ACUTE CARE

HANDBOOK for
PHYSICAL THERAPISTS
This page intentionally left blank

     
ACUTE CARE
HANDBOOK for
PHYSICAL THERAPISTS
Fifth Edition JAIME C. PAZ, PT, DPT, MS
Program Director / Professor
Physical Therapy Program
School of Behavioral and Health Sciences
Walsh University
North Canton, Ohio

MICHELE P. WEST, MS, PT

Physical Therapist
Inpatient Rehabilitation Services
St. Joseph Hospital
Nashua, New Hampshire

KATHRYN PANASCI, PT, DPT

Certified Brain Injury Specialist (CBIS)
Certified Wound Specialist (CWS)
Assistant Professor
Doctor of Physical Therapy Program
Department of Rehabilitation Sciences
Texas Tech University Health Sciences Center
Lubbock, Texas

KRISTIN CURRY GREENWOOD, PT, DPT, EdD, MS

Board-Certified Clinical Specialist in Geriatric Physical Therapy (GCS)
Department Chair and Associate Clinical Professor
Department of Physical Therapy, Movement and Rehabilitation Sciences
Northeastern University
Boston, Massachusetts
Elsevier
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ACUTE CARE HANDBOOK FOR PHYSICAL THERAPISTS, FIFTH EDITION ISBN: 978-0-323-63919-4
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 Contributors

Laura A. H. Blood, PT, DPT David M. Krause, PT, DPT

Board-Certified Clinical Specialist in Geriatric Physical Physical Therapist II
Therapy (GCS) Physical Medicine and Rehabilitation
Senior Physical Therapist University Medical Center
Home Care Rehabilitation Services Lubbock, Texas
Private Care Therapies, PLLC;
Part-Time Lecturer Harold Merriman, PT, PhD, CLT
Department of Physical Therapy, Movement and Associate Professor
­Rehabilitation Sciences Department of Physical Therapy
Northeastern University University of Dayton
Boston, Massachusetts Dayton, Ohio

Sean M. Collins, PT, ScD Lauren Mitchell, PT, DPT

Professor & Program Director Physical Therapist II
Physical Therapy Physical Medicine and Rehabilitation
Plymouth State University Johns Hopkins Hospital
Plymouth, New Hampshire; Baltimore, Maryland
Editor-in-Chief
Cardiopulmonary Physical Therapy Journal; Clare Nicholson, PT, DPT
Adjunct Professor Board-Certified Clinical Specialist in Cardiovascular and
Biomedical Engineering Pulmonary Physical Therapy (CCS)
University of Massachusetts—Lowell Clinical Team Leader Med Surg
Lowell, Massachusetts Cleveland Clinic Rehabilitation & Sports Therapy
Cleveland Clinic
Konrad J. Dias, PT, DPT Cleveland, Ohio
Board-Certified Clinical Specialist in Cardiovascular and
­Pulmonary Physical Therapy (CCS) Matthew Nippins, PT, DPT
Associate Professor Board-Certified Clinical Specialist in Cardiovascular and
Physical Therapy Pulmonary Physical Therapy (CCS)
Maryville University of St. Louis Assistant Clinical Professor
St. Louis, Missouri Department of Physical Therapy, Movement and
­Rehabilitation Sciences
Margarita V. DiVall, PharmD, MEd Northeastern University;
Associate Dean Senior Physical Therapist
Bouvé College of Health Sciences; Massachusetts General Hospital
Clinical Professor Boston, Massachusetts
School of Pharmacy
Northeastern University Marka Gehrig Salsberry, PT, DPT
Boston, Massachusetts Clinical Faculty
Physical Therapy
Laura C. Driscoll, PT, DPT The Ohio State University
Board-Certified Clinical Specialist in Geriatric Physical Columbus, Ohio
Therapy (GCS)
College of Health and Rehabilitation Sciences: Sargent College Julie Anna Snyder, PT, DPT
Department of Physical Therapy & Athletic Training Acute Care Physical Therapist
Boston University Rehabilitation Services
Boston, Massachusetts University Hospitals Ahuja Medical Center
Beachwood, Ohio
Karen Jeanne Hutchinson, PT, MS, DPT, PhD
Clinical Associate Professor
Department of Physical Therapy & Athletic Training
Boston University
Boston, Massachusetts
        v
vi CONTRIBUTORS

Erin M. Thomas, PT, DPT Kimberly Knowlton, PT

Assistant Professor of Practice Clinical Lead Physical Therapist
Physical Therapy Rehabilitation Services
The Ohio State University University of Massachusetts Memorial Medical Center
Columbus, Ohio Worcester, Massachusetts
Burns and Wounds
Alysha Walter, PT, DPT
Board-Certified Clinical Specialist in Cardiovascular and Eileen F. Lang, PT, DPT
Pulmonary Physical Therapy (CCS) Senior Physical Therapist
Assistant Clinical Professor Rehabilitation Services
Physical Therapy Program, School of Behavioral and Health Lahey Clinic North Shore
Sciences Peabody, Massachusetts
Walsh University Medical-Surgical Equipment in the Acute Care Setting
North Canton, Ohio
V. Nicole Lombard, MS, PT
Adam B. Woolley, PharmD, MEd Staff Physical Therapist
Associate Clinical Professor Department of Physical Therapy
Bouvé College of Health Sciences New England Baptist Hospital
Northeastern University Boston, Massachusetts
Boston, Massachusetts; Infectious Diseases
Clinical Pharmacist
Department of Pharmacy Rachael Maiocco, MSPT
VA Boston Healthcare System Physical Therapist
West Roxbury, Massachusetts Brigham and Women’s Hospital
   Boston, Massachusetts
Infectious Diseases
Contributors to Previous Editions
Cheryl L. Maurer, PT
Cathy S. Elrod, PhD, PT Senior Physical Therapist
Chair and Associate Professor Outpatient Physical Therapy Services
Department of Physical Therapy Massachusetts General Hospital
Marymount University Boston, Massachusetts
Arlington, Virginia Musculoskeletal System
Musculoskeletal System
Leah Moinzadeh, PT
James J. Gaydos, MS, PT Physical Therapist
Senior Physical Therapist Inpatient Rehabilitation
Department of Inpatient Acute Care Rehabilitation Services
New England Baptist Hospital Lahey Clinic
Boston, Massachusetts Burlington, Massachusetts
Musculoskeletal System Organ Transplantation

Jennifer Lee Hunt, MS, PT Jackie A. Mulgrew, PT, CCS

Physical Therapist Clinical Specialist
Rehabilitation Services Physical Therapy Services
Lahey Clinic Massachusetts General Hospital
Burlington, Massachusetts Boston, Massachusetts
Organ Transplantation Circulatory Assist Devices

Marie Jarell-Gracious, PT
Owner
Specialty Care
Mokena, Illinois
Burns and Wounds
 CONTRIBUTORS vii

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

In-Patient Physical Therapy Coordinator Senior Physical Therapist
Department of Rehabilitation Services Inpatient Complex Medical
Newton-Wellesley Hospital Spaulding Hospital–Cambridge
Newton, Massachusetts; Cambridge, Massachusetts
Clinical Instructor Nervous System
Department of Physical Therapy, Movement and
­Rehabilitation Sciences Paul E.H. Ricard, PT, DPT, CCS
Northeastern University Clinical Specialist
Boston, Massachusetts Rehabilitation Services
Gastrointestinal System Brigham and Women’s Hospital
Boston, Massachusetts;
Kara O’Leary, MS, PT, CCS Adjunct Faculty
Senior Physical Therapist Physical Therapy
Inpatient Physical Therapy and Outpatient Pulmonary University of Massachusetts–Lowell
­Rehabilitation Lowell, Massachusetts;
Rehabilitation Services Part-Time Lecturer
Lahey Clinic Department of Physical Therapy, Movement and
Burlington, Massachusetts ­Rehabilitation Sciences
Pulmonary System Northeastern University
Boston, Massachusetts
Susan Polich, PT, MA (ASCP), MEd Functional Tests
Assistant Clinical Specialist
Department of Physical Therapy, Movement and Jennifer A. Silva, MS, PT
­Rehabilitation Sciences Physical Therapist
Northeastern University Outpatient Rehabilitation Center
Boston, Massachusetts; South Shore Hospital
Adjunct Instructor South Weymouth, Massachusetts
Physical Therapy Assistant Program Functional Tests
Community College of Rhode Island
Newport, Rhode Island Timothy J. Troiano, PT
Oncology Senior Physical Therapist
Fluid and Electrolyte Imbalances Outpatient Physical Therapy Services
Massachusetts General Hospital
Danika Quinlan, PT, DPT Boston, Massachusetts
Staff Physical Therapist Oncology
Dayton VA Medical Center
Dayton, Ohio Falguni Vashi, PT, DPT
Acute Pain Management Physical Therapist
Rehabilitation Services
Jason D. Rand, PT St. Joseph Hospital
Physical Therapist Nashua, New Hampshire
Inpatient Physical Therapy Services Vascular System and Hematology
Winthrop University Hospital
Mineola, New York Karen Vitak, PT, DPT
Amputation Clinical Assistant Professor
Director of Clinical Education
Marie R. Reardon, PT School of Health Sciences
Clinical Specialist Cleveland State University
Inpatient Physical Therapy Services Cleveland, Ohio
Massachusetts General Hospital Organ Transplantation
Boston, Massachusetts
Musculoskeletal System
viii CONTRIBUTORS

Jessika Vizmeg, PT, DPT Kelsea A. Ziegler

Staff Physical Therapist
St. Vincent Charity Medical Center
Cleveland, Ohio
Endocrine System
Bouvé College of Health Sciences
School of Pharmacy
Northeastern University
Boston, Massachusetts
Pharmacologic Agents
 To Nay and Tay—my gratitude for a life full of blessings.
To Tallie, Will, and Henry—my joy and my life.
J.C.P.

For Isabelle and Genevieve, my sunshine!

For Amy Deck and Meredith King—you are champions,
steadfast and true.
For all the busy, hard-working, and devoted moms.
M.P.W.

For Michael, Ariana, and Luca—thank you for the craziness you
bring to life and to the many adventures we have ahead of us.
K.P.

For my husband, Jonathan, who inspires me to educate and lead

each day, and to my children, Alex and Hannah, who share how they see
the world through their eyes and seek to make change in the world.
For all the present and past students, faculty, and classmates that
provide me the privilege to teach and to learn alongside them.
K.C.G
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 Preface
In the early 1990s a handful of clinicians from Massachusetts
General Hospital in Boston, Massachusetts, sought to develop
a resource they believed was needed in the acute care setting.
With good fortune, a connection was made with Butterworth-
Heinemann, and the first edition of the Acute Care Handbook for
Physical Therapists was published. Twenty-two years later, with
Elsevier, the fifth edition of the Acute Care Handbook for Physical
Therapists has now published. Many ideas with lots of energy
were directed toward this project. Initially, the goal was to pro-
vide clinicians with a handy, pocket-sized reference for patient
care in the hospital setting. It was created primarily for physical
therapy students and clinicians unfamiliar with entry-level acute
care practice. This handbook was never intended to be a formal
comprehensive textbook; however, over the past four editions it
has evolved to become one of the resources available to students
and physical therapists seeking information for this content area.
Throughout the past 5 years, peer-reviewed literature and
clinical resources related to acute care physical therapy practice
have grown tremendously. Several efforts have been successfully
undertaken by collective stakeholders to maximize patient out-
comes and patient safety within the acute care setting, resulting
in position papers and references to help enhance practice in
real time. Many of the updates in this edition incorporate these
advances pertinent to the evolution of the care of patients in
the acute care environment as well as developments in medi-
cal science. Although it is impossible to keep up-to-date in the
moment of practice, we have provided categories and links, both
here and throughout the text, along with brief explanations of
their relevance, to extend the usefulness of this handbook into
practice. Some examples are provided:
• Resources available to members on the American Physical
Therapy Association website (apta.org):
• Physical Therapy Outcomes Registry: http://www.ptoutc
omes.com/home.aspx
• PTNow: https://www.ptnow.org/Default.aspx
• Clinical Practice Guidelines, including:
• Role of Physical Therapists in the Management of
Individuals at Risk for or Diagnosed with Venous
Thromboembolism: Evidence-Based Clinical Prac-
tice Guideline https://www.ptnow.org/clinical-
practice-guideline-detail/role-of-physical-
therapists-in-management-of-indiv
• Early Rehabilitation for Patients in the Intensive
Care Unit (ICU) https://www.ptnow.org/clinical-
summaries-detail/early-rehabilitation-patients-in-
intensive-care-unit
• Clinical Summaries:
• Stroke https://www.ptnow.org/clinical-summaries-
detail/stroke-2#ViewComplete
• D ocuments created by the Academy of Acute Care Physical
Therapy and available for free on their website (https://www
.acutept.org/):
• Laboratory values interpretation resources: 2017 Update
and Point-of-Care document: https://www.acutept.org/
store/ViewProduct.aspx?id=10758036
• Resources specific to entry-level education:
• Core Competencies for Entry-Level Practice in Acute
Care Physical Therapy https://www.acutept.org/store/
ViewProduct.aspx?id=10758435
• Core Competencies for Entry-Level Physical Therapy
Assistants in the Acute Care Setting https://www
.acutept.org/store/ViewProduct.aspx?id=10758519
• Interprofessional Practice Competencies:
• Interprofessional Education Collaborative: Core Compe-
tencies for Interprofessional Collaborative Practice: 2016
Update: https://www.ipecollaborative.org/resources.html.
With this fifth edition, editors Jaime Paz and Michele West
have recruited two talented associate editors, Kathryn Panasci
and Kristin Curry Greenwood, to help make the peer review
process more robust as well as to provide a transition for future
editions. For both Jaime and Michele, this will signal our last
edition as editors of the Acute Care Handbook. Since the first pub-
lication in 1997, we have been thankful to be able to contribute
to this area of clinical practice. Along with our new associate
editors, we acknowledge the work of past contributors, some
who have stayed on for many or all editions, and we welcome
the new contributors that have joined the team. Many of the
new and returning contributors are either faculty or clinicians in
highly specialized acute care centers. The overall combination of
our contributors allows material to remain current with litera-
ture while providing clinically relevant information.
This edition of the Acute Care Handbook for Physical Thera-
pists has been revised and updated to serve its original purpose.
All chapters include updated literature, available at the time of
revision, to assist with implementing evidence-based practice
in this setting. Each chapter centers on either a major body sys-
tem or health condition and includes:
• A review of body structure and function
• An overview of the medical-surgical evaluation of a patient
admitted to the hospital, including pertinent diagnostic pro-
cedures and laboratory tests
• A review of health conditions that emphasizes information
pertinent to physical therapy management
• Guidelines and considerations for physical therapy examina-
tion and intervention
Clinical Tips appear throughout each chapter. These helpful
hints are intended to maximize safety, quality, and efficiency
of care. As an essential member of the health care team, the
        xi
xii PREFACE
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 ICU to the
general ward. These Clinical Tips are suggestions from the edi-
tors and contributors that, from clinical experience, have proved
to be beneficial in acclimating therapists to the acute care set-
ting. With advances in literature pertaining to acute care, more
of these tips have become validated and thus are referenced
accordingly in this new edition.
It is important to remember that all information presented
in this book is intended to serve as a guide to stimulate indepen-
dent critical thinking within the scope of practice of physical
therapy and the spectrum of medical-surgical techniques and
trends. To implement evidence-based practice, this reference
should serve as one of the many resources involved with clinical
decision making. As health care continues to evolve, clinicians
will need to adapt information to the best of their ability. Devel-
oping and maintaining a rapport with the medical-surgical
team is essential to facilitate high-quality and safe patient care.
We believe the new edition of the Acute Care Handbook for Physi-
cal Therapists can enhance the content knowledge in the acute
care environment by providing valuable information to help
interpret medical record reviews, prepare for physical therapy
examination and intervention, assist in sound clinical decision
making, and support patient and interprofessional interaction.
J.C.P.
M.P.W.
K.P.
K.C.G
 Acknowledgments
We all offer sincere gratitude to the following people:
• Lauren Willis and Elsevier for their ongoing investment and
belief in working toward a fifth edition of this book.
• Maria Broeker for her professional guidance, support, and
immense patience with all of our questions during the entire
revision process.
• Jodi Willard for her welcoming assistance, flexibility, and
open communication in the production process.
• The contributors—both past and present. This textbook ob-
viously doesn’t exist without all of the hard work and dedica-
tion each of you has put toward this project. Both physical
therapists and patients have benefited from your expertise.
• The many patients and students who continually challenge
yet enrich our lives, both professionally and personally.
Personal thanks from Jaime to:
• Tallie, for continually reminding me what’s important in
life.
• Michele West, for all of your collaboration throughout the
years and editions.
• Kristin Curry Greenwood and Kate Panasci, for your will-
ingness to step up as Associate Editors—the future is in good
hands with you both.
• The PT faculty at Walsh University, who continue to be
great teammates.
• The dedicated clinicians, faculty, and researchers who have
helped advance the body of knowledge in this practice area.
• My faith and church community, who support me in ways I
didn’t know was possible.
Personal thanks from Michele to:
• Jaime Paz, for sharing your knowledge with me in the RICU
at the beginning of my career and for the countless hours of
work spanning decades as co-authors and editors.
• Kate Panasci and Kristin Curry Greenwood, for your hard
work and care of the fifth and future editions of the Acute
Care Handbook for Physical Therapists.
• Paula and Mike Panik, the best parents a daughter could
hope for, thank you for…everything.
• Marie Panik, a wonderful sister, for all of your quiet yet
strong support.
• Isabelle and Genevieve West, my beautiful daughters, for
your love and faith in me, and for sharing the computer
­nicely.
• Tracee Murphy, my lifelong friend, who has cheered me on
for all five editions of this book.
• My friends, both old and new, for your encouragement
throughout the publishing process.
• My co-workers and patients, who inspire me to become a
better clinician.
Personal thanks from Kate to:
• Jaime Paz, for the opportunity to be involved with this proj-
ect following a random email from a former student who
tracked you down.
• Jaime Paz, Michele West, and Kristin Curry Greenwood, for
all of your comradery, insight, and support throughout the
process.
• My Texas Tech University Health Sciences Center colleagues
and friends, for setting the bar high and providing a fun en-
vironment in which to strive to exceed it.
• My University Medical Center colleagues and friends, for all
that you have taught me and for keeping me on as part of the
team.
• My past, present, and future patients and students—you are
why I love what I do every day. Thank you.
Personal thanks from Kristin to:
• My husband and children, Alex and Hannah, who moti-
vate me to achieve my personal and professional goals each
day.
• Jaime Paz, for your education first as a professor and now as
a mentor in this Associate Editor role—thank you for your
belief and trust in my ability to add to this great text.
• To Michele West, for your guidance and oversight with
Chapter 18.
• To Kate Panasci, for your collaboration and teamwork tack-
ling this new challenge together, which has made this a more
rewarding experience.
• To the contributors whose chapters I edited, who share their
knowledge and patience with me in this new Associate Edi-
tor role.
• To the community of Northeastern University, who first
educated me, then embraced me as faculty and department
chair, and who continue to move the profession of physical
therapy forward every day.
• To the Elsevier staff, who provided guidance every step of the
way.
• To the Academy of Acute Care Physical Therapy, for their
agreement to allow links to their materials and for their on-
going dedication to the advancement of knowledge and the
advancement of acute care physical therapy.
        xiii
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 Contents

Part 1   Introduction 13 Infectious Diseases, 329

Harold Merriman
1 The Acute Care Setting, 1
Appendix 13A: Immune System Disorders, 350
Kathryn Panasci
14 Organ Transplantation, 353
2 The Medical Record, 13
Alysha Walter
   Kathryn Panasci 
15 Fluid and Electrolyte Imbalances, 379
Jaime C. Paz
Part 2   Body Systems
16 Amputation, 383
3 Cardiac System, 17 Jaime C. Paz
Konrad J. Dias, Sean M. Collins
17 Physical Therapy Considerations for Patients
 ppendix 3A: Description of Electrocardiography (ECG)
A Who Present With Chest Pain, 391
Characteristics and Associated Causes, 51 David M. Krause 
Appendix 3B: Common Rhythm Disturbances, 53

4 Pulmonary System, 57 Part 4   Interventions

Lauren Mitchell, Matthew Nippins
18 Medical-Surgical Equipment in the Acute Care
5 Musculoskeletal System, 89 Setting, 395
Marka Gehrig Salsberry Kathryn Panasci, Kristin Curry Greenwood
Appendix 18A:  Mechanical Ventilation, 409
6 Nervous System, 127
Sean M. Collins, Jaime C. Paz
Karen Jeanne Hutchinson, Laura C. Driscoll
Appendix 18B:  Mechanical Circulatory Support
7 Vascular System and Hematology, 171 Devices, 417
Laura A. H. Blood Alysha Walter, Jaime C. Paz

8 Gastrointestinal System, 209 19 Pharmacologic Agents, 431

Jaime C. Paz Margarita V. DiVall, Adam B. Woolley

9 Genitourinary System, 233 20 Anesthesia: Considerations for the Physical

Jaime C. Paz Therapist, 475
Clare Nicholson, Michele P. West
10 Endocrine System, 253
Jaime C. Paz  21 Acute Pain Management, 481
Jaime C. Paz

Part 3   Health Conditions 22 Airway Clearance, 491

Lauren Mitchell, Matthew Nippins
11 Oncology, 275
Julie Anna Snyder 23 Outcome Measures, 499
Erin M. Thomas
12 Integumentary System, 295
Appendix 23A: Functional Tests, 515
Kathryn Panasci

        xv
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 PA R T
1 INTRODUCTION
1 The Acute Care Setting
C H APT E R  
CHAPTER OUTLINE
Introduction
Safe Caregiver and Patient
Environment
Fall Risk
Use of Restraints
Medication Reconciliation
Latex Allergy
Effects of Prolonged Bed Rest
Intensive Care Unit Setting
Common Patient and Family
Responses to the Intensive Care
Unit
Critical Illness Myopathy,
Polyneuropathy, and
Polyneuromyopathy
Sleep Pattern Disturbance
Substance Use and Withdrawal
Severity of Injury and Illness
End-of-Life Considerations
Resuscitation Status
Withholding and Withdrawing
Medical Therapies
Palliative and Hospice Care
Advance Directives
Coma, Vegetative State, and Brain
Death
Kathryn Panascia
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . Review basic safety guidelines and principles for the physical therapist and patient in the hospital setting
2. Identify the multisystem effects of prolonged bed rest that can occur with hospitalization and the relevant
physical therapy considerations
3. Describe the unique characteristics of, and patient response(s) to, the intensive care unit
4. Review alcohol use disorders and alcohol withdrawal syndrome
5. Identify assessment scales used for defining severity of injury or illness
6. Discuss end-of-life considerations and palliative care concepts
Introduction
The physical therapist must have an appreciation for the distinct aspects of inpatient acute care.
This chapter provides a brief overview of the acute care environment, including safety and the
use of physical restraints; the effects of prolonged bed rest; end-of-life considerations; and some of
the unique circumstances, conditions, and patient responses encountered in the hospital setting.
The acute care or hospital setting is a unique environment 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 clinical expertise of the staff and the med-
ical-surgical equipment used in the acute care setting (see Chapter 18) reflect these needs. The
nature of the hospital setting is to provide 24-hour care; thus the patient, family, and caregivers
are faced with the physical, psychological, and emotional sequelae of illness and hospitaliza-
tion. This can include the response(s) to a change in daily routine, lack of privacy and inde-
pendence, or a potential lifestyle change, medical crisis, critical illness, or long-term illness.
Safe Caregiver and Patient Environment
Patient safety is a top priority. Physical therapists should strive to keep the patient safe at all
times, comply with hospital initiatives that maximize patient safety, and understand patient
safety goals established by their accrediting agency. Basic guidelines for providing a safe care-
giver and patient environment include the following:
• Reduce the risk of health care–associated infections by always following Standard Precautions,
including compliance with hand hygiene guidelines.1 Refer to Table 13.3 for a summary of
precautions to prevent infection, including standard, airborne, droplet, and contact precautions.
a The authors acknowledge Michele P. West for prior contributions to this chapter.
        1
2 CHAPTER 1     The Acute Care Setting
• B e familiar with the different alarm systems, including how
and when to use equipment such as code call buttons, staff
assist buttons, and bathroom call lights.
• Know the facility’s policy regarding accidental exposure to
chemicals, wastes, or sharps, as well as emergency procedures
for evacuation, fire, internal situation, and natural disaster.
Know how to contact the employee health service and hospi-
tal security.
• Confirm that you are with the correct patient before initiat-
ing physical therapy intervention, according to the facility’s
policy. Most acute care hospitals require two patient identi-
fiers (by patient report or on an identification bracelet), such
as name and hospital identification (ID) number, telephone
number, or another patient-specific number. A patient’s
room number or physical location may not be used as an
identifier.1 Notify the nurse if a patient is missing an ID
bracelet.
• Elevate the height of the bed as needed to ensure your use of
proper body mechanics when performing a bed-level inter-
vention (e.g., stretching, therapeutic exercise, bed mobility
training, or wound care).
• Leave the bed or chair (e.g., stretcher chair, recliner chair) in
the lowest position with wheels locked when the patient will
be seated at the edge of the surface, exiting or entering the
surface, and after physical therapy intervention is complete.
Leave the top bed rails up for all patients.
• Use only equipment (e.g., assistive devices, recliner chairs,
wheelchairs) that is in good working condition. 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 possible 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 equipment
used for physical therapy intervention (e.g., cuff weights,
Theraband) in a drawer or closet. Do not block the doorway
or pathway to and from the patient’s bed.
• Store assistive devices at the perimeter of the room when not
in use. However, when patients are allowed to ambulate in-
dependently with an assistive device, the device should be in
safe proximity to the patient.
• Provide enough light for the patient to move about the room
or clearly see reading materials.
• Reorient a patient who is confused or disoriented. Often,
patients who are confused are assigned rooms closer to the
nursing station.
• Always leave the patient with the call bell or other commu-
nication devices within close reach. These include eyeglasses
and hearing aids. Be sure to inquire if the patient will be
using the room telephone, personal cellular phone, or both,
and be sure it is within reach.
• Provide recommendations to nursing staff for the use of
bathroom equipment (e.g., tub bench, bedside commode,
or raised toilet seat) if the patient has functional limitations
that may pose a safety risk.
• Dispose of soiled linens, dressings, sharps, and garbage ac-
cording to the policies of the facility.
Fall Risk
A fall is defined as “an event which results in a person com-
ing to rest inadvertently on the ground or floor or other lower
level.”2 A fall by this definition applies to the conscious or
unconscious patient. For hospitalized patients, a fall is one of
the most common adverse events and accounts for increased hos-
pital personnel needs, length of stay, cost, and morbidity and
mortality, especially among older adults.3 Fall prevention dur-
ing hospitalization includes a fall risk assessment performed on
admission by nursing staff. Further prevention of falls involves a
multitude of strategies and safety initiatives, including personal
alarms, proper footwear, medication review, frequent toileting,
adequate room lighting, and routine mobilization. The stan-
dardized fall risk assessment performed on admission varies by
facility; however, common risk factors considered include prior
falls, advanced age, medications, visual acuity, muscle strength,
functional abilities (e.g., gait, balance, and mobility), and any
medical conditions associated with falls (e.g., neurologic, ortho-
pedic, or cognitive impairments; postural hypotension).4 On
the basis of the fall risk score and the subsequent designation
of increased fall risk, a patient is identified as such (depending
on hospital policy) by a specialized wristband and/or colored
hospital gown, on a sign at the doorway to the room, and in the
medical record. 
Use of Restraints
The use of a restraint may be indicated for the patient who is at
risk of self-harm or harm to others, including health care pro-
viders, facility staff, and other patients.5 A restraint is defined
as “any manual method, physical or mechanical device, mate-
rial or equipment that immobilizes or reduces the ability of a
patient to move his or her arms, legs, body or head freely; or
a drug or medication when it is used as a restriction to man-
age the patient’s behavior or restrict the patient’s freedom of
movement and is not a standard treatment or dosage for the
patient’s condition.”5 It should also be noted that “a restraint
does not include devices such as orthopedically prescribed
devices, surgical dressings or bandages, protective helmets, or
other methods that involve the physical holding of a patient
for the purpose of conducing routine physical examinations or
tests, or to protect the patient from falling out of bed, or to
permit the patient to participate in activities without the risk
of physical harm.”5
The most common types of physical restraints in the acute
care setting are wrist or ankle restraints, mitt restraints, vest
restraints, or an enclosure bed. Side rails on a bed are con-
sidered a restraint when they are elevated with the intent of
preventing the patient from exiting the bed, such as when all
four rails are raised.5 The use of restraints requires an order
from a licensed independent practitioner (LIP) that must be
updated approximately every 24 hours. At that time, an LIP
must assess the patient in person before documenting a new
order to continue restraint use.5 A patient on restraints must
be monitored frequently, either continuously or at predeter-
mined time increments, depending on the type of restraint
used and in accordance with facility policy and procedure and
state law.5

Although restraints are used with the intent to prevent
injury, morbidity and mortality risks are associated with physi-
cal restraint use. Most notably, the presence of the restraint and
the resultant limitation of patient mobility can increase agita-
tion. New-onset pressure ulcers or alterations in skin integrity,
urinary incontinence, constipation, and physical deconditioning
can also occur. Musculoskeletal or nerve injury from prolonged
positioning or from pushing or pulling on the restraint or stran-
gulation/asphyxiation from the restraint as a result of entrap-
ment can occur if the patient is not monitored closely. Many
clinical guidelines and hospital care plans and policies reflect
the trend of minimizing restraint use and deferring to alterna-
tives, including regular assessment for personal needs such as
scheduled toileting, food and fluids, sleep, and walking; bed
and chair alarms to alert staff when a patient has moved from
a bed or chair unassisted; diversions such as reading material,
activity kits, or movement activities; recruitment of help from
family or other patient care companions; relaxation techniques;
alternative methods of camouflaging or securing medical
devices, lines, or wires; and adequate pain management.6,7 Use
of restraints should be a last-resort option after all alternatives
have been explored.
General guidelines most applicable to the physical therapist
for the use of restraints include the following:
• Use a slipknot rather than a square knot to secure a restraint
if the restraint does not have a quick-release connector. This
ensures that the restraint can be untied rapidly in an emer-
gency.
• Do not secure the restraint to a movable object (e.g., the bed
rail), to an object that the patient is not lying or sitting on,
or within reach of the patient so that he or she could easily
remove it. If using restraints in the hospital bed, they should
be secured to a part of the bed that will move with the pa-
tient if the head or feet settings are adjusted for positioning.
• Ensure the restraint is secure but not too tight. Place two
fingers between the restraint and the patient to be sure cir-
culation and skin integrity are 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 have improved.
• Remember that the side effects of a chemical restraint may
make a patient drowsy or alter his or her mental status; thus
participation in a physical therapy session may be limited.  side. Hospitals will provide a special latex-free kit or cart, which
Medication Reconciliation
Medication reconciliation is the process of comparing a list
of the medication(s) a patient is taking with that ordered on
admission, on transfer between areas of the hospital, and on
discharge for the purpose of ensuring an up-to-date medication
list.8 Medication reconciliation is an important safety initiative
in hospitals to prevent medication errors, such as inadvertent
omission or duplication of a medication, incorrect dosing, and
drug interactions. This also ensures that all health care providers
can access the same complete medication list.8  the employee health office or a primary care physician.
The Acute Care Setting     CHAPTER 1 3
Latex Allergy
Latex allergy is a hypersensitivity to the proteins in natural rub-
ber latex. If the reaction is immediate, then it is immunoglobu-
lin E (IgE) mediated, with systemic symptoms resulting from
histamine release.9 If the reaction is delayed, typically 48 to 96
hours after exposure, it is T-cell mediated, with symptoms local-
ized at the area of contact and related to the processing chemi-
cals used in the production of natural rubber latex.9 Signs and
symptoms of an allergic reaction to latex range from mild to
severe and may include hives, edema, contact dermatitis, rhi-
nitis, headache, eye or throat irritation, abdominal cramping,
respiratory difficulty (e.g., wheezing or shortness of breath),
chest tightness, and possible anaphylaxis.9-11
Natural rubber latex is used in a multitude of products and
equipment found in the acute care setting. This commonly
includes gloves, stethoscopes, blood pressure cuffs, airway and
intravenous tubing, adhesive tape, dressings, electrode pads,
catheters, tubes, therapy/resistance bands, and hand grips on
assistive devices. Many hospitals have minimized or eliminated
latex products, replacing them with nonlatex or low-protein,
powder-free latex products for the benefit of both the patient
and health care provider.9-12 Effective January 1, 2018, the
U.S. Food and Drug Administration officially banned pow-
dered surgeon’s gloves, powdered patient examination gloves,
and absorbable powder for lubricating a surgeon’s glove because
of the “unreasonable and substantial risk of illness or injury…
including health care worker and patient sensitization to natural
rubber latex.”13
Less than 1% of the general population has a sensitization to
latex; health care workers have a greater incidence, between 8%
and 17%.9,10 Persons with spina bifida, congenital or urogeni-
tal defects, multiple childhood surgeries or medical treatments,
occupational exposures to latex, or certain food allergies are at
increased risk for latex allergy. 9,10 An association exists between
latex sensitivity and food allergies, in which a person can have a
cross-reactive allergy to a food (often a fruit) that is linked aller-
genically to natural rubber latex. This cross-reactivity is known
as latex–food syndrome or latex–fruit allergy, and the foods most
strongly associated with allergic reactions include banana, kiwi,
avocado, and chestnuts. Apples, carrots, celery, papaya, potato,
tomato, and melons have a moderate association with latex aller-
gies.9-11,14 Although not all people with latex sensitivity will also
be allergic to these foods, awareness of the possibility is important.
If a patient has an allergy or hypersensitivity to latex, then
it is documented in the medical record and at the patient’s bed-
consists of latex-free products for use during patient care. Health
care providers may be at risk for developing a latex allergy
because of their increased exposure to latex in the work setting.
The latex allergy protein reaches the skin during exposure to
the latex product. This risk is increased with powdered glove
use because the skin is exposed to increased amounts of the latex
protein through the powder. Aerosolized latex protein powder
can also become an irritant to the airways and eyes, resulting in
the respiratory and ocular symptoms noted previously.12 If you
suspect a latex hypersensitivity or allergy, seek assistance from
 
4 CHAPTER 1     The Acute Care Setting
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, the term
bed rest includes immobilization, disuse, and prolonged recum-
bency. The physical therapist must recognize that a patient in
the acute care setting is likely to have an alteration in physiol-
ogy (e.g., a traumatic or medical-surgical disease or dysfunc-
tion) superimposed on bed rest, a second abnormal physiologic
state.15 Many patients on bed rest have been in the intensive
care unit (ICU) for extended periods of time 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; multi-
ple trauma injuries; spinal cord injury; acute respiratory distress
syndrome (ARDS); or nonhealing, full-thickness wounds (e.g.,
stage 4 pressure injuries) of the lower extremity or sacrum.
Physiologic consequences of bed rest include, but are not
limited to, fluid volume redistribution, altered distribution
of body weight and pressure, muscular inactivity, and aerobic
deconditioning.16 The degree of impairment in each system is
directly related to the severity of illness or injury and the dura-
tion of bed rest. It has been noted that the cardiovascular and
pulmonary systems deteriorate more rapidly and recover more
slowly compared with the musculoskeletal system. This is seen
more dramatically in the older adult population.16 It is beyond
the scope of this book to discuss in detail the physiologic and
cellular mechanisms of the sequelae of prolonged bed rest;
­however, Table 1.1 lists the major systemic changes.
Physical Therapy Considerations
• Monitor vital signs carefully, especially during mobilization
at the edge and out of the bed.
• Progressively raise the head of the bed before or during a
physical therapy session to allow blood pressure to regulate.
Stretcher chairs (chairs that can position the patient from
supine to different degrees of reclined or upright sitting)
are also useful if orthostatic hypotension or activity intoler-
ance prevents standing activity or if the patient may need to
quickly return to the supine position.
• If hypotension persists after more than a few treatment ses-
sions, consider the use of lower extremity antiembolism
stockings, with or without elastic wrapping, when perform-
ing initial static sitting activities to minimize pooling of
blood in the lower extremities. An abdominal binder may
also be helpful to increase return from the abdominal vascu-
lature to the central system.
• 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 indepen-
dent 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.17 These feelings may manifest as emo-
tional lability or irritability, and caregivers may incorrectly
perceive the patient to be uncooperative.
• A s much as the patient wants to be off bed rest, he or she
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. Additional assistance (e.g.,
rehabilitation technicians, other licensed rehabilitation cli-
nicians, nurses) may be necessary the first time up to the
edge or out of the bed to ensure patient safety and medical
stability.
• After treatment, leave necessities and commonly used items
(e.g., call bell, television control, telephone, reading mate-
rial, beverages, food, tissues) within reach to minimize feel-
ings of confinement.
• Be sure to use bed or chair alarm systems or restraints, if
ordered, to minimize the risk of falls. 
Intensive Care Unit Setting
As its name suggests, the ICU is a place of intensive medical-
surgical care for patients who require continuous monitoring,
usually in conjunction with certain therapies or medical inter-
ventions, such as vasoactive medications, sedation, circulatory
assist devices, and mechanical ventilation. ICUs are often named
according to the specialized care that they provide, for example,
coronary care unit (CCU) or surgical ICU (SICU). The patient in
the ICU requires a high level of care; thus the nurse-to-patient
ratio is 1 : 1 or 1 : 2.
Common Patient and Family Responses to the
Intensive Care Unit
Admission to the ICU has an effect on both the patient and fam-
ily members that extends beyond the question of recovery from
injury or illness. Patients in the ICU experience psychological,
behavioral, and social challenges as a result of the stress expe-
rienced during their time in critical care.18,19 The stress expe-
rienced by the patient and family members is not attributed to
poor coping mechanisms or underlying psychological disorders;
rather, they become overwhelmed by the number and sever-
ity of environmental and psychological stressors experienced
in these care units.19 Patients are faced with environmental
stressors such as physical restrictions, sleep deprivation, unfa-
miliar medical equipment, crowding, excessive lighting, odors,
noises, and touch associated with procedures.18,19 Psychological
stressors can include diminished dignity and self-esteem, pow-
erlessness, loss of autonomy, vulnerability, boredom, pain, fear,
anxiety, isolation, uncertainty about the future, and spiritual
distress.18,19
The patient’s family can also become overwhelmed by the
ICU setting. Family members may experience fear, shock, anxi-
ety, stress, helplessness, anger, and denial.20,21 Like the patient,
the family may be overwhelmed by the stimuli and technology
of the ICU, in addition to the stress of a loved one’s critical
or life-threatening illness. Holistic, patient-centered care must
include family members and their well-being in addition to the
primary concern, which is care of the patient. Health care pro-
viders should make every effort to recognize the needs of the
family and identify and implement strategies to meet those
needs to the best of their ability.21
 The Acute Care Setting     CHAPTER 1 5

TABLE 1.1  Systemic Effects of Prolonged Bed Rest

Body System Effects
Cardiac Increased heart rate at rest and with submaximal exercise
Decreased stroke volume, VO2max, left ventricular volume, and cardiac output
Myocardial thinning
Orthostatic hypotension
Hematologic Decreased total blood volume, red blood cell mass, and plasma volume
Increased hematocrit
Venous stasis, hypercoagulability, and blood vessel damage (Virchow triad), causing increased risk of venous
thromboembolism
Respiratory Decreased lung volumes and capacities, especially FRC, FVC, and FEV1
Decreased mucociliary clearance
Increased risk of pneumonia, atelectasis, and pulmonary embolism
Decreased arterial oxygen saturation
Gastrointestinal Decreased appetite, fluid intake, bowel motility, and gastric bicarbonate secretion
Gastroesophageal reflux
Difficulty swallowing
Genitourinary Increased mineral excretion, kidney stones, difficulty voiding, and urinary retention
Increased risk of urinary tract infection
Endocrine Altered temperature and sweating responses, circadian rhythm, regulation of hormones, increased cortisol secre-
tion, and glucose intolerance
Decreased overall metabolism
Musculoskeletal Muscle: increased muscle weakness (especially in antigravity muscles), atrophy, decreased muscle endurance, risk of
contracture, weakened myotendinous junction, and altered muscle excitation
Bone: disuse osteoporosis
Joints: degeneration of cartilage, synovial atrophy, and ankylosis
Neurologic Sensory and social deprivation
Decreased dopamine, noradrenaline, and serotonin levels
Depression, restlessness, insomnia
Decreased balance, coordination, and visual acuity
Increased risk of compression neuropathy
Reduced pain threshold
Integumentary Increased risk of pressure injury formation
Immune system Increased risk of reactivation of latent viruses
Reduced immune response and immunity
Psychological Impaired self-worth and self-esteem
Increased risk of delirium, depression, and posttraumatic stress syndrome
Body composition Increased sodium, calcium, potassium, phosphorus, sulfur, and nitrogen loss
Increased body fat and decreased lean body mass
Fluid shift from the legs to the abdomen/thorax/head, diuresis, natriuresis, dehydration

FEV1, Forced expiratory volume in 1 second; FRC, functional residual capacity; FVC, forced vital capacity; VO2max, maximum oxygen update.
Data from Dean E, Butcher S. Mobilization and exercise: physiological basis for assessment, evaluation, and training. In: Frownfelter D, Dean E, ed. Cardiovascular and
Pulmonary Physical Therapy Evidence to Practice. 5th ed. St. Louis, Elsevier; 2012; Bartels M, Prince DZ. Acute medical conditions. In: Cifu DX, ed. Braddom’s Physical
Medicine and Rehabilitation. 5th ed. Philadelphia: Elsevier; 2016; Knight J, Nigam Y, Jones A. Effects of bed rest 1: cardiovascular, respiratory, and haemotological sys-
tems. Effects of bed rest 2: Gastrointestinal, endocrine, renal, reproductive, and nervous systems. Effects of bed rest 3: musculoskeletal and immune systems, skin and
self-perception (website): http://www.nursingtimes.net. Accessed August 27, 2018.

An acute state of delirium, often termed ICU delirium, ICU
syndrome, or ICU psychosis, is a state of delirium that can occur
during the stay in the ICU. Delirium is a “disturbance in con-
sciousness with inattention accompanied by a change in cogni-
tion or perceptual disturbance that develops over a short period
of time (hours to days) and fluctuates over time.”22 The exact
pathophysiology of ICU delirium is unknown, but research has
demonstrated that ICU patients may have 10 or more identi-
fied risk factors and are at a much higher risk for the develop-
ment of delirium compared with other populations.22 A strong
association has been found between delirium and variables such
as mechanical ventilation, emergency surgery, polytrauma,
organ failure, hypertension, metabolic acidosis, coma, history
of dementia, and advanced age.23 Other possible risk factors
include hypoxemia, use of certain benzodiazepine and narcotic
medications, infection, immobilization, and pain.22 ICU delir-
ium is associated with increased time on mechanical ventilation,
long-term cognitive impairments, extended length of ICU and
hospital stay, increased cost, and higher rates of mortality.22
ICU delirium may present as hyperactive (characterized
by agitation and restlessness), hypoactive (characterized by
withdrawal and flat affect or by decreased responsiveness), or
mixed (a fluctuation between the two).24 Most patients will
experience delirium of either mixed or hypoactive nature.
6 CHAPTER 1     The Acute Care Setting
Purely hyperactive delirium is reported in less than 5% of ICU
patients.24 It is important to recognize the distinction between
ICU delirium and dementia. ICU delirium has a sudden onset
of new cognitive and behavior changes attributed to the cur-
rent medical situation. Dementia has a more gradual onset and
would not be triggered by an ICU admission.24
Current practice guidelines recommend that adult ICU
patients be regularly assessed for ICU delirium. Accepted assess-
ment tools are the Confusion Assessment Method for the Inten-
sive Care Unit (CAM-ICU) and the Intensive Care Delirium
Screening Checklist (ICDSC).22 These tools are most appropri-
ately used in tandem with an additional validated assessment
of consciousness, one example being the Richmond Agitation-
Sedation Scale (RASS).24,25 Both the CAM-ICU and the ICDSC
have been validated for use with verbal patients as well as those
on mechanical ventilation.25
Management strategies for delirium include both pharma-
cologic and nonpharmacologic interventions. Pharmacologic
strategies focus on a thorough review of current medications to
identify and eliminate or decrease those that may be causing
or exacerbating the delirium (e.g., sedatives, benzodiazepines,
analgesics, and/or anticholinergic medications).22 Current liter-
ature is limited with regard to the use of specific medications for
the treatment of ICU delirium.22 Nonpharmacologic interven-
tions include minimizing all risk factors; repeated reorientation
and cognitive stimulation throughout the day; maximization of
the normal sleep pattern; hydration; pain management; early
mobility; removal of lines, wires, and restraints, when appropri-
ate; use of eyeglasses and hearing aids; and minimizing noxious
noises or environmental stimuli.22
The transfer of a patient from the ICU to a general floor unit
can be a stressful and anxiety-provoking event for the patient
and family. Referred to as relocation stress syndrome, the patient
and family may voice concerns about leaving staff members
whom they have come to recognize and know by name; they
may have to learn to trust new staff, or fear that the level of care
may be inferior to that in the ICU.20 To minimize this anxiety,
the physical therapist may continue to treat the patient (if staff-
ing allows), gradually transition the care to another therapist, or
assure the patient and family that the general goals of physical
therapy will remain unchanged.  Initial symptoms of CIM, CIP, and CIPNM are generally
Critical Illness Myopathy, Polyneuropathy, and
Polyneuromyopathy
Together, critical illness myopathy (CIM), critical illness poly-
neuropathy (CIP), and critical illness polyneuromyopathy
(CIPNM, a combination of both CIM and CIP) are the leading
causes of ICU-related neuromuscular weakness, often resulting
in difficulty or failure to successfully wean from mechanical
ventilation.26 These processes involve sensorimotor axons and
skeletal muscles, resulting in significant limb and respiratory
muscle weakness. Diagnosis is ideally confirmed through elec-
trodiagnostic studies (e.g., nerve conduction and electromy-
ography [EMG]); however, the feasibility of these studies can
be limited in the ICU setting. Therefore muscle biopsy and
examination of the phrenic nerve and diaphragm can also be
helpful diagnostic tools.26,27 Differential diagnoses may include
Guillain-Barré syndrome, amyotrophic lateral sclerosis, sar-
coidosis, myasthenia gravis, rhabdomyolysis, medication toxic-
ity, metabolic neuropathies, ongoing neuromuscular blockage,
and muscular dystrophy.26,27 Diagnosis is often first considered
when the patient demonstrates failure to wean from mechanical
ventilation. Because of the complex medical state of the patient
(e.g., sedation, drug-induced paralysis, and possible encepha-
lopathy), it is often difficult to determine the actual time of
onset.26 CIM and CIPNM are more often reported, with occur-
rence rates between 25% and 83%. The likelihood of pure CIP
is still being debated among experts.26 The patient’s underlying
medical condition is a large factor in determining the develop-
ment and severity of CIM, CIP, and CIPNM. Acute respiratory
distress, respiratory failure, mechanical ventilation, trauma, use
of vasopressors, intravenous steroid use, sepsis, systemic inflam-
matory response syndrome, multiple organ failure, inadequate
blood glucose control, renal replacement therapy, and prolonged
immobility have all been identified as possible variables that
increase the risk of developing CIM, CIP, or CIPNM.26,27
CIM presents as flaccid, symmetric weakness that is more
proximal than distal and includes respiratory muscles. Atrophy
will be noted as the illness progresses. Sensation is preserved,
but reflexes are generally decreased or absent.26-28 Electrodiag-
nostic testing demonstrates reduced amplitude of motor action
potentials and an inability to excite muscle tissue despite direct
stimulation. Sensory findings are near or at normal. Muscle
biopsy will reveal evidence of denervation and reinnervation
with fiber-type grouping and atrophy.26
CIP presents as flaccid, bilateral, distal extremity weakness,
sensory loss, and paresthesia. Although deep tendon reflexes
usually remain intact initially, they will likely decrease over
time.26-28 The lower extremities are generally affected more
compared with the upper extremities, and findings may not be
symmetric in nature.26 Nerve conduction studies demonstrate
decreased amplitude of both sensory and motor action potentials
without conduction velocity impairment.26,28 Nerve biopsy
reveals widespread motor and sensory nerve degeneration.26
CIPNM is a condition with overlap of both CIM and CIP
such that electrodiagnostic and clinical features of both will be
noted.26
noted within 2 weeks of admission to the ICU but have been
reported as soon as 72 hours.26 Medical management includes
supportive and symptomatic care, treatment of the causative
factor, and physical therapy. No proven cure exists; however, an
intensive insulin regimen is the only medical intervention with
notable clinical benefit.26 
Sleep Pattern Disturbance
The biological need for sleep is well understood. Ill and injured
individuals require increased amounts of sleep over the healthy
population to facilitate recovery. However, adequate sleep, in
both quantity and quality, can be difficult to obtain in the acute
care setting.29-32 Sleep disturbance is defined as “insufficient dura-
tion or stages of sleep that results in discomfort and interferes
with quality of life.”30 Inadequate or disrupted sleep can result
in impaired health and well-being (e.g., immune, metabolic,

cardiorespiratory, and neurologic system dysfunction); delayed
healing or recovery; decreased energy levels; alterations in cogni-
tion, mental status, and mood; and increased stress, anxiety, and
pain.29,31,32 The defining characteristics of sleep disturbance are
difficulty falling or remaining asleep with or without fatigue on
awakening, drowsiness during the day, decreased overall func-
tioning, inability to concentrate, and mood alterations.33
In the acute care setting, sleep disturbance may be related
to both environmental and nonenvironmental causes. Environ-
mental concerns include frequent awakenings associated with
a medical procedure or the need for nursing intervention (e.g.,
monitoring of vital signs); elevated noise levels, light exposure
(e.g., disruptive light at night and inadequate light during
the day), and the challenges of sleeping in an unfamiliar envi-
ronment.29,31,32 Nonenvironmental causes of disrupted sleep
may include the severity of the current disease or illness, pain,
medications, and certain medical interventions (e.g., ventila-
tion, dialysis, urinary catheters, external orthopedic hardware
or devices, and other lines and wires).29,31,32 Sleep disturbance
is often more prevalent in the older adult population because of
changes in circadian rhythms, coexisting health conditions, and
dementia.34
Possible interventions for sleep disruption include appro-
priate and adequate management of the current illness, injury,
and pain; review of possible sleep-related pharmacologic side
effects; reduction in night time noise, light, and interruptions;
increased daytime stimulation with reduction in daytime sleep-
ing; and relaxation techniques such as guided imagery, aroma-
therapy, or music.31,32 The physical therapist should be aware of
the patient who has altered sleep patterns or difficulty sleeping
because lack of sleep can affect a patient’s ability to participate
during a therapy session. The patient may have trouble concen-
trating and performing higher-level cognitive tasks. The pain
threshold may be decreased, and the patient also may exhibit
decreased emotional control.31  tions (described above) from DT-related halluciations.38
Substance Use and Withdrawal
Casual or habitual abuse of alcohol, illicit drugs (e.g., cocaine),
or medications (e.g., opioids) is a known contributing factor
in acute and chronic illness, traumatic accidents, drowning,
burn injury, and suicide.35 A patient in the acute care setting
may present with acute intoxication or drug overdose or with
a known (i.e., documented) or unknown substance abuse prob-
lem. When a patient with an unknown substance abuse disorder
is hospitalized, it becomes a challenge to the hospital staff when
substance withdrawal occurs. The physical therapist is not usu-
ally involved in the care of the patient admitted with substance
intoxication or overdose until medical stability is achieved.
However, the physical therapist may become involved when
the stabilized patient presents with impaired strength, balance,
coordination, or functional mobility. Physical therapy may also
be consulted to assist in developing a safe discharge plan.
This text will focus on alcohol withdrawal because of its
relatively high incidence. The Diagnostic and Statistical Man-
ual of Mental Disorders, fifth edition (DSM-V) has integrated
two previously identified disorders, alcohol abuse and alcohol
The Acute Care Setting     CHAPTER 1 7
dependence, into a single diagnosis, alcohol use disorder (AUD).
AUD is further divided into mild, moderate, and severe catego-
ries based on the number of identified symptoms.36
An estimated 15 million persons, age 18 years or older, in
the United States have an AUD.36 Data suggest that one in four
patients admitted to a hospital has an AUD.19 Alcohol with-
drawal syndrome (AWS) is the sudden reduction or cessation of
alcohol intake after heavy and prolonged alcohol consumption,
with the development of two or more physical manifestations
within hours to days.37 Noted signs and symptoms must result
in “significant distress or impairment in social, occupational,
or other important areas of functioning” and may not be attrib-
uted to any other condition or cause.37 Clinical manifestations
of AWS are classified as mild, moderate, or severe.19,38
• Mild signs/symptoms of AWS are observed within 3 to 6
hours after alcohol use is discontinued and typically last 1 to
2 days. Symptoms include tachycardia, palpitations, tremor,
diaphoresis, headache, nausea and vomiting, anxiety, and in-
somnia.37-39
• Moderate signs/symptoms of AWS include persistence or
worsening of the previously listed conditions and a new onset
of generalized tonic-clonic seizures (within 12–48 hours, but
may occur as soon as 1 hour after the last drink) and visual
hallucinations (within 12–24 hours of alcohol cessation). The
patient is aware, and often very distressed, that he or she is
hallucinating.37-39
• Severe AWS and delirium tremens (DT) symptoms begin 48
to 96 hours after the last drink and last up to 7 days. Clinical
manifestations include uncontrolled shaking, tachycardia,
hypertension, hallucinations, disorientation, agitation, dia-
phoresis, and fever.37-39 It should be noted that DT-related
hallucinations are more global in nature, with alterations in
vital signs. The timing of onset and the nature of the hallu-
cinations are the factors that distinguish alcoholic hallucina-
Medical interventions to prevent or minimize AWS include
hydration; electrolyte, vitamin, and glucose replacement (e.g.,
intravenous infusion of thiamine, folic acid, magnesium, and
a multivitamin in saline—often referred to as a “banana bag”);
adequate nutrition; and the use of benzodiazepines.38 Ideally,
an objective scale is used to grade AWS symptoms and dose
medication or other interventions accordingly. The Prediction
of Alcohol Withdrawal Severity Score (PAWSS) assessment tool
may be used to screen for risk of development of withdrawal
symptoms.37 The Clinical Institute Withdrawal Assessment for
Alcohol (CIWA-Ar) is a commonly used tool for grading with-
drawal severity and guiding medical treatment.19,38 
Severity of Injury and Illness
Determination of severity of injury and illness often focuses on
identifying the extent of actual or anticipated tissue damage and
the associated physiologic response of the body.40 Other dimen-
sions to consider are the cognitive, psychological, and functional
effects of the injury or illness on the patient.41 This information
may assist in predicting patient morbidity, disability, mortal-
ity, hospital readmission, and use of health care resources.40,42
8 CHAPTER 1     The Acute Care Setting
A multitude of host-related factors contribute to injury severity,
including preexisting medical, nutritional, and psychological
conditions; age; sex; prior level of function; environmental fac-
tors; and personal characteristics.40,41
Initial determination of injury and illness severity generally
occurs by first responders or emergency room and ICU physi-
cians. Table 1.2 outlines some commonly used injury and ill-
ness severity scoring systems. The acute care physical therapist
will encounter results of these assessments within the patients’
medical record and should have a basic understanding of their
implication in predicted outcomes.  different services to patients with a serious illness (e.g., chronic
End-of-Life Considerations
End-of-life care may include complex moral, ethical, or legal
dilemmas, or a combination of these, with regard to a patient’s
vital physiologic functions, medical-surgical prognosis, qual-
ity of life, and personal values and beliefs.43 End-of-life con-
siderations faced by patients, family, and caregivers include the
following:
• Resuscitation status
• Withholding and withdrawing medical therapies
• Palliative and hospice care
• Advance directives
• Coma, vegetative state, and brain death
Resuscitation Status
It is imperative that health care providers are aware of the
patient’s wishes regarding resuscitation should an emergency
situation arise. Therefore every patient has a “code” status,
which refers to the decision of whether or not life-saving inter-
ventions should be initiated after cardiopulmonary arrest. The
designation full code means all appropriate efforts will be made
to revive a patient after cardiopulmonary arrest. Do not resuscitate
(DNR) is the predetermined decision to decline cardiopulmo-
nary resuscitation (CPR), including defibrillation and pharma-
cologic cardioversion in the case of cardiopulmonary arrest. The
code status do not intubate (DNI) is the predetermined decision
to decline intubation for the purpose of subsequent mechanical
ventilation in the event of respiratory arrest. Either full code or
DNR and/or DNI status is officially documented in the medi-
cal record by the attending physician. If a patient is DNR or
DNI, he or she will wear a wristband with that designation.
The physical therapist must be aware of each patient’s resuscita-
tion or code status. DNR/DNI orders do not directly affect the
physical therapy plan of care.  Physical therapists are uniquely equipped to meet the needs of
Withholding and Withdrawing Medical Therapies
Withholding care is the decision to defer initiation of a treatment
because it is not beneficial for or desired by the patient. With-
drawing care refers to the discontinuation of a treatment that is
no longer beneficial or consistent with the goals of the patient
and/or family. In both situations, a specific medical intervention
is removed from the patient’s plan of care (e.g., mechanical ven-
tilation, hemodialysis, chemotherapy, or artificial nutrition and
hydration).44,45 By forgoing life-sustaining medical treatment,
the underlying disease process is allowed to take its course and
natural death occurs.44 In these situations, an order for “com-
fort measures only” (CMO) is written by the physician. The
patient on CMO status continues to receive care to maintain
overall comfort (e.g., medications for pain control or sedation
or to otherwise eliminate distress). Any intervention that causes
discomfort is discontinued.44 The patient on CMO status does
not receive physical therapy. 
Palliative and Hospice Care
Palliative and hospice care provide meaningful but distinctly
obstructive pulmonary disease [COPD], Parkinson’s disease,
cancer, Alzheimer’s disease). The goal of palliative care is the
management or relief of distressing symptoms of illness to
“achieve the best quality of life for patients and their families,
consistent with their values.”46,47 Palliative care is appropriate
for any patient, regardless of age, stage of illness, or progno-
sis.47 This team-based care model is applied alongside any other
medical treatments or interventions for the underlying disease
condition and focuses on physical, spiritual, and emotional well-
being; symptom management; family involvement and support;
and access to any therapies that may provide comfort or piece of
mind.46-48
Hospice care is a form of palliative care that is specific to any
patient with a life-limiting illness in his or her last 6 months
of life.46 Patients are no longer seeking curative intervention;
the focus is on comfort and relief of symptoms, maximizing
the quality of the remaining life, and providing support to the
patient and family.49 Like palliative care, hospice care has a
team-based approach and can occur in any setting (e.g., hospital,
long-term care facility, or the patients home).47
The role of physical therapy in patients receiving palliative
care or hospice services will depend on the needs and desires of
the patient and family. In either care situation, physical therapy
may be consulted to provide recommendations and interven-
tions for positioning, pain management, energy conservation,
mobility strategies, edema management, family education,
equipment training, and home modifications.50 Because the
focus of hospice is end-of-life care, intervention will be cen-
tered on comfort and maintenance of desired physical abili-
ties to enhance the quality of remaining life, while preparing
the patient and family for the anticipated decline as the dis-
ease progresses. Physical therapy intervention in the palliative
care population focuses on current symptom management and
optimizing physical function to improve the quality of life.50
this population because of the ability to provide a continuum of
care, to provide services when a patient has a change in medical
status, and to use a knowledge base encompassing movement
dysfunction, ergonomics, and pain management.51 The role of
physical therapy in hospital-based palliative care may be consul-
tative or ongoing. 
Advance Directives
An advance directive allows individuals to document their
wishes regarding medical decisions and end-of-life care should
they be unable to speak for themselves.52 This is a legal document
 The Acute Care Setting     CHAPTER 1 9

TABLE 1.2  Critical Illness and Injury Severity Scoring Systems

Scoring System Name Description
APACHE II Acute Physiologic As- Measurement of disease severity through assessment of 12 routine physiologic variables
sessment and Chronic (temperature; MAP; HR; RR; oxygenation; arterial pH; serum sodium, potassium, and
Health Evaluation creatinine; Hct; WBC; and GCS), age, and underlying health status. Scores range from
0 to 71, with higher scores indicating increased severity of disease and risk of mortal-
ity. A third and fourth version have been developed but are more cumbersome and less
widely utilized.
GCS Glasgow Coma Scale Rapid assessment of level of consciousness and severity of brain injury via eye open-
ing and verbal and motor responses. Scores range from 3 to 15. Lower scores indicate
increasingly compromised neurologic function, with a score of less than 8 typically
suggestive of a comatose state. Developed for determination of neurologic prognosis in
patients with head trauma but useful in monitoring severity of coma or impaired levels
of consciousness in other populations. Refer to Chapter 6 for more information.
MPM III Mortality Prediction Predictor of hospital mortality and length of stay through the assessment of three physi-
Model ologic variables (GCS, HR, SBP), presence of concurrent diagnoses, age, code status
at admission, and admission and medical management related variables. MPM II may
still be more widely used.
SAPS 3 3rd Simplified Acute Assessment of illness severity and prediction of mortality during hospitalization through
Physiology Score 20 variables including preadmission characteristics (age, health status and comorbidi-
ties, and medical management before current ICU admission), current admission
information (reason for admission, surgical status, and presence of infection), and nine
physiologic variables (HR, SBP, temperature, GCS, bilirubin, creatinine, leukocytes,
pH, platelets, and oxygenation). Scores range from 5 to 124, with higher scores indi-
cating increased likelihood of hospital mortality. It should be noted that SAPS II is
still in use in some facilities.
SOFA Sequential Organ Failure Measurement of organ failure severity through the assessment of six organ systems
Assessment (respiratory: PaO2/FiO2, coagulation: platelets, liver: bilirubin, cardiovascular: hypo-
tension, CNS: GCS, and renal: creatinine or urine output). Prediction of mortality is
not the focus, but can be estimated by SOFA score. Scores range from 0 to 24, with
higher scores indicating increased degree of organ failure and associated risk of adverse
outcomes and mortality.

BUN, Blood urea nitrogen; CNS, central nervous system; FiO2, fraction of inspired oxygen; Hct, hematocrit; HR, heart rate; MAP, mean arterial pressure; PaO2, partial
pressure of arterial oxygen; RR, respiratory rate; SBP, systolic blood pressure; WBC, white blood cells.
Data from Merck Manual Professional Version: Critical care scoring systems (website): https://merckmanuals.com. Accessed August 30, 2018; Rapsang AG, Shyam DC:
Scoring systems in the intensive care unit: a compendium, Indian J Crit Care Med. 18(4),220-228, 2014; Salluh JIF, Soares M: ICU severity of illness scores: APACHE,
SAPS, and MPM. Curr Opin Crit Care. 20:557-565, 2014. DOI:10.1097/MCC.0000000000000135; Moreno RP: SAPS 3—from evaluation of the patient to evaluation
of the intensive care unit. Part 2: development of a prognostic model for hospital mortality at ICU admission, Intensive Care Med. 10,1345-1355, 2005; Jentzer JC,
Bennett C, Wiley BM, et al. Predictive value of the sequential organ failure assessment score for mortality in a contemporary cardiac intensive care unit population.
J Am Heart Assoc. 18(7),e008169, 2018.

that remains in effect until the individual properly changes or
amends it. State laws regarding advance directives vary; there-
fore the advance directive documents in one state may not be
valid in another.52 Advance directives typically include the des-
ignation of a medical power of attorney (POA) (also referred to
as a durable power of attorney or health care proxy) and documenta-
tion of a living will. The medical POA is the individual who
will make medical decisions on behalf of the patient should he
or she be unable to do so.52,53 A living will is a written state-
ment that expresses the individual’s desires regarding treatment
decisions, such as resuscitation, mechanical ventilation, dialysis,
and artificial nutrition and hydration.52,53
It is imperative that the patient or family present advance
directive documents on admission to the hospital setting so that
the patient’s wishes may be honored in the event that he or she
is no longer able to communicate them. The medical POA and
living will go into effect only after a physician has determined
that the patient is no longer capable of making his or her own
medical decisions.52  lasts longer than 1 month after an acute trauma; it is considered
Coma, Vegetative State, and Brain Death
A diagnosis of coma, vegetative state, or brain death can be dev-
astating. These conditions involve unconsciousness and absence
of self-awareness but are distinct in terms of neurologic function
and recovery. Coma is a state of uninterrupted unconsciousness
without arousal or awareness, characterized by lack of eye open-
ing and sleep/wake cycles. While brainstem reflex responses
remain intact, no meaningful interaction with the environment
occurs.54,55 Coma is typically a symptom of another condition,
such as neurologic disease (e.g., stroke), a mass (e.g., brain
tumor), trauma (e.g., traumatic brain injury), or a metabolic
derangement (e.g., encephalopathy); drug or alcohol overdose;
poisoning; infection; or it may be psychogenic in nature.54 A
vegetative state (VS) is a transient state of wakefulness char-
acterized by cyclic sleep patterns, spontaneous eye opening,
involuntary movement, and normal body temperature, yet there
is a lack of purposeful awareness or responsiveness to stimuli,
cognitive function, and speech. VS is considered persistent if it
10 CHAPTER 1     The Acute Care Setting
permanent 3 months after a nontraumatic brain injury or 12
months after a traumatic brain injury.55 The clinical criteria
for brain death includes absence of brainstem reflexes, cerebral
motor responses, and spontaneous respirations in the setting of
a known irreversible cause.56,57 Brain death can be confirmed
with cerebral angiography, electroencephalography, transcra-
nial Doppler sonography, radionuclide imaging, or computed
tomography angiography.57 Refer to Chapter 6 for more infor-
mation on these neurologic diagnostic tests.
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37. The Ohio State University Wexner Medical Center. Alcohol
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://www.uptodate.com. Accessed August 23, 2018.
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44. Etland C. End of life care. In: Urden LD, Stacy KM, Lough ME,
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45. American Academy of Hospice and Palliative Medicine. State-
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46. American Hospice Foundation. Hospice care or pal-
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The Acute Care Setting     CHAPTER 1 11
47. American Academy of Hospice and Palliative Medicine (website):
http://www.aahpm.org. Accessed August 23, 2018.
48. National Hospice and Palliative Care Organization. Living with
a serious illness (website): http://www.caringinfo.org. Accessed
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49. American Cancer Society. What is hospice care? (website): http://
www.cancer.org. Accessed August 23, 2018.
50. Ries E. A special place: physical therapy in hospice and palliative
care, PT in Motion, 2007 (serial online): http://www.apta.org.
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51. The role of physical therapy in hospice and palliative care HOD
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53. Medicare.gov. Advanced directives & long term care (website):
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Nursing Diagnosis and Management. 8th ed. St. Louis: Elsevier;
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 2 The Medical Record
CH APT ER  

Kathryn Panascia

CHAPTER OUTLINE CHAPTER OBJECTIVES

Introduction The objectives for this chapter are the following:
Confidentiality 1 . Briefly describe the medical record, including related confidentiality and security regulations
Physical Therapist 2. Review documentation standards for the physical therapist
Documentation 3. Describe the different components of the medical record, including a detailed outline of the admission
Components of the Medical history and physical
Record
Orders
Admission Note Format Introduction
Progress Notes
Reports
The medical record is a legal document that contains information regarding a patient’s health
status, treatments received, provider plans, and an outline of delivery of care. Specifically, the
medical record contains information about past and present history of illness and medical condi-
tions, including current diagnosis; current medication list; known allergies and sensitivities and
patient reaction; physical examination findings; diagnostic test and laboratory results; treatment
plans and interventions; record of preventative services and screening; and follow-up plans.1 Both
primary care and ancillary service providers, such as physical therapists, will be contributing
information to the medical record. This document serves as the primary means of communication
among providers and a complete and accurate medical record aids in the continuity of quality
care.1 The medical record may also be used for educational purposes, performing quality improve-
ment studies, conducting research, and resolving legal issues such as competency or disability.2
In the past, medical records were paper-based and proved to have significant challenges and con-
sequences. The National Academy of Medicine highlighted that a paper-based health care system
resulted in “redundant tests; increased costs; uncoordinated and fragmented care; medical decisions
made with incomplete data, leading to adverse events; and potential clinical innovations left undis-
covered, hidden in patient files.”3 As a response, the Health Information Technology for Economic and
Clinical Health (HITECH) Act went into effect in February 2009 as a means to expand and protect
meaningful use of health information technology via electronic health records (EHRs).4 Federally
funded incentive programs were designed to encourage Medicare and Medicaid providers, both
individual and organizational, to adopt the use of EHRs with ongoing demonstration of risk assess-
ments to ensure compliance with the Health Insurance Portability and Accountability Act (HIPAA).4,5
All eligible providers were required to use EHRs by 2015, with increasing annual penalties for those
not in compliance.4,5 Data shows that nearly all U.S. hospitals and 80% of private practice providers
have adopted the use of EHRs. This has allowed for increased sharing of health-related information
among systems and a positive effect on quality, safety, and efficiency of health care services.3
  

Confidentiality

The HIPAA Privacy Rule e stablished standards for defining and protecting all “individually iden-
  

tifiable health information,” which is considered “protected health information (PHI)” and should
be kept confidential.6,7 All health care providers and covered entities (e.g., health care plans; health
care clearinghouses; and any business associates involved in data analysis, utilization review, bill-
ing, and claims processing) must safeguard the availability and integrity of PHI in oral, written,
media, or electronic forms.6 PHI includes any information that pertains to the past, present, or
future physical or mental health conditions of an individual, including provision of care, payment

a The authors acknowledge Michele P. West for prior contributions to this chapter.
        13
14 CHAPTER 2     The Medical Record

TABLE 2.1  Prohibitive Abbreviationsa

Do Not Use Potential Problem Use Instead
U, u (unit) Mistaken for “0” (zero), the number”4” (four) or “cc” Write “unit”
IU (International Unit) Mistaken for IV (intravenous) or the number 10 (ten) Write “International Unit”
Q.D, QD, q.d., qd (daily) Mistaken for each other Write “daily”
QOD., QOD, q.o.d., qod (every Period after Q mistaken for “I” and the “O” mistaken for the “I” Write “every other day”
other day) Mistaken for 3 times a day or twice in 1 week Write “3 times weekly”
TIW or tiw
Trailing zero (X.0 mg)b Decimal point is missed Write X mg
Lack of trailing zero (.X mg) Write 0.X mg
MS Can mean morphine sulfate or magnesium sulfate Write “morphine sulfate”
MSO4 and MgSO4 Confused for one another Write “magnesium sulfate”
> and < (greater than and less than) Mistaken as opposite of intended; mistakenly use the incorrect Write “greater than” or “less than”
symbol
aApplies to all orders and all medication-related documentation that is handwritten (including free-text computer entry) or on preprinted forms.
bException: A “trailing zero” may be used only where required to demonstrate the level of precision of the value being reported, such as for laboratory results, imaging
studies that report size of lesions, or catheter/tube sizes. It may not be used in medication orders or other medication-related documentation.
Data from The Joint Commission Official “Do Not Use” List. www.jointcommission.org. Last accessed August 24, 2018.; Institute for Safe Medication Practices: Unsafe
medical abbreviations (website): http://www.consumermedsafety.org. Accessed November 10, 2018.

of care, and demographics.6 The Privacy Rule does allow for, but
not require, disclosure of PHI without patient authorization for
the purposes of research and public health. It is recommended that
the covered entity rely on best judgment and professional ethics
when making the decision to disclose such information.6
The HIPAA Security Rule addresses the confidentiality of
electronic PHI (e-PHI).7 The Security Rule states that a covered
entity must ensure the integrity and availability of e-PHI that it
creates, receives, maintains, or transmits.7 The goal of the Secu-
rity Rule is to protect e-PHI as covered entities adopt new and
efficient technologies.7
All health care providers, individual and institutional, who
exchange health-related information electronically and for the pur-
poses of financial or administrative health care activities (e.g., refer-
ral, authorization, coordination of benefits, claims, and payment)
must comply with HIPAA.8,9 This would include the physical
therapist, who must also adhere to the American Physical Therapy
Association’s Guide for Professional Conduct and Code of Ethics for the
Physical Therapist,10,11 all policies and procedures of the facility,
and state law with regard to sharing medical record information
with the patient, family, caregivers, visitors, or third parties.
CLINICAL TIP
To ensure confidentiality of PHI in the acute care setting, the
physical therapist should log off the computer when not in use,
cover any paperwork kept on clipboards when moving within
the facility, and use discretion when discussing patient informa-
tion in shared rooms, hallways, and/or elevators.
 
Physical Therapist Documentation
The physical therapist should comply with documentation stan-
dards, including, but not limited to, the policies/procedures of
the organization, the state, and the American Physical Ther-
apy Association’s Guidelines: Physical Therapy Documentation of
Patient/Client Management.12
In general, documentation must be1,12:
• Completed for every visit/encounter, at the time of care or
soon after
• Dated and timed with authenticated signature and creden-
tials
• Legible and in blue or black ink (when applicable)
• Clearly labeled with the appropriate patient identification
(e.g., name and identification number)
• Complete, accurate, and objective
• Cosigned for a physical therapist assistant (if required by
state practice act) or student physical therapist
• Free of ambiguous acronyms or abbreviations to minimize
misinterpretation and prevent errors that could result in pa-
tient safety issues (Table 2.1)13
Errors on handwritten documentation should be corrected
with a single line through the error, followed by the author’s
initials and the date. Electronic documentation systems vary but
will allow the author to indicate a change without deleting the
original record.
These standards apply to documentation of the physical ther-
apy examination, evaluation, diagnosis, prognosis, and plan of
care (including interventions).12 Routine physical therapy doc-
umentation includes the initial examination/evaluation, visit/
encounter notes, reexamination, and discharge or discontinua-
tion summary.12 A documentation entry is required for every
physical therapist encounter and should include the following,
as applicable14:
• Phone calls or conversations with other health care providers,
referral sources, or payment entities
• Handouts provided to the patient, including exercise pro-
grams or educational materials
• Follow-up information provided to the patient
• The use of interpreter services
• Therapist response and assessment of an adverse event or
situation (completed outside the medical record via a facility
approved incident report form)

Physical Therapy Considerations
• Be sure to document when a patient/family member declines
or refuses therapy intervention or requests a specific time of
day for therapy, including a rationale for such.
• Documentation of deferring or “holding” therapy should in-
clude a rationale and the source of the deferral, whether it is from
the physician, nursing, physical therapist, or other provider.
• Documentation of patient unavailability (e.g., off the floor at
   a test or procedure) is also suggested.  and cause of death for immediate family members as
Components of the Medical Record
The organization of the medical record will vary from institu-
tion to institution; however, it is typically composed of the fol-
lowing basic sections:
Orders
The “orders” section is a log of all instructions within the plan
of care for the patient, including, but not limited to, medica-
tions, diagnostic or therapeutic tests and procedures, vital sign
parameters, activity level or restrictions, mobility precautions,
diet, request for consultation services, and resuscitation status.
Orders may be written by a physician, a physician assistant, or
a nurse practitioner. A verbal order, given either via telephone
or face to face, may be taken by a nurse or other licensed and
authorized health care provider, including a physical therapist,
according to departmental, facility, and state policies.15 In the
interests of patient safety and error prevention, the process of
taking a verbal order, especially for medications, has been mini-
mized in most facilities.15 In the event that a verbal order is
communicated, it must be read back to the ordering practitio-
ner and cosigned by that individual at a subsequent time.15
Physical Therapy Considerations
• The orders section of the patient’s medical record should be re-
viewed before the initial evaluation and any subsequent physi-
cal therapy intervention(s) for the following (as applicable):
the order for physical therapy services, patient activity level,
weight-bearing status, need for any bracing or orthotic devices,
vital sign parameters, and positioning restrictions. On subse-
quent physical therapy sessions, the review of the orders section
offers a “snapshot” of change(s) in the patient. Look for new or
discontinued medications, changes in PO (by mouth) status,
and new laboratory or diagnostic testing orders or results.
• If an order appears incomplete or ambiguous, the order
should be clarified before beginning physical therapy. 
Physical Therapy Considerations
Admission Note Format
The following outline summarizes the basic format of the initial
admission note (often referred to as the “H&P,” that is, history
and physical) written by a physician, a physician’s assistant, or a
nurse practitioner in the medical record.16 The italicized items
indicate the standard information the physical therapist should
review before beginning an initial evaluation.
I. History (subjective information)
A. Data that identify the patient, including the source and
degree of reliability of the information
The Medical Record     CHAPTER 2 15
B.  History of present illness (HPI), including the chief com-
plaint/concern (CC) and a chronological list of the events
associated with, and leading up to, arrival at the hospital
C. Past medical and surgical history (PMH, PSH), risk fac-
tors for disease, and if there are any known allergies and
sensitivities, including reactions, to medication, food, or other
substances
D.  Family health history, including age and health or age
well as a relevant familial medical history
E.  Personal and social history, including occupation, lifestyle,
leisure activities, substance use (e.g., tobacco, alcohol, illicit
drugs), functional mobility status, the need for home or out-
patient services, support system availability, and architectural
barriers at home
F.  Current medications, including over-the-counter and nontra-
ditional therapies, as well as overall level of compliance
II. Physical examination (objective information). Findings are
described in detail according to the following:
A. General information, including vital signs and physical
appearance
B. Skin
C. Head, eyes, ears, nose, throat (HEENT); oropharynx;
and thyroid
D. Neck, including lymph nodes and carotids
E. Heart
F. Lungs
G. Abdomen
H. Genitalia/pelvic/rectal examination
I.  Extremities, including range of motion (ROM),
strength, and pulses
J. Neurologic system (mental status, cranial nerves, mo-
tor strength, sensation, reflexes, cerebellar function/ob-
served ambulation)
III. Laboratory and test results (e.g., radiographic studies, elec-
trocardiography [ECG], etc.)
IV. Assessment. The assessment is a statement of the condi-
tion and prognosis of the patient in regard to the chief
complaint and/or medical-surgical status. If the etiology
of the problem(s) is unclear, then differential diagnoses are
listed.
V. Plan. The plan of care may include further observation,
tests, laboratory analysis, consultation with additional spe-
cialty services or providers, pharmacologic therapies, other
interventions, and discharge planning.
• It is always advisable to note if a patient has a preferred
name that may differ from the legal name documented in
the medical record. This may be reported to the physi-
cal therapist by nursing staff, documented in the patient’s
room, or learned via direct conversation with the patient or
their family.
• A patient’s gender identity may differ from that assigned
at birth or noted within the medical record. It is important
to inquire about the patient’s preferred name and pronouns
(e.g., he/she, him/her, they/them).17 
16 CHAPTER 2     The Medical Record
Progress Notes
A progress note is a shortened version of the initial admis-
sion note with an emphasis on any new findings, an updated
assessment, and plan. The progress note section is typically
multidisciplinary, with documentation from all caregivers
in chronological order. The nursing staff documents its own
admission assessment, problem list, and care plan(s). Medi-
cation reconciliation sheets, flow sheets, clinical pathways,
consult service notes from other physicians and health care pro-
fessionals, and operative and procedural notes are also included
in this section. 
Reports
A variety of reports are filed chronologically in individual
sections in the medical record (e.g., radiologic or laboratory
reports). Each report includes an interpretation or normal
reference ranges, or both, for various diagnostic or laboratory
test results. Other types of reports include those from pulmo-
nary function tests, electroencephalography (EEG), and stress
testing.
References
1. Kaiser Permanente. Medical records and documentation standards
(website). https://provider.ghc.org. Accessed August 24, 2018.
2. Monarch K. Documentation, part 1: principles for self-protection.
AJN. 2007;107(7):58.
3. Washington V, DeSalvo K, Mostashari F, Blumenthal D.
The HITECH era and the path forward. N Engl J Med.
2017;377:904–906.
4. Mennemeyer ST, Menachemi N, Rahurkar S, Ford EW. Impact
of the HITECH Act on physicians’ adoption of electronic health
records. J Am Med Inform Assoc. 2016;23:375–379.
5. HIPAA Journal. What is the HITECH Act? (website).
https://www.hipaajournal.com. Accessed August 24, 2018.
6. U.S. Department of Health and Human Services. Summary of
the HIPAA privacy rule (website). https://www.hhs.gov. Accessed
August 24, 2018.
7. U.S. Department of Health and Human Services. Summary of the
security rule (website). https://www.hhs.gov. Accessed August
24, 2018.
8. U.S. Department of Health and Human Services: Covered entities
and business associates (website): https://www.hhs.gov. Accessed
August 24, 2018.
9. Centers for Medicare & Medicaid Services. Transactions
overview (website). https://www.cms.gov/Regulations-and-
Guidance/Administrative-Simplification/Transactions/Transactio
nsOverview.html. Accessed August 24, 2018.
10. American Physical Therapy Association. Guide for professional
conduct (website). http://www.apta.org. Accessed August 24,
2018.
11. American Physical Therapy Association. Code of ethics for the
physical therapist (website). http://www.apta.org. Accessed Au-
gust 24, 2018.
12. American Physical Therapy Association, Guidelines: Physical
therapy documentation of patient/client management BOD G03-
05-16-41 (website). http://www.apta.org. Accessed August 24,
2018.
13. The Joint Commission. Facts about the official “do not use” list
of abbreviations (website). https://www.jointcommission.org/facts
_about_do_not_use_list/. Accessed August 24, 2018.
14. American Physical Therapy Association. Improving your clinical
documentation: reflecting best practice (website). http://integrity
.apta.org/Documentation/. Accessed August 24, 2018.
15. National Coordinating Council for Medication Error Report-
ing and Prevention. Recommendations to reduce medication errors
associated with verbal medication orders and prescriptions (website).
www.nccmerp.org. Accessed August 24, 2018.
16. University of California, San Diego. A practical guide to clinical
medicine (website). https://meded.ucsd.edu/clinicalmed/write
.htm. Accessed August 24, 2018.
17. Hayhurst C. Managing patients who are transgender. PT in Motion.
2016;8(6):16-22.
 PA R T
2 BODY SYSTEMS
3 Cardiac System
C H AP T E R  
CHAPTER OUTLINE
Introduction
Body Structure and Function
Cardiac Cycle
Cardiac Output
Coronary Perfusion
Systemic Circulation
Cardiac Evaluation
Patient History
Physical Examination
Diagnostic and Laboratory
Measures
Health Conditions
Hypertension
Acute Coronary Syndrome
Rhythm and Conduction
Disturbance
Valvular Heart Disease
Myocardial and Pericardial Heart
Disease
Heart Failure
Management
Revascularization and Reperfu-
sion of the Myocardium
Ablation Procedure
Cardioversion
Life Vest
Valve Replacement
Percutaneous Aortic Valvotomy
and Transcatheter Aortic Valve
Implantation
Cardiac Transplantation
Cardiac Medications
Physical Therapy Intervention
Patient Education
APPENDIX 3A: Description of
Electrocardiography (ECG)
Characteristics and Associated
Causes
APPENDIX 3B: Common Rhythm
Disturbances
Konrad J. Dias
Sean M. Collins
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . Provide a brief overview of the structure and function of the cardiovascular system
2. Give an overview of cardiac evaluation, including physical examination and diagnostic testing
3. Describe cardiac diseases and disorders, including clinical findings and medical and surgical management
4. Establish a framework on which to base physical therapy evaluation and intervention in patients with
cardiovascular disease
Introduction
Physical therapists in acute care facilities commonly encounter patients with cardiac system
dysfunction as either a primary morbidity or a comorbidity. The 2017 updated report from the
American Heart Association on heart disease and stroke statistics reported that cardiovascular
disease (CVD) accounts for approximately 800,000 deaths in the United States.1 This accounts
for one out of every three deaths in the United States. Globally CVD accounts for 31% of all
deaths, with an estimated cost of $1044 billion by 2030.1,2
Smoking, lack of physical activity, and obesity continue to be significant risk factors for
CVD. Physical therapists play a critical role in educating patients on the negative effects of
these risk factors and educate them on ways to modify lifestyle and reduce the risk for cardio-
vascular events. Smoking, including secondhand smoke, accounts for an estimated 6.3 million
deaths worldwide.1,2 Additionally, one in three adults in the United States do not meet cur-
rent recommendations for physical activity, with an estimated 37.7% of adults categorized as
obese.1,2
In the acute care setting, the role of the physical therapist in managing patients with CVD
is rooted in examination, evaluation, intervention, and discharge planning for the purpose of
improving functional capacity and maximizing participation. The physical therapist must be
prepared to safely accommodate for the effects of dynamic (pathologic, physiologic, medical,
and surgical interventions) 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, thus increas-
ing the oxygen demands of the heart. A variety of pathologic states can create impairments
in the cardiac system’s structure and function, ultimately leading to functional limita-
tions. To fully address these functional limitations, the physical therapist must understand
normal and abnormal cardiovascular structure, function, clinical tests, and medical and surgi-
cal management.
        17
18 CHAPTER 3     Cardiac System

Note: The mediastinum and the heart can be displaced from

Body Structure and Function their normal positions with changes in the lungs secondary to
various disorders. For example, a tension pneumothorax shifts
The heart and the roots of the great vessels (Fig. 3.1) occupy the
the mediastinum away from the side of dysfunction (see Chapter
pericardium, which is located in the mediastinum. The ster-
4 for a further description of pneumothorax).
num, the costal cartilages, and the medial ends of the third to
The cardiovascular system must adjust the amount of nutri-
fifth ribs on the left side of the thorax create the anterior border
ent- and oxygen-rich blood pumped out of the heart (cardiac
of the mediastinum. It is bordered inferiorly by the diaphragm,
output [CO]) to meet the spectrum of daily energy (metabolic)
posteriorly by the vertebral column and ribs, and laterally by
demands of the body.
the pleural cavity (which contains the lungs). Specific cardiac
The heart’s ability to pump blood depends on the following
structures and vessels and their respective functions are outlined
characteristics3:
in Tables 3.1 and 3.2.
• Automaticity: The ability to initiate its own electrical impulse

Aorta

Superior vena cava

Pulmonary artery

Conus branch
Sinus node branch

Ventricular branches
Right atrium

Posterolateral branch
Right coronary
artery
AV node branch
Inferior vena cava
Septal branches

Marginal branch
Posterior descending
artery

Aorta

Superior Pulmonary artery

vena cava
Left atrium
Right ventricular branch
Left main coronary
Right ventricle artery

Septal branch 1st diagonal branch

Left ventricle
Left circumflex artery
2nd diagonal branch
Obtuse
marginal branches
Left anterior
descending artery

Apical branches

FIG. 3.1
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.)
 Cardiac System     CHAPTER 3 19

• E xcitability: 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 circulatory
and cardiac pressure gradients. The right side of the heart is a
low-pressure system with little vascular resistance in the pulmo-
nary arteries, whereas the left side of the heart is a high-pressure
system with high vascular resistance from the systemic circula-
tion. The cardiac cycle is the period from the beginning of one
contraction, starting with sinoatrial (SA) node depolarization,
to the beginning of the next contraction. Systole is the period
of contraction, and diastole is the period of relaxation. Systole
and diastole can also be categorized into atrial and ventricular
components:
• Atrial diastole is the period of atrial filling. The flow of blood
is directed by the higher pressure in the venous circulatory
system.
• Atrial systole is the period of atrial emptying and contrac-
tion. Initial emptying of approximately 70% of blood occurs
as a result of the initial pressure gradient between the atria

TABLE 3.1  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 Lines the inner surface of the heart, valves, chordae
tissue 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 back flow of blood from the right ventricle to the
and ventricle atrium during ventricular systole
Right ventricle Heart chamber Pumps blood to the pulmonary circulation
Pulmonic valve Semilunar valve between right ventricle Prevents back flow of blood from the pulmonary artery to
and pulmonary artery 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 back flow of blood from the left ventricle to the
and ventricle atrium during ventricular systole
Left ventricle Heart chamber Pumps blood to the systemic circulation
Aortic valve Semilunar valve between left ventricle Prevents back flow of blood from the aorta to the left
and aorta ventricle during ventricular diastole
Chordae tendineae Tendinous attachment of atrioventricular Prevents valves from everting into the atria during
valve cusps to papillary muscles ventricular systole
Papillary muscle Muscle that connects chordae tendineae Constricts and pulls on chordae tendineae to prevent
to floor of ventricle wall eversion of valve cusps during ventricular systole

TABLE 3.2  Great Vessels of the Heart and Their Function

Structure Description Function
Aorta Primary artery from the left ventricle that ascends Ascending aorta delivers blood to neck, head, and arms
and then descends after exiting 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
20 CHAPTER 3     Cardiac System

and the ventricles. Atrial contraction then follows, squeezing
out the remaining 30%.3 This is commonly referred to as the
atrial kick.
• Ventricular diastole is the period of ventricular filling. It ini-
tially occurs with ease; then, as the ventricle is filled, atrial
contraction is necessary to squeeze the remaining blood vol-
ume into the ventricle. The amount of stretch placed on the
ventricular walls during 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.)
• Ventricular systole is the period of ventricular contraction.
The initial contraction is isovolumic (i.e., it does not eject
blood), which generates the pressure necessary to serve as the
catalyst for rapid ejection of ventricular blood. The left ven-
tricular ejection fraction (EF) represents the percent of end
diastolic volume ejected during systole and is normally ap-
proximately 60%.3  SV by increasing left ventricular end diastolic volume in addi-
Cardiac Output
CO is the quantity of blood pumped by the heart in 1 minute.
Regional demands for tissue perfusion (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 (HR—chronotropic) or stroke volume (SV—inotro-
pic).4 Normal resting CO is approximately 4 to 8 liters per min-
ute (L/min), with a resting HR of 70 beats per minute (bpm);
resting SV is approximately 71 mL/beat.3 The maximum value
of CO represents the functional capacity of the circulatory sys-
tem to meet the demands of physical activity.
CO (L/min) = HR (bpm) × SV (L)
CO also can 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 L/min/
m2. This wide normal range makes it possible for CO to decline
by almost 40% and still remain within the normal limits.
Although several factors interrupt a direct correlation between
CI and functional aerobic capacity, CI below 2.5 L/min/m2 rep-
resents a marked disturbance in cardiovascular performance and
is always clinically relevant.5
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
tion to pressure and therefore contraction.3 This relationship
is explained by the Frank-Starling mechanism and is demon-
strated in Fig. 3.2. 
Frank-Starling Mechanism.  The Frank-Starling mecha-
nism defines the normal relationship between the length and
tension of the myocardium.6 The greater the stretch on the myo-
cardium before systole (preload), the stronger is the ventricular
contraction. The length–tension relationship in skeletal muscle
is based on the response of individual muscle fibers; however,
relationships between cardiac muscle length and tension consist

Sympathetic tone
Catecholamines
Force-frequency relation
Systolic State of the Myocardium: Inotropic agents
The four lines provide an example of Anoxia/hypercapnia/
how the contractile state of the acidosis
myocardium influences the Loss of myocardium
relationship between LVEDV and Intrinsic depression
Ventricular ventricular performance.
performance

Elasticity of myocardium
Diastolic state of the myocardium Capacity of ventricular
chamber
Left Ventricular End
Diastolic Volume (LVEDV)

Total blood volume

Pump of skeletal muscles
Stretching of myocardium Venous return Body position
Intrathoracic pressure
Intrapericardial pressure
Venous tone

Atrial contribution to
ventricular filling
(atrial kick)

FIG. 3.2
Factors affecting left ventricular function. (Modified from Braunwal E, Ross J, Sonnenblick E et al. Mechanisms of Contraction of the Normal and Failing Heart.
2nd ed. Boston: Little, Brown; 1976.)
 Cardiac System     CHAPTER 3 21

of the whole heart. Therefore length is considered in terms of
volume; tension is considered in terms of pressure. 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 vol-
ume of blood is ejected during systole. The effectiveness of this
mechanism can be reduced in pathologic situations.4  tion can decrease CO (refer to the Health Conditions section for
Afterload.  Afterload is the force against which a muscle must
contract to initiate shortening.6 Within the ventricular wall, this is
equal to the tension developed across its wall during systole. The
most prominent force contributing 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 encoun-
tered by the ejecting ventricle. An example of afterload is the
amount of pressure in the aorta at the time of ventricular systole.3  Parasympathetic input travels through the vagus nerves. The
Cardiac Conduction System
A schematic of the cardiac conduction system and a normal elec-
trocardiography (ECG) result are presented in Fig. 3.3. Normal
conduction begins in the SA node and travels throughout the
atrial myocardium (atrial depolarization) via intranodal path-
ways to the atrioventricular (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.7 Disturbances in conduc-
a discussion of rhythm and conduction disturbances).8
Neural Input.  The SA node has its own inherent rate.
However, neural input can influence HR, heart rate variabil-
ity (HRV), and contractility through the autonomic nervous
system.3,9
Parasympathetic system (vagal) neural input generally decel-
erates cardiac function, thus decreasing HR and contractility.
right vagus nerve stimulates primarily the SA node and affects
rate, whereas the left vagus nerve stimulates primarily the AV
node and affects AV conduction.3,9
Sympathetic system neural input is through the thoracolum-
bar sympathetic system and increases HR and augment ven-
tricular contractility, thus accelerating cardiac function.3 
Endocrine Input.  In response to physical activity or stress,
a release in catecholamines increases HR, contractility, and
peripheral vascular resistance for a net effect of increased cardiac
function (Table 3.3).3 
Local Input.  Tissue pH, concentration of carbon dioxide
(CO2), concentration of oxygen (O2), and metabolic products
(e.g., lactic acid) can affect vascular tone.3 During exercise,
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. 

FIG. 3.3
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 Reflexes
Cardiac reflexes influence HR and contractility and can be
divided into four general categories: baroreflex (pressure), Bain-
bridge reflex (stretch), chemoreflex (chemical reflex), ergoreflex
(ergoreceptors).
Baroreflexes are activated through a group of mechanorecep-
tors located in the heart, great vessels, and intrathoracic and

TABLE 3.3  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 Tissue damage/inflammation Vasodilation, increased capillary permeability
in blood when activated
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) by Increased blood volume, kidneys excrete more
hypovolemia or decreased renal potassium
perfusion

Data from Guyton AC, Hall JE. Textbook of Medical Physiology. 13th ed. Philadelphia: Saunders; 2016.
22 CHAPTER 3     Cardiac System
cervical blood vessels. These mechanoreceptors are most plen-
tiful in the walls of the internal carotid arteries.3 Mechanore-
ceptors are sensory receptors that are sensitive to mechanical
changes, such as pressure and stretch. Activation of the mech-
anoreceptors by high pressures results in an inhibition of the
vasomotor center of the medulla that increases vagal stimula-
tion. This chain of events is known as the baroreflex and results in
vasodilation, decreased HR, and decreased contractility.
Mechanoreceptors located in the right atrial myocardium
respond to stretch. An increased volume in the right atrium
results in 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.3 Respiratory sinus arrhythmia,
an increased HR during inspiration and decreased HR during
expiration, may be facilitated by changes in venous return and
SV caused by changes in thoracic pressure induced by the respi-
ratory cycle. At the beginning of inspiration when thoracic pres-
sure is decreased, venous return is greater; therefore a greater
stretch is exerted on the atrial wall.10
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 also may result in
sinus arrhythmia.3
Ergoreceptors and the ergoreflex regulates hemodynamics
through activation of mechanosensitive afferents to inhibit the
sustained vagal effects on the heart caused by an increase heart
rate during physical loading.11  ter 2, the following pertinent information about patients
Coronary Perfusion
For a review of the major coronary arteries, refer to Fig. 3.1.
Blood is pumped to the large superficial coronary arteries during
Systemic
capillaries
Lung
CO2
O2
Pulmonary
capillaries
Pulmonary circulation
CO2 O2
Systemic circulation
FIG. 3.4
Schematic of systemic circulation. (From Thibodeau GA. Structure and Function of the Body. 13th ed. St. Louis: Mosby; 2007.)
ventricular systole. At this time, myocardial contraction limits
the flow of blood to the myocardium; therefore myocardial tis-
sue is perfused during diastole. 
Systemic Circulation
For a review of the distribution of systemic circulation, refer
to Fig. 3.4. Systemic circulation is affected by total peripheral
resistance (TPR), which is the 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. TPR, also called
systemic vascular resistance, and CO influence BP.3 This relation-
ship is illustrated in the following equation:
BP = CO × TPR  
  
Cardiac Evaluation
Cardiac evaluation uses patient history, physical examination
(which consists of observation, palpation, BP measurement,
and heart sound auscultation), laboratory tests, and diagnostic
procedures to summarize the patient’s situation by connecting
features of body structure, function, activity, and participation
to develop a plan of care.
Patient History
In addition to the general chart review presented in Chap-
with cardiac dysfunction should be obtained before physical
examination4,12–14:
• Presence of chest pain (see Chapter 17 for an expanded de-
scription of characteristics and etiology of chest pain)
CO2 O2
Circulation to
tissues of head
and upper body
Lung
CO2
O2
Circulation to
tissues of
lower body
 Cardiac System     CHAPTER 3 23

• L ocation and radiation

• Character and quality (crushing, burning, numbing, hot)
• Angina equivalents (what the patient feels as angina [e.g.,
jaw pain, shortness of breath, dizziness, lightheadedness, dia-
phoresis, burping, nausea, or any combination of these])
• Aggravating factors: Activity, recreational drugs
• Alleviating factors: Pain stops when activity ceases, relieved
by sitting forward or resting
• Precipitating factors
• Medical treatment sought and its outcome
• Presence of palpitations
• Presence of cardiac risk factors (Box 3.1)
• Family history of cardiac disease
• History of dizziness or syncope
• Previous myocardial infarction (MI), cardiac studies, or pro-
cedures
• Medications ordered: Nitroglyercin, beta-blockers, calcium chan-
nel blockers, antihypertensive medications, antiplatelet therapy
CLINICAL TIP
When discussing angina with a patient, use the patient’s terminol-
ogy. If the patient describes the angina as “crushing” pain, ask the
patient if he or she experiences the crushing feeling during treat-
ment 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 include the following4,8:
• Facial color, skin color and tone, or the presence of diaphoresis
• Obvious signs of edema, discoloration in the extremities
• Respiratory rate
• Signs of trauma (e.g., paddle burns or ecchymosis from car-
diopulmonary resuscitation)
• Presence of jugular venous distention (JVD), which results
from the backup of fluid into the venous system from right-
sided congestive heart failure (CHF) (Fig. 3.5)
• Make sure the patient is in a semirecumbent position (45
degrees).
• Have the patient turn his or her head away from the side be-
ing evaluated.
• Observe pulsations in the internal jugular neck region. Pulsa-
tions are normally seen 3 to 5 cm above the sternum. Pulsations
higher than this or absent pulsations indicate JVD. 
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 3.4,
Fig. 3.6)
• Extremities for pitting edema bilaterally (Table 3.5)

BOX 3.1  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, total (and LDL) Body mass index >30 kg/m2 Elevated homocysteine
Decreased HDL cholesterol Abdominal obesity (waist–hip ratio) Elevated lipoprotein (a)
Diabetes mellitus Men >40 inches Elevated inflammatory markers
Advancing age Women >35 inches C-reactive protein
Family history of premature heart disease Fibrinogen
Psychosocial factors
Job strain
Ethnic characteristics
LDL, Low-density lipoprotein; HDL, high-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; Belkic KL, Landsbergis PA, Schnall PL,
Baker D. Is job strain a major source of cardiovascular disease risk? Scand J Work Environ Health. 2004;30(2):85-128.

FIG. 3.5
Measurement of jugular venous distention (JVD). The JVD reading is the maximum height, in centimeters, above the sternal angle at which venous pulsa-
tions are visible. (Modified from Thompson JM, McFarland GK, Hirsch JE, et al. Mosby’s Clinical Nursing. 5th ed. St. Louis: Mosby; 2002.)
24 CHAPTER 3     Cardiac System

TABLE 3.4  Pulse Amplitude Classification and Pulse Abnormalities

Pulse Amplitude Classification
Scale Degree Description
0 Absent pulse No pulse—no 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)a 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 at normal heart rates
alternating with weak pulse waves
Bigeminal pulses Every other pulse is weak and early Result of premature ventricular contractions (bigeminy)
Pulsus paradoxus Reduction in strength of the pulse with May be caused by chronic obstructive lung disease, pericarditis,
an abnormal decline in blood pressure pulmonary emboli, restrictive cardiomyopathy, and cardiogenic
during inspiration shock
aCorrigan’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 Williams & Wilkins; 2000.

TABLE 3.5  Pitting Edema Scale

Temporal
pulse Scale Degree Description
Carotid pulse 1+ Trace Slight Barely perceptible depression
2+ Mild 0–0.6 cm Easily identified depression (EID)
Apical
(skin rebounds in <15 sec)
pulse
3+ Moderate 0.6–1.3 cm EID (rebound 15–30 sec)
Brachial 4+ Severe 1.3–2.5 cm EID (rebound >30 sec)
pulse
Data from Woods SL, Sivarajian Froelicher ES, Underhill-Motzer S, eds. Cardiac
Nursing. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2000; Hille-
Radial gass E. Essentials of Cardiopulmonary Physical Therapy. 4th ed. St. Louis: Elsevier;
pulse 2017.

irregular (e.g., during atrial fibrillation) or regularly irregular

Femoral (e.g., premature ventricular contractions [PVCs]), perform aus-
pulse
cultation of heart sounds to identify the apical HR for a full
Popliteal minute. In these cases, palpation of pulse cannot substitute for
pulse ECG analysis to monitor the patient’s rhythm, but it may alert
the therapist to the onset of these abnormalities.
Posterior
tibial pulse
CLINICAL TIP
Pedal pulse Use caution in palpating pulses because manual pressure on
(dorsalis pulse)
the carotid sinus may cause baroreflex drops in heart rate (HR),
FIG. 3.6
blood pressure (BP), or both.
Arterial pulses. (From Pierson FM. Principles and Techniques of Patient Care.  
4th ed. St. Louis: Saunders; 2008.)
Blood Pressure
When palpating HR, counting the pulse rate for 15 sec- BP measurement with a sphygmomanometer (cuff) and aus-
onds and multiplying by 4 is sufficient with normal rates and cultation is an indirect, noninvasive measurement of the
rhythms. If rates are faster than 100 bpm or slower than 60 bpm, force exerted against the arterial walls during ventricular sys-
palpate the pulse for 60 seconds. If the rhythm is irregularly tole (systolic blood pressure [SBP]) and during ventricular

TABLE 3.6  Normal Blood Pressure Ranges
Age Ranges Systolic Diastolic
Age 8 years 85–114 mmHg 52–85 mmHg
Age 12 years 95–135 mmHg 58–88 mmHg
Adult <120 mmHg <80 mmHg
Elevated 120–129 mmHg <80 mmHg
Hypertension
Stage 1 130–139 mmHg 80–89 mmHg
Stage 2 ≥140 mmHg ≥90 mmHg
Normal exercise Increases 5–12 mmHg ±g  mmHg
per MET increase in
workload
MET, Metabolic equivalent.
Data from Wright JD, Hughes JP, Ostchega Y, Yoon SS, Nwankwo T. Mean
systolic and diastolic blood pressure in adults aged 18 and over in the United
States, 2001-2008. Natl Health Stat Rep. 2011(35):1-22, 24; Whelton PK, Car-
ey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/
ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation,
and management of high blood pressure in adults: a report of the American
College of Cardiology/American Heart Association Task Force on Clinical Prac-
tice Guidelines. J Am Coll Cardiol. 2018;138:e426-e483; American College of
Sports Medicine, Armstrong LE, et al. ACSM’s Guidelines for Exercise Testing and
Prescription. Philadelphia: Lippincott Williams & Wilkins; 2005.
diastole (diastolic blood pressure [DBP]). BP is affected by
total peripheral resistance (blood volume and elasticity of
arterial walls) and CO. Table 3.6 lists normal BP ranges.
Occasionally, BP measurements can be performed only on
certain limbs secondary to the presence of such conditions
as a percutaneously inserted central catheter, arteriovenous
fistula for hemodialysis, blood clots, scarring from brachial
artery cutdowns, or lymphedema (e.g., status post mastec-
tomy). BP of the upper extremity should 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 mmHg between the right and left upper extrem-
ity are considered normal. Patients with arterial compres-
sion or obstruction may have differences of more than 10 to
15 mmHg.14
2. Use a properly fitting cuff. The inflatable bladder should
have a width of approximately 40% and length of approxi-
mately 80% of the upper arm circumference.15
3. Position the cuff 2.5 cm above the antecubital crease.
4. Rest the relaxed arm at the level of the heart.
5. To determine how high to inflate the cuff, palpate the radial
pulse, inflate until no longer palpable, and note the cuff in-
flation pressure. Deflate the cuff.
6. Place the bell of the stethoscope gently over the brachial
artery.
7. Reinflate the cuff to 30 to 40 mmHg greater than the value
in step 5. Then slowly deflate the cuff. Cuff deflation should
occur at approximately 2 to 3 mmHg per second.15
8. Listen for the onset of tapping sounds, which represents
blood flow returning to the brachial artery. This is the SBP.
9. As the pressure approaches diastolic pressure, the sounds
Cardiac System     CHAPTER 3 25
will become muffled and in 5 to 10 mmHg will be com-
pletely absent. These sounds are referred to as Korotkoff
sounds (Table 3.7).14,15
CLINICAL TIP
In situations when it is difficult to auscultate or discern a distinct
diastolic pressure, the patient’s blood pressure may be noted as
systolic BP/P (i.e., “BP is 90 over palp”) or systolic BP over 2
diastolic pressures (e.g., 140/85/62) denoting the onset of muf-
fling sounds and the disappearance of sounds.13  
Physical Therapy Considerations
• Recording preexertion, paraexertion, and postexertion BP is
important for identification of BP responses to activity. Dur-
ing 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 you are unable to obtain BP on the arm, the thigh is an
appropriate alternative, with auscultation at the popliteal ar-
tery.
• Falsely high readings 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 measure-
ments on the same arm 1 to 5 minutes after position chang-
es. The symbols that represent patient position are shown in
Fig. 3.7.
• The same extremity should be used when serial BP record-
ings will be compared for an evaluation of hemodynamic re-
sponse.
• 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 SBPs if the cuff is not inflated enough
(prevented by palpating for the disappearance of the pulse
before measurement), or falsely high DBPs 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 compliance, and ventricular compli-
ance.4 To listen to heart sounds, a stethoscope with a bell and
a diaphragm is necessary. For a review of normal and abnormal
heart sounds, refer to Table 3.8. The examination should fol-
low a systematic pattern using the bell (for low-pitched sounds)
and diaphragm (for high-pitched sounds) and should cover all
26 CHAPTER 3     Cardiac System
TABLE 3.7  Korotkoff Sounds
Phase Sound
1 First sound heard, faint tapping sound with
increasing intensity or sharp “thud” heard
2 Start blowing or swishing sound
3 Sounds increase in intensity with a distinct
tapping
4 Sounds become muffled
5 Disappearance
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S, eds. Cardiac Nursing. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2000; Bickley LS,
Szilagyi PG. Bates’ Guide to Physical Examination and History Taking. Philadelphia: Lippincott Williams & Wilkins; 2003; Ball JW, Dains JE, Flynn JA, Solomon BS,
Stewart RW. Seidel’s Guide to Physical Examination: An Interprofessional Approach. 9th ed. St. Louis: Elsevier; 2019.
Supine Sitting Standing
FIG. 3.7
Orthostatic blood pressure symbols.
auscultatory areas, as illustrated in Fig. 3.8. Abnormal sounds
should be noted with a description of the conditions in which
they were heard (e.g., after exercise or during exercise). 
Physical Therapy Considerations
• Always ensure proper function of a stethoscope by tapping
the diaphragm before use with a patient.
• Avoid rubbing any part of the stethoscope on extraneous ob-
jects because this can add noise and detract from the exami-
nation.
• Avoid auscultation of heart sounds over clothing, which can
muffle the intensity of normal and abnormal sounds.
• If the patient has an irregular cardiac rhythm, determine HR
through auscultation (apical HR). To save time, listen for
the HR during a routine auscultatory examination with the
stethoscope’s bell or diaphragm in any of the auscultation
locations (see Fig. 3.8).
• Heart sounds can be heard online at the Auscultation As-
sistant, available at: http://www.med.ucla.edu/wilkes/intro
.html.  this book. For a review of basic ECG rate and rhythm analysis,
Diagnostic and Laboratory Measures
The diagnostic and laboratory measures discussed in this
section provide information used to determine medical
diagnoses, guide interventions, and assist with determin-
ing prognoses. The clinical relevance of each test varies
according to the pathology. This section is organized across
Indicates
Systolic pressure (blood starts to flow through compressed artery)
Blood flow continues to be heard; sounds are beginning to change because of
the changing compression on the artery
Blood flow is increasing as artery compression is decreasing
Diastolic pressure in children <13 years of age and in adults who are exercis-
ing, pregnant, or hyperthyroid (see phase 5)
Diastolic pressure in adults—occurs 5–10 mmHg below phase 4 in normal
adults. In states of increased rate of blood flow, it may be >10 mmHg below
phase 4. In these cases, the phase 4 sound should be used as diastolic pres-
sure in adults
a spectrum—from the least invasive to the most invasive
measures. When appropriate, detailed information for test
results most pertinent to the physical therapist are provided.
For clinical decision making, physical therapists usually need
information that helps identify indications for intervention,
relative or absolute contraindications for intervention, pos-
sible complications during activity progression, and indi-
cators of performance. Box 3.2 provides the clinician with
important information to obtain from the medical record
before patient encounter. In addition, the clinician should
review the radiographic report, echocardiographic report and
other specialized tests to obtain valuable knowledge of the
patient’s cardiovascular status.
Oximetry
Oximetry (SaO2) is used to indirectly evaluate the oxygen-
ation of a patient and can be used to titrate supplemen-
tal oxygen. Refer to Chapter 4 for a further description of
oximetry. 
Electrocardiography
ECG provides a graphic analysis of the heart’s electrical activ-
ity. ECG commonly is used to detect arrhythmias, heart blocks,
and myocardial perfusion. It also can detect atrial or ventricular
enlargement. 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 usually is 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
refer to Table 3.9 and Fig. 3.3.
Holter and Event Monitoring.  Holter monitoring refers
to 24- or 48-hour ECG analysis conducted to detect cardiac
arrhythmias and corresponding symptoms during a patient’s
daily activity.14 Holter monitoring is different from telemetric
monitoring because the ECG signal is recorded and analyzed
later.
 Cardiac System     CHAPTER 3 27

TABLE 3.8  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 at apex Immediately after S2; occurs early in diastole and represents filling of the 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 at apex Immediately preceding S1; occurs late in ventricular diastole; associated with increased
resistance to ventricular filling; common in patients with hypertensive heart disease,
coronary heart disease, pulmonary disease, or myocardial infarction, or after coronary
artery bypass grafts
Murmur (abnormal) Over respective valves Indicates regurgitation of blood through valves; can also be classified as systolic or
diastolic murmurs. Common pathologies resulting in murmurs include mitral
regurgitation and aortic stenosis
Pericardial friction Third or fourth intercostal Sign of pericardial inflammation (pericarditis), associated with each beat of the heart;
rub (abnormal) space, anterior axillary line sounds like a creak or leather being rubbed together

Data from Bickley LS, Szilagyi PG. Bates’ Guide to Physical Examination and History Taking. Philadelphia: Lippincott Williams & Wilkins; 2003.

Pulmonic area
Aortic area

Tricuspid area
Mitral area /
apex
FIG. 3.8
Areas for heart sound auscultation. (Courtesy
Barbara Cocanour, PhD, Department of Physical
Therapy, University of Massachusetts, Lowell,
MA.)

Indications for Holter monitoring include the evaluation of
syncope, dizziness, shortness of breath with no other obvious
cause, palpitations, antiarrhythmia therapy, pacemaker func-
tioning, activity-induced silent ischemia, and risk of cardiac
complications with the use of HRV.
Event monitoring refers to extended ECG monitoring, with
recordings saved only when an event is either automatically
identified (device algorithms) or self-identified by the patient.  cardiac risk. Delayed HRR (<46 bpm) 3 minutes after an exer-
Heart Rate Variability.  HRV has been discussed in the
literature to possibly reflect cardiac autonomic nervous system
regulation. A common overall measure of HRV is the standard
deviation of all RR intervals on ECG during a 24-hour period
(SDNN).9 Evidence regarding the potential clinical utility of
HRV for cardiology is growing; however, HRV continues to be
used primarily in research.16 In healthy populations, low HRV
is a risk factor for all causes of cardiac mortality17–19 and for new
onset of hypertension.20 Low HRV is also a risk for mortality
in patients who have had an MI21–23 or have coronary artery
disease24 or CHF.25 Evidence suggests that altered HRV during
exercise may provide valuable information for risk assessment.26
This is likely related to the increasingly accepted relationship
between delayed heart rate recovery (HRR) after exercise and
cise test is a predictor of long-term (≈15 years) mortality.27
HRR is discussed further in the section on Physical Therapy
Intervention. 
Telemetric Electrocardiography Monitoring.  Telemet-
ric ECG monitoring provides real-time ECG visualization via
radiofrequency transmission of the ECG signal to a monitor.
Benefits of telemetry include monitoring with no hardwire
28 CHAPTER 3     Cardiac System
BOX 3.2  Medical Chart Review
Medical Test Rationale for Use of the Test
B-type natriuretic peptide Assesses biomarkers of heart failure,
(BNP) including natriuretic peptides that
include BNP and N-terminal pro-BNP
(NT-proBNP).6
Blood urea nitrogen Assesses renal function, which may be
(BUN), Plasma creatinine reduced in patients with HF.
levels, and urine output
Hemoglobin and hemato- Assess the oxygen carrying capacity
crit levels within the system.
Creatine kinase—myocar- Creatine kinase MB subunit (CK-MB),
dial band CK-MB index an isoenzyme, is released into blood and
elevates with an acute MI.8
Troponin I Troponin I is the most frequently used
marker to assess the presence of an acute
MI.8 Troponin I is an isotype found
exclusively in the myocardium and is
therefore 100% cardiac specific.
C-reactive CRP is a test that measures the amount of
protein (CRP) a protein in the blood that signals acute
inflammation. 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.
Electrolyte Appropriate levels of potassium, calcium,
assessment and magnesium allow for normal electri-
cal conduction through the heart.
Data from: Academy of Acute Care Physical Therapy. Laboratory Values Interpretation Resource. 2017 (Reference #: C)
TABLE 3.9  Electrocardiograph Interpretation
Wave/Segment Duration (seconds)
P wave <0.10
PR interval 0.12–0.20
QRS complex 0.06–0.10
ST segment 0.12
QT  interval (QTc) 0.42–0.47
T wave 0.16
Data from Meyers RS, ed. Saunders Manual of Physical Therapy Practice. Philadelphia: Saunders; 1995; Aehlert B, ed. ACLS Quick Review Study Guide. St. Louis: Mosby;
1994; Davis D, ed. How to Quickly and Accurately Master ECG Interpretation. 2nd ed. Philadelphia: Lippincott Williams & Wilkins; 1992.
Interpretation of the Test
Normal levels of BNP are less than 100 pg/mL.6 Values above 500 are
generally considered to be positive for heart failure. BNP has been
found to be a statistically significant (P < 0.05) prognostic indicator
of heart failure, and studies have discovered moderate to strong cor-
relations between BNP and peak oxygen uptake (VO2max)7
Normal BUN: 6–30 mg/dL
Normal creatinine: 0.5–2.0 mg/dL
Values above normal ranges indicate renal failure
Oliguria <400 mL of urine in 24 hours
Anuria: <100 mL of urine in 24 hours
Normal hemoglobin 12–14 gm/ 100 mL of blood in adult males
and 14–16 g/100 mL of blood in adult women
Normal hematocrit: 45% men; 40% women
Normal level: 0%–3%
Minor cardiac dysfunction: 5%
Major cardiac dysfunction: 10%
Peak Levels: 14–36 hours
Normal level: 0–0.2 mcg/mL
Minor cardiac dysfunction: 5 mcg/mL
Major cardiac dysfunction: 10 mcg/mL
Peak levels: 24–36 hours
hs-CRP lower than 1.0 mg/L indicates a low risk of developing
cardiovascular disease
hs-CRP between 1 and 3 mg/L indicates an average risk of develop-
ing cardiovascular disease
hs-CRP higher than 3.0 mg/L indicates a high risk of developing
cardio­vascular disease
Hypokalaemia, low potassium (usually <3.5 mEq/L), produces ar-
rhythmias with flattened T waves and depressed ST segments, as
well as bilateral lower extremity muscle cramping. An inverted
U-wave may also be noticed on the electrocardiogram. Hypocal-
caemia (low blood serum calcium levels) and hypomagnesaemia (low
magnesium in blood) have the potential of increasing ventricular
ectopy within the heart
Amplitude (mm) Indicates
1–3 Atrial depolarization
Isoelectric line Elapsed time between atrial
depolarization and ventricular
depolarization
25–30 (maximum) Ventricular depolarization and
atrial repolarization
–½ to +1 Elapsed time between end of
ventricular depolarization and
beginning of repolarization
Varies Elapsed time between beginning
of ventricular repolarization and
end of repolarization (QTc is
corrected for heart rate)
5–10 Ventricular repolarization

connection between the patient and the visual display unit and
real-time graphic display of the ECG signal using the standard
ECG monitor attachment.
CLINICAL TIP
Some hospitals use an activity log with Holter monitoring. If so,
document physical therapy intervention on the log. If no log is
available, record the time of day and physical therapy interven-
tion in the medical record.  
Complete Blood Cell Count
Relevant values from the complete blood cell count are hema-
tocrit, hemoglobin, and white blood cell counts (see Box 3.2).
Hematocrit refers to the number of red blood cells per 100 mL
of blood and therefore fluctuates with changes in the total red
blood cell count (hemoglobin) and with blood volume (i.e.,
reduced plasma volume results in relatively more red blood
cells in 100 mL of blood). Elevated levels of hematocrit (which
may be related to dehydration) indicate increased viscosity of
blood that can potentially impede blood flow to tissues.14 Hemo-
globin 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 tol-
erance or make patients more susceptible to ischemia second-
ary to decreased oxygen-carrying capacity.13,28 Slight decreases
in hematocrit resulting from 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.29
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 hematologic test, is a nonspecific index of
inflammation and commonly is elevated for 2 to 3 weeks after
MI.28 Refer to Chapter 7 for more information about these
values. 
Coagulation Profiles
Coagulation profiles provide information about the clotting
time of blood. Patients who undergo treatment with thrombo-
lytic therapy after the initial stages of MI or who are receiving
anticoagulant therapy because of various cardiac arrhythmias
require coagulation profiles to monitor anticoagulation in an
attempt to prevent complications, such as bleeding. The physi-
cian determines the patient’s therapeutic range of anticoagula-
tion using prothrombin time (PT), partial thromboplastin time
(PTT), and international normalized ratio (INR).28 Refer to
Chapter 7 for details regarding these values and their signifi-
cance to treatment.
The normal levels for PT-INR is 0.8 to 1.2.30 For patients
on heparin, the activated PTT is more appropriate to evaluate.
Normal PTT range is 21 to 35 seconds. Typically therapeutic
ranges for effectiveness of the anticoagulant is 2 to 2.5 times
normal range (60–109 seconds) with variability based on the
reagent utilized.30 Patients with low INR and activated partial
Cardiac System     CHAPTER 3 29
thromboplastin time (aPTT) are at higher risk of thrombosis,
especially if they have arrhythmias (e.g., atrial fibrillation) or val-
vular conditions (e.g., mitral regurgitation) that produce stasis
of the blood. Patients values greater than the therapeutic range
are at increased risk for bleeding and therefore should be care-
fully evaluated for balance and fall risk before mobilization.28 
Blood Lipids
Elevated total cholesterol levels in blood are a significant risk
factor for atherosclerosis and therefore ischemic heart disease.31
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 total
cholesterol greater 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-den-
sity 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 vas-
cular system. People with higher amounts of HDLs are at lower
risk for coronary artery disease.28,31 HDL levels of less than
33 mg/dL carry an elevated risk of heart disease. A more impor-
tant risk for heart disease is an elevated ratio of total cholesterol
to HDL. Normal ratios of total cholesterol to HDL range from
3 to 5.14
LDLs are formed by a diet excessive in fat and are related to
a higher incidence of coronary artery disease. LDLs are not as
readily transportable as HDLs because LDLs adhere to intimal
walls in the vascular system.28 Normal LDL levels are below
100 mg/dL.14
Triglycerides are fat cells that are free floating in blood.
When not in use, they are stored in adipose tissue. A person’s
triglyceride levels increase after he or she eats foods high in fat
and decrease with exercise. High levels of triglycerides are asso-
ciated with a risk of coronary heart disease.28
CLINICAL TIP
Cholesterol levels may be elevated falsely after an acute myocar-
dial infarction (MI); therefore preinfarction levels (if known) are
used to guide risk factor modification. Values will not return to
normal until at least 6 weeks after MI.  
C-Reactive Protein
C-reactive protein (CRP) is a test that measures the amount
of a protein in the blood that signals acute inflammation. To
determine a person’s risk for heart disease, a more sensitive CRP
test, called 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 (USA) and acute MI.
In addition, elevated hs-CRP levels are associated with lower
survival rates in these patients with cardiovascular disease (see
Box 3.2).32–34 
30 CHAPTER 3     Cardiac System
Biochemical Markers
After an initial myocardial insult, the presence of tissue necrosis
can be determined by increased levels of biochemical markers.
Levels of biochemical markers, such as serum enzymes (creatine
kinase [CK]) and proteins (troponin I and T), also can be used to
determine the extent of myocardial death and the effectiveness
of reperfusion therapy. In patients presenting with specific angi-
nal symptoms and diagnostic ECG, these biochemical markers
assist with confirmation of the diagnosis of an MI (refer to Box
3.2, Medical Chart Review). Enzymes play a more essential role
in the medical assessment of many patients with nonspecific or
vague symptoms and inconclusive ECG changes.35 Such analysis
also includes evaluation of isoenzyme levels.36 Isoenzymes are
different chemical forms of the same enzyme that are tissue spe-
cific and allow differentiation of damaged tissue (e.g., skeletal
muscle versus cardiac muscle).
CK (formally called creatine phosphokinase) is released after cell
injury or cell death. CK has three isoenzymes. The CK-MB iso-
enzyme is related to cardiac muscle cell injury or death. The
most widely used value is the CK-MB relative index calculated
as 100% (CK-MB/total CK).35 Temporal measurements of the
CK-MB relative index help physicians diagnose MI, estimate
the size of infarction, and evaluate the occurrence of reperfu-
sion and possible infarct extension. An early CK-MB peak with
rapid clearance is a good indication of reperfusion.14 Values may
increase from skeletal muscle trauma, cardiopulmonary resusci-
tation (CPR), defibrillation, and open-heart surgery. Coronary
artery bypass surgery tends to elevate CK-MB levels secondary
to the cross-clamp time in the procedure. Early postoperative
peaks and rapid clearance seem to indicate reversible damage,
whereas later peaks and longer clearance times with peak values
exceeding 50 U/L may indicate an MI.14 Treatment with throm-
bolytic 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.14,35
Troponins are essential contractile proteins found in skeletal
and cardiac muscles. Troponin I is an isotype found exclusively
in the myocardium and is therefore 100% cardiac specific. Tro-
ponin T, another isotype, is sensitive to cardiac damage, but its
levels also rise with muscle and renal failure.35 These markers
have emerged as sensitive and cardiac-specific clinical indicators
for the diagnosis of MI and for risk stratification.
CLINICAL TIP
Wait for the final diagnosis of location, size, and type of myo-
cardial infarction (MI) before beginning active physical therapy
intervention. This allows for compete information from the
medical team for the therapist’s clinical decision making and
decreases risk of harm. Withhold physical therapy geared toward
testing functional capacity or increasing the patient’s activity
until cardiac enzyme levels have peaked and begin to fall.  
Natriuretic Peptides
Three natriuretic peptides have been identified in humans. These
include atrial natriuretic peptide (ANP), B-type natriuretic
peptide (BNP), and C-type natriuretic peptide (CNP).5 ANP is
stored in the right atrium and released in response to increased
atrial pressures. BNP is stored 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 physi-
ologic role of CNP has not been clarified yet.
Circulating levels of ANP, BNP, and N-terminal (NT)–
proBNP (a variation of BNP) are elevated in plasma in patients
with heart failure (HF). In normal human hearts, ANP predom-
inates in the atria, with a low-level expression of BNP and CNP.
Patients with heart failure demonstrate an unchanged content of
ANP in the atria, with a marked increase in the concentrations
of BNP and NT-proBNP. The 2017 American Heart Associa-
tion (AHA)/American College of Cardiology (ACC) guidelines
provide a Class I recommendation (Level of Evidence: A) for
measurement of BNP or NT-proBNP for establishing prognosis
or disease severity in chronic HF.37 These natriuretic peptide
biomarkers in patients assist in the diagnosis and exclusion of
HF in those patients presenting with dyspnea.
No level of BNP perfectly distinguishes patients with HF
and those without HF. Normal levels include BNP less than
100 pg/mL (see Box 3.2).5,38 Research has indicated a correla-
tion between circulating BNP concentrations and the severity
of CHF, based on the New York Heart Association (NYHA)
functional classification system. Values between 100 and 300
pg/mL have been shown to be correlated with NYHA Class
I; values greater than 300 pg/mL are associated with Class II
heart failure; and values greater than 600 pg/mL and greater
than 900 pg/mL correlate with NYHA Class III and IV,
respectively.30 
Arterial Blood Gas Measurements
Arterial blood gas measurement may be used to evaluate the
oxygenation (PaO2), ventilation (PaCO2), and pH in patients
during acute MI and exacerbations of CHF in certain situa-
tions (i.e., obvious tachypnea, low SaO2). These evaluations can
help determine the need for supplemental oxygen therapy and
mechanical ventilatory support in these patients. Oxygen is the
first drug provided during a suspected MI. Refer to Chapters 4
and 18 for further description of arterial blood gas interpreta-
tion and supplemental oxygen, respectively. 
Chest Radiography
Chest radiography (“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 pulmonary vas-
culature markings, giving the appearance of congestion in the
vessels.4,8 Refer to Chapter 4 for further description of chest
radiography. 
Echocardiography
Transthoracic echocardiography (TTE), or “cardiac echo,” is
a noninvasive procedure that uses ultrasound to evaluate the
function of the heart. Evaluation includes the size of the ven-
tricular cavity, the thickness and integrity of the septum, valve

integrity, and the motion of individual segments of the ven-
tricular wall. Volumes of the ventricles are quantified, and EF
can be estimated.4
Transesophageal echocardiography (TEE) is an approach to
echocardiography that provides a better view of the mediasti-
num in cases of pulmonary disease, chest wall abnormality, and
obesity, which make standard echocardiography difficult.14,39
For this test, the oropharynx is anesthetized, and the patient is
given enough sedation to be relaxed but still awake because he
or she needs to cooperate by swallowing the catheter. The cath-
eter, a piezoelectric crystal mounted on an endoscope, is passed
into the esophagus. Specific indications for TEE include bac-
terial endocarditis, aortic dissection, regurgitation through or
around a prosthetic mitral or tricuspid valve, left atrial throm-
bus, intracardiac source of an embolus, and interarterial septal
defect. Patients usually are required to fast for at least 4 hours
before the procedure.39
Principal indications for echocardiography are to assist in the
diagnosis of pericardial effusion, cardiac tamponade, idiopathic
or hypertrophic cardiomyopathy, a variety of valvular diseases,
intracardiac masses, ischemic cardiac muscle, left ventricular
aneurysm, ventricular thrombi, and a variety of congenital heart
diseases.14
TTE also can be performed during or immediately after
bicycle or treadmill exercise to identify ischemia-induced wall
motion abnormalities or during a pharmacologically induced
exercise stress test (e.g., dobutamine stress echocardiography
[DSE]). This stress echocardiography adds to the information
obtained from standard stress tests (ECGs) and may be used as
an alternative to nuclear scanning procedures. Transient depres-
sion of wall motion during or after stress suggests ischemia.40
Contrast Echocardiography.  The ability of echocardiog-
raphy to diagnose perfusion abnormalities and myocardial
chambers is improved by using an intravenously injected con-
trast agent. The contrast allows for greater visualization of wall
motion and wall thickness and calculation of EF.41  ties, refer to Table 3.10. For a more thorough description of
Dobutamine Stress Echocardiography.  Dobutamine is
a potent alpha-1 (α1) agonist and a beta-receptor agonist with
prominent inotropic and less prominent chronotropic effects
on the myocardium. Dobutamine (which, unlike dipyridamole
(Persantine; see Persantine Thallium Stress Testing in this chap-
ter), increases contractility, HR, and BP in a manner similar to
exercise) is injected in high doses into subjects as an alternative
to exercise.40 Dobutamine infusion is increased in a stepwise
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
echocardiographic image of wall motion is obtained during the
final minute(s) of infusion. This image can then be compared
with baseline recordings.40 If needed, atropine occasionally is
added to facilitate a greater HR response for the test.40 Low-dose
DSE has the capacity to evaluate the contractile response of the
impaired myocardium. Bellardinelli et al.42 have demonstrated
that improvements in functional capacity after exercise can be
predicted by low-dose DSE. Patients with a positive contrac-
tile response to dobutamine were more likely to increase their
VO2max after a 10-week exercise program. Having a positive
Cardiac System     CHAPTER 3 31
contractile response on the low-dose DSE had a positive predic-
tive value of 84% and a negative predictive value of 59%.42
As this study indicates, research has demonstrated the prog-
nostic value of certain medical tests for determining functional
prognosis. Therefore physical therapists must be prepared to
assess this area of literature critically to assist the medical team
in determining the level of rehabilitative care for a patient dur-
ing 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 pur-
poses, which are not mutually exclusive. The most widespread
use of exercise testing is as a diagnostic tool for the presence
of coronary artery disease. Other uses include determination of
prognosis and severity of disease, evaluation of the effectiveness
of treatment, early detection of labile hypertension, evaluation
of CHF, evaluation of arrhythmias, and evaluation of functional
capacity.40 Exercise testing involves the systematic and pro-
gressive increase in intensity of activity (e.g., treadmill walk-
ing, bicycling, stair climbing, arm ergometry). These tests are
accompanied by simultaneous ECG analysis, BP measurements,
and subjective reports, commonly using Borg’s Rating of Per-
ceived Exertion (RPE).43,44 Occasionally, the use of expired gas
analysis can provide useful information about pulmonary func-
tion and maximal oxygen consumption.40 Submaximal tests,
such as the 12- and 6-minute walk tests, can be performed to
assess a patient’s function. For further discussion of the 6-min-
ute walk test, refer to Chapter 23.
Submaximal tests differ from maximal tests in that 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 maximum HR.45 For a comparison of
two widely used exercise test protocols and functional activi-
submaximal exercise testing, the reader is referred to the report
of Noonan and Dean.45
Contraindications to exercise testing include the following46:
• Recent MI (<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 exer-
cise prescription. On the basis of 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 also can 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 used to estimate metabolic equivalents of task
(METs) and oxygen consumption with the following equations:
32 CHAPTER 3     Cardiac System

TABLE 3.10  Comparison of Exercise Test Protocols and Functional Tasks—Energy Demands
Metabolic Treadmill: Bruce Bike Ergometer: for
Oxygen Requirements Equivalents Protocol 3-Minute 70 kg of Body Weight
(mL O2/kg/min) (METS) Functional Tasks Stages (mph/elevation) (kg/min)
52.5 15
49.5 14
45.5 13 4.2/16.0 1500
42.0 12 1350
38.5 11 1200
35.0 10 Jogging 3.4/14.0 1050
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. Exercise Testing and Training of Apparently Healthy Individuals: A Handbook for Physicians. Dallas: AHA;
1972; Brooks GA, Fahey TD, White TP, eds. Exercise Physiology: Human Bioenergetics and Its Applications. 2nd ed. Mountain View, CA: Mayfield Publishing; 1996.

V̇O2 mL /kg /min = (mph)(26.83 m / min)(0.1 mL / kg /min) 6.00

+ 3.5 mL/ kg /min
METs = V̇O2 mL/kg /min ÷ 3.5 5.00
Bruce Protocol - Stage 1
MPH = (pace [feet / min] × 60) ÷ 5280(feet /mile) Stair climbing

4.00 Raking lawn/gardening

A direct relationship exists between pace on a level surface
METs

Household tasks
and METs (oxygen consumption). A therapist can use walking 3.00

pace to estimate oxygen consumption and endurance for other Standing - light activity
2.00
functional tasks that fall within a patient’s oxygen consumption Sitting - light activity
(aerobic functional capacity). It is important to note METs can
1.00
only be calculated for individuals without biomechanical insuf-
METs = 0.0087 (feet/minute) + 1
ficiencies that may alter amount of energy needed, especially in 0.00
older adults.47 0 100 200 300 400 500 600
Feet per minute
Fig. 3.9 depicts the relationship between pace (feet/min)
and METs for level surface ambulation. Bruce Protocol Stage FIG. 3.9
1 (because of its incline when at 1.7 miles per hour [mph]) is Relationship between walking pace, metabolic equivalents of task (METs),
and oxygen consumption on level surfaces. (Data from Fletcher GF, Balady
similar to ambulation at 400 feet/min on a level surface. If a
GJ, Amsterdam EA, et al. Exercise standards for testing and training: a
patient cannot sustain a particular pace for at least 10 min- statement for healthcare professionals from the American Heart Associa-
utes, it can be concluded that this pace exceeds the patient’s tion. Circulation. 2001;104:1694-1740.)
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 CLINICAL TIP
pace below anaerobic threshold. For interval aerobic train- Synonyms for aerobic exercise tests include exercise tolerance
ing, work periods at walking paces that can be sustained for test (ETT) and graded exercise test (GXT).
1 to 10 minutes would be appropriate with an equal period
of rest. If a patient is required routinely to exceed maximal
oxygen consumption during daily tasks, he or she is much Thallium Stress Testing.  Thallium stress testing is a stress
more likely to experience signs of fatigue and exhaustion test that involves the injection of a radioactive nuclear marker
over time, such as during repeated bouts of activity through- for the detection of myocardial perfusion. The injection is given
out the day. typically (via an intravenous 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 evaluated for
myocardial perfusion by assessment of the distribution of thal-
lium uptake. The subject then returns 3 to 4 hours later to be
reevaluated for myocardial reperfusion. This test appears to be
more sensitive than stress tests without thallium for identifying
patients with coronary artery disease.14 
Persantine Thallium Stress Testing.  Persantine thallium
stress testing is the use of dipyridamole (Persantine) to dilate
the coronary arteries. Coronary arteries with atherosclerosis do
not dilate; therefore dipyridamole shunts blood away from these
areas. It is used typically in patients who are very unstable,
deconditioned, or unable to ambulate or cycle for exercise-based
stress testing.40 Patients are asked to avoid all food and drugs
containing methylxanthines (e.g., coffee, tea, chocolate, cola
drinks) for at least 6 hours before the test in addition to phos-
phodiesterase 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 (using
a large-vein intracatheter). Four minutes after the infusion is
completed, the perfusion marker (thallium) is injected, and the
patient is passed under a nuclear scanner to be evaluated for
myocardial perfusion by assessment of the distribution of thal-
lium uptake.40  • Some hospitals may use a knee immobilizer to assist with
Cardiac Catheterization
Cardiac catheterization, classified as either right or left, is an
invasive procedure that involves passing a flexible, radiopaque
catheter into the heart to visualize chambers, valves, coronary
arteries, great vessels, cardiac pressures, and volumes to evaluate
cardiac function (estimate EF, CO).
The procedure also is used in the following diagnostic and
therapeutic techniques14:
• Angiography
• Percutaneous coronary intervention (PCI)
• Electrophysiologic studies (EPSs)
• Cardiac muscle biopsy
Right-sided catheterization involves entry through a sheath
that is inserted into a vein (commonly subclavian) for evalua-
tion of right heart pressures; calculation of CO; and angiography
of the right atrium, right ventricle, tricuspid valve, pulmonic
valve, and pulmonary artery.14 It also is used for continuous
hemodynamic monitoring in patients with present or very
recent heart failure to monitor cardiac pressures (see Chapter
18). Indications for right heart catheterization include an intra-
cardiac shunt (blood flow between right and left atria or right
and left ventricles), myocardial dysfunction, pericardial con-
striction, pulmonary vascular disease, valvular heart disease, and
status post heart transplantation.
Left-sided catheterization involves entry through a sheath
inserted into an artery (commonly femoral) to evaluate the aorta,
left atrium, and left ventricle; left ventricular function; mitral
and aortic valve function; and angiography of coronary arteries.
Indications for left heart catheterization include aortic dissec-
tion, atypical angina, cardiomyopathy, congenital heart disease,
coronary artery disease, status post MI, valvular heart disease,
and status post heart transplant.  tals, these studies may be combined with a therapeutic procedure,
Cardiac System     CHAPTER 3 33
TABLE 3.11  Assessment Methods
Method Region Examined
Aortography Aorta and aortic valve
Coronary arteriography Coronary arteries
Pulmonary angiography Pulmonary circulation
Ventriculography Right or left ventricle and AV
valves
AV, Atrioventricular.
Data from Woods SL, Sivarajian Froelicher ES, Underhill-Motzer S, ed. Cardiac
Nursing. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2009.
Physical Therapy Considerations
• A fter catheterization, the patient is on bed rest for approxi-
mately 4 to 6 hours when venous access is performed, or for
6 to 8 hours when arterial access is performed.14
• The sheaths typically are removed from the vessel 4 to 6
hours after the procedure, and pressure is applied constantly
for 20 minutes after sheath removal.14
• The extremity should remain immobile with a sandbag over
the access site to provide constant pressure to reduce the risk
of vascular complications.14
immobilizing the lower extremity.
• Physical therapy intervention should be deferred or limited
to bedside treatment within the parameters of these precau-
tions.
• During the precautionary period, physical therapy inter-
vention, such as bronchopulmonary hygiene, or education
may be necessary. Bronchopulmonary hygiene is indicated if
pulmonary complications or risk of these complications ex-
ists. Education is warranted when the patient is anxious and
needs to have questions answered regarding his or her func-
tional mobility.
• After the precautionary period, normal mobility can progress
to the limit of the patient’s cardiopulmonary impairments;
however, the catheterization results should be incorporated
into the physical therapy treatment plan. 
Angiography
Angiography involves the injection of radiopaque contrast
material through a catheter to visualize vessels or cham-
bers. Different techniques are used for different assessments
(Table 3.11). 
Electrophysiologic Studies
EPSs are performed to evaluate the electrical conduction system of
the heart.14 An electrode catheter is inserted through the femoral
vein into the right ventricle apex. Continuous ECG monitoring
is performed internally and externally. The electrode can deliver
programmed electrical stimulation to evaluate conduction path-
ways, formation of arrhythmias, and the automaticity and refrac-
toriness of cardiac muscle cells. EPSs evaluate the effectiveness of
antiarrhythmic medication and can provide specific information
about each segment of the conduction system.14 In many hospi-
34 CHAPTER 3     Cardiac System
such as an ablation procedure (discussed in the Management sec-
tion). Indications for EPSs include the following14:
• Sinus node disorders
• AV or intraventricular block
• Previous cardiac arrest
• Tachycardia at greater than 200 bpm
• Unexplained syncope
CLINICAL TIP
Patients undergoing electrophysiologic studies (EPSs) typically
remain on bed rest for 4 to 6 hours after the test.
 
  
Health Conditions
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 perfusion is reduced, a vicious
cycle resulting in heart failure 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 (ACS), (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, sub-
cutaneous tissues, and serous cavities.5
Hypertension
Hypertension (HTN) is the most prevalent cardiovascular dis-
ease in the United States. The National Health and Nutrition
Examination Survey (NHAHES) conducted from 2005 to 2008
estimated that approximately 76 million Americans above age
20 years have HTN.48
In 2017 the ACC and the AHA published revised guide-
lines on the stages of HTN and the appropriate threshold values
to initiate antihypertensive drug treatment (see Table 3.6).49
Notably, hypertension is a predominant risk factor for several
additional cardiovascular diseases and often goes undetected for
decades.49 An important consideration for all health care profes-
sionals, including physical therapists, is the association between
undetected hypertension and risk, particular in ambulatory
(outpatient) and primary care settings.49 
Acute Coronary Syndrome
When myocardial oxygen demand is higher than supply, the
myocardium must use anaerobic metabolism to meet energy
demands. This system can be maintained for only a short period
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 circula-
tion; however, it is compromised in individuals with impaired
coronary blood flow. The following pathologies can result in
myocardial ischemia:
• C oronary 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 an-
gina).14
• Coronary atherosclerotic disease (CAD) is a multistep process
of the deposition of fatty streaks, or plaques, on artery walls
(atherosis). The presence of these deposits eventually leads to
arterial wall damage and platelet and macrophage aggrega-
tion, which then leads to thrombus formation and hardening
of the arterial walls (sclerosis). The net effect is a narrowing
of coronary walls. It can result in stable angina, unstable an-
gina, or MI.4,6,14
Clinical syndromes caused by these pathologies are as follows8,14:
• Stable (exertional) angina occurs with increased myocardial
demand, such as during exercise; is relieved by reducing ex-
ercise intensity or terminating exercise; and responds well to
nitroglycerin.
• Variant angina (Prinzmetal 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.
• Unstable angina is considered intermediate in severity be-
tween stable angina and MI. It usually has a sudden onset,
occurs at rest or with activity below the patient’s usual isch-
emic baseline and may be different from the patient’s usual
anginal pattern. Unstable angina 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 unstable angina is believed
to be a rupture of an atherosclerotic plaque.
• MI occurs with prolonged or unmanaged ischemia (Table
3.12). It is important to realize that an evolution occurs from
ischemia to infarction. Ischemia is the first phase of tissue re-
sponse when the myocardium is deprived of oxygen. It is re-
versible if sufficient oxygen is provided in time. However, if
oxygen deprivation continues, myocardial cells will become
injured and eventually will die (infarct). The location and
extent of cell death are determined by the coronary artery
that is compromised and the amount of time that the cells
are deprived. A clinical overview is provided in Fig. 3.10.
CLINICAL TIP
ST depression on a patient’s ECG of approximately 1 to 2 mm
generally is indicative of ischemia; ST elevation generally is
indicative of myocardial injury or infarction.
 
Rhythm and Conduction Disturbance
Rhythm and conduction disturbances can range from minor
alterations with no hemodynamic effects to life-threatening epi-
sodes with rapid hemodynamic compromise.4,6,8 Refer to the
tables in Appendix 3A for a description of atrial, ventricular, and
junctional rhythms and AV blocks. Refer to Appendix 3B for
examples of common rhythm disturbances. Physical therapists
must be able to identify abnormalities on ECG to determine
 Cardiac System     CHAPTER 3 35

TABLE 3.12  Myocardial Infarctions

Possible Occluded
MI/Wall Affected Coronary Artery Possible Complications
Anterior MI/anterior left ventricle LCA Left-sided CHF, pulmonary edema, bundle branch block,
AV block, and ventricular aneurysm (which can lead to CHF,
dysrhythmias, and embolism)
Inferior MI/inferior left ventricle RCA AV blocks (which can result in bradycardia) and papillary muscle
dysfunction (which can result in valvular insufficiency and
eventually CHF)
Anterolateral MI/anterolateral left ventricle LAD, circumflex Brady or tachyarrhythmias, acute ventricular septal defect
Anteroseptal MI/septal region—between LAD Brady or tachyarrhythmias, ventricular aneurysm
left and right ventricles
Posterior MI/posterior heart RCA, circumflex Bradycardia, heart blocks
Right ventricular MI RCA Right ventricular failure (can lead to left ventricular failure
and therefore cardiogenic shock), heart blocks, hepatomegaly,
peripheral edema
Transmural MI (Q-wave MI) Any artery Full wall thickness MI, as above
Subendocardial MI (non–Q-wave MI) Any artery Partial wall thickness MI, as above, potential to extend to
transmural MI

AV, Atrioventricular; CHF, congestive heart failure; LAD, left anterior descending; LCA, left coronary artery; MI, myocardial infarction; RCA, right coronary artery.
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S, eds. Cardiac Nursing. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2000.

Ischemic chest pain

Patients with ST elevation are 90%

likely to rule in with a Q-wave MI.
No ST elevation ST elevation They are also considered for
thrombolytic therapy or
revascularization procedures while
in the ER.
Rule in vs. rule
out MI
determined by Unstable angina Non–Q-wave MI Q-wave MI
biochemical (rule out MI) (rule in MI) (rule in MI)
markers

If patient has: If patient has no If patient has:

If patient has: ♦ Pulmonary edema complications and: ♦ Recurrent ischemia
♦ Normal ECG ♦ PAP >20 mmHg ♦ No h/o MI ♦ CHF
♦ No rest ♦ S3 gallop ♦ No ischemic pain ♦ Hypotension
angina ♦ Hypotension ♦ Stable rhythm ♦ Arrhythmias
♦ No nocturnal ♦ Dynamic ST changes ♦ No CHF ♦ Heart block
angina ♦ Ischemia ♦ No heart block May be considered:
♦ Prior MI ♦ Hemodynamically High risk/complicated/unstable
May be considered: stable
Low risk/stable May be considered: May be considered:
High risk—further medical Low risk/stable
work-up

Medical/surgical treatment
will depend on complication.
Revascularization No revascularization: Contraindicated Out of CCU 24-36 Diagnostics will likely
May undergo or patient refuses hours after admission. include a catheterization.
noninvasive If stays stable and Treatment may include some
stress test or asymptomatic MD may form of revascularization.
coronary consider d/c 24-48 Length of stay is variable.
arteriography; PTCA: CABG: hours later for
usually Uncomplicated Uncomplicated Prolonged outpatient management
discharged in 1-2 d/c day after d/c 4-7 days hospitalization
days procedure to decrease risk
and stabilize
for activity

FIG. 3.10
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 ST segment. (Data from American College of Cardiology/American Heart Associa-
tion. 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 [USA] and non-ST segment elevation myocardial infarction. J Am Coll Cardiol. 2000;36:971-1048.)
36 CHAPTER 3     Cardiac System

TABLE 3.13  Signs and Symptoms of Valvular Heart Disease

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 stroke
regurgitation failure, pulmonary edema, angina volume, loud S3, diastolic murmur, signs of ventricular
failure
Mitral stenosis Symptoms of pulmonary vascular congestion Left atrial hypertrophy, pulmonary hypertension, atrial
(dyspnea, orthopnea). If patient develops pulmonary fibrillation, can have embolus formation (especially
hypertension (which can cause hypoxia, hypotension), if in atrial fibrillation), long diastolic murmur
he or she may have angina, syncope
Chronic mitral Symptoms of pulmonary vascular congestion, angina, Left atrial enlargement, atrial fibrillation, elevated
regurgitation syncope, fatigue left atrial pressure
Acute mitral Rapid progression of symptoms of pulmonary vascular Sinus tachycardia, presence of S3 or S4, pulmonary
regurgitation congestion edema
Mitral valve prolapse Most commonly asymptomatic, fatigue, palpitation Systolic click, may have tachyarrhythmia syncope

Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S, eds. Cardiac Nursing. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2000; Cheitlin MD,
Sokolow M, McIlroy MB. Clinical Cardiology. 6th ed. Norwalk, CT: Appleton & Lange; 1993.

patient tolerance to activity. In particular, physical therapists
should understand progressions of common ECG abnormalities
so that they can identify, early on, when the patient is not toler-
ating an intervention. (Refer to the Physical Therapy Interven-
tion 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 abnor-
malities originate from depolarization of a cluster of cells in the
ventricle (an ectopic foci), which results in ventricular depolar-
ization. From the term ectopic foci, PVCs may be referred to as
ventricular ectopy.  • Right-sided failure—refers to failure of the right side of the
Valvular Heart Disease
Valvular heart disease encompasses valvular disorders of one or
more of the four valves of the heart (Table 3.13). The following
three disorders can occur4,6:
1. Stenosis, which involves narrowing of the valve
2. Regurgitation, the back flow of blood through the valve,
which occurs with incomplete valve closure
3. Prolapse, which involves enlarged valve cusps (The cusps
can become floppy and bulge backward. This condition may
progress to regurgitation.)
Over time, these disorders can lead to pumping dysfunction
and, ultimately, heart failure.  • Diastolic dysfunction—refers to a problem during diastole or
Myocardial and Pericardial Heart Disease
Myocardial heart disease affects the myocardial muscle tissue
and also is referred to as cardiomyopathy (Table 3.14); pericardial
heart diseases affect the pericardium (Table 3.15).  3.3. The AHA/ACC and the NYHA have created two classi-
Heart Failure
The syndrome of HF, evidenced by a decrease of CO, can be
caused by a variety of cardiac pathologies. Because CO is not
maintained, life cannot be sustained if HF continues without
treatment. HF results in the congestion of the pulmonary cir-
culation and, in certain cases, even the systemic circulation. In
light of this, clinically, therapists may see the abbreviation CHF
emphasizing the congestion within the heart failure syndrome.
The most common pathologic etiology of HF is some type of
cardiomyopathy (see Table 3.14).
The following terms are used to classify the types of cardiac
impairment in HF50:
• Left-sided heart failure—refers to failure of the left ventricle,
resulting in back flow into the lungs.
heart, resulting in back flow into the systemic venous sys-
tem.
• High-output failure—refers to heart failure that is secondary
to renal system failure to filter off excess fluid. The renal sys-
tem failure places a higher load on the heart, which 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 and is commonly
referred to as heart failure with reduced ejection fraction (HFrEF).
the ability of the ventricle to allow the filling of blood, and is
commonly referred to as Heart Failure with Preserved Ejec-
tion Fraction (HFpEF).
Possible signs and symptoms of HF are described in Box
fications of HF.1,51 From a structural perspective, HF is staged
on the basis of the extent of structural damage to heart tissue.
From a functional perspective, HF is classified on the basis of
the NYHA functional classification.52 The two classification
systems are combined in Table 3.16.
 Cardiac System     CHAPTER 3 37

TABLE 3.14  Myocardial Diseases—Cardiomyopathies

Functional Classification
Cardiomyopathy Dysfunction Description
Dilated Systolic Ventricle is dilated, with marked contractile dysfunction of myocardium
Hypertrophic Diastolic Thickened ventricular myocardium, less compliant to filling, and therefore
decreased filling during diastole
Restrictive Systolic and diastolic Endocardial scarring of ventricles, decreased compliance during diastole, and
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: Hillegass EA, Sadowsky HS, eds. Essentials of Cardiopulmonary Physical Therapy. 2nd ed. Philadelphia: Saunders;
2001; Hare JM. The dilated, restrictive, and infiltrative cardiomyopathies. In Libby P, Bonow RO, Mann DL, et al. Braunwald’s Heart Disease: A Textbook of Cardiovas-
cular Medicine. 8th ed. Philadelphia: Saunders; 2008.

TABLE 3.15  Signs and Symptoms of Pericardial Heart Diseases

Disease Symptoms Signs
Acute pericarditis Retrosternal chest pain (worsened by supine and/or Pericardial friction rub; diffuse ST segment elevation;
deep inspiration), dyspnea, cough, hoarseness, dysphagia, decreased QRS voltage in all ECG leads if pericardial
fever, chills, and weakness possible effusion also present
Constrictive Abdominal swelling, peripheral edema, fatigue, dyspnea, Jugular venous distention; QRS voltage diminished on
pericarditis dizziness and/or syncope, signs of pulmonary venous ECG; occasionally atrial fibrillation
congestion, vague nonspecific retrosternal chest pain
Chronic pericardial May have vague fullness in anterior chest, cough, Muffled heart sounds; may have pericardial friction rub;
effusion (without hoarseness, dysphagia QRS voltage diminished on ECG; chest x-ray with
tamponade) cardiomegaly without pulmonary congestion
Pericardial Symptoms of low cardiac output (dyspnea, fatigue, Jugular venous distention, cardiomegaly, diminished QRS
tamponade dizziness, syncope); may have retrosternal chest pain; voltage on ECG; becomes tamponade from effusion
may have cough, hiccoughs, hoarseness 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

ECG, Electrocardiography.
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S, eds. Cardiac Nursing. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2000; Cheitlin MD,
Sokolow M, McIlroy MB. Clinical Cardiology. 6th ed. Norwalk, CT: Appleton & Lange; 1993.

Activity progression for patients hospitalized with HF is
based on the ability of medical treatments (e.g., diuresis, ino-
tropes) to keep the patient out of heart failure. When a patient
with HF is medically stabilized, the heart is thought to be
“compensated.” Conversely, when the patient is unable to main-
tain adequate circulation, the heart would be “decompensated.”
Clinical examination findings allow the therapist to evaluate
continuously the patient’s tolerance to the activity progression.
Although MET tables are not commonly used clinically, they do
provide a method of progressively increasing a patient’s activ-
ity level. As greater MET levels are achieved with an appro-
priate hemodynamic response, the next level of activity can be
attempted. See Table 3.10 for MET levels for common activities
that patients can perform. 
38 CHAPTER 3     Cardiac System
  

high prevalence of coronary artery thrombosis during acute

Management MI. Thrombolytic agents, characterized as fibrin-selective and
nonselective agents, are administered to appropriate candidates
This section discusses surgical and nonsurgical procedures, via intravenous access. The most common agents include strep-
pharmacologic interventions, and physical therapy interven- tokinase (nonselective), anisoylated plasminogen streptokinase
tions for patients with cardiac health conditions activator complex (nonselective), and t-PA (fibrin-selective).14
Fibrin-selective agents have a high velocity of clot lysis, whereas
the nonselective agents have a slower clot lysis and more pro-
Revascularization and Reperfusion of the Myocardium
longed systemic lytic state.
Thrombolytic Therapy The indication for thrombolytic therapy includes chest pain
Thrombolytic therapy has been established as an acute man- suggestive of myocardial ischemia and associated with acute ST
agement strategy for patients experiencing MI because of the segment elevation on a 12-lead ECG or a presumed new left
ventricular bundle branch block. Hospital protocol regarding
the timing of thrombolytic therapy usually varies because clini-
BOX 3.3  Signs and Symptoms of Heart Failure cal trials have led to some controversy.14 Some studies show ben-
Signs Symptoms efits only if treatment is conducted within 6 hours of symptoms,
whereas others have demonstrated improvement with treatment
Cold, pale, possibly cyanotic Dyspnea
extremities Tachypnea up to 24 hours after onset of symptoms.14
Weight gain Paroxysmal nocturnal dyspnea The contraindications to thrombolytic therapy generally
Peripheral edema Orthopnea include patients who are at risk for excessive bleeding. Because
Jugular venous distention Cough of the variability that can occur among patients, many contra-
Tachypnea Fatigue
indications are considered relative cautions, and the potential
Crackles (rales)
Tubular breath sounds benefits of therapy are weighed against the potential risks.
S3 and S4 heart sounds Thrombolytic therapy is used in conjunction with other medi-
Sinus tachycardia cal treatments, such as with aspirin, intravenous heparin, intra-
Pulsus Alterans venous nitroglycerin, lidocaine, atropine, and a beta-blocker. As
Decreased exercise tolerance
previously discussed, early peaking of CK-MB is associated with
and physical
work capacity reperfusion.14 

Data from Hillegass E, Lowers ST, Barker E. Cardiac muscle dysfunction and Percutaneous Revascularization Procedures
failure. In: Hillegass EA. Essentials of Cardiopulmonary Physical Therapy. 4th ed.
St. Louis: Elsevier; 2017. Percutaneous revascularization procedures are used to return
blood flow through coronary arteries that have become occlusive

TABLE 3.16  AHA/ACC Stages and NYHA Functional Classes of Heart Failure
AHA/ACC NYHA
Stage Description Classa Description
Stage A At high risk for developing HF. No identified NA
structural or functional abnormality, no signs or
symptoms of HFb
Stage B Structural heart disease that is strongly I No limitation in physical activity; ordinary physical
associated with the development of HF activity does not cause fatigue, palpitations, or dys-
but no signs and symptoms of HF pnea
Stage C Symptomatic HF, associated with I No limitation in physical activity; ordinary physical
underlying structural heart disease activity does not cause fatigue, palpitations, or dyspnea
II Slight limitation of physical activity; comfortable at rest
but ordinary activity results in fatigue, palpitations,
or dyspnea
III Marked limitation of physical activity; comfortable at
rest, but less than ordinary activity results in fatigue,
palpitations, or dyspnea
IV Symptoms at rest; unable to do any physical activity
without symptomology
Stage D Advanced structural disease with marked sympto- IV Symptoms at rest; unable to do any physical activity
mology at rest despite maximal medical therapy without symptomology
aFunctional capacity refers to subjective symptoms of the patient. This aspect of the classification is identical to the New York Heart Association’s Classification.
bObjective structural assessment was added to the classification system by the American Heart Association in 1994. It refers to measurements such as electrocardio-
grams, stress tests, echocardiograms, and radiologic images.46
Data from Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA guideline for the management of heart failure: a
report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. J Card
Fail. 2017;23(8):628-651.

secondary to atherosclerotic plaques. The following list briefly
describes three percutaneous revascularization procedures14:
1. PCI is performed on atherosclerotic lesions that do not com-
pletely occlude the vessel. PCI can be performed at the time
of an initial diagnostic catheterization, electively at some
time after a catheterization, or urgently in the setting of an
acute MI. Refer to the Diagnostic and Laboratory Measures
section for a discussion on precautions after a catheterization
procedure.
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% diameter with a residual narrowing of less than 50%
in the vessel lumen.12 Because of some mild ischemia that
can occur during the procedure, patients occasionally require
temporary transvenous pacing, intraaortic balloon counter-
pulsation, or femorofemoral cardiopulmonary bypass circula-
tory support during PCI.
The use of endoluminal stents prevents the major limita-
tions of PCI, which include abrupt closure (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.45 Endo-
luminal stents are tiny springlike tubes that can be placed
permanently into the coronary artery to increase the intralu-
minal diameter. Stents are occasionally necessary when initial
attempts at revascularization (e.g., angioplasty) have failed.12
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 because of the expense of the equipment and a high
restenosis rate (greater than 40%).46
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 then can cut the atheroma and remove it from
the arterial wall. This also can 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 because of its in-
elastic properties as opposed to the elastic normal tissue.12
The debris emitted from this procedure is passed into the
coronary circulation and is small enough to pass through the
capillary beds. Commonly, PCI is used as an adjunct to this
procedure to increase final coronary diameter or to allow for
stent placement.  nary arteries, surgeons may opt to perform a hybrid procedure
Transmyocardial Revascularization
In transmyocardial revascularization, a catheter with a laser tip cre-
ates transmural channels from patent coronary arteries into an area
of the myocardium thought to be ischemic.53,54 It is intended for
patients with chronic angina who, because of medical reasons, can-
not have angioplasty or CABG. Ischemia is reduced by increasing
the amount of oxygenated blood in ischemic tissue. Angiogenesis
Cardiac System     CHAPTER 3 39
(the growth of new blood vessels) also has been proposed as a mech-
anism 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 does not change.55 Postcatheterization procedure pre-
cautions, as previously described, apply after this procedure. 
Coronary Artery Bypass Graft
CABG is performed when the coronary artery has become com-
pletely occluded or when it cannot be corrected by PCI, coronary
arthrectomy, or stenting. In this procedure a vascular graft is used
to revascularize the myocardium. The saphenous vein, radial artery,
left internal mammary artery (LIMA), or right internal mammary
artery (RIMA) commonly is used as a vascular graft. CABG most
commonly is performed through a median sternotomy, which
extends caudally from just inferior to the suprasternal notch to
below the xiphoid process and splits the sternum longitudinally.14
CLINICAL TIP
Because of the altered chest wall mechanics and the pain associ-
ated with a sternotomy, patients are at risk of developing pulmo-
nary complications after a coronary artery bypass graft (CABG).
The physical therapist should be aware of postoperative compli-
cation risk factors and postoperative indicators of poor pulmo-
nary function. Refer to Chapters 4 and 20 for further description
of postoperative pulmonary complications.
Minimally Invasive Coronary Artery Bypass Graft Sur-
gery.  Advances in medicine have led to a set of minimally
invasive cardiac surgical techniques using laparoscopic proce-
dures and robotics to enter the thoracic cavity through small
incisions in the chest in an effort to avoid a median sternotomy.
These procedures aim to reduce complications associated with
large surgical incisions and extensive periods on the cardiopul-
monary bypass pump. Endoscopic robotic surgery involves the
use of a computer-enhanced telemanipulation system to perform
the grafting procedure.56 The harvesting of the saphenous vein
also can be achieved through minimal incision by using video-
based surgical techniques.57 This minimally invasive procedure
decreases morbidity associated with large leg incisions (pain and
infection) in an effort to facilitate quicker recovery.57
Minimally invasive CABG techniques use a small thoracot-
omy incision as an alternate to median sternotomy.58 Through the
incision, the mammary arteries can be harvested and anastomosed
thorascopically or with robotic assistance. These minimally inva-
sive procedures performed through a small anterior thoracotomy
are found to be best suited for occlusions within the anterior
coronary vessels.58 For multiple blocks located in multiple coro-
involving the use of the minimally invasive CABG procedure
coupled with a percutaneous transluminal coronary intervention
procedure. The CABG procedure is used for restoring perfusion to
the anterior vessel, specifically the left anterior descending artery,
while the percutaneous procedure employs drug-eluting stents to
the right coronary artery and circumflex artery.59 
Off-Pump Coronary Artery Bypass Graft Procedure.  The
off-pump CABG procedure uses a standard median sternotomy
40 CHAPTER 3     Cardiac System
and grafting of the coronary arteries under conditions of a beat-
ing, normothermic heart.58 Regional ischemia is induced for 5-
to 15-minute periods, during which each anastomosis must be
constructed. The major advantage of the off-pump procedures is
to reduce the complications associated with artificial perfusion
induced by the cardiopulmonary bypass pump. Off-pump proce-
dures reduce markers of inflammatory response and intraopera-
tive troponin T release, thereby suggesting less myocyte injury.60 
Median Sternotomy and Sternal Precautions.  The primary
premise for the use of sternal precautions is to reduce the possi-
bility of sternal dehiscence. Interestingly, no direct evidence links
the use of arm movements or activity to an increased risk of ster-
nal complications after cardiothoracic surgery.61 El-Ansary et  al.
found that patients with chronic sternal instability demonstrated
the greatest sternal separation when pushing up from a chair with
sit-to-stand transfers and least sternal separation when elevating
both arms overhead.62 In normal healthy individuals, the great-
est amount of sternal skin movement was seen with sit-to-stand
and supine-to-long-sitting transfers, and the least movement was
noted when raising a unilateral weighted upper extremity (<8 lb)
above shoulder height.4,63 Patients with chronic sternal instability
tend to experience greater pain when raising a unilateral loaded
upper extremity compared with raising bilateral loaded upper
extremities.62
When prescribing sternal precautions for individuals after
median sternotomy, the many risk factors that increase the poten-
tial for sternal dehiscence must be considered. Some of these risks
include obesity, chronic obstructive pulmonary disease (COPD),
diabetes, repeat thoracotomy, smoking, peripheral vascular dis-
ease, female sex, and pendulous breasts. As the number of risk
factors increase, the therapist must be more vigilant regarding
sternal precautions. Sternal precautions usually are prescribed for
at least 8 weeks to prevent wound dehiscence and preserve the
integrity of sternal wiring. In managing the bariatric patient,
physical therapists should evaluate the operative report as often
the sternum is doubled wired during the surgical procedure to
prevent dehiscence. In general, sternal precautions include restric-
tions for upper extremity lifting greater than 10 lb, pushing or
pulling, scapular adduction, resistive exercises or loading of the
upper extremity past 90 degrees of flexion and abduction, and
minimal use of the arms for supine-to-sit and sit-to-stand trans-
fers.64 As evidence and guidelines continue to develop regarding
sternal precautions, consultation with the medical team for any
necessary clarification or modifications is essential for patient
safety
CLINICAL TIP
• To help patients understand the concept of lifting less than 10 lb,
inform them that a gallon of milk weighs approximately 8 lb.
• Additionally, when considering the use of an assistive device,
such as a rolling walker for balance, the amount of weight
bearing through the arms should be minimized.
• Before using an assistive device, consideration of the risk fac-
tors for sternal dehiscence, along with consultation from the
medical team is necessary to maximize safety.
 
Secondary Prevention After Revascularization
Improved medical and surgical interventions have reduced mor-
tality resulting from cardiovascular disease; however, incidence
and prevalence are still high.2 After revascularization procedures,
patients need education regarding cardiovascular disease risk fac-
tors. This ensures continued success of the procedures via second-
ary prevention of primary disease processes (refer to Box 3.1). 
Ablation Procedure
Catheter ablation procedures are indicated for supraventricular
tachycardia, AV nodal reentrant pathways, atrial fibrillation,
atrial flutter, and certain types of ventricular tachycardia.14
The procedure attempts to remove or isolate ectopic foci in an
attempt to reduce the resultant rhythm disturbance. Radio-
frequency ablation uses low-power, high-frequency alternat-
ing current to destroy cardiac tissue and is the most effective
technique for ablation.14 After the ectopic foci are located under
fluoroscopic guidance, the ablating catheter is positioned at the
site to deliver a current for 10 to 60 seconds.
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 to
recover after the procedure. Most of the postintervention care is
geared toward monitoring for complications. Possible complica-
tions include bleeding from the access site, cardiac tamponade
from perforation, and arrhythmias. After a successful procedure
(and the initial immobility to prevent vascular complications at
the access site), usually activity is not restricted.
Maze Procedure
Surgical ablation of atrial fibrillation is accomplished by the
maze procedure. This procedure was developed in 1990 and
aims to surgically create a “maze” along the atria to best direct
the electrical conduction appropriately to the AV node and the
ventricles.65 The procedure was so named for the appearance of
the surgical incisions, which often resembles a children’s maze.
The maze procedure is performed typically in conjunction with
CABG or valve replacement surgery.
The maze procedure has evolved over time. It is currently
the standard for nonpharmacologic treatment of atrial fibril-
lation.66,67 The initial surgery (maze I, or Cox maze) involves
several small incisions around the SA node, the atrial–superior
vena cava junction, and the sinus tachycardia region of the SA
node.68 The major complication of this procedure is chrono-
tropic incompetence.69 The procedure has been refined with the
creation of the maze II procedure and, most recently, the maze
III procedure. Maze III reduces the frequency of chronotropic
incompetence, improves atrial transport function, and involves
a shorter procedure time.70 It is important to note that atrial
fibrillation may not be reversed immediately after the proce-
dure; it may take months for the arrhythmia to be reversed. 
 Cardiac System     CHAPTER 3 41

various exercise modalities. For more detail, refer to the article

Cardioversion
Cardioversion is a procedure aimed to restore a normal heart
rhythm in people with tachycardic arrhythmias.71 Cardiover-
sion may be performed in two major ways. Electric shocks
are transmitted to the heart through electrodes placed on the
chest while the patient is sedated.71 A second method to car-
diovert the heart is to use medications. Clinically cardioversion
is associated with two major risks, including dislodgement of a
thrombus in a patient with atrial fibrillation and potential skin
burs.71 In patients undergoing elective cardioversion, physicians
will ensure that the patient is effectively anticoagulated before
the cardioversion procedure.
Cardiac Pacemaker Implantation and Automatic Implantable
Cardiac Defibrillator
Cardiac pacemaker implantation involves the placement of a
unipolar or bipolar electrode on the myocardium. This electrode
is used to create an action potential in the management of cer-
tain arrhythmias. Indications for cardiac pacemaker implanta-
tion include the following14,72,73:
• Sinus node disorders (bradyarrhythmias [HR lower than
60 bpm])
• Atrioventricular disorders (complete heart block, Mobitz
type II block)
• Tachyarrhythmias (supraventricular tachycardia, frequent ec-
topy)
• Improving atrioventricular and/or biventricular synchrony
Temporary pacing may be performed after an acute MI to
help control transient arrhythmias and after CABG. Table 3.17
presents various classes of pacemakers.
One of the most critical aspects of pacer function for a physi-
cal therapist to understand is rate modulation. Rate modulation
refers to the pacer’s ability to modulate HR based on activity
or physiologic demands. Not all pacers are equipped with rate
modulation; therefore some patients have HRs that may not
change with activity. In pacers with rate modulation, a variety
of sensors are available to allow adjustment of HR. The type
of sensor used may affect the ability of the pacer to respond to
by Collins and Cahalin.73
An automatic implantable cardiac defibrillator (AICD) man-
ages uncontrollable, life-threatening ventricular arrhythmias by
sensing the heart rhythm and defibrillating the myocardium, as
necessary, to return the heart to normal rhythm. Indications for
AICD include ventricular tachycardia and ventricular fibrillation.73 
Physical Therapy Considerations
• If the pacemaker does not have rate modulation, low-level
activity with small increases in metabolic demand is pre-
ferred. An assessment of RPE, BP, and symptoms should be
used to monitor tolerance.
• If the pacemaker does have rate modulation, then consider
the type of rate modulation used.
• With activity sensors, HR may respond sluggishly to activi-
ties that are smooth—such as on the bicycle ergometer.
• For motion sensors, treadmill protocols should include in-
creases in speed and grade because changes in only grade may
not trigger an increase in HR.
• QT sensors and ventilatory-driven sensors may require lon-
ger warm-up periods because of delayed responses to activity.
• Medication changes and electrolyte imbalance may affect re-
sponsiveness of HR with QT interval sensors.
• Know the upper limit of the rate modulation. When HR is
at the upper limit of rate, monitor BP to maintain safe activ-
ity levels.
• In individuals who do not have rate-modulated pacers, BP
response can be used to gauge intensity, as shown in the fol-
lowing equation:
Training SBP = (SBP max − SBP rest)(Intensity usually 60%−80%)
+ SBP rest
For example:
Training SBP = (180 − 120)(0.6 for lower limit to
0.8 for upper limit)+120
Training SBP = 156 -168 mmHg 

TABLE 3.17  Pacemaker Classification

Position One Position Two Position Three Response Position Four Rate Position Five
Chamber(s) Paced Chamber(s) Sensed to a Sensed Event 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 and D = Dual (inhibited and D = Dual (atrium and
ventricles) triggered) 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, Daubert JC, Fletcher RD, et al. The Revised NASPE/BPG (North American Society of Pacing and Electrophysiology/British Pacing and
Electrophysiology Group) Generic Code for antibradycardic, adaptive-rate, and multisite pacing. Pacing Clin Electrophysiol. 25(2):260-264.
42 CHAPTER 3     Cardiac System
Left Atrial Appendage Closure
Patients with atrial fibrillation are at increased risk for embolic
strokes. Left atrial appendage closure (LAAC) is a minimally
invasive procedure, which is used to reduce the risk of stroke. The
procedure works by sealing off the left atrial appendage, thereby
reducing the likelihood of emboli dislodging from the atria.
The left atrial appendage is a small, ear-shaped little pouch
in the muscle wall of the left atrium. Within this little atrial
pouch, blood is able to collect resulting in the formation of
blood clots within the left atrial appendage and the atria.
A minimally invasive procedure can help seal the left atrial
appendage thereby reduce the risk of stroke. The WATCHMAN
device is a parachute-shaped, self-expanding device that closes
the left atrial appendage. The WATCHMAN device was evalu-
ated in two randomized trials (PROTECT AF and PREVAIL) in
patients with nonvalvular atrial fibrillation and eligible for oral
anticoagulation.74,75 The efficacy for implantation of the device
was tested in these two large randomized controlled trials and
is currently approved for use by the US Food and Drug Admin-
istration and the Centers for Medicare and Medicaid Services.
On the basis of the results of these trials, anticoagulation ther-
apy can often be discontinued in patients after this procedure
because the risk of embolic stroke is eliminated.
CLINICAL TIP
The most common complication after this procedure is the pres-
ence of a pericardial effusion caused by intraoperative transsep-
tal puncture. Therefore it is important to ensure hemodynamic
stability before patient mobility and assess for signs and symp-
toms of a pericardial effusion and tamponade (see Table 3.15).  
Life Vest
Life Vest is a personal external defibrillator worn by patients
who are at risk for sudden cardiac arrest. It is an external device
that continuously monitors the patient’s heart rhythm and
delivers a shock in the event of a life-threatening arrhythmia.
The two major components of the life vest include a garment
and a monitor. The garment is worn under clothing and con-
tains electrodes to pick up ECG readings. The monitor can be
worn around the waist like a fanny pack or around the shoulder.
One advantage of this device is that it has the ability to sound
an alarm to notify the patient of a dangerous arrhythmia before
delivering the shock. If the patient is conscious, the patient has
time to respond to the alarms by pressing two buttons to stop the
treatment sequence in the event of a false alarm. If the patient is
unconscious and does not respond, the device warns bystanders that
a shock is to be delivered and then continues with the appropriate
treatment sequence. Both the implantable cardioverter defibrilla-
tor (ICD) and the Life Vest provide continuous protection to the
patient. However, the Life Vest can be used to provide protection
as a bridge to ICD implantation or cardiac transplantation. It also
can be useful in higher-risk patients who are being considered for
ICD implantation but do not meet the criteria for implantation.  expanding valve (Medtronic CoreValve, Minneapolis, MN), usu-
Valve Replacement
Valve replacement is the most common surgical treatment
for valvular disease. Patients with mitral and aortic stenosis,
regurgitation, or both are the primary candidates for this sur-
gery. Like CABG, a median sternotomy is the route of access
to the heart. Common valve replacements include mitral valve
replacements (MVRs) and aortic valve replacements (AVRs).
Prosthetic valves can be classified as mechanical (e.g., bi-leaflet
and tilting disk valves) or biologic valves (i.e., derived from
cadavers or porcine or bovine tissue).
Mechanical valves are preferred if the patient is younger
than 65 years of age and is already on anticoagulation therapy
(commonly because of 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 thrombogenic and therefore require lifelong adherence
to anticoagulation. For this reason, they may be contraindi-
cated in patients who have a history of previous bleeding-
related problems, wish to become pregnant, or have a history
of poor medication compliance. These patients may benefit
from biologic valves because anticoagulation therapy is not
necessary. Biologic valves also may be preferred in patients
older than 65 years of age.14 Postoperative procedures and
recovery from MVR and AVR surgeries are very similar to
those in CABG.14 
Percutaneous Aortic Valvotomy and Transcatheter
Aortic Valve Implantation
For patients with aortic stenosis, the mainstay treatment
involves an AVR executed through a median sternotomy. At
times, this procedure entails substantial risks, especially if the
patient has multiple comorbidities. Recent advances in medi-
cal technology have led to the development of catheter-based
techniques for aortic valve implantation for the management of
patients with symptomatic aortic stenosis.
Percutaneous aortic balloon valvotomy is a procedure in
which a balloon is placed across the stenosed valve and inflated
to relieve the stenosis.76 Stenosis is alleviated by stretching
the annulus and fracturing calcific deposits within the leaflets
of the valve. Despite reduction in transvalvular pressure and
overall reduction in symptoms after this procedure, patients
continue to present with varying degrees of persistent aortic
stenosis.76 The 2017 ACC/AHA guidelines state that this
procedure is not a substitute for valve replacement but may
be used as a bridge to surgery in hemodynamically unstable
patients at high risk for an AVR.77 In addition, the document
demarcates the frequent use of this procedure in children with
valvular aortic stenosis.
Another alternate to invasive open heart surgery involves a
minimally invasive transcatheter aortic valve implantation pro-
cedure.78 This procedure involves a replacement valve being
fed through a small incision in the vascular system and pro-
gressed into the heart or through direct aortic access either via
a mini-sternotomy or right anterior thoracotomy.78 Two stent
valve devices, including a balloon expandable valve (Edwards
SAPIEN, Edwards Lifesciences LLC, Irvine, CA) and a self-
ally are implanted retrograde through an incision in the femoral
artery.79 The Medtronic CoreValve also can be inserted retro-
grade via the subclavian/axillary artery or through direct access
to the heart by means of a mini-sternotomy or thoracotomy.78 
 Cardiac System     CHAPTER 3 43

patients who have cardiac impairment. This section discusses

Cardiac Transplantation basic treatment considerations for physical therapists working
Cardiac transplantation is an acceptable intervention for the with patients who have present or past cardiac impairments.
treatment of end-stage heart disease. A growing number of
facilities are performing heart transplantation, and a greater Goals
number of physical therapists are involved in the rehabilita- The primary goals in treating patients with primary or second-
tion of pretransplantation and posttransplantation recipients. ary cardiac pathology are the following80:
Physical therapy intervention is vital for the success of heart • Assess adequacy of cardiac blood flow and systemic hemody-
transplantation; recipients have often survived a long period of namic response in conjunction with medical or surgical man-
convalescence before and after surgery, rendering them decondi- agement during self-care activities and functional mobility
tioned. In general, heart transplant recipients are immunosup- • Maximize activity tolerance
pressed and are without neurologic input to their heart. These • Provide patient and family education regarding behavior
patients rely first on the Frank-Starling mechanism to augment modification and risk factor reduction (especially in patients
SV and then on the catecholamine response to augment both with CAD, status post MI, PTCA, CABG, or cardiac trans-
HR and SV. Refer to Chapter 14 for information on heart and plantation) 
heart–lung transplantation. 
Concepts for the Management of Patients With Cardiac
Cardiac Medications Dysfunction
Cardiac medications are classified according to functional indi- The patient’s medical or surgical status must be considered
cations, drug classes, and mechanism of action. Cardiac drug in intervention planning because it is inappropriate to treat a
classes occasionally are indicated for more than one clinical diag- hemodynamically unstable patient. A hemodynamically unsta-
nosis. Chapter 19 lists the functional indications, mechanisms ble patient is a patient who clearly requires medical intervention
of action, side effects, and the generic (trade names) of these to stabilize a life-threatening condition. A patient’s status may
cardiac medications: fluctuate on a daily or hourly basis. Box 3.4 provides general
• Table 19.1: Antiarrhythmic agents guidelines regarding when to withhold physical therapy (i.e.,
• Table 19.2: Anticoagulants instances in which further medical care should precede physical
• Table 19.3: Antihypertensives
• Table 19.3a: Combination drugs for hypertension
• Table 19.4: Antiplatelet agents BOX 3.4  Indications of Patient Instability
• Table 19.5: Lipid-lowering agents
• Table 19.6: Positive inotropes (pressors) Absolute Indications That Relative Indications That
• Table 19.7: Thrombolytics (also known as fibrinolytics) Patient Is Unstable and Treat- Patient Is Unstable and Treat-
Table 3.18 summarizes the presentation of digitalis toxicity.  ment Should Be Withheld ment Should Be Modified or
Withheld
Physical Therapy Intervention Decompensated congestive Resting heart rate >100 bpm
In the acute care setting, physical therapy intervention is indi- heart failure Hypertensive resting BP (sys-
Second-degree heart block tolic >160 mmHg, diastolic
cated for patients with cardiac impairments that result from coupled with PVCs of ven- >90 mmHg)
ACS, CHF, or status post invasive procedures, such as CABG. tricular tachycardia at rest Hypotensive resting BP (sys-
However, a great majority of patients who receive physical ther- Third-degree heart block tolic <80 mmHg)
apy present with one or many other cardiac impairments or diag- More than 10 PVCs per min- Myocardial infarction or ex-
noses. Given the prevalence of cardiac disease in the older adult ute at rest tension of infarction within
Multifocal PVCs, unstable the previous 2 days
population and number of hospital admissions for older adults, angina pectoris with recent Ventricular ectopy at rest
there is a high likelihood that physical therapists will manage changes in symptoms (less Atrial fibrillation with rapid
than 24 hours), and elec- ventricular response at rest
trocardiographic changes (HR >100 bpm)
TABLE 3.18  Signs and Symptoms of Digitalis Toxicity associated with ischemia/ Uncontrolled metabolic
injury diseases
System Affected Effects Dissecting aortic aneurysm Psychosis or other unstable
Central nervous Drowsiness, fatigue, confusion, visual New onset (less than 24 hours) psychological condition
system disturbances of atrial fibrillation with
rapid ventricular response at
Cardiac system Premature atrial and/or ventricular con- rest (HR >100 bpm)
tractions, paroxysmal supraventricular Chest pain with new ST seg-
tachycardia, ventricular tachycardia, ment changes on ECG
high degrees of atrioventricular block,
ventricular fibrillation BP, Blood pressure; bpm, beats per minute; ECG, electrocardiogram; HR, heart
Gastrointestinal Nausea, vomiting, diarrhea rate; PVCs, premature ventricular contractions.
Data from Cahalin LP. Heart failure. Phys Ther. 1996;76:520; Ellestad MH.
system
Stress Testing: Principles and Practice. 4th ed. Philadelphia: FA Davis; 1996; We-
gener NK. Rehabilitation of the patient with coronary heart disease. In: Schlant
Data from Woods SL, Sivarajian-Froelicher ES, Underhill-Motzer S, eds. Cardiac
RC, Alexander RW, eds. Hurst’s the Heart. 8th ed. New York: McGraw-Hill;
Nursing. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2000.
1994: 1227.
44 CHAPTER 3     Cardiac System

therapy).81 These are provided as absolute and relative indica-
tions of instability. Relative indications of instability should be
considered on a case-by-case basis. Box 3.5 provides a guide to
the assessment of impairments in body structure and function,
activity limitations, and participation restrictions to consider in
patients with cardiovascular disease.
Once it is determined that a patient is stable at rest, the
physical therapist is able to proceed with activity or an exer-
cise program, or both. Fig. 3.11 provides a general guide to
determining whether a patient’s response to activity is stable
or unstable. Ongoing vital sign monitoring is essential in this
process.

BOX 3.5  Assessment of Impairments in Body Structure and Function

Tests and Measures Purpose
Resting heart rate and rhythm Identify possible arrhythmia.
Exercise heart rate Assesses chrontropic incompetence (inability to increase heart rate with increasing demand).
Resting blood pressure Identify hypertension (BP >130/80 mmHg) or hypotension (mean arterial pressure
<60 mmHg).49
Exercise blood pressure Assess for changes in cardiac output during activity. Normal response, increase in SBP with
activity caused by increasing cardiac output. However, in patients with HF, BP that does not
increase with activity suggests compromised cardiac output.
Pitting edema before and after treatment Changes in edema post exercise indicate tolerance to exercise treatment.
Lung auscultation Increase in pulmonary crackles post treatment indicate intolerance to exercise intervention.
Maximal inspiratory pressure (MIP) Assesses strength of the inspiratory muscles. MIP <60 cm H2O signifies weak inspiratory
muscles.91
Dyspnea scale Useful in assessing the degree of dyspnea.
Pulse oximetry Assess changes in gas exchange (respiration).
Borg’s rate of perceived exertion Useful in understanding the intensity of exercise when heart rate responses are blunted by
medications.
Activity Limitations and Participation Restrictions
Tests and Measures Purpose
Gait speed, Timed Up and Go test, Berg A variety of functional tests including the Timed Up and Go Test,92 Berg Balance Test,93 and
balance test 10-meter Walk Test measuring gait speed,94 can be used in assessing a patient’s balance and
fall risk.
30-second chair rise test Measurement of lower limb muscle strength during transitional movement is helpful for docu-
menting changes over a period.
Six-minute walk (6MW) test, 2-minute Measurement of distance walked over 6 minutes, 2 minutes, or the number of steps
walk test, 2-minute step test completed in 2 minutes, can be used as a submaximal or maximal test of aerobic capacity.
Kommuri et al. found 6MW distances of less than 400 meters on the day of hospital
discharge revealed significantly greater 30 day readmission rates compared with patients
with HF and higher 6MWD scores.95
Activity measure for postacute care AM-PAC is an outcome measure that measures function in three major domains: basic
(AM-PAC) mobility, daily activities and applied cognitive.96,97 The primary goal for the development
of this measure was to create a single measure to effectively measure function across all care
settings within the continuum of care after an acute care stay. The AM-PAC is a patient
reported outcome measure and therefore captures the patient’s perspective. The measure is
available in two basic formats: a computer-based version and a short-form version.
Minnesota Living with Heart Failure A patient self-assessment of how heart failure affects a patient’s daily life. The content reflects
Questionnaire (MLHFQ) most frequent and important ways heart failure affects patients’ lives. All items are assessed
on a 1–5 Likert scale. Sum of item responses allow for total and individual dimension scores.
The test–retest/reproducibility assessed by Rector et al. is a Pearson correlation of 0.87.2,98
The minimally important difference is 5 points on the total score.98
Seattle Angina Questionnaire (SAQ) The SAQ is an outcome measure that is used to assess the effect of angina in a patient’s
quality of life within the previous 4 weeks of the assessment date.99,100 The survey uses 19
items to assess the severity of limitations in everyday life. There are two distinct sections
of the survey—the effect of angina on the patient’s ability for completing activities of daily
living (ADLs) and a second section involving several questions that assess the patient’s health
conditions. The measure has been a validated disease-specific health status instrument for
coronary artery disease (CAD) with high test-retest reliability, predictive power, and respon-
siveness, its use in routine clinical practice.101 However, its use has been limited by its length
(19 items). Therefore, in 2014, a short version (7 items) was developed, tested and validated
to increase the feasibility of measuring patient-reported outcomes in patients with CAD.101
 Cardiac System     CHAPTER 3 45

Determination of stable vs. unstable response to activity

or exercise is based on monitoring relevant patient
variables during examination or intervention and is
related to the patient’s physical capacity to support the
demands of the activity. The intensity of the activity is
Ischemic conditions always relative to the patient’s capacity. Pump failure: Congestive
heart failure

Unstable response may present as:
♦ Ischemic symptoms
♦ ST segment changes
♦ Onset of or increased frequency of
ventricular ectopy (stop Rx if >10/minute,
becomes symptomatic, or BP becomes
compromised)
♦ Unifocal PVCs become multifocal PVCs
♦ Onset of signs of CHF (see Table 3-17)
♦ Systolic blood pressure drops >10 mmHg
♦ Diastolic blood pressure increases or
decreases >10 mmHg
♦ Heart rate drops >10 bpm
♦ Diaphoresis, pallor, confusion
♦ Increased RPE despite no changes in vital
signs
♦ Cyanosis
♦ Diaphoresis
♦ Nasal flaring
♦ Increased use of accessory muscles of
respiration
Stable response may present as:
♦ Linear increase in HR and systolic BP
with increases in activity levels
♦ Blunted responses in HR and systolic
BP if on β-blockade, and some
calcium channel blockers
♦ Increased RPE with increased
workload
♦ If no changes in HR or systolic blood
pressure, there should be no change
in RPE. (During an examination low-
level workloads may not be significant
enough to produce vital sign
responses.)
♦ NOTE: Stable responses may include
increased respiratory rate, heart rate,
blood pressure, and RPE. However,
with the stable response, these
increases merely indicate the patient’s
response.
Unstable response may present as:
♦ Onset of or increased frequency of
ventricular ectopy (stop Rx if >10/minute,
becomes symptomatic, or BP becomes
compromised)
♦ Unifocal PVCs become multifocal PVCs
♦ Onset of signs of CHF (see Table 3-17)
♦ Systolic blood pressure drops >10 mmHg
♦ Diastolic blood pressure increases or
decreases >10 mmHg
♦ Heart rate drops >10 bpm
♦ Poor pulse pressure (<10 mmHg
difference between systolic and diastolic
blood pressure)
♦ Diaphoresis, pallor, confusion
♦ Increased RPE despite no changes in vital
signs
♦ Ischemic symptoms
♦ ST segment changes
♦ In patients being invasively monitored:
>10 mmHg increase in
° pulmonary artery pressure
Increase or decrease of >6 mmHg
° in central venous pressure
♦ Cyanosis
♦ Diaphoresis
♦ Nasal flaring
♦ Increased use of accessory muscles of
respiration

FIG. 3.11
Determination of stable vs. unstable responses to activity/exercise. BP, Blood pressure; CHF, congestive heart failure; HR, heart rate; PVC, premature ven-
tricular contraction; RPE, rating of perceived exertion; Rx, treatment.

Everything the physical therapist asks a patient to do is an
activity that requires energy and therefore must be supported by
the cardiac system. Although an activity can be thought of in
terms of absolute energy requirements (i.e., metabolic equiva-
lents [see Table 3.10]), an individual’s response to that activ-
ity 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 and close hemody-
namic monitoring is needed.
Unstable responses indicate that the patient is not able to
meet physiologic demands because of 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 activi-
ties create a stable response. If it is stable, can the patient func-
tion independently doing that level of work? For example, some
patients may be stable walking 10 feet to the bathroom without
stopping; however, this activity may require maximal exertion
for the patient and therefore 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 therapist
should try to discern why and find out if anything can be done
to make the patient stable (i.e., medical treatment may stabilize
this response). In addition, 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 must
determine whether a conditioning program would allow the
patient to meet the necessary energy demands without becom-
ing unstable. Proceeding with therapy at a lower level of activ-
ity 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 perform work. Often
becoming stronger—increased peripheral muscle strength and
endurance—will reduce the demands on the heart at a certain
absolute activity (work) level. Fig. 3.12 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 usually is per-
formed at a level of activity lower than the expected exercise
program. For example, it may consist of supine, seated, or stand-
ing 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.
46 CHAPTER 3     Cardiac System
CLINICAL TIP
Patients should be encouraged to report any symptom(s), even
those they consider trivial.
Listed below are various ways to monitor the patient’s activ-
ity tolerance:
1. HR: HR is the primary means of determining the exercise
intensity level for patients who are not taking beta-blockers
or who have rate-responsive pacemakers.
• A linear relationship exists between HR and work.
• In general, a 20- to 30-beat increase from the resting
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%–80%) of the
maximum HR achieved during the test can be calculated
to determine the exercise intensity.82
• An example of a disproportionate HR response to low-lev-
el activity (bed or seated exercises or ambulation in room)
is an HR of more than 120 bpm or less than 50 bpm.82
• HRR, which provides an indication of reduced parasym-
pathetic activity and an indicator of all-cause mortality,
can be used to document improvement of tolerance to
functional demands.83 HRR is the absolute difference
between peak HR achieved with exercise minus the HR at
60 seconds after the completion of exercise (HRR60sec).84
An abnormal HRR at 1 minute, after a treadmill test, is re-
ported to be a decrease of 12 bpm or less with a cool-down
period and less than 18 bpm without a cool-down period.85
• When prescribing activity intensity for a patient taking
beta-blockers, consider that HR should not exceed 20 beats
above the resting HR.
• If prescribing an activity intensity, with use of HR,
for patients with an AICD, remember that the exercise
target HR should be 20 to 30 beats below the threshold
rate on the defibrillator.82
• HR cannot be used to prescribe exercise status post heart
transplantation secondary to denervation of the heart dur-
ing transplantation.
• Baseline HR and recent changes in medications always
should be considered before beginning an exercise session.
2. BP: Refer to the Cardiac Evaluation section regarding BP
measurements and Table 3.6 for BP ranges. A clearly dis-
proportionate response to exercise includes SBP decrease of
10 mmHg below the resting value, a hypertensive systolic
response of greater than 180 mmHg, or a hypertensive dia-
stolic response of greater than 110 mmHg.82 A normoten-
sive systolic blood response should increase 5 to 12 mmHg
per increase in METs.86
• If the patient is on a pacemaker that does not have rate
modulation, BP response can be used to gauge inten-
sity. Refer to the Cardiac Pacemaker Implantation and
Automatic Implantable Cardiac Defibrillator section for
a discussion on pacemakers.
3. The Borg RPE scale: Provides clinicians with an assessment of
perceived exertion when heart rate responses do not provide an
accurate assessment of the intensity of exercise. This scale also
can be used to assess breathlessness and muscle fatigue.87,88
• The Borg CR10 Scale and the Borg CR100 (centiMax)
Scale are general scales for measuring intensities of most
kinds of perceptions, experiences, and feelings.87,88
• The Borg CR10 Scale also is used to measure RPE.
• The Borg CR100 (centiMax) Scale was developed because a
more finely graded scale was needed for certain situations.88
• These scales easily can be used to monitor exercise inten-
sity for the purpose of exercise prescription in a variety of
patient populations. They are the preferred method of pre-
scribing 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-to-20 scale.82
• For the scales to be used in the most safe, reliable, and
valid manner, complete instructions regarding the scale
and its use must be provided to the patient before its
implementation. These instructions are included with
the scales and should be followed exactly as designed and
not be modified.87,88
4. Rate pressure product (RPP), or double product, 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 calculated 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
3.8 for normal and abnormal heart sounds.
• The onset of murmurs, S3 heart sounds, or S4 heart
sounds during treatment may be detected and could in-
dicate a decline in cardiac function during activity. This
finding should be brought to the attention of the nurse
and the physician.
6. Breath sounds: Refer to Chapter 4 for a discussion of lung
auscultation and the interpretation of breath sounds.
• The presence of or increase in bi-basilar crackles during
activity may be indicative of acute HF. Activity should
be terminated and the nurse and the physician notified.
7. ECG rhythm: Refer to the Electrocardiography section and
the Rhythm and Conduction Disturbance section.
• When treating patients who are being continuously
monitored on ECG, know their baseline rhythm, the
most recently observed rhythm, what lead is being
monitored, and the reason for monitoring.
• Recognizing their normal rhythm and any deviations
from this norm in addition to changes that could indi-
cate a decline in cardiac status is important. Examples of
declining cardiac status include the following:
• Onset of ST changes (elevation or depression of more
than 1 mm), which could indicate ischemia
• Increased frequency of PVCs (trigeminy to bigeminy
or couplets)
• Unifocal PVCs to multifocal PVCs
• Premature atrial contractions to atrial flutter or atrial
fibrillation
 Cardiac System     CHAPTER 3 47

• A trial flutter to atrial fibrillation
• Any progression in heart blocks (first degree to Mob-
itz I)
• Loss of pacer spike capturing (pacer spike without
resultant QRS complex on ECG)
• Be able to recognize signs and symptoms of cardiac
decompensation, and immediately notify the physician if
any develop (see Fig. 3.11). Record any signs noted dur-
ing activity and other objective data at that time. Other
signs and symptoms include weakness, fatigue, dizzi-
ness, lightheadedness, angina, palpitations, and dyspnea.
Record any symptoms reported by the patient and any
objective information at that time (e.g., ECG readings;
BP, HR, and RPP measurements; breath sounds). 

Resting Examination of Patient Status

(Medical record review, speak with RN,
examine resting vital signs.)
Are there any contraindications to
Yes
treatment? Is the patient unstable at rest?

Assist is provided as needed
for these functional activities,
although determination of
stable or unstable has to do
with the cardiac response.
These two constructs must
both be considered by the
PT. Patients might be
moderate assist with a stable
response, or could be
independent with an
unstable response to an
activity (see text).
No
Speak with RN or MD regarding
decision to defer treatment, make note
in the patient’s record explaining
Active bed exercises: Distal LE first, moving
decision.
to distal UE, then proximal LE, finally
proximal UE. Avoid the use of the Valsalva
during exercise.
Monitor vital sign response.
Stable Response: Proceed Unstable Response: Inform RN or MD. If medical
as tolerated to bed mobility management can be altered to improve response, wait
activities, supine to sitting, for medical intervention; if nothing can be done to
seated exercise improve the patient’s medical status, attempt to modify
the intensity of the activity or proceed with PROM, and
bronchopulmonary hygiene as indicated.

Stable Response: Proceed Unstable Response: Inform RN or MD. If medical management can be
as tolerated to sit to altered to improve response, wait for medical intervention; if nothing
stand, transfer to chair, can be done you may attempt to provide more assistance (decreases the
sitting in chair patient’s contribution to the energy requirements) during the activity or
proceed with bedside AROM, and bronchopulmonary hygiene as
indicated.

Stable Response: Proceed Unstable Response: Inform RN or MD. If medical management

as tolerated to ambulation can be altered to improve response, wait for medical intervention;
on level surfaces. Monitor if nothing can be done you may attempt to provide more
gait, balance, time, and assistance during the activity or proceed with bed mobility
distance. Consider timed activities and seated exercise as tolerated.
walk test if the patient
ambulates independently
or with supervision.

Stable Response: Proceed Unstable Response: Inform RN or MD. If medical management can
as tolerated to ambulation be altered to improve response, wait for medical intervention; if
exercise program; depending nothing can be done, you may first attempt to reduce the energy
on gait and balance this may demands of the activity with modifications, otherwise proceed with
be performed with nursing staff sit to stand, transfers, and seated exercise as tolerated. If tolerated, a
or independently by patient. standing exercise program can also be initiated to include pregait
Proceed to stair climbing as activities (see text).
appropriate.

FIG. 3.12
Physical therapy activity examination algorithm. AROM, Active range of motion; LE, lower extremity; PROM, passive range of motion; UE, upper extremity.
48 CHAPTER 3     Cardiac System
Patient Education
Promoting appropriate self-care in patients with cardiovascular
disease is complex and therefore necessitates intensive patient
education. The physical therapist, along with other members of
the health care team, can play a vital role in appropriate patient
education to reduce cardiovascular risk, maximize activity, par-
ticipation and overall self-care.
A systematic review involving 35 intervention studies that
focused on education for patients with HF demonstrated that
education improved knowledge of the disease, self-monitoring,
medication adherence, time to hospitalization, and days in the
hospital.89 Further, in patients with HF, Gwadry-Sridhar et al.
found that patients who received in-hospital education had
higher knowledge scores at discharge and 1 year later compared
with those that did not receive in-hospital education.90 The fol-
lowing topics are appropriate to discuss within the education
phase of treatment or discharge visit.
• Self-monitoring techniques: Rate of perceived exertion, au-
tomatic blood pressure monitoring, pulse assessment, symp-
toms or signs that may suggest exercise intolerance, such as
light-headedness, mental confusion, dyspnea, and inability
to carry on a brief conversation while performing an activity.
• Symptom recognition and response: Weight gain of greater
than 2 lb overnight, or 5 lb in 2 days; increased dyspnea;
lower extremity swelling; need for increased number of pil-
lows for sleep; and the need to follow up with a physician or
a member of the medical team when these symptoms occur.
• Activity guidelines: Specific activity guidelines, which in-
clude planned exercise sessions as well as leisure time and
rests.
• Medication management: Medication reconciliation is a pro-
cess of comprehensively reviewing what the patient is taking,
comparing that with what the physician wants them to be
taking, checking for interactions, duplications, and omis-
sions, contacting the physician to collaborate, as needed, and
educating the patient regarding the same. The American
Physical Therapy Association has an official position state-
ment adopted from the House of Delegates that advocates
that therapists assist patients in medication management in
an effort to promote patient safety and reduce hospital read-
missions.
• Lifestyle modifications: Avoiding smoking and reducing
weight if overweight or obese.
• Nutrition: Monitoring salt and fluid intake, reducing fat in-
take, and decreasing alcohol consumption.  23. Doulalas A, Flather MD, Pipilis A, et al. Evolutionary pattern
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 Cardiac System     CHAPTER 3 51

  

APPENDIX 3A: Description of Electrocardiography (ECG) Characteristics and Associated Causes

TABLE 3A.1  Electrocardiographic Characteristics and Causes of Atrial Rhythms

Name ECG Characteristics
Supraventricular Regular rhythm; rate of 160–250 bpm;
tachycardia 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 “sawtooth” P
waves)
AF Irregular rhythm; atrial has no rate
(just quivers); ventricular rate varies
Premature atrial Irregular rhythm (can be regularly
contractions irregular, i.e., skip every third beat);
rate normal 60–100
Common Causes
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; PT would 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
PT until 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

AF, Atrial fibrillation; CAD, coronary artery disease; CHF, congestive heart failure; PT, physical therapy; RHD, rheumatoid heart disease.
Data from Aehlert B. ACLS Quick Review Study Guide. St. Louis: Mosby; 1993; Chung EK. Manual of Cardiac Arrhythmias. Boston: Butterworth-Heinemann; 1986.
52 CHAPTER 3     Cardiac System

TABLE 3A.2  Electrocardiographic Characteristics and Causes of Ventricular Rhythms

Name ECG Characteristics
Agonal rhythm Irregular rhythm, rate <20, no
P wave
Ventricular tachycardia Usually regular rhythm, rate
(VT) >100, no P wave or with
retrograde conduction and
appears after the QRS complex
Multifocal VT (torsades Irregular rhythm, rate >150, no
de pointes) P waves
Premature ventricular Irregular rhythm, (can be
contractions (PVCs) regularly irregular, i.e., skipped
(focal = one ectopic foci beat every fourth beat); rate
and all look the same; varies but is usually normal
multifocal = more than 60–100; couplet is 2 in a row;
one ectopic foci and will bigeminy is every other beat;
have trigeminy is every third beat
different waveforms)
Ventricular fibrillation Chaotic
Idioventricular rhythm Essentially regular rhythm, rate
20–40
Common Causes
Near death
CAD most common after acute MI; may
occur in rheumatoid heart disease,
cardiomyopathy, hypertension
Drug induced with antiarrhythmic
medicines (quinidine, procainamide);
hypokalemia; hypomagnesemia; MI;
hypothermia
In normal individuals, secondary
to caffeine, smoking, emotional
disturbances, CAD, MI,
cardiomyopathy, MVP, digitalis toxicity
Severe heart disease most common
after acute MI, hyperkalemia or
hypokalemia, hypercalcemia,
electrocution
Advanced heart disease; high degree
of atrioventricular block; usually a
terminal arrhythmia
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)—called pulseless VT.
Do not treat; patient needs
immediate medical assistance.
Frequency will dictate effect on
CO; monitor electrocardiograph
with treatment; can progress to
VT; more likely if multifocal in
nature or if >6 per minute; stop
treatment or rest if change in
frequency or quality.
Do not treat; patient needs
immediate medical assistance.
CHF is common secondary to
slow rates; do not treat unless
rhythm well tolerated.

CAD, Coronary artery disease; CHF, congestive heart failure; CO, cardiac output; ECG, echocardiographic; MI, myocardial infarction; MVP, mitral valve prolapse; PT,
physical therapy; VT, ventricular tachycardia.
Data from Aehlert B. ACLS Quick Review Study Guide. St. Louis: Mosby; 1994; Chung EK. Manual of Cardiac Arrhythmias. Boston: Butterworth-Heinemann; 1986.

TABLE 3A.3  Electrocardiographic Characteristics and Causes of Junctional Rhythms

Name ECG Characteristics Common Causes PT Considerations
Junctional escape Regular rhythm, rate 20–40; Usual cause is physiologic to If occasional and intermittent during bradycardia
rhythm inverted P wave before or after control the ventricles in AV or chronic AF, usually insignificant and can treat
QRS complex; starts with block, sinus bradycardia, (with close watch of possible worsening condition
ectopic foci in AV junction AF, sinoatrial block, drug via symptoms and vital signs); if consistent
tissue intoxication and present secondary to AV block, acute
myocardial infarction, or drug intoxication, can be
symptomatic with CHF (see Box 3.3).
Junctional Regular rhythm; rate 100–180; Most common with chronic May produce or exacerbate symptoms of CHF or
tachycardia P wave as above AF; also with coronary artery angina secondary to decreased cardiac output; PT
disease, rheumatoid heart treatment depends on patient tolerance—if new
disease, and cardiomyopathy onset, should wait for medical treatment.

AF, Atrial fibrillation; AV, atrioventricular; CHF, congestive heart failure; PT, physical therapy.
Data from Aehlert B. ACLS Quick Review Study Guide. St. Louis: Mosby; 1994; Chung EK. Manual of Cardiac Arrhythmias. Boston: Butterworth-Heinemann; 1986.
 Cardiac System     CHAPTER 3 53

TABLE 3A.4  Electrocardiographic Characteristics and Causes of Atrioventricular Blocks

Name ECG Characteristics Common Causes PT Considerations
First-degree AV Regular rhythm, rate normal 60–100, Elderly with heart disease, acute If chronic, need to be more
block prolonged PR interval >0.2 (constant) myocarditis, acute MI cautious of underlying heart
disease; if new onset, monitor
closely for progression to higher
level block.
Second-degree Irregular rhythm, atrial rate > ventricular Acute infection, acute MI Symptoms are uncommon, as
AV block type rate, usually both 60–100; PR interval above.
I (Wenckebach, lengthens until P wave appears without
Mobitz I) a QRS complex
Second-degree AV Irregular rhythm, atrial rate > ventricular Anteroseptal MI CHF is common; can have
block type II rate, PR interval may be normal or dizziness, fainting, complete
(Mobitz II) prolonged but is constant for each unconsciousness; may need
conducted QRS pacing and PT treatment;
should be held for medical
management.
Third-degree AV Regular rhythm, atrial rate > Anteroseptal MI, drug intoxication, Severe CHF; patient will need
block (complete ventricular rate infections, electrolyte imbalances, medical management; a pacer
heart block) coronary artery disease, degenerative (temporary or permanent,
sclerotic process of AV conduction depending on reversibility
system of etiology) is almost always
necessary.

AV, Atrioventricular; CHF, congestive heart failure; MI, myocardial infarction; PT, physical therapy.
Data from Aehlert B. ACLS Quick Review Study Guide. St. Louis: Mosby; 1994; Chung EK. Manual of Cardiac Arrhythmias. Boston: Butterworth-Heinemann; 1986.

  

APPENDIX 3B: Common Rhythm Disturbances

FIG. 3B.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.)

FIG. 3B.2
Atrial flutter. Note regular rhythm (P waves), but ventricular rhythm depends on conduction pattern. (From Walsh M, Crumbie A, Reveley S. Nurse Practi-
tioners: Clinical Skills and Professional Issues. Boston: Butterworth-Heinemann; 1993.)
54 CHAPTER 3     Cardiac System

FIG. 3B.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.)

FIG. 3B.4
Ventricular tachycardia. Rate 100 to 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.)

FIG. 3B.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.)
 Cardiac System     CHAPTER 3 55

FIG. 3B.6
Sinus rhythm with premature ventricular contractions. (From Chung EK. Manual of Cardiac Arrhythmias. Boston: Butterworth-Heinemann; 1986.)

FIG. 3B.7
Ventricular fibrillation. (From Walsh M, Crumbie A, Reveley S. Nurse Practitioners: Clinical Skills and Professional Issues. Boston: Butterworth-Heinemann;
1993.)
56 CHAPTER 3     Cardiac System

D
FIG. 3B.8
Degrees of heart block. (From Walsh M, Crumbie A, Reveley S. Nurse Practitioners: Clinical Skills and Professional Issues. Boston: Butterworth-Heinemann;
1993.)
 4 Pulmonary System
C H APT ER  

Lauren Mitchella
Matthew Nippins

CHAPTER OUTLINE CHAPTER OBJECTIVES

Introduction
Body Structure and Function
Structure
Function
Mechanics of Ventilation
Gas Exchange
Ventilation-to-Perfusion Ratio
Gas Transport
Examination
Patient History
Physical Examination
Inspection
Auscultation
Palpation
Chest Wall and Abdominal
Excursion
Posture and Musculoskeletal
Examination
Mediate Percussion
Cough Examination
Hemoptysis
Diagnostic Testing
Blood Gas Analysis
Chest X-Ray (Radiography)
Sputum Analysis
Flexible Bronchoscopy
Ventilation-Perfusion Scan
Computed Tomographic Pulmo-
nary Angiography
Pulmonary Function Tests
Health Conditions
Obstructive Pulmonary
Conditions
Restrictive Pulmonary Conditions
Restrictive Extrapulmonary
Conditions
Chest Wall Restrictions
Management
Pharmacologic Agents
Thoracic Surgery and Procedures
Physical Therapy Intervention
The objectives of this chapter are the following:
1 . Provide a brief review of the structure and function of the pulmonary system
2. Present an overview of pulmonary evaluation, including physical examination and diagnostic testing
3. Describe pulmonary diseases and disorders, including clinical findings, medical-surgical management, and
physical therapy intervention
Introduction
To safely and effectively provide physical therapy interventions of exercise, airway clearance
program(s), or both to patients with pulmonary system dysfunction, physical therapists require an
understanding of the pulmonary system and of the principles of ventilation and gas exchange. Ven-
tilation 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 inter-
faces. The term pulmonary primarily refers to the lungs, their airways, and their vascular system.1
Body Structure and Function
Structure
The primary organs and muscles of the pulmonary system are outlined in Tables 4.1 and 4.2,
respectively. A schematic of the lungs within the thorax is presented in Fig. 4.1. 
Function
To accomplish ventilation and respiration, the pulmonary system is regulated by many neural,
chemical, and nonchemical mechanisms, which are discussed in the sections that follow.
Neural Control
Ventilation is regulated by two separate neural mechanisms: one controls automatic ventila-
tion, and the other controls voluntary ventilation. The medullary respiratory center in the
brainstem, is responsible for the rhythmicity of breathing and controls automatic ventilation.
The pneumotaxic center, located in the pons, controls the rate and depth of ventilation. The
cerebral cortex, which sends impulses directly to the motor neurons of ventilatory muscles,
mediates voluntary ventilation.2 
Chemical Control
Arterial levels of CO2 (PCO2), hydrogen ions (H+), and O2 (PO2) can modify the rate and
depth of respiration. To maintain homeostasis in the body, specialized chemoreceptors on the
carotid arteries and aortic arch (carotid and aortic bodies, respectively) respond to either a rise
in PCO2 and H+ or a fall in PO2. Stimulation of these chemoreceptors results in transmission
of impulses to the respiratory centers to increase or decrease the rate, depth, or both, of respi-
ration. The respiratory center found in the medulla primarily responds to a rise in PCO2 and
H+.3,4 For example, an increase in PCO2 would increase the ventilation rate to help increase the
amount of CO2 exhaled and ultimately lower the PCO2 levels in arterial blood. 
aThe authors acknowledge Paul Ricard for prior contributions to this chapter.

        57
58 CHAPTER 4     Pulmonary System
TABLE 4.1  Structure and Function of Primary Organs of the Pulmonary System
Structure Description
Nose Paired mucosal-lined nasal cavities supported by bone and cartilage
Pharynx Passageway that connects nasal and oral cavities to larynx, and oral
cavity to esophagus
Subdivisions naso-, oro-, and laryngopharynx
Larynx Passageway that connects pharynx to trachea
Opening (glottis) covered by vocal folds or by the epiglottis during
swallowing
Trachea Flexible tube composed of C-shaped cartilaginous rings connected
posteriorly to the trachealis muscle
Divides into the left and right main stem bronchi at the carina
Bronchial Right and left main stem bronchi subdivide within each lung into
tree secondary bronchi, tertiary bronchi, and bronchioles, which contain
smooth muscle
Lungs Paired organs located within pleural cavities of the thorax
The right lung has three lobes, and the left lung has two lobes
Alveoli Microscopic sacs at end of bronchial tree immediately adjacent to
pulmonary capillaries
Functional unit of the lung
Pleurae Double-layered, continuous serous membrane lining the inside of the
thoracic cavity
Divided into parietal (outer) pleura and visceral (inner) pleura
Data from Marieb E. Human Anatomy and Physiology. 3rd ed. Redwood City, CA: Benjamin-Cummings; 1995; Moldover JR, Stein J, Krug PG. Cardiopulmonary physiol-
ogy. In: Gonzalez EG, Myers SJ, Edelstein JE, et al. Downey & Darling’s Physiological Basis of Rehabilitation Medicine. 3rd ed. Philadelphia: Butterworth-Heinemann; 2001.
Nonchemical Influences
The lungs have protective reflexes of coughing, bronchocon-
striction, and mucus secretion and react to irritants, such as
smoke or dust. Additional factors that can influence the rate
and depth of ventilation include emotions, stressors, pain, and
visceral reflexes from the lung tissue and other organ systems.3,5  expansion results in greater negative pressures being generated
Mechanics of Ventilation
Ventilation occurs as a result of changes in the potential space
(volume) and subsequent pressures within the thoracic cavity
created by the muscles of ventilation. The largest primary mus-
cle of inhalation, the diaphragm, compresses the contents of the
abdominal cavity as it contracts and descends, increasing the
volume of the thoracic cavity.
  CLINICAL TIP
The compression of the abdominal contents can be observed
with the protrusion of the abdomen. Clinicians use the term
“belly breathing” to denote diaphragmatic breathing.
The contraction of the intercostal muscles results in two
motions simultaneously: bucket and pump handle. These
motions are outlined schematically in Fig. 4.2. The combined
motions further increase the volume of the thorax. The overall
increase in the volume of the thoracic cavity creates a negative
intrathoracic pressure compared with the pressure outside the
body. As a result, air is pulled into the body and lungs via the
pulmonary tree, stretching the lung parenchyma, to equalize
the pressures within the thorax with those outside the body.
Function
Conduit that filters, warms, and humidifies air entering
lungs
Conduit for air and food
Facilitates exposure of immune system to inhaled anti-
gens
Prevents food from entering the lower pulmonary tract
Voice production
Cleans, warms, and moistens incoming air
Warms and moistens incoming air from trachea to alveoli
Smooth muscle constriction alters airflow
Contains air passageways distal to main stem bronchi,
alveoli, and respiratory membranes
Primary gas exchange site
Surfactant lines the alveoli to decrease surface tension and
prevent complete closure during exhalation
Produces lubricating fluid that allows smooth gliding of
lungs within the thorax
Potential space between parietal and visceral pleura
Accessory muscles of inspiration, noted in Table 4.2, are
generally not active at rest. Although not the primary actions
of the individual muscles, contractions of the accessory muscles
can increase the depth and rate of ventilation during progres-
sive activity by increasing the expansion of the thorax. Increased
and subsequent larger volumes of air entering the lungs.
  CLINICAL TIP
In healthy lungs, depth of breath or tidal volume (VT) generally
occurs before increases in respiratory rate.
Although inhalation is an active process, exhalation is gener-
ally passive. The muscles relax, causing a decrease in the tho-
racic volume while the lungs deflate to their natural resting
state. The combined effects of these actions result in an increase
of intrathoracic pressure and flow of air out of the lungs. Con-
traction of the primary and accessory muscles of exhalation (see
Table 4.2) results in an increase in intrathoracic pressure and
a faster rate of decrease in thoracic size, forcing air out of the
lungs.6
In persons with primary or secondary chronic pulmonary
health conditions, changes in tissue and mechanical properties
of the pulmonary system can result in accessory muscle use being
observed earlier in activity or even being present at rest. Deter-
mination of the impairment(s) resulting in the observed activity
limitation can help a clinician determine a plan of care. In addi-
tion, clinicians should consider the reversibility, or the degree
to which the impairment can be improved, when determining
a patient’s prognosis for improvement with physical therapy.

TABLE 4.2  Primary and Accessory Ventilatory Muscles With Associated Innervation
Pulmonary Muscles
Primary inspiratory muscles Diaphragm
External intercostals
Accessory inspiratory muscles Trapezius
Sternocleidomastoid
Scalenes
Pectorals
Serratus anterior
Latissimus dorsi
Primary expiratory muscles Rectus abdominis
External obliques
Internal obliques
Internal intercostals
Accessory expiratory muscles Latissimus dorsi
Data from Kendall FP, McCreary EK, eds. Muscles: Testing and Function. 3rd ed. Baltimore, MD: Lippincott, Williams, and Wilkins; 1983; Rothstein JM, Roy SH, Wolf
SL. The Rehabilitation Specialist’s Handbook. 2nd ed. Philadelphia: FA Davis; 1998; DeTurk WE, Cahalin LP. Cardiovascular and Pulmonary Physical Therapy: An Evidence-
Based Approach. New York: McGraw-Hill Medical Publishing Division; 2004.
If reversing a patient’s ventilatory impairments is unlikely,
facilitation of accessory muscle use can be promoted during
functional activities and strengthening of these accessory mus-
cles (e.g., use of a four-wheeled rolling walker with a seat and
accompanying arm exercises).7
  CLINICAL TIP
Patients with advanced pulmonary conditions may automati-
cally assume positions to optimize accessory muscle use, such
as forward leaning on their forearms (i.e., tripod posturing).  
Gas Exchange
Once air has reached the alveolar spaces, respiration or gas
exchange can occur at the alveolar-capillary membrane. Diffu-
sion of gases through the membrane is affected by the following8:
• A concentration gradient (partial pressure difference) in
which gases will diffuse from areas of high concentration to
areas of low concentration:
Alveolar O2 = 100 mmHg → Capillary O2 = 40 mmHg
• S urface area, or the total amount of alveolar-capillary in-
terface available for gas exchange (e.g., the breakdown
of alveolar membranes that occurs in emphysema will
reduce the amount of surface area available for gas ex-
change)
• 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)
• Diffusion coefficient of gas through a membrane, which is de-
pendent on the solubility of a particular gas in the membrane  aminohemoglobin and bicarbonate. A smaller percentage (3%)
Ventilation-to-Perfusion Ratio
Gas exchange is optimized when the ratio of air flow (ventilation
V̇) to blood flow (perfusion Q̇ ) approaches a 1 : 1 relationship.
However, the actual V̇/Q̇ ratio is 0.8 because alveolar ventilation
Pulmonary System     CHAPTER 4 59
Innervation
Phrenic nerve (C3–C5)
Spinal segments T1–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 segments T5–T12
Spinal segments T7–T12
Spinal segments T8–T12
Spinal segments T1–T9
Thoracodorsal nerve (C5–C8)
is approximately equal to 4 μL per minute and pulmonary blood
flow is approximately equal to 5 L per minute.9–11
Gravity, body position, and cardiopulmonary dysfunction
can influence this ratio. Ventilation is optimized in areas of least
resistance. For example, when a person is in the sitting position,
the upper lobes initially receive more ventilation than the lower
lobes; however, the lower lobes have the largest net change in
ventilation.12
Perfusion is greatest in gravity-dependent areas. For exam-
ple, when a person is in the sitting position, perfusion is the
greatest at the base of the lungs; when a person is in the left
side-lying position, the left lung receives the most blood.12
A V̇/Q̇ mismatch (inequality in the relationship between
ventilation and perfusion) can occur in certain situations. Two
terms associated with V̇/Q̇ mismatch are dead space and shunt.
Dead space occurs when ventilation is in excess of perfusion, as
with a pulmonary embolus. A shunt occurs when perfusion is in
excess of ventilation, as in alveolar collapse from secretion reten-
tion.12 These conditions are shown in Fig. 4.3. 
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 (oxyhemoglobin). 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.13
Approximately 97% of O2 transported from the lungs is car-
ried in chemical combination with hemoglobin. The majority
of CO2 transport (93%) occurs in the combined forms of carb-
of O2 and 7% of CO2 are transported in dissolved forms.13 Dis-
solved O2 and CO2 exert partial pressure within the plasma and
can be measured by sampling arterial, venous, or mixed venous
blood.14 (See the Arterial Blood Gas section for further descrip-
tion of this process.) 
60 CHAPTER 4     Pulmonary System

C
FIG. 4.1
(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) Posterior
view of the lungs in conjunction with bony landmarks. (From Ellis E, Alison J, eds. Key Issues in Cardiorespiratory
Physiotherapy. Oxford, UK: Butterworth-Heinemann; 1992:12.)
 Pulmonary System     CHAPTER 4 61

FIG. 4.2
Respiratory mechanics (bucket and pump handle motions). (From Snell RS, ed. Clinical Anatomy by Regions. 9th
ed. Baltimore, MD: Lippincott, Williams & Wilkins; 2012.)

Bronchiole

Alveoli

Capillary

A B C
FIG. 4.3
Ventilation and perfusion mismatch. (A) Normal alveolar ventilation. (B) Capillary shunt. (C) Alveolar dead
space.
62 CHAPTER 4     Pulmonary System
Examination
Pulmonary examination is composed of patient history, physical
examination, and interpretation of diagnostic test results.
Patient History
In addition to the general chart review presented in Chapter
2, other relevant information regarding pulmonary dysfunc-
tion that should be ascertained from the chart review or patient
interview is as follows14–16:
• History of smoking, including packs per day or pack-years
(packs per day × number of years smoked) and the amount
of time that smoking has been discontinued (if applicable).
Current or past exposure to secondhand smoke may also be
determined along with type of smoking the patient had been
performing (e.g., cigarette, cigar, pipe, vaporizing device).
• Presence, history, and amount of supplemental O2 therapy at
rest, with activity and at night. The choice of delivery meth-
ods of supplemental O2 therapy, such as intermittent versus
continuous flow or nasal cannula, versus an oxymizer is also
clinically important to determine.
• Exposure to environmental or occupational toxins (e.g., as-
bestos or occupational dusts).
• History of thoracic procedures, or surgery.
• History and frequency of pneumonia and other lung infections.
• History or current use of assisted ventilation or intubation
with mechanical ventilation.
• History or current reports of dyspnea either at rest or with exer-
tion. Dyspnea is the subjective complaint of difficulty with res-
piration, also known as shortness of breath. Measurement tools
are available to assess the multidimensional aspects of dyspnea.
Categories of these scales include sensory-perceptual scales that
measure ratings of intensity, such as the Modified Borg Scale
and visual analog scales; affective distress scales that measure
how distressing breathing feels to the patient, such as single or
multi-item ratings of distress or emotional responses, and lastly
symptom or impact burden scales measuring how dyspnea af-
fects function and quality of life, such as the Medical Research
Council (MRC) scale (Table 4.3).17,18 At this time, the American
Thoracic Society does not recognize a single standard measure.
• Prior level of activity, exercise and function.
• History of baseline sputum production, including color (e.g.,
yellow, green), consistency (e.g., thick, thin), and amount.
Familiar or broad terms can be applied as units of measure
for sputum (e.g., quarter-sized, tablespoon, or copious).
• Airway clearance techniques used currently and in the past,
along with their perceived effectiveness.
• Breathing treatments (e.g., metered-dose inhalers [MDIs]
and nebulized medications).
• Sleeping position and number of pillows used.
  CLINICAL TIP
Dyspnea may also be measured by counting the number of syl-
lables a person can utter per breath. For example, a patient with
one- to two-word dyspnea noticeably has more dyspnea com-
pared with a person who can speak a full sentence per breath.
TABLE 4.3  Medical Research Council Breathlessness Scale
Grade Degree
1 Is the patient’s breath as good as that of other men of his
age and build at work, on walking, and on climbing
hills or stairs?
2 Is the patient able to walk with normal men of own age
and build on the level but unable to keep up on hills
or stairs?
3 Is the patient unable to keep up with normal men on the
level, but able to walk about a mile or more at his own
speed?
4 Is the patient unable to walk more than about 100 yards
on the level without a rest?
5 Is the patient breathless on talking or undressing, or un-
able to leave his house because of breathlessness?
From Brooks SM. Surveillance for respiratory hazards. ATS News. 1982;8:12-16.
Used with the permission of the Medical Research Council.
  CLINICAL TIP
Dyspnea can be measured to further quantify functional activi-
ties or exercise, either as a primary or secondary measure-
ment of intensity. This is also especially useful in goal writing
(e.g., “Patient will ascend/descend 10 stairs using one rail with
reported dyspnea < 2/10.”)
 
Physical Examination
The physical examination of the patient with pulmonary
impairments consists of inspection, auscultation, palpation,
mediate percussion, cough examination, postural assessment
and musculoskeletal testing. Suggested guidelines for physi-
cal therapy intervention(s) that are based on examination find-
ings and diagnostic test results are found at the end of this
chapter. 
Inspection
A wealth of information can be gathered by simple observa-
tion of the patient at rest and with activity. Physical observa-
tion should proceed in a systematic fashion and include the
following14–16:
• General appearance and level of alertness
• Ease of phonation
• Skin color
• Posture and chest shape
• Ventilatory or breathing pattern
• Presence of digital clubbing
• Presence of supplemental O2 and other medical equipment
(refer to Chapter 18)
• Presence and location of surgical incisions
Observation of Breathing Patterns
Breathing patterns vary among individuals and may be influ-
enced by pain, emotion, body temperature, sleep, body position,
activity level, and the presence of pulmonary, cardiac, metabolic,
or nervous system disease (Table 4.4).
 Pulmonary System     CHAPTER 4 63

TABLE 4.4  Description of Breathing Patterns and Their Associated Conditions

Breathing Pattern Description Associated Conditions
Apnea Lack of airflow to the lungs for >15 seconds Airway obstruction, cardiopulmonary arrest, altera-
tions of the respiratory center, narcotic overdose
Biot’s respirations Constant increased rate and depth of respiration followed by Elevated intracranial pressure, meningitis
periods of apnea of varying lengths
Bradypnea Ventilation rate <12 breaths per minute Use of sedatives, narcotics, or alcohol; neurologic
or metabolic disorders; excessive fatigue
Cheyne-Stokes respira- Increasing depth of ventilation followed by a period of apnea Elevated intracranial pressure, CHF, narcotic
tions overdose
Hyperpnea Increased depth of ventilation Activity, pulmonary infections, CHF
Hyperventilation Increased rate and depth of ventilation resulting in decreased Anxiety, nervousness, metabolic acidosis
PCO2
Hypoventilation Decreased rate and depth of ventilation resulting in increased Sedation or somnolence, neurologic depression of
PCO2 respiratory centers, overmedication, metabolic
alkalosis
Kussmaul respirations Increased regular rate and depth of ventilation Diabetic ketoacidosis, renal failure
Orthopnea Dyspnea that occurs in a flat supine position. Relief occurs with Chronic lung disease, CHF
more upright sitting or standing
Paradoxical ventilation Inward abdominal or chest wall movement with inspiration and Diaphragm paralysis, ventilation muscle fatigue,
outward movement with expiration chest wall trauma
Sighing respirations The presence of a sigh >2–3 times per minute Angina, anxiety, dyspnea
Tachypnea Ventilation rate >20 breaths per minute Acute respiratory distress, fever, pain, emotions,
anemia
Hoover’s signa The inward motion of the lower rib cage during inhalation Flattened diaphragm often related to decompen-
sated or irreversible hyperinflation of the lungs
aHoover’s sign has been reported to have a sensitivity of 58% and specificity of 86% for detection of airway obstruction. Hoover’s sign is associated with a patient’s body
mass index, severity of dyspnea, and frequency of exacerbations and is seen in up to 70% of patients with severe obstruction.
CHF, Congestive heart failure; PCO2, partial pressure of carbon dioxide.
Data from Johnson CR, Krishnaswamy N, Krishnaswamy G. The Hoover’s sign of pulmonary disease: molecular basis and clinical relevance. Clin Mol Allergy. 2008;6:8;
Kersten LD. Comprehensive Respiratory Nursing: A Decision-Making Approach. Philadelphia: Saunders; 1989; DesJardins T, Burton GG. Clinical Manifestations and Assessment
of Respiratory Disease. 3rd ed. St. Louis: Mosby; 1995.

Observation of breathing pattern should include an
assessment of rate (12–20 breaths per minute is normal),
depth, ratio of inspiration to expiration (one to two is nor-
mal), sequence of chest wall movement during inspiration
and expiration, comfort, presence accessory muscle use, and
symmetry.14–16
  CLINICAL TIP
If possible, examine the patient’s breathing pattern when he
or she is unaware of the inspection, because knowledge of the
physical examination can influence the patient’s respiratory pat-
tern and/or rate. Objective observations of ventilation 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 ventilation rate or pattern that is 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 pass-
ing through the tracheobronchial tree and the alveolar spaces.
The sounds of airflow normally dissipate from proximal to distal
airways, making the sounds less audible in the periphery than in
the central airways. Alterations in airflow and ventilation effort
result in distinctive sounds within the thoracic cavity that may
indicate pulmonary disease or dysfunction.
Auscultation proceeds in a systematic, side-to-side, and
cephalocaudal fashion. Breath sounds on the left and right sides
are compared in the anterior, lateral, and posterior segments of
the chest wall, as shown in Fig. 4.4. The diaphragm (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 stetho-
scope to another lung segment.14–16
All of the following ensure accurate auscultation:
• Make sure stethoscope earpieces are pointing up and inward
(toward your patient) before placing them in your ears.
• Long stethoscope tubing may dampen sound transmission.
Length of tubing should be approximately 30 cm (12 in) to
55 cm (21–22 in).15
• Double tubing stethoscopes may cause the false appearance
of adventitious breath sounds when the two tubes touch dur-
ing auscultation.
64 CHAPTER 4     Pulmonary System
A B
FIG. 4.4
Landmarks for lung auscultation on (A) anterior, (B) posterior, and (C) lateral aspects of the chest wall. (Cour-
tesy Peter P. Wu.)
• A lways check proper function of the stethoscope before aus-
cultating by listening to finger tapping on the diaphragm
while the earpieces are in place.
• Apply the stethoscope diaphragm firmly against the patient’s
bare skin so that the diaphragm lays flat. Never auscultate
over clothes if it can be avoided.
• Observe chest wall expansion and breathing pattern while
auscultating to confirm the palpatory findings of breath-
ing pattern (e.g., sequence and symmetry). For example,
decreased chest wall motion, detected during palpation in
the left lower lung field, may present with decreased breath
sounds in that same area.
Breath sounds may be normal or abnormal (adventitious or
added) breath sounds; all breath sounds should be documented
according to the location and the phase of respiration (i.e., inspi-
ration, expiration, or both) and in comparison with the oppo-
site lung. Several strategies can be used to reduce the chance of
false-positive adventitious breath sound findings, including the
following:
• Ensure full, deep inspirations (decreased effort can be misin-
terpreted as decreased breath sounds).
• Ask the patient to breath in and out through the mouth in-
stead of the nose.
• Be aware of the stethoscope tubing touching other objects
(especially ventilator tubing) or chest hair.
• Periodically lift the stethoscope off the chest wall to help dif-
ferentiate extraneous sounds (e.g., chest or nasogastric tubes,
patient snoring) that may appear to originate from the thorax.
• Auscultate side to side to compare the sounds of a similar
region in the other lung.
C
  CLINICAL TIP
To maximize patient comfort, allow periodic rest periods between
deep breaths to prevent hyperventilation and dizziness. Instruct-
ing the patient to “Please stop if you get lightheaded or dizzy” is
also helpful to prevent these symptoms with auscultation.
Normal Breath Sounds
Clinically, tracheal, bronchial, and vesicular breath sounds gen-
erally are documented in the medical record as “normal” or
“clear” breath sounds; however, the use of tracheal or vesicular
breath sounds as descriptors is more accurate.
Tracheal, Bronchial, or Bronchovesicular Sounds.  Nor-
mal tracheal or bronchial breath sounds are loud tubular sounds
heard over the proximal airways, such as the trachea and main
stem bronchi. A pause is heard between inspiration and expira-
tion; the expiratory phase is longer than the inspiratory phase.
Normal bronchovesicular sounds are similar to bronchial breath
sounds; however, no pause occurs between inspiration and
expiration.14,15 
Vesicular Sounds.  Vesicular sounds are soft rustling sounds
heard over the more distal airways and lung parenchyma. Inspi-
ration is longer and more pronounced than expiration because a
decrease in airway lumen during expiration limits transmission
of airflow sounds.14,15
  CLINICAL TIP
The abbreviation CTA stands for “clear to auscultation.”
 
 Pulmonary System     CHAPTER 4 65

TABLE 4.5  Possible Sources of Abnormal Breath Sounds Discontinuous Sounds

Sound
Bronchial (abnormal if heard in
areas where vesicular sounds
should be present)
Decreased or diminished (less
audible)
Absent
Possible Etiology
Fluid or secretion consolidation
(airlessness) that could occur
with pneumonia
Hypoventilation, severe conges-
tion, or emphysema
Pneumothorax or lung collapse
Crackles.  Crackles are bubbling or popping sounds that rep-
resent the presence of fluid, secretions, or the sudden opening
of closed airways. Crackles that result from fluid (pulmonary
edema) or secretions (pneumonia or hypersecretion of mucus)
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.”15

Abnormal Breath Sounds
Breath sounds are abnormal if they are heard outside their usual
location in the chest or if they are qualitatively different from
normal breath sounds.19 Despite efforts to make the terminol-
ogy 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 docu-
mented or reported. Abnormal breath sounds with possible
sources are outlined in Table 4.5.  sound is heard as a loud grating sound, generally throughout
Adventitious Breath Sounds
Adventitious breath sounds occur from alterations or turbulence
in airflow through the tracheobronchial tree and lung paren-
chyma. These sounds can be divided into continuous (wheezes
and rhonchi) or discontinuous (crackles) sounds.15,19
The American Thoracic Society and the American College
of Chest Physicians have discouraged the use of the term rhon-
chi, recommending instead that the term wheezes be used for all
continuous adventitious breath sounds.20 Many health care pro-
viders in hospitals and clinics continue to use the term rhonchi;
therefore it is mentioned in this section.
Continuous Sounds
Wheeze.  Wheezes occur most commonly with airway obstruc-
tion from bronchoconstriction or retained secretions and com-
monly are heard on expiration. Wheezes also may be present
during inspiration if the obstruction is significant enough.
Wheezes can be high pitched (usually from bronchospasm or
constriction, as in asthma) or low pitched (usually from secre-
tions, as in pneumonia).15  to distal airways. Voice sounds that are more or less pronounced
Stridor.  Stridor is an extremely high-pitched wheeze that
occurs with significant upper airway obstruction and is pres-
ent during inspiration and expiration. The presence of stridor
indicates a medical emergency. Stridor is also audible without
a stethoscope.16
  CLINICAL TIP
Acute onset of stridor during an intervention session warrants
immediate notification of the nursing and medical staff.
 
Rhonchi.  Low-pitched or “snoring” sounds that are continuous
characterize rhonchi. These sounds generally are associated with large
airway obstruction, typically from secretions lining the airways.15  spaces or lung parenchyma is suspected.
  CLINICAL TIP
Wet crackles also can be referred to as rales; however, the Amer-
ican Thoracic Society and the American College of Chest Physi-
cians have moved to eliminate this terminology for purposes of
standardization.20
 
Extrapulmonary Sounds
These sounds are generated from dysfunction outside of the lung
tissue. The most common sound is the pleural friction rub. This
both phases of respiration, and almost always is associated with
pleuritis (inflamed pleurae rubbing on one another).15,19 The
sound is often described as that caused by two pieces of leather
rubbing together. The presence of a chest tube inserted into the
pleural space also may cause a sound similar to a pleural rub.15
  CLINICAL TIP
Auscultation should be used to guide selection of interventions,
assess for changes in patient status and determine the effective-
ness of treatment (i.e., high-pitched wheezes could justify inter-
ventions to promote opening airways, and location and degree
of wet crackles can help assess effectiveness of airway clearance
techniques).  
Voice Sounds
Normal phonation is audible during auscultation, with the
intensity and clarity of speech also dissipating from proximal
in distal lung regions, where vesicular breath sounds should
occur, may indicate areas of consolidation or hyperinflation,
respectively. The same areas of auscultation should be used when
assessing voice sounds. The following three types of voice sound
tests can be used to help confirm breath sound findings15,16:
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
 
66 CHAPTER 4     Pulmonary System
A Direct measurement of chest wall expansion can be used for
B ventilation impairments. Changes in these values after an inter-
C
FIG. 4.5
Palpation of (A) upper, (B) middle, and (C) lower chest wall motion. (Cour-
tesy Peter P. Wu.)
Palpation
The third component of the physical examination is palpation of
the chest wall, which is performed in a cephalocaudal direction.
Fig. 4.5 demonstrates hand placement for chest wall palpation
of the upper, middle, and lower lung fields. Palpation is per-
formed to examine the following:
• Presence of fremitus (a vibration caused by the presence of se-
cretions or voice production, which is felt through the chest
wall) during respirations14
• Presence, location, and reproducibility of pain, tenderness, or
both
• Skin temperature
• 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 sub-
cutaneous tissue). This finding is abnormal and represents air
that has escaped or is escaping from the lungs. Subcutaneous
emphysema can occur from a pneumothorax (PTX), a com-
plication from central line placement, after thoracic surgery,
or laparoscopic abdominal surgery.1
  CLINICAL TIP
To decrease patient fatigue while palpating each of the chest
wall segments for motion, all of the items listed above can be
examined simultaneously.
Chest Wall and Abdominal Excursion
objective data collection, intervention, or goal setting. Begin by
placing a tape measure snugly around the circumference of the
patient’s chest wall at three levels:
1. Angle of Louis
2. Xyphoid process
3. Umbilicus
Measure the change in circumference in each of these areas
with normal breathing and then deep breathing. The resulting
values can be used to describe breathing patterns or identify
vention may indicate improvements in breathing patterns and
can be used to evaluate treatment efficacy. Normal changes in
breathing patterns exist in the supine, sitting, and standing
positions.21
  CLINICAL TIP
By placing your thumb tips together on the spinous processes
or xyphoid process, you can estimate the distance of separation
between your thumb tips to qualitatively measure chest wall
motion.
 
Posture and Musculoskeletal Examination
Difficulty breathing can lead to trunk muscles shifting more
support to respiration while decreasing their ability to func-
tion as posture muscles. In addition to abnormal thoracic pres-
sures this change in function can lead to postural impairments.
These impairments and poor alignment, in turn, do not allow
for proper respiration mechanics. Particular attention should be
paid to the examination of alignment, range of motion (ROM),
flexibility, muscle balance and motor control of the shoulders,
scapulae, spine, rib cage and pelvis.22
  CLINICAL TIP
Writing goals that address pain and breathing mechanics can
help justify musculoskeletal interventions for patients with high
functional mobility.
Mediate Percussion
Mediate percussion can evaluate tissue densities within the tho-
racic cage and indirectly measure diaphragmatic excursion dur-
ing respirations. Mediate percussion also can be used to confirm
other findings in the physical examination. The procedure is
shown in Fig. 4.6 and is performed by placing the palmar sur-
face of the index finger, middle finger, or both from one hand

FIG. 4.6
Demonstration of mediate percussion technique. (From Hillegass EA, Sad-
owsky HS. Essentials of Cardiopulmonary Physical Therapy. 2nd ed. Philadel-
phia: Saunders; 2001.)
flatly against the surface of the chest wall within the intercos-
tal spaces. The tip of the other index finger, middle finger, or
a combination of both then strike the distal third of the fin-
gers resting against the chest wall. The clinician proceeds from
side to side in a cephalocaudal fashion, within the intercostal
spaces, for anterior and posterior aspects of the chest wall. Medi-
ate percussion is a difficult skill and is performed most profi-
ciently by experienced clinicians; mediate percussion also can be
performed over the abdominal cavity to assess tissue densities,
which is described further in Chapter 8.
Sounds produced from mediate percussion can be character-
ized 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)15
To evaluate diaphragmatic excursion with mediate percus-
sion, the clinician first delineates the resting position of the dia-
phragm by percussing down the posterior 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 diaphrag-
matic excursion. The other side is also examined, and a compari-
son then can be made of the hemidiaphragms.15,16 
Cough Examination
An essential component of airway clearance is cough effective-
ness. 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
Pulmonary System     CHAPTER 4 67
the cough mechanism can lead to impaired secretion clearance.
Cough examination includes the following components14,15:
• 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 oc-
curs)
• Sputum production (color, quantity, odor, and consistency)
The effectiveness of the patient’s cough can be examined
directly by simply asking the patient to cough or indirectly
by observing the above components when the patient coughs
spontaneously. 
Hemoptysis
Hemoptysis, the expectoration of blood during coughing, may
occur for many reasons. Hemoptysis is usually benign postop-
eratively if it is not sustained with successive coughs. The thera-
pist should note whether the blood is dark red or brownish in
color (old blood) or bright red (new or frank blood). The pres-
ence of new blood in sputum should be documented and the
nurse or the physician notified.23
Patients with cystic fibrosis may have periodic episodes of
hemoptysis with streaking or larger quantities of new blood.
During these episodes airway clearance techniques (ACTs) may
need to be modified. Current recommendations for patients who
have scant hemoptysis (<5 mL) are to continue with all ACT,
and those with massive hemoptysis (>240 mL) should discon-
tinue all ACTs. For persons with mild to moderate hemopty-
sis (≥5 mL), no clear recommendations exist for continuing or
discontinuing ACTs. However, expert consensus is that auto-
genic drainage and active cycle of breathing techniques are least
likely to exacerbate hemoptysis while maintaining the needs of
assisted sputum clearance.23 
Diagnostic Testing
Oximetry
Pulse oximetry is a noninvasive method of determining arte-
rial oxyhemoglobin saturation (SaO2) through the measurement
of the saturation of peripheral oxygen (SpO2). It also indirectly
examines the partial pressure of O2. Finger or ear sensors gener-
ally are applied to the patient on a continuous or intermittent
basis. O2 saturation readings can be affected by poor circulation
(cool digits), movement of sensor cord, cleanliness of the sensors,
nail polish, intense light, increased levels of carboxyhemoglobin
(HbCO2), jaundice, skin pigmentation, shock states, cardiac
dysrhythmias (e.g., atrial fibrillation), and severe hypoxia.24,25
  CLINICAL TIP
To ensure accurate oxygen (O2) saturation readings, (1) check
for proper waveform or pulsations, which indicate proper signal
reception, and (2) compare pulse readings on an O2 saturation
monitor with the patient’s peripheral pulses or electrocardiogra-
phy (ECG) readings (if available).
68 CHAPTER 4     Pulmonary System

Oxyhemoglobin saturation is an indication of pulmonary
reserve and is dependent on the PO2 level in the blood. Fig. 4.7
demonstrates the direct relationship of oxyhemoglobin satura-
tion and partial pressures of O2. As shown on the steep portion
of the curve, small changes in PO2 levels below 60 mmHg result
in large changes in oxygen saturation, which is considered mod-
erately hypoxic.11 The relationship between oxygen saturation
and PO2 levels is further summarized in Table 4.6. The affinity
or binding of O2 to hemoglobin is affected by changes in pH,
PCO2, temperature, and 2,3-diphosphoglycerate (a by-product
of red blood cell metabolism) levels. Note that pulse oxime-
try can measure only changes in oxygenation (PO2) indirectly
and cannot measure changes in ventilation (PCO2). Changes
100
SaO2 (O2 saturation %)
in ventilation must be measured by arterial blood gas (ABG)
analysis.26 This is especially important in patients who have
anemia, and thus lower oxygen-carrying capacity, but who may
have normal oxyhemoglobin saturation but lower PO2. 
Blood Gas Analysis
Arterial Blood Gas Analysis
ABG analysis examines acid-base balance (pH), ventilation
(CO2 levels), and oxygenation (O2 levels) and guides medical or
therapy interventions, such as mechanical ventilation settings
or breathing assist techniques.14 For proper cellular metabolism
to occur, acid-base balance must be maintained. Disturbances
in acid-base balance can be caused by pulmonary or metabolic
dysfunction (Table 4.7). Normally the pulmonary and meta-
bolic systems work in synergy to help maintain acid-base bal-
ance. Clinical presentation of carbon dioxide retention, which

80 can occur in patients with lung disease, is outlined in Box 4.1.

The ability to interpret ABGs provides the physical thera-
60 pist with valuable information regarding the current medical
status of the patient, the appropriateness for airway clearance or
40 exercise treatments, and the outcomes of medical and physical
therapy intervention.
20
ABG measurements usually are performed on a routine basis,
which is specified according to need in the critical care setting.
0
0 20 40 60 80 100 120 For the patient who is critically ill, ABG measurements may
PaO2 (O2 partial pressure) be done every 1 to 3 hours. In contrast, ABGs may be mea-
sured one or two times a day in a patient whose pulmonary or
FIG. 4.7 metabolic status has stabilized. Unless specified, arterial blood
The oxyhemoglobin dissociation curve. (Courtesy Marybeth Cuaycong.)
is drawn from an indwelling arterial line. Other sites of access
include arterial puncture, venous blood from a peripheral venous

TABLE 4.7  Potential Causes of Acid–Base Imbalances

TABLE 4.6  Relationship Between Oxygen Saturation, the Respiratory Metabolic
Partial Pressure of Oxygen, and the Signs and Symptoms
of Hypoxemia Acidosis Chronic obstructive Lactic acidosis
pulmonary disease Ketoacidosis:
Oxyhemoglobin Oxygen Partial Sedation Diabetes
Saturation (SaO2) Pressure (PaO2) Signs and Symptoms Head trauma Starvation
(%) (mmHg) of Hypoxemia Drug overdose Alcoholism
Pneumothorax Diarrhea
97–99 90–100 None Central nervous system Parenteral nutrition
95 80 Tachypnea disorders
Tachycardia Pulmonary edema
90 60 As above Sleep apnea
Restlessness Chest wall trauma
Malaise Alkalosis Pulmonary embolism Vomiting
Impaired judgment Pregnancy Nasogastric suction
Incoordination Anxiety/fear Diuretics
Vertigo Hypoxia Steroids
Nausea Pain Hypokalemia
85 50 As above Fever Excessive ingestion of
Labored respiration Sepsis antacids
Cardiac dysrhythmia Congestive heart failure Administration of bi-
Confusion Pulmonary edema carbonate (HCO3)
Asthma Banked blood transfu-
80 45 As above Acute respiratory distress sions
75 40 As above syndrome Cushing’s syndrome

From Frownfelter DL, Dean E. Principles and Practice of Cardiopulmonary Physical From George-Gay B, Chernecky CC, eds. Clinical Medical-Surgical Nursing: A
Therapy. 4th ed. St. Louis: Mosby; 2006. Decision-Making Reference. Philadelphia: WB Saunders; 2002.
 Pulmonary System     CHAPTER 4 69

puncture or catheter, and mixed venous blood from a pulmonary Normal Values.  The normal ranges for ABGs are as
artery catheter. Chapter 18 describes vascular monitoring lines follows28:
in more detail.
Terminology.  The following terms are frequently used in PaO2 Greater than 80 mmHg
ABG analysis27: PaCO2 35–45 mmHg
• PaO2 (PO2): Partial pressure of dissolved O2 in plasma pH 7.35–7.45
• PaCO2 (PCO2): Partial pressure of dissolved CO2 in plasma HCO3 22–26 mEq/L
• pH: Degree of acidity or alkalinity in blood
• HCO3: Level of bicarbonate in the blood ABGs generally are reported in the following format: pH/
• Percentage of SaO2 (O2 saturation): A percentage of the amount PaCO2/PaO2/HCO3 (e.g., 7.38/42/90/26). 
of hemoglobin sites filled (saturated) with O2 molecules (PaO2 Interpretation.  Interpretation of ABGs29 includes the abil-
and SaO2 are intimately related but are not synonymous)  ity to determine any deviation from normal values and hypoth-
esize a cause (or causes) for the acid-base disturbance in relation
BOX 4.1  Clinical Presentation of Carbon Dioxide to the patient’s clinical history. Acid-base balance—or pH—is
Retention and Narcosis the most important ABG value for the patient to have within
normal limits (Fig. 4.8). It is important to relate the ABG val-
•  ltered mental status
A ues to the patient’s medical history and the clinical course of the
• Lethargy disease. ABG values and vital signs generally are documented
• Drowsiness
• Coma on a daily flow sheet, which is an invaluable source of informa-
• Headache tion. Because changes in ABG are not immediately available in
• Tachycardia most circumstances, the value of this test is to observe changes
• Hypertension over time. Single ABG readings should be correlated with pre-
• Diaphoresis vious ABG readings, medical status, supplemental O2 or ven-
• Tremor
• Redness of skin, sclera, or conjunctiva tilator changes, and medical procedures. Be sure to note if an
ABG sample is drawn from mixed venous blood because the
From Kersten LD. Comprehensive Respiratory Nursing: A Decision-Making Ap- normal O2 value is lower. PO2 of mixed venous blood is 35 to
proach. Philadelphia: Saunders; 1989:351. 40 mmHg.

Evaluate pH & Blood Gases

pH < 7.40 pH > 7.40

Acidosis Alkalosis

Decreased HCO3– Increased PaCO2 Decreased PaCO2 Increased HCO3–

Metabolic Respiratory Respiratory Metabolic

Acidosis Acidosis Alkalosis Alkalosis

Decreased Normal Normal Increased Decreased Normal Normal Increased

PaCO2 PaCO2 HCO3– HCO3– HCO3– HCO3– PaCO2 PaCO2

Attempting to No Compensation Attempting to Attempting to No Compensation Attempting to

Compensate Compensate Compensate Compensate
FIG. 4.8
Methods to analyze arterial blood gases. (From Cahalin LP. Pulmonary evaluation. In: DeTurk WE, Cahalin LP,
eds. Cardiovascular and Pulmonary Physical Therapy. 2nd ed. New York: McGraw Hill; 2011:265.)
70 CHAPTER 4     Pulmonary System

Acid-base disturbances that occur clinically can arise from

pulmonary and metabolic disorders; therefore interpretation
of the ABG results may not prove to be as straightforward as
shown in Fig. 4.8. The clinician must use this information as
part of a complete examination process to gain full understand-
ing of the patient’s current medical status. 

Venous Blood Gas Analysis

Although not as common as ABG analysis, venous or mixed
venous blood gas (VBG) analysis30 also can provide important
information to the clinician. VBGs CO2 (PvCO2) and O2 (SvO2)
values represent the body’s metabolic workload and efficiency
for any given state. Large increases in PvCO2 values can rep-
resent inefficient/deconditioned peripheral muscles or overall
deconditioning associated with acute/chronic illness.
PvCO2 and cardiac output (estimated) values can be observed
in patients with central catheters and may be continuously A
monitored in those receiving tailored therapy for advanced heart
failure. Direct monitoring of SvCO2 values and cardiac output
during an exercise session can help direct your treatment and
recommendations. 

Chest X-Ray (Radiography)

Radiographic information of the thoracic cavity in combination
with a clinical history provides critical assistance in the differ-
ential diagnosis of pulmonary conditions. Diagnosis cannot be
made with chest x-ray (CXR, or radiography) alone; the thera-
pist should use CXR reports as a guide for decision making and
not as an absolute parameter for airway clearance evaluation and
treatment.

  CLINICAL TIP
CXRs sometimes lag behind significant clinical presentation
(e.g., symptoms of pulmonary infection may resolve clinically,
whereas CXR findings remain positive for infection). CXR also
can be a helpful tool to guide airway clearance interventions.
Indications for CXRs are as follows31,32:
• Assistance in the clinical diagnosis and monitor the progres-
sion or regression of the following:
• Airspace consolidation (pulmonary edema, pneumonia, adult
respiratory distress syndrome [ARDS], pulmonary hemor-
rhage, and infarctions)
• Large intrapulmonary air spaces and presence of mediastinal
or subcutaneous air, as well as pneumothorax
• Lobar atelectasis
• Other pulmonary lesions, such as lung nodules and abscesses
• Rib fractures
• Determination of proper placement of endotracheal tubes,
central lines, chest tubes, or nasogastric tubes
• Evaluation of structural features, such as cardiac or mediasti-
nal size and diaphragmatic shape and position
CXRs are classified according to the direction of projection
of the x-ray beam. The first word describes where the beam
enters the body, and the second word describes the exit. Com-
mon types of CXRs include the following:
B
FIG. 4.9
(A) Normal chest radiograph (posteroanterior view). (B) Same radiograph
as in (A) with normal anatomic structures labeled or numbered. (1, Trachea;
2, right main stem bronchus; 3, left main stem bronchus; 4, left pulmonary
artery; 5, pulmonary vein to the right upper lobe; 6, right interlobar artery;
7, vein to right middle and lower lobes; 8, aortic knob; 9, superior vena
cava; 10, ascending aorta.) (From Fraser RS, Müller NL, Colman N, Paré
MD. Diagnosis of Diseases of the Chest. 4th ed. Philadelphia: Saunders; 1999.)
• P osterior-anterior (P-A): Taken while the patient is upright
sitting or standing
• Anterior-posterior (A-P): Taken while the patient is upright
sitting or standing, semireclined, or supine
• Lateral: Taken while the patient is in the upright sitting or
standing position or in the decubitus position (lying on the side)
Upright positions are preferred to allow full expansion of
lungs without hindrance of the abdominal viscera and to visu-
alize gravity-dependent fluid collections. Lateral films aid in
three-dimensional, segmental localization of lesions and fluid
collections not visible in the 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, whereas air
appears black. Moderately dense structures, such as the heart,
 Pulmonary System     CHAPTER 4 71

aorta, and pulmonary vessels, appear gray, as do fluids, such as

pulmonary edema and blood.9 Fig. 4.9 outlines the anatomic BOX 4.2  Diagnostic and Therapeutic Indications for Flex-
structures used for chest x-ray (CXR) interpretation. ible Bronchoscopy
A systematic approach to a basic CXR interpretation is
Diagnostic Indications Therapeutic Indications
important. First, the densities of the various structures to iden-
tify air, bone, tissue, and fluid are examined, followed by deter- • E  valuation of neoplasms (benign • Removal of retained
or malignant) in air spaces and secretions, foreign bod-
mining whether the findings are normal or abnormal and are mediastinum, tissue biopsy ies, and/or obstructive
consistent on both sides of the lungs. Common CXR findings • Evaluation of the patient before endotracheal tissue
with various pulmonary diagnoses are discussed in the Health and after lung transplantation • Intubation or stent
Conditions section of this chapter.  • Endotracheal intubation placement
• Infection, unexplained chronic • Bronchoalveolar lavage
Sputum Analysis cough, or hemoptysis • Aspiration of cysts
• Tracheobronchial stricture and ­ordrainage of abscesses
Analysis of sputum includes culture and Gram stain to isolate stenosis • Pneumothorax or lobar
and identify organisms that may be present in the lower respi- • Hoarseness or vocal cord paralysis collapse
ratory tract.33 Refer to Chapter 13 for more details on culture • Fistula or unexplained pleural ef- • Thoracic trauma
and Gram stain. After the organisms are identified, appropri- fusion • Airway maintenance
• Localized wheezing or stridor (tamponade for bleed-
ate antibiotic therapy can be instituted. Sputum specimens • Chest trauma or persistent ing)
are collected when the patient’s temperature rises or the color pneumothorax
or consistency of sputum changes. These tests also can be used • Postoperative assessment of tra-
to evaluate the efficacy of antibiotic therapy. Sputum analy- cheal, tracheobronchial, bron-
sis can be inaccurate if a sterile technique is not maintained chial, or stump anastomosis
during sputum collection or if the specimen is contaminated
Data from Hetzed MR. Minimally Invasive Techniques in Thoracic Medicine and
with too much saliva, noted microscopically as the presence of Surgery. London, UK: Chapman & Hall; 1995; Rippe JM, Irwin RS, Fink MP,
many squamous epithelial cells. Therapists involved in airway et al. Procedures and Techniques in Intensive Care Medicine. Boston: Little, Brown;
clearance and sputum sample collection should have sterile 1994; Malarkey LM, McMorrow ME. Nurse’s Manual of Laboratory Tests and Di-
agnostic Procedures. 2nd ed. Philadelphia: Saunders; 2000.
sputum collection containers and equipment on hand before
beginning the treatment session to ensure successful sputum During a ventilation scan, inert radioactive gases or aero-
collection. sols are inhaled, and three subsequent projections (i.e., after the
first breath, at equilibrium, and during washout) of airflow are
  CLINICAL TIP recorded.
During a perfusion lung scan, a radioisotope is injected
Patients with a negative result on sputum analysis for active intravenously into a peripheral vessel, and six projections are
infection may still have retained secretions that could hinder gas taken (i.e., anterior, posterior, both laterals, and both posterior
exchange and tolerance to activity. Therefore therapists must obliques). The scan is sensitive to diminished or absent blood
evaluate clinically the need for secretion clearance techniques. flow, and lesions of 2 cm or greater are detected.
 
Perfusion defects can occur with pulmonary embolus,
asthma, emphysema, and virtually all alveolar filling, destruc-
Flexible Bronchoscopy tive or space-occupying lesions in lung, and hypoventilation.
A flexible, fiberoptic tube is used as a diagnostic and interven- CXR a few hours after the perfusion scan helps the differential
tional tool to visualize directly and aspirate (suction) the bron- diagnosis.
chopulmonary tree. If a patient is mechanically ventilated, the Ventilation scans are performed first, followed by perfusion
bronchoscope is inserted through the endotracheal or tracheal scan. The two scans are then compared to determine extent of
tube. Refer to Chapter 18 for more information on mechanical V̇/Q̇ matching. As described earlier in the Ventilation-to-Perfu-
ventilation and endotracheal and tracheal tubes. If the patient is sion Ratio section, average reference V̇/Q̇ ratio is approximately
breathing spontaneously, a local anesthetic is applied, and light equal to 0.8.34,36 
sedation via intravenous access is given before the bronchoscope
is inserted through one of the patient’s nares. Bronchoscopy also Computed Tomographic Pulmonary Angiography
can be performed with a rigid bronchoscope. This is primarily Computed tomographic pulmonary angiography (CT-PA) is
an operative procedure.34,35 a minimally invasive test that allows for direct visualization of
Box 4.2 summarizes the diagnostic and therapeutic indica- the pulmonary artery and subsequently facilitates rapid detec-
tions for bronchoscopy.  tion of a thrombus. CT-PA is most useful for detecting a clot in
the main or segmental vasculature. In recent years, CT-PA has
Ventilation-Perfusion Scan become the preferred method to diagnose acute PE, rather than
The V̇/Q̇ scan is used to rule out the presence of pulmonary V̇/Q̇ scanning.37,38 The benefits of CT-PA include its wide avail-
embolism (PE) and other acute abnormalities of oxygenation ability for testing, high sensitivity, and rapid reporting. The test
and gas exchange and as preoperative and postoperative evalua- is also useful in determining other pulmonary abnormalities that
tion of lung transplantation. may be contributing to a patient’s symptoms. The American and
72 CHAPTER 4     Pulmonary System

FIG. 4.10
Lung volumes. (From Yentis SM, Hirsch NP, Smith GB, eds. Anesthesia and Intensive Care A-Z: An Encyclope-
dia of Principles and Practice. 2nd ed. Oxford, UK: Butterworth-Heinemann; 2000:340.)

European Thoracic Societies have incorporated CT-PA into their
algorithms for diagnosing PE.39,40 The PIOPED II (Prospective
Investigation of Pulmonary Embolism Diagnosis) trial also rec-
ommended CT-PA as the first-line imaging test to diagnose PE.41 
Pulmonary Function Tests
Pulmonary function tests (PFTs) consist of measuring the
patient’s lung volumes and capacities, in addition to inspiratory
and expiratory flow rates. Lung capacities are composed of two
or more lung volumes. Quantification of these parameters helps
distinguish obstructive from restrictive respiratory patterns, in
addition to determining how the respiratory system contrib-
utes to physical activity limitations. The respiratory system’s
volumes and capacities are shown in Fig. 4.10. Alterations in
volumes and capacities occur with obstructive and restrictive
diseases; these changes are shown in Fig. 4.11.
Volume, flow, and gas dilution spirometers and body pleth-
ysmography are the measurement tools used for PFTs. A flow-
volume loop also is included as part of the patient’s PFTs and is
shown in Fig. 4.12. 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
4.8 outlines the measurements performed during PFTs. Forced
expiratory volume in 1 second (FEV1), forced vital capacity (FVC),
and the FEV1/FVC ratio are the most commonly interpreted PFT
values. These measures represent the degree of airway patency
during expiration, which affects airflow in and out of the lung.
The normal range of values for PFTs is variable and depends
on a person’s age, sex, height, ethnic origin, and weight (body
surface area). Normal predicted values for a person’s given age,
sex, and height are provided in the PFT report and determined
by prediction equations.29
  CLINICAL TIP
For example, based on a nomogram, the following predicted
values for forced vital capacity (FVC) and forced expiratory vol-
ume in 1 second (FEV1) would be approximately the following42:
•  FVC = 4.1 L; FEV1 = 3 L for a man who is 55 years old and
66 inches tall
•  FVC = 2.95 L; FEV1 = 2.2 L for a woman who is 55 years old
and 62 inches tall
•  More information can be obtained by comparing a patient’s
pulmonary function test (PFT) results with baseline values for
insight on the severity of an exacerbation or with trends over
time to understand the patient’s disease progression.
Indications for PFTs are as follows42–44:
• Detection and quantification of respiratory disease and type
of disease (e.g., restrictive versus obstructive)
• E valuation of pulmonary involvement in systemic dis-
eases
• Assessment of disease progression
• E valuation of impairment, activity limitation, or dis-
ability
• Assessment for bronchodilator therapy or surgical interven-
tion, or both, along with subsequent response to the respec-
tive intervention
• Preoperative evaluation (identification of high-risk patients) 
 Pulmonary System     CHAPTER 4 73

NORMAL LUNG OBSTRUCTED LUNG

RV, FRC, RV/TLC
VC, IC, ERV

IRV VT RV ERV TLC VC IC FRC

VC, RV, FRC, VT, VC, IC, ERV

and TLC

NORMAL LUNG RESTRICTED LUNG

IRV VT RV ERV TLC VC IC FRC

B
FIG. 4.11
(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 Des Jardins T, Burton GC, eds. Clinical Manifestations and Assessment of Respiratory Disease.
3rd ed. St. Louis: Mosby; 1995:40, 49.)

and restrictive processes, or with a combination of both as a

Health Conditions result of environmental, traumatic, orthopedic, neuromuscular,
nutritional, or drug-induced factors. These disorders may be
Respiratory disorders can be classified as obstructive or restric- infectious, neoplastic, or vascular or involve the connective tis-
tive. A patient may present with single or multiple obstructive sue of the thorax.14
74 CHAPTER 4     Pulmonary System

A B

C D
FIG. 4.12
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. (From Yentis 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.)

TABLE 4.8  Description and Clinical Significance of Pulmonary Function Tests

Test Description Significance
Lung Volume Tests
Tidal volume (VT) The volume of air inhaled or exhaled during a Decreased tidal volume could be indicative of atelectasis, fatigue,
single breath in a resting state. restrictive lung disorders, and tumors.
Inspiratory reserve vol- The maximum amount of air that can be in- Decreased IRV could be indicative of obstructive pulmonary
ume (IRV) spired after a normal inspiration. disease.
Expiratory reserve vol- The maximum amount of air that can be ex- ERV is necessary to calculate residual volume and FRC. De-
ume (ERV) haled after a normal exhalation. creased values could be indicative of ascites, pleural effusion, or
pneumothorax (PTX).
Residual volume (RV) The volume of air remaining in the lungs at RV helps differentiate between obstructive and restrictive disor-
the end of maximal expiration that cannot be ders.
forcibly expelled. An increased RV indicates an obstructive disorder, and a de-
creased RV indicates a restrictive disorder.
Total lung capacity (TLC) The volume of air contained in the lung at the TLC helps differentiate between obstructive and restrictive
end of maximal inspiration (TLC = VT + IRV disorders.
+ ERV + RV). An increased TLC indicates an obstructive disorder; a decreased
TLC indicates a restrictive disorder.
Vital capacity (VC) The maximum amount of air that can be ex- A decreased VC can result from a decrease in lung tissue distensi-
pired slowly and completely after a maximal bility or depression of the respiratory centers in the brain.
inspiration (VC = VT + IRV + ERV).
Functional residual The volume of air remaining in the lungs at the FRC values help differentiate between obstructive and restrictive
capacity (FRC) end of a normal expiration. respiratory patterns.
Calculated from body plethysmography (FRC = An increased FRC indicates an obstructive respiratory pattern,
ERV + RV). and a decreased FRC indicates a restrictive respiratory pattern.
Inspiratory capacity (IC) The largest volume of air that can be inspired Changes in IC usually parallel changes in VC.
in one breath from the resting expiratory level Decreased values could be indicative of restrictive disorders.
(IC = VT + IRV).
 Pulmonary System     CHAPTER 4 75

TABLE 4.8  Description and Clinical Significance of Pulmonary Function Tests—cont’d

Test Description Significance
Residual volume to total The percentage of air that cannot be expired in Values >35% are indicative of obstructive disorders.
lung capacity ratio relation to the total amount of air that can be
(RV : TLC × 100) brought into the lungs.
Ventilation Tests
Minute volume (VE) or The total volume of air inspired or expired in 1 VE is most commonly used in exercise or stress testing.
minute ventilation minute (VE = VT × respiratory rate). VE can increase with hypoxia, hypercapnia, acidosis, and exercise.
Respiratory dead space The volume of air in the lungs that is ventilated VD provides information about available surface area for gas
(VD) but not perfused in conducting airways and exchange.
nonfunctioning alveoli. Increased dead space = decreased gas exchange.
Alveolar ventilation (VA) The volume of air that participates in gas VA measures the amount of oxygen available to tissue, but it
exchange. should be confirmed by arterial blood gas measurements.
Estimated by subtracting dead space from tidal
volume (VA = VT − VD).
Pulmonary Spirometry Tests
Forced vital capacity The volume of air that can be expired forcefully FVC is normally equal to VC, but FVC can be decreased in
(FVC) and rapidly after a maximal inspiration. obstructive disorders.
Forced expiratory volume The volume of air expired over a time interval A decrease in FEV1 can indicate either obstructive or restrictive
timed (FEVt) during the performance of an FVC maneuver. airway disease.
The interval is usually 1 second (FEV1). With obstructive disease, a decreased FEV1 results from increased
After 3 seconds, FEV should equal FVC. 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% (usually FEV1/ The percent of FVC that can be expired over a FEV% is a better discriminator of obstructive and restrictive
FVC × 100) given time interval, usually 1 second. disorders than FEVt.
An increase in FEV1/FVC indicates a restrictive disorder, and a
decrease in FEV1/FVC indicates an obstructive disorder.
Forced expiratory flow The average flow of air during the middle 50% A decrease in (FEF25%–75%) generally indicates obstruction in the
25%–75% (FEF25%– of an FEV maneuver. small to medium-sized airways.
75%) Used in comparison with VC.
Represents peripheral airway resistance.
Peak expiratory flow rate The maximum flow rate attainable at any time PEFR can assist with diagnosing obstructive disorders such as
(PEFR) during an FEV. asthma.
Maximum voluntary The largest volume of air that can be breathed MVV measures status of respiratory muscles, the resistance of-
ventilation (MVV) per minute by maximal voluntary effort. fered by airways and tissues, and the compliance of the lung
Test lasts 10 or 15 seconds and is multiplied by and thorax.
6–4, respectively, to determine the amount of
air that can be breathed in a minute (liters/
minute [L/min]).
Flow-volume loop (F-V A graphic analysis of the maximum forced expi- The distinctive curves of the F-V loop are created according to
loop) ratory flow volume, followed by a maximum the presence or absence of disease.
inspiratory flow volume. Restrictive disease demonstrates an equal reduction in flow and
volume, resulting in a vertical oval loop. Obstructive disease
demonstrates a greater reduction in flow compared with vol-
ume, resulting in a horizontal tear-shaped loop.
Gas Exchange
Diffusing capacity of car- A known mixture of carbon monoxide and DLCO assesses the amount of functioning pulmonary capillary
bon monoxide (DLCO) helium gas inhaled and then exhaled after bed in contact with functioning alveoli (gas exchange area).
10 seconds, and the amount of gases are
remeasured.

Adapted from Thompson JM, McFarland GK, Hirsch JE, et al, eds. Clinical Nursing Practice. 5th ed. St. Louis: Mosby; 2002; and data from Malarkey LM, Morrow ME,
eds. Nurse’s Manual of Laboratory Tests and Diagnostic Procedures. 2nd ed. Philadelphia: Saunders; 2000:293-297.
76 CHAPTER 4     Pulmonary System
Common terminology often used to describe respiratory dys-
function is listed below:16,27,29
• 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 alveo-
lar air
• Hyperinflation: Overinflation of the lungs at resting volume as
a result of air trapping
• Hypoxemia: A low level of oxygen in the blood, usually a
PaO2 less than 60 to 80 mmHg
• Hypoxia: A low level of oxygen in the tissues available for cell
metabolism
• Respiratory distress: The acute or insidious onset of dyspnea,
respiratory muscle fatigue, abnormal respiratory pattern
and rate, anxiety, and cyanosis related to inadequate gas ex-
change; the clinical presentation that usually precedes respi-
ratory failure
• Respiratory failure: The inability of the pulmonary system to
maintain an adequate exchange of oxygen and carbon dioxide
(refer to Chapter 18A for information on mechanical ventilation)
Obstructive Pulmonary Conditions
Obstructive lung diseases or conditions may be described by
onset (acute or chronic), severity (mild, moderate, or severe), and
location (upper or lower airway). Obstructive pulmonary pat-
terns are characterized by decreased airflow out of the lungs as a
result of narrowing of the airway lumen. This causes increased
dead space and decreased surface area for gas exchange.45
The term chronic obstructive pulmonary disease (COPD) refers to
airflow limitation that is not fully reversible. The Global Initia-
tive for Obstructive Lung Disease (GOLD) states that the air-
flow limitation in COPD is usually progressive and associated
with an abnormal inflammatory response to noxious particles or
gases.46 The diagnosis of COPD is confirmed with spirometric
testing. Patients with COPD typically have a combination of
chronic bronchitis, emphysema, and small airway obstruction.47
Table 4.9 outlines obstructive disorders, their general physical
and diagnostic findings, and their general clinical management.
Asthma
Asthma is an inflammatory disorder with bronchial hyper-
responsiveness, characterized by episodes of coughing, wheez-
ing, breathlessness and chest tightness usually associated with
reversible airflow obstruction.48 The asthmatic exacerbation
may be immediate or delayed, resulting in air entrapment and
alveolar hyperinflation during the episode with symptoms dis-
appearing between attacks. The primary characteristics of an
asthma exacerbation are as follows:
• Bronchial smooth muscle constriction
• Mucus production (without infection) resulting from the in-
creased presence of leukocytes, such as eosinophils
• Bronchial mucosa inflammation and thickening resulting
from cellular and fluid infiltration49
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 40% of predicted
or personal best.48 Status asthmaticus is a severe, life-threatening
airway obstruction with the potential for cardiopulmonary com-
plications, such as arrhythmia, heart failure, and cardiac arrest.
Status asthmaticus is not responsive to basic medical therapies
and is characterized by severe hypoxemia and hypercarbia that
require assisted or mechanical ventilation.50 
Chronic Bronchitis
Chronic bronchitis is the presence of cough and pulmonary
secretion expectoration for at least 3 months, 2 years in a
row.28,51 Chronic bronchitis usually is linked to cigarette smok-
ing or, less likely, to air pollution or infection. It begins with
the following10:
• Narrowing of large, then small, airways because of inflam-
mation 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 bronchi-
tis is vague.52 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 produc-
tion 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 severity of symptoms, response to initial medi-
cal management, serious comorbidities, home support, and the
presence of acute respiratory failure or new physical signs.53 
Emphysema
Emphysema may be genetic (alpha1-antitrypsin protein defi-
ciency), in which the lack of proteolytic inhibitors allows the
alveolar interstitium to be destroyed, or it may be caused by
cigarette smoking, air pollutants, or infection. Three types of
emphysema occur: centrilobular (centriacinar), panlobular (pan-
acinar), 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.54
Emphysema leads to progressive destruction of alveolar walls
and adjacent capillaries secondary to the following10:
• Decreased pulmonary elasticity
• Premature airway collapse
• Bullae formation (a bulla is a pocket of air surrounded by
walls of compressed lung parenchyma)
These changes result in decreased lung elasticity, air trap-
ping, and hyperinflation.55 Reasons for hospital admission are
similar to those in a patient with chronic bronchitis, except that
cor pulmonale does not develop until the late stages of emphy-
sema. 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. 
 Pulmonary System     CHAPTER 4 77

TABLE 4.9  Characteristics and General Management of Obstructive Disorders

Disorder Observation Palpation Auscultation Cough Chest X-Ray Management
Asthma Tachypnea Tachycardia, with weak Polyphonic Tight, usually During exacerba- Removal of causative
(exacerba- Fatigue pulse on inspiration wheezing on nonproduc- tion: trans- agent
tion) Anxiety Increased A-P chest expiration > tive, then lucent lung Bronchodilators
Pursed lip breath- diameter inspiration slightly fields, flattened Corticosteroids
ing Decreased tactile and Diminished productive diaphragms, Supplemental O2
Active expiration vocal fremitus breath of benign increased A-P IV fluid administration
Cyanosis, if severe Hyperresonant percus- sounds sputum diameter of
Accessory muscle sion chest, more
use Pulsus paradoxus (sys- horizontal ribs
tolic blood pressure Chest x-ray
decreases on inspira- normal between
tion), if severe asthma exacer-
bations
Chronic “Blue bloater” Tachycardia Rhonchi Spasmodic Translucent lung Smoking cessation
bronchitis with stocky Hypertension Diminished cough fields Bronchodilator
build and depen- Decreased tactile and breath Sputum ranges Flattened dia- Steroids
dent edema vocal fremitus sounds from clear to phragms Expectorants
Tachypnea with Hyperresonant percus- Crackles purulent ± Cardiomegaly Antibiotics if infection
prolonged expi- sion Often most with increased exists
ratory phase Increased A-P chest productive in bronchovascular Diuretics if cor pulmo-
Pursed lip breath- diameter the morning markings nale present
ing Decreased lateral costal Supplemental O2
Accessory muscle expansion Airway clearance tech-
use, often with niques
fixed upper Assisted or mechanical
extremities ventilation, if severe
Elevated shoulders Pulmonary rehabilita-
Barrel chest tion
Fatigue
Anxiety
Emphysema “Pink puffer” with See Chronic bronchitis, Very dimin- Usually absent Translucent lung Bronchodilators
cachexia above ished breath and nonpro- fields Supplemental O2
Otherwise, see sounds ductive Flattened dia- Nutritional support
Chronic bronchi- Wheeze phragms Pulmonary rehabilita-
tis, above Crackles Bullae. tion
± Small heart
with decreased
vascular mark-
ings
Cystic Tachypnea See Chronic bronchitis, Crackles Chronic Translucent lung Antibiotics
fibrosis Fatigue above Diminished cough, either fields Bronchodilators
Accessory muscle breath controlled or Flattened dia- Mucolytics
use sounds spasmodic phragms Supplemental O2
Barrel chest Rhonchi Usually very Fibrosis Airway clearance tech-
Cachexia viscous, Atelectasis niques
Clubbing greenish spu- Enlarged right Aerobic exercise
tum ± blood ventricle Nutritional support
streaks Linear opacities Psychosocial support
Lung transplantation
Bronchiec- See Cystic fibrosis, See Chronic bronchitis, See Cystic fi- Purulent, odor- Patchy infiltrates Antibiotics
tasis above above brosis, above ous sputum ± Atelectasis Bronchodilators
± Hemoptysis + Honeycombing, Corticosteroids
if advanced Supplemental O2
Increased vascular IV fluid administration
markings Nutritional support
Crowded bron- Bronchopulmonary
chial markings hygiene
± Pain control for pleu-
ritic pain
Lung transplantation

±, With or without; A-P, anterior-posterior; O2, oxygen.

Ikeda B, Goodman C. The respiratory system. In: Goodman C, Fuller K, eds. Pathology Implications for the Physical Therapist. 4th ed. St. Louis: Saunders; 2014:742-827;
Dean E. Cardiovascular and pulmonary pathophysiology. In: Frownfelter DL, Dean E, eds. Cardiovascular and Pulmonary Physical Therapy: Evidence and Practice. 5th ed.
St. Louis:, Mosby; 2012:77-102.
78 CHAPTER 4     Pulmonary System
Cystic Fibrosis
Cystic fibrosis (CF) is an autosomal-recessive trait (chromosome
7) that affects exocrine glands of the entire body, particularly of
the respiratory, gastrointestinal, and reproductive systems. Mal-
function of this gene is associated with abnormal mucus secre-
tion. Respiratory pathogenesis follows the following sequela56:
• Airway obstruction caused by thick secretions
• Chronic lung infections
• Inflammation leading to bronchiectasis
These changes result in bronchospasm, atelectasis, V̇/Q̇ mis-
match, increased airway resistance, and hypoxemia.55 This pro-
gressive disease, with hallmark worsening lung function, is
accompanied with acute pulmonary exacerbations with common
symptoms of increased cough and sputum production, change
in sputum appearance, decreased exercise tolerance, fatigue, and
decreased appetite or weight loss.57
  CLINICAL TIP
A progressive exercise program in conjunction with airway clear-
ance during a hospitalization for exacerbation has been shown
to significantly improve secretion expectoration and increase
muscle strength and aerobic capacity, lasting up to 1 month
after discharge.58,59
 
Bronchiectasis
Bronchiectasis is an obstructive, restrictive disorder character-
ized by the following10:
• Destruction of the elastic and muscular bronchiole walls
• Destruction of the mucociliary escalator (in which normal epi-
thelium is replaced by nonciliated mucus-producing cells)
• Bronchial dilatation
• Bronchial artery enlargement
Bronchiectasis is defined as the permanent dilatation of airways
that have a normal diameter of greater than 2 mm.60 Bronchiec-
tasis results in fibrosis and ulceration of bronchioles, chronically
retained pulmonary secretions, atelectasis, and infection. The
etiology of bronchiectasis includes previous bacterial respiratory
infection, CF, tuberculosis (TB), chronic aspiration, and immobile
cilia syndromes.60 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.60 Hospitalization
usually occurs when complications of bronchiectasis arise, includ-
ing hemoptysis, pneumonia, PTX, empyema, or cor pulmonale.  cardiogenic or noncardiogenic. Cardiogenic pulmonary edema
Restrictive Pulmonary Conditions
Restrictive lung diseases or conditions are characterized by low
lung volumes and may be described by onset (acute or chronic)
or location (pulmonary or extrapulmonary). The characteristic
low lung volumes result is increased work of breathing. Table
4.10 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 segment(s), or lobe(s). It most commonly results from
hypoventilation or ineffective pulmonary secretion clearance.
The following conditions also may 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 V̇/Q̇ mismatch, transpulmonary
shunting, and pulmonary vasoconstriction of variable severity
depending on the amount of atelectasis.10 General risks for the
development of atelectasis include cigarette smoking or pulmo-
nary disease, obesity, and increased age. Perioperative or post-
operative risk factors include altered surfactant function from
anesthesia, emergent or extended operative time, altered con-
sciousness or prolonged narcotic use, hypotension, and sepsis.61 
Pneumonia
Pneumonia is the multistage inflammatory reaction of the distal
airways resulting from inhalation of bacteria, viruses, microor-
ganisms, foreign substances, gastric contents, dust, or chemicals
or occurs as a complication of radiation therapy.10 Pneumonia
often is described as community-acquired pneumonia or hospi-
tal (nosocomial)–acquired pneumonia. Hospital-acquired pneu-
monia is defined as pneumonia occurring after 48 hours within a
hospital stay and is associated with ventilator use, contaminated
equipment, or inadequate hand washing.62,63 The consequences
of pneumonia are V̇/Q̇ mismatch and hypoxemia.
Pneumonia may occur either unilaterally or bilaterally in single
or multiple lobes of the lung. The complete clearance of pneumonia
in a patient can take up to 6 weeks.62 Resolution of pneumonia is
slower with advanced age, previous pneumonia, positive smoking
history, poor nutritional status, or coexisting illness.
  CLINICAL TIP
Viral pneumonias may not produce the same quantity of secre-
tions as do bacterial pneumonias. Necessity and efficacy of
airway clearance techniques should be considered before pro-
viding these interventions to patients with viral pneumonias.  
Pulmonary Edema
The etiology of pulmonary edema can be categorized as either
is an imbalance of hydrostatic and oncotic pressures within the
pulmonary vasculature that results from backflow of blood from
the heart. This backflow increases the movement of fluid from
the pulmonary capillaries to the alveolar spaces. Initially, the
fluid fills the interstitium and then progresses to the alveolar
spaces, bronchioles, and, ultimately, the bronchi.64 A simulta-
neous 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 associa-
tion with left ventricular hypertrophy, mitral regurgitation, or
aortic stenosis. Cardiogenic pulmonary edema results in atelec-
tasis, V̇/Q̇ mismatch, and hypoxemia.10
 Pulmonary System     CHAPTER 4 79

TABLE 4.10  Characteristics and General Management of Restrictive Disorders

Disorder Observation Palpation Auscultation Cough Chest X-Ray Management
Atelectasis ± Tachypnea ± Tachycardia Crackles at involved Dry or wet Linear opacity of Incentive spirom-
± Fever Decreased tactile site Sputum varies involved area etry
± Shallow respira- fremitus and vo- Diminished breath widely, depend- If lobar collapse Supplemental O2
tions cal resonance sounds ing on reason for exists, white tri- Functional mobi-
If lobar collapse atelectasis angular density lization
exists, absent or Fissure and Airway clearance
bronchial (trans- diaphragmatic techniques
position) breath displacement
sounds
Pneumonia See Atelectasis See Atelectasis Crackles Initially dry to Well-defined Antibiotics
Fatigue Decreased chest Rhonchi more productive density at the Supplemental O2
± Accessory wall expansion at Bronchial breath Sputum may be involved lobe(s) IV fluid adminis-
muscle use involved site sounds over area of yellow, tan, ± Air bronchogram tration
Dull percussion consolidation green, or rusty ± Pleural effusion Functional mobi-
lization
Airway clearance
techniques
Pulmonary Tachypnea Increased tactile Symmetric wet Sputum may be Increased hilar vas- Diuretics
edema Orthopnea and vocal fremi- crackles, especially thin, frothy, cular markings Other medica-
Anxiety tus at bases clear, white, or Kerley’s B lines tions, depen-
Accessory muscle ± Wheeze pink (short, horizontal dent on etiology
use lines at lung field Supplemental O2
periphery) Hemodynamic
± Pleural effusion monitoring
Left ventricular
hypertrophy
Cardiac silhouette
Fluffy opacities
Adult respira- Labored breath- Hypotension Diminished breath Generally without Pulmonary edema Mechanical venti-
tory distress ing and altered Tachycardia or sounds sputum, al- with diffuse lation
syndrome mental status at bradycardia Crackles though sputum bilateral patchy Hemodynamic
(ARDS) onset Decreased bilateral Wheeze may be present opacities monitoring
Tachypnea chest wall expan- Rhonchi (rare) if infection “Ground glass” ap- IV fluid adminis-
Increased PA sion exists or from pearance tration
pressure Dull percussion the presence of Prone positioning
an endotracheal Glucocorticoids
tube
Pulmonary Rapid onset of Hypotension Diminished or ab- Usually absent Nondiagnostic for Anticoagulation
embolism tachypnea Tachycardia sent breath sounds PE Hemodynamic
(PE) ± Chest pain Decreased chest distal to PE May show den- stabilization
Anxiety wall expansion at Wheeze sity at infarct site Supplemental O2
Dysrhythmia involved site Crackles with lucency dis- or mechanical
Lightheadedness tal to the infarct ventilation
Decreased lung Inferior vena cava
volume filter placement
Dilated PA with Thrombolysis
increased vascular Embolectomy
markings
± Atelectasis
Lung contu- Tachypnea Hypotension Wet crackles Weak cough if Patchy, irregular Pain management
sion Chest wall ec- Tachycardia Diminished or ab- pain present, dry opacities localized Supplemental O2
chymosis Crepitus resulting sent breath sounds or wet to a segment or Mechanical venti-
Cyanosis, if severe from rib fracture at involved site Sputum may be lobe lation
clear, white, or ± Consolidation IV fluid adminis-
blood-tinged tration

±, With or without; IV, intravenous; O2, oxygen; PA, pulmonary artery.

Data from Thompson JM, McFarland GK, Hirsch JE et al., eds. Clinical Nursing Practice. St. Louis: Mosby; 1993; Malarkey LM, McMorrow ME, eds. Nurse’s Manual of
Laboratory Tests and Diagnostic Procedures. 2nd ed. Philadelphia: Saunders; 2000; Ikeda B, Goodman C. The respiratory system. In: Goodman C, Fuller K, eds. Pathology
Implications for the Physical Therapist. 4th ed. St. Louis: Saunders; 2014:742-827; Dean E. Cardiovascular and pulmonary pathophysiology. In: Frownfelter DL, Dean E,
eds. Cardiovascular and Pulmonary Physical Therapy: Evidence and Practice. 5th ed. St. Louis: Mosby; 2012:77-102.
80 CHAPTER 4     Pulmonary System
Noncardiogenic pulmonary edema can result from altera-
tions in capillary permeability (as in acute respiratory distress
syndrome [ARDS] or pneumonia), intrapleural pressure from
airway obstruction(s), or lymph vessel obstruction. The results
are similar to those of cardiogenic pulmonary edema.
  CLINICAL TIP
Beware of positioning the patient with pulmonary edema flat in
bed or in other positions that worsen dyspnea during physical
therapy intervention. Additional pillows may be used to elevate
the head in the supine position.  
Acute Respiratory Distress Syndrome
ARDS is acute inflammation of the lung, generally associated
with aspiration, drug toxicity, inhalation injury, pulmonary
trauma, shock, systemic infections, and multisystem organ fail-
ure.65 Despite advances in supportive care and mechanical ven-
tilation, the mortality rate still remains greater than 30% in
mild cases and increases with disease severity.66
The characteristics of ARDS include the following:
• An exudative phase (hours to days), characterized by increased cap-
illary permeability, interstitial and alveolar edema, hemorrhage,
and alveolar consolidation with leukocytes and macrophages
• A proliferative stage (days to weeks) characterized by hyaline
formation on alveolar walls and intraalveolar fibrosis result-
ing in atelectasis, V̇/Q̇ mismatch, severe hypoxemia, and pul-
monary hypertension
Latent pulmonary sequelae of ARDS are variable and range
from no impairments to mild exertional dyspnea to mixed
obstructive-restrictive abnormalities.67
  CLINICAL TIP
Prone positioning can be used in the intensive care unit (ICU)
setting as a treatment strategy in patients with acute respira-
tory distress syndrome (ARDS). Prone positioning facilitates
improved ventilation to the dorsal lung segments, improved
V̇/Q̇ matching, and improved secretion drainage.68,69 Prone
positioning should be performed only by experienced clinicians
and with proper equipment (specialty frames or beds).
Inspiratory muscle training has been shown to improve
inspiratory muscle strength after the patient is weaned from
mechanical ventilation.70
 
Pulmonary Embolism
Pulmonary embolism (PE) is the partial or full occlusion of the
pulmonary vasculature by material from one or more of the fol-
lowing possible sources: thromboembolism originating from
the lower extremity (>90% of the time),71 air entering the
venous system through catheterization or needle placement, fat
droplets from traumatic origin, or tumor fragments.
  CLINICAL TIP
Physical therapy intervention should be discontinued if the
signs and symptoms of PE arise during treatment (see Table
4.10). Ensure that the patient is secure on a stable surface and
call for help immediately.
A PE results in the following72:
• Decreased blood flow to the lungs distal to the occlusion
• Atelectasis and focal edema
• Bronchospasm from the release of humeral agents
• Possible parenchymal infarction
• Possible right heart strain
Emboli size and location determine the extent of V̇/Q̇ mis-
match, pulmonary shunt, and thus the degree of hypoxemia and
hemodynamic instability.71 The onset of a PE is usually acute
and may be a life-threatening emergency, especially if a larger
artery is obstructed.
  CLINICAL TIP
Physical therapists should recognize patients at high risk for pul-
monary embolism and, after conferring with the medical team,
initiate appropriate preventative measures, such as activity or
mobility and education.73
For patients diagnosed with PE, mobilization and therapy
should begin or continue once the patient’s anticoagulation
medications are at a therapeutic level or the appropriate period
has passed since administration.73 Refer to Chapter 7 for more
information on anticoagulation. 
Interstitial Lung Disease
Interstitial lung disease (ILD) is a general term for the destruc-
tion of the respiratory membranes in multiple lung regions.
This destruction occurs after an inflammatory phase, in which
the alveoli become infiltrated with macrophages and mono-
nuclear cells, followed by a fibrosis phase, in which the alveoli
become scarred with collagen.60 Fibrotic changes may extend
proximally toward the bronchioles. More than 100 suspected
predisposing factors exist for ILD, such as infectious agents,
environmental and occupational inhalants, and drugs; however,
no definite etiology is known.10,74 Clinically, the patient pres-
ents with exertional dyspnea, nonproductive cough, dry crackles
(classically sounding like Velcro being torn apart) and bilateral
diffuse chest radiographic changes and without pulmonary
infection or neoplasm.75 ILD has a variety of clinical features
and patterns, a discussion of which is beyond the scope of this
text; however, the general sequela of ILD is a restrictive pattern
with V̇/Q̇ mismatch. 
Lung Contusion
Lung contusion is the result of a sudden compression and decom-
pression of lung tissue against the chest wall from a direct blunt
(e.g., fall) or blast (e.g., air explosion) trauma. The compres-
sive force causes shearing of the alveolar-capillary membrane
and results in microhemorrhage, whereas the decompressive
force causes a rebound stretching of the parenchyma.76 Diffuse
accumulation of blood and fluid in the alveoli and intersti-
tium causes alveolar shunting, decreased lung compliance, and
increased pulmonary vascular resistance.77 The resultant degree
of hypoxemia is dependent on the size of contused tissue. Lung
contusion usually is located below rib fracture(s) and is associ-
ated with PTX and flail chest. 
 Pulmonary System     CHAPTER 4 81

TABLE 4.11  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 density If effusion is small and
± Discomfort from Decreased tactile decreased in dependent lung respiratory status is
pleuritis fremitus breath Fluid obscures stable, monitor only
Decreased chest Dull percussion sounds diaphragm and fills Supplemental O2
expansion on or bron- costophrenic angle Chest tube placement
involved side chial breath Fluid shifts with for moderate or
sounds at the change in patient large effusion
level of the position Thoracocentesis if
effusion Mediastinal shift to persistent
opposite side, if Pleurodesis
severe Diuretics
Workup to determine
cause if unknown
Pain management
if pleuritic pain
present
Pneumothorax See Pleural effusion, See Pleural effu- Diminished Usually absent Translucent area usu- If PTX is small and
(PTX) above sion, above breath ally at apex of lung respiratory status is
sounds near ± Associated de- stable, monitor only
involved site pressed diaphragm, If PTX is moderate-
Absent if ten- atelectasis, lung sized or large, chest
sion PTX collapse, mediasti- tube placement
nal shift, if severe Supplemental O2
Visceral pleura can Pain management
be seen as thin if pleuritic pain
white line present
Hemothorax See Pneumothorax, See Pleural effu- See Pneumo- Usually absent, See Pleural effusion, Supplemental O2
above sion, above thorax, above unless as- above Chest tube placement
sociated with Pain management
significant if pleuritic pain
lung contu- present
sion in which Monitor and treat for
hemoptysis shock
may occur Blood transfusion, as
needed

±, With or without; O2, oxygen.

Ikeda B, Goodman C. The respiratory system. In: Goodman C, Fuller K, eds. Pathology Implications for the Physical Therapist. 4th ed. St. Louis: Saunders; 2014:742-827;
Dean E. Cardiovascular and pulmonary pathophysiology. In: Frownfelter DL, Dean E, eds. Cardiovascular and Pulmonary Physical Therapy: Evidence and Practice. 5th ed.
St. Louis: Mosby; 2012:77-102.

Restrictive Extrapulmonary Conditions Pneumothorax

Disorders or trauma occurring outside of the visceral pleura also
may affect pulmonary function. Table 4.11 outlines restrictive
extrapleural disorders, their general physical findings, and their
general medical management.
Pleural Effusion
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 capil-
laries, which is associated with congestive heart failure, cirrho-
sis, PE, and pericardial disease.78 Exudative fluid (containing
cellular debris) occurs with pleural or parenchymal inflamma-
tion or altered lymphatic drainage, which is associated with
neoplasm, TB, pneumonia, pancreatitis, rheumatoid arthritis,
and systemic lupus erythematosus.78,79 Pleural effusions may be
unilateral or bilateral, depending on the cause of the effusion,
and may result in compressive atelectasis. Treatment is aimed at
the underlying cause.  • Tension: With air moving into the pleural space only during
PTX is the presence of air in the pleural space that can result from
(1) visceral pleura perforation with movement of air from within
the lung (spontaneous pneumothorax); (2) chest wall and parietal
pleura perforation with movement of air from the atmosphere
(traumatic or iatrogenic pneumothorax); or (3) formation of gas by
microorganisms associated with empyema. Spontaneous PTX can
be a complication of underlying lung disease, or it can occur idio-
pathically in tall persons secondary to elevated intrathoracic pres-
sures in the upper lung zones.80 Traumatic PTX results from rib
fracture, chest wounds, or other penetrating chest trauma. Compli-
cations of mechanical ventilation and central line placement are two
examples of iatrogenic PTX. PTX 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 dur-
ing inspiration and expiration (pleural space in contact with
the atmosphere)
inspiration
82 CHAPTER 4     Pulmonary System
PTX is usually unilateral. Complications of PTX include
atelectasis and V̇/Q̇ mismatch. A large or tension PTX can result
in lung collapse, mediastinal shift (displacement of the medias-
tinum) to the contralateral side, and cardiac tamponade (altered
cardiac function secondary to decreased venous return to the
heart from compression).10
Supplemental oxygen is often needed to manage hypoxemia
and to assist with absorption of the air. A needle aspiration or
a chest tube placement may also assist to drain the air from the
pleural space.
  CLINICAL TIP
Pneumothorax (PTX) is considered a contraindication for posi-
tive expiratory pressure (PEP) therapy. In addition, patients
should be advised to avoid breath holding because of the risk
of air leaks.81
 
Hemothorax
Hemothorax is characterized by the presence of blood in the
pleural space from damage to the pleura and great or smaller
vessels (e.g., interstitial arteries). Causes of hemothorax are pen-
etrating or blunt chest wall injury, draining aortic aneurysms,
pulmonary arteriovenous malformations, and extreme coagula-
tion therapy. Blood and air present together in the pleural space,
common after trauma, is called hemopneumothorax.55,76  Management
Flail Chest
Flail chest is caused by the double fracture of three or more adja-
cent ribs, resulting in this segment separating from the rest of
the ribcage, generally as a result of a crushing chest injury or
vigorous cardiopulmonary resuscitation (CPR). The sequelae of
this injury are as follows82:
• A paradoxical breathing pattern, with the discontinuous 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, with the
possibility of edema, hemorrhage, and necrosis.
• Involvement of large segments, which can also result in hy-
poventilation leading to atelectasis  tion or removal of medications from the regimen. If a patient
Empyema (Purulent Pleurisy)
Empyema is the presence of anaerobic bacterial pus in the pleu-
ral space, resulting from underlying infection (e.g., pneumonia,
lung abscess), which crosses the visceral pleura or chest wall and
parietal pleura penetration from trauma, surgery, or chest tube
placement. Empyema formation involves pleural swelling and
exudate formation, continued bacterial accumulation, fibrin
deposition on pleura, and chronic fibroblast formation.5  in Chapter 14 in addition to other transplantation procedures.
Chest Wall Restrictions
A restrictive respiratory pattern may be caused by abnormal
chest wall movement not directly related to pulmonary pathol-
ogy. Musculoskeletal changes of the thoracic cage can occur
with diseases such as ankylosing spondylitis, rheumatoid
arthritis, and kyphoscoliosis, or with conditions such as preg-
nancy and obesity. Neurologic diagnoses, such as cervical/tho-
racic spinal cord injury or Guillain-Barré syndrome, also can
create restrictive breathing patterns, depending on the level of
respiratory muscle weakness or paralysis. Refer to Chapter 6 for
more information 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 insuf-
ficiency, and parenchymal compression. Other consequences
of kyphoscoliosis are progressive alveolar hypoventilation,
increased dead space, hypoxemia with eventual pulmonary
artery hypertension, cor pulmonale, or mediastinal shift (in
very severe cases) toward the direction of the lateral curve of
the spine.10
Obesity (defined as body weight 20% to 30% above age-
predicted and sex-predicted weight) can cause an abnormally
elevated diaphragm position secondary to the upward displace-
ment 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, V̇/Q̇ mismatch, atelectasis and secre-
tion retention. Refer to Chapter 8 for more information on obe-
sity management with bariatric procedures. 
Pharmacologic Agents
The pharmacologic agents commonly used for the management
of respiratory dysfunction include adrenocortical steroids (glu-
cocorticoids) (see Table 19.8), antihistamines (see Table 19.9),
bronchodilators (see Table 19.10), leukotriene modifiers (see
Table 19.11), mast cell stabilizers (see Table 19.12), expecto-
rants (Chapter 22), and inhaled antibiotics (Chapter 22).
Generally, therapy sessions should be timed to coincide with
maximal medication benefit (Chapter 22).
  CLINICAL TIP
Be aware of respiratory medication changes, especially the addi-
has an inhaler, it is beneficial for the patient to bring it to physi-
cal therapy sessions in case of activity-induced bronchospasm.
Thoracic Surgery and Procedures
The most common thoracic operative and nonoperative pro-
cedures for respiratory disorders are described below in alpha-
betic order.9,83,84 Lung transplantation is described separately
Illustrations of many of the procedures described below are
shown in Fig. 4.13.
• Bronchoplasty: Also called a sleeve resection. Resection and re-
anastomosis (reconnection) of a bronchus; most commonly
performed for bronchial carcinoma (a concurrent pulmonary
resection also may be performed)
 Pulmonary System     CHAPTER 4 83

Procedure Definition Indications • R ib resection: Removal of a portion of one or more ribs for ac-
Pneumonectomy Removal of entire Malignant lesions
lung with or without cessing underlying pulmonary structures as a treatment for
Unilateral tuberculosis
resection of the
mediastinal lymph
thoracic outlet syndrome or for bone grafting
Extensive unilateral
nodes bronchiectasis • Segmentectomy: Removal of a segment of a lung; most com-
Multiple lung abscesses monly performed for a peripheral bronchial or parenchymal
Massive hemoptysis lesion
Bronchopleural fistula • Thoracentesis: Therapeutic or diagnostic removal of pleural
Lobectomy Resection of one or Lesions confined to a fluid via percutaneous needle aspiration
more lobes of lung single lobe
• Thoracoscopy (video-assisted thoracoscopic surgery [VATS]):
Pulmonary tuberculosis
Bronchiectasis
Examination, through the chest wall with a thoracoscope, of
Lung abscesses or cysts
the pleura or lung parenchyma for pleural fluid biopsy or
Trauma
pulmonary resection
• Tracheal resection and reconstruction: Resection and reanastomo-
Segmental resection Resection of Small peripheral lesions sis (reconnection) of the trachea, main stem bronchi, or both;
bronchovascular
segment of lung lobe Bronchiectasis most commonly performed for tracheal carcinoma, trauma,
Congenital cysts or blebs stricture, or tracheomalacia
• Tracheostomy: Incision of the second or third tracheal rings or
the creation of a stoma or opening for a tracheostomy tube;
preferred for airway protection and prolonged ventilatory
Wedge resection Removal of small Small peripheral lesions support or after laryngectomy, tracheal resection, or other
wedge-shaped section (without lymph node
of lung tissue involvement) head-and-neck surgery
Peripheral granulomas • Wedge resection: Removal of lung parenchyma without regard
Pulmonary blebs to segment divisions (a portion of more than one segment
but not a full lobe); most commonly performed for periph-
eral parenchymal carcinoma 
Bronchoplastic reconstruction Resection of lung Small lesions involving the
(also called sleeve resection) tissue and bronchus carina or major bronchus
with end-to-end without evidence of
reanastomosis of metastasis
bronchus
May be combined with
Physical Therapy Intervention
lobectomy
Goals
The primary focus of physical therapy goals in the treatment
of patients with primary lung pathology include promot-
FIG. 4.13
ing independence in functional mobility; maximizing gas
Images of thoracic surgeries: pneumonectomy, lobectomy, segmental resec-
tion, wedge resection, bronchoplastic resection (also known as sleeve re- exchange (by improving ventilation and airway clearance);
section). (From Urden L, Stacy K, Lough M, eds. Critical Care Nursing: and increasing aerobic capacity, respiratory muscle endurance,
Diagnosis and Management. 6th ed. St. Louis: Mosby; 2010.) and the patient’s knowledge of his or her condition. General
interventions to accomplish these goals are breathing retrain-
• L aryngectomy: The partial or total removal of one or more vo- ing exercises, airway clearance techniques, postural retraining,
cal cords; most commonly performed for laryngeal cancer musculoskeletal correction, positioning, functional activity
• Laryngoscopy: Direct visual examination of the larynx with a fi- and exercise with vital sign monitoring, and patient education.
beroptic scope; most commonly performed to assist with differ- Airway clearance techniques, including postural drainage, per-
ential diagnosis of thoracic pathology or to assess the vocal cords cussion, vibration, active cycle of breathing, autogenic drain-
• Lobectomy: Resection of one or more lobes of the lung; most age, high-frequency chest wall oscillation, positive expiratory
commonly performed for isolated lesions pressure (PEP) and oscillatory PEP are reviewed in more detail
• Lung volume reduction: The unilateral or bilateral removal of in Chapter 22. 
one or more portions of emphysematous lung parenchyma,
resulting in increased alveolar surface area
• Mediastinoscopy: Endoscopic examination of the mediastinum; Management of Patients With Respiratory Impairments
most commonly performed for precise localization and biopsy A physiologically based treatment hierarchy for patients
of a mediastinal mass or for the removal of lymph nodes with impaired oxygen transport, developed by Elizabeth
• Pleurodesis: The obliteration of the pleural space; most com- Dean, is a helpful tool in treating patients with cardiopul-
monly performed for persistent pleural effusions or pneu- monary impairments. The hierarchy is based on the princi-
mothoraces. A chemical agent is introduced into the pleural ple that physiologic function is best when an individual is
space via thoracostomy (chest) tube or with a thoracoscope upright and moving.55 Dean’s hierarchy is shown in Table
• Pneumonectomy: Removal of an entire lung; most commonly 4.12. Additional considerations for activity progression and
performed as a result of bronchial carcinoma, emphysema, musculoskeletal and postural problems are described in the
multiple lung abscesses, bronchiectasis, or TB following sections.
84 CHAPTER 4     Pulmonary System

TABLE 4.12  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 exer- Goal: To elicit an exercise stimulus that addresses one A
. Acute effects
cise of the three effects on the various steps in the oxy- . Long-term effects
B
gen transport pathway, or some combination thereof C . Preventive effects
II. Body positioning Goal: To elicit a gravitational stimulus that simulates . Hemodynamic effects related to fluid shifts
A
being upright and moving as much as possible: ac- B. Cardiopulmonary effects on ventilation and its distri-
tive, active-assisted, or passive bution, perfusion, ventilation, and perfusion match-
ing and gas exchange
III. Breathing control ma- Goal: To augment alveolar ventilation, to facilitate . Coordinated breathing with activity and exercise
A
neuvers mucociliary transport, and to stimulate coughing B. Spontaneous eucapnic hyperventilation
C. Maximal tidal breaths and movement in three dimen-
sions
D. Sustained maximal inspiration
E. Pursed-lip breathing to end-tidal expiration
F. Incentive spirometry
IV. Coughing maneuvers Goal: To facilitate mucociliary clearance with the . Active and spontaneous cough with closed glottis
A
least effect on dynamic airway compression and the B. Active-assisted (self-supported or supported by other)
fewest adverse cardiovascular effects C. Modified coughing interventions with open glottis
(e.g., forced expiratory technique, huff)
V. Relaxation and ener- Goal: To minimize the work of breathing and of the . Relaxation procedures at rest and during activity
A
gy-conservation in- heart and to minimize undue oxygen demand B. Energy conservation, (i.e., balance of activity and rest,
terventions performing activities in an energy-efficient manner,
improved movement economy during activity)
C. Pain-control interventions
VI. Ra nge-of-motion Goal: To stimulate alveolar ventilation and alter its A. Active
(ROM) exercises distribution B. Assisted-active
(cardiopulmo- C. Passive
nary indications)
VII. Postural drainage po- Goal: To facilitate airway clearance using gravita- A. Bronchopulmonary segmental drainage positions
sitioning tional effects
VIII. Manual techniques Goal: To facilitate airway clearance in conjunction A. Autogenic drainage
with specific body positioning B. Manual percussion
C. Shaking and vibration
D. Deep breathing and coughing
IX. Suctioning Goal: To facilitate the removal of airway secretions A. Open suction system
collected centrally B. Closed suction system
C. Tracheal tickle
D. Instillation with saline
E. Use of manual hyperinflation bag (bagging)

From Frownfelter D, Dean E. Cardiovascular and Pulmonary Physical Therapy: Evidence and Practice. 4th ed. St. Louis: Mosby; 2006.

Activity Progression.  The following concepts should be
considered when progressing activity in patients with respira-
tory dysfunction:
• Rating of perceived exertion or the dyspnea scale (see Table
4.3) are better indicators of exercise intensity than heart rate
because a patient’s respiratory limitations, such as dyspnea,
generally supersede cardiac limitations. Monitoring O2 satu-
ration also can assist in determining the intensity of the ac-
tivity.
• Shorter, more frequent sessions of activity are often better
tolerated than are longer treatment sessions. Patient educa-
tion regarding energy conservation and paced breathing con-
tributes to increased activity tolerance.
• A treatment session may be scheduled according to the pa-
tient’s other hospital activities to ensure that the patient is
not too fatigued to undergo therapy.
• D ocument the need and duration of seated or standing rest
periods during a treatment session to help measure function-
al activity progression or regression.
• Although O2 may not be needed at rest, supplemental O2
with exercise may decrease dyspnea and prolong exercise du-
ration and intensity. Titration of supplemental oxygen will
require an appropriate physician order indicating a saturation
goal rather than a dosage. Refer to the Supplemental Oxygen
Guidelines proposed by Hillegass et al. for additional detail.85
• Amount of O2 and vital signs need to be documented with
activity and at rest.
• Airway clearance before an exercise session may optimize ac-
tivity tolerance. Exercising before airway clearance may opti-
mize clearance.
Table 4.13 provides some suggested treatment interventions
based on common respiratory assessment findings. 

TABLE 4.13  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 effec- Ineffective cough
tiveness
DeTurk WE, Cahalin LP, eds. Cardiovascular & Pulmonary Physical Therapy: An Evidence-Based Approach. 2nd ed. New York: McGraw-Hill; 2010; Frownfelter DL, Dean
E, eds. Cardiovascular and Pulmonary Physical Therapy: Evidence and Practice. 5th ed. St. Louis: Mosby; 2012.
Posture and Musculoskeletal Intervention.  The following
concepts should be considered when addressing posture or muscu-
loskeletal impairments in patients with respiratory dysfunction:
• Exacerbations or acute illnesses can lead to patients reporting
worsening posture or musculoskeletal pain and impairments
• Manual therapies addressing impairments that affect breathing
mechanics are appropriate treatment techniques in the acute
care setting. Care should be taken in patients with comorbidi-
ties, such as osteoporosis caused by prolonged corticosteroid use.
• It is important to relate any posture or musculoskeletal goals
to function.
• Manual techniques (e.g., chest wall mobilization, rib spring-
ing and thoracic spine mobilization) used before mobility
may be useful in facilitating better breathing mechanics
• Inspiratory muscle training (IMT) may be used to strengthen
the primary and/or accessory muscles of inhalation in pa-
tients with poor maximal inspiratory pressure (MIP). This
is done by breathing against a resistor for some time to cre-
ate an overload on the respiratory muscles, resulting in an
increased MIP over time. IMT with exercise has been shown
to reduce dyspnea in patients with COPD.86
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Pulmonary System     CHAPTER 4 85
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 5 Musculoskeletal System
C H APT ER  
CHAPTER OUTLINE
Introduction
Structure and Function of the
Musculoskeletal System
Examination
Patient History
Medical Record Review
Patient Interview
Tests and Measures
Evaluation and Prognosis
Interventions
Decrease Pain and/or Muscle
Guarding
Prevent Circulatory and Pulmo-
nary Complications
Improve Range of Motion and
Strength Impairments
Improve Functional Mobility
While Protecting the Involved
Structures
Health Conditions
Traumatic Fracture
Joint Arthroplasty
Musculoskeletal Tumor Resection
Spinal Pathology
Soft Tissue Surgeries
Equipment Used in the
Management of Musculoskel-
etal Pathologies
Casts
External Fixators
Braces and Splints
Traction
Marka Gehrig Salsberrya
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . Provide a brief overview of the structure and function of the musculoskeletal system
2. Describe the physical therapist’s examination and management of the patient with musculoskeletal impair-
ments in the acute care setting
3. Give an overview of fracture management and common orthopedic surgeries seen in the acute care setting
4. Describe the equipment commonly used by patients with musculoskeletal impairments in the acute care
setting
Introduction
An understanding of musculoskeletal health conditions, medical-surgical interventions, and
use of orthotic and assistive devices, in conjunction with weight-bearing restrictions, is often
the basis of physical therapy evaluation and treatment planning for patients with acute muscu-
loskeletal impairments. Because a 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 physical
therapist is an integral member of the multidisciplinary health care team. 
Structure and Function of the Musculoskeletal System
The musculoskeletal system is made up of the bony skeleton and contractile and noncontractile
soft tissues, including muscles, tendons, ligaments, joint capsules, articular cartilage, and non-
articular cartilage. This matrix of soft tissue and bone provides individuals with the dynamic
ability of movement, giving them the capacity to move through space, absorb shock, convert
reactive forces, generate kinetic energy, and perform both gross and 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 com-
monly sustains traumatic injuries and degenerative changes. The impairments that develop
from injury or disease can significantly affect an individual’s ability to retain their functional
status and therefore can result in further pathologic compromise. 
Examination
Common orthopedic diagnoses seen by physical therapists in the acute care setting include
degenerative joint disease, spinal disorders, and fractures associated with trauma. Because many
patients with these conditions have undergone surgical interventions, physical therapists must
be familiar with physician-dictated precautions, such as weight-bearing limitations, range-of-
motion (ROM) restrictions, and therapeutic exercise restrictions.
aThe authors acknowledge Carol Elrod for prior contributions to this chapter.
        89
90 CHAPTER 5     Musculoskeletal System
Patients with orthopedic impairments often experience pain,
frustration, and anxiety while maneuvering through an environ-
ment that frequently includes peripheral lines, catheters, casts,
and drains. A challenge for physical therapists in the acute care
setting is to accurately interpret the patient’s presentation and
current and past health conditions to effectively achieve optimal
outcomes in a very short time frame. To do this, the therapist
must incorporate the judicious use of examination findings into
the decision-making process extracted from the history, systems
review, and tests and measures. Various factors influence a thera-
pist’s clinical reasoning when working with this patient popula-
tion. These factors include the therapist’s knowledge, expertise,
goals, values, beliefs, and use of evidence; the patient’s age, diag-
nosis, and medical history, as well as his or her own goals, values,
and beliefs; available resources; clinical practice environment;
level of financial and social support; and the intended use of the
collected information.1,2
Patient History
Information about the patient’s history can be obtained from
the medical record, the patient, and/or the patient’s care-
givers. According to the Guide to Physical Therapist Practice,
the different types of data that can be generated from the
patient history include general demographics, social history,
employment/work, growth and development, general health
status, social/health habits, family history, medical/surgical
history, current condition(s)/chief complaint(s), functional
status and activity level, medications, and results of clinical
tests.3  disk hernations.4
Medical Record Review
In addition to a standard medical review (see Chapter 2), infor-
mation pertaining to the patient’s musculoskeletal history
should include the following:
• Medical diagnosis
• Cause and mechanism of injury
• Medical treatment and/or surgical procedures
• Physician-dictated orders
• Weight-bearing status, limitations on ROM, positioning of
extremities
• Equipment, such as braces, orthotics, assistive device use
• Activity status
• Comorbidities and medical history
• Diagnostic test and laboratory results
• Medications (see Chapter 19)
Because many patients with musculoskeletal impairments
have undergone some type of surgical procedure in which blood
loss could have occurred, the physical therapist should review
and monitor the patient’s vital signs and laboratory results,
including hematocrit and hemoglobin levels. If these levels are
low, the patient is experiencing a reduction in the oxygen-car-
rying capacity of blood. Thus the patient may have decreased
exercise tolerance and complain of fatigue, weakness, and dys-
pnea on exertion.
Diagnostic test results should be reviewed by the physi-
cal therapist because they may indicate that certain activity
limitations are warranted and aid in the therapists decision-
making process. The most commonly used diagnostic tests for
the musculoskeletal system are discussed in the following sec-
tion. These tests may be repeated during or after a hospital stay
to assess bone and soft tissue healing and disease progression
and for any sudden changes in vascular or neurologic status
postoperatively.
Diagnostic Tests Review
Radiography.  More commonly referred to as “x-rays”
or “plain films,” radiographic images are the mainstay in the
detection of fractures, dislocations, bone loss, and foreign bodies
or air in tissue. Obtaining sequential x-rays is the standard pro-
cedure intraoperatively or postoperatively to evaluate compo-
nent position with joint arthroplasty, placement of orthopedic
hardware, or fracture reduction. 
Computed Tomography.  Computed tomography (CT)
combines the use of radiography with that of a computer to pro-
vide images that have greater sensitivity compared with plain
films alone. CT is the diagnostic test of choice for the evaluation
of subtle and complex fractures; degenerative changes; trauma
in which both soft tissue and bone injuries are suspected; and
loose bodies in a joint.4 
Magnetic Resonance Imaging.  Magnetic resonance
imaging (MRI) is superior to radiography or CT for the
evaluation of soft tissues. MRI is the imaging modality of
choice for the detection of partial or complete tendon, liga-
ment, or meniscal tears; bony and soft tissue tumors; and
 
Bone Scan.  A bone scan is the radiographic picture of the
uptake of a radionuclide tracer in bone. Bone scans reflect the
metabolic status of the skeleton at the time of the scan. They
can provide an early indication of increased bone activity and are
therefore used to detect skeletal tumors, subtle fractures, infec-
tions, and avascular necrosis.4 
Myelography.  A myelogram is a radiograph or CT image
of the spinal cord, nerve root, and dura mater with use of a
contrast dye. A myelogram can demonstrate spinal stenosis,
spinal cord compression, intervertebral disk rupture, and
nerve root injury.4 As with any test that includes contrast
media, contrast-related reactions may occur after arthrography
or myelography. 
Physical Therapy Implications
• Imaging may be ordered after any new event, such as an in-
hospital fall, abnormal angulation of an extremity, or pos-
sible loss of fixation or reduction or because of a dramatic
increase in pain. Regardless of the situation, defer physical
therapy intervention until results are reported or there is
confirmation that the patient can participate.
• Physical therapy intervention is typically deferred for the pa-
tient immediately after myelography secondary to specific
postprocedure positioning and possible bed rest restrictions.
If physical therapy is scheduled immediately after the com-
pletion of this test, the physical therapist should verify with
the medical team that the patient is able to participate in
rehabilitation. 

Medication Review
Physical therapists should also be aware of the patient’s medica-
tions. If the patient is being seen shortly after surgery, the resid-
ual effects of general anesthesia, including hypotension, may
be present. Specifically, the patient may be woozy, confused,
delirious, and/or weak.5 If a local anesthetic, such as an epidural
or spinal neural blockade, is used, the patient may experience
insufficient analgesia or diminished sensation or motor func-
tion.5 Refer to Chapter 20 for more detailed information on
anesthesia.
Pain medications, specifically opioid analgesics, may be
used in this patient population. The physical therapist needs
to be aware of the type of pain medication, its side effects,
and dosing schedule to enhance the patient’s participation in
rehabilitation. Refer to Chapter 21 for more information on
pain management.
Most patients’ status post orthopedic surgery are on an
anticoagulant, specifically a low-molecular-weight heparin
(LMWH). Other options include synthetic pentasaccharides
that inhibit factor Xa indirectly by binding to antithrombin
(e.g., fondaparinux) and vitamin K antagonists (e.g., warfarin).
Other venous thromboembolism deterrents include antiembo-
lism stockings (e.g., TED hose) and pneumatic compression
devices.
CLINICAL TIP
The coagulation profiles of patients on low-molecular-weight
heparin (LMWH) are not typically monitored via laboratory
testing, whereas unfractionated heparin is monitored via the
activated partial thromboplastin time (aPTT) test and warfarin
via the prothrombin time (PT) test. If the patient is bridging to
warfarin (Coumadin), the international normalized ratio (INR)  
level will determine appropriate anticoagulation.
Coordination With Other Providers
After reviewing the medical record and before interacting with
the patient, the physical therapist must discuss the patient’s
current medical status with the patient’s nurse. The physi-
cal therapist needs to determine whether there is any reason
why further examination of the patient should be modified
or deferred. The therapist should inquire about the following
information:
• Most recent laboratory values and current hemodynamic
­status
• Type and last dose of pain medication
• Patients activity and mobility since admission to the hospital  vation of the patient. The physical therapist should note the
Patient Interview
The physical therapist should also collect information from the
patient about his or her:
• Functional level before admission
• Previous use of assistive device(s)
• Recreation or exercise level and frequency
Musculoskeletal System     CHAPTER 5 91
• N eed for adaptive equipment or footwear on a regular basis
(e.g., a shoe lift)
• Any additional medical problems that limit use of assistive
devices, participation in physical therapy
• History of falls
• History of chronic pain
• Support system
• Anticipated discharge location to determine the presence of
stairs, railings, and other potential limitations in the home
environment
• Goals 
Tests and Measures
Based on the data from the review of patient history and the
medical record, the physical therapist determines the specific
tests and measures necessary to confirm his or her working
hypothesis as to the main reasons for the patient’s presenta-
tion. These tests can also be used as outcome measurement tools
to determine improvement. The following tests and measures
should be considered when examining patients with musculo-
skeletal impairments.
Mental Status
The screening of the patient’s mental status begins once the
physical therapist asks questions of the patient during the
patient interview/history. On the basis of the patient’s ability to
effectively communicate, the physical therapist is able to deter-
mine whether further specific testing is required. If a cognitive
impairment is present, the therapist must determine whether
onset occurred before or after the patient was hospitalized. The
therapist should also determine the patient’s hearing status to
ensure that the apparent impairment in mental status is not a
result of the patient’s inability to hear the questions that are
being asked.
CLINICAL TIP
Because the adverse effects of certain pain medications include
an altered mental status, the physical therapist needs to know
the medication side effects the patient may be experiencing and
his or her medication schedule.  
Observation
A wealth of information can be gathered through simple obser-
presence of any equipment and if it is being used correctly by
the patient. The therapist should also observe the patient’s:
• General appearance
• Level of anxiety or stress
• Position of extremities
• Willingness to move or muscle guarding
• Functional mobility
92 CHAPTER 5     Musculoskeletal System
It is important to observe the resting limb position of the
involved extremity. The therapist should note if the limb is
resting in its natural anatomic position or if it is being sup-
ported properly with a pillow, roll, or wedge. Proper position-
ing is needed for edema management and, in some situations,
for comfort; however, the use of a pillow, roll, or wedge can
predispose the limb to contracture development, in which case,
it is contraindicated.
CLINICAL TIP
Joints should be placed in a neutral resting position to preserve
motion and maintain the length of soft tissues. A limb in a
dependent position is at risk for edema formation, even if it is
dependent for only a short period. However, use of pillows or
raising the foot of the bed under the knee for a patient who has
undergone total knee arthroplasty is contraindicated because of
the risk of muscle shortening and therefore should be avoided.
Cardiovascular and Pulmonary.  The cardiovascular and
pulmonary systems should be assessed for any signs or symptoms
that indicate that the patient might not tolerate aerobic activi-
ties. As the energy expenditure (i.e., cardiopulmonary demand)
required for use of an assistive device is greater than the demand
imposed during ambulation without a device, it is important
for the physical therapist to examine the aerobic capacity of the
individual.6,7 Heart rate and rhythm, blood pressure, respiratory
rate, and oxygen saturation must be assessed at rest, before the
initiation of further tests and measures, as well as during and at
the completion of functional activities (e.g., mobility).
CLINICAL TIP
Because orthostatic hypotension is a side effect of opioid use,
anesthesia, and surgery, the physical therapist needs to ensure
that the patient’s cardiovascular system has accommodated to
positional changes before progressing with upright activities.
The therapist should be prepared for the patient to experience
symptoms associated with decreased mobility and pain medica-
tions; the patient may complain of dizziness, nausea, and light-
headedness. Patients should be taught to slowly transition from
sitting to standing activities, and standing to ambulatory activi-
ties. Orthostatic hypotension and syncope may be avoided by
waiting several minutes after each transition and encouraging
the patient to perform ankle pumps and to take two or three
deep breaths before standing.
CLINICAL TIP
The physical therapist should also examine the circulatory status
of the patient. With decreased mobility, the risk for the devel-
opment of deep venous thrombosis (DVT) increases. The lower
extremities should be observed for signs of a DVT. Deficits in skin
temperature, capillary refill, and peripheral pulses at the level of
or distal to the injury or surgical site should also be noted. Refer
to Chapter 7 for a further discussion on vascular examination.
 
Integumentary.  The patient’s skin should be assessed for
the presence and location of edema, bruising, lacerations, or sur-
gical incisions. Skin integrity and color should be examined,
especially around and distal to injuries and incisions. Pressure
sores from prolonged or increased bed rest after trauma or ortho-
pedic surgery can develop in anyone, regardless of age or previ-
ous functional abilities. The therapist should be aware of signs
and symptoms of infection, circulatory compromise, or pressure
ulcer development that would warrant further testing. Refer to
Chapter 12 for a further discussion of skin integrity. 
Sensation.  The neuromuscular system should be assessed
for impairments in sensation, especially in the involved extrem-
ity. Physical therapists should be aware of signs and symptoms
of sensory deficits in patients with diabetes, compartment
syndrome, and peripheral nerve injury (e.g., after total hip
arthroplasty (THA), acute foot drop may be present because of
injury to the sciatic nerve). Patients should be asked if they are
experiencing any changes in sensation. Light touch awareness
should be performed by lightly brushing different areas (dis-
tal and proximal, medial and lateral) on the extremity. With
eyes closed, the patient must recognize that a stimulus has been
applied for the system to be intact. If deficits are noted, more
formal testing is required. Refer to Chapter 6 for more detailed
information on the nervous system. 
Pain.  Musculoskeletal pain quality and location should be
determined subjectively and objectively. Pain scales appropriate
for the patient’s age, mental status, and vision should be used.
The physical therapist should understand the dosing schedule of
the patient’s pain medication if the patient is not using a patient-
controlled analgesia (PCA) pump to ensure that the patient can
optimally participate in rehabilitation. As an alternative to pain
medication, cold packs can be used for pain relief. An icing sched-
ule and related considerations should be reviewed with the patient.
The physical therapist should observe the patient through-
out the examination process (as well as during interventions)
to determine whether the patient is expressing or experiencing
pain. The patient might present nonverbal indicators of pain,
such as behavior changes, facial expressions, and body language.
The physical therapist should determine whether pain is con-
stant or variable and if movement or positioning increases or
decreases the pain. Refer to Chapter 21 for more detailed infor-
mation on acute pain assessment and management.
CLINICAL TIP
The patient’s experience of pain might be masked by medica-
tions, and thus the patient can be “overworked” if the intensity
of the intervention is too high. Providing the appropriate inter-
vention dosage and adapting intensity based on the patients’
response to treatment can limit the risk of “overworking.”
 
Range of Motion and Strength.  The musculoskeletal sys-
tem, including the uninvolved extremities, should be assessed
for impairments in ROM and muscle strength that might pre-
clude the patient from successfully performing mobility activi-
ties. For example, a patient with a fracture of the femur who will
require the use of an assistive device when ambulating should
 Musculoskeletal System     CHAPTER 5 93

have both upper extremities examined to ensure that the patient

TABLE 5.1  Normal Range-of-Motion Valuesa
can safely maintain the limited weight-bearing status.
It is optimal to determine whether any deficits exist in the Normal Range of Motion
patient’s ability to move the extremities before the performance Joint (Degrees)
of higher-level functional activities. A gross screen of upper Shoulder Flexion 0–180
extremity ROM can be performed by having the patient lift the Extension 0–60
arms over the head through the full ROM (i.e., shoulder flexion/ Abduction 0–180
abduction, external rotation, and elbow extension). The patient
Internal rotation 0–70
can then be asked to touch the shoulders (i.e., elbow flexion),
flex and extend the wrists, and make a fist. A gross screen of External rotation 0–90b
the lower extremities can include having the patient bring one Elbow Flexion 0–150
knee at a time up to the chest and then return it to the surface of Forearm Pronation 0–80
the bed (i.e., hip flexion and extension, knee flexion, and exten- Supination 0–80
sion). The patient can then bring the leg to the edge of the bed Wrist Flexion 0–80
and back to midline (hip abduction and adduction). Finally, the
Extension 0–70
patient can do dorsiflexion and plantarflexion of the ankle.
Hip Flexion 0–120
The ability to move through the full ROM gives the thera-
pist a gross estimate of minimal strength capabilities as well. Extension 0–30
If the patient is unable to move through the full available Abduction 0–45
ROM, the therapist will then need to move the limb passively Adduction 0–30
through the remaining range to determine whether it is a Internal rotation 0–45
strength deficit or loss of ROM. Further assessment of the mag- External rotation 0–45
nitude of the ROM impairment can be examined both passively
Knee Flexion 0–135
and actively via the use of a goniometer (e.g., after total knee
Ankle Dorsiflexion 0–20
arthroplasty). Table 5.1 outlines normal ROM values.
If the patient is able to move through the full available Plantar flexion 0–50
ROM, the therapist should provide some manual resistance to aValues are from the American Academy of Orthopedic Surgeons (AAOS), as
the major muscle groups to determine whether there are any reported in Appendix B of Reese NB, Bandy WD. Joint Range of Motion and
strength deficits that would affect the patient’s ability to suc- Muscle Length Testing. 3rd ed. St. Louis: Saunders; 2017.
bAs the AAOS does not report a value for external rotation of the shoulder, the
cessfully perform functional mobility activities and activities of value is from the American Medical Association (AMA), as reported in Appen-
daily living (ADLs). If there are no contraindications, the thera- dix B of Reese NB, Bandy WD. Joint Range of Motion and Muscle Length Testing.
pist can do formal manual muscle testing (MMT). 3rd ed. St. Louis: Saunders; 2017.
If MMT is not possible because of such conditions as altered
mental status and pain or if putting force across a fracture or surgi-
cal site is required when providing resistance, then strength should
be described in functional terms, such as how much movement CLINICAL TIP
occurred within the available ROM (e.g., active hip flexion is one- Safety awareness, or lack thereof, can be difficult to document.
third range in supine) or during the performance of a functional The physical therapist should try to describe a patient’s level of
activity (e.g., heel slide, ability to lift leg off and/or onto the bed).  safety awareness as objectively as possible (e.g., patient leaned
Posture.  The patient’s resting posture in the supine, sit- on rolling tray table, unaware that it could move). This can also
ting, and standing positions should be observed. An inspection be documented in a Min/Mod/Max manner when describing
of the head, trunk, and extremities for alignment, symmetry, level of verbal cues needed.
and deformity is warranted. Nearly all patients will fear or be anxious about moving out
of bed for the first time, especially if a fall or traumatic event
CLINICAL TIP led to the hospital admission. Before mobilization, the physical
A leg length discrepancy that could affect standing posture and therapist should use strategies such as clearly explaining what
gait may be present after some surgical procedures (e.g., total will be occurring and the sensations the patient may feel (e.g.,
hip arthroplasty [THA]) that may be temporary or permanent.8,9 “Your foot will throb a little when you lower it to the floor”) to
  decrease the patient’s apprehension.
Because orthopedic injuries can often be the final result
Locomotion and Balance.  A patient’s activity level, includ- of other medical problems (e.g., balance disorders or visual or
ing bed mobility, transfers, and ambulation on level surfaces and sensory impairments), it is important that the physical thera-
stairs, should be evaluated according to activity level, medical- pist take a thorough history, perform a physical examination,
surgical stability, and prior functional level. Safety is a key compo- and critically observe the patient’s functional mobility. Medical
nent of function. The patient’s willingness to follow precautions problems may be subtle in presentation but may dramatically
with consistency, as well as his or her ability to maintain weight influence the patient’s capabilities, especially with new variables,
bearing and comply with proper equipment use, must be evalu- such as pain or the presence of a cast. Collectively, these factors
ated. The patient’s self-awareness of risk for falls, speed of move- lead to a decreased functional level.
ment, onset of fatigue, and body mechanics should be monitored.
94 CHAPTER 5     Musculoskeletal System
CLINICAL TIP
It may be the physical therapist who first appreciates an addi-
tional fracture, neurologic deficit, or pertinent piece of medi-
cal or social history. Any and all abnormal findings should be
reported to the medical team.  
Evaluation and Prognosis
On completion of the examination, the physical therapist must
evaluate the data and use his or her clinical judgment to iden-
tify possible problems that require the skilled interventions
provided by physical therapists and/or referral to other health
care professionals. The therapist then determines the patient’s
impairments, activity limitations and participation restriction,
which will be the focus of the patient-related instruction and
direct interventions.3 A patient’s plan of care, including dis-
charge planning, includes many areas that require synthesis and
ongoing communication with the medical team. Factors such
as level of social support, potential destinations after acute care
(e.g., rehabilitation setting or home health care), premorbid
conditions and equipment needs are considered in designing a
successful plan of care and transition to the next level of care.3  equipment (e.g., braces, orthotics), the physical therapist
Interventions
Physical therapy interventions should be individualized to each
patient according to the patient’s goals and clinical presenta-
tion. General physical therapy goals for the patient with muscu-
loskeletal impairments include:
• Decrease pain and/or muscle guarding
• Prevent circulatory and pulmonary complications
• Improve ROM and strength impairments
• Improve functional mobility while protecting the involved
structures
When providing interventions to the patient, the physical
therapist must take into consideration the medical and/or sur-
gical management of the musculoskeletal impairment, physi-
cian orders, and need for equipment use during mobilization
activities. The patient’s medical status, social support system,
and ability to abide by all safety precautions will help guide
the therapist in his or her decision making about prioritizing
interventions.
Decrease Pain and/or Muscle Guarding
The physical therapist may choose to use relaxation and
active assisted ROM exercises within the patient’s toler-
ance to decrease the patient’s experience of pain and muscle
guarding. Cold, heat, and transcutaneous electrical nerve
stimulation (TENS) are also options available in the acute
care setting.  skin.
Prevent Circulatory and Pulmonary Complications
If edema is present, the limb can be elevated on pillows while
the patient is resting. Active muscle-pumping exercises, such
as ankle pumps, should be provided to all patients who have
decreased mobility to minimize the potential for the develop-
ment of DVT. The therapist should encourage the patient to
take two or three deep breaths several times a day, especially
on upright sitting, to minimize the development of pulmo-
nary complications and discourage shallow breathing that can
occur when a patient becomes anxious. Ultimately, having
the patient perform functional activities, especially ambu-
latory tasks, will combat circulatory stasis and pulmonary
impairments. 
Improve Range of Motion and Strength Impairments
The physical therapist should consider the use of isometrics to
minimize muscle atrophy around an immobilized joint. Active
ROM exercises can be used to maintain range of mobile joints.
If strength deficits are present or loss of strength is expected and
there are no contraindications to increasing the tension/force
production of the muscle, initiating a strengthening program
through progressive resistance exercises or the performance of
functional activities is warranted. 
Improve Functional Mobility While Protecting the
Involved Structures
While ensuring that the patient has donned all prescribed
must train the patient to perform all functional activities in a
manner that maximizes the patient’s capabilities and ensures
that the patient abides by all precautions (e.g., weight-bearing
status). If the injury is to the pelvis or lower extremity, use
of an assistive device will be required to maintain any lim-
ited weight-bearing status. Gait training must be provided
to minimize any inefficient gait deviations. Balance training
during static and dynamic activities must occur to ensure that
in different positions the patient is still able to abide by all
precautions. The patient must be educated on proper and safe
positioning and limb movements during the performance of
functional activities. 
Health Conditions
Traumatic Fracture
Traumatic Fracture Classification
The analysis and classification of fractures reveal the amount
of energy imparted to bone, the extent of soft tissue injury,
and optimal fracture management. Traumatic fractures can be
classified according to well-recognized classification systems,
such as the one established by the Orthopedic Trauma Asso-
ciation (OTA).10 They can also be described according to the
following11,12:
1. The maintenance of skin integrity:
a. A closed fracture is a fracture without disruption of the
b. An open fracture is a fracture with an open laceration of
the skin or protrusion of the bone through the skin.
2. The site of the fracture:
a. An articular fracture involves a joint.

b. An epiphyseal fracture involves the growth plate.
c. A diaphyseal fracture involves the shaft of a long bone.
3. The classification of the fracture:
a. A linear fracture lies parallel to the long axis of the bone.
b. An oblique fracture lies on a diagonal to the long axis of
the bone.
c. A spiral fracture encircles the bone.
d. A transverse fracture lies horizontal to the long axis of the
bone.
e. A comminuted fracture has two or more fragments; a but-
terfly (wedge-shaped) fragment may or may not be pres-
ent.
f. A segmental fracture has two or more fracture lines at dif-
ferent levels of the bone.
g. A compression fracture occurs when the bone is crushed;
it is common in the vertebrae.
4. The extent of the fracture:
a. An incomplete fracture has only one portion of the cortex
interrupted, and the bone is still in one piece.
b. A complete fracture has all cortices of bone interrupted,
and the bone is no longer in one piece.
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 abnormal anatom-
ic alignment of fracture fragments.  months, whereas in adults it typically takes 2 or more months.17
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.13 Early restoration of func-
tion 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 loca-
tion and type of fracture, presence of secondary injuries, and
hemodynamic stability. Elective or nonurgent management
(days to weeks) applies to stable fractures with an intact neu-
rovascular system or fracture previously managed with conser-
vative measures that have failed. Urgent management (24–72
hours) applies to closed, unstable fractures, dislocations, or
long bone stabilization with an intact neurovascular system.
Emergent management applies to open fractures, fractures/dis-
locations with an impaired neurovascular system or compart-
ment syndrome, and spinal injuries with increasing neurologic
deficits.13
Fracture reduction is the process of aligning and approxi-
mating fracture fragments. Reduction may be achieved by
either closed or open methods. Closed reduction is nonin-
vasive and is achieved by manual manipulation or traction.
Open reduction with internal fixation (ORIF) techniques
require surgery and fixation devices commonly referred to
as hardware. ORIF is the treatment of choice when closed
methods cannot maintain adequate fixation throughout the
healing phase. To decrease the extent of soft-tissue disruption
Musculoskeletal System     CHAPTER 5 95
that occurs when direct reduction is required, minimally
invasive surgical techniques for fracture fixation have been
developed. In minimal access surgery or minimally invasive
surgery (MIS), the surgeon uses the least invasive access por-
tal and mainly indirect reduction techniques to fixate the
fracture.14
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 (Fig.
5.1). Regardless of the method of immobilization, the goal is to
promote bone healing.
Fracture healing is complex and proceeds through two dif-
ferent processes. Primary cortical or direct healing occurs
when bone fragments are anatomically aligned via rigid inter-
nal fixation, encounter minimal strain, and are stable.15 More
commonly, fracture healing occurs through endochondral or
secondary bone healing (Fig. 5.2).16 The first stage (inflamma-
tory stage) of this process involves the formation of a hematoma
with a subsequent inflammatory response. The reparative phase
follows and includes the influx of fibroblasts, chondroblasts,
and osteoblasts, resulting in formation of a soft calcified carti-
lage callus. The remodeling phase begins with the transition of
the soft callus to a permanent hard callus consisting of lamel-
lar bone. In children, the healing of bone can take less than 2
Box 5.1 lists the multitude of factors that contribute to fracture
healing. 
Complications of Fracture
Complications of fracture may be immediate (within days),
delayed (weeks to months), or late (months to years). The imme-
diate or early medical-surgical complications of special interest
in the acute care setting include18:
• Loss of fixation or reduction
• DVT, pulmonary or fat emboli
• Nerve damage, such as paresthesia or paralysis
• Arterial damage, such as blood vessel laceration
• Compartment syndrome
• Infection
• Orthostatic hypotension
Delayed and late complications are as follows18:
• Loss of fixation or reduction
• Delayed union (fracture fails to unite in a normal time frame
in the presence of unfavorable healing factors)
• Nonunion (failure of fracture to unite)
• Malunion (fracture healed with an angular or rotary deformity)
• Pseudarthrosis (formation of a false joint at the fracture site)
• Posttraumatic arthritis
• Osteomyelitis
• Avascular necrosis
• Complex regional pain syndrome 
Fracture Management According to Body Region
Pelvis and Lower Extremity
Pelvic Fractures.  The pelvis is formed by the paired innom-
inate bones, sacrum, sacroiliac joints, and the symphysis
96 CHAPTER 5     Musculoskeletal System

Type of Fixation: Compression Plate and Screws

Biomechanics Stress shielding
Type of bone healing Primary
Speed of recovery Slow
Allows perfect alignment of the fracture
Advantages Holds bone in compression allowing for
primary healing
Stress shielding at the site of the plate
Disadvantanges
Some periosteal stripping inevitable
May initially need secondary support such
Other information
as a splint or cast
Tibial plateau fracture
Applications Displaced distal radial fracture

Type of Fixation: External Fixator Devices

Biomechanics Stress sharing

Type of bone healing Secondary
Speed of recovery Fast
Allows access to soft tissue
Advantages
if wounds are open
Pin tract infections
Disadvantanges
Cumbersome

Mainly used if patients have

associated soft tissue injuries
Other information that prevent ORIF or if patient
is too sick to undergo lengthy
surgery

Open tibial fractures

Applications Severely comminuted distal
radial fractures

Type of Fixation: Screws, Pins, or Wires

Biomechanics Stress sharing
Type of bone healing Secondary
Speed of recovery Fast
Minimal incision size often needed
Advantages Less chance of growth plate damage with
the use of smooth wires (Kirschner wires/
K-wires)
Difficult to get perfect alignment
Disadvantanges Hardware may need to be removed after
healing is achieved
Often needs secondary support such as
Other information
a splint or cast
Displaced patellar fractures
Applications Pediatric displaced supracondylar
humeral fractures
C
FIG. 5.1
Fracture fixation methods. (A) Compression plate and screws. (B) External fixator devices. (C) Screws, pins, or
wires. (D) Rods/nails. (E) Short or long cast of plaster or fiberglass; brace. ORIF, Open reduction with internal
fixation. (From Cameron MH, Monroe LG. Physical Rehabilitation. St. Louis: Saunders; 2007.)
 Musculoskeletal System     CHAPTER 5 97

Type of Fixation: Rods/Nails

Biomechanics Stress sharing

Type of bone healing Secondary
Speed of recovery Fast
Smaller incision than plates so often
Advantages less soft tissue damage caused by
surgery
Early weight bearing possible
Disruption of endosteal blood supply
Disadvantanges
Reaming may cause fat emboli
Other information Reamed rods are most commonly used

Applications Midshaft tibial and femoral fractures

D
Type of Fixation: Short or Long Cast of Plaster
or Fiberglass; Brace
Biomechanics Stress sharing
Type of bone healing Secondary
Speed of recovery Fast
Noninvasive
Advantages Easy to apply
Inexpensive
Skin breakdown or maceration
Reduction of fracture may be
Disadvantanges lost if cast becomes loose
Potential for harmful pressure
on nerve/blood vessels
Most commonly used means of
Other information
fracture support
Torus fracture of the wrist
Applications Nondisplaced lateral malleolar
fracture

E
FIG. 5.1, cont’d

pubis. Stability of the pelvis is provided by the posterior
sacroiliac ligamentous complex.19 Pelvic fractures are classi-
fied, according to the OTA classification system, based on the
mechanism of injury and the resultant stability of the pelvic
ring (Fig. 5.3).
Stable pelvic fractures (type A injuries), due to low-
impact direct blows or falls, do not disrupt the integrity of
the pelvic ring.10 Stable pelvic fractures include avulsion
and localized nondisplaced iliac wing, pubic rami, or sacral
fractures. When a pelvic fracture is described as stable, it is
typically treated nonsurgically. Mobilization of the patient
should occur as soon as stability is achieved to ensure opti-
mal outcomes. Consultation with Orthopedics is essential in
determining patient stability and appropriateness for physi-
cal therapy intervention.20,21 Ambulation with an assistive
device that allows for limited weight bearing on the affected
side is often prescribed.
Disruption of the pelvic ring is commonly the result
of high-energy injuries that result in concurrent damage
to the urinary, reproductive, and bowel systems as well as
soft tissues, blood vessels, and nerves.21 When two or more
components of the pelvic ring are injured, leading to rota-
tional instability, but the pelvis remains stable vertically
because the posterior osteoligamentous complex has been
only partially disrupted, the pelvic fracture is considered par-
tially stable (type B).10,19
If the posterior osteoligamentous complex is completely dis-
rupted, the pelvis becomes unstable both vertically and rotation-
ally (type C).10,19 Type B and C injuries are treated with external
fixation or internal fixation using plates and screws.20 On the
basis of the stability of the fracture and type of fixation, the
physician will determine the patient’s weight-bearing status,
which could range from non–weight bearing (NWB) to weight
bearing as tolerated (WBAT) on either one or both extremities.
Functional mobility training, with the use of an assistive device,
and active and active assisted ROM exercises for both lower
extremities are encouraged as soon as the patient is physiologi-
cally stable.20 
Acetabulum Fractures.  Acetabulum fractures occur when
a high-impact blunt force is transmitted through the femoral
head into the acetabulum. Depending on the direction of the
force, different components of the acetabulum may be injured
98 CHAPTER 5     Musculoskeletal System

Hematoma
Compact bone Medullary cavity BOX 5.1  Factors Contributing to Bone Healing

Favorable
• E  arly mobilization
• Early weight bearing
• Maintenance of
fracture reduction
• Younger age
A • Good nutrition
• Minimal soft tissue
Granulation tissue
damage
Fibrocartilage Spongy bone • Patient compliance
• Presence of growth
hormone
Unfavorable
• T  obacco smoking
• Presence of disease, such as diabetes,
anemia, neuropathy, or malignancy
• Vitamin deficiency
• Osteoporosis
• Infection
• Irradiated bone
• Severe soft tissue damage
• Distraction of fracture fragments
• Bone loss
• Multiple fracture fragments
• Disruption of vascular supply to bone
• Corticosteroid use

B 2017:2655-2711; Buckwalter JA, et al. Bone and joint healing. In: Bucholz R,
Bony callus
C Proximal Femur Fractures.  Fractures of the proximal femur
D dislocation and acetabular fracture, although the fracture can
FIG. 5.2
Fracture healing occurs in four stages. (A) Hematoma. (B) Granulation
tissue. (C) Bony callus. (D) Remodeling. (From Damjanov I. Pathology for
the Health Professions. 4th ed. St. Louis: Saunders; 2011.)
(Fig. 5.4). If the hip is flexed and a force is transmitted through
the femur posteriorly, as commonly occurs in a motor vehicle
accident, the posterior wall will fracture.22 An acetabulum frac-
ture is a complex injury and is associated with retroperitoneal
hematomas, injury to the lungs, shock, dislocation or fracture of
the femoral head, and sciatic nerve palsy.22,23 Acetabulum frac-
tures are, by nature, intraarticular; hence medical management
focuses on the restoration of a functional and pain-free weight-
bearing joint.24 Closed reduction via skeletal traction with bed
rest for the initial 6 to 8 weeks may be used if the patient is
unable to undergo surgery.24 Surgical management includes
percutaneous pinning, ORIF, and THA.
Upon stabilization of the fracture, functional mobility
activities should be initiated. Locomotion training with the
appropriate assistive device is required because the patient will
Data from Wood GW, II. General principles of fracture treatment. In: Canale ST,
Beaty JH, eds. Campbell’s Operative Orthopaedics. 13th ed. Philadelphia: Elsevier;
Heckman J, Court-Brown C, et al, eds. Rockwood and Green’s Fractures in Adults.
vol 1. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2010:90-97.
likely have limited weight bearing according to type of surgi-
cal intervention, typically touchdown weight bearing (TDWB)
or partial weight bearing (PWB), through the involved lower
extremity. Active assisted exercises to the involved hip should
be prescribed bearing in mind any hip precautions dictated by
the physician (e.g., following THA). 
include proximal trochanteric, neck, and head fractures.10 Col-
lectively they are often referred to as hip fractures. They can be
classified as intracapsular or extracapsular. In the older adult, a
femoral neck fracture can be caused by surprisingly little force
because of 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.
Femoral head fractures are associated with a posterior hip
occur in the absence of either of these conditions.25 Hip disloca-
tions require urgent reduction because the vascular supply to
the femoral head may be compromised.25 Management of hip
dislocation without fracture includes closed reduction under
conscious sedation and muscle relaxation possibly followed by
traction or open reduction if closed reduction fails. Rehabilita-
tion includes functional mobility activities with weight-bearing
limitations, exercise, and positioning per physician order based
on hip joint stability and associated neurovascular injury. Hip
dislocation with fracture warrants surgical repair.
CLINICAL TIP
After posterior hip dislocation, precautions typically include lim-
iting hip flexion to 90 degrees, internal rotation to 0 degrees,
and adduction to 0 degrees. Patients should be instructed to
avoid pivoting on involved lower extremity in weight-bearing
positions. For a patient that is confused or noncompliant, who
sustained a posterior hip dislocation, indirect restriction of hip
movement during rest or functional activity can be achieved
with the use of a knee immobilizer or hip abduction brace.
 Musculoskeletal System     CHAPTER 5 99

Intracapsular fractures are located within the hip joint cap-

A older adult who has a displaced femoral neck fracture, some sur-
B or intramedullary nail.28 Mobility and gait training focuses on
C proximal, middle, and distal third) and through descriptive
FIG. 5.3
Classification of pelvic fractures. (A) Lesions sparing (or with no displace-
ment of) the posterior pelvic arch. (B) Incomplete disruption of the poste-
rior arch (partially stable). (C) Complete disruption of the posterior arch
(unstable). (Courtesy the Orthopedic Trauma Association.)
sule and include the femoral head, subcapital, and femoral neck
regions. The four-stage Garden scale (Fig. 5.5) is used to classify
femoral neck fractures and is based on the amount of displace-
ment and the degree of angulation.
• Garden stage I fractures are impacted and incomplete.
• Garden stage II fractures are complete and nondisplaced.
• Garden stage III fractures are complete and partially dis-
placed.
• Garden stage IV fractures are completely displaced.
Femoral neck fractures require reduction and internal fixa-
tion, often through the use of cannulated screws.25,26 In the
geons may elect to use a prosthetic replacement of the femoral
head (hemiarthroplasty) to minimize the development of osteo-
necrosis or nonunion.25,26
Extracapsular fractures occur outside of the hip joint capsule.
They can be further classified as intertrochanteric or subtro-
chanteric. Intertrochanteric fractures occur between the greater
and lesser trochanters. Subtrochanteric fractures occur below the
lesser trochanter and end at a point 5 cm distally.27 Intertro-
chanteric and subtrochanteric fractures are shown in Fig. 5.6.
Extracapsular fractures are typically stabilized via open reduc-
tion and internal fixation through the use of a sliding hip screw
ensuring protected weight bearing. Active or assisted hip ROM
and strengthening exercises should be initiated to foster an early
restoration of function. 
Femoral Shaft Fractures.  Fractures of the femoral shaft
typically result from high-energy trauma and are associated
with concurrent injuries to the pelvis and ipsilateral lower
extremity.29 Femoral shaft fractures can be accompanied by
life-threatening systemic complications, such as hypovo-
lemia, shock, or fat emboli. There also can be significant
bleeding into the thigh with hematoma formation. Femoral
shaft fractures can be classified based on their location (e.g.,
terms (Fig. 5.7). In the presence of contamination or hemo-
dynamic instability, external fixation or skeletal traction may
be applied temporarily.30 For most surgeons, the treatment
of choice is the use of an intramedullary nail.29 After intra-
medullary nailing, the patient should avoid rotation of and
pivoting on the lower extremity because microrotation of the

A B C D
FIG. 5.4
The innominate bone and the acetabulum are divided into anterior and posterior columns to reference the
location of the trauma. Classification of acetabular fractures: (A) Anterior column. (B) Posterior column. (C)
Transverse, involving both columns. (D) Complex or T-shaped, involving both columns. (From McKinnis LM.
Fundamentals of Musculoskeletal Imaging. Philadelphia: FA Davis; 2010:348.)
100 CHAPTER 5     Musculoskeletal System
Grade I Grade II
Grade III Grade IV
FIG. 5.5
The Garden classification of femoral neck fractures. Grade I is an incom-
plete, impacted fracture in valgus malalignment (generally stable). Grade
II is a nondisplaced fracture. Grade III is an incompletely displaced frac-
ture in varus malalignment. Grade IV is a completely displaced fracture
with no engagement of the two fragments. The compression trabeculae
in the femoral head line up with the trabeculae on the acetabular side.
Displacement is generally more evident on the lateral view in grade IV.
For prognostic purposes, these groupings can be lumped into nondis-
placed/impacted (grades I and II) and displaced (grades III and IV)
because the risk of nonunion and aseptic necrosis is similar within these
grouped stages. (From Browner BD, Jupiter JB, Levine AM, et al. Skeletal
Trauma: Basic Science, Management, and Reconstruction. 4th ed. Philadelphia:
Saunders; 2009.)
intramedullary rod can occur and place stress on the fixation
device. Initially, weight bearing may be limited, as deter-
mined by the surgeon. Active and assisted ROM of the hip,
quadriceps setting, straight-leg raises, and hip abduction
exercises should be initiated.
CLINICAL TIP
The uninvolved leg or a single crutch can be used to assist the
involved lower leg in and out of bed if determined precautions
allow and if compensatory measures are needed to promote
independence.
Distal Femur Fractures.  Fractures of the distal femur are
classified according to the OTA classification system as extraar-
ticular (type A), partial articular (type B), or complete articu-
lar (type C).10 Involvement of the articular surface of the knee
joint complicates the fracture. Typically this type of fracture
is caused by high-energy impact to the femur, especially in
younger patients, or a direct force that drives the tibia cranially
b
a
FIG. 5.6
Fractures of the proximal femur: Neck (A); intertrochanteric (B); subtro-
chanteric (C). (From Pfenninger JL, Fowler GC, eds. Procedures for Primary
Care. 3rd ed. Philadelphia: Mosby; 2011.)
into the intercondylar fossa. Distal femur fractures may be
accompanied by injury to localized skin, muscle, and joint
ligaments and cartilage with the potential for decreased knee
joint mechanics.31
Postoperative rehabilitation will depend on the severity of
the fracture and surgical techniques used for reduction and
fixation. Early mobility and gentle active assisted knee ROM
exercises are encouraged for the majority of these patients.
Depending on the type of surgery, the physician will dictate
weight-bearing limitations—typically NWB, TDWB, or
PWB—and the need for any bracing (e.g., knee immobilizer or
locked hinged brace). 
Patella Fractures.  A patella fracture results from direct
trauma to the patella from a fall, blow, or motor vehicle accident
(e.g., dashboard injury) or indirect mechanisms from a forceful
contraction of the quadriceps with the knee flexed.32 Injury to
the patella may lead to alterations in the articular surface of the
patellofemoral joint and abnormal extensor mechanism mechan-
ics. Late complications include patellofemoral or hardware pain,
osteoarthritis, decreased terminal extension, quadriceps weak-
ness, or adhesions.32 Nonsurgical management through immo-
bilization of the knee in extension via a cast or brace may be
chosen for nondisplaced fractures or patients with significant
medical cormorbidities.33 Surgical treatment includes reduc-
tion and internal fixation, with a partial or total patellectomy
reserved for highly comminuted fractures. Postoperatively, the
knee is immobilized, and quadriceps setting exercises are ini-
tiated. Strong, forceful quadriceps contractions and straight-
leg raises should be avoided. Protected weight bearing should
ensue, abiding by the weight-bearing limitations prescribed by
the physician. 
 Musculoskeletal System     CHAPTER 5 101

A B

C
FIG. 5.7
Femur fracture patterns. (A) Transverse. (B) Oblique. (C) Spiral. (D) Butterfly fragment (arrow). (E) Commi-
nuted. (F) Segmental. (From Townsend CM, Beauchamp D, Evers M, Mattox KL. Sabiston Textbook of Surgery.
19th ed. Philadelphia: Saunders; 2012.)
102 CHAPTER 5     Musculoskeletal System
E F
FIG. 5.7, cont’d
Tibial Plateau Fractures.  Tibial plateau fractures typically
result from direct force on the proximal tibia (e.g., when a
pedestrian is hit by an automobile) and are considered extraar-
ticular, partial articular, or complete articular.10 The Schatzker
classification system is commonly used in cases of displaced frac-
tures (Fig. 5.8). This high-force injury often presents with open
wounds and soft tissue injuries, including capsular, ligamentous,
and meniscal disruption. Immediate or early complications of
tibial plateau fractures include popliteal or peroneal nerve com-
pression, compartment syndrome, infection, and DVT.29 Late
complications include abnormal patellofemoral mechanics, lack
of ROM or stability, and posttraumatic arthritis of the articular
surface. Surgical management via internal or external fixation
is used for fractures that are unstable or associated with liga-
mentous and articular disruption.29 The complexity of the tibial
plateau fracture will dictate the precautions for movement and
mobility after surgery. In most situations, no weight bearing
will be allowed during the initial healing phases, and gentle
active or active assisted knee ROM exercises may be delayed for
several days postoperatively.  long-axis compression throughout the proximal lower extrem-
Tibial Shaft and Fibula Fractures.  Tibial shaft and fibula
fractures typically result from high-energy trauma, such as
motor vehicle and skiing accidents. The higher the energy on
impact, the more is the soft tissue and bone damage, includ-
ing concomitant damage to the ankle (e.g., trimalleolar fracture,
syndesmotic disruption, or talar dome fracture). Complications
associated with tibial shaft fractures include anterior tibial
artery and peroneal nerve injury and compartment syndrome.
Tibial shaft fractures can be classified based on their location
(e.g., proximal, middle, and distal third) and through descrip-
tive terms (e.g., simple, wedge, and complex) from the OTA
classification system.10
Nonsurgical management through the use of casts or braces
may be provided for stable nondisplaced tibial and fibular frac-
tures associated with low-energy trauma.29 Surgical treatment
typically includes reduction followed by plate and screw fixation,
intramedullary nail insertion, or external fixation. Early mobility
with restricted weight bearing, as determined by the surgeon, is
encouraged. Knee and ankle (unless the foot is involved) ROM
and quadriceps strengthening exercises should also be initiated. 
Distal Tibia and Ankle Fractures.  Fractures of the distal tibia,
distal fibula, and talus are described together because of their
frequent simultaneous injury. Malleolar ankle fractures result
from rotational mechanisms, whereas distal tibial fractures (i.e.,
pilon fractures) are the result of high vertical loading forces,
such as falls from heights and motor vehicle accidents.34 Often,
ity can cause associated tibial plateau fracture, hip dislocation,
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 syndes-
mosis. Stability of the ankle depends on joint congruity and
 Musculoskeletal System     CHAPTER 5 103

FIG. 5.8
Tibial plateau fractures: Schatzker classification system. In this system, the treatment is more difficult and the
prognosis poorer with higher fracture types. Types I, II, and III fractures are low-energy injuries that often occur in
older persons and involve the lateral tibial plateau. Types IV, V, and VI fractures are higher-energy injuries and are
associated with fracture comminution and involvement of the medial aspect of the tibia or medial tibial plateau.
Type I injuries may also occur in young persons and are characterized by a split or wedge fracture line, although
the size of the wedge is variable. These fractures are commonly associated with lateral meniscal tears or entrapment.
Type II fractures are characterized by a lateral split fragment with or without articular depression just medial to the
split. Type III fractures are characterized by pure articular depression. Type IV fractures involve the medial tibial
plateau and may be further subdivided into those that are split fractures (type IVA) and those that are depression
injuries (type IVB). These fractures may extend to the lateral aspect of the midline. Type V fractures involve both
tibial plateaus and are often designated bicondylar fractures. Type VI fractures extend inferiorly to involve the
metaphysis and diaphysis of the tibia. (From Langford JR, Jacofsky DJ, Haidukewych. Tibial plateau fractures. In:
Insall JN, Scott WN, eds. Surgery of the Knee. 5th ed. New York: Churchill Livingstone; 2012:775.)

ligamentous integrity. The majority of distal tibial and ankle
fractures are managed through open reduction and internal fixa-
tion techniques. Surgical management for distal tibial and ankle
fractures typically includes reduction and internal fixation with
screws and plates. After fixation, the ankle may be immobilized
in a neutral position a short leg cast, posterior plaster splint,
removable splint, or fracture boot. Weight bearing will be lim-
ited. Knee ROM and proximal joint strengthening should be
prescribed.  bility must be provided to unstable segments. The standard of
Calcaneal Fractures.  The most commonly fractured bone of
the foot is the calcaneus, with fractures caused by axial loading
or a direct blow, such as a fall from a height or motor vehicle
accident. Calcaneal fractures, usually bilateral, are associated
with disruption of the subtalar joint. Nondisplaced fractures are
managed nonsurgically, whereas reduction and internal fixation
with plates and screws is used for displaced but reconstructable
articular fractures.35 Locomotion training with the appropriate
assistive device is required because the patient will be allowed
no weight bearing through the ankle joint. Depending on the
type of immobilization device, the physician may dictate spe-
cific ankle/forefoot motions. 
Spine.  Fractures to the vertebral column occur less fre-
quently than fractures to the extremities. Approximately half
the individuals with spinal trauma sustain spinal cord or periph-
eral nerve root injury as well (refer to the Spinal Cord Injury
section in Chapter 6).36 Preservation of neurologic function is
the primary goal of medical treatment. Thus mechanical sta-
treatment for most spinal injuries is closed reduction and sta-
bilization through the use of external braces and orthoses.36
The primary indication for surgical management is unstable
ligamentous injury or disruption of the vertebral column with
concomitant neurologic injury.36 If surgical reduction with fixa-
tion is required, it is performed as soon as the patient is medi-
cally stable. Secondary management of spinal fracture may also
include the following:
• Examination and treatment of associated extremity fracture,
or head or internal injuries
104 CHAPTER 5     Musculoskeletal System
• V
 ery frequent (every 15–30 minutes) neurovascular assess-
ment by nursing
Physical therapy management after spinal fracture without
neurologic injury focuses on protecting the fracture and surgi-
cal site during all functional mobility activities. Before initiat-
ing physical therapy in a patient with suspected spinal trauma,
the therapist must ensure that the spine has been “cleared” for
mobility. Reviewing the results of diagnostic imaging as well as
discussion with the surgical team will allow the therapist to ver-
ify the stability of the spine and the appropriateness of initiating
mobilization activities. Also, temporary immobilization devices
(e.g., a cervical collar) should not be removed until ordered by
the physician.
Once the spine has been “cleared,” instructing the patient
on proper mobility, including “logroll” techniques, is essential.
These precautions include having the patient roll nonsegmen-
tally with the head, torso, and hips as one unit (i.e., no rotation).
Patient education includes instruction on spinal precautions,
proper posture and body mechanics and use of any physician-
ordered braces or orthotics. Therapeutic exercises, including
strengthening and ROM exercises, will depend on the patient’s
clinical presentation. Refer to the Physical Therapy After Spinal
Surgery section for additional guidance on mobilizing a patient
after spinal stabilization.  any, will be dictated by the physician.
Upper Extremity
Shoulder Girdle Fractures.  Fractures of the scapula typically
occur during high-injury collisions; associated injuries include
rib fracture, pneumothorax, spinal injuries, and ipsilateral
upper extremity fracture.37 They are classified as extraarticu-
lar (not glenoid), partial articular (glenoid), or total articular
(glenoid).10 Fractures that do not involve the articular surface
often require minimal treatment (other than pain management)
because the surrounding musculature serves to protect and
immobilize the fracture site. Surgical reduction and fixation is
necessary for intraarticular fractures and fractures of the coracoid
with acromioclavicular separation.38
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
nonunion, neurovascular compromise, coracoclavicular ligament
tear, or floating shoulder (fracture of both the clavicle and surgical
neck of the scapula), as well as for separation of fracture fragments
by the deltoid or trapezius muscle.38 Short-term immobilization
in a sling or brace is typical after ORIF.  pronated forearm can cause a radial head or neck fracture. The
Proximal Humerus and Humeral Shaft Fractures.  Proxi-
mal humerus fractures occur when the humerus is subjected
to direct or indirect trauma and are associated with rotator
cuff injuries, and brachial plexus or peripheral nerve dam-
age.39 These fractures are typically defined as minimally dis-
placed or displaced and may be classified according to the OTA
classification system as an extraarticular, unifocal fracture (type
A); extraarticular, bifocal fracture (type B); or articular frac-
ture (type C).10 Minimally displaced fractures are managed
nonsurgically. A sling is provided for comfort, and pendulum
exercises initiated through physical therapy begin approxi-
mately 1 week after injury.38 Displaced proximal fractures may
be treated with closed reduction and percutaneous pinning,
intramedullary nailing, or screw and plate fixation. Rehabili-
tation focuses on active assisted ROM exercises of the shoulder
and functional mobility training while maintaining no weight
bearing through the shoulder.
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.
Humeral shaft fractures are often the result of high-energy
trauma, such as a fall from a height, a motor vehicle accident
in the younger patient, or a simple fall in the older adult.40
Humeral shaft fractures may be associated with radial nerve or
brachial plexus injury. Most humeral shaft fractures are man-
aged nonsurgically with closed reduction and immobilization
in a splint or brace. Functional mobility training while pro-
tecting the shoulder is encouraged. Typically, no weight bear-
ing through the involved upper extremity will be allowed. The
extent of assisted ROM exercises of the shoulder and elbow, if
CLINICAL TIP
Getting in and out of bed on the opposite side of an upper arm
fracture is usually more comfortable for the patient.
Distal Humeral and Proximal Forearm Fractures.  Dis-
tal humeral fractures are rare but complex fractures to manage
because of the bony configuration of the elbow joint, adjacent
neurovascular structures, and limited access to the articular sur-
face.39 Nonsurgical management is reserved for nondisplaced,
stable fractures. All other fractures typically require surgical treat-
ment, which consists of ORIF; total elbow arthroplasty (TEA) is
an option for severely comminuted intraarticular fractures.
Proximal forearm fractures involve the olecranon, the head
or neck of the radius, and the proximal third of the ulna. Olec-
ranon fractures result from direct trauma to a flexed elbow or
a fall on a partially flexed outstretched hand. If the fragments
are displaced, surgical treatment will include open reduction
and internal fixation. A fall onto an outstretched hand with a
majority of radial head fractures have good outcomes with non-
surgical management.38 Severely comminuted fractures, loose
bone fragments in the joint, and involvement of more than one-
third of the articular surface require surgical fixation.38 Any dis-
placed fracture of the radial neck and proximal ulna will also be
managed with surgical fixation.
Rehabilitation management of distal humerus and proximal
forearm fractures are similar. Initially the elbow is splinted, and
early active assisted elbow ROM exercises may be initiated sev-
eral days after surgery (physician dictated), although aggressive

passive ROM should be avoided. No weight bearing through
the involved arm should occur during any functional mobility
activities.  including medical and rehabilitation management, impair-
Fractures of the Shaft of the Radius and Ulna.  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. Because of the high-energy impact, the
fracture is usually displaced and is associated with neurovascular
injuries and compartment syndrome.41 A distal radial fracture is
often referred to as a Colles fracture if there is dorsal displacement
of the radius. Treatment options include closed reduction and
casting or percutaneous pinning, and ORIF. Immobilization
with braces or splints may be ordered by the physician after sur-
gical treatment. The physical therapist should note if there are
any orders to initiate elbow, wrist, and hand active ROM exer-
cises during the patient’s hospitalization. Functional mobility
training should occur while ensuring that no weight is applied
through the involved arm.
CLINICAL TIP
Edema management should be initiated by elevating the fore-
arm, wrist, and hand on pillows.  
Carpal, Metacarpal, and Phalangeal Fractures.  Carpal,
metacarpal, and phalangeal fractures are typically associated with
direct trauma from higher risk recreational, occupational, and
sports activities.42 Many of these fractures are accompanied by
soft tissue injuries that can result in treatment delay of several
days to allow for reduction of edema. Fractures are typically man-
aged either by closed reduction and immobilization via casts or
splints or by surgical fixation followed by immobilization with
a splint or cast. Patients with isolated carpal, metacarpal, or pha-
langeal fracture are usually treated in the ambulatory care setting.
CLINICAL TIP
For patients who have concurrent lower- and distal upper-
extremity injuries and require the use of a walker or crutches,
a platform attachment placed on the assistive device may allow
for weight bearing through the upper extremity proximal to the
wrist. Weight bearing restrictions and patient safety will dictate
the feasibility of this adaptation.
Joint Arthroplasty
Joint arthroplasty is the surgical reconstruction of articular sur-
faces with prosthetic components. It is reserved for the indi-
vidual 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. Its purpose is to restore function and motion to
the involved joint. This surgery is primarily elective and can be
unilateral or bilateral.
Joint arthroplasty typically 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 out-
comes. Physical therapists must consider various factors when
Musculoskeletal System     CHAPTER 5 105
designing the treatment plan for these patients. Specifically the
therapist needs to understand the patient’s preoperative history,
ments and activity limitations, surgical technique, prosthesis
type, fixation method, soft tissue disruption and repair, and type
of anesthesia, because all of these will dictate any postoperative
precautions or guidelines. Although total joint arthroplasty is
primarily considered an inpatient surgical intervention, a highly
selected group of patients are receiving total joint arthroplasty
on an outpatient basis. Evidence is showing improved patient
care, better satisfaction and lower overall cost.43 Thus preopera-
tive education and intervention for these predicted surgeries are
critical because patients are only in acute care for a short obser-
vation period postoperatively.
The following sections provide basic surgical information
and acute care hospital rehabilitation management strategies 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), avas-
cular necrosis (AVN), hip infection, or congenital disorders.
THA involves the replacement of both the femoral head and
the acetabulum with a combination of metal (titanium or
cobalt alloys), ceramic, and/or polyethylene components
(Fig. 5.9).
Fixation for the acetabular and femoral components may be
cemented, cementless with porous surface for bony ingrowth,
or cementless press-fit. With cementless components, weight
bearing may be limited by surgeon protocol, although WBAT is
more prevalent as evidence supports little adverse surgical effects
and increased patient outcomes.44,45 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 emphasis for the
FIG. 5.9
Bilateral total hip arthroplasty. (From Daniels AU, Tooms RE, Harkess
JW. Arthroplasty: Introduction and overview. In: Canale ST, ed. Campbell’s
Operative Orthopaedics, 9th ed. Vol. 1. St. Louis: Mosby; 1998:211-231.)
106 CHAPTER 5     Musculoskeletal System
patient should be the prevention of torque or twisting on the
operated leg while weight bearing. A cemented prosthesis allows
for early weight bearing to tolerance in the early recovery phase.
Surgical approaches for hip arthroplasty can be defined by how
the hip joint is accessed in relation to the greater trochanter (i.e.,
posterior or posterolateral, anterior or anterolateral, transtrochan-
ter or direct lateral), leg position for dislocating the femur (i.e.,
flexion = posterior dislocation, extension = anterior dislocation),
and status of the surrounding musculature (i.e., need for detach-
ment and repair of external rotators and abductors).45 Recent
studies suggest that there is no significant difference in clinical
benefit in regard to pain, function, and gait mechanics between
anterior and posterior approaches.46,47 For all approaches, patients
tend to walk faster and have an increased step length and stride
length postoperatively compared with preoperatively.46
A good understanding of the surgical approach taken to expose
the hip joint is necessary to determine movement precautions
that prevent dislocation postoperatively. Posterior dislocations
usually occur in the presence of excessive flexion, adduction, and
internal rotation, especially after surgery with a posterolateral
approach that has weakened the posterior capsule and soft tissue
structures. Anterior dislocation usually occurs during excessive
extension, adduction, and external rotation. In the acute care set-
ting, 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 dis-
location until these structures are well healed, edema is reduced,
and the surrounding musculature is strengthened. There is no
scientific evidence to support the benefit of incorporating hip
dislocation precautions into the immediate postoperative man-
agement of all patients who have undergone THA.48,49 Despite
these findings, THA precautions are often prescribed by sur-
geons, and the therapist should be aware of common hip disloca-
tion precautions to be followed after THA (Table 5.2).
CLINICAL TIP
If the physical therapist suspects that a patient has a hip dislo-
cation, the therapist should immediately contact the patient’s
nurse and physician so that further testing and appropriate
medical management can be initiated. Signs and symptoms of
hip dislocation include excessive pain with motion, abnormal
internal or external rotation of the limb with limited active and
passive motion, inability to bear weight through the limb, and
shortening of the limb.
Complications that may occur during or after THA include
fracture, aseptic loosening, hematoma formation, heterotopic
ossification, infection, dislocation, nerve injury, vascular dam-
age, thromboembolism that can cause pulmonary embolism,
myocardial infarction, cerebral vascular accident, and limb-
length discrepancy.50
Physical Therapy After Hip Arthroplasty.  Ideally, physi-
cal therapy should begin before the surgery. Preoperative physi-
cal therapy should focus on educating the patient and caregivers
on the expected course of rehabilitation after surgery and any
TABLE 5.2  Surgical Approaches and Common Hip
Dislocation Precautions for Total Hip Arthroplastya
Surgical Approach Dislocation Precautions
Posterolateral or No hip flexion beyond 90 degrees
posterior No internal rotation past neutral
No hip adduction past neutral
Anterolateral or anterior No hip extension and external rotation
In some cases, no active hip abduction
aHip surgery performed in conjunction with a trochanteric osteotomy (removal
and reattachment of the greater trochanter) will require an additional movement
restriction of no active abduction or passive adduction. Weight bearing of the
surgical limb may be limited further.
Data from Harkess JW, Crockarell JR. Arthroplasty of the hip. In: Canale ST,
Beaty JH, eds. Campbell’s Operative Orthopaedics. 13th ed. Philadelphia: Elsevier;
2017:165-321.
BOX 5.2  Common Activity Restrictions After Total Hip
Arthroplasty
• A  void hip motion into prohibited ranges based on dislocation
precautions dictated by the surgeon
• No sitting on low surfaces
• No sleeping on operative side
Data from Harkess JW, Crockarell JR. Arthroplasty of the hip. In: Canale ST,
Beaty JH, eds. Campbell’s Operative Orthopaedics. 13th ed. Philadelphia: Elsevier;
2017:165-321.
postoperative precautions, and training on proper transfer tech-
niques, appropriate assistive device use for locomotion, and
postoperative exercises.
Regardless of the surgery being performed on an outpatient
or inpatient basis, early postoperative physical therapy interven-
tion should be focused on functional mobility training, patient
education about movement precautions during ADLs, and
strengthening of hip musculature.51–53 Physical therapy may
assist in preventing complications, such as atelectasis, blockage
of the intestines because of decreased peristalsis secondary to
anesthesia (postoperative ileus), and DVT. Early mobilization
improves respiration, digestion, and venous return from the
lower extremities. Patients should be educated about these risks
to help prevent secondary complications. In addition, the poten-
tial for perioperative nerve compression exists; thus all periph-
eral innervations should be examined postoperatively, with
emphasis on the femoral nerve, which innervates the quadriceps,
and the sciatic nerve, which innervates the peroneals. Neura-
praxia of the femoral nerve can impact knee extension, and if
the peroneal muscles are affected, then foot drop may also occur
on the affected side. In such a situation, a custom-fit ankle–foot
orthosis may be indicated to optimize gait.
The priority of treatment is to achieve safe functional mobil-
ity (i.e., bed mobility, transfers, and ambulation with assistive
devices) to maximize independence and functional outcomes.
Because the stability of the hip is affected by the surgical
approach, the physical therapist must confirm the presence of
any activity restrictions with the patient’s surgeon (Box 5.2).
The physical therapist should educate the patient about hip dis-
location precautions and activity restrictions, while encouraging

No!
FIG. 5.10
Total hip arthroplasty: positions to be avoided and recommended alternatives. (From Cameron MH, Monroe
LG. Physical Rehabilitation. St. Louis: Saunders; 2007.)
use of the operated limb with functional activities. Verbal and
tactile cueing may assist a patient in precaution maintenance;
failure to do so may result in hip dislocation. As noted earlier in
the chapter, the use of a knee immobilizer reduces hip flexion
by maintaining knee extension. This technique can be helpful
in preventing dislocation in patients who are unable to main-
tain posterior hip dislocation precautions independently. A knee
immobilizer may also be necessary to provide stability if the
quadriceps lack adequate strength and stability for ambulation.
The therapist should also inform the patient that movement
of the operated hip can help decrease postoperative pain and
stiffness.
Physical therapy should be initiated on the day of or the first
day after surgery for those designated to receive an inpatient
postoperative course. For those specifically selected to receive
THA on an outpatient basis, physical therapy is initiated and
transferred to the next level of care on the day of surgery. The
patient should be premedicated for pain control before the treat-
ment session. Any surgical drains should be noted. Patients
commonly are prescribed antiembolism stockings and external
compression devices to reduce the risk of a thromboembolic
event.
Patient education should include the following:
• Proper positioning for comfort and maintenance of the integ-
rity of the surgical area
Musculoskeletal System     CHAPTER 5 107
Yes
• W hen supine, the operative leg should be positioned with
the patella and the toes pointing toward ceiling (Most pa-
tients are typically in a reclined position or sitting position
in a chair postoperatively, which allows for hip flexor tight-
ness. Lying flat in bed will allow the hip joint and sur-
rounding areas to adjust more comfortably to the neutral
position.)
• Use of abduction splint (Fig. 5.10), if ordered
• Hip dislocation precautions and activity restrictions, as dic-
tated by the surgeon (see Fig. 5.10)
• Limitations on weight-bearing
• Avoidance of low chairs
• Therapeutic exercise program
Muscle spasm often occurs in the musculature surrounding
the hip postoperatively. Instructing the patient in exercises to
gain control of the musculature around the hip can help reduce
muscle spasms and can also improve control of the limb during
functional activities. Patients should be encouraged to perform
all exercises several times a day. The patient should be educated
in and perform strengthening exercises on the noninvolved
limbs because the patient will be using them more to maintain
any weight-bearing limitations through the use of an assistive
device.
Isometric exercises for the quadriceps and gluteal muscles
can be performed immediately after surgery, progressing to
108 CHAPTER 5     Musculoskeletal System
active-assisted and active exercises as tolerated. As maxi-
mal gluteal isometrics have been shown to generate greater
acetabular contact pressures compared with weight-bear-
ing activities themselves, a submaximal effort should
be encouraged.54–56 Straight-leg raises should also be
avoided because they put rotational stresses on the femoral
component.50
Before establishing an advanced strengthening program
consisting of progressive resistive exercises or weight training,
the surgeon should be consulted to determine the appropriate
time frame for initiation of these exercises because excessive
strain can hinder healing of structures that were involved in
the surgery.
Therapeutic exercises during the immediate postoperative
phase should include:
• Deep breathing and antiembolism exercises (e.g., ankle
pumps)
• Passive, active assisted, and active ROM within the param-
eters of any hip movement precautions in supine
• Hip flexion and abduction within the parameters of any hip
movement precautions in the supine position
• Submaximal isometrics for gluteal muscles in the supine po-
sition
• Isometrics for the quadriceps muscles in the supine position,
progressing to active-assisted and active ROM as tolerated in
the supine and sitting positions
• As out-of-bed activities increase, initiation of active ROM,
gravity-only hip flexion, abduction, and extension within
the parameters of any hip movement or activity restriction
guidelines
Transfer and locomotion training with the appropriate
assistive device based on the patient’s weight-bearing restric-
tions should begin as soon as possible. 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 elevated position is especially helpful for
patients with bilateral THA. If available, a hip chair (or other
elevated seating surface) and commode chair should be used
to facilitate transfers, while maintaining hip movement pre-
cautions after a posterior or posterolateral approach. Preopera-
tive and postoperative education regarding use of furniture of
the appropriate height in the home should be initiated by the
physical therapist.
During gait training, the patient should be instructed to
avoid pivoting on the operated extremity when ambulating
by taking small steps and turning away from the operated leg
to maintain movement precautions. If appropriate, patients
should also be trained how to safely ascend and descend stairs
before discharge. Additionally, based on the patient’s pre-
sentation, an aerobic exercise program may be added to the
therapeutic exercise regimen because the patient’s limitations
in functional performance could be attributed to decondition-
ing and a decreased aerobic capacity. Patients should be pro-
vided with printed instructions on their therapeutic exercise
program, dislocation precautions and activity restrictions, and
signs and symptoms of dislocation as well as what they should
do if it occurs.
CLINICAL TIP
Implementing physical therapy examinations on postoperative
day 0 (POD 0) is becoming the standard for patients status post
uncomplicated joint arthroplasty. Early mobilization has shown
to increase functional mobility, lead to shorter length of stay, and
enhance recovery57 Patients need to be carefully monitored to
determine the appropriateness of an early mobilization protocol.
The considerations include hemodynamic stability, surgical sta-
bility, pain, current cognitive state, and response to anesthesia.
CLINICAL TIP
As the initial healing stages begin, the patient may feel as though
one leg is longer while ambulating. This condition is referred to
as “apparent leg length discrepancy” and is associated with the
newly restored joint space that was preoperatively lessened by
cartilage wearing.8,9 Patients are usually concerned because it
is a sudden noticeable increase in height, whereas the progres-
sive decrease in joint space preoperatively was gradual and less
noticeable. It is important to educate patients on this subject and
assure them 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
facilitate a sensation of more “evenness” during ambulation.
 
Trochanteric Osteotomy
A trochanteric osteotomy is a procedure that may be used dur-
ing hip arthroplasty to allow for easier dislocation of the hip and
exposure of the articular surfaces, especially in the presence of
distorted anatomy.50 If abductor muscle laxity has resulted in
hip instability, a trochanteric osteotomy can change the length
of the abductors and improve stability. 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 trochan-
ter is reattached to the femur with wires (Fig. 5.11).
Physical Therapy After Trochanteric Osteotomy.  As
most trochanteric osteotomies occur during hip arthroplasty,
physical therapy management follows the same general guide-
lines for patients who have undergone THA. Because a portion
of the greater trochanter with the abductor muscles attached
was resected and then reattached to the femur, activity restric-
tions will be required. Specifically, no active or active assistive
abduction is allowed. Procedures differ based on surgeon prefer-
ence, so the physical therapist should verify these and any other
weight-bearing or activity restrictions. Patients should be edu-
cated in how to perform all therapeutic exercises and functional
mobility activities while maintaining these precautions.
CLINICAL TIP
The patient can be instructed in using a leg lifter to support the
operative extremity and assist with positioning and getting the
limb in and out of bed to avoid active abduction of the hip.
 
 Musculoskeletal System     CHAPTER 5 109

B C
A
FIG. 5.11
Wire fixation of trochanter. (A) Two vertical wires are inserted in hole drilled in lateral cortex below abductor tu-
bercle; they emerge from cut surface of neck, and one is inserted in hole in osteotomized trochanter. Two vertical
wires are tightened and twisted, and transverse wire that was inserted in hole drilled in lesser trochanter and two
holes in osteotomized trochanter is tightened and twisted. (B) One-wire technique of Coventry. After component has
been cemented in femur, two anteroposterior holes are drilled in femur beneath osteotomized surface, and two holes
are drilled in osteotomized trochanter. One end of wire is inserted through lateral loop before being tightened and
twisted. (C) Oblique interlocking wire technique of Amstutz for surface replacement. (A, Modified from Smith &
Nephew, Memphis, TN. B and C, Redrawn from Markolf KL, Hirschowitz DL, Amstutz HC. Mechanical stability
of the greater trochanter following osteotomy and reattachment by wiring. Clin Orthop Relat Res. 1979;141:111.)

Hip-Resurfacing Arthroplasty
Hip-resurfacing arthroplasty (HRA) has evolved over time as
an alternative to THA in young, active patients with end-stage
osteoarthritis. It is desirable because of its femoral bone conserv-
ing properties and its ability to better preserve the biomechan-
ics of the hip, resulting in higher postoperative activity levels
compared with conventional THA.58–60 Modern implants use
metal-on-metal components with a cemented femoral stem and
cementless press-fit acetabular cup (Fig. 5.12). Complications
include infection, femoral neck fracture or notching, avascular
necrosis of the femoral head, component loosening, hypersensi-
tivity to metal ions, and higher incidence rates of revision than
for THA.58,60,61
Physical Therapy After Hip-Resurfacing Arthro-
plasty.  The postoperative pathway after HRA may vary, FIG. 5.12
depending on the surgical protocol, surgeon preference, com- Radiograph of a patient with a right total hip replacement and a left hip
plexity of the surgical procedure, and patient status. HRA may resurfacing. The total hip replacement consists of a longer stem placed in
the medullary canal of the femur. The hip resurfacing implant preserves
be performed on an outpatient basis in uncomplicated cases ,
the proximal femoral bone. (From Schafer AI, Goldman L. Goldman-Cecil
whereas in more complicated cases, patients may be admitted Medicine. 24th ed. Philadelphia: Saunders; 2012.)
for observation and continued intervention. Specific precautions
and therapeutic exercise restrictions should be confirmed with hip ROM and strength and maximizing independence with
the surgeon because they are dependent on the surgical approach functional activities and ambulation. 
and procedures performed. If the hip was approached postero-
laterally, hip dislocation precautions may be warranted. Full Knee Arthroplasty
weight bearing (FWB) immediately after surgery is commonly Knee arthroplasty involves the replacement of the articular
prescribed, although an initial period of restricted weight bear- surfaces of the knee with prosthetic implants. It is indicated
ing has been recommended when the surgeon is concerned for patients with end-stage arthritis. Pain reduction, gaining
about bone healing at the femoral neck–implant interface.62–64 intrinsic joint stability, and restoration of function are the pri-
Physical therapy should focus on bed mobility, transfer train- mary goals associated with knee arthroplasty and should only be
ing, and gait training, reflecting specific weight-bearing restric- considered when conservative measures have failed.
tions. Immediate postoperative functional outcomes should be A unicompartmental (unicondylar) knee arthroplasty is the
consistent with those of a THA, with emphasis on increasing replacement of the worn femoral and tibial articulating surfaces
110 CHAPTER 5     Musculoskeletal System

in either the medial or lateral compartment of the joint. This sur-

gery is indicated for individuals who have osteoarthritis or osteo-
necrosis confined to one compartment with intact cruciate and
collateral ligaments.65 In unicompartmental knee arthroplasty
(UKA), the goal is to maximize the preservation of the articular
cartilage of the healthier compartment and spare bone that may,
in turn, delay total knee arthroplasty. More of the joint is pre-
served, including the opposite tibiofemoral compartment and
the patellofemoral joint. Preservation of the joint helps maintain
the normal kinematics of the knee joint, allowing for a quicker
rehabilitation process because the patient can typically tolerate
more aggressive mobility training in the immediate postopera-
tive stage. Associated valgus deformities may also be corrected
by a tibial osteotomy and release of soft tissue during UKA. 65,66
The tricompartmental or total knee arthroplasty (TKA) is
A
the replacement of the femoral condyles, the tibial articulating
surface, and the dorsal surface of the patella. This type of knee
arthroplasty involves the medial and lateral compartments of
the joint, as well as resurfacing the patellofemoral articulation
with prosthetic components (Fig. 5.13A). The femoral condyles
are replaced with a metal-bearing surface that articulates with a
polyethylene tray implanted on the proximal tibia. The dorsal
aspect of the patella is often resurfaced if excessive erosion of the
cartilage has occurred; however, some surgeons refrain from the
patellar implant if the articular cartilage of the patella seems
reasonably intact, as shown in Fig. 5.13B.67
Prosthesis systems used in knee arthroplasty vary, depending
on the extent of tissue damage, varus or valgus deformity, and
joint laxity. Prostheses options include posterior cruciate liga-
ment (PCL)–retaining (mild deformity) or PCL-substituting
(more severe deformity) and fixed-bearing or mobile-bearing B
prostheses. The more recent mobile-bearing prosthesis has a FIG. 5.13
congruent rotating platform between the tibial and femoral (A) Anterior view of a right total knee arthroplasty. (B) Lateral view of a
right total knee arthroplasty. (From Tooms RE. Arthroplasty of ankle and
components and was designed to lower contact pressures and
knee. In: Canale ST, ed. Campbell’s Operative Orthopaedics, 9th ed. Vol. 1. St.
decrease long-term wear found in fixed-bearing devices.68,69 Louis: Mosby; 1998:389-439.)
The methods of fixation in TKA are similar to those of hip
arthroplasty. Cementing techniques can be used to fix the com- after TKA include thromboembolism, infection, joint instabil-
ponents, or the prosthetic design can allow for either porous ity, fractures, patellar tendon rupture, patellofemoral instability,
ingrowth or press-fit fixation. Weight bearing is typically lim- component failure or loosening, and peroneal nerve injury.67
ited initially with cementless fixation techniques, whereas early Physical Therapy After Knee Arthroplasty.  As with all
WBAT as tolerated is encouraged when cement is used. patients who are scheduled to have joint arthroplasty, physical
The most common surgical technique for accessing the knee therapy should begin before the surgery. Similar to THA, specif-
joint is an anterior midline incision and medial parapatellar ically selected patients will receive TKA on an outpatient basis,
retinacular approach.67 Some concern over the extent of quadri- warranting extensive physical therapy intervention in both the
ceps weakness with this technique has led to the development preoperative period and the immediate postoperative period
of other methods for accessing the knee, such as the subvas- before discharge. Preoperative physical therapy should focus
tus approach, which uses a more medial incision (Fig. 5.14A), on educating the patient and caregivers on the expected course
and the midvastus approach, which splits the vastus medialis of rehabilitation after surgery and any postoperative activity
oblique fibers (see Fig. 5.14B).67,70–72 restrictions, as well as training on proper transfer techniques,
Patients who undergo knee arthroplasty may also have asso- appropriate assistive device use, and postoperative exercises.
ciated preoperative soft tissue contractures. A lateral retinacu- Postoperative physical therapy after knee arthroplasty is focused
lar release can be performed to centralize patellar tracking. If on improving knee ROM and strength as well as maximizing inde-
performed, there may be an increased risk of patellar sublux- pendence and safety with all mobility activities (i.e., bed mobility,
ation with flexion. After use of this technique, the surgeon may transfers, and ambulation with assistive devices).73–75 The physi-
impose restrictions on ROM and weight bearing. Any additional cal therapist should verify with the surgeon if there are restrictions
procedures for soft tissue balance may prolong healing time sec- on weight bearing or any activity/movement precautions.
ondary to increased edema and pain, which limits the patient’s Physical therapy should be initiated on the day of or the first
functional mobility and tolerance to exercise. Complications day after surgery for those designated to receive an inpatient

Anteromedial
Midline
Subvastus
Anterolateral
A B
FIG. 5.14
(A) Preferred anterior approaches to the knee. (B) Midvastus approach. (A, Redrawn from Scott WN. The Knee.
vol 1. St. Louis: Mosby-Year Book; 1994. B, From Scott WN. Insall & Scott Surgery of the Knee. 5th ed. Philadel-
phia: Churchill Livingstone; 2012.)
postoperative course. For those preselected to receive THA on
an outpatient basis, physical therapy is initiated and transferred
to the next level of care on the day of surgery. The patient should
be premedicated for pain control before the treatment session.
Any surgical drains should be noted. Patients commonly are
prescribed antiembolism stockings and external compression
devices to reduce the risk of a thromboembolic event.
Knee immobilizers may be prescribed to protect the knee from
twisting and buckling because of decreased quadriceps strength.
With a lateral release, there may be increased pain and edema,
which might hinder quadriceps functioning; therefore a knee
immobilizer or brace may be required for a longer period. Proper
fit of the brace or the knee immobilizer should be determined to
maintain appropriate knee extension. The nursing team may need
to be educated about proper donning and doffing of the brace.
Positioning and edema control should be initiated immedi-
ately to help reduce pain and increase ROM. The patient should
be educated to elevate the operated extremity with pillows
or towel rolls under the calf to promote edema reduction and
knee extension. Ice should be applied after exercise or when-
ever needed for patient comfort. The therapist can also 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.
Patient education should include:
• Proper positioning for comfort and maintenance of the integ-
rity of the surgical area
• Avoidance of placing pillows directly under the knee, to
minimize the development of knee flexion contractures
Musculoskeletal System     CHAPTER 5 111
• U se of knee immobilizer, if ordered
• Any activity restrictions and weight-bearing limitations, as
dictated by the surgeon
• Therapeutic exercise program
ROM and strengthening exercises should begin immediately
after TKA. ROM must be gained early in the rehabilitation
process and is initially accomplished by passive, active-assisted,
or active exercises, progressing to passive and active stretching
exercises. A continuous passive motion (CPM) machine may be
used to assist in achieving knee flexion ROM.76 The limitations
in ROM are often attributed to pain, swelling, muscle guard-
ing, and apprehension, all of which can be addressed through
physical therapy interventions and patient education.
The focus of strengthening exercises is typically the oper-
ated limb, although addressing any deficits in the uninvolved
limb should be incorporated into the strengthening pro-
gram.77 Isometric progression to active-assisted and active
quadriceps and hamstring exercises through the full available
ROM should be performed to increase stability around the
operated knee and enhance performance of functional activi-
ties.78,79 Quadriceps retraining may be accomplished with
overflow from the uninvolved or distal limb. The patient
should be encouraged to perform exercises independently,
within the limits of comfort.
Therapeutic exercises during the immediate postoperative
phase should include:
• Deep breathing and antiembolism exercises (e.g., ankle
pumps)
• Passive, active-assisted, and active ROM
• Knee extension and flexion (e.g., heel slides)
112 CHAPTER 5     Musculoskeletal System

• G entle stretching at end ranges of knee flexion and extension

within limits of pain in the supine and sitting positions
• Minimization of tension on incision site to ensure that the
integrity of the surgical area is not compromised
• Isometrics for gluteal, quadriceps, and hamstring muscles in
the supine position, progressing to active-assisted and active
exercises in the supine, sitting, and standing (e.g., seated
long arc quads) positions
• Placing a small towel roll under the knee while performing
isometric quadriceps exercises (This position will produce a
stronger quadriceps contraction by reducing passive stretch
on joint receptors and pain receptors. It will also provide pos- A
terior support to the knee, providing increased tactile feed-
back for the patient.)
• Using hold/relax techniques to the hamstrings when perform-
ing active-assisted ROM (This technique assists in decreasing
muscle guarding and increases knee flexion through reciprocal
inhibition of the quadriceps muscle. It also provides a dorsal
glide to the tibia, preparing the posterior capsule for flexion.)
• Progression from active-assisted exercises to active exercises
for hip flexion with knee extension in the supine position
• Straight-leg raises with isometric quad setting to ensure full
knee-extension ROM before lifting the leg off the bed (i.e.,
no quad lag) B
• Active exercises for hip abduction and hip adduction in the
FIG. 5.15
supine or standing position to assist in controlling the limb (A) Minimally invasive knee: intraoperative measurement of incision line
when getting into and out of bed during MIS-TKA. (B) Minimally invasive hip: a typical length mini-inci-
Transfer, gait, and stair training with the appropriate assistive sion. (A, From Bonutti PM. Minimally invasive total knee arthroplasty: a
device should begin as soon as possible. Based on the patient’s 10-feature evolutionary approach. Orthop Clin North Am. 2004;35(2):217-
presentation, an aerobic exercise program may be added to the 226. B, From Sculco TP, Jordan LC, Walter WL. Minimally invasive total
hip arthroplasty: the Hospital for Special Surgery experience. Orthop Clin
therapeutic exercise regimen because the patient’s limitations North Am. 2004;35(2):137-142.)
in functional performance could be attributed to decondition-
ing and a decreased aerobic capacity. As the patient progresses
through rehabilitation, balance retraining should also be con- Shoulder Arthroplasty
sidered, especially if significant soft tissue trauma occurred dur- Shoulder arthroplasty is indicated for patients with severe pain
ing surgery; mechanoreceptor functioning around the knee joint and limited ROM that has not responded to conservative treat-
may be disrupted, leading to balance deficits.80  ment. Surgical options include replacing both the humeral
and glenoid surfaces (i.e., total shoulder arthroplasty [TSA]) or
Minimally Invasive Hip and Knee Arthroplasty replacing only the humeral head (i.e., hemiarthroplasty) with
The term minimally invasive surgery (MIS) refers to a variety of prosthetic components. The surgeon takes many factors into
procedures and techniques that are used to decrease the amount consideration when determining which surgical procedure to
of soft tissue injury during surgery. Surgeons use special instru- perform. Several systematic reviews suggest superior outcomes
mentation and smaller incision sites (Fig. 5.15) to access the hip with respect to pain, ROM, function, and revision rates after
or knee joint. The indications for MIS are very similar to those TSA compared with hemiarthroplasty.85,86
for traditional arthroplasty; however, this technique is not com- TSA involves the use of cemented or press-fit modular pros-
monly used for complex joint replacements or joint revisions. thetic designs that are unconstrained, semiconstrained, or con-
Physical therapy follows the same guidelines as presented for a strained (Fig. 5.16). The most commonly used prosthesis is the
patient who has undergone THA or TKA. unconstrained type, which relies on the soft tissue integrity
Proponents of minimally invasive techniques state that of the rotator cuff and deltoid muscles. If these structures are
these surgical methods have the potential to decrease postop- insufficient or damaged, soft tissue repair may be performed
erative pain, perioperative blood loss, and hospital length of during shoulder arthroplasty surgery, and this may prolong
stay, as well as increase healing times and speed of postopera- rehabilitation.
tive rehabilitation.50 A significant clinical advantage of MIS The shoulder is typically accessed anteriorly via the delto-
over conventional surgery has not been supported in the lit- pectoral approach. Surgeons may choose to access the humeral
erature. Some literature reports improved pain relief and early head via a subscapularis tenotomy or a lesser tubercle osteot-
functional mobility, whereas other reports suggest no clinical omy (LTO). The LTO approach has gained popularity because
improvement.81–84  some evidence suggests it decreases the extent of diminished
 Musculoskeletal System     CHAPTER 5 113

A B C
FIG. 5.16
A variable amount of constraint is incorporated in the various designs of total shoulder replacement. (A) Many
implants have their articular surfaces shaped much like a normal joint surface. (B) The system may be partially
constrained by virtue of a hooded or more cup-shaped socket. (C) The components may be secured to one an-
other as in a ball-in-socket prosthesis. (From Cofield RH. The shoulder and prosthetic arthroplasty. In: Evarts
CM, ed. Surgery of the Musculoskeletal System. New York: Churchill Livingstone; 1983125-143.)

subscapularis function after TSA.87,88 The success of TSA is asso-

ciated with accurate surgical placement of the prosthesis and the
ability of the surgeon to reconstruct the anatomic congruency of
the joint. Proper orientation of the prosthetic components and
preservation of structural length and muscular integrity are key
aspects of the surgery that ensure favorable outcomes. Peri- and
postoperative complications include rotator cuff tearing, gleno-
humeral instability, and humeral fracture.
A proximal humeral hemiarthroplasty can be performed
when arthritic changes have affected only the humeral head.
The humeral head is replaced with a prosthetic component
through a technique similar to that used in TSA. Results are
dependent on the integrity of the rotator cuff and deltoid
muscles, the precision of the surgeon, and the willingness of
the patient to commit to a continual rehabilitation program.
With hemiarthroplasty, there is less risk for shoulder insta-
bility than with TSA, but there is also less consistent pain
relief.89
Physical Therapy After Shoulder Arthroplasty.  Initial
postoperative rehabilitation after TSA or shoulder hemiarthro-
plasty should emphasize functional mobility training to ensure
independence with all ADLs, transfers, and safe ambulation and
patient education on therapeutic exercises to minimize adhesion
formation. Because the stability of the shoulder is dependent on
the rotator cuff and deltoid muscles, the rehabilitation program
will be dictated by their integrity. Thus the physical therapist
must confirm the presence of any precautions with the patient’s
surgeon (Box 5.3). Although some publications provide sug-
gested guidelines for rehabilitation after TSA,90–94 few studies
have examined the effectiveness of specific interventions. It is
imperative that the physical therapist maintain close commu-
nication with the patient’s surgeon to ensure that the patient-
specific surgical pathway after TSA is considered during the
development of the therapy plan.
BOX 5.3  Common Precautions After Total Shoulder
­Arthroplasty
• A  void shoulder active range of motion
• No lifting, pushing, or pulling objects with involved upper ex-
tremity
• No excessive shoulder motion behind back, especially into in-
ternal rotation
• No excessive stretching, especially into external rotation
• No supporting body weight by hand on involved side
• No driving for 3 weeks
Data from Wilcox RB, 3rd, Arslanian LE, Millett PJ. Rehabilitation following
total shoulder arthroplasty. J Orthop Sports Phys Ther. 2005;35(12):836.
Physical therapy should be initiated on the day of or the first day
after surgery if the patient is expected to follow an inpatient course
of treatment. If the patient is selected to receive surgical interven-
tion on an outpatient basis, physical therapy will intervene and
transfer services to the next level of care on the day of surgery. The
patient should be appropriately medicated for pain control before
the treatment session. Any surgical drains or postoperative slings
or immobilizers should be noted. Instruction should be given to
the patient and family/care providers on donning and doffing any
supportive braces. Typically, patients are allowed to remove the
sling or brace for exercise, dressing, and hygiene.
Patient education should include:
• Use of ice for the management of pain and inflammation
• Proper positioning for comfort, edema management, and
maintenance of the integrity of the surgical area
• Avoiding lying on the involved shoulder
• Use of a towel roll under the elbow when supine
• Bringing the hand to the mouth with the elbow held at the
side of the trunk
• Therapeutic exercise program
114 CHAPTER 5     Musculoskeletal System

A B
FIG. 5.17
(A) Top, Assisted external rotation exercise (supine). Elbows are flexed and held close to body, and movement
is assisted with stick. Position aids pain-free excursion of motion soon after surgery. Bottom, Assisted flexion
exercise (supine). Lifting power is provided by good arm. Early range of motion without stressing deltoid and
subscapularis repair is possible with this exercise. (B) Pendulum. (A, Redrawn from Hughes M, Neer CS, 2nd.
Glenohumeral joint replacement and postoperative rehabilitation. Phys Ther. 1975;55:850; B, From Gartsman
GM. Shoulder Arthroscopy. 2nd ed. Philadelphia: Saunders; 2009.)

To decrease distal edema, hand, wrist, and elbow active ROM
exercises and ice packs may be used. Having the patient squeeze
a ball or sponge will help maintain grip strength.
Therapeutic exercises during the immediate postoperative
phase should include89–91,93:
• Supine passive forward flexion with elbow flexed; patient
may passively move involved arm by using opposite hand to
guide the movement (Fig. 5.17A)
• Supine passive external rotation with arm at side and elbow
flexed to no more than 30 degrees; patient may passively
move involved arm by using a wand or cane
• Pendulum exercises, clockwise and counterclockwise (see
Fig. 5.17B)
Based on the patient’s surgical procedure, other therapeutic
exercises might be recommended by the surgeon; some of the listed
exercises might also be postponed until later in the rehabilitation
process. Outpatient physical therapy during which further ROM
and strengthening exercises will be initiated and progressed should
begin shortly after the follow-up visit with the surgeon.  Total Joint Arthroplasty Infection and Resection
Reverse Total Shoulder Arthroplasty
A reverse total shoulder arthroplasty (rTSA) is usually cho-
sen when the patient presents with rotator cuff arthropa-
thy, failed shoulder arthroplasty, multiple failed rotator cuff
repairs with poor function and anterosuperior instability, or
malunion of the tuberosity after fracture.89 The success of
this technique primarily results from positioning the cen-
ter of rotation of the shoulder more inferiorly and medially,
causing shoulder stability and function to rely heavily on the
deltoid muscle.95 The new position of the deltoid allows it to
elevate the arm in the presence of rotator cuff deficiency. The
great advantage to this semiconstrained technique is that it
is found to exhibit movement patterns similar to those of the
normal shoulder.96
Physical Therapy After Reverse Total Shoulder
Arthroplasty.  The physical therapy management and precau-
tions for an rTSA is similar to that of a TSA, as described previ-
ously. However, because of the significance of the deltoid muscle
resection in this procedure, patients are typically immobilized
in slight abduction and neutral rotation. The physical thera-
pist must consult with the surgeon to determine the surgical
approach to the shoulder because the extent of soft tissue injury
and reconstruction can vary, influencing the aggressiveness of
the immediate postoperative rehabilitation. For example, if the
standard deltopectoral approach was used, active ROM exer-
cises can be initiated on the first day after surgery, whereas if a
deltoid-splitting approach was used, only gentle passive forward
elevation and external rotation is started immediately postoper-
atively; active assisted exercises are performed for 2 to 3 weeks.97 
The percentage of total joint arthroplasties that become infected
(septic) is relatively small. However, a patient may present at any
time after a joint arthroplasty with fever, wound drainage, persis-
tent pain, or erythema. Infection is often diagnosed by aspirating
the joint, culturing joint fluid specimens, and laboratory analysis
of the aspirate. Once the type of organism is identified, several
avenues can be followed for treatment of the infection. Treatment
choices include antibiotic therapy, debridement with prosthesis
retention or removal, one- or two-stage reimplantation, arthrod-
esis, or, in life-threatening instances, amputation.50,67
Resection arthroplasty involves the removal of the infected
hardware and cement. The greatest potential for a functional
joint occurs with a reimplantation arthroplasty.67 The two-step

process includes the removal of the infected material, followed
by a course of intravenous antibiotics. Once the joint is cleared
of infection, new prostheses are implanted. In the interim, anti-
biotic spacers are typically placed between the joint surfaces.
Patients with an infection after THA, but for whom reimple-
mentation is not an option, commonly experience instability at
the hip and limited hip ROM and require the use of an assistive
device during ambulatory activities.50 If reimplantation is not
an option for the knee, the limb may be braced for 6 months
to maximize stability, although long-term function tends to be
poor because of instability and limited ROM.67 Because of these
results, arthrodesis with an intramedullary nail may be chosen
to provide stability at the knee.
Physical Therapy After Hip or Knee Resection
Arthroplasty.  Physical therapy after a resection arthroplasty
without reimplantation or a two-stage reimplantation is depen-
dent on the extent of joint or bone destruction caused by the
infection and the removal of the prosthetic components and
cement and debridement of soft tissue. Weight-bearing restric-
tions depend on use of cement spacers and range from NWB to
WBAT, as established by the surgeon. Physical therapy sessions
focus on functional mobility, safety, proper assistive device use,
and maintenance of muscle strength and endurance in anticipa-
tion of reimplantation of the joint.
Patients who have an infection and joint resection arthroplasty
may be compromised by general malaise and decreased endur-
ance secondary to the infection, as well as possibly from increased
blood loss during surgery. These conditions may lead to decreased
pain tolerance. 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 to patient tolerance.
Hip resection arthroplasty, also known as Girdlestone proce-
dure, may leave a patient with a significant leg-length discrep-
ancy.98 With decreased leg length, the musculature surrounding
the hip shortens. Shortened muscles may spasm; isometric exer-
cises should be encouraged to gain control of these muscles to
reduce spasm. For patients who are on NWB restrictions, 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.
CLINICAL TIP
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 because the significance of the discrepancy may
change from the acute stage to the chronic stage of healing.
THA precautions often do not apply after removal of the
prosthesis. The physical therapist should verify any other
precautions, such as trochanteric osteotomy precautions and
weight-bearing status, with the surgeon. Without movement
precautions, most isometric, active, and active-assisted exercises
Musculoskeletal System     CHAPTER 5 115
are appropriate. Progress the patient as tolerated to maximize
function, strength, and endurance in preparation for eventual
reimplantation of the prosthesis.
For patients who have undergone knee resection surgery,
strengthening exercises for the quadriceps muscle can be initi-
ated as long as the extensor mechanism is intact. Isometrics,
active-assisted exercises, and active straight-leg raises, as well
as active hip abduction and adduction exercises, can be initiated
according to patient comfort.
Edema should be controlled with ice and elevation. Position-
ing of the limb is important to decrease discomfort from muscle
spasm and the potential for deformities caused by muscle con-
tractures around the hip and knees. 
Musculoskeletal Tumor Resection
Limb Salvage Surgery
The primary goal of limb salvage surgery is to restore stability
and function in patients who face the threat of lower limb loss,
most commonly resulting from crush injuries, infection, dia-
betes, peripheral vascular disease, neuropathy, and cancer abla-
tion.99 Musculoskeletal tumors can originate in bones or in soft
tissues, such as muscle and cartilage. If the tumors are malig-
nant, they are considered sarcomas (e.g., osteosarcoma, chondro-
sarcoma). Although tumors of the musculoskeletal system are
uncommon, a major concern with regard to bone tumors is the
development of pathologic fractures. In many instances, when
the tumor occurs in an extremity, complete tumor resection is
necessary via either limb-salvaging (limb-sparing) techniques or
amputation.100
Limb-sparing procedures typically have three phases: tumor
resection, bone reconstruction, and soft tissue reconstruction for
wound closure.101 One example of a limb-salvaging procedure
is total femur replacement. Patients undergoing this procedure
achieve good long-term prosthetic survival; 90% have limb
survival.102 A major determining factor of the outcome is the
oncologic diagnosis and associated complications. Confounding
factors affecting patient outcomes include metastases, chemo-
therapy, and radiation therapy. Refer to Chapter 11 for sugges-
tions on physical therapy management of the patient with cancer.
Early postoperative rehabilitation is essential to minimize
the risks associated with immobility and to promote indepen-
dence with functional activities. Transfer and gait training in
the presence of restricted weight bearing, ROM and strength-
ening exercises for the involved and uninvolved extremities,
positioning for comfort, edema management, contracture pre-
vention, and aerobic conditioning should be components of the
physical therapy plan of care. 
Hip Disarticulation and Hemipelvectomy
Malignant soft tissue or bone tumors of the hip and pelvis are
treated in multiple ways. If the tumor is located on the femur
or thigh and cannot be managed with limb-salvaging tech-
niques, a hip disarticulation may be performed. This procedure
involves releasing key pelvic/hip musculature, dislocating the
hip joint, dividing the ligamentum teres, and removing the
lower limb.103
116 CHAPTER 5     Musculoskeletal System
FIG. 5.18
Internal hemipelvectomy. Anterior-posterior radiograph of pelvis dem-
onstrating 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. Hema-
tol Oncol Clin North Am. 2005;19(3):451-470.)
In contrast, an external hemipelvectomy is indicated when
the tumor involves the hip joint or a large portion of the ilium.
A hemipelvectomy is very similar to a hip disarticulation but is
more extensive because the resection encompasses more of the
pelvis. It typically begins at the posterior sacroiliac spine and
extends along the iliac crest to the pubic symphysis and requires
an osteotomy through the sacroiliac joint after the soft tissue
and neurovascular structures have been divided.103
In specific cases where the tumor has not interrupted the
neuromuscular system and obtains only a small portion of the
pelvis, an internal hemipelvectomy (Fig. 5.18) is a more favor-
able option because the lower extremity is typically spared
with this procedure.103 Internal hemipelvectomy is similar to
external hemipelvectomy, as described previously, because large
portions of the pelvis and soft tissue are resected. The critical
difference is the sparing of the extremity. There are many differ-
ent approaches for this surgical procedure that may or may not
involve internal fixation and/or THA.
These procedures are invasive and complex. It is important
to consider the entire patient in these situations because they
typically have multiple medical complications. Often these
patients are going thorough chemotherapy and/or radiotherapy.
In addition, the emotional component involved in this type of
amputation and the expected decrease in functional performance
should not be disregarded.104
There are also many postoperative complications to consider,
including infection, poor wound healing, blood loss, orthostatic
hypotension, and, when the lower limb is amputated, phantom
pain. With regard to the expected blood loss and anemia during
surgery and postoperatively, the patient will most likely have a
drain placed to remove excess blood from the surgical site. These
drains should be left intact and carefully monitored when per-
forming mobility activities. The physician should be notified
immediately if the drains become dislodged because the patient
is then at increased risk of infection and/or bleeding.
Physical Therapy After Hip Disarticulation or
Hemipelvectomy.  Physical therapy after a hip disarticulation
or hemipelvectomy is focused on increasing functional inde-
pendence. Compared with patients who have undergone joint
arthroplasty, these patients typically have a more difficult time
initiating mobility because they have more medical complica-
tions and limited activity tolerance at first. Because the amputa-
tion involves a large portion of the limb, many patients choose
not to use prosthetics, which can be awkward and cumbersome,
but instead opt to live an independent life with an appropriate
assistive device.
Rehabilitation should begin immediately postoperatively, as
soon as the patient is hemodynamically stable. Bed mobility,
transfer training, gait and balance training, and overall func-
tional strength and endurance training make up the primary
goals of rehabilitation.
Because mobility is encouraged from day 1, the patient
should begin to build tolerance for sitting because this is usually
the biggest challenge. Patients are typically unable to tolerate
prolonged sitting as a result of pain and orthostatic hypotension.
The patient should be educated on the importance of mobility,
but the concept of gradual and slow progression should also be
stressed and carefully monitored. Not uncommonly, it takes
months before a patient can tolerate prolonged sitting without
pain.
To alleviate pressure and pain during sitting, it is helpful
to have the patient transfer to a reclining wheelchair. When
the patient is no longer able to sit in the upright position, the
wheelchair can be reclined for comfort and to disperse pressure.
Using this type of wheelchair is an easy way to allow the patient
to quickly lie down without needing to be transferred 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. A seating consult should be initiated while the
patient is in the acute care setting.
Crutch and/or walker training is essential to promote func-
tional independence. Progression of these activities should
include increasing distance gradually and eventually incorpo-
rating stair training.
The patient should be instructed on ROM and strengthening
exercises for the noninvolved extremities, especially the upper
extremities, because they will be contributing significantly to
weight bearing.
CLINICAL TIP
The patient should be educated on proper scooting techniques
so that he or she can avoid shearing or irritation to the incision
while moving about in bed.  
Spinal Pathology
The vertebral column forms the central axial support of the
body and consists of bony segments and fibrocartilaginous disks
connected by ligamentous structures and supportive muscula-
ture. Degenerative, traumatic, or congenital changes can cause
compensation in the vertebral bodies, intervertebral disks, fac-
ets, and intervertebral foramen. Any changes in these structures
 Musculoskeletal System     CHAPTER 5 117

Omohyoid
Sternohyoid
Thyroid
cartilage Sternocleidomastoid
Cricoid
cartilage Skin incision

1 Thyroid 2
gland
A

L1

L5
L1
L2 Sacrum
L3
L4

B 1 2 C
FIG. 5.19
Surgical approaches to the spine. (A) Anterior approach to C3-7. 1, Incision. 2, Thyroid gland, trachea, and
esophagus have been retracted medially, and carotid sheath and its contents have been retracted laterally in op-
posite direction. (B) Anterior retroperitoneal approach. 1, Skin incisions for lumbar vertebrae. 2, Exposure of
spine before ligation of segmental vessels. (C) Posterior approach to lumbar spine. (From Canale ST, Beaty JH,
eds. Campbell’s Operative Orthopedics. 11th ed. Philadelphia: Mosby; 2007.)

can result in dysfunction, which, 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 disk, spinal stenosis with nerve
root compression, spondylolisthesis, and degenerative disease of
the disk, vertebral body, or facet joints. Any dysfunction can
present itself in the cervical, thoracic, and lumbar spine.
Although more conservative interventions for chronic back pain
are on the rise, back pain is the major indication for spinal surgery.
Pain can be disabling to a patient, limiting the ability to work or
complete ADLs.105 Any acute injury, such as muscle spasm, herni-
ated nucleus pulposus, or exacerbation of chronic low back pain,
should be managed conservatively before surgical treatment is rec-
ommended. Surgery may be indicated when these measures fail to
relieve a patient’s symptoms or if his or her neurologic status declines.
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 disk disease and herniation or
rupture of the intervertebral disk. Surgical procedures can be
performed to relieve the symptoms associated with degenerative
disk disease when conservative measures have failed. Spinal sur-
geries are also indicated for the management of fractures, hyper-
mobile spinal segments (e.g., subluxation), deformities (e.g.,
scoliosis), and spinal tumors.
The spinal column can be approached anteriorly (Figs. 5.19A
and B) and posteriorly (see Fig. 5.19C). A variety of surgical
procedures have been developed to meet the challenges of work-
ing on and around the spine (Table 5.3). The extent of soft tissue
trauma has diminished with the advent of minimally invasive
techniques. Minimally invasive procedures have evolved as a
favored approach to posterior lumbar spinal surgery. Because the
dorsal muscles of the lower back are large and deep, spinal inci-
sions can often cause more discomfort than the compromised
vertebral column. Given the significant muscle soreness postop-
eratively, it is advantageous to the patient if a smaller incision is
used. Techniques include the percutaneous approach with fluo-
roscopic imaging and the use of microendoscopes with tubular
retraction systems for lumbar discectomies and fusion.106,107
A discectomy removes disk fragments and herniated disk
material, which compress the adjacent nerve root. Microdiscec-
tomy is a minimally invasive procedure that uses magnification to
view the surgical area, allowing for decreased surgical exposure.108
118 CHAPTER 5     Musculoskeletal System

TABLE 5.3  Common Spinal Surgeries

Surgery Purpose Procedure
Fusion Stabilization of hypermobile or unstable Use of internal fixation (e.g., Harrington rods, plates, pedicle screws,
joints wires, interbody cages) and/or bone grafts
Laminectomy Relieve pressure on neural structures Removal of the lamina
Decompression Relieve pressure on neural structures Removal of elements of the vertebral column
Discectomy Excision of protruding or herniated Removal of a portion of or the entire intervertebral disk
interdiscal material Can be combined with laminectomy, decompression, and/or fusion
Corpectomy Removal of part of the vertebral body Use of special instruments to remove fragments or components of the
vertebral body
Total disk replacement Replacement of deranged vertebral disk Removal of damaged vertebra disk and replacement with artificial implant

Data from Baron E, Vaccaro A. Operative Techniques: Spine Surgery. 3rd ed. Philadelphia: Elsevier; 2018.

Most microdiscectomies can be performed on an outpatient basis,

and early return to activity is possible. If additional exposure of
the nerve root is needed, associated procedures, such as a laminec-
tomy, may be performed in conjunction with discectomy.
Spinal instability is commonly treated surgically with spinal
fusion. If neural structures are being compromised, a laminec-
tomy or decompression, in which elements of the vertebral col-
umn are removed, may also be performed. Stability is achieved
through implantation of various types of instrumentation and/
or bone struts. Spinal segments can be fixed by using different
types of rods, plates, pedicle screws, and interbody fusion cages
that are packed with bone graft harvested from the iliac crest
(autograft) or from a bone bank (Fig. 5.20).
Total disk replacement for the lumbar spine has been devel-
oped as an alternative to spinal fusion. It is designed to recon-
struct the disk, maintain disk height, and preserve the segmental
motion of the spine.109 Although the outcomes of total disk
replacement are better compared with those of spinal fusion sur-
geries, few high-quality clinical trials have evaluated its effec-
tiveness and efficacy in lumbar spine.110–112 Recent studies have
suggested that total disk replacement is safer, more effective and
a better alternative, providing statistical significant clinical and FIG. 5.20
functional outcomes, to traditional anterior cervical discectomy Lateral view of a posterior interbody fusion with pedicle screws. (From
and fusion in single-level disk disease.113 Wood GW. Lower back pain and disorders of intervertebral disc. In:
Canale ST, ed. Campbell’s Operative Orthopaedics, 9th ed. Vol. 3. St. Louis:
Perioperative complications of spinal surgery are neurologic Mosby; 1998:3014-3092.)
injury, infection, cauda equina syndrome, dural tear with cere-
brospinal fluid leak, and nonunion, as well as the general surgi- surgical procedures with an anterior approach, the patient should
cal complications noted in previous sections. be given a splinting pillow and be educated in its use to promote
Physical Therapy After Spinal Surgery.  In the acute care deep breathing and coughing. A corset may be prescribed to aid
setting, physical therapy should emphasize early functional patient comfort with activity.
mobilization, education on proper body mechanics, and locomo- Treatment should be coordinated with the administration of
tion training. Patients should be educated on movement precau- pain medication. Patients should be educated in relaxation tech-
tions, if applicable to their surgical procedure. Typically patients niques or breathing exercises to help manage their pain. They
who have undergone a decompression procedure without fusion, should be encouraged to limit the amount of time in the sitting
including microdiscectomy or laminectomy, only need to follow position to 30 minutes.
a 10-lb lifting precaution, as recommended by the surgeon. The Functional mobility training should begin on the first post-
patient should be encouraged to mobilize, as tolerated, and avoid operative day. The physical therapist should always check orders
any excessively painful motions. Decompression combined with to determine whether a brace has been prescribed by the sur-
a fusion or any type of instrumentation requires patients to fol- geon and if there are any restrictions on activity. Braces are worn
low specific precautions, which include minimizing bending and when the patient is out of bed but must be applied while the
twisting with activity, lifting restrictions as determined by the patient is supine. The patient needs to be instructed in proper
surgeon, and use of braces or corsets, if prescribed. In the case of donning and doffing techniques before mobilization.
 Musculoskeletal System     CHAPTER 5 119

1 2

A B 3 4
FIG. 5.21
(A) Vertebroplasty. At two levels, insertion via needle of radiopaque cement (arrows) has been used to arrest
compression fractures. (B) Kyphoplasty. Balloon kyphoplasty. (A, From Mettler FA, Jr. Essentials of Radiology.
2nd ed. Philadelphia: Saunders; 2005. B, Redrawn from Garfin S. What the experts say: treatment options for
VCF, including balloon kyphoplasty. In: Canale TS, Beaty JH, eds. Campbell’s Operative Orthopaedics. vol 2. 11th
ed. Philadelphia: Mosby; 2007.)

Patients should be taught to logroll to get out of bed by hav-
ing the body roll as one unit, minimizing any trunk rotation.
A walking program should be stressed as the only formal
exercise immediately after spinal surgery to promote healing of
all tissues. The patient must be informed of the need to discon-
tinue any previous exercises he or she was performing before
surgery. If an assistive device is necessary for safety, balance, and/
or pain reduction during ambulatory activities, a rolling walker
is useful to promote a step-through gait pattern and decrease
stress on the spine caused by lifting a standard walker. Patients
should quickly progress to a cane or no assistive device to pro-
mote upright posture. After several weeks of soft tissue healing,
initiating a progressive exercise program has been shown to be
beneficial in improving functional performance.114–117
Symptoms, such as radiating pain and sensory changes pres-
ent before surgery, may persist for a significant period postoper-
atively because of edema surrounding the surgical site. Patients
should be informed of 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.
CLINICAL TIP
If an iliac crest bone graft is harvested through a second inci-
sion, a patient may complain of increased pain at the surgical
site. Ice can decrease swelling at the donor site. With this type
of graft, a patient will likely need an assistive device to increase
safety with ambulation and decrease pain.
 
Kyphoplasty and Vertebroplasty
Vertebral augmentation is a surgical intervention used for
progressive symptomatic osteoporotic vertebral compression
fractures. These minimally invasive procedures are most
commonly referred to as vertebroplasty or kyphoplasty and have
been shown to be effective in restoring function and reliev-
ing acute pain associated with compression fractures.118
Conflicting reports, however, show that long-term out-
comes after vertebral augmentation are no different from
conservative management (e.g., bed rest, analgesics, and
braces).119,120
A vertebroplasty is a procedure that consists of injecting a
polymethylmethacrylate (PMMA) cement into the vertebral
space to stabilize the compression fracture (Fig. 5.21A).121
The cement is injected percutaneously in a fluid state and is
intended to permeate into the cancellous bone. There are sev-
eral benefits to this procedure, including stabilization of the
fracture and immediate pain relief; however, the lack of height
restoration and deformity restoration may lead to more chronic
pathologies.122
Kyphoplasty differs from vertebroplasty in that it creates a
space through percutaneously inserting an inflatable balloon to
allow accurate placement of the PMMA cement and restores the
height of the collapsed vertebral body and deformities of the
spine (see Fig. 5.21B).121 The advantages of this procedure com-
pared with vertebroplasty are the restoration of the vertebral
height and alignment of the spine.122
Physical Therapy After Vertebroplasty or
Kyphoplasty.  Although there are limited evidence-based prac-
tice guidelines for physical therapy after vertebral augmentation
procedures, the primary goal for the immediately postoperative
period is to increase functional mobility.123,124 As in most spi-
nal protocols, a walking program is the primary source of exer-
cise during the immediate postoperative period. However, the
physical therapist should consult with the surgeon to determine
120 CHAPTER 5     Musculoskeletal System

TABLE 5.4  Soft Tissue Repair and Reconstruction Surgeries of the Knee and Physical Therapy Intervention
Type of Repair and Reconstruction
Meniscectomy
Meniscal repair
Lateral retinacular release
Anterior cruciate ligament (ACL) reconstruction
Posterior cruciate ligament (PCL) reconstruction
Procedure
Removal of all or part of the medial or lateral meniscus secondary to an irreparable tear
Repair of a torn meniscus in the vascular portion of the meniscus, where the likelihood of
healing is greatest
Release of the synovium, capsular, and retinacular structures lateral to the patella, and
proximal muscle fibers of the vastus lateralis
Reconstruction of the ligament using autograft or allograft of the patellar tendon or ham-
string tendon
Reconstruction of the ligament with autograft or allograft using the central third of the
patellar tendon or Achilles tendon

Data from Canale ST, Beaty JH, eds. Campbell’s Operative Orthopaedics. 13th ed. Philadelphia: Elsevier; 2017:477-506.

whether there are any activity restrictions, especially in patients
with a medical diagnosis of osteoporosis.
The patient should also be encouraged and instructed to use
the logroll technique 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 both the acute and
chronic rehabilitation stages to help prevent any further injury.  compartment syndrome are pain (out of proportion to the injury,
Soft Tissue Surgeries
Soft tissue surgeries are primarily aimed at improving joint
stability by repairing the functional length of muscles, ten-
dons, and ligaments. Common soft tissue surgeries of the lower
extremity include tendon transfers, muscle repairs, fasciotomies,
cartilage resections or repairs, and ligament reconstructions
(Table 5.4). Many of these surgeries are performed arthroscopi-
cally in the setting of ambulatory surgery. However, in some
cases, discharge may be delayed because of complications, such
as disruption of articular cartilage, menisci, and fat pads; dam-
age to blood vessels, nerves, ligaments, and tendons; tempo-
rary paresis after tourniquet use; surgical instrument breakage;
hemarthrosis; thrombophlebitis; and infection.125 At this point,
physical therapy may be involved with functional activity pro-
gression and patient education before discharge.  • The physical therapist should notify the nurse and physician
Equipment Used in the Management of
Musculoskeletal Pathologies
Casts
A cast is a circumferential rigid external dressing used to main-
tain optimal skeletal alignment of a stable fracture. It is typi-
cally applied after closed reduction and encapsulates the joints
above and below the fracture site. Casts can be made of plaster,
fiberglass, or synthetic material and can be used on almost any
body part. Table 5.5 lists common types of casts. Some casts may
be split into two pieces (bivalved cast) to allow periodic visual-
ization of the involved area or to relieve pressure or be hinged
at joints (hybrid cast braces). Casts can also be used to provide
low-load, prolonged, passive stretch to soft tissue to improve
ROM. This application is known as serial casting.
Complications associated with casts include nerve compres-
sion of a peripheral nerve over a bony prominence by the cast,
skin breakdown, and compartment syndrome.126 Compartment
syndrome occurs when elevated interstitial pressures within a
closed fascial compartment lead to tissue hypoxia; the pressure
gradient becomes so high that perfusion to distal structures
diminishes.127 If compartment syndrome is left untreated, tis-
sue necrosis will occur. It may be caused by excessive swelling
or the improper fit of a cast. The classic signs and symptoms of
unrelieved by pain medicine, and increased by passive stretch-
ing of muscle groups), pressure, paresthesia, pallor, weakness
(paralysis), and decreased peripheral pulses (pulselessness).128
CLINICAL TIP
Cast wearing duration may vary from 1 to 2 days to 6 to 8 weeks,
depending on musculoskeletal stability. Regardless of the cast
duration, the therapist should instruct the patient to contact the
physician if any of the following develops: symptoms of burning
or warmth, numbness, or tingling; movement of the limb within
the cast; increased edema; a discolored and cool hand or foot;
or a strong odor from within the cast.
Physical Therapy Implications
immediately for any signs and symptoms of compartment
syndrome, nerve compression, suspected skin breakdown, or
new drainage from within the cast.
• The therapist should elevate all distal extremities 4 to 5 inches
above the heart to allow gravity to assist venous return. El-
evation of more than 5 inches can increase venous pressure,
causing increased cardiovascular workload, and may be contra-
indicated for patients with congestive heart failure.
• Casts, especially plaster casts, should not get wet. The therapist
should instruct the patient to wrap the cast in a waterproof bag
during bathing or showering. Exposing casting materials to wa-
ter weakens the structure and traps moisture against the skin.
• The therapist should discourage patients from sliding ob-
jects into the cast to scratch itchy skin. Such objects can be
lost in the cast or displace the stockinet beneath the cast and
cause a wound or increase the risk of pressure sore formation.
Because the cast provides a moist and warm environment,
bacterial growth can develop at an accelerated rate and prog-
ress to a gangrenous lesion.
 Musculoskeletal System     CHAPTER 5 121

TABLE 5.5  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 rear or midfoot fractures.
Immobilizes foot and ankle, usually 90 degrees neutral or slight dorsiflexion.
Plantar flexion immobilization is used for Achilles tendon rupture.
Patellar tendon–bearing cast (PTB) Extends from metatarsal heads to mid- or suprapatella.
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 the greater trochan-
ter (to stabilize the distal femur).
For proximal tibia and distal femur fractures.
Knee immobilized in 5 degrees flexion.
Hip spica cast 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 (1½ 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.
Forearm cast (Colles cast) Extends from metacarpal phalangeal (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 just below the axilla.
For distal humerus, elbow, and forearm fractures.
Elbow flexion typically immobilized at 90 degrees.
Spinal cast Extends from above sternal notch to pubic symphysis, enclosing the chest and abdomen.
For stable thoracolumbar spine injuries, such as burst fractures.
Immobilizes the thoracic and lumbar spine.

Data from Lusardi MM, Barringer WJ, Stills ML. Orthotics in the rehabilitation of congenital, developmental, and trauma-related musculoskeletal impairment of the
lower extremities. In: Lusardi MM, Nielsen CC, eds. Orthotics and Prosthetics in Rehabilitation. 3rd ed. St. Louis: Saunders; 2013:335-391; and Court-Brown CM. Prin-
ciples of nonoperative fracture treatment. In: Bucholz R, Heckman J, Court-Brown CM, et al, eds. Rockwood and Green’s Fractures in Adults. vol 1. 7th ed. Philadelphia:
Lippincott Williams & Wilkins; 2010:125-161.

• B ecause most casts are not rigid enough to withstand the
forces of weight bearing, the physical therapist must verify
any weight-bearing parameters with the physician.
• A nonslip cast shoe should be provided for patients who have
casts encompassing the foot and are allowed to bear weight
during transfers and ambulation.
• It is important to reinforce that the patient should move all joints
proximal and distal to the cast to maintain functional ROM.  and distal to the external fixator. A footplate can be attached
External Fixators
An external fixator is a device consisting of aluminum or tita-
nium percutaneous pins or wires inserted into the long axis of a
bone that connect externally to a frame. The frame provides the
alignment forces to fracture fragments and maintains reduction
while healing occurs.129 The pins and wires can be connected
to longitudinal connecting bars (monolateral external fixation)
or metal rings (circular external fixation).130 External fixation
devices are often the treatment of choice for severely commi-
nuted or open long-bone fractures; unstable pelvic fractures;
fractures with severe soft tissue or vascular injuries; or when
significant bone loss has occurred.130 An advantage of external
fixation is the ability to manage associated injuries, such as skin
grafts and areas of debridement. It also allows for early func-
tional mobilization; however, there is often a weight-bearing
restriction after external fixation placement.
Complications of external fixation devices include pin site
infection; nerve, blood vessel, or tendon damage; loss of fracture
reduction or new fractures; nonunion or malunion; joint and
muscle stiffness; and compartment syndrome.129
Physical Therapy Implications
• It is important to maintain full ROM of all joints proximal
to the lower leg fixator to maintain neutral ankle dorsiflex-
ion.
• The metal rods of the external fixator should not be used to
assist with movement of the extremity.
• Extra care should be taken to prevent the inadvertent tap-
ping or banging of the external fixator against objects, such
as a walker or a footstool, because the force (vibration) is
transferred to the bone and can be painful. 
Braces and Splints
Orthotic devices, such as braces, splints, and walking boots,
are used in conjunction with medical and surgical intervention
techniques for management of musculoskeletal impairments.
Functional bracing is based on the concept that continued
function during the fracture healing phase promotes osteo-
genesis (bone growth) and enhances soft tissue healing while
preventing joint hypomobility and disuse atrophy. Bracing and
122 CHAPTER 5     Musculoskeletal System

TABLE 5.6  Braces and Splints Commonly Used in the Acute Care Setting
Type of Orthosis Description
Spine
Soft cervical collar Foam cylinder with a cloth cover that secures with Velcro around the neck.
Used as a kinesthetic reminder to limit neck movement for injuries that do not require rigid cervical fixation.
Reinforced cervical collar (e.g., Bivalved total-contact soft inner padding reinforced within a semirigid plastic frame that secures with Velcro.
Philadelphia, Miami J, Aspen) Used to control motion of the cervical spine.
Cervicothoracic orthoses Reinforced cervical collars are connected via occipital and mandibular struts to thoracic shells.
Used to control motion of the lower cervical and upper thoracic spine.
Halo vest Percutaneous pins to the skull connect at the level of the forehead to a circumferential frame, which is at-
tached via vertical rods to a vest lined with sheepskin.
Used for strict immobilization of the cervical or high thoracic spine.
Hyperextension orthosis (e.g., Anterolateral aluminum frame with pads at the sternum, lateral midline of the trunk, pubis, and lumbar
Jewett, cruciform anterior spi- spine; three-point pressure system.
nal hyperextension [CASH]) Used to limit flexion and encourage hyperextension of low thoracic and upper lumbar vertebrae.
Molded thoracolumbosacral Custom-fabricated, total-contact thermoplastic shell (single unit or bivalved) secured with Velcro.
orthosis (TLSO) Used to limit flexion/extension, side bending, and rotation of the thoracic and upper lumbar spine.
Corset Fabric bands with or without stays sewn into the corset that encircle the thoracolumbar and/or sacral region.
Used for pain management; reduction of spinal and abdominal muscle activity.
Lower Extremity
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; plantar surface has a nonslip rubber grip.
Used for conditions that allow weight bearing but require immobilization (e.g., stable ankle fracture) or
cushioning (e.g., bruised calcaneus).
Ankle–foot orthosis (AFO) with Thermoplastic shell encompasses lower leg, ankle, and foot.
anterior shell Worn with standard lace-up shoes if weight bearing allowed.
Used to control ankle and distal tibial motion for patients with distal tibial or fibular fractures.
Knee immobilizer Cylinder-shaped foam secured with Velcro with either posterior or medial/lateral aluminum stays; extends
from the upper thigh to the lower calf.
Used to promote extension when rigid immobilization is not required.
Drop-lock brace (Bledsoe) Lateral and medial metal struts adhered to foam at the thigh and lower leg connect to a hinge mechanism at
the knee; hinge has a dial to select the desired degree of flexion or extension at the knee.
Used for knee injuries requiring intermittent rigid immobilization.
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; thigh cuff extends medially across the knee joint; may be
used with a spine orthosis or knee–ankle–foot orthosis (KAFO).
Used to keep hip in slight abduction while limiting hip flexion/extension.
Upper Extremity
Simple arm sling Fabric sling with a strap around the neck positions the elbow in approximately 90-degree flexion across the
chest with the shoulder internally rotated.
Used for comfort and gentle support of the shoulder and upper extremity.

Data from Lusardi MM, Nielsen CC. Orthotics and Prosthetics in Rehabilitation. 3rd ed. St. Louis: Saunders; 2013.

splinting can be used to maintain fracture and joint alignment
during healing and to unload weight-bearing forces. They can
be applied immediately at the time of injury or used as part of a
progressive treatment course after conventional casting or trac-
tion. They may be prefabricated or custom made.
CLINICAL TIP
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.
Patient education is vital for every patient receiving a brace,
splint, or orthosis. The patient or the 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.
Table 5.6 lists some of the most commonly used orthoses. 
Traction
Traction involves the use of a distractive force on an extrem-
ity to stabilize a fracture. For skeletal traction, a system
of weights and pulleys restores the alignment of bone and
muscle. It is most commonly used for fractures of the femur,
although internal or external fixation has become the pre-
ferred method of stabilization.131 The traction apparatus
connects to the patient (positioned in the supine position)
either directly into the bone via pins through the proximal
tibial metaphysis or indirectly via the skin through boots,

slings, or belts.132 It is maintained continuously; therefore
the patient is on strict bed rest.
Spinal traction can be used for the initial management of
cervical fractures and dislocations, allowing for decompression
of neural elements and stabilization of the spine. Frequently the
patient will be transitioned to halo rings (halo vest) or undergo
internal fixation.132 Cranial tongs are made up of a metal ring
with pins that are placed into the skull and a weighted pulley
system. Similar to skeletal traction, the patient is supine and on
strict bed rest while the cranial tongs are in place. Halo rings
allow the patient to have more mobility because the rings can be
incorporated into a brace or vest. They typically include two ante-
rior and two posterior pins that are inserted into the skull and are
then stabilized by metal struts attached to a plastic body brace.132
Complications associated with traction include generalized
muscle atrophy of the immobilized limb, deconditioning of the
cardiovascular system, the general side effects of prolonged bed
rest, skin breakdown or pressure ulcer formation of the immo-
bilized limb over high-pressure areas, pin tract infection, and
pin loosening.132
Physical Therapy Implications
• If loosening or any other complication or alteration of the
traction apparatus is suspected, the patient’s nurse and physi-
cian should be notified immediately. The physical therapist
should not adjust, remove, or reapply traction.
• 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.
• The weight should be hanging free when the patient is in
traction. The head of the bed should not be lowered to a level
at which the weight inadvertently rests on the floor.
• It is important to monitor the patient’s skin integrity, re-
ported pain, and lower extremity position when in skeletal
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).
• Isometric or active exercise of both the involved and unin-
volved extremities should be initiated, as appropriate, to
minimize strength loss, joint stiffness, and restlessness as-
sociated with prolonged bed rest.
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127. Prasarn ML, Ouellette EA. Acute compartment syndrome of the
upper extremity. J Am Acad Orthop Surg. 2011;19(1):49–58.
128. Olson SA, Glasgow RR. Acute compartment syndrome in
lower extremity musculoskeletal trauma. J Am Acad Orthop Surg.
2005;13(7):436–444.
129. Lavini F, Dall’Oca C, Renzi Brivio L. Principles of monolateral
external fixation. In: Bulstrode C, ed. Oxford Textbook of Trauma
and Orthopaedics. 2nd ed. Oxford: Oxford University Press;
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130. Watson JT. Principles of external fixation. In: Bucholz R, Heck-
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in Adults. 7th ed. Vol. 1. Philadelphia: Lippincott Williams &
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131. DeCoster TA, Xing Z. Femur shaft fractures. In: Bulstrode C,
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Oxford University Press; 2011:1328–1337.
132. Court-Brown C. Principles of nonoperative fracture treatment.
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pincott Williams & Wilkins; 2010:124–161.
 6 Nervous System
C H APT ER  
CHAPTER OUTLINE
Introduction
Body Structure and Function of
the Human Nervous System
Divisions of the Nervous System
Cells of the Nervous System
The Central Nervous System
Cortex
Brainstem and Cranial Nerves
Neurologic Clinical Examination
Traumatic Disorders of Frontal
Cortex and Brainstem
Sensory Components
Motor Components
Spinal Cord Injury
Cerebral Circulation
Protective Structures
Cerebrospinal Fluid
Blood-Brain Barrier
Cerebrovascular Diseases and
Disorders
The Peripheral Nervous System
Peripheral Nerve Injury
The Vestibular System
Vestibular Dysfunction
Peripheral Vestibular Disorders
Central Vestibular Disorders
Additional Prevalent Health
Conditions
Seizures
Neuroinfectious Diseases
Degenerative CNS Diseases
Myasthenia Gravis
Neoplasms
Physical Therapy Examination:
Chart Review
Evaluation: Diagnosis and
Prognosis
Plan of Care
Aging and the Nervous System
Karen Jeanne Hutchinson
Laura C. Driscoll
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1. Understand the gross structure and function of the central nervous system from a perspective of function
leading to acute assessment of integrity of structure
2. Analyze the clinical decision-making process for the acute care neurologic examination
3. Compare and contrast medical diagnostic examinations for patients with acute neurologic disorders
4. Describe the neurophysiologic basis for attention, arousal, and motor and sensory function, and analyze
the impact of dysfunction in certain health conditions
5. Appraise standard medical and surgical management of neurologic disorders in acute care and their impact
on examination and treatment by physical therapists
6. Synthesize evidence from the examination to make decisions on interventions, prognosis, outcomes, and
discharge planning in the acute care environment
Introduction
This chapter explores the human nervous system. The text is organized with an introduction
to the “Body Structure and Function” of the adult nervous system, followed by a discussion
of a typical neurologic examination provided by a physical therapist, and neurologic disor-
ders encountered in the acute care environment. Each examination technique is complemented
by review of the neurologic structure it’s intended to examine. Before initiating a neurologic
patient examination, a thorough chart review will be necessary. (Please stop, as needed, and
review Physical Therapy Examination: Chart Review for a summary of the chart review process).
Critical information, such as condition onset leading to hospitalization, the progression pattern
of signs and symptoms, stability of signs and symptoms, and specific medical precautions are
sought.1 The decision-making algorithm in Fig. 6.1 provides a foundational overview of how
the content is organized in this chapter. 
Body Structure and Function of the Human Nervous System
Divisions of the Nervous System
The human nervous system comprises two major divisions—central and peripheral. The
neuroanatomic organization of the central nervous system (CNS) contains the cerebral cortex
at the rostral, or top, position, followed by subcortical structures such as the basal ganglia,
thalamus, and hypothalamus, and then the brainstem and subsequent spinal cord sections
at the caudal or bottom section (Fig. 6.2A–C). Of note, bidirectional communication occurs
among all levels of the nervous system and is critical for proper neural function.2,3 In addi-
tion, a series of 12 paired cranial and 31 paired spinal nerves exit the CNS contributing to
the peripheral nervous system. These nerves are responsible for transmitting information to
and receiving information from the peripheral target organs and structures they innervate (see
also ANS, below) (Fig. 6.3). 
Cells of the Nervous System
There are an estimated 86 billion neuronal cells in the human nervous system,4 each con-
taining a cell body, dendrites, and at least one axon made up of excitable tissue that conducts
        127
128 CHAPTER 6     Nervous System

Bed level exam:

CN testing, Assess
language & ability to
Evaluate
hearing screen, bear weight,
transfers,
Yes UE/grip/LE stand,
ambulation,
strength screen, monitor HDR
monitor HDR
gross sensory with position
exam, supine changes
bed mobility
Chart review: Appropriate for PT

Follows Yes
Yes commands?
Cognitive
screen:
Arousal, Bed level Move to
attention, Arousable? exam: edge of Anticipatory
visual Language & bed with Hemodynamically Yes postural control,
tracking No hearing or without stable? displacement/ Select
screen, pain with mechanical recovery appropriate
movement, lift outcome
purposeful measure
movement with based on
functional activity results
No No

Return to Increase Targeted

supine, upright impairment
Provide noxious
implement tolerance, level testing:
stimulation,
turning assist with Strength,
No PROM,
schedule good skin sensation,
positioning for
and arousal hygiene and reflexes,
respiratory status,
routine if no resp status, coordination
skin integrity
spontaneous transfer to
movement chair

FIG. 6.1
Acute neuro exam algorithm. Starting on the left, follow the decision-making algorithm for a physical therapy
examination and/or treatment intervention in acute care. After chart review, the examination begins with as-
sessment of cognition, arousal, and attention.

action potentials (Fig. 6.4). Action potential conduction is

triggered by the instantaneous summation of synaptic inputs
onto neurons, resulting in a drop in membrane potentials
below a threshold level.5,6 Action potentials reaching the dis-
tal terminal axon can cause the release of neurotransmitter
molecules, which may diffuse across the synaptic cleft (space
between neurons) before binding with the postsynaptic neu-
ron and influencing its firing rate. Most neurologic processes
occur by a collection of neurons that carry out their mission,
whether that be transmitting nociceptive information up to
the cortex or sending motor signals down to the cerebellum
or the spinal cord.
In addition to neuronal cells, there are 85 billion glial/sup-
portive cells in the CNS that complement the function of neu-
rons.4 Astrocytes remove the metabolic byproducts of synaptic
activation, provide structural support by multiplying/upregu-
lating after trauma,7 and serve an important regulatory function
to what is called the blood–brain barrier, by its close approxima-
tion with blood vessels.8–10 Oligodendrocytes provide myelina-
tion, or a covering, to the axons, helping decrease energy
demands and accelerate action potential conduction.11,12 The
Schwann cell serves a similar function for the peripheral nervous
system (PNS).13 Finally microglia, described as immune cells
within the CNS, serve to clear away inflammation and cellu-
lar debris.12 Traumatic, tumorigenic, or vascular lesions of the
neurons can lead to a host of inflammatory responses, energy
disturbances, and neural/glial cell death, directly affecting the
functional capacity of the CNS.  nications between the spinal cord, cerebellar, subcortical, and
The Central Nervous System
Cortex
The cerebral cortex, functionally separated into lobes, con-
stitutes the outermost layer of gray matter, which comprises
neural and glial cell bodies. The dendrites of the cortical
neurons receive inputs from numerous other cortical, subcor-
tical, and brainstem structures. Divided into left and right
hemispheres, the cerebral cortex also gives rise to axons,
which project onto subcortical, brainstem, and spinal cord
targets. The outgoing pathways in the cortex also synapse on
adjacent cortical lobes and on the contralateral hemisphere,
with the latter traveling via the large white matter bundle
called the corpus callosum.
Clinical signs that may suggest impairment/involvement of
cortical structures include hemiparesis (weakness of one half of
the body), language-based disorders, and vision, hearing, hemi-
sensory, and/or perceptual loss. Disorders that lack such clini-
cal signs and symptoms are likely of subcortical, brainstem, or
spinal cord origin. Refer to Table 6.1 for a brief summary of the
clinical characteristics associated with damage to the respective
cortical lobes and the assessment strategies used to assess their
integrity. 
Brainstem and Cranial Nerves
The brainstem uniquely houses bidirectional axonal commu-
 Corpus callosum PARIETAL LOBE

Cingulate gyrus

FRONTAL LOBE

LIMBIC LOBE
OCCIPITAL
LOBE

Hippocampus
Thalamus
DIENCEPHALON
Hypothalamus Amygdala

Pituitary gland
CEREBELLUM
Midbrain

BRAIN STEM Pons SPINAL CORD

Medulla
A
Head of the
caudate nucleus

Claustrum
Putamen
Internal capsule Lentiform
Globus nucleus
pallidus
Thalamus
Tail of the
caudate nucleus

B Lateral ventricle Caudate

(anterior horn) nucleus
Thalamus

Internal
capsule

Putamen

Insula
Corpus
callosum
Claustrum

Anterior
commissure Globus
pallidus
Amygdala

Third
ventricle

Infundibulum Lateral ventricle

Hypothalamus (inferior horn)
C
FIG. 6.2
Cortical and subcortical structures related to movement schematic. (A) Midsagittal view of the brain shows the relationship among the cerebral cortex, sub-
cortical structures, brainstem, cerebellum, and spinal cord. (B) Horizontal section of the cerebrum showing the ventricles, basal ganglia, and thalamic nuclei.
(C) A three-dimensional image oriented in the coronal plane showing subcortical structures and descending white matter pathways. (A from Cech DJ, Martin
ST. Functional Movement Development Across the Life Span. 3rd ed. St. Louis: Saunders; 2012. B from Love RJ, Webb WG, eds. Neurology for the Speech-Language
Pathologist. 4th ed. Boston: Butterworth-Heinemann; 2001, p 38. C from Goodman, CC. Pathology: Implications for the Physical Therapist. 4th ed. Figure 28-13,
pg. 1385.)
130 CHAPTER 6     Nervous System

cortical structures.3 It is made up of three separate neuroana-
tomic subdivisions, namely the rostral midbrain, the caudal
Medulla and the intervening Pons (see Fig. 6.2A). In addition
to accommodating the ascending and descending pathways
between the brain and spinal cord, each brainstem structure
provides unique contributions to the function of the CNS.
Most of the cell bodies for the cranial nerves (CNs) are found
in the brainstem (olfactory nerve [CN I] and optic nerve [CN
II] cell bodies can be found in the orbitofrontal cortical region
and retinal fields, respectively).14 Having an understanding of
the brainstem anatomy allows for purposeful clinical examina-
tion of the 12 CNs (Table 6.2).15
CN examination results allow for (1) localizing brainstem
pathology, confirming signs/symptoms are consistent with the
medical diagnosis, and guiding further assessment of adjacent
neural structures; (2) documenting baseline and change in
baseline CN function within and/or between physical therapy
sessions, and (3) identifying and subsequently utilizing intact
CN pathways (e.g., visual tracking, auditory cueing, etc.) as
a therapeutic strategy to engage active patient participation.
Testing CNs that innervate optic, oculomotor, and vestibular
targets (e.g., CNs II, III, IV VI, VIII) are frequently utilized
by the physical therapist to properly examine and provide
intervention for patients with oculomotor, sensory, vestibular,
and balance-related disorders.

 CLINICAL TIP
A patient may present with nausea and lightheadedness. When
Afferent axon
these symptoms are associated with a deficit in one of the 12
cranial nerves (CNs), a brainstem level problem may exist.16
Efferent axon

Abductor digiti
minimi muscle
FIG. 6.3
Afferent and efferent axons of the peripheral nervous system. A single seg-
ment of the spinal cord is illustrated. The arrows illustrate the direction of
information in relation to the central nervous system. (From Lundy-Ekman
L. Neuroscience: Fundamentals for Rehabilitation. 2nd ed. Philadelphia: Saun-
ders; 2002, Fig. 1.4, p. 7.)
Visual/Oculomotor Examination
A visual examination includes an assessment of resting eye posi-
tion, presence of nystagmus, pupil size, and reactivity to light.
Pupils should appear equal in size, constrict in response to light
(approximately 2–4 mm) whether shone in the ipsilateral or con-
tralateral eye, and dilate in reduced light conditions (>4 mm in
darkness).17 Assessing range of motion (ROM) for the eye involves
facing a patient arm’s length away. Using a brightly colored pen
tip placed between you and the patient, ask the patient to track
an “H” trajectory along an area not wider than the patient’s shoul-
ders and to superior/inferior distance of 10 to 14 inches. Compare

Peripheral
axon
Dendrite
Cell body Dendrite
Cell body

Central Cell body

Axon axon

Axon

A B C
FIG. 6.4
Cell types of the central nervous system (CNS). (A) Motor neuron image. Note the direction of “information
flow” (anteroposterior [AP] conduction) in excitable cells. (B) Pseudounipolar sensory neuron. (C) Enlarged mo-
tor neuron image. Note the direction of “information flow” (AP conduction) in excitable cells. (A–C, From Lun-
dy-Ekman L. Neuroscience: Fundamentals for Rehabilitation. 2nd ed. Philadelphia: Saunders; 2002, Fig. 2.9, p. 32.)
 Nervous System     CHAPTER 6 131

the range of ocular motion for both eyes. Deficits in smooth pur-
suit tracking at a slow and/or fast rate, as well as deficits in sac-
cadic eye movement testing (fast eye movements between two
targets), can be indicative of central vestibular disorders. Both
examinations occur on horizontal and vertical planes.16 Assess-
ment of visual acuity using a Snellen chart is not frequently done
by physical therapists in the acute care environment; however,
inquiry about corrective lenses is necessary. Finally visual field cut
assessment (see Clinical Tip box) and convergence testing com-
plete the visuomotor examination.18,19
 CLINICAL TIP
Visual field cut testing involves covering up one eye and testing
the other eye. The patient maintains a steady forward gaze by
looking at the tester’s nose positioned at the same height. Move
a brightly colored pen tip on the diagonal from the periphery
(on the diagonal behind the subjects’ head) in toward the cen-
tral field of view, assessing at least four quadrants per eye. The
patient notes when the pen tip comes into view. See Fig. 6.5 for
interpretation of the field cut testing results.
Acute presentation of pupil malalignment, disconjugate
gaze, or pupils that are fixed and dilated (non-reactive to
light) require immediate action as these symptoms are indica-
tive of serious CN III dysfunction (i.e., compression), pos-
sible increased intracranial pressure (ICP), and/or brainstem
herniation.  ing (MRI) is the gold standard for diagnosis. Upon testing, 38%
Common Cranial Nerve Disorders
Bell’s palsy, a partial or complete unilateral injury of the periph-
eral nerve (CN VII), presents with idiopathic, acute onset of
weakness of one half of the face; however, some studies suggest
it can be triggered by herpes simplex or herpes zoster viral infec-
tion affecting the facial nerve nucleus.20 Complaints of mild
pain, facial numbness, and impaired taste (anterior two-thirds of
the tongue) are observed.20 Facial muscle testing, which reveals
sparing of the upper half of the face, suggests an upper motor
neuron (UMN) lesion and not a lower motor neuron (LMN)
lesion, although this has been challenged.21 With regard to
prognosis, 85% have clinically meaningful improvement in 3
to 4 weeks; the remaining 15% show improvement in 3 to 5
months.20 Lack of improvement in facial muscle weakness sug-
gests an alternate diagnosis. Facial muscle strengthening exer-
cises,22 corticosteroids, and antiviral medication appear to be
effective, although high-quality evidence for specific strength-
ening protocols is lacking.23
Acoustic neuromas (vestibular schwannomas) are benign tumors
found on the auditory portion of CN VIII. Clinical presentation
can be variable and includes unilateral sensorineural hearing loss,
tinnitus, and disequilibrium. If left untreated and with continued
growth, acoustic neuromas can affect additional CNs or the fourth
ventricle and cause hydrocephalus.24 The average rate of growth
of a schwannoma is 2 mm per year, although this is reported to be
quite variable.25 Gadolinium-contrast magnetic resonance imag-

TABLE 6.1  Characteristics and Screening of Cortical Function2,14

Characteristics
Lobe Right (R)/Left (L) Hemisphere Control Screening Tests
Frontal Typically refers to PFC areas bilaterally (e.g., in front of motor State months of the year backward; assess alertness (GCS),
cortices or precentral gyrus), responsible for affect; personality; orientation (full name, place, time); Yes/No reliability;
lability; memory; language; judgment Follows 1-, 2-, or 3-step commands
Lesions affect: personality; “restraint, initiative, and order”; learning For motor cortex: Assess isolated movement responses on
visuospatial material (R-sided lesion); learning verbal materials (L); contralateral half of the body
may lead to language-based disorders (e.g. Broca’s area for speech
production [L])
Medial PFC is involved in visceral motor control and implicated in
chronic pain states
Parietal Postcentral gyrus (primary sensory cortex) interprets sensory stimuli/ Pin prick testing; light touch with cotton ball; position
integrity of the anterior spinothalamic system via sharp/dull (i.e., sense (proprioception), movement sense (kinesthesia);
nociception) and thermal testing, and dorsal sensory columns perceptual sense (double simultaneous stimulation);
including: proprioception; kinesthesia; light touch; two-point line cancellation tests for neglect (the latter occurs most
discrimination; and vibration all received from the contralateral often with a R-sided lesion); impaired reading/writing
face and body; language functions (L) (supramarginal and angular (L)
gyrus affect reading/writing)
Temporal Primary and secondary auditory cortex; Wernicke’s area for speech Hearing screening (finger rub at each ear and confirm
interpretation; medial temporal lobe (hippocampus/memory) they hear it); ability to follow verbal cues/commands;
memory tests; introduce your name at the beginning of
a session, and see if the patient remembers it 5 minutes
later or at the end of the session
Occipital Interprets visual signals; inverted and backward representations of Homonymous hemianopsia with sparing of macula
the visual field are mapped onto occipital lobe
Limbica Visceral sensory processing, including chronic pain; modulates mood Assess arousal; resting vitals; lability, chronic pain
and arousal; facial recognition complaints; facial recognition (deficits = prosopagnosia)
aLimbiclobe includes cingulate cortex and occipitotemporal gyrus.
CN, Cranial nerve; GCS, Glasgow Coma Scale; PFC, prefrontal cortex.
132 CHAPTER 6     Nervous System

TABLE 6.2  Cranial Nerves14–16

Location of Cell Sensory, Screening Test
CN No. Bodies Motor, Both Functions (*Common Deficits)
CN I Orbital Frontal S Discriminate contrasting odorants or use Test one nostril at a time for contrasting
Olfactory Cortex noxious stimulus for testing arousal odorants; *anosmia
CN II Midbrain S Transmits light and visual information Snellen chart; field cut testing; each eye
Optic from retina to thalamus, hypothalamus, separately (see below); afferent limb
and superior colliculus; transmits color constricting pupil-to-light reflex
information
CN III Midbrain M Positions each eye to receive optic flow; “H” tracking; efferent limb constricting
Oculomotor EOM move up, down, in; eyelid elevation pupil for light reflex; *ptosis
CN IV Midbrain M Innervates superior oblique muscle of the Track eye movement with small target,
Trochlear eye; moves eye down and in down and in relative to the nose
(one eye at a time); *diplopia
CN V Pons/Medulla B Touch and nociception for the face; three Patient with eyes closed: Touch their
Trigeminal branches—forehead, cheek, jaw; muscles forehead; cheek bone; chin with cotton
of mastication; jaw jerk reflex; afferent tip … ask for location of touch; wisp of
limb corneal reflex cotton in corner of eye, assess blink
CN VI Caudal pons M Innervates lateral rectus for abduction of eye Track eye movement into abduction with
Abducens small target; no farther than shoulders;
Both eyes normally move together but
observe one eye at a time
CN VII Caudal pons B Innervates muscles of facial expression; Ask patient to close mouth and puff
Facial lacrimal glands; salivary glands; taste out cheeks; scrunch forehead muscles;
anterior two-thirds of the tongue; squeeze eyes shut tight; pucker; smile
weakness of full ipsilateral half of face = wide, showing teeth
LMN injury; Weakness of lower half of *Facial muscle weakness and loss of taste
face only = UMN lesion anterior two-thirds of the tongue; dry
eye, mouth
CN VIII Medulla S Integrate peripheral vestibular or cochlear Auditory—finger rub next to ear;
Vestibular information with central processing Weber/Rinne’ tests
and cochlear mechanisms; differentiates conductive vs Vestibular—Romberg’s sign; VOR;
divisions sensorineural hearing loss *balance and hearing loss
CN IX Medulla B Symmetric palate elevation; gag function Shine light at the back of the throat and
Glossopharyngeal say “aahh”; sensory branch of the gag
reflex; *hoarseness
CN X Medulla B “work horse” of the ANS, descends outside Motor branch of the gag reflex; Blood
Vagus of the spinal cord and provides PSNS pressure dysregulation
innervation to all organs and GI/GU tracts
CN XI Medulla M Bilateral shoulder shrug (upper trapezius; UMN trapezius weakness; LMN
Spinal accessory lateral cervical flexion with opposite trapezius and SCM weakness
rotation (SCM)
CN XII Medulla M Tongue control; prepare food for swallowing Ask for forward protrusion of tongue;
Hypoglossal assist with speech production LMN ipsilateral deviation

ANS, Autonomic nervous system; B, both; EOM, extraocular muscles; LGnT, lateral geniculate nucleus of the thalamus; LMN, lower motor neuron; M, motor; PSNS,
parasympathetic; S, sensory; SCM, sternocleidomastoid muscle; UMN, upper motor neuron; VOR, vestibular–ocular reflex.14

are found to have slowed facial nerve conduction velocity (NCV),
but patients are still able to move their facial muscles.24 Compli-
cations associated with surgical excision include new-onset facial
weakness, cerebrospinal fluid (CSF) leak, and infection.24  nuclei); ipsilateral Horner’s syndrome causing ptosis, miosis, and
Brainstem Blood Supply
Brainstem structures are susceptible to physical trauma as well
as vascular disorders, which may affect CN function (Fig. 6.6).
For example, vertebral artery lesions are associated with dysfunc-
tion of the medulla. Clinical signs and symptoms are associated
with the affected underlying cell bodies and pathways. Lateral
medullary syndrome, a common brainstem-level stroke, is caused
by posteroinferior cerebellar artery lesions. Clinical signs and
symptoms include deficits in CN functions as follows: ipsilat-
eral facial sensory loss (CN V); dysphagia, hoarseness, dimin-
ished gag reflex (CN IX and X); nystagmus, vertigo (vestibular
anhidrosis (descending hypothalamo-spinal fibers); and contra-
lateral nociception of body (disruption of spinothalamic tract).26 
Autonomic Nervous System in the Brainstem and Spinal Cord
In contrast to the volitional control of the somatic motor system
over skeletal muscle, the autonomic nervous system (ANS) pro-
vides involuntary control over smooth muscle, cardiac muscle,
and glands.2 The two major subdivisions of the ANS are the
sympathetic nervous system (SNS) and the parasympathetic
FIG. 6.5
Visual fields testing. Blackened area of circle demonstrates the loss of visual field detection during a field cut
examination. Specific visual pathway lesions include (1) the optic nerve; (2) the optic chiasm; (3) the optic tract;
(4) optic radiations; (5) a lower-quadrant visual cortex lesion; or (6) an upper-quadrant visual cortex lesion.
(From Love RJ, Webb WG, eds. Neurology for the Speech-Language Pathologist. 4th ed. Boston: Butterworth-
Heinemann; 2001, p 103.)

Anterior cerebral artery

Anterior communicating
artery

Internal carotid artery

Middle cerebral artery

Posterior
cerebral artery
Posterior communicating
Superior artery
cerebellar artery

Basilar artery

Anterior inferior
cerebellar artery

Posterior inferior
cerebellar artery

Vertebral artery

FIG. 6.6
Brainstem blood supply. Note the close approximation of cerebral blood vessels and brainstem cranial nerve lo-
cations. The “circle of Willis” is formed by the posterior cerebral artery; posterior communicating artery; inter-
nal carotid/middle cerebral artery; anterior cerebral artery; and anterior communicating arteries. (From Lundy-
Ekman L. Neuroscience: Fundamentals for Rehabilitation. 2nd ed. Philadelphia: Saunders; 2002, Fig. 1.16, p. 16.)
134 CHAPTER 6     Nervous System

nervous system (PSNS) (Fig. 6.7). Cell bodies of autonomic gan-
glia are located within the spinal cord and brainstem regions, as
well as outside of the CNS. The SNS is responsible for the “flight
or fight” response, which is characterized by extreme arousal
and activation (Box 6.1). Brainstem PSNS axons constitute the
“rest and digest” response and are associated with CN function
(i.e., CN III, Edinger-Westphal nu/pupillary light reflex; CN
VII, tear ducts and salivary gland activation). The medulla also
has major integrative functions for processing baroreceptor and
chemoreceptor information from the body via CN IX (glosso-
pharyngeal) and CN X (vagus) inputs to the nucleus of tractus
solitarius (NTS); both are integral to proper cardiovascular con-
trol.27 An example of suboptimal unconscious ANS processing
is lightheadedness upon standing, or failure of heart rate (HR)
and blood pressure (BP) regulation with position change. In
addition, reticular nuclei throughout the brainstem provide a
mechanism for hypothalamic control over the SNS and PSNS
cell bodies in the spinal cord.2 
Neurologic Clinical Examination
Arousal responses are mediated by the reticular activating system
(RAS), which consists of cell bodies (i.e., nuclei) in the brainstem
that give rise to axons projecting onto the hypothalamus and
the cortex, important in mediating arousal responses.28 Clini-
cal testing focused on assessing arousal, attention, and cognition
assesses the integrity of these pathways from the brainstem to
the subcortex and the cortex and is the first step in the clinical
examination in the acute care environment (see Fig. 6.1).28
Arousal, described as “bodily readiness for activity,” is impor-
tant in regulating consciousness, attention, alertness, and infor-
mation processing.28 Damage to the RAS from insult or injury
results in disorders of consciousness. The Glasgow Coma Scale

Plexus
Postganglionics
Ganglia
Postganglionics
with carotid
arteries and
cranial nerves

Carotid

Pulmonary
Upper limb
T1
Spinal nerve
Postganglionics Thoracic
Cardiac
Autonomic plexus
Preganglionics

Pilomotor ganglia
Splanchnic Celiac
Sudomotor Thoracic
Hepatic
Cholecystic
Vasomotor Splenic
Superior
mesenteric Gastric
L2 Intestinal
Lumbar
Suprarenal
Lower limb
Renal
Sac
ral

Colic
Sacral
Inferior
mesenteric Rectal
Pelvic

FIG. 6.7
The autonomic nervous system. (A) Sympathetic nervous system (SNS) axons leave the central nervous system
(CNS) from the spinal cord segments only. (B) Parasympathetic nervous system (PSNS) axons leave the CNS
from the brainstem and the caudal spinal cord levels only. Injury to the intervening spinal cord often spares the
brainstem descending PSNS axons. (A and B, From Goodman CC, Fuller KS. Pathology. 4th ed. Fig. 28.17 B,
p. 1392.)
 Nervous System     CHAPTER 6 135

Ganglia
Cranial preganglionic
Ciliary

Pterygopalatine
Nerves
Nuclei r
m oto
Edinger-Westphal ulo Otic
III Oc l Submandibular
Superior salivatory VII Facia
Inferior salivatory IX n g e al
Dorsal vagal o phary
X Gloss

Bronchial
and
bronchiolar

Vagus
Cardiac

a
nd its b
Cholecystic

ranche
Pancreatic
s
Esophageal
Sacral
preganglionic Gastric
S2 Intestinal
S3
S4

Rectal
Pelvic
B
FIG. 6.7, cont’d

BOX 6.1  Autonomic Nervous System (ANS) Signs of Activa-  CLINICAL TIP
tion2,14 Interpret the Glasgow Coma Scale (GCS) scores with caution
Sympathetic Increased heart rate, pupil and bronchial in the presence of the following; sedating drugs, cranial nerve
nervous system dilation, eyelid retraction, blood vessel injuries, intoxication, hearing impairment, intubation/trache-
(SNS) constriction to skin and gastrointestinal ostomy, limb or spinal cord injury, immobilization, preexisting
tract, blood flow increase to skeletal muscle
cognitive or psychiatric disorder, ocular trauma, orbital swelling,
readying for action
language barrier.31
Parasympathetic Decreased heart rate, increased blood flow to
nervous system skin and gastrointestinal tract, increased
(PSNS) peristalsis; relative pupillary constriction, Additional Resources for a link to the GCS). It is used for risk
increase salivation and tear production assessment (e.g., increased ICP/herniation), trend monitoring,
severity classification, and prognosis and has been in widespread
use since 1974.29 The three subscales help evaluate eye opening
(i.e., arousal, wakefulness), motor response (i.e., cortex, spinal
(GCS) helps assess impairment of consciousness, the hallmark cord integrity), and verbal response (i.e., cortex, brainstem func-
of traumatic brain injury (TBI), across a broad range of injury tion),30 which are scored on a 3-to-15 scale, with lower values
severities. As a rapid bedside examination tool, the GCS allows indicating more severe injury. The GCS has also been shown to
for triage and immediate intervention and supports continu- have predictive power regarding recovery of function after brain
ity of information for clinical care across different settings (see injury.
136 CHAPTER 6     Nervous System
The Richmond Agitation-Sedation Scale (RASS), typically
used for patients on mechanical ventilation, assesses alertness
and agitation, allowing for monitoring of sedation levels and
response to interventions. The scale ranges from −4 to +4, with
a score of 0 indicating calm and alert.28
Cognitive Assessment
A simple bedside cognitive examination includes assessment
of arousal and orientation to self, place, time, and situation
and tailors the physical therapy intervention approach. The
patient’s mood, personality, and reliability of yes/no question-
ing should be documented. Tests of attention, memory, lan-
guage, and cooperation are all indicators of brain function as
well as ability to participate in the rehabilitation plan. For
patients with compromised mental status, however, it is very
important to document specifically the questions they were
asked and how they answered to better standardize the exami-
nation and track changes over time (particularly with differ-
ent observers). Referral for neuropsychologic testing and/or
an Occupational Therapy consultation should be made if new
deficits are found.  the environment to support day/night schedule, place familiar
Delirium
Delirium is an acute change in cognition or the development
of a perceptual disturbance not otherwise explained by a pre-
existing condition. The essential features are an acute onset
with a fluctuating course, a disturbance of consciousness with
reduced ability to sustain, or a shift in attention and the pres-
ence of disorganized thinking.32,33 Three clinical variants of
delirium exist and may be present in the same person in each
form or may fluctuate between variants. Hyperactive delirium
is marked by restlessness, agitation, and autonomic arousal.33,34
People with hypoactive delirium present as lethargic, inactive,
and quiet. The third form is a mixture of the two variants.
Hypoactive delirium is often mistaken for depression or can
go undetected due to the nature of the presentation. Each year,
more than seven million Americans who are hospitalized expe-
rience delirium, its presence increasing the risk for mortality,
discharge to long-term care, increased length of hospitaliza-
tion, and increased risk of developing dementia.32,35 Effects
often persist even at 1 year after discharge. Sixty to eighty per-
cent of patients on mechanical ventilation develop delirium.
Intensive care unit (ICU) delirium is an independent predictor
of mortality at 6 months, with a 10% increase in risk of death
for each day of delirium.32,33
Diagnosis is made clinically by using the Confusion
Assessment Method (CAM), a standardized evidence-based
tool that enables nonpsychiatrically trained clinicians to
identify and recognize delirium quickly and accurately in
both clinical and research settings.34 The CAM includes four
features found to have the greatest ability to distinguish
delirium from other types of cognitive impairment (acute-
onset delirium, inattention, disorganized thinking, and
altered level of consciousness). Used routinely, the valid and
reliable CAM identifies the presence or absence of delirium
but does not assess the severity of the condition, making it
less useful to track clinical changes (see Additional Resources
for a link to the test).34
Delirium may have one or more causes, such as medica-
tions or drug toxicity, metabolic imbalances, severe illness,
acute infection, malnutrition or dehydration, sleep depriva-
tion or severe emotional distress, pain, surgery (especially
with general anesthesia), and immobility or may have no
known cause. Any condition that results in hospitalization
increases the risk of delirium, particularly in people with
dementia, stroke, Parkinson’s disease, visual or hearing
impairments, older age, multiple medical problems, or pre-
vious delirium episodes.33
 CLINICAL TIP
The prevention and treatment of delirium are similar and are
aimed at addressing the cause as well as modifying known risk
factors. Physical therapists should educate the interprofessional
team and seek involvement from family members to optimize
communication, create routines, encourage self-care and in-
teraction that involves frequent reorientation, optimization of
objects and pictures in the room, and, most importantly, assist
with mobility.34
 
Dementia
Various factors and disorders can contribute to the development
of dementia. There can often be an overlap in symptoms, but
there are some hallmark differences in the presentations of the
various types of dementia (Table 6.3).36 Differentiating between
delirium and dementia is often difficult; however, there are sev-
eral distinguishing features (Table 6.4).36,37 
Traumatic Disorders of Frontal Cortex and Brainstem
The average age of onset of TBI in the United States is 41
years. Seventy-four percent of the victims are males, with
causes reported as vehicle accidents (51%), falls (27%), vio-
lence (11%), and other causes (11%).38 Direct impact to the
head can cause neural cell death via necrotic processes, where
dead/dying cells release their excitotoxic contents to the local
cellular environment. The surrounding penumbral region is
vulnerable to progression of the primary insult as a result of
a host of inflammatory and toxic exposure mechanisms, caus-
ing a secondary injury and leading to a more severe clinical
presentation.39
Posttraumatic Amnesia
Posttraumatic amnesia (PTA), or the time from injury until
the patient is oriented and able to form and later recall new
memories, is an important index of TBI severity and functional
outcome.40 The duration of PTA has been associated with the
presence or extent of skull fracture, intracranial hemorrhage,
raised ICP, residual neurologic deficits, and extent of neuropa-
thology, as well as with longer-term functional outcomes and
return to employment.40 The average duration of PTA was 22
days, with 9% lasting less than 1 day, 18% 1 to 7 days (noted as
moderate/severe injury); 42% lasting 8 to 28 days (very severe);
 Nervous System     CHAPTER 6 137

TABLE 6.3  Dementia Types36

Type Onset/Progression Presentation Pathology/Imaging
Alzheimer’s Gradual, progressive onset Memory loss, especially recall of names and recent Generalized brain atrophy
disease events Beta amyloid plaques
Language deficits Neurofibrillary tangles
Impaired visuospatial skills
Normal gait and neurologic examination (early
after diagnosis)
Later affective changes with behavioral symptoms
such as aggression and wandering
Vascular Abrupt or gradual onset Focal neurologic signs Strokes and/or lacunar infarcts
Other vascular disease signs also present White matter lesions
Lewy body Insidious onset with Fluctuating cognition Generalized atrophy
fluctuations Visual hallucinations Lewy bodies in cortex and midbrain
Shuffling gait
Increased tone
Tremors
Frontotemporal Insidious onset, rapid Disinhibition Frontal and temporal atrophy
progression Poor executive function Pick cells and Pick bodies in cortex
Poor judgment
Apathy, decreased motivation
Subcortical Related to the presence of Reduced ability to attend to task Changes that involve primarily
multiple degenerative Absence of spontaneity the thalamus, basal ganglia, and
neurologic disorders Requires increased time to recall information (but related brainstem nuclei, with
(e.g., PSP, PD, HD, etc.) can eventually answer the question) relative sparing of the cerebral
cortex 

HD, Huntington’s disease; PD, Parkinson’s disease; PSP, progressive supranuclear palsy.

TABLE 6.4  Differentiating Between Delirium and Dementia36,37

Features Delirium Dementia
Onset Clear-cut, acute (hours to days) Insidious (months to years)
Identifiable precipitant Yes No
Course Fluctuating (“sun-downing” effect) Stability of symptoms within days
Duration Reversible resolution in days or weeks Not reversible, continuously progressive
Level of consciousness Impaired Usually not impaired (exceptions DLB, VaD)
Level of attention Impaired Usually not impaired (exceptions DLB, VaD, FTD)
Mood changes Frequent Rare (except VaD)
Hallucinations/illusions Frequent, predominantly visual Rare (except DLB)
Delusions Frequent (fluctuating, fragmented) Rare
Motor activity Hyperactive/Hypoactive/Mixed Without specific features

DLB, Dementia of Lewy body; FTD, frontotemporal dementia; VaD, vascular dementia.

and 31% lasting 29 days or longer (extremely severe).38 Lower
values on the GCS are associated with increases in the duration
of PTA.40
There is disagreement about the approach to assessing PTA,
although several standardized measures have emerged. The
Galveston Orientation and Amnesia test (GOAT) is a bedside
assessment performed by the therapists, nurses, or physicians
that examine basic biographic information, orientation, and for-
mation of new memories (see Additional Resources for a link
to test).41 The duration of PTA is defined as the period after
coma in which the GOAT score is less than 75. PTA is consid-
ered to have ended if a score of 75 or greater is achieved on three
consecutive administrations.42
Disorders of consciousness (DOCs) are categorized on the basis of
observable behavioral features and exist on a continuum (Table
6.5). Coma, which involves complete loss of spontaneous or
stimulus-induced arousal, is a self-limiting state that typically
resolves within 2 weeks and transitions into a vegetative state (VS)
or minimally conscious state (MCS).43 A VS is described as wakeful
unconsciousness. Spontaneous eye opening emerges, and sleep/
wake cycles are present. A VS that lasts for more than 1 month is
considered persistent vegetative state (PVS).43 A PVS is considered
permanent after 3 months in patients with nontraumatic injury
and after 12 months in those with a traumatic injury. A diag-
nosis of MCS is considered when there is awareness of self or the
environment. The hallmark feature of MCS is inconsistency, so
138 CHAPTER 6     Nervous System
TABLE 6.5  Clinical Features of Disorders of Consciousness
Disorder Arousal/Attention Cognition
Coma No sleep–wake cyclesa None
Vegetative state Intermittent periods of None
wakefulnessa
Minimally Intermittent periods of Inconsistent, signs
conscious state wakefulness of awareness
of self and/or
environment
Posttraumatic Extended periods of Confused and
confusional wakefulness disorienteda
state
aIndicates key distinguishing features.44
examination should include careful observation and documenta-
tion of time of day, anteceding activities, and specific techniques
employed to arouse the patient. Serial assessment is important
because of the fluctuating nature of MCS as well as the possible
masking of certain behaviors by concomitant complications.
Emergence from MCS is signaled by the reemergence of a func-
tional communication system or the use of functional objects.
Patients may present with disorientation, which can often
result in agitation, also called acute confusional state.43 Examina-
tion of the patient should identify the distinguishing features
of each DOC state, as early as possible, to prognosticate and to
direct appropriate interventions. Recent evidence suggests that
interventions aimed at neuromodulation can accelerate outcome
and enhance function. Accurate diagnosis of DOCs is difficult to
achieve but is imperative for prognostication and for planning
for postacute care. In the absence of an objective test, diagnosis
is made at the bedside on the basis of a behavioral assessment.
Neurobehavioral rating scales are used to assess consciousness in
a standardized, reliable way. According to the American Con-
gress of Rehabilitation task force, the Coma Recovery Scale–
Revised (CRS-R) has the highest recommendation.44  a region within a dermatome (e.g., peripheral nerve branch);
Sensory Components
The ability to discriminate light touch, perceive sharp sensa-
tions, or note limb position in space begins with activation of
peripheral sensory receptors triggering an action potential (AP)
on axonal pathways that enter the CNS (see Fig. 6.4). Encap-
sulated A-beta mechanoreceptors (e.g., Meissener’s, Merkel’s,
Pacinian’s, and Ruffini’s) (Fig. 6.8) are receptors that depolar-
ize secondary to mechanical deformation; their axons enter the
spinal cord and ascend ipsilaterally until synapsing on dorsal
column nuclei (DCN) in the caudal medulla. Table 6.6 provides
additional descriptions of the major ascending pathways in the
CNS. Activated neurons from the DCN cross to the contralat-
eral side, forming the medial lemniscal pathway and ascending
until synapsing in the thalamus.
Sensory “information” that is to be brought to conscious
awareness makes subsequent connections with the primary
Language Visual Perception Motor Function
No receptive or expressive None Primitive reflexes
language only
No receptive or expressive Inconsistent visual Involuntary
language startle movement only
Limited to single words or Visual pursuita Localization to
simple phrasesa Object noxious stimulia
Inconsistent following of recognitiona Object manipulationa
single-step commandsa Automatic movement
sequences
Sentence-level speech, Object recognition Functional use of
confused, perseverative. common objectsa
Yes/No reliablea
Consistently follows single-
step commands
sensory cortex, which interprets these incoming stimuli rela-
tive to past experiences (via various additional cortico-cortical
connections with the secondary somatosensory cortex, amyg-
dala, and hippocampal structures).2 Where and how a person is
being touched, however, actually activate two parallel processes
whereby both discriminative and affective systems are involved.
Cutaneous mechanosensory inputs (i.e., exteroceptive systems)
ultimately project onto somatosensory cortex for stimulus
identification. Concomitantly, a second interoceptive system
interprets inputs in the dorsal insular and anterior cingulate
cortices and regulates the “state of well-being,” relating the way
in which that sensory stimulus is experienced (e.g., more emo-
tional aspects of touch).2,45
Systematic assessment of discriminative sensory capacity
requires an understanding of the body’s sensory map represented
in the dermatome chart in Fig. 6.9. Each dermatome level
mapped onto the body represents the innervation pattern of the
respective spinal nerve.48 (Sensory capacity of the face is carried
predominantly by CN V and not by the spinal nerves; see Table
6.2.) It is important to assess if any sensory loss is relative to
the whole dermatome (e.g., potential single nerve root lesion);
the whole extremity (e.g., multiple nerve roots); distal but not
proximal limb (suggesting circulatory nature); or the whole half
of the body (e.g., high spinal cord location or higher lesion in
sensory pathways). Each of these clinical presentations reveals
different pathologic process of sensory loss and CNS damage.
Muscle spindles (e.g., intrafusal fibers) are sensory receptors
embedded within skeletal (extrafusal) muscle fibers and are
innervated by gamma motor neurons, which dictate their (spin-
dle) sensitivity. Type Ia and II sensory neurons wrap the spin-
dles and sense the length of the spindle (hence extent of muscle
stretch) and the rate of change in the length of the spindle
(hence detecting rate of muscle contraction) (see Table 6.7 for
details). This important proprioceptive/kinesthetic information
ascends to both cortical and cerebellar locations and is essential
for performing coordinated movements and for learning new
motor patterns.49,50
 Nervous System     CHAPTER 6 139

Ia Medial group
Αβ
Muscle spindle
primary ending Αδ
C Lateral
group
Pacinian
corpuscle
Pain or
temperature
Pain or
temperature

FIG. 6.8
Ascending sensory inputs. Sensory information (e.g., light touch, proprioception, kinesthesia) enters the spinal
cord and may immediately ascend in the dorsal columns of the spinal cord on its way to sensory cortex for inter-
pretation. Nociceptive information enters the spinal cord, synapses, and immediately crosses to the contralateral
side. (Crossing fibers not shown.) (From Lundy-Ekman L. Neuroscience: Fundamentals for Rehabilitation. 2nd ed.
Philadelphia: Saunders; 2002, Fig. 12.1, p. 269.)

TABLE 6.6  Ascending Sensory and Descending Motor Pathways

Tract
Fasciculus gracilis
Fasciculus cuneatus
Lateral spinothalamic
Ventral spinocerebellar
Dorsal spinocerebellar
Lateral corticospinal (pyramidal)
Anterior corticospinal (pyramidal)
Rubrospinal (extrapyramidal)
Tectospinal (extrapyramidal)
Vestibulospinal (extrapyramidal)
Function
Sensory pathway for lower-extremity and lower-trunk joint proprioception, vibration, two-point
discrimination, and graphesthesia
Sensory pathway for upper-extremity, upper-trunk, and neck joint proprioception, vibration, two-point
discrimination, and graphesthesia
Sensory pathway for nociception, temperature, and light touch
Sensory pathway for ipsilateral subconscious proprioception
Sensory pathway for ipsilateral and contralateral subconscious proprioception
Motor pathway for contralateral voluntary fine-muscle movement
Motor pathway for ipsilateral voluntary proximal movement46
Motor pathway from the red nucleus to the spinal cord for UE motion47
Motor pathway for contralateral gross postural muscle tone associated with auditory and visual stimuli
Motor pathway for ipsilateral gross postural adjustments associated with head movements

Adapted from Gilman S, Newman SW, eds. Manter and Gatz’s Essentials of Clinical Neuroanatomy and Neurophysiology. 7th ed. Philadelphia: FA Davis; 1989; and Marieb
EN, ed. Human Anatomy and Physiology. 5th ed. San Francisco: Benjamin-Cummings; 2001.

Nociception Versus Pain
Sharp/dull discrimination depends on nociceptor activation
(e.g., stimulation of unencapsulated free nerve endings), whose
depolarizing axons cross immediately upon entering the spinal
cord to the contralateral side and ascend in the anterior spinotha-
lamic tract within the anterior lateral system. This nociceptive
information ascends upward in the spinal cord and brainstem,
synapsing in the thalamus and ultimately interpreted in the pri-
mary sensory cortex. It is important, however, to separate the
discrimination of sharp/dull responses from the term pain.
Pain is defined by the International Association for the Study
of Pain (IASP) as “an unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or described in
terms of such damage.”53,54 Pain is a term related to perception and
has both discriminative and affective components but is not synony-
mous with sharp/dull testing.54 Testing sharp–dull discrimination
assesses the integrity of the anterior spinothalamic tract, on which
nociceptive information travels, but cortical and subcortical loops are
necessary for the interpretation/perception of that stimulus as being
painful and are something from which the body needs protection.54
 CLINICAL TIP
Fear of pain, sadness, anxiety, and threat can amplify ones expe-
rience of nociceptive inputs.55–58 Consequently, a single noxious
stimulus can have a range of interpretations.
Furthermore, descending pain modulation from cortical and
subcortical regions onto the periaqueductal gray nuclei of the
midbrain influences firing rates of other brainstem nuclei (e.g.,
reticular neurons, the parabrachial nucleus, the locus coeruleus,
and raphe nuclei), which all have descending axonal projec-
tions down to the level of the spinal cord.2 These descending
signals may subsequently inhibit the ascending “pain signals,”
 FIG. 6.9
Sensory axons carry representations of body parts, at each segmental level of the body, into the spinal cord and
ultimately up to cortex for interpretation. (From Maitland GD, ed. Vertebral Manipulation. 5th ed. Oxford,
UK, 1986, Butterworth-Heinemann, p. 46.)

TABLE 6.7  Central Nervous System (CNS) Cell Location and Function2
Cells of the CNS Location Function
Neurons: Located in the anterior horns cells of spinal cord Constitute the final common pathway; exit the CNS and
Alpha motor neurons or motor divisions of cranial nerves; highly innervate peripheral skeletal muscle, 40–50 m/s nerve
myelinated conduction velocity (NCV)51,52
Gamma motor Located in the anterior horns cells of spinal cord or Innervates and sets muscle spindle sensitivity to stretch;
neurons motor divisions of cranial nerves influences muscle tone
Ia and II sensory axons Wrap muscle spindles embedded in skeletal muscle Sends information about spindle length (and rate of change in
and project into the brainstem and spinal cord length) information into the CNS, NCV 80–120 m/s
Ib sensory axons Golgi tendon organs (GTOs) embedded within Transmits information about active contraction
muscle tendons
A-beta sensory axons Mechanoreceptors located within peripheral Transmit touch and pressure information from the surface of
surface tissues; receptors for these axons include the body into the CNS, NCV 35–75 m/s
Meissener’s, Merkel’s, Pacinian’s, and Ruffini’s
A-delta and C fibers Poorly myelinated and unmyelinated fibers in the Transmits nociceptive and temperature information into the
sensory axons body CNS, NCV 0.5–30 m/s
Glia: CNS cells located throughout the CNS; particularly Sequester metabolic byproducts of synaptic activation,
Astrocytes at the blood–brain barrier (BBB) neurotransmitter production; provide structural support
by multiplying/upregulating after trauma, and serve an
important regulatory function to what’s called the blood–
brain barrier by its close approximation with blood vessels
(see BBB below)
Oligodendrocytes Throughout the CNS A single cell myelinates multiple axons; a key mechanism
mediating NCV of CNS neurons
Microglia Throughout the CNS Immune mediated activation; “PAC man” type function in the
CNS; sequesters cellular debris after inflammation and/or
trauma for removal from CNS
Schwann cells Throughout the peripheral nervous system (PNS) Myelinate a single nerve cell; improves NCV in the PNS

thereby changing associated physiologic mechanisms, simply on
the basis of expectations that the descending pathways can be
influential (i.e., by engaging placebo effects).58 Conversely the
experience of nociceptive inputs may be made worse by nega-
tively affecting the activation of these descending modulatory
pathways, a term called nocebo effects.58 And, finally, chronic pain
has been classified by the IASP as a disease state in and of itself,
with its own underlying mechanisms53,59 and contrasts with
peripheral tissue damage or inflammation associated with an
acute pain state. Directed neuroscience education about these
modulatory pathways is being studied as a mechanism whereby
individuals experiencing pain may be able to harness the innate
descending pathways to affect their own pain states, simply by
understanding that such modulatory pathways exist and by
engaging them.54,58  3
Phantom Limb Pain
Recent studies have concluded that phantom limb pain,
which is the conscious experience of pain from a missing/
amputated limb, is correlated with excess activity within
the sensorimotor cortex originally dedicated to the missing
limb.60 Cells are still active and “remembering” the painful
limb. Engaging memory structures (e.g., that limb move-
ment is painful), seems advantageous to avoid repeated pain-
ful experiences. The neuroanatomic connections between the
medial thalamus (diencephalon) and the medial prefrontal
cortex (mPFC) have been observed to support this “working
memory” concept of the pain experience, despite the absence
of the inciting damaged tissues.61 Efforts to influence or erase
this lasting memory trace of previous painful tissue experi-
ences are likely to yield promising results.62  spindle system (e.g., intrafusal fibers) in skeletal muscle, setting
Motor Components
The motor control system can be divided into pyramidal (e.g.,
cortex/brainstem descending pathways) and extrapyramidal
(e.g., basal ganglia, cerebellar) systems. However, it is the seg-
mental motor system that is activated upon, and/or modulated
by, the actions of the pyramidal and extrapyramidal systems (see
Fig. 6.2).
At the start of a motor assessment, observation of any voli-
tional/functional activity is necessary. Noted restriction in
active motion means a passive ROM assessment may be war-
ranted. Resistance to passive movement throughout the avail-
able range may be described as hypertonic (yielding increased
resistance to passive movement), hypotonic (decreased resistance
to passive movement), or dystonic (fluctuating resistance). Vary-
ing the speed of passive limb testing allows for the assessment
of the presence of spasticity (e.g., a velocity-dependent increased
resistance to passive movement). The Modified Ashworth Scale
helps assess the amount of resistance to passive movement noted
on a four-point scale (Table 6.8).63
Segmental Motor Control
The alpha motor neuron is located in motor divisions of cranial
nerves in the brainstem and in the anterior horn cell of each seg-
ment of the spinal cord. Motor neurons have large myelinated
Nervous System     CHAPTER 6 141
TABLE 6.8  Modified Ashworth Scale for Grading
Abnormal Tone
Grade Description
0 No increase in muscle tone
1 Slight increase in muscle tone, manifested by a slight
catch and release or by minimal resistance at the end
of the range of motion when the affected part(s) is
moved in flexion or extension
1+ Slight increase in muscle tone, manifested by a catch,
followed by minimal resistance throughout the
remainder (less than half) of the range of motion
2 More marked increased in muscle tone through most of
the range of motion, but affected part(s) easily moved
Considerable increase in muscle tone; passive move-
ment 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. Phys Ther. 1987;67:206.
axons with fast nerve conduction velocities, exit the CNS, and
innervate skeletal muscle targets, creating the final common
pathway for movement generation. The alpha motor neuron is
modulated or acted upon by local interneurons, as well as by
descending inputs from the brainstem and the cortex and is
responsible for the orderly recruitment of specific motor unit
profiles needed to perform various movement tasks (e.g., fast
fatigable, fast fatigue-resistant, and slow motor unit activa-
tion). In addition, gamma motor neurons reside in the ante-
rior gray matter of the spinal cord and innervate the muscle
spindle sensitivity (see Sensory Components). This allows Ia and
II sensory fibers to precisely “sense” minute changes in spindle
length and transmit that information to central motor control
structures.2,64
Deep tendon reflex (DTR) testing assesses integrity of mus-
cle spindle sensory signal (muscle stretch) along with resul-
tant muscle activation and is scored on a 0 (areflexic) to 5+
(hyperreflexic) scale (a 2+ is considered normal on the reflex
scale).14,65 It is important to compare reflex responses within
and across limbs because it may be normal to be brisk/hyperre-
flexic upon testing (e.g., 3+) in all extremities but not normal
to have varying reflex grades throughout all joints of a single
extremity (see Table 6.9 for the DTR tests and the correspond-
ing neural level examined). Absent or hyporeflexic segmen-
tal stretch reflex responses (e.g., from L3 quadriceps) along
with corresponding muscle atrophy, decreased tone (or lack of
tone called atonia) and fasciculations within the muscles in the
tested limb, are hallmark signs of LMN syndrome.66 These
signs suggest that deficits are associated with the specific neu-
ral segment of the spinal cord and not with the descending
systems that activate them. 
Descending Motor Systems
Axons that project onto and modulate the LMNs are called upper
motor neurons (UMNs). These axons have cell bodies that are
142 CHAPTER 6     Nervous System
TABLE 6.9  Deep Tendon Reflexes of the Upper and
Lower Extremities
Reflex Spinal Level Normal Response
Biceps C5 Elbow flexion
Triceps C7 Elbow extension
Patellar L4 Knee extension
Posterior tibialis L5 Plantar flexion and
inversion
Achilles S1 Plantar flexion
located in the brainstem or the cortex and give rise to descending
pathways that directly influence LMN function.2,67,68 Descend-
ing projections from the primary motor, premotor, and supple-
mentary motor areas, as well as other cortical regions, give rise
to the corticospinal pathway.2,67,68 Some branches of the cortico-
spinal tract (CST) will synapse in the brainstem by innervating
the reticular neurons, which subsequently give rise to reticulo-
spinal axons (see Table 6.6 for a description of additional major
ascending/descending pathways). The remaining CST axons
continue to descend through the ipsilateral brainstem, where, at
the base of the medulla, the CST splits into the anterior and lat-
eral divisions. The anterior CST continues descending ipsilater-
ally down the anterior aspect of the spinal cord, where its axons
synapse on the motor neurons innervating the proximal muscles
groups bilaterally, contributing to core muscle strength. The
small axonal branches cross the midline to innervate the con-
tralateral motor neuron pools as well as the ipsilateral motor
neuron pools for proximal trunk musculature.46 The lateral
CST crosses in the caudal medulla and descends, contralaterally
from its origin, into the posterolateral region of the spinal cord,
where its axons exit the CST at each segmental level and syn-
apse on a variety of cell types, including the interneurons, local
circuit neurons, or alpha motor neurons.69 The CST is critical
for performing skillful, isolated movements particularly of the
distal extremities.68,70,71
 CLINICAL TIP
Isolated movement occurs when one joint moves without ob-
ligatory movement in another joint of the body. If the patient is
not able to move in an isolated fashion, do not perform manual
muscle testing (MMT) or provide resistance during testing of
muscle strength; instead describe any abnormal flexor or exten-
sor synergistic movement pattern observed.
The three main pathways descending from their brain-
stem nuclei to the spinal cord include the reticulospinal, the
tectospinal, and the vestibulospinal pathways. Ascending sen-
sory tracts, as well as descending cortical and cerebellar axons,
project onto these brainstem nuclear groups, influencing the
function of these cells and their subsequent descending activa-
tion. In addition, the rubrospinal pathway originates in the red
nucleus in the midbrain and is believed to descend to the spi-
nal cord and may preferentially activate upper extremity flexor
muscles groups.47 Increased activation of the reticulospinal and
rubrospinal pathways may be responsible for the characteristic
flexor synergy movement patterns associated with CST damage
from UMN lesions.47,64,72
UMN syndrome may occur after cortex or brainstem damage
and has the following clinical presentation: initial flaccid limb
paralysis, followed by (over the course of days to weeks after
stroke onset) increased resistance to passive movement (hyper-
tonicity) typically on one side of the body and contralateral to
the cerebrovascular accident (CVA). Hemiparesis, spasticity (e.g.,
velocity-dependent increased resistance to passive movement),
and hyperreflexia (i.e., positive Babinski sign) are hallmark signs
of UMN Syndrome.2,73 These clinical signs suggest deficits in
descending motor systems (e.g., not activating segmental inhibi-
tory interneurons as expected) and contrasts with the LMN syn-
drome previously described.2,73
 CLINICAL TIP
Strength deficits on one side of the body are called hemiparesis
(weakness) or hemiparalysis (paralysis).
 
Extrapyramidal Systems: Basal Ganglia and Cerebellum
The basal ganglia (BG) are a collection of subcortical and brain-
stem nuclei that modulate movement execution. The cell bod-
ies of the substantia nigra pars compacta and pars reticulata are
located in the midbrain, and their dopamine-releasing axons
project onto the corpus striatum (pc) and superior colliculus
(pr), representing control of movement of the body and the eyes,
respectively.2 Multiple disorders are associated with BG dys-
function; however, death of the neurons of the substantia nigra
causes the most common BG disorder, Parkinson’s disease (PD).
Because the BG do not project directly onto the LMNs, lesions
of the BG typically do not result in paralysis.
Basal Ganglia–Related Disorders. Parkinsonism is an umbrella
term for abnormalities of BG function. Idiopathic parkinsonism
(or PD) is a chronic disorder with an insidious onset; symptoms
start in one extremity and then slowly progress to the rest of the
body (Table 6.10).74,77 BG deficits secondary to tumors, viruses, or
adverse drug reactions, called secondary parkinsonism, has a similar
motor presentation to PD and may include resting tremor, brady-
kinesia, absent postural reflexes, rigidity, and “freezing” episodes.
These impairments contribute to hypometria, akinesia, slow shuf-
fling and/or festinating gait with limited arm swing, stooped
posture, the characteristic reduction in facial expression, as well
as speech and swallowing deficits (Table 6.11).74,78 Impairments
in the sensory, autonomic, gastrointestinal, and cardiopulmonary
systems can also be present, along with fatigue and behavioral
changes (e.g., cognitive decline and depression).74
Primary symptom management for PD includes dopamine
receptor agonists medication (Sinemet), although this medication
does not alter the course of the disease. A reduction in symptom
improvement at the end of the dose and as previously provided by
the drug (i.e. “on-off effect”) occurs after 2 years in 50% of Sinemet
users. Wearing off can also result in symptoms such as depression,
anxiety, akathisia, unpleasant sensations, and excessive sweating.
In the “on” phase, at peak dose levels, dyskinesias may appear.75
 Nervous System     CHAPTER 6 143

Prognosis. Individuals with postural or gait instability as

TABLE 6.10  Hoehn and Yahr Classification System of
their major symptom often have a faster rate of progression com-
Parkinson’s Disease (PD)77
pared with those with tremor as their major symptom.79 Akine-
Stage Characteristics sia is associated with an advanced rate of progression. The risk
I Unilateral involvement only, usually with minimal of mortality increases with the severity of PD, the increased rate
or no functional impairment of progression, and weak response to levadopa therapy.79 Treat-
II Bilateral or midline involvement, without impair- ment with implanted stimulating electrodes (called deep brain
ment of balance stimulation [DBS]) attempts to modulate the firing rates of BG
III Physically capable of independent living, “mild neurons to impact function, with some promising results.80–82
to moderate disability”; impaired righting Essential tremor (also known as benign, familial, or idiopathic tremor)
reactions; unsteadiness observed during turns is the most common movement disorder, affecting approximately
or when perturbed in standing feet together eyes- 4% of the population age 40 years or greater, with increasing preva-
closed condition; employment with modifications
possible, depending on demands lence with age.81 It is a distinct condition from PD, although people
can present with both. It is characterized by an action tremor, most
IV Fully developed, severely disabling disease; can
walk/stand unassisted but markedly incapacitated often isolated to the upper extremities, compared with the hall-
mark resting tremor found in PD. It usually presents as a bilateral
V Confinement to bed or wheelchair, unless aided
6- to 12-hertz tremor of the hands, followed by a kinetic and resting
component.81 The upper limbs are often symmetrically involved,
but with disease progression, the head and voice (less commonly
TABLE 6.11  Signs and Symptoms in Relation to Disease the legs, jaws, face, and trunk) may be involved.82 Although essen-
Progression/Phase of Parkinson’s Disease (PD)78 tial tremor has a benign effect on life expectancy, it can be socially
isolating, and in a small percentage of people, seriously disabling.
Early to Mid-Stage Late- or Advanced-
Essential tremor with tremor onset after age 65 years is associated
PD Stage PD End-Stage PD
with mild cognitive impairment and dementia.81,82 Symptoms
Initial symptom: Absent postural reflexes Dependent in
are typically progressive and potentially disabling, often forcing
resting tremor Freezing episodes all activities
Poor handwriting Dysphagia of daily patients to change jobs or seek early retirement.82
legibility Decreased cough; living (ADLs) Huntington’s disease (or Huntington’s chorea) is an autosomal
(micrographia) aspiration pneumonia Flexion dominant, progressive neurodegenerative disorder. Degenera-
Cogwheel rigidity risk contractures tion of the caudate/putamen and frontotemporal lobes is char-
present Flexed posture of neck/trunk
acterized by cognitive decline, psychiatric issues, and choreic or
Symptoms present Impaired movement: limit supine
in one extremity initiation and extension dance-like movements at rest, made worse by active conversa-
initially; as termination Assistive tion or movement. The average life span from onset of diagnosis
disease progresses, Sit-to-stand deficits device and is 21 years,83 although life span depends on age of onset. Juve-
symptoms occur present physical nile and late-onset cases have a shorter duration of illness (i.e.,
bilaterally Decreased step length assistance
shorter life span) compared with those with onset between ages
Reduced/absent arm (shuffling) in gait; fall required for
swing during gait risk ambulation 20 and 49 years.84,85 
Cerebellum-Related Disorders. Pathology of the cerebel-
lum may result from stroke; tumor/resection; degenerative
 CLINICAL TIP75,76 disorders (e.g., olivo-ponto-cerebellar atrophy [OPCA], Fried-
reich’s ataxia); multiple sclerosis [MS] lesions; cerebral palsy,
• Patients with PD may experience postprandial and/or post–
traumatic brain injury [TBI], or exposure to toxins (alcohol and
exercise-induced hypotension; monitor hemodynamic re-
chemotherapy).86–88 The cerebellum is largely responsible for
sponse (HDR), respectively.
producing highly coordinated movement patterns (e.g., limbs,
• Because of the risk of aspiration, consult the interprofessional
trunk, speech production, and eye movements) and coordinated
team before the provision of food/drink.
balance responses and is a major contributor to motor skill acqui-
• When selecting the time to work with patient, note the timing
sition (e.g., motor learning).86 In addition, the cerebellum plays
and dose of the PD medication relative to the “on-off” phe-
a role in attention, language, executive function, social cogni-
nomenon, as well as its effect on examination or treatment.
tion,87 and sleep-related motor memory consolidation.49,74,84,88
• Consider the effect of changes in the regular medication
Motor signs associated with cerebellar disorders include ataxia,
schedule related to comorbid conditions (e.g., nothing by
dysmetria, dysdiadochokinesia, and oculomotor and limb muscle
mouth [NPO] status for surgery).
weakness and intention tremor.84 These impairments contribute
to deficits in timing of movements, grading/scaling–appropriate
Comprehensive balance assessment is indicated in PD.
force production, inability to compensate for interactive torques
Prolonged movement initiation and postural rigidity contrib-
(e.g., adjusting force to account for the weight of one’s own limb
ute to impaired protective extension reactions and increased
movements), and impairment in predicting/anticipating motor
fall risk. In the later stages of PD, the individual may dem-
responses (see Table 6.12 for examination techniques).49,74,84,89,90
onstrate retropulsion in response to any anterior-to-posterior
Ensuring patient safety is critical because ataxia increases the risk
perturbation.75,79,80
144 CHAPTER 6     Nervous System

TABLE 6.12  Coordination Testing

Test Method Impairment
Upper Extremity
Finger to nose Ask the patient to touch the nose. Then ask patient to touch the nose and then touch Dysmetria
your finger (which should be held at arm’s length away). Ask the patient to repeat Intention tremor
this rapidly.
Finger Ask the patient to touch the thumb to each finger in sequence, gradually increasing Dysmetria
opposition the speed. Intention tremor
Supination and Ask the patient to rapidly and alternately supinate and pronate the forearms. Dysdiadochokinesia
pronation
Tapping Ask the patient to rapidly tap the hands on a surface simultaneously, alternately, or both. Dysdiadochokinesia
Arm bounce Have the patient flex the shoulder to 90 degrees, with elbow fully extended and wrist Cerebellar dysfunction—impaired
in the neutral position; then apply a brief downward pressure on the arm. (Excessive postural stability
swinging of the arm indicates a positive test.)
Rebound Ask the patient to flex the elbow to approximately 45 degrees. Apply resistance to Cerebellar dysfunction—impaired
phenomenon elbow flexion; then suddenly release the resistance. Normally the triceps would postural stability
contract and keep the elbow/arm in position. Be careful that the patient does not Triceps weakness
strike the face in the case of a positive test.
Lower Extremity
Heel to shin Ask the patient to move the heel up and down the opposite shin and repeat rapidly. Dysmetria
Tapping Ask the patient to rapidly tap the feet on the floor simultaneously, alternately, or both. Dysdiadochokinesia
Romberg test Ask the patient to stand (heels together) with eyes open. Observe for swaying or loss Inability to maintain balance
of balance. Have the patient repeat with eyes closed. when the eyes are closed is a
positive result, indicating loss
of proprioception, vestibular
dysfunction, or both
Gait Ask the patient to walk. Observe gait pattern, posture, and balance. Repeat with Ataxia
tandem walking to exaggerate deficits.

Data from Gilroy J, ed. Basic Neurology. 3rd ed. New York: McGraw-Hill; 2000; and O’Sullivan SB, Schmitz TJ, eds. Physical Rehabilitation. 5th ed. Philadelphia: FA
Davis; 2007.

of falling and being injured by a fall.84 Recommendations are to
teach slower movement strategies to patients with cerebellar dis-
orders so that they can use sensory feedback mechanisms to com-
pensate for the lack of (feedforward) somatosensory information
reaching the cerebellum in a timely manner.89–91
The Purkinje cell body is the only neural cell type that proj-
ects out from the cerebellar cortex. It projects onto the deep
cerebellar nuclei (DpCN). Modulation of Purkinje cell activa-
tion (called long-term depression [LTD]) is believed to be respon-
sible for motor adaptations that occur secondary to repetitive
task practice.91 The DpCN give rise to axons that subsequently
project onto the brainstem and the thalamic targets, from which
subsequent pathways project onto the cerebral cortex and the
spinal cord to do the cerebellum’s “work.”
The cerebellum receives movement instructions from the
cortex and sensory information from the spinal cord about what
movement is occurring or has just occurred. The difference
between the desired movement and the resultant movement
constitutes the movement error, and the next movement-iteration
cerebellar commands attempt to reduce the movement error. As
with the BG, the neurons that leave the cerebellum (projecting
onto the brainstem and the cortex) modify the activity patterns
of the UMNs but do not synapse directly on the LMNs. Lesions
of the cerebellum are more likely to develop hypotonia versus
spasticity and, importantly, have an ipsilateral affect. Lesions of
the inferior olive or its climbing fibers arising from the medulla
and projecting onto the cerebellum, leads to absent error correc-
tion and impaired motor learning.92 This is important because
patients who experience brainstem trauma or brainstem-level
stroke need to be assessed for the involvement of these pathways,
which may have a significant effect on motor learning.
Specific lesions of the cerebrocerebellum are believed to cause
deficits in highly skilled extremity movements (e.g., ataxia/
piano playing); spinocerebellar lesions affect proximal weakness,
whereas vestibulocerebellar lesions can result in hypotonia and
impairment of eye, head, and trunk movements in response to
motions of the head (e.g., vestibular stim associated with linear
motion and rotational accelerations). Finally slow degenerative
conditions of the cerebellum, such as OPCA, involve degenera-
tion of the pons and inferior olive bilaterally. A slowly progres-
sive disorder with no cure, OPCA carries a life expectancy of
approximately 20 years after diagnosis.2 
Spinal Cord Injury
In 2017 more than 17,000 new spinal cord injuries (SCIs) in
the United States occurred secondary to vehicular accidents
(38%); accidental falls (32%); violence (14%); sports/recreation
(8%); or other causes (8%).93 Nontraumatic spinal cord dam-
age may include arteriovenous malformation (AVM), throm-
bosis, embolus/hemorrhage; vertebral subluxation secondary to

TABLE 6.13  American Spinal Injury Association
Impairment Scale
A Complete No sensory function or motor function is
preserved in S4-S5.
B Incomplete The preservation of sensory function without
motor function below the neurologic level
and includes S4-S5.
C Incomplete The preservation of motor function below
the neurologic level. Muscle function of
more than half of key muscles below this
level is less than 3/5.
D Incomplete The preservation of motor function below
the neurologic level. Muscle function of at
least half of key muscles below this level is
equal to or greater than 3/5.
E Normal Motor function and sensory function are intact.
From American Spinal Injury Association. http://asia-spinalinjury.org/wp-
content/uploads/2016/02/International_Stds_Diagram_Worksheet.pdf. Accessed
July 31, 2018
rheumatoid arthritis or severe degenerative joint disease (DJD);
infections (syphilis, transverse myelitis); syringomyelia; spinal
cord abscesses; MS lesions; and amyotrophic lateral sclerosis
(ALS).74
Damage from SCIs can include sensory, motor, and auto-
nomic deficits, resulting in a wide range of functional dis-
abilities. The gold standard examination for classification of
SCI severity includes testing 10 myotome and 28 dermatome
sites on each side of the body with the patient in the supine
position.94 The extent of extremity and trunk impairment dic-
tates paraplegic (both legs and lower trunk involvement) ver-
sus tetraplegic (all four limbs and trunk) presentations. Further
identification of the specific segmental level of injury (e.g., T8,
T9, T10) coupled with severity indicators (Abbreviated Injury
Scale [AIS] Levels A, B, C or D; see Table 6.13) succinctly relays
information about level and extent of injury and helps predict
functional outcomes (Table 6.14).
Complete spinal cord injuries occurring above the sixth
thoracic spinal nerve level (T6 level), limit the SNS’s ability
to increase HR in response to activity and/or exercise (inter-
feres with hypothalamic projections onto the SNS neurons in
the spinal cord that subsequently innervate the sinoatrial node
to increase HR). This lack of sympathetic drive to the heart
and blood vessels of the extremities (e.g., limiting peripheral
vasoconstriction), along with a concomitant lack of abdomi-
nal muscle tone and blood pooling in legs during dependent
positioning, can lead to hypotensive episodes and necessitates
frequent monitoring of hemodynamic responses. Orthostatic
hypotension occurs with a 20-point drop in systolic blood pres-
sure (SBP), or a 10 mmHg drop in diastolic blood pressure
(DBP) when transitioning from supine to sitting (coupled with
an increased HR response) and frequently involves complaints
of lightheadedness or dizziness.95,96 Contraction of the available
muscle groups and utilization of compressive garments may
be able to partially increase BP and ameliorate these negative
symptoms.74
Nervous System     CHAPTER 6 145
TABLE 6.14  Level of Spinal Cord Injury with Expected
Return of Function
Level of Lesion Expected Return of Function
C4 Spontaneous breathing
C5 Elbow flexion
C6 Wrist extension
C7 Elbow extensiona
C8-T1 Finger flexion
T1-T12 Intercostal and abdominal muscles—trunk
control
L1-L2 Hip flexion
L3 Knee extension
L4 Ankle dorsiflexion
L5 Toe extension
S1-S2 Ankle plantarflexion
S2-S4 Rectal sphincter tone
aKey muscle group for reaching goal of independent transfers.
Autonomic dysreflexia (AD) occurs when SBP and DBP
increase to 20 mmHg or greater above the baseline and could
include sweating, piloerection, facial flushing, headache, com-
plaints of blurred vision and a stuffy nose.74,95 The diagnosis of
AD is based on changes in hemodynamic responses, regardless
of clinical signs. Low BP after cervical SCI is common (e.g., rest-
ing BP 90/50)96; awareness of baseline cardiovascular indicators
is critical for proper interpretation of hemodynamic responses
on the rising phase of a hypertensive crisis. To rule in an AD epi-
sode, both an increase in BP and a compensatory decrease in HR
must be observed.95 Pharmacologic management is dependent
on the HR response at the time of an elevated BP response. An
AD episode can be caused by a noxious (painful) tactile stimulus
or simply by bowel and/or bladder distention. Untreated hyper-
tension during a dysreflexic episode can lead to serious conse-
quences, such as retinal and/or cerebral hemorrhage, myocardial
infarction, congestive heart or kidney failure, or death.72
Because of the high risk of venous thromboembolism (VTE)
after SCI, therapists must encourage physical mobility, accord-
ing to tolerance, unless medical contraindications exist.97
Furthermore patient education, mechanical compression, hydra-
tion, and medication referral are indicated. Screening for the
presence of VTE includes assessment of pain, tenderness, swell-
ing, warmth, or discoloration in the lower extremity and should
always occur before initiating exercise activity. (Refer to Chap-
ter 7 for more information on VTE) Referral for anticoagulation
therapy and/or inferior vena cava (IVC) filter placement is the
current best clinical practice.97
Spinal Shock
“Spinal shock” can occur immediately after traumatic injury to
the spinal cord, when all reflexes below the injury are either
markedly decreased or absent; the resolution of spinal shock
marks the acute phase of SCI.95 Spinal shock can last 48 to 72
hours but, on average, lasts 4 to 6 weeks.95
146 CHAPTER 6     Nervous System

TABLE 6.15  Prediction Signs: Assessments Within 2 Weeks of SCI

Test Prognostic Sign/Interpretation Author
C4 Poor prognosis for recovery or conversion from cSCI to iSCI Kirshblum, 199899
C5 66%–90% improve one root level, not degree of completeness Kirshblum & O’Connor,
Sensory testing at 72 hours AIS B: 199899
after SCI If sharp/dull intact; 66%–89% achieve ambulation at 1 year
Only light touch intact = 11%–14% achieve ambulation at 1 year
Dual Dx SCI TBI 60% of SCI may be associated with some level of TBI Nott et al., 2014100
Requires longer LOS. If noncompliant, show difficulty learning, poor reaction Kushner, 2015101
to trauma or unmotivated…may have TBI component to their SCI Bradbury et al., 2008102
Macchiocchi et al., 2012103
Ambulation after SCI A patient with SCI walking ≥ 0.59 m/s will ambulate independently in com- Van Siflout et al., 2017104
munity versus be wheelchair dependent in community; suggests using this
speed for long-range planning
Dutch Clinical Prediction Tested within 15 days of injury onset, predicts ambulatory status at 1 year; Van Middendorp
Rule Uses age (≥ 65 years of age); light touch and motor score for L3 and S1 in et al., 2011105
the prediction equation
(I amb = e–3·273 + 0·267 × score/1 + e–3·279 + 0·267 × score)
<50 years of age; sharp/dull Tested baseline 2–4 weeks after injury; if <50 years of age with sharp/dull Oleson et al., 2016106
testing present in at least half of the lower extremity dermatomes (L2-S1) predicts
household ambulation at 1 year
INSCI testing within 1 week Less than 3% of pts with AIS A upon rehabilitation admission changed clas- Scivoletto et al., 2004107
sification
AIS A versus B; at discharge At 1-year post injury: AIS A more likely to still use indwelling catheter, have Kirshblum et al., 201194
from rehabilitation an inpatient hospital requirement over the first year; and require assistance
for self-care
C4-T10 AIS C Recovery of quad strength 3/5 by 2 months post injury; 100% became func- Crozier et al., 1992108
(n = 17) tional ambulators
Quadriceps strength <3/5 at 2 months; 25% functional ambulators

Amb, Ambulation; cSCI, complete spinal cord injury; I, independent; iSCI, incomplete spinal cord injury; LOS, length of stay.

Prognosis Cerebral Circulation

Predicting outcomes post SCI is critical for successful manage-
ment of recovery resources and is heavily influenced by injury
severity (Table 6.15).94,98–108 Digital examination of rectal tone
is the number one criterion for determining a complete versus
incomplete SCI98 and is important for prognostication. Life
expectancy is improved with incomplete injury but remains
reduced compared with that for nondisabled counterparts.
Physical therapy interventions in SCI include determining
cardiorespiratory control; circulation and hemodynamic responses
to position change; fracture stabilization; positioning/sleep man-
agement; skin and airway clearance; upright/out-of-bed tolerance;
classification of injury; strengthening and joint protection; and
initiation of functional mobility, as able. Strengthening programs
focus on all innervated muscle groups. No-weight repetitions or
body-weight resistance should be used for activities to increase
strength. Shoulder pathology is common among wheelchair users
post SCI. For individuals who are nonambulatory, exercise pro-
grams should focus on strengthening innervated muscles across
the shoulder girdle and providing support for all joints, as able,
particularly the upper extremity joints that may play a weight-
bearing role after injury (e.g., middle and lower trapezius, exter-
nal rotators, and scapular retractors); be sure to perform shoulder
extension without anterior impingement.109,110  blood flow. Assessing the integrity of these major cerebral vessels
Approximately 700 mL of blood flows through the adult brain
per minute,111 delivering oxygen and glucose to nervous tis-
sues. Brain damage associated with cerebral vascular disorders
elucidates the functions of different regions of the CNS because
blood vessel occlusions have revealed characteristic clinical pre-
sentations. Posterior versus anterior circulation in the brain
frames the clinical signs associated with damage in these respec-
tive regions.
The posterior circulation in the brain includes the vertebral
arteries, giving rise to the basilar artery, both of which perfuse
the brainstem before bifurcating into the right and left posterior
cerebral arteries. The latter blood vessel ultimately perfuses the
posterior aspect of the cortex, among other structures, but gives
off posterior communicating artery branches, forming the base
of the central vasculature, called the circle of Willis. Posterior
circulation strokes, therefore, typically present with brainstem,
cranial nerve, and posterior cortex damage.
Vertebral–basilar arterial insufficiency (VBI) may present as
transient dizziness, diplopia, dysarthria, diminished pupillary
light reflex, nystagmus, impaired sensation of the face, deviation
of the tongue with protrusion112 (affecting all the respective cra-
nial nerves), which resolve when no longer compromising this

Anterior cerebral artery
Posterior cerebral artery
A (“tough mother”) layer, which itself has an outer and inner com-
Branches of
middle cerebral
artery
B duits called arachnoid granulations, which transport CSF into the
FIG. 6.10
Large cerebral artery distributions. (A) The ACA (anteromedial) and PCA
(posteromedial) distributions. (B) The MCA perfusing the large lateral
hemisphere. ACA, Anterior cerebral artery; MCA, middle cerebral artery;
PCA, posterior cerebral artery. (Reprinted from Lindsay KW. Bone I, Cal-
lander R. Neurology and Neurosurgery Illustrated. New York: Churchill Liv-
ingstone; 1986.)
(e.g., vertebral/basilar arteries) before cervical spine manipula-
tions for neck pain or repositioning maneuvers for vestibular
dysfunctions has been of paramount importance. Clinical provo-
cation uses specific neck positioning to assess restriction in the
vertebral–basilar artery blood flow (thus detecting VBI). How-
ever, recent studies have questioned the sensitivity and utility
of these assessments.112 Thus results from VBI assessment must
note that negative test results do not mean that you proceed
without caution or that the procedure will not still have nega-
tive consequences.
Anterior circulation includes the internal carotid artery,
which also joins the circle of Willis and immediately dives lat-
erally as the middle cerebral artery (MCA), perfusing the BG
structures (via small lenticulostriate arteries) on its way to the
lateral hemispheres. Depending on the somatotopy of the pri-
mary motor and sensory cortices, lesions of the MCA result in a
characteristic pattern impairing upper extremity function more
than lower extremity function (Fig. 6.10A–B). The circle of
Willis continues anteriorly as the anterior cerebral artery (ACA),
perfusing the anteromedial aspects of each hemisphere and com-
pleting the “circle” when the left ACA and the right ACA join
via the anterior communicating artery. This creates a continuous
ring of blood flow to vital central structures in case of proxi-
mal vascular occlusion.113 Anterior circulation strokes affect the
Nervous System     CHAPTER 6 147
cortical structures (e.g., language, movement, perceptual defi-
cits), and specifically ACA strokes characteristically affect lower
extremity function more than upper extremity function. Finally
deoxygenated venous blood enters the major superior, inferior,
and laterally located dural venous sinuses and ultimately exits
the CNS via the internal jugular vein.114 
Protective Structures
The entire CNS is encapsulated with a protective and well-
vascularized connective tissue complex called the meninges.115,116
The three meningeal layers consist of the thick outer dura mater
partment, with the former adhering to its outer bony surface
and the inner layer adhering to the middle meningeal layer.
Within some sections of the dura lie large venous areas (sinuses),
which are responsible for collecting venous (and CSF) out-
flow. The potential subdural space (between the dura and the
middle arachnoid layer) houses “bridging veins,” which drain
the cerebral hemispheres as they make their way to the dural
venous sinuses, ultimately exiting the skull via the internal
jugular vein. The middle arachnoid (“spider-like”) layer gives
rise to the subarachnoid space for blood vessels and CSF to
travel around the brain and spinal cord and also provides con-
dural sinuses.14 Finally, the innermost meningeal layer, the pia
mater (“tender mother”), adheres directly to the surface of the
brain and provides a road map for blood vessel entry into brain
parenchyma.116
 CLINICAL TIP
Bridging veins are stretched in whiplash-type injuries and are re-
sponsible for slow bleeds that occur, often several hours to days
after injury to the head, giving rise to subdural hematoma.117,118
Veins have low pressure, which causes a slow leak, necessitating
close monitoring for the first few days after a head injury.
 
Cerebrospinal Fluid
Four brain cavities, called ventricles, contain choroid plexi, which
filter arterial blood via their choroidal capillaries, generating
CSF at this blood–CSF barrier (Fig. 6.11A).113 CSF flows from
the paired lateral ventricles through the single centrally located
third ventricle and via the cerebral aqueduct into the four ven-
tricles between the medulla/pons region and the cerebellum.
Openings at the caudal end of the fourth ventricle (foramen
of Magendie and Luschka) allow for CSF transfer into the sub-
arachnoid space. CSF subsequently circulates circumferentially
around the brain and spinal cord until it passes through struc-
tures called arachnoid granulations, collecting in the dural venous
sinuses for removal113 (see Fig. 6.11B). The pulsatile flow of
CSF is tied to the cardiac cycle. Capillary-to-venule fluid trans-
fer (i.e., CSF to interstitial fluid movement to removal) effec-
tively sweeps and removes metabolic waste products from brain
tissue.119,120 Failure of these removal systems (termed glymphatic
systems) have been recently implicated in neurodegenerative dis-
ease processes.113,120
148 CHAPTER 6     Nervous System

B
FIG. 6.11
The ventricular system of the brain. (A) 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. (B) Coronal section of
meningeal layers. Note the close approximation of the arachnoid layer and the superior sagittal sinus located
within the dural folds. (From Bogousslavsky J, Fisher M, eds. Textbook of Neurology. Boston: Butterworth-Heine-
mann; 1998: 656; Paz JC, West MP, eds. Acute Care Handbook for Physical Therapists. 4th ed. Fig. 6.2.)

CSF in the subarachnoid space goes through three to four
cycles in a day.14 Increased CSF production, decreased absorp-
tion, or blockage of CSF outflow has major consequences to
brain function (e.g., hydrocephalus and increased ICP). There-
fore monitoring for signs/symptoms of ICP is of paramount
clinical importance.
Intracranial Pressure and Cerebral Perfusion Pressure
Cerebral perfusion pressure (CPP), which is the pressure needed
to transfer blood from systemic circulation into cerebral circu-
lation, is determined by the difference between mean arterial
pressure (MAP) and ICP (CPP = MAP − ICP), with optimal
values between 65 to 95 mmHg.121 Low CPP is associated with
increased mortality after head injury, whereas high CPP has
been associated with more severe disability122 and progression
of secondary injury.123 Note that significant changes in ICP and/
or MAP can influence cerebral perfusion. For example, trauma to
the body leading to significant blood loss would negatively affect
MAP, whereas closed head injury can cause bleeding and inflam-
mation leading to increased ICP, both negatively affecting over-
all CPP and cerebral blood flow. Clinical signs of increased ICP
includes progressive deterioration in consciousness level, pupil-
lary dilation, ptosis, and irregular respiration.124,125 Decreased
ICP may occur spontaneously or result from a postlumbar punc-
ture procedure, causing headache.126 Lack of continuous or fre-
quent monitoring of BP during and between physical therapy
sessions can have negative consequences for both cardiac and
brain functions. 
Ventricular Dysfunction
Hydrocephalus. CSF is continually produced; therefore con-
ditions that block its normal flow or absorption will result in

overaccumulation of CSF. The resulting pressure of the fluid
against brain tissue results in hydrocephalus. CSF accumulation
may occur secondary to a blockage between the ventricles in the
brain (e.g., noncommunicating or obstructive hydrocephalus);
a blockage after CSF leaves the ventricles but within the sub-
arachnoid space (e.g., communicating hydrocephalus); or within
brain spaces vacated after endogenous removal of necrotic/
damaged tissue creating space for fluid collection (e.g., hydro-
cephalus ex vacuo).127 However, normal-pressure hydrocephalus
(NPH) may result from subarachnoid hemorrhage, head trauma,
infection, tumor, or complications of surgery, and many patients
develop NPH when none of these factors are present. An esti-
mated 375,000 older Americans have NPH, which is charac-
terized by urinary incontinence, subcortical dementia, and
gait dysfunctions, such as bradykinesia, shuffling, short stride
length with broad base of support, difficulty turning, decrease
foot clearance, and poor balance.127 Initially there may be an
increase in ICP; however, over time, it returns to normal ranges
(although it may be elevated compared with an individual’s
baseline value), and persistent ventricular enlargement causes
symptoms. A slow progressive onset caused by gradual blockage
of CSF drainage causes vague symptoms, which are often found
in other disorders; therefore NPH can be difficult to identify.
Hydrocephalus is most often treated by surgically inserting a
shunt system. This system diverts the flow of CSF from the CNS
to another area of the body where it can be absorbed as part of
the normal circulatory process.127 However, complications asso-
ciated with shunting include obstruction (symptoms improved
by shunting reappear); infection at the site (e.g., fever, mental
status changes); new-onset seizures; underdrainage of CSF; and
more drainage of CSF from ventricles than intended secondary
to position change (produces headaches and vomiting).127
 CLINICAL TIP
Physical therapists in acute care hospitals may be responsible
for performing objective measures on individuals as part of the
diagnostic process for normal-pressure hydrocephalus (NPH) to
help determine whether patients are candidates for shunting.
Patients who have positive outcomes to temporary CSF drain-
age or puncture on clinical testing may benefit the most from
shunt surgery.78
 
Post–Dural Puncture Headache. Disruption in the blood–
brain barrier (BBB) resulting from spinal anesthesia or lumbar
puncture can lead to a decrease in ICP with upright posture and
to complaints of headache, nausea, and vomiting. Symptoms
typically resolve spontaneously; however, severe symptoms are
treated with a blood patch. This involves venous blood injec-
tions into the area of the dural tear, and the coagulation that
occurs blocks the leak of CSF, providing symptom relief.78  Activity guidelines after receiving intraarterial tissue plasmin-
Blood-Brain Barrier
The term BBB refers to the tight junctions conferred by the
close approximation of the astrocyte’s terminal regions (end
feet) in the CNS and the ependymal cells, which line the brain
capillaries entering the CNS. These tight junctions allow for
Nervous System     CHAPTER 6 149
the regulation of oxygen and glucose across the BBB, as well
as maintenance of brain homeostasis.2,128 The tight junctions
also prevent toxic and nontoxic substances from passing directly
into the CNS, requiring diffusion across the ependymal cell’s
lipid membrane instead. A substance’s lipid solubility, there-
fore, dictates CNS access, which is a major challenge in CNS
drug delivery. Brain substances that are not lipid soluble would
require a special transport mechanism across the BBB (e.g., glu-
cose transporters).
Aquaporins (e.g., AQP4) are densely noted “pore-forming”
molecules on the astrocytic end feet allowing water to flow
across the BBB129 and helping to regulate interstitial fluid in
the CNS. A breech in BBB protections, caused by free radicals
(e.g., oxygen, nitrogen) and proteases (e.g., matrix metallopro-
teinases [MMPs] and cyclooxygenases), could potentially allow
unregulated passage of toxic molecules into the CNS.129 BBB
breakdown has been implicated in many CNS diseases (e.g.,
cerebral ischemia, brain trauma, meningitis, neuropathic pain,
ALS, MS, and brain tumors).8,128,129 
Cerebrovascular Diseases and Disorders
Stroke
A transient ischemic attack (TIA) is defined as the presence of focal
neurologic deficits lasting less than 24 hours, typically less than
60 minutes.78 The causes of a TIA are related to lack of cerebral
blood flow, either due to hypoperfusion from low blood pressure
or the presence of a thrombus or an embolus.
Acute cerebral vascular accidents (CVA) are categorized by isch-
emic (85%) or hemorrhagic (15%) mechanisms.130 A thrombus
from a cerebral origin or an embolus from a cardiac origin (e.g.,
atrial fibrillation [A Fib]) can lead to single or multiple blood
vessel occlusions and cerebral ischemia.130 The severity of the
sudden focal neurologic impairment depends on the duration of
vessel occlusion, the effectiveness of collateral circulation (e.g.,
circle of Willis; see Fig. 6.6), and the role of the area distal to the
occlusion.130 Chronic hypertension can generate small lesions
(<1.5 cm on MRI) called lacunar strokes in subcortical regions of
the BG, internal capsule, pons, and cerebellum.131
Rupture of cerebral arteries (e.g., hemorrhagic stroke) results
in bleeding into the neural tissue, which damages the neural
pathways and may increase ICP, requiring immediate interven-
tion. Intracerebral hemorrhages can cause ventricular compres-
sion, and cerebral herniation can occur (Fig. 6.12). Bleeding can
also occur within the meningeal spaces. This is usually caused
by a rupture of an aneurysm or an arteriovenous malformation
(AVM) and is referred to as subarachnoid hemorrhage.
Medical management and emergency treatment for isch-
emic strokes of thrombotic origins may include thrombolytics
if the patient receives care within 3 hours of symptom onset.130
ogen activator (tPA) vary by facility; generally a short period
of bed rest (6.48 hours) is imposed to prevent further injury
from bleeding, although recent research supports a shorter time
frame, indicating that early mobility is safe.132,133 Hemorrhagic
strokes may require surgical intervention for decompression of
the brain tissue due to swelling and clot burden. The physical
150 CHAPTER 6     Nervous System
A
B function, and lower extremity coordination.132-134 Recent stud-
FIG. 6.12
Herniation syndromes. Intracranial shifts from supratentorial lesions. (A)
Normal location of structures. (B) Various herniation syndromes are dem-
onstrated: 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 brainstem
through tentorial notch showing central herniation syndrome. (From Beare
PG, Myers JL, eds. Adult Health Nursing. 3rd ed. Philadelphia: Saunders;
1998, p 919.)
therapist should be aware of the surgical procedure and any pre-
cautions that may be subsequently imposed. If a craniectomy is
required for decompression, a helmet may be ordered for safe
out-of-bed activity until a cranioplasty can be completed, usu-
ally 6 to 8 weeks after injury.132,133
Prognostic factors for an unfavorable outcome for indepen-
dent living after 1 year are advanced age, female gender, nonla-
cunar stroke type, hemiparesis, prior hemiplegia, homonymous
hemianopia, urinary incontinence, low initial functioning in
activities of daily living (ADLs), an unalert initial level of con-
sciousness, visual extinction, constructional apraxia, visuospa-
tial construction problems, and absence of transfer to the stroke
unit.132 Inpatient rehabilitation has been shown to decrease hos-
pital length of stay and improve functional outcomes after an
acute stroke. Patients are significantly more likely to be alive,
independent, and living at home 1 year after stroke if they have
received specialized stroke rehabilitation versus nonspecialized
rehabilitation.132,134
Recovery of function after stroke is variable and also depends
on the type of stroke as well as the severity of damage. Ini-
tially mortality is higher with hemorrhagic strokes; however,
if patients survive a hemorrhagic stroke, they are more likely
to demonstrate larger functional improvement as the swelling
decreases.78 Those who have ischemic strokes demonstrate less
improvements compared with those with hemorrhagic strokes;
but, again, recovery of function is dependent on the location and
severity of injury, as well as patient age and comorbid condi-
tions. The National Institutes of Health Stroke Scale (NIHSS)
has been shown to be a predictor of both short-term and long-
term outcome of stroke patients. Documented at the time of
admission by the physician, the scale serves as both a data col-
lection tool for planning patient care as well as for improving
communication among health care providers.135
Prognosis. With regard to prognosis, the greatest predictor
of community ambulation is walking speed. However, survivors
of stroke who demonstrate mild to moderate motor impairment
and are functional ambulators have a 73% incidence of falls
within the first 6 months after the stroke.132–134 They are also at
increased risk for hip fractures, resulting in greater mortality and
morbidity compared with those who have not had a stroke.132
Clinical instruments predict functional outcomes after stroke
with better accuracy compared with lesion size and location.
Sitting balance, motor function, and ADL assessment in the sec-
ond week after the stroke predicts independence in ADLs at 1
year, while MRI imaging does not add predictive value. Other
predictors of participation and independence in ADLs over the
long term include age, comorbidity, cognition, upper extremity
ies suggest that earlier and more intensive out-of-bed activity
after stroke may reduce time to unassisted walking and improve
independence.132
 CLINICAL TIP
Pay close attention to maintaining blood pressure (BP) pa-
rameters after embolic strokes because of cardiac involvement.
Acute management of BP is a balancing act between maintain-
ing cerebral perfusion and avoiding adverse systemic events due
to persistently elevated BP.136
Review of the patient medical record and imaging before ini-
tiating the bedside evaluation, allows for prediction of patient
presentation and better preparation for mobility needs (Table
6.16). A physical therapy consultation is recommended within
24 hours of admission for acute stroke137,138 and continued
throughout recovery into the chronic phase. Strengthening
exercises and activity aimed at improving aerobic capacity and
cardiorespiratory function have been shown to improve out-
comes.139–143 Constraint-induced movement therapy (CIMT)
has been shown to be effective for improving outcomes of upper
extremity function in patients with some voluntary wrist exten-
sion as well as minimal finger extension. Metacarpophalangeal
and interphalangeal function is highly associated with integrity
of the CST system and is a strong clinical predictor of the return
of dexterity in the first days after stroke.139,144 Of note, use of
upper extremity prognostic indicators helps guide interven-
tions by identifying compensation mechanisms versus recovery
mechanisms needed to increase functional mobility.145 Most
 Nervous System     CHAPTER 6 151

TABLE 6.16  Neurologic Signs Associated With CVA by Locationa (See also Fig. 6.10)
Artery
Internal carotid
Middle cerebral
Anterior cerebral
Posterior cerebral
Vertebral or basilar
Posterior inferior
cerebellar
Anterior inferior and
superior cerebellar
aInterpreted
from table in: Paz J, West M. Acute Care Handbook for Physical Therapists. 4th ed. St. Louis: Saunders.
Data from Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg. 1968;28(1):14-20; Hunt WE, Mea-
gher JN, Hess RM. Intracranial aneurysm: a nine-year study. Ohio State Med J. 1966;62(11):1168-1171.
Area Affected
Diencephalon; Cerebral hemispheres via
MCA and ACA
Lobes: Frontal, parietal, and cortical
surfaces of temporal (communication;
language interpretation; perception and
interpretation of space, sensation, form,
and voluntary movement)
Superior surfaces of frontal and parietal
lobes and medial surface of cerebral
hemispheres (includes motor and
somesthetic cortex serving the legs), basal
ganglia, and corpus callosum
Lobes: Medial and inferior temporal,
medial occipital, thalamus, posterior
hypothalamus, and visual receptive area
Brainstem and cerebellum
Lateral and posterior portion of the medulla
Cerebellum
Neurologic Signs
Unilateral blindness; Profound aphasia
Severe contralateral hemiplegia and hemianesthesia
Contralateral homonymous hemianopsia
Contralateral motor and sensory loss, greater in the face and arm than
in the leg
Emotional lability; confusion, amnesia, personality changes; urinary
incontinence; contralateral hemiplegia or hemiparesis, greater in
the leg than in the arm
Hemianesthesia; Contralateral hemiplegia, greater in the face and
arm than in the leg; cerebellar ataxia, tremor; homonymous
hemianopsia, cortical blindness; receptive aphasia; memory deficits
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
Anterior portion of the pons = “Locked-in” syndrome (no movement
except eyelids; sensation and consciousness preserved)
Wallenberg syndrome
Dysphagia, dysphonia
Nystagmus, vertigo, nausea, and vomiting
Ipsilateral anesthesia of face and cornea for pain and temperature
(touch preserved), Horner syndrome, decompensation of movement
Contralateral anesthesia of trunk and extremities for pain and
temperature
Difficulty with articulation, gross movements of limbs—ipsilateral
ataxia
Nystagmus, vertigo, nausea, and vomiting
Ipsilateral Horner syndrome

interventions for the upper and lower limbs after stroke are TABLE 6.17  Unilateral Neglect132,146
driven by repetition and principles of task- and context-specific Type of Deficit Presentation
motor learning.
Memory and repre- Lack of awareness of the contralesional half
Unilateral neglect (Table 6.17) is a disabling feature of stroke, sentational deficits of a mental representation or visualization
defined as the failure to report, respond, or orient to stimuli pre- of a task or environment
sented contralateral to the brain lesion.146 Although unilateral Motor neglect Lack of spontaneous movement in the
neglect can occur after damage to either hemisphere, left neglect contralesional space that is not due to a
due to right hemisphere damage is much more common, longer deficit of the motor pathway
lasting, and more severe compared with right neglect due to left Sensory neglect Lack of awareness of sensory stimuli on the
hemisphere damage.132 (Inattention) contralesional side of the body or space
Patients with unilateral neglect often experience a visual spa- Personal neglect Inability to attend to one side of one’s body
tial midline shift, resulting in impaired balance and asymmetric Spatial neglect Failure to acknowledge stimuli on the
weight bearing in standing. Recovery from neglect is greatest contralesional side of space
in the first month after stroke and can range from persisting Peripersonal—inability to attend to the
neglect to complete recovery. From a prognostic standpoint, space within reaching distance
Extrapersonal—inability to attend to the
patients with neglect have longer lengths of stay in rehabili- space beyond reaching distance
tation facilities with lower Functional Independence Measures
152 CHAPTER 6     Nervous System
(FIM) scores and require more assistance at discharge compared
with those without neglect. The presence of neglect appears to
be a stronger indicator of poor prognosis compared with severity
of the lesion, presence of aphasia, or intellectual capacity and is
strongly related to an increased risk for injury and falls.132,146  and travel with arteries and veins as they exit the CNS en
Aneurysm
Weakening of the inner layer (the intima) of a blood vessel wall
can lead to abnormal focal dilation of a cerebral artery. The dila-
tion, potentially rupturing without warning, can bleed in to
subarachnoid space, causing stroke, coma, or death.147 Clips or
coils are typically used to stabilize the bleeding (see Surgical
Procedures section) or can be inserted prophylactically to pre-
vent hemorrhage if an aneurysm is found incidentally; however,
occlusion of blood beyond the aneurysm is a serious compli-
cation of both procedures.147 The pattern and distribution of
strokes varies, depending on the aneurysm location and the pro-
cedure type.
Subarachnoid hemorrhage due to trauma or aneurysm rupture
leaves patients vulnerable to vasospasm, delayed cerebral isch-
emia, and subsequent clinical decline, particularly in the first
2 weeks after onset.148 Current management includes ICU care,
with restricted activity; however, evidence for conservative man-
agement is lacking.78
Subdural hematomas occurring spontaneously (e.g., due
to anticoagulant medications) or secondary to head injury
involve tears in bridging veins and bleeding between the
dural and arachnoid meningeal layers. Burr holes into the
skull are commonly used for draining and decompression
of underlying brain tissue. Older adults have more subdu-
ral space due to brain atrophy associated with aging36 and
therefore experience less damage with an equal-sized subdu-
ral hemorrhage compared with younger patients. However,
slow bleeds can go unnoticed for longer (i.e., the time to
accumulate enough blood to create pressure on the surround-
ing tissue causing symptoms is longer). Therapists should
be aware of this time lag and routinely reevaluate and report
any changes in neurologic signs (e.g., gradual headaches and
increasing confusion).
Cerebral amyloid angiopathy (CAA), although often asymp-
tomatic, occurs when amyloid protein builds up on the walls
of the arteries in the brain. In severe CAA, protein deposits
cause the blood vessel walls to crack, resulting in hemorrhagic
stroke.78  (anterior, posterior, and lateral) (Fig. 6.14) and the two otolith
Arteriovenous Malformation
An AVM is a tangle of blood vessels that can occur anywhere in
the body but is most often found in the brain or spinal cord.78
Arteries and veins are usually connected by a capillary system;
however, in AVM, patients lack this capillary system, caus-
ing blood to flow from the artery to the vein without allowing
for perfusion of oxygen-rich blood to the surrounding tissues.
Symptoms usually do not appear until the malformation rup-
tures, causing hemorrhage. However, some AVMs grow and cre-
ate symptoms resulting from pressure created at the site of the
malformation; symptoms can range from headaches to seizures
as well as focal neurologic deficits.78  ance control.2
The Peripheral Nervous System
Peripheral nerves contain sensory, motor, and autonomic axons
route to their respective targets (see Fig. 6.3). Many of the
31 pairs of spinal nerves form functionally related nerve com-
plexes (brachial and lumbar plexuses), serving the upper and
lower extremities, respectively. Refer to Table 6.18 for descrip-
tions of the key nerve root designations for myotome testing.
Dermatomal distributions are represented in Fig. 6.9. Periph-
eral nerve bundles are encased by a protective connective tis-
sue layer: endoneurium (wraps a single axon), perineurium
(wraps a nerve fascicle), and ectoneurium (wraps bundles of
fascicles) (Fig. 6.13). Each individual axon, however, has its
own additional degree of myelination protection, which dic-
tates the speed of action potential conduction (NCV; see Table
6.7). CNS axons are myelinated by oligodendrocytes (one oligo
wraps multiple axons), but in the PNS, multiple Schwann
cells wrap/myelinate a single axon.2 Therefore the death of a
single oligodendrocyte has greater physiologic consequences
in the CNS compared with damage to its counterpart in the
periphery.
Peripheral Nerve Injury
Reversible compression injuries (i.e., neuropraxia), individual
axonal damage (i.e., axonotmesis), or severed nerves (i.e., neu-
rotmesis) result from a variety of trauma and overuse causes.
Peripheral nerve severance often triggers expression of growth
promoting substances from the damaged terminal axon. Sev-
ered CNS axons typically do not regrow; however, lesions of the
PNS’s axons result in measured growth (1 mm per day or 1 inch
per month),2 especially in the presence of Schwann cell axon
guidance channels. Potential regrowth and innervation of inap-
propriate targets can occur.51 
The Vestibular System
The vestibular system has both peripheral and central compo-
nents and is responsible for postural orientation with respect
to gravity, as well as for stabilizing visual images on the ret-
ina as the head moves. The paired (left/right) peripheral ves-
tibular apparatus includes three fluid-filled semicircular canals
organs, the utricle and the saccule. The semicircular canals work
in pairs (i.e., right anterior–left posterior canals) because they
have similar orientations in space and capture the rotational
accelerations of the head. The otolith organs contain otoconia
(i.e., salt crystals), which sit atop a gelatinous substance and
allows movement of the crystals en masse relative to gravity.
The otolith organs detect head position with respect to gravity
and linear acceleration of the head2; both structures send infor-
mation centrally to the brainstem and cerebellum. Central ves-
tibular pathways subsequently contribute to oculomotor control
and, along with visual and proprioceptive inputs (and without
conscious awareness), contribute to spatial orientation and bal-
 Nervous System     CHAPTER 6 153

TABLE 6.18  Major Peripheral Nerves of the Trunk, Upper Extremity, and Lower Extremity
Nerve Spinal Root Innervation
Trunk
Spinal accessory C3 and C4 Trapezius
Phrenic C3, C4, and C5 Diaphragm
Long thoracic C5, C6, and C7 Serratus anterior
Medial pectoral C6, C7, and C8 Pectoralis minor and major
Lateral pectoral C7, C8, and T1 Pectoralis major
Thoracodorsal C7 and C8 Latissimus dorsi
Intercostal Corresponds to nerve External intercostals, internal intercostals, levatores costarum longi and brevis
root level
Iliohypogastric and ilioinguinal L1 Transversus abdominis, internal abdominal oblique
Upper Extremity
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
Lower Extremity
Femoral L2, L3, and L4 Iliacus, psoas major, sartorius, pectineus, rectus femoris, vastus lateralis,
intermedius, and medialis, articularis genu
Obturator L2, L3, and L4 Obturator externus, adductor brevis, longus, and magnus, gracilis, pectineus
Superior gluteal L4, L5, and S1 Gluteus medius and minimus, tensor fasciae latae
Inferior gluteal L5, S1, and S2 Gluteus maximus
Sciatic L4, L5, S1, S2, and S3 Biceps femoris, adductor magnus, semitendinosus, semimembranosus
Tibial L4, L5, S1, S2, and S3 Gastrocnemius, soleus, flexor digitorum longus, tibialis posterior, flexor hallucis longus
Common peroneal L4, L5, S1, and S2 Peroneus longus and brevis, tibialis anterior, extensor digitorum longus, extensor
hallucis longus, extensor hallucis brevis, extensor digitorum brevis

Data from Netter FH, ed. Atlas of Human Anatomy. Summit City, NJ: Ciba-Geigy; 1989; Moore KL, Dalley AF, eds. Clinically Oriented Anatomy. 4th ed. Baltimore:
Lippincott Williams & Wilkins; 1999.

Vestibular Dysfunction Patients with cervicogenic dizziness complain of nausea, head-

Vestibular disorders may have an acute onset (i.e., within 2
weeks), subacute (i.e., 2 weeks to 3 months) or chronic (i.e., >3
months) presentation.149 Dizziness, frequently associated with
vestibular disorders, affects more than 30% of individuals over
age 60 years and 50% of individuals over age 85 years150,151
and can have a significant effect on fall risk/safety. However,
dizziness is not a localizing symptom, necessitating additional
descriptors and testing.152 Cervicogenic dizziness refers to dizzi-
ness coupled with neck or headache pain,153,154 which is com-
mon following whiplash injuries after motor vehicle accidents.
ache, and dizziness with neck motions, not head motions (e.g.,
the head stays still [no vestibular motion] and the body rolls
or rotates, producing neck motion on the head, triggering
symptoms).153
Additional Vestibular Dysfunction Terms
Vertigo is the perception that the self or the environment is
spinning in the absence of actual motion. Subsequently,
positional vertigo refers to spinning sensations that are posi-
tion dependent and relative to gravity.155
154 CHAPTER 6     Nervous System
Epineurium
around nerve
Fascicle
Perineurium
around
fascicle
Axon
Endoneurium around
individual axon
FIG. 6.13
Peripheral nerve structure. Connective tissue covering protects individual nerves (endoneurium), nerve fascicles
(perineurium), or collection of nerve fascicles (epineurium). Note blood vessels and autonomous nervous system
(ANS) axons travel with the peripheral nerve. (Latter not shown.) (From Lundy-Ekman L. Neuroscience: Funda-
mentals for Rehabilitation. 5th ed. St. Louis: Elsevier; 2018, Fig. 17.02A.)
A B
FIG. 6.14
Semicircular canals. (A) Lateral view: Note the 30-degree angle in the supe-
rior direction for the horizontal canal. (B) Superior view shows the pairing
of complementary canals. (From Goodman CC, Fuller KS. Pathology. 4th ed.
Fig. 38.4, pg. 1633.)
Lightheadedness can be caused by many factors, including low
BP; low blood glucose; or cardiac dysfunction, typically not
associated with vestibular deficits.
Disequilibrium refers to impaired balance or the sensation of
being off balance.74  Highly recommended vestibular tests include the Functional Gait
Peripheral Vestibular Disorders
Determination of unilateral versus bilateral peripheral ves-
tibular deficits is key for identifying the appropriate physi-
cal therapy intervention. Unilateral deficits (e.g., unilateral
vestibular hypofunction [ULVH], Meniere’s disease, and
vestibular neuritis) allow central compensations and recov-
ery, whereas bilateral deficits do not.149 Rehabilitation for
peripheral vestibular disorders (unilateral and bilateral) typi-
cally focuses on gaze stabilization with head movements (i.e.,
adaptation exercises), habituation exercises (i.e., repeated
exposure to offending positions intending to fatigue-pro-
voked symptoms), balance and gait training, as well as walk-
ing endurance.149
Peripheral
nerve
Blood vessels
Benign paroxysmal positional vertigo (BPPV) is an inner ear
disorder that presents as episodic positional vertigo155 (see Fig.
6.14). Calcium carbonate crystals dislodge from the otolith and
float into the semicircular canals, the posterior canal being the
most common. The Dix-Hallpike maneuver is the standard
assessment for posterior canal–related BPPV (Fig. 6.15).155 The
tested side is “ear down,” and treatment typically involves the
canalith repositioning manuever.19 Untreated BPPV leaves the
patient susceptible to falls and decreased quality of life.155 
Central Vestibular Disorders
Impaired smooth pursuit, or saccadic eye movement testing,
suggests a central vestibular disorder. These may be caused
by tumors, migraine, trauma, demyelination secondary to
MS or stroke, which affects the vestibulocerebellar structures.
Table 6.19156–159 compares CNS with PNS diagnostic criteria
and provides a description of common vestibular examination
procedures.
Current recommendations do not support the use of ves-
tibular suppressant medication for the diagnosis of BPPV155
or for imposing restrictions of body positioning after complet-
ing an BPPV treatment maneuver (e.g., Epley) (Fig. 6.16).158
Analysis, Dynamic Gait Index, Dynamic Handicap Index, Dix-
Hallpike Maneuver (see Fig. 6.15) tests, and recommended tests
include the Four Square Step Test, Dynamic Visual Acuity
(instrumented); Head Impulse Test; and the Activity-Specific
Balance Confidence (ABC) scale.
Meniere’s disease160 is caused by a buildup of endolymphatic
fluid affecting the vestibular and cochlear peripheral nerve
functions. Clinical symptoms include dizziness, tinnitus,
and hearing loss of the affected ear; abnormal nystagmus and
abnormal caloric testing have been observed, and 15% of those
diagnosed have bilateral symptoms.160 Patients with vestibular
migraine have similar complaints with the addition of headache,
light sensitivity, vomiting, and aura, not seen with Meniere’s
disease.156,160

FIG. 6.15
The Dix-Hallpike maneuver. Assessment for the presence of benign par-
oxysmal positional vertigo (BPPV). Have the patient recline with cervical
rotation and extension, and watch pupils for nystagmus. The tested side is
“ear down.” See Table 6.19. (From Herdman S: Treatment of benign parox-
ysmal positional vertigo. Phys Ther 70:381-3888, 1990.)
Acute vestibular neuritis refers to inflammation of the vestib-
ular nerve and results in paroxysmal attacks of severe vertigo
(dizziness) that is not accompanied by deafness or tinnitus. It
typically affects middle-aged adults and often follows an upper
respiratory tract infection. Medications may be indicated for the
acute phase only (meclizine or antinausea medications).156
Bilateral vestibular hypofunction is associated with ototoxicity
(i.e., systemic exposure to gentamycin, with bilateral effects).
Because bilateral peripheral vestibular organs are affected, a focus
on compensation versus driving recovery is recommended.149  terial or fungal infections include severe headache, back pain,
Additional Prevalent Health Conditions
Seizures
A seizure is defined as a “transient occurrence of signs and symp-
toms due to abnormal excessive or synchronous neuronal activity
in the brain.”161 Focal seizures originate within one part of a cere-
bral hemisphere, whereas generalized seizures are distributed in
bilateral cerebral hemispheres at onset.161 The clinical features of
seizures vary, depending on the underlying neuroanatomy. Sub-
jective symptoms at the onset of a seizure are called auras, which
are typically seen in patients with focal seizures, and provide
Nervous System     CHAPTER 6 155
the most localizing information of where in the brain seizures
might arise. Although seizures are fairly common, the differ-
ential diagnosis, particularly if the initial event is unwitnessed,
can be broad and includes migraine, syncope, TIA, psychogenic
nonepileptic seizures, movement disorders, sleep disorders, and
panic attacks. There is an approximately 35% chance of a seizure
recurrence within 5 years after new-onset seizure in adults.161
However, in persons who have had a second seizure, the risk
of a recurrent seizure increases to 75% during the following 5
years. Epilepsy is defined as “two or more unprovoked seizures
occurring more than 24 hours apart or one unprovoked seizure
and a high risk (at least 60%) of recurrent unprovoked seizures
over the next 10 years.”161 Excessive sleep deprivation and alco-
hol or illicit drug use can be precipitating factors for a seizure.
Additionally, certain medications (clozapine, cephalosporins,
fluoroquinolones, bupropion, and tramadol) have been shown to
reduce the seizure threshold. Metabolic derangements, altered
homeostasis caused by organ failure, and toxin exposure are also
common provoking factors for seizures.161
Electroencephalography (EEG) remains the most commonly
used study in the evaluation of patients with epilepsy. A routine
EEG may assist in diagnosis, classification of seizure type(s),
identification of treatment, and monitoring of therapy efficacy.
Video-EEG monitoring permits seizure classification, assess-
ment of psychogenic nonepileptic seizures, and evaluation of
candidacy for epilepsy surgery. MRI is pivotal in elucidating the
etiology of the seizure disorder and in suggesting the localiza-
tion of seizure onset.162
 CLINICAL TIP
Common adverse effects of antiepileptic drugs include somno-
lence, dizziness, blurry vision, and difficulties with concentration
and memory, all which may have an effect on physical therapy
examination and functional independence; this is particularly
important in the setting of new medications or acute changes
in dose.
 
Neuroinfectious Diseases
There are multiple types of neuroinfectious diseases. The caus-
ative agents may be bacteria, fungi, viruses, prions, and occa-
sionally protozoa or parasites. Infection of the brain results in
inflammation and subsequent damage. Symptoms of CNS bac-
stiff neck, confusion, weakness, fever, seizures, and paralysis.
Symptoms of CNS viral infections include fever, irritabil-
ity, anorexia, seizures, head and neck pain. Distinguishing
between an infectious and inflammatory disorder in the CNS
is sometimes a complex process because some conditions are
difficult to diagnose, and often there can be a great deal of
overlap. Some infections trigger an exaggerated inflammatory
reaction that causes neurologic damage independently of or
co-occurring with the infection, and in some inflammatory
conditions, new issues that arise may be related to the dis-
ease itself or may be infections in the setting of an abnormal
immune system.
156 CHAPTER 6     Nervous System

TABLE 6.19  Vestibular Tests and Measures156

Test
Static ocular observation
Saccadic eye movement
Smooth pursuit eye move-
ment
Heat thrust test or head
impulse test157
Head-shaking induced
nystagmus
Dix-Hallpike
Dynamic visual acuity (DVA) Sit or stand for testing; head motions at or above 120 degrees; ask
the patient lowest line seen on Snellen-type chart.
Procedure
Assess ocular alignment on forward gaze; gaze on a single focal
point will cause convergence.
Request eye movements on your command between two horizon-
tal or two vertical targets. (Do not place your face between the
two markers.)
Change speeds while tracking a brightly colored pencil-eraser
sized object. Contrast slow and fast tracking on horizontal and
vertical planes.
Hold neck in 30 degrees of flexion to place horizontal canal in
transverse plane; gently grasp head, ask patient to focus on
target. Next move 5–10 degrees (with high-velocity motion);
when movement stops, watch pupillary responses with eyes
open and their ability to stay on visual target.
Patient dons Frenzel’s goggles; flexes head 30 degrees and does 20 Presence of nystagmus reveals vestibular
horizontal head rotations. After 20 reps, patient eyes open; look “imbalance.”157,158 Sensitivity and speci-
for nystagmus.
45 degrees cervical rotation; 30 degrees quick cervical extension
over the edge of table (Fig. 6.15).
For those with C spine precautions: Lying upside down on a tilt
table may allow similar vestibular apparatus positioning with-
out need of or concern for neck extension.
Vestibular Pathology
Strabismus: Eyes do not align; an eye may
roll inward (esotropia); outward (exotro-
pia); upward (hypertropia) or downward
(hypotropia), (diplopia: double vision)
Look for dysmetria (over- and undershoot-
ing targets) or corrective catch-up sac-
cades to reach target
Impairments in tracking suggest saccadic
breakdowns
Uses VOR pathways to assess peripheral
vestibular hypofunction157
ficity vary; assesses central or peripheral
unilateral vestibular deficit
Nystagmus fatigues in 30–60 seconds of
triggering position if peripheral lesion;
lasts longer if central lesion
Compare with static acuity and norms159

Caloric testing
Rotary chair testing
Romberg test
VOR: X1 and X2 Viewing
Sensory Organization Test;
The is the clinical version of
the CDP test
Test tube water irrigation into the external auditory meatus;
watch pupillary response; typically used for nonresponsive
patient to test brainstem involvement after trauma.
Sitting in a chair in a small dark room;
EMG electrodes track eye movement responses to rotating-chair
displacement.
Standing with both shoulders flexed to 90 degrees; assess eyes-
open versus eyes-closed sway differences; Sharpened Romberg
refers to subject standing in tandem heel-toe position before the
eyes closed condition
Client starts with an extended arm holding a target. Head move-
ments to left and right are completed while maintaining eyes
on the target. Progression includes movement of target opposite
head motion.
Testing 30 seconds standing on floor or thick foam; with eyes
open, eyes closed, or eyes open and wearing a dome.
Normal response: cold opposite warm same
(COWS)
Cold water: eyes deviate direction op-
posite the ear irrigated
Warm water: eyes deviate to the same
side as the ear irrigated
Used to examine ocular responses during
VOR testing and to diagnose bilateral
vestibular hypofunction
Excess sway and asymmetry in hand posi-
tion after 30 seconds suggests vestibular
and/or proprioceptive deficits
Gaze Stabilization alone not recommended;
do X1 and X2 viewing for recovery
Difficulty with eyes open and dome (on
and/or off the foam) strongly suggest
vestibular dysfunction

CDP, Computerized dynamic posturography; VOR, vestibular ocular reflex.

Infections can cause inflammation of the brain (encephalitis).
The severity can be variable. Symptoms may include head-
ache, fever, confusion, stiff neck, and vomiting. Complications
may include seizures, hallucinations, aphasia, memory deficits,
and loss of hearing. Viruses are the most common causes of
encephalitis.
Infections can also cause inflammation of the meninges, called
meningitis. The most common symptoms are fever, headache,
and neck stiffness. Other symptoms include confusion or altered
consciousness, vomiting, and sensitivity to light or loud noises.
Often bacterial meningitis spreads to the brain itself, causing
encephalitis. Similarly, viral infections that cause encephali-
tis often also cause meningitis. When both the brain and the
meninges are infected, the disorder is called meningoencephalitis.
In encephalitis and meningitis, infection is not typically con-
fined to one area. It may occur throughout the brain itself or
 Nervous System     CHAPTER 6 157

Utriculus Posterior canal

Posterior-
Superior canal ampulla
canal Particles

Vantage
point

Gravity Vantage Gravity

A Particles point C Superior canal

Superior Posterior Superior canal

Posterior
canal canal Vantage canal
point Utriculus

Particles

Particles Vantage
BGravity point
B
Posterior-canal
ampulla

Gravity
D
FIG. 6.16
The Epley maneuver for the treatment of benign paroxysmal positional vertigo (BPPV) in the posterior canal.
(From Furman JM, Cass SP: Benign paroxysmal positional vertigo, N Engl J Med 341:1590-1596, 1999. Copy-
right 1999 Massachusetts Medical Society. All rights reserved.)

within meninges along the entire length of the spinal cord and
over the entire brain. But in some disorders, infection is a local-
ized abscess called an empyema.
The term encephalopathy, in most cases, is preceded by vari-
ous terms that describe the cause or condition of the patient
that leads to brain malfunction. For example, anoxic encepha-
lopathy means brain damage due to lack of oxygen, and hepatic
encephalopathy refers to brain malfunction due to liver disease.
Additionally some other terms either describe body conditions
or syndromes that lead to a specific set of brain malfunctions
(metabolic encephalopathy).  formed by the contact between a motor neuron and a muscle
Degenerative CNS Diseases
Amyotrophic lateral sclerosis (ALS) is the most common of the
motor neuron diseases and includes cortical and segmental
motor neuron degeneration preferentially targeting the fatigue
intermediate and fast fatigable motor units.163 Familial (10%)
or sporadic (90%) cases of ALS have an average age of onset of 50
to 70 years, with an average time from onset of clinical signs to
diagnosis being 14 months.163 Approximately 33% of patients
have onset of bulbar (brainstem) symptoms; 30% have onset
of upper extremity symptoms; and 34.4% have onset of lower
extremity symptoms.164 Twice-daily exercising, according to
patient tolerance, is recommended to offset disuse weakness,
which negatively affects ADLs.164 Average life expectancy is
3 to 5 years after onset,164 and ALS is often accompanied by
frontotemporal dementia. Use of assistive and adaptive equip-
ment to maintain functional capacity is recommended. Energy
conservation strategies, home modifications, and personal care
attendant information should also be included. 
Myasthenia Gravis
The term neuromuscular junction refers to a chemical synapse
fiber and where signal transmission by way of chemical neu-
rotransmitter (acetylcholine) occurs, causing muscle contrac-
tion.36,165 Myasthenia gravis (MG) is an autoimmune disease,
in which autoantibodies that block or destroy the acetylcho-
line receptors of the motor endplates are produced.36,165 When
acetylcholine binding is prevented, muscle contraction can-
not occur. This leads to excessive fatigue of the affected mus-
cles.36,165,166 Ocular myasthenia (15% of cases) affects only the
ocular muscles, causing ptosis and diplopia, and in generalized
myasthenia (85% of cases), other cranial and skeletal muscles
are also affected.165,166 The hallmark symptom of MG is fluc-
tuating weakness that worsens with exercise and improves with
158 CHAPTER 6     Nervous System
rest. Proximal muscles tend to be more affected compared with
distal muscles, and as the disease progresses, respiratory muscle
fatigue becomes problematic (up to 20% of patients require
mechanical ventilation).166
Exacerbations can result from surgery, stress, lack of sleep,
repeated activity, increased temperature, and pregnancy. A sud-
den loss of respiratory function or marked worsening of weakness
is called myasthenic crisis.36,165 This is a neurologic emergency
and often requires ICU-level care, with progression to acute
respiratory failure requiring ventilation. Glottal weakness can
cause recurrent aspiration pneumonia.165,166 Medical manage-
ment often includes thymectomy and/or plasmapheresis, which
can result in hypotension and worsened fatigue.165 MG is a very
treatable condition, with good survival rates and low mortality
rates (mortality rate has dropped from 75% to 4.5% over the
past 4 decades).166
 CLINICAL TIP
The visual analog scale (VAS) and/or the Borg ratings of per-
ceived exertion (RPE) scale help assess symptoms at differing
times of the day (at best, at worst, and with movement) to elu-
cidate a pattern. Teaching the patient how to manage fatigue is
one of the most important interventions. Activity modifications
should focus on rest, self-pacing, sleep, and stress reduction. The
addition of a seat to the walker may be indicated to accommo-
date the onset of fatigue while walking.
Multiple sclerosis (MS) is an autoimmune disorder of the CNS
and the most common among the demyelinating diseases. The
neurologic decline in MS is characterized by four main types of
clinical courses167:
1. Relapsing-remitting—inflammatory exacerbations with re-
covery
2. 
Secondary progressive—starts as relapsing–remitting but
progressive deterioration in neurologic function eventually
3. 
Progressive relapsing—episodic flare-ups leave persistent
sensorimotor deficits
4. Primary progressive—steady decline in neurologic function
from onset, without episodic flare-ups
A patient with MS can have almost any neurologic sign or
symptom, depending on the location of the lesions within the
CNS. Over 80% of individuals with MS report atypical and per-
sistent fatigue.78,167,168 The main symptom at onset or exacerba-
tion is often blurring of vision caused by optic neuritis.72,168,169
Demyelination is always part of the disease mechanism and
occurs during the inflammatory phases of the lesions. Demy-
elination can occur in the brainstem, cerebellum, cerebral hemi-
spheres, and spinal cord (i.e., almost anywhere in the CNS).78,168
The axons and oligodendrocytes in the CNS undergo demyelin-
ation in a seemingly random pattern and unpredictable order.
MS is associated with early thymus gland involution. Reduced
thymic output appears to disturb the homeostasis of CD4 T
cells, which produce an autoimmune response to myelin. Active
lesions are all characterized by T-cell and macrophage-domi-
nated inflammation. Heterogeneous sclerotic lesions (plaques)
are characteristic on MRI.168,169 Demyelination causes axonal
transection, which results in slowed nerve conduction.169 The
prevalence of MS is two to three times higher in females and is
often marked by onset in the young adult period (3rd and 4th
decades of life). There is a genetic component, with increased
risk for MS in those with a family history, Anglo-Scandinavian
or North Sea ancestry, living in a geographic area with increased
incidence of the disease (especially north of the 37th latitude),
Epstein-Barr virus infection, and optic neuritis (up to 60% of
patients have one or more bouts of optic neuritis preceding the
development of MS).169
 CLINICAL TIP
• Activity prescription should be modified, as needed, to mini-
mize exercise-induced MS symptoms; however, exercise in-
tervention alone (e.g., submax intensity) might reduce MS-
related fatigue.
• Environmental considerations should be made for patients
with Uhthoff’s phenomenon, an acute worsening in neuro-
logic symptoms in the presence of increased heat (e.g., sauna,
pool, hot climates, fever). Cooling exercise vests and cooler
pool temperatures have shown some success.170
Transverse myelitis (TM) is a similar neurologic disorder
caused by inflammation across both sides of one level or seg-
ment of the spinal cord.78,171 Inflammation can damage or
destroy myelin, resulting in loss of function. Pain is often (up
to 50% of the time) the first symptom of TM, beginning as a
sudden onset of lower back pain.171 The segment of the spinal
cord where the damage occurs determines which parts of the
body are affected. Other early symptoms can include allodynia
(up to 80% of people), weakness, sensory changes, bowel and
bladder incontinence, temperature sensitivity, and fatigue.78,171
Symptoms can develop over hours to several days or have a more
gradual onset of 1 to 4 weeks. Prognosis is variable, with some
people recovering with minor residual effects, whereas others are
left with permanent disability.78,171
TM can appear as the first symptom in MS or neuromyelitis
optica (NMO).172 A person with TM who also has an abnormal
brain MRI result and more than two lesions has an increased
risk (as high as 90%) of going on to develop MS. In the case of
NMO, also called Devic’s syndrome, the immune system cells and
antibodies primarily attack the optic nerves and the spinal cord
but may also attack the brain.78,172 The damage to the optic
nerves produces swelling and inflammation, causing pain and
loss of vision; the damage to the spinal cord causes weakness
or paralysis in the legs or arms, loss of sensation, and problems
with bladder and bowel functions. NMO is a relapsing–remit-
ting disease. During a relapse, new damage to the optic nerves
and/or the spinal cord can lead to accumulating disability.
Unlike MS, there is no progressive phase of this disease.172
The pathogenesis of Guillain-Barré syndrome (GBS) is still
somewhat unclear, although it appears to be related to an
autoimmune response where immune cells attack the myelin
sheaths, impairing or blocking nerve impulse conduction.173,174
Onset usually manifests as numbness or paresthesia, followed
by symmetric ascending muscle weakness. Acute respiratory

muscle failure can result from the combination of poor airway
protection, inadequate secretion clearance, and hypoventila-
tion.174,175 Although there are several clinical variants, the most
common type (seen in 85%–90% of individuals with GBS) is
acute inflammatory demyelinating polyradiculopathy (AIDP). The
typical presentation of GBS follows a viral or bacterial infection
or immunization; however, it can also occur with lymphoma,
trauma, surgery, or no identified trigger present.173–175
 CLINICAL TIP
• Exercise should be carefully prescribed, beginning with short-
er sessions because overexertion may be harmful. Intensity
can be increased with close attention paid to rating of per-
ceived exertion (RPE).
• A decline in vital capacity, lack of improvement or decline in
strength, increased pain, and substitution patterns with move-
ment are all signs to stop and report to the physician.
• Note the patients forced vital capacity (FVC) and oxygen satu-
ration levels—in the acute phase, up to 30% of patients with
GBS require mechanical ventilation.78,174
• Deep tendon reflexes are commonly diminished or absent.
• Closely monitor blood pressure when initiating therapeutic
standing because hypotension might develop.
The overall prognosis is generally good with most patients
returning to their prior functional status within 1 year after
onset. 80% of patients with pure demyelinating form of GBS
recover in 6 weeks, for the axonal form of GBS recovery is longer
(6 months to 3 years).78,173,174 Mortality is 5% to 10% world-
wide. Recurrence is uncommon (3%–5%). 20% of patients have
residual disability and 3% recurrence of acute polyneuropathy.
GBS in children has a shorter course and is associated with more
complete recovery than in adults.173
In case of recurrence, the patient might be diagnosed with
chronic inflammatory demyelinating polyneuropathy (CIDP). CIDP is
a chronic condition closely related to GBS and is diagnosed on
the basis of its pattern of progression and relapse. It typically has
a slower onset compared with GBS, but acute-onset CIDP might
be diagnosed when a patient diagnosed with GBS deteriorates
nine or more weeks after onset or when deterioration occurs three
or more times.173–175 In both GBS and CIDP, CSF might indi-
cate elevated protein. Electromyography (EMG) will indicate
muscle fibrillations and fasciculations and a reduced interference
pattern. Nerve conduction studies (NCSs) indicate a progressive
decline in NCV. Intravenous immunoglobulin (IVIg) and plasma
exchange are equally effective in hastening recovery.173,175
Features associated with worse outcomes in GBS are older
age, requirement for respiratory support, abnormal peripheral
nerve function, no plasmapheresis or IVIg performed, subgroup
of GBS with primary axonal degeneration, rapid onset, progres-
sion to quadriplegia, respiratory dependence, severe disease at
presentation, Campylobacter jejuni infection, no improvement at
3 weeks, or plateau of disease.173
Intensive care unit–acquired weakness (ICU-AW) is character-
ized by axonal degeneration with preservation of the myelin that
typically affects motor nerves (although sensory involvement can
Nervous System     CHAPTER 6 159
TABLE 6.20  Clinical Features of Intensive Care Unit–
Acquired Weakness (ICU-AW)
Feature CIP CIM
Weakness Flaccid Flaccid
Worse distal more Worse proximal more than
than proximal distal
Muscle atrophy May be present or May be present or absent
absent
Ventilatory May be present or May be present or absent
failure absent
Muscle stretch Hyporeflexia or are- Normal or hyporeflexia
reflexes flexia
Sensory loss May experience dis- Normal
tal sensory loss
Extraocular Intact Rare weakness, although
muscles facial muscle weakness
may occur
From Zorowitz RD. ICU-acquired weakness: a rehabilitation perspective of di-
agnosis, treatment, and functional management. Chest. 2016; 150(4):966-971.
https://doi.org/10.1016/j.chest.2016.06.006.
happen).176 The patient presents with symmetric weakness (prox-
imal more than distal limb) (Table 6.20).176,177 Many terms have
been used over the years, but the overarching term that is now
used is ICU-AW (critical illness myopathy [CIM], critical ill-
ness polyneuropathy [CIP]).176 Although the direct cause is still
unknown, multiple factors have been implicated in the patho-
genesis of ICU-AW: systemic inflammation, certain medications,
electrolyte disturbances, poor glycemic control, and immobility
in a patient who is critically ill.176 Diagnosis of ICU-AW is made
by using the Medical Research Council (MRC) strength score. A
score of less than 48 out of 60 indicates ICU-AW.176,177
In the short term, ICU-AW results in longer duration of
mechanical ventilation, longer ICU and hospital length of stay,
greater cost per patient, delayed return home after critical ill-
ness, and higher mortality (MRC <36 at discharge from ICU
hazard ratio 4.3).178,179 The long-term effect is also profound.
Effects of ICU-AW weakness persist in 60% of patients for up
to 1 year, with persistent functional limitations due to muscle
wasting (18% loss of body weight after ICU stay), continued
weakness and fatigue, entrapment neuropathy (foot drop, posi-
tioning in bed) and heterotopic ossification.178–180 In a recent
study, at 5 years after ICU discharge, all patients reported vary-
ing degrees of perceived weakness, 6-minute-walk test (6MWT)
median score was 436 m (76% of the age and gender matched
subjects) and the physical component of the Short-Form Health
Survey with 36 items (SF-36) remained approximately 1 stan-
dard deviation (SD) below the mean score for an age- and sex-
matched control population.180 
Neoplasms
Brain tumors are malignant or benign tumors occurring within
the intracranial space that can affect the brain tissue, meninges,
pituitary gland, or blood vessels.181 Primary brain tumors start in
the brain, whereas secondary (metastatic) brain tumors begin in
another part of the body and spread to the brain. Brain metastases
160 CHAPTER 6     Nervous System

are the most common intracranial tumors in adults and account for
more than one half of brain tumors.182 Brain tumors can be invasive
to the surrounding tissue, or space occupying, causing swelling,
increasing the pressure, and subsequently damaging the surround-
ing brain tissue. Symptoms vary, depending on the location, size,
and type of tumor. The rate of growth of brain tumor cells depends
on the type of brain tumor. Gliomas are the most aggressive type of
brain tumor, followed by astrocytomas.181 Meningiomas are benign
tumors that are generally managed and cured with surgery alone.
In general, the prognosis for patients with a brain tumor is not
favorable. Five-year survival among adults with malignant brain
tumors is 33.9%, whereas the survival rate for benign tumors is
better.181,183 Positive prognostic indicators include young age,
duration of symptoms (gradual onset of symptoms offers worse
prognosis), functional presentation at time of diagnosis, tumor
recurrence (recurring tumors offer worse prognosis than initial
tumors), and type of tumor (benign tumors).181,183
TABLE 6.21  Tumor Histology (Grades I–IV)182
I Low risk of recurrence; slow growing; may be cured
with surgery alone
II Also slow growing; has the ability to invade normal
tissue and the potential to recur with a higher grade
of malignancy
III Is composed of actively reproducing abnormal cells
(malignant) that can infiltrate adjacent normal cells
IV Most aggressive form of malignant brain tumor; rapid
proliferation and infiltration of adjacent tissues;
central area of necrosis
The World Health Organization (WHO) developed a clas-
sification system (Table 6.21) for all brain tumors based on
the resemblance of tumor cells to normal cells, rate of tumor
growth, presence of necrotic cells in the middle of the tumor,
tumor margins, and vascularity of the tumor.182
 CLINICAL TIP
It is important for the physical therapist to understand the stage,
prognosis, and expected progression of the brain tumor. End-of-
life and comfort measures only are not reasons for discontinua-
tion of services. Patients on hospice can often have goals that in-
volve mobility or compensatory techniques as well as caregiver
training needs to support their quality of life.
 
Physical Therapy Examination: Chart Review
Chapter 2 outlines the basic format and information found in
the medical record. In the acute care environment, the physical
therapist is called on to integrate information from multiple
sources (Tables 6.22 and 6.23) to determine the appropriate-
ness and timing of PT involvement and appropriate monitor-
ing parameters, plan for possibilities where movement might
compromise medical stability, and establish an activity sched-
ule outside of physical therapy. An understanding of the effect
of these factors on the patients’ body structure and function,
as well as activity limitations/participation, will aid interdis-
ciplinary communication and ultimately determine the best
discharge plan.

TABLE 6.22  Neurologic System-Specific Chart Review184

Provider orders Reason for consult; activity orders (including head of bed position, blood pressure parameters, ICP parameters),
resuscitation status, power of attorney, medical release authorizations, clinical pathways
Provider notes Results of history and physical examination by attending physician and/or consulting services can provide informa-
tion about onset, frequency, duration of symptoms
Loss of consciousness/memory loss/altered cognition
Alteration in speech/communication, headache/visual disturbance
Sleep pattern, handedness, fall history
Nursing notes: Behavior patterns, safety awareness, level of assistance, presences of drains/lines
Laboratory results Sodium (SIADH, cerebral salt wasting, diabetes insipidus)
Magnesium
Coagulation studies
Blood alcohol levels
Kidney function
Cardiac enzymes
C-reactive protein
ABGs
Vital signs Hemodynamic response to activity, CPP/ICP, Transcranial Doppler information
Operative reports Length of anesthesia, type of anesthesia, procedure done, complications
Imaging (Refer to Table 6.23)
Medications Timing, premedication, changes, interactions
Other interventions/ EEG monitoring, swallow studies, interventional radiology, NIF (GBS)
reports These can also provide information on whether the patient can leave the room

ABG, Arterial blood gas; CPP, cerebral perfusion pressure; EEG, electroencephalography; GBS, Guillain-Barré syndrome; ICP, intracranial pressure; NIF, negative
inspiratory force; SIADH, syndrome of inappropriate antidiuretic hormone secretion.
TABLE 6.23  Diagnostic Imaging78,185,186
Test Name
Method/General Infor- Precautions/Consider-
mation Conditions Detected Advantages Disadvantages ations
Radiography (X-Ray)
Image obtained by placing Quick screen for injury after Noninvasive, inexpensive, Small amount This method of imaging
a part of the patient in trauma fast of radiation is being replaced by
front of an x-ray detector Examines bone exposure, two- CT and/or MRI which
and then illuminating it Detects fracture, alignment, dimensional (2D) are more sensitive
with a short x-ray pulse erosion, spur images only examinations
Computed Tomography (CT)
Successive x-rays analyzed Used to identify neoplasm, Fast, noninvasive; can High doses of Contrast allergies; careful
by a computer to provide cortical atrophy, cerebral distinguish between radiation exposure consideration with use
three-dimensional (3D) aneurysm, intracerebral primary ischemic versus of contrast in patients
views with or without hemorrhage (ICH), hemorrhagic process to with renal disease,
contrast arteriovenous malformation determine treatment conventional scanners
(AVM), cerebral infarction, and (e.g., tissue plasminogen can only accommodate
ventricular displacement or activator [tPA]) patients up to 450
enlargement. CT of the spine pounds
and orbits can also evaluate for
fracture, neoplasm, spinal cord
compromise, or sinusitis
Computed Tomography Angiography (CTA)
Visualizes blood vessels Used to screen for subarachnoid Noninvasive, faster, and less High doses of Contrast allergies
hemorrhage (SAH), expensive than traditional radiation exposure
aneurysm, and vessel stenosis angiography
Xenon CT
Evaluate cerebral blood Detects cerebrovascular Noninvasive, fast High doses of Contrast material
flow by computer occlusive disease, increased radiation exposure allergies
detection of concentration intracranial pressure (ICP),
of inhaled xenon gas in intracranial bleeding, and
the bloodstream “brain death”
Magnetic Resonance Imaging (MRI)
Scanners use strong Detects neoplasm, degenerative Better than CT for contrast Not as sensitive Claustrophobia; patient
magnetic fields, radio disease, cerebral and spinal between normal and as CT for must remain still for
waves, and field gradients cord edema, ischemia, pathologic tissues allowing detecting or examination; must fit in
to form images of the hemorrhage, AVM, atrophy, for quicker identification of evaluating SAH, machine; cannot be per-
body and congenital anomalies areas of ischemia, improved calcification, formed in patients with
Used with or without visualization of blood or bony pacemakers, metallic
contrast vessels, less obscuring bone abnormalities implants, pain stimula-
artifact and can image in tor implants, or contrast
any plane allergy; caution must be
exercised in patient with
renal disorders
Magnetic Resonance Angiography (MRA)
Uses magnetic fields, radio MRA assesses intracranial Less invasive than traditional Takes longer than Claustrophobia; patient
waves and field gradients vasculature for cerebrovascu- angiography CTA to perform must remain still for
to form images of the lar accident (CVA), transient examination; must fit in
cerebral vasculature ischemic attack (TIA), venous machine; cannot be per-
sinus thrombosis, AVM, formed in patients with
vascular tumors, or carotid pacemakers, metallic
bifurcation stenosis implants, pain stimula-
tor implants, or contrast
allergy; caution must be
exercised in patient with
renal disorders
Doppler Flowmetry
Transcranial Doppler Sonography
Low frequency ultrasound Assesses atherosclerotic disease, Noninvasive; test can be Long test Very sensitive to motion,
waves over tempo- collateral circulation, vaso- interrupted for patient to so patient must be able
ral bones or gaps to spasm and brain death change position to be still
determine velocity and Identifies AVMs and their sup-
direction of blood flow in ply arteries
anterior, middle, poste-
rior, and basilar arteries
Continued
162 CHAPTER 6     Nervous System
TABLE 6.23  Diagnostic Imaging78,185,186—cont’d
Method/General Infor-
mation
Carotid Noninvasive Studies
High frequency ultrasound
over common, internal,
and external carotid arter-
ies to determine velocity
of blood flow
In color—carotid duplex
US
Angiography
Digital Subtraction Angiography (DSA)
Computer-assisted radio-
graphic visualization of
the carotids and cerebral
vessels with minimal
view of background
tissues
Intravenous contrast used
Cerebral Angiography (Intraarterial DSA)
Injection of contrast via
femoral artery catheter
(usually)
Lumbar Puncture
Collection of cerebrospinal
fluid (CSF) via needle
placed in subarachnoid
space below L1, usually
between L3 and L4
Positron Emission Tomography (PET)
Radioactive chemicals
administered
Mimics normal metabolic
brain processes
Positrons emitted are
sensed by detectors and
CT and recorded into
high-resolution 2D and
3D images
Conditions Detected
Assesses location, presence, and
severity of carotid occlusion
and stenosis
Assesses aneurysm, AVM, fis-
tula, occlusion, or stenosis
Also used in operating room
(OR) for examining integrity
of anastomoses or cardiovas-
cular repairs
Assesses aneurysm, AVMs, oc-
clusions, stenosis
As a single procedure or in the
OR to assess integrity after
repair (clipping or coiling)
CSF is tested for cytology, color, Can inject therapeutic
chlorine, glucose, protein, pH, agents, spinal anesthetics
opening and closing pressures
noted
Assists in diagnosis of primary or hydrocephalus [NPH])
metastatic brain or spinal cord
neoplasms, cerebral hemor-
rhage, meningitis, encephalitis,
degenerative brain disease,
autoimmune diseases involving
the central nervous system
(CNS), neurosyphilis, and
demyelinating disorders
Used to aid in diagnosis of
brain tumor, cardiovascular
disease (CVD), or trauma,
dementia, seizure disorders,
Parkinson’s disease (PD), and
psychiatric disorders
Areas that are more metabolically
active will show up more—
tumors
Areas less active show up less—
Alzheimer’s disease
Test Name
Advantages
Noninvasive; clear picture of
soft tissues
“Gold standard” for carotid
stenosis
Gold standard for imaging of
cervicocerebral vasculature
and flow
Can identify small lesions
missed by CTA and MRA
or reduce/drain the volume
of CSF (normal-pressure
Helps clarify diagnosis of
early stages of dementia or
seizure disorders
Precautions/Consider-
Disadvantages ations
No known risks Dressings, wounds, or
surgical scars might
impede images
Radiation exposure Contrast allergy or
higher dye load patients with renal
than CTA, more dysfunction
invasive than
CTA
More expensive and
carries small risk
of stroke or death
due to the invasive
nature of the test
(compared with
MRA or carotid
ultrasonography)
More invasive than Contrast allergy or
CTA and MRA patients with renal
dysfunction
Prolonged Usually bed rest × 1 hour;
patient position dural tear risk; headache
is difficult common and severe with
(hyperflexion of position changes; likely
spine and hips, caused by dural tear;
seated or side- either heals on its own
lying) or can have blood patch
Infection risk (injecting venous blood
into spinal column to
clot and close dural tear,
stopping the leak of CSF)
High cost Radiopharmaceuticals or
radiotracers used and
injected intravenously,
inhaled, or swallowed
Patients have to remain
still or stay in one
particular position
during imaging

TABLE 6.23  Diagnostic Imaging78,185,186—cont’d
Method/General Infor-
mation
Electroencephalography (EEG)
Recording of brain activity
by using electrodes af-
fixed to scalp
At rest, while sleeping,
after sleep deprivation,
after hyperventilation or
photic stimulation
Shows abnormalities in
brain wave amplitude,
speed, activity, or pattern
Evoked Potentials (EPs)
Derivative of EEG
Electrical response is gen-
erated by stimulation of a
sensory organ
Electromyography (EMG) and Nerve Conduction Velocity Studies
Records muscle activity
at rest, with voluntary
movement and with elec-
trical stimulation with
needle electrodes
Nerve conduction studies
are the measurement of
conduction time and
amplitude of electrical
stimulus along peripheral
nerves
Myelography
Uses x-ray and contrast
to show flow through
the subarachnoid space
and around the vertebral
column after the removal
of a small amount of CSF
and injection of dye. Via
lumbar puncture
Conditions Detected
Used in conjunction with other
tests to assess seizure focus,
sleep and metabolic disorder,
dementia, and brain death
Epileptic states shows rapid
spiking waves
Lesions, such as tumors or
infarctions, show slow EEG
waves, depending on the size
and location of the lesion
Can also be used in OR during
surgery when carotid vessel is
occluded to determine need
for temporary shunting to
avoid CVA
Measure and assess sensory
pathway from peripheral sen-
sory organ to the brain cortex
Conduction delays indicate
damage or disease along the
pathway
Detect the presence, loca-
tion, and extent of diseases
that damage the nerves and
muscles
Assesses bone displacement,
disk herniation, cord com-
pression, or tumor
Nervous System     CHAPTER 6 163
Test Name
Precautions/Consider-
Advantages Disadvantages ations
Noninvasive seizure monitor- Requires intense Patient may be hooked
ing interpretation just up to monitor and then
to hypothesize videotaped to record
what areas are activity
activated by a par- Often battery pack can be
ticular response disconnected, but there
Poorly measures is a time limit (usually
neural activity 15 minutes)
that occurs below Press button to record
the cortex if you suspect seizure
Time to set up the activity when with the
electrodes on pa- patient
tient is long and
requires precision
Signal to noise ratio
is poor
Visual evoked potential Slowly being 90% of patients with MS
(VEP) or visual evoked replaced by MRI, have decreased VERs
response (VER) is measured which can provide Certain factors, such as
by using electrodes over similar informa- severe visual or hearing
the occipital lobe to record tion along with impairments or muscle
cortex activity after patient other data spasms, can also affect
is shown flashing lights or the accuracy of the test
checkerboard pattern
VEP used to assess optic
neuropathies and optic
nerve lesions
Brainstem auditory evoked
response assesses lesions
in multiple sclerosis (MS),
brainstem function in pa-
tients who are in a coma
Somatosensory EP spinal cord
injury (SCI), cervical disk
disease, sensory dysfunction
(MS), parietal cortex tumor
Differentiate between my- Painful for brief Cannot be used in pa-
opathy and peripheral nerve periods tients with an internal
injury pacemaker or defibril-
lator
Less artifact than in MRI, Radiation exposure Contrast material aller-
which aids in surgical gies, renal dysfunction;
planning 24 hours after test,
restrict heavy lifting or
bending
Need hydration, elevation
of the head to limit con-
trast flowing intracrani-
ally and to prevent spinal
headache/dural tear
164 CHAPTER 6     Nervous System
Specific to the patient with an acute neurologic condition,
the ability of the physical therapist to analyze and synthesize
information discovered before entering the room helps with the
following:
• Formulation of a plan for examinations and interventions
• Prognostication of the patient’s ability to participate and
likelihood of a meaningful functional outcome
• Assistance in predicting the possible resources that will be
required both short term and long term
• The diagnostic and intervention process, as well as securing
insurance support for the best discharge plan  Aging and the Nervous System
Evaluation: Diagnosis and Prognosis
After all of the results from the tests and measures have been
collected, a physical therapist creates a clinical impression,
including the physical therapy diagnosis, prognosis, and plan
of care. Utilizing the International Classification of Function-
ing, Disability, and Health (ICF) framework for synthesizing
information, assessment in the acute care setting focuses on the
patient’s function within the hospital, determinants of safe dis-
charge disposition, contextual factors, and activity and partici-
pation restrictions for safe mobility.184
To link the diagnosis to outcomes and identify the need
for additional treatment, prognosis must be considered. This
involves determination of the predicted highest level of func-
tional improvement for the patient and the length of time
needed to reach that level of function. Disability resulting from
a neurologic disease or trauma can be extensive. With the con-
tinuing advances made in the emergent medical care of people
with significant neurologic trauma or disease, the number of
people living with permanent or progressive neurologic impair-
ments is increasing at a steady rate.78 Determination of an accu-
rate prognosis is essential to set realistic goals for care and to
appropriately educate the patient and family regarding optimal
functional outcomes that are as precise as possible.36
 CLINICAL TIP
There is a wealth of information (see Additional Resources be-
low) regarding expected outcomes for many of the neurologic
disorders and trauma discussed in this chapter. The physical
therapist should incorporate information about short-term and
long-term outcomes, predictors of ambulation, return to work or
readmission, and independence in ADLs and living when mak-
ing a case for reimbursement for a higher level of postacute care.
 
Plan of Care
The plan of care for the patient in the acute care setting consid-
ers both treatment goals and interventions to be provided dur-
ing the hospital stay as well as recommendations for discharge.
Determination of the patient’s most appropriate discharge plan
considers the patient’s baseline level of function and prognosis
of improvement with further physical therapy intervention. The
level of care that patient is discharged to must consider medical
conditions, anticipated length of stay, and insurance benefits, as
well as the goals of the patient and family.36 The physical thera-
pist in acute care has a strong role in the interprofessional team
and in patient and family education for patients with neuro-
logic disorders. Topics include communication regarding safety,
reorientation, and the appropriate level of participation/stimu-
lation for the current setting as well as expectations for transi-
tioning through levels of care. Knowledge of disease progression
and of the prognostic indicators facilitates these discussions.36 
The nervous system undergoes multiple changes with the aging
process, and these changes can present challenges to the older
adult. Changes occur in both the central and peripheral nerves
and receptors. Neuron loss is a feature of the aging nervous sys-
tem and presents as diminished gray and white matter content
in the cerebral and cerebellar187 hemispheres as well as reduced
cortical surface area. Ventricular dilation occurs as a result of the
shrinking of the brain structures, leaving an enlarged appear-
ance.188–190 Myelin degeneration is present and influences neu-
rotransmission.191 Changes also occur with neurotransmitters,
with depletion resulting in slowed effects. Additionally there
is less cerebral blood flow and reduced glucose metabolism,
resulting in less support for the energy demands of neural tis-
sue. Peripherally there is a loss of cells in the anterior horn of the
spinal cord, resulting in fewer motor units. The density of both
Meissner’s and Pacinian corpuscle receptors is reduced, leading
to altered sensation. NCV is decreased, and the neuromuscular
junction experiences deterioration.36
In the absence of acute or degenerative neurologic disorders,
physical therapists should be aware of the potential effects that
age-related changes have on a patient’s neurologic function.
Temperature regulation becomes more difficult because of a
decrease in sensitivity to feedback at the hypothalamus. Given
the multitude of sensory deficits, falls and related injuries are a
concern. Physical therapists should include in their assessment
the identification of age-related neural factors that can poten-
tially cause a fall.36
Additional Resources
Academy of Acute Care Physical Therapy
https://www.acutept.org/page/VTEGuidelines/VTE-Guidelines.htm
http://www.neuropt.org/
https://geriatricspt.org/
Cerebellar Disorders
https://www.ninds.nih.gov/disorders/all-disorders/olivopontocerebellar
-atrophy-information-page
Spinal Cord Injury
https://www.gaylord.org/Portals/0/PDFS/SCI%20Toolkit/2016%20F
ull%20TK%20Sum.pdf
http://asia-spinalinjury.org/information/
www.scipt.org
www.elearnsci.org
Delirium
http://www.icudelirium.org/docs/CAM_ICU_training.pdf
Traumatic Brain Injury
http://www.glasgowcomascale.org/

https://www.tbindsc.org
http://scale-library.com/pdf/Galveston_Orientation_Amnesia_Test.pdf
Amyotrophic Lateral Sclerosis
http://alsfamily.net/support/resources/
http://www.alsfoundation.org/
https://ccals.org/
http://www.alsa.org/
Epilepsy
https://epilepsychicago.org/2017/01/04/2017-revised-classification-
of-seizures/
https://www.epilepsy.com/
Parkinson’s Disease
https://www.michaeljfox.org/
http://parkinson.org/
https://www.davisphinneyfoundation.org/
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 7 Vascular System and
C H APT ER  
CHAPTER OUTLINE
Introduction
Vascular System
Hematologic System
Lymphatic System
Physical Examination
Vascular Evaluation
Hematologic Evaluation
Lymphatic Evaluation
Health Conditions
Vascular Disorders
Hematologic Disorders
Lymphatic Disorders
Management
Pharmacologic Therapy
Anticoagulation Therapy
Blood Product Transfusion
Vascular Surgical Procedures
Embolization Therapy
Transcatheter Thrombolysis
and/or Thrombectomy
Peripheral Vascular Bypass
Grafting
Endarterectomy
Aneurysm Repair and
Reconstruction
Physical Therapy Management
Hematology
Laura A. H. Blood
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . Review the structures and functions of the vascular, hematologic, and lymphatic systems
2. Review vascular, hematologic, and lymphedema evaluations, including physical examination and related
diagnostic and laboratory tests
3. Describe vascular, hematologic, and lymphatic health conditions, including clinical findings, medical and
surgical management, and physical therapy intervention
Introduction
Alterations in the integrity of the vascular and hematologic systems can alter a patient’s activ-
ity tolerance. The physical therapist must be aware of the potential effect that a change in blood
flow or blood composition has on a multitude of body functions. This includes cardiac output,
hemostasis, energy level, and healing. 
Vascular System
The network of arteries, veins, and capillaries composes the vascular system. These blood
vessels are composed of three similar layers (Fig. 7.1 and Table 7.1). Blood vessel diameter,
length, and wall thickness vary according to location and function (Table 7.2). Note that the
arteries are divided into three types based on their size and structural features. Veins also
possess a valve component that assists in prevention of backflow of blood. 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.1 
Hematologic System
The hematologic system is composed of living blood cells (Table 7.3) and nonliving plasma
solution within the blood vessels.1 Blood accounts for 8% of total body weight, or 4 to 5 L in
women and 5 to 6 L in men. Plasma is composed almost completely of water and contains more
than 100 dissolved substances. The major solutes include albumin, fibrinogen, protein glob-
ules, nitrogenous substances, nutrients, electrolytes, and respiratory gases.2 Blood has many
different functions, including immune defense, transportation of the respiratory gases, and
clotting (Table 7.4). 
Lymphatic System
The lymphatic system includes lymph vessels, lymph fluid, and lymph tissues and organs
(lymph nodes, tonsils, spleen, thymus, and the thoracic duct). The lymphatic system is
        171
172 CHAPTER 7     Vascular System and Hematology

Artery Vein

Endothelium
(tunica intima)

Valve

Elastic membrane
(thinner in veins)

Smooth muscle layer

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

FIG. 7.1
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.)

TABLE 7.1  Blood Vessel Layers TABLE 7.2  Characteristics of Blood Vessels
Layer Description Function Vessel Description
Tunica Innermost layer: Endothelial Provides a smooth Artery Large or elastic arteries—aorta and its large branches
intima layer over a basement mem- surface for laminar and pulmonary artery.
brane blood flow Medium or muscular arteries—composing other
Tunica Middle layer: Smooth muscle Constricts and dilates branches of aorta (i.e., coronary arteries).
media cells and elastic connective for blood pressure Small arteries and arterioles.
tissue with sympathetic regulation Thick tunica media layer allows arteries to readily
innervation accommodate to pressure changes from the heart.

Tunica Outermost layer: Composed of Protects and at-
adven- collagen fibers, lymph vessels, taches blood
titia and the blood vessels that vessels to nearby
supply nutrients to the blood structures
vessel
Data from Marieb EN. Human Anatomy and Physiology. 3rd ed. Redwood City,
CA: Benjamin-Cummings; 1995.
parallel to and works in conjunction with the venous sys-
tem. Lymph vessels are fragile and are more likely to collapse
under pressure compared with the veins. There are lymph
vessels located in all portions of the body except the cen-
tral nervous system and the cornea. The lymphatic system
assists the vascular system by draining unabsorbed plasma
from tissue spaces and returning this fluid 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 move-
ments, and gravity.1 Lymph fluid is first absorbed at the cap-
illary level, then channeled through the small vessels, and
finally picked up by the larger valved vessels. The primary
function of the lymphatic system is to facilitate the move-
ment of fluid between the bloodstream and the interstitial
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 systems
network 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., Philadelphia: Saunders; 2005.
spaces. This process assists in removing excess fluid, blood
waste, and protein molecules. Additionally, the lymphatic
system aides in protecting the body from infection and dis-
ease via the immune response.3 
Physical Examination
The vascular and hematologic systems are intimately linked,
and the examination of these systems is often similar. For the
purpose of this chapter, however, the evaluations of the vascular
and hematologic systems are discussed separately.
 Vascular System and Hematology     CHAPTER 7 173

Pain
TABLE 7.3  Blood Cell Types
• In arms and legs (Visceral pain and arthritis pain may radiate
Cell Description to the extremities.)
Erythrocyte Contains hemoglobin molecules responsible • Presence of intermittent claudication (IC) defined as pain,
(red blood cell for oxygen transport to tissues. ache, sense of fatigue, or other discomfort that occurs in the
[RBC]) Composed of four protein chains (two alpha affected muscle group with exercise, particularly walking,
and two beta chains) bound to four iron and resolves with rest (the speed, distance, and the site of
pigment complexes.
An oxygen molecule attaches to each iron
the pain, including what relieves the pain, should be not-
atom to become oxyhemoglobin. ed). The Claudication Scale [CLAU-S] is a questionnaire
Leukocyte (white Five types of WBCs (neutrophils, basophils,
that can be used to learn the effect IC has on a patient’s
blood cell eosinophils, lymphocytes, and monocytes) quality of life.9 The Claudication Pain Rating Scale allows a
[WBC]) are responsible for launching immune patient experiencing IC to rate his or her pain with activity.
defenses and fighting infection. The scale is defined as [1] minimal discomfort, [2] moder-
WBCs leave the circulation to gain access to ate but distractible pain, [3] intense pain, and [4] unbear-
a site of infection.
able pain.10
Thrombocyte Cell fragment responsible for clot formation. • Presence of nocturnal pain typically occurring when the pa-
(platelet [Plt])
tient is in bed or in the supine position (This pain can develop
Data from Marieb EN. Human Anatomy and Physiology. 3rd ed. Redwood City, as vascular occlusion worsens and is caused by a combination
CA: Benjamin-Cummings; 1995. of leg elevation and reduced cardiac output.)
• Presence of rest pain, specifically in the absence of activity
TABLE 7.4  Functions of Blood and with legs in a dependent position (rest pain suggests ad-
vanced occlusive disease, typically >90%).
Function Method
Oxygen and carbon dioxide transport Binding to hemoglobin;
dissolved in plasma CLINICAL TIP
Nutrient and metabolite transport Bound to plasma proteins;
Buttock, hip, or thigh claudication typically occurs in patients
dissolved in plasma
with obstruction of the aorta and iliac arteries. Calf claudica-
Hormone transport In plasma
tion characterizes femoral and popliteal artery stenosis. The
Transport of waste products to In plasma gastrocnemius muscle consumes more oxygen during walking
kidneys and liver
compared with other muscle groups in the leg and hence causes
Transport of cells and substances In plasma to site of infection the most frequent symptom reported by patients.
involved in immune reactions or foreign body
Clotting at breaks in blood vessels Hemostasis
Maintenance of fluid balance Blood volume regulation
Body temperature regulation Peripheral vasoconstriction CLINICAL TIP
or dilation Neurogenic claudication (symptoms often derived from spinal
Maintenance of acid–base balance Acid–base regulation stenosis) can often emulate IC. The stoop test should be per-
Data from Nettina S. The Lippincott Manual of Nursing Practice. 8th ed. Philadelphia: formed to rule out neurogenic claudication involvement. After
Lippincott Williams & Wilkins; 2005. the patient initiates walking and there is onset of claudication
pain, have the patient stop and rest in a stooped position.
The pain will not be relieved by the postural change if IC is
Vascular Evaluation
present.11,12  
Patient History
In addition to the general chart review discussed in Chapter 2,
it is important to gather any of the additional information listed Observation
below regarding suspected vascular dysfunction4-8: Observation of the following features can help delineate
• Medical history, including diabetes mellitus, hypertension, the location and severity of vascular disease and help deter-
hyperlipidemia, syncope or vertigo, and nonhealing ulcers mine whether these manifestations are arterial or venous in
• Social history, including exercise and dietary habits; use of origin1,4,5,13:
tobacco or alcohol • Skin color: Note the presence of any discoloration of the distal
• History of recent prolonged bed rest, surgery, or a long flight extremities/nail bed. Decreased color or pallor is indicative of
• Presence or history of acute or chronic peripheral edema (If decreased blood flow (mottled skin) or hemosiderin staining
chronic, determine the patient’s baseline level of edema.) (venous disease)
• Precautions, such as weight bearing or blood pressure param- • Hair distribution: Patchy hair loss on the lower leg may indi-
eters, after vascular surgery  cate arterial insufficiency.
174 CHAPTER 7     Vascular System and Hematology
• V enous pattern: Dilation or varicosities—dilated, purplish,
ropelike veins, particularly in the calf.
• Edema: Peripheral edema from right-sided congestive heart
failure occurs bilaterally in dependent areas; edema from
trauma, lymphatic obstruction, or chronic venous insuffi-
ciency is generally unilateral.
• Respiratory rate: Should be observed to collect a full set of
vital signs.
• 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 oxygen-
ation or circulation.
• Gait abnormalities.  may correspond to changes in the fluid volume status of the
Palpation
During the palpation portion of the examination, the physi-
cal therapist can assess the presence of pain and tenderness,
strength and rate of peripheral pulses, blood pressure, skin
temperature, and limb girth (if edema is present). A decreased
or absent pulse provides insight into the location of arterial
stenoses.7 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 peripheral pulses3:
• 0: Absent, not palpable
• 1+: Weak, barely palpable
• 2+: Palpable, but diminished
• 3+: Normal, easily palpable
• 4+: Bounding
Peripheral pulses can be assessed in the following arteries (see
Chapter 3, Fig. 3.6)14:
• Temporal
• Carotid
• Brachial
• Ulnar
• Radial
• Femoral
• Popliteal
• Posterior tibial
• Dorsalis pedis
CLINICAL TIP
A small percentage of the adult population may normally have
absent peripheral pulses; 10% to 17% lack dorsalis pedis pulses.1
The aorta can also be palpated in more slender people.
In addition to assessing for the presence of edema through
observation, edema should also be further assessed through pal-
pation of pitting edema (refer to Table 3.5 for grading of pitting
edema) and girth measurement. The girth measurements should
be taken on bilateral lower extremities and must remain consis-
tent from limb to limb and at each time examined. Measuring
boards or a precisely placed clipboard can be used to aide in
accuracy of the measurements between limbs. Bony landmarks
are often used; clinicians who commonly manage edema recom-
mend taking girth measurements every centimeter or at least
taking measurements using intervals of 4, 6, or 10 cm. The
smaller the interval, the more accurate the recording will be
documented and assessed. A difference between limbs of greater
than 1 cm just above the ankle or 2 cm at the calf is sugges-
tive of clinically significant edema.15 It is important to note
any additional pain or tenderness felt by the patient with edema
assessment. 
Physical Therapy Considerations
• Changes in heart rate, blood pressure, and respiratory rate
patient. For example, a decrease in fluid volume may result
in a decreased blood pressure, which results in a compensa-
tory increase in heart and respiratory rates. The decreased
fluid volume and resultant increased heart rate in this situa-
tion may then result in decreased strength of the peripheral
pulses on palpation.
• In patients who have disorders resulting in vascular compro-
mise (e.g., diabetes mellitus, peripheral vascular disease, or
hypertension), pulses should be monitored before, during,
and after activity. This allows for determination of any rate
changes and, more importantly, the determination of any
changes in the strength of the pulse.
• A note should be made if the strength of pulses is correlated
with complaints of pain, numbness, or tingling of the ex-
tremity.
• Compare the two extremities for color, temperature, and
swelling. Decreased temperature in bilateral extremities is
most often caused by a cold environment and/or anxiety.5
• Carotid arteries should never be palpated simultaneously
because excessive carotid sinus massage can cause slowing
of the pulse, resulting in a drop in blood pressure, and
compromise blood flow to the brain. If the pulse is dif-
ficult to palpate, the patient’s head should be rotated to
the side being examined to relax the sternocleidomastoid
muscle.14 
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 indica-
tive of accelerated blood flow velocity and flow disturbance
at sites of stenosis.7 Bruits are typically assessed by physicians
and nurses (see Chapter 3 for further details on blood pressure
measurement). 
Vascular Tests
Various tests that can be performed clinically to evaluate
vascular flow and integrity are described in Table 7.5. These
tests can be performed easily at the patient’s bedside with-
out the use of diagnostic equipment. The Wells Clinical
Decision Rule for Deep Venous Thrombosis is described in
Table 7.6. 
 Vascular System and Hematology     CHAPTER 7 175

TABLE 7.5  Vascular Tests

Test Indication Description Normal Results and Values
Ankle-brachial index To compare the perfu- Place the patient in supine at least 10 minutes The diagnosis of peripheral arterial
(ABI)a sion pressures in the before the test. Obtain the brachial pressure disease is based on the limb symptoms
lower leg with the up- in each arm, and record the highest pressure. or an ABI.
per extremity using a Obtain the ankle pressure in each leg. Place the Interpretation of ABIc:
blood pressure cuff and cuff around the lower leg 2.5 cm above the mal- ABI ≥ 1.2: falsely elevated, arterial
Doppler probe. This leolus. Apply acoustic gel over the dorsalis pedis ­disease, diabetes.
test is commonly used or posterior tibialis pulse location. Hold the ABI 0.95–1.19: normal.
to screen patients for Doppler probe lightly over the pedal pulse. In- ABI 0.75–0.94: mild arterial disease,
evidence of significant flate the cuff to a level 20–30 mmHg above the +IC.
arterial insufficiency. point at which the pulse is no longer audible. ABI 0.50–0.74: moderate arterial
Slowly deflate the cuff while monitoring for the disease, +rest pain.
return of the pulse signal; the point at which ABI ≤ 0.5: severe arterial disease.
the arterial signal returns is recorded as the
ankle pressure. Calculate the ABI by dividing
the higher of the two ankle systolic pressures by
the higher of the brachial systolic pressures.
Capillary refill timeb To assess vascular perfu- Nail beds of fingers or toes are squeezed until Blanching should resolve (capillary refill)
sion and indirectly blanching (whitening) occurs, and then they in less than 2 seconds.
assess cardiac output. are released.
Elevation of pallor To assess arterial perfu- Both limbs are elevated approximately 45 Observe the amount of time it takes for
sion. degrees for 60 seconds, and color changes are pallor to appear in the plantar surface
Normally color should observed over 60 seconds. of the foot.
not change. Pallor ≤ 25 seconds indicates severe
occlusive disease. Pallor within 25–40
seconds indicates moderate occlusive
disease.
Pallor within 40–60 seconds indicates
mild occlusive disease.
Rubor of dependency To assess arterial insuf- Both limbs are elevated approximately 45 de- Observe the amount of time and the de-
ficiency. grees for 60 seconds. gree of color to return to the lower limb
and dorsal surface of the foot.
Normal: <15 seconds with a slight pink
coloration.
Suspected PAD: >15 seconds with no-
table deep red color present.
Trendelenburg test To determine valvular Have the patient lie supine with legs raised If veins fully distend within 5 seconds
competence of the 45–90 degrees for 1–2 minutes. Then a tourni- before the tourniquet is released, val-
venous system. quet is placed around the thigh. The patient vular incompetence in the deep veins is
then stands up and the time for venous refill- suspected. If distention occurs within 5
ing is recorded. seconds after the tourniquet is released,
incompetence of superficial veins is
suspected.
aABI measurements may be of limited value in anyone with diabetes because calcification of the tibial and peroneal arteries may render them noncompressible.
bVariability is found in defining the time by different individuals, so capillary refill time should not be considered an observation with exquisite sensitivity and specific-
ity and should be used more to confirm clinical judgment.
cAn ABI of less than 0.95 is considered abnormal and is 95% sensitive for the angiographically verified peripheral arterial stenosis.

IC, Intermittent claudication; PAD, peripheral arterial disease.

Data from Seidel HM, Ball JW, Dains JE, et al. Mosby’s Guide to Physical Examination. 7th ed. St. Louis: Mosby; 2010; Lanzer P, Rosch J, eds. Vascular Diagnostics: Non-
invasive and Invasive Techniques, Peri-Interventional Evaluations. Berlin: Springer Verlag; 1994; Springhouse. Handbook of Medical-Surgical Nursing. 4th ed. Philadelphia:
Lippincott Williams & Wilkins; 2005; Newberry L, Sheehy S, eds. Sheehy’s Emergency Nursing: Principles and Practice. 6th ed. St. Louis: Mosby; 2009; Dormandy JA,
Rutherford RB. Management of peripheral arterial disease (PAD). TASC Working Group. J Vasc Surg. 2000;31:S1-S296; Hallet JW, Brewster DC, Darling RC, eds.
Handbook of Patient Care in Vascular Surgery. 3rd ed. Boston: Little, Brown; 1995; Goodman CC. The hematologic system. In: Goodman CC, Boisonnault WG, eds. Pa-
thology: Implications for the Physical Therapist. 3rd ed. Philadelphia: Saunders; 2009; DeTurk WE, Cahalin LP. Cardiovascular and Pulmonary Physical Therapy: An Evidence-
Based Approach. 3rd ed. New York: McGraw-Hill; 2018; O’Sullivan SB, Schmitz TJ, Fulk GD. Physical Rehabilitation. 6th ed. Philadelphia: FA Davis; 2014; O’Sullivan
SB, Schmitz TJ, Fulk GD. Physical Rehabilitation. 6th ed. Philadelphia: FA Davis; 2014.

Diagnostic Studies descriptions that are inclusive of the noninvasive tests described
Noninvasive Laboratory Studies. Various noninvasive pro- in Table 7.7. 
cedures can examine vascular flow. The phrases lower-extremity Invasive Vascular Studies. The most common invasive vascu-
noninvasive studies and carotid noninvasive studies are general lar study is arteriography, typically referred to as contrast angiography
176 CHAPTER 7     Vascular System and Hematology

TABLE 7.6  Wells Clinical Decision Rule (CDR) for Deep Venous Thrombosis (DVT)
Clinical Characteristic Scorea
Active cancer (treatment ongoing within previous 6 months or currently receiving palliative treatment) 1
Paralysis, paresis, or recent plaster immobilization of the lower extremities 1
Recently bedridden for more than 3 days or more, or major surgery within the previous 12 weeks, requiring general or regional 1
anesthesia
Localized tenderness along the distribution of the deep venous system 1
Entire leg swollen 1
Calf swelling by greater than 3 cm larger than that on the asymptomatic side (measured 10 cm below tibial tuberosity) 1
Pitting edema confined to the symptomatic leg 1
Collateral superficial veins (nonvaricose) 1
Previously documented deep venous thrombosis 1
Alternative diagnosis as likely as or more likely than deep venous thrombosis −2
aA score of two or higher indicates that the probability of DVT is likely; a score of less than two indicates that the probability of DVT is unlikely. In patients with
symptoms in both legs, the more symptomatic leg is used.
From Wells PS, Anderson DR, Rodger M, et al. Evaluation of D-dimer in the diagnosis of suspected deep-vein thrombosis. N Engl I Med. 2003;349:1227-1235.

TABLE 7.7  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 sensitivity
and specificity of approximately 95%.
Color duplex scan- Velocity patterns of blood flow along with visual images of vessel and plaque anatomy can be obtained by combing
ning or imaging ­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 pulse volume
­recordings (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 Chapters 3 and 4, respectively).
Computed tomog- CT is used to provide visualization of the arterial wall and its structures.
raphy (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 to visualize the arterial system
imaging (MRI) than arteriography. 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 of major blood vessels and the
angiography flow of blood through these vessels. The direction and rate of flow can also be quantified. MRA minimizes compli-
(MRA) cations that may be associated with contrast medium injection. Fig. 7.2 illustrates the MRA of the aorta and lower
extremity.
Data from Black JM, Matassarin-Jacobs E, eds. Luckmann and Sorensen’s Medical-Surgical Nursing: A Psychophysiologic Approach. 4th ed. Philadelphia: Saunders; 1993:1286;
Bryant RA, Nix DP. Acute and Chronic Wounds: Current Management Concepts. 4th ed. St. Louis: Mosby; 2012; Lanzer P, Rosch J, eds. Vascular Diagnostics: Noninvasive And
Invasive Techniques, Peri-Interventional Evaluations. Berlin: Springer Verlag; 1994; Kee JL, ed. Laboratory and Diagnostic Tests With Nursing Implications. 8th ed. Stamford,
CT: Appleton & Lange; 2009:606; Malarkey LM, Morrow ME, eds. Nurses Manual of Laboratory Tests and Diagnostic Procedures. 2nd ed. Philadelphia: Saunders; 2000:359;
Mettler FA. Essentials of Radiology. 2nd ed. Philadelphia: Saunders; 2005; Fahey VA, ed. Vascular Nursing. 4th ed. Philadelphia: Saunders; 2003; McCance KL, Huether
SE, eds. Pathophysiology: The Biologic Basis for Disease in Adults and Children. 6th ed. St. Louis: Mosby; 2009:1001; George-Gay B, Chernecky CC. Clinical Medical-Surgical
Nursing: A Decision-Making Reference. Philadelphia: Saunders; 2002; Schroeder ML. Principles and practice of transfusion medicine. In: Lee GR, Foerster J, Lukens J,
et al., eds. Wintrobe’s Clinical Hematology. vol 1, 10th ed. Baltimore: Lippincott Williams & Wilkins; 1999:817-874.
 Vascular System and Hematology     CHAPTER 7 177

(Fig. 7.2). This study is performed by injecting radiopaque dye Hematologic Evaluation
into the femoral, lumbar, brachial, or axillary arteries, fol-
The medical workup of the patient with a suspected hematologic
lowed by radiographic viewing. Blood flow dynamics, abnor-
abnormality includes the patient’s medical history and labora-
mal blood vessels, vascular anomalies, normal and abnormal
tory studies, in addition to the patient’s clinical presentation.
vascular anatomy, and tumors are easily seen during the radio-
graphic viewing. With the use of digital-subtraction angi- Patient History
ography (DSA), bony structures can be obliterated from the
In addition to the general chart review discussed in Chapter 2,
picture. DSA is useful when adjacent bone inhibits visualiza-
the following questions are especially relevant in the evaluation
tion of the blood vessel to be evaluated.16 An angiogram is a
of the patient with a suspected hematologic disorder18-20:
picture produced by using angiography. Angiography is gen-
• What are the presenting symptoms?
erally performed before or during therapeutic interventions,
• Was the onset of symptoms gradual, rapid, or associated with
such as percutaneous angioplasty, thrombolytic therapy, or
trauma or other disease?
surgical bypass grafting.
• Is the patient unable to complete daily activities secondary to
Post–angiography care includes the following17:
fatigue?
• Bed rest for 4 to 8 hours.
• Is there a patient or family history of anemia or other blood
• Pressure dressings to the injection site with assessment for
disorders, cancer, hemorrhage, or systemic infection?
hematoma formation.
• Is there a history of blood transfusion?
• Intravenous fluid administration to help with dye excretion.
• Is there a history of chemotherapy, radiation therapy, or other
Blood urea nitrogen (BUN) and creatinine are monitored to
drug therapy?
ensure proper renal function (refer to Chapter 9 for more in-
• Has there been an environmental or occupational exposure to
formation on BUN and creatinine).
toxins?
• Frequent vital sign monitoring, with pulse assessments.
• Have there been night sweats, chills, or fever?
• If a patient has been on heparin before angiography, it is not
• Is the patient easily bruised?
resumed for a minimum of 4 hours.17
• Is wound healing delayed?
• The complications of arteriography can be caused by
• Is there excessive bleeding or menses?
­catheterization or the contrast agent that is injected (Table 7.8). 
• Is there history of trauma to the area?
• What is the patient’s social history?
• Patient’s diet (for the evaluation of vitamin- or mineral-
deficiency anemia)
• History of weight loss (as a warning sign of cancer or
altered metabolism)
• Alcohol use (chronic alcohol abuse is a cause of anemia)
• What is the patient’s race (increased incidence of hemato-
logic conditions occurring in certain races)? 

Observation
During the hematologic evaluation, the patient is observed for
the following18,21,22:
• General appearance (for lethargy, malaise, or apathy).

TABLE 7.8  Complications of Contrast Arteriography

Cause Complication
Puncture site or Hemorrhage/hematoma
catheter related Pseudoaneurysm
Arteriovenous fistula
Atheroembolism
Local thrombosis
Contrast agent related Major (anaphylactoid) sensitivity reaction
Minor sensitivity reactions
Vasodilation/hypotension
Nephrotoxicity
Hypervolemia
FIG. 7.2 From Belkin M, Owens CD, Whittemore AD, et al. Peripheral arterial occlu-
Magnetic resonance angiography (MRA) of the aorta and lower extremity sive disease. In: Townsend CM, Beauchamp RD, Evers BM, et al., eds. Sabiston
arterial circulation. (From Adam A. Grainger & Allison’s Diagnostic Radiology. Textbook of Surgery: The Biological Basis of Modern Surgical Practice. 18th ed. Phila-
5th ed. London: Churchill Livingstone; 2008.) delphia: Saunders; 2007.
178 CHAPTER 7     Vascular System and Hematology

Palpation
TABLE 7.9  Signs and Symptoms of Hematologic
The examination performed by the physician includes palpation
Disorders by Body System
of lymph nodes, liver, and spleen as part of a general physical
Body System Sign/Symptom Associated Condition examination. For specific complaints, the patient may receive
Cardiac Tachycardia Anemia, hypovolemia more in-depth examination of a body system. Table 7.9 summa-
Palpitations Anemia, hypovolemia
rizes abnormal hematologic findings by body system on physi-
cal examination.
Murmur Anemia, hypovolemia
The physical therapist may specifically examine the following:
Angina Anemia, hypovolemia • The presence, location, and severity of bone or joint pain us-
Respiratory Dyspnea Anemia, hypovolemia ing an appropriate pain scale (see Chapter 21)
Orthopnea Anemia, hypovolemia • Joint range of motion (ROM) and integrity, including the
Musculoskel- Back pain Hemolysis presence of effusion or bony abnormality
etal Bone pain Leukemia • Presence, location, and intensity of paresthesia
• Blood pressure and heart rate for signs of hypovolemia (see
Joint pain Hemophilia
Physical Therapy Considerations in the Vascular Evalu-
Sternal tenderness Leukemia, sickle cell disease
ation section for a description of vital sign changes with
Nervous Headache Severe anemia, polycythemia, ­hypovolemia) 
metastatic tumor
Syncope Severe anemia, polycythemia Laboratory Studies
Vertigo, tinnitus Severe anemia In addition to the history and physical examination, the clinical
Paresthesia Vitamin B12 anemia, malig- diagnosis of hematologic disorders is based primarily on labora-
nancy tory studies.
Confusion Severe anemia, malignancy, Complete Blood Cell Count.  The standard complete blood
infection count (CBC) consists of a red blood cell (RBC) count, white
Visual Visual disturbances Anemia, polycythemia blood cell (WBC) count, WBC differential, hematocrit (Hct)
Blindness Thrombocytopenia, anemia measurement, hemoglobin (Hgb) measurement, and platelet
Gastrointesti- Dysphagia Iron-deficiency anemia (Plt) count (Table 7.10). Fig. 7.3 illustrates a common method
nal, urinary, Abdominal pain Lymphoma, hemolysis,
used by the medical-surgical team to document portions of the
and repro- sickle cell disease CBC in handwritten progress notes. If a value is abnormal, it
ductive is usually circled within this schematic. If electronic health
Splenomegaly or Hemolytic anemia
hepatomegaly records are used, then laboratory values are denoted by either
Hematemesis, Thrombocytopenia and symbols or abbreviations to relay their relationship to the ref-
melena clotting disorders erence value. Clinicians should ensure familiarity with their
Hematuria Hemolysis and clotting institutional medical records for specific information regarding
disorders documentation.
Menorrhagia Iron-deficiency anemia Physical Therapy Considerations 
• T he most important thing to consider when looking at Hgb
Integumen- Petechiae Iron-deficiency anemia
tary values is the patient’s oxygen supply versus demand. De-
Ecchymosis Hemolytic, pernicious creased Hgb levels can reduce oxygen transport capacity and
anemia
subsequently reduce the oxygen supply, which can reduce a
Flushing Iron-deficiency anemia
patient’s activity tolerance.
Jaundice Hemolytic anemia • It is important to consider the trends in Hgb and Hct lev-
Pallor Conditions with low els. If Hct/Hgb levels are low at baseline, these patients
hemoglobin may be able to tolerate activity. However, patients with
Data from Black JM, Matassarin-Jacobs E, eds. Medical-Surgical Nursing: Clinical acutely low levels of Hct/Hgb may or may not tolerate in-
Management for Continuity of Care. 5th ed. Philadelphia: Saunders; 1997. creased activity.
• A physical therapist should be aware of the signs and
symptoms of hypoxia to major organs: brain, heart, and
kidneys.
• D egree of pallor or flushing of the skin, mucous membranes, • Monitoring of tolerance and modifications in the therapeutic
nail beds, and palmar creases. Pallor can be difficult to assess plan may be indicated with low levels of Hct/Hgb.23 Hct
in dark-skinned individuals. In these individuals, the lips, is accurate in relation to fluid status; therefore Hct may be
tongue, mucosa, and nail beds should be monitored. falsely high if the patient is dehydrated and falsely low if the
• Presence of petechiae (purplish, round, pinpoint, nonraised patient is fluid overloaded.16
spots caused by intradermal or subcutaneous hemorrhage) or • Utilize facility guidelines along with consulting the medical
ecchymosis (bruising). team, to best determine activity levels in patients with low
• Respiratory rate.  levels of Hgb or Hct.
 Vascular System and Hematology     CHAPTER 7 179

TABLE 7.10  Complete Blood Cell Count: Values and Interpretationa

Test Description Value Indication/Interpretation
Red blood cell Number of RBCs per μL Female: 4.2–5.4 million/μL Blood loss, anemia, polycythemia.
(RBC) count of blood Male: 4.7–6.1 million/μL 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 per μL 5000–10,000/μL Presence of infection, inflammation, allergens, bone marrow
(WBC) count of blood integrity.
Monitors response to radiation or chemotherapy.
Increased: leukemia, infection, tissue necrosis.
Decreased: bone marrow suppression.
WBC differential Proportion (%) of the Neutrophils 55% to 70% Presence of infectious states.
different types of WBCs Lymphocytes 20% to 40% Detect and classify leukemia.
(out of 100 cells) Monocytes 2% to 8%
Eosinophils 1% to 4%
Basophils 0.5% to 1%
Hematocrit (Hct) Percentage of RBCs in Female: 37% to 47% Blood loss and fluid balance.
whole blood Male: 42% to 52% Increased: polycythemia, dehydration.
Decreased: anemia, acute blood loss, hemodilution.
Hemoglobin Amount of Hgb in 100 Female: 12–16 g/100 mL Blood loss, bone marrow suppression.
(Hgb) mL of blood Male: 14–18 g/100 mL Increased: polycythemia, dehydration.
Decreased: anemia, recent hemorrhage, fluid overload.

Platelets (Plt) Number of Plts per μL 150,000–450,000/μL Thrombocytopenia.

of blood Increased: polycythemia vera, splenectomy, malignancy.
Decreased: anemia, hemolysis, DIC, ITP, viral infections, AIDS,
splenomegaly, with radiation or chemotherapy.
aLaboratory values vary among laboratories. Refer to facility specific reference ranges. RBC, Hgb, and Plt values vary with age and sex.
AIDS, Acquired immunodeficiency syndrome; DIC, disseminated intravascular coagulation; ITP, idiopathic thrombocytopenic purpura.
Data from Elin RJ. Laboratory reference intervals and values. In: Goldman L, Bennett JC, eds. Cecil Textbook of Medicine. vol 2, 21st ed. Philadelphia: Saunders;
2000:2305; Matassarin-Jacobs E. Assessment of clients with hematologic disorders. In: Black JM, Matassarin-Jacobs E, eds. Medical-Surgical Nursing: Clinical Manage-
ment for Continuity of Care. 5th ed. Philadelphia: Saunders; 1997:1465; Mosby’s Diagnostic and Laboratory Test Reference. 8th ed. St. Louis: Mosby; 2007.

• T hrombocytopenia refers to a significant decrease in Plts.

FIG. 7.3
Illustration of portions of the complete blood cell count in shorthand
format. Hct, Hematocrit; Hgb, hemoglobin; Plt, platelet; WBC, white
blood cell.
• T he Hct value is approximately three times the Hgb value.
• A low Hct value may cause the patient to experience weak-
ness, 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.
• Pancytopenia refers to a significant decrease in RBCs, all types
of WBCs, and Plts.
• Neutropenia refers to an abnormal decrease in WBCs, particu-
larly neutrophils.
• Leukocytosis refers to an abnormal increase in circulating WBCs.
• Thrombocytosis refers to an abnormal increase in Plts. 
Erythrocyte Indices.  RBC, Hct, and Hgb values are used
to calculate three erythrocyte indices: (1) mean corpuscular vol-
ume (MCV), (2) mean corpuscular Hgb, and (3) mean corpuscu-
lar Hgb concentration (Table 7.11). At most institutions, these
indices are included in the CBC. 
Erythrocyte Sedimentation Rate.  The erythrocyte sedi-
mentation rate (ESR), often referred to as the sed rate, is a mea-
surement of how fast RBCs fall in a sample of anticoagulated
blood. Normal values vary widely according to laboratory
method used. According to the Westergren method, the normal
value for males is up to 15 mm per hour and the normal value
for females is up to 20 mm per hour.16
The ESR is a reflection of acute-phase reaction in inflam-
mation and infection. A limitation of the test is that it lacks
sensitivity and specificity for disease processes. In addition, ESR
cannot detect inflammation as quickly or as early as some other
tests can.24
ESR may be elevated in systemic infection, collagen vas-
cular disease, and human immunodeficiency virus (HIV). It
is a fairly reliable indicator of the course of disease. In gen-
eral, as the disease worsens, the ESR increases; as the disease
180 CHAPTER 7     Vascular System and Hematology
TABLE 7.11  Erythrocyte Indices: Values and Interpretationa
Test Description
Mean corpuscular volume Mean size of RBCs in a
(MCV) (Hct × 10/RBC) sample of blood
Mean corpuscular hemoglobin Amount of Hgb in one
(MCH) (Hgb × 10/RBC) RBC
Mean corpuscular hemoglobin Proportion of each RBC
concentration (MCHC) (Hgb/ occupied by Hgb
Hct × 100)
aLaboratory values vary among laboratories. Refer to facility specific reference ranges.
Hct, Hematocrit; Hgb, hemoglobin; RBC, red blood cell.
Data from Elin RJ. Laboratory reference intervals and values. In: Goldman L, Bennett JC, eds. Cecil Textbook of Medicine. vol 2, 21st ed. Philadelphia: Saunders;
2000:2305; Matassarin-Jacobs E. Assessment of clients with hematologic disorders. In: Black JM, Matassarin-Jacobs E, eds. Medical-Surgical Nursing: Clinical Manage-
ment for Continuity of Care. 5th ed. Philadelphia: Saunders; 1997:1466; and Pagana KD, Pagana TJ. Mosby’s Diagnostic and Laboratory Test Reference. 10th ed. St. Louis:
Mosby; 2011:830-833.
improves, the ESR decreases.16 ESR may be decreased in the
presence of sickle cell disease, polycythemia, liver disease, or
carcinoma.
CLINICAL TIP
ESR is often normal in patients with connective tissue disease or
neoplasms; heparin falsely increases the results.24
Peripheral Blood Smear.  A blood sample may be exam-
ined microscopically for alterations in size and shape of the
RBCs, WBCs, and Plts. RBCs are examined for size, shape,
and Hgb distribution. WBCs are examined for proportion and
the presence of immature cells. Finally Plts are examined for
number and shape.25 Peripheral blood smear results are corre-
lated with the other laboratory tests to diagnose hematologic
disease.  associated with high levels of D-dimer. The test accurately
Coagulation Profile.  Coagulation tests assess the blood’s
ability to clot. The tests used to determine clotting are pro-
thrombin time (PT) and partial thromboplastin time (PTT).
An adjunct to the measurement of PT is the international
normalized ratio (INR). The INR was created 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 expo-
nent (the sensitivity index of the reagent) provided by the
manufacturer.26
CLINICAL TIP
Because INR is more reliable and provides consistent measure-
ment of coagulation levels, the INR value is used more often
than PT.
The PT, PTT, and INR values are used in clinical condi-
tions in which an increased risk of thrombosis is present—for
Value Interpretation
80–100 μm3 Increased by macrocytic, folic acid, or vitamin B12 deficiency
anemias; liver disease; and recent alcohol use.
Decreased by microcytic, iron-deficiency, and hypochromic
anemias; thalassemia; and lead poisoning.
26–34 pg/cell Increased by macrocytic anemia.
Decreased by microcytic anemia.
Low mean corpuscular Hgb indicates Hgb deficiency.
31–37 g/dL Increased by spherocytosis (small round RBC).
Decreased by microcytic, hypochromic, and iron-deficiency
anemias and thalassemia.
example, treatment of deep venous thrombosis (DVT), throm-
bosis associated with prosthetic valves, and atrial fibrillation
(Table 7.12).27
CLINICAL TIP
When confirming an order for physical therapy in the physi-
cian’s orders, the therapist must be sure to differentiate between
  the order for physical therapy and that for the blood test (the
abbreviations for both physical therapy and prothrombin time
are PT).
 
D-Dimer.  The D-dimer assay provides (a highly specific)
measurement of the amount of fibrin degradation. D-dimer
tests have high sensitivity (95% to 99%) but are nonspecific
(40% to 60%). Thrombotic problems, such as DVT, pul-
monary embolism (PE), and thrombosis of malignancy, are
identifies patients with DVT because its high sensitivity
translates into a high negative predictive value. In other
words, if the D-dimer test result is negative, the patient has
a very low likelihood of having DVT. However, a positive
D-dimer test result is less helpful because of the multiple
conditions that may lead to elevated D-dimer titers (advanced
age, recent surgery, infection, inflammatory states, and ele-
vated liver enzyme levels). 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 throm-
bolytic therapy.16,28
CLINICAL TIP
A normal D-dimer value excludes pulmonary embolus in 30% of
patients,24 although a negative D-dimer result does not rule out
the possibility of a PE. False-negative D-dimers are not uncom-
mon for pulmonary emboli.24
 
 Vascular System and Hematology     CHAPTER 7 181

TABLE 7.12  Coagulation Profile

Test Description Valuea Indication/Interpretation
Prothrombin time (PT) Examines the extrinsic and PT 11–12.5 Used to assess the adequacy of warfarin (Coumadin)
­common clotting factors I, II, seconds therapy or to screen for bleeding disorders
V, VII, and X Increased: Coumarin therapy, liver diseases, bile duct
obstruction, diarrhea, salicylate intoxication, DIC, hered-
itary factor deficiency, alcohol use, or drug interaction
Decreased: Diet high in fat or leafy vegetables, or drug
interaction
INR Reflects standardized report- 0.8–1.1 Refer to PT
ing of PT so that results are
­comparable among laboratories
Partial thromboplastin time Examines the intrinsic and PTT 60–70 Used to assess the adequacy of heparin therapy and to
(PTT) (activated PTT ­common clotting factors I, II, seconds screen for bleeding disorders
[aPTT] is a rapid version of V, VIII, IX, X, XI aPTT 30–40 Increased: Heparin or coumarin therapy, liver disease,
PTT) seconds vitamin K or congenital clotting factor deficiency, DIC
Decreased: Extensive cancer, early DIC
aValues for PT and PTT vary between laboratories. Refer to facility specific reference ranges.
DIC, Disseminated intravascular coagulation.
Data from Pagana KD, Pagana TJ. Blood studies. In: Mosby’s Manual of Diagnostic and Laboratory Tests. St. Louis: Mosby; 1998; Mosby’s Diagnostic and Laboratory Test
Reference. 8th ed. St. Louis: Mosby; 2007.

Lymphatic Evaluation description should also include presence of edema or fibrosis

Patient History29
• R elevant history of cancer and/or cancer treatment, includ-
ing radiation or surgery
• History of trauma or surgery
• Onset of swelling at birth and/or puberty (primary lymph-
edema)3
• Duration of swelling episodes 
Observation
During the lymphatic examination, a physical therapist should
be aware of the following observations3:
• Skin integrity—ulcers, weeping, discoloration, fibrosis, un-
usual body contours
• Presence of Stemmer’s sign (the inability to pick up a fold of
skin on the base of the second toe3  again at 3 hours. The LAS, among other tests, can be used to
Palpation
Edema Assessment.  Circumferential measurements accu-
rately assess the shape and contour of a limb. Circumferential
measurements should be taken at consistent locations/sites rela-
tive to the anatomic landmarks for reliable comparison between
limbs and overtime. Volumetric measurements are useful to
measure the actual volume of the limb and are more helpful in
cases of bilateral extremity edema, when no “normal” limb can
be used for comparison. The water displacement method is reli-
able, but more inconvenient than other methods and therefore
done less in clinical settings. Both volumetric measurements
and girth measurements have been shown to be reliable, but
the two methods cannot be reliably interchanged.30 Pitting
edema testing should also be done to assess level of lymphedema
present.
Clinical evaluation should include a detailed description
of skin integrity, use of body diagrams, both anterior-pos-
terior (AP) and lateral to draw unusual body contours. This
on the trunk quadrants, the head, the neck, the limbs, and
the location and condition of scars, fibrotic area, and open
wounds.
CLINICAL TIP
Care should be taken to avoid indenting the edematous tissue
with the tape measure during circumferential measurements.
 
Diagnostics of Lymphedema.  A lymphoscintigraphy
(LAS) is currently the gold standard for lymphedema imag-
ing. Radioactive contrast is injected into the patient before
static images are taken for approximately 15 minutes. A whole
body scan is done as the camera moves centrally to follow the
flow of contrast. The scan is repeated after 30 minutes and
diagnose the severity of lymphedema; however, a special test is
not always needed for diagnosis of the condition. A combina-
tion of patient history, systems review, differential diagnosis,
and thorough physical examination can provide a diagnosis in
most cases.3,29 
Health Conditions
This section is divided into a discussion of vascular, hemato-
logic, and lymphatic disorders.
Vascular Disorders
Vascular disorders are classified as arterial, venous, or combined
arterial and venous disorders. Clinical findings differ between
arterial and venous disorders, as described in Table 7.13. 
Arterial Disorders
Atherosclerosis. Atherosclerosis is a diffuse and slowly
progressive process characterized by areas of hemorrhage and
182 CHAPTER 7     Vascular System and Hematology

TABLE 7.13  Comparison of Clinical Findings of Arterial BOX 7.1  Risk Factors for Atherosclerosis
and Venous Disorders
Reversible Irreversible
Clinical
• H  ypertension (controlled) • Male sex
Finding Arterial Disorders Venous Disorders
• Glucose intolerance and diabetes • Strong family history
Edema May or may not be Present (controlled) • G enetic abnormalities
present Worse at the end of the day • Lipid abnormalities (controlled)
Improves with elevation • High LDL cholesterol
Muscle mass Reduced Unaffected • Low HDL cholesterol
• Hypertriglyceridemia
Pain Intermittent claudica- Aching pain • Cigarette smoking
tion Exercise improves pain • Obesity
Cramping Better with elevation • Sedentary lifestyle
Worse with elevation Cramping at night • Cocaine
Paresthesias, pruritus • Depression
(severe itching)
Leg heaviness, especially
HDL, High-density lipoprotein; LDL, low-density lipoprotein.
at end of day Data from Bryant RA, Nix DP. Acute and Chronic Wounds. 3rd ed. St. Louis:
Pulses Decreased to absent Usually unaffected, but Mosby; 2007; Kumar V. Robbins and Cotran Pathologic Basis of Disease. 7th ed.
Possible systolic may be difficult to St. Louis: Saunders; 2005; Crawford MH, DiMarco JP, Paulus WJ. Crawford:
bruit ­palpate if edema is Cardiology. 3rd ed. St. Louis: Mosby; 2009.
present
Skin Absence of hair Broad, shallow, painless the stenosis, resulting in decreased blood perfusion past the
Small, painful ulcers ulcers of the ankle and
on pressure points, lower leg area of atherosclerosis. Generally, a 50% to 60% reduction in
especially lateral blood flow is necessary for patients to present with symptoms
malleolus (e.g., pain). Turbulence is increased when there is an increase
Normal toenails in blood flow to an area of the body, such as the lower extremi-
Tight, shiny skin ties during exercise. When atherosclerosis develops slowly,
Thickened toenails
collateral circulation develops to meet the needs.30 A patient
Color Pale Brown discoloration with no complaint of pain at rest may therefore experience leg
Dependent cyanosis (hemosiderin staining)
Dependent cyanosis pain (IC) during walking or exercise as a result of decreased
blood flow and the accumulation of metabolic waste (e.g., lac-
Temperature Cool May be warm in presence
of thrombophlebitis tic acid).4,34,35
The following are general signs and symptoms of
Sensation Decreased light touch Pruritus
Occasional itching, atherosclerosis36:
tingling, and numb- • Peripheral pulses that are slightly reduced to absent.
ness • Presence of bruits on auscultation of major arteries (i.e., ca-
Data from Black JM, Matassarin-Jacobs E, eds. Luckmann and Sorensen’s Medical-
rotid, abdominal aorta, iliac, and femoral).
Surgical Nursing: A Psychophysiologic Approach. 4th ed. Philadelphia: Saunders; • Coolness and pallor of skin, especially with elevation.
1993:1261. • Presence of ulcerations, atrophic nails, and hair loss.
• Increased blood pressure.
• Subjective reports of continuous burning pain in the lower
the cellular proliferation of monocytes, smooth muscle, con- extremities at rest that is aggravated with elevation (isch-
nective tissue, and lipids. The development of atherosclerosis emic pain) and relieved with placing the leg over the edge of
begins early in life. In addition to the risk factors listed in Box the bed.30 Pain at rest is usually indicative of severe (80% to
7.1, a high level of an inflammatory biomarker, C-reactive 90%) arterial occlusion.
protein, has been identified as a good predictive marker for • Subjective reports of calf or lower-extremity pain, ache or
early identification of atherosclerosis.31 Waist circumference cramp induced by walking (IC) and relieved by rest.
and weight gain are the strongest predictors of early athero-
sclerosis in healthy adults.32
Atherosclerosis is the underlying cause of approximately CLINICAL TIP
90% of all myocardial infarction and a large proportion of The distance a person can walk before the onset of pain indi-
strokes and ischemic gangrenes.33 cates the degree of circulatory inadequacy (e.g., two blocks or
Clinical manifestations of atherosclerosis result from decrea­ more is mild, one block is moderate, one half block or less is
sed bl­ood flow through the stenotic areas. Signs and symptoms severe).30 Progression of ambulation distance in the patient with
vary according to the area, size, and location of the lesion, along IC can be optimized if ambulation is performed at short, fre-
with the age and physiologic status of the patient. As blood quent intervals.
flows through a stenotic area, turbulence will occur beyond
 Vascular System and Hematology     CHAPTER 7 183

TABLE 7.14  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 or presence
Tightness of tingling, weakness, and clumsiness
Tiredness
Occurs with standing No Yes
Onset Occurs at the same distance each time with walking Occurs at variable distance each time with walking
on level surface on level surfaces
Unchanged or decreased distance walking uphill Increased distance when walking uphill
Unchanged or increased distance walking downhill Decreased distance when walking downhill
Relieved by Stopping activity Sitting
Data from Young JR, Graor RA, Olin JW, et al., eds. Peripheral Vascular Diseases. St. Louis: Mosby; 1991:183; Fritz JM. Spinal stenosis. In: Placzek JD, Boyce DA, eds.
Orthopaedic Physical Therapy Secrets. Philadelphia: Hanley & Belfus; 2001:344.

Symptoms similar to IC may have a neurologic origin from
lumbar canal stenosis or disk disease. These symptoms are
referred to as pseudoclaudication or neurologic claudication. Table
7.14 outlines the differences between true claudication and
pseudoclaudication.37
All patients with claudication should be strongly advised
to stop smoking. The beneficial effect of exercise training in
patients with IC is well proven. The improvement in walking
distance has been reported to be between 30% and 200%. (See
Physical Therapy Interventions for Vascular Disease for more
information regarding a walking program with IC.) A specific
exercise program can result in more improvement than if the
patient tries to exercise on his or her own. The greatest improve-
ment in walking distance until pain develops seems to occur
with exercise duration of longer than 30 minutes per session
and a frequency of at least three sessions per week. Walking
should be used as a mode of exercise, and it should be performed
at nearly maximum pain. The program should last at least 6
months.33
Medications that have been used in managing IC include
pentoxifylline and cilostazol.38
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 throm-
bolytics) 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.39,40  tensile strength of the arterial wall. Rupture is mostly likely to
Aneurysm. An aneurysm is a localized dilatation or out-
pouching of the vessel wall that results from degeneration
and weakening of the supportive network of protein fibers
with a concomitant loss of medial smooth muscle cells. Aneu-
rysms most commonly occur in the abdominal aorta or iliac
arteries, followed by the popliteal, femoral, and carotid ves-
sels.34,39,41,42 The exact mechanism of aneurysm formation
is not fully understood 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 nor-
mal diameter of the vessel42 and involves weakening of all three
layers of the arterial wall. True aneurysms are also generally
fusiform and circumferential in nature. False and saccular aneu-
rysms primarily affect the adventitial layer and are the result of
trauma from dissection (weakness or separation of the vascular
layers) or clot formation (Fig. 7.4).41
Abdominal aortic aneurysm (AAA) is dilatation of the
abdominal aorta to greater than 3 cm in diameter. These aneu-
rysms can be infrarenal, juxtarenal, or suprarenal, according to
the relationship to the renal arteries.33 Most abdominal aneu-
rysms are asymptomatic, but intermittent or constant pain in
the form of mild to severe midabdominal or lower back discom-
fort is present in some form in 25% to 30% of cases. Groin or
flank pain may also be experienced because of increasing pres-
sure on other structures.30
Most aneurysms are relatively asymptomatic until an
embolus dislodges from the aneurysm or the aneurysm rup-
tures.42 Approximately 80% of the aneurysms are identified
incidentally on abdominal ultrasound, computed tomography
(CT) scan, magnetic resonance imaging (MRI), or plain x-ray.43
Aneurysms will rupture if the intraluminal pressure exceeds the
occur in aneurysms that are 5 cm or larger.30
Surgical resection and graft replacement are generally the
desired treatments for aneurysms.44 However, endovascu-
lar repair of abdominal aneurysms is demonstrating favorable
results. Endovascular repair involves threading an endoprosthe-
sis through the femoral artery to the site of the aneurysm. The
endoprosthesis is then attached to the aorta, proximal to the site
184 CHAPTER 7     Vascular System and Hematology

Extravascular
connective
tissue

Extravasation
of
blood

Hematoma

True aneurysm Normal vessel False aneurysm

FIG. 7.4
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. 8th ed. Philadelphia: Saunders; 2010.)

of the aneurysm, and distal to the iliac arteries. This effectively DeBakey I DeBakey II DeBakey III
excludes the aneurysm from the circulation, which minimizes
the risk of rupture.42 Nonsurgical candidates must have blood
pressure and anticoagulation management.44
Physical Therapy Considerations.  The following are addi-
tional clinical manifestations of aneurysms that the physical
therapist should be aware of in clinical practice:
• An AAA may be visualized in more slender patients as a
pulsating swelling in the upper abdomen.33 Popliteal aneu-
rysms present as a pulsating mass, 2 cm or greater in diam-
eter. Femoral aneurysms present as a pulsating mass in the
femoral area on one or both sides.30
• Ischemic manifestations may be present if the aneurysm im-
pedes blood flow.
• Low back pain (aortic aneurysms can cause referred pain to
the low back).
• Cerebral aneurysms, commonly found in the circle of ­Willis,
present with increased intracranial pressure and its sequelae
(see Chapter 6 for more information on intracranial p­ ressure).41 Type A Type B
• Aneurysms that result in subarachnoid hemorrhage are also FIG. 7.5
discussed in Chapter 6. Classification of aortic dissections. (A) Dissection of ascending aorta
• Dysphagia (difficulty swallowing) and dyspnea (breathlessness) (type A). (B) Dissection of descending aorta (type B). (From Kumar V.
result from the enlarged vessel compressing adjacent organs.  Robbins and Cotran Pathologic Basis of Disease. 8th ed. Philadelphia:
Saunders; 2010.)
Aortic Dissection. Aortic dissection is caused by an intimal
tear, which allows for creation of a false lumen between the media
and the adventitia. A history of Marfan’s syndrome or hyperten- cardium, dissection or compression of the coronary arteries,
sion is usually present.45 Aortic dissection occurs at least twice acute aortic regurgitation, or acute blood loss.
as frequently in men than in women.7 Signs and symptoms • Syncope.
generally reflect the type of aortic dissection (whether type A • Hypertension: More than 50% of patients with distal dissec-
or type B [Fig. 7.5]) and the extent of cardiovascular involve- tion are hypertensive, and severe hypertension with diastolic
ment.46 Signs and symptoms of aortic dissection include46: pressure as high as 160 mmHg may be encountered with
• Pain: Sudden and excruciating pain in the chest (90% of distal dissection. Severe hypertension may be caused by renal
the patients) or the upper back is the most common initial ischemia.
symptom. Another important characteristic of the pain is its • Reduced or absent pulses.
tendency to migrate to the neck, abdomen, or groin, gener- • Murmur of aortic regurgitation. This may be present in 50%
ally following the path of dissection. of the patients with proximal dissection and may occur be-
• Shock: Cardiogenic or hypovolemic shock may be second- cause of widening of the aortic annulus or actual disruption
ary to cardiac tamponade from aortic rupture into the peri­ of the aortic valve leaflets.
 Vascular System and Hematology     CHAPTER 7 185

• P leural effusions: Occur most frequently in the left chest and

TABLE 7.15  Sources of Peripheral Emboli
can be caused by the rupture of the dissection into the pleural
space or by weeping of fluid from the aorta as the result of an Source Percentage
inflammatory reaction to the dissection.47 Cardiac 80%
• Neurologic manifestations (cerebrovascular accident and, Atrial fibrillation 50%
rarely, altered consciousness, coma).
Myocardial infarction 25%
Other 5%
CLINICAL TIP Noncardiac 10%
The pain of aortic dissection may mimic that of myocardial Aneurysmal disease 6%
ischemia.47 Proximal artery 3%
Paradoxical emboli 1%
A chest radiograph may be the first clue to the diagnosis
Other or idiopathic 10%
of aortic dissection, but the findings are nonspecific, subject
to interobserver variability, and, in many cases, completely From Belkin M, Owens CD, Whittemore AD, et al. Peripheral arterial occlu-
sive disease. In: Townsend CM, Beauchamp RD, Evers BM, et al., eds. Sabiston
normal.7 Textbook of Surgery: The Biological Basis of Modern Surgical Practice. 18th ed. Phila-
Electrocardiogram (ECG) findings in these patients are non- delphia: Saunders; 2007.
specific.7,45 Transesophageal echocardiography (TEE) and CT
scan are the primary diagnostic tests used by most institutions to be provided. Heat or cold application and massage are to be
diagnose aortic dissection.48 TEE is highly accurate for the evalua- avoided.30 Treatment of thrombi, emboli, or both includes
tion and diagnosis of acute aortic dissection, with 98% sensitivity anticoagulation with or without surgical resection of the
and 94% to 97% specificity. Contrast CT is also highly accurate atherosclerotic area that is predisposing the formation of
for diagnosing aortic dissection, with sensitivity and specificity of thrombi, emboli, or both. Medical management of arterial
95% to 98%, respectively. MRI is a highly accurate, noninvasive thrombosis can also include antithrombotic drugs (e.g., tis-
technique for evaluating aortic dissection but is rarely used as the sue factor or factor Xa inhibitors) or combined antithrom-
initial test for diagnostic evaluation of acute dissection. MRI is botic therapy with aspirin, as well as a thienopyridine,
known to have high sensitivity of 95% to 100% and specificity of warfarin, or both.50 
94% to 98% for the detection of aortic dissection.7 Hypertension. Hypertension is elevated arterial blood pres-
Management includes stabilizing the patient, aggressive sure, both systolic and diastolic, that is abnormally sustained at
control of blood pressure, and pain control. Patients may be rest (Table 7.16).51,52 Hypertension is frequently asymptomatic;
managed medically or surgically, depending on the site of the this creates a significant health risk for affected people.30 Signs
dissection and the patient’s comorbidities.  and symptoms that can result from hypertension and its effects
Arterial Thrombosis. Arterial thrombosis occurs in areas of on target organs are described in Table 7.17. Hypertension is a
low or stagnant blood flow, such as atherosclerotic or aneurys- risk factor for heart attack, stroke, and kidney failure. Systolic
mal areas. The reduced or turbulent blood flow in these areas blood pressure gradually increases through life, whereas diastolic
leads to Plt adhesion and aggregation, which then activates the blood pressure increases until 50 to 60 years of age. Women typi-
coagulation cycle to form a mature thrombus (clot). Blood flow cally have lower blood pressure compared with men until after
may then be impeded, potentially leading to tissue ischemia menopause.53
with subsequent clinical manifestations.41,44  Two general forms of hypertension exist: essential and sec-
Arterial Emboli. An arterial embolus is a fragment of ondary. Essential or idiopathic hypertension is elevation in blood
thrombus, fat, atherosclerotic plaque, bacterial vegetation, or pressure that results without a specific medical cause but is
air that mobilizes within the arterial vessels and obstructs flow related to the following risk factors41,54:
distal to the embolus.49 Arterial emboli arise from areas of stag- • Genetic predisposition
nant or disturbed blood flow in the heart or aorta. Acute arterial • Smoking
embolus is a surgical emergency. The likelihood of limb salvage • Sedentary lifestyle
decreases after 4 to 6 hours.48 The most common sources of arte- • Type A personality
rial emboli are listed in Table 7.15. • Obesity
Areas in which arterial emboli tend to lodge and interrupt • Diabetes mellitus
blood flow are arterial bifurcations and areas narrowed by ath- • Diet high in fat, cholesterol, and sodium
erosclerosis (especially in the cerebral, mesenteric, renal, and • Atherosclerosis
coronary arteries). Signs and symptoms of thrombi, emboli, or • Imbalance of vasomediator production, nitric oxide (vasodi-
both depend on the size of the occlusion, the organ distal to the lator), and endothelin (potent vasoconstrictor)
clot, and the collateral circulation available.41 Secondary hypertension results from a known medical cause,
When arterial thrombosis or embolism is suspected, such as renal disease and others listed in Table 7.18. If the caus-
the affected limb must be protected by proper positioning ative factors are treated sufficiently, systolic blood pressure may
below the horizontal plane, and protective skin care must return to normal limits.41
186 CHAPTER 7     Vascular System and Hematology

TABLE 7.16  Hypertension As It Relates to Different Age TABLE 7.17  Hypertensive Effects on Target Organs
Groups
Organ Hypertensive Effect Clinical Manifestations
Normal Blood Hypertensive Blood Brain Cerebrovascular Area of brain involved dictates
Pressure (Sys- Pressure (Systolic/Dia- ­accident presentation. May include
Age tolic/Diastolic) stolic) severe occipital headache, pa-
Infants 80/40 90/60 ralysis, speech and swallowing
disturbances, or coma
Children 100/60 120/80 Encephalopathy Rapid development of confu-
Children ≥13 <120/<80 Same as adults sion, agitation, convulsions,
years and death
Adults ≥18 <120/<80 Elevated: 120–129/<80 Eyes Blurred or impaired Nicking (compression) of reti-
years Stage 1 hypertension: vision nal arteries and veins, at the
130–139/80–89 point of their junction
Stage 2 hypertension: Encephalopathy Hemorrhages and exudates on
≥140/≥90 visual examination
Papilledema
Data from Bullock B. Pathophysiology: Adaptations and Alterations in Func-
tion. 4th ed. Philadelphia: Lippincott-Raven; 1996:517; Chobanian A, et al: Heart Myocardial Electrocardiographic changes
The seventh report of the Joint National Committee on Prevention, Detec- infarction Enzyme elevations
tion, Evaluation and Treatment of High Blood Pressure. The JNC 7 report. Congestive heart Decreased cardiac output
Hypertension. 2003;42:1206-1252; Flynn JT, Kaelber DC, et al. Subcommittee failure Auscultation of S3 or gallop
on screening and management of high blood pressure in children. Pediatrics. Cardiomegaly on radiograph
2017;140(3):e20171904; Whelton PK, Carey RM, Aronow WS, et al. 2017 Myocardial Increased angina frequency
ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guide- ­hypertrophy ST- and T-wave changes on
line for the Prevention, Detection, Evaluation, and Management of High Blood
Pressure in Adults: A Report of the American College of Cardiology/American
electrocardiogram
Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. Dysrhythmias Ventricular or conduction
2018;71(19):138. defects
Kidneys Renal insufficiency Nocturia
A rise in diastolic blood pressure from a sitting to a standing Proteinuria
position may suggest essential hypertension, whereas a fall in Elevated blood urea nitrogen
and creatinine levels
blood pressure from a sitting to a standing position may indi- Renal failure Fluid overload
cate secondary hypertension.9 Accumulation of metabolites
Management of hypertension consists of behavioral (e.g., Metabolic acidosis
diet, smoking cessation, activity modification) and phar-
Data from Bullock B. Pathophysiology: Adaptations and Alterations in Function. 4th
macologic intervention to maintain blood pressure within ed. Philadelphia: Lippincott-Raven; 1996:522.
acceptable parameters. Pharmacologic treatment can likely be
deferred in patients with hypertension who regularly partici-
pate in aerobic exercise. Exercise high in intensity and dura-
tion has a beneficial effect in the management of hypertension,
and the antihypertensive effect of regular training can be
maintained as long as 3 years.55 The primary medications used • R eview and clarify any strict blood pressure parameters that
are diuretics and angiotensin-converting enzyme inhibitors, the physician has designated for the patient. Some patients
along with beta blockers, calcium channel blockers, and vaso- need to have higher or lower systolic pressures than the ex-
dilators.41,56-58 A summary of these medications, their actions, pected normal ranges.
and their side effects can be found in Chapter 19, Tables 19.3 • If a patient has elevated blood pressure, make sure the cuff
and 19.3A. size is right for the patient’s arm, take the blood pressure in
Hypertensive crisis is a medical emergency. It occurs when the opposite extremity, and then notify the team.
the blood pressure is high enough to threaten target organs • In certain patient populations (e.g., patients who have had
acutely. Hypertensive emergency requires admission to an mastectomies, patients with a peripherally inserted central
intensive care unit and parenteral therapy.59 catheter [PICC] line), there are restrictions on taking blood
Physical Therapy Considerations pressure in the upper extremities. In these cases, blood pres-
• P hysical exertion increases blood pressure acutely and de- sure can be taken in the lower extremities—it is important
creases resting blood pressure over time.53 to document the change, if needed.
• Blood pressure is usually lowest in the morning when the • Patients receiving antihypertensive therapy, are at risk to ex-
metabolic rate is the lowest, rises throughout the day, and perience the signs and symptoms of low blood pressure, such
peaks in late afternoon when the person is mentally awake as dizziness, confusion, syncope, restlessness, or drowsiness,
and physically active.53 especially in older patients.
• Knowledge of medication schedule may facilitate activity • Elevated blood pressure can be present when patients are in
tolerance by having optimal blood pressures at rest and with pain, under stress, or apprehensive. It is important to attempt
activity. to make the patient calm and comfortable before repeating

TABLE 7.18  Causes of Secondary Hypertension
Origin Description
Coarctation of the Congenital constriction of the aorta at
aorta the level of the ductus arteriosus, which
results in increased pressure (proximal
to the area) of constriction and decreased
pressure (distal to the area) of constric-
tion
Cushing’s disease or See Pituitary Gland in Chapter 10
syndrome
Oral contraceptives May be related to an increased secretion of
glucocorticoids from adrenal or pituitary
dysfunction
Pheochromocytoma Tumor of the adrenal medulla causing
increased catecholamine secretion
Primary aldosteron- Increased aldosterone secretion primarily as
ism result of an adrenal tumor
Renin-secreting See Adrenal Gland in Chapter 10
tumors
Renovascular disease Parenchymal disease, such as acute and
chronic glomerulonephritis
Narrowing stenosis of renal artery as a
result of atherosclerosis or congenital
fibroplasia
Data from Bullock B. Pathophysiology: Adaptations and Alterations in Function. 4th
ed. Philadelphia: Lippincott-Raven; 1996:517.
the measurement to gain a more accurate representation of
blood pressure.  tract infection.37,40
Systemic Vasculitis. Systemic vasculitis is a general term
referring to 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, infec-
tious organisms, drugs, tumors, and allergic reactions are some
of the defined triggers. Pathogenetic factors include immune
complex disease, antineutrophil cytoplasmic antibodies, anti–
endothelial cell antibodies, and cell-mediated immunity. The
major ischemic manifestations of vasculitis are defined by
the type and size of blood vessels involved and the tissue and
organ damage caused by the ischemia related to the vascu-
lar occlusion.60 The secondary manifestations of vasculitis are
numerous and may include thrombosis, aneurysm formation,
hemorrhage, arterial occlusion, weight loss, fatigue, depres-
sion, fever, and generalized achiness that is worse in the morn-
ing. The recognized forms of vasculitis are discussed in the
following sections.35,61-63  and noninvasive methods. The noninvasive methods include
Polyarteritis Nodosa. Polyarteritis nodosa (PAN) is an
acute necrotizing vasculitis of small- and medium-sized arter-
ies.60 Most cases present with an unknown etiology; however,
hepatitis B virus has been emerging as one of the more com-
mon causative factors.62 PAN usually begins with nonspecific
symptoms, which may include malaise, fatigue, fever, myal-
gias, and arthralgias. Skin lesions are common, and a majority
of patients have vasculitic neuropathy.64 The most frequently
involved organs are the kidney, heart, liver, and gastrointesti-
nal tract, with symptoms representative of the dysfunction of
Vascular System and Hematology     CHAPTER 7 187
the involved organ. Aneurysm formation with destruction of
the medial layer of the vessel is the hallmark characteristic of
PAN. Pulmonary involvement can occur; however, most cases of
vasculitis in the respiratory tract are associated with Wegener’s
granulomatosis.
Current management of PAN includes corticosteroid ther-
apy, with or without concurrent cytotoxic therapy with cyclo-
phosphamide (Cytoxan). Antiviral agents may also be used if
there is an associated viral infection. Elective surgical correction
of PAN is not feasible, given its diffuse nature. Patients diag-
nosed with PAN have a 5-year survival rate of 12% without
medical treatment and 80% with treatment.61,62 
Wegener’s Granulomatosis. Wegener’s granulomatosis
is a granulomatous necrotizing disease that affects small- and
medium-sized blood vessels throughout the body, with pri-
mary manifestations in the upper respiratory tract, lungs, and
kidneys. The etiology is unknown; diagnosis and treatment are
still in development. It occurs most commonly in the fourth
and fifth decades of life and affects men and women with equal
frequency.45 Pulmonary signs and symptoms mimic those of
pneumonia (e.g., fever, productive cough at times with nega-
tive sputum cultures, and chest pain).56,62 The 1-year mor-
tality rate is 90% without therapy, 50% with corticosteroid
therapy, and 10% with combined corticosteroid and cytotoxic
therapy.62
Treatment of Wegener’s granulomatosis may consist of a
combination of immunosuppressive agents and corticosteroids
(methotrexate and prednisone, respectively). Antiinfective
agents may also be prescribed if there is associated respiratory
 
Thromboangiitis Obliterans. Thromboangiitis obliterans
(Buerger’s disease) is a vasculitis (inflammatory and thrombotic
process) affecting the peripheral blood vessels (both arteries
and veins), primarily in the extremities.30 It is found mainly
in young men age 20 to 45 years and is directly correlated with
a heavy smoking history.4,41,61 If abstinence from tobacco is
adhered to, the disease takes a favorable course. If smoking is
continued, the disease continues to progress, leading to gan-
grene and small-digit amputations.65 The disease is charac-
terized by segmental thrombotic occlusions of the small- and
medium-sized arteries in the distal lower and upper extremi-
ties. The thrombotic occlusions consist of microabscesses that
are inflammatory in nature, suggesting a collagen or autoim-
mune origin, although the exact etiology is still unknown.41,61
Rest pain is common, along with IC that occurs more in the
feet than in the calf region.3 The diagnosis is made by invasive
physical examination, Doppler ultrasound, plethysmography,
and ankle–brachial index (ABI). The invasive methods include
magnetic resonance angiography (MRA), other forms of angi-
ography, and spiral CT.66
Treatment of Buerger’s disease can include smoking cessation,
corticosteroids, prostaglandin E1 infusion, vasodilators, hemorhe-
ologic agents, antiplatelet agents, and anticoagulants.41,61 
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
188 CHAPTER 7     Vascular System and Hematology
by destruction of the internal elastic lamina. Two clinical pre-
sentations of GCA have been recognized: temporal arteritis and
Takayasu’s arteritis.41 Temporal artery biopsy (TAB) is the “gold
standard” for the diagnosis of GCA. ESR, C-reactive protein,
and Plt count are the primary serologic markers. Color ultraso-
nography of the temporal arteries detects characteristic signs of
vasculitis with high sensitivity and specificity. Vision loss is the
most dreaded complication of GCA, and when it occurs, it tends
to be profound and permanent.67
Temporal arteritis is a more common and mild presentation
of GCA that typically occurs after 50 years of age. The onset
of temporal arteritis is usually sudden, with a severe, continu-
ous, unilateral, throbbing headache and temporal pain as the
first symptoms. The pain may radiate to the occipital area, face,
or side of the neck. Visual disturbances range from blurring to
diplopia to visual loss. Irreversible blindness may occur in the
course of the disease from involvement of the ophthalmic artery.
Other symptoms include enlarged, tender temporal artery, scalp
sensitivity, and jaw claudication when involvement of the exter-
nal carotid artery causes ischemia of the masseter muscles. The
pain occurs in response to chewing, talking, or swallowing and
is relieved by rest.67 Polymyalgia rheumatica, a clinical syn-
drome characterized by pain on active motion and acute onset of
proximal muscular stiffness, is frequently associated with tem-
poral arteritis. The primary treatment for temporal arteritis is
prednisone.37,62
Takayasu’s arteritis generally affects young women of Asian
demographic but has been known to occur in both sexes in Afri-
can 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. The pulmonary circulation is involved
in approximately 50% of cases of Takayasu’s arteritis.64 Lower
extremity involvement is less common. Management of Takaya-
su’s arteritis may consist of prednisone and cyclophosphamide,
along with surgical intervention if the disease progresses to
aneurysm, gangrene, or both.37  system is unclear and because dystrophy is not an inevitable
Raynaud’s Disease. Raynaud’s disease is an episodic vaso-
spastic disorder characterized by color change in the digits
(white to blue to red—reflecting the vasoconstriction, cyano-
sis, and vasodilation process, respectively) with exposure to a
cold environment or emotional stress. Numbness, tingling,
and burning pain may also accompany the color changes. How-
ever, despite these vasoconstrictive episodes, peripheral pulses
remain palpable. If idiopathic, it is called Raynaud’s disease. If
associated with possible precipitation of a systemic or regional
disorder (e.g., autoimmune diseases, myeloproliferative disor-
ders, multiple myeloma, cryoglobulinemia, myxedema, macro-
globulinemia, or arterial occlusive disease), it is called Raynaud’s
phenomenon.4,37,56
Raynaud’s disease is symmetric by rule; the feet and toes are
infrequently involved. Between attacks, the affected extremi-
ties may be entirely normal. Raynaud’s disease is benign and
often controllable. It mostly causes mild discomfort on exposure
to cold and progressing very slightly over the years. The inci-
dence of disease is estimated to be as high as 10% in the general
population. 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 upregulation of
vascular smooth muscle alpha2-adrenergic receptors.
The distinction between Raynaud’s disease and Raynaud’s
phenomenon reflects a difference in prognosis.
In Raynaud’s phenomenon, the changes may be most
noticeable in one hand or even in one or two fingers only.
Raynaud’s phenomenon may progress to atrophy of the termi-
nal fat pads and development of fingertip gangrene. Women
16 to 40 years of age are most commonly affected, especially
in cold climates or during the winter season. The prognosis
of Raynaud’s phenomenon is that of the associated disease.45
Areas generally affected are the fingertips, toes, and the tip of
the nose.4,37,56
CLINICAL TIP
At the time of an exacerbation, gently rewarm fingers or toes as
soon as possible by placing hands in the axilla, wiggling fingers
or toes, and moving or walking around to improve circulation.
If possible, run warm water over the affected body part until
normal color returns.30
Management of Raynaud’s disease and Raynaud’s phenom-
enon 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 biofeedback;
acupuncture; and sympathectomy.37,45,68 
Complex Regional Pain Syndrome. Complex regional pain
syndrome (CRPS) is a rare disorder of the extremities character-
ized by autonomic and vasomotor 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
sequela of the syndrome.
The presenting symptom is constant, extreme pain that
occurs after the healing phase of minor or major trauma, frac-
tures, surgery, or any combination of these. Injured sensory
nerve fibers may transmit constant 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 prog-
ress 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.45
Three stages have been defined (Steinbrocker’s classification),
although all patients may not have evolved through the stages
or proceed in a temporal fashion60,65:
• Stage 1: Acute (occurring within hours to days after the in-
jury)—pain, tenderness, edema, and temperature changes
predominate.
• Stage 2: Dystrophic (3–6 months after the injury)—pain ex-
tends beyond the area affected; loss of hair and dystrophic
nails become apparent. Muscle wasting, osteoporosis, and
decreased ROM may occur.

• S tage 3: Atrophic or chronic (6 months after injury)—atro-
phy, demineralization, functional impairment, and irrevers-
ible damage are present.
Management of CRPS may consist of any of the following37,69-72:
• Physical or occupational therapy, or both (cornerstone therapy)
• Pharmacologic sympathetic blocks
• Surgical sympathectomy
• Spinal cord electrical stimulation
• Baclofen administration
• Prophylactic vitamin C administration after sustaining frac-
tures
• Bisphosphonate administration
The prognosis partly depends on the stage in which the
lesions are encountered and the extent and severity of associ-
ated organic disease. Early treatment offers the best prognosis
for recovery.45  can be either primary or secondary. Primary varicose veins originate
Compartment Syndrome. Compartment syndrome is a
condition in which the circulation within a closed compart-
ment is compromised by an increase in pressure within the
compartment. This causes necrosis of muscles and nerves and
eventually of the skin because of excessive swelling. Volk-
mann ischemic contracture is a sequela of untreated or inad-
equately treated compartment syndrome, in which necrotic
muscle and nerve tissue has been replaced with fibrous
tissue.73
Compartment syndrome can occur after traumatic injuries,
including fractures, crush injuries, hematomas, penetrating
injuries, circumferential burn injury, electrical injuries, and
revascularization procedures. External factors, such as casts
and circular dressings that are too constrictive, may also lead
to compartment syndrome.34,37,74 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.
Normal tissue pressure is between 0 and 8 mmHg. Compart-
ment pressures of 32 to 37 mmHg can cause compression of
capillaries.74
Permanent muscle damage can begin after 4 to 12 hours of
ischemia. Nerves appear to be more sensitive than muscles to
the effects of increased pressure, and damage can occur after
approximately 8 hours of pressure elevation.75
A common symptom of compartment syndrome is pain that
is associated with tense, tender muscle groups and that worsens
with palpation or passive movement of the affected area. Numb-
ness or paralysis may also be accompanied by a gradual diminu-
tion of peripheral pulses. Pallor, which indicates tissue ischemia,
can progress to tissue necrosis if appropriate management is not
performed.34,37,74
Management of compartment syndrome consists of prevent-
ing prolonged external compression of the involved limb, limb
elevation, and ultimately fasciotomy (incisional release of the
fascia) if compartment pressures exceed 37 to 52 mmHg. Man-
nitol can also be used to help reduce swelling.34,37,74
Physical Therapy Considerations.  Patient, staff, and family
education on proper positioning techniques can reduce the
risk of swelling and subsequent compartment syndrome.
Vascular System and Hematology     CHAPTER 7 189
In cases when compartment syndrome is present:
• E levation of the affected limb must be discontinued, and the
limb should be placed no higher than the heart level.
• Circumferential bandages must be removed.76
• The physical therapist should delineate any ROM precau-
tions that may be present after fasciotomies that cross a
joint line. 
Venous Disorders
Varicose Veins. Varicose veins are chronic dilations of the veins
that first result from a weakening in the venous walls, which leads
to improper closure of the valve cusps. Incompetence of the valves
further exacerbates the venous dilatation. The prevalence of varicose
veins in Western populations was estimated in one study to be about
25% to 30% in women and 10% to 20% in men.65 Varicose veins
in the superficial veins—the saphenous veins and their branches.
Primary varicose veins tend to run in families, affect both legs, and
are twice as common in females as in males. They can result from
congenital weakness of the valves or venous wall; from conditions
that produce prolonged venous stasis, such as pregnancy or wearing
tight clothing, or from occupations that necessitate standing for an
extended period.
Secondary varicose veins occur in the deep and perforating
veins. Usually secondary varicose veins occur in only one leg
and result from disorders of the venous system, such as deep
vein thrombophlebitis, trauma, and occlusion.9 Both primary
and secondary varicose veins are more common in middle
adulthood.
Risk factors include female sex, pregnancy, family history,
prolonged standing, and history of phlebitis.45 Patients gener-
ally complain of itchy, tired, heavy-feeling legs after prolonged
standing.34,77 Large varicose veins may produce anxiety and
cause major lifestyle changes. Trauma to a varicose vein may
result in severe bleeding, particularly in older adults because the
skin may be atrophic.78
Management of varicose veins may consist of any of the
following: behavioral modifications (e.g., avoiding pro-
longed sitting or standing and constrictive clothing), weight
loss (if there is associated obesity), elevating the feet for
10 to 15 minutes three or four times a day, gradual exer-
cise, applying well-fitting support stockings in the morn-
ing, showering or bathing in the evening, sclerotherapy (to
close dilated veins), ambulatory phlebectomy, endovenous
ablation, and surgical ligation and stripping of incompetent
veins.34,65,77 
Venous Thrombosis. Venous thrombosis can occur in the
superficial or deep veins (DVT) and can result from a combina-
tion of venous stasis, injury to the endothelial layer of the vein,
and hypercoagulability (Box 7.2). Venous stasis of the lower
extremities occurs as a consequence of immobility, whereas
hypercoagulability may occur as a result of inflammation, malig-
nancy, or tissue damage of intimal walls. Thrombus formation
usually occurs in legs, but its incidence in upper extremities
is growing, particularly because of increasing use of subclavian
venous catheters.79
190 CHAPTER 7     Vascular System and Hematology
BOX 7.2  Risk Factors for Deep Venous Thrombosis
• S urgery 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 complica-
tions of DVT. Mosby’s Nursing Consult. St. Louis: Mosby; 2007.
DVT places the patient at risk for PE, recurrent thrombo-
sis, and postphlebitic syndrome. There are two types of throm-
bus: (1) mural thrombus, where the thrombus is attached to
the wall of the vein but does not occlude the vessel lumen;
and (2) occlusive thrombus, which begins by attachment to
the vessel wall and progresses to completely occlude the vessel
lumen.30,34
There are two types of venous thrombosis: (1) superficial,
saphenous vein in the lower extremity; and (2) deep, usually of
the femoral or iliac veins of the lower extremities and pelvis.30
Superficial venous thrombosis of the upper extremity can occur,
although it is less common and is seen in people with systemic
illness in the presence of an indwelling central venous catheter,
malignancy, or, less often, hemodialysis.30
A 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.80
Signs and symptoms of venous thrombosis can include the
following37,81:
• 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
Patients with DVT in a lower extremity may complain of pain
around the general area of the thrombus with weight bearing,
although clinical presentation of DVT varies and physical exami-
nations are only 30% accurate.79
The primary imaging study to identify patients with DVT
is ultrasonography. It is relatively inexpensive, noninvasive, and
widely available. Ultrasound is considered to be 97% sensitive
and 96% specific for symptomatic patients with suspected DVT
of the proximal leg. The sensitivity of ultrasound for calf DVT
is well below 90%.64 Other diagnostic methods include venog-
raphy and impedance plethysmography. MRI is playing a grow-
ing role in the diagnosis of DVT, with sensitivity of 97% and
specificity of 95%.46 The Wells clinical decision rule (CDR) for
DVT, as described in the Vascular Tests section, has been shown
to be a reliable and valid tool for clinical assessment and predict-
ing the risk of DVT in the lower extremity.30,64,82,83
CLINICAL TIP
Homans’ sign (pain in the upper calf with forced ankle dorsi-
flexion) has been used as a screening tool for venous thrombo-
sis, but it is an insensitive and nonspecific test (sensitivity and
specificity are only about 50%) that has a very high false-positive
rate.46 Physical therapists should promote the use of the Wells
CDR based on its strong support in identifying risk of DVT.82,83
Patients admitted to the hospital and/or undergoing sur-
gery are often on DVT prophylaxis, which includes mechani-
cal and pharmacologic approaches80; lower-extremity elevation
or application of compression stockings (elastic or sequen-
tial pneumatic), or both, if bed rest is required; and antico-
agulation medications (intravenous heparin or oral warfarin
[Coumadin]).
Primary prevention of DVT is through the use of early
mobilization in low-risk individuals and prophylactic use of
anticoagulants in people with moderate to high risk for DVT.30
Prolonged sitting increases blood viscosity, Hct, and serum lac-
tate. It is important for postoperative patients to initiate early
ambulation, stay hydrated, wear nonrestrictive clothing, and
exercise their calf muscles frequently to reduce venous stasis and
improve venous return.64 Routine use of elastic stockings in all
postoperative patients along with the use of sequential compres-
sion also help prevent DVTs.30
The initial treatment for DVT is anticoagulation with
unfractionated heparin (UFH) or low-molecular-weight hepa-
rin (LMWH), such as enoxaparin (Lovenox) or fondaparinux
(Arixtra). The INR is used to assess the anticoagulation level for
unfractionated heparin as well as warfarin (Coumadin).84 PT/
INR is insensitive in measuring the anticoagulation effect of
LMWH. If enoxaparin (Lovenox) is administered at the correct
dosage for the patient, it is deemed to be at an immediate thera-
peutic level.85
CLINICAL TIP
Physical therapists should be alert for the signs and symptoms
of unusual bleeding in patients who are on anticoagulation after
the diagnosis of DVT.
Heparin blocks the extension of a 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
of several days to weeks. After initial anticoagulation with hepa-
rin, warfarin (Coumadin), and fondaparinux (Arixtra) are used.
Fondaparinux is more effective in decreasing the risk of DVT

after orthopedic surgery compared with LMWH. It is recom-
mended that patients have at least 3 to 6 months of treatment
for an initial event of DVT. After the first occurrence of DVT,
patients should receive 3 months of therapy in the setting of an
identifiable risk factor or surgery; patients with idiopathic DVT
should receive 6 months of therapy.84
If a patient cannot receive anticoagulation therapy, a device
called an inferior vena cava (IVC) filter can prevent lower extrem-
ity thrombi from embolizing to the lungs. The primary indi-
cations for IVC filter placement include contraindications to
anticoagulation, recurrent embolism while on adequate therapy,
and significant bleeding complications during anticoagulation.
IVC filters are sometimes placed in the setting of a massive PE
when it is believed that any further emboli might be lethal.
More recently, temporary 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.64 IVC filters prevent
approximately 97% of symptomatic PEs that originate from the
lower extremities.86 Management of venous thrombosis may
also consist of thrombolytic therapy (streptokinase and uro-
kinase), or both, and surgical thrombectomy (limited uses).34
However, the use of thrombolytic therapy is not recommended
for an isolated DVT.46
Traditionally all patients with a diagnosis of DVT were
required to be on bed rest for the first few days because of the
fear of dislodging clots that may result in PE. However, with
the introduction of LMWH (Lovenox), selected stable patients
are able to be 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. The incidence
of new PE and risk of thrombus propagation is not increased
in patients with uncomplicated DVT who are mobilized early;
however, there may be an increased risk of acute PE among
patients with DVT and known PE when ambulation begins
early, so these cases require careful consideration. Early ambula-
tion of patients with DVT, anticoagulation, and use of com-
pression stockings lead to a more rapid resolution of pain and
swelling associated with DVT, reduce the risk of extension of
proximal DVT, and decrease the incidence, severity, and recur-
rence of postthrombotic syndrome, in addition to preventing
venous stasis. Early ambulation is recommended in patients who
have not been diagnosed with PE in the setting of DVT and who
do not have cardiopulmonary impairment. Current evidence
suggests that patients with DVT who are receiving appropri-
ate anticoagulation and are at the appropriate therapeutic level
could be considered for early ambulation, provided they have
adequate cardiopulmonary reserve and no evidence of PE.82,87-89
Use of a compression stocking while ambulating has an added
advantage, and compression stockings are reported to help with
pain relief and leg circumference.46,90-92  nificant cause of either disorder. Fig. 7.6 illustrates the venous
Pulmonary Embolism. PE is the primary complication
of venous thrombosis, with emboli commonly originating in
the lower extremities. About 75% to 90% of PEs originate
from the lower extremities; the rest originate from the right
atrium and upper extremities,86 as well as the pelvic venous
plexus. Mechanical blockage of a pulmonary artery or capillary,
depending on clot size, results in an acute ventilation–perfusion
Vascular System and Hematology     CHAPTER 7 191
A B C
FIG. 7.6
Venous valves. (A) Open valves allow forward blood flow. (B) Closed
valves prevent backflow. (C) Incompetent valves are unable to fully close,
causing blood to flow backward and producing venous insufficiency.
(Redrawn from Bryant R, Nix D. Acute and Chronic Wounds: Current Man-
agement Concepts. 3rd ed. St. Louis: Mosby; 2007.)
mismatch that leads to a decrease in partial pressure of oxygen
and oxyhemoglobin saturation, ultimately manifesting as tis-
sue hypoxia. Chronic physiologic sequelae from PE include
pulmonary hypertension, chronic hypoxemia, and right conges-
tive heart failure. Refer to the Laboratory Studies section for
details on the D-dimer test. Refer to Chapter 4 for more details
on ventilation–perfusion mismatches, as well as the respiratory
sequelae (dyspnea, chest pain, hemoptysis, and tachypnea) of
PE.34,93
Management of PE consists of prevention of venous throm-
bosis formation (see the Venous Thrombosis section), early
detection, and thorough anticoagulation therapy with standard
heparin or LMWH. Thrombolytic therapy has also been used
in patients with PE. The placement of an IVC filter is indi-
cated when the patient cannot be anticoagulated or when there
is recurrence of PE despite anticoagulation.34,93
CLINICAL TIP
Physical therapy intervention should be discontinued imme-
diately if the signs and symptoms of an acute PE arise dur-
ing an examination or treatment session. The medical team
should be notified immediately because it is an emergent
situation.
Chronic Venous Insufficiency and Postphlebitic Syn-
drome. Chronic venous insufficiency and postphlebitic syn-
drome are similar disorders that result from venous outflow
obstruction, valvular dysfunction from thrombotic destruction
of veins, or both. Valvular dysfunction is generally the most sig-
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 charac-
teristics of both chronic venous insufficiency and postphlebitic
syndrome are the following1,8,34,66,94:
• Chronic swollen limbs, worsening while the limbs are in a
dependent position.
192 CHAPTER 7     Vascular System and Hematology
• S kin changes: (1) hemosiderin staining or hemosiderosis (dis-
coloration of soft tissue that results when extravasated RBCs
break down and release the pigment hemosiderin, resulting
in gray-brown pigmentation of the skin), also called hyperpig-
mentation or tissue staining; and (2) lipodermatosis (fibrosis
or hardening of the soft tissue in the lower leg), which is
indicative of longstanding venous disease.
• Venous stasis ulceration.
The goal of management is to prevent worsening of the dis-
ease to avoid additional medical complications. Management
of these disorders may consist of any of the following: leg
elevation above the level of the heart two to four times daily
for 10 to 15 minutes; application of proper elastic supports
(knee length preferable); skin hygiene; avoidance of cross-
ing legs, poorly fitting chairs, garters, and sources of pres-
sure 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.1,34,84 Refer to Chapter 12 for more information
on wound care.
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 malforma-
tions (AVMs) involve shunting of blood directly from the artery
to the vein, bypassing the capillary bed. The presence of an arte-
riovenous fistula in the AVM is usually the cause of the shunt.
The majority of AVMs occur in the trunk and extremities, with
a certain number of cases also presenting in the cerebrovascular
region.61
Signs of AVMs may include the following61:
• Skin color changes (erythema or cyanosis)
• Venous varices
• Edema
• Limb deformity
• Skin ulceration
• Pulse deficit
• Bleeding
• Ischemic manifestations in involved organ systems 
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 defined as a significant reduction in
the mass of circulating RBCs. As a result, the oxygen bind-
ing capacity of blood is diminished. Because blood volume is
normally maintained at a nearly constant level, patients with
anemia have a decrease in the concentration of RBCs or Hgb in
peripheral blood.64 Anemia can be described according to etiol-
ogy as (1) a decrease in RBC production, (2) abnormal RBC
maturation, or (3) an increase in RBC destruction.18 Anemia can
also be described according to morphology based on RBC size or
color.95 RBCs that are of normal size are referred to as 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 microchromic. Some of
the most common anemias are described in the next section.
Posthemorrhagic Anemia.  Posthemorrhagic anemia can
occur with rapid blood loss from traumatic artery severance,
aneurysm rupture, or arterial erosion from malignant or ulcer-
ative lesions or as a result of surgery. Blood loss results in nor-
mocytic, normochromic anemia. The signs and symptoms of
posthemorrhagic anemia depend on the amount of blood loss
and may include the following96:
• With 20% to 30% blood volume loss—dizziness and hypo-
tension when not at rest in a recumbent position; tachycardia
with exertion
• With 30% to 40% blood volume loss—thirst, dyspnea, dia-
phoresis, cold and clammy skin, hypotension and tachycar-
dia, decreased urine output, clouding or loss of consciousness
when at rest in a recumbent position
• With 40% to 50% blood volume loss—severe state of shock,
with potential for death
Management of posthemorrhagic anemia may consist of any
of the following: control of bleeding at the source, intravenous
and oral fluid administration, blood and blood product transfu-
sion, and supplemental oxygen.19,95,97 
Iron-Deficiency Anemia.  Iron-deficiency anemia is the most
common cause of anemia (Box 7.3), affecting at least one third of
the world’s population.66,98 When iron loss exceeds iron intake
for a time long enough to deplete the body’s iron stores, insuf-
ficient iron is available for normal Hgb production. Iron defi-
ciency is characterized by hypochromic microcytic anemia.98
The average American diet contains 10 to 15 mg of iron per
day, of which 10% is absorbed via the stomach, 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.45 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
BOX 7.3  Causes of Iron Deficiency
•  eficient diet
D
• Decreased absorption
• Increased requirements
• Pregnancy
• Lactation
• Blood loss
• Gastrointestinal
• Menstrual
• Blood donation
• Hemoglobinuria
• Iron sequestration
Data from McPhee SJ, Papadakis MA, Tierney LM. Current Medical Diagnosis
and Treatment. 46th ed. New York: McGraw-Hill Medical; 2007.

less than 10 mcg/L is diagnostic of iron-deficiency anemia.
Often iron-deficiency anemia is asymptomatic if the onset is
insidious.16,99,100 Signs and symptoms of iron-deficiency anemia
include the following78,98:
• Easy fatigability, tachycardia, palpitations, and dyspnea on
exertion
• Dizziness, headache, and irritability
• Dysphagia (Plummer-Vinson syndrome, formation of esoph-
ageal webs)
• Softening and spoon-shaped nails (koilonychias); pale ear-
lobes, palms, and conjunctivae (severe anemia)98
• Pica, which is the craving to eat unusual substances, such as
dirt or ice
Management of iron-deficiency anemia consists of a medi-
cal workup to identify the site of possible blood loss, as well as
iron supplementation and nutritional counseling.19,95,97,101 Iron
supplementation during pregnancy is almost always required.45  supplementation.101
Vitamin B12 Anemia.  Decreased levels of vitamin B12 cause
the production of macrocytic, normochromic RBCs. Vita-
min B12 deficiency is commonly caused by poor absorption
of vitamin B12 as a result of enteritis or iliac disease. It is less
commonly associated with Crohn’s disease and pancreatic insuf-
ficiency. Because 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 B12.45 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 great-
er than normal amounts of bilirubin in the blood)102
• Anorexia and diarrhea
• Oral ulceration
Neurologic symptoms may also present themselves in dif-
ferent stages of the deficiency. Early neurologic symptoms
include decreased vibratory sensation, loss of proprioception,
and ataxia.103 Later involvement results in spasticity, hyperac-
tive reflexes, and a positive Romberg’s sign. These neurologic
symptoms result from the formation of a demyelinating lesion
of the neurons of the spinal cord and cerebral cortex.78 Neu-
rologic symptoms are reversible if the onset was less than 6
months ago.63
Vitamin B12 deficiency is diagnosed on the basis of clini-
cal presentation, low serum vitamin B12 levels, elevated lactate
dehydrogenase and MCV values, and positive urine sampling
(Schilling’s test). Management of vitamin B12 anemia con-
sists of lifelong vitamin B12 supplementation and nutritional
counseling.19,95,97
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.  
Vascular System and Hematology     CHAPTER 7 193
Folic Acid Anemia.  A decrease in folic acid (folate) level
causes the production of macrocytic, normochromic RBCs.
The most common cause of folic acid deficiency is inadequate
dietary intake. Pregnant women, patients with alcoholism or
anorexia, those who do not eat fresh produce and those who
overcook their food are candidates for folate deficiency.101
The common occurrence of folic acid deficiency during the
growth spurts of childhood and adolescence and during the
third trimester of pregnancy is explained by the increased
demands for folate required for DNA synthesis in these cir-
cumstances.30 The presentation of folic acid anemia is similar
to that of vitamin B12 deficiency anemia, except that there
are no neurologic sequelae in folic acid anemia. Folic acid
anemia is diagnosed on the basis of clinical presentation, a
low serum folate level, and elevated lactate and MCV val-
ues.104 Management of folic acid anemia consists of folic acid
 
Aplastic Anemia.  Aplastic anemia is characterized by a
decrease in 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 pro-
duce RBCs, or alters the stem cell environment, which inhibits
RBC production. The exact mechanism of stem cell damage is
unknown; however, present theories include exposure to radia-
tion and chemotherapy or pharmacologic agents, the presence of
infection or malignancy, or an autoimmune response.105 RBCs
are normochromic and normocytic or macrocytic. WBC and Plt
counts are also decreased. The hallmark of aplastic anemia is
pancytopenia.45 Definitive diagnosis is made with bone marrow
biopsy. Signs and symptoms of aplastic anemia may include the
following:
• Bleeding, which is the most common symptom (easy bruis-
ability, gum bleeds, nose bleeds, petechiae, hematuria, heavy
menstrual flow, fecal blood)
• Fatigue and dyspnea
• Pallor on the mucosal membranes and palmar surfaces
• Fever or infection
• Sore throat
Management of aplastic anemia may include any of the fol-
lowing: investigation and removal of causative agent, RBC
and Plt transfusion, immunosuppression, bone marrow trans-
plantation and peripheral stem cell transplantation, cortico-
steroids, and antibiotics. Aplastic anemia can be fatal if untre
ated.9,19,45,95,97,98,106 
Hemolytic Anemia.  Hemolysis is the destruction or removal
of RBCs from the circulation before completion of 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.107 This condition is usually the result of an inherited
defect of the RBC membrane or structure, but it can be an auto-
immune process in which antibodies in the blood cause RBC
destruction through mononuclear phagocytosis.
194 CHAPTER 7     Vascular System and Hematology
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 of a genetic enzyme
deficit, attack of oxidants on RBCs, or infection. It may also
occur traumatically when RBCs are torn apart at sites of blood
flow turbulence, 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 (intravascular only)
Management of hemolytic anemia may include any of the
following: investigation and removal of the causative fac-
tor, fluid replacement, blood transfusion, corticosteroids, or
splenectomy.19,95,97  characterized by abnormal formation of Hgb chains in RBCs,
Sickle Cell Anemia.  Sickle cell anemia is an autosomal homo-
zygous (Hgb SS or HgSS) recessive trait characterized by RBCs
that become sickle (crescent) shaped when deoxygenated. Over
time, cells become rigid and occlude blood vessels, thus causing
tissue ischemia and infarction. The risk of cerebrovascular acci-
dent and infarction of other organs or muscles is high. Symp-
toms 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 usually nociceptive [secondary to tis-
sue damage] and is sharp and throbbing in nature.108)
A complication of sickle cell anemia that may require hospi-
talization is pain crisis, which is intense pain in any major organ
or body area. Pain crisis is usually treated with parenteral opi-
oids.108 Lasting from 4 to 6 days to weeks, pain crisis can be
precipitated by infection, dehydration, hypoxia, sleep apnea,
exposure to cold, or menstruation, or it may be of unknown
etiology.109
CLINICAL TIP
Tachycardia may be the first change observed when monitor-
ing vital signs during sickle cell crisis, usually accompanied by
a sense of fatigue, generalized weakness, loss of stamina, and
exertional dyspnea.30
Acute chest syndrome (ACS) is a pulmonary manifestation and
is an emergent situation that requires hospitalization. ACS may
be caused by intrapulmonary sickling, sickle cell emboli, or bone
marrow or fat embolism or by infection.110 The patient presents
with chest pain, dyspnea, hypoxemia, and infiltrates on chest x-ray,
perhaps with pleural effusion.110 ACS is currently defined as a new
infiltrate seen on the chest radiograph, in association with one or
more symptoms, such as fever, cough, sputum production, tachy-
pnea, dyspnea, or new-onset hypoxia.111 ACS is the leading cause of
death in adolescents and adults with sickle cell disease.21
Management of sickle cell anemia may include the prevention or
supportive treatment of symptoms with rest; hydration; analgesia;
supplemental oxygen; incentive spirometry; use of corticosteroids
or cytotoxic agents, such as hydroxyurea70; partial RBC exchange;
and psychosocial support.19,95,97,105,111 The average life expectancy
of a patient with sickle cell anemia is 40 to 50 years.101 Note that
sickle cell anemia is different from sickle cell trait. A patient with
sickle cell trait has a heterozygous trait of Hgb that is asymptom-
atic, without the signs and symptoms of anemia, although RBCs
may sickle under the conditions of high altitude, strenuous exer-
cise, or anesthesia.105 No treatment is usually necessary; however,
genetic counseling is a reasonable strategy.45 
Thalassemia.  Thalassemia is an autosomal recessive disease
resulting in RBC membrane damage and abnormal erythropoi-
esis and hemolysis.
Hgb is composed of two alpha and two beta chains.
α-Thalassemia is a defect in alpha-chain synthesis in which
one (alpha trait), two (α-thalassemia minor), or three (Hgb H
disease) genes are altered. Each type of α-thalassemia varies in
presentation from a lack of symptoms (alpha trait and minor)
to chronic severe hemolytic anemia (Hgb H).100 β-Thalassemia
minor is a defect in beta-chain synthesis in one of two beta chains
and is usually asymptomatic. β-Thalassemia major is a severe
reduction or absence in beta-chain production that results in
severe anemia, growth failure, bony deformities, hepatospleno-
megaly, and jaundice, causing a reduced life expectancy of 20 to
30 years as a result of complications of heart failure, cirrhosis,
and endocrinopathy.101
Patients with thalassemia are classified as having thalassemia
minor, thalassemia intermedia, or thalassemia major, depending
on the severity of their anemia. Patients with thalassemia minor
generally have little or no hematologic disease. Patients with
thalassemia intermedia may require occasional transfusions.
Patients with thalassemia major require lifelong chronic RBC
transfusion to maintain adequate Hgb levels.66
Management of thalassemia may include folate supple-
mentation, blood transfusion, iron-chelating agents, and
splenectomy.101
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 of chronic dis-
ease (ACD) designates an anemia syndrome typically found in
patients with chronic infections, inflammatory disorders, or
neoplastic disorders. ACD occurs in approximately 50% of hos-
pitalized patients, as identified by laboratory studies. ACD has
also been observed in acute trauma and critical care patients.
The clinical features are those of the causative condition. The
diagnosis should be suspected in patients with chronic diseases

and is confirmed by low serum levels, low total iron-binding
capacity, and normal or increased serum ferritin.
In most cases, no treatment is necessary. Purified recombinant
erythropoietin is effective in the treatment of anemia of renal fail-
ure or anemia related to cancer and inflammatory conditions.98  tropenia is considered mild (ANC between 1000 and 1500/μL),
Polycythemia.  Polycythemia is a chronic disorder charac-
terized by excessive production of RBCs, Plts, and myelocytes.
As these increase, blood volume, blood viscosity, and Hgb con-
centration increase, causing excessive workload for the heart and
congestion of some organs.21 The three types of polycythemia
are primary polycythemia (polycythemia vera), secondary polycythemia,
and relative polycythemia. Primary polycythemia, or polycythemia
vera, is an acquired myeloproliferative disorder,45 which causes
an increase in the number of RBCs, WBCs, and Plts.112 The ori-
gin of this disease is unknown; however, there is an autonomous
overproduction of erythroid stem cells from bone marrow, lead-
ing to increased blood viscosity and expanded blood volume.
Thus there is a risk for thrombus formation and bleeding.101
Primary polycythemia may convert to chronic myelogenous leu-
kemia or myelofibrosis. The hallmark of polycythemia vera is
Hct levels above normal, at times greater than 60%.45 Secondary
polycythemia is the overproduction of RBCs as a result of 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 hepa-
toma or cerebellar hemangioblastoma)100 or chronic low oxy-
genation 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.
Relative polycythemia is the temporary increase in RBCs second-
ary to decreased fluid volume (dehydration), resulting from exces-
sive vomiting, diarrhea, excessive diuretic use, or a burn injury.
Signs and symptoms of polycythemia may include48:
• Headache, dizziness, blurred vision, and vertigo, all result-
ing from hypervolemia
• Venous thrombosis, resulting from hyperviscosity
• Bleeding from the nose, gastrointestinal bleeding, and spon-
taneous bruising, all resulting from Plt 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 the
blood volume and decrease Hct to 45%. Every 2 to 4 days, 250
to 500 mL of blood is removed, depending on the age of the
patient, with the goal of bringing the Hct level to less than 42%
for females and less than 45% for males.21,64 Other treatments
used in polycythemia are myelosuppressive therapy (hydroxy-
urea); interferon30; antiplatelet therapy (aspirin); radiophospho-
rus (for primary polycythemia); smoking cessation; and fluid
resuscitation (for relative polycythemia).  Management of DIC may include treatment of the causative
Leukocytic Disorders
Neutropenia.  Neutropenia is defined as an absolute neu-
trophil count (ANC) of less than 1500/μL and is calculated
from the WBC differential ANC = WBC (cells/μL) × percent
Vascular System and Hematology     CHAPTER 7 195
(polymorphonuclear neutrophils + bands) ÷ 100.113 A variety of
bone marrow disorders (e.g., leukemia) and non–bone marrow
conditions (e.g., immunologic peripheral destruction, sepsis, or
hypersplenism) or chemotherapy may cause neutropenia. Neu-
moderate (ANC between 500 and 1000/μL), or severe (ANC
less than 500/μL).114 The risk of infection, typically bacterial, is
related to the severity of the neutropenia, with the risk of infec-
tion increasing at 1000/μL.114 The usual signs of inflammatory
responses to infection may be absent in a neutropenic patient;
however, fever in a patient with neutropenia should always be
assumed to be of infectious origin. Refer to Chapter 14 for more
information on neutropenia.
Medical therapy consists of symptomatic management
of fever, discontinuation of causative drugs, broad-spectrum
antibiotics or antifungal agents to treat infection, good den-
tal hygiene, the administration of myeloid growth factor, and
hematopoietic cell transplantation.45,114 
Coagulation Disorders
Disseminated Intravascular Coagulation. DIC involves
the introduction of thromboplastic substances into the circu-
lation that initiate a massive clotting cascade accompanied by
fibrin, plasmin, and Plt activation. It is a complex and para-
doxical disorder characterized by both hemorrhage and throm-
bus formation (Table 7.19). First, fibrin is deposited in the
microcirculation, leading to organ ischemia and the destruc-
tion of RBCs as they pass through these deposits. Second, Plts
and clotting factors are consumed and hemorrhage occurs.
Plasmin is activated to further decrease clotting factor, and
fibrin further inhibits Plt function, which further increases
bleeding.
DIC, either acute or chronic, is always a secondary process
mediated by inflammatory cytokines.115 DIC may be mild and
self-limiting or may be severe and is often associated with critical
illness.116 The onset of acute DIC usually occurs in the presence
of illness within hours or days of the initial injury or event. 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.100
Organ failure is common.6 Chronic DIC is associated with hem-
angioma 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
The diagnostic workup for DIC includes Plt count (throm-
bocytopenia), PT and activated PTT (aPTT) (prolonged),
INR (elevated), fibrinogen level (decreased), and presence of
d-dimer.117 The d-dimer test has high sensitivity and specific-
ity for diagnosing DIC.6
condition; hemodynamic and cardiovascular support, which
includes fluid management, oxygen supplementation, and inva-
sive monitoring; blood and blood product transfusion for active
bleeding; heparin therapy (this is controversial); and recombi-
nant protein factor therapy (experimental).21,115
196 CHAPTER 7     Vascular System and Hematology
TABLE 7.19  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.
CLINICAL TIP
Inflate the blood pressure cuff only as high as needed to obtain
a reading. Frequent blood pressure readings may cause bleeding
under the cuff, particularly in patients with thrombocytic disor-
ders, so rotate arm use to reduce repeated trauma.
 
Hemophilia. Hemophilia is a disease characterized by exces-
sive spontaneous hemorrhaging at the mucous membranes, into
the joint spaces (hemarthrosis) and muscles, or intracranially. It
is the result of a genetic deficiency of a clotting factor. There are
four basic types118:
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.101
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 characteristic of the disease. Muscle hemorrhages can
be more insidious and massive than joint bleeding and most
often involve the flexor muscle groups.30 Bleeding into joints
accounts for approximately 75% of bleeding episodes in severely
affected patients with hemophilia A.119 The knee is the most
frequently affected joint, followed by the ankle, elbow, hip,
shoulder, and wrist. Joints with at least four bleeds in 6 months
are called target joints. When blood is introduced into the joint,
the joint becomes distended, causing swelling, pain, warmth,
and stiffness.30 In seriously affected patients, major hemor-
rhages may dissect through tissue planes, ultimately leading
to compromise of vital organs. However, bleeding episodes are
intermittent, and some patients do not experience any hemor-
rhage for weeks or months.120
Symptoms and physical findings of bleeding episode from
hemophilia may include:
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
• P etechiae, purpura, and ecchymosis
• Hematoma (Intramuscular hematomas are common in he-
mophilia A, bleeding into the psoas muscle is common, and
femoral nerve involvement may be partial or complete.121)
• Disorientation
• Convulsions
• Tachycardia, tachypnea, and hypotension
• Intracranial bleeding, which is the major cause of death for
all age groups of patients with hemophilia6
• Pain
CLINICAL TIP
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. A large
iliopsoas hemorrhage can cause displacement of the kidney and
the ureter and can compress the neurovascular bundle. Iliopsoas
bleeds are considered a medical emergency requiring immediate
physician referral.30
Patients with acute hemarthrosis have pain, with objective
findings of warmth, a tense effusion, tenderness, and limitation of
motion, and the joint is usually held in flexion. Acute hemarthro-
sis of the knee is a common complication of hemophilia (Fig. 7.7).
It may be confused with acute infection unless the patient’s coagu-
lation disorder is known. Patients with subacute or chronic arthri-
tis (related to hemophilia) have chronically swollen joints, which
are usually painless and slightly warm to touch.122 Repeated hem-
arthrosis causes joint deformity and radiologic changes.
Management of hemophilia may include any of the follow-
ing: methods to stop active bleeding (e.g., direct pressure);
supportive therapy, depending on the location of the bleed
(e.g., joint debridement); factor replacement therapy; and pain
management.105
CLINICAL TIP
Watch for signs of joint effusion (warmth and edema) in patients
with hemophilia who are prone to hemarthrosis, especially dur-
ing weight-bearing activities.
 
Thrombocytopenia. Thrombocytopenia is an acute or
chronic decrease in the number of Plts (less than 150,000/μL)
in the circulation. It can result from decreased Plt production

FIG. 7.7
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.)
(caused by infection, drug or immune responses, or blood
vessel damage), increased Plt destruction (caused by malig-
nancy, antiplatelet antibodies, or the use of myelosuppressive
drugs), or altered Plt distribution (caused by cardiac sur-
gery–induced hypothermia, portal hypertension, or spleno-
megaly).118 Signs and symptoms of thrombocytopenia may
include123:
• 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 cranial bleeding is
present
• Renal failure
• Splenomegaly
Management of thrombocytopenia may include treatment
of the causative factor; immunosuppressive therapy; anticoagu-
lants in plasma transfusion or plasmapheresis; corticosteroids;
or splenectomy.118
Physical Therapy Considerations.  A physical therapist
should implement fall precautions during all physical ther-
apy interventions for the patient who has thrombocytopenia;
patients should also be educated about the fall risk precau-
tions and the potential for bleeding with activity.
Blood pressure cuffs and similar devices must be used with
caution. Elastic support stockings must be thigh high, never
knee high. Mechanical compression with a pneumatic pump
and soft tissue mobilization are avoided unless approved by a
physician.30  an immunoglobulin G (IgG) autoantibody is formed and binds
Heparin-Induced Thrombocytopenia. Heparin-induced
thrombocytopenia (HIT) is the most common type of drug-
induced thrombocytopenia and one of the most common causes
of thrombocytopenia in hospitalized patients.45 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 include124:
• Large, bilateral lower-extremity DVT
• Upper-extremity DVT at a venous catheter site
• Skin lesions at the injection site
• Aortic or ileofemoral thrombus with limb ischemia
• PE
• An acute systemic reaction to heparin
Vascular System and Hematology     CHAPTER 7 197
HIT may be type I (the asymptomatic aggregation of Plts)
or type II (an immune response resulting in Plt activation
and venous or arterial thrombi).125 Type I is more common
than type II, and type II is associated with greater risk of life-
threatening thrombosis.126 HIT is diagnosed on the basis of
clinical presentation, a Plt count less than 100 × 109/L, and
a positive Plt aggregation test. Heparin-PF 4 antibody test-
ing is recommended for patients suspected to have HIT.127
Management of HIT starts with the immediate discontinu-
ation of heparin and initiation of fast-acting, nonheparin
alternative anticoagulation. The direct thrombin inhibitors
argatroban, lepirudin, and bivalirudin are nonheparin anti-
coagulants that inhibit thrombin without interaction with
heparin-PF4 antibodies.127 Management of HIT also includes
plasmapheresis and immunoglobulin therapy, in addition
to supportive therapies for alteration in skin integrity and
pain.125 
Thrombotic Thrombocytopenic Purpura. Thrombotic
thrombocytopenic purpura (TTP) is the rapid accumulation
of thrombi in the small blood vessels. TTP is primarily seen
in young adults 20 to 50 years of age.101 The etiology of TTP
is unknown. It is associated with bacterial or viral infections,
estrogen use, certain drug use, pregnancy, and autoimmune
disorders, such as acquired immunodeficiency syndrome
(AIDS).101 The diagnosis of TTP is made by thrombocytope-
nia, anemia, and elevated serum lactate dehydrogenase. The
coagulation tests are normal.45 Signs and symptoms of TTP
may include:
• Hemolytic anemia, thrombocytopenia
• Fatigue and weakness
• Fever
• Pallor, rash, petechiae
• Waxing and waning headache, confusion, altered conscious-
ness from lethargy to coma
• Hemiparesis and seizures
• Abdominal pain and tenderness caused by pancreatitis
• Acute renal failure
Management of TTP may include emergent large-volume
plasmapheresis, plasma exchange, antiplatelet agents, corti-
costeroids, immunosuppressive agents, or splenectomy if not
refractory to initial therapy or if the condition recurs.101 
Idiopathic Thrombocytopenic Purpura. Idiopathic throm-
bocytopenic purpura (ITP) is an autoimmune disorder in which
to the Plts. Plts are not destroyed by direct lysis; rather, destruc-
tion takes place in the spleen without subsequent enlargement
(splenomegaly). An enlarged spleen should lead one to doubt a
diagnosis of ITP.
Patients are systemically well and usually not febrile. The
hallmark of the disease is thrombocytopenia. Bone marrow
appears normal, and coagulation study results will be entirely
normal.
The common symptoms are of bleeding and include epi-
staxis, oral bleeding, menorrhagia, purpura, and petechiae.
Most patients will require treatment, but some patients will
experience spontaneous remissions. Treatment is usually with
corticosteroids, most commonly prednisone and, in some cases,
198 CHAPTER 7     Vascular System and Hematology
TABLE 7.20  Stages of Lymphedema
Stage 0: Lymph transport capacity is reduced
Preclinical No clinical edema is present; however,
(Latent patients may begin to feel heaviness or
lymphedema) ­fullness in limb
Stage 1 Accumulation of protein-rich pitting edema
Reversible with elevation; area affected may
be normal size on waking in the morning
Increases with activity, heat, and humidity
Stage 2 Accumulation of protein-rich nonpitting
edema with connective scar tissue
Irreversible; does not resolve overnight;
minimal pitting despite increased swelling
Clinical fibrosis is present
Skin changes present in severe stage 2
Stage 3: Accumulation of protein-rich edema with
Lymphostatic significant increase in connective tissue and
elephantiasis scar tissue
Severe nonpitting fibrotic edema
Atrophic changes (hardening of dermal tissue,
skin folds, skin papillomas, and hyperkera-
tosis)
Data from Goodman CC. The hematologic system. In: Goodman CC, Boison-
nault WG, eds. Pathology: Implications for the Physical Therapist. 3rd ed. Philadel-
phia: Saunders; 2009; O’Sullivan SB, Schmitz TJ, Fulk GD. Physical Rehabilita-
tion. 6th ed. Philadelphia: FA Davis; 2014:594.
immunoglobulins. Splenectomy is the most definitive treat-
ment for ITP, and most patients will ultimately undergo sple-
nectomy. Plt transfusions are rarely used in the treatment of ITP
because exogenous Plts will survive no better than the patient’s
own and will usually last less than a few hours.45 
Lymphatic Disorders
Lymphedema
Lymphedema is a chronic disorder characterized by an abnor-
mal 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 sys-
tem. Lymphedema can be classified as primary or secondary.
Primary (idiopathic) lymphedema is caused by a condition that
is congenital or hereditary. In this case, the lymph node or
the lymph vessel formation is abnormal. Secondary (acquired)
lymphedema is caused by injury to one or more components
of the lymphatic system in some other manner. When part
of the lymphatic system is blocked, dissected, fibrosed, or
damaged, lymphedema can develop in any part of the body
or limb(s). The severity of lymphedema is graded by using
the scale from the International Society of Lymphology, as
described in Table 7.20. Signs and symptoms of lymphedema
include:3,29
• 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 nonpitting edema in later
stages, when fibrotic changes occur
• Fatigue and heaviness, pressure, tightness, tingling, and numb-
ness in the affected region—causing tremendous discomfort
• F ibrotic changes in the skin
• Increased circumferential limb girth
• Loss of ROM
Diagnosis of lymphedema can be made without the use of
special diagnostic tests (refer to the Lymphatic Evaluation sec-
tion for more details). When evaluating a patient with suspected
lymphedema, cardiac, renal, thyroid, and arteriovenous diseases
must be ruled out medically. Management includes manual
lymphatic drainage (MLD) and lymphedema bandaging. Early
intervention is of significance.
The physical therapist should have special training to treat this
patient population. MLD is a specialized manual therapy technique
that primarily affects the superficial lymphatic circulation. MLD
improves lymph transport capacity, redirects lymph flow toward
the collateral vessels, and mobilizes the excess lymph fluid.
CLINICAL TIP
Patients, particularly those with primary lymphedema of the
lower extremities, should be evaluated for abdominal and gen-
ital edema before they undergo any treatment to reduce the
extremity lymphedema to avoid the complication of moving
more fluid to an already overloaded abdominal area.30
Lymphedema bandaging is a highly specialized form of ban-
daging that uses multiple layers of unique padding materials
and short stretch bandages to create a supportive structure for
edematous and lymphedematous body segments. It is com-
monly used in between the MLD treatments.3 
Management
The management of vascular disorders includes pharmacologic
therapy and vascular surgical procedures. Hematologic disor-
ders may be managed with pharmacologic 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 Chapter 19, Table 19.2)
• Antiplatelet agents (see Chapter 19, Table 19.4)
• Thrombolytic agents (see Chapter 19, Table 19.7)
• Colony-stimulating factors (Chapter 19, Table 19.26) 
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,128 according to the values in Table 7.21.
Physical Therapy Considerations
The physical therapist should understand some basic concepts of
anticoagulation therapy to intervene safely and to estimate the
length of hospital 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.

TABLE 7.21  Therapeutic Values for International
Normalized Ratio (INR)
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
Data from Goldman L, Ausiello D. Cecil Textbook of Medicine. 24th ed. St. Louis:
Saunders; 2012 Gibbar-Clements T, Shirrell D, Dooley R, et al. The challenge
of warfarin therapy. Am J Nurs. 2000;100:38-40.
• P T/INR is insensitive to measuring the anticoagulation af-
fect for LMWH.82
• The therapeutic effect of heparin or LMWH is reached with-
in minutes or hours, whereas the effect of warfarin is reached
in 3 to 5 days; thus heparin or LMWH is usually prescribed
before warfarin. The dose of heparin or LMWH is increased
or decreased, depending on the PTT goal, then the patient is
transitioned to warfarin, as indicated.
• The term subtherapeutic level implies a coagulation level below
the anticoagulation goal. A subtherapeutic PT/INR or PTT
indicates a risk for thrombus formation, whereas a superther-
apeutic level indicates a risk for hemorrhage.
• The term supertherapeutic level implies a coagulation level
above the anticoagulation goal. Supertherapeutic antico-
agulation is rapidly reversed by vitamin K or fresh-frozen
plasma.
• Anticoagulant agents are temporarily discontinued before
surgery to minimize bleeding intraoperatively or postopera-
tively.
• The physical therapist should always monitor the patient
who is taking anticoagulants for signs and symptoms of
bleeding, as bleeding can occur even if the PT/INR is thera-
peutic.128
• The physical therapist should review fall risk education with
patients who are on anticoagulant agents.  and Hct to increase.59
Blood Product Transfusion
Blood and blood products are transfused to replenish blood vol-
ume, maintain oxygen delivery to tissues, or maintain proper
coagulation.129 The need for blood transfusion should be depen-
dent on the patient’s symptoms. It has been reported that refrig-
erated, banked blood loses its ability to deliver oxygen in a short
period.130 Table 7.22 lists the most common transfusion prod-
ucts 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 name of the
substance to be given must be typed and then crossed off after
administration. This process ensures that the correct type of
blood is given to a patient to avoid adverse reactions. A variety
Vascular System and Hematology     CHAPTER 7 199
of transfusion reactions can occur during or after the adminis-
tration of blood products (Table 7.23). These blood transfusion
reactions are usually not fatal, but they can extend a patient’s
length of hospital stay. Blood transfusions are a form of liquid
tissue transplantation, which can cause significant immuno-
suppression. This effect is known as transfusion-related immuno-
modulation (TRIM), and it happens every time a patient receives
blood. Transfusion reactions can be nonimmunologic and are
caused by the physical and chemical properties of the transfused
blood.131 There is a risk of transmission of infectious diseases via
blood transfusion.130
In addition to these reactions, complications of blood trans-
fusion include air embolism (if the blood is pumped into the
patient) or circulatory overload (from a rapid increase in vol-
ume). Circulatory overload occurs when the rate of blood (fluid)
transfusion is greater 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, HIV type 1
infection, or delayed hemolytic reaction (approximately 7–14
days posttransfusion).132
Physical Therapy Considerations
• If the patient is receiving blood products, the physical thera-
pist should observe the patient for signs or symptoms, or
both, of transfusion reaction before initiating physical thera-
py intervention.
• Depending on the medical status of the patient, the therapist
may defer out-of-bed or vigorous activities during the trans-
fusion. If medically stable, the patient may be appropriate to
mobilize during or following the completion of the transfu-
sion.
• Defer physical therapy intervention during the first 15 min-
utes of a blood transfusion because most blood transfusion
reactions occur within this time frame.
• During a blood transfusion, vital signs are usually taken ev-
ery 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
 
Vascular Surgical Procedures
Surgical management of coronary vascular disorders, such as
angioplasty, arthrectomy, and stent placement, is described in
Chapter 3 under Percutaneous Revascularization Procedures.
These same techniques are also used in peripheral arteries,
rather than coronary arteries. This section therefore concentrates
on embolization therapy, transcatheter thrombolysis/thrombec-
tomy, endarterectomy, bypass grafting, and aneurysm repair and
replacement with synthetic grafts. Endovascular procedures are
becoming more and more common in patients with peripheral
arterial disease. The basic concept of most endovascular proce-
dures is to obtain percutaneous access to a blood vessel and then
to gain access across the lesion (either stenosis or aneurysm) with
a guidewire.133 
200 CHAPTER 7     Vascular System and Hematology

TABLE 7.22  Common Blood Products and Their Clinical Indications and Outcomes
Product Content Clinical Indications Outcome
Whole blood Blood cells and plasma Acute major blood loss in setting of hypotension, tachy- Resolution of signs and symptoms
cardia, tachypnea, pallor, and decreased Hct and Hgb. of hypovolemic shock or anemia.
To treat oxygen-carrying deficit (RBC) and volume expan- Hct should increase 3% in a
sion (plasma). nonbleeding adult (per unit
When more than 10 units of blood are required in a 24- transfused).
hour period.
Whole blood is rarely used.
Red blood cells RBCs only Acute or chronic blood loss. Resolution of signs and symptoms
(RBCs) To treat oxygen-carrying deficit in setting of tachycardia, of anemia.
tachypnea, pallor, fatigue, and decreased Hct and Hgb. Hct should increase 3% in a
Anemia without need for volume expansion. nonbleeding adult (per unit
transfused).
Platelets (Plts) Concentrated Plts in To restore clotting function associated with or after blood loss. Resolution of thrombocytopenia.
plasma To increase Plt count in a bleeding patient with Plt <100,000, Prevention or resolution of bleeding.
in advance of a procedure with Plt <50,000, or prophylacti- Plts should increase by 5000 in a
cally with Plt <10,000. 70-kg adult (per unit).
Fresh-frozen All plasma components, To replace or increase coagulation factor levels. Improved or adequate coagulation
plasma (FFP) namely blood factors Acute disseminated intravascular coagulation. levels or factor assays.
and protein Thrombotic thrombocytopenic purpura. One unit of FFP should increase the
Factor XI deficiency. level of any clotting factor by 2%
Liver disease. to 3%.
Rapid reversal of warfarin therapy.
Albumin Albumin cells with few Volume expansion in situations when crystalloid (saline Acquire and maintain adequate
globulins and other or Ringer’s lactate) is inadequate, such as shock, major blood pressure and volume sup-
proteins hemorrhage, or plasma exchange. port.
Acute liver failure.
Burn injury.
Plasma protein Albumin, globulins, and See Albumin, above. See Albumin, above.
fraction (PPF) plasma proteins
Cryoprecipitate Factors VIII and XIII, Replacement of these factor deficiencies. Correction of these factor or fibrino-
von Willebrand’s fac- Replacement of fibrinogen when an increase in volume gen deficiencies.
tor, and fibrinogen in would not be tolerated with FFP. Cessation of bleeding in uremic
plasma Bleeding associated with uremia. patients.
Hct, Hematocrit; Hgb, hemoglobin.
Data from U.S. Department of Health and Human Services, National Institutes of Health. National Blood Resource Education Programs Transfusion Therapy Guidelines for
Nurses. Bethesda, MD: NIH; September 1990; Churchill WH. Transfusion therapy. Sci Am Med. 2001;4; Linker CA. Blood. In: McPhee SJ, Papadakis MA. Current
Medical Diagnosis and Treatment. 46th ed. New York: McGraw Hill; 2007; Rosenthal K. Avoiding bad blood: Key steps to safe transfusions. Nursing Made Incredibly
Easy! 2004;2(5):20-28.

Embolization Therapy
Embolizationa therapy is the process of purposely occluding
a vessel with Gelfoam, coils, balloons, polyvinyl 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.
Indications for embolization therapy include disorders char-
acterized by inappropriate blood flow, such as AVMs or, less
commonly, persistent hemoptysis. Complications of emboliza-
tion therapy include tissue necrosis, inadvertent embolization of
aThe
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 therapeu-
tic procedure described in this section. The context in which embolization
is discussed must be considered to avoid confusion.
normal tissues, and passage of embolic materials through arte-
riovenous communications.44 
Transcatheter Thrombolysis and/or Thrombectomy
Transcatheter thrombolysis is the process of directly infusing
thrombolytic agents, such as urokinase and tissue plasminogen
activator (tPA), into occluded vessels. The indications for this
procedure include lysis of clot in thrombosed bypass grafts,
acute carotid occlusions, and acute or chronic peripheral arterial
ischemia. Patients with an acute thrombotic arterial occlusion
are considered ideal candidates for lytic therapy.134 The tip of
the catheter is introduced into the center of the thrombus, and
a low dose of thrombolytic agent is administered. The catheter
is left in place for extended periods of time to allow for the clot
to lyse properly.135 This procedure may also include angioplasty,
if warranted, to open a stenotic area. By injecting the thrombo-
lytic agent into the area of occlusion, transcatheter thrombolysis
 Vascular System and Hematology     CHAPTER 7 201

TABLE 7.23  Acute Adverse Blood Reactions

Reaction Cause Signs and Symptoms Onset
Febrile reaction Patient’s blood (antileukocyte antibod- Chills followed by low-grade fever, headache, During transfusion or
ies) is sensitive to transfused plasma nausea and vomiting, flushed skin, muscle up to 24 hours after
protein, Plts, or white blood cells. pain, anxiety (mild). transfusion
Hypotension, tachycardia, tachypnea, cough
(severe).
Allergic reaction Patient’s blood (IgE, IgG, or both) is Hives, flushed or itchy skin, and bronchial Within minutes of
sensitive to transfused plasma protein. wheezing (mild). starting transfusion
Tachypnea, chest pain, cardiac arrest (severe).
Septic reaction Transfused blood components are con- Rapid onset of high fever, hypotension, chills, Within minutes to 30
taminated with bacteria. emesis, diarrhea, abdominal cramps, renal minutes after transfusion
failure, shock.
Acute hemolytic Patient’s blood and transfused blood are Fever with or without chills is the most Within minutes to hours
reaction not compatible, resulting in red blood common manifestation. after transfusion
cell destruction. Tachycardia, hypotension, tachypnea,
cyanosis, chest pain, headache or backache,
acute renal failure, cardiac arrest.
Anaphylactic reaction Patient is deficient in IgA and develops Hives (mild). Within a few seconds of
IgA antibody to transfused compo- Wheezing or bronchospasm, anxiety, cyanosis, starting transfusion
nents. nausea, emesis, bloody diarrhea, abdominal
cramps, shock, cardiac arrest (severe).
Transfusion-related Transfusion of antibodies in donor Chills, fever, chest pain, hypotension, cyano- Within several hours after
acute lung injury plasma is reactive with recipient granu- sis; chest radiograph shows florid pulmo- transfusion
locytes. nary edema.
Ig, Immunoglobulin.
Data from Linker CA. Blood. In: Tierney LM, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment. Stamford, CT: Appleton & Lange; 2001:505-558;
Kozier B, Erb G, Blais K, et al., eds. Fundamentals of Nursing: Concepts, Process and Practice. 8th ed. Redwood City, CA: Benjamin-Cummings; 2007:110; Larison PJ, Cook
LO. Adverse effects of blood transfusion. In: Harmening DM, ed. Modern Blood Banking and Transfusion Practices. Philadelphia, PA: FA Davis; 1999; U.S. Department
of Health and Human Services, National Institutes of Health. National Blood Resource Education Programs Transfusion Therapy Guidelines for Nurses. Bethesda, MD: NIH;
September 1990.

has fewer systemic complications of hemorrhage compared with
intravenous infusion of thrombolytic agents.17 The major risk
for thrombolytic therapy is bleeding.64
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
devices/catheters are used: “contact” and “noncontact” devices.
The contact catheters 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.134  • Infection
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 por-
tion of the saphenous vein or with a synthetic material, such as
Gore-Tex, Dacron, or Lycra. (This graft is referred to as a pros-
thetic graft). Vascular surgeons generally describe and illustrate
in the medical record what type of procedure was performed
on the particular vascular anatomy. The terminology used to
describe each bypass graft procedure indicates which vessels
were involved (e.g., a fem-pop [femoropopliteal] bypass graft
involves bypassing an occlusion of the femoral artery with
another conduit to the popliteal artery distal to the area of occlu-
sion). After a bypass procedure, patients require approximately
24 to 48 hours to return to hemodynamic stability (dependent
on premorbid physiologic status and extent of surgery). Patients
are usually monitored in an intensive care unit setting. Figs. 7.8
and 7.9 illustrate different types of vascular bypass procedures.
Complications that can occur after bypass grafting include
the following34:
• Hemorrhage (at graft site or in gastrointestinal tract)
• Thrombosis
• Pseudoaneurysm formation at the anastomosis
• 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 correct localized occlusive
vascular disease, commonly in the carotid arteries, eliminating
the need for bypassing the area.44
CLINICAL TIP
The abbreviation CEA is often used to refer to a carotid endar-
terectomy procedure.
 
202 CHAPTER 7     Vascular System and Hematology

A B C

D E F
FIG. 7.8
Peripheral arterial bypass procedures. (A) Aortoiliac bypass. (B) Aortobifemoral bypass. (C) Axillobifemoral bypass. (D) Femorofemoral bypass. (E) Femo-
ropopliteal bypass. (F) Femorotibial bypass. (From Urden LD, Stacy KM, Lough ME. Thelan’s Critical Care Nursing: Diagnosis and Management. 6th ed. St.
Louis: Mosby; 2010.)

Aneurysm Repair and Reconstruction
Aneurysm repair and reconstruction involves isolating the aneu-
rysm by clamping off the vessel proximal and distal to the aneu-
rysm, excising the aneurysm, and replacing the aneurysmal area
with a synthetic graft (Fig. 7.10). Performing the procedure
before the aneurysm ruptures (elective) is preferable to repairing
a ruptured aneurysm (emergent). A ruptured aneurysm presents
an extremely challenging and difficult operative course because of
the hemodynamic 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.
The surgical repair of AAAs can be accomplished by using a
transperitoneal or retroperitoneal approach. Transperitoneal repair
via a midline laparotomy incision is the most widely used approach.43
The endovascular procedure is less invasive and is associated
with good technical success and fair overall patency.43 Compli-
cations that may occur after aneurysm repair are similar to those
discussed in the Peripheral Vascular Bypass Grafting section.34
Physical Therapy Considerations
• Incisions should be inspected before and after physical ther-
apy interventions to assess the patency of the incision, as
 Vascular System and Hematology     CHAPTER 7 203

FIG. 7.9
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.)

• A bdominal incisions or other incisional pain can limit a pa-

A have a tendency to externally rotate the hip when resting in
C importance of avoiding the “frog leg” position.
B to ensure the patency of the graft area. Blood pressure below
FIG. 7.10
Surgical repair of an abdominal aortic aneurysm. (A) Incising the aneu-
rysmal 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.
6th ed. St. Louis: Mosby; 2004.)
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 un-
der the management of the nurse, document the incidence of
drainage accordingly in the medical record.
tient’s cough effectiveness and lead to pulmonary infection.
Diligent attention to position changes, deep breathing, as-
sisted coughing with splinting techniques, and manual tech-
niques (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.
• The patient with an incision on the medial aspect of the low-
er extremity (typically from a vascular graft procedure) will
bed. This is particularly true if the incision is lengthy and
crosses the knee joint. The physical therapist should promote
neutral leg position, with or without elevation as directed by
the surgeon, and educate the patient and caregivers on the
• After a patient is cleared for out-of-bed activity, specific or-
ders 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
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.18
• Patients who have undergone bypass grafting procedures
should have improved peripheral pulses. Any reduction in
the strength of distal peripheral pulses that occurs after sur-
gery should be brought to the attention of the interprofes-
sional team. 
Physical Therapy Management
The primary goals of physical therapy for patients with vascular
and hematologic disorders are to optimize functional mobility
204 CHAPTER 7     Vascular System and Hematology
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 hema-
tologic 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).
Progression of activity tolerance in patients with hematologic
disorders does not occur at the same rate as in patients with
normal blood composition; therefore the time frame for goal
achievement may need to be lengthened.
Patients who have either vascular and/or hematologic dys-
function will potentially have overlapping needs. For simplicity,
however, the following intervention considerations are divided.
Physical Therapy Interventions for Patients With Vascular
Disorders
Common comorbidities present with peripheral vascular dis-
ease are coronary artery disease, cerebrovascular disease, diabe-
tes mellitus, and chronic obstructive pulmonary disease. It is
important to be mindful of the risks associated with these diag-
noses; specifically signs and symptoms of angina, stroke, and
myocardial infarction. Continuing to monitor vital signs, pul-
monary limitations, and blood glucose levels is essential. This
patient population also has an increased risk for sensory impair-
ments; consequently, sensory testing is an important component
of the physical therapy evaluation, as well as patient education
on frequent and thorough skin checks.
As discussed in previous sections, a monitored walking pro-
gram is shown to improve the walking capacity of patients with
IC pain. An exercise regimen for patients with IC also lowers
cardiovascular mortality rates. In most cases walking is the rec-
ommended mode of exercise and should be done with short, fre-
quent intervals.136 It is recommended to continue ambulation
until experiencing a 2 (mild) to 3 (moderate) on the Claudi-
cation Pain Scale before resting.136,137 When participating in
a walking program, the patient should walk to a nearly maxi-
mum pain level in order to have improved long-term outcomes
of IC.33
For patients who are being evaluated for a possible diagnosis
of aortic dissection, the physical therapist may need to modify or
defer physical therapy intervention until the definitive diagno-
sis is established. The patient’s presentation and hemodynamic
status should be taken into consideration in the decision-mak-
ing process. Once the diagnosis is made, the option of medical
or surgical treatment should be a guide to the physical thera-
pist’s plan of care. In either case, if the patient is seen for physi-
cal therapy, vital signs should be monitored continuously, the
presenting symptoms should be kept in mind, and any changes
in the vital signs or in the symptoms should be reported to the
medical team.
Peripheral edema can result from a variety of disorders,
including venous insufficiency, liver disease, renal insufficiency
or renal failure, and heart failure. The physical therapist should
perform a thorough review of the patient’s medical history before
performing any edema management techniques. For example,
limb elevation may be helpful in chronic venous insufficiency but
may be detrimental in acute congestive heart failure. Compres-
sion is the primary treatment for venous insufficiency, however,
is contraindicated for other health conditions. An ABI should
always be performed by a clinician before application of newly
prescribed compression garments or any associated compression
pressure changes to check the perfusion of the lower extremities.3
It is the role of the physical therapist to educate patients who
are at risk for developing a lower extremity DVT regarding pre-
ventative measures. Specifically patient education for the signs
and symptoms of a DVT, continued activity avoiding bed rest,
increased hydration, compression, as needed and as appropri-
ate. If a patient presents at an increased risk of DVT, however,
anticoagulation is contraindicated, the physical therapist should
recommend mechanical compression be initiated.82
Once a patient is diagnosed with a DVT by the medical team,
anticoagulation therapy should be initiated. Physical therapy
should be put on hold until appropriate intervention has begun
as the patient presents at an increased risk of PE. Once the ther-
apeutic level of the anticoagulant has been reached, a patient
is cleared and recommended to mobilize with physical therapy.
If a patient diagnosed with a DVT is not on anticoagulation
therapy or does not have an IVC filter, the physical therapist
should discuss mobility clearance vs. bed rest with the medi-
cal team. Please refer to the Evidence-Based Practice Guideline
for detailed algorithms to assist in making clinical decisions to
mobilize patients diagnosed with DVT.82 
Physical Therapy Interventions for Patients With Hematologic
Disorders
For patients who have hematologic dysfunction, the physical
therapist should monitor the patient’s CBC and coagulation
profile on a daily basis and follow the trend30,138 to determine
the potential physical limitations and the risk for bruising or
bleeding, for thrombus formation, and for altered oxygen-car-
rying capacity at rest and 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 sever-
ity (mild, moderate, or severe) of the abnormal laboratory val-
ues; (3) the patient’s presentation and clinical symptoms; and
(4) whether the patient has a medical history or predisposing
condition that could be exacerbated by the abnormal laboratory
values. Given these considerations, the physical therapist must
determine the need to modify or defer physical therapy inter-
vention in the setting of abnormal blood laboratory values, most
commonly alterations in Hgb, Hct, Plt, and INR.
The patient’s diagnosis, presentation, and medical interven-
tion must be taken into consideration for patients with low Hgb
and Hct (H&H), especially postoperative patients and those who
are critically ill. Refer to Table 7.10 for Hgb and Hct reference
values. Discussion with the medical team will best help deter-
mine an appropriate plan of care. Monitoring of vital signs and
oxygen saturation at rest and with activity is crucial in patients
with low H&H because the hemodynamic sequelae of altera-
tions in blood volume or viscosity may be subtle or insidious in
onset and first noticed by the physical therapist in response to
exercise.

Patients with thrombocytopenia are at an increased risk of
bleeding, which may be associated with life-threatening hemor-
rhage. Physical therapy interventions must be tailored to the
individual’s Plt levels. Refer to Tables 7.10, 7.12, and 7.21 for
reference values. Interventions may require modification and/or
deferral based on careful examination of the patient’s presenta-
tion in the context of his or her overall medical status, along
with close consultation with the medical team.138 Of particular
consideration would be patients who are a significant fall risk or
are participating in functional activities and in activities of daily
living (ADLs) that may increase the risk of bruising or bleeding
(e.g., use of resistive bands, shaving).
In addition to decreased Plt counts, other conditions, includ-
ing anticoagulation medication use, can increase the risk of spon-
taneous bleeding and hemorrhage, resulting in a patient’s INR
value being increased. For patients with a venous thromboem-
bolism who are being managed with warfarin (Coumadin), the
Evidence-Based Practice Guideline provided by Hillegass et al.82
recommends continuing with mobilization activities as long as
the INR is between 2 to 5. When INR is greater than 5, con-
sultation with the physician should occur to determine the best
course of action.82 In general, the decision to mobilize a patient
whose INR is greater than 5 should be dependent on the patient’s
presentation (age, prior level of function, current functional sta-
tus, cognitive status, and current medical condition), the medical
intervention for the elevated INR, and institutional guidelines
along with the risk/benefit/goals of physical therapy interven-
tion. If INR is greater than 6, the medical team may consider
placing the patient on bed rest until the INR has been corrected.
This usually occurs within 2 days.139Although the preceding
information offers direction, variability may exist among facili-
ties with regard to guidelines and ongoing development of new
evidence; thus the decision to modify or defer physical therapy
needs to consider all the relevant information based on the indi-
vidual clinical presentation. The physical therapist should also
consider the fall risk/benefit when mobilizing a patient with
abnormal laboratory values (Hct, Hgb, INR, Plt) versus the
benefit of mobilizing the patient. For example, an older patient
who has a high INR, an unsteady gait pattern, and cognitive
impairments is at a higher risk for falling compared with a young
adult with a high INR and a steady gait. At the same time, the
negative effects of bed rest on the patient are significant. Com-
plications related to bed rest, such as pulmonary compromise,
muscle weakness, and functional decline,140 should be taken into
consideration when making the decision to mobilize a patient.
Ultimately, consultation and collaboration with other members
of the medical team will help facilitate the clinical decision mak-
ing and optimize the plan of care and safety for the patient.138
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 8 Gastrointestinal System
C H APT ER  
CHAPTER OUTLINE
Introduction
Body Structure and Function
Clinical Evaluation
History
Physical Examination
Diagnostic Studies
Health Conditions
Esophageal Disorders
Stomach Disorders
Intestinal Disorders
Anorectal Disorders
Morbid Obesity
Liver and Biliary Disorders
Pancreatic Disorders
Management
Pharmacologic Therapy
Surgical Procedures
Physical Therapy Management
Jaime C. Paz
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . Understand the structure and function of the gastrointestinal (GI) system
2. Describe information on the clinical evaluation of the GI system, including physical examination and
diagnostic studies
3. Identify the various health conditions of the GI system
4. Provide information on the management of GI disorders, including pharmacologic therapy and surgical
procedures
5. Discuss considerations for physical therapy intervention in patients with GI diseases and disorders
Introduction
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 and participation of a patient, which may influence physical therapy management.
Additionally, physical therapists must be aware of pain referral patterns from the GI system
that may mimic musculoskeletal symptoms (Table 8.1). 
Body Structure and Function
The basic structure of the GI system is shown in Fig. 8.1, with the primary and accessory
organs of digestion and their respective functions described in Tables 8.2 and 8.3. 
Clinical Evaluation
Evaluation of the GI system involves combining information gathered through history, physi-
cal examination, and diagnostic studies.
History
Before performing the physical examination, the presence or absence of items related to GI
pathology (Box 8.1) is ascertained through patient interview, questionnaire completion, or
chart review (see Chapter 2 for a description of the general medical record review). 
Physical Examination
Physical examination of the abdomen consists of inspection, auscultation, percussion, and pal-
pation.1 The medical team usually performs this examination on a daily basis in the acute care
setting; however, physical therapists can also perform this examination to help distinguish
between systemic and musculoskeletal symptoms.
Inspection
Fig. 8.2 demonstrates the abdominal regions associated with organ location. During inspec-
tion, the physical therapist should note asymmetries in size and shape in each quadrant, umbi-
licus appearance, and presence of abdominal scars indicative of previous abdominal procedures
or trauma.2
        209
 TABLE 8.1  Gastrointestinal System Pain Referral Patterns
Structure Segmental Innervation Areas of Pain Referral
Esophagus T4–T6 Substernal region
Upper abdomen
Stomach T6–T10 Upper abdomen
Middle and lower thoracic spine
Small intestine T7–T10 Middle thoracic spine
Pancreas T6–T10 Upper abdomen
Upper and lower thoracic spine
Gallbladder T7–T9 Right upper abdomen
Right, middle, and lower thoracic spine
Liver T7–T9 Right, middle, and lower thoracic spine
Right cervical spine
Common bile duct T6–T10 Upper abdomen
Middle lumbar spine
Large intestine T11–L1 Lower abdomen
Middle lumbar spine
Sigmoid colon T11–T12 Upper sacral region
Suprapubic region
Left lower quadrant of abdomen

From Boissonault WG, Bass C. Pathological origins of trunk and neck pain: part I. Pelvic and abdominal visceral disorders. J Orthop Sports Phys Ther. 1990;12:194.

Pharynx Tongue

Trachea

Esophagus

Liver
Stomach

Gallbladder
Spleen

Transverse colon
Jejunum

Ascending colon Descending colon

Ileum Sigmoid colon

Appendix Rectum
Anus
FIG. 8.1
Schematic representation of the gastrointestinal system.
 Gastrointestinal System     CHAPTER 8 211

TABLE 8.2  Structure and Function of the Primary TABLE 8.3  Structure and Function of the Accessory
Organs of Digestion Organs of Digestion
Structure Function Structure Function
Oral cavity Entrance to the gastrointestinal Teeth Break down food to combine with saliva
system; mechanical and chemical Tongue Provides taste sensations by cranial nerve VII (taste)
digestion begins here Keeps the food between the teeth to maintain
Pharynx Involved in swallowing and mechani- efficient chewing action for food to mix with
cal movement of food to esophagus saliva
Esophagus Connects mouth to the stomach; Salivary glands Produce saliva, which is necessary to dissolve
transports and disperses food food for tasting and moisten food for swallow-
Stomach (cardia, fundus, ing
Mechanical functions: Storage, mixing,
body, pylorus) and grinding of food and regulation Liver Regulates serum levels of fats, proteins, and
of outflow to small intestine carbohydrates
Exocrine functions: Secretion of Produces bile, which is necessary for the absorp-
hydrochloric acid, intrinsic factor, tion of lipids and lipid-soluble substances
pepsinogen, and mucus necessary Also assists with drug metabolism and red blood
for digestion cell and vitamin K production
Endocrine functions: Secretion of Gallbladder Stores and releases bile into the duodenum via
hormones that trigger the release the hepatic duct when food enters the stomach
of digestive enzymes from the
pancreas, liver, and gallbladder into Pancreas Bicarbonate and digestive enzymes secreted by
the duodenum exocrine portion into duodenum
Insulin, glucagon, and numerous other hormones
Small intestine (duode- Duodenum: Neutralizes acid in food secreted by endocrine portion into the blood-
num, jejunum, ileum) transported from the stomach and stream, all of which are essential in regulating
mixes pancreatic and biliary blood glucose levels
secretions with food
Jejunum: Absorbs nutrients, water, Spleena Filters out foreign substances and degenerates
and electrolytes blood cells from the bloodstream
Ileum: Absorbs bile acids and intrinsic Stores lymphocytes
factors to be recycled in the body— aThe spleen is not part of the gastrointestinal system but is located near other
necessary to prevent vitamin B12 gastrointestinal components in the abdominal cavity.
deficiency Data from Scanlon JC, Sanders T, eds. Essentials of Anatomy and Physiology.
Large intestine (cecum; Absorbs water and electrolytes 2nd ed. Philadelphia: FA Davis; 1993; Patton KT. Anatomy & Physiology (with
Media). 7th ed. St. Louis: Mosby; 2009:837-863.
appendix; ascending, Stores and eliminates indigestible
transverse, descend- material as feces
ing, and sigmoid colon;
rectum; anus)
BOX 8.1  Items Associated with Gastrointestinal Pathology
Data from Scanlon JC, Sanders T, eds. Essentials of Anatomy and Physiology. 2nd
ed. Philadelphia: FA Davis; 1993:362; Patton KT. Anatomy & Physiology (with Signs and Stool and Urine Associated
Media). 7th ed. St. Louis: Mosby; 2009:837-863. Symptoms Characteristics Disorders
• Nausea and vom- • C hange in stool • H istory of hernia
iting color • History of hepa-
• Hemoptysis • Change in urine titis or other
CLINICAL TIP • Constipation color liver diseases
• Incontinence • H ematochezia • Drug and
The physical therapist should document any changes in abdomi- • Diarrhea (bright red blood alcohol abuse
nal girth, especially enlargement, and notify the medical team. • Jaundice in stool) • Fatty food
Abdominal enlargement may hinder the patient’s respiratory and • Heartburn • Melena (black, intolerance
mobility status. Observe for abdominal distention in postopera- • Abdominal pain tarry stools) • Thyroid
tive patients receiving opioids for pain management because this • Dysphagia dysfunction
• Odynophagia • Diabetes
can be an early sign of reduced gastrointestinal motility3,4 or opi- (painful swal- mellitus
oid induced-constipation.4 lowing)
The physical therapist should also note the presence of inci-
sions, tubes, and drains during inspection because these may Data from Koopmeiners MB. Screening for gastrointestinal system disease.
require careful handling or placement during patient intervention.   In: WG Boisonnault, ed. Examination in Physical Therapy Practice. New York:
Churchill Livingstone; 1991:113; Peterson C, Goodman CC. The gastrointes-
tinal system. In: Goodman CC, Boisonnault WG, eds. Pathology: Implications for
the Physical Therapist. 4th ed. St. Louis: Elsevier; 2015:862-907; McQuaid K.
Auscultation Approach to the patient with gastrointestinal disease. In: Goldman L, Schafer
The abdomen is auscultated for the presence or absence of bowel AI, eds. Goldman’s Cecil Medicine. 24th ed. Philadelphia: Saunders; 2011:828-
844; Ball JW, Dains JE, Flynn JA, Solomon BS, Stewart RW. Abdomen. In:
sounds and bruits (murmurs) to help evaluate gastric motility Seidel’s Guide to Physical Examination: Interprofessional Approach. 9th ed. St. Louis:
and vascular flow, respectively. Bowel sounds can be altered Elsevier; 2019:393-411.
212 CHAPTER 8     Gastrointestinal System

Abdominal Quadrants
Right upper Left upper

Liver Stomach
Gallbladder Spleen
Colon (hepatic flexure and transverse) Pancreas
Kidney and adrenal gland Kidney and adrenal gland
Duodenum with head of pancreas Colon (splenic flexure and transverse)
Small intestine Small intestine (jejunum)

Right lower Left lower

Colon (ascending) Colon (descending)

Caecum Sigmoid colon
Appendix Small intestine
Small intestine

FIG. 8.2
The four abdominal quadrants, showing the viscera found in each. (From Palastanga N, Soames RW. Anatomy and Human Movement: Structure and Function.
6th ed. Edinburgh: Churchill Livingstone; 2012.)

postoperatively, as well as in cases of diarrhea, intestinal obstruc-

tion, paralytic ileus, and peritonitis. The presence of bruits over
the aorta or the renal, iliac, or femoral arteries may be indicative
of vascular disease.1  to as liver function tests (LFTs).
Percussion
Mediate percussion is used to evaluate liver and spleen size and
borders, as well as to identify ascitic fluid, solid- or fluid-filled
masses, and air in the stomach and bowel.1 The technique for
mediate percussion is described in the Physical Examination
section of Chapter 4.  aminotransferase (ALT; previously called serum glutamate pyruvate
Palpation
Light, moderate, and deep palpations are used to identify abdom-
inal tenderness, muscular resistance, and superficial organs and
masses. The presence of rebound tenderness (i.e., abdominal pain
worsened by a quick release of palpatory pressure) is an indication
of possible peritoneal irritation and requires immediate medical
attention. Muscle guarding during palpation may also indicate a
protective mechanism for underlying visceral pathology.1,5  Cholestasis is the impairment of bile flow from the liver to
Diagnostic Studies
Discussion of the diagnostic evaluation for the GI system is
divided into (1) the examination of the GI tract and (2) the
examination of the hepatic, biliary, pancreatic, and splenic sys-
tems. Examination of the GI tract includes the esophagus, stom-
ach, and intestines (small and large). Table 8.4 summarizes the
laboratory tests used to measure functional aspects of secretion,
digestion, absorption, and elimination within the GI tract.6-13
Table 8.5 summarizes the diagnostic procedures used to visual-
ize the GI tract.
Examination of the hepatic (liver), biliary (gallbladder and
cystic ducts), pancreatic, and splenic systems involve numerous
laboratory tests and diagnostic procedures, which are often per-
formed 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, disease or dysfunc-
tion in one organ can often extend into the other organs.14,15
CLINICAL TIP
Laboratory tests used to examine the liver are frequently referred
Hepatocellular disease results in cellular damage and poten-
tial cellular necrosis in the liver, which causes increased levels
of the following enzymes: aspartate aminotransferase (AST;
previously called serum glutamic-oxaloacetic transaminase), alanine
transaminase), and lactate dehydrogenase (LDH).15,16
Hepatocellular dysfunction can be identified when bilirubin
levels are elevated or when clotting times are increased (denoted
by an increased prothrombin time and the international normal-
ized ratio [INR]). The liver produces clotting factors, and there-
fore an increased prothrombin time or INR implicates impaired
production of coagulation factors. Refer to Chapter 7 for more
details on coagulation tests.
the duodenum and results in elevations of the following serum
enzymes: alkaline phosphatase (ALP), aspartate transaminase (pre-
viously known as γ-glutamine-oxaloacetic transaminase or γ-glutamyl
transpeptidase).15,16 Elevations in conjugated and unconjugated
bilirubin may also be found with hepatic obstruction.16
Table 8.6 summarizes the laboratory tests performed to mea-
sure hepatic, biliary, and pancreatic functions. Table 8.7 sum-
marizes 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 fiberoptic tube)
into the abdominal cavity through a small incision in the peri-
umbilical area. To perform this procedure, a local anesthetic is
 Gastrointestinal System     CHAPTER 8 213

TABLE 8.4  Laboratory Tests for the Gastrointestinal Systema

Test Description
Carcinoembryonic antigen (CEA) Purpose: Protein used to monitor recurrence of colorectal cancer and response to antineo-
Reference value: plastic therapy for both colorectal and breast cancer; presence of CEA in other body
Adult nonsmoker: <2.5 ng/mL fluids maybe indicative of metastasis.
Adult smoker: up to 5 ng/mL
Gastrin Hormone that stimulates the release of gastric acid in stomach.
Reference value: Adult: 0–180 pg/mL Purpose: To confirm the diagnosis of Zollinger-Ellison syndrome and monitor for recur-
rence of gastrinoma (gastrin-producing tumor).
Helicobacter pylori tests Purpose: To confirm the diagnosis of H. pylori infection, which is a risk factor for most
peptic ulcers and chronic gastritis and gastric carcinoma.
  Stool sample Purpose: To identify presence of H. pylori antigen.
  Reference value: Negative for H. pylori antigen
  Serologic test Purpose: To identify the presence of immunoglobulin G antibody to H. pylori in blood.
  Reference value: Immunoglobulin G negative
  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 exam-
ined.
5-Hydroxyindoleacetic acid (5-HIAA) Purpose: To detect a carcinoid tumor and provide ongoing evaluation of tumor stability.
Reference value: 2–8 mg/24 h (urine sample) 5-HIAA is a urinary metabolite of serotonin and is produced by most carcinoid tumors
found in the appendix, intestine, or lung.

Lactose tolerance test (oral lactose tolerance test) Purpose: To identify lactose intolerance or lactase deficiency as a cause of abdominal
Reference value: Adult cramps and diarrhea, as well as to help identify the cause of malabsorption or mal-
Blood glucose >20 mg/dL digestion syndrome.
An oral dose of lactose is provided to a fasting patient, and serial blood samples are
measured.
Minimal rise in blood glucose or urine lactose levels indicates lactose intolerance and/or
lactase deficiency.
Occult blood (fecal occult blood test [FOBT], fecal Purpose: A screening tool for early diagnosis of colon cancer.
occult blood [FOB], guaiac smear test) Multiple stool specimens over several days are collected and examined for the presence of
Reference value: Negative occult (nonvisible) blood in the feces, which can be indicative of adenocarcinoma and
premalignant polyps in the colon.
Serotonin (5-hydroxytryptamine) Purpose: To detect a carcinoid tumor.
Reference value: Less than or equal to 230  ng/mL Venous blood levels of serotonin are measured, as carcinoid tumors secrete excess
(blood) amounts of serotonin.
aWords or abbreviations in parentheses are synonyms for the test names.
Data from Pagana KD, Pagana TJ, Pagana TN. Mosby’s Diagnostic and Laboratory Test Reference. 13th ed. St. Louis: Mosby; 2017.

administered, and gas (i.e., nitric oxide or carbon dioxide) is
infused into the abdominal cavity to allow better visualization
and manipulation of the scope.17 A laparoscope is used for diag-
nostic for such purposes as evaluation of abdominal or pelvic
pain and suspicious masses. Therapeutically, laparoscopic inter-
ventions may include resection of structures in various abdomi-
nal health conditions.17,18  ogy to create color images of organs and their functions. Com-
Magnetic Resonance Imaging
The use of MRI of the GI system is primarily indicated for imag-
resecting colorectal tumors.21,22 MRI has also been successful in
helping delineate the etiology of cirrhosis between alcohol abuse
and viral hepatitis.23 
Positron Emission Tomography
PET is the use of positively charged ions and computer technol-
bination technology using both PET and CT is also available.
Clinical uses of PET for the GI system include evaluation of
pancreatic function and GI cancer.24,25 

ing of the liver for hepatic tumors, iron overload, and hepatic and
portal venous occlusion.19 Otherwise, computed tomography
(CT) scans are preferred for the visualization of other abdomi-
nal organs.20 Good success, however, has been reported recently
with the use of MRI in defining tissue borders for managing and
Health Conditions
GI disorders can be classified regionally by the structure
involved and are described in the following sections.
214 CHAPTER 8     Gastrointestinal System

TABLE 8.5  Diagnostic Procedures for the Gastrointestinal (GI) Systema

Test Description
Barium enema (BE) Purpose: To investigate and identify pathologic conditions that change the structure or
Reference value: No lesions, deficits, or abnor- function of the colon (large bowel).
malities of the colon are noted. The colon is emptied of feces, and contrast medium (barium) is instilled rectally. Fluoro-
scopic and x-ray images are then taken to identify the presence of any structural anomalies
as well as polyps, tumors, and diverticula.
Barium swallow (esophagography) Purpose: To identify pathologic conditions that change the structure or function of the
Reference value: No structural or functional esophagus.
abnormalities are visualized. The patient takes repeated swallows of barium liquid while x-ray and fluoroscopic images are
taken in various positions to examine the passage of contrast medium during swallowing
and peristaltic movement of the esophagus.
Colonoscopy (lower panendoscopy) Purpose: To perform routine screening of the colon for the presence of polyps or tumors and to
Reference value: No abnormalities of structure or investigate the cause of chronic diarrhea, bleeding, or other undiagnosed GI complaints.
mucosal surface are visualized in the colon or Patients are sedated, and a colonoscope is inserted into the rectum and passed through the
terminal ileum. various parts of the colon to the cecum. Tissue biopsy or polypectomy may be performed, if
indicated, during this procedure.
Computed tomography (CT) of the GI tract (CT, Purpose: To detect intraabdominal abscesses, tumors, aneurysms, infarctions, perforation,
computed axial tomography [CAT]) obstruction, inflammation, and diverticulitis. Metastases to the abdominal cavity can also
be detected. Intravenous or oral contrast may be used during the procedure.
Esophageal function studies:
Manometry Purpose: To evaluate esophageal motor disorders that could be causing dysphagia, reflux, or
Reference value: Lower esophageal sphincter (LES) rule out other possible diagnoses.
pressure: 10–20 mmHg.
Esophageal pH (acid reflux) Purpose: To evaluate changes in esophageal pH levels with wireless pH probes and a capsule
Reference value: No change in pH level. that is implanted into esophageal mucosa 5–6 cm above the gastroesophageal junction.
Monitoring takes place over 24–48 hours. Patients are able to eat and normally during this
time.
Acid perfusion test (Bernstein test) Purpose: To determine that heartburn is of esophageal rather than other causes.
Reference value: Negative. Hydrochloric acid is instilled into the esophagus through the endoscope or nasogastric tube.
Complaints of heartburn with acid instillation confirm the esophageal origin.
Esophagogastroduodenoscopy (EGD; upper Purpose: To identify and biopsy tissue abnormality; to evaluate the esophagus, stomach, and
gastrointestinal endoscopy; upper gastrointes- duodenum to investigate the cause of upper GI bleeding, dysphagia, dyspepsia, gastric
tinal [UG] endoscopy; gastroscopy) outlet obstruction, peptic ulcers, hiatal hernias, or epigastric pain.
Reference value: No abnormal structures or An endoscope is passed through the mouth into the esophagus to the stomach, pylorus, and
functions are observed in the esophagus, upper duodenum. Tissue biopsy or other interventions can be performed during the
stomach, or duodenum. procedure, as indicated.
GI bleeding scan (GI scintigraphy, abdominal Purpose: To evaluate the presence, source, or both, of GI bleeding.
scintigraphy) Radionuclide-labeled red blood cells are injected intravenously, followed by intermittent
Reference value: No evidence of focal bleeding. imaging studies of the abdomen and pelvis for up to 24 hours.
Paracentesis and peritoneal fluid analysis Purpose: To help delineate the cause of peritoneal effusion.
(abdominal paracentesis, ascitic fluid cytology, The peritoneal cavity is accessed with either a long thin needle or a trocar and stylet with the
peritoneal tap) patient under local anesthesia. Peritoneal fluid is collected and examined to determine the
Reference value: Clear, odorless, pale yellow. cause of effusion.
Peritoneal tissue biopsy can also be performed during this procedure for cytologic studies.
Sigmoidoscopy (proctoscopy, anoscopy) Purpose: Sigmoidoscopy is used as a screening tool for the anus, rectum, and sigmoid colon
Reference value: No tissue abnormalities are for cancer and to investigate the cause of rectal bleeding or monitor inflammatory bowel
visualized in the sigmoid colon, rectum, or disease. Proctoscopy is used to view the anus and rectum. Anoscopy is used to investigate
anus. the anus.
Upper GI (UGI) series and small bowel series Purpose: To detect disorders of structure or function of the esophagus, stomach, and
(Upper gastrointestinal x-ray study) duodenum. The jejunum and ileum are visualized for the small bowel series).
Small bowel follow-through study) Imaging studies of all these areas are performed while the patient drinks a barium solution.
Reference value: No structural or functional Passage of the barium through these structures can take from 30 minutes to 6 hours.
abnormalities are found.
aWords or abbreviations in parentheses are synonyms for the test names.
Data from Malarkey LM, McMorrow ME, eds. Nurse’s Manual of Laboratory Tests and Diagnostic Procedures. Philadelphia: Saunders; 2000:432-468; Pagana KD, Pagana
TJ, Pagana TN. Mosby’s Diagnostic and Laboratory Test Reference. 13th ed. St. Louis: Mosby; 2017; Andreoli TE, Benjamin IJ, Griggs RC, et al. Andreoli and Carpenter’s
Cecil Essentials of Medicine. 8th ed. Philadelphia: Saunders; 2010.
 Gastrointestinal System     CHAPTER 8 215

TABLE 8.6  Laboratory Tests for the Hepatic, Biliary, and Pancreatic Systemsa
Test Involved Systems Purpose
Alanine aminotransferase (ALT; serum glutamic- Hepatic To detect hepatocellular disease.
pyruvic transaminase [GPT], SGPT) Very specific in detecting acute hepatitis from viral causes.
Reference value: 4–36 IU/L
Alkaline phosphatase (ALP; total alkaline phospha- Hepatic, biliary Nonspecific indicator of liver disease, bone disease, or hyperpara-
tase [T-ALP]) thyroidism.
Reference value: 30–120 U/L or 0.5–2.0 King-Arm- Sensitive test for metastatic lesions to liver.
strong units/dL
Alkaline phosphatase isoenzymes (ALP1) Hepatic, biliary Used to distinguish between liver and bone pathology when total
serum ALP is elevated.
There are ALP isoenzymes for both liver (ALP1) and bone (ALP2).
Alpha fetoprotein (AFP) Hepatic, biliary A tumor marker for hepatocellular cancer in nonpregnant females.
Reference value: <40 ng/mL AFP normally exists during pregnancy; otherwise, levels are very
low.
Ammonia (NH3) Hepatic To evaluate or monitor liver disease, hepatoencephalopathy, and the
Reference value: Adult 10–80 mcg/dL effects of impaired portal vein circulation.
Ammonia is a by-product of protein metabolism and is converted
to urea in the liver.
Amylase, serum Pancreatic To assist in diagnosis of acute pancreatitis and traumatic injury to
Reference value: 30–220 U/L the pancreas or as surgical complication of the pancreas.
Amylase, urine Pancreatic To confirm diagnosis of pancreatitis later in the disease course,
Reference values: when serum amylase levels maybe normal or borderline elevated.
6.5–48.1 U/h (1-h test)
5000 Somogyi U/24 h (24-h test)
Aspartate aminotransferase (AST; formerly called se- Hepatic To assist in diagnosis of suspected hepatocellular disease.
rum glutamate oxaloacetate transaminase [SGOT]) AST is highly concentrated in the liver, but it is also present in
Reference value: 0–35 U/L skeletal muscle, kidney, and pancreas.
Bilirubin Hepatic, biliary Used to evaluate liver function, diagnose jaundice, and monitor
Reference values: progression of jaundice.
Total, 0.3–1.0 mg/dL Total bilirubin is the sum of direct and indirect bilirubin.
Direct (conjugated), 0.1–0.3 mg/dL Elevation in direct (conjugated) bilirubin or indirect (unconjugat-
Indirect (unconjugated), 0.2–0.8 mg/dL ed) bilirubin helps to determine cause of jaundice.
Carbohydrate antigen 19–9 (CA 19–9) Hepatic, pancre- An associated tumor marker used in the treatment surveillance of
Reference value: <37 U/mL atic pancreatic and hepatobiliary cancer.
Fecal fat (fat absorption, quantitative stool fat deter- Pancreatic, biliary To identify steatorrhea (high levels of fat in the feces). This can be
mination) caused by gallstones, pancreatic duct obstruction, cystic fibrosis,
Reference value: 2–6 g/24 h Crohn disease, and small intestine disease.
Gamma-glutamyl-transferase (GT), gamma-glu- Hepatic, biliary, Detects liver cell dysfunction. Accurate in detecting cholestasis,
tamyl-transpeptidase [GGT, GGTP]) pancreatic Sensitive to cholangitis, biliary obstruction, or cholecystitis.
Reference values:
Male and female 45 years or older—8–38 U/L
Female less than 45 years—5–38 U/L
Hepatitis virus studies Hepatic Distinguishes among the three common types of viral hepatitis
Reference value: Negative (no presence of antibodies) (caused by hepatitis A virus [HAV], hepatitis B virus [HBV],
hepatitis C virus [HCV]).
Presence of distinct antibodies or antigens for a specific virus will
help confirm the diagnosis and assist with treatment planning.
Lipase Pancreatic Used to diagnose pancreatitis and pancreatic disease. Lipase is a
Reference value: <160 U/L digestive enzyme used to digest fatty acids.
Elevated levels indicate onset of acute pancreatitis.
5-Nucleotidase (5N, 5-NT) Hepatic An enzyme specific to the liver.
Reference value: 0–1.6 units at 37°C Elevated levels help to identify extrahepatic or intrahepatic dis-
eases.
Protein electrophoresis Hepatic To identify the presence of abnormal proteins (multiple myeloma)
Reference value: Total protein 6.4–8.3 g/dL or absence of normal proteins (liver disease) and to detect high/
low amounts of different protein groups.
Continued
216 CHAPTER 8     Gastrointestinal System

TABLE 8.6  Laboratory Tests for the Hepatic, Biliary, and Pancreatic Systemsa—cont’d
Test Involved Systems Purpose
Serum proteins (albumin) Hepatic Provides general information about nutritional status, the oncotic
Reference value: 3.5–5.0 g/dL pressure of the blood, and the losses of protein associated with
liver, renal, skin, or intestinal diseases.
Sweat test (sweat chloride, cystic fibrosis sweat test, Pancreatic Standard test used to diagnose cystic fibrosis in children, as these
iontophorectic sweat test) children have higher contents of sodium and chloride in their
Reference value in children: sweat.
Sodium: <70 mEq/L
Chloride: <50 mEq/L
aWords or abbreviations in parentheses are synonyms for the test names.
Data from Knight JA. Liver function tests: their role in the diagnosis of hepatobiliary diseases. J Infus Nurs. 2005;28(2):108-117; Parad RB, Comeau AM, Dorkin HL,
et al. Sweat testing infants detected by cystic fibrosis newborn screening. J Pediatr. 2005;147(3 Supp 1):S69-S72; Davies JC. New tests for cystic fibrosis. Paediatr Respir
Rev. 2006;7(S1):S141-S143; Pagana KD, Pagana TJ, Pagana TN. Mosby’s Diagnostic and Laboratory Test Reference. 13th ed. St. Louis: Mosby; 2017.

TABLE 8.7  Diagnostic Procedures for the Hepatic, Biliary, Pancreatic, and Splenic Systemsa
Test Purpose
Computed tomography (CT) of the liver, Used to identify the presence of tumor, abscess, cyst, sites of bleeding or trauma, or hematoma in
biliary tract, pancreas, and spleen these organs.
Contrast medium may be used with CT of the liver and pancreas.
Endoscopic retrograde cholangiopancreatog- Used to investigate the cause of obstructive jaundice, persistent abdominal pain, or both.
raphy and pancreatic cytology (ECRP) Generally identifies stones, benign strictures, cysts, strictures and malignant tumors in the bili-
ary and pancreatic ducts.
Gallbladder nuclear scanning (hepatobiliary Purpose: to examine the gallbladder and the biliary ducts leading out of it. Radionuclide mate-
scintigraphy, cholescintigraphy, DISIDA rial is injected into the patient, absorbed by the liver, and excreted through biliary ducts; can
[diisopropyl iminodiacetic acid] scanning, diagnose obstructions in the ducts.
HIDA [hepatoiminodiacetic acid] scanning)
Liver biliary biopsy, percutaneous To diagnose pathologic changes in the liver and monitor disease progression.
Liver-spleen scan A radionuclide is injected intravenously, and imaging of the liver and spleen is performed.
Used to identify suspected hepatocellular disease and enlargement of the liver or spleen as well as
portal hypertension.
Magnetic resonance cholangiopancreatogra- Imaging test used to visualize gallbladder, biliary ducts, pancreas, and pancreatic ducts. Can
phy (MRCP) identify obstructions (stones) and other pathology (tumors, infection, inflammation) in the
gallbladder and ducts.
Ultrasound of the liver, biliary tract, pan- Imaging tool for examining the liver, spleen, gallbladder, and pancreas.
creas, and spleen Cyst, abscess, hematoma, primary neoplasm, and metastatic disease can be detected in the liver as
well as gallstones and pancreatic abscesses and tumors.
aWords or abbreviations in parentheses are synonyms for the test names.
Data from Knight JA. Liver function tests: their role in the diagnosis of hepatobiliary diseases. J Infus Nurs. 2005;28(2):108-117; Parad RB, Comeau AM, Dorkin HL,
et al. Sweat testing infants detected by cystic fibrosis newborn screening. J Pediatr. 2005;147(3 Supp 1):S69-S72; Davies JC. New tests for cystic fibrosis. Paediatr Respir
Rev. 2006;7(S1):S141-S143; Fulcher AS. MRCP and ERCP in the diagnosis of common bile duct stones. Gastrointest Endosc. 2002;56(6 Supp 1):S178-S182; Taylor ACF,
Little AF, Hennessy OF, et al. Prospective assessment of magnetic resonance cholangiopancreatography for noninvasive imaging of the biliary tree. Gastrointest Endosc.
2002;55(1):17-22; Miller AH, Pepe PE, Brockman CR, et al. ED ultrasound in hepatobiliary disease. J Emerg Med. 2006;30(1):69-74; Kalimi R, Gecelter GR, Caplin D,
et al. Diagnosis of acute cholecystitis: sensitivity of sonography, cholescintigraphy, and combined sonography-cholescintigraphy. J Am Coll Surg. 2001;193(6):609-613;
Pagana KD, Pagana TJ, Pagana TN. Mosby’s Diagnostic and Laboratory Test Reference. 13th ed. St. Louis: Mosby; 2017; Ferri’s Clinical Advisor 2013. St. Louis: Mosby; 2012.

Esophageal Disorders • I s it accompanied by pain?

Dysphagia
Dysphagia, or difficulty swallowing, can occur from various eti-
ologies (Table 8.8) and is generally classified by its location as
either oropharyngeal dysphagia, occurring in the pharynx or upper
esophagus, or esophageal dysphagia, occurring in the esophageal
body or lower esophageal sphincter.26,27
The following characteristics of dysphagia should also be
noted to aid in the diagnosis:
• Does it occur with ingestion of solids, liquids, or both?
• Is it intermittent, constant, or progressive?
• Does the patient complain of regurgitation/reflux or cough-
ing while eating?
• Where does the food get stuck?26
Diagnosis can be established with imaging studies,
such as video fluoroscopy, modified barium swallow study,
endoscopy, CT, and MRI. The primary goal of treatment
includes airway protection and maintenance of nutrition
with specific strategies employed once a definitive etiology
is established.28 
 Gastrointestinal System     CHAPTER 8 217

TABLE 8.8  Classification and Possible Etiologies of Dysphagia

Classification Possible Etiology
Oropharyngeal Neuromuscular: Stroke, Parkinson’s disease, multiple sclerosis, myasthenia gravis, head trauma, dementia, Bell’s palsy,
tumors of the central nervous system
Structural: Poor dentition, oropharyngeal tumor, infection of pharynx or neck, thyromegaly, esophageal webs, cleft
palate, goiter
Esophageal Neuromuscular: Achalasia, diffuse esophageal spasm, hypertensive lower esophageal sphincter, scleroderma, ineffective
esophageal motility
Structural: Peptic stricture, esophageal rings or webs, diverticuli, tumors, foreign bodies, vascular compression from
thoracic aneurysm, mediastinal masses, spinal osteophytes, mucosal injury from infection or gastric reflux

Data from Satpathy HK. Dysphagia. In: Ferri F, ed. Ferri’s Clinical Advisor 2013. St. Louis: Mosby; 2012. Smout A. Approach to the patient with dysphagia, odynopha-
gia, or noncardiac chest pain. In: Podolsky DK, Camilleri M, Gregory Fitz J, Kalloo AN, Shanahan F, Wang TC, eds. Yamada’s Textbook of Gastroenterology. 6th ed. New
York: Wiley & Sons, Ltd.; 2016:1629-1652.

Esophageal Motility Disorders and Angina-like Chest Pain
Poor esophageal motility from neuromuscular dysfunction can
result in dysphagia, chest pain, or heartburn. Achalasia, gastro-
esophageal reflux disease (GERD), and distal esophageal spasm
(DES) are the most common causes of primary esophageal motil-
ity disorders.29
Achalasia is a neuromuscular disorder of esophageal motil-
ity characterized by impaired lower esophageal sphincter
(LES) relaxation and aperistalsis (absence of peristalsis) in the
smooth muscle of the esophagus. Innervation to both the LES
and smooth muscle is thought to be disrupted, resulting in loss
of motility; however, the exact etiology and pathophysiology
remain unknown.30 In addition to the aforementioned symp-
toms, clinical manifestations may include chest pain, regurgita-
tion, hiccups, halitosis, weight loss, and aspiration pneumonia.
All patients with achalasia will have solid food dysphagia,
with variable degrees of liquid aphasia. Treatment is aimed at
compensating for poor esophageal emptying by reducing LES
pressure with pharmacologic therapy, pneumatic dilation, or
laparoscopic Heller myotomy and peroral endoscopic myotomy
(POEM).29-32
DES is characterized by the occurrence of normal peristalsis,
with intermittent nonperistaltic, simultaneous contractions in
the distal esophagus.30 Clinical manifestations include intermit-
tent chest pain that occurs with or without eating and may be
similar in character to angina, described as squeezing or crush-
ing in nature, radiating to the jaw, neck, arms, or midline of the
back.29 The etiology is unknown, and management is directed
at smooth muscle relaxation with pharmacologic agents, along
with behavior modification and biofeedback.29,33a Invasive
management may also include pneumatic dilation, laparoscopic
Heller myotomy and POEM.32  relative) of either Barrett’s esophagus or esophageal adenocar-
Gastroesophageal Reflux Disease
GERD is characterized by gastric acid backflow into the esopha-
gus as a result of an incompetent LES. Typical clinical manifes-
tations include complaints of heartburn (retrosternal burning
sensation) and regurgitation (perceived gastric reflux). Atypical
symptoms may include chest pain, nausea, gagging, cough, dys-
phagia, sore throat, or hoarseness.33b,34 GERD can be defined
by mild symptoms 2 or more days per week or moderate/severe
symptoms more than once a week.33b Although the exact etiology
of GERD is unknown, tobacco abuse, along with the consump-
tion of alcohol, coffee, peppermint, or chocolate, has been associ-
ated with this inappropriate relaxation. Esophageal and gastric
motility disorders may also contribute to GERD, as may hia-
tal hernia and/or obesity. Gastroesophageal reflux is a strong
predisposing factor for developing esophageal adenocarcinoma.
Depending on the severity of GERD, treatment can range
from dietary modifications (avoid risk factors and eat small fre-
quent meals in an upright position) to weight reduction, head
elevation while sleeping, antacids, proton pump inhibitors
(PPIs), histamine-2 (H2) blockers, or surgery.33b,35,36 Laparo-
scopic fundoplication, particularly the Nissen fundoplication,
have shown good long-term outcomes in improving GERD
symptoms.33b,34,37
CLINICAL TIP
Physical therapists should be aware of any positioning precau-
tions for patients with esophageal disorders that may exacerbate
their dysphagia or gastroesophageal reflux disease (GERD).
 
Barrett’s Esophagus
Barrett’s esophagus is a condition in which columnar epithe-
lium replaces the normal stratified squamous mucosa of the
distal esophagus. According to the American Gastrointestinal
Association, “intestinal metaplasia is required for the diagnosis
of Barrett’s esophagus as intestinal metaplasia is the only type of
esophageal columnar epithelium that is clearly associated with
malignancy.”38 Risk factors for developing Barrett’s esophagus
include males, older than 50 years of age, Caucasian race, obe-
sity, chronic GERD symptoms, and family history (first-degree
cinoma.39 The mechanism of cellular metaplasia is thought to
occur from chronic inflammatory injury from acid and pepsin
that refluxes from the stomach into the distal esophagus.40,41
Barrett’s esophagus is also a strong predisposing factor for devel-
oping esophageal adenocarcinoma, the incidence of which rose
in the 1990s.41-43
Associated signs and symptoms include dysphagia, esophagi-
tis, ulceration, perforations, strictures, bleeding, or adenocarci-
noma.41 Treatment for Barrett’s esophagus includes controlling
symptoms of GERD (e.g., use of PPIs) and healing reflux
218 CHAPTER 8     Gastrointestinal System
esophagitis. For patients with confirmed high-grade dysplasia
within Barrett’s esophagus, endoscopic eradication therapy with
radiofrequency ablation, photodynamic therapy, or endoscopic
mucosal resection is recommended.38,39 Low-grade dysplasia
may also be addressed with endoscopic ablation when confirmed
by an expert GI pathologist and seen to be persistent on a second
confirmatory examination.39  appropriateness for physical therapy management.
Esophageal Varices
Varices are dilated blood vessels in the lower third of the esopha-
gus caused by portal hypertension and may result in hemorrhage
that necessitates immediate medical and, usually, invasive man-
agement.44,45 Alcohol abuse and liver cirrhosis are associated
risk factors.46 Refer to the Cirrhosis section later in this chap-
ter for more information on portal hypertension and alcoholic
cirrhosis.  gastritis.44
Esophageal Cancer
A description of esophageal cancers with respect to evaluation
and management can be found in the Cancers in the Body Sys-
tems section in Chapter 11.
CLINICAL TIP
Patients who have undergone esophagectomy may likely have
chest tubes. Please refer to Chapter 18, Table 18.7, for chest
tube management.
 
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 occurs in
the esophagus, stomach, or duodenum47; an LGIB occurs in the
colon and anorectum. A UGIB can result from one or more of the
following: gastric or duodenal ulcers, gastric erosion, and gastric
or esophageal varices. An LGIB can result from one or more of
the following: (1) inflammatory bowel disease (e.g., diverticuli-
tis), (2) ischemic colitis, (3) anal and rectal lesions (e.g., hemor-
rhoids), and (4) ulcerated polyps or colorectal cancer.48-50
GI bleeds can be small and require minimal to no interven-
tion, or severe and constitute a medical emergency 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 hemoglobin are the primary
clinical manifestations of GI bleeds.50
Patients requiring medical management are generally stabilized
hemodynamically with intravenous (IV) fluids, blood transfusions,
or both before the cause of bleeding can be fully delineated. Naso-
gastric tubes (see Chapter 18) are typically used in the stabiliza-
tion 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 evaluate or treat
the source of upper or lower GI hemorrhage.49-51
CLINICAL TIP
Patients with ongoing GI bleeding may require their complete
blood count and coagulation profiles evaluated by the medical
team. Physical therapists should review ongoing trends in these
laboratory values in comparison with parameters to determine
Gastritis
Gastritis is the general term used to describe diffuse inflamma-
tory lesions in the mucosal layer of the stomach. Gastritis can
be subdivided as erosive, nonerosive, or specific types based
on histologic features and those found endoscopically.52 Clini-
cal features can also distinguish between acute and chronic
Common causes of gastritis include Helicobacter pylori infec-
tion, use of aspirin or nonsteroidal antiinflammatory drugs
(NSAIDs), alcohol use, radiation, chemotherapy, cocaine, stress,
and aging-related gastropathy.44 Clinical manifestations include
abdominal pain, nausea, and vomiting, typically occurring
when gastritis has led to ulceration; otherwise patients may be
asymptomatic. Symptoms of upper GI bleed may also be present
if ulceration occurs. Management of gastritis consists of address-
ing the underlying cause by using antimicrobial agents in the
case of H. pylori infection and acid suppression therapy.26,53-56 
Peptic Ulcer Disease
Peptic ulcer disease (PUD) is an ulceration in the stomach (gas-
tric ulcer) or duodenum (duodenal ulcer), resulting from an
imbalance between various mucosa-damaging substances and
mucosal protective factors, based on individual susceptibil-
ity.57 The two primary causes of PUD are H. pylori infection and
NSAID use.47 Other factors that can contribute to PUD include
incompetent LES, bile acids, impaired bicarbonate secretion,
decreased blood flow to gastric mucosa, cigarette smoking, and
alcohol use.26,58-61
Clinical manifestations of PUD may vary, depending on the
location of the ulcer. In duodenal ulcers, patient reports can
include “hunger-like” sensations or nocturnal pain. Pain can
occur 2 to 5 hours after a meal for patients with gastric ulcers,
along with complaints of nausea, vomiting, and weight loss.57
Ulcer pain can also radiate to the low back region. Hemorrhage
occurs in approximately 15% of patients with PUD.26
Management of PUD includes lifestyle changes (smoking
cessation and discontinuation of aspirin or alcohol use), discon-
tinuing NSAID use, and beginning PPI and/or antimicrobial
therapy for H. pylori.24,52 If a patient with PUD has bleeding
episodes, then timely endoscopic treatment and acid suppressive
therapy are indicated.57 Refer to the section on Gastrointestinal
hemorrhage for more details. 
Zollinger-Ellison Syndrome
Zollinger-Ellison syndrome (ZES) is a rare syndrome that includes
gastric acid hypersecretion, caused by a gastrin-producing neu-
roendocrine tumor (gastrinoma) in the pancreas and duodenum.
Symptoms include abdominal pain, heartburn, chronic diarrhea,

chronic reflux, nausea, and weight loss. Diagnosis of ZES is often
delayed, given the similarity to PUD or GERD. Management is
primarily directed at surgical resection of the gastrinoma, along
with decreasing gastric acid hypersecretion.62-65  Inflammation of the appendix of the large intestine can be
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 gastroparesis and may result from or be
associated with pyloric stenosis as a consequence of peptic ulcers,
diabetes mellitus, diabetic ketoacidosis, electrolyte imbalance,
autonomic neuropathy, gastric surgery, connective tissue dis-
orders, a variety of neurologic disorders and malignancy.66-68
Symptoms of gastroparesis may include epigastric pain, early
satiety, nausea, vomiting, and weight loss. Addressing the pri-
mary cause, as well as pharmacologic intervention to promote
gastric motility, is indicated for patients with decreased gas-
tric emptying disorders.67 If indicated for the patient, invasive
management may also be performed and may include any of the
following: placement of a temporary pyloric stent, gastric elec-
trical stimulation, laparoscopic pyloroplasty, or subtotal laparo-
scopic gastrectomy.68
Enhanced gastric emptying (also known as dumping syndrome
[DS]) is associated with an interruption of normal digestive
sequencing that results from vagotomy, gastrectomy, gastric
bypass, surgery for PUD, and Nissen fundoplication for GERD
in children.69 Gastric peristalsis, mixing, and grinding are dis-
turbed, resulting in rapid emptying of liquids, slow or increased
emptying of solids, and prolonged retention of indigestible sol-
ids.66 Symptoms of DS can be classified as either early or late,
referring to the timeframe following a meal. Early DS typically
occurs 30 minutes after a meal and can include systemic symp-
toms, such as palpitations, tachycardia, flushing, diaphoresis,
and potential for syncope. Abdominal symptoms also occur with
early DS and may include early satiety, bloating, cramps, nau-
sea, abdominal pain, and diarrhea. Late DS typically occurs 1
to 3 hours after a meal and includes symptoms consistent with
hypoglycemia, such as perspiration, decreased concentration,
and faintness. A combination of both early and late DS can also
exist.69 Dietary changes and pharmacologic management are the
usual treatment choices.67 Surgery is reserved as a last resort in
managing DS.69
CLINICAL TIP
Consultation with the medical team as well as understanding
the patient’s specific needs can facilitate the optimal treatment
schedule for an individual with dumping syndrome (DS), par-
ticularly in relation to meals.
 
Gastric Cancer
The most common malignant neoplasms found in the stom-
ach are adenocarcinomas,44 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 11.  open sigmoid colectomy44,75
Gastrointestinal System     CHAPTER 8 219
Intestinal Disorders
Appendicitis
classified as acute, gangrenous, or perforated. Acute appen-
dicitis involves an inflamed but intact appendix. Gangrenous
appendicitis is the presence of focal or extensive necrosis
accompanied by microscopic perforations. Perforated appen-
dicitis is a gross disruption of the appendix wall and can lead
to serious complications if it is not managed promptly.70 The
etiology of appendicitis includes a combination of obstruc-
tion in the appendix lumen, coupled with infection with
either bacterial or viral invasion.44,70,71 Obstruction can
result from lymphoid hyperplasia, tumor, fecal material, or
intestinal worms.44
The signs and symptoms of appendicitis may include44,71:
• Right lower quadrant (RLQ), epigastric, or periumbilical ab-
dominal pain that fluctuates in intensity
• Abdominal tenderness in the RLQ at McBurney’s point, lo-
cated approximately one third of the distance from the right
anterior superior iliac crest to the umbilicus72
• Vomiting, with presence of anorexia
• Constipation and failure to pass flatus
• Low-grade fever (no greater than 102°F [39°C])
Medical management of appendicitis involves early and
accurate diagnosis of acute appendicitis to prevent perforation.
Medical intervention requires surgical appendectomy and post-
operative antimicrobial agents.44,70 
Diverticular Disease
Diverticulosis is the presence of diverticula, which is an outpock-
eting, or herniation, of the mucosa of the large colon through the
muscle layers of the intestinal wall. Diverticular disease occurs
when the outpocketing becomes symptomatic. Diverticulitis is
the inflammation and infection of the diverticulum/diverticula
and may occur with such complications as perforation, obstruc-
tion, abscess formation, fistula, and bleeding.44,71,73-75
The signs and symptoms of diverticular disease may include
the following71,75,76:
• Achy, left lower quadrant (LLQ) pain and tenderness (pain
intensifies with acute diverticulitis)
• Urinary frequency
• Fever and elevated white blood cell (WBC) count (acute di-
verticulitis)
• Constipation, bloody stools, or both
• Nausea, vomiting, and anorexia
Management of diverticular disease is based on presentation and
includes any of the following71,73,75-77:
• Dietary modifications (increased fiber and decreased red
meat are advocated but lack supportive evidence)
• Bowel rest (clear liquids)
• IV fluids
• Pain medications
• Antimicrobial agents
• Invasive management is based on severity and may include
percutaneous abscess drainage, laparoscopic colectomy, or
 
220 CHAPTER 8     Gastrointestinal System
Hernia
Abdominal Hernia.  An abdominal hernia is an abnormal pro-
trusion of bowel that is generally classified by the area where the
protrusion occurs. These include the following common areas:
inguinal, femoral, ventral or incisional, and umbilical.44,78,79 A
hernia is referred to as reducible when its contents can be replaced
within the surrounding musculature and is irreducible or incarcer-
ated when it cannot be replaced. A strangulated hernia has com-
promised circulation, with the potential to be fatal. The signs
and symptoms of abdominal herniation include44,79:
• Abdominal distention, nausea, and vomiting
• Observable bulge with position changes, coughing, or laughing
• Paresthesia, if nerve compression occurs with hernia
• Pain of increasing severity with fever, tachycardia, and ab-
dominal rigidity (if the herniated bowel is strangulated)
Management of herniation includes any of the following44,79-81:
• “Watchful waiting” in asymptomatic cases
• Surgical repair with use of laparoscopy
• Open surgical reinforcement of weakened area with mesh,
wire, or fascia
• Temporary colostomy in cases of intestinal obstruction  • Insertion of a nasogastric tube in cases of severe abdominal
Hiatal Hernia.  A hiatal hernia is a protrusion of any
abdominal structure besides the esophagus upward through the
esophageal hiatus of the diaphragm into the thoracic cavity.82,83
Hiatal hernias are classified as types I through IV, according to
the anatomic structures that are involved.83 Clinical manifesta-
tions mimic those of GERD, including heartburn-like epigas-
tric pain, which usually occurs after eating and with recumbent
positioning, dysphagia, chest pain, dyspnea, or hoarseness.82
Management of hiatal hernia can include behavior modi-
fications, such as avoiding reclining after meals, drinking
caffeine or alcohol, and smoking tobacco. Eating small, fre-
quent, bland meals with a high fiber content may also be
beneficial. Pharmacologic intervention typically includes
acid-reducing medications. Surgical management of the hia-
tal hernia, if indicated, can be performed laparoscopically or
via open procedures.82,83
CLINICAL TIP
Positions associated with airway clearance techniques or func-
tional mobility may exacerbate pain in patients who have a her-
nia, particularly a hiatal hernia. Therefore careful modification
of these interventions will be necessary for successful comple-
tion of these activities. Refer to Chapter 22 for more informa-
tion on airway clearance techniques.  
Intestinal Obstructions
Failure of intestinal contents to be propelled forward in either
the small intestine or large intestine and can be caused by
mechanical or functional obstructions.
Mechanical Obstruction.  Blockage of the bowel by adhe-
sion, herniation, volvulus (twisting of bowel on itself), tumor,
inflammation, infarction, or invagination (intussusception) of a
bowel segment into an adjacent segment (much like a telescope)
constitutes mechanical obstruction.44,84,85  life-threatening situation.93
Functional Obstructions (Paralytic Ileus).  Paralytic ileus
is defined as “functional inhibition of propulsive bowel activ-
ity.”86 Obstructions may result from abdominal surgery, intes-
tinal distention, hypokalemia, peritonitis, severe trauma, spinal
fractures, ureteral distention, or use of narcotics.
Signs and symptoms of intestinal obstructions (either
mechanical or functional) include the following87:
• Sudden onset of crampy abdominal pain that may be inter-
mittent as peristalsis occurs
• Abdominal pain and/or distention
• Nausea, 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 dehydration or
peritonitis
• Bloody stools
Management of intestinal obstructions includes any of the
following86-89:
distention or intractable vomiting
• Restoration of intravascular volume
• Surgical resection (laparoscopic technique or open laparoto-
my) of mechanical obstructions from adhesions, necrosis, tu-
mor, or unresolved inflammatory lesions, particularly if the
obstruction is in the large intestine
• Colostomy placement and eventual colostomy closure (colos-
tomy closure is also referred to as colostomy takedown)
Constipation can occur after major orthopedic surgery (e.g.,
total joint arthroplasty) as a result of frequent narcotic use for
adequate pain control.3 In this patient population (and in all
postoperative surgical populations), early mobilization can help
lessen the likelihood of this complication. Abdominal distention
will also have an effect on other functions that may affect how
well patients are able to progress with their physical therapy
treatment. The ability to take deep breaths, reach for objects,
and mobilize will be much more difficult with the extra girth
associated with abdominal distention. 
Intestinal Ischemia
Ischemia within the intestinal tract can be acute or chronic, in
most cases occurring either in the colon or in areas supplied by
the superior mesenteric artery.90 Another form of intestinal isch-
emia is called ischemic colitis. Intestinal ischemia can be caused
by many factors, such as thrombosis or emboli to the superior
mesenteric artery (acute mesenteric ischemia); intestinal stran-
gulation; chronic vascular insufficiency; hypotension; oral con-
traceptives (combined with history of thrombophilic defects)91;
NSAIDs; and vasoconstrictors, such as vasopressin and dihy-
droergotamine. In situations when vasoconstriction occurs in
the absence of vascular disease, the term nonocclusive mesenteric
ischemia (NOMI) is used.92 Methamphetamine and cocaine have
vasoconstrictive properties that can also lead to intestinal isch-
emia. Significant ischemia that is not managed in a timely man-
ner can lead to intestinal necrosis or gangrene and prove to be a

The signs and symptoms of intestinal ischemia include90:
• 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 muscle
guarding
• Tachycardia, hypotension, and fever (with necrosis)
Management of intestinal ischemia may include any of the fol-
lowing90,92,94:
• Revascularization procedures, either via open or endovascu-
lar revascularization
• Resection of necrotic segments with temporary colostomy or
ileostomy placement and subsequent reanastomosis of func-
tional segments as indicated
• Antiinfective agents
• Vasodilators or vasopressors (blood perfusion enhancement)
• Anticoagulation therapy
• IV fluid replacement
• Insertion of nasogastric tube
• Analgesic agents  eryma whipplei)
Irritable Bowel Syndrome
Irritable bowel syndrome (IBS), also referred to as irritable or
spastic colon, is characterized by abdominal pain and altered bowel
habits. The Rome III diagnostic criteria include abdominal pain
or discomfort that persists for at least 3 days per month in the
past 3 months associated with two or more of the following95,96:
• Defecation relieves or improves pain.
• Onset is associated with a change in the frequency of bowel
movement.
• Onset is associated with a change in the form or appearance
of the stool.
Motility of the large bowel can be affected by emotions; history
of physical or sexual abuse; certain foods, such as milk products;
neurohumoral agents; GI hormones; toxins; prostaglandins; and
colon distention.97,98 Some evidence suggests that patients with
IBS may have bacterial overgrowth in their small intestines.99
Additional signs and symptoms of IBS include96,97:
• Diffuse abdominal pain, reports of feeling bloated, or both
• Constipation (<3 bowel movements/week) or diarrhea (>3
bowel movements/day)
• Abnormal stool form (hard or loose stool)
• Passing mucus
• Correlation of GI symptoms with eating, high emotional
states, or stress
• No weight loss
• Tender sigmoid colon on palpation
Management of IBS may include any of the following95-97,100:
• Laxatives or antidiarrheal (loperamide) agents
• Antispasmodic agents
• Antibiotic therapy
• Probiotics
• Dietary modifications, including a high-fiber diet
• Counseling or psychotherapy, with or without use of antide-
pressants
• Routine exercise  • Antibiotic therapy
Gastrointestinal System     CHAPTER 8 221
Malabsorption Syndromes
Malabsorption syndrome is a general term for acquired and con-
genital disorders that are characterized by the small intestine’s
failure to absorb and digest carbohydrates, proteins, fats, water,
vitamins, and electrolytes.101,102 The nutritional deficits that
result from malabsorption can lead to other chronic disorders,
such as anemia or osteoporosis. Undernutrition can be mea-
sured as a body mass index (BMI) of less than 18.5 in adults.103
Acquired malabsorption can result from numerous etiologies,
such as104,105:
• Pancreatic insufficiency (chronic pancreatitis, carcinoma)
• Short bowel syndrome
• Mechanical obstruction
• Crohn’s disease (see the Crohn’s Disease section)
• Celiac disease (small intestine mucosal damage from glutens
[e.g., wheat, barley, rye, and oats])
• Bariatric surgery
• Infection
• Liver disease (cirrhosis)
• Whipple’s disease (infection of the small intestine by Troph-
The signs and symptoms of malabsorption syndromes may in-
clude101,102,106:
• Diarrhea, steatorrhea (excessive fat excretion), or both
• Anorexia and weight loss
• Muscle wasting
• Anemia
• Abdominal bloating
Management of malabsorption syndromes includes any of the
following102,106,107:
• Antidiarrheal agents
• Dietary modifications and nutritional support
• Fluid hydration, electrolyte, vitamin, and mineral support
• Enteral or parenteral feeding 
Peritonitis
Peritonitis is general or localized inflammation in the peri-
toneal cavity and may be acute, chronic, septic or aseptic,
and primary or secondary. Etiologies for primary peritoni-
tis include ascites and bacterial infection, with secondary
peritonitis typically occurring as a result of perforation of
the GI tract, gangrene of the bowel, trauma, and surgical
irritants.5,44,108,109
The signs and symptoms of peritonitis include5,44,110:
• Generalized abdominal pain
• Fever, nausea, and/or vomiting
• Abdominal guarding, with diffuse tenderness and rigidity as
inflammation progresses
• Abdominal distention
• Diminished or absent bowel sounds
• Rebound tenderness
• Tachycardia, hypotension
Management of peritonitis includes any of the following5,44,108,110:
• Abdominal imaging
• Laparoscopic evaluation, with or without subsequent surgi-
cal correction of primary etiology
222 CHAPTER 8     Gastrointestinal System
• F luid management with electrolytes and colloids
• Pain management
• Nasogastric suctioning
• Invasive monitoring of central hemodynamic pressures  • Dehydration
Crohn’s Disease
Crohn’s disease, a form of idiopathic inflammatory bowel disease
(IBD), can occur in any part of the GI system. The small intes-
tine, particularly the terminal ileum and the proximal portion
of the colon, is most commonly involved, whereas the esophagus
and the stomach are rarely affected. Suspected causes of Crohn’s
disease include an interaction among genetic predetermination,
dysregulated immune mechanisms, infectious agents, psycho-
logical issues, dietary factors, smoking, and environmental
factors.109,111,-112
The signs and symptoms of Crohn’s disease may include the
following111,112:
• Constant crampy abdominal pain, often in RLQ, not relieved
by bowel movement
• RLQ abdominal mass
• Diarrhea
• Weight loss
• Fatigue
• Low-grade fever
Management of Crohn’s disease includes any of the follow-
ing109,111-113:
• Antiinflammatory medications (corticosteroids)
• Antibiotics, only in cases of abscess or fistula formation
• Immunosuppressants (thiopurines, methotrexate)
• Nutritional therapy
Biologic therapies include the following:
• Nasogastric suctioning
• Activity limitations (in acute phases)
• Surgical resection (in refractory or complicated cases) of in-
volved area, either with open laparotomy or video-assisted
laparoscopy, with or without ileostomy or stoma
The complications of Crohn’s disease can include111:
• Intestinal obstruction, possibly leading to fistula, abscess, or
perforations in the intestine
• Inflammation of the eyes, skin, and mucous membranes
• Arthritis and ankylosing spondylitis
• Gallstones
• Vitamin B12 deficiency
• Thromboembolism  matous polyps44
Ulcerative Colitis
Ulcerative colitis is a chronic idiopathic inflammatory bowel
disease (IBD) of the mucosal layer of the rectum and progress-
ing proximally to the colon. The definitive etiology of ulcer-
ative colitis is unknown, but suspected causes are similar to
those of Crohn’s disease. Inflammation can be mild, moderate,
or severe.109,114-116
The signs and symptoms of ulcerative colitis include114-116:
• Crampy lower abdominal pain that is relieved by a bowel
movement
• Bloody stools
• Diarrhea
• Incontinence
• Nocturnal defecations
• Fatigue with anorexia and weight loss
• Tachycardia
Management of ulcerative colitis includes any of the follow-
ing114-116:
• Antiinflammatory medications, including 5-acetylsalicylic
acid (5-ASA) drugs, and progressing to steroids, as indicated
• Immunosuppressants
• Biologic therapies
• Dietary modification
• Surgical intervention, when indicated, typically consists of
restorative protocolectomy with ileal pouch–anal anastomo-
sis (IPAA).
• Ongoing surveillance for colon cancer
Related manifestations and complications from ulcerative colitis
may include115,116:
• Arthritis, ankylosing spondylitis, osteomalacia, and osteoporosis
• Inflammation of the eyes, skin, and mucous membranes
• Hepatitis, bile duct carcinoma
• Primary sclerosing cholangitis
• Anemia, leukopenia, or thrombocytopenia 
Polyps
Polyps of the colon are mucosal lesions that project within the
bowel and consist of neoplastic and nonneoplastic (hyperplastic
and inflammatory) types. Adenomatous polyps are neoplastic
polyps and have the most potential to become a precursor to
colorectal cancer (adenocarcinoma).44,117,118
The signs and symptoms of polyps are as follows117,118:
• Rectal bleeding (occult or overt)
• Constipation or diarrhea
• Crampy pain in the lower abdomen
Management of polyps includes117,118:
• Beginning at age 45 years, screening and modification of
risk factors for colorectal cancer, such as excess body weight;
cigarette smoking; high consumption of alcohol and red meat
and processed meat; and low consumption of dietary fiber and
calcium, fruits, and vegetables; and physical inactivity119
• Colonoscopy, flexible sigmoidoscopy, and CT colonography
• Tissue biopsy to determine malignancy potential
• Polypectomy via a sigmoidoscope or colonoscope, for adeno-
• Surgical resection of involved area, if indicated, with or with-
out ileostomy 
Intestinal Tumors
Benign or metastatic neoplasms of the intestine include colonic
adenomas (polyps), villous or papillary adenomas, lipomas, leio-
myomas, and lymphoid hyperplasia. Tumors affect motility and
absorption functions in the intestine (see the Cancers in the
Body Systems section in Chapter 11 for further details). 
Anorectal Disorders
Disorders of the anus and rectum generally involve inflamma-
tion, obstruction, discontinuity from the colon, perforations, or

tumors. Anorectal disorders may include, hemorrhoids, anorec-
tal abscess and fistula, anal fissure, anorectal varices, anal steno-
sis rectal prolapse, pruritus ani, and anal carcinoma. Signs and
symptoms include pain with defecation and bloody stools. Man-
agement is supportive, depending on the disorder, and surgical
correction is performed as necessary.85,105,120  to 6 hours postoperatively and occurring every 2 to 4 hours
Morbid Obesity
Obesity is a complex disorder with many contributing meta-
bolic, psychological, and genetic factors.121 It is defined as a
chronic disease characterized by an excess of body fat.122 The
medical standard for measuring obesity is BMI.122 BMI is deter-
mined by dividing the person’s weight in kilograms by their
height in meters squared.122 Normal BMI ranges from 18.5 to
24.9; BMI of 25 to 29.9 is considered overweight; and BMI
of 30 or more is considered obese.123 Central adiposity (vis-
ceral or abdominal obesity) is estimated by measuring waist
circumference.124
Comorbidities, such as type 2 diabetes, cardiovascular dis-
ease, dyslipidemia, obstructive sleep apnea, degenerative joint
disease, renal disease, cholelithiasis, depression, and cancer,
have been linked to morbid obesity.125-127 An increased risk
of heart disease, hypertension, hyperlipidemia, and diabe-
tes are associated with central adiposity as waist circumfer-
ence exceeds greater than 40 inches (>102 cm) in males and
greater than 35 inches (>88 cm) in females.124 Conservative
treatment involves weight loss measures, with a goal of 10%
reduction in body weight; these measures include diet modi-
fications, pharmacotherapy, behavioral therapy, and increased
physical activity.124 Bariatric surgery is indicated for patients
with a BMI greater than 40 kg/m2 or a BMI greater than
35 kg/m2 and related comorbidities, including type 2 dia-
betes mellitus, cardiovascular disease, obstructive sleep
apnea, and physical difficulties with activities of daily living
(ADLs).124,127,128
Bariatric surgical options include121,127-129
• Roux-en-Y gastric bypass
• Laparoscopic adjustable gastric banding (LAGB)
• Vertical banded gastroplasty
• Biliopancreatic diversion with or without duodenal switch
• Jejunoileal bypass
• Sleeve gastrectomy
All of these bariatric procedures can be performed either
through open laparotomy or laparoscopically, except for bilio-
pancreatic diversion, which is typically performed as an open
procedure.127 One year after bariatric surgery, weight loss is pos-
itively associated with participation in an exercise program.130
Improved functional capacity and quality of life, measured by
the 6-minute walk test (6MWT) and Short Form Health Survey
(SF-36), respectively, have also been reported in patients 3 and 6
months after gastric bypass surgery.131
Physical Therapy Considerations
• Many facilities are outfitted with safe patient handling
equipment (e.g., ceiling lifts/mechanical lifts, gait/transfer
belts, and beds), which should be used to assist with safe
mobility for the patient and the therapist.
Gastrointestinal System     CHAPTER 8 223
• B e sure to check weight limits on devices, such as wheel
chairs and walkers of specialized bariatric equipment (e.g.,
gait/transfer belts, walkers, and wheel chairs); assistance
from several qualified personnel is recommended.132-135
• Early and frequent ambulation is recommended beginning 2
while awake.
• In patients who are critically ill after bariatric surgery, exer-
cise should be terminated until further consultation with the
physician if the following occur136:
• Increase of 20 mmHg or greater in systolic pressure
• Decrease of 20 mmHg or greater in diastolic pressure
• Heart rate increase or decrease by greater than 20 beats
per minute
• Severe dyspnea or paradoxical breathing
• Dizziness
• Excessive sweating
• Patient report of feeling faint
• In patients who are not critically ill immediately after bar-
iatric surgery, exercise intolerance can be monitored by the
presence of moderate dyspnea, heavy perspiration, muscle
weakness, or burning immediately after exercise or walk-
ing.137 Additional information on exercise after bariatric
surgery can be found in the meta-analysis by Ren et al.138
• To prevent pulmonary complications, active breathing
exercises and airway clearance techniques should be per-
formed.132,139
• To optimize skin integrity, consistent and diligent skin inspec-
tion is essential for bariatric surgery patients, especially in such
areas as surgical incision sites and skin folds because decreased
mobility and poor vascular supply to adipose tissue can facili-
tate the development of integumentary impairments.132,140,141 
Liver and Biliary Disorders
The liver is the only organ in the body with regenerative prop-
erties142; therefore patients with acute liver inflammation will
heal well with proper rest and medical treatment. To aid in the
proper healing of the liver, physical therapists should avoid
overfatiguing patients with functional activities.
Hepatitis
Hepatic inflammation and hepatic cell necrosis may be acute
or chronic and may result from viruses, autoimmune diseases,
alcohol abuse, certain medications, and Wilson’s disease (a rare
copper metabolism disorder).143,144 Viral hepatitis is the most
common type of acute hepatitis and can be classified as hepati-
tis A, B, C, D, and E (i.e., HAV, HBV, HCV, HDV, and HEV,
respectively).145,146
Hepatitis A, B, and C are the most common types of viral hepa-
titis. Hepatitis A is transmitted via the fecal–oral route, either from
person to person or from contaminated water sources; it is typi-
cally self-limiting and a vaccine is available. Hepatitis B is more
common than hepatitis C, but both are transmitted through blood
and body fluids. Vaccination is available only for hepatitis B. Acute
viral hepatitis generally resolves with appropriate medical manage-
ment, but in some cases, hepatitis B and C can become chronic and
result in end-stage cirrhosis or hepatocellular carcinoma.144,146,147
224 CHAPTER 8     Gastrointestinal System

The signs and symptoms of hepatitis include145,146: HEART

• Abrupt onset of malaise
• Fatigue and muscle weakness Esophagus
• Fever
• Loss of appetite, weight loss, or anorexia Esophageal varices
• Nausea, abdominal discomfort, and pain LIVER
(left lobe)
• Headache
Enlarged
• Jaundice spleen
• Dark-colored urine Collaterals
Management of hepatitis includes any of the following145,147:
CIRRHOTIC
• Adequate periods of rest LIVER
• Vaccinations (only against HAV, HBV, HDV) (right lobe)
• Fluid and nutritional support
• Removal of precipitating irritants (e.g., alcohol and toxins)
Portal
• Antiinflammatory agents
• Antiviral agents Splenic vein
Gallbladder Dilated
CLINICAL TIP portal vein
Hepatic artery Blood from bowel
Health care workers must ensure that they are properly vaccinated
against hepatitis B in case of exposure to blood and body fluids or Inferior vena cava Aorta
inadvertent needle stick during contact with the patient, or patient
surroundings (e.g., bed linens). Proper vaccination includes receiv-
FIG. 8.3
ing periodic measurements of antibody titers to the viruses and Portal hypertension. (From Goodman CC, Fuller KS, Boissonnault WG,
supplementation with booster shots, as needed, to maintain eds. Pathology: Implications for the Physical Therapist. 3rd ed. St. Louis:
appropriate immunity against these infections. Additionally, Saunders; 2009.)
proper use of personal protective equipment is essential.148  
Cirrhosis
Cirrhosis is a chronic disease state that is characterized by hepatic Management of cirrhosis includes149,151:
parenchymal cell destruction and necrosis, as well as fibrosis or scar • Addressing primary causes, such as viral hepatitis; cessation
tissue formation. The fibrosis that occurs in the liver reduces its of alcohol intake
ability to metabolize body fuels, hormones, toxins, and medications • Supportive care, including IV fluids, whole blood and blood
along with an inability to synthesize plasma proteins (albumin), products, colloid (albumin), vitamin and electrolyte replace-
clotting factors, and bilirubin.144 Progression of cirrhosis can be ment, and dietary and behavioral modifications (eliminate
measured by the model for end-stage liver disease (MELD) scores.149 alcohol consumption)
The primary complications that can occur from cirrhosis include • Medical (beta-blockade and corticosteroids) or surgical cor-
portal hypertension (Fig. 8.3), ascites, jaundice, impaired clotting rection (or both) of primary etiology or secondary complica-
ability, hepatic encephalopathy, and variceal bleeding.108,150,151 tions, as indicated
Cirrhosis may result from a variety of etiologies, including149,151: • Paracentesis to drain peritoneal edema (ascites)
• Viral hepatitis • Supplemental oxygen
• Autoimmune diseases • Liver transplantation (see Chapter 14) 
• Toxin exposure
• Drugs
• Alcohol abuse Hepatic Encephalopathy and Coma
• Cholestatic diseases Acute and chronic liver diseases, particularly cirrhosis, may
• Metabolic diseases lead to neuropsychiatric manifestations that may progress from
Signs and symptoms of cirrhosis include108,144,151: hepatic encephalopathy to precoma to coma. The neuropsychi-
• Recent weight loss or gain atric manifestations are linked to multiple factors, with ammo-
• Fatigability nia intoxication, changes in cerebral blood flow, and altered
• Jaundice neurotransmitters being involved.108,144,152,153
• Ascites (fluid accumulation in the peritoneum) The signs and symptoms of hepatic encephalopathy include
• Anorexia, nausea, or vomiting a combination of impaired mental status and neuromuscular
• Fever dysfunction occurring over a period of hours to days. Altered
• Decreased urine output (urine dark yellow or amber) consciousness may be present and includes a number of symp-
• Associated GI manifestations of esophageal varices, bowel toms ranging from changes in personality to disorientation,
habit changes, and GI bleeding sleep disturbance, stupor, and coma.152,153 Table 8.9 provides
• Altered mental status an overview of the evaluation for severity levels associated with
• Flapping tremor (asterixis) hepatic encephalopathy.
 Gastrointestinal System     CHAPTER 8 225

TABLE 8.9  West Haven Criteria of Altered Mental Status in Hepatic Encephalopathy
Grade Consciousness Intellect and Behavior Neurologic Findings
0 Normal Normal Normal; impaired psychomotor testing
1 Mild lack of awareness Shortened attention span; impaired addition Mild asterixis or tremor
or subtraction
2 Lethargic Disoriented; inappropriate behavior Obvious asterixis; slurred speech
3 Somnolent but arousable Gross disorientation; bizarre behavior Muscular rigidity and clonus; hyperreflexia
4 Coma Coma Decerebrate posturing

Data from Ferenci P, Lockwood A, Mullen K, et al. Hepatic encephalopathy—definition, nomenclature, diagnosis, and quantification: final report of the working party
at the 11th World Congresses of Gastroenterology, Vienna, 1998. Hepatology. 2002;35:716-721, in Sundaram V, Shaikh OS. Hepatic encephalopathy: pathophysiology
and emerging therapies. Med Clin North Am. 2009;93:819-836.

Management of hepatic encephalopathy and coma may con-
sist of any of the following152,153,154:
• Administering nonabsorbable disaccharides, such as lactu-
lose and lactitol, which is the mainstay of treatment to help
reduce ammonia levels
• Correction of fluid and electrolyte or acid–base imbalances,
or both
• Supplemental oxygen
• Removal of any precipitating factors
• Nutritional support
• Antibiotic therapy
• Probiotics/prebiotics/synbiotics
• Liver transplantation  plantation.
Cholecystitis with Cholelithiasis
Cholecystitis is acute or chronic inflammation of the gall-
bladder. It is commonly associated with obstruction by
gallstones.144,155,156 Gallstone formation (cholelithiasis) is asso-
ciated with three factors: gallbladder hypomobility, supersatu-
ration of bile with cholesterol (cholesterol stones), and crystal
formation from an increased concentration of insoluble biliru-
bin salts (pigment stones) in the bile. Cholelithiasis can lead
to secondary bacterial infection that further exacerbates the
cholecystitis.157-159
The signs and symptoms of cholecystitis include156-158:
• Pain in the right upper quadrant (RUQ), with possible pain
referral to the interscapular region or the right shoulder
• Rebound tenderness and abdominal rigidity
• Jaundice
• Anorexia
contributing factors are gallstones and alcohol and drug
abuse.144,161,162 Other contributing factors also include161,162:
• Trauma
• Endoscopic retrograde cholangiography (see Table 8.7)
• Hyperlipidemia/hypertriglycemia
• Hyperparathyroidism/ hypercalcemia
• Vasculitis
• Pancreatic obstruction with tumors
• Autoimmune pancreatitis
• Infections
• Medications
• Postoperative sequelae from cardiac surgery, including trans-
The signs and symptoms of acute pancreatitis160-162:
• Steady, dull abdominal pain in the epigastrium, LUQ, or
periumbilical area often radiating to back, chest, and lower
abdomen (Pain can be exacerbated by food, alcohol, vomit-
ing, and resting in the supine position.)
• Nausea, vomiting, and abdominal distention
• Fever, tachycardia, and hypotension (in acute cases)
• Abdominal tenderness or rigidity
Management of acute pancreatitis includes any of the follow-
ing160-162:
• Pain management, generally with opioids
• IV fluid and electrolyte replacement
• Enteral or parenteral feeding
• Removal of obstructions, such as cholecystectomy
• Supplemental oxygen and mechanical ventilation (as indi-
cated)
• Invasive monitoring (in more severe cases) 

• Nausea, vomiting, or both

• Fever
• Positive Murphy’s sign (inhibited inspiration on palpation)
in RUQ
Management of acute cholecystitis primarily involves laparo-
scopic cholecystectomy (gallbladder removal).156  modifications, and surgical procedures. Nutritional support and
Pancreatic Disorders
Pancreatitis
Inflammation of the pancreas can be acute or chronic, with acute
cases potentially progressing into chronic pancreatitis.144 Acute
pancreatitis can be categorized as necrotizing pancreatitis
or interstitial edematous pancreatitis.160 The most common
Management
General management of GI disorders may consist of any of the
following: pharmacologic therapy, nutritional support, dietary
dietary modifications are beyond the scope of this book. This sec-
tion focuses on pharmacologic therapy and surgical procedures.
A discussion of physical therapy intervention is also included.
Pharmacologic Therapy
Medications used to treat GI disorders can be broadly catego-
rized as (1) those that control gastric acid secretion and (2)
those that normalize gastric motility. Refer to Chapter 19 for
226 CHAPTER 8     Gastrointestinal System

an overview of these medications (Table 19.27, Antacids; Table
19.28, Antidiarrheal Medications; Table 19.29, Antispasmodic
Medications; Table 19.30, Cytoprotective Medications; Table
IV-31, Histamine-2 Receptor Antagonists [H2RAs]; Table
19.32 Laxatives; and Table 19.33, Proton Pump Inhibitors).
Other medications that do not fall into these categories are
mentioned in specific sections under Health Conditions earlier
in the chapter. 
Surgical Procedures
Surgical intervention is indicated in GI disorders when medical
intervention is insufficient. Table 8.10 provides an overview of

TABLE 8.10  Common Gastrointestinal (GI) Surgical Procedures

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 re-
moved (e.g., transverse colectomy is resection of the transverse colon). A colectomy may also have an associ-
ated colostomy or ileostomy. Performed either through open laparotomy or laparoscopically.
Colostomy A procedure used to divert stool from a portion of the diseased colon to the exterior. There are three general
types of colostomies: end, double-barrel, and loop colostomy.
End (Brooke) colostomy Involves bringing the functioning 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.
Double-barrel colostomy Two separate stomas are formed on the abdominal wall. The proximal stoma is the functional end that is con-
nected 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 colostomy Created by bringing a loop of 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. May be used as a temporary colostomy.
Fundoplication Upper curve of stomach (fundus) is wrapped around the esophagus at its juncture with the stomach.
Helps reinforce the esophageal sphincter in situations of hernia and/or manage gastroesophageal reflux disease
(GERD) to prevent acid reflux.32
Gastric bypass Creation of a small gastric pouch to limit oral intake in restrictive and malabsorptive disorders.105,107
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 (Fig. 8.4).105,107
Vertical banded gastroplasty Creates a small gastric pouch via 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 Fig. 8.4).105,106
Adjustable gastric banding Creates a small pouch in the upper stomach using an adjustable silicone band, with a resulting narrow outlet
to the small intestine (see Fig. 8.4).105,107
Gastrectomy Removal of a portion (partial) or all (total) of the stomach. Indicated for gastric cancer and peptic ulcer dis-
ease. Partial gastrectomy may either be a Billroth I or Billroth II procedure.
Billroth I (Antrectomy gastro- Resection of the lower portion of the antrum, pylorus, proximal duodenum and anastomosis with the remain-
duodenostomy) ing duodenum.
Billroth II (gastrojejunostomy) Resection of the distal portion of the stomach and the duodenum and anastomosis with the jejunum.
Ileostomy A procedure similar to a colostomy and performed in areas of the ileum (distal portion of the small intestine).
Resection and reanastomosis The removal (resection) of a 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 reanastomosed—for example, a pancreaticojejunostomy is the joining of the
pancreatic duct to the jejunum after a dysfunctional portion of the pancreas is resected.
Whipple procedure (resection) Consists of en bloc removal of the duodenum, a variable portion of the distal stomach and the proximal
(pancreaticoduodenectomy) jejunum, gallbladder, head of the pancreas, common bile duct, and regional lymph nodes. This removal
is followed by pancreaticojejunostomy, choledochojejunostomy, and gastrojejunostomy. This procedure is
reserved for the patient with chronic pancreatitis or pancreatic cancer.
GI transplantation Approved transplant procedures for patients with irreversible intestinal failure include isolated intestinal,
combined liver-small intestine and multivisceral transplantation. Refer to Chapter 14 for a description of
transplant considerations.

Data from Cox, JA, Rogers, MA, Cox, SD. Treating benign colon disorders using laparoscopic colectomy. AORN J. 2001;73(2):375; Beckingham IJ. ABC of diseases
of liver, pancreas, and biliary system, gallstone disease. BMJ. 2001;322(7278):91; Pedersen AG, Petersen OB, Wara P, et al. Randomized clinical trial of laparoscopic
versus open appendicectomy. Br J Surg. 2001;88(2):200-205; McMahon AJ, Fischbacher CM, Frame SH, et al. Impact of laparoscopic cholecystectomy: a population-
based study. Lancet. 2000;356(9242):1632; Ben-David K, Sarosi GA. Appendicitis. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s Gastrointestinal
and Liver Disease. 9th ed. Philadelphia: Saunders; 2010:2059-2071; Julka K, Ko CW. Infectious diseases and the gallbladder. Infect Dis Clin N Am. 2010;24:885-898;
Cima RR, Pemberton JH. Ileostomy, colostomy and pouches. In Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 9th
ed. Philadelphia: Saunders; 2010:2015-2025; Mann BD. Surgery: A Competency-Based Companion. Philadelphia: Saunders; 2011; Colquitt JL, Picot J, Loveman E, Clegg
AJ. Surgery for obesity. Cochrane Database Syst Rev. 2009;(2):CD003641.; Abrams P, Abu-Elmagd K, Felmet K, et al. Intestinal and multivisceral transplantation. In:
Vincent JL, Abraham E, Moore FA, et al., eds. Textbook of Critical Care. 6th ed. St. Louis: Elsevier; 2011:1443-1453; Hinkle JL, Cheever KH. Brunner and Suddarth’s
Textbook of Medical Nursing. 14th ed. Philadelphia: Wolters Kluwer; 2018:1299-1305, 1326-1334, 1449-1452.

COMMON BARIATRIC PROCEDURES
A B
Vertical-banded
gastroplasty
FIG. 8.4
Common bariatric procedures. (From Still CD, Jensen GL. Obesity. In: Rakel RE, Bope ET, eds. Conn’s Current Therapy. 60th ed. Philadelphia: Saunders; 2008.)
common GI surgical procedures. The location and extent of inci-
sions depend on the exact procedure. The decision to perform
either an open laparotomy or a laparoscopic repair will depend
on physician preference based on surgical difficulty and docu-
mented outcomes of specific techniques. Many open laparot-
omy procedures requiring large abdominal incisions are being
replaced with laparoscopic procedures. Laparoscopic procedures
have been shown to reduce length of hospital stay, many post-
operative complications, or both.73,157,163,164 Postoperative com-
plications may include pulmonary infection, wound infection,
and deconditioning resulting from prolonged bed rest. Refer to
Chapter 20 for further descriptions of the effects of anesthesia.
With a colostomy, an external, plastic 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, trans-
verse, or sigmoid portions of the colon. Sigmoid colostomies are
most commonly performed.
Physical Therapy Considerations
• Before mobilizing a patient, the therapist should ensure that
a patient’s 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 mini-
mize 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 while the
head of the bed is being lowered may also decrease incisional
discomfort.
• Patients with new colostomies may experience psychosocial
concerns postsurgery and have difficulty with acceptance
of the new device. Therapists need to be respectful of the
Gastrointestinal System     CHAPTER 8 227
C
Adjustable gastric Roux-en-Y gastric
banding bypass
p­ atient’s time frame for adjustment and modify treatment
accordingly. Examples include remaining in the hospital
room and keeping the colostomy area covered at all times. 
Physical Therapy Management
The following are general goals and considerations for the physi-
cal therapist when working with the patient who has GI dys-
function. These considerations should be adapted to a patient’s
specific needs.
Goals
The primary physical therapy goals for this patient popula-
tion are similar to those for other patients in the acute care set-
ting: (1) optimization of function, (2) maximization of activity
tolerance and endurance, and (3) prevention of postoperative
complications. 
Physical Therapy Considerations
In addition to considerations described in earlier sections of this
chapter, additional considerations include, but are not limited
to, the following:
1. Patients with GI dysfunction may have increased fatigue
levels as a result of poor nutritional status; therefore fatigue
level should be considered while determining frequency, in-
terventions, and goal setting.
a. Consultation with the registered dietitian nutritionist is
helpful in gauging the appropriate activity prescription,
which is based on the patient’s caloric intake, particularly
in patients with chronic liver disease.165 It is difficult to im-
prove the patient’s strength or endurance if his or her caloric
intake is insufficient for the energy requirements of exercise.
b. Review the patient’s laboratory values to determine treat-
ment parameters for that session.166 Refer to Chapters 7 and
14 for the pertinent sections on complete blood count, co-
agulation profile, and laboratory value guidelines for activity.
228 CHAPTER 8     Gastrointestinal System
2. Patients with GI dysfunction may have certain precautions
with positioning.
a. Dysphagia can be exacerbated in the supine position and
may also lead to aspiration pneumonia.167
b. Lying in the supine position can aggravate GERD, espe-
cially after a meal.
c. Portal hypertension can be exacerbated with activities
that increase intraabdominal pressure, therefore exercises
and/or positions may need modifications.144 If the patient
has associated esophageal varices resulting from portal
hypertension, then the risk of variceal rupture may be in-
creased with similar activities and positions that increase
intraabdominal pressure.
d. Examples include maneuvers that create the Valsalva ef-
fect, such as coughing. The increase in intraabdominal
pressure from the Valsalva maneuver can further exac-
erbate the esophageal varices.168 (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
rheumatic disease and GI dysfunction.
a. NSAID use is a causative/risk factor for many inflam-
matory and hemorrhagic conditions of the GI system
and may be withheld or modified in patients with any
exacerbation of these GI conditions. Patients who were
reliant on NSAIDs for pain management before admis-
sion may need additional pain management strategies
from the physical therapist to optimize functional
­mobility.
4. Patients with ascites or upper abdominal incisions are at risk
for pulmonary complications. Ascites and surgical incisions
create ventilation restrictions for the patient.165,169-171
a. Ascites and surgical incisions can hinder cough effective-
ness and functional mobility, both of which can further
contribute to pulmonary infection. Effective pain man-
agement before and during physical therapy intervention,
along with diligent position changes, can assist with air-
way clearance.
b. Instruction on incisional splinting during deep breathing
and coughing, as well as early mobilization with or with-
out assistive devices, will help prevent the development
of pulmonary complications and deconditioning.172
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 9 Genitourinary System
C H APT ER  
CHAPTER OUTLINE
Introduction
Body Structure and Function
Clinical Evaluation
Physical Examination
Diagnostic Tests
Health Conditions
Renal System Dysfunction
Lower Urinary Tract Dysfunction
Prostate Disorders
Endometriosis
Medical Management
Renal Replacement Therapy
Surgical Interventions
Physical Therapy Management
Jaime C. Paz
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . Review the structure and function of the genitourinary system
2. Describe the clinical evaluation of the genitourinary system, including physical examination and diagnostic
studies
3. Identify the various health conditions of the genitourinary system
4. Provide information about the medical and surgical management of genitourinary disorders, including
renal replacement therapy
5. Describe physical therapy management in patients with genitourinary diseases and disorders
  
Introduction
Health Conditions related to genitourinary dysfunction can affect a patient’s functional status
through impairment of activity, pain, and changes to hemodynamic responses. The genitouri-
nary system regulates fluid and is an essential component of cellular and cardiovascular func-
tions. Imbalance of fluids, electrolytes, or both can lead to hemodynamic changes or impaired
metabolism, which can ultimately influence the patient’s activity tolerance (see Chapter 15).
Genitourinary structures can also refer pain to the abdomen and the back. To help differentiate
neuromuscular and skeletal dysfunctions from systemic dysfunctions, physical therapists need
to be aware of pain referral patterns from these structures (Table 9.1). 
Body Structure and Function
The genitourinary system consists of two kidneys, two ureters, one urinary bladder, and one
urethra. The genitourinary system also includes the reproductive organs: the prostate gland,
testicles, and epididymis in males, and the uterus, fallopian tubes, ovaries, vagina, external
genitalia, and perineum in females. Of these reproductive organs, only the prostate gland and
the uterus are discussed in this chapter.
The anatomy of the genitourinary system is shown in Fig. 9.1. An expanded, frontal view of
the kidney is shown in Fig. 9.2. The functional unit of the kidney is the nephron, with approxi-
mately 1 million nephrons in each kidney. Urine is formed in the nephron through a process
consisting of glomerular filtration, tubular reabsorption, and tubular secretion.1
The following are the primary functions of the genitourinary system2:
• Excretion of cellular waste products (e.g., urea and creatinine [Cr],) through urine formation
and micturition (voiding).
• Regulation of blood volume by conserving or excreting fluids.
• Electrolyte regulation by conserving or excreting minerals.
• Acid–base balance regulation (H+ [acid] and HCO3− [base] ions are reabsorbed or ex-
creted to maintain homeostasis).
• Arterial blood pressure regulation via the renin angiotensin system. Sodium is excreted
and renin is secreted to maintain homeostasis. Renin is secreted from the kidneys during
states of hypotension, which results in formation of angiotensin I and II. Angiotensin causes
        233
234 CHAPTER 9     Genitourinary System

TABLE 9.1  Segmental Innervation and Pain Referral Areas of the Urinary System
Structure Segmental Innervation Possible Pain Referral Area
Kidney T10–L1 Lumbar spine (ipsilateral flank)
Upper abdomen
Ureter T11–L2, S2–S4 Groin
Upper and lower abdomen
Suprapubic region
Scrotum
Medial and proximal thigh
Thoracolumbar region
Urinary bladder T11–L2, S2–S4 Sacral apex
Suprapubic region
Thoracolumbar region

From Boissonault WG, Bass C. Pathological origins of trunk and neck pain: part 1. Pelvic and abdominal visceral
disorders. J Orthop Phys Ther. 1990;12:194.

Adrenal gland

Transversus
abdominis
Abdominal aorta
Kidney

Quadratus
lumborum
Inferior vena cava
Psoas major
and minor
Ureter
Iliacus

Bladder

Urethra

FIG. 9.1
Schematic illustration of the genitourinary system, including trunk musculature.

Medulla v­ asoconstriction to help increase blood pressure. Angiotensin

Pyramid also triggers the release of aldosterone, resulting in conserva-
Cortex tion of water by the kidney.
• Erythropoietin secretion (necessary for stimulating red blood
Papilla cell production).
The brainstem controls micturition through the autonomic
Hilum Minor calyces nervous system. Parasympathetic fibers stimulate voiding,
whereas sympathetic fibers inhibit it. The internal urethral
Major calyx sphincter of the bladder and the external urethral sphincter of
the urethra control the flow of urine.3 
  

Renal pelvis
Clinical Evaluation
Ureter
The clinical evaluation of the genitourinary system involves the
integration of patient history, physical findings, and laboratory
FIG. 9.2
Renal cross-section. data.

Physical Examination
History
Patients with suspected genitourinary pathology often present
with characteristic complaints or subjective reports. A detailed
history during a comprehensive patient interview and review of
the patient’s medical record provides a good beginning to the
diagnostic process for possible genitourinary system pathology.
The description of pain can offer clues as to its source: renal pain
can be described as aching and dull in nature, whereas urinary
pain is generally described as colicky (occurring in wavelike
spasms) and/or intermittent.4
Changes in voiding habits or a description of micturition pat-
terns are also noted during patient history and are listed here4-7:
• Dysuria (painful burning or discomfort during urination)
• Nocturia (urinary frequency, more than once, at night)
• Incomplete bladder emptying
• Difficulty initiating urinary stream
• Hematuria (blood in urine)
• Frequency (more often than every 2 hours)
• Hesitancy (weak or interrupted stream)
• Proteinuria (urine appears foamy)
• Oliguria (very low urine output, defined as less than 400 mL
in a 24-hour period)
 CLINICAL TIP
As a side effect of the medication phenazopyridine (Pyridium), a
patient’s urine may turn bright orange in color and be misinter-
preted as hematuria.8 Phenazopyridine (Pyridium) is prescribed
in the treatment of urinary pain and urgency. However, any new
onset of possible hematuria should always be alerted to the
medical team for proper delineation of the cause.  
Observation
When performing patient inspection, the presence of abdominal
or pelvic distention, peripheral edema, incisions, scars, tubes,
drains, and catheters should be noted because these may reflect
current pathology and recent interventions.7 Refer to Chapter
18 for more information on medical equipment. The physical
therapist must handle external tubes and drains carefully during
patient mobility and interventions.
 CLINICAL TIP
Patients with genitourinary disorders may present with skin
changes, such as pallor or rough, dry skin.6 Take caution in han-
dling patients with skin changes resulting from dehydration to
prevent any skin tears that can lead to infection.  
Palpation
The kidneys and a distended bladder are the only palpable struc-
tures of the genitourinary system. Distention or inflammation
of the kidneys results in sharp or dull pain (depending on sever-
ity) with palpation.6,7  indicative of decreased renal function. The reference range of plasma
Percussion
Pain and tenderness that occur with fist percussion of the kid-
neys can be indicative of kidney infection or polycystic kidney
Genitourinary System     CHAPTER 9 235
disease. Fist percussion is performed by placing one hand along
the dorsal costovertebral angle of the patient and striking the
dorsal surface of the examiner’s hand with a closed fist of the
other hand.6 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.7 
Auscultation
Auscultation is performed to examine the blood flow to the kid-
neys from the abdominal aorta and the renal arteries. The pres-
ence of bruits (murmurs) can indicate impaired perfusion to the
kidneys, which can lead to renal dysfunction.7 Placement of the
stethoscope is in the area of the costovertebral angles and the
four abdominal quadrants.6,7 Refer to Chapter 8, Fig. 8.2, for a
diagram of the abdominal quadrants. 
Diagnostic Testsa
Urinalysis
Urinalysis is a very common diagnostic tool used not only to
examine the genitourinary system, but also to evaluate for the
presence of other systemic diseases. Urine specimens can be col-
lected by bladder catheterization or suprapubic aspiration of
bladder urine or by having the patient void into a sterile speci-
men container. Urinalysis is performed to examine6,9,10:
• Urine color, appearance, and odor
• Specific gravity, osmolarity, or both (concentration of urine
ranges from 1.005–1.030)
• pH (4.6–8.0)
• Presence of glucose, ketones, proteins, bilirubin, urobilinogen,
nitrites, occult blood, red blood cells (RBCs), white blood cells
(WBCs), crystals, casts, bacteria or other microorganisms
• Urine abnormalities are summarized in Table 9.2.
 CLINICAL TIP
If the patient is having urine collected by the medical team, the
physical therapist should have the patient use the predesignated re-
ceptacle when the patient needs to urinate during a physical thera-
py session: this will ensure that the collection is not interrupted. The
predesignated receptacle can be a urinal for males or a collection
“hat” placed on the toilet or commode for females. If micturition
occurs during a physical therapy session and is collected in the des-
ignated receptacle, do not discard the urine because it may be nec-
essary to record or process the sample. Urine may also be collected
throughout the day to measure the patient’s urine output (UO)
relative to the patient’s fluid intake either orally or via intravenous
fluids (input). This provides a general estimate of the patient’s renal
function. Measurements of the patient’s input and output (I&O).  
Creatinine Tests
Two measurements of Cr (end product of muscle metabolism) are
performed: measurements of plasma Cr and Cr clearance. Plasma Cr
is measured by drawing a sample of venous blood. Increased levels are
Cr is 0.5 to 1.1 mg/dL for females and 0.6 to 1.2 mg/dL for males.10
aThe reference range of various laboratory values can vary among different
facilities. Be sure to verify the reference values located in the medical record.
236 CHAPTER 9     Genitourinary System

TABLE 9.2  Urine Abnormalities

Abnormality Etiology
Glycosuria (presence of glucose) Hyperglycemia and probable diabetes mellitus.
Reference: <15 mg/dL
Proteinuria (presence of proteins) Proteins are usually too large to be filtered; therefore permeability has abnormally increased.
Reference: 2–8 mg/dL Can occur with diabetes, acute or chronic kidney disease, nephrotic syndrome, congestive heart
failure, systemic lupus erythematosus.
Hematuria (presence of blood and red blood Possible urinary tract bleeding or kidney diseases (calculi, cystitis, neoplasm,
cells) glomerulonephritis, or miliary tuberculosis).
Reference: None
Bacteriuria (presence of bacteria) Generally indicates urinary tract infection.
Reference: None Urine is generally cloudy in appearance, with the possible presence of white blood cells.
Ketonuria (presence of ketones)a Can result from diabetes, fasting or starvation, a high-protein diet, and alcoholism.
Reference: None
Bilirubinuria (presence of bilirubin) Usually an early indicator of liver disease and hepatocellular jaundice.
Reference: None
Crystals (end products of food metabolism) Can occur with renal stones, gout, parathyroid, or malabsorption abnormalities.
Reference: Occasional
aKetones are formed from protein and fat metabolism.
Data from Bates P. Nursing assessment: urinary system. In: Lewis SM, Heitkemper MM, Dirksen SR, eds. Medical-Surgical Nursing: Assessment and Management of Clinical
Problems. 5th ed. St. Louis: Mosby; 2000:1241-1255; Abdomen. In: Seidel HM, Ball JW, Dains JE, et al., eds. Mosby’s Guide to Physical Examination. 5th ed. St. Louis:
Mosby; 2003:551; Weigel KA, Potter CK. Assessment of the renal system. In: Monahan FD, Neighbors M, Sands JK, eds. Phipps’ Medical-Surgical Nursing: Health and
Illness Perspectives. 8th ed. St. Louis: Mosby; 2008:943- 960; Pagana KD, Pagana TJ. Mosby’s Diagnostic And Laboratory Test Reference. 9th ed. St. Louis: Mosby; 2009;
Goodman CC, Heick J, Lazaro RT. Differential Diagnosis for Physical Therapists, Screening for Referral. 6th ed. St. Louis: Elsevier; 2018.

Cr clearance, also called the 24-hour urine test, specifically
measures glomerular filtration rate (GFR). Decreased clearance
(indicated by elevated levels of plasma Cr relative to Cr levels
in the urine) indicates decreased renal function. The reference
range of Cr clearance is 87 to 107 mL/min (females) and 107 to
139 mL/min (males).10  positions of the renal, ureteral, and bladder structures are delin-
Estimated Glomerular Filtration Rate
The 24-hour urine collection necessary to measure Cr clearance
has become time consuming and expensive to perform, resulting
in a prediction equation for estimated glomerular filtration rate
(eGFR). This estimate includes the patient’s age, gender, ethnic-
ity, and serum (blood) Cr with a reference value of greater than
60 mL/min/1.73 m2.10  are performed: intravenous pyelography (IVP), retrograde pyelog-
Blood Urea Nitrogen
As an end product of protein and amino acid metabolism, increased
blood urea nitrogen (BUN) levels can be indicative of any of the
following: decreased renal function, dehydration, increased muscle
(protein) catabolism, increased protein intake, congestive heart
failure, urinary obstruction, or acute infection. Levels of BUN need
to be correlated with plasma Cr levels to implicate renal dysfunc-
tion because BUN levels can be affected by the aforementioned
factors. Alterations in BUN and Cr levels can lead to an alteration
in a patient’s mental status and should be monitored. The refer-
ence range of BUN is 10 to 20 mg/dL in adults.6,9,10
 CLINICAL TIP
Reviewing BUN and Cr levels on a daily basis may help explain
changes in the patient’s mental status, participation in physical
therapy sessions, or both.
 
Radiographic Examination
Kidneys, Ureters, and Bladder Radiography. A radio-
graph (x-ray) of the kidneys, ureters, and bladder (a procedure
often abbreviated as “KUB”) is generally performed as an initial
screening tool for genitourinary disorders. The sizes, shapes, and
eated to identify renal calculi (kidney stones), tumor growth or
shrinkage (chronic pyelonephritis), and calcifications in the blad-
der wall. A KUB can also be performed when internal hemor-
rhage is suspected after major traumatic incidents. Identification
of any of these disorders requires further medical evaluation.6,9-11 
Pyelography. Radiopaque contrast materials are used to
radiographically examine the urinary system. Three types of tests
raphy, and antegrade pyelography.
IVP consists of (1) taking a baseline radiograph of the genito-
urinary system, (2) intravenous injection of contrast dye, and (3)
sequential radiographs to evaluate the sizes, shapes, and locations
of urinary tract structures and to assess renal excretory function.
The location of urinary obstruction or cause of nontraumatic
hematuria may be also be identified with this procedure.6,9-11
Retrograde pyelography consists of passing a catheter or cys-
toscope into the bladder and then proximally into the ureters
before injecting the contrast dye. This procedure is usually per-
formed in conjunction with a cystoscopic examination and is
indicated when urinary obstruction or trauma to the genitouri-
nary system is suspected. Evaluation of urethral stent or catheter
placement can also be performed with this procedure.5,6,9-11
Antegrade pyelography is conducted to visualize the renal
pelvis to accurately place nephrostomy tubes. This test is
indicated for patients with an obstruction in the ureter and
hydronephrosis.10 

Renal Arteriography. Renal arteriography consists of
injecting radiopaque dye into the renal artery (arteriography)
through a catheter that is inserted into the femoral or brachial
artery. Arterial blood supply to the kidneys can then be exam-
ined radiographically. Indications for arteriography include
suspected aneurysm, renal artery stenosis, renovascular hyper-
tension or trauma, palpable renal masses, chronic pyelonephri-
tis, renal abscesses, and determination of the suitability of a
(donor) kidney for renal transplantation.9,12
 CLINICAL TIP
Patients who are scheduled for procedures involving contrast
dye are generally restricted from eating or drinking 2 to 8 hours
before the procedure.10 A patient who is scheduled for an after-
noon procedure may therefore be fatigued from low nutrients
earlier in the day and may want to defer a scheduled therapy
session. Modifying the intended therapy session and respecting
the patient’s wishes at this time are both suitable alternatives.  
Bladder Examination: Cystoscopy
Cystoscopy consists of passing a flexible, fiberoptic scope
through the urethra into the bladder to examine the bladder
neck, urothelial lining, and ureteral orifices. The patient is gen-
erally placed under general or local anesthesia during this proce-
dure. Cystoscopy is performed to directly examine the prostate,
bladder, urethra, and ureters, to examine the causes of urinary
dysfunction, and to remove small tumors.9,10
 CLINICAL TIP
Patients may experience urinary frequency or dysuria after cys-
toscopic procedures; therefore the therapist should be prepared
for sudden interruptions during a therapy session conducted the
same day after this diagnostic procedure.  
Cystometry (Cystometrography)
Cystometry is used to evaluate motor and sensory function of
the bladder in patients with incontinence or suspicion of neu-
rologic bladder dysfunction. Obstructive or infectious causes
of bladder dysfunction can also be evaluated. The procedure
consists of inserting a catheter into the bladder, followed by
saline instillation and pressure measurements of the bladder
wall.6,10,11  by their etiology: prerenal, intrarenal, and postrenal.13,15-17
Renal Scanning
The structure, function, and perfusion of the kidneys can be
examined with a nuclear scan, using radioisotopes for different
testing procedures and structures.10  Intrarenal AKI involves primary damage to kidneys and is
Ultrasonography Studies
Ultrasound is used to (1) evaluate kidney size, shape, and posi-
tion; (2) determine the presence of kidney stones, cysts, and pre-
renal collections of blood, pus, lymph, urine, and solid masses;
(3) identify the presence of a dilated collecting system; and (4)
guide needle placement for biopsy or drainage of a renal abscess
or for placement of a nephrostomy tube.9,10  hypertrophy.13,15,16,18-21
Genitourinary System     CHAPTER 9 237
Computed Tomography
Indications for computed tomography (CT) of the genitourinary
system include defining renal parenchyma abnormalities and
differentiating solid mass densities. Kidney size and shape, as
well as the presence of cysts, abscesses, tumors, calculi, congeni-
tal abnormalities, infections, hematomas, and collecting system
dilation, can also be assessed with CT.5,9-11 
Magnetic Resonance Imaging and Angiography
Multiple uses for magnetic resonance imaging (MRI) and mag-
netic resonance angiography (MRA) include imaging the renal
vascular system for evaluation of stenosis, staging of renal cell car-
cinoma, identifying bladder tumors and their local metastases, and
distinguishing between benign and malignant prostate tumors.9,10 
Biopsies
Renal Biopsy. A renal biopsy consists of examining a small
portion of renal tissue that is obtained percutaneously with a
needle to determine the pathologic state and diagnosis of a renal
disorder (e.g., malignancy), monitor kidney disease progression,
evaluate response to medical treatment, or assess for rejection
of a renal transplant. A local anesthetic is provided during the
procedure, and accuracy of biopsy location is improved when
guided by ultrasound, fluoroscope, or CT scanning.6,9-11 
Bladder, Prostate, and Urethral Biopsies. Bladder, pros-
tate, and urethral biopsies involve taking tissue specimens from
the bladder, prostate, and urethra with a cystoscope, 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 perineal area and remov-
ing a wedge of prostate tissue. Examination for pain, hematuria,
and suspected neoplasm are indications for these biopsies.9 
Health Conditions
Renal System Dysfunction
Acute Kidney Injury
Acute kidney injury (AKI) (formerly known as acute renal failure
[ARF]) can result from a variety of causes and is defined as an
abrupt or rapid deterioration in renal function that results in a
rise in serum Cr levels with decreased urine output occurring
over hours or days.13,14 The three types of AKI are categorized
Prerenal AKI is caused by a decrease in renal blood flow from
injury or illness, reduced blood pressure, and/or volume deple-
tion. Contributing factors may include hemorrhage, shock, or
burns.13,15,16
caused by acute tubular necrosis (ATN), glomerulonephritis,
acute pyelonephritis, atheroembolic renal disease, malignant
hypertension, nephrotoxic substances (e.g., aminoglycoside
antibiotics or contrast dye), or blood transfusion reactions.13,16
Postrenal AKI involves obstruction (partial or complete) dis-
tal to the kidney and can be caused by urinary tract obstruc-
tion by renal stones, obstructive tumors, or benign prostatic
238 CHAPTER 9     Genitourinary System

• D iscontinuation of nephrotoxic agents or medications, if ap-

TABLE 9.3  Staging of Acute Kidney Injury
plicable
Stage Serum Creatinine Urine Output • Treatment of life-threatening conditions associated with
1 1.5–1.9 times baseline ≤0.5 mL/kg/h for AKI
OR ≥0.3 mg/dL (≥26.5 mmol/L) 6–12 hours • Monitoring and management of hematologic alterations
increase (e.g., anemia), transfusions and blood products, as indicated
2 2.0–2.9 times baseline ≤0.5 mL/kg/h for • Optimization of hemodynamics and fluid status
≥12 hours • Acid–base balance and electrolyte balance, particularly po-
3 3.0 times baseline OR <0.3 mL/kg/h for tassium levels
Increase in serum creatinine to ≥4.0 ≥24 hours • Intermittent hemodialysis or continuous renal replacement
mg/dL (≥353.6 mmol/L) OR OR Anuria for therapy as necessary (refer to the Renal Replacement Therapy
Initiation of renal replacement therapy ≥12 hours
OR, In patients <18 years,
section)
decrease in eGFR to <35 mL/ • Transfusions and blood products
min per 1.73 m2 • Nutritional support
From Table 2, Staging of AKI in Kidney Disease: Improving Global Outcomes
(KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guide-  CLINICAL TIP
line for Acute Kidney Injury. Kidney Int Suppl. 2012;2:1-138. Patients with acute kidney injury (AKI) will likely present in the
critical care setting because of multiple comorbidities leading to
AKI along with potential complications; therefore these factors
 CLINICAL TIP need to be considered to optimize physical therapy manage-
Patients who have acute kidney injury (AKI) may have heard the ment. Refer to Chapter 1 for an overview of intensive care unit
phrase “due to void” used when the medical team is awaiting (ICU) issues and Chapter 18 for a discussion of medical equip-
urine output after Foley catheterization. Hospital discharge may ment, mechanical ventilation, and circulatory assist devices.  
be dependent on patients’ ability to voluntarily void a significant
amount of urine. Chronic Kidney Disease
Chronic kidney disease (CKD) is an irreversible reduction in
The definition of AKI has been established by the Kidney renal function that occurs as a slow, insidious process as a result
Disease: Improving Global Outcomes (KDIGO) Acute Kidney of many systemic diseases that injure the kidney or of intrinsic
Injury Work Group as14: disorders of the kidney. CKD is defined decreased kidney func-
• Increase in serum Cr by ≥0.3 mg/dL (≥26.5 μmol/L) within tion as measured by a GFR of less than 60 mL/min per 1.73 m2,
48 hours; or the presence of markers indicating kidney structure damage, or
• Increase in serum Cr to ≥1.5 times from baseline, which is both, for at least 3 months regardless of an underlying cause.22,23
known or presumed to have occurred within the prior 7 days; Progression of CKD to complete renal failure is termed end-stage
or kidney disease (ESKD) or end-stage renal (ESRD).23 At this point,
• Urine volume <0.5 mL/kg/h for 6 hours. renal replacement therapy (RRT) is required for survival.15,24
The staging of AKI is outlined in Table 9.3. CKD can result from primary renal disease or other systemic
Clinical manifestations of AKI are based upon the specific diseases. Primary renal diseases that cause CKD are polycys-
type and severity level, including the following13-21: tic kidney disease, chronic glomerulonephritis, chronic pyelo-
• Malaise nephritis, atheroembolic renal disease, and chronic urinary
• Nausea and vomiting obstruction. The two primary systemic diseases that are associ-
• Altered mental status ated with CKD are diabetes and hypertension.25 Other systemic
• Anorexia diseases that can result in CKD include gout, systemic lupus
• Hypovolemic symptoms of thirst, hypotension, and de- erythematosus, amyloidosis, nephrocalcinosis, sickle cell ane-
creased urine output mia, scleroderma, and human immunodeficiency virus (HIV)
• Acid–base imbalance infection.15
• Electrolyte imbalance Clinical manifestations of CKD are numerous, given the
• Infection multisystem functions of the renal system and maybe similar
• Anemia to those of AKI and include anemia, hypertension, shortness of
• Peripheral edema breath, cognitive impairment, anorexia, vomiting, bone pain,
• Pulmonary vascular congestion, pleural effusion and extraosseous calcification.22,24 CKD is staged based on the
• Cardiomegaly, gallop rhythms, elevated jugular venous pres- severity of disease (as measured by GFR and level of albumin-
sure uria), from the KDIGO CKD Work Group.23 Stage 1 is nor-
• Hepatic congestion mal kidney function, whereas in stage 5 (kidney failure) renal
Management of AKI may include any of the following16: replacement therapy (RRT) is recommended.22,23
• Treatment of the primary etiology, including antimicrobial Management of CKD includes conservative management or
agents, if applicable RRT.25,26

Conservative management includes the following18,19,22,26,27:
• Nutritional support, dietary modifications (salt, protein, and
phosphate restrictions)
• Smoking cessation
• Calcium and vitamin D supplements
• Iron supplementation and recombinant erythropoietin for
anemia
• Cardiovascular disease management with antiplatelet agents;
statins for hyperlipidemia
• Fluid and electrolyte balancing
• Cancer screening
• Avoiding use of nonsteroidal antiinflammatory drugs
(NSAIDs), acetaminophen, bisphosphonates, oral estrogens,
or herbal therapies
Renal replacement therapy includes the following22:
• Peritoneal dialysis or hemodialysis to maintain fluid and
electrolyte balance
• Renal transplantation (see Chapter 14)
 CLINICAL TIP
Patients with limited mobility and activity especially status post
renal procedures are likely to be placed on anticoagulants to
prevent venous thromboembolism. In patients with chronic
renal disease, unfractionated heparin is the preferred medica-
tion for venous thromboembolism prophylaxis because most
medicines, including anticoagulants, are eliminated through the
kidneys, and patients with renal disease may have a higher likeli-
hood of bleeding if anticoagulant dosing is not titrated closely.28
Always monitor the patients’ clotting times before physical
therapy intervention.  
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 asso-
ciated with concurrent cystitis (bladder infection). The common
causative agents are bacterial, including Escherichia coli, and other
gram-negative bacilli. Predisposing factors for acute pyelonephri-
tis include urine reflux from the ureter to the kidney (vesicoure-
teral reflux), kidney stones, pregnancy, incontinence, spermicide
exposure, diabetes mellitus, and genetic predisposition.19,26,29,30
Resolution of acute pyelonephritis will typically occur with inter-
vention but, in some cases, can worsen with complications.30
The signs and symptoms of acute pyelonephritis include any
of the following30,31:
• Sudden onset of fever, chills, and malaise
• Pain and/or tenderness with deep palpatory pressure of one or
both costovertebral (flank) areas
• Urinary frequency, dysuria, and urgency
• Bacteriuria, pyuria (presence of WBCs [leukocytes])
• Nausea, vomiting, and diarrhea
Management of acute pyelonephritis includes any of the
following30,31:
• Fluid resuscitation, possibly administered intravenously, as
indicated.
Genitourinary System     CHAPTER 9 239
• A ntimicrobial therapy based on identified pathogens.
• Evaluation and treatment for contributing factors, such as
obstructions and inflammation in the urinary tract.
• In complicated cases requiring hospitalization, bed rest, in-
travenous fluids, and antipyretic agents are also indicated.31
 CLINICAL TIP
Kidney infection (pyelonephritis) may be referred to as an upper
urinary tract infection (upper UTI).
Chronic Pyelonephritis. Chronic pyelonephritis is charac-
terized by chronic interstitial inflammation and scarring of the
calices, resulting in destruction of nephrons. Chronic pyelone-
phritis may progress to CKD and is categorized into three forms:
reflux-associated, obstructive, and idiopathic. Reflux-associated
CKD is the most common form and occurs when there is a
reflux of urine from the bladder resulting in kidney scarring.
Obstructive chronic pyelonephritis occurs from recurrent epi-
sodes of kidney infection resulting from distal obstruction.32,33
The signs and symptoms of chronic pyelonephritis typically
occur once changes to kidney function have occurred. Once kid-
ney dysfunction occurs, the patient will have symptoms similar
to those described earlier in the AKI and CKD sections. If recur-
rent bouts of acute pyelonephritis are present, then a history of
intermittent symptoms of fever, flank pain, and dysuria may be
reported.31,33
Management of chronic pyelonephritis includes any of the
following31,33:
• Treatment of primary etiology and preserving renal function
• Prolonged antimicrobial therapy to maximize effectiveness
• Renal replacement therapy (dialysis or transplantation) 
Glomerular Diseases
Injury to the glomeruli with subsequent inflammation can
result from a variety of situations, either from primary kidney
disorders or as a secondary consequence of systemic diseases,
such as systemic lupus erythematosus, amyloidosis, Wegener’s
granulomatosis, diabetes mellitus, or hypertension. Primary glo-
merulonephritis may be idiopathic, be drug induced, or result
from streptococcal infection. Approximately 20% of glomeru-
lonephritis will result in CKD. Primary glomerulonephritis can
include acute nephritic syndrome, poststreptococcal glomerulo-
nephritis, and chronic glomerulonephritis. Immunoglobulin A
(IgA) nephropathy or Berger’s disease is a form of idiopathic glo-
merulonephritis and is the most common type worldwide.34-36
Glomerular diseases can result in any of these two syn­
dromes33,36:
• Nephritic syndrome, manifested by hematuria, proteinuria,
oliguria, edema, and hypertension
• Nephrotic syndrome, manifested by proteinuria (>3.5 g/
day), hypoalbuminemia, hyperlipidemia, lipiduria
Regardless of the type of glomerulonephritis, common signs
and symptoms may include34,35:
• Edema, joint pain, oral ulcers or malar rash, dark urine, hy-
pertension, heart murmurs, skin pallor, abdominal and/or
back tenderness
240 CHAPTER 9     Genitourinary System
Management for acute glomerulonephritis can include
nonpharmacologic strategies, such as diet or fluid restrictions;
or medical management, including diuretics, angiotensin-
converting enzyme (ACE) inhibitors, electrolyte correction,
antimicrobials, and/or immunosuppression.33,34  • Reduction in dietary consumption of predisposing factors, as
Acute Interstitial Nephritis
Acute interstitial nephritis (AIN) is inflammation of the renal
parenchyma affecting the tubules and the renal interstitial space
between glomeruli, tubules, and blood vessels.37 There are two
types, primary (idiopathic) or secondary, which can result from
hypersensitivity reactions to medications infections, or auto-
immune processes. Tubulointerstitial nephritis is a type of idio-
pathic AIN.37 The physical findings of AIN may include the
following37,38:
• Rash
• Fever
• Peripheral blood eosinophilia
• Leukocyturia
• Mild hematuria
• Mild proteinuria
• Flank pain
• Myalgias or arthralgias
Management of interstitial nephritis includes any of the
following18,37-39:
• Fluid and nutritional support
• Removal of causative medications while treating primary
infection (as indicated)
• Antimicrobial therapy if AIN is associated with concurrent
infection
• Renal replacement therapy (as indicated) 
Nephrolithiasis
Nephrolithiasis is characterized by renal calculi (kidney stones)
that form in the renal pelvis. There are four primary types of
kidney stones, which are categorized according to the stone-
forming substances: (1) calcium, (2) struvite (composed of
magnesium, ammonium, and phosphate), (3) uric acid, and
(4) cystine.40 Many factors contribute to stone formation and
include the following high-incidence risk factors41:
• Supplemental calcium, dietary oxalate (spinach, potatoes,
nuts), sucrose, fructose, sugar-sweetened soda, and punch
• Higher body mass index (BMI)
• Diabetes mellitus
• Cholelithiasis, urinary calcium, and/or oxalate excretion
• Hyperparathyroidism
• Crohn’s disease
The signs and symptoms of kidney stones include the following33,42:
• Colicky pain in the flank and/or lower abdominal region,
with possible radiation into the groin, depending on the
stone location (Pain increases greatly as the stone passes
through the ureters.)
• Hematuria, urinary frequency
• Nausea and vomiting
• Fever
• Variable urine pH
• Variable levels of serum calcium, chloride, phosphate, carbon
dioxide, uric acid, and Cr
After identification of the stones by using noncontrast heli-
cal CT scan, management of kidney stones includes any of the
following33,40,42:
• Analgesics (NSAIDs) and fluids
described earlier
• Alpha1 antagonists and calcium channel blockers may en-
hance passage of stones and alleviate related hypertension
• Ureteroscopic stone manipulation for larger stones, or in
situ extracorporeal shock wave lithotripsy (ECSWL) in cases
where smaller stones are not passed spontaneously 
Diabetic Nephropathy
Approximately 40% of people with type 1 or type 2 diabetes
will develop diabetic nephropathy, which is the primary cause
leading to renal replacement therapy and potentially progress-
ing to ESRD.43,44 Risk factors include sustained hyperglycemia,
hypertension, smoking, dyslipidemia, obesity, and diets high in
protein and fat.23 Patients with diabetic nephropathy are also at
high risk for cardiovascular disease, and therefore routine screen-
ing should be performed for coronary heart disease, carotid dis-
ease, peripheral artery disease, and atherosclerotic renal artery
stenosis.43
The signs and symptoms of diabetic nephropathy include the
following43:
• Microalbuminuria
• Decreased GFR
• Manifestations of AKI or CKD, as noted in earlier sec-
tions.
Management of diabetic nephropathy includes any of the
following18,45,46:
• Strict glycemic control as well as managing other comorbid
risk factors.47 (For detailed information, refer to National
Kidney Foundation: KDOQI Clinical Practice Guideline for
Diabetes and CKD.)47
• Management of risk factors including hypertension, smok-
ing, and dyslipidemia, including behavioral and medical
strategies (see Chapter 3)
• Nutritional support
• Renal replacement therapy 
Renal Artery Stenosis
Renal artery stenosis (RAS) commonly results from atheroscle-
rotic disease and concomitant risk factors for vascular disease,
such as advanced age, elevated cholesterol, smoking, and sys-
temic hypertension.48 Decreased renal perfusion results in reno-
vascular hypertension, which is a leading cause of secondary
hypertension and can have damaging effects on the cardiovascu-
lar and the kidney.48,49
The signs and symptoms of renal artery stenosis include the
following49,50:
• Unexplained hypertension
• Flank or upper abdominal pain
• Abdominal bruits
• Peripheral or pulmonary edema
• AKI after initiating ACE inhibitor or angiotensin receptor
blocker therapy51,52

Diagnosis can be established by renal duplex ultrasonography,
MRA, CT angiography, and invasive digital subtraction renal
angiography (which is the gold standard for diagnosis).51,52
Management of renal artery stenosis includes any of the
following50:
• Antihypertensive agents (ACE inhibitors or angiotensin re-
ceptor blockers, in appropriate cases)
• Antiplatelet therapy with aspirin
• Glycemic and lipid control
• Renal replacement therapy, as indicated
• Surgery—angioplasty with or without stent placement, as
indicated49,52  and/or night-time urinary frequency.”57 No specific etiology has
Renal Vein Thrombosis
Renal vein thrombosis (RVT) is primarily seen in children,
shortly after birth. Risk factors include prematurity, maternal
diabetes mellitus, sepsis, inherited prothrombotic disorders,
umbilical venous catheterization, conjoined twins, and patho-
logic states associated with thrombosis (e.g., dehydration,
cyanotic heart disease, and shock).53 In adults who have under-
gone surgery or have sustained trauma are also at risk for RVT,
along with adults who may have a hypercoagulable state, renal
tumors extending into the renal vein, or nephrotic syndrome.
Renal vein occlusion can increase renal vein pressure, creating
a decrease in renal artery blood flow.54 Diagnosis is confirmed
with renal Doppler ultrasound, CT scan, or MRI.
The signs and symptoms of renal vein thrombosis include
the following53:
• Flank or loin pain
• Palpable flank mass
• Fever
• Manifestations of acute kidney injury, including oliguria or
anuria
• Gross hematuria
• Hypertension
• Thrombocytopenia
RVT can be managed with antiplatelets or anticoagulants. In
situations when immediate thrombus lysis is required, throm-
bolytic therapy with tissue plasminogen activator (tPA) can be
administered either systemically or via catheter-directed tPA
therapy.53,54  bladder can include frequent urination, suprapubic or pelvic
Lower Urinary Tract Dysfunction
Cystitis
Inflammation of the urinary bladder may occur acutely or
extend to a chronic situation. Acute cystitis commonly occurs
from UTIs resulting from pathogens, such as E. coli, Staphylococ-
cus saprophyticus, Proteus, Klebsiella, and Enterobacter. Urinary tract
infections are also common causes of kidney infections (pyelone-
phritis). Prostatic enlargement, cystocele of the bladder, calculi
(stones), or tumors can also result in cystitis.55,56
The signs and symptoms of acute cystitis may include the
following55,56:
• Urinary frequency and urgency (as often as every 15–20 min-
utes)
• Dysuria
Genitourinary System     CHAPTER 9 241
• L ower abdominal or suprapubic pain
• Urinalysis may reveal pyuria, hematuria, and bacteriuria
Management of cystitis includes antimicrobial treatment
for approximately 3 days or less depending on the exact agent
prescribed.56
Associated conditions include bladder pain syndrome (BPS)
and chronic pelvic pain syndrome (CPPS). According to the
International Association for the Study of Pain, BPS occurs
when there is “persistent or recurrent pain perceived in the uri-
nary bladder region, accompanied by at least one other symp-
tom, such as pain worsening with bladder filling and daytime
been identified; rather BPS is associated with a wide variety of
disorders. Coexisting conditions include child abuse, fibromy-
algia, anxiety disorder, headache, esophageal reflux, gastritis,
depression, and irritable bowel syndrome.33
CPPS “is the occurrence of chronic pelvic pain where there is
no proven infection or other obvious local pathology that may
account for the pain.”57 Both males and females can experience
CPPS, which can be associated with dysfunction in a single pel-
vic organ, multiple pelvic organs, or systemic conditions, such
as fibromyalgia or chronic fatigue syndrome.57 
Urinary Calculi
Urinary calculi are stones (urolithiasis) that can form anywhere
in the urinary tract outside of the kidneys and are mostly com-
posed of calcium oxalate and phosphate.32 Formation of stones,
symptoms, and management are similar to that of kidney stones
(see the Nephrolithiasis section for further details on the forma-
tion and clinical presentation of kidney stones). 
Neurogenic Bladder
A neurogenic bladder is characterized by dysfunctional voiding
as a result of neurologic injury that interferes with urine storage
or voluntary coordinated voiding.33,58 Common causes include
dementia, Parkinson’s disease, multiple sclerosis, cerebrovascu-
lar accident, and brain tumors.33 Control of the bladder occurs
at multiple levels throughout the central nervous system, and
consequently injury at one or more of these levels can result
in voiding dysfunction. The range of symptoms of neurogenic
pain, urinary incontinence to urinary retention, urgency, incom-
plete voiding, paroxysmal hypertension with diaphoresis (auto-
nomic dysreflexia), urinary tract infection, and occult decline in
kidney function.33,58
Management consists of addressing the primary neurologic
disturbance (as able) and providing antimicrobial agents for any
associated infection to help preserve kidney function.58 A com-
plete approach also includes59,60:
• Bladder retraining, fluid regulation, pelvic floor exercises,
and biofeedback
• Detrusor relaxation achieved either by botulinum toxin (BTx)
injections into the detrusor muscle or antimuscarinic (AM)
treatment in patients with neurogenic detrusor overactivity
• Clean intermittent catheterization or indwelling catheteriza-
tion
• Surgical intervention 
242 CHAPTER 9     Genitourinary System
TABLE 9.4  Types of Chronic 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 because of inability to delay voiding after a sensation
of bladder fullness is perceived
Mixed Combination of stress and urge symptoms
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 Stiles M, Walsh K. Care of the elderly patient. In: Rakel RE, Rakel DP, eds. Textbook of Family Medicine. 8th ed. Philadelphia: Saunders; 2011:49.
Urinary Incontinence
Incontinence of urine can be transient or acute and can result
from situations such as fluid imbalance, stool impaction,
impaired mobility, delirium, and side effects of medications.
Inadequate resolution of these factors and/or repeated episodes
can contribute to chronic urinary incontinence.61 Table 9.4 pro-
vides a summary of the different types of chronic urinary incon-
tinence. Urinary incontinence can also contribute to fall risk in
older adults, skin breakdown, pressure injuries, UTI, depres-
sion, isolation, and institutionalization.33 The management of
the various types of chronic incontinence may include educa-
tion on risk factor prevention, scheduled voiding, pelvic floor
exercises, environmental modifications, antimuscarinic drugs,
surgical intervention, and catheterization.33,61
 CLINICAL TIP
If patients are incontinent of urine, observe whether bed linens
and/or the hospital gown is soiled before a physical therapy ses-
sion because these need to be changed to minimize skin break-
down. Adult incontinence undergarments can be applied before
an intervention to avoid disruption to the treatment session.  
Prostate Disorders
Benign Prostatic Hyperplasia
Benign prostatic hyperplasia (BPH) is characterized by a non-
malignant increase in the number of epithelial and stromal cells
in the prostate gland and may contribute to lower urinary tract
symptoms (LUTSs) in males over age 40 years.62,63 Digital rec-
tal examination can detect benign enlargement or abnormalities
that may be associated with prostate cancer. Urinalysis is also
performed to screen for other pathologies, such as UTIs.64 In
the presence of microscopic hematuria, CT urography, and cys-
toscopy are recommended, along with laboratory tests, such as
measurement of serum prostate-specific antigen (PSA).65 Test-
ing PSA values are withheld in patients over 75 years of age and
indicated in patients who have a life-expectancy of more than
10 years. Uroflowmetry is also used in the evaluation of BPH.64
Common Causes
Urethral sphincter dysfunction, or weakness in pelvic
floor muscles
Neurologic disorders, spinal cord injury, or detrusor
overactivity
Combination of stress and urge causes above
Anatomic obstruction by prostate, stricture, or cystocele
Diabetes mellitus or spinal cord injury
Neurologic disorders, detrusor failure
Mobility and/or cognitive impairment(s)
Enlargement of the prostate caused by BPH can result in uri-
nary tract obstruction; however, the factors described in Table
9.4 are also contributing issues to LUTSs in both males and
females.62 Thus there are overlapping signs and symptoms of
BPH and LUTSs, including62,64,66:
• Frequency of micturition, urgency
• Urge incontinence
• Decreased force and caliber of urinary stream
• Straining to void; hesitancy
• Postvoid dribble
• Nocturia, dysuria, and hematuria
Management of BPH includes any of the following62,63,67:
• Alpha1-adrenergic receptor antagonists act to relax the
smooth muscle in the neck of the bladder to facilitate void-
ing. Currently prescribed agents include tamsulosin (Flomax)
and prazosin (Minipress). Other medications include doxazo-
sin (Cardura), terazosin (Hytrin), and alfuzosin (Uroxatral).
• 5-alpha-reductase enzyme inhibitor used to inhibit male
hormones to the prostate, causing the gland to shrink over
time. Agents include finasteride (Proscar) and dutasteride
(Avodart).
• Antiinfective agents (if there is associated infection).
• Intermittent catheterization (as necessary).
Surgical options include transurethral incision of the prostate
(TUIP), transurethral resection of the prostate (TURP), trans-
urethral microwave thermotherapy (TUMT), laser surgery, or
open prostatectomy.68 
Prostatitis
Prostatitis is inflammation of the prostate gland. It can be divided
into four categories: (1) acute bacterial prostatitis, (2) chronic
bacterial prostatitis, (3) chronic pelvic pain syndrome, and (4)
asymptomatic prostatitis. Causative pathogens for acute and
chronic bacterial prostatitis can include E. coli, Pseudomonas aeru-
ginosa, Klebsiella pneumoniae, Proteus mirabilis, and Enteroccocus.69,70
The signs and symptoms of prostatitis include the fol­
lowing69:
• Suprapubic, perineal, or low back pain
• Fever, chills, malaise, nausea, and vomiting

• I ncreased urinary frequency or urgency to void
• Nocturia
• Painful urination (dysuria)
• Difficulty initiating a stream, interrupted voiding, or incom­
plete emptying
• Sexual dysfunction
Management of prostatitis includes any of the following69,70:
• Antimicrobial agents (for bacterial prostatitis)
• Alpha1-adrenergic blocking agents or antiinflammatory
agents
• Antipyretics
• Invasive management as a last resort  procedures. Considerations for physical therapy management for
Endometriosis
Females of childbearing age are at risk for developing endo-
metriosis. Endometriosis is the second most common cause of
dysmenorrhea and can be a confounding source of musculoskel-
etal pain. Aberrant growth of endometrial tissue occurs outside
of the uterus, particularly in the dependent parts of the pelvis
and ovaries. The exact nature of the pathogenesis and etiology
are currently unknown. Several theories are available: (1) direct
endometrial implantation caused by retrograde menstrual flow
into the pelvic cavity from the uterus, (2) transformation of
multipotential cells into endometrium-like cells, (3) transport
of endometrial cells by uterine vascular and lymphatic systems
to distant sites, and (4) disorder of immune surveillance allow-
ing growth of endometrial implants. Differential diagnosis of
endometriosis may include pelvic inflammatory disease, ectopic
pregnancy, appendicitis, hernia, irritable bowel syndrome, nerve
entrapment, interstitial cystitis, or muscle strain. Laparoscopic
examination will confirm the diagnosis of endometriosis.71-74
The signs and symptoms of endometriosis include the
following71-73:
• Classic triad of dysmenorrhea, dyspareunia (pain with inter-
course), and infertility
• Pelvic pain (hypogastric and perineal regions) related to the
menstrual cycle
• Pain in the low back and lower extremities
• Intermittent constipation/diarrhea, rectal bleeding, dysuria,
hematuria, and urinary frequency
• Abnormal bleeding (premenstrual spotting, menorrhagia)
Management of endometriosis includes any of the
following71-73
• NSAIDs for relief of symptoms associated with dysmenorrhea
• Conservative therapies aimed at enhancing fertility (for those
wishing to bear children)
• Hormonal therapy aimed at reducing hormone levels and
cyclic stimulation of ectopic endometrial tissue (Agents
used include estrogen-progesterone acetate, progestins, and
gonadotropin-releasing hormone (GnRH) agonists.)
• Laparoscopic ablation of endometrial implants (ectopic tis-
sue) with concurrent uterine nerve ablation to significantly
reduce pain
• Total abdominal hysterectomy and bilateral salpingo-
oophorectomy (TAH-BSO) followed by estrogen replace-
ment therapy (Refer to Table 11.11 in Chapter 11 for an
overview of TAH-BSO.)
Genitourinary System     CHAPTER 9 243
 CLINICAL TIP
Patients with recent uterine or prostate surgeries may have lift-
ing precautions that need to be ascertained prior to mobility.  
  
Medical Management
The specific management of various genitourinary disorders is
discussed earlier in the respective health conditions sections.
This section expands on renal replacement therapy and surgical
patients who have genitourinary dysfunction are also discussed.
Renal Replacement Therapy
The primary methods of managing fluid and electrolyte bal-
ance in patients with AKI or CKD are peritoneal dialysis, inter-
mittent hemodialysis, or continuous renal replacement therapy
(CRRT). For either type of dialysis (peritoneal or intermittent),
the principles of diffusion, osmosis, and ultrafiltration (convec-
tion) to balance fluid and electrolyte levels are used. Diffusion is
the movement of solutes, such as Cr, urea, or electrolytes, from
an area of higher concentration to an area of lower concentra-
tion. Osmosis is the movement of fluid from an area of lesser
solute concentration to an area of greater solute concentration.
Ultrafiltration, the removal of water and fluid, is accomplished
by creating pressure gradients between the arterial blood and
the dialyzer membrane or compartment.75-78 CRRT is generally
implemented in the critical care setting in patients with AKI.79
Kidney transplantation is described in Chapter 14.
Peritoneal Dialysis
Peritoneal dialysis (PD) involves using the peritoneal cavity as
a semipermeable membrane to exchange soluble substances and
water between the dialysate fluid and the blood vessels in the
abdominal cavity.20,75,76 Dialysate fluid is instilled into the peri-
toneal cavity through an indwelling catheter. After the dialysate
is instilled into the peritoneum, there is an equilibration period
when water and solutes pass through the semipermeable mem-
brane. Once equilibration is complete, then the peritoneal cavity
is drained of the excess fluid and solutes that the failing kidneys
cannot remove. Instillation, equilibration, and drainage consti-
tute one exchange.75,76 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.75
There are two delivery methods for PD: (1) automated PD
(APD), which uses an automatic cycling device to control the
instillation, equilibration, and drainage phases; and (2) continu-
ous ambulatory PD (CAPD), which is performed manually.80
CAPD is schematically represented in Fig. 9.3.75
PD is indicated for patients with CKD, who may or may
not be hospitalized. The choice to use PD versus intermittent
hemodialysis is dependent on whether there is a function-
ing peritoneal cavity as well as on the ability of the patient or
his or her care providers to manage the exchanges. In cases of
AKI, intermittent hemodialysis and CRRT are the preferred
modalities.79,81 
244 CHAPTER 9     Genitourinary System
A and is a valuable source of information regarding the patient’s
B Continuous Renal Replacement Therapy
FIG. 9.3
Schematic illustration of continuous ambulatory peritoneal dialysis. (A) In-
stillation of dialysate fluid. (B) Drainage of excess fluid and solutes.
Intermittent Hemodialysis
Kidney functions that are controlled by intermittent hemo-
dialysis 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 semi-
permeable tubing that is surrounded by a dialysate solution
in the dialyzer (artificial kidney). The dialysate fluid contains
vital solutes to permit diffusion of electrolytes into or out of the
patient’s blood. As the patient’s arterial blood is being filtered
through the dialyzer, “clean” blood is returned to the patient’s
venous circulation.76,79 Fig. 9.4 illustrates this process.
Vascular access is attained by three mechanisms: (1) a tun-
neled hemodialysis catheter, (usually for temporary dialysis); (2)
an arteriovenous fistula (AVF) (for chronic dialysis use); and (3)
an arteriovenous graft (AVG). The AVF is created by performing
a side-to-side, side-to-end, or end-to-end anastomosis between
the radial or brachial arteries and the basilic or cephalic veins. If
a native fistula cannot be created, then a synthetic graft (AVG) is
surgically anastomosed between the arterial and venous circula-
tion.75,82 Fig. 9.5 illustrates these various types of vascular access.
Patients who require intermittent hemodialysis for AKI are
generally required to replace 2 to 3 L of fluid per dialysis session
to fully achieve clear waste products and achieve osmotic bal-
ance. This large amount of fluid exchange can promote hypo-
tension and possible ischemia of nephrons in patients who are
critically ill.83 Hemodynamic instability may dictate the use
of CRRT preferred over intermittent hemodialysis; however,
strong evidence is lacking at this point in time.84
Patients who require chronic intermittent hemodialysis usu-
ally 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.20,85
 CLINICAL TIP
Airway clearance treatments can be performed during dialysis;
however, this depends on the hemodynamic stability of the
patient and is performed at the discretion of the nurse or the
physician. Extreme caution should be taken with the access site
to prevent accidental disruption.
 CLINICAL TIP
The dialysis team is generally nearby to monitor the procedure
hemodynamic stability. Also, inquiring about the length of time
for the hemodialysis may be helpful in scheduling therapy ses-
sions.  
The purpose of CRRT is to provide a continuous mechanism
that balances 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 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 hemodi-
alysis. The use of CRRT also appears to be beneficial in patients
with positive fluid balance.84 Predictable outcomes of CRRT
include79:
• Hemodynamic stability
• Continuous control of fluid status
• Control of acid–base status and electrolyte, calcium, and
phosphate balance
• Provision of protein-rich nutrition with excellent uremic
control
• Prevention of intracerebral water fluctuations
• Minimal risk of infection
There are several techniques to achieve CRRT, which
are outlined in Table 9.5. Vascular access is dependent
on the specific type of CRRT indicated for the patient.
Fig. 9.6 provides an illustration of continuous venovenous
hemofiltration.
 CLINICAL TIP
Limited evidence exists for mobility during CRRT; however,
Brownback86 and Talley87, in two separate articles, have report-
ed an ability to accomplish this successfully. Refer to these stud-
ies for more information, and always consult with the medical
team for specific considerations and parameters.  
Surgical Interventions
Surgical interventions for genitourinary system disorders can be
categorized broadly as procedures that remove diseased portions
of the genitourinary tract or procedures that restore urinary
flow. These interventions are briefly discussed in the following
sections. Refer to Chapter 20 for general anesthesia and postop-
erative considerations.
 Genitourinary System     CHAPTER 9 245

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
FIG. 9.4
Schematic representation of hemodialysis. (From Thompson JM, McFarland GK, Hirsch JE, et al. Mosby’s Clini-
cal Nursing. 3rd ed. St. Louis: Mosby; 1993:938.)

Nephrectomy • N ephron-sparing surgery (NSS)—removal of only the tumor

The primary indications for removing a part or all of the kidney
have included renal cell carcinoma, polycystic kidney disease,
severe traumatic injury to the kidney, and organ donation, as
well as removing a failing transplanted organ.88,89 Nephrectomy
can be performed as an open or laparoscopic procedure, with
laparoscopy nephrectomy typically resulting in shorter length
of hospital stays.88-93 Current trends lean toward more conserva-
tive and less invasive management.93 The types of nephrectomy
and their definitions follow:
• Radical nephrectomy—removal of the entire kidney, a section
of the ureter, the adrenal gland, and the fatty tissue sur-
rounding the kidney
• Simple nephrectomy—removal of the entire kidney with a sec-
tion of the ureter; generally performed when harvesting do-
nor organs for kidney transplantation
• Partial nephrectomy—removal of only the infected or diseased
portion of the kidney
while preserving the renal parenchyma; indicated for pa-
tients with small, localized tumors93
• Minimally invasive techniques—include cryoablation and
radiofrequency ablation to target localized masses92-94 
Urinary Incontinence Procedures
When conservative treatment of urinary stress incontinence is
unsuccessful or not desired, surgical management is considered.
One surgical approach involves open retropubic bladder sus-
pension, which can be achieved by using one of three methods;
Marshall-Marchetti-Kranz (MMK) procedure, Burch colposus-
pension, and paravaginal repair or obturator shelf procedure.95
These procedures are aimed at reestablishing the anatomic
support of the urethrovesical junction and proximal urethra to
provide stability during increases in intraabdominal pressure.
Another approach includes sling procedures, which involve
placement of synthetic mesh acting as a dynamic support in the
246 CHAPTER 9     Genitourinary System

Blood supply Blood return

to dialyzer to patient Vein

Fistula
(Anastomosis of artery and vein
A shunting arterial blood into vein) Radial artery

Antecubital vein

B Looped graft Brachial artery

Teflon connector
Radial artery

Teflon vessel tip

Silastic tubing Basilic vein

C (external segment)
FIG. 9.5
Methods of vascular access for hemodialysis. (A) Internal arteriovenous fistula. (B) Looped graft in forearm. (C)
External cannula or shunt. (From Lewis SM, Heitkemper MM, Dirksen SR, eds. Medical-Surgical Nursing: As-
sessment and Management of Clinical Problems. 6th ed. St. Louis: Mosby; 2004:1233.)

TABLE 9.5  Continuous Renal Replacement Therapy (CRRT) Techniques

Types of CRRT
Slow continuous ultrafiltration (SCUF)
Continuous venovenous hemofiltration
(CVVH)
Continuous venovenous hemodialysis
Continuous venovenous hemodiafiltration
(CVVHDF)
Continuous high-flux dialysis (CVVHFD)
Continuous plasma-filtration adsorption
(CPFA)
Description
Used for fluid control only
Can have arteriovenous or venovenous modes
Convective blood purification through a high-permeability membrane
Arteriovenous mode also available
Diffusive purification of blood through a low-permeability dialyzer
For small molecule clearance only
Diffusive and convective blood purification with a highly permeable membrane
Diffusive and convective blood purification with a highly permeable membrane and an accessory
pump to control ultrafiltration
A highly permeable plasma filter filters plasma, allowing it to pass through a bed of adsorbent
material (carbon or resins)
Fluid balance maintained throughout process

Data from Ronco C, Ricci Z, Bellomo R, et al. Renal replacement therapy. In: Vincent JL, Abraham E, Moore FA, et al., eds. Textbook of Critical Care. 6th ed. Philadel-
phia: Saunders; 2011:894-901.

Controlled infusion fluid
Infusion of substitution
Venous line
fluid, drugs, and nutrients
Hemofilter
Venous line
Closed graduated
filtrate collection
FIG. 9.6
Schematic representation of continuous venovenous hemofiltration.
midurethral region and can be performed via retropubic or tran-
sobturator approaches.33 Injection of urethral bulking agents,
such as collagen, can also be performed to help support the
urethra.33,96  tion or intervention can help the physical therapist decide
Urinary Diversion
Procedures aimed at diverting urinary flow are indicated in
patients who have undergone cystectomy or have a diseased
bladder. The three primary types of urinary diversion are ileal
conduit, continent cutaneous diversion, and orthotopic ileal
bladder. Continent cutaneous diversion involves the creation of
a stoma either in the right lower quadrant of the abdomen or in
the umbilicus. The stoma creates access for intermittent cath-
eterization. Different surgical procedures, including robotics,
are involved in these three types of urinary diversion and may
involve the use of either the small intestine or the large intestine
as a conduit or creation of an artificial bladder.97-99 
  
Physical Therapy Management
The following are general goals and considerations for the physi-
cal therapist when working with patients who have genitouri-
nary dysfunction. These should be adapted to a patient’s specific
needs.
The primary physical therapy goals in this patient popula-
tion are similar to those of other patients in the acute care set-
ting. These goals are to (1) optimize safe functional mobility,
(2) maximize activity tolerance and endurance, and (3) prevent
postoperative complications.
General physical therapy management considerations
revolve around the normal functions of the genitourinary system
that are disrupted by the various health conditions discussed
Genitourinary System     CHAPTER 9 247
Heparin infusion pump
earlier in this chapter. These include, but are not limited to, the
following:
• Evaluating the trends of laboratory values before examina-
which signs and symptoms to monitor as well as determine
the parameters of the session.100 Refer to Chapter 15 for
more information on fluid and electrolyte imbalance.
• The inability to regulate cellular waste products, blood vol-
ume, and electrolyte levels can result in:
• Mental status changes from a buildup of ammonia,
BUN, Cr, or a combination of these.33 If this situation
occurs, then the therapist may choose to modify or
defer physical therapy intervention, particularly educa-
tional activities that require concentration.
• Disruption of excitable tissues, such as peripheral
nerves and skeletal, cardiac, and smooth muscle, as
a result of altered levels of electrolytes.100,101 If this
situation occurs, then the therapist may need to reduce
exercise intensity during muscle-strengthening activi-
ties. In addition, 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.101 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 3.5 for a description of pitting edema
and refer to Chapter 4 for a description of pulmonary
edema.
248 CHAPTER 9     Genitourinary System
• F luid and electrolyte imbalance can also alter the he-
modynamic responses to activity; therefore vital signs
References
and symptoms should always be carefully monitored.
• Blood pressure regulation can be altered by the inability
to excrete body fluids and activate the renin–angiotensin
system.101
• Activity tolerance can be reduced by the factors mentioned
in this section, as well as anemia, which can result from a
decrease in erythropoietin secretion from kidneys, which is
necessary for stimulating RBC production.101
• Patients will likely demonstrate variable levels of fatigue
when receiving RRT102; some patients are more fatigued
before a dialysis session, whereas others are more fatigued
after a dialysis session. A variety of factors may contribute
to the development of fatigue and include coexisting chron-
ic illness, anemia, malnutrition, sleep disorders, depression,
and medication side effects.102 Hemodialysis sessions typi-
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• As stated in the introduction to this chapter, patients with geni-
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Physical therapists can play a role in differentiating the
source of a patient’s back pain and in providing symptom-
atic management of this referred pain.
• Patients who have undergone surgical procedures with ab-
dominal incisions are less likely to perform deep breathing
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nence.
• Patients who continue to be incontinent after hospital dis-
charge can benefit from a referral to a physical therapist
who specializes in pelvic floor management.
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 10
C H APT ER  
CHAPTER OUTLINE
Introduction
General Evaluation of Endocrine
Function
Thyroid Gland
Body Structure and Function
Thyroid Tests
Thyroid Disorders
Pituitary Gland
Body Structure and Function
Pituitary Tests
Pituitary Disorders
Adrenal Gland
Body Structure and Function
Adrenal and Metabolic Tests
Adrenal Disorders
Pancreatic Disorders
Insulin Resistance
Metabolic Syndrome
Diabetes Mellitus
Parathyroid Gland
Body Structure and Function
Parathyroid Tests
Parathyroid Disorders
Metabolic Bone Disorders
Osteoporosis
Osteomalacia
Paget’s Disease
Physical Therapy Management
Goals
Considerations
Endocrine System
Jaime C. Paza
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1. Provide an overview of normal functions of the endocrine system, including the thyroid, pituitary, adrenal,
and parathyroid glands, as well as the pancreas
2. Describe the clinical evaluation of these endocrine organs
3. Describe the health conditions associated with endocrine system dysfunction and relevant medical
management
4. Provide physical therapy considerations for working with patients who have endocrine system dysfunction
Introduction
The endocrine system consists of endocrine glands, which secrete hormones into the blood-
stream, and the target cells for those hormones. Target cells are the principal sites of action for
the endocrine glands. Fig. 10.1 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 weakness.1 Therefore it is important for the physical
therapist to carefully distinguish the source (endocrine system versus other systems) of
these symptoms to provide optimal care to the patient. For example, complaints of weak-
ness and muscle cramps can both result from hypothyroidism or inappropriate exercise
intensity. The physical therapist’s knowledge of the patient’s current endocrine system
status can better inform the decision making regarding the need for adjustments to a
patient’s intervention parameters.
Together the prevalence rate of endocrine and metabolic disorders is approximately 5% of
the U.S. population.2 According to the Centers for Disease Control and Prevention (CDC),
approximately 1.4% of the diagnoses in patients admitted to the emergency room in 2015 were
classified as endocrine disorders or metabolic disorders,3 and 7% of physician’s office visits are
a result of endocrine, metabolic, nutritional, and immunity disorders.4 
General Evaluation of Endocrine Function
Measurement of endocrine function can be performed by examining (1) the endocrine
gland itself, with the use of imaging techniques, or (2) the levels of hormones or hor-
mone-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 endo-
crine substances can indicate endocrine dysfunction. The most commonly used endocrine
tests are discussed in this chapter. Clinicians should refer to their institution’s laboratory
values for reference ranges of hormone or hormone-related substances referenced in their
setting.
aThe authors acknowledge Jessika Vizmeg for prior contributions to this chapter.
        253
254 CHAPTER 10     Endocrine System

TABLE 10.1  Target Sites and Actions of Thyroid Gland

Hypothalamic Hormones
nuclei Pituitary gland
Hormone(s) Target Site(s) Actions
Thyroxine (T4) Systemic Increases metabolic rate;
and triiodothy- stimulates growth, and
Parathyroid ronine (T3) development of all cells,
Thyroid gland
glands particularly of the nervous
system; and enhances the
effects of catecholamines
Adrenal
Thyrocalcitonin Bone Inhibits bone resorption
(suprarenal)
glands
Lowers blood levels of
calcium

Data from Brashers VL, Jones RE. Mechanisms of hormonal regulation. In: Mc-
Pancreas Cance KL, Huether SE, Brashers VL et al., eds. Pathophysiology: The Biologic Basis
for Disease in Adults and Children. 6th ed. St. Louis: Mosby; 2010:697-726; Hall
S. Prescribing in thyroid disease. Nurse Prescribing. 2010;8(8):382-387.

Ovaries
(in females) TABLE 10.2  Thyroid Hormone Tests
Reference Value
Hormone Test Description (Adults)
Serum thyrox- Free T4 measures the 0.8–2.8 ng/dL
Testes (in males) ine (T4) metabolically active,
FIG. 10.1 Free T4 unbound fraction of
Schematic representation of the primary endocrine glands in women and men. thyroxine
Serum thyrox- Total T4 measurements 4–12 mcg/dL male
ine (T4) include free and bound 5–12 mcg/dL
 CLINICAL TIP Total T4 fractions of thyroxine female
Serum triiodo- Measures total T3 levels 70–205 ng/dL
An imbalance of hormone levels can affect the patient’s toler- thyronine (T3) (20–50 years)
ance to activity. Knowledge of endocrine tests and values can 40–180 ng/dL (>50
help the clinician gauge the intended treatment parameters (i.e., years)
type, duration, frequency, and intensity) for the next session(s).
  Thyroid-
stimulating
Concentrations of TSH
help distinguish types
0.2–19 μU/mL

hormone of hypothyroidism
(TSH) (primary or secondary)
Thyroid Gland
Thyrotropin- Intravenous adminis- Baseline TSH levels,
Body Structure and Function releasing hor- tration of TRH to 10 μU/mL
mone (TRH) patients Hypothyroidism
The thyroid gland secretes three hormones: thyroxine (T4), tri- stimulation TRH augments the indicated by
iodothyronine (T3), and calcitonin, with T4 and T3 commonly test function of TSH in increased response
referred to as the thyroid hormones (Table 10.1). T4 and T3 require patients with to TRH
the presence of adequate amounts of iodine to be properly syn- hypothyroidism Hyperthyroidism
The expected response is indicated by no
thesized. Therefore dietary deficiencies of iodine can hinder thy- a rise in TSH levels response to TRH
roid hormone production, which is more common in developing
countries.5 The production and secretion of thyroid hormones Data from Pagana KD, Pagana TJ, Pagana TN. Mosby’s Diagnostic and Laboratory
Test Reference. 13th ed. St. Louis: Elsevier; 2017.
are regulated by thyrotropin (also called thyroid-stimulating hor-
mone [TSH]), which is secreted from the anterior pituitary gland.
TSH levels are directly influenced by T4 levels through a negative
feedback loop. Thyrotropin is further regulated by thyrotropin-  CLINICAL TIP
releasing hormone, which is secreted from the hypothalamus.6-8  Low levels of thyroid hormones T3 or T4 may result in weakness,
Thyroid Tests muscle aching, and stiffness. Based on this information, the
physical therapist may decide to alter treatment parameters to
T4 and T3 circulate throughout the bloodstream, either bound help optimize activity tolerance, minimize patient discomfort, or
to proteins or unbound; in the latter case, they are metabolically both. Radionuclide testing may also affect a patient’s mobility;
active by themselves. Thyroxine-binding globulin (TBG) is one patients may be placed on bed rest or precautions after radio-
of the major thyroid transport proteins.7 Table 10.2 describes nuclide studies. The physical therapist should consult with the
the tests used to measure thyroid hormones, and Table 10.3 medical team after testing to clarify the patient’s mobility status.
summarizes other tests used to measure thyroid function.  

TABLE 10.3  Thyroid Function Tests
Test Description
Thyroid imaging or Intravenous administration of radionuclides
scanning allows imaging or scanning of particular
areas of the thyroid gland.
Ultrasonography Increased or decreased uptake of the radio-
Needle biopsy nuclide can help diagnose dysfunction.
Nodules of the thyroid gland that are
palpable or detected by other imaging
modalities are indications for ultrasound
to help diagnose possible malignancy.
Fine-needle aspiration of thyroid cells may
help diagnose a suspected neoplasm.
Data from Sacher RA, McPherson RA, Campos JM, eds. Widman’s Clinical In-
terpretation of Laboratory Tests. 11th ed. Philadelphia: FA Davis; 2000:786-793;
Bastin S, Bolland MJ, Croxson MS. Role of ultrasound in the assessment of
nodular thyroid disease. J Med Imaging Radiat Oncol. 2009;53;177-187; McDer-
mott M. Endocrine Secrets. 5th ed. St. Louis: Mosby; 2009:279-282; Papadakis
MA, McPhee SJ. Current Medical Diagnosis and Treatment. 55th ed. New York:
McGraw Hill; 2016.
Thyroid Disorders
Disorders of the thyroid gland result from a variety of causes and
can be classified as hyperthyroidism or hypothyroidism.
Hyperthyroidism
Hyperthyroidism, which is a form of thyrotoxicosis, is primar-
ily characterized by excessive sympathomimetic and catabolic
activity resulting from overexposure of tissues to thyroid hor-
mones caused by an increase in thyroid hormone synthesis and
secretion.9,10 In addition, it has been reported that hyperthy-
roidism results in both an increased sympathetic activity with
concurrent decreased vagal (parasympathetic) tone.10 Spectral
analysis of heart rate variability has been shown to detect these
changes and is helpful in determining the severity of hyperthy-
roidism.10 Heart rate variability is discussed further in Chap-
ter 3. Patients may also present with subclinical hyperthyroidism,
which may or may not lead to overt hyperthyroidism. Subclini-
cal hyperthyroidism is defined by low TSH levels and normal T3
and T4 levels.11 The most common causes of hyperthyroidism
are outlined in Table 10.4.
The signs and symptoms of hyperthyroidism include the
following6,8,9,12:
• Nervousness, irritation, emotional lability, tremors, insomnia
• Hyperactivity, increased reflexes
• Palpitations, atrial fibrillation, tachycardia
• Hand tremor
• Proximal myopathy
• Moist and warm skin, or smooth and velvety skin
• Increased perspiration, heat intolerance
• Diarrhea, thirst, weight loss despite increased appetite
• Reduced menstruation
• Lid lag, retraction, or both
• Exophthalmos
• Fingernails that grow away from the nail bed, thinning or
loss of hair
• Thyroid bruit, presence of goiter
• Subclinical hyperthyroidism in some cases
Endocrine System     CHAPTER 10 255
TABLE 10.4  Common Causes of Hyperthyroidism
Cause Description
Graves’ A familial, autoimmune disorder responsible for
disease approximately 80% to 90% of hyperthyroid cases
in the United States.
Occurs more commonly in women than in men.
Distinguishing features include diffuse thyroid
enlargement, ophthalmopathy (double vision
and sensitivity to light), exophthalmos (exces-
sive 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, postpartum or chronic inflammation
with unknown etiology.
Pain may or may not be present on palpation of the
gland.
Toxic nodu- Areas of the enlarged thyroid gland (goiter)
lar and become autonomous and produce excessive
multinod- amounts of thyroid hormones.
ular goiter
Toxic ad- Solitary, benign follicular adenomas that function
enoma 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 Four types of malignancies in the thyroid gland:
carcinoma papillary carcinoma (most common), follicular
carcinoma, anaplastic carcinoma, and medullary
carcinoma.
Exogenous Ingestion of excessive amounts of thyroid hormone
hyperthy- or iodine preparation.
roidism Can be classified as iatrogenic hyperthyroidism,
factitious hyperthyroidism, or iodine-induced
hyperthyroidism.
Data from Woolf N, ed. Pathology, Basic and Systemic. London: Saunders;
1998:863-873; Mitrou P, Raptis SA, Dimitriadis G. Thyroid disease in older
people. Maturitas. 2011;70:5-9; Imam SK. Hyperthyroidism. In: Imam SK,
Ahmad SI, eds. Thyroid Disorders. Switzerland: Springer International Publish-
ing; 2016.
Management of hyperthyroidism primarily includes phar-
macologic therapy, which is summarized in Chapter 19, Table
19.44. Surgical management is indicated for patients with large
goiters or large “hot” nodules or if other options have been ruled
out.13 Surgical options (thyroidectomy) include six procedures
that remove portions or all of the thyroid gland.9,14 
Hypothyroidism
Hypothyroidism is either a decrease in thyroid hormone production
and/or impaired action of thyroid hormone in peripheral target tis-
sues. A person’s growth and development are affected by hypothy-
roidism, as well as many cellular processes. Primary hypothyroidism
is caused by decreased thyroid hormone production by the thyroid
gland and accounts for the majority of cases of thyroid disease. Central
or secondary hypothyroidism is caused by pituitary dysfunction result-
ing in reduced TSH levels. Tertiary hypothyroidism occurs if there is
hypothalamic dysfunction resulting in reduced TSH levels.5,12
The following are the causes of primary and central
hypothyroidism5,12,13:
256 CHAPTER 10     Endocrine System

TABLE 10.5  Target Sites and Actions of Pituitary Gland Hormones

Hormone(s) Target Site(s) Action(s)
Anterior Lobe
Growth hormone (GH) Systemic Stimulates body growth, lipolysis, inhibits insulin action on carbo-
hydrates and lipids
Thyrotropin (thyroid-stimulating hormone [TSH]) Thyroid Stimulates production of thyroid hormones
Adrenocorticotropic hormone (ACTH) Adrenal cortex Stimulates production of androgens and glucocorticoids by adrenal
cortex
Follicle-stimulating hormone Ovaries Development of ovarian follicles and secretion of estrogen
Testes Development of seminiferous tubules and regulates spermatogenesis
Luteinizing or interstitial cell–stimulating hormone Ovaries Ovulation, formation of corpus luteum, and stimulates secretion of
estrogen and progesterone
Testes Stimulates testosterone production
Prolactin or lactogenic hormone Mammary glands Stimulates milk production and secretion
Posterior Lobe
Antidiuretic hormonea (also called vasopressin) Kidney Controls rate of water excretion into the urine
Fluid and electrolyte balance
Oxytocina Uterus Contraction
Breast Expression of milk
aActually
produced in the hypothalamus but stored in the pituitary gland.
From Hall JE. Pituitary hormones and their control by the hypothalamus. In: Guyton and Hall Textbook of Medical Physiology. 13th ed. St. Louis: Saunders Elsevier;
2016:939-950.

• C ongenital maldevelopment, hypoplasia, or aplasia of the • A nemia

thyroid gland
• Hashimoto’s thyroiditis (autoimmune inflammation)
• Hypopituitarism or hypothalamic disease
• Iodine deficiency or excess
• Thyroid ablation from surgery, radiation of cervical neo-
plasms, or radioiodine therapy for hyperthyroidism
• Drug toxicity (from amiodarone, lithium, thionamides, in-
terferon-alfa, interleukin-2, tyrosine kinase inhibitors)
The general signs and symptoms of hypothyroidism vary, accord-
ing to the degree of thyroid deficiency and the area affected, and
include the following5,6,8,12:
• Lethargy, somnolence, and reduced cognitive function
• Constipation and ileus (decreased motility)
• Rough, scaly, dry, and cool skin; decreased perspiration; yel-
lowish complexion
• Dry and brittle hair
• Delayed deep tendon reflexes
• Cold intolerance
• Weakness, fatigue, muscle cramps, and aching and/or stiff
joints
• Slow speech, decreased hearing, tinnitus
• Paresthesia
• Nonpitting edema (myxedema) of eyelids, hands, and feet
• Sinus bradycardia with narrowing of pulse pressure, diastolic
hypertension
• Pleural effusion
• Coma and respiratory failure in severe cases
Additional laboratory findings that are associated with hypo-
thyroidism include the following5,15:
• Low glucose and serum sodium levels
• Elevated levels of cholesterol, creatinine phosphokinase (CK-
MM), serum myoglobin, lactate dehydrogenase, liver en-
zymes, homocysteine, and prolactin
• Proteinuria
• Increased serum creatinine
Management of hypothyroidism typically includes life-
long thyroid hormone replacement, primarily consist-
ing of generic and brand-name variations of levothyroxine
(L-T4).5,8,12 A complete list of medications is provided in
Chapter 19, Table 19.44.
 CLINICAL TIP
Properly managed hyperthyroidism or hypothyroidism should
not affect physical therapy intervention or activity tolerance. If
the signs or symptoms mentioned previously are present during
physical therapy evaluation, treatment, or both, then consulta-
tion with the medical team is indicated to help differentiate the
etiology of the physical findings.
 
Pituitary Gland
Body Structure and Function
Hormones secreted by the pituitary gland are responsible
for a variety of functions, which are summarized in Table
10.5. Secretions of hormones from the pituitary gland are
closely regulated by the hypothalamus and by negative feed-
back from the hormones that are secreted from the pituitary
gland.6 
 Endocrine System     CHAPTER 10 257

TABLE 10.6  Pituitary Hormone Tests

Hormone(s) Test Description
Growth hormone Serum level measurement; reference values for men are 0–5 ng/mL; normal values for women are 0–10 ng/mL.
(GH) Growth hormone–stimulation test. A baseline level of GH is established, then glucagon is administered to the patient, and
serial blood draws are performed to measure GH levels. GH should normally rise. Failure of GH levels to rise
significantly may indicate growth hormone deficiency.
Growth hormone suppression test (glucose load test). A baseline level of GH is established, followed by patient ingestion of a
glucose solution. Levels of GH are redrawn at timed intervals. Normally, glucose inhibits the secretion of GH. If GH
levels remain high despite the glucose load, then the likelihood of gigantism or acromegaly is increased.
Adrenocorticotropic Plasma ACTH levels are measured. Reference values are 6–58 pg/mL (female age >19 years) and 7–69 pg/mL (male age
hormone (ACTH) >19 years). ACTH-stimulation test (cortrosyn-stimulation test). Indicated for evaluating primary or secondary adrenal
insufficiency. Cosyntropin (cortrosyn, a synthetic form of ACTH) is administered to the patient after a baseline level
of cortisol is measured. ACTH acts to increase cortisol secretion from the adrenal gland. Expected results show an
increased plasma cortisol level after certain periods, depending on the type of test performed (rapid, 24-hour or 3-day).
ACTH-suppression test (dexamethasone suppression test). Dexamethasone is administered to the patient to determine
ACTH response, which should be a reduction in ACTH levels in nonobese individuals. May be used in the diagnosis of
Cushing’s syndrome.
Antidiuretic hor- Reference plasma levels of ADH are 2–12 pg/mL if serum osmolality is >290 mOsm/kg and <2 if serum osmolality is
mone (ADH or <290 mOsm/kg.
vasopressin) Water deprivation test (dehydration test or concentration test). Indicated to aid in the diagnosis of diabetes insipidus (DI),
either central or nephrogenic DI, or primary polydipsia.
Water loading test. Indicated to aid in the diagnosis of syndrome of inappropriate antidiuretic hormone (SIADH). During the
test, the patient ingests 20–25 mL/kg of fluid, with hourly serum and urine osmolality levels being measured for 4 hours.

Data from Malarkey LM, McMorrow ME, eds. Nurse’s Manual of Laboratory Tests and Diagnostic Procedures. Philadelphia: Saunders; 2000:580-584, 552-555, 613-614,
616-619; Wilson G, Mooradian A, Alexandraki I, Samrai G. Endocrinology. In: Rakel RE, Rakel DP, eds. Textbook of Family Medicine. 8th ed. Philadelphia: Elsevier
Saunders; 2011:756-784; Papadakis MA, McPhee SJ. Current Medical Diagnosis and Treatment. 55th ed. New York: McGraw Hill; 2016; Pagana KD, Pagana TJ, Pagana
TN. Mosby’s Diagnostic and Laboratory Test Reference. 13th ed. St. Louis: Elsevier; 2017.

Pituitary Tests Hyperpituitarism

Individual pituitary hormone levels can be measured by ana-
lyzing (1) random blood samples; (2) blood samples obtained
before and after the administration of specific releasing sub-
stances, such as serum TSH, during a thyrotropin-releasing
hormone test (see Table 10.2); or (3) blood samples obtained
before and after the administration of specific stimuli act-
ing directly on the pituitary or via the hypothalamus, such
as serum growth hormone (GH), serum cortisol, and plasma
adrenocorticotropic hormone (ACTH). Table 10.6 describes
common tests of pituitary function.
Pituitary function can also be evaluated by performing (1)
thyroid function tests, which are an indirect assessment of TSH
secretion from the pituitary; and (2) imaging to detect suspected
pituitary tumor or other structural changes.16,17  • Oligomenorrhea or amenorrhea in women
Pituitary Disorders
Dysfunction of the pituitary–hypothalamic system gener-
ally results from hypersecretion or hyposecretion of tropic
hormones. Hypersecretion of pituitary hormones (hyperpitu-
itarism) is most commonly caused by a benign adenoma in
the anterior lobe.18,19 Hyposecretion of pituitary hormones
(pituitary insufficiency) can result from pituitary disease
(e.g., nonsecreting pituitary tumors), diseases affecting the
hypothalamus or surrounding structures, hypophysectomy
(removal or destruction of the pituitary gland), or distur-
bance of blood flow around the hypothalamus and pituitary
(e.g., postpartum hemorrhage).18,20,21
The overproduction of the pituitary hormones GH, ACTH, and
antidiuretic hormone (ADH) is discussed next.
Growth Hormone Overproduction. Excessive GH secre-
tion is referred to as acromegaly in adults or gigantism in pre-
pubertal children. Excessive GH secretion has been linked
primarily to anterior pituitary adenomas and not necessarily to
excessive hypothalamic stimulation of the pituitary.21,22
Clinical manifestations for children with gigantism are char-
acterized by disproportionately long limbs.18
The signs and symptoms of acromegaly in adults include the
following21,23:
• Enlargement of hands and feet, coarse facial features with
furrowed brows
• Paresthesia of hands, carpal tunnel syndrome
• Sweating
• Headaches
• Impotence in men
• Diabetes mellitus
• Hypertension
• Joint pains, osteoarthritis
Management of acromegaly may include the following:
transsphenoidal surgical resection for microadenoma and
neurosurgery for macroadenomas.22,24 Medical therapy con-
sists of GH suppression with somatostatin receptor ligands
(SRLs), dopamine agonists (DAs), and GH receptor antago-
nists (GHRAs). Radiation therapy is considered the third-line
treatment.22,25
258 CHAPTER 10     Endocrine System
 CLINICAL TIP
Given the multisystem effects in patients with acromegaly, ac-
tivity progression should proceed cautiously, with a focus on
energy conservation, joint protection techniques, and fall pre-
vention strategies.
 
Adrenocorticotropic Hormone Overproduction. An incre­
ase 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 in carbohydrate,
protein, and fat metabolism; therefore excess cortisol levels affect
these cellular processes. Cushing’s syndrome results from gluco-
corticoid excess (hypercortisolism), resulting from benign tumor
hypersecretion of the adrenal gland, excess stimulation from the
pituitary gland or an excess of corticosteroid medication.19 Cush-
ing’s disease, however, is specific to ACTH-producing micro-
adenomas in the pituitary gland.26 Pituitary hypersecretion of
ACTH occurs in approximately 70% of patients with Cushing’s
syndrome. The hypersecretion of ACTH may originate either
from a tumor in the pituitary gland or from ectopic neuroendo-
crine tumors elsewhere in the body.6,27
The signs and symptoms of Cushing’s syndrome include the
following5,17,19,21,27:
• Truncal obesity with thin extremities (loss of type II muscle
fibers)18
• Redness and rounding of the face (moon face)
• Easy bruising, thinning of the skin, and presence of purple
striae and darker pigmentation
• Hirsutism, oligomenorrhea, or amenorrhea in females
• Hypertension
• Osteoporosis (radiographically confirmed)
• Peripheral muscle wasting
• Backache
• Glucose intolerance, glycosuria, and polydipsia, resulting in
diabetes mellitus
• Poor wound healing
Diagnosis of Cushing’s syndrome is established by detecting
increased levels of urine and serum cortisol.18,19 Additional confir-
matory tests are also performed to verify the diagnosis.19 Manage-
ment of Cushing’s syndrome may include the following: resection
of pituitary or adrenal glands through surgery or radiation, followed
by lifelong glucocorticoid replacement therapy after removal of the
pituitary or adrenal glands.19,27 Medical management may consist
of steroidogenic inhibitors (ketoconazole) or neuromodulators of
ACTH release with somatostatin analogs and dopamine agonists.27
Management of weakness, pain, edema, and osteoporosis
should be the focus of physical therapy intervention and should
be complementary to the medical management of the patient.
 CLINICAL TIP
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 the Diabetes
Mellitus section 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) caused by excessive water reabsorption. In this condition,
ADH secretion is poorly regulated resulting from increased produc-
tion, increased ectopic production, or increased sensitivity to ADH
in the periphery.28 Hyponatremia is fairly common in patients who
are hospitalized and can result in significant morbidity and mortal-
ity.29 Numerous etiologies of SIADH include28,30,31:
• Bacterial pneumonias, chronic obstructive pulmonary dis-
ease (COPD), asthma, tuberculosis, lung abscesses, pneumo-
thorax, atelectasis
• Malignancies of the nasopharynx, pancreas, gastrointestinal
tract, lymphoid tissue, pleural lining (mesothelioma)28
• Medication side effects caused by anticonvulsants, antipsychot-
ics, sedative-hypnotics, antidepressants, diuretics, angiotensin-
converting enzyme inhibitors, analgesics, cardiac drugs, non-
steroidal antiinflammatory drugs (NSAIDs), chemotherapy,
recreational drugs (e.g., ecstasy), and antibiotics28,32
• Head trauma, central nervous system (CNS) neoplasms,
Guillain-Barré syndrome
• Meningitis, encephalitis, abscesses, human immunodeficien-
cy virus, sarcoidosis28
Mild SIADH is usually asymptomatic. More severe cases,
however, can result in fluid and electrolyte imbalances, resulting
in interstitial edema resulting from lack of serum sodium. Many
systems will be affected by this edema, with the CNS being most
severely involved. Manifestations may include the following:
headaches, nausea, confusion, gait disturbances, falls, and cerebral
edema that leads to seizures and coma (in severe cases).18,29,30
Management of SIADH may include the following: treat-
ment of the underlying cause, including discontinuation of
contributing medications; fluid restriction; or administration of
select agents, such as demeclocycline, lithium, and urea. Intra-
venous administration of sodium chloride (saline) solution, or
administration of diuretics (furosemide) may also be used as
initial therapies but not for long-term management.19,29,30,32,33
The use of vaptans or vasopressin 2 receptor antagonists
for mild to moderate cases of SIADH has resulted in good
outcomes.29,33,34
 CLINICAL TIP
The physical therapist should be aware of fluid restriction guide-
lines for patients with SIADH, especially because activity during
physical therapy may increase the patient’s thirst. These guide-
lines are often posted at the patient’s bedside.
 
Hypopituitarism
Decreased secretion of pituitary hormones can result from either
pituitary or hypothalamic dysfunction. Complete anterior pitu-
itary hormone deficiency is referred to as panhypopituitarism.19,35
Most cases of pituitary hypofunction arise from destructive pro-
cesses involving the anterior pituitary, such as ischemic necrosis
occurring during the late stages of pregnancy (Sheehan’s syn-
drome). Additional causes may include pituitary adenomas,
traumatic brain injury, pituitary surgery, or radiation.19,35
 Endocrine System     CHAPTER 10 259

TABLE 10.7  Target Sites and Actions of Adrenal Gland Hormones

Hormone(s) Target Site(s) Action(s) Reference Valuesa
Cortex
Mineralocorticoids Kidney Reabsorption of sodium and water Upright positionb:
(aldosterone) Elimination of potassium 5–30 ng/dL (females)
6–22 ng/dL (males)
Urine:
2–26 mcg/24 h
Glucocorticoids Systemic Metabolism of carbohydrate, protein, and fat 5–23 mcg/dL (8–10 a.m.)
(cortisol) Response to stress 3–13 mcg/dL (4–6 p.m.)
Suppresses immune responses Urine:
Antiinflammation <100 mcg/dL in 24 hours
Sex hormones (andro- Systemic Preadolescent growth spurt, affects secondary Testosterone:
gens, progesterone, sex characteristics Serum values vary based on age and
and estrogen) stage of maturity indicated by Tanner
stages I–V
Estrogen:
10–50 pg/mL (adult males)
20–750 pg/mL (adult females,
menstrual phase dependent)
<20 pg/mL (postmenopausal female)
Medulla
Epinephrine Cardiac and smooth Emergency functions Epinephrine: <20 mcg/24 h (adults)
muscle, glands Stimulates the action of the sympathetic system
Norepinephrine Organs innervated by sym- Chemical transmitter substance Norepinephrine: <100 mcg/24 h
pathetic nervous system Increases peripheral resistance
aBlood levels unless otherwise specified.
bAldosterone levels vary from supine to upright positions.
Data from Fuller BF. Anatomy and physiology of the endocrine system. In: Hudak CM, Gallo BM, eds. Critical Care Nursing: A Holistic Approach. 6th ed. Philadelphia,
PA: Lippincott; 1994:875; Corbett JV, ed. Laboratory Tests and Diagnostic Procedures with Nursing Diagnoses. 5th ed. Upper Saddle River, NJ: Prentice Hall Health;
2000:391; ; Pagana KD, Pagana TJ, Pagana TN. Mosby’s Diagnostic and Laboratory Test Reference. 13th ed. St. Louis, MO: Elsevier; 2017.

Symptoms and physical findings depend on the extent of the
disorder and the specific hormone (GH, TSH, or ACTH) and
target cells involved, such as19,36:
• Decreased libido, impotence with loss of pubic and axillary
hair in males
• Secondary amenorrhea and infertility in women
• Pallor
• Short stature (in children)
• Hypothyroidism
• Hypoadrenalism
• Fatigue
• Headache
• Loss of visual acuity
Management of panhypopituitarism may include the following:
replacement therapy or pituitary hormones, such as T4, glucocor-
ticoids, and GH for children; desmopressin for diabetes insipidus
(DI); androgen therapy 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.17,37 
Diabetes Insipidus
DI involves the excretion of a large volume (i.e., >50 mL/kg per day)
of dilute urine (hypotonic polyuria). DI may result from an absence of
vasopressin or an inadequate response to vasopressin. Four categories
of DI exist: primary polydipsia, central (hypothalamic or posterior
pituitary) DI, transient (gestational) DI, and nephrogenic DI.38,39
The signs and symptoms of DI may be transient or perma-
nent, and include the following31,37,40,41:
• Polyuria, nocturia with resultant hypernatremia (increased
sodium)
• Thirst (especially for cold or iced drinks), polydipsia
• Dehydration
• Weight loss
• Dry skin with decreased turgor
• CNS manifestations (e.g., irritability, mental dullness, atax-
ia, hyperthermia, and coma) if unable to properly hydrate
Management of central DI may include pharmacologic
treatment, such as the following: vasopressin (Pitressin)
deamino-8-D-arginine vasopressin (desmopressin), chlor-
propamide (Diabinese), clofibrate (Atromid-S), carbamaze-
pine (Tegretol), and thiazide diuretics in combination with a
sodium-restricted diet.39,42 Nephrogenic DI is managed with
dietary modifications, inhibitors of prostaglandin synthesis
and thiazides.39 
Adrenal Gland
Body Structure and Function
The adrenal gland has two distinct areas, the outer cortex and
the inner medulla, which differ in function and embryologic
origin.6 Table 10.7 summarizes the target sites and actions of
the adrenal gland hormones. 
260 CHAPTER 10     Endocrine System
Adrenal and Metabolic Tests
Adrenal Tests
Evaluation of the adrenal cortical (glucocorticoids, androgens,
and mineralocorticoids) and medullary (epinephrine and norepi-
nephrine) hormones is typically performed by measuring plasma
and/or urinary levels. Reference values for adults for each hor-
mone are listed in Table 10.7. The primary method for evalu-
ating adrenal activity is by measuring plasma cortisol levels.
Levels are usually drawn at 8 a.m. and then 4 p.m. to evaluate
whether there is any deviation from the expected diurnal varia-
tion. Cortisol levels peak in the morning and taper during the
rest of the day. Increased levels indicate Cushing’s syndrome,
decreased levels suggest Addison’s disease. Normal serum levels
are 5 to 23 mcg/dL (8 to 10 am) and 3 to 13 mcg/dL (4 to 6
pm).43,44
Analysis of urine over a 24-hour period is used to deter-
mine the urinary levels of free cortisol. Normal levels are less
than 100 mcg/dL for a 24-hour period.43,44 ACTH levels are
usually examined concomitantly with cortisol levels, as ACTH
secretion from the pituitary gland is necessary for cortisol secre-
tion from the adrenal glands. Refer to Table 10.6 for details on
ACTH measurement.
Anatomic investigation of the adrenal glands may also be
performed to diagnose possible adrenal dysfunction. Common
methods to accomplish this are computed tomography (CT; to
identify adrenal tumors), radioisotope scanning using seleno-
cholesterol, ultrasound, arteriogram, adrenal venogram (allows
measurements of hormone levels), and intravenous pyelography
(see the Diagnostic Tests section in Chapter 9).43  by a tumor of the chromaffin cells in the adrenal medulla, which
Metabolic Tests
One of the tests for metabolism is described in this section, as
glucocorticoids (cortisol) affect carbohydrate, protein, and fat
metabolism.
Glucose Tolerance Test. To perform the test, a 75-g glucose
load is given to the subject. Blood glucose levels are then measured
at variable periods, ranging from every half hour to every hour for
the next 1 to 5 hours after the glucose administration. The subject
must remain inactive and refrain from smoking throughout the
duration of the test. Normally the blood glucose levels should fall
back to baseline values in a 2-hour period. Normal glucose value
for a fasting blood sugar (FBS) is less than 110 mg/dL. After 1
hour of ingesting the glucose load, expected levels of glucose are
less than 180 mg/dL and less than 140 mg/dL after 2 hours.44  • Dyspnea
Adrenal Disorders
Adrenal Hyperfunction
Increased secretion of glucocorticoids (hypercortisolism) results
in Cushing’s syndrome, which has been discussed in detail ear-
lier in this chapter.  use of alpha-adrenergic blockers, angiotensin receptor block-
Adrenal Insufficiency
Autoimmune dysfunction can lead to destruction of the adre-
nal cortex (i.e., primary adrenal insufficiency or Addison’s dis-
ease). Additionally, central ACTH deficiency from either the
hypothalamus or pituitary gland can lead to atrophy of the adre-
nal cortex (secondary and tertiary adrenal insufficiency). The
net result is an impaired adrenal system with decreased levels
of glucocorticoids (cortisols), mineralocorticoids (aldosterone),
and androgens. Given the systemic functions of these hormones,
Addison’s disease can have severe consequences if left untreated.
Fortunately, the incidence of Addison’s disease is rare.45,46
Cortisol deficiency results in decreased gluconeogenesis
(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.47,48
Symptoms and physical findings for adrenal insufficiency
may include the following45,46,49:
• Weakness, fatigue
• Weight loss, nausea, vomiting, vague abdominal pain
• Muscle and joint pain
• Salt craving (in <20% of patients)
• Skin hyperpigmentation
• Hypotension
• Headaches and visual deficits
Long-term management of adrenal insufficiency typically
includes pharmacologic intervention with any of the following
steroids: hydrocortisone, prednisone, dexamethasone fludrocor-
tisone, or cortisone.41,45,46 
Pheochromocytoma
Pheochromocytoma is a rare adrenomedullary disorder caused
results in excess secretion of the catecholamines, epinephrine,
and norepinephrine.50 Disease presentation can occur either in
childhood or early adulthood, with sporadic pheochromocy-
tomas occurring between 40 and 50 years of age.51 Given the
rare occurrence of this tumor, it often goes undiagnosed. Proper
diagnosis is essential, as the sustained release of catecholamines
can be life threatening.49,52,53
The signs and symptoms of pheochromocytoma include the
following47,49,50,52,53:
• Classic triad of palpitations, headaches, and sweating lasting
minutes to hours
• Sustained or paroxysmal hypertension
• Flushing or pallor, nausea, vomiting, tiredness, or weight loss
• Anxiety or panic attacks
• Abdominal pain, constipation, or chest pain
• Elevated blood glucose levels and glycosuria
Management of pheochromocytoma generally includes sur-
gical excision of the tumor with preoperative pharmacologic
management to block the effects of circulating catecholamine,
in all patients with catecholamine-producing tumors, with the
ers, and/or the calcium channel blockers nifedipine, diltiazem,
phenoxybenzamine, and doxazosin. Low-dose beta-blockade
with metoprolol, bisoprolol, or atenolol may also be imple-
mented preoperatively.50,53 Chemotherapy and radiation ther-
apy can offer palliative support to nonsurgical candidates.50 

TABLE 10.8  Criteria for Diagnosis of Metabolic
Syndrome
Sign Diagnostic Range
Elevated waist Population- and country-specific
circumferencea definitions
USA: >102 cm in men; >88 cm in
women
Elevated triglyceridesb ≥150 mg/dL (1.7 mmol/L)
Reduced HDL-Cb,c <40 mg/dL (1.0 mmol/L) in males
<50 mg/dL (1.3 mmol/L) in females
Elevated blood pressureb Systolic ≥130 and/or diastolic
85 mmHg
Elevated fasting glucoseb ≥100 mg/dL
aWaist
circumferences vary, depending on specific country definitions.
bIf values are not available, then presence of drug therapy is an alternate indicator.
cHDL-C indicates high-density lipoprotein cholesterol.
Data from Alberti KG, Eckel RH, Grundy SM et al. Harmonizing the metabol-
ic syndrome: a joint interim statement of the International Diabetes Federation
Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood
Institute; American Heart Association; World Heart Federation; International
Atherosclerosis Society; and International Association for the Study of Obesity.
Circulation. 2009;120:1640-1645.
Pancreatic Disorders
Insulin Resistance
Insulin resistance is an important link to the development of
metabolic syndrome, type 2 diabetes, cardiovascular disease
(CVD), and possibly some cancers. Insulin resistance is defined
as resistance to insulin-stimulated glucose.54 Patients who are
overweight or obese are more likely to develop insulin resis-
tance over time; however, patients who are not obese may also
have insulin resistance linked to an inherited genetic defect.54
Patients who have insulin resistance also present with com-
pensatory hyperinsulinemia and hyperglycemia. Furthermore,
insulin resistance in the absence of metabolic syndrome crite-
ria (see the next section) has also been shown to be indepen-
dently related to the development of CVD. Insulin resistance
has been detected 10 to 20 years before the development of
diabetes in individuals who are offspring of patients with type
2 diabetes.55-58  of insulin leads to increased levels of plasma glucose.63,64
Metabolic Syndrome
According to an international multiassociation statement,
“metabolic syndrome is a complex of interrelated risk fac-
tors for cardiovascular disease (CVD) and diabetes mellitus.
Patients with metabolic syndrome have twice the risk of devel-
oping CVD over the next 5 to 10 years compared with individ-
uals without the syndrome. Additionally, metabolic syndrome
confers a fivefold increase in risk for developing type 2 diabe-
tes mellitus.”59
Metabolic syndrome is defined as the cluster of clinical mani-
festations that are present just before the onset of type 2 diabe-
tes.60 Patients with metabolic syndrome have a high likelihood
of having concurrent insulin resistance. Metabolic syndrome
Endocrine System     CHAPTER 10 261
focuses on identifying patients who are at higher risk for type
2 diabetes and CVD and prescribing timely intervention to off-
set the development of these diseases and their complications.
Insulin resistance syndrome is also reported in the literature;
however, it is less clearly defined compared with metabolic
syndrome.55,61
The diagnosis of metabolic syndrome is established
when patients have at least three of the criteria outlined in
Table 10.8.
The cornerstone of the management of this syndrome is life-
style change, including calorie restriction, improved physical
activity, and improved health quality of foods.62 A modest reduc-
tion of 7% to 10% in initial weight has been reported to dem-
onstrate significant reduction in the development of diabetes and
CVD.60 In addition to this therapeutic lifestyle change, partici-
pation in an exercise program has been shown to either delay or
prevent the development of type 2 diabetes and to improve the
cardiovascular risk profile of patients by increasing high-density
lipoprotein (HDL) levels and lowering blood pressure.61 For some
patients, bariatric surgery may be considered. Concomitant medi-
cal management for dyslipidemia, hypertension, and hyperglyce-
mia is also prescribed as indicated for a patient.62
 CLINICAL TIP
In the acute care setting, physical therapists, unfortunately, do not
have a significant role in the establishment or progression of exer-
cise prescription to create the long-term changes necessary to mod-
ify metabolic syndrome. However, when working with patients who
have metabolic syndrome, acute care physical therapists should ei-
ther ensure that patients can continue with a previously established
exercise program or provide patient education and referral for physi-
cal therapy postdischarge to establish a long-term exercise program.
 
Diabetes Mellitus
Diabetes mellitus is a syndrome with metabolic, vascular, and
neural components and originates from glucose intolerance,
which, in turn, leads to hyperglycemic states (increased plasma
glucose levels). Hyperglycemia can result from insufficient insu-
lin production, insulin action, or both. Insulin promotes storage
of glucose as glycogen in muscle tissue and the liver. Deficiency
The diagnosis of diabetes is based on the presence of any one
of the following four factors6,65,66:
1. Presence of polyuria, polydipsia, weight loss, blurred vi-
sion, and random plasma glucose (regardless of last meal)
≥200 mg/dL (11.1 mmol/L).
2. Fasting plasma glucose (FPG) ≥125 mg/dL (6.9 mmol/L).
Fasting involves no caloric intake for at least 8 hours. Levels
between 100 and 125 mg/dL (between 5.5 and 6.9 mmol/L)
are considered prediabetic.
3. Two-hour postload glucose ≥200 mg/dL, during an oral glu-
cose tolerance test (OGTT) using a 75-g oral glucose load
dissolved in water, as described by the World Health Orga-
nization (WHO). Prediabetes is considered with values be-
tween 140 and 199 mg/dL. An OGTT is typically conducted
in pregnant individuals.
262 CHAPTER 10     Endocrine System

TABLE 10.9  Tests to Monitor Control of Diabetes

Test Description
Self-Monitoring
Blood glucose fingerstick Monitors immediate control of diabetes.
samples Very effective in establishing the correct insulin dosages and preventing complications from diabetes.
Reference, 74–106 mg/dL Capillary blood is obtained by a needlestick of a finger or an earlobe and placed on a reagent strip.
(fasting) The reagent strip is compared with a color chart or placed in a portable glucometer to read the glucose level.
≤200 mg/dL (nonfasting) 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 with a color chart to measure
Random specimen: negative 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 Hyperglycemia results in saturation of Hgb molecules during the life span of a red blood cell
(HgbA1C) (approximately 120 days).
Reference, 4% to 5.9% of Measuring the amount of HgbA1C in blood provides a weighted average of the glucose level over a period
total Hgb for a patient with and is a good indicator of long-term control of diabetes, without confounding factors such as a recent meal
controlled diabetes or insulin injection.
Measurements are performed every 3–6 months.
Data from: Pagana KD, Pagana TJ, Pagana TN. Mosby’s Diagnostic and Laboratory Test Reference. 13th ed. St. Louis: Elsevier; 2017.

4. Glycosylated hemoglobin A1C (HgbA1C) ≥6.5%, measured
with a standardized assay. HgbA1C is a widely used marker
for chronic glycemia and glycemic management. HgbA1C
readings between 5.7% and 6.4% are indicative of a predia-
betic state, necessitating intervention.
The diagnosis of diabetes is confirmed when one of the listed
factors is also found on a subsequent day or in situations when
hyperglycemia is unclear.6,64-66
The two primary types of diabetes mellitus are type 1 (pre-
viously known as insulin-dependent or juvenile-onset diabetes) and
type 2 (previously non–insulin-dependent or adult-onset diabetes).
After much debate on the classification of diabetes, the current
terminology for diabetes uses type 1 and type 2 diabetes to dis-
tinguish between the two primary types.63,65,67 Other forms of
glucose intolerance disorders exist but are not discussed in this
book.
A bi-directional association between diabetes and depression
has been reported with increased risk of depression among indi-
viduals who are being treated for type 2 diabetes.68-70 Depres-
sion has also been reported to contribute to central obesity,
which, in turn, is a risk factor for the development of diabe-
tes. Routine screening for depression should be considered if
clinicians note increased risk of elevated symptoms in patients
with diabetes or patients who have risk factors for diabetes.71
If a patient is found to be at risk for depression, referral may
be appropriate.68-70 Outcome measure tools that are useful to
assess depression include the Center for Epidemiologic Studies
Depression (CES-D) scale, the Mini-Mental State Examination
(MMSE), and the Patient Health Questionnaire.70,72,73
Type 1 Diabetes
Type 1 diabetes is an autoimmune disorder with a genetic–envi-
ronmental etiology that leads to the selective and progressive
destruction of beta cells in the pancreas. This destruction results
in decreased or absent insulin secretion necessary to for glucose
homeostasis.67 Other etiologies for type 1 diabetes are not dis-
cussed in this book.
The classic signs and symptoms of type 1 diabetes have been
described in the previous section, along with the diagnostic cri-
teria for diabetes.74
Management of type 1 diabetes may include the
following75-77:
• Close self-monitoring or medical monitoring of blood glu-
cose levels (Table 10.9).
• Continuous glucose monitoring (CGM) is a device that uses
a needle type electrode or small wire that measures inter-
stitial glucose subcutaneously and transmits glucose data to
a wireless monitor. The US Food and Drug Administration
(FDA) has approved the use of CGM for monitoring glucose
trends and patterns. Periodic calibration daily of the CGM is
required.78
• Insulin administration through oral medications, intramus-
cular injection, or continuous subcutaneous insulin infusion
(CSII) pump. A medication summary is provided in Chapter
19, Table 19.41.
The use of an insulin pump provides an ability to mimic a
more natural glycemic response in fasting and postprandial
states (Table 10.10). Pump technology includes communication
with glucose sensors (CGM) that detect rapid changes in blood
glucose.78
• New options for noninvasive insulin routes of administra-
tion, including insulin patch, artificial pancreas, and inhaled
insulin, have been in various stages of investigation and de-
velopment.79 These routes of administration are further de-
scribed later in this chapter.
• Diet modification based on caloric content, proportion of ba-
sic nutrients and optimal sources, and distribution of nutri-
ents in daily meals.
 Endocrine System     CHAPTER 10 263

TABLE 10.10  Summary of Insulin Pump Therapy

Parameter Description
Patient candidacy Patients with type 1 diabetes mellitus (DM) unable to meet glycosylated hemoglobin (HgbA1C) goal
Severe hypoglycemia or high glucose variability
Need for flexibility with insulin dosing and satisfaction regardless of glycemic control
Patients with type 2 DM unable to meet HbA1C goal despite the use of oral agents, intensive insulin therapy, and other
injectable drugs along with lifestyle changes
Demonstrated ability to self-monitor glucose and adjust insulin doses
Availability of resources to manage pump
Pump description Electromagnetic device that is portable and battery powered
Programmable user interface
Refillable reservoir of rapid acting insulin analog connected to narrow tubing with a needle and cannula for insertion
subcutaneously
Basal insulin delivered by controlled subcutaneous infusion
Infusion rates are adjustable
Bolus or mealtime insulin delivered by accelerated infusion via button push or programmable

Data from Galderisi A, Schlissel E, Cengiz E. Keeping up with the diabetes technology: 2016 endocrine society guidelines of insulin pump therapy and continuous
glucose monitor management of diabetes. Curr Diabetes Rep. 2017;17(11):1-7; Crasto W, Jarvis J, Davies MJ. Insulin management in type 1 diabetes. In: Handbook of
Insulin Therapies. Switzerland: Springer International Publishing.

• M eal planning. among females and minorities.84-88 According to the CDC,

• Exercise on a regular basis.
• Web-based and mobile phone applications are available
for patients to track glucose levels, assist with insulin dose
calculations and monitor activity, nutrition, and weight
management. Proper education by health care professionals
should be implemented before use of these technologies.78
Research directed at curing type 1 diabetes is aimed at
identifying the causative genes and permanent replacement of
lost beta-cell function, which could involve islet cell trans-
plantation.63 Islet cell transplantation, however, has had lim-
ited clinical success and is only reserved for a select subset
of patients. Drug studies have also been in place to alter the
autoimmune reaction by reeducating the immune system.80-82
The use of autologous hematopoietic stem cell transplan-
tation and autologous T-cell administration are also under
investigation.67,82  administration may also be used.75,77,91,92 Although insulin
Type 2 Diabetes
Type 2 diabetes accounts for the majority of cases worldwide.
Type 2 diabetes is significantly linked to obesity and insulin
resistance. Genetic predisposition has also been established;
however, lifestyle factors are also highly relevant.63,65,67,76 Pre-
vention of type 2 diabetes with diet and exercise interventions
may afford long-term benefits to patients compared with phar-
macologic therapies.83
The mechanism of type 2 diabetes involves increasing cel-
lular resistance to insulin, which results in a compensatory
hypersecretion of insulin from the pancreatic beta cells that ulti-
mately leads to a failure in insulin production.64,65,76,83 Other
etiologies for type 2 diabetes exist but are not discussed in this
text. A growing epidemic of concern in recent years is the num-
ber of children in the United States being diagnosed with type
2 diabetes. Of all people diagnosed with type 2 diabetes in the
United States, 0.18% to 0.24% of the total population are chil-
dren and adolescents under age 20 years. The onset generally
occurs between ages 12 and 16 years and has higher prevalence
between 2011 and 2012, 17,900 children and adolescents were
diagnosed with type 2 diabetes.89
The signs and symptoms of type 2 diabetes may be similar
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 diagnosed type 2 diabetes is similar to that
of type 1 diabetes, with an emphasis on medical nutritional
therapy (MNT) and exercise to control hyperglycemia. Bar-
iatric surgery may also be indicated in patients with severe
obesity.83 Monitoring carbohydrate intake by carbohydrate
counting, exchanges, or experience-based estimation, is a
component of MNT.90 Oral hypoglycemic agents and insulin
treatment is not as common in patients with type 2 diabetes,
insulin may be indicated in certain cases, when needed, to con-
trol glucose levels. Chapter 19 provides a summary of medica-
tions used to manage type 2 diabetes (see Table 19.41). CSII
has been shown to be as effective as multiple-dose injections
of insulin in patients with type 2 diabetes; however, it is not
in widespread use in these patients compared with those with
type 1 diabetes.83,93
Research has identified genetic associations with the devel-
opment of obesity and type 2 diabetes. Ongoing improve-
ments in the understanding of the mechanisms associated
with the pathophysiology of type 2 diabetes, including
insulin resistance has been underway.63,83 Targeted therapies
potentially aimed at individual (precision) medicine is being
investigated.83
 CLINICAL TIP
Blood sugar or glucose levels are denoted in the medical record
as BS or BG levels, respectively.
 
264 CHAPTER 10     Endocrine System
Physical Therapy Considerations
• 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, or postoperative recovery because
these new processes require added glucose metabolism. It
is important for the therapist to carefully monitor the pa-
tient’s blood glucose levels during therapeutic interventions
because the symptoms of diabetes may be exacerbated in a
patient with significant comorbidities.
• Patients with diabetes present with a wide range of their
individual “normal” values. Therefore establishing with the
medical team the tolerable high or low value for each patient
during the initial evaluation is very important in determin-
ing the parameters for physical therapy intervention.
• Patients with poor glycemic control can have wide fluctua-
tions in the BS levels on a daily basis. This is more common
when patients are in an acute medical state. Therefore be
sure to always verify their BS level before and after physical
therapy intervention.
• Consult with the nurse or physician to determine whether
therapy should be deferred for patients who were recently
placed on intravenous insulin to stabilize their glucose levels.
A preexercise glucose level less than 100 mg/dL may require
added carbohydrate ingestion before starting the activity.90
Patients who are hyperglycemic before exercise should be
monitored for ketosis (ketone bodies in blood or urine). If
the patient feels well and there is an absence of ketosis, then
monitored exercise can proceed.90
• Patients who were following a regular exercise program for
glycemic control before hospital admission will require edu-
cation 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 ill-
nesses.
• Hypoglycemia may occur during exercise or up to 16 hours
after exercise because of depleted stores of glycogen. 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 de-
crease the dose or rate of insulin injections or infusion, with
CSII.19
• 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
may be enhanced as a result of increased blood flow and tem-
perature. Alternative sites of insulin may need to be used in
these instances.19
• Insulin is necessary to modulate lipolysis and hepatic (liv-
er) glucose production during exercise. Performing exercise
without adequate insulin can lead to hyperglycemia and ke-
togenesis.19
• Coordinating physical therapy sessions with meals and in-
sulin injections is necessary to help optimize exercise toler-
ance.
• Keeping glucose sources, such as Graham Crackers, close by
is helpful in case hypoglycemia does occur with activity.  and stress.102,103
Insulin Routes of Administration
Subcutaneous injection of insulin has been the primary self-
insulin delivery option available until recent years. Compli-
cated equipment and the need for self-injections contribute
to noncompliance with medication and treatment. Subcutane-
ous injections tend to have slow absorption and can result in
peripheral hyperinsulinemia, as well as stress, pain, burden of
daily injections, high cost, infection, inability to handle insulin,
and localized subcutaneous deposits of insulin. These localized
deposits of insulin can lead to local hypertrophy and fat depos-
its, which can contribute to diabetic microangiography and
macroangiopathy.94-99
Alternative routes of insulin administration currently include
the CSII pump (see Table 10.10), implantable pump therapy, an
insulin pen, and an insulin patch pump. Under ongoing investi-
gation and development is a fully artificial pancreas.
In addition, there has been interest in developing new nonin-
vasive routes of insulin administration to improve convenience
and safety.79,98,106
 CLINICAL TIP
It is important to ascertain what form of insulin delivery a pa-
tient is using and have an understanding of the individual im-
plications. Specific PT considerations for newer routes of insulin
administration, which continue to be investigated and devel-
oped, include monitoring for adverse side effects in considera-
tion of both the mechanism of action of the drug as well as the
route of administration.
Implantable Pump Therapy. In individuals with type 1
diabetes, an implanted pump provides continuous subcuta-
neous insulin and eliminates multiple daily injections while
delivering a continuous basal rate for 24 hours. It also allows
for manual adjustments according to changes in glucose lev-
els. A catheter is surgically inserted into the peritoneal cavity,
and the pump is implanted into the abdominal wall and can
then be programmed by an external handheld device. Reduced
frequency of hypoglycemic episodes and better glucose reg-
ulation compared with subcutaneous injections have been
reported; however, robust evidence is still lacking, thus limit-
ing implantable pump therapy to select centers and patients
in Europe.84,85,100 
Artificial Pancreas. The fully artificial pancreas for type
1 diabetes has made steady progress toward implementation
and consists of three components: sensors that continuously
monitor glucose levels, controllers (decision-making algo-
rithms) and infusion mechanisms (pumps) for insulin.101-103
In 2016 the FDA approved a hybrid closed-loop system,
which monitors glucose every 5 minutes and provides the
necessary dose of insulin, but it requires manual adjustments
during mealtimes.104 Research indicates that these closed-
loop systems have advantages to open-loop systems or tra-
ditional management by injections, in controlling type 1
diabetes; however, more variables need to be interpreted to
account for glucose variability based on meals, exercise, sleep,

 CLINICAL TIP
A patient’s treatment plan may need to be altered to accom-
modate the use of an insulin pump. Before a treatment session
the therapist should ask the patient where the pump is located
for safe patient handling, determine how recently the pump was
put in, inspect the incision site as necessary, and verify if the
pump allows for fast-acting bolus insulin in response to meals
and exercise.
 
Insulin Pen. Currently approved for use, the insulin pen is
advantageous because it is easy to use, portable, and discreet. It
can be used for either type 1 or 2 diabetes and has a premeasured
amount of insulin. Different dose concentrations are available
for use with insulin pens; however, ensuring the proper time
for injection is required for optimal glucose management.105
Improved health-related quality of life and convenience are
reported advantages compared with use of a subcutaneous insu-
lin syringe.104,106  • Nausea, vomiting, abdominal pain, acute abdomen
Patch Pump. A patch pump consists of an insulin reservoir,
delivery system, and cannula integrated into a small, wearable,
disposable/semidisposable device. Patch pumps eliminate tub-
ing, are reported to be easy to use with simplified training, and
discreet. OmniPod, an example of the insulin patch pump cur-
rently approved for use, is attached to skin with an adhesive.
Benign to severe skin reactions are possible with the adhesives.
Other patch pumps are in various stages of review and approval.
Patch pumps communicate wirelessly to a personal data man-
ager and needs to be changed every 3 days.95,106-108  administration, hydration, electrolyte (sodium, potassium, and
Pulmonary Inhaled Insulin. Inhaled insulin is approved for
patients with either type 1 or 2 diabetes.104 It is an inhaler, mak-
ing it easy to transport. Inhaled insulin goes directly to the lungs,
which offer a large surface area for absorption. Mild to moderate
cough, decline in pulmonary function, and acute bronchospasm
are reported as side effects, as well as issues related to cost, con-
sistent delivery and need for pulmonary function compared with
oral agents. Inhaled insulin is contraindicated in patients with
chronic lung diseases, such as COPD.79,82,106,109,110  there is a higher mortality rate in patients with HHS compared
Complications of Diabetes Mellitus
Patients with diabetes mellitus, despite management, can
develop organ and organ-system damage linked to lesions in
small and large blood vessels. Complications can manifest at
variable rates after diagnosis and can be classified as (1) micro-
vascular, which causes retinopathy, nephropathy, and foot
ischemia; (2) macrovascular, which accelerates widespread ath-
erosclerosis; or (3) neuropathy.57,75,82,83 Another complication
of diabetes that is not directly linked to vascular damage is dia-
betic ketoacidosis (DKA).
Diabetic Ketoacidosis. Patients with type 1 diabetes have
the potential to develop this complication as a result of absolute
or relative insulin deficiency; it can progress from mild to mod-
erate glucose intolerance, to fasting hyperglycemia, to ketosis,
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.20 Patients with type 2 diabetes may also
Endocrine System     CHAPTER 10 265
develop DKA as well during acute onset of health conditions,
such as infection, trauma, congestive heart failure, and steroid
therapy.111
DKA is the end result of insulin deficiency, which lead to
elevated levels of ketone bodies in the tissues, a state referred
to as ketosis. Decreased insulin levels lead to uncontrolled
lipolysis (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 keto-
acidosis occurs.111 Ketoacidosis almost always results from
uncontrolled diabetes mellitus; however, it may also result
from alcohol abuse.6,20,76
The signs and symptoms of DKA include the following20,111
• Polyuria, polydipsia, dehydration
• Weakness and lethargy
• Muscle cramps, hypotonia
• Headache, difficulty paying attention, and confusion
• Anorexia
• Dyspnea, deep and sighing respirations (Kussmaul respira-
tions)
• Acetone-smelling (“fruity”) breath
• Tachycardia, orthostasis
• Hypothermia
• Stupor (coma), fixed, dilated pupils
• Uncoordinated movements
• Hyporeflexia
Management of DKA may include the following: insulin
phosphorus) replacement, and treatment of any underlying con-
tributing disorder, as well as supplemental oxygen and mechan-
ical ventilation, as needed.6,74,76,111 
Hyperosmolar Hyperglycemic State. Uncontrolled hyper-
glycemia can lead to this condition, which accounts for less than
1% of hospital admissions and is experienced by older indi-
viduals with type 1 or 2 diabetes. Although the hyperosmolar
hyperglycemic state (HHS) occurs less frequently than DKA,
with those with DKA. In addition to hyperglycemia, hyperos-
molality also occurs in the absence of ketosis. The most common
initial symptom is increased sugar in urine, and management
is aimed at controlling glucose levels with insulin, along with
hydration and electrolyte replacement. As HSS progresses, there
is risk of severe dehydration, seizures, and coma if it cannot be
managed adequately.112 
Skin Lesions. Skin lesions in patients with diabetes, particu-
larly on the feet, are common and multifactorial in nature. One
type of complication, diabetic dermopathy, will often look like
circular, scaly, light brown patches. It is most commonly seen on
the anterior aspect of the bilateral lower extremities.113 Addi-
tional skin complications include infections and ulcerations.
Lesions may result from any combination of the
following19,21,75,113:
• Loss of sensation from sensory neuropathy
• Skin atrophy from microangiopathy
• Decreased blood flow from macroangiopathy
266 CHAPTER 10     Endocrine System
• S ensory and autonomic neuropathy, resulting in abnormal
blood distribution that may cause bone demineralization and
Charcot’s joints (disruption of the midfoot)114
Proper foot care in individuals with diabetes helps prevent
complications, such as poor wound healing, which can progress
to tissue necrosis and ultimately lead to amputation.115 More
information regarding foot care for patients with diabetes can be
found at the American Diabetes Association website.116 Refer to
Chapter 12 for more details on diabetic ulcers.  • Strict glycemic control (primary method)
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 promote rapid prolifera-
tion of pathogens that enter the body; (4) decreased immune
response from reduced circulation, which leaves white blood
cells (WBCs) unable to get to the affected area; (5) impaired
WBC function, which leads to abnormal phagocytosis; and (6)
chemotaxis.19,74,117
Bacterial infections are most commonly caused by the Staph-
ylococcus species. Presentation includes boils, folliculitis, carbun-
cles, and infections around the nails. Fungal infections are also
commonly caused by Candida albicans in individuals with dia-
betes. These infections are often found in skin folds, including
under the breasts, around nails, and between fingers and toes.
Other areas of the body where it can be found are at the corners
of the mouth, axillae, and groin.113
 CLINICAL TIP
Skin checks are an especially important part of a physical thera-
pist’s screening process for those with diabetes because of the
increased likelihood of infections, particularly in less active or
bed-bound patients.
 
Diabetic Neuropathy. Of people with diabetes, 50% will
likely develop some form of neuropathy. Diabetic neuropathy
encompasses a diverse group of progressive syndromes affect-
ing many areas in the body.118,119 The exact link between neu-
ral dysfunction and diabetes is unknown; however, the vascular
and metabolic changes that occur with diabetes can promote
destruction of Schwann cells and therefore interfere with normal
nerve conduction.118,120
Neuropathies can be categorized as diffuse or focal. Diffuse
neuropathies include diabetic peripheral neuropathy and dia-
betic autonomic neuropathy. Diabetic peripheral neuropathy is
also known as sensorimotor polyneuropathy or distal symmet-
ric sensory neuropathy. Focal neuropathies are less common and
include mononeuropathy, radiculopathy, and cranial neuropa-
thy. Over time, patients may present with a mixture of these
various types of neuropathies.121
Sensory deficits present in a glove-and-stocking pattern, re-
sulting in either a loss of pinprick and light-touch sensations in
these areas or possibly “pins and needle” or “electrical” sensa-
tions.121 Foot ulcers and foot drop are also common manifesta-
tions of diabetic neuropathies.17,19,74-76,120
Patients with diabetic autonomic neuropathy may pres-
ent with difficulty controlling blood pressure, temperature,
sweating, and blood flow in the limbs. Additionally, patients
with cardiovascular autonomic neuropathy may have altered
exercise responses and decreased perception of ischemic heart
pain. Therefore vigilant monitoring of vital signs, including
electrocardiography (ECG), as appropriate, is necessary when
working with this patient population.19
Management of diabetic neuropathy may include the
following120,121:
• Tricyclic antidepressants, such as amitriptyline, nortripty-
line, imipramine, and desipramine
• Serotonin/norepinephrine reuptake inhibitors, such as dulox-
etine and venlafaxine
• Anticonvulsants, such as pregabalin, and gabapentin
• Topical agents, such as capsaicin cream or lidocaine ointment
• Opioids (use is controversial because of addiction potential);
agents currently used are tramadol and tapentadol
Additional complications from diabetes include coronary
artery disease, stroke, peripheral vascular disease, and nephropa-
thy. These are described in other chapters as listed next. 
Coronary Artery Disease. See Acute Coronary Syndrome in
Chapter 3 for a discussion of coronary artery disease. 
Stroke. See the Cerebrovascular Accident section in Chapter
6 for a discussion of stroke. 
Peripheral Vascular Disease. See the Atherosclerosis sec-
tion in Chapter 7 for a discussion of peripheral vascular disease. 
Nephropathy. See Chapter 9 for a discussion on nephropathy. 
Hypoglycemia. Hypoglycemia is a state of decreased BS
levels (<70 mg/dL serum glucose).122 Excess serum insulin
may result in decreased BS levels, which leads to symptoms of
hypoglycemia. Causes for this imbalance of insulin and sugar
levels can be grouped as fasting, postprandial, induced, or
spontaneous.31,57,122
Fasting hypoglycemia occurs before eating and can be caused
by insulin-producing beta-cell tumors (insulinomas), liver fail-
ure, chronic alcohol ingestion, GH deficiency, or extrapancre-
atic neoplasm, or it can be leucine induced. It can also occur in
infants whose mothers have diabetes.57
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.31
Hypoglycemia can also be induced by external causes, such as
exogenous insulin or oral hypoglycemic medications.6,31,122,123
Spontaneous hypoglycemia can occur in patients who are
hospitalized and is associated with the following risk factors;
malignancy, severe critical illness, renal failure, liver failure,
heart failure, and septic shock. Autonomic failure is a potential
related factor to developing spontaneous hypoglycemia.122
The signs and symptoms of hypoglycemia may
include6,31,122,123:
• Tachycardia and hypertension
• Tremor, irritability, pallor, and sweating
• Hunger
• Weight changes
• Headache
• Mental dullness, confusion, and amnesia
• Seizures

•  aralysis and paresthesias
P
• Dizziness
• Visual disturbance
• Loss of consciousness
Management of hypoglycemia may include the follow-
ing: glucose administration (fruit juice or glucose solutions);
strict monitoring of insulin and oral hypoglycemic adminis-
tration; dietary modifications; pharmacologic agents, such as
glucagon; surgery (e.g., subtotal pancreatectomy, insulinoma
resection); or a combination of these.31,122,124 The overall
goal of maintaining optimal glucose levels is the use of an
integrated patient-centered and hospital-centered approach,
utilizing available clinical guidelines, and reduction of
hypoglycemia.122  most cases and usually results from hyperplasia or an adenoma
Parathyroid Gland
Body Structure and 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.6,125  calcemia may then result in the following cascade of signs and
Parathyroid Tests
The primary measurements of parathyroid hormone are sum-
marized in Table 10.11. However, because PTH exerts its effects
on the intestines and kidneys, calcium metabolism can also be
evaluated by testing gastrointestinal and renal function. Refer
to Chapters 8 and 9, respectively, for a summary of diagnostic
tests for the gastrointestinal and renal systems.  • Hypertension, left ventricular hypertrophy
TABLE 10.11  Primary Tests Used to Evaluate
Parathyroid Hormone Function
Test Description
Serum calcium Measurement of blood calcium levels indirectly
examines PTH function. Normally, low cal-
cium levels stimulate PTH secretion, whereas
high calcium levels could be reflective of high
PTH levels.
Reference value for serum calcium is 9.0–
10.5 mg/dL in adults.
Calcium levels can also be measured in urine.
Reference value for urinary calcium is 50–
300 mg/dL.
Parathyroid PTH levels are measured in conjunction with
hormone serum calcium for patients with suspected
(PTH) parathyroid disease.
Reference value for serum levels is 10–65 pg/mL.
Data from Corbett JV, ed. Laboratory Tests and Diagnostic Procedures with Nursing
Diagnoses. 5th ed. Upper Saddle River, NJ: Prentice Hall Health; 2000:167-
176; Sacher RA, McPherson RA, Campos JM, eds. Widman’s Clinical Interpreta-
tion of Laboratory Tests. 11th ed. Philadelphia: FA Davis; 2000:803-804; Pagana
KD, Pagana TJ, Pagana TN. Mosby’s Diagnostic and Laboratory Test Reference. 13th
ed. St. Louis: Elsevier; 2017.
Endocrine System     CHAPTER 10 267
Parathyroid Disorders
Hyperparathyroidism
Hyperparathyroidism is a disorder caused by overactivity of one
or more of the parathyroid glands that leads to increased PTH
levels, resulting in increased blood calcium level (hypercalce-
mia), decreased bone mineralization, and decreased kidney func-
tion. This health condition is the third most common endocrine
disease and occurs more frequently in women than in men.126
Radiation therapy is also a risk factor for the development of
this disorder.127,128
Hyperparathyroidism can be classified as primary, second-
ary, or tertiary. Primary hyperparathyroidism represents the
in the parathyroid gland(s).126 Secondary hyperparathyroidism
results from another organ system disorder, such as renal fail-
ure, osteogenesis imperfecta, Paget’s disease, multiple myeloma,
lymphoma, or bone metastases from primary breast, lung, or
kidney tumors. Tertiary hyperparathyroidism occurs when
PTH secretion is autonomous despite normal or chronically
low serum calcium levels, particularly in patients undergoing
chronic hemodialysis.6,47,126,129
The primary clinical manifestations of hyperparathyroidism
are hypercalcemia and hypercalciuria (calcium in urine). Hyper-
symptoms47,126-129:
• Fatigue, weakness, bony pain
• Depression, memory loss, decreased concentration, sleep dis-
turbances
• Osteopenia, osteoporosis and increased fracture risk
• Polyuria, polydipsia, dehydration
• Kidney stone formation (nephrolithiasis)
Management of hyperparathyroidism may include the follo­
wing31,74,129:
• Minimally invasive surgery is the current standard for symp-
tomatic primary parathyroidism.126,128,130
• Addressing any underlying causes for secondary hyperpara-
thyroidism126
• Pharmacologic intervention for nonsurgical candidates (sum-
marized in Chapter 19, Table 19.42)
• Fluid replacement
• Dietary modification (a diet low in calcium and high in vita-
min D) 
Hypoparathyroidism
Hypoparathyroidism is a disorder caused by underactiv-
ity of one or more of the parathyroid glands that leads to
decreased PTH levels and thus to low serum calcium lev-
els. Decreased levels of PTH occur most commonly as a
result of damage to the parathyroid glands during thyroid
or parathyroid surgery (postoperative hypoparathyroidism).
Less common causes may include radiation-induced dam-
age, infiltration by metastatic cells, rare genetic disorders
in parathyroid glands, iron or copper overload, and autoim-
mune dysfunction.47,129,131,132
268 CHAPTER 10     Endocrine System
The signs and symptoms of hypoparathyroidism include the
following47,131-133:
• Osteomalacia in adults; rickets in children
• Increased neuromuscular irritability (tetany); painful muscle
spasms; muscle weakness
• Paresthesias
• Laryngospasm; bronchospasm
• Dysrhythmias, QRS and ST segment changes seen on elec-
trocardiogram
• Thin, patchy hair; brittle nails; dry, scaly skin
• Altered mental status; seizures
• Extrapyramidal disorders
• Visual impairment from cataracts
• Nephrolithiasis, renal insufficiency
Management of hypoparathyroidism may include the follo­
wing31,47,130,131,134:
• Pharmacologic intervention with the following:
• PTH replacement
• Vitamin D supplements: calcitriol or alfacalcidol; calcif-
erol
• Calcium carbonate, calcium citrate, calcium malate
• Magnesium sulfate
• Thiazide diuretics
• Parathyroid autotransplantation—indicated for patients who
demonstrate parathyroid dysfunction either during or from
thyroid procedures (The remaining parathyroid glands are
autotransplanted into the brachioradialis muscle to preserve
function. Other sites for autotransplantation include the
sternocleidomastoid muscle, pectoralis major, and subcuta-
neous tissue of the forearm.)135  ward head posture
Metabolic Bone Disorders
Osteoporosis
Osteoporosis is a multifactorial skeletal disorder that leads to
decreased bone density and organization, which ultimately
reduces bone strength.136
 CLINICAL TIP
Always consult with the physician to determine whether there
are any weight-bearing precautions or range-of-motion limita-
tions in place for patients with osteoporosis.
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 absorptiometry (DXA) measurement is currently the
gold standard for determining bone mineral density, which is
reported as T- and Z-scores. The Z-score for bone density is used
in premenopausal women, young men, and children. Accord-
ing to the WHO, the T-score is to be used in postmenopausal
white women.121,137 The use of biochemical markers in blood
and urine to help detect bone loss and possibly to predict risk of
fracture in patients have also been investigated.138 The Fracture
Risk Assessment (FRAX) tool, developed by the WHO, inte-
grates information on the 10-year fracture risk on the basis of
clinical risk factors and can be used to target individuals at high
risk for fracture.139,140
Osteoporosis can be classified as primary or secondary. Pri-
mary osteoporosis is the deterioration of bone mass not associ-
ated with other illnesses.121,137 It can occur in both genders at
all ages but often occurs after menopause in females and later in
life in males. Secondary osteoporosis is a result of medications
(e.g., glucocorticoids or anticonvulsants), alcoholism, other
chronic conditions (e.g., hypogonadism or hypoestrogenism), or
diseases (e.g., hyperthyroidism).136,140
There is no clear etiology for osteoporosis. However, many
risk factors have been elucidated. These risk factors include Cau-
casian, Asian, Hispanic, or Native American females; a petite
frame; inadequate dietary intake of calcium; positive family
history of osteoporosis; alcohol abuse; cigarette smoking; high
caffeine intake; sedentary lifestyle; depression; reduced bone
mineral content (most predictive factor); and early menopause
or oophorectomy (removal of ovary).130,136,140
The signs and symptoms of osteoporosis may include the
following121,130,137,140:
• Loss of height
• Back pain (aggravated by movement or weight bearing, re-
lieved by rest)
• Muscle spasm
• Low body weight
• Renal disease
• Vertebral deformity (kyphosis and anterior wedging); for-
• Presence of vertebral compression fractures, Colles’ fracture,
hip and pelvic fractures
• Pulmonary embolism and pneumonia, which are complica-
tions that can occur secondary to these fractures141
Management of osteoporosis may include the following136,142,143:
• Regular bone density screening
• Daily supplementation with calcium and vitamin D. For specific
recommendations, refer to the National Osteoporosis Founda-
tion.144
• Hormone replacement therapy with estrogen or with estro-
gen 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 therapy141
• Physical therapy for exercise prescription (A systematic re-
view on resistance exercises have been found to increase
physical function in older adults with osteoporosis and os-
teopenia.145 Weight bearing exercises should be prescribed
as appropriate for the individual patient. Whole body vibra-
tion or oscillating plate therapy is another modality under
investigation.140)

• A n abdominal corset can provide additional support for sta-
ble vertebral compression fracture(s). A rolling walker that
is adjusted higher than normal can promote a more upright
posture. Both of these techniques may also help decrease
back pain in patients with osteoporosis.
• Fracture management, if indicated (refer to Chapter 5).
 CLINICAL TIP
Although evidence supports resistive exercises, caution should
still be taken with resistive exercises and manual contacts dur-
ing therapeutic activities in patients with severe osteoporosis
to avoid risk of microtrauma or fracture of osteoporotic bones.
Excessive spinal flexion exercises should be avoided to decrease
loading on the spine.
Osteomalacia
Osteomalacia, or rickets in children, is a disorder characterized
by decreased bone mineralization, reduced calcium absorption
from the gut, and compensatory hyperparathyroidism. The
etiology of osteomalacia stems from any behavior or condi-
tion that lowers serum levels of phosphate, calcium, or vitamin
D.17,130,146 Osteoporosis is often a preexisting condition.121
The signs and symptoms of osteomalacia include the
following17,121,130,146:
• Bone pain and tenderness
• Softening of cranial vault (in children)
• Swelling of costochondral joints (in children)
• Predisposition to femoral neck fractures (in adults)
• Pathologic fractures
• Proximal myopathy later in disease course
• Waddling gait
Medical management of osteomalacia may include treating
the underlying or predisposing condition or supplementation
with calcium and vitamin D.17,146,147 Exercise is recommended
to address weakness or deficits in mobility.147  Considerations
Paget’s Disease
Paget’s disease, a bone disease of unknown etiology, usually
presents after the age of 55 years. It may affect one bone (mono-
stotic) or more than one bone (polyostotic); only 27% of indi-
viduals are symptomatic at diagnosis.119 The primary feature is
thick, spongy bone that is unorganized and brittle as a result of
excessive osteoclastic and subsequent osteoblastic activity. Some
evidence points to an inflammatory or viral origin. The axial
skeleton, including the pelvis and lumbar spine, and the femur
are involved in a majority of cases, with the tibia, ilium, skull,
and humerus being less involved.141,148 Fractures and compres-
sion of the cranial nerves (especially cranial nerve VIII) and spi-
nal cord are complications of Paget’s disease.130,148,149
Paget’s disease is generally asymptomatic; however, the fol-
lowing clinical manifestations may present119,130,148,149:
• Bone pain that is unrelieved by rest and persists at night
• Bone deformity (e.g., skull enlargement, bowing of leg and
thigh, increased density and width)
• Increased warmth of overlying skin of affected areas
Endocrine System     CHAPTER 10 269
• Headaches or hearing loss
• Chalk-stick fractures from softening of bone
• Kyphosis
Management of Paget’s disease primarily includes the use of bis-
phosphonates, including alendronate, etidronate, ibandronate,
pamidronate, risedronate, and zoledronic acid.148-150
Other interventions may include the following130,148,149:
• Calcitonin, when bisphosphonates are contraindicated
• Calcium supplementation (if necessary)
• Promotion of mobility
• Adequate hydration
• Symptomatic pain relief with NSAIDs and/or antineuro-
pathic drugs 
Physical Therapy Management
Clinical management of endocrine dysfunction has been dis-
cussed earlier in the sections on specific endocrine-gland and
metabolic disorders. The following are general physical ther-
apy goals and considerations for working with patients who
have endocrine or metabolic dysfunction. These considerations
should be adapted to a patient’s specific needs. Clinical tips have
been 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 (1) to optimize functional mobility; (2) to maximize activ-
ity tolerance and endurance; (3) to prevent skin breakdown
in the patient with altered sensation (e.g., diabetic neuropa-
thy); (4) to decrease pain (e.g., in patients with osteoporosis or
hyperparathyroidism); and (5) to maximize safety for preven-
tion of falls, especially in patients with altered sensation or
muscle function. 
Patients with diabetes or osteoporosis represent the primary
patient population for which the physical therapist intervenes.
Physical therapy considerations for these patients have been dis-
cussed in earlier sections, Diabetes Mellitus and Osteoporosis,
respectively.
For other patients with endocrine or metabolic dysfunction,
the primary physical therapy treatment considerations are the
following:
1. To improve activity tolerance, it may be necessary to decrease
exercise intensity when the patient’s medication regimen is
being adjusted. For example, a patient with insufficient thy-
roid hormone replacement will fatigue more quickly than
will a patient with adequate thyroid hormone replacement.
In this example, knowing the normal values of thyroid hor-
mone and reviewing the laboratory tests help the therapist
gauge the appropriate treatment intensity.
2. Consultation with a registered dietician to help determine
the appropriate activity level based on the patient’s caloric
intake because caloric intake and metabolic processes are af-
fected by endocrine and metabolic disorders.
270 CHAPTER 10     Endocrine System
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 PA R T
3 HEALTH CONDITIONS

11 Oncology
C H APT ER  

Julie Anna Snydera

CHAPTER OUTLINE CHAPTER OBJECTIVES

Introduction The objectives of this chapter are the following:
Terminology 1. An understanding of the medical assessment and diagnosis of a patient with cancer, including staging and
Nomenclature classification
Risk Factors 2. An understanding of the various medical and surgical methods of cancer management
Signs and Symptoms 3. An overview of the different body system cancers, including common sites of metastases
4. Examination, evaluation, and intervention considerations for the physical therapist
Diagnosis
Staging and Grading
Management
Surgery
Introduction
Radiation Therapy
Chemotherapy Cancer is a term that applies to a group of diseases characterized by the abnormal division and
Biotherapy growth of cells. The physical therapist requires a foundational understanding of underlying
Gene Therapy cancer disease processes, as well as the side effects, considerations, and precautions related to
Cancers in the Body Systems cancer care. This knowledge enhances clinical decision making to safely and effectively man-
Respiratory Cancers age the patient with cancer, and it also assists the physical therapist with the early detection of
Bone and Soft Tissue Cancers previously undiagnosed cancer. Please note that the field of oncology is vast; this chapter only
Breast Cancer highlights specific information pertinent to physical therapy management. 
Gastrointestinal and Genitouri-
nary Cancers Terminology
Hepatobiliary Cancers
Pancreatic Cancer
Several terms are used in oncology to describe cancer or cancer-related processes, which are out-
Hematologic Cancers
lined in Table 11.1. Neoplasms, or persistent abnormal dysplastic cell growth, are classified by
Head and Neck Cancers
Neurologic Cancers cell type, growth pattern, anatomic location, degree of dysplasia, tissue of origin, and the abil-
Skin Cancer ity to spread or remain in the original location. Two general classifications for neoplasms are
Physical Therapy Management benign tumors and malignant tumors. Benign tumors generally consist of differentiated cells that
reproduce at a higher rate than normal and are often encapsulated, allowing expansion, but do
Rehabilitation and Cancer-Related
Fatigue not spread to other tissues.1 Benign tumors are considered harmless unless their growth becomes
large enough to encroach on surrounding tissues and impair their function. Malignant neoplasms,
or malignant tumors, consist of undifferentiated cells, are unencapsulated, and grow uncontrol-
lably, invading normal tissues and causing destruction to surrounding tissues and organs. Malig-
nant neoplasms may spread, or metastasize, to distant sites of the body.1,2 Tumors may also be
classified as primary or secondary. Primary tumors are the original tumors in the original location.
Secondary tumors or cancers are metastases that have moved from the primary site to form new
tumors. Secondary tumors are of the same original type of cancer cells as the primary tumors.3,4 

aThe authors acknowledge Jaime C. Paz for prior contributions to this chapter.

        275
276 CHAPTER 11    Oncology

TABLE 11.1  Cancer Terminology

Term Definition
Neoplasm “New growth” pertaining to an abnormal mass of tissue that is excessive, persistent, and unregulated by physiologic stimuli.
Classified as benign or malignant.3
Tumor Common medical term for a neoplasm.
Cancer A term for diseases in which abnormal cells divide without control and can invade nearby tissues. Malignant tumors are
referred to as cancers.3
Dysplasia General term denoting variability of cell size, shape, and organization as viewed under a microscope. This situation may be
reversible or potentially progress to cancer.
Metaplasia Abnormal change of one mature cell type to another mature cell type, resulting from certain stimuli, such as cigarette smoking.
Hyperplasia An increased number of cells resulting in an enlarged tissue mass. It may be a mechanism to compensate for increased demands,
or it may be pathologic when there is a hormonal imbalance. Normal appearing, noncancerous cells that may develop into
malignant cells.3
Differentiation The extent to which a cell resembles the normal morphology and function of the original cell. A cell that is well differentiated
is physiologic and functions as intended. A poorly differentiated cell does not resemble a normal cell in both morphology
and function. Poorly differentiated cells also spread more quickly.3
Data from Stricker TP, Kumar V. Neoplasia. In: Kumar V, Abbas AK, Fausto N, et al., eds. Robbins Basic Pathology. 8th ed. Philadelphia: Saunders; 2007:174-175;
Gould B, Dyer R. Pathophysiology for the Health Professions. 4th ed. Philadelphia: Saunders; 2010:8; McGarvey CL, Vanhoose L, Calys M, Friaetta JA. Oncology. In: Good-
man CC, Fuller KS. Pathology: Implications for the Physical Therapist. 4th ed. Philadelphia: Elsevier; 2015:366; National Institute of Health. NCI dictionary of cancer
terms. National Cancer Institute website. https://www.cancer.gov/publications/dictionaries/cancer-terms/. Accessed October 23, 2018.

system(s) affected and are described later in the chapter in those

Nomenclature
Benign and malignant tumors are named by their cell of origin
(Table 11.2). 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 the
epithelium and sarcoma if they originate in mesenchymal tissue.2
Variations to this naming exist, such as melanoma and leukemia.  • Change in bowel or bladder habits or function
Risk Factors
There are numerous carcinogens (cancer-causing agents) and risk
factors that are thought to predispose a person to cancer. Most
cancers probably develop from a combination of genetic and
environmental factors. According to the World Cancer Research
Fund, a combination of preventable risk factors is responsible for
an estimated 20% of all cancers diagnosed in the United States.
These modifiable risk factors include excess body weight, physi-
cal inactivity, excess alcohol consumption, and poor nutrition.5
The use of tobacco, especially cigarette smoking, is also a widely
known preventable risk factor for cancer.5 Infectious agents, such
as the hepatitis B virus (HBV), human papillomavirus (HPV),
human immunodeficiency virus (HIV), and Helicobacter pylori (H.
pylori), have also been related to certain cancers, such as cervical
cancer (HPV).5 A complete overview of risk factors is beyond the
scope of this text. As specific cancers are described later in the
chapter, relevant etiologic agents or risk factors are stated.  represent significant clinical problems, and/or mimic metastatic
Signs and Symptoms
The signs and symptoms of cancer are most often caused by the
tumor’s growth and invasion of surrounding tissues. Specific
manifestations will depend on the particular cancer and body
respective sections. General signs and symptoms that may be
indicative of early or progressive cancer include1,6
• Unusual bleeding or discharge
• Unexplained weight loss of 10 pounds or more
• Fever
• Fatigue
• Headache that does not improve with treatment
• Development of a lump in the breast or other body location
• Pain
• Persistent cough or hoarseness without a known cause
• Skin, wart, or mole changes
• Hyperpigmentation (darker-looking skin)
• Jaundice (yellowish skin and eyes)
• Erythema (reddened skin)
• Pruritus (itching)
• Excessive hair growth
Paraneoplastic syndromes are rare disorders that are triggered
by an abnormal immune system response to the presence of a
tumor.7 These syndromes are defined by a collection of symp-
toms that occur remotely from the primary tumor. They are a
result of the substances produced by the tumor (e.g., abnormal
hormonal secretions). They cannot be related directly to the can-
cer’s growth and invasion of tissues.7 The documented frequency
of paraneoplastic syndromes ranges from 2% to 20% in those
diagnosed with cancer and often are the first sign of malignancy,
disease.7 The most common initial presentation of paraneoplas-
tic syndrome is fever. However, clinical presentation is often
similar to endocrinopathies (Cushing’s syndrome, hypercalce-
mia), nerve and muscle syndromes (myasthenia), dermatologic
disorders (dermatomyositis), vascular and hematologic disorders
(venous thrombosis, anemia), and various other disorders.2,7 
 Oncology     CHAPTER 11 277

TABLE 11.2  Classification of Benign and Malignant Tumors

Tissue of Origin Benign Malignant
Epithelial Tissue
Surface epithelium (skin) and mucous membrane Papilloma Squamous cell, basal cell, and
transitional cell carcinoma
Epithelial lining of glands or ducts Adenoma Adenocarcinoma
Pigmented cells (melanocytes of basal layer) Nevus (mole) Malignant melanoma
Connective Tissue and Muscle
Fibrous tissue Fibroma Fibrosarcoma
Adipose Lipoma Liposarcoma
Cartilage Chondroma Chondrosarcoma
Bone Osteoma Osteosarcoma
Blood vessels Hemangioma Hemangiosarcoma
Smooth muscle Leiomyoma Leiomyosarcoma
Striated muscle Rhabdomyoma Rhabdomyosarcoma
Nerve Tissue
Nerve cells Neuroma —
Glia — Glioma or neuroglioma
Ganglion cells Ganglioneuroma Neuroblastoma
Nerve sheaths Neurilemmoma Neurilemmal sarcoma
Meninges Meningioma Meningeal sarcoma
Retina — Retinoblastoma
Lymphoid Tissue
Lymph nodes — Lymphoma
Spleen — —
Intestinal lining — —
Hematopoietic Tissue
Bone marrow — Leukemias, myelodysplasia, and
myeloproliferative syndromes
Plasma cells — Multiple myeloma

From McGarvey CL, Vanhoose L, Calys M, Friaetta JA. Oncology. In: Goodman CC, Fuller KS. Pathology: Implications for the Physical Therapist. 4th ed. Philadelphia:
Elsevier; 2015:367.

used to scrape or brush tissue cells from the cervix to be

Diagnosis
After obtaining a medical history and performing a physical
examination, specific medical tests are employed to diagnose
cancer. These tests may include medical imaging (x-ray, posi-
tron emission tomography [PET] or computed tomography
[CT] scan, magnetic resonance imaging [MRI], ultrasound,
nuclear scans, etc.), endoscopic procedures, blood tests for
cancer markers, several types of biopsy, and cytology test-
ing. Biopsy, or the removal and examination of tissue, is
the definitive test for cancer identification. Table 11.3 lists
different types of biopsy. Cytology involves sampling flu-
ids from body cavities for tumor cells. Fluids sampled may
include urine, sputum, cerebrospinal fluid (CSF), pleural
fluid, pericardial fluid, and ascitic fluid.8 An example of
cytology testing includes the Papanicolaou test (“Pap test”)
in females. Termed scrape or brush cytology, an instrument is
tested for abnormal or cancer cells. Scrape cytology is also
used for identifying pathology in the esophagus, stomach,
bronchi, and oral cavity.8
Tumor markers are substances produced by cells in response
to cancer or some benign conditions.9 These substances are found
in body fluids and may be used to detect, diagnose, and manage
some types of cancer.9 Examples of some common tumor mark-
ers currently in use include BRCA1 and BRCA2 gene mutations
and prostate-specific antigen (PSA). BRCA1 and BRCA2 muta-
tions identify breast and ovarian cancers, and PSA identifies
prostate cancer. These markers indicate the potential presence
and recurrence of cancer and the potential benefits of certain
medications or treatment modalities for patients.9 There is no
one specific tumor marker used for cancer identification.9 More
substances are being discovered and used as tumor markers as
time passes. Therefore a complete list of tumor markers is well
beyond the scope of this text. 
278 CHAPTER 11    Oncology
TABLE 11.3  Types of Biopsy
Test Name Description of Procedure
Needle biopsy Removal of a small amount of fluid or tissue
(Fine needle by using a thin, hollow needle. May be im-
biopsy or fine age guided through ultrasound or computed
needle aspira- tomography (CT), depending on the location
tion) of the tumor.85
Core needle Removal of a cylinder of tissue with a large
biopsy needle. This biopsy is used with local anesthe-
(Core biopsy) sia, and it may be image guided depending on
tumor location. The “core” removed is typically
1
⁄16 inch in diameter to ½ inch in length.85
Excisional/ Surgical procedure to completely remove a
Incisional tumor (excisional biopsy) or the removal of
biopsy a smaller portion of a large tumor (incisional
biopsy).85
Endoscopic An endoscope is used to remove tissue samples
biopsy from the esophagus, nose, sinuses, and throat.
A bronchoscope looks at the lungs and the
bronchi, and a colonoscope is used for visual-
izing the colon and the rectum.85
A laparoscope is used to access the abdomen
with a small incision.79 Laparoscopes are also
used in the chest, and these procedures are
referred to as thoracoscopy and mediastinoscopy.85
Laparotomy Laparotomy—A surgical procedure with gen-
open proce- eral anesthesia where the abdomen is incised
dures and a surgeon is able to visualize and biopsy
tissues. Termed thoracotomy if completed in
the chest.85
Skin biopsy Shave biopsy—removal of the superficial layers
of skin for tissue sample. Punch biopsy (ex-
cisional biopsy)—removal of deep skin layers
for tissue samples.85
Sentinel lymph A surgical procedure where the specific lymph
node biopsy nodes that drain fluid from a targeted tumor
(SLNB) are identified and removed through an exci-
sional biopsy.85
Staging and Grading
After the diagnosis of cancer is established, staging is performed
to describe the location and size of the primary site of the
tumor, the extent of lymph node involvement, and the presence
or absence of metastasis. Staging helps determine treatment
options, predict life expectancy, and determine the prognosis for
complete resolution.
The most commonly used method to stage cancer is the
TNM system. Tumors are classified according to the American
Joint Committee on Cancer (AJCC) system, which is based on
the extent (size and/or number) of the primary tumor (T), lymph
node involvement (N), and the presence or absence of metastasis
(M) (Table 11.4).2,10 Certain types of cancers will have specific
staging criteria, and these are identified later in this chapter for
the various cancers.
TABLE 11.4  TNM System
Stage Parameters
T: Primary tumor TX: Primary tumor cannot be 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 lymph NX: Nodes cannot be assessed.
node involvement N0: No metastasis to local lymph nodes.
N1, N2, N3: Progressive involvement of
local lymph nodes.
M: Distant metastasis MX: Presence of distant metastasis
cannot be assessed.
M0: No distant metastasis.
M1: Presence of distant metastasis.
From Stricker TP, Kumar V. Neoplasia. In: Kumar V, Abbas AK, Faus-
to N, et al., eds. Robbins Basic Pathology. 8th ed. Philadelphia: Saunders;
2007:174-223; Cancer staging. American Cancer Society website. https://
www.cancer.org/treatment/understanding-your-diagnosis/staging.html?_
ga=2.10900148.1694555549.1537880130-1514946149.1524067701. Up-
dated March 25, 2015. Accessed September 25, 2018.
TABLE 11.5  Grading of Neoplasms
Grade Description
GX Undetermined-grade, cannot be assessed
G1 Low-grade, well-differentiated tumor
G2 Intermediate-grade, moderately differentiated tumor
G3 High-grade, poorly differentiated tumor
G4 High-grade, undifferentiated tumor
From National Cancer Institute website. cancer.gov/cancertopics/factsheet/de-
tection/tumor-grade. Accessed June 27, 2012; American Joint Committee on
Cancer. AJCC Cancer Staging Manual. 6th ed. New York: Springer; 2002.
Grading reports the degree of dysplasia, or differentia-
tion, from the original cell type. Cells that are more highly
differentiated resemble the original cells more strongly and
this is associated with a lower grade and a less aggressive
tumor. A higher grade is linked to aggressive, fatal tumors
(Table 11.5). 
Management
The focus of cancer treatment is on quality of life. Four major
treatment options include:
• Surgical removal of the tumor
• Radiation therapy
• Chemotherapy
• Biotherapy (including immunotherapy, hormonal therapy,
stem cell transplantation, and monoclonal antibodies)
Additional treatments may include physical therapy, nutri-
tional support, acupuncture, chiropractic treatment, alternative
medicine, and hospice care. Treatment protocols differ from
physician to physician and from cancer to cancer. Standard

treatment includes some combination of surgery, radiation, and/
or chemotherapy.
Surgery
Surgical intervention is determined by the size, location, and
type of cancer, as well as the patient’s age, general health, and
functional status. Successful localization and resection of recur-
rent and/or metastatic lesions found on positive PET scans may
be optimized with the intraoperative use of a hand-held PET
probe.11 The following are indications for invasive surgical
management12:
• Removal of precancerous lesions or of organs at high risk for
cancer
• Establishing a diagnosis by biopsy and subsequent histo-
pathologic analysis
• Assisting in staging by sampling lymph nodes
• Definitive treatment by removing the primary tumor
• Reconstruction of a limb or organ with or without skin graft-
ing
• Palliative care, such as decompressive or bypass procedures
Specific surgical procedures relevant to musculoskeletal and
neurologic cancers are discussed in Chapters 5 and 6, respec-
tively. Additional surgical procedures for specific cancers are
covered later in the chapter.
 CLINICAL TIP
Range of motion (ROM) and muscle contraction in newly recon-
structed limbs or regions should be tailored according to physi-
cian’s orders to help facilitate surgical healing.
 
Radiation Therapy
The primary objective in administering radiation therapy13,14
is to eradicate tumor cells, either benign or malignant, while
minimizing damage to healthy tissue. This objective can further
be divided into six different indications based on disease presen-
tation and the practitioner’s intentions:
1. Definitive treatment with the intent to cure
2. Neoadjuvant treatment to improve the chances of successful
surgical resection
3. 
Adjuvant treatment to improve local control of cancer
growth after chemotherapy or surgery
4. Prophylactic treatment to prevent growth of cancer in as-
ymptomatic, yet areas at high risk for metastasis
5. Control to limit growth of existing cancer cells
6. Palliation to relieve pain, prevent fracture, and enhance mo-
bility when cure is not possible
Before a patient receives radiation therapy, a simulation
procedure is performed to circumscribe the tumor and adja-
cent tissues and organs to prepare for delivery of ionizing
radiation. Simulation can be performed with CT, virtual
simulation software, or MRI. Further mapping is then per-
formed to synchronize the radiation energy with the patient’s
respiratory cycle, and PET is also used to specifically map
the tumor.15
Oncology     CHAPTER 11 279
 CLINICAL TIP
A patient will need sufficient active and passive ROM to undergo
a simulation procedure. For example, a patient undergoing ra-
diation therapy after lumpectomy or mastectomy will require
sufficient bilateral shoulder flexion and abduction to allow the
hands to be clasped behind the neck or the arms to rest on a ta-
ble in end-range passive flexion and abduction while the patient
is supine. This allows markings to be placed for radiation treat-
ment and will likely also be the position a patient must assume
for radiation treatment sessions. An exercise program emphasiz-
ing active and passive shoulder stretching would be indicated in
this case to facilitate comfort and allow radiation treatments to
proceed.
Radiation therapy is delivered by two different modalities.
The most common clinical approach is external beam radiation
therapy (EBRT). External beam radiation is delivered from out-
side a patient’s body by aiming high-energy rays into the tumor
location. The second method is known as internal radiation,
or brachytherapy. Internal radiation is accomplished through
the placement of radioactive sources sealed in seeds or cathe-
ters directly into the tumor site. This type of treatment has a
shorter-range effect than EBRT.16
Technologic advances have allowed EBRT to be further
divided into different modalities that allow better localiza-
tion of tumor margins along with gradation of radiation dose.
Both of which can minimize damage to surrounding tissues
and maximize the therapeutic effect. These different forms
of EBRT include three-dimensional conformal radiotherapy
(3DCRT), intensity-modulated radiation therapy (IMRT),
image-guided radiotherapy (IGRT), stereotactic body radiation
therapy (SBRT), radiosurgery, and image-guided CyberKnife
radiosurgery.13,15,16
Brachytherapy involves the placement (temporary or perma-
nent) of selected radioactive sources directly into a body cav-
ity (intracavitary), into tissue (interstitial), into passageways
(intraluminal), or onto tissue surfaces (plaque).15 The following
malignancies can be treated with brachytherapy: gynecologic,
breast, lung, esophageal, head and neck, brain, and prostate
tumors, as well as certain types of melanoma. Brachytherapy can
be used alone or in combination with EBRT.
3DCRT is based on CT imaging and has essentially replaced
two-dimensional (2D) radiation therapy which was based on
x-ray imaging.16 IMRT allows clinicians to deliver irregular-
shaped radiation doses which adhere to tumor margins. This
helps avoid critical organs and body structures during radiation
treatments.16 IGRT involves daily medical imaging before each
radiation treatment, and both IGRT and IMRT are now used
for the treatment of head and neck cancers and prostate cancers.
IMRT also is used with gynecologic cancers.16
These advancements in technology enabled the develop-
ment of SBRT. SBRT accurately delivers very high individual
radiation doses over fewer treatment sessions to ablate small,
well-defined tumors anywhere in a patient’s body.16 SBRT is
280 CHAPTER 11    Oncology
used to treat prostate, head and neck, hepatic, and renal cancers;
oligometastases; and spinal and pancreatic cancers, as well as
early-stage non–small cell lung cancer (NSCLC) in nonsurgical
candidates.16
Intraoperative radiation therapy (IORT) consists of deliv-
ering a single, large fraction of radiation to an exposed tumor
or to a resected tumor bed during a surgical procedure. IORT
is generally used in the management of gastrointestinal (GI),
genitourinary, gynecologic, and breast cancers.13 Advances in
radiation therapy include use of high-intensity magnetic res-
onance–guided focused ultrasound (MRgFUS) and selective
internal radiation therapy (SIRT).15
 CLINICAL TIP
A patient may be prescribed antiemetics (see Chapter 19, Table
19.24) after radiation treatment to control nausea and vomit-
ing. Notify the physician if antiemetic therapy is insufficient to
control the patient’s nausea or vomiting during physical therapy
sessions.
General side effects that commonly occur with radiation
therapy include skin reactions, fatigue, and myelosuppression
(bone marrow suppression). Numerous site-specific toxicities
may include limb edema, alopecia, cerebral edema, esophagitis,
visual disturbances, pneumonitis, fibrosis, esophagitis, nausea,
vomiting, diarrhea, cystitis, and cardiomyopathy. These side
effects may occur immediately after radiation therapy and/or
reappear at a later time. In addition, radiation-induced malig-
nancies, including breast cancer, leukemia, and sarcoma, may
occur.17
A progressive condition called radiation fibrosis syndrome
(RFS) may also develop years after radiation treatment. The
neuromuscular and musculoskeletal complications of RFS are
caused by the direct and indirect effects of progressive fibro-
sis on the nerves, muscles, tendons, ligaments, skin, bones, and
lymphatic system.16 RFS may cause muscle weakness and dys-
function, as well as nerve dysfunction. Clinical symptoms may
include pain, sensory loss, fatigue, and weakness.16
 CLINICAL TIP
Radiation may lead to decreased skin distensibility and result in
decreased ROM. Special care should be taken with the skin and
other tissues in the radiated area because of the fragility of the
tissues. Promotion of active or passive ROM may help prevent
contracture.
 
Chemotherapy
The overall purpose of chemotherapy is to inhibit the various
signaling pathways that control cancer cell proliferation, inva-
sion, metastasis, angiogenesis, and cell death. Chemotherapy
agents can potentially provide a cure or manage metastatic
disease and reduce the size of the tumor for surgical resection
or palliative care.18 Chemotherapy can be implemented preop-
eratively, postoperatively, or both preoperatively and postop-
eratively. Chemotherapy is usually delivered systemically, via
intravenous or central lines, but may be directly injected into
or near a tumor. Refer to Chapter 18, Table 18.7 for informa-
tion regarding tunneled central venous catheters often used for
chemotherapy. Patients may receive single or multiple rounds
of chemotherapy over time to treat their cancers and to possibly
minimize side effects. Side effects of chemotherapy include nau-
sea, vomiting, “cancer pain,” hair loss, and the loss of other fast-
growing cells, including platelets, red blood cells (RBCs), and
white blood cells (WBCs). A variety of chemotherapy agents
have different mechanisms of action and are described in Chap-
ter 19, Table 19.25.
Physical Therapy Considerations
• Patients receiving chemotherapy can become neutropenic
and are at risk for infections and sepsis.19 (A neutrophil is
a type of leukocyte or WBC that is often the first immu-
nologic cell at the site of infection; neutropenia is an ab-
normally low neutrophil count. Absolute neutrophil count
[ANC] will determine whether or not a patient is neutrope-
nic and any necessary precautions to be taken subsequently.)
Chemotherapy-induced neutropenia typically occurs 3 to 7
days after administration of chemotherapy. The areas with
the highest rate of infection include the GI tract, sinuses,
lungs, and skin.20 It is important for all clinicians to practice
good hand hygiene techniques, specifically with antimicro-
bial products. There is no noted evidence that rehabilitation
interventions are contraindicated due to neutropenia. How-
ever, modifications may be needed for patients who have
increased fatigue, malaise, dizziness, or lethargy.20 Inter-
ventions completed in public therapy spaces or public areas
where potential pathogen exposure is increased should also
be reduced or avoided, when possible.20 Patients undergo-
ing chemotherapy may be on facility-specific “neutropenic
precautions,” “protective precautions,” or “reverse isolation
precautions.” Follow the institution’s guidelines for isolation
precautions when treating these patients to help reduce the
risk of infection. Examples of these guidelines can be found
in the Stem Cell Transplantation section in Chapter 14.
• Nausea and vomiting after chemotherapy varies 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 physi-
cal therapy, whereas others allow patients to tolerate activity.
• Patients may be taking antiemetics, which help control nau-
sea and vomiting after chemotherapy. The physical therapist
should alert the physician when nausea and vomiting limits
the patient’s ability to participate in physical therapy so that
the antiemetic regimen can be modified or enhanced. Anti-
emetics are listed in Chapter 19, Table 19.24.
• Chemotherapy agents affect the patient’s appetite and
ability to consume and absorb nutrients. This decline in
nutritional status can inhibit the patient’s progression in
strength and conditioning programs. Proper nutritional
support should be provided and directed by a nutrition-
ist. Consulting with a nutritionist may be beneficial when
planning the appropriate activity level based on a patient’s
caloric intake.

• A nemia is known to reduce exercise tolerance and endur-
ance. Symptoms of anemia include fatigue, dizziness, and
hemodynamic instability.20 In the acute care setting, moder-
ate- and high-intensity aerobic exercises should be avoided
in patients with severe anemia. Conversely, low-intensity
exercise is thought to be beneficial in promoting improve-
ments in blood counts.20 Low-intensity exercise also may
also have a protective effect against anthracycline-induced
cardiotoxicity.20 Platelet, RBC, and WBC counts should
be monitored closely in patients undergoing chemotherapy
treatment. Patients should be monitored for reports of chest
pain, lightheadedness, and inappropriate dyspnea. Those
with thrombocytopenia (<20,000 cells/μL) generally should
be restricted to walking and performance of activities of daily
living (ADLs).20 The Stem Cell Transplantation section in
Chapter 14 suggests appropriate therapeutic activities in
the presence of altered blood cell counts. Consult with the
medical team or facility policies and procedures for specific
guidelines on activity with low or abnormal blood counts, as
appropriate.
• Vital signs should always be monitored, especially when pa-
tients are taking the more toxic chemotherapy agents that
affect the heart, lungs, and central nervous system (CNS).20
• Chemotherapy-induced peripheral neuropathy (CIPN) is
a well-known complication of taxane- and platinum-based
chemotherapeutic agents.20 This neuropathy typically pres-
ents in a “stocking/glove pattern.” When severe, motor
nerves can be affected, typically the lower extremity motor
nerves.20 CIPN symptoms tend to subside after chemother-
apy treatment is completed. There is evidence that patients
treated with neurotoxic agents have a significantly increased
fall risk. Patients with a history of neurotoxic chemotherapy
have a fall risk two to three times greater than that in the
general population.20
• Patients should be aware of the possible side effects of che-
motherapy and understand the need for modification or delay
of rehabilitation efforts. Patients should be given emotional
support and encouragement when they are unable to achieve
their initial goals. Intervention may be coordinated around
the patient’s medication schedule.  to smoking.5 Symptoms associated with lung cancer include
Biotherapy
Biologic therapy is also referred to as immunotherapy, biological
response modifier therapy, and BRM therapy.21 Biotherapy involves
the use of living organisms or materials derived from sub-
stances produced naturally or synthetically by living organisms
to treat cancer or disease.21,22 Some biotherapy methods use a
patient’s native host defense system (the immune system) as a
mechanism to treat cancer as well as other diseases. This form
of therapy can be highly targeted while minimizing toxicity.
Agents currently used for biotherapy include cytokines, mono-
clonal antibodies, vaccines, and bacteria; genes therapy; and
targeted therapy.16,17,23 Table 19.25 in Chapter 19 provides a
list of monoclonal antibodies used for cancer management, as
well as their side effects and physical therapy considerations.
Vaccines are currently used to prevent viral infections that have
been shown to lead to cancer. HPV infection has been linked to
Oncology     CHAPTER 11 281
cervical cancer, and hepatitis B can lead to liver cancer. Vaccina-
tion is available for both HPV and HBV.24 
Gene Therapy
The potential exists for treating many genetic disorders, auto-
immune disorders, cancer, and infectious diseases by geneti-
cally modifying cells that may have defective genetic material.
A common therapeutic approach is performed by introducing
healthy genes into a patient’s cell nuclei to enhance, repair,
or replace altered genetic material.25 The carriers most often
used to insert genetic material (RNA and DNA) into cells are
viruses. Liposomes and nanoparticles are also being used and
studied for future use.22 Treatment approaches differ for gene
therapy because some methods are aimed directly at cancer cells
whereas other methods target healthy cells to better enable
them to fight the cancer cells.20 Gene therapy continues to be
experimental but is being studied in clinical trials for cancer
treatment.22 Somatic gene therapy is approved in the United
States and involves somatic, nonreproductive cells of the body,
including skin, muscle, bone, and liver.25 
Cancers in the Body Systems
Cancers can invade or affect any organ or tissue in the body. The
following is an overview of various cancers in each body system.
Respiratory Cancers
Cancer can affect any structure of the respiratory system, in-
cluding the larynx, lungs, and bronchus. There are two major
categories of lung cancer—NSCLC and small cell lung cancer
(SCLC). Lung carcinoid or lung neuroendocrine tumors make
up the third category of lung cancer, and account for only 5%
of all lung cancers. These tumors are very slow growing and
typically do not spread.26 Approximately 85% of lung cancers
are NSCLCs, which are further divided into three subtypes:
squamous cell carcinoma, adenocarcinoma, and large cell carci-
noma.26-28 The risk of developing lung cancer is 13 to 23 times
higher, respectively, in female and male smokers compared with
nonsmokers. Eighty percent of lung cancer deaths are related
chronic cough, dyspnea, hoarseness, chest pain, and hemoptysis.
Additional symptoms may also include weakness, weight loss,
anorexia, and, in rare cases, fever.5,6 Common sites of metas-
tases of lung cancer include the adrenal glands, liver, bone,
intraabdominal lymph nodes, brain and spinal cord, and skin
(20%).28,29
Bronchoscopy, biopsy, and imaging techniques, such as radi-
ography, CT, and PET, can be used to stage lung cancer.28-30 In
addition to the TNM staging, NSCLC is further staged to help
guide interventions and prognosis. Table 11.6 outlines the spe-
cific TNM components, and Table 11.7 illustrates the staging
components (Ia to IV).
SCLC is defined as either limited-stage or extensive-stage
disease, according to the Veterans Administration Lung Study
Group. Limited-stage disease is defined as stages I through III
(T any, N any, M0) tumors that can be safely managed with
definitive radiation therapy.31
 TABLE 11.6  Staging of Non–Small-Cell Lung Cancer
Descriptors Definitions
T Primary Tumor
T0 No primary tumor
T1 Tumor ≤3 cm in the greatest dimension, surrounded by lung or visceral pleura, not more proximal than the lobar bronchus
T1a Tumor ≤2 cm in the greatest dimension
T1b Tumor >2 but ≤3 cm in the greatest dimension
T2 Tumor >3 but ≤7 cm in the greatest dimension or tumor with any of the followinga:
Invades visceral pleura
Involves main bronchus ≥2 cm distal to the carinab
Atelectasis/obstructive pneumonia extending to hilum but not involving the entire lung
T2a Tumor >3 but ≤5 cm in the greatest dimension
T2b Tumor >5 but ≤7 cm in the greatest dimension
T3 Tumor >7 cm; or directly invading chest wall, diaphragm, phrenic nerve, mediastinal pleura, or parietal pericardium; or
tumor in the main bronchus <2 cm distal to the carinab; or atelectasis/obstructive pneumonitis of entire lung; or separate
tumor nodules in the same lobe
T4 Tumor of any size with invasion of heart, great vessels, trachea, recurrent laryngeal nerve, esophagus, vertebral body, or
carina; or separate tumor nodules in a different ipsilateral lobe

N Regional Lymph Nodes

N0 No regional node metastasis
N1 Metastasis in ipsilateral peribronchial and/or perihilar lymph nodes and intrapulmonary nodes, including involvement by
direct extension
N2 Metastasis in ipsilateral mediastinal and/or subcarinal lymph nodes
N3 Metastasis in contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular lymph
nodes

M Distant Metastasis
M0 No distant metastasis
M1a Separate tumor nodules in a contralateral lobe; or tumor with pleural nodules or malignant pleural disseminationc
M1b Distant metastasis
Special Situations
TX, NX, MX T, N, or M status not able to be assessed
Tis Focus of in situ cancer
T1b Superficial spreading tumor of any size but confined to the wall of the trachea or mainstem bronchus
aTwo tumors with these features are classified as T2a if ≤5 cm.
bThe uncommon superficial spreading tumor in central airways is classified as T1.
cPleural effusions are excluded that are cytologically negative, nonbloody, transudative, and clinically judged not to be caused by cancer.

From Detterbeck FC, Boffa DJ, Tanoue LT. The new lung cancer staging system. Chest. 2009;136(1):260.

TABLE 11.7  Staging Components of Non–Small-Cell Lung Cancer

T/M Subgroup N0 N1 N2 N3
T1 T1a Ia IIa IIIa IIIb
T1b Ia IIa IIIa IIIb
T2 T2a Ib IIa IIIa IIIb
T2b IIa IIb IIIa IIIb
T3 T3 > 7 IIb IIIa IIIa IIIb
T3lev IIb IIIa IIIa IIIb
T3Satell IIb IIIa IIIa IIIb
T4 T4lev IIIa IIIa IIIb IIIb
T4Ipsi Nod IIIa IIIa IIIb IIIb
M1 M1aContra Nod IV IV IV IV
M1aPl Disem IV IV IV IV
M1b IV IV IV IV

From Detterbeck FC, Boffa DJ, Tanoue LT. The new lung cancer staging system. Chest. 2009;136(1):260.
 Oncology     CHAPTER 11 283

Surgery is the treatment of choice for stage I and II NSCLC,

TABLE 11.8  Malignant Tumors in Bone and Soft Tissue
with lobectomy considered the gold standard for definitive
surgery. Wedge resection, sleeve resection, segmentectomy, Sarcoma Subtype Involved Tissue or Cells
or pneumonectomy can also be performed in patients with Angiosarcoma Blood vessels
NSCLC.5 Early-stage NSCLC, typically located near the periph- Hemangiosarcoma
ery of the lung, is now also treated with video-assisted thoracic Hemangioendothelioma
surgery (VATS). This procedure allows for a smaller incision site Kaposi’s sarcoma Lymph vessels
than with a traditional thoracotomy.32 Lymphangiosarcoma
Surgical intervention for SCLC is not standard practice.31,33 Lymphosarcoma
Chemotherapy or a combination of chemotherapy and radiation Chondrosarcoma Cartilage
therapy administered at the same time, known as “concurrent Endochondroma
Chondroblastoma
chemoradiation,” is the standard treatment for SCLC.5,34 Osteochondroma
Osteosarcoma (osteogenic sarcoma) Bone
 CLINICAL TIP
Leukemia Bone marrow
Thoracic surgery generally results in a very painful incision. Multiple myeloma
Surgical incisions into the pleural space will cause deflation of Ewing sarcoma
the lung. Deep-breathing exercises (along with airway clearance Hodgkin’s lymphoma of bone
techniques with incisional splinting and ROM exercises of the Liposarcoma Adipose tissue
upper extremity on the side of the incision) are important to Fibrosarcoma Fibrous tissue
prevent postoperative pulmonary complications and restore Malignant fibrous histiocytoma
shoulder and trunk mobility. Note that patients may have chest (MFH)
tubes in place immediately after surgery (see Chapter 18). Ox- Neurofibrosarcoma Neural/peripheral nerves
ygen supplementation may be required in patients who have Neurogenic sarcoma
undergone thoracic surgery. Oxyhemoglobin saturation (SaO2) Glioma
should be monitored to ensure adequate oxygenation, especial- Rhabdomyosarcoma Skeletal muscle
ly when increasing activity levels. Leiomyosarcoma Smooth muscle
 
Synovial sarcomas Synovial tissue

Bone and Soft Tissue Cancers
Tumors of bone are most commonly discovered after an injury or
fracture or during a medical evaluation for pain. A majority of
tumors in bone arise from other primary sites. Common primary
tumors that metastasize to bone include breast, lung, prostate,
kidney, and thyroid tumors.35
 CLINICAL TIP
Patients commonly experience fractures as a result of metastatic
disease in the vertebrae, proximal humerus, and femur.36 The
literature reflects the effectiveness of rehabilitation in preserv-
ing function, promoting safety, and preventing additional frac-
tures in patients with bony metastases.20 Interventions should
include falls risk assessment and strategies for safety during
ADLs to prevent further trauma in the patient with bony me-
tastases. A patient with bony metastases must also receive clear-
ance from the physician or the medical team before initiating
mobility, along with clarification of the patient’s weight-bearing
status. This also applies to patients who have undergone surgical
interventions. Assistive devices may be prescribed based on the
patient’s weight-bearing and functional status.
Nonspecific pain, nighttime pain, a palpable mass (fixed
or mobile), possible bony tenderness, and increasing altera-
tions in mobility are the main clinical manifestations of pri-
mary or secondary bone cancer as well as soft tissue cancers.37
Soft tissue cancers can be found in tissues that surround,
connect, or support body organs and structures. Types of
Adapted from Table 26-1 in Helgeson K. Musculoskeletal neoplasms. In: Good-
man CC, Fuller KS. Pathology: Implications for the Physical Therapist. 4th ed. St.
Louis: Elsevier; 2015:1253.
primary bone and soft tissue cancers, both of which occur
less frequently,35 are described in Table 11.8. Treatment of
bone and soft tissue cancers can include radiation, chemo-
therapy, amputation, and surgery on involved limbs.35 Risk
factors for both bone and soft tissue cancers include prior
radiation and certain inherited conditions.5 Although not
all metastases to bone cause pathologic fractures, surgical
intervention can be used for a patient with a bone metasta-
sis because of the risk of pathologic fracture. These proce-
dures may include the use of intramedullary rods, plates,
and prosthetic devices (e.g., total joint arthroplasty) and are
described in Chapter 5. 
Breast Cancer
Breast cancer, although more prevalent in women, is also diag-
nosed in men, but to a lesser extent. The risk for developing
breast cancer in women is related to increasing age, family his-
tory, and carrying either of the two breast cancer genes BRCA1
and BRCA2.38 The U.S. Preventive Services Task Force (USP-
STF) recommends “biennial screening with mammography”
for women. Women who are at average risk for breast cancer
benefit the most from biennial screening from age 50 to 74
years; women aged 60 to 69 years are the most likely to prevent
breast cancer death through mammography screening.39 For
women ages 40 to 49 years, the USPSTF states that biennial
284 CHAPTER 11    Oncology

TABLE 11.9  Stages of Breast Cancer

Stage TNM Description
Stage 0 Tis, N0, M0 Ductal carcinoma in situ (DCIS).
Stage IA T1, N0, M0 Tumor is 2 cm or less and has not spread to lymph nodes or distant sites.
Stage IB T0 or T1, Tumor is 2 cm or less across (or is not found) with micrometastases in 1–3 axillary lymph nodes and no dis-
N1mi, M0 tant metastases.
Stage IIA T0 or T1, N1 The tumor is 2 cm or less across (or is not found) and either:
(two (but not • It has spread to 1–3 axillary lymph nodes, with the cancer in the lymph nodes larger than 2 mm across
possible N1mi), M0 (N1a), OR.
situations) • Tiny amounts of cancer are found in internal mammary lymph nodes on sentinel lymph node biopsy (N1b),
OR.
• It has spread to 1–3 lymph nodes under the arm and to internal mammary lymph nodes (found on sentinel
lymph node biopsy) (N1c).
T2, N0, M0 The tumor is larger than 2 cm across and less than 5 cm (T2) but has not spread to the lymph nodes (N0) or
to distant sites (M0).
Stage IIB T2, N1, M0 The tumor is larger than 2 cm and less than 5 cm across (T2). It has spread to 1–3 axillary lymph nodes and/
(two or tiny amounts of cancer are found in internal mammary lymph nodes on sentinel lymph node biopsy (N1).
possible The cancer has not spread to distant sites (M0).
situations) T3, N0, M0 The tumor is larger than 5 cm across but does not grow into the chest wall or skin and has not spread to
lymph nodes (T3, N0) or to distant sites (M0).
Stage IIIA T0 to T2, N2, The tumor is not more than 5 cm across (or cannot be found) (T0 to T2). It has spread to 4–9 axillary lymph
(two M0 nodes, or it has enlarged the internal mammary lymph nodes (N2). The cancer has not spread to distant
possible sites (M0).
situations) T3, N1 or N2, The tumor is larger than 5 cm across but does not grow into the chest wall or skin (T3). It has spread to 1–9
M0 axillary nodes, or to internal mammary nodes (N1 or N2). The cancer has not spread to distant sites (M0).
Stage IIIB T4, N0 to N2, The tumor has grown into the chest wall or skin (T4), and one of the following applies:
M0 • It has not spread to the lymph nodes (N0).
• It has spread to 1–3 axillary lymph nodes and/or tiny amounts of cancer are found in internal mammary
lymph nodes on sentinel lymph node biopsy (N1).
• It has spread to 4–9 axillary lymph nodes, or it has enlarged the internal mammary lymph nodes (N2).The
cancer has not spread to distant sites (M0).
Stage IIIC Any T, N3, The tumor is any size (or cannot be found), and one of the following applies:
M0 • Cancer has spread to 10 or more axillary lymph nodes (N3).
• Cancer has spread to the lymph nodes under the clavicle (collar bone) (N3).
• Cancer has spread to the lymph nodes above the clavicle (N3).
• Cancer involves axillary lymph nodes and has enlarged the internal mammary lymph nodes (N3).
• Cancer has spread to 4 or more axillary lymph nodes, and tiny amounts of cancer are found in internal mam-
mary lymph nodes on sentinel lymph node biopsy (N3).The cancer has not spread to distant sites (M0).
Stage IV Any T, any N, The cancer can be any size (any T) and may or may not have spread to nearby lymph nodes (any N). It has
M1 spread to distant organs or to lymph nodes far from the breast (M1). The most common sites of spread are
the bone, liver, brain, or lung.

From American Joint Committee on Cancer TNM system, American Cancer Society website. http://www.cancer.org/Cancer/BreastCancer/DetailedGuide/breast-cance
r-staging. Accessed June 29, 2012.

screening should be an individual decision; women with a par-
ent, sibling, or child with breast cancer are at a higher risk for
breast cancer and may benefit from earlier screening begin-
ning in their 40s.39
The American Cancer Society (ACS) screening guidelines
were also recently updated and are similar to the current USP-
STF recommendations. The ACS recommends that “women 40
to 44 years of age have the option to begin annual mammog-
raphy; those 45 to 54 should undergo annual mammography;
and those 55 years of age and older may transition to biennial
mammography or continue annual mammography.”5 It has also
been recommended that mammography screening be completed
as long as a woman’s overall health is good and life expectancy is
10 years or more. For those at a high risk of breast cancer, annual
MRI is recommended in addition to mammography beginning
at age 30 years.5 In contrast, the American College of Radiology
and the Society of Breast Imaging recommend annual screen-
ing with mammography for women beginning at the age of 40
years.40
Progression of breast cancer is staged according to the
growth and spread of the tumor (Table 11.9). Areas that are
prone to metastases from breast cancer, in order of occurrence,
are the lungs, bones, liver, adrenal glands, brain, and menin-
ges. Advancement in the treatment of breast cancer includes
inhibition of growth factor receptors, stromal proteases, and
angiogenesis by pharmacologic agents or specific antibodies.41
Common surgical procedures for the treatment of breast cancer
are described in Table 11.10.

TABLE 11.10  Surgical Interventions for Breast Cancer
Surgery Description
Local treatment Removal of involved tissue determines type
of procedure, including lumpectomy, total
mastectomy, total skin-sparing mastectomy,
and bilateral mastectomy.
Axillary and Performed to help determine prognosis and risk
sentinel lymph for recurrence.
node mapping Sentinel node is the first node that receives
and dissection primary lymphatic flow from the tumor
and has been found to predict the histologic
characteristics of the remaining lymph nodes
in the region.
Breast Types include alloplastic implant-based recon-
restoration struction, autogenous breast reconstruction,
consisting of pedicle flaps or free flaps.
Pedicle flaps consist of the transverse rectus
abdominis myocutaneous (TRAM) procedure
and the latissimus dorsi procedure.
Free flaps include microsurgery consisting of a
TRAM procedure, the deep inferior epigastric
perforator (DIEP) flap, the superficial inferior
epigastric (SIEA) flap.
Data from Lester J. Early stage breast cancer. In Yarboro CH, Wujcik D, Gobel
BH, eds. Cancer Nursing. 8th ed. Sudbury, MA: Jones & Bartlett; 2018:1279-
1334.
Physical Therapy Considerations
• The physical therapist should clarify the physician’s orders
regarding upper extremity ROM restrictions, particularly
after surgery involving muscle transfers. The therapist must
know what muscles were resected or transferred during the
procedure, the location of the incision, and whether there
was any nerve involvement before mobilization. Once this
information is clarified, the therapist should proceed to ex-
amine the ROM of the shoulder and neck region because
it may have been affected during surgical interventions for
breast cancer. When to begin shoulder and arm mobility is
dependent on the specific aspects of the procedure and needs
to be clarified with the medical team.42
• Patients may exhibit postoperative pain, lymphedema, or
nerve injury caused by trauma or traction during the opera-
tive procedure.
• Postoperative drains may be in place immediately after sur-
gery, and the physical therapist should take care to avoid ma-
nipulating these drains. ROM exercises may cause the drain
to be displaced; therefore caution should be used.
• Incisions resulting from muscle transfer flaps involving the
rectus abdominis, pectoralis, and latissimus dorsi muscles
should be supported when the patient coughs.
• The physical therapist should instruct the patient in the log-
roll technique, which is used to minimize contraction of the
abdominal muscles while the patient is getting out of bed.
The therapist should also instruct the patient to minimize
contraction of the shoulder musculature during transfers.
• Lymphedema may need to be controlled with lymphedema
massage, elevation, exercise while wearing nonelastic wraps,
elastic garments, or compression pneumatic pumps, especial-
Oncology     CHAPTER 11 285
ly when surgery involves the lymph nodes that are near the
extremities. These techniques have been shown to be of val-
ue in decreasing lymphedema.43-45 Circumferential or water
displacement measurements of the involved upper extremity
may be taken to record girth changes and to compare with
the noninvolved extremity. When possible, a baseline or pre-
operative circumferential measurement of the bilateral upper
extremities should be recorded to assist with monitoring for
the development of lymphedema.
• The physical therapist should consider the effect of recon-
structive breast surgery on the patient’s sexuality, body im-
age, and psychological state.46 
Gastrointestinal and Genitourinary Cancers
GI cancers can involve the esophagus, stomach, colon, and
rectum, and colorectal cancer is the most prevalent type of GI
cancer.
The risk of colorectal cancer increases with age (over 50
years), obesity, physical inactivity, a diet rich in processed or
red meat, alcohol consumption, low calcium, very low fruit and
vegetable consumption, and long-term smoking.5 Common
areas for metastases for colorectal cancer, in order of occurrence,
include regional lymph nodes, liver, lungs, and bones.47 Cancers
of the liver and pancreas, although considered GI cancers, are
discussed separately in this chapter. Surgical procedures used to
treat GI cancers involve resection of the involved region (e.g.,
gastrectomy or colectomy), with or without accompanying che-
motherapy or radiation therapy.5
 CLINICAL TIP
Patients who have undergone gastrointestinal (GI) surgery may
have resultant colostomy placements. Please refer to Chapter 8
for details regarding this procedure.
Genitourinary cancers can involve the uterus, ovaries, vulva,
vagina, penis, testicles, prostate, bladder, and kidney. It has
been estimated that 75% of vaginal, 69% of vulvar, and 63%
of penile cancers are associated with HPV infection.5 Prostate
cancer is the second most common cancer diagnosed in men,
and early-stage prostate cancer often has no clinical signs or
symptoms. Changes in urination frequency, flow, urge, or pain
with urination are signs of advancing disease. Later-stage pros-
tate cancer also typically metastasizes to bone, which can cause
bone pain.5 Routine prostate cancer screening for men at aver-
age risk for the development of the disease is not currently rec-
ommended because of the high potential for overdiagnosis.5 The
ACS recommends those at average risk for prostate cancer who
have at least a 10-year life expectancy have a conversation with
their physician or health care provider regarding routine screen-
ings starting at age 50 years.5 Treatment includes surveillance,
surgery, EBRT, brachytherapy, and hormonal therapy or com-
binations of these, and the 5-year relative survival rate is near
100%.5
Testicular cancer is the most common cancer diagnosed
in men between ages 15 and 44 years.5 The two main types
of testicular germ cell tumors (TGCTs) are seminomas and
286 CHAPTER 11    Oncology

Metastatic cancer to the liver from breast, lung, or colon

TABLE 11.11  Surgical Interventions for Genitourinary
cancer is a common source of secondary hepatic cancer.54 Par-
System Cancers
tial hepatectomy is the standard treatment for resectable HCC
Area Involved Surgical Intervention Excision in patients without cirrhosis. In patients with cirrhosis, liver
Uterus Hysterectomy Uterus through abdominal transplantation is the standard surgical management of HCC in
wall or vagina appropriate candidates.53 Chapter 8 describes cirrhosis in fur-
Total abdominal Body of uterus and ther detail, and Chapter 14 reviews liver transplantation.
hysterectomy cervix through Cancer of the biliary tract consists of gallbladder cancer and
abdominal wall bile duct cancer. Associations with gallstones or chronic inflam-
Subtotal abdominal Uterus (cervix mation in the region have been reported. Surgical resection can
hysterectomy remains) be curative if the tumor is contained; however, the median sur-
Ovary Oophorectomy One ovary vival rate is 3 months for all patients with gallbladder cancer,
Ovaries and Bilateral salpingo- Both ovaries and and the 5-year survival rate is 19%.55
oviducts oophorectomy fallopian tubes
Testes Orchiectomy One or both testes  CLINICAL TIP
Data from McCaughey J. Management of patients with female reproductive dis-
Hepatic cancers can result in metabolic complications involving
orders, and Copel LC. Assessment and management of problems related to male glucose metabolism, which primarily occurs in the liver. The pa-
reproductive disorders. In: Hinkle JL, Cheever KH, eds. Brunner and Suddarth’s tient may therefore have subsequent energy deficits.
Textbook of Medical Surgical Nursing. 14th ed. Philadelphia: Wolters Kluwer;  
2018:1686, 1705, 1714, 1752.

nonseminomas.5 Seminomas are slow-growing tumors, and non-
seminomas are typically more aggressive than seminomas. Risk
factors include cryptorchidism (undescended testicle), personal
or family history of testicular cancer, exposure to organochlorine
pesticides, and Northern European ancestry. The 5-year relative
rate of survival for testicular cancer is 95%.5
 CLINICAL TIP
Patients with genitourinary cancer may experience urinary in-
continence. Bladder control training, pelvic floor exercises, and
biofeedback or electrical stimulation may be necessary to re-
store control of urinary flow.48-50 Patients with GI cancer may
experience bowel as well as urinary incontinence. Both bowel
and bladder incontinence can lead to areas of dampened skin,
which are prone to breakdown.51 Therefore physical therapists
should be careful to minimize shearing forces in these areas dur-
ing mobility.
Renal cell carcinoma tends to metastasize widely before
symptoms are recognized, which generally results in a more
advanced stage upon diagnosis. In addition, renal cell carcinoma
is usually discovered on unrelated imaging scans of the abdomen
and occurs twice as often in men as in women.5,52
Surgical interventions are the primary treatment modalities
for kidney cancer. Ablation therapy is now often used for non-
surgical candidates and targeted therapy for metastatic disease.5
Surgical interventions for the prostate and kidneys are described
in Chapter 9. Additional surgical procedures used to treat geni-
tourinary cancers are listed in Table 11.11.  There are four main groups of leukemia: acute lymphocytic
Hepatobiliary Cancers
Hepatocellular carcinoma (HCC) accounts for 80% of primary
liver cancers and carries high rates of mortality. Risk factors
for developing HCC include hepatitis B virus or hepatitis C
virus infection, cirrhosis of any etiology, smoking, obesity, and
diabetes.5,53
Pancreatic Cancer
Pancreatic cancer is the fourth leading cause of cancer death in
men and women and has a 5-year survival rate of 8%.5,56 Most
pancreatic tumors arise from the pancreatic duct and are found
in the head of the pancreas. Symptoms may include weight loss,
pain in the upper abdomen with or without radicular pain to
the back, and jaundice if bile duct obstruction is caused by the
tumor.5 Risk factors for developing pancreatic cancer include
tobacco smoking and smokeless tobacco use, family history and
personal history of pancreatitis, diabetes, obesity, and high lev-
els of alcohol consumption. Treatment usually focuses on slow-
ing tumor growth with chemotherapy and radiation therapy. As
detection typically occurs after tumor cells have spread from the
pancreas, fewer than 20% of patients are surgical candidates.5 
Hematologic Cancers
Leukemia
Leukemias are malignancies of hematopoietic stem cells origi-
nating in bone marrow. Hematopoietic stem cells are immature
blood cells that have the potential to differentiate into mature
blood cells, such as RBCs, platelets, or WBCs (lymphocytes).57
Because the malignant cells first occupy bone marrow, they can
occlude the space occupied by normal bone marrow cells. As a
result, patients can have anemia, thrombocytopenia, and leuko-
penia. Often the clinical manifestations of leukemia are fever,
fatigue, bone pain, pale skin, easy bruising, weight loss, and
infections.5 (Refer to Chapter 7 for hematological information.)
leukemia (ALL), chronic lymphocytic leukemia (CLL), acute
myeloid leukemia (AML), and chronic myeloid leukemia (CML).
Leukemia is classified according to the cell type involved as well
as the rate of growth of the cancer cells.5 These four groups have
further subtypes that are determined by numerous factors, such
as the characteristics of bone marrow and the clinical presen-
tation. It is beyond the scope of this text to outline all of the

TABLE 11.12  Epidemiology of Leukemia in the United
States
Median Age at Survival Rate
Type Diagnosis (years) (5-year)
Acute lymphocytic 14 70.7%
leukemia
Acute myeloid leukemia 67 26.8%
Chronic myeloid leukemia 64 65.9%
Chronic lymphocytic 71 85.1%
leukemia
Adapted from Kurtin SE. Leukemia and myelodysplastic syndromes, Table 58-
1. In: Yarboro CH, Wujcik D, Gobel BH, eds. Cancer Nursing. 8th ed. Burling-
ton, MA: Jones & Bartlett; 2018:1614.
different subtypes. Table 11.12 outlines the median age at diag-
nosis as well as the 5-year survival rate for each group. Leukemia
can be managed by systemic therapies, such as chemotherapy,
immunotherapy, targeted therapies, or stem cell transplantation
(see Chapter 14).58
Myelodysplastic syndrome (MDS) is a distinct entity from leu-
kemia; however, an overlap in clinical presentation with leu-
kemia exists. Common to both diagnoses, general symptoms
such as anemia, thrombocytopenia, and neutropenia create dif-
ficulties in establishing an early diagnosis of MDS. MDS occurs
commonly in the elderly but can be present at any age.58,59 Bone
marrow transplantation is the primary therapeutic approach,
with proven potential to cure MDS in younger patients. Several
chemotherapy agents are also currently used in this population
for supportive care.58,60
 CLINICAL TIP
Complete blood count (CBC) should be assessed to determine
a safe level of activity or exercise. Refer to the Stem Cell Trans-
plantation section in Chapter 14 for further information.
Lymphomas
Lymphomas are malignancies of lymphocytes and may be of
T-cell, B-cell, or natural killer (NK) cell origin.61-63 Unlike
leukemic cells that primarily occupy bone marrow, lympho-
mas occupy lymph tissue (lymph nodes and spleen). Lymphoma
results in painless enlargement (lymphadenopathy) of involved
lymph nodes, which can also be firm and rubbery. Fever, night
sweats, itching, unexplained weight loss, and fatigue may also
be reported.5,61,62,64
 CLINICAL TIP
Discovery of enlarged lymph nodes without a known cause may
necessitate physician referral.
There are two primary types of lymphoma: Hodgkin’s lym-
phoma (HL) and non–Hodgkin’s lymphoma (NHL). More cases
of NHL were estimated to occur in the United States in 2017
compared with HL (72,240, compared with 8260 cases of HL).5
Oncology     CHAPTER 11 287
TABLE 11.13  Characteristics of Hodgkin’s and Non-
Hodgkin’s Lymphomas
Non-Hodgkin’s
Hodgkin’s Lymphoma Lymphoma
Cell Presence of Reed-­ Wide variety of cell
characteristics Sternberg cells, which types involving B
are large, multinucle- cells, T cells, and
ated cells found in natural killer (NK)
involved lymph nodes cells
Extranodal Uncommon Common
disease
5-year survival 85% (men); 87% 69% (men) 72%
rate5 (females) (females)
Data from Roper K. Hodgkin lymphoma. In Yarboro CH, Wujcik D, Gobel
BH, eds. Cancer Nursing. 8th ed. Burlington, MA: Jones & Bartlett; 2018:1599-
1612; Sorensen E, Johnson J, Gilliam M. Lymphomas. In: Yarboro CH, Wujcik
D, Gobel BH, eds. Cancer Nursing. 8th ed. Burlington, MA: Jones & Bartlett;
2018:1721-1752; American Cancer Society. Cancer Facts & Figures 2017. At-
lanta: American Cancer Society; 2017.
Accounting for this difference is the fact that NHL includes
a wide variety of disease subtypes.5 Characteristics of HL and
NHL can be found in Table 11.13. Clinical staging for lym-
phoma is based on the Cotswolds Modification of the Ann Arbor
Staging Classification (Table 11.14). Treatment for both HL and
NHL involves chemotherapy, radiation therapy, and/or stem cell
transplantation.5,61-63 Stem cell transplantation, targeted ther-
apy, and immunotherapy are also treatments for some forms of
NHL.5
 CLINICAL TIP
In a patient with diagnosed lymphoma, awareness of the ar-
eas of lymphadenopathy is advisable before working with the
patient. Caution should be used with manual techniques, and
disease progression should be monitored.
Multiple Myeloma
Multiple myeloma is a malignancy of plasma cells, which are
derived from B lymphocytes (B cells) and are responsible for cre-
ating antibodies. The disease is characterized by infiltration of
the myeloma cells into bone and, eventually, other organs. These
malignant cells produce monoclonal proteins that may increase
the viscosity of blood. Classically the disease produces bone
pain and a decreased number of normal hematologic cells (e.g.,
RBCs, WBCs, and platelets).65 Staging of the disease has been
updated from the Durie-Salmon Classification to the Interna-
tional Myeloma Working Group Staging System (Table 11.15).
 CLINICAL TIP
Patients with advanced stages of multiple myeloma may be de-
hydrated. Ensure proper hydration before intervention.66
The median age of patients diagnosed with multiple
myeloma66 is approximately 70 years, with only 2% being
younger than 40 years of age. Bone pain is usually the first
288 CHAPTER 11    Oncology
TABLE 11.14  Cotswolds Modification of Ann Arbor
Staging Classification
Stagea Description
I Involvement of a single lymph node region or
lymphoid structure (e.g., spleen, thymus)
IE Involvement of a single extralymphatic site or
extranodal organ or site
II Involvement of two or more lymph node regions
on the same side of the diaphragm
IIE Localized contiguous involvement of only one
extranodal organ or side and its regional lymph
nodes with or without other lymph node regions
on the same side of the diaphragm
III Involvement of lymph node regions on both sides
of the diaphragm
IIIS Involvement of both sides of the diaphragm
including the spleen
IIIE Localized contiguous involvement of only one
extranodal organ side
IIIES Localized contiguous involvement of only one
extranodal organ side and the spleen
IV Disseminated (multifocal) involvement of one
or more extranodal organs or tissues, with or
without associated lymph node involvement or
isolated extralymphatic organ involvement with
distant (nonregional) nodal involvement
A: No symptoms.
B: Fever, drenching night sweats, unexplained weight loss during the previous
6 months.
X: Bulky disease, defined as greater than 10 cm in the long axis or for a medias-
tinal mass as measuring greater than one third of the internal transverse thoracic
diameter of a standard 5th or 6th thoracic vertebral body.
E: Involvement of an extranodal site that is contiguous or proximal to the
known nodal site.
aAny disease stage can have any of the further designations:
Data from Lister TA, Crowther DM, Sutcliffe SB, et al. Report of a commit-
tee convened to discuss the evaluation and staging of patients with Hodgkin’s
disease: Cotswolds meeting. J Clin Oncol. 1989;7:1630-1636; Matasar MJ, Zele-
netz AD. Overview of lymphoma diagnosis and management. Radiol Clin North
Am. 2008;46;75-198; Roper K. Hodgkin lymphoma. In: Yarboro CH, Wujcik
D, Gobel BH, eds. Cancer Nursing. 8th ed. Burlington, MA: Jones & Bartlett;
2018:1605.
TABLE 11.15  International Myeloma Working Group
Staging System
Stage Criteria
I β2-microglobulin <3.5 μg/mL and albumin ≥3.5 g/dL
II β2-microglobulin <3.5 μg/mL and albumin <3.5 g/dL or
β2-microglobulin = 3.5–5.5 μg/mL
III β2-microglobulin ≥5.5 μg/mL
From Ng AK, Anderson KC, Mahindra A. Multiple myeloma and other plasma
cell neoplasms. In: Gunderson LL, Tepper JE, eds. Clinical Radiation Oncology.
3rd ed. Philadelphia: Saunders; 2012:1576.
symptom, with lesions by the malignant cells potentially
causing osteoporosis and pathologic fractures, especially in
the vertebral bodies. As more bone is destroyed, calcium is
released, resulting in hypercalcemia. Acute kidney injury is
present in approximately 20% of patients with myeloma.
Treatment can include chemotherapy, radiation therapy,
and stem cell transplantation.66 The 5-year survival rate is
approximately 41%.5
 CLINICAL TIP
Activity clearance and potential clarification of weight-bearing
status should be obtained from the physician before mobilizing
anyone with bone lesions.
Head and Neck Cancers
Cancers in this anatomic region involve the paranasal sinuses,
nasal and oral cavities, salivary glands, pharynx, nasopharynx,
oropharynx, hypopharynx, larynx, and upper cervical lymph
nodes.67 Risk factors for developing cancer in the oral cavity
and pharynx include use of all forms of smoked and smokeless
tobacco products and excessive consumption of alcohol. An asso-
ciation with HPV infection has also been documented in both
men and women.5
Symptoms can include sore throat, a poorly healing sore in
the mouth, ear pain, a neck mass, or hemoptysis (coughing up
blood). Difficulty chewing may present as the disease advances.
Cancer management includes radiation therapy and/or surgery,
along with chemotherapy in the advanced stages.5
A tumor with clear margins and no cervical lymph node
involvement can be successfully resected or treated with radia-
tion. However, when lymph node involvement occurs, a radi-
cal neck dissection (RND) or modified neck dissection (MND)
is performed.67 A RND includes removal of the sternocleido-
mastoid muscle (SCM), cervical lymph nodes, spinal accessory
nerve, internal jugular vein, and submaxillary gland. An MND
does not include resection of the SCM, spinal accessory nerve, or
internal jugular vein.68 Reconstructive surgery, including a skin
flap, muscle flap, or both, may also be performed to cover the
resected areas of the neck and face.67
 CLINICAL TIP
Proper positioning is important to prevent aspiration and exces-
sive edema that may occur after face, neck, and head surgery.
Clarify the surgeon’s orders regarding head and neck position-
ing: patients may require a tracheostomy, artificial airway, or
both to manage the airway and secretions (refer to Chapter 18,
Appendix 18A).
Physical Therapy Considerations
• 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 pa-
tients with oral cancer is the use of tobacco (both chewing
and smoking). Therefore possible underlying lung disease
must also be considered. During physical therapy examina-
tion, the patient should be assessed for adventitious breath
sounds and effectiveness of airway clearance. Oral secretions
should be cleared thoroughly before assessing breath sounds.

• A fter a surgical procedure, the physician should be contacted
to determine activity and ROM parameters, especially after
skin and muscle flap reconstructions. Physical therapy to re-
store posture, as well as 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, in-
cluding smell, taste, hearing, and sight.
• Because the patient may have difficulty communicating and
swallowing, referring the patient to a speech therapist and
registered dietitian may be necessary. If these disciplines are
already involved in the care of the patient, be aware of any
posted guidelines to facilitate communication, including the
use of an electronic larynx (electropharynx).  small, reddish, and translucent with telangiectases (small, wid-
Neurologic Cancers
Primary tumors of the CNS include gliomas, neuronal tumors,
poorly differentiated neoplasms, primary CNS lymphomas, and
meningiomas.69 Secondary tumors can be the result of another
systemic cancer (lung, breast, melanoma, kidney, and GI tract)
that has metastasized to the CNS.69 Symptoms related to can-
cers of the nervous system depend on the size of the tumor and
the area of the CNS involved. Because of the compressive nature
of CNS tumors, clinical manifestations can occur whether they
are malignant or benign.70 Neurologic symptoms can persist
after tumor excision because of the destruction of neurologic
tissues. Changes in neurologic status resulting from compres-
sion of tissues within the CNS 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 dysfunction, and the need for assistive
devices and positioning devices.70
After resection of a brain tumor, patients may demonstrate
many other neurologic sequelae, including hemiplegia and
ataxia. Radiation therapy to structures of the CNS may also
cause transient neurologic symptoms. Refer to Chapter 6 for
more details on neurologic examination and intervention.
 CLINICAL TIP
A patient with neurologic cancer may have a variety of needs, de-
pending on the location and extent of the cancer. Consequently
the therapist should evaluate the patient’s needs for skin care,
splinting, positioning, cognitive training, gait and balance train-
ing, assistive devices, special equipment, and assistance with
activities of daily living (ADLs).
 
Skin Cancer
There are two major groups of skin cancers: melanoma and non-
melanoma. Melanoma comprises 5% of all diagnosed cancers in
the United States, with 15% turning out to be fatal.71 Nonmel-
anoma skin cancers are divided into the following categories:
keratinocytic (including basal cell and squamous cell carci-
noma), melanocytic, appendageal, soft tissue, neural, and cuta-
neous tumors.71 Risk factors for developing melanoma include
a personal or family history of melanoma, as well as numerous
Oncology     CHAPTER 11 289
and/or atypical moles. Additional risk factors include sun sen-
sitivity; history of excessive sun exposure, including sunburns;
use of indoor tanning; presence or history of immunosuppressive
treatments or diseases; and a history of basal cell or squamous
cell skin cancers.5 Skin cancer risk is reducible by minimizing
exposure to intensive ultraviolet (UV) radiation. According to
the ACS, “many of the more than 5 million skin cancer cases
that are diagnosed annually could be prevented by protecting
skin from excessive sun exposure and not using indoor tanning
devices.”5
Basal cell carcinoma is potentially the most common cancer
diagnosed in humans.71 It is usually found in areas exposed to
the sun, including the head and neck regions. Lesions caused by
basal cell carcinoma are mostly noduloulcerative, appearing as
ened blood vessels on skin). Diagnosis is made with biopsy and
tissue analysis, and surgical excision is the treatment of choice.71
Squamous cell cancer is the second most common cancer in
the United States but is more likely to be fatal compared with
basal cell carcinoma.71 Lesions may be variable in presentation
and include small, pink, erythematous, and scaly plaques or
large, ulcerated, and indurated plaques. The lesions may also
bleed and be painful, and there may be peripheral neural symp-
toms depending on the location of the lesion. Surgical excision
is the treatment of choice for squamous cell cancer.71
Malignant melanoma is a neoplasm that arises from melano-
cytes. Moles or pigmented spots exhibiting the following signs
(called the ABCDE rule) may indicate malignant melanoma5:
• A = Asymmetry
• B = Irregular border
• C = Varied color, pigmentation
• D = Diameter of more than 6 mm
• E = Evolution or change in appearance over time
Management of malignant melanoma can range from surgi-
cal excision with or without lymph node dissection, radiation
therapy, chemotherapy, immunotherapy, or palliative care.5 The
5-year survival rate for localized melanoma is 98%, with rates
declining as the disease spreads.5
 CLINICAL TIP
After resection of skin lesions, proper positioning is important
to prevent skin breakdown. The use of positioning or splinting
devices may be necessary. The physical therapist should deter-
mine the location of the lesion and the need for ROM exer-
cises to prevent contractures. If the lesion involves an area that
will be stressed (e.g., joints), the physical therapist should seek
clarification from the physician’s orders for precautions limiting
motion.
 
Physical Therapy Management
In a systematic review of the cancer literature by Stout et al., it
was noted that exercise is beneficial to patients with cancer. “The
impact of exercise is positive and significantly improves a wide
range of functional, psychological, and physiological markers in
290 CHAPTER 11    Oncology
individuals before, during, and after cancer treatment.”72 It has
also been well documented that exercise and mobility performed
immediately postoperatively “may reduce the risk of adverse
events, affect overall length of stay, and reduce readmissions and
complications in various cancer populations.”20 Therefore the
role of the physical therapist in the acute care setting is vital in
this patient population.
The following are general goals and considerations for the
physical therapist working with the patient who has cancer.
These considerations should be adapted to a patient’s spe-
cific needs. Although there is similarity in the goals for other
patients, in the acute care setting, the systemic nature of the
cancer will necessitate modification of either the goals and/or
time frames for achievement.
These goals are to (1) optimize functional mobility, (2) mini-
mize or prevent cancer-related fatigue (CRF), (3) prevent joint
contracture and skin breakdown, (4) prevent or reduce limb
edema, and (5) prevent postoperative pulmonary complications.
General considerations include, but are not limited to, the
following:
• Knowing the stage and grade of cancer can help the physical
therapist prescribe and modify appropriate treatment param-
eters and establish realistic goals and intervention.
• Patients may be placed on bed rest postoperatively and/
or while receiving cancer treatment and will be at risk for
developing pulmonary complications, deconditioning, and
skin breakdown. Deep-breathing exercises,73 frequent po-
sition changes, and an exercise program that can be per-
formed in bed are beneficial in counteracting these compli-
cations.
• Patients who have metastatic processes, especially to bone,
are at high risk for pathologic fracture. Fall prevention and
education for lifting precautions are essential in this patient
population. Patients at high risk for fracture may benefit
from the use of an assistive device or orthoses to safely en-
hance function and mobility.20 According to a literature re-
view by Maltser et al., there are several specific safety mea-
sures that should be implemented for patients with bone
metastasis.20 The restriction of extreme resistive, compres-
sive, or rotational torque-like forces on an affected extremity
or body region are the main focus of the following general
safety measures20:
1. Manual muscle testing should not be performed in the
affected extremity.
2. Progressive resistive exercises should be avoided in the
affected extremity.
3. Use an assistive device to assist with weight bearing of the
affected extremity, as needed.
4. Avoid excessive spinal flexion, extension, and rotation;
clarify the need for bracing or orthotics in the presence of
fracture or high fracture risk.
5. Patients should be monitored closely for increased pain
with functional mobility.
• Airway clearance is indicated for most patients who undergo
surgical procedures. Care should be taken with patients who
have metastatic processes during the performance of manual
secretion clearance techniques.
• P atients undergoing chemotherapy treatment should be
monitored for reduced exercise tolerance, significantly im-
paired baseline vital signs, and various malicious physiologic
responses to mobility.20 Patients should be monitored for
excessive sweating, disproportionate fatigue, pallor changes,
and severe shortness of breath during therapy interventions
and mobility.20
• Provide patient and caregiver education regarding safety
management, energy conservation, postural awareness, and
body mechanics during ADLs.20
• An assessment of the appropriate assistive devices, prosthet-
ics, and required orthotics should also be performed. De-
creased sensation requires special attention when prescribing
and fitting adaptive devices.
• For patients on isolation precautions, place exercise equip-
ment, such as stationary bicycles or upper extremity ergom-
eters (after being thoroughly cleaned or disinfected with
facility-approved solutions), in their room. Assessment is
necessary for the appropriateness of this equipment, along
with the safety of independent use. Interventions performed
in public therapy spaces or public areas where potential
pathogen exposure is increased should also be reduced or
avoided, when possible, in patients with neutropenic precau-
tions.20
• When performing mobility or exercise treatments, care
should be taken to prevent bruising or bleeding into joint
spaces when patients have low platelet counts.
• Emotional support for both the patient and family is at times
the most appreciated and effective method in helping accom-
plish the physical therapy goals.
• Timely communication with the entire health care team is
essential for safe and effective care. Communication should
minimally include the patient’s current functional status,
progress toward the patient’s goals, and any factors that are
interfering with the patient’s progress.74
• Trends in laboratory values, especially hemoglobin/hemato-
crit, WBC count, platelet count, and international normal-
ized ratio (INR) should be monitored daily.75 The term nadir
is sometimes used to denote when the patient’s blood count
is at its lowest point.75 
Rehabilitation and Cancer-Related Fatigue
CRF affects between 70% to 100% of patients with cancer.76 It is
reported to be the most documented and most distressing cancer
symptom.77 CRF may occur during or after the completion of
cancer treatments, and the specific cause of CRF is unknown.76
This subjective symptom of fatigue is characterized by sudden
onset, is not caused by an activity or exertion, and is not alle-
viated by rest.77 According to a literature review by McNeely
and Courneya,78 aerobic and resistive exercise programs may
help to improve mood and to minimize the complications of
CRF, including a reduction in psychological stress, the physi-
cal side effects of cancer treatment, and anxiety.76 Similarly, the
American College of Sports Medicine (ACSM) has published
roundtable consensus-derived guidelines on exercise for cancer
survivors. The ACSM states that exercise is safe both during and

after cancer treatments and “results in improvements in physical
functioning, quality of life, and cancer-related fatigue” in the
References
cancer survivor.79
The cause of CRF is multifactorial and patient dependent,
there is no distinct etiology. Therefore using several instru-
ments to monitor CRF is essential.80 There are unidimensional
measures, single-question scales that focus on the presence or
absence and severity of the symptom, and multidimensional
measures that emphasize the effect of CRF on the cognitive,
physical, and emotional domains. Single-question assessments
are the most regularly used assessment tools. Refer to Jean-
Pierre et al. for a review of CRF assessments.81
A commonly used tool used for CRF is the Brief Fatigue
Inventory (BFI).77,82 This unidimensional, self-reported patient
tool includes measuring nine items on the severity and effect of
fatigue during the previous 24 hours. The BFI is short and simple,
taking less than 5 minutes to complete, and it is able to include
psychological and physical aspects. It is useful for screening and
outcome assessments and had been validated in both male and
female patients with cancer.82 In the acute care physical therapy
setting, the tool enables a quick assessment of fatigue levels in
patients with cancer and recognizes patients with severe fatigue.
To minimize the sequelae of CRF, the following guidelines
are recommended83:
• Before prescribing an exercise program, evaluate the patient’s
fatigue level, and determine the need for more medical in-
tervention. If the patient is cleared for exercise, then use the
following:
• Begin an exercise program when patients start cancer
treatment, and continue until the end of treatment.
• Before exercise sessions, evaluate the patient to rule out
instability and/or decline in medical status.84
• Before, several times during, and after exercise sessions,
be sure to monitor vital signs, including heart rate,
blood pressure, and oxygen saturation.20,84
• Emphasize the importance of an exercise log or diary to help
monitor progress and promote adherence to the exercise pro-
gram. Patient adherence is crucial to alleviating CRF.77
The ACSM states that exercise prescriptions should be indi-
vidualized and based on the precautions associated with the
patient’s specific cancer, fitness level, surgical or nonsurgical
intervention, comorbidities, and response to treatment.76,79
Normal daily activities and exercise should be continued as
much as possible during and post–nonsurgical treatment.79
Those with known metastasis to bone will require specific mod-
ifications to avoid fracture, and those with cardiac conditions
may also require increased monitoring or modifications.20,79
Patients experiencing extreme fatigue, anemia, or ataxia should
not participate in exercise.79 It is important to remember that
exercise and activity tolerance of patients during and immedi-
ately post–cancer treatment may vary from session to session.
Patients who are immediately post–surgical intervention should
also adhere to the specific precautions relating to their surgery,
which may last for several weeks depending on the procedure.79
Refer to the ACSM Roundtable on Exercise Guidelines for Can-
cer Survivors79 for specific recommendations by cancer type and
for exercise prescription in the postacute setting.
Oncology     CHAPTER 11 291
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 12 Integumentary System
C H APT ER  

Kathryn Panasci

CHAPTER OUTLINE CHAPTER OBJECTIVES

Introduction The objectives of this chapter are the following:
Structure and Function of the 1 . Describe the structure and function of the integumentary system
Integumentary System 2. Recognize the normal process of integumentary repair after injury, including factors which will delay
Structure wound closure
Function 3. Discuss the common causes and etiologies of burn and wound injuries
BURNS 4. Understand the local and systemic effects of a burn
Pathophysiology of Burns 5. Review physical therapy evaluation and management of burn and wound injuries
Physiologic Sequelae of Burn Injury 6. Identify options for medical and surgical management of burn and wound injuries
Types of Burn Injuries
Assessment and Acute Care
­Management of a Burn Injury
Determining Surface Area and Introduction
Depth of Tissue Involvement
Acute Care Management
Managing a patient with an injury to the integumentary system is often a specialized area of
Physical Therapy Examination in
physical therapy practice. All physical therapists should, however, have a fundamental under-
Burn Care
standing of normal and abnormal skin integrity, including the etiology of skin breakdown and
History
Inspection and Palpation the factors that influence wound healing. For the purpose of this chapter, an alteration in skin
Pain Assessment integrity secondary to a burn injury is referred to as a burn. Alteration in skin integrity from
Range of Motion any other etiology is referred to as a wound. 
Strength
Functional Mobility Structure and Function of the Integumentary System
Physical Therapy Intervention
Structure
WOUNDS
Pathophysiology of Wounds The integumentary system consists of the skin and its appendages (hair and hair shafts, nails,
Types of Wounds and sebaceous [oil] and sudoriferous [sweat] glands), as shown in Fig. 12.1. Skin is composed
Phases of Wound Healing of two major layers: the superficial, thinner epidermis and the deeper, thicker dermis. Skin
Factors That Can Delay Wound varies in thickness from 0.5 to 6 mm, depending on the area of the body, with an average of
Healing approximately 1 to 2 mm thickness.1-4 The epidermal and dermal layers are supported by the
Age deeper hypodermis (e.g., adipose, fascia) and other subcutaneous tissues and structures (e.g.,
Lifestyle and Psychological muscle, tendon, cartilage, bone).1,2,4 Table 12.1 presents the cellular composition and function
Well-being of each skin layer.
Nutrition The avascular epidermis is composed primarily of keratinocytes. These cells produce kera-
Vascular Status tin, which is imperative for integumentary structure and protection. Keratinocytes present
Medical Status in different stages of maturity and degeneration and are therefore seen as five distinct layers
Medications within the epidermis. The deepest layer, the stratum basale, is one cell thick and is the point
Bioburden and Infection
of active cellular differentiation. The most superficial layer, the stratum corneum, is composed
Appropriate Plan of Care and
Patient Compliance
of dead, flattened keratinocytes which are constantly shedding. Cellular maturation and move-
ment between epithelial layers from cellular division to death and sloughing is approximately
Wound Evaluation and Acute
Care Management
30 days.1-4 Other cell types found in the epidermis include Langerhans cells, Merkel cells, and
History melanocytes.1-4
Physical Examination The highly vascularized dermis is divided into two layers and is composed primarily of
Wound Assessment collagen and elastin, along with amorphous extracellular matrix, or ground substance. Col-
Wound Cleaning and lagen and elastin are produced by fibroblasts, the predominant cell in the dermis. The der-
Debridement mis also contains and supports structures such as hair follicles, sudoriferous glands, sebaceous
Dressings and Topical Agents glands, vasculature, lymphatics, and nerve endings.1-4 The epidermis and dermis are connected
Advanced Therapies
Physical Therapy Management
        295
296 CHAPTER 12     Integumentary System
Stratum corneum
Sweat duct EPIDERMIS
Capillary
Sebaceous
gland
Arrector pili
muscle DERMIS
Nerve
endings
Hair
follicle
Dermal
papilla
Sweat
gland SUBCUTANEOUS
Fat TISSUE
Blood vessels
FIG. 12.1
Three-dimensional representation of the skin and subcutaneous connective
tissue layer showing the arrangement of hair, glands, blood vessels, and
other structures. (From Black JM. Medical-Surgical Nursing: Clinical Man-
agement for Positive Outcomes. 8th ed. St. Louis: Saunders; 2009.)
at the dermal–epidermal junction by a basement membrane.
The dermal–epidermal junction is an irregular surface of hills
and valleys, allowing for increased contact, and thus anchoring,
between the epidermis and the dermis. The basement mem-
brane is semipermeable, which allows for nutrient diffusion to
occur from the vascularized dermis to the deeper layers of the
avascular epidermis.1,3,4
The skin has a number of clinically significant variations: (1)
compared with women’s skin, men’s skin is thicker and drier
and demonstrates increased rate of sebum production, suscepti-
bility to infection, and sensitivity to environmental conditions
(e.g., ultraviolet [UV] radiation)5; (2) skin thickness varies with
age6,7; and (3) skin on different parts of the body varies in thick-
ness, number of appendages, and blood flow.2,3 These variations
affect the severity of integumentary breakdown, as well as the
process of wound closure.  unless additional tissue injury occurs.6,9-11
Function
The integument has several major functions1,3,7,8:
1. Protection: The skin provides physical, chemical, and biologi-
cal barriers to protect the body from microorganisms, UV
radiation, physical trauma, chemicals, and dehydration.
2. Thermoregulation: Local vasodilation results in increased blood
flow to the skin. Together with sweating, these processes as-
sist in lowering core body temperature. Vasoconstriction
shunts blood internally to increase core temperature and pre-
vent heat loss.
3. Sensation: Multiple sensory cells within the skin detect pain,
temperature, pressure, vibration, and touch.
4. Immunity: Epithelial cells act as first responders, initiating
the immune response to pathogens. Additionally, the intact
integumentum creates a physical barrier, and the relatively
acidic pH (4.0–6.5) of the skin’s surface provides chemical
protection from microorganism invasion.
5. Blood reservoir: The skin normally holds approximately 5% of
the body’s blood supply, which can be shunted between the
skin and the central organs, as needed. The cutaneous blood
reservoir can drop to zero in extremely cold temperatures
to help increase core temperature. The blood reservoir can
increase to 60% of total cardiac output during severe heat
conditions to decrease core temperature.
6. Metabolism: Modified cholesterol molecules are converted to
previtamin D when exposed to UV radiation.
7. Aesthetics: The skin plays a significant role in one’s overall
psychological well-being with regard to cosmesis and ap-
pearance. Impairments in the skin (e.g., acne, pigmentation
disorders, sun damage, scarring) can have a profound effect
on self-confidence and societal responses. 
BURNS
Pathophysiology of Burns
Skin and tissue destruction occur after a burn injury as a result
of the absorption of heat energy. The effect of heat energy on
the exposed tissues is observed in distinct zones based on loss
of blood flow and severity of the overall injury (Fig. 12.2). The
zone of coagulation, located in the center of the burn, is the area
of greatest damage with no remaining viable tissue.6,9,10 The
zone of stasis, also referred to as the zone of ischemia, surrounds
the zone of coagulation and contains marginally viable tissue,
which has a potential for salvage but which can easily be further
damaged from processes such as hypoperfusion, desiccation of
tissues, edema, or infection.6,9-11 Proper wound care and medi-
cal care (e.g., debridement, infection prevention, restoration of
perfusion, fluid resuscitation, temperature regulation, and man-
agement of underlying chronic disease processes) can preserve
the integrity of the viable tissue in this zone. The zone of hyper-
emia, the outermost area, is the least damaged and heals rapidly
Two systems exist for documenting the severity of a burn
injury. The classic nomenclature of first, second, and third degree
injury and the more conventional classification system of super-
ficial, partial, or mixed thickness (further divided into superficial
partial thickness and deep partial thickness), and full thickness12
(Fig. 12.3). Burn depth is most commonly determined through
observation of clinical presentation, including appearance (e.g.,
tissue coloration and presence of blistering or eschar), capillary
refill, degree of intact sensation (including pain), and presence
of edema, as described in Table 12.2. Superficial burns have no
significant structural damage and therefore no zone of stasis or
coagulation. Differentiation between superficial and deep partial-
thickness burns can be made based on the presence of the zones
of coagulation, stasis, and hyperemia in the deeper burns, whereas
superficial partial-thickness burns will only present with zones of
stasis and hyperemia. Full-thickness burns contain a significant
and easily identifiable zone of coagulation in addition to the zones
of stasis and hyperemia.13 Newer technologies, such as thermal,
nuclear, and laser imaging; ultrasound; computer-enhanced pho-
tography; and serial tissue biopsy are emerging to assist in accu-
rate and objective determination of depth of injury.6,12
 TABLE 12.1  Normal Skin Layers: Structure and Function
Layer Cellular/Structural Composition Function
Epidermis
Stratum corneum Dead, flattened keratinocytes Tough outer layer that protects deeper layers of epidermis.
Stratum lucidum Dead keratinocytes Only present in areas with “thick skin” (i.e., palms, soles).
Stratum granulosum Mature keratinocytes Slowly dying as they migrate farther from vascularized dermis.
Langerhans cells Involved in immunoregulation.
Stratum spinosum Keratinocytes Maturing as they move superficially.
Langerhans cells See above.
Stratum basale or germina- Keratinocytes Primary epidermal cell, undergoes mitosis and moves superficially.
tivum Produces keratin, a structural protein providing structural and water-
proofing properties.
Melanocytes Produce melanin, which determines skin pigmentation and protects
from ultraviolet absorption.
Merkel cells Mechanoreceptors.
Dermal–Epidermal Junction Irregular surface anchoring the epidermis to the dermis, which flattens
(Basement membrane) with age, decreasing contact between the layers of skin.
Dermis
Papillary layer Collagen, elastin, and extracellular Thin, superficial, dermal layer produced by fibroblasts; conforms into
matrix/ground substance overlying basement membrane.
Vasculature and lymph network Provides blood supply and drainage to deeper layers of the avascular
epidermis.
Reticular layer Collagen, elastin, and reticular fibers Produced by fibroblast cells, provides tensile strength and elasticity.
Macrophages, mast cells Immunoregulation.
Meissner’s corpuscles Detect light touch.
Pacinian cells Detect pressure.
Free nerve endings Detect temperature, pain, and mechanical stimulation.
Vasculature and lymph vessels Circulation and drainage.
Hair follicles Sensation, temperature regulation.
Sweat glands Thermoregulation.
Sebaceous glands Sebum production, lubricates skin and hair.
Hypodermis
Subcutaneous fat (adipose) Attaches dermis to underlying structures. Provides insulation, shock
absorption, and source of energy reserve.
Fascia Fibrous connective tissue separating and facilitating movement be-
tween adjacent structures.

Data from Myers BA. Wound Management: Principles and Practice. 3rd ed. Upper Saddle River, NJ: Pearson Education; 2012:4; Baronoski S. Integumentary anatomy:
skin—the largest organ. In: McCulloch JM, Kloth LC, eds. Wound Healing: Evidence-Based Management. 4th ed. Philadelphia: FA Davis; 2010:1; Khan SA, Bank J,
Song DH, Choi EA. The skin and subcutaneous tissue. In: Brunicardi FC, et al., eds. Schwartz’s Principles of Surgery. 10th ed. New York: McGraw-Hill AccessMedicine;
2015; Chu DH. Development and structure of skin. In: Goldsmith LA, et al., eds. Fitzpatrick’s Dermatology in General Medicine. 8th ed. vol 1. New York: McGraw Hill
AccessMedicine; 2012.

Epidermis
Zone of
coagulation

Zone of
stasis

Dermis
Zone of
hyperemia

FIG. 12.2
Zones of injury after a burn. The zone of coagulation is the portion irreversibly injured. The zones of stasis and hyper-
emia are defined in response to the injury. (From Townsend CM, Jr., Beauchamp RD, Evers BM, Mattox KL. Sabiston
Textbook Of Surgery: The Biological Basis of Modern Surgical Practice. 19th ed. Philadelphia: Saunders; 2012.)
298 CHAPTER 12     Integumentary System

A B

C D
FIG. 12.3
The depth of burn injuries from (A) superficial to (D) full thickness. (From Walsh M, ed. Nurse Practitioners:
Clinical Skills and Professional Issues. Oxford, UK: Butterworth-Heinemann; 1999.)

TABLE 12.2  Burn Depth Characteristics

Depth
Superficial (first-degree):
Epidermal injury
Superficial partial-thickness Pink or red with edema
(second-degree): superficial Moist appearance with blisters
dermal injury
Deep partial-thickness
(second-degree):
Deep dermal injury; deeper
skin appendage
structures may remain intact
Full-thickness (third-
degree):
Entire dermis injured with
possible extension into
subcutaneous tissue
Appearance Estimated Closure Pain
Pink to red 3–5 days through epidermal regenera- Very tender to
Little to no edema tion (reestablishment of epidermal touch, painful
Dry appearance without blisters layers from intact stratum basale)
Blanches with brisk refill No scarring
Sensation intact
1–2 weeks through epithelialization Very painful,
without significant risk of scarring hypersensitive
Blanches with brisk capillary refill Pigmentation changes likely
Sensation intact Minimal to no risk of hypertrophic
scarring
Pale pink to mottled red or white ≥3 weeks through epithelialization Pain present
Blistered but dry in appearance Will likely undergo skin grafting if but decreasing
Possible blanching with slow capillary refill healing time expected to be >3 weeks with depth of
Decreased sensation to pinprick Scar formation likely destruction
Hair readily removed
White, red, brown, or black; possibly waxy charred, >3 weeks through granulation followed Insensate
leathery, mottled, or depressed. Clotted capillaries by reepithelialization, although of-
may be visible ten will not heal spontaneously and
Dry appearance without blanching or capillary refill requires surgical intervention
Insensate to pinprick

Data from Brownson EG, Gibran NS. Evaluation of the burn wound: management decisions. In: Herndon DN, ed. Total Burn Care. 5th ed. St. Louis: Elsevier; 2018:87-
92.e2; Hettiaratchy S, Papini R. ABC of burns—initial management of a major burn: II-assessment and resuscitation. BMJ. 2004;329:101-103; Cleland H. Thermal
burns assessment and acute management in the general practice setting. Austral Fam Physician. 2012;41(6);371-375.
 Integumentary System     CHAPTER 12 299

Burn injury

Release of vasoactive substances

Increased vascular permeability

Cell membrane destruction

Edema formation Electrolyte changes Hematologic changes

Risk of compartment
syndrome
Increased body weight
Low protein content
Decreased levels of K+
Increased levels of Na+, Cl–
Increased levels of BUN
(protein catabolism)
Increased Hct
(plasma volume loss)
Decreased numbers of
RBCs (hemolyzed cells)
Increased numbers of
WBCs (hemoconcentration)
Decreased numbers of
thrombocytes
(platelet destruction)

Decreased intravascular volume Increased blood viscosity

Decreased urine output

(hypovolemia)
Myoglobinuria
(muscle damage)

Increased peripheral resistance

Decreased cardiac output

Decreased O2 delivery to vital organs and tissues

in the setting of decreased body temperature and increased heart rate
FIG. 12.4
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 Marvin J.
Thermal injuries. In: Cardona VD, Hurn PD, Bastnagel Mason PJ, et al., eds. Trauma Nursing from Resuscitation
Through Rehabilitation. 2nd ed. Philadelphia: Saunders; 1994; Demling RH, LaLonde C. Burn Trauma. New
York: Thieme; 1989:99.)

Physiologic Sequelae of Burn Injury Electrical Burns

A series of physiologic events occurs after a burn (Fig. 12.4). An electrical burn occurs with exposure to a low voltage current
The physical therapist must appreciate the multisystem effects source (<1000 volts) or a high voltage current source (≥1000
of the burn injury and their effect on physical function. Tissue volts).14 Electrical burn injuries demonstrate varied degrees of
damage and organ dysfunction may be immediate or delayed, tissue damage related to both the electrical current as well as
minor or severe, and local or systemic. A summary of common the associated high-intensity thermal energy produced. There
systemic complications after burn injury is presented in Table is also the possibility of other mechanical trauma if the patient
12.3. Patient age, total body surface area (TBSA) involved, and experiences a fall, blast forces, or sustained muscle contraction
the presence of inhalation injury are the primary risk factors for as a result of the exposure to electrical energy.14 The external
mortality after a burn injury.13  and visible damage to the integumentum is generally confined
to the point where the current entered and exited the body,
commonly referred to as entry and exit wounds or contact wounds.14
Types of Burn Injuries
Entry wounds are located at the point of initial contact, whereas
Thermal Burns exit wounds indicate the location the current exited the body,
Thermal burns are the result of contact with a hot object, liquid, typically where the patient was in contact with the ground.15
flame, steam, or intense heat. Common types of thermal burns Tissue necrosis of deeper structures (e.g., vasculature, muscle,
are scald, flame, flash, and contact injuries (Table 12.4).6,10 The nerve, bone, organs) occurs from the intense heat created by
severity of the burn depends on the location of the burn, the tem- the flow of the current and the electrical disruption of cellular
perature of the source, and the duration of contact or exposure.  membranes.15 Electrical burns may be limited to significant
300 CHAPTER 12     Integumentary System

TABLE 12.3  Systemic Complications of Burn Injury TABLE 12.4  Thermal Burns: Types and Characteristics
Body System Complications Burn Type Description Characteristics
Cardiovascular Hypovolemia, hypotension, alterations in Scald burn Spill of or im- Often causes deep partial- or
cardiac output (decreased or increased mersion in a full-thickness burns.
depending on fluid resuscitation and cardiac hot liquid (e.g., Exposure to thicker liquids
response), tachycardia, arrhythmias, coagu- boiling water, or immersion causes a
lopathy disorders, hemorrhage, anemia, deep over heated bath deeper burn from increased
venous thrombosis water, cooking contact time.
Endocrine Hyperglycemia, insulin resistance, decreased oil, or tar) or ex- Immersion burns commonly
cortisol levels posure to steam cover a larger total body
surface area than do spills.
Gastrointestinal/ Ulceration, decreased gut motility, ileus, ab-
genitourinary dominal compartment syndrome, pancreati- Flame burn Flame exposure Often causes deep partial-
tis, constipation or diarrhea, and decreased from fire or flam- thickness burns.
urinary output mable liquids, Associated with carbon
or ignition of monoxide poisoning and
Neurologic Increased intracranial pressure and cerebral clothing inhalation injuries.
edema; central nervous system dysfunc-
tion, including confusion, agitation, ataxia, Flash burn Explosion of flam- Often causes partial-­
posturing, seizures, shock; critical illness mable liquid, thickness burns.
polyneuropathy such as natural Burns may be distributed
gas, gasoline, or over all exposed skin.
Skeletal Muscle Critical illness related muscle wasting, rhabdo- propane. High Clothing can be protective
myolysis, cachexia voltage electri- but may also ignite result-
Renal Acute renal insufficiency, acute tubular necro- cal sources can ing in a flame burn as well.
sis, nephrotoxicity, renal hypoperfusion also create a high Associated with upper air-
intensity flash way thermal damage.
Respiratory Inhalation injury, restrictive pulmonary pat-
burn without con-
tern (which may occur with a burn on the
comitant typical
trunk), atelectasis, pneumonia, pulmonary
electrical injury
edema, pulmonary embolism, and acute
respiratory distress syndrome Contact burn Exposure to hot Often causes deep partial- or
objects full-thickness burns.
Data from Culnan DM, Sherman WC, Chung KK, Wolf SE. Critical care in the Most common cause of seri-
severely burned: organ support and management of complications. In: Herndon ous burns in older adults.
DN, ed. Total Burn Care. 5th ed. St. Louis: Elsevier; 2018:328-354.e4; Nielson
CB, Duethman NC, Howard JM, Moncure M, Wood JG. Burns: pathophys- Data from Brownson EG, Gibran NS. Evaluation of the burn wound: manage-
iology of systemic complications and current management. J Burn Care Res. ment decisions. In: Herndon DN, ed. Total Burn Care. 5th ed. St. Louis: Elsevier;
2017;38(3):e469-e481. 2018:87-92.e2; Hettiaratchy S, Dziewulski P. ABC of burns—pathophysiology
and types of burns. BMJ. 2004;328(7453):1427-1429.
cutaneous damage at the point of contact or may include an
entry wound, deep tissue damage along the path of travel, exit (ECG) be performed on all patients who sustain electrical
wound, and possible arc burns.6 As electricity travels through injuries. Typically, patients with low-voltage injuries who
body tissues, the trunk is able to dissipate heat energy more are asymptomatic and have normal ECG will not develop
efficiently than the extremities; therefore it is typical to see late arrhythmias. Any patient with a documented loss of
more significant tissue damage in the fingers, hands, and feet consciousness or the immediate presence of arrhythmia after
with high-voltage electrical burn injuries.6 An arc burn can an electrical injury should be admitted for telemetry moni-
occur when joint segments are in close apposition with each toring. Bradycardia caused by disruption of normal cardiac
other and the current takes the path of least resistance, such as conduction, as well as cardiac muscle damage secondary to
across the popliteal fossa when the knee is bent or the antecu- ischemia or direct tissue necrosis, can also occur.
bital fossa with a flexed forearm.6 The severity of an electrical • Vascular: Coagulation disorders and clotting may occur as a
injury depends on the type, frequency, and voltage of the elec- result of vessel damage following thermal injury or direct
trical current; duration of contact with the source; and path- tissue necrosis. Ischemia to all distal tissues and organs is a
way of and resistance to the flow of current through the bodies concern.
tissues.14,15 • Respiratory: Diaphragm and respiratory muscle paralysis can
Multisystem complications specific to electrical injury occur as a result of electrical disruption of neural impulses.
include13-16: • Neurologic: Injury to the nervous system is common as a
• Cardiac: Arrhythmias (sinus and ventricular tachycardia, ex- result of the low resistance to electrical current by nerve
trasystoles, and fibrillations) are the most common complica- tissue. Dysfunctions may include loss of consciousness or
tion of electrical injury. Cardiac arrest is more likely to occur coma, seizure, peripheral nerve injury, and spinal cord in-
after a high-voltage injury but may also occur in low-voltage jury (including progressive demyelination). Patients may
related injuries as well. Cardiac arrhythmias can develop also experience impaired attention, memory, and learning
up to 12 hours after exposure; therefore the American Burn as well as posttraumatic stress disorder, depression, and
Association (ABA) recommends that an electrocardiogram chronic neuropathic pain.

• O  rthopedic: Dislocations or fractures may occur secondary to
sustained muscular contraction or from a fall during the elec-
trical injury. Direct damage to muscle tissue, compartment
syndrome, and rhabdomyolysis may also be observed.
• Other: Aphasia, visual disturbances, blindness, and renal fail-
ure may also occur.
Lightning. Lightning, considered a form of very high
electrical current, typically results in injury via one of four
mechanisms14,17:
1. Direct strike, in which the person is the grounding site for the
lightening discharge
2. Side flash, in which a nearby taller object is struck first, fol-
lowed by a portion of the lightening jumping to strike the
shorter victim
3. Ground current, in which lightning strikes an object or the
ground with resulting energy (ground current) traveling
outward along the ground surface. The person is within the
grounding area and creates a pathway for the current.
4. Conduction or contact strike, in which lightning comes into con-
tact with and travels along metal or electrical wires, plumb-
ing, or metal surfaces. A victim coming into contact with
anything connected to these (e.g., fencing, electrical outlet,
corded phone, shower) will be injured.  • Gastrointestinal: Cramping, nausea, vomiting, diarrhea, and
Chemical Burns
Chemical burns occur as a result of integumentary contact with
acid or alkali substances in which injury is the result of a chemical
reaction rather than a thermal based exposure.6,18,19 In general,
acids tend to cause tissue necrosis and the formation of localized
thick, leathery nonviable tissue (eschar), which limits overall
penetration of the offending chemical.18,19 Alkaline substances
are more damaging because they cause liquefaction necrosis of
tissues with deeper penetration and injury.18,19 The severity of
a chemical burn depends on the type, amount, and concentra-
tion of the chemical; manner and duration of contact; affected
body region and surface area; extent of penetration; mechanism
of action; physical state of the chemical (e.g., gas, solid, liquid);
and immediate care after exposure (e.g., removal of chemical-
soaked clothing followed by irrigation).18,19 In addition to the
effect on the integumentary system, chemical burns can cause
multisystem complications, including cardiac arrhythmias,
alterations in electrolyte levels, multiple organ failure, respira-
tory and mucous membrane irritation, massive hemolysis, cen-
tral nervous system (CNS) toxicity, and nephrotoxicity.19  rule of nines, or the Lund and Browder formula. TBSA is only
Ultraviolet and Ionizing Radiation Burns
A nonblistering sunburn is an epidermal injury consistent with
a superficial burn following overexposure of the skin to UV
radiation.6 More severe burns can occur due to UV exposure
and would be described as partial- or full-thickness burns, as
outlined in Table 12.2. Ionizing radiation burns, with or with-
out thermal injury, occur when radiation energy is transferred
to body tissues, resulting in the formation of chemical free radi-
cals.20 Ionizing radiation burns occur in laboratory or indus-
trial settings but can also be seen in the medical setting after
radiation treatment, most often for cancer. The severity of the
radiation burn is dependent on the dose, dose rate, sensitivity of
Integumentary System     CHAPTER 12 301
exposed cells, body surface area exposed, and duration of expo-
sure. Cells that typically divide and turn over more rapidly are
most susceptible (e.g., skin, bone marrow, and the gastrointes-
tinal tract).20
The effect of radiation exposure may be localized or affect
the entire body (acute radiation syndrome). Mild damage to the
integumentary system presents initially as erythema, similar
to a superficial thermal burn, with possible concurrent pruri-
tus and hyperesthesia. These symptoms will typically develop
within hours of exposure and resolve within 48 to 72 hours.
A second phase of superficial erythema appears 2 to 3 weeks
later, with associated sloughing of the epidermis. Hair loss is
also possible. Partial-thickness radiation related burns present
as blisters, typically 3 weeks after exposure, depending on the
dosage amount. Both superficial and partial-thickness radiation
burns appear identical to thermal burns of the same severity.21
Higher doses of radiation may result in full-thickness wounds,
which appear months after treatment exposure. The wounds are
necrotic in nature, with fibrotic changes in the intact periwound
skin. It is not uncommon for these lesions to develop into skin
cancers.20 Systemic complications of ionizing radiation exposure
include20,21:
bowel ischemia
• Hematologic: Pancytopenia, granulocytopenia, thrombocyto-
penia and hemorrhage (Refer to Chapters 7 and 11 for more
information.)
• Vascular: Endothelium destruction which can result in neu-
rologic, respiratory, and cardiovascular symptoms, distress,
or collapse 
Assessment and Acute Care Management of a
Burn Injury
Determining Surface Area and Depth of Tissue
Involvement
Accurate assessment of TBSA and depth of tissue destruction
in a burn injury is necessary to determine appropriate medi-
cal treatment (e.g., fluid volume resuscitation, airway manage-
ment) and local wound management (e.g., type of debridement,
dressing selection, need for surgical intervention). Total body
surface area is a reliable predictor of morbidity and mortal-
ity13,22 and can be calculated by using the palmar method, the
calculated for partial- and full-thickness burns; superficial burns
are not assessed in this manner.23 Depth of the burn injury is
most commonly described as superficial, partial-thickness, or
full-thickness.
Palmar Method
This method of assessing TBSA relies on the estimate that the
patient’s palmar surface area (PSA) is 1% of their TBSA. PSA is
calculated as the area of the palm and fingers, with the thumb
extended and the fingers adducted.24 The palmar method is the
least accurate method of assessment, although it can be benefi-
cial in young children whose body proportions do not follow the
traditional rule of nines. It can also be useful when estimating
302 CHAPTER 12     Integumentary System
the TBSA of small burns (<15%) or large burns (>85%), where
the unaffected TBSA is calculated and subtracted from 100% to
determine the TBSA of the burn injury.24,25 Use of the palmar
method may overestimate burn TBSA.24  adjustments for age and growth.24,25
Rule of Nines
The rule of nines divides the adult body into sections, each of
which is assigned a percentage of TBSA. Each lower extremity
and the anterior and posterior trunk are assigned 18%, upper
extremities 9% each, the head 9%, and the genitalia 1% (Fig.
12.5).23 To use the rule of nines, the areas of partial- and full-
thickness burns are estimated for each affected body segment,
and the percentages are added up to calculate TBSA. Modifica-
tions are made if a portion of a body section is burned. For exam-
ple, if only the posterior left arm is involved, TBSA is calculated
as 4.5%. 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.23 There is concern related to accuracy in pedi-
atric and obese adult patients, and therefore specific recommen-
dations, not discussed in this text, are available for calculating
TBSA in these populations.23,24  occur as a result of inadequate management of the burn wound,
Lund and Browder Formula
The Lund and Browder formula divides the body into 19 sections,
each of which is assigned a different percentage of TBSA (Table 12.5).
These percentages vary with age from infant to adult to account for
FIG. 12.5
The rule of nines method of assessing the extent of a burn injury. (From
Walsh M, ed. Nurse Practitioners: Clinical Skills and Professional Issues. Ox-
ford: Butterworth-Heinemann; 1999.)
the relative changes in TBSA with normal growth. The Lund and
Browder formula is the most accurate predictor of TBSA because
of the inclusion of a greater number of body segments, along with
 
Depth of Tissue Involvement
The degree to which the skin and the underlying tissues have
been affected by a burn will determine the manner in which the
injury heals and affects medical and therapeutic decision making.
Accurate assessment of burn depth provides a clinical basis for the
determination of appropriate conservative, or nonsurgical, burn
care or surgical intervention and to predict the expected func-
tional and cosmetic outcomes. Refer to Fig. 12.3 and Table 12.2
to review the depth of tissue destruction in burn injuries.
A burn is considered a dynamic wound that can change
in appearance, especially during the first 3 days after injury.6
Therefore the exact classification of depth of injury cannot be
determined definitively until the burn has developed fully.6 As
previously discussed, one must also consider that later conver-
sion of a burn from a superficial injury to a deeper injury may
tissue perfusion, fluid resuscitation, temperature regulation,
and infection; the presence of edema or infection; or the effect of
other underlying chronic medical conditions.6,9-11 
Acute Care Management
The ABA has defined criteria for admission of a burn victim to
a designated burn center.26 The following section discusses these
guidelines as well as the role of medical and wound care personnel
in the resuscitative and reparative phases of burn management.
Burn Center Admission Guidelines
In addition to such factors as TBSA and depth of tissue destruc-
tion, the presence of other associated injuries and premorbid
medical conditions determine the optimal level of care for the
patient. The ABA recommends medical care in a verified burn
center if the patient has any of the following26:
• Partial-thickness burns greater than 10% of 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 medical disor-
ders that could complicate management, prolong recovery, or
affect mortality
• Burns and concomitant trauma (e.g., fractures) in which the
burn injury poses the greatest risk of morbidity or mortal-
ity (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
will be necessary in such situations and should be in concert
with the regional medical control plan and triage protocols.)
• Children with burn injuries admitted to hospitals without
qualified personnel or equipment for the care of children
• Burn injury in patients who require special social, emotional,
or rehabilitative intervention 
 Integumentary System     CHAPTER 12 303

TABLE 12.5  Lund and Browder Method of Assessing the Extent of Burnsa
Birth 1–4 yr 5–9 yr 10–14 yr 15 yr 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
aValuesrepresent percentage of total body surface area.
Adapted from McManus WF, Pruitt BA. Thermal injuries. In: Feliciano DV, Moore EE, Mattox KL, eds. Trauma. Stamford, CT: Appleton & Lange; 1996:941; Lund
CC, Browder NC. The estimation of areas of burns. Surg Gynecol Obstet. 1944;79:355.

Medical Care in the Resuscitative Phase
In addition to the burn injury, this patient population may
have other associated traumatic injuries to consider. The objec-
tives of on-scene and emergency room medical management of
the patient who has a major burn injury include simultaneous
general systemic stabilization as well as burn care.26,27 Initial
emergent care in the form of the medical ABCDEs (airway,
breathing, circulation, disability, exposure) should be followed,
and thus general systemic stabilization involves27-29:
• Airway with cervical spine protection: Assessment of respiratory
distress, inhalation injury, carbon monoxide (CO) poisoning,
airway obstruction, and maintenance of airway patency; stabili-
zation of the cervical spine if there is obvious or suspected injury
• Breathing and ventilation: Provision of supplemental oxygen to
any patient with suspected inhalation injury; bronchoscopy to
assess and clear airways, as indicated; prevention of pneumo-
nia and other ventilator-associated respiratory disorders; and
determination and management of appropriate supplemental
oxygen or mechanical ventilation (refer to Chapter 18)
• Circulation and cardiac status: Assessment and ongoing moni-
toring of vital signs, particularly pulses in extremities with
circumferential burns; obtaining vascular access to initiate flu-
id resuscitation to replace lost volume and maintain perfusion
• Disability: Neurologic assessment for consciousness and ob-
servation of any other gross deformities
• E xposure: Removal of clothing, jewelry, and contact lenses to
cease the burning process and prevent further injury; irriga-
tion of the burned area with tepid water; covering the patient
with clean linens to prevent heat loss and to maintain a warm
environmental temperature, if possible
• Secondary injuries: Survey of the patient for other concomitant
injuries and stabilization, as appropriate (e.g., spinal precau-
tions); follow-up with medical testing (e.g., ECG, imaging,
and laboratory studies) to guide management
Medical stability remains a priority in the hours and days
after a major burn injury. In addition to other traumatic inju-
ries and underlying chronic conditions, the medical team will
continue to observe for and manage burn-specific issues, such as
inhalation injury, fluid resuscitation, maintenance of body tem-
perature, and pain control.
Inhalation Injury and Carbon Monoxide Poisoning.
Inha­lation injury is defined as “the toxic and deleterious effects
of heat and the chemical products of combustion on the air-
ways”30 and may present as a chemical injury, thermal injury,
systemic toxicity, or a combination of these.31 Inhalation inju-
ries can cause direct cellular injury, alterations in blood flow and
perfusion, toxin and inflammatory cytokine release, and airway
obstruction.32 The severity of the injury is largely dependent
on environmental factors, such as ignition source, temperature,
concentration, and solubility of the gases, as well as the duration
304 CHAPTER 12     Integumentary System
of exposure.32,33 Although diagnostic and intervention strate-
gies have evolved, inhalation injury continues to significantly
increase the risk of morbidity and mortality.31,33,34 Inhalation
injury is suspected based on a combination of history and physi-
cal examination findings and confirmed with diagnostic stud-
ies, such as fiberoptic bronchoscopy, carboxyhemoglobin values,
chest computed tomography (CT), and pulmonary function test-
ing.32,34 Many facilities will also rely on the Abbreviated Injury
Scale (AIS) to determine the severity of inhalation injury.32 His-
tory and physical examination findings include knowledge of
exposure to noxious inhalants, especially in an enclosed space,
and if the patient demonstrates any of the following31,32,34:
• Altered mental status or loss of consciousness, confusion, agi-
tation
• Burns on the face, neck, or upper chest
• Singed eyebrows or nose hair
• Airway obstruction, including mucosal damage, edema, or stridor
• Alterations or hoarseness of voice
• The presence of soot in the mouth, nose, or sputum
• Respiratory distress
Inhalation injuries are classified by the following categories:
upper airway, lower airway, or parenchymal injury; and systemic
toxicity.32,33 Upper airway injuries are the result of microvascular
changes caused by direct thermal injury, resulting in significant
airway edema, peaking 24 to 48 hours after injury. Endotracheal
intubation is often indicated with this type of injury because the
progressive edema can lead to airway obstruction.13,32,33 Adequate
cooling of inspired air occurs before the toxic gases and chemicals
reach the lower airways; therefore lower airway injury is generally
related to chemical irritation caused by the gases themselves. The
rapid proinflammatory response after chemical exposure in the
lower airways results in increased permeability and destruction
of the bronchial epithelium, sloughing of the mucosa, edema,
bronchoconstriction, and copious production of secretions. Air-
way obstruction often occurs as a result of these processes.13,32,33
Parenchymal injuries are also the result of chemical exposure, as
opposed to a direct thermal injury, and present as edema, inactive
surfactant, and decreased tissue compliance, with related hypox-
emia and acute respiratory distress syndrome (ARDS).32,33 Sys-
temic toxicity occurs when inhalation of chemicals, liquids, mists,
fumes, and gases results in metabolic acidosis, tissue hypoxia, and
impaired cerebellar oxygen usage.32 General complications of
inhalation injuries include increased airway resistance and work of
breathing, increased metabolic demand, and decreased lung com-
pliance possibly leading to pneumonia or ARDS.13 Management
of inhalation injuries may include the use of bronchodilators,
mucolytic agents, anticoagulants, nitric oxide, bronchopulmo-
nary hygiene (e.g., coughing, percussion and vibration, postural
drainage, serial bronchoscopy, and airway suctioning), respiratory
and ventilatory support, and early mobilization.13,32
CO is a colorless, odorless, tasteless, combustible, nonirritat-
ing gas produced by incomplete combustion of organic material.
Inhalation of CO is cited as one of the most frequent causes of
immediate mortality after smoke-related inhalation injury.13 CO
molecules have a 200 to 250 times higher affinity to hemoglo-
bin than that of oxygen molecules. Upon inspiration, CO mol-
ecules rapidly bind to hemoglobin to form carboxyhemoglobin.
The result is a shift of the oxyhemoglobin curve to the left, with
subsequent impairment in oxygen availability, decreased oxy-
gen delivery, and ultimately severe hypoxia.13 Elevated carboxy-
hemoglobin levels can cause headache, disorientation, nausea,
visual changes, tachycardia, syncope, coma, or death, depending
on the concentration of the gas and exposure time.13 Current
initial management of CO poisoning focuses on administration
of high concentrations of oxygen via a nonrebreather mask or a
mechanical ventilator, as indicated.13,31 
Fluid Resuscitation. Patients with burn injuries, particularly
those in excess of 20% TBSA, are at risk of developing burn-
related shock due to rapid loss of blood volume as the resulting
inflammatory response leads to increased capillary permeability
and a massive fluid shift out of the microvasculature.35,36 Other
contributing factors include vasoconstriction following the burn
injury, decreased myocardial contractility and cardiac output, and
insufficient end organ perfusion.27,35 The gold standard inter-
vention to counteract this fluid shift and prevent burn shock is
immediate and ongoing fluid resuscitation.27,35 Delayed initia-
tion of fluid resuscitation beyond 2 hours after the initial injury
has been shown to increase patient mortality.27
The goals of fluid resuscitation include infusion of fluids to
counteract loss of blood volume and maintain adequate organ
perfusion, monitoring and altering treatment (e.g., titrating fluid
infusion rate) as necessary based on patient response, and pre-
vention or correction of subsequent edema formation.35,36 Fluid
administration should be determined based on the needs of the
individual patient, but in general considers patient age, burn
depth and TBSA, presence of inhalation injury or other associated
injuries, preexisting comorbidities, and current hemodynamic
status.27,37 The ABA practice guidelines do not support a stan-
dard treatment for fluid resuscitation35,36; therefore the specific
formula and fluids used vary according to hospital preference.27,35
Close monitoring is imperative to ensure adequate resuscitation
while avoiding under- or overresuscitation. Urinary output, vital
signs (e.g., heart rate and blood pressure), central venous pres-
sure, laboratory values (e.g., electrolytes, blood glucose, complete
blood count, hematocrit, hemoglobin, acid–base status, and base
deficit), and echocardiogram are commonly used medical assess-
ments in determining optimal resuscitation efforts.36,37 
Body Temperature Maintenance. Patients with a major
burn injury are at risk for hypothermia as a result of loss of the
integumentum, specifically the dermis, and the subsequent
inability to thermoregulate.38 Initially, dry dressings or lin-
ens may be placed on the patient to minimize heat loss.39 The
patient should be placed in a warm environment to maintain
body temperature, which may include the use of warming blan-
kets, heat lamps, and warmed IV fluids. The patient’s room and
the burn unit may have overhead radiant heat panels and may
be humidified in an effort to preserve the patient’s body heat.27 
Pain Management. Pain is the most common complaint after
a burn injury, and every patient’s pain threshold, coping mecha-
nisms, and response to treatment will vary.40,41 A patient with a
burn injury can experience pain as a result of any of the following41:
• Nerve ending exposure
• Hyperactive (hyperalgesia) or exaggerated (allodynia) noci-
ceptive responses

• I nflammation related cytokine and chemokine release
• Manipulation of the burned and adjacent tissues (e.g., de-
bridement, dressing changes, range of motion [ROM], thera-
peutic exercise, mobility)
• Secondary injury (e.g., fracture)
Patients may also experience psychoaffective responses, such
as fear, anxiety, depression, fatigue, and helplessness, which
can exacerbate the individual’s perception of pain.41 Pain in
the patient with burns can be categorized as background pain
(i.e., directly related to the injury and present at all times),
breakthrough pain (i.e., intense and episodic in nature, directly
related to minor activities of daily living [ADLs] that require
movement of the affected area), and procedural pain (i.e., occur-
ring with specific procedures such as wound care, placement
of intravascular catheters, physical therapy, occupational ther-
apy).40,41 Pharmacologic pain management strategies should
be implemented immediately, and current practice guidelines
recommend the use of regularly scheduled intravenous opioids
to manage background pain.27,40,41 The addition of benzodi-
azepines, nonsteroidal antiinflammatory drugs (NSAIDs), and
anticonvulsants provide a multimodal approach to pain man-
agement. The varied mechanisms of action of these drug classes
has shown to improve pain control and reduce opioid doses.41
Breakthrough pain is managed with as-needed doses of analge-
sia, typically short acting in nature.27,40,41 The drug class and
the delivery route are determined based on the needs of the indi-
vidual patient.40,41 Procedural pain may be managed through
the previously discussed analgesia options or possibly through
sedation.27,40,41 Refer to Chapters 19 and 21 for more informa-
tion about pharmacologic agents.
Nonpharmacologic pain management options include the
use of cognitive interventions (e.g., strategies to modify a
patient’s thought process about pain), virtual reality technology,
hypnosis, massage, and transcutaneous electrical nerve stimula-
tion (TENS).40,41  be performed by the patients themselves, family members,
Burn Care in the Resuscitative Phase
Medical management and stability is of the utmost importance in
the hours and days after a burn injury. The team will also initiate
management of the burn injury itself, including infection preven-
tion and management and initial burn care, which may include
debridement and possibly escharotomy or fasciotomy procedures.
Infection Prevention and Management.42 Burn wound
infection is a major risk factor for mortality in the patient with
burns. The intact integumentary system provides physical, chem-
ical, and biological barriers against microorganisms. Thus infec-
tion becomes a significant problem after an injury to the skin.
Additional risk factors for localized infection (i.e., at the site of
the burn injury) include decreased blood supply and the presence
of nonviable tissue. Systemic infection, including sepsis and sep-
tic shock, are also of concern in this patient population.
Prevention of infection is the ideal management approach.
Facility and caregiver strategies to minimize transmission of
pathogens to the burned patient include:
• Individual patient rooms with positive pressure airflow system
• Terminal cleaning of all patient rooms after discharge or
transfer
Integumentary System     CHAPTER 12 305
• T horough decontamination of equipment (e.g., toilet, show-
er, bath bench, bedside commode, mobile diagnostic and
procedural devices)
• Caregiver use of personal protective equipment (PPE) (e.g.,
gown, glove, hair cap, face mask)
• Routine hand hygiene before and after every patient
­encounter
• Prohibiting health care providers from wearing ties, watches,
and rings or using cellular phones because these are objects
likely to carry infectious pathogens
• Tetanus prophylaxis upon admission
• Use of clean or aseptic techniques, as appropriate, during
procedures and burn dressing changes
Early identification and management of infection strategies
include:
• Observation of the burn wound for signs of localized infec-
tion (see the Bioburden and Infection and Wound Cultures
sections in Chapter 12)
• Observation of the patient for signs and symptoms of sepsis
(see the Sepsis section in Chapter 13)
• Use of topical antimicrobial agents or systemic antibiotics, as
needed
 CLINICAL TIP
To minimize the risk of infection, the physical therapist must
follow burn unit isolation procedures whenever entering a pa-
tient’s room. The physical therapist should be familiar with the
institution’s policies regarding the use and disposal of PPE, such
as gloves, gowns, caps, and masks. Family members and visitors
should be encouraged to comply with these policies when visit-
ing the patient as well.
 
Initial Burn Care. Initial care of patients with burns may
other observers present at the time of injury, or emergency first
responders. The ABCDE strategies, as previously discussed,
encompass the best practice guidelines for initial medical sta-
bilization and management.27-29 Initial care specific to the burn
wound begins with removing the patient from the source of
injury and ceasing the burning process. This includes removal
of burned or chemically soaked clothing and all accessories (e.g.,
contact lenses, belts, watches, rings, and other jewelry).28,29,37,39
The burn site should be irrigated with water to neutralize chem-
icals, cool tissues, minimize depth of injury, and decrease pain.
Neutral temperatures should be used; cold water and ice can
induce peripheral vasoconstriction with subsequent increased
tissue damage as well as hypothermia.29,39 The patient should be
covered with clean, dry linens to maintain body temperature.29
Once the patient is medically stable, large blisters or
those that are painful or limit function are deroofed (i.e.,
removal of the dead, blistered skin and drainage of the blis-
ter fluid), nonviable tissue and debris are debrided from the
wound bed, and the burn is cleaned and covered with the
hospital’s or burn unit’s topical agent and dressing of choice
(see Table 12.12). Cleaning solutions commonly used include
mild soap and water or chlorhexidine washes.27,37 Topical
306 CHAPTER 12     Integumentary System
antimicrobial agents may be used to prevent or minimize
colonization and replication of microorganisms.37 A vari-
ety of antimicrobial agents are available, each with its own
advantages, disadvantages, and application procedures. Con-
siderations when determining the most appropriate topical
antimicrobial agent include the antimicrobial’s spectrum
of coverage, risk of tissue and systemic toxicity, ability to
penetrate eschar, and overall effect on wound healing.39,42
If antimicrobial coverage is not necessary or desired, other
topical ointments (e.g., petroleum jelly–based products) may
be used to maintain moisture levels and promote wound clo-
sure. The medical team will determine the depth of tissue
destruction, TBSA, estimated time for wound closure, and
need for surgical intervention.  cosmetically important body regions where multiple surger-
Decompression Intervention: Escharotomy and Fas-
ciotomy. Circumferential or near-circumferential burns can
create extremity, thoracic, or abdominal compartment syn-
dromes.13,43,44 Inelastic eschar paired with edema creates a
tourniquet effect around the trunk, neck, or extremity, result-
ing in increased compartment pressures and possible ischemia
and tissue necrosis, nerve compression, impaired chest expan-
sion, hypoventilation, decreased urine output, or hemody-
namic compromise.13,43,44 In the extremities, loss of limb can
occur if compartment syndrome is left untreated. Likewise, in
the trunk, respiratory and organ functions may be impaired in
the absence of decompressive intervention.13,43 An escharot-
omy is the creation of longitudinal surgical incisions through
eschar (necrotic skin and tissue) to decompress the subcutane-
ous tissues.13,43,44 A 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 decompressive intervention include decreased
or absent oxygen saturation or Doppler flowmetry signal,
increased compartment pressure measurements (considered if
≥25 mmHg and necessary if ≥40 mmHg), or sudden onset of
neurologic compromise.43  • T he therapist should check with the physician to determine
Burn Care in the Reparative Phase
Burn management is divided into two major approaches: (1)
surgical management and (2) nonsurgical management, includ-
ing routine wound cleaning, debridement, bioburden manage-
ment, and dressing selection. It is beyond the scope of this book
to discuss in great detail the indications, advantages, and dis-
advantages of surgical interventions that facilitate burn closure.
A brief discussion and description of such procedures will be
presented.
Surgical Procedures. The cornerstone of present surgi-
cal management is early excision and grafting in deep burns
that are unlikely to heal in a reasonable time frame (less than 3
weeks) through conservative treatment.9,13,44,45 Excision (escha-
rectomy) is the surgical removal of all nonviable tissue with
exposure of bleeding, viable tissue. The subsequent wound may
undergo immediate closure (e.g., staples or sutures), immedi-
ate graft placement (e.g., temporary or permanent skin graft
or substitute, or flap closure), or delayed closure (e.g., remain
open for granulation formation and possibly additional surgical
intervention).13,44 Grafting is the placement of skin or skin sub-
stitute onto a prepared wound bed.44 Early burn closure mini-
mizes scarring, infection, the incidence of multisystem organ
failure, and morbidity; increases chances of graft take; improves
functional and cosmetic outcomes; and decreases the length of
hospital stay.9,44,45
Permanent graft placement at the time of excision is
ideal; however, grafting may be temporary, providing short-
term closure to assist in pain control, minimize infection
risk, maintain a moist wound environment and prevent tis-
sue desiccation, and protect the integrity of the underlying
wound tissue.44,45 Temporary grafting may be indicated for
small burns that are expected to heal by secondary intention,
ies are planned, large burns for which permanent coverage
is not available or in which immediate grafting may not be
well tolerated or successful, or in the medically unstable
patient.9,44,45 Table 12.6 describes common types of excision
and grafting procedures. Table 12.7 describes artificial and
biologic skin substitutes available for use when there is a
lack of viable autograft sites. Many of these are used in the
management of other wound etiologies as well.
Graft adherence and vascularization, commonly referred to
as “graft take,” occurs in approximately 5 days.44 The timing
of the first postoperative dressing change will vary by surgeon
and facility protocol, although typically occurring between 3 to
4 days postsurgery.46 Graft adherence may be compromised by
any of the following44,45:
• Grafted area greater than 60% of TBSA
• Incomplete eschar excision
• Movement or shear of the graft on the recipient site
• Infection, inadequate blood flow, or hematoma formation at
the recipient site
• Poor nutritional status
Physical Therapy Considerations
whether the graft crosses a joint or how closely it may border
a joint. If possible, observe the graft during dressing changes
to obtain a visual understanding of its exact location.
• To promote grafting success, postoperative restrictions on
weight bearing and movement of a specific joint or entire
limb may be present. The therapist should become familiar
with the surgeon’s procedures and protocols and alter posi-
tioning, ROM, therapeutic exercise, and functional mobility
accordingly.
• Donor sites are oriented longitudinally and are commonly
located on the thigh, buttocks, or low back. Once reepithe-
lialized, donor sites may be reharvested if more grafting is
necessary. The donor site is often more painful than the burn
itself. 
Nonsurgical Procedures. Burn wound cleaning, debride-
ment, and dressing selection decisions are dependent on
wound characteristics (e.g., depth of destruction, drainage,
bioburden status, presence of nonviable tissue, edema man-
agement), patient comfort, clinician preference, and product
availability. The goals of conservative, nonsurgical man-
agement are maintenance of a moist wound environment,
 Integumentary System     CHAPTER 12 307

TABLE 12.6  Types of Excision and Grafting

Procedure Description
Tangential excision Surgical removal of eschar in successive layers down to viable dermis; typically performed on deep partial-thick
burns
Full-thickness excision Surgical removal of eschar as a single layer down to viable subcutaneous tissue
Split-thickness skin graft Graft consisting of the entire epidermis and a portion of the dermis (exact thickness is determined by the sur-
(STSG) geon); most common type of graft for permanent coverage
Full-thickness skin graft Graft consisting of the entire epidermis and dermis, including skin appendages and nerve endings. Typically
(FTSG) used on small, functionally and cosmetically important regions (i.e., face, hands)
Mesh graft Harvested skin is placed through a mesher to expand the size before placement on the recipient site; allows for
passive drainage of fluid
Sheet graft Harvested skin placed on the recipient site as a single piece without meshing; improved cosmesis over meshed
graft; must closely monitor for pockets of fluid postoperatively as there is no allowance for passive drainage
Autograft Surgical transfer of a patient’s own skin from another part of the body (donor site) and placing it permanently
on the wound (recipient site)
Allograft (homograft) Temporary graft from donated human cadaver skin
Xenograft (heterograft) Temporary graft from another animal species, typically of porcine skin
Amnion graft Temporary graft from placental membrane
Cultured epidermal autograft Autograft of unburned epidermal cells cultured in the laboratory, which provides epidermal replacement only
(CEA)
Composite skin substitute Epidermal and dermal cells cultured in the laboratory to provide dermal and epidermal skin replacement.
Temporary coverage if cells are allograft or xenograft (more common); permanent coverage option if autogenic
(less common)

Data from Kagan JR, Peck MD, Ahrenholz DH, et al. Surgical management of the burn wound and use of skin substitutes: an expert panel white paper. J Burn Care
Res. 2013;34(2):e60-e79.; Middelkoop E, Sheridan RL. Skin substitutes and “the next level.” In” Herndon DN, ed. Total Burn Care. 5th ed. St. Louis: Elsevier; 2018:
167-173.e2.

prevention or management of infection, and minimizing tis-
sue trauma to promote wound closure and functional out-
come. Occasionally, conservative wound care goals are to
prepare the burn wound for upcoming surgical intervention.
Refer to the Wound Cleaning and Debridement section for
more information on these interventions. A discussion of
common dressing types is found in Table 12.12. Conserva-
tive burn wound management may be performed by a nurse,
a physician, or a physical therapist, depending on the hospi-
tal’s or burn unit’s protocol.  are elevated in appearance and extend beyond the boundaries
Scar Formation
Wound closure occurs over days to months, according to the
depth of tissue destruction, and is described in the Phases of
Wound Healing section. For a discussion of variables that can
impede the process of wound closure and healing, see the Fac-
tors That Can Delay Wound Healing section. In brief, superfi-
cial burns heal through epithelial regeneration, or restoration
of the damaged epithelial layers. Superficial partial-thickness
burns undergo very minimal granulation formation and close
primarily through reepithelialization, or migration of kera-
tinocytes from the wound margins across the wound surface
to restore the epithelium. In both cases, the skin appendages
remain intact, and little to no scarring results when closure
occurs within 2 to 3 weeks of injury.44,47 In contrast, closure of
deep partial-thickness and full-thickness burns requires depo-
sition of granulation tissue, and thus these wounds undergo
scar formation and remodeling.47 Following the remodeling
phase of healing, a normal burn scar is flat in appearance as
dermal collagen fibers are arranged in an organized parallel
formation.47 Hypertrophic scars are abnormal and appear firm
and raised as a result of the overproduction of collagen, abnor-
mal ratio of collagen types, and wavy alignment of dermal col-
lagen fibers.47,48 Another pathologic scar type is a keloid scar,
which is also related to abnormal collagen production and type
ratio, as well as overall collagen fiber alignment. Keloid scars
of the primary wound, whereas a hypertrophic scar remains
within the boundaries of the wound.47,48 Keloid scars are more
likely to occur in dark-skinned individuals of African descent
who have a positive familial history.47 
Physical Therapy Examination in Burn Care
Physical therapy services for the patient with a burn injury
may include wound management and/or functional based
interventions, depending on the delineation of services within
the facility. A functional mobility–based evaluation is often
initiated within 48 hours of hospital admission, with consid-
eration for the patient’s overall medical stability and indi-
vidual rehabilitation needs. The physical therapist should be
aware of any surgical procedures that have occurred, as they
may prevent some or all physical therapy intervention until
postoperative graft dressings have been taken down and graft
adherence assessed.
308 CHAPTER 12     Integumentary System

TABLE 12.7  Skin Substitutes for the Treatment of Burns and Wounds
Product Description
Biobrane (Smith & Temporary, two-layered dressing composed of nylon mesh impregnated
Nephew, Andover, with porcine dermal collagen and silicone; the outer silicone layer is
MA) semipermeable allowing vapor transmission but hydrophilic to liquid
and bacteria. Spontaneously separates from the wound as the epithe-
lium is reestablished.
Dermagraft Organo- Dermal substitute composed of human fibroblasts (which produce
genesis Inc, La Jolla, collagen, proteins, growth factors, and cytokines), extracellular
CA) matrix, and a bioreabsorbable scaffold.
Derived from newborn foreskin tissue.
Remains in wound, assisting in restoration of the dermal bed in
preparation for reepithelialization.
AlloDerm (Allergan, Cadaver dermis aseptically treated to remove epidermal antigenic
Dublin, Ireland) cellular components so that it is immunologically inert.
Provides dermal and basement layer replacement.
Integra (Integra Life Two-layered material composed of a disposable outer silicone film
Sciences, Plainsboro, that acts as a barrier to evaporative water loss and bacteria, and an
NJ) inner layer of bovine collagen and glycosaminoglycan that becomes
a scaffold for dermal regeneration. When the neodermis becomes
vascularized, the silicone covering is removed and replaced with split-
thickness autografts.
GRAFTJACKET Acellular dermal matrix from donated human cadaver skin and applied
(LifeCell, Branch- to provide a scaffold for repair of integumentary tissue.
burg, NJ)
Apligraf Bilayered skin substitute containing bovine collagen and human fibro-
(Organogenesis, blasts (which produce growth factors and proteins for dermal regrowth) ulcers
Canton, MA) and keratinocytes (which reproduce to replace the epithelial surface).
Human cellular components are derived from neonatal foreskin.
OASIS Wound Matrix Bioresorbable matrix derived from porcine small intestinal submucosa.
(Cook Biotech, West
Lafayette, IN)
Epicel (Vericel Postage stamp–sized sample is taken from unburned skin and treated
Corporation, with growth factors, hormones, and antibiotics to encourage cellular
Cambridge, MA) and tissue growth. The resulting cultured epidermal autograft (CEA)
is a 2- to 8-cell thick, permanent epidermal replacement.
Use
Debrided partial-thickness burns
Split-thickness donor sites
Excised burn; may be placed directly on
wound bed or over meshed autograft
Full-thickness diabetic foot ulcers without
underlying structure exposure
Repair or replacement of damaged integu-
ment, no specific limitations to wound type
Can be applied to a debrided burn with an
ultrathin split-thickness autograft
immediately applied over it
Partial- and full-thickness wounds of most
etiologies (including donor sites and grafts)
Not indicated for use in third-degree burns
Any wound with damaged or inadequate
integumental tissue
Chronic venous leg ulcers and diabetic foot
Partial- and full-thickness wounds of most
etiologies (including donor sites and grafts)
Not indicated for use in third-degree burns
Deep partial-thick and full thickness burns
that are ≥30% TBSA
May be used in conjunction with a split thick-
ness skin graft, Integra, or Alloderm or alone
when other donor sites are not available

Data from Kagan JR, Peck MD, Ahrenholz DH, et al. Surgical management of the burn wound and use of skin substitutes: an expert panel white paper. J Burn Care Res.
2013;34(2):e60-e79.; Middelkoop E, Sheridan RL. Skin substitutes and “the next level.” In: Herndon DN, ed. Total Burn Care. 5th ed. St. Louis: Elsevier; 2018:167-
173.e2; smith-nephew.com; dermagraft.com; hcp.alloderm.com; integralife.com; acelity.com; apligraf.com; oasiswoundmatrix.com; epicel.com; kci1.com/KCI1/tissue-
regeneration.

History • W as the burn self-inflicted? If so, is there a history of self-

In addition to the general chart review (see Chapter 2), the injury or attempted suicide?
following information is especially relevant in the evaluation, • Were friends or family members also injured? 
treatment planning, and understanding of the physiologic sta-
tus of a patient with a burn.
• How, when, where, and why did the burn occur? Inspection and Palpation
• Did the patient get thrown (as in an explosion) or fall during To assist with treatment planning, pertinent data that can be
the burn incident? gathered from the direct observation of a patient or palpation
• Is there an inhalation injury or CO poisoning? include the following:
• What are the secondary injuries? • Level of consciousness
• What is the extent, depth, and location of the burn? • Presence of agitation, pain, and stress
• Does the patient have a condition(s) that might impair tissue • Location of the burn or graft, including the proximity of the
healing? burn to a joint

• P resence and location of dressings, splints, or pressure gar-
ments
• Presence of lines, tubes, or other equipment
• Presence and location of edema
• Posture
• Position of head, trunk, and extremities
• Heart rate and blood pressure, respiratory rate and pattern,
and oxygen saturation
 CLINICAL TIP
When examining a patient with burn injuries:
• Avoid rupturing 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.
• Be cautious with gait belt placement where trunk burns are
present. Nylon belts are preferred for easier cleaning and in-
fection management.
 
Pain Assessment
Adequate pain control increases patient participation and activ-
ity tolerance, and pain assessment should occur at each therapy
interaction. For the conscious patient, the physical therapist
should note the presence, quality, and grade of pain before (rest-
ing), during, and after all physical therapy interventions. It is
beneficial to inquire about pain at both the burn and donor sites.
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
the patient is as comfortable as possible. Restlessness and vital
sign monitoring (e.g., 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
Chapter 21 for information on various pain assessment scales.
The Visual Analogue Scale and the Faces Pain Rating Scale are
most commonly used by burn centers for pain assessment.40  status post burn injury.49 General considerations for physical
Range of Motion
ROM of the involved joints typically requires goniometric mea-
surements. ROM can be difficult to perform and exact gonio-
metric values difficult to obtain when the patient has bulky
dressings in place; therefore some estimation of ROM may
be necessary. If possible, the therapist should coordinate with
nursing or the physical therapy wound care team to evaluate
ROM when the dressings are temporarily off. This will also
allow the physical therapist to visualize the extremity during
ROM exercise and to observe for banding, or areas of tissue that
appear white when stretched, which is an initial sign of scar
contracture. This observation may not be possible if dressings
are in place. The uninvolved joints or extremities can be grossly
addressed actively or passively, depending on the patient’s level
of alertness or participation.
The physical therapist should pay attention to the position
of adjacent joints when measuring ROM to account for any
length-tension deficits of healing tissues. The physical therapist
Integumentary System     CHAPTER 12 309
should also be aware of the presence of tendon damage before
ROM assessment; ROM should not be performed on joints with
exposed tendons. 
Strength
Strength on an uninvolved extremity is usually assessed grossly
by function, unless more specific testing is indicated. Formal
strength testing, such as resisted isometrics or manual muscle
testing, is often indicated on the involved side. The physical
therapist should be aware of burn wound and donor site loca-
tions when determining manual contact points for stabilization
and application of resistance during strength assessment. 
Functional Mobility
Examination of functional mobility may be limited, depending
on the patient’s current state of illness, medication side effects,
the need for isolation or a warm or sterile environment, and
pain. The physical therapist should evaluate functional mobil-
ity according to medical stability, precautions, and patient
tolerance.
 CLINICAL TIP
The skin at both grafted and donor site areas (once closed) is
more fragile than normal, intact skin. These areas should be
protected to avoid shearing forces and friction blister forma-
tion. Compression dressings (e.g., ace bandages, elastic tubular
bandages) are routinely used to assist with graft adherence and
venous return.
Physical Therapy Intervention
The primary goal of physical therapy intervention for patients
with burn injuries is to maximize independent and safe function.
Significant improvements in functional outcomes have been
demonstrated following inpatient rehabilitation for patient’s
therapy intervention by impairment are listed in Table 12.8.
The physical therapist should also recognize the following:
• This population may have multisystem organ involvement
and be in a hypermetabolic state; thus the physical therapist
needs to be aware of cardiac, respiratory, and neurologic sta-
tus, as well as musculoskeletal and integumentary issues.
• Fluid resuscitation and pain medications can affect blood
pressure, heart rate, respiratory pattern and rate, and level of
alertness. Monitoring these variables will help the therapist
gauge the patient’s pain level and determine how aggres-
sively to intervene during the therapy session.
• The patient with a burn may require more frequent re-
evaluations than other patient populations because the
patient’s status and therapy intervention can change dra-
matically as swelling decreases, wound debridement and
closure occur, hemodynamic and respiratory stability are
achieved, and mental status improves. The goals and plan
of care need to be updated throughout the patient’s hospi-
tal stay.
310 CHAPTER 12     Integumentary System
TABLE 12.8  Physical Therapy Considerations for Burn
Injury
Variable Considerations
Decreased ROM Most patients have full ROM on admission
and altered limb but may readily begin to exhibit decreased
position ROM because of edema (localized or sys-
temic), pain, and immobility.
Devices that help properly position the
patient include splints (off the shelf or
custom fabricated), abduction wedges, arm
boards attached to the bed, pillows, and
blanket rolls.
Incorporate the use of a modality (i.e., pulley)
into stretching activities.
Decreased strength Active exercise is preferred unless sedation
or the patient’s level of consciousness or
cognition prevents it.
Active exercise (i.e., proprioceptive neu-
romuscular facilitation) provides muscle
conditioning, increased blood flow, edema
reduction, and contraction prevention and
helps reduce hypertrophic scar formation.
Decreased endur- Prolonged bed rest (see Chapter 1) may be
ance and func- necessary for weeks or months secondary
tional mobility to medical status or to accommodate graft-
ing, especially of the lower extremity.
Orthostatic hypotension may occur as a
result of prolonged bed rest. The use of a
tilt table and/or pressure supportive stock-
ings may assist toleration to progressively
upright mobilization.
Assistive devices may need adaptations (e.g.,
platform walker, built-up handgrips) to ac-
commodate for ROM and strength deficits
or weight-bearing restrictions.
Consider the use of active exercises (e.g.,
restorator, recumbent bike, treadmill) that
address cardiovascular conditioning while
increasing ROM and strength.
Risk for scar devel- Healing of deeper burns and skin grafts is
opment accompanied by scarring.
Hypertrophic scarring can be decreased
through the use of pressure garments, sili-
cone gel sheets, ROM, and scar massage.
Patient/family Patient/family education emphasizes infor-
knowledge deficit mation about the role of physical therapy,
related to burns exercise, positioning, pain and edema
and physical control, and skin care.
therapy Education before discharge is of the utmost
importance to improve compliance, confi-
dence, and independence.
ROM, Range of motion.
Data from Simons M, King S, Edgar D. Occupational and physiotherapy for
the patient with burns: principles and management guidelines. J Burn Care Res.
2003;24(5):323-335.
• A
 portion(s) of the plan of care is often withheld for a pe-
riod of time after skin grafting to prevent shearing forces
on the new graft. 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.
TABLE 12.9  Preferred Positions for Patients with Burn
Injury
Area of Body Position
Neck Neutral (0 degrees) or slight extension (10–15
degrees), no rotation or side bend
Shoulder Abduction (90 degrees)
Horizontal flexion (15–20 degrees)
Elbow and Extension minus 5–10 degrees to minimize
forearm pain from full extension
Forearm neutral or slight supination (≈10
degrees)
Wrist Neutral or slight extension (10–15 degrees)
Hand MCP joint flexion (70–90 degrees)
Proximal and distal IP joints in full extension
Thumb CMC joint in radial and palmar abduc-
tion and MCP joint in neutral or full extension
Hip Neutral extension/flexion (0 degrees)
Neutral rotation (0 degrees)
Slight abduction (10–15 degrees)
Prone position naturally promotes ideal hip
alignment, though may not be possible to
achieve in many patients
Knee Near-full extension (3- to 5-degree bend)
Foot and ankle Neutral ankle dorsiflexion/plantarflexion
Avoidance of inversion
Neutral toe extension/flexion
CMC, Carpometacarpal; IP, interphalangeal; MCP, metacarpophalangeal.
Adapted from Serghiou MA, Niszczak J, Parry I, Richard R. Clinical practice
recommendations for positioning of the burn patient. Burns. 2016;42:267-275.
• T ime frames for physical therapy goals vary widely and are
generally based on TBSA affected, the location of the burn,
patient age, and preexisting functional status.
• Joints at risk for contracture formation need to be properly po-
sitioned (Table 12.9) and positioning protocols must be con-
sistently carried out by all caregivers and documented in the
patient care plan. Proper positioning will decrease edema and
prevent contracture formation to facilitate maximal recovery.
• The therapist should be creative in treating the patient with a
burn. Traditional exercise works well; however, incorporating rec-
reational activities and other modalities into the plan of care can
often increase functional gains and compliance, with less pain.
• The plan of care must be comprehensive and address all af-
fected body regions.
• The therapist should attend bedside rounds or any multidis-
ciplinary team meetings/conferences to be involved in care
planning and inform the team of therapy progression. 
WOUNDS
Pathophysiology of Wounds
The processes behind wound formation vary, based on the under-
lying etiology (e.g., vascular insufficiency, pressure, autoimmune
disorders, hypersensitivity reactions, infection, other medical
 Integumentary System     CHAPTER 12 311

TABLE 12.10  Clinical Indicators of Common Lower Extremity Wounds

Wound Etiology Clinical Indicators
Arterial insufficiency Intermittent claudication
Extreme pain or cramping, decreased with rest and dependent positioning, increased with exercise and elevation
Decreased or absent pedal pulses; delayed capillary refill; decreased temperature of the distal lower limb
Full-thickness wound depth with distinct, well-defined wound edges; typically located on the anterolateral leg, distal
foot, and toes
Pale granulation (if any), presence of nonviable tissue (e.g., eschar), and minimal drainage
Shiny, anhydrous, pale to cyanotic skin
Venous insufficiency Lower limb discomfort, heaviness, and edema; decreased with elevation and activity and increased with rest and depen-
dency
Pedal pulses present unless arterial disease also present
Irregularly shaped, shallow wound typically located on the medial lower leg and malleolus
Fibrous slough covered wound bed and moderate to copious drainage
Hemosiderin staining and lipodermatosclerotic changes
Diabetic foot ulcer Painless ulcer; however, lower-limb neuropathic pain patterns may be present
(neuropathic) Absent pedal pulses if arterial disease is present, otherwise may be normal
May demonstrate decreased temperature secondary to arterial insufficiency or hyperperfusion due to autonomic neu-
ropathy component or in areas of repetitive trauma
Full-thickness wound located at pressure points on the foot and toes (e.g., plantar surface of foot, metatarsal heads)
often surrounded by areas of callus
Pale wound bed often with nonviable tissue and minimal drainage
Trophic changes of skin, hair, and nails due to autonomic neuropathy (e.g., dry, cracked, hairless, callus formation)
Pressure injury Pain generally present if sensation intact
Present over areas of pressure, most commonly bony prominences
Vary significantly in depth and appearance from superficial epidermal injury to full-thickness wound with exposed
subcutaneous structures, undermining, and tunneling
Periwound may be intact/normal in appearance or characterized by nonblanchable erythema or induration
Pulses intact unless vascular compromise is also present

Data from Singer AJ, Tassiopoulos A, Kirsner RS. Evaluation and management of lower-extremity ulcers. New Engl J Med. 2017;377(16):1559-1567; Elftman N, Con-
lan JE. Management of the neuropathic foot. In: Sussman C, Bates-Jensen B, eds. Wound Care: A Collaborative Practice Manual for Health Professions. 4th ed. Philadelphia:
Lippincott Williams & Wilkins; 2012:325-367; Bonham PA. Assessment and management of patients with wounds due to lower-extremity arterial disease (LEAD). In:
Doughty DB, McNichol LL, eds. Core Curriculum Wound Management. Philadelphia: Wolters Kluwer; 2016:420-465; Myers BA. Pressure ulcers. In Myers BA. Wound
Management: Principles and Practice. 3rd ed. Upper Saddle River, NJ: Pearson Education; 2012:257-295.

conditions) or the source of injury (e.g., trauma, burn, surgery).
It is beyond the scope of this text to address all wound types and
causes; however, common types of wounds, the pathophysiology
behind their formation, and factors that contribute to or delay
wound healing are discussed in the following sections.
Types of Wounds
Traumatic Wounds
A traumatic wound is an injury caused by an external force, such
as a laceration from broken glass, a cut from a knife, a bite by
another person or animal, or penetration of a bullet. Contamina-
tion, infection, and the presence of foreign bodies are concerns,
depending on the exact origin of injury.50 Management will be
determined based on the specific presentation (e.g., presence
of contamination, infection, or nonviable tissue and ability to
approximate edges for suture placement) of the wound.  tes mellitus (DM)–related macro- and microvascular diseases,
Surgical Wounds
A surgical wound is the residual skin defect after a surgical inci-
sion. Typically these wounds are closed by primary intention
(i.e., the use of sutures or staples to bring wound edges together
at the time of the surgery), and healing occurs through granula-
tion formation between the wound walls and reepithelialization
of the incision line.51,52 Surgical wound closure may be delayed
when complications, such as infection, vascular insufficiency, or
underlying medical conditions, are present that may prevent or
limit wound healing or the ability to approximate wound edges.
Wound closure by secondary intention occurs as the wound is
left open and allowed to progress though the stages of wound
healing (see Phases of Wound Healing section). The surgi-
cal team may also opt to leave the wound open initially after
surgery with later use of sutures or staples to approximate the
wound edges (i.e., delayed primary closure or tertiary closure).52 
Arterial Ulcers
A wound resulting from arterial insufficiency occurs secondary
to impaired perfusion, which results in tissue ischemia, necrosis,
and subsequent ulcer formation. Most commonly these wounds
are the result of atherosclerosis, although microthrombi, diabe-
and vasculitis are other possible sources of impaired perfusion
in the lower extremity.53,54 Arterial ulcers, described in Table
12.10, occur most commonly in the distal, anterolateral lower
leg and distal foot and toes as a result of lack of collateral cir-
culation in this area. Arterial ulcers may also be found in areas
where repeated pressure or trauma has occurred on the already
ischemic limb (e.g., phalangeal heads, heels).53,54 
312 CHAPTER 12     Integumentary System
Venous Ulcers
A wound resulting from venous insufficiency occurs secondary
to improper functioning of the venous system, which results
in venous hypertension, persistent inflammation, capillary bed
congestion, impaired oxygen delivery, destruction of dermal
tissues, and subsequent ulcer formation.53,55 Venous system
impairment may include damaged or dilated veins, improp-
erly functioning valves, or an obstruction to venous flow (e.g.,
stenosis or thrombosis). All of these result in impaired venous
return, subsequent retrograde flow, and increased pressure
within the venous system (i.e., venous hypertension).53,55,56 The
exact mechanism by which venous system impairments and
venous hypertension result in wound formation has not been
established, although some theories do exist (e.g., the fibrin cuff
theory and white blood cell [WBC] trapping theory).55,56
Venous ulcers, described in Table 12.10, present most com-
monly on the medial calf and malleolus but can occur anywhere
on the lower leg.53,55,56 As red blood cells (RBCs) extravasate
from the vasculature and break down, iron is released from
hemoglobin. This, combined with increased stimulation of
melanin, results in hemosiderin staining, the characteristic
hyperpigmentation of the ankle and the lower leg.53,55,56 Lipo-
dermatosclerosis is the result of inflammation of the subcuta-
neous adipose tissue, which becomes sclerotic over time. The
skin appears thickened, hard, and contracted with an inverted
champagne-bottle or bowling-pin appearance.55,56 Other char-
acteristics of venous insufficiency include significant gravity-
dependent edema of the lower extremity, telangiectasia (small
blood vessels visible under the skin, i.e., spider veins), and atro-
phie blanche (areas of ivory or porcelain white skin with visible
telangiectasias).53,55,56 Compression therapy is the gold standard
management strategy for venous insufficiency; however, the cli-
nician must always consider the possibly concomitant presence
of arterial insufficiency.55  of neuropathy, peripheral artery disease, and impaired immune
Diabetic Foot Ulcers
Lower extremity neuropathic disease (i.e., peripheral neuropa-
thy) is a feature of many systemic diseases, although most com-
mon to subsequent wound formation is the underlying diagnosis
of DM.57 Diabetic foot ulcer formation is multifactorial, but it
generally occurs as a result of poorly controlled DM contribut-
ing to peripheral artery disease and peripheral neuropathy.53,57
The development of lower extremity and foot wounds in patients
with diabetes is the leading cause of nontraumatic amputation
of the lower extremity in the United States.57,58
Diabetes mellitus is a major risk factor for peripheral artery
disease. Sustained hyperglycemia, dyslipidemia, and insulin
resistance result in vascular inflammation, vessel damage, and
atherosclerotic plaque formation.58 Refer to the Arterial Ulcers
section for a review of the effect of peripheral artery disease on
the formation of lower extremity wounds.
Diabetic peripheral neuropathy is characterized by sensory,
motor, and autonomic dysfunctions.53,57,59 Progressive loss of
protective sensation decreases the patients ability to sense pain,
pressure, and trauma at the foot (e.g., a small object in the shoe,
stepping on a nail, poorly fitting footwear), increasing the risk
of physical trauma and subsequent ulceration.53,57,59 Loss of
temperature discrimination increases the risk of burns, such as
with hot bath water.57 Sensation can be examined using sev-
eral methods, including vibration testing with a 128-Hz tuning
fork, position sense testing, reflex testing, and pressure assess-
ment with Semmes-Weinstein monofilaments.57 Monofilament
sensory testing should be done on intact, noncallused skin.53,57
Structural deformities, contractures, impaired strength,
abnormal weight-bearing patterns, and altered gait can occur as
a result of the peripheral motor neuropathy present in patients
with diabetes.57,59 Achilles tendon contractures, foot drop, claw
toe deformity, hallux rigidus, and hallux valgus are commonly
observed deformities, all of which lead to altered weight distri-
bution, creating areas of increased pressure and shear. The result
is tissue ischemia and ulceration.57,59 These abnormal mechani-
cal forces also stimulate callus formation.57 Callus formation, in
itself, also increases pressure and shear forces to the underlying
tissues, resulting in ulceration beneath the callus.57
Autonomic neuropathy is characterized by the loss of
sweat and oil production in the feet, resulting in severely dry,
cracked, and inelastic skin; callus formation; and frequent toe-
nail infections.53,57,59 Vascular changes also occur as persistent
vasodilation of pedal vessels increases blood flow to the foot
and contributes to demineralization of bone.57 The resulting
osteopenic bones are highly susceptible to fracture, which often
goes unnoticed in the insensate foot, leading to additional frac-
tures and possible bony collapse of the plantar arch. This rocker
bottom foot deformity, known as Charcot neuroarthropathy or
Charcot foot, leads to increased plantar pressures, ulceration, and
possible amputation.57,60
Diabetic foot ulcers, described in Table 12.10, present most
commonly in areas of repeated pressure, shear, or trauma (e.g.,
tips of and between the toes, plantar surface of the foot, site
of bony deformities).53,57 Because of the underlying presence
function, diabetic foot ulcers are at an increased risk of infection,
particularly osteomyelitis.53
 CLINICAL TIP
• The patient with diabetes or a family member or caregiver
should be instructed on daily foot inspections and routine
foot protection (e.g., appropriately fitting footwear, avoidance
of walking in bare feet, professional foot and nail care).57
• Evaluation of the patient’s footwear, if available, is essential to
observe wear pattern (indicator of abnormal pressure points
and gait patterns) and fit, both of which can contribute to
ulcer formation, particularly in the presence of foot deformi-
ties.57
 
Pressure Injuries
A pressure injury is defined by the National Pressure Ulcer
Advisory Panel (NPUAP) as “localized damage to the skin
and underlying soft tissue usually over bony prominence or
related to a medical or other device.”61 Pressure injuries occur
as the result of tissue ischemia caused by intense and/or sus-
tained pressure on localized areas of skin and subcutaneous
tissue. Detrimental pressure forces may be of low intensity

TABLE 12.11  Pressure Injury Staging
Stage Definition
Stage 1 Pressure Intact, reddened skin that does not blanch.
Injury Skin with darker pigmentation may present
as a differing color from surrounding areas.
Stage 2 Pressure A partial-thickness wound with exposed, viable
Injury dermis that may appear red or pink.
Granulation, slough, and eschar are not
present. Can present as an intact or open/
ruptured serum-filled blister.
Stage 3 Pressure Full-thickness wound in which subcutaneous
Injury fat may be visible; however, no underly-
ing structures (e.g., muscle, tendon, fascia,
ligaments, cartilage, bone) are exposed. May
include epibole, tunneling, and undermining.
Slough or eschar may be present, but does not
obscure the depth of tissue loss.
Stage 4 Pressure Full-thickness wound in which muscle, tendon,
Injury fascia, ligaments, cartilage, or bone is exposed
or directly palpable. Often includes epibole,
tunneling, and undermining. Slough or
eschar may be present, but cannot obscure the
depth of tissue loss.
Unstageable Full-thickness wound in which slough and/or
Pressure Injury eschar covers the wound bed. True depth can-
not be determined until nonviable tissue has
been debrided and wound base is exposed. It
is recommended not to disrupt stable eschar
(i.e., dry, adherent, intact without erythema
or fluctuance) on the heel or ischemic limb.
Deep Tissue Intact or nonintact skin appearing as non-
Pressure Injury blanchable red, maroon, or purple in color.
(DTPI) Can also present as a blood filled blister.
Adapted from NPUAP Pressure Injury Stages. National Pressure Ulcer Advi-
sory Panel website. www.npuap.org. Accessed November 12, 2018.
over long periods or higher intensity applied over short peri-
ods of time.62 Shear forces, moisture, heat, nutritional status,
tissue perfusion, and underlying comorbidities are additional
confounding factors that increase the risk of pressure-related
skin and tissue breakdown.61,62 Superficial pressure injuries
are generally the result of friction or shear. Deeper pressure
injuries may result from a worsening superficial injury if the
damaging forces are not removed, or if pressure over a bony
prominence persists, causing localized internal ischemia at the
point of contact. The muscle–bone interface deep to the point
of pressure is where tissue death first occurs, and the tissues
continue to necrotize externally until a wound is created at
the skin surface. By this time, there is significant internal tis-
sue damage.62,63 Refer to the Wound Staging and Classifica-
tion section and Table 12.11 for detailed information on the
NPUAP pressure injury staging system.
Pressure injuries, described in Table 12.10, present most
commonly over bony prominences.53,62,63 High risk areas are
related to patient positioning and include62-64:
• Supine—occiput, scapula, sacrum, calcaneus
• Side-lying—greater trochanter, medial and lateral femoral
condyles, malleoli
• Sitting—ischial tuberosity, sacrum/coccyx
Integumentary System     CHAPTER 12 313
• P
 rone (e.g., after extended positioning during surgery)—an-
terior tibia, patella, iliac crest, chin
Blanchable erythema indicates an area of pressure that still
has sufficient perfusion and capillary refill. Pressure relief strate-
gies (e.g., turning schedule, specialized pressure relief support
surfaces, increased mobility) should be incorporated into the
general care plan. If the pressure forces are not relieved, clini-
cians will observe nonblanching erythema, which is the first
sign of tissue damage (i.e., stage 1 pressure injury).62-64 
Phases of Wound Healing
There are four overlapping phases of wound healing: hemosta-
sis, inflammation, proliferation, and remodeling. Although dis-
tinct in their purposes, these phases overlap, and the progression
into and through each phase is dependent on a variety of fac-
tors, including cellular and chemical signals from the previous
phase.65-67 Acute wounds have a known cause, occur suddenly,
move through the phases of healing within a reasonable time-
frame, and attain successful closure. The length of time it takes
for an acute wound to progress through the phases of healing
will depend on the size and type of the wound, in addition to
other patient-related and environmental factors (refer to the Fac-
tors that Can Delay Wound Healing section). Chronic wounds
are typically the result of an underlying process (e.g., vascular
insufficiency, neuropathy, pressure) or localized negative effect
on the wound (e.g., infection, desiccation, repeated trauma to
wound tissue). With chronic wounds, healing is delayed in one
of the phases, closure is not attained in a timely manner, or
wound closure is not sustained and dehiscence (i.e., reopening)
occurs.65,66,68,69
Hemostasis occurs in acute injuries extending beyond the
epidermis, resulting in bleeding. This phase begins immedi-
ately after injury and serves to minimize blood loss and to create
a barrier from contamination (i.e., blood clot).65-67,69 Vascular
injury triggers localized vasoconstriction; activation of platelets,
which then release growth factors and cytokines; and the clot-
ting cascade. The blood clot created provides a scaffolding for
the incoming cells of the inflammation phase.65,66,69
The primary goals of the inflammation phase are to control
bioburden and to establish a clean wound bed prepared to move
into the proliferation phase.65,66,69 The inflammatory response
begins approximately 10 to 15 minutes after injury once bleed-
ing has been controlled and the platelet-released growth factors
and cytokines chemically signal an influx of WBCs and inflam-
matory mediators to the site of injury.65-67 Localized vasodilation
and increased capillary permeability assist in bringing cellular-
rich fluid (i.e., exudate) into the wound bed.65,66,69 Neutro-
phils, followed by macrophages and lymphocytes, migrate to
the wound and begin to eliminate debris and bacteria. They also
release a host of growth factors, which serve to stimulate pro-
gression to the next phase of wound healing.65-67,69 It should
be noted that inflammation often demonstrates clinical signs
similar to those of infection (increased temperature, erythema,
edema, pain, and impaired function); however, these signs are
localized to the site of injury (i.e., no systemic signs, such as
fever or malaise) and are reasonable for the size of injury.67,69
314 CHAPTER 12     Integumentary System
The proliferation phase begins approximately 2 to 5 days
postinjury as inflammation is subsiding. It is characterized by
restoration of vascular integrity (i.e., neoangiogenesis), forma-
tion of connective tissue (i.e., granulation) to fill the wound
defect, wound contraction to further decrease wound size, and
reepithelialization to close the wound surface.65-67,69 A mul-
titude of cells are active in the proliferation phase; however,
fibroblasts are the primary cells responsible for the formation
of granulation tissue. Granulation is primarily collagen with
extracellular matrix and is deposited around the newly formed
vascular network, filling in the depth of the wound bed. Granu-
lation coloration is directly related to blood supply, and healthy
granulation tissue is often described as “beefy red.”65–67,69 A
secondary type of fibroblast—myofibroblasts—exert tractional
forces on the wound bed to contract the wound margins together
and decrease the overall size and depth of the defect.65-67,69
Reepithelialization occurs as keratinocytes migrate across gran-
ulation tissue from either intact wound margins (partial- and
full-thickness wounds) or skin appendages (partial-thickness
wounds only) to resurface the wound. The initial wound cover-
ing is a single cell layer thick and reestablishment of the normal
epidermal layers will occur over the next 3 to 4 weeks. Wounds
are considered closed when reepithelialization is completed.65-67
Wound healing continues into the remodeling phase, which
can last up to 2 years after the initial injury.65,66 During the
remodeling phase, immature collagen is reorganized into
mature collagen, thus increasing overall tensile strength of the
scar tissue, although it will never exceed 80% of normal, intact
skin.65-67,69 New scar tissue is characterized by its dark pink
to purple coloration, the result of the highly vascularized net-
work of capillaries necessary for granulation formation. As the
capillary bed recedes, scar coloration will fade. It should also be
noted that scar tissue lacks elastin; therefore it is often stiffer or
more rigid than unimpaired skin.65-67
Superficial (epidermal) wounds retain an intact stratum
basale and therefore heal through regeneration, or reestablish-
ment, of the damaged epidermal layers. No scarring occurs.47
Superficial partial-thickness wounds also heal through epider-
mal regeneration, although in these wounds, the keratinocytes
migrate medially from the intact wound edges as well as laterally
from the dermal appendages within the wound. After epidermal
resurfacing has occurred, the new skin will also undergo reestab-
lishment of the epidermal layers. Superficial partial-thickness
wounds move through the phases of hemostasis, inflammation,
and reepithelialization. No granulation or contraction occurs,
and generally no scarring results.65,69 Deep partial-thickness
and full-thickness wounds undergo all phases of wound heal-
ing (hemostasis, inflammation, proliferation, and maturation).
It can be expected that scarring will occur.65,69  There are major metabolic abnormalities associated with
Factors That Can Delay Wound Healing
Normal wound healing follows a predictable sequence of events.
Delayed healing occurs when there is an interruption to this
process. Many patient-related and environmental factors can
delay wound healing, and any wound that is not progressing
through the phases within a reasonable timeframe should be
assessed for an underlying cause.70 It is beyond the scope of this
text to discuss all of the possible factors that might delay wound
healing. The following section addresses select patient-, envi-
ronmental-, and management-related causes that the physical
therapist should consider.
Age
Skin, just like other tissues and organs, changes with age.
Age-related thinning of the epidermis and flattening of the
dermal–epidermal junction increases the risk of skin tears
and wound formation.70,71 Decreased cellular activity leads to
impaired keratinocyte and fibroblast production.66,70,71 Subse-
quent impaired collagen and elastin production in intact skin
results in dermal atrophy and decreased elasticity. Granulation
formation, wound contraction, and reepithelialization is slowed
in the event a wound does occur.70,71 Comorbidities that delay
wound healing, such as diabetes, peripheral neuropathy, and
vascular insufficiency, occur with greater frequency in older
individuals.66,70,71 
Lifestyle and Psychological Well-being
A patient’s lifestyle and psychological well-being can have a
significant effect on the prognosis for healing, decision mak-
ing 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 traumatic situations, such
as construction workers, are also more likely to reinjure heal-
ing wounds. Behaviors such as cigarette smoking can impede
wound healing significantly because of the vasoconstriction that
nicotine creates.
Stress, depression, and lack of adequate sleep have a negative
hormonal effect on wound healing.66,70,71 Stress and depressive
states both induce the release of cortisol, a regulatory hormone
known to adversely affect wound healing (e.g., immunosup-
pression, decreased fibroblast production).66,70,71 Interrupted
or short duration of sleep limits the release of essential growth
hormones in the deepest sleep stages.70 
Nutrition
Proper nutrition is necessary for the growth and maintenance
of all body tissues. Macronutrients (e.g., carbohydrates, fats,
and proteins) and micronutrients (e.g., amino acids, vitamins,
and minerals) are necessary for cell metabolism, division, and
growth. Suboptimal nutritional status can result in impaired
immune function, collagen synthesis, and resulting tensile
strength of scar tissue, and malnutrition is a common factor in
the development of chronic wounds.72
injury that can deplete nutritional stores, including increased
output of catabolic hormones; decreased output of anabolic
hormones; increased metabolic rate; sustained increase in body
temperature; increased glucose demands; rapid skeletal muscle
breakdown, with amino acids used as an energy source; lack
of ketosis; and unresponsiveness to catabolism to nutrient
intake.73 Overall caloric needs increase during wound healing,
and the composition and method of consumption of calories

consumed should be individualized to the patient’s needs and
desires.72,74 Protein-calorie malnutrition (PCM) results from a
decrease in overall calories but, more specifically, protein-based
calories. This leads to a decreased lean body mass. PCM may
occur in critically ill patients with hypermetabolism/hyperca-
tabolism, or in any patient with poor eating behaviors.72 Pro-
tein is essential in all phases of wound healing, and inadequate
protein intake and stored reserves slow the progression of heal-
ing, decrease immune function, and increase skin fragility.72
Fluid levels should also be closely monitored in patients with
wounds because insufficient fluid intake affects glucose levels,
waste removal, tissue perfusion and oxygenation, and overall
skin health.72,74
The relationship between nutrition and wound healing is
multifaceted; therefore a nutritional assessment by a registered
dietitian, nutritional supplements, and careful monitoring of
the patient’s nutritional status and weight are important com-
ponents of a comprehensive assessment and treatment program
for the patient with a wound.
 CLINICAL TIP
Measurement of blood glucose, serum albumin, and prealbumin
levels are commonly assessed to determine nutritional status.
These values must be considered as part of the holistic assess-
ment because they are affected by factors other than nutritional
deficiencies (e.g., infection, stress, trauma, inflammation, fluid
status, and hepatic function).72,74
 
Vascular Status
Impaired vascular status (e.g., arterial and venous insufficiency)
can be a direct cause of wound formation. In addition, all phases
of wound healing require adequate perfusion for delivery of oxy-
gen and nutrients. Therefore any compromise in vascular status
may contribute to the development of a wound and/or delay
wound healing.71  with the developed plan of care can contribute to proper wound
Medical Status
In general, underlying chronic disease and compromised health
negatively affect the normal function of the body’s systems.
This includes the ability to maintain intact integumentum and,
when a wound occurs, to progress through the phases of wound
healing. Immunosuppression, diabetes, cardiopulmonary dis-
orders, hematologic conditions, neurologic impairment, and
altered cognitive status are just a few underlying medical condi-
tions that may affect wound healing.68,70,71 
Medications
Anticoagulants (e.g., warfarin, heparin), antiplatelet aggrega-
tion agents (e.g., aspirin), and antiinflammatory agents (e.g.,
NSAIDs) interfere with platelet activation. This results in an
increased risk of prolonged bleeding during hemostasis and
decreased release of the platelet-derived growth factors and cyto-
kines necessary to move forward to the inflammation phase.70,71
NSAIDs can be of benefit in controlling inflammation but may
also blunt its normal occurrence.71 Steroids delay all phases
Integumentary System     CHAPTER 12 315
of wound healing by inhibiting cellular production and func-
tion.70,71 Chemotherapy interrupts normal cellular proliferation
with a profound effect on wound healing.70,71 Radiation therapy
impairs endothelial cell and fibroblast production, with both
immediate and delayed (i.e., years after treatment) effects on
wound healing.70,71 Application of local anesthetics may impair
cellular function and long-term antibiotic use has demonstrated
correlation with decreased rates of wound healing.71 
Bioburden and Infection
All wounds will have some level of contamination (see Wound
Cultures section). The presence of nonviable tissue or foreign
debris in the wound bed and poor wound care management
strategies (e.g., ineffective cleaning or debridement, failure to
monitor for signs of infection, exposure to environmental con-
taminants) contribute to the proliferation of microorganisms.
Microorganisms in the wound bed compete with fibroblasts
and keratinocytes for oxygen and nutrients. The by-products
released by the microorganisms also have a negative effect on
wound healing.70 The development of critical colonization,
infection, or a biofilm creates a barrier to wound healing and an
increased risk of chronic wound formation.70,71 In the medically
compromised patient, a local wound infection can easily lead to
sepsis. 71 
Appropriate Plan of Care and Patient Compliance
Knowledge of current care standards and practices is paramount
in promoting a wound environment that is conducive to heal-
ing (see Wound Cleaning, Wound Debridement, Dressings
and Topical Agents, and Advanced Therapy sections).70,71 An
appropriate plan of care (e.g., proper moisture balance, appro-
priate use of cleaning and topical agents, avoidance of repetitive
trauma to the wound bed, minimizing environmental exposure,
proper dressing application technique) will promote normal
and timely progression through the phases of healing.71 Addi-
tionally, patient and caregiver comprehension and compliance
healing.70 
Wound Evaluation and Acute Care Management
The evaluation of a patient with a wound includes a general his-
tory, including identification of factors that may affect healing,
a physical examination (e.g., sensation, pain, ROM, strength,
edema, circulation, self-care, and functional mobility), and a
specific examination of the wound itself.
History
In addition to the general chart and medical history review (see
Chapter 2), 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?
316 CHAPTER 12     Integumentary System
• W hat 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?  assessment.
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? Drink alcohol? Use illicit drugs?
• Is the patient generally well-nourished and hydrated? 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 is the patient taking? What are their ef-
fects on wound healing?  ally, the AGS advocates stating “patient reports pain” rather than
Psychosocial Factors
• Does the patient have a good support system, including
physical assistance, if necessary?
• What are the patient’s self-care and mobility needs?
A review of laboratory values and results of vascular tests,
radiographic studies, and tissue biopsies also provide valu-
able information about the integrity of the body systems and
the presence of any underlying disease that may affect wound
healing.  increases weight bearing or pressure may contribute to wound
Physical Examination
Sensation
Sensation to light touch, pressure, pain, temperature, vibra-
tion, and proprioception should be examined.71 Varied methods
exist to accurately assess each of these aspects of sensation. It is
imperative to test for protective sensation in the patient with
neuropathy, and the gold standard is with the Semmes-Wein-
stein monofilaments.71 Impaired or absent sensation should be
addressed through instruction on appropriate wound prevention
techniques, such as daily foot checks, custom or modified foot-
wear, assistive device use and offloading, nail care, and water
temperatures for bathing.  the weight-bearing status is changed. In addition, if the patient
Pain
The evaluation of pain in the patient with a wound is not unlike
the evaluation of pain in any other patient, and pain should be
assessed regularly and appropriate management provided.71
The therapist should evaluate the nature of the pain, including
the location, onset, intensity (using a pain-rating scale), qual-
ity, duration, aggravating and alleviating factors, the effect on
ADLs, and response to treatment efforts.75,76 Understanding the
nature of the pain will ultimately allow the physical therapist
to provide or recommend the appropriate intervention. Refer to
Chapter 21, Acute Pain Management, for more details on pain
It is good practice for the clinician to assume that all wounds
are painful until it has been reported or proven otherwise.76 A
variety of terminology exists to distinguish between types of
wound pain experienced. Acute pain is temporary and serves a
protective purpose as a warning of possible mechanical, thermal,
or chemical related tissue damage. Chronic (persistent) pain is
typically not indicative of current tissue injury but instead rep-
resents the physical and emotional aspects of pain perception.
Nociceptive pain is the appropriate response from harmful stim-
ulation of nociceptors. Neuropathic pain is the result of abnor-
mal function of the nervous system and is present regardless of
painful stimuli. Pain may also be classified as procedure-related
pain or background pain (i.e., pain at rest).75-77
 CLINICAL TIP
The American Geriatric Society (AGS) promotes use of the term
persistent pain rather than “chronic pain” to help lessen nega-
tive connotations that accompany the term chronic. Addition-
“patient complains of pain,” again to maximize positive interac-
tions with patients.78
Range of Motion
Specific measurement of ROM may not be necessary in a patient
with a wound unless the wound crosses a joint line, if contrac-
tures are observed, or if decreased ROM is limiting mobility
and/or self-care. Decreased ROM that inhibits mobility or
development.79 Therefore passive or active ROM exercise, or
both, should be included, as necessary, in the treatment plan. 
Strength
Strength should be evaluated for its effect on the patient’s func-
tional mobility and risk of pressure-related wound develop-
ment. 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 and maintain this precaution
while ambulating. If the patient does not have adequate upper
extremity strength, then he or she may be nonambulatory until
is unable to maintain correct postures or perform pressure relief
strategies and position changes, the risk of pressure related tis-
sue breakdown will increase.79 
Edema
The evaluation of edema is important because it is frequently an
indicator of an underlying pathology (e.g., congestive heart fail-
ure, renal disease, venous insufficiency, lymphatic dysfunction,
inflammation, or infection).71,80 The presence of edema may

predispose skin to breakdown. Wound healing is also impaired
through the accumulation of breakdown products in the edema
fluid, which suppress cellular function.80 Examination of edema
should include distribution, symmetry, relationship to time of
day or physical activity, type (i.e., pitting or nonpitting), mea-
surement, vascular assessment, and skin condition (e.g., texture,
color, temperature, hydration, and integrity).55,71,80 Refer to
Table 3.5 for the Pitting Edema Scale. Additional information
on edema measurements is discussed in Chapter 7.
Therapists should also consider that lymphedema and chronic
wounds may be closely linked. Lymphedema is commonly asso-
ciated with individuals who have undergone a mastectomy;
however, it can also occur secondary to venous insufficiency
(phlebolymphedema) and after surgeries and traumatic injuries
that affect the integrity of the lymphatic system.55 Folliculi-
tis, fungal infections, and cellulitis are common skin conditions
observed in the patient with lymphedema.55 Refer to Chapter 7
for a description of lymphedema. 
Circulation
Adequate perfusion is imperative to tissue integrity and
wound healing. Circulation can be indirectly assessed by
examining skin temperature, distal limb coloration, capillary
refill, nail bed appearance, presence of muscle wasting, tro-
phic changes (e.g., thin and shiny skin, hair loss, nail deformi-
ties, and infection), and the presence of pedal pulses.81 Other
noninvasive assessment methods include ankle brachial index
(ABI) and transcutaneous oxygen monitoring (TCOM, TCO2,
or TCPO2).82 The ABI compares the pressures in the brachial
arteries with those in the posterior tibial or dorsalis pedis arter-
ies. Differences indicate severity of arterial disease and guide
intervention strategies.81 Transcutaneous oximetry assesses
arterial circulation through the use of surface electrodes that
measure oxygen content in periwound tissues.81 Recom-
mended cutoff values vary but, in general, values greater than
40 mmHg are normal, values of 30 mmHg or greater are
likely adequate for healing and safe for debridement, and val-
ues less than 20 mmHg indicate poor healing potential and
a need for surgical intervention.81,82 Refer to Chapter 7 for
more information on the evaluation of circulation. The thera-
pist should notify the physician when any significant changes
in circulatory status occurs and must be aware of any arterial
compromise before using compression therapy.  11 12
Self-Care and Functional Mobility
The ability of the patient to manage his or her ADLs, including
skin and wound care, must be assessed to determine whether
assistance is required. In some cases, family members are avail-
able and can assist the patient with bathing, foot checks, nail
care, and dressing management. Otherwise, hired assistance
(i.e., home health aide, nail care professional, wound care clini-
cian) may be needed. Functional mobility, including bed mobil-
ity, transfers, and ambulation or wheelchair mobility, should be
evaluated. The therapist should consider that the patient’s func-
tion may have changed because of the presence of the wound.
For example, balance may be compromised if the patient
requires orthotics or shoe modifications. Gait training with an
Integumentary System     CHAPTER 12 317
assistive device is often necessary to decrease weight bearing on
an affected lower extremity. Specialized pressure relief seating
and sleeping surfaces or customized foot wear may be appropri-
ate to assist in off-loading areas of increased pressure and weight
bearing. 
Wound Assessment
Assessment of wound-specific characteristics creates an
objective record of the baseline status of a wound and can
help determine the most appropriate intervention to facili-
tate healing.
 CLINICAL TIP
During every interaction with the patient, the clinician should
screen the wound for any overt and concerning changes in sta-
tus and determine whether there is a need to consult additional
services (e.g., vascular, dermatology, infectious disease).
Location, Orientation, Size, and Depth
The location of the wound should be documented in relation
to anatomic landmarks. Body diagrams are often used to depict
wound location; however, written documentation should use
appropriate anatomic terminology to describe wound loca-
tion. If there is more than one wound in the same area, they
should be identified by different letters, numbers, or references
(e.g., medial, lateral, proximal, distal).83,84 Wound orientation,
length, width, depth, and presence of undermining or tunneling
are essential measurements.
Wound orientation must be determined to ensure con-
sistent length and width measurements, particularly for a
wound with an abstract shape or uncommon location. One
method of determining wound orientation is to consider the
wound in terms of clock positions, with the patient’s head
being at 12 o’clock (Fig. 12.6).83-85 The clock method is most
1
10 2
9 3
8 4
7 5
6
FIG. 12.6
Clockwise method of measuring wound size. (From Hamm RL. Tissue heal-
ing and pressure ulcers. In: Cameron MH, Monroe LG, eds. Physical Reha-
bilitation: Evidence-Based Examination, Evaluation, and Intervention. St. Louis:
Saunders; 2007.)
318 CHAPTER 12     Integumentary System

commonly applied as though the patient is in anatomic posi-

tion, which can be difficult depending on the actual position
of the patient or if the wound is in an uncommon location.
If it is more convenient to orient the 12 o’clock position to
an alternative anatomic landmark, be sure to document it as
such.83
Currently there is no gold standard method for wound
measurements, and no method is completely reliable. Ruler-
based measurements are common and will be discussed here;
however, other measurement methods may be observed.
Wound tracings on an acetate sheet with a calibrated grid
placed over the wound are useful for measuring irregularly
shaped wounds. Digital photography and volumetric meth- A
ods of measurement can also be used.83,85 Whatever method
selected, it is imperative to be consistent so that subsequent
measurements can be compared to determine progress and
goal achievement.
Length and width are the most common linear measure-
ments and are measured from one wound edge to the opposite
wound edge.83 Two methods may be utilized for measuring
length and width: (1) the clock method and (2) the greatest
length by greatest width method. If using the clock method, the
length will always be assessed from the 12 o’clock to 6 o’clock
positions and the width from the 3 o’clock to 9 o’clock posi-
tions.83-85 The greatest length by greatest width measurement
considers length to be the longest vertical distance and width
the greatest horizontal distance.83-85 These measurements may
or may not coincide with the length and width measured via the
clock method.
B
FIG. 12.7
Undermining (A) and tunneling (B). (From Myers B. Examination of pa-
 CLINICAL TIP tients with open wounds. In: Myers B, ed. Wound Management: Principles and
To ensure consistency and accuracy in wound assessments, use Practice. 3rd ed. Upper Saddle River, NJ: Pearson Education; 2012.)
a consistent unit of measurement among all individuals measur-
ing the wound. Centimeters, rather than inches, are universally
used, as reported in the literature. Multiple wounds can be docu- The term undermining describes wound erosion underneath the
mented relative to each other if the wounds are numbered—for intact skin at the wound perimeter, resulting in a large wound
example, “Wound #1: left lower extremity, 3 cm proximal to the with a small opening.83,84,86 This is evaluated by probing under-
medial malleolus. Wound #2: 2 cm proximal to wound #1.” neath the skin parallel to the wound bed and grasping or mark-
When taking a photograph of a wound, create or follow a con- ing the applicator at the point of the wound edge. Assessment of
sistent procedure, as changes in the distance of the camera from undermining should be done circumferentially around the wound
the wound as well as the position of the patient can affect the edge and can be documented by using the clock orientation (e.g.,
appearance of the wound. “Undermining: 2 cm at 12 o’clock, 5 cm at 4 o’clock”).83,84,86 A
sinus or a tract, sometimes also referred to as a “tunnel,” is a single
linear channel into subcutaneous tissue that should be measured
Depth is the distance from the skin edge to the wound bed by probing the depth and marking the applicator at the point of
and is measured by placing a sterile cotton-tipped applicator the wound edge. Tunnel may also refer to a linear channel connect-
or wound probe perpendicular to the wound bed. The appli- ing two wounds. Documentation should contain both location
cator is then grasped or marked at the point of the wound (using clock method) and length in centimeters.83,84,86 Caution
edge and measured.83,86 Common practice is to assess depth must be taken when measuring the extent of undermining and
at the deepest site of the wound; however, this location can tunneling to avoid traumatic separation of tissues or increasing
be difficult to reproduce. It may be more reliable to measure the areas of depth. Refer to Fig. 12.7 for undermining and tunnel
depth at the 12 o’clock, 3 o’clock, 6 o’clock, and 9 o’clock measurement and documentation strategies. 
positions.83 Always consider that depth may decrease as a
result of formation of granulation tissue or nonviable tissue. Wound Bed Composition
Depth may appear to increase after debridement of nonviable Wound bed tissue composition and color must be assessed. Doc-
tissue.83 umentation should include a percentage estimate of tissue type

and color (e.g., 50% red granulation, 50% yellow slough).84
Granulation tissue can vary in coloration, from beefy red to
pale pink, depending on the amount of vasculature associated
with it.71,84,86 Healthy adipose tissue often appears yellow in
coloration, although it darkens to a more brown coloration if
it desiccates. New epithelium will often appear shiny, dry, and
pink, regardless of the tone of the underlying skin.84 Nonvia-
ble, necrotic tissue can be described by its color and consistency.
Slough is generally yellow to tan, moist and possibly stringy
and mucinous or adherent. Eschar will typically appear gray to
black and may be soft and soggy or hard and leathery.71,84,86
Anatomic structures (e.g., fascia, muscle, bone, tendon) and
medically implanted devices (e.g., plates, screws, hernia repair
mesh) may also be observed in the wound bed and will vary in
appearance.  Obtaining a wound culture involves the sampling of micro-
Wound Edges
Wound edges can be described as distinct and well defined
when there is definitive depth, whereas indistinct, diffuse edges
are observed where intact skin blends into the wound bed.84
Wound clinicians should pay attention to wound edges that are
calloused (hyperkeratosis; common in neuropathic foot wounds)
or rolled under (epibole). Both will result in delayed closure and
require intervention.  Results of aerobic and anaerobic cultures have been found to
Drainage
Wound drainage is described by type, color, and amount. Drain-
age can be documented as (1) serous (clear to pale yellow and
thin; may be present in a healthy, healing wound); (2) serosan-
guineous (containing blood; may also be present in a healthy,
healing wound); (3) sanguineous (primarily blood); or (4) puru-
lent (thick, white to brown, and pus-like; may be indicative of
infection and should be cultured). Drainage that is blue-green
in color is usually indicative of Pseudomonas infection and should
be cultured. The amount of drainage is generally documented
as absent, scant, minimal, moderate, large, or copious; however,
there is no consistent objective measurement that correlates
with these descriptions.71,84,86  ment, rather than those of the internal environment.86,88
Odor
Wounds may present with an odor for a variety of reasons, such
as the type of dressing used, the solubilization of necrotic tissue,
presence of infection, or hygiene.71,86 The presence of wound
odor should be assessed after wound irrigation to determine
whether it is transient or not.71 Assessment of wound odor is
subjective, and no standard or reliable method of documenta-
tion exists.87 Odor may be documented on a three- or four-point
rating scale, using descriptive terms (e.g., foul, sweet, putrid,
mild, medium, strong), or simply as “present” or “absent.”87
Odor in combination with other clinical signs (e.g., nature of
drainage, fever) may indicate the need for cultures to assess for
infection.71  not appropriate. In other words, a stage 4 wound does not
Wound Cultures
All wounds will have some level of contamination, which
refers to the presence of nonreplicating microorganisms
Integumentary System     CHAPTER 12 319
on the surface of the wound without immune response or
negative effect on wound healing. Colonization occurs when
microorganisms begin multiplying; however, there is still
no need for an immune response, and therefore no clinical
symptoms are present. Increased presence and multiplica-
tion of microorganisms on the surface of the wound elic-
its a localized response in critical colonization.88,89 Topical
antimicrobials and aggressive debridement are appropriate
interventions at this time.86 Infection is the invasion, mul-
tiplication, and penetration of microorganisms in body tis-
sues, resulting in increased local, and likely systemic, clinical
symptoms.88,89 Intervention usually includes a combination
of local and systemic management strategies (e.g., topical
and systemic antimicrobials, serial debridement).86
organisms from the wound surface or tissue and subsequently
growing them in a nutrient medium for the purpose of iden-
tifying the type and number of organisms present. Wound
cultures are indicated if there are clinical signs of critical
colonization or infection, such as purulent drainage, increased
drainage, increased local or systemic temperature, abnormal
granulation tissue, erythema, edema, and foul odor, or if a
clean wound is failing to respond to standard care practices.90
underrepresent the presence and type of microorganisms pres-
ent; however, they are commonly used to determine whether
antimicrobial therapy is indicated.90 Methods of culturing
include tissue biopsy, needle aspiration, curettage, and swab
cultures. Physical therapists may administer swab cultures.
Tissue biopsy, curettage, and needle aspirations are performed
by a nurse or a physician, depending on the protocol of the
institution.88,90,91
 CLINICAL TIP
Unless specifically prescribed otherwise, culture specimens
should be taken after debridement of eschar and necrotic mate-
rial and wound cleaning; otherwise the culture will reflect the
growth of the microorganisms of the external wound environ-
Wound Staging and Classification
Wounds are often described by depth of tissue destruction,
and several staging and classification systems exist. The
NPUAP Pressure Injury Staging scale (see Table 12.11) is
specific to pressure-related injuries and is not appropriate for
use in wounds of any other etiology.61 Wounds are staged on
a continuum of progression of depth and tissue destruction.
Stage 3 and 4 pressure injuries will close through granula-
tion formation, contraction, and epithelialization; however,
references to the wound should always denote the maximum
anatomic depth of tissue damage, and reverse staging is
improve to a stage 3; rather it would be referred to as a heal-
ing stage 4.71,92 Clinicians can also use descriptive terms to
denote improved wound characteristics or use available tools,
such as the Pressure Ulcer Scale for Healing (PUSH) tool or
320 CHAPTER 12     Integumentary System
the Bates-Jensen Wound Status Tool (formerly known as the
Pressure Score Status Tool [PSST]), to monitor progress over
time.71
All other wounds can be described by depth of tissue destruc-
tion. Superficial injuries involve only the epidermis. Partial-
thickness wounds involve varying degrees of the dermis, and
full-thickness wounds continue into subcutaneous tissues and
often expose underlying body structures. The Wagner Ulcer
Grade Classification is used to classify depth and presence of
infection in wounds of arterial origin.93 The University of Texas
Wound Classification System is appropriate for use in the neu-
ropathic foot.94  less than 1 week) may help control the proliferation of micro-
Periwound Assessment
The area surrounding the wound should be evaluated and com-
pared with noninvolved areas and monitored and protected from
damage and breakdown.95 Skin color, texture, temperature,
hydration, induration, hair distribution, presence of old scars,
edema, and changes in nails should all be examined and docu-
mented accordingly.71,84,95
 CLINICAL TIP
Increased localized temperature can indicate infection; de-
creased temperature can indicate decreased blood supply. In-
creased temperature, erythema, and edema can occur with both
inflammation and infection processes, and the therapist should
be aware of other clinical signs to determine appropriate course
of action. Darker underlying skin tones may make changes in
coloration more difficult to observe.
 
Wound Cleaning and Debridement
It is beyond the scope of this book to discuss in detail methods
for wound cleaning and debridement. Instead, general descrip-
tions and indications of each are provided. Wound cleaning and
debridement can be performed by physical therapists, nurses,
or physicians, depending on state practice acts and the policies
of an individual facility. Specifically, physical therapists should
verify their state practice act regarding the ability to perform
sharp debridement. Management considerations for physical
therapists who work with patients with wounds are described
in the Physical Therapy Intervention section at the end of this
chapter.
Wound Cleaning
The purpose of cleaning a wound is to remove loosely attached
debris, necrotic tissue, contaminants, superficial slough, and
dressing materials to prepare the wound for healing and to
prevent infection.88,96,97 Wound cleaning can be achieved
through a variety of methods, such as irrigation, soaking,
swabbing, or scrubbing.88,97 Although widely used the past,
use of a whirlpool is generally no longer indicated for rou-
tine wound cleaning but may be of benefit in grossly contami-
nated or necrotic wounds.88 To avoid damaging new tissue,
discontinue aggressive cleaning techniques and use wound
irrigation, with forces between 4 to 15 pounds per square inch
(psi), when the majority of the wound bed is granulating or
when reepithelialization is occurring.88
The use of sterile saline or potable tap water is safe for use
when managing healthy, clean wounds. If bioburden manage-
ment is desired, cleaning or irrigating with an antimicrobial
solution (e.g., povidone-iodine, chlorhexidine, acetic acid,
hydrogen-peroxide, Dakin’s solution) may be more appropri-
ate.88,96,97 It must be considered that most antimicrobial solu-
tions are cytotoxic and thus delay healing. Short-term use (i.e.,
organisms while minimizing the negative effect on healthy
wound cells.88
 CLINICAL TIP
Sterile saline expires 24 to 48 hours after opening the bottle and
must be discarded. A saline solution can be made by adding 2
teaspoons of salt to 1 quart of boiling water.88 This recipe may
be an inexpensive alternative to purchasing saline for the patient
who will be cleaning wounds at home. If the water source is
known or suspected to be contaminated, it should not be used
for wound cleaning.96,97 If the physical therapist is unsure, the
water can be tested in the hospital laboratory.
There are many commercial skin and wound cleansers on
the market. Skin cleansers have been developed for external use
and should not be used for wound cleaning.88 Wound-specific
cleansers contain surfactants that help break the bonds between
contaminants and debris and the wound surface.98 There is also
a concern that some wound cleansers may be cytotoxic, thus
having adverse effects on normal wound healing.99 In general,
the most neutral solution that will meet the needs of the patient
should always be used.
 CLINICAL TIP
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.96,100
Clean Versus Sterile Technique. Although clean versus ster-
ile technique remains somewhat controversial, clean technique is
sufficient for local care to most wounds and is generally accepted
in the medical community. Sterile technique includes the use of
a sterile field, instruments, and PPE. This method is typically
reserved for surgical or invasive procedures, possibly including
sharp debridement, and for patients at high risk for infection.88
Otherwise, the use of clean gloves and a clean field is adequate
during routine procedures and dressing changes in the nonim-
munocompromised patient.88 Sterile dressings, once opened, can
still be used as long as they are kept in a clean, controlled area. 
Wound Debridement
Debridement is the removal of devitalized tissue, for-
eign debris, or callus from the wound bed and edges to

minimize infection risk and promote wound closure.101-104
The presence of nonviable tissue provides a medium for
microorganism growth and poses a barrier to granula-
tion and epithelialization, preventing normal progression
through the phases of wound healing. Debridement is a key
component in wound bed preparation.101-105 Debridement
is generally indicated for any nonviable tissue (i.e., slough,
eschar, callus) or foreign debris present in or around a wound
with the exception of stable eschar on the heel or ischemic
limb.61 The NPUAP defines stable eschar as “dry, adherent,
intact without erythema and fluctuance” and recommends
not softening or removing it in the previously mentioned
patient situations.61
There are two categories of debridement: selective and
nonselective. Selective debridement removes nonviable tis-
sue only and includes sharp, autolytic, and enzymatic (chemi-
cal) debridement techniques.103 Hydrosurgery and biologic
debridement (i.e., use of medical grade maggot larvae) are addi-
tional forms of selective debridement beyond the scope of this
text. Nonselective debridement removes both viable and non-
viable tissues. Mechanical debridement is a method of nonse-
lective debridement.103 Surgical debridement is also a form of
nonselective debridement; however, this is not within the scope
of practice for the physical therapist and will not be discussed
here. Most wounds will require more than one form of debride-
ment throughout the healing process. It is the responsibility of
the therapist to understand all indications, contraindications,
and safety considerations for any form of debridement used. The
following will present brief descriptions of selective and non-
selective debridement options available to the physical thera-
pist. Readers are directed to other sources for more detailed
information.
Selective Debridement
Sharp Debridement. Sharp debridement involves the use
of scalpels, scissors, and forceps to remove necrotic tissue. It
is considered selective debridement because a thin margin of
nonviable tissue is left untouched, thus minimizing harm to
the underlying viable tissue.101,102,104,105 It is a highly skilled
technique best performed by or under the direct supervi-
sion of an experienced clinician.99,102,104,105 Because the true
selectivity of sharp debridement depends on the skill of the
clinician, sharp debridement can result in unintentional dam-
age to healthy tissues, which may cause bleeding.102 Sharp
debridement is especially expedient in the removal of large
amounts of thick, leathery eschar, although some eschar may
need to be softened beforehand to increase the effectiveness of
removal.102,105
Sharp debridement can be painful; it is therefore recom-
mended that pain medications or topical analgesics be admin-
istered before treatment. When debriding, the clinician must
be able to distinguish viable tissue from nonviable tissue and
must be cautious to have the technique remain selective by not
removing viable tissue.104 Because of the potential for bleeding,
extra care should be taken with patients who are taking antico-
agulants or have bleeding disorders.  Whirlpools use mechanical agitation of a liquid, typically
Autolytic Debridement. Autolytic debridement is a natu-
rally occurring process and the safest and most selective form
Integumentary System     CHAPTER 12 321
of debridement. The body uses its own endogenous enzymes
to selectively lyse necrotic tissue, a normal process that occurs
in any wound. It is painless and does not harm healthy tis-
sues.102-105 Applying a moisture-retentive dressing, such as
films, hydrocolloids, hydrogels, or calcium alginates, facilitates
autolytic debridement in a pain-free manner in patients with
adequate tissue perfusion.99,102-105 Wound irrigation should
occur at each dressing change to remove partially degraded tis-
sue.102 Because it takes time for autolytic debridement to occur,
sharp debridement and/or cross-hatching of eschar may be of
benefit, if tolerated, before dressing application to expedite the
removal of necrotic tissue.102 Conversely, autolytic debride-
ment may be of benefit to soften necrotic tissues before sharp
debridement.105 Autolytic debridement is contraindicated in
patients with a known infection, those with increased risk for
infection, or those who require quick elimination of nonviable
tissue.103,105 
Enzymatic Debridement. Enzymatic, or chemical, debride-
ment is achieved through the topical application of exogenous
enzymes that selectively break down nonviable tissue.101-103
Enzymatic debridement agents are available only by prescrip-
tion.102 Sharp debridement of the wound may be performed
before the application of enzymes to facilitate their effective-
ness. When applying an enzymatic debriding agent to eschar
that cannot be immediately sharp debrided, it is beneficial to
crosshatch the eschar to facilitate penetration of the enzymes.102
Manufacturer guidelines for application and use should always
be followed.102
 CLINICAL TIP
Certain metals, such as silver and zinc oxide, which are present
in some cleansing agents and dressings, can inactivate enzymes
and interfere with enzymatic debridement.102
 
Nonselective Debridement
Mechanical Debridement. Mechanical debridement uses
physical force to remove nonviable tissue and debris from the
wound bed.101,102,104 It is nonselective in nature because of
the risk of harm to healthy, viable tissue as the wound bed and
underlying tissue is exposed to the required forces.101 Gauze
dressings, whirlpool, irrigation, and pulsed lavage are examples
of mechanical debridement.
Wet-to-dry dressings use the application of a moistened
gauze dressing to the wound, allowing it to dry, and then
removing the dressing. The dried dressing will adhere to, and
forcefully remove, any tissue, viable or nonviable, or debris from
the wound bed.102-106 Wet-to-dry dressings were once routinely
used for all wounds, but it has been recognized that they are
painful, detrimental to viable tissue, prolong inflammation,
and do not promote a moist wound environment.106 Therefore
these dressings have fallen out of favor and are only indicated
for use if nonselective, mechanical debridement is desired and
appropriate.102,106
water, to debride loosely adherent tissue, debris, and exudate
and deodorize the wound. It may also help prepare a wound
322 CHAPTER 12     Integumentary System
for sharp debridement by softening necrotic tissue and sepa-
rating desiccated tissues from the wound bed, or it can be
used to soak off adhered dressings. If the intention is to use a
wet-to-dry technique for mechanical debridement, the dress-
ings should not be soaked off, as necrotic tissue will not be
removed.107
Irrigation is the pressurized (4–15 psi) application of a
solution (typically saline) to clean and debride wounds. Con-
current suction in the form of pulsatile lavage may also be
used to loosen nonviable tissue and to aid in the removal of
debris and the irrigation solution.101,108 The negative pres-
sure of pulsatile lavage also stimulates granulation forma-
tion.108 Pulsatile lavage may be a more appropriate option
than whirlpool in patients who are incontinent, have venous
insufficiency, should not be in a dependent position, have an
indwelling catheter or line, or are mechanically ventilated.
Various rigid and flexible tunneling tips are available from
manufacturers to assist the clinician in accessing narrow tun-
nels.108 One must also consider risk of contamination from
aerosolization of droplets during irrigation, pulsed lavage,
and whirlpool treatments.108  goal of complete wound closure, which may occur over many
Dressings and Topical Agents
Although traditional wound care practices included regular
exposure to air and maintenance of a clean, dry wound bed,
it is now understood that limiting exposure and facilitat-
ing a moist environment is optimal for wound healing.100,109
When determining appropriate dressing selection for a
wound, the clinician must consider multiple factors, includ-
ing tissue composition, moisture level, bioburden status,
size, location, odor, pain, and periwound condition. Other
significant factors include the patient’s and caregiver’s cog-
nitive and physical ability to apply the dressing, availability
of physical therapy or nursing services to assist the patient,
cost, and accessibility of supplies.100,110
A wealth of wound care products are available, and it is
virtually impossible for the physical therapist to be aware of
the purpose and application instructions of every available
dressing. It is therefore the responsibility of the therapist to
know the purpose of the dressing, to read the manufacturer’s
instructions for application, and to make educated decisions
when choosing the appropriate dressing for a given wound at
each stage of the healing process. Although it is not feasible
to identify every available dressing, it is possible to catalog
most dressings into basic categories: gauze, transparent film,
hydrocolloids, hydrogels, foams, calcium alginates, collagen
matrix, and topical ointments. Table 12.12 is a summary of
the indications, advantages, and disadvantages of various
dressings.  of the following: physician, nurse, specialized skin and wound
Advanced Therapies
Chronic wounds fail to progress through the phases of heal-
ing in an orderly and timely manner despite standard wound
care practices. Adjunctive therapies may be used in addi-
tion to standard wound practices in the care of chronic and
nonhealing wounds. These include negative-pressure wound
therapy, ultrasound, electrical stimulation, UV light therapy,
laser therapy, and hyperbaric oxygen. It is beyond the scope
of this text to discuss each of these at length. Table 12.13 is
a brief summary of their methods of action, indications, and
contraindications. Reimbursement for the use of adjunctive
therapies varies, and therapists should be aware of third-party
payer regulations. 
Physical Therapy Management
The responsibility and autonomy of the physical therapist
in the treatment of wounds varies greatly among facilities
and by state practice act. The physical therapist in any set-
ting can, and should, play a key role in the patient’s clini-
cal course of wound prevention, initiation of a wound care
plan, and recommendations for activity and footwear modi-
fications and positioning aids. The physical therapist in the
acute care setting can also make recommendations regarding
ongoing wound care upon discharge from the hospital. Unless
the wound is superficial, wound closure is not likely to occur
during the acute care phase. Therefore the ultimate long-term
months, occurs at a different level of care, usually outpatient
or home care.
The following are the primary goals of physical therapy for
wound treatment in the acute care setting:
• To promote wound healing through wound assessment,
cleaning, bioburden management, debridement, and dress-
ing selection and application
• To educate patients and caregivers regarding appropriate
management for an existing wound and the prevention of
further breakdown and future wounds
• To maximize patient mobility and function while accom-
modating needs for wound healing (e.g., maintaining non–
weight-bearing status)
• To minimize pain
• To provide recommendations for interdisciplinary 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 intervention. 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 be
part of an interdisciplinary team that may include one or more
care nurse (enterostomal therapist), dietitian, and others. The
physical therapist should be aware of and make proper recom-
mendations to the appropriate personnel for all of the patient’s
needs for healing.
Specific considerations for physical therapy intervention
with a patient who has a wound include pain management,
ROM, strengthening, functional mobility, edema management,
and wound prevention (Table 12.14).

TABLE 12.12  Indications and Uses of Basic Types of Dressings
Type of Dressing Description
Gauze, including Highly porous; available in woven
impregnated and nonwoven forms (pads, strips,
gauze rolls)
Transparent film Polyurethane sheet with an adhesive
layer on one side
Hydrocolloids 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
Hydrogels Water- or glycerin-based dressings
available in sheets, amorphous gels,
or impregnated gauzes
Foams Polyurethane foam with a hydrophilic
inner surface and a hydrophobic
outer surface
Calcium alginates, Calcium alginate: Fibrous sheet or
hydrofibers rope derived from seaweed-based
calcium and sodium salts. Upon
contact with wound exudate, ion
exchanges convert the
dressing to a viscous gel
Hydrofiber: similar in appearance and
action though composed of sodium
carboxymethylcellulose
Collagen matrix Collagen derived from bovine
material, processed and shaped into
sheets, particles, or gels
Topical ointments Water- or petrolatum-based creams,
gels, and ointments (antimicrobials,
growth factors, silver, enzymes,
anesthetics)
Data from Bryant RA, Nix DP. Principles of wound healing and topical management. In: Bryant R, Nix D, eds. Acute and Chronic Wounds: Current Management Concepts.
5th ed. St. Louis: Elsevier; 2016:307-324; Powers JG, Higham C, Broussard K, Phillips TJ. Wound healing and treating wounds: chronic wound care and management.
J Am Acad Dermatol. 2016;74(4):607-625; Sussman G. Management of the wound environment with dressings and topical agents. In: Sussman C, Bates-Jensen B, eds.
Wound Care: A Collaborative Practice Manual for Health Professions. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2012:502-521.
Integumentary System     CHAPTER 12 323
Indications Advantages/Disadvantages
May be used for any type of Readily available and inexpensive
wound if properly applied and Dry gauze does not maintain a moist wound
removed (although other dress- environment, but may be useful in
ings may be more effective) management of highly exudating wounds
Some come impregnated with Impregnated gauzes used as a contact layer can
petroleum, hydrogel, hyper- minimize adherence to granulation tissue
tonic saline, bismuth, or zinc Topical ointments can be added to some gauze
dressings
Autolytic debridement, to Conforms and adheres well to dry skin surface,
reduce friction, superficial promotes autolysis, allows visualization of the
wounds with minimal drainage wound with dressing in place, permeable to
gaseous exchange, impermeable to water and
bacteria, cost-effective
Minimal to no absorptive qualities
Partial- or full-thickness wounds Prevent secondary wound infection
with low to moderate drainage, Impermeable to contaminants
including partially necrotic Available in many forms (pastes, powders, and
wounds sheets)
Promotes a moist wound May come with adhesive edging or require
environment, autolysis, and secondary dressing to secure
granulation formation Changed infrequently (every 3–5 days)
May not be able to manage copiously draining
wounds
Any wound with minimal Requires secondary dressing to cover
drainage; promotes moist Monitor periwound for maceration
environment and autolysis
Beneficial in rehydrating
desiccated nonviable tissue for
debridement or maintaining
moisture content and viability
of exposed structures
Partial- or full-thickness wounds Nonadherent to wound surface unless drainage
with moderate to heavy dries; may come with adhesive edging or
drainage require tape or secondary dressing to secure
Highly absorbable and conformable
Permeable to oxygen (reduced risk of anaerobic
infection)
Partial- and full-thickness Highly conformable; requires secondary
wounds with moderate to dressing to cover
heavy amounts of drainage, Alginates possess hemostatic properties as a
infected or noninfected wounds result of released calcium; hydrofibers do not
Provides a moist wound have this same property
environment to facilitate
autolysis
Any recalcitrant, full-thickness Conforms to wound bed; requires secondary
wound dressing to cover
Facilitates deposition of Promotes granulation
collagen Hemostatic properties
Wounds requiring topical agents Provides local application of antimicrobials,
to minimize infection or pain bypassing systemic administration
or to promote wound healing May assist in maintaining moist environment
324 CHAPTER 12     Integumentary System

TABLE 12.13  Adjunctive Therapies in Wound Care

Intervention Method of Action
Negative-pressure Application of continuous or intermit-
wound therapy tent localized subatmospheric pressure
(NPWT); via a specialized porous dressing and
vacuum-assisted mechanical vacuum pump
closure Removal of exudate, reduction in edema
and bioburden, maintenance of moist
wound environment, increase in blood
flow
Produces a mechanical deformation of
cells, stimulating all phases of wound
healing
Ultrasound (US) Transmission of acoustic energy to tissues
Stimulation of growth factor release
and cellular activity in all phases of
healing; increase in capillary perfusion;
improved collagen deposition and scar
tensile strength; debridement; and
reduction in pain, edema, and bioburden
Benefits vary depending on settings
(e.g., frequency and intensity)
Electrical Transfer of electrical current into tissues
stimulation Stimulation of cellular migration and
proliferation, increase in localized
blood flow and perfusion, and
reduction in edema and bioburden
Ultraviolet (UV) Exposure to nonthermal UV radiation
light therapy for bactericidal effects. UVC most
effective with 99.99% eradication of
common pathogens
Low-level laser Exposure to infrared light in the
therapy (LLLT) 600–1200 nm range
Stimulation of cellular proliferation
and activity in all phases of healing;
enhanced rates of tissue repair and
healing; and decreased inflammation,
pain, and edema
Hyperbaric oxygen Inhalation of 100% O2 at greater than 1.4 Specific to wound care in-
therapy (HBOT, atmospheres absolute pressure (ATA)
HBO) Typically at 2–2.5 ATA
Tissue hyperoxygenation, edema
reduction, stimulation of angiogen-
esis and granulation formation, and
reestablishment of normal cellular
metabolism
Indications Contraindications
Acute, subacute, chronic, Presence of eschar, untreated osteomyelitis, or
traumatic, and dehisced malignancy in the wound; exposed vascu-
wounds (including surgical, lature, nerves, anastomotic sites, or organs;
neuropathic, pressure, and and nonenteric and unexplored fistulas
venous in origin); partial- Precaution: High risk of bleeding or
thickness burns; flaps; and hemorrhage, including concurrent use of
grafts anticoagulants, weakened blood vessels or
organs in the vicinity of the wound
Infected wounds must be monitored closely
with more frequent dressing changes than
the noninfected wound
Adjunct intervention for Over reproductive organs; eye; heart; carotid
chronic wounds—not de- sinus; exposed central nervous system tissue;
pendent on wound etiology malignancy or precancerous lesions; deep
venous thrombosis, emboli, severe athero-
sclerosis, or thrombophlebitis; pacemaker
Precaution: Over active epiphyseal plates,
implanted metal or plastic components,
sensory neuropathy, superficial bony areas,
acute infection
Adjunct intervention for In region of malignancy, active osteomyeli-
chronic wounds—not de- tis, or known peripheral vascular disease;
pendent on wound etiology over electrical implants, eyes, pregnant
uterus, or central nervous system
structures, such as carotid bodies and
phrenic nerve
In combination with topical agents
containing metal ions
Precaution: Cardiac dysfunction, seizure
disorders
Chronic wounds with high History of skin cancer; radiation therapy
levels of bioburden or ne- anywhere on the body in the last 3
crotic tissue months; systemic lupus erythematosus;
sarcoidosis; over the eye; presence of fever
or erythema from previous treatment;
malignancy; tuberculosis; cardiac, renal,
or liver disease; diabetes; HIV/AIDS;
hyperthyroidism; herpes simplex
Acute, chronic, and nonheal- Over a malignancy, the thyroid gland, or
ing wounds; infected or during the first trimester of pregnancy
colonized wounds Avoid direct exposure to eyes
Untreated pneumothorax, concurrent use of
cludes diabetic foot ulcers, certain chemotherapeutic agents
chronic osteomyelitis, nec- Precaution: Seizures, claustrophobia,
rotizing fasciitis, peripheral chronic obstructive pulmonary disease,
arterial insufficiency, acute, any condition impairing ability to
traumatic ischemia, and equalize ear pressure, pregnancy
preservation of compromised
skin grafts

Data from V.A.C. therapy clinical guidelines: a reference source for clinicians. Acelity website. https://www.acelity.com/healthcare-professionals/instructions-for-use.
Accessed November 20, 2018; Cordrey R. Ultraviolet light and ultrasound. In: Bryant R and Nix D, eds. Acute and Chronic Wounds: Current Management Concepts. 5th
ed. St. Louis: Elsevier; 2016:377-385; Sussman C, Dyson M. Therapeutic and diagnostic ultrasound. In: Sussman C, Bates-Jensen B, eds. Wound Care: A Collaborative
Practice Manual for Health Professions. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2012:684-726; Thakral F, LaFontaine J, Najafi B, et al. Electrical stimula-
tion to accelerate wound healing. Diabet Foot Ankle. 2013;4:22081; Sussman C. Electrical stimulation for wound healing. In: Sussman C, Bates-Jensen B, eds. Wound
Care: A Collaborative Practice Manual for Health Professions. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2012:577-628; Connor-Kerr T, Albaugh KW, Bell A.
Phototherapeutic applications for wound management. In: Sussman C, Bates-Jensen B, eds. Wound Care: A Collaborative Practice Manual for Health Professions. 4th ed.
Philadelphia: Lippincott Williams & Wilkins; 2012:669-683; Rashini S, Yadollahpour A, Mirzaiyan M. Low level laser therapy for the treatment of chronic wound:
clinical considerations. Biomed Pharmacol J. 2015;8(2):1121-1127; Niezgoda JA. Hyperbaric oxygen therapy: management of the hypoxic wound. In: Sussman C,
Bates-Jensen B, eds. Wound Care: A Collaborative Practice Manual for Health Professions. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2012:781-793; Latham E.
Hyperbaric oxygen therapy (website): https://emedicine.medscapte.com. Accessed November 20, 2018.
 Integumentary System     CHAPTER 12 325

TABLE 12.14  Physical Therapy Considerations for Wound Care

Physical Therapy Intervention Consideration
Pain management Coordinate physical therapy session with pain premedication.
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.
ROM, strength, and functional Adequate ROM is necessary for proper positioning and minimizing the risk of pressure injury formation.
mobility Care should be taken with manual contacts over fragile skin and to not disturb dressings during exercise.
Adequate strength is necessary for weight shifting and functional mobility with the maintenance of
weight-bearing precautions.
Edema management Depending on the etiology, intervention options to manage edema include exercise, compression therapy,
lymphatic drainage, limb elevation, or a combination of these. The therapist should be aware of any
medically related contraindications for these interventions.
Prevention 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, management of incontinence).
Pressure reduction surfaces (e.g., air mattress, wheelchair cushion).
Footwear adaptations (e.g., orthotics, inserts, extra-depth shoes).

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94. Armstrong DG, Laverly LA, Harkless LB. Validation of a
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95. Dowsett C, Gronemann MN, Harding K. Taking wound assess-
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96. Wilkins R, Unverdorben M. Wound cleaning and wound heal-
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97. Lloyd-Jones M. Wound cleansing: is it necessary, or just a
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the TIME paradigm. J Wound Care. 2016;25(suppl 3):S7–S9.
99. Wilson JR, Mills JG, Prather ID, Dimitrijevich SD. A toxicity
index of skin and wound cleansers used on in vitro fibroblasts
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102. Bates-Jensen BM, Serena T. Management of necrotic and nonvi-
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103. Kamoz LP, Wild T. Wound bed preparation: the impact of de-
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104. Atkin L. Understanding methods of wound debridement. Br J
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328 CHAPTER 12     Integumentary System
105. Gray D, Acton C, Chadwick P, et al. Consensus guidance
for the use of debridement techniques in the U. Wounds UK.
2011;7(1):77–84.
106. Dale BA, Wright DH. Say goodbye to wet-to-dry wound care
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107. Sussman C. Hydrotherapy. In: Sussman C, Bates-Jensen B, eds.
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108. Loehne HB. Pulsatile lavage with suction. In: Sussman C, Bates-
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109. Sibbald RG, Elliott JA, Ayello EA, Somayajo R. Optimizing
the moisture management tightrope with wound bed prepara-
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2016:307–324.
 13
C H APT ER  
CHAPTER OUTLINE
Introduction
Definition of Terms
Body Structure and Function
Evaluation
History
Physical Examination
Laboratory Studies
Health Conditions
Health Care–Associated or
Nosocomial Infections
Respiratory Tract Infections
Cardiac Infections
Neurologic Infections
Musculoskeletal Infections
Skin Infections
Gastrointestinal Infections
Immune System Infections
Sepsis
Management
Prevention
Medical Intervention
Lifestyle Management
Physical Therapy Management
APPENDIX 13A: Immune System
Disorders
Systemic Lupus Erythematosus
Sarcoidosis
Amyloidosis
Rheumatoid Arthritis
Infectious Diseases
Harold Merriman
CHAPTER OBJECTIVES
The objectives of this chapter are to provide a description of the following:
1. Clinical evaluation of common infectious diseases and immune system disorders, including physical exami-
nation and laboratory studies
2. Frequently encountered infectious diseases and immune system disorders, including etiology, pathogen-
esis, clinical presentation, and management
3. Precautions and guidelines that a physical therapist should implement when treating a patient with an
infectious diseases and immune system disorders
Introduction
A patient may be admitted to the hospital setting with an infectious disease process acquired in the
community or may develop one as a complication caused by the hospital environment. The cur-
rent terminology is to call this latter type of infection a health care–associated infection (HAI). It is
difficult to obtain recent numbers of HAIs in the United States, although in 2002, the estimated
number of HAIs in U.S. hospitals was 1.7 million, resulting in about 99,000 deaths.1 More recent
estimates of HAI rates is that 1 out of every 25 hospitalized patients is affected by an HAI.2 The
major source of HAI is likely the patient’s endogenous flora, but up to 40% of HAIs can be caused
by cross-infection via the hands of health care workers.3 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 dis-
ease processes is useful in designing, implementing, and modifying physical therapy treatment pro-
grams. The physical therapist may also provide treatment for patients who have immune system
disorders. These disorders are mentioned in this chapter because immune system reactions can be
similar to those of infectious diseases (see Appendix 13A for a discussion of four notable immune
system disorders: systemic lupus erythematosus, sarcoidosis, amyloidosis, and rheumatoid arthritis).
Definition of Terms
To facilitate understanding of how infectious diseases occur, terminology that is commonly
used when referring to infectious diseases is presented in Table 13.1.4-7 
Body Structure and Function
A person’s immune system is composed of many complex, yet synergistic, components that
defend against pathogens (Table 13.2).4 Any defect in this system may lead to the development
of active infection. Patients in the acute care setting often present with acquired factors that
can create some or most of these defects, which can ultimately affect their immune system (Box
13.1).5 Congenital factors, such as lymphocyte deficiency, occur rarely.
Evaluation
When an infectious disease 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 laboratory tests are further required to identify specific pathogens.8 
        329
330 CHAPTER 13     Infectious Diseases

TABLE 13.1  Terminology Associated with Infectious Diseases and Immune System Disorders
Term
Antibody
Antigen (immunogen)
Carrier
Colonization
Communicable
Disseminated host
Health care–associated
infection (HAI)
Immunocompromised
Immunodeficiency
Immunosuppression
Nosocomial infection
Opportunistic
Pathogen
Subclinical infection
Definition
A highly specific protein that is manufactured in response to antigens and defends against subsequent infection
An agent that is capable of producing antibodies when introduced into the body of a susceptible person
A person who harbors an infectious agent that can cause a specific disease but who demonstrates no evidence of the disease
The process of a group of organisms living together; the host can carry the microorganism without being symptom-
atic (no signs of infection)
The ability of an infective organism to be transmitted from person to person, either directly or indirectly
Distributed over a considerable area
The person whom the infectious agent invades and from whom it gathers its nourishment
Localized or systemic condition resulting from an adverse reaction to the presence of an infectious agents(s) or its
toxin(s); there must be no evidence that the infection was present or incubating at the time of admission to the
acute care setting
An immune system that is incapable of a normal response to pathogenic organisms and tissue damage
Decreased or compromised ability to respond to antigenic stimuli by appropriate cellular immunity reaction
The prevention or diminution of the immune response, as by drugs or radiation
Infection acquired in the hospital setting; note that this has been replaced by the term HAI (see above)
An infectious process that develops in immunosuppressed individuals (Opportunistic infections normally do not
develop in individuals with intact immune systems.)
An organism capable of producing a disease
A disease or condition that does not produce clinical symptoms, or the period before the appearance of disease-
specific symptoms

TABLE 13.2  Components of the Immune System

Lines of Defense Components Description
First line of defense Skin, conjunctivae, mucous membranes Physical barriers to pathogens.
Second line of defense Inflammatory response Inflammatory response acts to (1) contain pathogens and (2) bring
immune cells to antigens 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)a B cells produce antibodies.
Cellular immunity (T cells)a T cells (1) augment production of antibodies; (2) directly kill
antigens; and (3) turn off immune system.
aB cells and T cells can also be referred to as B lymphocytes and T lymphocytes, respectively.
Data from Rote NS. Immunity. In: Huether SE, McCance KL, eds. Understanding Pathophysiology. 2nd ed. St. Louis: Mosby; 2000:125-150; Marieb EN, ed. Human
Anatomy and Physiology. 2nd ed. Redwood City, CA: Benjamin Cummings; 1992:690-723; Guyton AC, Hall JE. Textbook of Medical Physiology. 9th ed. Philadelphia:
Saunders; 1996:445-455.

History BOX 13.1  Factors Affecting the Immune System

Potential contributing factors of the infection are sought out,
such as immunocompromise, immunosuppression, recent expo-
sure to infectious individuals, or recent travel to foreign coun-
tries. Also, a qualitative description of the symptomatology is
discerned, such as onset or nature of symptoms (e.g., a nonpro-
ductive versus productive cough over the past days or weeks).  • Age
Physical Examination
Observation
Clinical presentation of infectious diseases is highly variable
according to the specific system involved. However, common
physical findings that occur with infection include sweating
• P  regnancy
• Preexisting infections
• Malignancies (Hodgkin’s disease, acute or chronic leukemia,
nonlymphoid malignancy, or myeloma)
• Stress (emotional or surgical—anesthesia)
• Malnutrition (insufficiency of calories, protein, iron, and zinc)
• Chronic diseases (diabetes, alcoholic cirrhosis, sickle cell anemia)
• Lymph node dissection
• Immunosuppressive treatment (corticosteroids, chemotherapy,
or radiation therapy)
• Indwelling lines and tubes
Data from Rote NS, Heuther SE, McCance KL. Hypersensitivities, infection,
and immunodeficiencies. In: Heuther SE, McCance KL, eds. Understanding
Pathophysiology. 2nd ed. St. Louis: Mosby; 2000:204-208.

and inflammation, both of which are related to the metabolic
response of the body to the antigen. The classic signs of inflam-
mation (redness [rubor], and swelling [tumor]) in certain areas
of the body can help delineate the source, location(s), or both of
infection. Delineating the source of infection is crucial to the
diagnostic process.  (WBC) count, and antibody measurement.11
Palpation
The presence of warmth (calor) and possible pain (dolor) or ten-
derness is another typical classic sign of inflammation that may be
consistent with active infection. Lymphoid organs (lymph nodes
and spleen) can also be swollen and tender with infection because
lymphocytes (processed in these organs) are multiplying in response
to the antigen. Inflammation and tenderness in these or other areas
of the body can further help delineate the infectious process.  from baseline, termed leukopenia, can indicate altered immunity
Vital Signs
Heart Rate, Blood Pressure, and Respiratory Rate. Mea-
surement of vital signs helps in determining whether an infec-
tious process is occurring. (Infections result in an increased
metabolic rate, which presents as increased heart rate and respi-
ratory rate.) Blood pressure may also be elevated when the rate of
metabolism is increased, or blood pressure can be decreased sec-
ondary to vasodilation from inflammatory responses in the body.  of these changes can assist in identification of the type of infec-
Temperature. Monitoring the patient’s temperature over
time (both throughout the day and daily) provides information
regarding the progression (a rise in temperature) or a regres-
sion (a fall in temperature) of the infectious process. With an
infectious process, some of the bacteria and extracts from normal
leukocytes are pyrogenic, causing the thermostat in the hypo-
thalamus to rise, resulting in an elevated body temperature.9 A
fall in body temperature from a relatively elevated temperature
may also signify a response to a medication.
 CLINICAL TIP
An afebrile status is not always indicative of absence of infection.
If a patient is on antipyretics, the fever symptoms may be con-
trolled. Check the medication list, and ask about the administra-
tion schedule. A patient must be afebrile for at least 24 hours
before being discharged from an inpatient setting.
 
Auscultation
Heart and lung sounds determine whether infectious processes
are a direct result of any disorders in these areas or are indirectly
affecting these areas. Refer to Chapters 3 and 4, respectively, for
more information on heart and lung auscultation.  Gram stain is used to differentiate similar organisms by cat-
Laboratory Studies
Most of the evaluation process for diagnosing an infectious dis-
ease is based on laboratory studies. These studies are performed
to (1) isolate the microorganisms from various body fluids or
sites; (2) directly examine specimens by microscopic, immu-
nologic, or genetic techniques; or (3) assess specific antibody
responses to the pathogen.10 This diagnostic process is essential
for prescribing the most specific medical regimen possible for
the patient.
Infectious Diseases     CHAPTER 13 331
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 procedures used to diagnose
infection include leukocyte count, differential white blood cell
Leukocyte Count. Leukocyte, or WBC, count is measured
to determine whether an infectious process is present and should
range between 5000 and 10,000 cells/mm3.4 An increase in the
number of WBCs, termed leukocytosis, is required for phagocy-
tosis (cellular destruction of microorganisms) and can indicate
the presence of an acute infectious process.12 Leukocytosis can
also be present with inflammation and may occur after a surgery
with postoperative inflammation.9 A decreased WBC count
or the presence of an infection that exhausts supplies of certain
WBCs.12 A decreased WBC count relative to a previously high
count (i.e., becoming more within normal limits) may indicate
the resolution of an infectious process.12 
Differential White Blood Cell Count. Five types of WBCs
exist: lymphocytes, monocytes, neutrophils, basophils, and
eosinophils. Specific types of infectious processes can trigger
alterations in the values of one or more of these cells. Detection
tion present. For example, an infection caused by bacteria can
result in a higher percentage of neutrophils, which have a nor-
mal range of 2 to 7.5 × 109/L. In contrast, a parasitic infection
will result in increased eosinophils, which have a normal count
of 0 to 0.45 × 109/L.12 
Antibody Measurement. Antibodies develop in response
to the invasion of antigens from new infectious agents. Iden-
tifying the presence and concentration of specific antibodies
helps in determining past and present exposure to infectious
organisms.13 
Microbiology
In microbiology studies, specimens from suspected sources of
infection (e.g., sputum, urine, feces, wounds, and cerebrospinal
fluid) are collected by sterile technique and analyzed by stain-
ing, culture, or sensitivity or resistance testing, or a combina-
tion of all of these.
Staining. Staining allows for morphologic examination 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 differen-
tial Gram stain is the most common.13
egorizing them as gram positive or gram negative. This separa-
tion assists in determining subsequent 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.14 A red
specimen at completion indicates a gram-negative organism,
whereas a violet specimen indicates a gram-positive organism.14 
Culture. The purpose of a culture is to identify and produce
isolated colonies of organisms found within a collected speci-
men. Cells of the organism are isolated and mixed with specific
media that provide the proper nourishment and environment
332 CHAPTER 13     Infectious Diseases
(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.14 
Sensitivity and Resistance. When an organism has been
isolated from a specimen, its sensitivity (susceptibility) to anti-
microbial agents or antibiotics is tested. An infectious agent is
sensitive to an antibiotic when the organism’s growth is inhib-
ited 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 changing constantly.15  diagnostic studies can be performed to help with the differential
Cytology
Cytology is a complex method of studying cellular structures,
functions, origins, and formations. Cytology assists in differen-
tiating between an infectious process and a malignancy and in
determining the type and severity of a present infectious process
by examining cellular characteristics.13,16 It is beyond the scope
of this text, however, to describe all of the processes involved in
studying cellular structure dysfunction. 
Body Fluid Examination
Thoracocentesis. Thoracocentesis also known as thoracente-
sis or pleural tap, 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 thoracocentesis may also
be performed to drain excessive pleural fluid in large pleural
effusions.17  the Centers for Disease Control and Prevention (CDC) has used
Pericardiocentesis. Pericardiocentesis is a procedure 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.18  staphyloccoci.32,27,28 Patients who are at risk for developing
Synovial Fluid Analysis. Synovial fluid analysis, or arthro-
centesis, involves aspirating synovial fluid from a joint capsule.
The fluid is then analyzed and used to assist in diagnosing infec-
tions, rheumatic diseases, and osteoarthritis, all of which can
produce increased fluid production within the joint.19  tes, or acquired immunodeficiency syndrome [AIDS])
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 tuber-
culosis (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 confirm the
diagnosis of TB.17,20 Historically, gastric lavage has also been
administered as a medical intervention to prevent absorption of
ingested toxins in the acutely poisoned patient, although its use
for this purpose is now rarely recommended.21  6. Agitation: Resulting in removal of medical equipment, such as
Peritoneal Fluid Analysis. Peritoneal fluid analysis, or
paracentesis, is the aspiration of peritoneal 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 systemic
malfunctions, diseases, infections, such as spontaneous bacterial
peritonitis (SBP), or malignancies; and (3) help detect the pres-
ence of abdominal trauma.17,20,22 
Other Studies
Imaging with plain x-rays, computed tomography (CT) scans,
positron emission tomography (PET), and magnetic resonance
imaging (MRI) can also help identify areas with infectious
lesions.23,24 Minuscule amounts of pathogens can be detected
by using molecular biology techniques, such as enzyme-linked
immunosorbent assay (ELISA), radioimmunoassay (RIA), and
polymerase chain reaction (PCR).25,26 In addition, the following
diagnosis of the infectious process. For a description of these
studies, refer to the sections and chapters indicated below:
• Sputum analysis (see Chapter 4)
• Cerebrospinal fluid (see Chapter 6)
• Urinalysis (see Chapter 9)
• Wound cultures (Chapter 12) 
Health Conditions
Various infectious diseases, which are commonly encountered in
the acute care setting, are described in the following sections. Cer-
tain diseases that are not included in this section are described in
other chapters. (Please consult the index for assistance.)
Health Care–Associated or Nosocomial Infections
Nosocomial infection is an older general term that refers to an
infection that is acquired in the hospital setting. Since 2008,
the generic term health care–associated infections instead of nosoco-
mial infections.7 Many pathogens can cause an HAI, but the most
commonly reported bacteria in past years have been Clostridium
difficile, Escherichia coli, Staphylococcus aureus, Enterococcus faecalis,
Pseudomonas aeruginosa, Candida albicans, and coagulase-negative
HAIs are those with the following characteristics29:
1. Age: The very young or the very old
2. Immunodeficiency: Chronic diseases (cancer, chronic renal dis-
ease, chronic obstructive pulmonary disease [COPD], diabe-
3. Immunosuppression: Chemotherapy, radiation therapy, or corti-
costeroids
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/or therapeutic procedures: Indwell-
ing urinary catheters, monitoring devices, intravenous (IV)
catheters, and mechanical ventilation with intubation
central venous catheters or self-extubation of artificial airways
7. Surgery: Incisions provide access to pathogens
8. Burns: Disrupt the skin’s first line of defense
9. Length of hospitalization: Increases exposure to pathogens and
medical interventions
 Infectious Diseases     CHAPTER 13 333

TABLE 13.3  Summary of Precautions to Prevent Infection

Precaution Description Potential Pathogens
Standard Wash hands before and after each patient contact. Wear a different set of gloves with each pa- Treat all patient situations
tient. Also, equipment or items in the patient environment likely to have been contaminated as potentially infectious.
with infectious body fluids must be handled in a manner to prevent transmission of infectious
agents (e.g., wear gloves for direct contact, contain heavily soiled equipment, properly clean
and disinfect or sterilize reusable equipment before use on another patient).
The application of Standard Precautions during patient care is determined by the nature of the
HCW-patient interaction and the extent of anticipated blood, body fluid, or pathogen expo-
sure. If splashing of body fluids is likely, wear a mask or face shield, or both, and a gown.
Respiratory Hygiene/Cough Etiquette is a new element of Standard Precautions and includes
source control measures (e.g., covering the mouth/nose with a tissue when coughing, promptly
disposing of used tissues, using surgical masks on the coughing person when tolerated and ap-
propriate); hand hygiene after contact with respiratory secretions; and spatial separation, ideally
>3 feet, of persons with respiratory infections in common waiting areas when possible. Cover-
ing sneezes and coughs and placing masks on coughing patients are proven means of source
containment that prevent infected persons from dispersing respiratory secretions into the air.
Airbornea A respirator (preferable) or mask is required in situations in which contagious pathogens can be Rubeola virus (measles),
transmitted by airborne droplet nuclei, which can stay in the air for more than an hour and varicella (chickenpox),
can travel >10 feet because of their small size (<5 μm). tuberculosis, and possibly
The preferred placement for patients who require Airborne Precautions is in an airborne infec- SARS (severe acute respi-
tion isolation room (AIIR). An AIIR is a single-patient room that is equipped with special air ratory syndrome).
handling and ventilation capacity (e.g., negative pressure).
In settings where Airborne Precautions cannot be implemented due to limited engineering
resources (e.g., physician offices), masking the patient, placing the patient in a private room
(e.g., office examination room) with the door closed, and providing N95 or higher level
respirators or masks if respirators are not available for health care personnel will reduce the
likelihood of airborne transmission.
Health care personnel caring for patients on Airborne Precautions should don a mask or respi-
rator (depending on the disease-specific recommendations) before room entry. Whenever pos-
sible, nonimmune health care workers should not care for patients with vaccine-preventable
airborne diseases.
Patients on Airborne Precautions who must be transported outside of the room should wear a
mask if tolerated and follow Respiratory Hygiene/Cough Etiquette.
Dropleta A mask or face shield, or both, are required when large-particle (>5 μm in size) droplet transmission Haemophilus influenzae,
(usually 3 ft or less) is likely. Droplets can be generated from coughing, sneezing, and talking. Neisseria meningitidis,
Spatial separation of ≥3 feet and drawing the curtain between patient beds is especially impor- mycoplasmal pneumonia,
tant for patients in multi-bed rooms with infections transmitted by the droplet route. streptococcal pneumonia,
Health care personnel should wear a mask (a respirator is not necessary) for close contact with mumps, and rubella.
infectious patients, and the mask is generally donned upon room entry.
Patients on Droplet Precautions who must be transported outside of the room should wear a
mask if tolerated and follow Respiratory Hygiene/Cough Etiquette.
Contacta Gown and gloves are required when pathogens are transmitted by direct person-to-person Acinetobacter baumannii,
contact or person-to-object contact. It is important to use disposable or dedicated patient-care Clostridium difficile, Esch-
equipment (e.g., gait belt) and to don PPE upon room entry and discard it before exiting the erichia coli, herpes simplex
patient room. virus, herpes zoster, meth-
Patients on Contact Precautions who must be transported outside of the room should have the icillin-resistant Staphy-
infected or colonized areas of the patient’s body covered or contained. lococcus aureus (MRSA),
The term enteric contact precautions may be used when a person is infected with C. difficile, norovirus, rotavirus and
rotavirus, or norovirus to stress that the health care worker must clean the hands after patient vancomycin-resistant
contact with soap and water hand washing instead of using an alcohol-based handrub. Enterococcus (VRE).
aThese precautions are in addition to practicing Standard Precautions.
PPE, Personal protective equipment.
Data from Centers of Disease Control, https://www.cdc.gov/infectioncontrol/basics/standard-precautions.html, https://www.cdc.gov/infectioncontrol/basics/transmission-
based-precautions.html, https://www.cdc.gov/infectioncontrol/pdf/guidelines/isolation-guidelines-H.pdf. Accessed June 26, 2019.

The mode of transmission for pathogens that cause HAIs are
contact, droplet, and airborne. Pathogens can also cause oppor-
tunistic infections in patients who are immunocompromised or
immunosuppressed. Medical devices, such as catheters, venti-
lators, and central lines, frequently cause infection. Common
sites for HAIs are the urinary tract, surgical wounds, joints, and
the lower respiratory tract (e.g., pneumonia). Clinical manifes-
tations and management of HAIs vary, according to the type
of pathogen and the organ system involved. However, the pri-
mary management strategy for HAIs is prevention by follow-
ing the standard and specific precautions outlined in Table
13.3.10,27,30,31
334 CHAPTER 13     Infectious Diseases
 CLINICAL TIP
Prevention or minimizing the risk of developing pneumonia in
patients who have been on bed rest and/or on mechanical inter-
vention can be achieved through airway clearance and increased
mobility. (Refer to Table 4.12, Dean’s Hierarchy for Treatment
of Patients with Impaired Oxygen Transport.)
Antibiotic-Resistant Infections
The number of antibiotic-resistance infections is still a major
concern in health care facilities. According to the CDC, approxi-
mately 30% to 50% of antibiotic use in hospitals and in long-
term care facilities is unnecessary or inappropriate.32 In response
to this problem, the CDC has launched a program called “Be
Antibiotics Aware,” whose goals include reducing unneces-
sary antibiotic use (resulting in less antimicrobial resistance),
decreasing health care costs, and improving patient outcomes in
hospitals and long-term care facilities.33
Microbial experts from the European Centre for Disease Pre-
vention and Control and from the CDC in the United States have
recently developed interim standard terminology to describe
this resistance.34 They developed three major definitions for
resistance: multidrug-resistant (MDR), extensively drug-resis-
tant (XDR), and pandrug-resistant (PDR) bacteria. The agreed-
on definitions are as follows: MDR as acquired nonsusceptibility
to at least one agent in three or more antimicrobial categories;
XDR as nonsusceptibility to at least one agent in all but two
or fewer antimicrobial categories (i.e., remaining susceptible to
only one or two categories); and PDR as nonsusceptibility to all
agents in all antimicrobial categories.
Methicillin-Resistant Staphylococcus aureus Infection.
Methicillin-resistant S. aureus (MRSA) is a strain of Staphylo-
coccus that is resistant to methicillin or similar agents, such as
oxacillin and nafcillin. Methicillin is a synthetic form of peni-
cillin 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 methi-
cillin. Community-acquired MRSA typically manifests itself
as a skin infection, whereas in health care settings MRSA can
cause serious problems such as sepsis, pneumonia, and surgical
site infections. Indiscriminate use of antibiotic therapy is sug-
gested to have a primary role in the increased incidence of this
HAI.31,35
In addition, patients who are at risk for developing MRSA
infection in the hospital are those who35-37:
• Are debilitated, of advanced age, 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 through person-to-person
contact or person-to-object-to-person contact. MRSA can
survive for prolonged periods of time on inanimate objects,
such as gait belts, walkers, wheelchairs, telephones, bed rails,
and tray tables, unless such objects are properly sanitized. Hos-
pital personnel can be primary carriers of MRSA because the
bacterium can colonize healthy adults. MRSA infections can be
diagnosed via nasal swabs.38,39
Management of MRSA infections is difficult and may consist
of combining local and systemic antibiotics, increasing antibi-
otic 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. aureus [VISA]).31 Therefore pre-
vention of MRSA infection is the primary treatment strategy
and includes the following27,35-37:
• 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 Enterococcus Infection. Vanco-
mycin-resistant Enterococcus (VRE) infection is another HAI
that has become resistant to vancomycin, aminoglycosides, and
ampicillin. The infection can develop as endogenous entero-
cocci (normally found in the gastrointestinal tract or the female
reproductive tract) become opportunistic pathogens in patient
populations similar to those with MRSA. VRE infections can be
diagnosed via rectal swab.27,31,40,41
Transmission of the infection can also occur via (1) direct
patient-to-patient contact, (2) indirect contact through asymp-
tomatic 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 entero-
cocci can withstand harsh environments and easily survive on
the hands of health care workers and on hospital objects. Treat-
ment options are very limited for patients with VRE infection,
and the best intervention plan is to prevent the spread of the
infection.31 Strategies for preventing VRE infections include
the following40:
• The controlled use of vancomycin
• Timely communication between the microbiology laborato-
ry and appropriate personnel to initiate contact precautions
as soon as VRE is detected
• Implementation of screening procedures to detect VRE infec-
tion 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 pa-
tient’s room), and washing hands immediately after working
with an infected patient
• Designating commonly used items, such as stethoscopes,
blood pressure cuffs, and rectal thermometers, to be used
only with VRE patients
• Disinfecting any item that has been in contact with VRE
patients with a hospital-approved cleaning agent 

Multidrug-Resistant Acinetobacter baumannii. Over
the past decade, infection with Acinetobacter baumannii (AB)
has become one of the most difficult to effectively treat because
this pathogen easily acquires a wide spectrum of antimicrobial
resistance, resulting in the commonly found MDR and the
much more serious, but fortunately rarer, PDR forms. It is a
gram-negative coccobacillus that has become one of the most
important pathogens, particularly in the intensive care unit
(ICU). AB infections in the hospital can cause serious com-
plications, such as ventilator-associated pneumonia (VAP),
bloodstream infection, wound infections, and nosocomial
meningitis.42,43
AB is remarkable in that it is ubiquitous, exists in diverse
habitats (e.g., human skin), can survive for long periods of
time on dry inanimate surfaces (e.g., hospital bed rails) and,
as already mentioned, can acquire antimicrobial resistance
extremely rapidly. These factors combined, especially the
latter two, greatly facilitate MDR-AB outbreaks in the ICU,
in physical therapy wound clinics and even multifacility
outbreaks.44,45 Fortunately, strict infection-control measures
(e.g., contact isolation precautions outlined in Table 13.3
and in guidelines for physical therapy intervention at the
end of the chapter) can decrease health care staff and envi-
ronmental colonization and/or contamination.46 MDR-AB
and PDR-AB infections can also be prevented by following
the previously mentioned guidelines effective against MRSA
and VRE.
 CLINICAL TIP
Equipment used during physical therapy treatments for patients
with antibiotic-resistant bacteria (e.g., MRSA, VRE, or MDR-AB),
such as assistive devices, gait belts, stethoscopes, 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 equip-
ment shortage, thorough cleaning of equipment is necessary
before using it with other patients. Linens, hospital curtains,
and laboratory coats also need to be properly cleaned to avoid
transmission of infection. Health care workers should change
their clothes before leaving the facility especially if the clothes
are soiled.
 
Respiratory Tract Infections
Infections of the respiratory tract can be categorized as upper
respiratory tract infections and lower respiratory tract infec-
tions. Upper respiratory tract infections (affecting the nose,
nasal passages, paranasal sinuses, pharynx, and larynx above
the vocal cords) that are discussed in this section include aller-
gic and viral rhinitis, sinusitis, influenza, and pertussis. Lower
respiratory tract infections (affecting the larynx below the vocal
cords, trachea, bronchi, and lungs) that are discussed in this sec-
tion include TB, histoplasmosis, legionellosis, and severe acute
respiratory syndrome. Pneumonia is the most common lower
respiratory tract infection and is discussed under Health Condi-
tions in Chapter 4.
Infectious Diseases     CHAPTER 13 335
 CLINICAL TIP
Measles is a highly contagious viral respiratory illness that is ap-
pearing with increasing frequency in areas of the United States
with lower vaccination rates. A maculopapular rash appears
about 14 days after a person is exposed, and an infected person
is contagious from 4 days before to 4 days after appearance of
the rash. A single dose of the measles-mumps-rubella (MMR)
vaccine is 93% effective at preventing measles.
Airborne precautions should be followed. If a health care
worker without evidence of immunity is exposed to measles, he
or she should be given the MMR vaccine within 72 hours and
should not report to work from day 5 after first exposure to day
21 after last exposure. Pregnant women should not be given the
MMR vaccine.
Upper Respiratory Tract Infections
Rhinitis. Rhinitis is inflammation of the nasal mucous
membranes and can result from an allergic reaction or a viral
infection. Allergic rhinitis is commonly a seasonal reaction from
allergens, such as pollen, or a perennial reaction from environ-
mental 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 dis-
charge. In addition to these, clinical manifestations of viral
rhinitis include fever, malaise, headache, and thicker nasal
discharge.
Management of allergic rhinitis includes antihistamines,
decongestants, nasal corticosteroid sprays, and allergen avoid-
ance. Management of viral rhinitis includes rest, fluids, anti-
pyretics, and analgesics.47-50 
Sinusitis. Sinusitis is the inflammation or hypertrophy of
the mucosal lining of any or all of the facial sinuses (frontal, eth-
moid, 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, con-
gestion, fever, and malaise.
Management of sinusitis includes antibiotics (as appropri-
ate), decongestants or expectorants, and nasal corticosteroids.48
 CLINICAL TIP
Despite the benign nature of rhinitis and sinusitis, the manifes-
tations (especially nasal drainage and sinus pain) of these infec-
tions can cause significant discomfort to the patient and to the
physical 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 activ-
ity accordingly.
 
336 CHAPTER 13     Infectious Diseases
Influenza. Influenza (“the flu”) is caused by any of the influ-
enza viruses (A, B, or C and their mutagenic strains) that are
transmitted via aerosolized mucus droplets. These viruses have
the ability to change over time and is the reason 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 com-
munity. According to the CDC, with rare exceptions, everyone
6 months and older, including health care workers, should be
vaccinated annually against the influenza virus to decrease the
risk of influenza transmission.49
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 profuse discharge), and (8)
mild sore throat. Gastrointestinal signs and symptoms of
nausea, vomiting, abdominal pain, and diarrhea can also be
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 pneumonia,
especially in older adults and in individuals with chronic
diseases.4,5,17,48
 CLINICAL TIP
A rapid flu nasal swab test can help diagnose influenza. If results
have not come back or if they are positive, a simple face mask
should be worn to prevent transmission.
If management of influenza is necessary, it may include the
following4,5,17,48:
• Antiinfective agents
• Antipyretic agents
• Adrenergic agents
• Antitussive agents
• Active immunization by vaccines
• Supportive care with IV fluids and supplemental oxygen, as
needed  tions should be observed.
Pertussis. Pertussis, or whooping cough, is an acute bacte-
rial infection of the mucous membranes of the tracheobronchial
tree, and recently the number of cases has been increasing in the
United States.51 It occurs most commonly in children younger
than 1 year of age and in children and adults in lower socio-
economic groups. 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 contagious.52
Management of pertussis may include any of the
following17,52:
• 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  derivative of the bacilli.
Lower Respiratory Tract Infections
Tuberculosis. TB is a chronic pulmonary and extrapulmo-
nary infectious disease caused by the bacillus Mycobacterium
tuberculosis. It is transmitted through airborne particles, which
are expelled into the air when an individual with pulmonary or
laryngeal TB coughs or sneezes.53 When M. tuberculosis reaches
the alveolar surface of a new host, it is attacked by macro-
phages, and one of two outcomes can result: Macrophages kill
the particles, terminating the infectious process, or the par-
ticles 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 with TB and will test positive on
tuberculin skin tests, such as the Mantoux test, which uses
tuberculin purified protein derivative,a or the multiple punc-
ture test, which uses tuberculin. At this point, the infection
enters a latent period (most common) or develops into active
TB.53,54
A six-category classification system has been devised by the
American Thoracic Society (ATS) and the CDC to describe the
TB status of an individual.53,55
1. No TB 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)
 CLINICAL TIP
Patients with TB are placed in negative-pressure isolation rooms,
if available. This results in air flowing into but not out of the
isolation room, thus preventing the escape of contaminated air
into the rest of the building. Patients who are suspected of hav-
ing TB but have not been diagnosed with it are generally placed
on a “rule-out TB” protocol, in which case respiratory precau-
Populations at high risk for acquiring TB include (1) older
adults; (2) Native Americans, Eskimos, and African Ameri-
cans (in particular if they are homeless or economically disad-
vantaged); (3) incarcerated individuals; (4) immigrants from
Southeast Asia, Ethiopia, Mexico, and Latin America; (5) mal-
nourished individuals; (6) infants and children younger than 5
years of age; (7) those with decreased immunity (e.g., because of
AIDS or leukemia, or after chemotherapy); (8) those with dia-
betes mellitus, end-stage renal disease, or both; (9) those with
silicosis; and (10) those in close contact with individuals with
active TB.6,53
Persons with normal immune function do not normally
develop active TB after acquisition and are therefore not con-
sidered contagious. Risk factors for the development of active
aA 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
 Infectious Diseases     CHAPTER 13 337

TB after infection include age (children younger than 8 years

of age and adolescents are at greatest risk), low weight, and  CLINICAL TIP
immunosuppression.56 Facilities should provide health care workers with personal
When active TB does develop, its associated signs and protective equipment (PPE) effective against TB, such as either
symptoms include (1) fever, (2) an initial nonproductive specialized masks (e.g., N-95) or powered air-purifying respira-
cough, (3) mucopurulent secretions that present later, and tors (PAPRs) (Fig. 13.1) to wear around patients on respiratory
(4) hemoptysis, dyspnea at rest or with exertion, adventitious precautions even if the patient is in a negative-pressure isolation
breath sounds at lung apices, pleuritic chest pain, hoarseness, room. These types of PPE are protective against the airborne TB
and dysphagia, all of which may occur in the later stages. Chest mycobacteria. Always verify with the nursing staff or physician
films also show abnormalities, such as atelectasis or cavitation before working with these patients to determine which type of
involving the apical and posterior segments of the right upper PPE to wear.
lobe, the apical-posterior segment of the left upper lobe, or  
both.53
Extrapulmonary TB occurs with less frequency than pulmo- Histoplasmosis. Histoplasmosis is a pulmonary and sys-
nary TB but affects up to 70% of human immunodeficiency temic infection that is caused by infective spores (fungi), most
virus (HIV)–positive individuals diagnosed with TB.57 Organs commonly found in the soil of central and eastern United States.
affected include the meninges, brain, blood vessels, kidneys, Histoplasmosis is transmitted via inhalation of dust from the
bones, joints, larynx, skin, intestines, lymph nodes, peritoneum, soil or bird and bat feces. The spores form lesions within the
and eyes. When multiple organ systems are affected, the term lung parenchyma that can be spread to other tissues. The inci-
disseminated TB or miliary TB is used.57 Signs and symptoms dence of fungal infection is rising, particularly in immuno-
that manifest are dependent on the particular organ system or compromised, immunosuppressed, and chronically debilitated
systems involved. individuals who may also be receiving corticosteroid, antineo-
Because of the high prevalence of TB in HIV-positive plastic, and multiple antibiotic therapies.58,59
individuals (up to 60% in some states),57 it should be noted Different clinical forms of histoplasmosis are (1) acute,
that the areas of involvement and clinical features of the benign respiratory disease, which results in flulike illness and
disease in this population differ from those normally seen, pneumonia; (2) acute disseminated disease, which can result
particularly in cases of advanced immunosuppression. Brain in septic-type fever; (3) chronic disseminated disease, which
abscesses, lymph node involvement, lower lung involve- involves lesions in the bone marrow, spleen, and lungs and can
ment, pericarditis, gastric TB, and scrotal TB are all more result in immunodeficiency; and (4) chronic pulmonary disease,
common in HIV-positive individuals. HIV also increases which manifests as progressive emphysema.
the likelihood that TB infection will progress to active TB
by impairing the body’s ability to suppress new and latent
infections.57
Management of TB may include the following4,5,17:
• Antiinfective agents (see Chapter 19, Table 19.38, Antitu-
bercular Agents)
• Corticosteroids
• Surgical intervention to remove cavitary lesions (rare) and
areas of the lung with extensive disease or to correct hemop-
tysis, spontaneous pneumothorax, abscesses, intestinal ob-
struction, 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 puncture test)
• Vaccination for prevention
In recent years, new strains of M. tuberculosis that are resis-
tant to antitubercular drugs (e.g., isoniazid, rifampin, and
pyrazinamide) have emerged. These MDR-TB strains are
associated with fatality rates as high as 89% and are common
in HIV-positive 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 FIG. 13.1
Powered air-purifying respirator (PAPR). (From the National Person Pro-
they take their medications for the entire treatment regimen tective Technology Laboratory, The National Institute for Occupational
or for a brief period, respectively, in hopes of minimizing Safety and Health (NIOSH), Centers for Disease Control and Prevention,
resistance.57 Morgantown, WV.)
338 CHAPTER 13     Infectious Diseases
Management of histoplasmosis may include the
following17,58,60,61:
• Antiinfective agents
• Corticosteroids
• Antihistamines
• Antifungal therapy (see Chapter 19, Table 19.37, Antifungal
Agents)
• Supportive care appropriate for affected areas in the various
forms of histoplasmosis  Infections of the cardiac system can involve any layer of the
Legionellosis. Legionellosis is commonly referred to as Legion-
naire’s disease after a pneumonia outbreak in people who attended
an American Legion Convention in Philadelphia in 1976. It is
an acute bacterial infection primarily resulting in high fever
and pneumonia (patchy or confluent consolidation). Legionella
pneumophila causes more than 80% of all cases of legionellosis.
However, organs beside the lungs may also become involved,
especially in the immunocompromised patient. Other risk fac-
tors include underlying chronic pulmonary disease, smoking
history, and age greater than 50 years. Legionellosis is transmit-
ted by inhalation of aerosolized organisms from infected water
sources, such as air-conditioning cooling towers for large build-
ings, including hospitals. Additional examples of infected hos-
pital water sources have included shower heads, tap water from
respiratory devices, ice machines, decorative fountains, and even
distilled water.4,62-64
Primary clinical manifestations include high fever, pneu-
monia, malaise, myalgia, headache, and nonproductive cough.
Other manifestations can also include diarrhea, confusion and
other gastrointestinal symptoms. The disease is rapidly progres-
sive during the first 4 to 6 days of illness, with complications
that may include renal failure, bacteremic shock, and respiratory
failure.4,63
Management of legionellosis may consist of the following4:
• Antiinfective agents
• Supplemental oxygen with or without assisted ventilation
• Temporary renal dialysis
• IV fluid and electrolyte replacement  previously are then managed specifically. The general interven-
Severe Acute Respiratory Syndrome. The single-
stranded RNA coronavirus is responsible for severe acute
respiratory syndrome (SARS), which affects the epithelial
cells of the lower respiratory tract. Pathogenesis is not lim-
ited to the lungs but often includes mucosal cells of the
intestines, tubular epithelial cells of the kidneys, and brain
neurons. This new disease was first identified in China in late
2002 and then spread to the rest of the world in the spring
and summer of 2003, resulting in the first pandemic of the
twenty-first century. Of the approximately 8000 world-
wide cases that occurred during this pandemic, about 25%
of patients required mechanical ventilation in the ICU, and
about 10% of infected patients died.
SARS has flulike symptoms of fever, chills, cough, and mal-
aise along with frequent shortness of breath. A common cause of
death during this pandemic was diffuse alveolar damage (DAD).
In addition, SARS typically compromises the immune response,
which increases lung injury.
The 2003–2004 SARS pandemic showed that a prompt,
coordinated worldwide response could help contain the disease.
Although SARS was rapidly spread throughout the world by
international air travelers, the virus itself was not transmitted
through the air. Thus adherence to the basic infection control
practice of thorough hand washing, implemented with droplet
precautions, was able to ultimately stop this particular SARS
pandemic.65,66 
Cardiac Infections
heart (endocardium, myocardium, or pericardium) and gener-
ally result in acute or chronic depression of the patient’s cardiac
output. Infections that result in chronic cardiomyopathy most
likely require cardiac transplantation. Refer to Chapters 3 and
14 for a discussion of cardiomyopathy and cardiac transplanta-
tion, 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 β-streptococcal 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 (does not produce pus)
inflammatory lesions occurring in any or all of the connec-
tive tissues of the heart, joints, subcutaneous tissues, and cen-
tral nervous system (CNS). 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 dam-
age to the heart from the inflammatory process of rheumatic
fever.17,36,67,68
Cardiac manifestations can include pericarditis, myocarditis,
left-sided endocarditis, and valvular stenosis 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.17,36,67
Management of rheumatic fever follows the treatment for
streptococcal infection. The secondary complications mentioned
tion scheme may include the following17,36,67:
• 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 CNS and fortunately is in rapid decline, with global
eradication becoming a distinct possibility.69 There were
fewer than 200 cases of wild poliovirus worldwide in 2016
and 2017, and these cases occurred in only three countries
(Afghanistan, Nigeria, and Pakistan).70 Polioviruses are a
type of enteroviruses that multiply in the oropharynx and
intestinal tract.17,71

Poliomyelitis is usually transmitted directly via the fecal–
oral route from person to person but can also be transmitted
indirectly through consumption of water from contaminated
sources.71
Clinical presentation can range from subclinical infection,
to afebrile illness (24–36 hours), to aseptic meningitis, to
paralysis (after 4 days), and possibly to death. If paralysis
does occur, it is generally associated with fever and muscle
pain. The paralysis is usually asymmetric and involves mus-
cles of respiration, swallowing, and the lower extremities.
Paralysis can resolve completely, leave residual deficits, or
be fatal.17,71
Management of poliomyelitis primarily consists of preven-
tion with inactivated poliovirus (IPV) vaccine given in four
doses to children from 2 to 6 years of age.71 If a patient does
develop active poliomyelitis, then other management strategies
may include the following17:
• Analgesics and antipyretics
• Bronchopulmonary hygiene
• Bed rest with contracture prevention with positioning and
range of motion (ROM)
Postpoliomyelitis Syndrome. Postpoliomyelitis syndrome,
also known as postpolio syndrome, occurs 30 to 40 years after an
incidence 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 endurance. Muscle atrophy and
fasciculations may also be present. Patients who are older or
critically ill, have had a previous diagnosis of paralytic poliomy-
elitis, and are female are at greater risk for development of this
syndrome.71-73  enter a person’s nasal passages while he or she is swimming.
Meningitis
Meningitis, an inflammation of the meninges that cover the
brain and the spinal cord, results from acute infection by bac-
teria, viruses, fungi, or parasitic worms or from chemical irri-
tation. The route of transmission is primarily inhalation of
infected airborne mucus droplets released by infected individ-
uals or through the bloodstream via open wounds or invasive
procedures.74,75
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 respi-
ratory tract infection; and (4) viral (aseptic or serous) meningi-
tis, which is generally benign and self-limiting.
Bacterial meningitis is more severe than viral meningitis and
affects the pia mater, arachnoid and subarachnoid spaces, ven-
tricular system, and cerebrospinal fluid. The primary complica-
tions of bacterial meningitis 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,
or VIII) dysfunction.74,75
Infectious Diseases     CHAPTER 13 339
Management of any form of meningitis may include the
following17,74,76:
• Antimicrobial therapy, antiinfective agents, or immunologic
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 the brain and
spinal cord, commonly resulting from viral or amebic infection.
Types of encephalitis include infectious viral encephalitis, mos-
quito-borne viral encephalitis, and amebic meningoencephalitis.
Infectious viral encephalitis is transmitted via direct contact
with droplets from respiratory passages or other infected excre-
tions and is most commonly associated with herpes simplex type
1 virus (HSV-1). Viral encephalitis can also occur as a complica-
tion of systemic viral infections, such as poliomyelitis, rabies,
mononucleosis, measles, mumps, rubella, and chickenpox. Man-
ifestations of viral encephalitis can be mild to severe, with HSV
encephalitis having the highest mortality rate among all types
of encephalitides.17,74,75
Mosquito-borne viral encephalitis is transmitted via infec-
tious mosquito bites and cannot be transmitted from person to
person. The incidence of this type of encephalitis can be epi-
demic and typically varies according to geographic regions and
seasons.17,74,75
Amebic meningoencephalitis is transmitted in water and can
Amebic meningoencephalitis cannot be transmitted from per-
son to person.
General clinical presentation of encephalitis may include the
following17,74,75:
• Fever
• Signs of meningeal irritation from increased intracranial
pressure (e.g., severe frontal headache, nausea, vomiting, diz-
ziness, 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 following17:
• Antiinfective agents
• Intracranial pressure management
• Mechanical ventilation, with or without tracheostomy (as in-
dicated)
• Sedation
• IV fluids and electrolyte replacement
• Nasogastric tube feedings
340 CHAPTER 13     Infectious Diseases
 CLINICAL TIP
Mosquitos, ticks, lice, and fleas are common vectors that trans-
mit a variety of infectious diseases found in North America.
Common symptoms are fever, chills, headache, sore muscles,
skin rash, nausea, and stomach pain. Possible vector-borne dis-
eases include viral diseases transmitted by mosquitos (dengue,
chikungunya, West Nile virus infection, yellow fever, and Zika),
bacterial diseases transmitted by ticks (Lyme disease, Rocky
Mountain spotted fever, and tularemia) or by fleas (plague and
typhus fevers) and babesiosis, the malaria-like parasitic disease
transmitted by ticks. Vaccines already offer protection from
some of these diseases (e.g., yellow fever, dengue), and new
vaccines for other diseases (e.g., Lyme disease, West Nile virus
infection, Zika) are in development.77
 
Musculoskeletal Infections
Osteomyelitis is an acute infection of the bone that can result
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 hematogenous osteo-
myelitis and usually results from the spread of a systemic infec-
tion. Both these types can potentially progress to subacute and
chronic osteomyelitis. The term 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.78,79
Acute contagious osteomyelitis is an extension of the concur-
rent infection in soft tissues to the adjacent bony area. Trauma
resulting in compound fractures and tissue infections is a com-
mon example. Prolonged orthopedic surgery, wound drainage,
and chronic conditions such as diabetes or alcoholism also pre-
dispose patients to acute contagious osteomyelitis.79,80
Acute hematogenous osteomyelitis is a blood-borne infection
that generally results from S. aureus infection (80%)4 and occurs
mostly in infants; children (in the metaphysis of growing long
bones); or patients undergoing long-term IV therapy, hyperalimen-
tation, hemodialysis, or corticosteroid or antibiotic therapy. Patients
who are malnourished, are obese, have diabetes, or have chronic joint
disease are also susceptible to acute hematogenous osteomyelitis.78,79
 CLINICAL TIP
Performing electrical stimulation on untreated osteomyeli-
tis present in the base of the bone is contraindicated to avoid
premature wound closure, which can lead to abscess forma-
tion. Once the osteomyelitis responds favorably to antibiotic
treatment, then electrical stimulation may be used to promote
wound healing and closure.
Clinical presentations of both types of acute osteomyelitis
include (1) delayed onset of pain, (2) tenderness, (3) swelling,
and (4) warmth in the affected area. Fever is present with hema-
togenous osteomyelitis. The general treatment course for acute
osteomyelitis is early and aggressive administration of the appro-
priate antibiotics to prevent or limit bone destruction.4,60,78,79
Chronic osteomyelitis is an extension of the acute form
discussed previously. It results in marked bone destruction,
draining sinus tracts, pain, deformity, and the potential for
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 antibiotic
therapy. If the infection has spread to the surrounding soft tis-
sue and skin regions, then grafting, after debridement, may be
necessary. Good treatment results have also been shown with
hyperbaric oxygen therapy for chronic osteomyelitis.78,79
 CLINICAL TIP
Clarify weight-bearing orders with the physician when perform-
ing gait training with patients who have any form of osteomyeli-
tis. Both upper and lower extremities can be involved; therefore
choosing the appropriate assistive device is essential to prevent-
ing pathologic fractures.
 
Skin Infections
Cellulitis, or erysipelas, is a bacterial infection of the dermis
and the subcutaneous tissue that can remain localized or be dis-
seminated into the bloodstream, resulting in bacteremia (rare).
Cellulitis occurs most commonly on the face, neck, and legs and
is associated with an increased incidence of lymphedema.81
Groups A and G Streptococcus and S. aureus are the usual caus-
ative agents for cellulitis and generally gain entry into the skin
layers when there are open wounds (surgical wounds or ulcers).
Patients who are at most risk for developing cellulitis include
postsurgical patients and those immunocompromised as a result
of chronic diseases or medical treatment. The primary manifes-
tations of cellulitis are fever, with abrupt onset of hot, sting-
ing, and itchy skin and painful, red, thickened lesions that have
firm, raised palpable borders in the affected areas. Identify-
ing the causative agent through blood cultures is often diffi-
cult; therefore localized cultures, with samples collected from
open wounds if possible, may be more sensitive in helping to
delineate the appropriate antibiotic treatment.80,82,83 Other
skin infections frequently encountered in health care settings
are caused by viruses and parasites. HSV infections are usually
asymptomatic. HSV-1 causes oral herpes (“cold sores”) and can
be spread through kissing, sharing lip balm, or eating from the
same utensils, whereas HSV-2 causes genital herpes, a sexually
transmitted infection.84 Shingles is caused by varicella zoster
virus (VZV), which lies dormant in persons who had chick-
enpox in childhood and is characterized by a painful rash that
often presents in a dermatomal pattern on one side of the torso.
VZV can easily spread through direct contact with unscabbed
shingles blisters, but if these blisters are covered, the risk of
infection is low.85 Body lice and head lice infestations and sca-
bies are examples of parasitic infections that are spread through
close person-to-person contact as well as through contact with
an infected person’s clothing, personal items, or linens.86-88 
Gastrointestinal Infections
Gastroenteritis is a global term used for inflammation of the diges-
tive tract, typically as a result of infection. Bacterial sources of

gastroenteritis are often caused by E. coli, Shigella (which causes
bacterial dysentery), C. difficile, or Salmonella. In a study pub-
lished in 2014, C. difficile was estimated to be the single most
common pathogen causing 17.1% of all infections, including
gastroenteritis, in U.S. hospitals.2 Thus it is not surprising that
C. difficile infections are the leading cause of gastroenteritis-
associated death (14,000 deaths estimated in 2007).89 However,
most cases of gastroenteritis are caused by a variety of viruses
that are less deadly. Rotavirus and norovirus are, by far, the most
frequent causes of gastroenteritis; adenovirus and astrovirus also
commonly cause gastroenteritis, especially in children. Trans-
mission of both bacterial and viral gastroenteritis is usually
through ingestion of contaminated food, water, or both or via
direct and indirect fecal–oral transmission.
 CLINICAL TIP
Strict contact precautions with thorough hand washing using
water and soap and not an alcohol-based handrub (also known
as enteric precautions) should be observed with patients who
have a diagnosis of a C. difficile infection (whose spores can
persist on fomites and environmental surfaces for months) as
well as a rotavirus or norovirus infection. All of these pathogens
are relatively resistant to waterless alcohol-based antiseptics,
and they have been associated with contamination of both hos-
pital room surfaces and health care workers’ hands.
Of these aforementioned organisms, rotavirus (a double-
stranded RNA virus) infection is the most important cause of
severe diarrheal disease in young children. Historically rotavirus
has caused 500,000 childhood deaths annually in developing
countries around the world. In the United States, 50% of pediat-
ric gastroenteritis cases requiring hospitalization or emergency
room visits are caused by rotavirus, and the total health and
societal costs of rotavirus infections are estimated to exceed $1
billion per year. Fortunately the annual pediatric death rate in
the United States is relatively low (20 to 60 deaths). Rotavirus is
very contagious in that the virus can survive on dry surfaces for
up to 10 days and on human hands for up to 4 hours. It also has a
low infectious dose (10 or fewer particles) and the infected stool
can contain up to 1 × 1011 particles per gram, present before and
up to 2 weeks after the onset of symptoms. Because of the highly
contagious nature of rotavirus infections, it is estimated that for
every 4 children admitted to the hospital with a rotavirus infec-
tion, 1 additional child acquires it as an HAI. Rotavirus infec-
tions also may be transmitted to adults who are around infected
children, immunocompromised individuals, and older adults
in nursing homes. Fortunately the newly developed second-
generation rotavirus vaccines have proven to be effective and
have fewer serious side effects (e.g., intussusception [intestinal
invagination]).90-93
Norovirus (formally known as Norwalk virus, calicivirus, or
small round-structured viruses) is a single-stranded positive sense
RNA virus and is the most common cause of nonbacterial gas-
troenteritis worldwide. These outbreaks occur where groups
of individuals gather, including nursing homes, hospitals,
restaurants, and cruise ships. Like rotavirus, norovirus is very
Infectious Diseases     CHAPTER 13 341
contagious (fewer than 10 particles can cause infection) and can
survive for up to 4 weeks in a dried state at room temperature.
In hospitals, the most common contaminated sites include toi-
let tops, door handles, and telephone receivers, and contami-
nated hands can spread norovirus to up to seven clean surfaces.
Although considerably less pathogenic than C. difficile, norovi-
rus was estimated to cause nearly 1000 gastroenteritis-related
deaths in the United States in 2007.89
 CLINICAL TIP
Norovirus and rotavirus can be transmitted through aerosoliza-
tion, so health care workers should wear a mask when disposing
of vomitus and feces from infected individuals.
Research has shown that 1 minute of hand washing with
soap and water, followed by rinsing the hands for 20 seconds
and then drying them with a disposable towel, completely
removes norovirus from hands contaminated by infected stools.
Unlike rotavirus, there is no fully developed vaccine for noro-
virus, although vaccines for norovirus are in the early stages of
development.94-96
The primary manifestations of any form of gastroenteritis
are crampy abdominal pain, nausea, vomiting, and diarrhea, all
of which vary in severity and duration, according to the type
of infection. Gastroenteritis is generally a self-limiting infec-
tion, with resolution occurring in 3 to 4 days. However, in
the hospital setting, patients with reduced immunity can have
longer periods of recovery, with dehydration being a primary
concern.17,60,97
Management of acute gastroenteritis may include the
following17,60:
• Antiinfective agents
• IV fluid and electrolyte replacement
• Antiemetic agents (if nausea and vomiting occur) 
Immune System Infections
Human Immunodeficiency Virus Infection
Two types of HIV exist: HIV-1 and HIV-2, with HIV-1 being
the more prevalent and the one discussed here. It is a retrovirus
that occurs in pandemic proportions and primarily affects the
function of the immune system. Eventually, however, all systems
of the body become affected directly (e.g., the immune system),
indirectly (e.g., the cardiac system), or through both methods
(e.g., the nervous system). The virus is transmitted in blood,
semen, vaginal secretions, and breast milk through sexual, peri-
natal, and blood or blood-product contact. Proteins on the sur-
face of the virus attach to CD4+ receptors, found primarily on
T4 lymphocytes.98 Other types of cells found to house the virus
include monocytes, macrophages, uterine cervical cells, epithe-
lial cells of the gastrointestinal tract, and microglial cells.98
Upon entering the cell, viral DNA and cellular DNA com-
bine, making the virus part of the cell. The exact pathogenesis
of cellular destruction caused by HIV is not completely under-
stood, and several methods of destruction may be entailed. It
is known that immediately after initial infection, HIV enters
342 CHAPTER 13     Infectious Diseases
a latent period, or asymptomatic stage, in which viral replica-
tion is minimal, but CD4+ T-cell counts begin to decline.98
Continued reduction results in decreasing immunity, eventually
leading to symptomatic HIV, in which diseases associated with
the virus begin to appear.98 This eventually leads to the onset
of AIDS, which the CDC defines as occurring when the CD4+
T-lymphocyte count falls below 200 cells/μL (reference = 1000
cells/μL) or below 14%; when one of 26 specific AIDS-defining
disorders is contracted, most of which are opportunistic infec-
tions; or a combination of these factors is present.99,100
Six laboratory tests are available to detect HIV infection101-104:
1. ELISA: This procedure tests for the presence of antibodies
to HIV proteins in the patient’s serum. A sample of the pa-
tient’s blood is exposed to HIV antigens in the test reagent.
If HIV antibodies are identified, it is inferred that the virus
is present in the patient.
2. Western blot test: This test detects the presence of antibodies in
the blood of 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 tool to confirm a positive ELISA test result.
3. Immunofluorescence assay: In this test, the patient’s blood is di-
luted and placed on a slide containing HIV antigens. The
slide is then treated with antihuman globulin mixed with
a fluorescent dye that will bind to antigen–antibody com-
plexes. If fluorescence is visible 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 pres-
ence of the p24 antigen located on HIV virions. It can be
used to diagnose acute infection, to screen blood for HIV an-
tigens, to determine HIV infection in difficult-to-diagnose
cases, or to evaluate the treatment effects of antiviral agents.
5. PCR for HIV nucleic acid: This highly specific and extremely
sensitive test detects viral DNA molecule in lymphocyte nu-
clei 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 re-
quires a sample of blood, serum, plasma, or oral fluid to de-
tect HIV antibodies. This test can be completed in 20 min-
utes.
 CLINICAL TIP
Any clinician who sustains a needle-stick injury when working
with a patient with a suspected HIV infection should alert em-
ployee health/occupational health and have an HIV test. A false-
negative HIV test result can occur if an individual has not yet
developed HIV antibodies. If an individual has been exposed to
HIV, he or she should have a repeat HIV test to ensure a true-
negative result.105
Once HIV has been detected, it can be classified in a num-
ber of ways. The Walter Reed staging system has six categories
grouped according to the quantity of helper T cells and charac-
teristic signs, such as the presence of an HIV antigen or anti-
body.106 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/μL.
2. Category 2 consists of counts ranging between 200 and 499
cells/μL.
3. Category 3 contains cell counts less than 200 cells/μL.
These groups are then subdivided into A, B, and C, accord-
ing to the presence of specific diseases.99
A major advancement in the medical treatment of HIV has
been antiretroviral therapy. There are currently six classes of
medications (see Chapter 19, Table 19.39). Each of these thera-
pies 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 (HAART).106 There is a sig-
nificant need for more effective and cost-efficient prevention
methods for HIV infection. The HIV Vaccine Trials Network
(HVTN) is an international collaboration working to develop
HIV preventive vaccines.107 Although the results of some clini-
cal trials are promising, as of yet, there is no commercially avail-
able HIV-1 vaccine.108
As HIV progresses and immunity decreases, the risk for and
the severity of infections, not normally seen in a person with
a healthy immune system, increase. These opportunistic infec-
tions, combined with disorders that are caused directly by the
virus, often result in multiple diagnoses and medically complex
cases. 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 13.4 lists common complications 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 CNS lymphoma, toxoplasmosis, and neuropathies. These
manifestations may cause paresis, decreased sensation, ataxia,
aphasia, spasticity, altered mental status, and visual deficits.109
In the pulmonary system, TB, cytomegalovirus (CMV) infection,
and pneumonia can result in cough, dyspnea, sputum production,
and wheezing.110 In the cardiac system, cardiomyopathy, arrhyth-
mias, and congestive heart failure can cause chest pain, dyspnea,
tachycardia, tachypnea, hypotension, fatigue, peripheral edema,
syncope, dizziness, and palpitations.111
Physical therapy intervention can assist in minimizing the
effect of these deficits on functional ability, thus helping to
maximize the independence and quality of life of the individual.
However, the course of rehabilitation in HIV-positive individ-
uals can often be difficult owing to concurrent opportunistic
infections, an often-rapid downhill disease course, low energy
state, and frequent hospitalizations. 
Mononucleosis
Mononucleosis is an acute viral disease that has been primar-
ily linked to Epstein-Barr virus (EBV) and less commonly to
CMV. Mononucleosis is transmitted generally through saliva
from symptomatic or asymptomatic carriers (EBV can remain
infective for 18 months in the saliva).17,112
 Infectious Diseases     CHAPTER 13 343

TABLE 13.4  Common Complications of HIV and AIDS and Associated Medical Treatment
Complication Medication
Cardiomyopathy May be reversed with reduction or discontinuation of interleukin-2, adriamycin, α2-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 infection Clarithromycin, rifabutin, ciprofloxacin, ethambutol
Oral hairy leukoplakia Acyclovir if symptoms present
Pneumocystis jirovecii pneumonia Trimethoprim-sulfamethoxazole, dapsone, clindamycin, pentamidine isethionate
Progressive multifocal leukoencephalopathy Antiretroviral therapy, acyclovir, IV cytosine, adenosine-arabinoside, interferon-alphas
Pulmonary hypertension Low-flow oxygen if hypoxia present; vasodilators, including nitroglycerin, hydralazine, nifedip-
ine, lisinopril, and prostaglandin E
Toxic neuronal neuropathy: neuropathy May be reversed with discontinuation or reduction in the following: zalcitabine, didanosine, and
caused by certain medications stavudine
Tuberculosis Four-drug regimen: isoniazid, rifampin, pyrazinamide, and ethambutol

AIDS, Acquired immunodeficiency syndrome; HIV, human immunodeficiency virus; IV, intravenous.
Data from Zwolski K. Viral infections. In: Kirton CA, Talotta D, Zwolski K, eds. Handbook of HIV/AIDS Nursing. St. Louis: Mosby; 2001:303, 310-311, 313, 315;
Cheitlin MD. Cardiovascular complications of HIV infection. In: Sande MA, Volberding PA, eds. The Medical Management of AIDS. Philadelphia: Saunders; 1999:278,
280; Boss BJ, Farley JA. Alterations in neurologic function. In: Heuther SE, McCance KL, eds. Understanding Pathophysiology. 2nd ed. St. Louis: Mosby; 2000:403-406;
Smith L. Management of bacterial meningitis: new guidelines from the IDSA. Am Fam Physician. 2005;71(10):2003-2008; Rhuda SC. Nursing management, muscu-
loskeletal problems. In: Lewis SM, Heitkemper MM, Dirksen SR, eds. Medical-Surgical Nursing, Assessment and Management of Clinical Problems. 5th ed. St. Louis: Mosby;
2000:1795-1798; McCance KL, Mourad LA. Alterations in musculoskeletal function. In: Heuther SE, McCance KL, eds. Understanding Pathophysiology. 2nd ed. St.
Louis: Mosby; 2000:1046-1048; Rowland BM. Cellulitis. In: Boyden K, Olendorf D, eds. Gale Encyclopedia of Medicine. Farmington Hills, MI: Gale Group; 1999:616.

The disease is characterized by fever, lymphadenopathy
(lymph node hyperplasia), and exudative pharyngitis. Spleno-
megaly, hepatitis, pneumonitis, and CNS involvement may
occur as rare complications of mononucleosis. The infection is
generally self-limiting in healthy individuals, with resolution
in approximately 3 weeks without any specific treatment.17,112
If management of mononucleosis is necessary, it may include
the following17,112,113:
• Corticosteroids, in cases of severe pharyngitis
• Adequate hydration
• Bed rest during the acute stage
• Saline throat gargle
• Aspirin or acetaminophen for sore throat and fever  following17,114:
Cytomegalovirus Infection
CMV, a member of the herpesvirus group, can be found in all
body secretions, including saliva, blood, urine, feces, semen,
cervical secretions, and breast milk. CMV infection is a common
viral infection that may be asymptomatic or symptomatic. CMV
infection can remain latent after the initial introduction into the
body and can become opportunistic at a later point.
If CMV infection is symptomatic, the clinical presentation
of mononucleosis may be relatively benign in adults, or more
serious manifestations, such as pneumonia, hepatitis, encephali-
tis, esophagitis, colitis, and retinitis, can occur in patients with
HIV infection.
CMV is usually transmitted via prolonged contact
with infected body secretions, as well as congenitally or
perinatally.17,114
Management of CMV infection may include the
• Antiviral agents
• Corticosteroids
• Immunoglobulins
• Blood transfusions for anemia or thrombocytopenia
• Antipyretics 
344 CHAPTER 13     Infectious Diseases
Toxoplasmosis
Toxoplasmosis is a systemic protozoan infection caused by
the parasite Toxoplasma gondii. Transmission typically results
from three mechanisms: (1) eating raw or inadequately cooked
infected meat (especially pork or wild game meat) or eating
uncooked foods that have come in contact with contaminated
meat; (2) inadvertently ingesting sporulated 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 (termed congenital toxoplasmosis). Congenital trans-
mission of T. gondii can result in mental retardation, blindness
from ocular lesions, and epilepsy in the infant.115 Transmission
can also occur from an infected to an uninfected person by blood
transfusion or organ transplantation.116
Almost half of the world’s population is infected with toxo-
plasmosis. In the United States, the overall infection rate is
23%, ranging from 18% in the western region to 29% in the
northeast region, with 1.1 million new infections reported each
year. Fortunately most people are asymptomatic, with no evi-
dence of fever (subclinical infection), although severe general-
ized infection can occur, particularly in immunocompromised
individuals. Toxoplasmosis is the second leading cause of food-
borne illness deaths in the United States, causing more than 300
deaths annually.116
The primary way to treat toxoplasmosis is through preven-
tion with safe eating habits (thoroughly cooking meats, peel-
ing and washing fruits and vegetables) and minimizing contact
with cat feces while pregnant, along with keeping cats indoors
to prevent contamination.115  by 49% to 87% in the Veterans Affairs system, with the highest
Sepsis
Sepsis is a general term that describes three progressive infec-
tious conditions: bacteremia, septicemia, and shock syndrome
(or septic shock).17
Bacteremia is a generally asymptomatic condition that
results from bacterial invasion of blood from contaminated
needles, catheters, monitoring transducers, or perfusion fluid.
Bacteremia can also be caused by a preexisting infection from
another body site. Patients with prosthetic heart valves may
need to take prophylactic antibiotics for dental surgery because
bacteremia may progress to endocarditis. Bacteremia can resolve
spontaneously or progress to septicemia.
Septicemia is a symptomatic extension of bacteremia
throughout the body, with clinical presentations that are rep-
resentative 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 following17:
• Removal of suspected infective sources (e.g., lines or tubes)
• Antiinfective agents
• B lood pressure maintenance with adrenergic agents and cor-
ticosteroids
• IV fluids
• Blood transfusions
• Cardiac glycosides
• Supplemental oxygen, mechanical ventilation, or both
• Anticoagulation 
Management
Prevention
Reducing HAIs is critical because about 1 in 20 patients receiv-
ing treatment in U.S. hospitals contracts an HAI. In 2011 the
CDC published a strategic framework for preventing infectious
diseases, which outlines three critical elements: (1) strong pub-
lic health fundamentals, including infectious disease surveil-
lance, laboratory detection, and epidemiologic investigation;
(2) high-impact interventions, such as handwashing and vaccines;
and (3) sound health policies. It is within critical element 2 that
the therapist typically has the greatest opportunity to prevent
the spread of infectious disease. The CDC has developed specific
measures to reduce HAIs, specifically, central line–associated
bloodstream infections (CLABSIs), catheter-associated urinary
tract infections (CAUTIs), ventilator-associated events (VAEs),
surgical site infections (SSIs), laboratory-identified hospital-
onset C. difficile events, and laboratory-identified hospital-onset
MRSA bacteremia. These concerted infection control practices
and measures have led to a significant reduction in HAIs.117 For
example, from 2007 to 2015 MRSA HAIs rates were reduced
reductions occurring in the ICU setting.118 
Medical Intervention
Medical management of the various infectious diseases discussed
in this chapter is described in the specific sections of the respec-
tive disorders. Chapter 19 (Table 19.36, Antibiotics; Table
19.37, Antifungal Agents; Table 19.38, Antitubercular Agents;
Table 19.39, Antiretroviral Medications; and Table 19.40, Anti-
viral Medications) also lists common antiinfective agents used
in treating infectious diseases. 
Lifestyle Management
The critical importance of encouraging healthy lifestyles to
combat disease is indicated by the National Prevention and
Health Promotion Strategy that was announced in the summer
of 2011. The objective of this strategy is to “move the nation
away from a health care system focused on sickness and disease
to one focused on wellness and prevention.”119 That same year,
the American Physical Therapy Association’s president encour-
aged physical therapists to support this national prevention
initiative by “expanding quality preventative services in both
clinical and community settings, empowering people to make
healthful choices, and eliminating health disparities” and to
become “leaders in their communities to advance these direc-
tions and priorities.”120 Although the physical therapist may
have limited treatment options that emphasize prevention and
wellness during the patient’s acute care stay, the therapist has

greater opportunities to effect meaningful lifestyle changes in
other settings, such as in nursing homes and home health care.
At a minimum, the physical therapist can play a key role in
all health care settings in helping patients understand the link
between lifestyle factors and infectious diseases. These impor-
tant links, which may be poorly understood by the typical
patient, are discussed in this section.
Many of the same lifestyle and nutrition factors that can
delay wound healing (see Chapter 12) also affect the immune
system and the infection rate. To have an optimally functioning
immune system, a person should eat plenty of fresh fruits and
vegetables, as well as foods rich in fiber. Also, it is important to
obtain adequate amounts of the micronutrients zinc; selenium;
iron; copper; vitamins A, C, E, and B6; and folic acid. Vitamin
D, which is produced through exposure to sunlight, is known to
activate one’s innate immunity (i.e., regulatory T cells) by the
production of antimicrobial peptides. Excess sugar also decreases
the ability of WBCs to destroy bacteria (leukocytic phagocyto-
sis). Moreover, a healthy immune system is promoted not only
by eating proper foods but also by staying well hydrated, which
is a key consideration in combating septic shock.121-127
Exposure to fresh, unpolluted air benefits the immune sys-
tem. It is a well-studied fact that the higher the ventilation rate
(amount of outdoor air circulated per unit time), the lower is the
infection rate of airborne diseases, such as measles, TB, influ-
enza, and SARS. The cross-infection problem of the 2002–2003
SARS epidemic was particularly evident where people congre-
gated, such as in airplanes, buses, and hospitals. This would
imply a strong benefit in exposing patients to as much fresh
air as medically prudent, which is reminiscent of the philoso-
phy behind the “open-air treatment” TB hospitals of the past
century.128,129
When one achieves the proper balance between exercise and
rest, it helps the immune system fight off infection. Exercise
and adequate rest are key factors in promoting a healthy psy-
chological state, which also reduces the negative effects of stress
(e.g., high levels of cortisol) on the immune system. However,
it should be mentioned that the beneficial effects of resistance
exercise (as opposed to cardiovascular exercise) on immunity are
less clear, although excessive cardiovascular exercise may lead
to immunosuppression. The key role that melatonin, the cru-
cial rest-promoting hormone, plays in influencing our circadian
rhythm (sleep–wake cycle) and immune system (specifically
T-cell populations) is still being unraveled. Melatonin’s peak
production occurs at night, which is the inverse of another key
immunoregulatory hormone, vitamin D. To maximize melato-
nin levels, which promote sleep efficiency and restfulness, one
should exercise regularly; be exposed to natural light (sunlight),
especially early in the day; minimize exposure to artificial light
at night; and go to bed 2 to 3 hours before midnight in a com-
pletely dark room. It is important to follow this advice every
day because melatonin has a short half-life and thus must be
produced every 24 hours.126,130-135
Alcohol consumption has a well-known immunosuppressive
effect, which includes negative effects on lymphocyte activation,
cytokine production by macrophages and T cells, and neutrophil
function. This results in increased susceptibility to infection
Infectious Diseases     CHAPTER 13 345
and reduces the body’s ability to heal after injury. People who
smoke and those who are exposed (especially children) to pas-
sive or environmental tobacco smoke (ETS) are at greater risk
of impairing their immune system, which can cause infections
such as influenza and TB in adults and serious respiratory tract
infection and pneumonia in children. Caffeine is largely antiin-
flammatory in nature and thus has an overall negative effect on
the immune system. Specifically caffeine suppresses lymphocyte
function, antibody production, and neutrophil and monocyte
chemotaxis. Illicit drug users also have well-documented higher
infection rates involving bacteria, viruses, fungi, and protozo-
ans. These rates are even higher in injection drug users.136-139
Finally obesity has now been associated with increased infec-
tion risk. Increased infection has been observed in obese patients
with conditions as diverse as urinary tract infection (UTI), influ-
enza, hepatitis C, and a history of total hip arthroplasty. With
obesity rates increasing throughout the world, the exact mecha-
nism of the link between obesity and infections warrants more
study.140-143 
Physical Therapy Management
The following are general physical therapy goals and consider-
ations to be used when working with patients who have infec-
tious diseases and those with immune system disorders. These
guidelines should be adapted to a patient’s specific needs.
Goals
The primary physical therapy goals in this patient population
are similar to those of patient populations in the acute care set-
ting: (1) to optimize the patient’s functional mobility, (2) to
maximize the patient’s tolerance and endurance, (3) to maximize
ventilation and gas exchange in the patient who has pulmonary
involvement, and (4) when appropriate, to educate the patient
in proper lifestyle management (see previous section). 
Considerations for Physical Therapy Intervention
General physical therapy considerations 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
(Box 13.2).144
a. Warning or labeling systems for biohazards and infectious
materials may vary slightly among facilities.
b. Be sure to check the patient’s medical record or signs
posted on doors and doorways for indicated precautions.
c. Table 13.3 provides an outline of the types of PPE that
should be worn with specific precautions.
2. Personally follow and also educate patients concerning prop-
er coughing and sneezing hygiene etiquette to prevent the
spread of disease and illness.
a. Cover the mouth and nose with a tissue when coughing or
sneezing.
b. Put used tissues in a waste basket.
c. If no tissue is available, cough or sneeze into the upper
sleeve and not into the hands.
d. Wash the hands after coughing or sneezing (see Box 13.2).
346 CHAPTER 13     Infectious Diseases
BOX 13.2  Proper Hand Washing Technique
Hand washing with soap and water is the best method to remove
pathogens, including highly contagious pathogens (e.g., norovirus,
Clostridium difficile spores), from your hands.
1. Wet your hands with clean running water (warm or cold), and
apply soap.
2. Lather your hands by rubbing them together with the soap. Be
sure to lather the backs of your hands, between your fingers, and
under your nails.
3. Scrub your hands for at least 20 seconds (as previously men-
tioned, some pathogens, such as norovirus, require a longer
time [at least 60 seconds] to remove stool contamination from
hands).
4. Rinse your hands well under running water (stool-contaminated
norovirus hands should be rinsed for at least 20 seconds).
5. Dry your hands using a clean disposable towel, or air-dry them.
If soap and water are not available, use an alcohol-based hand
sanitizer that contains at least 60% alcohol (continue to rub the
sanitizer over all hand and finger surfaces until dry). Alcohol-based
hand sanitizers can quickly reduce the number of pathogens but do
not remove all pathogen types (e.g., norovirus, C. difficile spores).
3. The dangers of aerosolization of pathogens during common
hygiene activities and physical therapy treatment are often
not fully recognized.
a. Flushing the toilet (even with the lid down) causes aero-
solization of pathogens; it is greatest with the first flush
and then diminishes with each subsequent flush.
b. Aerosolization danger is greatest when the patient has di-
arrhea (in contrast to normal stools) and/or vomits into
the toilet.
c. Viral pathogens that cause gastroenteritis are especially
easy to spread as described previously because each gram
of feces can contain up to 1 × 1011 viral particles.
d. Pulsatile lavage is a common wound physical therapy mo-
dality that can cause aerosolization of pathogens.
e. In addition to the therapist wearing appropriate PPE dur-
ing pulsatile lavage, patients receiving treatment should
wear surgical masks, and all IV lines and other wounds
should be covered during treatment. The procedure
should be performed in a private room, with minimal
equipment and supplies. The room should be thoroughly
cleaned and disinfected after each procedure.
4. Patients who have infectious processes have an elevated meta-
bolic rate, which will most likely manifest itself as a high rest-
ing heart rate. As a result, the activity intensity level should be
modified, or more frequent rest periods should be incorporated
during physical therapy treatment to enhance activity tolerance.
Patients with infectious processes will also be prone to
orthostatic hypotension, hypotension with functional activi-
ties, or both as a result of the vasodilation occurring from
the inflammation associated with infection. Therefore slow
changes in positions, especially from recumbent to upright
positions, and frequent blood pressure monitoring are essen-
tial to promoting tolerance for functional activities.
5. Monitoring the temperature curve and WBC count of pa-
tients with infectious processes helps determine the appro-
priateness of physical therapy intervention.
a. Rest may be indicated during an exacerbation or progres-
sion of an infection process.
b. Clarification with the physician or nurse regarding the
type of intended physical therapy intervention is helpful
in making this decision.
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113. Ebell MH. Epstein-Barr virus infectious mononucleosis. Am
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when-how-handwashing.html. Accessed August 14, 2018.
350 CHAPTER 13     Infectious Diseases
APPENDIX 13A: IMMUNE SYSTEM DISORDERS
Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE) is a chronic, multisystem
autoimmune disease with a strong genetic predisposition. 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 expo-
sure, can trigger the onset of this disease. Women who are of
African American, Asian, or Native American descent, ages 20
to 40 years, are more susceptible than men in acquiring this dis-
ease. SLE is characterized by a systemic, remitting-and-relaps-
ing clinical presentation.1-4
The primary laboratory test for the diagnosis of SLE is as
antinuclear antibody titer.5 Diagnosis of SLE is confirmed if a
patient has 4 of the following 11 manifestations of SLE: malar
rash, discoid rash (individual round lesions), photosensitivity,
oral ulcers, arthritis, serositis, renal disorder, neurologic disor-
der, hematologic disorder, immunologic disorder, and the pres-
ence 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 central nervous system dysfunction.1-3
Clinical presentation of SLE may include the following1-4:
• Arthritis or arthralgias (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
• Pleurisy, pericarditis
• Headache, seizures
• Hemolytic anemia, thrombocytopenia, leukopenia
• Renal disease or failure
Management of SLE may consist of nonsteroidal antiin-
flammatory drugs; glucocorticoids; immunosuppressive agents
(cyclophosphamide); dialysis; and renal transplantation in severe
cases.1,2,4,6  in firmer, less distensible tissues that compromise organ func-
Sarcoidosis
Sarcoidosis is a systemic granulomatous disorder that primarily
affects women and non-white adults in the third decade of their
life. The definitive etiology is unknown, although an autoim-
mune process that is environmentally triggered is the gener-
ally agreed-on hypothesis. Sarcoidosis may present as acute or
chronic and have periods of progression and remission.6-10
Multiple body systems may be affected by sarcoidosis. The
lungs are the primary organs affected, with dyspnea, dry cough,
and chest pain being common symptoms. Pulmonary involve-
ment can be staged according to the following radiographic
evidence7,8:
• Stage 0: No radiographic abnormalities
• Stage I: Bilateral hilar lymphadenopathy
• Stage II: Bilateral hilar adenopathy and parenchymal infiltration
• S tage 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, with symp-
toms 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. In addi-
tion, cytotoxic agents (methotrexate and azathioprine), anti-
malarial agents (chloroquine and hydroxychloroquine), and
nonsteroidal antiinflammatory drugs may be used. In severe
cases of pulmonary disease, single- and double-lung transplan-
tations may be performed.6-8 
Amyloidosis
Amyloidosis is a group of disorders characterized by deposi-
tion of amyloid (a type of protein) in various tissues and organs.
Amyloidosis is classified according to protein type and tissue
distribution and affects men more than women, between ages
60 and 70 years.11 The most common type is caused when the
bone marrow produces abnormal antibodies, which are depos-
ited as amyloid. Clinical signs and symptoms are representative
of the affected areas, with common manifestations including11:
• Fatigue
• Shortness of breath
• Edema
• Paresthesia
• Weight loss
• Diarrhea
• Peripheral neuropathy
In general, the deposition of protein in these areas will result
tion. Management of amyloidosis consists of controlling any
primary disease process that may promote deposition of amyloid
into the tissues.11 
Rheumatoid Arthritis
Rheumatoid arthritis (RA) is an autoimmune disease character-
ized by uncontrolled proliferation of synovial tissue.12 It is a
chronic disease involving systemic inflammation, with periods
of exacerbation and remission.13 The etiology is not fully under-
stood, but it is believed that there is a correlation between envi-
ronmental and genetic factors. Females have an increased risk of
developing RA, as do individuals with a positive family history,
silicate exposure, or a smoking history.12
There are two forms of RA: juvenile idiopathic arthritis (JIA)
and adult RA. JIA occurs most often during the toddler and
early adolescent developmental phases, whereas adult RA has a
 Infectious Diseases     CHAPTER 13 351

TABLE 13A.1  Comparison of Osteoarthritis and Rheumatoid Arthritis

Osteoarthritis Rheumatoid Arthritis
Onset Majority of adult age >65 Adult: ages 25–50
Gradual onset Sudden onset
Incidence 12% 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 with multifactorial components
Genetic, environmental factors
Manifestations Unilateral joint involvement Symmetric, bilateral joint involvement
Affects: spine, hips, knees, feet, hands Affects any joint, predominantly upper-extremity joints
Inflammation present in 10% of cases Inflammation present in most cases
Brief morning stiffness Prolonged morning stiffness
Systemic symptoms None Fatigue, malaise, weight loss, fever
Laboratory values ESR: mildly-moderately increased ESR: increased during inflammatory process (exacerbation)
Rheumatoid factor: absent Rheumatoid factor: present but not diagnostic for disease

ESR, Erythrocyte sedimentation rate.

peak onset in the third and fourth decades of life. Both forms of
RA have an inflammatory component in disease development
and have similar medical management strategies.13
With RA, an interaction between autoantibodies (rheuma-
toid factors) and immunoglobulins initiates the inflammatory
process, which involves an increased infiltration of leukocytes
from the peripheral circulation into the synovial joint. Pannus—
a destructive granulation tissue that dissolves periarticular tis-
sues—can develop, ultimately leading to joint destruction.13
Clinical manifestations of RA can include articular and
extraarticular symptoms. Most body systems may be involved,
including the pulmonary, cardiovascular, neurologic, and gas-
trointestinal systems.13 The joints most commonly affected by
RA are those with the highest ratio of synovium compared with
articular cartilage, including the wrist, proximal interphalan-
geal, and metacarpophalangeal joints.12 Common deformities
References
associated with RA are ulnar drift, swan-neck, and boutonniere
deformities.13 Other symptoms include anorexia, low-grade
fever, fatigue, and malaise.12 Osteoarthritis (OA), also called
degenerative joint disease, may result in joint changes and defor-
mation. Table 13A.1 compares OA and RA.13
Diagnosis of RA can be made through the following seven
criteria established by the American Rheumatism Association12:
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
(CBC) count with differential, rheumatoid factor, and erythro-
cyte sedimentation rate (ESR) or C-reactive protein (CRP).11
Management of RA may include the following12,13:
• Nonsteroidal antiinflammatory drugs
• Glucocorticoids
• D isease-modifying antirheumatic drugs (DMARDs) (Chap-
ter 19, Table 19.13)
• 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 plat-
form walker may more appropriate than a standard walker,
and Lofstrand crutches may be more appropriate than axillary
crutches.
1. Rote NS. Alterations in immunity and inflammation. In: Mc-
Cance KL, Heuther SE, Brashers VL, et al., eds. Pathophysiology:
The Biologic Basis for Disease in Adults and Children. 6th ed. St.
Louis: Mosby; 2010:256–272.
2. Kimberly RP. Research advances in systemic lupus erythemato-
sus. J Am Med Assoc. 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 Muscu-
loskelet Med. 1999;16(9):531.
5. Gill JM, Quisel AM, Rocca PV, et al. Diagnosis of systemic lu-
pus erythematosus. Am Fam Physician. 2003;68(11):2179–2186.
6. Chandrasoma P, Taylor CR. Concise Pathology. 2nd ed. East Nor-
walk, CT: Appleton & Lange; 1995.
7. Morey SS. American Thoracic Society Issues consensus statement
on sarcoidosis. Am Fam Physician. 2000;61(2):553.
8. Johns CJ, Michele TM. The clinical management of sarcoidosis.
A 50-year experience at the Johns 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.
352 CHAPTER 13     Infectious Diseases
10. Peterson C, Goodman CC. Problems affecting multiple systems.
In: Goodman CC, Fuller K, eds. Pathology: Implications for the
Physical Therapist. 3rd ed. Philadelphia: Saunders; 2009:180.
11. Naqvi BH, Ferri FF. Amyloidosis. In: Ferri FF, ed. Ferri’s Clinical
Advisor. Philadelphia: Elsevier; 2013.
12. Rindfleisch JA, Muller D. Diagnosis and management of rheu-
matoid arthritis. Am Fam Physician. 2005;72(6):1037–1047.
13. Goodman CC. Soft tissue, joint, and bone disorders. In: Goodman
CC, Fuller K, eds. Pathology: Implications for the Physical Therapist.
3rd ed. Philadelphia: Saunders; 2009:1235–1317.
 14
C H APT ER  
CHAPTER OUTLINE
Introduction
Types of Organ Transplants
Criteria for Transplantation
Transplant Donation
Cadaveric Donors
Living Donors
Donor Shortage
Donor Matching/Allocation
General Posttransplantation Care
and Complications
Postoperative Care for Living
Donors
Postoperative Care for Transplant
Recipients
Rejection
Types of Graft Rejection
Infection
Renal Transplantation
Cadaveric Versus Living Donor
Renal Transplantation
Renal Transplantation Procedure
Indication of Renal Function
Posttransplantation
Postoperative Care and
Complications
Physical Therapy for Renal
Transplant Recipients
Liver Transplantation
Pretransplantation Care
Types of Liver Transplantations
Liver Transplantation Procedure
Indication of Liver Function
Posttransplantation
Postoperative Care and
Complications
Physical Therapy for Liver
Transplant Recipients
Combined Liver–Kidney
Transplantation
Pancreas Transplantation
Indication for Pancreas
Transplantation
Enteric Drainage Versus Bladder
Drainage
Indication of Pancreatic Function
Posttransplantation
Postoperative Care and
Complications
Pancreatic Islet Cell
Transplantation
Organ Transplantation
Alysha Waltera
CHAPTER OBJECTIVES
The objectives of this chapter are to describe the following:
1. The transplantation process, including the 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. Considerations for physical therapy intervention with the transplant recipient
Introduction
With advances in technology and immunology, organ and tissue transplantations have become
a more standard practice. There were 33,610 organ transplants performed in the United States
in 2016.1 Physical therapists are frequently involved in the rehabilitation process for pre-
transplant and posttransplant recipients.2 Owing to limited organ donor availability, physical
therapists often treat more potential recipients than transplant recipients. Patients awaiting
transplantations 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 dur-
ing their stay. The goals of physical therapy for transplantation candidates are conditioning
in preparation for the transplantation procedure and postoperative course. Additional goals
include increasing functional mobility and endurance and educating patients on their post-
operative precautions, all of which aim to return patients to a safe functional level at home.
Some transplantation candidates may be too acutely sick and may no longer qualify for trans-
plantation 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 in pretransplantation or posttransplantation status, physical thera-
pists focus on conditioning patients to their maximum functional level and should have a basic
knowledge of the patient’s end-stage organ disease.3 
Types of Organ Transplants
The kidney, liver, pancreas, heart, lung, and intestine are organs that are procured for transplan-
tation. The most frequent of those are the kidney, liver, and heart.4 Double transplantations,
such as liver–kidney,5 kidney–pancreas,5 heart–kidney,5 and heart–lung transplantations, are
performed if the patient has multiorgan failure. In addition to these solid organ transplanta-
tions, stem cell transplantation, which involves the replacement of abnormal cells with healthy
cells, is discussed.
Intestinal transplantation is not addressed in this text because it is performed in much
smaller numbers, with only 147 transplantations in 2016.1 Candidates for this procedure
include individuals with various disorders involving poor intestinal function and who are
unable to be maintained with other nutritional support.
aThe authors acknowledge Karen Vitak for prior contributions to this chapter.
        353
354 CHAPTER 14     Organ Transplantation
Pancreas–Kidney Transplantation
Types of Pancreas–Kidney
Transplantations
Postoperative Care and
Complications
Cardiac Transplantation
Pretransplantation Care
Orthotopic and Heterotopic Heart
Transplantations
Indication of Cardiac Function
Posttransplantation
Postoperative Care and
Complications
Physical Therapy for Cardiac
Transplant Recipients
Lung Transplantation
Types of Lung Transplants
Preoperative Care
Indication of Lung Function
Posttransplantation
Postoperative Care and
Complications
Physical Therapy for Lung Trans-
plant Recipients
Heart–Lung Transplantation
Hematopoietic Stem Cell
Transplantation
Patient Preparation
Harvesting
Reinfusion and Indication of
Postprocedure Function
Postprocedure Care and
Complications
Physical Therapy for Stem Cell
Transplant Recipients
Physical Therapy Management
Goals
General Physical Therapy Consider-
ations for Transplant Recipients
Physical Therapy Consideration
for Transplant Recipients
Activity Progression
Patient Education
 CLINICAL TIP
It is recommended that physical therapists who may be involved
in care for patients with intestinal transplantation seek addition-
al information from their transplantation center as well as from
the Intestinal Transplant Association (https://www.tts.org/irta-
home/home/welcome-to-ita).
 
Criteria for Transplantation
Transplantation is offered to patients who have end-stage organ disease when alternative
medical or surgical management has failed. The patient typically has a life expectancy of
less than 1 to 3 years.6-8 Criteria for organ recipients vary, depending on the type of organ
transplant needed and the transplantation facility.
The general criteria for transplantation include the following9:
• 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 irreversible infection
• The absence of disease that would attack the transplanted organ or tissue
In addition to these criteria, transplantation candidates must demonstrate emotional and
psychological stability, have an adequate support system, and be willing to comply with
lifelong immunosuppressive drug therapy. Other criteria, such as age limits and absence
of drug or alcohol abuse, are specific to the transplantation facility. To determine whether
transplantation is the best treatment option for the individual, all transplantation candidates
are evaluated by a team of health care professionals, consisting of a transplantation surgeon,
transplantation nurse coordinator, infectious disease physician, psychiatrist, social worker,
nutritionist, and, sometimes, a physical therapist. The patient undergoes many laboratory
and diagnostic studies during the evaluation process. Acceptable candidates for organ trans-
plantation are placed on a waiting list. Waiting times for an organ may range from days to
years, depending on the organ and an individual’s medical status.4 Improvements in the
medical management of transplant recipients, including immunosuppressants and postop-
erative care protocols, have increased the survival rates. As a result, organs are now being
offered to recipients who were previously considered “at risk,” including older patients with
multiple comorbidities and accompanying activity limitations.10 
Transplant Donation
Cadaveric Donors
Cadaveric donors are generally individuals who have been determined to be dead according
to neurologic criteria after severe trauma, such as from head or spinal cord injury, cerebral
hemorrhage, or anoxia.11,12 Death must occur at a location where cardiopulmonary support
is immediately available to maintain the potential organ donor on mechanical ventilation,
cardiopulmonary bypass, or both to preserve organ viability.11 To a more limited extent,
death can also be determined on the basis of circulatory criteria, and organs can be expedi-
tiously procured after specific criteria have been met (e.g., asystole for generally between 2
and 5 minutes). However, ethical issues remain surrounding the precise determination of
death and decisions to withdraw support. In addition, these organs are subject to potentially
greater ischemic injury, which, in turn, increases the risk for delayed graft function and graft
failure.4,13 Both types of cadaveric donors must have no evidence of malignancy, sepsis, or
communicable diseases, such as hepatitis B or human immunodeficiency virus (HIV).9,14,15 
Living Donors
Living donor transplantation offers an alternative means of organ donation that helps expand
the donor pool and allows for greater evaluation of the organs before transplantation. In
2017 more than 6000 transplantations were made possible because of living donors.16 Liv-
ing organ donation is when a living individual donates an organ or part of an organ for

transplantation to another person.17 Living donors are always
used for stem cell transplantations (SCTs), often used for kid-
ney transplantations, and sometimes used for liver, lung, and
pancreas transplantations. They may be genetically related (i.e.,
blood relative), emotionally related to the recipient (i.e., spouse
or close friend), or perhaps even a stranger in the case of a donor
chain. Direct donation occurs when a donor gives an organ to
a specific person, whereas nondirect donation occurs when an
individual donates an organ, but does not know the recipient.17
Living donors also are evaluated by the transplantation team to
determine medical suitability.
The age of a potential donor generally ranges from a term
newborn to 65 years, depending on the organ considered for
donation and the recipient. There are benefits to the recipient
of a living donor donation in that the donated organ is typically
from a young, healthy person who has undergone an intensive
medical evaluation, and surgery can be planned for when the
recipient’s medical status is most stable.18 Donors do not have
a history of drug or alcohol abuse, chronic disease, malignancy,
syphilis, tuberculosis, hepatitis B, or HIV infection. Ideally, the
donor’s height and weight approximate those of the recipient
for the best “fit.”  performed in several ways; however, the most conventional
Donor Shortage
As of December 2018, there were more than 114,000 indi-
viduals on the transplant waiting list, with more than 75,000
of those listed as medically suitable for transplantation.1 How-
ever, there were just over 14,500 donors from January through
October 2018.1 As a result of this shortage, many patients die
while waiting for a suitable organ to become available. Numerous
efforts have been undertaken to address the organ donor shortage,
including educational campaigns and technologic advancements.
Increased use of what are termed expanded criteria donor (ECD)
grafts is occurring with many transplants, including kidneys.
These are organs that may have previously gone unused because
of advanced age or other complicating donor factors, such as
hypertension or death resulting from stroke.10
Regenerative medicine entails the development of cellular,
tissue, and organ substitutes to help restore function.19 Engi-
neers continue to work on the development of implantable bio-
artificial organs, including artificial kidneys and lungs; however,
none of these devices has yet gained approval for use in humans
in the United States. Stem cell research also has the potential to
provide an alternative to solid organ transplants. The goal is for
immature stem cells to be directed to differentiate into specific
cell types and repair or replace tissues that have been damaged
because of injury. For example, stem cells have been shown in
animal studies and a few small human studies to repair injured
heart tissue and improve cardiac function.20  patient who has undergone major abdominal or cardiothoracic
Donor Matching/Allocation
In the United States, organ procurement and distribution for
transplantation are administered by the United Network for
Organ Sharing (UNOS) under contract with the federal govern-
ment. The UNOS sets standards for transplantation centers and
teams, tissue typing laboratories, and organ procurement orga-
nizations. Organ allocation is a complex process, and UNOS
Organ Transplantation     CHAPTER 14 355
policies attempt to balance justice and medical utility. Factors
that are involved in determining allocation and how they are
weighted in the decision making vary, depending on the organ
but generally include the following21:
• ABO blood type
• Tissue (histocompatibility) type
• Size
• Waiting time
• Severity of illness/degree of medical urgency
• Geographic location (distance between potential recipient
and donor)
The donor and recipient must be ABO blood type identi-
cal or compatible for all organ transplantations.22 Tissue typ-
ing typically involves a series of several tests to determine how
likely a potential recipient is to develop a rejection response
with transplantation, which include:
• Human leukocyte antigen (HLA) typing attempts to match
HLAs, which are the antigens that mostly cause graft rejec-
tion. The better the histocompatibility match and degree of
genetic similarity between the donor and the recipient, the
less severe is the potential rejection response. This may be
method involves mixing a serologic sample of the potential
recipient’s lymphocytes with a standard panel of antisera and
observing for lymphocytotoxicity.23
• White blood cell (WBC) cross-matching is performed by
mixing the lymphocytes from the donor with the serum from
the recipient and then observing for immune responses. A
negative cross-match indicates no antibody reaction and that
the recipient’s antibodies are compatible with those of the
donor. A negative cross-match is required for successful kid-
ney and kidney–pancreas transplantations.24
Although pretransplantation tissue typing is ideal, it is not
always performed because of insufficient time. The time that an
organ remains viable after it is recovered varies, depending on
the organ. Average viability times range from 4 to 6 hours for
the heart and lungs, 24 hours for the pancreas, 24 to 30 hours for
the liver, and 48 to 72 hours for kidneys.4 When there is insuf-
ficient time, other factors become the major considerations.23,25
For example, in lung transplantation, the Lung Allocation Score
(LAS) is used to estimate the severity of illness and the chances
for survival to assist with allocation.21 
General Posttransplantation Care and
Complications
Postoperative Care for Living Donors
Postoperative care for living donors is similar to that for any
surgery. These patients are taken off mechanical ventilation
in the recovery room and transferred to the general surgery or
transplantation ward. Vital signs and blood counts are moni-
tored closely for possible postoperative bleeding. Patients are
usually out of bed and ambulating on postoperative day 1. Phys-
ical therapists are rarely involved in the care of donors but may
become involved if complications arise affecting the donors’
functional mobility. 
356 CHAPTER 14     Organ Transplantation
Postoperative Care for Transplant Recipients
Once an organ is transplanted, postoperative care of the recipient
focuses on the monitoring and/or treatment of the following26:
• Allograft function
• Rejection
• Infection
• Adverse effects of immunosuppressive drugs
General postoperative care for transplant recipients is also
similar to the care patients receive after a major abdominal or
cardiothoracic surgery. Kidney and liver transplant recipients are
often taken off mechanical ventilation before leaving the operat-
ing room.27,28 Most other solid organ recipients are transferred
from the operating room to the surgical intensive care unit (ICU),
where they are weaned from mechanical ventilation (extubated)
within 24 to 48 hours.4,22,26,29,30 Once extubated and hemody-
namically stable, recipients are transferred to a step-down floor,
which may be specialized transplantation units in some facili-
ties. The 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 of postoperative transplantation may contrib-
ute to increased length of hospital stay or hospital readmissions.
These complications are grouped as follows:
• Surgical
• Medical
• Rejection
• Infection
Surgical complications include vascular problems, such as
thrombosis, stenosis, leakage at anastomotic sites, and post-
operative bleeding. Medical complications may include fluid
overload or dehydration, electrolyte imbalance, or hypotension/
hypertension.  account when designing treatment plans. Refer to Chapter 19
Rejection
Rejection, or the tendency of the recipient’s body to reject any-
thing that is “nonself,” is one of the leading problems with organ
transplantation. This 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
will be completely rejected and cease to be viable.4 Transplant
recipients must receive immunosuppressants for the rest of their
lives to minimize rejection of their transplanted organs. The
pharmacologic agents most often used to prevent organ rejec-
tion include double or triple drug therapy, which allows for the
use of smaller doses of individual drugs.31
These immunosuppressive drugs decrease the body’s abil-
ity to fight infection. A delicate balance must be reached
between suppressing rejection and avoiding infection. Insuffi-
cient immunosuppression may result in rejection that threatens
the survival of the allograft and the patient, whereas excessive
immunosuppression increases the risk of infection and malig-
nancy.32 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 posttransplantation including the individual patient’s con-
dition, organ transplanted, transplant center–specific practices,
and recent literature. There are three general approaches to post-
transplantation immunosuppression31:
• Induction immunosuppression: Encompasses high-dose immu-
nosuppressive medications given to prevent acute rejection
immediately after transplantation (usually only in the first
30 days)
• Maintenance immunosuppression: Includes all medications used
for long-term immunosuppression
• Antirejection immunosuppression: Includes all immunosuppres-
sive medications given for managing a specific acute rejec-
tion episode at any point posttransplantation
The main classes of drugs used for transplant immunosuppres-
sion include corticosteroids, calcineurin inhibitors, antimetabo-
lites, target of rapamycin inhibitors, monoclonal antibodies, and
polyclonal antilymphocyte antibodies. Individual drug classes
have different mechanisms, which include inhibition of gene
transcription, DNA and RNA production, T-cell activation and
proliferation, and lymphocyte and antibody production.33 Please
refer to Chapter 19 on Pharmacologic Agents for additional infor-
mation on pharmacology and the physical therapy implications
for immunosuppressants used in organ transplantation.
 CLINICAL TIP
Immunosuppressants used in the management of organ trans-
plantation have significant side effects. Drug protocols promote
the rapid tapering of steroids after transplantation, which helps
diminish the harsh side effects of those drugs.34 The most com-
mon side effects include hypertension, bone marrow suppres-
sion, electrolyte disturbances, decreased bone density, renal
dysfunction, and hepatotoxicity. Physical therapists must rou-
tinely monitor for these adverse side effects and take these into
on Pharmacologic Agents for more information on immunosup-
pressive agents.
 
Types of Graft Rejection
Hyperacute Rejection
Hyperacute rejection, characterized by ischemia and necrosis of
the graft, occurs from the time of transplantation to 48 hours after
transplantation.9 It is believed to be caused by the response of cyto-
toxic antibodies present in the recipient to tissue antigens on the
donor organ. The manifestations of hyperacute rejection include
general malaise and high fever. Rejection occurs before vasculariza-
tion of the graft takes place. Plasmapheresis may be used to attempt
to remove circulating antibodies from blood. However, usually
hyperacute rejection is unresponsive to treatment, and removal of
the rejected organ with immediate retransplantation is required.4,23 
Acute Rejection
Acute rejection is a treatable and reversible form of rejection that
typically occurs within the first 3 months to 1 year after trans-
plantation. However, changes in the immunosuppressive manage-
ment may also cause later acute rejection episodes.4 Almost every
patient has some degree of acute rejection after transplantation. It
may be caused by an antibody-mediated immune response and/or
 Organ Transplantation     CHAPTER 14 357

a T cell–mediated immune response. More commonly, 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 the thrombosis is left untreated.4,14 The first signs of
acute rejection may be detected within 4 to 10 days postopera-
tively.9,19,23 The actual manifestations of rejection vary, depend-
ing on the affected organ. General signs and symptoms of acute
rejection include the following1,4,14:
• Fever, chills, sweating, body aches/pains
• Swelling and/or tenderness at the graft site
• Malaise and/or fatigue
• Nausea, diarrhea, vomiting, loss of appetite
• Peripheral edema
• Dyspnea, arrhythmia, increased blood pressure (BP)
• Sudden weight gain (6 lb in less than 3 days)
• Decreased urine output
• Abnormal laboratory findings (depending on the organ)—
electrolyte imbalances, increased blood urea nitrogen (BUN)
and serum creatinine levels, increased bilirubin and liver en-
zymes (alanine transaminase [ALT], aspartate transaminase
[AST]), increased urine amylase
Early intervention is key to the reversal of acute rejection,
and treatment usually includes use of antirejection drugs.  viral, antibacterial, and antifungal medications prophylactically.
Chronic Rejection
Chronic rejection of the graft occurs after the first few months of
transplantation and is characterized by gradual and progressive
deterioration of the graft. It is believed to result from a combina-
tion of B cell–mediated and T cell–mediated immunity, frequent
episodes of acute rejection, and infection. Persistent inflamma-
tion leads to graft necrosis and deterioration in function. Increas-
ing immunosuppressive medications may slow the process, but
it cannot stop chronic rejection, and eventually retransplantation
is required. Chronic rejection presents differently, depending on
the transplanted organ. Individuals who have undergone kid-
ney and liver transplantations may present with a more gradual
rise in laboratory values (i.e., creatinine, BUN, bilirubin, liver
function tests [LFTs]) compared with what is seen in acute rejec-
tion.9,14,35 Cardiac transplant recipients may experience coronary
allograft vasculopathy, in which there is accelerated graft athero-
sclerosis or myocardial fibrosis, leading to myocardial ischemia
and infarction.9 Chronic rejection of lung transplants manifests
as bronchiolitis obliterans, with symptoms of increasing airflow
obstruction.6,7 In pancreas transplant recipients, the pancreatic
vessels thicken, leading to fibrosis, and there is a decrease in insu-
lin secretion with resultant hyperglycemia.9 
Infection
Suppression of the immune response prevents rejection of the
transplanted organ; however, the recipient is more susceptible
to bacterial, fungal, and viral infections. Infection is one of the
leading causes of critical illness, hospitalization, morbidity, and
mortality after organ transplantations.36 The high risk of infec-
tions after transplantation requires that recipients be given anti-
Active infections are treated with a reduction of immunosup-
pressants and addition of other medications targeting the patho-
gen.4 Please refer to Chapter 19 on Pharmacologic Agents for
information about specific medications used to treat infections.
An overview of the timeline for infection after organ transplan-
tation is shown in Fig. 14.1.

Donor-derived Nosocomial, technical Activation of latent infection

Community-acquired
infection (donor or recipient) (relapsed, residual, opportunistic)

Transplant Dynamic assessment of risk infection

Common infections in solid-organ transplant recipients

Recipient-derived <1 month 1-6 months >6 months

infection Infection with antimicrobial-
resistant species:
MRSA
VRE
Candida species (non-albicans)
Aspiration
Catheter infection
Wound infection
Anastomotic leaks and ischemia
Clostridium difficile colitis
Donor-derived infection
(uncommon):
HSV, LCMV, rhabdovirus
(rabies), West Nile virus,
HIV, Trypanosoma cruzi
Recipient-derived infection
(colonization):
Aspergillus, Pseudomonas
With PCP and antiviral (CMV, HBV)
prophylaxis:
Polyomavirus BK infection, nephropathy
C. difficile colitis
HCV infection
Adenovirus infection, influenza
Cryptococcus neoformans infection
Mycobacterium tuberculosis infection
Anastomotic complications
Without prophylaxis:
Pneumocystis
Infection with herpesviruses (HSV,
VZV, CMV, EBV)
HBV infection
Infection with Listeria, Nocardia,
Toxoplasma, Strongyloides,
Leishmania, T. cruzi
Community-acquired pneumonia,
urinary tract infection
Infection with aspergillus, atypical
molds, Mucor species
Infection with Nocardia,
Rhodococcus species
Late viral infections:
CMV infection (colitis and
retinitis)
Hepatitis (HBV, HCV)
HSV encephalitis
Community-acquired (SARS,
West Nile virus infection)
JC polyomavirus infection (PML)
Skin cancer, lymphoma (PTLD)

FIG. 14.1
Changing timeline of infection after organ transplantation. (Data from Fishman JA. Infection in solid-organ
transplant recipients. N Engl J Med. 2007;357:2601. In Auerbach PS. Wilderness Medicine. 6th ed. Philadelphia:
Mosby/Elsevier; 2012.)
358 CHAPTER 14     Organ Transplantation
General signs and symptoms of infection include the
following24:
• Temperature greater than 38°C (100.5°F)
• Fatigue
• Shaking, chills, body aches
• Sweating
• Diarrhea lasting longer than 2 days
• Dyspnea
• Cough or sore throat
 CLINICAL TIP
Some signs of activity intolerance are similar to signs of rejec-
tion and infection. In addition, it can be difficult to distinguish
clinically between rejection and infection. It is important for the
physical therapist to monitor for signs and symptoms of both
and to communicate these to the transplantation team.
 
Renal Transplantation
Renal or kidney transplantation is the most common organ
transplantation procedure.4 In 2016, 19,060 kidney transplan-
tations were performed in the United States.21 As of August
2018, there were 94,863 individuals awaiting renal transplanta-
tion in the United States.1
The goal of renal transplantation is to restore normal renal
function in patients with irreversible end-stage renal failure.
The most frequent causes of end-stage renal disease requiring
transplantation include the following23:
• Primary uncontrolled hypertension
• Glomerulonephritis
• Chronic pyelonephritis
• Diabetic nephropathy
• Polycystic kidney disease
Contraindications to renal transplantation include the following23:
• Advanced cardiopulmonary disease
• Active vasculitis
• Morbid obesity
Cadaveric Versus Living Donor Renal Transplantation
Kidney transplants may come from a cadaveric donor or a 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 preferred over cadaveric transplants. Most
living donor nephrectomies are performed laparoscopically with a
2- to 3-inch incision in the lower quadrant, minimizing pain and
allowing donors to mobilize quickly after surgery.1,12,37 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.24
The benefits of a living donor transplant for the recipient
include longer survival rates for both the allograft and the
patient. According to the UNOS data as of December 2018,
the 5-year survival rate for kidney grafts from living donors is
85.6% compared with 74.4% for those from cadaveric donors,
and patient 5-year survival rates are 92.1% and 83.2%, respec-
tively.1 The higher success rate of the recipients of living donor
transplants can be attributed to the following: potentially
healthier recipients who are undergoing the procedure elec-
tively, more thorough pretransplantation evaluation resulting in
closer genetic matches, lower incidence of acute tubular necrosis
(ATN) postoperatively, and reduced requirement for immuno-
suppressive medications resulting in a lower risk for infection/
malignancy.24,38 Risks to an individual who donates a kidney
include hernia, high BP after pregnancy, new or continuing
high BP, and organ failure.39 The average length of hospital stay
for living kidney donors is approximately 2 to 3 days.39
Unfortunately, the shortage of donor kidneys continues, with
more than 4400 individuals removed from the waiting list as a
result of death in 2017.1 Strategies to expand the donor pool are
evolving and include the following37:
• Use of more ECD kidneys
• Desensitization protocols—use of intravenous immunoglobulin
and plasmapheresis before transplantation to modulate antibod-
ies and reduce the recipient’s potential immune response (This
may allow the use of organs that are traditionally deemed in-
compatible based on blood type and/or a positive cross-match.)
• Kidney Paired Donation (KPD)—a potential recipient with a
willing but incompatible donor is matched to another incom-
patible donor recipient pair with reciprocal incompatibility38
(Donor chains that incorporate this concept are developing.) 
Renal Transplantation Procedure
The renal allograft is not placed in the same location as that of the
native kidney. It is placed extraperitoneally in the iliac fossa through
an oblique lower abdominal incision.4,12,40 The renal artery and
vein of the donated kidney are attached to the recipient’s internal
iliac artery and iliac vein, respectively. The ureter of the donated
kidney is sutured to the bladder, and a urinary catheter is placed for
approximately 5 days to allow time for healing.12 The recipient’s
native kidney is not removed unless it is a source of infection or
uncontrolled hypertension. The residual function may be helpful
if the transplant fails and the recipient requires hemodialysis.40,41
The advantages of renal allograft placement in the iliac fossa
include the following42:
• A decrease in postoperative pain because the peritoneal cav-
ity 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 Posttransplantation
Restoration of renal function is characterized by:
• Immediate production of urine and massive diuresis (excel-
lent renal function is characterized by a urine output of 800–
1000 mL per hour)30

• D
 eclining levels of BUN and serum creatinine
However, there is a 20% to 30% chance of delayed graft
function, and dialysis may be required for a few days to several
weeks.40 Dialysis is discontinued once urine output increases
and serum creatinine and BUN levels begin to normalize. With
time, normal kidney function is restored, and the dependence on
dialysis is eliminated.40  from rehabilitation, it is often underused in this population.
Postoperative Care and Complications
Volume status is strictly assessed, and intake and output val-
ues 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 parameters 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.23
The most common signs of rejection specific to the kid-
ney are an increase in BUN and serum creatinine, decrease in
urine output, increase in BP, weight gain greater than 1 kg
in a 24-hour period, and ankle edema.23,24,40 A percutaneous
renal biopsy under ultrasound guidance is the most definitive
test for acute rejection.40 ATN may occur posttransplantation
because of ischemic damage resulting from prolonged preser-
vation, and dialysis may be required until the kidney starts to
function.24
Ureteral obstruction may occur owing to compression of
the ureter by a fluid collection or by blockage from a blood
clot in the ureter and may be visible on ultrasound. The place-
ment of a nephrostomy tube or surgery may be required to
repair the obstruction and prevent irreversible damage to the
allograft.40
Urine leaks may occur at the level of the bladder, ureter,
or renal calyx. Symptoms of urine leak posttransplantation
include fever, pain over the graft, fluid leak from wound, per-
sistent Jackson-Pratt (JP) drain output and increasing serum
creatinine.43 The leaks usually occur within the first few days
of transplantation.41 Renal ultrasounds are performed to assess
for fluid collections, and radionucleotide scans view the per-
fusion of the kidney. Other potential complications include
posttransplantation diabetes mellitus (PTDM); renal artery
thrombosis or leakage at the anastomosis; hypertension;
hyperkalemia; renal abscess or decreased renal function; and
pulmonary edema.4,25,40 Thrombosis most often occurs within
the first 2 to 3 days after transplantation.40 Venous thrombosis
is more common than arterial thrombosis and is confirmed by
ultrasound. Thrombosis is an indication for emergent surgical
exploration. There is also risk for injuries to the iliac artery on
the ipsilateral leg, most often resulting from application of a
vascular cross clamp during surgery. Peripheral pulses should
be monitored, and signs of vascular compromise should be
reported to the medical team.43 The most common cause of
decreased urine output in the immediate postoperative period
is occlusion of the urinary catheter caused by clot retention, in
which case, aseptic irrigation is required.23
Organ Transplantation     CHAPTER 14 359
 CLINICAL TIP
Individuals who have undergone a kidney transplantation tend
to have impaired exercise capacity for a number of reasons, in-
cluding renal osteodystrophy, anemia, and muscle dysfunction/
wasting.44 Although kidney transplant recipients will benefit
Physical therapists should advocate for physical therapy services
at discharge for appropriate individuals.
 
Physical Therapy for Renal Transplant Recipients
• D aily fluid intake of 2 to 3 L is generally recommended for
kidney transplant recipients.27,45 Therapists should assist pa-
tients in adhering to fluid recommendations from the medi-
cal team during therapy sessions.
• In the immediate postoperative period, BP needs to be main-
tained to ensure adequate perfusion to the newly grafted kid-
ney. Therapists should check with the physician for specific
parameters, but generally the systolic BP should be kept
above 110 mmHg. Untreated hypertension poses a risk for
bleeding.43 Kidney transplant recipients may be normoten-
sive at rest; however, they respond to exercise with a higher-
than-normal blood pressure.46
• Consistent BP monitoring for the life span of the transplant
recipient is necessary because many transplant recipients de-
velop hypertension over time, and cardiovascular disease is
the leading cause of death in kidney transplant recipients.47 
Liver Transplantation
The liver is the second most commonly transplanted organ in
the United States.
In 2016, 7841 liver transplantations were performed.1 As
of 2016, Hepatitis C virus was no longer the leading indica-
tion for transplantation, with the most common indication now
being “other/unknown,” including non–alcoholic fatty liver dis-
ease (NAFLD) and alcoholic liver disease.48 As of August 2018,
13,723 individuals were awaiting liver transplantation in the
United States.1
Indications for liver or hepatic transplantation include the
following9,49,50:
• End-stage hepatic disease
• Primary biliary cirrhosis
• Chronic hepatitis B or C
• Fulminant hepatic failure (FHF) resulting from an acute vi-
ral, toxic, anesthetic-induced, or medication-induced liver
injury
• Congenital biliary abnormalities
• Sclerosing cholangitis
• Wilson’s disease
• Budd-Chiari syndrome
• Biliary atresia
• Confined hepatic malignancy (hepatocellular carcinoma)
• Hereditary metabolic diseases (e.g., familial amyloid poly-
neuropathy)
360 CHAPTER 14     Organ Transplantation

TABLE 14.1  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
Impaired cerebral function
Clinical Effects
Jaundice
Dark, tea-colored urine
May induce nausea and anorexia
Abdominal pain
Itching of the skin
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, elevated international
normalized ratio (INR)
Thrombocytopenia
Low blood sugar
Systemic and splanchnic vasodilation
Presence of esophageal varices
May lead to hepatic encephalopathy
Spontaneous bacterial peritonitis or
cholangitis
Osteoporosis may result
Lack of awareness, decreased attention span,
lethargy, personality changes, disorienta-
tion, coma
Physical Therapy Implications
Abdominal discomfort may affect patient comfort
during therapy
Monitor symptoms to determine appropriateness
and parameters of intervention
Decreased thoracic compliance. May cause pressure
on the diaphragm, leading to respiratory and
nutritional difficulties
Monitor for dyspnea and altered SpO2 with activity
Patient may have an altered center of gravity and
decreased balance
May lead to muscle atrophy and skin fragility
Prolonged bleeding time
Patient bruises easily
Monitor patient safety and prevention of falls
Patient may have decreased energy
Monitor for hypotension
Bleeding may occur spontaneously
Patient may have altered mental status and
decreased safety awareness
May have an increased risk of infection
May develop compression or pathologic fractures
Patient may be confused with treatment
Maintain safety and monitor for changes to com-
municate with medical team

↑, Elevated; ↓, decreased.
Data from: Sigardson-Poor KM, Haggerty LM. Nursing Care of the Transplant Recipient. St. Louis: Saunders; 1990:149-151; Braddom RL, ed. Physical Medicine and Re-
habilitation. 2nd ed. Philadelphia: Saunders; 2000 and 2007:139, 1145; Findlay JY, Fix OK, Paugam-Burtz C, et al. Critical care of the end-stage liver disease patient
awaiting liver transplantation. Liver Transpl. 2011;17:496-510; Olson JC, Karvellas CJ. Critical care management of the patient with cirrhosis awaiting liver transplant
in the intensive care unit. Liver Transpl. 2017;23(11):1465-1476; Grek A, Arasi L. Acute liver failure. AACN Adv Crit Care. 2016;27(4):420-429; and Sargenti K, Prytz
H, Nilsson E, Kalaitzakis E. Predictors of mortality among patients with compensated and decompensated liver cirrhosis: the role of bacterial infections and infection-
related acute-on-chronic liver failure. Scand J Gastroenterol. 2015;50(7):875-883.

Contraindications to hepatic transplantation include the

following4,35,49:
• Advanced cardiac disease
• Myocardial infarction within the previous 6 months
• Severe chronic obstructive pulmonary disease (COPD)
• Active alcohol use/other substance abuse (required time to
be substance free is determined by the center but is usually
greater than 6 months)
Pretransplantation Care
Patients awaiting liver transplantation are often deconditioned
and malnourished, with resulting weakness and muscle loss
caused by breakdown of muscle protein and fat, which are used
as alternative energy sources.51 Additionally, anasarca and asci-
tes often lead to overall weight gain with associated balance
impairments. The goals of preoperative physical therapy include
aerobic conditioning, strength training, postural education,
and maximizing functional mobility with a focus on education
regarding postoperative follow-up, fall prevention, home exer-
cise program, and lifestyle modification.
Table 14.1 provides some characteristics of liver failure, clin-
ical effects, and implications for physical therapy.  this, the use of living donors of liver transplants has declined
Types of Liver Transplantations
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. 
Cadaveric Split Liver Transplantation
Split liver transplants are sometimes used to expand the donor
pool. Surgeons divide an adult cadaveric liver in situ into two
functioning allografts.21 Usually, the smaller left lobe is donated
to a child, and the larger right lobe is given to an adult.52 
Living Adult Donor Liver Transplantation
A single lobe of the liver from a living adult is transplanted
into the recipient. Because of the unique ability of the liver to
regenerate, the donor’s and recipient’s livers will grow back
to normal size within several months.24 At 1-year follow-up,
there was no significant difference in the bilirubin, albumin,
and international normalized ratio (INR) values in the donors
compared with their pretransplantation values. In spite of

steadily since its peak in 2001, likely as a result of concerns
about higher donor morbidity and mortality relative to what
is seen among kidney donors.21 Risks to an individual who
donates part of the liver include organ failure, wound infection
or hernia, bile leakage, and intestinal blockage.38 The average
length of hospital stay for an individual donating part of the
liver is about 5 days.38  patient with an elevated INR and communicate with the medical
Domino Liver Transplantation
Domino liver transplantation (DLT) is a technique used in the
treatment of several hereditary metabolic diseases, including
familial amyloid polyneuropathy (FAP). Patients with these dis-
eases have aberrant or deficient protein production in the liver;
however, the liver is structurally and functionally normal. In
a domino liver transplantation, individuals receive a donated
cadaveric liver and, in turn, donate their explanted liver to the
domino recipient, another patient on the waiting list. Because
of the natural history of these disease processes, it can take years
for any symptomatic disease to develop in domino recipients, if
at all. Individuals who are chosen to receive these domino livers
are usually older and more marginal transplantation candidates,
and it is thought that they might not otherwise be offered a
transplant.41  Physical therapists should monitor the output of the drains.
Liver Transplantation Procedure
The procedure for liver transplantation takes between 4 to 12
hours.48 Common incisions used include the bilateral subcostal
with midline extension also called the Mercedes incision, and the
“inverted J” incision called the Makuuchi incision.53 
Indication of Liver Function Posttransplantation
• O nce the graft is vascularized in the operating room, the
functioning liver starts to produce bile.23 Thus prompt out-
flow 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.14 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.14
• The most sensitive laboratory indices of liver function are
the values for coagulation, prothrombin time (PT), partial
thromboplastin time (PTT), and 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.23
• LFTs should reveal a progressive decline after transplanta-
tion. The exact values can vary from patient to patient and
with volume status; more accurate levels are determined 6 to
12 hours after surgery.23
• In the immediate postoperative period, hypokalemia is an-
other sign that the liver is functional. Once the graft is vas-
cularized, hepatocytes extract potassium from blood. On the
other hand, hyperkalemia often signifies cell death and that
the hepatocytes are nonfunctional.23
• Normal to slightly elevated blood glucose levels indicate
that the liver is able to store glycogen and convert it to
glucose.4
Organ Transplantation     CHAPTER 14 361
 CLINICAL TIP
Patients may have prolonged clotting time reflected in the labo-
ratory results (PT/PTT/INR). An INR greater than 4.0 increases
the risk of uncontrolled bleeding with injury. Check the guide-
lines at your facility for physical therapy intervention for the
team.
 
Postoperative Care and Complications
Postoperatively, liver transplant recipients may emerge with
several JP suction drains and a biliary T tube. The JP drains
lie over the superior surface of the liver and drain blood-tinged
fluid. The JP drains are gradually removed after surgery as the
drainage decreases, but often one is left in place for up to a week
after surgery.24,30 The T tube, which is placed in the bile duct,
allows for monitoring the amount, color, and consistency of the
bile. It remains in place for up to 12 weeks postoperatively and
is removed once the bilirubin level falls.24,35
 CLINICAL TIP
JP drains should be monitored for bleeding, increased output,
and bile. These abnormalities should be reported to the medical
team. T-tube drains should be monitored for the amount and
consistency of bile output.48
Primary graft failure (PGF) is a sign of acute hepatic failure
that may be seen immediately postoperatively. It is character-
ized by a markedly abnormal liver function; prolonged PT, PTT,
or both; oliguria; metabolic acidosis; hyperkalemia; hypoglyce-
mia; and coma. In the event of primary graft failure, retrans-
plantation is immediately required.
Acute kidney injury (AKI) is relatively common after liver
transplantation. Several factors influence the development of
AKI after liver transplantation, including intraoperative hypo-
tension, severity of liver disease, preoperative renal function,
and drug-induced toxicity. Calcineurin inhibitors are frequently
used after liver transplantation but may lead to renal injury, and
they are now used in reduced doses and at a later time postsur-
gery.36 Other potential medical complications include PTDM,
abscess, atelectasis, and pneumonia secondary to ascites or
peritonitis.9
Acute rejection specific to a transplanted liver includes ele-
vated LFTs (especially an increase in bilirubin) and prolonged
PT, PTT, or both; jaundice; right upper-quadrant pain; clay-col-
ored stools; tea-colored urine; decreased quantity of bile; thin,
watery, light-colored bile through the T tube; and increased
ascitic drainage. A liver biopsy is the definitive diagnostic test
for rejection and is able to distinguish between early rejection
and ischemic injury.35
Surgical complications include hepatic artery thrombosis,
biliary leak, or stricture. These complications present with a ris-
ing bilirubin level and are identical in appearance to an acute
rejection episode.4 Consequently, recipients undergo routine
362 CHAPTER 14     Organ Transplantation
Doppler ultrasound of the abdomen to check for fluid collections
and patency of the hepatic artery and portal vein.35 A cholan-
giogram, which examines the patency of the biliary tree drain-
age system, may be performed to rule out bile duct obstruction.
Surgical intervention is indicated if the biliary obstruction can-
not be corrected by a percutaneous transhepatic cholangiogram.
Portal vein thrombosis is evident if ascites persists or variceal
hemorrhage develops.25
Long-term evidence shows cardiovascular complications
related to obesity, diabetes, and hyperlipidemia in liver trans-
plant recipients. Corticosteroids used to treat rejection are the
primary risk factor for the development of these postoperative
complications; however, studies indicate a significant decrease
in these complications when steroids are withdrawn by 3 to 4
months posttransplant.54 Exercise and diet modification can
play a role in preventing these complications.55 Survival rates
for liver transplant recipients are improving, with 91.2%
to 92.3% 1-year survival and 75% to 33.9% 5-year survival
(higher in living versus cadaveric donor transplants).1 Fatigue
has also been found to be a significant chronic problem after
liver transplantation.2
 CLINICAL TIP
Typical length of stay (LOC) in the hospital after liver trans-
plantation ranges from 1 to 3 weeks.12 An individualized home
exercise program with follow-up home or outpatient physical
therapy is recommended because of the high incidence of obesi-
ty and diabetes in liver transplant recipients. In addition, energy
conservation techniques may help reduce activity limitations in
recipients during periods of increased fatigue.
 
Physical Therapy for Liver Transplant Recipients
• A n intensive early rehabilitation program, described by Maf-
fei et al. in 2017, has been reported to be feasible and well
tolerated, with few adverse events noted and none requiring
specific medical intervention.56
• 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 a large incision that hinders
full chest expansion and cough effectiveness. Postoperatively,
many recipients still have ascites from weeping of sodium-
rich and albumin-rich fluid from the liver’s surface.14
• Along with ascites and postoperative fluid retention, liver
transplant recipients have an increased abdominal girth and
lower extremity edema, which lead to a shift in the patient’s
center of gravity and thus to impaired balance. Often pa-
tients have increased lumbar lordosis and complain of low
back pain.  leaks and infections. Bladder drainage is obtained by anasto-
Combined Liver–Kidney Transplantation
It has been estimated that approximately one quarter of all liver
transplantation candidates have impaired renal function; conse-
quently, renal transplantation may also be indicated. Consen-
sus statements have been developed to describe indications for
combined liver–kidney transplantations. Factors used in this
determination include the degree and duration of renal injury,
length of time undergoing renal replacement therapy, the degree
of proteinuria, and findings from renal biopsy.57 
Pancreas Transplantation
Indication for Pancreas Transplantation
In 2016 there were 215 individuals who received a pancreas
transplant in the United States.21 As of August 2018, in
the United States, 880 individuals were awaiting pancreas
transplantation.1
Pancreas transplantation candidates have insulin-dependent,
type 1 diabetes mellitus and are preuremic (without urea in
blood). These patients have severe brittle diabetes and metabolic
imbalances, such as hypoglycemic unawareness and subcutane-
ous insulin resistance.58,59 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.4 Ideally pancreas
transplantation should be performed before secondary compli-
cations of diabetes (e.g., retinopathy, peripheral neuropathy,
vasculopathy, and end-stage renal disease) develop. Because
pancreas transplantation alone is not a lifesaving procedure and
has a high incidence of rejection and surgical complications, the
patient’s condition is evaluated carefully to determine whether
the benefits outweigh the risks of transplantation.60
Contraindications to pancreas transplantation include the
following59,60:
• Age greater than 50 years (relative)
• Morbid obesity
• Active smoking
• Severe cardiovascular disease
Living donor pancreas transplantation, in which a segment
of the body and the tail of the pancreas from a living donor
are used, may be performed; however, whole-organ cadaveric
pancreas transplantation is preferred. The donor pancreas is
placed intraperitoneally in the right iliac fossa through either
an oblique lower-abdominal incision or a midline incision.25,61
The recipient’s native pancreas is left intact. The vasculature of
the new pancreas is anastomosed to the iliac vessels, and insulin
is delivered to the systemic circulation.60 
Enteric Drainage Versus Bladder Drainage
Pancreatic exocrine secretions can be drained through two dif-
ferent techniques. For both approaches, the pancreas is trans-
planted with a segment of the donor duodenum. In an enteric
approach, the duodenum is anastomosed to a loop of the recipi-
ent’s small bowel. Concerns with this technique have included
the risk of contaminating the field with the bowel and associated
mosing the donor duodenum with the recipient’s urinary blad-
der.59,60,62 This permits expulsion of the exocrine secretions with
urine and allows for monitoring of urine amylase as a marker
for rejection.59,62 The disadvantage of bladder drainage is that
urologic and metabolic complications are common, including
metabolic acidosis, volume depletion, dehydration, pancreatitis

from reflux of urine, urinary tract infections, and urethral stric-
ture formation.63 Enteric conversion may be required if there
are persistent metabolic issues.59,62 Because of the significant
complications noted with bladder drainage, enteric drainage has
become the preferred technique at most transplantation centers,
with more than 80% of transplantations using enteric drainage
since 2003.60 Ultimately, the decision regarding which tech-
nique to use is the choice of the transplantation surgeon.59 
Indication of Pancreatic Function Posttransplantation
Within 24 hours, the transplanted pancreas should be produc-
ing insulin. Analysis of blood glucose response and C-peptide
levels (a protein produced by the pancreas) is used to deter-
mine the success of the pancreatic transplantation. Immedi-
ately after transplantation, blood sugar levels are monitored
every hour because glucose levels typically drop 50 mg/dL
each hour, and dextrose infusion may be necessary.62 The blood
glucose level should range between 80 and 150 mg/dL within
a few hours after the transplantation.25 C-peptide levels are
elevated, and blood sugar level returns to normal within 2 to
3 days postoperatively.9 After a diet is started, serum glucose
is monitored four times a day. Recipients should return to nor-
mal or near-normal fasting plasma glucose levels, glycosylated
hemoglobin levels (which represent the average blood glucose
level over the previous several weeks), and glucose tolerance
tests.58,64 Generally within a week to 10 days, the recipient is
weaned from insulin and becomes insulin independent, with
normal carbohydrate metabolism for an indefinite period.25,64
The need for strict adherence to a diet and constant blood sugar
monitoring should diminish.9 Long-term follow-up studies
indicate that the insulin independence can be sustained for at
least 5 years.64  Typically, simultaneous pancreas–kidney (SPK) transplanta-
Postoperative Care and Complications
The recipient may be 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 pancreas.25 A Foley cath-
eter is left in place for at least the first week to prevent disten-
tion of the bladder and leakage from a bladder anastomosis.25
During the first postoperative day, a baseline radionuclide blood
flow study of the pancreas and Doppler ultrasonography of the
allograft vasculature are performed. Repetition of these studies
and operative intervention are performed urgently with any sign
of pancreatic dysfunction.25
Acute rejection after pancreas transplantation is difficult to
diagnose. Nonspecific clinical criteria, such as fever, allograft
tenderness, weight gain, ileus, abdominal pain, hematuria, leu-
kocytosis, and hyperglycemia, can be used in combination to
detect acute pancreas rejection.59,63 Hyperglycemia does not
occur until 80% to 90% of the graft has been destroyed.30 A
decrease in bicarbonate, urine pH, or urine amylase levels of
greater than 25% from baseline, an elevation of serum amy-
lase, or a combination of these factors also indicates acute
pancreas rejection in a bladder-drained pancreas transplant
recipient.23,25,63 Percutaneous ultrasound-guided or cystoscopic
biopsy of the transplanted pancreas is used as a sensitive histo-
logic method to confirm acute graft rejection.59,65
Organ Transplantation     CHAPTER 14 363
 CLINICAL TIP
Remind patients who are status-post pancreas transplantation
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.62
 
Pancreatic Islet Cell Transplantation
Pancreatic islet beta cells are responsible for the production
of insulin. In this experimental procedure for type 1 diabetes
being performed at some U.S. centers, islet cells are first iso-
lated and removed from the pancreas of a deceased donor. Radio-
graphic (x-ray or ultrasound) guidance is used to place a catheter
through the recipient’s abdomen and into the portal vein. After
purification, the cells are injected through the catheter, and
once implanted, they begin to produce and release insulin in the
recipient. The clear advantage of this technique is its minimally
invasive nature, typically requiring only local anesthesia. How-
ever, there is still a risk for hemorrhage and thrombosis, and the
immunosuppression requirements have significant side effects.
Preliminary results show that insulin independence is achieved
in the majority of recipients; however, it has been difficult to
maintain over time.66 
Pancreas–Kidney Transplantation
Types of Pancreas–Kidney Transplantations
Simultaneous Pancreas–Kidney Transplantations
tions are offered to patients who have type 1 diabetes mellitus
with diabetic nephropathy and renal insufficiency. SPK trans-
plantations are more common than a non-lifesaving pancreas
transplantation alone, accounting for approximately 80% of
pancreas transplantations, because physicians are reluctant to
use potent immunosuppressive drugs in patients with diabetes
before they need concomitant renal transplantation.60,64 The
benefits of a successful SPK transplantation include normo-
glycemia, elimination of dialysis, prevention of reoccurring
diabetic nephropathy in the kidney graft, higher quality of
life compared with that in individuals on dialysis, and higher
10-year survival compared with individuals receiving a kidney
transplant alone.58,64
SPK transplants may be cadaveric or from living donors, in
which case a segmental pancreas transplantation is performed.
Using an abdominal midline incision, the pancreatic graft is
implanted first on the right side of the pelvis, after which the
kidney graft is implanted on the left.61,65 
Pancreas-After-Kidney Transplantations
A pancreas-after-kidney (PAK) transplantation is performed on
a patient with type 1 diabetes who has already received a func-
tioning kidney or on individuals after an SPK with a failing
pancreas graft. 
364 CHAPTER 14     Organ Transplantation
Postoperative Care and Complications
In SPK transplantations, pancreas rejection episodes frequently
occur concurrently with renal allograft rejection. Rejection of
the donor pancreas is more difficult to diagnose; therefore acute
rejection of both allografts is recognized with deterioration in
kidney function.62,64 When rejection is clinically suspected,
kidney biopsy specimens are obtained.
The SPK transplantation involves a more complex surgi-
cal procedure, with more complications, longer hospitaliza-
tion, more frequent rehospitalizations, greater morbidity, and
a higher incidence of rejection, and greater immunosuppression
required compared with renal transplantation alone.60,62 The
advantages noted earlier, including near-perfect glucose metab-
olism and the prevention of further secondary diabetic compli-
cations, help justify the increased risk.62  procedure and helping to maximize quality of life in the hospital.
Cardiac Transplantation
In 2016, 3191 heart transplantations were performed in the
United States.1,21 Over half of the individuals who underwent
transplantations in 2016 had a ventricular assist device (VAD) at
the time of their transplantation.1 As of August 2018, 3950 indi-
viduals were awaiting heart transplantation in the United States.1
Candidates for heart transplantation have irreversible end-
stage cardiac disease, no other surgical or medical options, and
a poor prognosis of survival longer than 6 to 12 months.2,4,14
Patients typically present with low exercise tolerance, cachexia,
generalized weakness, decreased muscle mass, marginal BP, dys-
pnea, and poor peripheral perfusion.67
Common indications for heart transplantation include the
following2,4,8,14:
• Severe left ventricular disease (ejection fraction less than
20% to 25%)
• Cardiomyopathy
• Ischemic heart disease
• Congenital heart disease
• Valvular disease
• Inoperable coronary artery disease, with angina refractory to
medical management
• Malignant cardiac dysrhythmias unresponsive to medical or
surgical therapy, or both
• Primary cardiac tumors with no evidence of spread to other
systems
Contraindications to cardiac transplantation include the
following4,8,23,68:
• Autoimmune disorders
• Irreversible kidney, liver, or lung disease
• Fixed pulmonary hypertension
• Unresolved pulmonary infarction
• Relative contraindications—active peptic ulcer disease, type
1 diabetes mellitus with secondary complications, COPD
with a forced expiratory volume in 1 second (FEV1) of less
than 50%, age greater than 65 years.
Pretransplantation Care
Although heart failure continues to be a significant problem, the
number of cardiac transplantations performed (approximately 2300
annually) has remained relatively unchanged.1 With demand for
donor hearts much higher than the supply, VADs and total artificial
heart (TAH) are being used as bridges to cardiac transplantation.69
Physical therapists often treat patients who have these devices and
are awaiting cardiac transplantation. A thorough understanding of
not only the precautions and contraindications but also the evidence
related to physical therapy intervention and outcomes is essential.
Please refer to Chapter 18 for information on pertinent physical
therapy implications when working with patients who have these
devices. The management of individuals with end-stage heart fail-
ure requiring transplantation is often very intensive and requires
ongoing hospitalization compared with those requiring other solid
organ transplantations. The physical therapist may be involved
with helping to condition transplantation candidates before the
 
Orthotopic and Heterotopic Heart Transplantations
Orthotopic and heterotopic transplantations are the two types of
heart transplantation procedures. The more common orthotopic
procedure involves a median sternotomy, with removal of the
recipient’s heart and the insertion of the donor heart in the normal
anatomic position.8,15,70,71 There are two variations on the ortho-
topic technique. In the standard biatrial technique, the recipient’s
native atria are left in place, and a large atrial anastomosis is used to
connect the donor with the recipient. In the bicaval technique, the
recipient’s native atria are totally excised. The bicaval technique
maintains the normal anatomy of the atria; evidence suggests that
it may result in fewer surgical and postoperative complications,
including reduced sinoatrial node dysfunction.72,73
Heterotopic or “piggy-back” transplants, which retain the
diseased heart, are rare and are used for patients with pulmonary
hypertension. Whether orthotopic transplantation or hetero-
topic transplantation is performed, temporary epicardial pacing
wires and mediastinal and pleural chest tubes are inserted before
closure of the chest wall (see Chapter 18).22,74 
Indication of Cardiac Function Posttransplantation
After the initial separation of the heart from cardiopulmonary
bypass support, the allograft requires active hemodynamic sup-
port and management. The exact type of support (pharmaco-
logic, epicardial pacing, and/or mechanical) and how long it will
be required varies tremendously between recipients. Important
indicators of function include arterial pressure, right atrial pres-
sure or central venous pressure, left atrial or pulmonary artery
wedge pressure, cardiac output, and ejection fraction. Hemo-
dynamic monitoring devices typically include a pulmonary
artery catheter and an arterial line (see Chapter 18).74 In addi-
tion, transesophageal echocardiography (TEE) and transthoracic
echocardiography (TTE) can be used to assess heart function
both intraoperatively and postoperatively. After surgery, con-
tinuous pulse oximetry and electrocardiography (ECG) is used,
and the patient’s complete blood count (CBC), arterial blood gas
(ABG), serum electrolyte, metabolic functions, and immuno-
suppressant levels are monitored closely.8,73
With reperfusion in the operating room, most recipients dis-
play a normal sinus rhythm. Sinus node dysfunction may occur
after surgical trauma or ischemia and result in bradycardia or a

slow junctional rhythm. Although this occurs less frequently
with the bicaval technique, sinus node dysfunction is treated
with atrial or atrioventricular pacing or chronotropic drugs when
it does occur. It may take the new heart a few days to achieve a
stable intrinsic rhythm, and heart rate may vary from bradycardia
to tachycardia. The target is to maintain heart rate between 90
and 100 beats per minute (bpm) to optimize cardiac output.8,73
It is typical for the transplanted heart to demonstrate functional
decline over the first 12 hours because of the effects of ischemia,
reperfusion, and myocardial edema. During this period of myocar-
dial depression, the transplanted heart may be affected temporarily
by decreased diastolic compliance, diminished systolic function,
and impaired contractility.8,24 Treatment of heart dysfunction
typically begins with pharmacotherapy, including inotropes, and
advances to an intraaortic balloon pump (IABP) and mechani-
cal support, such as with VADs, only when initial measures have
failed. Cardiac rate and function usually return to normal within
3 to 4 days, at which time the patient is weaned off intravenous
medications, mechanical support, and pacing systems.8  under fluoroscopy and local anesthesia, using a catheter inserted
Postoperative Care and Complications
Immediate postoperative care for cardiac transplant recipients
is similar to that of patients who have undergone cardiothoracic
surgery. In the initial postoperative period, mediastinal drain-
age is promoted by elevating the head of the bed to a 30-degree
angle and turning the patient every 1 to 2 hours.6 Chest tubes
are typically removed once the drainage is less than the amount
specified by the facility, and pacing wires are removed when
there are no episodes of arrhythmias, such as bradycardia.
Early postoperative management is focused on maintain-
ing hemodynamic stability, as described previously. Aside from
sinus node dysfunction and myocardial depression, other poten-
tial complications after heart transplantation include mediasti-
nal bleeding, thrombosis or leakage of anastomosis, PGF, right
heart failure, biventricular heart failure, pulmonary hyperten-
sion, pericardial effusion, renal dysfunction, immunosuppres-
sant-induced hypertension, and PTDM.8,15,26,68,73
Heart transplant recipients have an increased risk of exces-
sive postoperative bleeding and cardiac tamponade.25 Owing to
chronic congestive heart failure, patients usually have passive
liver congestion, which increases the risk of bleeding.68 Many
patients also receive anticoagulation therapy preoperatively
to prevent thrombus formation. However, inadequate heparin
reversal may occur; depending on the severity of anticoagula-
tion, treatment includes transfusion of platelets or fresh-frozen
plasma.68
PGF occurs within 24 hours after transplantation when
there is severe mechanical dysfunction without an obvious ana-
tomic or immunologic cause (e.g., hyperacute rejection), which
requires two or more inotropes or mechanical support. This can
result in left ventricular, right ventricular, or biventricular fail-
ure.73 Right heart failure is the most common cause of cardiac
dysfunction postoperatively.68 It may be caused by a preexisting
elevated pulmonary vascular resistance (PVR); donor size mis-
match, in which the donor heart is too small for the recipient;
long ischemic time; and acute rejection.68 Clinical evidence of
right ventricular heart failure includes hypotension, low cardiac
Organ Transplantation     CHAPTER 14 365
output, elevated central venous pressure, and low urinary out-
put.25 Right atrial pressure, pulmonary artery pressure, PVR,
cardiac output, and signs of right-sided heart failure are moni-
tored closely.8
Many cardiac transplant recipients have preexisting renal
insufficiency as a result of their low cardiac output, congestive
heart failure, and long-term diuretic use.8,68 After transplanta-
tion, cardiopulmonary bypass and use of nephrotoxic immuno-
suppressants can cause renal failure in the transplant recipient.8
Objective characteristics of acute rejection specific to cardiac
transplant recipients include new cardiac arrhythmias, hypoten-
sion, pericardial friction rub, ventricular S3 gallop, decreased
cardiac output, peripheral edema, pulmonary crackles, and jug-
ular vein distention.15,22,23 Recipients may report vague subjec-
tive symptoms of decreased exercise tolerance, fatigue, lethargy,
or dyspnea. However, the most reliable technique to diagnose
rejection is by performing periodic endomyocardial biopsy. The
initial biopsy is performed 5 to 10 days after transplantation
through the right internal jugular vein into the right ventri-
cle.22,68 The frequency of surveillance biopsies varies between
transplantation institutions and tends to decrease over time.22,25
If the cardiac transplant recipient has frequent arrhythmias
(which often indicate ischemia), periodic coronary angiography
is performed to detect allograft coronary disease.23,52
 CLINICAL TIP
• When managing a patient who is awaiting cardiac transplan-
tation, physical therapists should consider the guidelines for
activity in the patient population with heart failure.
• A small study performed by Forestieri et al. in 2016 in Bra-
zil demonstrated that individuals who were hospitalized with
heart failure and were awaiting heart transplantation while
on inotropic support showed positive improvements in func-
tional capacity, as demonstrated by the 6-minute walk test
(6MWT) and inspiratory muscle strength.75
 
Physical Therapy for Cardiac Transplant Recipients
Phase I cardiac rehabilitation usually begins 2 to 3 days post-
operatively, once the patient is hemodynamically stable. It is
important to recognize that the transplanted heart is physiolog-
ically different because of several factors (Table 14.2):
1. Ischemia: Procurement of the organ subjects the heart to isch-
emia and reperfusion, which may reduce myocardial contrac-
tility and impair function.76
2. Denervation: The extrinsic nervous supply to the donor heart
is severed during the procurement surgery, so the heart re-
ceives no efferent input from the autonomic nervous system
and provides no direct afferent input to the central nervous
system. The heart is unaffected by the recipient’s sympa-
thetic and parasympathetic nervous systems, which normally
control the rate and contractility. In the absence of this neu-
ral regulation, the denervated heart depends on circulating
catecholamines and the Frank-Starling mechanism to regu-
late cardiac output.8,15,22,76,77
366 CHAPTER 14     Organ Transplantation

TABLE 14.2  Physiologic Changes After Cardiac Transplantation

Maximal Posttransplanta- Physical Therapy Implica-
Resting Submaximal Exercise Exercise tion Activity tions
Heart rate Higher than normal Delayed increase (≈3–5 min) from Reduced peak Max HR achieved Use Borg Rating of Perceived
(HR) (≈90–115 beats per circulating catecholamines (≈150 bpm) in first few min- Exertion (RPE) scale with
minute (bpm); rate of HR reserve utes of recovery target 11–13 in postopera-
sinoatrial node) less than Delayed return to tive phase16
normal baseline Extend warm-up and cool-
down by 5–10 minutes
Blood Higher than normal Higher than normal systolic Slightly Delayed return to Monitor BP before, during,
pressure systolic and diastolic Appropriate response with reduced baseline and after activity
(BP) Orthostatic hypotension exercise peak Target resting BP: systolic
common (absence of Diastolic may fall with reduced BP 80–150 mmHg; dia-
reflex tachycardia)6 peripheral resistance stolic BP <90 mmHg60
Allow time to adapt to posi-
tion changes76
Cardiac Normal to slightly less Delayed increase Below Delayed return to Extend warm-up and cool-
output than normal Initial increase due to increase normal baseline down by 5–10 minutes
(CO) of stroke volume via Frank- Watch for signs/symptoms of
Starling law activity intolerance
Later due to increased HR from
circulating catecholamines

Data from: Squires RW. Exercise therapy for cardiac transplant recipients. Prog Cardiovasc Dis. 2011;53(6):429-436.

3. Diastolic dysfunction: Impaired filling is fairly common as a
result of myocardial scarring and fibrosis.76,77
4. Skeletal muscle structural and biochemical abnormalities: Heart
transplant recipients have been found to have impaired aero-
bic metabolic enzyme activity, lower capillary density, endo-
thelial dysfunction with impaired peripheral and coronary
vasodilation during exercise, and an increased proportion of
type II fibers.76,77
Additional considerations for physical therapy include the
following:
• Patients may be asked to follow sternal precautions, which
may limit shoulder range of motion (ROM), pushing, pull-
ing, and lifting for up to 6 to 8 weeks.76 However, the ex-
act definition of these precautions varies by institution and
also often by surgeon. Emerging evidence suggests that tra-
ditional sternal precautions may be overly restrictive and
impede healing and restoration of functional mobility.78,79
In transplant recipients, however, immunosuppressants may
contribute to delayed healing. It is recommended that thera-
pists consult with the medical team to assess the patient’s
risk for sternal complications and determine restrictions on
an individualized basis.
• Exercise prescription should be progressive and based on the
patient’s activity tolerance, typically beginning with active
supine exercises without resistance to ambulation and sta-
tionary biking. Extended warm-up and cool-down periods
are essential, and the RPE scale should be used to monitor
and prescribe exercise. Vital signs are monitored before, dur-
ing, and immediately after exercise. For most, oxygen satura-
tion will be normal at rest and with exercise.76
• Most recipients will not experience typical anginal symp-
toms as a result of denervation, although there is some
evidence for limited regeneration in the first few months
to years posttransplantation.76,77 The physical therapist
should monitor ECG readings for arrhythmias and stay
alert for other sign/symptoms of activity intolerance, in-
cluding fatigue, dyspnea, lightheadedness, and increased
RPE.15,22,23,71,80
• When monitoring ECG readings, there may be two P-waves
if both donor and recipient sinoatrial nodes are present. The
recipient-generated P-wave does not cross the surgical suture
line, however, so there should only be one QRS wave from
the donor heart.68,81
• Overall, adult heart transplant recipients have an approx-
imately 30% to 40% lower exercise capacity (oxygen con-
sumption) than do healthy age-matched and sex-matched
controls.82 The cause of this is likely multifactorial,
with potential factors including the physiologic differ-
ences outlined previously, tissue damage from rejection
episodes, general pretransplantation deconditioning, and
long-term immunosuppressant use.82 Because early car-
diac rehabilitation has been found to improve exercise
capacity83 and posttransplantation quality of life, discuss-
ing potential participation in outpatient cardiac rehabili-
tation with the medical team should occur before hospital
discharge.84
 CLINICAL TIP
Complaints of chest pain from the recipient may result from the
sternal incision and musculoskeletal manipulation during sur-
gery but are likely noncardiac because of denervation.85
 
Lung Transplantation
In 2016, 2327 lung transplantations were performed in
the United States.1,21 Of these, 1757 were bilateral lung

transplantations,1, and 588 were single lung transplantations.
As of August 2018, 1455 individuals were awaiting lung trans-
plantation in the United States.1
Lung transplantation is indicated for end-stage pulmonary
disease caused by a variety of medical conditions. Major indica-
tions include the following6,7,29:
• COPD (with FEV1 of less than 20% of predicted value)
• Cystic fibrosis (with FEV1 of less than 30% of predicted
value)
• Emphysema
• Bronchiectasis
• Primary pulmonary hypertension
• Pulmonary fibrosis
• Eisenmenger’s syndrome (a congenital heart disease)
• Alpha1-antitrypsin deficiency
Less-frequent indications include the following:
• Sarcoidosis (see Appendix 13.A)
• Eosinophilic granuloma
• Scleroderma
Contraindications to lung transplantation include the
following4,29:
• Absolute86:
• Adults with a recent history of malignancy
• Poorly controlled significant dysfunction of another ma-
jor organ, unless multiorgan transplant is being consid-
ered
• Uncorrected coronary artery disease (CAD) with end-
organ ischemia or dysfunction and/or CAD not amenable
to revascularization
• Unstable medical condition (acute sepsis, myocardial
infarction, liver failure)
• Uncorrectable bleeding disorder
• Poorly control infection with virulent and/or resistant
microbes
• Evidence of Mycobacterium tuberculosis infection
• Chest wall or spinal deformity expected to cause severe
restriction after transplantation
• Class II or III obesity (body mass index [BMI] ≥35 kg/
m2)
• Current nonadherence to medical therapy or a history of
repeated or prolonged nonadherence
• Psychiatric or psychological issues that affect the ability
to comply with a complicated medical regimen
• Inadequate social support
• Functionally limited with inability to participate in
rehabilitation program
• History of illicit substance abuse or dependence
• Relative86:
• Age greater than 65 years, with low physiologic reserve
and/or other relative contraindications
• Class I obesity (BMI 30.0–34.9 kg/m2)
• Significant malnutrition
• Significant osteoporosis
• Extensive prior chest surgery with lung resection
• Mechanical ventilation and/or extracorporeal life support
(ECLS) (However, transplantation may be successful in
carefully selected patients.)
Organ Transplantation     CHAPTER 14 367
• Colonization with resistance or highly virulent pathogens
• H epatitis B and/or C—lung transplantation should be
performed in centers with experienced hepatology units
• HIV infection—lung transplantation should be per-
formed in centers with expertise in caring for HIV-posi-
tive patients
• CAD—disease burden enough to put the candidate at
risk after transplantation
• Extrapulmonary conditions that have not resulted in
significant end-organ damage (e.g., diabetes mellitus
or systemic hypertension)—should be well-controlled
before transplantation
Types of Lung Transplants
There are three types of surgical procedures for lung transplan-
tation, discussed in the following sections.
Single-Lung Transplantation
This is the most common surgical technique and is indicated
for all types of end-stage lung disease, except cystic fibrosis and
bronchiectasis.6 It involves a single anterolateral or posterolat-
eral thoracotomy in which the right or left cadaveric lung is
transplanted into the recipient.29 
Double-Lung or Bilateral Lung Transplantation
With double-lung transplantation, the left and right lungs are
transplanted sequentially into one recipient, with the least func-
tional lung resected and replaced first.29 The incision used is a
bilateral anterior thoracotomy in the fourth or fifth intercostal
space, or the surgeon may choose a transverse sternotomy to cre-
ate a “clamshell revision.”29 This may be used in individuals with
cystic fibrosis, bronchiectasis, or pulmonary hypertension.6,30 
Living Donor Lobar Transplantation
Transplantation of lobes involves bilateral implantation of lower
lobes from two blood-group–compatible living donors.6 The
donor’s lungs are larger than the recipient’s in order for the
donor lobes to fill each hemithorax.6 This procedure is rare and
is performed primarily in patients with cystic fibrosis.25 
Preoperative Care
Patients awaiting lung transplantation often present with
decreased work capacity in both respiratory and skeletal muscles,
significantly lower daily physical activity than what has been
found in individuals with chronic disease.87 Preoperative physical
therapy should focus on improving functional mobility and exer-
cise capacity with the goal of increasing quality of life and activ-
ity tolerance postoperatively. The preoperative program should
include resistive training with focus on the proximal muscles of
the upper and lower extremities, core muscles, and respiratory
muscles, as well as aerobic training. Interval training may allow
potential recipients to better tolerate exercise. Caution should be
used with upper extremity exercise because it may lead to dys-
synchronous thoracoabdominal breathing and dyspnea in indi-
viduals with severe respiratory disease.2 The literature supports
using tools, such as the 6MWT (see Chapter 23 on Outcome
Measures), muscle endurance test (using timed stair climbing),
368 CHAPTER 14     Organ Transplantation
and shuttle test, to assist in objectively demonstrating training
effects. The 6MWT has been has been found to be a strong pre-
dictor of mortality both before and after lung transplantation;
however, further research is needed to determine whether reha-
bilitation focused on improving this before transplantation will
increase survival.88 Physical therapists also play a role in using
airway clearance techniques (see Chapter 22) because patients are
often admitted with pulmonary decompensation while waiting
for transplantation.89  and detect early rejection, especially in bilateral lung transplant
Indication of Lung Function Posttransplantation
For patients with pulmonary vascular disease, single-lung or
double-lung transplantation results in an immediate and sus-
tained normalization of pulmonary vascular resistance and
pulmonary arterial pressures.6 This is accompanied by an imme-
diate increase in cardiac output. Arterial oxygenation gener-
ally returns to normal, and supplemental oxygen is no longer
required, usually by the time of hospital discharge.6
The maximum improvement in lung function and exercise
capacity is achieved within 3 to 6 months after transplantation,
once the limiting effects of postoperative pain, altered chest
wall mechanics, respiratory muscle dysfunction, and acute lung
injury have subsided.6,7 After double-lung transplantation, nor-
mal pulmonary function is usually achieved. However, in sin-
gle-lung transplantation, lung function improves but does not
normalize fully owing to the disease and residual impairment
of the remaining nontransplanted lung. Lung volumes and flow
rates improve to two thirds of normal in single-lung transplan-
tation.7 Most lung transplant recipients are therefore able to
resume an active lifestyle free of supplemental oxygen, with less
dyspnea, and with improved exercise tolerance.  use of pulmonary rehabilitation (PR), both on inpatients and
Postoperative Care and Complications
Ineffective postoperative airway clearance occurs after lung trans-
plantation. Recipients present with an impaired cough reflex,
incisional pain, altered chest wall musculoskeletal function,
and diminished mucociliary clearance.89 Bronchopulmonary
hygiene is a crucial part of postoperative care because it helps
mobilize secretions and prevents atelectasis and mucus plug-
ging. It may also help improve activity tolerance if performed
before exercise because airflow obstruction has been found to
limit daily physical activity levels in transplant recipients.87
Postoperative complications that may develop in the dener-
vated transplanted lung include pulmonary edema or effusion,
acute respiratory distress syndrome, dehiscence of the bronchial
anastomosis, and anastomotic stenosis.6 Single-lung transplant
recipients may experience complications of ventilation–perfu-
sion mismatch and hyperinflation owing to the markedly dif-
ferent respiratory mechanics in each hemithorax.25 The rate of
infection in lung transplant recipients is higher than that in
other organ transplant recipients because the graft is exposed to
the external environment through the recipient’s native airway.
The patient’s WBC and absolute neutrophil counts are moni-
tored closely.9 Bacterial pneumonia and bronchial infections are
very common complications that usually occur in the first 30
days.5,25 Bronchoalveolar lavage is used to diagnose opportunis-
tic infections.2
Clinical manifestations of acute pulmonary rejection in lung
transplant recipients include dyspnea, nonproductive cough,
leukocytosis, hypoxemia, pulmonary infiltrates as seen on chest
x-ray (CXR), sudden deterioration of pulmonary function tests
(PFTs), elevated WBC count, need for ventilatory support, fever,
and fatigue.9,23,29 The rejection typically presents with a sudden
deterioration of clinical status over 6 to 12 hours.30 Daily docu-
mentation of oxygen saturation and FEV1 is used to monitor
recipients, because a decline in oxygen saturation or spirometry
values in excess of 10% commonly accompany episodes of rejec-
tion or infection.6,7,85 Bronchoscopic lung biopsy, bronchiolar
lavage, and cytoimmunologic monitoring of the peripheral
blood may be used to diagnose acute rejection.6,30,85
Bronchoscopy is performed routinely, and whenever rejection
is suspected, to assess airway secretions, healing of the anasto-
mosis, and the condition of the bronchial mucous membrane.23
The first bronchoscopy is performed in the operating room to
inspect the bronchial anastomosis.30 To prevent infection and
atelectasis, routine fiberoptic bronchoscopy with saline lavage
and suctioning are used to reduce accumulation of secretions
that the recipient is unable to clear.25 
Physical Therapy for Lung Transplant Recipients
Pretransplantation
• Physical rehabilitation can optimize physical function pre-
transplantation and facilitate recovery posttransplantation.90
A recent systematic review by Hoffman et al. examined the
outpatients, and showed that PR can improve exercise capac-
ity and quality of life over time regardless of the underlying
pulmonary disease. The study also reported that PR can be a
beneficial and effective treatment for patients with advanced
lung disease on the waiting list for transplantation.91
• There is limited research on the physical therapy manage-
ment of individuals awaiting lung transplantation on an
inpatient basis. Before transplantation, the goal is to keep
the patient as physically active as possible and to provide
education on the upcoming surgery and postoperative expec-
tations.
• Exercises chosen in the preoperative period include those
that decrease ventilatory needs and could include interval
training, resistance training, or single leg exercises.92 Sug-
gested guidelines from evidence-based and expert-informed
clinical approaches are available in the literature for patients
awaiting lung transplantation or posttransplantation.90,93
Wickerson et al. further classified the conditions of patients,
according to their pretransplantation courses, as “compli-
cated” or “uncomplicated” and provided their expert recom-
mendations.90 
Posttransplantation
After lung transplantation and after extubation, aggressive
bronchopulmonary hygiene should be performed every 2 to 4
hours while the patient is awake.23

An effective bronchopulmonary hygiene program should
include the following23:
• Reeducation in coughing techniques after denervation
(splinted cough with a pillow may assist with pain control)
• Education in breathing techniques, including diaphragmatic
breathing
• Suctioning to remove secretions and help maintain adequate
oxygenation (when intubated, a premeasured catheter can be
used to prevent damage to the anastomosis)
• Vibration and gentle percussion (see Chapter 22)
• Incentive spirometry and use of a flutter device to maximize
lung expansion and prevent atelectasis and pneumonia (see
Chapter 22)
• Chest and upper extremity mobilization exercises, which
can be used to help improve thoracic mobility with caution
taken to protect the incision2
• Postural drainage and positioning (see Chapter 22)
• During the first 24 hours after surgery, patients with
double-lung transplants should be turned side to side.
Turning is initiated gradually, beginning with 20- to
30-degree turns, assessing vital signs, and then increas-
ing gradually to 90 degrees each way, every 1 to 2 hours.
Prolonged periods in the supine position are avoided to
minimize secretion retention.23
• Patients with single-lung transplants should lie on their
nonoperative side to reduce postoperative edema, assist
with gravitational drainage of the airway, and promote
optimal inflation of the new lung.23
• There is limited research regarding the rehabilitation of pa-
tients during hospitalization early after lung transplantation.
There are suggested elements of rehabilitation based on con-
sensus or experience of clinicians.92
Suggested elements of rehabilitation after lung transplantation,
according to Rochester et al., include93:
• Beginning rehabilitation 24 hours postoperatively with an
emphasis on early mobilization
• Early inpatient postoperative rehabilitation, which should
include breathing retraining, reassessing supplemental oxy-
gen requirements, balance activities, building upper and
lower extremity ROM, and management of any neuropathic
pain:
• Hillegass et al. provided guidelines for physical thera-
pists regarding the assessment and management of
supplemental oxygen for patients with cardiopulmonary
disease.94
• Direction and encouragement to cough secondary to inci-
sional pain and denervated cough reflex of the donor lung
• Transfer training, and ambulation using a specialized walker,
with care managing chest tubes and pain
• Exercise progression to gradually incorporate lower limb re-
sistance training
• Lifting and upper limb ROM precautions and limitations,
which may be maintained up to 6 weeks postoperatively, de-
pending on the surgical approach
• Ensuring adequate lower extremity strength, balance, and
gait to promote patient safety and to minimize the risk for
falls before hospital discharge
Organ Transplantation     CHAPTER 14 369
• P
 rovision of necessary medical and adaptive equipment at
discharge
 CLINICAL TIP
Initially, most lung transplant recipients are asked to follow
thoracotomy precautions, which include lifting restrictions. The
restrictions generally include not lifting anything heavier than
5 lb95 to 10 lb.96-98 Patients are generally restricted to partial
weight bearing on their upper extremities, which may limit the
use of an assistive device, at least temporarily. It is important to
check with the medical team about specific precautions and to
determine when it is safe to incorporate assistive devices and up-
per extremity resistance exercises (generally after 6–12 weeks).
In spite of improved lung function posttransplantation,
exercise capacity continues to be impaired (40% to 60% of pre-
dicted).99 Studies indicate that lower extremity skeletal muscle
dysfunction, rather than dyspnea, is the primary limiting factor
impairing exercise tolerance in patients after lung transplan-
tation.100 This muscle dysfunction includes decreased muscle
mass and strength, reduced proportion of type I fibers, decreased
mitochondrial enzyme activity, impaired calcium uptake and
release, and an impaired capacity for oxidative metabolism.99-101
Several factors may contribute to this, such as pretransplanta-
tion skeletal muscle changes as a result of the disease process and
the side effects of immunosuppressive drugs given pretransplan-
tation and posttransplantation, as well as inactivity.99
Evidence suggests that structured exercise training programs,
including aerobic conditioning and upper and especially lower
limb strengthening, may improve functional exercise capacity,
skeletal muscle strength, and lumbar bone mineral density in
lung transplant recipients.101 However, further research is still
needed to determine optimal exercise guidelines for this popu-
lation. Multiple rest periods may be required during activity at
the beginning of the postoperative period to limit the amount
of dyspnea and muscle fatigue. Rest periods can be gradually
decreased so that the patient advances toward periods of con-
tinuous exercise as endurance improves.
 CLINICAL TIP
Always monitor the recipient’s oxygen saturation before, dur-
ing, and after exercise. If the patient is on room air at rest, sup-
plemental oxygen may be beneficial during exercise to reduce
dyspnea and improve activity tolerance. The lung transplant
recipient should maintain an arterial oxyhemoglobin saturation
greater than 90% with activity.102
Heart–Lung Transplantation
In 2016, 18 heart–lung transplantations (HLTs) were performed
in the United States.21 As of August 2018, in the United States,
50 individuals were awaiting HLT.1
HLT is performed on patients who have coexisting end-stage
pulmonary disease and advanced cardiac disease that produces
right-sided heart failure.23
370 CHAPTER 14     Organ Transplantation
Indications for HLT include the following6,81:
• 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 dys-
function 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.25 Postoperative
care after HLT is similar to that after heart and lung posttrans-
plantation as previously discussed. Rejection of the heart and
lung allografts occurs independently of each other.81 Bacterial
pneumonia from contamination in the donor tracheobronchial
tree is the most common cause of morbidity and mortality after
HLT.  Patient Preparation
Hematopoietic Stem Cell Transplantation
According to the Center for International Blood and Bone Mar-
row Transplant Research, in 2014, 19,862 hematopoietic stem
cell transplantations (HSCTs) were performed in the United
States.103
Hematopoietic stem cells (HCTs), which are primitive cells
found in bone marrow, circulating blood, or umbilical cord,
have the capacity to evolve into specialized cells, including
mature blood cells (WBCs, red blood cells [RBCs], and plate-
lets).104,105 Blood-forming cells for HSCT can be harvested
from blood, bone marrow, or the umbilical cord.104,105 HSCT is
performed for a variety of conditions to replace defective blood
cells and restore hematologic and immunologic functions.
However, this approach is only used after conventional meth-
ods of treatment have failed. Indications for HSCT include the
following14,80,105-108:
• Malignant disorders (e.g., myelodysplastic syndromes, acute
lymphocytic or myelogenous leukemia, chronic myelog-
enous leukemia, lymphoma, multiple myeloma, neuroblas-
toma, and selected solid tumors, including breast, ovarian,
and testicular cancers)
• Nonmalignant hematologic disorders (e.g., aplastic anemia,
sickle cell anemia, and thalassemia)
• Solid tumors (medulloblastomas and germ cell tumors)
• Immunodeficiency disorders (severe combined immunodefi-
ciency disease)
Contraindications to SCT include the following108:
• 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)
When the stem cells are harvested from bone marrow, the
procedure is referred to as bone marrow transplantation (BMT),
and when the cells are taken from blood, it is referred to as
peripheral blood stem cell transplantation (PBSCT).
The three types of HSCT are allogeneic, syngeneic, and autolo-
gous transplantations104:
1. In allogeneic transplantation, cells are harvested from an HLA-
matched donor, who may be related or unrelated. Umbilical
cord blood can also be used. A move has been made from
standard serologic tissue typing toward DNA-based proce-
dures to improve HLA matching. Improved matching has
been shown to decrease time to engraftment, decrease in-
cidence of graft-versus-host disease (GVHD), and improve
overall transplant survival.109
2. In syngeneic transplantation, cells are harvested from an identi-
cal twin.
3. In autologous transplantation, the donor and the recipient are
the same person. Cells harvested from the patient when he or
she is healthy or in complete remission are frozen and stored
for future reinfusion.
Before SCT, the recipient’s body is deliberately immunosuppressed
to gain the greatest acceptance of the graft. The recipient undergoes
a 2- to 4-day cytoreduction protocol, consisting of ablative chemo-
therapy, radiation, or both, designed to destroy malignant cells and
to create space in bone marrow for the engraftment of new mar-
row.7,14,106 New protocols for nonmyeloablative transplantations or
reduced-intensity transplantations are evolving; these procedures
use lower, less toxic doses of chemotherapy or radiation during the
cytoreduction phase for allogenic transplantations. This process
will eliminate some, but not all, of the patient’s bone marrow. It
is believed that donor graft cells may help attack the remaining
malignant cells when they react immunologically, a process called
the graft-versus-tumor (GVT) effect.104,105 
Harvesting
In BMT, bone marrow is harvested via multiple needle aspira-
tions, most commonly from the posterior and anterior iliac crests
of the donor or, less commonly, from the sternum.105 About 500
to 2500 mL of aspirated marrow is filtered, heparinized, mixed
with peripheral blood, frozen, and stored.14 The donor may
experience some soreness and stiffness at the graft site; however,
the body replaces the lost marrow, and most donors recover fully
within 3 to 4 weeks.105
For PBSCT, the cells are harvested through apheresis or leu-
kapheresis. During apheresis, the patient’s blood is removed via
a central venous catheter or from a large vein in the arm. It is
then circulated through a high-speed cell separator in which
the peripheral stem cells are removed, frozen, and stored. The
plasma cells and erythrocytes are reinfused into the patient.
Donors may be given a hematopoietic growth factor before
apheresis to increase the number of cells available. The process
of apheresis takes about 4 to 6 hours. Apheresis may cause some
temporary constitutional symptoms such as minor bone and
muscle aches, headache, fatigue, nausea, vomiting, and/or dif-
ficulty sleeping.9,105 
Reinfusion and Indication of Postprocedure Function
One to 3 days after the last dose of chemotherapy or radiation,
the cells are then infused into the patient, much like a blood

transfusion, through a central venous access device or Hickman
right atrial catheter. The most common side effects of reinfusion
are fever, chills, nausea, headache, and flushing.9,110
The stem cells that were infused migrate to the recipient’s
marrow cavities and begin to produce new blood cells, a pro-
cess known as engraftment. A successful engraftment, which is
indicated by an increase in the platelet, RBC, and WBC counts,
is determined 10 to 21 days after transplantation.82,110,111
Generally the minimum criteria for engraftment includes (1)
absolute neutrophil count (ANC) of 500 mm3 or greater for 3
consecutive days; (2) platelet count of 20,000 mm3 or greater
for 3 consecutive days (and without transfusions for 7 days);
and (3) hematocrit 25% or greater for at least 20 days without
transfusion.111 General timelines for engraftment vary, based on
the type of graft and the location from which the HSCs were
harvested—between 9 and 14 days from transplant infusion for
PBSCT, between 12 and 18 days from transplant infusion for
BMT, and 25 to 56 days from transplant infusion for cord blood
transplantation (CBT).80 Recovery of platelet production is
more delayed, with transfusion independence usually occurring
within 5 to 7 weeks after transplant infusion.111 The hemato-
logic recovery after PBSCT is approximately a week earlier than
with BMT because the stem cells procured from the peripheral
blood are more mature than those in bone marrow.80  1 to 3 weeks after transplantation and spontaneously resolves
Postprocedure Care and Complications
Complications during or after HSCT include marrow failure,
infection, hemorrhage, pulmonary,112 cardiac gastrointestinal
(GI) infections, acute renal failure, venoocclusive disease of the
liver, engraftment syndrome, and GVHD.113 Complications can
be classified as acute or chronic, with acute complications occur-
ring through the conditioning phase through the first 100 days
after HSCT.113
All recipients undergoing HSCT 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 to 4
weeks after transplantation. Recipients will likely present with
pancytopenia, a marked reduction in RBCs, WBCs, and plate-
lets.12,76,80 During this time, recipients may receive daily trans-
fusions of platelets, lymphocytes, and granulocytes (preferably
from the donor) and antimicrobial therapy to counteract the
side effects of hemorrhage and infection.9,76 Daily bone mar-
row aspirations and CBCs are performed to monitor the progress
of the grafts and to check for recurrence of malignancy. HSCT
recipients are at risk for fatal infection because normal immune
function may not be regained for 12 to 18 months when the
transplanted immune system has fully matured.12,80 Hemor-
rhage is also a significant threat because of impaired clotting
from the loss of platelets. Because of prolonged neutropenia and
immunosuppression, the patient undergoing HSCT is at severe
risk for many types of infection.113 The hemodynamic response
to infection poses the greatest threat to patients.
Pulmonary complications after HSCT result from chemo-
therapy or direct radiation therapy.113
Complications include112,113:
• Idiopathic pneumonia syndrome
• Diffuse alveolar hemorrhage
Organ Transplantation     CHAPTER 14 371
•  hemotherapy or traditional associated pulmonary toxicity
C
• Pulmonary embolism
• Pulmonary edema
• Infection
• Bronchiolitis obliterans syndrome (BOS)
Cardiac complications can arise from dysfunction of the
cardiac muscle, valvular abnormality, or dysfunction of the
conduction system.114 Cardiac toxicity can occur during the
conditioning phase and the recovery phase after the transplanta-
tion. Common complications include cardiomyopathy, pericar-
ditis, and arrhythmia. Risk factors for cardiomyopathy include
the use of chest irradiation, age between 45 and 59 years, and
the use of anthracyclines. The most common arrhythmias are
atrial dysrhythmia and supraventricular tachycardia. Arrhyth-
mias can be caused by chemotherapy, radiation, infection, and
fluid volume shifts.113
Venoocclusive disease, also known as sinusoidal obstruction syn-
drome,114 is characterized by obstruction of the hepatic venules
by deposits of collagen and fibrin formed as a result of endo-
thelial cell damage with chemotherapy and radiation. Clinical
manifestations of venoocclusive disease include sudden weight
gain,113 increased LFTs, hepatomegaly,113 right upper quadrant
pain, ascites, and jaundice.106 Venoocclusive disease may occur
within 2 to 3 weeks in approximately half of those affected.14
Engraftment syndrome (ES) presents as a combination of
signs and symptoms, including fever, rash, fluid retention,
weight gain, hypoxia, noncardiogenic pulmonary edema, pul-
monary infiltrates, and/or diffuse alveolar hemorrhage.111 It
typically presents within 96 hours of neutrophil recovery.111
GVHD is a complication that occurs in approximately
20% to 70% of allogeneic transplant recipients and may be
either acute or chronic.115 It is caused by activated produc-
tion of T lymphocytes in the donor marrow that react immu-
nologically to the host recipient and attack the host cells.114
Acute GVHD occurs typically between 3 and 30 days after
transplantation.9,106,116 Typical sites of tissue damage occur
at the mucus membranes.113 Major organs affected by GVHD
are the skin, liver, GI tract, and lymphoid system.9,106,113,114
Skin involvement manifests as an erythematous rash that can
progress to blistering and desquamation. Liver manifestations
include increased liver enzymes and bilirubin, right upper
quadrant pain, hepatomegaly, and jaundice. GI tract manifesta-
tions include nausea, vomiting, diarrhea, malabsorption, ileus,
sloughing of intestinal mucosa, abdominal pain, cramping, and
bloody stools.9,106 Diagnosis of GVHD is made via biopsy of the
tissue.114 GVHD is treated with immunosuppressive medica-
tions,110 via steroids.113 GVHD does, however, appear to have
a protective effect against some leukemias because the donor
cells may also attack the malignancy in the host and prevent
relapse.115 
Physical Therapy for Stem Cell Transplant Recipients
Physical therapy is beneficial to SCT recipients during their pro-
longed hospital stay, with an average duration of 5 weeks.116 Pro-
longed bouts of malaise, fever, diarrhea, nausea, and pain resulting
from inflammation of the mucous membranes of the mouth and
372 CHAPTER 14     Organ Transplantation
digestive tract, which usually accompanying SCT, can be debilitat-
ing. Initially physical therapists provide a gentle exercise program
to prevent deconditioning and muscle atrophy 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. Evidence demonstrates
the benefits of a posttransplantation exercise program, including
decreased fatigue and time in the hospital, as well as minimized
WBC and platelet drops frequently seen after transplantation.117
A systematic review and meta-analysis examining exercise for
individuals undergoing HSCT suggests that it is beneficial to
start an exercise program before or just after transplantation.118
Immediately posttransplantation, the role of the rehabilita-
tion professional is to maintain function, reduce symptom bur-
den, maintain muscle mass, reduce the risk for pneumonia and
atelectasis, and improve aerobic exercise.118 Structured exercise
is also reported to be more beneficial than simple encourage-
ment to perform exercise.118
Current research suggests that physical activity is effective
at reducing fatigue in patients with cancer and those who have
undergone HSCT. Physical activity should therefore be promoted
in the management of fatigue in this patient population.119
SCT recipients typically require 6 months to a year before
they recover their full strength and return to their normal
lifestyle.110
It is important that physical therapists routinely moni-
tor the CBC and consider the implications of abnormal values
when designing treatment plans. Values especially important in
this patient population include hemoglobin/hematocrit, WBC
count (especially the absolute neutrophil count), and platelets
(Table 14.3). Caution should also be used with patients who
present with temperature above 99.5°F.117  counts122 between 20,000 and 40,000 mm3,123 or below
Physical Therapy Management
Physical therapists play an integral role in the rehabilitation of
transplant recipients. With the exception of SCT recipients, the
LOS in an acute care hospital ranges from 3 to 16 days depend-
ing on the type of organ transplantation and barring any compli-
cations. The shortest LOS is generally for kidney recipients and
the longest for SPK recipients. Some factors that may prolong
hospitalization include the following: advanced recipient age and
comorbidities, use of ECD organs, organs donated after cardiac
death, or those with increased cold ischemic time.10,13,25,26,71
Given the short LOS for many transplant recipients, physical
therapists are consulted in the early postoperative period to pro-
vide treatment and assist the transplantation team with a safe dis-
charge plan. If patients are medically stable but need assistance for
activities of daily living and ambulation, they will require transfer
to a rehabilitation facility for further physical and occupational
therapy before being discharged home.
Goals
In the acute care setting, the primary physical therapy goals are
similar to those for postoperative abdominal or cardiothoracic
surgical patients. These goals include maximizing functional
mobility and endurance; improving ROM, 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 years before receiving their transplant and may pres-
ent with other medical comorbidities. As a result, they are
usually physically deconditioned and present with a marked
reduction in exercise capacity and skeletal muscle strength
owing to longstanding pretransplantation physical inactivity.
Generalized weakness results from the disease process, fluid and
electrolyte imbalance, and poor nutrition. After transplantation,
recipients generally require a longer time frame to regain their
strength and endurance and to achieve their goals. 
General Physical Therapy Considerations for Transplant
Recipients
• C oordinate the best time for physical therapy with the pa-
tient’s nurse each day. The patient may be fatigued after
other interventions or medically inappropriate for exercise
owing to a decline in medical status, especially in the ICU
or early in the postoperative course. Visits should also ideally
be scheduled after patients have received their pain medica-
tions and any breathing treatments. Incisional pain can limit
activity progression, deep breathing exercises, and coughing.
• During the ICU stay, it is recommended to keep mean arte-
rial pressure (MAP) above 60 to 70 mmHg to maintain safe
organ perfusion.120
• Analyze laboratory values daily, as they may change dramati-
cally from day to day (see Table 14.3):
• Many recipients have very low platelet counts imme-
diately posttransplantation. Patients with low platelet
counts or increased PT/INR, PTT, or both are at risk
for bleeding. Coagulopathy121,122,124 and low platelet
20,000 per mm3,70,124 are conditions that should be
considered relative contraindications or precautionary to
deliver percussion as a manual therapy airway clearance
technique and caution should be used with suctioning.
Other aspects of bronchopulmonary hygiene, as described
under Lung Transplantation, may still be performed.
• Anemia is also common posttransplantation, and recipi-
ents may present with reduced activity tolerance.
• WBCs, especially neutrophils, are also commonly af-
fected after transplantation and should be monitored
carefully in light of the high risk of infection.
• Each type of solid organ transplant has other specific
values that help indicate graft function and should be
followed (e.g., creatinine for kidney, blood glucose and
C-peptide levels for pancreas).
• Infection control is vitally important after transplanta-
tion. Depending on the type of transplantation and the
medical status, patients may be placed in a protective
isolation room and positive-pressure flow rooms may be
used to limit the transfer of airborne pathogens. Strict
hand washing and standard precautions are essential, and
the use of a face mask is often required of the health care
worker entering the room and/or for patients when they
are leaving their room.71
 Organ Transplantation     CHAPTER 14 373

TABLE 14.3  Laboratory Values in Transplantation

Laboratory Value Reference Value Abnormal Value Physical Therapy Implications
White blood cell 5–10 109/L <4.0 109/L (leukopenia) Symptoms-based approach when determining appropriateness for activ-
ity; especially in the presence of fever
Risk for infections
<1.5 109/L (neutropenia) Neutropenic precautions (dependent on facility guidelines)
0.5–1 109/L (moderate Symptoms-based approach when determining appropriateness for activ-
neutropenia) ity; especially in the presence of fever
<0.5 109/L (severe neu- Risk for infections
tropenia) Absolute neutrophil count of ≤0.5: avoid activities that increase risk of
bacterial infection
Platelets 140,000– <150,000/μL Fall risk awareness (risk of spontaneous hemorrhage)
400,000/μL (thrombocytopenia) Check for petechiae
Check for active signs of bleeding (e.g. bleeding gums, coughing up
blood, painful swollen joints, etc.)
>50,000/μL: active resistive movements
<20,000/μL (severe Symptoms-based approach when determining appropriateness for activ-
thrombocytopenia) ity; collaborate with interprofessional team (regarding possible need
for/timing of transfusion before mobilization)
Fall risk awareness (risk of spontaneous hemorrhage)
Check for petechiae
Check for active signs of bleeding (e.g. bleeding gums, coughing up
blood, painful swollen joints, etc.)
<20,000/μL: active movements; no resistive motions
<5000/μL: only active assistive movements/no Valsalva
Hemoglobin Male: 14–17.4 g/dL Trending down (anemia) Monitor vitals including SpO2 to predict tissue perfusion
Female: 12–16 g/dL <8 g/dL May present with tachycardia and/or orthostatic hypotension
Symptoms-based approach when determining appropriateness for activ-
ity; collaborate with interprofessional team (regarding possible need
for/timing of transfusion before mobilization)
Consultation with the interprofessional team as well as monitoring of
signs and symptoms imperative because hemoglobin levels and blood
transfusions are individualized
Patients with hematologic disorders, oncologic disorders, and severe
thrombocytopenia or chronic transfusion-dependent anemia: no trans-
fusion threshold recommendation available
Fatigue, increased rest periods, increased heart rate
<8 g/dL: defer therapy if symptomatic
8–10 g/dL: monitor patient closely (shorten therapy session)
<10 g/dL: resistive exercise
<5–7 g/dL Low critical values (<5–7 g/dL) can lead to heart failure or death
Hematocrit Male: 42% to 52% Trending down (anemia) If <25%: Symptoms-based approach when determining appropriateness
Female: 37% to 47% for activity; collaborate with interprofessional team (regarding pos-
sible need for/timing of transfusion before mobilization)
<20% can result in cardiac death/failure
<25%: defer therapy
25% to 30%: ADL and exercise as tolerated
30%: can add resistive exercise

Data obtained from APTA Task Force on Lab Values. Laboratory Values Interpretation Resource. Academy of Acute Care Physical Therapy website. https://cdn.ymaws.c-
om/www.acutept.org/resource/resmgr/docs/2017-Lab-Values-Resource.pdf. Published 2017. Accessed September 25, 2018; Shin KY. Cancer. New York: Demos Medical;
2014. http://wa.opal-libraries.org/login?url=http://search.ebscohost.com/login.aspx?direct=true&db=nlebk&AN=654885&site=ehost-live. Accessed October 3, 2018.

• S upine therapeutic exercise in the acute care setting is im-
plemented only if necessitated by the recipient’s condition,
such as high fever, chills, bed rest restriction, or low platelet
count. A high temperature will result in elevated respiratory
and heart rates; therefore it is important to avoid strenuous
cardiovascular and resistance exercises during this time.
• Timeline to mobilization out of bed after transplantation is
variable and depends on several factors, including preopera-
tive status, type of transplantation, and complications. Early
ambulation helps decrease the risk of cardiovascular and pul-
monary infections, increases blood circulation, stimulates GI
function, relieves gas pains, and maintains muscle tone.24,125
• Many posttransplantation patients retain fluid, especially
in the lower extremities. Weight bearing may be painful;
however, ambulation for short periods should still be encour-
aged. The recipient’s balance may be altered secondary to in-
creased fluid retention, 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 maintain maxi-
mum safety.
374 CHAPTER 14     Organ Transplantation
• A lways monitor and document vital signs, oxygen satura-
tion, and RPE (for cardiac transplant recipients) before,
during, and after physical therapy intervention. 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 document daily progress or decline as well as vital sign
responses.
• Many patients experience some form of organ rejection. If ap-
proved by the transplantation team, exercise generally con-
tinues if the rejection episode is mild to moderate.22,99
• The adverse effects of immunosuppressants may produce
delayed wound healing and can contribute to osteoporosis.
Upper extremity resistance training is important; however,
it should be delayed for cardiac and lung transplant recipi-
ents until cleared by the medical team (generally around 6–8
weeks posttransplantation), when wound and tissue healing
is complete. All recipients should be instructed in postural
awareness, alignment, exercise, and optimal body mechanics
to combat the effects of osteoporosis.67
• Consider the implementation of standardized outcomes mea-
sures to objectively assess and document patient status and
improvement. For example, the 6MWT has been frequently
used in patients after heart and lung transplantations and
also with patients after liver transplantation in the immedi-
ate postoperative period.76,126 Other tests, such as the sit-to-
stand (STS)-10 and the STS-60, have been studied in patients
undergoing dialysis and may be appropriate for patients after
kidney transplantation.127  *“This work was supported in part by Health Resources and
Activity Progression
Activity posttransplantation is progressed gradually by the
physical therapist, according to foundational exercise principles,
while monitoring for signs and symptoms of activity intolerance
and making appropriate adjustments. Physical therapists should
refer to the individual transplantation sections for special con-
siderations when designing and implementing programs. Ini-
tially most transplant recipients will fatigue easily and require
frequent rest periods. Thus shorter and more frequent treatment
sessions may be beneficial.  in exercise in solid organ transplantation. Am J Transplant.
Patient Education
• P
 hysical therapists assist in the education of transplant re-
cipients. Recipients must assume an active role in health
care after transplantation. Patients are educated preopera-
tively about what to expect after transplantation. Initially,
the recipient is very weak and may have difficulty learning
during the early posttransplantation rehabilitation phase.
The physical therapist reinforces the activity protocol with
the patient. The transplantation team usually provides the
recipient with a comprehensive guide that includes informa-
tion on medications, proper diet, exercise, and psychosocial
changes. The patient must adhere to the posttransplantation
medication protocol and be able to monitor for signs and
symptoms of infection, rejection, and toxicity of the medi-
cations. Patients are instructed to monitor temperature and
weight daily, inspect the mouth and gums, maintain proper
oral hygiene, and report any fever or infectious symptoms.
• U pon discharge home, transplant recipients should partici-
pate in a daily home exercise routine. The physical therapy
department or the organ transplantation team may have pre-
printed exercise protocols. Otherwise the physical therapist
should customize an individual exercise program that con-
sists of stretching and strengthening exercises and a walking
or aerobic program that includes warm-up and cool-down
periods. A gradual increase in ambulation to at least 30 min-
utes 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 at-
tending physician. Contact sports should be avoided for life after
transplantation to prevent trauma to the transplanted organ.24
Organ transplantation provides a patient with end-stage
organ disease the 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.
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115. Hymes SR, Alousi AM, Cowen EW. Graft-versus-host disease.
Part I: pathogenesis and clinical manifestations of graft-versus-
host-disease. J Am Acad Dematol. 2012;66(4):515.e1–515.e18.
116. Leger CS, Nevill TJ. Hematopoietic stem cell transplan-
tation: a primer for the primary care physician. CAMJ.
2004;170(10):1569–1577.
117. Scalzitti DA, Sternisha C. Does exercise during hospitaliza-
tion after stem cell transplantation decrease reports of fa-
tigue and reduce the duration of the hospital stay? Phys Ther.
2002;82(7):716–721.
118. van Haren IEPM, Timmerman H, Potting CM, Blijlevens
NMA, Staal JB, Nijhuis-van der Sanden MWG. Physical
exercise for patients undergoing hematopoietic stem cell trans-
plantation: systematic review and meta-analyses of randomized
controlled trials. Phys Ther. 2013;93(4):514–528.
119. Oberoi S, Robinson PD, Cataudella D, et al. Physical activity
reduces fatigue in patients with cancer and hematopoietic stem
cell transplant recipients: a systematic review and meta-analysis
of randomized trials. Crit Rev Oncol Hematol. 2018;122:52–59.
120. Saner FH, et al. Intensive care unit management of liver
transplant patients: a formidable challenge for the intensivist.
Transplant Proc. 2008;40:3206–3208.
121. AARC Clinical Practice Guideline. Postural drainage therapy.
American Association for Respiratory Care. Respir Care.
1991;36:1418–1426.
122. Tecklin JS. The patient with airway clearance dysfunction-
preferred practice pattern 6C. In: Irwin S, Tecklin JS, eds.
Cardiopulmonary Physical Therapy: A Guide to Practice. 4th ed. St.
Louis: Mosby; 2004:285–329.
123. Watchie J. Cardiovascular and Pulmonary Physical Therapy. 2nd
ed. St. Louis: Saunders; 2010.
124. Hillegass E. Essentials of Cardiopulmonary Physical Therapy. 4th
ed. St. Louis: Elsevier; 2017.
125. Luckmann J, ed. Medical-surgical Nursing. Philadelphia: Saun-
ders; 1980:167, 1011.
126. Foroncewicz B, Mucha K, Szparaga B, et al. Rehabilitation and
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127. Segura-Orti E, Martinez-Olmos FJ. Test-retest reliability and
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grip strength in people undergoing hemodialysis. Phys Ther.
2011;91:1244–1252.
This page intentionally left blank

     
 15 Fluid and Electrolyte
C H APT ER  

Imbalances
Jaime C. Paz

CHAPTER OUTLINE CHAPTER OBJECTIVES

Introduction
Fluid Imbalance
Fluid Volume Deficiency
Fluid Volume Excess
Fluid Shift
Electrolyte Imbalance
Physical Therapy Considerations
The objectives of this chapter are the following:
1. Provide a description of fluid and electrolyte imbalance, including clinical manifestations and contributing
health conditions.
2. Outline relevant medical management for fluid and electrolyte imbalance.
3. Describe considerations for physical therapy management.
  

Introduction

Maintaining homeostasis between intracellular fluid, extracellular fluid, and electrolytes is nec-
essary for 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
• Renal function
Many variables can alter a patient’s fluid and electrolyte balance. For more detail, refer to
Guyton and Hall Textbook of Medical Physiology.1 An imbalance of either fluids or electrolytes
may result in numerous clinical manifestations, which can subsequently affect a patient’s par-
ticipation in daily activities. Being cognizant of fluid and electrolyte imbalance is therefore an
important aspect of physical therapy management. In addition, the physical therapist must be
aware of which patients may be at risk for these imbalances, as well as the concurrent health
conditions
   and related medical management. 

Fluid Imbalance

The total amount of fluid in the body is circulated between the intracellular and extracellular
compartments. Intracellular fluid makes up approximately two thirds of the body’s fluid and
consists of water, sodium, potassium, glucose, and proteins. Extracellular fluid, the remaining
one third of the body’s total fluid volume, includes blood plasma, interstitial fluid, and cere-
brospinal fluid.1-3 Fluid imbalance occurs when there is a deficit or an excess in one or both of
these compartments.1-6 Table 15.1 provides an overview of fluid imbalances.

Fluid Volume Deficiency

A deficit in bodily fluids can occur from inadequate fluid intake, loss of blood, loss of plasma,
or loss of body water. These situations can result in insufficient fluid volume to meet cellular
needs (dehydration), loss of circulating blood (hypovolemia), or inadequate blood flow to body
tissues (shock) in extreme cases.1-9
Clinical manifestations may 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 hypotension.1-8 Clinical manifestations
in children also include poor capillary refill, absence of tears, and dry mucous membranes.8 

        379
380 CHAPTER 15     Fluid and Electrolyte Imbalances

TABLE 15.1  Fluid and Electrolyte Imbalances

Imbalance Definition
Hypovolemia Decreased blood volume
Fluid volume deficit Decreased fluid volume in
either the extracellular or
intracellular spaces
Hypervolemia Increased blood volume
Fluid volume excess Increased fluid volume in
either the extracellular or
intracellular spaces
Hyponatremia Sodium deficiency (serum
sodium level <135 mEq/L)
Hypernatremia Sodium excess (serum sodium
level >145 mEq/L)
Hypokalemia Potassium deficiency (serum
potassium level <3.5 mEq/L)
Hyperkalemia Potassium excess (serum
potassium level >5 mEq/L)
Hypocalcemia Calcium deficiency (serum
calcium level <8.5 mg/dL)
Hypercalcemia Calcium excess (serum calcium Hyperparathyroidism, bone metastases,
>10.5 mg/dL)
Hypophosphatemia Phosphate deficiency (serum
phosphate level <2.6 mg/dL)
Hyperphosphatemia Phosphate excess (serum
phosphate >4.5 mg/dL)
Hypomagnesemia Magnesium deficiency
(serum magnesium
<1.5 mEq/L)
Hypermagnesemia Magnesium excess (serum
magnesium >2.5 mEq/L)
Possible Contributing Factors
Vomiting, diarrhea, fever, blood loss,
uncontrolled diabetes mellitus
Renal failure, congestive heart failure,
liver disease, blood transfusion,
prolonged corticosteroid therapy
SIADH (see Chapter 10); vomiting;
diarrhea; diuretic therapy; renal disease;
cirrhosis; excessive sweating; hyperglycemia;
NPO status; congestive heart failure; side
effects from anticonvulsants, glycemic
agents, antineoplastics, antipsychotics,
and sedatives
Fluid volume deficit; diabetes insipidus
(see Chapter 10); diarrhea; hyperventilation; restlessness; thirst; dry, flushed skin;
excessive administration of corticosteroid,
sodium bicarbonate, or sodium chloride
Inadequate potassium intake, diarrhea,
vomiting, renal dysfunction, gastric
suction, polyuria, corticosteroid therapy,
digoxin therapy, diuretics
Excessive potassium intake, renal
insufficiency, Addison’s disease, burns,
use of potassium-conserving diuretics,
ACE inhibitors, angiotensin II blockers,
NSAIDs, chronic heparin therapy
Inadequate intake or absorption of
calcium, bone or soft-tissue deposition,
decreased PTH and vitamin D, thyroid or
parathyroid diseases, chronic kidney disease
sarcoidosis, prolonged immobilization
Intestinal malabsorption, diarrhea,
increased renal excretion, vitamin D
deficiency, hyperparathyroidism
Hematopoietic malignancies, laxatives,
hypoparathyroidism, chronic renal failure
Malnutrition, intestinal malabsorption,
vomiting, diarrhea, alcoholism, renal
dysfunction, use of loop and thiazide
diuretic agents
Renal failure, excessive antacid intake
Potential Clinical Manifestations
Weak, rapid pulse; decreased BP;
dizziness; thirst; cool, pale skin over
extremities; confusion; muscle cramps
Shortness of breath, increased BP,
bounding pulse, presence of an S3
heart sound and cough if heart is
failing, dependent edema
Anxiety, nausea, headache, muscle
cramps, muscular twitching, confu-
sion (in severe states), seizure
Altered mental status; lethargy or
weakness; irritability; hyperreflexia;
ataxia; tremors; tachycardia; oliguria;
seizure
Fatigue, muscle weakness, arrhythmias,
paresthesias, leg cramps, constipation,
decreased BP
Vague muscle weakness, nausea, initial
tachycardia followed by bradycardia,
dysrhythmia, muscle cramping,
flaccid paralysis, paresthesia,
irritability, anxiety
Confusion, anxiety, paresthesias,
muscle spasms, tetany, hyperreflexia,
arrhythmias
Fatigue, muscle weakness, lethargy,
headaches, abdominal/flank pain, bone
pain, anorexia, nausea, constipation
Thrombocytopenia, muscle weakness,
irritability, confusion, numbness,
respiratory failure
Confusion, paresthesias, muscle
weakness, spasms, hyperreflexia
Depression, lethargy, confusion,
irritability, hyperreflexia, muscle
weakness, tremors, paresthesias,
ataxia, nystagmus, tetanus,
convulsions, arrhythmias
Lethargy, confusion, nausea,
vomiting, muscle weakness,
decreased DTRs, flaccid paralysis

ACE, Angiotensin-converting enzyme; BP, blood pressure; BUN, blood urea nitrogen; DTRs, deep tendon reflexes; ECG, electrocardiography; NPO, nothing by mouth;
NSAIDs, nonsteroidal antiinflammatory drugs; PTH, parathyroid hormone; SIADH, syndrome of inappropriate antidiuretic hormone secretion.
Data from Maday KR. Understanding electrolytes: important diagnostic clues to patient status. JAAPA. 2013;26:26-31; The body fluid compartments: extracellular
and intracellular fluids; edema. In: Hall JE, ed. Guyton and Hall Textbook of Medical Physiology. 13th ed. Philadelphia: Saunders; 2011; McGloin S. The ins and outs of
fluid balance in the acutely ill patient. Br J Nursing. 2015;24( 1):14-18; Peterson C, Wampler MA, Cohn JC, Firrone LA. Problems affecting multiple systems. In:
Goodman CC, Fuller KS, eds. Pathology: Implications for the Physical Therapist. 4th ed. St. Louis: Elsevier; 2015; Huether SE. The cellular environment: fluids and electro-
lytes, acids and bases. In: McCance KL, Huether SE, Brashers VL, et al., eds. Pathophysiology, the Biologic Basis for Disease in Adults and Children. 6th ed. St. Louis: Mosby;
2010; Porth CM. Alterations in fluids and electrolytes. In: Porth CM, ed. Pathophysiology, Concepts of Altered Health States. 6th ed. Philadelphia: Lippincott; 2002;
Gorelick MH, Shaw KN, Murphy KO. Validity and reliability of clinical signs in the diagnosis of dehydration in children. Pediatrics. 1997;99(5):E6; Mulvey M. Fluid
and electrolytes: balance and disorders. In: Smeltzer SC, Bare BG, eds. Brunner and Suddarth’s Textbook of Medical-Surgical Nursing. 8th ed. Philadelphia: Lippincott; 1996;
Fall PJ. Hyponatremia and hypernatremia: a systematic approach to causes and their correction. Postgrad Med. 2000;107(5):75-82; Marieb EN, ed. Human Anatomy and
Physiology. 2nd ed. Redwood City, CA: Benjamin Cummings; 1992.

Fluid Volume Excess
An excess of bodily fluids can occur when there is an imbalance
in favor of either sodium or fluid as a result of excessive intake
or retention. Acute kidney injury or chronic kidney disease
may contribute to these situations.1-6,8 Clinical manifestations
of fluid volume excess include weight gain, pulmonary edema,
peripheral edema, and a bounding pulse.1-6,8
 CLINICAL TIP
During casual conversation among physicians and nurses, pa-
tients who are volume depleted may be referred to as being dry,
whereas patients who are volume overloaded are referred to
as being wet. Fluid volume depletion or overload can occur for
many reasons, please refer to Table 15.1 for examples.
 
Fluid Shift
Fluid movement between the intracellular and extracellular com-
partments is an ongoing process aimed at homeostasis. At times,
the shifting of fluid between compartments may result in either
a deficit or an excess of fluid volume. Among many other pos-
sible causes, excessive pressure in the vasculature (e.g., ventricular
failure), loss of serum albumin (e.g., liver failure), or fluid over-
load (e.g., excessive rehydration during surgery) may result in
this fluid shift.3,9 A shift of plasma into the interstitial spaces can
result in a fluid volume deficit if the fluid becomes sequestered,
such as in ascites caused by liver failure or in pleural effusion
resulting from heart failure.3 Clinical manifestations of a fluid
shift may also resemble those of dehydration (e.g., tachycardia
and hypotension) caused by the resultant decrease in intravascular
fluid volume.1-6,8 In situations when the fluid is able to return
to the blood vessels from the interstitial spaces, a fluid volume
excess may occur, manifesting as engorged vessels with a bound-
ing pulse.9 Patient presentation will likely vary over the course of
medical management for a particular health condition; therefore
consider the aforementioned examples to be dynamic in nature.
 CLINICAL TIP
Interstitial edema may often be referred to as third spacing,
which is the shift of fluid volume from the intravascular spaces
to the extravascular spaces.10
 
Electrolyte Imbalance
Fluid imbalances are often accompanied by changes in electrolyte
balance. Similarly, an alteration in electrolyte balance often affects
fluid balance. Cellular functions that are reliant on proper electro-
lyte balance include neuromuscular excitability, secretory activity,
and membrane permeability.11 Clinical manifestations will vary,
depending on the severity of the imbalance, and can include those
noted in the Fluid Imbalance section. In extreme cases, muscle
tetany and coma can occur. Common electrolyte imbalances are
further summarized in Table 15.1. Alterations in arterial blood
gas (ABG) levels are also considered electrolyte imbalances.12
Refer to Chapter 4 for more information on ABGs.
Electrolyte levels can be found in the laboratory report section
of the medical record or may be represented schematically in the
Fluid and Electrolyte Imbalances     CHAPTER 15 381
Na Cl BUN
BS
K HCO3 Cr
FIG. 15.1
Schematic representation of electrolyte levels. BUN, Blood urea nitrogen;
BS, blood sugar; Cl, chloride; Cr, creatinine; HCO3, bicarbonate; K, potas-
sium; Na, sodium.
daily progress note by using a sawhorse figure, as shown in Fig.
15.1. Electrolyte levels that are out of reference range are denoted
by either symbols or abbreviations to relay the relationship to the
reference value (e.g., low, high, critically high). Clinicians should
ensure that they are familiar with their institutional medical
records with regard to specific information on documentation.
Medical management of electrolyte imbalances includes iden-
tification of causative factors and ongoing monitoring with labo-
ratory testing of blood and urine. These tests include measuring
sodium, potassium, chloride, and calcium levels in blood and
urine; arterial blood gases; and serum and urine osmolality. Treat-
ment involves managing the primary cause of the imbalance(s),
accompanied by supportive care with intravenous or oral fluids,
electrolyte
   supplementation, and diet modifications. 
Physical Therapy Considerations
• R eview the medical record closely for any fluid restriction
orders in patients with fluid volume excess.13 These restric-
tions may also be posted at the patient’s bedside.
• Patients with a sodium deficit may have fluid restrictions to
minimize the risk of hyponatremia.
• If allowed, ensure proper fluid intake before, during, and af-
ter physical therapy management with patients who have a
fluid volume deficit.
• Patients who have a fluid volume deficit are at risk for or-
thostatic hypotension; therefore monitor vital signs carefully
and proceed with upright activities gradually.
• Slight potassium imbalances can have significant effects on
cardiac rhythms; therefore carefully monitor the patient for
any arrhythmias before, during, and after physical therapy
intervention. If the patient is not on a cardiac monitor, con-
sult with the nurse or the physician regarding the appropri-
ateness of physical therapy intervention.
• Patients who are taking antihypertensive medications are at
risk for electrolyte imbalances. These medications include
thiazide, loop, and potassium-sparing diuretics; beta-block-
ers; angiotensin-converting enzyme (ACE) inhibitors; and
angiotensin receptor blockers (ARBs).14
• Refer to Chapter 3 for more information on cardiac arrhythmias.
• Refer to Chapter 9 for more information on fluid and electro-
lyte imbalances caused by renal dysfunction.
• Refer to Chapter 10 for more information on fluid and elec-
trolyte imbalances caused by endocrine dysfunction.
• Refer to Chapter 19 for more information on antihyperten-
sive medications.
382 CHAPTER 15     Fluid and Electrolyte Imbalances
References
1. The body fluid compartments: extracellular and intracellular flu-
ids. Edema. In: Hall JE, ed. Guyton and Hall Textbook of Medical
Physiology. 13th ed. Philadelphia: Elsevier; 2016:306–321.
2. Huether SE. The cellular environment: fluids and electrolytes,
acids and bases. In: McCance KL, Huether SE, Brashers VL, et al.,
eds. Pathophysiology, the Biologic Basis for Disease in Adults and
Children. 6th ed. St. Louis: Mosby; 2010:96–125.
3. Porth CM. Alterations in fluids and electrolytes. In: Porth CM,
ed. Pathophysiology, Concepts of Altered Health States. 6th ed. Phila-
delphia: Lippincott; 2002:693–734.
4. Rose BD, ed. Clinical Physiology of Acid-Base and Electrolyte Disor-
ders. 2rd ed. New York: McGraw-Hill; 1984.
5. Cotran RS, Kumar V, Robbins S, et al., eds. Robbins Pathologic
Basis of Disease. Philadelphia: Saunders; 1994.
6. Kokko J, Tannen R, eds. Fluids and Electrolytes. 2rd ed. Philadel-
phia: Saunders; 1990.
7. McGee S, Abernethy 3rd WB, Simel DL. Is this patient hypov-
olemic? J Am Med Assoc. 1999;281(11):1022–1029.
8. Springhouse. Portable Fluids & Electrolytes. Philadelphia: Lippin-
cott William & Wilkins; 2008.
9. Peterson C, Wampler MA, Cohn JC, Firrone LA. Problems affect-
ing multiple systems. In: Goodman CC, Fuller KS, eds. Pathology:
Implications for the Physical Therapist. 4th ed. St. Louis: Elsevier;
2015:202–2015.
10. McGloin S. The ins and outs of fluid balance in the acutely ill
patient. Br J Nurs. 2015;24(1):14–18.
11. Marieb EN, ed. Human Anatomy and Physiology. 2nd ed. Redwood
City, CA: Benjamin Cummings; 1992:911.
12. Fukagawa M, Kurokawa K, Papadakis MA. Fluid & electrolyte
disorders. In: Tierney LM, McPhee SJ, Papadakis MA, eds. Current
Medical Diagnosis & Treatment. New York: McGraw-Hill; 2007.
13. Greenwood K, Stewart E, Milton E, Hake M, Mitchell L, Sanders
B. Core competencies for entry-level practice in acute care physi-
cal therapy. Academy of acute care physical therapy. Am Phys Ther
Assoc. 2015.
14. Liamis G, Milionis H, Elisaf M. Blood pressure drug therapy
and electrolyte disturbances. Int J Clin Pract. 2008;62(10):
1572–1580.
 16 Amputation
C H APT ER  

Jaime C. Paz

CHAPTER OUTLINE CHAPTER OBJECTIVES

Introduction
Lower Extremity Amputation
Upper Extremity Amputation
Physical Therapy Management
Wound Healing
Edema Control
Pain Management
Limb and Trunk Motion,
The objectives of this chapter are the following:
1 . Provide an overview of the possible causes and types of upper and lower extremity amputation
2. Outline physical therapy management, pertinent to the acute care setting, for patients with either upper or
lower extremity amputation
3. Provide an overview of applicable standardized outcome measures for this patient population
  

Strengthening, and Functional

Mobility Introduction
Holistic Care
Outcome Measures This chapter provides a brief overview of the most common types of lower extremity amputa-
tion (LEA) and upper extremity amputation (UEA), as well as subsequent physical therapy
management pertinent to the acute care setting. For more detailed information on this topic,
readers are referred to the most recent edition of Lusardi et al.’s Orthotics and Prosthetics in Reha-
bilitation.1 Although the incidence of UEA is quite low compared with LEA, it is important
that the acute care physical therapist have an understanding of all types of amputations to
properly
   plan for the management of this patient population. 

Lower Extremity Amputation

Vascular disease and trauma are the primary causes of LEA. Among other conditions, vascular
disease can occur as a complication of diabetes mellitus (refer to Chapters 7 and 10, respec-
tively, for more information). Reported incidence rates of LEA in persons with and without
diabetes mellitus vary depending on the methodology of the studies.2 However, the number of
people living in the United States with the loss of a limb is projected to increase from 1.6 to
3.6 million by the year 2050 if the current health status of individuals remains unchanged.3
Traumatic amputation appears to occur less frequently in people with diabetes as opposed to
those without.2
Surgical site options for LEA are shown in Fig. 16.1 and described in Table 16.1. 
  

Upper Extremity Amputation

Trauma, such as automobile collisions, industrial accidents, or penetrating injuries, are com-
mon causes of UEA.4-6 Malignant disease and congenital limb deficiency are also contributors
to UEA.7,8 Despite peripheral vascular disease being a major cause of LEA, it often does not
create the need for UEA.5
Surgical site options for UEA are shown in Fig. 16.2 and described in Table 16.2. 
  

Physical Therapy Management

The focus of physical therapy in the acute care setting for patients with a new limb ampu-
tation is facilitating functional mobility, in conjunction with a thorough assessment of the

        383
384 CHAPTER 16    Amputation

Hemipelvectomy
Wound Healing
To facilitate prosthetic fitting, the integumentary condition of
Hip the residual limb needs to be thoroughly examined for signs of
disarticulation wound healing.10,11 A surgical incision with delayed or ineffec-
tive closure can lead to infection, increased risk of decondition-
ing, and delays in functional mobility.9 In addition, wound
closure failure is associated with decreased success in ambula-
tion with a prosthetic.12 Refer to Chapter 12 for more informa-
Above-knee tion on wound care management.
(transfemoral)
amputation  CLINICAL TIP
Patients with peripheral arterial disease and diabetes are at an
increased risk for skin breakdown in the sound (nonamputated)
lower extremity because this limb will be required to support
Knee
disarticulation more weight during the preprosthetic period.10 Additionally, sin-
gle limb ambulation, or hopping, with an assistive device may
promote unnecessary shifts in the patient’s center of mass to-
ward the sound limb, and this can interfere the development of
Below-knee a smooth gait pattern upon receiving a prosthetic.9
(transtibial)  
amputation

Edema Control
Syme’s Management of edema in the early postoperative stages has
amputation many benefits, including reduction of pain, promotion of
Transmetatarsal
wound closure, and facilitation of appropriate prosthetic fit-
amputation ting.9 Approaches to managing edema include soft dressings
Toe (elastic bandages and elastic shrinker socks), semirigid dress-
Ray
amputation amputation ings (air splints and Unna boot), removable rigid dressings, and
FIG. 16.1 rigid cast dressings. One type of rigid dressing is an immediate
Levels of amputation. Lower extremity. (From Cameron MH, Monroe LG. or early postoperative prosthesis (IPOP or EPOP, respectively)
Physical Rehabilitation: Evidence-Based Examination, Evaluation, and Interven- which includes an attachment for prosthetic components to
tion. St. Louis: Saunders; 2007.) facilitate early ambulation.9 Elastic bandages should be applied
in a “figure-of-eight” pattern to minimize a tourniquet effect.10
patient’s potential to use a prosthetic.9 Physical therapists Semirigid dressings, such as the Unna boot, have been shown
function within a multidisciplinary team during the post- to foster wound closure and possibly better prepare the resid-
operative phase and should collaborate on a consistent basis ual limb for prosthetic fitting13; however, no specific type of
with the involved disciplines to optimize patient outcomes.9 dressing has proven to be the most effective.10 The choice of
Prosthetic training, if appropriate, most often occurs in the dressings for edema management is determined by a variety of
subacute, outpatient, or home setting and is not discussed factors, including the patient’s medical status and functional
specifically in this chapter. Alternatively, a patient with a condition, potential prosthetic use, preference and experience of
preexisting amputation may be admitted to the acute care the surgeon, and any existing hospital protocols.9
hospital with another diagnosis and require physical therapy
to augment mobility during his or her hospital stay.  CLINICAL TIP
The primary components of acute care physical therapy man- Coordinate with nursing or wound care staff during dressing
agement for the patient who has undergone limb amputation, as changes to visualize the skin and the incision without causing
observed throughout examination, evaluation, and plan of care unnecessary disruption to the dressings. Monitor for drainage
development, are as follows9,10: strikethrough, particularly after therapeutic activities with the
• Wound healing limb in a dependent position.
• Edema control  
• Pain management
• Joint mobility Pain Management
• Strengthening Pain after limb amputation can occur in many areas of the body;
• Functional mobility however, the majority of pain complaints occur in the residual
• Holistic care (including meeting psychosocial needs and limb. Several descriptions of pain after amputation exist, but
management of comorbidities) they are generally categorized into three types: phantom limb

TABLE 16.1  Types of Lower Extremity Amputations
Type
Toe
Ray
Transmetatarsal
Syme’s amputation (ankle disarticulation)
Transtibial
Through-the-knee (disarticulation)
Transfemoral
Hip disarticulation (femoral head from acetabulum)
Hemipelvectomy (half of the pelvis is
removed along with the entire lower limb)
Data from Thompson A, Skinner A, Piercy J, eds. Tidy’s Physiotherapy. 12th ed. Oxford: Butterworth-Heinemann; 1992:260; Engstrom B, Van de Ven C, eds. Therapy
for Amputees. 3rd ed. Edinburgh: Churchill Livingstone; 1999:149-150, 187-188, 208; May B, ed. Amputations and Prosthetics: A Case Study Approach. Philadelphia: FA
Davis; 1996:62-63; Sanders G, ed. Lower Limb Amputations: A Guide to Rehabilitation. Philadelphia: FA Davis; 1986:101-102; Edelstein JE. Prosthetic assessment and
management. In: O’Sullivan SB, Schmitz TJ, eds. Physical Rehabilitation: Assessment and Treatment. 4th ed. Philadelphia: FA Davis; 2001:645-673. Lusardi M, Pepe
JL. Amputation surgeries for the lower limb. In: Lusardi M, Jorge M, Nielson C, eds. Orthotics and Prosthetics in Rehabilitation. 3rd ed. St. Louis: Elsevier Saunders;
2013:499-531.
pain, phantom limb sensation, and stump (residual limb) pain.
Phantom limb pain is a type of neuropathic pain defined as pain-
ful sensations perceived in the missing limb as though it were
still intact. Phantom limb sensation is any sensation, except for
pain, in the missing limb. Examples of phantom limb sensa-
tion include tingling, prickling, or a “pins and needles” sensa-
tion. Stump or residual limb pain is pain in the residual portion
of the amputated limb and may be caused by neuromas, bone
spurs, or infection.14,15 Phantom limb pain/sensation and stump
pain can affect up to 80% of patients after amputation.15 Fac-
tors reported to affect the frequency of experiencing phantom
Amputation     CHAPTER 16 385
Description
Digital amputation can occur at any level: proximal, middle, or distal interphalangeal
joints. Toe amputation can occur with metatarsal head amputation. Patients will
initially be non–weight bearing and progress to weight bearing according to the
surgeon’s guidelines.
Single or multiple rays may be amputated, depending on the patient’s diagnosis,
which can include neuropathic ulcer, osteomyelitis, or vascular disease. If the first
ray is amputated, balance is often affected because weight is transferred to the lateral
border of the foot, and this may also cause ulceration and skin breakdown. Postop-
erative weight-bearing status will range from non–weight bearing to partial weight
bearing according to the physician’s orders. Orthotics or custom footwear may be
necessary after healing has occurred to minimize altered forces during ambulation.
The metatarsal bones are transected with this procedure compared with other types of
partial foot amputations, which may disarticulate the metatarsals from the cuboid
and cuneiform bones. Balance is facilitated with a transmetatarsal amputation
because the residual limb is symmetric in shape and major muscles remain intact.
At times, tendon transfers or other procedures may be necessary to minimize muscle
imbalances. An adaptive shoe with a rocker bottom is used to help facilitate push-off
in gait. Additional orthoses to stabilize the foot and ankle may also be indicated.
Often performed to treat traumatic injury or infection, this type of amputation is
preferred over more distal, partial foot amputations (ray and transmetatarsal) because
of the ease of prosthetic management at this level. Uncomplicated cases may begin
prosthetic fitting 6–8 weeks postoperatively.
Ideal amputation site for a variety of diagnoses. In cases with vascular compromise,
the residual limb incision may be slow to heal. Outcomes appear to be optimized
when 40% to 50% of the tibia is preserved.
Maximum prosthetic control can be achieved after this procedure because of the abil-
ity to be fully weight bearing on the residual limb. The long muscular lever arm and
intact hip musculature also contribute to improved prosthetic mobility. The intact
femoral condyles, however, leave a cosmetically poor residual limb.
Vascular disease, trauma, malignancy, and nonhealing infection may result in this
level of amputation. Traditional transfemoral amputation preserves 50% to 66% of
femoral length. Prosthetic ambulation with an artificial knee joint will be necessary
and requires increased metabolic demand.
Often performed in cases of trauma, significant infection, or malignancy. The pelvis
remains intact; however, patients may experience slow wound healing and may
require secondary grafting to fully close the amputation site. Refer to Chapter 5 for
more information.
Possibly indicated in cases of malignancy. A muscle flap covers the internal organs
after loss of the protective bony structure. Prosthetic support may be necessary for
the abdominal contents along with assisting in symmetry while sitting. Refer to
Chapter 5 for more information.
limb pain include gender (women experience this more com-
pared with men), UEA versus LEA (less incidence in LEA), and
time elapsed since amputation (patients experience less pain as
more time passes).16 Patients with chronic and severe preopera-
tive pain related to vascular disease may also be more likely to
experience phantom pain.9 Refer to Chapter 6 for more informa-
tion on phantom limb pain.
Managing pain after amputation includes both medical and
rehabilitation components. Preoperative analgesia with non-
steroidal antiinflammatory drugs (NSAIDs) has demonstrated
equivocal results in reducing postoperative pain. Postoperative
386 CHAPTER 16    Amputation
Shoulder
disarticulation
Humeral neck
Short above elbow
Standard above elbow
Elbow disarticulation
Very short below elbow
Short below elbow
Long below elbow
Wrist disarticulation
FIG. 16.2
Upper extremity amputation. (From Burke SL, Higgins JP, McClinton
MA, et al., eds. Hand and Upper Extremity Rehabilitation: A Practical Guide.
3rd ed. St. Louis: Churchill Livingstone; 2006:716.)
pain management may include pharmacologic and nonpharma-
cologic methods. Pharmacologic interventions include the use of
opioids; patient-controlled analgesia; local anesthetics, such as
epidural infusion; NSAIDs; antidepressants; anticonvulsants14;
muscle relaxants; and sympathetic blocks.15 Nonpharmacologic
pain interventions may include compression bandages, desensi-
tization, relaxation, transcutaneous electrical nerve stimulation
(TENS), imagery, biofeedback, and, if necessary, surgical revi-
sion of the residual limb.9,10 Currently, there is a lack of robust
evidence to determine the effectiveness or harm from the use of
TENS for patients with phantom limb pain or stump pain.15  helpful for both facilitating mobility and preventing falls.
Limb and Trunk Motion, Strengthening, and Functional
Mobility
Ensuring sufficient motion and strength to optimize functional
movement are critical aspects of patient management after limb
amputation. Limb and trunk motion, strengthening, and func-
tional mobility are interrelated aspects of rehabilitation and
may allow the therapist to achieve different goals with a sin-
gle therapeutic activity. For example, to prevent contractures,
active movements of all of the joints proximal to the level of
the amputation should be performed. Active range-of-motion
(ROM) exercises and passive stretching or positioning should be
incorporated as well.5,8,17-20
For patients with LEA, the physical therapist can provide the
patient, family members, and members of the nursing staff with
education on residual limb positioning, proper pillow place-
ment, and the use of splint boards. Patients with a transtibial
amputation will be most susceptible to knee flexion contracture.
A small towel roll should be placed under the tibia rather than
under the knee to promote extension. Patients with transfemo-
ral amputations or hip disarticulations will be most susceptible
to hip flexor and abductor contractures. Positioning the patient
in the prone or flat supine positions (as medically allowed) can
promote a neutral hip posture.5,8,9,17-20
During ambulation, patients with UEA tend to flex the
trunk toward the side of the amputation and maintain a stiff
gait pattern that lacks normal arm swing. Patients often need
gait training, balance exercises, posture retraining, or a combi-
nation of these to facilitate an efficient gait pattern.5,8,17-20
Upper extremity movements that are required for powering
an upper extremity prosthetic can vary, depending on the length
of amputation and type of prosthetic. For patients with myo-
electric prostheses, specific muscle reeducation will be depen-
dent on the specific type of device prescribed. For patients with
body-powered prosthesis, the patient will need to strengthen
both involved and uninvolved shoulder musculature. Ensur-
ing the maximum available ROM in the following directions
should also be facilitated5,8,17-21:
• 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
Functional mobility training for patients with LEA includes
bed mobility and transfer training, as well as gait training or
wheelchair mobility. Patients with bilateral above-knee ampu-
tations 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.9
 CLINICAL TIP
Be mindful of hand placement for ROM exercises to prevent
excessive stress on new incisions, particularly with transtibial
amputations. During functional training for patients with LEA,
patients should wear good footwear on the sound limb. This is
 
Holistic Care
Patients who undergo limb amputation may experience post-
operative psychological challenges,22 including depression,
anxiety, body-image anxiety, concerns over social functioning,
social discomfort, and difficulty adapting to a new self-iden-
tity. A higher rate of depression appears to occur immediately
after the amputation and between 1 and 2 years postampu-
tation. After this period, rates of depression may decrease to
those in the general population. Anxiety is also likely to be
increased in the first year postamputation. A more specific
form of anxiety in this population includes perceptions of
 Amputation     CHAPTER 16 387

TABLE 16.2  Types of Upper Extremity Amputations

Type Description
Wrist disarticulation Distal radial ulnar joint function is often retained to maintain rotation of the radius.
Transradial Optimal residual limb length for eventual prosthetic fitting is 8 cm above the ulnar styloid. Active
prosthetic devices are operated by elbow extension and shoulder flexion, shoulder girdle protrac-
tion, or both. Length of residual limb will vary, depending on amount of viable tissue below the
elbow. Refer to Fig. 16.2 for approximate length of these amputations.
Elbow disarticulation Not an optimal location for amputation due to the poor cosmetic appearance and decreased
postoperative function of the prosthesis.
Transhumeral Often performed as a result of primary malignancy or metastatic disease. Optimal residual limb
length for eventual prosthetic fitting is 10 cm above the elbow joint. Length of residual limb will
vary depending on amount of viable tissue below the elbow. Refer to Fig. 16.2 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. Less than 30% of the
humerus is maintained, or the acromion process and clavicle are trimmed to create a rounded
appearance. Prosthetic use is variable.
Forequarter Often performed as a result of primary malignancy or metastatic disease. Consists of removal of the
patient’s clavicle, scapula, and arm. Limited prosthetic options.

Data from Engstrom B, Van de Ven C, eds. Therapy for Amputees. 3rd ed. Edinburgh: Churchill Livingstone; 1999:243-257; Zenie JR. Prosthetic Options for persons
with upper extremity amputation. In: Lusardi M, Jorge M, Nielson C, eds. Orthotics and Prosthetics in Rehabilitation. 3rd ed. St. Louis: Elsevier Saunders; 2013:795-796;
Banerjee SN, ed. Rehabilitation Management of Amputees. Baltimore: Williams & Wilkins; 1982:30-33; Ham R, Cotton L, eds. Limb Amputation: From Aetiology to Reha-
bilitation. London: Chapman & Hall; 1991:136-143; Theisen L. Management of upper extremity amputations. In: Burke SL, Higgins JP, McClinton MA, et al., eds.
Hand and Upper Extremity Rehabilitation: A Practical Guide. 3rd ed. St. Louis: Churchill Livingstone; 2006:716. Ovadia SA, Askari MA. Upper extremity amputations
and prosthetics. Semin Plast Surg. 2015;29:55-61.

body-image distortion. Development of body image–related TABLE 16.3  Outcome Measures for Patients with Limb
anxiety has been associated with depression, decreased percep- Amputation
tion of quality of life, higher levels of anxiety, and lower lev-
els of self-esteem. Social discomfort and perceived stigma may Type Measurement Tool
also affect physical and social activities. The literature concern- Self-report Amputee Activity Survey
ing adaptations to a new self-identity is currently limited.22 Sickness Impact Profile
Because of the various psychological challenges experienced by Reintegration to Normal Living
this patient population, physical therapists must be mindful Prosthetic Profile of the Amputee
SF-36 Health Status Profile
during patient care and refer patients to appropriate practitio- Prosthetic Evaluation Questionnaire
ners if these issues arise.9  Orthotic Prosthetic User’s Survey
Patient Specific Functional Scale
Outcome Measures
Professional report Barthel Index
Numerous tools are available to measure function and out- Physical 2-Minute Walk Test
comes in patients with limb amputation (Table 16.3). The performance Functional Ambulation Profile
Amputee Mobility Predictor (AMP) has been reported to instruments Tinetti Performance-Oriented Assessment
determine functional level and predict functional ability of Mobility
Timed Up and Go test
in amputees23 and can be used for patients both before and
Berg Balance Measurement
after prosthetic fitting and rehabilitation.24,25 Reliability and Duke Mobility Skills Profile test
validity have been established for the AMP.25 Additionally, Functional Reach Test
the modified Prosthetic Evaluation Questionnaire (PEQ), the Amputee Mobility Predictor
SF-36 for veterans (SF-36V), the Orthotics and Prosthetics Wheelchair Skills Test v. 4.1
User’s Survey (OPUS), the Patient-Specific Functional Scale Data from Gailey RS. Predictive outcome measures versus functional outcome
(PSFS), the 2-Minute Walk Test (2MWT), the 6-Minute Walk measures in the lower limb amputee. J Prosthet Orthot. 2006;18(1S):51-60;
Test (6MWT), the Timed Up and Go (TUG) test, and the Resnik L, Borgia M. Reliability of outcome measures for people with lower-
limb amputations: distinguishing true change from statistical error. Phys Ther.
AMP have been studied to examine test–retest reliability, as 2011;91:555-565; Wong CK, Chen CC, Welsh J. Preliminary assessment of
well as to calculate the minimal detectable change (MDC) of balance with the Berg Balance Scale in adults who have a leg amputation and
each measure.26 All of these aforementioned tools have dem- dwell in the community: Rasch rating scale analysis. Phys Ther. 2013;93:1520-
1529; Lusardi M. Postoperative and preprosthetic care. In: Lusardi M, Jorge
onstrated good reliability (interclass coefficient [ICC] > 0.8) M, Nielson C, eds. Orthotics and Prosthetics in Rehabilitation. 3rd ed. St. Louis:
when used in patients with one LEA. Elsevier Saunders:532-594.
388 CHAPTER 16    Amputation

TABLE 16.4  Medicare Functional Classification Level (MFCL) Descriptions

MFCL Description HCFA Modifier
0 Does not have the ability or potential to ambulate or transfer safely with or without K0
assistance, and prosthesis does not enhance quality of life or mobility.
1 Has the ability or potential to use prosthesis for transfers or ambulation on level surfaces at K1
fixed cadence. Typical of the limited and unlimited household ambulator.
2 Has the ability or potential for ambulation with the ability to traverse low-level environmental K2
barriers such as curbs, stairs, or uneven surfaces. Typical of the limited community ambulator.
3 Has the ability or potential for ambulation with variable cadence. Typical of the community K3
ambulator who has the ability to traverse most environmental barriers and may have vocational,
therapeutic, or exercise activity that demands prosthetic use beyond simple locomotion.
4 Has the ability or potential for prosthetic ambulation that exceeds the basic ambulation skills, K4
exhibiting high-impact, stress, or energy levels typical of the prosthetic demands of the child,
active adult, or athlete.

HCFA, Health Care Financing Administration.

Adapted from Hafner B, Smith D. Differences in function and safety between Medicare Functional Classification Level-2 and -3 transfemoral amputees and influence of
prosthetic knee joint control. J Rehabil Res Dev. 2009; 46(3):417-433.

With regard to the MDC, the following should be used as a
guide to measure true change from previous to current measure-
ments in patients who have single-limb LEA26:
• 2-Minute Walk Test: 34.3 m
• 6-Minute Walk Test: 45 m
• TUG test: 3.6 seconds
• AMP: 3.4 points
The Medicare Functional Classification Level (MFCL)
descriptions are used as a guideline by health care practitioners
to determine prosthetic candidacy (Table 16.4). The MFCL is
also used by third-party payers to guide their reimbursement for
certain types and components of prosthetics.27
References
1. Lusardi M, Jorge M, Nielson C, eds. Orthotics and Prosthetics in
Rehabilitation. 3rd ed. Elsevier: Saunders; 2013.
2. Narres M, Kvitkina T, Claessen H, et al. Incidence of lower extrem-
ity amputations in the diabetic compared with the non-diabetic
population: a systematic review. PLoS One. 2017;12(8):e0182081.
https://doi.org/10.1371/journal.pone.0182081.
3. Ziegler-Graham K, MacKenzie E, Ephraim P, et al. Estimating
the prevalence of limb loss in the United States: 2005 to 2050.
Arch Phys Med Rehabil. 2008;89(3):422–429.
4. Barmparas G, Inaba K, Teixeira PGR, et al. Epidemiology of
post-traumatic limb amputation: a national trauma databank
analysis. Am Surg. 2010;76(11):1214–1222.
5. Engstrom B, Van de Ven C, eds. Therapy for Amputees. 3rd ed.
Edinburgh, Scotland: Churchill Livingstone; 1992.
6. 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.
7. Ovadia SA, Askari M. Upper extremity amputations and pros-
thetics. Semin Plast Surg. 2015;29(1):55–61. https://doi.org/10.10
55/s-0035-1544171.
8. Karacoloff LA, Schneider FJ, eds. Lower Extremity Amputation: A
Guide to Functional Outcomes in Physical Therapy Management. Rock-
ville, MD: Aspen; 1985.
9. Lusardi M. Postoperative and preprosthetic care. In: Lusardi M,
Jorge M, Nielson C, eds. Orthotics and Prosthetics in Rehabilitation.
3rd ed. Elsevier: Saunders; 2013:532–594.
10. Edelstein JE. Amputations and prostheses. In: Cameron MH,
Monroe LG, eds. Physical Rehabilitation: Evidence-Based Examination,
Evaluation, and Intervention. St. Louis: Saunders; 2007:267–299.
11. Esquenazi A. Amputation rehabilitation and prosthetic restora-
tion. From surgery to community reintegration. Disabil Rehabil.
2004;26(14/15):831–836.
12. Munin MC, Espejo-De Guzman MC, Boninger ML, et al. Predic-
tive factors for successful early prosthetic ambulation among
lower-limb amputees. J Rehabil Res Dev. 2001;38(4):379–384.
13. Wong CK, Edelstein JE. Unna and elastic postoperative
dressings: comparison of their effects on function of adults
with amputation and vascular disease. Arch Phys Med Rehabil.
2000;81(9):1191–1198.
14. Chapman S. Pain management in patients following limb ampu-
tation. Nurs Stand. 2011;25(19):35–40.
15. Johnson MI, Mulvey MR, Bagnall AM. Transcutaneous electri-
cal nerve stimulation (TENS) for phantom pain and stump pain
following amputation in adults. Cochrane Database Syst Rev.
2015;(Issue 8):CD007264. https://doi.org/10.1002/14651858.
CD007264.pub3.
16. Bosmans JC, Geertzen JHB, Post WJ, et al. Factors associated
with phantom limb pain: a 3½-year prospective study. Clin Reha-
bil. 2010;24(5):444–453.
17. May B, ed. Amputations and Prosthetics: A Case Study Approach.
Philadelphia: FA Davis; 1996:86–88.
18. Banerjee SN, ed. Rehabilitation Management of Amputees. Vols.
30–33. Baltimore: Williams & Wilkins; 1982:255–258.
19. Ham R, Cotton L, eds. Limb Amputation: From Aetiology to Reha-
bilitation. London: Chapman & Hall; 1991:136–143.
20. Theisen L. Management of upper extremity amputations. In:
Burke SL, Higgins JP, McClinton MA, et al., eds. Hand and
Upper Extremity Rehabilitation: A Practical Guide. 3rd ed. St. Louis:
Churchill Livingstone; 2006:716.
21. Wise M. Rehabilitation for persons with upper extremity
amputation. In: Lusardi M, Jorge M, Nielson C, eds. Orthot-
ics and Prosthetics in Rehabilitation. 3rd ed. Elsevier: Saunders;
2013:814–829.

22. Horgan O, MacLachlan M. Psychosocial adjustment to lower-
limb amputation: a review. Disabil Rehabil. 2004;26(14/15):
837–850.
23. Helm P, Engel T, Holm A, et al. Function after lower limb am-
putation. Acta Orthop Scand. 1986;57:154–157.
24. Gailey RS. Predictive outcome measures versus functional
outcome measures in the lower limb amputee. J Prosthet Orthot.
2006;18(1S):51–60.
Amputation     CHAPTER 16 389
25. May BJ, Lockhard MA. Prosthetics & Orthotics in Clinical Practice:
A Case Study Approach. Philadelphia: FA Davis; 2011:107.
26. Resnik L, Borgia M. Reliability of outcome measures for people
with lower-limb amputations: distinguishing true change from
statistical error. Phys Ther. 2011;91:555–565.
27. Hafner B, Smith D. Differences in function and safety between
Medicare Functional Classification Level-2 and -3 transfemoral
amputees and influence of prosthetic knee joint control. J Rehabil
Res Dev. 2009;46(3):417–433.
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 17
C H APT ER  
CHAPTER OUTLINE
Introduction
Physiology of Chest Pain
Presentation of Chest Pain
Diagnostic Considerations
Physical Therapy Considerations
Physical Therapy
Considerations for Patients
Who Present With Chest Pain
David M. Krause­­a
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . To describe the physiology and incidence of chest pain
2. To discuss the difference in symptomology of cardiogenic versus noncardiogenic chest pain, including
atypical chest pain patterns in select patient populations
3. To distinguish between stable versus unstable angina
4. To provide the physical therapist with a clinical framework of ways to proceed if a patient presents with
chest pain
Introduction
Chest pain, also referred to as angina, is a common complaint for which many patients seek
medical attention and accounts for approximately 7.3 million emergency department visits per
year in the United States.1 Of those patients, 30% are diagnosed with acute coronary syndrome
(ACS), which is an operational term used to define the disruption of the blood supply to the
heart, more commonly referred to as myocardial ischemia or myocardial infarction (MI), and
unstable angina (USA).2,3 Thus the physical therapist in the acute care setting should be famil-
iar with the various etiologies of cardiogenic (cardiac related) and noncardiogenic (non–cardiac
related) chest pain and should be competent in taking an efficient history when a patient
reports chest pain. 
Physiology of Chest Pain
Cardiogenic chest pain may be ischemic or nonischemic in origin. Ischemic chest pain is typi-
cally caused by atherosclerosis, coronary spasm, systemic or pulmonary hypertension, aortic
stenosis, aortic or mitral regurgitation, hypertrophic cardiomyopathy, endocarditis, tachycardia
(caused by dysrhythmia, such as atrial fibrillation), or severe anemia.4 Nonischemic chest pain is
often the result of aortic dissection or aneurysm, mitral valve prolapse, or pericarditis.4 Refer to
the Acute Coronary Syndrome section in Chapter 3 for a detailed description of stable angina,
USA, and variant (Prinzmetal’s) angina and to Fig. 3.10 for the possible clinical courses of
patients admitted with cardiogenic chest pain.
Briefly, stable angina is considered to be predictable, episodic, reproducible, triggered by
physical or psychological stressors, occurring with a constant frequency over time, and relieved
by rest or nitroglycerin.5,6 USA is considered to be of new onset, occurring at rest or with
minimal exertion, progressive in nature with increased frequency and duration of episodes, and
refractory to previously effective medication.5,6 During an episode of USA, an electrocardio-
gram may reveal ST segment elevation or depression with or without T-wave inversion that
reverses when anginal pain decreases.6 These electrocardiographic changes are depicted in Fig.
17.1. Vital sign findings during cardiogenic (USA) chest pain will typically include:
aThe authors acknowledge Michele P. West for prior contributions to this chapter.
        391
392 CHAPTER 17     Physical Therapy Considerations for Patients Who Present With Chest Pain

• H ypotension or hypertension
• Bradycardia or tachycardia
• Irregular pulse
Noncardiogenic chest pain can arise from a wide range of
diseases and disorders, which makes the differential diagnosis of
Pathologic chest pain challenging. Afferent fibers from the heart, lungs, and
Q wave
esophagus enter the same thoracic dorsal ganglia and produce
Dead myocardium
an indistinct quality and location of pain.5 With overlapping
of the dorsal segments, disease that is thoracic in origin may
produce pain anywhere between the jaw and the epigastrium.5
Table 17.1 describes the most common differential diagnoses of
noncardiogenic chest pain, each with its own distinctive associ-
ated signs and symptoms. Refer to Table 8.1 for gastrointestinal
pain referral patterns. 
Raised ST
segment
Presentation of Chest Pain
Acutely damaged myocardium
When a patient presents with chest pain, it is imperative to
understand the differences between typical and atypical pain
patterns. Table 17.2 outlines commonly reported symptoms of
cardiogenic (typical) chest pain and noncardiogenic (atypical)
chest pain seen in the general patient population.
Some patient populations may present with atypical pain
Inverted
T wave
patterns. Female patients may not have midchest pain (ster-
nal) but rather may have midback pain, left-sided chest pain,
Myocardial ischemia
Note: There are a range of other
heaviness, squeezing, or pain in the abdomen.7 Other atypical
causes for T wave inversion cardiogenic-related chest pain symptoms frequently observed
FIG. 17.1 in females include dyspnea, unusual fatigue, dizziness, nau-
Ischemic changes on electrocardiography (ECG). sea, sleep disturbance, and unexplained severe weakness (spe-
cifically heaviness in the upper extremities) which reduces
the capacity for activities of daily living (ADLs).5,7 Elderly
patients typically present with weakness, congestive heart

TABLE 17.1  Possible Etiologies, Pain Patterns, and Associated Signs of Noncardiogenic Chest Pain
Origin Possible Etiology Pain Pattern and Associated Signs and Symptoms
Pulmonary/pleural Pneumonia, pulmonary embolus, tuberculosis, Pain with respiration, of sudden onset, usually well localized (lateral to
pleuritis, pneumothorax, mediastinitis, midline) and prolonged
chronic obstructive pulmonary disease, Associated with abnormal breath sounds, increased respiratory rate,
tracheobronchitis cough, hemoptysis, or pleural rub
Gastrointestinal Hiatal hernia, esophagitis, esophageal spasm, Epigastric, visceral, or burning in nature of moderate duration or prolonged;
gastroesophageal reflux, motility disorder, acute and usually related to food, alcohol, or medication/alcohol intake
pancreatitis, peptic ulcer, or cholecystitis Relieved by antacids, milk, or warm liquids
Nausea, vomiting, burping, or abdominal pain may be present
Musculoskeletal Muscle strain, rib fracture, costochondritis, Achy, increased with movement of the head/neck/trunk or upper
cervical disk disease, shoulder bursitis or extremity, or reproducible with palpation
tendonitis, thoracic outlet syndrome, trauma, Signs of inflammation may be present, or there may be a history of
or strain overuse/trauma
Psychological Panic disorder, anxiety, depression, or self-gain Pain is often precordial (anterior chest over the heart), with report of
pain moving from place to place, of moderate duration or situational,
and unrelated to movement or exertion
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
Localized with a vesicular rash in the area of discomfort

Data from Bonaca MP, Sabatine MS. Approach to the patient with chest pain. In: Zipes DP, Libby P, Bonow RO, et al., eds. Braunwald’s Heart Disease: A Textbook of
Cardiovascular Medicine. 11th ed. Philadelphia: Elsevier; 2019; Goldman L. Approach to the patient with possible cardiovascular disease. In: Goldman L, Schafer AI, eds.
Goldman-Cecil Medicine. 25th ed. Philadelphia: Saunders; 2016; Runge MS, Ohman EM, Stouffer GA. The history and physical examination. In: Runge MS, Patterson
C, Stouffer GA, eds. Netter’s Cardiology. 2nd ed. Philadelphia: Saunders; 2010.
 Physical Therapy Considerations for Patients Who Present With Chest Pain     CHAPTER 17 393

TABLE 17.2  Symptoms of Angina

Noncardiogenic (Atypical) Chest Pain Cardiogenic (Typical) Chest Pain
Signs and symptoms Pain that is choking, knifelike, piercing, Perception of chest aching, bandlike discomfort, burning,
pleuritic, prickling, pulsating, or sharp heaviness, pressure, squeezing, tightness, weight
Onset Random Relatively predictable
Duration Seconds, minutes, hours, or all day 3-15 minutes
Potential referral patterns and Chest wall is involved Radiation to shoulder, neck, jaw, inner arm, epigastrium (can
characteristics Pain is positional, tender to palpation occur without chest component)
Pain can be inframammary
Radiation patterns are highly variable
Relief Response to nitroglycerin is variable Subsides with nitroglycerin use or when stressor is eliminated
Data from Abrams J. Chronic stable angina. N Engl J Med. 2005;352:2524-33; and Sangareddi V, Chockalingam A, Gnanavelu G, et al. Canadian Cardiovascular Society
classification of effort angina: an angiographic correlation. Coron Artery Dis. 2004;15(2):111-114.

TABLE 17.3  Angina Rating Scale

Rating Description
1 Mild, barely noticeable
2 Moderate, bothersome
3 Moderately severe, very uncomfortable
4 Most severe or intense pain ever experienced

Data from American College of Sports Medicine. ACSMs Guidelines for Exercise Testing and Prescription. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2014:132.

failure, and chest tightness.6 Patients with diabetes commonly
report dyspnea, indigestion, and even vague symptoms, such
as weakness, unusual fatigue, cold sweats, sleep disturbance,
anxiety, and dizziness.5 Evidence to support contrasting pre-
sentations across racial and ethnic populations, which could
help distinguish between typical or atypical chest pain, is cur-
rently lacking.5 
Diagnostic Considerations
Clinical prediction rules can help guide the practitioner toward
an accurate diagnosis of chest pain. One prediction rule is the
Marburg Heart Score, which predicts the likelihood of a diag-
nosis of coronary artery disease (CAD) when a patient presents
with at least three of the following variables (sensitivity: 87.1;
specificity: 80.8; 95% confidence interval)8:
• Age 55 years or older in men; 65 years or older in women
• Known CAD or cerebrovascular disease
• Pain not reproducible by palpation
• Pain worse during exercise
• Patient’s assumption that pain is cardiogenic in origin
Guidelines from the American College of Cardiology (ACC)
and the American Heart Association (AHA) provide the follow-
ing pain descriptions that are not characteristic of myocardial
ischemia9:
• Pleuritic pain (i.e., sharp or stabbing pain brought on by
respiratory movements or cough)
• Primary or sole location of discomfort in the middle or lower
abdominal region
• Pain that may be localized at the tip of one finger, par-
ticularly over the left ventricular apex or a costochondral
junction
• P ain reproduced with movement or palpation of the chest
wall or arms
• Brief episodes of pain that last a few seconds or less
• Pain that radiates into the lower extremities 
Physical Therapy Considerations
If a patient reports chest pain during physical therapy interven-
tion, the therapist should discontinue the activity being per-
formed and allow the patient to rest in a comfortable position
(e.g., standing, sitting, supine). It is important to gather objec-
tive data about the patient’s active presentation of chest pain
during the event. This includes measuring and continuously
monitoring the patient’s vital signs (e.g., heart rate, blood pres-
sure, pulse oximetry) and telemetry (if applicable), obtaining the
patient’s pain rating, using the angina rating scale (Table 17.3),
and applying the Canadian Cardiovascular Society classification
of angina according to the impact on physical therapy activity
(Table 17.4). It is also important to continuously observe the
patient for signs of altered cardiac output (e.g., low blood pres-
sure), and it may be necessary to provide supplemental oxygen.
The therapist should determine whether the source of chest
pain is cardiogenic in nature, and if it is stable or unstable (refer to
Pathophysiology of Chest Pain section). If the patient presents with
one or more of the previously described unstable vital sign find-
ings, the therapist should immediately discontinue treatment and
notify the nurse and/or the physician. If appropriate, nitroglycerin
can be used to relieve acute pain. Further physical therapy interven-
tions should be deferred until workup and treatment are completed
by the medical team. When a patient presents with stable angina,
nitroglycerin may be useful, as well as physical rest or modification
of physical therapy evaluation or treatment, based on the stressor.
394 CHAPTER 17     Physical Therapy Considerations for Patients Who Present With Chest Pain

TABLE 17.4  Canadian Cardiovascular Society Classification of Angina According to Impact on Physical Activity
Level Impact of Physical Activity on Occurrence of Angina
Class I Ordinary physical activity, such as walking or climbing stairs, does not cause angina.
Angina occurs with strenuous, rapid, or prolonged exertion at work or recreation.
Class II Slight limitation of ordinary activity.
Angina occurs on walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind,
under emotional stress, or only during the first few hours of awakening.
Angina occurs on walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal
pace and in normal conditions.
Class III Marked limitations of ordinary physical activity.
Angina occurs on walking one to two blocks on the level and climbing one flight of stairs in normal conditions and at a normal
pace.
Class IV Inability to carry out any physical activity without discomfort.
Angina symptoms may be present at rest.

Data from Sangareddi V, Chockalingam A, Gnanavelu G, et al. Canadian Cardiovascular Society classification of effort angina: an angiographic correlation. Coron Artery
Dis. 2004;15(2):111-114.

The medical team and the nursing staff should still be notified
of the patient’s complaints and whether the pain has resolved.
Finally, if noncardiogenic chest pain is detected, it is the profes-
sional judgment of the physical therapist, in conjunction with
current practice guidelines and consideration of overall patient
safety, that determines whether the therapy intervention should
be continued or modified.
To ensure the continued safety of the patient in and out of
the acute care setting, patients who have a history of cardiogenic
chest pain must have an understanding of the presentations of
stable and unstable chest pain. It is the role of the physical ther-
apist to provide education on the differences between the two
conditions so that patients can determine whether they need
to rest, modify their activity, or seek out medical attention, as
appropriate.
Regardless of the etiology of the patient’s complaint of chest
pain, the physical therapist must be prepared to gather a reliable
description of chest pain and respond and/or refer accordingly
for prompt medical attention. It is always recommended to
report anything out of the physical therapists scope of practice
to the appropriate clinical professional.
References
1. Centers for Disease Control and Prevention. National Hospital Am-
bulatory Medical Care Survey: 2015 Emergency Department Survey
Tables. U.S. Department of Health and Human Services, Centers for
Disease Control and Prevention, National Center for Health Statis-
tics. http://www.cdc.gov. Accessed September 30, 2018.
2. Anderson JL, Adams CD, Antman EM, et al. 2012 ACCF/AHA
focused update incorporated into ACCF/AHA 2007 guidelines
for the management of patients with unstable Angina/non-ST-
elevation myocardial infarction: a report of the American College
of Cardiology foundation/American heart association task force on
practice guidelines: 2007 writing committee members: developed
in collaboration with the American College of emergency physi-
cians, society for cardiovascular angiography and interventions, and
society of thoracic surgeons. Endorsed by the American association
of cardiovascular and pulmonary rehabilitation and the society for
academic emergency medicine. Circulation. 2013;127:e683.
3. American Heart Association. Acute Coronary Syndrome. http://ww
w.heart.org. Accessed September 20, 2018.
4. Runge MS, Ohman EM, Stouffer GA. The history and physical
examination. In: Runge MS, Patterson C, Stouffer GA, eds. Netter’s
Cardiology. 2nd ed. Philadelphia: Saunders; 2010:3–14.
5. Thomas JJ, Brady WJ. Acute Coronary Syndrome. In: Walls RM,
et al., ed. Rosen’s Emergency Medicine. 9th ed. Philadelphia: Elsevier;
2018:204–212.
6. Brown JE. Chest pain. In: Walls RM, et al., ed. Rosen’s Emergency
Medicine. 9th ed. Philadelphia: Elsevier; 2018:204–212.
7. Goodman CC, Heick J, Lazario RT. Screening for cardiovascular
disease. In: Goodman CC, Heick J, Lazario RT, eds. Differential
Diagnosis for Physical Therapists: Screening for Referral. 6th ed. St.
Louis: Elsevier; 2018:224–237.
8. Bösner S, Haasenritter J, Becker A, et al. Ruling out coronary ar-
tery disease in primary care: development and validation of a sim-
ple prediction rule. CMAJ (Can Med Assoc J). 2010;182(12):1295–
1300.
9. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC
guideline for the management of patients with non-ST-elevation
acute coronary syndromes: executive summary: a report of the
American College of Cardiology/American heart association task
force on practice guidelines. Developed in collaboration with the
society for cardiovascular angiography and interventions and the
society of thoracic surgeons. Endorsed by the American association
for clinical chemistry. Circulation. 2014;130:2354–2394. https://
doi.org/10.1161/CIR.0000000000000133.
 PA R T
4 INTERVENTIONS
18
C H APT ER  
CHAPTER OUTLINE
Introduction
Oxygen Therapy
Physical Therapy Considerations
Hemodynamic Monitoring
Intracranial Pressure Monitoring
Physical Therapy Considerations
Multimodal Monitoring of
the Patient With Neurologic
Diagnoses
Medical-Surgical Management
Devices
Physical Therapy Considerations
APPENDIX 18A: Mechanical
Ventilation
Objectives of Mechanical
Ventilation
Types of Mechanical Ventilatory
Support
Complications of Mechanical
Ventilation
Weaning From Mechanical
Ventilation
Physical Therapy Considerations
APPENDIX 18B: Mechanical
Circulatory Support Devices
Objectives
Introduction
Short-Term Percutaneous Devices
Short-Term Surgically Placed
Devices
Long-Term Devices
Total Artificial Heart
Medical-Surgical Equipment
in the Acute Care Setting
Kathryn Panasci
Kristin Curry Greenwooda
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1. Describe the various types of medical-surgical equipment commonly used in the acute care setting, includ-
ing oxygen (O2) therapy and noninvasive and invasive monitoring and management devices
2. Provide a framework for the safe use of medical-surgical equipment during physical therapy practice
Introduction
Medical-surgical equipment is used in all areas of the hospital. Some types of equipment are
used only in specialty areas, such as the intensive care unit (ICU). The ICU, also known as the
critical care unit, is a highly specialized care unit for patients with life-threatening illness or
injury, requiring constant and close monitoring by the medical team. The equipment needed
to provide life-sustaining care in the ICU is numerous. Regardless of the unit or patient status,
the presence of certain types of equipment in a patient’s room can provide the physical therapist
with a preliminary idea of the patient’s general medical condition and the appropriateness of
therapeutic physical therapy intervention, prophylactic physical therapy intervention, or both.
The physical therapist may initially be intimidated by the medical-surgical equipment in use;
however, proper orientation to this equipment allows the physical therapist to intervene appro-
priately, safely, and with confidence.
Oxygen Therapy
The general indication for O2 therapy is hypoxemia. Hypoxemia is considered to be present
when the arterial oxyhemoglobin saturation (SaO2) is less than 90%, corresponding to an arte-
rial blood O2 partial pressure (PaO2) of less than 60 mmHg.1 Refer to Table 4.6 for the rela-
tionship between O2 saturation as measured by pulse oximetry (SpO2) and PaO2 and to Fig. 4.7
for the oxyhemoglobin dissociation curve. Other indications for O2 therapy are severe trauma,
shock, acute myocardial infarction, surgery, or carbon monoxide or cyanide poisoning.1,2 The
goal of O2 therapy is to prevent or reverse hypoxemia by increasing oxygen levels both in the
alveoli and in arterial blood, thereby improving tissue oxygenation, decreasing the work of
breathing, and decreasing myocardial work.1,2
aThe authors acknowledge Michele P. West for prior contributions to this chapter.
        395
396 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting
Supplemental O2 is delivered by variable-performance (Table
18.1) or fixed-performance (Table 18.2) systems. Each cannula
or mask is designed to provide a range of fraction of inspired
oxygen (FiO2). Variable-performance systems are not intended
to meet the total inspiratory requirements of the patient and
should not be used if a specific FiO2 is required. The actual
FiO2 for a given flow rate in a variable system is dependent on
a patient’s tidal volume; inspiratory/expiratory ratio; 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-performance systems deliver a specific FiO2
despite breathing pattern or other variables.2,3 Mechanical ven-
tilation is a form of fixed-performance delivery and will be dis-
cussed in Appendix 18A.
O2 delivery devices 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 stor-
age capacity of the mask or reservoir is increased, the FiO2 for a
given flow rate is also increased.2
The supplemental O2 requirements of a patient may fluctu-
ate with activity. Monitoring SaO2 with pulse oximetry (identi-
fied as SpO2) and subsequent titration (increasing or decreasing
the FiO2) of O2 may be indicated during exercise. The physician
may order specific parameters for resting and exercise SpO2 if a
patient has a low activity tolerance or an abnormally low SpO2
at baseline.
A patient with chronic obstructive pulmonary disease
(COPD) who has chronic carbon dioxide (CO2) retention may
become desensitized to the respiratory stimulant effects of CO2.
In these patients, ventilation is driven by means of a reflex ven-
tilatory response to a decrease in PaO2 and in theory, provid-
ing supplemental O2 may lead to a reduction in the hypoxic
peripheral chemoreceptor ventilatory drive. The hypoxic drive
is not usually suppressed until the PaO2 increases to 60 mmHg
or greater.1,4 However, potential respiratory depression or
hypercapnia should never contraindicate O2 therapy in the
case of hypoxemia. In fact, long-term continuous supplemen-
tal O2 therapy is the recommended intervention in patients
with COPD and severe resting hypoxemia (PaO2 ≤55 mmHg
or SpO2 ≤88%), demonstrating reductions in mortality risk
for this fragile patient population.5 If acute respiratory failure
occurs in the patient with COPD, other support measures, such
as noninvasive positive-pressure ventilation or invasive mechan-
ical ventilation, can be used.6
Physical Therapy Considerations
• A green label designates the O2 supply on hospital walls. A
similar gauge supplies pressurized air and is designated by a
yellow label.
• The FiO2 for a given system is dependent on its proper fit
and application. Ensure that all connections are intact, that
the O2 is flowing as indicated, and that the cannula or mask
is properly positioned.
• Provide extra lengths of O2 extension tubing if functional
mobility will occur farther than 5 to 6 feet from the bedside
(i.e., the wall O2 source) and without use of a portable O2
tank. Keep in mind that adding more than one extension
tubing can require an increase in FiO2 because O2 is lost in
the gradient. Ensure that the plastic adaptor between two
lengths of oxygen supply tubing is secure.
• When used, ensure that portable O2 tank valves are open,
turned on to the desired flow rate, and have sufficient levels of
O2 before mobilizing the patient. Have backup tanks available.
Be sure to secure the tank in a rolling O2 cart during mobility.
Return used O2 cylinders to the designated storage area.
• Observe masks for the accumulation of mucus or clogging.
Clear or change the cannula or mask, if needed.
• Monitor the patient’s skin for potential breakdown caused by
pressure from the cannula or mask. Provide appropriate pad-
ding (e.g., foam ear protectors) without interfering with the
fit of the cannula or mask.
• 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 during breathing, confu-
sion, pallor, or cyanosis.
• Document the type and amount of supplemental O2 used
during physical therapy intervention. This may include dif-
ferent amounts of FiO2 for rest, exertion, and recovery period
after exercise, with corresponding vital signs.
• O2 is a medication that must be prescribed and is typically
titrated according to physician orders or hospital protocol.
The physical therapist should only titrate oxygen if an order
to do so exists or if the situation is clinically appropriate,
such as an acute desaturation. Communicate any changes in
O2 to the medical team.
• There may be specific guidelines set forth by third-party
payers regarding the eligibility for home O2 use. For exam-
ple, Medicare requires that patients meet all of the following
criteria for home O2: documented diagnosis of a medical con-
dition known to improve with O2 therapy, documentation of
O2 saturation levels by a qualified provider within 48 hours
of durable equipment delivery, and alternative treatments
deemed ineffective. Oximetry studies must demonstrate one
of the following: a resting (awake) room air SaO2 of 88% or
less, room air SaO2 of 88% or less during exercise and doc-
umented improvement of hypoxemia during exercise with
oxygen, or room air SaO2 of 88% or less for at least 5 minutes
during sleep.7 
Hemodynamic Monitoring
Monitoring hemodynamic (blood flow) status provides informa-
tion about the function of the cardiovascular system, including
adequacy of a patient’s circulation, perfusion, and oxygenation
of tissues and organ systems.8 The objective of hemodynamic
monitoring is to ensure optimal tissue perfusion and oxygen
delivery while maintaining adequate mean arterial blood pres-
sure and blood gas levels.9,10 Multiple measures of cardiac and
intravascular pressures and volumes are interpreted to direct the
therapeutic plan of care with the goal of preventing or treat-
ing organ failure.10 Ideally, hemodynamic monitoring is accu-
rate and reproducible, as noninvasive as possible, and minimizes
 TABLE 18.1  Variable-Performance Oxygen Delivery for Spontaneously Breathing Adultsa
Device Purpose Clinical Implications
Nasal cannula Delivers supplemental O2 mixed with The rule of thumb for the cannula system is that FiO2 is increased by 3% to
(Fig. 18.1A) RA, usually 1–6 lpm 4% for each lpm of O2. Mouth breathing does not necessarily indicate that
RA ≈21% FiO2 a patient is not receiving supplemental O2. If nasal passages are obstructed,
1 lpm ≈24% FiO2 O2 is able to collect in the oral and nasal cavities and is drawn in on inspira-
2 lpm ≈28% FiO2 tion. Flow rates greater than 6 lpm are unlikely to further increase delivered
3 lpm ≈32% FiO2 O2 and may prove uncomfortable because of mucosal irritation. Provide
4 lpm ≈36% FiO2 patients who are mobile with adequate lengths of extension tubing or a por-
5 lpm ≈40% FiO2 table O2 tank to enable functional mobility. Patients should be instructed
6 lpm ≈44% FiO2 on how to avoid tripping over or becoming tangled in the tubing. Ensure
that the cannula is in place and the tubing is without kinks or external
compression during and after the physical therapy session. Observe skin on
the face and ears for any irritation or breakdown from the tubing.
Open face tent Provides humidified, supplemental O2 A significant amount of mixing with RA occurs, although the capacity of
(Fig. 18.1B) mixed with RA the mask allows O2 to collect about the nose and mouth. May be more
FiO2 ≈30% to 55% Can also be used for nebulized comfortable than a closed face mask for patients who are claustrophobic
­medications or have sustained facial trauma. Moisture may collect in the tubing and
should be drained before moving the patient. The mask can easily shift;
reposition under the chin, if necessary. The aerosol system is 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 alternatively used when mobilizing the patient.
Closed face mask, Delivers supplemental O2 mixed with The closed face mask interferes with coughing, talking, eating, drinking,
Simple oxygen RA and facial and airway care. They may be very drying and uncomfortable
mask (Fig. 18.1C) Mask capacity is limited but does allow with resultant skin irritation. Patients often remove the mask for these
5–6 lpm ≈40% FiO2 for the collection of O2 about the nose reasons. Educate the patient on the importance of keeping the mask in
6–7 lpm ≈50% FiO2 and mouth place.
7–8 lpm ≈60% FiO2
Transtracheal oxygen Used for long-term O2 therapy Patients with uncompensated respiratory acidosis, severe coagulopathy,
(TTO) catheter Indicated when there are complications upper airway obstruction, medical instability, and an inability to practice
with or suboptimal nasal cannula use, self-care of insertion site are excluded from the use of this device. De-
nocturnal hypoxemia despite na- pending on the surgical technique, the use of this device for O2 delivery
sal c­ annula use, in situations when is delayed from 1 day to 1 week postoperatively to ensure that a perma-
a ­patient needs more freedom to nent tract is formed between the trachea and skin. This device requires
­mobilize, or for patient preference care and attention to hygienic maintenance. The most serious complica-
Provides continuous supplemental O2 tion is tracheal obstruction resulting from the accumulation of mucus
mixed with RA on the outside of the catheter, which can be avoided by routine secretion
clearance multiple times per day. There is risk of infection around the
catheter site and risk of catheter dislodgement.
Tracheostomy mask Provides supplemental, humidified O2 Significant mixing with RA occurs. Humidification is particularly important
or collar or air at a tracheostomy site for a patient with a tracheostomy, as the tracheostomy bypasses the natural
(Fig. 18.1D) humidification system. Moisture or pulmonary secretions may collect in
FiO2 ≈28% to 100% the mask or tubing and should be drained before moving the patient or
lowering the head of the bed (HOB). The mask can easily shift; reposition
over the site, if necessary. Gently pull the mask away from the patient to
access the tracheostomy site for bronchopulmonary secretion clearance.
Partial non- Mix of supplemental O2 and RA The partial non-rebreather mask provides similar FiO2 to the non-
rebreather mask Provides a high FiO2 to the patient while rebreather mask at lower flow rates. The closed face mask may interfere
FiO2 ≈40% to 60% conserving the O2 supply with talking, eating, and drinking. High O2 concentration may be
Two-way valves in the mask allow for RA drying and uncomfortable; however, humidification is not used with this
inhalation in addition to supplemental O2. method because it interferes with O2 delivery. The reservoir bag should
A two-way valve allows for the O2-rich remain at least ⅓–½ full on inspiration.
portion of the exhaled breath to reenter the
reservoir bag so that inhalation consists of
both exhaled air and supplemental O2
The remaining exhaled air exits through
the RA valves in the mask
Non-rebreather Provides the patient with the highest This mask delivers the highest concentration of FiO2 available without
mask (NRB) concentration of supplemental mechanical ventilation. Physical therapy intervention is usually deferred
(Fig. 18.1E) O2 available via a face mask in a if a patient requires this type of device to maintain oxygenation. How-
FiO2 ≈60% to 80% variable-performance system ever, after consultation with the medical team, in some cases bronchopul-
One way valves control inflow of monary hygiene may still be indicated.
­supplemental O2 and outflow of
exhaled air so that the patient is
only breathing the supplied O2
aListedfrom least to most oxygen support.
FiO2, Fraction of inspired oxygen; lpm, liters per minute; O2, oxygen; RA, room air.
Data from References 4, 21-23.
398 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

B C D

E
FIG. 18.1
(A) Nasal cannula with humidification. (B) Open face mask or tent. (C) Closed face mask. (D) Tracheostomy
mask or collar. (E) Non-rebreather mask. (A, Redrawn from Kersten LD, ed. Comprehensive Respiratory Nursing: A
Decision-Making Approach. Philadelphia: Saunders; 1989. In: Hillegass E, ed. Essentials for Cardiopulmonary Physi-
cal Therapy. 4th ed. St. Louis: Elsevier; 2011. B to E, From Williams P. deWit’s Fundamental Concepts and Skills for
Nursing. 5th ed. St. Louis: Elsevier; 2017.)
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18 399

TABLE 18.2  Fixed-Performance Oxygen Delivery

Device
Air entrainment mask
(AEM) (Venti-mask,
Venturi mask) (Fig. 18.2)
FiO2 ≈24% to 50%
BiPAP (Bi-level positive
airway pressure)
FiO2 ≈21% to 100%
Purpose
Provides a specific concentration of
supplemental O2 using color-coded
diluter pieces to ensure accurate FiO2
delivery
Pressure supported, noninvasive ventila-
tion that provides positive inspiratory
and end expiratory pressure
Pressures are set at different levels to
decrease the work of breathing by
reducing the airway pressure necessary
to generate inspiration
May be used to avoid intubation and
mechanical ventilation
Often used in the hospital or home set-
ting for the management of obstructive
sleep apnea
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. When humidification is used, monitor
for accumulation of moisture in the tubing. Useful for patients with
COPD who require a fixed precise FiO2.
BiPAP may deliver supplemental O2 at a specific concentration, or
it may deliver RA. Patients may feel claustrophobic because of the
tight fit of the mask. The equipment may be noisy; thus the thera-
pist may need to speak loudly to communicate with the patient.
Air leaks can occur around the mask. 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. May also cause nasal congestion, nasal dryness, or rhinorrhea.
Depending on the patient’s oxygen requirements, BiPAP may be
turned off when mobilizing and alternate methods of O2 deliv-
ery 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.

COPD, Chronic obstructive pulmonary disease; FiO2, fraction of inspired oxygen; lpm, liters per minute; O2, oxygen; RA, room air.
Data from References 2, 4, 24.

of the heart, or both. The cannula or catheter is attached to

FIG. 18.2
Air entrainment mask or Venturi mask. (From Williams P. deWit’s Fun-
damental Concepts and Skills for Nursing. 5th ed. St. Louis: Elsevier; 2017.)
harm to the patient.9,10 Hemodynamic monitoring can be
accomplished by using noninvasive (Table 18.3) or invasive
(Table 18.4) methods.
Noninvasive, or indirect, hemodynamic monitoring pro-
vides physiologic information without the risks of invasive
monitoring and can be used in most settings. Invasive, or
direct, measurements are obtained by penetrating the skin and
inserting a cannula or catheter into a blood vessel, chamber
a monitoring system, which consists of a transducer, ampli-
fier, and oscilloscope for the display of the vascular waveforms
and pressure measurements.11 Direct monitoring can pro-
vide continuous, accurate data; however, thrombosis, air or
clot embolisms, vessel perforations, dysrhythmias, infections,
skin necrosis, and trauma to nearby structures are potential
complications.8,9
During invasive hemodynamic monitoring, the level of the
right atrium is the standard zero reference point and is identi-
fied by the phlebostatic axis—the intersection of the midaxillary
line and the fourth intercostal space (Fig. 18.3).11 The system
is “leveled” by using a carpenter’s level or laser-light level to
align the patient’s phlebostatic axis with the transducer. Reposi-
tioning the patient may artificially alter waveforms by applying
pressure to the catheter, shifting the catheter or stopcock, or
shifting the phlebostatic axis relative to the transducer.11 The
transducer is releveled when clinically indicated. Raising the
level of the phlebostatic axis relative to the transducer gives
falsely high readings; lowering the phlebostatic axis gives falsely
low readings.11
Patients with critical illness will have an alarm set on the
hemodynamic monitoring system that sounds when vital sign
measurements are out of the desired parameters.11 
Intracranial Pressure Monitoring
Intracranial pressure (ICP) and cerebral perfusion pressure
(CPP) are monitored in patients with acute brain injuries and
suspected intracranial hypertension.12 It has also been sug-
gested that ICP monitoring be initiated in patients when clin-
ical assessment, imaging assessment, or both has identified an
400 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

TABLE 18.3  Noninvasive Medical Monitoring

Device Purpose Clinical Implications
BP cuff (sphygmomanometer) Indirectly measures arte- Do not use a BP cuff on an extremity with an arterial line, lymphedema, AV
Normal (adults): rial BP fistula or graft, blood clot, or ipsilateral mastectomy. Best to avoid measur-
<120/<80 mmHg ing BP in an extremity with a peripheral or central intravenous line. Look for
Elevated (adults): signs posted at the patient’s bedside stating whether the use of a BP cuff on a
120–129/<80 mmHg particular extremity is contraindicated. Use an appropriately sized cuff. The
Stage 1 HTN: cuff bladder should be no less than 80% of limb circumference. Incorrect cuff
SBP 130–139 size will lead to measurement error. Ideal cuff placement is proximal to the
or DBP 80–89 mmHg elbow with auscultation of the brachial artery. Alternative sites include: distal
Stage 2 HTN: to the elbow with auscultation of the radial artery, proximal to the popliteal
SBP ≥140 or DBP ≥90 mmHg space with auscultation of the popliteal artery, and proximal to the ankle with
auscultation of the posterior tibial artery. Avoid contact between stethoscope
tubing and the cuff tubing to minimize extraneous sounds. The nondominant
arm should be used and placed at the level of the heart, in full extension, with
the antecubital fossa facing upward. A Doppler probe may be used to take a
BP measurement if it is too difficult to hear Korotkoff sounds, such as in the
situation of hypotension. Automatic cuffs may be helpful when serial BPs are
needed, or when the therapist needs both hands (simultaneously) to guard a
patient. While an automatic BP cuff is inflating/deflating, be sure to keep the
patient’s arm and hand still, and free from movement. Be sure to document the
location where a BP measurement is taken in your note.
Telemetry (ECG) Continuous monitor- Communicate with the nurse before physical therapy intervention because many
ing of heart rate and activities may alter the rate or rhythm or cause artifact (e.g., chest percussion).
rhythm and respiratory If electrodes become dislodged, reconnect them. One way to remember elec-
rate (see Table 3.9) trode 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
abdomen), and “smoke over fire” (black electrode is placed on the upper-left
rib cage superior and lateral to the left nipple, and red electrode is placed
below the black one on the anterolateral left abdomen). The brown electrode is
usually placed centrally in the fourth intercostal space. Do not place electrodes
over a pacemaker or defibrillator. Artifact or poor signal quality can appear on
telemetry because the strength and consistency of the electrical current are in-
terrupted. Causes of artifact include patient movement, poor electrode contact
with the skin, or manual techniques for bronchopulmonary hygiene. Patients
on telemetry should be instructed to stay in the area monitored by telemetry
antennas. Watch the telemetry monitor to get a baseline heart rate and rhythm
before physical therapy intervention and to ensure that the telemetry unit is
actively connected. Telemetry may be put on hold temporarily for the patient
to travel off the floor, or the batteries in an individual patient box may need
replacement. The telemetry box may fit in the pocket of a hospital gown or in
a small pocket carrier that is placed around the patient’s neck or shoulder for
exercise. 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). At some institutions, a designated
nurse is stationed at the nursing desk to watch the main telemetry monitor for
all patients. If indicated, check in with this nurse and request that the patient’s
telemetry be carefully watched during physical therapy intervention. Other
telemetry boxes may have a screen the physical therapist can monitor during
activity.
Pulse oximeter A noninvasive, trans- Typically taken on the finger; can also use the nose, ear lobe, forehead, or toe.
Normal SpO2 (at sea level) 95% cutaneous method of Generally, SpO2 ≤88% indicates the need for supplemental oxygen. The wave-
to 100%. monitoring the per- form or pulse rate reading should match the ECG or palpated pulse. Monitor
Caution below 90% centage of hemoglobin changes in pulse oximetry during exercise and position changes. Certain medi-
saturated with O2 in cal conditions (e.g., peripheral vascular disease, anemia, cardiac dysrhythmia,
arterial blood sepsis, hypothermia, vasoconstriction, hypotension, and carbon monoxide
poisoning), sunshine or excessive ambient light, poor probe position, motion
artifact, dark skin pigmentation, or nail polish may lead to a false or unreli-
able readings. 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 to Table 4.6 and Fig. 4.7.

AV, Arteriovenous; BP, blood pressure; ECG, electrocardiography; SaO2, arterial oxyhemoglobin saturation; SpO2, measurement of SaO2 with pulse oximetry.
Data from References 25-29.
 TABLE 18.4  Invasive Medical Monitoring
Device Purpose
Arterial line (A-line) Direct and continuous monitoring of
Normal values: systolic, diastolic, and MAP; source
Systolic: 90–140 mmHg for repeated arterial blood gas
Diastolic: 60–80 mmHg
MAP: 70–100 mmHg
Central venous catheter Indicated for a patient with signifi-
(CVC) cant fluid volume deficit and is used Greatly reduces the need for repeated venipuncture and reduces risk of
CVP Normal value: as a guide to overall fluid balance
2–5 mmHg or 3–8 cm Measurement of CVP is a direct re-
water (H2O) flection of right heart function (See or water manometer, which must be leveled to the phlebostatic axis.
the Pulmonary artery catheterization
section later.)
Also provides vascular access for
parenteral nutrition, large fluid
volumes, or noxious medications
that cause irritation when adminis-
tered peripherally; obtain repeated
blood sampling; or the initiation of
transvenous cardiac pacing
Pacemaker (temporary) Provides temporary supportive or
prophylactic cardiac pacing post-
operatively, for bradydysrhythmias
(e.g., heart block), tachydysrhythmias and range of motion (ROM) restrictions. Temporary pacing wires and
(e.g., supraventricular tachycardia),
patients post myocardial infarction,
EPS diagnostic studies, or perma-
nent pacemaker failure (Refer to the
Management section in Chapter 3 for
more information on pacemakers.)
Pulmonary artery catheter- Measures PAS, PAD, PAP, PAOP,a
ization (PAC) (PA line, LVEDP, RAP, CVP, CI, and CO in
Swan-Ganz) (Fig. 18.4B) cases of hemodynamically unstable
Normal values: patients with suspected or diagnosed rectly aligned with the phlebostatic axis, accurate readings are possible
PAS: 20–30 mmHg cardiogenic shock
PAD: 5–10 mmHg Invasive and most often used during
PAP (mean): 10– or after cardiac surgery
15 mmHg Some use in the clinically stable pa-
PAOP (mean): tient for diagnosis and management
5–12 mmHg of unexplained dyspnea or pulmo-
CVP: 2–5 mmHg nary HTN
CO: 4–6 lpm (at rest)
aPAOP (formerly called pulmonary capillary wedge pressure or PAWP).
A-line, Arterial line; ARDS, acute respiratory distress syndrome; CI, cardiac index; CO, cardiac output; CVP, central venous pressure; EPS, electrophysiology study;
HTN, hypertension; ICU, intensive care unit; LAP, left atrial pressure; LVEDP, left ventricular end-diastolic pressure; MAP, mean arterial pressure; PAP, pulmonary ar-
tery pressure; PAOP, pulmonary artery occlusion pressure; PAD, pulmonary artery diastolic pressure; PAS, pulmonary artery systolic pressure; RAP, right atrial pressure.
Data from References 11, 30-34.
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 de-
cline (Fig. 18.4A). A damped (flattened) waveform may indicate hypoten-
sion, or it may result from pressure on the line. If a waveform changes dur-
ing treatment, in the absence of other clinical signs, reposition the patient
or limb and reassess. If the waveform does not return to baseline, notify
the nurse. Traditionally a patient with a femoral A-line is seen bedside due
to mobility precautions of limiting hip flexion past 60–80 degrees. Newer
guidelines may allow for safe mobility in the presence of a femoral A-line.
After femoral A-line removal, the patient is usually on strict bed rest for
a period of time to be determined by the medical team with a sandbag
placed over the removal site. 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. Upper extremity insertion sites are usually splinted
with an arm board to stabilize the catheter. The transducer may be taped
to the patient’s hospital gown at the level of the phlebostatic axis (see Fig.
18.3) during mobilization. If the transducer is too low, blood pressure (BP)
will read high; if the transducer is too high, BP will read low.
Do not use a blood pressure cuff on an extremity with a central line.
vein irritation. A chest x-ray is taken to confirm placement and to rule
out iatrogenic pneumothorax. The CVC is connected to a transducer
When correctly aligned, accurate CVP readings are possible with
the head of the bed (HOB) elevated up to 60 degrees. Complications
include thrombus or thromboembolism formation, air embolus, and
infection.
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
electrodes should be kept dry. Be aware of the location of the generator
and wires at all times, especially during mobility activities. If a tem-
porary pacemaker is placed after cardiac surgery, the wires are removed
when the patient is hemodynamically stable and without indication for
further pacing. 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 monitor-
ing to evaluate pacemaker function. Pacemaker malfunctions can occur
and include failure to pace due to a mechanical problem with the pacer,
“loss of capture” when the pacing stimulus fails to initiate myocardial
depolarization, “rate drift” when pacing occurs at inappropriate times,
“undersensing” when the pacer does not detect spontaneous myocardial
depolarizations, and “oversensing” when the pacer detects extraneous
electrical input, then inappropriately triggers or inhibits output.
Traditionally, the patient with a PA line is on bed rest but does not need
to remain in the supine position for accurate readings. Newer guide-
lines may allow for mobility out of bed. When the transducer is cor-
with the HOB elevated up to 60 degrees. PAOP is an indirect measure
of LVEDP. CO equals stroke volume (SV) × heart rate (HR). Possible
complications include hemorrhage, pneumothorax, thromboembolism,
infection, vessel trauma, valve damage, and arrhythmias.
402 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

increased risk for elevation in ICP.13,14 Intracranial hyperten-

sion may lead to decreased cerebral blood flow and oxygenation
4 ICS and can have significant, and potentially fatal, neurologic
outcomes.15 ICP and CPP may be measured in a variety of
ways, depending on how urgently values are needed and the
patient’s neurologic and hemodynamic stability. The purpose
of ICP monitoring is prevention, early detection, and/or man-
agement of secondary injuries (e.g., intracranial hypertension,
cerebral ischemia, arterial hypotension, hypoxemia) to main-
tain adequate cerebral blood flow and oxygenation.14-16 (See
also Chapter 6.)
Table 18.5 describes the different types of ICP monitors. Some
Midpoint
A-P Chest Wall
ICP monitors, such as the intraventricular catheter, require that
FIG. 18.3
the sensor and transducer be leveled. Although the anatomi-
The phlebostatic axis at the intersection of the fourth intercostal space (ICS) cal reference point is the foramen of Monro, clinically the zero
and the midpoint of the anterior (A) and posterior (P) chest wall. (Courtesy point for leveling the transducer is most often at the external
Edwards Lifesciences LLC.) auditory meatus.17 A normal ICP waveform has a triphasic sinu-
soidal waveform and should correspond to the cardiac cycle.16

Aorta

Radial artery

Dorsalis pedis artery

A Time

Balloon inflated
for PCWP
Static venous
blood flow to
left atrium

Lungs
Proximal
(PA) LA PCWP
infusion Distal (PA) REFLECTS
line infusion line LAP
Distal port LV
Syringe to balloon in branch of
inflation valve pulmonary artery

Thermistor port
Thermistor connector RV
to cardiac output Proximal port
computer in right atrium
B
FIG. 18.4
(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, From Yentis SM, Hirsh NP, Smith GB,
eds. Anaesthesia and Intensive Care A-Z. An Encyclopedia of Principles and Practice. 2nd ed. Oxford: Butterworth-
Heinemann; 2000:45. B, From Kersten LD, ed. Comprehensive Respiratory Nursing: A Decision-Making Approach.
Philadelphia: Saunders; 1989:758.)
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18
TABLE 18.5  Intracranial Pressure Monitors
Device Purpose
Epidural sensor Inserted into the epidural space via burr
hole to monitor intracranial pressure
(ICP)
Subarachnoid bolt Direct monitoring of ICP through a
hollow screw placed into the skull
and dura
Intraventricular catheter Direct monitoring of ICP and access for
(IVC), external ventricu- the sampling and drainage of cerebro-
lar drain (EVD), ventricu- spinal fluid (CSF) and intraventricular
lostomy blood via placement in the third
ventricle
Fiberoptic transducer- Used to monitor ICP and drain CSF;
tipped catheter both can be done intermittently or
continuously
Data from References 17, 35-37.
Although noninvasive methods to monitor ICP are available,
invasive monitoring remains the most accurate and reliable source
of information for clinical management.14,16 Risks of invasive
ICP monitoring include malfunction, poor positioning, catheter
obstruction, infection, and intracranial hemorrhage.16
Physical Therapy Considerations
• B e aware of both the ICP value and the corresponding wave-
form on the monitor. Waveform characteristic changes can
indicate evolving pressure issues before critical elevations of
ICP values.12
• Transient elevations in ICP will occur normally and without
concern. A sustained elevation lasting longer than 5 minutes
is indicative of intracranial hypertension, which is a medical
concern13 and should be reported to the medical team. Signs
and symptoms of elevated ICP include nausea and vomiting,
altered mental status, headache, and possible Cushing’s triad
(hypertension, bradycardia, and irregular breathing or ap-
nea).13,14
• Patients with elevated ICP should be positioned with the
head of the bed (HOB) at a level which maximizes cerebral
venous return, thus lowering ICP. There are varying recom-
mendations as to what degree is optimal, but the general
consensus is a minimum of 30 degrees.13,14,18,19 Therefore be
aware that lowering the HOB below 30 degrees may increase
ICP and position changes should be verified with the medi-
cal team. Other positions that increase ICP are the prone
position, Trendelenburg position, excessive neck flexion or
rotation, and hip flexion.14,18
• Additional conditions that may transiently increase ICP are
the Valsalva maneuver; noxious stimuli; coughing; sneezing;
403
Clinical Implications
The transducer does not need to be releveled with position changes.
Least invasive monitoring option, but also less reliable than intraven-
tricular measures of ICP.
Poor reliability with less accuracy than the ventricular devices de-
scribed below. Complications include infection, hemorrhage, and
blockage of the bolt by clot or brain tissue. Declined use over recent
years.
The nondominant frontal hemisphere is the preferable insertion site.
The transducer must be positioned (leveled) with the foramen of
Monro, which is approximately the external auditory meatus, and
must be repositioned with position changes. Intermittent drain-
age systems allows CSF drainage (1–2 mL/minute for 2–3 minutes
at a time), as needed, by opening a stopcock when the ICP exceeds
the parameters set by the physician. A continuous system allows
the drainage of CSF to occur whenever the intraventricular pressure
is higher than the pressure set by the height of the collection bag
(determined by the physician). Very reliable and considered the gold
standard due to a high level of precision. Complications can include
hemorrhage, incorrect placement in brain tissue, infection, ventricu-
litis, or catheter occlusion by blood or brain tissue.
The transducer is on the fiberoptic catheter and must be zeroed before
placement. It does not need to be adjusted (releveled) with position
changes. The drip chamber does need to be leveled with the foramen
of Monro. Very reliable.
suctioning; isometric muscle contractions; overstimulation,
such as with clustering of care or treatment interventions;
pain; and stress.14,18,19 
Multimodal Monitoring of the Patient
With Neurologic Diagnoses
Multimodal monitoring (MMM) is the use of multiple types
of neuromonitoring modalities to obtain information regard-
ing cerebral pressure, perfusion, metabolism, oxygenation,
and electrocortical activity. Such values are imperative in
the management of patients in the neurologic critical care
unit because of the high risk of inflammation, ischemia, and
edema after the initial injury.20 This sequelae of injury can
result in irreversible secondary brain injury. Therefore the
goal of MMM is early detection and prevention of secondary
brain injury.20 An overview of select monitoring technologies,
which are typically used in larger hospitals with n­ eurotrauma
or neurosurgery specific units, are listed in Table 18.6. 
Medical-Surgical Management Devices
A wide variety of lines, tubes, catheters, and access devices
make up the array of medical-surgical equipment that is
routinely 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 guidance) or in the oper-
ating room. Table 18.7 describes the medical-surgical man-
agement devices most commonly encountered in the acute
care setting.
404 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

TABLE 18.6  Multimodal Brain Monitoring Technologies

Device Purpose Clinical Implications
Cerebral Assessment of cerebral metabolism through The recovered metabolites represent 70% of the true interstitial fluid
­microdialysis specific metabolic marker levels (glucose, concentrations and are compared with normal values. A result toward a
lactate, pyruvate, glutamate, and glycerol) threshold value requires intervention, such as permissive hyperglycemia,
via a catheter inserted into the injured hypoglycemia prevention, vasopressor use, or positioning. A second
brain tissue catheter may be placed in an uninjured area of the brain for comparison.
Typically used in patients with severe head Allows for dynamic, real-time monitoring versus the static information
trauma snap shot provided by traditional imaging.
Cerebral blood Bedside monitoring of cerebral blood flow TDP reflects real-time perfusion of the brain. The patient may need to be
flow (CBF) and circulation cooled if brain temperature is >38.5°C. A second catheter may be placed
Perfusion is measured directly through a in an uninjured area of the brain for comparison. The probe can be seen
thermal diffusion probe (TDP) inserted on computed tomography and radiography; however, it is not compatible
into the white matter to monitor thermal with magnetic resonance imaging.
convection as a result of blood flow
Can also be measured indirectly via tran-
scranial Doppler (TCD) which assesses
flow velocities and can detect vasospasm
Brain tissue oxy- Directly measures brain oxygen and temper- Lower PBTO2 values (<20mm) may represent impending hypoxia and
genation ­tension ature as a marker of cerebral ischemia and intervention should be considered. Elevated PBTO2 values may represent
(PBTO2) secondary brain injury in the mechanically hyperemia or excessive cerebral blood flow, which could increase ICP.
ventilated patient PBTO2 results can be improved during ischemic conditions by decreas-
ing ICP with barbiturates, CSF drainage, or craniotomy. Cerebral oxygen
delivery can be increased with isotonic fluid administration, vasopressors,
or blood transfusion. Conditions such as pain, shivering, or agitation that
decrease brain oxygenation can be managed with sedatives, antiinflam-
matory agents, or cooling devices.

ATP, Adenosine triphosphate; CSF, cerebrospinal fluid; FiO2, fraction of inspired oxygen; ICP, intracranial pressure.
Data from References 20, 38.

Physical Therapy Considerations
The following information applies to medical-surgical equip-
ment, including the O2 therapy and hemodynamic and ICP
monitoring equipment previously discussed.
• Before entering a patient’s room, review the medical record,
particularly new orders; recent progress notes; test results; and
charted vital signs, noting trends or variations from the norms.
• Note whether any particular precautions protecting the pa-
tient or the caregiver from specific pathogens are in place
(e.g., contact, droplet, airborne, or neutropenic precautions).
Refer to Table 13.3 for a summary of infection prevention
precautions.
• Practice standard precautions. The likelihood of encounter-
ing bodily fluids is increased in the acute care setting.
• Discuss your planned intervention with the nurse. Sched-
uled procedures may take precedence over physical therapy
intervention, or it may coordinate well with another planned
procedure, such as standing x-ray to view fracture position in
weight bearing.
• Upon 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. Devel-
op a consistent method of surveying the room: left to right or
top of bed to bottom of bed, to ensure that all lines and equip-
ment 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 as a result
of position changes or artifact.
• 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 attempt-
ing to move the patient.
• 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 beginning
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 recom-
mended that the physical therapist disable an alarm.
• If available and appropriate, use a portable telemetry moni-
tor to maintain the continuity of electrocardiography (ECG)
monitoring when mobilizing a patient who has been placed
on continuous ECG monitoring away from the bedside.
• At the completion of your treatment, ensure that all equip-
ment is plugged into a power source, that the patient is not
lying on top of any lines and wires (risk of pressure injury),
that appropriate alarms are turned on, and that the patient
is positioned with the appropriate safety and communication
measures in place. Notify the nurse of any change in the pa-
tient’s status.
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18
TABLE 18.7  Medical-Surgical Management Devicesa
Device Purpose
Arteriovenous (AV) Provides access for long-term hemo-
fistula or graft dialysis
Chest tube (CT) Removes and prevents the reentry of
(Fig. 18.5) air or fluid from the pleural or me-
diastinal space and provides negative
intrapleural pressure
Used to treat pneumothorax, hemo-
thorax, pleural effusion, empyema,
or chylothorax
May also be used for chemical
pleurodesis to treat recurrent pleural
effusion or pneumothorax
Lumbar drain (lum- Drainage of cerebral spinal fluid (CSF)
bar drainage device from the subarachnoid space in the
[LDD]) lumbar spine
Treatment of CSF leaks/dural tears,
shunt infections, or traumatic dural
fistulae or to reduce intracranial
pressure
Nasoenteric feeding Placed for enteral feedings when pa-
tube (Dobhoff tube) tients are unable to take in adequate
nutrition by mouth. Short-term use,
days to several months, depending
on composition of tubing
405
Clinical Implications
The surgeon may order upper extremity elevation and non–weight bearing on
the involved extremity for 24 hours after surgical procedure. The involved
extremity should not be used for phlebotomy, intravenous (IV) infusions,
or blood pressure measurements. Avoid pressure or constriction over the
site (e.g., tight clothing, sleeping on, or bending the accessed limb for pro-
longed periods of time). Palpable turbulence is normal in the graft or fistula,
which will have a raised, ropelike appearance. Complications may include
thrombosis, infection, pseudoaneurysm, and vascular steal syndrome.
Chest tubes may cause discomfort, which may inhibit effective coughing,
deep breathing, mobility, or lying on the involved side. The patient may
benefit from premedication for pain before treatment if the CT has been
removed from suction, often referred to as “chest tube to water seal.”
The drainage system should be below the level of CT 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 CT itself becomes dislodged, stop the activity,
place a gloved hand over the insertion site, and notify nursing immedi-
ately. When able, cover the site with an occlusive dressing to minimize
influx of air (e.g., petroleum gauze) and secure with dry gauze and tape.
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 respiratory distress. Do not apply pressure over the insertion
site. Prevent kinks in the tubing. The presence of a CT should not, in and
of itself, limit activity. Position changes and mobility can facilitate drain-
age. Ask the nurse or the physician whether the CT may be temporarily
disconnected from suction during mobility activities. If the suction must
remain connected, additional lengths of tubing may be added, or a por-
table suction device may be used. Serial chest x-rays are often performed
to determine chest tube placement and effectiveness, and to assist the
medical-surgical team in determining the CT weaning process.
The position of the patient and the collection bag are determined by the
physician and the rationale for the LDD intervention. Changes in the pa-
tient’s position, the level of the collection bag, or the intrathecal pressure
can all affect the amount and rate of drainage. Maintain head, neck, and
back in neutral to minimize impedance of flow. CSF is drained to a specif-
ic level within the drainage bag, a specific volume per hour, or a specific
pressure. 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,
sneezing, straining, or the Valsalva maneuver. Complications of LDD by
relative presence or overdrainage/underdrainage include infection, lower
extremity nerve root irritation, tension pneumocranium, central hernia-
tion of the brain, compression of the brainstem, and subdural hematoma.
Monitor the patient for any changes in neurologic status. Notify nursing
immediately if any changes are noted.
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 the
mouth and taped to the forehead or cheek. The tube can be dislodged
easily; always check that the tape is secure and notify nursing if the tube
becomes dislodged. The tube may also be affixed with a safety-pin to
the patient’s hospital gown for reinforcement. The patient may be on
aspiration precautions and is typically positioned with the head of the bed
(HOB) elevated a minimum of ≥ 25–30 degrees during feedings. Place
feedings on hold when the HOB is flat for an extended period in order to
minimize the risk of regurgitation or aspiration. This small-diameter tube
can clog easily; irrigating with 20–30 mL of water assists in maintaining
patency. Facility protocol may include flushing every 3–4 hours when on
continuous feeds, before and after intermittent feeds, and with medica-
tions. Be aware of facility policy on flushing the tubing after use of the
hold feature on the tube feeding pump.
Continued
406 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

TABLE 18.7  Medical-Surgical Management Devicesa—cont’d

Device Purpose Clinical Implications
Nasogastric tube (NGT) Keeps the stomach empty after See Nasoenteric feeding tube section for positioning tips. Review the orders
surgery and rests the bowel by limit- to determine whether the patient’s NGT may be temporarily disconnect-
ing the passage of gastric contents. ed from suction. Ask the nurse to disconnect or “clamp” the NGT from
Also used for gastric decompression suction in order to mobilize the patient. If/when disconnected, monitor
(to relieve pressure and prevent the patient for nausea or abdominal distention. When disconnected from
vomiting), for gastric lavage, and to suction, the open end should be capped and monitored to prevent leak-
provide access to gastric specimens ing. Tubing should be secured when not connected to suction to avoid
for laboratory analysis accidental dislodging. This is commonly done by placing the loose end in
Some NGTs allow access to the the pocket of the hospital gown or draping around the neck.
stomach for medications or tube
feedings (See Nasoenteric Feeding
Tube section.)
Nebulizer Delivers aerosolized water or medica- Some patients may experience increased airway resistance and bronchospasm
tions to the respiratory tract, lungs, with high-density or cold air aerosols. Patients may be better prepared for
throat, or nose mobility activities or airway clearance after nebulizer treatments.
Percutaneous endoscopic Provides long-term access for nourish- Place tube feedings on hold when the HOB is flat to minimize the risk of
gastrostomy/ jejunos- ment to patients who are unable to regurgitation/aspiration. PEJ tube is considered postpyloric; therefore the
tomy tube (PEG/PEJ tolerate food by mouth or have a na- risk of aspiration from regurgitation is minimized. This small-diameter
tube) soenteral obstruction, or for a patient tube can clog easily; be aware of facility protocol for flushing the tubing
with confusion/ agitation at risk for to prevent occlusion (see Nasoenteric feeding).
nasoenteral tube dislodgement
May be used to supplement nutrition
taken by mouth
Peripheral IV line Provides temporary access for delivery Avoid using blood pressure cuff on the involved extremity, if possible. Watch
of medications, fluids, electrolytes, IV tubing for kinks or occlusions. Position the patient to avoid occluding
nutrients, or blood product transfu- flow. If inserted over a joint or in the dominant hand, a splint may be used
sions to minimize risk of occlusion or dislodging. Observe the patient for signs
Cannot be used to draw blood of infiltrated IV or phlebitis: localized pain, edema, erythema, or tender-
ness. Notify the nurse if signs of infiltration or phlebitis are present, if the
IV dressing is not intact or appears infiltrated, or if the IV has become
dislodged. If the IV is accidentally removed, 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.
Peripherally inserted Provides IV access for administration A single- or multilumen catheter placed via the basilic, cephalic, or brachial
central catheter (PICC of total parenteral nutrition (TPN), vein, terminating in the superior vena cava. Exterior tubing is taped to the
line) medications, fluid, blood products, or arm and covered with a transparent dressing. Site usually needs to be covered
chemotherapy. Generally placed for for protection during showering. Bathing or swimming is prohibited. Axil-
midterm access (weeks to months) lary crutch use may be contraindicated to avoid excess pressure on the veins.
Rectal pouch/tube Catheter inserted into rectum temporar- Very easily dislodged, particularly with increased sheer during bed mobility
ily collects and contains bowel drain- or scooting. Consider using a draw sheet when moving the patient in
age (typically large amounts of liquid bed if there is concern of pulling out the tubing. Keep the collection bag
stool) into external collection bag below the level of insertion. Upright sitting may be limited because of
Protects fragile skin from contact with discomfort resulting from the catheter exiting the rectum.
feces
Also used for infection-control
purposes (e.g., Clostridium difficile
infection diagnosis)
Sequential compression Provides intermittent pressure to the Usually worn when the patient is in bed, but can be worn when sitting in a
device (SCD) (pneu- lower extremities via gradual and chair. Should be removed during ambulation as tubing can be a tripping
matic compression sequential inflation and deflation of hazard; reapply when patient returns to bed. Best fit occurs when sleeves
boots) the air-filled sleeves are applied without air in them. Consult with the medical team to discon-
Promotes venous return and prevents tinue use when the patient is ambulating on a regular basis. Contraindi-
deep vein thrombosis (DVT) and cated in an extremity in which there is a known DVT because of concerns
venous thromboembolism (VTE) of thromboembolus, although no empirical evidence supports this theory.
secondary to prolonged or postopera- Not used directly over the lower extremity with a fracture, open wound,
tive bed rest or inactivity or compartment syndrome.
Suprapubic catheter Surgically placed catheter to drain the Keep the collection bag below the level of the bladder. The collection
bladder temporarily or permanently tubing and/or leg bag may be secured to the patient’s thigh. Avoid pres-
after some bladder or gynecologic sure over the insertion site. May be removed after a successful voiding
surgeries in cases of urinary retention trial with the tube clamped. Often more comfortable and allows greater
(possibly caused by an obstruction, mobility than a urethral catheter. The collection bag should be emptied
tumor, stricture, periurethral ab- frequently to avoid leaking. Be sure to ask nursing for assistance in the
scess) or a severe voiding dysfunction event that exact output measurements are needed.

TABLE 18.7  Medical-Surgical Management Devicesa—cont’d
Device
Surgical drain (e.g. Pen-
rose, Jackson-Pratt,
Hemovac)
Texas catheter (condom
catheter)
Vascular access port
(VAP) (Port-A-Cath,
MediPort, Pass-port,
Infuse-A-Port, Bard-
Port)
Tunneled central venous
catheter (Hickman,
Broviac, Quinton, and
Groshong catheters)
Urinary catheter (Foley
catheter)
Ventriculoperitoneal
shunt (VP); ventricu-
loatrial shunt (VA)
Yankauer suction
AV, Arteriovenous; CSF, cerebrospinal fluid; CVP, central venous pressure; TPN, total parenteral nutrition.
aListed in alphabetical order.
Data from References 39-60.
Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18 407
Purpose Clinical Implications
Removes excess air, blood, or fluid (se- Many options available. Some drain by gravity; others through self-
rum, lymph, bile, pus, or intestinal contained or external negative pressure. Be aware of the location of the
secretions) from a surgical site that drain when mobilizing the patient. The drain or tubing may be taped to
would otherwise collect internally; the patient’s skin or pinned to the hospital gown or clothing to prevent
to control ecchymosis; and to pre- tugging. Ask the nurse to temporarily disconnect a drain from suction,
vent deep wound infection if necessary/appropriate. Before mobilization, visually inspect the drain
for output. If the drain is close to full, ask the nurse to empty it to ensure
proper function and allow for exact measurements to be recorded. Position
changes can cause increased output. Monitor for leakage during a physical
therapy session, and report this to the nurse.
Noninvasively collects urine via a Very easily dislodged; may be held in place with a Velcro strap. The drainage
sheath placed over the penis bag should always be below the level of the bladder to prevent backflow
Does not provide assistance with in the tubing. Secure the collection bag or catheter tubing to patient’s
drainage of urine from the bladder 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 and should be emptied frequently to avoid
leaking and to increase the ease of mobilization. Be sure to ask nursing for
assistance in the event that exact output measurements are needed. Be alert
for possible penile irritation if attached too tightly.
Used for long-term (months to years) Surgically implanted subcutaneously. Once healed and cleared by physician,
chemotherapy, hemodialysis, TPN, physical activity is not limited. Patients can usually swim, bathe, and
or other intermittent infusion exercise without limitation. Appears as a slight protrusion under the skin.
therapy
Used for long-term (months to years) Surgically implanted in the chest, neck, or groin with external access
continuous or intermittent chemo- lumens. The external tailed portion should be taped down to prevent
therapy, acute hemodialysis, TPN, or dislodging. Do not perform manual techniques directly over the tail.
other infusion therapy needs Patients are allowed to shower once the insertion site is healed; however,
tub bathing and swimming are usually limited.
Catheter inserted through the urethra Be aware of the position of the catheter. The collection bag should always
in both men and women in order to be below the level of the bladder to allow drainage by gravity. Secure the
temporarily (<3 weeks) drain and collection bag or tubing to the patient’s leg, clothing, or assistive device
collect urine from the bladder to prevent the patient from tripping or becoming tangled in the tubing
Used for urinary incontinence and during mobility activities. The collection bag should be kept off the floor
retention, to assist with postoperative and should be emptied frequently to avoid leaking and make mobilization
bladder drainage, when accurate mea- easier. Be sure to ask nursing for assistance in the event that exact output
surement of urine output is necessary, measurements are needed.
or to prevent contamination in pa-
tients with a stage 2, 3, or 4 pressure
injury on the buttocks/perineum
Drains excess CSF from the ventricles The patient may be on bed rest for a specified period of time after place-
into the abdominal cavity/perito- ment. The shunt can often be palpated under the skin; avoid excess
neum (VP) or right atrium of the pressure over this area. Monitor for signs of increased intracranial pressure
heart (VA) (ICP).
Clears secretions from the oral cavity Some patients use this independently; if so, place within the patient’s reach.
or the oropharynx To keep the Yankauer as clean as possible, it is often stored in the original
packaging and rinsed with saline. 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. Gentle Yankauer 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 the
Yankauer, do not attempt to pull on the device. Wait for the patient to
relax, and then gently slide the Yankauer from the patient’s mouth.
408 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

Water seal 11. Lough ME. Cardiovascular diagnostic procedures. In: Urden LD,
chamber Stacy KM, Lough ME, eds. Critical Care Nursing: Diagnosis and
To suction From patient
Management. 8th ed. St. Louis: Elsevier; 2018:199–289.
12. Mariano GSL, Fink ME, Hoffman C, Rosengart A. Intracranial
pressure: monitoring and management. In: Principles of Criti-
cal Care. 4th ed. New York: McGraw Hill; 2014. http://access
medicine.mhmedical.com/content.aspx?bookid=1340&section
B 200
2000 1090 D Collection id=72041588. Accessed July 25, 2018.
180
Suction A chamber 13. Stevens RD, Shoykhet M, Cadena R. Emergency Neurological
1000
control 1900 160

chamber 140 Life Support: intracranial hypertension and herniation. Neurocrit

900
1800 120
1700
800
100
90
700
80
1600
70
600
1500
60
50
500
40
Air leak C 1400
400 30
monitor 1300
20
300
1200
10
FIG. 18.5
Tubing attachment to three-chamber collection unit. (From Phillips N.
Berry and Kohn’s Operating Room Technique. 12th ed. St. Louis: Mosby; 2013.)
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APPENDIX 18A:  MECHANICAL VENTILATION
Sean M. Collins
Jaime C. Paz
Objectives of Mechanical Ventilation
Mechanical ventilatory support provides positive pressure to
inflate the lungs. Patients with acute illness, serious trauma,
exacerbation of chronic illness, or progression of chronic illness
may require mechanical ventilation.1
409
46. Houston A. Enteral feeding: indications, complications, and
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60. Altobelli H. Airway management. In: Kacmarek RM, Stoller JK,
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St. Louis: Elsevier; 2017:740.
Physiologic Objectives of Mechanical Ventilation2-4
• Support or manipulate pulmonary gas exchange
• Increase lung volume
• Reduce or manipulate the work of breathing 
Clinical Objectives of Mechanical Ventilation2,3,5,6
• Reverse hypoxemia and acute respiratory acidosis
• Relieve respiratory distress
• Reverse ventilatory muscle fatigue
• Permit sedation, neuromuscular blockade, or both
410 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

Noninvasive Mechanical Ventilation

Noninvasive mechanical ventilation (NIV) primarily includes
continuous positive airway pressure (CPAP) and bi-level posi-
tive airway pressure (BiPAP). NIV consists of an interface to
Depth connect the patient to the ventilator tubing from the machine.
Standard 15 mm markings
connector Six types of interfaces are available: full-face (or oronasal) mask,
total facemask, mouthpieces, nasal mask, nasal pillows or plugs,
and a helmet.10 Indications for NIV include patients with sleep
apnea, exacerbations of or hypercarbic chronic obstructive pul-
monary disease (COPD), or cardiogenic pulmonary edema when
the airway cannot be protected.10
Pilot balloon CPAP provides continuous positive pressure (above atmo-
and valve
spheric pressure) throughout the entire respiratory cycle. It
is intended to decrease the work of spontaneous breathing by
reducing the airway pressure necessary to generate inspiration.
BiPAP includes two levels of positive pressure support, trig-
gered during spontaneous breathing. BiPAP provides a higher
pressure during inspiration to augment inspiratory airflow,
and a lower pressure during exhalation to help maintain air-
way patency and prevent collapse. The use of NIV is increasing
because it is being used for the treatment of sleep apnea, to pre-
Murphy vent the need for invasive ventilation, and during the weaning
eye
process to avoid the need to return to invasive ventilation.10,11 
Tracheal
Invasive Mechanical Ventilation
cuff
Invasive mechanical ventilation is the use of an artificial airway
FIG. 18A.1 to provide ventilatory support and is described further in the
A typical endotracheal tube. (From Durbin CG. Airway management. In: following sections.
Cairo JM, Pilbeam SP, eds. Mosby’s Respiratory Care Equipment. 7th ed. St. Process of Invasive Mechanical Ventilation
Louis: Mosby; 2004.) Intubation. Intubation is the passage of an artificial air-
way (tube) into the patient’s trachea (Fig. 18A.1), most often
through the mouth (endotracheal tube intubation), but occa-
• D ecrease systemic or myocardial oxygen consumption and sionally through the nose (nasotracheal intubation), or by
intracranial pressure surgical incision through the neck directly into the trachea
• Stabilize the chest wall (tracheostomy). The process of removing the artificial airway is
• Provide access to tracheal-bronchial tree for pulmonary hy- called extubation.
giene Intubation is considered for the following reasons6,7:
• Provide access for delivery of anesthetic, analgesic, or seda- • The presence of upper airway obstruction
tive medication  • Inability to protect the lower airways from aspiration
• Inability to clear pulmonary secretions
Indications for Mechanical Ventilation2,6-9: • Hypoxemia despite supplemental oxygen
• Apnea (including sleep apnea) • Respiratory acidosis
• Acute hypercapnia that is not quickly reversible with stan- • Progressive general fatigue including mental status deterio-
dard treatment ration
• Partial pressure of arterial oxygen of less than 50 mmHg • The need for positive pressure ventilation
with supplemental oxygen When patients require ventilatory support for a prolonged
• Respiratory rate of more than 30 breaths per minute period, defined as more than 21 days by the Centers for Medi-
• Vital capacity less than 10 liters per minute care and Medicaid,12 a tracheostomy is considered. A trache-
• Negative inspiratory force of less than 25 cm H2O ostomy tube is an artificial airway inserted directly into the
• Protection of airway from aspiration of gastric contents anterior trachea below the vocal cords, generally performed in
• Reversal of respiratory muscle fatigue  the operating room but may be done emergently at the bedside,
if needed. Benefits of tracheostomy include6:
Types of Mechanical Ventilatory Support • Reduced laryngeal injury
There are two primary methods to deliver mechanical ven- • Improved oral comfort
tilatory support: noninvasive and invasive. The use of either • Decreased airflow resistance
method is dependent on several variables, which are described • Increased effectiveness of airway care
next.10,11 • Feasibility of oral feeding and vocalization
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18
Depending on the patient’s medical condition, other consid-
erations for tracheostomy may include intubation greater than
1 week1 or transfer out of the intensive care unit (ICU) with the
need for ongoing mechanical ventilation.13 However, a patient
may also be intubated for many weeks without tracheostomy,
based on the clinical situation.
If the patient with a tracheostomy is able be weaned from
ventilatory support but still requires an artificial airway, then
humidified oxygen can be delivered through a tracheostomy
mask (see Table 18.1).  the preset pressure limit was reached. Dual-targeted ventila-
Cuff. Approximately 0.5 inches proximal from the inserted
end of an endotracheal or tracheal tube is a cuff (balloon). The
cuff is inflated with air to (1) ensure that all of the supplemental
oxygen delivered by the ventilator via the artificial airway enters
the lungs and (2) help maintain placement of the artificial air-
way.6 Cuff inflation pressure should be adequate to ensure that
no air is leaking around the tube; however, cuff pressures, typi-
cally measured by respiratory therapists, should not exceed 20
to 30 mmHg. High cuff pressures have been linked to tracheal
damage and scarring, which can cause tracheal stenosis.14
 CLINICAL TIP
A cuff leak should be suspected if the patient is able to phonate
or audible sounds come from the mouth. Leaks can occur if the
endotracheal or tracheal tube is shifted (positional leak) or if
the pressure decreases in the cuff. If a cuff leak is suspected,
then the respiratory therapist or the 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.
 
Mechanical Ventilators. Mechanical ventilators provide
positive pressure ventilation and are classified based on the
method used to stop the inspiratory phase and allow expiration
to occur, referred to as the cycling method.6
There are three primary cycling methods8,15:
1. Pressure-cycled
2. Volume-cycled
3. Time-cycled9
Ventilators can also be classified by control mode16:
1. Pressure-controlled
2. Volume-controlled
3. Dual-targeted
For our purposes, these two classification approaches are
interchangeable. Pressure-cycled (or controlled) ventilators stop
inspiration at a preset pressure, volume-cycled (or controlled)
ventilators stop inspiration at a preset volume, and time-cycled
ventilators stop inspiration at a preset time interval. Dual-
targeted ventilators combine features from both pressure and
volume control systems.17 These methods allow for increased
control of certain variables during inspiration. However, hold-
ing only one variable constant for the termination of positive
pressure inhalation allows other factors, such as position changes
or manual airway clearance techniques, to affect inspiration and
potentially cause barotrauma (lung tissue damage caused by
excessive airway pressure)12 or reduced inspiratory volumes.
411
For example, with a volume-cycled ventilator, a preset vol-
ume will be delivered regardless of the patient’s position, and
reductions in chest wall expansion caused by a patient’s position
(e.g., side lying) may increase the pressure placed on the depen-
dent 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. However,
because the patient’s position may hinder chest expansion, a
resultant lower volume of inspired air may be delivered because
tors provide more than one cycling option, and certain modes
of ventilation allow for more than one parameter to determine
the inspiratory phase.
Wide-bore plastic tubing is used to create the mechanical
ventilator’s circuit. The terminal end of this circuit directly con-
nects to an endotracheal, nasotracheal, or tracheal tube.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.6
 CLINICAL TIP
Knowledge of the cycling (control) method used allows the
physical therapist to monitor for any changes in pressure and
tidal volumes (VT) that may occur during interventions.
Modes of Ventilation. Ventilation mode options range from
provision of total support (no work performed by the patient)
to minimal support (near-total work performed by the patient).
The mode of ventilation selected ideally allows the patient to do
as much of the work of breathing as is physiologically possible
while meeting the intended objectives of ventilatory support.
Even short periods (12 days) of complete dependence on posi-
tive pressure ventilation can lead to respiratory muscle atrophy
and concomitant reductions in diaphragm strength and endur-
ance.18 Many modes of mechanical ventilation exist and are
beyond the scope of this text. Characteristics of commonly used
conventional and additional modes of ventilation are presented
in Tables 18A.1 and 18A.2, respectively. 
Ventilatory Settings. Ventilatory settings are parameters
established to provide the necessary support to meet the patient’s
individual ventilatory and oxygenation needs.9,19 Establishment
of the ventilatory settings requires consideration of the patient’s
(1) arterial blood gas levels, (2) vital signs, (3) airway pressures,
(4) lung volumes, and (5) pathophysiologic condition, includ-
ing the patient’s ability to breathe spontaneously.9,19 Ventilator
settings, subdivided into those that influence oxygenation and
those that influence ventilation, are presented in Table 18A.3. 
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 capacity
(resting volume) before the onset of the next inspiration.6 The
process leading to auto-PEEP is referred to as dynamic hyperinfla-
tion.2,6,9 The primary consequence of dynamic hyperinflation is
412 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

TABLE 18A.1  Conventional Modes of Ventilation

Modes
Control ventilation (CV)
Also referred to as Continuous
mandatory ventilation (CMV)
Assist control (AC)
Also referred to as assist con-
trolled ventilation (ACV)
Synchronized intermittent man-
datory ventilation (SIMV)
Pressure-supported ventilation
(PSV)
Characteristics
Total control of the patient’s ventilation: preset rate, FiO2, VT, flow rate, I : E ratio.
Either volume or pressure cycled.
Patients may be sedated or pharmacologically paralyzed.
No active respiratory muscle activity is necessary.
Patient-initiated breaths and respiratory rate create negative airway pressure in the circuit and are
augmented with either a preset volume or pressure and flow rate.
Respiratory muscles are still active.
Patient can trigger RRs that are too high, leading to respiratory alkalosis or auto PEEP (refer to
Complications of Mechanical Ventilation section).
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.
Like AC, this mode will assist the patient-initiated breath. Mandatory breaths are only delivered when the
patient is not initiating a sufficient number of breaths to achieve a preset minute ventilation.
Patient-initiated breaths are augmented with a preset flow of pressure.
Patient controls RR, inspiratory time, and flow; patient and ventilator determine VT and minute ventilation.

FiO2, Fraction of inspired oxygen; I:E ratio, inspiratory time to expiratory time ratio; PEEP, positive end-expiratory pressure; RR, respiratory rate; VT, tidal volume.
Data from: Chandrashekar R, Perme C. Monitoring and life support equipment. In: Hillegass EA, ed. Essentials of Cardiopulmonary Physical Therapy. 4th ed. St. Louis:
Saunders; 2016; Chatburn RL. Recognising, describing and comparing modes of mechanical ventilation. Ind J Resp Care. 2014;3(2):469-78. Pham T, Brochard LJ,
Slutsky AS. Mechanical ventilation: state of the art. Mayo Clin Proc. 2017;92(9):1382-1400.

TABLE 18A.2  Additional Modes of Ventilation

Mode
Pressure control ventilation
(PCV)
High-frequency oscillation
ventilation (HFOV)
Proportional assist ventila-
tion (PAV)
High-frequency jet ventila-
tion (HFJV)
Airway pressure release venti- A variation of CPAP, APRV consists of two levels of positive pressure during both inhalation and exhalation.
lation (APRV)
Neurally adjusted ventilatory
assist (NAVA)
Characteristics
Delivers a preset airway pressure for a predetermined inspiratory time interval.
Patients may be 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 underlying acute lung
injury (e.g., ARDS); now also available in AC or SIMV modes.
A technique of ventilation that is administered with frequencies of 180–400 breaths per minute and conse-
quently small tidal volumes of 1–4 mL/kg.
Decreases peak airway pressure, promotes alveolar recruitment, and prevents lung injury.
All breaths are initiated and terminated by the patient. Pressure assistance by the ventilator is calculated in
real-time and proportional to automated measurements of respiratory system compliance and resistance.
Offers increased patient autonomy with respiration over other ventilator modes.
Uses a nozzle and injector to deliver jets of gas directly into the lungs at high rates.
Indicated for the neonatal population with pulmonary hypoplasia, restrictive lung disease, and persistent pul-
monary hypertension. Typically used in tandem with a conventional ventilator.
The release consists of a very short pause between inhalation and exhalation.
Helps lower airway pressure in situations of low lung compliance, such as ARDS.
Synchronizes ventilator support based on diaphragmatic contractions.
Requires placement of an enteral catheter to sense electrical activity of diaphragm. Varies the level of support
based on amplitude of signals.
Reduces patient and ventilator dyssynchrony.

AC, Assist/control ventilation; ARDS, adult respiratory distress syndrome; CPAP, continuous positive airway pressure; SIMV, synchronized intermittent mandatory
ventilation; VT, tidal volume.
Data from: DeTurk WE, Cahalin LP. Cardiovascular & Pulmonary Physical Therapy: An Evidence-Based Approach. 2nd ed. New York: McGraw-Hill; 2011; Chandrashekar
R, Perme C. Monitoring and life support equipment. In: Hillegass EA, ed. Essentials of Cardiopulmonary Physical Therapy. 4th ed. St. Louis: Elsevier; 2016; Pham T,
Brochard LJ, Slutsky AS. Mechanical ventilation: state of the art. Mayo Clin Proc. 2017;92(9):1382-1400; Goldworthy S, Graham L. Compact Clinical Guide to Mechanical
Ventilation: Foundations of Practice for Critical Care Nurses. New York: Springer Publishing Co.; 2014.

increased air trapping, which results in physiologic dead space
caused by pulmonary shunting (perfusion is delivered to alveolar
units that are not receiving fresh ventilation), which decreases
gas exchange.6 Ultimately, air trapping leads to an increased
work of breathing as a result of higher respiratory demand, as
well as altered length–tension relationships of the inspiratory
muscles resulting from the hyperinflation.8 Auto-PEEP and
concomitant air trapping can occur when the expiratory time, in
a given ventilatory mode, is not long enough to allow the lung
volumes to return to resting position.8 This is of particular con-
cern in patients with COPD6 who are on ventilator modes that
allow them to initiate ventilator-assisted breaths (e.g., assisted
ventilation, assist control ventilation, synchronized intermit-
tent mandatory ventilation [SIMV], and pressure-supported
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18 413

TABLE 18A.3  Ventilator Settings

Purpose Setting Characteristic
Oxygenation Fraction of inspired oxygen The percentage of inspired air that is oxygen. At normal respiratory rate (RR), tidal vol-
(FiO2) ume (VT), and flow rates, an FiO2 of 21% (ambient air) yields a normal oxygen partial
pressure of 95–100 mmHg. 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-expiratory The pressure maintained by the mechanical ventilator in the airways at the end of expira-
pressure (PEEP) tion. Normal physiologic PEEP, 5 cm H2O, is maintained by sufficient surfactant levels
in the alveoli.
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 based on the number of spontaneous ventilatory efforts initiated by the patient. Differ-
ent ventilatory modes, described in Tables 18A.1 and 18A.2, are prescribed according to
the patient’s needs.
Patients who are unable to generate any spontaneous breaths are fully ventilated at respi-
ratory 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, therefore pressures are routinely
monitored to prevent barotrauma.
At times, hypercapnia is induced in order to prevent high lung pressures due to the deliv-
ered volume and noncompliance of lung tissue. This is termed permissive hypercapnia.
Inspiratory flow rate Set to match the patient’s peak inspiratory demands. If this match is not correct, 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 which ultimately prevents hyperinflation. This can lead 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-expiratory Set with the goal of allowing the ventilator to be as synchronous as possible with the
(I : E) ratio patient initiated respiratory ratio.
For patients who are not spontaneously breathing, this ratio is set to maintain adequate
ventilation and oxygenation.
Sensitivity Pressure change is required in the airway to trigger an AC or PSV breath; typically −1 to
−3 cm H2O.
If mechanical sensors respond poorly, then respiratory muscle fatigue can occur. If the sen-
sors 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. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2006; Slutsky AS. Mechanical ventilation. American College of Chest Physi-
cians’ Consensus Conference. Chest. 1993;104:1833; Howman SF. Mechanical ventilation: a review and update for clinicians. Hosp Physician. 1999;December:26-36.
Goldworthy S, Graham L. Compact Clinical Guide to Mechanical Ventilation: Foundations of Practice for Critical Care Nurses. New York: Springer Publishing Co.; 2014.

ventilation [PSV]). The therapist should realize that activ-
ity may increase the patient-generated respiratory rate. Some
modes (e.g., assisted ventilation, assist control ventilation, and
SIMV) will then, given the initiation of a breath, provide a set
volume of air that could increase the likelihood of hyperinflation
owing to auto-PEEP. This can also occur in modes that do not
deliver a set volume of air (PSV) because inspiration is assisted
with positive pressure.17  trauma are bypassed, and lung pressures may become exces-
Barotrauma
Barotrauma refers to damage (injury or rupture) of the alveoli
caused by excessive airway pressure.12 Many additional modes
of ventilation are aimed at reducing this complication (see
Table 18A.2). In the normal lung, spontaneous inhalation
without ventilatory support takes place as a result 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 pressure,
these normal physiologic mechanisms for preventing such
sive. Another consideration is that many of the lung condi-
tions requiring mechanical ventilation do not uniformly affect
the lungs (e.g., adult respiratory distress syndrome, pneumo-
nia). In these situations, inhalation volumes are delivered to
those areas that are still normal, which can overdistend and
414 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting
increase pressure as a result. This can produce stress fractures
in the walls of the alveoli, thus exacerbating the acute lung
condition.20,21 For example, infants who are mechanically ven-
tilated are five times more likely to develop the complication
of bronchopulmonary dysplasia than infants who are not.22
Excessive positive pressure may also exacerbate the acute lung
injury associated with adult respiratory distress syndrome,1
referred to as ventilator-induced lung injury (VILI)8 Other com-
plications associated with barotrauma include pneumothorax
and subcutaneous emphysema.5  and is a powerful predictor of an unsuccessful wean.
Additional Complications of Mechanical Ventilation
• Improper intubation technique can result in esophageal or
tracheal tears.2,9,19
• Oxygen toxicity may result from oxygen levels that are too
high (elevated inhaled oxygen partial pressure beyond neces-
sary requirements)8 and maintained for a prolonged period
of time (hours to days).12 An inverse relationship exists be-
tween inhaled oxygen partial pressure and time. Oxygen tox-
icity can result in the following2,9,19:
• Substernal chest pain that is exacerbated by deep breath-
ing
• Dry cough
• Tracheal irritation
• Pleuritic pain with inspiration
• Dyspnea
• Nasal stiffness and congestion
• Sore throat
• Eye and ear discomfort
• Decreased cardiac output may result from high positive
pressures that can compress the great vessels by overinflated
lungs.
• Ventilator-associated pneumonia (VAP) is a health care–associ-
ated infection that occurs in patients who are mechanically ven-
tilated longer than 48 hours. VAP results in both an increased
length of stay and patient mortality (by 27% to 43%). Risk
factors include immunosuppression, underlying lung condi-
tions, body position, level of consciousness, endotracheal tub-
ing, ventilator circuit setup, and lack of compliance to standard
precautions by hospital personnel. Prevention of VAP includes
oral hygiene before intubation, avoiding saline lavage during
suctioning, changing positions frequently, and preventing as-
piration by keeping the head of the bed (HOB) at or above 30
degrees.12,23  NIV.24 This recommendation is made specifically for patients
Weaning From Mechanical Ventilation
The process of decreasing or discontinuing mechanical ven-
tilation is referred to as the weaning process or liberation.17,19 A
contributing factor to successfully weaning from ventilatory
support is the resolution or stability of the condition that led to
the need for mechanical ventilation.24
Criteria for an attempt at weaning from mechanical ventila-
tion are as follows12,25-27:
• Spontaneous breathing with a tidal volume of 5 L/kg.
• Adequate gas exchange with a fraction of inspired oxygen (FiO2)
less than 50% and PEEP less than 5 cm H2O with oxygen satu-
ration, as measured by pulse oximetry, greater than 90%.
• I nspiratory pressures greater than −20 to −30 cm H2O. Pres-
sures greater than −30 cm H2O have been associated with
successful extubation. An inability to maintain spontaneous
breathing is associated with an inspiratory pressure of ap-
proximately −15 cm H2O.
• Respiratory rate less than 35 breaths per minute.
• Minute ventilation of 5 to 10 L/min.
• Respiratory rate/VT ratio less than 105. A respiratory rate/VT
ratio greater than 105 indicates shallow and rapid breathing
A spontaneous breathing trial (SBT) is typically performed
to evaluate a patient’s readiness to begin the weaning process.8
The trial consists of the patient breathing spontaneously for 15
to 30 minutes while being closely monitored.15
Examples of weaning methods are as follows6,12,27:
• Intermittent mandatory ventilation (IMV) or synchronized
intermittent mandatory ventilation (SIMV)—decreasing the
number of machine breaths per minute from the ventila-
tor 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 ventilator support for an extended period of time
and do not usually have an underlying lung condition that
required intubation 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—an adaptor is connected to the ventilator tubing
which allows for progressively longer trials of spontaneous
breathing while still intubated. Patients must have the respira-
tory drive to breathe spontaneously and the capability to gener-
ate adequate VT to attempt this weaning method. The process
aims to improve respiratory muscle strength and endurance
with prolonged time periods of independent ventilation.
• PSV—the patient spends specific periods of time with de-
creased pressure support to increase effective spontaneous
ventilation. Two factors can be manipulated with PSV: (1) re-
duce the PSV to increase strength of the respiratory muscles,
and (2) increase the length of time that PSV is reduced to in-
crease the endurance requirement on the respiratory muscles.
Current guidelines recommend an initial SBT is attempted
with inspiratory pressure augmentation (PSV methods) rather
than without (T-piece.).24 It is also recommended that some
patients may benefit from extubation followed by preventive
who have been mechanically ventilated for more than 24 hours,
are considered a high risk for difficulty to wean from the venti-
lator, and who have passed an SBT. However, it continues to be
a challenge to identify patients at high risk for difficulty wean-
ing.15 Furthermore, the influence of sedation during the early
period of mechanical ventilation may also limit the liberation
process, enough to warrant guidelines specifically recommend-
ing protocols that attempt to minimize sedation.24
In addition, proportional-assist ventilation (PAV) is a
mode that has been developed to enhance the patient’s ability
to wean off the ventilator. With PAV, the resistive load of the
artificial airways and associated ventilator tubing is lessened,
thus decreasing the patient’s work of breathing and possibly
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18
increasing tolerance of the weaning process.25 Refer to Table
18A.2 for more information on PAV.
Five major factors to consider during the weaning process
are15,19,24:
1. Respiratory demand (the need for oxygen for metabolic pro-
cesses and the need to remove carbon dioxide produced dur-
ing 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 the weaning process
are9,12,19,27:
• Change in level of consciousness
• Increased tachypnea (more than 30 breaths per minute)
• Decrease in PaO2 or increase in PaCO2 of 5 mmHg, in pa-
tients with a pH less than 7.30
• Paradoxical breathing pattern (discoordination in move-
ments of the abdomen and thorax during inhalation; see
Chapter 4)
• Oxygen saturation, as measured by pulse oximetry, less than
90%
• Change in heart rate or blood pressure greater than 20%
from baseline
• Agitation, panic, diaphoresis, cyanosis, angina, or arrhyth-
mias  performed without glottis closure, which cannot be achieved
Physical Therapy Considerations
A patient who is mechanically ventilated may require ventila-
tory support for a prolonged period of time. This population
is at risk for developing pulmonary complications, skin break-
down, joint contractures, and deconditioning from bed rest.
Physical therapy intervention can help prevent, minimize, or
reverse these complications despite ongoing mechanical ventila-
tion and assist with the weaning process.
Assistance With Weaning and Functional Mobility
The physical therapist can play a vital role on the interdisciplin-
ary team involved in the weaning process. Physical therapists
offer a combined understanding of the respiratory difficulties
faced by the patient, the biomechanics of ventilation, the prin-
ciples of exercise (weaning is a form of exercise), and the general
energy requirements of functional activities. Physical therapists
should work with the multidisciplinary team to optimize the
conditions under which the patient attempts each weaning trial
(e.g., time of day, activities before and after attempted weaning,
position during the trial period) and parameters to be manipu-
lated (frequency, intensity, duration). Patients should be placed
in a position that facilitates the biomechanics of their ventila-
tion.28 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.29 The literature supports the use of inspira-
tory muscle-resistive training to increase respiratory muscle
strength and endurance, which facilitates weaning success,
415
particularly in patients who have previously demonstrated fail-
ure to wean.18
Evidence indicates that patients who are mechanically venti-
lated for more than 4 days can safely participate in some activi-
ties, such as sitting at the edge of the bed, sitting in a chair,
and ambulation.30 These patients were determined to be physi-
ologically ready for activity if they were responsive to verbal
stimulation, if FiO2 was 0.6 or less, if PEEP was 10 cm H2O
or less, if there was an absence of orthostatic hypotension, and
if catecholamine drips were not in use.30 Furthermore, recent
reviews provide evidence that early mobilization of critically ill
patients provided by a multidisciplinary team, including physi-
cal therapy, reduces ventilatory-dependent days, shortens the
ICU and hospital length of stay, improves functional outcomes,
and is safe and effective.31,32 Despite these findings, barriers still
exist, and optimization of outcomes requires additional studies
on the timing and intensity of functional activity.32 
Airway Clearance
Patients on ventilatory support are frequently suctioned as
part of their routine care. Physical therapists working with
patients on airway clearance should use suctioning as the last
attempt to remove secretions. Encouraging the process of huff-
ing and coughing during treatment will maintain, and pos-
sibly improve, cough effectiveness as a result of activation of
the expiratory muscles. It is important to note that huffing is
while intubated. This technique would only be feasible in
patients on NIV. If patients have difficulty with a deep inspi-
ration for an effective huff or cough, then manual techniques,
postural changes, or assistive devices, such as an adult manual
breathing unit (AMBU bag), can be used to facilitate depth of
inspiration. 
Noninvasive Mechanical Ventilation and Exercise
A limitation to prolonged exercise in patients with COPD is
the development of dynamic hyperinflation. Increased end-expi-
ratory volume, resulting from expiratory flow limitations, and
increased respiratory rate both contribute to dynamic hyperin-
flation. To help offset this concern, interest has developed in
the use of NIV during exercise training to improve respiratory
capacity. However, current evidence is inconclusive on the use
of NIV during exercise. NIV has been shown to improve the
6-minute walk test (6MWT) and/or endurance test results when
coupled with exercise, compared with exercise without NIV, in
both controlled and uncontrolled studies.33,34 Despite these
findings, a literature review of available systematic reviews and
meta-analyses was not able to recommend the addition of NIV
during exercise therapy because of lack of supporting evidence.35
This is certainly an area worthy of additional investigation.34
References
1. Marino PL. Marino’s the ICU Book. Philadelphia: Lippincott Wil-
liams & Wilkins; 2014.
2. Slutsky AS. Mechanical ventilation. American College of chest
Physicians’ Consensus Conference. Chest. 1993;104:1833.
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3. Huang YT, Singh J. Basic modes of mechanical ventilation. In:
Papadakos PJ, Lachman B, eds. Mechanical Ventilation. Philadel-
phia: Saunders; 2007:247–256.
4. Pupella RA. Basic ventilation modes. In: Mechanical Ventilation in
Patient with Respiratory Failure. Singapore: Springer; 2018.
5. Joanne Elliot Z, Charlton Elliot S. An overview of me-
chanical ventilation in the intensive care unit. Nurs Stand.
2018;32(28):41. https://doi.org/10.7748/ns.2018.e10710.
6. Chandrashekar R, Perme C. Chapter 13, Monitoring and life
support. In: Hillegass E, ed. Essentials of Cardiopulmonary Physical
Therapy. 4th ed. 2017:429–437.
7. Chessnutt AN, Chessnutt MS, Prendergast TJ. Pulmonary disor-
ders. In: Tierney LM, McPhee SJ, Papadakis MA, eds. Current Medi-
cal Diagnosis & Treatment. 57th ed. New York: McGraw-Hill; 2018.
8. Pham T, Brochard LJ, Slutsky AS. Mechanical ventilation: state
of the art. Mayo Clin Proc. 2017;92(9):1382–1400. https://doi.org
/10.1016/j.mayocp.2017.05.004.
9. Tol G, Palmer J. Principles of mechanical ventilation. Anaesth
Intensive Care Med. 2010;11(4):125–128.
10. Rochwerg B, Brochard L, Elliott MW, et al. Official ERS/
ATS clinical practice guidelines: noninvasive ventilation
for acute respiratory failure TASK FORCE REPORT ERS/
ATS GUIDELINES. Eur Respir J. 2017;50:1–20. https://doi.
org/10.1183/13993003.02426-2016.
11. Cabrini L, Landoni G, Oriani A, et al. Noninvasive ventilation
and survival in acute care settings: a comprehensive system-
atic review and metaanalysis of randomized controlled trials.
Crit Care Med. 2015;43(4):880–888. https://doi.org/10.1097/
CCM.0000000000000819.
12. Goldworthy S, Graham L. Compact Clinical Guide to Mechanical
Ventilation: Foundations of Practice for Critical Care Nurses. Spring
Publishing Co; 2014.
13. Huntziner A. NAMDRC recommendations for prolonged me-
chanical ventilation. Am Fam Physician. 2006;73(7):1277–1284.
14. Jaillette E, Martin-loeches I, Artigas A, Nseir S. Optimal care
and design of the tracheal cuff in the critically ill patient. Ann
Intensive Care. 2014;4(1):1–9. https://doi.org.wa.opal-libraries.o
rg/10.1186/2110-5820-4-7.
15. Rose L. Strategies for weaning from mechanical ventilation: a
state of the art review. Intensive Crit Care Nurs. 2015;31(4):189–
195. https://doi.org/10.1016/j.iccn.2015.07.003.
16. Ciesla ND, Kuramato JD. Physical therapy associated with res-
piratory failure. In: DeTurk WE, Cahalin LP, eds. Cardiovascular
& Pulmonary Physical Therapy: An Evidence-Based Approach. 3rd ed.
New York: McGraw-Hill; 2018.
17. Chatburn RL. Recognising, describing and comparing modes of
mechanical ventilation. Ind J Resp Care. 2014;3(2):469–478.
18. Ahmed S, Daniel Martin A, Smith BK. Inspiratory muscle train-
ing in patients with prolonged mechanical ventilation: narrative
review. Cardiopulm Phys Ther J. 2019;30(1):1–7. https://doi.
org/10.1097/CPT.0000000000000092.
19. Gerold KB. Physical therapists’ guide to the principles of me-
chanical ventilation. Cardiopulm Phys Ther. 1992;3(8).
20. Costello ML, Mathieu-Costello O, West JB. Stress fracture of
alveolar epithelial cells studied by scanning electron microscopy.
Am Rev Respir Dis. 1992;145:1446–1455.
21. Mathieu-Costello O, West JB. Are pulmonary capillaries suscep-
tible to mechanical stress? Chest. 1994;105(suppl):102S–107S.
22. Heimler R, Huffman RG, Starshak RJ. Chronic lung disease in
premature infants: a retrospective evaluation of underlying fac-
tors. Crit Care Med. 1988;16:1213–1217.
23. Augustyn B. Ventilator-associated pneumonia: risk factors and
prevention. Crit Care Nurse. 2007;27(4):32–36, 38–39; quiz 40.
24. Ouellette DR, Patel S, Girard TD, et al. Liberation from me-
chanical ventilation in critically ill adults: an Official American
College of chest Physicians/American Thoracic Society clinical
practice guideline. Chest. 2017;151(1):166–180. https://doi.
org/10.1016/j.chest.2016.10.036.
25. Eskandar, Siner JM. Liberation from mechanical ventilation: what
monitoring matters? Crit Care Clin. 2007;23(3):613–638.
26. Yang KL, Tobin MJ. A prospective study of indexes predicting
the outcome of trials of weaning from mechanical ventilation. N
Engl J Med. 1991;324:1446–1495.
27. Sciaky A, Pawlik A, Johansen M, Lahart M. Interventions for
acute cardiopulmonary conditions. In: Hillegass E, ed. Essentials
of Cardiopulmonary Physical Therapy. 4th ed. St. Louis: Elsevier;
2016:554–557.
28. Shekleton ME. Respiratory muscle condition and the work of
breathing—a critical balance in the weaning patient. AACN Clin
Issues Crit Care. 1991;2:405–414.
29. Holliday JE, Hyers TM. The reduction of wean time from me-
chanical ventilation using tidal volume and relaxation biofeed-
back. Am Rev Respir Dis. 1990;141:1214–1220.
30. Baily P, et al. Early activity is feasible and safe in respiratory
failure patients. Crit Care Med. 2007;35(1):139–145.
31. Adler J, Malone D. Early mobilization in the intensive care unit:
a systematic review. Cardiopulm Phys Ther J. 2012;23(1):5–13.
32. Cameron Ian Ball Gediminas Cepinskas Karen Choong Timo-
thy Doherty SJ, Kevin J. Early mobilization in the critical care
unit: A review of adult and pediatric literature. J Crit Care.
2015;30:664-672. https://doi.org/10.1016/j.jcrc.2015.03.032.
33. Shah NM, D’Cruz RF, Murphy PB. Update: Non-invasive ventilation
in chronic obstructive pulmonary disease. J Thorac Dis. 2018;10(suppl
1):S71–S78. https://doi.org/10.21037/jtd.2017.10.44.
34. Vitacca M, Kaymaz D, Lanini B, et al. Non-invasive ventilation dur-
ing cycle exercise training in patients with chronic respiratory failure
on long-term ventilatory support: a randomized controlled trial.
Respirology. 2018;23(2):182–189. https://doi.org/10.1111/resp.13181.
35. Menadue C, Piper A, Van’t Hul A, Wong K. Non-invasive venti-
lation during exercise training for people with chronic obstructive
pulmonary disease (Review). Cochrane Database Syst Rev. 2014;5.
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18 417

APPENDIX 18B:  MECHANICAL CIRCULATORY SUPPORT DEVICES

Alysha Walter increased myocardial oxygen supply) by increasing diastolic

Jaime C. Paz pressure in the aorta and thereby displacing blood proximally
into the coronary arteries.5,9
Fig. 18B.1 illustrates balloon inflation during ventricular
filling (diastole) and deflation during ventricular contraction
Objectives (systole). The deflation of the balloon just before aortic valve
1. To provide an overview of mechanical circulatory support de- opening decreases afterload and thereby reduces resistance
vices to the ejection of blood during systole. The blood in the
2. To describe the implications of mechanical circulatory sup- aorta is then propelled forward into the systemic circulation.
port devices in physical therapy management 

Introduction
Mechanical circulatory support (MCS) devices are designed to
support patients in hemodynamic collapse, cardiogenic shock,
cardiopulmonary arrest, or prophylactically during invasive pro-
cedures. MCS devices can be classified as (1) acute, short-term,
temporary support devices or (2) long-term durable devices.1,2
Short-term devices can further be classified according to their
Balloon
method of implantation: devices placed percutaneously and inflated
those which require surgical implantation.2,3 Long-term devices
are all surgically implanted.
Acute, short-term temporary devices covered in this appen-
dix include:
1. Percutaneous devices
A. Intraaortic balloon pump (IABP)
B. Temporary ventricular assist devices (temporary VAD)
a. Impella
b. TandemHeart
2. Surgically placed devices
A. CentriMag A
B. Extracorporeal membrane oxygenation (ECMO)
Long-term durable devices covered in this appendix include:
1. Ventricular assist device (VAD)
2. Total artificial heart (TAH) 

Short-Term Percutaneous Devices

Intraaortic Balloon Pump
The IABP is the most common form of mechanical support for Balloon
the failing heart.4,5 The IABP consists of a catheter with a sau- deflated
sage-shaped balloon at the terminal end, connected to an exter-
nal pump-controlling device. The catheter is typically inserted
percutaneously into the femoral artery and is threaded antegrade
until it reaches the proximal descending thoracic aorta. Occa-
sionally placement in the subclavian or axillary artery is used as
a means of long-term ambulatory support (refer to the Intraaor-
tic Balloon Pump via the Subclavian or Axillary Artery section).
This placement location also decreases the mobility restrictions
encountered with femoral artery placement.6-8
The main function of the IABP is to lessen the work (i.e., B
decreased myocardial oxygen demand) of the heart by decreas- FIG. 18B.1
ing afterload in the proximal aorta. This is accomplished via Mechanisms of action in intraaortic balloon pump. (A) Diastolic balloon
a vacuum effect created by rapid intravascular balloon defla- inflation augments coronary blood flow. (B) Systolic balloon deflation de-
creases afterload. (From Urden LD. Thelan’s Critical Care Nursing: Diagnosis
tion. The IABP also improves coronary artery perfusion (i.e.,
and Management. 5th ed. St. Louis: Mosby; 2006.)
418 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting
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 phases of the heart.5 Balloon inflation is trig-
gered through synchronization with either electrocardio-
gram (ECG) or pressure changes, with ECG being the most
common10
Indications for IABP include the following5,6,9,11-16:
• Acute left ventricular failure, refractory to other manage-
ment
• Unstable angina, refractory to other management
• Recent acute myocardial infarction (MI)
• Cardiogenic shock
• Acute mitral valve regurgitation
• Assisting patients to wean from cardiopulmonary bypass
• Ventricular septal defect
• Refractory ventricular dysrhythmias
• Adjunctive therapy in high-risk or complicated catheteriza-
tion and angioplasty
• Preoperative management of patients undergoing high-risk
cardiac surgery
The ratio of counterpulsations of the IABP to heartbeats
indicates the amount of circulatory support an individual
requires (e.g., a ratio of 1:1 is one counterpulsation to one
heartbeat; a ratio of 1:4 is one counterpulsation to every
fourth heartbeat; the 1:1 ratio provides maximum circula-
tory support). Weaning a patient from an IABP typically
involves gradually decreasing the ratio of counterpulsations
to heartbeats, with the goal being 1 counterpulsation for
every fourth heartbeat, as tolerated, before discontinuing
the IABP. Weaning also can be accomplished by gradually
decreasing the amount of balloon inflation pressure in the
aorta.1
Potential complications of IABP include the
following5,10,16-20:
• Transient loss of peripheral pulse
• Limb ischemia
• Thromboembolism
• Compartment syndrome
• Aortic dissection
• Local vascular injury—hematoma, pseudoaneurysm (false
aneurysm)
• Thrombocytopenia, hemolysis
• Cerebrovascular accident (CVA)
• Infection
• Balloon rupture
• Balloon entrapment
• Bleeding
Physical Therapy Considerations
• Length of time on IABP, poor ejection fraction, and a history
of vascular disease increase the risk of limb ischemia and vas-
cular complications.21,22
• During IABP, the lower extremity in which femoral access
is obtained cannot be flexed at the hip, and the head of bed
(HOB) cannot be raised higher than 30 degrees to prevent
the intraaortic balloon catheter from migrating.23
• I f the IABP becomes dislodged, allow 1 to 2 seconds of bleed-
ing so that any blood clots can pass before applying firm pres-
sure. Nursing and the physician should then be notified.23
• Once the IABP is removed, the patient will be on bed rest
for a specified amount of time as determined by the medi-
cal team and should avoid exercising the involved extremity
during that time to prevent bleeding.23
• Patients may require range of motion (ROM) or strength-
ening exercises for the hip and knee after IABP remov-
al. The ankle can be ranged while the patient is on the
IABP.23
• The patient is at risk for skin breakdown as a result of lim-
ited mobility and decreased perfusion to the affected extrem-
ity. Therefore patients benefit from pressure-reducing or
pressure-relieving mattresses; frequent repositioning; and
assessment of vascular, motor, and sensory function.14
• To prevent pulmonary complications while on bed rest, pa-
tients benefit from frequent repositioning and deep breath-
ing and coughing exercises.
Intraaortic Balloon Pump via the Subclavian or Axillary
Artery. The literature also describes IABP insertion via the sub-
clavian artery (sIABP) or the axillary artery. An advantage to
these placement options is that patients are not required to be
immobile.7,8,24 It is important to monitor extremity perfusion,
neurologic status, surgical site bleeding, and the overall hemody-
namic status of the patient.24 Blood pressure differences between
the upper extremities should be reported to the medical team.24
Tachyarrhythmias may impair the ability of the balloon to sense
and trigger appropriately.24 Proper securement and anchoring of
the tubing is critical to prevent kinking of the catheter. One pos-
sible method is the use of the Centurion urinary catheter (Centu-
rion Medical Products, Williamston, MI) to secure both the IABP
tubing and cardiac monitoring leads. Mobility has been reported
to be allowed once the patient with sIABP has recovered from
anesthesia and any groin catheters have been removed.24
Complications with sIABP are similar to IABP inserted
via the femoral artery and include aortic dissection, bleeding,
plaque rupture and embolism, balloon rupture, limb ischemia,
balloon catheter migration, lymphocele, infection, and mesen-
teric artery occlusion.24
As reported in two studies, additional mobilization and
activity considerations include the following8,24:
• Nursing presence is required during ambulation to address
problems with the console or pump, difficulty with catheter
tubing, or patient complications.8,24
• Ensure pump console batteries are fully charged and battery
life is assessed during ambulation periods.24
• Murks et  al. have reported successful implementation of
progressive ambulation and core and strength training ex-
ercises in patients with sIABP while awaiting heart trans-
plantation.24
• Shumock et al. described a case study regarding the feasibil-
ity and physical therapy plan of care for an individual with
an axillary IABP. Highlights of this article included consul-
tation with the multidisciplinary team and establishing he-
modynamic parameters to ensure safety during the physical
therapy interventions.8 
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18
Impella® Recover System
The Impella Recover System is a minimally invasive percuta-
neous axial flow ventricular unloading catheter. The Impella
draws blood from the ventricle and empties it into the aor-
tic root or pulmonary artery.25,26 This device allows the heart
to rest and recover by actively unloading the ventricle and
reducing myocardial workload and oxygen consumption.26 It
also helps increase cardiac output, coronary perfusion, and end
organ perfusion. The Impella is available in four options to
provide left heart support: Impella 2.5, Impella CP, Impella
5.0, and Impella LD. A fifth option, the Impella RP, is the
only device available for right heart support.25,26 The Impella
2.5 is able to provide up to 2.5 L/min of cardiac output and
can support a patient for up to 4 days.26 The Impella CP
can provide up to 4.3 L/min support for up to 4 days.26 The
Impella 5.0 and Impella LD are able to provide up to 5 L/min
of cardiac output and can support a patient for up to 6 days.26
The Impella RP can provide up to 4.0 L/min flow and can
support a patient for up to 14 days.26 Fig. 18B.2 illustrates
an Impella 2.5.
The Impella catheters are inserted percutaneously in the car-
diac catheterization laboratory by one of several methods: into
the femoral artery (Impella 2.5, CP), via a small cut-down of
the femoral or axillary artery (Impella 5.0), through open chest
procedures (Impella LD), or via insertion through the femoral
vein (Impella RP).26 The Impella 2.5, CP, 5.0, and LD all pull
blood from the left ventricle and expel blood from the catheter
to the ascending aorta. The Impella RP pulls blood from the
inferior vena cava and delivers it to the pulmonary artery.26 An
advantage of the Impella over the TandemHeart is that there is
no need for a transseptal puncture and no extracorporeal (exter-
nal) blood flow occurs.27,28
FIG. 18B.2
Illustration of the Impella LP 2.5. (Courtesy AbioMed, Danvers, MA.)
419
Indications for the Impella include the following27, 29:
Impella 2.5 and Impella CP26
• High-risk percutaneous coronary interventions
• Post–percutaneous coronary intervention support
• Advanced heart failure
• Cardiogenic shock
• Post–cardiotomy cardiogenic shock 
Impella LD 5.026
• Postcardiotomy low cardiac output syndrome
• Post–percutaneous coronary intervention support
• Myocarditis
• Cardiogenic shock
• Acute heart failure
• Bridge to next decision 
Impella RP26
• Decompensated right heart failure after:
• Myocardial infarction
• Left ventricular assist device implantation
• Heart transplantation
• Open heart surgery
Potential complications of the Impella device include the
following27,28:
• Bleeding
• Thromboembolism
• Critical limb ischemia
• Pump displacement
• Infection
 CLINICAL TIP
There are currently no specific guidelines that relate to hip
ROM or mobility during use of the Impella. Typically, these
patients are critically ill, so if you are consulted to evaluate a
patient with an Impella, follow your hospital’s guidelines re-
lated to ROM and mobility. Consider the risk of kinking or dis-
placing the femoral cannula in your clinical decision making.  
TandemHeart
The TandemHeart is an extracorporeal (external) continuous
flow centrifugal, left VAD (Fig. 18B.3).25 Pump components
include an inflow cannula inserted into the femoral vein with
transseptal placement into the left atria, outflow cannula placed
in the femoral artery, a centrifugal pump, and a control con-
sole.10 The pump propels blood by means of a magnetically
driven impeller through the outflow port and returns it to
one or both femoral arteries via arterial cannulas.10,29 Some of
the blood in the femoral arteries continues in a forward flow
through the arterial system to perfuse the lower extremities, and
some of the blood returns in a reverse flow backup 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, the TandemHeart can provide a cardiac
output of up to 4 to 5 L/min.10,25,27,30
By unloading the left ventricle, decreasing myocardial oxy-
gen consumption, and decreasing left atrial filling pressures,
420 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting
FIG. 18B.3
TandemHeart percutaneous VAD. (Courtesy Cardiac Assist, Pittsburgh, PA.)
this percutaneous VAD can provide short-term support (i.e., a
few hours up to 14 days) in the intensive care unit (ICU). This
allows time for the native heart to recover.10,29
Indications for the TandemHeart include the following27-30:
• High-risk percutaneous coronary interventions
• Cardiogenic shock
• Bridge to cardiac transplantation
• Bridge to long-term mechanical circulatory support, such
as a surgically implanted left ventricular assist device
(LVAD)
Potential complications of the TandemHeart include the
following27,28,31:
• Bleeding
• Thromboembolism
• Transseptal cannula dislocation
• Arterial cannula dislocation
• Lower extremity ischemia
• Infection
Physical Therapy Considerations
• Avoid hip flexion greater than 20 degrees to prevent the can-
nula from kinking or displacing. A knee immobilizer is use-
ful in preventing unwanted hip flexion.
• Avoid HOB elevation greater than 20 degrees.
• Do not exceed 30 degrees in reverse Trendelenburg posi-
tion.
• After cannula removal, hip flexion is prohibited for at least 4
to 6 hours.
• Because of the location of cannula insertion, monitor distal
perfusion of extremities.10  ECMO. However, less positive pressure is required to oxygenate
Short-Term Surgically Placed Devices
CentriMag
CentriMag is a continuous-flow, extracorporeal, centrifugal-type
rotary blood pump.25 Components include a single-use pump,
motor, and monitoring console. It can deliver flows up to 9.9 L/
min. The device is designed to provide temporary right, left, or
bi-ventricular support.25
The CentriMag is approved by the US Food and Drug
Administration (FDA) under the humanitarian device designa-
tion for use in patients with cardiogenic shock caused by right
ventricular failure for up to 30 days. It is also indicated for use
up to 6 hours as an extracorporeal pump system for left ven-
tricular or bi-ventricular failure.32
 CLINICAL TIP
• There are limited reports in the literature and guidelines re-
garding mobilization of this patient population are scarce.
Following facility guidelines, support and guidance from the
multidisciplinary team, ensuring that the appropriate num-
ber of trained staff are available to assist with mobilization
and protection of cannula, and analyzing the risk and benefit
of mobilization of this population are important factors to
consider.33
• Cannula placement may either prohibit or allow for mobiliza-
tion. Centrally placed cannulas allow for progressive mobility,
whereas femoral placement creates limitations.34
• Physical therapists should conduct a risk assessment before
physical therapy and mobilization to ensure hemodynamic
stability. Parameters to consider include33:
• Stable mean arterial pressure (MAP)
• No acute cardiac arrhythmia
• Stable CentriMag flow rates (no unexplained drop in
flow >0.5 L/min within an hour of treatment)
• Firmly secured VAD cannulae
• No indication of infection or drainage
• Stability in clotting parameters (mobilization not per-
formed if activated partial thromboplastin time (aPTT) ra-
tio is ≥3.0 or the activated clotting time is ≥240 seconds)
• Patient’s ability to follow instructions  
Extracorporeal Membrane Oxygenation
Extracorporeal membrane oxygenation (ECMO) uses an exter-
nal device for direct oxygenation of blood, assistance with the
removal of carbon dioxide, or both. The primary indication for
ECMO is cardiac or respiratory failure that is unresponsive to
maximal medical therapy and conventional mechanical ventila-
tion. The pediatric population with respiratory failure appears
to benefit from ECMO therapy the most; however, successful
use in the adult population has improved as a result of tech-
nologic advances.35,36 The pumping device is used to help a
failing ventricle circulate blood, whereas the oxygenator device
assists the failing respiratory system to fully oxygenate the
patient. Patients who have respiratory failure may require con-
current mechanical ventilation to prevent atelectasis while on
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18
FIG. 18B.4
Illustration of extracorporeal membrane oxygenation. (From Shanley CJ, Bartlett RH. Extracorporeal life sup-
port: techniques, indications, and results. In: Cameron JL, ed. Current Surgical Therapy. 4th ed. St. Louis: Mosby-
Year Book; 1992:1062-1066.)
blood when on ECMO, resulting in a decreased incidence of
barotrauma.35
As illustrated in Fig. 18B.4, the ECMO system consists of
a venous drainage cannula, a reservoir for blood, a pumping
device that uses a centrifugal or roller system, an oxygenator,
and an arterial or second venous return cannula.35,37 A variety
of configurations of ECMO may occur; however, there are fun-
damental components, including a drainage and perfusion can-
nula, centrifugal roller pump, and membrane oxygenator.10
The venous drainage to arterial return cannula system (V-A
mode) is used primarily with patients who require cardiac or
cardiorespiratory support. V-A mode can be achieved in the fol-
lowing three ways35:
1. Femoral vein to the ECMO system with return to the femo-
ral artery
2. Right atrium to the ECMO system with return to the as-
cending aorta
3. Femoral vein to the ECMO system with return to the ascend-
ing aorta
The venous drainage to venous return cannula system (V-V
mode) is used with, and is the preferred mode for, patients
requiring only respiratory support. V-V mode can be achieved
in the following two ways35:
1. Internal jugular vein to the ECMO system with return to the
common femoral vein
2. Common femoral vein drainage to the ECMO system with
return to the contralateral common femoral vein
421
Patients who are on V-A mode ECMO are typically anticoag-
ulated with heparin and may require the use of IABP to further
assist the ventricle. Patients on V-V mode may require sedation
and/or medical paralysis to help improve oxygenation to organs
and tissues by minimizing the metabolic demands of a conscious
individual.35
According to the Extracorporeal Life Support Organization
(ELSO), adults with respiratory failure have a 58% survival
rate to discharge. Use of extracorporeal life support (ECLS) in
adults with respiratory failure has seen the most growth among
all ECLS indications, with the majority of patients supported
on VV-ECMO.38 Survival rates of patients on VV-ECMO
were found to be higher than those of patients supported on
VA-ECMO. With regard to adults receiving cardiac ECLS, the
registry included 9025 adults, with 41% surviving to hospital
discharge. Cardiogenic shock was the most common diagnosis
indicating ECLS use.38
Indications for ECMO include the following:
Cardiac Support: VA ECMO39
• Cardiogenic shock (severe cardiac failure, numerous
possible causes)
• Inability to be weaned from cardiopulmonary bypass
after cardiotomy
• Primary graft failure after heart transplantation or heart–
lung transplantation
• Chronic cardiomyopathy
• Periprocedural support for high-risk percutaneous car-
diac interventions
422 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting
Respiratory Support: VV or VA ECMO39
• Acute respiratory distress syndrome (ARDS)
• Extracorporeal assistance to provide lung rest
• Lung transplantation
• Primary graft failure
• Intraoperative ECMO
• Lung hyperinflation
• Status asthmatics
• Pulmonary hemorrhage or massive hemoptysis
• Congenital diaphragmatic hernia, meconium aspiration
Contraindications to ECMO include the following39:
Absolute Contraindications
• Unrecoverable heart and not a candidate for transplanta-
tion or destination therapy VAD
• Disseminated malignancy
• Known severe brain injury
• Unwitnessed cardiac arrest
• Prolonged cardiopulmonary resuscitation (CPR) without
adequate tissue perfusion
• Unrepaired aortic dissection
• Severe aortic regurgitation
• Severe chronic organ dysfunction
• Limited compliance with complete medical regimen
• Peripheral vascular disease (PVD) in peripheral VA ECMO
• VV ECMO in cardiogenic failure and in severe chronic
pulmonary hypertension (mean pulmonary artery pres-
sure [PAP] >50 mmHg)
Relative Contraindications
• Contraindication for anticoagulation
• Advanced age
• Obesity  indications to transplantation that are expected to resolve.3,50
Potential complications and adverse events for adults on ECMO
include the following37,38,40:
• Surgical- or cannula-related hemorrhage
• Infection
• Renal failure
• Hyperbilirubinemia
• Central nervous system (CNS) or pulmonary hemorrhage
• CNS infarction
• Lower limb ischemia
• Thrombocytopenia
• Thromboembolism
• Mechanical: pump malfunction or oxygenator failure  Indications for VAD include51,52:
Physical Therapy Considerations
• Physical therapy involvement with patients receiving ECMO
may depend on the facility; proficiency, skill, expertise, and
advanced training of the physical therapist; and the experi-
ence and culture of the multidisciplinary team. Early, active
physical therapy mobilization for patients on ECMO may be
feasible and safe at an ECMO center when a qualified, mul-
tidisciplinary team is present.41-43,44 Caution should be used
in hospitals with smaller ECMO programs or when physical
therapists have less training in this area of care.43
• Screening tools are available to determine safety to partici-
pate in rehabilitation.43,45
• Recent studies have focused on early mobilization of patients
on VV ECMO. There is little guidance on intervention for
those on VA ECMO.46
• I f working with a patient on ECMO, reducing the patient’s
stress level may decrease the amount of energy expenditure
by the patient and improve tolerance to activity.37
• Rolling or turning the patient is not recommended because
of risk of dislodging the cannula.
• ROM should only be performed if the benefits heavily out-
weigh 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 neurologic impairments,
such as cognitive changes, developmental dysfunction, and
hypotonia.47 
Long-Term Devices
Ventricular Assist Device
A VAD is a mechanical pump that provides prolonged circula-
tory assistance in patients who have acute or chronic ventricular
failure. Since the initial use several decades ago, multiple devices
have been designed and clinically tested, with ongoing clinical
trials developing the future generation of pumps.48 Left ven-
tricular assist devices (LVADs) are described as first-generation,
second-generation, and now third-generation devices. Patients
are appropriate for VAD implantation if they are categorized
as a New York Heart Association (NYHA) Class III or IV or
an American College of Cardiology/American Heart Association
Stage D.49
There are four objectives for the use of a VAD:
• Bridge to transplantation (BTT): heart transplantation candi-
dates who are medically labile or who have temporary contra-
• Destination therapy (DT): individuals who are ineligible for
transplantation and for whom the VAD is the final therapy
for advanced heart failure.3,50
• Bridge to recovery (BTR): the patient’s myocardium is expect-
ed to recover after an insult.3,50
• Bridge to decision: the best long-term option is not clear at the
time of VAD implantation.
Short-term VADs, discussed previously in this appendix, may
be used as a bridge to bridge, for individuals with severe cardio-
genic shock because their clinical course will determine whether
they are candidates for a long-term VAD.49,50
• Heart failure refractory to conventional therapy
• Patients with a peak oxygen consumption (VO2) of less than
14 mL/kg/min or less than 50% predicted for age, sex, and
body surface area on cardiopulmonary stress test
• Cardiac index less than 2 L/min2, despite treatment with
inotropic agents
• Pulmonary capillary wedge pressure greater than 25 mmHg
• Systolic blood pressure less than 90 mmHg
Reports in the literature indicate that VAD therapy is
highly beneficial in alleviating symptoms and improving out-
comes, including survival rates and quality of life in patients
with Class IV heart failure.53 The life expectancy of patients
who receive VAD implantation for DT is approximately 1 to
2 years.54,55
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18 423

The VAD restores cardiac output and blood pressure, as well
as providing a reduction in left ventricular pressure and vol-
ume. A reduction in left ventricular workload further produces
a decrease in pulmonary venous and arterial pressures along with
reduced pulmonary vascular resistance. The VAD also improves
perfusion to all body organs, which results in improved auto-
nomic function and normalization of the neurohormonal and
cytokine milieu that is present in heart failure.52
VADs can be used to assist the left ventricle (LVAD), the
right ventricle (RVAD), or both ventricles (BiVAD). The most
commonly used is the LVAD. For more severe situations, both
ventricles need to be assisted (BiVAD).3 In 20% to 30% of cases
where the LVAD provides pressure and volume unloading of the
left ventricle, the increase in venous return to the right ven-
tricle results in right ventricle volume overload. Pharmacologic
support with angiotensin-converting enzyme inhibitors, angio-
tensin receptor blockers, and beta-blockers, such as carvedilol,
is provided to patients with an LVAD to minimize systemic
hypertension and help preserve right heart function.56 While
this situation can be treated with inotropes or pulmonary vaso-
dilators, in some instances, an RVAD is necessary.52
VADs consist of a pump, a driveline providing electric or
pneumatic energy, a system controller, and a console.50 The
pumps generally fall into two main categories: pulsatile pumps
and continuous flow pumps. Continuous flow pumps can be fur-
ther classified as either axial-flow or centrifugal-flow devices.
Pulsatile pumps tend to be larger than continuous flow pumps
because of 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 L/min of blood flow.
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 pericardial, preperitoneal,
or intraabdominal position. The inflow conduit drains the left
ventricle through the apex of the heart, and an outflow conduit
ejects blood into the ascending aorta (Fig. 18B.5A).The power
source line, known as the drive line, exits the abdomen and leads
to an external system controller. An extracorporeal VAD can be
univentricular or bi-ventricular 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 (see Fig. 18B.5B). This type of VAD may
be placed paracorporeally (lying on top of the abdomen) and
may be referred to as a “paracorporeal VAD.”57 Extracorporeal
pump cannulae must be adequately supported during functional
mobility.58 Support of the cannulae minimizes disruption of the
insertion site to ensure healing and avoid dislodgement. This
support will also ensure that there is no kinking of the cannulae
or disruption of flow from the device to the patient.58 Support
can be provided by securing the cannulae with an anchoring
device or abdominal binder. The physical therapist may confer

A B
FIG. 18B.5
(A) The HeartMate intracorporeal left ventricular assist device and system controller. (B) The Thoratec paracor-
poreal ventricular assist device. (A, Heartmate 3 is a trademark of Abbott or its related companies. Reproduced
with permission of Abbott © 2019. All rights reserved. B, Courtesy Thoratec Corporation, Pleasanton, CA.)
424 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting

with the medical team to select the most appropriate method for
cannulae securement.58
 CLINICAL TIP
Continuous flow pumps provide continuous flow, so there are no
distinct systolic or diastolic phases. For this reason, a traditional
blood pressure measurement cannot be obtained. Instead, an
average blood pressure, or mean arterial pressure (MAP), can be
measured by using a manual blood pressure cuff and Doppler
ultrasound.59 The suggested range for blood pressure during ac-
tivity and at rest to maintain systemic perfusion and decrease
risk for stroke is a MAP between 70 and 90 mmHg.58,60,61
The various types and general characteristics of intracorporeal
and extracorporeal VADs are described briefly in Table 18B.1.
The VADs described in this table are either FDA approved or
in investigational 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 this population must be famil-
iar with the type of device the patient is using, as well as the
safety features of the VAD. A brief overview is provided below
for frequently encountered intracorporeal LVADs.
Heartmate II. The HeartMate II (Abbott, North Chicago,
IL) is a second-generation LVAD, which has been implanted
in more than 26,000 patients.62 The Heartmate II can be pro-
grammed at speeds between 6000 to 15,00063 revolutions per
minute (rpm) and can deliver flow up to 10 L/min.62  the physical therapist must be competent in hand pump-
HeartWare (HVAD). The HeartWare (HVAD) (HeartWare,
Inc., Framingham, MA) is a continuous-flow, centrifugal pump
which was approved by the FDA in 2012. It consists of an inflow
cannula (placed in the left ventricle), an ascending aorta out-
flow graft, and percutaneous drive line.64 It can generate blood
flow up to 10 L/min and operate at speeds between 2400 and
3200 rpm.63,64 The pump is positioned in the pericardial space,
eliminating the need for the creation of a pump pocket. The
external system includes a microprocessor control unit, lithium-
ion batteries with chargers, and AC (alternating current) or DC
(direct current) power adaptors. The controller unit is powered
by internal, rechargeable batteries and is connected to the moni-
tor. Patient information is displayed on the monitor.64 
Heartmate 3. The HeartMate 3 LVAD (Abbott, North Chi-
cago, IL) is a continuous-flow, centrifugal pump. The pump is
capable of delivering up to 10 L/min of blood through the body.
The HeartMate 3 is smaller than previous VADs, is placed in
the pericardial space, and can create an “artificial” pulse via peri-
odic increase and decrease in pump speed.65
Complications of VAD implantation can either be machine-
related or patient-related and include the following:
• Device-related complications: disconnection of the lead and
drivelines, valve dysfunction, and/or deterioration in the
pump mechanism requiring either repair or replacement
with another VAD.54,66 Each VAD has an educational man-
ual outlining the relevant details of the components, opera-
tion, and safety features. 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 and
ing should an emergency situation arise.67 Continuous flow
pumps cannot be hand pumped, so in the presence of pump
failure, follow the hospital’s emergency code procedure.

TABLE 18B.1  Ventricular Assist Devices

Device Pump Mechanism Position Purpose
Thoratec Centrimaga Continuous Extracorporeal TCS
Thoratec PVADa Pulsatile Extracorporeal BTT
HeartMate II (Abbott) Continuous/Axial Intracorporeal BTT, DT
HeartMate 3 (Abbott)a Continuous/Centrifugal Intracorporeal BTT, DT
Berlin Heart INCOR Ib Continuous Intracorporeal BTR, BTT, DT
Berlin Heart EXCOR Pediatrica Pulsatile Extracorporeal BTR pediatric population
Jarvik 2000 (JarvikHeart, Inc.)b Continuous/Axial Intracorporeal BTT, DT
HeartWare HVADa (Medtronic) Continuous/Centrifugal Intracorporeal BTT, DT

BTR, Bridge to recovery; BTT, bridge to transplant; DT, destination therapy; PVAD, paracorporeal ventricular assist device; TCS, temporary circulatory support.
aFDA approved.
bInvestigational.

Data for chart from: Thoratec Corporation. CentriMag website. http://www.thoratec.com/medical-professionals/vad-product-information/thoratec-centrimag.aspx.

Published 2018. Accessed December 18, 2018; Thoratec Corporation. Thoratec PVAD website. http://www.thoratec.com/medical-professionals/vad-prod-
uct-information/thoratec-pvad.aspx. Published 2018. Accessed December 18, 2018; Berlin Heart. INCORE website. https://www.berlinheart.de/en/medi
cal-professionals/incorr/. Published 2018. Accessed December 2018, 2018; Berlin Heart. EXCORE Pediatric website. https://www.berlinheart.com/patients-
relatives/excorr-pediatric/. Published 2018. Accessed December 18, 2018; Jarvik Heart. The Jarvik 2000 website. https://www.jarvikheart.com/products/. Published
2018. Accessed December 18, 2018; Feldmann C, Charrerjee A, Haverich A, Schmitto J. Heart failure: From research to clinical practice. In: Islam MS, ed. Left Ventricu-
lar Assist Devices—A State of the Art Review. Vol 3. Basel, Switzerland: Springer International Publishing AG; 2018. Accessed November 27, 2018;HeartMate 3 LVAD
Abbott website. https://www.heartmate.com/healthcare-provider/heartmate-3-lvad. Published 2018. Accessed November 27, 2018; HeartWare. HeartWare website.
https://www.heartware.com/clinicians/destination-therapy. Published 2018. Accessed November 26, 2018.
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18
• P
 atient-related complications: infection; arrhythmias; gas-
trointestinal distress; and thromboembolic events, includ-
ing stroke, respiratory failure, and death.54,55 Patients with
pulsatile pumps who require defibrillation can be defibril-
lated after the pump is disconnected from the power source
and hand pumping is started. Patients with continuous flow
pumps can be defibrillated per Advanced Cardiac Life Sup-
port (ACLS) guidelines without disconnecting the pump
from the power source.
The combination of technologic improvements and a lack
of donor organs has increased the use of VADs in patients with
advanced heart failure. Current literature indicates that patients
with a VAD can be mobilized safely in the hospital and that
their exercise tolerance (as demonstrated by the 6-minute
walk test [6MWT], peak VO2, and subjective reports) can be
improved while awaiting transplantation or while continuing
with destination therapy.59,67,70 Patients with LVAD implants
have also demonstrated quality-of-life improvements, as mea-
sured by the Kansas City Cardiomyopathy questionnaire and
the Minnesota Living with Heart Failure questionnaire, which
correlate to an improved functional capacity denoted by NYHA
classification.59,65  mechanical factors. The patient’s native heart is still con-
Physical Therapy Considerations
The following are general goals and guidelines for the physical
therapist when working with a patient who has a VAD.
• The postoperative rehabilitation of a patient after VAD
placement is similar to that of patients who have undergone
other cardiothoracic surgeries. Differences in the rehabilita-
tion for LVAD patients include increased complexity of their
preoperative condition and safety issues related to device
management.71
• It is the physical therapist’s responsibility to identify any red
flags and consider the appropriateness of the patient to par-
ticipate in therapy. Therapists should consider the patient’s
mental status, cooperation, and hemodynamic status.58,71
• Common physical therapy interventions for patients with an
LVAD include gait training, balance exercises (sitting and/
or standing), therapeutic exercise, stair training, and patient
and family education. Early ambulation after LVAD place-
ment has been shown to be predictive of shorter length of
hospital stay and discharge home.72
• Whether a patient is awaiting heart transplantation (BTT)
or not (DT), the primary goals of physical therapy for the
patient with an implanted VAD are to optimize mobility and
functional capacity. The patient’s length of stay and achieve-
ment of goals is likely dependent on their overall medical
status, along with the primary purpose of VAD implantation
(BTT or DT). Patients with VADs can benefit from outpa-
tient cardiac rehabilitation once discharged from the hospi-
tal. Physical therapy can be initiated on postoperative day
1, depending on hemodynamic stability.59,67 In some cases,
physical therapy may already be working with patients pre-
operatively.
• Open-heart surgery via sternotomy is required to implant
the VAD and its components. Refer to Chapter 3 for more
information regarding sternal precautions.
425
• P ostoperatively, patients may have pain at the driveline exit
site and sternal incision and may need appropriate premedi-
cation with analgesics before initiation of physical therapy.68
Pain at exit sites can result in a kyphotic or scoliotic posture,
which could lead to an obstruction in the LVAD driveline,
resulting in a possible reduction in flow rates to meet activ-
ity demands.67 Patients may also have symptoms of nausea
because of the position of the internal pump within the peri-
toneal region and may need antiemetic medication before
therapy.
• An abdominal binder or other anchoring system (e.g., Foley
catheter anchor) should be used to secure the driveline and
protect its exit site during all activity. This will allow for
wound healing and formation of scar tissue around the drive-
line and will reduce shearing forces at the exit site, thereby
decreasing the risk of infection. Abdominal binders may
need to be customized to fit the patient appropriately and
modified to provide an attachment for the system controller.
Additional types of carriers have been designed to hold the
smaller controllers for systems, such as Heartmate II.
• Hemodynamic monitoring is affected by both patient and
tracting; therefore the patient’s electrocardiogram will re-
flect the native heart’s electrical activity. The native heart
rate response at rest and with activity will likely be blunted
as a result of taking beta-blockers. A peripheral pulse can
typically be palpated in a patient with a pulsatile pump, and
a traditional blood pressure can be measured. Furthermore,
because the VAD is performing the majority of the patient’s
cardiac output, the patient’s peripheral pulse is indicative of
the parameters set on the VAD.73 A flow rate of 3 to 4 L/min
is considered adequate in most devices to achieve a sufficient
cardiac output, which is displayed on the screen of the power
base monitor of the VAD.59,67 To help maintain an adequate
flow rate, fluids are often not restricted in these patients,59
but it is helpful to ascertain any precautions before working
with them.
• The speed, occasionally referred to as rate, of a VAD can
be fixed or automatic/adaptive. VADs that have automatic
speeds are able to adjust according to the demands of the
patient. However, keeping the pump at a fixed speed im-
proves the pump’s longevity, if the patient can tolerate
it.42,67 Physical therapists can monitor several parameters
to gauge the appropriate intensity and response to exercise
and activity. These parameters may include the patient’s rat-
ing of perceived exertion (RPE) (e.g., Borg Scale), Dyspnea
Scale,58 BP or MAP, and oxygen saturation. An RPE of 11
to 13 out of 20 has been reported as an appropriate intensity
level at which to safely exercise and achieve training benefits
in this patient population.67 Based on the type of VAD and
its settings, a MAP between 70 and 95 mmHg at rest and
with activity has been reported as a reference value for most
patients.59
• Patients with VADs can still experience heart failure;
therefore a supervised resistance exercise program, once
medically cleared, is an important part of their therapeutic
plan of care.74 According to the American Association for
426 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting
­ ardiovascular Rehabilitation, a period of 12 weeks or more
C pulsatile, pneumatically driven pump, thus avoiding the need
after device implantation, should pass before initiating a
light resistance exercise program.75
• Indications to stop exercise in a patient with a VAD are the
same as when treating a patient with cardiac disease (refer to
Chapter 3 for more guidelines). In addition, a drop in pump
flow or speed may indicate pump failure, occlusion of tub-
ing, and/or bleeding.67 Therefore stop the exercise, investi-
gate the cause, and seek assistance, as necessary.
• VADs with electric pumps can be battery powered during
mobility, making the patient independent to move without
the need for an electrical power source. Physical therapists
must be knowledgeable about battery life. It is important
to always carry extra batteries and a system controller when
mobilizing the patient away from his or her room. Most
hospitals require the patient and caregivers to be able to in-
dependently switch batteries before mobilizing away from
the unit. Patients with electric pumps can be discharged to
home once they reach the appropriate level of independence.
Pneumatic pumps cannot be battery powered, and thus these
patients are confined to the hospital.
• Because patients will need to learn to mobilize independent-
ly with the VAD equipment, physical therapists can include
specific training to assist patients in preparation for this ac-
tivity. The equipment that these patients need to carry is
between 2 and 2.5 kg (or ∼4.4 to 5.5 lb), which can affect
their posture and balance.71 Therefore postural and balance
exercises may assist patients in improving strength and de-
creasing fall risk so that they can safely carry the necessary
equipment and increase their independence with mobility.
• Patients should be educated to avoid strong static discharges
(e.g., television or computer screens), swimming, and con-
tact sports. Patients can shower, provided they use a water-
proof shower kit that protects the VAD.76  via a standard electrical outlet or car charger.84
Total Artificial Heart
An implantable and sustainable TAH has been under investiga-
tion for several decades.77 The Syncardia/CardioWest temporary
TAH (SynCardia Systems, Tucson, AZ) is the only commercially
available TAH approved by the FDA and is for use in patients
with end-stage congestive heart failure as a BTT.78,79 The TAH’s
primary role is in patients with end-stage bi-ventricular failure
who are not candidates for an LVAD.78
Specific indications for the TAH include78:
• Eligibility for heart transplantation in those with NYHA
Class IV symptoms and the appropriate chest size (body sur-
face area 1.7–2.5 m2)
• Hemodynamic insufficiency requiring cardioactive medica-
tions or mechanical support
• Not being a candidate for LVAD therapy
• Other clinical conditions with end-stage heart failure that
are not adequately treated with an LVAD (e.g., small/nondi-
lated ventricles, patients requiring concomitant repair, such
as septal defects or congenital heart disease)
• Eligibility for heart transplantation
Implantation of the TAH involves removal and subsequent
replacement of the native atria, ventricles, and valves with a
for medications, such as inotropic or antiarrhythmic agents.80-82
The TAH is implanted via median sternotomy. Additionally,
two small incisions are made in the left upper abdomen, and
intramuscular tunnels are created through the left rectus abdo-
minus, from which the drivelines exit.78 Patients with TAH
typically receive long-term anticoagulation to prevent throm-
boembolic complications. Anticoagulation strategies may vary
by institution. Target international normalization ratio (INR)
goals with use of warfarin is 2 to 3.78,81
There are two versions of the TAH—50 cc and 70 cc. The 50 cc
TAH is a smaller version that has been designed as a BTT for indi-
viduals with a smaller stature.83The 50 cc TAH has a stoke volume
up to 50 mL and can attain a cardiac output between 5 and 7.5 L/
min.84 A maximum stroke volume of 70 mL is attainable with
cardiac output in the range of 7 to 9 L/min for the 70 cc TAH.82
The TAH consists of an external drive console that sends
pneumatic pulses from compressor-generated air tanks through
7-foot drivelines into two independent ventricles that have uni-
directional inflow and outflow valves.84 There are a variety of
external drivers used in practice, including the Companion 2
(C2) Hospital Drive and the Freedom Driver (Fig. 18B.6A).
Some health care systems may also continue to use the “Big
Blue” (Fig. 18B.6B) console as the external driver. The C2
Hospital Driver supports the patient during initial recovery
from surgery. As the patient becomes more stable, he or she
can be switched from the C2 Hospital Driver to the C2 Caddy,
and then to the Freedom Driver, a smaller, lighter pneumatic
pump.84 See Fig. 18B.6A to compare the different external driv-
ers available. Stable patients who meet the necessary criteria can
be discharged home with the Freedom Driver, which weighs
13.5 pounds and can be worn as a backpack or shoulder bag.84 It
is powered by two lithium-ion batteries, which can be recharged
When on the C2 Hospital Driver, noninvasive monitoring,
including beat rate, dynamic fill volumes, calculated outputs,
and hourly cardiac output, is provided by a full-color liquid
crystal display (LCD) touch screen.84 Typical programmed
ranges include a beat rate between 100 and 130 beats per min-
ute , systolic duration of 50% to 60%, right ventricular driv-
ing pressure 30 mmHg above the PAP (approximately 50–70
mmHg), left ventricular driving pressure 60 mmHg above sys-
temic pressure (approximately 180–200 mmHg), and filling
volumes around 50 to 60 mL per beat.82 Fig. 18B.7 illustrates
the CardioWest TAH.
Major TAH complications include78:
• Stroke
• Infection
• Bleeding
• Renal failure
• Chronic anemia
Physical Therapy Considerations
• Hemodynamic stability must be established by the medical
team before out-of-bed mobility can occur. Reports in the
literature indicate that rehabilitation begins approximately
4 to 7 days postimplantation.80,85,86
 Medical-Surgical Equipment in the Acute Care Setting     CHAPTER 18 427

A B
FIG. 18B.6
(A) SynCardia TAH external drivers (Freedom Portable Driver and Companion 2 Hospital Driver). (B) “Big Blue” Driver for SynCardia TAH. (A and B,
Courtesy syncardia.com.)

Aorta Aorta
Venae Pulmonary Venae Pulmonary
cavae artery cavae artery

Right Left Right Left

atrium atrium atrium atrium

Right Left Left

Right
Ventricle Ventricle Ventricle
Ventricle

TOTAL ARTIFICIAL HEART HUMAN HEART

FIG. 18B.7
Syncardia CardioWest total artificial heart. (Courtesy syncardia.com.)
428 CHAPTER 18     Medical-Surgical Equipment in the Acute Care Setting
• S afe exercise and increased endurance with TAH devices has
also been documented.80,85,86 See the articles by Nicholson
et al. and Kohli et al. for exercise parameters.
• Limited evidence exists regarding specific exercise parame-
ters for individuals with TAH. Therefore monitoring guide-
lines and exercise progression are similar to those in patients
with cardiac disease or implanted VADs.80,86
• Specific training needs to be completed by staff working
with the CardioWest TAH before initiating care and reha-
bilitation.80,86
• Device rate, flow, and volume; blood pressure; symptoms
of orthostasis; oxygen saturation; and exercise intolerance
(RPE) should be monitored throughout each treatment ses-
sion. The device is typically set at a fixed beat rate of 90 to
130 beats per minute with the cardiac output automatically
increasing up to 9.5 L/min.80,86
• Physical therapy should be modified or terminated if the pa-
tient is short of breath (at least 5/10 on the modified 10-grade
dyspnea scale) or reports exercise intolerance (greater than
13/20 on the Borg RPE scale), if the patient becomes or-
thostatic, if systolic blood pressure is less than 80 mmHg or
decreases by greater than 20 mmHg, if the device flow is less
than 3 L/min, if the device alarm is triggered, or if the thera-
pist notices neurologic changes (e.g., ataxia) or bleeding. The
medical team should be consulted for assistance during these
events.80,86
• Patients with TAH demonstrate a blunted blood pressure
response during exercise, and therefore clinicians should be
watchful for potential episodes of hypotension.86
• Ensuring pain control and proper posture can help prevent
driveline occlusion during splinting and/or altered trunk po-
sitions. Patients should not be positioned on the side of the
driveline or in the prone position.80
• Infection control is essential, particularly where drivelines
exit the body.80,85
• Sternal protection will be necessary if working with the pa-
tient for the first 8 to 10 weeks after implantation.80,86 Con-
sult with the medical team to determine specific time frames
and movement restrictions.
• Ensure all equipment is operational before ambulation. As-
sistance will be needed to move the large console during am-
bulation.80,85,86
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81. Platis A, Larson DF. CardioWest temporary total artificial heart.
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82. Yaung J, Arabia FA, Nurok M. Perioperative care of the patient
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 19
C H APT ER  
CHAPTER OUTLINE
Introduction
Cardiovascular System
Respiratory System
Musculoskeletal System
Central Nervous System
Oncology
Vascular System and Hematology
Gastrointestinal System
Genitourinary System
Infectious Disease
Endocrine System
Diabetes
Organ Transplantation
Pharmacologic Agents
Margarita V. DiVall
Adam B. Woolley
CHAPTER OBJECTIVE
The objective of this chapter is to provide the following:
1. An overview of the pharmacologic agents that are commonly prescribed as an adjunct to the medical-
surgical management of a wide variety of diseases and disorders to inform clinical practice in the acute care
setting
Introduction
Pharmacology is multifactorial in nature and applies to many body systems. The medications
in this chapter are organized according to systems (see the following index table). Both generic
and common brand name(s) are listed for each agent. Depending on the practice setting, you
may see generic names being used all the time (acute, inpatient setting) or brand names used
(outpatient setting). Many drugs are available as extended-release formulations. In that case,
several letters may be added to the generic/brand name of the drug. Among the common
abbreviations are XL, XT, and ER (extended release); SR (sustained release); and CR (controlled
release). It is likely that new drug formulations of previously approved agents may become
available on the market under various brand names after publication of this edition. Our rec-
ommendation is to identify the generic names of medications by utilizing Tables 19.1 to 19.45.
Pharmacy laws mandate the dispensing of a generic medication if it is available, even if the
physician writes a prescription using a brand name. A physician may indicate “No substitu-
tion” on the prescription if he or she desires only the proprietary drug to be dispensed.
For each type of medication in this chapter, a description of the indication(s), mechanism of
action, and side effects, as well as important physical therapy considerations are presented in
tables.1,2 Note that some pharmacologic agents specific to a certain subset are listed in another
chapter or appendix.
        431
The following is a list of tables in this chapter, organized according to body system and drug classes:
Table Topic
Cardiovascular System
Table 19.1 Antiarrhythmic Agents
Table 19.2 Anticoagulants
Table 19.3 Antihypertensive Agents
Table 19.3a Combination Drugs for Hypertension
Table 19.3b Medications for Pulmonary Hypertension
Table 19.4 Antiplatelet Agents
Table 19.5 Lipid-Lowering Agents
Table 19.6 Positive Inotropes (Pressors)
Table 19.7 Thrombolytics (Also Known as Fibrinolytics)
Respiratory System
Table 19.8 Adrenocortical Steroids (Glucocorticoids)
Table 19.9 Antihistamines
Table 19.10 Bronchodilators
Table 19.11 Leukotriene Modifiers and Other Nonsteroidal Antiinflammatory
Agents
Table 19.12 Mast Cell Stabilizers
Musculoskeletal System
Table 19.13 Disease-Modifying Antirheumatic Drugs (DMARDs)
Table 19.14 Muscle Relaxants and Antispasmodic Agents
Central Nervous System
Table 19.15 Antianxiety Medications
Table 19.16 Anticonvulsants
Table 19.17 Antidepressants
Table 19.18 Antipsychotics
Table 19.19 Mood Stabilizers
Table 19.20 Stimulants
Table 19.21 Medications for Substance Use–Related Disorders
Table 19.22 Multiple Sclerosis Medications
Table 19.23 Parkinson’s Disease Medications
Oncology
Table 19.24 Antiemetic Medications
Table 19.25 Chemotherapy
Vascular System and Hematology
Table 19.26 Colony-Stimulating Factors
Gastrointestinal System
Table 19.27 Antacids
Table 19.28 Antidiarrheal Medications
Table 19.29 Antispasmodic Medications
Table 19.30 Cytoprotective Medications
Table 19.31 Histamine-2 Receptor Antagonists (H2RAs)
Table 19.32 Laxatives
Table 19.33 Proton Pump Inhibitors (PPIs)
Genitourinary System
Table 19.34 Benign Prostatic Hyperplasia (BPH) Therapy
Table 19.35 Oral Contraceptives
Infectious Disease
Table 19.36 Antibiotics
Table 19.37 Antifungal Agents
Table 19.38 Antitubercular Agents
Table 19.39 Antiretroviral Medications
Table 19.40 Antiviral Medications
Endocrine System
Table 19.41 Hypoglycemic Agents
Table 19.42 Treatment of Hyperparathyroidism
Table 19.43 Treatment of Osteoporosis
Table 19.44 Treatment of Thyroid Disorders
Organ Transplantation
Table 19.45 Immunosuppressants
 

Cardiovascular System
TABLE 19.1  Antiarrhythmic Agents
Indications: Treatment and prevention of arrhythmias.
Precautions: All antiarrhythmic drugs are proarrhythmic. Monitor vital signs, ECG, and side effects.
Class: Mechanism of Action
Class I: Sodium channel blockers—
slow the fast sodium channels,
thereby controlling rate of
depolarization
Class Ia
Class Ib
Class Ic
Class II: Beta-blockers
Class III: Prolong the action
potential and refractory period in Pacerone), dronedarone
myocardial tissue; decrease AV
conduction and sinus node function
Class IV: Nondihydropyridine
calcium channel blockers
Miscellaneous
Slows conduction time through the
AV node, interrupting the reentry
pathways through the AV node
Direct suppression of the AV node
conduction to increase effective
refractory period and decrease
conduction velocity
AV, Atrioventricular node; CHF, chronic heart failure; ECG, electrocardiogram; GI, gastrointestinal; IV, intravenous.
Generic Name (Common
Brand Name[s])
disopyramide (Norpace)
procainamide (Pronestyl)
quinidine (Biquin,
Cardioquin)
lidocaine (Xylocaine),
tocainide (Tonocard),
mexiletine (Mexitil)
flecainide (Tambocor)
propafenone (Rythmol)
See Table 19.3.
amiodarone (Cordarone,
(Multaq)
dofetilide (Tikosyn)
ibutilide (Corvert)
sotalol (Betapace,
Betapace AF)
See Table 19.3.
adenosine (Adenocard,
Adenoscan)
digoxin (Lanoxin)
Pharmacologic Agents     CHAPTER 19 433
Physical Therapy
Adverse Effects Considerations
Class common side effects: Monitor for orthostasis.
anticholinergic, nausea, vomiting,
dizziness, drowsiness, fatigue
CHF Monitor for orthostasis.
Lupus, fever, hematologic toxicity
Hypotension, diarrhea, tinnitus
Disorientation, slurred speech, tinnitus, Monitor for orthostasis.
seizures, tremor
Visual disturbances, dyspnea, Monitor for orthostasis.
tachycardia, syncope
Angina, CHF, AV block, ECG
abnormalities, syncope, constipation
Amiodarone—ECG abnormalities, This drug concentrates
bradycardia, hypotension (IV form), in tissues and causes
pulmonary fibrosis, hepatotoxicity, toxicities in the heart,
thyroid dysfunction, corneal deposits, eyes, thyroid, and lungs.
photosensitivity, constipation, Any new symptoms should
blue-gray skin discoloration be reported. This agent
Dronedarone—designed to reduce has numerous drug–drug
toxicities associated with amiodarone, interactions.
but possibly less effective;
postmarketing case reports of acute
liver and renal failure, torsades de
pointes
Arrhythmias, dizziness, insomnia, Requires initiation in
headache, GI side effects inpatient setting with
constant telemetry
monitoring because of high
risk of arrhythmias in the
first 3 days.
Arrhythmias, hypotension,
bradycardia, headaches
Bradycardia, chest pain, fatigue, Has beta-blocking properties
dizziness, dyspnea, CHF, GI side and is associated with
effects similar side effects.
Facial flushing, headache, dizziness,
chest pressure, dyspnea
Anorexia, lethargy, confusion, visual
disturbances, ECG abnormalities,
arrhythmias
434 CHAPTER 19     Pharmacologic Agents

TABLE 19.2  Anticoagulants

Indications: Prevention and treatment of DVT and 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.
Physical therapy considerations for all of these agents: Do not perform deep tissue massage; implement 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 of Generic Name (Common Physical Therapy

Action
Coumarin derivatives—interfere
with synthesis of vitamin K–
dependent clotting factors that
decrease prothrombin
Direct thrombin
inhibitors—directly inhibit
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
Brand Name[s])
warfarin (Coumadin)
Intravenous—argatroban
(Argatroban), bivalirudin
(Angiomax), desirudin
(Iprivask)
Oral—dabigatran (Pradaxa)
Injection— fondaparinux
(Arixtra)
Oral— rivaroxaban (Xarelto),
apixaban (Eliquis),
edoxaban (Savaysa),
betrixaban (Bevyxxa)
heparin sodium
dalteparin sodium (Fragmin),
enoxaparin sodium
(Lovenox)
Adverse Effects
Systemic cholesterol
microembolism (purple toe
syndrome); rare
Gastrointestinal symptoms
(dyspepsia, gastritis) with
dabigatran
Thrombocytopenia
Heparin-induced
thrombocytopenia type 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
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 aPTT values are
associated with increased
bleeding risk; argatroban
causes false-positive
elevations in INR, and goal
INR during concomitant
argatroban warfarin therapy
is 4–5; dabigatran does
not require laboratory
monitoring.
Monitor neurologic
impairment if patient
is receiving neuraxial
anesthesia or is undergoing
spinal puncture; laboratory
monitoring of anticoagulant
effect not required.
aPTT monitoring is necessary
with goal values 1.5–2.5
times control. Goal range
differs by institution
(typically 60–80 seconds);
high aPTT values are
associated with increased
bleeding risk. Low doses
administered subcutaneously
for prophylaxis do not
require aPTT monitoring.
No special laboratory
monitoring required.
Anti-Xa monitoring may
be considered in select
populations (obesity,
pregnancy).

ACS, Acute coronary syndrome; aPTT, activated partial thromboplastin time; DVT, deep vein thrombosis; Hct, hematocrit; Hgb, hemoglobin; INR, international nor-
malized ratio; MI, myocardial infarction; PE, pulmonary embolism.

TABLE 19.3  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
Class: Mechanism of Action Brand Name[s])
Adrenergic agonists—stimulate alpha2- clonidine (Catapres, Catapres
adrenoceptors in the brainstem, thus TTS—transdermal patch)
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 (Minipress), tamsulosin
receptors, which results in vasodilation (Flomax), terazosin (Hytrin)
of veins and arterioles and a decrease
in total peripheral resistance and blood
pressure
Angiotensin-converting enzyme (ACE) captopril (Capoten),
inhibitors—inhibit conversion of enalapril (Vasotec),
angiotensin I to angiotensin II and fosinopril (Monopril),
therefore act to decrease excess water lisinopril (Prinivil, Zestril),
and sodium retention while also perindopril (Aceon),
preventing vasoconstriction quinapril (Accupril),
ramipril (Altace),
trandolapril (Mavik),
moexipril (Univasc),
benazepril (Lotensin)
Angiotensin II receptor blockers azilsartan (Edarbi),
(ARBs)—selectively antagonize candesartan (Atacand),
angiotensin II and therefore act to eprosartan (Teveten),
decrease excess water and sodium irbesartan (Avapro), losartan
retention while also preventing (Cozaar), olmesartan
vasoconstriction (Benicar), telmisartan
(Micardis), valsartan
(Diovan)
Beta-blockers—decrease myocardial oxygen Beta-1 selective—acebutolol
demand by decreasing sympathetic input (Sectral), atenolol (Tenormin),
to myocardium, therefore decreasing heart bisoprolol (Zebeta), esmolol
rate and contractility (Brevibloc), metoprolol
(Lopressor, Toprol XL)
Nonselective beta 1 and 2—
nadolol (Corgard), pindolol
(Visken), propranolol (Inderal)
Alpha- and beta-blockers—
carvedilol (Coreg), labetalol
(Normodyne)
Pharmacologic Agents     CHAPTER 19 435
Physical Therapy
Adverse Effects Considerations
Drowsiness, Clonidine can also be used
dizziness, dry as an epidural to control pain.
mouth, orthostasis, It takes 2–3 days to
headache, lethargy, see full efficacy after the first
weakness application of the transdermal
patch. Clonidine levels will
slowly decline over 2–3 days
after patch removal.
Drowsiness, dizziness, These agents should not
first dose syncope, be used for treatment of
palpitations, HTN caused by increased
orthostasis, weakness cardiovascular mortality
(ALLHAT trial) compared
with 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
males and females).
Common—cough, Report to other providers
hypotension, changes in urine output,
dizziness, muscle cramps (indicative
hyperkalemia of hyperkalemia), and swelling
Serious—renal or redness in the face and
failure, angioedema, neck area (indicative of
anaphylaxis, angioedema).
neutropenia
Common— Refer to ACE inhibitors above.
hypotension,
dizziness,
hyperkalemia
Serious—renal
failure, angioedema,
anaphylaxis
Common—smooth Negative inotropic effects
muscle spasm prevent heart rate to increase in
(bronchospasm), response to exercise; use Borg
exaggeration RPE scale to monitor exertion
of therapeutic rather than checking the pulse;
cardiac actions check blood sugar in patients
(bradycardia), fatigue, with diabetes before exercise
insomnia, masking and administer a carbohydrate
of hypoglycemic snack with blood sugar ≤
symptoms in diabetics 100 mg/dL before exercise.
(except diaphoresis),
impaired glucose
tolerance, lipid
abnormalities, exercise
intolerance
Serious—AV block
Continued
436 CHAPTER 19     Pharmacologic Agents

TABLE 19.3  Antihypertensive Agents—cont’d

Generic Name (Common Physical Therapy
Class: Mechanism of Action Brand Name[s]) Adverse Effects Considerations
Calcium channel blockers—inhibit calcium Non-DHP: verapamil (Isoptin, Bradycardia, Non-DHP CCB will decrease
ion from entering the “slow channels” or Calan, Verelan, Covera-HS), hypotension, AV block, the heart rate and prevent
select voltage-sensitive areas of vascular diltiazem (Cardizem, Tiazac, CHF, constipation and heart rate increase in response
smooth muscle and myocardium during Cartia XT) gingival hyperplasia to exercise, similarly to beta-
depolarization, producing a relaxation DHP: amlodipine (Norvasc), (with verapamil) blockers.
of coronary vascular smooth muscle felodipine (Plendil), nifedipine Hypotension, peripheral DHP-CCBs have more effects
and coronary vasodilation; increase (Procardia XL, Adalat CC), edema, flushing, in the peripheral vasculature
myocardial oxygen delivery in patients isradipine (DynaCirc), palpitations, headaches, versus non-DHP CCBs, which
with vasospastic angina; non-DHP CCB nicardipine (Cardene), gingival hyperplasia have more central cardiac
also slow automaticity and conduction of nimodipine (Nymalize) (with nifedipine) effects.
AV node
Diuretics
Thiazide diuretics—inhibit sodium chlorthalidone (Hygroton), Hypotension, orthostasis, All diuretics can cause volume
reabsorption in the distal tubules causing hydrochlorothiazide (Esidrix, volume depletion, depletion. Monitor weight,
increased excretion of sodium and water as HydroDIURIL), indapamide hypokalemia, urine output for changes in
well as potassium and hydrogen ions (Lozol), metolazone hyponatremia, renal function, orthostasis,
(Zaroxolyn), methyclothiazide photosensitivity, serum electrolytes (will
(Aquatensen) hyperuricemia, decrease), signs and symptoms
hyperglycemia of gout (caused by increase in
uric acid).
Loop diuretics—inhibit reabsorption of bumetanide (Bumex), furosemide Hyperglycemia,
sodium and chloride in the ascending loop (Lasix), torsemide (Demadex) hyperuricemia,
of Henle, thus causing increased excretion hypokalemia,
of water, sodium, chloride, magnesium, hypocalcemia,
phosphate, and calcium hypomagnesemia,
hypotension, excessive
urination, dehydration,
orthostasis
Potassium-sparing diuretics—interfere amiloride (Midamor), eplerenone Hyperkalemia, dizziness,
with potassium/sodium exchange (active (Inspra), spironolactone hypotension
transport) in the distal tubule, cortical (Aldactone, CaroSpir), With spironolactone—
collecting tubule, and collecting duct; triamterene (Dyrenium; Gynecomastia, breast
spironolactone is an aldosterone antagonist Maxzide [in combination with pain, hyperkalemia,
hydrochlorothiazide]) hyponatremia,
dehydration,
hyperchloremic
metabolic acidosis in
decompensated hepatic
cirrhosis, inability to
achieve or maintain
an erection, irregular
menses, amenorrhea,
postmenopausal
bleeding
Carbonic anhydrase inhibitors—inhibit acetazolamide (Diamox), di- Flushing, dizziness, Because of toxicities, these are
carbonic anhydrase enzyme, resulting in chlorphenamide (Daranide), drowsiness, fatigue, not used as diuretics, but can
reduction of hydrogen ion secretion at methazolamide (Neptazane) allergic reactions, be used to treat glaucoma,
renal tubule and an increased renal excre- hyperglycemia or hy- acute mountain sickness, or
tion of sodium, potassium, bicarbonate, poglycemia, hypoka- metabolic alkalosis.
and water lemia, hyponatremia,
metabolic acidosis,
kidney stones, hepatic
insufficiency, myopia

TABLE 19.3  Antihypertensive Agents—cont’d
Class: Mechanism of Action
Nitrates—relax vascular smooth muscle;
decrease venous ratios and arterial blood
pressure; reduce left ventricular work;
decrease myocardial O2 consumption;
in addition to hypertension indication,
often used in patients with ischemic heart
disease
Renin inhibitors—inhibit renin, resulting
in blockade of the conversion of angioten-
sinogen to angiotensin I
Vasodilators—direct vasodilation of arte-
rioles (with little effect on veins) with
decreased systemic resistance
Sacubitril—prodrug; inhibits neprilysin,
leading to increased levels of natriuretic
peptides
Valsartan—produces direct antagonist of the
angiotensin II receptors
Miscellaneous—selectively inhibits
hyperpolarization-activated cyclic
nucleotide-gated (HCN) channels within
the sinoatrial node of cardiac tissue,
resulting in disruption of the ion current
flow prolonging diastolic depolarization,
slowing firing in the SA node and reduc-
ing heart rate
ACE, Angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BPH, benign prostatic hyperplasia; CCB, calcium channel blockers; CK, creatinine kinase;
CNS, central nervous system; DHP, dihydropyridine; HTN, hypertension; IV, intravenous; NTG, nitroglycerin; RPE, rating of perceived exertion.
Generic Name (Common
Brand Name[s])
amyl nitrite (Aspirol, Vapor-
ole; inhalation), nitroglycerin
(NTG) (dosage forms: sublin-
gual, spray, percutaneous oint-
ment, oral, sustained release,
IV) (Nitro-Bid, Nitrostat;
Nitro-Dur, Transderm-Nitro,
Nitrodisc; transdermal patch),
isosorbide dinitrate (Isordil,
Sorbitrate; sublingual, oral,
chewable), isosorbide mononi-
trate (ISMO)
aliskiren (Tekturna)
hydralazine (Apresoline), minoxi- Headache, hypotension,
dil (Loniten)
sacubitril/valsartan (Entresto)
ivabradine (Corlanor)
Pharmacologic Agents     CHAPTER 19 437
Physical Therapy
Adverse Effects Considerations
Hypotension, orthostasis, Patients with ischemic heart dis-
flushing, tachycardia, ease should always carry rapid-
headache, dizziness acting NTG (sublingual or
spray). In acute care settings,
find out where rapid-acting
NTG is stored (e.g., nursing
station, medication dispensing
cabinet, etc.) to help patient
gain access quickly. Patients
may take a dose to prevent
exercise induced angina. In
case of angina, sit down and
administer 1 tablet (under the
tongue) or spray up to 3 times
every 5 minutes. If no relief
5 minutes after the first dose,
call 911. Sublingual NTG
tablets have specific storage
requirements that should be
followed (avoid heat, moisture,
light). If tablets no longer have
their shape, NTG is likely to
be expired and may not be ef-
fective. Monitor for orthostasis.
Avoid heat/ice near nitro paste/
patch.
Dizziness, rash, hyperka- Monitor muscle cramps associ-
lemia, increases in se- ated with hyperkalemia. Moni-
rum creatinine, cough, tor urine output and weight
increase in serum CK, for renal dysfunction.
diarrhea
Monitor blood pressure and
compensatory sympa- heart rate. Patients are at risk
thetic reflex causing for orthostasis. Use caution.
increased heart rate,
lupus with long-term
hydralazine
Hypotension, hyperkale- Monitor for hypersensitivity re-
mia, cough, increased actions (angioedema). Patients
serum creatinine are at risk for orthostasis.
Bradycardia, hyperten- Monitor blood pressure and
sion, atrial fibrillation, heart rate.
vision changes (phos-
phene)
438 CHAPTER 19     Pharmacologic Agents

TABLE 19.3A  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 are many 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 as generic drugs. The fixed-dose combinations may also be more difficult to
titrate at the start of drug therapy as opposed to individual components. Physical therapists should consider the side effects, and monitor all
individual components of the combination antihypertensives, especially when the team is working on determining the correct therapeutic dose.
(See Table 19.3.)

Combination Type Fixed-Dose Combination, mga Trade Name

ACEIs and CCBs
ACEIs and diuretics
ARBs and diuretics
ARB and rennin inhibitor
ARBs, CCB, and diuretics
BBs and diuretics
Centrally acting drug and
diuretic
Diuretic and diuretic
HTN and lipid lowering
agents
Renin inhibitor and CCB
Renin inhibitor, CCB, and
diuretic
aSome 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; CCB, calcium channel blocker; HTN, hypertension.
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
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
Azilsartan medoxomil–chlorthalidone (40/12.5, 40/25) Edarbyclor
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 (20/12.5, 40/12.5, 40/25) Benicar HCT
Telmisartan–hydrochlorothiazide (40/12.5, 80/12.5) Micardis-HCT
Valsartan–hydrochlorothiazide (80/12.5, 160/12.5, 160/25) Diovan-HCT
Valsartan–aliskiren (160/150), (320/300) Valturna
Olmesartan medoxomil–amlodipine–hydrochlorothiazide (20/5/12.5), Tribenzor
(40/10/25)
Valsartan–amlodipine–hydrochlorothiazide (320/10/25) Exforge HCT
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
Methyldopa–hydrochlorothiazide (250/15, 250/25, 500/30, 500/50) Aldoril
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
Amiloride–hydrochlorothiazide (5/50) Moduretic
Spironolactone–hydrochlorothiazide (25/25, 50/50) Aldactazide
Triamterene–hydrochlorothiazide (37.5/25, 75/50) Dyazide, Maxzide
Amlodipine–atorvastatin (5/10, 5/20, 5/40, 5/80, 10/10, 10/20, 10/40, 10/80) Caduet
Aliskiren–amlodipine (150/5), (300/10) Tekamlo
Aliskiren–amlodipine–hydrochlorothiazide (300/10/25) Amturnide
 Pharmacologic Agents     CHAPTER 19 439

TABLE 19.3B  Medications for Pulmonary Hypertension

Indications: Vasodilatory agents used in the treatment of pulmonary arterial hypertension.

Generic Name (Common

Mechanism of Action
Phosphodiesterase-5 (PDE5)
inhibitors—inhibit
hydrolysis of cyclic
guanosine monophosphate,
resulting in vasodilation
Prostacyclin analogs—
promote direct arterial
vasodilation and inhibits
platelet aggregation
Endothelial receptor
antagonists—antagonize
endothelin (ET) receptor
Soluble guanylate cyclase
stimulator—stimulates
soluble guanylate cyclase,
both independently and
synergistically to the nitric
oxide signaling path
Brand Name[s])
sildenafil (Revatio, Viagra),
tadalafil (Cialis, Adcirca)
epoprostenol (Flolan, Veletri),
treprostinil (Remodulin)
bosentan (Tracleer),
ambrisentan, Macitentan
(Opsumit)
riociguat (Adempas)
Adverse Effects
Headache, flushing, visual
disturbances, dyspepsia,
epistaxis
Headache, nausea and
vomiting, hypotension,
bradycardia, flushing,
diarrhea
Respiratory tract infection,
headache, edema,
hepatotoxicity
Palpitations, peripheral
edema, headache, nausea,
anemia, hypotension
Physical Therapy Considerations
Monitor for signs and symptoms of
low blood pressure, vision loss, or
priapism.
These agents are very potent
vasodilators. Monitor for signs and
symptoms of hypotension.
Monitor for signs and symptoms
of liver injury (e.g., jaundice,
abdominal pain, nausea and
vomiting) and fluid retention.
Monitor for signs and symptoms of
serious bleeding, hypotension, and
fluid retention.

TABLE 19.4  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 Physical Therapy

Class: Mechanism of Action Brand Name[s]) Adverse Effects Considerations
Glycoprotein IIb/IIIa inhibitors— abciximab (ReoPro) Produce potent Only used for short-term therapy,
block the platelet glycoprotein IIb/ eptifibatide (Integrilin) antiplatelet effect with typically, in combination
IIIa receptor, the binding site for tirofiban (Aggrastat) high risk of bleeding with other antiplatelet and
fibrinogen, von Willebrand factor, and anticoagulant agents; high risk
other ligands. Inhibition of binding of bleeding.
at this final common receptor blocks
platelet aggregation and prevents
thrombosis
Salicylates—inhibit cyclooxygenase; aspirin (many brand names, Well tolerated at Many NSAIDs may decrease the
block prostaglandin synthetase available OTC) 81–325 mg antiplatelet effects of aspirin;
action, which prevents formation of aspirin/dipyridamole Common—dyspepsia, if used concomitantly, patient
the platelet-aggregating substance (Aggrenox) minor bleeding should take aspirin 2 hours
thromboxane A2 Serious—anaphylaxis, before NSAID.
bronchospasm, severe
bleeding
Thienopyridine—blocks ADP Intravenous—cangrelor Common—dyspepsia, High risk of bleeding.
receptors, which prevent fibrinogen (Kengreal) gastritis, minor
binding at that site and thereby Oral—clopidogrel (Plavix), bleeding, dyspnea
reduce the possibility of platelet prasugrel (Effient), (ticagrelor)
adhesion and aggregation ticagrelor (Brilinta) Serious—bleeding
Reversible antagonist of the protease- vorapaxar (Zontivity) Hemorrhage (including
activated receptor-1 (PAR-1) expressed GI), anemia
on platelets—inhibits platelet
aggregation induced by thrombin and
thrombin receptor agonist peptides.
Used in patients with thrombosis and
history of myocardial infarction or
peripheral arterial disease

ADP, Adenosine diphosphate; NSAID, nonsteroidal antiinflammatory drug.

440 CHAPTER 19     Pharmacologic Agents

TABLE 19.5  Lipid-Lowering Agents

Indications: Treatment of dyslipidemia.

Generic Name (Common

Class: Mechanism of Action Brand Name[s]) Adverse Effects Physical Therapy Considerations
Bile acid sequestrants—bind bile cholestyramine (Questran), Constipation, dyspepsia, These drugs cause significant GI
acids including glycocholic acid colesevelam (Welchol), flatulence discomfort. Ask the patient when
in the intestine, impeding their colestipol (Colestid) the symptoms are less severe to
reabsorption. Increase the fecal loss of schedule your sessions.
bile salt–bound LDL-C.
Cholesterol absorption inhibitor— ezetimibe (Zetia) Dizziness, headache, This medication is well tolerated.
inhibits absorption of cholesterol diarrhea Often combined with a statin for
at the brush border of the small additional LDL reduction.
intestine; leads to 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 bezafibrate (Bezalip), Constipation, LFT Monitor for hepatotoxicity: yellow
acid is believed to increase VLDL fenofibrate (Antara, abnormalities skin/sclera, abdominal pain. If
catabolism by enhancing the Lipofen, Tricor), combined with a statin, higher
synthesis of lipoprotein lipase; gemfibrozil (Lopid) potential for hepatotoxicity and
as a result of a decrease in VLDL muscle toxicity.
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)— fish oil—available in Dyspepsia, fishy odor,
mechanism not completely defined many formulations taster perversion
yet; possible mechanisms include OTC; because of concern
inhibition of acetyl CoA:1,2 over impurities in OTC
diacylglycerol acyltransferase, formulations, there is
increased hepatic beta-oxidation, or a one product (Omacor)
reduction in the hepatic synthesis of available by prescription
triglycerides. only
HMG-CoA reductase inhibitors atorvastatin (Lipitor, Headache, GI toxicity, LFTs must be monitored routinely,
(statins)—inhibit 3-hydroxy- Liptruzet [in hepatotoxicity, muscle monitor for hepatotoxicity.
3-methylglutaryl coenzyme A combination with pain and weakness, Patients with muscle pain not
(HMG-CoA) reductase, the rate- ezetimibe]), fluvastatin rhabdomyolysis (rare) related to exercise should be
limiting enzyme in cholesterol (Lescol), lovastatin referred to their providers to check
synthesis (reduces the production of (Mevacor), pitavastatin for muscle breakdown (CK levels
mevalonic acid from HMG-CoA); (Livalo), pravastatin are typically checked).
results in a compensatory increase (Pravachol), rosuvastatin
in the expression of LDL receptors (Crestor), simvastatin
on hepatocyte membranes and a (Zocor)
stimulation of LDL catabolism
Nicotinic acid—inhibits synthesis of niacin (Niacor; Niaspan; Edema, flushing, Monitor blood pressure and heart
VLDLs Slo-Niacin [OTC]). hypotension, rate and orthostasis, signs and
orthostasis, symptoms of hyperglycemia, and
palpitations, gout. Monitor for hepatotoxicity.
tachycardia,
hyperglycemia,
hyperuricemia,
hepatotoxicity
PCSK9 inhibitors—inhibit proprotein evolocumab (Repatha), Hypertension, dizziness, Monitor for signs and symptoms of
convertase subtilisin kexin 9; cause alirocumab (Praluent) fatigue, rash, nausea, hypersensitivity reactions.
decreased degradation of LDL nasopharyngitis,
receptors and increased clearance of injection site reactions
LDL

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 19.6  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 Brand Name[s]) Adverse Effects Physical Therapy Considerations
Agents in this class increase dopamine, dobutamine, Increase BP and HR, chest These agents are used acutely,
cardiac output via epinephrine (Adrenalin, pain, ischemia, ACS, typically in unstable patients
stimulating alpha, beta, and/ EpiPen), norepinephrine arrhythmia in the ICU setting. Outpatient
or dopaminergic receptors (Levophed), phenylephrine intermittent infusions can be used
(Neo-Synephrine), in severe heart failure. Monitor
vasopressin (Pitressin) vitals and avoid exertion.
ACS, Acute coronary syndrome; BP, blood pressure; HR, heart rate; ICU, intensive care unit.

TABLE 19.7  Thrombolytics (Also Known as Fibrinolytics)

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

Generic Name (Common Physical Therapy

Mechanism of Action
Agents in this class initiate
fibrinolysis by binding
to fibrin and converting
plasminogen to plasmin
IV, Intravenous.
Brand Name[s])
alteplase (Activase, Cathflo),
reteplase (Retavase),
tenecteplase (TNKase),
Adverse Effects
Bleeding at various sites,
including intracranial
hemorrhage
Considerations
These agents are used acutely IV,
typically in unstable patients.
Risk of bleeding is very high
and may outweigh the benefit
of clot lysis and restoration of
blood flow. Physical therapy
is often withheld in patients
immediately after thrombolysis.

   
Respiratory System

 
TABLE 19.8  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 Brand

Mechanism of Action Name[s])
Agents in this Systemic—dexamethasone
class prevent the (Decadron), fludrocortisone
accumulation of (Florinef), hydrocortisone (Cortef,
inflammatory Solu-Cortef), methylprednisolone
cells at the (Depo-Medrol, Medrol), prednisone
infection site, (Deltasone, Sterapred, Sterapred
inhibit lysosomal DS), prednisolone (Orapred,
enzyme release Pediapred, Prelone), triamcinolone
and chemical (Aristocort)
mediators of Inhaled—beclomethasone (Beclovent,
inflammatory Vanceril), budesonide (Pulmicort),
response, reduce flunisolide (AeroBid), fluticasone
capillary dilatation propionate (Flovent, Advair [in
and permeability combination with salmeterol]),
fluticasone furoate (Arnuity Ellipta),
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
Physical Therapy 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—implement
caution when exercising and
prescribe weight-bearing exercises
that promote bone health; reinforce
compliance—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 increase the risk
of systemic side effects, especially
osteoporosis
442 CHAPTER 19     Pharmacologic Agents
TABLE 19.9  Antihistamines
Indications: To decrease inflammation and bronchoconstriction associated with hypersensitivity reactions, such as allergic rhinitis.
Mechanism of Action
Agents in this class reduce
or prevent the physiologic
effects of histamine by
competing for histamine
binding sites
TABLE 19.10  Bronchodilators
Indications: To relieve bronchospasm associated with obstructive pulmonary disease, asthma, and exercise-induced bronchospasm.
Mechanism of Action
Anticholinergics—block
the action of acetylcholine
at parasympathetic sites in
bronchial smooth muscle
causing bronchodilation;
also decrease mucous
secretion and play greater
role in the management of
COPD
Beta-2 agonists—relax
bronchial smooth muscle
by action on beta-2-
receptors with little effect
on heart rate
Theophylline—causes
bronchodilation, diuresis,
CNS and cardiac
stimulation, and gastric
acid secretion by blocking
phosphodiesterase,
which increases tissue
concentrations of cyclic
adenine monophosphate
(cAMP)
Combination: Advair (fluticasone + salmeterol); Combivent (albuterol + ipratropium); Dulera (mometasone + formoterol); Symbicort (budesonide + formoterol); Breo
Ellipta (vilanterol + fluticasone furoate); Anoro Ellipta (vilanterol + umeclidinium bromide).
CNS, Central nervous system; COPD, chronic obstructive pulmonary disease; GI, gastrointestinal; PVC, premature ventricular contraction.
Generic Name (Common
Brand Name[s])
azelastine (Astelin),
chlorpheniramine maleate
(Chlor-Trimeton), cetirizine
(Zyrtec), clemastine (Tavist),
desloratadine (Clarinex),
diphenhydramine (Benadryl,
various), fexofenadine
(Allegra), loratadine (Alavert,
Claritin)
Generic Name (Common
Brand Name[s])
ipratropium bromide
(Atrovent), tiotropium
(Spiriva), Umeclidinium
bromide (Incruse Ellipta)
Short-acting—albuterol
(Proventil, Ventolin),
arformoterol (Brovana),
epinephrine (various),
isoproterenol (Isuprel),
levalbuterol (Xopenex),
metaproterenol (Alupent),
pirbuterol (Maxair)
Long-acting—formoterol
(Foradil), salmeterol
(Serevent), vilanterol
(Trelegy Ellipta)
Ultralong-acting—indacaterol
(Arcapta Neohaler)
theophylline (Elixophyllin,
Quibron, Theo-24,
TheoCap, Theochron,
Uniphyl)
Adverse Effects
Drowsiness, dizziness,
decreased coordination,
orthostatic hypotension,
hypotension, hypertension,
palpitations, bradycardia,
tachycardia, epigastric
distress, urinary frequency,
thickening of bronchial
secretions, dry mouth
Adverse Effects
Bronchitis, palpitations, dizziness,
dry mouth
Common—tachycardia,
palpitations
Rare—increased blood pressure,
angina, hypokalemia
Appropriate therapeutic range is
5–20 mcg/mL
At therapeutic concentrations—
nervousness, insomnia,
tachycardia, nausea and vomiting
15–25 mcg/mL—GI upset,
diarrhea, nausea/vomiting,
abdominal pain, nervousness,
headache, insomnia, agitation,
dizziness, muscle cramp, tremor
25–35 mcg/mL—tachycardia,
occasional PVCs
>35 mcg/mL: Ventricular
tachycardia, frequent PVCs,
seizure
Physical Therapy
Considerations
If patient experiences drowsiness,
avoid scheduling physical
therapy session within a few
hours of administration with
short-acting formulations.
Many are available in 12-hour
and 24-hour formulations, so
ask patient and medical team
when he or she feels the most
sedation.
Physical Therapy
Considerations
Short-acting beta-2 agonists
are often referred to as
“rescue” inhalers. In patients
with asthma and COPD,
maintenance therapy should
minimize the use of short-
acting beta-2 agonists. Observe
if patients are using their
rescue inhalers too often, and
refer them to their health care
provider to titrate maintenance
therapy.
Encourage patients who have
exertion- or exercise-induced
bronchospasm to administer
beta-2 agonists 10–15 minutes
before therapy sessions.
Bronchodilator administration
can also facilitate airway
clearance therapy effectiveness.
Monitor for signs and symptoms
of toxicity. Theophylline has
many drug interactions, and
levels can rapidly change.
Caffeine intake will exacerbate
side effects.
 Pharmacologic Agents     CHAPTER 19 443

TABLE 19.11  Leukotriene Modifiers and Other Nonsteroidal Antiinflammatory Agents

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

Generic Name (Common Physical Therapy

Mechanism of Action
Leukotriene receptor
antagonist—selective
competitive inhibitor of
LTD4 and LTE4 receptors;
5-lipoxygenase inhibitor
Phosphodiesterase type 4
inhibitor
Brand Name[s])
montelukast (Singulair),
zafirlukast (Accolate), zileuton
(Zyflo)
roflumilast (Daliresp)
Adverse Effects
Montelukast and zafirlukast
well tolerated with infrequent
cough, dizziness, fatigue,
dyspepsia; zileuton can cause
hepatotoxicity
Nausea, reduced appetite and
weight loss, abdominal pain,
diarrhea, sleep disturbances,
headache, back pain, dizziness
Considerations
Monitor for abdominal pain,
yellow skin, and sclera
appearance with zileuton.
This medication has a lot of drug
interactions, educate patients
to avoid making medication
changes without discussions
with providers.

COPD, Chronic obstructive pulmonary disease; LTD4, leukotriene D4; LTE4, leukotriene E4.

TABLE 19.12  Mast Cell Stabilizers

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

Generic Name (Common Physical Therapy

Mechanism of Action Brand Name[s]) Adverse Effects Considerations
Agents in this class decrease cromolyn (Intal), nedocromil Well tolerated; May take up to 2 weeks to see
histamine release from mast cells; (Tilade) unpleasant taste with complete response, which
block early and late reaction to nedocromil can be seen after patient is
allergen; inhibit acute response to discharged. Effective to prevent
exercise, cold dry air, and sulfur exercise-induced asthma.
oxide

  

Musculoskeletal System

TABLE 19.13  Disease-Modifying Antirheumatic Drugs (DMARDs)

Indications: Treatment of rheumatoid arthritis (RA). Refer to Chapter Appendix 13A.
Unlike nonsteroidal antiinflammatory drugs (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 erythrocyte sedimentation rate and C-reactive protein (CRP) levels, and/or radiographic evidence of joint damage. Methotrexate is
considered a first-line agent among DMARDs because of 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 antiinflamma-
tory agents that can lead to immunosuppression. Physical therapists should follow infection-control measures, such as good hand hygiene, sani-
tizing of equipment, and avoiding contact with patients if feeling sick. DMARDs are listed in alphabetical order, not in the order of preference,
in the table below. Corticosteroids are frequently used as part of RA therapy, typically for short courses (see Table 19.8).

Generic Name (Common

Mechanism of Action
Selective costimulation
modulator; inhibits T-cell
(T-lymphocyte) activation.
Activated T lymphocytes are
found in the synovium of
rheumatoid arthritis patients
Blocks biologic activity of
interleukin-1 (IL-1)
Brand Name[s])
abatacept (Orencia)
anakinra (Kineret)
Adverse Effects
Headache, nausea, high risk of
infections (54% incidence), COPD
exacerbations, hypertension,
dizziness, cough, back pain, infusion-
related reactions
Injection site reactions are very
common; also, headache, nausea,
diarrhea, sinusitis, flulike symptoms,
abdominal pain, and infections
Physical Therapy Considerations
Monitor blood pressure (may
increase). Monitor for and report
any new symptoms associated
with infections: increase in
WBC count, fever, cough, skin
infections.
Monitor skin appearance for
injection site reactions. Exercise
infection-control measures.
Continued
444 CHAPTER 19     Pharmacologic Agents

TABLE 19.13  Disease-Modifying Antirheumatic Drugs (DMARDs)—cont’d

Mechanism of Action
Bind and inhibit tumor necrosis
factor (TNF), which produces
potent antiinflammatory effect
Antagonizes purine metabolism azathioprine (Imuran)
and may inhibit synthesis of
DNA, RNA, and proteins; may
also interfere with cellular me-
tabolism and inhibit mitosis
Mechanism of action unknown;
appear to suppress the synovitis gold sodium thiomalate
possibly through stimulation of
protective IL-6 and IL-10.
May inhibit IL-1 release by
monocytes, thereby decreasing
macrophage chemotaxis and
phagocytosis
Inhibits dihydro-orotate dehy-
drogenase (an enzyme involved
in the de novo pyrimidine syn-
thesis) and has antiproliferative
and antiinflammatory effect
Inhibits dihydrofolate reduc-
tase and interferes with DNA
synthesis, repair, and cellular
replication
Sulfasalazine—broken down by
intestinal flora into 5-amino-
salicylic acid and sulfapyridine;
sulfapyridine—likely inhibits
endothelial cell proliferation,
reactive oxygen species, and
cytokines
IL-6 inhibitor
Janus kinase (JAK) inhibitor—
interferes with hematopoiesis
and immune cell function
Generic Name (Common
Brand Name[s])
Anti–tumor necrosis factor Rash, headache, nausea, cough
therapy: adalimumab Serious: associated with infections,
(Humira), certolizumab
pegol (Cimzia), etanercept
(Enbrel), golimumab
(Simponi), infliximab
(Remicade)
gold compounds
(Myochrysine), auro-
thioglucose (Solganal),
auranofin (Ridaura)
hydroxychloroquine
(Plaquenil)
leflunomide (Arava)
methotrexate (Rheumatrex)
sulfasalazine (Azulfidine)
tocilizumab (Actemra)
tofacitinib (Xeljanz)
Adverse Effects
including serious mycobacterial, fun-
gal, and opportunistic complications
Dose-related bone marrow suppression,
stomatitis, diarrhea, rash, and liver
failure
With IM injections, patients can Monitor skin appearance for rash.
experience injection reactions—flush- Avoid scheduling physical therapy
ing, weakness, dizziness, sweating,
syncope, hypotension
Common—rash ranging from simple
erythema to exfoliative dermatitis;
oral formulation causes nausea, diar- the injection site has no adverse
rhea, taste disturbances
Rare—renal disease, leukopenia,
thrombocytopenia
Rash, abdominal cramping, diarrhea,
myopathy, skin pigment changes,
peripheral neuropathy
Serious: retinal damage that can lead to extremities. Patients should be
vision loss
Diarrhea, alopecia, hypertension, rash,
hepatotoxicity, peripheral neuropathy
Common—nausea, vomiting, and
stomatitis
Serious—hepatotoxicity, bone marrow
suppression, pulmonary toxicity
Headache, GI intolerance, taste percep- Ask patient about GI side effects
tion disturbances, rash, leukopenia,
thrombocytopenia
Serious—severe infections
Increased HDL/LDL, headache, urinary
tract infections, nasopharyngitis, GI
perforation, anemia, increased risk of
cancers, opportunistic infections
Physical Therapy Considerations
Patients are at high risk for
infection. Monitor for any signs
and symptoms including fever,
productive cough, and increase in
WBC count. Exercise infection-
control measures.
Monitor WBC count (will decrease;
patients will be at high risk
for infection), hematocrit (will
decrease; patient will complain of
fatigue), platelets (will decrease;
the risk of bleeding will increase).
sessions immediately and soon
after the IM injection (injections
are scheduled every 2–3 weeks
and then monthly). Ensure that
reaction before initiating therapy.
Monitor for muscle pain not as-
sociated with exercise. Monitor
for tingling and numbness of the
evaluated by ophthalmologist
every 6–12 months. Report any
vision changes.
Monitor liver function (abdominal
pain, yellow skin and sclera).
Risk of hepatotoxicity is higher
when used in combination with
methotrexate.
Ask patients about GI side effects
to optimize scheduling physical
therapy sessions. Monitor WBC
count (will decrease; use infec-
tion-control measures), hemato-
crit (will decrease; patient will
complain of fatigue), and platelets
(will decrease; patient will be at a
higher risk of bleeding).
to optimize scheduling of the
session. Use infection-control
measures if WBC count decreases
(wash hands, sanitize equipment,
avoid contact with patient if
sick). Use caution if the platelet
count decreases (patient will be at
higher risk of bleeding).
Monitor for signs and symptoms of
infection. Monitor liver function
in adults and children.
Monitor patients for signs and
symptoms of new infections.
Encourage patient to report symp-
toms to providers.

COPD, Chronic obstructive pulmonary disease; GI, gastrointestinal; HDL, high-density lipoprotein; IM, intramuscular; LDL, low-density lipoprotein; WBC, white
blood cell.

TABLE 19.14  Muscle Relaxants and Antispasmodic Agents
Baclofen, tizanidine, dantrolene, and botulinum toxin are best reserved for spasticity, as opposed to acute musculoskeletal conditions. Adverse
effects common to all muscle relaxants include drowsiness, dizziness, and GI effects. CNS depression is additive with other CNS depressants
(e.g., opioids).
Mechanism of Action
Structural analog of
GABA; inhibits spinal
reflexes
Acetylcholine release
inhibitor and a
neuromuscular
blocking agent used
to relieve spasm and
cervical dystonia
Acts in brainstem and
spinal cord to relieve
muscle spasm, pain,
and tenderness
Interferes with calcium
release from the
sarcoplasmic reticulum
Muscle relaxation
through neuronal
inhibition via GABA
receptors
Inhibits motor neurons
by stimulating alpha-2
receptors; structurally
related to clonidine
Unknown mechanism;
may act as an analgesic
Unknown mechanism;
may act as a sedative
CNS, Central nervous system; GABA, gamma-aminobutyric acid.
Generic Name (Common Brand
Name[s])
baclofen (Lioresal [available for
intrathecal administration])
botulinum toxin A (Botox,
Dysport, Myobloc)
cyclobenzaprine (Flexeril, Amrix
extended-release capsules)
dantrolene (Dantrium)
diazepam (Valium), lorazepam
(Ativan), and other
benzodiazepines
tizanidine (Zanaflex)
orphenadrine (Norflex)
carisoprodol (Soma),
chlorzoxazone (Parafon
Forte), metaxalone (Skelaxin),
methocarbamol (Robaxin)
Pharmacologic Agents     CHAPTER 19
Adverse Effects
Withdrawal syndrome (e.g.,
hallucinations, psychosis,
seizures)
Muscular weakness, dysphagia,
dry mouth, injection site
discomfort, fatigue, headache,
neck pain, musculoskeletal
pain, dysphonia, injection site
pain, and eye disorders
Sedation, anticholinergic side
effects (e.g., dry mouth), can
cause cardiovascular side effects
at higher doses
Dose-dependent hepatotoxicity
(onset between 3 and 12
months of therapy)—most
common in females over
35 years and can be severe
(fatalities reported); dose-
dependent diarrhea
Sedation
Hypotension, hepatotoxicity
(usually reversible, rarely fatal),
hallucinations/ delusions,
withdrawal (hypertension,
tachycardia, hypertonia)
Anticholinergic (e.g., dry mouth,
urinary retention)
Sedation; some will exhibit
hypersensitivity with these
agents; mild withdrawal
syndrome; methocarbamol
causes urine discoloration
(brown, black, green)
445
Physical Therapy Considerations
Useful for spasticity and muscle
spasms. Causes only transient
drowsiness. Be aware of
withdrawal syndrome, and
educate patients on avoiding
abrupt discontinuation.
Monitor for side effects and efficacy
of injections.
Structurally related to a tricyclic
antidepressant; has drug
interactions—advise your
patients to alert health care
providers about any medication
change; schedule physical therapy
sessions when patient is least
drowsy.
Monitor for signs and symptoms of
hepatotoxicity (e.g., abdominal
pain, icterus, and jaundice);
establish optimal time for
physical therapy based on side
effects.
Schedule physical therapy sessions
when patient is least drowsy.
Monitor blood pressure; avoid
abrupt discontinuation; this
agent has many drug interactions
(avoid drugs that prolong QT
interval)—advise patients
to notify providers of any
medication changes.
Has long half-life, which may be
problematic if side effects are
serious.
Sedation is common, so time
physical therapy sessions
during times of least sedation.
Metaxalone is least drowsy of
these agents.
446 CHAPTER 19     Pharmacologic Agents

   
Central Nervous System

TABLE 19.15  Antianxiety Medications

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

Generic Name (Common

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

GABA, Gamma-aminobutyric acid; GI, gastrointestinal; 5-HT, 5-hydroxytryptamine.

TABLE 19.16  Anticonvulsants

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

Generic Name (Common Physical Therapy

Mechanism of Action
Multiple mechanisms of
action—enhancement of
sodium channel inactivation,
reducing current through
T-type calcium channels,
enhancement of GABA
activity, antiglutamine activity
Brand Name[s])
carbamazepine (Tegretol,
Carbatrol)
ethosuximide (Zarontin)
ezogabine (Potiga)
Adverse Effects Considerations
Rash, nausea, vomiting, Many drug interactions, complex
drowsiness, dizziness, pharmacokinetics, therapeutic
neutropenia, SIADH, drug level 4–12 mcg/mL.
osteomalacia, folic acid deficiency, Monitor for hepatotoxicity.
hepatotoxicity, aplastic anemia
Aggressiveness, ataxia, disturbance Monitor changes in mood,
in sleep, dizziness, drowsiness, aggression, suicidal ideations.
euphoria, fatigue, headache,
hyperactivity, inability to
concentrate, irritability, lethargy,
mental depression (with cases of
overt suicidal intentions), night
terrors, paranoid psychosis
The most common adverse Fatigue and somnolence can
reactions (incidence ≥ 4% and affect physical therapy; examine
approximately twice placebo) are balance and include balance
dizziness, somnolence, fatigue, interventions in plan of care.
confused state, vertigo, tremor,
abnormal coordination, diplopia,
disturbance in attention, memory
impairment, asthenia, blurred
vision, gait disturbance, aphasia,
dysarthria, and balance disorder
 Pharmacologic Agents     CHAPTER 19
TABLE 19.16  Anticonvulsants—cont’d
Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects
fosphenytoin (Cerebyx), Nausea, vomiting, drowsiness,
phenytoin (Dilantin), dizziness, peripheral neuropathy,
ethotoin (Peganone) acne, hirsutism, gingival
hyperplasia, folate deficiency,
hepatic failure, Stevens-Johnson
syndrome.a
felbamate (Felbatol) Weight loss, hepatotoxicity,
aplastic anemia
gabapentin (Neurontin), Well-tolerated, somnolence, ataxia,
pregabalin (Lyrica) weight gain
lamotrigine (Lamictal) Rash, Stevens-Johnson syndrome
levetiracetam (Keppra), Behavioral symptoms (aggression,
brivaracetam (Briviact) hyperkinesias, irritability,
neurosis), somnolence, fatigue
oxcarbazepine (Trileptal), Dizziness, somnolence, headache,
tiagabine (Gabitril), ataxia, fatigue, vertigo. Stevens-
eslicarbazepine Johnson syndrome, suicidal
(Aptiom) ideation
phenobarbital (Barbital, Drowsiness, dizziness,
Luminal, Solfoton), incoordination, decreased
primidone (Mysoline) cognition, hepatic failure,
Stevens-Johnson syndrome
topiramate (Topamax, Drowsiness, dizziness, difficulty
Qudexy XR), with concentration, loss of
zonisamide (Zonegran) appetite, mood changes,
metabolic acidosis, kidney
stones, weight loss, oligohydrosis
(inability to sweat)
valproic acid (Depacon, Nausea and vomiting, significant
Depakene, Depakote) weight gain, alopecia, tremor,
thrombocytopenia, fatal
hepatotoxicity, fatal hemorrhagic
pancreatitis
lacosamide (Vimpat) Dizziness, ataxia, blurred vision,
diplopia, somnolence, atrial
fibrillation
zonisamide (Zonegran) Headache, anorexia, dizziness,
somnolence, tremor
perampanel (Fycompa) Abnormal gait, ataxia, dizziness,
headache, loss of equilibrium,
somnolence, irritability, mood
disorders, fatigue, aggressive
behavior, homicidal & suicidal
thoughts
BLACK BOX WARNING—
serious or life-threatening adverse
reactions, including aggression,
hostility, irritability, anger, and
homicidal ideation and threats,
anger
447
Physical Therapy
Considerations
Many drug interactions;
therapeutic drug levels
10–20 mcg/mL.
Popular for treatment of
neuropathic pain. Can assist
with patient’s ability in
participating in therapy by
reducing pain with activity.
Refer to the prescriber if rash
develops.
High potential for abuse, very
sedating, therapeutic drug levels
15–40 mcg/mL.
Make sure patient stays well
hydrated; patients who develop
oligohydrosis may overheat
easily and need to stay well
hydrated.
Design an exercise regimen to
minimize weight gain; monitor
abdominal pain for liver and
pancreatic toxicity.
Potential for abuse
Patients are counseled to avoid
driving, other activities
requiring mental alertness until
drug effects are stabilized.
Monitor for severe
hypersensitivity reactions.
Potential for abuse. Monitor
patients for mood changes.
Abnormal gait, dizziness may
affect physical therapy.
Continued
448 CHAPTER 19     Pharmacologic Agents

TABLE 19.16  Anticonvulsants—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s])
rufinamide (Banzel)
trimethadione (Tridione)
vigabatrin (Sabril)
aSteven-Johnson
syndrome is a severe and life-threatening hypersensitivity complex, which affects skin and mucous membranes.
GABA, Gamma-aminobutyric acid; REMS, Risk Evaluation and Mitigation Strategy; SIADH, syndrome of inappropriate antidiuretic hormone secretion.
Physical Therapy
Adverse Effects Considerations
Nausea/vomiting, ataxia, dizziness, Monitor patient to report any
headache, somnolence, blurred signs of rash to medical team.
vision, fatigue, status epilepticus, Monitor for blurred vision,
suicidal behavior, Stevens- dizziness.
Johnson syndrome
Somnolence, acneiform/ Monitor patient for signs and
morbilliform eruptions, symptoms of myasthenia gravis.
pancytopenia, hepatitis,
myasthenia gravis, day blindness,
suicidal behavior
Fetal risk has been demonstrated—
in females of child-bearing
potential, administer only if
benefit outweighs risk
Weight gain, arthralgia, Coordination problems, memory
confusion, coordination impairment may require
problems, memory impairment, alterations to physical therapy
somnolence, tremors, blurred regimen.
vision, nystagmus, otitis Offer exercise regimen to
media, aggressive behavior, minimize weight gain.
dysmenorrhea, bronchitis, upper
respiratory infections, fatigue,
liver failure, visual field defects,
psychotic disorder, suicidal
thoughts
REMS program—communication
plan, medication guide,
elements to assure safe use,
implementation system to ensure
patients are aware of risk of vision
loss

TABLE 19.17  Antidepressants

Indications: Treatment of depression and other psychological disorders, such as panic, obsessive compulsive disorder, and so on; some agents in
this class can be used to treat neuropathic pain (TCAs) or to prevent migraines (TCAs, SSRIs). It takes 4 to 6 weeks before full efficacy of drug
therapy can be assessed.

Generic Name (Common

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
Brand Name[s])
phenelzine (Nardil),
tranylcypromine (Parnate),
rasagiline (Azilect),
safinamide (Xadago),
selegiline (Eldepryl,
Zelapar)
bupropion (Wellbutrin,
Zyban)
citalopram (Celexa),
escitalopram (Lexapro),
fluoxetine (Prozac,
Sarafem), fluvoxamine
(Luvox), paroxetine (Paxil),
sertraline (Zoloft)
Adverse Effects
Orthostatic hypotension, weight
gain, sexual dysfunction,
anticholinergic effects,
hypertensive crisis, dyskinesia,
hallucinations, impulse control
disorder, serotonin syndrome
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
Physical Therapy 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-HT
and/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 because of good
tolerability profile. Patients should
not abruptly discontinue SSRIs
(taper over 2–4 weeks, with the
exception of fluoxetine).

TABLE 19.17  Antidepressants—cont’d
Mechanism of Action
Serotonin-norepinephrine
reuptake inhibitors
(SNRI)—inhibit reuptake of
NE and 5-HT
Serotonergic (dual-acting)—
inhibit serotonin reuptake
similar to SSRIs and serve as
partial agonists at 5-HT1A
receptor
Tricyclic antidepressants
(TCAs)—increase synaptic
concentration of 5-HT and/
or NE in the CNS
Mirtazapine—increases 5-HT
and NE in the synapses;
antagonizes 5-HT2A and
5-HT3 receptors
Nefazodone—inhibits 5-HT
and NE uptake and blocks
5-HT2A receptors
Trazodone—inhibits 5-HT
reuptake and blocks 5-HT2A
receptors
Vortioxetine—inhibits
reuptake of serotonin (5-HT)
and blocks select serotonin
receptors (5-HT3, 5-HT1D,
5-HT7)
CNS, Central nervous system; GI, gastrointestinal; 5-HT, 5-hydroxytryptamine; LFTs, liver function tests; MAO, monoamine oxidase; NE, norepinephrine; SDRI,
serotonin-dopamine reuptake inhibitor; SNRI, serotonin-norepinephrine reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor; TCA, tricyclic antidepressant;
TG, triglycerides.
TABLE 19.18  Antipsychotics
Indications: Treatment of various schizoaffective disorders, such as schizophrenia. Can be used to treat aggressive behaviors associated with
bipolar disorders and dementia.
Mechanism of Action
Typical (conventional
antipsychotics)—block
postsynaptic dopamine-2
receptors; share
anticholinergic, antihistamine,
and alpha-blocking properties
(often producing undesirable
side effects)
Generic Name (Common
Brand Name[s])
duloxetine (Cymbalta),
venlafaxine (Effexor),
desvenlafaxine (Khedezla),
levomilnacipran (Fetzima),
milnacipran (Savella)
vilazodone (Viibryd)
amitriptyline (Elavil),
clomipramine (Anafranil),
desipramine (Norpramin),
doxepin (Sinequan),
nortriptyline (Pamelor)
mirtazapine (Remeron)
nefazodone (Serzone)
trazodone (Desyrel)
vortioxetine (Brintellix)
Generic Name (Common Brand
Name[s])
chlorpromazine (Thorazine),
fluphenazine (Prolixin),
haloperidol (Haldol),
thioridazine (Mellaril)
Pharmacologic Agents     CHAPTER 19
Adverse Effects
GI upset, anxiety, headache,
dose-related hypertension,
increased heart rate, palpitations,
diaphoresis, hot sweats, serotonin
syndrome
Diarrhea, nausea, dizziness, dry
mouth, insomnia, and decreased
libido
Orthostatic hypotension,
tachycardia, sedation,
anticholinergic effects,
arrhythmias (prolongs QT
interval), weight gain, sexual
dysfunction
Fewer GI side effects and less
anxiety; sedation, increased
appetite, weight gain,
constipation, elevation of LFTs
and TG
GI upset, sedation, dry mouth,
constipation, lightheadedness,
minimal sexual dysfunction,
orthostasis, high incidence of
hepatotoxicity
Extremely sedating, orthostatic
hypotension, priapism; no
anticholinergic and cardiovascular
side effects
Hyponatremia, hypomania, mania,
suicidal thoughts, serotonin
syndrome, nausea
Adverse Effects
Sedation, orthostasis, weight
gain, anticholinergic side
effects (dry mouth, urinary
retention, constipation,
confusion), EPS effects
(dystonia, akathisia,
pseudoparkinsonism, TD)
449
Physical Therapy Considerations
Duloxetine has an indication for the
treatment of diabetic neuropathic
pain. Monitor blood pressure.
Duloxetine and milnacipran can also
treat fibromyalgia.
This agent appears to be as effective
as SSRIs but causes more GI
upset; dose titration can minimize
GI upset. Schedule physical
therapy sessions when patients are
experiencing fewer side effects.
Establish the time of the day when
sedation is minimal to schedule
PT sessions. TCAs are deadly in
overdose (they block sinoatrial
node). Drug serum levels can be
obtained to guide therapy.
Sedation is more pronounced with
this medication. Schedule physical
therapy sessions when patient
is most alert. Design exercise
program to minimize weight gain.
Monitor abdominal pain and yellow
appearance for hepatotoxicity.
Commonly used for insomnia
because of its sedating properties.
Schedule sessions later in the
afternoon if sedation persists into
the morning.
Monitor for behavioral changes.
Physical Therapy
Considerations
Monitor for orthostasis and
sedation. EPS effects can
interfere with therapy sessions.
TD is irreversible. Report first
signs of TD to health care
providers. (Symptom triad
characteristic of TD: splayed
writhing fingers; grimacing,
bruxism, lip smacking;
protrusion of tongue.) Design
exercise programs to minimize
weight gain.
Continued
450 CHAPTER 19     Pharmacologic Agents

TABLE 19.18  Antipsychotics—cont’d

Mechanism of Action
Atypical antipsychotics—weak
dopamine and dopamine-2
receptor blockers that
block serotonin and alpha-
adrenergic, histamine, and
muscarinic receptors in the
CNS
In management of tardive
dyskinesia—reversibly inhibits
the vesicular monoamine
transporter 2 (VMAT2),
which prevents the uptake of
monoamines into the synaptic
vesicle in the cytoplasm
Generic Name (Common Brand
Name[s])
aripiprazole (Abilify),
asenapine (Saphris), clozapine
(Clozaril), iloperidone
(Fanapt), lurasidone (Latuda),
olanzapine (Zyprexa),
paliperidone (Invega),
quetiapine (Seroquel,
Seroquel XR), risperidone
(Risperdal), ziprasidone
(Geodon), Brexpiprazole
(Rexulti), Cariprazine
(Vraylar), Pimavanserin
(Nuplazid)
valbenazine (Ingrezza)
Adverse Effects
Sedation, orthostasis,
weight gain, new-onset
diabetes, possible dose-
related EPS with some
agents (incidence of EPS
is significantly less than
with conventional agents),
QT interval prolongation;
hypersalivation and
agranulocytosis with
clozapine
Somnolence, dizziness,
impairment of balance,
restlessness
Physical Therapy
Considerations
Monitor for sedation, orthostasis,
QT interval prolongations,
signs and symptoms of
hyperglycemia (excessive thirst,
urination). Design programs
to minimize weight gain.
With clozapine, WBC count
is monitored every 2 weeks; if
patient becomes neutropenic,
use precautions to minimize
exposure to viral and bacterial
infections.
Assess patient for somnolence
before initiating activities that
require mental alertness.

CNS, Central nervous system; EPS, extrapyramidal side; TD, tardive dyskinesia; WBC, white blood cell.

TABLE 19.19  Mood Stabilizers

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

Generic Name (Common Physical Therapy

Mechanism of Action Brand Name[s]) Adverse Effects Considerations
Lithium—mechanism of lithium (Lithobid, Eskalith Tremor, polydipsia, polyuria, Lithium has narrow therapeutic
action unknown; facilitates CR, Cibalith-S) nausea, diarrhea, weight range. Therapeutic levels are
GABA and influences gain, hypothyroidism, mental 0.6–1.2 mEq/L (acute) and
reuptake of serotonin and dulling 0.8–1.0 mEq/L (maintenance).
norepinephrine Monitor signs and symptoms of
lithium toxicity.a
aMild 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 im-
paired consciousness, coma, seizures, respiratory complications, death.
Note: Divalproex sodium (Depakote and Carbamazepine (Tegretol) are anticonvulsant medications that can be used as mood stabilizers. See Table 19.16.
GABA, Gamma-aminobutyric acid.

TABLE 19.20  Stimulants

Mechanism of Action
Acts on the brainstem
arousal system and cortex
to stimulate the CNS;
exact mechanism is not
known, but is suspected
to block reuptake of
norepinephrine and
dopamine into presynaptic
neuron, increasing their
concentration in the
extraneural space
Generic name (Common
Brand Names)
amphetamine/
dextroamphetamine (Adderall)
dextroamphetamine (Dexedrine,
ProCentra)
methylphenidate (Concerta,
Metadate, Methylin, Ritalin)
Physical Therapy
Adverse effects Considerations
Tachycardia, diaphoresis, Monitor patients for mood
weight loss, abdominal changes.
pain, xerostomia, Monitor patient’s weight, body
dizziness, anxiety, growth, if applicable.
depression, irritability,
myocardial infarction,
Raynaud’s phenomenon,
decreased body growth,
gastrointestinal
obstruction, cerebral artery
occlusion, hemorrhage,
seizures, blurred vision,
mania, psychotic disorders,
priapism
 Pharmacologic Agents     CHAPTER 19 451

TABLE 19.21  Medications for Substance Use–Related Disorders

Mechanism of Action
Synthetic opioid with mixed mu
receptor agonist and NMDA
receptor antagonist activity
Buprenorphine—a mu receptor
agonist and a kappa receptor
antagonist with a ceiling effect
at higher doses
Naloxone—an antagonist at
the mu receptor that causes
symptoms of withdrawal when
administered parenterally;
inclusion in oral and sublingual
dosage forms serves as a
deterrent for abuse
Naltrexone—an opioid antagonist
that competitively binds to
opioid receptors to block effects
of opioid agonists
Disulfiram—inhibits a step in
the metabolism of alcohol,
leading to accumulation of the
metabolite acetaldehyde, which
causes unpleasant symptoms,
including hypotension,
flushing, nausea, and vomiting
Interacts with glutamate and
GABA neurotransmitter
systems to create a dose-
dependent reduction of
alcohol intake without causing
anticonvulsant, antidepressant,
or anxiolytic effects
Generic name (Common
Brand Names)
methadone (Dolophine,
Methadose)
buprenorphine/naloxone
(Suboxone)
naltrexone (Vivitrol [IM],
Revia [oral])
disulfiram (Antabuse)
acamprosate (Campral)
Adverse Effects
Hypotension, diaphoresis,
asthenia, dizziness
Hyperhidrosis, insomnia,
pain, headache, respiratory
depression, serotonin
syndrome
Abdominal cramps,
arthralgia, myalgia,
headache, difficulty
sleeping, lack of energy,
anxiety, hepatotoxicity,
suicidal ideation
Hepatitis, optic neuritis
When patients are exposed
to alcohol—can cause
respiratory depression,
cardiovascular collapse,
arrhythmias, myocardial
infarction, acute
congestive heart failure,
unconsciousness and death
Pruritus, dizziness, insomnia,
cardiomyopathy, deep
thrombophlebitis, heart
failure, mesenteric arterial
occlusion, shock, suicidal
intent
Physical Therapy
Considerations
Monitor patients for acute
changes in blood pressure,
dizziness.
Ensure adequate hydration
in patients experiencing
hyperhidrosis. Monitor for
respiratory depression, serotonin
syndrome.
Monitor patients for mood
changes, signs and symptoms of
hepatotoxicity.
Patients are advised to carry
an identification card with
information on their disulfiram
treatment and physician contact
information.
Avoid using any alcohol-
containing products, including
hand sanitizer, while working
with these patients.
Monitor patients for dizziness,
pruritus, suicidal changes.

TABLE 19.22  Multiple Sclerosis Medications

Indications: To prevent relapse and/or maintain remission and/or delay multiple sclerosis (MS) progression.
MS is a complex disorder. Pharmacologic treatment of MS falls into three categories: symptomatic therapy, treatment of acute attacks, and
disease-modifying therapies. Acute exacerbations are managed with high doses of systemic corticosteroids (e.g., methylprednisolone), whereas
many of the medications described in other tables are used for managing symptoms of MS, such as agents to treat constipation, spasticity,
depression, and other symptoms. This table reviews disease-modifying agents used to prevent relapse, maintain remission, and delay disease
progression.

Generic Name (Common Physical Therapy

Mechanism of Action
First disease-modifying oral drug
for MS; a sphingosine 1-phosphate
receptor agonist
Brand Name[s])
fingolimod (Gilenya)
Adverse Effects
Pronounced first-dose bradycardia
(rarely bradyarrhythmia or first-
degree AV block); can rarely cause
infections, macular edema, decrease
in FEV1, elevated LFTs, and
increase in blood pressure
Considerations
Avoid scheduling therapy after
first dose administration.
Monitor vision changes,
exercise tolerance, and blood
pressure.
Continued
452 CHAPTER 19     Pharmacologic Agents
TABLE 19.22  Multiple Sclerosis Medications—cont’d
Mechanism of Action
Mechanism not completely
understood, but glatiramer
appears to mimic the antigenic
properties of myelin basic protein
and induce antiinflammatory
lymphocytes, thereby reducing
inflammation, demyelination, and
axonal damage
Interferon (INF)—mechanism not
completely understood, but it is
likely that the effect is caused via
immunomodulation; augments
suppressor cell function; reduces
INF-gamma secretion by activated
lymphocytes, and activates
macrophages; also suppresses
T-cell proliferation and increases
the production of natural killer
cells
Chemotherapeutic agent that works
in MS by suppressing T cells, B
cells, and macrophages that are
thought to lead the attack on the
myelin sheath
Monoclonal antibody; blocks
T-lymphocyte migration into the
CNS
Monoclonal antibody;
binds to CD52 to exert
immunomodulatory effects,
which may include alteration in
the number, proportions, and
properties of some lymphocyte
subsets after treatment
Unknown mechanism in
MS; believed to result from
its antiinflammatory and
cytoprotective properties via
activation of the Nrf2 pathway
Immunomodulatory agent that
inhibits pyrimidine synthesis,
resulting in antiproliferative and
antiinflammatory effects:
AV, Atrioventricular; FEV1, forced expiratory volume over 1 second; LFTs, liver function tests.
Generic Name (Common
Brand Name[s])
glatiramer (Copaxone)
INF beta1a (Avonex,
Rebif); INF beta1b
(Betaseron, Extavia);
peginterforeonbeta1a
(Plegridy)
mitoxantrone
(Novantrone)
natalizumab (Tysabri)
alemtuzumab (Lemtrada)
dimethyl fumarate
(Tecfidera)
teriflunomide (Aubagio)
Adverse Effects
Mild pain and itching at the injection
site; approximately 10% experience
a one-time transient reaction
consisting of chest tightness,
flushing, and dyspnea beginning
several minutes after injection and
lasting up to 20 minutes
Common—injection site redness
and swelling, as well as flulike
symptoms (fevers, chills, myalgias)
Less common—tachycardia,
depression, thyroid dysfunction,
elevated LFTs, thrombocytopenia
Cardiotoxic with maximum lifetime
dose of 140 mg/m2; other side
effects include nausea, alopecia, and
upper respiratory and urinary tract
infections
Commonly cause headache, fatigue,
depression, nausea and vomiting,
influenza, flu-like symptoms,
respiratory tract infections,
arthralgia, gastroenteritis, and
abdominal distress.
Headache, fatigue, insomnia,
paresthesia, skin rash, thyroid
disease, GI upset, urinary tract
infection, arthralgia, flushing,
edema
Commonly causes flushing, diarrhea,
nausea, and infection; may cause
lymphocytopenia
Headache, alopecia,
hypophosphatemia, diarrhea,
nausea, neutropenia, increased
serum alanine aminotransferase,
hypertension, paresthesia,
neuropathy, arthralgia
Physical Therapy
Considerations
This agent is relatively well
tolerated. The one-time
transient injection reaction
presents similarly to angina,
so be aware of it if working
with patients initiated on
glatiramer.
Flulike symptoms typically
occur for up to 24 hours after
injection (most patients receive
injections once a week), so
scheduling therapy sessions
at least a day after injection is
best. Monitor injection sites
for signs and symptoms of
possible infection.
Monitor for signs and symptoms
of congestive heart failure,
such as edema, shortness
of breath, and exercise
intolerance.
Monitor for signs and symptoms
hepatotoxicity (e.g., jaundice,
abdominal pain, nausea
and vomiting), meningitis,
encephalitis (e.g., stiff
neck, severe headache), and
hypersensitivity reactions (e.g.,
rash, peeling of skin, swelling).
Monitor for signs and
symptoms of hepatic injury
(e.g., jaundice, abdominal
pain, nausea and vomiting)
and progressive multifocal
leukoencephalopathy (e.g.,
general weakness, gait
instability, changes of vision).
Monitor patient closely for
paresthesia, peripheral
neuropathy, and arthralgia.

TABLE 19.23  Parkinson’s Disease Medications
Indications: Treat signs and symptoms associated with Parkinson’s disease.
Mechanism of Action
Antiparkinsonian activity,
likely resulting from blocking
of reuptake of dopamine
into presynaptic neurons or
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
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).
CNS, Central nervous system; MAO, monoamine oxidase.
Pharmacologic Agents     CHAPTER 19
Generic Name (Common
Brand Name[s]) Adverse Effects
amantadine (Symmetrel) Orthostasis, peripheral edema,
anxiety, ataxia, dizziness,
hallucinations, insomnia,
somnolence, anorexia, GI upset
benztropine (Cogentin), Dry mouth, blurred vision,
biperiden (Akineton) constipation, nausea, urinary
procyclidine retention, tachycardia,
(Kemadrin), somnolence, confusion
orphenadrine
(Disipal, Norflex),
trihexyphenidyl
hydrochloride (Artane,
Trihexy-5)
entacapone (Comtan, Nausea, dyskinesias, orthostasis,
Stalevo [in combination dizziness, hallucinations,
with levodopa/ diarrhea, brown-orange urine
carbidopa]), tolcapone discoloration; hepatotoxicity
(Tasmar) with tolcapone
bromocriptine mesylate Nausea and vomiting,
(Parlodel), pergolide dizziness or fainting; sudden,
mesylate (Permax), unpredictable attacks of
pramipexole (Mirapex), sleepiness (these can be very
ropinirole hydrochloride dangerous if they occur while a
(Requip), rotigotine person is driving); orthostatic
(Neupro), apomorphine hypotension; confusion or
(Apokyn) hallucinations; depression;
insomnia; dyskinesias; irregular
heart rate and chest pain
levodopa (Dopar, Orthostasis, hypertension,
Larodopa), carbidopa arrhythmias, dizziness,
(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, LFT elevations,
choreiform and involuntary
movements, paresthesia, bone
pain, shoulder pain, muscle
cramps, weakness, hiccups,
dyskinesias
selegiline (Deprenyl, Headache, insomnia, dizziness,
Eldepryl, Emsam, nausea, hypotension,
Zelapar), Zydis orthostasis, diarrhea, weight
selegiline, rasagiline loss
(Azilect), safinamide
453
Physical Therapy Considerations
Rarely used; often combined with
other agents.
First-line agents for tremor-
predominant diseases; can
be used to treat motor
complications (dyskinesias) of
dopaminergic agents.
These drugs are added to levodopa
to optimize motor function and
reduce motor complications.
Patients should be taking one of
these with each dose of levodopa.
These are first-line agents in
younger patients. Compared
with levodopa, 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
because of heart valve damage
(March 2007).
Many side effects occur because
of 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.
454 CHAPTER 19     Pharmacologic Agents
Oncology
TABLE 19.24  Antiemetic Medications
Indications: Prevention and treatment of nausea and vomiting from any causes, including chemotherapy and radiation-induced and postopera-
tive nausea and vomiting.
Mechanism of Action
5-HT3 receptor antagonists—
selective 5-HT3-receptor
antagonists; block serotonin,
both peripherally on vagal nerve
terminals and centrally in the
chemoreceptor trigger zone
Benzamides—block dopamine
receptors and (when given
in higher doses) also blocks
serotonin receptors in
chemoreceptor trigger zone of
the CNS
Butyrophenones—antiemetic
effect is a result of blockade of
dopamine stimulation of the
chemoreceptor trigger zone
Cannabinoids—mechanism
unknown; may inhibit
endorphins in the brain’s emetic
center; suppress prostaglandin
synthesis, and/or inhibit
medullary activity through an
unspecified cortical action
Doxylamine succinate/Pyridoxine
Hydrochloride—mechanism
unknown
Neurokinin-1 (NK1) receptor
antagonists—antagonize
substance P and NK1 receptors
CNS, Central nervous system; ECG, electrocardiography; 5-HT, 5-hydroxytryptamine.
Generic Name (Common
Brand Name[s])
dolasetron (Anzemet),
granisetron (Kytril),
ondansetron (Zofran),
palonosetron (Aloxi)
metoclopramide (Reglan)
droperidol (Inapsine),
haloperidol (Haldol)
dronabinol (Marinol)
doxylamine succinate/
pyridoxine hydrochloride
(Diclegis, Bonjesta)
aprepitant or
fosaprepitant (Emend),
casopitant (Rezonic),
rolapitant (Varubi),
netupitant/palonosetron
(Akynzeo)
Adverse Effects
Well tolerated; headache,
constipation, dizziness
Drowsiness, fatigue, acute
dystonic reactions, akathisia,
confusion, neuroleptic
malignant syndrome (rare),
parkinsonian-like symptoms,
diarrhea
QT interval prolongation,
restlessness, anxiety,
extrapyramidal symptoms,
seizure, altered central
temperature regulation,
sedation, drowsiness
Palpitations, vasodilation/facial
flushing, euphoria, dizziness,
paranoia, somnolence, amnesia,
anxiety, ataxia, hallucinations
Somnolence
Asthenia, fatigue, diarrhea,
headache, dizziness, cough,
pruritus, and cough
Physical Therapy
Considerations
Nausea and vomiting are
common for the first 24 hours
after chemotherapy, but can
occur for up to 5 days. Assess
severity and frequency before
scheduling therapy.
Monitor vitals and
extrapyramidal symptoms.
Monitor for QT interval
prolongation on ECG (high
risk for torsades); schedule the
session when the patient is least
sedated.
Assess adverse side effects before
scheduling the session; can
also be used as an appetite
stimulant in cachexia.
Often used to treat morning
sickness during pregnancy.
 Pharmacologic Agents     CHAPTER 19 455

TABLE 19.25  Chemotherapy

Indications: Treat malignancy; some chemotherapeutic agents 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, and 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: Most chemotherapeutic agents cause nausea and
vomiting, mucosal ulceration, myelosuppression (decreased white blood cells, red blood cells, and platelets), and alopecia. As the result of my-
elosuppression, these patients are often immunocompromised and are at high risk for infection and bleeding. Most chemotherapeutic agents are
also carcinogenic, teratogenic, and mutagenic. Most 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 the nadir (lowest point) and right after a cycle
of chemotherapy administration (nausea and vomiting are most common in the first 24 hours but can occur for up to 5 days). However, a full
evaluation of the patient and conversation with the medical team will ultimately determine whether physical therapy intervention, depending on
its nature, is appropriate. Always use infection-control measures when working with patients with cancer. Make sure that your hands are cleaned
properly and that any equipment used has been cleaned/sterilized. Avoid close contact with patients with cancer if you are sick. Special measures,
such as facial masks and isolation from other patients, may be necessary with patients who have neutropenia (decreased white blood cell count).
Although this table attempts to highlight the major side effects of each class of chemotherapeutic agents, adverse event profiles vary among
agents within the same class, and careful review of a specific agent’s side effects is recommended when working with patients with cancer.

Generic Name (Common Brand Physical Therapy

Mechanism of Action Name[s]) Adverse Effects Considerations
Alkylating agents—form carmustine (BICNU), Pulmonary fibrosis (carmustine) and Monitor for signs of
covalent bonds with nucleic cyclophosphamide (Cytoxan, interstitial pneumonitis, hemorrhagic pulmonary toxicity,
acids and proteins resulting Neosar), dacarbazine (DTIC- cystitis (cyclophosphamide and renal function—urinary
in cross-linking of DNA Dome), ifosfamide (Ifex), melphalan ifosfamide), encephalopathy output, and blood in
stands and inhibition of (Alkeran), temozolomide (Temodar), (ifosfamide) urine. Mesna (an adjuvant
DNA replication thiotepa (Thioplex) medication) and hydration
are administered with
cyclophosphamide and
ifosfamide to decrease the
risk of hemorrhagic cystitis.
Antimetabolites—act by capecitabine (Xeloda), cytarabine Hand–foot syndrome (redness, Monitor for tingling and
falsely inserting themselves (Cytosar-U, DepoCyt), fludarabine tenderness, and possibly peeling of swelling of palms and soles,
in place of a pyrimidine (Fludara), fluorouracil (5-FU, the palms and soles), severe diarrhea, bruising, bleeding, and
or purine ring, causing Adrucil), gemcitabine (Gemzar), fatigue, neurotoxicity (cytarabine, diarrhea.
interference in nucleic acid mercaptopurine (Purinethol), fludarabine, methotrexate), rash
synthesis methotrexate (Rheumatrex) and fever, flulike symptoms
(gemcitabine), renal toxicity,
conjunctivitis (cytarabine), hemolytic
uremic syndrome (gemcitabine),
tumor lysis syndrome, hepatotoxicity
(methotrexate, mercaptopurine)
Antitumor antibiotics— Anthracyclines—doxorubicin Severe nausea and vomiting, stomatitis, All anthracyclines have
block DNA and/or RNA (Adriamycin, Doxil), daunorubicin and alopecia; acute and chronic heart limits on cumulative
synthesis through various (Cerubidine, DaunoXome), failure (anthracyclines); secondary lifetime dosing because
mechanisms idarubicin (Idamycin), mitoxantrone acute myelogenous leukemia; of cardiotoxicity. Delayed
(Novantrone) pulmonary fibrosis and interstitial nausea and vomiting
Alkylating-like—mitomycin pneumonitis with bleomycin; renal are common with
(Mutamycin) toxicity with dactinomycin anthracyclines. Monitor
Chromomycin—dactinomycin vitals, shortness of breath,
(Cosmegen) fatigue, and edema for
Miscellaneous—bleomycin signs of heart failure.
(Blenoxane), pralatrexate (Folotyn)
Biologic response modifiers Immunologic therapies—aldesleukin Hypotension and hypersensitivity Patients are typically
and monoclonal (Proleukin), interferon alfa-2b on infusion; cardiac, pulmonary, premedicated with Tylenol
antibodies—biologic (Intron A), levamisole (Ergamisol) and renal impairment; depression, and Benadryl to decrease
response modifiers activate Monoclonal antibodies—alemtuzumab diarrhea (brentuximab), infusion-related reactions.
the body’s immune- (Campath), bevacizumab (Avastin), fever, fatigue, chills, nausea, Monitor for hypertension,
mediated host defense brentuximab vedotin (Adcetris), musculoskeletal pain; tumor lysis fever, and organ toxicity
mechanisms to cancerous cetuximab (Erbitux), denileukin (rituximab); bleeding, hemorrhage, (lung—respiratory
cells; monoclonal antibodies diftitox (Ontak), gemtuzumab hypertension, proteinuria, rash problems; heart—blood
bind to specific antigens on (Mylotarg), ibritumomab (Zevalin), (bevacizumab and brentuximab); pressure, pulse, exercise
malignant cells and cause ipilimumab (Yervoy), ofatumumab cutaneous and infusion reactions, tolerance; kidney—urine
apoptosis, an antibody- (Arzerra), rituximab (Rituxan), interstitial lung disease (cetuximab); output, weight, serum
mediated toxicity, or sipuleucel-T (Provenge), tositumomab hypothyroidism (tositumomab), creatinine).
complement-mediated lysis (Bexxar), trastuzumab (Herceptin) sensory neuropathy (brentuximab)
Continued
456 CHAPTER 19     Pharmacologic Agents
TABLE 19.25  Chemotherapy—cont’d
Mechanism of Action
Histone deacetylase
inhibitor—induces cell
cycle arrest and apoptosis
Hormones and antagonists—
act on hormone-dependent
tumors by inhibiting or
decreasing the production
of disease-causing hormone
Microtubule inhibitors—
inhibit growth phase of
microtubules leading to
cell death (apoptosis)
Plant alkaloids—inhibit
replication of cancerous
cells through various
mechanisms
Platinum compounds—
alkylating-like; cause
inhibition of DNA
synthesis
Kinase inhibitors—inhibit
tyrosine kinase, rapamycin
kinase (everolimus),
serine-threonine kinase
(vemurafenib)
DNA, Deoxyribonucleic acid; DVT, deep venous thrombosis; GI, gastrointestinal; GNRH, gonadotropin-releasing hormone, LHRH, luteinizing hormone–releasing
hormone; PE, pulmonary embolism; RNA, ribonucleic acid.
Generic Name (Common Brand
Name[s])
romidepsin (Istodax)
Androgens—testosterone
(Delatestryl), fluoxymesterone
(Halotestin)
Antiandrogens—abiraterone (Zytiga),
dutasteride/tamsulosin (Jalyn),
flutamide (Eulexin), bicalutamide
(Casodex), nilutamide (Nilandron)
Antiestrogens—tamoxifen (Nolvadex)
Aromatase inhibitors: exemestane
(Aromasin), anastrozole (Arimidex),
letrozole (Femara)
Estrogens—ethinyl estradiol (Estinyl)
GNRH agonists—abarelix (Plenaxis)
LHRH agonists—goserelin (Zoladex),
leuprolide (Lupron, Eligard),
triptorelin (Trelstar)
Progestins—megestrol (Megace),
medroxyprogesterone (Provera)
cabazitaxel (Jevtana), eribulin
(Halaven)
Camptothecins—irinotecan
(Camptosar), topotecan (Hycamtin)
Epipodophyllotoxins—etoposide
(VePesid), Teniposide (Vumon)
Taxanes—docetaxel (Taxotere),
paclitaxel (Taxol, Abraxane)
Vinca alkaloids—vinblastine (Velban), inappropriate antidiuretic hormone
vincristine (Oncovin), vinorelbine
(Navelbine)
carboplatin (Paraplatin), cisplatin
(Platinol-AQ), oxaliplatin (Eloxatin)
crizotinib (Xalkori), dasatinib
(Sprycel), erlotinib (Tarceva),
everolimus (Afinitor), gefitinib
(Iressa), imatinib (Gleevec),
pazopanib (Votrient), sunitinib
(Sutent), vandetanib (Caprelsa),
vemurafenib (Zelboraf)
Adverse Effects
Loss of appetite, nausea, vomiting,
fatigue, infections
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)
Diarrhea, nausea, fatigue, anemia,
leukopenia, neutropenia, and
thrombocytopenia
Edema (docetaxel), hypotension/
hypersensitivity upon administration
(paclitaxel), neurotoxicity
(vincristine), diarrhea, headache,
secondary malignancies
(epipodophyllotoxins), syndrome of
secretion (vinca alkaloids)
Nephrotoxicity, peripheral
neurotoxicity, ototoxicity
Hepatotoxicity, hypertension, fluid
retention, weight gain, neutropenia,
GI effects, muscle cramps (imatinib);
rash, interstitial lung disease
(erlotinib); rash, acne (gefitinib);
disorder of vision (crizotinib), anemia
(imatinib, sorafenib, sunitinib)
Physical Therapy
Considerations
Monitor blood cells for
anemia, leukopenia,
neutropenia, and
thrombocytopenia.
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).
Monitor blood cell counts;
fatigue caused by anemia
may interfere with physical
therapy; patients with low
platelet count have high
risk of bleeding.
Monitor for peripheral
neuropathy, blood pressure
decrease. Acute and late-
onset diarrhea may interfere
with therapy sessions.
These agents are associated
with severe acute and
delayed nausea and
vomiting; monitor hearing
and urinary output, as well
as symptoms of peripheral
neuropathy.
 Pharmacologic Agents     CHAPTER 19 457

   
Vascular System and Hematology

TABLE 19.26  Colony-Stimulating Factors

Indications: Stimulate formation of white blood cells and red blood cells.

Generic Name (Common Physical Therapy

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
Brand Name[s])
darbepoetin alfa (Aranesp),
epoetin alfa (Epogen,
Procrit)
filgrastim (Neupogen,
G-CSF), pegfilgrastim
(Neulasta, G-CSF),
sargramostim (Leukine,
GM-CSF)
Adverse Effects Considerations
Hypertension, thrombotic and Monitor hemoglobin
vascular events, edema, DVT, and hematocrit; higher
fever, dizziness, insomnia, values are associated
headache, pruritus, GI upset, with thromboembolic
arthralgias, seizures (rare) complications; monitor blood
pressure.
Hypertension, edema, chest pain, Monitor for musculoskeletal
fever, headache, chills, rash, pain and vital signs. G-CSF
pruritus, weakness, bone pain, and GM-CSF is often used in
arthralgias, myalgias, GI upset; severely neutropenic patients
increase in serum creatinine, (high infection risk)—use
bilirubin, serum glucose, and infection-control measures.
cholesterol (sargramostim)

G-CSF, Granulocyte-colony stimulating factor; GI, gastrointestinal; GM-CSF, granulocyte-macrophage colony-stimulating factor; GI, gastrointestinal; DVT, deep
venous thrombosis.

   
Gastrointestinal System

TABLE 19.27  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, magne-
sium, or a combination. Sodium bicarbonate can also be used as an antacid. Only the most common antacids are presented below. Antacids that
contain calcium or magnesium have more acid neutralizing capacity (ANC) per milliliter 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
Alginic acid—reacts with
sodium bicarbonate in saliva to
form sodium alginate viscous
solution, which floats on the
surface of gastric contents and
acts as a protective barrier
Brand Name[s])
Aluminum based—
aluminum carbonate
(Basaljel), aluminum
hydroxide (Amphojel,
ALternaGEL)
Calcium based—calcium
carbonate (TUMS)
Magnesium based—
magnesium hydroxide
sodium bicarbonate
(Alka-Seltzer)
Adverse Effects
Constipation,
hypophosphatemia and bone
demineralization; toxicity in
patients with renal disease—
bone abnormalities
Constipation
Diarrhea; toxicity in patients
with renal disease—deep
tendon reflex reduction,
muscle weakness, arrhythmias
Water retention, edema,
exacerbation of hypertension,
and heart failure
Physical Therapy Considerations
Constipation can interfere with
physical therapy; monitor for
aluminum toxicity in patients with
reduced renal function. Encourage
mobility to address constipation.
Constipation can interfere with
physical therapy. Encourage
mobility to address constipation.
Diarrhea can interfere with physical
therapy; monitor for signs and
symptoms of toxicity in patients
with reduced renal function.
Avoid in patients with cardiovascular
disease.

Combination therapy: aluminum hydroxide + magnesium hydroxide (Maalox), magaldrate (Riopan), alginic acid + aluminum hydroxide + magnesium hydroxide
(Gaviscon), calcium carbonate + magnesium hydroxide (Mylanta).
GERD, gastroesophageal reflux disease; GI, Gastrointestinal; H2RA, histamine-2 receptor antagonist; PPI, proton pump inhibitor.
458 CHAPTER 19     Pharmacologic Agents

TABLE 19.28  Antidiarrheal Medications

Indications: Treatment of diarrhea.

Generic Name (Common Physical Therapy

Mechanism of Action Brand Name[s]) Adverse Effects Considerations
Inhibit/decrease GI diphenoxylate/atropine (Lomotil), Constipation; sedation, drowsiness, Assess for presence of CNS
motility loperamide (Imodium), opium dizziness (especially with opium depression and timing of
tincture, bismuth subsalicylate tincture); black tarry stools (with diarrhea to optimize scheduling
(Pepto-Bismol) bismuth subsalicylate) of the physical therapy session.
CNS, Central nervous system; GI, gastrointestinal.

TABLE 19.29  Antispasmodic Medications

Indications: Treatment of irritable bowel syndrome.

Generic Name (Common Brand Physical Therapy

Mechanism of Action
Selectively inhibit gastrointestinal
smooth muscle (via anticholinergic
properties) and reduce stimulated
colonic motor activity
Name[s]) Adverse Effects Considerations
dicyclomine (Bentyl), hyoscyamine Dizziness, lightheadedness, Monitor for dizziness
(Hyosyne, Levsin, Levbid), drowsiness, xerostomia, nausea, and blurred vision.
promethazine (Phenergan) constipation, blurred vision

TABLE 19.30  Cytoprotective Medications

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

Generic Name (Common Brand Physical Therapy

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

TABLE 19.31  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 Helicobacter pylori.

Generic Name (Common Brand Physical Therapy

Mechanism of Action Name[s]) Adverse Effects Considerations
Suppress gastric acid secretion by cimetidine (Tagamet), famotidine Very well tolerated; headache, Drug therapy should not
reversibly blocking histamine-2 (Pepcid), nizatidine (Axid), nausea, diarrhea, constipation influence PT; however, report
receptors on the surface of the ranitidine (Zantac) have been reported; confusion any new signs and symptoms of
gastric parietal cell can occur in elderly who take GI upset or bleeding, which can
high doses; gynecomastia and occur in case of therapy failure.
impotence (cimetidine)
Combination therapy: Ranitidine bismuth citrate (Tritec)—used specifically for the treatment of H. pylori; calcium carbonate + magnesium hydroxide + famotidine
(Pepcid Complete OTC).
GERD, Gastroesophageal reflux disease; GI, gastrointestinal; NSAID, nonsteroidal antiinflammatory drug.
 Pharmacologic Agents     CHAPTER 19 459

TABLE 19.32  Laxatives

Indications: Treatment of constipation.

Generic Name (Common Brand Physical Therapy

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

TABLE 19.33  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 Helicobacter pylori.

Generic Name (Common Brand Physical Therapy

Mechanism of Action Name[s]) Adverse Effects Considerations
Suppress gastric acid secretion esomeprazole (Nexium), Very well tolerated; headache, Drug therapy should not
specifically by inhibiting omeprazole (Prilosec), nausea, diarrhea, constipation influence physical therapy;
the H+- ATPase, K+- lansoprazole (Prevacid have been reported; increase however, report any new signs
ATPase enzyme system of SoluTab), pantoprazole the incidence of Clostridium and symptoms of GI upset or
the secretory surface of the (Protonix), rabeprazole difficile–associated diarrhea bleeding that can occur in case
gastric parietal cell (Aciphex) of therapy failure.
Combination therapy: lansoprazole + amoxicillin + clarithromycin (Prevpac)—this 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 used H. pylori regimen.
ATP, Adenosine 5′-triphosphate; GERD, gastroesophageal reflux disease GI, gastrointestinal; NSAID, nonsteroidal antiinflammatory drug.
460 CHAPTER 19     Pharmacologic Agents

   
Genitourinary System

TABLE 19.34  Benign Prostatic Hyperplasia (BPH) Therapy

Indications: Treatment of symptomatic BPH.

Generic Name (Common Physical Therapy

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

TABLE 19.35  Oral Contraceptives

A variety of formulations are 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
chapter, numerous contraceptive formulations are not listed. Physical therapists are advised to recognize the active ingredients of the particular
contraceptive preparation and refer to this table for drug information.

Generic Name (Common Physical Therapy

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

FSH, Follicle-stimulating hormone.

 Pharmacologic Agents     CHAPTER 19 461

   
Infectious Disease

TABLE 19.36  Antibiotics

Indications: Treatment and prophylaxis of infections.

Physical Therapy
Mechanism of Action Generic Name (Common Brand Name[s]) Adverse Effects Considerations
Aminoglycosides— amikacin (Amikin), gentamicin Nephrotoxicity, ototoxicity Serum levels of aminoglycosides
inhibit bacterial (Garamycin), neomycin (Kantrex), require monitoring. High
protein synthesis streptomycin, tobramycin (AKTob, trough levels (at the end
by binding to 30S TOBI, Tobrex) of the dosing interval) are
ribosomal subunit and associated with renal toxicity.
inhibiting bacterial Trough levels for gentamicin
RNA synthesis and tobramycin should be
<2 mcg/mL. Monitor urine
output, serum creatinine for
renal function. Report any
changes in patient’s hearing.
Carbapenems—inhibit ertapenem (Invanz), imipenem-cilastatin Nausea, vomiting, Monitor for GI side effects.
cell wall synthesis, (Primaxin), meropenem (Merrem, diarrhea, leukopenia,
thereby causing cell Vabomere [in combination with thrombocytopenia, seizures
lysis and death vaborbactam]) (imipenem-cilastatin only)
Cephalosporins— First generation—cefadroxil (Duricef), Allergic/hypersensitivity Monitor for rash, hives,
inhibit mucopeptide cefazolin (Ancef, Kefzol), cephalexin reactions swelling in the face and
synthesis in the (Keflex), cephapirin (Cefadyl), GI side effects with oral neck for allergic reactions.
bacterial cell wall, cephradine (Anspor) administration—nausea, Ask patients about GI side
which leads to cell Second generation—cefaclor (Ceclor), vomiting, diarrhea effects to optimize the time of
lysis and death cefonicid (Monocid), cefotetan Serious—seizure, therapy session. Monitor for
(Cefotan), cefoxitin (Mefoxin), cefprozil nephrotoxicity resolution of infection.
(Cefzil), cefuroxime (Ceftin), loracarbef
(Lorabid)
Third generation—cefixime (Suprax),
cefdinir (Omnicef), cefoperazone
(Cefobid), cefotaxime (Claforan),
cefpodoxime (Vantin), ceftazidime
(Fortaz), ceftibuten (Cedax), ceftizoxime
(Cefizox), ceftriaxone (Rocephin)
Fourth generation—cefepime (Maxipime)
Fifth generation—ceftaroline (Teflaro)
Fluoroquinolones— ciprofloxacin (Cipro), gatifloxacin Nausea, dyspepsia, Monitor blood sugar (may
inhibit bacterial (Tequin), levofloxacin (Levaquin), headache, dizziness, increase or decrease),
DNA topoisomerase lomefloxacin (Maxaquin), moxifloxacin insomnia, hypoglycemia or especially in patients with
and disrupts DNA (Avelox), ofloxacin (Floxin) hyperglycemia, QT interval diabetes. ECG should be
replication prolongation, tendonitis, checked for QT interval
photosensitivity, rash, prolongation, which
urticaria predisposes patients to
arrhythmias. Tendon rupture
has been reported; avoid any
exercise that can increase
that risk further. Use caution
if using UV light as part of
therapy.
Macrolides and Macrolides—azithromycin (Zithromax), GI upset—erythromycin Ask patients about GI side
ketolides—bind to clarithromycin (Biaxin), erythromycin can stimulate GI motility effects to optimize the
50S RNA subunit, (Ery-tab, various), fidaxomicin (Dificid) and result in diarrhea; time of the therapy session.
thereby inhibiting Ketolide—telithromycin (Ketek) clarithromycin has the least Predisposes patients to
RNA synthesis GI side effects; QT interval arrhythmias; monitor ECG
prolongation, ototoxicity; for QT interval prolongation.
fidaxomicin is used to
treat Clostridium difficile–
associated diarrhea
Continued
462 CHAPTER 19     Pharmacologic Agents

TABLE 19.36  Antibiotics—cont’d

Physical Therapy
Mechanism of Action Generic Name (Common Brand Name[s]) Adverse Effects Considerations
Lipoglycopeptides— telavancin (Vibativ), oritavancin Taste disturbance, nausea, Ask patients about GI side
inhibit bacterial (Orbactiv), dalbavancin (Dalvance) vomiting, and foamy urine effects to optimize the time of
wall synthesis and the therapy session.
disrupt bacterial cell
membrane function
Penicillins—bind to Natural penicillins—penicillin G Allergic/hypersensitivity Monitor for rash, hives,
penicillin-binding (Pfizerpen), penicillin G procaine reactions in 3% to 10% of swelling in the face and
proteins and inhibit (Wycillin), penicillin G benzathine patients neck for allergic reactions.
cell wall synthesis in (Bicillin LA), penicillin V (Pen-Vee K) GI side effects with oral Ask patients about GI side
the bacteria, causing Penicillinase-resistance penicillins— administration—nausea, effects to optimize the time of
lysis and cell death oxacillin (Prostaphlin), Nafcillin (Nafcil, vomiting, diarrhea therapy session. Monitor for
Unipen), Dicloxacillin (Dynapen, Dycill) Serious—seizure (rare), resolution of infection.
Aminopenicillins—ampicillin hepatotoxicity (oxacillin,
(Omnipen), amoxicillin (Amoxil, nafcillin)
Trimox)
Carboxypenicillins—carbenicillin
(Geopen), ticarcillin (Ticar)
Ureidopenicillins—mezlocillin (Mezlin),
piperacillin (Pipracil)
Extended-spectrum penicillins plus
beta-lactamase inhibitors—amoxicillin-
clavulanic acid (Augmentin),
ampicillin-sulbactam (Unasyn),
piperacillin-tazobactam (Zosyn),
ticarcillin-clavulanic acid (Timentin),
ceftazidime-avibactam (Avycaz),
ceftolozane-tazobactam (Zerbaxa)
Sulfonamides— sulfadiazine, sulfamethizole (Urobiotic), Hypersensitivity reactions, Monitor for changes in skin
interfere with sulfamethoxazole/trimethoprim dermatologic reactions—rash, appearance; use caution when
bacterial folic acid (Septra), sulfisoxazole (Gantrisin) urticaria, Stevens-Johnson using UV light therapy.
synthesis syndrome, photosensitivity
Tetracyclines—inhibit demeclocycline (Declomycin), Photosensitivity reactions, Use caution if using UV
bacterial protein doxycycline (Vibramycin), minocycline hepatotoxicity, diarrhea, light therapy. Monitor for
synthesis by binding (Minocin), tetracycline (Sumycin) nausea, anorexia; vestibular side effects of
to 30S ribosomal minocycline use associated minocycline therapy.
subunit with dizziness, ataxia,
vertigo, skin and mucous
membrane pigmentation
Oxazolidinones—bind linezolid (Zyvox), Tedizolid phosphate Myelosuppression Monitor WBC (will decrease;
to 23S ribosomal (Sivextro) use infection-control
subunit of the 50S measures), hematocrit (will
RNA subunit, thus decrease; patient will complain
inhibiting bacterial of fatigue), and platelets (will
translation decrease; patient will be at a
higher risk of bleeding).
Miscellaneous
Inhibits 50S subunit, clindamycin (Cleocin) Nausea, vomiting, Monitor for GI side effects.
thereby inhibiting diarrhea, abdominal pain, Diarrhea can be especially
RNA synthesis thrombophlebitis problematic with this drug;
high incidence of C. difficile
colitis (do not recommend
over-the-counter antidiarrhea
medications).
Binds to components daptomycin (Cubicin) Diarrhea, nausea, vomiting, CPK should be checked at
of the cell membrane constipation, weakness, baseline and monitored
of susceptible arthralgias, increase in CPK periodically.
organisms and causes
rapid depolarization,
inhibiting intracellular
synthesis of DNA,
RNA, and protein

TABLE 19.36  Antibiotics—cont’d
Mechanism of Action
After diffusing into the
organism, interacts
with DNA to cause a
loss of helical DNA
structure and strand
breakage resulting in
inhibition of protein
synthesis and cell
death in susceptible
organisms
Quinupristin—inhibits
late-phase protein
synthesis
Dalfopristin—inhibits
early-phase protein
synthesis through
binding to 50S
subunit of bacterial
RNA
Inhibit bacterial
cell wall synthesis;
may inhibit RNA
synthesis
CPK, Creatine phosphokinase; DNA, deoxyribonucleic acid; ECG, electrocardiography; GI, gastrointestinal; RNA, ribonucleic acid; UV, ultraviolet; WBC, white blood
cells.
TABLE 19.37  Antifungal Agents
Indications: Treatment and prevention of fungal infections.
Mechanism of Action
Bind 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
β-(1,3)-d-glucan, an
essential component
of the cell wall of
susceptible fungi
GI, Gastrointestinal; LFTs, liver function tests.
Generic Name (Common Brand Name[s])
metronidazole (Flagyl)
quinupristin-dalfopristin (Synercid)
IV—vancomycin (Vancocin)
PO—vancomycin (not systemically
absorbed, concentrates in GI tract to
treat C. difficile infections)
Generic Name (Common
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)
Pharmacologic Agents     CHAPTER 19
Adverse Effects
Nausea, vomiting, unusual/
metallic taste, dark urine,
dizziness, headache
Thrombophlebitis and severe
injection site reactions,
hyperbilirubinemia,
arthralgias, and myalgias
Nephrotoxicity, ototoxicity,
thrombophlebitis,
histamine release during
or after infusion (red man
syndrome), causing swelling
and redness in the neck and
face
Adverse Effects
Infusion reactions—fevers, chills,
hypotension, rigors, pain,
thrombophlebitis, anaphylaxis;
nephrotoxicity (common and dose-
limiting)
Electrolyte disturbances—
hypokalemia, hypocalcemia,
hypomagnesemia; anemia; increase
LFTs and bilirubin
Lower incidence of renal and
infusion-related side effects with
lipid formulations
Nausea, vomiting, abdominal
pain, diarrhea, increase in LFTs,
rash, pruritus, photosensitivity
(voriconazole only)
Increased LFTs, histamine-release
reactions, such as rash, pruritus,
anaphylaxis; infusion reactions:
fever, nausea, vomiting, myalgias
463
Physical Therapy
Considerations
Monitor for GI adverse effects.
Monitor bilirubin (will
increase, patient’s skin and
mucosal membranes will
become more yellow, patient
will complain of itching).
Arthralgias and myalgias are
common and can lead to drug
discontinuation.
Avoid scheduling sessions
immediately after vancomycin
infusion because of possibility
of “red man syndrome.”
Monitor urine output and
serum creatinine for renal
toxicity. Report any changes
in patient’s hearing.
Physical Therapy
Considerations
Avoid scheduling physical
therapy sessions immediately
after amphotericin infusion.
Monitor urine output and
serum creatinine for renal
toxicity; LFTs, abdominal
pain, yellow skin appearance
for hepatic failure; electrolytes
(will decrease); hematocrit and
hemoglobin (will decrease).
Monitor for GI side effects;
abdominal pain, yellow skin
appearance for hepatotoxicity.
Avoid scheduling therapy
sessions immediately after
caspofungin infusion. Monitor
for hypersensitivity reactions.
464 CHAPTER 19     Pharmacologic Agents
TABLE 19.38  Antitubercular Agents
Indications: Treatment and prevention of mycobacterial infections, including tuberculosis.
Mechanism of Action
Inhibits folic acid synthesis
Cyclic polypeptide
antimicrobial; mechanism of
action unknown
Structurally similar to d-
alanine; inhibits cell wall
synthesis by competing
for incorporation into the
bacterial cell wall
Inhibits bacterial cellular
metabolism
Inhibits peptide synthesis
Mechanism unknown, but may
include inhibition of mycolic
acid synthesis, resulting in
disruption of the bacterial
cell wall
Converted to pyrazinoic acid
in susceptible strains of
Mycobacterium, which lowers
the pH of the environment;
exact mechanism of action
unknown
Inhibits RNA synthesis
Combinations: rifampin + isoniazid (IsonaRif; Rifamate), rifampin + isoniazid + pyrazinamide (Rifater).
CNS, Central nervous system; GI, Gastrointestinal; LFTs, liver function tests; RNA, ribonucleic acid; WBC, white blood cells.
Generic Name (Common
Brand Name[s])
aminosalicylic acid (Paser)
capreomycin (Capastat)
cycloserine (Seromycin)
ethambutol (Myambutol)
ethionamide (Trecator)
isoniazid (Nydrazid),
commonly abbreviated
as INH
pyrazinamide (Tebrazid),
commonly abbreviated
as PZA
rifampin (Rifadin)
Adverse Effects
Nausea, vomiting, abdominal
pain, diarrhea, hypersensitivity
reactions—fever, joint pain, skin
eruptions
Nephrotoxicity and ototoxicity in
30% of patients; elevated LFTs;
hypersensitivity reactions
Headache, vertigo, confusion,
psychosis, seizures
Optic neuritis with decreased
visual acuity, loss of red-green
color discrimination
Hepatitis (rare)
Peripheral neuropathy,
hepatotoxicity, agranulocytosis,
thrombocytopenia
Hepatotoxicity, gout
Nausea, vomiting, diarrhea,
abdominal pain, headache,
dizziness, mental
confusion, hepatotoxicity,
thrombocytopenia, leukopenia,
renal insufficiency
Physical Therapy
Considerations
Monitor for GI side effects and
allergic reactions.
Monitor urine output and serum
creatinine. Report any changes
in patient’s hearing.
Assess CNS toxicity before
therapy.
Report any changes in vision.
Monitor for hepatotoxicity
(abdominal pain, yellow skin
discoloration).
Monitor for tingling and pain in
the extremities; hepatotoxicity
(abdominal 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).
Monitor for hepatotoxicity
(abdominal 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); urine output and
serum creatinine for renal
insufficiency.
 Pharmacologic Agents     CHAPTER 19 465

TABLE 19.39  Antiretroviral Medications

Indications: Treatment of HIV/AIDS.
At the time of publication, there are currently six classes of antiretroviral drugs. Antiretroviral therapy (ART) typically consists of three to five agents
from different drug classes. Newer combination drugs allow patients to decrease the number of pills taken per day. ART is associated with much toxic-
ity. Class-common toxicities: All nucleoside reverse transcriptase inhibitors (NRTIs) can cause nausea, vomiting, and hepatic steatosis with lactic aci-
dosis. Nonnucleoside reverse transcriptase inhibitors (NNRTIs) are associated with rash and hepatotoxicity (rash to one agent in this class does not pre-
dict 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 use 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 medica-
tions 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 regimens. 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. Each antiretroviral drug has a commonly used abbreviation, which may lead to confusion and medical errors.

Mechanism of Generic Name (Common Brand

Action Name[s], Abbreviation[s])
NRTIs—nucleotide abacavir (Ziagen, ABC)
analogs that
compete with
nucleotides for
incorporation into
replicating DNA,
thereby aborting
viral replication
process
didanosine (Videx EC, ddI)
emtricitabine (Emtriva, FTC),
lamivudine (Epivir, 3TC)
stavudine (Zerit, D4T)
tenofovir disoproxil fumarate
(Viread, TDF)
Available combinations—
elvitegravir + cobicistata +
emtricitabine + TDF (Viread),
TDF + emtricitabine (Truvada),
efavirenz + TDF + emtricitabine
(Atripla), rilpivirine +
emtricitabine + TDF (Complera).
tenofovir alafenamide (Vemlidy,
TAF)
Available combinations—
elvitegravir + cobicistata +
emtricitabine + TAF (Genvoya),
emtricitabine + rilpivirine + TAF
(Odefsey)
zidovudine (Retrovir, AZT, ZDV)
Adverse Effects
Hypersensitivity reactions (can
present as combination of the
following symptoms—fever,
rash, nausea, vomiting, diarrhea,
abdominal pain, dyspnea, cough,
pharyngitis, malaise, fatigue;
HLA-B*5701 testing performed
before initiation to identify those
at risk for hypersensitivity; possible
increased risk of cardiovascular
disease in patients with risk factors
Peripheral neuropathy, pancreatitis,
diarrhea, nausea
Well tolerated; increased
pigmentation on palms/soles
Peripheral neuropathy, pancreatitis,
lipoatrophy, hyperlipidemia,
rapidly ascending progressive
neuromuscular weakness
Diarrhea, flatulence, renal
insufficiency, asthenia, headache
Headache, hyperpigmentation of skin
and nails, anemia, neutropenia,
myopathy
Physical Therapy Considerations
Physical therapists should monitor for
symptoms of hypersensitivity. Patient
should be referred to the prescriber
at once if hypersensitivity is detected
because of the potential for serious
anaphylactic reactions if therapy is
not discontinued. In patients with
multiple cardiovascular risk factors,
report any new symptoms.
This medication must be taken on an
empty stomach. Ask patients about
diarrhea to optimize scheduling
therapy sessions. Monitor abdominal
pain for pancreatitis and tingling
and numbness in the extremities for
peripheral neuropathy.
These agents are also active against
hepatitis B. Acute withdrawal of it
can result in hepatitis flare—monitor
for new/increased abdominal pain.
Monitor abdominal pain for pancreatitis
and tingling and numbness in the
extremities for peripheral neuropathy.
Report any neuromuscular weakness
to the prescriber.
Monitor urine output and serum
creatinine for renal failure. This
agent is also active against hepatitis
B. Acute withdrawal of it can result
in hepatitis flare—monitor for new/
increased abdominal pain.
Monitor WBC count (will decrease) and
hematocrit (will decrease; patient will
report fatigue). Report any muscle
pain/weakness not associated with
exercise.
Continued
466 CHAPTER 19     Pharmacologic Agents
TABLE 19.39  Antiretroviral Medications—cont’d
Mechanism of Generic Name (Common Brand
Action Name[s], Abbreviation[s])
NNRTIs—inhibit efavirenz (Sustiva, EFV)
reverse transcriptase,
an enzyme involved
in viral replication
etravirine (Intelence, ETR)
nevirapine (Viramune, Viramune
XR, NVP)
rilpivirine (Edurant, RPV)
Protease inhibitors— atazanavir (Reyataz, ATV, Evotaz
inhibit protease, an [in combination with cobicistata)
enzyme involved in
viral replication
darunavir (Prezista, DRV, Prezcobix Rash, abdominal pain, constipation
[in combination with cobicistata])
fosamprenavir (Lexiva, FPV)
indinavir (Crixivan, IDV)
lopinavir/ritonavir (Kaletra, KAL,
LPV/r)
nelfinavir (Viracept, NFV)
ritonavir (Norvir)
saquinavir (Invirase-HBC or tab,
SQV)
tipranavir (Aptivus, TPV)
Adverse Effects
Drowsiness, dizziness, insomnia,
abnormal dreaming, agitation,
hallucinations
Nausea, hypersensitivity reactions
with rash, hepatic failure
Severe rash and hepatotoxicity;
medication should be titrated up
to decrease the incidence of rash;
should be avoided in men and
females with CD4 counts >250
and >400 cells/mm3, respectively,
because of higher risk of liver
toxicity
Depression, insomnia, headache, rash
Hyperbilirubinemia, prolonged PR
interval on ECG, asymptomatic
first-degree heart block,
nephrolithiasis; does not have a
negative effect on lipids
Rash, nausea, diarrhea
Nephrolithiasis (kidney stones),
hyperbilirubinemia
GI intolerance, asthenia, prolonged
PR, rare cases of second- and third-
degree heart blocks, prolonged QT
interval
Diarrhea
Severe GI intolerance, taste
disturbances, asthenia, paresthesias
GI intolerance, increases QTc
interval—avoid in patients with
cardiovascular disease or drugs that
cause QT interval prolongation
Hepatotoxicity, GI intolerance,
increased risk of intracranial
hemorrhage, rash
Physical Therapy Considerations
Assess CNS side effects when
scheduling physical therapy sessions.
Afternoon may be a preferred time
because patients take this medication
at bedtime and may still complain of
side effects in the morning.
Should be taken after a meal; tablets
can be dispersed in water if patient
has difficulty swallowing. Monitor for
rash, nausea, and abdominal pain.
Report any indication of rash,
abdominal pain, yellow skin
appearance.
Should be taken with food; interacts
with acid-reducing agents and can
prolong QTc interval—monitor.
Monitor mood and sleep.
Report yellow skin/sclera appearance.
Monitor HR and ECG. Encourage
patients to drink a lot of
noncaffeinated fluids to prevent
kidney stones.
Incidence of rash is higher in those with
sulfa allergy (but not contraindicated).
Incidence of rash is higher in those with
sulfa allergy (but not contraindicated);
interacts with acid-reducing
medications.
Remind patients to consume at least
48 ounces of fluid per day to prevent
kidney stones.
Tablets should be swallowed whole and
can be taken with or without food.
Solution should be taken with food to
improve absorption. Ask patients about
GI side effects to optimize the time of
the therapy session. Monitor ECG.
Ask patients about GI side effects to
optimize the time of the therapy
session. Should be taken with food.
Commonly used in small doses to boost
pharmacokinetics of another PI and is
better tolerated in lower doses.
Ask patients about GI side effects to
optimize the time of the therapy
session; monitor ECG.
Monitor LFTs; ask patients about GI
side effects to optimize the time of
the therapy session. Rash is more
common in those with sulfa allergy
(not contraindicated); interacts with
antacids.
 Pharmacologic Agents     CHAPTER 19 467

TABLE 19.39  Antiretroviral Medications—cont’d

Mechanism of Generic Name (Common Brand
Action Name[s], Abbreviation[s]) Adverse Effects Physical Therapy Considerations
Fusion inhibitor enfuvirtide (Fuzeon, T-20, ENF) Injection-site reactions occur in all Monitor injection-site reactions for
—inhibits the patients: itching, swelling, redness, signs and symptoms of infection
fusion of HIV-1 pain or tenderness, induration, (warm, swollen). Report any signs
virus with CD4 nodules and cysts; hypersensitivity and symptoms associated with
cells by blocking reactions: rash, fever, nausea, hypersensitivity.
the conformational vomiting, chills, rigors,
change in gp41 hypotension, elevated LFTs
required for
membrane fusion
and entry into CD4
cells
CCR5 inhibitor— maraviroc (Selzentry, MVC) Hepatotoxicity (maybe preceded by Monitor and report pruritic rash,
binds to CCR5 systemic hypersensitivity reaction), abdominal pain. Be aware of postural
coreceptor on CD4 dizziness/postural hypotension, hypotension.
cell and prevents cough, rash, musculoskeletal
HIV entry into the symptoms, abdominal pain
cell in CCR5-tropic
infections (note
that genetic testing
to establish CCR5
tropism is required)
Integrase inhibitor— raltegravir (Isentress, RAL), Diarrhea, nausea, headache, Typically well tolerated; monitor for
inhibits the catalytic dolutegravir (Tivicay), elvitegravir increased LFTs, myopathy, and abdominal pain, GI intolerance.
activity of HIV-1 (Vitekta) rhabdomyolysis have been reported Report any new muscle pain not
integrase, an HIV-1 associated with exercise; risk of
encoded enzyme that myopathy is higher in combination
is required for viral with other drugs that can cause
replication myopathy, such as statins.
aCobicistat interferes with the metabolism of HIV medications and increases amount in blood.
Additional combinations: abacavir + dolutegravir + lamivudine (Triumeq), lamivudine + zidovudine (Combivir), lamivudine + abacavir (Epzicom), lamivudine +
abacavir + zidovudine (Trizivir)
AIDS, Acquired immunodeficiency syndrome; ART, antiretroviral therapy; CNS, central nervous system; DNA, deoxyribonucleic acid; EC, enteric coated; ECG, electro-
cardiogram; GI, gastrointestinal; HIV, human immunodeficiency virus; HR, heart rate; LFTs, liver function tests; NNRTI, nonnucleoside reverse transcriptase inhibitor;
NRTI, nucleoside reverse transcriptase inhibitor; PI, protease inhibitor; WBC, white blood cell.

TABLE 19.40  Antiviral Medications

Indications: Treatment and prevention of viral illnesses.

Generic Name (Common Physical Therapy

Mechanism of Action
Inhibit DNA synthesis
and viral replication
by competing with
deoxyguanosine triphosphate
for viral DNA polymerase
and being incorporated into
viral DNA
Protease inhibitor indicated
for treatment of genotype 1
hepatitis C in combination
with peginterferon alfa and
ribavirin.
Brand Name[s])
acyclovir (Zovirax,
Sitavig), famciclovir
(Famvir), ganciclovir
(Cytovene, Vitrasert),
penciclovir (Denavir),
valganciclovir (Valcyte;
rapidly converts into
ganciclovir in the body)
boceprevir (Victrelis)
Adverse Effects
Malaise, headache, nausea,
vomiting; topical administration
can produce local redness and
irritation; acyclovir IV can lead
to nephrotoxicity; ganciclovir
can cause neutropenia, anemia,
thrombocytopenia
Rash (discontinue all treatment
components if progressive or
severe), fatigue, itching, nausea,
anemia
Considerations
With IV acyclovir, monitor urine
output and serum creatinine for
renal function; monitor blood
counts (will decrease).
Monitor for rash and report to the
prescriber. Fatigue that can be
related to anemia may interfere
with effective physical therapy.
Continued
468 CHAPTER 19     Pharmacologic Agents

TABLE 19.40  Antiviral Medications—cont’d

Mechanism of Action
Cidofovir diphosphate—
suppresses CMV replication
by selective inhibition
of viral DNA synthesis;
incorporation of cidofovir
into growing viral DNA
chain results in reductions
in the rate of viral DNA
synthesis
Noncompetitive inhibitor of
many viral RNA and DNA
polymerases as well as HIV
reverse transcriptase
Exert immunomodulating effect
through suppression of cell
proliferation, enhancement
of the phagocytic activity of
macrophages and augmentation
of the specific cytotoxicity
of lymphocytes for target
cells, and inhibition of virus
replication in virus-infected
cells
Inhibits influenza virus
neuraminidase, with the
possibility of alteration of virus
particle aggregation and release.
Inhibits replication of RNA and ribavirin (Copegus; Rebetol)
DNA viruses; inhibits influenza
virus RNA polymerase activity
and inhibits the initiation and
elongation of RNA fragments
resulting in inhibition of viral
protein synthesis
First-generation protease telaprevir (Incivek),
inhibitors—indicated for
treatment of genotype 1
hepatitis C in combination with
peginterferon alfa and ribavirin
Second-generation protease
inhibitors—Direct acting
antiviral agent against hepatitis
C through various mechanisms
Generic Name (Common
Brand Name[s])
cidofovir (Vistide)
foscarnet (Foscavir)
interferon-alfa-2b (Intron A)
and peginterferon-alfa-2b
(peg-Intron, Sylatron)
oseltamivir (Tamiflu),
zanamivir (Relenza)
Boceprevir
simeprevir (Olysio),
Grazoprevir, sofosbuvir
(Sovaldi), dasabuvir,
elbasvir, ledipasvir,
daclatasvir (Daklinza),
ombitasvir, velpatasvir
Adverse Effects
Chills, fever, pain, nausea, vomiting,
diarrhea, anemia, neutropenia,
weakness, renal failure
Fever, headache, hypokalemia,
hypocalcemia, hypomagnesemia,
hypophosphatemia, nausea, diarrhea,
vomiting, anemia, granulocytopenia,
renal toxicity
Most frequently reported adverse
reactions were “flulike” symptoms,
particularly fever, headache, chills,
myalgia, and fatigue; poorly tolerated
and affect almost every organ system.
Serious effects—hypotension,
arrhythmia, cardiomyopathy,
hemorrhagic stroke, depression and
suicidal behavior, bone marrow
suppression, thyroid abnormalities,
peripheral neuropathy, and
hepatotoxicity
Nausea, vomiting, abdominal pain,
neuropsychiatric events (self-injury,
confusion, delirium)
Fatigue, headache, insomnia, nausea,
anorexia, anemia, fever, depression,
irritability, dizziness, alopecia,
pruritus, neutropenia, anemia,
thrombocytopenia, myalgia,
arthralgias, muscle pain, cough,
dyspnea, flulike syndrome
Fatigue, anemia (over 40% of patients
need erythropoiesis-stimulating
agent), nausea, headache, dysgeusia
(distortion of the sense of taste)
Fatigue, headache, nausea, pruritus,
skin reactions, insomnia, anemia
Physical Therapy
Considerations
This drug is administered every
other week. Ask patients about
toxicity to optimally schedule
therapy. Monitor urine output
and serum creatinine for renal
function. Monitor WBC (will
decrease) and hematocrit (will
decrease, patient will report
fatigue).
Monitor temperature (will
increase), electrolytes (will
decrease), blood counts
(will decrease).
If working with patients on
interferon therapy, become
familiar with the adverse event
profile and monitor for new
symptoms, which should be
reported to the prescriber.
Fatigue and flulike symptoms
will likely interfere with
physical therapy.
Monitor for CNS toxicity.
This medication is very toxic,
with a high incidence of side
effects. Careful determination
of readiness for physical therapy
should be performed.
Fatigue and anemia (patient will
complain of fatigue and exercise
intolerance) are most likely to
interfere with physical therapy.
Anemia should be corrected
to facilitate effective physical
therapy.

Combinations: Elbasvir + grazoprevir (Zepatier), ledipasvir + sofosbuvir (Harvoni), sofosbuvir + velpatasvir (Epclusa), sofosbuvir + velpatasvir + voxilaprevir (Vosevi),
ombitasvir + paritaprevir + ritonavir + dasabuvir (Viekira Pak), ombitasvir + paritaprevir + ritonavir (Technivie)
CMV, Cytomegalovirus; CNS, central nervous system; DNA, deoxyribonucleic acid; HIV, human immunodeficiency virus; IV, intravenous; RNA, ribonucleic acid.
 Pharmacologic Agents     CHAPTER 19 469

    be shut off, thereby maintaining muscle glucose uptake and

Endocrine System
Diabetes
Physical therapists should be familiar with the signs and
symptoms of hyperglycemia (polyuria, polydipsia, poly-
phagia, fatigue), hypoglycemia (shakiness, dizziness, sweat-
ing, hunger, headache, pale skin color, sudden moodiness or
behavior changes, clumsy or jerky movements, seizure, diffi-
culty paying attention, confusion, tingling sensations around
the mouth), and ketoacidosis (shortness of breath, breath that
smells fruity, nausea and vomiting, very dry mouth, coma).
Because of the effect of exercise on blood glucose, physi-
cal therapists must pay special attention to patients with
diabetes.
Patients with well-controlled blood glucose levels and
adequate serum insulin concentrations will usually have an
exercise-induced fall in blood glucose concentrations that
is much larger than that in normal patients. Several factors
contribute to this response: (1) Exogenous insulin cannot
inhibiting hepatic glucose output; and (2) increased tem-
perature and blood flow associated with exercise may speed
insulin absorption from subcutaneous depots (storage/collec-
tion sites where a drug remains before its release into the
bloodstream).
In contrast, exercise can cause a paradoxical elevation in
blood glucose concentrations in patients with diabetes who
have 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
mediated by counterregulatory hormones. Blood glucose should
be managed before, during, and after exercise. If the blood sugar
(BS) level is greater than 250 mg/dL, exercise should be delayed
until better control is achieved. Alternatively, if the BS level 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 risk of skin ulcer
formation. 

TABLE 19.41  Hypoglycemic Agents

Indications: Treatment of hyperglycemia in patients with diabetes mellitus (DM) or drug-induced hyperglycemia.

Generic Name (Common

Mechanism of Action
Alpha-glucosidase inhibitors—
Inhibit pancreatic alpha-amylase
and intestinal brush border alpha-
glucosidases, resulting in delayed
hydrolysis of ingested complex
carbohydrates and disaccharides and
absorption of glucose
Amylin analog—synthetic analog
of human amylin cosecreted with
insulin by pancreatic beta cells;
prolongs gastric emptying time,
reduces postprandial glucagon
secretion, and reduces caloric intake
through centrally mediated appetite
suppression
Biguanides—decrease hepatic glucose
production, decreasing intestinal
absorption of glucose, and improves
insulin sensitivity (increases
peripheral glucose uptake and
utilization)
Brand Name[s])
acarbose (Precose), miglitol
(Glyset)
pramlintide (Symlin)
metformin (Glucophage)
Adverse Effects Physical Therapy Considerations
Abdominal pain, GI side effects may interfere with
diarrhea, flatulence physical therapy session; has an
advantage of decreasing postprandial
blood sugars; should be taken
with each meal (skip a meal,
skip a dose). These agents do not
cause hypoglycemia if used as
monotherapy (i.e., the only agent
used). Use only simple sugars (i.e.,
glucose tabs) to treat hypoglycemic
episodes, because these drugs
delay the breakdown of complex
carbohydrates.
Nausea (in 50% Administered subcutaneously with
of patients), meals; can be used in type 1 and
hypoglycemia type 2 DM as adjunct therapy with
(when combined insulin. Can cause weight loss.
with insulin)
Nausea, vomiting, No hypoglycemia and possible weight
diarrhea, flatulence, loss are advantages of this agent;
lactic acidosis GI side effects may interfere with
physical therapy session; lactic
acidosis is rare, but fatal in 50% of
cases; risk factors for lactic acidosis
include age >80 years, reduced renal
function, liver disease, ischemic/
acidotic states, use of contrast dye for
imaging (hold metformin for at least
48 hours after procedure).
Continued
470 CHAPTER 19     Pharmacologic Agents

TABLE 19.41  Hypoglycemic Agents—cont’d

Generic Name (Common
Mechanism of Action Brand Name[s]) Adverse Effects Physical Therapy Considerations
Dopamine receptor agonist—activates bromocriptine mesylate Constipation, Oral therapy for type 2 DM; should
the postsynaptic dopamine receptors (Cycloset) diarrhea, nausea, be taken with food within 2 hours
to inhibit prolactin secretions and also asthenia, dizziness, of waking. Patients should avoid
stimulates the receptors to improve headache, rhinitis, activity until drug effects are
motor function; mechanism of action fatigue realized. This should be taken as an
of improving glycemic control poorly adjunct with other hypoglycemic
understood; contributes to resetting agents, such as metformin. Although
circadian rhythms in individuals it does not cause hypoglycemia, it
with type 2 DM; central effects may can be poorly tolerated and has only
reverse some of the metabolic changes modest benefit, so other alternatives
associated with insulin resistance and should be tried first.
obesity
DPP-IV inhibitors—inhibit dipeptidyl linagliptin (Tradjenta) Infrequent— Oral therapy for type 2 DM; does not
peptidase IV (DPP-IV) enzyme saxagliptin (Onglyza) headache, diarrhea cause hypoglycemia when used as
resulting in prolonged active incretin sitagliptin (Januvia) monotherapy (i.e., the only agent
levels; incretin hormones (e.g., alogliptin (Nesina) used).
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)— exenatide (Byetta, Hypoglycemia Administered subcutaneously with
analog of the hormone incretin Bydureon) (when combined morning and evening meals to type
(glucagon-like peptide 1 or GLP-1), liraglutide (Victoza) with sulfonylurea), 2 DM patients; can cause weight
which increases insulin secretion, dulaglutide (Trulicity) nausea (45%); loss. Liraglutide is contraindicated
increases B-cell growth/replication, albiglutide (Tanzeum) constipation, in patients with a history of multiple
slows gastric emptying, and may vomiting, diarrhea, endocrine neoplasia type 2 and
decrease food intake nausea (less medullary thyroid carcinoma.
with Bydureon), Bydureon is the long-acting form of
headache exenatide and is only to be used once
weekly.
Insulin—acts via specific membrane- Ultrarapid acting—aspart Atrophy or Be aware of the time of onset and peak
bound receptors on target tissues to (Novolin), glulisine hypertrophy of effect and duration to peak effect to
regulate metabolism of carbohydrate, (Apidra), insulin subcutaneous determine when the hypoglycemia
protein, and fats; normally secreted inhalation (Exubera), fat tissue; and hyperglycemia are most likely
by the pancreas; insulin products insulin human inhalation hypoglycemia, to occur.
manufactured for pharmacologic powder (Afrezza), lispro weight gain; Rapid-acting insulins—onset within
use through recombinant DNA (Humalog) respiratory 30 minutes, peak 1–2 hours,
technology and categorized on the Rapid acting—regular infection, cough, duration 3–5 hours.
basis of promptness and duration of (Humulin R, Novolin R) pharyngitis (with Regular—onset 30 minutes, peak 2–4
effect Intermediate—NPH insulin inhalation; hours, duration 6–8 hours.
(Humulin N, Novolin N) contraindicated NPH—onset 1–2 hours, peak 6–12
Intermediate to long- in smokers and hours, duration 18–24 hours.
acting—detemir patients with Detemir—onset 3–4 hours, duration
(Levemir) respiratory disease) (dose-dependent): 6–23 hours.
Long-acting—glargine Glargine—onset 3–4 hours, no peak,
(Lantus), insulin degludec duration 24 hours.
(Tresiba)
Meglitinides (nonsulfonylurea nateglinide (Starlix), Hypoglycemia, These are short-acting agents, which
secretagogues)—stimulates insulin repaglinide (Prandin) weight gain are advantageous in controlling
release from the pancreatic beta cells postprandial blood glucose. They
should be taken with meals (skip a
meal, skip the dose).
Sulfonylureas—stimulate insulin release glimepiride (Amaryl), Hypoglycemia, Monitor for hypoglycemia; design
from the pancreatic beta cells; reduces glipizide (Glucotrol), weight gain, an exercise regimen to minimize
glucose output from the liver; insulin glyburide (Micronase, photosensitivity weight gain; use caution when using
sensitivity is increased at peripheral DiaBeta, Glynase) ultraviolet (UV) light for therapy.
target sites
 Pharmacologic Agents     CHAPTER 19 471

TABLE 19.41  Hypoglycemic Agents—cont’d

Generic Name (Common

Mechanism of Action Brand Name[s]) Adverse Effects Physical Therapy Considerations
Thiazolidinediones—lower blood pioglitazone (Actos), Edema, heart These drugs do not cause
glucose by improving target rosiglitazone (Avandia) failure, weight hypoglycemia when used as
cell response to insulin, without gain; low risk of monotherapy; however, when added
increasing pancreatic insulin hepatotoxicity— to existing insulin therapy, the risk
secretion; mechanism of action requires periodic of hypoglycemia is very high. These
dependent on the presence of insulin monitoring agents also have positive effects on
for activity; agonists for peroxisome of LFTs; lipid. Because of edema and heart
proliferator-activated receptor-gamma postmarketing data failure risk, they should be avoided
(PPARgamma), which influences revealed increased in patients with NYHA class III and
the production of a number of gene risk of CVD with IV heart failure. Postmarketing data
products involved in glucose and lipid rosiglitazone revealed increased risk of CVD with
metabolism rosiglitazone, which led to majority
of prescribers switching their
patients to pioglitazone.
Sodium glucose cotransporter -2 ertugliflozin (Steglatro, Genital fungal
(SGLT-2) inhibitors—block glucose Synjardy [in combination infections, urinary
transporter (SGLT-2) in proximal with metformin]), tract infections,
tube, resulting in increased excretion canagliflozin (Invokana), hypotension,
of glucose in urine dapagliflozin (Farxiga), weight loss,
empagliflozin (Jardiance) diuretic effect;
low risk of
hypoglycemia

Oral combinations: glimepiride + pioglitazone (Duetact), glimepiride + rosiglitazone (Avandaryl), glipizide + metformin (Metaglip), glyburide + metformin (Gluco-
vance), metformin + rosiglitazone (Avandamet), metformin + saxagliptin (Kombiglyze XR), 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).
BS, Blood sugar; CVD, cardiovascular disease; DNA, deoxyribonucleic acid; GLP-1, glucagon-like peptide 1; LFTs, liver function tests.

TABLE 19.42  Treatment of Hyperparathyroidism

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

Generic Name (Common Physical Therapy

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

GI, Gastrointestinal; PTH, parathyroid hormone.

472 CHAPTER 19     Pharmacologic Agents
TABLE 19.43  Treatment of Osteoporosis
Indications: Prevention and treatment of osteoporosis.
In addition to medications described below, patients with osteopenia and osteoporosis should receive adequate calcium and vitamin D supple-
mentation.
Mechanism of Action
Bisphosphonates—inhibit
osteoclast-mediated bone
reabsorption and induces
osteoclast apoptosis
(zoledronic acid)
Calcitonin—reduces number
of osteoclasts and prevents
the resorptive activity, also
increases osteoblast activity
Estrogen/hormone therapy—
binds to estrogen-responsive
tissues and reduce the
levels of gonadotropins,
luteinizing hormone,
and follicle-stimulating
hormone in postmenopausal
females
Estrogen agonists/
antagonists—reduce bone
resorption and increases
bone mineral density
by selectively activating
and blocking estrogenic
pathways
Parathyroid hormone—
reduces the number of
osteoclasts and prevents
resorptive activity of the
bone
RANK inhibitor—binds
to the protein RANKL,
inhibiting the formation,
function, and survival of
osteoclasts
DVT, Deep vein thrombosis; GI, gastrointestinal; RANK, receptor activator of nuclear factor kappa-Β; RANKL, receptor activator of nuclear factor kappa-Β ligand.
Generic Name (Common
Brand Name[s])
alendronate (Fosamax
or Fosamax plus D),
ibandronate (Boniva),
risedronate (Actonel or
Actonel with Calcium),
zoledronic acid (Reclast)
salmon calcitonin (Fortical
and Miacalcin)
conjugated estrogens
(Premarin),
conjugated estrogens/
medroxyprogesterone
acetate (Premphase
and Prempro), ethinyl
estradiol/norethindrone
acetate (Femhrt), estradiol
(Climara, Estrace,
Vivelle dot), estradiol/
norethindrone acetate
(Activella), estropipate
(Ogen, Ortho-Est)
raloxifene (Evista)
teriparatide (Forteo)
denosumab (Prolia)
Adverse Effects
GI issues (mostly esophageal),
fever (alendronate), nausea,
visual disturbances
Zoledronic acid—atrial
fibrillation, bone metastasis
Mild—nausea
Mild—headache, edema,
nausea
Serious—breast cancer, DVT,
myocardial infarction,
pulmonary emboli, stroke
Mild—hot flashes
Serious—DVT
Constipation, indigestion, leg
cramps, nausea, spasms
Diarrhea, headache, fatigue,
musculoskeletal pain,
nausea, vomiting
Physical Therapy Considerations
Zoledronic acid is given as an
injection once yearly.
The other agents are oral and must be
taken on an empty stomach with a
full glass of water; the patient then
must wait 30–60 minutes upright
before eating, drinking, or taking
other medications.
Available as an intranasal spray or
injection.
Females who have not had a
hysterectomy require one of
the compounds containing
medroxyprogesterone acetate or
norethindrone acetate.
Monitor for abnormal vaginal
bleeding; estrogens can increase the
risk of endometrial cancer.
Activella, Climara, Estrace, and
Premarin come in different
formulations.
Avoid in females with a history of
venous thromboembolism.
Causes an increase in the incidence of
osteosarcoma.
 Pharmacologic Agents     CHAPTER 19 473

TABLE 19.44  Treatment of Thyroid Disorders

Indications: Treatment of hypothyroidism and hyperthyroidism.

Generic Name (Common Physical Therapy

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
to T3
Iodides—block hormone release, inhibit strong iodide solution (Lugol’s
thyroid hormone synthesis
Hypothyroidism
Thyroid hormones—enhance oxygen
consumption by most tissues and
increase basal metabolic rate and
metabolism of carbohydrates, lipids,
and proteins
Brand Name[s])
methimazole (Tapazole),
propylthiouracil (commonly
abbreviated as PTU)
solution), saturated solution
of potassium iodide (SSKI)
desiccated thyroid (Armour
Thyroid, Nature-Throid),
levothyroxine (Levothroid,
Levoxyl, Synthroid,
Thyro-Tabs, Unithroid),
liothyronine (Cytomel,
Triostat), liotrix (Thyrolar)
Adverse Effects
Fever, headache, paresthesias, rash,
arthralgia, urticaria, jaundice,
hepatitis, agranulocytosis,
leukopenia, bleeding
Rash, swelling of salivary
glands, metallic taste, burning
of the mouth, GI distress,
hypersensitivity, goiter
Tachycardia, arrhythmia, angina,
myocardial infarction, tremor,
headache, nervousness, insomnia,
hyperactivity, diarrhea, nausea,
vomiting, cramps, weight loss,
fatigue, menstrual irregularities,
excessive sweating, heat
intolerance, fever, muscle weakness,
decreased bone mineral density
Considerations
Monitor for improvement
of signs and symptoms
of hyperthyroidism;
monitor blood counts
(will decrease, patient will
complain of fever, malaise,
sore throat).
Monitor for improvement
of signs and symptoms of
hyperthyroidism.
Mostly well tolerated as
long as patient maintains
normal thyroid state.
Dose that is too high
will produce signs
and symptoms of
hyperthyroidism.

  

Organ Transplantation

TABLE 19.45  Immunosuppressants

Immunosuppressive therapy is essential to prevent organ rejection after transplantation. Immunosuppression protocols vary depending on the
transplantation center and the specific organ transplanted. The principles remain the same, however. Initially, immunosuppression is more ag-
gressive, with the ultimate goal of reducing the doses and number of agents used to optimize graft and patient survival. To achieve this, several
immunosuppressive agents must be monitored by serum concentration levels (these levels vary, depending on time since transplant and other
concomitant agents). Multidrug regimens are common to reduce doses of individual agents and, therefore, side effects, while maintaining the
efficacy. Systemic corticosteroids (see Table 19.8) are often used immediately posttransplantation but can also be used for maintenance immu-
nosuppression at low doses. Patients on immunosuppressive therapy are at high risk for typical and atypical infections, and infection control
measures must be used to reduce their exposure to bacteria and viruses. Most immunosuppressants have drug–drug interactions, so advise your
patients to notify providers of any medication changes. Grapefruit and grapefruit juice have potential to interact with many immunosuppressive
drugs, so avoid their use or check for drug interaction potential with a specific regimen.
Indications: For treatment and prevention of graft rejection in solid organ transplant recipients.

Generic Name (Common Physical Therapy

Mechanism of Action Brand Name[s]) Adverse Effects Considerations
Antimetabolites—azathioprine is a prodrug azathioprine Nausea, vomiting,
of 6-MP; through the process of metabolism (Azasan, Imuran), thrombocytopenia,
these agents are converted to active metabolites 6-mercaptopurine (6-MP, leukopenia,
that, when incorporated into the nucleic acid, Purinethol) increased risk of
disrupt DNA, RNA, and protein synthesis melanoma
decreasing proliferation of immune cells
Antimetabolites—mycophenolate inhibits mycophenolate mofetil Diarrhea, nausea, Strategies to reduce diarrhea
inosine monophosphate dehydrogenase (CellCept), mycophenolic vomiting, include dose decrease,
resulting in decreased nucleotide synthesis, acid (Myfortic) leukopenia separating dose into 3–4
ultimately reducing lymphocyte proliferation times a day administration,
or taking it with food; assess
patient side effects before
scheduling physical therapy.
Continued
474 CHAPTER 19     Pharmacologic Agents

TABLE 19.45  Immunosuppressants—cont’d

Generic Name (Common Physical Therapy

Mechanism of Action Brand Name[s]) Adverse Effects Considerations
Antithymocyte globulins—polyclonal ATG (Atgam), RATG Dose-limiting These are very potent
antibodies that bind to a wide array of (Thymoglobulin) myelosuppression; immunosuppressants used
lymphocyte receptors, leading to cell lysis and anaphylaxis, short term as induction
subsequent lymphocyte depletion hypotension, therapy or for treatment of
hypertension, acute rejection.
tachycardia,
dyspnea, urticaria,
rash
Calcineurin inhibitors—block T-cell cyclosporin modified Both—nephrotoxicity, Monitor blood pressure
proliferation by inhibiting the production of (Gengraf, Neoral), hypertension, (cyclosporin causes
interleukin-2 (IL-2) and other cytokines by cyclosporin nonmodified hyperglycemia, more hypertension than
T cells (Sandimmune), tremor tacrolimus). Hyperlipidemia
tacrolimus (FK506, Cyclosporin— is more common with
Prograf) hyperlipidemia, cyclosporin, whereas
gingival hyperplasia, hyperglycemia is more
hirsutism common with tacrolimus
Tacrolimus: (monitor signs such as
diarrhea, nausea, increase in thirst and
hepatotoxicity, urination). Monitor and
headache, report changes in urine
hyperkalemia, output.
hypomagnesemia
IL-2 receptor antagonist—binds to the alpha basiliximab (Simulect) Hypersensitivity Follow infection-control
chain on the surface of activated T cells and reactions and measures.
to IL-2 receptors, preventing IL-2 mediated increase in risk of
activation and proliferation of T cells infections
Mammalian target of rapamycin (mTOR) everolimus (Afinitor, Dose-related Monitor complete blood
inhibitors—bind to FKBP12, forming a Zortress), sirolimus myelosuppression— counts. Patients with low
complex that binds to mTOR, which inhibits (also called rapamycin; thrombocytopenia, platelets are at an elevated
the response to cytokines; ultimately this Rapamune) anemia, and risk of bleeding; low
inhibits T-cell proliferation neutropenia hemoglobin—will complain
(all improve of fatigue; low WBC count
with continued —puts patients at higher
treatment); risk of infection.
hyperlipidemia
Muromonab-CD3—murine monoclonal muromonab-CD3 Cytokine release This is a very potent
antibody; binds to the CD3 receptor of (Orthoclone OKT3) syndrome is immunosuppressants used
mature T cells, leading to T-cell depletion and common with first short term as induction
functional alteration dose—fever, chills, therapy or for treatment of
rigors, pruritus, acute rejection.
changes in blood
pressure

WBC, White blood cell.

References
1. Ciccone CD. Chapters 6 through 37. In: Pharmacology in Rehabili-
tation. 5th ed. Philadelphia: FA Davis; 2016.
2. Lexicomp Online®, Lexi-Drugs®, Hudson. Ohio. Lexi-Comp, Inc;
2018.
 20
CH APT ER  
CHAPTER OUTLINE
Introduction
Types of Anesthesia
Intraoperative Effects of
Anesthesia
Postoperative Effects of
Anesthesia
Immediate Postoperative Phase
Postoperative Complications
Operative Positioning
Physical Therapy Considerations
Anesthesia: Considerations for
the Physical Therapist
Clare Nicholson
Michele P. West
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . Describe the types of anesthesia and the physiologic effects of anesthesia on the body
2. List the potential complications that can occur with anesthesia
3. Provide an introduction to the basic operative body positions and discuss the potential for complications
related to positioning
4. Discuss physical therapy considerations related to the effects of anesthesia on the patient
  
Introduction
The physical therapist should have a general understanding of the types of anesthesia com-
monly used and the physiologic effect that anesthesia can have on a patient in the perioperative
phase: that is, before (preoperative), during (intraoperative), and after (postoperative) surgery.
This includes an understanding of the intraoperative effects, postoperative recovery phases,
and the potential complications of anesthesia. Insight into 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 hospital stay, discharge disposi-
tion, and physical therapy goals.
Surgery may be classified by urgency (elective, required, urgent, or emergent) and purpose
(diagnostic, explorative, reconstructive, transplant, curative, or palliative). The surgical clas-
sification determines the preoperative preparations, operative setting, and type of anesthesia
used. 1 
Types of Anesthesia
There are two types of anesthesia: general and regional. General anesthesia is a reversible state
of unconsciousness consisting of four components (amnesia, analgesia, inhibition of noxious
reflexes, and skeletal muscle relaxation) and is achieved through the use of intravenous and
inhalation anesthetics, analgesics, and muscle relaxants.2 Regional anesthesia is used for site-
specific surgical procedures of the upper or lower extremity or lower abdomen and is achieved
through spinal (subarachnoid), epidural (thoracic or lumbar), or peripheral nerve blockade.2
Local anesthesia is considered a subset of regional anesthesia and involves the topical or direct
application of an anesthetic to the skin or mucosa and/or the injection of a local anesthetic to
a superficial site.1
The administration of anesthesia can occur outside of the operating room for brief diagnos-
tic or surgical procedures (e.g., port or central line placement, percutaneous endoscopic gastros-
tomy (PEG) tube placement, kyphoplasty, endoscopy, bronchoscopy, electrical cardioversion).3
Procedural sedation with analgesia (formerly called conscious sedation) involves the use of seda-
tive agents to reduce discomfort and awareness during procedures while avoiding the need for
mechanical ventilation. It is characterized by the patient’s ability to maintain a patent airway
without intervention, ventilate spontaneously, maintain cardiovascular function, and respond
purposely to verbal or tactile stimulation.2 
        475
476 CHAPTER 20     Anesthesia: Considerations for the Physical Therapist
Intraoperative Effects of Anesthesia
The major intraoperative effects of general anesthesia include
the following4:
1. Neurologic effects: Decreased cortical and autonomic function
2. Metabolic effects: Hypothermia or malignant hyperthermia (in
patients with a genetic predisposition)
3. Cardiovascular effects: Risk of arrhythmia, hypotension, hy-
pertension, decreased myocardial contractility, and decreased
peripheral vascular resistance5
4. Respiratory effects6:
• Multiple effects, including decreased or altered:
• Arterial oxygenation
• Response to hypercarbia or hypoxia
• Vasomotor tone and airway reflex
• Respiratory pattern
• Minute ventilation
• Functional residual capacity
• Alterations in chest shape and motion because of de-
creased muscle tone, which causes the following:
• Decreased anteroposterior diameter
• Increased lateral diameter
• Increased cephalad position of the diaphragm
• Patient and surgical factors that increase the risk of post-
operative respiratory failure (i.e., prolonged mechanical
ventilation, unplanned reintubation) include the follow-
ing7:
• Underlying pulmonary diseases, such as chronic
obstructive pulmonary disease (COPD)
• Pain, especially if there is a thoracic or upper abdomi-
nal incision
• Smoking history
• Obesity
• Obstructive sleep apnea
• Advanced age
• The need for large intravenous fluid administration
intraoperatively
• Prolonged operative time (>180 minutes)
   • Emergency surgery  • Airway obstruction
Postoperative Effects of Anesthesia
Immediate Postoperative Phase
In the immediate postoperative phase, the patient is transported
from the operating room (OR) to a postanesthesia care unit
(PACU) (after general anesthesia) or to an ambulatory surgery
recovery room (after regional anesthesia); both provide for con-
tinuous nursing care. The recovery period after surgery is char-
acterized as a time of physiologic alteration resulting from the
operative procedure and the effects of anesthesia.2 During this
initial postoperative phase, the priorities of care are to assess
emergence from anesthesia and the status of the surgical site, to
determine the patient’s physiologic status and vital sign trends,
and to identify actual or potential postoperative complications,
described in the next section.8
Discharge from the PACU is dependent on clinical criteria,
rather than time-based criteria. Specific discharge criteria and/or
the use of scoring systems (e.g., Aldrete, Post Anesthetic Discharge
Scoring System [PADSS]) vary among institutions; however, the
general criteria for discharge from the PACU includes stable vital
signs with normothermia, adequate respiratory function, return to
baseline level of consciousness, return of motor function, satisfac-
tory pain control, satisfactory management of nausea and vomit-
ing, and control of surgical wound bleeding/drainage.1
The criteria for discharge from the ambulatory recovery room
are similar to those for the PACU and include recovery from
sedation or nerve blockade. 
Postoperative Complications
During the days to weeks of the postoperative phase, the patient
is monitored for proper return of function in all major body sys-
tems. Prevention and prompt recognition of potential or actual
postoperative complications is the cornerstone of high-quality
care by all health care providers, including physical therapists.
The development of postoperative complication(s) in the imme-
diate or secondary postoperative phase may be expected or unex-
pected and determines further medical-surgical management
and treatment parameters. Common postoperative complica-
tions include the following9:
1. Neurologic complications
• Delayed arousal, altered consciousness, agitation, de-
lirium
• Cerebral edema, seizure, stroke
• Peripheral muscle weakness
• Altered sensation
2. Cardiovascular and hematologic complications
• Hypotension, cardiogenic shock, or both
• Hypertension
• Dysrhythmia
• Myocardial ischemia and/or infarction (MI)
• Hemorrhage
• Deep vein thrombosis (DVT)
• Pulmonary embolism (PE)
3. Respiratory complications
• Hypoxemia or hypercapnia
• Atelectasis
• Pneumonia, pulmonary edema
• Acute respiratory distress syndrome (ARDS)
• Aspiration of gastric contents
• Hypoventilation
• Acute lung injury
4. Renal complications
• Acute renal failure/acute kidney injury (ARF/AKI)
• Urine retention
• Urinary infection
5. Gastrointestinal complications
• Nausea and vomiting
• Hiccups
• Abdominal distention
• Paralytic ileus or obstruction
 Anesthesia: Considerations for the Physical Therapist     CHAPTER 20
6. Integumentary complications
• Wound infection
• Wound dehiscence, evisceration, or both
• Hematoma or seroma
7. Other complications
• Fever
• Sepsis
• Hyperglycemia
• Fluid overload or deficit
• Electrolyte imbalance
• Acid–base disorders
  • Shivering  of anesthesia; operative time; and medications given intraop-
Operative Positioning
Occasionally, a patient may experience pressure-induced nerve
or skin damage as a result of operative positioning, especially
during a lengthy procedure. The physiologic effects of anesthe-
sia, such as hypothermia, hypotension, and pharmacologically
blocked pain and pressure receptors, make a patient susceptible
to pressure injuries.10 When combined with risk factors, such
as advanced age, poor skin integrity, altered nutrition, diabe-
tes, peripheral vascular disease, or the presence of cancer or
neurologic or cardiac disease, the incidence of pressure injury
increases.10 Judicious and proper operative positioning utiliz-
ing pads, limb holders, and drawsheets can prevent or minimize
these injuries.
Standard operative positions include supine (dorsal decubi-
tus), prone (ventral decubitus, low or full jackknife), side-lying
(left or right lateral decubitus, jackknife, or flexed lateral), seated,
and lithotomy (standard, low, or exaggerated) (Fig. 20.1).11 The
supine surgical position is most frequently used. The patient’s
upper extremities are padded and secured in abduction less than
90 degrees with hands supinated or tucked with a drawsheet at
the patient’s side with the hands and thumbs facing up.12
The physical therapist may be consulted in the postoperative
phase to evaluate for extremity weakness related to neuropa-
thy resulting from stretch, compression, ischemia, metabolic
derangement, and/or surgical injury. Peripheral nerve injury
is the second most prevalent adverse event, after death, among
all claims in the Anesthesia Closed Claims database.13 Brachial
plexus injury is the most common, followed by ulnar nerve
injury.13
Postoperative pain, including back pain caused by the loss of
lordosis in supine surgical positioning,12 and joint pain related
to stiffness from immobility or connective tissue injury may also
lead
   to physical therapy consultation.  should adhere to their postoperative mobility plans and re-
Physical Therapy Considerations
• T
 ypically the patient’s chart will contain a brief operative
note and a more detailed report regarding the surgery, as dic-
477
tated by the attending surgeon. The brief note is similar to
a procedure note and may be helpful to confirm the date and
time of surgery as well as the type of surgery performed. The
full operative report specifically states the patient’s position
during surgery, the exact surgical technique used, specimens
that were taken, estimated blood loss, unexpected findings,
and/or complications.
• A review of the anesthesiologist’s notes can provide informa-
tion about the patient’s surgical procedure(s) and type of an-
esthesia; intraoperative hemodynamic status and vital signs,
including electrocardiographic changes; unexpected effects
eratively.
• The physical therapist should closely monitor vital signs,
such as heart rate, blood pressure, oxygen saturation, and re-
spiratory rate, when intervening in the postoperative period
because of the altered, or potentially altered, physiology of
multiple body systems after general anesthesia.
• Careful examination of sensation and motor control in the
lower extremity following local or regional anesthesia (e.g.,
after knee arthroplasty) is important to prevent falls, espe-
cially when the patient is not fully aware of the impairment.
• Nausea and vomiting are among the most common patient
complaints after anesthesia and may continue for days. Nau-
sea and vomiting may make the patient reluctant to mobilize
out of bed. The physical therapist may need to consider the
timing of the physical therapy session relative to these symp-
toms as well as antiemetic medication use, mealtimes, and
rest between patient position changes or other activities in
the day.
• Hyperglycemia can be caused by medications (e.g., cortico-
steroids), stress, acute pain, blood loss, and lengthy surgical
procedures.14 Therefore blood glucose levels may be elevated
postoperatively in patients with or without diabetes. Check
for the current blood glucose levels as you would other vital
signs.
• Document the development and/or resolution of any post-
operative complications or changes in the physical therapy
evaluation and/or treatment notes. Discuss the relevance and
effect of these changes on the patient’s performance in the
assessment portion of the note.
• Discuss the patient’s performance and the plan of care with
nursing staff so that the patient may be safely mobilized
outside of therapy, if appropriate, during the postoperative
phase.
• Educating the postsurgical patient on how and why they
lated surgical restrictions or precautions is of the utmost im-
portance to their rehabilitation success and to the outcome of
their surgeries.
478 CHAPTER 20     Anesthesia: Considerations for the Physical Therapist

FIG. 20.1
(A) Supine position. Patient is placed on the back, with arms at the sides or extended to less than 90 degrees
and the head in alignment with the body. Legs are uncrossed, with a safety strap placed above the knees. (B)
Prone position. Patient is usually anesthetized while supine and then turned. Arms are placed at the sides,
with rolls beneath the axillae 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 the back, and the foot section of operating table is removed or lowered to a 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. Philadelphia: Saunders; 2003; Cassorla L, Lee JW. Patient positioning and associated
risks. In: Miller RD, Eriksson LI, Wiener-Kronish JP, et al., eds. Miller’s Anesthesia. 8th ed. Philadelphia:
Elsevier; 2015:1242-1248.)
 Anesthesia: Considerations for the Physical Therapist     CHAPTER 20
References
1. Moe KL. Perioperative nursing. In: Craven RF, et al., ed.
Fundamentals of Nursing: Human Health and Function. 7th ed.
Philadelphia: Wolters Kluwer Lippincott Williams & Wilkins;
2013:534–563.
2. Hernandez A, Sherwood E. Anesthesiology principles, pain
management, and conscious sedation. In: Townsend CM, et al.,
ed. Sabiston Textbook of Surgery. 20th ed. Philadelphia: Elsevier;
2017:360–391.
3. Neumayer L, Ghalyaie N. Principles of preoperative and opera-
tive surgery. In: Townsend CM, et al., ed. Sabiston Textbook of
Surgery. 20th ed. Philadelphia: Elsevier; 2012:237.
4. Wadlund DL. Prevention, recognition, and management of nurs-
ing complications in the intraoperative and postoperative surgical
patient. Nurs Clin North Am. 2006;41:151–171.
5. Wilson RS. Anesthesia for thoracic surgery. In: Baue AE, Geha
AS, Hammond GL, et al., eds. Glenn’s Thoracic and Cardiovascular
Surgery. 6th ed. Stamford, CT: Appleton & Lange; 1996:23.
6. Kavanagh BP, Hedenstierna G. Respiratory physiology and
pathophysiology. In: Miller RD, et al., ed. Miller’s Anesthesia. 8th
ed. Philadelphia: Elsevier; 2015:444–471.
7. Stentz MJ, Cereda M. Postoperative respiratory failure. In: Atlee
RL, ed. Complications of Anesthesia. 3rd ed. Philadelphia: Elsevier;
2018:663–665.
479
8. O’Brien D. The perianesthesia patient. In: Urden LD, Stacy KM,
Lough ME, eds. Critical Care Nursing: Diagnosis and Management.
8th ed. St. Louis: Elsevier; 2018:989.
9. Nicholau D, Haehn M. Postanesthesia recovery. In: Miller RD,
Pardo MC, eds. Basics of Anesthesia. 7th ed. Philadelphia: Elsevier;
2018:675–690.
10. Primiano M, Friend M, McClure C, et al. Pressure ulcer preva-
lence and risk factors during prolonged surgical procedures.
AORN J. 2011;94(6):555–566.
11. O’Connell MP. Positioning impact on the surgical patient. Nurs
Clin North Am. 2006;41:173–192.
12. Walls J. Patient Positioning during Anesthesia: Supine Position; 2017.
Retrieved from https://www.clinicalpainadvisor.com/anesthesiol-
ogy/patient-positioning-during-anesthesia-supine-position/artic
le/582929/.
13. Chui J, Murkin JM, Posner KL, Domino KB. Perioperative nerve
injury after general anesthesia: a qualitative systematic review.
Anesth Analg. 2018;127(1):134–143.
14. Rutan L, Sommers K. Hyperglycemia as a risk factor in the perio-
perative patient. AORN J. 2012;95(3):352–361.
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 21 Acute Pain Management
C H APT ER  

Jaime C. Paza

CHAPTER OUTLINE CHAPTER OBJECTIVES

Introduction
Pain Evaluation
Physical Therapy Considerations
Pain Management
Pharmacologic Pain Management
Physical Therapy Considerations
The objectives of this chapter are to provide the following:
1 . An overview of pain assessment scales most applicable to the acute care setting
2. A description of physical therapy considerations when evaluating pain
3. An overview of commonly used pharmacologic management strategies for acute pain
4. A description of physical therapy management strategies for acute pain

Introduction

This chapter provides information on the evaluation and management of acute pain within
the context of facilitating patient care. The characteristics of acute pain include a duration of
less than 6 months, an association with tissue damage such as surgery or traumatic injury, an
easily recognized cause, an ability to be treated readily, and a predictable time period.1 Acute
pain in the medical patient may result from numerous sources, including, but not limited to,
nonsurgical abdominal pain, ischemic pain, renal or biliary stones, and phantom limb pain.2,3

Pain Evaluation

The subjective complaint of pain is often difficult to objectify in the inpatient setting. Patients
may be mechanically ventilated, pharmacologically sedated, cognitively impaired, or in too much
pain to articulate their discomfort.4 Furthermore, cognitively impaired patients are at a higher risk
for undertreatment of pain with a resultant decrease in quality of life.5-7 Despite these difficulties,
an effective pain treatment plan depends on an accurate evaluation of the patient’s pain.8,9
Every evaluation requires a complete physical examination and diagnostic evaluation of the
patient’s pain, including imaging, as necessary.3 The criterion for pain assessment is self-report by the
patient because it is the most accurate indicator of the existence or intensity of pain, or both.5,6,10,11
The goal for evaluation should be directed toward individualization while maintaining consistent
assessment standards between patients. To assist with this process, various pain-rating tools have
been developed to evaluate pain in both verbal and nonverbal, as well as conscious and unconscious,
patients. Those presented in this chapter are commonly used and referenced in the literature:
• Verbal pain scales (Table 21.1) include:
• Numeric rating scale (NRS)
• Visual analog scale (VAS)
• Wong-Baker FACES Pain Rating Scale
• Faces Pain Scale, Revised (FPS-R)
• Verbal Rating Scale (VRS)
• Functional Pain Scale
• Nonverbal pain scales include:
• Adult Nonverbal Pain Scale (NVPS) (Table 21.2)
• Behavioral Pain Scale (BPS) (Table 21.3)
• Pain scales used for both verbal and nonverbal patients include:
• Face, Legs, Activity, Cry, Consolability (FLACC) scale (Table 21.4)
• Critical-Care Pain Observation Tool (CPOT) (Table 21.5)

aThe authors acknowledge Danika Vengrow for prior contributions to this chapter.
        481
482 CHAPTER 21     Acute Pain Management

TABLE 21.1  Verbal Pain Scales

Tool Description
Numeric rating The patient reports a number from 0–10 to rate his or her pain, with 0 indicating no pain and 10 indicating
scale (NRS) 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 FACES The patient chooses one of six faces, portrayed on a scale that depicts graduated levels of distress, to repre-
Pain Rating Scale sent his or her pain level.
Faces Pain Scale The patient chooses the face that corresponds to his or her current level of pain intensity. The faces consist
Revised (FPS-R) of endpoints with “no pain” and “very much pain.” Can be converted to a 0–10 rating scale with the
faces having equal intervals.
Verbal Rating Scale (VRS) The patient describes pain by choosing from a list of adjectives representing gradations of pain intensity.
Functional Pain Scale A 0–5 scale with corresponding pain descriptions
0 = No pain
1 = Tolerable (and does not prevent any activity)
2 = Tolerable (but does prevent some activities)
3 = Intolerable (but can use telephone, watch TV, or read)
4 = Intolerable (cannot use telephone, watch TV, or read)
5 = Intolerable (and unable to verbally communicate because of pain)

Data from Kittelberger KP, LeBel AA, Borsook D. Assessment of pain. In: Borsook D, LeBel AA, McPeek B, eds. The Massachusetts General Hospital Handbook of Pain
Management. Boston: Little, Brown; 1996:27; Carey SJ, Turpin C, Smith J, 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; Puntillo K, Pasero C, Li D, et al. Evaluation of pain in ICU patients. Chest. 2009;135:1069-1074; Gloth FM, Cheve AA, Stober CV, et al. The
functional pain scale: reliability, validity, and responsiveness in an elderly population. J Am Med Dir Assoc. 2001;2:110-114; Chanques G, Viel E, Constantin JM, et al.
The measurement of pain in intensive care unit: comparison of 5 self-report intensity scales. Pain. 2010;151:711-721. Zaccagnino MP, Nedeljkovic SS. Pain assessment
tools. In: Yong R, Nguyen M, Nelson E, Urman R, eds. Pain Medicine. Basel, Switzerland: Springer, Cham; 2017.

TABLE 21.2  Adult Nonverbal Pain Scale

Categories 0 1 2
Face No particular expression or smile Occasional grimace, tearing, Frequent grimace, tearing, frown-
frowning, wrinkled forehead ing, wrinkled forehead
Activity Lying quietly, normal position Seeking attention through movement Restless, excessive activity and/or
(movement) or slow, cautious movement withdrawal reflexes
Guarding Lying quietly, no positioning of Splinting areas of the body, tense Rigid, stiff
hands over areas of body
Physiologic I Stable vital signs (no change Change over past 4 hours in any Change over past 4 hours in any of
(vital signs) in past 4 hours) of the following: SBP >20 mmHg, the following: SBP >30 mmHg,
HR >20/min, RR >10/min HR >25/min, RR >20/min
Physiologic IIa Warm, dry skin Dilated pupils, perspiring, flushing Diaphoretic, pallor
a Arevised version of the NVPS scale includes a Respiratory category in the place of the Physiologic II category35:
0 points = Baseline RR/SpO2, Complaint with ventilator
1 point = RR >10 above baseline or 5% ↓ SpO2, mild asynchrony with ventilator
2 points = RR >20 above baseline or 10% ↓ SpO2, severe asynchrony with ventilator
HR, Heart rate; RR, respiratory rate; SBP, systolic blood pressure.
From Odhner M, Wegman D, Freeland N, et al. Assessing pain control in nonverbal critically ill adults. Dimens Crit Care Nurs. 2003;22:260-267.
The validity of these scales may be improved by asking the hemodynamic stress.14 The Adult NVPS is targeted toward
patient about his or her current level of pain, rather than asking the adult patients who are critically ill, mechanically ventilated,
patient to speculate about “usual” or “previous” levels of pain.12 and sedated and has demonstrated good interrater reliability
and validity.14-16 The NVPSa (see Table 21.2) has been adapted
 CLINICAL TIP from the FLACC Pain Assessment scale (see Table 21.4).14 Good
construct validity (P < 0.001) has been reported for the FLACC
The therapist should be sensitive to, and respectful of, cultural
variances in perception and outward expression of pain.6,13 a Arevised version of the NVPS scale includes a Respiratory category in the
place of the Physiologic II category35:
The therapist should be aware that some physiologic mani- 0 points = Baseline RR/SpO2, Complaint with ventilator
1 point = RR >10 above baseline or 5% ↓ SpO2, mild asynchrony with
festations of pain are expected in critically ill patients. One ventilator
needs to analyze the behavioral trend and differentiate pain from 2 points = RR >20 above baseline or 10% ↓ SpO2, severe asynchrony with
physiologic changes, such as elevated vital signs occurring from ventilator
 Acute Pain Management     CHAPTER 21 483

scale, as evidenced by decreased pain scores following admin- been established for both the BPS (>5) and CPOT (>2) to
istration of analgesics and between painful situations to non- denote the presence of pain.11
painful situations. The FLACC scale also has good interrater
reliability when assessing pain in critically ill patients15 and is Physical Therapy Considerations
currently recommended for assessment of postoperative pain in • O bserve pain-related behaviors (e.g., verbal reports, facial
patients 3 to 18 years of age.17 expressions, elevated vital signs) to appropriately select an
The BPS (see Table 21.3) is appropriate for use with assessment tool. Use nonverbal assessment tools when self-
mechanically ventilated, sedated patients in the intensive report cannot be obtained.6
care unit (ICU) and demonstrates very good psychometric • Select the appropriate tool based on the clinical environ-
properties.5,11 Validity is noted by the change in scores of ment, current available evidence, and relevance to the spe-
the BPS with increased painful stimuli.18 In other words, cific patient population.6
as the patient’s pain increases, BPS scores increase accord- • Table 21.6 provides a comparison of various pain scales to aid
ingly. The CPOT (see Table 21.5) was developed to assess in selecting an appropriate tool. The reader is referred to the
pain in critically ill ICU patients and is mainly used with specific articles in the table references for more information re-
those recovering from cardiac surgery. It is reliable and valid garding the psychometric properties. The VAS and NRS are the
in this population and has also been shown to have robust most commonly used scales in a majority of clinical settings.6,20
psychometric properties11,19 The CPOT can be used with • Patients report a preference for the NRS because of its ease of
both verbal and nonverbal patients.5,19 Cutoff scores have use and accuracy.11
• In consideration of accreditation requirements, each patient
interaction must include a pain rating, even if the patient
TABLE 21.3  Behavioral Pain Scale reports 0 out of 10 on the NRS.
Item Description Score • A pain rating is generally accompanied by location, descrip-
Facial Relaxed 1 tion, and most importantly, an “intervention,” especially if
expressions pain is reported greater than 4/10 on the NRS.
Partially tightened (e.g., brow 2
lowering) • The physical therapist should recognize when the patient is
being weaned from pain medication (e.g., transitioning from
Fully tightened (e.g., eyelid 3
closing) intravenous to oral administration) because they may report
increased pain and concurrent reduced activity tolerance dur-
Grimacing 4
ing this period.
Movements No movement 1
• To optimize consistency among health care team members,
of upper Partially bent 2
limbs the physical therapist should use the same pain rating tool as
Fully bent with finger flexion 3 the medical-surgical team to determine the adequacy of pain
Permanently retracted 4 management.
Compliance Tolerating movement 1 • Often, the best way to communicate the adequacy of a pa-
with ventilation Coughing but tolerating ventilation 2 tient’s pain management to nurses or physicians is in terms
for most of the time of the patient’s ability to complete a given task or activity
Fighting ventilator 3 (e.g., the patient is or is not effectively coughing and clearing
secretions). Therapists should communicate to the medical
Unable to control ventilation 4
team both verbally and in their documentation if the cur-
From Payen JF, Bru O, Bosson JL, et al. Assessing pain in critically ill sedated rent pain management strategies are insufficient to allow the
patients by using a behavioral pain scale. Crit Care Med. 2001;29(12):2258-2263. patient to accomplish functional tasks. 

TABLE 21.4  FLACC Pain Assessment Scale

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/ Arched, rigid, or jerking
moves easily forth, tense
Cry No cry (awake or asleep) Moans or whimpers, Crying steadily, screams or
occasional complaint sobs, frequent complaints
Consolability Content, relaxed Reassured by occasional touching, Difficult to console or comfort
hugging, or “talking to,” distractible

Indication: For nonverbal patients, particularly the postoperative pediatric population aged 3 to 18.
FLACC, Face, Legs, Activity, Cry, Consolability.
From Merkel SI, Voepel-Lewis T, Shayevitz JR, et al. The FLACC: a behavioral scale for scoring postoperative pain in young children. Pediatr Nurs. 1997;23(3):293-297.
484 CHAPTER 21     Acute Pain Management

TABLE 21.5  Critical Care Pain Observation Tool (CPOT)

Indicator Descriptor Score
Facial expression No muscular tension observed 0 = Relaxed, neutral
Presence of frowning, brow lowering, orbit tightening and levator 1 = Tense
contraction
All of the above facial movements plus eyelid tightening 2 = Grimacing
Body movements Does not move at all (does not necessarily mean absence of pain) 0 = Absence of movement
Slow cautious movements, touching or rubbing the pain site, 1 = Protection
seeking attention through movements
Pulling tube, attempting to sit up, moving limbs/thrashing, not 2 = Restlessness
following commands, striking at staff, trying to climb out of bed
Muscle tension (evaluation No resistance to passive movements 0 = Relaxed
by passive flexion and Resistance to passive movements 1 = Tense, rigid
extension of upper
extremities) Strong resistance to passive movements, inability to complete them 2 = Very tense, rigid
Compliance with mech- Alarms not activated, easy ventilation 0 = Tolerating ventilator or movement
anical ventilator (intubated Alarms stop spontaneously 1 = Coughing but tolerating machine
patient)
Asynchrony: blocking ventilation, alarms frequently activated 2 = Fighting ventilator
Vocalization (extubated Talking in normal tone or no sound 0 = Talking in normal tone or no
patient) sound
Sighing, moaning 1 = Sighing, moaning
Crying out, sobbing 2 = Crying out, sobbing

Modified from Gélinas C. Nurses’ evaluations of the feasibility and the clinical utility of the Critical-Care Pain Observation Tool. Pain Manag Nurs. 2010;11(2):115-125.

of opioid agents. Recommendations27 from the American Pain

Pain Management
The primary goal in acute pain management is to promote
the resolution of the underlying cause(s) of pain while provid-
ing effective analgesia.21 Acute pain can be managed by using
both pharmacologic and nonpharmacologic methods, includ-
ing physical therapy, either in isolation or, more often, in
combination.22,23
 CLINICAL TIP
Communication among therapists, nurses, physicians, and pa-
tients 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 physician’s orders by
the physical therapist before initiating any modalities or thera-
peutic exercises.
Pharmacologic Pain Management
Pharmacologic management of acute pain has traditionally been
based on the World Health Organization (WHO) Analgesic Lad-
der,24,25 originally designed to promote ongoing assessment of
pain management during palliative care of patients with can-
cer.20 The WHO ladder is a stepwise process in which step 1 is
for patients with mild pain, step 2 is for patients with moder-
ate pain, and step 3 is for patients with severe pain.23,26 Over
time, however, new approaches and guidelines have been devel-
oped to more effectively address acute pain while minimizing
adverse drug effects, such as addiction and abuse with the use
Society and the American Society of Anesthesia include the use of
multimodal analgesia in children and adults with postoperative
pain, including a variety of analgesic medications coupled with
nonpharmacologic interventions, such as relaxation, massage,
and transcutaneous electrical nerve stimulation (TENS). Multi-
modal analgesia is focused on the use of nonopioid analgesics to
decrease the use of opioids and thus their potential side effects or
dependency. Adverse drug effects resulting from opioids include
sedation, respiratory depression, nausea, vomiting, constipation,
and urinary retention.28 Additional recommendations include
providing acetaminophen and nonsteroidal antiinflammatory
drugs (NSAIDs) to both children and adults as part of the mul-
timodal approach to postoperative pain, provided that there are
no contraindications to their administration. The use of neur-
axial analgesia for major thoracic or abdominal surgery is also
recommended, particularly for high-risk patients likely to expe-
rience pulmonary and/or cardiac complications, as well intestinal
motility issues (e.g., ileus) postoperatively. Lastly, surgical site–
specific regional anesthetic techniques in adults and children are
also recommended,27 when supportive evidence exists.
For older adults (>60 years) experiencing acute pain, defined
as greater than 4 on the 0 to 10 NRS, the initial priority is
rapid pain assessment and treatment, followed by comprehen-
sive pain assessment and establishment of a plan for the remain-
der of the pain episode.28 Ideally, if there will be an anticipated
painful event, such as a diagnostic procedure or surgery, then
the comprehensive assessment should occur before this event.
The subsequent pain management plan should be multifaceted,
including patient education in addition to pharmacologic and
 Acute Pain Management     CHAPTER 21 485

TABLE 21.6  Comparison of Pain Assessment Scales

Verbal or
Tool Targeted Population Benefits Reliability Validity Non-verbal
Numeric Rating Adults Easy to use Spearman rank p < 0.001 compared to Verbal
Scale (NRS)a,b,k ­correlation VDS (r = 0.86), VAS, BPS
Coefficient = 0.87b (r = 0.40)a
Visual Analog Scale Adults Visual face and num- Intraclass correlation p < 0.001 compared to Verbal
(VAS)a,c,k ber scale to rate pain coefficients range NRS (r = 0.86) and VDS
0.95–0.98c (r = 0.75)a
Functional Pain Older adults Relates pain to func- Interrater reliability r = 0.62 compared to VASd Verbal
Scale (FPS)d tion coefficient 0.97d
Verbal Descriptor Adults, older adults Descriptions aid pa- Spearman rank correla- p ≤ 0.0001 compared to Verbal
Scale (VDS)a,b,k tient to rate pain tion coefficient = 0.86b VAS (r = 0.75) and BPS
(r = 0.42)a
Face, Legs, Activity, Primarily pediatrics, Clinically useful and Intraclass correla- Criterion validity p < 0.01 Both
Cry, Consolability may also be used in efficient in the ICU tion coefficient = compared to Checklist of
(FLACC)e,f critically ill adults 0.98 (adults), 0.85 Nonverbal Pain Indica-
(children)e tors (adults) and COM-
FORT scale for childrenf
Critical-Care Pain Verbal and nonverbal Good reliability Weighted kappa coef- Criterion validity Both
Observation Tool mechanically venti- and validity when ficient = 0.52–0.88 p < 0.001 compared with
(CPOT)f,g lated patients applied to cardiac based on different patient’s assessment of
surgical patients assessment periodsg paing
Nonverbal Pain Sedated ICU patients, Assessment of burn Interrater reliability = Criterion validity p < 0.05 Nonverbal
Scale (NVPS)f,h conscious adults and trauma patients 94.7% original NVPS, (original NVPS) com-
90.8% revised NVPSh pared to FLACC
(r = 0.86)i
Behavioral Pain Unconscious, critically Widely used for Inter-rater reliability Construct validity Nonverbal
Scale (BPS)f ill, mechanically sedated patients Intraclass correlation p < 0.001 when used for
ventilated, sedated coefficient = 0.95j measuring pain in non-
ICU patients verbal ICU patientsj

ICU, Intensive care unit.

aChanques G, Viel E, Constantin JM, et al. The measurement of pain in intensive care unit: comparison of 5 self-report intensity scales. Pain. 2010;151:711-721.
bWare LJ, Epps CD, Herr K, Packard A. Evaluation of the revised faces pain scale, verbal descriptor scale, numeric rating scale, and Iowa pain thermometer in older

minority adults. Pain Manage Nurs. 2006;7:117-125.

cBijur PE, Silver W, Gallagher EJ. Reliability of the Visual Analog Scale for measure of acute pain. Acad Emerg Med. 2001;8:1153-1157.
dGloth FM, Cheve AA, Stober CV, Chow S, Prosser J. The functional pain scale: reliability, validity, and responsiveness in an elderly population. J Am Med Dir Assoc.

2001;2:110-114.
eVoepel-Lewis T, Zanotti J, Dammeyer JA, Merkel S. Reliability and validity of the Face, Legs, Activity, Cry, Consolability behavioral tool in assessing acute pain in

critically ill patients. Am J Crit Care. 2010;19:55-61.

fCade CH. Clinical tools for the assessment of pain in sedated critically ill adults. Br Assoc Crit Care Nurs. 2008;13:288-297.
gGelinas C, Fillion L, Puntillo K, Viens C, Fortier M. Validation of the critical-care pain observation tool in adult patients. Am J Crit Care. 2006;15:420-427
hKabes AM, Graves JK, Norris J. Further validation of the nonverbal pain scale in intensive care patients. Crit Care Nurse. 2009;29:59-66.
iOdhner, M, Wegman D, Freeland N, Steinmetz A, Ingersoll GL. Assessing pain control in nonverbal critically ill adults. Dimens Crit Care Nurs. 2003;22:260-267.
jAissaoui Y, Zeggwagh AA, Zekraoui A, Abidi K, Abouqal R. Validation of a behavioral pain scale in critically ill, sedated, and mechanically ventilated patients. Anesth

Analg. 2005;101:1470-1476.
kKarcioglu O, Topacoglu H, Dikme O. A systematic review of the pain scales in adults: which to use? Am J Emerg Med. 2018;36(4):707-714.

nonpharmacologic interventions. In older patients with mild to
moderate pain, acetaminophen should be the preferred nonopi-
oid agent, with caution not to exceed the recommended doses.
All NSAIDs should be used cautiously in this population, with
the lowest effective dose prescribed for the shortest possible
period of time and ongoing monitoring for adverse effects. An
opioid may be used as a coanalgesic as part of a multimodal anal-
gesia plan in older adults with moderate to severe acute pain,
provided there are no contraindications and the use of more than
one opioid agent at a time is avoided.28
Nonopioid options include acetaminophen (paracetamol)
and NSAIDs (Table 21.7). Acetylsalicylic acid (aspirin) is the
oldest NSAID prescribed to help manage pain and inflam-
mation, as well as to provide antiplatelet effects for vascular
conditions.23
Acetaminophen is a centrally acting analgesic that interacts
with the cyclooxygenase system.21,22,29 It also has antipyretic
effects and is an effective analgesic when used alone or as an
adjunct to opioid analgesia.21 However, acetaminophen does not
have anticoagulant or antiinflammatory effects compared with
NSAIDs.23
As a group, NSAIDs are nonselective cyclooxygenase (COX)
inhibitors. COX is an enzyme that exists in two primary
forms (COX-1 and COX-2).30 The homeostatic pathways,
486 CHAPTER 21     Acute Pain Management

TABLE 21.7  Nonsteroidal Antiinflammatory Drugs (NSAIDs)

Indications To decrease inflammation
Sole therapy for mild to moderate pain; useful alternative to opioid therapy.
Used in combination with opioids for moderate pain, especially when weaning from stronger medications
Prevention of myocardial ischemia, transient ischemic attack, or stroke (aspirin)
Useful in children younger than 6 months of age
Contraindicated in patients undergoing anticoagulation therapy or with peptic ulcer disease, gastritis, renal dys-
function, or NSAID-induced asthma
Mechanism of action Inhibition of the enzyme cyclooxygenase (COX), which, in turn, stops the production of prostaglandins, resulting
in antiinflammatory effects (prostaglandin is a potent pain-producing chemical)
General side effects Platelet dysfunction, gastritis, nausea, abdominal pain, anorexia, dizziness, and drowsiness
Severe reactions that include nephrotoxicity (dysuria, hematuria) and cholestatic hepatitis
Medications: generic aspirin/acetylsalicylic acid (Bayer, and many others)
name (Trade name) celecoxib (Celebrex)
diclofenac (Cataflam, Voltaren)
diflunisal (Dolobid)
etodolac (Lodine)
fenoprofen (Nalfon)
flurbiprofen (Ansaid)
ibuprofen (Motrin, Advil, and many others)
indomethacin (Indocin, Indocin SR, Indomethacin, Novomethacin, Nu-Indo)
ketoprofen (Orudis, Oruvail, others)
ketorolac (Toradol)
meclofenamate (Meclomen)
nabumetone (Relafen)
naproxen (Anaprox, Naprosyn, Aleve)
oxaprozin (Daypro)
piroxicam (Feldene)
sulindac (Clinoril)
tolmetin (Tolectin)
Data from Nonsteroidal anti-inflammatory drugs. In: Ciccone CD. Pharmacology in Rehabilitation. 5th ed. Philadelphia: FA Davis; 2016:219-236; Frampton C, Quinlan
J. Evidence for the use of non-steroidal anti-inflammatory drugs for the acute pain in the post anaesthesia care unit. J Perioper Pract. 2009;19(12):418-423; Cox F. Basic
principles of pain management: assessment and intervention. Nurs Stand. 2010;25(1):36-39; Musculoskeletal and anti-inflammatory drugs. In: Woodrow R, Colbert
BJ, Smith D, eds. Essentials of Pharmacology for Health Occupations. 6th ed. Clifton Park, NY: Delmar; 2011:389; Drugs affecting the musculoskeletal system. In: Panus
PC, Katzung B, Jobst EE, et al., eds. Pharmacology for the Physical Therapist. New York: McGraw-Hill; 2009:522-523.

which include production of prostaglandins and thrombox- Physical Therapy Considerations

ane, primarily involve the COX-1 enzyme, whereas COX-2
is involved in pathways that produce pain and inflammation.
Prostaglandins have a protective role for the mucosal lining of
the gastrointestinal tract; therefore nonselective inhibition of
these substances can result in gastrointestinal (GI) dysfunction
(see Chapter 8). Selective inhibition of COX-2 was found to
decrease injury to the mucosal lining of the stomach, lead-
ing to the development of COX-2 selective agents, which aim
to reduce inflammation without adverse GI effects. Unfortu-
nately, these medications were correlated with an increased
risk of cardiovascular events in susceptible individuals, result-
ing in rofecoxib (Vioxx) and valdecoxib (Bextra) being taken
off the market. Currently, celecoxib (Celebrex) is the only
COX-2 selective agent available.29-31 Careful patient selection
regarding all NSAIDs and overall cardiovascular risk need to
be considered.30
Opioid agents and NSAIDs can be administered via oral,
intravenous, or intramuscular routes. Table 21.8 provides an
overview of opioid agents commonly used in the management of
acute pain. Alternative routes of administration for pain medi-
cations include local anesthetics (Tables 21.9A and 21.9B) and
patient-controlled analgesia (PCA) (Table 21.10).  support a painful area during functional mobility.
• T he physical therapist should be aware of the patient’s avail-
able pain medications, their dosing schedules, and their du-
ration of effectiveness when scheduling treatment sessions,
particularly if premedication is necessary to optimize inter-
vention.
• Patients should be educated to request pain medicine or push
their PCA button when they need it, particularly when they
are on an “as needed” (PRN) pain medication schedule.32
• Patients should be asked about the specific type of pain that
the medication is intended for, such as postsurgical incisional
pain. Pain medications, such as opioids, may mask the occur-
rence of a new type of pain, such as angina.32
• The physical therapist should educate patients regarding the
use of a pillow, blanket, or his or her hands to splint or sup-
port a painful area. Examples include pain when the patient
coughs following abdominal or thoracic procedures or rib
fractures or when performing functional mobility tasks, such
as going from the side-lying position to sitting at the edge of
the bed.33 If the patient is unable to perform these tasks in-
dependently, the physical therapist can assist with splinting,
as needed. Use of a corset, binder, or brace can also be used to
 Acute Pain Management     CHAPTER 21 487

TABLE 21.8  Systemic Opioids

Indication
Mechanism of action
General side effects
Medications: generic
name (Trade name)
aOpioid antagonist.
Data from Opioid analgesics. In: Ciccone CD. Pharmacology in Rehabilitation. 5th ed. Philadelphia: FA Davis; 2016:201-218; Opioid analgesics and antagonists. In:
Panus PC, Katzung B, Jobst EE, et al., eds. Pharmacology for the Physical Therapist. New York: McGraw-Hill; 2009:278-279; Analgesics, sedatives and hypnotics. In:
Woodrow R, Colbert BJ, Smith D, eds. Essentials of Pharmacology for Health Occupations. 6th ed. Clifton Park, NY: Delmar; 2011:327-333.
Moderate to severe pain
Block transmission of pain from the periphery to the cerebrum through interaction with opioid receptors
Can be administered orally, intravenously, intramuscularly, subcutaneously, and intrathecally
Decreased gastrointestinal motility, nausea, vomiting, and cramping
Mood changes and sedation
Pruritus (itching)
Urinary retention
Bradycardia, hypotension
Respiratory and cough depression
Pupillary constriction, blurred vision
Physical dependence
alfentanil (Alfenta, Rapifen)
buprenorphine (Buprenex, Subutex)
butorphanol (Stadol)
codeine (Paveral)
fentanyl (Actiq, Sublimaze, Duragesic)
hydrocodone (Hycodan)
hydromorphone (Dilaudid, Hydrostat)
levorphanol (Levo-Dromoran, Levorphan)
meperidine (Demerol, Pethidine)
methadone (Methadose)
morphine (MS Contin, Kadian, Morphine sulfate, and others)
nalbuphine (Nubain)
oxycodone (OxyContin, Roxicodone, Percocet [oxycodone with acetaminophen], Percodan [oxycodone with aspirin])
oxymorphone (Opana)
pentazocine (Talwin)
propoxyphene (Darvon)
remifentanil (Ultiva)
sufentanil (Sufenta)
tapentadol (Nucynta)
tramadol (Ultram)
naloxone (Narcan)a

TABLE 21.9A  Local Anesthetics

Type
Topical administration
Transdermal administra-
tion
Infiltration anesthesia
Peripheral nerve block
Central nerve block
Sympathetic block
Intravenous regional
anesthesia (“Bier block”)
Indication
Minor injuries, surgical procedures, adminis-
tered before intravenous (IV) line insertion,
premedication for wound care, hypertonicity
Pain relief in subcutaneous structures, such as
tendons and bursae
Suturing of skin lacerations
Minor surgical procedures, management for
chronic pain, specific nerve pain
Obstetric procedures; alternative anesthesia for
orthopedic procedures, such as lumbar sur-
gery; acute or chronic pain management
Complex regional pain syndrome
Short surgical procedures
Description
Direct application to skin, mucous membrane, cornea, or other
areas requiring anesthesia
Direct application to skin or other surfaces in concentrations to
allow penetration to deeper tissues; iontophoresis (electrical
current), phonophoresis (ultrasound), or transdermal patches
may also be used to facilitate drug administration
Injection directly into selected tissue for diffusion to sensory
nerve endings
Injection close to a single nerve trunk or several nerves/plexus
to interrupt signal transmission
Injection within the epidural space, referred to as epidural nerve
blockade, or intrathecal space, referred to as spinal nerve blockade
Selective interruption of sympathetic efferent pathways
Injection into a peripheral distal limb vein with a proximally
placed tourniquet to isolate limb circulation

Data from Local anesthetics. In: Panus PC, Katzung B, Jobst EE, et al., eds. Pharmacology for the Physical Therapist. New York: McGraw-Hill; 2009:218-225. Local
anesthetics. In: Ciccone CD. Pharmacology in Rehabilitation. 5th ed. Philadelphia: FA Davis; 2016:165-176.
488 CHAPTER 21     Acute Pain Management

TABLE 21.9B  Local Anesthetics

Mechanism of action
General side effects
Medications: generic
(Trade name)
Block action potential propagation, thereby preventing transmission of sensation from the periphery to the central
nervous system
Somnolence, confusion, agitation, restlessness
Hypotension, bradycardia, fatigue, dizziness
articaine (Septocaine)
benzocaine (Americaine)
bupivacaine (Marcaine, Sensorcaine)
butamben picrate (Butesin Picrate)
chloroprocaine (Nesacaine)
dibucaine (Nupercainal)
etidocaine (Duranest)
levobupivacaine (Chirocaine)
lidocaine (Xylocaine)
mepivacaine (Carbocaine)
pramoxine (Tronothane)
prilocaine (Citanest)
procaine (Novocain)
tetracaine (Pontocaine)

Data from Local anesthetics. In: Panus PC, Katzung B, Jobst EE, et al., eds. Pharmacology for the Physical Therapist. New York: McGraw-Hill; 2009:218-225; Local
anesthetics. In: Ciccone CD. Pharmacology in Rehabilitation. 5th ed. Philadelphia: FA Davis; 2016:165-176.

TABLE 21.10  Patient-Controlled Analgesia

Indications For patients with moderate to severe acute pain who are not cognitively impaired and are capable of properly
using the pump
Considerations Preoperative education of the patient on the use of patient-controlled analgesia (PCA)
Ensuring that only the patient doses himself or herself
Dosage, dosage intervals, maximum dosage per set time, and background (basal) infusion rate can be pro-
grammed
Pump apparatus, tubing, and power lines could limit mobility
Side effects Similar to those of opioids (see Table 21.8)
Medications Alfentanil, buprenorphine, morphine, meperidine, fentanyl, hydromorphone, methadone, nalbuphine, oxy-
morphone, pentazocine, sufentanil

Type
Intravenous patient-controlled
analgesia (IV-PCA)
Patient-controlled epidural
analgesia (PCEA)
Patient-controlled regional
analgesia (PCRA)
Patient-controlled intranasal
analgesia (PCINA)
Fentanyl iontophoretic trans-
dermal system (ITS), also
referred to as patient controlled
transdermal analgesia (PCTA)
Description
An IV line to a peripheral vein is connected to a microprocessor pump and a patient is provided with a
button to allow for self-dosing. Surgical catheter implantation can be performed if IV-PCA is required for
longer periods of time.
The tip of a small catheter is placed in either the epidural or the subarachnoid space of the spinal cord, at a
specific level, 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 in the patient’s abdomen and
exits through the front for patient control. Alternatively, the catheter may be connected to an implanted
drug reservoir or access port.
A catheter tip is inserted directly into a specific anatomic site, such as a wound (incisional PCRA), near a
peripheral nerve (perineural PCRA), or into a peripheral joint (intraarticular [IA] PCRA).
The other end of the catheter is attached to a pump with a button for patient control.
Ropivacaine and bupivacaine are also used in PCRA.
Intranasal opioids are delivered using a syringe, nasal spray, dropper, or nebulized inhaler (either in dry pow-
der, water, or saline solution). A pump mechanism is adapted to provide PCINA.
This is a needle-free, self-contained fentanyl delivery system that does not require venous access for adminis-
tration.
System secures to the outer arm or chest with an adhesive backing and, via iontophoresis, delivers fentanyl
across intact skin.
Patient has on-demand dosing up to 6 doses per hour.

Data from Patient-controlled analgesia. In: Ciccone CD. Pharmacology in Rehabilitation. 5th ed. Philadelphia: FA Davis; 2016:261-275; Viscusi E. Patient-controlled
drug delivery for acute postoperative pain management: a review of current and emerging technologies. Region Anesth Pain Med. 2008;33(2):146-158; Chumbley G,
Mountford L. Patient-controlled analgesia infusion pumps for adults. Nurs Stand. 2010;25(8):35-40.

• P
 atients may experience pain induced by exercise or mobi-
lization (PIEM), which can be perceived by patients as a de-
creased quality of life and result in fears about participation
in physical therapy and refusal of care. Enhanced communi-
cation among care providers and with the patient about ex-
pected pain responses during therapy may lessen the adverse
results of PIEM.34
 CLINICAL TIP
Patients, particularly postsurgical patients, are often prescribed
more than one type of pain medication and/or different dosages
to help manage breakthrough pain.
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inhibitors: a journey so far. Curr Med Chem. 2010;17:1563–1593.
32. Chumbley G, Mountford L. Patient controlled analgesia infusion
pumps for adults. Nurs Stand. 2010;25(8):35–40.
33. Cahalin L, Lapier T, Shaw D. Sternal precautions: is it time for
change? Precautions versus restrictions—a review of literature
and recommendations for revision. Cardiopulm Phys Ther J.
2011;22(1):5–15.
34. Alami S, Desjeux D, Lefèvre-Colau MM, et al. Management
of pain induced by exercise and mobilization during physical
therapy programs: views of patients and care providers. BMC
Musculoskelet Disord. 2011;12:172.
35. Kabes AM, Graves JK, Norris J. Further validation of the non-
verbal pain scale in intensive care patients. Critical Care Nurse.
2009;29:59–66.
This page intentionally left blank

     
 22 Airway Clearance
C H APT ER

Lauren Mitchell
Matthew Nippins

CHAPTER OUTLINE CHAPTER OBJECTIVES

Introduction
Methods of Airway Clearance
Cough
Forced Expiratory Technique
(Huff)
Active Cycle of Breathing
Technique
Autogenic Drainage
Positive Expiratory Pressure
Oscillatory Positive Expiratory
Pressure
High-Frequency Chest Wall
Oscillation
Percussion, Postural Drainage,
and Vibration/Shaking
Exercise
Pharmacologic Breathing
Treatments
Creating an Airway Clearance
Program
The objectives of this chapter are the following:
1 . Define secretion retention and airway clearance.
2. Describe select methods of airway clearance available to the physical therapist, including indications,
contraindications, and mechanism of action.
3. Discuss select pharmacologic management options used in conjunction with airway clearance techniques.
4. Review factors to consider when developing an airway clearance program.
Introduction
Mucus secretion is a major contributing factor to the symptomology and disease progression
of many pulmonary conditions. Observed sequela of secretion retention progresses on a con-
tinuum of airway obstruction, airflow limitation, ventilation–perfusion (V/Q) mismatch, and
finally impaired gas exchange.1 Additionally, secretion retention contributes to bacterial colo-
nization and significantly increases the risk for infection, which propagates inflammation and
further mucus secretion and retention.1 Secretion clearance is essential for effective respiratory
function and immune protection of the airways and is considered a cornerstone therapy for
diseases of hypersecretion.2
Airway clearance techniques (ACTs) aim to facilitate secretion clearance, improve ventila-
tion, manage breathlessness and discomfort, and increase cough effectiveness. The mechanism
of action is dependent on the specific method of airway clearance used, but generally consists
of altering the viscoelasticity of the secretions, promoting collateral airflow distal to the secre-
tions, and increasing expiratory flow to promote secretion mobilization from the distal airways
proximally through the bronchial tree.3
The following principles form the basis for how various airway clearance techniques help to
optimize ventilation behind obstructed airways:
1. Interdependence, in which traction forces of expanding alveoli during deep inhalation lead
to the expansion of adjacent, collapsed alveoli, thus allowing air into the obstructed airways
2. Collateral ventilation, where channels bypass blocked airways by using pressure from adja-
cent lung segments to move air into the obstructed airway
3. The 3-second inspiratory breath hold, which allows time for the above two principles to
ventilate obstructed airways.4

 CLINICAL TIP
A basic understanding of respiratory pathophysiology is necessary before selecting airway clear-
ance as an intervention because airway clearance is not indicated for certain conditions (e.g.,
pleural effusion, pulmonary edema, or fully obstructive bronchial tumors) and requires careful
consideration or may be contraindicated for others (e.g., pneumothorax, hemoptysis, and rib or
 
spine fractures).

        491
492 CHAPTER 22     Airway Clearance
Methods of Airway Clearance
Cough
The most basic airway clearance technique is the cough. Cough-
ing serves to clear secretions from the proximal one-third of the
bronchial tree.1,3 All other ACTs function to mobilize secretions
from the distal airways. Their primary goal is to move the secre-
tions into the proximal one-third so as to allow for a cough to
expectorate the secretions as efficiently as possible.3
An effective cough is characterized by dynamic compression
of the airways and increased expiratory flow. It occurs in a series
of phases:
1. Deep inhalation, wherein at least 60% of the patient’s pre-
dicted vital capacity, or 1.5 times tidal volume, increases
elastic recoil.
2. Subsequent closure of the glottis combined with contraction
of the abdominal muscles results in an increase of intratho-
racic pressure. This phase may be lengthened with a 3 second
breath hold to increase collateral ventilation, thus maximiz-
ing air and pressure behind the secretions blocking alveoli.
3. Upon reopening of the glottis, the expiratory flow rate in-
creases, functioning to shear secretions from the distal bron-
chial walls and mobilize them toward more proximal air-
ways. In addition, this increase in airflow can cause dynamic
compression of the airways, which may help move secretions
more proximally as well.5
All of the phases of cough should be assessed to determine
effectiveness before performing ACTs and continually reassessed
throughout the therapy session. Refer to Table 22.1 to review
the benefits of and considerations for coughing as an ACT.
 CLINICAL TIP
Care should be taken to assess the cough to ensure the per-
ceived dynamic compression of the airways is not actually dy-
namic collapse. This can be recognized by a high-pitched, tight,
or spastic cough. This should be avoided as collapse of the
airway dramatically lessens the effectiveness of the cough. The
forced expiratory technique (FET) may be an excellent alterna-
tive for these patients.6
 
Forced Expiratory Technique (Huff)
The forced expiratory technique (FET), otherwise known as
huffing, uses high velocity airflow with an open glottis to move
secretions proximally within the bronchial tree while minimiz-
ing the airway constriction, which occurs during coughing. By
maintaining an open glottis, the equal pressure point (EPP),
an isolated area of airway collapse occurring where airway pres-
sure is equal to intrapleural pressure, is shifted upward in the
bronchial tree.5 The open glottis lowers the risk of dynamic
airway collapse and the movement of the EPP creates a wave
of turbulent airflow to move secretions proximally. This is fur-
ther accomplished by initially huffing at low lung volumes and
progressing to medium and then larger volumes; this progres-
sively moves the EPP from peripheral airways toward the larger
central airways.3 After the gradual volume increase, the FET
includes a subsequent period of relaxed diaphragmatic breaths.
This cycle can be repeated until secretions are proximal enough
to be expectorated with a cough.2,7 Refer to Table 22.1 to review
the benefits of and considerations for FET as an ACT.
 CLINICAL TIP
A clinical cue that is useful for patient instruction on the forced
expiratory technique (FET) technique is to have the patient ex-
hale as though trying to fog a mirror by making a “H/Hu” sound
from the back of the throat. The patient should avoid contrac-
tion of the throat muscles or adding any vocal sounds.
 
Active Cycle of Breathing Technique
The Active Cycle of Breathing Technique (ACBT)8 is a com-
bination of breathing patterns performed in a cyclic fashion to
maximize secretion clearance. The three phases of ACBT are
breathing control (BC), thoracic expansion exercises (TEEs),
and the FET.
• In BC, the patient is instructed to take relaxed tidal volume
breaths, emphasizing diaphragmatic expansion. This is done
to decrease the work of breathing and any airway constric-
tion. Care should be taken to position the patient to mini-
mize the use of accessory muscles.
• BC is followed by TEEs, in which slow, deep breaths are per-
formed, with a 2- to 3-second hold at the end of inspira-
tion to facilitate chest expansion and maximize ventilation.
Tactile and verbal cues may be used to maximize segmental
breathing, based on the breathing pattern and auscultation
assessment performed by the therapist before the interven-
tion. Positioning may also be employed to maximize seg-
mental ventilation, again based on the preintervention as-
sessment.
• TEEs are followed by another round of BC before advancing
to FET. The FET is performed in the same way as described
in the previous section. BC should be reinstituted after the
FET and the cycle may be started again.
The amount of time spent in each phase and the order of
stage progression are based on the individual patient and the
observation of the therapist during the treatment. For example,
if after TEEs the patient displays a significant increase in acces-
sory muscle use, more time would be spent in BC before FET to
decrease the patient’s work of breathing and maximize the effec-
tiveness of the FET. Suggested cycles are visually represented
in Fig. 22.1. Refer to Table 22.1 to review the benefits of and
considerations for ACBT as an ACT. 
Autogenic Drainage
Autogenic drainage (AD)6, or self-drainage, consists of three
phases and relies on the movement of the EPP to facilitate
advancement of secretions from the deep, distal airways to the
larger, more proximal ones. It requires the patient to progress
from breathing at low lung volumes to larger lung volumes.
The patient and therapist use sensory and auditory feedback to
move through the phases of AD. The three phases of AD are the
unsticking phase, the collection phase, and the evacuation phase
(Table 22.2).
 Airway Clearance     CHAPTER 22 493

TABLE 22.1  Benefits of and Considerations for Airway Clearance Techniques (ACTs)
ACT Benefits Considerations
Cough Easy to perform Effectiveness may be limited by pain
Reflexive (or volitional) May cause dynamic airway collapse
No cost Not feasible in patients with tracheostomies
No equipment required May elicit bronchospasm
Patient can be independent with this form of ACT May require assistance to increase intrathoracic pressure in patients
with neuromuscular impairments
Only clears secretions in proximal one-third of airway
Forced expiratory Easy to learn Cognitive integrity imperative to be able to follow instructions and
technique (FET) No cost learn the technique
No equipment required May be limited by pain (less so than cough)
Patient can be independent with this form of ACT Forceful FET may cause bronchospasm
Limits dynamic airway collapse
Minimizes bronchoconstriction compared to a cough
Can be combined with other ACTs
Active Cycle of Easy to learn Cognitive integrity imperative to be able to follow instructions and
Breathing Tech- No cost learn the technique
nique (ACBT) No equipment required Forceful FET may cause bronchospasm
Patient can be independent with this form of ACT
Limits dynamic airway collapse
Useful in patients with pain complaints
Allows for breathing pattern intervention to be done
simultaneously with ACT
Autogenic drain- No cost Cognitive integrity imperative to be able to follow instructions and
age (AD) No equipment required learn the technique
Patient can be independent with this form of ACT Patient must be in tune with his or her breathing cycle to learn this
Limits dynamic airway collapse technique
Useful in patients with pain complaints May increase dyspnea during the teaching of the technique
Positive expira- Easy to learn Cognitive integrity imperative to be able to follow instructions and
tory pressure Inexpensive learn the technique
(PEP), includ- Patient can be independent with this form of ACT Device requires cleaning
ing oscillatory Limits dynamic airway collapse Care should be taken when using PEP or OPEP in patients with
PEP (OPEP) Useful in patients with pain complaints pneumothoraces because increasing positive pressure within the
Excellent for reversing atelectasis lungs may be contraindicated
OPEP may cause bronchospasm
High frequency Easy to learn and use Passive treatment
chest wall Patient can be independent with this form of ACT Expensive
oscillation Can be used in patients unable to follow commands Air bladder devices are larger pieces of equipment and patients are
(HFCWO) Motor oscillating devices increase freedom of move- tethered to them during treatment
ment Due to the possible intensity of the intervention, may be uncom-
fortable for patients with pain complaints within the trunk
May require modifications and padding around ports and tubes
Contraindicated with patients with unstable head and neck injuries
or hemodynamic instability
Some motor oscillating HFCWO units use magnets that require
modified use in the presence of other medical devices (e.g., im-
planted insulin pumps, pacemaker)
Exercise Inexpensive May be limited by functional or musculoskeletal impairments
Additional health benefits outside of airway clearance May require vital sign monitoring or supplemental oxygen

Data from Button BM, Button B. Structure and function of the mucus clearance system of the lung. Cold Spring Harb Perspect Med. 2013;3: pii: a009720; Pryor
JA, Weber BA, Hodson ME, et al. Evaluation of the forced expiration technique as an adjunct to postural drainage in the treatment of cystic fibrosis. Br Med J.
1979;2(6187):417-418; Lapin CD. Airway physiology, autogenic drainage, and active cycle of breathing. Respir Care. 2002;47:778-785; Physiotherapy for people with
cystic fibrosis: from infant to adult. International Physiotherapy Group for CF website. http://www.cfww.org/docs/ipg-cf/bluebook/bluebooklet2009websiteversion.
pdf. Accessed November 30, 2018; McIlwaine M, Button B, Dwan K. Positive expiratory pressure physiotherapy for airway clearance in people with cystic fibrosis.
Cochrane Database Syst Rev. 2015;(6):CD003147; Morrison L, Agnew J. Oscillating devices for airway clearance in people with cystic fibrosis. Cochrane Database Syst Rev.
2009:CD006842; Fink JB, Mahlmeister MJ. High-frequency oscillation of the airway and chest wall. Respir Care. 2002;47:797-807; Thomas J, Cook KJ, Brooks D.
Chest physical therapy management of patients with cystic fibrosis. Am J Respir Crit Care Med. 1995;151:846-850; Osman LP, Roughton M, Hodson ME, et al. Short-
term comparative study of high frequency chest wall oscillation and European airway clearance techniques in patients with cystic fibrosis. Thorax. 2010;65:196-200;
Thomas J, Cook KJ, Brooks D. Chest physical therapy management of patients with cystic fibrosis. Am J Respir Crit Care Med. 1995;151:846-850; Mazzocco MC, Owens
GR, Kirilloff LH, Rogers RM. Chest percussion and postural drainage in patients with bronchiectasis. Chest. 1985;88(3):360-363.
494 CHAPTER 22     Airway Clearance

Breathing
Control

Thoracic
FET/Huff
Expansion

FIG. 22.1
Active Cycle of Breathing Technique (ACBT) patterns. (Courtesy L. Mitchell.)

FIG. 22.2
TheraPep.
TABLE 22.2  Autogenic Drainage: For Use During Patient
Education of the technique. The number of breaths performed in each
phase and the number of cycles completed should be individ-
Forced ualized to meet the needs of the patient and may vary as the
­Expiratory patient’s pulmonary status changes.
 Phase Unsticking Collection Evacuation Technique
Refer to Table 22.1 to review the benefits of and consider-
Inhalation Small/ Larger Deep inha- 2–3 huffs from ations for AD as an ACT.
normal than lation smaller to larg-
breath normal er inhalations
 CLINICAL TIP
Pause 3–4 second 3–4 second 3–4 second
hold hold hold Autogenic drainage (AD) may be conceptually difficult for pa-
Exhalation Full exha­ Large, but Normal tients to comprehend. Use of a chart or drawings may help in
lation not full, exhala- instructing the technique, as well as maximizing their independ-
exhala- tion ence outside of therapy sessions. While teaching this technique,
tion a “rescue breath” may be required. This is a deep breath in the
Clears Distal Middle Upper middle of any of the cycles due to dyspnea. The patient is to
airways airways airways return to where he or she left off in the cycle after the rescue
breath.
Adapted from Lapin CD. Airway physiology, autogenic drainage, and active  
cycle of breathing. Respir Care. 2002;47:778-785.

• U nsticking phase—breathing at low lung volumes mo- Positive Expiratory Pressure

bilizes secretions in the distal airways. This is achieved
through exhalation to the end of the expiratory reserve vol-
ume, followed by inhalation within the lower end of the
vital capacity.
• Collection phase—breathing at medium lung volumes mo-
bilizes secretions in the middle airways. This is achieved
through exhalation just short of the expiratory reserve vol-
ume, followed by inhalation slightly over the prior phases’
range of vital capacity.
• Evacuation phase—breathing at high lung volumes mobiliz-
es secretions in the upper airways. This is achieved through
normal sized exhalation, followed by inhalation breaths that
are in the upper end of the vital capacity.
The evacuation phase should be followed by a huff/FET or
cough to expectorate the mobilized secretions. A cycle of AD
starts with the unsticking phase and advances to the collection
and evacuation phases, thus moving the secretions up the bron-
chial tree.
It is important for the huff/FET or cough to be suppressed
until the end of the last phase because of the progressive nature
Positive expiratory pressure (PEP)9 is achieved by using a device
that provides 10 to 20 cm H2O of pressure during exhalation
(Fig. 22.2). The action of PEP is twofold: Expiratory pressure
maximizes collateral ventilation while also serving to dislodge and
advance retained secretions proximally. Additionally, PEP main-
tains airway patency during exhalation. This allows secretions to
be moved up the bronchial tree while resisting airway collapse.9
The pressure in PEP is attained via a mouthpiece or mask
with variable or interchangeable resistors. Resistance is adjusted
to obtain the desired 10 to 20 cm H2O pressure while main-
taining an inspiratory-to-expiratory ratio of 1:3. A 2- to 3-sec-
ond breath hold is commonly used at the end of each inhalation
to further maximize collateral ventilation. A cycle of 10 to 20
breaths is performed with the PEP device, followed by the FET
or cough. The patient is most often in the seated position, but
this ACT can be used in postural drainage positions as well. To
further decrease the patient’s work of breathing, a tripod sitting
position may be used, with the patient’s elbows on a bedside
table or counter. Refer to Table 22.1 to review the benefits of
and considerations for PEP as an ACT. 

C
FIG. 22.3
Oscillatory positive expiratory pressure (OPEP) devices. (A) Acapella. (B) Flutter. (C) Aerobika.
Oscillatory Positive Expiratory Pressure
Oscillatory positive expiratory pressure (OPEP)10 uses the same
mechanism of action as PEP, with the addition of a vibratory force
during exhalation. OPEP devices contain an oscillating resistor,
which functions to achieve both the desired 10 to 20 cm H2O
pressure and the added vibratory component. During exhalation,
oscillation forces vibrate airway walls, both loosening and chang-
ing the physical properties of retained secretions. This occurs in
Airway Clearance     CHAPTER 22 495
addition to the actions of PEP described above. There are sev-
eral types of OPEP devices currently available, with the Acapella,
Flutter, and Aerobika being the most commonly used (Fig. 22.3).
OPEP is used in a manner similar to PEP devices in that it
is performed in cycles of 5 to 20 breaths with a 2- to 3-second
hold at the end of each inspiration. This cycle is followed by an
FET or cough. Patient positioning for both Acapella and Aero-
bika is also similar to that for PEP devices, and the PEP can be
496 CHAPTER 22     Airway Clearance
FIG. 22.4
High-frequency chest wall oscillation (HFCWO).
mechanically adjusted on each. The Flutter device is position
dependent because the orientation of the device can be maneu-
vered to adjust the PEP. Refer to Table 22.1 to review the ben-
efits of and considerations for OPEP as an ACT.  tural drainage, percussion, and vibration/shaking as an ACT.15
High-Frequency Chest Wall Oscillation
High-frequency chest wall oscillation (HFCWO), or “vest” ther-
apy, delivers oscillatory pulsed airflow into an air bladder vest
worn by the patient. The subsequent pressure on the chest wall
results in increased peak expiratory flow as well as alterations
in the physical properties of the secretions by shearing them
from the lining of the bronchial walls. The increased expiratory
airflow also has the effect of moving the secretions proximally
within the bronchial tree.11
There are multiple brands of HFCWO devices available, and the
settings are manufacturer specific. Current best practice involves
progressing from low frequencies to high frequencies while adjust-
ing pressure settings according to patient comfort.12 Pauses every 3
to 5 minutes for huffing and secretion clearance during HFCWO
are critically important. Total treatment time of 15 to 30 minutes,
one to two times per day, is recommended.13 Combining HFCWO
and nebulized medications may be indicated to decrease the burden
of care in these patients. Refer to Table 22.1 to review the benefits
of and considerations for HFCWO as an ACT. Fig. 22.4 provides
examples of HFCWO options.
Newer models of HFCWO therapy devices have introduced
motor oscillating vests, which offer patients wireless options.
The oscillation is different from that of the air bladder HFCWO,
with more of a percussive force being applied and less increase
in peak expiratory flow.14 With these differences in mind, the
motor oscillating vests need to be assessed for effectiveness sepa-
rately from the traditional air bladder vests.  Pharmacologic Breathing Treatments
Percussion, Postural Drainage, and Vibration/
Shaking1,15
Sometimes referred to as chest physical therapy or manual tech-
niques, percussion is a rhythmical motion performed with a cupped
hand on the chest wall during normal tidal volume breathing. The
percussion, or clapping, creates a pressure wave, which is transmitted
into the airways to loosen secretions. This is typically done for 2 to 5
minutes in each drainage position and is often combined with vibra-
tion or shaking during exhalation to further mobilize secretions
toward the proximal airways. High-frequency vibration and low-
frequency shaking are vibratory forces transmitted via flat hands on
the chest wall during exhalation. Selection between either vibration
or shaking is largely based on clinician and patient preference and
comfort. Number of repetitions needed may vary, but these tech-
niques are commonly performed during two to three exhalations
or until secretions are expectorated. Percussion and vibration/shak-
ing are commonly performed with the patient in postural drainage
positions (Fig. 22.5) to use gravity in mobilizing secretions toward
the proximal airways. Percussion and vibration/shaking may be per-
formed by a health care provider (e.g., physical therapist, respiratory
therapist, or nurse) or taught to a caregiver for home carryover.
These techniques have been shown to assist with secretion
clearance but are generally recommended to be combined with
other ACTs, such as huffing, deep breathing, or PEP/OPEP ther-
apy.12 The addition of these interventions provides the benefits
of collateral ventilation and increased expiratory flow. Refer to
Table 22.3 to review the benefits of and considerations for pos-
 
Exercise
Aerobic exercise can be a powerful supplement to ACTs. Exercise
serves to increase ventilation and respiratory flow, thus increasing
overall secretion clearance.16 There is also evidence to suggest that
exercise modalities that create chest oscillations, such as tread-
mill use instead of a stationary bike, may decrease the mechani-
cal impedance of secretions.17 Exercise and moderate levels of
physical activity have been correlated with slower advancement
of disease progression and decreased hospitalizations in patients
with chronic obstructive pulmonary disease (COPD) and cystic
fibrosis (CF).18,19 Adding another form of ACT to aerobic exercise
or physical activity to increase expiratory flow may be beneficial
in maximizing secretion mobilization.20 Refer to Table 22.1 to
review the benefits of and considerations for exercise as an ACT.
 CLINICAL TIP
Timing of exercise with airway clearance techniques (ACTs)
should vary depending on the patient’s goals. If the goal is to
maximize secretion production, then exercise should immedi-
ately precede the ACT. If maximizing physical activity tolerance
is the goal, then the ACT should be performed before exercise,
with enough time to recover from any airway irritation or con-
striction that patients may experience.
Most ACTs are recommended to be coordinated with the
patient’s pharmacologic breathing treatments. Medications pre-
scribed will vary, but the following recommendations should be
considered when used in conjunction with ACTs21:
• Bronchodilators—open airways; used before airway clear-
ance22
 Airway Clearance     CHAPTER 22 497

A G

C I

F
FIG. 22.5
Recommended postures for segmental drainage from the upper lobe of the lung. (A–F) Patient positions for
postural drainage of S1, S2, S1-2, S3, and S6 as recommended by Potter and Perry. (G–I) Positions recom-
mended 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, whereas Miyagawa included another five postures (8 postures in
total). (A) Bending backward to drain S1. When bending backward or forward (see C), the craniocaudal axis of
the lung is tilted at 45 degrees from the horizontal. (B) 45 degrees 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 that in the prone or
supine position, but the coronal plane of the lung is tilted at 45 degrees. (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) 45 degrees relative prone with head-raised position, which is recom-
mended for S1-2 drainage in the left lung. “Head raised” means that the craniocaudal axis of the lung is raised
to 30 degrees. (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) 45 degrees rotative prone positions with right and left
sides up, respectively. These positions are recommended for S2 and S1-2 drainage during intubation. (From
Takahashi N, Murakami G, Ishikawa A, et al. Anatomic evaluation of postural bronchial drainage of the lung
with special reference to patients with tracheal intubation. Chest. 2004;125(3):935-944.)

• E xpectorants—induce cough or increase volume of secre-

tions; used before airway clearance
• Mucolytics—reduce viscosity23
• Hypertonic saline—used before or during airway clear-
ance21
• Dornase alfa—used 30 minutes before airway clearance21
• Inhaled steroids—reduce inflammation; used after airway
clearance
• Inhaled antibiotics—treat bacterial infections; used after air-
way clearance24
It is important to allow the patient adequate time to resolve
any increase in cough following ACTs before initiating inhaled
steroids or antibiotics. This will increase absorption, rather than
clearance, of the medication.25  time. With these in mind, physical therapists must then apply
Creating an Airway Clearance Program
The ACTs discussed represent some of the most commonly used
and researched methods of secretion clearance, but several other
options are available to patients and clinicians. Other devices
include intrapulmonary percussive ventilators (IPVs), acoustic
percussors, mechanical percussors, and cough assist machines.
Although regional preferences may exist and multiple techniques
may be effective, a personalized approach to the selection of an air-
way clearance program should be used to best meet each patient’s
needs. Factors to consider include disease, patient preference,
comfort, cost, access to devices, lifestyle, adherence, maturity, and
498 CHAPTER 22     Airway Clearance

TABLE 22.3  Percussion, Postural Drainage, and Vibration/Shaking

Benefits Considerations Contraindications
Feasible for use Most beneficial when used in conjunction with additional airway High intracranial pressure (>20 mmHg)
with patients clearance techniques (ACTs) Uncontrolled hypertension
who are unable Patient cannot be independent with percussion or vibration/shaking; Uncontrolled or unprotected airway with risk of
to follow com- requires caregiver assistance aspiration
mands Passive Recent esophageal surgery
Can individualize Time and effort intensive Significantly distended abdomen
treatment to May be uncomfortable if pain is present Pulmonary edema and/or orthopnea
target specific Modification of postural drainage positions may be required with pa- Integumentary abnormalities over the area to be
lobes based on tients with increased intracranial pressure, decreased cardiac output, percussed or vibrated, such as burns, skin grafts,
patient disease pulmonary hemorrhage, and severe dyspnea or open wounds
process Postural drainage should be modified to remove head down position- Rib fractures, flail chest, rib metastases
ing in infants and patients with gastroesophageal reflux disease Acute hemorrhage and/or hemodynamic instability
Unstable head or neck injury
Data from Thomas J, Cook KJ, Brooks D. Chest physical therapy management of patients with cystic fibrosis. Am J Respir Crit Care Med. 1995;151:846-850; Mazzocco
MC, Owens GR, Kirilloff LH, Rogers RM. Chest percussion and postural drainage in patients with bronchiectasis. Chest.1985;88(3):360-363.

their knowledge of the physiologic basis for each technique to
make the best selection and optimize its effectiveness.4
The most effective or appropriate selection of an ACT may
vary depending on a patient’s current state. What is most effec-
tive during hospitalization for an exacerbation or acute illness
may differ from what best fits into the patient’s lifestyle and
general maintenance program at home. Additionally, the param-
eters of a single type of ACT may be altered to fit the patient’s
current status. For example, during an exacerbation a patient
may need to decrease the number of breaths per cycle on their
PEP device before the FET or cough as a result of the increased
irritability of their airways or increased sputum production.
References
1. Frownfelter D, Dean E. Cardiovascular and Pulmonary Physical
Therapy: Evidence to Practice. St. Louis: Elsevier; 2012.
2. Irwin S, Tecklin J. Cardiopulmonary Physical Therapy: A Guide to
Practice. St. Louis: Mosby; 2004.
3. Button BM, Button B. Structure and function of the mucus clear-
ance system of the lung. Cold Spring Harb Perspect Med. 2013;3.
4. McIlwaine M, Bradley J, Elborn JS, Moran F. Personalising
airway clearance in chronic lung disease. Eu Respir Rev. 2017;23.
5. Knudson RJ, Mead JERE, Knudson DE. Contribution of air-
way collapse to supramaximal expiratory flows. J Appl Physiol.
1974;36(6):653–667.
6. Lapin CD. Airway physiology, autogenic drainage, and active
cycle of breathing. Respir Care. 2002;47:778–785.
7. Pryor JA, Weber BA, et al. Evaluation of the forced expiration
technique as an adjunct to postural drainage in the treatment of
cystic fibrosis. Br Med J. 1979;2(6187):417–418.
8. International Physiotherapy Group for CF. Physiothera-
py for people with Cystic Fibrosis: from infant to adult.
http://www.cfww.org/docs/ipg-cf/bluebook/bluebooklet2009webs
iteversion.pdf. Accessed November 30, 2018.
9. McIlwaine M, Button B, Dwan K. Positive expiratory pressure
physiotherapy for airway clearance in people with cystic fibrosis.
Cochrane Database Syst Rev. 2015;(6):CD003147.
10. Morrison L, Milroy S. Oscillating devices for airway clear-
ance in people with cystic fibrosis. Cochrane Database Syst Rev.
2017:CD006842.
11. Fink JB, Mahlmeister MJ. High-frequency oscillation of the
airway and chest wall. Respir Care. 2002;47:797–807.
12. Thomas J, Cook KJ, Brooks D. Chest physical therapy manage-
ment of patients with cystic fibrosis. Am J Respir Crit Care Med.
1995;151:846–850.
13. Osman LP, Roughton M, Hodson ME, et al. Short-term compara-
tive study of high frequency chest wall oscillation and European
airway clearance techniques in patients with cystic fibrosis.
Thorax. 2010;65:196–200.
14. Hill-Rom. Where Therapy is Moving - Monarch® Air-
way Clearance System. May 8, 2018 Available at:
https://respiratorycare.hill-rom.com/globalassets/media/produ
ct-media/monarch-system/pdfs/202183r7—-monarch-clinician-
brochure-lr.pdf. Accessed December 16, 2018.
15. Mazzocco MC, Owens GR, Kirilloff LH, Rogers RM. Chest
percussion and postural drainage in patients with bronchiectasis.
Chest. 1985;88(3):360–363.
16. Burtin C, Hebestreit H. Rehabilitation in patients with chronic
respiratory disease other than chronic obstructive pulmonary dis-
ease: exercise and physical activity interventions in cystic fibrosis
and non-cystic fibrosis bronchiectasis. Respiration. 2015;89:
181–189.
17. Dwyer TJ, Alison JA, McKeough ZJ, et al. Effects of exercise on
respiratory flow and sputum properties in patients with cystic
fibrosis. Chest. 2011;139:870–877.
18. Schneiderman-Walker J, Wilkes D, Strug L, et al. Sex differences
in habitual physical activity and lung function decline in children
with cystic fibrosis. J Pediatr. 2005;147:321–326.
19. Spruit M. Pulmonary rehabilitation. Eur Respir Rev. 2014;23:
55–63.
20. Dwyer TJ, et al. Effects of exercise on respiratory flow and
­sputum properties in patients with cystic fibrosis. Chest.
139(4):870–877
21. The Cystic Fibrosis Foundation. Mucus Thinners. Accessed
December 2nd, 2018. https://www.cff.org/Life-With-CF/
Treatments-and-Therapies/Medications/Mucus-Thinners/.
22. The Cystic Fibrosis Foundation. Bronchodilators. Accessed
December 2nd, 2018. https://www.cff.org/Life-With-CF/
Treatments-and-Therapies/Medications/Bronchodilators/.
23. Rogres D. Mucoactive agents for airway mucus hypersecretory
diseases. Respir Care September. 2007;5 2(9):1176–1197.
24. The Cystic Fibrosis Foundation. Antibiotics. Accessed December
2nd, 2018. https://www.cff.org/Life-With-CF/Treatments-and-
Therapies/Medications/Antibiotics/
25. Agent P, Parrott H. Inhaled therapy in cystic fibrosis: agents,
devices and regimens. Breathe (Sheff). 2015;11(2):110–118.
 23
C H APT ER  
CHAPTER OUTLINE
Introduction
Berg Balance Scale
Procedure
Interpretation of Results
Gait Speed
Timed Up and Go Test
Procedure
Interpretation of Results
Dynamic Gait Index
Procedure
Interpretation of Results
Tinetti Performance-Oriented
Mobility Assessment
Procedure
Interpretation of Results
Sit-to-Stand Tests
Interpretation of Results
Acute Care Index of Function
Function in Sitting Test
Procedure
Exercise Testing
Six-Minute Walk Test
Procedure
Interpretation of Results
Self-Paced Walk Test
Interpretation of Results
Psychometric Properties
Activity Measure for Post–Acute
Care “6 Clicks” Inpatient Short
Form
Intensive Care Unit–Specific
Outcome Measures
Confusion Assessment Method
for the Intensive Care Unit
Interpretation of Results
Intensive Care Unit Mobility Scale
Functional Status Score for the
Intensive Care Unit
Procedure
Interpretation of Results
Perme Intensive Care Unit Mobil-
ity Score
Interpretation of Results
Physical Function in Intensive
Care Test—Scored
Procedure
Interpretation of Results
Conclusion
Appendix 23A: Functional Tests
Outcome Measures
Erin M. Thomas
CHAPTER OBJECTIVES
The objectives of this chapter are the following:
1 . Describe outcome measures applicable to patient populations in the inpatient acute care setting
2. Provide an overview of how to select, administer and interpret outcome measures
Introduction
Performing objective measures of patient’s performance in the acute care setting is best practice.
Clinicians frequently look for the “best” test for particular functional activities (e.g., balance).
Several contributing factors are that functional activities have multisystem components and
outcomes can vary based on the environment, time of day, or prior patient practice. The pur-
pose of this chapter is therefore to describe more common outcome measures for various patient
populations in the acute care setting to assist the therapist with selection and administration of
specific tests and not to compare one test with another.
Fortunately the literature on outcome measures is consistently expanding. Although atten-
tion should be paid to the patient population used to validate each test described in this sec-
tion, a particular outcome measure still may be useful for patient examination and evaluation
in a population not yet specifically studied. A clinician should consider all factors when inter-
preting the results of any clinical test and continue to read current literature to keep abreast of
changes in test validation and interpretation. Given the acuity of patients in the hospital set-
ting, modifications of objective functional tests may be required. It is important to document
any modifications you make when using a functional test.
 CLINICAL TIP
The American Physical Therapy Association (APTA) has developed an evidence-based web por-
tal called PTNow to assist clinicians with making evidence-based practice decisions.1 PTNow
provides clinically relevant information on typically treated conditions. PTNow includes such
resources as an article search, clinical summaries, tests and measures, clinical practice guidelines
(CPGs), Cochrane reviews, and a rehabilitation reference center. The test and measures section
of PTNow allows members to download tests, tools, and measurement instruments for patient
examination.
It is also important for clinicians to reference the Evaluation Database to Guide Effectiveness
(EDGE) documents created by specified taskforces within the APTA Academies and Sections.2
The EDGE documents are key resources to assist clinicians in identifying a core set of recom-
mended tests/measures for a specific population or practice area.3 An example of the Stroke
EDGE II recommendations for acute care can be found at the Academy of Neurologic Physical
Therapy site (http://neuropt.org/docs/default-source/edge-documents/strokedge-ii-acute-care.
pdf?sfvrsn=14fc5443_2).4
The outcome measures presented in this chapter were selected because of their ease of use,
reliable and valid test results, and the appropriate population in the acute care setting. Where
applicable, interrater (tested by different therapists) and intrarater (retested over time by a
        499
500 CHAPTER 23     Outcome Measures

TABLE 23.1  Overview of the Berg Balance Scale

Population Equipment Time Reliability Validity
Older adults who have Ruler 10–20 minutes Interrater reliability: ICC = 0.98 Concurrent validity:
experienced acute cerebrovas- Stopwatch required to complete rs = 0.88 Tinetti, r = 0.91
cular accident and/or are in a Chair test Intrarater reliability: Get up and go, r = −0.76
rehabilitation setting Step stool ICC = 0.98 Predictive validity:
Flat surface Internal consistency: <45 score predicts falls
Cronbach’s alpha = 0.96 (sensitivity 53%)

ICC, Intraclass correlation coefficient; r, correlation coefficient; rs, Spearman’s rank correlation coefficient.
Data from Thorbahn L, Newton R. Use of the Berg Balance Test to predict falls in elderly persons. Phys Ther. 1996;76(6):576-583; Conradsson M, Lundin-Olsson L, Lin-
delof 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. Phys
Ther. 2007;87:1155-1163; Thompson M, Medley A. Performance of community dwelling elderly on the timed up and go test. Phys Occup Ther Geriatr. 1995;13(3):17-
30; Whitney S, Poole J, Cass S. A review of balance instruments for older adults. Am J Occup Ther. 1998;52(8):666-671; Berg K, Wood-Dauphinee S, Williams JI, et al.
Measuring balance in the elderly: preliminary development of an instrument. Physiother Can. 1989;41:304.

single therapist) reliability3 and content,a construct,b and pre-

dictivec validity will be noted in the respective description of BOX 23.1  Short Form of Berg Balance Scale
each test.5  Items:
• Reaching forward with outstretched arm
• Standing with eyes closed
Berg Balance Scale • Standing with one foot in front
• Turning to look behind
The Berg Balance Scale (BBS) is a 56-point scale that evaluates • Retrieving object from floor
14 tasks. Katherine Berg developed this test to assess the level • Standing on one foot
of function and balance in various patient populations.6 Table • Sitting to standing
23.1 describes the appropriate population, required equipment, Data from Chou CY, Chien CW, Hsueh IP, et al. Developing a short form of
completion time, reliability, and validity of the BBS. the Berg Balance Scale for people with stroke. Phys Ther. 2006;86(2):195-204.

Procedure levels are reduced to three (0, 2, 4). This modified BBS has been
The patient is evaluated and graded on a sequence of balance shown to have excellent criterion, construct and content validity
activities, such as sitting unsupported with arms folded, rising, as well as excellent test–retest reliability (intraclass correlation
standing, transfer from one surface to another, reaching forward coefficient [ICC] = 0.99) in patients who have had a cerebrovas-
in standing, picking up objects off the floor, turning around in a cular accident (CVA).7,8 Box 23.1 outlines the seven items on
full circle, and standing on one leg.6 Scoring for each task ranges this modified BBS.
from 0 to 4. A score of 0 indicates that the patient is unable to
complete a particular task. A score of 4 indicates that the patient
can completely carry out the task.6 The 14 tasks consist of 6:  CLINICAL TIP
• Sitting to standing The short-form Berg Balance Scale (SF BBS) was originally de-
• Standing unsupported veloped for patients who have had a stroke, and its use has more
• Sitting unsupported recently been studied in patients with hip and knee arthroplasty
• Standing to sitting and older adults.9,10
 
• Transfers
• Standing with eyes closed
• Standing with feet together Interpretation of Results
• Reaching forward with an outstretched arm Clinicians can use the BBS in clients who have goals to improve
• Retrieving object from floor static and dynamic sitting and standing balance and have the
• Turning to look behind capacity to change in this area.11 Once you have administered
• Turning 360 degrees the BBS and have a score, you can interpret or apply this infor-
• Placing alternate foot on stool mation in several different ways:
• Standing with one foot in front of the other foot 1. Track the score over time—the BBS can be used to estab-
• Standing on one foot lish a baseline in acute care to show change over time in the
A short form of the BBS (SF BBS) demonstrates psychomet- course of a person’s episode of care. Note: Even if the patient
ric test properties similar to those of the original BBS. The SF in acute care scores a “0” on the BBS, this baseline score has
BBS includes seven activities rather than 14, and the scoring value to show changes at a later time point in their rehabili-
tation.
a Content validity: Degree to which a test actually measures what it was 2. Use evidence to draw a conclusion(s) or set a goal for your
designed for. patient.
b Construct validity: Degree to which a theoretical construct is measured
Use minimal detectable change (MDC) values for the BBS
against the test.
c Predictive validity: Ability of a test to predict future performance. that have been established for various populations (e.g., acute

TABLE 23.2  Overview of the Timed “Up and Go” Test
Population Time Equipment
Geriatric population with 1–3 minutes to complete Armchair
various diagnoses test Stopwatch
Persons with spinal cord Assistive devicea
injury
aIf necessary, an assistive device may be used while performing this test.
ICC, Intraclass correlation coefficient; r, correlation coefficient.
Data from Whitney S, Poole J, Cass S. A review of balance instruments for older adults. Am J Occup Ther. 1998;52(8):666-671; Posiadlo D, Richardson S. The timed “up
and go”: a test of basic functional mobility for frail elderly persons. J Am Geriatr Soc. 1991;39:142-148; Berg KO, Wood-Dauphinee SL, Williams JI, et al. Measuring
balance in the elderly: validation of an instrument. Can J Public Health. 1992;83:S7-S11; Van Hedel HJ, Wirz M, Dietz V. Assessing walking ability in subjects with
spinal cord injury: validity and reliability of 3 walking tests. Arch Phys Med Rehabil. 2005;86:190-196; Portney LG, Watkins MP. Foundations of Clinical Research Ap-
plications to Practice. 3rd ed. Philadelphia: F.A. Davis; 2015:77-118.
stroke, MDC of 6)12 to set a short-term goal. It will be impor-
tant to consider the acuity level of your patient when select-
ing the goal for a change score. Also, when retesting, consider
the change in the score and compare it with this MDC value
to confirm if the change detected exceeds the referenced MDC.
MDC change values for stroke and Parkinson’s disease have been
established. According to Stevenson, a change of +6 points on
the BBS was necessary to be 90% confident of a genuine change
in a person who has suffered an acute stroke.12 Although Steffen
and Seney found that change of 5 points on the BBS was nec-
essary to demonstrate change that was clinically significant in
patients with Parkinson’s disease.13
 CLINICAL TIP
In patients who are over 65 years of age and are dependent in
at least one personal activity of daily living, a change of 8 points
on the Berg Balance Scale (BBS) is necessary to demonstrate a
genuine change in function.14
Gait Speed
Gait speed has been designated the “sixth vital sign.”15 Gait
speed is a valuable measure both clinically and for research
purposes in evaluating and monitoring functional capacity and
a person’s general health status. Age-based and gender-based
norms have been established for this test. Although gait speed
can be affected by age, gender, and anthropometric properties,
the range for a normal walking speed is 1.2 to 1.4 m/s.16 It is
a valid, reliable measure that is predictive of various outcomes,
such as response to rehabilitation, functional dependence, fra-
gility, mobility disability, cognitive decline, falls, institution-
alization, cardiovascular-related events, and mortality. Gait
speed can be assessed at self-selected speeds or at a fast pace.15
A clinician can also assess a person’s gait speed trajectory by
determining the rate of change. Walking speed trajectories that
demonstrate a rapid decline are more strongly associated with
mortality compared with trajectories that are more stable.15
Gait speed test protocols vary widely, no standardized proto-
col has been established. The variations used include distances (2
to 40 meters), start (static versus dynamic), speed (self-selected
versus fast), path (straight versus turn), instructions (“walk at
a comfortable pace” versus “walk as if you are taking a stroll in
Outcome Measures     CHAPTER 23 501
Reliability Validity
Interrater reliability: Content validity: none
r = 0.99 reported
Intrarater reliability: Concurrent validity: Berg
r = 0.99 ICC = 0.99 Balance Scale
the park”), and timing instrument (stopwatch, automatic timer,
instrumented walkway).15 Therefore it is important to docu-
ment the exact testing parameters used so that the same condi-
tions can be used on subsequent testing sessions.
 CLINICAL TIP
Clinicians should consider administering the gait speed test with
a straight path 5 to 10 meters in length because this is more
clinically feasible.16 No significant difference was found among
5-, 8-, or 10-meter walkways in older adults or in persons who
have had a stroke.17 Clinicians may also want to incorporate an
acceleration phase of approximately 2.5 meters for self-selected
speeds and 3 to 3.25 meters for maximal speeds.15 Clinicians
are referred to the article by Middleton et al. for a helpful visual
graphic summarizing the current literature for cutoff scores of
walking speeds and correlated expected outcomes.15
Timed Up and Go Test
The “up and go” test was originally developed in 1986 to serve
as a clinical measure of balance in older adults.18 The original
test used a numeric scoring system to determine a patient’s level
of balance, but it was modified in 1991 to a timed version by
Podsiadlo and Richardson.19 The Timed Up and Go (TUG) Test
uses a time score to assess gait and balance in the older adult
population and in clients with spinal cord injury (SCI) and is
summarized in Table 23.2.20-24
Procedure
The patient is timed during a five-part mobility task from start
to finish. The task consists of the following19:
1. Rising from an armchair
2. Walking 3 meters
3. Turning around
4. Walking 3 meters back to the armchair
5. Sitting down
It is important to instruct the patient to walk at a comfort-
able and normal pace to ensure safety throughout the test. Test
instructions and video can be accessed at the website of the U.S.
Centers for Disease Control and Prevention (CDC) at https://w
ww.cdc.gov/steadi/materials.html#tabs-2-5 (2) under the Func-
tional Assessments tab.25 
502 CHAPTER 23     Outcome Measures

TABLE 23.3  Overview of the Dynamic Gait Index

Population Equipment Time Reliability Validity MCD/MCID
Older adult Shoe box Less than 10 Intrarater reli- Predictive /concurrent validity: MDC = 2.9 for
Stroke 2 cones minutes ability: Berg , r = 0.67; Community-dwelling
Parkinson’s Stairs ICC = 0.90 Content validity: older adults
disease 20-foot walkway Interrater reli- Each of the four rating scale cat- MCID = 1.80 for sub-
Multiple ability: egories distinctly identified sub- jects with DGI scores
sclerosis ICC = 0.92 jects at different ability levels; <21/24 and 0.60 for
Brain injury eight items appear to represent a subjects with DGI
single construct scores >21/24

ICC, Intraclass correlation coefficient; MCD, minimal detectable change; MCID, minimally clinically important difference; r, correlational coefficient.
Data from: Chui YP, Fritz SL, Light KE, Velozo CA. Use of item response analysis to investigate measurement properties and clinical validity of data for the dynamic
gait index. Phys Ther. 2006;86:778-787; Pardasaney PK, Latham NK, Jette AM, et al. Sensitivity to change and responsiveness of four balance measures for community
dwelling older adults. Phys Ther. 2012;92:388-397; Romero S, Bishop MD, Velozo CA, Light K. Minimum detectable change of the berg balance scale and dynamic
gait index in older persons at risk for falling. J Geriatr Phys Ther. 2011;34:131-137; Jonsson LR, Kristensen MT, Tibaek S, Andersen CW, Juhl C. Intra- and interrater
reliability and agreement of the Danish version of the dynamic gait index in older people with balance impairments. Arch Phys Med Rehabil. 2011;92:1630-1635.

Interpretation of Results
Shumway-Cook and colleagues determined that community-
dwelling older adults who took longer than 13.5 seconds to
complete the test were classified as “fallers.” 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 func-
tion, and (3) increased familiarity of the test, or a combination
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 with baseline results.
As described in Table 23.2, compared with other func-
tional tests (i.e., BBS), with regard to balance testing, the
TUG test is a consistent test of the balance characteristics in
the frail community-dwelling elderly population. The ability
or inability to complete the TUG test helps stratify patients
according to their fall risk. Patients who are unable to com-
plete the TUG test for nonphysical reasons (including refusal
or inability to follow instructions [e.g., dementia or delirium])
appear to have higher rates of falling compared with patients
who are unable to perform the TUG test for physical reasons
(inability to sit, stand, or walk independently, or with standby
assistance).26
Additionally, patients who have undergone hip fracture sur-
gery and are discharged from the acute care setting with a TUG
score of 24 seconds or more are more likely to have a fall in
the next 6 months than are patients with scores of less than
24 seconds.27 When used in an acute care setting, this test can
objectively demonstrate improvements in balance and ambula-
tion. Over the course of therapy, it is expected that the time
the patient takes to complete the TUG test will decrease as the
patient’s condition improves.24
Dynamic Gait Index
Procedure
The Dynamic Gait Index (DGI) was designed to assess the like-
lihood of falling in older adults by testing eight different tasks
with gait with varying demands, such as walking at different
speeds, walking with head turns, negotiating over and around
obstacles, making quick turns, and stair climbing. A possible
total score of 24 is determined by scoring each item on a four-
level ordinal scale (no gait dysfunction, minimal impairment,
moderate impairment, severe impairment). This test takes
about 15 minutes to administer and requires a box, two cones,
stairs, and a 20-foot walkway (Table 23.3).
 CLINICAL TIP
The DGI has been studied in patients with multiple sclerosis,
Parkinson’s disease, stroke, and vestibular disorders. The DGI
has been recommended or highly recommended by the MS
Edge and Stroke Edge groups for use in the acute care setting.2,29
The DGI has excellent interrater and intrarater reliabilities for
use in community-dwelling older adults with baseline impair-
ment in the hospital setting, with an intraclass correlation of inter-
rater and intrarater reliability of 0.92 and 0.90, respectively.30 
Interpretation of Results
A higher score on the DGI denotes a higher level of indepen-
dent functional mobility. Several studies have found that a score
less than 19 indicates an increased risk of falls for community-
dwelling older adults.31,32 

 CLINICAL TIP Tinetti Performance-Oriented Mobility Assessment

Caution should be exercised in interpreting the scores of the
TUG test when administered to a frail older adult who has mul-
tisystem impairments. Patients with these characteristics may
have TUG scores as low as 10 seconds but may still be at risk
for falling.28
 
The Tinetti performance-Oriented Mobility Assessment
(POMA) has several adapted versions, such as Tinetti Mobil-
ity Test (TMT). The TMT is a performance test of balance and
gait maneuvers used during normal daily activities.33 The TMT
is a modified version of the original POMA test.34 It has been
 Outcome Measures     CHAPTER 23 503

TABLE 23.4  Overview of the Tinetti Performance-Oriented Mobility Assessment

Population Equipment Time Reliability Validity
Balance portion: adult or Chair 10–15 minutes to Interrater reliability: Concurrent validity: Berg, r = 0.91
geriatric population with a Stopwatch complete test 85% ± 10% agreement Predictive validity: ≤ 19 total score
wide variety of diagnoses 15-foot walkway balance portion predicts fall risk

r, Correlation coefficient.
Data from Tinetti ME. Performance oriented assessment of mobility problems in elderly patients. J Am Geriatr Soc. 1986;34(2):119-126; Kegelmeyer DA, Kloos AD,
Thomas KM, Kostyk SK. Reliability and validity of the Tinetti Mobility Test for individuals with Parkinson disease. Phys Ther. 2007;87:1369-1378; Kloos AD,
Bello-Haas VD, Thome R, et al. Interrater and intrarater reliability of the Tinetti balance test for individuals with amyotrophic lateral sclerosis. J Neurol Phys Ther.
2004;28(1):12-19.

TABLE 23.5  30-Second Chair Stand Test: Criterion-Referenced Fitness Standards for Maintaining Independence in Older
Adults
Age-Groups
60–64 65–69 70–74 75–79 80–84 85–89 90–94
Number of chair stands in 30 secondsa
Women 15 15 14 13 12 11 9
Men 17 16 15 14 13 11 9
aData from Rikli RE, Jones CJ. Development and validation of criterion referenced clinically relevant fitness standards for maintaining physical independence in later
years. Gerontologist. 2013;53(2):255-267.

studied in the older adult population and in conditions for pain
management, Parkinson’s disease, stroke, and amyotrophic
lateral sclerosis.34-37 This test has two subscales—balance and
gait—as described in Appendix 23A. In the TMT, there are nine
maneuvers in the balance portion and seven maneuvers in the
gait portion. The balance subscale on the TMT can be used indi-
vidually as a separate test of balance.35
Procedure
The balance maneuvers are graded on an ordinal scale as normal (2
points), adaptive (1 point), or abnormal (0 points). The gait maneu-
vers are graded as “normal” or “abnormal,” with the exception of
a few items. A combination of the total points for the balance and
gait portions are summed together to determine the final score.18,38
A summary overview of the TMT can be found in Table 23.4.  adults.54-64 Overall, the 5×STS tends to have excellent reliabil-
Interpretation of Results
A total combined score on the balance and gait subscales of the TMT
correlates with the patient’s relative risk of falling. A score of 19 or
less out of 28 is indicative of a fall risk.39 The TMT is an effective
and objective measure to predict fall risk in the older adult popula-
tion and to assist in determining progress over time in therapy.  from nonfallers on the 5×STS.60 In 2008 Tiedemann found a
Sit-to-Stand Tests
There are several sit-to-stand tests40-50 currently being used in
the clinical setting; these include the 30-second chair stand test
(30CST) and the five-time sit-to-stand test (FTSTS or 5×STS).
These tests have been used for the assessment of balance or lower
extremity strength and function. The 30CST is a component of
the Fullerton Functional Fitness Test Battery, also known as the
senior fitness test, and was developed to overcome the floor effects
of the five- or 10-repetition sit-to-stand test in older adults.51,52
The 30CST is a criterion and norm-referenced test that has
established cutoff scores (Table 23.5) for moderately function-
ing older adults in maintaining physical independence. Table
23.6 provides an overview of the 30CST. Rikli et al. determined
criterion validity by comparing weight-adjusted leg press per-
formances in independent, functioning, community-dwelling
older adults over the age of 60 years.52 Construct validity was
established in a study by Gill et al. for participants who were
awaiting a total hip or knee replacement with moderately high
correlations seen with 36-Item Short Form Survey (SF-36; physi-
cal function and mental health components) and the 50-feet
timed walk test.53
The 5×STS has been studied in patients with pulmonary
diseases, multiple sclerosis, arthritis, joint pain, fractures, Par-
kinson’s disease, stroke, or vestibular disorders and in older
ity and adequate to excellent validity (concurrent/predictive and
construct) in each of these populations.
Interpretation of Results
In 2011 Duncan et al. determined that a cutoff score of 16 sec-
onds in patients with Parkinson’s disease distinguished fallers
cutoff score of 12 seconds or more identified a need for further
assessment for fall risk in community-dwelling older adults aged
74 to 98 years.65 Age-related norms are reported in Table 23.7.66
The procedures for sit-to-stand tests have included timing
the patient’s ability to complete five or 10 repetitions; counting
the number of stands completed by the patient in 30 seconds;
and varying the conditions, such as the use of arms to stand
up. A meta-analysis by Bohannon cautiously reports normative
values for the five-repetition sit-to-stand test in older adults. In
persons who are 60 to 69 years of age, mean times to complete
this test were 11.4 seconds, whereas in persons 80 to 89 years of
age, mean times were 12.7 seconds.50
504 CHAPTER 23     Outcome Measures

TABLE 23.6  Overview of the 30-Second Chair Stand Test

Population Equipment Time Reliability Validity MCID MCD
Primarily for Chair without Under 5 min- Interrater reliability: Construct valid- Range 2.0–2.6 2.96 in pa-
those age >60 arms—seat utes for set up, Excellent: r = 0.95 ity ranged from in patients tients with
years height 17 instruction, (95% CI = 0.84, 0.97) excellent to poor with osteoar- osteoar-
Hip osteoar- inches procedure Intrarater reliability: for patients with thritis thritis
thritis Stopwatch Excellent: osteoarthritis;
ICC (1.1) values Criterion validity—
ranged from .0.97 excellent for com-
(95% CI 0.94–0.98) munity dwelling
to 0.98 (95% CI elderly
0.97–0.99)

CI, Confidence interval; ICC, intraclass correlation coefficient; MCD, minimal detectable change; MCID, minimally clinically important difference.
Data from: Rikli RE, Jones CJ. Development and validation of criterion referenced clinically relevant fitness standards for maintaining physical independence in later
years. Gerontologist. 2013;53(2):255-267; Jones C, Rikli R, Beam WC. A 30-s chair stand test as a measure of lower body strength in community-residing older adults.
Res Q Exerc Sport. 1999;70(2):113-119; Gill SD, de Morton NA, Mc Burney H. An investigation of the validity of six measures of physical function in people await-
ing joint replacement surgery of the hip or knee. Clin Rehabil. 2012;26(10):945-951; Wright AA, Cook CE, Baxter GD, Dockerty JD, Abbott JH. A comparison of 3
methodological approaches to defining major clinically important improvement of 4 performance measures in patients with hip osteoarthritis. J Orthop Sports Phys Ther.
2011;41(5):319-327.

TABLE 23.7  Descriptive Statistics for Time (in seconds) for Five Sit-to-Stand Repetitions
Measurement (n) Mean + SD Minimum–Maximum
Trial 1: all ages (94) 7.8 + 2.8 4.0–16.3
Trial 2: all ages (94) 7.5 + 2.8 4.0–17.0
Mean: all ages (94) 7.6 + 2.7 4.0 + 16.0
Mean 19–49 years (39) 6.2 + 1.3 4.1–11.5
Mean: 50–59 years (15) 7.1 + 1.5 4.4–9.1
Mean 60–69 years (18) 8.1 + 3.1 4.0–15.1
Mean 70–79 years (16) 10.0 + 3.1 4.5–5.5
Mean 80–89 years (6) 10.6 + 3.4 7.8–6.0

Reprinted from Bohannon RW, Shove ME, Barreca SR, Masters LM, Sigouin CS. Five-repetition sit-to-stand test performance by community-dwelling adults: a preliminary
investigation of times, determinants, and relationship with self-reported physical performance. Isokinet Exerc Sci. 2007;15(2):77-81 with permission from IOS Press.

Despite some of the inconsistencies reported in the literature,
performing a suitable version of the sit-to-stand test during the
examination of patients can still yield helpful information because
a relationship exists between the sit-to-stand test with instrumen-
tal activities of daily living and balance. In addition, a sit-to-stand
test can be used to describe the limitations during a functional
activity and measure improvement over time. Repeating the same
procedure within the same clinical scenario (e.g., same chair/same
bed height) will help improve the reliability of these results.
 CLINICAL TIP
When documenting a sit-to-stand test, make sure to describe
the test characteristics, such as seat height, use of arms or no
arms, repetitions (5 or 10), and time to complete the test, as
well as when to stop timing, either at the last stand or the last sit.
Acute Care Index of Function
The Acute Care Index of Function (ACIF) was developed
in 1988 to standardize the assessment of functional status in
patients with acute neurologic deficits.67,68 The test is based on
patient performance measured in four domains: mental status,
bed mobility, transfers, and mobility. Higher scores denote bet-
ter patient performance.
For the functional aspects of the examination (bed mobility,
transfers, and mobility) there are three possible choices for scor-
ing the patient’s performance: “unable,” “dependent,” or “inde-
pendent,” with point values of 0, 4, and 10, respectively.67 For
the mental status portion of the test, only the absence or pres-
ence of patient performance is issued point values. The sums of
all the scores for all of the domains are then averaged.67 Finally,
each domain is independently weighted by a multiplier to help
detect changes in performance and to determine the patient’s
discharge disposition.68
This test has good validity (rs = 0.81; p < 0.01) and good
interrater reliability (weighted kappa 0.88–0.98), except in the
area of “impaired safety awareness” (weighted kappa 0.60), as a
result of the more subjective nature of the question.67,68 The test
has subsequently been used to describe the functional status of
patients with lower extremity orthopedic health conditions.69 To
date, the minimal clinically detectable change score for this test
has not been calculated.68 A systematic review article in 2018
by Peterson and colleagues on the psychometric properties of
physical function measures used in the intensive care unit (ICU)
found that the ACIF was one of only four other measures that
were the most comprehensive in examining physical function.70
 Outcome Measures     CHAPTER 23 505

TABLE 23.8  Overview of the Function in Sitting Test (FIST)

Population Equipment Time Reliability Validity MCD MCID
Acute stroke Standard hospital 15 minutes Vestibular disorders: Concurrent validity: Acute stroke: Vestibular
Vestibular bed (without or less Test–retest reliability: Good to excellent with 5.63 disorders:
disorders air mattress) excellent ICC = 0.097a Berg Balance Scale Vestibular MCID >6.5
Multiple Stopwatch Interrater reliability: (BBS) and Functional disorders:
sclerosis Excellent ICC = 0.991a Independence Measure 5.5
Intrarater reliability: (FIM) at admission and
Excellent ICC = 0.99a discharge
Spearman ρ = −0.71–0.85

aMedical diagnoses of the balance participants included Parkinson’s disease, multiple sclerosis, and stroke.
ICC, Intraclass correlation coefficient; MCD, minimal detectable change; MCID, Minimally Clinically Important Difference.
Data from Gorman SL, Radtka S, Melnick M, Abrams G, Byl NN. Development and validation of Function in Sitting Test (FIST) in adults with acute stroke. J Neurol
Phys Ther. 2010;34(3):150-160; Gorman SL, Harro C, Platko C. Validity and responsiveness of the function in sitting test (FIST) in adults in inpatient rehabilitation:
preliminary results. J Rehab Med. 2013;6(suppl 53):99; Sung JH, Ousley CM, Shen S, et al. Reliability and validity of the function in sitting test in nonambulatory
individuals with multiple sclerosis. Int J Rehabil Res. 2016;39(4):308-312.

 CLINICAL TIP Procedure

Clinicians may want to consider using the ACIF to make appro-
priate discharge recommendations, thereby reducing readmis-
sions and helping patients get to the appropriate level of care.
Function in Sitting Test
The Function in Sitting Test (FIST) was developed to be a per-
formance-based bedside evaluation of sitting balance that assesses
the static and dynamic components of sitting balance. The FIST
consist of 14 items on an ordinal 0 to 4 rating scale. A score
of 0 indicates that the individual is dependent, requires com-
plete assistance to perform the task, or is unable to perform the
task even with physical assistance; 1 indicates that the individual
needs assistance, with documentation of the assist level as min,
mod, or max; 2 means the person requires upper extremity sup-
port to complete the task; 3 indicates that the person requires
verbal cues or increased time to complete the task, but is able to
complete the task independently; and 4 indicates that the person
is able to complete the task independently and successfully.71 The
range of scores is 0 to 56 points. The 14 items are listed below:
• Anterior (superior sternum)/posterior (between scapular
spines)/lateral nudge (dominate side at acromion)—random-
ly administered once
• Static sitting—30 seconds
• Sitting, shake “no”—left and right
• Sitting, eyes closed—30 seconds
• Sitting, lift foot—dominant side, lift foot 1 inch twice
• Pick up object from behind—object at midline, hands
breadth posterior
• Forward reach—use dominant arm, must complete full motion
• Lateral reach—use dominate arm, clear opposite ischial tu-
berosity
• Pick up object from the floor—from behind feet
• Posterior scooting/anterior scooting—move backward 2
inches/move forward 2 inches
• Lateral scooting—move to dominant side 2 inches
Testing involves the following:
1. One trial of each item is allowed.
2. 
Verbal instructions and demonstration are permitted, as
needed, by the therapist.
3. Standard position—the person is seated at the edge of the
hospital bed with half of the femur on the surface, hips and
knees at 90 degrees, and feet flat either on the floor or using
a stool
4. Hands are placed in the person’s lap unless they are needed
for support.
Table 23.8 summarizes the characteristics of the FIST.70
The FIST has been found to be valid and reliable for assessing
patients with acute stroke, multiple sclerosis, and vestibular
disorders.71-73 
Exercise Testing
Although maximal exercise testing with evaluation of exhaled
gases is considered the gold standard to evaluate a person’s car-
diopulmonary capacity, maximal testing is not commonly per-
formed in the acute care setting. Submaximal tests are often
performed by the medical team in the hospital setting when
cardiac disease is suspected. Aerobic capacity field tests can be
used safely to help a clinician in the differential diagnosis of
the etiology of a patient’s fatigue or shortness of breath (SOB),
describing a person’s current aerobic capacity, estimating aero-
bic capacity, or prescribing exercise or in outcome assessment.74
Despite their submaximal design, these exercise tests may result
in a symptom-limited test that, in some patient populations,
approaches a maximal effort, particularly in very deconditioned
patients.
Although not within the scope of this text, exercise prescrip-
tion based on actual effort during an exercise test can be more
accurate than exercise prescribed on heart rate (HR) or perceived
effort alone. Refer to American College of Sports Medicine Guideline
for Exercise Testing and Prescription75 for further details on exercise
testing and prescription. 
506 CHAPTER 23     Outcome Measures

TABLE 23.9  Overview of the Six-Minute Walk Test (6MWT)

Population Equipment Time Reliability Validity
Patients with cardiac and/ Chair 10–15 minutes to Test–retest reliability: Responsiveness
or pulmonary disease and Stopwatch complete test ICC = 0.93 index validity:
osteoarthritis of the knee Pulse oximeter 0.6
Portable blood pressure cuff
Rate of perceived exertion scale
Visual analog scale for pain
Measuring wheel

ICC, Intraclass correlation coefficient.

Data from King MB, Judge JO, 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; Woo MA, Moser DK, Stevenson LW, et al. Six-minute walk test and heart rate variability: lack of association in advanced stages of heart
failure. Am J Crit Care. 1997;6(5):348-354; Kovar PA, Allegrante JP, 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; Guyatt GH, Sullivan MJ, Thompson PJ, et al. The 6-minute walk: new measure of exercise capacity
in patients with chronic heart failure. Can Med Assoc J. 1985;132:919-923; McGavin CR, Gupta SP, McHardy GJR. Twelve-minute walking test for assessing disability
in chronic bronchitis. BMJ. 1976;1:822; Butland RJ, Pang J, Gross ER, et al. Two-, six-, and twelve-minute walking tests in respiratory disease. BMJ. 1982;284:1607.

Six-Minute Walk Test
The 6-minute walk test (6MWT) is a time-limited measure of
functional capacity in which a patient walks as far as possible
on a course for 6 minutes.76 This test evolved from the 12-min-
ute walk test, originally designed to assess disability levels in
patients with chronic bronchitis.77 The 6MWT was found to
provide similar measures of exercise tolerance and therefore was
adopted by clinicians for its convenience (Table 23.9).77,78
Although this test is considered a time-limited, submaximal
exercise test, it may cause patients with advanced heart disease
and end-stage lung disease to approach their maximal work
effort.76,79 In patients with advanced heart disease, regression
equations have been used to predict peak oxygen uptake (peak
VO2) values.80
 CLINICAL TIP
There is also a 2-minute walk test that has been used for the
functional capacity assessment of patients after cardiac surgery,
those patients with chronic obstructive pulmonary disease, and
for persons after amputation.81-83 Although the 2-minute walk
test may lack normative data and the 6MWT is preferred when
possible, the 2-minute walk test may be considered as an al-
ternative to functional walking when a patient is known to be
compromised and will not be able to complete walking for more
than 2 minutes.
Procedure
Premeasure the course in a flat, straight, enclosed corridor,
approximately 30 meters (100 feet) in length to minimize
turns.84 Patients should have rested in a chair for 10 minutes
before the start of the test and use their usual walking aid and
footwear for the test. For standardization of the test, patients are
encouraged to carry their own oxygen delivery system, are asked
not to talk to anyone during the test, and are not accompanied
by the clinician during the test. Standardized encouragement,
or the lack thereof, has been shown to influence the results of the
BOX 23.2  Standardized Instructions for the 6-Minute Walk
Test (6MWT)
“The object of this test is to walk as far as possible for 6 minutes.
You will walk back and forth in this hallway. Six minutes is a long
time to walk, so you will be exerting yourself. You will probably
get out of breath or become exhausted. You are permitted to slow
down, to stop, and to rest as necessary. You may lean against the
wall while resting, but resume walking as soon as you are able. You
will be walking back and forth around the cones. You should pivot
briskly around the cones and continue back the other way without
hesitation. Now I’m going to show you. Please watch the way I
turn without hesitation.” Demonstrate by walking one lap yourself.
Walk and pivot around a cone briskly. “Are you ready to do that? I
am going to use this counter to keep track of the number of laps you
complete. I will click it each time you turn around at this starting
line. Remember that the object is to walk AS FAR AS POSSIBLE
for 6 minutes, but don’t run or jog. Start now or whenever you are
ready.”
From American Thoracic Society Board of Directors. ATS Statement: guidelines
for the six-minute walk test. Am J Resp Crit Care Med. 2002;166:111-117.
walking test.85 Standard statements of encouragement, if used,
should be made in normal tone and identify only the time left
(i.e., “You have 2 minutes left. You are doing a good job.”).85
The standardized initial instructions to the patient, according to
the American Thoracic Society (ATS), can be found in Box 23.2.
Although following ATS guidelines is preferred, it is recom-
mended that the performance of the 6MWT in the acute setting
be altered to maximize patient safety in recognition of the larger
potential for medical or physical variability in this patient pop-
ulation. During the test, it is recommended that the therapist
walk slightly behind the patient to allow for close monitoring
of HR and saturation of peripheral oxygen (SpO2), but also to
guard the patient if necessary. Because of the potential for varia-
tions in vital signs from baseline values, HR, SpO2, respiratory
rate (RR), rate of perceived exertion (RPE), and rate of perceived
dyspnea (RPD) should be monitored every 2 minutes and for
at least 2 minutes after the end of the test to assess for patient
recovery. If the patient is unable to complete the full 6 minutes,
then the distance covered upon termination is measured along
with establishing the reason for test termination by the patient.

TABLE 23.10  Prediction Equations for 6-Minute Walk
Test (6MWT) Distance
Author Equation
Enright, 199863 Healthy men age between 40 and 80 years
Expected 6MWD = (7.57 × height in cm)
− (5.02 × age) − (1.76 × weight in kg) −
309 meters
Healthy women age between 40 and 80
years
Expected 6MWD = (2.11 × height in cm)
− (2.29 × weight in kg) − (5.78 × age) +
667 meters
Troosters, 199964 Age range = 50–85 years of age
Expected 6MWD = 218 + (5.14 × height
in cm − 5.32 × age) − (1.80 × weight in
kg) + (51.31 × gender*)
*Male = 1; female = 0
Gibbons, 200165 Age range = 22–79 years of age
Expected 6MWD = 868.8 − (2.99 × age) −
(74.7 × gender*)
*Male = 0; female = 1
Enright, 200366 Age range ≥ 65 years
Healthy females:
Expected 6MWD = 493 + (2.2 × height in
cm) − (0.93 × weight in kg) − (5.3 × age)
Healthy men: Add 17 meters to results of
above equation
6MWD, 6-Minute walk distance.
 CLINICAL TIP
• Although the 6MWT was initially performed in a 30-meter
hallway, studies have attempted to validate the test in other
formats, such as on a treadmill, because of space, safety, and
monitoring issues frequently found in the acute care patient
population. The conclusions reached in the literature thus far
regarding a 6MWT performed on a treadmill are currently
mixed.86-89 It is important to consider the validity of the test
and patient safety when choosing how to perform the 6MWT.
• Patient safety takes priority over standardization of the test.
For patients who are unable to ambulate without assistance,
an alternative exercise test, such as a seated test or cycle test,
should be chosen.
Interpretation of Results
Many studies have examined the usefulness of the 6MWT in
specific populations and have found it to be effective in predict-
ing oxygen consumption and determining the efficacy of surgi-
cal intervention on functional mobility.77,78,80,90 A number of
regression equations have been developed to predict the 6MWT
distance in healthy adults (Table 23.10).91-94 These prediction
equations can be used by physical therapists as a means of deter-
mining the level of deficits in their patients and ultimately in
prescribing exercise and measuring progress in patients’ func-
tional activity tolerance. A minimal change in walking distance
of 54 to 70 meters has been shown to be clinically significant for
improving functional status in patients with chronic obstructive
Outcome Measures     CHAPTER 23 507
pulmonary disease (COPD).95 In frail, older adults with chronic
heart failure, the 6MWT is a responsive measure of cardiac
status.96 
Self-Paced Walk Test
The self-paced walk test (SPWT) examines the time it takes an
individual to walk a set distance, typically less than 150 feet.
The individual is asked to walk quickly and safely without
overexertion, and assistive device use is permitted and docu-
mented. The time it takes to complete the specified distance is
recorded in seconds but can also be recorded as meters divided
by the time (m/s) to establish the person’s walking speed. This
test takes less than 5 minutes to administer and requires a
tape measure, a marked walkway, and a stopwatch. This test is
ideal for use in persons with hip and knee osteoarthritis (OA),
recent joint replacements, or rheumatoid arthritis and older
adults.
Interpretation of Results
Kennedy (2005) and Gill and colleagues (2008) determined
the MDC for a 40-meter and 50-meter fast pace SPWT as
4.04 seconds or 0.33 m/s and 3.08 s or 0.2 m/s, respectively,
for persons with end-stage hip and knee OA before total joint
replacement.97,98 
Psychometric Properties
Test–retest reliability for 50-foot, 40-meter, 6-meter, and
25-meter SPWT ranged from excellent (0.97) to good (0.74)
in individuals with hip and knee OA. Interrater and intra-
rater reliabilities were found to be excellent for the 50-foot
and 40-meter SPWT for people with hip and knee OA.98,99
Construct validity varied widely in different populations,
from no significant correlation between the 25-meter SPWT
and the Western Ontario McMaster Universities Osteoarthri-
tis Index (WOMAC) to modest correlation with the Lower
Extremity Functional Scale (r = 0.44, 95% confidence interval
[CI] 0.26–0.59).100,101 However, Butler et al. did find signifi-
cant correlations between seven tests of functional mobility
(stair ascent and descent, coordinated stability test, near tan-
dem balance test, 6MWT, 5×STS, and the alternate step test)
suggestive of a common mobility construct in older adults
aged 75 to 98 years.102 Butler and colleagues concluded from
these findings that older individuals who perform poorly on
one test are more likely to perform poorly on other tests as
well.102 Discriminant validity has been established between
the 400-meter SPWT and the Short Physical Performance
Battery (SPPB) in high-functioning older adults, suggesting
that the SPWT may be better at distinguishing functional
levels in this patient population.103 Predictive validity has
determined that a decrease in the SPWT from 0.80 m/s to
0.43 m/s in community-dwelling older adults was consistent
with individuals who had documented disabilities in activi-
ties of daily living 4 years later. In predicting falls, when older
adults 70 years of age or older demonstrated slow gait speeds
of greater than equal to 70 m/s, there is a 1.5-fold increase
risk of falls.104,105 
508 CHAPTER 23     Outcome Measures
TABLE 23.11  Activity Measure for Post-Acute Care
(AM-PAC) “6 Clicks” Mobility and Daily Activity Items
and Rating Scale
Mobility Daily Activity
Turning over in bed Feeding
Supine to sit Oral and facial hygiene
Bed to chair Dressing—uppers
Sit to stand Dressing—lowers
Walk in room Toilet (toilet, urinal, bed pan)
3–5 steps with rail Bathing (wash, rinse, dry)
1 = Unable (total assist)
2 = A lot (mod/max assist)
3 = A little (min assist/supervision)
4 = None (independent)
Activity Measure For Post–Acute Care “6 Clicks”
Inpatient Short Form
The Activity Measure for Post-Acute Care (AM-PAC) “6 Clicks”
is a standardized functional assessment tool created by the
Cleveland Clinic Health System. The AM-PAC “6 Clicks” is
a shortened acute care version derived from the full version of
AM-PAC that was developed by researchers at Boston Uni-
versity. The AM-PAC “6 Clicks” incorporates the conceptual
framework of the International Classification of Functioning,
Disability, and Health (ICF) and measures functional outcomes
in basic mobility and daily activity.106 The AM-PAC basic
mobility and daily activity short forms are a six-item assess-
ment, which uses a four-point ordinal scale for each, for a total
of 24 points, with lower scores indicating a greater deficit in
mobility. Table 23.11 outlines the six items and the rating
scale.106 The AM-PAC “6 Clicks” demonstrates excellent inter-
rater and test–retest reliability for both physical therapists and
nurses in a study conducted by Hoyer et al.107 A 2014 study
by Jette and colleagues noted that the “6 Clicks” basic mobil-
ity and daily activity scores documented at the first physical
or occupational therapy encounter were accurate in predict-
ing a patient’s discharge destination.108 A cutoff score of 42.9
for basic mobility and 39.4 for daily activity on the first visit
demonstrated fair to good accuracy at predicting a person’s dis-
charge destination.108
 CLINICAL TIP
As multiple members of the medical team use the AM-PAC, it is
important for there to be intrarater and interrater reliability and
standardization within a facility with regard to score calculation
to aid in communication and discharge planning.
Intensive Care Unit–Specific Outcome Measures
Outcomes testing in the ICU is an area that is challenging
because of the variety of diagnoses and the fluctuations in level
of acuity. Despite these challenges, researchers are developing
tools specific to this specialized area of acute care practice to aid
physical therapists in objective measurement of patients whose
physical function can vary widely hour to hour and day to day.
A few of these tests are described in the following sections. In
addition, clinicians are encouraged to refer to the 2017 study by
Parry and colleagues that summarizes the current clinical utility
and practical considerations of functional measures in the ICU
setting.109 
Confusion Assessment Method for the Intensive
Care Unit
The Confusion Assessment Method for the Intensive Care Unit
(CAM-ICU) is a tool used in the ICU setting to monitor for the
presence or absence of delirium. This tool can be used in non–
mechanically ventilated and mechanically ventilated critically
ill patients. The CAM-ICU has four diagnostic features110:
1. Acute change or fluctuating course of mental status
2. Inattention
3. Altered levels of consciousness—assessed using the Rich-
mond Agitation Sedation Scale (RASS)
4. Disorganized thinking
Interpretation of Results
A person is considered to test positive for delirium if he or
she manifests features 1 and 2 and exhibits either feature 3
or 4.111 In a study by Guenther and colleagues, CAM-ICU
flowsheets demonstrated sensitivity ranging from 88% to
92% and specificity of 100% with a CI of 95% and accuracy
reported as 94% to 96% between two clinicians.112 A sys-
tematic review by Shi et al. in 2013 found similar sensitivity
and specificity when pooling data from 11 different studies
(sensitivity: 81% to 95% [CI = 57% to 93%] and specificity
of 98% [95% CI = 86% to 100%]).113 The interrater reli-
ability in several studies has been found to be good to very
high.112 The CAM-ICU tool has been found to have criterion
validity, according to the Diagnostic and Statistical Manual of
Mental Disorders, 4th edition (DSM-IV), as well as positive
predictive validity.110
 CLINICAL TIP
The CAM-ICU is commonly used in nursing; however, this is
also a beneficial tool for physical therapists, who can use it as a
screening tool before intervention to assess a person’s ability to
retain or carryover information provided during a session.
Intensive Care Unit Mobility Scale
The Intensive Care Unit Mobility Scale (IMS) is a tool
designed to quickly document (in ≤1 minute) in a stan-
dardized manner the highest level of functional mobility
for patients in the ICU environment. The IMS consist of 11
items rated on a categorical scale. Table 23.12 outlines the
classifications and definitions according to Hodgson.114 The
IMS is considered a reliable tool when used by both junior
 Outcome Measures     CHAPTER 23 509

TABLE 23.12  Intensive Care Unit (ICU) Mobility Scale (IMS)

Classification
0 = Nothing (lying in bed)
1 = Sitting in bed, exercises in bed
2 = Passively moved to chair (no standing)
3 = Sitting over edge of bed
4 = Standing
5 = Transferring bed to chair
6 = Marching on spot (at bedside)
7 = Walking with assistance of two or more
people
8 = Walking with assistance of one person
9 = Walking independently with a gait aid
10 = Walking independently without a gait
aid
Definition
Passively rolled or passively exercised by staff, but not actively moving
Any activity in bed, including rolling, bridging, active exercises, cycle ergometry and active
assisted exercises; not moving out of bed or over the edge of the bed
Hoist, passive lift or slide transfer to the chair, with no standing or sitting on the edge of the
bed
May be assisted by staff, but involves actively sitting over the side of the bed with some trunk
control
Weight bearing through the feet in the standing position, with or without assistance; may
include use of a standing lifter device or tilt table
Able to step or shuffle through standing to the chair; involves actively transferring weight
from one leg to another to move to the chair; if the patient has stood with the assistance of a
medical device, he or she must step to the chair (not included if the patient is wheeled in a
standing lifter device)
Able to walk on the spot by lifting feet alternately (must be able to step at least four times,
twice on each foot) with or without assistance
Walking away from the bed/chair by at least 5 meters (5 yards) assisted by two or more people
Walking away from the bed/chair by at least 5 meters (5 yards) assisted by one person
Walking away from the bed/chair by at least 5 meters (5 yards) with a gait aid, but no assis-
tance from another person; in a wheelchair-bound person, this activity level includes wheel-
ing the chair independently 5 meters (5 yards) away from the bed/chair
Walking away from the bed/chair by at least 5 meters (5 yards) without a gait aid or assistance
from another person

From Hodgson C, Needham D, Bailey M, et al. Feasibility and inter-rater reliability of the ICU Mobility Scale, Heart & Lung 2014;43(1):19-24.

physical therapists (≤2 years’ experience) and senior physical
therapists (≥2 years’ ICU experience).114 Construct validity
was demonstrated through a moderate correlation between
the IMS and the Medical Research Council (MRC) sum score
at ICU discharge and significantly higher IMS values for par-
ticipants without ICU-acquired weakness. Predictive validity
was illustrated with increasing IMS values being associated
with survival to 90 days and discharge home.115 Parry et al.
also found that lower age and higher scores on the IMS at
ICU discharge were significant factors that predicted dis-
charge to the patient’s home.116 High criterion validity was
seen between the Physical Function in Intensive Care Test–
Scored (PFITs) and the IMS (rho = 0.81; 95% CI 0.70–0.88;
p < 0.005).116  nursing facility, long-term care/hospice/expired, and transfer to
Functional Status Score for the
Intensive Care Unit
The Functional Status Score for the Intensive Care Unit (FSS-
ICU) is an outcome tool that is commonly used in the ICU set-
ting and in long-term acute care hospitals (LTACHs).117 The
FSS-ICU is derived from the Functional Independence Measure
(FIM).
Procedure
The tool scores five functional tasks (rolling, transferring supine
to sit, sitting at the edge of the bed, transferring sit to stand,
ambulation) using the FIM rating system based on a scale of
1 (total assist) to 7 (complete independence). A score of 0 is
assigned if a patient is unable to perform a task, as a result of
either physical limitations or medical status. The simple sum of
the five scores is the reported score for the FSS-ICU, with the
available range of scores being 0 to 35.118 The reported time to
administer this test is 10 to 30 minutes. 
Interpretation of Results
The higher the total score, the more independent the individual.
Thrust et al. found that (1) cumulative FSS-ICU scores signifi-
cantly improved from admission to discharge in the LTACH
setting and (2) the FSS-ICU tool was able to distinguish the
discharge categories (home, inpatient rehabilitation, skilled
a short stay hospital).117 The FSS-ICU has demonstrated good
construct validity, both convergent and concurrent with sig-
nificant and positive correlations with other physical function
measures. The FSS-ICU has also demonstrated good to excellent
internal consistency.119
The interrater reliability of the FSS-ICU was determined
by Ragavan and colleagues in 2016 to be high among physi-
cal therapists who routinely worked in the ICU setting (ICC =
0.992, 95% CI = 0.984–0.996).120 Similar to the findings of
Thrush et al., Ragavan and colleagues also found that FSS-ICU
scores were significantly different among each of the discharge
categories—home, inpatient rehabilitation, skilled nursing
home, and other discharge destinations (mental health unit or
left against medical advice).120 
510 CHAPTER 23     Outcome Measures
TABLE 23.13  Physical Function in Intensive Care Test–Scored (PFIT-s) Scoring
Marching on the Spot Cadence
Sit-to-Stand Assistance (steps/minute)
0 = unable 0 = unable
1 = assist ×2 1 = 0–49
2 = assist ×1 2 = 50–80
3 = no assistance 3 = 80 +
From Denehy L, de Morton NA, Skinner EH, et al. A physical function test for use in the intensive care unit: validity, responsiveness, and predictive utility of the Physical
Function ICU Test (scored). Phys Ther. 2013;93:1636-1645.
Perme Intensive Care Unit Mobility Score
The Perme Intensive Care Unit Mobility Score is a test to mea-
sure a patient’s mobility status and takes into account the limita-
tions of equipment specifically related to the ICU environment
that could potentially be barriers to progressive mobility. This
15-item test is organized into seven different categories (men-
tal status, potential mobility, functional strength, bed mobil-
ity transfers, gait, and endurance). It is designed to capture a
patient’s performance at a specific moment in time.121 The time
to administer this test varies from 15 minutes to 60 minutes.
For more detailed information regarding how to administer the
test, refer to the article by Perme et al.,121 which can be found
at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4051334/?r
eport=reader.
Interpretation of Results
The total score for the Perme ICU mobility test ranges from
0 to 32 and is achieved by grading each of the 15 items. The
score uses a maximum range of 2 to 4 points for each of the
15 items and provides a total score that will document the
patient’s mobility status at a given moment. A high score
indicates few potential mobility barriers and decreased need
for assistance, whereas a low score indicates more poten-
tial barriers to mobility and more need for assistance with
mobility.
The interrater reliability has been reported as follows: ICC =
0.9880, 95% CI 0.97743–0.99859.122  See Table 23.13 for ways to score each item on the PFIT-s.
Physical Function in Intensive Care Test—Scored
The Physical Function in Intensive Care Test—Scored (PFIT-s)
was designed as an outcome measure specifically for patients
who are critically ill in the ICU. This test can be used not only
to guide exercise prescription in the ICU setting but also as a
measure of progress in functional recovery. The original PFIT
consisted of five items; however, the modified version (PFIT-
s) includes only four tasks: sit-to-stand assistance, marching on
the spot cadence, shoulder flexor strength, and knee extensor
strength.
Procedure
The PFIT-s should be administered to patients who are alert and
able to follow verbal commands. Norton-Craft et al., in 2014,
Shoulder Flexion Strength Knee Extension Strength
(Oxford Grading System) (Oxford Grading System)
0 = grade 0, 1, or 2 0 = grade 0,1, or 2
1 = grade 3 1 = grade 3
2 = grade 4 2 = grade 4
3 = grade 5 3 = grade 5
recommended that grip strength should be tested in addition to
confirming that the patient can follow commands.123
Patients must perform, in order, the following items124:
1. Sit to stand from a standardized chair, with assistance re-
corded as 0 to 3 people. The use of an assistive device is not
scored as assistance. Note: Measurements are not provided
to define the parameters of a standardized chair.
2. Marching on the spot as long as possible—time in seconds,
steps, and cadence (steps/min) are recorded. When patients
are able to sit out of bed, a practice session of standing
and marching on the spot is performed. Standardized in-
structions must be given for marching on the spot. The
standardized instructions for marching on the spot are as
follows:
“Once you are in the standing position, we will ask you
to march on the spot. We would like you to march on the
spot for as long as you can. We are going to record how
long you can march and for how many steps. This test is
designed to record your maximum exercise ability, so it
is very important that you march on the spot for as long
as you possibly can.”
You are allowed to give standardized encouragement every
10 seconds: “Keep going for as long as you can,” You’re do-
ing well,” “Well done.”
3. 
Muscle strength testing (Oxford scale, graded 0–5)—for
knee extension and shoulder flexion. 
Interpretation of Results
A score of 12 out of 12 is the highest score available on this
test. Excellent test–retest reliability has been determined for
cadence measurement (ICC = 0.996).124 Intrarater reliability
has not been studied because ICU patients are unable to repeat
the test in a single session. Face, criterion, predictive, con-
struct, convergent, and discriminant validities have been estab-
lished for the PFIT-s. Criterion validity was established with
a moderate to large positive relationships between the PFIT-s
and the FSS-ICU, IMS, and SPPB.116 The PFIT-s has excellent
construct validity, as demonstrated by a large positive rela-
tionship with the MRC sum score and moderate relationships
with the FSS-ICU and MRC sum score and with the IMS and
MRC sum score.116 Convergent validity was found with mod-
erate correlation with the TUG test (r = −0.60, 95% CI −0.70
to −0.46, p <.001), the 6MWT (r = 0.41, 95% CI 0.24 to
0.55, p <.001), and the MRC sum score (rho = 0.49. 95% CI

0.33 to 0.62, p <.001).125 Divergent validity was established
with a low correlation between body mass index (BMI) and
PFIT-s scores (r = −0.011, 95% CI −0.18 to 0.16).125 Denehy
et al. reported the following: “At ICU admission, the PFIT-s
demonstrated predictive utility for several patient and hospi-
tal outcomes, and higher PFIT-s scores (better function) were
positively associated with obtaining a higher MRC sum score
(being stronger) (>48) (odds ratio [OR] = 1.28, p < 0.001),
discharge to home (OR= 1.20, p < 0.001), and reduced likeli-
hood of discharge to inpatient rehabilitation (OR = 0.86, p =
0.02).”125 In addition, higher admission PFIT-s scores (better
function) were also associated with reduced lengths of hospital
stays.125  while reducing the overall cost of care.
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 Outcome Measures     CHAPTER 23 515

Appendix 23A: Functional Tests

TABLE 23A.1  Tinetti Mobility Test (Performance Oriented Mobility Assessment)

Element Scoring
Balance Tests
Subject is seated in hard, armless chair. The following maneuvers are tested:
1. Sitting balance 0 = Leans, slides in chair
1 = Steady, safe
2. Arises 0 = Unable without help
1 = Able, uses arms to help
2 = Able without using arms
3. Attempts to arise 0 = Unable without help
1 = Able, requires >1 attempt
2 = Able to rise, 1 attempt
4. Immediate standing balance (first 5 seconds) 0 = Unsteady (swaggers, moves feet, trunk sway)
1 = Steady, but uses walker or other support
2 = Steady without walker or other support
5. Standing balance 0 = Unsteady
1 = Steady but wide stance (heels >10.16 cm [4 inches] apart and uses
a cane or other support
2 = Narrow stance without support
6. Nudge (subject with feet as close together as possible, examiner 0 = Begins to fall
pushes with lightly on subject’s sternum three times) 1 = Staggers, grabs, catches self
2 = Steady
7. Eyes closed (subject with feet as close together as possible) 0 = Unsteady
1 = Steady
8. Turning 360 degrees 0 = Discontinuous steps
1 = Continuous
0 = Unsteady (grabs, staggers)
1 = Steady
9. Sitting down 0 = Unsafe (misjudges distance, falls into chair)
1 = Uses arms or not smooth motion
2 = Safe, smooth motion
Gait Tests
Subject stands with examiner, walks hallway or across room, first at “usual pace,” then back at “rapid, but safe pace” (using usual walking aids).
1. Initiation of gait 0 
= Any hesitancy or multiple attempts to start
1 
= No hesitancy
2. Step length and height 0 
= Right swing foot does not pass left stance foot with step
1 
= Passes left stance foot
0 
= Left swing foot does not pass right stance foot with step
1 
= Passes right stance foot
0 
= Right foot does not clear floor completely with step
1 
= Right foot completely clears floor
0 
= Left foot does not clear floor completely with step
1 
= Left foot completely clears floor
3. Step symmetry 0 
= Right and left step lengths not equal (estimate)
1 
= Right and left steps appear equal
4. Step continuity 0 = Stopping or discontinuity between steps
1 = Steps appear continuous
5. Path (estimate in relation to floor tiles, 30.48 cm [12 inches] di- 0 
= Marked deviation
ameter; observe excursion of 1 foot over about 3 meters [10 feet] 1  = Mild/moderate deviation or uses a walking aid
of the course) 2 
= Straight without walking aid
6. Trunk 0 
= Marked sway or uses walking aid
1 
= No sway but flexion of knees or back or spreads arms
2 
= No sway; no flexion of knees or back or spread arms

Continued
516 CHAPTER 23     Outcome Measures

TABLE 23A.1  Tinetti Mobility Test (Performance Oriented Mobility Assessment)—cont’d

Element Scoring
7. Walk stance 0 
= Heels apart
1 
= Heels almost touching while walking
Balance score: ___/16
Gait score: ___/12
Balance score + gait score: __/28

Modified from Tinetti ME. Performance-oriented assessment of mobility problems in elderly patients. J Am Geriatr Soc. 1986;34:119-126; Kegelmeyer DA, Kloos AD,
Thomas KM, Kostyk SK. Reliability and validity of the Tinetti Mobility Test for individuals with Parkinson disease. Phys Ther. 2007;87:1369-1378.

Note: Page numbers followed by b indicate boxes, f indicate illustrations, and t indicate tables.
A Acute care setting (Continued)
AAA. see Abdominal aortic aneurysm
Abacavir (Ziagen, ABC), for HIV/AIDS,
465t
Abarelix (Plenaxis), in chemotherapy, 455t
Abatacept (Orencia), for rheumatoid arthritis,
443t
Abbreviations, prohibitive, 14t
Abciximab (ReoPro), as antiplatelet agents,
439t
Abdominal aortic aneurysm (AAA), 183
Abdominal excursion, 66, 66b
Abdominal quadrants, 212f
Abducens nerve (CN VI), 132t
A-beta sensory axons, 140t
ABI. see Ankle-brachial index
Abiraterone (Zytiga), in chemotherapy, 455t
Ablation procedure, for rhythm disturbances,
40, 40b
Abnormal breath sounds, 65, 65t
ACA. see Anterior cerebral artery
Acamprosate (Campral), for substance
use-related disorders, 451t
Acarbose (Precose), for hyperglycemia, 469t
ACBT. see Active cycle of breathing
technique
Accessory muscles of inspiration, 58, 59t
ACD. see Anemia of chronic diseases
Acebutolol (Sectral), as antihypertensive
agents, 435t
Acetabulum fractures, 97–98, 99f
Acetaminophen (paracetamol), in pain
management, 485
Acetazolamide (Diamox), as antihypertensive
agents, 435t
Acetylsalicylic acid (Bayer), in pain
management, 487t
Achalasia, 217
Acid-base balance, arterial blood gas analysis
and, 69
Acid-base imbalances, potential causes of, 68t
Acidosis, causes of, 68t
Acoustic neuromas, 131–132
Acquired immunodeficiency syndrome
(AIDS), complications from, 343t
Acromegaly, 257
ACS. see Acute chest syndrome
ACTH. see Adrenocorticotropic hormone
Active cycle of breathing technique (ACBT),
492, 493t, 494f
Activity, patient response to, evaluating, 44,
45f
Activity Measure for Post-Acute Care
(AM-PAC), 508, 508t, 508b
Activity progression, 84
ACTs. see Airway clearance techniques
Acute Care Index of Function, 504–505,
505b
Acute care setting, 1–12
end-of-life considerations in, 8–10
Index
intensive care unit in, 4–7. see also
Intensive care unit (ICU)
medical-surgical equipment in, 395–430.
see also Medical-surgical equipment, in
acute care setting
pain management in, 481–490
safe caregiver and patient environment in,
1–4
sleep pattern disturbance in, 6–7
substance abuse and withdrawal in, 7
Acute chest syndrome (ACS), 194
Acute confusional state, 138
Acute contagious osteomyelitis, 340
Acute coronary syndrome, 34, 34b, 35f, 35t
Acute hematogenous osteomyelitis, 340
Acute inflammatory demyelinating
polyradiculopathy (AIDP), 158–159
Acute interstitial nephritis, 240
Acute kidney injury (AKI), 237–238, 238t,
238b, 361
Acute pyelonephritis, 239, 239b
Acute respiratory distress syndrome (ARDS),
79t, 80, 80b
Acute tubular necrosis (ATN), 358
Acute vestibular neuritis, 155
Acyclovir (Zovirax, Sitavig), as antiviral
medications, 467t
AD. see Autogenic drainage
Adalimumab (Humira), for rheumatoid
arthritis, 443t
Addison’s disease, 260
A-delta sensory axons, 140t
Adenoma, thyroid, hyperthyroidism from, 255t
ADH. see Antidiuretic hormone
Admission note format, 15
Adrenal cortical hormones, tests of, 259t,
260
Adrenal gland, 259–260
disorders of, 260
hormones of, target sites and actions of,
259t
structure and function of, 259, 259t
Adrenal hyperfunction, 260
Adrenal insufficiency, 260
Adrenal medulla
hormones of, tests of, 259t
tumor of, pheochromocytoma from, 260
Adrenergic agonists, as antihypertensive
agents, 435t
Adrenergic antagonists, as antihypertensive
agents, 435t
Adrenocortical steroids, 441t
for respiratory system, 441t
Adrenocorticotropic hormone (ACTH)
overproduction of, 258, 258b
tests of, 257t
Advance directives, 8–9
AFO. see Ankle-foot orthosis
Afterload, cardiac output and, 21
Age, wound healing and, 314
Agonal rhythm, ECG characteristics and
causes of, 52t
AICA. see Anterior inferior cerebellar artery
AIDP. see Acute inflammatory demyelinating
polyradiculopathy
AIDS. see Acquired immunodeficiency
syndrome
Air entrainment mask, in oxygen delivery,
399f, 399t
Air trapping, in respiratory dysfunction, 76
Airway clearance, 415
Airway clearance techniques (ACTs), 83, 491
benefits and considerations for, 493t
methods of, 492–496
active cycle of breathing technique, 492,
493t, 494f
autogenic drainage (AD), 492–494,
493t–494t, 494b
chest physical therapy, 496
cough, 492, 492b, 493t
exercise, 493t, 496, 496b
forced expiratory technique (FET), 492,
493t
high-frequency chest wall oscillation
(HFCWO), 496, 496f
oscillatory positive expiratory pressure
(OPEP), 493t, 495–496, 495f
positive expiratory pressure (PEP), 493t,
494
pharmacological breathing treatments,
496–497
principles of, 491
program, creating, 497–498
respiratory physiology for, 491b
Airway pressure release ventilation (APRV),
412t
AKI. see Acute kidney injury
Alanine aminotransferase (ALT), in hepatic
testing, 215t–216t
Albiglutide (Tanzeum), for hyperglycemia,
469t
Albumin, clinical indications and outcomes
for, 200t
Albuterol (Proventil, Ventolin), as
bronchodilators, 442t
Alcohol use disorder (AUD), in acute care
setting, 7
Aldesleukin (Proleukin), in chemotherapy,
455t
Aldosterone
cardiac effects of, 21t
target sites and actions of, 259t
Alemtuzumab (Campath, Lemtrada)
in chemotherapy, 455t
for multiple sclerosis, 451t
Alendronate (Fosamax, Fosamax plus D), for
osteoporosis, 472t
Alfuzosin (Uroxatral), for benign prostatic
hyperplasia, 460t
        517
518 INDEX
Alirocumab (Praluent), as lipid-lowering
agent, 440t
Aliskiren (Tekturna), as antihypertensive
agents, 435t
Alkaline phosphatase (ALP), in hepatic and
biliary testing, 215t–216t
Alkaline phosphatase isoenzymes, in hepatic
and biliary testing, 215t–216t
Alkalosis, causes of, 68t
Alkylating agents, in chemotherapy, 455t
Allergic rhinitis, 335
Allergy, latex, 3
AlloDerm, in burn and wound treatment,
308t
Allogeneic transplantation, 370
Allogenic graft, for burns, 307t
Allograft, for burns, 307t
Alogliptin (Nesina), for hyperglycemia, 469t
ALP. see Alkaline phosphatase
Alpha fetoprotein, in hepatic and biliary
testing, 215t–216t
Alpha motor neurons, 140t
Alprazolam (Xanax), as antianxiety
medication, 446t
ALS. see Amyotrophic lateral sclerosis
ALT. see Alanine aminotransferase
Alteplase (Activase, Cathflo), as
thrombolytics, 441t
Aluminum carbonate (Basaljel), as antacid,
457t
Aluminum hydroxide (Amphojel,
ALternaGEL), as antacid, 457t
Alveolar ventilation (VA), description and
clinical significance of, 74t–75t
Alveoli, description and function of, 58t
Alzheimer’s disease, 137t
Amantadine (Symmetrel), for Parkinson’s
disease, 453t
Amebic meningoencephalitis, 339
American College of Chest Physicians, 65
American Physical Therapy Association
(APTA), 499b
American Spinal Injury Association (ASIA)
Impairment Scale, 145, 145t
American Thoracic Society, 65
Amiloride (Midamor), as antihypertensive
agents, 435t
Aminoglycosides, for infectious diseases,
461t
Aminopenicillins, for infectious diseases,
461t
Aminosalicylic acid (Paser), as antitubercular
agent, 464t
Amiodarone (Cordarone, Pacerone), for
arrhythmias, 433t
Amitriptyline (Elavil), as antidepressant,
448t
Amlodipine (Norvasc), as antihypertensive
agents, 435t
Ammonia, in hepatic testing, 215t–216t
Amnion graft, for burns, 307t
Amoxicillin (Amoxil, Trimox), for infectious
diseases, 461t
Amoxicillin-clavulanic acid (Augmentin), for
infectious diseases, 461t
AM-PAC. see Activity Measure for Post-
Acute Care
Amphetamine/dextroamphetamine
(Adderall), as stimulants, 450t
Amphotericin B (Fungizone), as antifungal
agents, 463t
Amphotericin B cholesteryl sulfate complex
(Amphotec), as antifungal agents, 463t
Amphotericin B lipid complex (Abelcet), as
antifungal agents, 463t
Amphotericin B liposomal (AmBisome), as
antifungal agents, 463t
Ampicillin (Omnipen), for infectious
diseases, 461t
Ampicillin-sulbactam (Unasyn), for
infectious diseases, 461t
Amputation, 383–390
edema control in, 384, 384b
functional mobility after, 386, 386b
holistic care after, 386–387
limb and trunk motion after, 386, 386b
lower extremity, 383. see also Lower
extremity amputation
outcomes measures for, 387–388, 387t
pain management after, 384–386
physical therapy management of,
383–388
prosthetic candidacy after, 388, 388t
strengthening after, 386, 386b
upper extremity, 383. see also Upper
extremity amputation
wound healing after, 384, 384b
Amyl nitrite (Aspirol, Vaporole), as
antihypertensive agents, 435t
Amylase
serum, in pancreatic testing, 215t–216t
urine, in pancreatic testing, 215t–216t
Amyloidosis, 350
Amyotrophic lateral sclerosis (ALS), 157
Anakinra (Kineret), for rheumatoid arthritis,
443t
Analgesia, patient-controlled, 488t
Androgens, target sites and actions of,
259t
Anemia, 192–195
Anemia of chronic diseases (ACD), 194–195
Anesthesia
considerations for the physical therapist,
475–480
intraoperative effects of, 476
local, 487t
operative positioning and, 477, 478f
physical therapy considerations, 477
postoperative complications o, 476–477
postoperative effects of, 476–477
types of, 475
Aneurysm, 183–184, 184f
abdominal aortic, 183
false, 183, 184f
physical therapy considerations for, 184
repair and reconstruction of, 202–203,
203f
physical therapy considerations for,
202–203
saccular, 183
true, 183, 184f
Angina
Canadian Cardiovascular Society
Classification of, 394t
rating scale, 393t
stable (exertional), 34
physical therapy considerations for, 391
symptoms of, 393t
Angina (Continued)
unstable, 34, 35f
physical therapy considerations for, 391
variant (Prinzmetal), 34
Angiography
in cardiac evaluation, 33, 33t
contrast, in vascular evaluation, 175–177,
177f
pulmonary, computed tomographic, 71–72
Angioplasty, laser, coronary, 39
Angiotensin, cardiac effects of, 21t
Angiotensin-converting enzyme (ACE)
inhibitors, as antihypertensive
agents, 435t
Angiotensin II receptor blockers (ARBs), as
antihypertensive agents, 435t
Ankle, fracture of, 102–103
Ankle-brachial index (ABI), in vascular
evaluation, 175t
Ankle-foot orthosis (AFO), 122t
Anorectal disorders, 222–223
Anoxic encephalopathy, 157
ANS. see Autonomic nervous system
Antacids, 457t
Anterior cerebral artery (ACA), 147, 147f, 151t
Anterior corticospinal tract, function of, 139t
Anterior cruciate ligament (ACL)
reconstruction, 120t
Anterior inferior cerebellar artery (AICA),
151t
Antiandrogens, in chemotherapy, 455t
Antianxiety medications, 446t
Antiarrhythmic agents, 433t
Antibiotic-resistant infections, 334–335
Antibiotics
for infectious diseases, 461t
inhaled, 497
Antibody(ies), definition of, 330t
Antibody measurement, in infectious disease
evaluation, 331
Anticholinergics, as bronchodilators, 442t
Anticoagulants, 434t
Anticoagulation
in DVT management, 190
therapy, in vascular disorders management,
198–199, 199t
physical therapy considerations for,
198–199
Anticonvulsants, 446t
Antidepressants, 448t
Antidiarrheal medications, 458t
Antidiuretic hormone (ADH)
absence of/inadequate response to, 258
overproduction of, 258, 258b
tests of, 257t
Antiemetic medications, 454t
Antifungal agents, for infectious diseases,
463t
Antigen, definition of, 330t
Antihistamines, 442t
for respiratory system, 442t
Antihypertensive agents, 435t
combination, 438t
Antimetabolites, in chemotherapy, 455t
Antiplatelet agents, 439t
Antipsychotics, 449t
Antirejection immunosuppression, 356
Antiretroviral medications, 465t
for HIV infection, 342

Antispasmodic agents, 458t
for musculoskeletal system, 445t
Antitubercular agents, for infectious diseases,
464t
Antitumor antibiotics, in chemotherapy, 455t
Antiviral medications, 467t
Aorta, description and function of, 19t
Aortic aneurysm, abdominal, 183
Aortic regurgitation, signs and symptoms
of, 36t
Aortic stenosis, signs and symptoms of, 36t
Aortic valve
description and function of, 19t
replacement of, 42
transcatheter implantation in, 42
stenosis of
percutaneous aortic valvotomy for, 42
transcatheter aortic valve implantation
for, 42
Aortobifemoral bypass, 202f
Aortofemoral graft, 203f
Aortoiliac bypass, 202f
Apixaban (Eliquis), as anticoagulants, 434t
Aplastic anemia, 193
Apligraf, in burn and wound treatment, 308t
Apnea, description and conditions associated
with, 63t
Apomorphine (Apokyn), for Parkinson’s
disease, 453t
Appendectomy, 226t
Appendicitis, 219
APRV. see Airway pressure release ventilation
APTA. see American Physical Therapy
Association
Aquaporins, 149
Arachnoid granulations, 147
ARDS. see Acute respiratory distress
syndrome
Arformoterol (Brovana), as bronchodilator,
442t
Argatroban, as anticoagulant, 434t
Aripiprazole (Abilify), as antipsychotic, 449t
Arm sling, 122t
Aromatase inhibitors, in chemotherapy, 455t
Arousal, 134–135
Arterial blood gas
analysis of, in pulmonary examination,
68–70, 69f, 69b
interpretation of, 69–70
measurement of, in cardiac evaluation, 30
normal values in, 69
terminology in, 69
Arterial disorders
aneurysm as, 183–184, 184f
aortic dissection as, 184–185, 184f, 185b
arterial emboli as, 182t, 185
arterial thrombosis as, 185
arteriovenous malformations as, 192
atherosclerosis as, 181–183, 182b
compartment syndrome as, 189
complex regional pain syndrome as,
188–189
giant cell arteritis as, 187–188
hypertension as, 185–187, 186t–187t
polyarteritis nodosa as, 187
Raynaud’s disease as, 188, 188b
systemic vasculitis as, 187
thromboangiitis obliterans as, 187
Wegener’s granulomatosis as, 187
Arterial emboli, 185, 185t
Arterial insufficiency wounds, 311, 311t
Arterial line, in hemodynamic monitoring,
401t, 402f
Arterial pulses, 24f
Arterial thrombosis, 185
Arteriography
contrast
complications of, 177t
in vascular evaluation, 175–177
renal, in genitourinary evaluation, 237,
237b
Arteriovenous (AV) fistula, in medical-
surgical management, 405t–407t
Arteriovenous malformations (AVMs), 152,
192
Arteritis, giant cell, 187–188
Artery(ies)
characteristics of, 172t
disorders of, 181–187. see also Arterial
disorders
structure of, 172f
Arthritis, rheumatoid, 350–351, 351b
osteoarthritis compared with, 351t
Arthroplasty, joint, 105–115
Articaine (Septocaine), for local anesthesia,
488t
Asenapine (Saphris), as antipsychotics, 449t
Aspartate aminotransferase (AST), in hepatic
testing, 215t–216t
Aspirin (Bayer), in pain management, 487t
Aspirin/dipyridamole (Aggrenox), as
antiplatelet agents, 439t
Assist control ventilation, 411–413
Assist ventilation, 412t
Asthma, 76, 77t
Astrocytes, 140t
Atelectasis, 78, 79t
Atenolol (Tenormin), as antihypertensive
agents, 435t
Atherectomy, coronary, directional, 39
Atherosclerosis, 181–183, 182b
ATN. see Acute tubular necrosis
Atonia, 141
Atorvastatin (Lipitor), as lipid-lowering
agent, 440t
Atrial diastole, 19
Atrial fibrillation, 54f
Maze procedure for, 40
Atrial flutter, 53f
ECG characteristics and causes of, 51t
Atrial kick, 19–20
Atrial natriuretic peptides, 30
cardiac effects of, 21t
Atrial rhythms, ECG characteristics and
causes of, 51t
Atrial systole, 19–20
Atrioventricular (AV) blocks, ECG
characteristics and causes of, 53t
Atrioventricular (AV) node, 21, 21f
Atrium, description and function of, 19t
AUD. see Alcohol use disorder
Auranofin (Ridaura), for rheumatoid
arthritis, 443t
Aurothioglucose (Solganal), for rheumatoid
arthritis, 443t
Auscultation
in cardiac evaluation, 25–26, 27f, 27t
in gastrointestinal evaluation, 211–212
INDEX 519
Auscultation (Continued)
in genitourinary evaluation, 235
in infectious disease evaluation, 331
in pulmonary examination, 63–65, 64f,
64b–65b
in vascular evaluation, 174
Auto positive end-expiratory pressure,
complicating mechanical ventilation,
411–413
Autogenic drainage (AD), 492–494,
493t–494t, 494b
Autograft, for burns, 307t
Autologous transplantation, 370
Autolytic debridement of wound, 321
Automatic implantable cardiac defibrillator,
41
Automaticity, of heart, 18
Autonomic dysreflexia (AD), 145
Autonomic nervous system (ANS), 132–134,
134f–135f, 135b
AVMs. see Arteriovenous malformations
Axillary artery, intraaortic balloon pump via,
418
Axillobifemoral bypass, 202f
Azathioprine (Azasan, Imuran)
as immunosuppressants, 473t
for rheumatoid arthritis, 443t
Azelastine (Astelin), for respiratory system,
442t
Azilsartan (Edarbi), as antihypertensive
agents, 435t
Azithromycin (Zithromax), for infectious
diseases, 461t
B
Back pain, spinal surgery for, 117
Baclofen (Lioresal), for spasticity, 445t
Bacteremia, 344
Bacterial meningitis, 339
Bacteriuria, etiology of, 236t
Bainbridge reflex, 22
Balance, in musculoskeletal evaluation,
93–94, 93b
Balloon pump, intraaortic, 417–418,
417f
Bandaging, lymphedema, 198
BardPort, in medical-surgical management,
405t–407t
Barium enema (BE), in gastrointestinal
evaluation, 214t
Barium swallow, in gastrointestinal
evaluation, 214t
Baroreflexes, 21–22
Barotrauma, complicating mechanical
ventilation, 413–414
Barrett’s esophagus, 217–218
Basal cell carcinoma, 289
Basal ganglia (BG), 142–144
-related disorders, 142–143, 143b
prognosis of, 143
Basement membrane, function of, 297t
Basilar artery, 151t
Basiliximab (Simulect), as
immunosuppressants, 473t
BBB. see Blood-brain barrier
BC. see Breathing control
BE. see Barium enema
Beclomethasone (Beclovent, Vanceril), for
respiratory system, 441t
520 INDEX
Beclomethasone dipropionate (Beconase,
Vancenase), for respiratory disorders,
441t
Behavioral Pain Scale (BPS), 481, 483t, 485t
Bell’s palsy, 131
“Belly breathing”, 58b
Benazepril (Lotensin), as antihypertensive
agents, 435t
Benign paroxysmal positional vertigo
(BPPV), 154
Benign prostatic hyperplasia (BPH), 242
therapy for, 460t
Benign tremor, 143
Benign tumor(s)
classification of, 277t
definition of, 275
Benzocaine (Americaine), for local anesthesia,
488t
Benzodiazepines, as antianxiety medications,
446t
Benztropine (Cogentin), for Parkinson’s
disease, 453t
Berg Balance Scale, 500–501, 500t,
500b–501b
interpretation of results of, 500–501
procedure, 500
Beta-2 agonists, as bronchodilators, 442t
Beta-blockers
as antiarrhythmic agents, 433t
as antihypertensive agents, 435t
Betrixaban (Bevyxxa), as anticoagulants, 434t
Bevacizumab (Avastin), in chemotherapy,
455t
Bezafibrate (Bezalip), as lipid-lowering agent,
440t
BG. see Basal ganglia
Bicalutamide (Casodex), in chemotherapy,
455t
Bier block, 487t
Bilateral lung transplantation, 367
Bilateral vestibular hypofunction, 155
Bile acid sequestrants, as lipid-lowering
agents, 440t
Bilevel positive airway pressure (BiPAP), in
oxygen delivery, 399t
Biliary system
diagnostic procedures for, 216t
disorders of, 223–225
disorders of, cancer as, 286
laboratory tests for, 215t–216t
Bilirubin, in hepatic and biliary testing,
215t–216t
Bilirubinuria, etiology of, 236t
Billroth I procedures, 226t
Billroth II procedures, 226t
Biobrane, in burn and wound treatment,
308t
Biochemical markers, in cardiac evaluation,
30, 30b
Biopsy(ies)
in cancer diagnosis, 278t
in genitourinary evaluation, 237
liver biliary, 216t
needle, of thyroid gland, 255t
Biotherapy, for cancer, 281
Biot’s respirations, description and conditions
associated with, 63t
BiPAP. see Bilevel positive airway
pressure
Biperiden (Akineton), for Parkinson’s disease,
453t
Bisacodyl (Dulcolax), as laxative, 459t
Bismuth subsalicylate (Pepto-Bismol), for
diarrhea, 458t
Bisoprolol (Zebeta) , as antihypertensive
agents, 435t
Bivalirudin (Angiomax), as anticoagulant,
434t
Bladder
biopsy of, in genitourinary evaluation, 237
drainage, from transplanted pancreas,
enteric drainage versus, 362–363
examination of, in genitourinary
evaluation, 237, 237b
neurogenic, 241
X-ray of, with kidneys and ureters, in
genitourinary evaluation, 236
Bleb, in emphysema, 76
Bleomycin (Blenoxane), in chemotherapy,
455t
Blood
cholesterol levels in, 29
whole, clinical indications and outcomes
for, 200t
Blood-brain barrier (BBB), 149
Blood cell types, 173t
Blood gas
arterial
analysis of, 68–70, 69f, 69b
measurement of, in cardiac evaluation,
30
venous, analysis of, 70
Blood lipids, 29, 29b
Blood pressure (BP)
cardiac transplantation and, 366t
elevated, 185, 186t–187t. see also
Hypertension
in infectious disease evaluation, 331
measurement of, 24–25, 25b
orthostatic, symbols for, 26f
ranges for, 25t
Blood pressure cuff, in hemodynamic
monitoring, 400t
Blood product transfusion
adverse reactions to, 201t
physical therapy considerations for, 199
for vascular disorders, 199, 200t
Blood urea nitrogen (BUN), in genitourinary
evaluation, 236, 236b
Blood vessels, 171. see also Vascular system
characteristics of, 172t
great, description and function of, 19t
layers, 172t
BMT. see Bone marrow transplant
Boceprevir (Victrelis), as antiviral
medications, 467t
Body composition, prolonged bed rest and,
4, 5t
Body temperature, maintenance of, in burn
care, 304
Bone
cancer of, 283, 283t, 283b
metabolic disorders of, 268–269
Bone marrow transplant (BMT), 370
bone marrow harvesting for, 370
Bone scan, in musculoskeletal evaluation, 90
Borg CR10 Scale, 46b
Borg CR100 Scale, 46b
Borg RPE scale, 46b
Bosentan (Tracleer), for pulmonary
hypertension, 439t
Botulinum toxin A (Botox, Dysport,
Myobloc), for spasticity, 445t
BP. see Blood pressure
BPH. see Benign prostatic hyperplasia
BPPV. see Benign paroxysmal positional
vertigo
BPS. see Behavioral Pain Scale
Braces, 121–122, 122t, 122b
Brachytherapy, 279
Bradykinin, cardiac effects of, 21t
Bradypnea, description and conditions
associated with, 63t
Brain
hypertensive effects on, 186t
monitoring of, multimodal, equipment for,
403, 404t
vestibular system of, 148f
Brain death, 9–10
Brain tissue oxygenation, in brain
monitoring, 404t
Brainstem, 128–134
autonomic nervous system in, 132–134
blood supply, 132, 133f
traumatic disorders of, 136–138
Breast cancer, 283–285
physical therapy considerations in, 285
stages of, 284t
surgical interventions for, 285t
Breath sounds, 46b
abnormal, 65, 65t
adventitious, 65
discontinuous, 65
extrapulmonary, 65
normal, 64
in pulmonary examination, 63
Breathing control (BC), 492
Breathing patterns, observation of, 62–63,
63t, 63b
Brentuximab vedotin (Adcetris), in
chemotherapy, 455t
Brexpiprazole (Rexulti), as antipsychotics,
449t
Brivaracetam (Briviact), as anticonvulsants,
446t
Bromocriptine mesylate (Cycloset, Parlodel,
for Parkinson’s disease, 453t
Bronchial breath sounds, 64
Bronchial tree, description and function of,
58t
Bronchiectasis, 77t, 78
Bronchitis, chronic, 76, 77t
Bronchodilators, 442t, 496
for respiratory system, 442t
Bronchophony, 65
Bronchoplasty, 82, 83f
Bronchoscopy, flexible, for pulmonary
examination, 71, 71b
Bronchospasm, in respiratory dysfunction, 76
Bronchovesicular sounds, 64
Brooke colostomy, 226t
Broviac catheter, in medical-surgical
management, 405t–407t
Budesonide (Pulmicort, Rhinocort)
for respiratory disorders, 441t
for respiratory system, 441t
Buerger’s disease, 187

Bullae formation, in emphysema, 76
Bumetanide (Bumex), as antihypertensive
agents, 435t
BUN. see Blood urea nitrogen
Bupivacaine (Marcaine, Sensorcaine), for local
anesthesia, 488t
Buprenorphine (Buprenex, Subutex), in pain
management, 487t
Buprenorphine/naloxone (Suboxone), for
substance use-related disorders, 451t
Bupropion (Wellbutrin, Zyban), as
antidepressants, 448t
Burns, 296–301
admission guidelines, 302
assessment of, 301–307, 302f, 303t
chemical, 301
depth of, 296, 298f, 298t
assessing, 301–302
electrical, 299–301
ionizing radiation, 301
from lightning, 301
management of
acute care, 301–307, 307t–308t
physical therapy examination in,
307–309
reparative phase of, 306–307, 307t–308t
nonsurgical procedures in, 306–307
surgical procedures in, 306,
307t–308t
resuscitative phase of, 303–305
body temperature maintenance in, 304
fluid resuscitation in, 304
infection control in, 305, 305b
initial burn care in, 305–306
pain management in, 304–305
pathophysiology of, 296–301
physical therapy intervention for,
309–310, 310t
physiologic sequelae of, 299, 299f, 300t
preferred positions for patients
with, 310t
thermal, 299, 300t
types of, 299–301
ultraviolet, 301
zones of injury after, 296, 297f
Buspirone (BuSpar), as antianxiety
medications, 446t
Butamben picrate (Butesin Picrate), for local
anesthesia, 488t
Butorphanol (Stadol), in pain management,
487t
Bypass grafting, peripheral vascular, 201,
202f–203f
C agent, 464t
C fibers sensory axons, 140t
CAA. see Cerebral amyloid angiopathy
Cabazitaxel (Jevtana), in chemotherapy, 455t
CABG. see Coronary artery bypass graft
CAD. see Coronary atherosclerotic disease
Cadaveric organ donors, 354
liver, split, 360
renal, versus living donors, 358
Calcaneal fractures, 103
Calcimimetic, for hyperparathyroidism, 471t
Calcitriol (Calcijex, Rocaltrol), for
hyperparathyroidism, 471t
Calcium alginate dressings, 323t
Calcium carbonate (TUMs), as antacid, 457t
Calcium channel blockers
as antiarrhythmic agents, 433t
as antihypertensive agents, 435t
Calculi, urinary, 241
Caloric testing, for vestibular dysfunction,
156t
CAM. see Confusion Assessment Method
CAM-ICU. see Confusion Assessment Method
for the Intensive Care Unit
Camptothecins, in chemotherapy, 455t
Canagliflozin (Invokana), for hyperglycemia,
469t
Cancer(s)
biotherapy for, 281
bone and soft tissue, 283, 283t, 283b
breast, 283–285, 284t–285t
chemotherapy for, 280–281
definition of, 276t
diagnosis of, 277, 278t
esophageal, 218, 218b
gastric, 219
gastrointestinal, 285–286, 285b–286b
gene therapy for, 281
genitourinary, 285–286, 285b–286b, 286t
head and neck, 288–289, 288b
hematologic, 286–288, 287t–288t
hepatobiliary, 286, 286b
liver, 286, 286b
management of, 278–281
neurologic, 289, 289b
pancreatic, 286
paraneoplastic syndromes and, 276
physical therapy guidelines for patients
with, 289–290
radiation therapy for, 279–280,
279b–280b
rehabilitation and cancer-related fatigue,
290–291
respiratory, 281–283, 282t, 283b
risk factors for, 276
signs and symptoms of, 276
skin, 289, 289b
staging and grading of, 278
surgery for, 279, 279b
Candesartan (Atacand), as antihypertensive
agents, 435t
Cangrelor (Kengreal), as antiplatelet agents,
439t
Capecitabine (Xeloda), in chemotherapy,
455t
Capillary network, characteristics of, 172t
Capillary refill time, in vascular evaluation,
175t
Capreomycin (Capastat), as antitubercular
Captopril (Capoten), as antihypertensive
agents, 435t
Carbamazepine (Tegretol, Carbatrol), as
anticonvulsants, 446t
Carbapenems, for infectious diseases, 461t
Carbenicillin (Geopen), for infectious
diseases, 461t
Carbidopa (Lodosyn), for Parkinson’s disease,
453t
Carbohydrate antigen, in hepatic and
pancreatic testing, 215t–216t
Carbon dioxide retention, clinical
presentation of, 69b
Carbon monoxide (CO) poisoning, 303–304
INDEX 521
Carbonic anhydrase inhibitors, as
antihypertensive agents, 435t
Carboplatin (Paraplatin), in chemotherapy,
455t
Carboxypenicillins, for infectious diseases,
461t
Carcinoembryonic antigen (CEA), in
gastrointestinal evaluation, 213t
Carcinogens, 276
Carcinoma
basal cell, 289
hepatocellular, 286
thyroid, hyperthyroidism from, 255t
tissue of origin of, 276
Cardiac catheterization, 33
Cardiac cycle, 19–20
Cardiac dysfunction, management of,
concepts for, 43–47, 43b–44b, 46b, 47f
Cardiac evaluation
angiography in, 33, 33t
arterial blood gas measurements in, 30
biochemical markers in, 30
blood lipids in, 29
blood pressure in, 24–25
cardiac catheterization in, 33
chest radiography in, 30
coagulation profiles in, 29
complete blood cell count in, 29
C-reactive protein in, 29
diagnostic and laboratory measures in,
26–34, 28t, 28b, 32t
echocardiography in, 30–31
electrocardiography in, 26–29, 28t
electrophysiologic studies in, 33–34
exercise testing in, 31–33, 32f, 32t
natriuretic peptides in, 30
oximetry in, 26
patient history in, 22–23, 23b
physical examination in, 23–26
Cardiac output (CO), 20–22
cardiac transplantation and, 366t
Cardiac pacemaker, 41, 41t
Cardiac reflexes, 21–22
Cardiac system, 17–56
acute coronary syndrome and, 34, 34b,
35f, 35t
coronary perfusion and, 22
evaluation of, 22–34. see also Cardiac
evaluation
health conditions affecting, 34–37
heart failure and, 36–37, 38t, 38b
hematologic disorders and, 178t
infections of, 338
management of, 38–47
myocardial and pericardial heart disease
and, 36, 37t
prolonged bed rest and, 4, 5t
rhythm and conduction disturbance of,
34–36
structure and function of, 18, 18f, 19t
systemic circulation and, 22, 22f
valvular heart disease and, 36, 36t
Cardiac transplantation, 43, 364–366
cardiac function after, indication of,
364–365
contraindications to, 364
indications for, 364–365
lung transplantation combined with,
369–370
522 INDEX
Cardiac transplantation (Continued)
orthotopic and heterotopic, 364
physical therapy for recipients of,
365–366, 366b
physiologic changes following, 366t
postoperative care and complications of,
364–365, 365b
pretransplantation care, 364
Cardiogenic chest pain, 393t
Cardiogenic pulmonary edema, 78
Cardiomyopathy
from cardiac infections, 338
classification of, 37t
as HIV and AIDS complication, 343t
Cardiovascular system, 433–441
antiarrhythmic agents for, 433t
anticoagulants for, 434t
antihypertensive agents for, 435t
antiplatelet agents, 439t
complications of burns affecting, 300t
lipid-lowering agents, 440t
in musculoskeletal evaluation, 92
positive inotropes for, 441t
thrombolytics for, 441t
Cardioversion, 41–42
Caregiver, safe, 1–4
guidelines for, 1
Cariprazine (Vraylar), as antipsychotics, 449t
Carisoprodol (Soma), as muscle relaxants,
445t
Carmustine (BICNU), in chemotherapy,
455t
Carotid noninvasive studies, 175
Carpal fractures, 105, 105b
Carrier, definition of, 330t
Carvedilol (Coreg), as antihypertensive
agents, 435t
Casopitant (Rezonic), as antiemetic, 454t
Caspofungin (Cancidas), as antifungal agents,
463t
Casts, 120–121, 120b, 121t
Catheter
central, peripherally inserted, in medical
surgical management, 405t–407t
condom, in medical-surgical management,
405t–407t
fiberoptic transducer-tipped, in ICP
monitoring, 403t
intraventricular, in ICP monitoring,
403t
suprapubic, in medical-surgical
management, 405t–407t
Swan-Ganz, in hemodynamic monitoring,
401t
Texas, in medical-surgical management,
405t–407t
transtracheal, in oxygen delivery, 397t
urinary (Foley), in medical-surgical
management, 405t–407t
Catheterization, cardiac, 33
CBC. see Complete blood cell count
CBF. see Cerebral blood flow
CCR5 inhibitor, for HIV/ AIDS, 465t
Cefadroxil (Duricef), for infectious diseases,
461t
Cefazolin (Ancef, Kefzol), for infectious
diseases, 461t
Cefdinir (Omnicel), for infectious diseases,
461t
Cefepime (Maxipime), for infectious diseases,
461t
Cefonicid (Monocid), for infectious diseases,
461t
Cefoperazone (Cefobid), for infectious
diseases, 461t
Cefotaxime (Claforan), for infectious diseases,
461t
Cefotetan (Cefotan), for infectious diseases,
461t
Cefoxitin (Mefoxin), for infectious diseases,
461t
Cefpodoxime (Vantin), for infectious diseases,
461t
Cefprozil (Cefzil), for infectious
diseases, 461t
Ceftaroline (Teflaro), for infectious diseases,
461t
Ceftazidime (Fortaz), for infectious diseases,
461t
Ceftazidime-avibactam (Avycaz), for
infectious diseases, 461t
Ceftibuten (Cedax), for infectious diseases,
461t
Ceftolozane, for infectious
diseases, 461t
Cefuroxime (Ceftin), for infectious diseases,
461t
Celecoxib (Celebrex), in pain management,
487t
Cellulitis, 340
Central nerve block, 487t
Central nervous system (CNS), 128–152,
131t, 446–454
antianxiety medications for, 446t
anticonvulsants for, 446t
antidepressants for, 448t
antipsychotics for, 449t
blood-brain barrier, 149
brainstem, 128–134
cancers of, 289
cerebral circulation, 146–147
cerebrospinal fluid, 147–149
cerebrovascular disease/disorders and,
149–152
cognitive assessment of, 136
cranial nerves, 128–134, 130b, 132t
delirium and, 136, 136b, 137t
dementia and, 136, 137t
disease, degenerative, 157
infections of, 338
mood stabilizers for, 450t
motor components of, 141–144
descending motor systems, 141–142,
142b
extrapyramidal systems, 142–144
segmental motor control, 141
multiple sclerosis and, medications for,
451t
neurologic clinical examination of,
134–136
Parkinson’s disease and, medications for,
453t
protective structures of, 147, 147b
sensory components of, 138–141,
139f–140f, 139t–140t
spinal cord injury to, 144–146, 145t
stimulants for, 450t
ventricular dysfunction and, 148–149
Central venous catheter
in hemodynamic monitoring, 401t
in medical-surgical management, 405t–407t
tunneled, in medical-surgical management,
405t–407t
Central vestibular disorders, 154–155
Centrilobular emphysema, 76
CentriMag, 420, 420b
Cephalosporins, for infectious diseases, 461t
Cerebellum, 142–144
-related disorders, 143–144
Cerebral amyloid angiopathy (CAA), 152
Cerebral angiography, in neurologic
examination, 161t–163t
Cerebral blood flow (CBF), in brain
monitoring, 404t
Cerebral circulation, 146–147
Cerebral microdialysis, in brain monitoring,
404t
Cerebral perfusion pressure (CPP), 148
monitoring of, equipment for, 399–402,
403t
Cerebral toxoplasmosis, as HIV and AIDS
complication, 343t
Cerebral vascular accidents (CVA)
acute, 149
neurologic signs associated with, 151t
Cerebrospinal fluid (CSF), 147–149
Cerebrovascular disease/disorders, 149–152,
150b
acute cerebral vascular accidents as, 149
aneurysm as, 152
arteriovenous malformation as, 152
prognosis of, 150–152
stroke as, 149–152
subarachnoid hemorrhage as, 149, 152
transient ischemic attack as, 149
Certolizumab pegol (Cimzia), for rheumatoid
arthritis, 443t
Cervical collar, 122t
Cervicogenic dizziness, 153
Cervicothoracic orthoses, 122t
Cetirizine (Zyrtec), as antihistamines, 442t
Cetuximab (Erbitux), in chemotherapy, 455t
Chemical burns, 301
Chemoreceptors, 22
as chemical control, 57
Chemotherapy
for cancer, 280–281
physical therapy considerations on,
280–281
medications for, 455t
Chest, flail, 82
Chest pain
angina-like, 217
diagnostic considerations, 393
etiologies, patterns, and signs associated
with, 392t
patients with, physical therapy
considerations for, 391–394
physical therapy considerations, 393–394
physiology of, 391–392
presentation of, 392–393
Chest radiography, in cardiac evaluation, 30
Chest tube, in medical-surgical management,
405t–407t, 408f
Chest wall
excursion of, 66, 66b
restriction, 82

Chest X-ray, in pulmonary examination,
70–71, 70f, 70b
Cheyne-Stokes respirations, description and
conditions associated with, 63t
CHF. see Congestive heart failure
Chlordiazepoxide (Librium), as antianxiety
medication, 446t
Chloroprocaine (Nesacaine), for local
anesthesia, 488t
Chlorpheniramine maleate, as antihistamines,
442t
Chlorpromazine (Thorazine), as
antipsychotic, 449t
Chlorthalidone (Hygroton), as
antihypertensive agents, 435t
Chlorzoxazone (Parafon Forte), as muscle
relaxant, 445t
Cholangiopancreatography
magnetic resonance, 216t
retrograde, endoscopic, 216t
Cholecystectomy, 226t
Cholecystitis, 225
Cholelithiasis, 225
Cholesterol, total, 29
Cholesterol absorption inhibitor, as lipid-
lowering agents, 440t
Cholestyramine (Questran), as lipid-lowering
agent, 440t
Chordae tendineae, description and function
of, 19t
Christmas’ disease, 196
Chronic bronchitis, 76, 77t
Chronic graft rejection, 357
Chronic inflammatory demyelinating
polyneuropathy (CIDP), 159
Chronic kidney disease (CKD), 238–239,
239b
Chronic obstructive pulmonary disease
(COPD), 76
Chronic osteomyelitis, 340
Chronic pyelonephritis, 239
Chronic venous insufficiency, 191–192, 191f,
192b
Cidofovir (Vistide), as antiviral medications,
467t
CIDP. see Chronic inflammatory
demyelinating polyneuropathy
CIM. see Critical illness myopathy
Cimetidine (Tagamet), in gastric acid
suppression, 458t
CIMT. see Constraint-induced movement
therapy
Cinacalcet (Sensipar), for
hyperparathyroidism, 471t
CIP. see Critical illness polyneuropathy
Ciprofloxacin (Cipro), for infectious diseases,
461t
Circle of Willis, 146
Circulation
cerebral, 146–147
posterior, 146
systemic, 22, 22f
in wound assessment, 317
Circulatory assist devices, 417–430
long-term devices, 422–426
total artificial heart, 426–428, 427f
ventricular assist device, 422–425, 423f,
424t, 424b
short-term percutaneous, 417–420
Circulatory assist devices (Continued)
Impella® Recover System, 419, 419f,
419b
intraaortic balloon pump as, 417–418,
417f
TandemHeart, 419–420, 420f
short-term surgically placed, 420
CentriMag, 420, 420b
extracorporeal membrane oxygenation
(ECMO), 420–422, 421f
Circulatory complications, of
musculoskeletal, interventions to
prevent, 94
Cirrhosis, 224, 224f
Cisplatin (Platinol-AQ), in chemotherapy,
455t
Citalopram (Celexa), as antidepressants, 448t
CK. see Creatine kinase
CKD. see Chronic kidney disease
Clarithromycin (Biaxin), for infectious
diseases, 461t
Claudication
neurologic, in atherosclerosis, 183
pseudoclaudication differentiated from,
183, 183t
Claudication Scale (CLAU-S), 173
Clavicle fractures, 104
Cleaning, wound, 320, 320b
“Clear to auscultation”, 64b
Clemastine (Tavist), as antihistamines, 442t
Clindamycin (Cleocin), for infectious
diseases, 461t
Clobazam (Onfi), as antianxiety medication,
446t
Clomipramine (Anafranil), as antidepressant,
448t
Clonazepam (Klonopin), as antianxiety
medication, 446t
Clonidine (Catapres, Catapres TTS-
transdermal patch), as antihypertensive
agents, 435t
Clopidogrel (Plavix), as antiplatelet agents,
439t
Closed face mask, in oxygen delivery, 397t,
398f
Clozapine (Clozaril), as antipsychotics, 449t
CMV. see Cytomegalovirus infection
CNS. see Central nervous system
CO. see Cardiac output
Coagulation disorders, 195–198
disseminated intravascular coagulation as,
195–196, 196t, 196b
hemophilia as, 196, 196b, 197f
heparin-induced thrombocytopenia, 197
idiopathic thrombocytopenic purpura as,
197–198
thrombotic thrombocytopenic purpura as,
197
Coagulation profiles
in cardiac evaluation, 29
in hematologic evaluation, 180, 180b
Coccidioidomycosis, as HIV and AIDS
complication, 343t
“Code” status, 8
Codeine (Paveral), in pain management, 487t
Colesevelam (WelChol), as lipid-lowering
agent, 440t
Colestipol (Colestid), as lipid-lowering agent,
440t
INDEX 523
Colitis, ulcerative, 222
Collagen matrix dressings, 323t
Collateral ventilation, airway clearance
techniques, 491
Collection phase, of autogenic drainage (AD),
494
Colles cast, 121t
Colonization, definition of, 330t
Colonoscopy, in gastrointestinal evaluation,
214t
Colony-stimulating factors, in hematology,
457t
Color duplex scanning, in vascular
evaluation, 176t
Colorectal cancer, 285
Colostomy, 226t
Coma, 9–10, 137–138, 138t
hepatic encephalopathy and, 224–225,
225t
Coma Recovery Scale-Revised (CRS-R), 138
Communicable, definition of, 330t
Compartment syndrome, 189
Complete blood cell count (CBC)
in cardiac evaluation, 29
in hematologic evaluation, 178–179, 179f,
179t
Complete heart block, ECG characteristics
and causes of, 53t
Complex regional pain syndrome (CRPS),
188–189
Composite skin graft, for burns, 307t
Computed tomographic pulmonary
angiography, for pulmonary
examination, 71–72
Computed tomography (CT)
in gastrointestinal evaluation, 214t
in genitourinary evaluation, 237
in hepatic/biliary/pancreatic/splenic
evaluation, 216t
in musculoskeletal evaluation, 90
in neurologic examination, 161t–163t
in vascular evaluation, 176t
Computed tomography angiography (CTA),
in neurologic examination, 161t–163t
Concentration gradient, in gas exchange, 59
Condom catheter, in medical-surgical
management, 405t–407t
Conduction disturbance, 34–36
Conduction system, cardiac, 21, 21f
Conductivity, of heart, 19
Confidentiality, medical record and, 13–14
Confusion Assessment Method (CAM), 136
Confusion Assessment Method for the
Intensive Care Unit (CAM-ICU), 508,
508b
Congestive heart failure (CHF), 36, 38b
as HIV and AIDS complication, 343t
Conjugated estrogens (Premarin), for
osteoporosis, 472t
Connective tissue, tumors originating from,
277t
Conscious sedation, 475
Consolidation, in respiratory dysfunction, 76
Constraint-induced movement therapy
(CIMT), 150–151
Contact burn, 300t
Continuous positive airway pressure (CPAP),
412t
Contractility, of heart, 19
524 INDEX
Contrast angiography, in vascular evaluation,
175–177, 177f
Contrast echocardiography, 31
Control ventilation, 412t
Coordination, in neurologic examination,
143–144, 144t
COPD. see Chronic obstructive pulmonary
disease
Coronary arterial spasm, 34
Coronary artery(ies), anatomy of, 18f
Coronary artery bypass graft (CABG), 39–40,
39b
Coronary artery disease, 266
Coronary atherectomy, directional, 39
Coronary atherosclerotic disease (CAD), 34
Coronary laser angioplasty, 39
Coronary perfusion, 22
Corpectomy, 118t
Corpus callosum, 128, 131t
Corset, 122t
Cortex, 128
Cortisol
deficiency of, 260
target sites and actions of, 259t
Cotswolds modification of Ann Arbor
Staging Classification for lymphomas,
288t
Cough
airway clearance techniques, 492, 492b,
493t
examination, 67
whooping, 336
Coumarin derivatives, 434t
as anticoagulants, 434t
CPAP. see Continuous positive airway pressure
CPOT. see Critical-Care Pain Observation
Tool
CPP. see Cerebral perfusion pressure
Crackles, 65
Cranial nerves, 128–134, 130b, 132t
disorders, common, 131–132
C-reactive protein (CRP), 29
in atherosclerosis, 181–182
Creatine kinase (CK), 30
Creatinine tests, in genitourinary evaluation,
235–236
Critical-Care Pain Observation Tool (CPOT),
481, 484t–485t
Critical illness myopathy (CIM), 6
Critical illness polyneuropathy (CIP), 6
Crizotinib (Xalkori), in chemotherapy, 455t
Crohn’s disease, 222
Cromolyn (Intal), for respiratory system, 443t
CRP. see C-reactive protein
CRPS. see Complex regional pain syndrome
CRS-R. see Coma Recovery Scale-Revised
Cruciate ligament reconstructions, 120t
Cryoprecipitate, clinical indications and
outcomes for, 200t
Cryptococcal meningitis, as HIV and AIDS
complication, 343t
Crystals, in urine, etiology of, 236t
CSF. see Cerebrospinal fluid
CTA. see Computed tomography angiography
Cuff, in mechanical ventilation, 411, 411b
Culture
in infectious disease evaluation, 331–332
wound, 319, 319b
Cultured epidermal autograft, for burns, 307t
Cushing’s syndrome, 258
CVA. see Cerebral vascular accidents
Cyclobenzaprine (Flexeril, Amtrix extended
release capsules), as muscle relaxant, 445t
Cyclophosphamide (Cytoxan, Neosar), in
chemotherapy, 455t
Cycloserine (Seromycin), as antitubercular
agent, 464t
Cyclosporin modified (Gengraf, Neoral), as
immunosuppressants, 473t
Cyclosporin nonmodified (Sandimmune), as
immunosuppressants, 473t
Cystic fibrosis, 77t, 78
hemoptysis in, 67
Cystitis, 241
Cystometry, in genitourinary evaluation, 237
Cystoscopy, in genitourinary evaluation, 237,
237b
Cytarabine (Cytosar-U, DepoCyt), in
chemotherapy, 455t
Cytology, in infectious disease evaluation, 332
Cytomegalovirus, as HIV and AIDS
complication, 343t
Cytomegalovirus infection (CMV), 343
Cytoprotective medications, 458t
D Dexamethasone (Decadron), for respiratory
Dabigatran (Pradax), as anticoagulants, 434t
Dacarbazine (DTIC-Dome), in chemotherapy,
455t
Daclatasvir (Daklinza), as antiviral
medications, 467t
Dactinomycin (Cosmegen), for chemotherapy,
455t
Dalbavancin (Dalvance), for infectious
disease, 461t
Dalteparin sodium (Fragmin), as
anticoagulant, 434t
Dantrolene (Dantrium), for spasticity, 445t
Dapagliflozin (Farxiga), for hyperglycemia,
469t
Daptomycin (Cubicin), for infectious
diseases, 461t
Darbepoetin alfa (Aranesp), for colony-
stimulating factor, 457t
Dasabuvir, as antiviral medications, 467t
Dasatinib (Sprycel), in chemotherapy, 455t
Daunorubicin (Cerubidine, DaunoXome), in
chemotherapy, 455t
DBS. see Deep brain stimulation
D-dimer assay, in hematologic evaluation,
180, 180b
Dead space, 59
Dean, Elizabeth, 83
Dean’s hierarchy for treatment of patients
with impaired oxygen transport, 84t
Death, brain, 9–10
Debridement, wound, 320–322
Decompression, spinal, 118, 118t
Decubitus ulcer, 311–312, 312b, 313t
Deep brain stimulation (DBS), 143
Deep tendon reflex (DTR), 141, 142t
Deep venous thrombosis (DVT), 92b, 189
early ambulation and, 191
imaging studies for, 190
prophylaxis for, 190
risk factors for, 190b
treatment of, 190
Wells Clinical Decision Rule for, 176t
Defibrillator, cardiac, automatic implantable,
41
Delirium, 136, 136b, 137t
ICU, 5
Demeclocycline (Declomycin), for infectious
diseases, 461t
Dementia, 136, 137t
Denileukin diftitox (Ontak), in
chemotherapy, 455t
Denosumab (Prolia), for osteoporosis,
472t
Dermagraft, in burn and wound treatment,
308t
Dermis, structure and function of, 297t
DES. see Distal esophageal spasm
Desensitization protocols, 358
Desiccated thyroid (Armour Thyroid,
Nature-Thyroid), for hypothyroidism,
473t
Desipramine (Norpramin), as antidepressant,
448t
Desirudin (Iprivask), as anticoagulants, 434t
Desloratadine (Clarinex), as antihistamines,
442t
Desogestrel, as oral contraceptive, 460t
Detemir (Levemir), for hyperglycemia, 469t
system, 441t
Dextroamphetamine (Dexedrine, ProCentra),
as stimulants, 450t
DI. see Diabetes insipidus
Diabetes insipidus (DI), 259
Diabetes mellitus, 261–267, 469
complications of, 265–267
physical therapy considerations for, 264
type 1, 262–263
control of, tests monitoring, 262t
insulin pump therapy for, 263t
type 2, 263, 263b
Diabetic complications
coronary artery disease as, 266
diabetic ketoacidosis as, 265
diabetic neuropathy as, 266
hyperosmolar hyperglycemic nonketotic
syndrome/coma as, 265
hypoglycemia as, 266–267
infection as, 266, 266b
nephropathy as, 266
peripheral vascular disease as, 266
skin lesions as, 265–266
stroke as, 266
Diabetic ketoacidosis (DKA), 265
Diabetic nephropathy, 240
Diabetic neuropathy, 266
Diagnostic and laboratory measures, in
cardiac evaluation, 26–34, 28t, 28b, 32t
Dialysis, peritoneal, for genitourinary
dysfunction, 243, 244f
Diaphragm, in inspiration, 58, 61f
Diaphragmatic excursion, 67
Diastole, 19
Diastolic dysfunction, 36
Diazepam (Valium)
as antianxiety medication, 446t
as muscle relaxants, 445t
Dibucaine (Nupercainal), for local anesthesia,
488t
Dichlorphenamide (Daranide), as
antihypertensive agents, 435t

Diclofenac (Caraflam, Voltaren), in pain
management, 487t
Dicloxacillin (Dynapen, Dycill), for
infectious diseases, 461t
Dicyclomine (Bentyl), for irritable bowel
syndrome, 458t
Didanosine (Videx EC, ddI), for HIV/AIDS,
465t
Diet, wound healing and, 314–315, 315b
Differentiation, definition of, 276t
Diffusing capacity of carbon monoxide
(DLCO), 74t–75t
Digestion, organs of
accessory, structure and function of, 211t
primary, structure and function of, 211t
Digital-subtraction angiography (DSA), in
neurologic examination, 161t–163t
Digitalis toxicity, signs and symptoms of, 43t
Digoxin (Lanoxin), for arrhythmias, 433t
Diltiazem (Cardizem, Tiazac, Cartia XT) , as
antihypertensive agents, 435t
Dimethyl fumarate (Tecfidera), for multiple
sclerosis, 451t
Diphenhydramine (Benadryl), as
antihistamines, 442t
Diphenoxylate/atropine (Lomotil), for
diarrhea, 458t
Direct thrombin inhibitors, as
anticoagulants, 434t
Directional coronary atherectomy, 39
Disarticulation, 115–116, 116b
Discectomy, 117–118, 118t
Discontinuous sounds, 65
Disease-modifying antirheumatic drugs
(DMARDs), for musculoskeletal system,
443t
Disequilibrium, in vestibular dysfunction,
154
Disopyramide (Norpace), for arrhythmias,
433t
Disorders of consciousness (DOCs), 137–138,
138t
Disseminated host, definition of, 330t
Distal esophageal spasm (DES), 217
Distal symmetric polyneuropathy, as HIV
and AIDS complication, 343t
Disulfiram (Antabuse), for substance use-
related disorders, 451t
Diuretics, as antihypertensive
agents, 435t
Diverticular disease, 219
Dix-Hallpike maneuver, 155f
Dix-Hallpike test, 156t
DKA. see Diabetic ketoacidosis
DLCO. see Diffusing capacity of carbon
monoxide
DMARDs. see Disease-modifying
antirheumatic drugs
DNI. see Do not intubate
DNR. see Do not resuscitate
Do not intubate (DNI), 8
Do not resuscitate (DNR), 8
Dobbhoff tube, in medical-surgical
management, 405t–407t
Dobutamine, as positive inotropes, 441t
Dobutamine stress echocardiography (DSE),
31
Docetaxel (Taxotere), in chemotherapy, 455t
DOCs. see Disorders of consciousness
Documentation, physical therapist, 14–15
Docusate (Colace), as laxative, 459t
Dofetilide (Tikosyn), for arrhythmias, 433t
Dolasetron (Anzemet), as antiemetic, 454t
Dolutegravir (Tivicay), for HIV/AIDS, 465t
Domino liver transplantation, 361
Donors, organ, 353
cadaveric, 354
living, 354–355
postoperative care for, 355
matching/allocation of, 355
shortage of, 355
Dopamine, as positive inotropes, 441t
Dopamine receptor agonist, for
hyperglycemia, 469t
Doppler flowmetry, in neurologic
examination, 161t–163t
Doppler ultrasound, in vascular evaluation,
176t
Dorsal spinocerebellar tract, function of, 139t
Double-barrel colostomy, 226t
Double-lung transplantation, 367
Doxazosin (Cardura)
as antihypertensive agents, 435t
for benign prostatic hyperplasia, 460t
Doxepin (Sinequan), as antidepressants, 448t
Doxercalciferol (Hectorol), for
hyperparathyroidism, 471t
Doxorubicin (Adriamycin, Doxil), in
chemotherapy, 455t
Doxycycline (Vibramycin), for infectious
diseases, 461t
Doxylamine succinate/pyridoxine
hydrochloride (Diclegis, Bonjesta), as
antiemetic, 454t
Drainage, from transplanted pancreas, enteric
versus bladder, 362–363
Dressings, wound, 322, 323t
Dronabinol (Marinol), as antiemetic, 454t
Dronedarone (Multaq), for arrhythmias, 433t
Droperidol (Inapsine), as antiemetic, 454t
Drop-lock brace, 122t
DSA. see Digital-subtraction angiography
DSE. see Dobutamine stress echocardiography
DTR. see Deep tendon reflex
Dual-energy X-ray absorptiometry (DXA),
268
Dulaglutide (Trulicity), for hyperglycemia,
469t
Duloxetine (Cymbalta), as antidepressants,
448t
Dumping syndrome, 219
Dutasteride (Avodart), for benign prostatic
hyperplasia, 460t
Dutasteride/tamsulosin (Jalyn), in
chemotherapy, 455t
DVT. see Deep venous thrombosis
DXA. see Dual-energy X-ray
absorptiometry
Dynamic Gait Index, 502, 502t
interpretation of results, 502
procedure, 502, 502b
Dynamic hyperinflation, 411–413
Dynamic visual acuity (DVA) test, for
vestibular dysfunction, 156t
Dysphagia, 216, 217t
Dysplasia, definition of, 276t
Dyspnea, pulmonary examination
of, 62, 62b
INDEX 525
E
EBRT. see External beam radiation therapy
ECD. see Expanded criteria donor
ECG. see Electrocardiography
Echocardiography, 30–31
ECMO. see Extracorporeal membrane
oxygenation
Edema
assessment, 181, 181b
control of, postamputation, 384, 384b
management of, in wound care, PT
considerations for, 325t
pitting, scale for, 24t
in wound assessment, 316–317
EDGE. see Evaluation Database to Guide
Effectiveness
Edoxaban (Savaysa), as anticoagulants, 434t
EEG. see Electroencephalography
Efavirenz (Sustiva, EFV), for HIV/AIDS,
465t
EGD. see Esophagogastroduodenoscopy
Egophony, 65
EHRs. see Electronic health records
Elbasvir, as antiviral medications, 467t
Electrical burns, 299–301
Electrical stimulation, in wound care, 324t
Electrocardiography (ECG), 26–29
atrial rhythm characteristics on, 51t
changes in, ischemic, 392f
in hemodynamic monitoring, 400t
interpretation of, 28t
junctional rhythm characteristics on, 52t
rhythm of, 46b
ventricular rhythm characteristics on, 52t
Electroencephalography (EEG), 155
in neurologic examination, 161t–163t
Electrolyte imbalance, 381, 381f
physical therapy considerations for, 381
Electromyography (EMG), in neurologic
examination, 161t–163t
Electronic health records (EHRs), 13. see also
Medical record(s)
Electrophoresis, protein, in hepatic testing,
215t–216t
Electrophysiologic studies (EPSs), in cardiac
evaluation, 33–34, 34b
Elevation pallor, in vascular evaluation, 175t
Elvitegravir (Vitekta), for HIV/AIDS, 465t
Embolism, pulmonary, 79t, 80, 80b, 191
Embolization therapy, 200
Embolus(i), arterial, 185, 185t
EMG. see Electromyography
Empagliflozin (Jardiance), for hyperglycemia,
469t
Emphysema, 76, 77t
Empyema, 82, 156–157
Emtricitabine (Emtriva, FTC), for HIV/
AIDS, 465t
Enalapril (Vasotec), as antihypertensive
agents, 435t
Encephalitis, 156, 339–340, 340b
Encephalopathy, 157
hepatic, 224–225, 225t
End (Brooke) colostomy, 226t
Endarterectomy, 201, 201b
Endocardium, description and function of,
19t
Endocrine function, evaluation of, 253–254,
254b
526 INDEX

Endocrine input, to cardiac conduction Erysipelas, 340 Evolocumab (Repatha), as lipid-lowering

system, 21, 21t
Endocrine system, 253–274, 254f, 469
adrenal gland of, 259–260
dysfunction of, physical therapy
management of, 269
metabolic bone disorders and, 268–269
pancreas in, 261–267
parathyroid gland in, 267–268
pituitary gland of, 256–259
prolonged bed rest and, 5t
thyroid gland of, 254–256
End-of-life considerations, 8–10
Endometriosis, 243, 243b
Endoscopic retrograde
cholangiopancreatography and
pancreatic cytology (ECRP), 216t
Endothelial receptor antagonists, for
pulmonary hypertension, 439t
Endotracheal tube, 410, 410f
Enema, barium, in gastrointestinal
evaluation, 214t
Enfuvirtide (Fuzeon, T-20, ENF), for HIV/
AIDS, 465t
Enoxaparin sodium (Lovenox), as
anticoagulant, 434t
Enteric drainage, from transplanted pancreas,
bladder drainage versus, 362–363
Enterococci infection, vancomycin-resistant,
334
Enzymatic debridement of wound, 321, 321b
Epicardium, description and function of, 19t
Epidermis, structure and function of, 297t
Epidural analgesia, patient-controlled, 488t
Epidural sensor, in ICP monitoring, 403t
Epinephrine (Adrenalin, EpiPen)
as bronchodilators, 442t
cardiac effects of, 21t
as positive inotropes, 441t
target sites and actions of, 259t
Epipodophyllotoxins, in chemotherapy, 455t
Epithelial tissue, tumors originating from,
277t
Eplerenone (Inspra), as antihypertensive
agents, 435t
Epley maneuver, 154, 157f
Epoetin alfa (Epogen, Procrit), for colony-
stimulating factor, 457t
Epoprostenol (Flolan, Veletri), for pulmonary
hypertension, 439t
EPP. see Equal pressure point
Eprosartan (Teveten), as antihypertensive
agents, 435t
EPSs. see Electrophysiologic studies
Epstein-Barr virus, mononucleosis from, 342
Eptifibatide (Integrilin), as antiplatelet
agents, 439t
Equal pressure point (EPP), 492
Ergocalciferol (Drisdol, Calciferol), for
hyperparathyroidism, 471t
Eribulin (Halaven), in chemotherapy, 455t
Erlotinib (Tarceva), in chemotherapy, 455t
Ertapenem (Invanz)
for infectious diseases, 461t
for infectious diseases, for infectious
diseases, 461t
Ertugliflozin (Steglatro), for hyperglycemia,
469t
ERV. see Expiratory reserve volume
Erythrocyte index, in hematologic evaluation,
179, 180t, 180b
Erythrocyte sedimentation rate (ESR), in
hematologic evaluation, 179–180
Erythrocytes
description of, 173t
disorders of, 192–195
anemia as, 192–195
neutropenia as, 195
polycythemia as, 195
Erythromycin (Ery-tab), for infectious
diseases, 461t
Escitalopram (Lexapro), as antidepressants,
448t
Eslicarbazepine (Aptiom), as anticonvulsants,
446t
Esomeprazole (Nexium), as proton pump
inhibitors, 459t
Esophageal dysphagia, 216, 217t
Esophageal function studies, in
gastrointestinal evaluation, 214t
Esophageal motility disorders, 217
Esophageal varices, 218
Esophagogastroduodenoscopy (EGD), in
gastrointestinal evaluation, 214t
Esophagus
Barrett’s, 217–218
disorders of, 216–218
function of, 211t
Essential tremor, 143
Estazolam (ProSom), as antianxiety
medication, 446t
Estradiol/norethindrone acetate (Acivella), for
osteoporosis, 472t
Estrogens
in chemotherapy, 455t
as oral contraceptive, 460t
target sites and actions of, 259t
Eszopiclone (Lunesta), as antianxiety
medication, 446t
Etanercept (Enbrel), for rheumatoid arthritis,
443t
Ethambutol (Myambutol), as antitubercular
agent, 464t
Ethinyl estradiol (Estinyl), for chemotherapy,
455t
Ethinyl estrogen, as oral contraceptive, 460t
Ethionamide (Trecator), as antitubercular
agent, 464t
Ethosuximide (Zarontin), as anticonvulsants,
446t
Ethotoin (Peganone), as anticonvulsants,
446t
Ethynodiol diacetate, as oral contraceptive,
460t
Etodolac (Lodine), in pain management, 487t
Etoposide (VePesid), in chemotherapy, 455t
Etravirine (Intelence, ETR), for HIV/AIDS,
465t
Evacuation phase, of autogenic drainage
(AD), 494
Evaluation Database to Guide Effectiveness
(EDGE), 499
Everolimus (Afinitor, Zortress)
in chemotherapy, 455t
as immunosuppressants, 473t
Evoked potentials (EPs), in neurologic
examination, 161t–163t
agent, 440t
Excision, in burn care, 306, 307t
Excitability, of heart, 19
Exenatide (Byetta, Bydureon), for
hyperglycemia, 469t
Exercise, 415
airway clearance techniques, 493t, 496,
496b
isometric, for quadriceps and gluteal
muscles
after knee arthroplasty, 111
after total hip arthroplasty, 107–108
therapeutic
after knee arthroplasty, 111
after shoulder arthroplasty, 114, 114f
patient response to, evaluating, 44, 45f
Exercise testing, 505
in cardiac evaluation, 31–33, 32f, 32t, 32b
in vascular evaluation, 176t
Exertional angina, 34
Exhalation, in ventilation, 58
Expanded criteria donor (ECD), 355
Expectorants, 497
Expiratory muscles, innervation of, 59t
Expiratory reserve volume (ERV), description
and clinical significance of, 74t–75t
External beam radiation therapy (EBRT), 279
Extracorporeal membrane oxygenation
(ECMO), 420–422, 421f
Extrapleural disorders, characteristics and
general management of, 81t
Extrapulmonary conditions, restrictive,
81–82, 81t
Extrapulmonary sounds, 65
Extrapyramidal tracts, function of, 139t
Extremities
lower
braces and splints for, 122t
fractures of, 95–103
upper
braces and splints for, 122t
fractures of, 104–105
Exudative fluid, in pleural effusion, 81
Eyes, hypertensive effects on, 186t
Ezetimibe (Zetia), as lipid-lowering agent,
440t
Ezogabine (Potiga), as anticonvulsants, 446t
F
Face mask, in oxygen delivery, 397t, 398f
Facial nerve (CN VII), 132t
Factor Xa inhibitor, as anticoagulant, 434t
Fall
definition of, 2
risk for, in acute care setting, 2
Famciclovir (Famvir), as antiviral
medications, 467t
Familial tremor, 143
Famotidine (Pepcid), in gastric acid
suppression, 458t
Fasciculus cuneatus, function of, 139t
Fasciculus gracilis, function of, 139t
Fecal fat, in pancreatic and biliary testing,
215t–216t
Fecal occult blood test (FOB), in
gastrointestinal evaluation, 213t
Felbamate (Felbatol), as anticonvulsants,
446t
 INDEX 527

Felodipine (Plendil), as antihypertensive Fluid volume excess, 380t Fracture (Continued)

agents, 435t Flunisolide (AeroBid), for respiratory system, carpal, 105
Femoral head fractures, 98 441t classification of, 94–95
Femoral neck fractures, 99, 100f Fluoroquinolones, for infectious diseases, complications of, 95
Femorofemoral bypass, 202f 461t extremity
Femoropopliteal bypass, 202f Fluorouracil (5-FU, Adrucil), in lower, 95–103
Femorotibial bypass, 202f chemotherapy, 455t upper, 104–105, 104b
Femur Fluoxetine (Prozac, Sarafem), as femur
distal, fracture of, 100, 100b antidepressants, 448t distal, 100
proximal, fracture of, 98–99, 98b, 100f Fluoxymesterone (Halotestin), in proximal, 98–99, 100f
shaft of, fracture of, 99–100, 101f–102f chemotherapy, 455t shaft, 99–100, 101f–102f
Fenofibrate (Antara, Lipofen, Tricor), as Fluphenazine (Prolixin), as antipsychotic, fibula, 102
lipid-lowering agent, 440t 449t healing of, 95, 98f, 98b
Fentanyl (Actiq, Sublimaze, Duragesic), in Flurazepam (Dalmane), as antianxiety humeral, 104
pain management, 487t medication, 446t immobilization of, 95, 96f–98f
Fentanyl iontophoretic transdermal system Flurbiprofen (Ansaid), in pain management, management of
(ITS) for analgesia, 488t 487t by body region, 95–105
FET. see Forced expiratory technique Flutamide (Eulexin), in chemotherapy, 455t clinical goal of, 95
Fexofenadine (Allegra), as antihistamines, Fluticasone furoate (Arnuity Ellipta), for metacarpal, 105
442t respiratory system, 441t patella, 100
FFP. see Fresh-frozen plasma Fluticasone propionate (Flonase, Flovent, pelvic, 95–97, 99f
Fiberoptic transducer-tipped catheter, in ICP Advair) phalangeal, 105
monitoring, 403t for respiratory disorders, 441t proximal forearm, 104–105
Fibric acid derivatives, as lipid-lowering for respiratory system, 441t radial, 105
agents, 440t Fluvastatin (Lescol), as lipid-lowering agent, reduction of, 95
Fibrin cuff theory, of venous insufficiency 440t shoulder girdle, 104
wounds, 312 Fluvoxamine (Luvox), as antidepressants, spine, 103–104
Fibrinolytics, 441t 448t tibia
Fibula, fracture of, 102 Foam dressings, 323t distal, 102–103
Fidaxomicin (Dificid), for infectious diseases, FOB. see Fecal occult blood test shaft, 102
461t Foley catheter, in medical-surgical tibial plateau, 102, 103f
Finasteride (Proscar), for benign prostatic management, 405t–407t traumatic, 94–95
hyperplasia, 460t Folic acid anemia, 193 Frank-Starling mechanism, cardiac output
Fingolimod (Gilenya), for multiple sclerosis, Fondaparinux (Arixtra), as anticoagulant, and, 20–21, 20f
451t 434t FRC. see Functional residual capacity
First-degree AV block, ECG characteristics Foot care, for diabetic patients, 266 Free thyroxine index, 254t
and causes of, 53t Forced expiratory flow 25%-75%, Fremitus, palpation of, 66
First line of defense, 330t description and clinical significance of, Fresh-frozen plasma (FFP), clinical
Fish oil, as lipid-lowering agent, 440t 74t–75t indications and outcomes for, 200t
FIST. see Function in Sitting Test Forced expiratory technique (FET), 492, Frontal cortex, traumatic disorders of, 136–138
Fistula, arteriovenous, in medical-surgical 492b, 493t Frontal lobe, structure, function, and
management, 405t–407t Forced expiratory volume in 1 second (FEV1) dysfunction of, 131t
Five-time sit-to-stand test (FTSTS), 503, description and clinical significance of, Frontotemporal dementia, 137t
504t 74t–75t FSS-ICU. see Functional Status Score for the
Fixed performance oxygen delivery, 396, predicted values for, 72b Intensive Care Unit
399f, 399t Forced expiratory volume timed (FEVt), FTSTS. see Five-time sit-to-stand test
FLACC Pain Assessment Scale, 481, 483t, description and clinical significance of, Full-thickness excision, for burns, 307t
485t 74t–75t Function in Sitting Test (FIST), 505, 505t
Flail chest, 82 Forced vital capacity (FVC) Functional incontinence, 242t
Flame burn, 300t description and clinical significance of, Functional mobility, 415
Flash burn, 300t 74t–75t training, after spinal surgery, 118
Flecainide (Tambocor), for arrhythmias, 433t predicted values for, 72b Functional Pain Scale (FPS), 485t
Flexible bronchoscopy, for pulmonary Forearm cast, 121t Functional residual capacity (FRC),
examination, 71, 71b Formoterol (Foradil), as bronchodilators, description and clinical significance of,
Flow-volume loop, 72, 74f 442t 74t–75t
description and clinical significance of, Fosamprenavir (Lexiva, FPV), for HIV/AIDS, Functional Status Score for the Intensive Care
74t–75t 465t Unit (FSS-ICU), 509
Fluconazole (Diflucan), as antifungal agents, Fosaprepitant (Emend), as antiemetic, 454t Functional tests, 515
463t Foscarnet (Foscavir), as antiviral medications, Acute Care Index of Function as, 504–505
Fludarabine (Fludara), in chemotherapy, 455t 467t Berg Balance Scale as, 500–501, 500t,
Fludrocortisone (Florinef), for respiratory Fosinopril (Monopril), as antihypertensive 500b
system, 441t agents, 435t exercise testing as, 505
Fluid imbalance, 379–381, 380t Fosphenytoin (Cerebyx), as anticonvulsants, Short Physical Performance Battery as, 507
fluid shift, 381, 381b 446t sit-to-stand tests as, 503–504
fluid volume deficiency, 379 FPS. see Functional Pain Scale six-minute walk test as, 506–507, 506t,
fluid volume excess, 381, 381b Fracture 506b
physical therapy considerations for, 381 acetabulum, 97–98, 99f timed “up and go” test as, 501–502, 501t
Fluid resuscitation, in burn care, 304 ankle, 102–103 Tinetti Performance Oriented Mobility
Fluid volume deficit, 380t calcaneal, 103 Assessment as, 502–503, 503t
528 INDEX
Fundoplication, 226t
Furosemide (Lasix), as antihypertensive
agents, 435t
Fusion inhibitor, for HIV/ AIDS, 465t
FVC. see Forced vital capacity
G Gatifloxacin (Tequin), for infectious diseases,
Gabapentin (Neurontin), as anticonvulsants,
446t
Gait speed, 501, 501b
Gait training
after knee arthroplasty, 112
after total hip arthroplasty, 108, 108b
Gallbladder
cancer of, 286
function of, 211t
nuclear scanning, 216t
Galveston Orientation and Amnesia test
(GOAT), 137
Gamma-glutamyl-transferase, in hepatic,
biliary, and pancreatic testing,
215t–216t
Gamma motor neurons, 140t
Ganciclovir (Cytovene, Vitrasert), as antiviral
medications, 467t
Garden classification, 99, 100f
Gas exchange, 59
tests for, description and clinical
significance of, 74t–75t
Gas transport, 59
Gastrectomy, 226t
Gastric banding, adjustable, 226t, 227f
Gastric bypass, 226t
Roux-en-Y, 226t, 227f
Gastric emptying disorders, 219, 219b
Gastric lavage, body fluid examination of,
332
Gastric retention, 219
Gastrin, in gastrointestinal evaluation, 213t
Gastritis, 218
Gastroduodenostomy, 226t
Gastroenteritis, 340–341
Gastroesophageal reflux disease (GERD),
217, 217b
Gastrointestinal disorders
management of, 225–228
physical therapy in, 227–228
pharmacologic therapy for, 225–226
surgical procedures for, 226–227, 226t
Gastrointestinal evaluation
auscultation in, 211–212
diagnostic studies in, 212–213, 212b,
213t–216t
history in, 209, 211b
inspection in, 209–211, 211b, 212f
laparoscopy in, 212–213
magnetic resonance imaging in, 213
palpation in, 212
percussion in, 212
physical examination in, 209–212
positron emission tomography in, 213
Gastrointestinal hemorrhage, 218, 218b
Gastrointestinal system, 209–232, 457–460
cancers of, 285–286, 285b–286b
clinical evaluation of, 209–213
complications of burns affecting, 300t
hematologic disorders and, 178t
infections of, 340–341, 341b
pain referral patterns in, 210t
Gastrointestinal system (Continued)
prolonged bed rest and, 5t
structure and function of, 209, 210f, 211t
Gastrojejunostomy, 226t
Gastroparesis, 219
Gastroplasty, vertical banded, 226t, 227f
461t
Gauze dressings, 323t
GBS. see Guillain-Barré syndrome
GCA. see Giant cell arteritis
GCS. see Glasgow Coma Scale
Gefitinib (Iressa), in chemotherapy, 455t
Gemcitabine (Gemzar), in chemotherapy,
455t
Gemfibrozil (Lopid), as lipid-lowering agent,
440t
Gemtuzumab (Mylotarg), in chemotherapy,
455t
Gene therapy, for cancer, 281
General anesthesia, 475
Genitourinary dysfunction
endometriosis as, 243, 243b
intermittent hemodialysis for, 244, 244b,
245f–246f
lower urinary tract dysfunction as,
241–242
management of, 243–247
physical therapy in, 247–248
nephrectomy for, 245
peritoneal dialysis for, 243, 244f
prostate disorders as, 242–243
renal, 237–241
renal replacement therapy for, 243–244
continuous, 244, 244b, 246t, 247f
surgical interventions for, 244–247
urinary diversion for, 247
urinary incontinence procedures for,
245–247
Genitourinary evaluation, 234–237
angiography in, 237
auscultation in, 235
biopsies in, 237
bladder examination in, 237, 237b
blood urea nitrogen in, 236, 236b
computed tomography scan in, 237
creatinine tests in, 235–236
cystometry in, 237
diagnostic tests in, 235–237
estimated glomerular filtration rate in, 236
history in, 235, 235b
KUB X-ray in, 236
magnetic resonance imaging in, 237
observation in, 235, 235b
palpation in, 235
percussion in, 235
physical examination in, 235
pyelography in, 236
radiographic examination in, 236–237
renal arteriography in, 237, 237b
renal scanning in, 237
ultrasonography studies in, 237
urinalysis in, 235, 235b, 236t
Genitourinary system, 233–252, 460–461
cancers of, 285–286, 285b–286b, 286t
clinical evaluation of, 234–237
complications of burns affecting, 300t
health conditions involving, 237–243
prolonged bed rest and, 5t
Genitourinary system (Continued)
segmental innervation and pain referral in,
234t
structure and function of, 233–234, 234f
Gentamicin (Garamycin), for infectious
diseases, 461t
GERD. see Gastroesophageal reflux disease
GFR. see Glomerular filtration rate
GH. see Growth hormone
GI bleeding scan, in gastrointestinal
evaluation, 214t
GI transplantation, 226t
Giant cell arteritis (GCA), 187–188
Gigantism, 257
Glasgow Coma Scale (GCS), 134–135, 135b
Glatiramer (Copaxone), for multiple sclerosis,
451t
Glia, 140t
Glimepiride (Amaryl), for hyperglycemia, 469t
Glipizide (Glucotrol), for hyperglycemia, 469t
Global Initiative for Obstructive Lung
Disease (GOLD), 76
Glomerular diseases, 239–240
Glomerular filtration rate (GFR), estimated,
in genitourinary evaluation, 236
Glossopharyngeal nerve (CN IX), 132t
Glucocorticoids, 441t
target sites and actions of, 259t
Glucose tolerance test, 260
Gluteal muscles, isometric exercises for, after
total hip arthroplasty, 107–108
Glyburide (Micronase, Diabeta, Glynase), for
hyperglycemia, 469t
Glycerin (Fleet glycerin suppositories), as
laxative, 459t
Glycoprotein IIb/IIIa inhibitors, as
antiplatelet agents, 439t
Glycosuria, etiology of, 236t
Glymphatic systems, 147
GNRH agonists, in chemotherapy, 455t
GOAT. see Galveston Orientation and
Amnesia test
Goiter, hyperthyroidism from, 255t
GOLD. see Global Initiative for Obstructive
Lung Disease
Gold sodium thiomalate (Myochrysine), for
rheumatoid arthritis, 443t
Golimumab (Simponi), for rheumatoid
arthritis, 443t
Goserelin (Zoladex), in chemotherapy, 455t
Graft, arteriovenous, in medical-surgical
management, 405t–407t
Graft rejection
chronic, 357
hyperacute, 356
types of, 356–357
Grafting
in burn care, 306, 307t–308t
bypass, peripheral vascular, 201, 202f–203f
GRAFTJACKET, in burn and wound
treatment, 308t
Granisetron (Kytril), as antiemetic, 454t
Granulomatosis, Wegener’s, 187
Graves’ disease, hyperthyroidism from, 255t
Grazoprevir, as antiviral medications, 467t
Great vessels of heart, description and
function of, 19t
Groshong catheter, in medical-surgical
management, 405t–407t

Growth hormone (GH)
overproduction of, 257–258, 258b
tests of, 257t
Guillain-Barré syndrome (GBS), 158–159
chest wall restriction in, 82
H cardiac reflexes influencing, 21
Haemophilus meningitis, 339
HAI. see Health care-associated infection
Halazepam (Paxipam), as antianxiety
medication, 446t
Halo vest, 122t
Haloperidol (Haldol)
as antiemetic, 454t
as antipsychotic, 449t
Hamstring muscles, isometric exercises for,
after knee arthroplasty, 111
Hand washing, proper technique for, 346b
HCC. see Hepatocellular carcinoma
HDLs. see High-density lipoproteins
Head and neck cancers, 288–289, 288b
Head impulse test, in testing for vestibular
dysfunction, 156t
Head-shaking-induced nystagmus, in testing
for vestibular dysfunction, 156t
Head thrust test, in testing for vestibular
dysfunction, 156t
Healing, wound
factors delaying, 314–315
phases of, 313–314
Health care-associated infection (HAI),
definition of, 330t, 332–335, 334b
Health Information Technology for Economic
and Clinical Health (HITECH)
Act, 13
Health Insurance Portability and
Accountability Act (HIPAA),
confidentiality and, 13–14
Heart
blood pumping ability of, characteristics
facilitating, 18
conduction system of, 21, 21f
diseases of
functional classification of, 36
myocardial, 36. see also Myocardial
infarction (MI)
pericardial, 36
valvular, 36, 36t
displacement of, 18
evaluation of, 22–34. see also Cardiac
evaluation
failure of, 36–37
great vessels of, 19t
hypertensive effects on, 186t
structures of, 19t
transplantation of, 364–366
cardiac function after, indication of,
364–365
contraindications to, 364
indications for, 364–365
lung transplantation combined with,
369–370
orthotopic and heterotopic, 364
physical therapy for recipients of,
365–366, 366b
physiologic changes following, 366t
postoperative care and complications in,
364–365, 365b
pretransplantation care, 364
Heart block
complete, ECG characteristics and causes
of, 53t
degrees of, 56f
Heart-lung transplantation (HLT), 369–370
Heart rate (HR)
cardiac transplantation and, 366t
hormonal influences on, 21, 21t
in infectious disease evaluation, 331
neural influences on, 21
palpation of, 24
variability of, 27
Heart rate variability (HRV), 21
Heart sounds, 46b
normal and abnormal, 27t
Heartmate II, 424
Heartmate 3, 424–425
HeartWare (HVAD), 424
Helicobacter pylori
gastritis from, 218
tests, in gastrointestinal evaluation, 213t
Hemarthrosis, acute, in hemophilia, 196, 197f
Hematocrit, in organ transplantation, 373t
Hematologic disorders, 192–195
cancer as, 286–288, 287t–288t
coagulation, 195–198. see also Coagulation
disorders
erythrocytic, 192–195. see also
Erythrocytes, disorders of
leukemia as, 286–287, 287t, 287b
leukocytic, 195. see also Leukocytic
disorders
lymphomas as, 287, 287t, 287b
multiple myeloma as, 287–288,
287b–288b, 288t
physical therapy interventions for patients
with, 204–205
signs and symptoms of, by body system,
178t
Hematologic evaluation, 177–180
history in, 177
laboratory studies in, 178–180, 179f,
179t–181t
observation in, 177–178
palpation in, 178, 178t
Hematologic system, 171–208, 173t
disorders of, 192–195. see also Hematologic
disorders
evaluation of, 177–180. see also
Hematologic evaluation
physical examination of, 172–181
prolonged bed rest and, 5t
Hematology
in infectious disease evaluation, 331
pharmacologic agents for, 457
Hematopoietic tissue, tumors originating
from, 277t
Hematuria, etiology of, 236t
Hemiarthroplasty, humeral, proximal, 113
Hemiparalysis, 142b
Hemiparesis, 142b
Hemipelvectomy, 115–116, 116f
Hemodialysis, intermittent, for genitourinary
dysfunction, 244, 244b, 245f–246f
Hemodynamic monitoring, 396–399, 402f
invasive, 399, 401t
noninvasive, 399, 400t
objectives of, 396–399
INDEX 529
Hemoglobin, in organ transplantation, 373t
Hemolytic anemia, 193–194
Hemophilia, 196, 196b
Hemoptysis, 67
Hemorrhage, gastrointestinal, 218
Hemothorax, 81t, 82
Heparin
as anticoagulant, 434t
in DVT management, 190
Heparin sodium, as anticoagulant, 434t
Hepatic encephalopathy, 157, 224–225,
225t
Hepatitis, 223–224, 224b
Hepatitis virus studies, in hepatic testing,
215t–216t
Hepatobiliary cancers, 286, 286b
Hepatocellular carcinoma (HCC), 286
Hernia
abdominal, 220
hiatal, 220, 220b
Herniation syndromes, 150f
Herpes simplex, as HIV and AIDS
complication, 343t
Herpes zoster (shingles), as HIV and AIDS
complication, 343t
Heterograft, for burns, 307t
Heterotopic heart transplantation, 364
HFCWO. see High frequency chest wall
oscillation
HFJV. see High-frequency jet ventilation
HFOV. see High-frequency oscillation
ventilation
Hickman catheter, in medical-surgical
management, 405t–407t
High-density lipoproteins (HDLs), 29
High frequency chest wall oscillation
(HFCWO), airway clearance techniques,
493t, 496, 496f
High-frequency jet ventilation (HFJV), 412t
High-frequency oscillation ventilation
(HFOV), 412t
High-output failure, 36
High-sensitivity C-reactive protein (Hs-CRP)
assay, 29
Hip abduction orthosis, 122t
Hip arthroplasty, 105–108
infected, resection for, 114–115
physical therapy after, 115
physical therapy after, 106–108, 106b
positions to avoid after with alternatives,
107f
resurfacing, 109, 109f
surgical approaches for, 106, 106t
total
activity restrictions after, 106b
dislocation precautions for, 106, 106t
trochanteric osteotomy in, 108, 108b, 109f
Hip disarticulation, 115–116
Hip spica cast, 121t
HIPAA. see Health Insurance Portability and
Accountability Act
Histamine, cardiac effects of, 21t
Histamine-2 receptor antagonists, 458t
Histone deacetylase inhibitor, in
chemotherapy, 455t
Histoplasmosis, 337–338
as HIV and AIDS complication, 343t
HIV. see Human immunodeficiency virus
infection
530 INDEX
HIV-associated dementia complex, as HIV
and AIDS complication, 343t
HLT. see Heart-lung transplantation
HMG-CoA reductase inhibitors (statins), as
lipid-lowering agents, 440t
Hodgkin’s lymphoma, 287, 287t
Holter monitoring, 26–27
Hoover’s sign, description and conditions
associated with, 63t
Hormones
cardiac effects of, 21, 21t
in chemotherapy, 455t
pituitary, 256–259, 256t–257t
thyroid, 254–256
Hospice care, 8
HRV. see Heart rate variability
Huffing, 492
Human immunodeficiency virus infection
(HIV), 341–342, 342b, 343t
Humeral fractures, 104–105, 104b
Humeral hemiarthroplasty, proximal, 113
Huntington’s chorea, 143
Huntington’s disease, 143
Hydralazine (Apresoline), as antihypertensive
agents, 435t
Hydrocephalus, 148–149, 149b
Hydrochlorothiazide (Esidrix,
HydroDIURIL), as antihypertensive
agents, 435t
Hydrocolloid dressings, 323t
Hydrocortisone (Cortef, Solu-Cortef), for
respiratory system, 441t
Hydrogel dressings, 323t
Hydromorphone (Dilaudid, Hydrostat), in
pain management, 487t
Hydroxychloroquine (Plaquenil), for
rheumatoid arthritis, 443t
5-Hydroxyindoleacetic acid (5-HIAA), in
gastrointestinal evaluation, 213t
Hyoscyamine (Hyosin, Levsin, Levbid), for
irritable bowel syndrome, 458t
Hyperacute graft rejection, 356
Hyperbaric oxygen therapy, in wound care,
324t
Hypercalcemia, 380t
Hyperextension orthosis, 122t
Hyperinflation
dynamic, 411–413
in respiratory dysfunction, 76
Hyperkalemia, 380t
Hypermagnesemia, 380t
Hypernatremia, 380t
Hyperosmolar hyperglycemic nonketotic
syndrome/coma, 265
Hyperparathyroidism, 267
treatment of, 471t
Hyperphosphatemia, 380t
Hyperplasia, definition of, 276t
Hyperpnea, description and conditions
associated with, 63t
Hypersensitivity, latex, 3
Hypertension, 34, 185–187
by age group, 186t
aortic dissection and, 184
essential (idiopathic), 185
management of, 186
physical therapy considerations for,
186–187
portal, in cirrhosis, 224, 224f
Hypertension (Continued)
secondary, causes of, 185, 187t
target organ effects of, 186t
Hypertensive crisis, 186
Hyperthyroidism, 255, 255t
Hyperventilation, description and conditions
associated with, 63t
Hypocalcemia, 380t
Hypodermis, composition and function of,
297t
Hypoglossal nerve (CN XII), 132t
Hypoglycemia, complicating diabetes,
266–267
Hypoglycemic agents, 469t
Hypokalemia, 380t
Hypomagnesemia, 380t
Hyponatremia, 380t
Hypoparathyroidism, 267–268
Hypophosphatemia, 380t
Hypopituitarism, 258–259
Hypothyroidism, 255–256, 256b
Hypoventilation, description and conditions
associated with, 63t
Hypovolemia, 380t
Hypoxemia
oxygen therapy for, 395
in respiratory dysfunction, 76
signs and symptoms of, 68t
Hypoxia, in respiratory dysfunction, 76
I body fluid examination of, 332
Ia and II sensory axons, 140t
IABP. see Intraaortic balloon pump
Iatrogenic pneumothorax, 81
Ib sensory axons, 140t
Ibandronate (Boniva), for osteoporosis, 472t
Ibritumomab (Zevalin), in chemotherapy, 455t
IBS. see Irritable bowel syndrome
Ibuprofen (Motrin, Advil), in pain
management, 487t
Ibutilide (Corvert), for arrhythmias, 433t
ICA. see Internal carotid artery
ICP. see Intracranial pressure
ICU. see Intensive care unit
ICU-AW. see Intensive care unit-acquired
weakness
Idarubicin (Idamycin), in chemotherapy, 455t
Idiopathic thrombocytopenic purpura,
197–198
Idiopathic tremor, 143
Idioventricular rhythm, ECG characteristics
and causes of, 52t
Ifosfamide (Ifex), in chemotherapy, 455t
Ileostomy, 226t
Ileus, paralytic, 220
Iliac crest bone graft, 119b
Iloperidone (Fanapt), as antipsychotics, 449t
Imatinib (Gleevec), in chemotherapy, 455t
Imipenem-cilastatin (Primaxin), 461t
for infectious diseases, 461t
Immobilization, fracture, 95, 96f–98f
Immune system
components of, 330t
factors affecting, 330b
infections of, 341–344
prolonged bed rest and, 5t
terminology associated with infectious
diseases and, 330t
Immunocompromised, definition of, 330t
Immunodeficiency, definition of, 330t
Immunogen, definition of, 330t
Immunosuppressants, 473t
in graft rejection prevention, 356
in organ transplantation, 473t
Immunosuppression, definition of, 330t
Impella® Recover System, 419, 419f, 419b
IMS. see Intensive Care Unit Mobility Scale
Incontinence, urinary, 242, 242t, 242b
Indacaterol (Arcapta Neohaler), as
bronchodilators, 442t
Indapamide (Lozol), as antihypertensive
agents, 435t
Indinavir (Crixivan, IDV), for HIV/AIDS, 465t
Indomethacin (Indocin, Indocin SF,
Novomethacin, Nu-Indo), in pain
management, 487t
Induction immunosuppression, 356
Infection(s)
complicating diabetes, 266, 266b
complicating joint arthroplasty, resection
for, 114–115
complicating organ transplantation,
357–358, 357f, 358b
control of, in burn care, 305, 305b
Infectious diseases, 329–352
antibiotic-resistant, 334–335
antibiotics for, 461t
antifungal agents for, 463t
antitubercular agents for, 464t
body structure and function of, 329–332
cardiac, 338
evaluation of, 329
history in, 330
laboratory studies in, 331–332
hematology, 331
physical examination in, 330–331
gastrointestinal, 340–341, 341b
health care-associated, 329
health conditions of, 332–344
immune system and, 330t, 330b, 341–344
lifestyle management in, 344–345
management of, 344–346
medical intervention for, 344
methicillin-resistant Staphylococcus aureus
as, 334
multidrug-resistant Acinetobacter baumannii
as, 335, 335b
musculoskeletal, 340, 340b
neurologic, 338–340
nosocomial, 332–335, 334b
pharmacologic agents for, 461–469
physical therapy intervention for,
345–346, 346b
considerations for, 345–346
goals, 345
prevention of, 344
respiratory tract, 335–338, 335b
sepsis as, 344
skin, 340
summary of precautions to prevent
infection, 333t
terminology associated with, 329, 330t
vancomycin-resistant Enterococcus as, 334
Inferior vena cava (IVC)
description and function of, 19t
filter, in DVT management, 191
Infiltration anesthesia, 487t

Infliximab (Remicade), for rheumatoid
arthritis, 443t
Influenza, 336, 336b
Infuse-A-Port, in medical-surgical
management, 405t–407t
Inhalation, in ventilation, 58
Inhalation injury, 303–304
Injury/illness, severity of, 7–8, 9t
INR. see International normalized ratio
Inspiration, accessory muscles of, 58
Inspiratory capacity (IC), description and
clinical significance of, 74t–75t
Inspiratory muscles, innervation of, 59t
Inspiratory reserve volume (IRV), description
and clinical significance of, 74t–75t
Insulin
for hyperglycemia, 469t
routes of administration of, 264–265, 264b
Insulin aspart (Novolin), for hyperglycemia,
469t
Insulin glargine (Lantus), for hyperglycemia,
469t
Insulin glulisine (Apidra), for hyperglycemia,
469t
Insulin human inhalation powder (Afrezza),
for hyperglycemia, 469t
Insulin inhalation (Exubera), for
hyperglycemia, 469t
Insulin pen, 265
Insulin pump
implanted, 264
therapy, for type 1 diabetes, 263t
Insulin resistance, 261
Integra, in burn and wound treatment, 308t
Integrase inhibitor, for HIV/ AIDS, 465t
Integumentary system, 295–328
cancer of, 289, 289b
function of, 296, 297t
hematologic disorders and, 178t
in musculoskeletal evaluation, 92
prolonged bed rest and, 5t
structure of, 295–296, 296f, 297t
Intensive care unit (ICU), 4–7
Confusion Assessment Method for, 508
Functional Status Score for, 509
Mobility Scale, 508–509, 509t
patient and family responses to, 4–6
Perme Intensive Care Unit Mobility Score,
510
Physical Function in Intensive Care Test-
Scored, 510–511
specific outcome measures, 508
Intensive Care Unit Mobility Scale (IMS),
508–509, 509t
Intensive care unit-acquired weakness
(ICU-AW), 159, 159t
Interdependence, airway clearance
techniques, 491
Interferon (INF), for multiple sclerosis, 451t
Interleukin-6 (IL-6) inhibitor, for rheumatoid
arthritis, 443t
Intermittent claudication, pseudoclaudication
differentiated from, 183t
Internal carotid artery (ICA), 151t
International normalized ratio (INR),
360–361
in hematologic evaluation, 180, 181t
physical therapy and, 29
therapeutic values for, 198, 199t
Interstitial lung disease, 80
Interstitial nephritis, acute, 240
Intertrochanteric fractures, 99, 100f
Intestinal disorders, 219–222
appendicitis as, 219
Crohn’s disease as, 222
diverticular disease as, 219
hernia as, 220
intestinal ischemia as, 220–221
intestinal obstructions as, 220
irritable bowel syndrome as, 221
malabsorption syndromes as, 221
paralytic ileus as, 220
peritonitis as, 221–222
polyps as, 222
tumors as, 222
ulcerative colitis as, 222
Intestinal obstructions, 220
Intraaortic balloon pump (IABP), 417–418,
417f
Intracapsular fractures, 99, 100f
Intracranial pressure (ICP), 148
monitoring of, equipment for, 399–402,
403t
Intranasal analgesia, patient-controlled,
488t
Intraoperative radiation therapy
(IORT), 280
Intravenous patient-controlled analgesia,
488t
Intravenous regional anesthesia, 487t
Intraventricular catheter, in ICP monitoring,
403t
Intubation, for mechanical ventilation,
410–411, 410f
Invasive vascular studies, in vascular
evaluation, 175–177
Ionizing radiation, burns from, 301
IORT. see Intraoperative radiation therapy
Ipratropium bromide (Atrovent), as
bronchodilators, 442t
Irbesartan (Avapro), as antihypertensive
agents, 435t
Irinotecan (Camtosar), in chemotherapy,
455t
Iron-deficiency anemia, 192–193, 192b
Irritable bowel syndrome (IBS), 221
IRV. see Inspiratory reserve volume
Ischemia
intestinal, 220–221
myocardial, electrocardiographic changes
in, 392f
Isometric exercises, for quadriceps and
gluteal muscles, after total hip
arthroplasty, 107–108
Isoniazid (Nydrazid), as antitubercular agent,
464t
Isoproterenol (Isuprel), as bronchodilators,
442t
Isosorbide dinitrate (Isordil, Sorbitrate), as
antihypertensive agents, 435t
Isosorbide mononitrate (ISMO), as
antihypertensive agents, 435t
Isradipine (DynaCirc), as antihypertensive
agents, 435t
Itraconazole (Sporanox), as antifungal agents,
463t
Ivabradine (Corlanor), as antihypertensive
agents, 435t
INDEX 531
J
Jackknife position, 478f
Janus kinase (JAK) inhibitor, for rheumatoid
arthritis, 443t
Joint arthroplasty, 92b, 105–115, 105b
hip, 105–108, 105f, 106t, 106b
infected, resection for, 114–115
knee, 109–112, 110f–111f
shoulder, 112–114, 113f, 113b
Jugular venous distention (JVD),
measurement of, 23, 23f
Junctional escape rhythm, ECG
characteristics and causes of, 52t
Junctional tachycardia, ECG characteristics
and causes of, 52t
JVD. see Jugular venous distention
K
Kaposi’s sarcoma, as HIV and AIDS
complication, 343t
Keloid scar, from burn wound, 307
Ketoacidosis, diabetic, 265
Ketoconazole (Nizoral), as antifungal agents,
463t
Ketolides
as antibiotics, 461t
for infectious diseases, 461t
Ketonuria, etiology of, 236t
Ketoprofen (Orudis), in pain management,
487t
Ketorolac (Toradol), in pain management,
487t
Kidney(s)
biopsy of, in genitourinary
evaluation, 237
chronic disease of, 238–239, 239b
complications of burns affecting, 300t
dysfunction of, 237–241
hypertensive effects on, 186t
injury to, acute, 237–238, 238t, 238b
posttransplant function of, indication of,
358–359
scanning of, in genitourinary evaluation,
237
transplantation of, 358
liver transplantation combined with,
362
pancreas transplantation combined with,
363–364
X-ray of, with ureters and bladder, in
genitourinary evaluation, 236
Kidney Paired Donation (KPD), 358
Kinase inhibitors, in chemotherapy, 455t
Knee arthroplasty, 109–112
minimally invasive, 112, 112f
physical therapy after, 110–112
resection, physical therapy after, 115
surgical approaches to, 112f
tricompartmental, 110, 110f
unicompartmental, 109–110
Knee immobilizer, 122t
Korotkoff sounds, 25, 26t
KPD. see Kidney Paired Donation
KUB X-ray, in genitourinary
evaluation, 236
Kussmaul respirations, description and
conditions associated with, 63t
Kyphoplasty, 119–120, 119f
Kyphoscoliosis, chest wall restriction in, 82
532 INDEX
L Levomilnacipran (Fetzima), as
Labetalol (Normodyne), as antihypertensive
agents, 435t
LAC. see Long arm cast
Lacosamide (Vimpat), as anticonvulsants,
446t
Lactose tolerance test, in gastrointestinal
evaluation, 213t
Lactulose (Enulose, Generlac), as laxative,
459t
Lacunar strokes, 149
Laminectomy, 117–118, 118t
Lamivudine (Epivir, 3TC), for HIV/AIDS,
465t
Lamotrigine (Lamictal), as anticonvulsants,
446t
Lansoprazole (Prevacid SoluTab), as proton
pump inhibitors, 459t
Laparoscopy, in gastrointestinal evaluation,
212–213
Large intestine, function of, 211t
Laryngectomy, 83
Laryngoscopy, 83
Larynx, description and function of, 58t
Laser angioplasty, coronary, 39
Laser therapy, low-level, in wound care, 324t
Lateral corticospinal tract, function of, 139t
Lateral medullary syndrome, 132
Lateral retinacular release, 120t
Lateral spinothalamic tract, function of, 139t
Latex allergy, 3
Latex-food syndrome, 3
Latex-fruit allergy, 3
Laxatives, 459t
LDLs. see Low-density lipoproteins
Ledipasvir, as antiviral medications, 467t
Leflunomide (Arava), for rheumatoid
arthritis, 443t
Left atrial appendage closure, 42, 42b
Left atrium, description and function of, 19t
Left coronary artery, anatomy of, 18f
Left-sided heart failure, 36
Left ventricle, description and function of,
19t
Leg length discrepancy, 108b
Legionellosis, 338
Leukemia, 286–287, 287t, 287b
Leukocyte count, in infectious disease
evaluation, 331
Leukocytes, description of, 173t
Leukocytic disorders, 195
Leukotriene modifiers, 443t
for respiratory system, 443t
Leuprolide (Lupron, Eligard), in
chemotherapy, 455t
Levalbuterol (Xopenex), as bronchodilators,
442t
Levamisole (Ergamisol), in chemotherapy,
455t
Levetiracetam (Keppra), as anticonvulsants,
446t
Levobupivacaine (Chirocaine), for local
anesthesia, 488t
Levodopa (Dopar, Larodopa), for Parkinson’s
disease, 453t
Levodopa/carbidopa (Sinemet, Sinemet CR),
for Parkinson’s disease, 453t
Levofloxacin (Levaquin), for infectious
diseases, 461t
antidepressants, 448t
Levonorgestrel, as oral contraceptive, 460t
Levorphanol (Levo-Dromoran), in pain
management, 487t
Levothyroxine (Levothroid, Levoxyl,
Synthroid, Thyro-Tabs), for
hypothyroidism, 473t
Lewy body dementia, 137t
LHRH agonists, in chemotherapy, 455t
Lidocaine (Xylocaine)
for arrhythmias, 433t
for local anesthesia, 488t
Life vest, 42
Lifestyle, wound healing and, 314
Lightheadedness, in vestibular dysfunction,
154
Lightning, injury from, 301
Limb salvage surgery, 115
Linagliptin (Tradjenta), for hyperglycemia,
469t
Linezolid (Zyvox), for infectious diseases,
461t
Liothyronine (Cytomel, Triostar), for
hypothyroidism, 473t
Liotrix (Thyrolar), for hypothyroidism, 473t
Lipase, in pancreatic testing, 215t–216t
Lipid-lowering agents, 440t
Lipoproteins, 29
Liraglutide (Victoza), for hyperglycemia,
469t
Lisinopril (Prinivil, Zestril), as
antihypertensive agents, 435t
Lispro (Humalog), for hyperglycemia, 469t
Lithium (Lithobid, Eskalith CR, Cibalith-S),
as mood stabilizer, 450t
Lithotomy position, 478f
Liver
diagnostic procedures for, 216t
disorders of, 223–225
cancer as, 286, 286b
cirrhosis as, 224, 224f
hepatic encephalopathy and coma as,
224–225
hepatitis as, 223–224
failure of, medical characteristics of, 360t
function of, 211t
laboratory tests for, 215t–216t
Liver biliary biopsy, 216t
Liver-spleen scan, 216t
Liver transplantation, 359–362
kidney transplantation combined with,
362
physical therapy for recipients of, 362
postoperative care and complications of,
361–363, 361b, 363b
posttransplant function of, indication of,
361, 361b–362b
pretransplantation care of, 360
procedure, 361
types of, 360–361
Living organ donors, 354–355
liver, adult, 360–361
lung, lobar, 367
postoperative care for, 355
renal, versus cadaveric donors, 358
LLC. see Long leg cast
LMN. see Lower motor neuron
LMWH. see Low-molecular-weight heparin
Lobectomy, 83, 83f
Local anesthesia, 475
Local anesthetics
indication of, 488t
mechanism of action of, 488t
Local input, 21
Lomefloxacin (Maxaquin), for infectious
diseases, 461t
Long arm cast (LAC), 121t
Long leg cast (LLC), 121t
Long-term depression (LTD), 144
Long-term devices, circulatory for assist,
422–426
total artificial heart, 426–428, 427f
ventricular assist device, 422–425, 423f,
424t, 424b
Loop colostomy, 226t
Loop diuretics, as antihypertensive agents,
435t
Loperamide (Imodium), for diarrhea, 458t
Lopinavir/ritonavir (Kaletra, KAL, LPV/r),
for HIV/AIDS, 465t
Loracarbef (Lorabid), for infectious diseases,
461t
Loratadine (Alavert, Claritin), as
antihistamines, 442t
Lorazepam (Ativan)
as antianxiety medication, 446t
as muscle relaxants, 445t
Losartan (Cozaar), as antihypertensive agents,
435t
Lovastatin (Mevacor), as lipid-lowering
agent, 440t
Low-density lipoproteins (LDLs), 29
Low-level laser therapy, in wound care, 324t
Low-molecular-weight heparin (LMWH), 91b
as anticoagulant, 434t
Low-output failure, 36
Lower extremity amputation, 383
levels of, 384f
types of, 385t
Lower-extremity noninvasive studies, 175
Lower motor neuron (LMN), 131
Lower respiratory tract infections, 336–338
Lower urinary tract dysfunction, 241–242
LTD. see Long-term depression
Lubiprostone (Amitiza), as laxative, 459t
Lumbar drain, in medical-surgical
management, 405t–407t
Lumbar puncture (LP), in neurologic
examination, 161t–163t
Lund and Browder formula, in burn
assessment, 301, 303t
Lung(s)
cancer of, 281–283, 282t, 283b
contusion of, 79t, 80
description and function of, 58t
position of, in thorax, 60f
posttransplant function of, indication of,
368
transplantation of, 366–369
heart transplantation combined with,
369–370
physical therapy for recipients, 368–369,
369b
postoperative care and complications,
368
preoperative care, 367–368
types of, 367

Lung volume, 72f
alterations in, 72, 73f
reduction, 83
tests for, 74t–75t
Lurasidone (Latuda), as antipsychotics, 449t
Lymphatic system, 171–172
disorders of, 198, 198t
evaluation of, 181
history in, 181
observation in, 181
palpation in, 181
Lymphedema, 198, 198t, 198b
diagnostics of, 181
Lymphoid tissue, tumors originating from,
277t
Lymphomas, 287, 287t, 287b
as HIV and AIDS complication, 343t
M conventional, 412t
Macitentan (Opsumit), for pulmonary
hypertension, 439t
Macrolides, for infectious diseases, 461t
Magnesium citrate (Citroma), as laxative,
459t
Magnesium hydroxide, as antacid, 457t
Magnesium sulfate, as laxative, 459t
Magnetic resonance angiography (MRA)
in genitourinary evaluation, 237
in neurologic examination, 161t–163t
in vascular evaluation, 176t, 177f
Magnetic resonance
cholangiopancreatography (MRCP),
216t
Magnetic resonance imaging (MRI)
in gastrointestinal evaluation, 213
in genitourinary evaluation, 237
in musculoskeletal evaluation, 90
in neurologic examination, 161t–163t
in vascular evaluation, 176t
Maintenance immunosuppression, 356
Malabsorption syndromes, 221
Malignant melanoma, 289
Malignant tumor(s)
classification of, 277t
definition of, 275
MAP. see Mean arterial pressure
Maraviroc (Selzentry, MVC), for HIV/AIDS,
465t
Marfan’s syndrome, aortic dissection and, 184
Mask
air entrainment/Venturi, in oxygen
delivery, 399f, 399t
face, in oxygen delivery, 397t, 398f
non-rebreather, in oxygen delivery, 397t,
398f
Mast cell stabilizers, 443t
for respiratory system, 443t
Maximum voluntary ventilation (MVV),
description and clinical significance of,
74t–75t
MCA. see Middle cerebral artery
MCH. see Mean corpuscular hemoglobin
MCHC. see Mean corpuscular hemoglobin
concentration
MCS. see Minimally conscious state
MCV. see Mean corpuscular volume
MDS. see Myelodysplastic syndrome
Mean arterial pressure (MAP), 148
Mean corpuscular hemoglobin (MCH), 180t
INDEX 533
Mean corpuscular hemoglobin concentration MediPort, in medical-surgical management,
(MCHC), 180t 405t–407t
Mean corpuscular volume (MCV), 180t Medroxyprogesterone (Provera), in
Mechanical circulatory assist devices, 417– chemotherapy, 455t
430. see also Circulatory assist devices Medullary respiratory center, of pulmonary
Mechanical debridement of wound, system, 57
321–322 Megestrol (Megace), in chemotherapy, 455t
Mechanical obstruction, 220 Meglitinides, for hyperglycemia, 469t
Mechanical ventilation, 409–416 Melanoma, 289
complications of, 411–414 malignant, 289
invasive Melphalan (Alkeran), in chemotherapy, 455t
cuff in, 411, 411b Meniere’s disease, 154
intubation in, 410–411, 410f Meningitis, 156, 339
positive pressure ventilators in, 411, Meningococcal meningitis, 339
411b Meningoencephalitis, 156
process of, 410–411 Meniscal repair, 120t
modes of, 411 Meniscectomy, 120t
additional modes, 412t Mental status, evaluation of, 91
Meperidine (Demerol, Pethidine), in pain
noninvasive, 410 management, 487t
objectives of, 409–415 Mepivacaine (Carbocaine), for local
physical therapy considerations for, 415 anesthesia, 488t
types of, 410–411 6-Mercaptopurine (6-MP, Purinethol), as
ventilatory settings for, 411, 413t immunosuppressants, 473t
weaning from, 414–415 Mercaptopurine (Purinethol), in
Mechanoreceptors, 22 chemotherapy, 455t
Median sternotomy, sternal precautions after, Meropenem (Merrem), for infectious diseases,
40, 40b 461t
Mediastinoscopy, 83 Mesh graft, for burns, 307t
Mediastinum, 18 Mestranol, as oral contraceptive, 460t
displacement of, 18 Metabolic acidosis, causes of, 68t
Mediate percussion, 66–67, 67f Metabolic alkalosis, causes of, 68t
Medical record(s), 13–16 Metabolic bone disorders, 268–269
admission note format for, 15 Metabolic syndrome, 261, 261t, 261b
components of, 15–16 Metacarpal fractures, 105, 105b
confidentiality and, 13–14, 14b Metaplasia, definition of, 276t
documentation in, 14–15 Metaproterenol (Alupent), as bronchodilators,
orders in, 15 442t
progress notes in, 16 Metaxalone (Skelaxin), as muscle relaxant,
reports in, 16 445t
review of, in musculoskeletal evaluation, Metformin (Glucophage), for hyperglycemia,
90–91 469t
Medical Research Council (MRC) scale, 62, Methadone (Dolophine, Methadose)
62t in pain management, 487t
Medical status, wound healing for substance use-related disorders, 451t
and, 315 Methazolamide (Neptazane), as
Medical-surgical equipment, in acute care antihypertensive agents, 435t
setting, 395–430 Methicillin-resistant Staphylococcus aureus
for hemodynamic monitoring, 396–399, (MRSA), 334
400t–401t, 402f Methimazole (Tapazole), for hyperthyroidism,
for intracranial pressure monitoring, 473t
399–403, 403t Methocarbamol (Robaxin), as muscle
management devices as, 403–404, relaxant, 445t
405t–407t, 408f Methotrexate (Rheumatrex)
for mechanical ventilation, 409–416. see in chemotherapy, 455t
also Mechanical ventilation for rheumatoid arthritis, 443t
for multimodal neuromonitoring, 403, Methyclothiazide (Aquatensen), as
404t antihypertensive agents, 435t
for oxygen therapy, 395–396, 397t, Methylcellulose (Citrucel), as laxative, 459t
398f–399f, 399t Methylphenidate (Concerta, Metadate,
Medical therapies, withholding and Methylin, Ritalin), as stimulants, 450t
withdrawing, 8 Methylprednisolone (Depo-Medrol, Medrol),
Medication(s) for respiratory system, 441t
cardiac, 43 Metoclopramide (Reglan), as antiemetic,
review of, in musculoskeletal evaluation, 454t
91 Metolazone (Zaroxolyn), as antihypertensive
wound healing and, 315 agents, 435t
Medication reconciliation, in acute care Metoprolol (Lopressor, Toprol XL), as
setting, 3 antihypertensive agents, 435t
534 INDEX
Metronidazole (Flagyl), for infectious
diseases, 461t
Mexiletine (Mexitil), for arrhythmias, 433t
Mezlocillin (Mezlin), for infectious diseases,
461t
MG. see Myasthenia gravis
MI. see Myocardial infarction
Microbiology, in infectious disease
evaluation, 331–332
Microdiscectomy, 117–118
Microglia, 140t
Microtubule inhibitors, in chemotherapy,
455t
Middle cerebral artery (MCA), 147, 147f,
151t
Miglitol (Glyset), for hyperglycemia, 469t
Milnacipran (Savella), as antidepressants,
448t
Mineral oil (Fleet miner oil enema), as
laxative, 459t
Mineralocorticoids, target sites and actions
of, 259t
Minimally conscious state (MCS), 137–138,
138t
Minimally invasive surgery (MIS)
coronary artery bypass graft, 39
hip and knee arthroplasty, 112, 112f
spine, 117–119
Minocycline (Minocin), for infectious
diseases, 461t
Minoxidil (Loniten), as antihypertensive
agents, 435t
Minute ventilation, 74t–75t
Minute volume (VE), description and clinical
significance of, 74t–75t
Mirtazapine (Remeron), as antidepressants,
448t
MIS. see Minimally invasive surgery
Misoprostol (Cytotec), 458t
Mitomycin (Mutamycin), in chemotherapy,
455t
Mitoxantrone (Novantrone)
in chemotherapy, 455t
for multiple sclerosis, 451t
Mitral regurgitation, signs and symptoms
of, 36t
Mitral valve
description and function of, 19t
prolapse of, signs and symptoms of, 36t
stenosis of, signs and symptoms of, 36t
Mixed incontinence, 242t
Mobility, functional
in burn patient evaluation, 309, 309b
in musculoskeletal evaluation, 94
postamputation, 386, 386b
in wound assessment, 317
in wound care, PT considerations for, 325t
Mobitz I blocks, ECG characteristics and
causes of, 53t
Mobitz II blocks, ECG characteristics and
causes of, 53t
Modified Ashworth Scale, 141, 141t
Modified Borg Scale, 62
Moexipril (Univasc), as antihypertensive
agents, 435t
Mometasone furoate monohydrate (Nasonex),
for respiratory system, 441t
Monoamine oxidase (MAO) inhibitors, as
antidepressants, 448t
Mononucleosis, 342–343
Montelukast (Singulair), for respiratory
system, 443t
Mood stabilizers, 450t
Morbid obesity, 223
Morphine (MS Contin, Kadian, Morphine
sulfate), in pain management, 487t
Moxifloxacin (Avelox), for infectious diseases,
461t
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
Mucolytic, 497
Mucus secretion, 491
Multidrug-resistant Acinetobacter baumannii,
335, 335b
Multifocal ventricular tachycardia, ECG
characteristics and causes of, 52t
Multimodal neuromonitoring, equipment
for, 403, 404t
Multinodular goiter, hyperthyroidism from,
255t
Multiple myeloma, 287–288, 287b–288b,
288t
Multiple sclerosis (MS), 158
medications for, 451t
Muromonab-CD3 (Orthoclone OKT3), as
immunosuppressants, 473t
Muscle, tumors originating from, 277t
Muscle guarding, physical therapy
interventions to decrease, 94
Muscle relaxants, for musculoskeletal system,
445t
Musculoskeletal evaluation, 94, 94b
balance in, 93–94
cardiovascular system in, 92
diagnostic tests review in, 90
functional mobility in, 93
integumentary system in, 92
medical record review in, 90–91
mental status in, 91
observation in, 91–94
pain in, 92
patient history, 90
patient interview in, 91
posture in, 93
prognosis and, 94
pulmonary system in, 92
range of motion in, 92–93, 93t
sensation in, 92
strength in, 92–93
tests and measures in, 91–94
Musculoskeletal system, 89–126, 443–446
antispasmodic agents for, 445t
disease-modifying antirheumatic drugs
for, 443t
examination of, 89–94
fractures and, 94–105
hematologic disorders and, 178t
infections of, 340, 340b
interventions for, 94
joint arthroplasty and, 105–115
muscle relaxants for, 445t
pathologies of, equipment in management
of, 120–123
Musculoskeletal system (Continued)
braces and splints as, 121–122, 122t
casts as, 120–121, 121t
external fixators as, 121
traction as, 122–123
prolonged bed rest and, 4, 5t
soft-tissue surgeries and, 120t
spinal pathology and, 116–120, 117f, 118t
structure and function of, 89
tumor resection in, 115
MVV. see Maximum voluntary ventilation
Myasthenia gravis (MG), 157–159,
158b–159b
Myasthenic crisis, 158
Mycobacterium avium complex infection, as
HIV and AIDS complication, 343t
Mycophenolate mofetil (CellCept), as
immunosuppressants, 473t
Mycophenolic acid (Myfortic), as
immunosuppressants, 473t
Myelodysplastic syndrome (MDS), 287
Myelography
in musculoskeletal evaluation, 90
in neurologic examination, 161t–163t
Myocardial heart disease, 36
Myocardial infarction (MI), 34, 35f
coronary artery involvement and
complications of, 35t
evolution of, 34
Myocardial ischemia, electrocardiographic
changes in, 392f
Myocardium
description and function of, 19t
percutaneous, 38–39
revascularization and reperfusion of, 38–40
coronary artery bypass graft in, 39–40
secondary prevention after, 40
transmyocardial, 39
thrombolytic therapy in, 38
Myopathy, critical illness, 6
N
Nadolol (Corgard), as antihypertensive
agents, 435t
Nalbuphine (Nubain), in pain management,
487t
Naloxone (Narcan), in pain management,
487t
Naproxen (Anaprox, Naprosyn, Aleve), in
pain management, 487t
Narcosis, clinical presentation of, 69b
Nasal cannula, in oxygen delivery,
397t, 398f
Nasoenteric feeding tube, in medical-surgical
management, 405t–407t
Nasogastric tube (NGT), in medical-surgical
management, 405t–407t
Natalizumab (Tysabri), for multiple sclerosis,
451t
Nateglinide (Starlix), for hyperglycemia,
469t
National Institutes of Health Stroke Scale
(NIHSS), 150
Natriuretic peptides, in cardiac evaluation,
30
NAVA. see Neurally adjusted ventilatory
assist
NDRI. see Norepinephrine-dopamine
reuptake inhibitor

Nebulizer, in medical-surgical management,
405t–407t
Neck cancers, 288–289, 288b
Nedocromil (Tilade), for respiratory system,
443t
Needle biopsy, in thyroid function testing,
255t
Nefazodone (Serzone), as antidepressants,
448t
Negative-pressure wound
therapy, 324t
Neomycin (Kantrex), for infectious diseases,
461t
Neoplasms, 159–160, 160t, 160b
definition of, 275, 276t
Nephrectomy, for kidney disorders, 245
Nephritis, interstitial, acute, 240
Nephrolithiasis, 240
Nephron, 233
Nephron-sparing surgery, 245
Nephropathy, 266
diabetic, 240
Nerve conduction velocity studies, in
neurologic examination, 161t–163t
Nerve tissue, tumors originating
from, 277t
Nerves, cranial, 128–134, 130b, 132t
Nervous system, 127–170, 128f
additional prevalent health conditions,
155–160
aging and, 164
cells of, 127–128, 130f
central, 128–152, 131t
chart review, 160–164, 160t–163t
diagnosis and prognosis, 164, 164b
divisions of, 127, 129f–130f
hematologic disorders and, 178t
peripheral, 153t, 154f
plan of care, 164
structure and function of, 127–128
vestibular system, 152–155
Netupitant/palonosetron (Akynzeo), as
antiemetic, 454t
Neural input, to cardiac conduction system,
21
Neurally adjusted ventilatory assist (NAVA),
412t
Neurogenic bladder, 241
Neuroinfectious diseases, 155–157
Neurologic diagnoses, chest wall restriction
in, 82
Neurologic dysfunction, cancer causing, 289,
289b
Neurologic system, prolonged bed rest and,
5t
Neuromonitoring, multimodal, equipment
for, 403, 404t
Neuromuscular junction, 157–158
Neuromyelitis optica (NMO), 158
Neuropathic ulcers, 311t, 312
Neuropathy
diabetic, 266
ICU, 6
Neutropenia, 195
Nevirapine (Viramune, Viramune XR, NVP),
for HIV/AIDS, 465t
NGT. see Nasogastric tube
Niacin (Niacor, Niaspan, Slo-Niacin), as
lipid-lowering agent, 440t
Nicardipine (Cardene), as antihypertensive
agents, 435t
Nicotinic acid, as lipid-lowering agent, 440t
Nifedipine (Procardia XL, Adalat CC), as
antihypertensive agents, 435t
NIHSS. see National Institutes of Health
Stroke Scale
Nilutamide (Nilandron), in chemotherapy,
455t
Nimodipine (Nymalize), as antihypertensive
agents, 435t
Nitrates, as antihypertensive
agents, 435t
Nitroglycerin (NTG, Nitro-Bid, Nitrostat,
NitroDur, Transderm-Nitro, Nitrodisc),
as antihypertensive agents, 435t
Nizatidine (Axid), in gastric acid
suppression, 458t
NMO. see Neuromyelitis optica
Nocebo effects, 139–141
Nociception, 139–141
Noncardiogenic chest pain, 393t
Noncardiogenic pulmonary edema, 80
Non-Hodgkin’s lymphoma, 287, 287t
Noninvasive laboratory studies,, in vascular
evaluation, 175
Noninvasive mechanical ventilation, 415
Non-rebreather masks, in oxygen delivery,
397t, 398f
Non-small-cell lung cancer (NSCLC), 281,
282t
Nonsteroidal antiinflammatory drugs
(NSAIDs), 443t
in pain management, 484, 486t
for respiratory system, 443t
Nonverbal pain scale, adult, 482t, 485t
Norepinephrine (Levophed)
cardiac effects of, 21t
as positive inotropes, 441t
target sites and actions of, 259t
Norepinephrine-dopamine reuptake
inhibitor (NDRI), as antidepressants,
448t
Norethindrone, as oral contraceptive, 460t
Norethindrone acetate, as oral contraceptive,
460t
Norethynodrel, as oral contraceptive, 460t
Norgestrel, as oral contraceptive, 460t
Normal breath sounds, 64
Normal-pressure hydrocephalus (NPH),
148–149
Norovirus infections, 341, 341b
Nortriptyline (Pamelor), as antidepressants,
448t
Nose, description and function of, 58t
Nosocomial infection(s), definition of, 330t,
332–335, 334b
NPH. see Normal-pressure hydrocephalus
NSAIDs. see Nonsteroidal antiinflammatory
drugs
NSCLC. see Non-small-cell lung cancer
Nuclear scanning, gallbladder, 216t
5-Nucleotidase, in hepatic testing,
215t–216t
Numeric rating pain scale, 485t
Nutrition, wound healing and, 314–315,
315b
Nystagmus, head-shaking-induced, in testing
for vestibular dysfunction, 156t
INDEX 535
O
OASIS Wound Matrix, in burn and wound
treatment, 308t
Obesity, chest wall restriction in, 82
Observation
in cardiac evaluation, 23, 23f
in hematologic evaluation, 177–178
in musculoskeletal evaluation, 91–94
in vascular evaluation, 173–174
Obstructive pulmonary conditions, 76–78,
77t
asthma as, 76, 77t
bronchiectasis as, 77t, 78
chronic bronchitis as, 76, 77t
cystic fibrosis as, 77t, 78
emphysema as, 76, 77t
Occipital lobe, structure, function, and
dysfunction of, 131t
Oculomotor nerve (CN III), 132t
Ofatumumab (Arzerra), in chemotherapy, 455t
Off-pump coronary artery bypass graft
procedure, 39–40
Ofloxacin (Floxin), for infectious diseases, 461t
Ointments, topical, in dressings, 323t
Olanzapine (Zyprexa), as antipsychotics, 449t
Olecranon fractures, 104
Olfactory nerve (CN I), 132t
Oligodendrocytes, 140t
Olmesartan (Benicar), as antihypertensive
agents, 435t
Ombitasvir, as antiviral medications, 467t
Omeprazole (Prilosec), as proton pump
inhibitors, 459t
Oncology, 275–294
medications in, 454–457
nomenclature in, 276
terminology for, 275
Ondansetron (Zofran), as antiemetic, 454t
Open face mask, in oxygen delivery, 397t,
398f
OPEP. see Oscillatory positive expiratory
pressure
Opioids, systemic, in pain management, 484,
487t
Opium tincture, for diarrhea, 458t
Opportunistic, definition of, 330t
Optic nerve (CN II), 132t
Oral cavity
cancer of, 288
function of, 211t
Oral contraceptives, 460t
Oral hairy leukoplakia, as HIV and AIDS
complication, 343t
Orders, in medical record, 15
Organ transplantation, 353–378, 473–474
activity progression of, 374
care and complications after, 355–358
criteria for, 354
donors for, 354–355
infection complicating, 357–358, 357f,
358b
patient education in, 374
recipients of
laboratory values in, importance, 373t
physical therapy guidelines for, 372–374
physical therapy management for,
372–374
postoperative care for, 356
types of, 353–354, 354b
536 INDEX
Oritavancin (Orbactiv), for infectious
diseases, 461t
Oropharyngeal dysphagia, 216, 217t
Orphenadrine (Disipal, Norflex)
as muscle relaxants, 445t
for Parkinson’s disease, 453t
Orthopnea, description and conditions
associated with, 63t
Orthosis, in acute care setting, 122t
Orthostatic blood pressure, symbols for, 26f
Orthostatic hypotension, 92b, 145
Orthotopic cadaveric liver transplantation,
360
Orthotopic heart transplantation, 364
Oscillatory positive expiratory pressure
(OPEP), 495–496, 495f
Oseltamivir (Tamiflu), as antiviral
medications, 467t
Osteoarthritis, rheumatoid arthritis
compared with, 351t
Osteomalacia, 269
Osteomyelitis, 340
Osteoporosis, 268–269, 268b–269b
treatment of, 472t
Osteotomy, trochanteric, in hip arthroplasty,
108, 109f
Overflow incontinence, 242t
Oxacillin (Prostaphilin), for infectious
diseases, 461t
Oxaliplatin (Eloxatin), in chemotherapy, 455t
Oxaprozin (Daypro), in pain management,
487t
Oxazepam (Sertax), as antianxiety
medication, 446t
Oxcarbazepine (Trileptal), as anticonvulsants,
446t
Oximetry
in cardiac evaluation, 26
in pulmonary examination, 67–68, 67b
Oxycodone (Oxycontin, Roxicodone,
Percocet, Percodan), in pain
management, 487t
Oxygen partial pressure, 68t
Oxygen therapy
equipment for, 395–396, 397t, 398f–399f,
399t
indications for, 395
oxygen delivery in, 396
cannula/masks for, 396, 397t,
398f–399f, 399t
fixed-performance, 396, 399f, 399t
variable-performance systems in, 396,
397t, 398f
Oxygen toxicity, complicating mechanical
ventilation, 414
Oxygen transport, impaired, Dean’s hierarchy
for treatment of patients with, 84t
Oxygenation, ventilator settings supporting,
413t
Oxyhemoglobin dissociative curve, 68f
Oxyhemoglobin saturation, 68, 68t
Oxymorphone (Numorphan), in pain
management, 487t
P Pancreatic disorders
Pacemaker
cardiac, 41, 41t
temporary, in hemodynamic monitoring,
401t
Paclitaxel (Taxol, Abraxane), in
chemotherapy, 455t
Paget’s disease, 269
Pain, 139–141, 139b
acute, management of, 481–490, 484b,
489b
pharmacological, 484–486
physical therapy considerations for,
486–489
in burn patient
assessment of, 309
management of, 304–305
chest
diagnostic considerations, 393
etiologies, patterns, and signs associated
with, 392t
patients with, physical therapy
considerations for, 391–394
physical therapy considerations,
393–394
physiology of, 391–392
presentation of, 392–393
evaluation of, 481–483, 482b
management of
postamputation, 384–386
in wound care, PT considerations for,
325t
in musculoskeletal evaluation, 91b, 92
physical therapy interventions to decrease,
94
referral patterns for, in gastrointestinal
system, 210t
in vascular evaluation, 173, 173b
in wound assessment, 316, 316b
Pain crisis, 194
Pain scales, comparison of, 485t
Paliperidone (Invega), as antipsychotics, 449t
Palliative care, 8
Pallor, elevation, in vascular evaluation, 175t
Palonosetron (Aloxi), as antiemetic, 454t
Palpation
in burn patient evaluation, 308–309, 309b
in cardiac evaluation, 23–24, 24t, 24b
in gastrointestinal evaluation, 212
in genitourinary evaluation, 235
in hematologic evaluation, 178, 178t
in infectious disease evaluation, 331
in pulmonary examination, 66, 66f, 66b
in vascular evaluation, 174, 174b
PAN. see Polyarteritis nodosa
Pancreas
artificial, 264–265, 265b
diagnostic procedures for, 216t
disorders of, 225, 261–267
function of, 211t
laboratory tests for, 215t–216t
posttransplant function of, indication of,
362
transplantation of, 362–363
bladder drainage, enteric drainage versus,
362–363
indication of, posttransplantation, 363
kidney transplantation combined with,
363–364
cancer as, 286
diabetes mellitus as, 261–267
insulin resistance as, 261
metabolic syndrome as, 261, 261t, 261b
Pancreatic islet cell transplantation, 363
Pancreaticoduodenectomy, 226t
Pancreatitis, 225
Panhypopituitarism, 258
Panlobular emphysema, 76
Pantoprazole (Protonix), as proton pump
inhibitors, 459t
Papillary layer of dermis, composition and
function of, 297t
Papillary muscle, description and function
of, 19t
PAPR. see Powered air-purifying respirator
Paracentesis, in gastrointestinal evaluation,
214t
Paradoxical ventilation, description and
conditions associated with, 63t
Paralytic ileus, 220
Paraneoplastic syndromes, 276
Paraseptal emphysema, 76
Parasympathetic nervous system (PNS),
132–134
Parathyroid gland, 267–268
disorders of, 267–268
tests of, 267, 267t
Paricalcitol (Zemplar), for
hyperparathyroidism, 471t
Parietal lobe, structure, function, and
dysfunction of, 131t
Parkinsonism, 142
Parkinson’s disease (PD), 142, 143t
medications for, 453t
Paroxetine (Paxil), as antidepressants, 448t
Paroxysmal supraventricular tachycardia, 53f
Partial non-rebreather mask, in oxygen
delivery, 397t, 398f
Partial thromboplastin time (PTT)
in hematologic evaluation, 180, 181t
physical therapy and, 29
Pass-port, in medical-surgical management,
405t–407t
Patch insulin pump, 265
Patella fractures, 100
Patellar tendon-bearing (PTB) cast, 121t
Pathogen, definition of, 330t
Patient-controlled analgesia (PCA), 488t
Patient environment, safe, 1–4
guidelines for, 1
Patient history
in cardiac evaluation, 22–23, 23b
in musculoskeletal evaluation, 90
in pulmonary examination, 62
in vascular evaluation, 173
Patients
instability of, indications of, 43b
response of
to activity/exercise, evaluating, 44, 45f
to ICU, 4–6
PAV. see Proportional assist ventilation
Pazopanib (Votrient), in chemotherapy, 455t
PBSCT. see Peripheral blood stem cell
transplant
PCA. see Patient-controlled analgesia
PCSK9 inhibitors, as lipid-lowering agent,
440t
PD. see Parkinson’s disease
PE. see Pulmonary embolism
Peak expiratory flow rate (PEFR), description
and clinical significance of, 74t–75t
PEFR. see Peak expiratory flow rate

Pegfilgrastim (Neulasta, G-CSF), in
hematology, 457t
Pelvic fractures, management of, 95–97, 99f
Pelvic ring fractures, 95–97, 99f
Penciclovir (Denavir), as antiviral
medications, 467t
Penicillin G (Pfizerpen), for infectious
diseases, 461t
Penicillin G benzathine (Bicillin LA), for
infectious diseases, 461t
Penicillin V (Pen-Vee K), for infectious
diseases, 461t
Penicillinase-resistance penicillins, for
infectious diseases, 461t
Pentazocine (Talwin), in pain management,
487t
PEP. see Positive expiratory pressure
Peptic ulcer disease (PUD), 218
Perampanel (Fycompa), as anticonvulsants, 446t
Percussion, 496, 498t
in gastrointestinal evaluation, 212
in genitourinary evaluation, 235
Percutaneous aortic balloon valvotomy, 42
Percutaneous endoscopically inserted
gastrostomy/jejunostomy (PEG/PEJ)
tube, in medical-surgical management,
405t–407t
Percutaneous revascularization procedures,
38–39
Perfusion
coronary, 22
ratio of ventilation to, 59
scan, for pulmonary examination, 71
Pergolide mesylate (Permax), for Parkinson’s
disease, 453t
Pericardial effusion, signs and symptoms of,
37t
Pericardial heart disease, 36, 37t
Pericardial tamponade, signs and symptoms
of, 37t
Pericardiocentesis, body fluid examination
of, 332
Pericarditis, signs and symptoms of, 37t
Pericardium, description and function of, 19t
Perindopril (Aceon), as antihypertensive
agents, 435t
Peripheral blood smear, in hematologic
evaluation, 180
Peripheral blood stem cell transplant
(PBSCT), 370
harvesting for, 370
Peripheral intravenous (IV) line, in medical
surgical management, 405t–407t
Peripheral nerve block, 487t
Peripheral nerve injury, 152
Peripheral nervous system, 153t, 154f
Peripheral pulses, in vascular evaluation, 174
Peripheral vascular bypass grafting, 201,
202f–203f
Peripheral vascular disease, 266
Peripheral vestibular disorders, 154
Peripherally inserted central catheter (PICC
line), in medical-surgical management,
405t–407t
Peritoneal dialysis (PD), for genitourinary
dysfunction, 243, 244f
Peritoneal fluid analysis
body fluid examination of, 332
in gastrointestinal evaluation, 214t
Peritonitis, 221–222
Periwound assessment, 320, 320b
Perme Intensive Care Unit Mobility Score,
510, 510t
Persantine thallium stress testing, 33
Persistent vegetative state (PVS), 137–138,
138t
Pertussis, 336
PET. see Positron emission tomography
PGF. see Primary graft failure
Phalangeal fractures, 105, 105b
Phantom limb pain, 141
Pharmacologic agents, 431–474, 432t
for cardiovascular system, 433t
for central nervous system, 446–454
for gastrointestinal system, 457–460
for genitourinary system, 460–461
for hematology, 457
for musculoskeletal system, 443–446
for oncology, 454–457
for respiratory system, 441
for vascular system, 457
Pharynx
description and function of, 58t
function of, 211t
Phenelzine (Nardil), as antidepressants, 448t
Phenobarbital (Barbital, Lumina, Solfoton),
as anticonvulsants, 446t
Phenylephrine (Neo-Synephrine), as positive
inotropes, 441t
Phenytoin (Dilantin), as anticonvulsants,
446t
Pheochromocytoma, 260
Phosphodiesterase-5 (PDE5) inhibitors, for
pulmonary hypertension, 439t
Physical examination
auscultation in, 25–26, 27f, 27t
blood pressure in, 24–25, 25t
in cardiac evaluation, 23–26, 23f–24f, 24t
in infectious disease, 330–331
observation in, 23, 23f
palpation in, 23–24, 24f, 24t
physical therapy considerations for, 25, 26f
in pulmonary system, 62
auscultation in, 63–65, 64f, 64b–65b
cough examination in, 67
hemoptysis in, 67
inspection in, 62–63
mediate percussion in, 66–67, 67f
palpation in, 66, 66f, 66b
in wound assessment, 316–317
Physical Function in Intensive Care Test-
Scored, 510–511
Physical therapist, documentation by, 14–15
Physical therapy, in hematologic evaluation,
178–179
Pia mater, 147
PICA. see Posterior inferior cerebellar artery
Pimavanserin (Nuplazid), as antipsychotics,
449t
Pindolol (Visken), as antihypertensive agents,
435t
Pioglitazone (Actos), for hyperglycemia,
469t
Piperacillin (Pipracil), for infectious diseases,
461t
Piperacillin-tazobactam (Zosyn), for
infectious diseases, 461t
Pirbuterol (Maxair), as bronchodilators, 442t
INDEX 537
Pitavastatin (Livalo), as lipid-lowering agent,
440t
Pitting edema scale, 24t
Pituitary gland
disorders of, 257–259
diabetes insipidus as, 259
hyperpituitarism as, 257–258
hypopituitarism as, 258–259
hormones of
target sites and actions of, 256t
tests of, 257t
structure and function of, 256
Plant alkaloids, in chemotherapy, 455t
Plasma, fresh-frozen, clinical indications and
outcomes for, 200t
Plasma protein fraction (PPF), clinical
indications and outcomes for, 200t
Platelets
clinical indications and outcomes for, 200t
in organ transplantation, 373t
Platinum compounds, in chemotherapy, 455t
Plethysmography, in vascular evaluation,
176t
Pleurae, description and function of, 58t
Pleural effusion, 81, 81t
Pleural friction rub, 65
Pleural tap, body fluid examination of, 332
Pleurodesis, 83
Pneumatic compression boots, in medical
surgical management, 405t–407t
Pneumococcal meningitis, 339
Pneumocystis jirovecii pneumonia, as HIV and
AIDS complication, 343t
Pneumonectomy, 83, 83f
Pneumonia, 78, 78b, 79t
ventilator-associated (VAP), 414
Pneumotaxic center, of pulmonary system, 57
Pneumothorax (PTX), 81–82, 81t, 82b
PNS. see Parasympathetic nervous system
Poisoning, carbon monoxide, 303–304
Poliomyelitis, 338–339
Polyarteritis nodosa (PAN), 187
Polycarbophil (Fiber-lax, FiberCon), as
laxative, 459t
Polycythemia, 195
Polyethylene glycol (MiraLax), as laxative,
459t
Polyneuropathy, critical illness, 6
Polyps, 222
Port-A-Cath, in medical-surgical
management, 405t–407t
Portal hypertension, in cirrhosis,
224, 224f
Positioning, operative, injuries from, 477
Positions, advanced pulmonary conditions,
59b
Positive expiratory pressure (PEP), airway
clearance techniques, 493t, 494
Positive inotropes, 441t
Positive pressure ventilators, in mechanical
ventilation, 411
Positron emission tomography (PET)
in gastrointestinal evaluation, 213
in neurologic examination, 161t–163t
Post-dural puncture headache, 149
Posterior cerebral artery, 151t
Posterior circulation, 146
Posterior cruciate ligament (PCL)
reconstruction, 120t
538 INDEX
Posterior inferior cerebellar artery (PICA),
151t
Posthemorrhagic anemia, 192
Postphlebitic syndrome, 191–192, 192b
Postpoliomyelitis syndrome, 339
Posttraumatic amnesia (PTA), 136–138
Postural drainage positions, 496, 497f, 498t
Posture, in musculoskeletal evaluation,
93, 93b
Potassium-sparing diuretics, as
antihypertensive agents, 435t
Powered air-purifying respirator (PAPR),
337f
PPF. see Plasma protein fraction
Pralatrexate (Folotyn), in chemotherapy, 455t
Pramipexole (Mirapex), for Parkinson’s
disease, 453t
Pramlintide (Symlin), for hyperglycemia,
469t
Pramoxine (Tronothane), for local anesthesia,
488t
Prasugrel (Effient), as antiplatelet agents,
439t
Pravastatin (Pravachol), as lipid-lowering
agent, 440t
Prazepam (Centrax), as antianxiety
medication, 446t
Prazosin (Minipress)
as antihypertensive agents, 435t
for benign prostatic hyperplasia, 460t
Prednisolone (Orapred, Pediapred, Prelone),
for respiratory system, 441t
Prednisone (Deltasone, Sterapred, Sterapred
DS), for respiratory system, 441t
Pregabalin (Lyrica), as anticonvulsants,
446t
Preload, cardiac output and, 20
Premature atrial contractions, ECG
characteristics and causes of, 51t
Premature ventricular contractions (PVCs),
36
ECG characteristics and causes of, 52t
sinus rhythm with, ECG appearance of,
24, 55f
Pressure control ventilation, 412t
Pressure-cycled ventilators, 411
Pressure-supported ventilation (PSV), 412t
Pressure wounds, 311t, 312–313, 313t
Prilocaine (Citanest), for local anesthesia,
488t
Primary graft failure (PGF), 361
Primary polycythemia, 195
Primidone (Mysoline), as anticonvulsants,
446t
Prinzmetal angina, 34
Procainamide (Pronestyl), as antiarrhythmic
agents, 433t
Procyclidine (Kemadrin), for Parkinson’s
disease, 453t
Progesterone, target sites and actions
of, 259t
Progestins
in chemotherapy, 455t
as oral contraceptive, 460t
Progress notes, 16
Progressive exercise program, obstructive
pulmonary conditions and, 78b
Progressive multifocal leukoencephalopathy,
as HIV and AIDS complication, 343t
Prolonged bed rest
effects of, 4
systemic, 5t
physical therapy considerations for, 4
Promethazine (Phenergan), for irritable bowel
syndrome, 458t
Prone position, 478f
for acute respiratory distress syndrome
(ARDS), 80b
Propafenone (Rythmol), for arrhythmias,
433t
Proportional assist ventilation (PAV), 412t
Propoxyphene (Darvon, Dolene, Doloxene,
Novopropoxyn), in pain management,
487t
Propranolol (Inderal), as antihypertensive
agents, 435t
Prostacyclin analogs, for pulmonary
hypertension, 439t
Prostate gland
biopsy of, in genitourinary evaluation, 237
disorders, 242–243
hyperplasia of, benign, 242
Prostatitis, 242–243
Prosthesis
for knee arthroplasty, 110
for shoulder arthroplasty, 112, 113f
Prosthetic graft, 201
Protease inhibitors, for HIV/AIDS, 465t
Protein electrophoresis, in hepatic testing,
215t–216t
Proteins, serum, in hepatic testing,
215t–216t
Proteinuria, etiology of, 236t
Prothrombin time (PT)
in hematologic evaluation, 180, 181t
physical therapy and, 29
Proton pump inhibitors, 459t
Proximal humeral hemiarthroplasty, 113
PSV. see Pressure-supported ventilation
Psychological system, prolonged bed rest
and, 5t
Psyllium (Metamucil), as laxative, 459t
PT. see Prothrombin time
PTA. see Posttraumatic amnesia
PTNow, 499b
PTT. see Partial thromboplastin time
PTX. see Pneumothorax
PUD. see Peptic ulcer disease
Pulmonary artery, description and function
of, 19t
Pulmonary artery catheterization, in
hemodynamic monitoring, 401t
Pulmonary complications, of musculoskeletal
dysfunction, physical therapy
interventions to prevent, 94
Pulmonary edema, 78–80, 79t, 80b
Pulmonary embolism (PE), 79t, 80, 80b, 191
Pulmonary function tests, 72, 72f–74f,
74t–75t
Pulmonary hypertension
as HIV and AIDS complication, 343t
medications for, 439t
Pulmonary inhaled insulin, 265
Pulmonary spirometry tests, 74t–75t
Pulmonary system, 57–88
assessment of, in musculoskeletal
evaluation, 92
auscultation of, 63–65, 64f, 64b–65b
Pulmonary system (Continued)
cancers of, 281–283, 282t, 283b
examination of, 62–72
blood gas analysis in, 68–70, 69f, 69b
chest wall and abdominal excursion in,
66, 66b
chest X-ray, 70–71, 70f, 70b
computed tomographic pulmonary
angiography in, 71–72
diagnostic testing for, 67–68
flexible bronchoscopy in, 71, 71b
inspection in, 62–63
palpation in, 66, 66f, 66b
patient history in, 62
physical examination in, 62
of posture and musculoskeletal, 66–67,
66b
pulmonary function tests for, 72,
72f–74f, 74t–75t
sputum analysis in, 71, 71b
ventilation-perfusion scan for, 71
function of, 57–58, 58t
chemical control as, 57
neural control as, 57
nonchemical influences as, 58
gas exchange in, 59
health conditions affecting, 73–82
chest wall restriction as, 82
obstructive pulmonary conditions as,
76–78, 77t
restrictive extrapulmonary conditions as,
81–82, 81t
restrictive pulmonary conditions as,
78–80, 79t
infections of, 342
management of, 82–85
pharmacologic agents for, 82, 82b
physical therapy intervention for, 83–85
thoracic surgery and procedures for,
82–83, 83f
mechanics of ventilation in, 58–59, 61f
obstructive pulmonary conditions of,
76–78, 77t
asthma as, 76
bronchiectasis as, 78
chronic bronchitis as, 76
cystic fibrosis as, 78
emphysema as, 76
physical therapy intervention for,
83–85, 85t
goals for, 83
management concepts for patients with
respiratory impairments, 83–85
posture and musculoskeletal intervention
in, 85
restrictive extrapulmonary conditions of,
81–82, 81t
emphysema as, 76
flail chest as, 82
hemothorax as, 82
pleural effusion as, 81
pneumothorax (PTX) as, 81–82, 82b
restrictive pulmonary conditions as,
78–80, 79t
acute respiratory distress syndrome
(ARDS) as, 80, 80b
atelectasis as, 78
interstitial lung disease as, 80
lung contusion as, 80

Pulmonary system (Continued)
pneumonia as, 78, 78b
pulmonary edema as, 78–80, 80b
pulmonary embolism (PE) as, 80, 80b
structure of, 57, 58t–59t, 60f
ventilation-to-perfusion ratio in, 59
Pulmonic valve, description and function of,
19t
Pulse amplitude classification and
abnormalities, 24t
Pulse oximetry, 67
in hemodynamic monitoring, 400t
Pulsed lavage, in wound debridement, 322
Pulses, arterial, 24f
Pump, balloon, intraaortic, 417–418, 417f
Purpura, thrombocytopenic
idiopathic, 197–198
thrombotic, 197
Purulent pleurisy, 82
PVCs. see Premature ventricular contractions
PVS. see Persistent vegetative state
Pyelography, in genitourinary evaluation,
236
Pyelonephritis, 239
Pyramidal tracts, function of, 139t
Pyrazinamide (Tebrazid), as antitubercular
agent, 464t
Q Remifentanil (Ultiva), in pain management,
Quadriceps muscles isometric exercises for
after knee arthroplasty, 111
after total hip arthroplasty, 107–108
Quazepam (Doral), as antianxiety medication,
446t
Quetiapine (Seroquel, Seroquel XR), as
antipsychotics, 449t
Quinapril (Accupril), as antihypertensive
agents, 435t
Quinidine (Biquin, Cardioquin), for
arrhythmias, 433t
Quinupristin-dalfopristin (Synercid), for
infectious diseases, 461t
R chronic kidney disease as, 238–239, 239b
RA. see Rheumatoid arthritis
Rabeprazole (Aciphex), as proton pump
inhibitors, 459t
Radiation
ionizing, burns from, 301
therapy, for cancer, 279–280, 279b–280b
Radiography
chest, in cardiac evaluation, 30
in genitourinary evaluation, 236–237
KUB, in genitourinary evaluation, 236
in neurologic examination, 161t–163t
in pulmonary examination, 70–71, 70f,
70b
Radius fractures, 105
Rales, 65b
Raloxifene (Evista), for osteoporosis, 472t
Raltegravir (Isentress, RAL), for HIV/AIDS,
465t
Ramelteon (Rozerem), as antianxiety
medication, 446t
Ramipril (Altace), as antihypertensive agents,
435t
Range of motion (ROM)
after knee arthroplasty, 110
exercises for, 111
Range of motion (ROM) (Continued)
in burn patient evaluation, 309
deficits in, physical therapy interventions
to prevent, 93
in musculoskeletal evaluation, 92–93, 92b,
93t
in wound assessment, 316
in wound care, PT considerations for, 325t
Ranitidine (Zantac), in gastric acid
suppression, 458t
RAS. see Renal artery stenosis
Rasagiline (Azilect), as antidepressants, 448t
RASS. see Richmond Agitation-Sedation Scale
Rate pressure product (RPP), 46b
Raynaud’s disease, 188, 188b
Raynaud’s phenomenon, 188
Rectal pouch/tube, in medical-surgical
management, 405t–407t
Red blood cells (RBCs), clinical indications
and outcomes for, 200t
Reflex(es), cardiac, 21–22
Regional analgesia, patient-controlled, 488t
Regional anesthesia, 475
Rejection, 356b
graft, 356–357
acute, 356–357
hyperacute, 356
Relative polycythemia, 195
487t
Renal arteriography, in genitourinary
evaluation, 237, 237b
Renal artery stenosis (RAS), 240–241
Renal failure, acute, 237–238, 238b
Renal replacement therapy
continuous, for genitourinary dysfunction,
244, 244b, 246t, 247f
for genitourinary dysfunction, 243–244
Renal scanning, in genitourinary evaluation,
237
Renal system dysfunction, 237–241
acute interstitial nephritis as, 240
acute kidney injury as, 237–238, 238t
diabetic nephropathy as, 240
glomerular diseases as, 239–240
nephrolithiasis as, 240
pyelonephritis as, 239
renal artery stenosis as, 240–241
renal vein thrombosis as, 241
Renal transplantation, 358–359
cadaveric versus living donor, 358
indication of posttransplantation, 358–359
postoperative care and complications of,
359, 359b
procedure, 358
recipients, physical therapy for, 359
Renal vein thrombosis (RVT), 241
Renin inhibitors, as antihypertensive agents,
435t
Repaglinide (Prandin), for hyperglycemia,
469t
Reparative phase, in burn management,
306–307, 307t–308t
Reperfusion, of myocardium, 38–40
Reports, in medical record, 16
Reproductive system, hematologic disorders
and, 178t
Resection and reanastomosis, 226t
INDEX 539
Residual volume (RV), description and
clinical significance of, 74t–75t
Residual volume to total lung capacity ratio,
74t–75t
Respiration, 57
Respiratory acidosis, causes of, 68t
Respiratory alkalosis, causes of, 68t
Respiratory dead space (VD), description and
clinical significance of, 74t–75t
Respiratory distress, in respiratory
dysfunction, 76
Respiratory failure, in respiratory
dysfunction, 76
Respiratory rate, in infectious disease
evaluation, 331
Respiratory system, 441
adrenocortical steroids for, 441t
antihistamines for, 442t
bronchodilators for, 442t
cancers of, 281–283, 282t, 283b
complications of burns affecting, 300t
hematologic disorders and, 178t
leukotriene modifiers for, 443t
mast cell stabilizers for, 443t
nonsteroidal antiinflammatory agents for,
443t
prolonged bed rest and, 4, 5t
Respiratory tract, infections of, 335–338,
335b
Restraint usage, in acute care setting, 2–3
Restrictive extrapulmonary conditions,
81–82, 81t
Restrictive pulmonary conditions, 78–80,
79t
acute respiratory distress syndrome
(ARDS) as, 79t, 80, 80b
atelectasis as, 78, 79t
interstitial lung disease as, 80
lung contusion as, 79t, 80
pneumonia as, 78, 78b, 79t
pulmonary edema as, 78–80, 79t, 80b
pulmonary embolism (PE) as, 79t, 80, 80b
Resuscitation status, 8
Resuscitative phase, of burn management,
303–305
Reteplase (Retavase), as thrombolytics, 441t
Reticular layer of dermis, composition and
function of, 297t
Retinacular release, lateral, 120t
Revascularization, of myocardium, 38–40
Reverse total shoulder arthroplasty, 114
Rheumatic fever, rheumatic heart disease
from, 338
Rheumatoid arthritis (RA), 350–351, 351b
osteoarthritis compared with, 351t
Rhinitis, 335
Rhonchi, 65
Rhythm disturbance, 34–36
ablation procedures for, 40
Rhythmicity, of heart, 19
Rib resection, 83
Ribavirin (Copegus, Rebetol), as antiviral
medications, 467t
Richmond Agitation-Sedation Scale (RASS),
136
Rifampin (Rifadin), as antitubercular agent,
464t
Right atrium, description and function of,
19t
540 INDEX
Right coronary artery, anatomy of, 18f
Right-sided failure, 36
Right ventricle, description and function
of, 19t
Rilpivirine (Edurant, RPV), for HIV/AIDS,
465t
Riociguat (Adempas), for pulmonary
hypertension, 439t
Risperidone (Risperdal), as antipsychotics,
449t
Ritonavir (Norvir), for HIV/AIDS, 465t
Rituximab (Rituxan), in chemotherapy, 455t
Rivaroxaban (Xarelto), as anticoagulant, 434t
Roflumilast (Daliresp), for respiratory
system, 443t
Rolapitant (Varubi), as antiemetic, 454t
ROM. see Range of motion
Romberg test, in testing for vestibular
dysfunction, 156t
Romidepsin (Istodax), in chemotherapy, 455t
Ropinirole hydrochloride (Requip), for
Parkinson’s disease, 453t
Rosiglitazone (Avandia), for hyperglycemia,
469t
Rosuvastatin (Crestor), as lipid-lowering
agent, 440t
Rotary chair testing, in testing for vestibular
dysfunction, 156t
Rotavirus infections, 340–341, 341b
Rotigotine (Neupro), for Parkinson’s disease,
453t
Roux-en-Y gastric bypass, 226t, 227f
RPP. see Rate pressure product
Rubor of dependency, in vascular evaluation,
175t
Rubrospinal tract, function of, 139t
Rufinamide (Banzel), as anticonvulsants,
446t
Rule of nines, in burn assessment, 302, 302f
RVT. see Renal vein thrombosis
S Septicemia, 344
SA (sinoatrial) node, 21, 21f
rate of, 21
Saccadic eye movement, in testing for
vestibular dysfunction, 156t
Sacubitril, as antihypertensive agents, 435t
Safety, caregiver and patient, 1–4
guidelines for, 1
Safinamide (Xadago), as antidepressants,
448t
Salicylates, as antiplatelet agents, 439t
Salivary glands, function of, 211t
Salmeterol (Serevent), as bronchodilators,
442t
Salmon calcitonin (Fortical, Miacalcin), for
osteoporosis, 472t
Saquinavir (Invirase-HBC or tab, SQV), for
HIV/AIDS, 465t
Sarcoidosis, 350
Sarcoma
tissue of origin of, 276
tissue/cells involved in, 283t
Sargramostim (Leukine, GM-CSF), in
hematology, 457t
SARS. see Severe acute respiratory syndrome
Saxagliptin (Onglyza), for hyperglycemia,
469t
SCA. see Superior cerebellar artery
Scald burn, 300t
Scapula fractures, 104
Scar, burn, 307
SCD. see Sequential compression device
Schatzker classification, of tibial plateau
fractures, 102, 103f
Schwann cells, 140t
SCI. see Spinal cord injury
Scintigraphy, GI, in gastrointestinal
evaluation, 214t
SCLC. see Small-cell lung cancer
Second line of defense, 330t
Secondary parkinsonism, 142
Secondary polycythemia, 195
Second-degree AV block, ECG characteristics
and causes of, 53t
Secretion, mucus, 491
Sedative-hypnotic agents, as antianxiety
medications, 446t
Segmentectomy, 83
Seizures, 155, 155b
Selective costimulation modulator, for
rheumatoid arthritis, 443t
Selective serotonin reuptake inhibitors
(SSRIs), as antidepressants, 448t
Selegiline (Deprenyl, Eldepryl, Emsam,
Zelapar)
as antidepressants, 448t
for Parkinson’s disease, 453t
Self-care ability, wound healing and, 317
Self-paced walk test (SPWT), 507
interpretation of results, 507
psychometric properties of, 507
Semicircular canals, 154f
Senna (Senokot), as laxative, 459t
Sensation
in musculoskeletal evaluation, 92
in wound assessment, 316
Sensitivity/resistance, in infectious disease
evaluation, 332
Sepsis, 344
Sequential compression device (SCD),
in medical-surgical management,
405t–407t
Serotonin, in gastrointestinal evaluation,
213t
Sertraline (Zoloft), as antidepressants, 448t
Serum proteins, in hepatic testing,
215t–216t
Serum thyroxine, tests of, 254t
Serum triiodothyronine, tests of, 254t
Severe acute respiratory syndrome (SARS), 338
Sex hormones, target sites and actions of,
259t
Sharp debridement of wound, 321
Sheet graft, for burns, 307t
Shift, fluid, 381, 381b
Shock syndrome, 344
Short leg cast (SLC), 121t
Short leg walking boot, 122t
Short Physical Performance Battery (SPPB),
507
Short-term percutaneous devices, 417–420
Impella® Recover System, 419, 419f,
419b
intraaortic balloon pump as, 417–418,
417f
TandemHeart, 419–420, 420f
Short-term surgically placed devices, 420
CentriMag, 420, 420b
extracorporeal membrane oxygenation
(ECMO), 420–422, 421f
Shoulder arthroplasty, 112–114, 113f, 113b
Shoulder girdle fractures, 104
Shunt, 59
ventriculoatrial, in medical-surgical
management, 405t–407t
ventriculoperitoneal, in medical-surgical
management, 405t–407t
Sickle cell anemia, 194, 194b
Sighing respirations, description and
conditions associated with, 63t
Sigmoidoscopy, in gastrointestinal
evaluation, 214t
Sildenafil (Revatio, Viagra), for pulmonary
hypertension, 439t
Simeprevir (Olysio), as antiviral medications,
467t
Simultaneous pancreas-kidney (SPK)
transplantations, 363
Simvastatin (Zocor), as lipid-lowering agent,
440t
Sinoatrial (SA) node, 21, 21f
rate of, 21
Sinusitis, 335, 335b
Sipuleucel-T (Provenge), in chemotherapy,
455t
Sirolimus (Rapamune), as
immunosuppressants, 473t
Sitagliptin (Januvia), for hyperglycemia, 469t
Sit-to-stand tests, 503–504, 503t
interpretation of results, 503–504, 504b
Six-minute walk test (6MWT), 506–507,
506t–507t, 506b–507b
Sixth vital sign, 501
Skin
cancer of, 289, 289b
infection of, 340
structure of, 295–296, 296f, 297t
substitutes for, for grafts, 308t
Skin lesion, complicating diabetes, 265–266
SLC. see Short leg cast
SLE. see Systemic lupus erythematosus
Sleep pattern disturbance, in acute care
setting, 6–7
Sleeve resection, 82, 83f
Sling, arm, 122t
Small-cell lung cancer (SCLC), 281, 282t
Small intestine, function of, 211t
Smoking, history of, 62
Smooth pursuit eye movement, in testing for
vestibular dysfunction, 156t
SNS. see Sympathetic nervous system
Sodium bicarbonate (Alka-Seltzer), as
antacid, 457t
Sodium channel blockers, 433t
Sofosbuvir (Sovaldi), as antiviral medications,
467t
Soft tissues, cancer of, 283, 283t, 283b
Soft-tissue surgery, musculoskeletal, 120t
Soluble guanylate cyclase stimulator, for
pulmonary hypertension, 439t
Sotalol (Betapace, Betapace AF), for
arrhythmias, 433t
Sphygmomanometer, 24–25
in hemodynamic monitoring, 400t
Spinal accessory nerve (CN XI), 132t

Spinal cast, 121t
Spinal cord, autonomic nervous system in,
132–134
Spinal cord injury (SCI), 144–146, 146t
impairment from, scale for, 145t
level of, expected return of function and,
145t
Spinal fusion, 118, 118f, 118t
Spinal shock, 145–146
prognosis of, 146
Spinal traction, 123
Spine
braces and splints for, 122t
fractures, 103–104
pathology of, 116–120
surgeries of, 117–119, 117f, 118t
physical therapy after, 118–119
Spirometry tests, pulmonary, 74t–75t
Spironolactone (Aldactone, CaroSpir), as
antihypertensive agents, 435t
Spleen
diagnostic procedures for, 216t
function of, 211t
Splints, 121–122, 122t, 122b
Split-thickness skin graft, for burns, 307t
Spontaneous pneumothorax, 81
SPPB. see Short Physical Performance Battery
Sputum, analysis of, in pulmonary
examination, 71, 71b
SPWT. see Self-paced walk test
Squamous cell cancer, 289
SSRIs. see Selective serotonin reuptake
inhibitors
Stable angina, 34
physical therapy considerations for, 391
Staining, in infectious disease evaluation, 331
Stair training, after knee arthroplasty, 112
Staphylococcus aureus infection, methicillin-
resistant, 334
Static ocular observation, in testing for
vestibular dysfunction, 156t
Stem cell transplantation (SCT),
hematopoietic, 367, 370–372
harvesting, 370
patient preparation of, 370
postprocedure care and complications, 371
recipients of, physical therapy
for, 371–372
reinfusion and indication of postprocedure
function of, 370–371
Sternotomy, medial, sternal precautions after,
40
Steroids, 497
Stimulants, 450t
Stomach
disorders of, 218–219
function of, 211t
Stool sample, in gastrointestinal evaluation,
213t
Stratum basale, composition and function of,
297t
Stratum corneum, composition and function
of, 297t
Stratum germinativum, composition and
function of, 297t
Stratum granulosum, composition and
function of, 297t
Stratum lucidum, composition and function
of, 297t
Stratum spinosum, composition and function
of, 297t
Strength
after amputation, 386, 386b
in burn patient evaluation, 309
deficits in, physical therapy interventions
to prevent, 93
in musculoskeletal evaluation, 92–93
in wound assessment, 316
in wound care, PT considerations for, 325t
Streptomycin, for infectious diseases, 461t
Stress incontinence, 242t
surgical procedures for, 245–247
Stress testing, in cardiac evaluation, 31–33,
32f, 32t, 32b
Stridor, 65, 65b
Stroke, 149–152, 266
Subarachnoid bolt, in ICP monitoring, 403t
Subarachnoid hemorrhage, 149, 152
Subclavian artery, intraaortic balloon pump
via, 418
Subclinical infection, definition of, 330–331,
330t
Subcortical dementia, 137t
Subcutaneous emphysema, palpation of, 66
Subdural hematomas, 152
Substance abuse and withdrawal, in acute
care setting, 7
Subtherapeutic level, 199
Subtrochanteric fractures, 99, 100f
Sucralfate (Carafate), as cytoprotective
medication, 458t
Sufentanil (Sufenta), in pain management,
487t
Sulfadiazine, for infectious diseases, 461t
Sulfamethizole (Urobiotic), for infectious
diseases, 461t
Sulfamethoxazole/trimethoprim (Septra), for
infectious diseases, 461t
Sulfasalazine (Azulfidine), for rheumatoid
arthritis, 443t
Sulfisoxazole (Gantrisin), for infectious
diseases, 461t
Sulfonylureas, for hyperglycemia, 469t
Sulindac (Clinoril), in pain management,
487t
Sunburn, 301
Sunitinib (Sutent), in chemotherapy, 455t
Superior cerebellar artery (SCA), 151t
Superior vena cava, description and function
of, 19t
Supertherapeutic level, 199
Supine position, 478f
Suprapubic catheter, in medical-surgical
management, 405t–407t
Supraventricular tachycardia, ECG
characteristics and causes of, 51t
Surface area, in gas exchange, 59
Surgical drain, in medical-surgical
management, 405t–407t
Surgical wounds, 311
Swallowing, difficulty with, 216
Swan-Ganz catheter, in hemodynamic
monitoring, 401t
Sweat test, in pancreatic testing, 215t–216t
Sympathetic nerve block, 487t
Sympathetic nervous system (SNS), 132–134
Syndrome of inappropriate antidiuretic
hormone (SIADH) secretion, 258
INDEX 541
Syngeneic transplantation, 370
Synovial fluid analysis, body fluid
examination of, 332
Systemic circulation, 22, 22f
Systemic lupus erythematosus
(SLE), 350
Systemic vasculitis, 187
Systole, 19
Systolic dysfunction, 36
T
Tachycardia
junctional, ECG characteristics and causes
of, 52t
paroxysmal supraventricular, 53f
ventricular, ECG characteristics and causes
of, 52t
Tachypnea, description and conditions
associated with, 63t
Tacrolimus (FK506, Prograf), as
immunosuppressants, 473t
Tadalafil (Cialis, Adcirca), for pulmonary
hypertension, 439t
Takayasu’s arteritis, 188
Tamoxifen (Nolvadex), in chemotherapy,
455t
Tamsulosin (Flomax)
as antihypertensive agents, 435t
for benign prostatic hyperplasia, 460t
TandemHeart, 419–420, 420f
Tangential excision, for burns, 307t
Taxanes, in chemotherapy, 455t
TB. see Tuberculosis
TBI. see Traumatic brain injury
TBSA. see Total body surface area
TCAs. see Tricyclic antidepressants
Tectospinal tract, function of, 139t
Tedizolid phosphate (Sivextro), for infectious
disease, 461t
TEE. see Transesophageal echocardiography
TEEs. see Thoracic expansion exercises
Teeth, function of, 211t
Telaprevir (Incivek), as antiviral medications,
467t
Telavancin (Vibativ), for infectious diseases,
461t
Telemetric electrocardiography monitoring,
27–29, 29b
Telemetry, in hemodynamic monitoring,
400t
Telithromycin (Ketek), for infectious diseases,
461t
Telmisartan (Micardis), as antihypertensive
agents, 435t
Temazepam (Restoril), as antianxiety
medication, 446t
Temozolomide (Temodar), in chemotherapy,
455t
Temperature, in infectious disease evaluation,
331, 331b
Temporal arteritis, 188
Temporal lobe, structure, function, and
dysfunction of, 131t
Tenecteplase (TNKase), as thrombolytics,
441t
Tenofovir alafenamide (Vemlidy, TAF), for
HIV/AIDS, 465t
Tenofovir disoproxil fumarate (Viread, TDF),
for HIV/AIDS, 465t
542 INDEX
Terazosin (Hytrin)
as antihypertensive agents, 435t
for benign prostatic hyperplasia, 460t
Teriflunomide (Aubagio), for multiple
sclerosis, 451t
Teriparatide (Forteo), for osteoporosis, 472t
Testosterone (Delatestryl), in chemotherapy,
455t
Tetracaine (Pontocaine), for local anesthesia,
488t
Texas catheter, in medical-surgical
management, 405t–407t
Thalassemia, 194, 194b
Thallium stress testing, 32–33
Theophylline (Elixophyllin, Quibron, Theo-
24, TheoCap, Theochron, Uniphyl)
as bronchodilators, 442t
TheraPep, 494f
Thermal burns, 299, 300t
Thiazide diuretics, as antihypertensive
agents, 435t
Thienopyridine, as antiplatelet agents, 439t
Thioridazine (Mellaril), as antipsychotic,
449t
Thiotepa (Thioplex), in chemotherapy, 455t
Third-degree AV block, ECG characteristics
and causes of, 53t
Third line of defense, 330t
30-second chair stand test (30CST), 503,
503t–504t
Thoracentesis, 83
Thoracic expansion exercises (TEEs), 492
Thoracic surgery and procedures, 82–83, 83f
Thoracocentesis, body fluid examination of,
332
Thoracolumbosacral orthosis (TLSO), 122t
Thoracoscopy, 83
Thorax, lung position in, 60f
3-second inspiratory breath hold, airway
clearance techniques, 491
Thrombectomy, 200–201
Thrombin inhibitors, direct, as
anticoagulants, 434t
Thromboangiitis obliterans, 187
Thrombocytes, description of, 173t
Thrombocytopenia, 196–197
physical therapy considerations for, 197
Thrombocytopenic purpura
idiopathic, 197–198
thrombotic, 197
Thrombolysis, transcatheter, 200–201
Thrombolytic therapy, 38, 441t
Thrombosis
arterial, 185
deep vein, Wells Clinical Decision Rule
for, 176t
renal vein, 241
Thrombotic thrombocytopenic purpura, 197
Thyrocalcitonin, target sites and actions of,
254t
Thyroid disease, treatment of, 473t
Thyroid function tests, 254t
Thyroid gland, 254–256
adenoma of, hyperthyroidism from, 255t
carcinoma of, hyperthyroidism from, 255t
disorders of, 255–256
hyperthyroidism as, 255, 255t
hypothyroidism as, 255–256, 256b
imaging/scan of, 255t
Thyroid gland (Continued)
needle biopsy of, 255t
structure and function of, 254
ultrasonography of, 255t
Thyroid hormones
target sites and actions of, 254t
tests of, 254, 254t, 254b
Thyroiditis, hyperthyroidism from, 255t
Thyroid-stimulating hormone (TSH), 254t
Thyrotoxicosis, 255
Thyrotropin-releasing hormone (TRH), 254t
Thyroxine (T4)
serum, tests of, 254t
target sites and actions of, 254t
TIA. see Transient ischemic attack
Tiagabine (Gabitril), as anticonvulsants, 446t
Tibia
distal, fracture of, 102–103
shaft of, fracture of, 102
Tibial plateau fractures, 102, 103f
Ticagrelor (Brilinta), as antiplatelet agents,
439t
Ticarcillin (Ticar), for infectious diseases,
461t
Ticarcillin-clavulanic acid (Timentin), for
infectious diseases, 461t
Tidal volume (VT), 58b
description and clinical significance of,
74t–75t
Timed “up and go” test, 501–502, 501t,
502b
interpretation of results of, 502
procedure, 501
Tinetti Performance Oriented Mobility
Assessment (POMA), 502–503, 503t,
515t–516t
interpretation of results, 503
procedure, 503
Tiotropium (Spiriva), as bronchodilators,
442t
Tipranavir (Aptivus, TPV), for HIV/AIDS,
465t
Tirofiban (Aggrastat), as antiplatelet agents,
439t
Tizanidine (Zanaflex), for spasticity, 445t
TKA. see Total knee arthroplasty
TLC. see Total lung capacity
TLSO. see Thoracolumbosacral orthosis
TM. see Transverse myelitis
TNM cancer staging system, 278, 278t
Tobramycin (AKTob, TOBI, Tobrex), for
infectious diseases, 461t
Tocainide (Tonicard), for arrhythmias, 433t
Tocilizumab (Actemra), for rheumatoid
arthritis, 443t
Tofacitinib (Xeljanz), for rheumatoid
arthritis, 443t
Tolcapone (Tasmar), for Parkinson’s disease,
453t
Tolmetin (Tolectin), in pain management,
487t
Tongue, function of, 211t
Topical agents, in wound care, 322
Topical anesthetics, 487t
Topical ointments in dressings, 323t
Topiramate (Topamax, Qudexy XR), as
anticonvulsants, 446t
Topotecan (Hycamtin), in chemotherapy,
455t
Torsades de pointes, ECG characteristics and
causes of, 52t
Torsemide (Demadex), as antihypertensive
agents, 435t
Tositumomab (Bexxar), in chemotherapy,
455t
Total artificial heart, 426–428, 427f
Total body surface area (TBSA), in burn
assessment, 301, 302f, 303t
Total knee arthroplasty (TKA), 110
Total lung capacity (TLC), description and
clinical significance of, 74t–75t
Total shoulder arthroplasty (TSA), reverse,
113f, 113b, 114, 115b
Toxic neuronal neuropathy, as HIV and AIDS
complication, 343t
Toxic nodular goiter, hyperthyroidism from,
255t
Toxoplasmosis, 344
Trachea
description and function of, 58t
resection and reconstruction of, 83
sounds of, 64
Tracheostomy, 83
Traction, 122–123
Tramadol (Ultram), in pain management,
487t
Trandolapril (Mavik), as antihypertensive
agents, 435t
Transcatheter aortic valve implantation, 42
Transcatheter thrombolysis, 200–201
Transcranial Doppler sonography, in
neurologic examination, 161t–163t
TransCyte, in burn and wound treatment,
308t
Transdermal administration of anesthetics,
487t
Transesophageal echocardiography (TEE),
30–31
Transfer training
after knee arthroplasty, 112
after total hip arthroplasty, 109
Transfusion, blood product, adverse reactions
to, 201t
Transfusion-related immunomodulation
(TRIM), 199
Transient ischemic attack (TIA), 149
Transmyocardial revascularization, 39
Transparent film dressings, 323t
Transplantation
cardiac, 43
GI, 226t
organ, 353–378
Transthoracic echocardiography (TTE),
30–31
Transtracheal catheter, in oxygen delivery,
397t
Transudative fluid, in pleural effusion, 81
Transverse myelitis (TM), 158
Tranylcypromine (Parnate), as
antidepressants, 448t
Trastuzumab (Herceptin), in chemotherapy,
455t
Traumatic brain injury (TBI), monitoring of,
multimodal, equipment for, 403, 404t
Traumatic pneumothorax, 81
Traumatic wounds, 311
Trazodone (Desyrel), as antidepressants,
448t

Trendelenburg’s test, in vascular evaluation,
175t
Treprostinil (Remodulin), for pulmonary
hypertension, 439t
TRH. see Thyrotropin-releasing hormone
Triamcinolone (Aristocort), for respiratory
system, 441t
Triamcinolone acetonide (Azmacort,
Nasacort), for respiratory disorders, 441t
Triamterene (Dyrenium), as antihypertensive
agents, 435t
Tricuspid valve, description and function of,
19t
Tricyclic antidepressants (TCAs), 448t
Trigeminal nerve (CN V), 132t
Triglycerides, 29
Trihexyphenidyl hydrochloride (Artane,
Trihexy-5), for Parkinson’s disease, 453t
Triiodothyronine (T3)
serum, tests of, 254t
target sites and actions of, 254t
TRIM. see Transfusion-related
immunomodulation
Trimethadione (Tridione), as anticonvulsants,
446t
Triptorelin (Trelstar), in chemotherapy, 455t
Trochanteric osteotomy, in hip arthroplasty,
108, 109f
Trochlear nerve (CN IV), 132t
Troponins, 30
TSH. see Thyroid-stimulating hormone
TTE. see Transthoracic echocardiography
Tuberculosis (TB), 336–337, 336b–337b
as HIV and AIDS complication, 343t
Tumor(s)
benign, 275
classification of, 277t
definition of, 276t
grading of, 278t
intestinal, 222
malignant, 275
musculoskeletal, resection for, 115–116
nomenclature for, 276
Tunica adventitia, 172t
Tunica intima, 172t
Tunica media, 172t
Tunneled central venous catheter, in medical
surgical management, 405t–407t
Tunneling, in wound, 318, 318f
U replacement of, 42
Ulcer(s)
decubitus, 311t, 312, 312b, 313t
neuropathic, 311t, 312
peptic, 218
Ulcerative colitis, 222
Ulipristal, as oral contraceptive, 460t
Ultrasonography
in deep venous thrombosis, 190
in genitourinary evaluation, 237
in thyroid function testing, 255t
in wound care, 324t
Ultraviolet burns, 301
Ultraviolet (UV) light therapy, in wound
care, 324t
Umeclidinium bromide (Incruse Ellipta), as
bronchodilators, 442t
UMNs. see Upper motor neurons
Undermining, in wound, 318, 318f
Unilateral neglect, 151, 151t
United Network for Organ Sharing (UNOS),
355
UNOS. see United Network for Organ
Sharing
Unstable angina, 35f
physical therapy considerations for, 391
Unsticking phase, of autogenic drainage
(AD), 494
“Up and go” test, timed, 501–502, 501t
Upper extremity amputation, 383
levels of, 386f
types of, 387t
Upper GI (UGI) series, in gastrointestinal
evaluation, 214t
Upper motor neurons (UMNs), 131,
141–142
Upper respiratory tract infections, 335–336
Ureidopenicillins, for infectious diseases,
461t
Ureters, X-ray of, with kidneys and bladder,
in genitourinary evaluation, 236
Urethra, biopsy of, in genitourinary
evaluation, 237
Urge incontinence, 242t
Urinalysis, in genitourinary evaluation, 235,
235b, 236t
Urinary calculi, 241
Urinary catheter, in medical-surgical
management, 405t–407t
Urinary diversion, 247
Urinary incontinence, 242, 242t, 242b
procedures for, 245–247
Urinary tract
hematologic disorders and, 178t
lower, dysfunction of, 241–242
Urine abnormalities, etiologies of, 236t
V physical examination of, 172–181. see also
Vagus nerve (CN X), 132t
Valbenazine (Ingrezza), as antipsychotics,
449t
Valganciclovir (Valcyte), as antiviral
medications, 467t
Valproic acid (Depacon, Depakene,
Depakote), as anticonvulsants, 446t
Valsartan (Diovan, Entresto), as
antihypertensive agents, 435t
Valve, cardiac
description and function of, 19t
Valvotomy, aortic, percutaneous, 42
Valvular heart disease, 36, 36t
for infectious diseases, 461t
Vancomycin-resistant Enterococcus
(VRE), 334
Vandetanib (Caprelsa), in chemotherapy, 455t
VAP. see Vascular access port
Variable-performance oxygen delivery, for
spontaneously breathing adults, 396,
397t, 398f
Variant angina, 34
Varices, esophageal, 218
Varicose veins, 189
Vascular access, for hemodialysis,
244, 246f
Vascular access port (VAP), in medical-
surgical management, 405t–407t
Vascular dementia, 137t
INDEX 543
Vascular disorders, 181–192, 182t
anticoagulation therapy for, 198–199, 199t
arterial, 181–187, 182t–183t, 182b
blood product transfusion for, 199,
200t–201t
pharmacologic therapy for, 198
physical therapy interventions for patients
with, 204–205
vascular surgical procedures for, 199. see
also Vascular surgical procedures
venous, 189–192, 190b, 191f. see also
Venous disorders
Vascular evaluation, 173–177
auscultation in, 174
diagnostic studies in, 175–177,
176t–177t, 177f
history in, 173
observation in, 173–174
pain in, 173, 173b
palpation in, 174, 174b
physical therapy considerations in, 174
tests in, 174, 175t–176t
Vascular status, wound healing and, 315
Vascular surgical procedures, 199
aneurysm repair and reconstruction as,
202–203, 203f
embolization therapy as, 200
endarterectomy as, 201, 201b
peripheral vascular bypass grafting as, 201,
202f–203f
physical therapy management
for, 203–205
thrombectomy as, 200–201
transcatheter thrombolysis as, 200–201
Vascular system, 171–208, 172f, 172t
disorders of, 181–192, 182t. see also
Vascular disorders
pharmacologic agents for, 457
Vascular evaluation
Vasculitis
acute necrotizing, 187
systemic, 187
Vasodilators, as antihypertensive
agents, 435t
Vasopressin (Pitressin)
cardiac effects of, 21t
as positive inotropes, 441t
VATS. see Video-assisted thoracoscopic
surgery
VBI. see Vertebral-basilar arterial
insufficiency
VDS. see Verbal Descriptor Scale
Vegetative state (VS), 9–10, 137–138, 138t
Vein
characteristics of, 172t
disorders of, 189–192. see also Venous
disorders
structure of, 172f
varicose, 189
Velpatasvir, as antiviral medications, 467t
Vemurafenib (Zelboraf), in chemotherapy,
455t
Vena cava, description and function
of, 19t
Venlafaxine (Effexor), as antidepressants,
448t
Venous blood gas analysis, in pulmonary
examination, 70
544 INDEX
Venous disorders, 189–192
arteriovenous malformations as, 192
chronic venous insufficiency as, 191–192,
191f, 192b
postphlebitic syndrome as, 191–192, 192b
pulmonary embolism as, 191, 191b
varicose veins as, 189
venous thrombosis as, 189–191, 190b
Venous insufficiency
chronic, 191–192, 191f, 192b
wounds, 311t, 312
Venous thrombosis, 189–191
deep. see Deep venous thrombosis
types of, 190
Ventilation
chemical control of, 57
definition of, 57
gas exchange in, 59
mechanical, 409–416
mechanics of, 58–59, 61f
neural control of, 57
nonchemical influences in, 58
paradoxical, description and conditions
associated with, 63t
ventilator settings supporting, 413t
Ventilation-perfusion scan, for pulmonary
examination, 71
Ventilation tests, description and clinical
significance of, 74t–75t
Ventilation-to-perfusion ratio, 59
mismatch, 59, 61f
Ventilator-associated pneumonia (VAP), 414
Ventral spinocerebellar tract, function of,
139t
Ventricles, 147
description and function of, 19t
Ventricular assist device, 422–425, 423f,
424t, 424b
Ventricular diastole, 20
Ventricular dysfunction, 148–149
tests and measures, 156t
Ventricular ectopy, 54f
Ventricular fibrillation, 55f
ECG characteristics and causes of, 52t
Ventricular rhythms, ECG characteristics and
causes of, 52t
Ventricular systole, 20
Ventricular tachycardia (VT), 54f
ECG characteristics and causes of, 52t
Ventriculoperitoneal (VP) shunt, in medical
surgical management, 405t–407t
Ventriculostomy, in ICP monitoring, 403t
Venturi mask, in oxygen delivery, 399f, 399t
Verapamil (Isoptin, Calan, Verelan,
Covera-HS), as antihypertensive agents,
435t
Verbal Descriptor Scale (VDS), for pain, 485t
Verbal Pain Scales, 482t
Vertebral artery, 151t
Vertebral augmentation, 119, 119f
Vertebral-basilar arterial insufficiency (VBI),
146–147
Vertebral column
fracture of, 103
pathology of, 116–120
Vertebroplasty, 119–120, 119f
Vertical banded gastroplasty, 226t, 227f
Vertigo, in vestibular dysfunction, 153
Vesicular sounds, 64
Vestibular dysfunction, 153–154
Vestibular migraine, 154
Vestibular schwannomas, 131–132
Vestibular system, 152–155
Vestibulocochlear nerve (CN VIII), 132t
Vestibulospinal tract, function of, 139t
Vibration, airway clearance techniques, 498t
Video-assisted thoracoscopic surgery (VATS),
83
Vigabatrin (Sabril), as anticonvulsants, 446t
Vilanterol (Trelegy Ellipta), as
bronchodilators, 442t
Vilazodone (Viibryd), as antidepressants,
448t
Vinblastine (Velban), in chemotherapy, 455t
Vinca alkaloids, in chemotherapy, 455t
Vincristine (Oncovin), in chemotherapy, 455t
Vinorelbine (Navelbine), in chemotherapy,
455t
Viral encephalitis, infectious, 339
Viral meningitis, 339
Viral pneumonia, 78b
Viral rhinitis, 335
Vision, hematologic disorders and, 178t
Visual Analog Pain Scales, 485t
Visual/oculomotor examination, 130–131,
131b, 133f
Vital capacity (VC), description and clinical
significance of, 74t–75t
Vital signs, in infectious disease evaluation,
331
Vitamin B12 anemia, 193, 193b
Voice sounds, 65
Volume, fluid
deficiency, 379
excess, 381, 381b
Volume-cycled ventilators, 411
von Willebrand’s disease, 196
Vorapaxar (Zontivity), as antiplatelet agents,
439t
Voriconazole (Vfend), as antifungal agents,
463t
Vortioxetine (Brintellix), as antidepressants,
448t
VRE. see Vancomycin-resistant Enterococcus
VS. see Vegetative state
VT. see Ventricular tachycardia
W Zanamivir (Relenza), as antiviral
Walking pace, metabolic equivalents and
oxygen consumption related to, 32, 32f
Walking program, after spinal surgery, 119
Warfarin (Coumadin), as anticoagulant, 434t
Weaning, from mechanical ventilation,
414–415
Wedge resection, 83, 83f
Wegener’s granulomatosis, 187
Wells Clinical Decision Rule (CDR), for deep
vein thrombosis, 176t
Wenckebach block, ECG characteristics and
causes of, 53t
Wet crackles, 65b
Wet-to-dry dressings, in wound
debridement, 321
Wheezes, 65
Whipple procedure, 226t
Whirlpool, in wound debridement, 321–322
Whispered pectoriloquy, 65
White blood cell (WBC)
count, in infectious disease evaluation, 331
in organ transplantation, 373t
White blood cell-trapping hypothesis, of
venous insufficiency wounds, 312
Whole blood, clinical indications and
outcomes for, 200t
Whooping cough, 336
Withdrawal, alcohol, 7
Wounds, 310–313
arterial insufficiency, 311, 311t
assessment of, 317–320, 317b
chronic, advanced therapies for, 322, 324t
cleaning of, 320, 320b
debridement of, 320–322
dressings for, 322, 323t
healing of
after amputation, 384, 384b
factors delaying, 314–315
phases of, 313–314
inspection and evaluation of
bed composition in, 318–319
drainage in, 319
location, orientation, size, and depth in,
317–318, 317f–318f, 318b
periwound assessment in, 320, 320b
staging and classification in, 319–320
wound culture in, 319, 319b
pathophysiology of, 310–313
physical therapy intervention in care of,
322, 325t
pressure, 311t, 312–313, 313t
surgical, 311
traumatic, 311
types of, 311–313
venous insufficiency, 311t, 312
X
Xenograft, for burns, 307t
Xenon CT, in neurologic examination,
161t–163t
X-rays. see Radiography
Z
Zafirlukast (Acculate), for respiratory system,
443t
Zaleplon (Sonata), as antianxiety medication,
446t
medications, 467t
ZES. see Zollinger-Ellison syndrome
Zidovudine (Retrovir, AZT, ZDV), for HIV/
AIDS, 465t
Zileuton (Zyflo), for respiratory system, 443t
Ziprasidone (Geodon), as antipsychotics,
449t
Zoledronic acid (Reclast), for osteoporosis,
472t
Zollinger-Ellison syndrome (ZES), 218–219
Zolpidem (Ambien), as antianxiety
medication, 446t
Zonisamide (Zonegran), as anticonvulsants,
446t
Zydis selegiline, rasagiline (Azilect), for
Parkinson’s disease, 453t