have
secretion. It has a positive effects on lipid. Due to
mechanism of action that edema and heart failure risk, they
is dependent on the should be avoided in patients
presence of insulin for with NYHA class III and IV
activity. Agonists for heart failure
peroxisome proliferator-
activated receptor-gamma
(PPARgamma), which
influences the production
of a number of gene
products involved in
glucose and lipid
metabolism
BS, Blood sugar; DNA, deoxyribonucleic acid; GLP-1, glucagon-like peptide 1; LFTs, liver function tests.
Oral combinations: glimeperide + pioglitazone (Duetact), glimeperide + rosiglitazone (Avandaryl), glipizide + metformin (Metaglip),
glyburide + metformin (Glucovance), metformin + rosiglitazone (Avandamet), pioglitazone + sitagliptin (Janumet).
Combination insulin products are designed to decrease the number of injections and necessity to mix rapid-acting and long-acting insulins.
The disadvantage of mixed insulin products is that it is more difficult to titrate the dose for tight glycemic control: insulin aspart
suspension + insulin aspart (Novolog mix 70/30), regular + NPH (Novolin 70/30, Humulin 70/30), lispro suspension + lispro (Humalog mix
75/25 or 50/50).
 Pharmacologic Agents APPENDIX IV 529

Table IV-38 TREATMENT OF HYPERPARATHYROIDISM

Indications: Decrease parathyroid hormone and prevent complications associated with hyperparathyroidism.

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects PT Considerations
Calcimimetic: binds with the Cinacalcet (Sensipar) Hypocalcemia, nausea, Monitor calcium
calcium-sensing receptor on the vomiting, diarrhea, (will decrease);
parathyroid gland and increases myalgias myalgias, GI side
sensitivity of the receptor to effects
extracellular calcium, thereby
decreasing the stimulus for
PTH secretion
Vitamin D and analogs: vitamin D Calcitriol (Calcijex, Hypercalcemia, Monitor calcium
promotes absorption of calcium Rocatrol), doxecalciferol hyperphosphatemia, (will increase),
in the intestines and retention at (Hectorol), adynamic bone disease phosphate (will
the kidneys thereby increasing ergocalciferol (Drisdol, increase), PTH
calcium levels in the serum; Calciferol), paricalcitol (should decrease)
decreases excessive serum (Zemplar)
phosphatase levels, parathyroid
hormone levels; decreases bone
resorption; increases renal
tubule phosphate resorption
PTH, parathyroid hormone

Table IV-39 TREATMENT OF THYROID DISORDERS

Indications:Treatment of hypothyroidism and hyperthyroidism.

Generic Name (Common

Mechanism of Action
Hyperthyroidism
Inhibit synthesis of thyroid
hormones by preventing the
incorporation of iodine into
iodotyrosines and by
inhibiting the coupling of
monoiodotyrosine and
diiodotyrosine to form
thyroxine (T4) and
triiodothyronine (T3); PTU
also inhibits peripheral
conversion of T4 toT3
Iodides: block hormone
release, inhibit thyroid
hormone synthesis
Brand Name[s]) Adverse Effects PT Considerations
Methimazole (Tapazole), Fever, headache, paresthesias, Monitor for
propylthiouracil rash, arthralgia, urticaria, improvement of signs
(commonly abbreviated jaundice, hepatitis, and symptoms of
as PTU) agranulocytosis, leukopenia, hyperparathyroidism;
bleeding monitor blood counts
(will decrease, patient
will complain of fever,
malaise, sore throat)
Strong iodide solution Rash, swelling of salivary glands, Monitor for
(Lugol’s solution), metallic taste, burning of the improvement of signs
saturated solution of mouth, GI distress, and symptoms of
potassium iodide hypersensitivity, goiter hyperparathyroidism
(SSKI)
Continued
530 APPENDIX IV Pharmacologic Agents

Table IV-39 TREATMENT OF THYROID DISORDERS—cont’d

Mechanism of Action
Hypothyroidism
Thyroid hormones: enhance
oxygen consumption by
most tissues and increase
basal metabolic rate and
metabolism of
carbohydrates, lipids,
and proteins
Generic Name (Common
Brand Name[s]) Adverse Effects PT Considerations
Desiccated thyroid Tachycardia, arrhythmia, angina, Mostly well tolerated as
(ArmourThyroid, MI, tremor, headache, long as patient
Nature-Throid), nervousness, insomnia, maintains normal
levothyroxine hyperactivity, diarrhea, nausea, thyroid state.
(Levothroid, Levoxyl, vomiting, cramps, weight loss, Dose that is too high
Synthroid,Thyro-Tabs, fatigue, menstrual will produce signs
Unithroid), irregularities, excessive and symptoms of
liothyronine (Cytomel, sweating, heat intolerance, hyperthyroidism.
Triostat), liotrix fever, muscle weakness,
(Thyrolar) decreased bone mineral
density

References
1. Ciccone CD. Pharmacology in Rehabilitation (4th ed). 2. Lacy CF. Drug Information Handbook (15th ed).
Philadelphia: FA Davis, 2007. Hudson, OH: Lexi-Comp, 2007.
 Anesthesia:
Perioperative and
Appendix V Postoperative Considerations
Michele P. West
The physical therapist should have a general under-
standing of the types of anesthesia and the impact that
anesthesia can have on a patient in the perioperative
phase.This includes an understanding of the intraoper-
ative effects, postoperative recovery phases, and poten-
tial complications of anesthesia. Insight of these
factors allows the physical therapist to intervene as
safely as possible, prioritize the plan of care, modify
interventions and treatment parameters, and more
accurately predict length of stay, discharge disposition,
and physical therapy goals.
TYPES OF ANESTHESIA
There are two types of anesthesia: general and regional.
General anesthesia is a reversible state of unconscious-
ness consisting of four components (amnesia, analgesia,
inhibition of noxious reflexes, and skeletal muscle
relaxation) and is achieved by the use of intravenous
and inhalation anesthetics, analgesics, and muscle relax-
ants.1 Regional anesthesia is used for site-specific surgi-
cal procedures of the upper or lower extremity or
lower abdomen and is achieved by spinal (subarach-
noid), epidural (thoracic or lumbar), or peripheral
nerve blocks.1
The administration of anesthesia to a patient for a
brief diagnostic or surgical procedure has transitioned
from the operating room (OR) to other inpatient and
outpatient settings.2 Procedural sedation (formerly con-
scious sedation) is characterized by the patient’s ability
to maintain a patent airway without intervention, spon-
taneously ventilate, maintain cardiovascular function,
and respond purposely to verbal or tactile
stimulation.1,2
INTRAOPERATIVE EFFECTS OF
ANESTHESIA
The major intraoperative effects of general anesthesia
include the following3:
A. Neurologic effects. Decreased cortical and
autonomic function.
B. Metabolic effects. Hypothermia or malignant
hyperthermia (in patients with a genetic
predisposition).
C. Cardiovascular effects. The potential for arrhyth-
mia, hypotension, hypertension, decreased myocar-
dial contractility, and decreased peripheral vascular
resistance.4
D. Respiratory effects5,6
1. Anesthesia has multiple effects on the lung,
including decreased or altered:
a. Arterial oxygenation
b. Response to hypercarbia or hypoxia
c. Vasomotor tone and airway reflex
d. Respiratory pattern
e. Minute ventilation
f. Functional residual capacity
2. The shape and motion of the chest are altered sec-
ondary to decreased muscle tone, which causes
the following7:
a. Decreased anteroposterior diameter
b. Increased lateral diameter
c. Increased cephalad position of the diaphragm
3. Other factors that affect respiratory function and
increase the risk of postoperative pulmonary
complications (e.g., atelectasis, pneumonia, lung
collapse) include the following:
a. Underlying pulmonary disease
b. Incisional pain, especially if there is a thoracic
or abdominal incision
531
532 APPENDIX V Anesthesia: Perioperative and Postoperative Considerations

c. Smoking history further medical-surgical management and treatment

d. Obesity parameters. The most common postoperative compli-
e. Increased age cations include the following8-10:
f. The need for large intravenous fluid adminis- A. Neurologic complications
tration intraoperatively 1. Delayed arousal, altered consciousness, agitation,
g. Prolonged operative time or delirium
2. Cerebral edema, seizure, or stroke
3. Peripheral muscle weakness or altered sensation
THE IMMEDIATE POSTOPERATIVE PHASE B. Cardiovascular and hematologic complications
1. Hypotension, cardiogenic shock, or both
In the immediate postoperative phase, the patient 2. Hypertension
is transported from the OR to a postanesthesia care 3. Dysrhythmia
unit (PACU) (after general anesthesia) or to an ambula- 4. Myocardial ischemia and/or infarction
tory surgery recovery room (after regional anesthesia); 5. Hemorrhage
both are located near the operating room for continu- 6. Deep vein thrombosis
ous nursing care. The recovery period after surgery is 7. Pulmonary embolism
characterized as a time of physiologic alteration as a C. Respiratory complications
result of the operative procedure and the effects of 1. Airway obstruction
anesthesia.7 During this initial postoperative phase, 2. Hypoxemia or hypercapnia
the priorities of care are to assess emergence from 3. Atelectasis, pneumonia, or both
anesthesia, the status of the surgical site, to determine 4. Aspiration of gastric contents
the patient’s physiologic status and vital sign trends, 5. Hypoventilation
and to identify actual or potential postsurgical 6. Pulmonary edema, acute lung injury, ARDS
problems.8 D. Renal complications
Discharge from the PACU is often now dependent 1. Acute renal failure (ARF)
upon clinical criteria rather than time-based criteria. 2. Urine retention
Score-based discharge criteria systems such as the 3. Urinary infection
Modified Aldrete Score or the Postanesthesia Dis- E. Gastrointestinal complications
charge Scoring System are commonly used to deter- 1. Nausea and vomiting
mine when a patient has adequately recovered from 2. Hiccups
anesthesia.9 Components of both these scales include 3. Abdominal distention
activity, respiration, circulation, consciousness, and 4. Paralytic ileus or obstruction
oxygen saturation, with the Postanesthesia Discharge F. Integumentary complications
Scoring System further evaluating pain, nausea/vomit- 1. Wound infection
ing, and surgical bleeding.9 2. Wound dehiscence, evisceration, or both
The criteria for discharge from the ambulatory 3. Hematoma or seroma
recovery room are similar to that of the PACU and G. Other complications
include recovery from sedation or nerve block. 1. Fever
2. Sepsis
3. Hyperglycemia
POSTSURGICAL COMPLICATIONS 4. Fluid overload or deficit
5. Electrolyte imbalance
During the days to weeks of the postsurgical phase, the 6. Acid-base disorders
patient is monitored for the proper function and
return of all of the major body systems. The prompt
prevention and recognition of potential or actual post- CLINICAL TIP
surgical complications is the cornerstone of high-  A review of the anesthesia and surgical notes can
quality care by all health care providers, including provide information about the patient’s surgical
physical therapists. The development of postsurgical procedure(s) and findings, hemodynamic and general
complication(s) in the immediate or secondary phase surgical status, unexpected anesthetic effects,
may be expected or unexpected and determines
Continued
A

FIGURE V-1
A, Supine position. Patient is placed on back with arms at sides or extended to 90 degrees and head in
alignment with body. Legs are uncrossed, with a safety strap placed above knees. B, Prone position.
Patient is usually anesthetized while supine, and then turned. Arms are placed at sides, with rolls beneath
axilla to facilitate respiration. C, Jackknife position. Patient is usually anesthetized while supine, and then
turned. Knees are flexed slightly to reduce lumbosacral stress. D, Lithotomy position. Patient is on back,
and foot section of operating table is removed or lowered to 90-degree angle. Buttocks are moved to
table’s edge. Feet are suspended in straps to flex knees. Legs are placed into or removed from the stirrups
simultaneously to avoid hip injuries. (From Ballweg R. Physician Assistant: A Guide to Clinical Practice
[3rd ed]. Saunders: Philadelphia, 2003.)
534 APPENDIX V Anesthesia: Perioperative and Postoperative Considerations
operative time, position during surgery, vital signs,
electrocardiographic changes, and degree of blood
loss.
OPERATIVE POSITIONING
Occasionally, a patient may experience postoperative
pressure-induced nerve or skin damage as a result of
operative positioning, especially during a lengthy pro-
cedure. The physiologic effects of anesthesia such as
hypothermia, hypotension, and pharmacologically
blocked pain and pressure receptors make a patient vul-
nerable to pressure injuries.11 When combined with
References
1. Sherwood E,Williams CG, Prough DS. Anesthesiology
Principles, Pain Management, and Conscious Sedation.
In CM Townsend, et al. (eds): SabistonTextbook of
Surgery (17th ed). Philadelphia: Saunders, 2004;297-330.
2. O’DonnellJM, Bragg K, and Sell S. Procedural
Sedation: Safely Navigating theTwilight Zone. Nursing
2003;33(4):36-41, 44-45.
3. Wadlund DL. Prevention, Recognition, and Management
of Nursing Complications in the Intraoperative and
Postoperative Surgical Patient. Nurs Clin N Am
2006;41:151-171.
4. Wilson RS. Anesthesia forThoracic Surgery. In AE Baue,
AS Geha, GL Hammond, et al. (eds), Glenn’sThoracic
and Cardiovascular Surgery (96th ed). Stamford, CT:
Appleton & Lange, 1996;23.
5. Conrad SA, Jayr C, Peper EA.ThoracicTrauma, Surgery,
and Perioperative Management. In DB George,
RW Light, MA Matthay, et al. (eds), Chest Medicine:
Essentials of Pulmonary and Critical Care Medicine
(3rd ed). Baltimore: Williams & Wilkins, 1995;629.
risk factors such as advanced age; poor skin integrity;
altered nutrition; diabetes; peripheral vascular disease;
or the presence of cancer, neurologic, or cardiac dis-
ease, the incidence of pressure injury increases.11
Judicious proper operative positioning with pads,
limb holders, and drawsheets can prevent or minimize
these injuries.
Standard operative positions include supine (dorsal
decubitus), prone (ventral decubitus, low or full jack-
knife), side-lying (left or right lateral decubitus, jack-
knife, or flexed lateral), seated, lithotomy (standard,
low, or exaggerated) (FigureV-1).11
The physical therapist may be consulted in the post-
operative phase to evaluate for extremity weakness
related to neuropathy from stretch, compression, ische-
mia, metabolic derangement, and/or surgical injury11
or for back or joint pain related to joint stiffness from
immobility or connective tissue injury.
6. Wilson WC, Benumof JL. Respiratory Physiology and
Respiratory Function during Anesthesia. In RD Miller
(ed), Anesthesia,Vol. 1 (6th ed). Philadelphia: Churchill
Livingstone, 2005;705-715.
7. Litwack K. Immediate Postoperative Care: A Problem-
Oriented Approach. In JS Vender, BD Spiess (eds),
Post-Anesthesia Care. Philadelphia: Saunders, 1992;1.
8. Litwack K. Postoperative Patient. In SM Lewis, MM
Heitkemper, SR Dirksen (eds), Surgical Nursing:
Assessment and Management of Clinical Problems.
St. Louis: Mosby, 2000;390-399.
9. FeeleyTW, Macario A.The Postanesthesia Care Unit.
In RD Miller (ed), AnesthesiaVol. 2 (6th ed).
Philadelphia: Churchill Livingstone, 2005;2708.
10. Dayton MT. Surgical Complications. In CM Townsend,
et al. (eds): SabistonTextbook of Surgery (17th ed).
Philadelphia: Saunders, 2004;4201-4421.
11. O’Connell MP. Positioning Impact on the Surgical
Patient. Nurs Clin N Am 2006;41:173-192.
 Appendix VI Pain Management
Jaime C. Paz
In the acute care setting, physical therapists encounter
patients who are experiencing pain for a variety of rea-
sons, most commonly from surgical intervention. This
appendix provides information on tools to evaluate
and manage pain that can facilitate the therapist’s ability
to provide care for a patient.
EVALUATION
The subjective complaint of pain is often difficult to
objectify in the clinical setting. However, an effective
pain treatment plan depends on an accurate evaluation
of the patient’s pain.1,2 Each evaluation requires a com-
plete physical and diagnostic examination of the
patient’s pain. The goal for evaluation should be
toward individualization while maintaining consis-
tency among patients. To assist with this process, vari-
ous pain-rating tools have been developed. Tables VI-1
and VI-2 describe some of the pain-rating tools that
are used in the acute care setting, with the visual ana-
logue and numeric rating scales being the most com-
monly used.1,3,4
CLINICAL TIP
 The validity of these scales may be improved
by asking the patient about his or her current
level of pain, rather than asking the patient
to speculate about ‘‘usual’’ or ‘‘previous’’ levels
of pain.5
 The patient’s self-reporting of pain is the most
accurate indicator of the existence or intensity of his
or her pain, or both.10
 Be sensitive to and respectful of how different
cultures perceive pain, as certain cultures may be
very stoic about their pain, whereas others are very
demonstrative.
Physical Therapy Considerations for Pain
Evaluation
 In consideration of Joint Commission requirements,
each patient interaction needs a pain rating, even if
the patient reports 0/10 on the NRS.
 A pain grade is generally accompanied by location,
description, and most importantly, an ‘‘intervention’’
especially if pain is graded >4/10 on the NRS.
 Be aware of the nonverbal indicators of pain, such as
behavior changes, facial expressions, and body lan-
guage, in patients with an impaired ability to com-
municate pain, as with an unconscious patient or an
adult with dementia.
 Monitoring vital signs during the pain evalua-
tion may provide insight into the sympathetic
tone of the patient, which can be indicative
of their level of pain. This can be performed easily
in the intensive care setting, because the patient’s
hemodynamic status is being continuously
monitored.
 The physical therapist should recognize when the
patient is weaning from pain medication (e.g., transi-
tioning from intravenous to oral administration), as
the patient may complain of increased pain with a
concurrent reduced activity tolerance during this
time period.
 To optimize consistency in the health care team, the
physical therapist should use the same pain rating
tool as the medical-surgical team to determine ade-
quacy of pain management.
 Often the best way to communicate the adequacy of a
patient’s pain management to the nurses or physi-
cians is in terms of the patient’s ability to complete a
given task or activity (e.g., the patient is effectively
coughing and clearing secretions). Therapists
should communicate both verbally and in written
form to the medical team if the pain management is
insufficient to allow the patient to accomplish their
functional tasks.
535
536 APPENDIX VI Pain Management
Table VI-1 PAIN ASSESSMENT TOOLS
Tool Description
Verbal descriptor The patient describes pain by
scales choosing from a list of
adjectives representing
gradations of pain intensity.
Numeric rating The patient picks a number from
scale (NRS) 0 to 10 to rate his or her pain,
with 0 indicating no pain, and
10 indicating the worst pain
possible.
Visual analog scales
(VAS)
Line scale The patient marks his or her pain
intensity on a 10-cm line, with
one end labeled ‘‘no pain,’’and
the other end labeled ‘‘worst
pain possible.’’
Wong-Baker The patient chooses one of six
Faces scale faces, portrayed on a scale that
depicts graduated levels of
distress, to represent his or her
pain level.
Pain diary A daily log is kept by the patient
denoting pain severity, by using
the numeric rating scale, during
activities of daily living.
Medication and alcohol use (if out
of the hospital), along with
emotional responses, are also
helpful pieces of information
to record.
Data from KP Kittelberger, AA LeBel, D Borsook. Assessment of
Pain. In D Borsook, AA LeBel, B McPeek (eds),The Massachusetts
General Hospital Handbook of Pain Management. Boston: Little
Brown, 1996;27; Carey SJ,Turpin C, SmithJ, et al. Improving Pain
Management in an Acute Care Setting:The Crawford Long
Hospital of Emory University Experience. Orthop Nurs
1997;16(4):29;Wong, DL, Hockenberry-Eaton M,Wilson D, et al.:
Wong’s Essentials of Pediatric Nursing (6th ed). St. Louis: Mosby,
2001;1301.
MANAGEMENT
Nonsteroidal antiinflammatory drugs (NSAIDs) (Table
VI-3) and systemic opioids (Table VI-4) are the most
common pharmacologic agents prescribed for postop-
erative pain. Aspirin and acetaminophen (Tylenol) are
also common medications prescribed for pain relief
and are categorized as non-narcotic analgesic and
antipyretic drugs.11,12 A majority of NSAIDs are nonse-
lective cyclooxygenase inhibitors. Cyclooxygenase
(COX) is an enzyme that exists in two forms (COX-1
and COX-2) and leads to the production of prostaglan-
dins and thromboxane, which are substances that pro-
duce pain and inflammation. Prostaglandins are also
beneficial to the mucosal lining of the gastrointestinal
tract, therefore nonselective inhibition of these sub-
stances can result in GI dysfunction (refer to Chapter 8).
However, selective inhibition of COX-2 can result in
decreased injury to the mucosal lining of the stomach,
a discovery that led to the development of COX-2
selective agents. Unfortunately, these agents were also
shown to lead to an increased risk of heart attack or
stroke in susceptible individuals, resulting in agents
such as rofecoxib (Vioxx) and valdecoxib (Bextra) to be
discontinued. Currently celecoxib (Celebrex) is the only
COX-2 selective agent still available.13 Alternatives
to oral, intravenous, or intramuscular drug delivery
for pain are described in Tables VI-5 and VI-6.
Communication among therapists, nurses, physicians,
and patients on the effectiveness of pain management is
essential to maximize the patient’s comfort.This includes
a thorough review of the patient’s medical history and
the doctor’s orders by the physical therapist before
prescribing any modalities or therapeutic exercises.
CLINICAL TIP
 Aspirin and acetaminophen are often lumped under
the term ‘‘NSAID’’ because these agents are not
manufactured from steroid properties, however
aspirin and acetaminophen do not have the
antiinflammatory effects that NSAIDs possess.
Physical Therapy Considerations for Pain
Management
 The physical therapist should be aware of the
patient’s pain medication schedule and the duration
of the effectiveness of different pain medications
when scheduling treatment sessions. (Pharmacist,
nurse, physician, and medication reference books
are good resources.)
 Patients should be educated on the need to request
pain medicine or push their PCA button when
they need it, particularly when they are on an
‘‘as needed’’or PRN pain medication schedule.
 The physical therapist should also use a pillow, blan-
ket, or his or her hands to splint or support a painful
area, such as an abdominal or thoracic incision or
 Table VI-2 FLACC PAIN ASSESSMENT TOOL

Indication: For nonverbal patients, particularly the pediatric population

Categories Score = 0 Score = 1 Score = 2

Face No particular expression or smile Occasional grimace or frown, Frequent to constant frown,
withdrawn, disinterested clenched jaw, quivering chin
Legs Normal position or relaxed Uneasy, restless, tense Kicking, or legs drawn up
Activity Lying quietly, normal position, Squirming, shifting back/forth, Arched, rigid, or jerking
moves easily tense
Cry No cry (awake or asleep) Moans or whimpers, occasional Crying steadily, screams or
complaint sobs, frequent complaints
Consolability Content, relaxed Reassured by occasional Difficult to console or comfort
touching, hugging, or ‘‘talking
to,’’distractible
Source: Renee CB, Manworren RCB, et al. Clinical Validation of FLACC: Preverbal Patient Pain Scale. Pediatr Nurs 2003;29(2):140-146.

Table VI-3 NONSTEROIDAL ANTIINFLAMMATORY DRUGS

Indications
Mechanism of action
General side effects
Medications: Generic
name (trade name)
*Rarely used
Data from reference numbers 6-8, 12, 13.
 To decrease inflammation
 Used as the sole therapy for mild to moderate pain
 For patients with osteoarthritis, rheumatoid arthritis, and dysmenorrhea
 Used in combination with opioids for moderate postoperative pain, especially when weaning
from stronger medications
 Useful in children younger than 6 months of age
 Contraindicated in patients undergoing anticoagulation therapy, with peptic ulcer disease, or
with gastritis
 Accomplish analgesia by inhibiting prostaglandin synthesis, which leads to antiinflammatory
effects (Prostaglandin is a potent pain-producing chemical)
 A useful alternative or adjunct to opioid therapy
 Platelet dysfunction and gastritis, nausea, abdominal pain, anorexia, dizziness, and drowsiness
 Severe reactions include nephrotoxicity (dysuria, hematuria) and cholestatic hepatitis
 Celecoxib (Celebrex)
 Diclofenac potassium (Cataflam,Voltaren, Rapide)
 Diclofenac sodium (Apo-Dilo, Novo-Difenac,Voltaren,Voltaren-XR)
 Diflunisal (Dolobid)*
 Etodolac (Lodine)
 Fenoprofen (Nalfon)*
 Flurbiprofen (Ansaid)
 Ibuprofen (Motrin, Advil, Bayer Select Ibuprofen, Excedrin, Medipren, Menadol, Midol,
Nuprin, Pamprin, Pedia Profen)
 Indomethacin (Apo-Indomethacin, Indameth, Indocin, Indomethacin, Novomethacin,
Nu-Indo)
 Ketoprofen (Apo-Keto, Orudis, Oruvail, Rhodis)
 Ketorolac (Toradol)
 Nabumetone (Relafen)
 Naproxen (Anaprox, Naprosyn, Naxen, Novo-naprox, Nu-naprox)
 Naproxen sodium (Aleve)
 Oxaprozin (Daypro)
 Phenylbutazone (Cotylbutazone)
 Piroxicam (Apo-Piroxicam, Feldene, Novo-Pirocam)
 Sulindac (Apo-Sulin, Clinoril, Novo-Sundac, Sulindac)
 Tolmetin (Tolectin)
538 APPENDIX VI Pain Management

Table VI-4 SYSTEMIC OPIOIDS

Indication  Moderate to severe postoperative pain, can also be used preoperatively
Mechanism of action  Blocks transmission of pain from the spinal cord to the cerebrum by interacting with
opioid receptors
 Can be administered orally, intravenously, intramuscularly, subcutaneously, and
intrathecally
General side effects  Decreased gastrointestinal motility, nausea, vomiting, and cramps
 Mood changes and sedation
 Pruritus (itching)
 Urinary retention
 Respiratory and cough depression
 Pupillary constriction
Medications: Generic name  Alfentanil (Alfenta, Rapifen)*
(trade name)  Buprenorphine (Buprenex, Subutex)
 Butorphanol (Stadol)
 Codeine (Paveral)
 Fentanyl (Actiq, Fentanyl Oralet, Sublimaze)
 Fentanyl transdermal (Duragesic)
 Hydromorphone (Dilaudid, Hydrostat)
 Levorphanol (Levo-Dromoran)
 Meperidine (Demerol, Pethidine)
 Methadone (Dolophine, Methadose)
 Morphine (MS Contin, Roxanol, Anamorph, Astramorph, Morcap, Duramorph,
Epimorph, Infumorph, Oramorph, Rescudose, Statex, Kadian, Morphine sulfate,
Morphitec)
 Nalbuphine (Nubain)
 Naloxone (Narcan){
 Oxycodone (Oxycontin, Roxicodone, Supeudol, Endodan,Tylox, Percocet [oxycodone
with acetaminophen], Percodan [oxycodone with aspirin])
 Oxymorphone (Numorphan)
 Pentazocine (Talwin)
 Propoxyphene (Darvon, Dolene, Doloxene, Novopropoxyn)
 Remifentanil (Ultiva)
*Rarely used.
{
Opioid antagonist.
Data from reference numbers 6, 8, 9, 12.

rib fractures when the patient coughs or performs

functional mobility tasks, such as going from side-
lying to sitting at the edge of the bed.
 The physical therapist can also use a corset, binder, or
brace to support a painful area during intervention
sessions that focus on functional mobility.
 The physical therapist should instruct the patient not
to hold his or her breath during mobility, because
doing so increases pain.
CLINICAL TIP
 Patients, particularly those who are
postsurgical, are often prescribed more than
one type of pain medication in order to
achieve ‘‘breakthrough’’ pain levels. In order
words, they require additional medicine to
break their pain.
 Pain Management APPENDIX VI 539

Table VI-5 CENTRAL NEURAL BLOCKADE

Types  Epidural nerve blockadeçinjection of medications into the epidural space
 Spinal nerve blockage (intrathecal anesthesia)çinjection of medications within the
subarachnoid space
Indications  Obstetric procedures, including caesarean delivery
 Surgeries of the thorax or upper and lower abdomen, especially in patients with
significant pulmonary disease
 Surgery of the lower extremity, especially when early mobilization is important
 Vascular procedures of the lower extremity, when sympathetic blocks are used
Mechanism of action  Prevent transmission of pain signals to the cerebrum at the spinal level
 A mixture of opioids and local anesthetics is often used.This drug combination
provides a synergistic effect for pain relief with a decreased incidence of side effects.
 If patients do experience adverse side effects, nonsteroidal antiinflammatory drugs can
be added to the mixture, and the dosages of the opioids or local anesthetics are
reduced.
General side effects  Epidural opioids: Pruritus (itching), nausea, sedation and respiratory depression,
decreased gastrointestinal motility
 Local anesthetics: Hypotension, temporary lower-extremity weakness, urine retention,
local anesthetic toxicity (ringing in the ears, metallic taste, slow speech, irritability,
cardiac arrhythmias, and seizures)
Medications: Generic  Epidural opioids: Morphine, fentanyl, sufentanil, alfentanil, hydromorphone
(trade name) (Dilaudid), and meperidine (Demerol)
 Local anesthetics: Bupivacaine, chloroprocaine (Nesacaine), etidocaine (Duranest),
levobupivacaine, lidocaine (Xylocaine), mepivacaine (Carbocaine, Polocaine), procaine
(Novocain), tetracaine (Pontocaine)
 Nonsteroidal antiinflammatory drugs: Acetaminophen, ketorolac (Toradol), or
ibuprofen
Data from reference numbers 6, 13-15.
540 APPENDIX VI Pain Management

Table VI-6 PATIENT-CONTROLLED ANALGESIA

Indications For moderate to severe postoperative pain in patients who are capable of properly using
the pump
For patients with chronic pain, such as those with cancer or rheumatologic diseases
Considerations Pumps are either external or internal (implantable) depending on patient’s needs.
Preoperative education of the patient on the use of patient-controlled analgesia
Ensuring that only the patient doses himself or herself
Dosage, dosage intervals, maximum dosage per set time, and background (basal) infusion
rate can be programmed.
Side effects Similar to those of opioids (TableVI-3)
Medications: Generic (trade Morphine, Meperidine, tramadol, fentanyl and fentanyl derivatives (alfentanil,
name) remifentanil)

Types Mechanism of Action

Patient-controlled intravenous
analgesia (PCIA)
Patient-controlled epidural
analgesia (PCEA)
Patient-controlled transdermal
analgesia (PCTA)
Patient-controlled regional
analgesia (PCRA)
Data from reference numbers 6, 13, 16-19.
An intravenous line to a peripheral vein is connected to a microprocessor pump, and a
patient is provided a button to allow self-dosing.This setup is for short-term use,
generally postoperatively.
For long-term use, a catheter is implanted surgically into a large central vein with the tip
of this catheter being placed into the right atrium.The other end of the catheter is then
tunneled through the subcutaneous tissues and brought out through the patient’s skin
to allow PCA administration.
The tip of a small catheter is placed in either the epidural or the subarachnoid space and
connected to a pump.
For short-term use, the catheter exits through the back to connect to a pump.
For long-term use, the catheter is tunneled through the subcutaneous tissue and exits
through the front for patient control.
A credit card—sized patch is impregnated with opioid and adhered to a the patient’s skin
surface.
The patient self-doses by pushing a button directly on the patch
The catheter tip is inserted directly into a specific anatomical site such as a wound, near a
peripheral nerve or into a peripheral joint.
The other end of the catheter is attached to a pump with a button for patient control.

References
1. Kittelberger KP, LeBel AA, Borsook D. Assessment
of Pain. In D Borsook, AA LeBel, B McPeek (eds),
The Massachusetts General Hospital Handbook of
Pain Management. Boston: Little, Brown, 1996;26.
2. Cristoph SD. Pain Assessment:The Problem Of Pain
in the Critically Ill Patient. Crit Care Nurs Clin N Am
1991;3(1):11-16.
3. Carey SJ,Turpin C, SmithJ, et al. Improving Pain
Management in an Acute Care Setting:The Crawford
Long Hospital of Emory University Experience.
Orthop Nurs 1997;16(4):29.
4. Haggell P. Pain Management. J Neurosci Nurs
1999;31(4):251.
5. Turk DC, Okifuji A. Assessment of Patients’ Reporting
of Pain: An Integrated Perspective. Lancet
1999;353(9166):1784.
6. JC Ballantyne, D Borsook. Postoperative Pain.
In D Borsook, AA LeBel, B McPeek (eds),The
Massachusetts General Hospital Handbook of Pain
Management. Boston: Little, Brown, 1996;247, 249.
7. Nursing 2001 Drug Handbook (21st ed). Springhouse,
PA: Springhouse Corporation, 2001;346-367.
8. Skidmore-Roth L (ed). Mosby’s Nursing Drug Reference
(21st ed). St. Louis: Mosby, 2007.
9. Fields HL (ed). Pain. NewYork: McGraw-Hill, 1987;253.
Pain Management APPENDIX VI 541
10. Acello B. Meeting JCAHO Standards for Pain Control.
Nursing 2000;30(3):52-54.
11. Nursing 2001 Drug Handbook (21st ed). Springhouse,
PA: Springhouse Corporation, 2001;337-342.
12. Skidmore-Roth L (ed), Mosby’s Nursing Drug
Reference. St. Louis: Mosby, 2001;56-57, 70,135,924.
13. Ciccone CD: Pharmacology in Rehabilitation (4th ed).
Philadelphia: FA Davis, 2007;183-249.
14. Pasero C, McCaffery M. Providing Epidural Analgesia.
Nursing 1999;29(8):34.
15. Davis WM,Vinson MC. New Drug Approvals of 2000,
Part 2. DrugTopics 2001;145(5):89.
16. White CL, Pokrupa RP, Chan MH. An Evaluation of the
Effectiveness of Patient-Controlled Analgesia After
Spinal Surgery. J Neurosci Nurs 1998;30(4):225.
17. Hoare K, Sousa KH, Person L, et al. ComparingThree
Patient Controlled Analgesia Methods. Medsurg Nurs
2000;9(1):33.
18. Valentino L, Pillay KV,WalkerJ. Managing Chronic
Nonmalignant Pain with Continuous Intrathecal
Morphine. J Neurosci Nurs 1998;30(4):233.
19. York M, PaiceJA.Treatment of Low Back Pain with
Intraspinal Opioids Delivered via Implanted Pumps.
Orthop Nurs 1998;17(3):61.
This page intentionally left blank.
 Appendix VII Amputation
Jason D. Rand and Jaime C. Paz
This appendix describes the most common types of
lower-extremity and upper-extremity amputations.
The etiology of these amputations and the physical ther-
apy management that is pertinent to the acute care set-
ting are described. Although the incidence of upper-
extremity (UE) amputation is quite low compared to
lower-extremity (LE) amputation, it is important that
the acute care physical therapist have an understanding
of all types of amputations to properly plan for the
evaluation and treatment of the patient.
LOWER-EXTREMITY AMPUTATION
Peripheral vascular disease accounts for approximately
85% to 90% of LE amputations in the developed
world, with 25% to 50% of this percentage resulting
from diabetes mellitus.1-3 Refer to Chapter 11 for more
information on the complications of diabetes mellitus.
Trauma is the second highest cause of amputation in
developed countries and is the primary cause in devel-
oping parts of the world.1 Traumatic amputation often
results from environmental injury or land mines in var-
ious parts of the world.1 The various locations of LE
amputation are shown in FigureVII-1and are described
inTableVII-1.
UPPER-EXTREMITY AMPUTATION
UE amputation is most often the result of trauma, such
as automobile or industrial accidents.1,3 Disease and
congenital limb deficiency are also major causes of UE
amputation.4 Despite peripheral vascular disease being
a major cause of LE amputation, it often does not
create the need for UE amputation.1 The various loca-
tions of UE amputations are shown in Figure VII-2
and are described inTableVII-2.
PHYSICAL THERAPY INTERVENTION FOR
PATIENTS WITH AN AMPUTATION
The focus of physical therapy intervention in the acute
care setting is on preprosthetic evaluation and training.
Prosthetic training, if appropriate, most often occurs
in the subacute, outpatient, or home setting. The pri-
mary components of the evaluation for a patient who
is status post amputation in the acute care setting are
as follows5:
 The onset and type of amputation
 Premorbid lifestyle and functional mobility
 Current level of functional mobility
 Discharge plans
TableVII-3 outlines general physical therapy consid-
erations and treatment suggestions for the care of
patients who are status post new UE or LE amputa-
tions. Table VII-4 outlines specific clinical concerns
for these patients.
543
544 APPENDIX VII Amputation

Hemipelvectomy

Hip
disarticulation

Above-knee
(transfemoral)
amputation

Knee
disarticulation

Below-knee
(transtibial)
amputation

Syme’s
amputation

Transmetatarsal
amputation

Ray Toe
amputation amputation

FIGURE VII-1
Levels of amputation. Lower extremity. (From Cameron MH, Monroe LG: Physical Rehabilitation:
Evidence-Based Examination, Evaluation, and Intervention. St Louis: Saunders, 2007.)
 Amputation APPENDIX VII 545

Table VII-1 TYPES OF LOWER-EXTREMITY AMPUTATIONS*

Type Description
Ray Single or multiple rays can be amputated depending on the patient’s diagnosis.
If the first ray is amputated, balance is often affected, as weight is transferred to
the lateral border of the foot, which may also cause ulceration and skin
breakdown. Postoperative weight-bearing status will range from non—weight-
bearing to partial weight bearing status according to the physician’s orders.
Transmetatarsal The metatarsal bones are transected with this procedure as compared to other
types of partial foot amputations, which may disarticulate the metatarsals from
the cuboid and cuneiform bones. Balance is maintained with a transmetatarsal
amputation, because the residual limb is symmetric in shape and major muscles
remain intact. An adaptive shoe with a rocker-bottom is used to help facilitate
push-off in gait.
Syme’s amputation (ankle Often performed with traumatic and infectious cases, this type of amputation
disarticulation) is preferred to more distal, partial foot amputations (ray and transmetatarsal)
because of the ease of prosthetic management at this level.
Patients may ambulate with or without a prosthesis.
Below the knee (transtibial) Ideal site for amputation for patients with a variety of diagnoses. Increased
success rate with prosthetic use. In cases with vascular compromise, the
residual limb may be slow to heal. Residual limb length ranges from 12.5 cm
to 17.5 cm from the knee joint.
Through-the-knee (disarticulation) Often performed on elderly and young patients. Maximum prosthetic control can
be achieved with this procedure because of the ability to fully bear weight on
the residual limb. Also, a long muscular lever arm and intact hip musculature
contribute to great prosthetic mobility.The intact femoral condyles, however,
leave a cosmetically poor residual limb.
Above the knee (transfemoral) Traditional transfemoral amputation preserves 50%-66% of femoral length.
Prosthetic ambulation with an artificial knee joint requires increased metabolic
demand.
Hip disarticulation (femoral head Often performed in cases of trauma or malignancy.The pelvis remains intact;
from acetabulum) however, patients may experience slow wound healing and may require
secondary grafting to fully close the amputation site.
Hemipelvectomy (half of the pelvis Also indicated in cases of malignancy. A muscle flap covers the internal organs.
is removed along with the entire
lower limb)
*Unless otherwise stated, the etiology of these amputations is from peripheral vascular disease.
Data fromThompson A, Skinner A, PiercyJ (eds).Tidy’s Physiotherapy (12th ed). Oxford, UK: Butterworth-Heinemann, 1992;260;
Engstrom B,Van de Ven C (eds).Therapy for Amputees (3rd ed). Edinburgh, UK: Churchill Livingstone, 1999;149-150, 187-188, 208; May B
(ed). Amputations and Prosthetics: A Case StudyApproach. Philadelphia: FA Davis, 1996;62-63; Sanders G (ed). Lower Limb Amputations:
A Guide to Rehabilitation. Philadelphia: FA Davis, 1986;101-102; Lusardi M, Nielsen C (eds). Orthotics and Prosthetics in Rehabilitation.
Boston: Butterworth-Heinemann, 2000;370-373; EdelsteinJE. Prosthetic Assessment and Management. In O’Sullivan SB, SchmitzTJ (eds),
Physical Rehabilitation; Assessment and Treatment (4th ed). Philadelphia: FA Davis, 2001;645-673.
546 APPENDIX VII Amputation

FIGURE VII-2
Upper extremity amputation. (From Burke SL, HigginsJP, McClinton MA, et al [eds]: Hand and Upper
Extremity Rehabilitation: A Practical Guide [3rd ed]. St. Louis: Churchill Livingstone, 2006;716.)
 Amputation APPENDIX VII 547

Table VII-2 TYPES OF UPPER-EXTREMITY AMPUTATIONS*

Type Description
Wrist disarticulation Distal radial ulnar joint function is often retained to maintain rotation of the radius.
Below elbow (transradial) Optimum residual limb length for eventual prosthetic fitting is 8 cm above the ulnar
Long below styloid. Active prosthetic devices are operated by elbow extension and shoulder
Short below flexion, shoulder girdle protraction, or both. Length of residual limb will vary
Very short below depending on amount of viable tissue below the elbow. Refer to FigureVII-2 for
approximate length of these amputations.
Elbow disarticulation Not a choice location for amputation secondary to the poor cosmetic look created and
decreased postsurgical function of the prosthesis.
Above elbow (transhumeral) Often performed as a result of primary malignancy or metastatic disease. Optimum
Standard above residual limb length for eventual prosthetic fitting is 10 cm above the elbow joint.
Short above Length of residual limb will vary depending on amount of viable tissue below the
elbow. Refer to FigureVII-2 for approximate length of these amputations.
Humeral neck Occurs between the glenohumeral joint and deltoid tuberosity. Allows for some
attachment of prosthesis.
Shoulder disarticulation Often performed as a result of primary malignancy or metastatic disease.The head of
the humerus is maintained, or the acromion process and clavicle are trimmed to
create a rounded appearance.
Forequarter Often performed as a result of primary malignancy or metastatic disease. Consists of
removal of the patient’s clavicle, scapula, and arm.
*Unless otherwise stated, the etiology of these amputations is from trauma.
Sources: Data from Engstrom B,Van de Ven C (eds).Therapy for Amputees (3rd ed). Edinburgh, UK: Churchill Livingstone, 1999;243-257;
Lusardi M, Nielsen C (eds). Orthotics and Prosthetics in Rehabilitation. Boston: Butterworth-Heinemann, 2000;573; Banerjee SN (ed).
Rehabilitation Management of Amputees. Baltimore: Williams & Wilkins, 1982;30-33; Ham R, Cotton L (eds). Limb Amputation: From
Aetiology to Rehabilitation. London: Chapman & Hall, 1991;136-143;Theisen L. Management of Upper ExtremityAmputations. In Upper
ExtremityAmputation (Reprinted with permission from Burke SL, HigginsJP, McClinton MA, et al. (eds). Hand and Upper Extremity
Rehabilitation: A Practical Guide (3rd ed). St. Louis: Churchill Livingstone, 2006;716.
548 APPENDIX VII Amputation

Table VII-3 GENERAL PHYSICAL THERAPY CONSIDERATIONS AND TREATMENT SUGGESTIONS

Considerations Treatment Suggestions
Psychological impact of Patients who undergo an amputation, especially of the upper extremity, often experience
amputation psychological changes during the acute stage of their care.
Patients may experience grief, anger, denial, and sadness. It is important to establish a
rapport with the patient based on trust and respect.
To help the patient regain his or her self-esteem, encourage him or her to take an active
role in the therapy session, and highlight successes in therapy.
The physical therapist should request a psychiatric or social service consult if the
patient’s psychosocial issues are interfering with physical therapy intervention.
Residual limb edema Physical therapy techniques may involve the use of ace wraps, shrinker socks, rigid
dressings (lower extremity), or a combination of these according to the patient’s needs
along with the physician’s or facility’s protocols.
Safe residual limb wrapping involves the use of a figure eight or angular pattern,
anchoring turns around the most proximal joint, increased distal pressure, and a
smooth or wrinkle-free application.
The physical therapist should elevate the residual limb in a position that prevents joint
contracture formation.
In patients with upper-extremity amputation, a sling may be used to help manage edema.
Phantom limb pain Often described as a cramping, squeezing, shooting, or burning pain felt in the part of
the extremity that has been removed.The physical therapist may use desensitizing
techniques (e.g., massaging the residual limb), exercise, hot and cold therapy, electrical
stimulation, or other modalities when phantom limb pain is determined as the cause
of the patient’s pain.
Hypersensitivity Patient should be encouraged to rub the residual limb with increasing pressure as
tolerated.
Skin condition Ensure stability of new incision(s) before, during, and after physical therapy
intervention.
Examine the incision for any changes in the appearance (size, shape, open areas, color),
temperature, and moisture level.
Instruct patient and nursing staff on importance of frequent position changes to prevent
skin breakdown. Implement out-of-bed activities as soon as possible.
Instruct patient in active movements and bed mobility activities such as bridging,
rolling, and moving up and down in the bed.
Data from Engstrom B,Van deVen C (eds).Therapy for Amputees (3rd ed). Edinburgh, UK: Churchill Livingstone, 1999;27-37, 43-45; May B
(ed). Amputations and Prosthetics: A Case StudyApproach. Philadelphia: FA Davis, 1996;73, 86-88; Banerjee SN (ed). Rehabilitation
Management of Amputees. Baltimore: Williams & Wilkins, 1982;30-33, 255-258; Pomeranz B, Adler U, Shenoy N, et al. Prosthetics and
Orthotics for the Older Adult with a Physical Disability. Clin Geriatr Med 2006;22(2):377-394.
 Amputation APPENDIX VII 549

Table VII-4 SPECIFIC CONSIDERATIONS AND TREATMENT SUGGESTIONS FOR PATIENTS WITH
UPPER- OR LOWER-EXTREMITY AMPUTATION

Consideration Treatment Suggestions

Joint contracture (upper Physical therapy should consist of active movements of all of the joints above the level
extremity) of the amputation, including movements of the scapula. Patients who use upper-
extremity slings to fixate the arm in elbow flexion and shoulder internal rotation
should be examined regularly for contractures.
Joint contracture (lower The physical therapist should provide the patient and members of the nursing staff with
extremity) education on residual limb positioning, proper pillow placement, and the use of splint
boards.
Patients with a below-the-knee amputation will be most susceptible to knee flexion
contraction. A pillow should be placed under the tibia rather than under the knee to
promote extension.
Patients with above-the-knee amputations or disarticulations will be most susceptible to
hip flexor and abductor contractures.
The physical therapist should begin active range-of-motion exercises and provide passive
stretching as indicated.
Decreased functional mobility During ambulation, patients tend to flex their trunk toward the side of the amputation
(upper extremity) and maintain a stiff gait pattern that lacks normal arm swing. Patients often need gait,
balance, posture retraining, or a combination of these.
It is important to work on active movements, specifically the movements that might be
used for powering a prosthesis, such as in the following:
Below elbow body powered prosthesis: elbow extension, shoulder flexion, shoulder
girdle protraction, or a combination of these
Above elbow body powered prosthesis: elbow flexion, shoulder extension, internal
rotation, abduction and shoulder girdle protraction and depression.
Decreased functional mobility Techniques should range from bed mobility training to transfer training to ambulation
(lower extremity) or wheelchair mobility. Patients with bilateral above-knee amputations will need a
custom wheelchair that places the rear axle in a more posterior position to
compensate for the alteration in the patient’s center of gravity when sitting.
Sources: Data from Karacoloff LA, Schneider FJ (eds). Lower ExtremityAmputation: A Guide to Functional Outcomes in Physical Therapy
Management. Rockville, MD: Aspen, 1985; Engstrom B,Van deVen C (eds).Therapy for Amputees (3rd ed). Edinburgh, UK: Churchill
Livingstone, 1999;27-37, 43-45, 243-257; May B (ed). Amputations and Prosthetics: A Case StudyApproach. Philadelphia: FA Davis,
1996;86-88; Banerjee SN (ed). Rehabilitation Management of Amputees. Baltimore: Williams & Wilkins, 1982;30-33, 255-258; Ham R,
Cotton L (eds). Limb Amputation: From Aetiology to Rehabilitation. London: Chapman & Hall, 1991;136-143;Theisen L. Management of
Upper ExtremityAmputations. In Upper ExtremityAmputation (Reprinted with permission from Burke SL, HigginsJP, McClinton MA,
et al (eds). Hand and Upper Extremity Rehabilitation: A Practical Guide (3rd ed). St. Louis: Churchill Livingstone, 2006;716.

References
1. Engstrom B,Van deVen C (eds),Therapy for Amputees
(3rd ed). Edinburgh, UK: Churchill Livingstone,
1999;27-37, 43-45, 149-150, 187-188, 208.
2. Huang ME, JohnsJS,WhiteJ, et al.Venous
Thromboembolism in a Rehabilitation Setting after
Major Lower ExtremityAmputation. Archives of
Physical Medicine & Rehabilitation 2005;86(1):73-78.
3. Pomeranz B, Adler U, Shenoy N, et al. Prosthetics and
Orthotics for the Older Adult with a Physical Disability.
Clin Geriatr Med 2006;22(2):377-394.
4. Karacoloff LA, Schneider FJ (eds), Lower Extremity
Amputation: A Guide to Functional Outcomes in
Physical Therapy Management. Rockville, MD: Aspen,
1985.
5. Thompson A, Skinner A, PiercyJ (eds).Tidy’s
Physiotherapy (12th ed). Oxford, UK: Butterworth-
Heinemann, 1992;260.
This page intentionally left blank.
 Appendix VIII Postural Drainage
Michele P. West
Postural drainage is the positioning of a patient with an
involved lung segment as close to perpendicular to the
floor as possible to facilitate the drainage of broncho-
pulmonary secretions by gravity.1 FigureVIII-1 demon-
strates the twelve traditional postural drainage
positions. The use of postural drainage as an adjunct
to other techniques (mainly breathing exercises and
chest wall manipulation) can be highly effective for
mobilizing retained secretions and maximizing gas
exchange.The physical therapist should note that there
are many clinical contraindications and considerations
for postural drainage.
The relative contraindications for the use of the
Trendelenburg position (placing the head of the bed
in a downward position) include the following2:
 Patient with an intracranial pressure (ICP) greater
than 20 mm Hg or in whom increased intracranial
pressure should be avoided
 Uncontrolled hypertension
 Uncontrolled or unprotected airway with a risk of
aspiration
 Recent gross hemoptysis
 Recent esophageal surgery
 Significantly distended abdomen
 Orthopnea
The contraindications for the reverseTrendelenburg
position (placing the head of the bed in an upward
position) include the following2:
 Hypotension
 Use of vasoactive medications
The following are absolute and relative contraindi-
cations for postural drainage in conjunction with
other manual bronchopulmonary hygiene techniques
such as vibration, shaking, or percussion.2
 Acute hemorrhage with hemodynamic instability
(absolute contraindication)
 Unstabilized head or neck injury (absolute
contraindication)
 ICP greater than 20 mm Hg
 Unstable cardiac dysrhythmia
 Bronchopleural fistula (BPF)
 Empyema
 Large pleural effusion(s)
 Unstable pneumothorax
 Subcutaneous emphysema (air in the subcutaneous
tissue)
 Pulmonary embolism
 Pulmonary edema or congestive heart failure
 Active hemoptysis
The use of postural drainage with or without
other bronchopulmonary hygiene techniques should
be considered on an individual patient basis if any of
the aforementioned relative contraindications exist.
This can include a discussion with the medical-surgical
team, an analysis of the risk(s) versus benefit(s) for
the patient, as well as any possible modifications of
therapy.
Postural drainage positions with or without airway
clearance techniques may require modification to max-
imize patient safety, comfort, and/or tolerance. In the
acute care setting, there are many situations and con-
ditions in which the patient cannot obtain or main-
tain traditional postural drainage positions nor
tolerate chest wall manipulation. These situations
and conditions include the following1,3,4:
 The presence of multiple lines and tubes or mechan-
ical ventilation
 Obesity
 Massive ascites
 Diaphragmatic hernia or reflux
 Chest wall abnormalities such as skin grafting, open
wound, the presence of a vacuum-assisted wound
closure dressing, rib fracture, flail chest, or rib
metastasis
 The elderly or long-term bedridden patient with
cachexia or a spinal deformity
 Anxiety or confusion
 Inadequate pain control, especially in the postsurgi-
cal patient
 Recent pacemaker placement
 Platelet count less than 20,000 per mm3
Examples of postural drainage position modifica-
tions frequently used in the acute care setting are
shown in FigureVIII-2.
551
552 APPENDIX VIII Postural Drainage
FIGURE VIII-1
The twelve postural drainage positions. LLL, Left lower lobe; RUL right upper lobe; LUL, left upper
lobe; RLL, right lower lobe; RML, right middle lobe.
Physical therapy considerations and clinical tips for
the use of postural drainage include the following:
 The timing of postural drainage after pain medica-
tion or bronchodilators can improve its
effectiveness.
 Monitor vital signs with position changes to evaluate
patient tolerance, especially for critically ill patients
or those status post cardiothoracic surgery with a
history of blood pressure and heart rate changes
when turned to one side.
 Modify the position of the patient if anxiety, pain,
skin breakdown, abnormal posture, decreased range
of motion, or positioning restrictions exist.
 To improve patient tolerance of postural drainage,
consider modifying the time spent in each position,
the angle of the bed, or patient position.
 Postural Drainage APPENDIX VIII 553

FIGURE VIII-2
Recommended postures for segmental drainage from the upper lobe of the lung. A through F, Patient
positions for postural drainage of S1, S2, S1-2, S3, and S6 as recommended by Potter and Perry. G through
I, Positions recommended for patients with tracheal intubation by Miyagawa. Potter and Perry described
another six postures (i.e., 12 postures in all) to cover all lung segments, while Miyagawa included another
five postures (eights postures total). A, Bending backward to drain S1.When bending backward or
forward (see C), the craniocaudal axis of the lung is tilted at 458 from the horizontal. B, 458 rotative prone
with right-side-up position for draining the right S2. In this position, the craniocaudal axis of the lung is
the same as in the prone or supine positions, but the coronal plane of the lung is tilted at 458. C, Bending
forward is recommended for drainage of the posterior portion of the left and right upper lobes.
D, Supine position for draining S3. E, Prone position for draining S6 and S10. F, 458 relative prone with
head-raised position, which is recommended for S1-2 drainage in the left lung.‘‘Head raised’’ means
that the craniocaudal axis of the lung is raised to 308. G,The supine position is also useful for S3 drainage
during tracheal intubation. It is also useful for S1 drainage during tracheal intubation. H and I, 458
rotative prone positions with right and left sides up, respectively.These positions are recommended for
S2 and S1-2 drainage during intubation. (From Anatomic Evaluation of Postural Bronchial Drainage of the
Lung with Special Reference to Patients withTracheal Intubation. Chest 2004;125[3].)
554 APPENDIX VIII Postural Drainage
 Provide time for the patient to rest or become
acclimated to position changes if necessary.
 Use pillows, blankets, foam rolls, or wedges to
maximize comfort or provide pressure relief.
 Bed mobility training can be incorporated during
position changes with patients who have decreased
independence with rolling or supine-to-sit transfers.
References
1. Downs AM. Physiological Basis for Airway Clearance
Techniques. In D Frownfelter, E Dean (eds), Principles
and Practice of Cardiopulmonary Physical Therapy
(3rd ed). St. Louis: Mosby, 1996;323.
2. AARC Clinical Practice Guideline: Postural
DrainageTherapy. Respir Care 1991;36(12):1418-
1426Available at: www.rcjournal.com. Accessed
January 23, 2008.
 Have a good working knowledge of the controls on
the patient’s bed that are needed to position the
patient for postural drainage. Each bed model, espe-
cially pressure relief or rotating beds, has different
controls, locks, and alarms.
3. SciakyA, StockfordJ, Nixon E.Treatment of Acute
Cardiopulmonary Conditions. In EA Hillegass, HS
Sadowsky (eds), Essentials of Cardiopulmonary Physical
Therapy (2nd ed). Saunders, 2001;647-651.
4. Downs AM. Clinical Application of Airway Clearance
Techniques. In D Frownfelter, E Dean (eds), Principles
and Practice of Cardiopulmonary Physical Therapy
(3rd ed). St. Louis: Mosby, 1996;339-347.
 Appendix IX Functional Tests
Jaime C. Paz and Jennifer A. Silva
The purpose of this appendix is to describe various
objective measures that can be used to determine the
functional levels of various patient populations in the
acute care setting. The Berg balance scale (BBS), timed
‘‘up and go’’ (TUG) test, Tinetti performance oriented
mobility assessment (POMA), functional reach test,
and the 6-minute walk test will be reviewed here.
These functional tests were selected because of their
ease of use, reliable and valid test results, and the popu-
lation that can use these tests in the acute care setting.
All of these tests showed high interrater (tested by dif-
ferent therapists) and intrarater (retested over time by a
single therapist) reliability.1 These tests also show high
content,* construct,{ and predictive{ validity unless
otherwise noted in the respective description of each
test.1
BERG BALANCE SCALE
The BBS is a 56-point scale that evaluates 14 tasks.
Katherine Berg developed this test to assess the level
of function and balance in various patient populations.2
Procedure
The patient is evaluated and graded on a sequence of
balance activities, such as sitting unsupported with
arms folded, rising, standing, and transferring between
one surface and another, reaching forward in standing,
picking up objects off the floor, turning around in a
full circle, and standing on one leg.2 Figure IX-1 out-
lines the evaluation form for this test. Table IX-1
describes the appropriate population, required equip-
ment, completion time, reliability, and validity of the
BBS.4
*Content validity: Degree in which a test actually measures what it
was designed for.
{
Construct validity: Degree to which a theoretical construct is
measured against the test.
{
Predictive validity: Ability of a test to predict future performance.
Scoring for each task ranges from 0 to 4. A score of 0
indicates that the patient is unable to complete a partic-
ular task. A score of 4 indicates that the patient can
completely carry out the task.2
A short form of the BBS has been developed and
demonstrates similar psychometric test properties as
the original BBS. The short form of the BBS includes
seven activities rather than 14, and the scoring levels
are reduced to three (0, 2, 4). This modified BBS has
been shown to have good validity and reliability in
patients who are status post CVA. Box IX-1 outlines
the seven items on this modified BBS.
CLINICAL TIP
 Because the modified BBS was developed with
patients who are status post CVA, then it should
only be utilized with this population until further
evidence is gathered for other patient diagnoses.
Interpretation of Results
A total score of less than 45 predicts that the patient is at
risk for falls.5,6 In contrast, higher scores on the BBSindi-
cate greater independence and better ability to balance.7
In patients who are over 65 years of age and are depen-
dent in at least one personal activity of daily living,
a change of 8 points on the BBS is necessary to demon-
strate a genuine change in function.8 For patients with
multiple sclerosis, the BBS is reported to be less efficient
in discriminating between patients who tend to fall as
compared to patients less likely to fall.9
TIMED ‘‘UP AND GO’’ TEST
The ‘‘get up and go’’ test was originally developed in
1986 to serve as a clinical measure of balance in elderly
people.10 The original test used a numeric scoring
system to determine a patient’s level of balance but was
later modified to a timed version by Posiadlo and
Richardson in 1991.11 The TUG test uses a time score
555
556 APPENDIX IX Functional Tests

FIGURE IX-1
Berg Balance Scale. (Reprinted with permission of Katherine Berg. Data from Wood-Dauphinee S,
Berg K, Bravo G, et al.The Balance Scale: Responding to Clinically Meaningful Changes. Can J Rehabil
1997;10:35-50; Berg K,Wood-Dauphinee S,WilliamsJI.The Balance Scale: ReliabilityAssessment for
Elderly Residents and Patients with an Acute Stroke. ScandJ Rehab Med 1995;27:27-36; Berg K, Maki B,
WilliamsJI, et al. A Comparison of Clinical and Laboratory Measures of Postural Balance in an Elderly
Population. Arch Phys Med Rehabil 1992;73:1073-1083; Berg K,Wood-Dauphinee S,WilliamsJI, et al.
Measuring Balance in the Elderly:Validation of an Instrument. CanJ Public Health 1992;[suppl 2]:S7-S11;
Berg K,Wood-Dauphinee S,WilliamsJI, et al. Measuring Balance in the Elderly: Preliminary
Development of an Instrument. Physiother Can 1989;41:304-311.)
 Functional Tests APPENDIX IX 557

Equipment required for testing are a stopwatch or watch with second

hand, and a ruler or other indicator of 2, 5, and 10 in. (5, 12.5, and 25 cm).
Chairs used during testing should be of reasonable height. Either a step or
a stool (of average step height) may be used for item #12.

1. Sitting to Standing
Insturctions: Please stand up. Try not to use your hands for support.
( ) 4 able to stand without using hands and stabilize independently
( ) 3 able to stand independently using hands
( ) 2 able to stand using hands after several tries
( ) 1 needs minimal aid to stand or to stablilize
( ) 0 needs moderate or maximal assist to stand

2. Sitting Unsupported
Insturctions: Please stand for miniutes without holding.
( ) 4 able to stand safely 2 minutes
( ) 3 able to stand 2 minutes with supervision
( ) 2 able to stand 30 seconds unsupported
( ) 1 needs several tries to stand 30 seconds unsupported
( ) 0 unable to stand 30 seconds unassisted
if a subject is able to stand 2 minutes unsupported, score full points for
sitting unsupported. Proceed to item #4.

3. Sitting with Back Unsupported But Feet Supported on Floor or on a

Stool
Insturctions: Please sit with arms folded for 2 minutes.
( ) 4 able to sit safely and securely 2 minutes
( ) 3 able to sit 2 minutes under supervision
( ) 2 able to sit 30 seconds
( ) 1 able to sit 10 seconds
( ) 0 unable to sit without support 10 seconds

4. Standing to Sitting
Instructions: Please sit down.
( ) 4 sits safely with minimal use to hands
( ) 3 controls descent by using hands
( ) 2 uses back of legs against chair to control descent
( ) 1 sits independently but has uncontrolled descent
( ) 0 needs assistance to sit

5. Transfers
Instructions: Arrange chair(s) for a pivot transfer. Ask subject to transfer
one way toward a seat with armrests and one way toward a seat without
armrests. You may use to chairs (one with and one without armrests) or a
bed and a chair.

FIGURE IX-1. cont’d Continued

558 APPENDIX IX Functional Tests

( ) 4 able to transfer safely with minor use of hands

( ) 3 able to transfer safely definite need of hands
( ) 2 able to transfer with verbal cueing and/or supervision
( ) 1 needs one person to assist
( ) 0 needs two people to assist or supervise to be safe

6. Standing Unsupported with Eyes Closed

Insructions: Please close your eyes and stand still for 10 seconds.
( ) 4 able to stand 10 seconds safely
( ) 3 able to stand 10 seconds with supervision
( ) 2 able to stand 3 seconds
( ) 1 unable to keep eyes closed 3 seconds but stays steady
( ) 0 needs help to keep from falling

7. Standing Unsupported with Feet Together

Instructions: Place your feet together and stand without holding.
( ) 4 able to place feet together independently and stand 1 minute safely
( ) 3 able to place feet together independently and stand for 1 minute with
supervision
( ) 2 able to place feet together independently and to hold for 30 seconds
( ) 1 needs help to attain position but able to stand 15 seconds feet
together
( ) 0 needs help to attain position and unable to hold for 15 seconds

8. Reaching Forward with Outstretched Arm while Standing

Instructions: Lift arm to 90 degrees. Stretch out your finges and reach
forward as far as you can. (Examiner places a ruler at end of fingertips when
arm is at 90 degrees. Fingers should not touch the ruler while reaching
forward. The recorded measure is the distance forward that the fingers reach
while the subject is in the most forward lean position. When possible, ask
subject to use both arms when reaching to avoid rotation of the trunk.)
( ) 4 can reach forward confidently >25 cm ( 10 in.)
( ) 3 can reach forward >12.5 cm safely (5 in.)
( ) 2 can reach forward >5 safely (2 in.)
( ) 1 reaches forward but needs supervision
( ) 0 loses blance while trying, requires external support

9. Pick Up Object from the Floor from a Standing Position

Instructions: Pick up the shoe/slipper that is placed in front of your feet.
( ) 4 able to pick up slipper safely and easily
( ) 3 able to pick up slipper but needs supervision
( ) 2 unable to pick up but reaches 2–5 cm (1–2 in.) from slipper and
keeps balance independently
( ) 1 uable to pick up and needs supervision while trying
( ) 0 unable to try, needs assist to keep from losing balance or falling

FIGURE IX-1. cont’d

 Functional Tests APPENDIX IX 559

10. Turning to Look Behind Over Left and Right Shoulders while
Standing
Instructions: Turn to look directly behind you over left shoulder. Repeat to
the right.
Examiner may pick an object to look at directly behind the subject to
encourage a better twist turn.
( ) 4 looks behind from both sides and weight shifts well
( ) 3 looks behind one side only, other side shows less weight shift
( ) 2 turns sideways only but maintains balance
( ) 1 needs supervision when turning
( ) 0 needs assist to keep from losing balance or falling

11. Turn 360 Degrees

Instructions: Turn completely around in a full circle. Pause. Then turn a full
circle in the other direction
( ) 4 able to turn 360 degrees safely in 4 seconds or less
( ) 3 able to turn 360 degrees safely one side only in 4 seconds or less
( ) 2 able to turn 360 degrees safely but slowly
( ) 1 needs close supervision or verbal cueing
( ) 0 needs assistance while turning

12. Placing Alternate Foot on Step or Stool while Standing Unsupported

Instructions: Place each foot alternately on the step/stool. Continue until
each foot has touched the step/stool four times.
( ) 4 able to stand independently and safely and complete 8 steps in 20
seconds
( ) 3 able to stand independently and complete 8 steps >20 seconds
( ) 2 able to complete 4 steps without aid with supervision
( ) 1 able to complete >2 steps, needs minimal assist
( ) 0 needs assistance to keep from falling, unable to try

13. Standing Unsupported with One Foot in Front

Instructions: (demonstrate to subject)
Place one foot directly in front of the other. If you think that you cannot
place your foot directly in front, try to step far enough ahead that the heel of
your forward foot is ahead of the toes of the other foot. (To score 3 points, the
length of the step should exceed the length of the other foot and the width of
the stance should approximate the subject’s normal stride width.)
( ) 4 able to place foot tandem independently and hold 30 seconds
( ) 3 able to place foot ahead of other independently and hold 30 seconds
( ) 2 able to take small step independently and hold 30 seconds
( ) 1 needs help to step but can hold 15 seconds
( ) 0 loses balance while stepping or standing
FIGURE IX-1. cont’d Continued
560 APPENDIX IX Functional Tests

14. Standing on One Leg

Instructions: Stand on one leg as long as you can without holding.
( ) 4 able to lift leg independently and hold >10 seconds
( ) 3 able to lift leg independently and hold 5–10 seconds
( ) 2 able to lift leg independently and hold ≥3 seconds
( ) 1 tries to lift leg unable to hold 3 seconds but remains standing
independently
( ) 0 unable to try or needs assist to prevent fall

( ) Total Score (maximum = 56)

FIGURE IX-1. cont’d

to assess gait and balance in the elderly population and

is summarized inTable IX-2.12 BOX IX-1 SHORT FORM OF BERG
Procedure BALANCE SCALE
The patient is timed during a five-part mobility task Item
from start to finish.The task consists of the following13:
1. Rising from an armchair  Reaching forward with outstretched arm
2. Walking 3 m  Standing with eyes closed
3. Turning around  Standing with one foot in front
4. Walking 3 m back to the armchair  Turning to look behind
5. Sitting down  Retrieving object from floor
It is important to instruct the patient to walk at a  Standing on one foot
comfortable and normal pace to maintain safety  Sitting to standing
throughout the test. It is appropriate to provide assis-
tance for the patient if it is needed. Documenting the Data from Chou CY, Chien CW, Hsueh IP, et al. Developing a
level of assistance (i.e., assistive device, contact guard) Short Form of the Berg Balance Scale for People with Stroke.
is essential in demonstrating progress when perform- PhysTher 2006;86:199.
ing the test over time.

Table IX-1 OVERVIEW OF THE BERG BALANCE SCALE

Population Equipment Time Reliability Validity
Elderly patients who Ruler 10-20 minutes Interrater reliability: Concurrent validity:
have sustained acute Stopwatch required to ICC = 0.98 Tinetti, r = 0.91
cerebrovascular Chair complete test rs = 0.88 Get up and go, r =
accident and/or are Step stool Intrarater reliability: —0.76
in a rehabilitation Flat surface ICC = 0.98 Predictive validity:
setting Internal consistency: <45 score predicts falls
Cronbach’s alpha = 0.96
ICC, Intraclass correlation coefficient; r, correlation coefficient; rs, Spearman’s rank correlation coefficient.
Data from reference numbers 3, 5, 6, 10.

Table IX-2 OVERVIEW OF THE TIMED ‘‘UP AND GO’’ TEST
Population Time
Geriatric population 1 to 3 minutes to
with various complete test
diagnoses
ICC, Intraclass correlation coefficient; r, correlation coefficient.
*If necessary, an assistive device may be used while performing this test.
Data from reference numbers 1, 5, 10, 11.
Interpretation of Results
Test completion in fewer than 20 seconds indicates
that the patient is independent with functional
mobility.13 The time needed to complete the test may
improve for many reasons, including: (1) Altering the
use of an assistive device, (2) Actual change in function,
and (3) Increased familiarity of the test, or a combina-
tion of these. Therefore, it is important to periodically
perform this test over the course of a patient’s physical
therapy intervention to allow for comparison to their
baseline results.
As described in Table IX-2, when compared to
other functional tests (i.e., BBS), with regards to bal-
ance testing, theTUG test is a consistent test of the bal-
ance characteristics in this population. The ability or
inability to complete the TUG test helps to stratify
patients according to their fall risk. Patients who are
unable to complete the TUG test for nonphysical rea-
sons (including refusal, inability to follow instructions
[e.g., dementia or delirium]) appear to have higher
rates of falling as compared to patients who are unable
to do the TUG test for physical reasons (inability to
sit, stand, or walk independently, or with standby
assistance).14
Additionally, in patients who are status post hip
fracture surgery and are discharged from the acute
care setting with a TUG score of 24 seconds or more
are more likely to fall in the next six months as
compared to those patients with scores of less than
24 seconds.15 When used in an acute care setting, this
test can objectively demonstrate improvements in
balance and ambulation. Over the course of therapy, it
is expected that the time the patient takes to complete
the timed up and go test will decrease as the patient
improves.12
Functional Tests APPENDIX IX 561
Equipment Reliability Validity
Armchair Interrater reliability: Content validity:
Stopwatch r = 0.99 none reported
Assistive Intrarater reliability: Concurrent
device* r = 0.99 validity: Berg
ICC = 0.99 balance scale
CLINICAL TIP
 Caution should be exercised in interpreting the
scores of the TUG test when administered to a frail
elder who has multisystem impairments and
cognitive deficits. Patients with these characteristics
may have TUG scores as low as 10 seconds but may
still be at risk for falling.16
FUNCTIONAL REACH TEST
The functional reach test was developed to assess the
risk for falls in the elderly population and is a dynamic
measure of stability during a self-initiated movement.17
The functional reach test evaluates balance by measur-
ing the maximum distance an elderly person can reach
forward, backward, and sideward while standing on
the floor at a fixed position.7
Procedure
The procedure involves a series of three trials of the dis-
tance a patient is willing to reach from a fixed surface.7
After every reach, distance is measured with a yardstick
attached to the wall at shoulder level.The difference in
inches between a person’s arm length and maximal for-
ward, backward, and sideward reach with the shoulder
flexed to 90 degrees while maintaining a fixed base of
support in standing is then recorded.10,18 The mean of
their three trials is their score. Refer toTable IX-3 for a
summary of the functional reach test.
Interpretation of Results
The functional reach in inches correlates with the
patient’s relative risk for falling.17
562 APPENDIX IX Functional Tests

Table IX-3 OVERVIEW OF THE FUNCTIONAL REACH TEST

Population Equipment Time Reliability Validity
Elders who are community Yardstick <5 minutes Test-retest Concurrent validity:
ambulators, patients Level to complete reliability: Walking speed, r = 0.71
who are status post hip Assistive test r = 0.89 Tandem walk, r = 0.71
fracture surgery. device* Interrater Center of pressure, r = 0.71
Population limitation, reliability: Predictive validity:
excluding patients with ICC = 0.99 >10 in.: not likely to fall
dementia, extreme spinal 6-10 in.: two times more likely
deformities, severely to fall
restricted upper extremity 1-6 in.: four times more likely
function, frail elders, and to fall
nursing home residents. 0 in.: 28 times more likely to fall
ICC, Intraclass correlation coefficient; r, correlation coefficient.
*An assistive device may be used while performing this test if it is necessary.
Data from reference numbers 1, 17, 19, 20.

Reach Likelihood of falling TINETTI PERFORMANCE ORIENTED

>10 inches Not likely
6-10 inches 2 times more likely
1-6 inches 4 times more likely
Subject unwilling 28 times more likely
to reach
When working with an elderly patient in an acute
care setting, this test may be an objective way to quickly
gauge balance abilities and determine the need for
balance treatment, an assistive device, or both. It is
important to remember that there are limitations to
the population that can participate in this test. Elders
who are frail, demented, or both, are excluded, because
participation in this test may lead to unnecessary
injury or falls.
CLINICAL TIP
 If the procedure of the functional reach test is
followed correctly, then scores of either their first
trial, second trial, or the mean of their first two
trials will have no significant difference from
that of the mean of the three trials.21 This may
be useful for clinicians who do not have time
to perform three trials or if their patients may not
have the endurance to perform three trials.
MOBILITY ASSESSMENT
The Tinetti POMA is a performance test of balance
and gait maneuvers used during normal daily
activities.22 This test has two subscales of balance
and gait, as described in Table IX-4. There are
13 maneuvers in the balance portion and nine
maneuvers in the gait portion. The balance subscale,
the performance oriented assessment of balance
(POAB), can be used individually as a separate test
of balance.
Procedure
The balance maneuvers are graded on an ordinal
scale as normal (2 points), adaptive (1 point), or
abnormal (0 points). The gait maneuvers are
graded as normal or abnormal, with the exception
of a few items (see Table IX-4). A combination of
the total points for the balance and gait portions are
summed together to determine the final score.10,23
A summary of the Tinetti POMA can be found in
Table IX-5.
Interpretation of Results
A total combined score on the balance and gait sub-
scales of theTinetti POMA correlates with the patient’s
relative risk of falling.26

Table IX-4 PERFORMANCE ORIENTED MOBILITY ASSESSMENT I
Element
Balance
1. Sitting balance
2. Arising from chair
3. Immediate standing balance
(first 5 seconds)
4. Standing balance
5. Balance with eyes closed
(with feet as close together
as possible)
6.Turning balance
(360 degrees)
7. Nudge on sternum (patient
standing with feet as close
together as possible,
examiner pushes with light
even pressure over sternum
three times)
8. Neck turning (patient asked
to turn to side and look up
while standing with feet as
close together as possible)
9. One leg standing balance
10. Back extension (ask patient
to lean back as far as
possible, without holding
onto object)
11. Reaching up (have patient
attempt to remove an object
from a shelf high enough to
require stretching or
standing on toes)
Functional Tests APPENDIX IX 563
Scoring
Instructions: Subject is seated in hard, armless chair. The following
maneuvers are tested.
2 = steady, stable
1 = holds onto chair to keep upright
0 = leans, slides down in chair
2 = able to rise in a single movement without use of arms
1 = uses arms (on chair or walking aid) to pull or push up; and/or moves forward
in chair before attempting to arise
0 = multiple attempts required or unable without human assistance
2 = steady without holding onto walking aid or other object for support
1 = steady, but uses walking aid or other object for support
0 = any sign of unsteadiness
2 = steady, able to stand with feet together without holding object for support
1 = steady, but cannot put feet together
0 = any sign of unsteadiness regardless of stance or holds onto object
2 = steady without holding onto any object with feet together
1 = steady with feet apart
0 = any sign of unsteadiness or needs to hold onto an object
2 = no grabbing or staggering; no need to hold onto any objects; steps are
continuous (turn is a flowing movement)
1 = steps are discontinuous (patient puts one foot completely on floor before
raising other foot)
0 = any sign of unsteadiness or holds onto an object
2 = steady, able to withstand pressure
1 = needs to move feet, but able to maintain balance
0 = begins to fall, or examiner has to help maintain balance
2 = able to turn head at least halfway side to side and able to bend head back to
look at ceiling; no staggering, grabbing, or symptoms of lightheadedness,
unsteadiness, or pain
1 = decreased ability to turn side to side or to extend neck, but no staggering,
grabbing, or symptoms of lightheadedness, unsteadiness, or pain
0 = any sign of unsteadiness or symptoms when turning head or extending neck
2 = able to stand on one leg for 5 seconds without holding object for support
1 = some staggering, swaying, or moves foot slightly
0 = unable
2 = good extension without holding object or staggering
1 = tries to extend, but decreased range of motion (compared with other patients
of same age) or needs to hold object to attempt extension
0 = will not attempt or no extension seen or staggers
2 = able to take down object without needing to hold onto other object for
support and without becoming unsteady
1 = able to get object but needs to steady self by holding onto something for
support
0 = unable or unsteady
Continued
564 APPENDIX IX
Table IX-4 PERFORMANCE ORIENTED MOBILITY ASSESSMENT I—cont’d
Element
12. Bending down (patient is
asked to pick up small
objects [e.g., a pen] from
the floor)
13. Sitting down
Gait
1. Initiation of gait (patient is
asked to begin walking down
hallway)
2. Step height (begin observing
after first few steps; observe
one foot, then the other;
observe from side)
3. Step length (observe distance
between toe of stance foot
and heel of swing foot;
observe from side; do not
judge first few or last few
steps; observe one side
at a time)
4. Step symmetry (observe the
middle part of walking, not
the first or last steps; observe
from side; observe distance
between heel of each
swing foot and toe of
each stance foot)
5. Step continuity
6. Path deviation (observe from
behind; observe one foot
over several strides; observe
in relation to line on floor
[e.g., tiles] if possible;
difficult to assess if patient
uses a walker)
7.Trunk stability (observe from
behind; side to side motion
of trunk may be a normal
gait pattern, need to
Functional Tests
Scoring
2 = able to bend down and pick up the object and able to get up easily in a single
attempt without needing to pull self up with arms
1 = able to get object and get upright in a single attempt but needs to pull self up
with arms or hold onto something for support
0 = unable to bend down or unable to get upright after bending down, or takes
multiple attempts to become upright
2 = able to sit down in one smooth movement
1 = needs to use arms to guide self into chair, or movement is not smooth
0 = falls into chair, misjudges distances (lands off center)
Instructions: Subject stands with examiner, then walks 15 ft down a
premeasured hallway, turns, and walks back to starting point. Subject should
use customary walking aid as necessary.
1 = begins walking immediately without observable hesitation; initiation of gait
is single, smooth motion
0 = hesitates; multiple attempts; initiation of gait is not a smooth motion
1 = swing foot completely clears floor but by no more than 1 to 2 inches.
0 = swing foot is not completely raised off floor (may hear scraping) or is raised
too high (>2 inches)
1 = at least the length of individual’s foot between the stance toe and swing heel
(step length usually longer, but foot length provides basis for observation)
0 = step length less than the individual’s foot
1 = step length same or nearly same on both sides for most step cycles
0 = step length varies between sides or patient advances with same foot with
every step
1 = begins raising heel of one foot (toe off) as heel of other foot touches the floor
(heel strike); no breaks or stops in stride; step lengths equal over most cycles
0 = places entire foot (heel and toe) on floor before beginning to raise other foot;
or stops completely between steps; or step length varies over cycles
2 = foot follows close to straight line as patient advances
1 = foot deviates from side to side or toward one direction, or patient uses a
walking aid
0 = marked deviation from straight line
2 = trunk does not sway; knees or back are not flexed; arms are not abducted in
effort to maintain stability
1 = no sway but flexion of knees or back or spreads arms out while walking
0 = any of the preceding features are present
 Functional Tests APPENDIX IX 565

Table IX-4 PERFORMANCE ORIENTED MOBILITY ASSESSMENT I—cont’d

Element Scoring
differentiate this from
instability)
8.Walk stance (observe from 1 = feet should almost touch as one passes the other
behind) 0 = feet apart with stepping
9.Turning while walking 2 = no staggering or use of a walking aid; turning is continuous with walking;
and steps are continuous while turning
1 = steps are discontinuous but no staggering, or uses walking aid
0 = staggers; unsteady; stops before initiating turn
Data fromTinetti ME. Performance-Oriented Assessment of Mobility Problems in Elderly Patients. J Am Geriatr Soc 1986;34:119-126;
Tinetti ME,WilliamsTF, Mayewski R. Fall Index for Elderly Patients Based on Number of Chronic Disabilities. Am J Med 1986;80:429-434.

possible on a premeasured course for 6 minutes. This

Score Risk test evolved from the 12-minute walk test, originally
<18 High designed to assess disability levels in patients with
19-23 Moderate chronic bronchitis. The 6-minute walk test was found
>24 Low to provide similar measures of exercise tolerance
and therefore was adopted by clinicians for its
This functional test is an effective and objective convenience.32,33
measure to predict falls in elderly and adult population,
as well as assist in determining progress over time in Procedure
therapy. The patient is instructed to walk as far as possible for
6 minutes within a designated test area of a premea-
sured distance. The patient is instructed to report if he
SIX-MINUTE WALK TEST or she experiences shortness of breath, muscular pain,
dizziness, or anginal symptoms, at which time the test
The 6-minute walk test is a symptom-limited measure is terminated. The patient is also instructed to rest
of functional capacity in which a patient walks as far as whenever necessary during the test but asked to

Table IX-5 OVERVIEW OF THE TINETTI PERFORMANCE ORIENTED MOBILITY ASSESSMENT

Population Equipment Time Reliability Validity
Balance portion: adult Chair 10-15 minutes to Interrater reliability: Concurrent validity:
or geriatric Stopwatch complete test 85% =  10% Berg, r = 0.91
population with a agreement Balance Predictive validity:
wide variety of portion 18 total score predicts
diagnoses high fall risk
r, Correlation coefficient.
Data from reference numbers 2, 7, 23-26.
566 APPENDIX IX Functional Tests

Table IX-6 OVERVIEW OF THE SIX-MINUTE WALK TEST

Population Equipment Time Reliability Validity
Patients with Chair 10-15 minutes to Test-retest reliability: Responsiveness index
cardiac and/or Stopwatch complete test ICC = 0.93 validity: 0.6
pulmonary Pulse oximeter
disease and Portable blood pressure cuff
osteoarthritis Rate of perceived exertion scale
of the knee Visual pain analog scale
Measuring wheel
ICC, Intraclass correlation coefficient.
Data from reference numbers 24, 27-31.

continue as soon as he or she is able. Timing begins
when the tester states ‘‘go’’ or ‘‘start.’’ During the test,
the tester should walk alongside the patient and offer
appropriate guarding as needed. (Walking behind or
ahead of the patient influences his or her pace.)
Vital signs should be taken at rest, one or two times
during the test, and immediately at the end of the 6 min-
utes or on completion of the test. If the patient is
unable to complete the full 6 minutes, then the distance
covered on termination is measured along with estab-
lishing the reason for termination by the patient.

Table IX-7 PREDICTION EQUATIONS FOR Interpretation of Results

6-MINUTE WALK TEST DISTANCE Many studies have examined the usefulness of the
6-minute walk test in specific populations (Table IX-6)
Author Equation and have found it to be effective in predicting oxygen
Enright, Healthy men between 40 and 80 years consumption and determining the efficacy of surgical
1998 of age intervention on functional mobility.32-35 A number of
Expected 6 MWD = (7.57  height in cm) regression equations have been developed to predict
— (5.02  age) — (1.76  weight in kg) 6-minute walk test distance in healthy adults
— 309 (Table IX-7). These prediction equations can be used
Healthy women between 40 and 80 years
of age by physical therapists as a means of determining the
Expected 6 MWD = (2.11  height in cm) level of deficits in their patients and ultimately in pre-
— (2.29  age) — (1.76  weight in kg) scribing exercise and measuring progress in patients’
+ 667 functional activity tolerance. A minimal change in
Troosters, Age range = 50 to 85 years of age walking distance of 54 to 70 meters has been shown to
1999 Expected 6 MWD = 218 + (5.14  height be clinically significant for improving functional
in cm — 5.32  age) — (1.80  weight in status for patients with chronic obstructive pulmonary
kg + (51.31  gender*) disease (COPD). For patients with congestive heart fail-
*male = 1, female = 0 ure (CHF), a minimal change in walking distance of
Gibbons, Age range = 22 to 79 years of age 43 meters resulted in improvement of quality of life
2001 Expected 6 MWD = 868.8 — (2.99  age)
— (74.7  gender*) for these patients.40,41
*male = 0, female = 1
Enright, Age range greater than or equal to 68 years
2003 of age CONCLUSION
Healthy women:
Expected 6 MWD = 493 + (2.2  height The use of functional tests is becoming more common
in cm) — (0.93  weight in kg) — among physical therapists in the acute care setting.
(5.3  age) With the profession moving into an era of evidence-
Healthy men: Add 17 meters to results of based practice, it is important to become aware of
above equation these effective, objective measures that can be used to
6 MWD, 6-Minute walk distance. determine the functional level of various patient popu-
Data from reference numbers 36-39. lations.The functional tests described in this appendix

offer objective, reliable, and valid measurement options
that examine the functional mobility of varying popu-
lations. In the current health care system, evidence-
based practice is required to survive the ongoing
References
1. Portney LG,Watkins MP (eds). Foundations of Clinical
Research Applications to Practice. Norwalk, CT:
Appleton & Lange, 1993;680, 689.
2. WeeJYM, Bagg SD, Palepu A.The Berg Balance
Scale as a Predictor of Length of Stay and
Discharge Destination in an Acute Stroke
Rehabilitation Setting. Arch Phys Med Rehabil
1999;80(4):448-452.
3. Thorbahn L, Newton R. Use of the Berg BalanceTest
to Predict Falls in Elderly Persons. PhysTher
1996;76(6):576-583.
4. Chou CY, Chien CW, Hsueh IP, et al. Developing a
Short Form of the Berg Balance Scale for People with
Stroke. PhysTher 2006;86:195-204.
5. Berg KO,Wood-Dauphinee SL,WilliamsJI, et al.
Measuring Balance in the Elderly:Validation of an
Instrument. CanJ Public Health 1992;83:S7-S11.
6. Berg K,Wood-Dauphinee S,WilliamsJI, et al. Measuring
Balance in the Elderly: Preliminary Development of an
Instrument. Physiother Can1989;41:304.
7. Nakamura DM, Holm MB,Wilson A. Measures of
Balance and Fear of Falling in the Elderly: A Review.
Phys OccupTher Geriatr 1998;15(4):17-32.
8. Conradsson M, Lundin-Olsson L, Lindelof N, et al.
Berg Balance Scale: intrarater test-retest reliability
among older people dependent in activities of daily
living and living in residential care facilities. PhysTher
2007;87:1155-1163.
9. Cattaneo D, Regola A, Meotti M.Validity of Six Balance
Disorders Scales in Persons with Multiple Sclerosis.
Disability and Rehabilitation, June 2006;28(12):789-795.
10. Whitney S, PooleJ, Cass S. A Review of Balance
Instruments for Older Adults. AmJ OccupTher
1998;52(8):666-671.
11. Posiadlo D, Richardson S.TheTimed ‘‘Up and Go’’:
A Test of Basic Functional Mobility for Frail Elderly
Persons. J Am Geriatr Soc 1991;39:142-148.
12. Thompson M, MedleyA. Performance of Community
Dwelling Elderly on theTimed Up and GoTest. Phys
OccupTher Geriatr 1995;13(3):17-30.
13. WhiteJ. Functional assessment toolsçuse them! Phys
Ther Case Rep 2000;3(4):188-189.
14. LargeJ, Gan N, Basic D, et al. Using theTimed Up and
GoTest to Stratify Elderly Inpatients at Risk of Falls.
Clin Rehabil 2006;20:421-428.
Functional Tests APPENDIX IX 567
changes in insurance reimbursement. These tests
are quick, effective measures that can objectively dem-
onstrate fall risk and progress with functional mobility
in the acute care setting.
15. Kristensen MT, Foss NB, Kehlet H.Timed ‘‘Up & Go’’
Test as a Predictor of Falls Within 6 Months After Hip
Fracture Surgery. PhysTher 2007;87:24-30.
16. Nordin E, Rosendahl E, Lundin-Olsson L.Timed ‘‘Up
& Go’’ Test: Reliability in Older People Dependent in
Activities of Daily LivingçFocus on Cognitive State.
PhysTher 2006;86(5):646-655.
17. Duncan PW,Weiner DK, ChandlerJ, et al. Functional
Reach: A New Clinical Measure of Balance. J Gerontol
1990;45:M192-M197.
18. Newton R. Reach in Four Directions as a Measure of
Stability in Older Adults. PhysTher 1996;76:S23.
19. Thapa PB, Gideon P, Fought RL, et al. Comparison of
Clinical and Biomechanical Measures of Balance and
Mobility in Elderly Nursing Home Residents. J Am
Geriatr Soc 1994;42:493-500.
20. Sherrington C, Lord SR. Reliability of Simple
PortableTests of Physical Performance in Older
People After Hip Fracture. Clin Rehabil
2005;19:496-504.
21. Billek-Sawbney B, GayJ.The Functional ReachTest;
Are 3 Trials Necessary? Topics in Geriatric
Rehabilitation 2005;21(2):144-148.
22. Umphred DA (ed), Neurological Rehabilitation (3rd ed).
St. Louis: Mosby, 1995;808-809, 812, 816-817, 822-823,
828-829.
23. Tinetti M. Performance Oriented Assessment of
Mobility Problems in Elderly Patients. J Am Geriatr
Soc 1986;41:479.
24. King MB, JudgeJO,Whipple L, et al. Reliability and
Responsiveness of Two Physical Performance Measures
Examined of a Functional Training Intervention. Phys
Ther 2000;80(1):8-16.
25. Anemaet W, Moffa-Trotter M. Functional tools for
assessing balance and gait impairments.Top Geriatr
Rehabil 1999;15(1):66-83.
26. Tinetti ME,WilliamsTF, Mayewski R. Fall Index for
Elderly Patients Based on Number of Chronic
Disabilities. AmJ Med 1986;80:429-434.
27. Woo MA, Moser DK, Stevenson LW, et al. Six-Minute
WalkTest and Heart RateVariability: Lack of
Association in Advanced Stages of Heart Failure. AmJ
Crit Care 1997;6(5):348-354.
28. Guyatt GH, Sullivan MJ,Thompson PJ, et al.The
6-Minute Walk: New Measure of Exercise Capacity in
568 APPENDIX IX Functional Tests
Patients with Chronic Heart Failure. Can Med AssocJ
1985;132:919-923.
29. Guyatt GH, Pugsley SO, Sullivan MJ, et al. Effect of
Encouragement onWalkingTest Performance.Thorax
1994;39:818-822.
30. KavanaughT, Myers MG, Baigrie RS, et al. Quality of
Life and Cardiorespiratory Function in Chronic Heart
Failure: Effects of 12 Months AerobicTraining. Heart
1996;76:42-49.
31. Kovar PA, AllegranteJP, MacKenzie CR, et al.
Supervised Fitness Walking in Patients with
Osteoarthritis of the Knee: A Randomized Controlled
Trial. Ann Intern Med 1992;116:529-534.
32. McGavin CR, Gupta SP, McHardy GJR.Twelve-Minute
WalkingTest for Assessing Disability in Chronic
Bronchitis. BMJ 1976;1:822.
33. Butland RJ, Pang J, Gross ER, et al.Two-, Six-, and
Twelve-Minute WalkingTests in Respiratory Disease.
BMJ 1982;284:1607.
34. Cahalin LP, Mathier MA, Semigran MJ, et al.The Six-
Minute WalkTest Predicts Peak Oxygen Uptake and
Survival in Patients With Advanced Heart Failure.
Chest 1996;110:310.
35. Laupacis A, Bourne R, Rorabeck C, et al.The Effect
of ElectiveTotal Hip Replacement on Health-
Related Quality of Life. J BoneJoint Surg [Am]
1993;75:1619.
36. Enright PL, Sherrill DL. Reference Equations for the
Six Minute Walk in HealthyAdults. AmJ Respir Crit
Care Med 1998;158:1384-1387.
37. TroostersT, Gosselink R, Decramer M. Six Minute
Walking Distance in Healthy Elderly Subjects. Eur
RespirJ 1999;14:270-274.
38. Gibbons WJ, Fruchter N, Sloan S, et al. Reference
Values for a Multiple Repetition 6-Minute WalkTest in
HealthyAdults OlderThan 20 Years. J Cardiopulm
Rehabil 2001;21:87-93.
39. Enright PL, McBurnie MA, Bittner V, et al.The
6 Minute WalkTest: a Quick Measure of Functional
Status in ElderlyAdults. Chest 2003;48(8):783-785.
40. Redelmeier DA, Bayoumi AM, Goldstein RS, et al.
Interpreting Small Differences in Functional Status:
The Six Minute WalkTest in Chronic Lung Patients.
AmJ Respir Crit Care Med 1997;155:1278-1282.
41. O’Keefe St, Lye M, Donnellan C, et al. Reproducibility
and Responsiveness Of Quality Of Life Assessment
And Six Minute WalkTest In Elderly Heart Failure
Patients. Heart 1998;80:377-382.
 Physical Therapy
Considerations for Patients
Appendix X Who Complain of Chest Pain
Michele P. West
Chest pain, a common complaint for which many
patients seek medical attention, accounts for approxi-
mately 7 million emergency department visits per
year in the United States of which 15% to 25% are diag-
nosed with acute coronary syndrome (ACS).1 Thus the
physical therapist in the acute care setting should be
familiar with the different etiologies of cardiogenic
and noncardiogenic chest pain and be competent
taking an efficient history when a patient complains of
chest pain.
Cardiogenic chest pain may be ischemic or nonis-
chemic. Ischemic chest pain may be caused by athero-
sclerosis, coronary spasm, systemic or pulmonary
hypertension, aortic stenosis or regurgitation, hypertro-
phic cardiomyopathy, or endocarditis.2 Nonischemic
chest pain may be owing to aortic dissection or aneur-
ysm, mitral valve prolapse, pericarditis, or myocarditis.2
(Refer to the Acute Coronary Syndrome section in
Chapter1for a description of stable, unstable, and variant
[Prinzmetal’s] angina and to Figure 1-10 for the possible
clinical courses of patients admitted with cardiogenic
chest pain.)
Noncardiogenic chest pain can arise from a wide
range of diseases and disorders, which makes the differ-
ential diagnosis of chest pain challenging. Afferent
fibers from the heart, lungs, great vessels, and esophagus
enter the same thoracic dorsal ganglia and produce an
indistinct quality and location of pain.3 With overlap-
ping of the dorsal segments, disease that is thoracic in
origin may produce pain anywhere between the jaw and
epigastum.3 Table X-1 describes the most common dif-
ferential diagnoses of noncardiogenic chest pain, each
with its own distinctive associated signs and symptoms.
Refer to Table 8-1 for gastrointestinal pain referral
patterns.
The mnemonic OLD CART can be used as a rapid
survey for the differential diagnosis of chest pain
during a physical therapy session4:
 Onset: Sudden versus insidious, with exertion or
stress versus rest? (Cardiogenic chest pain is usually
of sudden onset.)
 Location: Substernal or on the left side of the chest?
(Cardiogenic chest pain typically occurs in this
location, but can also present in any area above the
waist.)
 Duration: Lasts longer than 20 to 30 minutes?
(Cardiogenic chest pain related to stable angina
pectoris typically lasts 2 to 20 minutes, and pain
related to acute myocardial infarction usually lasts
30 minutes or slightly longer.)
 Characteristics: Pressure, tightness, or heaviness
versus other feelings, such as sharpness, or with
inspiration? (Cardiogenic chest pain is usually
described as chest pressure or heaviness unchanged
with respiration.)
 Accompanying symptoms: Associated with diaphor-
esis, nausea, dyspnea, or lightheadedness versus a
lack of these symptoms? (Cardiogenic chest pain
is typically associated with one or more of these
accompanying symptoms.)
 Radiation: Does the pain radiate to the arm(s),
shoulder(s), back, neck, jaw, or teeth? (Cardiogenic
chest pain can radiate widely.)
 Treatment: Relieved by rest, oxygen, or nitrogly-
cerin? (Cardiogenic chest pain is usually relieved by
these interventions.)
As this information is ascertained, the physical
therapist should discontinue the activity (if not resting)
and determine the need for seated or supine rest,
observe the patient for signs of altered cardiac output
569
570 APPENDIX X Physical Therapy Considerations for Patients Who Complain of Chest Pain

Table X-1 POSSIBLE ETIOLOGIES, PAIN PATTERNS, AND ASSOCIATED SIGNS OF NONCARDIOGENIC
CHEST PAIN

Pain Pattern and Associated Signs

Origin Possible Etiology and Symptoms
Pulmonary/ Pneumonia, pulmonary embolus, tuberculosis, Pain with respiration, of sudden onset, usually
pleural pleuritis, pneumothorax, mediastinitis well localized (lateral to midline) and
prolonged.
Pain is associated with abnormal breath sounds,
increased respiratory rate, cough, hemoptysis,
or pleural rub
Gastrointestinal Hiatal hernia, esophagitis, esophageal reflux or Pain is epigastric, visceral or burning in nature,
motility disorder, acute pancreatitis, peptic of moderate duration or prolonged, and is
ulcer, cholecystitis usually related to food/alcohol intake.
Pain is relieved by antacids, milk, or warm liquids
Nausea, vomiting, burping, or abdominal pain
may be present.
Musculoskeletal Muscle strain, rib fracture, costochondritis, Pain is achy, increased with movement of the
cervical disc disease, shoulder bursitis, or head/neck/trunk or upper extremity, or
tendonitis reproducible with palpation.
Signs of inflammation may be present, or there
may be a history of overuse/trauma.
Psychological Panic disorder Pain is often precordial with report of pain
moving from place to place, moderate duration
or situational, and unrelated to movement or
exertion.
Pain is associated with sighing respirations and
accompanied by other evidence of emotional
distress/disorder.
Infectious Herpes zoster (shingles) Burning itching pain that is prolonged and in a
dermatomal pattern.
Pain is localized with a vesicular rash in the area
of discomfort.
Data from Cannon CP, LeeTH. Approach to the Patient with Chest Pain. In P Libby, RO Bonow, DL Mann, et al. (eds), Braunwald’s Heart
Disease: A Textbook of Cardiovascular Medicine (8th ed). Philadelphia: Saunders, 2008; Goldman L. Approach to the Patient with Possible
Cardiovascular Disease. In L Goldman, D Ausiello (eds), Cecil Medicine (23rd ed). Philadelphia: Saunders, 2008.

(decreased blood pressure), take vital signs, and moni-
tor telemetry as appropriate. If the chest pain appears
cardiogenic, the physical therapist must determine
whether it is stable or unstable. During an episode of
unstable angina, an electrocardiograph may reveal ST
segment elevation or depression with or without
T-wave inversion that reverses when anginal pain
decreases.4 These electrocardiograph changes are
depicted in Figure X-1.Vital sign findings include:
 Hypotension or hypertension
 Bradycardia or tachycardia
 Irregular pulse
If the patient presents with one or more of these
unstable anginal findings, the therapist should stop or
defer treatment and immediately notify the nurse.
Regardless of the etiology of the patient’s complaint
of chest pain, the physical therapist must be prepared
to expedite a reliable chest pain description and
respond and/or refer accordingly for prompt medical
therapies or for further investigation of the cause of
noncardiogenic chest pain.
 Physical Therapy Considerations for Patients Who Complain of Chest Pain APPENDIX X 571

FIGURE X-1
Ischemic electrocardiographic changes.

References
1. Cannon CP, LeeTH. Approach to the Patient with Chest
Pain. In P Libby, RO Bonow, DL Mann, et al. (eds),
Braunwald’s Heart Disease: A Textbook of Cardiovascular
Medicine (8th ed). Philadelphia: Saunders, 2008.
2. Becker RC (ed). Chest Pain. Boston: Butterworth-
Heinemann, 2000.
3. BrownJE, Hamilton GC. Chest Pain. InJA Marx (ed),
Rosen’s Emergency Medicine: Concepts and Clinical
Practice (6th ed). Philadelphia: Mosby, 2006.
4. McAvoyJA. Cardiac Pain: Discover the Unexpected.
Nursing 2000;30:34.
This page intentionally left blank.
 Index
A Acetabular fracture, 94^95 Activity intensity, prescribing.
ABCD rule, 214^215 classification, 95f See Automatic implantable
Abdomen management, 140t cardiac defibrillator
auscultation, 298 occurrence, 94^95 beta blockers, impact, 33
physical examination, 298 physical therapy intervention, 140t Activity program, initiation, 31
Abdominal aneurysms, 234 Achalasia, 309 Activity tolerance, maximization, 31
Abdominal aortic aneurysm, surgical Acid-base balance (pH), 342 Acute adverse blood reactions, 253t
repair, 258f ABG analysis, 60 Acute bacterial prostatitis, 340
Abdominal binder, 130^131t ABG value, importance, 61^62b Acute care setting
wearing, 480^481b regulation, 328 introduction, 430
Abdominal bloating, 314 Acid-base disturbances medical-surgical equipment,
Abdominal contraction, 58^59 knowledge, 61 introduction, 441
Abdominal corset, support, 397b occurrences, 62b physical therapy, focus, 184
Abdominal distention Acid-base imbalance ROM values, applicability, 90t
impact, 312^313b causes, 61b Acute chest syndrome (ACS),
presence, 329^330 compensation, 60 245^246
Abdominal hernia, 312 correction, 60^61 Acute confusional state, 434
classification, 312 Acidemia, occurrence, 60 Acute contagious osteomyelitis, 365
Abdominal herniation, signs/ Acidosis, process, 60 Acute coronary syndrome (ACS), 21^22
symptoms, 312 Acid perfusion test, 303^304t diagnosis, 569
Abdominal incisions, impact, 255b ACL. See Anterior cruciate ligament usage, 21^22
Abdominal quadrants, viscera, 301f Acquired factors, 356t Acute demyelinating
Abdominal tenderness, palpation, Acquired immunodeficiency polyneuropathy, 175
298^299 syndrome (AIDS) Acute gastritis, etiology, 310
Abducens nerve, 167^169t complications, 368t Acute gastroenteritis, management, 366
ABG. See Arterial blood gas onset, 366 Acute glomerulonephritis, signs/
ABI. See Ankle-Brachial Index Acromegaly symptoms, 335
Ablation procedure, 28^29 management, 383^384 Acute hemarthrosis, 248
Abnormal breath sounds, 55^56 signs/symptoms, 383 Acute hematogenous osteomyelitis, 365
Abnormal heart sounds, 12t ACS. See Acute chest Acute illness, alcohol/drug abuse
Abnormal muscle tone (grading), syndrome; Acute coronary (impact), 435
Modified Ashworth Scale syndrome Acute inflammatory demyelinating
(usage), 171t ACTH. See Adrenocorticotropic polyradiculopathy, 189^190
Above elbow amputation, 547t hormone Acute kidney failure (AKF), 333^334
Above the knee amputation, 545t Activated partial prothrombin time Acute osteomyelitis, clinical
Absence seizure, 185t (APPT), 232t presentation, 365
Absolute neutrophil count (ANC), Active abduction/flexion, limitation, 111 Acute pancreatitis
205^206b Active assisted ROM, 104 management, 318
level, 247 Active-assistive ROM, performing, signs/symptoms, 318
monitoring, 417 108^109b Acute pericarditis, 18
ACA. See Anterior cerebral artery ActiveTB, development, 362 Acute peripheral edema, presence/
ACD. See Anemia of chronic diseases Activities of daily living (ADLs) history, 222
ACE. See Angiotensin converting impact, 122 Acute pulmonary rejection, clinical
enzyme movement precautions, 104^105 manifestations, 417^418
Acetabular components, cementing Activity/exercise, stable/unstable Acute pyelonephritis, 335
options, 103 responses (determination), 33f cystitis, association, 335

Page numbers followed by f indicate figures; t, tables; b, boxes.

573
574 INDEX

Acute quadriplegic myopathy, 434^435
Acute rejection
signs, 404^405
treatment, potential.
See Organ transplantation
Acute renal failure (ARF), 333^334
clinical manifestations, 334
diuretic phase, 334
indication, 329
late/recovery period, 334
management, 334
mortality rate, 334
oliguric/anuric phase, 334
stages, 334
Acute rheumatic fever, clinical sequela, 363
Acute steroid myopathy, 434^435
Acute tubular necrosis (ATN), 334
incidence, 407
Acute vestibular neuronitis (vestibular
neuritis), 186^187
Adaptive support ventilation, 467^468t
Adenocarcinomas, 311
ADH. See Antidiuretic hormone
Adjustable gastric banding, 319^320t
Adjuvant treatment, 204
ADLs. See Activities of daily living
Admission note format.
See Medical record
Adrenal cortical hormones, evaluation,
386^387
Adrenal disorders, 388
Adrenal gland, 386^395
function, 386
hormones, target
sites/actions, 386t
Adrenal hyperfunction, 388
Adrenal insufficiency, 388
management, 388
symptoms/physical findings, 388
Adrenal tests, 386^388
Adrenergic agonists, 489^491t
Adrenergic antagonists, 489^491t
Adrenocortical steroids
(glucocorticoids), 496t
Adrenocorticotropic hormone (ACTH)
increase, 384^385
levels, examination, 387
overproduction, 384^385
stimulation test, 384t
test, 384t
Adrenocorticotropin, 383t
Adult manual breathing unit (AMBU)
bag, 471
Adult-onset diabetes. SeeType 2 diabetes
Adult RA, 375
Adult respiratory distress syndrome
(ARDS), 62, 76, 318
characteristics, 76
exudative phase, 76
Adult respiratory distress syndrome Alveolar membranes, breakdown, 49
(ARDS)çContinued Alveolar walls, progressive
latent pulmonary sequelae, 76 destruction, 73
proliferative stage, 76 Amantadine, 506^507t
Adventitious breath sounds, 56 AMBU. See Adult manual breathing unit
AFO. See Solid ankle-foot orthosis Amebic meningoencephalitis,
Afterload, 4 transmission, 364
CO factor, 4 Amenorrhea, 383, 385
AICA. See Anterior inferior American Physical TherapyAssociation.
cerebellar artery See Guide for Professional
AICD. See Automatic implantable Conduct and Code of Ethics
cardiac defibrillator American Spinal InjuryAssociation
AIDS. See Acquired immunodeficiency (ASIA), 177
syndrome AmericanThoracic Society Dyspnea
Air, rapid expulsion, 58^59 Scale, 53t
Air entrainment mask, 446t Aminoglycosides, 517^520t
example, 447f Ammonia (NH3) test, 305^306t
Airspace consolidation, 62 Amnion graft, 274t
Air trapping, 70 Amorphous dressing, 291^292t
Airway pressure release ventilation Amputation. See Lower extremity;
(APRV), 467^468t Upper extremity
Airways level, 544f
dilatation, 73 physical therapy
monitoring, 99^100 considerations, 548t
AKF. See Acute kidney failure intervention, 543
Alanine aminotransferase (ALT) test, psychological impact, 548t
211, 299, 305^306t treatment suggestions, 548t
Albumin-rich fluid, weeping, 411b Amylase. See Serum amylase;
Alcoholic cirrhosis, impact. Urine amylase
See Liver failure Amylin analog, 526^528t
Aldosterone. See Mineralocorticoids Amyloidosis, 213, 314, 374^375
Alert and oriented to person, place, and clinical signs/symptoms, 375
time (A&Ox3), 163b management, 375
Alertness, appearance/level, 53 rarity, 374^375
A-line. See Arterial line Amyotrophic lateral sclerosis
Alkalemia, occurrence, 60 (ALS), 187^189
Alkaline phosphatase (ALP), 211, 410 progressive degeneration, 187^189
test, 305^306t Anastomosis, 413^414
Alkalosis, process, 60 ANC. See Absolute neutrophil count
Alkylating agents, 509^511t Androgens, 387, 386t
Allen’s test, 225^226t levels, measurement, 387
Allergic rhinitis, 360 Anemia, 243^246
clinical manifestations, 361 description, 243
management, 361 postoperative phase, 532
AlloDerm, usage, 228t RBC decrease, 243
Allogenetic transplant, usage, 419 Anemia of chronic diseases (ACD), 246
Allogenic graft, 274t clinical features, 246
Allograft function, 403 occurrence, 246
ALP. See Alkaline phosphatase Anesthesia. See General anesthesia;
Alpha1-antitrypsin deficiency, 416 Regional anesthesia
Alpha-1 blockers, 516t administration, 531
Alpha-glucosidase inhibitors, 526^528t intraoperative effects, 531^532
ALS. See Amyotrophic jackknife position, 533f
lateral sclerosis lithotomy position, 533f
ALT. See Alanine aminotransferase operative positioning, 534
Alveolar-capillary interface, availability, 49 postsurgical complications, 532^534
Alveolar-capillary membrane prone position, 533f
oxygen, movement, 441 supine position, 533f
shearing, 77 types, 531

Aneurysmal sac, incision, 258f
Aneurysms, 234^235.
See also Cerebral aneurysm; False
aneurysms;True aneurysms
clinical manifestations, 234^235
clipping, 194t
focal signs, 183t
graft replacement, 235
ischemic manifestations, 234
localized dilatation/outpouching, 234
repair/reconstruction, 255
surgical resection, 235
Angina. SeeVariant angina
equivalents, 7
instability, 18
stability. See Stable angina
Angina-like chest pain, 309
Angiography, 20, 174. See also Digital-
subtraction angiography
radiopaque contrast material,
injection, 20
Angiotensin converting enzyme (ACE)
inhibitors, 489^491t
Angiotensin II receptor blockers
(ARBs), 489^491t
Ankle-Brachial Index (ABI), 225^226t
Ankle disarticulation. See Syme’s
amputation
Ankle fractures, 97^98
medical-surgical management, 145t
physical therapy intervention, 145t
results, 98
Ankle stirrup, 130^131t
Ann Arbor classification, 212. See also
Lymphomas
Anorectal disorders, 315
Anoscopy, 303^304t
Antacids, 512^513t
Antagonists, impact, 509^511t
Anterior cerebral artery (ACA), 159t
Anterior cruciate ligament (ACL) repair,
124
Anterior horn, motor cells, 187^189
Anterior inferior cerebellar artery
(AICA), 159t
Anterolateral thoracotomy, 416
Antianxiety medications, 501t
Antiarrhythmic agents, 486^487t
Antibiotic-resistant infections, 359^360
Antibiotics, 517^520t
misuse, 358
Antibody
development, 357
measurement, 357
responses, assessment, 354
term, 355t
Anticholinergics, 497^498t
usage, 506^507t
Anticoagulants, 488t
INDEX 575
Anticoagulation agents, ARBs. See Angiotensin II receptor
discontinuation, 251 blockers
Anticoagulation therapy ARDS. See Adult respiratory distress
INR goal, 251 syndrome
physical therapist understanding, 251 ARF. See Acute renal failure
Anticonvulsants, 502t Arginine test. See Growth hormone
Antidepressants, 503^504t stimulation test
Antidiarrheal medications, 513t Arterial abnormalities, sites, 180f
Antidiuretic hormone (ADH) Arterial blood gas (ABG)
(vasopressin), 383t analysis, 59^60
overproduction, 385 interpretation, 60^62
Antiembolic exercises, 105 ability, 60
patient instruction, 108 measurements, 16
Antiemetic medications, 508t performing, 60
Antiemetics, prescribing, 205b usage, 16
Antifungal agents, 520t normal values, 60
Antigen, term, 355t terminology, 60
Antihistamines, 497t Arterial blood pressure
Antihypertensive agents, 489^491t elevation, 236
Antilymphocyte globulin, usage, regulation, 328
405^406 Arterial circle of Willis, schematic
Antimetabolites, 509^511t representation, 158f
Antiplatelet agents, 493t Arterial damage, 93
Antipsychotics, 505t Arterial disorders, 231^240
Antiretroviral medications, 522^524t clinical findings, comparison, 232t
Antispasmodic medications, 513t risk factors, 231^233
Antithymocyte globulin, usage, 405^406 venous disorders, combination, 243
Antitubercular agents, 521^522t Arterial emboli, impact, 236
Antitumor antibiotics, 509^511t Arterial insufficiency wounds, 279
Antiviral medications, 524^525t result, 279
Anuria, 329 Arterial line (A-line), 449^450t
Aorta tracing, 451f
coarctation, 238t usage, 414
MRA, 228f Arterial pulses, 10f
Aortic dissection, 235 Arterial thrombosis, 235
cause, 235 occurrence, 235
Aortic valve, 3t Arterial walls, elasticity, 9^11
Aortic valve replacement (AVR), 30 Arteries, structure, 221f
Aortobifemoral bypass, 256f Arteriovenous (AV) graft/fistula, 454t
Aortobifemoral grafts, 255b Arteriovenous malformation (AVM), 174,
Aortofemoral graft, 257f 181, 243
Aortography, 20 occurrence, 181
Aortoiliac bypass, 256f signs, 243
A&Ox3. See Alert and oriented to Arthrography, 92
person, place, and time Arthroscopic surgery, commonness, 124
Aplasia. SeeThyroid gland Arthroscopy, complications, 124b
Aplastic anemia, 245 Ascites, presence, 411b
characterization, 245 ASIA. See American Spinal Injury
management, 245 Association
signs/symptoms, 245 Aspartate aminotransferase (AST),
Apligraf, 292 211, 299
Appendectomy, 319^320t test, 305^306t
Appendicitis, 311 Assist/control ventilation, 466t
signs/symptoms, 311 Assisted ventilation, history, 52
Appendix, inflammation, 311 Asthma, 70
APPT. See Activated partial prothrombin exacerbation, characteristics, 70
time ATC. See Automatic tube
APRV. See Airway pressure release compensation
ventilation Atelectasis, 73
576 INDEX
Atherosclerosis, 231^234
characterization, 231
clinical manifestations, 233
risk factors, 233t
signs/symptoms, 233
Atherosclerotic damage. See Collagen;
Elastin
Atonic seizure, 185t
Atrial depolarization, 4
Atrial diastole, 2
Atrial fibrillation, 35
catheter ablation procedures,
indication, 28
irregular rhythm, 43f
P waves, normality (absence), 43f
surgical ablation, 28^29
Atrial flutter, 35
catheter ablation procedure,
indication, 28
rhythm, consideration, 42f
Atrial kick, 3^4
Atrial rhythms, ECG characteristics/
causes, 18t
Atrial systole, 3^4
Atrioventricular (AV) blocks, ECG
characteristics/causes, 41t
Atrioventricular (AV) disorders, 29
Atrioventricular (AV) nodal reentrant
pathways, catheter ablation
procedures (indication), 28
Atrioventricular (AV) node, 4
conduction, 486^487t
Atrophy, observation, 223
Atypical antipsychotics, 505t
Aura, 185^186t
Auscultation, 11^12, 55^57
accuracy, ensuring, 57b
landmarks. See Lungs
process, 55
systematic/cephalocaudal
fashion, 55
Auscultatory areas, coverage, 11^12
Autograft, 274t
Autoimmune dysfunction, 388
Autologous chondrocyte implantation
procedure, 128f
Autologous transplant, usage, 419
Autolytic debridement, 289
Automated PD, 342
Automatic implantable cardiac
defibrillator (AICD)
activity intensity, prescribing, 33
usage, 30
Automatic tube compensation
(ATC), 470
Autonomic dysreflexia, 179^180b
Autonomic nervous system, 158
neuropathy, 281
Autonomic neuropathy, 393
Auto positive end-expiratory pressure
(Auto PEEP), 466^468
AV. See Arteriovenous; Atrioventricular
Avascular necrosis (AVN), 91, 94
AVM. See Arteriovenous malformation
AVR. See Aortic valve replacement
Axial flow pumps, 479
Axillary nerve, 160t
Axillobifemoral bypass, 256f
Azathioprine, usage, 405t
Azoles, 520t
B Berger’s disease. See Immunoglobulin
Babinski skin, observation, 172b
Back pain, indication. See Spinal surgery
Bacteremia, 369
Bacterial cellular metabolism,
inhibition, 521^522t
Bacterial meningitis, 364
Bacteriuria, 331t
Balloon, proximal slippage, 474
Balloon inflation, 473
Balloon kyphoplasty, 123f
Bariatric procedures, 320f
Barium enema (BE), 303^304t
Barium swallow, 303^304t
Baroflexes, activation, 6
Barotrauma, 468^470
definition, 468
Barrett’s esophagus, 309
chronic GERD association, 309
Barrier thickness, 49
Basal cell carcinoma, 214
risk factors, 214
Baseline HR, consideration, 33
Baseline pupil changes, observation,166b
Baseline sputum production
documentation, 81
history, 53
Basilar artery, 159t
Basophils, 357
BBS. See Berg Balance Scale
BE. See Barium enema
Bed-bound patients, 280
Bed mobility, 90^91
Bed rest, effects. See Prolonged bed rest
Behavior modification, patient/family
education, 31
Below elbow amputation, 547t
Below the knee amputation, 545t
Benign MS, 192b
Benign positional paroxysmal vertigo
(BPPV), 186^187
characterization, 187
Benign prostatic hyperplasia (BPH),
339^340
enlargement, 339^340
management, 340
signs/symptoms, 339^340
Benign prostatic hypertrophy (BPH)
therapy, 516t
Benign tumors, classification, 200t
Benzamides, 508t
Benzodiazepines, 501t
Berg Balance Scale (BBS), 555
example, 556^560f
overview, 560t
procedure, 555
results, interpretation, 555
short form, 560b
development, 555
A nephropathy
Beta2 agonists, 497^498t
Beta blockers, 489^491t
Biguanides, 526^528t
Bilateral anterior thoracotomy, incision
(usage), 416
Bilateral cutaneous ureterostomies, 348f
Bilateral lung transplantation, 416
Bilateral ROM, evaluation, 89
Bilateral total hip arthroplasty, 103f
Bilateral upper-extremity strength,
maintenance, 115
Bilateral ventricular assist device
(BiVAD), 479
Bilateral vestibular hypofunction
(BVH), 187
Bile acid sequestrants, 493^495t
Biliary atresia, 408
Biliary disorders, 316
Biliary systems
diagnostic procedures, 307t
laboratory tests, 305^306t
Biliary tract, cancer, 211
Bilirubin test, 211, 305^306t
Bilirubinuria, 331t
Billroth I/II, 319^320t
Biobrane, usage, 228t
Biochemical markers, 15^16
list, 16t
Biological fixation, advantage, 103
Biologicals, usage, 292
Biologic response modifiers, 509^511t
Biologic valves, usage, 30
Biopsies, 333. See also Needle biopsy
Biosynthesis, inborn deficiencies, 380
Biotherapy, 203. See also Cancer
BiPAP, 446t
Bipolar prosthesis, components, 103
Bisphosphonate supplementation, 397
BiVAD. See Bilateral ventricular
assist device
Biventricular synchrony, improvement,
29
Bladder
biopsies, 333
distention, 330
 INDEX 577
BladderçContinued Body position, changes, 163b BrainçContinued
drainage Body systems, cancer, 206^215 blood supply, 159t
complications, 412 Body temperature maintenance, 272 death, 433
contrast. See Enteric drainage Body tissue destruction, occurrence, 222 diagnosis, 433
disadvantage, 411^412 Bone marrow division, 152
examination, 333 evaluation, 91 herniation, 193t
inflammation, occurrence, 339 harvesting injury, indication, 171^172
irritation, 411^412 multiple aspirations, usage, 420 posterior circulation, 159t
removal, 347 procedure, 420 protective mechanisms, 152^156
x-ray, 332 malignant cells, occupation, 211 stem, structure/function/dysfunction,
Bladder neck suspension, 333 Bone marrow transplantation (BMT), 155^156t
procedure, 347 419^421 tissues, inflammation, 364
Blood-brain barrier, 156 complications, 421 tumor, diagnosis, 175
physiologic mechanism, 156 contraindications, 420 ventricular system, 158f
Blood cell types, 221t graft disease, host disease Breast cancer, 208^209
Blood clotting time information, 14 (complication), 421 prevalence, 208^209
Blood functions, 222t indications, 419 stages, 209t
Blood glucose concentrations, patient preparation, 420 surgical interventions, 209t
paradoxical elevation, 526 postprocedure care/complications, Breathing, monitoring, 99^100
Blood glucose finger stick 420^421 Breathing patterns, description/
samples, 390t recipients conditions, 54t
Blood lipids, 15 fatal infection, risk, 420^421 Breath sounds, 35, 55. See also Abnormal
analysis, 15 physical therapy, 421 breath sounds; Normal
Blood pressure (BP), 4, 9^11, 356 physical therapy, benefits, 421 breath sounds
change, 471 types, 419 findings, 56^57
control, ICP treatment option, 194t Bones terminology, variation, 56b
measurement, 9^11 displacement, assessment, 176 Bridge to heart transplantation
monitoring, 408b healing (BTT), 479
ranges, 10t contributing factors, 94t Bridge to recovery (BTR), 479
Blood products occurrence, 93 Broad-spectrum antibodies, usage, 358
clinical indications/outcomes, primary tumors, 208b Bronchial artery enlargement, 73
252^253t scan, 91 Bronchial dilatation, 73
transfusion, 251^254 Bone tumors, 208 Bronchial gland, hypertrophy, 73
Blood reactions. See Acute adverse blood treatment, 116 Bronchial mucosa inflammation/
reactions Bony abnormalities, presence, 57^58 thickening, 70
Blood reservoir, 264 Bony landmarks, assistance, 50^51f Bronchial smooth muscle
Blood transfusion, 251 Bony skeleton, 88 constriction, 70
complications, 251^254 Borg’s Rating of Perceived Exertion Bronchial sounds, 55
Blood urea nitrogen (BUN), 332 (RPE), 17^18 Bronchial walls, inflammation, 73
increase, 405 proposal/evolution, 34^35 Bronchiectasis, 73
Blood vessels usage, 18 characteristics, 73
characteristics, 220t BP cuff, 448^449t Bronchiolar lavages, usage, 418
function, 221 BPH. See Benign prostatic hyperplasia; Bronchiolar walls, inflammation, 73
laceration, 93 Benign prostatic hypertrophy Bronchoconstriction, protective
layers, 220t BPPV. See Benign positional paroxysmal reflex, 49
Blood viscosity, exercise-related vertigo Bronchodilators, 497^498t
decreases, 14 Brace immobilizer, usage, 108^109b Bronchoplastic resection, image, 80f
Blood volume, regulation, 328 Braces, 127^128 Bronchoplasty, 80
Blunt injuries, 177t acute care setting, 130^131t Bronchopulmonary hygiene, 81^83
BMI. See Body mass index medical/surgical intervention care plan, development, 81
BMT. See Bone marrow transplantation techniques, combination, component, 58^59
Bodily fluid 127^128 concepts, implementation, 81^83
excess, occurrence, 437 Brachial artery impact, 418^419b
loss, 437 bell placement, 10 programs, 47
Bodily water, loss, 437 sheath insertion, 27 therapists, involvement, 63b
Body cast, 129t Brachytherapy, 204^205 tolerance, monitoring, 81
Body fluid examination, 358 Brain, 152^157 usage, 471
Body mass index (BMI), 315 anterior circulation, 159t Bronchopulmonary tree,
Body plethysmography, 65 attack, 180 visualization/aspiration, 63^64
578 INDEX

Bronchoscope lung biopsy, BurnsçContinued CancerçContinued

usage, 418 surgical procedures, 273^274 sites, risk factors, 202t
Bronchoscopy. See Flexible treatment, temporary/permanent skin surgery, 203^204
bronchoscopy substitutes, 275t term, usage, 199^200
performing, 64b Burns injury treatment protocols, 203
Bronchospasm, 70 acute care management, 268^275, Candida albicans, 358
Bronchovesicular sounds, 55 269^275 Cannabinoids, 508t
Broviac catheter, 454t admission guidelines, 269 Capillary refill time, 225^226t
Bruits, presence, 223 body temperature maintenance, 272 Capreomycin, 521^522t
BTR. See Bridge to recovery depth, 271f Carbapenems, 517^520t
BTT. See Bridge to heart transplantation emergency room management, Carbidopa, 506^507t
Buck traction, 132t objectives, 269^270 Carbohydrate antigen, 305^306t
Budd-Chiari syndrome, 408 extent, Rule of Nines assessment, 269f Carbon dioxide (CO2)
Buerger’s disease. SeeThromboangiitis fluid resuscitation, 272 arterial levels, 48^49
obliterans infection control, 272 decrease, 23
Bulk-forming laxatives, 515t pain management, 272^273 impact, 6
BUN. See Blood urea nitrogen patient treatment concepts, 277^279 retention. See Chronic carbon dioxide
Burkitt’s lymphomas, 211^212 physical therapy considerations, 278t retention
Burns physiologic sequelae, 264^265 clinical presentation, 62b
assessment, 268^275 schematic representation, 266f Carbonic anhydrase inhibitors,489^491t
care. See Initial burn care preferred positions, 279t Carbon monoxide (CO)
history, 275^276 resuscitative phase, 269^273 inhalation, 272
physical therapy examination, burn care, 272^273 poisoning, 270^272
275^277 systemic complications, 267t Carcinoembryonic antigen (CEA),
classification, 268^269 Burr hole, 194t 302^303t
cleaning/debridement, 274^275 Burst fracture, 99f Cardiac abnormalities, sites, 180f
depth Busipirone, 501t Cardiac arrest, 222
assessment, 269 Butyrophenones, 508t Cardiac catheterization, 20
characteristics, 271t BVH. See Bilateral vestibular classification, 20
description, 269 hypofunction Cardiac conduction system, 4
dressing, 276t CO factor, 4
extent, assessment, 268 C Cardiac cycle, 2^4
Lund and Browder method, 270t CABG. See Coronary artery bypass graft Cardiac decompensation, signs/
extremity strength, 277 CAD. See Coronary atherosclerotic symptoms (recognition), 35
function, 264, 264 disease Cardiac disease, family history, 7
functional mobility, 277 Cadaveric donors, 402 Cardiac dysfunction
inspection/palpation, 276 donation, insufficiency, 402 patient response, instability, 31^32
introduction, 263 living donors, contrast, 407 patient stability, 31
management, reparative phase, matching, 403 treatment concepts, 31^35
273^275 renal transplantation, 407 unstable responses, 31
neutralization, 273 Calcaneal fractures, 98 Cardiac echo. SeeTransthoracic
nonsurgical procedures, 274^275 association, 98 echocardiography
pain management, 146t Cardiac function posttransplant,
assessment, 276^277 physical therapy intervention, 146t indication, 414
control, 276^277 Calcimimetic, 529t Cardiac impairments, physicaltherapy
pathophysiology, 264^268 Calcitonin supplementation, 397 intervention (indication), 30^31
physical therapy goals, time frame, Calcium alginates, 291^292t Cardiac index (CI), 4
278 Calcium-channel blockers, 489^491t Cardiac infections, 363
physical therapy intervention, Calcium oxalate kidney stones, 337 manifestations, 363
277^279 Caloric testing, 188^189t Cardiac medications, 30
goals, 277 Cancer. See Body systems classification, 30
physiologic events, 264^265 biotherapy, 206 Cardiac muscle biopsy, 20
reevaluations, 278 diagnostic tests, 203t Cardiac output (CO), 2
ROM, 277 etiologies, 201t calculation, 4
involvement, 277 physical therapy, 215 description, 4
scar, 273 goals, 215 factors, 4
shock, 272 guidelines, 215^216 Cardiac pacemaker
sites, tissue healing, 284 radiation, usage, 204^205 classification, 29t
structure, 264, 264 sequelae, 215^216 function, critical aspects, 29^30

Cardiac pacemakerçContinued
implantation, 29^30
temporary pacing, performing, 29
Cardiac reflexes, 6
CO factor, 6
Cardiac risk factors
presence, 7
primary/secondary prevention, 8t
Cardiac status, decline (examples), 35
Cardiac studies/procedures, 7^8
Cardiac system
function, 2^7
infections, 363
structure, 2
Cardiac system, introduction, 1^2
Cardiac transplantation, 30, 413^416
acute rejection, objective
characteristics, 415^416
complications, 414^416
potential, 414
contraindications, 413
indications, 413
intervention, acceptability, 30
positive-pressure flow rooms,
recommendation, 415^416b
postoperative care, 414^416
pretransplantation care, 413
recipients
cardiac tamponade, risk
(increase), 415
postoperative bleeding, risk
(increase), 415
renal insufficiency,
preexistence, 414^415
resting heart rate, 415^416b
variable global myocardial
depression, manifestation, 414
Cardiogenic chest pain, 569
Cardiogenic pulmonary edema,
occurrence, 76
Cardiogenic syncope, 186
Cardiomyopathies, 24t
Cardiopulmonary assist devices, 473, 475
Cardiopulmonary support, 475
indications, 475
Cardiopulmonary support (CPS), 473
Cardiovascular disease (CVD), types, 1
Cardiovascular involvement, extent, 235
Cardiovascular/pulmonary disorders,
primary prevention/risk
reduction, 1
Cardiovascular system
function, 2^7
pumping force, 1
tables, 486
Cardiovascular system,
deconditioning, 132
Caregiver environment, safety, 430^431
guidelines, 430^431
Carotid noninvasive studies, 174
Carotid ultrasound, 174
Carpal fractures, 102
reasons, 102
Carrier, term, 355t
Casts
circumferential rigid dressing,
124^125
complications, 125^127
dryness, 127b
rigidity, 127b
types, 99f
usage, 124^127
Catecholamines, 387
Catechol-O-methyltransferase (COMT)
inhibitors, 506^507t
Catheter ablation procedures,
indication, 28
Catheter-based firbinolysis, 181
Catheterization. See Left-sided
catheterization; Right-sided
catheterization
CAUTION, cancer signs, 201
CAVH. See Continuous arteriovenous
hemofiltration
Cavitary lesions, surgical
intervention, 362
CBC. See Complete blood cell
CBF. See Cerebral blood flow
CCU. See Coronary care unit
CD4+
receptors, 366
Tcell counts, decline, 366
T-lymphocyte counts, 367
CEA. See Carcinoembryonic antigen;
Cultured epidermal autograft
Celiac sprue, 314
Cellular debris, presence, 77
Cellular waste products, excretion, 328
Cellulitis, 365
manifestations, 365
presence, 223
Cemented prosthesis, usage, 103
Centers for Medicare and Medicaid
Services (CMS), wet-to-dry
dressings (statements), 289
Central brain systems, 156^157
Central DI, 386
Central line (venous line), 454t
Central nervous system (CNS), 152^157
components, 152
diabetes, impact, 281
diseases. See Degenerative central
nervous system diseases
tables, 499^501
Central neural blockade, 539t
Central vestibular pathology,
symptoms, 189t
Cephalosporins, 517^520t
INDEX 579
Ceramic-on-ceramic implant, 102^103
Cerebellum, structure/function/
dysfunction, 155^156t
Cerebral aneurysm, 181, 234
description, 181
Cerebral angiography, 175
radiographic visualization, 175
Cerebral blood flow (CBF), 174
Cerebral concussion, 178t
Cerebral contusion, 178t
Cerebral hemispheres, structure/
function/dysfunction, 154t
Cerebral laceration, 178t
Cerebral perfusion pressure (CPP),
192^193
neurosurgical procedures, 193^195
pharmacologic therapy, 193
physical therapy intervention, 195
Cerebrospinal fluid (CSF)
flow, 153
ICP treatment options, 194t
leak, 184^185
management, 184^185
pressure, 192
Cerebrovascular accident (CVA),
180^181. See also Hemorrhagic
CVA; Ischemic CVA;
Lacunar CVA
characterization, 180
description, 181
experimental treatment options, 181
neurologic signs, association, 182t
risk factors, 180^181
signs/symptoms, 181
Cerebrovascular disease/disorders,
180^183
Cerebrum, horizontal section, 153f
Ceruloplasmin, 305^306t
Cervical fracture, description/
management, 99^100
Cervical spine fracture
breathing, close monitoring, 99^100
clearance, 99^100b
management, 147t
physical therapy intervention, 147t
Cervical traction, 132t
CF. See Cystic fibrosis
Chair-bound patients, 280
Chemical burns, 269, 268
Chemical control. See Respiratory system
Chemical exposure, 430
Chemoreceptors, location, 6
Chemotherapeutic agents
toxicity, 205^206b
types, 205
Chemotherapy, 203, 205^206
nausea/vomiting, 205^206b
purpose, 205
usage, 509^511t
580 INDEX

Chest drainage system, 461f
Chest expansion, symmetry
(relationship), 58
Chest pain
complaints
commonness, 569
etiology, 570
Chest pain, presence, 7
Chest radiograph, posteroanterior
view, 62f
Chest radiography, 16
order, 16
Chest tube, 454t
Chest wall
expansion, observation, 57b
motion, palpation, 57f
restrictions, 79
Chest x-ray (CXR)
chest structures, appearance, 63
classification, 63
indications, 62^63
interpretation, 62
formation, 63
types, 63
CHF. See Congestive heart failure
Cholecystectomy, 319^320t
Cholecystitis, 317^318
management, 318
signs/symptoms, 317^318
Cholelithiasis, 317^318
Cholestasis, 301
Cholesterol absorption inhibitor,
493^495t
Cholesterol embolization, 474
Chordae tendineae, 3t
Chronic bacterial prostatitis, 340
Chronic bronchitis, 70
acute exacerbation, definition, 70
Chronic carbon dioxide retention,
441^445
Chronic erosive gastritis, etiology, 310
Chronic glomerulonephritis, 336^337
management, 336
signs/symptoms, 336
Chronic illness, alcohol/drug abuse
(impact), 435
Chronic intermittent hemodialysis,
requirement, 342
Chronic nonerosive gastritis,
etiology, 310
Chronic obstructive pulmonary disease
(COPD), 70
carbon dioxide, respiratory stimulant
effects (desensitization), 441^445
value, prediction, 416
Chronic osteomyelitis, 365
Chronic pancreatitis, 314
Chronic peripheral edema,
presence/history, 222
Chronic pyelonephritis, 332, 335, 406 Colonization, term, 355t
Chronic rejection. See Organ Colonoscopy, 303^304t
transplantation Colony-stimulating factors, 512t
Chronic renal failure (CRF), 334^335 usage, 206
conservative management, 334 Color duplex scanning/imaging, 227t
management, 334 Colostomy, 319^320t
reduction, 334 Coma, 317, 433
result, 334 diagnosis, 433
Chronic respiratory diseases, 81 management, 317
Chronic swollen limbs, 242 signs/symptoms, 317
Chronic venous insufficiency, 221^222 Comfort measures only (CMO), 433
Chronic wounds, 283 Comminuted fracture, 92
CI. See Cardiac index Commode chair, usage, 105b
Cidofovir diphosphate, 524^525t Communicable, term (usage), 355t
CIM. See Critical illness myopathy Communicating hydrocephalus, 184
CIP. See Critical illness polyneuropathy Co-morbidities, 315
Circulation quality, pulses, 8 Compartment syndrome, 93,
Circulatory assist devices 128^132, 240
design, 473 condition, 240
physical therapy considerations, impact, 132
481^482 management, 240
Circumferential burns, 224 neurovascular compromise, 125
Cirrhosis, 316^317 occurrence, 240
characterization, 316 symptom, 240
etiologies, 316 Complete blood cell (CBC) count, 14,
management, 317 227^228
CK. See Creatine phosphokinase interpretation, 230t
CK-MM. See Creatinine phosphokinase monitoring, 258
Clamshell incision, creation, 416 shorthand format, 231f
Clavicle, fractures, 100 values, 14, 230t
Clonic seizure, 185t Completed stroke, 181t
Closed face mask, 442^444t Complete fracture, 92
example, 444^445f Complex partial seizure, 185t
Clostridium difficile, 359t Complex regional pain syndrome
CMO. See Comfort measures only (CRPS), 239^240
CMV. See Cytomegalovirus rarity, 239
CN. See Cranial nerves stages, Steinbrocker
CNS. See Central nervous system classification, 240
CO. See Cardiac output symptom, 239
Coagulation factors, 410 Compliance level, notation, 428
test, 211 Composite skin graft, 274t
Coagulation level, subtherapeutic/ Computed tomography (CT), 91, 174
supertherapeutic noninvasive vascular studies, 227t
implication, 251 scan, 333
Coagulation profiles, 14^15, 229^231 successive x-ray films, series, 174
blood clotting time information, 14 tests, 307t
tests, 232t Computerized tomographic pulmonary
Coagulation zones, 265f angiography (CT-PA),64^65
location, 264 invasiveness, 64^65
Cobalt alloys, 102^103 COMT. See Catechol-O-
Cognition, 163 methyltransferase
Cognitive function, tests, 165t Concentration gradient, 49
Cognitive testing, 163 Condom catheter (Texas catheter), 454t
Colectomy, 319^320t Conduction disturbance, 22
Collagen Confidentiality, 427
atherosclerotic damage, 234 Confined hepatic malignancy
genetic abnormality, 234 (hepatocellular carcinoma), 408
matrix, 291^292t Congenital biliary abnormalities, 408
Colles’ fracture, 397 Congenital dysphagia, 308t
 INDEX 581
Congenital factors, 356t Cord compression, assessment, 176 CRF. See Chronic renal failure
Congestive heart failure (CHF), 8. See also Corneal reflex, 171^172 Critical illness myopathy (CIM), 434^435
Decompensated CHF Coronary arterial spasm, 21 definition, 434^435
activity progression, 26 Coronary arteries, dilation, 19 Critical illness polyneuropathy
cardiac impairment, classification, Coronary arteriography, 20 (CIP), 434
23^26 Coronary artery bypass graft definition, 434
evaluation, 17^18 (CABG), 28 Crohn’s disease, 314, 314
reference, 23 minimally invasive technique, management, 314
signs/symptoms, 25, 25b usage, 28 occurrence, 314
Consciousness performing, 28 signs/symptoms, 314
abnormal states, 164t surgery, 27 CRP. See C-reactive protein
elements, 163 Coronary artery disease, 394 CRPS. See Complex regional
level, 163 Coronary atherosclerotic disease pain syndrome
description, 163b (CAD), 21 CRRT. See Continuous renal
loss, 222 Coronary care unit (CCU), 433 replacement therapy
normal states, 164t Coronary heart disease, 13 Crystals, abnormality, 331t
Consolidation, 70 Coronary laser angioplasty, laser energy CSF. See Cerebrospinal fluid
Constrained TSA prostheses, 110 (usage), 27 CT. See Computed tomography
Contact burn, 267t Coronary perfusion, 6 CT-PA. See Computerized tomographic
Continent urinary diversion, 347 CO factor, 6 pulmonary angiography
internal urine reservoirs, 347 Coronary vascular disorders, surgical Cuff, 464. See also BP cuff
Continuous ambulatory PD, 342 management, 254 external pressure, release, 475
schematic illustration, 342f Corrigan’s pulse, 9t inflation, determination, 10
Continuous arteriovenous Cortical bone, evaluation, 91 Culture, 357
hemofiltration (CAVH), 344^345 Corticospinal tract, motor cells, 187^189 purpose, 357
schematic representation, 345f Corticosteroids, usage, 405^406, 405t Cultured epidermal autograft
Continuous passive motion (CPM) Cortisol deficiency, 388 (CEA), 274t
machine, usage, 108 Cough effectiveness, enhancement, 81 Current medications, notation, 428
ordering. See Shoulder CPM Cough examination, 58^59 Cushing’s disease/syndrome, 238t
Continuous positive airway Coughing, protective reflex, 49 diagnosis, 385
pressure, 466t Cough mechanism, phases, 58^59 signs/symptoms, 384^385
Continuous renal replacement therapy Coumarin derivatives, 488t Custom seating cushions, importance,
(CRRT), 341, 343^346 Counterpulsation devices, 473^475 117^118b
indications, 345^346 COX. See Cyclooxygenase CVA. See Cerebrovascular accident
purpose, 343^344 C-peptide levels, usage, 412 CVVH. See Continuous venovenous
Continuous sounds, 56 CPM. See Continuous passive motion hemofiltration
Continuous venovenous CPP. See Cerebral perfusion pressure CVVHD. See Continuous venovenous
hemodiafiltration CPS. See Cardiopulmonary support hemodialysis
(CVVHDF), 345 Crackles, 56 CVVHDF. See Continuous venovenous
Continuous venovenous hemodialysis fluid/secretions, presence, 56 hemodiafiltration
(CVVHD), 345 Cranial meninges, coronal section,157f CXR. See Chest x-ray
Continuous venovenous hemofiltration Cranial nerves (CN), 166 Cyclooxygenase (COX), 536
(CVVH), 344^345 origin/purpose/testing, 167^169t Cyclophosphamide, usage, 405^406
venous system usage, 345 testing, 166 Cyclosporine, usage, 405^406, 405t
Contractile soft tissues, 88 Craniectomy, 194t Cystectomy, 347
Contrast arteriography, Cranioplasty, 194t Cystic fibrosis (CF), 73
complications, 228t Craniotomy, 194t value, prediction, 416
Contrast dye, intravenous injection, 332 Cranium, 152 Cystine kidney stones, 337
Contrast echocardiograph, 17 brain enclosure, 152 Cystitis, 339
usage, 17 Cr clearance, 332 management, 339
Contused lung parenchyma, 79 C-reactive protein (CRP), 15 signs/symptoms, 339
Coordination, 172 protein measurement, 15 Cystoscopy, 333
tests test, 375 Cytology, 357
limitation, 172^173 Creatine phosphokinase (CK), release, complexity, 357
list, 173t 15^16 Cytomegalovirus (CMV), 367
COPD. See Chronic obstructive Creatinine phosphokinase infections, 368^369
pulmonary disease (CK-MM), 381 clinical presentation, 369
Coracoid process, articulation Creatinine tests, 331^332 commonness, 368
(fracture involvement), 100 Crescentic glomerulonephritis, 336 management, 369
582 INDEX

Cytoprotective drugs, 181 Diabetes mellitus, 389^395 Direct hemodynamic monitoring.

Cytoprotective medications, 514t complications, 392^395 See Invasive hemodynamic
diagnosis, 387 monitoring
D basis, 389 Directional coronary atherectomy,
DAI. See Diffuse axonal injury types, 389 performing, 27
DBS. See Deep brain stimulator Diabetic dermopathy, 393 Direct observational therapy,
D-dimer, 231 Diabetic ketoacidosis (DKA), short-course (DOTS), 362^363
assay, 231 392^393 Direct observational therapy (DOT),
Dean, Elizabeth, 81 management, 393 362^363
Debridement. See Wounds result, 392 Direct thrombin inhibitors, 488t
purposes, 288 signs/symptoms, 392 Disc herniation, assessment, 176
types, 288 Diabetic nephropathy, 338, 406 Discontinuous sounds, 56
Debulking, 204 commonness, 338 Disease-modifying antirheumatic drugs
Decompensated CHF, 18 management, 338 (DMARDs), 375,499^501t
Decubitus ulcer. See Pressure ulcer reoccurrence, prevention, 412 Displaced fracture, 92
Deep brain stimulator (DBS), signs/symptoms, 338 Disseminated host, term (usage), 355t
190^192 Diabetic neuropathy, 393^394 Disseminated intravascular coagulation
Deep inspirations, ensuring, 57b commonness, 393^394 (DIC), 247
Deep partial thickness burn, 271f signs/symptoms, 394t diagnostic workup, 247
Deep tendon reflexes (DTRs), 170. Diabetic ulcers, clinical indicators, 280t management, 247
See also Lower extremity; Diagnostic measures, cardiac evaluation, secondary process, 247
Upper extremity 12^21 signs/symptoms, 247t
grades/interpretation, 171t Diagnostic testing, 59^67 thromboplastic substances,
testing, 170 Dialysate fluid, instillation, 341 introduction, 247
Deep vein thrombosis (DVT), 93, 94^95, Dialysis, elimination, 412 Disseminated TB, 362
104^105 Diaphoresis, presence, 8 Distal dysphagia, 308
association, 241 Diaphragmatic restriction, 73 Distal femoral fractures, 96^97
disorders, management, 243 Diaphragm sellae, 156t types, 96^97
initial treatment, 241^242 Diastole, 2^4 Distal femur fractures, management/
MRI role, 241 Diastolic dysfunction, 23 physical therapy
prevention, assistance, 104^105 DIC. See Disseminated intravascular intervention, 142t
prophylaxis, 241 coagulation Distal fibula fractures, 97^98
risk factors, 241b Diencephalon, structure/function/ Distal humeral fractures, 100^102
treatment, 229^231 dysfunction, 155^156t rarity, 100
Defense lines, 355t Differential white blood cell count, 357 Distal tibial fractures, 97^98
Degenerative central Diffuse axonal injury (DAI), 178t medical-surgical management, 145t
nervous system diseases, Diffuse esophageal spasm, physical therapy intervention, 145t
187^192 characterization, 309 Diuretics, 489^491t
Degloving injury, 94^95 Digestion Diverticular disease, 311^312
Delayed union, 94 accessory organs, structure/ signs/symptoms, 311^312
Delta III procedures, 113 function, 300t Diverticulitis, 311
Dementia, 183^184 primary organs, structure/ Diverticulosis, 311
syndrome, 183 function, 300t Dizziness
Dermagraft, 292 Digital clubbing complaint, 186
TC, usage, 228t observation, 223 history, 7
Dermatomal innervations, 105b presence, 54 DKA. See Diabetic ketoacidosis
Dermatome chart, embryologic segment Digitalis toxicity, signs/symptoms, 31t DLT. See Domino liver transplant
basis, 162f Digital subtraction angiography (DSA), DMARDs. See Disease-modifying
Destination therapy (DT), 479 174, 224 antirheumatic drugs
DEXA. See Dual Energy X-ray computer-assisted radiographic DNAR. See Do not attempt resuscitation
Absortiometry visualization, 174 DNA synthesis, inhibition, 524^525t
Diabetes, 526 Dihydrofolate reductase, inhibition, DNR. See Do not resuscitate
complication, 394 499^501t Dobbhoff tube. See Nasoenteric
foot care, 393b Dihydro-orotate dehydrogenase, feeding tube
infection, 393 inhibition, 499^501t Dobutamine, alpha-1 agonist, 17
Diabetes insipidus (DI), 385, 386. Seealso Dilutional hyponatremia, 385 Dobutamine stress echocardiograph
Central DI; Peripheral DI Dipeptidyl peptidase IV (DPP-IV) (DSE), 17
involvement, 386 inhibitors, 526^528t usage, 17
signs/symptoms, 386 Dipyridamole (Persantine), usage, 19 Documentation. See Medical record
 INDEX 583
Domino liver transplant (DLT), 409 Dysphagia, 308 Electrolyte balance, 342
performing, UNOS report, 409 characterization, 308 management, 341
Donors. See Cadaveric donors; classification/etiologies, 308t Electrolyte imbalance, 437^439
Living donors occurrence, 308 characteristics, 438t
heart, removal, 419 Dysplasia, degree (grading reports), 202 medical management, 439
lung removal, 419 Dyspnea, history/reports, 52^53 Electrolyte imbalances, 405
matching, 403 Dysuria, 329, 339 Electrolyte levels
Donor sites, dressings, 229t representation, 439b
Do not attempt resuscitation E schematic representation, 439f
(DNAR), 433 Ear sensors, application, 59^60 Electrolyte regulation, 328
Do not resuscitate (DNR), 433 EBRT. See External beam radiation Electromyography (EMG), studies, 176
Dopamine therapy Electrophysiologic studies (EPSs),
agonists, 506^507t ECA. See External carotid artery 20^21
precursor, 387 ECG. See Electrocardiogram indications, 20^21
Doppler flowmetry, 174. See also Laser Echocardiograph image, 17 usage, 20^21
Doppler flowmetry Echocardiography, 17 Elevation pallor, 225^226t
ultrasound usage, 174 indications, 17 ELISA. See Enzyme-linked
Doppler ultrasonography, 412 noninvasive procedure, 17 immunosorbent assay
Doppler ultrasound, 227t ECMO. See Extracorporeal membrane Emboli
Dorsal scapular nerve, 160t oxygenation impact. See Arterial emboli
DOT. See Direct observational therapy Ectopic bone, presence, 91 size/location, 77
DOTS. See Direct observational therapy, Ectopic foci, 22 treatment, 236
short-course Ectopic thyroid hormone Embolization, 194t
Double-barrel colostomy, 319^320t production, 382t therapy, 254
Double-lung transplantation, 416 Edema process, 254
Double simultaneous stimulation, control Emergency room management,
testing, 172t exercises, usage, 111 objectives, 269^270
DPP-IV. See Dipeptidyl peptidase IV initiation, 108^109 EMG. See Electromyography
Dressings, 290. See also Primary management, 385b Emollients, 515t
dressings; Secondary observation, 223 Emotional state, 163^164
dressings signs, 8 assessment, 163^164
types, indications/uses, 291^292t EDH. See Epidural hematoma Emphysema, 70^73
Drop-lock brace, 130^131t EECP. See Enhanced external etiology, 70^73
Drug toxicity, 381 counterpulsation Empyema, 79
DSA. See Digital-subtraction EEG. See Electroencephalography anaerobic bacterial pus, presence,79
angiography EF. See Ejection fraction Encephalitis, 364^365
DSE. See Dobutamine stress Eisenmenger’s syndrome, 416 clinical presentation, 364^365
echocardiograph Ejection fraction (EF), 4 management, 365
DT. See Destination therapy EKG. See Electrocardiogram Encephalopathy, 434
DTRs. See Deep tendon reflexes Elastic bronchiole walls, destruction, 73 Endarterectomy, 255
Dual Energy X-rayAbsortiometry Elastic recoil, 4 process, 255
(DEXA), 396 Elastin End colostomy, 319^320t
Dumping syndrome. See Enhanced aging/degeneration, 234 Endocardium, 3t
gastric emptying atherosclerotic damage, 234 Endocrine dysfunction, screening, 378
Duodenal-bladder anastomotic leak, 412 Electrical brain activity, recording, 175 Endocrine function
Duodenal stump leak, 412 Electrical burns, 269, 266^268 evaluation, 378^379
Duodenal ulcer, 311 cause, 266^267 measurement, 378
commonness, 311 characterization, 267 Endocrine glands, schematic
disease, clinical manifestations, 311 Electrical injury, complications, 267^268 representation, 378f
Dural folds, 156t Electrocardiogram (ECG), 4, 13^14 Endocrine input, 5
DVA. See Dynamic visual acuity rhythm, 35 CO factors, 5
DVT. See Deep vein thrombosis usage, 448^449t Endocrine system, 519^526
Dye, usage, 176b Electrocardiogram (EKG) management, 398
Dynamic hyperinflation, 466^468 findings, 235 goals, 398
Dynamic visual acuity (DVA) test, Electrocardiographic (ECG) guidelines, 398
188^189t characteristics, 38t metabolic tests, 387^388
Dysequilibrium, 186 Electrocardiograph interpretation, 14t Endocrine system, introduction, 377
Dysmenorrhea, endometriosis Electroencephalography (EEG), 175 End-of-life issues, 432^433
(impact), 341 electrodes, usage, 175 complexity, 432^433
584 INDEX

Endoluminal stents Esophageal cancer, 309^310 Extracorporeal VAD, types/

placement, 27
usage, 27
Endometriosis, 341
impact. See Dysmenorrhea
management, 341
signs/symptoms, 341
Endoscopic retrograde
cholangiopancreatography, 307t
Endothelin, imbalance, 236
Endotracheal tube, 464f
End-stage hepatic disease, 408
End-stage renal disease (ESRD), 329
causes, 406
End-to-end proximal anastomosis, 257f
Energy demands, 18t
Enhanced external counterpulsation
(EECP), 473, 475
definition, 475
illustration, 475f
pneumatic cuff inflation, usage, 475
Enhanced gastric emptying (dumping
syndrome), 311
Enteric conversion, requirement,
411^412
Enteric drainage, bladder drainage
(contrast), 411^412
Enterococcus faecalis, 358
Environmental toxins, exposure, 52
Enzymatic debridement, 289
Enzyme immunoassay test, 366
Enzyme-linked immunosorbent assay
(ELISA), 366
Eosinophilic granuloma, 416
Eosinophils, 357
Epicardium, 3t
Epidermal wounds, healing, 236
Epidural hematoma (EDH), 178t
Epidural sensor, 453t
Epidural space, 157t
Epilepsy, 185^186t
Epinephrine, 387, 386t
Epiphyseal fracture, 92
Epithalamus, 155^156t
Epley maneuver, 187b
illustration, 191f
EPs. See Evoked potentials
EPSs. See Electrophysiologic studies
Epstein-Barr virus, infective ability, 367
Erysipelas, 365
Erythrocytes. See Red blood cells
Erythrocyte sedimentation rate (ESR),
228^229, 375
values, 228^229
Erythrocytic disorders, 243^246
Erythropoiesis-stimulating action, 512t
Erythropoietin secretion, 328
Escharotomy, 273
Escherichia coli, 358, 359t
description, 309^310
Esophageal disorders, 308^310
Esophageal manometry, 303^304t
Esophageal motility, 312^313
Esophageal pH, 303^304t
Esophageal varices, 309
Esophageal webs, formation, 244
Esophagogastric balloon tamponade
tube, 454t
Esophagogastroduodenoscopy, 303^304t
ESR. See Erythrocyte sedimentation rate
ESRD. See End-stage renal disease
Essential hypertension, 236
Estrogen, 386t
impact, 516t
Evacuation, 194t
Evoked potentials (EPs), 175^176
Excessive plantar callus formation,
development, 236
Excision, types, 274t
Excisional surgery, 203^204
Exercise intensity
monitoring, RPE usage, 34
prescribing, 34
Exercise log, importance (emphasis), 215
Exercise prescription, physical therapist
role, 389b
Exercise program, initiation, 31
Exercise testing, 17^19, 227t
contraindications, 18
Exercise test protocols, comparison, 18t
Exogenous hyperthyroidism, 382t
Experimental soft-tissue surgery, 124
Expired gas analysis, usage, 17^18
Exploratory surgery, 203
External beam radiation therapy
(EBRT), 204
irradiation, 205b
External cannula/shunt, 344f
External carotid artery (ECA), 159t
External fixation devices, complications,
128^132
External fixators, 128^132
aluminum/titanium percutaneous
pins, insertion, 128^132
tapping/banging, prevention, 132b
External rotation, usage, 111
Extracapillary glomerulonephritis, 336
Extracapsular fractures, 96
Extracorporeal mechanical pump,479^480
Extracorporeal membrane oxygenation
(ECMO), 473, 477^479
complications, 478^479
illustration, 478f
involvement, 477
pumping device, 477
requirement, 477
system components, 477
characteristics, 480^481
Extrapleural disorders, characteristics/
general management, 78t
Extrapulmonary sounds, 56
ExtrapulmonaryTB, occurrence, 362
Extravascular hemolytic anemia, 245
Extremities, circumferential burns, 224
Extubation, 463
F
Face, redness/rounding, 385
Facial nerve, 167^169t
Facial prosthesis, 213^214
Facial tumors, 213^214
physical therapy intervention, 213^214
Factor Xa inhibitor, 488t
False aneurysms, 234f
definition, 234
False-positive adventitious breath sound
findings, minimization, 57b
Falx cerebelli, 156t
Falx cerebri, 156t
Familial amyloidotic polyneuropathy
(FAP), 409
Fasciculus cuneatus, 160t
Fasciculus gracillis, 160t
Fasciotomy, 273
Fasting hypoglycemia, 395
Fasting plasma glucose, 389
Fat emboli, 93
FDG. See Fluorodeoxyglucose
Fecal fat (test), 305^306t
Femoral access, 474^475b
Femoral artery
sheath insertion, 27
usage, 344^345
Femoral components, cementing
options, 103
Femoral head AVN, 96
Femoral head fractures, 96
hip fractures, similarity, 96
Femoral nerve, neuropraxia, 105b
Femoral shaft fracture, 96
management, 141t
physical therapy intervention, 141t
result, 96
Femorofemoral bypass, 256f
Femoropopliteal bypass, 256f
Femorotibial bypass, 256f
FHF. See Fulminant hepatic failure
Fiberoptic transducer-tipped
catheter, 453t
Fibric acid derivatives, 493^495t
Fibrinolysis, initiation, 495t
Fibrinolytics. SeeThrombolytics
Fibrotic changes, 77
Fibula fractures, 97
result, 97

Fibular motion, elimination, 113
FIM. See Functional independence
measure
Finger sensors, application, 59^60
FiO2. See Fraction of inspired oxygen
Fish oil, 493^495t
Fitting cuff, usage, 10
5-Alpha-reductase inhibitors, 516t
5-HT3 receptor, 508t
5-hydroxyindoleacetic acid (test),
302^303t
5’-Nucleotidase, 305^306t
Fixation, loss, 93, 94
Fixation devices (hardware), 93
Fixators. See External fixators
Fixed performance oxygen delivery,446t
FLAAC pain assessment tool, 537t
Flail chest, 79
fracture, impact, 79
Flame burn, 267t
Flash burn, 267t
Flexible bronchoscopy, 63^64
diagnostic/therapeutic
indications, 64b
Flow-volume loop, 65
characteristics, 67f
Fluid balance, management, 341
Fluid imbalance, 437
characteristics, 438t
medical management, 439
Fluid intake, ensuring, 439b
Fluid resuscitation, impact, 278
Fluid volume, 342
Fluorescein fluorometry, 269
Fluorodeoxyglucose (FDG), 175
Fluoroquinolones, 517^520t
Foams (dressings), 291^292t
Focal mononeuropathy, 393
Focal neuropathies, 394t
Foley catheter. See Urinary catheter
Folic acid
anemia, 244^245
deficiency, decrease, 244^245
synthesis, inhibition, 521^522t
Follicle-stimulating hormone
(FSH), 383t
Forced expiratory volume in 1 second
(FEV1), 65^67
Forced vital capacity (FVC), 65^67
Forearm, looped graft, 344f
Forearm fractures, 102
management, 150t
physical therapy intervention, 150t
Forefoot fractures, 98
management, 146t
occurrence, 98
physical therapy intervention, 146t
Foreign body, presence, 73
Forequarter amputation, 547t
INDEX 585
Forward elevation, initiation, 111 Functional reach testçContinued
Fourth intercostal space (ICS), procedure, 561
intersection (phlebostatic results, interpretation, 561^562
axis), 451f Functional safety, 90^91
Fraction of inspired oxygen (FiO2), 445 Functional tasks, comparison, 18t
criteria, 470 Functional tests
Fracture description, 555
angular/rotary deformity, 94 usage, increase, 566^567
bony union, 93 Fundoplication, 319^320t
complications, 93^94 Fusion inhibitors, 522^524t
timing, 93^94 FVC. See Forced vital capacity
configuration, 92
extent, 92 G
fragments, aligning/ Gag reflex, 171^172
approximating, 93 Gait abnormalities, observation, 223
management, 92^102 Gallium scan, 303^304t
body region, 94^102 Gamma-glutamine-oxaloacetic
clinical goal, 93 transaminase, 301
equipment, 124^132 Gamma-glutamyltransferase test, 211,
nonoperative management, 93 305^306t
operative management, 93 Gas dilution spirometers, 65
pattern, orientation, 92f Gas exchange. See Respiratory system
reduction, 93 Gas transport. See Respiratory system
loss, 128 Gastrectomy, 319^320t
site, 92 Gastric acid
false joint formation, 94 secretion, suppression, 515t
uniting, failure, 94 suppression, 514t
Fragments, relative position, 92 Gastric bypass, 319^320t
Frank-Starling mechanism, 4 surgery, 315^316b
CO factor, 4 Gastric cancer, 311
Free thyroxine index, test, 380t Gastric emptying
Fremitus, presence, 57 disorders, 311
Frontal lobe, 154t scan, 303^304t
Fructosamine protein, test, 390t Gastric lavage, 358
FSH. See Follicle-stimulating hormone Gastric retention, 311
FTSG. See Full-thickness skin graft Gastric simulation test, 302^303t
Full inspiration, 58^59 Gastric ulcer, 310
Full thickness burn, 271f management, 310
Full thickness excision, 274t symptoms, 310
Full-thickness skin graft (FTSG), 274t Gastrin test, 302^303t
Full-thickness wounds, 287 Gastritis, 310
Fulminant hepatic failure (FHF), 408 etiology. See Acute gastritis; Chronic
Functional aerobic capacity, 4 erosive gastritis; Chronic
Functional bowel disorder, 313 nonerosive gastritis
Functional capacity. See Heart term, usage, 310
Functional independence measure Gastroenteritis, 366
(FIM), 234 management. See Acute gastroenteritis
Functional mobility, 90^91. manifestations, 366
See also Burns Gastroesophageal reflux disease
achievement, 104 (GERD), 309
decrease, 549t characterization, 309
evaluation, 108, 285 Gastrografin study, 303^304t
treatment, 108 Gastrointestinal (GI) bleeding, 246
Functional obstructions (paralytic ileus), scan, 303^304t
312^313 Gastrointestinal (GI) bleeds,
observation, 312^313b characteristics, 310
Functional reach test, 561^562 Gastrointestinal (GI) cancer,
elderly, interaction, 562 209^210
overview, 562t involvement, 209
586 INDEX
Gastrointestinal (GI) cytologic studies,
303^304t
Gastrointestinal (GI) disorders
management, 318
pharmacologic therapy, 318
surgical procedures, 319^321
Gastrointestinal (GI) dysfunction
fatigue levels, increase, 321
nonpharmacologic pain management
techniques, 321
physical therapy intervention, 321
positioning precautions, 321
Gastrointestinal (GI) hemorrhage, 310
Gastrointestinal (GI) infections, 366
Gastrointestinal (GI) injury, 94^95
Gastrointestinal (GI) pathology, 301b
Gastrointestinal (GI) polyps, 315
Gastrointestinal (GI) surgical
procedures, 319^321
addition, 319^320t
Gastrointestinal (GI) system
auscultation, 298
bleeding, 310
cancers, surgical interventions, 210t
clinical evaluation, 298^307
diagnostic evaluation, 299
diagnostic procedures, 303^304t
diagnostic studies, 299^301
history, 298
inspection, 298
introduction, 297
laboratory tests, 302^303t
management, 318^322
MRI, 307
pain referral patterns, 298t
palpation, 298^299
pathophysiology, 307^318
percussion, 298
PET, 307
physical examination, 298
physical therapy intervention, 321^322
guidelines, 321^322
schematic representation, 299f
structure/function, 297
surgical intervention, indication, 319
tables, 512
Gastrointestinal (GI) tract, CTscan,
303^304t
Gastroparesis, 311
Gauze dressings, 291^292t
GBS. See Guillain-Barre¤ syndrome
GCA. See Giant cell arteritis
GCS. See Glasgow Coma Scale
General anesthesia, 531
intraoperative effects, 531^532
Generalized muscle atrophy, 132
Generalized seizures, 185t
Genitourinary cancers, 209^210
involvement, 210
Genitourinary system
anatomy, 328
auscultation, 331
performing, 331
baseline radiograph, 332
biopsies, 333
cancers, surgical interventions, 210t
clinical evaluation, 328^333
components, 327^328
CTscan, 333
diagnostic tests, 331^333
disorders, surgical interventions, 346
history, 328^329
introduction, 327
management, 341^347
MRI, 333
observation, 329^330
palpation, 330
pathophysiology, 333^341
percussion, 330
physical examination, 328^331
physical therapy intervention,
347^349
primary functions, 328
radiographic examination,
332^333
radioisotope studies, 333
schematic illustration, 329f
structure/function, 327^328
surgical interventions, 346^347
tables, 512^516
ultrasonography studies, 333
urodynamic studies, 333
Gentle ROM, definition, 138
GERD. See Gastroesophageal reflux
disease
GH. See Growth hormone
GHB. See Glycosylated hemoglobin
Giant cell arteritis (GCA), 239
inflammatory disorder, 239
Gigantism, clinical manifestations, 383
Girth measurements, taking, 90b
Glasgow Coma Scale (GCS), 163
calculation, 163b
consciousness/responsiveness
measurement, 163
score, 164t
Glenohumeral dislocation,
occurrence, 100
Glenohumeral joint, articulation
(fracture involvement), 100
Global Initiative for Obstructive Lung
Disease (GOLD), 70
Glomerulonephritis, 335^337, 406
IgA nephropathy, impact, 335^336
inflammation, 335
Glossopharyngeal nerve, 167^169t
Glottis, closure, 58^59
GLP-1 analogs. See Incretin mimetic
Glucocorticoids (cortisol), 387, 386t.
See also Adrenocortical
steroids
deficiency, 385
evaluation, 387
Gluconeogenesis, 328
Glucose load test. See Growth hormone
suppression test
Glucose tolerance test, 387^388
performing, 387^388
usage, 387
Gluteal muscles, isometric
exercises, 104
Glycated protein, test, 390t
Glycemic control, 392b
Glycoprotein IIb/IIIa inhibitors, 493t
Glycosuria, 331t
Glycosylated hemoglobin (GHB),
test, 390t
Goblet cells, hypertrophy, 73
GOLD. See Global Initiative for
Obstructive Lung Disease
Grafting
success, 274b
types, 274t
Graft rejection, types. See Organ
transplantation
Gram’s stain, usage, 357
Granulocyte-stimulating action, 512t
Graphesthesia, testing, 172t
Graphs, bone fragments (fixation), 125f
Graves’disease, 382t
Groshong catheter, 454t
Group A streptococcus, 365
Group G streptococcus, 365
Growth hormone (GH), 383t
overproduction, 383^384
test, 384t
Growth hormone stimulation test
(arginine test) (insulin tolerance
test), 384t
Growth hormone suppression test
(glucose load test), 384t
Guide for Professional Conduct and
Code of Ethics (American
Physical Therapy
Association), 427
Guide to Physical Therapist Practice
(American Physical Therapy
Association), 47
Guillain-Barre¤ syndrome (GBS),
189^190, 434
H
HAART. See Highly active antiretroviral
therapy
Haemophilus meningitis, 364
Hair distribution, observation, 222
Hallpike-Dix maneuver, 190f
 INDEX 587
Hallpike-Dix test, 188^189t HEENT. See Head, eyes, ears, nose, Hemoglobin (Hgb), 14
contraindications, 187b and throat composition, 249
Halo vest, 130^131t Heliobacterpylori tests, 302^303t measurement, 227^228
Hardware. See Fixation devices Hematocrit (Hct), 14 values/interpretation, 230t
Hashimoto’s thyroiditis, 381 accuracy, 228b Hemolysis, RBC destruction/
Hct. See Hematocrit measurement, 227^228 removal, 245
HDLs. See High-density lipoproteins values/interpretation, 230t Hemolytic anemia, 245
Head, eyes, ears, nose, and throat Hematologic cancers, 211^213 management, 245
(HEENT) findings, 428 Hematologic disorders, 243^250 signs/symptoms, 245
Headache, complaint, 175b body system signs/symptoms, 229t Hemophilia, 248^249
Head CT, 174 drug classifications, 250^251 bleeding episode, symptoms/physical
Head shaking-induced nystagmus, evaluation, 224 findings, 248
188^189t management, 250 characterization, 248
Head thrust test, 188^189t physical therapy interventions, experience, 248
Head tumors, 213^214 255^259 management, 248^249
physical therapy intervention, Hematologic system structure, 220 Hemophilia A, 248
213^214 Hematology, 357 Hemorrhagic CVA, 180^181
Healthcare Insurance Portability and auscultation, 223 Hemosiderin staining (hemosiderosis),
AccountabilityAct (HIPAA), diagnostic studies, 224 242^243
physical therapist evaluation, 224^231 Hemostatic condition, insight, 258
compliance, 427 function, 221^222 Hemothorax, 79
Heart history, 224 characteristics, 79
block. See Second-degree heart block; inspection, 224 Heparin, 488t
Third-degree heart block introduction, 219 therapeutic effect, 251
degrees, 46f invasive vascular studies, 224 Heparin-induced thrombocytopenia
blood pumping ability, factors, 2 laboratory studies, 227^231 (HIT), 249
diseases, functional capacity/objective noninvasive laboratory studies, 224 Heparin-PF4 antibodies,
assessment (AHA), 26t palpation, 223 interaction, 249
displacement, 2 pathophysiology, 231^250 Hepatic adenomas (benign hepatic cell
electricity activity, graphic analysis, 13 physical examination, 222^231 tumors), 210^211
excitation, sequence (schematic history, 222 Hepatic encephalopathy, 317
representation), 5f inspection, 222^223 management, 317
failure, 23^26 structure, 220^221 signs/symptoms, 317
causae, 23 tables, 509^512 Hepatic systems
great vessels, function, 3t Hematoma, 248 diagnostic procedures, 307t
intrinsic rhythm, stability Hematuria, 329, 339 laboratory tests, 305^306t
(achievement), 414 blood, presence, 331t Hepatic transplantation
primary structures, 3t Hemipelvectomy, 116^118, 545t. See also contraindications, 408
transplants. See Cardiac Internal hemipelvectomy indications, 408
transplantation evaluation/treatment, 117 Hepatitis, 316
Heart-lung transplantation, 419 mobility, encouragement, 117 management, 316
indications, 419 physical therapy intervention, 117^118 signs/symptoms, 316
HeartMate intracorporeal LVAD, ROM/strengthening exercises, virus tests, 305^306t
480f 117^118 Hepatobiliary cancers, 210^211
Heart rate (HR), 4, 356 similarity. See Hip disarticulation Hepatocellular carcinoma. See Confined
change, 471 Hemiresurfacing arthroplasty, 105^106 hepatic malignancy
palpation, 8 Hemisected brain, medial/midsagittal Hepatocellular dysfunction, 299^300
prescription, absence, 33 view, 153f Hepatocellular injury, 299
pulses, 8 Hemodialysis, 335 Heptoiminodiacetic acid (HIDA)
response, 17 contraindications, 343 scan, 307t
disproportion, 32 indications, 342^343 Hernia, 312. See also Abdominal hernia;
work, linear relationship, 32 vascular access methods, 344f Hiatal hernia
Heart rate recovery (HRR), 32^33 Hemodynamic events, monitoring, 447 Herniation syndromes, 192f
Heart rate variability (HRV), 13 Hemodynamic monitoring, 447. See also Heterograft (xenograft), 274t
Heart sounds, 35. See also Abnormal heart Direct hemodynamic Heterotopic heart transplantation,
sounds; Normal heart sounds monitoring; Indirect 413^414
auscultation, areas, 13f hemodynamic monitoring Heterotopic transplantation (piggy-back
evaluation, 11^12 physical therapy considerations, 447 transplantation), 413^414
Heating modalities, 205b Hemodynamic response, assessment, 31 Heterotropic bone, presence, 94
588 INDEX
Hgb. See Hemoglobin
Hiatal hernia, 312
causative risk factors, 312
management, 312
Hickman catheter, 454t
HIDA. See Heptoiminodiacetic acid
High-density lipoproteins (HDLs), 15
formation, 15
High-frequency jet ventilation,
467^468t
High-frequency oscillation ventilation,
467^468t
Highly active antiretroviral therapy
(HAART), 522^524t
High-output heart failure, 23
High-risk patient identification, 67
High-sensitivity C-reactive protein
(hs-CRP) assay, availability, 15
HIPAA. See Healthcare Insurance
Portability and
AccountabilityAct
Hip abduction orthosis, 130^131t
Hip arthroplasty, 102^105.
See also Bilateral total hip
arthroplasty;Total hip
arthroplasty
performing, 102
physical therapy intervention, 104^105
Hip chair, usage, 105b
Hip disarticulation, 116^118, 545t
complexity, 116
evaluation/treatment, 117
hemipelvectomy, similarity, 116
mobility, encouragement, 117
physical therapy
focus, 117
intervention, 117^118
ROM/strengthening exercises, 117^118
Hip dislocation, 95^96
management, 95^96
precautions. See Posterior hip
dislocation
result, 95
Hip flexion, avoidance, 476b
Hip fractures, 397
Hip Girdlestone procedure, 114^115b
Hip joint grafts, 255b
Hip movement, indirect restriction, 96b
Hip resection arthroplasty, 114
Hip spica, 129t
Hirsuitism, 385, 387
Histamine-2 receptor antagonists
(H2RAs), 514t
Histoplasmosis, 363
clinical forms, 363
management, 363
pulmonary/systemic infection, 363
History and Physical (H&P), 428
History of present illness (HPI), 428
HIT. See Heparin-induced
thrombocytopenia
HIV. See Human immunodeficiency virus
HLAs. See Human leukocyte antigens
HMG-CoA reductase inhibitors,
493^495t
Hodgkin’s lymphoma, 211^212
characteristics, 212t
Hold/relax techniques, usage, 108^109b
Holter monitoring, 13
ECG analysis, 13
Homan’s sign, 225^226t
usage, 241b
Homograft, 274t
Hormonal therapy
importance, 206
usage, 206
Hormone levels, 378
imbalance, 379b
Hormone replacement therapy, 397
Hormones, impact, 509^511t
Hormone secretion, 382
Hospital admission, occurrence, 70
Hospitalization, length, 358
Hospitals, rotational beds (usage), 83
H&P. See History and Physical
HPI. See History of present illness
HR. See Heart rate
HR:HR, exercise intensity level, 32^33
HRR. See Heart rate recovery
HRV. See Heart rate variability
hs-CRP. See High-sensitivity C-reactive
protein
Human fibroblasts, addition, 292
Human immunodeficiency virus (HIV)
infection, 366^367
classification, 367
complications, 368t
detection, 367
laboratory tests, availability,
366^367
medical treatment, advancement, 367
physical therapy intervention, 367
progression, 367
types, 366
Human leukocyte antigens (HLAs), 403
Humeral neck amputation, 547t
Humeral shaft fractures, 100
management, 149t
physical shaft intervention, 149t
results, 100
Hunt and Hess scale. See Subarachnoid
hemorrhage
Hydrocephalus, 183, 184.
See also Communicating
hydrocephalus;
Noncommunicating
hydrocephalus; Normal-pressure
hydrocephalus
Hydrocolloids, 291^292t
Hydrogels, 291^292t
Hyperactive reflexes, symptom, 244
Hyperacute rejection, characterization.
See Organ transplantation
Hypercalcemia, result, 396
Hypercarbia, occurrence, 60
Hyperglycemia, occurrence, 412
Hyperinflation, 70
Hyperinsulinism. See Hypoglycemia
Hypernatremia, characteristics, 438t
Hyperparathyroidism, 396
causing, 396
classification, 396
clinical manifestations, 396
management, 396
treatment, 529t
Hyperpigmentation (tissue staining),
242^243
Hyperpituitarism, 383^385
Hypersensitivity, 548t
Hypertension, 385. See also Essential
hypertension; Idiopathic
hypertension; Portal
hypertension; Secondary
hypertension
age group relationship, 236t
combination drugs, 492t
control, absence, 406
forms, 236
management, 236
Hypertensive crisis, 236^237
Hypertensive effects. SeeTarget organs
Hyperthyroidism (thyrotoxicosis),
379^380
causes, 382t
management, 381^382b, 380
signs/symptoms, 380
Hypervolemia, characteristics, 438t
Hypodermis, 265t
Hypoglossal nerve, 167^169t
Hypoglycemia (hyperinsulinism), 395
BS levels, decrease, 395
inducing, 395
management, 395
occurrence, 390^391b. See also Fasting
hypoglycemia; Postprandial
hypoglycemia
signs/symptoms, 395
Hypoglycemic agents, 526^528t
Hypogonadism, 385
Hyponatremia, characteristics, 438t
Hypoparathyroidism, 396
causes, 396
management, 396
signs/symptoms, 396
Hypopituitarism, 381, 385^386
Hypoplasia, 380
Hypotension, 248

Hypothalamic disease, 381
Hypothalamus, 155^156t
Hypothermia, 181
Hypothyroidism, 380^382
causes, 380^381
laboratory findings, 381
management, 381^382,
381^382b
signs/symptoms, 381
Hypovolemia, 437
characteristics, 438t
Hypovolemic patients, 437b
Hypoxemia, 70
result, 73^76
signs/symptoms, 59t
Hypoxia, 70
occurrence, 60
I IMV. See Intermittent mandatory
IABP. See Intraaortic balloon pump
IBS. See Irritable bowel syndrome
ICA. See Internal carotid artery
ICH. See Intracerebral hematoma
ICP. See Intracranial pressure
ICU. See Intensive care unit
Identification bracelet, absence, 430
Idiopathic endolymphatic hydrops.
See Me¤ nie' re’s disease
Idiopathic hypertension, 236
Idiopathic thrombocytopenic purpura
(ITP), 250
characteristics, 250
symptoms, 250
ILD. See Interstitial lung disease
Ileal loop (ileal conduit), 348f
Ileostomy, 319^320t
Iliac crest bone graft, harvesting,
121^122b
Immersion hydrotherapy, 274^275b
Immune response, suppression, 406
Immune system
components, 355t
factors, 356t
glucose levels, impact, 236
history, 354^356
infections, 366^369
overview, 354
Immunity, decrease, 367
Immunocompromised, term
(usage), 355t
Immunodeficiency, 358
term, 355t
Immunofluorescence assay, 366
Immunoglobulin A (IgA) nephropathy
(Berger’s disease), 335^336
management, 336
signs/symptoms, 336
Immunoglobulin G (IgG) levels,
increase, 190
Immunosuppression, term, 355t
Immunosuppressive drugs
adverse effects, 403
usage. See Organ transplantation
Immunotherapy, importance, 206
Impaired aerobic capacity/endurance,
1^2
Impaired myocardium, response, 17
Impaired oxygen transport, patient
treatment (Dean’s hierarchy), 82t
Impella, 476^477
catheter insertion, 476^477
complications, 477
illustration, 477f
indications, 477
types, 476
IMRT. See Intensity modulated radiation
therapy
ventilation
Incisional infection, 93
Incomplete fracture, 92
Incontinence, 329
Incontinent urinary diversion, 347
urine flow, diversion, 347
Incretin mimetic (GLP-1 analogs),
526^528t
Indirect hemodynamic monitoring.
See Noninvasive hemodynamic
monitoring
Infection
control. See Burns injury
prevention, 224
precautions, 359t
risk, minimization, 241b
Infectious diseases, 358^369
antibiotic-resistant infections,
359^360
auscultation, 356
body fluid examination, 358
cardiac infections, 363
CMV infection, 368^369
cytology, 357
encephalitis, 364^365
evaluation, 354^358
GI infections, 366
hematology, 357
history, 354^356
HIV infection, 366^367
immune system infections,
366^369
introduction, 353^354
laboratory studies, 356^358
lower respiratory tract infections,
361^363
management, 369^370
goals, 369^370
medical intervention, 369
meningitis, 364
INDEX 589
Infectious diseasesçContinued
methicillin-resistant staphylococcus
aureus infection, 359^360
microbiology, 357
mononucleosis, 367^368
musculoskeletal infections, 365
neurologic infections, 363^365
nosocomial infections, 358^360
observation, 356
palpation, 356
physical examination, 356
physical therapy intervention,
369^370
guidelines, 370
poliomyelitis, 363^364
postpoliomyelitis syndrome, 364
processes, terminology, 355t
respiratory tract infections, 360^363
sepsis, 369
skin infections, 365
studies, 358
tables, 517
terms, definitions, 354
toxoplasmosis, 369
upper respiratory tract infections,
360^361
vancomycin-resistant enterococci
infection, 360
vital signs, 356
Infectious dysphagia, 308t
Infectious viral encephalitis, 364
Inferior patellar capsular releases,
allowance, 109
Inferior vena cava (IVC) filter, 241^242
Inflammatory dysphagia, 308t
Influenza, 361
clinical manifestations, 361
management, 361
viruses, mutagenic strains, 361
Infuse-A-Port, 454t
Inhalation injury, 269, 270^272
pathophysiology, 272
Inhalation volumes, delivery, 468
Initial burn care, 273
INR. See International Normalized
Ratio
Inspiratory flow rate, 469t
Inspiratory-to-expiratory ratio, 469t
Insulin, 526^528t
circulation, 390^391b
tolerance test. See Growth hormone
stimulation test
Insulin-dependent diabetes. SeeType 1
diabetes
Insulin pump
complications, 391t
description, 391t
therapy, 391t
Insulin resistance syndrome, 388
590 INDEX

Insulin-treated diabetic patients, Interstitial nephritis, 337 Intraventricular catheter

control, 526 management, 337 (ventriculostomy), 453t
Insulin types, 391t physical findings, 337 Intubation, 463^464
Integra, usage, 228t Intertrochanteric fractures definition, 463
Integument, functions, 274 Evans classification, 141t history, 52
Integumentary system management/physical therapy problems, 468
components, 264 intervention, 141t Invasive diagnostic procedures,
functions, 264 Russell-Taylor classification, 141t usage, 358
Intensity modulated Intestinal disorders, 311^312 Invasive hemodynamic
radiation therapy Intestinal ischemia, 313 monitoring (direct
(IMRT), 204 signs/symptoms, 313 hemodynamic monitoring), 447
Intensive care unit (ICU), 441. Intestinal obstructions, 312^313 Invasive medical monitoring,
See also Surgical ICU functional obstructions 449^450t
bed rest, 431 (paralytic ileus), Invasive therapeutic procedures,
delirium, 434 312^313 usage, 358
neuropathy, 436 mechanical obstruction, 312 Invasive vascular studies, 224
patient/family signs/symptoms, 313 Inverse ratio ventilation, 467^468t
problems, 434 Intestinal tumors, 315 Iodine deficiency, 381
responses, 434 Intraaortic balloon pump (IABP), Ionizing radiation burns, 268
psychosis, 434 473^475 IORT. See Intraoperative radiation
setting, 433^435 action, mechanisms, 474f therapy
transfer, 463 complications, 474^475 Iron deficiency, causes, 244b
stress, 434 function, 473 Iron-deficiency anemia, 243^244
Interbody fusion cages, usage, heartbeats to counterpulsation ratio, Irregularly shaped burns, extent
121^122b, 120 473^474 (estimation), 268
Intercondylar distal femoral fractures, indications, 473 Irritable bowel syndrome (IBS), 313
96^97 time, expenditure, 474^475b signs/symptoms, 313
Intercondylar fracture, 100 usage, 414 Ischemic colitis, 313
Interleukin-1 Intraarticular fracture, 92 Ischemic CVA, 180
biologic activity, blockage, 499^501t Intracapsular hip fractures Ischemic electrocardiographic
inhibition, 499^501t Garden classification, 140t changes, 571f
Intermittent hemodialysis, 341, 342^343 management/physical therapy Ischemic stroke, impact sites, 180f
requirement, 342 intervention, 140t Isometric exercises. See Gluteal muscles;
Intermittent mandatory ventilation Intracerebral hematoma (ICH), 178t Quadriceps
(IMV), 466t. See also Intracorporeal mechanical pump, ITP. See Idiopathic thrombocytopenic
Synchronized intermittent 479^480 purpura
mandatory ventilation Intracorporeal VAD, types/ IVC. See Inferior vena cava
criteria, 470 characteristics, 480^481 IVP. See Intravenous pyelography
Internal arteriovenous fistula, 344f Intracranial pressure (ICP), 192^193
Internal capsule, 155^156t death cause, 248 J
Internal carotid artery (ICA), 159t decrease, treatment options, 194t Jackknife position. See Anesthesia
Internal fixation, techniques, 93f dynamic variables, 192^193 Jejunal/duodenal biopsy, 302^303t
Internal hemipelvectomy, 118 increase, early/late signs, 193t Jewitt brace, 130^131t
complexity, 118 maintenance, 192 Joint arthroplasty, 102^119
illustration, 117f monitoring, 447^452 indication, 102
physical therapy intervention, 118 physical therapy considerations, 452 postoperative course, 102
Internal jugular neck region, pulsations monitors, 453t Joint contracture, 549t
(observation), 8 neurosurgical procedures, 193^195 Joint resection arthroplasty,
International Normalized Ratio (INR), pharmacologic therapy, 193 compromise, 114
229^231, 258 physical therapy intervention, 195 Joint resurfacing, 105^106
goal. See Anticoagulation therapy terms, usage, 193 evolution, 105^106
increase, 299^300 ventricular pressure, 192 physical therapy, 106
level, 258^259 Intraoperative radiation therapy Joints
Interstitial cell-stimulating (IORT), 205 articulation, facilitation, 105^106
hormone, 383t Intrapulmonary air spaces, 62 dislocation, incidence (rarity), 109
Interstitial lung disease (ILD), 77 Intrarenal ARF, 334 effusion, 91
predisposing factors, 77 Intravascular hemolytic anemia, 245 hypomobility, 132
respiratory membranes, RBC membrane destruction, 245 integrity, emphasis, 106
destruction, 77 Intravenous pyelography (IVP), 332 protection, 375
 INDEX 591
JointsçContinued Lactase deficiency, 314 Light touch, testing, 172t
ROM Lactate dehydrogenase (LDH) test, 211 Limb
improvement, 110 Lactic acid, impact, 6 edema formation, risk, 88^89b
maintenance, 132b Lactogenic hormone, 383t ischemia, 474
Jugular venous distention, presence, 8 Lactose tolerance test, 302^303t Limbic system, 156^157
Junctional rhythms, ECG Lacunar CVA, 181 Limb position, 88^89
characteristics/causes, 40t Language ability, 164^165 observation. See Resting limb position
Juvenile-onset diabetes. SeeType1diabetes Language assessment, performing, Limb salvage surgery, 115
Juvenile RA, 375 164^165 Limb salvage techniques, 115
LAP. See Left atrial pressure Limb-sparing techniques, 115
K Laparoscopic utilization, 308b Linear fracture, 92
Kaposi’s sarcoma, 214 Laparoscopy, 301 Line scale, 536t
Keloid scar, 273 performing, 301 Lipase, 305^306t
Ketolides, 517^520t Large bowel, motility, 313 Lipid-lowering agents, 493^495t
Ketonuria, 331t Large intestine, appendix Lipodermatosis, 242^243
Kidneys (inflammation), 311 Lithium, usage, 505t
cross-section, 330f Laryngectomy, 80 Lithotomy position. See Anesthesia
fist percussion, 330 Laryngoscopy, 80 Liver biliary biopsy, 307t
functions, 342 Laser Doppler flowmetry, 269 Liver biliary scan, 307t
palpation, 330 Lateral plateau,Type 2 wedge Liver biopsy, usage, 410
radiographic examination, 332 fracture, 98f Liver disorders, 316
stones. See Renal calculi Lateral tibial plateau,Type 1 wedge Liver failure
transplantation. See Pancreas-kidney fracture, 98f alcoholic cirrhosis, impact, 408
transplantation Latex allergy, 431 medical characteristics, 409t
transplants, maintenance, 407 definition, 431 clinical effects/physical therapy
Kidneys Ureters Bladder (KUB) X-ray, Laxatives, 515t implications, 409t
332, 303^304t, 332b LDH. See Lactate dehydrogenase Liver function postransplant,
Knee arthroplasty, 106^109. LDLs. See Low-density lipoproteins indication, 410
See also Minimally invasive knee Left atrial pressure (LAP), 451f Liver functions, indices, 410
arthroplasty Left coronary artery, anatomy, 2f Liver function tests (LFTs), 410
indication, 106 Left-sided catheterization, 20 Liver-spleen scan, 307t
physical therapy intervention, 107^109 Left-sided endocarditis, 363 Liver transplantation, 408^411
preoperative soft-tissue contractures, Left-sided heart failure, 23 ascites, 411b
107 Left total elbow arthroplasty, exercise/diet modification, 410^411
Knee immobilizer, 130^131t flexion, 112f graft, vascularization, 410
prescribing, 108 Left ventricle, unloading, 476 indications, 408
usage, 105b, 108^109b; 476b Left ventricular assist devices (LVADs), long-term evidence, 410
Knee resection 473, 475^476. See also HeartMate medical complications, 410
arthroplasty, 114 intracorporeal LVAD postoperative care/complications,
ROM minimization, 114^115b Left ventricular end diastole pressure 410^411
surgery, 114 (LVEDP), 4 preoperative physical therapy,
Knees Left ventricular function, factors, 5f goals, 408
acute hemarthrosis, 248f Leg length, decrease, 114^115b pretransplantation care, 408
arthroscopy, 124 Lesions, identification, 214 surgical complications, 410
soft-tissue repair/reconstruction Leukemia, 211 Liver transplants, types, 408^409
surgeries, 126t Leukocytes. See White blood cells Living adult donor liver transplant,
Korotoff sounds, 11t count, 357 408^409
reference, 11 Leukocytosis, 228b, 357 Living donor lobar transplantation, 417
KUB. See Kidneys Ureters Bladder Leukopenia, 357 Living donors, 402^403
Kyphoplasty, 122^123. See also Balloon Leukotriene modifiers, 498t matching, 403
kyphoplasty Leukotriene receptor antagonist, 498t renal transplantation, 407
guidelines, 123 Level surface ambulation, METs transplant recipients, 407, 407
percutaneous procedure, 112 (usage), 19 LLC. See Long leg cast
physical therapy, 123 Levodopa, 506^507t LMWH. See Low-molecular-weight
LFTs. See Liver function tests heparin
L LGIB. See Lower gastrointestinal bleed Lobar transplantation. See Living donor
Laboratory measures, cardiac evaluation, Lightheadedness, 186 lobar transplantation
12^21 Lightning, 268 Lobectomy, 80
LAC. See Long arm cast injury, 269 image, 80f
592 INDEX
Local input, 6
CO factor, 6
Locking pin device, 112^113
Log-roll technique, 208^209b
Long above amputation, 547t
Long arm cast (LAC), 129t
Long butterfly fragment, screws, 93f
Long leg cast (LLC), 129t
Long oblique fracture, screws, 93f
Long-term bed rest, effects, 431
Loop colostomy, 319^320t
Lou Gehrig’s disease, 192
Low-density lipoproteins (LDLs), 15
formation, 15
Lower extremity
amputation, 543
considerations/treatment
suggestions, 549t
examples, 545t
illustration, 544f
arterial circulation, MRA, 228f
coordination test, 173t
DTRs, 171t
fracture management, 94^98
major peripheral nerves, 161t
skeletal muscle dysfunction,
indication, 418^419
Lower gastrointestinal bleed (LGIB), 310
result, 310
Lower-quarter screen, 89^90
list, 90t
sequencing, 89^90
Lower respiratory tract infections,
361^363
Lower subscapular nerve, 160t
Low-frequency ultrasound waves,
passage, 174
Low-molecular-weight heparin
(LMWH), 488t
usage, 242
Low-output heart failure, 23
LP. See Lumbar puncture
LSH. See Luteinizing-stimulating
hormone
Lubiprostone, 515t
Lumbar drain, 454t
Lumbar puncture (LP), 175
CSF collection, 175
Lumbar spine, fracture (clearance),
99^100b
Lund and Browder formula, 268
Lund and Browder method. See Burns
Lung function
improvement, maximum, 417
postransplant indication, 417
Lungs
auscultation, landmarks, 55f
cancers, categories, 206
capacities, alteration, 66f
LungsçContinued Magnetic resonance imaging (MRI), 91,
contusion, 77 174, 333
result, 77 noninvasive vascular studies, 227t
parenchyma, compression, 73 Major ascending/descending white
posterior view, 50^51f matter tracts, 160t
Lung transplantation, 416^419. Malabsorption syndromes, 313^314
See also Heart-lung characterization, 313^314
transplantation management, 314
contraindications, 416 result, 313^314
multiple rest periods, 418^419b Malignant melanoma, 214^215
postoperative airway clearance, Malignant MS, 192b
occurrence, 417 Malignant soft-tissue tumors,
postoperative care/complications, treatment, 116
417^419 Malignant tumor, classification, 200t
preoperative care, 417 Malunion, 94, 128
work capacity, decrease, 417 Management, 26^35
Lung transplants Mandatory minute ventilation, 467^468t
chronic rejection, 406 Mantoux test, 362
thoractomy precautions, Manual compression test, 225^226t
418^419b Manual muscle testing
Lung volume, 65f possibility, absence, 90b
alteration, 66f usage, 90
reduction, 80 MAO. See Monoamine oxidase
Luteinizing-stimulating hormone Massage modalities, 205b
(LSH), 383t Mass effect, 193t
LVADs. See Left ventricular assist Mast cell stabilizers, 499t
devices Maximal inspiratory pressure, 470
LVEDP. See Left ventricular end diastole MCA. See Middle cerebral artery
pressure MCH. See Mean corpuscular
Lymphatic disorders, 250 hemoglobin
Lymphatic evaluation, 231 MCHC. See Mean corpuscular
Lymphatic system hemoglobin concentration
function, 221^222 MCV. See Mean corpuscular volume
structure, 220^221 Mean corpuscular hemoglobin
Lymphatic thyroiditis, 381 concentration (MCHC), 231t
Lymphedema, 250. See also Primary Mean corpuscular hemoglobin
lymphedema; Secondary (MCH), 231t
lymphedema Mean corpuscular volume (MCV), 231t
classification, 250 values, 244^245
control, 208^209b Mechanical clot retrieval devices, 181
diagnosis, 250 Mechanical debridement, 289^290
signs/symptoms, 250 Mechanical obstruction, 312
Lymph node dissection, 204 Mechanical valves, preference, 30
Lymphomas, 211^212 Mechanical ventilation
prognosis, 212 clinical objectives, 469t
stages, Ann Arbor classification, 212t complications, 466^470
treatment, 212 alternatives, 467t
types, 211^212 criteria, 470
Lympocytes, 357 physical therapy considerations, 471
physiologic objectives, 469t
M process, 463^465
Macrolides, 517^520t weaning, 470^471
Macrophages, impact, 281^282, 361^362 methods, examples, 470
Magnetic resonance angiography Mechanical ventilation, ICP treatment
(MRA), 174 options, 194t
noninvasive vascular studies, 227t Mechanical ventilator modes,
Magnetic resonance schematic, 465f
cholangiopancreatography Mechanoreceptors, location, 6
(MRCP), 307t Medial epicondyle, fracture, 101f

Median nerve, 160t
Median sternotomy, performing, 28
Mediastinal air, presence, 62
Mediastinoscopy, 80
Mediastinum, displacement, 2
Mediate percussion, 58
performing, difficulty, 58b
technique, demonstration, 58f
usage, 298. See alsoTissue densities
Medical record
admission note format, 428
components, 427^428
documentation, 427
introduction, 427
orders, 427^428
progress notes, 428
review, 439b
sections, 427
Medical-surgical equipment. See Acute
care setting
Medical-surgical management devices,
452^461
physical therapy considerations,
452^461
Medical therapies, withholding/
withdrawing, 433
MediPort, 454t
Medulla, vasomotor center (inhibition), 6
Medullary hormones, evaluation,
386^387
Meglitinides, 526^528t
Melanocyte-stimulating hormone, 383t
Me¤ nie' re’s disease (idiopathic
endolymphatic hydrops),
186^187, 187
Meninges, 152
connective tissue layers, 152
coronal section. See Cranial meninges
inflammation, 364
Meningitis, 364
management, 364
types, 364
Meningococcal meningitis, 364
Mental status examination, 163^165
Mesh graft, 274t
Metabolic bone disorders, 396^398
Metabolic disorders
definition, 388^389
impact, 60
Metabolic dysfunction, screening, 378
Metabolic equivalents (METs), 18
contrast. See Walking pace
levels, usefulness, 31
tables, clinical usage (rarity), 26
Metabolic products, 6
Metabolic syndrome, 388^389
diagnosis, 389
insulin resistance, importance, 388
management, 389
Metabolic tests, 386^388, 387^388
Metacarpal fractures, 102
result, 102
Metal-on-metal implant, 102^103
Metal-to-polyethylene articulation,
112^113
Metatarsal fracture, occurrence, 98
Methicillin-resistant staphylococcus
aureus (MRSA)
infection, 359^360
infection, development (risk), 359
management, 360
Staphylococcus strain, 359
survival, 359^360
transmission, 359^360
MI. See Myocardial infarction
Micturition patterns, description, 328^329
Midbrain, 155^156t
Middle cerebral artery (MCA), 159t
Midline catheter, 454t
Midline shift, 193t
MiliaryTB, 362
Mineralocorticoids (aldosterone),
387, 386t
evaluation, 387
Minimally conscious state, 433
Minimally invasive hip, 109f
Minimally invasive hip arthroplasty,109
Minimally invasive knee, 109f
Minimally invasive knee arthroplasty,109
Minimally invasive procedures
connulated screws/portal systems,
usage, 122
evolution, 119
Minimally invasive spine surgeries,122
Minimally invasive surgery (MIS), 109
hip arthroplasty, benefits, 109
joint arthroplasty, rehabilitation,109
knee arthroplasty, benefits, 109
rapid recovery approach, 110
Minimally invasive total joint
arthroplasty, physical therapy
intervention, 109
Minnesota tube, 454t
Mirtazapine, 503^504t
MIS. See Minimally invasive surgery
Misoprostol, 514t
Mitral valve replacement (MVR), 30
Modified bipolar cap, 104f
Mohs’surgery, 204
Molded thoracolumbosacral orthosis
(TLSO), 130^131t
Monoamine oxidase (MAO) inhibitors,
503^504t
Monoclonal antibodies, 509^511t
usage, 206
Monocytes, 357
Mononucleosis, 367^368
characterization, 367^368
INDEX 593
Mood stabilizers, 505t
Moon face, 385
Morbid obesity, 315^316
surgical options, 315^316
Mosquito-borne viral encaphalitis, 364
Motility disorders, 309
Motor function, 170^173
MRA. See Magnetic resonance
angiography
MRCP. See Magnetic resonance
cholangiopancreatography
MRI. See Magnetic resonance imaging
MRSA. See Methicillin-resistant
staphylococcus aureus
MS. See Multiple sclerosis
Mucociliary clearance, decrease, 73
Mucociliary escalator, destruction, 73
Mucosal lining, inflammation/
hypertrophy, 361
Mucous membranes, acute bacterial
infection, 361
Mucus production, 70
Mucus secretion, protective reflex, 49
Multifocal neuropathies, 394t
Multifocal PVCs, 35
Multiple myeloma, 212^213
international staging system, 213t
progression, 213
Multiple sclerosis (MS), 175, 190
CNS white matter, demyelination, 190
description, definitions/terminology
(usage), 192b
Multisystem effects, 383^384b
Multisystem organ failure,
incidence, 273
Muromonab-CD3, usage, 405^406, 405t
Muscle impingement, 128
Muscle mass, increase, 387
Muscle tone, 170
description, 170
evaluation, 170
grading, Modified Ashworth
Scale (usage). See Abnormal
muscle tone
Muscle transfer flaps, 208^209b
Muscular bronchiole walls, destruction,
73
Muscular resistance, palpation, 298^299
Musculocutaneous nerve, 160t
Musculoskeletal cancers, 208
Musculoskeletal disease/injury, medical-
surgical management, 88
Musculoskeletal examination, 88^92
Musculoskeletal infections, 365
Musculoskeletal pain, 88
Musculoskeletal system
components, 88
diagnostic tests, 91^92
healing stages, 105b
594 INDEX
Musculoskeletal systemçContinued
introduction, 87
observation, 88^89
patient history, 88
structure/function, 88
tables, 499
Mycobacterium tuberculosis
strains, resistance, 362^363
Mycophenolate mofetil, usage, 405t
Myelin protein, increase, 190
Myelography, 92, 176
studies. See Electromyography
Myeloma. See Multiple myeloma
treatment, 213
Myelosuppressive therapy, 246
Myobacteriumtuberculosis, 361^362
Myocardial diseases, 24t
Myocardial infarction (MI)
diagnosis, 15
history, 7^8
list, 22t
occurrence, 21^22
Myocarditis, 363
Myocardium, 3t
revascularization/reperfusion, 26^28
Myoclonic seizure, 185t
Myopathy, management, 385b
Myositis ossificans, 91
heterotropic bone, presence, 94
Myotomal innervations, 105b
N division, 152
Nails, softening/spooning, 244
Narcosis, clinical presentation, 62b
Nasal cannula, 442^444t
humidification, inclusion, 444^445f
Nasal mucous membranes,
inflammation, 360
Nasoenteric feeding tube
(Dobbhoff tube), 454t
Nasogastric tube (NGT), 454t
National Patient Safety Goals (TJC),
430^431
Natriuretic peptides, 16
identification, 16
Natural rubber latex
health care providers, sensitization/
symptoms (increase), 431
presence, 431
NDRI. See Norepinephrine-dopamine
reuptake inhibitor
Nebulized medications, activeness, 80b
Nebulizer, 454t
Neck fractures, 96
cause, 101^102
hip fractures, similarity, 96
Neck tumors, 213^214
physical therapy intervention, 213^214
Needle biopsy, 381t
Nefazadone, 503^504t
Negative pressure ventilators, 467^468t
Negative pressure wound therapy,
290^292
Neoadjuvant treatment, 204
Neoplasms, 200
grading, 204t
resection/excision, 203^204
term, usage, 199^200
Nephrectomy, 346
types, 346
Nephrolithiasis, 337^338
occurrence, 337
Nephrolithotomy, 347
Nephropathy, 395
Nephrostomy, 348f
Nephrotic syndrome, 337
management, 337
physical findings, 337
symptoms, group, 337
Nerve compression, 125
Nerve conduction velocity (NVC),
187^189
studies, 176
Nerve damage, 93
Nervous system. See Autonomic nervous
system; Central nervous system;
Peripheral nervous system
data, inclusion, 162^163
diagnostic procedures, 173^176
disorders, impact, 367
introduction, 151^152
management, 192^195
neurologic examination, 161^173
observation, 162^163
pathophysiology, 176^192
patient history, 161^162
structure/function, 152^158
tumors, 214
Neural control. See Respiratory system
Neural dysfunction, diabetes
(connection), 393
Neural input, 5
CO factor, 5
Neurogenic bladder, 339
characterization, 339
lesions, 339
management, 339
symptoms, 339
Neuroinfectious diseases, 186
Neurologic cancers, 214
sequelae, 214
Neurologic dysfunction
diagnostic tests/procedures, 173
treatment concepts, 195
Neurologic dysphagia, 308t
Neurologic infections, 363^365
Neurologic status, indirect measure, 165
Neurologic syncope, 186
Neuromuscular excitability,
decrease, 396
Neuropathic/neurotropic ulcers, 281
secondary complication,
occurrence, 281
Neuropathies. See Diabetic neuropathy
manifestation, 393
Neuropathy of critical illness, 434
Neurosurgical procedures, 193^195
Neurovascular assessment, 99
Neutropenia, 205^206b, 247
definition, 247
Neutrophil, 205^206b, 357
NewYork Heart Association (NYHA)
Functional Classification of
Heart Disease, 25
NGT. See Nasogastric tube
Nicotinic acid, 493^495t
Nitrates, 489^491t
Nitric oxide, imbalance, 236
Nitrogeneous wastes, filtration, 342
NNRTIs. See Non-nucleoside reverse
transcriptase inhibitors
Nocturia, 339
Nocturnal pain, presence, 222
Nonbacterial prostatitis, 340
Noncardiogenic chest pain, 569
etiologies, 570t
pain patterns, 570t
signs, 570t
Noncardiogenic pulmonary edema, 76
Nonchemical influences. See Respiratory
system
Noncommunicating
hydrocephalus (obstructive
hydrocephalus), 184
Noncontractile soft tissues, 88
Noncyclic acute wound pain, 284
Nondisplaced fracture, 92
Non-Hodgkin’s lymphomas, 211^212
characteristics, 212t
Noninsulin-dependent diabetes. SeeType
2 diabetes
Noninvasive hemodynamic monitoring
(indirect hemodynamic
monitoring),447
Noninvasive laboratory studies, 224
Noninvasive medical monitoring,
448^449t
Noninvasive positive pressure
ventilators (NPPV), 467^468t
Noninvasive vascular studies, 227t
Non-nucleoside reverse transcriptase
inhibitors (NNRTIs), 367,
522^524t
Nonoperative lower extremity strength,
maintenance, 115
Nonprimary system, failure, 60

Non-rebreather mask, 442^444t
Nonselective debridement, 288,
289^290
Non-small cell lung cancer
(NSCLC), 206
staging, 207t
Nonsteroidal antiinflammatory drugs
(NSAIDs), 536
characteristics, 537t
Nonunion, 94, 128
Norepinephrine, 387, 386t
Norepinephrine-dopamine
reuptake inhibitor (NDRI),
503^504t
Normal breath sounds, 55, 55
Normal heart sounds, 12t
Normal phonation, 56^57
Normal-pressure hydrocephalus
(NPH), 184
Normoglycemia, 412
Nosocomial infection, 358^360
acquisition, risk, 358
term, 355t
term, reference, 358
NPH. See Normal-pressure
hydrocephalus
NPPV. See Noninvasive positive pressure
ventilators
NRS. See Numeric rating scale
NRTIs. See Nucleoside reverse
transcriptase inhibitors
NSAIDs. See Nonsteroidal
antiinflammatory drugs
NSCLC. See Non-small cell lung cancer
Nucleoside analog reverse transcriptase
inhibitors, 367
Nucleoside reverse
transcriptase inhibitors (NRTIs),
522^524t
Numeric rating scale (NRS), 536t
NVC. See Nerve conduction velocity
Nystagmus
elicitation, 161t
presence, 166^170
reduction, techniques, 166^170b
O (avoidance), 105b
Obesity. See Morbid obesity
complexity, 315
impact, 79
Objective assessment. See Heart
Observation, physical examination
component, 8
Obstructive disorders,
characteristics/general
management, 71^72t
Obstructive dysphagia, 308t
Obstructive lung diseases/conditions, 70
Obstructive lung disorders, 66f
Obstructive pulmonary conditions,
70^73
Obstructive pulmonary disorder, 81
Occipital lobe, 154t
Occult blood test, 302^303t
Occupational toxins, exposure, 52
Oculomotor nerve, 167^169t
Odontoid peg fractures, 99f
OLD CART. See Onset Location
Duration Characteristics
Accompanying surprises
RadiationTreatment
Olecranon fractures, 100^102
illustration, 101f
management, 150t
physical therapy intervention, 150t
result, 100^101
Olfactory nerve, 167^169t
Oligomenorrhea, 383, 385
Oliguria, 329
Oncology
definitions, 199^200
diagnosis, 201
etiology, 201
grading, 201^202
introduction, 199
management, 202^206
nomenclature, 200
risk factors, 201
signs/symptoms, 201
staging, 201^202
tables, 501^508
Onset Location Duration Characteristics
Accompanying surprises
RadiationTreatment (OLD
CART), 569
Open face mask/tent, example, 444^445f
Open face tent, 442^444t
Open prostatectomy, 346
surgical removal process, 346
Open reduction internal fixation
(ORIF), 93, 102
requirement, 100
Open urologic surgery, 347
surgical procedures, 347
Operated extremity, pivoting
Operated limb, elevation, 108^109b
Opportunistic, term (usage), 355t
Optic nerve, 167^169t
Oral contraceptives, 238t
table, 516t
Oral prostatectomy, 346
Orders. See Medical record
Organisms
morphologic examination, 357
sensitivity/resistance, 357
Organ posttransplantation care/
complications, 403^406
INDEX 595
Organ procurement/distribution,
UNOS administration, 403
Organ transplantation
acute rejection
reversal, early intervention
(importance), 405^406
signs/symptoms, 404^405
treatment, potential, 404
allograft function, 403
criteria, 402, 402
graft
chronic rejection, 406
rejection, types, 404^406
graft site, swelling/tenderness, 405
hyperacute rejection,
characterization, 404
immunosuppressive drugs, usage,
405t
infection, 403, 406
introduction, 401^402
postoperative complications, 403^404
rejection, 403, 404^406
surgical complications, 404
Organ transplants
candidates, stability
(demonstration), 402
donation, 402^403
recipients, postoperative care,
403^404
types, 402
ORIF. See Open reduction internal
fixation
Oropharynx tree, damage, 270
Orthopedic injuries, 91
Orthoses, acute care setting, 130^131t
Orthostatic blood pressure symbols, 12f
Orthostatic hypotension, 94
Orthostatic syncope, 186
Orthotopic cadaveric liver
transplantation, 408
Orthotopic heart transplantation,
413^414
Orthotopic neobladder, 347
distal ileum reshaping, 347
Oscillatory positive expiratory pressure,
providing, 81
Osmolar agents, 515t
Osmotherapy, 194t
Osteoarthritis, 110
Osteoinductive growth
factors, bone graft
supplementation, 120
Osteomalacia (rickets), 397
characterization, 397
medical management, 397
signs/symptoms, 397
Osteomyelitis, 94
infection, 132
Osteonecrosis, severity, 105^106
596 INDEX
Osteoporosis, 385, 396^397
classification, 397
etiology, absence, 397
management, 385b, 397
multifactorial skeletal disorder, 396
signs/symptoms, 397
Osteotomy, 118^119. See alsoTibial
osteotomy
Ototoxicity, 186^187
Outstretched hand, pronated forearm
(impact), 101^102
Overhead 90-90 traction, 132t
Oximetry (SaO2), 13, 59^60
usage, 13
Oxygenated blood, withdrawal, 475^476
Oxygenation, 469t
O2 levels, 60
Oxygenation (PaO2), evaluation, 16
Oxygen-carrying capacity, decrease, 14
Oxygen consumption, 18
contrast. See Walking pace
Oxygen (O2)
delivery. See Fixed performance oxygen
delivery; Spontaneously
breathing adults
devices, 441
extension tubing, providing, 447
movement, 441
saturation
criteria, 471
partial pressure, relationship, 59t
readings, ensuring, 60b
supplementation, 207^208b
system, humidification
(supplementation), 445^447
toxicity, 470
transport, 51
percentage, 51
Oxygen (O2) therapy, 441^447
indication, 441
physical therapy considerations,
445^447
presence/history/amount, 52
Oxyhemoglobin dissociation curve, 59f
P Panendoscopy, 333
p24 antigen assay, 366
PA. See Pulmonary artery
Pacemaker. See Cardiac pacemaker
PACU. See Postanesthesia care unit
Paget’s disease, 397^398
asymptomatic characterization,
397^398
management, 398
Pain, 88. See also Musculoskeletal pain
assessment, 276^277
tools, 536t. See also FLAAC pain
assessment tool
diary, 536t
PainçContinued
evaluation, 240, 535
physical therapy considerations,
535, 536t
management, 272^273, 385b,
536^541
physical therapy considerations,
536^541
medications, impact, 278
subjective complaint, 535
testing, 172t
Pain/tenderness, presence/location/
reproducibility, 57
PAK. See Pancreas after kidney
Palliation, 204
Palliative care, 433
Palpation, 8^9, 57^58
physical examination component, 8^9
Palpitations, presence, 7
PAN. See Polyarteritis nodosa
Pancreas after kidney (PAK)
transplants, 413
Pancreas-kidney transplantation,
412^413
Pancreas transplant
candidates, diabetic
characteristics, 411
indication, 411
insulin production, 412
Pancreas transplantation, 411^412
acute rejection, 412
duodenum, usage, 411^412
postoperative care/complications, 412
Pancreatic carcinoma, 314
Pancreatic disorders, 318, 388^395
Pancreatic function posttransplant,
indication, 412
Pancreaticoduodenectomy. See Whipple
procedure
Pancreatic systems
diagnostic procedures, 307t
laboratory tests, 305^306t
Pancreatitis, 318. See also Acute
pancreatitis
contributing factors, 318
Panhypopituitarism, 385
management, 385^386
Papillary layer, 265t
Papillary muscle, 3t
Paracentesis, 303^304t
Paradoxical breathing pattern, 79
criteria, 471
Paralysis, 93
ICP treatment option, 194t
Paralytic ileus. See Functional
obstructions
Paraneoplastic syndromes, 201
Paraplegia, 177
Parasympathetic system
neural input (vagal neural
input), 5
Parathyroid disorders, 396
Parathyroidectomy, 396
Parathyroid gland, 395^396
function, 395
Parathyroid hormone (PTH), 395
function, evaluation tests, 395t
measurements, 395
test, 395t
Parathyroid tests, 395
Paresthesia, 93, 246, 383
Parietal lobe, 154t
Parkinson’s disease (PD), 190^192
neurodegenerative disorder, 190^192
Parkinson’s medications, 506^507t
Paroxysmal supraventricular
tachycardia, 42f
Partial knee arthroplasty, 106
Partial liquid ventilation, 467^468t
Partial nephrectomy, 346
Partial non-rebreather mask, 442^444t
Partial prothrombin time (PTT), 14
test, 229
Partial seizures, 185t
Partial-thickness burns, 271f, 269
Partial thickness wounds, 287
Passive ROM, 104
impact, 125
Pass-port, 454t
Patella eversion, absence, 109
Patellar fractures, 97
management, 143t
physical therapy intervention, 143t
result, 97
Patellar tendon-bearing cast, 129t
Patellar tracking abnormalities,
detection, 91
Pathogen
term, 355t
transmission, mode, 359
Pathophysiology, 21^26, 67^79
Patient-controlled analgesia (PCA), 540t
Patient-controlled epidural analgesia
(PCEA), 540t
Patient-controlled intravenous analgesia
(PCIA), 540t
Patient-controlled regional analgesia
(PCRA), 540t
Patient-controlled transdermal analgesia
(PCTA), 540t
Patient history, 51^53. See also
Musculoskeletal system
cardiac evaluation, 7^8
Patient instability, indications, 32b
Patients
activity tolerance, monitoring, 32^35
behavioral changes, 434

PatientsçContinued
candidacy, 391t
clinical course, example, 23f
comfort, maximization, 57b
disturbances, 434
environment, safety, 430^431
guidelines, 430^431
inspection, 53^55
pH change, determination, 61
pH level, examination, 61
reorientation, 430
responses, instability, 31^32
self-awareness, monitoring, 90^91
severity, stages, 25
PAV. See Proportional-assist
ventilation
PBSC. See Peripheral blood stem cell
PCA. See Patient-controlled analgesia;
Posterior cerebellar artery
PCEA. See Patient-controlled epidural
analgesia
PCIA. See Patient-controlled intravenous
analgesia
PCRA. See Patient-controlled regional
analgesia
PCS. See Postconcussive syndrome
PCTA. See Patient-controlled
transdermal analgesia
PCWP. See Pulmonary capillary wedge
pressure
PD. See Parkinson’s disease; Peritoneal
dialysis
PDGF. See Platelet-derived growth
factor
PE. See Pulmonary embolism
PEEP. See Positive end-expiratory
pressure
PEG/PEJ. See Percutaneous
endoscopically inserted
gastrostomy/jejunostomy
Pelvic distention, presence, 329^330
Pelvic fracture, 397
examples. See Unstable pelvic fractures
instability, 94
stability, 94
Pelvic ring fracture, 94
management, 139t
physical therapy intervention, 139t
Young classification, 139t
Pelvic traction, 132t
Pelvis, fracture management, 94^98
Pendulum exercises, patient
instruction, 111
Penetrating injuries, 177t
Penicillins, 517^520t
Peptic ulcer
disease, 310^311
mucosal surface loss, 310
Perceived exertion, rating, 83
INDEX 597
Percutaneous devices, 473^479 Peripheral vascular bypass grafting,
types, 473 254^255
Percutaneous endoscopically inserted complications, 255
gastrostomy/jejunostomy (PEG/ Peripheral vascular disease, 257, 395
PEG) tube, 454t chronic obstructive pulmonary
Percutaneous introducer sheath, 454t disease, 257
Percutaneous nephroscopic stone impaired sensation, 257
removal, 346^347 LE amputation percentage, 543
Percutaneous revascularization Peripheral vascular resistance (PVR),
procedures, 27 decrease, 414
usage, 27 Peripheral vestibular pathology,
Percutaneous transluminal coronary symptoms, 189t
angioplasty (PTCA), 20 Peripheral vestibular system pathology,
limitations, prevention, 27 186^187
performing, 27 Peritoneal dialysis (PD), 335,
Performance-oriented mobility 341^342. See also Automated PD;
assessment, 563^565t. See also Continuous ambulatory PD
Tinetti performance-oriented indications, 342
mobility assessment process, 341
Perfusion types, 342
lung scan, 64 usage, 341
presence, 51 Peritoneal fluid analysis,
Perfusion ratio. See Respiratory system 358, 303^304t
Perianal reflex, 171^172 Peritonitis, 314
Pericardial disease, 77 management, 314
Pericardial heart diseases, signs/ signs/symptoms, 314
symptoms, 25t Perivascular lymphocytic infiltrates,
Pericardiocentesis, 358 presence, 418
procedure, 358 Pernicious anemia, 244
Pericarditis, 363 PERRLA. See Pupil function,
Pericardium, 3t Pupils Equal, Round, and
Peripheral arterial bypass Reactive to Light and
procedures, 256f Accommodation
Peripheral blood smear, 229 Persantine thallium stress
Peripheral blood stem cell (PBSC) testing, 19
transplant, commonness, 419 usage, 19
transplantation, 419^421 Persistent abnormal dysplastic cell
usage, 419 growth, 200
Peripheral DI, 386 Pertussis (whooping cough), 361
Peripheral edema, result, 257 management, 361
Peripheral emboli, sources, 235t PET. See Positron emission
Peripheral innervations, 105b tomography
Peripheral intravenous line, 454t Petechiae, 248
Peripherally inserted central catheter presence, 223
(PICC), 454t PFTs. See Pulmonary function tests
line, 234b Phalangeal fractures, 102
Peripheral nerve injury, 222 result, 102
Peripheral nerve innervations, 89 Phantom limb pain, 548t
Peripheral nervous system (PNS), Pharmacologic agents, 79^80
157^158 purpose, 485
components, 152, 157^158 variety, 193
diabetes, impact, 281 Pharmacologic therapy, 193
division, 152 Pheochromocytoma, 238t, 388
Peripheral pulses management, 388
assessment, 223 rarity, 388
grades, denotation, 223b signs/symptoms, 388
system/scale grading, 223 Physical examination, 53^59
Peripheral symmetric polyneuropathy, cardiac evaluation, 13^14
393^394 observation, 8
598 INDEX
Physical therapy. SeeJoint resurfacing
activity examination algorithm, 34f
deferral, 205b
focus, 184
goals, time frames, 432b
Physical therapy intervention, 30^31,81^84
deferral, 92b
orthopedic impairments, 88
suggestions, 83t
warm-u phase, inclusion, 32
PICA. See Posterior inferior cerebellar
artery
Pica, development, 244
PICC. See Peripherally inserted central
catheter
Piggy-back transplantation. See
Heterotopic transplantation
Pigment layer, 265t
Pin site infection, 128
PIOPED II. See Prospective
Investigation of Pulmonary
Embolism Diagnosis
Pitting edema scale, 10t
Pituitary disorders, 382^386
Pituitary function, description, 382
Pituitary gland, 155^156t, 382^386
function, 382
hormones, target sites/actions, 383t
Pituitary hormones
deficiency, 385
levels, measurement, 382
overproduction, 383
tests, 384t
Pituitary-hypothalamic system,
dysfunction, 382
Pituitary tests, 382
Plant alkaloids, 509^511t
Plasma Cr, measurement, 331^332
Plaster casts, dryness, 127b
Platelet-derived growth factor
(PDGF), 292
Platelet-rich plasma (PRP), 292
Platelets. SeeThrombocytes
aggregation, 281^282
count, 227^228
values/interpretation, 230t
Platinum compounds, 509^511t
Plethysmography, 227t
Pleural effusion, 77
Pleural tap (thoracentesis), 358
Pleurodesis, 80
Plummer-Vinson syndrome, 244
PMMA. See Polymethylmethacrylate
Pneumatic cuffs, inflation, 475
Pneumococcal meningitis, 364
Pneumonectomy, image, 80f
Pneumonia, 76
development, risk (prevention/
minimization), 359b
Pneumonia, history, 52
Pneumothorax (PTX), 77^79
PNS. See Peripheral nervous system
Poliomyelitis, 363^364
clinical representation, 363^364
transmission, 363
Polyarteritis nodosa (PAN), 238
characteristics, 238
management, 238
Polycystic kidney disease, 406
Polycythemia, 246. See also Primary
polycythemia; Relative
polycythemia; Secondary
polycythemia
management, 246
Polycythemia vera. See Primary
polycythemia
Polymerase chain reaction, 366^367
Polymethylmethacrylate (PMMA)
cement, injection, 122^123
Polyneuropathy. See Peripheral
symmetric polyneuropathy
Polyps, 315. See also Gastrointestinal
polyps
signs/symptoms, 315
Polyuria, presence, 389
Pons, 155^156t
Port-A-Cath, 454t
Portal hypertension, 317f
Positioning
guidelines, clarification, 207^208b
ICP treatment option, 194t
importance, 213^214b
initiation, 108^109
Positive end-expiratory pressure (PEEP),
469t. SeealsoAuto positive end-
expiratory pressure
Positive inotropes (pressors), 495t
Positive pressure ventilators, 464
Positron emission tomography
(PET), 175
FDG, administration, 175
scans, 301
technology, advancements, 201
Postanesthesia care unit (PACU), 532
Postangiogram care, inclusion, 224
Postconcussive syndrome (PCS), 178t
Posterior cerebellar artery (PCA), 159t
Posterior hip dislocation,
precautions, 96b
Posterior inferior cerebellar artery
(PICA), 159t
Posterior interbody fusion, pedicle
screws (lateral view), 121f
Posterolateral thoracotomy, 416
Posthemorrhagic anemia, 243
occurrence, 243
signs/symptoms, 243
Postictal state, 185t
Postinfectious glomerulonephritis, 336
renal system inflammation, 336
Postobstructive pneumonia, 73
Postoperative drains, 208^209b
Postphlebitic syndrome, 221^222
Postpoliomyelitis syndrome (postpolio
syndrome), 364
occurrence, 364
Postprandial hypoglycemia, 395
Postrenal ARF, 334
Poststreptococcal glomerulonephritis
management, 336
signs/symptoms, 336
Posttraumatic arthritis, 94
Postural drainage
absolute/relative contraindications,
551
definition, 551
physical therapy considerations, 552
positions
illustration, 552f
modification, 551
usage, 551
Postural stability, maintenance, 186
Posture, 88
observation. See Resting posture
Potassium imbalances, impact, 439b
Potassium-sparing diuretics,
489^491t
PPIs. See Proton pump inhibitors
PPMS. See Primary-progressive MS
Preload, 4
CO factor, 4
Premature atrial contractions, 35
Preoperative aortogram, schematic
illustration, 257f
Prerenal ARF, 334
Press-fit prostheses, 103
Pressors. See Positive inotropes
Pressure control ventilation, 467^468t
Pressure-cycled ventilators, 464
Pressure-regulated volume control,
467^468t
Pressure Score StatusTool (PSST), 287
Pressure sores, development, 89b
Pressure-supported ventilation (PSV),
466^468, 466t
criteria, 470
Pressure testing, 172t
Pressure ulcer (decubitus ulcer), 280
formation, 132
size, clockwise method
measurement, 285f
staging, 287t
Pressure Ulcer Scale for Healing
(PUSH), 287
Pressure wounds, 280
Pretransplant tissue typing,
usefulness, 403

Primary aldosteronism, 238t
Primary cardiac pathology, goals, 31
Primary dressings, 290
Primary hypopituitarism, 385
Primary hypothyroidism, 380
causes, 380^381
Primary liver tumors, appearance, 210
Primary lung pathology, physical
therapy goals, 81
Primary lymphedema, 250
Primary metabolic process,
determination, 61
Primary polycythemia (polycythemia
vera), 246, 246
Primary process, 60
Primary-progressive MS (PPMS), 192b
Primary SCI, 177
Primary varicose veins, 240
occurrence, 240
Prinzmetal’s angina. SeeVariant angina
Prodrome, 185^186t
Progesterone, 386t
Progestins, 516t
Progress notes. See Medical record
initial note emphasis, 428
Prolactin (hormone), 383t
Prolapse, involvement, 22
Prolonged bed rest
effects, 431^432
psychosocial aspects, 432b
systemic effects, 432t
Pronator drift test, 173
Prone position. See Anesthesia
Prophylaxis treatment, 204
Proportional-assist ventilation
(PAV), 470
Proprioception
decrease, 244
testing, 172t
Propulsive bowel activity, functional
inhibition, 312^313
Prospective Investigation of Pulmonary
Embolism Diagnosis (PIOPED
II), 64^65
Prostate biopsies, 333
Prostate disorders, 339^341
Prostatitis, 340^341
categories, 340
inflammation, 340
management, 341
signs/symptoms, 340^341
Prostatodynia, 340
Prosthetic designs, types, 113
Prosthetic graft, 254^255
Prosthetic valves, classification, 30
Protease inhibitors, 367
characteristics, 522^524t
Protective sensation, loss, 281
Protein electrophoresis, 305^306t
INDEX 599
Proteinuria, 331t Pulmonary function tests (PFTs), 65^67
Proteolytic enzyme activity, comparison, 65^67
increase, 234 components, 65
Proteolytic inhibitors, absence, 70^73 description/clinical significance,
Prothrombin time/international 68^69t
normalized ratio (PT/INR), 232t deterioration, 417^418
Prothrombin time (PT) indications, 65^67
increase, 299^300 values, range, 65^67
low level, 14^15 Pulmonary hygiene treatments, 346b
test, 229, 305^306t Pulmonary infections, recurrence, 73
usage, 14 Pulmonary reserve, indication,
Proton pump inhibitors (PPIs), 515t 59^60
Provocative testing, 378^379 Pulmonary vascular disease, 417
Proximal dysphagia, 308 Pulse abnormalities, 9t
Proximal femur, fractures, 97f Pulse amplitude classification, 9t
occurrence, 100 Pulse oximeter, 448^449t
Proximal hemiarthroplasty. See Right Pulse oximetry (SpO2), 59^60
shoulder Pupil function, Pupils Equal, Round,
Proximal humeral fractures, 100 and Reactive to Light and
complications, 100 Accommodation
management, 149t (PERRLA), 166b
physical therapy intervention, 149t Pupils
Proximal humeral hemiarthroplasty, 110 changes, observation. See Baseline
Proximal tibial osteotomy, 118 pupil changes
PRP. See Platelet-rich plasma examination, 166
Pseudarthrosis, 94 reactivity, 166
Pseudoclaudication, differentiation, 233t shape, 166
Pseudomonas aeruginosa, 358 size/equality, 166
PSST. See Pressure Score StatusTool Purine metabolism, antagonism,
PSV. See Pressure-supported ventilation 499^501t
Psychogenic seizures, 185 Purkinje fibers, 4
PT. See Prothrombin time PUSH. See Pressure Ulcer Scale for
PTCA. See Percutaneous transluminal Healing
coronary angioplasty PVCs, frequency increase, 35
PTH. See Parathyroid hormone PVR. See Peripheral vascular
PT/INR. See Prothrombin time/ resistance
international normalized ratio Pyelography, 332
PTT. See Partial prothrombin time Pyelolithotomy, 347
PTX. See Pneumothorax Pyelonephritis, 335. See also Acute
Pulmonary angiography, 20 pyelonephritis; Chronic
Pulmonary artery (PA) catheter, 451f pyelonephritis
usage, 414
Pulmonary artery (PA) catheterization, Q
449^450t Quadriceps
Pulmonary cancers, 206^208 isometric exercises, 104
nonsurgical techniques, 206^208 sparing, 109
surgical interventions, 207t strength, improvement, 110
Pulmonary capillary wedge pressure Quadriplegia, 177
(PCWP), 451f Quinton catheter, 454t
Pulmonary edema, 76. See also
Noncardiogenic pulmonary R
edema RA. See Rheumatoid arthritis
etiology, 76 Radial artery, sheath insertion, 27
occurrence. See Cardiogenic Radial head fractures, 100^102
pulmonary edema cause, 101^102
Pulmonary emboli, 93 management, 150t
Pulmonary embolism (PE), 76^77, 94^95 physical therapy intervention, 150t
management, 242 Radial neck, fractures, 101f
result, 76^77 Radial nerve, 160t
600 INDEX
Radiation
administration. SeeTherapeutic
radiation
therapy, 203
side effects, 205
Radical cystectomy, 347
Radical neck dissections (RND),
213^214
Radical nephrectomy, 346
Radiculopathy, 393
Radiography, 91
Radioimmunoassay (RIA), 378
Radioisotope studies, 333
Radiopaque dyes, usage, 332
Radius, shaft/distal portion
(fractures), 102
Rales. See Wet crackles
Range of motion (ROM). See Active
assisted ROM; Passive ROM
evaluation. See Bilateral ROM
exercises, 108
increase, 110
involvement. See Burns
usage. SeeTotal knee arthroplasty
values, applicability. See Acute care
setting
Rapid arrhythmias, 18
Rapid HIV testing, 367
Rapidly progressive glomerulonephritis
(RPGN), 336
RAS. See Reticular activating system
Rate pressure product (RPP), 35
Ray amputation, 545t
Raynaud’s disease, 239
episodic vasospastic disorder, 239
Raynaud’s phenomenon, 239
RBCs. See Red blood cell
Reanastomosis, 319^320t
Rebleeding, 183
Reconstructive surgery, 204
Rectal pouch/tube, 454t
Red blood cells (RBCs) (erythrocytes),
205^206b
count, 227^228
values/interpretation, 230t
indices, 228
values/interpretations, 231t
production, decrease, 243
sedimentation rate, 228^229
Reduction, loss, 94
Reepithelialization, 236
Reflexes, 170^172
motor response, 170
Reflexive syncope, 186
Reflex sympathetic dystrophy
(RSD), 239
Refracture, loss, 128
Regional anesthesia, 531
Regurgitation, occurrence, 22
Reinforced cervical collar, 130^131t
Rejection. See Organ transplantation
Relapsing-remitting MS
(RRMS), 192b
Relative polycythemia, 246, 246
Renal allograft, 407
Renal allograft, evaluation, 407
Renal arteriography, 332^333
Renal artery occlusion, 338
diagnosis, 338
management, 338
signs/symptoms, 338
Renal artery stenosis, 338
diagnosis, 338
management, 338
narrowing, 338
signs/symptoms, 338
Renal biopsy, 333
Renal calculi (kidney stones), 332
formation, factors, 337
identification, 338
removal, 347, 347
signs/symptoms, 337
types, 337
Renal cross-section, 330f
Renal function
postransplant, indication, 407
restoration, 407
Renal incisions, 347
Renal replacement therapy, 335, 341^346
Renal system dysfunction, 333^338
Renal transplantation, 335, 406^408
benefits, 407
contraindications, 407
postoperative care/complications,
407^408
rejection, signs, 407^408
Renal transplants
procedures, 407
Renal vascular abnormalities,
338^339
Renal vein thrombosis, 338^339
rarity, 338
signs/symptoms, 338^339
Renin inhibitors, 489^491t
Renin-secreting tumors, 238t
Renin secretion, 328
Renovascular disease, 238t
Reperfusion. See Myocardium
Resection arthroplasty, 114
physical therapy
dependence, 114^115
intervention, 114^115
Residual limb edema, 548t
Resistance, impact, 357
Respiration, regulation, 48
Respiratory disorders, impact, 60
classification, 67
Respiratory distress, 70
Respiratory dysfunction
activity progression, 83^84
description, 70
Respiratory evaluation, 51^67
composition, 51
findings, 83t
Respiratory failure, 70
Respiratory impairments, treatment
(concepts), 81^84
Respiratory isolation, 362
Respiratory mechanics, 49
bucket and pump handle motion, 52f
Respiratory medication changes,
awareness, 80b
Respiratory muscles, motions
(occurrence), 49
Respiratory pathophysiology,
understanding, 81
Respiratory pattern, 53^54
Respiratory rate, 356
criteria, 470
observation, 8
Respiratory system
chemical control, 48^49
function, 48^51
gas exchange, 49
gas transport, 51
impairment, 213^214b
introduction, 47
management, 79^84
neural control, 48
nonchemical influences, 49
palpation, 57^58
perfusion ratio, 49^51
pharmacologic agents, 79^80
physical examination, 53
respiratory mechanics, 49
structure, 48
tables, 486^496
ventilation ratio, 49^51
Respiratory tract infections, 360^363
Resting hand splint, 130^131t
Resting limb position, observation, 88^
89
Resting posture, observation, 88
Resting value, beat increase, 32
Rest pain, presence, 222
Restraints, usage, 431
indication, 431
physical therapist guidelines, 431
Restrictive disorders, characteristics/
general management, 74^75t
Restrictive extrapulmonary conditions,
77^79
Restrictive lung disorders, impact, 66f
Restrictive pulmonary conditions, 73^77
Restrictive pulmonary disorder,
therapeutic activities
(impact), 83

Restrictive respiratory pattern, cause, 79
Resuscitation studies, 433
Reticular activating system (RAS),
156^157
Reticular layer, 265t
Retina, visual images (stabilization),186
Retrograde filling test, 225^226t
Retrograde urography, 332
Retroperitoneal hematoma, 94^95
Revascularization. See Myocardium
secondary prevention, usage, 28^30
Reverse total arthroplasty, 112
physical therapy intervention, 112
physical therapy protocol/
precautions, 112
TSA, similarity, 112
ReverseTrendelenburg position,
contraindications, 551
RevisionTHA, 103
Rheumatic fever
clinical sequela. See Acute rheumatic
fever
management, 363
Rheumatoid arthritis (RA), 77, 110,
375^376
autoimmune disease, 375
clinical manifestations, 375
diagnosis, 375
forms, 375
laboratory diagnostic tests, 375
leukocytes, increase, 375
management, 375^376
Rheumatoid factor, 375
Rhinitis, 360^361
Rhinorrhea, 184^185
Rhomberg test, 188^189t
Rhonchi, 56
AmericanThoracic Society/American
College of Chest Physicians, usage
discouragement, 56b
Rhythm disturbance, 22
form, 22
RIA. See Radioimmunoassay
Rib fractures, presence, 57^58
Rib resection, 80
Rickets. See Osteomalacia
Right coronary artery, anatomy, 2f
Right lung
configuration, identification,
50^51f
positioning, 50^51f
Right medial compartment,
unicompartmental knee
arthroplasty, 106f
Right shoulder, proximal
hemiarthroplasty, 110f
Right-sided catheterization, 20
Right-sided heart failure, 23
Right TKA, anterior view, 107f
Right ventricular assist device
(RVAD), 479
Risk factor reduction, patient/family
education, 31
RNA synthesis, inhibition, 521^522t
RND. See Radical neck dissections
Rolling walkers
usage, 397b
usefulness, 121^122b
Romberg’s sign, 244
Rotary chair test, 188^189t
Roux-en-Y, 319^320t
Rowe sling, 130^131t
RPE. See Borg’s Rating of Perceived
Exertion
RPGN. See Rapidly progressive
glomerulonephritis
RPP. See Rate pressure product
RRMS. See Relapsing-remitting MS
RSD. See Reflex sympathetic dystrophy
RT3U. SeeTriiodothyronine resin uptake
Rule of Nines, 268
assessment. See Burns injury
Russell traction, 132t
S Selective costimulation modulator,
SA. See Sinoatrial
SAC. See Short arm cast
Saccades, examination, 188^189t
Saccular aneurysms, 234
Safety awareness, documentation
(difficulty), 91b
SAH. See Subarachnoid hemorrhage
Salicylates, 493t
Sarcoidosis, 374, 416
impact, 374
management, 370
systemic granulomatous disorder, 374
SBP. See Systolic blood pressure
SCA. See Superior cerebellar artery
Scald burn, 267t
Scapula , fracture, 100
SCD. See Sequential compression device
Schwann cells, breakdown, 189^190
SCI. See Spinal cord injury
Sciatic nerve injury, 94^95
SCLC. See Small-cell lung cancer
Sclerosing cholangitis, 408
Sclerosis, 21
SDH. See Subdural hematoma
SDNN, 13
S.E.A. Port, 454t
Secondary brain injury,
occurrence, 177
Secondary cardiac pathology, goals, 31
Secondary dressings, 290
Secondary hypertension, 236
causes, 238t
Secondary hypopituitarism, 385
INDEX 601
Secondary hypothyroidism, 380
causes, 380^381
Secondary lymphedema, 250
Secondary polycythemia, 246, 246
Secondary prevention, usage.
See Revascularization
Secondary-progressive MS (SPMS), 192b
Secondary SCI, 177
Secondary varicose veins,
occurrence, 240
Second-degree heart block, 18
Sedation, ICP treatment option, 194t
Sedative-hypnotic agents, 501t
Sed rate, 228^229
Segmental drainage, postures
(recommendations), 553f
Segmental fracture, medullary nail, 93f
Segmental resection, image, 80f
Segmentectomy, 80
Seizure, 183, 185^186
control, ICP treatment option, 194t
description, 185
disorder, 185^186t
occurrence, 185
terms, usage, 185^186
499^501t
Selective debridement, 288, 288^289
Selective Estrogen Receptor Modulation
(SERM), 397
Selective serotonin reuptake inhibitors
(SSRIs), 503^504t
Selegiline, 506^507t
Semiconstrained articulation,
creation, 113
Semiconstrained TSA prostheses, 110
Sengstaken-Blakemorre tube, 454t
Sensation, 172
testing, 172
list, 172t
Sensitivity, impact, 357
Sensory impairment, presence, 257
Sensory organization test, 188^189t
Sensory testing, importance, 90b
Sepsis, 369
management, 369
progression, 369
Septicemia, 369
Sequential compression device
(SCD), 454t
Sequential x-rays, 91
SERM. See Selective Estrogen Receptor
Modulation
Serologic test, 302^303t
Serotonin-norepinephrine reuptake
inhibitors (SNRI), 503^504t
Serotonin test, 302^303t
Serum amylase, 305^306t
Serum calcium, tests, 395t
602 INDEX
Serum cortisol levels, measurement, 387
Serum creatinine levels, increase, 405
Serum ferritin, diagnostic test, 243^244
Serum glutamate-pyruvate transaminase
(SGPT), 410
Serum glutamicoxaloacetic transaminase
(SGOT), 410
Serum LDH, elevation, 249
Serum proteins test, 211, 305^306t
Serum thyroxine, test, 380t
Serum triiodothyronine, test, 380t
Sex hormones, 386t
SGOT. See Serum glutamicoxaloacetic
transaminase
SGPT. See Serum glutamate-pyruvate
transaminase
Sharps exposure, 430
Sheet graft, 274t
Shock, 94
syndrome, 369
Short above amputation, 547t
Short-acting spinal analgesics, 110
Short arm cast (SAC), 129t
Short butterfly fragment, plates/
screws, 93f
Short leg cast (SLC), 129t
Short leg walking boot, 130^131t
Short oblique fracture, plates/screws, 93f
Short-term bed rest, effects, 431
Short-term immobilization, usage, 100
Shoulder
disarticulation, 547t
physical therapy intervention, 126t
spica, 129t
Shoulder arthroplasty, 110^111
indication. SeeTotal shoulder
arthroplasty
physical therapy intervention, 111
Shoulder arthroscopy, 124
Shoulder CPM, ordering, 111b
Shoulder girdle fractures, 100
Shoulder surface replacement
arthroplasty, 111
Shunt placement, 194t
SIADH. See Syndrome of
inappropriate ADH
Sickle cell anemia, 245^246
autosomal homozygous recessive
trait, 245
complication, 245^246
management, 246
symptoms/physical findings, 245
SICU. See Surgical ICU
Side arm traction, 132t
Sigmoidoscopy, 303^304t
Silastic catheter, 454t
Simple nephrectomy, 346
Simple partial seizure, 185t
Simultaneous pancreas-kidney (SPK) Sleep pattern disturbance, 435
transplants, 412 Sling, usage, 111
cadaveric/living donors, usage, 412 Small bowel series, 303^304t
SIMV. See Synchronous intermittent Small-cell lung cancer (SCLC), 206
mandatory ventilation Small intestine submucosa (SIS)
Single-lung transplantation, 416 dressings, 291^292t
Sinoatrial (SA) node Smoking, history, 51^52
depolarization, 2^4 Snap-it device, usage, 112^113
inherent rate, 5 Snoring sounds, 56
Sinusitis, 361 SNRI. See Serotonin-norepinephrine
clinical manifestations, 361 reuptake inhibitors
management, 361 Sodium channel blockers, 486^487t
Sinus node disorders, 29 Sodium excretion, 328
Sinus node dysfunction, 414 Sodium-rich fluid, weeping, 411b
Sinus rhythm, premature ventricular Soft-tissue dysfunctions, shoulder
contractions (presence), 44f surgeries, 124
Sirolimus, usage, 405t Soft-tissue injuries
SIS. See Small intestine submucosa management, equipment, 124^132
Sitting pressure/pain, alleviation, x-ray detection, 91
117^118b Soft-tissue masses, detection/
Sitting tolerance, 117^118b localization, 91
Sit-to-stand transfers, facilitation,105b Soft-tissue repair/reconstruction, 126t
Six-minute walk test, 565^566 Soft-tissue surgeries, 123^124.
distance, prediction equations, 566t See also Experimental soft-tissue
overview, 566t surgery
procedure, 565^566 variety, 123^124
results, interpretation, 566 Solid ankle-foot orthosis (AFO),
symptom-limited measure, 565 130^131t
Skin Somatic nervous system (voluntary
breakdown, 132 nervous system), 152
occurrence, 125^127 Space-occupying lesion, 193t
cancer, 214^215 Spastic colon, 313
change, 242^243 Spatial orientation, maintenance, 186
color, observation, 222 Specimens, examination, 354
condition, 548t Speech ability, 164^165
destruction, occurrence, 222 Speech assessment, performing, 164^165
grafting, 204 Speech-language pathologist,
grafts. See Composite skin graft consultation, 165
dressings, 229t Sphygmomanometer, 448^449t
incision, decrease, 109 Spinal accessory, 167^169t
infections, 365 Spinal cord, 157
layers, structure/function, 220t cross-section, 159t
mechanical properties, changes, 236 placement, 157
substitutes, 292 tissues, inflammation, 364
temperature, 57 Spinal cord injury (SCI), 177^180. See also
three-dimensional Primary SCI; Secondary SCI
representation, 264f early mobilization, 179^180b
variations, 264 function, loss (association), 179t
Skin integrity, 89 impact, 177
inspection, 89 management, 180
maintenance, 92 severity, classification, 177
Skin lesions syndromes, 179t
observation, 223 Spinal instability, pain, 120
resection, 215b Spinal pathologies, 119^123
SLC. See Short leg cast Spinal shock, 179^180
SLE. See Systemic lupus erythematosus Spinal surgery, 120^123
Sleep, interruption/deprivation advances, 120
(interference), 435 back pain indication, 119
Sleeping position, 53 functional mobilization, 121^122
 INDEX 603
Spinal surgeryçContinued Strengthening program, Supracondylar distal femoral fractures,
indications, 120t establishment, 105 96^97
physical therapy intervention, 121^122 Stridor, 56 Suprapubic catheter, 454t
Spine, 98^100 acute onset, 56b Suprascapular nerve, 160t
Spine/trunk soft cervical collar, 130^131t high-pitched wheeze, 56 Supraventricular tachycardia, catheter
Spiral fracture, screws, 93f Stroke, 180, 394 ablation procedures (indication),
SPK. See Simultaneous pancreas-kidney Stroke-in-evolution, 181t 28^29
Splenic systems, diagnostic Stroke volume (SV), 4 Supravesical diversion, 347
procedures, 307t Structural deformities, occurrence, 281 Surface area, 49
Splenomegaly, 246 Struvite kidney stones, 337 Surface replacement arthroplasty, 111
Splints, 127^128 STSG. See Split-thickness skin graft Surgery, history, 52
acute care setting, 130^131t Subacute glomerulonephritis, 336 Surgical devices, 479^481
medical/surgical intervention Subarachnoid bolt, 453t Surgical drain, 454t
techniques, combination, Subarachnoid hemorrhage (SAH), Surgical ICU (SICU), 433
127^128 181^183 Surgical incisions, presence/location,
Split liver transplant, 409 complications, 183 54^55
Split-thickness skin graft (STSG), 274t diagnosis, 183 Surgical subtotal-thyroidectomy, 380
SPMS. See Secondary-progressive MS Hunt and Hess scale, 181^183 Surgical wounds, 279
Spontaneously breathing adults, variable Subarachnoid space, 157t residual skin defects, 279
performance oxygen delivery, Subcapital fractures, 96 Sussman Wound HealingTool
442^444t Sub capital fractures, garden (SWHT), 287
Spontaneous PTX, 77^79 classification, 96f SV. See Stroke volume
Sputum analysis, 63 Subclinical infection, term, 355t Swallowing reflex, 171^172
culture/Gram stain, inclusion, 63 Subcutaneous air, presence, 62 Sweat test, 305^306t
Squamous cell cancer, occurrence, 214 Subcutaneous connective tissue layer, SWHT. See Sussman Wound
SSRIs. See Selective serotonin reuptake three-dimensional HealingTool
inhibitors representation, 264f Syme’s amputation (ankle
Stable angina, 21 Subcutaneous emphysema, presence, 58 disarticulation), 545t
occurrence, 21 Subdural hematoma (SDH), 178t Symmetric polyneuropathies, 394t
Staining, usage, 357 Subdural space, 157t Symmetric sensorimotor
Standard above amputation, 547t Submaximal tests, 18 neuropathy, 393
Staphylococcus aureus, 358, 359t Substance abuse/withdrawal, 435 Sympathetic system neural input, 5
Static ocular observation, 188^189t Subthalamus, 155^156t Synchronous intermittent mandatory
Stationary bicycles, usage, 215 Subtotal cystectomy, 339 ventilation (SIMV),
Status epilepticus, 185^186t Subtrochanteric fractures 466^468, 466t
STchanges, onset, 35 Evans classification, 141t criteria, 470
Steinbrocker classification. See Complex management/physical therapy Syncope, 186
regional pain syndrome intervention, 141t characteristics, 186
Stem cell research, 402 Russell-Taylor classification, 141t diagnosis, 186
Stenosis, involvement, 22 Sucralfate, 514t history, 7
Stereognosis, testing, 172t Sulfasalazine, breakdown, 499^501t Syndesmosis, two-component
Stereotaxis, 194t Sulfonamides, 517^520t design, 113
Stethoscope earpieces, direction, 57b Sulfonylureas, 526^528t Syndrome of inappropriate ADH
Stimulants, 515t Superficial burn, 271f (SIADH), 385
Stimuli Superficial organs/masses, palpation, condition, 385
patient identification, 172b 298^299 etiologies, 385
progressive intensity, usage, 163b Superficial reflex, muscle contraction, management, 385
Stomach disorders, 310^311 171^172 Syngenetic transplant, 419
Stomach ulceration, 310 Superficial wounds, epidermal Synovial fluid analysis, 358
Stratum basale, 265t involvement, 287 Synthetic graft
Stratum corneum, 265t Superior cerebellar artery (SCA), 159t insertion, 258f
Stratum granulosum, 265t Superior gluteal nerve injury, 94^95 native aortic wall,
Stratum spinosum, 265t Superior patellar capsular releases, suturing, 258f
Strength allowance, 109 Systemic blood pressure, 223
force output, 170 Supine position. See Anesthesia Systemic circulation, 6^7
gradations, 170 Supplemental O2 CO factor, 6^7
testing, 170 delivery, 441 schematic, 7f
Strengthening exercises, postoperative presence, 54 Systemic complications, control,
initiation, 108 requirements, 441 375^376
604 INDEX

Systemic lupus erythematosus (SLE), Texas catheter. See Condom catheter Thrombolytics (fibrinolytics), 495t
77, 374 THA. SeeTotal hip arthroplasty Thrombolytic therapy, 26^27
clinical presentation, 374 Thalamus, 155^156t acute management strategy, 26
laboratory test, 374 Thalassemia, 249 contraindications, 27
management, 370 autosomal-recessive disease, 249 indication, 27
prognosis, 374 management, 249 Thrombotic thrombocytopenic purpura
Systemic opioids, 536 patient classification, 249 (TTP), 249^250
characteristics, 538t Thallium stress testing, 19. See also management, 250
Systemic vasculitis, 237^239 Persantine thallium stress testing signs/symptoms, 249^250
factors, 237^238 usage, 19 Through-the-knee amputation, 545t
Systole, 2^4 TheJoint Commission (TJC). See Thyrocalcitonin, 379t
onset, 475 National Patient Safety Goals Thyroid ablation, 381
Systolic blood pressure (SBP), 9^11 requirements, 535 Thyroid adenoma, 382t
limitations, 255b standards, 427 Thyroidal 24-hour radioactive iodine
Systolic dysfunction, 23 Theopylline, 497^498t uptake, 381t
Therapeutic hydrodistention, 339 Thyroid carcinoma, 382t
T Therapeutic radiation, administration Thyroid disorders, 379^382
Tacheostomy, consideration, 463 (purpose), 204 treatment, 485t
Tachyarrhythmias, 29 Thermal burns, 265^266 Thyroid function tests, 381t
Tachycardia, 248 result, 265^266 Thyroid gland, 379^382
Tachypnea, 248 types/characteristics, 267t aplasia, 380
Tacrolimus, usage, 405t Thiazolidinediones, 526^528t function, 379
Takayasu’s arteritis, 239 Thienopyridine, 493t hormones, target sites/actions, 379t
Talus, fractures, 97^98 Third-degree burns, 269 Thyroid hormones (T3/T4)
TandemHeart, 475^476 Third-degree heart block, 18 action, 380
complications, 476 Thoracentesis, 80. See also Pleural tap levels, 379b
extracorporeal continuous flow Thoracic incisional pain, 73 synthesis, inhibition, 485t
centrifugal assist device, 475^476 Thoracic procedures, 80^81 tests, 380t
indications, 476 history, 52 Thyroid imaging/scan, 381t
percutaneous VAD, 476f Thoracic spine, fracture (clearance), Thyroiditis, 382t
Tangential excision, 274t 99^100b Thyroid-stimulating hormone
Tapping sounds, listening, 11 Thoracic surgeries (TSH), 380t
Target organs, hypertensive effects, 237t images, 80f Thyroid tests, 379
TB. SeeTuberculosis incisions, involvement, 207^208b Thyrotoxicosis. See Hyperthyroidism
TBG. SeeThyroxine-binding globulin Thoracolumbar fracture, Thyrotropin, 383t
TBI. SeeTraumatic brain injury description/management, Thyrotropin-releasing hormone
TBSA. SeeTotal body surface area 99^100 (TRH), 380t
TCAs. SeeTricyclic antidepressants Thoracolumbar spine fractures Thyroxine-binding globulin
TCD. SeeTranscranial Doppler management, 148t (TBG), 379
sonography physical therapy, 148t Thyroxine (T4), 379t
TEA. SeeTotal elbow arthroplasty Thorascopy, 80^81 TIA. SeeTransient ischemic attack
TEE. SeeTransesophageal Thoratec paracorporeal VAD, 481f Tibial osteotomy, 118^119. See also
echocardiography Thrombectomy, 254 Proximal tibial osteotomy
Telemetric electrocardiogram method, 254 physical therapy, 118^119
monitoring, 13^14 Thrombi focus, 118
real-time ECG visualization, 13^14 accumulation, 249 ROM tolerance, 118
Telemetry, Holter monitoring (benefit), treatment, 236 strengthening exercises, 119, 119
13^14 Thromboangiitis obliterans (Buerger’s Tibial plateau fracture, 97
Temperature disease), 238^239 classification, 98f
control, ICP treatment option, 194t treatment, 239 complexity, 97
monitoring, 356 Thrombocytes (platelets), 221t management, 143t
regulation, 264 Thrombocytic disorders, 247^250 physical therapy intervention, 143t
testing, 172t Thrombocytopenia, 249. result, 97
Temporal arteritis, 239 See also Heparin-induced Tibial shaft fractures, 97
Temporal lobe, 154t thrombocytopenia medical-surgical management, 144t
Tendon calcification, 91 exercise guidelines, 258 physical therapy intervention, 144t
Tendon impingement, 128 management, 249 result, 97
Tentorium cerebelli, 156t result, 249 Tidal volume, 470
Tetracyclines, 517^520t signs/symptoms, 249 Tilt table, usage, 432b

Timed up and go (TUG) test,
555^561
completion, 561
overview, 561t
procedure, 560
results, interpretation, 560^561
Tinetti performance-oriented mobility
assessment (Tinetti POMA),
562^565
balance maneuvers, grading, 562
overview, 565t
procedure, 562
results, interpretation, 562^565
Tinnitus, 187
Tissue biopsy, 302^303t
Tissue damage, occurrence,
266^267
Tissue densities (evaluation), mediate
percussion (usage), 58
Tissue hypoxia, 125
Tissue necrosis, 266^267
Tissue pH, impact, 6
Tissue plasminogen activator (tPA), 174
Tissue staining. See Hyperpigmentation
Titanium alloys, usage, 102^103
TJC. SeeTheJoint Commission
TKA. SeeTotal knee arthroplasty;
Tricompartmental knee
arthroplasty
TLSO. See Molded thoracolumbosacral
orthosis
TNM. SeeTumor Node Metastasis
Toe touch weight bearing,
limitation, 118
Tonic-clonic seizure, 185t
Tonic seizure, 185t
Topical agents, 290
Topical dressings, 291^292t
Total ankle arthroplasty, 113
popularity, problems, 113
Total body surface area (TBSA), 268
changes, 268
Total cholesterol levels, elevation, 15
Total cystectomy, 339
Total disc replacement, experimental
designs, 120^121
Total elbow arthroplasty (TEA),112^113
complications, 113
early results, 112^113
flexion. See Left total elbow
arthroplasty
reliability, 112
Total femur replacement, 115
complication, 115
illustration, 116f
indication, 115
patient-specific procedure, 115
patient tolerance, 115
physical therapy intervention, 115
Total hip arthroplasty (THA), 102^103.
See also RevisionTHA;
Uncemented THA
medical complications, 104
precautions, 114
protocol, 106
surgical approaches/movement
precautions, 103^104
surgical approaches/precautions, 96f
Total joint arthroplasty
early postoperative period, 113
infection/resection, 113^115
rapid recovery program, 110
Total joint resurfacing, 105^106
Total knee arthroplasty (TKA),
106^107
anterior view. See Right TKA
complications, 107b
fixation, methods, 107
medical complications, 107
proximal tibial osteotomy,
alternative, 118
ROM, usage, 108^109b
Total peripheral resistance (TPR), 6^7
impact, 6^7
Total shoulder arthroplasty (TSA)
glenoid articulating surface,
replacement, 110
glenoid fixations/designs, 111
indication, 110
prostheses, types (availability), 110
rehabilitation, 111
ROM exercises, usage, 111
similarity. See Reverse total
arthroplasty
Toxic nodular/multinodular goiter, 382t
Toxoplasmosis, 369
clinical manifestations, 369
management trend, 369
tPA. SeeTissue plasminogen activator
T-piece, criteria, 470
TPR. SeeTotal peripheral resistance
Tracheal resection/reconstruction, 81
Tracheal sounds, 55
Tracheobronchial tree, 55
damage, 270
Tracheostomy, 81
mask/collar, 442^444t
example, 442^444t
Traction, 132
complications, 132
pin sites, infection, 132
types, 132t
Transcatheter thrombolysis, 254
process, 254
Transcranial Doppler sonography
(TCD), 174
Transcutaneous ureterostomy, 348f
TransCyte, usage, 228t
INDEX 605
Transesophageal echocardiography
(TEE), 17, 176
diagnostic tests, 235
usefulness, 176
Transfer anxiety, 434
Transient ischemic attack (TIA), 180
characterization, 180
Transmetatarsal amputation, 545t
Transmyocardial revascularization,
27^28
Transparent film dressing, 291^292t
Transplantation. See Organ
transplantation
Transplant recipients
activity progression, 422
patient education, 422^423
physical therapy
goals, 421^422
guidelines, 413^416
treatment concepts, 422
Transthoracic echocardiography
(TTE), 176
cardiac echo, noninvasive
procedure, 17
Transtracheal catheter, 442^444t
Transurethral resection, 346
surgical approach, 346
Transverse fracture, plates/screws, 93f
Trauma, signs, 8
Traumatic arthritis, 110
Traumatic brain injury (TBI),
176^177
clinical findings, 178t
extent, 176
injury mechanism, 176
location, 176
management, 178t
medical-surgical treatment, 176
severity, 176
Traumatic PTX, 77^79
Trauma wounds, 241
Trazadone, 503^504t
Trendelenburg position, contraindications,
551
Trendelenburg’s test, 225^226t
TRH. SeeThyrotropin-releasing
hormone
Tricompartmental knee arthroplasty
(TKA), 106^107
Tricyclic antidepressants (TCAs),
503^504t
Trigeminal nerve, 167^169t
Triglycerides, 15
Triiodothyronine resin uptake
(RT3U), 381t
Triiodothyronine (T3), 379t
Trochanteric osteotomy, 119
abductor precautions, 119
physical therapy intervention, 119
606 INDEX
Trochanteric osteotomyçContinued
postoperative evaluation/
treatment, 119
ROM/strengthening, 119
surgical fixation, usage, 119
Trochlea, ulna (impact), 100
Trochlear nerve, 167^169t
Troponin I/T, 15
True aneurysms, 234f
definition, 234
True intermittent claudication,
differentiation, 233t
Truncal obesity, 384
Trunk
circumferential burns, 224
major peripheral nerves, 161t
TSH. SeeThyroid-stimulating hormone
TTE. SeeTransthoracic
echocardiography
TTP. SeeThrombotic thrombocytopenic
purpura
T tube/piece, 446t
Tuberculosis (TB), 361^363
acquisition risk, 362
development. See ActiveTB
development, absence, 362
high-risk populations, 362
management, 362
occurrence. See ExtrapulmonaryTB
presence, 358
status, ATS/CDC category
classification, 362
TUG. SeeTimed up and go
Tumor
classification, 200
surgical removal, 203
term, usage, 199^200
Tumor Node Metastasis (TNM) system,
201, 212
Tunneled central venous catheter, 454t
TURP, 346
24-hour urinary corticosteroids, 387
24-hour urine test, 332
Two-hour postload glucose, 389
Two-point discrimination, testing, 172t
Type 1 diabetes (insulin-dependent
diabetes / juvenile-onset
diabetes), 389, 389^391
autoimmune disorder, 389
management, 389
medication summary, 389
monitoring tests, 390t
research, 389^391
signs/symptoms, 389
Type 2 diabetes (noninsulin-dependent
diabetes / adult-onset diabetes),
389, 391^392
commonness, 391
management, 391^392
Type 2 diabetes (noninsulin-dependent
diabetes / adult-onset
diabetes)çContinued
mechanism, 391
monitoring tests, 390t
onset, 388^389
research, 392
signs/symptoms, 391
Typical antipyschotics, 505t
Tyrosine kinase inhibitors, 509^511t
U Ureteral obstruction, 408
UGIB. See Upper gastrointestinal bleed
UKA. See Unicompartmental knee
arthroplasty
Ulcerative colitis, 314^315
etiology, 314^315
management, 315
manifestations, 315
signs/symptoms, 315
Ulna, shaft/distal portion
(fractures), 102
Ulnar nerve, 160t
Ultra-high-molecular-weight
polyethylene implant, 102^103
Ultrasonography studies, 333
Ultrasound, 381t
tests, 307t
Ultraviolet burns, 268
UMN lesions, indication, 171^172
Uncemented THA, 103
Unconstrained TSA prostheses, 110
Unicompartmental knee arthroplasty
(UKA), 106. See also Right medial
compartment
Unicondylar distal femoral fractures,
96^97
Unicondylar knee arthroplasty, 106
Unifocal PVCs, 35
United Network for Organ Sharing
(UNOS), 403
procurement/distribution. See Organ
procurement/distribution
Unstable angina (USA), 21
severity, 21
Unstable pelvic fractures, examples, 95f
Upper abdominal pain, 73
Upper extremity, 100^102
amputation, 543
considerations/treatment
suggestions, 549t
illustration, 546f
types, 547t
coordination test, 173t
DTRs, 171t
ergometers, usage, 215
major peripheral nerves, 160t
Upper extremity Simple arm sling,
130^131t
Upper gastrointestinal bleed
(UGIB), 310
result, 310
Upper GI series, 303^304t
Upper-quarter screen, 89^90
list, 89t
sequencing, 89^90
Upper respiratory tract infections,
360^361
Upper subscapular nerve, 160t
Urea breath test, 302^303t
Ureteroileosigmoidostomy, 348f
Ureterolithotomy, 347
Ureterostomy, 348f
Ureters, radiographic examination, 332
Urethral biopsies, 333
Uric acid kidney stones, 337
Urinalysis, 331
performing, 331
Urinary calculi, 339
stones, formation, 339
Urinary catheter (Foley catheter), 454t
Urinary diversion, 347. See also Continent
urinary diversion; Incontinent
urinary diversion
methods, 348f
Urinary flow, obstruction, 347
Urinary frequency, 339
Urinary incontinence, types, 340t
Urinary stone, removal, 347
Urinary system
pain referral areas, 328t
segmental innervation, 328t
Urinary tract dysfunction, 339
Urinary tract obstruction, 337
Urinary tract structures (evaluation),
sequential radiographs
(usage), 332
Urinary urgency, 329, 339
Urine abnormalities, 331t
Urine amylase, 305^306t
Urine leaks, occurrence, 408
Urine output, decrease, 405
Urine testing, 390t
Urine urobilinogen, 305^306t
Urobilinogen. See Urine urobilinogen
Urodynamic studies, 333
Urolithiasis, 339
Urologic injury, 94^95
V
VA. SeeVentriculoatrial
Vacuum Assisted Closure (V.A.C.),
290^292
VAD. SeeVentricular assist devices
Vagal neural input. See Parasympathetic
system neural input
Vagus nerve, 167^169t

Valve replacement, 30
Valvular heart disease, 22
disorders, occurrence, 22
signs/symptoms, 24t
Valvular stenosis, 363
V-A mode, achievement, 477^478
Vancomycin, usage (control), 360
Vancomycin-resistant
enterococci (VRE)
infection, 360
detection, screening procedures
(implementation), 360
management, 360
transmission, 360
patients, stethoscopes/rectal
thermometers (usage), 360
transmission, prevention, 360
VAP. SeeVascular Access Port;Ventilator-
associated pneumonia
Variable global myocardial depression,
manifestation. See Cardiac
transplantation
Variable performance oxygen
delivery. See Spontaneously
breathing adults
Variant angina (Prinzmetal’s angina), 21
Varices. See Esophageal varices
characterization, 309
Varicose veins, 240^241
chronic dilations, 240
management, 241
occurrence. See Primary varicose
veins; Secondary varicose veins
risk factors, 240
symptoms, 240^241
Vascular access, 342
methods. See Hemodialysis
Vascular Access Port (VAP), 454t
Vascular compliance/resistance, 4
Vascular compromise, 223b
Vascular disease, location/severity
(observation), 222^223
Vascular disorders, 231^243
anticoagulation therapy, 251
drug classifications, 250^251
management, 250^259
pharmacologic therapy, 250^251
physical therapy interventions,
255^259
Vascular evaluation, 222^224
Vascular insufficiency wounds, clinical
indicators, 280t
Vascular laceration, 474
Vascular occlusion, bypass, 254^255
Vascular smooth muscle
alpha2-adrenergic receptors,
up-regulation theory, 239
Vascular surgical procedures,
254^255
Vascular system
auscultation, 223
diagnostic studies, 224
function, 221^222
history, 224
inspection, 224
introduction, 219
invasive vascular studies, 224
laboratory studies, 227^231
noninvasive laboratory studies, 224
palpation, 223
pathophysiology, 231^250
physical examination, 222^231
history, 222
inspection, 222^223
structure, 220^221
tables, 509^512
Vascular tests, 224
list, 225^226t
Vasodilators, 489^491t
Vasomediator production,
imbalance, 236
Vasopressin. See Antidiuretic
hormone
Vasospasm, 183
VASs. SeeVisual analog scales
Vegetative state (VS), 433^435
diagnosis, 433
Veins, structure, 221f
Venography, 332^333
Veno-occlusive disease, 421
Venous disorders, 240^243
clinical findings, comparison, 232t
combination. See Arterial
disorders 243
Venous drainage, usage, 477^478
Venous insufficiency wounds, 279^280
result, 279^280
Venous pattern, observation, 223
Venous stasis ulceration, 243
Venous thrombosis, 241^242
management, 242
occurrence, 241
PE complication, 242
Venous ulcers, 280
Venous valves, 242f
Ventilation (PaCO2), 16
modes, 465
alternates, 467^468t
list, 466t
range, 465
ratio. See Respiratory system
scan, 64
settings, 469t
: :
Ventilation-perfusion ( V/ Q)
mismatch, 51, 79
extent, determination, 77
scan, 64
usage, 64
INDEX 607
Ventilator-associated pneumonia (VAP),
468^470
Ventilators. See Positive pressure
ventilators; Pressure-cycled
ventilators;Volume-cycled
ventilators
settings, 469t
weaning, distress (signs), 470^471
Ventilatory settings, 465
parameters, establishment, 465
Ventilatory support
consideration, 463
weaning, 471
Ventricular arrhythmias, 18
Ventricular assist devices (VAD), 413,
479^481. See alsoThoratec
paracorporeal VAD
cessation, indications, 482
components, 479
education manual, usage, 481
heart failure, occurrence, 482
indication, 479
list, 482t
manufacture, 473
physical therapy considerations, 479
power, 482
therapy, superiority, 479
usage, increase, 481
ventricular arrhythmias, risk, 481
Ventricular contraction, 4
Ventricular depolarization, result, 22
Ventricular diastole, 4
Ventricular dysfunction,
184^185
Ventricular ectopy, 22
refractory period, inclusion, 43f
Ventricular fibrillation, 45f
Ventricular pressure, 153^156
Ventricular rhythms, ECG
characteristics/causes, 39t
Ventricular system, 153^156
brain nourishment, 153
Ventricular systole, 4
Ventricular tachycardia
catheter ablation procedures,
indication, 28
characteristics, 43f
Ventriculoatrial (VA) shunt, 454t
Ventriculography, 20
Ventriculoperitoneal (VP) shunt, 454t
Ventriculostomy. See Intraventricular
catheter
Venturi mask, 447f
VEP. SeeVisual evoked potential
VER. SeeVisual evoked response
Verbal descriptor scales, 536t
Vertebral artery, 159t
Vertebral augmentation, 122
Vertebral column, axial support, 119
608 INDEX

Vertebral compression fractures, W WoundsçContinued

presence, 397 Walking pace, METs/oxygen clean technique, sterile technique
Vertebral compression fractures, consumption (contrast), 19f (contrast), 288
treatment, 122^123 Waste exposure, 430 clinical indicators. SeeVascular
Vertebroplasty, 118^119 Water-based dye, usage, 176b insufficiency wounds
guidelines, 123 Water deprivation test, 384t cognition, impact, 283
percutaneous procedure, 122^123 Water loading test, 384t color, 286
physical therapy, 123 Watershed stroke, 181t contamination, 286^287
radio-opaque cement, needle Weakness, management, 385b culture, 286^287
insertion, 123f Wedge resection, 81 debridement, 287^290, 288^290
Vertical banded gastroplasty, 319^320t image, 80f depth, 285^286
Vertigo, 186 Wegener’s granulomatosis, 238 measurement, 286
elicitation, 190f necrotizing disease, 238 drainage, 286
Very short above amputation, 547t treatment, 238 dressing, 290, 276t
Vesicular sounds, 55 Weight-bearing orders, edema, impact, 285
hearing, 55 clarification, 365b enzymatic debridement, 289
Vestibular dysfunction, 186^187 Weight-bearing restrictions, evaluation, 285^287
tests/measures, 188^189t 114^115 function, 264, 264
Vestibular neuritis. See Acute vestibular Western blot test, 366 functional mobility,
neuronitis Wet crackles (rales), 56b evaluation, 285
Vestibulocochlear nerve, 167^169t Wet-to-dry dressings, mechanical healing
Vibration, testing, 172t debridement, 289 factors, 282^283
Viral rhinitis, 360 Wheeze, 56 process, 281^282
clinical manifestations, 361 occurrence, 56 history, 283^284, 283^284
Viral RNA/DNA polymerases, non- Whipple procedure inflammatory phase, 281^282
competitive inhibition, 524^525t (pancreaticoduodenectomy), inspection, 285^287
Visceral pleura, disorders/trauma, 77 319^320t introduction, 263
Vision Whipple’s disease, 314 length, documentation, 285^286
testing, importance, 166 White blood cells (WBCs) lifestyle, impact, 282
Visual analog scale/ratio (leukocytes), 221t location, 285^286
scale, 52^53 counts, 14, 205^206b, 227^228. mechanical debridement, 289^290
Visual analog scales (VASs), 536t See also Differential white blood medical status, 283
Visual evoked potential (VEP), 175^176 cell count medications, 283
Visual evoked response (VER), 175^176 elevation, 417^418 nonselective debridement,
abnormal latencies, 175^176 monitoring, 417 289^290
Visual field defects, 169f values/interpretation, 230t nutrition, impact, 282^283
Visual pathway, lesion sites, 169f differential, 230t orientation, 285^286
Vital signs, 165^166 existence, 357 pain, 284. See also Noncyclic acute
monitoring, 432b malignancies, 211 wound pain
neurologic measure, 165 White blood cell-trapping evaluation, 284
trends, therapist awareness, 165^166b hypothesis, 280 experience, 284
Vitamin B12 anemia, 244 White matter tracts. See Major pathophysiology, 279^281
neurologic symptoms, 244 ascending/descending white physical examination, 284^285
Vitamin B12 deficiency, 244 matter tracts psychosocial factors, 284
Vitamin D, 529t Whooping cough. See Pertussis risk factors, 284
synthesis, 264 Wilson’s disease, 408 ROM, 284
Voice change, 387 Wong-Baker Faces scale, 536t selective debridement, 288^289
Voice sounds, 56^57 Wounds self-care ability, impact, 283
Voiding habits, changes, 328^329 acute care management, sensation, examination, 284
Volume-cycled ventilators, 464^465 283^292 sharp debridement, 288^289
Volume status, assessment, 407 advanced therapies, 290^292 pain, 289
Voluntary nervous system. age, impact, 282 size, 285^286
See Somatic nervous system assessment, 283^292 strength, evaluation, 284^285
VP. SeeVentriculoperitoneal autolytic debridement, 289 structure, 264, 264
: :
V/ Q. SeeVentilation-perfusion care, physical therapy surrounding areas, evaluation, 287
VRE. SeeVancomycin-resistant considerations, 293t therapy. See Negative pressure wound
enterococci intervention, 292^293 therapy
VS. SeeVegetative state circulation, impact, 285 topical agents, 290
V-Vmode, 478 cleaning, 287^290, 287^288 types, 279^281
 INDEX 609
WoundsçContinued X Y
vascular status, 283 Xenograft. See Heterograft Yankauer suction, 454t
wet-to-dry dressings, 289 X-rays, 173^174. See also Chest x-ray;
whirlpools Sequential x-rays Z
limitation, 290 ordering, 92b Zollinger-Ellison syndrome, 314, 311
usage, 289 usage, 173^174 clinical triad, 311
Wrist disarticulation, 547t
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