Primary Care Mentor

Primary Care
Your Clerkship &

Shelf Exam Companion
Mentor
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Mentor
Primary Care
Your Clerkship &
Shelf Exam Companion
Marianne M. Green, MD
Associate Dean for Medical Education and Competency
Achievement and Assistant Professor of Medicine
Division of General Internal Medicine
Northwestern University Feinberg School of Medicine
Chicago, Illinois
Jennifer A. Bierman, MD
Chicago, Illinois
James J. Foody, MD
Professor of Medicine
Vice Chairman of Medicine for Clinical Affairs
Chicago, Illinois
Russell G. Robertson, MD
Professor and Chair
Department of Family Medicine
Chicago, Illinois
Gary J. Martin, MD
Raymond J. Langenbach, MD Professor of Medicine and
Vice Chair for Faculty Affairs and Education, Department of Medicine
Chicago, Illinois
Mentor
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F. A. Davis Company
1915 Arch Street
Philadelphia, PA 19103
www.fadavis.com
Copyright 2009 by F. A. Davis Company
All rights reserved. This product is protected by copyright. No part of it may be reproduced,
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As new scientific information becomes available through basic and clinical research, recom-
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dards at the time of publication. The author(s), editors, and publisher are not responsible for er-
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Library of Congress Cataloging-in-Publication Data
Primary care mentor : your clerkship & shelf exam companion / [edited by] Marianne
M. Green [et al.].
p. ; cm.
ISBN 978-0-8036-2125-1 (pbk. : alk. paper) 1. Primary care (Medicine)Outlines, syllabi,
etc. 2. Clinical clerkshipOutlines, syllabi, etc. I. Green, Marianne M.
[DNLM: 1. Ambulatory CareHandbooks. 2. Clinical ClerkshipHandbooks.
3. Diagnostic Techniques and ProceduresHandbooks. WB 39 P9525 2009]
RC59.P75 2009
616.0076dc22
2009001350
Authorization to photocopy items for internal or personal use, or the internal or personal use of
specific clients, is granted by F. A. Davis Company for users registered with the Copyright
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The fee code for users of the Transactional Reporting Service is: 8036-2125-1/09 0 + $.25.
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To the patients, whose lives we endeavor to improve
To the students, residents, and fellows who have stimulated
our development as teachers
To our families, for everything
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vi
FOREWORD
The final 2 years of medical school are a critical period of physician
development. Students make the final leap across the chasm separating
educated layperson from medical professional. Fortified by 2 years of
medical school instruction in basic and medical sciences and armed with
fledgling clinical skills, students suddenly find themselves thrust into the
real worlda world where practice subjects are replaced by bona
fide patients with real medical needs and expectations. It is a world that
no longer revolves around the student, a world with neither a structured
curriculum nor controlled clinical settings. It is a time of discovery, a time
when teaching moments do not occur on a schedule, when a days
lessons are not known until they occur, and when students really begin to
appreciate just how much more there is to learn.
Although hospital-based rotations may appear to students, on the
surface, to be the most demanding of all, in reality students play an
apprentice role in this settingbeing handed a working diagnosis at the
time of a patients admission and learning principally by observing and
following in the steps of others. A far greater challenge lies in the ambulatory
arena, where students are placed in the role of physician and can find
themselves in a sink-or-swim situation. This challenge is only heightened
in the primary care setting, where students must also grapple with the
uncertainties of first contact and undifferentiated symptoms. This can be
a humbling time because students are ill-prepared to attend to the broad
clinical agenda that is the hallmark of primary care. Not surprisingly,
many students find themselves growing increasingly frustrated and
discouraged as they struggle to see the forest for the trees.
Although numerous primary care texts directed at practicing clinicians
exist, ready references in primary care designed for novice clinicians are
sorely lacking. Stepping up to help fill this void is Primary Care Mentor.
This carefully crafted compendium, edited by five master clinician-teachers,
was developed specifically to provide guidance and direction to medical
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student clerks making their initial ventures into primary care. Each chap-
ter in this thoughtfully written manual is presented in a structured outline
format to provide the reader with a succinct, no-frills, nuts-and-bolts
approach to the subject covered.
Including insightful introductory information on patient communica-
tions skills and clinical epidemiology are 37 chapters covering a wide
array of topics, ranging from preventive medicine to common symptoms
and complaints to chronic conditions seen in primary care. In addition to
providing the working knowledge needed to approach problems, each
chapter is replete with clinical pearls, instructive figures, and handy
tables. Each chapter concludes with a Mentor Tips Digest highlighting
major teaching points, a list of key references and recommended read-
ings, and a set of self-test questions designed to help learners gauge their
understanding of the material presented.
In reviewing this book, I could not help but think back to an early
lesson taught to me and my classmates on our first day of medical school.
In an effort to provide us with a glimpse of what the next 4 years held in
store, a sagacious professor shared his version of the There must be a
pony. vignette. He began by telling us that medical school could be
likened to entering a room full of horse manure. Pessimists in the class
would immediately be repulsed by the excrement, whine about the smell,
strive to stay away from it, and plea to be let out. He said optimists would
joyously throw themselves into the muck and, using their bare hands,
cheerfully burrow and shovel through it with glee. Why? one might ask.
Because optimists would figure that with so much horse manure in the
room, there just had to be a pony in there!
Although this book wont spare novice clinicians from having to
shovel their way through the challenges of primary care, it certainly
figures to make them feel more optimistic.
Martin A. Quan, MD
Professor of Clinical Family Medicine
Director of Continuing Medical Education
David Geffen School of Medicine
University of California Los Angeles
FOREWORD vii
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viii
PREFACE
Primary care medicine continues to advance, furthering its mission of
maximizing the health of patients throughout their lives. In order to give
the next generation of clinicians the very best possible study tools, we
have created Primary Care Mentor: Your Clerkship & Shelf Companion
for the primary care clerkship rotation and shelf examinations.
This book will also be helpful to mid-level providers, residents in
primary care fields, and even attending physicians who want to update
and review their knowledge base. Primary Care Mentor is a collaborative
effort between internal medicine and family medicine faculty, with
additional input from relevant subspecialists.
We sincerely believe the information contained in this book will help
students who go on to any medical specialty. It covers common problems
they will encounter as students and on into their practice. Primary care is
a rewarding area. Being able to provide comprehensive care to patients
and having longitudinal relationships with them energizes us as physicians
and is a cost-effective strategy for providing health care to the nation.
We hope this book helps in your quest to practice medicine, wherever it
might be.
James J. Foody, MD
Gary J. Martin, MD
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ix
CONTRIBUTORS
Stephen L. Adams, MD
Division of Sports Medicine
Chicago, Illinois
Chapter 13: Musculoskeletal Pain
Martin J. Arron, MD, MBA
Vice President for Ambulatory Operations
Beth Israel Medical Center
New York, New York
Chapter 15: Fatigue
Assistant Professor of Medicine
Chicago, Illinois
Chapter 1: Office Management and the Principles of Diagnosis
and Management of Ambulatory Patients
Chapter 32: Hormone Replacement Therapy
John E. Butter, MD
Chicago, Illinois
Chapter 8: Dizziness
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Raymond H. Curry, MD
Dean for Education
Chicago, Illinois
Chapter 2: Communicating with Patients
Aarati D. Didwania, MD
Chicago, Illinois
Chapter 31: Preconception Care
Deborah L. Edberg, MD
Assistant Professor
Chicago, Illinois
Chapter 33: Menstrual Disorders
James J. Foody, MD
Vice Chairman of Medicine for Clinical Affairs
Chicago, Illinois
Chapter 6: Headache
Chapter 36: Osteoporosis
Chapter self-test questions and testbank
Jordana Friedman, MD
Chicago, Illinois
Ellen J. Gelles, MD
x CONTRIBUTORS
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Case Western Reserve University School of Medicine
Cleveland, Ohio
Chapter 35: Pap Smear and Cervical Cancer Screening
Joseph P. Gibes, MD
Instructor, Department of Family Medicine
Chicago, Illinois
Chapter 28: Otitis Media in Children
Robert M. Golub, MD
Associate Professor of Medicine
Chicago, Illinois
Chapter 3: Clinical Epidemiology and Principles of Quantitative
Decision Making
Associate Dean for Medical Education and Competency Achievement
and Assistant Professor of Medicine
Chicago, Illinois
Chapter 34: Female Genital Symptoms
Heather Heiman, MD
Chicago, Illinois
Chapter 10: Sinusitis, Bronchitis, and Pharyngitis
Mitchell S. King, MD
Associate Professor of Family Medicine
Associate Dean for Academic Affairs
University of Illinois College of Medicine at Chicago
Chicago, Illinois
Chapter 11: Abdominal Pain
CONTRIBUTORS xi
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Elizabeth Nguyen Kirchoff, DO
Resident
McGaw Northwestern Family Medicine Residency
Chicago, Illinois
Michael Kornfeld, MD
Instructor, Department of Medicine
Division of Hospital Medicine
Chicago, Illinois
Chapter 5: Preoperative Evaluation
Robert F. Kushner, MD
Professor, Department of Medicine
Chicago, Illinois
Chapter 25: Obesity
Cynthia A. Lagone, MD
Clinical Instructor, Department of Medicine
Chicago, Illinois
Chapter 14: Dermatology in Primary Care
Martin S. Lipsky, MD
Regional Dean and Professor
University of Illinois College of Medicine at Rockford
Rockford, Illinois
Chapter 12: Diarrhea
Chapter 23: Diabetes
Chapter 29: Geriatric Conditions
Janice A. Litza, MD
Assistant Professor
Chicago, Illinois
Chapter 26: Well-Child Visit
xii CONTRIBUTORS
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Melissa Yvette Liu, MD
Chief Resident
Chicago, Illinois
Gregory Makoul, PhD
Chief Academic Officer
Senior Vice President for Innovation and Quality Integration
Saint Francis Hospital and Medical Center
Hartford, Connecticut
Gary J. Martin, MD
Raymond J. Langenbach, MD Professor of Medicine and Vice Chair for
Faculty Affairs and Education, Department of Medicine
Chicago, Illinois
Chapter 4: Prevention and Screening
Chapter 6: Headache
Chapter 9: Chest Pain
Chapter 18: Somatization
Chapter 19: Congestive Heart Failure
Chapter 24: Hyperlipidemia
Helen Gartner Martin, MD
Division of Pulmonary and Critical Care Medicine
Chicago, Illinois
Chapter 7: Common Sleep Disorders
Kevin T. McVary, MD
Director, Center for Sexual Health and Director Prostate Diseases
Minimally Invasive Program
Associate Professor of Urology
Chicago, Illinois
Chapter 16: Erectile Dysfunction
CONTRIBUTORS xiii
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Michael J. Moore, MD
Division of Pulmonary and Critical Care Medicine
Chicago, Illinois
Chapter 21: Asthma
Chapter 22: Chronic Obstructive Pulmonary Disease
David B. Neely, MD
Director, Undergraduate Education
Chicago, Illinois
Chapter 20: Hypertension
Kevin OLeary, MD
Division of Hospital Medicine
Chicago, Illinois
Sandra A. Pagan, MD, MPA
Resident
Chicago, Illinois
Chapter 27: Fever in Children
Karin G. Patterson, DO
Clinical Faculty
St. Vincents Family Medicine Residency Program
Indianapolis, Indiana
Chapter 27: Fever in Children
Michael J. Polizzotto, MD
Assistant Professor of Family Medicine
Rockford, Illinois
xiv CONTRIBUTORS
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Eduard Porosnicu, MD
Director, Palliative Care Service
Clinical Assistant Professor of Medicine
State University of New York Downstate Medical Center
Brooklyn, New York
Chapter 15: Fatigue
Aparna Priyanath, MD
Chicago, Illinois
Chapter 30: Benign Breast Disease
Douglas R. Reifler, MD
Associate Professor of Medicine
Chicago, Illinois
Chapter 17: Anxiety and Depression
Professor and Chair
Chicago, Illinois
Editorial review
Phillip E. Roemer, MD
Chicago, Illinois
Adam D. Rosenfeld, DO
Resident
Chicago, Illinois
CONTRIBUTORS xv
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Jeffrey S. Royce, MD
Director, Swedish-American Center for Headache Care
Clinical Assistant Professor of Family Medicine
Rockford, Illinois
Herbert Sier, MD
Associate Chief of Geriatric Medicine
Division of Geriatrics
Chicago, Illinois
Lenore F. Soglin, MD
Instructor, Department of Medicine
Chicago, Illinois
Chapter 37: Intimate Partner Violence
Christopher Varona, DO
Resident
Chicago, Illinois
xvi PREFACE
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xvii
CONTENTS
P A R T
one
OVERVIEW OF PRIMARY CARE 1
CHAPTER 1 OFFICE MANAGEMENT AND THE PRINCIPLES OF DIAGNOSIS
AND MANAGEMENT OF AMBULATORY PATIENTS 1
CHAPTER 2 COMMUNICATING WITH PATIENTS 8
CHAPTER 3 CLINICAL EPIDEMIOLOGY AND PRINCIPLES OF QUANTITATIVE
DECISION MAKING 17
CHAPTER 4 PREVENTION AND SCREENING 47
CHAPTER 5 PREOPERATIVE EVALUATION 59
P A R T
two
DIAGNOSIS AND MANAGEMENT OF COMMON OUTPATIENT
SYMPTOMS 77
CHAPTER 6 HEADACHE 77
CHAPTER 7 COMMON SLEEP DISORDERS 91
CHAPTER 8 DIZZINESS 107
CHAPTER 9 CHEST PAIN 118
CHAPTER 10 SINUSITIS, BRONCHITIS, AND PHARYNGITIS 126
CHAPTER 11 ABDOMINAL PAIN 142
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xviii PREFACE
CONTENTS xviii
CHAPTER 12 DIARRHEA 167
CHAPTER 13 MUSCULOSKELETAL PAIN 180
CHAPTER 14 DERMATOLOGY IN PRIMARY CARE 199
CHAPTER 15 FATIGUE 221
CHAPTER 16 ERECTILE DYSFUNCTION 233
CHAPTER 17 ANXIETY AND DEPRESSION 250
CHAPTER 18 SOMATIZATION 260
P A R T
three
DIAGNOSIS AND MANAGEMENT OF COMMON
CHRONIC ILLNESSES 269
CHAPTER 19 CONGESTIVE HEART FAILURE 269
CHAPTER 20 HYPERTENSION 278
CHAPTER 21 ASTHMA 294
CHAPTER 22 CHRONIC OBSTRUCTIVE PULMONARY DISEASE 309
CHAPTER 23 DIABETES 324
CHAPTER 24 HYPERLIPIDEMIA 337
CHAPTER 25 OBESITY 346
P A R T
four
DIAGNOSIS AND MANAGEMENT OF AGE-RELATED
CONDITIONS 359
CHAPTER 26 WELL-CHILD VISIT 359
CHAPTER 27 FEVER IN CHILDREN 376
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PREFACE xix
xix CONTENTS
CHAPTER 28 OTITIS MEDIA IN CHILDREN 391
CHAPTER 29 GERIATRIC CONDITIONS 400
P A R T
five
WOMENS HEALTH 409
CHAPTER 30 BENIGN BREAST DISEASE 409
CHAPTER 31 PRECONCEPTION CARE 418
CHAPTER 32 HORMONE REPLACEMENT THERAPY 426
CHAPTER 33 MENSTRUAL DISORDERS 438
CHAPTER 34 FEMALE GENITAL SYMPTOMS 450
CHAPTER 35 PAP SMEAR AND CERVICAL CANCER SCREENING 462
CHAPTER 36 OSTEOPOROSIS 472
CHAPTER 37 INTIMATE PARTNER VIOLENCE 482
APPENDIX A ANSWERS TO SELF-TEST QUESTIONS 489
APPENDIX B ABBREVIATIONS 505
APPENDIX C KEY CONTACTS AND NOTES 512
INDEX 517
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OVERVIEW OF
PRIMARY CARE
OVERVIEW OF
PRIMARY CARE
1
one
P A R T
I. Introduction to Ambulatory Medicine
A. The majority of medical care is received in the outpatient setting.
B. The ambulatory physician is what most patients consider their
doctor.
II. Differences in Inpatient Versus Ambulatory Care
A. Inpatient care focuses on curing or resolving an acute condition,
such as an exacerbation of congestive heart failure.
B. Ambulatory care may focus on curing or resolving an acute
medical problem such as treating a bacterial sinus infection.
OFFICE MANAGEMENT AND
THE PRINCIPLES OF
DIAGNOSIS AND
MANAGEMENT OF
AMBULATORY PATIENTS
CHAPTER
1
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2 one OVERVIEW OF PRIMARY CARE
P A R T
C. Further goals of ambulatory care include:
1. Providing longitudinal care of a patients chronic medical
problems; e.g., diabetes over years, not days
2. Preventing further health problems
a. Primary prevention by screening for and treating
hypertension to prevent Coronary Heart Disease
b. Secondary prevention by lowering the cholesterol of a
patient who is post myocardial infarction (MI) with
medication to prevent a future MI.
3. Improving the patients quality of life
D. Diagnosis
1. Inpatient care typically involves a disease process that is
already differentiated, and the focus is on treating that process;
e.g., intravenous (IV) antibiotics for pneumonia.
2. Ambulatory care typically involves undifferentiated symptoms;
e.g., fatigue, cough. The goal is to make a correct diagnosis in a
cost-conscious manner, which often leads to symptoms being
treated presumptively.
III. Principles of Diagnosis and Treatment
A. Clinical presentation
1. Patients may present with symptoms that need a diagnosis and
treatment plan.
2. Patients may present for the management of a known health
problem.
3. Patients may present for a prevention visit.
B. History and physical
1. Diagnosis-specific
2. Interview should focus on the presenting symptoms
i. Using a mnemonic is helpful to focus the history of present
illness (HPI) and to minimize the chance of omitting impor-
tant information.
ii. Example: OLDCARTS
O Onset of symptoms
L Location
D Duration
C Characteristics
A Aggravating and alleviating factors
R Radiation
T Treatment
S Significance
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3. Physical examination needs to be focused on organ system
related to the complaint.
i. Use your initial differential diagnosis to focus your physical
examination.
4. Manage a chronic disease
a. Interview should:
i. Explore how the disease affects the individual
(1) Does an asthmatic patient have any nighttime
symptoms?
(2) Does a diabetic patient have any hypoglycemic
episodes?
ii. Determine the patients response to previous treatments
iii. Monitor compliance with prescribed treatments
iv. Monitor for side effects of treatment
b. Physical examination
i. It may be very brief, e.g, in a known hypertensive
patient, may include only checking blood pressure (BP)
and listening to the heart
c. Review the chart for results of recent tests, and identify
recent treatments the patient may have undergone.
d. Order needed testing.
e. Change the treatment plan as needed, and ensure the
patient understands the plan.
i. Patient understanding and compliance are essential in the
ambulatory setting
1 DIAGNOSIS AND MANAGEMENT OF AMBULATORY PATIENTS 3
C H A P T E R
Use the teach-back technique by having the
patient tell you the plan to ensure understanding.
5. Prevention
a. The interview needs to focus on a complete review of
systems (ROS), family history, and any risk factors the
patient may have, especially related to heart disease, cancer,
infections.
b. The physical examination should be complete.
c. Know the indications for routine health maintenance testing
(e.g., Pap smears, mammograms, colonoscopies, immuniza-
tions), and schedule appropriately.
d. Counsel patients on the role of a healthy diet and exercise
program for their long-term health.
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C. Diagnostic and therapeutic plan
1. Pace of ambulatory care can be hectic.
a. Each return patient is seen and managed in 1020 minutes.
New patients are often given longer appointments.
2. Physicians need to assemble clinical information from the
history, physical examination, and old records efficiently.
3. The differential diagnoses should be grouped into 1) most
likely, 2) most worrisome, and 3) least likely.
4. A plan needs to be formulated in a stepwise fashion regarding
diagnosis and treatment.
a. Serial testing versus parallel testing
i. In the inpatient setting parallel testing is often
undertaken.
(1) Patients are often very ill, and determining a
diagnosis quickly is imperative.
(2) Hospital care is very expensive, and there is pressure
to limit the length of stay for each patient.
(3) Ordering several tests at once is an efficient way to
achieve both these goals.
(A) For example, a patient with chest pain and short-
ness of breath undergoes simultaneous testing for
cardiac ischemia and pulmonary embolus.
ii. In the outpatient setting, serial testing is often undertaken.
(1) Cost-effective care is a priority.
(2) A test or treatment plan is ordered, and the results are
analyzed prior to further testing.
(3) Diagnostic studies that are minimally invasive are
preferred.
(4) Symptoms are often treated empirically, based on a
presumptive diagnosis.
(A) For example, a young female with 1 day of dysuria
without fever may be treated with antibiotics for
presumed cystitis without any further testing.
(5) A treatment failure or worsening of symptoms may
then prompt further testing.
D. Management
1. Reevaluate the patient after initial testing and treatment.
2. Educate and advise patients on their symptoms, disease
process, and goals of therapy.
P A R T
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IV. Role of Students
A. Learn to focus on a specific complaint.
1. Interview and examine patients in a concise manner appropriate
to specific complaints.
2. Formulate a diagnostic hypothesis without laboratory or radio-
logic testing.
3. Learn to treat symptoms when appropriate.
4. Learn to follow a patients response to treatment.
a. Monitor for side effects to medications.
b. Monitor for compliance.
c. Learn to adjust treatment based on the above factors.
B. Prevention
1. Know how to modify risk factors for chronic diseases.
a. This is especially important for risks related to heart
disease, stroke, cancer, and infections.
2. Learn to counsel patients effectively to promote behavioral
change.
a. Effectively counsel a patient on smoking cessation.
b. Give appropriate dietary and exercise advice.
c. Effectively and empathetically give advice on how to limit
sexually transmitted infections.
d. Improve patients compliance with health maintenance issues.
C. Time management
1. Learn the benefits of reviewing a patients chart to improve
efficiency and quality of the visit.
2. Learn to set the agenda based on office visit type: 1) chronic
disease management; 2) new problem; or 3) prevention issue.
3. Learn to help an office run efficiently.
a. Having a student in the office slows down the flow of
patients and can upset patients.
i. A student typically adds an hour of work to the attending
physicians day.
ii. Most physicians are not paid or are paid nominally to
have a student in their office.
iii. Patients present to see their doctor and are often fearful
when a student is present.
b. There are ways to alleviate time pressures and patients fears.
i. Alleviate tension with patients by letting them know that
the attending physician is present and will see them.
C H A P T E R
1389_Ch01_001-007 2/2/09 1:21 PM Page 5
(1) Say, e.g., Hi. My name is John Doe. I am a medical
student working with Dr. X. Dr X asked me to get
started and he/she will be in shortly.
(2) This statement can allay the patients fears and let
them know that they will see their doctor.
ii. Perform bedside presentations as often as possible.
(1) Patients enjoy learning from this interaction.
(2) It improves face time with the attending physician
and avoids the need to repeat the HPI for the attending
physician.
(3) It saves time overall.
iii. Offer to move on to the next patient while the attending
physician is finishing charting.
iv. Orient yourself to the triage and rooming nurses to help
facilitate patient flow.
V. Learn What It Means to Be Someones Doctor
A. Observe the attending physicians interactions with patients the
physician has known for many years.
1. Observe to see how the attending physician makes a personal
connection with patients.
a. The physician may relate by talking about common
hobbies, sports.
b. The physician may review the chart to refresh his/her
memory about the patients recent life stressors. Employment
changes and marriage issues are important themes.
P A R T
Understand the broader context of your contact
with patients: their work, their family life, their
chronic illnesses (if any).
B. Learn the role of work and family life in a patients long-term
health.
1. Review a patients chart to see how work and family life
stressors have affected health.
a. Job losses may lead to difficulty purchasing needed medica-
tions or inability to see a physician for periods of time.
b. Family stressors (especially the illness of a loved one) can
affect a patients compliance with a medical regimen.
1389_Ch01_001-007 2/2/09 1:21 PM Page 6
2. Review a patients chart to see how medical illnesses have
affected employment and family life.
a. Sometimes patients need to modify their job, given their illness.
b. A patient on dialysis may not be able to continue with a job
that requires travel.
C H A P T E R
MENTOR TIPS DIGEST
Use the teach-back technique by having the patient tell you
the plan to ensure understanding.
Learn what it means to be someones doctor. Understand
the broader context of your contact with patients: their work,
their family life, their chronic illnesses (if any).
Chapter Self-Test Questions
Fill in the answers. When youre done, check your answers in Appendix A.
1. List 23 life stressors that may negatively affect a patients management
of his/her chronic illness.
_____________________________________________________________
_____________________________________________________________
_____________________________________________________________
2. Patients can be nervous about medical students because patients want
to know that they will still see their doctor. Write an example of how
you can introduce yourself in a way that allays patient fears:
_____________________________________________________________
_____________________________________________________________
_____________________________________________________________
3. List 23 differences in general approach between outpatient care and
inpatient care.
_____________________________________________________________
_____________________________________________________________
_____________________________________________________________
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8
COMMUNICATING
WITH PATIENTS
Phillip E. Roemer, MD, Gregory Makoul, PhD,
and Raymond H. Curry, MD
CHAPTER
2
I. Overview
A. Communication: a transactional process in which messages are
filtered through the perceptions, emotions, and experiences of
those involved
B. Increasing volume of medical literature strongly suggests that effec-
tive communication is associated with improved patient outcomes
1. An accurate diagnosis is more frequently made when the
history is obtained effectively and directly from the patient.
2. Effective communication leads to improved adherence to the
treatment plan and, in some studies, better physiologic
outcomes (e.g., blood pressure control).
3. Effective communication empowers patients and allows them
to take responsibility for their health.
C. Physician education in communication skills shown to result in
better patient satisfaction and even reduction in malpractice suits
D. Better communication makes patient-physician encounter more
productive and rewarding for both the patient and physician
II. Structured Framework Is Key to Effective Interview
A. SEGUE is an acronym that outlines the transition through the
stages in the patient interview. Box 2.1 shows the basic meaning.
The text below discusses each idea in more detail.
1. Set the stage
a. When entering the room, greet your patient appropriately,
which, unless you know the patient well, generally involves
saying both the patients name and your name. For instance,
1389_Ch02_008-016 2/2/09 1:21 PM Page 8
if Dr. Robert Franklin is meeting Ms. Jane Smith, we
suggest that he say: Jane Smith? Hi, Im Bob Franklin.
Adopting this strategy of using parallel identity terms
communicates respect and reciprocity.
b. Be sure to provide for a private setting by shutting the
door/drawing the curtain and asking the patient if others
in the room may stay. There are several strategies for
establishing the reason for the visit, including What can
I do for you? How can I help you today? What brings
you in today?
c. Listening skills
2 COMMUNICATING WITH PATIENTS 9
C H A P T E R
Outline an agenda for the visit during the first few
minutes.
Allow the patient to speak without interruption,
especially at the beginning of the encounter.
i. This listening usually takes only a minute or two and pro-
vides the best opportunity for patients to make sure you
have heard what they came to say.
ii. Your careful listening during this phase can also be an
invaluable opportunity to discern nuances of the patients
perceptions and expectations and other aspects of their
affective and psychological state.
d. Determining an agenda
BOX
2.1
The SEGUE Approach to Communicating With Patients
Set the stage
Elicit information
Give information
Understand the patients perspective (and show the patient that you
understand)
End the encounter
1389_Ch02_008-016 2/2/09 1:21 PM Page 9
P A R T
i. What else can I do for you? Is there anything else you
would like to discuss? This efficiently establishes an
outline for the visit and allows the patient to highlight
concerns, which can then be prioritized early in the
encounter. Otherwise, patients may delay additional
concerns until the end of the encounter when you may
not be able to handle them effectively. Accomplishing
this task will facilitate a more organized encounter.
2. Elicit information
a. It is important to obtain information both about the patients
condition (i.e., symptoms) and the patients perceptions of the
health problem.
i. What does the patient believe is causing the symptoms?
ii. What are the patients major concerns about the problem
(even unspoken concerns)? e.g., with headaches: Are
you concerned about what they might mean? Well,
one of my coworkers was just diagnosed with a brain
tumor.
iii. Explore the physical and physiologic factors contributing
to the patients symptoms. Do certain kinds of food
cause or worsen your headaches? Do the headaches
correlate with your menstrual cycle?
iv. Explore psychosocial and emotional factors influencing
the patients condition. Is your headache worse during
certain times of the day or week? Is it related to work?
Assess how the problem affects the patients life. How
do your headaches limit your activities at home and
work?
v. Has the patient already attempted to address the problem?
Review antecedent treatments to better determine the
patients perspective on the condition. What have you
tried to relieve your headaches? What treatments are
acceptable to the patient? For example, many people prefer
not to take even over-the-counter medications. What is
the patient willing to do to improve the situation (e.g.,
exercising regularly to better control diabetes or reducing
fat intake in order to lower cholesterol)? There are many
effective strategies for eliciting information, as discussed
below.
1389_Ch02_008-016 2/2/09 1:21 PM Page 10
b. Asking open-ended questions allows patients to tell you in
their own words what is wrong.
i. The use of close-ended questions is also appropriate
when you need to focus on a specific point. Do you ever
experience nausea? How many cigarettes do you smoke
daily?
ii. Avoid leading questions. You dont have any chest pain,
do you? Answers formulated by the patient are much
more accurate and unbiased.
iii. Listen attentively at all times, and allow the patient
uninterrupted time to speak.
iv. Repeatedly check and clarify information. So let me
recap to make sure I understand: You have been experi-
encing pressure in the middle of your chest on and off
for the last 6 weeks associated with nausea and shortness
of breath?
C H A P T E R
Listen carefully and actively.
(1) Give the patient your undivided attention.
Patients satisfaction and sense of well-being
have been shown to correlate more closely with
the quality of the attention given them by the
physician than with the quantity of time devoted
to the encounter.
3. Give information
a. Communication involves sending, giving, or exchanging
(information, ideas, etc.). The physicians role includes
giving information as well as obtaining it. Information is
better provided if it is presented at the level of understanding
of the patient. Explain in laymans terms the rationale behind
your diagnosis and recommendations for further testing and
treatment
b. Review findings of the physical examination and laboratory
tests in the context of the patients situation. The pain in
your upper belly and the findings from your recent tests
strongly suggest that you have something called gastroe-
sophageal reflux disease.
1389_Ch02_008-016 2/2/09 1:21 PM Page 11
c. Encourage patients to ask questions about their problem.
Doctor, what causes reflux disease?
d. Teach the patient about the body and the condition. A valve
between your stomach and esophagus, the tube that leads
from your mouth to your stomach, leaks and allows stomach
acid to back up into the esophagus causing your heartburn
pain. Use written diagrams to more concretely describe a
patients problem
e. Review recommendations for improving the patients
situation. There are several strategies for helping your con-
dition. Lets review these, and I will also provide you with
some written information. In addition, I believe this medica-
tion should help.
f. Explain the likely benefits of treatment options. This
antacid medication should reduce the acid in your stomach
and the acid that then refluxes into your esophagus, reducing
the pain you are experiencing.
g. Explain likely and possible side effects of treatment. Most
people tolerate this medication without problems. Possible
side effects include cramping and diarrhea.
h. Acknowledge other possible diagnoses and symptoms
with which to be concerned. This encourages an interactive
encounter and allows the patient more control. If your
cough does not improve using these treatments for acid
reflux, then we should consider other possible problems
such as asthma or other gastrointestinal disorders. Please
contact me if you do not have any improvement over the
next 2 weeks.
4. Understand the patients perspective (and show the patient that
you understand)
a. Most important: acknowledge the patients accomplish-
ments, progress, and challenges. Its great that youve been
able to stop smoking. Keep it up!
b. Try to make a link between the patients perspective of the
situation and your recommendations. You mentioned that
your headache seems to worsen when you are pressured at
work. Can you think of any opportunities for reducing your
stress level at work, such as relaxing or exercising during
your breaks?
P A R T
1389_Ch02_008-016 2/2/09 1:21 PM Page 12
c. Discuss improvement or worsening of patients situation in
the context of your findings. Acknowledge challenges to
improving the patients circumstances, e.g., financial barriers.
Explore your patients expectations and goals for treatment
and/or prevention.
5. End the encounter
a. At the end of the encounter, ask if there is anything else the
patient would like to discuss. Major concerns will have been
addressed early on when setting the agenda for the visit.
b. Review the next steps with the patient. Schedule next visits
or tests. It is very important to provide hope as well as
expectations in more serious situations and when bad news
is given. There are effective options for approaching this
kind of cancer, and many people have been treated
successfully.
B. Utilizing effective strategies for communication
1. One way to facilitate better communications is to make a per-
sonal connection. This provides a more comfortable environ-
ment for communication. I understand how stressful caring for
your children can be. I also have two little ones at home.
2. Pay attention to nonverbal messages you are sending the
patient as well as those you receive from the patient. A judg-
mental tone of voice will often reduce a patients willingness to
speak freely with you. Patients will often communicate how
they feel without speaking or before they speak. For example, a
patient pacing the room with arms folded may suggest angry
feelings or anxiety.
3. Maintain a respectful tone at all times. This conveys to the
patient that you care and that you are serious about helping.
Express caring, concern, and empathy with your words, voice
inflections, and body posture. Patients reactions to your
recommendations often reflect how you say something rather
than what you say.
C. Difficult encounters
C H A P T E R
It is especially important in difficult encounters to stop
and think for a moment about the communication skills
and strategies you can use to facilitate the interaction.
1389_Ch02_008-016 2/2/09 1:21 PM Page 13
1. Angry patientneed to defuse intense feelings
a. Acknowledge the patients apparent feelings.
b. Determine the reason for anger.
c. Provide an explanation, if pertinent.
d. If the patient has reason to be angry with you,
apologize.
e. Reinforce your commitment to help.
2. Breaking bad news
a. Provide a comfortable and private setting in which
to meet.
b. Establish how much information the patient has about the
current condition, and provide updates before communicat-
ing the bad news.
c. Provide the news in a clear and concise way.
d. Allow for questions, and give information in small bits.
e. Discuss the next steps.
f. Offer hope in some form.
g. Plan for follow-up.
3. Taking a sexual history
a. Start by telling the patient why you are asking the
questionshealth risks or sexual health/function.
b. Do not assume anything regarding sexual orientation or
practices.
c. Remember to be nonjudgmental when asking questions
and receiving answers.
4. Talking to patients from different cultures
a. It is better to ask questions than resort to stereotypesget
the patients perspective on the problem and its cause.
b. Be sure to confirm your interpretations.
c. Check the patients understanding and acceptance of your
recommendations.
P A R T
MENTOR TIPS DIGEST
Allow the patient to speak without interruption, especially at
the beginning of the encounter.
Outline an agenda for the visit during the first few minutes.
1389_Ch02_008-016 2/2/09 1:21 PM Page 14
Resources
Makoul G. The SEGUE Framework for teaching and assessing communi-
cation skills. Patient Education & Counseling 45:2334, 2001.
Reviews several years of experience with the SEGUE Framework, the
most widely used model for teaching and assessing communication
skills in North America.
Makoul G (for the Bayer-Fetzer Conference on Physician-Patient Commu-
nication in Medical Education). Essential elements of communication in
medical encounters: The Kalamazoo consensus statement. Academic
Medicine 76:390393, 2001.
Reports consensus of leading educators and researchers regarding
communication tasks that should be accomplished in medical encounters.
Platt FW, Gordon GH. Field Guide to the Difficult Patient Interview.
Philadelphia: Lippincott, Williams & Wilkins, 2004.
Circle the correct answer. After you have responded to the questions,
check your answers in Appendix A.
1. Fill in the expanded meaning of the SEGUE acronym.
S
________________________________________________________
E
________________________________________________________
G
________________________________________________________
U
________________________________________________________
E
________________________________________________________
C H A P T E R
Listen carefully and actively.
It is especially important in difficult encounters to stop and
think for a moment about the communication skills and
strategies you can use to facilitate the interaction.
1389_Ch02_008-016 2/2/09 1:21 PM Page 15
2. When asking questions of a patient, one style of question that is usu-
ally not appropriate is a style in which you are more or less coaching
the patient to give you the answer that you expect. This style of ques-
tion is called what?
_________________________________________________________
.
3. Sometimes patients biggest concern is something they are hesitant to
bring up, e.g., presenting with headaches. You may ask, Are you con-
cerned about what they might mean? What do you think this patient
may be worried about, more than minor pain relief?
_________________________________________________________
P A R T
See the testbank CD for more self-test questions.
1389_Ch02_008-016 2/2/09 1:21 PM Page 16
17
CLINICAL EPIDEMIOLOGY
AND PRINCIPLES OF
QUANTITATIVE DECISION
MAKING
*
Robert M. Golub, MD
CHAPTER
3
I. Consider These Two Problems
A. Problem 1: In the emergency room you are seeing a 32-year-old
female who yesterday developed pleuritic chest pain and shortness
of breath. She has had a painful, warm, and swollen left calf for
the last 3 days, with tenderness and edema on examination. She
takes oral contraceptives (OCPs) and smokes. In addition to the
leg findings, her examination is notable for a heart rate of 112;
when she was in the office for a Pap smear 2 weeks ago her heart
rate was 88. Several questions arise:
1. What is the likelihood that she has had a pulmonary
embolism (PE)?
2. Does taking an OCP or smoking make her predisposed
to a PE?
3. Would a D-dimer test help to make the diagnosis?
4. What is the best treatment for her?
5. If she has had a PE, what problems can she expect in the
future?
B. Problem 2: Should you be advocating screening mammograms
for your patients between the ages of 40 and 50 years?
*Data used in examples have been excerpted from the medical literature. However, they
have been adapted for teaching purposes; the risk measures calculated in these examples are
therefore different from those reported in the articles, and the reader should refer back to the
original study for the true risk measures as well as confidence intervals.
1389_Ch03_017-046 2/2/09 1:20 PM Page 17
P A R T
II. Overview
A. These are the types of questions that you face in making
decisions with all of your patients. The approaches that you
use to answer them in the best way come from the discipline of
clinical epidemiology, which is the application of epidemio-
logic principles and methods to problems encountered in
clinical medicine.
B. The core idea is that issues such as diagnosis and treatment out-
come are uncertain for individual patients, are therefore expressed
as probabilities, and are best estimated by referring to past experi-
ence with groups of similar patients. In other words, information
is taken from (ideally large) studies and applied one-on-one with
each patient. This requires understanding and being able to use
certain basic quantitative methods.
C. These decisions should be made using the approach of evidence-
based medicine. This involves:
1. Framing the question in a precise way that will facilitate
finding needed information.
2. Accessing that information efficiently (e.g., searching primary
literature, reading textbooks, speaking to local experts).
3. Evaluating the quality of that information critically, using
methodical approaches to determine its validity.
4. Determining how to apply valid information to the specific cir-
cumstances of the individual patient.
D. This chapter briefly considers the key concepts of clinical
epidemiology as they relate to these common questions, the
types of measures you will encounter, and how to apply them. A
textbook of clinical epidemiology, such as that by Fletcher and
Fletcher,
1
will provide more background. Methodical approaches
to critiquing the studies you will be reading are essential, but they
go beyond the scope of this book; a number of texts address these
well, such as that by Guyatt and Drummond.
2,3
III. Topics of Clinical Epidemiology and Medical Decision
Making. Problem 1 illustrates the categories of typical epidemiologic
questions. To understand the measures used with each, it is helpful to
divide them into questions of frequency, diagnosis, and association.
A. How common is a condition? (frequency and prevalence)
1. For Problem 1, in deciding whether to pursue the diagnostic
possibility of a PE, you should be interested in knowing the
1389_Ch03_017-046 2/2/09 1:20 PM Page 18
probability that someone who presents like this patient has a
PE. When considering the likelihood of disease in a patient,
the starting point is usually the prevalence of the disease in the
relevant population, which is defined as:
number of people with a condition
number of people at risk for having a condition
2. The best way to estimate this prevalence is a cross-sectional
study that looks at a population of people similar to the patient
to find out what percentage had a PE and what percentage had
another diagnosis. In looking for prevalence studies, try to find
ones in which the denominator (population at risk) matches
your patient as closely as possible. For example, look for
studies that were done only on people who presented as
outpatients with pleuritic pain, or only on women, or only on
women who smoke and take OCPs. Unfortunately, this is not
always possible, and in applying studies in which the popula-
tion is different from your patient you have to use your judg-
ment to adjust the probability up or down.
3. It is important not to confuse prevalence (which is a snapshot
of a population at a single point in time) with incidence, which
is a measure of the number of new cases in a population that
occur over a specified length of time and is discussed later in
the chapter.
B. Does my patient have a particular disease? (choice and interpre-
tation of diagnostic tests) To decide whether a particular diagnostic
test is useful to do, you need to combine three pieces of informa-
tion: the treatment threshold for the diagnosis under consideration,
the test characteristics of the diagnostic test under consideration,
and your patients pre-test probability (the likelihood of disease
before getting new information).
1. The treatment threshold and the threshold model
a. In thinking about diagnostic tests, it is useful to conceptualize
your patient having the disease as a probability falling along
a continuum between 0 (absolute certainty that she does not
have it) and 1 (absolute certainty that she does have it)
(Fig. 3.1A). As you gain new information about the patient,
whether from additional history, physical examination find-
ings, or test results, the patient moves right or left along the
3 CLINICAL EPIDEMIOLOGY 19
C H A P T E R
1389_Ch03_017-046 2/2/09 1:20 PM Page 19
continuum as you become more certain she does or does not
have the disease of interest (Fig. 3.1B). One is almost never
100% sure about presence or absence of disease because
information is rarely perfect. Given this, how certain do you
need to be that someone has a disease before you are willing
to label the patient with it and to take the necessary action?
Because this could involve mistakenly treating some people
who in fact do not have disease or failing to treat some
people who do have it, you must consider the tradeoffs
between the benefits and risks of treatment for those with
and without disease.
b. In general, if the benefit of treatment is high and/or the risks
are low, you are willing to treat someone even if there is a low
probability the patient has the disease. Conversely, if the
benefit of treatment is relatively low and/or the risks are high,
you require a high probability that the patient has the disease
before deciding to treat. These tradeoffs are incorporated in
the treatment threshold: the lowest probability that someone
could have a disease whereby, in the absence of any further
available information, you would be willing to treat the
patient as if he or she did (Fig 3.1C) (Chapter 9 of Sox et al
4
).
If you can estimate the relative risks and benefits, the formula
for the treatment threshold is:
risk
benefit
risk
1
benefit
c. For example, if you consider the risk of complication from
anticoagulation against the benefit of preventing a future pos-
sibly fatal PE, a reasonable risk/benefit ratio might be 1/5. This
would result in a treatment threshold of 0.17. This means
that, in the absence of further information, if you believed
your patients probability of a PE was any less than 0.17 you
should not anticoagulate, despite the possibility of missing
someone with a PE; alternately, if probability is any greater
than 0.17 (even 0.18), you should anticoagulate, recognizing
that you may be unnecessarily anticoagulating some people
without a PE.
P A R T
1389_Ch03_017-046 2/2/09 1:20 PM Page 20
d. To decide whether to order a test or to interpret the test
results, you can then use the threshold model that says that
you should only perform a test if it could potentially move
C H A P T E R
FIGURE 3.1 The threshold model for choice and interpretation of test results.
Post-test
probability
Post-test
probability
Pre-test
probability
New
information
New
information
0 1.0
0 1.0
Dont treat Treat
Treatment threshold
0 1.0
Pre-test Post-test
Treatment threshold
0 1.0
Pre-test Post-test
Treatment threshold
0 1.0
Post-test Pre-test
Treatment threshold
0 1.0
Post-test Pre-test
Treatment threshold
0 1.0
Post-test neg Pre-test Post-test pos
0.17
Treatment threshold
.42 .72 .76
0 1.0
A
B
C
D
E
F
G
H
1389_Ch03_017-046 2/2/09 1:20 PM Page 21
you from a pre-test probability on one side of the threshold
to a post-test probability (the probability of a disease after
you have gained new information) on the other side of the
threshold. For example, the test shown in Figure 3.1D, in
which the patients pre-test probability is less than the
threshold, should not be done because a positive result
would not make you certain enough of the diagnosis to
change how you would label the patient. However, the test in
Figure 3.1E will change this if it is positive, and therefore it
is reasonable to perform. If you start with a pre-test proba-
bility above the threshold, you are interested in whether a
negative test will cross the threshold. Figure 3.1F shows a
test in which that will not happen; thus, the test should not
be used. In Figure 3.1G, the test will change how you treat
the patient and can give useful information.
e. To use this approach, you need to be able to calculate post-
test probability. Before you can do that, you have to know
the tests characteristics (which tell you how accurate the
test is) and your patients pre-test probability.
2. Test characteristics
a. Most tests in medicine are not perfect; those that are tend to
be invasive, expensive, or autopsies (usually not the ideal
diagnostic approach). The accuracy of an imperfect test is
measured in two ways: sensitivity/specificity and likelihood
ratios.
i. Sensitivity and specificity are determined by a cross-
sectional study of a population with and without disease,
as determined by everyone getting a gold-standard test
(a test that is considered to define presence or absence of
disease) and everyone getting the index test (the partic-
ular test of interest). By looking at the results as a
2 2 table (Fig 3.2), there are four subgroups: true
positives (disease present and index test positive), true
negatives (disease absent and index test negative), false
negatives (disease present but index test negative), and
false positives (disease absent but index test positive).
Sensitivity is then defined as the probability of a posi-
tive index test given the knowledge that someone actu-
ally has the disease. Specificity is the probability of a
P A R T
1389_Ch03_017-046 2/2/09 1:20 PM Page 22
C H A P T E R
Gold standard
Totals
Totals
Disease
present
Index
test
result
Positive
Negative
Sensitivity =
Pre-test probability (prevalence) =
Positive predictive value = post-test probability (+) =
Post-test probability () =
Negative predictive value = 1 post-test probability () =
Converting between probability and odds
Likelihood ratios, and odds-likelihood ratio calculation of post-test probability
a b
a + b
c + d
a+b+c+d a + b
a
a + c
a
a + b
Specificity =
d
b + d
c
c + d
d
c + d
a + c
a + b + c + d
probability
Odds =
1 (probability)
probability of a result given disease
Likelihood ratio =
probability of the same result given no disease
odds
Probability =
1+ (odds)
sensitivity
Likelihood ratio (+) =
1 (specificity)
prevalence
Pre-test odds =
Post-test odds = (pre-test odds) x (likelihood ratio)
Treatment threshold =
R
B
R
1 +
B
, where R is net risk (all types of harm) and B is benefits
=
1 (prevalence)
post-test odds
Post-test probability =
post-test odds + 1
pre-test probability
1 (pre-test probability)
1 (sensitivity)
Likelihood ratio () =
specificity
c + d
Disease
absent
True
positives
False
positives
c d
False
negatives
True
negatives
FIGURE 3.2 Formulas for diagnostic test use and calculating post-test
probability.
1389_Ch03_017-046 2/2/09 1:20 PM Page 23
negative index test given the knowledge that someone
does not have the disease. These criteria indicate how of-
ten the index test is correct if you start out knowing about
presence or absence of disease, but unfortunately this is
not the clinically important information. You need the op-
posite: what you are looking for, because you do not al-
ready have the knowledge about your patients presence
or absence of disease, is the probability that disease is
present given either a positive or negative test resultthe
post-test probability.
ii. Likelihood ratio is defined as
probability of a particular result given presence of disease
probability of the same result given absence of disease
(1) For a test that can only have a positive or negative
result, there are therefore two likelihood ratios: likeli-
hood ratio positive and likelihood ratio negative (see
Fig. 3.2). The better the test is, the higher the likeli-
hood ratio positive (infinity would represent a perfect
test) and the lower the likelihood ratio negative (0 would
represent a perfect test). Using likelihood ratios pro-
vides a second, often easier, way to calculate post-test
probability.
(2) Considering the D-dimer test, in one study
5
the measure
of accuracy was sensitivity 0.93, specificity 0.25.
From this, the likelihood ratio positive of 1.24, and
likelihood negative of 0.28 can be calculated.
b. Pre-test probability
i. As noted above, one common way to establish your
patients pre-test probability of disease is to find a study
that looks at prevalence of that disease in patients simi-
lar to yours. If such a study has not been done, you may
need to rely on an expert opinion. However, there are
many prediction rule studies in the literature that allow
you to determine a score for your patient based on clinical
characteristics and to translate that score into a proba-
bility. Using one published rule for a PE (Le Gal et al
6
),
a pre-test probability for a PE of 0.72 for this patient
could be calculated.
P A R T
1389_Ch03_017-046 2/2/09 1:20 PM Page 24
c. Calculating Post-Test Probability
i. Two ways to calculate this number are the tree method,
which uses sensitivity/specificity, and the odds-likelihood
ratio method.
d. Using the Tree Diagram (Fig 3.3)
i. Assume you begin with a large round number of patients
(e.g., 10,000) exactly like yours. You perform the
gold standard test for each member of this group, the pul-
monary angiogram, so that you could know for certain
whether each had had a PE. The pre-test probability of
0.72 would mean that 7200 would have disease, and
2800 would not.
C H A P T E R
10,000 patients exactly like yours
all get the gold standard test
Everyone
gets the
gold standard
test
Everyone
gets the
index test
7200
(Pretest
probability x 10,000) (10,0007200)
(Sensitivity
x 7200)
(Specificity
x 2800)
6696
True
positives
504
False
negatives
2800
Disease present by
positive gold
standard test
Index test
positive
Index test
negative
2100
False
positives
700
True
negatives
Index test
positive
Index test
negative
Disease absent by
negative gold
standard test
Post-test probability positive = = = 0.76
True positives
All positives
6696
6696 + 2100
Post-test probability negative = = = 0.42
False negatives
All negatives
504
504 + 700
FIGURE 3.3 The tree method of calculating post-test probability.
1389_Ch03_017-046 2/2/09 1:20 PM Page 25
ii. Assume all 10,000 patients also had a D-dimer test.
Sensitivity is 0.93; using the definition of sensitivity
above means that 93% of the 7200 with a PE (6696)
would have a positive test, leaving 504 with a PE having a
negative test. Similarly, using the specificity of 0.25 and
its definition, 25% of the 2800 without a PE (700) would
have a negative test, leaving 2100 without a PE having a
positive test.
iii. What is the post-test probability of a PE given a
positive result? This is the number of patients with a
PE, out of all of the patients with a positive test, or
6696/(6696 2100) 0.76. What is the post-test
probability of a PE given a negative result? This is the
number of patients who still have a PE, out of all of
the patients with a negative test, or 504/(504 700)
0.42. You now know what you should conclude about
the patients updated likelihood of a PE if you decide
to go ahead and do the D-dimer test. But should you do
the test in the first place? You need to return to the
threshold model with this new information. However,
there is an alternative way to get to the post-test proba-
bility that in some cases is easier: the odds-likelihood
ratio method.
e. Using Odds-Likelihood Ratio
i. Although uncertainty is usually expressed as a probabil-
ity, it can easily be converted to odds, which is defined
as the probability of an event occurring divided by
the probability of the same event not occurring. The
formulas for converting back and forth between
probability and odds are simple and are given in
Figure 3.2.
ii. The main reason to do this is that it gives you a very easy
way to calculate post-test probability. The formula is
post-test odds pre-test odds likelihood ratio, using
likelihood ratio positive or negative, depending on the
particular test result.
iii. Using the example of possible PE and D-dimer, convert
pre-test probability to pre-test odds:
P A R T
1389_Ch03_017-046 2/2/09 1:20 PM Page 26
pre-test odds 0.72/(1 - 0.72) 2.6
If the D-dimer test is positive:
post-test odds 2.6 1.24 3.2
To convert odds back to post-test probability:
probability 3.2/(1 3.2) 0.76
This is the same answer obtained by using the tree
method. Similarly, if the D-dimer test is negative:
post-test odds 2.6 0.28 0.73
Converting odds back to post-test probability:
probability 0.73/(1 0.73) 0.42
This is, again, the same answer obtained with the tree
method. Not only is the arithmetic somewhat easier
with this odds-likelihood ratio method, but it also
becomes very easy to substitute different pre-test odds
to see the effect of applying the same test to different
patients or to substitute different likelihood ratios to see
the impact of choosing different tests.
3. Applying this to the threshold model
a. After calculating the possible post-test probabilities, positive
and negative, what is done about doing the D-dimer test? The
probabilities are placed on the continuum, along with the
pre-test probability of 0.72 and the treatment threshold of
0.17 (Fig. 3.1H). In this case, even a negative D-dimer result
would be well above the treatment threshold, even if you
were not sure precisely what that threshold value should be.
Given this, your conclusion should be that the D-dimer test
would not be useful to do for the patient because it would
not change any action you would take. You would in fact
need a more accurate test or combination of tests, one that
would move you further to the left along the continuum, to
accomplish that.
b. In general, how far you move left along the continuum is
determined by the sensitivity of a test (or likelihood ratio
negative), so you need one with a higher sensitivity (or lower
C H A P T E R
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likelihood ratio negative); conversely, how far you move
right along the continuum is determined by the specificity
(or likelihood ratio positive).
4. Receiver operating characteristic (ROC) curve
a. Rather than consider sensitivity and specificity using a single
cutoff of positive versus negative for the index test, much
more information is gained by examining an ROC curve. The
cutoff level is varied, and the resulting sensitivity and speci-
ficity at each level are plotted against each other; it reveals the
inherent tradeoff between the two. Its value is in allowing you
the flexibility to choose where you want to set the cutoff for
your own patients and to know the resulting sensitivity and
specificity. It also allows you to compare two or more differ-
ent diagnostic tests for the same disease, because the best test
has the largest area under the curve.
b. An example of an ROC curve for D-dimer is shown in
Figure 3.4.
5
Traditionally the sensitivity is plotted on the
y axis from 0 to 1 and the specificity on the x axis from 1 to
0. The sensitivity and specificity that have been used so far
P A R T
100
200
500
1000
1500
1
0.8
0.93
0.42
0.6
0.4
0.2
0
1 0.8
0.73 0.25
0.6
S
e
n
s
i
t
i
v
i
t
y
Specificity
0.4 0.2 0
2000
3000
>8000
FIGURE 3.4 ROC curve for D-dimer, varying cutoff.
1389_Ch03_017-046 2/2/09 1:20 PM Page 28
correspond to setting a cutoff of 500 ng/dL for positive, but
you can now see what happens if you decide that a different
cutoff is more relevant for your own decision making. For
example, if you set a cutoff of 3000, you have improved
your specificity to 0.73, but you have traded that off for
a lower sensitivity of 0.42.
C. Is there an association? (risk, prognosis, treatment, and
prevention)
1. The other epidemiologic questions that occur with patients are
related to possible associations between some type of exposure
and some type of outcome, although what is considered expo-
sure and what is considered outcome changes depending on the
particular question. Various common measures of association to
express how strongly the two are related come from clinical
studies.
2. Risk
a. Does the presence of one factor increase (or decrease) the
likelihood of getting a particular disease or having a particu-
lar event? This is the question of risk. In Problem 1, you
want to know if either smoking or using OCPs is a risk
factor for having a PE.
b. For risk, exposure usually means having a risk factor among
a group of people who are initially free of the disease (non-
exposure is absence of the risk factor), and outcome is the
development of the disease or occurrence of the event of
interest. Look to see if there is a difference in the proportion
getting the outcome, depending on exposure or nonexposure.
Exposure might be an environmental toxin, a family history,
or a behavior. Sometimes you look at a protective risk;
for example, you might be interested in whether exposure to
bicycle helmet use actually decreases the likelihood of the
bad outcome of head trauma.
c. The two most common study designs to look for a risk
association are the cohort study and the case-control study.
i. A cohort study starts with a group of people who are free
of the outcome, some of whom have the exposure, and
others do not; they are then followed forward to see how
many develop the outcome and how many do not. This
information is placed in a 2 2 table (Fig. 3.5) The
following measures of association can be calculated:
C H A P T E R
1389_Ch03_017-046 2/2/09 1:20 PM Page 29
P A R T
Outcome
Totals
Totals
Present
O
+
Exposure
Yes (cohort 1)
E
+
No (cohort 2)
E
Absolute risk = Incidence

Absolute risk difference (AR) = (I ) (I )
Relative risk (RR) = =
Incidence (exposed)
Incidence (non-exposed)
Number needed to treat or harm =
1
Attributable risk
a b a + b
c+d
a + c
Incidence (exposed) = I
a
a + b
a
c
a + b
c + d
b + d
Absent
O
c d
E
+
=
Incidence (non-exposed) = I
c
c + d
E
E
+
=
Cohort studies or RCTs:
Incidence cannot be measured.
Therefore, relative risk cannot be measured.
It is estimated by the Odds Ratio (OR) = =
Case-control studies:
a
b
c
c x b
a x d
d
Outcome
Totals
Totals
Present
(case)
O
+
Exposure
Yes
E
+
No
E
a b a + b
c + d
a + c b + d
Absent
(control)
O
c d
FIGURE 3.5 Formulas for interpreting studies of risk, prognosis, treatment,
and prevention.
1389_Ch03_017-046 2/2/09 1:20 PM Page 30
(1) Incidence (absolute risk): This is the number of new
cases in a population, divided by the number of people
initially free of disease and potentially able to get it,
over a specified time interval. There is an incidence
for the cohort of people who were exposed (I
E
), and
another incidence for those not exposed (I
E
).
(2) Relative risk (RR): This is the ratio of the incidence
in those exposed divided by the incidence in those not
exposed; it represents the strength of the association.
An RR of 1 means no association, an RR 1 means
a direct association, and an RR 1 means an inverse
association. A risk factor that is linked to a bad outcome
(e.g., number dying) will have an RR 1, and a risk
factor that is protective against a bad outcome will
have an RR 1. (Sometimes studies give their out-
comes as good ones, e.g., using number surviving
instead of number dying, in which case the interpreta-
tion of RR is the opposite). Whereas RR may be
important in looking for risk associations, it may
distort the real risk for your own particular patient
who has a risk factor: if the baseline risk of a disease
in a population is very low, then you may find a very
high RR despite only a small actual risk for the indi-
vidual patient.
(3) Absolute risk difference (AR): This is the difference
in the incidence between those exposed and those not
exposed and represents the individual increased risk
that a person has by virtue of being exposed. This is
the number that is most relevant to decision making
with individual patients, but it often is not given
within a study, so you must be able to calculate it
yourself.
(4) Number needed to harm (NNH): This is 1/AR and
gives information that is analogous to AR but in a way
that may be more intuitive for both the patient and the
physician. A low NNH means that only a few people
need to be exposed for one person to have a bad out-
come, compared with a nonexposed person, and there-
fore means that an individual has a high risk of the
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outcome. Alternately, a high NNH means that many
people need to be exposed for one person to have the
bad outcome, and the individual therefore is at low
risk for the outcome. What constitutes a low NNH or
a high NNH? There is no single answer because it
depends on the outcome and its consequences, along
with the nature of reducing risk. For an outcome that
is relatively minor (transient pain that resolves
completely) or for which modifying the risk factor
would be expensive or would itself induce harm, one
would need a very low NNH to be concerned about it.
However, for an outcome that is devastating (death,
disabling myocardial infarction, or stroke) and a risk
factor that can be modified without itself causing
harm, you would then consider a much higher NNH,
one that is worth intervening.
i. As an example, consider a cohort study that looked at
the risk of PE in women who were taking oral contracep-
tives.
7
Among approximately 2186 women currently
using OCPs who were followed for 10 years, there were
5 new cases of PE; among approximately 82,924 women
who never used OCPs there were 76 new cases. After
putting this information in a 2 2 table (Fig 3.6), an
RR of 2.5, an AR of 0.0014, and an NNH of 714 can be
calculated. An interpretation of this would be that there is
a direct association between OCP use and a PE (RR 1),
but the magnitude of risk for an individual user is not
high. This is because the AR means that a user has only
a 0.0014 increased risk over 10 years of having a PE,
compared with a nonuser; the NNH means that for every
729 users, only 1 will have a PE over 10 years who
would not otherwise have had one if she did not use an
OCP. This is not a very high risk.
ii. An alternative to the cohort study design is the case-
control study, in which a group of participants who have
already had the outcome is entered (cases), along with
another group that is comparable with the exception that
the group has not had the outcome (controls). The
groups, having been defined on the basis of outcome, can
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then be observed backward to see how many in each
group had been exposed in the past. Place this informa-
tion in another 2 2 table (see Fig. 3.5). The advantages
of this over the cohort study are that it is generally less
expensive, faster (particularly important in the setting of a
toxin or infectious epidemic), and may be the only rea-
sonable way to deal with rare diseases (as there may be
too few outcomes to be able to have a successful cohort
study). The main disadvantage is that it is potentially
prone to many more biases in design and execution and
must be read very carefully for assessing validity. The
other disadvantage is that, because it involves participants
who already have or do not have the outcome incidence
of outcome cannot be measured; therefore, RR, AR, or
NNH cannot be measured. There is only one measure of
association:
iii. This is the odds ratio (OR). This is the ratio of the odds
of exposure among the cases divided by the odds of
exposure among the controls. If the study is valid, and
if the disease is relatively rare (prevalence 0.01 in the
C H A P T E R
Outcome
Totals
Totals
PE
Exposure
OCP users
OCP non-users
I =
Relative risk (RR) =
Absolute risk difference (AR) = 0.00229 0.00092 = 0.0014/10 years
Number needed to harm (NNH) = = 714/10 years
= 2.5
= 0.00229/10 years
5 2,181
5
2,186
No PE
76 82,848
2,186
82,924
92,110 81 85,029
E
+
I = = 0.00092/10 years
76
82,924
1
0.0014
0.00229
0.00092
E
FIGURE 3.6 Example of measuring risk in a cohort study.

1389_Ch03_017-046 2/2/09 1:20 PM Page 33
unexposed population), it is a close approximation of the
relative risk. Unfortunately, like the RR it does not allow
one to know what the actual increased risk is for the indi-
vidual patient, so it limits the practical information con-
siderably. (If you know the risk of disease in the baseline
population of patients similar to yours, you can infer the
AR and NNH, but this may be very inaccurate.)
(1) As an example, one case-control study also looked at
association between PE and OCP use.
8
The researchers
found 26 cases of PE and 111 comparable controls
without a PE. Among the cases, 17 were contraceptive
users; among the controls, 25 were contraceptive
users. Placing this information in a 2 2 table
(Fig. 3.7), you can calculate an odds ratio of 6.5.
The interpretation is that there is a direct association
between OCP use and a PE.
3. Prognosis
a. A prognosis attempts to predict the future for someone
who already has a disease. In Problem 1, you want to know
what this patient can expect in the future if she currently
has a PE.
b. For prognosis studies, exposure means having a disease
(nonexposure means not having the disease), and outcome
P A R T
Outcome
Totals
Totals
Cases
PE
Exposure
OCP users
OCP non-users
Odds Ratio (OR) = = 6.5 =
17 25
17
9
25
86
17 x 86
9 x 25
Controls
No PE
9 86
42
95
137 26 111
FIGURE 3.7 Example of measuring risk in a case-control study.
1389_Ch03_017-046 2/2/09 1:20 PM Page 34
means a later complication related to the disease. Prognosis
studies are sometimes called natural history studies,
although this can be misleading because patients are often
getting some treatment for the disease. Although there are
some similarities between risk and prognosis, the main
difference is that with risk the patients are exposed at a
time they are disease-free, and with prognosis the
exposure starts by having the disease. These terms also gen-
erally reflect different medical concerns. With risk, you are
most often interested in seeing if there is something that
can be modified with the goal of preventing a disease in the
future. With prognosis, there is rarely something that can be
modified, and you are more interested in knowing what to
expect, with the goal being able to inform the patient and be
alert for specific problems. In addition, outcomes tend to be
relatively infrequent in risk studies and relatively frequent in
prognosis studies.
c. Because prognosis considers future problems in someone
starting out with an exposure, these are always grouped into
cohort studies. The same measures of association as with
risk are often used: incidence, RR, AR, and NNH, compar-
ing people with a disease to those without a disease. Other
measures that are commonly used are survival (Kaplan-Meier)
curves and mortality rates (such as 5-year survival).
d. Also consider prognostic factors, specific characteristics of
patients with a disease that make it more or less likely that
they will have an outcome of interest. In that case, exposure
is defined as having a disease and having a prognostic
factor, and nonexposure is having the disease but not having
the prognostic factor.
e. One PE study
9
followed 2454 patients with acute PE and
found that the mortality rate at 3 months was 15.3%. The
investigators discovered there were several prognostic factors
that increased the likelihood of dying during this time:
age 70 years (RR 1.6), presence of cancer (RR 2.3),
congestive heart failure (RR 2.4), chronic obstructive pul-
monary disease (RR 1.8), hypotension (RR 2.9), and
tachypnea (RR 2.0).
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4. Treatment
a. Treatment considers if making an intervention will change
what happens to a patient. Although treatment includes
giving drugs or performing surgery, it is important to think
of it more broadly as any type of intervention. This can
include actions as diverse as:
i. Counseling about smoking cessation (an individual
intervention).
ii. Fluoridating water to prevent dental caries (a societal
intervention).
iii. Raising taxes on cigarettes (a societal intervention).
b. For treatment, exposure generally means receiving an inter-
vention (nonexposure being no intervention), with outcome
being occurrence of a disease or other event of interest. In
some studies there may be multiple categories of exposure
representing alternative treatments rather than a nonexposure
group. Either way, the proportion getting the outcome in
each group is compared to see if there is a difference.
c. Treatment questions are studied using a randomized
controlled study design. This is similar to a cohort study,
except that the participants do not choose whether they are
exposed; this is done by the researcher, using some chance
method. Having been assigned to one exposure group or
another, the patients are then followed, and the number in
each group getting the outcome is recorded. The advantage
of this over cohort studies is that, ideally, the randomization
process should make each exposure group identical as far as
likelihood of developing the outcome, except for the possible
effect of the exposure itself. This does not always happen,
but when it does it eliminates biases that can be present in
cohort studies.
d. As with cohort studies, the numbers measured are placed in
a 2 2 table (see Fig 3.5), and the following measures of
association are calculated.
i. Incidence. This is the same as in cohort studies.
ii. RR. This is the same as in cohort studies. Sometimes a
study will report the relative risk reduction (RRR).
This is 1 - RR and indicates by what percentage the like-
lihood of a bad outcome is reduced in the exposed group
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compared with the nonexposed group. As with cohort
studies, RRR gives a measure of the strength of associa-
tion but does not give the relevant information to apply to
individual patient benefit.
iii. AR. This is the same as in cohort studies and is some-
times referred to as the absolute risk reduction (ARR).
This indicates the actual amount of benefit a person will
get because of the treatment itself and is therefore the
number that is important in applying a studys informa-
tion to an individual patient. As with cohort studies, this
number frequently is not given so you have to be able to
calculate it yourself.
iv. Number needed to treat (NNT). This is 1/AR and gives
information analogous to AR, but like NNH it may be more
intuitive to use. A low NNT means that only a few people
need to be treated for one person to have a good outcome,
compared with a nonexposed person, and therefore means
that an individual has a high likelihood of benefiting from
treatment. A high NNH means that many people need to be
treated unnecessarily for one person to get benefit, and the
individual therefore is at low likelihood for being helped.
As with NNH, there is no single number for NNT that is
acceptable for all diseases and all treatments. For a benefit
that is relatively minor or for which the treatment would be
expensive or could itself induce harm, a very low NNT
would be required to consider a treatment worthwhile.
However, for preventing an outcome that is devastating and
a treatment that itself is not harmful or expensive, a much
higher NNT is needed to not consider the treatment.
e. With respect to Problem 1, consider the best way to treat
a PE. A study
10
compared 6 weeks of oral anticoagulant
therapy with 6 months of the same therapy: 107 participants
with a first-time PE were enrolled, with 56 randomized
to receive treatment for 6 weeks and 51 randomized to
6 months. Follow-up was for the next 2 years, with the
outcome measure being recurrent PE. In the 6-week group
there were 15 episodes of recurrent PE, and in the 6-month
group there were 7 episodes of recurrent PE. Putting this
information into a 2 2 table (Fig. 3.8), the measures of
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association can be calculated: RR 1.93, ARR 0.13,
and NNT 7.7. In addition, there was no difference in
anticoagulation side effects between the groups. Because
the outcome measured in this treatment study was a bad
one, an interpretation of this would be:
i. There is a harmful relationship between short-term anti-
coagulation and prevention of recurrent PE, compared
with the longer treatment (RR 1).
ii. Using the long-term anticoagulation provides a fairly
high likelihood of benefiting the individual patient (the
AR means that there is a 13% lower chance of a PE
in the next 2 years if long-term treatment is used as com-
pared with short-term treatment).
iii. The NNT means that around eight people need to be
treated with long-term anticoagulation unnecessarily in
P A R T
Outcome
Totals
Totals
Recurrent
PE
Exposure
6 weeks of
anticoagulant
6 months of
anticoagulant
I =
Relative risk (RR) =
Absolute risk difference (AR) = 0.27 0.14 = 0.13/2 years
Number needed to treat (NNT) = = 7.7/2 years
= 1.93
= 0.27/2 years
15 41
15
56
1
0.13
0.27
0.14
No
recurrent
PE
7 44
56
51
107 22 85
E
+
I = = 0.14/2 years
7
51
E
FIGURE 3.8 Example of measuring benefit in a treatment study.

1389_Ch03_017-046 2/2/09 1:20 PM Page 38
order to prevent a PE in one patient as compared with
short-term anticoagulation. If you believe this study is
valid, a reasonable conclusion is that long-term treatment
is the better approach.
5. Prevention and screening
a. Both of these should be considered subcategories of treat-
ment because they constitute intervening in a persons life
with the goal of having better health in the future. Look for
randomized controlled trials as evidence that a purported
prevention maneuver or screening test is worthwhile.
Cohort studies are particularly prone to bias with prevention
and screening and should never in themselves be considered
definitive proof of benefit.
b. Because study design is the same as for treatment, use the
same measures of association (RR, AR, and NNT) in
deciding whether to advocate these interventions.
c. Screening tests, because they are recommended to be widely
used across an asymptomatic population, have other criteria
that must be met (Fletcher and Fletcher,
1
Chapter 9):
i. The disease should represent a substantial burden at the
public health level.
ii. The disease should have a prevalent asymptomatic
critical point (a point in the course of the disease where
there is evidence that intervening earlier will result in a
better outcome than intervening later).
iii. This critical point must be recognizable by some test.
iv. A good screening test should be available: it must have
reasonable sensitivity, specificity, and predictive value; it
must have low risk and low cost; and it must be accept-
able to both the screener and person screened.
v. Curative potential should be substantially better in early
compared with advanced stages of disease.
vi. Treatment of screen-detected patients should improve
outcome as measured by cause-specific mortality rate,
functionality, and quality of life.
vii. Patients in whom an early diagnosis is achieved will
comply with your subsequent recommendations and
treatment regimens.
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IV. Decision Making in Uncertainty: Decision Analysis
A. When we face decisions that have tradeoffs, it may be obvious
whether the benefits of one option outweigh the drawbacks.
However, in medicine the complexity of decisions may make it
impossible to use intuition as the sole guide to the best choice.
This may be due to the intricate ramifications of any one decision,
to the various ways that different patients may value different
outcomes, or to a combination of both. In these difficult situations,
decision analysis may be a helpful tool to inform (but not
substitute for) decision making (Sox et al,
4
Chapter 6).
B. As an example of how this technique could be used, consider
whether to treat the patient in Problem 1 with long-term anticoag-
ulation. The main potential benefit is preventing a future PE that
could be fatal. However, this has to be balanced against the
bleeding risks associated with anticoagulation use, which could
result in a major but nonfatal stroke, among other complications.
What makes the decision even more difficult is that, even after
testing, it may not be certain that the patient actually has a PE, so
there is risk of causing a stroke in someone who potentially would
not benefit from the treatment. How do we put all of this together?
C. A simplified version of a decision analysis for addressing this is
shown in Figure 3.9. The first step is to diagram the problem in a
decision tree, a graphic device that shows the decisions or choices
that have to be made, the chance events that can ensue, the proba-
bilities of each chance event, and the eventual outcomes. Decision
points are shown with boxes, and chance events (not under the
control of the decision maker) are shown with circles. At the end
of each branch is the ultimate outcome of traveling down that
pathway.
D. After creating the tree, you need to find information on the
probability of each chance event and then assign a value to each
outcome. By straightforward arithmetic, it is then possible to
determine which decision option is, on average, most likely to
result in the best outcome (Sox et al,
4
Chapter 6).
E. An important piece of this approach is that it allows you to take
into account an individual patients values for different health
outcomes and to measure the patients preferences for health
states. This allows you to use the generic decision tree information
(the chance events and probabilities) and then individualize the
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tree to the particular values and personality of your patient.
Techniques for this are described in standard textbooks (e.g., Sox
et al,
4
Chapters 7 and 8). The answer units are utilities (a measure
of quality of life) and quality-adjusted life expectancy (which
takes the actual life expectancy in a given health state and adjusts
it downward, based on how bad that health state is for your
particular patient).
V. Costs and Cost-Effectiveness
A. If there were no limits on the resources used to deliver health care,
the relative costs of different tests and treatments would not need
to be considered. For example, on a societal level, there are limits
to the amount of money the U.S. government has available to fund
Medicare. On a hospital level, there are limits to the number of in-
tensive care unit (ICU) beds available at any given moment. Both
of these factors can result in someone needing to make a choice in
what care to cover or who should be given an ICU bed. It is in a
situation of limited resources that considering cost-effectiveness
is of value.
C H A P T E R
Alive-with-a-stroke
Alive-with-a-stroke
Alive-with-a-stroke
Dead
Dead
Dead
Survive
Recurrent PE
Stroke
Stroke
No stroke
No stroke
No recurrent PE
Recurrent PE
No recurrent PE
Recurrent PE
Really had a PE
Anticoagulate
Dont anticoagulate
Didnt have a PE
Really had a PE
Didnt have a PE
No recurrent PE
Die
Survive
Die
Survive
Die
Alive-without-a-stroke
FIGURE 3.9 Simplified decision tree for a PE.
1389_Ch03_017-046 2/2/09 1:20 PM Page 41
B. Cost-effectiveness is a term that is frequently used incorrectly.
11
A strategy or approach to a medical problem cannot be described
as cost-effective in isolation; cost-effectiveness always requires
comparing two or more treatment options (even if one of the
options is do nothing as there are still costs that result from
doing nothing that need to be considered).
C. Other erroneous uses are equating cost-effective solely with the
most effective approach or with the least costly approach.
D. A strategy can be described properly as cost-effective in two
situations:
1. It is both more effective and less costly than the alternative.
This option should always be chosen, but this situation is
unusual because in medicine it tends to cost more to get more
effectiveness.
2. It is more effective but also more costly. However, the increased
cost is low enough to make it worthwhile to get that increased
effectiveness. This is the more common situation, but it creates
a problem because it is not obvious how much is reasonable
to spend to get a unit of effectiveness. For this reason, cost-
effectiveness analyses often do not give an answer as to what
is the best strategy but merely inform the decision maker of the
relative costs; the ultimate decisions of what to fund have to be
based on other issues, which commonly include social equity,
ethics, and politics.
E. For this reason, in most cases cost-effectiveness analysis results do
not give a direct answer as to what to do with a patient, and in fact
there may be a tension between what is in societys best interest
and what is in your own patients best interest. Nevertheless,
physicians have a responsibility to society as well as to individual
patients; they cannot ignore issues of cost.
F. The proper measure of cost-effectiveness analysis is marginal
(or incremental) cost-effectiveness, which is the increased
amount that must be paid to obtain one unit of effectiveness as
compared with the next cheapest strategy. This gives the correct
picture of what benefits are provided as resources are diverted to
increasingly expensive options. This is in contrast to average
cost-effectiveness (the cost of a particular strategy divided by its
effectiveness), which will often be misleadingly low and does not
give any comparative information.
P A R T
1389_Ch03_017-046 2/2/09 1:20 PM Page 42
G. Costing needs to consider both the immediate cost of a particular
treatment or test and the downstream costs that are incurred because
of a particular choice. Costs should be comprehensive, including
drug or test costs, physician fees, hospital fees, and any other re-
sources that can be used (opportunity costs). Effectiveness units
can be anything that is clinically meaningful, but the most common
one is quality-adjusted life expectancy. The advantage of using the
same unit of effectiveness in most cost-effectiveness analyses is that
it allows direct comparisons of very disparate options (e.g., childhood
immunizations versus screening treadmill tests in middle-aged men).
H. As an example, consider Problem 2, the question of whether to
advocate screening mammography for women in their 40s as
compared with women in their 50s. A study
12
addressed this by
comparing three options: no screening, annually screening women
age 5069 years, and annually screening women age 4069 years.
The results are shown in Figure 3.10.
1. The marginal cost-effectiveness means that $45,700 must be
spent for each additional year of life gained by screening women
ages 5069 years as compared with no screening. Furthermore,
an additional $159,000 must be spent for each additional
year of life then gained by screening women ages 4069 years
as compared with screening women ages 5069 years.
C H A P T E R
Strategy
No
screening
50-69
annual
40-69
annual
Cost
($ millions)
Effectiveness
(Total life-years)
Marginal cost
(additional
$ millions)
Marginal
effectiveness
(additional
years of life)
Average CE
($/year of life)
Marginal CE
(additional
$/additional
year of life
gained)
C/D A/B D C B A
$112 241,950
B1
27.03
A1
$45,700 $174 329
(B2-B1)
15.05
(A2-A1)
242,279
B2
42.08
A2
$159,000 $216 64
(B3-B2)
10.19
(A3-A2)
242,343
B3
52.27
A3
FIGURE 3.10 Example of CE analysis (in a hypothetical population of
10,000 women).
1389_Ch03_017-046 2/2/09 1:20 PM Page 43
Although the average cost-effectiveness looks trivially
different among the different strategies, once the marginal
cost-effectiveness is examined, you see that in fact almost
all of the effectiveness in expanding the screening age down
to 40 years is still coming from screening the women who
are older than 50 years.
2. What is the right choice? Although there is not a single
reasonable marginal cost-effectiveness, many people set an
upper limit between $50,000 and $100,000 per additional year
of life gained. Given that, one interpretation of these results
would be that screening women 5069 years is definitely
worth the increased cost, but as there are limited dollars in the
United States that can be used for screening as well as all other
health care, it is too expensive to divert the money to screening
women 4049 years; instead those resources could be used
more efficiently elsewhere (e.g., trying to get more women in
their 50s to get screened.)
P A R T
MENTOR TIPS
The core idea of clinical epidemiology is that issues such as
diagnosis and treatment outcome are uncertain for individual
patients, are therefore expressed as probabilities, and are
best estimated by referring to past experience with groups
of similarpatients.
Information from (ideally large) studies is taken and possibly
applied one-on-one with each individual patient.
Most tests in medicine are not perfect; those that are tend to
be invasive, expensive, or autopsies (usually not the ideal diag-
nostic approach). The accuracy of an imperfect test is mea-
sured in two ways: sensitivity/specificity and likelihood ratios.
With questions of treatment, will making an intervention change
what happens to a patient? Although treatment certainly includes
giving drugs or performing surgery, it is important to think of it
more broadly as any type of intervention.
In prevention and screening, randomized controlled trials are
the best evidence that a purported prevention maneuver or
screening test is worthwhile. Cohort studies are particularly
prone to bias with prevention and screening and should never in
themselves be considered definitive proof of benefit.
When there are decisions that have tradeoffs, it may be
obvious whether the benefits of one option outweigh the
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C H A P T E R
drawbacks. However, in medicine the complexity of decisions
may make it impossible to use intuition as the sole guide to
the best choice. In these difficult situations, decision analysis
may be a helpful tool to inform (but not substitute for)
decision making.
A strategy or approach to a medical problem cannot be de-
scribed as cost-effective in isolation; cost-effectiveness
always requires comparing two or more treatment options
(even if one of the options is do nothing).
Marginal (or incremental) cost-effectiveness (which is the in-
creased amount that must be paid to obtain one unit of
effectiveness as compared with the next cheapest strategy) is
usually more important than average cost-effectiveness.
Definitions of cost need to consider the immediate cost of a
particular treatment or test as well as the downstream costs
that are incurred because of the particular choice and the
opportunity costs (the other activities could have been done
with the money).
References
1. Fletcher RH, Fletcher SW. Clinical epidemiology: The essentials,
3th ed. Lippincott Williams & Wilkins, 2005.
This is an extremely clear and practical introductory textbook on the
principles of clinical epidemiology and their direct use in patient care.
Its great strength is its clinical (rather than research) focus and
organization, with excellent use of medical examples. All clinicians
would benefit from reading this, and it could be considered a core
piece of a personal medical library.
2. Guyatt G, Drummond R (eds). Evidence-based medicine working
group, users guides to the medical literature: A manual for evidence-
based clinical practice. AMA Press, 2002.
This is a reference that presents formal but practical methods for
finding and evaluating medical literature critically.
3. Guyatt G, Drummond R (eds). Evidence-based medicine working
group, users guides to the medical literature: Essentials of
evidence-based clinical practice. AMA Press, 2002.
A concise pocket-sized version of the preceding textbook.
4. Sox HC, Blatt MA, Higgins MC, et al. Medical decision making.
American College of Physicians, 2007.
1389_Ch03_017-046 2/2/09 1:20 PM Page 45
This is a very straightforward introduction to decision analysis and
cost-effectiveness analysis and the ways to quantify individual patient
preferences for health states and incorporate those preferences into
medical decisions.
5. Goldhaber SZ, Simons GR, Elliott CG, et al. Quantitative plasma
D-dimer levels among patients undergoing pulmonary angiography
for suspected pulmonary embolism. Journal of the American Medical
Association 270:28192822, 1993.
6. Le Gal G, Righini M, Roy PM, et al. Prediction of pulmonary
embolism in the emergency department: The revised Geneva score.
Annals of Internal Medicine 144:165171, 2006.
7. Grodstein F, Stampfer MJ, Goldhaber SZ, et al. Prospective study of
exogenous hormones and risk of pulmonary embolism in women.
Lancet 348:983987, 1996.
8. Parkin L, Skegg DC, Wilson M, et al. Oral contraceptives and fatal
pulmonary embolism. Lancet 355:21332134, 2000.
9. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism:
Clinical outcomes in the International Cooperative Pulmonary
Embolism Registry (ICOPER). Lancet 353:13861389, 1999.
10. Schulman S, Rhedin AS, Lindmarker P, et al. A comparison of
six weeks with six months of oral anticoagulant therapy after a first
episode of venous thromboembolism. New England Journal of
Medicine 332:16611665, 1995.
11. Doubilet P, Weinstein MC, McNeil BJ. Use and misuse of the term
cost effective in medicine. New England Journal of Medicine
314:253256, 1986.
This term has become a catchword in recent years, but at the expense
of major misunderstanding about its meaning, interpretation, and
proper application. This article very clearly points out the correct and
incorrect ways to use the term.
12. Salzmann P, Kerlikowski K, Phillips K. Cost-effectiveness of
extending screening mammography guidelines to include women 40 to
49 years of age. Annals of Internal Medicine 127:955965, 1997.
P A R T
1389_Ch03_017-046 2/2/09 1:20 PM Page 46
47
CHAPTER
PREVENTION AND
SCREENING
Gary J. Martin, MD
4
I. Epidemiology
A. The general principles that apply to screening are listed in Box 4.1.
Frequency and severity of the disease and a long latency period
where the disease can be found (or risk factors treated effectively)
are key principles.
TABLE
4.1
Lifetime Cumulative Risks
Pathology Lifetime Cumulative Risk
Breast cancer for women 10%
Colon cancer 6%
Cervical cancer* 2%
Domestic violence for women Up to 15%
Hip fracture for white women 16%
*Assuming an unscreened population
BOX
4.1
Principles of Screening
Find disease early while curable (long latency)
Focus on common problems, major burden of illness
Consider cost/benefit issues
Does it make a difference, or did you just find out about it?
B. Table 4.1 lists the lifetime cumulative risk of a number of conditions
for which screening is done. This helps put into perspective what the
potential yield is and why, as the number gets smaller, false positives
become a significant counterbalancing factor for benefit.
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C. While thinking critically about tests, remember that:
Tobacco use, diet and activity, and alcohol use represent
the majority of factors for preventable deaths and close
to half of all deaths. That is why general counseling is an
important preventive measure in addition to screening tests.
In fact, probably the single greatest accomplishment a physician
can achieve for patients is to help them quit smoking.
D. Box 4.2 lists some of the benefits of screening and prevention.
This can help physicians prioritize and make decisions on what
to include in their efforts. Some examples of these different
measures follow.
1. Number needed to screen: using a DEXA machine to screen for
osteoporosis and then treating patients, one would have to
screen 731 women age 65 to 69 years in order to prevent one
hip fracture.
2. The related number of absolute impact can be exemplified
by looking at breast cancer screening. A meta-analysis of
all of the Swedish mammography trials for breast cancer
noted that approximately 1.2 fewer women per thousand
would die from breast cancer with screening for women
age 40 to 70 years if they were screened over a 12-year
period.
3. Although a different population is involved, it is interesting
to compare the preceding number to the approximately
three lives per thousand saved from colon cancer death in
a population of 50- to 75-year-olds screened with annual
fecal occult blood testing (8.8/1000 versus 5.9/1000). Based
on this, colon cancer screening may actually save more
womens lives than mammography. The relative impact
BOX
4.2
Methods of Measuring Health Benefits
Number of patients needed to screen in order to prevent one event
Absolute and relative impact on morbidity and mortality
Cost per year of life saved
Increase in average life expectancy for a population
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4 PREVENTION AND SCREENING 49
C H A P T E R
often sounds more impressive, but both figures are important.
The relative impact for occult blood testing from the same
data can be stated as a 30% reduction in colon cancer
deaths.
4. Cost per year of life data have been estimated for many screen-
ing and prevention strategies. Typically, strategies that cost less
than $30,000$50,000/year of life saved are considered cost-
effective. One example at this threshold of approximately
$30,000/year of life saved is alendronate use for a 65-year-old
woman with osteoporosis.
E. Table 4.2 lists the increases in life expectancy for a population for
a number of screening procedures.
F. There are two important concepts to keep in mind while looking at
this list:
1. The first is that the average time increase actually applies to no
one. In reality, the majority of people screened will not derive
any benefit, or possibly a slight negative, from false positives.
There will be a small subset of patients who benefit a great
deal from being screened. These numbers average out to the
reported value. One example is cervical cancer patients. Pap
smears cannot benefit the 98% of women who will never get
cancer of the cervix, but for the 2% who would develop
TABLE
4.2
Estimated Average Increase in Life Expectancy
for a Population
Test or Intervention Increase
Mammography:
Women 4050 years old 05 days
Women 5070 years old 1 month
Pap smears 1865 years old 23 months
Screening treadmill for asymptomatic men 8 days
50 years old
Prostate-specific antigen (PSA) and digital rectal Up to 2 weeks
examination for men over 50 years old
Getting a 35-year-old smoker to quit 35 years
Beginning regular exercise for 40-year-old men 9 months to 2 years
(30 minutes 3 times a week)
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P A R T
cervical cancer, Pap smears may lead to preventing invasive
cervical cancer and add as much as 25 years onto those
individuals lives.
2. The second is that although the average numbers appear modest,
they are averaged over the entire population so that the number
of patient months is a fairly large number. Some physicians
have recommended that the gain of a month for a preventive
strategy aimed at the general population represents an important
intervention.
II. Diseases for Which to Screen in Most Adults
A. The U.S. Preventive Services Task Force (USPSTF) has attempted
to balance all these issues rigorously. Table 4.3 lists the majority
of its recommendations. However, there are additional procedures
to consider for individuals at higher risk for a given disease than
TABLE
4.3
Clinical Preventive Services Recommended
by the USPSTF for Normal-Risk Adults
Screening
Blood pressure,
height, and weight
Cholesterol
Diabetes
Pap smear
Chlamydia
Mammography
Colorectal cancer
Osteoporosis
Abdominal aortic
aneurysm
Alcohol use
Vision, hearing
Periodically, 18 years and older
Men, every 5 years, 35 years and older
Women, every 5 years, 45 years and older
Periodically, adults with hypertension or
hyperlipidemia
Women, every 13 years, within 3 years of
onset of sexual activity, or 2165 years old
1825 years old
Every 12 years, 40 years and older
Periodically, 50 years and older (fecal occult
blood annually, and/or sigmoidoscopy every
5 years, or colonoscopy every 10 years)
depending on family history
Women, routinely 65 years old or 60 years
old at increased risk for fractures
Once in men who have ever smoked
6575 years old using ultrasound
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C H A P T E R
TABLE
4.3
Clinical Preventive Services Recommended by
the USPSTF for Normal-Risk Adults (Continued)
Immunization (www.cdc.gov/nip/recs/adult-schedule.htm)
HPV
Tetanus-diphtheria
(Td)
Varicella (VZV)
Measles, mumps,
rubella (MMR)
Pneumococcal
Influenza
Meningococcal,
hepatitis A and B
Chemoprevention
Aspirin
Breast cancer
chemoprevention
Counseling
Calcium intake
Folic acid
Tobacco cessation,
drug and alcohol
use, STDs and HIV,
nutrition, physical
activity, sun exposure,
oral health, injury
prevention (loaded
handgun, seat belts,
bicycle helmet), and
polypharmacy
In elderly patients, some measures become the priority. For example: vision, hearing, dental
evaluations, immunizations (pneumococcal, influenza), fall prevention, hot water heater at
less than 120 degrees, and avoidance of polypharmacy.
Adapted from U.S. Preventive Services Task Force: Guide to Clinical Prevention Services,
2nd and 3rd ed. (www.ahrq.gov/clinic/uspstfix.htm).
Females 26 years old: three doses
Every 10 years, 18 years and older (substitute
one Tdap)
Susceptibles onlyTwo doses, 18 years and older
One dose, 18-50 years old if not given series
as child or born before 1957
Women of childbearing age: caution
One dose, 65 years and older
Yearly, 50 years and older
Can be considered based on risk
Discuss aspirin to prevent cardiovascular (CV)
events: CV risk needs to be enough to justify it
Men, periodically, 40 years and older
Women, periodically, 50 years and older
(especially 65 years)
Discuss breast cancer chemoprevention with
women at high risk
Women, periodically, 18 years and older
Women of childbearing age, 1850 years old
Periodically, 18 years and older; upper age
limits should be individualized for each patient
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P A R T
the general population. In general, family history and social his-
tory can identify these patients and are illustrated in the USPSTF
report, which is available at www.ahrq.gov/clinic/uspstfix.htm.
B. Regarding age:
Screening for many conditions begins at age 50 years;
however, for those with a significant family history,
starting 10 years earlier than when the youngest family
member developed a condition is also prudent.
1. For example, if the patients mother had colon cancer diag-
nosed at age 55 years, start screening as early as 45 years for
the patient.
2. This 10-year advance is also reasonable for breast and prostate
cancer screening (although prostate cancer screening with PSA
is not mandated by the USPSTF).
C. Some interventions that the USPSTF believes are of uncertain
value because of lack of data are recommended by other groups.
Some examples are screening the general population for diabetes
(with fasting blood sugars), domestic violence, HIV, and
depression.
D. The Agency for Healthcare Research and Quality and the Centers
for Disease Control and Prevention (CDC) have numerous flow
sheets as part of their Put Prevention Into Practice program
(www.ahcpr.gov/clinic/ppipix.htm).
E. There are fewer data about when to sunset some of these services.
1. Certain cancers, such as cancer of the cervix, become less com-
mon in older populations; age 65 years has been offered for
consideration as a stopping point, assuming the previous recent
Pap smears have been negative.
2. For breast, colon, and prostate cancer, an age of approximately
75 years may be a reasonable time to reevaluate the need for
some of these procedures. Because of comorbidities and
the fact that so many screening procedures benefits set in
approximately 10 years after screening, a useful approach is
estimating the patients life expectancy.
3. For some older patients with advanced comorbidities, such
as severe chronic obstructive pulmonary disease (COPD),
congestive heart failure, or immobility, the benefits of some
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C H A P T E R
screening procedures are likely to be close to zero, and other
priorities emerge if the patients life expectancy is less than
10 years. This type of shift in focus needs to be conveyed
tactfully, so the patient does not receive the wrong message.
The fact that greater attention will be paid to functional
capacity, activities of daily living, and optimizing their
comorbidities can be explained to both patients and families.
III. Cancer
A. Screening for lung cancer and other cancers as well as coronary
artery disease (CAD) with computed tomography/magnetic reso-
nance imaging (CT/MRI) scanning has been commercialized.
1. There is no proven benefit to lung cancer screening, and
nonrandomized comparison group studies offer mixed results.
2. A 50,000-patient National Institutes of Health (NIH)-funded
randomized controlled study has started, using CT scanning for
lung cancer screening. Use for abdominal cancers has not been
proved.
3. Screening for CAD with CT is very controversial and unproven
but is also the subject of an ongoing 10-year Multiethnic Study
of Atherosclerosis (MESA) trial funded by the NIH. Screening
for CAD may be worthwhile in higher- (intermediate) risk
patients with hypercholesterolemia.
B. Most authorities agree that screening for cancer of the cervix is
valuable. For low-risk women, the frequency may be as seldom
as every 3 years because increasing the frequency adds little
benefit. However, in women at higher risk (for example, a history
of multiple sexually transmitted illnesses [STIs], multiple sexual
partners, dysplasia), more frequent testing is advisable.
1. Using a cytobrush to collect cells in the cervical os markedly
increases the yield of some practitioners abilities to collect
endocervical cells.
2. The use of the liquid-based tests as part of the cervical cancer
screening collection technique has become a first-line approach
in many parts of the country, although its primary benefit is for
women who have borderline cytology.
3. Both the American Cancer Society (ACS) and USPSTF still
recommend the traditional collection as acceptable. The
USPSTF believes more data are needed before routinely using
the liquid-based technologies.
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P A R T
C. There is a lifetime cumulative risk of approximately 10% of
developing breast cancer. Pooled data from Scandinavian studies
demonstrate a reduction in breast cancer deaths of approximately
1.2 women/1000 screened over a 12-year period. Approximately
5.1/1000 women who are not screened will die of breast cancer
over a 12-year period versus 3.9/1000 women who are screened
with mammography.
1. Mammography between the ages of 40 and 50 has always
been controversial, but in the United States it has become
|generally accepted. Although the absolute benefit in this age
group is quite small and the number of false positives that lead
to unnecessary biopsies is relatively large, the USPSTF has
recommended that women in this age group continue to have
mammography.
a. Mammography is particularly difficult in this group because
breast cancer is less common (only about 1%1.5% of
women will get breast cancer between 40 and 50 years of
age), the density of premenopausal breast tissue makes the
interpretation of mammography more difficult, and it may be
a faster-growing tumor in this premenopausal age group
when it does occur and spread earlier.
b. Although an overall frequency between 1 and 2 years is rec-
ommended, it probably makes some sense to use the shorter
interval for women between 40 and 50 years of age if one is
going to screen this age group. A carefully done breast ex-
amination has been a component in some studies and proba-
bly adds value.
c. In recent years, breast cancer deaths have been declining,
presumably correlated with the marked decline in hormone
replacement therapy since the Womens Health Initiative
study results became available.
D. A persons lifetime cumulative risk for colon cancer is
approximately 6%. The percentage is a bit lower for those
without a family history and higher for those with first-degree
relatives who had colon cancer at younger ages.
1. There are three accepted screening techniques for colon cancer.
a. Fecal occult blood testing annually has led to a 15%30%
reduction in colon cancer deaths in controlled studies.
b. Flexible sigmoidoscopy is thought to reduce colon cancer
deaths by approximately 60%.
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C H A P T E R
c. Although the benefit of flexible sigmoidoscopy may last for
up to 10 years, most experts would recommend a screening
sigmoidoscopy every 5 years.
2. Although colonoscopy has not had as much data regarding
a mortality benefit, it is generally believed that it offers at
least the potential benefit of flexible sigmoidoscopy.
Colonoscopy does, however, have additional costs and risks.
No head-to-head comparisons between these techniques have
been performed in the same population, but the most impor-
tant point is that some type of colon cancer screening be of-
fered to patients.
Colonoscopy is estimated to reduce colon cancer by
as much as 80% by removing adenomatous polyps
before they progress to colon cancer and by early detection
of cancers at a curable stage.
3. Screening generally starts at age 50 years; however, for those
patients with a significant family history, starting 10 years
earlier from when the youngest family member developed
colon cancer is also prudent (e.g., if the patients mother had
colon cancer diagnosed at age 55, one would start as early as
45 for the patient).
4. Either endoscopic technique may offer more benefit than fecal
occult blood testing, and the choice between them can also be
based on the patients preferences and family history.
5. Relative to flexible sigmoidoscopy, colonoscopy is more complete
but is much more expensive and has a modestly increased risk.
6. Virtual colonoscopy with imaging techniques is evolving, but it
misses mucosal lesions and smaller polyps and cannot deal with
polyps even if they are seen. It may have a role in the future.
E. The lifetime cumulative risk of prostate cancer in men in the
United States is approximately 15%, with three fourths of those
being diagnosed after age 65 years.
1. The likelihood of a man in the United States dying from prostate
cancer is only about 3%, so it should be clear that many men
diagnosed with prostate cancer would die from other causes,
particularly older men. It is also well known that at autopsy, an
even higher percentage of men have occult prostate cancer that
did not lead to any morbidity during their lifetime.
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2. Many experts, including the USPSTF, recommend an individu-
alized discussion between physicians and their patients
about prostate cancer screening as the risk-benefit ratio is
complicated, and therefore personal preferences weigh
highly.
3. Although the early detection of prostate cancer seems desirable,
the risks include false-positive results, unnecessary anxiety,
biopsies, and even potential complications from treating some
early cancers that may never have affected a patients health
or well-being. These include:
a. Erectile dysfunction.
b. Urinary incontinence.
c. Bowel dysfunction from surgery and radiation treatment.
4. An ongoing National Cancer Institute randomized clinical
trial expected to end later this decade may help clarify the net
benefits of prostate cancer screening. Until then the current data
are considered inconclusive.
IV. Immunizations, Chemoprevention, and Counseling
A. Childhood immunizations are covered in Chapter 26.
B. Table 4.3 lists key immunizations, chemoprevention, and counsel-
ing issues for adults. As mentioned earlier, the counseling can be
just as important as any screening test, and smoking cessation is
probably the single biggest event a clinician can help a patient
accomplish.
MENTOR TIPS DIGEST
Tobacco use, diet and activity, and alcohol use represent the
majority of factors for preventable deaths and close to half of
all deaths. That is why general counseling is an important
preventive measure in addition to screening tests. In fact,
probably the single greatest support a physician can provide
for patients is to help them quit smoking.
Screening for many conditions begins at age 50 years;
however, for those with a significant family history, starting
10 years earlier than when the youngest family member devel-
oped a condition is also prudent.
Colonoscopy is estimated to reduce colon cancer by as much
as 80% by removing adenomatous polyps before they
progress to colon cancer in addition to early detection.
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C H A P T E R
Resources
Albertson R. A 72-year-old man with localized prostate cancer. Journal of
the American Medical Association 274:6974, 1995.
Ask yourself if patient is likely to live another 10 years.
CDC recommendations and guidelines: Adult immunization schedule
(2007). www.cdc.gov/nip/recs/adult-schedule.htm
Clinical Preventive Services for Normal-Risk Adults Recommended by
the U.S. Preventive Services Task Force. Put prevention into practice.
January 2003. Agency for Healthcare Research and Quality, Rockville,
Md. www.ahrq.gov/ppip/adulttm.htm
Elmore JE, Barton MB, Moceri VM, et al. Ten-year risk of false positive
screening mammograms and clinical breast examinations. New England
Journal of Medicine 338:10891096, 1998.
Of women screened with mammography, 24% had at least one
false-positive result.
Harris R, Leininger L. Clinical strategies for breast cancer screening:
Weighing and using the evidence. Annals of Internal Medicine
122:539547, 1995.
Good overview of mammography data and risks. Two to four fewer
50-year-old women out of 1000 will die from breast cancer with
10 years of screening.
Olsen O, Gotzsche PC: Cochrane review on screening for breast cancer
with mammography. Lancet 358:1340, 2001.
Calls into question the quality of earlier studies of mammography benefit.
U.S. Preventive Services Task Force: Screening for breast cancer: Recom-
mendations and rationale. Annals of Internal Medicine 137:344, 2002.
Start at age 40 years.
U.S. Preventive Services Task Force. Screening for colorectal cancer:
Recommendations and rationale. Annals of Internal Medicine
137:129131, 2002.
U.S. Preventive Services Task Force. Screening for prostate cancer: A
recommendation from the U.S. Preventive Services Task Force. Annals
of Internal Medicine 2002 137:148, 2002.
Still an individualized decision.
Winawer SJ, Zauber AG, Ho MN, et al. Prevention of colorectal cancer by
colonoscopic polypectomy. The National Polyp Study Workgroup.
New England Journal of Medicine 329:19771981, 1993.
Compared with nonrandomized reference groups, this approach
reduced colon cancer incidence by 76%90%.
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P A R T
Writing Group for the Womens Health Initiative Investigators. Risks and
benefits of estrogen plus progestin in healthy postmenopausal women.
Journal of the American Medical Association 288:321, 2002.
Risks somewhat outweighed benefits.
1. Applying the general principles for screening, which one of the
following diseases is most suitable for screening?
a. Small cell lung cancer
b. Ovarian cancer
c. Pancreatic cancer
d. Rectal cancer
2. Which one of these interventions would have the greatest population
impact to decrease preventable deaths?
a. Encourage aerobic exercise 30 minutes 3 times a week.
b. Facilitate smoking cessation.
c. Obtain mammography for women age 5065 years.
d. Perform flexible sigmoidoscopy for men age 5075 years.
3. Screening and treatment in women for which of the following
malignancies would yield the greatest impact on longevity?
a. Ovaries
b. Colon
c. Breast
d. Cervical
1389_Ch04_047-058 2/2/09 1:20 PM Page 58
59
PREOPERATIVE EVALUATION
Michael Kornfeld, MD, and Kevin OLeary, MD
CHAPTER
5
I. Overview
A. The purposes of the preoperative evaluation:
1. To assess the patients risk for surgery
2. To take measures to reduce this risk
B. Communicating the assessment and plan to the surgeon and
patient is critical. The more specific and concise the recom-
mendations, the more likely the recommendations will be
followed.
C. Anesthesia is generally safe, with an overall mortality rate of
0.3%. The choice of anesthetic is best left to the anesthesiologist.
It is important for the medical consultant to have a basic under-
standing of anesthetic techniques.
1. General anesthesia is drug-induced reversible absence of
sensation and consciousness. This is usually done using
inhaled anesthetics delivered through an endotracheal tube.
Neuromuscular blocking agents are often used.
2. Neuroaxial anesthesia includes spinal and epidural
anesthesia.
a. Spinal anesthesia is accomplished by injecting local
anesthetics and/or opioids into the subarachnoid space
using a needle or catheter.
d. Epidural anesthesia is accomplished by injecting local
anesthetics and/or opioids into the epidural space.
i. Both carry a very small risk of epidural hematoma;
therefore, the effect of antiplatelet agents and anti-
thrombotic agents needs to have worn off by the time
of insertion of the needle.
1389_Ch05_059-076 2/2/09 1:20 PM Page 59
P A R T
II. Preoperative Testing
A. The general principle for all preoperative testing is that it should
be done only if the results will alter clinical management.
B. Preoperative laboratory tests should be ordered for patients who
would otherwise require testing, regardless of the plans for
surgery. Additional factors to consider include the following.
1. Complete blood count (CBC) may be useful as a baseline
for patients expected to have a large amount of perioperative
bleeding.
2. Prothrombin time (PT) and partial thromboplastin time (PTT)
are not indicated unless the patient is on anticoagulants or has a
history suggestive of a bleeding disorder.
3. Low-risk patients going for low-risk surgeries can safely
proceed to surgery with no laboratory testing.
4. If laboratory testing is indicated and tests have been done
within the past 6 months, there is no need to repeat testing, as
long as no change in the patients clinical status has occurred.
C. Men over 40 and women over 50 years of age who are scheduled
for intermediate- to high-risk surgery should have a preoperative
electrocardiogram (ECG).
D. Chest x-ray (CXR) indications include symptoms or examination
findings suggestive of heart or lung disease.
III. Preoperative Cardiac Assessment and Perioperative
Management
A. Perioperative cardiac complications occur in 1.4% of patients
50 years of age and older. Although the incidence of cardiac
complication is not very high, the mortality rate of cardiac
complications is 15%50%.
1. Risk assessmentthe Revised Cardiac Risk Index (RCRI)
provides a practical method to estimate a patients risk for
cardiac complications related to surgery (Table 5.1). By adding
up the number of Risk Factors in the Index, one can estimate
the risk for perioperative cardiac events.
2. Need for noninvasive testingbeyond estimating a patients
risk using the RCRI, noninvasive cardiac testing may further
clarify the risk for select patients.
a. Options for noninvasive cardiac testing include:
i. Exercise ECG.
1389_Ch05_059-076 2/2/09 1:20 PM Page 60
ii. Exercise or dobutamine stress echocardiography.
iii. Exercise or pharmacologically induced stress myocardial
perfusion imaging.
b. The American College of Cardiology/American Heart
Association (ACC/AHA) Task Force has published evidence-
based guidelines on preoperative cardiac risk assessment and
management. These guidelines provide a stepwise approach to
help the physician decide which patients may benefit from
noninvasive cardiac testing (Fig. 5.1)
i. Assess the urgency of surgery. If the patient needs to
go to surgery emergently, there is no time for risk
assessment. The medical consultants role in this situation
is to determine whether measures can be taken to
reduce the risk for complications intraoperatively and
postoperatively.
ii. Determine if the patient has significant active cardiac
conditions, such as unstable or severe angina, recent
myocardial infarction (MI), decompensated or new-onset
heart failure, high-grade arrhythmia, or severe valvular
disease. If any one of these conditions is present, it
should be evaluated and treated preoperatively.
iii. Surgical procedures may be classified according to the
rate of perioperative complications (Table 5.2). Cardiac
5 PREOPERATIVE EVALUATION 61
C H A P T E R
TABLE
5.1
Revised Cardiac Risk Index
Risk Factor Points
High-risk surgery* 1
Established coronary artery disease 1
Congestive heart failure 1
Cerebrovascular accident or transient ischemic attack 1
Diabetes mellitus (insulin requiring) 1
Chronic renal insufficiency (cr 2.0) 1
*Defined as intraperitoneal, intrathoracic, and suprainguinal vascular procedures.
Rates of complications in patients with 0, 1, 2, 3 points were 0.5%, 0.9%1.3%,
4%7%, and 9%11%.
From Lee TH, Marcantonio ER, Mangione CM, et al: Derivation and prospective valida-
tion of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation
1999;100(10):10431049.
1389_Ch05_059-076 2/2/09 1:20 PM Page 61
P A R T
Step 1 Yes
No
No
No
Need for emergency
noncardiac surgery?
Step 4
Step 5
Yes
No or unknown
Vascular
surgery
Consider testing
if it will change
management
*Active cardiac conditions include unstable or severe angina, recent MI, decompensated
or new-onset heart failure, high-grade arrhythmia, or severe valvular disease.
See Table 5.3 for estimated MET equivalent.
See Table 5.1 for clinical risk predictors.
Intermediate
risk surgery
Vascular surgery Intermediate
risk surgery
Proceed with planned surgery with HR control
or consider noninvasive testing if it will
change management
3 or more clinical
risk factors
1 or 2 clinical
risk factors
No clinical
risk factors
Good functional capacity
(MET level ? 4) without
symptoms
Operating
room
Step 2 Yes
Active cardiac
conditions?*
Evaluate and treat per
ACC/AHA guidelines
Step 3 Yes
Low-risk
surgery?
Proceed with
planned surgery
Consider
operating room
Proceed with
planned surgery
Proceed with
planned surgery
Perioperative
surveillance and
postoperative risk
stratification and risk
FIGURE 5.1 Cardiac evaluation and care algorithm for noncardiac surgery
based on active clinical conditions, known cardiovascular disease, or cardiac
risk factors. (Based in part on recommendations from Eagle KA, Berger PB,
Calkins H, et al: ACC/AHA guideline update for perioperative cardiovascular
evaluation for noncardiac surgeryexecutive summary: A report of the American
College of Cardiology/American Heart Association Task Force on Practice Guide-
lines [Committee to Update the 1996 Guidelines on Perioperative Cardiovascular
Evaluation for Noncardiac Surgery]. J Am Coll Cardiol 2002;39[3]:542553.)
1389_Ch05_059-076 2/2/09 1:20 PM Page 62
C H A P T E R
testing rarely changes management of patients going for
low-risk procedures. It is appropriate in these cases to
proceed with planned surgery without further cardiac
testing.
iv. Management of patients going for vascular or intermediate-/
high-risk nonvascular surgery depends on assessment of
their functional capacity. Functional capacity is measured
in metabolic equivalents (METs), with 4 METs consid-
ered poor functional capacity (Table 5.3). Patients who
are not symptomatic and have good functional capacity
can generally proceed to planned surgery without further
cardiac testing.
v. If functional capacity is poor or cannot be assessed, the
decision to perform additional preoperative testing
depends on presence of RCRI risk factors. If none of
these risk factors is present, patients can generally pro-
ceed to planned surgery without further testing. If one
or more risk factor is present, additional testing may be
considered (see Fig. 5.1).
c. Keep in mind that testing should be ordered only if the
results will change the physicians management. In the case
of an abnormal noninvasive test result, the physician may
TABLE
5.2
Cardiac Risk Stratification for Noncardiac
Surgical Procedures
Risk Stratification Procedure Examples
Vascular (reported cardiac Aortic and other major vascular surgery
risk often more than 5%) Peripheral vascular surgery
Intermediate (reported Intraperitoneal and intrathoracic surgery
cardiac risk generally Carotid endarterectomy
1%5%) Head and neck surgery
Orthopedic surgery
Prostate surgery
Low (reported cardiac risk Endoscopic procedures
generally less than 1%) Superficial procedures
Cataract surgery
Breast surgery
Ambulatory surgery
1389_Ch05_059-076 2/2/09 1:20 PM Page 63
consider revascularization, adjustment of medications, and/or
postoperative surveillance for myocardial damage.
3. Determining the need for revascularizationrevascularization
can be accomplished with percutaneous coronary angioplasty
(PTCA, with or without stent placement) or with coronary
artery bypass surgery (CABG).
a. Issues with PTCAthe majority of patients undergoing
PTCA have stents placed in an effort to reduce the risk for
restenosis.
i. Studies show that patients who undergo surgery soon
after stent placement may be at high risk for complica-
tions. Patients must be on two antiplatelet agents for
46 weeks after bare metal stent placement to allow the
lumen to become endothelialized.
P A R T
TABLE
5.3
Estimated Energy Requirements for Various
Activities
1 MET 4 METs
Can you take care of yourself? Climb a flight of stairs or walk up a hill?
Eat, dress, or use the Walk on level ground at
toilet? 4 mph?
Walk indoors around Run a short distance?
the house?
Walk a block or two on Do heavy work around the house
level ground at 23 miles like scrubbing floors or lifting or
per hour? moving heavy furniture?
Participate in activities such as golf,
bowling, dancing, doubles tennis?
4 METs Greater than 10 METs
Do light work around the Participate in strenuous sports like
house like dusting or swimming, singles tennis, football,
washing dishes? basketball, or skiing?
From Eagle KA, Berger PB, Calkins H, et al: ACC/AHA guideline update for perioperative
cardiovascular evaluation for noncardiac surgeryexecutive summary: A report of the
American College of Cardiology/American Heart Association Task Force on Practice
Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular
Evaluation for Noncardiac Surgery). J Am Coll Cardiol 2002;39(3):542553.
1389_Ch05_059-076 2/2/09 1:20 PM Page 64
(1) If antiplatelet agents are stopped too early, the
patient is at risk for in-stent thrombosis.
(2) If antiplatelet agents are continued perioperatively, the
patient is at risk for bleeding.
ii. Drug-eluting stents have been used to further reduce risk
for restenosis.
(1) Drug-eluting stents require a longer period of dual
antiplatelet therapy, necessitating a longer delay
before surgery can be safely performed.
b. Assessing the potential benefit of revascularizationthe
Coronary Artery Revascularization Prophylaxis (CARP)
study evaluated whether PTCA with stent or CABG prior to
major vascular surgery in high-risk patients reduced the risk
of cardiac complications.
i. Revascularization prior to surgery did not reduce the risk
for perioperative cardiac complications.
ii. Certain patients were excluded from the study, including
patients with:
(1) Low ejection fraction.
(2) Severe aortic stenosis.
(3) Left main coronary artery disease.
4. Medication to reduce riskstudies have evaluated the potential
benefit of beta blockers, alpha-2 agonists, calcium channel
blockers, statins, and nitrates in reducing the risk for periopera-
tive cardiac events.
a. Beta blockersstudies have shown reduced ischemia
and mortality for high-risk patients who are treated with
beta blockers perioperatively. Indications for beta blockers
include:
i. Patients who are already being treated with beta blockers.
ii. Patients with abnormal results on noninvasive cardiac
testing who are going for vascular surgery.
iii. Patents with known coronary artery disease who are
going for vascular surgery.
iv. Patients with one or more cardiac risk factors going for
vascular or intermediate-/high-risk nonvascular surgery,
as defined in Table 5.2.
(1) The strength of evidence in support of the use of
perioperative beta blockers varies with indication.
C H A P T E R
1389_Ch05_059-076 2/2/09 1:20 PM Page 65
(2) When possible, beta blockers should be adjusted to
achieve a resting heart rate of 5060, as long as the
blood pressure tolerates.
b. Alpha-2 agonistsclonidine has been shown to reduce
perioperative cardiac events. Clonidine is most useful for
patients who cannot tolerate beta-blocker treatment.
c. Calcium channel blockersthere is evidence that these
medications reduce ischemia and supraventricular
tachycardia, although their use in perioperative setting is not
well established.
d. Statinsthere are observational data that suggest that statins
may have a protective effect in term of reducing
perioperative cardiac complications.
e. Nitratesoral and intravenous nitrates have not been
shown to decrease the risk of perioperative cardiac
complications and may induce hypotension.
5. Surveillancethe majority of postoperative myocardial
ischemia and infarction cases occur in the absence of typical
symptoms. Unfortunately, the optimal strategy to detect
perioperative ischemia remains to be determined.
a. Postoperative ECGfor patients with known or suspected
coronary artery disease who are undergoing high- or
intermediate-risk procedures, the most cost-effective
strategy is to obtain a 12-lead ECG immediately after
surgery and on the first 2 postoperative days.
b. Computerized ST segment monitoringthis should be
considered for patients with coronary artery disease or
patients undergoing vascular surgery.
c. Cardiac markerscardiac troponin I is useful to rule out
myocardial infarction should symptoms, ECG changes, or
ST monitoring suggest myocardial ischemia.
IV. Preoperative Pulmonary Evaluation, Risk Assessment,
and Risk Reduction Strategies for Patients Undergoing
Noncardiothoracic Surgery
A. Overview
1. Postoperative pulmonary complications (PPCs) are common
and contribute significantly to mortality and morbidity of
surgical patients.
P A R T
1389_Ch05_059-076 2/2/09 1:20 PM Page 66
2. PPCs predict long-term mortality.
3. Validated patient-related and procedure-related risk factors
predict PPCs.
4. The goal of preoperative pulmonary evaluation is to identify
risk factors, optimize preoperative conditions, and to anticipate
postoperative interventions that may reduce risk.
B. Scope of significant pulmonary complications
1. PPCs that are known to contribute to mortality and morbidity or
prolong hospital stay include the following:
a. Atelectasis
b. Bronchospasm
c. Exacerbation of chronic obstructive pulmonary disease (COPD)
d. Pneumonia
e. Respiratory failure with prolonged mechanical ventilation
C. Interview, physical examination, and laboratory assessment
1. Focus of the interview
a. Assess baseline lung disease, such as asthma, COPD,
obstructive sleep apnea (OSA), and recent lung infections.
b. Assess baseline cardiac disease, congestive heart failure
(CHF) in particular.
c. Assess baseline neuromuscular disease.
d. Assess baseline functional status.
e. Assess nutritional status, and identify patients with recent
weight loss.
f. Identify patients with unexplained shortness of breath or cough.
g. Identify patients with significant alcohol use.
2. Focus of the physical examination
a. Assess nutritional status
b. Baseline lung examination important for identifying
patients who may need further preoperative evaluation
3. Laboratory assessment
a. Preoperative spirometry may be helpful in patients with
active asthma, recent COPD exacerbation, or unexplained
cough or shortness of breath.
b. Preoperative arterial blood gas (ABG) is not indicated in
most patients. Patients with abnormal baseline ABG are at
higher risk for PPCs, but these patients can be identified as
high-risk based on findings in history and/or physical
examination.
C H A P T E R
1389_Ch05_059-076 2/2/09 1:20 PM Page 67
c. Chest x-ray (CXR) should be considered for:
i. Patients over the age of 50 years scheduled for
intermediate- to high-risk surgery.
ii. Patients with a history of heart or lung disease scheduled
for intermediate- to high-risk surgery.
D. Patient-related risk factors
1. Age is an important risk factor, even after adjustment for
comorbid conditions
2. Albumin 3.5 g/dL significant independent risk factor for PPCs
3. American Society of Anesthesiologists (ASA) class 2 (Table 5.4)
identifies patients at increased (at least twofold) risk for PPCs
4. Asthma
a. Mild or moderate asthma is not a significant risk factor for
PPCs.
b. Risk factors for bronchospasm include recent asthma symp-
toms, recent treatment for active asthma, and a history of
tracheal intubation.
c. A short course of perioperative steroids does not increase the
rate of PPCs in patients with asthma.
d. For elective surgery, patients with asthma should be
optimized to achieve at least 80% of personal best FEV
1
and no wheezing on lung auscultation
5. COPD
a. Clinical practice suggests that COPD is a risk factor for
PPCs, but the magnitude of this risk is not well established.
b. No threshold spirometric value has been established that
should preclude surgery. Experience with lung reduction
P A R T
TABLE
5.4
The ASA Physical Status Classification
Class 1
Class 2
Class 3
Class 4
Class 5
Healthy patient; no medical problems
Mild systemic disease
Severe systemic disease but not incapacitating
Severe systemic disease that is a constant threat to life
Moribund; not expected to live 24 hours irrespective of
operation
1389_Ch05_059-076 2/2/09 1:20 PM Page 68
surgery suggests that even patients with severe COPD may be
appropriate candidates for surgery in selected cases.
6. CHF is an established risk factor for PPCs
7. Functional status
a. Functional dependence defined as inability to perform
activities of daily living
b. Functional dependence is significant risk factor for PPCs
8. Obesity not an independent risk factor for PPCs
9. OSA may increase risk of PPCs
10. Smoking
a. Cessation of smoking 2 months before surgery may
decrease risk of PPCs.
b. Cessation of smoking within 2 weeks of surgery may
increase risk of PPCs.
E. Procedure-related risk factors
1. High-risk surgeries
a. Abdominal aortic aneurysm repair
b. Thoracic surgery
c. Neurosurgery
d. Upper abdominal surgery
e. Neck surgery
f. Vascular surgery
g. Emergency surgery
2. Duration of surgery (over 3 hours) is independent risk
factor
F. Strategies to reduce postoperative pulmonary complications
1. Optimization of baseline cardiopulmonary disease
2. Lung expansion maneuvers, including incentive spirometry
and chest physical therapy, reduce risk for PPCs; chest
physical therapy involves one or more of the following:
deep breathing exercises, percussion and vibration, suctioning
and mobilization
3. Postoperative pain control important to promote deep
breathing
4. Nasogastric decompression should be used in patients post
abdominal surgery who develop symptomatic abdominal
distention, nausea, vomiting
5. No conclusive evidence that regional anesthesia superior to
general anesthesia in terms of reducing PPCs
C H A P T E R
1389_Ch05_059-076 2/2/09 1:20 PM Page 69
V. Preoperative Evaluation of Patients on Antithrombotic
or Anticoagulant Therapy
A. Overview
1. Optimal perioperative management of antithrombotic or
anticoagulant therapy depends on the original indication for
therapy, comorbid conditions, and anticipated bleeding risk
associated with the planned procedure.
2. Risk of postoperative bleeding has to be balanced against the
risk of postoperative thrombosis.
3. Perioperative strategy must be designed in close consultation
with the surgeon.
B. Common antithrombotic medications
1. Aspirinmechanism of action is irreversible inhibition of
platelet function
2. Clopidogrel and ticlopidinework by inhibiting adenosine
diphosphate (ADP)dependent platelet aggregation
3. Warfarinmechanism of action is inhibition of vitamin K
dependent clotting factors
C. Patient-specific considerations
1. Age is risk factor for venous thromboembolism
2. Prior history of bleeding raises risk for subsequent bleeding
3. Comorbid conditions
a. Many cancers raise the risk of thrombosis.
b. Chronic liver and kidney disease may raise the risk for
hemorrhage.
4. Concurrent use of warfarin and antiplatelet agents increase risk
for bleeding
5. Common indications for antiplatelet therapy
a. Cardiac stents
b. Stroke prevention
c. Coronary artery disease
6. Common indications for warfarin
a. Primary or secondary prevention of venous thromboem-
bolism (VTE)
b. Atrial fibrillation with or without structural heart disease
c. Mechanical heart valve(s)
d. Ventricular aneurysm
e. Hypercoagulable state
f. Inferior vena cava filter
P A R T
1389_Ch05_059-076 2/2/09 1:20 PM Page 70
C H A P T E R
D. Procedure-specific considerations
1. Most dental procedures do not require discontinuation of
anticoagulation.
2. Neurosurgical procedures and other procedures that involve
tissues where even minimal bleeding may result in significant
morbidity and mortality require discontinuation of antiplatelet
medications and warfarin.
E. Common perioperative strategies
1. Low bleedingrisk procedures: warfarin may be continued
(International Normalized Ratio [INR] should be adjusted to
low end of therapeutic range); antiplatelet agents should be
continued
2. High bleedingrisk procedures
a. Low thrombotic risk
i. Discontinue warfarin 35 days before the procedure
ii. Restart warfarin immediately post procedure if allowable
from surgical standpoint
iii. Consider IV heparin 2448 hours after procedure if allow-
able from surgical standpoint and INR subtherapeutic
b. High thrombotic risk
i. Discontinue warfarin 35 days before procedure
ii. Initiate IV heparin or subcutaneous (SQ) low molecular
weight heparin (LMWH) when INR becomes subtherapeutic
iii. Proceed with surgery when INR 1.5
iv. Discontinue heparin 6 hours prior to procedure or
LMWH 24 hours prior to procedure
v. Start IV heparin as soon after procedure as is safe from
surgical standpoint
vi. Restart warfarin the night of procedure unless contraindi-
cated from surgical standpoint
VI. Preoperative Evaluation and Management
of Endocrine Disorders
A. Preoperative patient with diabetes mellitus
1. Goals of preoperative assessment
a. Identify the type and duration of diabetes.
b. Assess adequacy of glycemic control.
c. Identify any complications of diabetes.
d. Evaluate cardiac and renal function.
e. Establish strategy for perioperative glycemic control.
1389_Ch05_059-076 2/2/09 1:20 PM Page 71
P A R T
2. Perioperative monitoring
a. Patients on insulin or oral diabetic medications should have
blood glucose checked before surgery, every 12 hours
during surgery, and every 6 hours post surgery.
b. Patients whose diabetes is controlled with diet should have
their blood glucose checked preoperatively.
3. Perioperative management of diabetic medications
a. Oral diabetic medications should be held on day of surgery
and restarted once patients resume diet
b. Patients on insulin therapy
i. Short-acting insulin should be held the morning of
surgery and restarted once patients resume diet.
ii. Patients should be given half to two thirds of their long-
acting insulin on the day of surgery.
iii. Many patients will require IV insulin drips during major
surgery.
B. Stress dose corticosteroids
1. Who is at risk for perioperative adrenal insufficiency?
a. Patients with history of adrenal insufficiency, either
primary or secondary
b. Patients who have received prolonged courses of systemic
corticosteroids in the year preceding surgery at risk for
secondary adrenal insufficiency
i. Patients who have received 20 mg of prednisone or an
equivalent dose of another corticosteroid medication for
3 weeks or longer.
ii. Patient who have received multiple short courses of
corticosteroids in the past year.
c. Patients with severe hyperthyroidism undergoing emergent
surgery
2. ACTH stimulation test may be helpful for assessment of
hypothalamic-pituitary-adrenal axis in patients with suspected
adrenal suppression
3. Perioperative stress corticosteroid regimens for patients at risk
for perioperative adrenal insufficiency
a. Major surgerygive 100 mg IV hydrocortisone prior to
surgery, then 50 mg hydrocortisone every 8 hours for
4872 hours, then resume usual dose of steroids
b. Minor proceduregive usual dose of steroids, no
additional supplementation
1389_Ch05_059-076 2/2/09 1:20 PM Page 72
C. Preoperative patient with thyroid disease
1. Surgery in patients with hypothyroidism
a. Mild to moderate hypothyroidism does not increase periop-
erative risk.
b. Patients with severe hypothyroidism or myxedema coma
should be treated prior to surgery.
2. Surgery in patients with hyperthyroidism
a. Mild hyperthyroidismpatients should be started on a beta
blocker and proceed to surgery
b. Severe hyperthyroidism
i. Patients can be started on antithyroid agents and prepared
for surgery in 38 weeks.
ii. Patients who are hyperthyroid at the time of surgery are
at risk for atrial fibrillation, adrenal insufficiency, and
thyroid storm.
iii. Thyrotoxic patients undergoing urgent surgery should be
treated with antithyroid medications, beta blockers, and
stress dose steroids and receive very close hemodynamic
monitoring.
C H A P T E R
MENTOR TIPS
Communicating the assessment and plan to the surgeon and
patient is critical. The more specific and concise the recom-
mendations, the more likely the recommendations will be
followed.
Anesthesia is generally safe, with an overall mortality rate of
0.3%.
In general, preoperative testing should only be done if the
results might alter clinical management.
Men over 40 and women over 50 years of age who are planned
for
intermediate- to high-risk surgery should have a preoperative
ECG.
A thorough history and exam is essential in preoperative risk
assessment. Special attention should be made to identifying
active symptoms and underlying risk factors for cardiac
disease.
Surgeries that carry a high risk for perioperative cardiac compli-
cations include emergent surgeries, aortic and peripheral
1389_Ch05_059-076 2/2/09 1:20 PM Page 73
P A R T
vascular surgeries, and prolonged surgeries with large fluid
shifts and/or blood loss.
Revascularization prior to noncardiac surgery has not been
shown to reduce the risk for perioperative cardiac
complications.
Beta blockers have been shown to reduce ischemia and
mortality in high-risk patients.
Cessation of smoking 2 months prior to surgery decreases the
risk for postoperative pulmonary complications. However,
cessation of smoking within 2 weeks of surgery may
paradoxically increase risk.
Lung expansion maneuvers reduce the risk for postoperative
pulmonary complications.
Optimal perioperative management of antithrombotic or anti-
coagulant therapy depends on the original indication for
therapy, comorbid conditions, and anticipated bleeding risk
associated with planned procedure.
Patients who have received prolonged courses of systemic
corticosteroids in the year preceding surgery are at risk for
secondary adrenal insufficiency.
Mild hypothyroidism does not confer an increased risk for
perioperative complications. Similarly, mild hyperthyroidism
does not confer an increased risk for perioperative
complications.
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1. A 65-year-old man with history of kidney transplant, atrial fibrillation
treated with warfarin, and stroke needs to undergo kidney biopsy to
evaluate worsening renal function. What is the optimal perioperative
strategy with respect to management of his anticoagulation?
a. Continue warfarin throughout the operative interval.
b. Discontinue warfarin 35 days before the procedure, and restart
immediately after the procedure.
c. Discontinue warfarin 35 days before the procedure; when INR
2 start heparin infusion until 46 hours before the procedure.
Resume heparin infusion several hours after the procedure, and
resume warfarin the night of the procedure.
d. Discontinue warfarin 35 days before the procedure; when INR
2 start subcutaneous heparin 5000 units every 12 hours. Resume
warfarin the night of the procedure.
C H A P T E R
1389_Ch05_059-076 2/2/09 1:20 PM Page 75
2. Which of the following statements accurately describes the rationale
for preoperative evaluation?
a. Clear the patient for surgery.
b. Order and evaluate routine preoperative tests.
c. Recommend the safest type of anesthesia.
d. Take measures to reduce perioperative risk.
3. A 65-year-old male with a history of hypertension will undergo
cataract surgery. He has no additional past medical or surgical history
or symptoms. The physical examination result is normal. His only
medication is hydrochlorothiazide 25 mg daily. What preoperative test
should he have?
a. No testing
b. Electrocardiogram
c. Exercise cardiac stress test
d. Exercise cardiac stress test with perfusion imaging
P A R T
1389_Ch05_059-076 2/2/09 1:20 PM Page 76
DIAGNOSIS AND
MANAGEMENT
OF COMMON
OUTPATIENT
SYMPTOMS
DIAGNOSIS AND
MANAGEMENT
OF COMMON
OUTPATIENT
SYMPTOMS
77
two
P A R T
I. Background
A. Headache is one of the most common complaints a primary care
clinician will encounter
B. Features
1. Only intracranial structures with sensation are meninges and
circle of Willis and a few centimeters of its branches
2. Primary headache results from neurogenic mistakes in
processing pain information
HEADACHE
Gary J. Martin, MD, and James J. Foody, MD
CHAPTER
6
1389_Ch06_077-090 2/2/09 1:27 PM Page 77
78 two DIAGNOSIS AND MANAGEMENT OF COMMON OUTPATIENT SYMPTOMS
P A R T
3. Term vascular headaches is a misnomer: blood vessels are
not the cause of headaches, although vascular response is a
component of some primary headaches
4. Episodic primary headache runs across continuum of clinical
presentations from typical migraine with aura to common
everyday headache that people self-treat with over-the-counter
analgesics
5. Secondary headache is result of anatomical pathology
Primary headaches arise from brain dysfunction.
C. Headache classification
1. Primary headache
a. Migraine
b. Tension-type
c. Chronic daily
d. Cluster
2. Secondary headache
a. Increased intracranial pressure
b. Intracerebral hemorrhage
c. Trauma
d. Tumor
e. Post concussion
D. Clinical manifestation of primary headache
1. Migraine
a. Aura precedes a headache in fewer than 20% of all
migraineurs. Aura is a neurologic disturbance of the
cerebral cortex due to spreading electrochemical depres-
sion followed by cortical oligemia. Aura, especially
visual aura, may precede headache onset by as much
as an hour and typically lasts about 20 minutes.
b. Migraine pain has any or all of following characteristics:
throbbing; unilateral; accompanied by nausea with or without
vomiting; gastroparesis; light, smell, or sound hyper-
sensitivity; severity that is moderate or worse and lasts
472 hours.
1389_Ch06_077-090 2/2/09 1:27 PM Page 78
c.Migraine syndrome is ~4 times more common in women.
Many women have variation of frequency and severity that
correlates with menses (catameneal migraine).
d. Migraine exhibits a strong familial pattern.
e. Most people with migraine will exhibit one or more of
the following: tendency for motion sickness, pain on
chilling of roof of mouth (freezer brain), ice picklike
head pains lasting for seconds, or personal history of colic
in infancy.
2. Tension-type
a. Hypothetical pathologic mechanism is same as migraine
i. Studies demonstrate there is no muscle tension in
tension-type headache.
ii. Stress or tension as headache inducer is not different from
migraine.
b. Distinguished by lesser severity and absence of patterns
typical for migraine
c. ~90% of people have some headaches during lifetime
d. Most of these headaches never require medical attention
because acetaminophen or nonsteroidal anti-inflammatory
drug (NSAID) analgesics relieve pain
3. Chronic daily headache
a. Occurs with background of frequent primary headache
treated with analgesic
b. Headache rebounds after treatment until rebound headache
and primary headache overlap
c. Recurrent episodic primary headache can transform into
headache that is present on most days
6 HEADACHE 79
C H A P T E R
Migraine is a primary headache characterized by
moderate to severe unilateral throbbing pain
lasting 472 hours, often accompanied by nausea and
vomiting.
Tension-type headache is an old term for primary
headaches that do not fit migraine characteristics.
1389_Ch06_077-090 2/2/09 1:27 PM Page 79
4. Cluster
a. Manifested by severe, boring type of pain perceived behind
one eye; is always unilateral
b. Male-to-female prevalence 10:1
c. Clustering of headaches multiple times daily for a few
to several days, followed by weeks to months of no
episodes
d. Initial headache of a cluster episode almost always begins
during sleep at night
e. Each episode of headache lasts 2030 minutes, often
repeated several times a night
5. Diagnostic guidelines
a. Sinus headache is almost always a primary headache
syndrome. Head pain from sinusitis is usually easy to
distinguish.
b. No one seeks medical care without first trying self-medication
with over-the-counter drugs.
c. History of chronic episodic headache and normal neurologic
examination is sufficient for diagnosis. Primary headache is
not a diagnosis of exclusion.
d. Patients with cluster headache often have a peculiar history
of hitting their head against the wall because pain is so severe.
E. Clinical manifestations of secondary headache
1. History of new onset headache in adult or change in pattern of
chronic primary headache should alert to possibility of pain
caused by something else.
2. Neurologic examination is normal in primary headache.
Abnormal neurologic examination results suggest secondary
headache caused by another disorder. Neurologic abnormalities in
setting of headache always need thorough evaluation.
P A R T
Frequent use of medicine that aborts primary
headache can cause chronic daily headache.
Cluster headaches strike as brief, severe, and retro-
orbital, often disrupting sleep, clustering together
for several days with longer headache-free intervals.
1389_Ch06_077-090 2/2/09 1:27 PM Page 80
3. Cluster headache can be an exception to the rule about normal
physical examination. During a headache, it is possible to
demonstrate ipsilateral Horner syndrome.
4. Head computed tomography (CT) scan without infusion is 100%
sensitive for clinically significant intracerebral hemorrhage.
5. Subarachnoid hemorrhage, meningitis, and meningeal malig-
nancy require examination of cerebrospinal fluid (CSF). Imaging
is seldom, if ever, diagnostic.
II. Approach to the Patient
A. History
1. Inquire about age at onset. Primary headache syndromes start in
childhood or adolescence. However, patients may not recognize
any pattern until adulthood.
2. Ask patient to describe typical headache duration. If headaches
are episodic, attempt to identify typical intervals between
headaches.
3. Ask what measures have been used to treat headaches and what
response to treatment has been.
4. Listen for triggers
5. A headache that exists on awakening in the morning means
nothing. The notion that such a headache suggests brain tumor
is wrong.
6. Ask about family history, symptoms of motion sickness, cold-
induced head pain, and ice picklike head pains. Positive
responses may bolster the diagnosis of primary headache.
a. Note that many patients may deny family history of migraine
but report that mothers used to get sinus headaches.
b. Parents need to provide history of colic.
6 HEADACHE 81
C H A P T E R
Change in pattern of headache is an important alert
for secondary headache. Head CT scan and/or CSF
examination would be necessary.
Identify common lifestyle triggers, including sleep
deprivation, occasional excessive sleep, caffeine,
caffeine withdrawal, alcohol, fasting, life stresses, or any
relationship to menstrual cycle.
1389_Ch06_077-090 2/2/09 1:27 PM Page 81
B. Physical examination
1. Primary headache syndromes do not cause physical examination
abnormalities
2. Palpation of entire head and auscultation for intracranial bruit
rarely yield abnormality yet may be only early clue for secondary
headache
3. Mandatory elements
1. Failure to thus reassure often results in treatment failure.
III. Treatment
A. Headache treatment is not simple; lifestyle interventions are
effective and safe; drugs may be necessary to abort a headache
episode or prevent headache recurrences; no distinct line in the
spectrum of headache delineating which should require more
specific drug treatment
C. Laboratory evaluation
1. Consider complete blood count and glucose.
2. If intracranial hemorrhage is a possibility, head CT scan without
contrast is an emergency procedure.
3. If subarachnoid hemorrhage or meningitis is a possibility, CSF
examination is an emergency procedure. Many would choose
an imaging procedure first to exclude increased intracranial
pressure.
4. Magnetic resonance imaging (MRI) is more sensitive for small
tumors, encephalitis, some unusual infections, stroke, and
demyelinating disease but not as an emergency procedure.
D. Remember to consider reason that patients with primary headache
seek medical attention; they often worry about brain tumor; careful
history and competent physical examination are adequate to rule
out brain tumor
P A R T
Physical examination for headache must include head,
cranial nerves, reflexes, stance, gait, frontal release,
and funduscopy.
If true, then always tell patients that they do not have a
brain tumor, even if they do not ask.
1389_Ch06_077-090 2/2/09 1:27 PM Page 82
1. Transformation to chronic daily headache is a limiting factor
with drugs that relieve episodic headaches. Transformation
is unlikely if fewer than 10 doses are required in a month;
transformation is common when abortive drugs are generally
used three or more times a week. Any abortive drug, even
acetaminophen, can result in transformation to chronic daily
headache. Compound medicines that contain caffeine or barbi-
turate are more prone to cause transformation.
B. Lifestyle
1. Regularize sleeping hours; oversleeping is as likely to trigger
headache as sleep deprivation.
2. Avoid fasting; eat something for breakfast.
3. Standardize caffeine intake.
a. Most people tolerate two to three cups of coffee or equiva-
lent in a day.
b. Some may need to avoid caffeine totally.
c. Include caffeinated soft drinks in estimating total daily intake.
4. Regulate alcohol.
a. Red wines may be especially provocative.
b. Alcohol can interfere with sleep maintenance, leading to
headache.
5. Observe for any consistent trigger.
6. Contrary to popular belief, chocolate does not induce migraine.
C. Abortive (Table 6.1)
1. Acetaminophen
a. Least side effects, but almost everyone has tried it prior to
medical consultation
2. Aspirin or NSAID
a. Aspirin maximal dose 650 mg
b. NSAIDs have higher maximal equivalent dose
i. Ibuprofen 200 mg naproxen 220 mg aspirin 650 mg
ii. No comparative evidence demonstrating superiority of
any NSAID
iii. COX-2 inhibitors not superior to standard NSAIDs
6 HEADACHE 83
C H A P T E R
Transformation of episodic headaches to chronic daily
headache is unlikely if abortive drug use does not
exceed 10 doses per month.
1389_Ch06_077-090 2/2/09 1:27 PM Page 83
3. Triptans
a. Gastroparesis is often a part of migraine, so oral drug
availability may be impaired, but oral drugs may have a
longer duration of effectiveness.
b. The subcutaneous route is fastest.
c. Intranasal spray is absorbed as quickly as injected.
d. The sublingual route is almost as quickly absorbed as injected.
e. Oral tablets have variable absorption but greatest patient
acceptance.
4. Ergot derivatives
a. DHE
i. Most effective early at headache onset; effectiveness
diminishes quickly with headache duration
ii. Intranasal spray for outpatients
iii. Intravenous bolus or infusion for inpatients
b. Constituent of many unregulated homeopathic and
natural compounds
P A R T
TABLE
6.1
Drug Classes to Stop Primary Headache
Drug Class Route(s) of Administration
Acetaminophen Oral
Aspirin Oral
NSAID Oral
Triptans Oral
Intranasal
Transbuccal
Subcutaneous
Dihydroergotamine (DHE) Intranasal
Intramuscular
Intravenous
Narcotics Intranasal
Parenteral
Oral
Triptans have the greatest efficacy. Early treatment is
best. They differ primarily in route of administration.
1389_Ch06_077-090 2/2/09 1:27 PM Page 84
5. Narcotics
a. Using potentially addictive agent for lifelong disorder
is troublesome; migraine-specific drugs (i.e., triptans
and DHE) as potent or more effective than narcotic
analgesics
b. Oral narcotics
i. Poor pharmacologic availability due to delayed
absorption
ii. Slow onset of action can lead to excessive dosing
iii. Caution with potentially addictive agent for a chronic
condition
iv. Lipophilic preparations, such as oxycodone and meperi-
dine, have extremely high abuse potential
c. Parenteral narcotics
i. Quick pharmacologic availability
ii. Occasionally used in emergency room setting
d. Intranasal narcotics
i. Butorphanol available as intranasal spray
ii. Mixed agonist-antagonist activity theoretically less prone
to addiction
iii. Use in pregnancy not unusual; no studies exist demon-
strating relative safety
e. Anti-nausea drugs
i. Drugs that prevent or relieve nausea have no direct effect
on primary headache but may be useful as adjunct treat-
ment (e.g., metoclopramide, promethazine)
D. Preventive (Table 6.2)
6 HEADACHE 85
C H A P T E R
TABLE
6.2
Drugs to Prevent Primary Headache
Drug Dosing Suggestion
Divalproex 1252500 mg/day
Amitriptyline/nortriptyline 1050 mg at bedtime
Topiramate
Beta blockers
Verapamil 40320 mg/day
Cyproheptadine 416 mg/day
1389_Ch06_077-090 2/2/09 1:27 PM Page 85
1. Frequent use of any drug that aborts primary headache will
lead to transformation to chronic daily headache. When
patients require abortive treatment more than two to three
times a week, they can prevent headaches by taking daily
preventive medication. Several drug classes are effective.
Clinical trials, in particular comparative trials, have been small.
2. Lack of efficacy of one drug class does not predict failure of
drugs from other classes. Switching drugs within a class might
improve side effects, but drugs within a class likely have the
same beneficial effects.
3. Preventive benefits may not be apparent for 26 weeks.
4. There are no clinical trials for use in pregnancy. Almost all pre-
ventive drugs are potent CNS serotonin antagonists, suggesting
possible fetal intrauterine developmental risk.
5. Divalproex
a. Comparative results suggest modestly greater effectiveness
than other agents.
b. The initial dose is small, 125 mg once or twice a day.
c. The dose is gradually increased until successful or until
reaching maximal anticonvulsant dose.
d. Ill-defined malaise and fatigue are not uncommon side
effects.
e. Hepatotoxicity occurs in children and adolescents. Hepato-
toxicity occurs rarely, if at all, in adults.
f. Clinical effectiveness is 60%80%.
6. Tricyclic drugs
a. Amitriptyline and nortriptyline most commonly used
b. Effective dose much lower than dose necessary for antide-
pressant properties; 1050 mg is usual range
c. Little or no antidepressant effect at this dose
d. Sedating side effect can be advantageous if sleep disorder
contributes to triggering headaches
e. Mild weight gain common and problematic.
f. Dry mouth common limiting side effect
g. Clinical effectiveness approximates that of divalproex
P A R T
Low-dose tricyclic drugs are useful in preventing
primary headache. Their sedating side effect can be
useful if sleeping is a problem.
1389_Ch06_077-090 2/2/09 1:27 PM Page 86
7. Beta-adrenergic blockers
a. First agent to demonstrate preventive effectiveness
b. Dose range identical to that for treating hypertension
c. Clinical effectiveness ~40%
8. Topiramate
a. Dose range identical to anticonvulsant dosage
b. Lacks substantial comparative trials
c. Hypothetical mechanism of action differs from that of
divalproex
d. Mild weight gain common
e. Subjective adverse effects common
9. Calcium channel blockers
a. Verapamil 40320 mg daily
b. Bradycardia, constipation, and hypotension frequent side
effects
c. Mild weight gain common
d. Clinical effectiveness 20%40%
10. Antihistamine serotonin antagonist
a. Cyproheptadine 416 mg daily
b. Extensive experience in childhood migraine makes it drug
of choice for children and adolescents
c. Sedation often prominent at initiation but typically
improves with continued use
d. Weight gain very common and problematic
e. Dry mouth very common and problematic
11. SSRI antidepressants
a. It is questionable if SSRI agents are effective in headache
prevention.
b. Depression is a frequent co-morbid condition with
primary headache syndromes. Untreated depression
can aggravate underlying headache.
E. Nonspecific treatment
1. Therapies such as stress reduction techniques, biofeed-
back, massage therapies, stretching exercises, and
relaxation training all may be useful adjuncts for selected
patients. There are no clinical trials demonstrating
effectiveness.
2. Vitamin and nutritional supplement therapy lacks evidence-
based support.
6 HEADACHE 87
C H A P T E R
1389_Ch06_077-090 2/2/09 1:27 PM Page 87
3. Many over-the-counter nutritional supplements and homeopathic
remedies contain compounds that interact with pharmaceutical
treatment.
P A R T
MENTOR TIPS DIGEST
Primary headaches arise from brain dysfunction.
Migraine is a primary headache characterized by moderate to
severe unilateral throbbing pain lasting 472 hours, often
accompanied by nausea and vomiting.
Tension-type headache is an old term for primary
headaches that do not fit migraine characteristics.
Frequent use of medicine that aborts primary headache can
cause chronic daily headache.
Cluster headaches strike as brief, severe, and retro-orbital,
often disrupting sleep, clustering together for several days
with longer headache-free intervals.
Change in pattern of headache is an important alert for
secondary headache. Head CT scan and/or CSF examination
would be necessary.
Identify common lifestyle triggers, including sleep depriva-
tion; occasional excessive sleep; caffeine; caffeine
withdrawal; alcohol; fasting; life stresses; or any relation-
ship to menstrual cycle.
Physical examination for headache must include head, cranial
nerves, reflexes, stance, gait, frontal release, and funduscopy.
If true, then always tell patients that they do not have a brain
tumor, even if they do not ask.
Transformation of episodic headaches to chronic daily
headache is unlikely if abortive drug use does not exceed
10 doses per month.
Triptans have the greatest efficacy. Early treatment is best.
They differ primarily in route of administration.
Low-dose tricyclic drugs are useful in preventing primary
headache. Their sedating side effect can be useful if sleeping
is a problem.
Resources
Dodick D, Freitag F. Evidence-based understanding of medication-overuse
headache: Clinical implications. Headache 46:S202S211, 2006.
1389_Ch06_077-090 2/2/09 1:27 PM Page 88
This article discusses the problem of medication-overuse headache
from a variety of perspectives, based on the best available
evidence.
Lipton RB, Bigal ME. Migraine prevalence, disease burden, and the need
for preventive therapy. Neurology 68: 343349, 2007.
Objectives: to reassess the prevalence of migraine in the United
States; to assess patterns of migraine treatment in the population;
and to contrast current patterns of preventive treatment use with
recommendations for use from an expert headache panel
Rothrock, JF. Lets put mixed headache to rest. Headache 47:
9497, 2007.
1. Primary headache differs from secondary headache in that:
a. Primary headache describes the first headache of a persons
life.
b. Primary headache describes neurogenic headache.
c. Aura precedes secondary headache.
d. Triptans are the drugs of choice for secondary headache.
2. The following statement about headache is true:
a. Most persons with headache will sometime seek medical attention
for their headache.
b. Almost all people will experience headache.
c. Women are four times more likely than men to have
headaches.
d. Prevention is a critical factor in treating most headaches.
3. The aura of migraine headache typically demonstrates:
a. A sharp jabbing pain that can feel as if an ice pick is jammed in the
head.
b. Sudden onset of visual scotoma (circumscribed vision loss) often
relieved by using triptan drugs
6 HEADACHE 89
C H A P T E R
1389_Ch06_077-090 2/2/09 1:27 PM Page 89
c. Gradual onset of vision distortion that becomes progressively
greater over 20 minutes.
d. Cerebral ischemia due to constriction of middle or posterior cerebral
artery.
P A R T
1389_Ch06_077-090 2/2/09 1:27 PM Page 90
91
COMMON SLEEP
DISORDERS
Helen Gartner Martin, MD
CHAPTER
7
I. Introduction
A. Sleep disturbances are very common problems in primary care.
B. Sleep disturbances can affect quality of life and be significant
medical problems.
C. Questions to ask patients to evaluate their sleep include:
1. How is your sleep at night?
2. Are you too sleepy during the day?
3. Does anything unusual happen during your sleep?
D. Some of the most common sleep disorders are insomnia, obstruc-
tive sleep apnea (OSA), and restless leg syndrome/periodic leg
movements of sleep.
II. Insomnia
A. Definition/epidemiology
1. Insomnia is defined as difficulty with sleep initiation, duration, or
consolidation or quality, despite adequate time and opportunity for
sleep.
2. There should be an associated complaint of some daytime
impairment (e.g., lack of energy, difficulty concentrating,
irritability).
30%40% of adults experience insomnia within any
given year.
10%15% of adults have chronic insomnia, defined as
persisting for at least several weeks.
1389_Ch07_091-106 2/2/09 1:26 PM Page 91
P A R T
B. Classification
1. Acute insomnia
a. Insomnia occurring in association with identifiable stressor
b. Should resolve within several days to weeks as stressor
resolves
C. Chronic insomnialasting more than several weeks
1. Psychophysiologic insomnia
a. The patient learns sleep-preventing associations, commonly
after an acute stressor, and develops excessive anxiety concern-
ing sleep
2. Paradoxical insomnia
a. Also called sleep state misperception
b. Characterized by marked overestimate of lack of sleep as
well as overestimate of daytime impairment
3. Insomnia associated with psychiatric disorder
a. Insomnia commonly associated with depression, bipolar
disorder, anxiety
4. Insomnia associated with drug or substance abuse
a. Insomnia commonly associated with caffeine, ampheta-
mines, other central nervous system (CNS) stimulants
b. Insomnia may be unintended side effect of some prescription
medications (e.g., antidepressants, antihypertensives,
antiepileptics, theophylline)
c. Acute and chronic alcohol abuse as well as abrupt with-
drawal from alcohol may disrupt sleep
5. Insomnia due to a medical condition
a. Chronic pain
b. Respiratory disorders, e.g., asthma
c. Gastroesophageal reflux disorder
d. Medical conditions associated with nocturia
e. Neurologic disorders
f. Menopause
6. Insomnia not otherwise classified
D. Evaluation of patient with insomnia
1. History
A complete sleep history is the most important tool in
evaluating insomnia.
1389_Ch07_091-106 2/2/09 1:26 PM Page 92
a. History should be tailored based on whether insomnia is
acute or chronic.
i. Acute insomnia
(1) Has there been a recent stressful life event?
(2) Has there been a recent change in sleeping
environment?
(3) Are there any acute medical or surgical issues?
(4) Has the patient started taking any new medications or
stopped any chronic medications?
(5) Has the patient experienced any recent time changes
(e.g., shift work or jet lag?)
ii. Chronic insomnia
(1) Has the patient had a long history of difficulty
sleeping?
(2) What are the duration and frequency of the problem?
(3) What are usual bedtime and waking times for week-
days and weekends?
(4) What are the patients sleep-related habits? Does the
patient read or watch television in bed? If not able
to sleep, does the patient remain in bed or leave the
bedroom?
(5) Does the patient have a medical or psychiatric prob-
lem which might be interfering with sleep?
(6) Does the patient use caffeine, alcohol, or tobacco?
When, and how much?
(7) Does the patient snore or have leg movements
during sleep? These questions are frequently better
answered by a bed partner.
(8) Is the patients sleep disrupted by bed partner
(including pets)?
(9) Has the patient traveled?
(10) What are the patients work hours?
(11) What are the daytime consequences of the patients
insomnia?
2. Physical examination
a. Looking for signs of thyroid disorders (tremor, goiter, lid
lag) or congestive heart failure (CHF) (edema, rales, jugular
venous distention [JVD], S
3
) is reasonable.
7 COMMON SLEEP DISORDERS 93
C H A P T E R
1389_Ch07_091-106 2/2/09 1:26 PM Page 93
4. Polysomnography
a. Occasionally, a formal sleep study may be indicated if a
problem such as sleep apnea or nocturnal leg movements is
suspected as a cause of sleep disruption.
b. If a sleep study is performed, the comparison of the recorded
information with the patients perception of the nights sleep
may help physician better evaluate patients complaints.
E. Treatment
1. Review of sleep hygiene measures is appropriate in most cases.
2. Acute insomnia
a. Alter, if possible, any precipitating factor (e.g., stop medica-
tion causing problem, treat nocturnal pain adequately).
b. Treatment with hypnotics may be valuable for current symp-
toms and help avoid the development of learned or condi-
tioned insomnia.
3. Chronic insomnia
a. Treat any sleep-disturbing issues, such as apnea and leg
movements.
b. Optimize any medical conditions disturbing sleep.
c. It is very important to establish reasonable goals and
expectations at the beginning of treatment.
d. Medications:
i. The use of medications for chronic insomnia is controver-
sial, as most hypnotics have been approved for short-term
use only. However, more recently, at least one hypnotic has
been approved for long-term use.
P A R T
Recording daily sleep diary for 12 weeks can help
determine extent of problem and may uncover poor
sleep habits. Information includes wake and sleep times,
nocturnal awakenings, time spent awake during the night,
and quality of sleep as determined by patient and bed
partner.
The best therapy for chronic insomnia involves both
medications and cognitive behavioral therapy.
3. Sleep diary
1389_Ch07_091-106 2/2/09 1:26 PM Page 94
(1) Benzodiazepine (BDZ) receptor agonists
(A) Almost all drugs approved for treatment of insom-
nia in the United States are BDZ receptor agonists
or similar agents because of overall safety and
(at least short-term) efficacy
(B) Include estazolam, eszopiclone, flurazepam,
temazepam, triazolam, zaleplon, and zolpidem
(C) All generally well-tolerated but recommended for
short-term use
(D) Eszopiclone has been studied over 6 months, and
it retains efficacy; eszopiclone and the extended-
release form of zolpidem are the only medications
not limited to short-term treatment of insomnia;
effects longer than 612 months have not been
documented
(E) Potential side effects include tolerance; these med-
ications are frequently prescribed on an intermit-
tent basis to avoid tolerance, but this approach has
not been systematically studied
(F) Another side effect is complex sleep related
behaviors; in March 2007 U.S. Food and Drug
Administration (FDA) requested labeling to
include stronger warnings
(2) Melatonin receptor agonists
(A) Ramelteon approved for treatment of insomnia.
(B) Data supporting efficacy still evolving
(3) Antidepressants
(A) Although not specifically indicated for treatment of
insomnia, trazodone, amitriptyline, and mirtazapine
identified as three of top four drugs prescribed to
treat insomnia in 2002
(B) Little systematic evidence that these drugs are
effective
(4) Other
(A) Over-the-counter medications frequently contain
antihistamines. These drugs may promote drowsi-
ness but generally do not improve the quality of
sleep and have the disadvantage of long half-lives
and may result in morning hangover effects.
C H A P T E R
1389_Ch07_091-106 2/2/09 1:26 PM Page 95
(B) Melatonin is a normal product of the pineal gland,
but it has had limited efficacy in most patients
with insomnia.
(C) Valerian is a commonly used herbal supplement,
but few data support efficacy in promoting sleep.
e. Cognitive behavioral therapy:
i. Components of treatment include combinations of several
of the following:
(1) Stimulus control therapya set of instructions
designed to promote the association of the bed and
bedroom with sleep and to help establish a consistent
sleep schedule
(2) Sleep restriction therapymethod designed to limit
the time in bed to time spent actually sleeping. As
sleep becomes more consolidated, time in bed is
gradually increased.
(3) Relaxation trainingtraining to reduce tension and
intrusive thoughts interfering with sleep onset
(4) Cognitive therapypsychological training aimed at
changing perceptions of insomnia and its effect on
daytime function
(5) Sleep hygiene educationgeneral guidelines for
optimizing conditions for sleep, including:
(A) Maintaining regular sleep-wake schedule
(B) Establishing a relaxing pre-sleep ritual
(C) Going to bed only when sleepy
(D) Using bed for sleep and sex only
(E) Avoiding naps, especially past early afternoon
(6) Avoid stimulants (e.g., caffeine and nicotine) and
alcohol before bedtime
(7) Maintain comfortable sleep environment (comfortable
temperature; dark, quiet room)
(8) Avoid heavy exercise or stimulating activity
(including computer work) in late afternoon
(9) Exercise regularly in the morning or afternoon
(10) Do not eat heavy meals close to bedtime
P A R T
Cognitive behavioral therapy is as effective as
medication in long-term treatment of insomnia.
1389_Ch07_091-106 2/2/09 1:26 PM Page 96
ii. Cognitive behavioral therapy and medications have
additive effects on treatment of insomnia; ideally an
approach combining both is used.
III. Obstructive Sleep Apnea (OSA)
A. Definition
1. An obstructive apnea is defined as an obstruction to airflow
during sleep for at least 10 seconds with continued respiratory
effort.
2. An obstructive hypopnea is an incomplete apnea with some air-
flow maintained and should be associated with either an arousal
or a decrease in oxygen saturation.
3. Apneas and hypopneas are grouped together in the Apnea/
Hypopnea Index (AHI), the number of apneas and hypopneas
per hour.
4. OSA syndrome defined as:
a. Five or more respiratory events/hour associated with
either:
i. Excessive daytime sleepiness or
ii. Symptoms of (two or more):
(1) Choking or gasping episodes during sleep
(2) Recurrent awakenings
(3) Unrefreshing sleep
(4) Daytime fatigue
(5) Impaired concentration
5. Severity of OSA defined by frequency of respiratory events:
a. Mild: AHI between 5 and 15
b. Moderate: AHI between 15 and 30
c. Severe: AHI 30
B. Prevalence of OSA
1. Defined as AHI 5, with symptoms of daytime sleepiness, ages
3060 years
C H A P T E R
Prevalence of OSA: 4% in men; 2% in women.
C. Signs and symptoms of OSA
1. Nocturnal symptoms
a. Loud snoring
b. Witnessed apneas (often interrupt snoring)
1389_Ch07_091-106 2/2/09 1:26 PM Page 97
c. Gasping and/or choking episodes that arouse patient from sleep
d. Restless sleep (tossing and turning)
e. Nocturia
2. Daytime symptoms
a. Excessive daytime sleepiness (EDS)
b. Sense that sleep was nonrestorative
c. Personality changes, problems with concentration or memory
d. Dry throat and mouth on awakening
e. Impotence
D. Pathophysiology of OSA
1. Promoting airway patency
a. Pharyngeal dilator muscles
b. Increased lung volume
2. Promoting airway collapse
a. Negative pressure in airway on inspiration
b. Extraluminal positive pressure
i. Small anatomic airway
ii. Excess fat deposition in neck or airway
iii. Excess tissue (e.g., large tongue, uvula, or tonsils) in
airway
iv. Small or posteriorly placed mandible
E. Pertinent physical examination for OSA
1. Examine face for retro- or micrognathia
2. Examine nose for deviated septum, obstruction, or narrowing
of nares
3. Examine upper airway for evidence of obstruction: small
oropharynx, excessive tissue in pharynx, enlarged tonsils, large
uvula, large tongue
4. Measure neck (size 17 inches increased risk of OSA)
5. Cardiovascular and respiratory examination
F. Diagnosis of OSA
P A R T
OSA involves abnormal balance between forces maintain-
ing airway patency and forces promoting airway collapse.
Standard is overnight study monitored in laboratory.
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1. Study includes recordings of:
a. Sleep stages
b. Heart rate and rhythm
c. Airflow and respiratory effort
d. Oxygen saturation
e. Leg movements
2. Avariety of portable devices are available, often for home use,
that can record some of the standard data (e.g., oxygen
saturation, respiratory effort)
a. Not well standardized
b. Can be useful for screening large populations
G. Consequences of OSA
1. Impairment of cognitive function and performance
a. Patients with OSA have more auto accidents
2. Cardiovascular (CV) function
a. Increased incidence of hypertension
b. Increased risk of CV events (e.g., myocardial infarction and
stroke)
3. Metabolic dysfunction
a. Increased glucose intolerance
b. Increased insulin resistance
H. Treatment of OSA
1. Conservative measures
a. Avoid use of alcohol and central nervous system depressants
close to time of sleep
b. Avoid sleep in the supine position
c. Lose weight (if patient overweight or obese)
2. Medications
a. Little role in treatment of OSA
b. Small studies have shown mild improvement in AHI with
protriptyline and mirtazapine
c. Oxygen, especially transtracheal oxygen, may improve
apneas slightly; oxygen can also prolong apneas;
patients must have sleep study on oxygen before it is
prescribed
C H A P T E R
OSA has far-reaching consequences across many
domains of health and safety.
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3. Surgical options may improve apnea in appropriately selected
candidates; surgical options include:
a. Nasal surgery (repair of deviated septum, etc).
b. Uvulopalatopharyngoplasty (removal of excess tissue from
posterior pharynx).
c. Mandibular advancement for retrognathia.
d. Radiofrequency ablation for reduction in size of tongue and
other tissue.
e. Tracheotomy: ultimate (but drastic) treatment of OSA as it
bypasses the upper airway obstruction entirely.
4. Mechanical devices
a. Mandibular advancement devices are worn at night to move
mandible forward; may be helpful in appropriate
patient with mild apnea
b. Continuous positive airway pressure (CPAP)
i. CPAP is effective in almost all patients, although not all
patients choose to use CPAP.
ii. Treatment consists of a bedside device (CPAP unit) that
compresses room air. The compressed air is fed into the
patients airway via a mask (commonly a mask that covers
only the nose) that maintains airway patency with the
positive pressure of the compressed air.
iii. CPAP has been documented to reverse the CV effects of
OSA. Various types of CPAP and many masks are avail-
able to increase patient comfort and compliance.
IV. Restless Leg Syndrome (RLS)/Periodic Leg Movements
of Sleep (PLMD)
A. Introduction
1. Restless legs syndrome (RLS) and periodic leg movement
disorder (PLMD) are closely related syndromes, with signifi-
cant clinical overlap.
P A R T
CPAP is the standard of care for OSA.
RLS is an intense urge to move the legs and is an
awake phenomenon. PLMD is a series of repetitive
involuntary movements occurring during sleep.
1389_Ch07_091-106 2/2/09 1:26 PM Page 100
2. Approximately 80% of RLS patients also have PLMD.
3. RLS is not as common in association with PLMD.
4. Research studies of treatment often combine the two phenomena.
B. Prevalence
1. The prevalence of RLS is estimated to be approximately
10%15%. It can be severe during pregnancy.
2. PLMD is rare earlier than age 30 years but increases dramati-
cally after age 50 years. The estimated prevalence is estimated
to be 45% in the elderly.
C. Diagnosis
1. RLS
C H A P T E R
RLS is a clinical diagnosis requiring four criteria:
PLMD is a diagnosis made by sleep study.
a. There is an urge to move the legs, usually accompanied by
paresthesias or dysesthesias.
b. Symptoms of RLS begin or worsen during periods of rest or
inactivity.
c. Symptoms are relieved or significantly improved by
movement.
d. Symptoms are worse in the evening or at night.
2. PLMD
a. A sequence of four or more leg movements, each with
duration of 0.55 seconds, and separated by intervals of
590 seconds
b. Periodic leg movement index (PLMI), number of leg
movements/hour, should exceed 15
c. Movements may be asymptomatic or may disturb sleep
d. Although movements typically involve legs, they may also
involve arms and, occasionally, trunk
D. Evaluation of patients with RLS and PLMD
a. Frequently normal results
b. Look for evidence of peripheral neuropathy, which can be
associated with RLS/PLMD
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2. Laboratory tests
a. Serum ferritin (low levels may worsen symptoms)
b. Renal function (can have RLS/PLMD in association with
severe renal insufficiency)
c. Diagnostic test for pregnancy (if indicated)
E. Pathophysiology of RLS/PLMD
1. Not clearly established
2. Significant inherited component
3. Likely involves dopaminergic system
F. Treatment
1. Substances to avoid include nicotine, alcohol, and
caffeine
2. Medications that can worsen symptoms include some antide-
pressants, many antihistamines, most anti-nausea drugs, many
antipsychotics
3. Anecdotal evidence for hot baths, leg massage, counterstimula-
tion, heat or ice packs, regular exercise, supplemental
calcium, folate, vitamin E, vitamin C, magnesium
4. Iron supplementation: serum ferritin levels of 50 mcg/L
(normal 20300) associated with increased symptoms and
supplementation can improve symptoms
5. Four types of medications used for treatment
a. Dopaminergic agentspramipexole (0.1250.5 mg qhs) and
ropinirole (0.252.0 mg qhs)
i. Problems with these medications include rebound
(symptoms worsen at end of dosing period), augmenta-
tion (symptoms develop earlier in the day or become
more severe), and tolerance (decreased effectiveness
with time).
ii. Pathologic gambling or other compulsive behaviors have
rarely been reported with these medications).
P A R T
Dopaminergic agents are the only medications
approved by the FDA for treatment of RLS/ PLMD.
They are considered first-line therapy.
1389_Ch07_091-106 2/2/09 1:26 PM Page 102
b. Anticonvulsants
i. Gabapentin (1001200 mg qhs) best studied
ii. May produce drowsiness (sometimes beneficial)
c. Benzodiazepinese.g., clonazepam (0.52.0 mg qhs)
i. Some of the first drugs used to treat RLS/PLMD
ii. Generally less effective than dopaminergic agents and
gabapentin
d. Opioidse.g., oxycodone (515 mg) and propoxyphene
(100200 mg)
i. Can probably generalize effects to most narcotics
6. General principles of use of medications in treating
RLS/PLMD
a. Start with one of the dopaminergic agents, unless there is
pain or insomnia; then consider starting with gabapentin.
b. Use medications at lowest effective dose, and increase
dose slowly.
c. Combinations of medications may be needed.
d. Medications may need to be administered in divided doses
(dinner and bedtime) to control early evening symptoms
of RLS.
e. Optimal treatment is often determined empirically.
C H A P T E R
MENTOR TIPS DIGEST
30%40% of adults experience insomnia within any given
year.
10%15% of adults have chronic insomnia, defined as persist-
ing for at least several weeks.
A complete sleep history is the most important tool in evaluat-
ing insomnia.
Recording in a daily sleep diary for 12 weeks can help
determine extent of a problem and may uncover poor sleep
habits. Information includes wake and sleep times, nocturnal
awakenings, time spent awake during the night, and quality of
sleep as determined by patient and bed partner.
The best therapy for chronic insomnia involves both medica-
tions and cognitive behavioral therapy.
Cognitive behavioral therapy is as effective as medication in
long-term treatment of insomnia.
Prevalence of OSA: 4% in men; 2% in women.
1389_Ch07_091-106 2/2/09 1:26 PM Page 103
Resources
Insomnia
Edinger JD, Sampson WS. A primary care friendly cognitive behavioral
insomnia therapy. Sleep 26:177182, 2003
This study demonstrates efficacy of cognitive behavioral therapy and
also describes how it is performed.
National Institutes of Health state of the science conference statement
on manifestations and management of chronic insomnia in adults,
June 1315, 2005. Sleep 28:10491057, 2005.
Overview of the scope of the problem, with many classic references.
Schenck CH, Mahowald MW, Sack RL. Assessment and management of
insomnia. Journal of the American Medical Association.
289:24752479, 2003.
A more clinical approach to managing insomnia.
Obstructive Sleep Apnea
Drager LF, Bortolotto LA, Figueiredo AC, et al. Effects of continuous
positive airway pressure on early signs of atherosclerosis in obstructive
sleep apnea. American Journal of Respiratory and Critical Care Medicine
176:706712, 2007.
Documents efficacy of CPAP in reversing adverse CV effects of OSA.
P A R T
OSA involves abnormal balance between forces maintaining
airway patency and forces promoting airway collapse.
For diagnosis of OSA, the standard is overnight study moni-
tored in laboratory.
OSA has far-reaching consequences across many domains of
health and safety (from auto accidents to cardiovascular
events and many others).
CPAP is the standard of care for OSA.
RLS is an intense urge to move the legs and is an awake
phenomenon. PLMD is a series of repetitive involuntary move-
ments occurring during sleep.
RLS is a clinical diagnosis requiring four criteria (discussed
in text).
PLMD is a diagnosis made by sleep study.
Dopaminergic agents are the only medications approved by
the FDA for treatment of RLS/PLMD. They are considered
first-line therapy.
1389_Ch07_091-106 2/2/09 1:26 PM Page 104
C H A P T E R
Yaggi HK, Concato J, Kernan WN, et al. Obstructive sleep apnea as a risk
factor for stroke and death. New England Journal of Medicine
353:20342041, 2005.
One of the articles documenting OSA as a risk factor for increased CV
mortality.
Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered
breathing among middle-aged adults. New England Journal of Medicine
328:12301235, 1993.
One of the classic studies measuring prevalence of OSA in employed
adults.
RLS/PLMD
Bogan RK, Fry JM, Schmidt MH, et al. Ropinirole in the treatment of
patients with restless legs syndrome: A U.S.-based randomized,
double-blind, placebo-controlled clinical trial. Mayo Clinic Proceedings
81:1727, 2006.
One of the classic articles demonstrating efficacy of treatment with
dopaminergic agents.
Phillips B, Young T, Finn L, et al. Epidemiology of restless legs symp-
toms in adults. Archives of Internal Medicine 160:21372141, 2000.
A study measuring prevalence of restless leg syndrome in adults;
documents increasing prevalence with increasing age.
Trenkwalder C, Paulus W, Walters AS. The restless legs syndrome. Lancet
4:465475, 2005
A recent, thorough review with specific recommendations for
treatment.
1. How common is chronic insomnia among American adults?
a. 1%
b. 15%20%
c. 50%70%
d. 90%
1389_Ch07_091-106 2/2/09 1:26 PM Page 105
P A R T
2. A 47-year-old woman presents to you because she has difficulty falling
asleep. She typically will lie in bed awake for hours. There have been
nights during which she did not sleep at all. She has trouble concentrat-
ing at work. Her difficulty sleeping began 1 week ago when her
husband told her he wanted a divorce. Which of these choices is most
appropriate for your response?
a. She should immediately begin to take lorazepam 0.51 mg every
46 hours to relieve anxiety.
b. She should have a polysomnogram (overnight sleep study).
c. She should begin to drink 12 glasses of wine before bedtime.
d. You can reassure her that her insomnia is very likely to remit
spontaneously, and zolpidem can be used short-term along with
counseling if necessary.
3. A 56-year-old man complains of insomnia with daytime difficulty
maintaining attention since hospital discharge 6 weeks ago. His hospi-
tal stay was due to angina, treated with coronary angioplasty and stent.
His discharge medicines, all newly prescribed, include clopidogrel,
aspirin, atorvastatin, fluoxetine, and lisinopril. Which of his medicines
is most likely to cause sleep disturbance?
a. Clopidogrel
b. Atorvastatin
c. Fluoxetine
d. Lisinopril
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107
CHAPTER
8
DIZZINESS
John E. Butter, MD
I. Background
A. Dizziness is a common disorder that can be challenging for
patients to describe and physicians to evaluate.
B. Complexity and vagueness of symptoms arise from interaction of
multiple systems that maintain a persons proper perception of
relationship to the environment.
C. Disturbances in the cardiovascular, visual, vestibular, and proprio-
ceptive pathways can produce dizziness. Dizziness may be related
to multiple causative factors in nearly half of all patients.
D. Patients descriptions are frequently vague due to difficulty com-
municating what disturbs them.
II. Epidemiology
A. Dizziness common in all age groups but more common in elderly
and women
B. Over 7 million office visits for dizziness in the United States each year
C. 15%30% of patients experience dizziness severe enough to seek
medical attention at some time in their lives
D. Most patients present to primary care physicians
III. Approach to the Patient
A. History is the most crucial part of the evaluation.
B. A common mistake is for the physician to say too much. Avoid
putting words in patients mouths or offering them a list of
descriptors from which to choose.
When eliciting the history from patients who are dizzy,
allow them to describe the sensation in their own words
before offering multiple choices.
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P A R T
C. Facilitative questions or comments include Tell me what you
mean by dizzy, or Im not sure I understand what you mean
when you say you are dizzy; please tell me more.
IV. Classification of Type of Dizziness
A. Each category has its own differential diagnosis and treatment.
B. Typical statements include the following:
1. I feel like the room is spinning (vertigo).
2. I feel like Im going to pass out (presyncope).
3. I feel like Im off balance, like Im going to fall down
(disequilibrium).
4. I just feel dizzy, like Im woozy (vague lightheadedness).
C. The evaluation can proceed when the dizziness has been placed in
one (or more) of these categories.
V. Vertigo
A. A rotatory sensation is hallmark
B. Caused by disturbance in the vestibular system, which normally
functions to provide an awareness of the bodys position in space.
C. Key questions are:
1. How long do the symptoms last?
2. Does a change in head position provoke symptoms?
3. Is there hearing loss?
4. Are there other neurologic symptoms such as dysphagia,
diplopia, dysarthria, hemiparesis, or ataxia?
D. Differential diagnosis
1. Benign positional vertigo
2. Vestibular neuronitis
3. Labyrinthitis
4. Mnire disease
5. Central nervous system (CNS) disorders
E. Benign positional vertigo (BPV)
1. Classic history: When I turned over in bed, I felt like the room
was spinning for a few minutes.
2. Symptoms resolve spontaneously after a few minutes.
3. Hearing is not affected.
Categorize the diagnosis into one (or more) of four cate-
gories: vertigo, presyncope, disequilibrium, or vague light-
headedness.
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8 DIZZINESS 109
C H A P T E R
4. The cause may include accumulation of organic debris in the
posterior circular canal.
5. Clinical test:
BPV can be confirmed by reproduction of symptoms
with the Dix-Hallpike maneuver, also known as the
Brny test (Fig. 8.1).
FIGURE 8.1 Dix-Hallpike maneuver (A). With the patient sitting, the neck is
extended and turned to one side. The patient is then placed supine rapidly
so that the head hangs over the edge of the bed. The patient is kept in this
position and observed for nystagmus for 30 seconds. Nystagmus usually
appears with a latency of a few seconds and lasts less than 30 seconds.
It has a typical trajectory, beating upward and torsionally, with the upper
poles of the eyes beating toward the ground. After it stops and the patient
sits up, the nystagmus will recur but in the opposite direction. Therefore,
the patient is returned to upright and again observed for nystagmus for
30 seconds. If nystagmus is not provoked, the maneuver is repeated with
the head turned to the other side (B). If nystagmus is provoked, the patient
should have the maneuver repeated to the same (provoked) side; with each
repetition, the intensity and duration of nystagmus will diminish. (Modified
from Foster CA, Baloh RW: Episodic vertigo. In Rakel [ed]: Conns Current Therapy,
47th ed. WB Saunders, Philadelphia, 1995, p. 873.)
A
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P A R T
a. To perform this test, have the patient sit on the examination
table, then move the patients head down over the end of the
examination table to about 30 degrees below the horizontal
plane, and then turn the head toward one side. Frequently, the
patient will say Its coming on nowI feel dizzy. If there is
no response after about 30 seconds, return the patient to the
sitting position, and repeat the maneuver, but this time turn the
head in the opposite direction so the other ear is dependent.
b. Classic positive response on the Dix-Hallpike maneuver
(Brny test) is:
i. Vertigo, which occurs after a latency of a few seconds.
ii. Nystagmus.
iii. Fatigabilitythe symptoms are less severe if the maneuver
is repeated.
F. Vestibular neuronitis
1. Classic history: The room has been spinning for days, and Im
nauseous and have been vomiting.
2. Symptoms last much longer than those of BPVgenerally a
few days, then resolve spontaneously.
FIGURE 8.1 Continued
B
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8 DIZZINESS 111
C H A P T E R
3. Residual unsteadiness may last for weeks after the attack.
4. Hearing is not affected.
5. Spontaneous nystagmus may be present.
G. Labyrinthitis
1. Classic history: The room is spinning, my hearing is diminished,
and I hear ringing in my ears.
2. Labyrinthitis, unlike BPV or vestibular neuritis, causes dimin-
ished hearing.
3. Symptoms typically follow a viral upper respiratory tract
infection.
4. Symptoms last a few weeks, then resolve without
recurrence.
H. Mnire disease
1. Classic history: My ears feel full, I cant hear so well, theres
ringing in my ears, and I feel dizzy.
2. There is a triad of hearing loss, vertigo, and tinnitus, frequently
accompanied by aural fullness.
3. Hearing loss is frequently low-frequency and fluctuates.
4. The typical patient is a 3060-year-old male.
5. Cause of Mnire disease is abnormal collection of endolym-
phatic fluid in the inner ear.
I. Other causes of peripheral vestibular disturbances include ototoxic
drugs such as loop diuretics, aspirin, quinine, caffeine, alcohol,
aminoglycosides, and cisplatinum.
J. CNS:
1. Clues to a CNS cause of vertigo include more gradual onset
and less intense symptoms.
2. The lower brainstem or cerebellum is frequently involved,
producing symptoms such as diplopia, dysarthria, paresthesias,
and changes in sensory or motor function.
3. Cerebellar dysfunction may be difficult to separate from a
peripheral vestibular disorder. Difficulty with rapidly alternat-
ing movements and finger-nose-finger testing supports a
cerebellar cause. In contrast, patients with a peripheral cause
of vertigo are able to complete finger-nose-finger testing
CNS causes of vertigo are manifested by additional
neurologic symptoms, not dizziness alone.
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P A R T
accurately because visual fixation partly compensates for the
vestibular defect.
4. Causes of CNS vertigo include neoplastic, vascular, and
demyelinating disorders. Neoplasms such as acoustic neuromas
grow slowly and often cause imbalance, tinnitus, and hearing
loss. Multiple sclerosis may cause vertigo. Stroke or transient
ischemic attack (TIA) may cause dizziness but in conjunction
with other neurologic symptoms. One of the most common
brainstem syndromes is Wallenberg syndrome, caused by
infarction of the lateral medulla by occlusion of the posterior
inferior cerebellar artery (PICA). Wallenberg syndrome pro-
duces a characteristic clinical picture of vertigo, ataxia,
diplopia, dysphagia, Horner syndrome, ipsilateral facial
numbness, and contralateral decreased pain and temperature
sensation.
K. Nystagmus from peripheral causes usually evokes horizontal
beating. Vertical nystagmus (up and down beating) is suggestive
of central causes of vertigo. Table 8.1 compares and contrasts
central versus peripheral causes.
VI. Presyncope
A. Classic history: I feel faint, like Im going to black out.
B. Presyncope is the impending loss of consciousness caused by
decreased blood flow to the brain.
TABLE
8.1
Central Versus Peripheral Vertigo
Central Peripheral
Duration Long Brief
Intensity Moderate Severe
Nausea and/or vomiting Mild Moderate to severe
Neurologic symptoms Common Rare
Hearing loss Rare May be present
Affected by head position Not usually Frequently
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8 DIZZINESS 113
C H A P T E R
C. Differential diagnosis includes vasovagal hypotension and cardio-
vascular disease and disorders that produce orthostatic hypotension.
D. Vasovagal reaction (neurocardiogenic presyncope)
1. Most common cause of presyncope and syncope in young
adults
2. Episodes often precipitated by stressful or painful stimuli that
lead to drop in heart rate and peripheral resistance.
3. Vasovagal syncope often accompanied by prodrome of
diaphoresis, pallor, and nausea
4. Tilt table test, which demonstrates an exaggerated fall in blood
pressure and pulse on assuming an upright posture, may be
helpful in diagnosing vasovagal syncope
E. Orthostatic hypotension may be the result of dehydration,
hemorrhage, diarrhea, vomiting, or excessive diuresis. Drugs
are a common cause and include antihypertensives, anticonvul-
sants, antipsychotics, and antiparkinson medications.
F. Peripheral neuropathy, such as that caused by diabetes or alcohol,
can contribute to orthostatic hypotension.
G. Cardiovascular disease
1. The mechanism of cardiovascular causes is valvular disease or
arrhythmias.
2. Valvular disease such as aortic stenosis causes presyncope
during or shortly after exercise due to the inability of the heart
to augment cardiac output combined with exercise-induced
vasodilation leading to a fall in blood pressure. Physical exami-
nation followed by echocardiography can confirm this diagnosis.
3. Arrhythmias usually have a short or absent prodrome. Advanced
age; history of coronary artery disease; depressed ejection frac-
tion; or an electrocardiogram (ECG) showing left-axis devia-
tion, left ventricular hypertrophy (LVH), or left bundle branch
block (LBBB), should raise suspicion of arrhythmias.
VII. Disequilibrium
A. Classic history: I feel unbalanced when I walklike I might fall.
B. Disequilibrium-type dizziness commonly causes dizziness when
walking but not when sitting or supine.
C. Disequilibrium is common in the elderly.
D. Disequilibrium results from a constellation of impaired sensory
deficits, including visual impairments, neuropathy, vestibular
disorders, and musculoskeletal disturbances.
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P A R T
VIII. Vague Lightheadedness
A. Classic history: a vague description of dizziness often accompa-
nied by anxiety and/or a positive review of systems.
B. Dizziness is common in patients with anxiety, panic disorder,
depression, or somatization.
C. Frequent accompanying symptoms include palpitations,
headaches, weakness, chest pain, dyspnea, and paresthesias.
D. A subset of anxiety disorders with dizziness is provoked by
hyperventilation.
IX. Treatment
A. Effective treatment depends on reaching a probable diagnosis.
B. Treatment for vertigo
1. Vestibular suppressants such as meclizine do not alter the
natural history of the disease but can reduce symptoms.
2. The canalith respositioning maneuver (Eply maneuver)
(Fig. 8.2), which involves turning the patient 360 degrees to
reposition the otoliths in the semicircular canals, is one of the
most effective treatments for BPV. Patients with BPV can be
cured with this maneuver.
3. Methylprednisolone has been shown to induce a more rapid
and complete recovery in patients with vestibular neuritis.
4. Salt restriction and diuretics can be helpful for patients with
Mnire disease.
C. Treatment for presyncope
1. For orthostatic hypotension, eliminating offending medica-
tions or volume depletion can be curative.
2. Support stockings may be helpful to augment venous return.
3. Fludrocortisone or midodrine are pharmacologic treatments
that may be helpful.
4. Valvular heart disease such as aortic stenosis requires surgical
evaluation.
5. Arrhythmias may require pharmacologic therapy, ablation, or
treatment with an automatic implantable cardiac defibrillator
(AICD).
D. Treatment dysequilibrium
1. Patients with disequilibrium usually have multiple sensory
deficits that are not easily corrected.
2. Correcting any visual problems such as refractive errors or
cataracts may be helpful.
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8 DIZZINESS 115
C H A P T E R
5
1
2
3
4
Patient is seated upright facing
examiner, grasping examiners
forearm with both hands for
stability, then moved rapidly into
supine position with head
extending just beyond examin-
ing table, right ear
downward.
Head is quickly rotated to
the left, stopping with right
ear upward. Position is
held for 30 seconds.
Patient rolls onto left
side while examiner
rapidly rotates head
until nose is angled
toward floor. Position
is held for 30
seconds.
Patient is rapidly
lifted into sitting
position. Entire
sequence is
repeated until no
nystagmus can
be elicited.
Examiner
moves to head
of table,
repositioning
hands as
shown.
Utricle
Posterior
semicircular
canal
FIGURE 8.2 Particle repositioning maneuver. In patients with benign paroxys-
mal positional vertigo due to canalithiasis, the particle repositioning maneuver
encourages the calcium carbonate debris to migrate toward the common
crus of the anterior and posterior canals and exit into the utricular cavity.
Step 1 is the standard Dix-Hallpike positioning test. (Modified from Foster
CA, Baloh RW: Episodic vertigo. In Rakel [ed]: Conns Current Therapy, 47th ed.
WB Saunders, Philadelphia, 1995, p. 873.)
1389_Ch08_107-117 2/2/09 1:26 PM Page 115
P A R T
3. Physical therapy and devices such as a cane or walker can be
helpful.
E. Treatment for vague lightheadedness
1. For patients with anxiety, panic disorder, or depression, a selec-
tive serotonin reuptake inhibitor is effective.
2. Psychological counseling and cognitive behavioral therapy can
be helpful.
F. Vestibular rehabilitation helpful for chronic or multifactorial
dizziness of various causes, including BPV, psychological factors,
head injury, and multifactorial dizziness common in elderly
Resources
Eaton DA, Roland PS. Dizziness in the older adult, part 1: Evaluation and
general treatment strategies. Geriatrics 58:2836, 2003.
Hoffman RM, Einstadter D, Kroenke K. Evaluating dizziness. American
Kroenke K, Hoffman RM. How common are various causes of dizziness?
A critical review. Southern Medical Journal 93:160167, 2000.
Radtke A, Von Brevern M, Tiel-Wilck K, et al. Self-treatment with a
modified Eply procedure resolved positional vertigo. Neurology
63:150152, 2004.
Sloan PD, Coeytaux RR, Beck RS, et al. Dizziness: State of the science.
Annals of Internal Medicine 134:Supplement, 823832, 2001.
Strupp M, Zingler VC, Arbusow V, et al. Methylprednisolone, valacy-
clovir, or the combination for vestibular neuritis. New England Journal
of Medicine 351:354361, 2004.
MENTOR TIPS DIGEST
When eliciting the history from patients who are dizzy, allow
them to describe the sensation in their own words before
offering multiple choices.
Categorize the diagnosis into one (or more) of four categories:
vertigo, presyncope, disequilibrium, or vague
lightheadedness.
BPV can be confirmed by reproduction of symptoms with the
Dix-Hallpike maneuver, also known as the Brny test.
CNS causes of vertigo are manifested by additional neuro-
logic symptoms, not dizziness alone.
1389_Ch08_107-117 2/2/09 1:26 PM Page 116
8 DIZZINESS 117
C H A P T E R
Tusa R. Dizziness. Medical Clinics of North America 87: 609641, 2003.
Warner EA, Wallach PM, Adelman HM, et al. Dizziness in primary care
patients. Journal of General Internal Medicine 7:45463, 1992.
1389_Ch08_107-117 2/2/09 1:26 PM Page 117
118
9
CHEST PAIN
Gary J. Martin, MD
I. Pathophysiology
A. Chest pain can be caused by any of the structures within or adjacent
to the chest, including the chest wall and upper abdomen. The vascu-
lar causes are the most concerning.
II. Epidemiology
A. It is useful to separate acute causes of chest pain from chronic
causes. Box 9.1 lists many of the causes of acute chest pain.
Box 9.2 lists some of the common causes of episodic or chronic
recurrent chest pain.
BOX
9.1
Common Causes of Acute Chest Pain
Myocardial infarction
Aortic dissection
Pulmonary embolism
Pericarditis
Esophageal reflux or spasm
Pneumonia
Chest wall disorders (musculoskeletal, zoster, breast disease)
Psychogenic
Upper abdominal causes (pancreatitis, peptic ulcer, cholelithiasis)
In a primary care setting, the most common causes of
chest pain are musculoskeletal followed by gastrointesti-
nal and cardiac causes. Less common are psychiatric and
pulmonary causes.
CHAPTER
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9 CHEST PAIN 119
C H A P T E R
III. Signs and Symptoms
A. Classic patterns of chest pain include:
1. Angina: central pressure associated with exertion, lasting
approximately 12 minutes and relieved with rest; myocardial
infarction is similar but typically lasts 30 minutes to 2 hours or
longerunusual to last more than 6 hours
2. Pericarditis: central pain that can be aggravated when lying
down and relieved when sitting up; duration can be hours
to days
3. Esophageal pain: typically described as burning (reflux)
or squeezing (spasm) and aggravated by lying down after a
meal or triggered by certain foods or alcohol; patients mouth
may also have a bitter taste; duration may be minutes to
an hour
4. Pleuritic chest pains: by definition are aggravated by taking a
deep breath
5. Chest wall pain: can also be aggravated by taking a deep breath
or by other position changes; can last for minutes or hours
IV. History and Physical
A. History
1. Key points to collect information on include:
a. Classic cardiac risk factors such as smoking, diabetes, hyper-
tension, hyperlipidemia, and family history
BOX
9.2
Common Causes of Episodic or Recurrent Chest Pain
Esophagitis
Esophageal spasm
Biliary colic
Chest wall pain
Psychogenic causes including anxiety, depression, and panic attacks
Stable angina from coronary artery disease (CAD)
Classic angina is usually a pressure sensation, and
patients may even deny pain. Less often it can be
described as a burning, ache or, although rarely, a sharp pain.
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P A R T
b. Quality, location, duration, radiation, precipitating factors,
relieving factors
c. Past medical history of cardiac and gastrointestinal disease
and psychiatric disorders
2. Box 9.3 lists criteria for classic angina, atypical chest pain, and
nonanginal/nonischemic chest pain
a. Using these categories for pain, along with the patients age
and gender, a reliable estimate of the likelihood of finding
significant CAD can be made. Table 9.1 demonstrates the
probabilities based on a large number of patients.
BOX
9.3
Criteria to Classify Chest Discomfort
Criteria
1. Precipitated by exercise
2. Brief duration (215 min)
3. Relieved promptly by rest or nitroglycerin
4. Substernal location
5. Radiation from chest to jaw, left arm, or neck
6. Absence of other causes for pain
Classification
I. Typical angina pectoris
Criteria 13 all positive
Any four criteria positive
II. Atypical chest pain
Any two criteria positive
Only criteria 46 positive
III. Nonanginal chest pain
Only one criterion positive
From Patterson RE, Horowitz SF: Importance of epidemiology and biostatistics in
deciding clinical strategies for using diagnostic tests: A simplified approach using
examples from coronary artery disease. JACC 1989; 13:16531665.
Your history-taking skills are able to classify patients
into these three useful categories.
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9 CHEST PAIN 121
C H A P T E R
1. Comparison of blood pressure in each arm can be useful for
detecting aortic dissection.
2. Chest auscultation can detect pleural rubs, consolidation sug-
gesting pneumonia, or decreased breath sounds consistent with
a pneumothorax.
3. Cardiac examination can detect pericardial rubs, an aortic steno-
sis murmur, and other evidence of underlying heart disease.
4. Pressure on the chest wall or certain arm or shoulder maneuvers
may reproduce the patients pain, but patients with serious
internal conditions including myocardial infarction can say
yes to chest wall tenderness, so the clinician needs to be
careful not to eliminate such possibilities prematurely.
V. Laboratory Tests
A. Even though for most patients chest pain can be diagnosed by
history with additional help from the physical examination, a
subset of patients benefit from additional tests.
TABLE
9.1
Approximate Clinical Probability (%) of Coronary
Disease
Nonanginal Atypical Typical
Age Chest Chest Angina
(yr) Pain Pain Pectoris
Females 35 .5-1 4 27
45 5 13 57
55 12 37 80
65 20 55 89
Males 35 6 23 71
45 15 46 88
55 21 58 91
65 27 72 93
Adapted from Patterson RE, Horowitz SF. Importance of epidemiology and biostatistics in
deciding clinical strategies for using diagnostic tests: A simplified approach using examples
from coronary artery disease. JACC 1989;13(7):16531665.
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P A R T
1. An electrocardiogram (ECG) during the pain is quite helpful in
diagnosing cardiac disease. However, an ECG test result can be
quite normal after an episode of angina. ST segment changes
and T-wave inversions are usually associated with ischemia.
ST segment elevation may also be present (and, classically,
PR depression) in pericarditis. For prolonged chest pain, tro-
ponin levels are quite sensitive for cardiac ischemia.
2. A chest x-ray is another useful test for detecting pneumothorax,
pneumonia, pleural effusions, and even a dilated aorta associated
with a dissection.
3. More advanced testing could include esophageal manometry,
pH monitoring, and stress testing with or without imaging.
Transesophageal echo, computed tomography (CT) and magnetic
resonance imaging (MRI) can help with acute pain syndromes
such as aortic dissection and pulmonary embolism.
VI. Management
A. Acute coronary problems:
1. Initial office treatment includes chewable aspirin and trans-
portation as soon as possible to a monitored setting or a cardiac
catherization laboratory for possible thrombolytic therapy or
percutaneous coronary intervention. Time is critical because
opening the occluded artery within 6090 minutes gives the
best results.
B. For chronic CAD, long-term use of aspirin, beta blockers, and
statins are the mainstay of therapy. Angiotensin-converting
enzyme (ACE) inhibitors are particularly helpful for the subset
of coronary patients with a prior myocardial infarction or left
ventricular dysfunction. Control of other risk factors, such as
smoking, hypertension, and diabetes, is important.
Unstable angina and acute myocardial infarction
(acute coronary syndromes) need immediate attention.
Control of cholesterol with statins, use of aspirin, and use
of beta blockers all have a major impact on recurrent
events and mortality in patients with chronic coronary disease.
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9 CHEST PAIN 123
C H A P T E R
C. Reflux disease is usually improved with proton pump inhibitors.
Some patients can be managed with just diet or over-the-counter
H
2
blockers.
D. Chest wall pain usually only requires reassurance, but local physi-
cal therapy measures such as cold packs and pain medications
would be useful adjuncts.
Resources
ACC/AHA 2002 guideline update of the management of patients with
chronic stable anginasummary article: A report of the American
College of Cardiology/American Heart Association task force on prac-
tice guidelines (committee on the management of patients with chronic
stable angina). Circulation 107:149158, 2003.
Use of aspirin, statins, beta blockers, and in some cases ACE
I
are key
interventions for these patients.
Goldman L. A computer-derived protocol to aid in the diagnosis of
emergency room patients with acute chest pain. New England Journal
of Medicine 588596, 1982.
A decision tree for acute chest pain that has been validated.
Klinkman MS, Stevens D, Gorenflo DW. Episodes of care for chest pain:
A preliminary report from Michigan Research Network. Journal of
Family Practice 38:345, 1994.
MENTOR TIPS DIGEST
In a primary care setting, the most common causes of chest
pain are musculoskeletal followed by gastrointestinal and
cardiac causes. Less common are psychiatric and pulmonary
causes.
Classic angina is usually a pressure sensation, and patients
may even deny pain. Less often it can be described as a
burning, ache or, although rarely, a sharp pain.
Your history-taking skills are able to classify patients into three
useful categories: classic angina, atypical chest pain, and
non-anginal/nonischemic chest pain.
Unstable angina and acute myocardial infarction (acute coro-
nary syndromes) need immediate attention.
Control of cholesterol with statins, use of aspirin, and use of
beta blockers all have a major impact on recurrent events and
mortality in patients with chronic coronary disease.
1389_Ch09_118-125 2/2/09 1:26 PM Page 123
P A R T
Episodes of chest pain totaling 399 were collected and used for analysis
from a community-based network. Musculoskeletal chest pain accounted
for 20.4% of all diagnoses, followed by reflux esophagitis (13.4%) and
costochondritis (13.1%). Stable angina pectoris was the primary diag-
nosis in only 10.3% of episodes, unstable angina or possible myocar-
dial infarction in 1.5%.
Patterson RE, Horowitz SF. Importance of epidemiology and biostatistics
in deciding clinical strategies for using diagnostic tests: A simplified
approach using examples from coronary artery disease. JACC
13:16531665, 1989.
Useful evidence-based overview of the diagnosis of CAD, using proba-
bility to enhance the approach.
1. Which is characteristic of typical angina?
a. Retrosternal pressure chest pain lasting for a few seconds
b. Retrosternal pressure chest pain lasting for 25 minutes associated
with exertion
c. Retrosternal pressure chest pain lasting for a few hours to days,
exacerbated by supine posture
d. Retrosternal burning chest pain lasting for seconds to an hour
2. Which is characteristic of pericarditis?
a. Retrosternal pressure chest pain lasting for seconds and associated
with exertion
b. Retrosternal pressure chest pain lasting for 215 minutes
c. Retrosternal pressure chest pain lasting for hours to days, exacerbated
by supine posture
d. Retrosternal burning chest pain lasting for seconds to an hour
3. A 47-year-old man comes to the emergency department because of
chest pain. He describes a squeezing retrosternal pain that began
shortly after he went to bed. He had attended a party that evening and
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9 CHEST PAIN 125
C H A P T E R
imbibed adult beverages. The pain lasted for over an hour and remitted
when paramedics administered sublingual nitroglycerin. What is the
most appropriate management at this time?
a. Reassure him that he experienced esophageal reflux and to control
alcohol intake.
b. Prescribe a proton pump inhibitor, and arrange for follow-up later in
the week.
c. Obtain an ECG.
d. Admit to CCU for observation.
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126
CHAPTER
10
SINUSITIS, BRONCHITIS,
AND PHARYNGITIS
Heather Heiman, MD
I. Sinusitis
A. Pathophysiology
1. Viruses lead to rhinosinusitis, also known as the common cold
and viral upper respiratory infection.
2. Blockage of the osteomeatal complex from viral rhinosinusitis
can lead to acute bacterial sinusitis.
3. The microbes causing sinusitis depend on the host.
a. Immunocompetent hosts
i. Streptococcus pneumoniae and Haemophilus influenza
are the most common.
ii. Moraxella catarrhalis, Streptococcus pyogenes,
Staphylococcus aureus, and anaerobic bacteria are
less common.
b. Patients having diabetes may also get fungal infections such
as mucormycosis
4. Chronic sinusitis, which lasts longer than 12 weeks, more
commonly involves different bacteria.
a. Anaerobic bacteria
b. S. aureus
c. Gram-negative rods
Clinicians use the term sinusitis to imply acute
bacterial sinusitis.
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10 SINUSITIS, BRONCHITIS, AND PHARYNGITIS 127
C H A P T E R
B. Epidemiology
1. Occasional upper respiratory infection (URI) comorbidity
2. Other risk factors for sinusitis include environmental, anatomic,
and genetic conditions:
a. Allergic rhinitis
b. Swimming
c. Anatomic disorders such as nasal polyps
d. Ciliary dysmotility syndromes such as cystic fibrosis
e. Immunodeficiency states such as HIV
3. Uncommon complications:
C. Prevention
1. Hand hygiene has been shown to prevent the spread of viral URIs.
Sinusitis complicates about 0.5%2% of URIs.
Antimicrobial agents do not alter the course of the
common cold or prevent bacterial sinusitis.
History and physical examination in the office focus on
differentiating viral rhinosinusitis from bacterial sinusitis.
About 1/10,000 cases of sinusitis lead to severe com-
plications such as local or central nervous system
(CNS) infection.
Mental status changes or vision changes are red
flags for CNS spread.
D. History and physical
1. Some symptoms increase the likelihood of a bacterial cause.
a. Maxillary toothache is specific for bacterial sinusitis.
b. History of colored nasal discharge is usually described.
c. Poor response to decongestants is common.
d. The presence of symptoms for more than 7 days is needed to
diagnose sinusitis.
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P A R T
2. The physical examination can be helpful but is less so than the
history.
a. Tenderness to sinus palpation is neither sensitive nor specific.
b. Abnormal sinus transillumination may be helpful: opaque or
dull transillumination predicts bacterial source.
i. Transillumination is done by shining a light source on the
sinus in a darkened room and watching the transmission
of light through the sinus.
ii. Transillumination can be done for the frontal and maxillary
sinuses.
c. Purulent secretions in the nares increase the likelihood of
bacterial sinusitis.
d. Periorbital edema is a red flag for orbital cellulitis or
osteomyelitis.
E. Differential diagnosis
1. Radiologic studies do not differentiate bacterial from viral
sinusitis, as over 80% of viral rhinosinusitis cases show abnor-
malities on plain film or computed tomography of the sinuses.
2. Sinus aspirate by puncture is invasive and not performed
routinely.
Diagnosis of acute sinusitis is made empirically.
National guidelines endorsed by the U.S. Centers for
Disease Control and Prevention (CDC) recommend reserving
the diagnosis of acute bacterial rhinosinusitis for patients
with rhinosinusitis symptoms lasting 7 days or more with
maxillary pain or tenderness in the face or teeth (especially
when unilateral) and purulent nasal secretions.
3. Sinus symptoms are occasionally caused by noninfectious illness.
a. Rhinitis medicamentosum (overuse of topical decongestants
leading to rebound congestion)
b. Allergic rhinitis
c. Idiopathic (vasomotor) rhinitis
d. Migraine headache
e. Wegener granulomatosis
E. Management
1. Antimicrobial therapy
a. Two thirds of cases of acute bacterial sinusitis will get better
on their own.
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C H A P T E R
b. Amoxicillin and penicillin have a small, statistically significant
benefit over placebo in terms of cure or improvement of
symptoms.
i. Patients who are allergic to penicillin may be treated with
doxycycline or trimethoprim-sulfamethoxazole.
ii. Patients who used antibiotics in the past month should
be treated with broader-spectrum antibiotics such as
amoxicillin/clavulanic acid or quinolones.
2. Supportive therapy
a. Antihistamines and intranasal steroids are effective for
patients with a history of allergic rhinitis.
b. Patients without a history of allergic rhinitis are not known
to benefit from antihistamines, intranasal corticosteroids, or
decongestants.
3. Referral to an otolaryngologist for consideration of surgical
therapy reasonable for patients with more than three episodes of
sinusitis per year
II. Acute Bronchitis
A. Pathophysiology
1. Infection leading to inflammation and desquamation of the
bronchial epithelium
2. Microbiology
Newer, non-penicillin antibiotics are not shown to
be more effective than amoxicillin.
Amoxicillin (500 mg three times daily in adults) is
first-line therapy for acute sinusitis.
Acute bronchitis is almost always viral.
a. Viruses involved
i. Influenza
ii. Respiratory syncytial virus
iii. Adenovirus
iv. Rhinovirus
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v. Coronavirus
vi. Parainfluenza
b. Atypical bacteria
i. Bordatella pertussis probably accounts for 1% of cases of
acute bronchitis.
ii. Chlamydia pneumoniae accounts for 5% of cases.
iii. Mycoplasma pneumoniae accounts for 1% of cases.
c. Intubated patients or patients with chronic obstructive
pulmonary disease may get bronchitis from typical bacteria
such as S. pneumoniae, H. influenza, or M. catarrhalis
B. Epidemiology
1. Bronchitis affects about 5% of adults each year.
2. It is most common in winter.
3. Recurrent episodes of bronchitis are associated with develop-
ment of adult-onset asthma, but the link is poorly understood.
C. Prevention
1. Hand hygiene prevents spread of viruses.
2. Pertussis immunization is given in childhood, and a booster
dose is given once in adulthood.
1. A cough is almost always the presenting manifestation of
bronchitis.
a. The common cold is associated with a cough, which usually
follows sore throat, sneezing, and congestion.
b. Cough in bronchitis is persistent.
Atypical bacterial causes of acute bronchitis are
thought to be far less common than viral.
In bronchitis, cough persists for more than 5 days,
usually 1020 days.
Dyspnea is typically absent in bronchitis.
c. Cough may be productive or nonproductive.
2. Chest pain may be present and is often pleuritic.
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C H A P T E R
3. The vital signs follow.
a. Fever may not occur
i. Usually present in patients with influenza and adenovirus
ii. Most often absent in patients with rhinovirus or coronavirus
b. Others
E. Chest examination
1. Signs of consolidation (rales, egophony) should not be present.
F. Differential diagnosis
1. Other possible diagnoses
a. Asthma may present jointly with bronchitis or be the sole
diagnosis.
b. Bronchiolitis presents with wheezing, tachypnea, and
hypoxemia.
c. Bronchiectasis presents with a chronic cough with dilation
of the bronchi on imaging.
d. Chronic bronchitis occurs in smokers who have cough with
sputum on most days for more than 3 months of the year for
2 years running.
e. Upper respiratory infection typically manifests with cough
less than a week.
f. Pneumonia usually presents with consolidation or vital sign
abnormalities, although patients over 75 years may lack
these findings.
2. Laboratory testing in patients with a clinical presentation of
bronchitis
a. Chest x-ray (CXR) for certain indications
Tachypnea, tachycardia, and hypoxemia should not
be present in bronchitis and are concerning for
pneumonia, bronchiolitis, or severe asthma.
Either normal breath sound or wheezing is heard in
bronchitis.
CXR is recommended for patients with signs of consol-
idation on lung examination, or with tachycardia,
tachypnea, hypoxemia, or fever 101F (38.3C)
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P A R T
b. Nasopharyngeal swabs can detect pertussis, mycoplasma, and
influenza in epidemics
c. 40% of patients have transient decrement in forced expiratory
volume in the first second, but pulmonary function testing is
not necessary routinely
G. Management
1. Antimicrobial therapy
a. Nevertheless, 60% of patients with bronchitis receive
antibiotics.
b. Patients with influenza benefit from initiation of neuraminidase
inhibitors within the first 48 hours of symptoms.
c. Spread of pertussis can be reduced by initiating macrolide
therapy during the paroxysmal (cough) phase, although therapy
after 14 days of the illness does not reduce symptoms for the
individual.
d. Tetracyclines or macrolides treat M. pneumoniae and
C. pneumoniae.
2. Supportive therapies
a. Nonsteroidal anti-inflammatory medications with or without
antihistamines reduced cough in some studies.
b. No consistent benefit has been seen with use of beta agonist.
c. Trials of mucolytic or antitussive agents, such as guaifenesin
and codeine, have had mixed results.
III. Pharyngitis
A. Pathophysiology
1. Viral
Bronchitis is a self-limited illness; antibiotics reduce
cough by a fraction of a day but have no benefit for
overall quality of life.
Viruses are the most common cause of pharyngitis.
a. Rhinoviruses are the leading viral cause.
b. Coronavirus, adenovirus, and herpes simplex virus are also
frequent.
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C H A P T E R
c.Less commonly, pharyngitis is caused by parainfluenza,
influenza, Epstein-Barr virus (EBV), cytomegalovirus, HIV,
coxsackievirus
2. Streptococcus causes almost all bacterial pharyngitis.
a. Groups C and G beta-hemolytic streptococci are common
causes as well.
b. Arcanobacterium hemolyticum may cause pharyngitis that
mimics a streptococcal infection.
B. Epidemiology
1. There are 18 million office visits yearly in the United States for
pharyngitis.
2. Winter is the most common time for pharyngitis outbreaks.
3. S. pyogenes often colonizes the oropharynx, especially in
school-age children.
C. Prevention
1. Prevention of strep throat through tonsillectomy in patients with
recurrent episodes is controversial.
2. Influenza vaccination in October through May can prevent
influenza pharyngitis.
1. Streptococcal pharyngitis
a. Symptoms
i. Sometimes patients have headaches, abdominal pain, and
chills.
b. Signs
Streptococcus pyogenes (group A beta-hemolytic
streptococcus) accounts for 15%30% of pharyngitis
episodes in children and 10% in adults.
Key signs are temperature above 101F (38.3C),
exudate on the tonsils, and tender cervical
adenopathy.
Frequent symptoms are sore throat, painful
swallowing, and fever.
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P A R T
i. Other signs
(1) Significant erythema of the throat
(2) Edema of the uvula
(3) A white blood cell count of greater than 12,000/mm
3
c. Be alert for complications of streptococcal pharyngitis
i. Suppurative complications
(1) Peritonsillar abscess
(2) Retropharyngeal abscess, jugular venous throm-
bophlebitis, otitis media, mastoiditis can complicate
strep throat
ii. Nonsuppurative complications
(1) Acute rheumatic fever
(2) Poststreptococcal glomerulonephritis may occur in
children
(3) Reactive arthritis may occur
2. Viral pharyngitis
a. Exudative pharyngitis often observed with adenovirus
and EBV
b. Ulcers, vesicles occur with herpes simplex and coxsackievirus
c. Diphtheria, occurring occasionally in the United States,
presents with grayish pseudomembrane
d. Possibilities with HIV
In peritonsillar abscess, the tonsil may be
displaced toward the midline, and the voice
may sound muffled, classically described as a hot
potato.
Acute rheumatic fever occurs in 3% of patients
with untreated streptococcal tonsillitis (one case
per million people annually in the United States) and
manifests with heart and joint involvement, chorea,
subcutaneous nodules, and fever.
Acute HIV can manifest with fever and a nonexudative
pharyngitis.
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C H A P T E R
e. Mild nonexudative pharyngitis occasionally occurs with oral
infection with Neisseria gonorrhea
f. Influenza may present with nonexudative pharyngitis, muscle
aches, headache, cough
1. It is critical to distinguish between streptococcal infection,
which requires antimicrobial therapy to prevent suppurative and
nonsuppurative complications, and viral causes of pharyngitis.
a. Although only 10% of adults with sore throat have a strep
infection, 75% of adults receive antibiotics.
i. Fever
ii. Tonsillar exudates
iii. Tender cervical lymphadenopathy
iv. Absence of cough
v. Age sometimes included in modification of the criteria,
with age under 14 years giving one point and over
45 years taking away one point
b. Guidelines for use of Centor criteria, according to the
American College of Physicians:
i. Patients with zero or one Centor criterion do not need
further testing, because risk of strep is 10% or less.
ii. Patients with two Centor criteria should be tested with
one of the methods discussed in the following section.
iii. Patients with three or more Centor criteria can be tested
or empirically treated because risk is at least 28%.
2. Laboratory testing for strep
a. Rapid strep enzyme immunoassay
The Centor criteria are a validated clinical prediction
rule to help diagnose strep; one point is given for
each of the following criteria.
In this rapid test, specificity is great at over 90%;
sensitivity is only 80%90%.
i. Advisory committees consider that the rapid test is
not sensitive enough to be used alone in children and
adolescents.
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P A R T
ii. Because adults have lower incidence of strep and less
risk of rheumatic fever, relying on rapid antigen test is
considered reasonable in adults.
b. Throat culture
3. Laboratory testing for other causes
a. Heterophile antibody can be checked to evaluate for EBV.
b. Testing for gonorrhea requires culture on Thayer-Martin
medium.
c. Rapid testing on an oropharyngeal swab can detect influenza
virus.
F. Management
1. Antimicrobial therapies
a. Penicillin cures group A strep, and essentially no resistance
has been seen.
i. 10 days of oral penicillin VK
ii. Injection of benzathine penicillin
b. Patients with mononucleosis (EBV) who are treated with
ampicillin or amoxicillin for presumed strep often get a
diffuse, pruritic skin eruption.
2. Supportive therapies
a. OTC pain relievers
b. Warm saltwater gargles, throat lozenges may also help.
Throat culture is the gold standard and should be
done in children if results of rapid testing are negative.
Treatment within 9 days of onset of symptoms is
sufficient to prevent rheumatic fever.
Ibuprofen is more effective than acetaminophen in
relieving pain in the throat in children.
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C H A P T E R
MENTOR TIPS DIGEST
Sinusitis
Clinicians use the term sinusitis to imply acute bacterial
sinusitis.
Sinusitis complicates about 0.5%2% of URIs.
About 1/10,000 cases of sinusitis lead to severe complications
such as local or CNS infection.
Antimicrobial agents do not alter the course of the common
cold or prevent bacterial sinusitis.
History and physical examination in the office focus on differ-
entiating viral rhinosinusitis from bacterial sinusitis.
Mental status changes or vision changes are red flags for CNS
spread.
Diagnosis of acute sinusitis is made empirically. National
guidelines endorsed by the CDC recommend reserving the
diagnosis of acute bacterial rhinosinusitis for patients with
rhinosinusitis symptoms lasting 7 days or more with maxillary
pain or tenderness in the face or teeth (especially when uni-
lateral) and purulent nasal secretions.
Newer, non-penicillin antibiotics are not shown to be more effec-
tive than amoxicillin.
Amoxicillin (500 mg three times daily in adults) is first-line
therapy for acute sinusitis.
Bronchitis
Acute bronchitis is almost always viral.
Atypical bacterial causes of acute bronchitis are thought to be
far less common than viral.
In bronchitis, cough persists for more than 5 days, usually
1020 days.
Dyspnea is typically absent in bronchitis.
Tachypnea, tachycardia, and hypoxemia should not be
present in bronchitis and are concerning for pneumonia,
bronchiolitis, or severe asthma.
Either normal breath sound or wheezing is heard in bronchitis.
CXR is recommended for patients with signs of consolidation
on lung examination, or with tachycardia, tachypnea,
hypoxemia, or fever >38.3C.
Bronchitis is a self-limited illness; antibiotics reduce cough by
a fraction of a day but have no benefit for overall quality of life.
1389_Ch10_126-141 2/2/09 1:25 PM Page 137
P A R T
Resources
Bisno A. Acute pharngitis. New England Journal of Medicine
344:205211, 2001
This is a helpful review article that pays special attention to the differ-
ential diagnosis of pharyngitis and the clinical characteristics of the
various viral and bacterial etiologies.
Bisno A. Pharyngitis. In Mandell GL, Bennett JE , Dolin R, eds.
Principles and practice of infectious diseases, 6th ed. Elsevier,
Philadelphia, 2005.
Pharyngitis
Viruses are the most common cause of pharyngitis.
Streptococcus pyogenes (group A beta-hemolytic streptococ-
cus) accounts for 15%30% of pharyngitis episodes in
children and 10% in adults.
Frequent symptoms in streptococcal pharyngitis are sore
throat, painful swallowing, and fever.
Key signs in streptococcal pharyngitis are temperature above
39.4C, exudate on the tonsils, and tender cervical adenopathy.
In peritonsillar abscess, the tonsil may be displaced toward
the midline, and the voice may sound muffled, like a hot
potato.
Acute rheumatic fever occurs in 3% of patients with untreated
streptococcal tonsillitis (one case per million people annually in
the United States) and manifests with heart and joint involve-
ment, chorea, subcutaneous nodules, and fever.
Acute HIV can manifest with fever and a nonexudative
pharyngitis.
The Centor criteria are a validated clinical prediction rule to
help diagnose strep; one point is given for each criterion
(see text).
In rapid strep enzyme immunoassay, specificity is great at
over 90%; sensitivity is only 80%90%.
Throat culture of strep is the gold standard and should be
done in children if results of rapid testing are negative.
Penicillin cures group A strep. Treatment within 9 days of
onset of symptoms is sufficient to prevent rheumatic fever.
Ibuprofen is more effective than acetaminophen in relieving
pain in the throat in children.
1389_Ch10_126-141 2/2/09 1:25 PM Page 138
C H A P T E R
This comprehensive chapter explains the pathophysiology,
clinical syndromes, diagnosis, and treatment of all causes of
pharyngitis.
Brook I. Acute and chronic bacterial sinusitis. Infectious Disease Clinics
of North America 427448, 2007.
This is a detailed review article about the microbes causing acute and
chronic sinusitis.
Ebell MH, et al. The rational clinical examination: Does this patient
have strep throat. Journal of the American Medical Association
29122918, 2000.
This article is a focused exploration of the sensitivity and speci-
ficity of signs and symptoms for diagnosing strep pharyngitis. It
explores available clinical prediction rules such as the Centor
criteria.
Gonzalez R, et al. Principles of appropriate antibiotic use for treatment of
nonspecific upper respiratory infections in adults: Background. Annals
of Internal Medicine 134:490494, 2001.
A clinical practice guideline for treating ambulatory patients with
suspected sinusitis.
Gwaltney J. Acute bronchitis. In Mandell GL, Bennett JE , Dolin R, eds.
Philadelphia, 2005.
Gwaltney explores the pathogenesis and clinical manifestations of the
viral and nonviral causes of acute bronchitis.
Gwaltney J. Sinusitis. In Mandell GL,Bennett JE, Dolin R, eds.
Philadelphia, 2005.
Gwaltney explores sinusitis.
Hahn RG, Knox LM, Forman TA. Evaluation of poststreptococcal illness.
American Family Physician 19491954, 2005.
This article details the suppurative and nonsuppurative complications
of streptococcal pharyngitis.
Piccirillo J. Acute bacterial sinusitis. New England Journal of Medicine
351:902910, 2004.
Excellent review article.
Snow V, et al. Principles of appropriate antibiotic use for acute pharyngitis
in adults. Annals of Internal Medicine 506517, 2001.
This is a brief clinical guideline focusing on the diagnosis of strep
throat and avoidance of unnecessary antibiotic use.
1389_Ch10_126-141 2/2/09 1:25 PM Page 139
P A R T
Steinman MA, et al. Changing use of antibiotics in community-based
outpatient practice, 19911999. Annals of Internal Medicine
525533, 2003.
Cross-sectional study showing a high incidence of antibiotic prescribing
for common viral diagnoses such as acute bronchitis.
Wenzel RP, Fowler AA. Acute bronchitis. New England Journal of Medi-
cine 2006;355:212530.
This article offers a practical approach to the common clinical presen-
tation of acute bronchitis.
Williams JW, et al. Antibiotics for acute maxillary sinusitis. The Cochrane
Database of Systematic Reviews 2007.
A compilation of the high-quality studies of antibiotics for sinusitis,
which in summary show a marginal benefit of antibiotics.
Williams JW, Simel DL. Does this patient have sinusitis: Diagnosing
acute sinusitis by history and physical examination. Journal of the
American Medical Association 12421246, 1993.
An installment in the rational clinical examination series that explores
utility of signs and symptoms in distinguishing bacterial sinusitis from
the common cold.
1. What is the most effective proven technique for preventing the common
cold?
a. Hand washing
b. Paper face masks covering nose and mouth
c. Decongestant nasal spray
d. Prophylactic antibiotic therapy
1389_Ch10_126-141 2/2/09 1:25 PM Page 140
C H A P T E R
2. A 32-year-old man presents to you because his wife has a sinus
infection for which a provider prescribed amoxicillin/clavulanate. He
is aware of extensive news coverage of MRSA in the community. He
would like a prescription to prevent a sinus infection. Which is the
most appropriate response?
a. Prescribe amoxicillin/clavulanate.
b. Prescribe clindamycin.
c. Reassure and explain that sinus infections are not contagious.
d. Reassure and recommend temporary change in home sleeping
arrangements.
3. Which is the most common organism causing acute bacterial sinusitis
in immunocompetent adults?
a. Staphylococcus aureus
b. Streptococcus pneumoniae
c. Legionella pneumoniae
d. Escherichia coli
1389_Ch10_126-141 2/2/09 1:25 PM Page 141
142
CHAPTER
11
ABDOMINAL PAIN
Mitchell S. King, MD
I. Introduction
A. Common with a variety of presenting symptoms and potential
etiologies.
B. Diagnostic possibilities from chronic and benign illnesses, such as
irritable bowel syndrome, to acute and life-threatening conditions,
such as abdominal aortic aneurysm (AAA).
C. Differential diagnosis includes intra-abdominal conditions;
pulmonary, cardiac, musculoskeletal, and dermatologic disease
(Table 11.1).
D. Chronic abdominal pain not assumed as benign
TABLE
11.1
Differential Diagnosis of Abdominal Pain by
Location
Location Differential Diagnosis
Poorly localized Abdominal aortic aneurysm (AAA)
Mesenteric ischemia
Early obstruction
Early appendicitis
Inflammatory bowel disease
Gastroenteritis
Pancreatitis
Peritonitis
Sickle cell anemia crisis
Epigastric Gastroesophageal reflux disease
Peptic ulcer disease
Gastritis
1389_Ch11_142-166 2/2/09 1:25 PM Page 142
11 ABDOMINAL PAIN 143
C H A P T E R
Differential Diagnosis of Abdominal Pain by Location (Continued)
Pancreatitis
Cholecystitis
Musculoskeletal
Cardiac (myocardial infarction/pericarditis)
Right upper quadrant Cholecystitis
Other liver disease (hepatitis, cholangitis,
abscess)
Gastritis
Renal (stones, pyelonephritis)
Pulmonary (pneumonia, pleural disease,
pulmonary embolus)
Musculoskeletal
Herpes zoster
Appendicitis
Subdiaphragmatic abscess
Left upper quadrant Peptic ulcer disease
Gastritis
Splenic (splenomegaly, infarction, injury)
Pancreatitis
AAA
Cardiac (infarction, pericarditis)
Pulmonary (pneumonia, pleural disease,
pulmonary embolus)
Musculoskeletal
Herpes zoster
Right lower quadrant Appendicitis
Mesenteric adenitis
Crohn disease
Diverticular disease, including Meckel
Cholecystitis/biliary tract
Musculoskeletal
Pancreatitis
Herpes zoster
Gynecologic (pelvic inflammatory disease,
ectopic pregnancy, endometriosis)
Renal (stones, infection)
(continued on page 144)
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P A R T
II. Approach to the Patient
A. Initial evaluation of abdominal pain
1. History (Box 11.1): characterizing the pain and assessing risk
for the different diseases that can cause abdominal pain are
important elements of the history.
TABLE
11.1
Differential Diagnosis of Abdominal Pain by
Location (Continued)
Left lower quadrant Diverticular disease
Colitis
Crohn disease
Bowel obstruction
Colon cancer
Musculoskeletal
Renal (stones, infection)
Gynecologic (pelvic inflammatory disease,
ectopic pregnancy, endometriosis)
Herpes zoster
BOX
11.1
Important History Elements to Evaluate in Patients
With Abdominal Pain
Onset of pain
Location of pain
Aggravating/alleviating factors
Associated symptoms
Fever
Past medical and surgical history
Medication use
Family history
Smoking history
Dietary history
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C H A P T E R
a. Onset
i. Onset of pain with peptic ulcer disease, diverticulitis,
appendicitis, bowel obstruction, biliary or renal colic,
and pancreatitis is generally over minutes to hours.
ii. The exact onset of pain with chronic abdominal pain is
often difficult to define.
b. Location of pain (see Table 11.1)
i. Pain radiation patterns: e.g., midepigastric pain of pancre-
atitis is referred through to the back; pain of biliary colic
may be referred to the scapular region
ii. Evolution of the pain: e.g., pain of appendicitis starts in
periumbilical region but as process progresses, pain can
localize to right lower quadrant
c. Aggravating/alleviating factors: ingesting food, passing
bowel movements, or changing position
i. Food may alleviate the symptoms of ulcer disease but
worsen the symptoms associated with bowel obstruc-
tion, cholecystitis, pancreatitis, and irritable bowel
syndrome.
ii. Bowel movements may bring some relief to patients with
irritable bowel syndrome.
iii. The reclining position may aggravate the symptoms
of pancreatitis and gastroesophageal reflux disease
(GERD).
Pain that develops suddenly suggests a vascular
etiology (e.g., organ infarction, AAA) or perforation/
rupture of an abdominal organ (perforated ulcer,
esophageal rupture).
In patients with chronic abdominal pain, the pres-
ence of alarm symptoms such as onset at older
than 50 years of age, rectal bleeding, weight loss, or
recent change in bowel function raises suspicion for
organic disease.
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P A R T
iv. Body movement may aggravate the pain in conditions
with peritoneal inflammation, such as appendicitis,
diverticulitis, or ruptured viscus. The pain of renal colic
occurs independently of the above factors.
d. Associated symptoms
i. Nausea and vomiting are common.
ii. Hematemesis, or coffee ground emesis, occurs with
upper gastrointestinal (GI) bleeding seen with peptic
ulcer disease, gastritis, esophagitis, or esophageal varices.
iii. Heme-positive stools (can occur with either upper or
lower GI blood loss) and abdominal pain may be caused
by peptic ulcer disease, gastritis, inflammatory bowel
disease, infectious colitis, mesenteric ischemia, diverticular
disease, or colon cancer.
iv. Diarrhea associated with crampy abdominal pain is pre-
sent with gastroenteritis, colitis, lactose intolerance, and
inflammatory bowel disease.
v. Jaundice in association with abdominal pain suggests
liver disease or biliary tract obstruction.
vi. Colicky or wavelike discomfort is consistent with an
intestinal obstruction. Vomiting is common, particularly
in proximal obstruction. Obstruction that is more distal
tends to be less painful and is associated with less vomit-
ing than proximal obstruction.
vii. Fatigue and weight loss may indicate inflammatory
bowel disease or a malignancy as the underlying cause
for abdominal pain.
viii. Extraintestinal manifestations such as iritis, arthritis,
aphthous ulcers, and dermatologic findings of erythema
nodosum and pyoderma gangrenosum may occur with
inflammatory bowel disease.
ix. Referred pain from a cardiac or pulmonary process should
be considered if patients complain of shortness of breath,
cough, or chest pain. For patients with stigmata of alcohol
Pain that precedes emesis suggests a potential
surgical condition, whereas emesis that is
followed by pain points more toward a nonsurgical
condition.
1389_Ch11_142-166 2/2/09 1:25 PM Page 146
C H A P T E R
abuse, such as spider hemangioma, palmar erythema, or
testicular atrophy, pancreatitis should be considered.
x. Gynecologic conditions should be considered in female
patients. Timing of the pain in relation to the menstrual
cycle may point to either endometriosis or mittelschmerz.
Finally, vaginal discharge and a history of sexually trans-
mitted disease may indicate the possibility of pelvic
inflammatory disease.
xi. Fever is common with infectious enteritis, diverticulitis,
appendicitis, cholecystitis, intra-abdominal abscesses
(psoas, subdiaphragmatic), and pulmonary, gynecologic,
and urinary tract infections.
2. Past medical and surgical history may suggest etiologies:
a. Gallstones, nephrolithiasis, or diverticular disease may indicate
a recurrence.
b. Previous abdominal surgery should lead to consideration of
bowel obstruction due to adhesions.
c. Known hypertension or vascular disease is a risk factor for a
vascular cause, such as AAA, or mesenteric infarction.
d. Cholelithiasis and alcohol abuse are the most common con-
ditions associated with pancreatitis.
e. Prior ectopic pregnancies, a history of a sexually transmitted
disease, or pelvic inflammatory disease may suggest a gyne-
cologic etiology.
Symptoms that are significantly associated with
ovarian cancer are pelvic/abdominal pain, urinary
urgency/frequency, increased abdominal size/bloating,
and difficulty eating/feeling full when present for 1 year
and occurring 12 days per month.
Of the adult Western population, 10%15% will
develop gallstones.
Ectopic pregnancy and ovarian torsion are two of
the most common causes of acute abdominal pain
in early pregnancy.
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P A R T
f. Ketoacidosis may present with abdominal pain and should
be considered in diabetic individuals.
3. Medication use:
a. Nonsteroidal anti-inflammatory medications (NSAIDs) may
cause Helicobacter pylorinegative ulcer disease.
b. Fenofibrate and gemfibrozil are associated with gallstone
formation.
c. Azathioprine, 6-mercaptopurine, didanosine, and other
medications can cause pancreatitis.
B. Physical examination (Table 11.2)
TABLE
11.2
Diagnostic Clues to Etiologies of Abdominal Pain
Diagnosis Typical Symptoms
Gastroesophageal reflux Regurgitation, dysphagia
disease
Peptic ulcer disease Gnawing epigastric pain, nausea,
vomiting, bloating
Gastritis Same as peptic ulcer disease
Nonulcer dyspepsia Upper abdominal/epigastric pain,
bloating, belching, flatulence, nausea
Cholelithiasis Colicky right upper quadrant pain,
worse with meals, radiation to
scapular region
Pancreatitis Severe constant midabdominal pain
Inflammatory bowel disease Chronic diarrhea, hematochezia,
weight loss, anorexia, fever
Irritable bowel syndrome Chronic abdominal cramps, alternating
diarrhea and constipation; no weight
loss, fever, or hematochezia
Gastroenteritis Acute illness with nausea, vomiting,
diarrhea
Bowel obstruction Pain followed by absent stool, flatus,
nausea, vomiting, abdominal
distention
Peritonitis Severe abdominal pain, worsens
with movement, cough; fever
Nephrolithiasis Flank pain radiating to the groin,
intense, writhing to get comfortable,
hematuria
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C H A P T E R
1. Vital signs
a. Hypotension may signify AAA, rupture of an intra-
abdominal organ, significant blood loss, dehydration, or
sepsis.
b. Fever may occur with appendicitis, diverticulitis, pancreatitis,
and cholecystitis as well as with pulmonary, gynecologic, or
urinary tract infections.
2. General appearance and posture
a. Patients in severe pain should generally be evaluated in an
emergency room setting.
b. A patient with pancreatitis may prefer to sit up and lean
forward and may be more uncomfortable in the supine
position.
Diagnostic Clues to Etiologies of Abdominal Pain (Continued)
Diagnosis Typical Symptoms
Appendicitis Periumbilical pain followed by anorexia,
vomiting; pain subsequently in right
lower quadrant; fever
Diverticulitis Left lower quadrant pain, anorexia,
fever
Mesenteric ischemia Postprandial intense diffuse pain;
benign examination
Abdominal aortic aneurysm Abdominal pain radiating to back or
groin; pain out of proportion to
examination; pulsatile mass; possibly
hemodynamic instability
Ovarian cancer Pelvic/abdominal pain, urinary
urgency/frequency, increased
abdominal size/bloating, and difficulty
eating/feeling full when present for
1 year and occurring 12 days per
month
Patients with renal colic or an intestinal obstruction
may be restless, whereas patients with peritonitis
tend to be still.
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P A R T
3. Chest
a. Evaluate for pericardial or pleural rubs and signs of lower
lobe consolidation.
4. Abdomen
a. Inspection
i. Abdominal distention may indicate bowel obstruction
(however, it is nonspecific).
ii. Scars from prior surgeries should be noted.
iii. Rash could indicate presence of herpes zoster.
iv. Skin discoloration or bruising should be noted and may indi-
cate retroperitoneal bleeding as may occur with hemorrhagic
pancreatitis. Jaundice suggests biliary disease or hepatitis.
b. Auscultation
i. Hyperactive bowel sounds occur with gastroenteritis or
bowel obstruction, with high-pitched, tinkling bowel
sounds being characteristic of the latter.
ii. Hypoactive bowel sounds may be present with divertic-
ulitis or appendicitis and late bowel obstruction. A silent
abdomen often indicates generalized peritonitis.
iii. Abdominal bruits suggest potential vascular pathology.
c. Palpation
i. Begin with light palpation in areas away from the abdom-
inal pain.
ii. Abdominal guarding, presence of masses, hernias, or
organomegaly should be noted during palpation.
iii. Rebound tenderness can be elicited by asking the patient
to cough.
iv. Localization of the pain is very helpful in narrowing the
differential diagnosis (see Table 11.1). For example, a
positive Murphy sign, increased pain on palpation of the
right upper quadrant while the patient inspires, suggests
cholecystitis.
v. Generalized severe abdominal tenderness indicates
diffuse peritoneal inflammation.
Carnett test: Identify the site of maximal pain,
ask the patient to attempt to sit up while apply-
ing pressure to the forehead. An increase in pain sug-
gests an abdominal wall etiology, whereas no change
suggests a visceral source.
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C H A P T E R
5. Rectal examination
a. Evaluate for masses, and check the stool for occult blood.
6. Pelvic examination
a. Evaluate for pelvic masses, cervical/vaginal discharge, and
presence of cervical motion tenderness.
7. Testicular examination
a. Evaluate for testicular torsion or epididymitis.
C. Diagnostic studies (Table 11.3)
Significant abdominal pain in the absence of
significant physical examination findings may sug-
gest mesenteric ischemia. (However, be circumspect;
this finding is also common in somatoform disorder and
malingering.)
TABLE
11.3
Diagnostic Testing to Evaluate Abdominal Pain
Laboratory test Useful for
Complete blood count
Urinalysis
Liver panel
Amylase
Lipase
Serum calcium
Basic metabolic panel
Lipids
Human chorionic gonadotropin
Hemoccult testing of stool
Stool for leukocytes
Stool culture
Stool for ova and parasites
Stool for Clostridium difficile
toxin
Anemia/hemorrhage, infection
Renal infection, renal stones, diabetes
Cholecystitis, hepatitis
Pancreatitis
Pancreatitis
Pancreatitis
Nausea/vomiting/diarrhea, dehydration,
impaired renal function, diabetes
Pancreatitis
Pregnancy/ectopic pregnancy
Gastrointestinal blood loss (any
source)
Bacterial gastroenteritis, inflammatory
bowel disease
Bacterial gastroenteritis
Diarrhea/abdominal pain due to
parasites
Diarrhea/abdominal pain from
pseudomembranous colitis
1389_Ch11_142-166 2/2/09 1:25 PM Page 151
P A R T
TABLE
11.3
Diagnostic Testing to Evaluate Abdominal
Pain (Continued)
Perforated viscus, bowel obstruction,
renal stones
Organ infection, infarction or tumor,
bowel obstruction, pancreatitis,
appendicitis, diverticulitis, hemor-
rhage, abdominal aortic aneurysm
(AAA)
Imaging patients for whom the risk of
radiation or the potential nephrotoxi-
city of iodinated contrast is a major
concern; evaluating pregnant
patients with acute lower abdominal
pain believed to have an extrauter-
ine cause such as appendicitis or
torsion. MRI with gadolinium should
be avoided in patients with end
stage renal disease.
Cholecystitis, pancreatitis, renal
infection/obstruction, AAA in women
and children: appendicitis, gyneco-
logic disease
Renal stones/obstruction, hematuria
evaluation
Esophageal cancer, stricture, diverticula,
reflux, spasm
Small bowel source of blood loss when
other source negative, bowel obstruc-
tion, inflammatory bowel disease,
small bowel malignancies (rare)
Colon cancer, polyps, colitis, Crohn
disease, bowel obstruction
Gastroesophageal reflux disease,
esophageal stricture, cancer, peptic
ulcer disease, gastritis, gastric cancer
Colon cancer, colitis, polyps, inflam-
matory bowel disease
Radiologic test Useful for
Plain film
Computer tomography scan
Magnetic resonance scan
Ultrasound
Intravenous pyelogram
Barium swallow
Upper gastrointestinal series
Barium enema
Esophagogastroduodenoscopy
Colonoscopy
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C H A P T E R
1. Laboratory studies
a. Complete blood count (CBC): detects the presence of anemia
or an elevated white blood cell count suggesting the presence
of an acute inflammatory or infectious process; in elderly
patients, the differential is extremely important because a
shift to immature forms of white blood cells can indicate
significant disease in patients with just mildly elevated or
normal white blood cell counts
b. Urinalysis: look for pyuria and/or hematuria, thus pointing
to urinary tract as potential source for abdominal pain
c. Liver function tests and amylase/lipase: when elevated, may
signify liver and/or pancreatic disease; when a patient has had
recurrent episodes of hepatitis and pancreatitis, this may not
be true
d. Basic metabolic panel: can assess hydration, renal function,
and electrolytes; an elevated glucose with low serum bicar-
bonate is consistent with ketoacidosis
e. H. pylori testing (Table 11.4): in patients who are not taking
ulcerogenic medications, H. pylori accounts for almost 90%
of ulcer disease
TABLE
11.4
Diagnostic Tests for Helicobacter pylori
Test Comments
Rapid urease test
Histologic staining
Serology
Most commonly used test
Performed on endoscopically obtained
tissue sample
Test is inexpensive but requires endoscopy
Results promptly obtained
Sensitive/very specific
Requires endoscopy culture
Often performed in conjunction with rapid
urease test
Takes longer to receive results
More expensive than rapid urease test
Noninvasive
Inexpensive
Documents exposure but not active disease
1389_Ch11_142-166 2/2/09 1:25 PM Page 153
P A R T
i. Rapid urease test analyzes tissue samples obtained during
endoscopy for the presence of urease (the presence of
urease is consistent with H. pylori infection). This test has
a sensitivity of approximately 90% and a specificity of
98%. The test itself is inexpensive and quickly performed
but requires endoscopy to obtain tissue.
ii. Histologic staining can also detect H. pylori and may be
performed if the rapid urease test is negative in a patient
with ulcers or gastritis. Histologic staining has an excel-
lent sensitivity and specificity; however, it is slower and
more expensive than the urease test.
iii. Serologic testing for H. pylori has the advantage of being
noninvasive, inexpensive, and highly sensitive and spe-
cific (90%). The disadvantages are that serology will re-
main indefinitely positive, and a positive test does not
distinguish between prior or current infection. Patients in
their twenties are rarely positive, whereas those in their
sixties are positive more than 50% of the time.
TABLE
11.4
Diagnostic Tests for Helicobacter pylori (Continued)
Test Comments
Urea breath tests
Stool antigen testing
Cannot document eradication
Used more in younger patients (age
40 years)
High rate of positive tests in asymptomatic
elderly limits usefulness
Noninvasive
Variable cost but can be inexpensive
Sensitive/specific
Can document eradication
Requires stool sample
95% sensitive and specific
Can document eradication
This test is useful in younger populations and
for diagnosing H. pylori in radiographically diag-
nosed duodenal ulcers, but it cannot be relied on in
older patients with gastric ulcers or for following ther-
apeutic response.
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C H A P T E R
iv. H. pylori stool antigen testing requires collecting a stool
sample. It can be used to test for cure of the disease and
is 95% sensitive and specific.
v. Urea breath testing involves having the patient ingest
urea labeled with radioactive carbon. If H. pylorus is
present, urease hydrolyzes the urea, and the patient
exhales labeled carbon dioxide. The test is both sensitive
and specific but is expensive and not readily available.
2. Radiologic testing
a. Plain film is useful for detecting intestinal obstruction and free
air, which suggests a perforated viscus. Plain film has a sensi-
tivity of 30%60% for detecting free air and is diagnostic for
50%60% of cases of bowel obstruction. Additional informa-
tion from plain films is limited.
b. Computed tomography (CT) has become one of the most
widely used tests for evaluating undifferentiated acute
abdominal pain as well as cases of pancreatitis, appendicitis,
and diverticulitis. The CT scan has a sensitivity and speci-
ficity of over 90% for appendicitis and diverticulitis.
c. Magnetic resonance imaging (MRI) is a useful modality for
patients for whom the risk of radiation or the potential
nephrotoxicity of iodinated contrast is a major concern. MRI
is also useful in evaluating pregnant patients with acute
lower abdominal pain that is believed to have an extrauterine
cause, such as appendicitis or torsion.
d. Ultrasound is commonly used to evaluate patients with
abdominal pain and suspected gallstones, renal stones,
pyelonephritis, appendicitis, or gynecologic disease. Ultra-
sound is commonly the first radiologic study performed for
patients being evaluated for cholecystitis. The ultrasound can
detect the presence of gallstones, gallbladder wall edema, and
biliary duct obstruction. For renal disease, ultrasound can
detect ureteral obstruction and demonstrate parenchymal dis-
ease or abscess formation. In women with lower quadrant
pain, ultrasound is commonly the test first used because of
lower cost and lack of radiation exposure. Ultrasound has a
sensitivity of approximately 85% and specificity of approxi-
mately 90% for diagnosing appendicitis. Ultrasound can also
assess the uterus, fallopian tubes, and ovaries for gynecologic
disease in patients with abdominal pain.
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P A R T
e. Intravenous pyelogram can demonstrate urinary tract obstruc-
tion and is useful for evaluating patients with hematuria and the
renal system for traumatic damage. However, CT scan is usu-
ally the initial test for patients with abdominal trauma; it can
also detect internal bleeding and kidney or other organ damage.
f. Barium studies can be useful in evaluating the colon (barium
enema) and upper GI tract (barium swallow or upper GI with
small bowel follow through). This test is useful in detecting
anatomical abnormalities and esophageal spasm, and it may
detect esophageal reflux. However, barium studies have a lower
sensitivity than endoscopy for detecting ulcerations, erosions,
polyps, and tumors, and they do not allow tissue diagnosis.
3. Endoscopy
a. Esophagogastroduodenoscopy (EGD) is the diagnostic tool
most frequently used in evaluating symptoms of heartburn or
dysphagia and in assessing the upper GI tract in patients with
GI blood loss. EGD detects esophagitis, erosions, ulcerations,
malignancies, webs, diverticula, and strictures, and it can be
therapeutically useful in treating ulcer disease and strictures.
b. Colonoscopy is most commonly used in assessing patients
with suspected lower intestinal blood loss. In patients with
negative CT scans, it is often used to rule out colonic
sources of abdominal pain.
III. Management (Tables 11.5, 11.6, and 11.7)
A. Acute abdomen
1. Patients typically present in emergency rooms but may, rarely,
present to physicians office
2. Often present with sudden onset of severe abdominal pain with
associated generalized tenderness
3. Acute abdominal pain presenting with rigid abdomen and
hemodynamic instability may be due to perforation, infarction,
obstruction of abdominal organ, or ruptured aneurysm
4. Patients require urgent surgical consultation, stabilization
5. Clinicians have historically withheld opiate analgesics from
patients with acute abdominal pain until after surgical evalua-
tion, based on concern that physical findings may be altered;
new evidence shows whereas physical findings may be altered,
no significant increase in management errors occurs.
1389_Ch11_142-166 2/2/09 1:25 PM Page 156
C H A P T E R
TABLE
11.5
Medical Therapies for Some Common Causes
of Abdominal Pain
Cause Medical Therapies
Gastroesophageal reflux
disease
(PUD)
Behavioral changes
No food or drink 2 hours before
reclining
Lose weight
Avoid overeating, tight clothing, and
certain foods (spicy, citrus, mints,
alcohol, caffeine)
Elevate head of bed
Medications
H
2
blockers (cimetidine, famotidine,
nizatidine, ranitidine)
Proton pump inhibitors (lansopra-
zole, omeprazole)
Motility agents (metoclopramide)
H. pyloripositive disease
714 days of antibiotics: clarithromycin
and ampicillin or metronidazole;
bismuth subsalicylate, metronidazole,
and tetracycline.
48 weeks of H
2
blocker or proton
pump inhibitor therapy for duodenal
ulcers and 612 weeks for gastric
ulcers
Follow-up EGD to document eradica-
tion of gastric ulcers
H. pylorinegative disease
H
2
blockers or proton pump inhibitor
therapy as for H. pyloripositive
disease
Follow-up EGD as for H. pyloripositive
disease
Removal of causative agents (e.g.,
NSAIDs)
Misoprostol can help prevent NSAID-
induced ulcers
1389_Ch11_142-166 2/2/09 1:25 PM Page 157
P A R T
TABLE
11.5
Medical Therapies for Some Common Causes
of Abdominal Pain (Continued)
Cause Medical Therapies
Nonulcer dyspepsia
Pancreatitis
Cholecystitis
Diverticulitis
Behavioral changes
Physician reassurance of nonserious
nature of the disease
Avoidance of provocative foods and
medications
Medications
H
2
blockers or proton pump inhibitors
for PUD and GERD-like symptoms
With dysmotility symptoms, motility
agents can be tried
Can try to step down or use intermit-
tent therapy after about 4 weeks of
therapeutic success
Intravenous (IV) hydration
Nothing by mouth until pain subsides,
pancreatic enzymes decline
Pain relief as appropriate
Monitor for complications: necrosis,
abscess, pseudocyst, hypocalcemia,
hyperglycemia, hypotension, renal
failure, shocks
IV hydration, antibiotics, surgery
For nonsurgical candidates and
chronic symptoms, ursodiol may
be used
IV hydration
Nothing by mouth until pain subsides
Antibiotic therapy (see Table 11.6)
Monitor for complications: peritonitis,
abscess formation, strictures,
fistulae
Follow-up colonoscopy to document
no other underlying cause for the
patient
Symptoms (i.e., colon cancer)
1389_Ch11_142-166 2/2/09 1:25 PM Page 158
C H A P T E R
TABLE
11.6
Examples of Antibiotic Coverage for GI Organism
Route and Indication Examples
Outpatient/oral (for
diverticulitis)
Outpatient/oral
(for H. pylori)
Inpatient/intravenous
(for diverticulitis)
Trimethoprim/sulfamethoxazole
160/800 mg bid
or
Ciprofloxacin 500 mg bid plus metronida-
zole 500 mg qid
or
Amoxicillin/clavulanic acid 500 mg tid or
875 mg bid
Omeprazole 40 mg qd and clarithromycin
500 mg tid and ampicillin 500 mg or
metronidazole 250 mg qid
or
Ranitidine 150 mg bid and bismuth
subsalicylate 2 tabs qid and metron-
idazole 250 mg qid and tetracycline
500 mg qid
Ciprofloxacin 400 mg IV q 12 h
or
Gentamicin 2 mg/kg loading dose then
1.7 mg/kg IV q 8 h
or
Cefotaxime 2 g IV q 48 h
or
Aztreonam 2 g IV q 8 h plus metronida-
zole 500 mg IV q 6 h
or
Clindamycin 450900 mg IV q 8 h
plus ampicillin/sulbactam 3 g IV q 6 h
or
Cefoxitin 2 g IV q8 h
or
Cefotetan 2 g IV q 12 h
or
Ticarcillin/clavulanic acid 3.1 g IV q 6 h
or
Piperacillin/tazobactam 3.375 g IV q 6 h
1389_Ch11_142-166 2/2/09 1:25 PM Page 159
P A R T
TABLE
11.7
Indications for Abdominal Pain Referral
Referral Type Indications
Gastroenterology referral
Surgical referral
Dysphagia
Evidence of bleeding
Early satiety
Recurrent vomiting
Weight loss
Atypical symptoms
Diagnostic uncertainty
Refractory to therapy
For possible endoscopic retrograde
cholangiopancreatography in
patients with pancreatitis or
cholecystitis
Suspected colon cancer
Follow-up endoscopy for gastric
ulcers and diverticulitis
Appendicitis
Diverticulitis
Bowel obstruction/perforation
Abdominal aortic aneurysm
Mesenteric ischemia
Resectable malignancy
Cholecystitis
Nephrolithiasis
B. Surgical conditions
1. Abdominal aortic aneurysm, mesenteric ischemia, and appen-
dicitis are surgical conditions.
2. Cholecystitis is generally treated surgically; however, for
patients who have chronic disease who are not surgical candi-
dates, ursodiol may be utilized.
3. Bowel obstruction is initially treated with bowel rest, support-
ive care, and nasogastric suction. In instances when the obstruc-
tion is caused by adhesions, these measures may resolve the
obstruction. Surgery is needed for persistent obstruction and
for those with mechanical lesions such as colon cancer.
1389_Ch11_142-166 2/2/09 1:25 PM Page 160
C H A P T E R
4. Therapy for peritonitis is dictated by the underlying cause. Antibi-
otic therapy and other supportive measures are important for all
patients; for those with peritonitis from an organ perforation (e.g.,
peptic ulcer, appendicitis, diverticulitis), surgery is indicated.
5. Patients with painful renal stones need intravenous hydration,
narcotic pain medications, and often antibiotics until their
stones pass. Stones that have not passed within 4872 hours or
that are associated with infection or uncontrollable pain require
surgical intervention.
C. Medical conditions
1. Acute pancreatitis
a. Typically hospitalized
b. Nothing by mouth to limit stimulation of pancreatic enzyme
secretion and provided intravenous hydration and pain med-
ication until symptoms resolve
c. Monitoring for hypotension, infection, respiration, renal and
fluid/electrolyte abnormalities are cornerstones of therapy
2. Chronic pancreatitis
a. Chronic pain, steatorrhea, and diabetes are complications
that may require therapy.
i. Chronic pain should be treated initially with nonnarcotic
pain medication.
ii. Cautious use of narcotic medications is recommended
along with monitoring the patients use of these medica-
tions for potential abuse.
iii. Consider pancreatic enzymes.
Even in the absence of clinical signs of malab-
sorption, empiric therapy with pancreatic
enzymes may ameliorate the pain.
iv. Refractory pain may require nerve blocks or surgical
intervention.
3. Pancreatic pseudocysts
a. They are a complication of either acute or chronic pancreatitis.
b. Pseudocysts may resolve spontaneously.
1389_Ch11_142-166 2/2/09 1:25 PM Page 161
P A R T
c. Pseudocysts present for more than 6 weeks are less likely to
resolve spontaneously.
d. Pseudocysts that are more than 5 cm in size have an increased
rate of complication that includes rupture, hemorrhage, or
infection.
e. Ultrasound or CT can be used to monitor the presence and
size of pseudocysts.
f. For patients at increased risk of complications, surgical or
gastroenterology consultation should be considered for
possible operative or endoscopic surgical drainage.
4. Diverticulitis
a. Patients with mild diverticulitis can be managed as outpa-
tients with antibiotics active against gram-negative rods and
anaerobes (see Table 11.6).
b. Patients may be placed on a clear liquid diet, with advance-
ment of the diet as tolerated, if clinical improvement is noted
within the following 23 days.
c. Antibiotic therapy is continued for 714 days.
d. Outpatient evaluation (CT scan) and follow-up colonoscopy
are often recommended.
e. To prevent further episodes, fiber supplements or high-fiber
diets are prescribed.
5. GERD
a. Spectrum ranges from minimal symptoms and objective
findings to severe disease with associated complications
such as stricture, bleeding, or Barrett esophagus.
b. Therapy should be tailored to the patient.
i. Mild GERD: behavioral or lifestyle modifications (see
Table 11.5), along with over-the-counter (OTC) H
2
blockers
or antacids.
ii. For patients with more severe symptoms or patients
unresponsive to OTC medications, prescription H
2
blockers,
proton pump inhibitors, or motility agents can be
prescribed, along with continued reinforcement of
lifestyle modifications.
c. If symptoms are relieved, then maintenance therapy can be
initiated.
d. Symptoms persisting beyond 6 weeks merit referral for
endoscopy.
1389_Ch11_142-166 2/2/09 1:25 PM Page 162
C H A P T E R
e. Recurrence of GERD is very high because the underlying
pathophysiologic process is unchanged when therapy is dis-
continued.
f. Therapy for moderate to severe esophagitis may require long-
term treatment. Nonetheless, attempts to step down therapy
should be attempted after 8 weeks of symptom control.
g. Some patients may require only intermittent therapy along
with continued lifestyle modifications.
6. Peptic ulcer disease and gastritis
a. Therapy is dependent on the presence of H. pylori.
i. If H. pylori is present, then therapy directed against this
organism is indicated (see Tables 11.5 and 11.6).
ii. After completion of the antibiotic regimen, proton pump
inhibitors are generally continued for 48 weeks for
duodenal ulcers and for 612 weeks for gastritis or
gastric ulcers.
b. NSAID-related ulcers are generally treated with acid sup-
pression therapy and discontinuing the NSAID.
i. If NSAIDs must be used, options include switching
the patient to a non-acetylated salicylate, such as
salsalate (Disalcid), with an enterically coated prepara-
tion, using a COX-2 inhibitor, and prescribing the low-
est effective dose.
ii. If NSAIDs must be used in patients with a history of
ulcer, misoprostol (Cytotec) can help prevent recurrence.
Severe esophagitis, Barrett esophagus, and
stricture are markers of severe reflux and require
long-term treatment and follow-up, even in the absence
of symptoms, in order to reduce the risk of esophageal
carcinoma, bleeding, or disease progression.
Patients with gastric ulcer require follow-up EGD
to document ulcer healing and to exclude the
possibility of malignancy as the underlying cause of
the ulcer.
1389_Ch11_142-166 2/2/09 1:25 PM Page 163
P A R T
7. Nonulcer dyspepsia
a. For patients with ulcer-like or reflux symptoms, acid-
suppressing agents can be used.
b. For patients with dysmotility-related symptoms, e.g., nausea,
bloating, or early satiety, motility agents such as metoclo-
pramide can be tried.
c. If treatment is initially successful, 4 weeks of continuous
therapy can be employed, followed by a trial off medication.
d. Some patients may benefit from intermittent therapy,
whereas others may require continuous treatment. In such
cases, periodic trials off medication should be attempted to
see if medication is still necessary.
IV. Referral or Consultations
A. Whereas many of the conditions associated with abdominal pain
can be managed medically, many require specialty referral for
further evaluation or therapy. Indications for gastroenterology
and surgical referral are outlined in Table 11.7.
Therapy involves avoidance of precipitating foods
or medications, reassurance regarding the absence
of serious disease, and medications directed at the predom-
inant symptoms.
MENTOR TIPS DIGEST
Pain that develops suddenly suggests a vascular etiology
(e.g., organ infarction, AAA) or perforation/rupture of an ab-
dominal organ (perforated ulcer, esophageal rupture).
In patients with chronic abdominal pain, the presence of
alarm symptoms such as onset at older than 50 years of
age, rectal bleeding, weight loss, or recent change in bowel
function raises suspicion for organic disease.
Pain that precedes emesis suggests a potential surgical
condition, whereas emesis that is followed by pain points more
toward a nonsurgical condition.
Symptoms that are significantly associated with ovarian cancer
are pelvic/abdominal pain, urinary urgency/frequency, increased
abdominal size/bloating, and difficulty eating/feeling full when
present for 1 year and occurring 12 days per month.
1389_Ch11_142-166 2/2/09 1:25 PM Page 164
C H A P T E R
Resources
Ables AZ, Simon I, Melton ER. Update on Helicobacter pylori treatment.
American Family Physician 75: 351358, 2007.
Reviews the epidemiology of H. pylori disease along with a discussion
of the various tests and treatments available.
Of the adult Western population, 10%15% will develop
gallstones. Ectopic pregnancy and ovarian torsion are two of
the most common causes of acute abdominal pain in early
pregnancy.
Patients with renal colic or an intestinal obstruction may be
restless, whereas patients with peritonitis tend to be still.
Carnett test: Identify the site of maximal pain, ask the patient
to attempt to sit up while applying pressure to the forehead.
An increase in pain suggests an abdominal wall etiology,
whereas no change suggests a visceral source.
Significant abdominal pain in the absence of significant physi-
cal examination findings may suggest mesenteric ischemia.
(However, be circumspect; this finding is also common in
somatoform disorder and malingering.)
Serologic testing for H. pylori is useful in younger populations
and for diagnosing H. pylori in radiographically diagnosed
duodenal ulcers, but it cannot be relied on in older patients
with gastric ulcers or for following therapeutic response.
In chronic pancreatitis, even in the absence of clinical signs of
malabsorption, empiric therapy with pancreatic enzymes may
ameliorate the pain.
Severe esophagitis, Barrett esophagus, and stricture are
markers of severe reflux and require long-term treatment and
follow-up, even in the absence of symptoms, in order to
reduce the risk of esophageal carcinoma, bleeding, or disease
progression.
Patients with gastric ulcer require follow-up EGD to document
ulcer healing and to exclude the possibility of malignancy as
the underlying cause for the ulcer.
In nonulcer dyspepsia, therapy involves avoidance of
precipitating foods or medications, reassurance regarding the
absence of serious disease, and medications directed at the
predominant symptoms.
1389_Ch11_142-166 2/2/09 1:25 PM Page 165
P A R T
Camilleri M. Management of patients with chronic abdominal pain in
clinical practice. Neurogastroenterology and Motility 18:499506,
2006.
Dickerson LM, King DE. Evaluation and management of nonulcer
dyspepsia. American Family Physician 70:107114, 2004.
Presents an approach to evaluating the patient with dyspepsia
along with different treatment options for patients with nonulcer
dyspepsia.
Dominguez EP, Sweeney JF, Choi YU. Diagnosis and management of
diverticulitis and appendicitis. Gastroenterology Clinics of North
America 35:367391, 2006.
Review of diagnosis and care for diverticulitis and appendicitis.
Flaser MH, Goldberg E. Acute abdominal pain. Medical Clinic of
North America 90:481503, 2006
Presents an approach to assessment of patients with acute abdominal
pain.
Goff BA, Mandel LS, Drescher CW, et al. Development of an ovarian
cancer symptom index: Possibilities for earlier detection. Cancer
109:221227, 2007.
Mayerle J, Simon P, Lerch MM. Medical treatment of acute pancreatitis.
Gastroenterology Clinics of North America 33:855869, 2004.
Reviews diagnosis, treatment, and complications for acute pancreatitis.
Smith L. Updated ACG guidelines for diagnosis and treatment of GERD.
American Family Physician 71:23762381, 2005.
For self-test questions, see the testbank CD.
1389_Ch11_142-166 2/2/09 1:25 PM Page 166
167
DIARRHEA
Michael J. Polizzotto, MD, and Martin S. Lipsky, MD
I. Definitions and Overview
A. Diarrhea is one of the most common conditions seen in a primary
care setting. Acute diarrhea is defined as the passage of more
than three abnormally loose stools per 24 hours during fewer than
2 weeks. Chronic diarrhea is recurrent diarrhea or diarrhea that
persists for more than 30 days.
B. Acute diarrhea has the following features.
1. Acute diarrhea can be divided into two clinical presentations:
a watery noninflammatory diarrhea and an inflammatory
diarrhea with the presence of either blood or white blood
cells in the stool.
2. Diarrhea can also be classified as mild (no effect on daily activity),
moderate (some activity limitations), or severe (patient is
confined to bed).
3. It is important to ask about exposure to individuals
with similar symptoms; recent travel; intake of caffeine,
alcohol, and sorbitol; and antibiotic or other medication
use.
Antibiotic use within 2 weeks suggests that diarrhea may
be from either an alteration of bowel flora or Clostridium
difficile infection.
4. Grossly bloody diarrhea indicates mucosal damage and is most
commonly seen with an invasive bacterial infection or inflam-
matory bowel disease.
CHAPTER
12
1389_Ch12_167-179 2/2/09 1:25 PM Page 167
P A R T
5. Most acute diarrhea cases are caused by infection.
a. Viral cases have the following features.
i. Typically, stools are watery and accompanied by a low-
grade fever, nausea, or vomiting and achiness.
ii. Rotavirus is the most common cause in infants and chil-
dren, and norovirus (formerly Norwalk virus) is the leading
adult cause.
iii. Although infectious diarrhea in adults is usually viral, it
is more likely to be bacterial than in children.
b. Invasive bacterial infections, such as Shigella, Salmonella, and
Campylobacter, typically present with a prodrome of fever,
headache, fatigue, anorexia, and stools that may initially be
watery before becoming bloody. Crampy abdominal pain
is common. Travelers diarrhea usually lasts 35 days and
presents with symptoms similar to viral gastroenteritis.
Toxigenic Escherichia coli is a common cause of travelers
diarrhea.
6. Severe abdominal pain associated with acute diarrhea in an
older patient suggests the possibility of an ischemic bowel.
Other noninfectious causes of acute diarrhea include fecal
impaction, diverticular disease, acute presentation of inflamma-
tory bowel disease and, rarely, colonic neoplasm.
C. Chronic diarrhea has the following features.
1. The differential diagnosis for chronic diarrhea is extensive
(Figs. 12.1 and 12.2). However, the diagnosis can be broken
down into major groups based on stool characteristics: watery,
inflammatory (bloody), and fatty. Watery diarrhea is further
divided into secretory and osmotic diarrhea.
Viral gastroenteritis accounts for most cases of
acute infectious diarrhea.
The most common causes for persistent diarrhea in
the primary care setting are irritable bowel syndrome
(IBS), inflammatory bowel disease (IBD), lactose intolerance,
and chronic or relapsing gastrointestinal infections (such as
giardiasis, amoebiasis, and C. difficile).
1389_Ch12_167-179 2/2/09 1:25 PM Page 168
12 DIARRHEA 169
C H A P T E R
History
Categorize
Physical
examination
Stool
analysis
Onset
Congenital
Abrupt
Gradual
Epidemiology
Travel
Food
Water
Pattern
Continuous
Intermittent
Duration
Stool
characteristics
Watery
Bloody
Fatty
Fecal
Incontinence
Abdominal pain
Inflammatory
bowel disease
Irritable
bowel syndrome
Ischemia
Aggravating
factors
Diet
Stress
Iatrogenic
diarrhea
Drugs
Radiation
Surgery
Systemic diseases
Hyperthyroidism
Diabetes mellitus
Collagen-vascular
diseases
Tumor syndromes
AIDS
Ig deficiencies
Anorectal
Sphincter
competence
Fecal occult
blood test
Abdomen
Hepatomegaly
Mass
Ascites
Tenderness
Skin
Flushing
Rashes
Dermato-
graphism
General
Fluid
balance
Nutrition
Routine
laboratory
tests Complete blood count
Anemia
Leukocytosis
Chemistry screen
Fluid/electrolyte status
Nutritional staus
Serum protein/globulin
Extremities
Edema
Chest
Wheezing
Electrolytes
Osmotic gap
Stool WBCs
Inflammation
pH
Carbohydrate
malabsorption
Fat output
Sudan stain
Quantitative
Fecal occult
blood test
Bleeding
Heart
Murmur
Thyroid
Mass
Weight
Watery diarrhea
Secretory Osmotic
Fatty diarrhea Inflammatory diarrhea
Laxative screen
Factitious
diarrhea
Laxatives
Mitigating
factors
Diet
OTC drugs
Rx drugs
Previous
evaluation
Weight loss
Malabsorption
Neoplasm
FIGURE 12.1 Workup of chronic diarrhea, part 1. (Reprinted from Gastroen-
terology, Vol 116, Issue 6, Kenneth D. Fine and Lawrence R. Schiller, AGA Technical
Review on the Evaluation and Management of Chronic Diarrhea, Pages 14641486,
Copyright 1999, with permission from Elsevier.)
1389_Ch12_167-179 2/2/09 1:25 PM Page 169
P A R T
Secretory
diarrhea
Exclude
infection
Exclude
infection
Selective
testing
Bacterial pathogens
Standard
Aeromonas
Plesiomonas
Osmotic
diarrhea
Fatty
diarrhea
Stool
analysis
Low pH
Carbohydrate
malabsorption
Dietary review
Breath H
2
test (lactose)
Lactase assay
High Mg output
Inadvertent ingestion
Laxative abuse
Plasma peptides
Gastrin
Calcitonin
VIP
Somatostatin
Other tests
TSH
ACTH stimulation
Serum protein electrophoresis
Immunoglobulins
Urine
5-HIAA
Metanephrines
Histamine
Other pathogens
Standard ova + parasites
Coccidia
Microsporidia
Giardia antigen
Bacterial pathogens
Standard
Aeromonas
Plesiomonas
Tuberculosis
Other pathogens
Parasites
Viruses
Inflammatory
diarrhea
Exclude
structural
disease
Exclude
structural
disease
Exclude
pancreatic
exocrine
insufficiency
Exclude
structural
disease
Cholestyramine
trial for bile acid
diarrhea
Small-bowel
radiographs
CT scan of
abdomen
Small-bowel biopsy
and aspirate for
quantitative culture
Small-bowel
biopsy and
aspirate for
quantitative
culture
Sigmoidoscopy
or colonoscopy
with biopsy
Small-bowel
radiographs
CT scan of
abdomen
Small-bowel
radiographs
CT scan of
abdomen
Secretin
test
Bentiromide
test
Stool
chymotrypsin
activity
Small-
bowel
biopsy
Sigmoidoscopy
or colonoscopy
with biopsy
FIGURE 12.2 Workup of chronic diarrhea, part 2. (Reprinted from Gastroen-
terology, Vol 116, Issue 6, Kenneth D. Fine and Lawrence R. Schiller, AGA Technical
Review on the Evaluation and Management of Chronic Diarrhea, Pages 14641486,
Copyright 1999, with permission from Elsevier.)
1389_Ch12_167-179 2/2/09 1:25 PM Page 170
12 DIARRHEA 171
C H A P T E R
2. IBS accounts for about half of the gastrointestinal complaints
seen by primary care providers. It typically affects young or
middle-aged adults, with a 2:1 female-to-male predominance.
Box 12.1 lists criteria for IBS.
3. IBD refers either to ulcerative colitis or to Crohn disease.
a. IBD has a bimodal age distribution for both ulcerative colitis
and Crohn disease. The largest peak occurs in the third
decade of life, with a smaller peak in the sixth decade of life.
b. Table 12.1 lists some of the characteristics that differentiate
ulcerative colitis from Crohn disease.
BOX
Criteria for Irritable Bowel Syndrome
1. Continuous or recurrent symptoms associated with abdominal pain relieved
by defecation or associated with a change in frequency or stool consistency.
2. A varied pattern of disturbed defecation occurring 25% of the time and
consisting of two or more of the following:
Change in frequency or consistency of stool
Needing to strain to pass stool
Feeling an urgent need to defecate
Bloating
Passing mucus in the stool
Feeling incomplete evacuation
12.1
TABLE
12.2
Comparison of Ulcerative Colitis
and Crohn Disease
Feature Ulcerative Colitis Crohn Disease
Clinical diarrhea Common Common
Rectal bleeding Common Common
Abdominal pain Less prominent Prominent
Abdominal mass Rare Common
Perianal disease Uncommon Common
Fistula Rare Common
Weight loss Occasional Common
Risk of malignancy Increased Slightly increased
Distribution of lesions Continuous Skip lesions
Rectal involvement Almost 100% Occasionally occurs
1389_Ch12_167-179 2/2/09 1:25 PM Page 171
P A R T
4. Lactose intolerance is common and to some extent affects more
than half the worlds population. There are three categories:
congenital, primary with delayed onset, and secondary.
a. The most common type is delayed onset, in which as
individuals age the level of the enzyme lactase decreases.
b. A secondary deficiency occurs when enzyme activity
decreases because of a diffuse intestinal insult, such as in
Crohn disease.
5. Giardia and other parasitic infections can present with chronic
diarrhea. Recent travel to an area where these organisms are
endemic increases the likelihood of these infections.
6. Stools that contain fat globules suggest malabsorption, often
due to pancreatic insufficiency. Infections, enzyme deficiencies
(e.g., lactose intolerance), and mucosal abnormalities such as
those seen in celiac disease are among the other most common
causes of malabsorption in the primary care setting. Once
thought to be rare, celiac disease (due to an abnormal immune
response to gluten, a protein found in wheat, barley, and rye)
has been estimated to affect 1 in 133 Americans. It is most
common in those of European ancestry.
II. Evaluation
A. Acute diarrhea
Most cases of acute diarrhea are mild, self-limiting
illnesses, and diagnostic testing is unnecessary.
1. Box 12.2 lists indications suggesting a need for a more detailed
evaluation.
2. Examining the stool for leukocytes and occult blood is a useful
first test.
a. A stool specimen that has fewer than three to four white blood
cells per high-powered field reflects a noninflammatory process
that is usually self-limited and requires no further investigation.
b. The presence of more than five fecal leukocytes per high-
powered field suggests an inflammatory process; when com-
bined with a history of an abrupt onset of more than four
stools per day and no vomiting before the onset of diarrhea,
it has a positive predictive value of 60%70% for bacterial
diarrhea (Shigella, Salmonella, Campylobacter.)
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12 DIARRHEA 173
C H A P T E R
i. If an inflammatory process is suspected, stool cultures
should be sent to detect Salmonella, Shigella, Campy-
lobacter, and Shiga-toxin producing E. coli (such as
O157:H7).
ii. Stool examinations for ova and parasites have been
recommended for patients at risk for Giardia or other
parasitic infections; however, enzyme immunoassays are
now considered to be more sensitive.
B. Chronic diarrhea
1. The workup for chronic diarrhea should be individualized.
Reviewing stool characteristics, past medical illnesses and
surgeries, travel history, diet, and medications helps focus the
approach.
2. For patients who have no red flags to suggest serious illness
and whose physical examination suggests a benign illness, only
a limited diagnostic evaluation may be needed.
a. For example, patients suspected of having lactose intolerance
that responds to a lactose-free diet need no further testing.
3. Look for offending foods or drugs.
Findings that suggest serious underlying disease
include new-onset diarrhea in patients older than
40 years, nocturnal diarrhea, progressive or persistent
symptoms, weight loss, rectal fissure, anemia, elevated
erythrocyte sedimentation rate (ESR), greasy stools that are
difficult to flush, and extraintestinal symptoms.
BOX
Indications for Evaluation of Acute Diarrhea
Evidence of dehydration
More than six stools per 24 hours
No improvement after 4872 hours
Presence of bloody stool
Temperature higher than 38.5C (101F)
Severe abdominal pain
Diarrhea in an older or immunocompromised individual
12.2
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a. Box 12.3 lists several medications that may cause diarrhea.
Generally, no further evaluation is needed in those patients
whose diarrhea responds to decreasing or stopping a
medication.
4. For patients with chronic diarrhea whose cause is not readily
apparent from the history and physical examination, an initial
evaluation consists of a complete blood count (CBC), ESR, and
checking the stool for occult blood, leukocytes, ova, and parasites.
a. An assay for C. difficile toxin is indicated for patients with
recent antibiotic exposure.
b. For patients with associated left lower quadrant pain or
bloody diarrhea, early sigmoidoscopy examination to detect
mucosal ulcerations, friability, and masses and to biopsy for
suspected IBD is indicated.
c. If an amoebic infection is suspected, mucosal smears obtained
during sigmoidoscopy can be examined for amoeba.
d. Biopsy can also detect less common diseases such as amy-
loidosis and collagenous colitis.
As many as 4% of cases of chronic diarrhea may be
due to medications and food additives.
BOX
Medications That May Cause Diarrhea
Alpha-glucosidase inhibitors
Antacids
Antibiotics
Antidepressants
Colchicine
Lactulose
Laxatives
Loop diuretics
Proton pump inhibitors
Quinidine
Theophylline
Thyroxine
12.3
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12 DIARRHEA 175
C H A P T E R
a. A CBC can detect anemia or leukocytosis.
b. Serum electrolytes can detect abnormalities associated with
fluid loss.
c. Tests for celiac disease include IgA antiendomysial antibody
and antitissue transglutaminase (tTGA). In cases of
immunoglobulin A deficiency, antigliaden IgG improves
sensitivity.
6. Often cases with chronic diarrhea of unclear etiology or suspected
IBD need referral to a gastroenterologist for evaluation.
III. Management
A. Oral rehydration is usually adequate.
1. Commercial rehydration solutions such as Pedialyte and
Ricelyte are designed for fluid and electrolyte replacement
and are most commonly used for infants and children.
2. Sports drinks, fruit drinks, and flavored soft drinks augmented
with crackers, soup, or broth are usually adequate to replace
fluids in adults or older children with diarrhea.
B. More severely dehydrated individuals may require intravenous
fluids.
C. Other diet tips comprise the following.
1. Avoiding milk products and caffeine-containing foods may be
helpful.
2. Boiled starches (potatoes, rice, and noodles) with some salt are
good foods for patients with acute diarrhea.
3. For children, a BRAT diet (bananas, rice, apples, and toast) is
commonly recommended, although there is limited evidence
documenting the effectiveness of this strategy.
4. Lactose intolerance options follow.
5. Blood tests have the following features.
Blood tests may be useful but are rarely diagnostic.
Fluid therapy, an alteration in diet, and monitoring the
patient for resolution of symptoms are sufficient for most
patients with acute diarrhea.
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a. Taking lactase capsules orally before consuming dairy products
is also an effective treatment.
D. Medications consist of the following.
1. Several preparations are available for symptomatic treatment.
Preparations containing kaolin and pectate (Kaopectate) are
available over the counter; however, despite wide usage their
efficacy is uncertain. Bismuth subsalicylate (Pepto-Bismol) is
also used for diarrhea and may have an antisecretory effect.
2. The antimotility drugs, such as loperamide, are the drugs of
choice for most nonspecific treatment. These medications slow
gut motility, facilitating intestinal absorption. They should not
be used in febrile patients with inflammatory infectious diarrhea.
3. Specific management depends on the underlying cause of the
diarrhea. For patients with bacterial diarrhea, the use of antibi-
otics depends on the organism, health of the individual, and
systemic symptoms. All cases of Shigella should be treated
with either a fluoroquinolone or trimethoprim-sulfamethoxazole
(TMP-SMZ). Salmonella infections causing mild to moderate
symptoms should generally not be treated because antibiotics
may prolong the carrier state. Patients with salmonella who
have severe symptoms or those at risk for bacteremia (e.g.,
HIV-infected patients or elderly individuals) should be treated
with a fluoroquinolone.
4. Treating patients with a culture-proven Campylobacter infec-
tion shortens the duration of the illness if symptoms are still
present when the culture results become available. Erythromycin
is the drug of choice, but quinolones are also effective. E. coli
causes a wide spectrum of disease. Invasive E. coli with bloody
diarrhea should be treated with a fluoroquinolone or TMP-SMZ.
Travelers diarrhea due to toxigenic E. coli responds to either a
short course of a fluoroquinolone or TMP-SMZ. C. difficile
infection should be treated with metronidazole; an alternative is
oral vancomycin. Giardia is also treated with metronidazole.
E. Patients with IBS whose predominant symptom is diarrhea should
do the following.
For patients with lactose intolerance, a 1- to 2-week
trial of lactose-free diet is usually sufficient to see
improvement in symptoms.
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12 DIARRHEA 177
C H A P T E R
1. Using an antimotility agent such as loperamide (Imodium),
24 mg up to four times a day, or diphenoxylate hydrochloride
with atropine (Lomotil), 1020 mg up to four times per day,
may provide relief.
2. Antispasmodics such as dicyclomine (Bentyl) 1020 mg before
meals may benefit patients with associated abdominal cramping
and pain. A high-fiber diet is helpful for IBS patients with diar-
rhea alternating with constipation. (New FDA restricted use
only severe refractory cases.)
F. Patients with celiac disease must follow a lifelong gluten-free
diet. Foods and beverages that contain wheat, barely, rye, and
possibly oats should be eliminated completely.
G. Management goals for IBD are to control active disease, maintain
remission, detect complications, and refer to surgery when appropri-
ate. Most patients should be co-managed by a gastroenterologist
experienced in managing IBD.
MENTOR TIPS DIGEST
Antibiotic use within 2 weeks suggests that diarrhea may be
from either an alteration of bowel flora or Clostridium difficile
infection.
Viral gastroenteritis accounts for most cases of acute
infectious diarrhea.
The most common causes for persistent diarrhea in the pri-
mary care setting are IBS, IBD, lactose intolerance, and
chronic or relapsing gastrointestinal infections (such as
giardiasis, amoebiasis, and C. difficile).
Most cases of acute diarrhea are mild, self-limiting illnesses,
and diagnostic testing is unnecessary.
Findings that suggest serious underlying disease include
new-onset diarrhea in patients older than 40 years, nocturnal
diarrhea, progressive or persistent symptoms, weight loss,
rectal fissure, anemia, elevated ESR, greasy stools that are
difficult to flush, and extraintestinal symptoms.
As many as 4% of cases of chronic diarrhea may be due to
medications and food additives.
Blood tests may be useful but are rarely diagnostic.
Fluid therapy, an alteration in diet, and monitoring the patient
for resolution of symptoms are sufficient for most patients
with acute diarrhea.
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Resources
American Gastroenterological Association: American Gastroenterological
Association medical position statement: Guidelines for the evaluation
and management of chronic diarrhea. Gastroenterology 116:14611463,
1999.
Even almost 10 years after they were produced, these guidelines for
chronic diarrhea are useful.
Camilleri M. Therapeutic approach to the patient with irritable bowel
syndrome. American Journal of Medicine 107:275325, 1999.
IBS is one of the most common problems seen in primary care. The
article reviews the diagnostic criteria for IBS and the evidence to
support current therapies.
Schmulson MW, Chang L. Diagnostic approach to the patient with irritable
bowel syndrome. American Journal of Medicine 107:205265, 1999.
Thielman NM, Guerrant RL. Clinical practice: Acute infectious diarrhea.
A concise, clinically oriented review of the diagnosis and management
of acute infectious diarrhea.
Wilson JF. Irritable bowel syndrome. Annals of Internal Medicine 147:
ITC1ITC17, 2007.
1. Acute diarrhea is:
a. Explosions of flatus accompanying defecation.
b. A watery loose stool.
c. More than three loose bowel movements in 24 hours.
d. More than five formed or unformed stools in 24 hours.
For patients with lactose intolerance, a 1- to 2-week trial of
lactose-free diet is usually sufficient to see improvement in
symptoms.
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12 DIARRHEA 179
C H A P T E R
2. Types of acute diarrhea are differentiated by:
a. Greater or less than 1 L in 24 hours.
b. Presence of white blood cells in feces.
c. Phosphorus concentration in feces.
d. Litmus paper measurement of pH.
3. Diarrhea associated with antibiotic usage commonly features:
a. Clostridium difficile toxin.
b. Clostridium difficile mucosal invasion.
c. Candida albicans mucositis.
d. Crohn disease.
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180
CHAPTER
13
MUSCULOSKELETAL PAIN
Marianne M. Green, MD, and Stephen L. Adams, MD
I. Introduction
A. Musculoskeletal pain is a very common presenting symptom.
B. It is among the most frequent chief complaints during office visits
to the primary care physician.
C. Etiologies are myriad. Symptoms may be due to trauma (either acute
or chronic), overuse, mechanical problems, metabolic disorders, or
infection.
1. Ask all patients about a history of trauma.
2. Fever and chills suggest an infectious cause.
3. Weight loss or prior history of cancer suggests an underlying
malignancy.
4. The age of the patient can be very useful in estimating likelihood
of certain diagnoses. For example, an elderly person is more at
risk for an osteoporotic fracture than is a young person.
The physician must ascertain the circumstances behind
an acute musculoskeletal injury.
For a persistent pain (1 month) especially in patients
over age 50, consider malignancy as a possibility, and
imaging may be needed.
D. The diagnostic approach after the appropriate tailored history and
physical may include radiographic studies, examination of joint
aspirate to look for infection or crystals, or nerve conduction studies
when neuropathy is a consideration.
E. Treatment for most acute musculoskeletal injuries includes rest,
ice, compression, and elevation (the RICE protocol).
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13 MUSCULOSKELETAL PAIN 181
C H A P T E R
F. This chapter will review several of the most common conditions:
shoulder pain, carpal tunnel syndrome, osteoarthritis, low back
pain, and patellofemoral syndrome.
II. Shoulder Pain
A. Pathophysiology
1. Inflammation or injury to the rotator cuff causes most shoulder
pain.
a. The muscles of the rotator cuff can be remembered using the
SITS mnemonic: Supraspinatus, Infraspinatus, Teres Minor,
and Subscapularis.
b. The major function of the first three muscles is externally to
rotate the humerus. The supraspinatus also abducts the
humerus. The subscapularis serves as an internal rotator of
the shoulder.
2. Other causes of shoulder pain include biceps tendonitis, deltoid
bursitis, adhesive capsulitis (frozen shoulder), glenohumeral
instability, acromioclavicular (AC) injury, fracture, and metabolic
and infectious causes.
B. Epidemiology
1. Younger patients are most susceptible to traumatic injuries,
such as AC joint subluxation and glenohumeral instability.
2. Rotator cuff injury is the most common shoulder problem
seen in athletes. Impingement of the rotator cuff tendons
beneath an arthritic AC joint may be the presenting problem in
the elderly.
a. The supraspinatus is the muscle involved in the majority of
rotator cuff injuries.
3. The proximal humerus is a bone commonly fractured in elderly
women with osteoporosis.
A complete rotator cuff tear is unlikely in patients
younger than 30 years unless they are major athletes
or have sustained significant trauma.
Always consider the possibility of referred pain, such
as atypical angina presenting as shoulder pain or an
abdominal aortic aneurysm presenting as low back pain.
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4. Conditions that increase in frequency with age are impingement
syndrome, adhesive capsulitis, and rotator cuff tear.
C. Patient history
1. Elicit a history of chronic overuse, acute trauma, or both.
a. Patients may not recall a specific causal incident.
b. Patients may report a history of glenohumeral instability
(I dislocated my shoulder).
2. Pain is the predominant complaint, often worse at night.
a. Most patients have pain in the lateral or anterior shoulder.
3. Patients may complain of weakness, especially if there is a tear
in the rotator cuff.
D. Physical examination
1. Inspection
a. May reveal atrophy of the rotator cuff muscles
b. With the patient in the seated position and arm at the side,
traction on humerus may cause posterior gap between
humerus and acromion; this sulcus sign may be present in
patients with glenohumeral dislocation
c. If present, note superficial signs of inflammation,
e.g., erythema, swelling
2. Palpation
a. Palpate all bones surrounding the shoulder.
b. Deltoid bursa and biceps tendon should be specifically
located and palpated for tenderness.
c. Tenderness of the AC joint seldom occurs in impingement
syndrome.
d. Assess neurovascular integrity.
3. Range of motion
a. Test abduction by asking the patient to make the touchdown
sign: raising both arms in the plane of the body.
b. To assess adduction, perform the drop arm test. If the test
result is positive, the patient is unable to control slowly low-
ering the involved arm back to the sides. This is an insensi-
tive but very specific test for a complete supraspinatus tear.
c. Test internal rotation by having the patient reach over the
head to touch the back. Inability to reach the thoracic spine
is abnormal.
Posterior shoulder pain is rare and is usually due to
cervical spine disease.
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d. Test external rotation with elbow flexed and upper arm at the
side. First passively, then actively, rotate the hand and arm
away from the body at both 0 and 90 degrees.
e. Compare the affected and unaffected arms internal and
external rotation.
4. Special maneuvers
a. Tests for impingement (rotator cuff impingement due to
decreased subacromial space) include the Neer and Hawkins
tests.
i. Neer test. Internally rotate the patients arm at the side;
then bring the arm forward in flexion until it is straight
up. Press down on the affected AC joint to prevent
scapula motion. The test result is positive if the maneuver
causes pain (Fig. 13.1).
Adhesive capsulitis, also called frozen shoulder,
is present when there is loss of both active and
passive range of motion.
FIGURE 13.1 Neer test. (Redrawn from Woodward TW, Best TM: The painful shoulder:
part I. Clinical evaluation. Am Fam Physician 2000;61(10):30793088, Figure 5.)
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ii. Hawkins test. Flex the patients elbow and arm, holding
the arm in the horizontal position. The test result is
positive if internal rotation causes pain with impingement
(Fig. 13.2).
b. Perform the apprehension test with the patient supine
or seated, raising the arm to 90 degrees flexion. While
pressing on the anterior glenohumeral joint, externally
rotate the arm. Patients with glenohumeral instability
report pain or apprehension that the shoulder would
dislocate (Fig. 13.3).
5. Strength testing
a. Supraspinatus is tested with the empty can test. Abduct
both patient arms to 90 degrees, positioned 30 degrees ante-
rior to the coronal plane of the body and pronated with the
thumb pointing down as if emptying a can. Push down on
both arms while the patient resists. Weakness in the affected
arm is a positive test result (Fig. 13.4).
FIGURE 13.2 Hawkins test. (Redrawn from Woodward TW, Best TM: The painful
shoulder: part I. Clinical evaluation. Am Fam Physician 2000;61(10):30793088,
Figure 6.)
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C H A P T E R
FIGURE 13.3 Apprehension test. (Redrawn from Woodward TW, Best TM: The
painful shoulder: part I. Clinical evaluation. Am Fam Physician 2000;61(10):
30793088, Figure 8.)
FIGURE 13.4 Supraspinatus examination (empty can test). (Redrawn from
Woodward TW, Best TM: The painful shoulder: part I. Clinical evaluation. Am Fam
Physician 2000;61(10):30793088, Figure 3.)
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b. The infraspinatus and teres minor muscles are external
rotators. Position the patients arms at the side with elbows
flexed. Decreased strength in external rotation against
resistance (Fig 13.5) reflects weakness of these muscles
of the rotator cuff.
1. To evaluate possible infectious or metabolic cause of shoulder
pain, perform arthrocentesis of joint for cell count, culture,
crystal analysis
2. Radiography
3. Shoulder MRI necessary to evaluate for surgical repair of a
rotator cuff or if diagnosis unclear
FIGURE 13.5 Infraspinatus/teres minor examination. (Redrawn from Woodward
TW, Best TM: The painful shoulder: part I. Clinical evaluation. Am Fam Physician
2000;61(10):30793088, Figure 4.)
Plain radiographs are required if there is a history of
trauma.
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C H A P T E R
F. Management
1. Nonsurgical treatment modalities for acute and chronic inflam-
mation of the rotator cuff include nonsteroidal anti-inflammatory
drugs (NSAIDs), ice, and a program of physical therapy.
2. Impingement and adhesive capsulitis may respond to physical
therapy, although orthopedic referral for severe or refractory
cases is necessary.
3. Refer rotator cuff tears to orthopedists for consideration of
surgical repair.
4. Metabolic or infectious etiologies of shoulder pain require
specific treatment.
III. Carpal Tunnel Syndrome
A. Pathophysiology
1. The carpal tunnel contains the median nerve and nine flexor
tendons that course through the wrist. The carpal bones and
flexor retinaculum, also known as the transverse carpal liga-
ment, form the carpal tunnel.
2. Flexor tenosynovitis causes swelling that compresses the
median nerve as it traverses the carpal tunnel.
3. The median nerve is on the palmar side of the wrist and provides
sensory innervation to part of the thumb, the second and third
fingers, as well as to the radial aspect of the fourth finger. It pro-
vides the sole motor innervation to the abductor pollicis brevis.
B. Epidemiology
1. Carpal tunnel syndrome is the most common entrapment
neuropathy.
Repetitive activities that flex the wrist, such as typing,
assembly line work, or playing a musical instrument,
put patients at increased risk for carpal tunnel syndrome.
2. Associated conditions include rheumatoid arthritis, history of
Colles fracture, pregnancy, and hypothyroidism.
3. There is a genetic predisposition to carpal tunnel syndrome.
C. History
1. Ask patient about a history of repetitive wrist flexion.
2. The patient often complains of paresthesia in the median nerve
distribution. These symptoms are often worse at night.
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3. More severe compression can cause radiation of pain into the
forearm.
4. Ask about a history of thyroid disease or symptoms of
hypothyroidism.
1. Examination results may be normal early in the course of
disease.
2. Sensory examination may reveal a diminished response to
pinprick over the palmar aspect of the median nerve distribution.
3. Thumb abduction may be weak, and thenar atrophy may be
present.
4. Phalen sign and Tinel sign
a. Phalen sign. With the patients elbows resting on the table,
let the wrists fall freely into maximum flexion. This results
in passive hyperflexion of the wrist. A positive test result
occurs when the patient develops symptoms of pain, numb-
ness, and tingling within 3 minutes.
b. Tinel sign. Tap over the route of the median nerve on the
volar side of the patients wrist at the distal wrist crease. A
positive test result occurs when this provokes paresthesia in
the median nerve sensory distribution.
1. Cervical radiculopathy, thoracic outlet syndrome, generalized
neuropathy, and syringomyelia.
F. Management
1. Early treatment includes rest and modification of the activity
related to wrist flexion.
2. Wearing a wrist splint initially at night places the wrist in a
neutral position.
3. Inject corticosteroid into or near the carpal tunnel.
These are two classic physical examination signs. Their
sensitivity is only 20%50%.
Nerve conduction velocity (NCV) and electromyography
(EMG) studies may be necessary to differentiate
conditions.
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4. Systemic corticosteroids may be effective.
5. Severe cases may require surgery to divide the transverse carpal
ligament.
IV. Osteoarthritis (OA)
A. Pathogenesis
1. OA results from a complex mixture of biomechanical and
biochemical causes.
2. Although idiopathic OA with no known predisposing factors is
the most common form, OA occurs most often in weight-
bearing joints as a result of wear and tear on the articulations
caused by joint injury, obesity, laxity of the joints, and muscle
weakness.
3. Genetics and dietary factors may play a role.
4. There are various patterns of joint involvement.
a. Other affected joints besides the hip and the knee include the
base of the thumb and the spine. Idiopathic OA rarely affects
the elbows, wrists, and ankles.
b. In generalized OA more than three joints are affected.
5. OA does not have systemic manifestations.
B. Epidemiology
1. Age, female sex, obesity, occupation, prior injury, genetics, and
history of sports activities all increase risk.
2. OA of the hip and knee is the most common reason for total
knee and hip replacement.
C. History
1. OA causes pain that is localized to the involved joint and is
described as a deep ache.
2. An early manifestation of OA is pain that is worse during use
of the joint and relieved with rest. As the disease progresses,
The interphalangeal joints are most commonly
affected in idiopathic OA.
The National Health and Nutrition Examination Survey
reported the prevalence of OA as 0.1% in 2534-year-olds
and 80% in people over the age of 55.
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the pain may occur earlier in onset with joint use and may
persist even with the joint at rest.
1. Heberden nodes are bony enlargements of the distal interpha-
langeal (DIP) joints.
2. Bouchard nodes are bony enlargements on the proximal
interphalangeal joints (PIP).
3. There is usually tenderness over the joint lines of involved
joints.
4. There may be crepitus with movement of the joint, especially in
the knee.
5. There is restricted range of motion of involved joints.
6. There is pain with passive range of motion.
1. Calcium pyrophosphate deposition (CPPD), rheumatoid arthritis,
and infection all are alternative considerations.
2. X-rays of the affected joint may show joint space narrowing
and osteophyte formation, but their presence does not prove
that OA is the cause of the patients pain.
F. Management
1. Treatment is both nonpharmacologic and pharmacologic in an
effort to keep the patient pain-free.
2. Muscle conditioning and aerobic exercise can help slow down
progression of disease.
3. More advanced cases may require physical therapy as well as
assistance with daily living activities.
4. Acetaminophen or an NSAID is appropriate initial analgesia.
Topical NSAIDs and capsaicin are useful adjunctive therapy.
5. Many patients will use alternative therapies such
glucosamine/chondroitin and acupuncture.
a. Two meta-analyses failed to show effectiveness of
glucosamine/chondroitin.
b. Acupuncture may be effective for some types of osteoarthritis.
6. Joint replacement is an option for severe cases.
Obtain erythrocyte sedimentation rate, rheumatoid factor,
and synovial fluid analysis in all patients in whom the
diagnosis is not certain.
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V. Low Back Pain
A. Pathophysiology
1. Etiology is myriad, varying from seemingly minor strains or
spasms to metastatic spread of malignant tumors.
2. Specific problems of the lumbar spine include spondylosis
(stress injury of the pars interarticularis), spondylolisthesis (the
sliding of one vertebra over another), herniated nucleus pulposus,
spinal stenosis, vertebral fractures, and ankylosing spondylitis.
3. Infectious causes such as osteomyelitis and epidural abscess are
possible in the right setting.
4. Referred pain has the following feature.
B. Epidemiology
1. Some studies estimate that 2.5 % of all outpatient visits to the
primary care office are due to low back pain.
2. Low back pain is second only to the common cold as a major
cause of lost work time.
3. Some data suggest that 60%80% of all adults will experience
low back pain during their adult lives.
C. Patient history
1. The onset and timing of the pain are essential. A history of
trauma or onset while trying to lift a heavy load is helpful in
developing a likely cause of the pain.
2. Ask about radiation of the pain into the extremities, which sug-
gests a radicular component and increases the likelihood of disc
herniation.
3. Ask about the presence of paresthesia, numbness, or weakness
in the lower extremities. Bowel or bladder incontinence suggests
a serious underlying neurologic involvement and should result
in immediate imaging and referral.
Always consider referred pain from abdominal aortic
aneurysms, kidney stones, dissections of the aorta,
and testicular torsion.
The primary goal of the clinical examination is to identify
patients who require an immediate surgical evaluation
and those whose symptoms suggest a more serious underlying
condition such as malignancy or infection.
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4. A history of cancer or fever often lowers the threshold for
imaging.
5. A detailed psychosocial history may predict outcome in
chronic low back pain because concurrent issues can affect
pain or perception.
1. Examination includes vital signs and thorax, abdomen, lower
extremities, and vascular and neurologic evaluation.
2. Inspect the back, looking for abnormality in curvature and in
range of motion.
3. Palpate each of the lumbar vertebrae and paraspinous muscles
for signs of bony or soft-tissue involvement.
4. Neurologic evaluation includes a good sensory examination
including over the medial foot (L4), the web space
between the great and the second toe (L5), and the lateral
foot (S1).
5. Evaluate deep tendon reflexes for evidence of nerve root
involvement.
6. Motor examination includes evaluation of hip flexors and
adductors (L2L3), knee extension (L3L4), and foot dorsiflexion,
inversion, and plantar flexion (L4L5, S1).
7. Perform straight leg raise test to assess compression or irritation
of the nerve roots.
8. Assess heel walking and toe walking. Inability to walk on
the heels indicates weakness in L5, the foot dorsiflexors,
and inability to walk on the toes indicates an S1 root
involvement.
9. Watching a patient pick up a piece of paper from the floor can
be very helpful in confirming poor bending technique, even in
patients who say they know to bend their knees.
E. Imaging
1. The American College of Radiology has developed guidelines
for imaging patients presenting with low back pain.
a. Plain radiography
Most patients presenting with acute low back pain will
not require immediate imaging because conditions requir-
ing immediate intervention are rare.
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i. Plain radiography is recommended for patients with:
(1) Possible vertebral compression fractures (history of
osteoporosis or corticosteroid use).
(2) Unexplained weight loss.
(3) Significant trauma.
(4) Failure to improve after 1 month.
(5) Age over 50 years.
(6) History of cancer.
(7) Unrelenting night pain or pain at rest.
b. Magnetic resonance imaging (MRI)
F. Treatment
1. Self-care management that has been shown to be effective
includes:
a. Remaining active.
b. Education booklets and handouts.
c. Application of heat to area.
2. Medication options include acetaminophen, NSAIDs muscle
relaxants, and opioid analgesics.
3. Studies fail to show systemic corticosteroids benefit treatment
of low back pain, with or without radicular symptoms.
4. Physicians should consider the following treatments with
proven benefit for patients who do not improve with self-care.
MRI is the preferred imaging for patients with
severe or progressive neurologic defects or when
underlying conditions such as infection or malignancy are
likely. Perform MRI when back pain has persisted and
patients are candidates for intervention such as surgery
or epidural corticosteroid injection.
Most patients with acute back pain, with or without sciatica,
improve within 1 month with noninvasive management.
There is no evidence that routine plain radiography
of patients with nonspecific low back pain results in
improved outcomes.
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a. Physical therapy
b. Acupuncture
c. Massage therapy
d. Yoga
e. Cognitive behavioral therapy
f. Spinal manipulation
g. Tricyclic antidepressants
h. Gabapentin
5. Reserve surgery for patients who have severely debilitating
neurologic deficits or pain that has persisted despite noninva-
sive therapies.
VI. Patellofemoral Syndrome
A. Pathophysiology
1. The patella is a sesamoid bone that protects the knee from
direct trauma and serves as a fulcrum for the quadriceps in
extension. It articulates with the trochlear groove of the femur.
2. Irritation and inflammation in the patellofemoral groove cause
pain in this syndrome. Implicated causes include overuse,
biomechanical problems (e.g., widened Q angle of the hips,
abnormal pronation of the foot), and muscular dysfunction.
B. Epidemiology
1. Anterior knee pain is one of the most common musculoskeletal
complaints in physically active persons.
2. Up to 25% of runners may have symptoms of anterior knee
pain at one time or another.
3. One study noted over 10% of musculoskeletal problems
presenting to primary care were for anterior knee pain.
C. History
1. Patients may describe a dull, aching discomfort and stiffness in
the anterior knee. Symptoms are often bilateral.
2. The condition is often exacerbated by prolonged sitting and
knee flexion (theatre sign).
3. A history of trauma is usually absent.
4. A family history of anterior knee pain may be present.
5. Consider locking or giving out.
Ask all patients with knee pain about these signs. They
may indicate a meniscus or ligament problem.
1389_Ch13_180-198 2/2/09 1:24 PM Page 194
C H A P T E R
1. Physical examination may show swelling, effusion, and crepitus
below the patella.
2. A grind test result is positive when the examiner puts pressure
on the patella, pushing it into the femoral groove, and elicits pain.
1. Locking often indicates meniscus injury, although this
usually presents with medial or lateral knee pain.
2. Giving out indicates a ligament injury. Anterior cruciate
ligament (ACL) rupture presents with anterior knee pain, but
more swelling and a history of trauma will be present.
3. Other causes of anterior knee pain include patellar tendonitis,
bursitis, overuse syndrome, plica, Osgood-Schlatter disease,
Legg-Calv-Perthes disease, infections, neoplasm, and inflam-
matory disease.
4. Plain radiography is not usually helpful unless there is a history
of trauma.
5. For prolonged symptoms that do not respond to treatment, MRI
can aid in making the diagnosis.
F. Treatment
1. Modification of activities that increase patellofemoral pressure,
such as squatting and kneeling, may be helpful.
2. Short periods of ice applied to the knee reduce symptoms.
3. Exercise, including strengthening of the vastus medialis oblique
muscle, is useful.
MENTOR TIPS DIGEST
General
The physician must ascertain the circumstances behind an
acute musculoskeletal injury.
For a persistent pain (1 month) especially in patients over
age 50, consider malignancy as a possibility, and imaging may
be needed.
Always consider the possibility of referred pain, such as atypi-
cal angina presenting as shoulder pain or an abdominal aortic
aneurysm presenting as low back pain.
Shoulder Pain
A complete rotator cuff tear is unlikely in patients younger
than 30 years unless they are major athletes or have sus-
tained significant trauma.
1389_Ch13_180-198 2/2/09 1:24 PM Page 195
P A R T
Posterior shoulder pain is rare and is usually due to cervical
spine disease.
Adhesive capsulitis, also called frozen shoulder, is present
when there is loss of both active and passive range of motion.
Plain radiographs are required if there is a history of trauma.
Carpal Tunnel Syndrome
Repetitive activities that flex the wrist, such as typing, assem-
bly line work, or playing a musical instrument, put patients at
increased risk for carpal tunnel syndrome.
Two classic physical examination signs are the Phalen sign and
Tinel sign. Their sensitivity is only 20%50%.
NCV and EMG studies may be necessary to differentiate
conditions.
Osteoarthritis
The interphalangeal joints are most commonly affected in
idiopathic OA.
The National Health and Nutrition Examination Survey re-
ported the prevalence of OA as 0.1% in 2534-year-olds and
80% in people over the age of 55.
Obtain erythrocyte sedimentation rate, rheumatoid factor, and
synovial fluid analysis in all patients in whom the diagnosis is
not certain.
Low Back Pain
Always consider referred pain from abdominal aortic
aneurysms, kidney stones, dissections of the aorta and
testicular torsion.
The primary goal of the clinical examination is to identify
patients who require an immediate surgical evaluation and
those whose symptoms suggest a more serious underlying
condition such as malignancy or infection.
Most patients presenting with acute low back pain will not
require immediate imaging because conditions requiring im-
mediate intervention are rare.
There is no evidence that routine plain radiography for
patients with nonspecific low back pain results in improved
outcomes.
MRI is the preferred imaging for patients with severe or pro-
gressive neurologic defects or when underlying conditions
such as infection or malignancy are likely. Perform MRI when
1389_Ch13_180-198 2/2/09 1:24 PM Page 196
Resources
Chou R, et al. Diagnosis and treatment of low back pain: A joint
clinical practice guideline from the American College of Physicians
and the American Pain Society. Annals of Internal Medicine
147:478491, 2007.
Chou R, Huffman L. Nonpharmacological therapies for acute and chronic
low back pain: A review of the evidence for an American Pain Society/
American College of Physicians clinical practice guideline. Annals of
Internal Medicine 147: 492504, 2007.
DArcy CA, McGee S. Does this patient have carpal tunnel syndrome?
Deyo RA, Weinstein JN. Low back pain. New England Journal of Medi-
cine 344:363370, 2001.
Hunter DJ. In the clinic: Osteoarthritis. Annals of Internal Medicine.
147:ITC8-1-ITC8-16, 2007.
Woodward TW, Best TM. The painful shoulder, part 1: Clinical evaluation.
American Family Physician 61, 2000.
1. A 45-year-old male carpenter has leg pain and fever. On examination,
passive and active movements of the knee cause pain. Based on this
information, what is the most likely cause of his leg pain?
a. Osteoarthritis
b. Rheumatoid arthritis
C H A P T E R
back pain has persisted and patients are candidates for
intervention such as surgery or epidural corticosteroid injection.
Most patients with acute back pain, with or without sciatica,
improve within 1 month with noninvasive management.
Patellofemoral Syndrome
Ask all patients with knee pain for the presence of locking
or giving out. These may indicate a meniscus or ligament
problem.
1389_Ch13_180-198 2/2/09 1:24 PM Page 197
P A R T
c. Gout
d. Septic arthritis
2. A 45-year-old male carpenter has leg pain and 25 pound unex-
plained weight loss in the past month. On examination, the hip
and knee are normal, but there is tenderness on palpation of the
mid-femur. Based on this information, what is the most likely
cause of his leg pain?
a. Malignancy
b. Osteoarthritis
c. Tenosynovitis
d. Gout
3. A 45-year-old male carpenter has low back pain. He admits to having
similar pain in the past, usually lasting for weeks. This episode started
with bending at work. On examination, there is tenderness on palpation
of lumbar paraspinous muscles; knee jerk reflexes are 1 and bilaterally
symmetric; ankle jerks are absent. The straight leg raising test produces
posterior thigh pain with both legs. Which is the most appropriate diag-
nostic test?
a. MRI of lumbosacral spine
b. Plain x-ray of lumbosacral spine
c. EMG of lower legs
d. No test
1389_Ch13_180-198 2/2/09 1:24 PM Page 198
199
DERMATOLOGY IN
PRIMARY CARE
Cynthia A. Lagone, MD
CHAPTER
14
I. Overview
A. The skin is the largest organ of the body. Diseases of the skin can
be a primary disorder or a secondary disorder as a manifestation
of a systemic disease. The most common primary skin disorders
are discussed in this chapter.
B. General principles consist of the following.
1. History
a. Obtain a directed history, including onset, duration, location,
and associated symptoms.
b. Occupation and new exposures are important.
c. Any previously prescribed treatments should be noted.
d. Review medications, including any over-the-counter (OTC)
medicines.
e. A brief past medical history and family history should be
included when appropriate.
2. Physical
a. It is important to have a patient disrobe to perform a
thorough examination.
b. Examine the skin, noting characteristics and distribution of
lesions.
Dermatology is a morphologically oriented specialty.
It is very important to identify and be able to
describe the lesions accurately.
c. Tables 14.1 and 14.2 define common terms used in the
description of skin lesions.
1389_Ch14_199-220 2/2/09 1:24 PM Page 199
P A R T
TABLE
14.1
Primary Lesions
Primary Lesion Description
Macule A flat, circumscribed discoloration
Papule An elevated, solid lesion up to 5 mm
Nodule A palpable, solid lesion greater than 5 mm
Plaque A superficial, circumscribed, elevated flat lesion
greater than 5 mm
Wheal A transient, slightly edematous lesion with a
characteristic pale red color
Vesicle A circumscribed collection of free fluid less than
5 mm
Bulla A circumscribed collection of free fluid greater than
5 mm
Pustule A circumscribed, superficial cavity of the skin that
contains purulent material
Petechia A visible collection of red blood cells less than 5 mm
Purpura A visible collection of red blood cells greater than
5 mm
Telangectasia Dilated superficial blood vessels
TABLE
Secondary Lesions
Secondary Lesion Description
Scale Thickened, loose excess stratum corneum that
sheds readily
Crust Dried exudate; a scab
Excoriation An often linear erosion caused by scratching
Ulcer A focal loss of epidermis and dermis
Fissure A linear loss of epidermis and dermis, with
sharp vertical walls
Lichenification An area of thickened skin with accentuated lines,
giving the skin a washboard appearance
Scar An abnormal collection of connective tissue
from dermal damage
Atrophy Thinning of the epidermis or dermis, resulting
in a depression of the skin
14.2
1389_Ch14_199-220 2/2/09 1:24 PM Page 200
3. Develop differential diagnosis based on data gathered
4. Testing
a. For most skin diseases, testing is minimal. The diagnosis is
made by history and appearance.
b. Lesions can be scraped with a scalpel and examined with
potassium hydroxide (KOH) or saline.
c. A skin biopsy can be performed.
d. Serum testing for infectious or autoimmune processes may
be done.
5. Initiate treatment; monitor lesions for improvement
C. There are literally hundreds of different skin disorders. The rest of
this chapter focuses on those most commonly seen in primary care.
II. Acne Vulgaris
A. Pathophysiology
1. Acne vulgaris is an inflammation of the pilosebaceous units of
the skin. The pilosebaceous unit consists of a small hair follicle
associated with a large sebaceous gland.
2. Acne begins in predisposed patients when sebum production is
increased. Sebum is partly controlled by androgen stimulation
thus the emergence of acne in adolescence. Increased sebum
causes a change in the lining of the follicle, and a plug develops.
Behind this blockage, there is an overgrowth of the bacterium
Propionibacterium acnes.
3. Irritation and inflammation develop, which provokes an immune
response. Inflammatory mediators lead to follicular rupture and
leakage of lipids, bacteria, and fatty acids into the dermis.
B. Epidemiology
1. Acne is the most common skin disease. It affects almost every-
one in varying amounts in their lifetime.
2. It is most common during adolescence, affecting 80%85% of
all teenagers. It can persist into the second and third decades.
3. Acne tends to be more frequent and severe in males.
4. Extrinsic factors can aggravate acne.
a. Emotional stress
b. Mechanical pressure
i. Straps from sports helmets or just pressure from leaning
face on hand can trigger outbreaks.
ii. Friction from frequent and overzealous washing worsens
acne. Many laypersons think that more or better washing
is the cure for acne. Explain to patients that there are
14 DERMATOLOGY IN PRIMARY CARE 201
C H A P T E R
1389_Ch14_199-220 2/2/09 1:24 PM Page 201
histologic reasons for acne that harder scrubbing does not
negate.
c. Occlusive products (e.g., cosmetics)
d. Endocrine factors that increase androgens, e.g., normal fluc-
tuations in menstrual cycle, polycystic ovarian syndrome
e. Medications
i. Glucocorticoids
ii. Anabolic steroids
iii. Progestin-only birth control pills
f. Diet
i. Many patients insist that their acne is exacerbated by
certain foods.
ii. There is no conclusive evidence that diet plays a role.
C. History and physical examination
1. Determine the onset, and ask about possible aggravating factors.
2. Review current or previous treatments, including OTC treatments.
3. On physical examination, note the characteristics and distribution.
a. Acne is most common in areas with a dense population of
pilosebaceous units such as the face, chest, and back.
b. Acne characteristically presents as closed comedones (white-
heads), open comedones (blackheads), papules, pustules and,
in severe cases, nodules, cysts, and scarring.
c. Acne is typically graded as mild, moderate, or severe
(Table 14.3).
1. Acne rosacea, folliculitis, perioral dermatitis, pseudofolliculitis
barbae, drug eruption
P A R T
TABLE
Acne Grades
Acne Grade Principal Lesion
Mild Comedones
Moderate Comedones
Papules
Pustules
Severe Papules
Pustules
Nodules
Cysts
14.3
1389_Ch14_199-220 2/2/09 1:24 PM Page 202
E. Laboratory tests
F. Treatment
1. General principles
a. Treatment is chosen based on acne severity (Table 14.4).
b. Treatment is tailored depending on side effects.
i. Many therapies cause dryness and skin irritation.
c. Treatment takes time.
2. Specific treatments
a. Topical retinoids
i. Mechanism is via anti-inflammatory effect and promoting
normal keratinocyte desquamation
C H A P T E R
Laboratory tests are generally not helpful for acne.
TABLE
Acne Management
Acne Grade Management
Mild Topical treatments (antibacterials, benzoyl peroxide,
retinoids)
Moderate Topical therapies, systemic antibiotics, hormones
Severe Isotretinoin
14.4
Topical preparations come in several forms. For
dry skin use a cream or lotion. For oily skin
choose a gel or solution.
All acne therapies can take weeks for results to be
apparent. Patients must be counseled regarding
realistic expectations.
Retinoids are widely used and very effective.
1389_Ch14_199-220 2/2/09 1:24 PM Page 203
ii. Tretinoin, adapalene, tazarotene are examples
iii. Primary limiting factors are their irritant potential
and that they are degraded by light and benzoyl
peroxide (BP)
iv. Best applied at night
b. BP
i. Mechanism is via comedolytic activity and antibacterial
activity against P. acnes
ii. Primary limiting factor is irritant potential
c. Topical antibiotics
i. Mechanism is via antibacterial activity against P. acnes
ii. Clindamycin and erythromycin are available agents
iii. Resistance minimized by combining with BP.
d. Systemic antibiotics
i. Mechanism is via antibacterial activity against P. acnes
and possibly anti-inflammatory effect.
ii. Erythromycin, clindamycin, and tetracycline and its
derivatives have been used.
(1) Erythromycin is rarely used given rising resistance
rates.
(2) Systemic clindamycin is generally avoided given its
propensity to cause pseudomembranous colitis.
(3) Tetracycline and its derivatives are the preferred
agents.
(A) Use of tetracycline is limited given gastrointestinal
(GI) side effects, need for frequent dosing, and
less overall effectiveness than newer agents.
(B) Doxycycline is a good option; however, use may
be limited by photosensitivity (dose 50100 mg
once to twice daily).
P A R T
BP should be part of most patients treatment.
The limiting factor in the use of topical antibiotics
is increasing resistance.
1389_Ch14_199-220 2/2/09 1:24 PM Page 204
e. Hormonal therapy: oral contraceptive pills (OCPs)
i. They work by antagonizing the actions of circulating
androgens.
ii. Up to 83% of patients will have clinical improvement in
their acne symptoms.
iii. Most OCPs should act similarly to reduce acne lesions,
although only Ortho Tri-Cyclen and Estrostep have
received U.S. Food and Drug Administration approval
for the treatment of acne.
f. Systemic retinoid
i. Mechanism is by reducing sebum production, normaliz-
ing keratinization, and anti-inflammatory effects
ii. Only medication that is curative; up to 60% of patients
will have prolonged remission after treatment course
iii. Limited by its side-effect profile
(1) It has skin irritant properties. It may cause leucopenia
or transaminitis as well as lipid abnormalities.
(2) The principal concern is teratogenicity.
(A) Most physicians recommend two forms of birth
control in young women taking isotretinoin.
(3) More recent concerns have been associations of
isotretinoin with mood disorders.
C H A P T E R
Minocycline is the preferred agent given
its lower risk of GI side effects and photo-
sensitivity (dose 50100 mg once or twice daily).
Isotretinoin is the most effective treatment for acne.
Isotretinoin is potently teratogenic.
Patients should be monitored closely on
isotretinoin; however, it is the only medication
that is potentially curativeall others are suppressive.
1389_Ch14_199-220 2/2/09 1:24 PM Page 205
III. Eczema
A. Overview
1. The terms eczema and dermatitis are often used
interchangeably.
2. Erythema, scale, and vesicles characterize eczematous
inflammation.
3. There are three stages of eczema/dermatitis: acute, subacute,
and chronic.
a. Acute dermatitis has an inflamed, oozing epidermis. On
biopsy there is an area of edema in the epidermis that pushes
apart keratinocytes and causes vesicles and small blisters.
b. Subacute dermatitis has a visible scale and crust associated
with inflamed skin. On biopsy there are scaling and epider-
mal infiltration of lymphocytes among the keratinocytes.
c. Chronic dermatitis has a thickened, often violaceous, plaque.
On biopsy there is epidermal acanthosis or thickening with a
lymphocytic infiltrate in the papillary dermis.
4. The most common disorders in this group are atopic dermatitis,
contact dermatitis, and seborrheic dermatitis.
B. Contact dermatitis
1. Pathophysiology
a. It is inflammation secondary to substances that come in
direct contact with the skin.
b. It can be either allergic or irritant.
i. Allergic contact dermatitis occurs in patients who have
been previously sensitized with a contact allergen. It is a
classic, delayed, cell-mediated hypersensitivity reaction.
(1) Other common triggers are nickel perfumes and
topical medicine such as neomycin.
ii. Irritant dermatitis occurs when the substance directly
damages the skin.
2. Clinical manifestations
P A R T
The most common triggers in North America
are poison ivy and poison oak.
It is typically an intense pruritic rash.
1389_Ch14_199-220 2/2/09 1:24 PM Page 206
a. Erythematous, edematous papules and plaques are character-
istic. Blisters and vesicles may be involved.
b. The location may be a clue to the trigger; e.g., around the
neck from nickel jewelry, in a line along the legs with
poison ivy.
3. Differential diagnosis
a. Atopic dermatitis, seborrheic dermatitis, fungal infections,
psoriasis, nummular eczema
4. Laboratory testing
a. Skin biopsy may be helpful but is usually not necessary.
b. Patch testing may be helpful to help identify the offending
allergen.
5. Treatment
a. Identify and remove the offending agent.
b. Topical treatment includes cold, wet dressing or topical
corticosteroids.
c. Oral antihistamines may be helpful.
d. In severe cases oral steroids may be used.
i. 2040 mg of prednisone daily, tapered over 12 weeks
C. Atopic dermatitis
1. Pathophysiology
a. The exact mechanism in atopic dermatitis is incompletely
understood. It appears to be IgE-mediated with allergic trig-
gers generating an immune response.
b. Most patients have a personal or family history of asthma,
allergic rhinitis, or atopy.
c. Patients often have immediate positive skin tests in response
to a number of food and environmental allergens.
d. Patients have decreased cell-mediated immunity, a decreased
number of immunoregulatory T cells, and usually increased
serum IgE.
a. It presents as red scaling and crusting lesions. In adults the
lesions may be thickened or lichenified.
C H A P T E R
Most patients with atopic dermatitis are diagnosed
in childhood, and over 40% of these cases resolve
by adulthood.
1389_Ch14_199-220 2/2/09 1:24 PM Page 207
b. Patients always have dry skin that is pruritic.
c. Atopic dermatitis flares in dry winter months and improves
in the summer.
d. Atopic dermatitis has a predilection for elbow, knee, and
buttock flexures; the ankles; neck; wrists; and the dorsa of
feet and hands.
e. Secondary bacterial and fungal infections are a common
complication.
3. Differential diagnosis: contact dermatitis, seborrhea, psoriasis,
fungal infections
a. No specific test is usually required to confirm the
diagnosis.
b. Radioallergosorbent test (RAST) and skin testing may be
helpful in certain cases.
5. Treatment
a. Patient education is extremely important.
i. Emollients are key and should be used daily.
ii. Excessive rubbing and scratching can lead to lichenifica-
tion and refractory lesions.
b. Oral antihistamines are helpful in treating the pruritus.
c. Mild-to-moderate atopic dermatitis should be treated with
topical steroids. Initially, higher potency is used for the acute
flare, then a lower-to-intermediate strength is used two to
three times a week for maintenance.
d. Topical calcineurin inhibitors are helpful in moderate flares
and for maintenance.
i. Their advantage is that there is no skin atrophy.
ii. They are equivalent to low-potency steroids.
iii. There is some concern that they induce cancers.
iv. Two examples are tacrolimus and pimecrolimus.
e. Ultraviolet light therapy is helpful.
f. Severe cases are treated with oral cyclosporine or other
immunosuppressants, such as methotrexate, azathioprine,
and mycophenolate.
P A R T
Skin dehydration exacerbates atopic dermatitis.
Patients should avoid long hot baths and frequent
hand washing.
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D. Seborrheic dermatitis
1. Pathophysiology
a. It is a common, chronic dermatosis with scaling and erythema.
It occurs in areas where sebaceous glands are most active,
such as the scalp, face, and body folds.
b. Biopsy results show mounds of parakeratotic scale around hair
follicles with mild superficial inflammation and lymphocytes.
a. It has a gradual onset.
b. It can occur in infants (cradle cap) or adults.
c. The condition is worse in the winter and improves in the
summer.
d. The scales are frequently yellow or oily in appearance.
There is underlying erythema. Pruritus is not characteristic.
e. Skin lesions can be diffuse, such as on the scalp, or scattered
and discrete on the face and trunk.
3. Differential diagnosis
a. Psoriasis, contact dermatitis, pityriasis versicolor, tinea,
subacute lupus erythematosus
a. Laboratory testing is usually not necessary.
5. Treatment
a. Mild scalp involvement is treated with over-the-counter sham-
poos containing tar preparations, selenium sulfide, or zinc.
i. Examples are Selsun Blue, Head and Shoulders, and T/Gel.
b. Antifungal shampoo with ketoconazole or ciclopirox can
be used.
i. These can also be lathered onto the face and body.
c. Topical ketoconazole cream and intermittent low-potency
corticosteroid creams are effective for nonscalp seborrheic
dermatitis.
C H A P T E R
The exact cause is not known; however, the yeast
Malassezia furfur (formerly Pityrosporum ovale) is
thought to play a role in pathogenesis.
The shampoo should be left on the scalp for
35 minutes before rinsing.
1389_Ch14_199-220 2/2/09 1:24 PM Page 209
d. Seborrheic blepharitis, which is seborrhea of the eyelids,
is treated by gently removing the scales once a day with a
diluted solution of baby shampoo on a cotton ball.
IV. Psoriasis
A. Overview
P A R T
Psoriasis is a common skin disease affecting about
1%3% of the population.
Although most patients with psoriasis have a normal life
span, the disease can be highly disabling emotionally.
Patients often shun outdoor activities and intimacy because
they are self-conscious of their appearance.
The principle abnormality is abnormal cell proliferation.
The epidermal cells have a shortened cycle time with
36 hours as compared with over 300 hours in normal skin. This
results in significant increase in the normal production of epider-
mal cells and keratinization. The result is scaling.
1. It affects men and women equally, with a bimodal distribution
in adolescence and age 5060 years.
2. It is a lifelong condition with recurrent exacerbations and
remissions.
3. There are several types: plaque (most common), guttate, pustular,
and nail.
4. Approximately, 5%10% of patients have accompanying arthritis.
This tends to be more common in young women and in those with
nail involvement.
B. Pathophysiology
1. The dermis has large tortuous capillaries that are close to the
surface and give plaques their characteristic red hue.
2. Etiology of abnormal cell proliferation is unknown; however,
psoriasis is genetically linked with a higher incidence in fami-
lies, and there is some association with the human leukocyte
antigen (HLA) system.
1389_Ch14_199-220 2/2/09 1:24 PM Page 210
C. Clinical manifestations
1. Psoriasis is characterized by red scaling papules that coalesce
to form plaques. The scale is silvery white and can become
very thick.
E. Laboratory testing
1. Diagnosis is usually made by physical examination and history.
F. Differential diagnosis
1. Lichen planus, seborrheic dermatitis, secondary syphilis, pityriasis
rosacea, mycosis fungoides, systemic lupus erythematosus
G. Treatment
1. Treatment is lifelong, avoiding triggers and treating exacerbations.
2. Mild disease (which is defined as involving 20% of the body)
is treated as summarized in Table 14.5. Topical steroids and
creams, such as calcipotriol, tazarotene, anthralin, and tar, can
be used with or without ultraviolet light.
3. Localized plaques can be treated with intralesional steroids.
4. Patients with more diffuse disease (20% body) are treated
with a number of different therapies: ultraviolet light B (UVB)
phototherapy and tar, psoralen and ultraviolent light A (PUVA),
methotrexate, acitretin, cyclosporine, and biologic agents:
infliximab, etanercept, alefacept.
2. Psoriasis can present anywhere but has a predilection for the
elbows, knees, scalp, and gluteal cleft.
3. In the skin folds, the plaques appear smooth and red.
4. Nail findings are pitting, hyperkeratosis, and onycholysis.
D. Triggers of exacerbations
1. Triggers are stress, infection, ethanol, and medications. Lithium,
beta blockers, and antimalarials are well documented triggers
and should be avoided in a patient with psoriasis.
C H A P T E R
When the scale is removed there is pinpoint bleeding
characteristic of psoriasis that is called the Auspitz sign.
Psoriasis can develop in traumatic sites such as
scars, sunburns, and scratches. This is known as the
Koebner phenomenon.
1389_Ch14_199-220 2/2/09 1:24 PM Page 211
P A R T
TABLE
14.5
Therapeutic Options for Persons With Psoriasis
on Less Than 20% of the Body
Treatment Advantages Disadvantages Comments
Topical
steroids
Calcipotriol
(Dovonex)
Tazarotene
(Tazorac)
Anthralin
Tar
UVB and
lubricating
agents
or tar
Rapid response,
controls
inflammation
and itching,
best for inter-
triginous ar-
eas and face,
convenient,
not messy
Well tolerated,
long remis-
sions possible
Effective, long
remissions
possible
Convenient
short contact
programs,
long remis-
sions, effec-
tive for scalp
New prepara-
tions are
pleasant
Insurance may
cover part or
all of treat-
ment, effec-
tive for 70%
of patients,
no need for
topical
steroids
Temporary relief
(tolerance occurs),
less effective with
continued use,
atrophy and
telangiectasia
occur with contin-
ued use, brief
remissions, very
expensive
Burning, skin irrita-
tion, expensive
Irritating, expensive
Purple-brown stain-
ing, irritating,
careful application
(only to plaque)
required
Only moderately
effective in a few
patients
Expensive, office-
based therapy
Best results occur
with pulse
dosing (e.g.,
2 weeks of
medication
and 1 week
of lubrication
only), plastic
occlusion is
very effective
Best for moderate
plaque psoriasis
Topical steroids
can control irri-
tation and
enhance
effectiveness
Used on chronic
(not inflamed)
plaques, best
results occur
when used with
UVB light
Most effective
when combined
with UVB light
(Goeckerman
regimen)
Used only on
plaque and
guttate psoria-
sis, travel and
time required
1389_Ch14_199-220 2/2/09 1:24 PM Page 212
5. Those with psoriatic arthritis are treated with nonsteroidal anti-
inflammatory drugs (NSAIDs): methotrexate, sulfasalazine,
cyclosporine, and the biologic agents.
6. Patients treated with UV therapy should be monitored for skin
cancer due to increased incidence.
V. Superficial Fungal Infections
A. Overview
1. Dermatophytes are fungi that infect and survive on dead keratin.
2. Dermatophytes cause skin infections called tinea and are further
categorized by their location (i.e., tinea pedis, tinea capitus)
3. Dermatophytes are ubiquitous and routinely infect healthy
people. However, patients with a compromised immune system
are more susceptible.
4. Infections are spread by human-to-human contact or by animal-
to-human.
5. Three types of dermatophytes are responsible for the majority
of skin infections: Epidermophyton, Trichophyton, and
Microsporum.
B. Pathophysiology
C H A P T E R
Therapeutic Options for Persons With Psoriasis on Less Than
20% of the Body (Continued)
Treatment Advantages Disadvantages Comments
Tape or
occlusive
dressing
Intralesional
steroids
From Habif TP: Clinical Dermatology: A Color Guide to Diagnosis and Therapy, 4th ed.
Mosby, 2003.
Convenient, no
mess
Convenient,
rapidly effec-
tive, long
remissions
Expensive, only for
limited disease
Only for limited
areas, atrophy
and telangiectasia
occur at injection
site
May be used to
occlude topical
steroids
Ideal for chronic
scalp and body
plaques when
small and few
in number
Dermatophytes produce keratinases that digest keratin
and sustain their existence on skin structures.
1389_Ch14_199-220 2/2/09 1:24 PM Page 213
1. There may be genetic susceptibility, but host factors that facilitate
infection are atopy, steroids, and diabetes. Local factors that
promote infection are sweating and occlusion.
C. Clinical manifestations
1. The rash appearance can vary based on the area of the body
infected.
2. The rash may be pruritic.
3. The infection is usually an erythematous, scaling, well-demarcated
patch with a distinct border when it occurs on the trunk, face,
or extremities. There may be central clearing of the rash.
4. Tinea pedis appears as painful, erythematous vesicular lesions
between the toes and on the soles.
1. Differential diagnosis is often based on location. Consider
contact dermatitis, and atopic dermatitis, pityriasis infection,
erythema migrans, and subacute lupus.
E. Laboratory testing
P A R T
The best tool for diagnosis is visualization of branching
hyphae under the microscope. Scrape the scale from the
active border, and place it on a slide with 10% KOH solution.
Terbinafine 1% applied one to two times daily has higher
cure rates than older azole agents and has fewer side
effects.
1. A fungal culture may also be obtained in cases where the
diagnosis is less clear.
2. Dermatophyte infections of the hair shaft infected by Microsporum
canis show a diagnostic brilliant green when examined under
the Wood lamp.
F. Treatment
1. Most dermatophyte infections of the skin can be treated success-
fully with topical antifungals.
a. Topical polyene and azoles have been mainstays of therapy,
but there is emerging resistance.
i. Examples: nystatin and ketoconazole
b. Terbinafine is an allylamine that is fungicidal as well as
fungistatic.
1389_Ch14_199-220 2/2/09 1:24 PM Page 214
2. Oral agents are usually necessary to treat hair and nail infections.
They can also be used on patients with extensive skin involve-
ment. These include griseofulvin, ketoconazole, itraconazole, and
terbinafine. They are all associated with potential side effects and
should be used with caution.
a. Terbinafine has fewer side effects and for most infections is
more effective.
G. Special considerations
1. Candidiasis is a cutaneous yeast infection that can occur on
moist skin sites, including the mucous membranes. Candida
albicans is the most common cause of candidiasis in humans.
It lives on the normal flora of the mouth, vagina, and GI tract.
It can become pathogenic in a number of conditions including
areas of increased moisture, pregnancy, diabetes, and oral con-
traceptive pills. It is usually treated with controlling the exacer-
bating factors and topical imidazoles. Oral agents can be used
for severe infections.
2. Pityriasis versicolor is an asymptomatic fungal infection of the
trunk due to M. furfur. The lesions have a fine scale. On pale
skin the lesions are hyperpigmented. On dark skin the lesions
are depigmented. Topical antifungals work well, but recurrence
is common.
3. Onychomycosis is a nail infection caused by any fungus,
including yeasts and nondermatophyte molds.
a. KOH examination of nail scrapings can be diagnostic, but
often a fungal culture of subungual debris or nail clippings is
needed to make the diagnosis. In proximal infections, a nail
plate biopsy may be needed.
b. Treatment consists of the following.
i. Oral treatment includes terbinafine and itraconazole,
which are more effective then griseofulvin.
C H A P T E R
Topicals are usually not effective. Oral therapy is
effective only two thirds of the time, with a high
rate of recurrence.
Treat onychomycosis of the fingernails for a mini-
mum of 6 weeks and the toenails for 12 weeks.
Terbinafine 250 mg daily is a good option.
1389_Ch14_199-220 2/2/09 1:24 PM Page 215
VI. Skin Cancer
A. Overview
1. Skin cancer is the most common type of cancer.
2. A primary care physician must be able to identify suspicious
neoplasms and refer for removal when appropriate.
3. The three main types of skin cancer are basal cell, squamous
cell, and melanoma.
B. Pathophysiology
1. Studies clearly show a relationship between early childhood sun
exposure and the development of skin cancer.
2. Genetic factors also play a role, especially in melanoma.
C. Basal cell carcinoma
1. This is the most prevalent type of skin cancer.
2. Risk factors include fair skin and sun exposure. It is most com-
monly found on the face and skin appendages.
3. It is locally invasive, destructive, and aggressive, but it rarely
metastasizes.
4. Appearance:
P A R T
The typical appearance is a pearly white, pink, or red,
dome-shaped papule with characteristic fine telangiec-
tasia. The center frequently ulcerates and bleeds, causing a
crust or scale.
5. Treatment is usually surgery, although cryotherapy and radiation
are used in certain situations. Mohs surgery is a microscopic, tis-
sue-sparing technique especially useful on the face.
D. Squamous cell carcinoma (SCC)
1. This lesion is a malignant tumor arising from the keratinocytes.
2. It usually develops in sun-damaged skin, often in an actinic
keratosis (AK).
a. AK is a SCC confined to the epidermis.
b. Almost all AKs are considered to be from sun damage.
c. AKs can be treated with topical 5-fluorouracil or Imiquimod.
3. SCC usually presents as a hyperkeratotic ulcerated or expand-
ing nodule. It has the potential to metastasize to local lymph
nodes.
4. Treatment is generally the same as for basal cell carcinoma:
surgery, cryotherapy, or radiation.
1389_Ch14_199-220 2/2/09 1:24 PM Page 216
E. Malignant melanoma (MM)
1. MM is one of the most dangerous forms of cancer, and its
incidence is rapidly increasing.
2. It can occur at any age and on any area of the skin, and it can
metastasize to any organ.
3. The goal is early recognition; a thorough skin examination is
extremely important.
4. Remember the ABCDs of malignant melanoma recognition.
a. Asymmetrytwo halves of the lesion not identical
b. Borderirregular, notched, or poorly circumscribed
c. Colorpure black or haphazard display of red, blue, brown,
or black
d. Diametergreater than 6 mm (size of a pencil eraser)
5. MM can begin de novo or in a preexisting mole; this is why
any changing mole needs to be taken seriously.
6. The diagnosis is made with excisional biopsy. The patient
should be referred to a specialist for staging and treatment.
C H A P T E R
The most important prognostic factor is tumor thickness
in millimeters.
MENTOR TIPS DIGEST
Overview
Dermatology is a morphologically-oriented specialty. It is very
important to identify and be able to describe the lesions
accurately.
Acne Vulgaris
Laboratory tests are generally not helpful for acne.
Topical preparations come in several forms. For dry skin use a
cream or lotion. For oily skin choose a gel or solution.
All acne therapies can take weeks for results to be apparent.
Patients must be counseled regarding realistic expectations.
Retinoids are widely used and very effective.
BP should be part of most patients treatment.
The limiting factor in the use of topical antibiotics is in-
creasing resistance.
Among systemic antibiotics, minocycline is the preferred agent
given its lower risk of GI side effects and photosensitivity.
1389_Ch14_199-220 2/2/09 1:24 PM Page 217
P A R T
Isotretinoin is the most effective treatment for acne. However,
it is teratogenic. Patients should be monitored closely on
isotretinoin; however, it is the only medication that is
potentially curativeall others are suppressive.
Eczema
For contact dermatitis, the most common triggers in North
America are poison ivy and poison oak.
It is typically an intense pruritic rash.
Most patients with atopic dermatitis are diagnosed in child-
hood, and over 40% of these cases resolve by adulthood.
Skin dehydration exacerbates atopic dermatitis. Patients
should avoid long hot baths and frequent hand washing.
The exact cause of seborrheic dermatitis is not known; how-
ever, the yeast Malassezia furfur (formerly Pityrosporum ovale)
is thought to play a role in pathogenesis.
The shampoo should be left on the scalp for 35 minutes before
rinsing.
Psoriasis
Psoriasis is a common skin disease affecting about 1%3% of
the population.
Although most patients with psoriasis have a normal life span,
the disease can be highly disabling emotionally. Patients
often shun outdoor activities and intimacy because they are
self-conscious of their appearance.
The principle abnormality is abnormal cell proliferation. The
epidermal cells have a shortened cycle time with 36 hours as
compared with over 300 hours in normal skin. This results in
significant increase in the normal production of epidermal
cells and keratinization. The result is scaling.
When the scale is removed there is pinpoint bleeding
characteristic of psoriasis that is called the Auspitz sign.
Psoriasis can develop in traumatic sites such as scars,
sunburns, and scratches. This is known as the Koebner
phenomenon.
Superficial Fungal Infections
Dermatophytes produce keratinases that digest keratin and
sustain their existence on skin structures.
1389_Ch14_199-220 2/2/09 1:24 PM Page 218
C H A P T E R
The best tool for diagnosis is visualization of branching
hyphae under the microscope. Scrape the scale from the
active border, and place it on a slide with 10% KOH solution.
Terbinafine 1% applied one to two times daily has higher cure
rates than older azole agents and has fewer side effects.
In onychomycosis, topicals are usually not effective. Oral
therapy is effective only two thirds of the time, with a high
rate of recurrence.
Treat onychomycosis of the fingernails for a minimum of
6 weeks and the toenails for 12 weeks. Terbinafine 250 mg
daily is a good option.
Skin Cancer
With basal cell carcinoma, the typical appearance is a pearly
white, pink, or red, dome-shaped papule with characteristic
fine telangiectasia. The center frequently ulcerates and
bleeds, causing a crust or scale.
With malignant melanoma, the most important prognostic
factor is tumor thickness in millimeters.
Resources
DermIS.net Dermatology Information System: www.dermis.net
This Web site also provides a quick reference and color atlas with
additional references cited.
Fitzpatrick TB, et al. Color atlas and synopsis of clinical dermatology,
4th ed. New York: McGraw Hill, 2005.
This is a quick reference guide. It has a number of color pictures and
lists key points in epidemiology and etiology, history, physical exami-
nation findings, differential diagnoses, and treatment plans.
Fyhrquist VN. Contact dermatitis. Dermatological Clinics 25:613623, 2007.
Habif TP. Clinical dermatology: A color guide to diagnosis and therapy,
4th ed. Mosby, 2003.
Yan, AC. Current concepts in acne management. Adolescent Medicine
Clinics 17:613637, 2006.
Zhang AY. Advances in topical and systemic antifungals. 25:165183, 2007.
1389_Ch14_199-220 2/2/09 1:24 PM Page 219
1. What is the most common type of skin cancer?
a. Adenocarcinoma
b. Squamous carcinoma
c. Basal cell carcinoma
d. Melanoma
2. Which type of skin cancer causes the most deaths?
a. Adenocarcinoma
c. Basal cell carcinoma
d. Melanoma
3. What skin disease has the highest prevalence?
a. Plantar wart
b. Acne vulgaris
c. Psoriasis
d. Eczema
P A R T
1389_Ch14_199-220 2/2/09 1:24 PM Page 220
221
CHAPTER
15
FATIGUE
Eduard Porosnicu, MD, and Martin J. Arron, MD, MBA
I. Definition
A. Refers to a perceived decline in a patients ability to perform
physical or mental activity
B. Subjective: tiredness, malaise, adversity to activity, sensation of
exhaustion, weariness
C. Objective: impaired physical or mental (cognitive and affective)
performance
II. Classification
A. Acute fatigue: 30 days
B. Prolonged fatigue: 30 days
1. Chronic fatigue: persistent or relapsing fatigue for a minimum
of 6 consecutive months
2. Chronic fatigue syndrome (CFS): idiopathic chronic fatigue and
four or more of the following:
a. Sore throat
b. Tender cervical or axillary lymph nodes
c. Myalgias
d. Polyarthralgias
e. New headaches
f. Unrefreshing sleep
g. Malaise after exertion
h. Impaired memory or concentration
Fatigue should be distinguished from weakness, hyper-
somnolence, dyspnea, or apathy.
1389_Ch15_221-232 2/2/09 1:24 PM Page 221
P A R T
III. Epidemiology
A. Prevalence
1. 20%30% of primary care patients report significant fatigue
that interferes with their life quality
2. 5% of primary care patients seek medical advice for fatigue
3. 50% of primary care patients admit being fatigued when asked
(secondary complaint)
4. Prevalence of CFS in United States is approximately 0.4%, or
more than one million people
5. CFS is diagnosed in only 20% of those who have the syndrome
6. Prevalence of chronic fatigue in African Americans and Hispanics
is equal to or greater than in the white population
B. Risk factors
1. Gender
2. Early childhood psychological abuse, sexual abuse, or physical
trauma
3. Adverse parenting styles
4. Limited participation in sports during childhood
5. Middle age, with peak between 4059 years
6. Lower income (contrary to popular belief)
7. History of psychiatric disease
C. Precipitating factors
1. Acute medical illness
2. Acute or chronic psychological stress
D. Perpetuating factors
1. Sleep disorders
2. Physical inactivity
Given the stressful circumstances in life, fatigue is a com-
mon symptom occurring in 20%25% of the population.
CFS accounts for only 1%9% of patients with chronic
fatigue.
Fatigue is twice as common in women as men.
1389_Ch15_221-232 2/2/09 1:24 PM Page 222
15 FATIGUE 223
C H A P T E R
3. Psychiatric disorders
4. Social stress
E. CFS comorbid conditions
1. Fibromyalgia
2. Irritable bowel syndrome
3. Multiple chemical sensitivities
4. Gulf War syndrome
5. Temporomandibular joint disorder
6. Interstitial cystitis
F. Economics of chronic fatigue
1. Total economic cost in the United States is estimated at $9.1
billion annually.
2. Average lost annual household earning from CFS is $20,000.
3. Fully 25% of chronically fatigued patients are unemployed or
receive disability.
IV. Etiology
A. General
1. It is frequently multifactorial in origin.
B. Psychiatric causes are encountered in 60%70% of cases of chronic
fatigue.
1. Depression
2. Anxiety
3. Somatization
4. Personality disorder
5. Substance abuse
C. Infections
1. Viral: Epstein-Barr virus (mononucleosis), cytomegalovirus, HIV
2. Bacterial: osteomyelitis, endocarditis, abscesses
3. Mycobacterial: tuberculosis
4. Systemic fungal infections
Fatigue is expensive to the overall economy because of
impaired productivity.
Fatigue is a symptom associated with a wide variety of
acute and chronic medical and psychological disorders.
1389_Ch15_221-232 2/2/09 1:24 PM Page 223
D. Medications:
1. Antidepressants: tricyclics, trazodone, nefazodone
2. Antihypertensives: beta blockers, clonidine
3. Immunomodulators: corticosteroids, interferon, tumor necrosis
factor, interleukins
4. Sedatives-hypnotics: benzodiazepines, barbiturates
5. Antipsychotics: chlorpromazine, haloperidol
6. Anticonvulsants: phenytoin, valproic acid
7. Antihistamines: hydroxyzine, diphenhydramine
8. Chemotherapy
9. Muscle relaxants: cyclobenzaprine, carisoprodol
10. Antispasmotics: dicyclomine
11. Analgesics: narcotics
E. Endocrine disorders
1. Diabetes mellitus
2. Hypothyroidism and hyperthyroidism
3. Hypocortisolism and hypercortisolism
4. Hyperparathyroidism
5. Hypogonadism
F. Metabolic and fluid-electrolyte imbalance
1. Dehydration
2. Hypercalcemia
3. Hypophosphatemia
4. Hyponatremia or hypernatremia
5. Liver failure
6. Chronic kidney disease
G. Neurologic disorders
1. Parkinson disease
2. Lou Gehrig disease
3. Multiple sclerosis
4. Restless leg syndrome
5. Autonomic failure (e.g., Shy-Drager)
6. Neurally mediated hypotension
7. Postural tachycardia syndrome
H. Pulmonary disease
1. Chronic obstructive pulmonary disease (COPD)
2. Sleep apnea
3. Asthma
4. Interstitial lung disease
P A R T
1389_Ch15_221-232 2/2/09 1:24 PM Page 224
I. Cardiac disease
1. Coronary artery disease
2. Congestive heart failure
3. Valvular disease
4. Cardiomyopathies
J. Connective tissue diseases
1. Rheumatoid arthritis
2. Polymyalgia rheumatica
3. Giant cell arteritis
4. Sarcoidosis
5. Systemic lupus erythematosus
V. Pathophysiology
A. General
1. The pathophysiology of fatigue remains unclear.
2. Most of the studies have focused on patients with CFS.
3. Premorbid physical deconditioning may play a role.
4. Some of the hypotheses to explain chronic fatigue are listed
below.
B. Hypofunctional hypothalamic-pituitary-adrenal (HPA) axis
1. Patients with CFS were found to have a mildly depressed
serum cortisol response to stress and abnormally high release of
proinflammatory cytokines.
2. An association exists between CFS and variations in the gluco-
corticoid receptor gene.
C. Genetic disorders
1. Studies have demonstrated that variations in certain genes are
associated with CFS. One study predicted whether an individ-
ual had CFS with 76% accuracy.
2. Three of the most relevant genes were associated with stress
reactions, emotional responses, memory, and other central
nervous system activity.
3. No definitive genetic markers have been identified; the role of
genetic profiling in the diagnosis of CFS remains unclear.
D. Brainstem dysfunction
1. Postulated for postviral fatigue syndromes
2. Entails viral damage to the dopaminergic pathways and the
ascending reticular activating system from brainstem to the
cortex
15 FATIGUE 225
C H A P T E R
1389_Ch15_221-232 2/2/09 1:24 PM Page 225
P A R T
E. Orthostatic intolerance
1. Some patients with chronic fatigue have postural or neurally
mediated hypotension
2. Reduction in blood pressure when ambulating may result in
fatigue, lightheadedness, impaired concentration, and other
nonspecific symptoms
VI. Clinical Assessment
A. General
1. Physicians may sometimes perceive fatigue as less important
because it is diagnostically nonspecific.
2. Fatigue is an important symptom for the patient and can be
disabling.
3. Chronic fatigue patients can be as debilitated as patients with
multiple sclerosis, renal failure, or heart disease.
B. History
1. History should be developed with open-ended, nonjudgmental
questions
2. Fatigue characteristics
a. Duration
b. Timing
c. Triggering factors
d. Relieving factors
e. Associated symptoms
3. Contextual history
a. Psychosocial history
b. Sleep history
c. Sexual history
d. Recreational drug use
e. Acute or chronic environmental toxin exposure (e.g., lead,
carbon monoxide (CO)
C. Physical examination
The history is the most important part of the evaluation.
The physical examination needs to be thorough.
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15 FATIGUE 227
C H A P T E R
1. The list of possible diagnostic clues to a potential causal illness
is extensive
a. Orthostatic hypotension
b. Low-grade fever
c. Skin pallor, jaundice, cyanosis, malar rash, bruises
d. Oral thrush, mucosal pallor
e. Lymph node enlargement
f. Thyromegaly
g. Breast masses
h. Cardiac murmurs; jugular venous distention (JVD), S3,
pedal edema, rales
i. Wheezing
j. Hepatosplenomegaly and/or ascites
k. Muscle atrophy and/or decreased strength
l. Clubbing
m. Joint deformities (swan neck, boutonnire)
n. Poor balance, coordination
o. Cognitive defects
D. Diagnostic testing
1. General
a. Fatigue is a nonspecific symptom.
Unless clues in the history or physical examination
significantly increase the pretest probability for a
certain disease, there is limited benefit from testing
beyond age- and gender-appropriate screening.
2. Suggested battery of routine tests
a. Complete blood count with differential
b. Erythrocyte sedimentation rate or reactive protein
c. Serum urea nitrogen, creatinine, electrolytes
d. Serum calcium and phosphate
e. Liver transaminases
f. Thyroid-stimulating hormone
g. Fasting blood glucose
h. Creatine kinase
i. Urinalysis
j. Urine pregnancy test (in reproductive-age women)
k. Globulin and albumin
l. Antinuclear antibodies and rheumatoid factor
1389_Ch15_221-232 2/2/09 1:24 PM Page 227
P A R T
3. Specialized testing may be indicated if suggested by clinical
findings
a. Polysomnography and other sleep studies
b. Tilt table testing
4. Psychiatric referral
a. Psychiatric or psychological consultation is indicated when
such an etiology is suspected or the fatigue remains unex-
plained despite a thorough medical evaluation by the primary
care provider.
VII. Management
A. General
1. Idiopathic chronic fatigue can be challenging to treat for both
medical and psychological reasons.
Many patients have preconceived ideas regarding the
causes and treatments of their symptoms.
Cognitive behavioral therapy and graded exercise pro-
grams are the only proven therapies for chronic fatigue.
2. Patients with chronic fatigue may experience more side effects
from treatment and may require lower starting doses.
3. Early intervention may facilitate better outcomes.
B. Disease-specific therapies
1. Are directed to the diagnosed condition such as infection,
medication side effect, or organ dysfunction
2. Fatigue due to a psychiatric illness often responds to:
a. Reassurance.
b. Stress management.
c. Sleep hygiene.
d. Sedative-hypnotic or anxiolytic medications.
e. Psychotropic medication and/or psychotherapy.
C. Coping strategies
1. Develop effective adaptive strategies for improving functioning,
limiting symptoms, and increasing quality of life
2. Helpful strategies include
a. Acknowledging the disability and establishing reasonable
treatment goals
1389_Ch15_221-232 2/2/09 1:24 PM Page 228
b. Recognizing and addressing counterproductive beliefs
c. Lifestyle management
d. Balanced diet and, if necessary, calorie reduction
e. Graded exercise program
f. Cognitive behavioral therapy
i. Focuses on the illness experience of patients and the
impact the fatigue has on their lives
ii. Therapy incorporates:
(1) Cognitive element: focuses on modification of
thoughts and beliefs relevant to disease process
(2) Behavioral element: graded increase in activity.
(3) A skilled psychotherapist
D. Symptom-specific strategies
1. For pain
a. Acetaminophen, nonsteroidal anti-inflammatory drugs
(NSAIDs), corticosteroids (avoid opiates, if possible)
2. For sleep disturbance
a. Sleep hygiene
b. Over-the-counter sedatives
c. Cautious use of hypnotics
3. For depression
a. Antidepressants
b. Psychostimulants
i. Psychostimulants such as methylphenidate, pemoline, and
modafinil have been used in chronic fatigue with varied
results.
ii. In a randomized trial, methylphenidate diminished fatigue
and increased concentration significantly in only 17% of
CFS patients.
iii. These medications should be prescribed by experienced
clinicians who are familiar with their side effects.
E. Alternative therapies
1. Many unproven interventions are often tried in chronic fatigue.
2. Pharmacologic therapy with fludrocortisone, corticosteroids,
vitamin B
12
, and acyclovir has not been proven to be effective.
3. L-carnitine, coenzyme Q10, monoclonal antibodies, serum
immunoglobulins, galantamine, and a variety of herbal remedies
have been used without clear evidence of efficacy.
4. Acupuncture, massage, meditation, and yoga are often pre-
scribed but are of unproven benefit.
15 FATIGUE 229
C H A P T E R
1389_Ch15_221-232 2/2/09 1:24 PM Page 229
P A R T
VIII. Prognosis
A. Acute fatigue has a good prognosis. It is usually not the primary
symptom at presentation.
B. Chronic fatigue has a variable course with unpredictable remis-
sions and exacerbations.
C. Patients with idiopathic chronic fatigue may have undiagnosed
cancers or other major disorders as a cause of their symptoms.
D. The mortality rate of idiopathic chronic fatigue is low (0.01%).
E. Although the majority of patients improve over time, a signifi-
cant proportion of patients do not fully recover.
Children with chronic fatigue have a good chance of
recovery (50%95%). (This is a better rate than seen in
adults.) Reassure children and their parents.
MENTOR TIPS DIGEST
Fatigue should be distinguished from weakness,
hypersomnolence, dyspnea, or apathy.
Given the stressful circumstances in life, fatigue is a common
symptom occurring in 20%25% of the population.
CFS accounts for only 1%9% of patients with chronic fatigue.
Fatigue is twice as common in women as men.
Fatigue is expensive to the overall economy because of
impaired productivity.
Fatigue is a symptom associated with a wide variety of acute
and chronic medical and psychological disorders.
The history is the most important part of the evaluation.
The physical examination needs to be thorough.
Unless clues in the history or physical examination signifi-
cantly increase the pretest probability for a certain disease,
there is limited benefit from testing beyond age- and gender-
appropriate screening.
Many patients have preconceived ideas regarding the causes
and treatments of their symptoms.
Cognitive behavioral therapy and graded exercise programs
are the only proven therapies for CFS.
Children with chronic fatigue have a good chance of recovery
(50%95%). (This is a better rate than seen in adults.)
Reassure children and their parents.
1389_Ch15_221-232 2/2/09 1:24 PM Page 230
Resources
Blockmans D, Persoons P, Van Houdenhove B, et al. Does methylphenidate
reduce the symptoms of chronic fatigue syndrome? American Journal of
Medicine 119:167.e2330, 2006.
Chaudhuri A, Behan PO. Fatigue in neurological disorders. Lancet
363:978988, 2004.
Cornuz J, Guessous I, Favrat B. Fatigue: A practical approach to diagnosis
in primary care. Canadian Medical Association Journal 174: 2006.
Goertzel B, Pennachin C, deSouza L, et al: Combinations of single
nucleotide polymorphisms in neuroendocrine effector and receptor
genes predict chronic fatigue syndrome. Pharmacogenomics.
7:475483, 2006.
Price JR, Couper J. Cognitive behaviour therapy for chronic fatigue
syndrome in adults. Cochrane Database of Systematic Reviews Issue
4, 1998.
Prins JB, van der Meer JW, Bleijenberg G. Chronic fatigue syndrome.
Lancet. 367:346355, 2006.
Reyes M, et al. Prevalence and incidence of chronic fatigue syndrome in
Wichita, Kansas. Archives of Internal Medicine 163:15301536, 2003.
U.S. Department of Health and Human Services, Centers for Disease
Control and Prevention. CFS toolkit for healthcare professionals
1. Which of the following suggests objective evidence of fatigue?
a. Slow, deep tendon reflexes
b. Diminished deep tendon reflexes
c. Impaired cognitive performance
d. Impaired muscle tone
2. What is the approximate frequency of fatigue as the primary complaint
in primary care?
a. 0.5%
b. 5%
15 FATIGUE 231
C H A P T E R
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c. 50%
d. 95%
3. Which of these symptomatic complaints are most consistent with
fatigue?
a. Excess daytime sleepiness
b. Unremitting weariness
c. Lack of caring about matters that should be important
d. Difficulty breathing at rest
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233
CHAPTER
ERECTILE DYSFUNCTION
Kevin T. McVary, MD
CHAPTER
I. Epidemiology
A. Erectile dysfunction (ED) is defined as the condition when a man
cannot acquire or sustain an erection of sufficient rigidity to have
sexual intercourse.
B. The estimated prevalence of ED in the United States is approxi-
mately 30 million and is associated with approximately $330 million
in annual expenditures.
C. ED is not considered a normal part of the aging process.
II. ED Risks
Both the prevalence and incidence of ED increase with
age.
ED has been associated independently with several risk
factors and disease comorbidities. These are listed in
Table 16.1.
A. ED may be the presenting symptom of one of the risk factors in
Table 16.1, and health-care providers should view ED as a potential
symptom of a systemic disease.
III. Erectile Physiology
A. At rest the penis is kept flaccid both through sympathetic outflow
onto
1
receptors as well as through the action of local endothelial
factors, which work together to cause tonic contraction of cavernosal
smooth muscle.
16
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P A R T
B. Erection is initiated by parasympathetic stimulation of penile
blood vessels, vascular endothelium, and corpus cavernosal smooth
muscle, causing relaxation via a nitric oxide (NO)/cGMPmediated
mechanism.
1. The smooth muscle relaxation allows increased blood flow
and compression of venous outflow by the tunica albugenea.
IV. Pathophysiology of Erectile Dysfunction
A. Several diseasesdiabetes mellitus (DM), metabolic syndrome,
chronic renal failure (CRF), benign prostatic hyperplasia
Factors contributing to the pathogenesis of ED can be
divided into the following six categories: arteriogenic,
venogenic, neurogenic, endocrine, psychogenic, and medication-
related. More than one category may be involved in an individual
patient.
TABLE
16.1
Risk Factors for Organic ED
Disease Age-Adjusted Odds Ratio
Diabetes mellitus 4.08
Coronary artery disease 1.79
Hypertension 1.58
Hyperlipidemia 1.63
Peripheral vascular disease 2.63
Alcohol abuse 1.53
BPH/LUTS 2.93
Obesity 1.96
Smoking 1.972.45
Metabolic syndrome 33%40%*
Prior pelvic surgery 25%*
Chronic renal failure 20%50%*
Endocrine disorders:
Hyperthyroid 14.7%*
Hypothyroid 64.3%*
Hyperprolactinemia 50%75%*
Depression 1.822.03
*Indicates population prevalenceor not available
1389_Ch16_233-249 2/2/09 1:28 PM Page 234
16 ERECTILE DYSFUNCTION 235
C H A P T E R
(BPH)associated with increased risk of developing ED, with
underlying pathology as one or several of the six categories
B. Arteriogenic: disturbance in flow of blood into penis
1. The commonly accepted mechanism involves endothelial cell
dysfunction.
2. Damage to the vascular endothelium can prevent sufficient
NO-dependent vasodilation to allow adequate blood inflow.
This is often due to atherogenesis for which DM, hypertension
(HTN), cardiovascular disease, and smoking are risk factors.
a. Many consider men with ED and no cardiovascular symptoms
to be vascular patients until proved otherwise.
3. Other causes of arteriogenic ED include pelvic trauma and
radiation therapy.
C. Cavernous (venogenic): disturbance in flow of blood out of penis
1. Insufficient compression of the subtunical venous plexuses
allows venous blood to escape and prevents sufficient penile
engorgement to attain an erection. No increase in arterial inflow
can compensate for the unrestricted venous outflow.
2. Suggested causes include decreased cavernous smooth muscle
content due to smooth muscle cell apoptosis, loss of compliance
of venous sinusoids, abnormal vascular structures, degenerative
tunical changes, and damage to the tunica albugenea.
D. Neurogenic:
1. Includes central, peripheral, and iatrogenic causes and may
account for up to 20% of all cases of ED
a. Disorders that affect the sacral spinal cord or the peripheral
autonomic fibers to the penis prevent autonomic relaxation
of penile smooth muscle.
2. In patients with spinal cord injury, extent of ED depends on
completeness and level of spinal lesion
3. Other disorders commonly associated with ED include
multiple sclerosis and peripheral neuropathy due to DM or
alcoholism
Prostate Cancer Prevention Trial data demonstrated
that men with ED who have no symptoms of vascular
disease should be screened for cardiovascular disease and
its associated risk factors.
1389_Ch16_233-249 2/2/09 1:28 PM Page 235
P A R T
1. Hyperprolactinemia can result in sexual dysfunction with loss
of libido, ED, galactorrhea, gynecomastia, and infertility, as it
is associated with low levels of testosterone.
2. Hypothyroidism and hyperthyroidism are both associated with ED.
F. Diabetes:
1. In studies using exclusively diabetic populations, the preva-
lence of ED is estimated anywhere from 35% to 75%.
4. Pelvic surgery may result in ED through disruption of auto-
nomic nerve supply leading to smooth muscle cell apoptosis
E. Endocrinologic:
Androgens contribute to, but are not essential for, normal
libido, and their complete role in erectile function remains
unclear.
Symptoms of ED may be the presenting symptom of
diabetes in up to 12% of men.
2. ED in diabetic men has been most strongly associated with
poor glycemic control, insulin dependence, long duration of
disease, concurrent smoking ,and diabetic complications such
as neuropathy, nephropathy, or retinopathy.
3. Diabetic ED is a result of a combination of arteriogenic and
neurogenic mechanisms.
G. Metabolic syndrome:
1. The metabolic syndrome is defined by three of the five factors
present: 1. abdominal obesity; 2. HTN; 3. glucose intolerance;
4. hypertriglyceridemia; and 5. low HDL cholesterol.
2. The metabolic syndrome is an independent risk factor for car-
diovascular disease and has also been associated with endothe-
lial dysfunction and decreased NO release.
H. Lower urinary tract symptoms (LUTS)/benign prostatic hyperplasia
(BPH):
1. LUTS secondary to BPH have a reported prevalence ranging
from 30% in men in their 50s up to 60% in men over the age of
70 years.
a. Up to 90% of men over the age of 80 years have histologic
evidence of BPH on autopsy.
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C H A P T E R
2. Although sexual dysfunction has not been linked definitively to
any one specific type of LUTS (obstructive versus irritative ver-
sus overall bother), it appears that the overall severity of LUTS
is associated with more severe sexual dysfunction.
3. The underlying mechanism is still not clear, but suggested etiolo-
gies include increased sympathetic tone, alterations in smooth
muscle contraction, endothelial dysfunction, atherosclerosis-
induced pelvic ischemia, and age-related hormone imbalances.
Thus, all men presenting with LUTS/BPH should be
evaluated for ED, and all men experiencing sexual
dysfunction should be evaluated for LUTS.
I. Chronic kidney disease (CKD):
1. There is a reported prevalence of ED ranging from 20% to 50%
in patients with CKD, especially among transplant and dialysis
patients.
2. The underlying cause is likely secondary to endothelial damage
from underlying vascular disease, diabetes, or prolonged uremia.
J. Psychogenic:
1. It is defined as the persistent inability to achieve or maintain
erections satisfactory for sexual performance due predomi-
nantly or exclusively to psychological or interpersonal factors.
a. The most common causes of psychogenic ED are performance
anxiety, depression, relationship conflict, loss of attraction,
history of sexual abuse, conflicts over sexual preference, or
fear of pregnancy or STD.
2. Men who present with ED who have nocturnal erections have at
least an element of psychogenic ED, but an underlying organic
cause still cannot be ignored (Table 16.2).
Many cases of ED have some aspect of psychogenic
ED involved and are called mixed ED.
3. There are two mechanisms that may be involved in
psychogenic ED.
a. Increased psychogenic stimuli to the sacral cord, which may
inhibit reflexogenic erections and prevent the activation of
the vasodilator outflow to the penis
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P A R T
b. Excess of sympathetic outflow or plasma catecholamine levels,
which can increase penile smooth muscle tone
K. Medication and substance-related:
1. Many patients presenting with ED have a history of prescription
drug use.
TABLE
16.2
Classification of ED Characteristics
Organic ED Psychogenic ED
Slow onset Rapid onset
No situational correlate Situational dysfunction
Dysfunction constant Dysfunction comes and goes
Absence of nocturnal and Presence of nocturnal or early
early morning erections morning erections
History of systemic disease, Presence of psychological
such as diabetes or coronary factors, relationship
artery disease, or lifestyle difficulties, or emotional
factors stressors
There is a consensus that drugs are implicated in
a large percentage of ED cases, but the exact
mechanisms are complex (Box 16.1).
Thiazide diuretics and nonselective beta blockers have
been implicated most often.
BOX
Medications Associated With ED
Cardiovascular
Clonidine
Calcium channel blockers (Verapamil)
Hydralazine
Methyldopa
Nonselective beta blockers
(Propranolol)
Hormones
GnRH agonists (Leuprolide)
Estrogens
Progesterone
Corticosteroids
Cyproterone acetate
5 -reductase inhibitors
16.1
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C H A P T E R
BOX
Medications Associated With ED (continued)
Reserpine
Guanethidine
Disopyramide
Fibrates (Gemfibrozil)
Amiodarone
Digoxin
Psychiatric
SSRIs (Paroxetine)
Haloperidol
Tricyclic antidepressants
(Imipramine)
Doxepin
Lithium
MAO inhibitors (Phenelzine)
Trazodone
Phenothiazines (Thioridazine)
Gastrointestinal
H2 blockers (Cimetidine)
Metoclopramide
Anti-inflammatory
Indomethacin
Naproxen
Cytotoxic
Chemotherapy
Sulfasalazine
Methotrexate
Cyclophosphamide
Roferon-A
Genitourinary
Prazosin
Diuretics
Acetazolamide
Thiazides
Spironolactone
Central Nervous System
Opiates
Anticholinergics
Benzodiazepines (Diazepam)
Barbiturates
Carbamazepine
Bromocriptine
Phenytoin
Antiviral
Protease inhibitors
Recreational
Ethanol
Nicotine
Cocaine
Marijuana
16.1
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P A R T
2. Antidepressant and antipsychotic agents, particularly neuroleptics,
tricyclic antidepressants, monoamine oxidase (MAO) inhibitors,
and selective serotonin uptake inhibitors (SSRIs), are associated
with erectile, ejaculatory, and sexual desire difficulties.
3. Anti-androgen medications may be associated with decreased
sexual desire.
4. Cigarette smoking induces systemic vasoconstriction, is athero-
genic, and may directly cause endothelial dysfunction.
Smoking cessation may decrease the risk of ED.
5. Alcohol causes central sedation, and large amounts can cause
liver failure, with longstanding use leading to hyperestrogenemia
and ED.
V. Approach to the ED Patient
A. A complete medical and sexual history should be taken during the
initial evaluation of any man with ED.
1. Initial questions should focus on the onset of symptoms,
progression, and the presence, quality, and duration of erections.
The absence of nocturnal erections is often a crucial
piece of information differentiating organic from
psychogenic ED.
a. Organic causes are generally characterized by a gradual and
persistent change in rigidity or ability to sustain nocturnal,
coital, or self-stimulated erections.
b. Psychogenic ED is often associated with the presence of
nocturnal erections, may be situational, and may have an
abrupt onset without obvious cause (see Table 16.2).
c. Although a patient may demonstrate symptoms of psychogenic
ED, it is important to understand he may also be suffering
from an organic cause of ED.
2. Relevant risk factors should be identified (such as DM, lipid
disorders, HTN, peripheral vascular disease, smoking, alcoholism,
and obesity).
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3. It is recommended that the physician administer the International
Index of Erectile Function (IIEF) score, or another accepted
quantitative form, which measures the severity of the dysfunction
and details which domains are affected.
Decreased libido may be one of the earliest signs
of altered testosterone or prolactin.
Signs of thyroid, hepatic, hypertensive, cardiovascular,
or renal disease should be evaluated.
Peripheral pulses, reflexes, and visual fields should be
examined.
Assess the external genitalia by palpating the penis to
check for fibrotic plaques, suggestive of Peyronie disease;
also, perform a testicular examination in search of small testes
or reduced secondary sexual characteristics, suggestive of
hypogonadism.
4. Questions should be asked about whether ejaculation is normal,
premature, delayed, or absent.
a. Retrograde ejaculation is often present in diabetic men with
autonomic neuropathy.
5. The patient should also be questioned about the presence of
penile curvature or pain with coitus to assess for any structural
abnormalities.
6. The patients surgical history should be probed, with emphasis
on bowel, bladder, prostate, or vascular diseases.
7. A complete drug history should be taken, including alcohol
consumption and cigarette smoking.
B. The physical examination is a crucial part of the assessment
of ED.
C. Select laboratory testing is recommended in many cases.
1. Serum chemistries, complete blood count (CBC), fasting blood
glucose, lipid profiles
2. Measuring free and total testosterone can be important,
especially in cases of advanced age, obesity
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3. Serum prolactin should be measured, although admittedly
low-yield
4. Thyroid function studies should be considered
VI. Indications for Specialty Referral
A. Most patients with ED do not need further workup; some require
specialized testing.
B. Situations that support specialized vascular, neurologic, or
psychiatric evaluation include the following.
1. Complicated endocrinopathies
2. Complicated psychiatric disturbances
3. Penile abnormalities (e.g., Peyronie disease)
4. Pelvic/perineal trauma
5. Necessity of vascular or neurosurgical intervention
6. Patient wishes a more comprehensive diagnostic evaluation or
understanding prior to selection of a treatment
7. Failure of initial treatment
8. Presence of medical/legal issues
C. The major classes of diagnostic testing (invasiveness and cost
should be weighed) for ED include the following.
1. VascularDuplex Doppler ultrasound, injection of vasoactive
substances followed by penile stimulation, dynamic infusion
cavernosography/cavernosometry
2. Neurologicnocturnal penile tumescence and rigidity,
biothesiometry, somatosensory-evoked potentials
3. Endocrinologichypothalamic and/or pituitary function studies,
brain magnetic resonance imaging (MRI), thyroid function studies
4. Psychodiagnostic
VII. Management
A. Patient education
1. Patient and partner education is essential in the treatment of ED.
2. Discussion of the treatment options helps clarify how to best
offer treatment.
B. Nonpharmacologic therapies
1. The initial therapy for a patient with obesity, excess alcohol
consumption, and cigarette smoking involves lifestyle changes
including weight loss and smoking and drinking cessation.
a. Studies have proved weight loss to be an effective treatment
for ED in obese men with no other comorbidities.
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2. Review the patients medications to determine if any are associated
with ED.
a. Consider changing a patients antidepressant medication
to one with fewer sexual side effects, such as bupropion,
mirtazapine, sertraline, or fluoxetine.
b. If the therapeutic benefits of the patients medication outweigh
the sexual side effects, it is appropriate to give a trial of oral
phosphodiesterase-5 (PDE-5) inhibitor therapy.
C. Psychosexual therapy
1. Group therapy, cognitive-behavioral interventions, behavioral
desensitization, individual and couples therapy
2. Psychosexual therapy may help treat organic ED along with
first-line pharmacologic or surgical therapy, as there may be
mixed disorder
D. Oral PDE-5 inhibitors
1. PDE-5 inhibitors are oral agents that potentiate the release of
NO to enhance erection in men who already have functional
NO release.
PDE-5 inhibitors are effective across a broad range of
etiologies, including vascular disease, DM, LUTS, spinal
cord injury, and medication-related ED (specifically SSRIs).
2. They do not effect ejaculation, orgasm, or sexual drive.
3. Both vardenafil (Levitra) and sildenafil (Viagra) are semise-
lective inhibitors of PDE-5 (predominant isoform found in
the penis) and have some PDE-6 inhibition (isoform found
in the eye), whereas tadalafil (Cialis) inhibits PDE-5 and
PDE-11 (isoform found in the prostate, skeletal muscle,
and testis).
4. These three medications show similar efficacy, tolerability, time
to onset of action, and side effects.
a. Tadalafil has a significantly longer half-life, allowing it to be
active for up to 36 hours, whereas the other two have a
significantly shorter duration of action.
5. The side effects of these drugs are secondary to inhibition of
vascular and smooth muscle PDE-5 and include the following.
a. Minor side effects such as headaches, facial flushing,
dyspepsia, myalgia, nasal congestion
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P A R T
b. Approximately 7% of men may experience transient altered
color vision with sildenafil and vardenafil
c. Rare but serious side effect of nonarteritic anterior ischemic
optic neuropathy (NAION) reported for all three drugs
d. Vardenafil may cause QT prolongation; contraindicated for
patients who take class 1A and III antiarrythmic drugs or
who have prolonged QT syndrome
e. These drugs can potentiate hypotensive effects of nitrates
and may result in profound shock and even death; no antidote
to nitrate-PDE-5 inhibitor interaction
Androgen replacement is associated with increased libido
in hypogonadal men but not necessarily with improved
erectile ability.
These drugs are strictly contraindicated for all men
receiving any form of nitrate therapy.
6. Exercise caution in prescribing these drugs for those with active
coronary disease, heart failure, left ventricle low outflow states,
and patients on complex antihypertensive regimens because
PDE-5 inhibitors have a vasodilatory effect and may cause
hypotension.
a. There is an increase in cardiovascular activity with sexual
activity.
b. PDE-5 inhibitors do not increase the risk of MI or cardiac
mortality in patients with known coronary disease or heart
failure.
E. Androgen therapy
1. The goals of replacement therapy are to increase sexual interest
and desire, attain serum levels close to physiologic levels, and
replicate physiologic diurnal rhythm.
2. Replacement methods include depot intramuscular (IM)
injections, oral preparations, and transdermal preparations of
testosterone.
a. The long-acting IM depots of testosterone are the most cost-
effective, safe, and practical preparations available.
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C H A P T E R
3. It has not been demonstrated that replicating the diurnal rhythm
provides any physiologic advantage.
a. Oral androgen preparations are associated with increased
risk for hepatotoxicity.
b. The transdermal delivery of testosterone is convenient and
reliable and more closely mimics the physiologic testos-
terone levels.
4. Androgen supplementation in the face of normal testosterone is
discouraged because adverse side effects may result without
any effect on erectile function.
5. Side effects of unnecessary testosterone administration include
infertility, erythrocytosis, hepatotoxicity, worsening of sleep
apnea, and dyslipidemia.
6. Hepatic function and a CBC should be measured before and
during testosterone therapy.
Androgen therapy is contraindicated in men with
androgen-sensitive cancers.
It is considered wise to perform a digital rectal exami-
nation and measure PSA prior to giving androgens.
F. Intracavernosal self-injection
1. If oral therapy fails or is contraindicated, the self-injection of
intracavernosal vasoactive substances is a reasonable next
choice.
2. There are three different vasoactive medications that are used
for intracavernosal injection: alprostadil (prostaglandin E1),
papaverine, and phentolamine.
3. In the long term, anywhere from 13% to 60% of patients
discontinue.
4. The side effects include local adverse events such as prolonged
erections, priapism (especially with alprostadil preparations),
pain, and fibrosis with chronic use.
a. It is contraindicated in men with a history of hypersensitivity
to the drug or who are at risk for priapism (hypercoagulable
states, sickle cell disease).
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P A R T
G. Intraurethral treatments
1. Intraurethral alprostadil (Medicated Urethral System for
ErectionMUSE) in a semisolid pellet placed into the
urethra is a type of local therapy.
2. Approximately 65% of men receiving intraurethral alprostadil
respond with an erection adequate for intercourse when tested
in the office, but only 50% of those achieve successful coitus
at home.
3. The associated side effects are similar to those of the intracav-
ernous injection (see below), except for a markedly reduced
incidence of priapism.
H. Vacuum constriction devices
1. In select situations they are a reasonable treatment alternative for
patients who do not desire any of the preceding interventions.
2. The majority of men (68%83%) who use this device report
self- and partner satisfaction even though the primary dropout
rate is around 60%.
3. The adverse events include pain, numbness, bruising, and altered
ejaculation.
I. Surgery
1. Surgical implantation of a penile prosthesis.
2. Surgical treatments invasive; associated with potential compli-
cations and generally reserved for treatment-refractory ED
3. Despite cost and invasiveness, penile prosthesis associated with
high rates of patient satisfaction (83% men, 70% partner)
4. American Urological Association Panel on Erectile Dysfunction
recommends prosthetic implantation as only surgical standard
of care for ED
J. Penile revascularization
1. Has largely fallen out of favor, except for patients who have
suffered traumatic injury, and still largely considered experi-
mental surgery
a. Finding a discrete lesion on penile angiography, especially
in a young patient with a history of trauma and no other
comorbid vascular risks, is the only indication for revascu-
larization therapy.
2. Venous surgery for dysfunctional cavernosal veno-oclusion
possible; has long-term success rate of only 40%50%.
1389_Ch16_233-249 2/2/09 1:28 PM Page 246
C H A P T E R
MENTOR TIPS DIGEST
Both the prevalence and incidence of ED increase with age.
ED has been independently associated with several risk
factors and disease comorbidities.
Factors contributing to the pathogenesis of ED can be
divided into the following six categories: arteriogenic,
venogenic, neurogenic, endocrine, psychogenic, and medication-
related. More than one category may be involved in an individual
patient.
Men with ED who have no symptoms of vascular disease
should be screened for cardiovascular disease and its
associated risk factors.
Androgens contribute to, but are not essential for, normal
libido, and their complete role in erectile function remains
unclear.
Symptoms of ED may be the presenting symptom of diabetes in
up to 12% of men.
All men presenting with LUTS/BPH should be evaluated for ED,
and all men experiencing sexual dysfunction should be evalu-
ated for LUTS.
Many cases of ED have some aspect of psychogenic ED
involved and are called mixed ED.
There is a consensus that drugs are implicated in a large
percentage of ED cases, but the exact mechanisms are
complex.
Thiazide diuretics and nonselective beta blockers have been
implicated most often.
Smoking cessation may decrease the risk of ED.
The absence of nocturnal erections is often a crucial piece of
information differentiating organic from psychogenic ED.
Decreased libido may be one of the earliest signs of altered
testosterone or prolactin.
Signs of thyroid, hepatic, hypertensive, cardiovascular, or renal
disease should be evaluated.
Peripheral pulses, reflexes, and visual fields should be examined.
Assess the external genitalia by palpating the penis to check for
fibrotic plaques, suggestive of Peyronie disease; also, performa
testicular examination in search of small testes or reduced
secondary sexual characteristics, suggestive of hypogonadism.
PDE-5 inhibitors are effective across a broad range of etiolo-
gies, including vascular disease, DM, LUTS, spinal cord injury,
and medication-related ED (specifically SSRIs).
1389_Ch16_233-249 2/2/09 1:28 PM Page 247
P A R T
These drugs are strictly contraindicated for all men receiving
any form of nitrate therapy.
Androgen replacement is associated with increased libido in
hypogonadal men but not necessarily with improved erectile
ability.
Androgen therapy is contraindicated in men with andro-
gensensitive cancers
It is considered wise to perform a digital rectal examination
and measure PSA prior to giving androgens.
Resources
Brown JS, Wessells H, Chancellor MB, et al.: Urologic complications of
diabetes. Diabetes Care 28:177, 2005.
Burnett AL: The role of nitric oxide in erectile dysfunction: Implications
for medical therapy. Journal of Clinical Hypertension (Greenwich)
8:53, 2006.
Chiurlia E, DAmico R, Ratti C, et al.: Subclinical coronary artery athero-
sclerosis in patients with erectile dysfunction. Journal of the American
College of Cardiology 46:1503, 2005.
Derby CA, Mohr BA, Goldstein I, et al.: Modifiable risk factors and erectile
dysfunction: Can lifestyle changes modify risk? Urology 56:302, 2000.
Jackson G, Rosen RC, Kloner RA, et al.: The second Princeton consensus
on sexual dysfunction and cardiac risk: New guidelines for sexual
medicine. Journal of Sexual Medicine 3:28, 2006.
Kirby M, Jackson G, Simonsen U: Endothelial dysfunction links erectile
dysfunction to heart disease. International Journal of Clinical Practice
59: 225,2005.
Lewis RW, Fugl-Meyer KS, Bosch R, et al.: Epidemiology/risk factors of
sexual dysfunction. Journal of Sexual Medicine 1:35, 2004.
Lue TF: Physiology of penile erection and pathophysiology of erectile dys-
function. In Wein AJ, Novick AC, Partin AW (eds), et al.: Campbell-
Walsh Urology, 9th ed. Philadelphia: WB Saunders, pp. 718749, 2007.
Lue TF, Broderick GA: Evaluation and nonsurgical management of erec-
tile dysfunction and premature ejaculation. In Wein AJ, Novick AC,
Partin AW, et al. (eds): Campbell-Walsh Urology, 9th ed. Philadelphia:
WB Saunders, pp. 750787, 2007.
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McVary KT, Carrier S, Wessells H: Smoking and erectile dysfunction:
Evidence-based analysis. Journal of Urology 166:1624, 2001.
Wein AJ, Van Arsdalen KN: Drug-induced male sexual dysfunction. Urology
Clinics of North America 15:23, 1988.
1. How is ED related to age?
a. Often a congenital disorder manifesting at puberty
b. Prevalence increases with age
c. Normal part of aging process
d. Universal in men older than 80 years
2. What occult cause of ED is common and warrants screening in otherwise
healthy men?
a. Colorectal cancer
b. Depression
c. Pituitary hypogonadism
d. Occult Chlamydia infection
3. What occult cause of ED is common and warrants screening in otherwise
healthy men?
a. Colorectal cancer
b. Pituitary hypogonadism
c. Peripheral vascular disease
d. Osteoarthritis
C H A P T E R
1389_Ch16_233-249 2/2/09 1:28 PM Page 249
250
ANXIETY AND DEPRESSION
Douglas R. Reifler, MD
CHAPTER
17
I. Background and Epidemiology
A. Anxiety and depression are very common, affecting 11%35% of
primary care patients, and these disorders can be as debilitating as
advanced cardiovascular disease. More patients who have mental
disorders visit primary care physicians than visit psychiatrists.
In spite of their ubiquity, mental disorders are either
missed or not addressed in 50% of primary care patients
who have them.
B. Mental disorders often coexist with somatic disorders, compounding
symptoms and even increasing mortality rates.
C. Point prevalences of common mood and anxiety disorders in primary
care patients are as follows.
1. Major depressive disorder: 5%10%
2. Dysthymia: 2%4%
3. Bipolar disorder: 1%2%
4. Panic disorder: 3%7%
5. Generalized anxiety disorder: 5%8%
6. Obsessive-compulsive disorder: 1%2%
D. Twice as many women as men have major depression, but this
condition is common in both sexes.
II. Diagnostic Approach
A. Any patient who gives clues of mental distress should be asked
about symptoms in a routine and nonjudgmental way.
1. Clues can include overt mention of feeling sad, depressed, or
anxious; nonverbal signals such as being tearful or agitated; and
subtler hints such as an excessive focus on somatic symptoms.
1389_Ch17_250-259 2/2/09 1:29 PM Page 250
B. The Diagnostic Statistical Manual of Mental Disorders, 4th Edition
(DSM-IV) criteria for major depressive disorder and panic disorder
are listed in Table 17.1.
17 ANXIETY AND DEPRESSION 251
C H A P T E R
The greater the number of somatic symptoms, the
more likely the presence of a mental disorder35%
of patients with four or five unrelated symptoms have
a mental disorder.
2. Fatigue, insomnia, or headaches can be somatic manifestations of
depression or anxiety. In one study, nearly half of patients referred
for Holter monitoring to evaluate palpitations had an underlying
mental disorder, including almost 20% with panic disorder.
TABLE
17.1
DSM-IV Diagnostic Criteria for Major Depressive
Episode and Panic Disorder*
Diagnosis Criteria
Major Depressive Episode At least five of the following nine
symptoms for 2 weeks:
Depressed mood
Anhedonia
Weight loss or gain
Sleep disturbance
Psychomotor retardation or agitation
Fatigue
Guilt or sense of worthlessness
Difficulty concentrating or making
decisions
Suicidal ideation
Panic Disorder Recurrent unexpected panic attacks,
characterized by sudden intense
fear peaking within 10 minutes
and at least 4 of the following
13 symptoms:
Palpitations
Sweats
Trembling
Dyspnea
Choking
continued on page 252
1389_Ch17_250-259 2/2/09 1:29 PM Page 251
C. Dysthymia describes less intense but more chronic symptoms of
depression, including two or more symptoms of major depression
lasting at least 2 years.
D. Generalized anxiety disorder reflects chronic excessive worry that
impairs function (accompanied by restlessness, fatigue, difficulty
concentrating, irritability, muscle tension, or sleep disturbance)
without discrete panic episodes.
E. To identify or exclude bipolar disorder, patients who have depres-
sion should be asked about manic episodesperiods of excessive
elation with grandiosity, decreased need for sleep, excessive talk-
ing, flight of ideas, agitation, or uncontrolled pleasure-seeking
(sexual, financial, thrill-seeking, etc.).
F. Anxiety disorders can occur alone or can accompany a mood disorder.
G. Panic disorder symptoms are typically intense, do not have a clear
precipitant, peak in under 10 minutes, and then subside.
P A R T
TABLE
17.1
DSM-IV Diagnostic Criteria for Major Depressive
Episode and Panic Disorder* (continued)
Diagnosis Criteria
Chest pain
Nausea
Dizziness
Derealization
Fear of losing control
Fear of dying
Paresthesias
Chills/hot flushes
*For either diagnosis, symptoms must cause functional impairment and must not be due to a
medical illness or substance abuse.
Two brief case-finding questions can exclude or identify
depression: During the past month have you often been
bothered by: 1) feeling down, depressed, or hopeless? or
2) little interest or pleasure in doing things? A no to both ques-
tions makes depression unlikely. A yes to one or both should
prompt questioning about the full list of DSM-IV criteria for
depression.
1389_Ch17_250-259 2/2/09 1:29 PM Page 252
H. Patients who have mood or anxiety disorders should always be
asked about alcohol and drug use, which can cause, mimic, or
worsen symptoms.
I. It is also critical to assess suicidal ideation and risk.
J. Thyroid disorder and occasionally pheochromocytoma can
cause some similar symptoms and should be considered in
select patients.
III. Treatment
A. Choice of therapy
1. Patients diagnosed with major depressive disorder or panic
disorder should be offered psychotherapy, medication, or both.
Often the choice depends on patient preference and financial
or insurance limitations.
C H A P T E R
An alternative explanation should be sought for panic-
like symptoms that last longer than 1015 minutes.
Half of all patients who have panic disorder have agoraphobia,
or fear of being in public. All patients with panic disorder
should be asked about agoraphobia because it can be very
debilitating.
Randomized trials have proved that certain forms of
psychotherapy, particularly cognitive-behavioral therapy
and interpersonal therapy, are as effective as antidepressant
medication for mild-to-moderate major depressive disorder.
2. Psychotherapy may produce more lasting responses than
medication produces for panic disorder.
3. Medication has also proved effective, and the benefit can be
additive.
4. Patients who have more severe symptoms should receive both
medication and psychotherapy.
5. If impairment is extreme or there is an active risk of suicide or
homicide, urgent hospitalization is required.
6. Dysthymia and generalized anxiety disorder are, by definition,
more chronic conditions.
7. For some patients, symptoms respond to the medications used
for major depression and panic disorder.
1389_Ch17_250-259 2/2/09 1:29 PM Page 253
8. Certain medicationsparticularly selective serotonin reuptake
inhibitors (SSRIs)can work for all of these conditions.
9. Patients who have bipolar disorder or obsessive-compulsive
disorder should be referred to a psychiatrist for treatment.
B. Medication
1. A variety of effective medications for mood and anxiety disorders
can be used in primary care settings (Tables 17.2 and 17.3).
2. The tricyclic antidepressants (TCAs), such as imipramine,
desipramine, and nortriptyline, were the most frequently used
category several years ago.
P A R T
TABLE
Antidepressant Medication Side-Effect Profiles
Postural Sexual
Medication Sedation Hypotension Function Other
17.2
SSRIs
(citalopram,
fluoxetine,
paroxetine,
sertraline)
TCAs
(imipramine,
nortriptyline,
desipramine,
others)
Bupropion
Mirtazapine
Nefazodone
Trazodone
Venlafaxine
Key:
little to no
change
increase
decrease
Variable
(paroxetine
> fluoxetine)
(except
paroxetine
)
or
Priapism
Anxiety
early,
headaches,
GI upset,
weight
Toxic in
overdose,
mild
weight,
inexpensive
Seizure
threshold,
smoking
urge
Weight
Many drug
interactions
Mild weight
Hypertension
1389_Ch17_250-259 2/2/09 1:29 PM Page 254
3. TCAs are effective for depression, and imipramine has proved
effective for panic disorder. TCAs have the advantage of being
less expensive.
4. The choice of medication for depression is often based on side-
effect profiles, because all antidepressant medications work in
about 70% of patients who use them (see Table 17.2).
5. SSRIs as a group have fewer anticholinergic side effects (dry
mouth, orthostatic hypotension, sedation) than TCAs.
6. Although SSRIs are generally well tolerated, they can cause
gastrointestinal (GI) disturbances, headache, and sexual dysfunc-
tion. Their sedating or activating effects are not fully predictable,
but paroxetine tends to be the most sedating and fluoxetine the
most activating of the SSRIs.
7. Various other antidepressants are also available (see Table 17.2).
8. Before prescribing any antidepressant, a primary physician
should become familiar with the side-effect profiles and
contraindications.
C H A P T E R
TABLE
Common Medications for Anxiety
Medication Advantages Disadvantages
17.3
Benzodiazepines
(alprazolam,
lorazepam, clon-
azepam, others)
SSRIs
Buspirone
Immediate-acting, can
be used as needed
if addiction and
suicide risks are low
Effective long-term, low
suicide risk
Effective long-term, low
suicide risk
Sedation, potential
addiction, suicide
risk
(Anxiety early, delayed
onset of action
Delayed onset
of action
The SSRIs are now first-line medications for many
conditions because of their simplicity of dosing, relatively
fewer side effects, and lower toxicity, particularly in overdose.
Bupropion, nefazodone, and mirtazapine cause less
sexual dysfunction than SSRIs and can be good alter-
natives when patients do not tolerate SSRIs for this reason.
1389_Ch17_250-259 2/2/09 1:29 PM Page 255
9. The antidepressant medications typically require 46 weeks to
achieve their full beneficial effect.
10. SSRIs are also effective for anxiety disorders, particularly
panic disorder, although they can worsen anxiety symptoms in
the first 2 weeks.
11. When using SSRIs for panic disorder or depression accompanied
by anxiety, the lowest possible dose (10 mg of citalopram, 5 mg
of fluoxetine or paroxetine, 12.5 mg of sertraline) should be used
at the start.
P A R T
Anxiety induced by starting an SSRI can be avoided
by concurrent regular doses of a benzodiazepine for
a limited time (e.g., alprazolam 0.25 mg three times a day
for the first 14 days).
12. Benzodiazepines alone are also effective for anxiety disorders,
particularly when medication is needed only intermittently.
Because these medications are addictive and are potentially
fatal in overdose, the individual patients risk of addiction and
suicide must be weighed against the medications potential
benefit (see Table 17.3).
13. Slow-to-intermediate-onset, long-acting benzodiazepines such
as clonazepam tend to have lower addiction risk than shorter-
acting ones such as alprazolam or lorazepam. Buspirone is an
alternative long-term antianxiety treatment that takes 46
weeks to achieve its full effect.
IV. Follow-Up and Referral
A. Patients treated in primary care settings for depression and panic
disorder should be seen in follow-up soon after initiation of therapy.
They should return at least once in the first 46 weeks of therapy
sooner if their symptoms are more severeto gauge the initial
effect of medication and make any necessary adjustments.
Patients starting an SSRI, TCA, or other antidepressant
should be cautioned not to give up on a medication too
soon before it has had 46 weeks to reach its full beneficial effect.
1389_Ch17_250-259 2/2/09 1:29 PM Page 256
B. If depression or panic attacks abate with medication, treatment
should continue for at least 6 months before an attempt is made to
stop the medication.
C H A P T E R
Patients whose medication is effective should be cau-
tioned not to stop too soon because their symptoms will
return. If symptoms remain in remission for 69 months, med-
ication can be gradually tapered off.
C. If an initial antidepressant medication is not working, it is
reasonable to try switching medicines, again basing the choice
on side-effect profiles. If symptoms do not respond to two
treatment attempts, psychiatric referral is warranted. Some
patients require two or more agents simultaneously, and
psychiatrists are better equipped to manage more complex
regimens. Other indications for referral include severe or
worsening symptoms.
D. Patients who have multiple recurrences of major depression, panic
disorder, or the more chronic conditions of dysthymia and general-
ized anxiety disorder often require long-term medication to main-
tain adequate symptom control.
MENTOR TIPS DIGEST
In spite of their ubiquity, mental disorders are either missed or
not addressed in 50% of primary care patients who have them.
The greater the number of somatic symptoms, the more likely
the presence of a mental disorder35% of patients with four
or five unrelated symptoms have a mental disorder.
Two brief case-finding questions can exclude or identify
depres-sion: During the past month have you often been
bothered by: 1) feeling down, depressed, or hopeless? or
2) little interest or pleasure in doing things? A no to both ques-
tions makes depression unlikely. A yes to one or both should
prompt questioning about the full list of DSM-IV criteria for
depression.
An alternative explanation should be sought for panic-like
symptoms that last longer than 1015 minutes. Half of
patients who have panic disorder have agoraphobia, or fear
of being in public. All patients with panic disorder should be
asked about agoraphobia because it can be very debilitating.
1389_Ch17_250-259 2/2/09 1:29 PM Page 257
Resources
American Psychiatric Association. Diagnostic and statistical manual of
mental disorders, fourth edition. American Psychiatric Association,
Washington DC, 1994.
This reference defines current psychiatric diagnoses. An alternative
primary care version of the manual published in 1995 recognizes the
more somatic presentations of mental disorders in primary care settings.
Depression Guideline Panel. Depression in primary care: volume 1:
Detection and diagnosis. Clinical Practice Guideline, Number 5.
Rockville, Md. US Department of Health and Human Services,
Public Health Service, Agency for Health Care Policy and Research.
AHCPR Publication No. 93-0550. April 1993.
Depression Guideline Panel. Depression in primary care: volume 2: Treat-
ment of major depression. Clinical Practice Guideline, Number 5.
Rockville, Md. US Department of Health and Human Services, Public
Health Service, Agency for Health Care Policy and Research. AHCPR
Publication No. 93-0551. April 1993.
P A R T
Randomized trials have proved that certain forms of psy-
chotherapy, particularly cognitive-behavioral therapy and
interpersonal therapy, are as effective as antidepressant
medication for mild-to-moderate major depressive disorder.
The SSRIs are now first-line medications for many conditions
because of their simplicity of dosing, relatively fewer side
effects, and lower toxicity, particularly in overdose.
Bupropion, nefazodone, and mirtazapine cause less sexual
dysfunction than SSRIs and can be good alternatives when
patients do not tolerate SSRIs for this reason.
Anxiety induced by starting an SSRI can be avoided by
concurrent regular doses of a benzodiazepine for a limited
time (e.g., alprazolam 0.25 mg three times a day for the first
14 days).
Patients starting an SSRI, TCA, or other antidepressant should
be cautioned not to give up on a medication too soon before it
has had 46 weeks to reach its full beneficial effect.
Patients whose medication is effective should be cautioned not
to stop too soon because their symptoms will return. If symp-
toms remain in remission for 69 months, medication can be
gradually tapered off.
1389_Ch17_250-259 2/2/09 1:29 PM Page 258
These companion books established federal (Agency for Health Care
Policy and Research) clinical guidelines for the diagnosis and treatment
of depression in primary care settings.
Spitzer RL, Williams JBV, Kroenke K, et al.: PRIME MD: Primary care
evaluation of mental disorders. Pfizer, 1995.
1. How common are depression and anxiety disorders in patients seen in
primary care practice?
a. 1 in 100
b. 1 in 20
c. 1 in 5
d. More than half
2. Concerning mental illness, which is most true?
a. Most patients see psychiatrists.
b. Relatively few patients with mental disorders ever see a primary
care physician.
c. Most patients with mental illnesses are not recognized by primary
care physicians.
d. All patients with mental illness should have psychiatric referral.
3. Which mental illness diagnosis is most common in primary care
practice?
a. Obsessive-compulsive disorder
b. Bipolar disorder
c. Dysthymia
d. Major depressionBLE 17.1
C H A P T E R
1389_Ch17_250-259 2/2/09 1:29 PM Page 259
260
CHAPTER
SOMATIZATION
Gary J. Martin, MD
18
I. Pathophysiology
A. Somatization is a term that in its broadest sense applies commonly
to many people. It is a phenomenon in which unexplained or ampli-
fied physical symptoms may be related to psychological factors.
The process of somatization is commonly involved in many
difficult patients.
B. Somatoform symptoms have the following features.
1. At one end of the spectrum are ordinary patients who present
with a symptom but who appear to worry about it more or focus
on it excessively in the setting of additional stressors. These
patients are not malingering, and this is different from the rare
patient with factitious illness. However, positive reinforcement
including a sick role can be a contributing factor.
The process of somatization is very common in patients
and in milder forms may just be related to situational
stress and not major psychological problems.
2. The amplification of normal bodily processes appears to be part
of the pathophysiology. Examples of this amplification might
include heightened sensitivity to colon dilatation in patients
with irritable bowel syndrome or increased sensitivity to pain
in patients with fibromyalgia.
3. Somatic complaints may be an alternative that is more acceptable
for a patient to seek help for rather than present for the psycho-
logical stressors.
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18 SOMATIZATION 261
C H A P T E R
4. Primary care physicians gestalt about a symptom being med-
ically unexplained is quite good. Few patients with symptoms
judged to be somatoform are later found to have occult serious
physical disorders at follow-up.
5. Childhood illness or illnesses in the family and abuse can also
be contributing factors. Family, cultural, and religious norms
for expressing pain or emotion may be issues. Major loss and
inner conflicts can contribute.
C. Somatoform disorders
1. Somatoform disorder is a much more restrictive term (versus
somatoform symptom) that applies to a much smaller number
of patients at one end of the spectrum. Only focusing on the
uncommon somatoform disorder misses the much larger impor-
tant group of patients with an element of somatization who have
functional impairment, psychiatric comorbidity, difficult doctor-
patient relationships, and increased health-care utilization.
II. Signs and Symptoms
A. Box 18.1 lists verbal and nonverbal clues that should attract the
clinicians attention and raise the possibility of somatization as a
contributing factor. Many times, patients with somatization are dif-
ficult historians. They may be vague and tangential in their answers.
B. These patients may have a positive review of systems, have
dramatic descriptions of their symptoms, may have seen multiple
doctors already for their symptoms, and may have failed many
therapeutic trials.
C. None of the features in Box 18.1 makes a diagnosis of somatization,
but they should raise the clinicians suspicions and lead to additional
explorations of the possibility of a psychological component to the
patients problems.
D. Many times these patients will appear more preoccupied with their
symptoms than the clinician would expect.
E. At the far end of the spectrum, patients may have seen multiple
specialists or had multiple surgeries or be on disability for their
problems.
A somatoform symptom can be defined as a symptom
that does not have an adequate (based on the physi-
cians clinical judgment) physical explanation to explain its
severity and associated disability.
1389_Ch18_260-268 2/2/09 1:29 PM Page 261
P A R T
III. History and Physical Examination
A. Box 18.2 lists questions that are particularly helpful in eliciting
additional useful information in the setting of possible somatization.
1. Past medical history including previous physicians evaluations
and family history can be useful.
2. Social history is particularly helpful, including how patients
spend their day, who they live with, and how things are going
at work and home.
3. Patients who have a relative short history of symptoms may be
more open to the possibility of psychological contributions. For
these patients, more direct questions about psychosocial stressors
can be effective.
4. For patients who have a more chronic presentation and may
have already seen other providers for their problems, many of
these questions are worked into the social history. This gives
patients the perception that they are not being targeted, that the
information is a routine part of the social history. For example,
BOX
Verbal and Nonverbal Clues of Somatoform Symptoms
Verbal
Vague history
Multiple prior physicians
Multiple prior surgeries
Multiple allergies
Positive review of systems
Dramatic, emotionally charged description of symptoms
Excessive research or paper recordings by patient (some of this is
commonly done in the current Internet-connected society)
Patients concern out of proportion to what you would expect
Patients concern much less than what you would expect
Nonverbal
Poor eye contact
Sighing
Depressed or anxious affect
Who comes with patient to visit
Inconsistent examination
18.1
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18 SOMATIZATION 263
C H A P T E R
What do you do for a living? Do you smoke? Drink?
How are things at work? Who do you live with? can all be a
routine part of the social history.
5. Time correlations can be helpful. For example, do the patients
symptoms disappear when the patient is on vacation or on
weekends? Is there some correlation with a major event like the
death of a family member; anniversary of an event?
IV. Differential Diagnosis
A. The process of somatization can occur in many different psychi-
atric diseases, including major affective disorders such as depres-
sion, panic disorder, and even schizophrenia and dementia.
B. At times, patients may be diagnosed with a specific psychiatric
condition. For example, a patient might meet the criteria for
depression or panic attacks. Disturbed sleep and loss of enjoyment
are the two most sensitive questions for detecting depression.
C. Box 18.3 lists the diagnostic criteria for somatoform disorders. Many
patients, however, will not be this severe or as well differentiated.
D. The broad collection of patients with unexplained somatic symp-
toms is quite common and may represent up to 30% to 50% of
BOX
18.2
Useful Questions for Patients With Suspected
Somatoform Symptoms
1. What is going on at home?
2. What new things are coming up in your life?
3. What are you concerned may be the problem?
4. How is this affecting your life?
5. Would you walk me through a typical day?
6. How were things in your family when you were growing up?
7. If there is a window of opportunity: Things were pretty bad then
(pause)
8. Are there any experiences that you havent discussed yet that were
difficult?
9. It is not uncommon for people to be emotionally, sexually, or physically
victimized at some time in their life. Has this ever happened to you?
10. How do you spend your spare time?
11. How do you keep busy?
12. Anniversary dates (for major loss)?
1389_Ch18_260-268 2/2/09 1:29 PM Page 263
P A R T
BOX
Diagnostic Criteria for Somatization Disorder
A history of many physical complaints beginning before age 30 that occur
over a period of several years and that result in treatment being sought or
significant impairment in social, occupational, or other important areas of
functioning.
Each of the following criteria must be met, with individual symptoms
occurring at any time during the course of the disturbance:
Four pain symptoms: a history of pain related to at least four different sites
or functions (e.g., head, abdomen, back, joints, extremities, chest, rectum,
during menstruation, during sexual intercourse, or during urination)
Two gastrointestinal symptoms: a history of at least two gastrointestinal
symptoms other than pain (e.g., nausea, bloating, vomiting other than
during pregnancy, diarrhea, or intolerance of several different foods)
One sexual symptom: a history of at least one sexual or reproductive
symptom other than pain (e.g., sexual indifference, erectile or ejaculatory
dysfunction, irregular menses, excessive menstrual bleeding, vomiting
throughout pregnancy)
One pseudo-neurologic symptom: a history of at least one symptom or
deficit suggesting a neurologic condition not limited to pain (conversion
symptoms such as impaired coordination or balance, paralysis or localized
weakness, difficulty swallowing or lump in throat, aphonia, urinary reten-
tion, hallucinations, loss of touch or pain sensation, double vision, blind-
ness, deafness, seizures, dissociative symptoms such as amnesia, or loss
of consciousness other than fainting)
Either of the following:
After appropriate investigation, none of the symptoms can be fully
explained by a known general medical condition or the direct effects of
a substance (e.g., a drug of abuse, a medication).
When there is a related general medical condition, the physical complaints
or resulting social or occupational impairment are in excess of what
would be expected from the history, physical examination, or laboratory
findings.
The symptoms are not intentionally produced or feigned (as in Factitious
Disorder or Malingering).
Adapted from American Psychiatric Association. Task Force on DSM-IV. Diagnostic
and Statistical Manual of Mental Disorders, 4th ed. Text Revision (DSM-IV-TR).
Washington, DC: American Psychiatric Association, 2000.
18.3
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18 SOMATIZATION 265
C H A P T E R
physician encounters in the primary care setting. It is by no means
limited to primary care, and every specialty has examples of this
problem. Milder cases occur that do not meet the DSM criteria but
that do have significant impairment, difficult relationships, and
increased utilization. These can be suspected when patients have 3
somatoform symptoms (as defined before) from a list of 15 symp-
toms: stomach pain, back pain, headache, chest pain, dizziness,
faintness, palpitations, shortness of breath, bowel complaints
(constipation or diarrhea), dyspeptic symptoms (nausea, gas, or
indigestion), fatigue, trouble sleeping, pain in the joints or limbs,
menstrual pain or problems, and pain or problems during sexual
intercourse.
E. Occasionally patients with certain personality traits and personality
disorders may present with somatic complaints.
V. Laboratory Evaluations
A. As a general rule, laboratory evaluations are best used sparingly in
this patient population.
B. Classic biomedical diseases can appear in these patients; be care-
ful not to reinforce the sick role, and avoid testing that leads to
false positives and increased anxiety.
C. Questionnaires that screen for anxiety disorders and depression
can be used in the office for a subset of these patients, and
more formal psychometric testing may be indicated in a small
subset.
VI. Management
A. Physicians have learned over the years that relatively frequent
visits with follow-up are most helpful for patients with chronic
somatization.
1. Visits may need to be as frequent as a week apart initially. This
is preferable to having a 3-month return visit scheduled, only to
have the patient present to the emergency room or call in the
middle of the night with additional symptoms.
Although these patients are not malingering, some of
them have noted that a symptom is a ticket for an
office visit and by scheduling frequent visits a patient does
not need to focus on other problems in order to be able to
see the physician.
1389_Ch18_260-268 2/2/09 1:29 PM Page 265
P A R T
2. Patients responses to reassurance vary.
a. Positive response:
i. An explanation about the autonomic nervous system and
how functional disorders can cause symptoms can be helpful
to some patients. The clinician does not dismiss the problem
but can explain it as a heightened sensitivity to bodily
sensations.
b. Negative response:
A subset of patients can benefit from reassurance
and explanation.
There is, however, a subset of patients, particularly
those with a more chronic presentation, who will
respond negatively to reassurance, particularly if given
prematurely. These patients need a different approach.
i. These patients need to understand that you are going to
evaluate their problems thoroughly and thoughtfully and
without prejudice.
ii. Typically, after several visits, some rapport will be devel-
oped with such patients.
iii. Two related approaches can then be tried.
(1) Some psychiatrists recommend offering the patient
help with coping with their illness. For example, the
patient presents with, e.g., chronic abdominal pain,
and in the course of several visits the physician
determines that the problem is associated with a
great deal of distress in the patients life, which is
interfering with social activities and work. The
physician at that point can recommend that the
patient return soon again to continue to evaluate the
disorder. The physician would also like the patient to
get help coping with the distress that the problem is
causing. The key here is that you are not trying to
make the point that stress is causing the problem but
that the problem is associated with a great deal of dis-
ruption in the patients life. Many patients are willing
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18 SOMATIZATION 267
C H A P T E R
to accept seeing a psychiatrist or other mental health
worker under those circumstances, particularly if
they do not believe that the primary care clinician is
dismissing them.
(2) The other approach is that, in the course of several
visits and collecting psychosocial information, the
clinician may identify the presenting problem but
notes that the patient may also have some stress, not
drawing any particular relationship between the two.
Occasionally, some patients are willing to see a men-
tal health worker for help with the stress in their life
without any attempt on the physicians part to link
their somatic complaints to their stress. This is partic-
ularly likely to happen if the physician keeps close
follow-up on the presenting problem so the patient
does not feel dismissed.
iv. Many patients over time resolve their somatic problems
or greatly minimize them if they are able to connect with
a mental health worker using either of the two preceding
approaches.
v. Going forward, one of several paths may be best, depend-
ing on the individual patient:
(1) Some patients have a specific diagnosis (for example,
depression, panic attacks, or generalized anxiety dis-
order), and a therapeutic trial can be instituted.
(2) Cognitive behavioral therapy may be an option for
some patients.
(3) Thorough primary care may continue to be the best
option.
For the rare true somatoform disorder patient,
a long-term relationship with a caring physician,
including frequent office visits and physical exami-
nations, can be the most cost-effective solution.
(4) The preceding options are preferable to referring the
patient to multiple different specialists, all of whom
may generate tests and false positives and reinforce a
sick role or precipitate complications from down-
stream testing.
1389_Ch18_260-268 2/2/09 1:29 PM Page 267
P A R T
Resources
American Psychiatric Association. Task Force on DSM-IV. Diagnostic
and Statistical Manual of Mental Disorders, 4th ed, Text Revision (DSM-
IV-TR). Washington, DC: American Psychiatric Association, 2000.
Goldberg RJ, Novack DH, Gask L. The recognition and management of
somatization: What is needed in primary care training. Psychosomatics
1992;3: 5561.
Very useful management strategies.
Kroenke K, Spitzer RL, DeGruy FV, et al. A symptom checklist to screen for
somatoform disorders in primary care. Psychosomatics 1998;39:263272.
Useful checklist of symptoms for the more common, less advanced patient.
MENTOR TIPS DIGEST
The process of somatization is commonly involved in many
difficult patients.
The process of somatization is very common in patients and
in milder forms may just be related to situational stress and
not major psychological problems.
A somatoform symptom can be defined as a symptom that
does not have an adequate (based on the physicians clinical
judgment) physical explanation to explain its severity and
associated disability.
Although these patients are not malingering, some of them
have noted that a symptom is a ticket for an office visit and
by scheduling frequent visits a patient does not need to focus
on other problems in order to be able to see the physician.
A subset of patients can benefit from reassurance and explanation.
There are, however, a subset of patients, particularly those
with a more chronic presentation, that will respond negatively to
reassurance, particularly if done prematurely. These patients
need a different approach. (Discussed in text.)
For the rare true somatoform disorder patient, a long-term rela-
tionship with a caring physician, including frequent office visits and
physical examinations, can be the most cost-effective solution.
See the testbank CD for self-test questions.
1389_Ch18_260-268 2/2/09 1:29 PM Page 268
DIAGNOSIS
AND MANAGEMENT
OF COMMON
CHRONIC ILLNESSES
DIAGNOSIS
AND MANAGEMENT
OF COMMON
CHRONIC ILLNESSES
269
three
P A R T
I. Overview
A. In the past decade, congestive heart failure (CHF) has become
much more prominent. There is greater appreciation of its
significance in terms of frequency (particularly with aging of
population) and potential severity (given that its 5-year survival
can be worse than that of many malignancies).
B. CHF has become one of the most frequent reasons for admission
to the hospital, and major disease management programs have been
developed to optimize outpatient care to minimize admissions.
CONGESTIVE HEART
FAILURE
Gary J. Martin, MD
CHAPTER
19
1389_Ch19_269-277 2/2/09 1:29 PM Page 269
270 three DIAGNOSIS AND MANAGEMENT OF COMMON CHRONIC ILLNESSES
P A R T
C. Another underappreciated point is that more than half of deaths
related to heart failure come from asymptomatic patients suffering
sudden cardiac death.
D. This highlights the need for earlier diagnosis and treatment.
Fortunately, in the past few years, there has been a growing num-
ber of carefully done randomized trials to provide better data for
treatment of this disease.
II. Approach to CHF Patient
A. Diagnosis of CHF is made based on a constellation of signs and
symptoms, including dyspnea on exertion, fatigue, jugular venous
distention, inspiratory rales, a third heart sound, hepatojugular
reflux, and edema.
1. Initial imaging and laboratory tests
a. Chest x-ray evidence of pulmonary congestion or increased
heart size is often helpful.
b. Electrocardiogram may give clues to etiology, showing
Q waves, left ventricular hypertrophy (LVH), or left bundle
branch block.
B. Two key questions must be asked for every CHF patient.
Always ask yourself: (1) What is the underlying cause of
the patients CHF? and (2) What precipitated the current
exacerbation?
1. Understanding underlying cause (Box 19.1) can be very important
in terms of treatment. Coronary artery disease and hypertension
are the most common causes of underlying CHF. Also important
are identifying and treating less common etiologies such as
valvular heart disease or pericardial disease. Symptomatic
treatment of CHF alone is not appropriate.
BOX
19.1
What Is Underlying Cause of Patients CHF?
Hypertension
Coronary artery disease
Valvular heart disease
Cardiomyopathy
Pericardial disease
1389_Ch19_269-277 2/2/09 1:29 PM Page 270
2. Box 19.2 lists common causes for exacerbation of CHF.
Attention to these can help minimize future exacerbations.
3. Box 19.3 lists clues in the history and physical examination
that can be particularly helpful with regard to these two key
questions.
4. The single most useful diagnostic test for patients with CHF is
the echocardiogram. In general, almost all patients warrant at
least one echocardiogram in the evaluation of their condition.
An echocardiogram can help sort out systolic from diastolic
dysfunction, which has major ramifications for treatment. It
can help identify underlying etiology, particularly wall-motion
abnormalities suggestive of coronary disease and valvular
abnormalities that may not always be detected by auscultation.
III. Management
A. Management can be divided into two broad categories.
1. General treatment to be considered for all patients with CHF
2. Etiology-specific treatment
B. Box 19.4 lists the most validated treatments for CHF.
19 CONGESTIVE HEART FAILURE 271
C H A P T E R
BOX
19.2
Common Causes of CHF Exacerbation
Factors That Increase Demand on Heart
Increased salt intake or physical activity
Infection, surgery, fluid therapy, transfusions
Pulmonary embolism
Anemia
Hyperthyroidism
Salt- and water-retaining medications (e.g., nonsteroidal anti-inflammatory
drugs, steroids)
Pregnancy
Factors That Decrease Cardiac Output
Discontinuation of medications (digoxin, angiotensin-converting enzyme
inhibitor [ACEI])
Arrhythmia (e.g., atrial fibrillation, heart block)
Myocarditis or infarction
Toxic substances (e.g., ethyl alcohol [ETOH])
Thiamine deficiency
1389_Ch19_269-277 2/2/09 1:29 PM Page 271
C. General treatment guidelines follow.
1. Diuretics can be the mainstay of symptomatic treatment by
relieving pulmonary congestion and edema, particularly when
the patient first presents.
2. Digoxin has proved to be helpful in symptomatic patients in
reducing both symptoms and hospitalizations, which have no
overall effect on mortality. For asymptomatic patients with
systolic dysfunction it is probably not beneficial.
3. ACEIs have become a mainstay in treatment of CHF because
of their proven value in reducing symptoms and improving
survival. Mortality benefits of over 20% have been well
P A R T
BOX
19.3
Important Clues About CHF in History and Physical
Examination
These clues can help you answer the two key questions:
(1) What is the underlying cause of this patients CHF (2) What precipi-
tated the current exacerbation?
History of angina or myocardial infarction
History of rheumatic fever, or a recent flu-like illness
History of TB, malignancy (pericardial disease)
Recent pregnancy
Family history of CHF
Dietary indiscretion, lapses in medication, or use of new salt-retaining
medications
Evidence of valvular heart on examination (especially aortic or mitral
stenosis or regurgitation)
Displaced point of maximum impulse (PMI) suggesting a dilated heart
BOX
19.4
Most Validated CHF Treatments
ACEIs
Beta blockers
Aldosterone antagonists
Revascularization for selected patients with coronary artery disease (CAD)
Implantable defibrillator and cardiac resynchronization in selected patients
1389_Ch19_269-277 2/2/09 1:29 PM Page 272
documented. Aspirin may blunt some of the benefit of ACEI
via effect on kinins and probably should be reserved only for
patients with known CAD. In long-term trials, ACEI benefits
extend to even asymptomatic patients with ejection fractions
lower than 40%. Whether angiotension receptor blockers
(ARBs) are equally efficacious is somewhat controversial, but
they are a reasonable substitute for the patient who cannot
tolerate ACEI. Data suggest ARBs may have additive benefit on
top of ACEIs. Hydralazine and nitrates may also have additive
benefit in the African-American population.
4. In recent years use of beta blockers has emerged. In the past
these drugs were avoided in patients with CHF because of their
negative inotropic effect, but they have been shown to help stop
the downhill spiral of CHF pathophysiology involving elevated
levels of catecholamines and increased afterload. In this setting,
these drugs must be introduced cautiously at doses 5%10%
of ultimate target dose to which they will be titrated. They are
initiated when the patient is otherwise optimized and compen-
sated. The majority of data exist for use of metoprolol and
carvedilol in this setting. Surprisingly for both ACEIs and beta
blockers, ejection fraction may significantly improve over time
after these drugs have been instituted. Mortality benefits of beta
blockers may also be related to their potential effect at raising
the threshold for ventricular fibrillation and preventing sudden
cardiac death.
5. Spironolactone has recently been added to the multidrug approach
to CHF patients. A large randomized trial showed that, in addi-
tion to standard therapy, the drug was able to further reduce
mortality by approximately 27%. A dose of 25 mg per day was
used in this study (RALES study). The mechanism of this bene-
fit is probably less related to its effect on potassium and sodium
excretion and more related to decreasing progressive fibrosis.
C H A P T E R
ACEIs, beta blockers, and spironolactone have been
documented to improve mortality in patients with CHF.
6. Salt restriction, using a no-salt-added diet, is a useful adjunct to
treatment.
1389_Ch19_269-277 2/2/09 1:29 PM Page 273
7. Cardiac rehabilitation including a carefully tailored exercise
program may also benefit CHF patients.
8. If the patient has atrial fibrillation, cardioversion should ideally
be considered, but if this is not possible, rate control and efforts
to prevent embolic disease are important. Rate response in atrial
fibrillation may appear to be controlled at rest but frequently is
poorly controlled with exercise when digoxin alone is used.
Beta blockers or alternatively low doses of verapamil and dilti-
azem may be necessary to control heart rate to a reasonable
level with activity. Warfarin is of proven value in decreasing
cardioembolic events in patients with atrial fibrillation, particu-
larly in the setting of CHF. Aspirin at 325 mg per day may be
an acceptable alternative of lesser value in patients who cannot
take warfarin safely. Tachycardia can contribute to systolic
dysfunction, and ejection fraction can improve dramatically
over time with cardioversion.
D. Disease-specific treatment guidelines follow.
1. If a patient is found to have CAD contributing to CHF, some
type of stratification of risk is appropriate, utilizing treadmill
testing with or without additional imaging such as stress echo or
perfusion studies including magnetic resonance imaging (MRI)
techniques. Pharmacologic stress testing with adenosine or
dobutamine may also be necessary. These studies can help select
which patients would benefit most from angiography, although
some clinicians would recommend angiography in all patients
with CHF when CAD is suspected as a significant contributor.
2. Nitrates and beta blockers are useful in most patients with
symptomatic coronary disease.
3. Aspirin is generally indicated in all such patients too, although
aspirin may partially reduce the benefits of ACEIs through its
effect on kinins. Therefore, aspirin should be limited to patients
with CAD or some patients with atrial fibrillation in the setting
of CHF.
4. Aggressive lipid therapy has been documented to have major
benefits in the setting of CAD (see also Chapter 24). Of course,
other risk factor modifications, including cessation of smoking,
can be critical success factors in these patients.
P A R T
1389_Ch19_269-277 2/2/09 1:29 PM Page 274
5. Optimal control of hypertension can frequently benefit patients
with CHF and even lead to some reversal of left ventricular
hypertrophy (LVH) and diastolic dysfunction.
6. When valvular heart disease contributes to CHF, an experienced
cardiologist can be particularly helpful. Mild-to-moderate mitral
regurgitation can often be secondary to left ventricular dilatation
and may not be the primary problem in some patients. Timing
of valve surgery is a difficult decision, although in general
patients with symptoms of CHF related to their valve problem
should be considered for surgery. Increasing skill with repair
of regurgitant valves has lowered the threshold for surgical
intervention in some patients as compared with replacement
with prosthetic devices. Endocarditis prophylaxis must also
always be remembered in this patient population.
7. With regard to cardiomyopathies, addressing underlying
etiology may be helpful. Many patients with alcohol-induced
cardiomyopathy benefit from alcohol abstinence. In patients
with active myocarditis, selected patients may benefit from
aggressive anti-inflammatory therapy anecdotally, although
this has been difficult to demonstrate in controlled trials. For
patients with end-stage heart failure, heart transplantation
remains a potentially life-saving intervention in appropriately
selected patients.
8. For patients with advanced ventricular arrhythmias, particularly
those with symptoms, treatment with implantable defibrillator
or carefully chosen antiarrhythmic therapy such as amiodarone
may also be beneficial. Cardiac resynchronization therapy
can also help symptoms and survival in certain subsets of
patients.
C H A P T E R
MENTOR TIPS DIGEST
Always ask yourself: (1) What is the underlying cause of
the patients CHF? and (2) What precipitated the current
exacerbation?
ACEIs, beta blockers, and spironolactone have been docu-
mented to improve mortality in patients with CHF.
1389_Ch19_269-277 2/2/09 1:29 PM Page 275
Resources
American College of Cardiology Foundation, American Heart Association.
Diagnosis and management of chronic heart failure in the adult [booklet].
Bristow MR, Saxon LA, Boehmer J, et al. Cardiac-resynchronization
therapy with or without an implantable defibrillator in advanced chronic
heart failure. New England Journal of Medicine 350:21402150, 2004.
Kadish A, Dyer A, Daubert JP, et al. Prophylactic defibrillator implantation
in patients with nonischemic dilated cardiomyopathy. New England
Journal of Medicine 350:21512158, 2004
1. What is the most frequently occurring proximate cause of death in
persons with heart failure?
a. Lethal arrhythmia
b. Embolic stroke
c. Pulmonary edema
d. End-stage kidney disease
2. Heart failure often causes which of these electrocardiogram
abnormalities?
a. High peaked T waves
b. Mobitz type 1 second-degree AV block
c. Mobitz type 2 second-degree heart block
d. Left bundle branch block
3. A 74-year-old woman has long-standing hypertension that is well
controlled with nifedipine. She complains of gradual onset difficulty
breathing when lying flat in bed. She notes ankle swelling in the
morning. On examination, pulse is 90 and regular; blood pressure is
120/70. There are crackles only in the lung bases and a third heart
sound. Electrocardiogram shows regular sinus rhythm, left ventricular
P A R T
1389_Ch19_269-277 2/2/09 1:29 PM Page 276
hypertrophy, and no ischemic changes. Serum electrolytes and creati-
nine levels are normal. What is the initial most appropriate next step?
a. Begin digoxin 0.125 mg daily, and observe over a few weeks.
b. Begin furosemide 20 mg daily, and observe over a few weeks.
c. Discontinue nifedipine, and observe over a few weeks.
d. Order transthoracic echocardiogram.
C H A P T E R
1389_Ch19_269-277 2/2/09 1:29 PM Page 277
278
HYPERTENSION
David B. Neely, MD
CHAPTER
20
I. Overview
A. Hypertension (HTN) is common.
Approximately 26% of adults in the United States have
HTN.
A reduction of 5 mm Hg diastolic blood pressure (DBP) is
associated with a 35%40% decreased incidence of stroke.
B. Unfortunately, fewer than 50% of these patients have their blood
pressure (BP) controlled adequately.
C. HTN is a risk factor for coronary heart disease (CHD), stroke, re-
nal insufficiency, renal failure, and other types of vascular disease.
II. Benefits of Treatment
A. Stroke risk reduction
1. The benefits occur quickly; therefore, there is no upper age
limit for treatment.
B. CHD amelioration
1. In the last 50 years, cardiovascular mortality has decreased
significantly, in part secondary to better control of HTN.
2. The risk of myocardial infarction (MI) is reduced 20%25%
with 5 mm Hg reduction in DBP.
C. Decrease in other risks
The risks of heart failure and renal disease are clearly re-
duced with lower BP; however, the major mortality benefits
of BP treatment depend on the reduction of CHD and stroke.
1389_Ch20_278-293 2/2/09 1:28 PM Page 278
III. Definition
A. The definition of HTN is systolic BP (SBP) greater than 140 and
diastolic BP (DBP) greater than 90.
20 HYPERTENSION 279
C H A P T E R
1. The risk of CHD doubles with each increment of 20/10 above
this goal.
B. Patients should be treated to a goal less than 140/90; patients with
diabetes or renal disease should be treated to a goal of less than
130/80.
IV. Etiology
A. First distinction: primary (essential) HTN versus secondary HTN.
The Joint National Committee (JNC) on Prevention, Detec-
tion, Evaluation, and Treatment of High Blood Pressure
has released a new classification scheme for HTN (Table 20.1).
Management is determined by the highest category, either
systolic or diastolic.
According to the JNC, 115/75 is the optimal BP as defined
as the BP that predicts the longest life.
95% of patients with high BP have primary HTN.
TABLE
20.1
BP Classification Scheme
BP Classification SBP DBP
Normal 120 80
Prehypertension 120139 8089
Stage I 140159 9099
Stage II 160 100
B. 5% of patients with high BP may have secondary HTN.
1. The incidence of a secondary cause of HTN may be increased in:
a. Patients younger than 35 without a family history of HTN.
1389_Ch20_278-293 2/2/09 1:28 PM Page 279
b. Patients whose HTN has a sudden onset or is severely
elevated.
c. Patients whose HTN is resistant to three medications, one of
which is a diuretic.
2. Secondary causes:
a. Parenchymal renal disease
P A R T
i. This occurs in about 3% of all patients with hypertension
and is easily ruled out by a serum creatinine.
b. Renovascular HTN is next most common form
i. Fibromuscular dysplasia is common in young women.
ii. Atherosclerotic renovascular disease is often found in older
patients with significant cardiovascular disease (CVD).
c. Primary hyperaldosteronism
i. Classically the patient has a low potassium level (3.5),
although in many patients the potassium could be at a
low normal level.
ii. The most common cause is bilateral adrenal hyperplasia.
iii. Primary hyperaldosteronism is treated medically.
iv. Plasma renin activity (PRA) and plasma aldosterone
activity (PAC) and the ratio of PRA to PAC can be a
helpful diagnostic screening test.
d. Pheochromocytoma
i. This is rare.
ii. The patient classically has paroxysm of HTN, sweats,
and palpitations.
iii. However, over half of patients with pheochromocytoma
present with a steady elevation of BP.
iv. A 24-hour urine collection for metanephrines is a simple
screen.
e. Cushing disease
i. This is a rare cause of secondary HTN.
ii. Patients classically are obese with stria.
iii. A 24-hour urine collection for cortisol is a good screen.
f. Sleep apnea newly recognized cause of secondary HTN
i. Patients are often obese with daytime somnolence.
The most common cause of secondary HTN is
parenchymal renal disease.
1389_Ch20_278-293 2/2/09 1:28 PM Page 280
V. BP Measurement
A. BP can easily fluctuate 1020 mm Hg throughout the day; the
higher the BP, the greater the fluctuation.
1. The BP readings of the nurse, student, and attending physician
may vary.
B. Accurate BP measurement is key.
1. The patient should be seated quietly for at least 5 minutes.
2. The patients feet should be flat on the floor, and the arm
should be supported at the level of the heart.
3. An appropriately-sized cuff should be used.
20 HYPERTENSION 281
C H A P T E R
The most frequent mistake in BP measurement is using
a cuff that is too small.
4. Two measurements should be made after the preceding
conditions are met.
VI. Evaluation
A. Initial evaluation of patient with HTN should focus on three factors
1. Other cardiovascular risk factors that will influence the prognosis
2. Evidence of target organ damage that will influence the urgency
of treatment and the target BP
3. Causes for secondary HTN, which are relatively rare but impor-
tant to discover
B. History
1. History is primarily focused on assessing risk for acquiring CHD
a. Personal history of diabetes
b. Family history of HTN, CHD, stroke, renal disease
c. Lifestyleexercise, cigarette smoking, alcohol, diet, illicit drugs
1. The physical examination should focus on the heart, lungs,
pulses, abdominal bruits, presence of peripheral edema, and a
funduscopic examination looking for evidence of target organ
damage and searching for clues to secondary causes.
D. Laboratory examination
1. Electrolytes, blood urea nitrogen (BUN), creatinine (Cr),
urinalysis
2. Lipid panel, glucose
3. Electrocardiogram (ECG)
1389_Ch20_278-293 2/2/09 1:28 PM Page 281
VII. Patients to Treat
A. It is helpful to consider HTN as a risk factor for CVD rather than
a disease in itself.
P A R T
Left ventricular hypertrophy
(ECG, echocardiogram,
or radiogram)
Proteinuria and/or slight
elevation of plasma
creatinine in concentra-
tion (1.22.0 mg/dL)
Ultrasound or radiologic
evidence of atheroscle-
rotic plaque (carotid,
iliac, and femoral
arteries; aorta)
Generalized or focal nar-
rowing of retinal arteries
Cerebrovascular
disease
Ischemic stroke
Cerebral
hemorrhage
Transient ischemic
attack
MI
Angina
Coronary
revascularization
Congestive heart
failure (CHF)
TABLE
20.2
Factors Influencing Prognosis in Hypertension
Risk Factors for
CVDs Used for Risk Associated
Stratification Target Organ Damage Clinical Conditions
High levels of SBP
and DBP
Men 55 years
Women 85 years
Smoking
Total cholesterol
65 mmol/L
(250 mg/dL)
Diabetes
Family history of
premature CVD
The decision about BP treatment should not be deter-
mined solely by the level of BP.
1. See Tables 20.2 and 20.3.
B. Age: the risks of CHD and stroke increase markedly with age.
The absolute benefits of HTN treatment increase with age.
C. Sex: CHD risk is 23 times higher in men than women.
D. Diabetes: Diabetes triples the risk of CHD and stroke.
E. Smoking: Smoking doubles the risk of heart disease.
F. Lipids: High cholesterol is a major risk for CHD; as cholesterol
rises, the need to treat blood pressure rises.
G. Pre-existing vascular disease in self or family increases the
patients risk of CHD.
1389_Ch20_278-293 2/2/09 1:28 PM Page 282
VIII. Nonpharmacologic Treatment (Table 20.4)
A. Dietary Approaches to Stop Hypertension (DASH) diet
1. This is a diet rich in fruits, vegetables, and whole grains.
2. All patients with prehypertension, stages I and II, should be
prescribed the DASH diet.
20 HYPERTENSION 283
C H A P T E R
Grade 1
(Mild hypertension)
SBP 140159 or
DBP 9099
Low risk
Medium risk
High risk
Very high risk
Medium risk
High risk
Very high risk
High risk
Very high risk
Very high risk
Very high risk
Grade 2
(Moderate
hypertension)
SBP 160179 or
DBP 100109
Medium risk
Grade 3
(Severe
hypertension)
SBP 180 or
DBP 110
TABLE
20.3
Stratification of Risk to Quantify Prognosis
BP (mm Hg)
Other risk
factors
and disease
history
No other
risk factors
12 risk
factors
3 or more
risk factors
or target
organ
damage or
diabetes
Associated
clinical con-
ditions (see
Table 20-2
An otherwise healthy patient with a BP of 185/115 has a similar CV risk as a patient with
diabetes and a BP of 145/95. A young patient without other risk factors with a BP of 150/95
can be managed without medicine for months, even years. A patient with a BP of 150/95
and a previous MI probably needs prompt pharmacologic treatment.
DASH diet compliance can lower BP as much as
814 mm Hg.
1389_Ch20_278-293 2/2/09 1:28 PM Page 283
B. Weight reduction
1. A loss of only 10 kg may reduce BP 520 mm Hg.
2. It is difficult for patients to lose weight; however, weight loss
should be encouraged.
C. Sodium restriction
1. Limiting salt intake to 4 g or less will reduce BP 28 mm Hg.
a. This may be higher in patients who are black, obese, or elderly.
b. There may be no benefit to salt reduction in about half of all
patients.
2. The average American consumes about 10 g of sodium per day.
P A R T
TABLE
20.4
Lifestyle Modifications to Manage HTN
Approximate SBP
Modification Recommendation Reduction, Range
Weight
reduction
Adopt DASH
eating plan
Dietary sodium,
reduction
Physical activity
Moderation of
alcohol
consumption
520 mm Hg/10-kg
weight loss
814 mm Hg
28 mm Hg
49 mm Hg
24 mm Hg
Maintain normal body weight
(BMI, 18.524.9)
Consume a diet rich in fruits,
vegetables, and low-fat
dairy products, with a
reduced content of
saturated and total fat
Reduce dietary sodium intake
to no more than 100 mEq/L
(2.4 g sodium or 6 g sodium
chloride)
Engage in regular aerobic
physical activity such as
brisk walking (at least
30 minutes per day, most
days of the week)
Limit consumption to no more
than two drinks per day
(1 oz or 30 mL ethanol [e.g.,
24 oz beer, 10 oz wine, or
3 oz 90-proof whiskey]) for
most men and no more than
one drink per day for women
and lighter-weight persons
1389_Ch20_278-293 2/2/09 1:28 PM Page 284
D. Exercise
1. Aerobic exercise lasting 30 minutes 3 times a week can lower
blood pressure by 49 mm Hg.
E. Alcohol moderation
1. Male patients should limit their alcohol intake to two drinks
per day or fewer.
2. Female patients should limit their alcohol intake to one drink
per day or fewer.
3. Limiting alcohol intake to these levels can lower BP by
24 mm Hg.
F. Tobacco cessation
20 HYPERTENSION 285
C H A P T E R
Smoking cigarettes is the most important modifiable risk
factor to prevent CHD.
Use a thiazide diuretic, beta blocker, or angiotensin-
converting enzyme inhibitor (ACEI) as first-line therapy.
1. Smoking cessation does not affect HTN itself very much
(BP drops by only 12 mm Hg), but it is still very important
because of the many other ways that it reduces disease risk.
IX. General Principles of Drug Treatment
A. Drug types
1. These drugs have been shown to reduce mortality rates in large
randomized studies.
2. They are inexpensive.
B. Monotherapy
1. Begin with low doses of the drug.
2. If no or minimal BP lowering is not achieved, consider chang-
ing to another drug class.
Monotherapy is effective in 70% of patients.
Stage II HTN generally requires two BP medications.
1389_Ch20_278-293 2/2/09 1:28 PM Page 285
C. Side effects
1. Doubling the initial dose will double the incidence of side
effects without necessarily doubling the BP-lowering effects.
P A R T
Physicians routinely underestimate the side effects
and overestimate the benefits of interventions.
a. When physicians were asked how many of their patients had
side effects from their BP medications, they indicated 10%.
b. When patients were asked the same question, they
indicated 50%.
D. Cost of drugs (Table 20.5)
E. Renin and HTN
1. Elderly and black patients tend to have low renin HTN.
a. Diuretics (D) and dihydropyridine calcium channel blockers
(C) tend to work better in low renin HTN.
2. Young and white patients tend to have high renin HTN.
a. Beta blockers (B) and ACEIs (A) tend to work better in high
renin HTN.
3. Measuring a patients renin level has not been shown to be
clinically helpful; however, the above guidelines are often
helpful in initiating therapy.
a. Use an A or B drug in young or white patients.
b. Use a C or D drug in elderly or black patients.
F. Be aware of the major advantages and disadvantages of the major
drugs (Table 20.6).
X. Medications
A. Diuretics
1. Diuretics are inexpensive, effective, and well tolerated in low
doses.
TABLE
20.5
Cost of HTN Drugs
Drug Cost
Diuretics $5/month
Beta blockers $10/month
ACE inhibitors $40/month
Calcium channel blockers $70/month
1389_Ch20_278-293 2/2/09 1:28 PM Page 286
20 HYPERTENSION 287
C H A P T E R
TABLE
20.6
Advantages/Disadvantages of HTN Drugs
Major Advantages/ Major Disadvantages/
Indications Contraindications
Diuretics
Beta blockers
ACEIs
Angiotensin
receptor
blockers
Calcium
channel
blockers
Clonidine
Alpha
blockers
Inexpensive
Heart failure
Inexpensive (if generic)
Angina
Post-MI
Heart failure
Tachyarrhythmia
Heart failure
Ejection fraction 40%
Post-MI
Diabetic nephropathy
Early trials suggest may
be as good as ACEIs
Use in patients with
ACEI-induced cough
Angina
Systolic HTN in the elderly
or African Americans
Very effective BP lowering
Inexpensive (generic)
Patchfewer side effects,
more expensive
Benign prostatic
hypertrophy (BPH)
Gout
Increase incidence of
diabetes
Asthma
Chronic obstructive
pulmonary disease
Heart block
Very physically active
patients
Pregnancy
Bilateral renal artery
stenosis
Renal insufficiency
Experience much less
than with ACEIs
Very expensive
CHF
Very expensive
No proven mortality
benefits
Many nuisance side
effects such as
sedation, dry mouth
Increased heart failure
in a major BP trial
(ALLHAT)
1389_Ch20_278-293 2/2/09 1:28 PM Page 287
2. They are drastically underutilized.
a. One reason is that older studies used doses of 50100 mg
that produced many more side effects than the currently used
doses of 12.525 mg of hydrochlorothiazide.
b. A major reason may be the powerful influence of drug
representatives and advertising. The influence of marketing
in general is well documented, and the need for doctors to be
mindful of this influence is well documented.
3. Hypokalemia has the following diuretic profile.
a. Mild hypokalemia is not a problem for most patients taking
a diuretic.
b. There have been case-controlled studies demonstrating a reduc-
tion of sudden death as a result of using potassium-sparing
diuretics in combination with thiazide diuretics.
c. In patients at risk of arrhythmias or any patient with heart
disease, a potassium-sparing diuretic should be considered.
B. Beta blockers
1. Beta blockers have been used in most major trials that have
demonstrated a mortality rate benefit.
2. In addition, beta blockers have mortality rate benefits when
used in patients post-MI or CHF.
3. They are useful for symptom control in patients with tach-
yarrhythmia and angina.
4. However, in the last few years there have been concerns raised that
in patients without an MI or CHF (the majority of patients with
HTN), beta blockers prevent fewer cardiovascular endpoints, espe-
cially stroke, than other antihypertensive medicines. Given that two
thirds of the beta-blocker studies have used atenolol, it is difficult
to sort out whether this is a class effect or an atenolol effect.
C. ACEIs
1. There have been multiple trials suggesting that ACEIs as a class
may have beneficial effects on cardiovascular and renal morbid-
ity and mortality rates that exceed their BP-lowering effects.
2. The mechanisms of ACEI beneficial effects are often uncertain.
3. The advantages are as follows.
P A R T
Diuretics have been used in the major trials that have
demonstrated a reduction in mortality and cardiovas-
cular events.
1389_Ch20_278-293 2/2/09 1:28 PM Page 288
a. Diabetes incidence is not increased.
b. The incidence of MI is reduced.
c. Proteinuria is reduced.
d. Mortality due to CHF is reduced.
20 HYPERTENSION 289
C H A P T E R
An ACEI should be considered for most hypertensive
patients with diabetes, proteinuria, renal insufficiency,
or CVD.
The most common cause of refractory HTN is poor
compliance.
4. Cough is the most common side effect, occurring in up to 5%
of patients.
a. If coughing is present, changing to an angiotensin receptor
blocker is the recommendation.
b. Angioedema is a rare side effect of ACEI therapy, occurring
in 0.1%0.2% of patients.
D. All other medications, including calcium channel blockers, an-
giotension receptor blockers, alpha blockers, and clonidine, should
be added only if the preceding agents are not tolerated due to side
effects or unsuccessful in lowering BP.
XI. Refractory HTN
A. Poor compliance can happen for understandable reasons, but it
needs to be identified and improved in order to make treatment
effective.
1. Several factors may lead patients to comply poorly.
a. Cost: medicines are often expensive.
b. Side effects: medicines can often produce side effects.
c. Lack of immediate reward: HTN medicines rarely produce
any improvement in short-term well-being.
d. Effort: it can be challenging to stick to dietary or exercise
plans.
2. The physician needs to ask directly but nonjudgmentally, In a
week, how many pills do you miss?
3. An assessment of compliance is one of the most important
tasks of the physician when seeing patients with HTN.
B. After poor compliance, secondary causes of HTN should be
considered.
1389_Ch20_278-293 2/2/09 1:28 PM Page 289
C. Look for medication interactions.
1. Review the patients drug list to find potential interactions.
2. Over-the-counter medications can be the cause.
a. Decongestants raise BP and are a commonly used class of
drugs.
b. Nonsteroidal anti-inflammatory drugs (NSAIDs) can negate
the effects of BP therapy.
D. Consider diuretic changes.
P A R T
More diuretics is often the answer.
1. Renal insufficiency and high sodium intake are well-understood
problems.
2. A less well-recognized mechanism is that the kidney seems to
retain sodium in response to most BP medications.
3. Once a patient requires three different medications, the use of
furosemide can be helpful. As these patients are usually not
fluid-overloaded, they usually do not lose large amounts of
water and potassium.
MENTOR TIPS DIGEST
Approximately 26% of adults in the United States have HTN.
A reduction of 5 mm Hg DBP is associated with a 35%40%
decreased incidence of stroke.
The risks of heart failure and renal disease are clearly reduced
with lower BP; however, the major mortality benefits of BP
treatment depend on the reduction of CHD and stroke.
The JNC on Prevention, Detection, Evaluation, and Treatment
of High Blood Pressure has released a new classification
scheme for HTN.
Management is determined by the highest category, either
systolic or diastolic.
According to the JNC, 115/75 is the optimal BP as defined as
the BP that predicts the longest life.
95% of patients with high BP have primary HTN.
The most common cause of secondary HTN is parenchymal
renal disease.
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20 HYPERTENSION 291
C H A P T E R
The most frequent mistake in BP measurement is using a cuff
that is too small.
The decision about BP treatment should not be determined
solely by the level of BP.
DASH diet compliance can lower BP as much as 814 mm Hg.
Smoking cigarettes is the most important modifiable risk
factor to prevent CHD.
Use a thiazide diuretic, beta blocker, or ACEI as first-line
therapy for HTN.
Monotherapy is effective in 70% of patients.
Stage II HTN generally requires two BP medications.
Physicians routinely underestimate the side effects and
overestimate the benefits of interventions.
Diuretics have been used in the major trials that have demon-
strated a reduction in mortality and cardiovascular events.
An ACEI should be considered for most hypertensive patients
with diabetes, proteinuria, renal insufficiency, or CVD.
The most common cause of refractory HTN is poor compliance.
With refractory HTN, more diuretics is often the answer.
Resources
Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack
Trial (ALLHAT). Major outcomes in high-risk hypertensive patients
randomized to angiotensin-converting enzyme inhibitor or calcium
channel blocker vs. diuretic. Journal of the American Medical Associa-
tion 288:29812997, 2002.
Cialdini R. Influence, science and practice, 4th ed., Allyn and Bacon Pub-
lishers, Delaware, 2000.
Dickerson JEC, et al. Optimization of antihypertensive treatment by
crossover rotation of four major classes. Lancet 353:20082013,
1999.
Graves JW. Management of difficult-to-control hypertension.
Mayo Clinic Procedures 75:278284, 2000.
Hansson L, et al. Effects of intensive blood-pressure lowering and
low-dose aspirin in patients with hypertension: Principal results of the
hypertension optimal treatment (HOT) randomised trial. Lancet
351:17551762, 1988,
1389_Ch20_278-293 2/2/09 1:28 PM Page 291
Haynes RB, et al. Increased absenteeism from work after detection and
labeling of hypertensive patients. New England Journal of Medicine
299:741744, 1978.
No Free Lunch website: http://www.nofreelunch.org/index.htm
This Web site encourages health care providers to practice medicine
on the basis of scientific evidence rather than on the basis of pharma-
ceutical promotion.
Seventh Report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure:
The JNC 7 report. Journal of the American Medical Association
289:25602572, 2003.
Siscovick D, et al. Diuretic therapy for hypertension and the risk of
primary cardiac arrest. New England Journal of Medicine
330:18521857, 1994.
U.S. National Heart, Lung, and Blood Institute. DASH diet booklet:
http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf
This booklet explains the DASH diet to patients.
U.S. National Heart, Lung, and Blood Institute. Risk assessment tool for
estimating your 10-year risk of having a heart attack:
http://hp2010.nhlbihin.net/atpiii/calculator.asp
Risk assessment tool (based on the Framingham Heart Study) for
estimating 10-year risk of having a heart attack.
1. What is the prevalence of hypertension among adults in the
United States?
a. Less than 10%
b. 20%30%
c. 50%60%
d. Greater than 90%
2. What is the correct classification for a BP of 125/85 according to
JNC-7?
a. Normal
b. Pre-hypertension
P A R T
1389_Ch20_278-293 2/2/09 1:28 PM Page 292
c. Stage 1 hypertension
d. Stage 2 hypertension
3. What is the correct classification for a BP of 140/85 according to
JNC-7?
a. Normal
b. Pre-hypertension
c. Stage 1 hypertension
d. Stage 2 hypertension
20 HYPERTENSION 293
C H A P T E R
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294
CHAPTER
ASTHMA
21
I. Definition
A. Good general definition of asthma:
Asthma is a chronic disease of the airways that is
complex and characterized by variable and recurring
symptoms, airflow obstruction, bronchial hyperreactivity, and
airways inflammation.
B. National Institutes of Health (NIH) working definition of asthma:
1. Asthma is a chronic inflammatory disorder of the airways in
which many cells and cellular elements play a role; in particu-
lar, mast cells, eosinophils, T lymphocytes, macrophages,
neutrophils, and epithelial cells.
2. In susceptible individuals, this inflammation causes recurrent
episodes of wheezing, breathlessness, chest tightness, and
coughing, particularly at night or in the early morning.
3. These episodes are usually associated with widespread but
variable airflow obstruction that is often reversible either spon-
taneously or with treatment.
4. The inflammation also causes an associated increase in the
existing bronchial hyperresponsiveness to a variety of stimuli.
II. Burden of Asthma: Epidemiology and Economics
A. Prevalence
1. Worldwide distribution and estimated global prevalence of
300 million patients.
U.S. prevalence estimate is 10.9% of population.
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21 ASTHMA 295
C H A P T E R
B. Morbidity and mortality rates
1. The World Health Organization (WHO) estimates 15 million
disability-adjusted life years lost annually due to asthma.
2. Estimated worldwide deaths: 250,000 per year.
3. U.S. case fatality rate is 5.2 deaths per 100,000 cases.
C. Social and economic data
1. Total cost (direct and indirect) of asthma-related illness was
estimated at $6.2 billion in 1990.
2. Emergency room use, hospitalization, and death comprise
43% of the economic impact.
III. Pathogenesis
A. Host factors (genetics)
1. Asthma has a clear heritable component with multiple genes
playing a role.
2. Genetic factors are also involved in the response to asthma
therapy.
B. Environmental
1. Allergens: indoor and outdoor allergens can cause asthma exac-
erbations; play important but undefined role in development of
asthma
2. Infections
a. Some viral infections (respiratory syncytial virus [RSV],
parainfluenza virus) in infancy share many features of
childhood asthma.
b. Approximately 40% of children admitted to the hospital with
documented RSV will continue to wheeze or have asthma
later in childhood.
c. The hygiene hypothesis follows.
Patients with asthma commonly miss school or work and
suffer a decreased quality of life.
The factors involved in the development of asthma are
complex, interactive, and highly dependent on the interplay
between host factors (primarily genetics) and environmental
exposures.
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P A R T
i. Early childhood infections influence development of
immune system along a nonallergic pathway
ii. May explain observation that children at increased
risk of infection (e.g., attend day care) have decreased
incidence of asthma and other allergic diseases later
in life.
IV. Pathophysiology
A. Asthma is caused by a complex interaction between cells,
mediators, and cytokines that result in airway inflammation.
B. This results in important physiologic changes in airway structure
and function, including airway smooth muscle contraction, hyper-
trophy and hyperplasia, stimulation of mucous secretion, and
airway epithelial dysfunction.
C. Infiltrating inflammatory cells produce a wide variety of
mediators including histamine, platelet activating factor, and
derivatives of the arachidonic cascade that can result in
bronchoconstriction.
V. Natural History
Asthma can develop at any age.
A. Early-onset asthma
1. Children with early-onset disease may outgrow their asthma
in 30%50% of cases; this asthma is more common in males
than females.
2. Risk factors for persistent asthma include severe atopy, marked
bronchial hyperreactivity, and a history of difficult-to-control
asthma.
3. Lung growth appears to be normal but can be decreased in
more severe disease.
B. Adult-onset asthma
1. Patients with adult-onset asthma, severe disease, and abnormal
pulmonary function tests (PFTs) are less likely to have
remission.
2. Some patients over time develop irreversible airflow obstruction
that may be related to structural changes in the airways (airway
remodeling) in the setting of chronic inflammation.
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21 ASTHMA 297
C H A P T E R
VI. Diagnosis
A. History
1. Cough or dyspnea can be isolated features
2. Symptoms tend to be episodic, often with acute onset; may be
historically linked to exposures to known triggers and can have
periods of prolonged remission
3. Cough in asthma
a. Can predate a formal diagnosis of asthma by years and be an
isolated feature of asthma, i.e., cough-variant asthma
b. Typical triggers include cigarette smoke, cold air, laughter,
deep inhalation, forced exhalation
c. Coughing paroxysms triggered by deep breathing maneuver
suggests bronchial hyperreactivity; can be useful bedside test
4. Other symptoms: chest tightness, substernal pressure, chest
pain, nocturnal awakenings
B. Physical findings/examination
1. Acute asthma
a. Wheeze
i. Characteristic diffuse musical wheeze
ii. Presence or intensity does not reliably predict severity of
airflow obstruction
b. Tachypnea and tachycardia (universal)
c. Prolonged expiratory phase
d. Hyperinflation of chest
e. Mild hypoxemia
2. Severe asthma
a. Wheeze
i. Loud, high-pitched, and inspiratory and expiratory wheezing
is generally associated with more severe obstruction.
ii. Wheezing may be absent, suggesting poor air movement
and impending respiratory failure.
Asthma is a clinical diagnosis that is made based on history,
physical examination, and diagnostic testing including
objective measurement of lung function.
Classic triad of symptoms: shortness of breath, wheeze,
and cough with or without sputum production.
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P A R T
b. Respiratory distress including the inability to speak in full
sentences
c. Accessory muscle use
d. Pulsus paradoxus
e. Diaphoresis
f. Severe hypoxemia and mental status changes possibly in
extreme cases
C. Objective measures of lung function
1. Spirometry
a. Measures forced expiratory volume in 1 second (FEV
1
),
forced vital capacity (FVC), and FEV
1
/FVC ratio
b. Airflow obstruction demonstrated by decreased FEV
1
,
decreased FEV
1
/FVC ratio, and scooping in the expira-
tory flow limb of flow volume loop
Reversible airflow obstruction is the sine qua non
of asthma and is considered significant with a 12%
improvement in FEV
1
and an absolute increase of 200 mL
after administration of a short-acting beta agonist.
Bronchoprovocation testing is useful for supporting
the diagnosis of asthma in cases when spirometry is
normal.
2. Bronchoprovocation testing
a. Inducible bronchial hyperreactivity is demonstrated by a
significant decrease in FEV
1
after nebulized administration
of an agonist (e.g., methacholine, histamine).
b. The test is highly sensitive but not specific for asthma.
VII. Differential Diagnosis
A. Acute viral tracheobronchitis
1. Can result in persistent cough following typical upper respira-
tory infection (URI) symptoms
2. Bronchial hyperresponsiveness persisting for up to 6 weeks
3. May also be manifestation of mild intermittent asthma
B. Chronic obstructive pulmonary disease (COPD)
1. Also associated with symptom triad of shortness of breath
(SOB), wheeze, and cough.
2. Can be difficult to differentiate from asthma.
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21 ASTHMA 299
C H A P T E R
C. Gastroesophageal reflux
1. Can present with cough and chest tightness with or without
classic dyspepsia
2. Can exacerbate asthma; treatment of gastroesophageal reflux
disease (GERD) can improve asthma control
D. Cardiac ischemia (chest tightness, chest pain/pressure, dyspnea)
E. Upper airway obstruction
F. Congestive heart failure
G. Vocal cord dysfunction
H. Parasitic infections (Strongyloides)
I. Cough secondary to drugs
J. Eosinophilic pneumonia
VIII. Management
A. Successful management of asthma
1. Routine monitoring of symptoms and objective measures of
lung function
2. Control of asthma triggers
3. Pharmacologic therapy
4. Patient education
B. Goals of asthma care
1. Avoid frequent, severe, and troublesome asthma symptoms
(e.g., cough/breathlessness during night, early morning, or
after physical activity).
2. Prevent acute exacerbations that require urgent medical
intervention.
3. Maintain ability to pursue daily activities including participa-
tion in athletics without limitation due to asthma symptoms.
4. Optimize lung function.
5. Optimize pharmacotherapy while minimizing or avoiding
side effects.
6. Provide effective education.
C. Pharmacologic therapy
1. Controller therapy: chronic pharmacotherapy to prevent
symptoms of asthma
Basic distinction: controller therapy versus reliever
therapy.
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P A R T
2. Reliever therapy: short-acting pharmacotherapy used on
as-needed (PRN) basis to treat current asthma symptoms
3. Route of administration
a. Asthma therapy can be delivered by inhalation, orally, and
intravenously.
i. Inhalation therapy has the major benefit of delivery of
drug directly to the airways, resulting in a higher local
concentration with fewer systemic side effects.
4. Classes of asthma medications
a. Anti-inflammatory agents (generally used as controller
medications)
i. Reduce airway inflammation and improve lung function,
decrease bronchial hyperreactivity, decrease symptoms,
reduce frequency and severity of asthma exacerbations,
reduce mortality, improve quality of life
ii. Prevent migration and activation of inflammatory cells,
interfere with production of prostaglandins and
leukotrienes, reduce microvascular leak, enhance action
of beta-adrenergic receptors on airway smooth muscle
iii. Corticosteroids
(1) May be inhaled, oral, or intravenous
(A) Inhaled corticosteroids (ICSs) are most effective
medications for treatment of persistent asthma.
(B) Examples of inhaled agents are fluticasone,
beclomethasone, and flunisolide.
(C) Oral and intravenous corticosteroids are generally
used for acute asthma exacerbations.
iv. Mast cell stabilizers
(1) Limited role as controller therapy in adult asthma but
have excellent safety profile
(2) May be useful for some adults with mild persistent
asthma or exercise-induced asthma
(3) Cromolyn sodium and nedocromil sodium available in
inhaled form
v. Leukotriene modifying agents
(1) Includes 5-lipoxygenase inhibitors (Zileuton) and
cysteinyl leukotriene receptor blockers (Zafirlukast,
Montelukast)
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21 ASTHMA 301
C H A P T E R
(2) Shown to have small and variable bronchodilator
effect, reduce symptoms including cough, improve
lung function, and reduce airway inflammation and
asthma exacerbations
(3) May be useful in mild persistent asthma, preventing
allergen-induced asthma, exercise-induced asthma,
and aspirin-induced bronchospasm
Leukotriene-modifying agents are less effec-
tive than ICSs as monotherapy and less
effective than long-acting beta agonists (LABA) as
add-on therapy for poorly controlled asthma.
Regular use without concomitant use of
an ICS is associated with poor asthma
control and heightened bronchial hyperreactivity.
LABAs have been associated with increased
risk of asthma-related death and are not
appropriate for monotherapy as asthma controller
therapy.
b. Bronchodilators
i. Short-acting
(1)
2
-adrenergic agonists (albuterol, pirbuterol,
levalbuterol)
(A) Used as reliever therapy for acute asthma
symptoms
(2) Inhaled anticholinergic agent (ipratropium)
(A) Provides bronchodilation via decreased vagal tone
of airways
(B) Primarily used for the treatment of COPD but
often combined with albuterol (Combivent/
Duoneb) for treatment of acute asthma
ii. LABAs: (salmeterol, formoterol)
(1) Used as asthma controller therapy and to control noc-
turnal asthma symptoms
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P A R T
(2) Fixed-dose combination therapy of ICS and LABA
(Advair) associated with increased patient compliance
and assures LABA always delivered with ICS.
iii. Theophylline
(1) Bronchodilator with modest anti-inflammatory effects
(2) Sustained-release formulations can be used as add-on
agent to ICS, but less effective than LABA
(3) Side effects, especially in high doses, limit usefulness
c. Immunomodulating agents
i. Various agents have been investigated for their ability to
maintain long-term asthma control or steroid-sparing effects.
ii. These agents include methotrexate, cyclosporin A, intra-
venous immunoglobulin (IVIG), clarithromycin, omal-
izumab (anti-IgE), and others.
iii. Omalizumab has the following profile.
(1) Only agent approved by the U.S. Food and Drug
Administration (FDA) for asthma
(2) Recombinant DNA-derived humanized anti-IgE mon-
oclonal antibody that prevents IgE from binding to
mast cells and basophils
(3) Indicated as adjunctive therapy in patients with aller-
gies and severe persistent asthma that is inadequately
controlled with the combination of high-dose ICS and
LABA
(4) Local side effects common; urticaria and anaphylactic
reactions reported in 0.1%0.2% of treated patients
D. Step therapy approach (Fig. 21.1)
1. Treatment should be adjusted in a continuous cycle, determined
by the patients asthma control.
Adding a LABA to an ICS has been shown
to be more effective at controlling asthma
symptoms than increasing the dose of an ICS.
Data suggest that it is not effective as a
first-line controller medication.
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21 ASTHMA 303
C H A P T E R
Level of Control
Step 1 Step 2 Step 3 Step 4 Step 5
Controller
options***
*ICS=inhaled glucocorticosteroids
**=Receptor antagonist or synthesis inhibitors
***Preferred controller options are shown in shaded boxes
Alternative reliever treatments include inhaled anticholinergics, short-acting oral
2
-agonists,
some long-acting
2
-agonists, and short-acting theophylline. Regular dosing with short- and
long-acting
2
-agonist is not advised unless accompanied by regular use of an inhaled
glucocorticosteroid.
As needed rapid-acting
2
-agonist
Select one Select one Add one or more Add one or both
As needed rapid-
acting
2
-agonist
Asthma education
Environmental control
Medium- or
high-dose ICS
plus long-acting
2
-agonist
Low-dose inhaled
ICS*
Low-dose ICS plus
long-acting
2
-agonist
Oral
glucocorticosteroid
(lowest dose)
Leukotriene
modifier**
Leukotriene
modifier
Medium- or
high-dose ICS
Sustained-release
theophylline
Low-dose ICS plus
leukotriene modifier
Low-dose ICS plus
sustained-release
theophyline
Anti-IgE
treatment
Treatment Action
Controlled Maintain and find lowest controlling step
Partly controlled Consider stepping up to gain control
Uncontrolled Step up until controlled
Exacerbation Treat as exacerbation
Management Approach Based on Control
for Children Older Than 5 Years, Adolescents and Adults
Treatment Steps
R
e
d
u
c
e
I
n
c
r
e
a
s
e
Increase Reduce
FIGURE 21.1 Asthma management approach, based on level of control,
ages 5 through adult. (From Global Initiative for Asthma: GINA Report 2006:
Global Strategy for Asthma Management and Prevention, Chapter 4, page 59.
http://www.ginasthma.com/)
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P A R T
2. Therapy should be stepped up when symptoms are partly
controlled or uncontrolled until control is achieved.
3. Therapy should be stepped down when control is achieved
for at least 3 months.
4. Reliever therapy is used at each step for quick relief of symp-
toms as needed.
E. Monitoring
1. Ongoing monitoring is essential to maintain control and to
establish the lowest step and dose to minimize cost and
maximize safety.
2. Symptom assessment consists of the following.
a. Suggested points of inquiry
i. Frequency of short-acting bronchodilator use
ii. Frequency of daytime symptoms
iii. Frequency of nocturnal symptoms
iv. Limits to physical activity or missed work/school
v. Asthma exacerbations since last visit
b. Well-controlled asthma: daytime symptoms no more than
two times per week and nighttime symptoms no more than
two times per month.
c. Frequent use of short-acting bronchodilators, generally more
than two to three puffs per day, is a marker for poorly con-
trolled asthma.
d. Patient perception of dyspnea/severity
i. Patient perception of control poorly correlates with objec-
tive measures of lung function
ii. May be linked to near-fatal or fatal asthma
iii. Objective monitoring of lung function is essential
3. Objective measures of lung function consists of the following.
a. Peak expiratory flow rate (PEFR)
i. Simple, inexpensive measure of airflow obstruction for
home use
ii. Repeated measurements used to determine relative
changes and track trends in asthma control
iii. Single measurements not accurate for airflow obstruction
or useful for diagnosis of asthma
b. Spirometry
i. Serial measurements used to monitor asthma control
ii. Generally limited to clinician office use
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21 ASTHMA 305
C H A P T E R
F. Control of triggers
Identification and avoidance of asthma triggers are criti-
cal components of asthma management.
Asthma action plans can result in one third to two
thirds reduction in hospitalizations, emergency room
visits, unscheduled physician office visits for asthma,
missed days of work or school, and nocturnal awakenings.
1. Common triggers include allergens, respiratory infections,
inhaled irritants, physical activity, emotional distress, gastroe-
sophageal reflux, and medicines (nonselective beta blockers,
aspirin).
G. Asthma action plans
1. Written, customized plan for patient-initiated changes in therapy,
based on individual patients range of peak flow measurements
and/or asthma symptoms
2. Examples can be found at www.ginasthma.com or
www.nhlbi.nih.gov/guidelines/asthma.
IX. Referral to Pulmonary Specialist
A. Diagnostic uncertainty
B. Difficulty in achieving or maintaining asthma control
C. Need for Step 4 care.
MENTOR TIPS DIGEST
Asthma is a chronic disease of the airways that is complex
and characterized by variable and recurring symptoms,
airflow obstruction, bronchial hyperreactivity, and airways
inflammation.
U.S. prevalence estimate is 10.9% of population.
Patients with asthma commonly miss school or work and
suffer a decreased quality of life.
The factors involved in the development of asthma are
complex, interactive, and are highly dependent on the interplay
between host factors (primarily genetics) and environmental
exposures.
1389_Ch21_294-308 2/2/09 1:30 PM Page 305
P A R T
Asthma can develop at any age.
Asthma is a clinical diagnosis that is made based on history,
physical examination, and diagnostic testing including
objective measurement of lung function.
Classic triad of symptoms in asthma: shortness of breath,
wheeze, and cough with or without sputum production.
Reversible airflow obstruction is the sine qua non of asthma
and is considered significant with a 12% improvement in FEV
1
and an absolute increase of 200 mL after administration of a
short-acting beta agonist.
Bronchoprovocation testing is useful for supporting the
diagnosis of asthma in cases when spirometry is normal.
Basic distinction in pharmacologic therapy: controller therapy
versus reliever therapy.
Leukotriene-modifying agents are less effective than ICSs as
monotherapy and less effective than long-acting beta agonists
(LABA) as add-on therapy for poorly controlled asthma.
Regular use of
2
-adrenergic agonists without concomitent
use of an ICS is associated with poor asthma control and
height-enced bronchial hyperreactivity.
LABAs have been associated with increased risk of asthma-
related death and are not appropriate for monotherapy as asthma
controller therapy.
Adding a LABA to an ICS has been shown to be more effective
at controlling asthma symptoms than increasing the dose of
an ICS.
Data suggest that theophylline is not effective as a first-line
controller medication.
Identification and avoidance of asthma triggers are critical
components of asthma management.
Asthma action plans can result in one third to two thirds
reduction in hospitalizations, emergency room visits, unsched-
uled physician office visits for asthma, missed days of work or
school, and nocturnal awakenings.
Resources
Busse WW, Lemanske RF. Advances in immunology: Asthma. New England
1389_Ch21_294-308 2/2/09 1:30 PM Page 306
21 ASTHMA 307
C H A P T E R
1. Among Americans who have asthma, about how many die each year?
a. 510/100,000
b. 50100/100,000
c. 5001000/100,000
d. 500010000/100,000
2. Based on the Global Initiative for Asthma prevalence data, how
many of the approximately 300 million persons who live in the
United States have asthma?
a. About 30,000
b. About 300,000
c. About 3,000,000
d. Over 30,000,000
Global initiative for asthma: GINA report 2006: Global strategy for
asthma management and prevention. Accessed 5/1/07 at http://www.
ginasthma.com/
National Asthma Education and Prevention Program. Expert panel 2
report: Guidelines for the diagnosis and treatment of asthma.
Accessed 5/1/07 at http://www.nhlbi.nih.gov/guidelines/asthma/
asthgdln.pdf
Wechsler ME, Lehman E, Lazarus SC, et al. Beta-adrenergic receptor
polymorphisms and response to salmeterol. American Journal of
Respiratory and Critical Care Medicine 173:519526, 2006.
Weiss KB, Gergen PJ, Hodgson TA. An economic evaluation of asthma
in the United States. New England Journal of Medicine 326:862866,
1992.
1389_Ch21_294-308 2/2/09 1:30 PM Page 307
P A R T
3. According to the NIH, which characterizes the primary pathophysiol-
ogy of asthma?
a. Reversible constriction of airways
b. Irreversible constriction of airways
c. Inflammation of airways
d. Anxiety-medicated airways disease
1389_Ch21_294-308 2/2/09 1:30 PM Page 308
309
CHAPTER
CHRONIC OBSTRUCTIVE
PULMONARY DISEASE
22
I. Definition
A. There is no universally accepted definition of chronic obstructive
pulmonary disease (COPD).
B. Most recent published consensus definition by the Global Initiative
of Obstructive Lung Disease (GOLD).
GOLD defines COPD as a disease state characterized by
airflow obstruction that is no longer fully reversible, usually
progressive, and associated with an abnormal inflammatory
response to noxious particles or gases.
C. Other expert panels have defined COPD as a disease state charac-
terized by chronic airflow limitation due to chronic bronchitis and
emphysema.
1. Chronic bronchitis can be defined clinically as a chronic pro-
ductive cough for at least 3 consecutive months in 2 consecutive
years.
2. Emphysema can be defined pathologically as abnormal
enlargement of airspaces distal to the terminal bronchioles
accompanied by destruction of their walls.
II. Epidemiology
COPD is underdiagnosed and undertreated, and it is a major
cause of morbidity and mortality globally.
1389_Ch22_309-323 2/2/09 1:30 PM Page 309
P A R T
A. Approximately 24 million people in the United States showing
evidence of impaired lung function
B. Data from 2000 indicate COPD responsible for:
1. 8 million outpatient visits
2. 1.5 million emergency department visits
3. 726,000 hospitalizations
C. Mortality
COPD was the fourth leading cause of death in 2002
(125,500).
1. Significantly increased rate of death from COPD among
women since 1980.
2. Among the six leading causes of death in the United States;
only COPD has been increasing steadily since 1970.
III. Risk Factors
A. Cigarette smoking
Cigarette smoking is most important risk factor, involving
85%90% of all cases.
1. However, only 15%25% of smokers will be diagnosed with
COPD, but a majority will develop some loss of lung function.
2. Pipe and cigar smoking as well as passive smoking may confer
risk for adult COPD.
B. Some occupations (e.g., coal miners, grain handlers, and cement
and cotton workers) at increased risk, especially with concomitant
exposure to tobacco smoke
C. Environmental factors (e.g., indoor use of biomass fuels, exposure
to urban pollution and particulate matter)
D. Genetic factors
1.
1
-antitrypsin deficiency responsible for <1% of COPD in
United States
2. Multiple gene polymorphisms associated with increased risk
E. Gender: males more at risk than females
F. Low socioeconomic status
G. Bronchial hyperresponsiveness: strong predictor of progressive
airflow obstruction in smokers
1389_Ch22_309-323 2/2/09 1:30 PM Page 310
22 CHRONIC OBSTRUCTIVE PULMONARY DISEASE 311
C H A P T E R
H. Asthma: many adult nonsmokers develop fixed airflow limitation
over time
I. Childhood illness: prematurity, low birth rate, frequent respiratory
tract infections, symptomatic childhood asthma
J. Dietary: vitamin C and E deficiency
IV. Pathophysiology
A. Chronic exposure to noxious gases and particulate matter
induce a chronic innate and adaptive inflammatory immune
response.
1. Important cell mediators of inflammation include macrophages,
neutrophils, CD8 T cells, and eosinophils.
2. Other mediators of inflammation include inflammatory
cytokines, chemotactic factors, growth factors, and proteases.
B. Airway inflammation leads to small airway disease and parenchymal
destruction and results in airflow limitation.
C. Emphysematous destruction of lung parenchyma leads to loss of
alveolar attachments and decreases the maximum expiratory flow
secondary to decreased elastic recoil.
D. Other important changes include goblet cell hyperplasia, mucous
gland hyperplasia, and mucus hypersecretion.
V. Natural History
COPD is characterized by a prolonged preclinical period
of 2040 years, with a marked continuous decline in lung
function (Fig. 22.1).
The diagnosis of COPD should be considered in current or
former smokers and in never-smokers with other risk factors
who present with cough, sputum production, or dyspnea.
A. Exertional dyspnea generally develops when the FEV
1
is 40%50%
of predicted.
B. Disability is common when the FEV
1
is approximately 30% of
predicted.
VI. Diagnosis
1389_Ch22_309-323 2/2/09 1:30 PM Page 311
P A R T
100
Gold 0+1
Never smoked
or not susceptible
to smoke
Stopped at 50 years
Stopped at 65 years
Gold 2
Gold 3
Gold 4 Disability
Death
75
50
25
25 50 75
Age (years)
F
E
V
1

(
p
e
r
c
e
n
t
a
g
e

o
f

v
a
l
u
e

a
t

a
g
e

2
5
)
100
0
FIGURE 22.1 Rate of decline in FEV
1
with age. (From Hogg JC. Pathophysiology
of airflow limitation in chronic obstructive pulmonary disease. Lancet 2004;
364:709721, Figure 1, p. 709.)
A. Symptoms usually present in fifth decade and after smoking a
pack per day for at least 20 years
1. Chronic cough sputum production
2. Dyspnea with exertion
3. Wheezing
1. Prolonged expiratory phase
2. Wheeze
3. Chest wall hyperinflation
4. Limited diaphragmatic excursion
5. Distant breath and heart sounds
6. Severe signs including cyanosis, accessory muscle use, and
pursed-lip breathing
C. Imaging
1. Chest x-ray findings
a. Low flat diaphragm
b. Increased retrosternal airspace
c. Pruning of arterial tree
d. Bullae
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C H A P T E R
2. Computed tomography findings
a. Focal areas of low attenuation with Swiss cheese appearance
b. Low attenuation areas small (1 cm), round or oval, with-
out definable walls
D. Pulmonary function testing
1. Spirometry
Spirometry measures expiratory airflow and is most
important for diagnosis and staging.
The FEV
1
is best correlated with morbidity and
mortality.
a. Decreased FEV
1
b. Decreased ratio of FEV
1
/FVC
c. Flow-volume loop shows scooping in expiratory limb
2. Lung volumes
a. Total lung capacity (TLC): increased when hyperinflation
is present
b. Residual volume (RV): increased when air trapping is
present
3. Diffusing capacity (DLCO)
a. Indirect measure of gas exchange
b. Predicts loss of alveolar-capillary units and suggests presence
of emphysema
E. Laboratory
1. CBC: chronic hypoxemia may lead to secondary polycythemia
2.
1
-antitrypsin levels in selected patients
3. Highly sensitive C-reactive protein: increased regardless of
smoking status; associated with increased morbidity and
mortality
VII. Differential Diagnosis
A. Asthma
B. Acute bronchitis
C. Cystic fibrosis
D. Upper airway obstruction
E. Congestive heart failure
1389_Ch22_309-323 2/2/09 1:30 PM Page 313
P A R T
F. Sarcoidosis
G. Some pneumoconioses
VIII. Staging of COPD
A. Multiple respiratory/thoracic societies have severity staging
scores
1. All based on FEV
1
2. Most recent from GOLD
B. GOLD stage criteria
1. Stage 0: at risk group
a. Normal spirometry
b. Chronic symptoms (cough, sputum production)
2. Stage I: mild COPD
a. FEV
1
/FVC 70%
b. FEV
1
80% predicted
c. With or without chronic symptoms
3. Stage II: moderate COPD
a. FEV
1
/FVC 70%
b. FEV
1
between 50% and 79% predicted
i. Stage IIa: FEV
1
between 50% and 70%
ii. Stage IIb: FEV
1
between 30% and 49%
4. Stage III: severe COPD
a. FEV
1
/FVC 70%
b. FEV
1
30% and 50% predicted
5. Stage IV: very severe COPD
a. FEV
1
/FVC 70%
b. FEV
1
30% predicted or
c. FEV
1
50% and respiratory failure or clinical signs of
right heart failure
IX. Management
A. Stable COPD
1. Smoking cessation
Stopping smoking can slow the loss of lung function
and decrease symptoms at any point in time.
1389_Ch22_309-323 2/2/09 1:30 PM Page 314
C H A P T E R
a. First-line treatments include nicotine replacement therapy
and either buproprion or varenicline.
b. See smoking cessation guidelines at www.surgeongeneral.gov/
tobacco/default.htm
2. Pharmacologic therapy
All symptomatic patients warrant a trial of drug
treatment.
a. Goals of pharmacologic therapy
i. Reduce or eliminate symptoms.
ii. Increase exercise capacity.
iii. Decrease the number or severity of exacerbations.
iv. Improve health status.
b. Bronchodilators
i. Three types in common clinical use: beta-agonists,
anticholinergics, and methylxanthines
ii. Documented clinical outcomes
(1) Short-acting bronchodilators can acutely increase
exercise tolerance.
(2) Anticholinergics given four times a day can improve
health status over a 3-month period compared with
placebo.
(3) Long-acting inhaled beta-agonists improve health
status, reduce symptoms, decrease rescue medication,
use and increase the time between exacerbations com-
pared with placebo.
(4) Combination therapy has the following profile.
(A) Short-acting agents (albuterol/ipratropium) produce
a greater change in spirometry over 3 months than
either agent alone.
(B) Combination therapy with long-acting inhaled
beta-agonists and ipratropium leads to fewer
exacerbations than either drug alone.
(C) Combination therapy with long-acting beta-
agonists and theophylline appear to produce a
greater spirometric response than either drug
alone.
1389_Ch22_309-323 2/2/09 1:30 PM Page 315
P A R T
c. Inhaled corticosteroid (ICS)
i. Available agents: beclomethasone, budesonide, triamci-
nolone, fluticasone, flunisolide
ii. Generally used for patients with more advanced disease
(usually classified as an FEV
1
50% predicted or presence
of frequent exacerbations).
iii. Documented clinical outcomes
(1) Decrease in exacerbations per year
(2) Decreased rate of deterioration in health status
(3) No clear evidence of effect on rate of change of FEV
1
in any severity category of COPD
d. Clinical use
i. Intermittent symptoms (cough, wheeze, exertional dyspnea)
(1) Short-acting inhaled beta-agonist or
(2) Short-acting inhaled anticholinergic agent
ii. Persistent symptoms (dyspnea, nocturnal symptoms)
(1) Scheduled short-acting beta-agonist four times a day
(2) Combination short-acting bronchodilators
(albuterol/ipratropium)
(3) Consider adding long-acting beta-agonist or long-acting
anticholinergic short-acting reliever agents as needed
iii. Persistent symptoms refractory to preceding therapies
(1) Try alternate-class bronchodilator
(2) Combine long-acting bronchodilator and ICS
(A) Indication for ICS includes FEV
1
50% of
predicted or frequent exacerbations
(B) Single-inhaler combination therapy with LABA
and ICS (Advair) appears to have benefits greater
than each agent alone
iv. Benefit still limited or side effects
(1) Add or substitute long-acting theophylline
e. Other therapies
i. Systemic corticosteroids
(1) No role in stable COPD
(2) Important for acute exacerbations
ii. Vaccination
(1) Yearly influenza vaccination reported to reduce serious
illness and death in COPD
(2) Pneumococcal vaccine
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C H A P T E R
3. Oxygen therapy
Long-term oxygen therapy (LTOT) improves survival,
exercise tolerance, sleep quality, and cognitive
performance.
a. Treating hypoxemia more important versus concern for
carbon dioxide (CO
2
) retention
b. Indications for supplemental oxygen
i. P
A
O
2
55 mm Hg
ii. SaO
2
88%
iii. SaO
2
88% with presence of cor pulmonale
c. Therapeutic goal SaO
2
90% during rest, sleep, and exertion
4. Pulmonary rehabilitation
a. Multidisciplinary program individually designed to optimize
physical and social performance and preserve patient autonomy
b. Typically includes exercise training, education, psychosocial/
behavioral intervention, nutritional therapy, outcome assess-
ment, promotion of long-term adherence to rehabilitation
recommendations
c. Documented benefits are decreased dyspnea, improved exercise
tolerance and health status, decreased health-care utilization.
5. Nutrition
a. COPD associated with negative energy and protein balance;
weight loss or being underweight associated with increased
mortality risk
b. Nutritional therapy
i. Goal: prevention of weight loss, preservation of
energy/protein balance
ii. Most effective when combined with exercise
6. Surgery for COPD
In highly selected patients, bullectomy and lung
volume reduction surgery may result in improved
spirometry, lung volume, exercise capacity, dyspnea, and
health-related quality of life.
a. In highly selected patients, lung transplantation can result in
improved pulmonary function, exercise capacity, and quality
of life as well as possible survival.
1389_Ch22_309-323 2/2/09 1:30 PM Page 317
P A R T
B. Acute exacerbation
1. Definition
a. Change in natural course of disease, characterized by increased
dyspnea, cough, and/or change in sputum quantity or quality,
which requires a change in management
2. Assessment
a. Assess severity of symptoms, perform physical examination,
and look for presence of high-risk comorbid conditions to
determine need for inpatient or outpatient care.
b. High-risk comorbid conditions include pneumonia, congestive
heart failure (CHF), new cardiac arrhythmia, renal or liver
failure, and history of previous exacerbations.
c. A physical examination looks for the following.
i. Tachypnea, tachycardia, and hyper- or hypotension
ii. Respiratory distress indicated by inability to speak in full
sentences, air movement on chest auscultation, and use of
accessory muscles
d. Pulse oximetry or arterial blood gas looks for presence of
hypoxemia and/or hypercapnia.
e. Selected patients should get chest x-ray (CXR), laboratory
evaluation, electrocardiogram (EKG), and sputum culture.
3. Outpatient treatment
a. Patient education to ensure proper inhaler technique and use
of spacer device (if not already using one)
b. Bronchodilators
i. Short-acting bronchodilators (albuterol/ipratropium)
ii. Consider nebulizer
iii. Consider LABA (if not already using)
c. Corticosteroids
i. Oral prednisone 3040 mg/day 510 days
ii. Consider ICS (if not already using)
d. Antibiotics
i. Particularly in patients with change in quantity or quality
of sputum
ii. First-line drugs: amoxicillin, doxycycline, macrolides
4. Inpatient
a. Indications for hospitalization
i. Presence of high-risk comorbidities
ii. Failure of outpatient therapy
iii. Marked increase in dyspnea
1389_Ch22_309-323 2/2/09 1:30 PM Page 318
C H A P T E R
iv. Inability to sleep or eat due to symptoms
v. New or worsening hypercapnia
vi. New or worsening hypoxemia
vii. Change in mental status
viii. Lack of home support
ix. Uncertain diagnosis
b. Bronchodilators
i. Short-acting bronchodilators (albuterol/ipratropium)
with spacer or nebulizer
ii. Increase dose and/or frequency
c. Supplemental oxygen
d. Systemic corticosteroids
i. Oral (if tolerates) or intravenous steroids
ii. Dose variable; trial of higher-dose steroids may be
indicated depending on severity and response
e. Antibiotics
i. Particularly in patients with change in quantity or quality
of sputum
ii. Base on local resistance patterns for Streptococcus
pneumoniae, Haemophilus influenza, and Moraxella
catarrhalis
f. Ventilatory support
Ventilatory support is indicated for patients with
severe exacerbations that may be indicated by
respiratory distress, accessory muscle use, hypercapnia
and acidemia, hypoxemia, and changes in mental status.
i. Ventilatory support can be invasive or noninvasive.
ii. Noninvasive positive-pressure ventilation (NIPPV)
is first-line therapy and has been shown in multiple
randomized controlled trials to decrease intubation rates,
mortality, infection, and hospital length of stay
X. End-of-Life Planning
A. Acute exacerbations of COPD can result in respiratory failure and
need for mechanical ventilation.
B. It is currently not possible to determine which patients will have
greater benefit versus burden with advanced life support, i.e., need
for tracheostomy and long-term ventilator assistance.
1389_Ch22_309-323 2/2/09 1:30 PM Page 319
P A R T
C. End-of-life planning should occur in periods of stable disease.
1. Prepare patients for life-threatening exacerbations.
2. Provide information regarding probable outcomes and existence
of palliative care options.
3. Enquire about patient preferences regarding end-of-life care.
4. Help patient execute a living will and durable power of attorney
for health care.
XI. Prognosis
A. FEV
1
is the most commonly used predictor of clinical outcomes.
B. Other factors associated with poor clinical outcomes include
presence of prior acute exacerbations with or without respiratory
failure, low body mass index (BMI), poor functional capacity,
presence of hyperinflation, and current cigarette smoking.
C. BODE index consists of the following (Fig. 22.2).
1.0
0.8
0.6
Quartile 1
Quartile 2
Quartile 3
Quartile 4
P<0.001
0.4
0.2
0.0
0 4
P
r
o
b
a
b
i
l
i
t
y

o
f

S
u
r
v
i
v
a
l
8 12 16 20 24
Months
No. at Risk 625 611 574 521 454 322 273 159 80
28 32 36 40 44 48 52
FIGURE 22.2 Kaplan-Meier survival curves for the four quartiles of the body
mass index, degree of airflow obstruction and dyspnea, and exercise capacity
index. Quartile 1 is a score of 02, quartile 2 is a score of 34, quartile 3 a
score of 56, and quartile 4 a score of 710. Survival differed significantly
among the four groups (p 0.001 by the log-rank test). (From Celli BR, Cote CG,
Marin JM, et al: The body-mass index, airflow obstruction, dyspnea, and exercise
capacity index in chronic obstructive pulmonary disease. New England Journal of
Medicine 2004; 350(10):10051012, Figure 1A, p. 1010.)
1389_Ch22_309-323 2/2/09 1:30 PM Page 320
C H A P T E R
1. Validated multidimensional index developed to predict death
in individual patients
2. Four components
a. Body mass index (B)
b. Airflow obstruction (O)
c. modified Medical Research Council (MMRC) dyspnea
score (D)
d. Exercise capacity (E)
3. 10-point scale, with higher numbers predictive of death
XII. Referral to Pulmonary Specialist
A. Referral to specialist care: confirm diagnosis, perform additional in-
vestigations, optimize and initiate treatment, exclude other illnesses
B. Possible indications for referral
1. Disease onset at age 40 years
2. Frequent exacerbations (two or more per year) despite
adequate treatment
3. Rapidly progressive course of disease
4. Severe COPD (FEV
1
50% predicted) despite optimal
treatment
5. Need for oxygen therapy
6. Onset of comorbid illness (osteoporosis, heart failure,
bronchiectasis, lung cancer)
MENTOR TIPS DIGEST
GOLD defines COPD as a disease state characterized by
airflow obstruction that is no longer fully reversible, usually
progressive, and associated with an abnormal inflammatory
response to noxious particles or gases.
COPD is underdiagnosed and undertreated, and it is a major
cause of morbidity and mortality globally.
COPD was the fourth leading cause of death in 2002 (125,500).
Cigarette smoking is the most important risk factor for COPD,
involving 85%90% of all cases.
COPD is characterized by a prolonged preclinical period of
2040 years with a marked continuous decline in lung function.
The diagnosis of COPD should be considered in current or
former smokers and in nonsmokers with other risk factors
who present with cough, sputum production, or dyspnea.
1389_Ch22_309-323 2/2/09 1:30 PM Page 321
P A R T
Resources
American Thoracic Society. Standards for the diagnosis and care of
patients with chronic obstructive pulmonary disease. American
Journal of Respiratory and Critical Care Medicine 152:S77S121,
1995.
Celli BR, Cote CG, Marin JM, et al. The body-mass index, airflow
obstruction, dyspnea, and exercise capacity index in chronic obstruc-
tive pulmonary disease. New England Journal of Medicine
350:10051012, 2004
Chapman KR, Mannino DM, Soriano JB, et al. Epidemiology and costs
of chronic obstructive pulmonary disease. European Respiratory
Journal 2006; 27:188207
Mannino DM, Homa DM, Akinbami LJ, et al. Chronic obstructive
pulmonary disease surveillanceUnited States, 19712000. MMWR
Surveillance Summary 51:116, 2002.
Pauwels RA, Buist AS, Calverley PM, et al. Global strategy for the diag-
nosis, management and prevention of chronic obstructive pulmonary
disease. NHLBI/WHO global initiative for chronic lung disease (GOLD)
workshop summary. American Journal of Respiratory Critical Care
Medicine 163:12561276, 2001.
Rabe KF, Begh B, Luppi F, et al. Update in chronic obstructive pulmonary
disease 2006. American Journal of Respiratory Critical Care Medicine
175:12221232, 2007.
Spirometry measures expiratory airflow and is most important
for diagnosis and staging.
The FEV
1
is best correlated with morbidity and mortality.
Stopping smoking can slow the loss of lung function and
decrease symptoms at any point in time.
All symptomatic patients warrant a trial of drug treatment.
Long-term oxygen therapy (LTOT) improves survival, exercise
tolerance, sleep quality, and cognitive performance.
In highly selected patients, bullectomy and lung volume
reduction surgery may result in improved spirometry, lung
volume, exercise capacity, dyspnea, and health-related quality
of life.
Ventilatory support is indicated for patients with severe exacer-
bations that may be indicated by respiratory distress, acces-
sory muscle use, hypercapnia and acidemia, hypoxemia, and
changes in mental status.
1389_Ch22_309-323 2/2/09 1:30 PM Page 322
C H A P T E R
Sutherland ER, Cherniack RM. Current concepts: Management of chronic
obstructive pulmonary disease. New England Journal of Medicine
350:26892697, 2004.
1. Which description is characteristic of COPD?
a. Airways obstruction that improves 20% with albuterol
b. Airways obstruction that is not fully reversible with albuterol
c. Restrictive lung disease due to chronic tobacco exposure
d. Alveolar infiltration with inflammatory cells
2. Which is minimal manifestation in order to make a diagnosis
of COPD?
a. Daily cough for more than 6 months
b. Daily sputum-producing cough for more than 6 months
c. Productive cough for at least 3 months in 2 consecutive years
d. Productive daily cough for at least 3 months
3. Concerning the relationship between cigarette smoking and COPD,
which of the following statements is correct?
a. Most persons who smoke pipe tobacco will develop COPD.
b. Most persons who smoke cigarettes will develop COPD.
c. Among persons with COPD, 15%25% have been cigarette smokers.
d. Among cigarette smokers, 15%25% will develop COPD
(85%90% of COPD patients had been smokers).
1389_Ch22_309-323 2/2/09 1:30 PM Page 323
324
DIABETES
Jeffrey S. Royce, MD, and Martin S. Lipsky, MD
CHAPTER
23
I. Introduction
A. Diabetes is a group of metabolic disorders characterized by hyper-
glycemia caused by two types of anomalies.
1. Defects in insulin secretion
2. Insulin resistance
II. Epidemiology
A. Diabetes is one of the most common diseases seen in a primary
care setting.
1. In the United States, 21 million people have diabetes (7% of
the population).
2. Diabetes accounts for one-sixth of all health-care expendi-
tures.
III. Classification and Diagnosis
A. Classification
1. Type 1 diabetes
a. Results from beta-cell destruction
b. An absolute insulin deficiency
c. Requires insulin to avoid ketoacidosis
2. Type 2 diabetes
a. Formerly known as noninsulin-dependent diabetes mellitus
b. Accounts for 90% of all cases of diabetes
c. Caused by insulin resistance and a progressive secretory
defect of insulin
3. Other specific types
a. Genetic defects
b. Endocrinopathies such as Cushing disease
1389_Ch23_324-336 2/2/09 1:30 PM Page 324
c. Pancreatic disease
d. Chemical- /drug-induced, e.g., thiazides and corticosteroids
4. Gestational diabetes mellitus
B. Diagnosis (Table 23.1)
1. Plasma glucose
a. The criteria for diagnosing diabetes in adults include a single
plasma glucose level greater than or equal to 200 mg/dL
accompanied by classic symptoms such as polyuria, polydipsia,
or an unexplained weight loss.
b. Additional criteria include fasting blood glucose of at least
126 mg/dL on two occasions or a 2-hour postprandial
glucose of 200 mg/dL or higher.
c. Blood glucose meters are not always accurate, and a finger-
stick testing result should be verified with a plasma glucose
level.
23 DIABETES 325
C H A P T E R
Measuring the fasting plasma glucose (FPG) is the
most common means of testing for diabetes.
Oral glucose tolerance testing is used primarily to
screen for diabetes during pregnancy.
d. The benefits of using the FPG include ease of testing, patient
acceptability, and low cost when compared with a glucose
tolerance test.
TABLE
Diagnostic Criteria for Diabetes
Glucose Level Type Values
23.1
Fasting blood glucose 126 on two or more separate
occasions
Random blood glucose 200 mg/dL with polyuria,
polydipsia, and polyphagia
2-hour postprandial glucose 200 mg/dL
1389_Ch23_324-336 2/2/09 1:30 PM Page 325
2. Glycosylated hemoglobin
a. Although a glycosylated hemoglobin (Hgb
A1c
) is not part
of the diagnostic criteria, it is an essential component for
measuring overall glucose control.
b. Hgb
A1c
is formed when glucose is bound non-enzymatically
to the hemoglobin molecule and reflects the average level
of glucose over the preceding 120 days.
c. The Hgb
A1c
provides an objective index that correlates with
the risk of diabetic complications.
d. If a patient is self-monitoring blood sugar levels at home,
the Hgb
A1c
can validate the accuracy.
e. Although the optimal frequency is not certain, experts
recommend two assays per year in stable type 2 diabetes.
f. Testing three or four times per year may be indicated when
adjusting therapy.
IV. Complications
A. Patients with diabetes often develop long-term complications in
addition to the symptoms related to elevated blood sugars.
P A R T
Maintaining glucose control as close to normal as possi-
ble reduces the risk of diabetic complications.
1. The Diabetes Control and Complication Trial (DCCT) firmly
established the benefit of good control in type 1 diabetics
for reducing the risk of microvascular (such as retinopathy
or neuropathy) complications. However, the DCCT did not
establish that good glycemic control reduced macrovascular
complications (atherosclerotic disease).
2. The United Kingdom Prospective Diabetes Study (UKPDS)
demonstrated that maintaining near normal glucose levels in
type 2 diabetics also reduces microvascular complications.
The American Diabetes Association (ADA) recom-
mends trying to achieve an Hgb
A1c
of 7%. Levels
above 8% suggest the need to reexamine treatment, either
by reemphasizing the adherence to current therapy or by
changing management.
1389_Ch23_324-336 2/2/09 1:30 PM Page 326
B. Macrovascular complications
1. Atherosclerotic disease, commonly referred to as macrovascular
disease, accounts for approximately 75% of all excess mortality
in patients with type 2 diabetes mellitus.
2. Most of the excess mortality rate is due to cardiovascular disease
and to complications from cerebral vascular or peripheral vascular
disease.
3. In addition to maintaining good glycemic control, it is critically
important to address other cardiovascular risk factors such as
smoking, hypertension, and hyperlipidemia.
4. The Seventh Report of the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure (JNC-VII) recommends a blood pressure of
less than 130/80 mm Hg for patients with diabetes.
23 DIABETES 327
C H A P T E R
ACE inhibitors are first-line antihypertensive agents
for patients with diabetes because of their potential
benefits on renal function and their lack of adverse effects
on lipid and glucose levels.
5. Many patients with type 2 diabetes have hyperlipidemia. Because
of the high prevalence of coronary artery disease with diabetes,
the National Cholesterol Education Panel (NCEP) recommends
annual screening for diabetic patients and initiating pharmaco-
logic treatment at low-density lipoprotein (LDL) levels of
130 mg/dL or higher, with an LDL target of 100 mg/dL or lower.
6. The ADA also recommends prophylactic aspirin use for patients
age 50 or older or those with cardiovascular risk factors.
7. Type 2 diabetes is often associated with a cluster of risk factors
known as the metabolic syndrome or insulin-resistance syndrome,
characterized by hyperinsulinemia and insulin resistance.
a. The metabolic syndrome is characterized by central obesity,
dyslipidemia, impaired fibrinolysis, and hypertension, each
of which is a risk factor for macrovascular disease.
C. Microvascular complications
1. Retinopathy is one of earliest signs of microvascular disease
a. The ADA recommends annual dilated eye examinations for
patients with diabetes.
1389_Ch23_324-336 2/2/09 1:30 PM Page 327
b. Any evidence of retinopathy merits an evaluation by an
ophthalmologist as timely appropriate laser therapy may
be effective in preserving vision.
c. Diabetes accounts for about 12% of all new cases of adult
blindness.
2. Nephropathy
P A R T
Nephropathy is one of the most common diabetic
complications.
a. The ADA recommends screening for microalbuminuria to
detect early nephropathy. Microalbuminuria is defined as the
presence of 30300 mg of urinary protein excreted over
24 hours (more than 300 mg is considered macroalbuminuria).
b. Microalbuminuria is most commonly measured using a spot
urine to determine the albumin:creatinine ratio. This measure-
ment correlates very well with a 24-hour urine collection.
c. The presence of microalbuminuria should signal the clini-
cian to do a careful retinal examination because retinopathy
may also be a marker for cardiovascular disease.
Intensifying glycemic control, reducing blood pressure
to less than 130/80 mm Hg, and reducing protein
intake are all strategies that may slow the progression of
nephropathy.
d. Angiotensin-converting enzyme (ACE) inhibitors have been
shown to have renal protective effects independent of their antihy-
pertensive effects. For patients who cannot take ACE inhibitors,
angiotensin-II receptor blockers (ARBs) are an alternative.
e. Diabetic nephropathy accounts for about a third of all patients
with end-stage renal disease.
3. Neuropathy
a. Diabetic autonomic neuropathy can cause bladder and bowel
dysfunction, impotence, orthostatic hypotension, and diarrhea.
b. Patients with diabetes may also experience serious sensory
neuropathy.
c. The presence of a neuropathy and vascular insufficiency
makes the diabetic patient prone to foot problems.
1389_Ch23_324-336 2/2/09 1:30 PM Page 328
V. Management
A. Diet (Table 23.2) and exercise
1. Overview
23 DIABETES 329
C H A P T E R
Painful neuropathies may respond to tricyclic antide-
pressants, gabapentin (Neurontin), pregabalin (Lyrica),
or duloxetine (Cymbalta).
Diet and exercise are the cornerstones of therapy for
type 2 diabetes.
a. Of patients with type 2 diabetes, 80%90% are overweight,
making weight loss a common and important goal.
b. Often a modest loss of 1020 pounds may be sufficient to
improve glycemic control.
c. Reducing fat intake is also important because of the risk of
developing vascular disease and dyslipidemia.
2. Exercise
a. The ADA recommends that individuals with diabetes try to
achieve 3045 minutes of moderate exercise at least three
times per week.
b. Before starting an exercise program, patients with diabetes
merit a thorough evaluation, including an assessment for
macrovascular and microvascular complications that might
be aggravated by physical activity.
TABLE
Nutritional Recommendations for Diabetes
Nutritional Component Recommendations
23.2
Protein 10%20% of calories; lower in patients with
nephropathy
Fat 30% of caloric intake, 10% from
saturated fats
Carbohydrates 60%70% of caloric intake
Fiber 2530 g/day dietary fiber
Alcohol 2 oz per day for men, 1 oz for women
1389_Ch23_324-336 2/2/09 1:30 PM Page 329
c. Many experts recommend that individuals undergo EKG
stress testing before embarking on a vigorous exercise program.
d. Patients with peripheral neuropathy need to avoid exercise
regimens that might damage their feet, and individuals with
retinopathy should avoid exercises that require straining.
B. Pharmacologic treatment with oral agents
1. Overview
a. Diet and exercise are often insufficient to achieve glycemic
control. Pharmacologic therapy should be considered when
glycemic goals are not met by diet and exercise alone within
3 months.
b. In addition to insulin, five classes of oral agents are available
for treating type 2 diabetes. All these medications need the
presence of endogenous or exogenous insulin to be effective.
2. Biguanide
a. The only biguanide on the market in the United States is
glucophage (Metformin).
b. It acts by inhibiting hepatic gluconeogenesis and by increas-
ing glucose uptake in the peripheral tissues.
c. Metformin when used alone does not cause hypoglycemia
but can potentiate hypoglycemia when used in conjunction
with insulin or sulfonylureas.
d. The most common side effects of Metformin are gastroin-
testinal (GI) (e.g., diarrhea, nausea, or dyspepsia).
e. These are generally mild and often resolve spontaneously
within 12 weeks.
f. A rare (1:100,000) but potentially fatal complication is
lactic acidosis.
g. Avoiding the use of Metformin in patients with renal dys-
function (creatinine 1.5 mg/dL in men; 1.4 mg/dL in
women), congestive heart failure, acute or chronic acidosis,
and hepatic dysfunction reduces the risk of lactic acidosis.
h. Metformin is similar in effectiveness to sulfonylureas and
reduces fasting blood sugar by 3060 mg/dL and the Hgb
A1C
by 1.5%.
P A R T
Because Metformin tends not to increase weight
and has a modest beneficial effect on lipid levels,
some experts view it as a first choice for monotherapy in
obese individuals with type 2 diabetes.
1389_Ch23_324-336 2/2/09 1:30 PM Page 330
3. Sulfonylureas
a. Sulfonylureas enhance insulin release from pancreatic beta
cells.
b. All sulfonylureas have the same mechanism of action and
differ only in their pharmacokinetic properties.
c. Contraindications include allergy, pregnancy, and significant
renal dysfunction.
d. The most common serious side effect of these medications is
hypoglycemia.
e. Therapy should begin with the lowest dose and titrated
slowly upward until glycemic control is achieved.
f. About 50%70% of patients with diabetes can be initially
controlled solely with a sulfonylurea.
g. As beta-cell function deteriorates, an additional 5%10%
per year of patients formerly controlled on sulfonylureas
will lose glycemic control.
23 DIABETES 331
C H A P T E R
Typically, patients with significant residual beta-cell
function respond best to sulfonylureas. These indi-
viduals have usually had diabetes for fewer than 5 years
and tend to be lean.
h. Sulfonylureas generally improve fasting blood sugars by
3060 mg/dL and Hgb
A1C
by 1.5%.
4. Thiazolidinediones (TZD)
a. These medications (rosiglitazone, pioglitazone) work by
increasing the sensitivity to insulin in the skeletal muscle,
liver, and adipose tissue.
b. They are used in combination with insulin and the other oral
medications.
c. The Hgb
A1C
is lowered approximately 0.5%1.4% by these
agents.
d. The most common side effects are weight gain and fluid
retention. For rosiglitazone, recent safety data from controlled
clinical trials revealed a potentially significant increase in the
risk of heart attack and heart-related deaths.
5. Alpha-glucosidase inhibitors
a. Alpha glucosidase is an enzyme that hydrolyzes disaccharides.
Inhibiting it limits the rate of carbohydrate absorption, reducing
postprandial elevation of glucose.
1389_Ch23_324-336 2/2/09 1:30 PM Page 331
b. The major side effects are flatulence, diarrhea, and abdominal
pain.
c. It has a smaller effect on fasting blood sugar than the other
oral agents and lowers Hgb
A1C
approximately 0.5%.
6. Dipeptidyl peptidase-4 (DPP-4) inhibitor
a. Currently sitagliptin is the only FDA-approved DPP-4 inhibitor.
b. DPP-4 is an enzyme that inactivates the incretins glucagon-like
peptide-1 (GLP-1) and glucose-dependent insulin-releasing
polypeptide (GIP).
c. GLP-1 is excreted by small-intestine L cells.
i. Stimulates glucose-dependent insulin receptor from
pancreatic beta cells
ii. Suppresses postprandial glucagon secretion from pancre-
atic 2 cells
iii. Slows gastric emptying
d. Currently DPP-4 inhibitors are used as an adjuvant therapy
with Metformin and the TZDs.
e. Glycosylated Hgb
A1C
is lowered by a modest 0.6%0.8%.
f. There is no weight gain caused by DPP-4 inhibitors.
P A R T
The DPP-4 inhibitors are eliminated renally; thus, dose
adjustment in moderate renal disease is necessary.
C. Parental medications administered subcutaneously
1. Incretin mimetic (exenatide) mimics action of GLP-1
a. Lowers postprandial glucose
b. Used in type 2 diabetics in combination with sulfonylureas
and Metformin.
c. Appears to lower Hgb
A1C
by 0.5%1%
d. Is associated with weight loss
e. High frequency of GI side effects
f. Administered twice daily before a meal
2. Amylin agonist (pramlintide)
a. Pramlintide is a synthetic analogue of the beta-cell hormone
amylin.
b. Its mechanism of action is suppression of glucagon secretion,
slowing of gastric emptying, induction of satiety, and reduction
of food intake.
1389_Ch23_324-336 2/2/09 1:30 PM Page 332
c. It is used with insulin for the treatment of type 1 or type
2 diabetes.
d. Pramlintide is administered subcutaneously before meals.
e. The Hgb
A1C
reduction is in the 0.5%0.7% range.
f. GI side effects such as nausea predominate.
g. Weight loss is associated with this medication.
3. Insulin
a. Insulin is the oldest treatment of diabetes.
b. Eventually almost 50% of type 2 diabetics require it.
c. Unlike other medications, there is no maximum dosage of
insulin.
d. Characteristics of insulin preparations vary in terms of onset
of action and duration of action.
e. Patients on insulin are best managed in conjunction with
self-monitoring at home using a glucometer.
D. Combination therapy
1. Type 2 diabetes is a progressive disease. Monotherapy may be
ineffective at the outset or may become ineffective with disease
progression.
2. Combination therapy with two or more agents that work by
different mechanisms may reduce the blood sugar to an
acceptable level.
3. A biguanide combined with a sulfonylurea is the most widely
studied combination.
23 DIABETES 333
C H A P T E R
The effects of these two medications are additive;
switching from a biguanide to a sulfonylurea generally
does not improve control.
4. The benefit of using insulin with oral agents over insulin alone
has yet to be clearly demonstrated, but insulin and a sulfonylurea,
insulin and a biguanide, or insulin and a thiazolidinedione are
commonly combined.
1389_Ch23_324-336 2/2/09 1:30 PM Page 333
P A R T
MENTOR TIPS DIGEST
Measuring the fasting plasma glucose (FPG) is the most com-
mon means of testing for diabetes.
Oral glucose tolerance testing is used primarily to screen for
diabetes during pregnancy.
Maintaining glucose control as close to normal as possible
reduces the risk of diabetic complications.
The ADA recommends trying to achieve an Hgb
A1c
of 7%.
Levels above 8% suggest the need to reexamine treatment,
either by reemphasizing the adherence to current therapy or by
changing management.
ACE inhibitors are first-line antihypertensive agents for patients
with diabetes because of their potential benefits on renal
function and their lack of adverse effects on lipid and glucose
levels.
Nephropathy is one of the most common diabetic compli-
cations.
Intensifying glycemic control, reducing blood pressure to less
than 130/80 mm Hg, and reducing protein intake are all
strategies that may slow the progression of nephropathy.
Painful neuropathies may respond to tricyclic antidepressants,
gabapentin (Neurontin), pregabalin (Lyrica), or duloxetine
(Cymbalta).
Diet and exercise are the cornerstones of therapy for type
2 diabetes.
Because Metformin tends not to increase weight and has a
modest beneficial effect on lipid levels, some experts view it
as a first choice for monotherapy in obese individuals with
type 2 diabetes.
Typically, patients with significant residual beta-cell function
respond best to sulfonylureas. These individuals usually have
had diabetes for less than 5 years and tend to be lean.
The DPP-4 inhibitors are eliminated renally; thus, dose adjust-
ment in moderate renal disease is necessary.
The effects of biguanides and sulfonylureas are additive;
switching from a biguanide to a sulfonylurea generally does
not improve control.
1389_Ch23_324-336 2/2/09 1:30 PM Page 334
Resources
American Diabetes Association. Clinical practice recommendations 2007.
Diabetes Care 23:S1S65, 2007.
This position paper provides guidelines for care in terms of treat-
ment goals, monitoring patients, and prevention strategies. It
reflects a combination of evidence from the medical literature
and expert opinion.
American Diabetes Association. http://www.diabetes.org/ada/facts.asp
This Web site is an excellent resource for information about diabetes
and complications, epidemiology, demographics, and management in
special populations.
DCCT Research Group. The effect of intensive diabetes management on
long-term complications in insulin-dependent diabetes mellitus. New
England Journal of Medicine 329:97786, 1993.
A landmark study that provided evidence that tight control for patients
with type 1 diabetes reduced complications.
Nathan D, et al. Management of hyperglycemia in type 2 diabetes: A
consensus algorithm for the initiation and adjustment of therapy.
Diabetes Care 29:19631972, 2006.
1. What is the most common cause of diabetes mellitus in the
United States?
a. Autoimmune beta-cell destruction with absolute insulin
deficiency
b. Progressive beta-cell insulin secretory failure associated with insulin
resistance
c. Pancreatic disease with beta-cell destruction
d. Glucocorticoid-induced hyperglycemia
23 DIABETES 335
C H A P T E R
1389_Ch23_324-336 2/2/09 1:30 PM Page 335
2. A 53-year-old man has polyuria, polydipsia, and 5-pound weight
loss for a month. His body mass index is 31. Past medical history
and physical examination are otherwise unremarkable. Which of
the following test results would confirm your clinical suspicion of
diabetes?
a. Non-fasting plasma glucose 215 mg/dL
b. Single-fasting plasma glucose 185 mg/dL
c. 2-hour postprandial plasma glucose 185 mg/dL
d. Hgb
A1c
8.1%
3. A 53-year-old man has polyuria, polydipsia, and 5-pound weight loss for
a month. His body mass index is 31. Past medical history and physical
examination are otherwise unremarkable. You have confirmed the diag-
nosis of type-2 diabetes by appropriate testing. What should be initial
therapy in order to achieve Hgb
A1c
7.0%?
a. Glyburide 1.252.5 mg daily
b. Metformin 1000 mg daily
c. Insulin glargine 1020 units every morning
d. Initiate calorie-restricted diet and vigorous exercise at least three
times weekly
P A R T
1389_Ch23_324-336 2/2/09 1:30 PM Page 336
337
HYPERLIPIDEMIA
Gary J. Martin, MD
CHAPTER
24
I. Pathophysiology and Epidemiology
A. Hyperlipidemia has many causes and in most patients is multifac-
torial. The basic causes are related to liver metabolism, genetic
traits, and diet. In some patients the genetic tendencies are strong
enough to be apparent, and the patient has a familial hyperlipi-
demia. Most patients have either pure hypercholesterolemia or a
mixed pattern with increased triglycerides also.
B. Metabolic syndrome is a fairly common presentation with low
high-density lipoprotein (HDL) and elevated triglycerides as well
as often an elevated blood sugar, blood pressure, and excess
abdominal fat. It is associated with inflammatory and prothrom-
botic markers. Table 24.1 has the most widely accepted criteria
in the United States.
Metabolic syndrome has become increasingly common
in the United States. It is estimated that more than
50 million Americans have it.
II. Signs and Symptoms
A. Patients with hyperlipidemia should always have their history
explored for signs of hypothyroidism, nephrotic syndrome, and
such target organ damage as coronary artery disease, peripheral
vascular disease, and cerebral vascular disease.
B. Clues may be found on physical examination, including checking
the Achilles tendon for thickening, the skin for xanthelasma, and
the cornea for premature arcus senilis.
1389_Ch24_337-345 2/2/09 1:31 PM Page 337
III. History and Physical Examination
A. Key parts of the history include:
1. A history of diabetes
2. Coronary artery disease (angina, prior myocardial infarction)
3. Peripheral vascular disease (claudication or transient ischemic
attacks)
4. Drugs that may adversely affect lipids, including progestins,
anabolic steroids, corticosteroids, and anti-retrovirals
B. Key parts of the physical examination include:
1. Waist circumference, as it may provide additional information
beyond body mass index.
2. Carotid and femoral bruits, as possible signs of atherosclerosis
A. Liver disease, hypothyroidism, and nephrotic syndrome should be
ruled out initially in patients with hyperlipidemia because the
secondary causes are often quite treatable and might need atten-
tion independently.
P A R T
TABLE
Definition of Metabolic Syndrome
The American Heart Association (AHA) and the U.S. National Heart, Lung,
and Blood Institute (NHLBI) recommend that the metabolic syndrome
be identified as the presence of three or more of these components:
Components Values
Elevated waist circumference Men: Equal to or greater than
40 inches (102 cm)
Women: Equal to or greater than
35 inches (88 cm)
Elevated triglycerides Equal to or greater than 150 mg/dL
Reduced HDL cholesterol Men: Less than 40 mg/dL
Women: Less than 50 mg/dL
Elevated blood pressure Equal to or greater than 130/85 mm Hg
Elevated fasting glucose Equal to or greater than 100 mg/dL
24.1
Mild hypothyroidism can contribute to significant eleva-
tion of lipids, and treatment can improve cholesterol
levels.
1389_Ch24_337-345 2/2/09 1:31 PM Page 338
V. Laboratory Testing
A. Thyroid-stimulating hormone (TSH), basic chemical panel, and a
hepatic panel including an albumin test are appropriate tests.
B. Fasting lipids are the gold standard, although there is increasing
evidence that measuring triglycerides postprandial may have
even more predictive value for atherosclerosis. Testing urine for
proteinuria is also a useful screen for nephrotic syndrome.
VI. Management
A. Management is divided into primary prevention for patients with
no apparent end-organ damage and secondary prevention for
patients with known coronary or peripheral vascular disease.
B. Diet is the mainstay of treatment and is appropriate for all patients
and adequate for many.
C. American Heart Association has a recommended diet based on
many epidemic studies. This diet is low in fat and cholesterol.
1. The Mediterranean diet has been tested in randomized trials
and has been shown to reduce recurrent myocardial infarctions
in patients with a previous infarct. This is a diet that is high in
grains and low in meat and that uses olive oil.
D. Many patients need medication for their cholesterol to get to a
low-density lipoprotein (LDL) goal. Table 24.2 lists the risk
factors that should be weighed in this decision.
E. For primary prevention patients, an LDL goal is generally 160
(Table 24.3).
F. For most patients with coronary or peripheral vascular disease, or
diabetes that is now being used as a proxy for atherosclerosis, the
goal is an LDL 100. Recent data suggest that patients with acute
coronary syndromes and even stable coronary disease may be better
off with an LDL of 5070 mg/dL. At these levels, patients have
fewer recurrent events and possibly more regression of plaque.
G. Most information is available for the statins, particularly atorvas-
tatin, pravastatin, and simvastatin.
1. Pravastatin, lovastatin, and simvastatin are available as generic
drugs. Many statins average about $100/month for patients.
2. Two national chains offer pravastatin and lovastatin for
$4/month.
H. Statins vary in their potency and dose-response curve, providing a
30%50% reduction in LDL. The most potent statins are atorvastatin
and rosuvastatin.
24 HYPERLIPIDEMIA 339
C H A P T E R
1389_Ch24_337-345 2/2/09 1:31 PM Page 339
P A R T
TABLE
24.2
Major Risk Factors (Exclusive of LDL Cholesterol)
That Modify LDL Goals*
Risk Factor Details
Cigarette smoking Counsel on means of cessation
Hypertension BP 140/90 mm Hg or on antihypertensive
medication
Low HDL cholesterol 40 mg/dL
Family history of CHD in male first-degree

premature coronary relative 55 years
heart disease (CHD) CHD in female first-degree
relative 65 years
Age Men 45 years
Women 55 years*
*In ATP III, diabetes is regarded as a CHD risk equivalent.
HDL cholesterol 60 mg/dL counts as a negative risk factor; its presence removes
one risk factor from the total count.
Adapted from U.S. National Institutes of Health. Third Report of the National Cholesterol
Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults (Adult Treatment Panel) Executive Summary. May 2001; NIH
Publication Number 01-3670.
TABLE
24.3
Treatment Goals Based on Patient Risk
LDL Level to LDL Level to
Initiate Therapeutic Consider Drug
Risk Category LDL Goal Lifestyle Change Therapy
CHD or CHD
risk equi-
valents
(10-year
risk 20%)
2+ risk
factors
(10-year
risk 20%)
100
mg/dL
130
mg/dL
130 mg/dL
(100129
mg/dL: drug
optional)*
10-year risk at
10%20%:
130 mg/dL
10-year risk
10%: 160
mg/dL
100
mg/dL
130
mg/dL
1389_Ch24_337-345 2/2/09 1:31 PM Page 340
I. Fibrates are used for patients who have low HDLs and elevated
tryglycerides, i.e., triglycerides greater than at least 200 mg/dL.
There is much less information documenting benefits for fibrates,
but some studies suggest fewer recurrent myocardial infarctions in
patients treated with these drugs.
J. Niacin is an inexpensive alternative. It does have relatively modest
LDL-lowering effects but can raise HDL significantly.
K. The following are important facts about statins.
C H A P T E R
Treatment Goals Based on Patient Risk (continued)
LDL Level to LDL Level to
Initiate Therapeutic Consider Drug
Risk Category LDL Goal Lifestyle Change Therapy
01 risk
factor
*Some authorities recommend use of LDL-lowering drugs in this category if an LDL cholesterol
100 mg/dL cannot be achieved by therapeutic lifestyle changes. Others prefer use of drugs
that primarily modify triglycerides and HDL, e.g., nicotinic acid or fibrate. Clinical judgment
may also call for deferring drug therapy in this subcategory.
Almost all people with 01 risk factor have a 10-year risk 10%; this 10-year risk
assessment in people with 01 risk factor is necessary.
Adapted from U.S. National Institutes of Health. Third Report of the National Cholesterol
Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High
Blood Cholesterol in Adults (Adult Treatment Panel) Executive Summary. May 2001; NIH
Publication Number 01-3670.
160
mg/dL
190 mg/dL
(160189
mg/dL: LDL-
lowering drug
optional)
160
mg/dL
Statins for the most part are well-tolerated drugs, but rare
cases of rhabdomyolysis occur (1%). More frequently,
cases of myalgias are seen with normal or mild creatinine
phosphokinase (CPK) elevations.
1. Mild liver function abnormalities (transaminase elevations) can
also be seen in up to 2% of patients. However, these are rarely
clinically significant.
2. Combination treatment is generally reserved for patients with
known atherosclerosis that is otherwise poorly controlled.
1389_Ch24_337-345 2/2/09 1:31 PM Page 341
Fibrates and niacin may be combined with statins; however,
they may increase the risk of rhabdomyolysis.
3. The best monitoring for rhabdomyolysis is an activated
patient who understands what the symptoms may be and
knows to stop the drug and contact the physician the same day
diffuse unexplained muscle aches occur.
4. Periodic CPK monitoring, although sometimes done, is not
particularly helpful unless used to evaluate symptoms of myalgia
5. One needs to be sensitive that many additional medications can
elevate statin levels and thereby precipitate rhabdomyolysis.
This includes fairly common drugs such as antifungals and
macrolides and even grapefruit juice.
L. Bile sequestrant agents, such as cholestyramine, colesevelam, and
cholestipol, are also used in some patients who do not reach a
goal with a statin or who cannot tolerate a statin. These drugs are
limited by the fact that they also absorb other medications and
need to be separated by a number of hours from other doses.
They can worsen hypertriglyceridemia.
M. Ezetimibe has had the most impressive impact as an adjunct
therapy with statins. This drug has been documented to be safe
in terms of drug interactions with statins and can provide an addi-
tional 25% reduction in LDL levels. It may also be an option for
patients who cannot tolerate statins. Unfortunately, ezetimibe has
not been studied in any clinical outcome trials, but several are in
progress.
P A R T
MENTOR TIPS DIGEST
Metabolic syndrome has become increasingly common in
the United States. It is estimated that more than 50 million
Americans have it.
Mild hypothyroidism can contribute to significant elevation
of lipids, and treatment can improve cholesterol levels.
Statins for the most part are very well tolerated drugs, but rare
cases of rhabdomyolysis occur (1%). More frequently, cases
of myalgias are seen with normal or mild CPK elevations.
1389_Ch24_337-345 2/2/09 1:31 PM Page 342
Resources
Blankenhorn DM, et al. Beneficial effects of combined colestipol-niacin
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Journal of the American Medical Association 257:32333240, 1987
The first report of regression of coronary atherosclerosis in subjects
intensively treated with lipid-lowering medications.
Cannon CP, Braunwald E, McCabe CH, et al. Comparison of intensive
and moderate lipid lowering with statins after acute coronary syndromes.
This study from 2004 supported getting to LDL levels of approximately
6080 mg/dL.
Downs JR, Clearfield M, Weiss S, et al. Primary prevention of acute coro-
nary events with lovastatin in men and women with average cholesterol
levels: Results of AFCAPS/TexCAPS. Journal of the American Medical
Association 279:16151622, 1998.
Forrester JS, et al. Lipid lowering versus revascularization: An idea whose
time (for testing) has come. Circulation 96:13601362, 1997
Haffner SM, Lehto S, Ronnemaa T, et al. Mortality from coronary heart
disease in subjects with type 2 diabetes and in nondiabetic subjects
with and without prior myocardial infarction. New England Journal of
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La Rosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with
atorvastatin in patients with stable coronary disease. New England
Journal of Medicine 352: 14251435, 2005.
MRC/BHF Heart Protection study Collaborative Group. MRC/BHF heart
protection study of cholesterol lowering with simvastatin in 20,536
high-risk individuals: A randomized placebo-controlled trial. Lancet
360:722, 2002.
National Institute of Health. Third report of the national cholesterol edu-
cation program expert panel on detection, evaluation, and treatment of
high blood cholesterol in adults (adult treatment panel) executive
summary. May 2001; NIH Publication Number 01-3670.
Nissen SE, Tuzcu EM, Schoenhagen P, et al. Effect of intensive compared
with moderate lipid-lowering therapy on progression of coronary
atherosclerosis. JAMA 2004; 291:10711080.
This is another study from 2004 that supported getting to LDL levels
of approximately 6080.
C H A P T E R
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Nissen SE; Nicholls SJ; Sipahi I, et al. Effect of very high-intensity statin
therapy on regression of coronary atherosclerosis: The ASTEROID trial.
Pasternak RC, Smith SC, Bairey-Merz CN, et al. ACC/AHA/NHLBI
clinical advisory on the use and safety of statins. Circulation
106:10241028, 2002.
Pitt B, Waters D, Brown WV, et al. Aggressive lipid-lowering therapy
compared with angioplasty in stable coronary artery disease. New England
Lipid lowering actually led to lower event rate than PCI in low-risk patients.
Rubins HB, Robins SJ, Colins D, et al. Gemfibrozil for the secondary
prevention of coronary heart disease in men with low levels of high-
density lipoprotein cholesterol: Veterans Affairs high-density lipopro-
tein cholesterol intervention trial study group. New England Journal
of Medicine 341:410418, 1999.
Sacks FM. High-intensity statin treatment for coronary heart disease.
Scandinavian Simvastatin Survival Study Group. Randomized trial of
cholesterol lowering in 4444 patients with coronary heart disease: The
Scandinavian simvastatin survival study. Lancet 344:13831389, 1994.
Simvastatin results in decreased CHD incidence and mortality and a
30% decrease in all-cause mortality. Coronary artery disease patients
LDL 187122 with simvastatin: mortality 12% versus 8% (5.4 yr F/U).
Shepherd J, et al. Prevention of coronary heart disease with pravastatin in
men with hypercholesterolemia. New England Journal of Medicine
333:13011307, 1995.
Primary prevention (west of Scotland study) LDL 192140.
Approximately 10% versus 6% major event rate over 6 years.
Singh RB, Dubnov G, Niaz MA, et al. Effect of an Indo-Mediterranean
diet on progression of coronary artery disease in high risk patients
(Indo-Mediterranean diet heart study): A randomized single-blind trial.
Lancet 360:14551461, 2002.
Smith SC, Allen J, Blair SN, et al. AHA/ACC guidelines for secondary
prevention for patients with coronary and other atherosclerotic vascular
disease: 2006 Update. Journal of the American College of Cardiology
47:21302139, 2006.
Most recent guidelines that advocate for LDL 70, beta blockers (BB),
angiotensin-converting enzyme inhibitor (ACEI), exercise, BMI 25, blood
pressure (BP) control <130140/8090, ASA, and quitting smoking.
P A R T
1389_Ch24_337-345 2/2/09 1:31 PM Page 344
1. What is a physical finding that suggests hyperlipidemia?
a. Subcutaneous cholesterol-filled nodules
b. Flare-shaped red deposits in retina
c. Periarticular swelling of the distal phalangeal joints of hands
d. Third heart sound
2. What ocular physical finding suggests hyperlipidemia?
a. Cloudiness in lens
b. Brown deposit around periphery of cornea seen with slit-lamp
c. White-gray deposit around periphery of cornea
d. Blue sclerae
3. A 64-year-old woman has been under your care for years. Several
screening total cholesterol measurements had been 180200 mg/dL.
Now random total cholesterol is 286 mg/dL. Which test is most
appropriate?
a. Serum Apo-B
b. Serum direct LDL
c. ACTH
d. TSH
C H A P T E R
1389_Ch24_337-345 2/2/09 1:31 PM Page 345
346
OBESITY
Robert F. Kushner, MD
CHAPTER
25
I. Pathophysiology
A. Etiology
The etiology of obesity is multifactorial.
1. Obesity is brought about by an interaction between predisposing
genetic and metabolic factors and a rapidly changing environment.
2. Interactive influences include social, behavioral, physiologic,
metabolic, cellular, and molecular factors.
3. By definition, obesity is a disease of energy imbalance, in
which energy
in
exceeds energy
out
. The resultant accretion of
body fat and, to a lesser extent, lean body mass, is a function
of time (months or years) surplus energy (kcalories). This
concept is consistent with the First Law of Thermodynamics,
or the Law of Conservation of Energy.
4. There is a positive energy balance produced whenever energy
intake is increased, energy output is lowered, or both occur.
5. Energy balance is critical. A daily calorie mismatch of only
1% would theoretically lead to a gain of approximately
2.5 pounds of fat per year.
6. Heredity clearly plays a role in human obesity. The evidence
for a genetic basis for obesity comes from several areas of
investigation, including animal models, human inherited disor-
ders (e.g., Prader-Willi syndrome), adoption studies, human
twin studies, family metabolic studies, and human intervention
studies.
1389_Ch25_346-358 2/2/09 1:31 PM Page 346
B. Pathology
25 OBESITY 347
C H A P T E R
Obesity is a pervasive and insidious disorder affecting
nine organ systems and over 40 conditions and diseases.
1. Obesity-related comorbidities
a. Endocrine: type 2 diabetes, dyslipidemia, metabolic
syndrome, polycystic ovarian syndrome (PCOS)
b. Cardiovascular: hypertension, congestive heart failure
(CHF), atrial fibrillation, left ventricular hypertrophy (LVH)
c. Respiratory: reduced lung compliance, asthma, obstructive
sleep apnea (OSA), obesity hypoventilation syndrome
d. Gastrointestinal: gallstones, gastroesophageal reflux disease
(GERD), nonalcoholic fatty liver disease (NAFLD)
e. Genitourinary: urinary incontinence, hypogonadism (male),
complications of pregnancy, uterine cancer, obesity-related
nephropathy
f. Integument: carbuncles and furuncles, intertrigo, stretch
marks, venous stasis pigmentation
g. Musculoskeletal: arthralgias and arthritis, Blount disease
(childhood)
h. Psychological: reduced quality of life, depression, poor self-
esteem and body image
2. Pathophysiology
The pathophysiology of obesity is multifactorial.
a. It is the result of changes in diet, physical inactivity, hemo-
dynamics, weightbearing mechanics, and metabolic and
endocrine abnormalities.
b. Alterations in function are often insidious, progressing from
subclinical physiologic changes to reduction in quality of
life and symptomatic disease states.
c. New insights include the following.
1389_Ch25_346-358 2/2/09 1:31 PM Page 347
i. The VAT adipocytes and adipose connective tissue secrete
products called adipokines. These bioactive peptides act
locally and distally through autocrine, paracrine, and
endocrine effects.
ii. Secreted factors include the energy balance-regulating
hormone leptin, cytokines such as interleukin (IL)-6 and
tumor necrosis factor (TNF)-alpha, prothrombotic agents
such as plasminogen activator inhibitor 1 (PAI-1), and a
component of the blood-pressure regulating system:
angiotensinogen.
iii. In obesity, increased production of most adipokines affects
multiple functions such as appetite and energy balance,
immunity, insulin sensitivity, angiogenesis, blood pressure,
lipid metabolism, and hemostasis. For example, IL-6
leads to hypertriglyceridemia by stimulating lipolysis
and hepatic triglyceride secretion; TNF-alpha directly
decreases insulin sensitivity and increases lipolysis in
adipocytes.
II. Epidemiology
A. The prevalence of obesity is increasing to epidemic proportions in
the United States.
P A R T
Recent studies have linked the metabolic and inflam-
matory abnormalities seen in obesity to the visceral
adipose tissue (VAT) compartment.
About two-thirds of American adults are overweight, and
about one-third is obese.
About one-third of American children and adolescents
(age 619 years) is overweight or obese.
1. An analysis based on the 19992000 data from the National
Health and Nutrition Examination Survey (NHANES) esti-
mated the adult numbers at 64.5% (overweight) and 30.5%
(obese); 31% of children and adolescents were overweight
or obese.
1389_Ch25_346-358 2/2/09 1:31 PM Page 348
2. Differences in prevalence exist in many segments of the popula-
tion, particularly among blacks and Mexican Americans. Of adult
African American women, 50% are obese, and 40% of Hispanic
women are obese, compared with 30% of white women. Mexican
American men have a higher prevalence of overweight and
obesity (75%) than non-Hispanic white men (67%) and non-
Hispanic black men (61%).
B. Obesity is now considered a global health problem. The World
Health Organization (WHO) has concluded that overweight
and obesity are now so common that they are replacing the more
traditional public health concerns such as undernutrition and
infectious diseases as some of the most significant contributors
to ill health.
III. Prevention
A. Maintaining a healthy body weight by balancing dietary calories
with physical activity is recommended by all professional guide-
lines including the 2005 USDA Dietary Guidelines for Healthy
Americans.
25 OBESITY 349
C H A P T E R
Clinicians should provide behavioral counseling on
preventing weight gain as part of preventive counseling.
The number and severity of organ-specific comorbid
conditions usually rise with increasing levels of obesity.
IV. Signs and Symptoms
A. Obese patients at very high absolute risk who trigger the need for
intense risk-factor modification and management include those
with the following pathology.
1. Established coronary heart disease
2. Presence of other atherosclerotic diseases such as peripheral
arterial disease, abdominal aortic aneurysm, or symptomatic
carotid artery disease
3. Type 2 diabetes
4. Sleep apnea
B. Additional triggers for treatment include development of any other
obesity-related comorbid condition listed earlier.
1389_Ch25_346-358 2/2/09 1:31 PM Page 349
V. History and Physical Examination
A. A comprehensive history that addresses issues and concerns
specific to obesity should be taken.
1. Chronological history of weight gain; age at onset, description
of weight gain (and loss), and inciting events
2. Response to previous weight-loss attempts
3. Effect of excess body weight on health; important to elicit
patients own perceptions regarding how overweight affects
them physically, psychologically, and socially
4. Expectations from a weight management program
5. A thorough medication history to uncover possible drug-
induced weight gain and medications interfering with weight
loss (such as antipsychotics, antidepressants, mood stabilizers,
antidiabetic agents, and steroids)
6. Determination of fitness level; cardiorespiratory fitness (mea-
sured by maximal treadmill exercise test) is important predictor
of all-cause mortality independent of body mass index (BMI)
and body composition
B. For the physical examination, the following insights apply.
P A R T
Assessment of risk status due to overweight or obesity is
based on the patients BMI, waist circumference, and the
existence of comorbid conditions.
1. BMI is calculated as weight (kg)/height (m)
2
, or as weight
(pounds)/height (inches)
2
703.
A desirable or healthy BMI is 18.524.9 kg/m
2
, over-
weight is 2529.9 kg/m
2
, and obesity is 30 kg/m
2
.
Obesity is categorized as class I (30.034.9 kg/m
2
), class II
(35.039.9 kg/m
2
), and class III (40 kg/m
2
).
Measurement of waist circumference should be
obtained in those individuals with a BMI 35 kg/m
2
.
a. Abdominal fat is clinically defined as a waist circumference
102 cm (40 inches) in men and 88 cm (35 inches)
in women according to the APT III report. Lower waist
circumference thresholds exist for Asian populations.
1389_Ch25_346-358 2/2/09 1:31 PM Page 350
2. Special attention needs to be given to measurement of blood
pressure.
a. A bladder cuff that is not the appropriate width for the
patients arm circumference will cause a systematic error
in blood pressure measurement. The error in blood pressure
measurement is larger when the cuff is too small relative to
the patients arm circumference than when it is too largea
situation commonly encountered among the obese.
b. It has been demonstrated that the most frequent error in
measuring blood pressure is mis-cuffing, with undercuffing
large arms accounting for 84%.
VI. Differential Diagnosis
A. In the majority of patients, obesity is the result of environmental
exposure to increased caloric intake and reduced energy expendi-
ture associated with a poorly defined genetic vulnerability.
1. Single-gene disorders are uncommon and include the syn-
dromes of Prader-Willi, Bardet-Biedl, Cohen, and Alstrm,
along with deficiencies in the leptin and MC4 receptors.
B. Laboratory tests consist of the following.
1. There is no single laboratory test or diagnostic evaluation that
is indicated for all patients with obesity. The specific evaluation
performed should be based on presentation of symptoms, risk
factors, and index of suspicion; however, many screening
guidelines recommend a fasting lipid panel and blood glucose
measurement at presentation.
2. Other tests to consider include the liver function tests alanine
aminotransferase (ALT) and aspartate aminotransferase
(AST) (for NAFLD), thyroid-stimulating hormone (TSH)
(for hypothyroidism), and a polysomnogram for patients
presenting with symptoms consistent with obstructive
sleep apnea.
25 OBESITY 351
C H A P T E R
An increased waist circumference has been found
to be predictive of the risk of having hypertension,
diabetes, dyslipidemia, and the metabolic syndrome
compared with those who have normal waist circumference.
1389_Ch25_346-358 2/2/09 1:31 PM Page 351
VII. Management
A. Lifestyle modification
P A R T
Lifestyle management incorporates the three essential
components of obesity care: dietary therapy, physical
activity, and behavior therapy.
The diet needs to produce a calorie deficit of 5001000
kcal/day, resulting in a weight loss of 12 lb/week.
1. Obesity is a disease of energy imbalance; patients must learn
how and when energy consumed (diet), how and when energy
expended (physical activity), and how to incorporate this infor-
mation into daily life (behavior therapy)
2. Diet
a. This is usually consistent with a diet containing 10001200
kcal/day for most women and 12001600 kcal/day for men.
b. The diet may be instituted using a broad range of acceptable
macronutrient levels consisting of 45%65% of total calories
from carbohydrates, 20%35% of total calories from fat, and
10%35% of total calories from protein.
3. Physical activity
a. In addition to increasing calorie expenditure, physical activity
is beneficial for improved cardiorespiratory fitness, cardio-
vascular disease and cancer risk reduction, and improved
mood and self-esteem.
b. The minimum public health recommendation for physical
activity is 30 minutes of moderate intensity physical activity
on most, preferably all, days of the week (150 minutes
per week).
c. For long-term weight loss, higher amounts of exercise (e.g.,
200300 minutes per week or 2000 kcal/week) are needed.
4. Behavior therapy
a. The most commonly used approaches include motivational
interviewing, transtheoretical model and stages of change,
and cognitive behavioral therapy (CBT).
b. CBT incorporates various strategies intended to help
change and reinforce new dietary and physical activity be-
1389_Ch25_346-358 2/2/09 1:31 PM Page 352
haviors. Strategies include self-monitoring techniques
(e.g., journaling, weighing and measuring food and activ-
ity), stress management, stimulus control, social support,
problem solving, and cognitive restructuring, i.e., helping
patients develop more positive and realistic thoughts
about themselves.
25 OBESITY 353
C H A P T E R
When recommending any behavioral lifestyle change,
have the patient identify what, when, where, and how
the behavioral change will be performed.
c. Have the patient and yourself keep a record of the antici-
pated behavioral change, and monitor progress at the next
office visit.
d. Combined interventions of diet, physical activity, and behavior
therapy provide the most successful therapy for weight loss
and weight maintenance.
B. Pharmacotherapy
Adjuvant pharmacologic treatments should be considered
for patients with a BMI 30 kg/m
2
or with a BMI 27 kg/m
2
who also have concomitant obesity-related risk factors or dis-
eases and for whom dietary and physical activity therapies have
not been successful.
1. Centrally acting anorexiant medications
a. Sibutramine (Meridia) functions as a serotonin and norepi-
nephrine reuptake inhibitor (SNRI).
i. Sibutramine produces a dose-dependent weight loss
(available doses are 5-, 10-, and 15-mg capsules), with
an average loss of about 5%9% of initial body weight
at 12 months.
ii. The most commonly reported adverse events are headache,
dry mouth, insomnia, and constipation. A dose-related
increase in blood pressure and heart rate may require
discontinuation of the medication. A dose of 1015 mg/day
causes an average increase in systolic and diastolic blood
pressure of 24 mm Hg and an increase in heart rate of
46 beats/min.
1389_Ch25_346-358 2/2/09 1:31 PM Page 353
b. Phentermine is a centrally acting anorectic drug and a deriv-
ative of amphetamine.
i. The development of drug tolerance, a characteristic feature
of amphetamine and other drugs in this class, is commonly
reported by patients after a few weeks or months.
ii. Because phentermine was originally approved for short-
term use only, there are no published studies of phenter-
mine monotherapy beyond 9 months.
iii. There are several trade brands of phentermine. Initial dose
is typically 15 mg/day, with maximum dose at 30 mg/day.
iv. Side effects include those associated with central nervous
system stimulation, such as elevation of blood pressure,
increased heart rate, palpitations, insomnia, and dry mouth.
2. Peripherally acting medication
a. Orlistat (Xenical) is a potent, slowly reversible inhibitor of pan-
creatic, gastric, and carboxyl ester lipases and phospholipase
A
2
, which are required for the hydrolysis of dietary fat in the
gastrointestinal tract into fatty acids and monoacylglycerols.
Orlistat (Alli) was approved as a 60-mg over-the-counter
medication in February 2007.
i. Taken at a therapeutic dose of 120 mg three times a day,
orlistat blocks the digestion and absorption of about 30%
of dietary fat.
ii. Orlistat produces a weight loss of about 9%10% com-
pared with a 4%6% weight loss in the placebo-treated
groups.
iii. Gastrointestinal tract adverse effects occur in at least 10%
of orlistat-treated patients. Effects include oily spotting,
flatus with discharge, fecal urgency, fatty/oily stool, oily
evacuation, and increased defecation.
C. Surgical (bariatric) treatment
P A R T
Bariatric surgery should be considered for patients with
severe obesity (BMI 40 kg/m
2
) or those with moderate
obesity (BMI 35 kg/m
2
) associated with a serious medical
condition.
1. Weight loss surgeries are in one of two categories: restrictive
and restrictive malabsorptive.
1389_Ch25_346-358 2/2/09 1:31 PM Page 354
a. Restrictive surgeries limit the amount of food the stomach
can hold and slow the rate of gastric emptying. Laparoscopic
adjustable silicone gastric banding (LASGB) is an example.
b. Restrictive malabsorptive bypass procedures combine the
elements of gastric restriction and selective malabsorption.
The Roux-en-Y gastric bypass (RYGB) is an example.
2. These procedures are generally effective in producing an
average weight loss of approximately 30%35% of total body
weight that is maintained in nearly 60% of patients at 5 years.
25 OBESITY 355
C H A P T E R
Bariatric surgery is the most effective weight loss
therapy for patients with clinically severe obesity.
3. The restrictive-malabsorptive procedures produce a pre-
dictable increased risk for micronutrient deficiencies of
vitamin B
12
, iron, folate, calcium, and vitamin D, based
on surgical anatomical changes. The patients require life-
long supplementation with these micronutrients and should
be managed by a team of specialists including a registered
dietitian.
MENTOR TIPS DIGEST
The etiology of obesity is multifactorial.
Obesity is a pervasive and insidious disorder affecting
nine organ systems and over 40 conditions and diseases.
The pathophysiology of obesity is multifactorial.
Recent studies have linked the metabolic and inflammatory
abnormalities seen in obesity to the visceral adipose tissue
(VAT) compartment.
About two-thirds of American adults are overweight, and about
one-third is obese.
About one-third of American children and adolescents
(age 619 years) is overweight or obese.
Clinicians should provide behavioral counseling on preventing
weight gain as part of preventive counseling.
The number and severity of organ-specific comorbid condi-
tions usually rise with increasing levels of obesity.
1389_Ch25_346-358 2/2/09 1:31 PM Page 355
Resources
Buchwald H, et al. Bariatric surgery: A systematic review and meta-
analysis. Journal of the American Medical Association 292:1724,
2004.
Haslam DW, James WPT. Obesity. Lancet 366:1197, 2005.
P A R T
Assessment of risk status due to overweight or obesity is
based on the patients BMI, waist circumference, and the
existence of comorbid conditions.
A desirable or healthy BMI is 18.524.9 kg/m
2
, overweight is
2529.9 kg/m
2
, and obesity is kg/m
2
. Obesity is categorized
as class I (30.034.9 kg/m
2
), class II (35.039.9 kg/m
2
), and class
III (40 kg/m
2
).
Measurement of waist circumference should be obtained in
those individuals with a BMI 35 kg/m
2
.
An increased waist circumference has been found to be pre-
dictive of the risk of having hypertension, diabetes, dyslipi-
demia, and the metabolic syndrome compared with those
who have normal waist circumference.
Lifestyle management incorporates the three essential com-
ponents of obesity care: dietary therapy, physical activity, and
behavior therapy.
The diet needs to produce a calorie deficit of 5001000 kcal/day,
resulting in a weight loss of 12 lb/week.
When recommending any behavioral lifestyle change, have
the patient identify what, when, where, and how the behav-
ioral change will be performed.
Adjuvant pharmacologic treatments should be considered for
patients with a BMI 30 kg/m
2
or with a BMI 27 kg/m
2
who
also have concomitant obesity-related risk factors or diseases
and for whom dietary and physical activity therapies have not
been successful.
Bariatric surgery should be considered for patients with
severe obesity (BMI 40 kg/m
2
) or those with moderate
obesity (BMI 35 kg/m
2
) associated with a serious medical
condition.
Bariatric surgery is the most effective weight loss therapy for
patients with clinically severe obesity.
1389_Ch25_346-358 2/2/09 1:31 PM Page 356
25 OBESITY 357
C H A P T E R
Jakacic JM, et al: Appropriate intervention strategies for weight loss and
prevention of weight regain for adults. Medicine and Science in Sports
and Exercise 33:2145, 2001.
Kushner RF. Roadmaps for clinical practice: Case studies in disease
prevention and health promotionassessment and management of
adult obesity: A primer for physicians. www.ama-assn.org/ama/pub/
category/10931.html
McTigue KM, et al: Screening and interventions for obesity in adults:
Summary of the evidence for the U.S. Preventive Services Task Force.
Annals of Internal Medicine 139:933, 2003.
National Heart, Lung, and Blood Institute (NHLBI) and North American
Association for the Study of Obesity (NAASO). Practical guide to
identification, evaluation, and treatment of overweight and obesity
in adults. Bethesda, MD: National Institutes of Health, NIH Pub.
00-4084, Oct. 2000.
National Heart, Lung, and Blood Institute (NHLBI). Clinical guide-
lines on the identification, evaluation, and treatment of overweight
and obesity in adults. The evidence report. Obesity Research
6:51S, 1998.
Padwal R, Li SK, Lau DCW. Long-term pharmacotherapy for over-
weight and obesity: A systematic review and meta-analysis of
randomized controlled trials. International Journal of Obesity
27:1437, 2003.
U.S. Preventive Services Task Force. Screening for obesity in adults:
Recommendations and rationale. Annals of Internal Medicine
139:930, 2003.
Yanovski S, Yanovski JA: Obesity. New England Journal of Medicine
346:591, 2002.
1. There is an association between obesity and which of the
following?
a. Type 1 diabetes mellitus
b. Diabetes insipidus
1389_Ch25_346-358 2/2/09 1:31 PM Page 357
c. Polycystic ovarian syndrome
d. Interstitial pulmonary fibrosis
2. There is an association between obesity and which cardiovascular
disease?
a. Hypertrophic cardiomyopathy
b. Pulmonic stenosis
c. Rheumatic valvular disease
d. Myocardial infarction
3. A 60-year-old woman who was previously healthy presented with
hematemesis. Subsequent testing demonstrated esophageal varices and
hepatic cirrhosis. She admits to one to two glasses of wine in an average
week and denies binge drinking. She denies taking any prescription or
over-the-counter medicine. After her condition has been stabilized, her
physical examination is notable for BMI 33 and normal ophthalmological,
lung, and cardiovascular systems. Serum AST = 68 IU/L, ALT = 86 IU/L.
TSH and iron results are normal. What is the most likely cause of
cirrhosis in this patient?
a. Obesity
b. Chronic alcoholism despite her denial
c. Chronic acetaminophen use despite her denial
d. Hepatic atherosclerosis
P A R T
1389_Ch25_346-358 2/2/09 1:31 PM Page 358
DIAGNOSIS
AND MANAGEMENT
OF AGE-RELATED
CONDITIONS
DIAGNOSIS
AND MANAGEMENT
OF AGE-RELATED
CONDITIONS
359
four
P A R T
I. Fundamentals of Well-Child Examination
A. The purpose of the examination is to assess the overall well-
being of the child and child-family unit and to provide guid-
ance how the family can stimulate the physical and mental
growth of the child. Most of the time the child is well, and
physicians provide reassurance to the parents. Visit sched-
ules are set according to major age groups and comprise the
following.
1. Newborn: within 12 weeks of birth
2. Infant: at 2, 4, 6, 9, and 12 months
WELL-CHILD VISIT
Janice A. Litza, MD, and Adam D. Rosenfeld, DO
CHAPTER
26
1389_Ch26_359-375 2/2/09 1:32 PM Page 359
360 four DIAGNOSIS AND MANAGEMENT OF AGE-RELATED CONDITIONS
P A R T
3. Toddler: at 12, 15, and 18 months; 2 and 3 years old
4. Preschool: annual visits beginning at 3 years old
5. Elementary school age: annual visits 5 through 10 years old
6. Middle school age: annual visits 10 through 13 years old
7. Teenager: annual visits 13 through 18 years old
B. Each examination should include a review of the medical history
and assess family dynamics.
1. Any parental and child concerns that begin at school age and
allow opportunity to interact and build trust with the child
2. Review of interval medical problems (active, chronic, resolved)
3. Urgent-care history versus well-child examination history
Many young children just starting in day care or school
have numerous colds with frequent urgent-care exami-
nations and need to be monitored for more serious underly-
ing issues. Urgent-care examinations do not substitute for
well-child examinations.
Birth history and key highlights should be documented
in past medical history for review and assessed in any
new patient.
4. Review of medications and supplements, including vitamins
and over-the-counter medications that can cause serious injury
to children if not used correctly.
5. Birth history
a. Birth history should include:
i. Prenatal course
ii. Labor and delivery method (cesarean section, normal sponta-
neous vaginal delivery [NSVD], instrument-assisted delivery)
iii. Gestational age (full term/preterm)
iv. Birth weight
v. Apgar scores (low numbers indicate there may have been
problems at birth, which parents were not aware of or
forgot after a couple of years, at a time when development
may be lagging as a first indication of birth trauma)
vi. Bonding: postpartum depression, substance use, sibling
rivalry
6. Family history: can be very dynamic and must be updated every
examination; includes family history of genetic abnormalities
1389_Ch26_359-375 2/2/09 1:32 PM Page 360
7. Immunization history: for timing, appropriateness, and
assessment of any reactions or refusal of any immunizations
8. Social history and home environment: parent involvement with
child including marital status, who lives in the home, other
adults who spend time interacting with child (grandparents,
aunts, uncles, step-family, siblings, day care, babysitters), day-
care/babysitter/school information, passive exposure to smoking,
lead potential in very old houses, peeling paint, fire and carbon
monoxide alarms present and working, neighborhood safety
C. Examine physical characteristics for possible disease, develop-
mental assessment, appropriate growth, and abuse concerns.
1. Development divided into milestones in a few key areas; impor-
tant to review these milestones to ensure child progressing and
that appropriate anticipatory guidance according to the childs
developmental stage being provided
a. Motor
b. Cognitive
c. Language
d. Social and emotional
2. Observation: parent-child interactions, appropriate behavior to-
ward physician, activity with toys and items in examination room
3. Build trust: playfully including child in discussion early on or using
a book to build trust (critical for ease of physical examination)
26 WELL-CHILD VISIT 361
C H A P T E R
D. All well-child examinations have anticipatory guidance packed into
them. It is best done while taking history and performing the exam-
ination. Otherwise, parents and children will not remember a
checklist of what to do and what not to do. Use any opportunity
to reinforce positive parental and child behaviors, and frame a few
key other areas around safety and normal development of the child.
E. One mechanism for remembering general areas for well-child
examination is the mnemonic SNASI (safety, nutrition, activity,
socialization, immunizations). Document a few key points of
discussion so that following examinations can build on what was
discussed previously.
As with any other patient, examining in the easiest and
least invasive areas first and finishing with the most
invasive or uncomfortable is key (may vary).
1389_Ch26_359-375 2/2/09 1:32 PM Page 361
ii. Fall protection: infant beginning to roll and move
iii. Choking hazard: remove objects smaller than 1 inch or with
small parts; no ribbons or string to attach pacifier to child
F. Immunizations are often the dreaded part of well-child examina-
tion for parents and children. See full immunization schedule, and
use Centers for Disease Control as updated source for immuniza-
tions. The schedule can be downloaded into a hand-held device.
Review possible immunization reactions.
II. Age-Specific Examination Guidelines
A. Newborn and infant examinations
1. In the first year of life, major transitions are made along all of the
developmental milestones, and much opportunity exists to educate
parents on nurturing their child and keeping the child safe. Most
parental concerns center around nutrition, elimination, and social-
ization. Most critical times for changes in family dynamics and
home environment and childs well-being depend on the well-being
and functioning of the caregivers. Leading causes of death in this
age group are suffocation, motor vehicle accidents, and homicide.
B. 2-month examination
1. Common parental concerns: nutrition: starting solids (not yet),
breastfeeding, spitting up; parent(s) returning to work; crying
responsivenesslet cry or pick up (pick up); assessment of
social/home environment: caregivers other than parents; focus on
attention to growth curve and deviations from normal pattern;
developmental milestones include motorlifts head in prone,
eyes follow past midline and fix on objects, pulls to sit with head
lag; socialsmiles responsively, consoled by being held; and
languagelistens and responds when speaker is quiet, coos
2. Anticipatory guidance
a. Safety:
i. Incorrect use of child safety seats accounting for many
deaths at this age
P A R T
The SNASI areas of anticipatory guidance are safety,
nutrition, activity, socialization, and immunizations.
Stress car-seat safety: rear-facing in middle of
back seat (can turn car seat around when baby
is 20 pounds).
1389_Ch26_359-375 2/2/09 1:32 PM Page 362
iv. Sleeping safety
v. Burn caution: infant begins to grab for things, including
cups that may contain hot liquid
b. Nutrition:
i. Stools: normal stooling pattern; will push with bowel
movements; less frequent with formula-fed infants; stool
usually yellow and liquid in exclusively breast-fed infants;
stress the wide range of normal bowel habits in infants;
constipationstool is small-caliber and hard; cries with
bowel movement; anal fissures present
c. Activity:
i. Encourage tummy time while awake; infant sleeps most
of night except for one or two feedings. Parents have been
so compliant with placing their children on their backs to
prevent sudden infant death syndrome (SIDS), they fail to
place the child on its stomach when awake, which leads
to developmental delays in upper body and neck strength.
d. Social:
i. Cuddling/holding and talking encourages bonding and
does not spoil the baby.
ii. Respond to crying promptly to provide reassurance to
infant. Crying will decrease in time as infant knows
needs will be met quickly. Maximum hours of crying per
day occur at 6 weeks and coincide with incidence of
shaken baby syndrome.
C H A P T E R
Infant sleeps on back; if infant rolls over, then
keep crib clear of soft pillows, comforters, and
toys to prevent suffocation.
No water, juice, or solids; no cereal in bottle unless
indicated for reflux; do not have baby lie down with
bottle.
Prevent shaken baby syndrome by advising par-
ents and caregivers that, when they become
frustrated, it is safest to place child gently in a safe
place and walk away to call for help or take a break
until they are calm.
1389_Ch26_359-375 2/2/09 1:32 PM Page 363
iii. Assess signs of postpartum depression that may affect
bonding negatively.
e. Immunizations:
i. Inactivated polio vaccine (IPV); hepatitis B (Hep B) No.
2; pneumococcal; Haemophilus influenzae type b (Hib);
diphtheria, tetanus, and pertussis (DTaP); rotavirus
C. 4-month examination
1. Development
a. Motor: pulls to sit without head lag, holds rattle, lets go of
objects, rolls over, bears some weight on legs
b. Social: regards strangers with interest, laughs and smiles,
initiates social contact
c. Cognitive: stares at own hand, crumples paper happily
d. Language: recognizes sounds such as parents voices
a. Safety: rear-facing car seat, small object caution, child more
mobile and can get under furniture, keep cords from window
blinds and appliances high and wrapped up
b. Nutrition:
i. First tooth may show up; Tylenol and chew toys best for
discomfort (can have fever with teething)
c. Activity: floor time important; cannot spoil child by respond-
ing to basic needs when crying; lie down to sleep when
drowsy, not asleep to develop routine; child sleeps all night;
parents may want to start childproofing house
d. Social: child enjoys people and being talked to, music, cuddling
e. Immunizations: DTaP No. 2, IPV No. 2, pneumococcal No. 2,
Hib No. 2, rotavirus No. 2; Hep B may be extra dose in
combination vaccine, but not required
D. 6-month examination
1. Development
a. Motor: raking grasp with fingers, passes cube from hand to
hand, will grab book with two hands and put in mouth, pulls
to sit with head forward, turns head to localize sounds
b. Cognitive: looks for fallen objects, more attentive to surroundings
c. Language: babbles, smiles at other babies and familiar
things in books
P A R T
Child can begin solids with rice cereal mixed with
milk in bowl with spoon.
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a. Safety: outlets need covers; poisonous substances, including
medications, locked away; car seat may be facing front in
back seat if child heavier than 20 lbs; child starting to crawl
and pull up on furniture; keep stairs blocked, secure furniture,
and put objects higher on shelves or away
b. Nutrition:
i. Introduce new solid every 3 days to assess for intolerance
allergies
C H A P T E R
ii. Meats at 78 months; allow child to feed self with hands
and begin to use spoon; introduce cup
iii. Brush or clean teeth with washcloth (fluoride if needed)
c. Activity: child should be sitting up; crawling begins; enjoys
books and listening to reading
d. Socialization: begin routine for bedtime and anticipate
beginning of separation anxiety
e. Immunizations: DTaP No. 3, IPV No. 3, Hep B No. 3, pneumococ-
cal No. 3, Hib No. 3, rotavirus No. 3, consider flu shot if in season
E. 9-month examination
1. Development/examination
a. Motor: thumb-finger or pincer grasp, grabs items efficiently,
crawls, pulls to stand, sits without support
b. Cognitive: inspects object, puts things in mouth, bangs
cubes, looks for hidden object
c. Language: babbles, begins mama/dada sounds
d. Social: plays peek-a-boo and pat-a-cake; shy with strangers
a. Safety: keep in car seat at all times; electrical outlet and cord
cautions; can strangle self with cords
Avoid fish, milk products, eggs, peanut butter.
Choking caution for round and small hard foods
such as grapes, peanuts, and sliced hot dogs
Do not leave child alone in bath, near toilet, or pool.
b. Nutrition: child should eat meals with family; supplement
with milk in cup and occasional bottle; transition continues
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to cup; some decrease in appetite is normal; assure adequate
growth on pediatric growth charts; brush teeth, no bottle or
cup in bed to avoid dental caries; minimal juice
c. Activity: continue to establish bedtime routine; child more
mobile so needs constant supervision, enjoys simple games
d. Socialization: stranger anxiety; separation anxiety; use books
for language development; talks frequently throughout the day
e. Immunizations: usually none unless needed for catch-up; flu
shot second dose during flu season (4 weeks after first dose)
3. Toddler years: ages 1 to 3 years. child is more mobile, fearlessly
curious, independent with increasing language skills; most
parental concerns center around speech development and disci-
pline; conflict frequent between toddlers and parents over picky
eating, bedtime, and toileting; leading safety issues and causes
of death include motor vehicle accidents, drowning, burns
F. 12-month examination
1. Development
a. Motor/examination: intoe-ing, either as a result of femoral
anteversion, tibial torsion, or metatarsus adductus is common;
normal bruising of shins with active children; first steps;
stands alone
b. Cognitive: looks for hidden objects
c. Language: first words in addition to mama/dada and jargoning
d. Social: consolable; explores present environment under
parental observation
a. Safety: street safety, electrical cord, water safetyno buck-
ets of water; small pools; bath time alone; burnskeep bath
water at 100 degrees and water thermostat at 120 degrees;
chokingsmall objects and food caution; lower crib mat-
tress; child requires constant supervision
b. Nutrition:
P A R T
Red flag: if no pointing, babbling, other gestures by
12 months: consider autistic spectrum disorder.
Phase out bottle by using for water only; everything
else in cup.
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c. Activity: enjoys outside playground; gauge activities to
temperament and plan for transition to quieter activities;
naps two or three times a day
d. Socialization: positive reinforcement; books along with
familiar objects; will want same book read repeatedly
e. Immunizations: MMR No. 1, varicella No. 1, Hib No. 4,
pneumococcal No. 4, annual flu shot
i. Lead and Hgb/hematocrit screens for high-risk populations
G. 15- and 18-month examinations
1. Development/examination
a. Motor: walks well, scribbles spontaneously, rolls ball, by
18 months can walk up steps and backward, stacks two cubes
b. Cognitive: uses objects correctly in play; can point to body
parts; works wind-up toys and on-off buttons
c. Language: follows single-step command without gesture;
has at least one word; by 18 months should have six words,
not echolalic, and indicates desired objects with index finger
d. Social: reads parents expressions; uses feeling words
(sad, happy, scared)
C H A P T E R
Red flag: if no single words by 16 months: consider
autism spectrum disorder.
a. Safety: car seat, water/electrical safety, poisons
b. Nutrition: variety of healthy foods offered at meals;
fruits/vegetables that are favorite at most meals
c. Activity: more advanced toys such as riding cars; naps once
or twice per day; enjoys books and points to objects
No television recommended under 2 years old.
d. Socialization: substitution of activities and praise for
discipline; limited choices reduce power struggles
e. Immunizations: DTaP No. 4, annual flu shot
H. 2-year examination
1. Development
a. Motor: walks backward and up and down steps independently;
copies a circle by 30 months, kicks ball
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b. Social: may be clingy (normal); dresses self mostly, with
supervision
c. Cognitive: can substitute one thing for another in play; com-
bines play actions (rocks doll and puts to bed) by 30 months;
wants same books over and over
d. Language: two-word phrases, vocabulary of 20 words,
points to at least one body part, names several body parts by
30 months, follows two-prepositional commands with block
(behind, under, next to, in)
a. Safety: disciplinepick battles carefully to minimize
power struggles; respond directly and in timely manner to
undesired behavior; may still distract or substitute activity
unless unsafe, then need to clarify why activity unsafe
b. Nutrition: all types of solid foods with an abundance of
foods containing calcium
c. Activity:
P A R T
Red flag: if no two-word spontaneous phrases by
24 months of age: consider autism spectrum disorder.
Red flag: loss of previously learned language or
social skills at any age: consider autism spectrum
disorder.
Toilet training: do not rush the toddler! Positive
reinforcement is the key.
d. Socialization: parents should ask questions and interact with
books and relate stories to childs life
e. Immunizations: review and annual flu shot; lead and
hematocrit screenings for high-risk population
I. Preschool-age (3- to 5-year-old) examinations
1. Child fine-tuning early skills in all areas of development;
speech development most critical and often area of concern
for parents; age for toilet training if not already accomplished.
2. Development
a. Motor:
i. 3-year-old: jumps with both feet off floor, stacks tower,
mature crayon grasp, holds book without help
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ii. 4-year-old: balances on one foot for 45 seconds, copies
the equal sign =, makes three-part or more person,
turns book pages one at a time
iii. 5-year-old: balances on one foot for 510 seconds, copies
square and triangle
b. Social:
i. 3-year-old: separates more easily from caregivers; on aver-
age, diapers dry all night; sits for 5-minute story or longer
ii. 4-year-old: understands taking turns; uses words, not
hitting; retells familiar story; makes up tall tale
iii. 5-year-old: plays well with group of children; dresses
with little help
c. Cognitive:
i. 3-year-old: plays out familiar events and changes out-
comes; duplicates simple actions
ii. 4-year-old: talks for doll and assigns roll to other children
in play; pretends to read and write
iii. 5-year-old: plays out imaginary scripts (e.g., space voyage);
understands simple concepts: If I cut an apple in half, how
many pieces will I have? What do you do to make water
boil? Candy and ice cream are both good to _____?
d. Language:
i. 3-year-old: forms three- or four-word sentences; speech
easily understood; gives full name; knows cold, tired,
hungry; likes rhymes and nonsense words
ii. 4-year-old: forms sentences with mostly correct gram-
mar; asks questions
iii. 5-year-old: correct use of me and I; uses past tense
and plurals
a. Safety: water safety, seat belts
b. Nutrition: bedwetting common and accidents still occur and
can escalate as a response to stress or change in home envi-
ronment (e.g., new sibling) but generally resolves by 12 years;
picky eatingparents advised to continue to offer healthy
choices and can be creative to offer fruits with dinner if
needed versus giving in to junk food
c. Activity: encourage imaginative and interactive play; books
important for beginning letter recognition and writing
C H A P T E R
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d. Socialization: should be interacting with other children; par-
allel play lessens; preschool introduces routine, structure;
will listen to reading up to 1020 minutes; parents should
ask What will happen next? and encourage story telling
e. Immunizations: At 4 or 5 years, child needs booster shots for
MMR, IPV, DtaP, and varicella; annual flu shot
J. Elementary-age (5- to 10-year-old) examinations
1. Development
a. Motor: walks backward heel to toe; begins sports/dance;
copies diamond shape
b. Social: plays rule-based games; has best friend; parents assess
school performance and possible learning disabilities, ADHD.
c. Cognitive:
i. 6-year-old: Asks, e.g., how are peaches and plums alike?
why do we wear shoes?; able to repeat 4-digit strings and
calculate simple math
ii. 7-year-old: repeats five digits forward and three digits
backward; asks, e.g., how are a cat and a mouse alike?
how are a penny and a nickel alike?; knows left and right;
able to write and calculate simple math
iii. 8-year-old: asks how similar things are alike and different
(fish/boat, dime/nickel, book/video) and calculates more
advanced math
iv. 910-year-old: repeats four digits in reverse; gives names of
the days of the week in reverse order; knows month order;
simple recall of three objects; can tell time in minutes and
hours
d. Language:
i. 6-year-old: fluency, names four or five things to eat or wear
in 20 seconds; knows names of most letters and recognizes
a few words; reads books aloud, early chapter books
ii. 7-year-old: can read simple paragraph story and tell what
happened in summary; spells three-letter words
iii. 8-year-old: more spelling and comprehension of stories
a. Safety: protective gear, seat belts, water safety
b. Nutrition:
P A R T
Television time should be less than 2 hours per day.
1389_Ch26_359-375 2/2/09 1:32 PM Page 370
c. Activity: television time maximum of 2 hours and includes
all television/computer activity; organized sports
d. Socialization: bullying assessment, school activities
e. Immunizations: reviewed, annual flu shot
K. Preteen or middle-school-age (10- to 13-year-old) examinations
1. Development
a. Motor/examination: puberty changes begin; review Tanner
staging; screen for obesity; menses (may not begin until
15 years old); acne
b. Cognitive: assess school performance and for any learning
difficulties
a. Safety: drowning risk, protective gear with sports
b. Nutrition: tends to fall into junk-food habits, skips meals;
needs healthy encouragement; preventive health screening con-
sidered especially for cholesterol and diabetes if overweight;
increase calcium intake
C H A P T E R
Healthy food and beverage choices encouraged
limit junk.
c. Activity: begins to focus on a few sports and extracurricular
activities in which excels
d. Socialization: bullying: identify who might be object of
bullying as well as teens who are bullying; provide counsel-
ing for intervention
Eating disorders may begin to appear more clearly
in this age group.
Discuss influence of drugs, alcohol, and sex. Easiest
to ask when parent not in room. Begin in the context
of their friends, and then assess their own feelings to peer
pressure and if/how they respond. Discuss Internet safety.
e. Immunizations: HPV series, annual flu shot
L. Teen (13- to 18-year-old) examinations
1. Development at this age is physical, with puberty changes;
address common concerns such as acne, menses, bodys sex-
ual responses, hormonal fluctuations that lead to emotional
1389_Ch26_359-375 2/2/09 1:32 PM Page 371
changes; struggles for independence yet needs the limit-setting
and support of parents for protection from external influences;
may struggle with body image, self-esteem, and peer pressure
despite external appearances of confidence, school success,
athletic ability, and social acceptance; fears should be assessed
and normalized; parenting should have real-life consequences
with responsibilities, goal setting, rules/limits, and rewards;
calmness and consistency are critical for parentsengaging other
adults in school, church, family for reinforcement is helpful.
2. Development
a. Motor/examination: physical maturity and puberty; Tanner
staging; sports physical examination separate from normal well-
child and includes hernia and musculoskeletal examination
b. Cognitive: School performance and career goals
a. Safety: driving safety; high-risk behavior at various levels
with sense of invincibility; leading cause of deaths in this
group are motor vehicle accidents, drowning, suicide, and
homicide; explore Internet safety and predator awareness;
discuss sexual activity and diseases
b. Nutrition: discuss junk food versus healthy habits for life-
time, eating disorders, body image; consider screening for
diabetes and cholesterol
c. Activity: encourage activity of any kind to get teens away
from television, Internet, gaming systems that are not
physically interactive
d. Socialization: assess for peer pressure, depression, coping
mechanisms for stress, self-esteem issues for all teens and
pressure for performance from parents and coaches; cutting,
tattooing, piercing health hazards
e. Immunizations: HPV, DTaP, meningococcal, annual flu shot
P A R T
MENTOR TIPS DIGEST
General Tips
Many young children just starting in day care or school have
numerous colds with frequent urgent-care examinations and
need to be monitored for more serious underlying issues.
Urgent-care examinations do not substitute for well-child
examinations.
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C H A P T E R
Birth history and key highlights should be documented in past
medical history for review and assessed in any new patient.
As with any other patient, examining in the easiest and least
invasive areas first and finishing with the most invasive or
uncomfortable is key (may vary).
The SNASI areas of anticipatory guidance are safety, nutrition,
activity, socialization, and immunizations.
2-Month Examination
Stress car-seat safety: rear-facing in middle of back seat (can
turn car seat around when baby is 20 pounds).
Infant sleeps on back; if infant rolls over, then keep crib clear
of soft pillows, comforters, and toys to prevent suffocation.
No water, juice, or solids; no cereal in bottle unless indicated
for reflux; do not have baby lie down with bottle.
Prevent shaken baby syndrome by advising parents and care-
givers that, when they become frustrated, it is safest to place
child gently in a safe place and walk away to call for help or
take a break until they are calm.
4-Month Examination
Child can begin solids with rice cereal mixed with milk in bowl
with spoon.
6-Month Examination
Avoid fish, milk products, eggs, peanut butter. Choking cau-
tion for round and small hard foods such as grapes, peanuts,
and sliced hot dogs
9-Month Examination
Do not leave child alone in bath, near toilet, or pool.
12-Month Examination
Red flag: if no pointing, babbling, other gestures by 12 months:
consider autistic spectrum disorder.
Phase out bottle by using for water only; everything else in cup.
15- and 18-Month Examinations
Red flag: if no single words by 16 months: consider autism
spectrum disorder.
No television recommended under 2 years old.
2-Year Examination
Red flag: No two-word spontaneous phrases by 24 months of
age: consider autism spectrum disorder.
1389_Ch26_359-375 2/2/09 1:32 PM Page 373
P A R T
Red flag: Loss of previously learned language or social skills
at any age: consider autism spectrum disorder.
Toilet training: do not rush the toddler! Positive reinforcement
is the key.
Preschool-Age (3- to 5-Year-Old) Examinations
Television time should be less than 2 hours per day.
Elementary-Age (5- to 10-Year-Old) Examinations
Healthy food and beverage choices encouragedlimit junk.
Preteen or Middle-School-Age (10- to 13-Year-Old) Examinations
Eating disorders may begin to appear more clearly in this
age group.
Discuss influence of drugs, alcohol, and sex. Easiest to ask
when parent not in room. Begin in the context of their friends,
and then assess their own feelings to peer pressure and
if/how they respond. Discuss Internet safety.
Resources
American Academy of Family Physicians. www.aafp.org
Specific articles on newborn examination and sports physical through
AAFP journal articles.
American Academy of Family Physicians Family Doctor.
www.familydoctor.org
Teen and parent information on a variety of anticipatory guidance
topics.
Reach Out and Read (ROR). www.reachoutandread.org
Developmental milestones and parent/patient handouts on language
development and book use.
U.S. Centers for Disease Control and Prevention (CDC). www.cdc.gov
Many tools available, including immunization chart, off-cycle timing.
1. A mother of a 9-month-old boy brings him in for an urgent examination
for a respiratory infection. Chart review shows only urgent-care exami-
nations. When you recommend that she bring him for a well-child
1389_Ch26_359-375 2/2/09 1:32 PM Page 374
examination, she asks why she cannot have the childs immunizations
from the nurse to save on fees? What is an appropriate response?
a. Your practice policy requires well-child examinations yearly.
b. A concern about potential litigation requires well-child
examinations.
c. You need to observe the childs activity and socialization
development.
d. You need to assess for child abuse.
2. Which of the following is among the three most common mortality
causes in the first year for a child in the United States?
a. Suffocation
b. Intussusception
c. Volvulus
d. Retinoblastoma
3. A 5-year-old child has a positive test screening for lead. Subsequent
blood lead is high. Which of these environmental conditions would
likely be responsible for this finding?
a. Both parents smoke cigarettes in the home.
b. The family lives in a high-rise apartment building in a smoggy city.
c. The family lives in a 100-year-old home undergoing extensive
renovation.
d. The tap water in a suburban area has a municipal well for water
supply.
C H A P T E R
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376
FEVER IN CHILDREN
Karin G. Patterson, DO, and Sandra A. Pagan, MD, MPA
CHAPTER
27
I. Definition
A. No universally recognized definition of fever
B. Consensus: fever is rectal temperature higher than 100.4F
(38C)
C. If temperature higher than 106F: much higher risk of bacterial
infection
D. Fever of unknown origin (FUO): illness lasting more than 3 weeks
with a temperature higher than 101F and an uncertain diagnosis
after a 1-week investigation in the hospital
E. Fever without localizing signs (FWLS): brief febrile illness for
which there are no localizing findings
II. Epidemiology
A. Fever in children is common.
III. Pathophysiology
A. Generation of fever in response to hypothalamic stimuli,
such as:
1. Cutaneous vasoconstriction
2. Skin temperature falls
3. Cold receptors in the skin sense this as cold
B. Defervescence: body temperature falls in response to:
1. Cutaneous vasodilation
2. Drenching sweats; typically terminate an episode of fever
Most children undergo evaluation for a febrile illness
before age 3 years.
Almost a third of pediatric outpatient visits are for fever.
1389_Ch27_376-390 2/2/09 1:33 PM Page 376
C. Fever detrimental if:
1. Convulsion risk
2. Extreme hyperthermia (>108F); may cause:
a. Direct cellular damage (especially to vascular endothelium,
brain, muscle, and heart; frequently associated with dissemi-
nated intravascular coagulation (DIC)
b. Metabolic derangements (hypoxia, acidosis, hyperkalemia),
which may further contribute to coma, seizures, arrhythmias,
or hypotension.
3. Body temperatures of 113F uniformly lethal
A. Infectious
1. Viral (majority of infections): most are nonspecific, self-
limiting illnesses
a. Upper respiratory infection (croup, bronchiolitis, etc.);
pharyngitis; otitis media; sinusitis; gastroenteritis; exanthem
2. Bacterial
a. Urinary tract infection (UTI); meningitis; pneumonia;
sinusitis; cellulitis; otitis media; pelvic inflammatory disease;
osteomyelitis
B. Neoplasms
1. Lymphoma, leukemia, renal cell carcinoma, atrial myxoma,
metastases to bone or liver
C. Collagen-vascular and other multisystem disease
1. Juvenile rheumatoid arthritis (JRA), systemic lupus erythemato-
sus (SLE), polyarteritis nodosa, Wegener granulomatosis,
mixed connective tissue disease, sarcoidosis
27 FEVER IN CHILDREN 377
C H A P T E R
In children, high fevers should be suppressed to pre-
vent convulsions.
Majority of fevers in children are due to an infectious
cause.
UTI is the main source of bacterial infection among
febrile infants and young children.
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D. Other
1. Appendicitis, noninfectious granulomatous diseases, inflamma-
tory bowel disease, drug fever (especially to antibiotics), facti-
tious fever, miscellaneous uncommon diseases (familial
Mediterranean fever, Whipple disease), undiagnosed
V. History and Physical Examination
A. Should reveal diagnostic clues so that laboratory and study results
may be used selectively
B. Assess host for vulnerability (immunocompromised) and for
exposure (travel, drugs, sick contacts) (Table 27.1).
P A R T
TABLE
27.1
Fever in Children: History and Physical
Examination Clues
History:
Assess for Physical:
Localizing Assess for Potential
System Symptoms Focal Signs Diagnoses
Vital Signs
Head, ears,
eyes, nose,
throat
Temperatures
reported
Heart racing
Breathing
history
Urine output
Headache
Ear pain or
drainage
Eye pain or
discharge
Rhinorrhea
Sinus
tenderness
Sore throat
Toothache
Fever
Tachycardia
Tachypnea
Hypotension
Hypoxia
Anterior oral
ulcers
Pharyngeal
vesicles
Tonsillary
hypertrophy
Pharyngeal
erythema or
exudates
Tooth/gum
abnormalities
Salivary gland
tenderness
Strawberry tongue
Need to incorporate
vitals with other
findings; impor-
tant in determin-
ing toxicity of
patients and
hydration status
Herpes simplex
virus (HSV)
gingivostomatitis
Coxsackievirus
Pharyngitis
Dental abscess
Kawasaki disease
Mononucleosis
Otitis media
Sinusitis
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C H A P T E R
Fever in Children: History and Physical Examination
Clues (Continued)
History:
Neck
Respiratory
Cardiovascular
Gastrointesti-
nal
Neck pain or
stiffness
Neck swelling
or mass
Cough
Dyspnea
Wheeze
Dyspnea
Chest pain
Vomiting
Diarrhea
Petechiae at
junction of hard
and soft palate
Tympanic
membrane with
erythema or
effusion, may be
bulging
Sinus tenderness
with percussion,
transillumina-
tion
Nuchal rigidity
(Kernig
Brudzinski
signs)
Lymphadenopathy
Thyroid
tenderness
Quality of cough
Nasal flaring,
retractions
Rhonchi, rales,
wheeze
Murmur (?new)
Pulses, capillary
refill
Organomegaly,
masses
Meningitis
Pharyngitis,
mononucleosis
Thyroiditis
Croup
Bronchiolitis
(/ respiratory
syncytial virus
[RSV])
Pneumonia
(bacterial or
viral)
Endocarditis
Dehydration
Gastroenteritis
Appendicitis
1389_Ch27_376-390 2/2/09 1:33 PM Page 379
P A R T
TABLE
27.1
Fever in Children: History and Physical
Examination Clues (Continued)
History:
Genitourinary
Neurologic
Dermatologic
Muscu-
loskeletal
Abdominal
pain
Dysuria
Hematuria
Flank pain
Vaginal
discharge
Pelvic pain
Testicular
pain
Confusion
Seizures
Rash
Change in
consistency
Pruritis
Painful lesions
Joint or bone
pain
Trauma
Tenderness,
guarding,
rebound
Hernia
CVA tenderness
Female: cervical
motion tender-
ness, abnormal
discharge,
adnexal
tenderness
Male: testicular
pain, mass or
color changes
Focal deficits
Alteration in
consciousness
(confusion,
delirium, stupor)
Petechiae
Pustular lesions
Cellulitis
Exanthem
Erythema chron-
icum migrans
Turgor
Range of motion
of joints involved
Swelling or
effusion of joints
Strength,
symmetry
Bony deformities
Strangulated,
incarcerated
hernia
Urinary tract
infection
Pyelonephritis
Pelvic inflammatory
disease
Testicular torsion
Meningitis
Encephalitis
Meningococcemia
Rocky Mountain
spotted fever
Gonococcemia
Staphylococcus
infection
Viral
Lyme disease
Dehydration
Septic arthritis
Osteomyelitis
1389_Ch27_376-390 2/2/09 1:33 PM Page 380
VI. Diagnostic Evaluation
A. Overview
1. A thorough history and physical will typically uncover the obvious
source of infection (e.g. otitis media, gastroenteritis, upper respira-
tory infection). However, 20% of febrile children have no apparent
source of infection after history and physical examination.
B. Diagnostic approach by age
b. Workup includes hospitalization, blood culture, urine cul-
ture, lumbar puncture, and empiric antibiotics (Table 27.2)
pending culture results.
2. Young infant (13 months):
a. 7%10% of young infants with temperature 100.4F (38C)
or higher have SBI
1. Neonates (028 days):
a. 10%20% of well-appearing neonates with a temperature
100.4F (38C) or higher have a serious bacterial infection.
C H A P T E R
A small percentage of children with fever will have
an occult serious bacterial infection (SBI), including
bacteremia, urinary tract infection, occult pneumonia, or
meningitis.
All temperatures should be taken rectally.
Clinical impression is not reliable in this age group.
Rectal temperature 100.4F(38C) or higher requires
a full septic workup.
The diagnostic and clinical criteria in Table 27.3
are used to identify febrile young infants at low
risk for SBI.
1389_Ch27_376-390 2/2/09 1:33 PM Page 381
P A R T
TABLE
27.2
Common Pediatric Infectious Sources
of Fever*
Diagnostic
Infection Evaluation Pathogens Treatment
Gastroen-
teritis
Basic metabolic
panel
electrolyte
imbalances
Bloody diarrhea
stool
culture, fecal
leukocytes
(Campylobac-
ter, Shigella,
Yersinia, or
toxic strains of
Escherichia
coli)
Winter
Rotavirus test
of stool
Stool culture for
ova, parasites,
C. difficile (if
prolonged)
Blood culture if
clinical
suspicion
Community-
acquired:
Viruses, E. coli
Salmonella
Shigella
Yersinia
Campylobacter
Nosocomial:
C. difficile (antibi-
otics use, immuno-
compromised,
hospitalized)
Supportive
6 mo,
bacteremia,
toxic or
immunocom-
promised:
cefotaxime or
ceftriaxone
Ceftriaxone or
oral cefixime
Bacteremia,
extraintesti-
nal infection,
immunocom-
promised:
trimethoprim/
sulfamethoxa-
zole (TMP/
SMX), amino-
glycoside, ce-
fotaxime, tetra-
cycline (8 y)
Azithromycin or
erythromycin
Metronidazole
1389_Ch27_376-390 2/2/09 1:33 PM Page 382
C H A P T E R
Common Pediatric Infectious Sources of Fever* (continued)
Diagnostic
Meningitis
Pneumonia
Blood culture
Lumbar punc-
ture
Urinalysis and
urine culture
Chest radi-
ograph:
Focal infiltrate
bacterial
Bilateral diffuse
infiltrates
atypical
or viral
Culture for
influenza,
RSV, or other
viruses
Blood culture if
clinical suspi-
cion
Neonate: Group B
streptococci,
Enterobacter
(esp. E. coli),
Listeria spp.
13 mo: GBS,
Streptococcus
pneumoniae,
Haemophilus
influenzae,
Neisseria
meningitidis,
Enterobacter spp.
3 mo: S. pneumo-
niae, N. meningi-
tidis, H. influenzae,
neonatal pathogens
Neonate: E. coli,
GBS, Staphylo-
coccus aureus,
Listeria monocy-
togenes, Chlamy-
dia trachomatis
3 wk4 mo:
S. pneumoniae,
C. trachomatis,
virus
6 wk4yr:
Lobar:
S. pneumoniae
Ampicillin
cefotaxime
(alternative:
ampicillin
gentamycin)
Ampicillin
cefotaxime
Cefotaxime or
ceftriaxone
( van-
comycin for
S. pneumo-
niae resis-
tance)
Ampicillin
gentamycin
or ampicillin
cefotaxime
Febrile
IV ceftriaxone
or cefotaxime
Erythromycin
(alternative:
oral azithro-
mycin)
PO: amoxicillin
(or clin-
damycin)
IV: ceftriaxone
or cefotaxime
1389_Ch27_376-390 2/2/09 1:33 PM Page 383
P A R T
TABLE
27.2
Common Pediatric Infectious Sources
of Fever* (Continued)
Diagnostic
Atypical: Bordetella
pertussis
RSV
Influenza
4 yr:
Lobar:
S. pneumoniae
Atypical: My-
coplasma
pneumoniae,
Chlamydia
pneumoniae
Influenza
Macrolide
(erythromycin,
azithromycin,
or clar-
ithromycin)
Supportive care:
hydration /
albuterol
nebulizer
/ oxygen
In 36 h:
1 yr,
influenza A/B
oseltamivir
1 yr, influenza
A amanta-
dine
PO: amoxicillin
(or ery-
thromycin)
IV: ceftriaxone
or cefotaxime
PO/IV
macrolide
Clarithromycin
or azithromycin
Zanamir or
oseltamivir
(if onset of
symptoms
in 36 h)
1389_Ch27_376-390 2/2/09 1:33 PM Page 384
C H A P T E R
Common Pediatric Infectious Sources of Fever* (continued)
Diagnostic
Pharyngitis
Urinary tract
infection
*CBC often helpful in most cases: WBC 15,000: increased risk of occult bacteremia
Left shiftincrease in immature form of neutrophils (bands, myelocytes, metamyelo-
cytes) or increased neutrophils bacterial
Elevated lymphocytes viral
Elevated eosinophils parasitic, malignancy, allergic
*First follow management as recommended by age group
Monospot
Rapid strepto-
coccus
streptococcus
culture if neg-
ative and high
suspicion
Urinalysis and
culture
elevated white
blood cell
count, nitrites,
leukocyte
esterase, bac-
teria, positive
Gram stain
CVA tenderness
computer
tomography
(CT) abdomen/
pelvis
pyelonephritis
Blood culture
(if clinical
suspicion)
Group A strepto-
cocci,
group C and
G streptococci
Viral, mononucleo-
sis
Uncomplicated:
E. coli, Proteus
spp., Staphylo-
coccus sapro-
phyticus, enter-
ococci
Complicated
(immunocom-
promised/urinary
tract): above +
Pseudomonas
spp.
PO: penicillin
VK
IM: benzathine
penicillin
G 1
Supportive
PO: TMP/SMX
IV: cefotaxime
OR amp and
gent
Ampicillin +
gentamycin,
Zosyn, or
Timentin
1389_Ch27_376-390 2/2/09 1:33 PM Page 385
(1) Includes blood and urine culture, lumbar puncture,
parenteral antibiotics (see Table 27.2).
ii. Otherwise:
(1) Rectal temperature 38C (100.4F) or higher, if
nontoxic-appearing and low risk:
(A) Blood and urine culture alone; follow outpatient
within 24 hours or
(B) Blood culture, urine culture, lumbar puncture,
single dose of ceftriaxone 50 mg/kg IM in hospital;
follow outpatient within 24 hours
3. Older infant or toddler (336 months):
a. Fewer than 2% of well-appearing in age group with temper-
ature higher than 39C (102.2F) manifest bacteremia
P A R T
TABLE
Fever at 13 Months: Low-Risk Criteria
Diagnostic Clinical
White blood cell (WBC) count
500015,000 and <1500 bands
Normal urinalysis (<5 WBC/HPF
on Gram-stain smear)
When diarrhea present: <5
WBC/HPF in stool
When respiratory symptoms
present: normal chest radiograph
27.3
Previously healthy
Nontoxic-appearing (negative for
weak cry, irritability, inconsola-
bility, poor perfusion, poor tone,
decreased activity, lethargy,
hypoventilation, hyperventilation)
No focal bacterial infection on
examination (excluding otitis
media)
No increased work of breathing
b. Deciding workup plan
i. Most important:
Rectal temperature 38C (100.4F) or higher, if
toxic-appearing or not low risk, requires full
septic workup.
1389_Ch27_376-390 2/2/09 1:33 PM Page 386
b. Deciding workup plan
i. Toxic-appearing
C H A P T E R
Refer to Table 27.2 for most common infections, diag-
noses, pathogens, and management.
Admit to the hospital for full septic workup.
Clinical impression is reliable in this age group.
Most have localizing sources of infection.
ii. Nontoxic appearing and temperature 39C (102.2F)
or higher
(1) Blood culture regardless of WBC count
(2) Urine culture for males younger than 6 months or
females younger than 2 years
(3) Chest x-ray if respiratory symptoms involved
(4) Stool culture, if blood and mucus in stool or 5
WBC/HPF or more in stool
(5) Empiric antibiotics (after cultures) if temperature
39C (102.2F) or higher or if temperature 39C or
higher and WBC count 15,000 or more
(6) Follow-up in 2448 hours
iii. Nontoxic-appearing and temperature lower than 39C
(102.2F), follow clinically
4. Children 3 years and older: an apparent source of infection
usually present on history and physical examination; target
diagnostic evaluation to findings
VII. Management
A. Viral infection (most common): supportive care (e.g., hydration,
antipyretics, supplemental oxygen, albuterol)
B. Management by age if no apparent source of infection (all tem-
peratures taken rectally)
1389_Ch27_376-390 2/2/09 1:33 PM Page 387
P A R T
In this age group, S. pneumoniae cause 90% of
cases of occult bacteremia.
Suggested empiric antibiotics are ampicillin and
gentamicin or ampicillin and cefotaxime.
Common pathogens are group B streptococcus,
E. coli, other gram-negative rods and, less com-
monly, Listeria monocytogenes.
1. Neonates (028 days):
a. Rectal temperature 38C (100.4F): hospitalization, blood
culture, urine culture, lumbar puncture, and empiric antibi-
otics pending culture results
2. Young infant (13 months):
a. Temperature higher than 38C (100.4F)
i. Toxic-appearing or not low risk: admit for full sepsis
workup
ii. Nontoxic-appearing and low risk: may or may not give
empiric antibiotics in hospital (ceftriaxone 50 mg/kg
IM 1); follow outpatient within 24 hours
3. Older infant or toddler (336 months):
a. S. pneumoniae primary suspect
b. Less common causes N. meningitides, Salmonella, and
H. influenza.
c. Toxic-appearing: admit to the hospital for full septic workup
d. Nontoxic-appearing and temperature 39C (102.2F) or
higher: diagnostics as preceding and empiric antibiotics
(ceftriaxone 50 mg/kg IM 1) regardless of WBC count;
follow up in 2448 hours
e. Nontoxic-appearing and temperature 39C (102.2F) or
lower: follow clinically and return in 48 hours if child febrile
4. Children 3 years and older: an apparent source of infection is
usually present on history and physical examination (see
Table 27.1)
1389_Ch27_376-390 2/2/09 1:33 PM Page 388
C H A P T E R
MENTOR TIPS DIGEST
General Tips
Most children undergo evaluation for a febrile illness before
age 3 years.
Almost a third of pediatric outpatient visits are for fever.
In children, high fevers should be suppressed to prevent
convulsions.
Majority of fevers in children are due to an infectious cause.
UTI is the main source of bacterial infection among febrile
infants and young children.
A small percentage of children with fever will have an occult
serious bacterial infection (SBI), including bacteremia, urinary
tract infection, occult pneumonia, or meningitis.
All temperatures should be taken rectally.
Diagnosis in Neonates
Rectal temperature higher than or 100.4F (38C) requires a full
septic workup.
Diagnosis in Young Infants
The diagnostic and clinical criteria in Table 27.3 are used to
identify febrile young infants at low risk for SBI.
Rectal temperature 38C (100.4F) or higher, if toxic-appearing
or not low risk, requires full septic workup.
Diagnosis in Older Infant or Toddler
Clinical impression is reliable in this age group. Most have
localizing sources of infection.
Admit to the hospital for full septic workup.
Management
Refer to Table 27.2 for most common infections, diagnoses,
pathogens, and management.
In neonates, suggested empiric antibiotics are ampicillin and
gentamicin or ampicillin and cefotaxime.
In neonates, common pathogens are group B streptococcus,
E. coli, other gram-negative rods and, less commonly, Listeria
monocytogenes.
In older infants or toddlers, S. pneumoniae cause 90% of
cases of occult bacteremia.
1389_Ch27_376-390 2/2/09 1:33 PM Page 389
P A R T
Resources
Ahmed, S. et al. Evaluation and treatment of urinary tract infections in
children. American Family Physician 57, 1998.
Alpern ER, Alessandrini EA, Bell LM, et al. Occult bacteremia from a
pediatric emergency department: Current prevalence, time to detection,
and outcome. Pediatrics 106:505511, 2000.
Baraff LJ. Management of fever without source in infants and children.
Annals of Emergency Medicine 36:602614, 2000.
Baraff LJ, Bass JW, Fleisher GR, et al. Practice guideline for the manage-
ment of infants and children to 36 months of age with fever without
source. Pediatrics 92:112, 1993
Baskin MN. The prevalence of serious bacterial infections by age in
febrile infants during the first 3 months of life. Pediatric Annals
22:462466, 1993.
Chiu CH, Lin TY, Bullard MJ. Identification of febrile neonates unlikely
to have bacterial infections. Pediatric Infectious Disease Journal
16:5963, 1997.
Jaskiewicz JA, McCarthy CA, Richardson AC, et al. Febrile infants at low
risk for serious bacterial infection: An appraisal of the Rochester crite-
ria and implications for management. Pediatrics 94:390396, 1994.
Krauss BS, Harakal T, Fleisher GR. The spectrum and frequency of ill-
ness presenting to a pediatric emergency department. Pediatric Emer-
gency Care 7:6771, 1991.
Lee GM, Harper MB. Risk of bacteremia for febrile young children in the
post-Haemophilus influenzae type B era. Archives of Pediatric Adoles-
cent Medicine 152:624628, 1998.
Lutfiyya, N, et al. Diagnosis and treatment of community-acquired pneu-
monia. American Family Physician 73, 2006.
See the testbank CD for self-test questions.
1389_Ch27_376-390 2/2/09 1:33 PM Page 390
391
CHAPTER
OTITIS MEDIA
IN CHILDREN
Elizabeth Nguyen Kirchoff, DO, Christopher Varona, DO,
and Joseph P. Gibes, MD
I. Infectious Versus Noninfectious Otitis Media
A. Otitis media (OM) can be divided into two categories:
1. Infectious: suppurative or acute otitis media (AOM)presence
of symptoms of acute illness and signs of tympanic membrane
(TM) under positive pressure (full or bulging)
2. Noninfectious: nonsuppurative secretory OM, or otitis media
with effusion (OME)
II. Anatomy and Function
A. Middle ear anatomy
1. Delineated laterally by tympanic membrane (TM)
2. TM attached to middle ears bones: ossicles
3. Ossicles consist of malleus (most lateral, attached to TM),
incus, and stapes
4. Medial wall of middle ear consists largely of promontory of
cochlea
5. Within medial wall are round window and oval window
(stapes footplate)
6. Anterior wall contains petrous carotid artery, eustachian tube,
semicanal of the tensor tympani muscle
B. Middle ear function
1. To increase efficiency of sound energy transfer from
surrounding air-filled environment to fluid-filled inner
ear
2. Sound pressure waves conducted from TM through ossicles
to oval window (connected to the vestibule of inner ear)
28
1389_Ch28_391-399 2/2/09 1:32 PM Page 391
P A R T
3. Two mechanisms of amplifying sound wave energy
a. Difference in surface area of TM to stapes footplate
(pressure force/area)
b. Difference in length of long process of malleus and incus
provides mechanical lever that increases energy
III. Pathophysiology of AOM
Usually AOM is preceded by an upper respiratory
infection (URI).
Negative pressure created in the middle ear causes
serous fluid buildup.
Serous fluid provides medium for bacterial or viral
growth.
Most common bacteria are Streptococcus pneumoniae,
untypeable Haemophilus, influenza, and Moraxella spp.
Top three risk factors are: day care (predisposes to URI);
bottle feeding; and cigarette smoking in the house.
A. Inflammation and secretions from URI cause occlusion of the
eustachian tubes.
B. Middle ear mucosa continues to absorb air as usual; air is not
replaced because of occlusion of the eustachian tubes.
C. URI provides source of bacteria or viruses.
IV. Microbiology
A. Other less common causes are Mycoplasma spp. and viruses.
V. Risk Factors
1389_Ch28_391-399 2/2/09 1:32 PM Page 392
28 OTITIS MEDIA IN CHILDREN 393
C H A P T E R
A. Other risk factors are:
1. Increased number of siblings in the house
2. Male gender
3. Cleft palate
4. Immunodeficiencies
a. IgG subclass deficiencies
b. AIDS
c. Complement deficiencies
d. Immunosuppression secondary to medications
VI. Epidemiology
A. Frequency
1. 50% of children have one episode prior to first birthday.
2. 80% of children have one episode prior to third birthday.
B. Age
1. Most common in children 6 months to 3 years; may be due to
immunologic factors (lack of antibodies) and low angle of
eustachian tubes in relation to nasopharynx
2. May occur in all age groups
C. Sexmales slightly more affected than females; unknown cause
D. Race
1. White Americans and Hispanics more susceptible than African
Americans
2. Native Americans and Inuit Indians at higher risk
VII. Examining the Ear
A. Otoscopecan use regular otoscope and/or pneumatic
Pneumatic otoscope has a bulb attachment that can be
squeezed and released to view mobility of the TM in
response to positive and negative pressure.
1. Should have a properly sized speculum to permit seal in
external auditory canal
2. Bright otoscopic illumination critical to adequately visualize TM
3. May require cerumen removal before examination (cerumen
can limit visualization)
4. Particular attention should be paid to position and mobility of TM
1389_Ch28_391-399 2/2/09 1:32 PM Page 393
P A R T
VIII. Diagnosis
A diagnosis of AOM must fulfill the following requirements:
history of acute onset of signs and symptoms, presence of
middle ear effusion (MEE), and signs and symptoms of middle
ear inflammation.
A. Elements of preceding requirements
1. Recent or abrupt onset of signs and symptoms of middle ear
inflammation and MEE
a. Otalgia (pain, or pulling of ear in infant)
b. Irritability in infant or toddler
c. Otorrhea (drainage in ear)
d. Fever
2. MEEcommonly confirmed by pneumatic otoscopy (must
use a properly sized speculum to permit a seal in the external
auditory canal); can be found in both AOM and OME
a. Fullness or bulging of TMhighest predictive value for
presence of MEE
b. Air fluid level behind TM
c. Limited or no mobility of TMadditional evidence of
fluid in middle ear
d. Otorrhea
3. Signs or symptoms of middle ear inflammation
a. Distinct erythema of TMmust be distinguished from
other elements that may cause redness of TMcrying,
cerumen removal, fevers
b. Distinct otalgia (discomfort) that interferes with regular
activity or sleep
B. Typical TM findings
1. Color
a. Normal is pearly gray
b. Can have erythema from inflammation; must differentiate
from redness caused by crying, fevers, or irritation from
cerumen removal
c. Abnormal whiteness; can be from scarring or fluid in
middle ear
1389_Ch28_391-399 2/2/09 1:32 PM Page 394
C H A P T E R
2. Contour
a. Normal is slightly concave
b. In AOMcan be full or bulging
c. In OMEusually retracted or in neutral position
3. Translucence
a. Normal is translucent
b. Opacity commonly from underlying MEE
i. Can sometimes reflect scarring
4. Structural changes
a. Scarring
b. Perforation
c. Retraction pockets
5. Mobility
TM mobility is most sensitive and specific in determin-
ing presence or absence of MEE. In MEE, TM has
decreased or absent mobility.
Mobility is seen using pneumatic otoscopy.
C. Other tests that may assist with diagnosis of MEE
1. Tympanometry
a. Simple, rapid, atraumatic test
b. Gives objective evidence of presence or absence of MEE
c. Gives information about TM compliance in electroacoustic
terms: basically equivalent to mobility of TM as visualized
via pneumatic otoscopy
d. Can be helpful in office with patients who are difficult to
examine
e. Can be used to confirm/refine/clarify otoscopic findings
f. Can predict probability of MEE but cannot distinguish OME
from AOM
2. Acoustic reflectometry
a. Small, portable; gives readings rapidly
b. Estimates condition of middle ear by assessing response of
TM to sound stimulus
c. More limited than tympanometry
d. Can predict probability of MEE but cannot distinguish OME
from AOM
1389_Ch28_391-399 2/2/09 1:32 PM Page 395
P A R T
IX. Management
A. Definitions
Severe illness is defined here as moderate to severe otalgia
or temperature higher than 102F (39C) in past 24 hours.
For nonsevere illness, high-dose amoxicillin
(8090 mg/kg/day) is used.
Nonsevere illness is defined here as mild otalgia and
temperature lower than 102F.
B. AOM
1. Antibiotic treatment
a. Severe illness or amoxicillin failure: high-dose amoxicillin/
clavulanate (8090 mg/kg/day of amoxicillin component)
b. Nonanaphylactic penicillin (PCN) allergy: cefdinir
(14 mg/kg/day in one or two doses), cefpodoxime
(10 mg/kg/day, once daily), cefuroxime (30 mg/kg/day
in two divided doses)
c. Severe PCN allergy: azithromycin (multiple regimens avail-
able: one 30mg/kg dose; or 10 mg/kg every day for 3 days;
or 10 mg/kg on first day, followed by 5 mg/kg daily on
second through fifth days) or clarithromycin (7.5 mg/kg
twice daily)
d. Unable to tolerate oral: ceftriaxone 50 mg/kg IM once
e. Other options: erythromycin-sulfisoxazole (50 mg/kg/day of
erythromycin) or sulfamethoxazole-trimethoprim (10 mg/kg/
day of trimethoprim)
f. Alternative therapy for PCN-allergic patient being treated for
infection known or presumed to be caused by PCN-resistant
S. pneumoniae: clindamycin (3040 mg/kg/day in three
divided doses)
2. Observation: period of watchful waiting with close clinical
follow-up; Association of American Physicians (AAP)
and American Academy of Family Physicians (AAFP)
guidelines
1389_Ch28_391-399 2/2/09 1:32 PM Page 396
C H A P T E R
a. Acceptable for children 6 months to 2 years old with
nonsevere symptoms (see below) and uncertain diagnosis
b. Acceptable for older children with nonsevere symptoms,
regardless of certainty of diagnosis
Observation is an appropriate option only when
follow-up can be ensured and antibacterial agents
started if symptoms persist or worsen.
c. Strategies for monitoring children being managed with initial
observation include parent-initiated visit and/or phone contact
for worsening condition or no improvement at 4872 hours,
a scheduled follow-up appointment in 4872 hours, routine
follow-up phone contact, or use of a safety-net antibiotic pre-
scription to be filled if illness does not improve in 4872 hours
3. Pain management: for all children with pain whether or not
antibiotics are prescribed
a. Acetaminophen: 1015 mg/kg every 46 hours
b. Ibuprofen: 510 mg/kg every 68 hours
C. OME
In OME, antibiotics, steroids, antihistamines/decongestants,
and mucolytics afford no long-term benefit.
1. Surgery for persistent OME should be reserved for children
with significant hearing loss, persistent symptoms, risk factors
for developmental difficulties, or structural damage to the
tympanic membrane or middle ear.
2. Antibiotics, with or without steroids, can be considered if the
parents or caregivers are strongly opposed to surgery.
MENTOR TIPS DIGEST
Usually AOM is preceded by a URI.
Negative pressure created in the middle ear causes serous
fluid buildup.
Serous fluid provides medium for bacterial or viral growth.
1389_Ch28_391-399 2/2/09 1:32 PM Page 397
P A R T
Most common bacteria are S. pneumococcus, untypeable
Haemophilus, influenza, and Moraxella.
Top three risk factors are: day care (predisposes to URI); bottle
feeding; and cigarette smoking in the house.
Pneumatic otoscope has a bulb attachment that can be
squeezed and released to view mobility of the TM in response
to positive and negative pressure.
A diagnosis of AOM must fulfill the following requirements: his-
tory of acute onset of signs and symptoms, presence of middle
ear effusion (MEE), and signs and symptoms of middle ear
inflammation.
TM mobility is most sensitive and specific in determining pres-
ence or absence of MEE. In MEE, TM has decreased or absent
mobility.
Mobility is seen using pneumatic otoscopy.
Severe illness is defined here as moderate to severe otalgia or
temperature higher than 102F (39C) in past 24 hours.
Nonsevere illness is defined here as mild otalgia and tempera-
ture lower than 102F.
For nonsevere illness, high-dose amoxicillin (8090 mg/kg/day)
is used.
Observation is an appropriate option only when follow-up can
be ensured and antibacterial agents started if symptoms per-
sist or worsen.
In OME, antibiotics, steroids, antihistamines/decongestants,
and mucolytics afford no long-term benefit.
Resources
Paradise, JL. Otitis media. In Behrman RE, et al (eds): Nelson Textbook
of Pediatrics, 17th ed. WB Saunders, 2004.
Pichichero, ME. Acute otitis media: Improving diagnostic accuracy.
American Family Physician 61:19901992, 2000.
Subcommittee on Management of Acute Otitis Media. Diagnosis and
management of acute otitis media: Clinical practice guideline.
Pediatrics 113: 14511465, 2004.
1389_Ch28_391-399 2/2/09 1:32 PM Page 398
C H A P T E R
1. What is the usual cause of suppurative acute otitis media?
a. Exacerbation of chronic bacterial otitis media
b. Complication of antecedent viral upper respiratory infection
c. Tympanic membrane trauma from cotton-tip swab
d. Primary bacterial infection acquired from another person
2. How does bottle-feeding an infant affect risk of acquiring suppurative
acute otitis media?
a. No risk difference
b. Increased risk compared with breastfed infants
c. Decreased risk compared with breastfed infants
d. Increased risk if bottle nipples are not sterile
3. During which of these ranges are children most at risk of acute otitis
media?
a. Younger than 6 months of age
b. 6 months to 3 years of age
c. 710 years of age
d. Older than 10 years of age
1389_Ch28_391-399 2/2/09 1:32 PM Page 399
400
GERIATRIC CONDITIONS
Gary J. Martin, MD, Martin S. Lipsky, MD,
and Herbert Sier, MD
CHAPTER
29
I. Overview
A. The aging of the population is a situation that physicians need to
consider.
1. Most specialties will be caring for older patients.
2. Some of these tactics have been garnered from geriatric evalua-
tion services. Many randomized trials have documented these
approaches.
3. Box 29.1 lists issues that are routinely evaluated in
geriatric evaluation programs. In addition to an appropriate
history and physical, special assessments of home safety,
cognition, advance directives, and social support are
helpful.
BOX
Geriatric Programs: Issues for Evaluation
Thorough history, physical examination, and:
Activities of daily living (e.g., bathroom, bathing, eating)
Instrumental activities of daily living (e.g., shopping, checkbook)
Mobility
Advance directives
Medications
Social network/resources
Cognition
Affect
Nutrition
Environmental safety
Alcohol use/abuse
29.1
1389_Ch29_400-408 2/2/09 1:33 PM Page 400
B. Issues that are particularly helpful to address in the management
of older patients are listed in Box 29.2. In general, optimizing the
care for any chronic condition such as congestive heart failure and
diabetes can often improve the overall functioning of the elderly
patient.
1. Addressing issues such as vision, dental conditions, and hearing
can often be neglected in routine practice and yet may be a
major determinant of how a patient functions.
2. Medications have a tendency to be added and added, particu-
larly for older patients. A careful reevaluation of everything a
patient is taking and dosages from all providers (and on their
own) needs to be done periodically.
29 GERIATRIC CONDITIONS 401
C H A P T E R
In the frail elderly, addressing home safety, social sup-
port, functional capacity, and special senses can have
a high yield.
BOX
Geriatric Programs: Management Strategies
Address chronic conditions.
Identify the following:
Sensory and cognitive impairments
Dental conditions
Polypharmacy
Substance abuseespecially excessive alcohol intake
Pain
Depression
Incontinence
Social isolation
Environmental hazards
Caregiver stress
Advise patient about and help patient take steps toward the following:
Health maintenance/vaccinations
Nutrition
Exercise
Smoking cessation
Advance directives
29.2
1389_Ch29_400-408 2/2/09 1:33 PM Page 401
II. Assessment
A. As part of the functional assessment of an older patient, a number
of areas can be addressed quickly.
1. Vision can be tested with a Jaeger card.
2. Hearing can be checked by whispering an easily asked question
in each ear.
3. A brief range-of-motion test of the arms and legs can be
performed.
4. Careful observation of a patient getting out of a chair and
walking can be very enlightening. Patients who have difficulty
walking should have a full neurologic and musculoskeletal
evaluation and may benefit from physical therapy.
5. Basic questions include the following.
a. Do you often feel sad or depressed?
b. Are you able to get out of bed yourself?
c. Can you dress yourself?
d. Can you make your own meals?
e. Can you do your own shopping?
f. Do you have trouble with stairs inside or outside of your
home?
g. Who would be able to help you in case of an illness or
emergency?
h. Are you losing weight?
i. Have you fallen in the last year?
j. Are you having any problems with your memory?
6. Depending on the answers to the preceding questions, further
evaluation may be warranted.
7. Inquire about urinary incontinence. For example, Do you ever
lose your urine and get wet? Incontinence can lead to the insti-
tutionalization of a patient. Appropriate treatment may allow a
patient to remain home.
P A R T
Controlling urinary incontinence can make the differ-
ence between a patient being able to stay with the
family versus going to a nursing home.
B. The following syndromes are particularly relevant to older
patients.
1. Dementia increases in frequency with age. It approaches
10%20% in patients over 80 years of age.
1389_Ch29_400-408 2/2/09 1:33 PM Page 402
a. If there is any suspicion in an older patient, a full Mini-
Mental Status Examination is recommended.
b. There are several potentially reversible causes of dementia
that can be pursued, including medications, metabolic abnor-
malities, and depression.
c. Nonreversible causes of dementia include Alzheimer
disease, vascular dementia, and Lewy body dementia.
d. Treatment with drugs such as donepezil may be warranted in
some patients, although the overall impact of these drugs is
relatively modest.
2. Depression can present as dementia, and the two can be hard to
separate at times in older patients.
a. The Geriatric Depression Scale can be helpful in the initial
evaluation of a patient suspected of depression (see Lachs,
et al, 1990).
b. If there is uncertainty, at times a therapeutic trial may be
warranted or an evaluation by a psychiatrist familiar with
geriatric evaluation.
3. Incontinence has the following profile.
a. Incontinence can be divided into categories.
i. Stress incontinence, which is leakage associated with intra-
abdominal pressure such as coughing, laughing, or bending
ii. Urge incontinence, which is usually associated with a
precipitant urge to void
iii. Overflow incontinence, which can be due to mechanical
factors such as an enlarged prostate or less commonly to
a contractile bladder
iv. Functional incontinence, which is inability or unwillingness
to get to a toilet or toilet substitute; can be due to a cogni-
tive or physical functional impairment and, occasionally, a
psychological factor such as depression, anger, or hostility
b. After initial evaluation for incontinence, depending on the
physicians knowledge and skills, it is usually helpful to ad-
dress any potentially reversible conditions that contribute to
urinary incontinence. If this is unsuccessful, then urologic
consultation is generally warranted.
c. Examples of some of the more readily treatable conditions
include urinary tract infection, atrophic vaginitis, hyper-
glycemia, hypercalcemia, and fluid overload related to
venous insufficiency with edema or congestive heart failure.
C H A P T E R
1389_Ch29_400-408 2/2/09 1:33 PM Page 403
d. Drugs and side effects may contribute, such as short-acting
diuretics. If the timing of these can be adjusted, this can also
be helpful. As well, some patients may not realize that BID
(twice a day) does not necessarily mean before bedtime for
the second dose, that it may be appropriate for the second
dose to be as early as 3:00 p.m. Many blood pressure med-
ications and psychotropic drugs and other anticholinergics
may be factors contributing to urinary problems.
e. For urge and stress urine incontinence, behavioral therapies
are the first management strategies. Examples include blad-
der training and pelvic muscle exercise.
4. Iatrogenesis can be a significant issue.
a. Avoid hospitalizations whenever possible.
b. Forgoing surgery if surgical indications are marginal can
avoid a downhill spiral for some patients.
P A R T
Ask whether any test or procedure will truly change
the management of the patient in the context of the
patients overall condition and life expectancy.
c. Inappropriate prescribing of medications can be avoided by
avoiding treating side effects of one medication with another.
d. Remember appropriate dosing in patients whose renal func-
tion is lower than their creatinine level as this may suggest
age-related loss of muscle mass.
e. For hospitalized frail elderly patients, avoid sedative
hypnotics, benzodiazepine, and medications with anticholin-
ergic properties if possible.
5. Falls and gait disturbances have the following profile.
a. Falls and gait disturbances may need to be addressed, based
on the patients history or functional status assessment,
including visual impairment; drug side effects causing
orthostasis or vestibular disturbances; peripheral neuropathy;
musculoskeletal diseases such as arthritis; foot disorders;
central nervous system disease; and sedating medications
including anxiolytics, sedatives, anticholinergics, and
antidepressants.
b. Addressing these contributing factors as well as aggressive
physical therapy to improve a patients balance and walking
1389_Ch29_400-408 2/2/09 1:33 PM Page 404
can be very beneficial. Even small improvements in strength
and balance can make the difference between falling and not
falling. Use of assistive devices and footwear can be very
helpful.
III. Other Important Concepts
A. Involving the aid of dentists, otologists, and ophthalmologists
rather than depending on the patient to utilize these services is a
necessary part of primary care.
B. Elder abuse and neglect are issues that must be addressed and in
general reported to the appropriate state agency when identified.
C. Remember the nonspecific presentations of disease in the elderly.
For example, myocardial infarction can present as sudden pro-
found fatigue, and major infections can present with just a decline
in functional status without a noticeable fever.
C H A P T E R
MENTOR TIPS DIGEST
In the frail elderly, addressing home safety, social support,
functional capacity, and special senses can have a high yield.
Controlling urinary incontinence can make the difference
between a patient being able to stay with the family versus
going to a nursing home.
Ask whether any test or procedure will truly change the
management of the patient in the context of the patients
overall condition and life expectancy.
Resources
American Geriatrics Society (AGS). Core competency.
www.americangeriatrics.org/education/competency.html
Overview of what a panel of experts believes every medical student
should know about geriatric issues.
Geldmacher DS, ed. Dementia update: Overview from the first annual
dementia congress. Journal of the American Geriatric Society 51:
S281326, 2003.
Grossman H, Bergmann C, Parker S. Dementia: A brief overview. Mount
Sinai Journal of Medicine 73:985992, 2006.
Inouye SK. Delirium in older persons. New England Journal of Medicine
354:11571165, 2006.
1389_Ch29_400-408 2/2/09 1:33 PM Page 405
Kane RL, Ouslander JG, Abrass IB, eds. Functional assessment. In Essen-
tials of Clinical Geriatrics, 5th ed. New York, McGraw Hill, 2004,
pp. 4956.
Lachs MS, Feinstein AR, Cooney LM, et al. A simple procedure for
general screening for functional disability in elderly patients. Annals
of Internal Medicine 112:699706, 1990.
An excellent overview of how to incorporate a comprehensive evalua-
tion efficiently into an office visit. Includes the Mini-Mental State
Examination and Geriatric Depression Scale.
Landefeld CS, Palmer RM, Kresevic DM, et al. A randomized trial of
care in a hospital medical unit especially designed to improve the
functional outcomes of acutely ill patients. New England Journal of
Medicine 332:13381344, 1995.
Morley JE. Urinary incontinence and the community dwelling elder: A
practical approach to diagnosis and management for the primary care
geriatrician. Clinical Geriatric Medicine 20: 427435, 2004.
Pogo Web site for medical students. www.POGO.org
Rubenstein LZ, Josephson KR, Wieland GD, et al. Effectiveness of a
geriatric evaluation unit: A randomized trial. New England Journal of
Medicine 311:16641670, 1984.
Tinetti ME. Preventing falls in elderly persons. New England Journal of
Medicine 348:4249, 2003.
1. In contrast to routine medical care of adults, geriatric assessments also
include attention to which of these additional concerns?
a. Tobacco use
b. Living conditions, including stairs, floor coverings, and bathing
facilities
c. Screening for common malignancies
d. Over-the-counter medication use
2. In periodic health assessment of elderly persons who deny visual com-
plaints, what is the most appropriate way to evaluate visual acuity?
a. Funduscopic examination
b. Assess cranial nerves III, IV, and VI
P A R T
1389_Ch29_400-408 2/2/09 1:33 PM Page 406
c. Jaeger or Snellen test
d. Referral to ophthalmologist
3. Medical treatment can reverse which of these cognitive illnesses?
a. Depression
b. Alzheimer disease
c. Lewy body disease
d. Multiple vascular infarcts
BOX 29.1
O
C H A P T E R
1389_Ch29_400-408 2/2/09 1:33 PM Page 407
1389_Ch29_400-408 2/2/09 1:33 PM Page 408
409
five
P A R T
I. Introduction
A. Benign breast disease encompasses a heterogeneous group of
disorders and conditions.
B. In the United States, approximately 16% of primary care office
visits involved breast symptoms.
C. The clinical history is paramount in formulating a diagnosis in
breast disease.
1. Age
2. Menopausal status
3. Symptoms relation to the menstrual cycle
4. Quality and duration of pain
5. Location of the symptoms
D. The diagnostic workup should include a thorough physical
examination, breast imaging with mammography or ultrasound
if necessary, and possibly a fine-needle aspiration or biopsy.
BENIGN BREAST DISEASE
Aparna Priyanath, MD
CHAPTER
30
WOMENS HEALTH
WOMENS HEALTH
1389_Ch30_409-417 2/2/09 1:33 PM Page 409
410 five WOMENS HEALTH
P A R T
Women seeking an evaluation of breast symptoms often
experience a great deal of anxiety. Therefore, it is often
helpful to explain to the patient that the majority of benign
breast diseases arise from cyclical changes within the ducts
and lobules that occur throughout reproductive life.
The palpation of a breast lump at any age warrants a
workup.
Figure 30.1 is an algorithm for the evaluation of a palpable
breast mass.
Palpable mass
Fine-needle aspiration
? Solid
Mammogram and ultrasound
Cystic
Complex
Cyst
No further
workup
Probably
benign/
suspicious
Probable
fibroadenoma
Complex
Cyst
Aspirate
Disappears.
No further
workup
Does not
disappear
Biopsy
Core biopsy
Malignant Benign or
equivocal
Staging
workup
and
treatment
Excisional
biopsy
Core biopsy or
short-term
follow-up based
on clinical
judgment
Monitor or
offer excisional
biopsy
Solid
Simple
Cyst
FIGURE 30.1 Algorithm for the evaluation of a palpable breast mass.
II. Fibrocystic Disease
A. Fibrocystic disease is a generalized term that has been used to
describe benign, palpable thickening or nodularity in the breast
tissue, which is usually associated with pain.
1389_Ch30_409-417 2/2/09 1:33 PM Page 410
30 BENIGN BREAST DISEASE 411
C H A P T E R
B. Variations in the texture of the breast may cause thickening or nodu-
larity that is sometimes difficult to distinguish from a true mass.
C. A persistent asymmetrical area of breast tissue thickening or nodularity
that is suspicious for a breast mass should prompt further evaluation.
D. The term disease is a misnomer as the majority of breast
changes described by the term are physiologic.
E. The etiology of the changes referred to as fibrocystic disease is
unknown, and clear risk factors have not been identified.
F. A clinically useful strategy, which is supported by the College of
American Pathologists, classifies benign breast disease into strictly
defined histologic groups (Table 30.1)
1. Nonproliferative lesions
2. Proliferative lesions without atypia
3. Atypical hyperplasia, each associated with a different risk for
developing subsequent cancer
Areas of nodularity or thickening should be compared
with the corresponding area of the other breast, as sym-
metrical changes are rarely pathologic. Often these changes
fluctuate with the menstrual cycle.
In the National Surgical Adjuvant Breast and Bowel
Project P-1 Study, tamoxifen was found to reduce the
5-year risk of invasive breast cancer by 86% in women with
a history of atypical hyperplasia. Recent results from the
Study of Tamoxifen and Raloxifene showed similar benefits
with raloxifene; however, there has not been United States
Food and Drug Administration approval for this indication.
G. Thus, in women with a previous history of a benign breast biopsy,
it is important to obtain histologic diagnosis and consider
chemoprevention for those at higher risk of developing cancer.
H. Treatment is generally directed at the symptoms of mastalgia
(see later). Although the avoidance of substances that contain
methylxanthine, such as coffee, tea, cola, and chocolate, has been
recommended by clinicians, there is no definite evidence that it
offers a therapeutic benefit.
III. Breast Pain
A. Breast pain, or mastalgia, is a common complaint in the primary
care setting.
1389_Ch30_409-417 2/2/09 1:33 PM Page 411
B. Mastalgia is more common in premenopausal than postmenopausal
women and is rarely associated with breast cancer.
C. It is useful to consider the classification of breast pain based on its
relationship to the menstrual period:
1. Cyclic mastalgiarelated to the onset of the menstrual period
a. More common in younger women (younger than 35 years)
and is often relieved after the menstrual period
b. Usually bilateral, diffuse, and described as heaviness or
soreness that radiates to the axilla or arm
c. Usually begins 14 days prior to menses; however, in
women who experience moderate-to-severe mastalgia, the
duration can extend 514 days pre-menses
2. Noncyclic mastalgia
a. Most common in women in the 4th decade
b. Unilateral, localized, and described as sharp or burning in quality
D. In cases of severe mastalgia, nodularity may be associated with
the pain; however, the extent of mastalgia does not correlate with
the amount of nodularity.
P A R T
TABLE
30.1
Relative Risk (RR) of Breast Cancer Based on
Benign Breast Disease Histological Categories
(Nonproliferative Type)
Proliferative Without Atypical
Nonproliferative Atypia Hyperplasia
Epithelial-related Intraductal papilloma, Atypical ductal or
calcifications sclerosing adenosis, lobular hyperplasias
moderate hyperplasias
of the usual type
RR 1.0 RR 1.3 (0.82.2) RR 4.3 (1.711.0)
Mammography is required as part of the workup for
mastalgia in women over the age of 35 years to rule out
malignancy.
E. Treatment choices consist of the following.
1. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the
first-line treatment of breast pain.
1389_Ch30_409-417 2/2/09 1:33 PM Page 412
C H A P T E R
Fibroadenomas are benign tumors occurring most frequently
in women between the ages of 20 and 50 years.
2. If NSAIDs fail, a trial of evening primrose oil or vitamin E may
relieve breast pain, with little or no side effects.
IV. Breast Cysts
A. Cysts are a common cause of a dominant breast mass and are often
difficult on physical examination to distinguish from a solid mass.
B. Ultrasound examination is used to distinguish between a cystic
versus a solid lesion.
C. Cysts may fluctuate with the menstrual cycle and occur most
frequently in perimenopausal women in their 40s.
D. In premenopausal women, fine-needle aspiration of the cyst
should be performed. If the mass disappears and is nonbloody, no
further evaluation is required. If the fluid is bloody or the palpable
abnormality persists or recurs after multiple aspirations in a short
time interval, a biopsy is required.
E. Cytologic examination of cystic fluid for malignancy provides lit-
tle value.
V. Fibroadenomas
A. Histologically, fibroadenomas display a considerable amount of
morphologic variability and consist of a mixture of proliferated fi-
brous stroma and increased epithelial ductal structures.
B. These tumors are usually asymptomatic and are often found by
either breast self-examination or incidentally during the clinical
breast examination.
C. Fibroadenomas typically present as solitary masses but may be
multiple in about 10%15% of cases.
D. Classically, these tumors are smooth, nontender, discrete, and
freely moveable.
1. They are usually 12 cm when detected and do not often
increase in size beyond 23 cm.
2. A diagnosis based on clinical examination alone is accurate
only 50%73% of the time.
E. Ultrasound examination is disappointing as there is significant
overlap in the ultrasonographic appearance of benign and
malignant masses.
1389_Ch30_409-417 2/2/09 1:33 PM Page 413
1. Because of the inadequacy of the examination and ultrasound
alone in the diagnosis of fibroadenoma, many investigators
advocate triple assessment with clinical examination, ultrasound,
and aspiration with cytology.
P A R T
If the diagnosis of fibroadenoma cannot be established
with certainty, excisional biopsy is the procedure of
choice.
Most nipple discharge is benign in origin.
A. Galactorrhea
1. Milk or milk-like discharge from the breast
2. Usually bilateral, spontaneous, or intermittent
3. May be due to chronic breast stimulation
4. Common drugs implicated include:
a. Oral contraceptives
b. Dopamine antagonists (methyldopa, phenothiazine)
5. Laboratory evaluation should include:
a. Pregnancy test
b. Prolactin level
c. Thyroid studies
B. Features associated with an increased risk of cancer include:
1. Unilateral discharge
2. Spontaneous appearance
3. Bloody or guaiac-positive
4. Association with a mass
5. Patient older than 40 years
1. Elicit discharge by massaging breast from periphery to center
or applying warm compresses.
2. Identify breast masses or lymphadenopathy.
3. Determine skin color changes, nipple position, erythema,
ulceration, or retraction of skin.
VI. Nipple Discharge
1389_Ch30_409-417 2/2/09 1:33 PM Page 414
4. Observe the number of ducts involved.
a. Flow from one duct is concerning for intraductal papilloma
or intraductal breast carcinoma.
b. Bilateral or multiductal discharge should be evaluated for
endocrinological causes.
D. Diagnostic evaluation
1. Guaiac tests
2. Mammography
3. Ductography or ductoscopy
C H A P T E R
MENTOR TIPS DIGEST
Women seeking an evaluation of breast symptoms often
experience a great deal of anxiety. Therefore, it is often helpful
to explain to the patient that the majority of benign breast
diseases arise from cyclical changes within the ducts and
lobules that occur throughout reproductive life.
The palpation of a breast lump at any age warrants a workup.
Figure 30.1 is an algorithm for the evaluation of a palpable
breast mass.
Areas of nodularity or thickening should be compared with
the corresponding area of the other breast, as symmetrical
changes are rarely pathologic. Often these changes fluctuate
with the menstrual cycle.
In the National Surgical Adjuvant Breast and Bowel Project
P-1 Study, tamoxifen was found to reduce the 5-year risk of
invasive breast cancer by 86% in women with a history of
atypical hyperplasia. Recent results from the Study of Tamoxifen
and Raloxifene showed similar benefits with raloxifene; how-
ever, there has not been United States Food and Drug Admin-
istration approval for this indication.
Mammography is required as part of the workup for mastalgia
in women over the age of 35 years to rule out malignancy.
Fibroadenomas are benign tumors occurring most frequently in
women between the ages of 20 and 50 years.
If the diagnosis of fibroadenoma cannot be established with
certainty, excisional biopsy is the procedure of choice.
Most nipple discharge is benign in origin.
1389_Ch30_409-417 2/2/09 1:33 PM Page 415
Resources
Barton MB, Elmore JG, Fletcher SW. Breast symptoms among women
enrolled in a health maintenance organization: Frequency, evalua-
tion, and outcome. Annals of Internal Medicine 130:651657, 1999.
Dupont WD, Parl FF, Hartman WH, et al. Breast cancer risk associated
with proliferative breast disease and atypical hyperplasia. Cancer
71:1258, 1993.
Fisher B, Constantino JP, Wickerham DL, et al. Tamoxifen for prevention
of breast cancer: Report of the National Surgical Adjuvant Breast and
Bowel Project P-1 Study. Journal of the National Cancer Institute
90:13711388, 1998.
Hansen N, Morrow M. Breast disease. Medical Clinics of North America
82: 203222, 1998.
Harris J, Lippman ME, Morrow M, et al. Diseases of the Breast, 2nd ed.
Philadelphia, Lippincott Williams & Wilkins, 2000.
Vogel VG, Costantino JP, Wickerham DL, et al. Effects of tamoxifen vs
raloxifene on the risk of developing invasive breast cancer and other
disease outcomes: the NSABP Study of Tamoxifen and Raloxifene
(STAR) P-2 Trial. Journal of the American Medical Association
295:27272741, 2006.
1. A 24-year-old woman found a lump in her right breast 2 days ago. The
lump is mildly tender on palpation. She has no family history of breast
cancer. Menarche was at age 13. Menses are regular; last menstrual
period began 24 days ago. On examination, you feel a 2-cm tender firm
nodule in the upper outer quadrant. The axillary examination result is
negative. What is the next appropriate medical response?
a. Reassurance that this is not malignant
b. Reassurance that this is common; return for breast examination in 2 weeks
c. Reassurance that this is common; return for breast examination in
3 months
d. Diagnostic mammogram and ultrasound imaging
P A R T
1389_Ch30_409-417 2/2/09 1:33 PM Page 416
2. A 24-year-old woman found a lump in her right breast 2 weeks ago. The
lump is mildly tender on palpation. She has no family history of breast
cancer. Menarche was at age 13. Menses are regular; last menstrual period
began 10 days ago. On examination 2 weeks ago, you felt a 2-cm tender
firm nodule in the upper outer quadrant. The axillary examination result
was negative. Examination now is unchanged. What is the next appropriate
medical response?
a. Diagnostic mammogram and ultrasound imaging
b. Fine-needle aspiration of nodule
c. Excisional or core biopsy of nodule
d. Magnetic resonance image of right breast
3. A 35-year-old woman is your regular patient. While out of town, she
felt a breast lump and consulted a physician. She reports that she
promptly underwent needle aspiration of the mass and that the mass
disappeared. She observed that the aspirated fluid was yellow and
translucent. The other physician told her that nothing further would be
necessary. She is a healthy mother of children ages 8 and 10 years.
Menses are regular. She uses a diaphragm for contraception. On exami-
nation, you are unable to palpate any abnormality. What is the most
appropriate response in answer to what intervention is necessary next?
a. Tamoxifen 10 mg twice daily for 5 years
b. Obtain previously aspirated fluid sample for cytologic examination
c. Bilateral screening mammogram
d. Reassurance and observation only
C H A P T E R
1389_Ch30_409-417 2/2/09 1:33 PM Page 417
418
PRECONCEPTION CARE
Aarati D. Didwania, MD
CHAPTER
31
I. Preconception Evaluation
A. Complete medical history should be taken, with particular
attention paid to the presence of the following:
1. Known medication allergies, particularly antibiotics
2. Autoimmune disorders
3. A history of blood transfusions and date at which each
transfusion was received
4. Breast disorders including history of biopsies and
pathologies
5. Cardiovascular conditions
6. Domestic violence or other safety concerns at home or work
7. Endocrine disorders
8. Family history of any known hereditable disorders
9. Gastrointestinal disease
10. Hematologic disorders
11. Kidney disease
12. A list of all medications the patient is taking
a. Prescription
b. Over-the-counter
c. Herbal or vitamin supplements
13. Neurologic disorders
14. Psychiatric disease
15. Pulmonary disorders
16. Substance abuse
17. Surgical procedures
B. Medications can present teratogenic risk to the fetus. The list of
medications in Box 31.1 includes common teratogens that need to
be changed prior to conception. There is a risk/benefit ratio to
consider when changing or discontinuing medications. If the
1389_Ch31_418-425 2/2/09 1:34 PM Page 418
disease process cannot be controlled with a change in regimen, a
decision may be needed on which risk to the fetus is greaterthe
risk posed by the medication or the risk posed by uncontrolled
disease in the mother. This is a decision that should be made by a
high-risk obstetrician.
C. Advanced maternal age, defined as older than 35 years at the
time of delivery, can affect pregnancy outcomes.
1. Maternal age older than 35 years at time of delivery is
associated with:
a. Decrease in fecundity (ability to become pregnant) with
advancing age
i. 50% for women age 1926 years
ii. 40% for women age 2734 years
iii. 30% for women age 3539 years
31 PRECONCEPTION CARE 419
C H A P T E R
Consider the relative risks and benefits of each
medication change.
BOX
31.1
Common Teratogenic Medications
ACE inhibitors
Anticholinergic drugs
Antithyroid
Carbamazepine
Cyclophosphamide
Danazol
Hypoglycemic drugs
Lithium
Methotrexate
Misoprostol
Nonsteroidal anti-inflammatory drugs
Phenytoin
Psychoactive drugs
Systemic retinoids
Tetracycline
Thalidomide
Valproic acid
Warfarin
1389_Ch31_418-425 2/2/09 1:34 PM Page 419
P A R T
Eliminate alcohol or tobacco for women who are planning
to conceive. Suggest minimal caffeine use as well.
More than 250 mg of caffeine per day is associated
with a decrease in fertility.
1. Tobacco use is associated with an increased risk of the following.
a. Miscarriage
b. Prematurity
c. Low birth weight
2. Alcohol use can adversely affect pregnancy outcomes.
a. Moderate intake is associated with subtle growth retardation
and neurobehavioral effects.
b. Fetal alcohol syndrome is associated with excessive alcohol use.
3. Caffeine content varies between products.
b. Increased risk of spontaneous abortion due to decline in
oocyte quality
c. Increased risk of aneuploidy
d. Coexisting medical conditions that can increase the risk of com-
plications; risks further amplified in even older women; condi-
tions such as hypertension and diabetes should be optimized
2. A medical assessment of women over the age of 35 years
should include:
a. Infertility evaluation if conception difficulty
b. Prenatal diagnosis via:
i. Amniocentesis or chorionic villus sampling (CVS)
ii. Maternal serum testing/nuchal translucency evaluation
c. Diabetes screening
D. Substance use can affect pregnancy and fetal outcomes.
As a woman gets older, conception gets harder.
Do an infertility evaluation after 6 months if the
woman is unable to become pregnant.
1389_Ch31_418-425 2/2/09 1:34 PM Page 420
4. Pelvic examination with sexually transmitted illness (STI) screen
5. Thyroid evaluation for size and nodules
F. Laboratory evaluation should include the following.
1. Complete blood count (CBC) to assess for anemia
2. Rubella titer
3. Varicella titer
4. Hepatitis B surface antigen
5. HIV
6. Plasma glucose for patients at high-risk for diabetes
II. Specific Preconception Counseling
A. Optimizing maternal medical conditions
B. Promoting smoking cessation
C. Encouraging alcohol abstinence
D. Medication adjustment and assessment of disease process effects
with a change in medication regimen
C H A P T E R
Pseudoephedrine has the best safety record during
pregnancy and is preferred over other decongestants.
Dental disease is associated with a higher rate of
premature birth and spontaneous abortion.
Acetaminophen is considered the nonnarcotic analgesic
of choice because of its well-established safety profile in
all trimesters.
E. A thorough physical examination should be performed and include
the following.
1. Complete breast examination: symmetry, nipple morphology, pal-
pable change in breast tissue, axillary adenopathy, skin changes
2. Cardiovascular examination including pulse, blood pressure,
and rhythm assessment
3. Dental evaluation by a trained professional
More than 500 mg of caffeine per day is associated
with an increase in spontaneous abortion.
1389_Ch31_418-425 2/2/09 1:34 PM Page 421
1. All medications are assigned a United States Food and Drug
Association (FDA) pregnancy risk factor category. These cate-
gories are defined in Table 31.1.
E. Genetic counseling for those with heritable disorders
F. Nutritional evaluation and recommendations should include:
1. Vitamins
2. Vegetarian diet assessment for presence of essential amino
acids and iron
3. Avoidance of shark, swordfish, king mackerel, tuna steaks, or
tilefish because of methylmercury exposure
4. Recommend limiting caffeine consumption to less than
250 mg/day
G. Maintenance of regular exercise
H. Perform social service assessment for those at risk for domestic
violence
I. Provide immunizations as needed
P A R T
Recommend a multivitamin supplement with 400 mcg
of folate to prevent neural tube defects.
Advise women not to alter their regular exercise regimen.
TABLE
31.1
FDA Pregnancy Risk Categories
Risk Category Profile
A Safety established using human studies
B Presumed safe (animal studies)
C Uncertain safety; animal studies show an adverse
effect, no human studies
D Unsafe; evidence of human fetal risk that may in
certain clinical circumstances (i.e. life-threatening)
be justifiable
X Highly unsafe; risk of use outweighs any possible
benefit
1389_Ch31_418-425 2/2/09 1:34 PM Page 422
C H A P T E R
1. Influenza during flu season
2. Measles, mumps, rubella, tetanus, diphtheria, poliomyelitis,
varicella
a. Varicella for those without previous clinical disease and neg-
ative titers
3. Hepatitis B for those at high risk
Live viruses should be administered 1 month prior to
conception.
MENTOR TIPS DIGEST
Consider the relative risks and benefits of each medication
change.
As a woman gets older, conception gets harder.
Do an infertility evaluation after 6 months if the woman is
unable to become pregnant.
Eliminate alcohol or tobacco for women who are planning to
conceive. Suggest minimal caffeine use as well.
More than 250 mg of caffeine per day is associated with a
decrease in fertility.
More than 500 mg of caffeine per day is associated with an
increase in spontaneous abortion.
Dental disease is associated with a higher rate of premature
birth and spontaneous abortion.
Pseudoephedrine has the best safety record during pregnancy
and is preferred over other decongestants.
Acetaminophen is considered the nonnarcotic analgesic of
choice because of its well-established safety profile in all
trimesters.
Recommend a multivitamin supplement with 400 mcg of folate
to prevent neural tube defects.
Advise women not to alter their regular exercise regimen.
Live viruses should be administered 1 month prior to conception.
1389_Ch31_418-425 2/2/09 1:34 PM Page 423
Resources
Johnson K, Posner SF, Biermann J, et al. Recommendations to improve
preconception health and health care: United StatesReport of the
CDC/ATSDR Preconception Care Work Group and the Select Panel
on Preconception Care. MMWR 55:1, 2006.
Lee RV, Rosene-Montella K, Barbour LA, et al. Medical care of the preg-
nant patient. American College of Physicians Womens Health Series.
Philadelphia, 2000.
1. Which of these antihypertensives should not be prescribed for women
who may become pregnant?
a. Ramipril
b. Metoprolol
c. Hydrochlorothiazide
d. Alpha methyldopa
2. Which of these drugs is least likely to cause fetal complications
when used by a pregnant woman who has type 2 diabetes
mellitus?
a. Metformin
b. Pioglitazone
c. Glyburide
d. Insulin
3. A 39-year-old primigravida at 8 weeks gestation and with no med-
ical history develops a swollen leg. Noninvasive vascular Doppler
imaging shows a thrombosis extending to the mid-femoral vein.
P A R T
1389_Ch31_418-425 2/2/09 1:34 PM Page 424
C H A P T E R
Which of these is the most appropriate treatment to prevent
pulmonary embolism?
a. Warfarin adjusted to INR 23 for pregnancy duration
b. Warfarin adjusted to INR 23 for 6 weeks
c. Low molecular weight heparin for pregnancy duration
d. Inferior vena cava filter
TABLE 31.1 FDA Pregnancy Risk Categories
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426
HORMONE REPLACEMENT
THERAPY
CHAPTER
32
I. Background
A. Hormone replacement therapy (HRT) consists of estrogen and/or
progestin.
B. HRT is often used for treatment of menopausal complaints.
Vasomotor symptoms or hot flashes are among the most
common menopausal complaints and occur in up to 80%
of women during their menopause transition. Of these women,
20% have disabling symptoms.
C. In the past estrogen/progestin was routinely used also for the pre-
vention of chronic diseases such as osteoporosis and coronary
heart disease (CHD).
1. This was based on observational studies showing a beneficial
effect of estrogen on bone and heart health.
2. Most physicians recommended HRT to all menopausal women
for chronic disease prevention.
3. More recent randomized controlled trials including the
Womens Health Initiative (WHI) trial have refuted the
long-term benefits of HRT and have shown an increased risk
of some chronic diseases such as CHD and strokes (Tables 32.1
and 32.2).
4. Media stories abounded making it confusing for patients who
were on HRT or considering this therapy for the treatment of
menopausal symptoms.
5. The WHI trial was a landmark study and changed how
physicians and patients viewed HRT.
1389_Ch32_426-437 2/2/09 1:34 PM Page 426
II. Epidemiology and Diagnosis of Menopause
A. Menopause is a component of natural process of aging
1. Early menopause is associated with:
a. Lower body weight
b. Nulliparity
c. Smoking
d. Absence of oral contraceptive use
e. Lower socioeconomic status
32 HORMONE REPLACEMENT THERAPY 427
C H A P T E R
TABLE
Risk-Benefit: Estrogen and Progestin
10,000 women taking estrogen and progestin for 1 year might
experience:
Risks Benefits
7 more CHD events
8 more strokes
8 more pulmonary emboli (PEs)
and 10 more deep venous
thromboses (DVTs)
8 more invasive breast cancers
Data from Womens Health Initiative (WHI) trial
32.1
6 fewer colorectal cancer deaths
5 fewer hip fractures
6 fewer vertebral fractures
TABLE
Risk-Benefit: Estrogen Alone
10,000 women taking estrogen alone for 1 year might experience:
Risks Benefits
12 more strokes
3 more PEs and 4 more DVTs
No difference in CHD, breast, or colon cancer
Data from Womens Health Initiative (WHI) trial
32.2
6 fewer hip fractures
6 fewer vertebral fractures
HRT is still the most effective therapy for the treatment
of hot flashes; however, it should no longer be used
for chronic disease prevention.
1389_Ch32_426-437 2/2/09 1:34 PM Page 427
B. Diagnosis
P A R T
The median age is 50 years plus or minus 2 years.
80% of women are affected by hot flashes; 10%20%
have severe symptoms.
Menopause is diagnosed after 12 consecutive months of
amenorrhea not associated with a physiologic (pregnancy/
lactation) or pathologic cause.
1. A high follicle-stimulating hormone (FSH) level is often used
but not essential for diagnosis.
2. Premature ovarian failure is cessation of menses in a woman in
her 30s or early 40s.
III. Symptoms of Menopause
A. Vasomotor symptomsoften called hot flashes or flushes
1. Described as a sudden sensation of intense heat with sweating
and flushing typically lasting 46 minutes
2. Onset typically occurs 612 months prior to menopause when
periods may still be present although irregular
a. Severity ranges from mild, i.e., several per week, to severe,
with more than six per day.
b. Surgical- or chemotherapy-induced menopause leads to
higher incidence and severity of hot flashes.
3. Risk factors for more severe hot flashes
a. Higher body mass index (BMI)
b. Little or no exercise
c. Smoking
d. Ethnicity
i. African Americans have higher incidence than whites
ii. Whites have a higher incidence than Asians
iii. May be cultural differences with respect to reporting
symptoms
iv. Diet may play role
1389_Ch32_426-437 2/2/09 1:34 PM Page 428
4. Natural history
C H A P T E R
For most women, hot flashes last for about 1 year and
then resolve spontaneously.
a. 50% of women have symptoms that last up to 4 years.
b. 10% of women have symptoms that last up to 12 years.
5. Pathophysiology
a. Exact mechanism unknown
b. Believed to be secondary to thermoregulatory dysfunction
B. Vaginal dryness and painful intercourse
1. Low estrogen levels are associated with cellular changes in the
vaginal epithelium, resulting in atrophy of the tissues.
C. Sleep disturbances
1. Common in men and women as they age but tied to
menopausal transition in women
2. Vasomotor symptoms often contribute to sleep disturbance
D. Mood symptoms
1. Depression and anxiety may occur at the time of menopause.
2. It has been difficult to establish whether menopause is the
cause of these symptoms as mood changes are often of
multifactorial origin.
3. There is very little evidence that treatment with HRT
results in improvement of mood symptoms associated with
menopause.
4. Cognitive disturbances, somatic complaints, sexual dysfunc-
tion, and quality of life have been linked to the menopausal
transition, but the majority of studies show no association
between the prevalence of these symptoms and menopausal
status.
E. Most studies limited to reduction of frequency and severity of hot
flashes; little evidence on reduction of other symptoms.
IV. Benefits of HRT (see Tables 32.1 and 32.2)
HRT improves hot flashes in 80%90% of women.
1389_Ch32_426-437 2/2/09 1:34 PM Page 429
A. Vaginal dryness and painful intercourse are reduced.
B. Hip and vertebral fractures due to osteoporosis are reduced.
1. However, there are more focused treatments for osteoporosis
without the HRT-associated risks of CHD and stroke. HRT
should not be used as first-line management for osteoporosis
treatment or prevention.
C. Colorectal cancer deaths are reduced; however, given the risks,
HRT currently does not have a role in colon cancer prevention.
V. Risks of HRT (see Tables 32.1 and 32.2)
A. Endometrial hyperplasia and cancer
1. Unopposed estrogen is linked to both.
P A R T
Women with an intact uterus need progestin when taking
estrogen to minimize the risk of hyperplasia and cancer.
2. Women who have undergone a hysterectomy may be given
estrogen alone.
B. Venous thromboembolism (VTE) including deep venous thrombosis
(DVT) and pulmonary embolus (PE)
1. Users of HRT are at two to three times higher risk for VTE
C. CHD
1. HRT users risk increases 29%
2. Of 10,000 women on HRT for 1 year, seven more CHD events
expected
3. Secondary analyses have evaluated risk of CHD by age and
years since menopause; seems to be no increased risk in CHD
or stroke in women age 5059 years
D. Cerebrovascular accident (CVA)
2. Of 10,000 women on HRT for 1 year, eight more strokes expected
E. Invasive breast cancer
F. Dementia
1. Womens Health Initiative Memory Study (WHIMS) trial
revealed increased risk of dementia after 4 years of HRT.
VI. Side Effects of HRT
A. Breast tenderness
B. Irregular vaginal bleeding
C. Headaches
1389_Ch32_426-437 2/2/09 1:34 PM Page 430
D. Nausea
E. Weight gain
F. Rare elevations in triglycerides
VII. Contraindications to HRT
A. Breast cancer/ovarian cancer
B. Undiagnosed vaginal bleeding
C. History of VTE events
D. Coronary artery disease
E. Cerebrovascular disease
VIII. Formulations of HRT
A. Oral estrogen preparations
1. Low-dose and high-dose formulations available
2. Advantage: ease of use and dosing
3. Premarin, FemHRT, Estrace
B. Progestin preparations
1. Medroxyprogesterone acetate (Provera) most extensively
studied and used
a. Can be used in continuous or cyclical regimens
2. Micronized progesterone (Prometrium)
3. Drospirenone
C. Cyclic versus continuous regimens
1. Cyclic: daily estrogen and progestin on days 1 to 1214
a. Advantage: cyclical bleeding
b. Often used in women near menopause to prevent irregular
bleeding
c. Example: Premphase, Ortho-Prefest
2. Continuous regimen
a. Advantage: more convenient
b. May have irregular bleeding early although amenorrhea
eventually results in most cases
c. Examples: Prempro, Activella, FemHRT
D. Transdermal patches
1. Estrogen alone or combination patches
2. Advantage: ease of use
E. Estrogen vaginal ring
1. Femrin delivers estradiol for 3 months
a. Used for vasomotor and genitourinary (GU) symptoms
b. Need to use with progestin if uterus intact
C H A P T E R
1389_Ch32_426-437 2/2/09 1:34 PM Page 431
2. Estring
a. Low-dose estrogen for treatment of GU symptoms
b. No increases of serum estradiol levels or endometrial
hyperplasia
c. No need to use with progestin
d. May be safe in women with breast cancer
F. Topical estrogen
1. Estrasorb and EstroGel are foil patches and gel, respectively,
applied to arm or leg daily
2. Vaginal estrogen creams: most often used for GU symptoms of
vaginal dryness
a. May be used in low-dose or high-dose regimen
b. If using high doses, need progestin also
c. Lower doses do not need a progestin: estradiol serum levels
not increased
IX. Alternatives to HRT
A. Most of these therapies aimed at reducing hot flashes
B. Behavioral
1. Exercise, weight loss, tobacco cessation, paced respirations
2. No good studies proving these therapies effective
C. Complementary and alternative medicine (CAM)
P A R T
46% of women use CAM therapies for menopausal
symptoms.
Most CAM users do not tell their physicians. Physicians
should routinely ask about alternative treatments used.
1. Many CAM therapies have not been studied well. Studies often
do not have an adequate placebo arm.
2. Many products are advertised for menopause, but most are
without any evidence of benefit.
a. Red clover, wild yam, dong quai, evening primrose oil,
flaxseed
3. Soy
a. Postulated that dietary intake of soy may partly explain
lower reporting of hot flashes by Asian women
b. Most common plant containing phytoestrogens
c. In 11 randomized controlled trials (RCTs)
1389_Ch32_426-437 2/2/09 1:34 PM Page 432
i. Six demonstrated no difference
ii. Five demonstrated soy superior to placebo, with reduction
of hot flashes by 45% compared with placebo of 30%
d. No significant side effects
e. Phytoestrogens may increase risk of breast cancer and
antagonize antitumor effect of tamoxifen
f. Long-term use results in questions of safety; endometrial
hyperplasia may be induced
g. Dosages: 50100 mg/day
C H A P T E R
Studies are contradictory and difficult to evaluate
given variation in soy preparations; however, soy is
probably safe in these doses.
No conclusive supportive data for use; however,
German health authorities, World Health Organiza-
tion, and North American Menopause Society recommend
black cohosh as a treatment option for mild menopausal
symptoms.
4. Black cohosh
a. Most commonly used CAM therapy
b. Mechanism unclear
c. Indigenous North American rhizome
d. Five RCTs but results may not be conclusive: many without
placebo arm
e. No adverse effects
f. Dose: 40160 mg/day
g. Remifemin, Menofem
D. Bio-identical hormones
1. Often called natural hormone therapy; e.g., Biest, Triest
2. Individually compounded recipes of steroids in various dosage
forms, including estrone, estradiol, estriol, progesterone,
dehydroepiandrosterone (DHEA), testosterone, pregnenolone
3. Patients tested via salivary hormone level; steroid doses
individualized to need
a. Salivary levels vary with time of day
b. Poor reproducibility of assays
1389_Ch32_426-437 2/2/09 1:34 PM Page 433
c. No standardized or recognized recommendations based on
salivary data
4. Dosages based and titrated on symptoms, not testing
5. Some formulations have more estrogen than conventional
preparations
P A R T
There are no proven advantages over conventional or
synthetic hormones and potentially the same risks.
E. Medications
1. Antidepressants
a. Selective serotonin reuptake inhibitor (SSRI): best evidence
with paroxetine
b. Selective norepinephrine reuptake inhibitor (SNRI):
venlafaxine
c. Mechanism: two serotonin sites in hypothalamus associated
with temperature control
d. Studies show greater reduction in hot flashes 40%65%
versus placebo 14%38%
2. Gabapentin
a. Mechanism: may regulate calcium channels in hypothalamus
that are involved in thermoregulation
b. Modest reductions in hot flashes
X. Summary
A. HRT is very effective in alleviating menopausal symptoms.
B. Given the increased risk of CHD, CVA, breast cancer, and VTE,
HRT should no longer be recommended for chronic disease
prevention. It is not generally used for osteoporosis treatment or
prevention.
C. Avoid use in women at risk for dementia, stroke, CHD, VTE, and
breast or ovarian cancer.
D. Most women have spontaneous resolution of hot flashes within the
first year.
E. Stop HRT after 612 months to reevaluate.
F. Use low-dose vaginal therapy for GU symptoms.
When using oral hormone therapy, use the lowest dose
possible for the shortest period of time.
1389_Ch32_426-437 2/2/09 1:34 PM Page 434
C H A P T E R
MENTOR TIPS DIGEST
Vasomotor symptoms or hot flashes are among the most com-
mon menopausal complaints and occur in up to 80% of
women during their menopause transition. Of these women,
20% have disabling symptoms.
HRT is still the most effective therapy for the treatment of hot
flashes; however, it should no longer be used for chronic dis-
ease prevention.
Menopause is diagnosed after 12 consecutive months of
amenorrhea not associated with a physiologic (pregnancy/
lactation) or pathologic cause.
The median age is 50 years plus or minus 2 years.
80% of women are affected by hot flashes; 10%20% have
severe symptoms.
For most women, hot flashes last for about 1 year and then
resolve spontaneously.
HRT improves hot flashes in 80%90% of women.
Women with an intact uterus need progestin and estrogen to
minimize the risk of hyperplasia and cancer.
46% of women use CAM therapies for menopausal symptoms.
Most CAM users do not tell their physicians. Physicians
should routinely ask about alternative treatments used.
Studies are contradictory and difficult to evaluate given variation
in soy preparations; however, soy is probably safe in these
doses.
No conclusive supportive data for use; however, German
health authorities, World Health Organization, and North
American Menopause Society recommend black cohosh as
a treatment option for mild menopausal symptoms.
For bio-identical hormones, there are no proven advantages over
conventional or synthetic hormones and potentially the same
risks.
When using oral hormone therapy, use the lowest dose possible
for the shortest period of time.
1389_Ch32_426-437 2/2/09 1:34 PM Page 435
P A R T
Resources
Grady D, Herrington D, Bittner V, et al. Cardiovascular disease outcomes
during 6.8 years of hormone therapy: Heart and estrogen/progestin
replacement study follow-up. Journal of the American Medical
Association 288:4957, 2002.
Hickey M, Saunders CM, Stuckey BG. Nonhormonal treatments for
menopausal symptoms. Maturitas 57:8589, 2007.
Hulley S, Furberg C, Barrett-Connor E, et al. Noncardiovascular disease
outcomes during 6.8 years of hormone therapy: Heart and
estrogen/progestin replacement study follow-up. Journal of the
American Medical Association 288:5864, 2002.
Nelson, Heidi D. Postmenopausal estrogen for the treatment of hot
flashes. Journal of the American Medical Association 291: 16211625,
2004.
NIH State of the Science Panel. Management of menopause-related
symptoms. Annals of Internal Medicine 142:10031013, 2005.
Politi MC, Schleinitz MD, Col NF. Revisiting the duration of vasomotor
symptoms: A meta-analysis. Journal of General Internal Medicine
9:15071533, 2008.
Rossouw JE, Anderson GL, Prentice RL, et al. Risks and benefits of
estrogen plus progestin in healthy postmenopausal women: Principal
results from the Womens Healthy Initiative Randomized Controlled
Trial. Journal of the American Medical Association 288:321333,
2002.
1. Postmenopausal estrogen replacement reduces long-term risk of which
condition ?
a. Osteoporosis
b. Cardiac mortality
c. Breast cancer
d. Depression and anxiety
1389_Ch32_426-437 2/2/09 1:34 PM Page 436
2. Estrogen replacement therapy is the preventive treatment of choice for
which condition?
a. Osteoporosis
b. Endometrial cancer
c. Colorectal cancer
d. Prevention is not a use of estrogen
3. What is the most effective proven hormonal treatment for peri-
menopausal depression and anxiety?
a. Estrogen replacement
b. Estrogen and progestin replacement
c. Dietary soy
d. There is no proven hormonal treatment
LE 32.1
C H A P T E R
1389_Ch32_426-437 2/2/09 1:34 PM Page 437
438
MENSTRUAL DISORDERS
Deborah L. Edberg, MD, Melissa Yvette Liu, MD,
and Joseph P. Gibes, MD
CHAPTER
33
I. Normal Menstrual Cycle
A. Normal cycle: mean interval between menses of 28 days
(/ 7 days); mean duration of 4 days; blood loss about 35 mL
B. Menstrual cycle has three phases
1. In the first part of the cycle, estrogen causes menstrual flow to
stop and promotes endometrial proliferation.
2. In the second phase, after ovulation, progesterone stops
endometrial proliferation and promotes maturation of the
endometrium.
3. In the third phase, as the corpus luteum regresses, progesterone
production falls, which causes the endometrium to shed its lin-
ing, resulting in menstrual bleeding.
II. Primary Amenorrhea
A. Definition
Primary amenorrhea is no menarche by 16 years old in a
girl with normal secondary sexual characteristics (puber-
tal development).
1. May be defined as young as 14 years old in a girl with no
secondary sexual characteristics
B. Evaluation
1. History: clarify if patient has any history of vaginal bleeding
that may constitute menses; ask about sexual history and screen
for abuse to evaluate for pregnancy
1389_Ch33_438-449 2/2/09 1:37 PM Page 438
2. Physical examination: assess for signs of secondary sexual
characteristic (pubertal development)breast development,
pubic hair, underarm hair, body odor, acne.
C. Diagnostic tests
33 MENSTRUAL DISORDERS 439
C H A P T E R
Check pregnancy test.
Constitutional delay in growth and puberty is most
common explanation.
1. If no pregnancy and if patient has normal secondary sexual
characteristics:
a. Ultrasound uterusif present, then evaluate for outflow
obstruction
b. Imperforate hymen
c. Transverse vaginal septum
2. If uterus is absent, then check karyotyping:
a. If normal XX: mullerian agenesis
b. If abnormal XY: androgen insensitivity
3. If patient does not have secondary sexual characteristics:
a. Check follicle-stimulating hormone (FSH) and luteinizing
hormone (LH)
b. If FSH 20 IU and LH 40 IU, then check karyotyping
i. If normal XX: premature ovarian failure
ii. If abnormal XO: Turner syndrome
c. If FSH and LH 5, then work up for hypogonadism
i. Other possibilities:
(1) Excessive exercise
(2) Anorexia/bulimia
(3) Malnutrition
(4) Chronic illness (liver disease/renal disease)
(5) Hypothalamic or pituitary destruction
(6) Central nervous system tumor
1389_Ch33_438-449 2/2/09 1:37 PM Page 439
III. Secondary Amenorrhea
A. Definition:
P A R T
Secondary amenorrhea is absence of menses for 3 months
in women with previously normal menstruation or absence
of menses for 9 months in women with previous oligomenorrhea.
B. Evaluation
1. History
a. Determine frequency and duration of periods, amount of
bleeding, and changes in character of period.
b. Inquire about symptoms of metabolic disorders (e.g., galac-
torrhea, which suggests hyperprolactinemia, symptoms of
thyroid disease), medications (e.g., tricyclic antidepressants,
selective serotonin reuptake inhibitors, steroids, herbal
substances), alcohol use, polycystic ovarian syndrome (signs
of androgen excess such as acne, hirsutism, and obesity),
hepatic disease, hypothalamic suppression (secondary to
eating disorders, stress, excessive exercise).
c. Inquire regarding possibility of pregnancy.
a. Vital signs, body mass index (BMI), signs of androgen ex-
cess (such as acne and hirsutism), thyroid size, galactorrhea
(suggests hyperprolactinemia, which can cause anovulation),
visual field defects (may be caused by a pituitary tumor),
signs of hepatitis, Pap smear, sexually transmitted disease
(STD) screening, pelvic examination.
3. Diagnostic tests
Check thyroid-stimulating hormone (TSH) and prolactin
levels.
a. If both normal, then do progesterone challenge test (give
patient Provera 10 mg daily for 710 days and expect
withdrawal bleed)
1389_Ch33_438-449 2/2/09 1:37 PM Page 440
b. If patient bleeds, there is ovarian malfunction (such as
polycystic ovarian syndrome [PCOS])
c. If patient does not bleed, do estrogen/progesterone challenge
(Premarin for 21 days)
i. If patient bleeds, check follicle-stimulating hormone
(FSH)/luteinizing hormone (LH) levels
(1) If FSH/LH levels high, patient has ovarian failure
(Turner syndrome)
(2) If FSH low, check MRI to evaluate for pituitary tumor
ii. If patient does not bleed, evaluate for outflow obstruction
(i.e., cervical stenosis)
d. If TSH abnormal, treat thyroid disease
e. If TSH normal and prolactin level high
i. If prolactin 100, consider medications, breastfeeding,
hypothyroidism
ii. If prolactin 100, check magnetic resonance imaging
(MRI) to evaluate for prolactinoma
IV. Dysfunctional Uterine Bleeding (DUB)
A. Definitions
1. Abnormal uterine bleeding (AUB) is any bleeding that differs
in regularity, frequency, duration, or volume from the patients
usual menses.
C H A P T E R
DUB is abnormal uterine bleeding for which no
systemic or anatomic cause has been identified.
DUB is a diagnosis of exclusion.
a. Likely a disturbance of the hypothalamic-pituitary-ovarian
axis that results in irregular, prolonged, and sometimes
heavy menstrual bleeding
2. AUB can take many forms.
a. Polymenorrheauterine bleeding at regular intervals of
fewer than 21 days
b. Oligomenorrheauterine bleeding at intervals of more than
35 days
1389_Ch33_438-449 2/2/09 1:37 PM Page 441
c. Menorrhagiaregularly occurring menstrual bleeding that is
prolonged or excessive
d. Metrorrhagiableeding at irregular intervals or between
periods
e. Menometrorrhagiaheavy or prolonged uterine bleeding
occurring at irregular intervals
B. Impact of DUB
1. Frequency: 5%10% of outpatient complaints
2. Morbidity/mortality:
a. A single episode usually has no sequelae.
b. Repetitive episodes increase the chance of iron deficiency
anemia (up to 30% of cases).
c. Up to 20% of adolescents with persistent menorrhagia have a
concomitant bleeding disorder.
d. Heavy flow can cause need for fluid management, blood
transfusion, or intravenous (IV) hormone therapy (i.e.,
estrogen/progesterone).
e. DUB can lead to unnecessary surgical evaluation (i.e.,
uterine curettage, endometrial ablation, hysterectomy).
f. Continuous unopposed estrogen stimulation of the endometrium
increases the risk for endometrial adenocarcinoma.
g. Infertility is associated with chronic anovulation, particularly
in patients with polycystic ovarian syndrome, obesity, and
chronic hypertension.
C. Pathophysiology of DUB
1. Most frequent:
P A R T
DUB usually represents anovulatory cycles.
a. During a cycle in which ovulation does not occur, there is an
absence of progesterone production, which in a normal
ovulatory cycle acts to stop endometrial proliferation.
b. The result is constant, noncycling estrogen stimulation of
endometrial growth and proliferation, which causes the
endometrium to outgrow its blood supply, and leads to
irregular breakdown and sloughing.
2. DUB occurs with ovulatory cycles, most often in adolescence
and perimenopause; ovulatory dysfunctional bleeding may
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C H A P T E R
present as polymenorrhea, oligomenorrhea, midcycle spotting,
menorrhagia
Because DUB is a diagnosis of exclusion, organic causes
must be ruled out.
1. Systemic disease (coagulopathy, hypothyroidism, liver disease)
2. Pregnancy-related (implantation bleeding, threatened abortion,
ectopic pregnancy)
3. Malignancy (endometrial or cervical cancer)
4. Anatomic abnormalities (endometrial hyperplasia, submucous
myoma, cervical lesions)
5. Foreign bodies (e.g., intrauterine device [IUD])
6. Iatrogenic (e.g., medications, herbal substance)
E. Taking the history
1. Determine frequency and duration of periods, amount of bleed-
ing, changes in character of period
Rule out pregnancy.
2. Inquire about symptoms of metabolic disorders (e.g., galactor-
rhea, which suggests hyperprolactinemia; symptoms of thyroid
disease), bleeding disorders (e.g., easy bruising, bleeding gums,
epistaxis), medication causes (e.g., anticoagulants, tricyclic
antidepressants, selective serotonin reuptake inhibitors, steroids,
herbal substances), alcohol use, polycystic ovarian syndrome
(signs of androgen excess such as acne, hirsutism, obesity),
hepatic disease, hypothalamic suppression (secondary to eating
disorders, stress, excessive exercise)
F. Physical examination
1. Vital signs, BMI, signs of androgen excess (such as acne and
hirsutism), thyroid size, galactorrhea (suggests hyperprolactinemia,
which can cause anovulation), visual field defects (may be caused
by a pituitary tumor), ecchymosis and purpura (which suggest a
bleeding disorder), signs of anemia, signs of hepatitis, Pap smear,
sexually transmitted disease screening, pelvic examination
1389_Ch33_438-449 2/2/09 1:37 PM Page 443
G. Diagnostic tests
1. Laboratory
a. Beta-HCG
P A R T
The hallmark of DUB is a negative pelvic examination
(that is, no palpable uterine enlargement suggesting
fibroids or polyps).
Most common cause of AUB is pregnancy-related.
b. Complete blood count to evaluate for anemia, platelets,
evidence of hematologic disease
c. Pap smear to rule out cervical cancer (most common gyneco-
logic cancer)
d. Thyroid function tests, prolactin; abnormalities can cause
ovulatory dysfunction and can be treated
e. Liver function tests to evaluate for alcoholism or hepatitis,
both of which can affect metabolism of estrogen
f. Coagulation studies, hormone assays (such as FSH/LH)
g. Endometrial evaluation with imaging or sampling recom-
mended for women with risk factors for endometrial cancer,
such as chronic anovulatory cycles, obesity, nulliparity, age
older than 35 years, tamoxifen therapy
H. Imaging
1. Consider transvaginal ultrasound in patients who cannot
tolerate bimanual examination, obese patients, or if ovarian or
uterine pathology is suspected.
2. Ultrasound can identify endometrial hyperplasia, carcinoma,
polyps, or uterine fibroids.
3. Saline-infusion sonohysterography increases the diagnostic
accuracy of ultrasonography.
I. Procedures to rule out endometrial carcinoma
1. Endometrial sampling: aspiration, curetting, hysteroscopy or
dilation and curettage (D&C)
2. Ultrasound to measure the width of the endometrial stripe
J. Treatment
1. Medical:
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C H A P T E R
a. Acute, severe bleeding: conjugated equine estrogen
(Premarin) 25 mg IV q4h for 24 hours, or orally in divided
doses up to 10 mg/day; once acute bleeding stabilized, one
monophasic oral contraceptive pill (OCP) twice a day until
bleeding stops (usually 57 days); a withdrawal bleed
usually occurs when pills stopped; on day 5 of bleeding,
start regular regimen of OCPs
b. Less severe bleeding: OCPs two to four times daily until
bleeding stops, then start regular regimen of OCPs
c. OCPs suppress endometrial development, reestablish cycle,
decrease menstrual flow, lower risk of iron-deficiency
anemia and endometrial carcinoma; first-line therapy in
anovulatory DUB
d. Progestins suppress endometrial growth and mature
endometrium so withdrawal bleeding organized; may be
administered 510 mg/day for 21 days of the cycle or for
the last 10 days of the cycle; especially useful for patients
with anovulatory DUB for whom estrogen therapy is con-
traindicated (e.g., smokers over the age of 35 years, women
at risk for thromboembolism)
e. Levonorgestrel-releasing intrauterine device (Mirena)
releases low-level progestin, suppressing endometrial
proliferation and reducing blood loss; useful in menorrhagic
ovulatory DUB
f. Nonsteroidal anti-inflammatory drugs (NSAIDs) useful in
menorrhagic ovulatory DUB; these are prostaglandin
synthetase inhibitors: by blocking conversion of arachidonic
acid to prostaglandins, they reduce prostaglandin levels,
decreasing uterine bleeding
g. Antifibrinolytic agents (e.g., tranexamic acid [Cyklokapron])
reduce heavy bleeding by inhibiting breakdown of blood
clots; most useful in women with menorrhagic ovulatory
DUB; best to combine with OCP therapy (off-label use)
h. Androgens (Danazol) cause endometrial atrophy; seldom
used due to side effects (including possibility of irreversible
signs of masculinization)
i. Gonadotropic-releasing hormone (GnRH) agonists limited to
women with severe blood loss who fail to respond to medical
therapy and who do not want to resort to surgical intervention
1389_Ch33_438-449 2/2/09 1:37 PM Page 445
2. Surgical (appropriate when medical therapy fails or is
contraindicated):
a. D&C: for those who fail hormonal management
b. Hysterectomy: for those who fail or refuse hormonal
therapy, have symptomatic anemia, or altered quality of life
c. Endometrial ablation: less invasive and costly than hysterec-
tomy; options include thermal balloon, rollerball, microwave,
cryoablation, radiofrequency, electrocautery, laser
V. Dysmenorrhea
A. Definition
P A R T
Dysmenorrhea is painful menses in women with normal
pelvic anatomy.
It affects 20%90% of adolescent women.
It is caused by release of prostaglandins in the menstrual
fluid, which causes uterine contractions and menstrual pain.
1. Crampy pelvic pain begins at or shortly before the onset of
menses, lasting 13 days.
B. Prevalence
1. Of those, 15% say cramping severe enough to cause them to
miss school.
C. Pathogenesis
1. Increased vasopressin also increases uterine contractility.
D. Risk factors
1. Age younger than 20 years
2. Attempts to lose weightparticularly in women 1420 years
of age
3. Depression/anxiety
4. Smoking
5. Nulliparity
6. Disruption of social networks
1389_Ch33_438-449 2/2/09 1:37 PM Page 446
E. Diagnosis
1. History: abnormal vaginal discharge, sexual activity, fever, pain
not during time of menses, abnormal cycles, infertility, possibility
of pregnancy
2. Physical: evaluate for discharge, pelvic tenderness not during
time of menses, enlarged ovaries, pelvic masses
3. Laboratory: Pap smear, STD cultures, wet mount
4. Imaging: for severe dysmenorrhea not responsive to treatment
check ultrasound to rule out ovarian cyst
5. Note: relationship between endometriosis and dysmenorrhea
not clear
F. Treatment:
1. NSAIDsbegin before onset of menstrual pain and flow to
block prostaglandin release
2. OCPs
3. Depo-Provera injections
4. Mirena IUD
5. Intravaginal administration of normal birth control
6. Lifestyle modificationlow-fat vegetarian diet, exercise
7. Alternative treatments (limited data):
a. Thiamine
b. Vitamin E
c. Omega-3 polyunsaturated fatty acids
d. Acupuncture/acupressure
e. Transcutaneous electrical nerve stimulator (TENS)
C H A P T E R
MENTOR TIPS DIGEST
Primary amenorrhea is no menarche by 16 years old in a girl
with normal secondary sexual characteristics (pubertal
development).
Constitutional delay in growth and puberty is most common
explanation.
Secondary amenorrhea is absence of menses for 3 months in
women with previously normal menstruation or absence of
menses for 9 months in women with previous oligomenorrhea.
Check thyroid-stimulating hormone (TSH) and prolactin levels.
1389_Ch33_438-449 2/2/09 1:37 PM Page 447
Resources
Albers H., et al. Abnormal uterine bleeding. American Family Physician
69:19151926, 2004 (available at
www.aafp.org/afp/20040415/1915.html).
Behera M. Dysfunctional uterine bleeding. eMedicine. Available at
www.emedicine.com/med/topic2353.html
French L. Dysmenorrhea. American Family Physician 71, 2005.
Gaunt AM, Mayeaux EJ Diagnosis and management of dysfunctional
uterine bleeding. CME Bulletin 6, 2007 (available at www.aafp.org/
online/en/home/cme/selfstudy/cmebulletin/dub.html).
Master-Hunter T, Heiman DL. Amenorrhea: Evaluation and
treatment. American Family Physician, 2006, 73 (8): 1374-82.
Stenchever M, et al. Comprehensive gynecology, 4th ed., 10791098.
St Louis: Mosby, 2001.
P A R T
DUB is abnormal uterine bleeding for which no systemic or
anatomic cause has been identified.
DUB is a diagnosis of exclusion.
DUB usually represents anovulatory cycles.
Because DUB is a diagnosis of exclusion, organic causes must
be ruled out.
The hallmark of DUB is a negative pelvic examination (that is,
no palpable uterine enlargement suggesting fibroids or
polyps).
Most common cause of AUB is pregnancy-related.
Dysmenorrhea is painful menses in women with normal pelvic
anatomy.
It affects 20%90% of adolescent women.
It is caused by release of prostaglandins in the menstrual fluid,
which causes uterine contractions and menstrual pain.
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C H A P T E R
1. In the first phase of the menstrual cycle when the endometrium prolif-
erates, what is the responsible hormone?
a. Estrogen
b. Progesterone
c. Beta-hCG
d. Prolactin
2. In the second phase of the menstrual cycle when endometrial proliferation
stops and the endometrium matures, what is the responsible hormone?
a. Estrogen
b. Progesterone
c. Beta-hCG
d. Prolactin
3. The corpus luteum produces which hormone?
a. Estrogen
b. Progesterone
c. Beta-hCG
d. Prolactin
1389_Ch33_438-449 2/2/09 1:37 PM Page 449
450
CHAPTER
FEMALE GENITAL
SYMPTOMS
34
I. Pathophysiology
A. Vulvar
1. Dermatologic conditions
a. Lichen sclerosus: benign, chronic inflammatory condition
with epithelial thinning of unknown etiology
b. Lichen planus: benign inflammatory condition that is more
widespread; involves skin, nails, and mucous membranes
c. Contact dermatitis: may be irritant (80%) or allergic (20%)
2. Infectious conditions
a. Condyloma acuminatum: sexually transmitted human
papillomavirus (HPV), most commonly types 6 and 11
b. Genital ulcer disease (syphilis, herpes simplex [HSV]):
sexual transmission, e.g., HSV-1 and HSV-2 chancroid
(Table 34.1)
3. Unknown etiology
a. Vestibulitis: inflammation of the minor vestibular glands
b. Vulvodynia: possibly type of peripheral neuropathy
B. Vaginal
1. Infectious
a. Bacterial vaginosis: a decrease in the normal lactobacillus
leads to an overgrowth of gram-negative and variable rods in
vaginal flora
b. Candida: overgrowth of yeast after disruption of the vaginal
ecosystem (85% Candida albicans; 15% other Candida spp.)
c. Trichomonas: sexually transmitted infection with protozoan
Trichomonas vaginalis
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34 FEMALE GENITAL SYMPTOMS 451
C H A P T E R
2. Atrophic: noninfectious form of vaginitis affecting the epithelium
due to lack of estrogen
C. Cervical
1. Infectious
a. Chlamydia: infection of the upper genital tract caused by
obligate intracellular bacteria, Chlamydia trachomatis
b. Gonorrhea: gram-negative diplococci infecting the columnar
epithelium of the upper genital tract
II. Epidemiology
A. Acute vulvovaginitis accounts for more than 10 million health-care
visits per year.
1. Bacterial vaginosis is the most common cause of acute vaginitis,
accounting for 15%50% of cases depending on the population
studied.
2. Women with bacterial vaginosis and trichomoniasis are at
increased risk of infection with HIV.
3. 75% of women have at least one candidal (yeast) infection in
their lifetime, and 40%45% have more than one.
4. A single exposure to a partner infected with trichomonas will
infect 85% of females.
B. Vulvar syndromes and dermatologic conditions are less common
causes of vaginal symptoms.
1. Contact dermatitis accounts for a third to half of womens
vulvar complaints.
C. Cervicitis is a serious condition affecting millions of women,
many of whom are asymptomatic, leading to infertility.
TABLE
Painful Versus Painless Genital Ulcers
Painful
Painless
Herpes simplex virus
Chancroid
Chancre (primary syphilis)
Condyloma latum (secondary syphilis)
Lymphogranuloma venereum
Granuloma inguinale
Molluscum contagiosum
34.1
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P A R T
1. Chlamydia is the most common bacterial sexually transmitted
disease (STD) in the United Sates, with nearly 3 million new
cases every year.
2. The U.S. Centers for Disease Control (CDC) estimate at least
700,000 new cases of gonorrhea in the United States each year.
III. Patient History
A. Chief complaint
1. Symptom and its duration
Symptoms alone cannot be used to localize the site
of infection and may not correlate with the presence
of infection.
B. History of present illness
1. Obstetric history, including past and current pregnancies
2. Gynecologic history, including last menstrual period, sexual
history, number of partners, new partners, and form of contra-
ception if indicated
3. Presence of pain, itching, irritation, discharge, lesions
a. Discharge: describe color, texture, location, odor
b. Lesions: describe number, size, location, whether painful or
painless
4. Include associated symptoms of dysuria, dyspareunia, abdominal
or pelvic pain, fever, inguinal adenopathy
C. Past medical history
1. Previous infections, diabetes, immunosuppression
D. Medications
1. Recent antibiotic use, over-the-counter treatments, oral
contraceptives
E. Allergies
1. History of drug rash
IV. Physical Examination
A. Vital signs
1. Note presence or absence of fever.
B. Abdominal examination
1. Palpate for left or right lower quadrant tenderness.
2. Palpate the inguinal area for adenopathy.
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C H A P T E R
C. Pelvic examination
1. Examine the external genitalia for lesions, erythema, or
edema.
a. About 25% of patients with vaginal candidiasis have excori-
ations on their external genitalia.
2. With the speculum, examine the vagina and cervix, noting the
presence, location (from the cervix or in the vagina only), and
character of the discharge.
a. The classic strawberry cervix represents erythematous
punctuations on the cervix associated with Trichomonas
infection but is only present in 2%5% of cases.
3. Obtain a vaginal pH from the side walls of the vagina with a
cotton-tipped swab wiped onto commercially available pH paper.
a. The normal vaginal pH is 4.0.
b. Candidal vaginitis will not alter the normal pH.
pH of 4.5 is present in over 95% of women with
bacterial vaginosis and trichomoniasis.
c. Trichomonas vaginitis and atrophic vaginitis are associated
with the highest vaginal pH.
d. The presence of sperm or blood raises the vaginal pH.
4. Bimanual examination consists of the following.
a. Determine if there is any cervical motion tenderness.
b. Feel the uterus and adnexa for any tenderness or masses.
V. Differential Diagnosis
A. Vulvar conditions
1. L. sclerosus
a. Symptoms include intense pruritus, dyspareunia, and
burning pain.
b. The skin appears thin and white.
c. Biopsy reveals a thin epithelium with loss of rete ridges
and inflammatory cells lining the basement membrane.
2. L. planus
a. Symptoms may include itching.
b. Examination reveals slightly purple polygonal papules that
have overlying fine white lines called Wickham striae.
3. Vestibulitis
a. Symptoms include severe dyspareunia at the introitus.
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P A R T
b. On examination over the vestibula, there may be erythematous
papules 14 mm that are extremely tender to touch with a
cotton-tipped swab.
4. Vulvodynia
a. Symptoms include a nonspecific burning, itching, and pain
involving some or all of the external genitalia.
b. Examination results are usually normal.
5. C. acuminatum
a. Painless cauliflower-like growths on the vulva and vagina
and sometimes involving the rectal mucosa.
Types 6 and 11 are most common cause of warts,
and types 16 and 18 have been associated with
cervical cancer.
6. Herpes simplex
a. Symptoms include painful ulcerations on skin and mucosal
surfaces. Vaginal discharge and dysuria may also be present.
Burning pain may occur before outbreak of lesions. Primary
infection may be accompanied by fever and flu-like symptoms.
b. Examination reveals multiple painful grouped vesicles on
an erythematous base. Vesicles erupt and form ulcerations.
Inguinal adenopathy may be present.
c. Viral shedding always occurs when lesions are present and
may also occur when patients are asymptomatic.
d. Diagnosis consists of the following.
i. Viral culture of active lesion
ii. Serologic tests for HSV-1 and HSV-2 antibodies may be
helpful but do not differentiate present from past infection
B. Vaginal infections and conditions (Table 34.2)
1. Bacterial vaginosis
a. May occur in women who are not sexually active
b. Symptoms sometimes include discharge with fish-like odor;
usually no pruritus
c. Examination reveals thin homogenous often gray or white
vaginal discharge; vaginal pH >4.5
Diagnosis is by Amsels criteria (Box 34.1).
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C H A P T E R
2. Candidiasis
a. Risk is increased in patients with recent antibiotic use, dia-
betes mellitus, immunosuppression, and increased estrogen
states (pregnancy and oral contraceptive use).
TABLE
Diagnosis of Vaginitis
Diagnostic Bacterial Atrophic
Study Candida Vaginosis Trichomonas Vaginitis
pH
Saline wet
mount
Potassium
hydroxide
(KOH)
wet
mount
Culture
34.2
3.84.2
(normal)
Budding
yeast
Pseudohy-
phae
Candida
spp.
>4.5
Clue cells
No white
blood
cells
(WBCs)
Gram-
negative
>5.0
Flagellated
organisms
WBCs
Trichomonas
with
Diamond
media
>5.0
Parabasal
epithelial
cells
BOX
Amsels Criteria for Bacterial Vaginosis
Three of four criteria should be met for diagnosis:
Positive whiff (amine) test with application of 10% KOH
Clue cells (epithelial cells with stippled borders due to adherent bacteria)
present on saline wet mount
Presence of thin, homogenous vaginal discharge
Vaginal pH >4.5
Absence of odor has strong negative likelihood ratio for bacterial vaginosis.
34.1
Bacterial vaginosis is associated with an increased
risk of upper genital tract infections, spontaneous
abortion, and premature labor.
1389_Ch34_450-461 2/2/09 1:36 PM Page 455
P A R T
b. Symptoms include itching and thick white cottage
cheeselike discharge.
c. Diagnosis consists of the following.
i. Normal vaginal pH
ii. KOH wet mount showing yeast elements (sensitivity
around 60%)
iii. Culture for Candida
iv. Erythema found on examination increases likelihood of
candidiasis
3. Trichomoniasis
Half of both males and females with trichomoniasis
may be asymptomatic despite infection.
a. Symptoms include thin, green frothy discharge, vulvovaginal
irritation, and sometimes dyspareunia and dysuria.
b. Physical examination may reveal hemorrhages on the
endocervix (strawberry cervix).
c. Diagnosis consists of the following.
i. Saline wet mount reveals mobile flagellated organisms
and a high number of WBCs (only 70% sensitive).
ii. Culture should be performed when wet mount is negative
(90% sensitive and specific).
4. Atrophic vaginitis
a. Noninfectious form of vaginitis that occurs in postmenopausal
females due to lack of estrogen
b. Symptoms include vaginal soreness, discharge, dysuria,
dyspareunia
c. Physical examination reveals thin vaginal mucosa with
diffuse erythema and lack of vaginal folds
d. Vaginal pH elevated
C. Cervical infections (Table 34.3)
1. Chlamydia
a. 40% of women are asymptomatic.
b. Progression of the infection can lead to pelvic inflammatory
disease and infertility.
c. Symptoms may include vaginal discharge, dyspareunia, and
postcoital bleeding.
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C H A P T E R
d. Physical examination may reveal mucopurulent cervical
discharge and a friable cervix.
e. Diagnosis is made with nucleic acid amplification tests such
as PCR (highly sensitive and specific) on cervical swabs
and/or urine.
f. Expert panels recommend screening for chlamydia for all
women younger than 25 years, who have new or multiple
sexual partners, or who use non-barrier contraceptives.
2. Gonorrhea
a. Up to 50% of women may be asymptomatic.
b. Symptoms can occur up to 2 weeks post exposure and
include vaginal discharge, dyspareunia, and vaginal irritation.
c. Physical examination may reveal mucopurulent cervical
discharge and a friable cervix.
d. Untreated infections may develop pelvic inflammatory
disease and infertility. Widespread dissemination may occur.
e. Diagnosis is made with culture on chocolate agar or PCR of
cervical discharge.
TABLE
Diagnostic Tests for Cervical Infections
Diagnosis Test
Herpes *Culture, PCR, serologic studies, Tzanck smear
Chlamydia *PCR of cervical discharge or urine
Gonorrhea *Culture with chocolate agar, PCR of cervical discharge
*gold standard
PCR = polymerase chain reaction
34.3
If either chlamydia or gonorrhea is suspected,
patients should be treated for both, as coinfection
frequently occurs.
VI. Management
A. Vulvar
1. Dermatologic conditions such as L. sclerosus and L. planus
should be referred to a dermatologist because biopsies may be
necessary to distinguish these conditions from vaginal cancer.
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P A R T
Contact dermatitis may be treated with sitz baths and a low-
potency topical steroid preparation.
2. C. acuminatum has the following profile.
a. Cases may resolve spontaneously 20%30% of the time.
b. Medical therapies can be topical cryodestructive or
immunoablative preparations.
c. Surgical treatment may be necessary for more aggressive
cases.
d. Annual Pap smears are essential to detect early cervical
dysplasia.
3. Herpes simplex has the following profile.
Treatment with oral antivirals such as acyclovir, famci-
clovir, and valacyclovir will reduce the duration of
symptoms if taken within the first 72 hours.
a. Treatment of the first outbreak may reduce the number of
recurrent infections.
b. Theses oral agents can be used as suppressive therapy for
patients with frequent outbreaks and may reduce the rate of
asymptomatic viral shedding.
c. Topical treatments have little effect on the herpes virus.
4. Vestibulitis and vulvodynia have the following profile.
a. Avoid vulvar irritants.
b. Tricyclic antidepressants have been useful.
c. Surgical treatment including vestibulectomy is controversial.
B. Vaginal
1. Bacterial vaginosis
a. Topical treatments are metronidazole gel 0.75% or clindamycin
cream 2% applied intravaginally for 5 days.
b. Oral treatment is metronidazole 500 mg twice daily for 7 days.
c. There is no need to treat sexual partners.
2. Candida
a. Topical antimycotics cure more than 80% of all infections.
b. A one-time dose of oral fluconazole (150 mg) can be used
but has a lower rate of efficacy.
c. A variety of treatments are available for recurrent candidiasis.
d. There is no need to treat sexual partners.
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C H A P T E R
3. Trichomonas
a. The only treatment available is oral metronidazole.
All sexual partners of patients with trichomoniasis
should be treated, and both partners should be
screened for other STDs.
4. Atrophic vaginitis
a. Topical or oral estrogens are effective.
C. Cervical
1. Chlamydia
a. Treatment for the patient and her partner includes a single
dose of azithromycin or a 1-week course of doxycycline.
Alternate regimens include 1 week of erythromycin,
levofloxacin, or ofloxacin.
b. Patients should be treated for gonorrhea.
c. All sexual partners should be treated.
d. Patients should be tested for other STDs and counseled
about HIV and safe sex practices.
2. Gonorrhea
a. A single dose of ceftriaxone 250 mg IM is effective.
b. A variety of single-dose oral quinolone regimens is
effective, but the resistance of gonorrhea to quinolones is
increasing.
c. The CDC considers gonorrhea in Hawaii and California to
be quinolone-resistant.
d. Patients should be treated empirically for chlamydia.
e. All sexual partners should be treated, and patients should be
counseled about safe sex and HIV as well as tested for other
sexually transmitted infections.
MENTOR TIPS DIGEST
In general, symptoms alone cannot be used to localize the
site of infection and may not correlate with the presence of
infection.
pH of 4.5 is present in over 95% of women with bacterial
vaginosis and trichomoniasis.
1389_Ch34_450-461 2/2/09 1:36 PM Page 459
P A R T
Resources
Anderson MR, Klink K, Cohrssen A. Evaluation of vaginal complaints.
Journal of the American Medical Association 291:13681379,
2004.
Beck WW. National medical series: Obstetrics and gynecology, 4th ed.
Baltimore, Williams & Wilkins, 1997.
Excellent textbook that provides further details on vaginal
symptoms.
Eckert LO: Acute vulvovaginitis. New England Journal of Medicine
355:12441252, 2006.
Excellent review with table on sensitivity and specificity of diagnostic
tests as well as costs of treatment regimens.
Sobel JD: Vaginitis. New England Journal of Medicine 337:18961903,
1997.
Well-organized vaginitis review authored by a national expert.
Condyloma acuminatum types 6 and 11 are most common
cause of warts, and types 16 and 18 have been associated
with cervical cancer.
Bacterial vaginosis is diagnosed using Amsel criteria.
Bacterial vaginosis is associated with an increased risk of
upper genital tract infections, spontaneous abortion, and
premature labor.
Half of both males and females with trichomoniasis may be
asymptomatic despite infection.
If either chlamydia or gonorrhea is suspected, patients should
be treated for both, as coinfection frequently occurs.
In herpes simplex, treatment with oral antivirals such as
acyclovir, famciclovir, and valacyclovir will reduce the duration
of symptoms if taken within the first 72 hours.
All sexual partners of patients with trichomoniasis should
be treated, and both partners should be screened for other
STDs.
1389_Ch34_450-461 2/2/09 1:36 PM Page 460
1. Which of the following vulvovaginal conditions is infectious?
a. Lichen planus
b. Lichen sclerosus
c. Atrophic vaginitis
d. Condyloma acuminatum
2. What is the cause of Lichen sclerosus?
a. Scleroderma (progressive systemic sclerosis)
b. Estrogen deficiency
c. Trichomonas vaginalis
d. Unknown
3. Human papillomavirus (HPV) causes:
a. Condyloma acuminatum
b. Increased risk of spontaneous miscarriage
c. Painless genital ulcers
d. Painful genital ulcers
C H A P T E R
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462
CHAPTER
PAP SMEAR AND CERVICAL
CANCER SCREENING
Ellen J. Gelles, MD
35
I. Pathophysiology of Cervical Cancer
A. Types include squamous cell carcinoma and adenocarcinoma;
squamous by far most common
B. Role of human papillomavirus (HPV)
HPV infections are believed to be the cause of most
cervical cancers.
1. Serotypes 16, 18, 31, 33, and 35 are among the high-risk, or
oncogenic, HPV strains; serotypes 6 and 11 are examples of the
low-risk types.
2. Most HPV infections are transient; other factors are likely
necessary for HPV to progress to dysplasia (Box 35.1).
BOX
Risk Factors for Cervical Cancer
Early onset of sexual activity (younger than 17 years)
Multiple sexual partners (more than two per lifetime)
History of herpes simplex virus or other sexually transmitted diseases
Immunosuppression, such as HIV infection or chemotherapeutic agents
Cigarette smoking
Low socioeconomic status
Radiation exposure
High-risk sexual partner
Prolonged use of contraceptive hormones
High parity
35.1
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35 PAP SMEAR AND CERVICAL CANCER SCREENING 463
C H A P T E R
C. Cervical intraepithelial neoplasia (CIN)
1. CIN pre-invasive stage of cervical cancer
2. Precedes invasive cervical cancer by years to decades
3. Biopsy specimens classified as CIN IIII, depending on how
much cervical epithelium involved with dysplastic changes
a. CIN I is known as low-grade dysplasia.
b. CIN II and III are known as high-grade dysplasia.
II. Epidemiology of Cervical Cancer
A. Affects 10,000 women in the United States per year; more than
4000 U.S. women die from cervical cancer annually
B. Incidence higher in developing countries without access to
screening
C. Median age of diagnosis 48 years; rarely occurs in women
younger than 35 years
D. Risk factors listed in Box 35.1
III. Prevention of HPV and Cervical Cancer
A. Modifying risk factors
1. Smoking cessation
Smoking cessation can reduce the risk of cervical
cancer two- to threefold.
2. Limiting number of sexual partners, delaying onset of sexual
activity, and using barrier contraception reduce HPV infection
rates
B. Screening for cervical dysplasia and HPV
1. Papanicolaou (Pap) smear
2. Testing for high-risk HPV DNA
a. Up to 95% sensitive for detecting cervical dysplasia
b. Can be performed on same sample as liquid Pap smear;
collected by people with little medical training or by patient
Disadvantages of HPV testing include its low speci-
ficity, particularly in young women. As most HPV
infections are transient and never develop into cervical
cancer, detection of every HPV infection is of question-
able value.
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c. Not usually used alone as a primary screening tool; used to
triage women with minor Pap smear abnormalities to decide
whether further testing needed; also used in combination
with Pap smear to decide which women are very low-risk for
cervical cancer and can be screened less frequently; guide-
lines for this combination Pap smear being developed
C. HPV vaccine
HPV vaccine targets four serotypes: 6, 11, 16, and
18. Types 16 and 18 cause the vast majority of cervical
cancers; 6 and 11 are associated with genital warts.
1. In women who have not yet been exposed to these serotypes,
the vaccine has been shown to be highly effective in preventing
high-grade cervical dysplasia.
2. Three-dose vaccine is approved for use in females age
926 years and ideally should be given prior to the onset
of sexual activity.
IV. Pap Smear
A. Features that make this a good screening test
1. Inexpensive
2. Easy to perform as part of a routine office visit
3. Minimally uncomfortable to patients
4. Targets a disease with a long, identifiable, precancerous stage,
during which treatment and cure are possible
B. Current Pap smear screening guidelines
1. Screening at some regular intervals is crucial; a single Pap
smear may miss cervical dysplasia 30%50% of the time.
The United States Preventive Services Task Force
(USPSTF) and the National Cancer Institute (NCI) advise
screening at least every 3 years, starting 3 years after a
woman becomes sexually active, or at age 21 years. In
average-risk women, annual screening does not provide a
higher yield for detecting high-grade dysplasia than screening
every 3 years.
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C H A P T E R
2. After age 6570 years (exact guidelines vary), Pap smear
screening is no longer necessary, as long as the patient has
undergone previous regular screening with normal test results.
3. Immunosuppressed women (those with HIV/AIDS and those on
immunosuppressant drugs) should be screened more often as
should those who have been sexually active and have not had
regular screening in the past.
4. Women who have no cervix because they have undergone total
hysterectomies for noncancerous conditions do not need Pap
smears.
C. Tips and techniques for obtaining a good Pap smear
1. The patient should be made as comfortable as possible and
draped appropriately. With newer liquid-based Pap smear
collection systems (see later), use of small amounts of lubri-
cants is fine and does not affect the adequacy of the specimen.
2. Avoid collecting specimens when the patient is menstruating or
has an active vaginal or cervical infection.
3. Collect from best location.
During the speculum examination, obtain the Pap
smear sample from the transformation zone (the
junction between the darker-colored columnar epithelium
and the paler squamous epithelium), as this is where most
cervical cancers arise.
a. Hormonal changes of pregnancy or hormonal contraceptives
can cause the transformation zone to migrate outward,
whereas in postmenopausal women it can be located inside
the os where it is not visible to the examiner.
b. To maximize chances of getting transformation-zone cells on
the specimen, both the endocervix and the ectocervix are
sampled. An extended-tip spatula is used to sample the
ectocervix, and a Cytobrush is used for the endocervix.
4. Conventional Pap smear is performed as follows.
a. Samples are spread directly on a slide in the examination
room and fixed with a spray fixative.
b. This technique is more cumbersome and prone to sampling
problems. Leaving the slide sitting in air before it is sprayed
with fixative, the presence of blood or inflammatory vaginal
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discharge and use of examination lubricant can lower the
sensitivity and lead to more unsatisfactory smears.
5. Liquid-based Pap smears are collected as follows.
a. Cervical cells are collected in a container of liquid fixative
rather than on a slide. In the laboratory, the specimen is
filtered to remove blood and noncellular debris and trans-
ferred to a slide for interpretation.
b. This method is more convenient, is higher-sensitivity for
detecting cervical dysplasia, and fewer smears are deemed
unsatisfactory for interpretation.
c. This method is more expensive than the conventional Pap
smear and has a longer processing time.
V. Interpretation and Management of Pap Smear Results
A. Reports contain the following information:
1. Assessment of specimen adequacy allows pathologist to comment
if correct cell types (transformation zone) not present in specimen,
smear not well labeled, or if blood or inflammatory cells comprise
too much of the specimen for an adequate reading
2. General categorization: (normal or other)
3. Descriptive diagnosis that names any abnormalities on the smear
B. Squamous cell abnormalities and management
1. Cervical carcinomaimmediate referral to gynecologist
2. High-grade squamous intraepithelial lesion (HSIL)
a. Cytologic equivalent to high-grade dysplasia (CINII-III); in
practice, this correlation not always true: sometimes HSIL
reading is false alarm and pathology more benign
b. High rate of progression to invasive cervical carcinoma;
patients should be referred for colposcopy with cervical biopsy
3. Low-grade squamous intraepithelial lesion (LSIL)
a. Correlates with mild dysplasia (CINI) and cellular changes
associated with HPV infection
b. Progression to invasive cervical cancer much lower than with
HSIL
Pap smear cytology results are reported with a standardized
system (the Bethesda System for Reporting Cervical/Vaginal
Cytological Diagnoses).
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c. Management controversial; most experts advise referral for
colposcopy
There is no role in testing for HPV in patients with
LSIL, as nearly all test positive.
4. Atypical squamous cells (ASCs)
a. Cells appear abnormal but not severe enough to meet criteria
for LSIL or HSIL
b. ASC not a clear step in progression from mild precancerous
changes to cervical cancer
c. Can be caused by a variety of factors including non-HPV
infections and postmenopausal atrophy
d. Subclassified into atypical squamous cells, favor high-grade
dysplasia (ASC-H), and atypical squamous cells of uncertain
significance (ASC-US); women with ASC-H should be
referred for colposcopy
e. Management options for women with ASC-US
i. Send the same Pap smear specimen (if collected with a
liquid-based collection system) for HPV (reflex HPV)
testing. Only women who test positive for high-risk strains
need to be referred for colposcopy. Women with ASC-US
who are high-risk HPV-negative are at very low risk for
having HSIL and can have their Pap smear repeated in
12 months. This approach limits the anxiety and cost of
referring women unnecessarily for colposcopy and the
inconvenience of needing to follow up for repeat Pap
smears.
ii. Repeat serial Pap smears every 36 months, and refer for
colposcopy only if the patients Pap smear progresses in
severity. This is a good plan for women younger than
30 years in whom HPV infection is often transient and
high-grade dysplasia is extremely uncommon.
iii. Refer directly for colposcopy. For average-risk women,
this strategy has become less desirable now that HPV
testing is available. It is still a reasonable option when
HPV testing is not available or when reliable follow-up
for repeat Pap smears is not feasible.
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C. Glandular cell abnormalities and their management
1. All patients with glandular abnormalities seen on a Pap smear
need referral for further evaluation; the Pap smear is designed
to screen for squamous cell abnormalities.
2. The glandular cells can originate from either the endocervix or
endometrium, so adenocarcinoma of the cervix or endometrial
cancer needs to be considered.
3. Follow-up with serial Pap smears or reflex HPV testing alone is
never appropriate for glandular abnormalities.
4. Specific glandular abnormalities require the following.
a. Adenocarcinoma in situ (AIS): immediate referral to
gynecologist
b. Atypical glandular cells (AGCs): referred for colposcopy;
women older than 40 years should also be referred for
endometrial biopsy to rule out endometrial cancer
c. Endometrial cell abnormalities:
i. Atypical endometrial cells: referred for endometrial biopsy,
then colposcopy if the endometrial biopsy result abnormal
Immunosuppressed women, including those who are
HIV-positive, should always be referred for immediate
colposcopy, with any epithelial cell abnormality on a Pap
smear, including ASC-US.
Specimens from postmenopausal women should
not have endometrial cells. If endometrial cells are
present, whether atypical or not, endometrial biopsy is
indicated. The same holds true for any woman with
endometrial cells present that do not correspond to the
reported time of her last menstrual period and in women
with irregular or heavy bleeding, suggesting endometrial
abnormalities.
D. Other Pap smear results and their management
1. Unsatisfactory for evaluation: repeat Pap smear in 3 months
2. Satisfactory but limited:
a. Repeat Pap smear in 3 months if the patient is at high risk
for cervical cancer or in 1 year if average or low risk.
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C H A P T E R
b. Treat any obvious causes of inflammation, such as infection,
before repeating cytology.
c. If no endocervical cells are present, a good sample from the
transformation zone was not obtained.
3. Benign cellular changes, inflammation/cellular repair: routine
follow-up unless specimen unsatisfactory
4. Infection (chlamydia, herpes simplex virus, Trichomonas):
with the exception of Trichomonas, which can be accurately
diagnosed on a liquid-based Pap smear, infections should be
clinically evaluated and treated.
MENTOR TIPS DIGEST
HPV infections are believed to be the cause of most cervical
cancers.
Smoking cessation can reduce the risk of cervical cancer
two- to threefold.
Disadvantages of HPV testing include its low specificity, par-
ticularly in young women. As most HPV infections are transient
and never develop into cervical cancer, detection of every HPV
infection is of questionable value.
HPV vaccine targets four serotypes: 6, 11, 16, and 18. Types
16 and 18 cause the vast majority of cervical cancers; 6 and
11 are associated with genital warts.
The United States Preventive Services Task Force (USPSTF)
and the National Cancer Institute (NCI) advise screening at
least every 3 years, starting 3 years after a woman becomes
sexually active, or at age 21 years. In average-risk women,
annual screening does not provide a higher yield for detect-
ing high-grade dysplasia than screening every 3 years.
During the speculum examination, obtain the Pap smear
sample from the transformation zone (the junction between the
darker-colored columnar epithelium and the paler squamous
epithelium), as this is where most cervical cancers arise.
Pap smear cytology results are reported with a standardized
system (the Bethesda System for Reporting Cervical/Vaginal
Cytological Diagnoses).
There is no role in testing for HPV in patients with LSIL, as
nearly all test positive.
Immunosuppressed women, including those who are HIV-positive,
should always be referred for immediate colposcopy, with any
epithelial cell abnormality on a Pap smear, including ASC-US.
1389_Ch35_462-471 2/2/09 1:35 PM Page 469
P A R T
Resources
A human papillomavirus vaccine. The Medical Letter on Drugs and
Therapeutics 1241:6566, 2006.
Naucler P, Ryd W, Trnberg S, et al: Human papillomavirus and
Papanicolaou tests to screen for cervical cancer. New England
Screening for Cervical Cancer in U.S. Preventive Services Task
Force Guidelines. Available at http://www.ahrq.gov/clinic/uspstf/
uspscerv.htm
1. Which type of cervical cancer is most common?
a. Adenocarcinoma
c. Myosarcoma
d. T-cell lymphoma
2. What is the cause of most or all cases of cervical carcinoma?
a. Human immunodeficiency virus (HIV)
b. Human papillomavirus (HPV)
c. Chlamydia trachomatis
d. Cigarette smoking
Specimens from postmenopausal women should not have
endometrial cells. If endometrial cells are present, whether
atypical or not, endometrial biopsy is indicated. The same holds
true for any woman with endometrial cells present that do not
correspond to the reported time of her last menstrual period
and in women with irregular or heavy bleeding, suggesting
endometrial abnormalities.
1389_Ch35_462-471 2/2/09 1:35 PM Page 470
3. Which of the following statements accurately describes HPV and
cervical cancer?
a. All HPV strains are likely to lead to cervical cancer.
b. Only some HPV serotypes are associated with high risk for cervical
cancer.
c. HPV serotypes that cause genital warts also have the highest risk of
association with cervical cancer.
d. HPV requires a co-infection to develop into cervical cancer.
C H A P T E R
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472
CHAPTER
OSTEOPOROSIS
Jordana Friedman, MD, and James J. Foody, MD
36
I. Definitions
A. Osteoporosis is a disease characterized by a decrease in bone mass
and bone quality, which results in increased bone fragility and
susceptibility to fracture (1993 consensus definition).
B. Primary osteoporosis is due to aging and menopause.
C. Secondary osteoporosis is due to underlying diseases or conditions.
Fractures cause the morbidity and mortality associated
with osteoporosis.
Bone loss is a normal part of aging that menopause
accelerates.
II. Pathophysiology
A. Remodeling, replacing old bone with new bone tissue maintains
bone health.
1. Active phases of remodeling are resorption and formation.
a. Resorption: osteoclasts remove old bone tissue
b. Formation: osteoblasts produce new bone matrix
B. If resorption exceeds formation, there is net loss of bone mass.
1. Peak bone mass ages 2030 years
2. Age-related bone loss 0.5%1% per year
3. Menopausal estrogen deficiency accelerates bone loss 2%5%
annually for 5 years
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36 OSTEOPOROSIS 473
C H A P T E R
III. Epidemiology
A. U.S. prevalence is 10 million.
B. Thirty four million people have low bone mass (osteopenia)
with increased risk for osteoporosis.
C. The cost of osteoporosis was $17 billion in 2001.
D. Osteoporosis is responsible for more than 1.5 million fractures
per year.
E. Approximately half of 50-year-old women will sustain an
osteoporotic fracture during their remaining life.
F. Vertebral fractures are the most common type of osteoporotic
fracture.
G. Hip fractures are the second most common type of osteoporotic
fracture and have the most serious consequences.
1. 10%25% of people with a hip fracture will die within the
first year after the fracture.
a. Increased risk for infection (urine, wound, pneumonia)
b. Thromboembolic disease
2. 25% of hip fracture survivors require institutionalization in
long-term care facilities.
IV. Risk Factors
A. The more risk factors from Box 36.1 a patient has, the higher the
risk of osteoporosis.
V. History Key Components
A. Medical conditions
B. Medications
C. Smoking history
D. Alcohol history
E. Prior fractures
F. Loss of teeth (can indicate alveolar bone loss)
G. Loss of height
H. Activity level
I. Loss of mobility
J. Menstrual history (early menopause or amenorrhea)
K. Calcium and vitamin D intake
L. Family history
Secondary causes of osteoporosis are common in post-
menopausal women.
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VI. Physical Examination Findings Suggesting Osteoporosis
A. Loss of height
B. Kyphosis
C. Fewer than 20 teeth
D. Forward head position
BOX
Risk Factors for Osteoporosis
Female:male 4:1
White or Asian
Advancing age
First-degree relative with low
trauma fracture
Personal history of fracture after
age 50 years
Thin body habitus or low body weight
Loss of estrogen
Early menopause (younger than
age 45 years)
Previous amenorrhea
Medication
Glucocorticoids
Aromatase inhibitors
Heparin
Phenobarbital, phenytoin,
carbamazapine, lithium
Cyclosporine, tacrolimus,
methotrexate
Sustained progestins (e.g.,
Depo-Provera)
Excessive exogenous thyroid
replacement, excessive vitamin A
Antacids containing aluminum
Cigarette smoking
Excess alcohol intake
Sedentary lifestyle
Low calcium diet
Lack of vitamin D
Low dietary intake
Inadequate sunlight exposure
Endocrine diseases
Primary hyperparathyroidism
Hyperthyroidism
Cushing syndrome
Adrenal insufficiency
Testosterone deficiency in men
Hyperprolactinemia
Chronic kidney disease
Chronic liver disease
Malabsorption
Celiac disease
Gastric or small bowel
resection
Hematologic diseases
Multiple myeloma
Lymphoma
Leukemia
Pernicious anemia
Rheumatoid arthritis
Genetic diseases
Glycogen storage diseases
Marfan syndrome
Ehler-Danlos syndrome
Turner syndrome
Hemochromatosis
Organ transplant
Immobilization
36.1
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36 OSTEOPOROSIS 475
C H A P T E R
VII. Screening Guidelines
A. Many organizations publish screening guidelines; there is
currently no set of consensus guidelines, but differences are
minor.
B. United States Preventive Services Task Force, National Osteoporosis
Foundation, American Academy of Clinical Endocrinology, North
American Menopause Society, and International Society for Clinical
Densitometry all recommend the following.
Screen all women at age 65 years or older for osteoporo-
sis. In women with increased risk, screen before age 65.
Central DXA is the gold standard for evaluating bone
density and is the only testing modality that can
establish the diagnosis of osteoporosis.
VIII. Diagnosis
A. Fragility fracture (occurs with less force than would be expected
to cause a fracture [e.g., fall from a standing height]) can estab-
lish diagnosis of osteoporosis.
B. Decreased bone mineral density (BMD) measurement can diag-
nose osteoporosis.
1. Dual energy x-ray absorption (DXA) is standard for
measuring BMD.
2. Central DXA measures density of proximal femur, lumbar
spine, forearm, or total body.
3. T-score represents the standard deviation from mean bone
density of a healthy young adult population.
4. Relative risk of fracture increases 1.52.5 for each T-score
decrease in bone density.
5. Z-score is the comparison of the patients BMD with that of
an age-matched population. Z-score of -2.0 or lower is below
the expected range for age.
6. The World Health Organization established definitions based
on central DXA results in postmenopausal white women.
a. T-score -2.5 is osteoporosis
b. T-score between -1.0 and -2.5 is osteopenia
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7. Other modalities for measuring BMD that may be useful for
screening but not diagnosis include the following.
a. Peripheral DXA of wrist, heel or finger
b. Quantitative ultrasound of calcaneus, tibia, or patella
c. Quantitative computed tomography (CT) scan
C. Bone biomarkers have the following features.
1. Biochemical markers of remodeling are markers of formation
and resorption
2. High levels of markers indicate high remodeling rate.
a. High rate of remodeling usually indicates higher rate of bone
loss as resorption exceeds formation with advancing age.
b. Biomarkers are independent predictors for fracture.
3. Changes in biomarkers typically precede changes in BMD.
4. Biomarkers cannot diagnose osteoporosis.
5. Potential uses of biomarkers are the following.
a. Assessing rate of remodeling prior to starting therapy
b. Selecting therapy
c. Monitoring response to therapy
IX. Evaluation for Secondary Osteoporosis
A. Underlying secondary causes of osteoporosis occur in 20%30%
of postmenopausal women.
B. Consider the following secondary causes.
1. Z-score <-2.0
2. Premenopausal women with osteoporosis
3. Men with osteoporosis
4. Unexplained fragility fracture (e.g., fracture with normal BMD)
5. Less than expected response to therapy
6. High suspicion for secondary cause based on history and physical
T-score compares BMD with that of healthy young
adults. Z-score compares BMD with age- and sex-
matched controls. Low Z-score raises alert to possibility
of secondary osteoporosis.
C. Laboratory testing consists of the following.
1. Routine laboratory testing
a. Complete blood count (CBC)
b. Chemistry panel (renal function, liver function, alkaline
phosphatase, calcium, phosphorous, albumin)
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36 OSTEOPOROSIS 477
C H A P T E R
c. Thyroid-stimulating hormone (TSH)
d. Parathyroid hormone (PTH)
e. 24-hour urinary calcium and creatinine
f. 25-hydroxy vitamin D
g. Testosterone level in males
2. Specialized testing
a. Urine-free cortisol or overnight dexamethasone suppression
test (for Cushing syndrome)
b. Serum and urinary electrophoresis
c. Sedimentation rate
d. Celiac antibodies and small-bowel biopsy if needed (evaluate
for celiac disease)
e. Bone biopsy when needed to diagnose osteomalacia or renal
osteodystrophy
X. Management
A. Nonpharmacologic treatment
1. Calcium
a. Best absorbed in doses of 500 mg or less
b. Adequate calcium intake can slow rate of bone loss
c. Recommended daily dose of calcium
i. 1000 mg/day for premenopausal women and post-
menopausal women on hormone replacement therapy
ii. 12001500 mg/day for postmenopausal women not on
hormone replacement therapy
2. Vitamin D 800 IU/day
3. Weight-bearing (e.g., walking) and resistance (e.g., weight-
lifting) exercises
4. Healthy lifestyle; avoid smoking and excess alcohol intake
5. Monitoring home environment to decrease risk of falls
Lifestyle factors, including supplemental calcium and
vitamin D, exercise, tobacco cessation, and limiting
alcohol, are both preventive for everyone and a component
of treatment for persons with osteoporosis.
B. Pharmacologic treatment
1. Antiresorptives decrease rate of bone remodeling
a. Bisphosphonates
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i. Decrease osteoporotic fractures 39%56%
ii. Gastrointestinal (GI) side effects most common (e.g.,
abdominal pain, nausea/vomiting (N/V), acid reflux,
dyspepsia, dysphagia, esophageal or gastric ulcer)
iii. Osteonecrosis of jaw (ONJ) rare side effect that can be
associated with bisphosphonates
(1) ONJ is the death of bone tissue in the jaw and typically
presents as infection and necrosis in the mandible.
(2) ONJ is less common with oral than IV bisphosphonates.
(3) The estimated incidence is 7 cases per year for every
million people taking oral bisphosphonates.
(4) ONJ is seen after dental surgery or local infection.
(5) Risk factors for ONJ include use of IV bisphosphonate,
diagnosis of cancer (majority of patients with ONJ
had either multiple myeloma or breast cancer), and
dental surgery.
b. Selective estrogen receptor modulators (SERMs)
i. Act as estrogen agonist or antagonist, depending on site
(estrogen agonist at bone)
ii. 30%50% reduction in vertebral fractures; no reduction
in nonvertebral fractures.
Oral bisphosphonates and SERMs are the
mainstay of osteoporosis treatment.
c. Nasal calcitonin
i. 35% reduction in vertebral fracture; no reduction in
nonvertebral fracture
ii. May relieve fracture pain
2. Anabolic agent: teriparatide
a. Recombinant parathyroid hormone
b. Increases rate of bone formation
i. Stimulates osteoblast function
ii. Increases GI calcium absorption
iii. Increases renal tubular reabsorption of calcium
c. 65% decrease in new vertebral fracture, 53% decrease in risk
of nonvertebral fragility fracture
d. Daily subcutaneous injection; limited to 2 years because of
oncogenic concern
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36 OSTEOPOROSIS 479
C H A P T E R
Teriparatide is the only osteoporosis treatment that
stimulates bone formation.
XI. Monitoring
A. Frequency of screening with DXA depends on the measurement
site, type of therapy, patient factors, and precision of the testing
center.
B. Gains in spine BMD with treatment usually occur within 1 year.
C. General recommendations for follow-up DXA comprise these
guidelines.
1. Recheck 1 year after starting or changing therapy; extend
interval if BMD is stable or increasing.
2. Monitor more often in patients on glucocorticoids (bone loss
seen as soon as 6 months).
D. Appropriate response to therapy is stable or increasing BMD.
E. Significant decrease in BMD while on therapy merits investigation
for secondary causes of osteoporosis.
MENTOR TIPS DIGEST
Fractures cause the morbidity and mortality associated with
osteoporosis.
Bone loss is a normal part of aging that menopause accelerates.
Secondary causes of osteoporosis are common in post-
menopausal women.
Screen all women at age 65 years or older for osteoporosis.
In women with increased risk, screen before age 65.
Central DXA is the gold standard for evaluating bone density
and is the only testing modality that can establish the diagnosis
of osteoporosis.
T-score compares BMD with that of healthy young adults.
Z-score compares BMD with age- and sex-matched controls.
Low Z-score raises alert to possibility of secondary osteoporosis.
Lifestyle factors, including supplemental calcium and vitamin D,
exercise, tobacco cessation, and limiting alcohol, are both
preventive for everyone and a component of treatment for
persons with osteoporosis.
Oral bisphosphonates and SERMs are the mainstay of
osteoporosis treatment.
Teriparatide is the only osteoporosis treatment that stimulates
bone formation.
1389_Ch36_472-481 2/2/09 1:35 PM Page 479
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Resources
Cummings S. A 55-year-old woman with osteopenia. Journal of the
American Medical Association 296:26012610, 2006.
Renowned expert on osteoporosis discusses osteoporosis diagnosis,
risk factors, and treatment in the framework of a case study; highlights
the importance of individualizing treatment plans and provides a
patient perspective on the disease.
Gass M, Dawson-Hughes B. Preventing osteoporosis-related fractures:
An overview. American Journal of Medicine 119:3S11S, 2006.
This article provides a concise overview of the pathophysiology, epidemi-
ology, risk factors, and diagnosis of osteoporosis, followed by an in-depth
discussion of osteoporosis treatment. The U.S. Surgeon General pyrami-
dal approach to treatment of osteoporosis is used as the framework for
approaching osteoporosis treatment. Level one is lifestyle changes; level
two involves treating secondary causes of osteoporosis; level three is
pharmacotherapy. The article reviews the role of each intervention in
maintenance of bone health and fracture risk reduction.
Goroll H, Mulley A, eds. Prevention and management of osteoporosis.
Primary care medicine, 5th ed. Lippincott, Williams & Wilkins, 2007.
Comprehensive textbook chapter that reviews bone physiology and
pathophysiology as well as the risk factors, clinical presentation, diag-
nosis, prevention, and treatment of osteoporosis; briefly addresses the
management of osteoporosis-related vertebral and hip fracture.
Stein E, Shane E. Secondary osteoporosis. Endocrinology and Metabolism
Clinics 32:115134, 2003.
Excellent, detailed discussion of secondary causes of osteoporosis
including inherited disorders, hypogonadal states, endocrine disorders,
GI diseases, hematologic disorders, rheumatologic conditions, medica-
tions, and organ transplantation. The article ends with overview of the
diagnostic evaluation for secondary causes.
1. Which of the following is characteristic of osteoporosis?
a. Most cases of osteoporosis in the United States result as a complication
of a separate disease.
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36 OSTEOPOROSIS 481
C H A P T E R
b. Most cases of osteoporosis in the United States result from vitamin D
deficiency.
c. Most cases of osteoporosis in the United States result from calcium
deficiency.
d. Most cases of osteoporosis in the United States result from
accelerated age-related changes.
2. How does osteoporosis cause increased mortality?
a. Fractures
b. High output heart failure
c. Chronic calcium depletion
d. Nephrocalcinosis
3. Which statement describes osteoporosis?
a. Bone remodeling stops, leading to increased bone fragility.
b. Osteoclast activity decreases.
c. Aging causes osteoclasts to be relatively more active than osteoblasts.
d. Formation of new bone matrix exceeds resorption of bone.
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482
CHAPTER
INTIMATE PARTNER
VIOLENCE
Lenore F. Soglin, MD
37
I. Overview
A. Intimate partner violence (IPV) is an endemic problem. Medical
providers are in a unique position to help identify and assist IPV
victims.
B. This chapter helps providers identify victims of IPV, learn to
screen for IPV, and teach intervention strategies.
II. Definition of IPV
IPV is defined as a pattern of coercive behaviors that are
designed to dominate and control an intimate partner
through fear and intimidation.
A. Perpetrators use a variety of tactics to control their partners. These
tactics may include:
1. Threats and intimidation
2. Isolation
3. Physical abuse
4. Forced sex
5. Economic deprivation
III. Demographics
A. IPV occurs in both heterosexual and homosexual relationships, but
90% of the victims are women and perpetrators are men. For discus-
sion, IPV victims are called her or she, and the perpetrators are
called he or him. (The author acknowledges that women are not
the only victims nor are men the only perpetrators.)
B. IPV is the leading cause of injuries to women 1544 years old.
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37 INTIMATE PARTNER VIOLENCE 483
C H A P T E R
C. In the emergency department, battering may account for
22%35% of women seeking care for any reason. In the primary
care setting, 10%22% of women report physical assault by a
partner in the last year, and 30%40% have suffered abuse in their
adult lifetime.
D. IPV occurs at all ages and in all socioeconomic strata of society.
IV. Description of Relationship Pattern in IPV
The abusive relationship often involves a combination of
physical, sexual, and psychological abuse.
A. The abuse is usually chronic and intensifies in a cyclic pattern.
1. During the initial phase, the abuser exerts increasing control
over his partner by using coercion, intimidation, and threats.
2. The abuser often isolates the victim from family and friends
and may withhold money to exert his power.
3. The victim often has low self-esteem at the onset of the relation-
ship, and her partner further undermines her self-confidence
with his intimidating behavior.
4. This initial phase may be followed by an episode of physical
battering.
5. This is followed by the honeymoon phase, during which
the abuser shows great remorse and promises to change his
behavior.
6. The cycle may begin again. Over time, the violent episodes
may become more frequent and more severe.
V. Medical Presentation of IPV
A. Vague medical complaints, for which physical cause is hard to
find, are common: e.g., dizziness, shortness of breath, headache
B. Specific medical complaints common to IPV
1. Chronic abdominal pain/irritable bowel syndrome (IBS)
2. Pelvic pain/dyspareunia
3. Acute physical injuries
4. Bilateral injuries in different stages of healing
5. Multiple sites of injuries
6. Contusions on ulnar surfaces of arms
7. Injuries to the breasts and genitalia
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P A R T
C. Common psychiatric presentations
1. Depression
2. Anxiety
3. Panic attacks
4. Suicidal ideation or attempts
5. Substance abuse
D. Behavioral clues during office visit
1. Patient may be late for or miss appointment
2. Abuser may accompany patient and answer questions for her
or refuse to leave examination room
E. Despite association between some specific medical conditions
and a higher rate of IPV, any woman presenting to the medical
setting may be struggling with IPV
VI. Barriers to IPV Identification
A. Despite high prevalence rate of IPV, only 5%7% of women have
been queried about IPV by their physician; lack of disclosure
compounded by physician discomfort and patients reluctance to
discuss; fewer than 25% of victims of IPV have brought up the
issue with health-care providers
B. Barriers to physician inquiry
1. Fear of offending patient
2. Sense of powerlessness to help patient
3. Lack of physician education
4. Lack of time
C. Barriers to patient disclosure
1. Fear of jeopardizing safety
2. Shame and humiliation
3. Feeling protective of partner
4. Partners promise to change
VII. Screening for IPV
A. Screening for IPV important part of social history of all female
patients
1. Privacy essential; others asked to leave, including partners,
family translators
2. Screening questions should be asked calmly after establishing
initial contact with patient
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C H A P T E R
B. Approaching patient about IPV
1. Frame the question by making a statement that makes your
questions seem part of your routine.
Because violence is common in womens lives, I now
routinely ask every woman in my practice about IPV.
Are you in a relationship in which you have been
physically hurt or threatened by your partner?
Have you ever been hit, kicked, slapped, pushed,
or shoved by your partner?
2. The framing statement is followed by simple questions about IPV.
3. Avoid words such as abuse or violence in your direct
question because they mean something different to each person.
VIII. Assessing Safety
A. If the patients response to the screening questions indicates
abuse is present in her relationship, the provider or a social
worker must assess the level of violence and the safety of the
home by determining the following:
1. Type and frequency of abuse
2. Presence of weapons in the home
3. Safety of the children
4. Extent of patients isolation
B. Determine if plans are in place for escaping from the home in an
emergency.
C. Documentation in the medical record should be in the patients
own words.
D. Physical findings of injuries should be well described or de-
picted in sketches or photographs.
IX. Intervention Strategies
A. Treat injuries.
B. Physicians can play an invaluable role in helping patients change
their lives.
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P A R T
1. Validate the patients feelings by stating that IPV is wrong and
that no one deserves such treatment.
2. Communicate empathy and concern; this lets patient know that
her physician is a resource and confidante.
3. Provide referrals to social workers, shelters, and legal services.
A safety plan should be formulated for each patient,
usually by a social worker: home safety, abuse protec-
tion orders, safety on the job, and emergency escape plans.
X. Legal Concerns
A. Most states provide women with the right to confidentiality and do
not require the reporting of partner abuse unless children are in
danger or a firearm is involved.
B. Providers need to learn the legal requirements in their areas
regarding reporting IPV.
XI. Summary
A. IPV is a common but under-recognized problem.
B. Routine screening and enhanced awareness among physicians can
improve identification of victims of IPV.
C. Medical practitioners can help IPV victims transition to safer lives.
MENTOR TIPS DIGEST
IPV is defined as a pattern of coercive behaviors that are
designed to dominate and control an intimate partner through
fear and intimidation.
The abusive relationship often involves a combination of physical,
sexual, and psychological abuse.
Say, Because violence is common in womens lives, I now
routinely ask every woman in my practice about IPV.
Ask, Are you in a relationship in which you have been physically
hurt or threatened by your partner?
Ask, Have you ever been hit, kicked, slapped, pushed, or
shoved by your partner?
A safety plan should be formulated for each patient, usually by
a social worker: home safety, abuse protection orders, safety
on the job, and emergency escape plans.
1389_Ch37_482-488 2/2/09 1:34 PM Page 486
C H A P T E R
Resources
Eisenstat SA, Bancroft L. Intimate partner violence. New England Journal
of Medicine 341:886892, 1999.
Good review article on IPV.
McCauley J, Kern DE, et al. Relation of low severity violence to womens
health. Journal of General Internal Medicine 13:687691, 1998.
Clearly shows relationship between violence in the home and multiple
medical complaints.
Warshaw C, Ganley AL. Improving the health care response to intimate
partner violence: A resource manual for health care providers. Produced
by The Family Violence Prevention Fund, San Francisco, CA 1996.
A practical guide for screening for IPV and developing a comprehensive
response to the problem.
For self-test questions, see the testbank CD.
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489
ANSWERS TO SELF-TEST
QUESTIONS
APPENDI X
A
Part I: Overview of Primary Care
Chapter 1: Office Management and the Principles of
Diagnosis and Management of Ambulatory Patients
1. job change
job loss
marital difficulties
illness of a family member
being a caregiver
2. Hi, my name is John Doe. I am a medical student working with
Dr. X. Dr X asked me to get started and he/she will be in shortly.
3. Outpatient care is often focused on prevention and on longitudinal care
of chronic illnesses, whereas inpatient care tends to focus on acute
exacerbations.
Outpatient care very often involves undifferentiated symptoms, which
are often treated presumptively, whereas inpatient care more often
involves a disease process that is already differentiated, and the focus
is on treating that process.
Outpatient care tends to involve serial testing, whereas inpatient care
often involves parallel testing.
Chapter 2: Communicating With Patients
1. Set the stage
Elicit information
Give information
Understand the patients perspective (and show the patient that you
understand)
End the encounter
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2. Leading question
3. Brain tumor/cancer
Chapter 4: Prevention and Screening
1. d. Rectal cancer
Response: Successful screening requires both effective treatment and to
screen before a disease becomes untreatable. Lung, ovarian, and pancreatic
cancer have not demonstrated either characteristic. Screening for rectal
cancer enables detection before it becomes symptomatic. Surgical treat-
ment of rectal cancer is highly successful.
2. b. Facilitate smoking cessation.
Response: Overwhelming evidence demonstrates cigarette smoking is the
most important preventable cause of death. Lack of exercise is associated
with increased mortality, but proof of benefit from encouraging more
exercise is lacking. Mammography decreases mortality of breast cancer,
and flexible sigmoidoscopy decreases mortality of colorectal cancer, but
the benefit of smoking cessation exceeds them.
3. b. Colon.
Response: Breast cancer is the most common cause of cancer death in
women. Colon cancer is almost half as common, but efficacy of colorectal
cancer screening is superior to that of mammography for breast cancer.
Screening for cervical cancer is very effective but has a lifetime incidence
of 2%, which is one-fifth the incidence of breast cancer. No effective
screening exists for ovarian cancer.
1. c. Discontinue warfarin 35 days before procedure; when INR <2 start
heparin infusion until 46 hours before the procedure. Resume
heparin infusion several hours after the procedure, and resume
warfarin the night of procedure.
Response: Bridge anticoagulation is necessary when there is high risk of
thrombosis and bleeding from the surgical procedure would be difficult to
control. Atrial fibrillation and history of stroke are associated with high
risk for thrombosis. Visceral organ biopsy can cause bleeding without a
means of direct control.
2. d. Take measures to reduce perioperative risk.
Response: The preoperative consultant evaluates potential risks of surgery
and makes recommendations to attenuate risk. The concept of clearing
a patient for surgery is archaic because it ignores a comprehensive risk
490 A ANSWERS TO SELF-TEST QUESTIONS
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evaluation and does not include risk reduction. It is inappropriate to ad-
vise the anesthesiologist on the technique of anesthesia; it is better to ad-
vise about risks that warn of potential complications.
3. a. No testing.
Response: There is no general recommendation for any testing in general
for low-risk surgery.
Part II: Diagnosis and Management of Common
Outpatient Symptoms
Chapter 6: Headache
1. b. Primary headache describes neurogenic headache.
Response: Primary headache is the result of neurologic malfunction.
Secondary headache has a definable anatomical origin.
2. b. Almost all people will experience headache.
Response: At least 90% of people experience headache. Most never seek
medical attention. Although the female:male prevalence of migraine
headache is 4:1, there is no gender difference for headache generally.
Prevention is important for persons with frequent episodic headache.
3. c. Gradual onset of vision distortion that becomes progressively greater
over 20 minutes.
Response: Aura is a spreading cortical depression preceding migraine
headache that most often affects vision. Triptans have no effect on aura.
Chapter 7: Common Sleep Disorders
1. b. 15%20%
Response: Chronic insomnia is not rare. More than twice as many people
experience insomnia in a year, but most episodes are limited. Chronic
insomnia lasts for 6 weeks or longer.
2. d. You can reassure her that her insomnia is very likely to remit
spontaneously.
Response: Stressful life events may precipitate insomnia. Most insomnia
remits within days or a couple of weeks. Reassurance is appropriate.
Sometimes prescribing a short course of hypnotic sleeping medicine helps
prevent habituation to sleeplessness. Benzodiazepine drugs are useful to
decrease anxiety symptoms, but anxiety likely requires a higher dose to
induce sleep than a person could tolerate all day. Polysomnogram is not indi-
cated for acute insomnia; it is the diagnostic tool for obstructive sleep apnea
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and periodic leg movement in sleep. Alcohol is a very inefficient sleep aide
because it disrupts normal sleep rhythm and can become habituating quickly.
3. c. Fluoxetine.
Response: SSRI antidepressants can cause initial insomnia. Clopidogrel
is an antiplatelet agent; atorvastatin is a lipid-lowering agent; and lisino-
pril is an ACE inhibitor. None of these has an association with insomnia.
Chapter 9: Chest Pain
1. b. Retrosternal pressure chest pain lasting for 215 minutes.
Response: There are many causes of retrosternal chest pain. Angina pectoris
is chest pain resulting from ischemic coronary disease. If ischemic pain lasts
much longer than 15 minutes, there will likely be some myocardial necrosis
or infarction. Pain lasting seconds is more likely to be from a noncardiac
cause. Although the usual description of typical angina is pressure pain, the
type of pain is neither sensitive nor specific enough to be very helpful.
2. c. Retrosternal pressure chest pain lasting for hours to days, exacer-
bated by supine posture.
Response: The exacerbation of the pain by lying down suggests pericardi-
tis because the source of the pain is friction of the pericardium against the
epicardium. The long duration is inconsistent with other alternative diag-
noses. Pericardial pain is seldom fleeting. Angina usually lasts minutes.
Myocardial infarction can cause a pericarditis.
3. c. Obtain an ECG.
Response: He has two of the criteria for angina: squeezing retrosternal
pain relieved by nitroglycerin. This description is also typical for esophageal
reflux with spasm. Ischemic pain lasting more than an hour likely would
cause infarction, so EEG is critical. Depending on clinical acumen and judg-
ment, a physician might consider a normal EEG to be the most likely cause.
If the description for a man this age meets one angina criterion, probability
for ischemia is 6%; two criteria yield a 46% probability. Even a negative
EEG might not be adequate reassurance to discharge the patient, but the EEG
is the first test.
Chapter 10: Sinusitis, Bronchitis, and Pharyngitis
1. a. Hand washing.
Response: The common cold describes a syndrome resulting from one
of a very large number of viruses. Studies demonstrate hand washing
decreases person-to-person transmission. There is no evidence that a
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paper face mask prevents transmission of respiratory viruses. Neither
decongestants nor antibiotics have any effect.
2. c. Reassure and explain that sinus infections are not contagious.
Response: Sinusitis is a bacterial complication of sinus osteomeatal
occlusion leading to effusion that is susceptible to infection with colo-
nized nasopharyngeal bacteria. Sinusitis is not contagious. Preventive
antibiotic therapy is ineffective.
3. b. Streptococcus pneumoniae.
Response: Chronic, not acute sinusitis, commonly involves Staphylococcus
aureus and gram-negative rods. Legionella pneumoniae infects any part of
the respiratory tract but much less commonly than S. pneumoniae.
1. c. More than three loose bowel movements in 24 hours.
Response: Flatus does not define diarrhea. Diarrhea must be loose or
watery feces. Acute diarrhea lasts no more than 2 weeks.
2. b. Presence of white blood cells in feces.
Response: White blood cells in loose feces point to inflammation present
in the gut. Malabsorption causes watery feces without white blood cells.
3. a. Clostridium difficile toxin.
Response: C. difficile typically does not invade colonic mucosa. It is
often found in small numbers as one of the anaerobic flora of the colon.
Antibiotic therapy can alter the normal flora, permitting C. difficile over-
growth. C. difficile secretes a toxin that causes watery diarrhea.
1. d. Septic arthritis.
Response: Fever accompanying a joint or skeletal complaint suggests the
possibility of infection. If there is joint effusion, it requires arthrocentesis
and evaluation for infection. If the joint is normal, plain radiography or
MRI scanning can identify osteomyelitis. Passive joint pain is a late find-
ing of osteoarthritis. Rheumatoid arthritis rarely starts in the knee and has
a strong predilection for women. Gout is possible, although it is typically
extremely painful and more likely to occur initially in the first metatarsal-
phalangeal joint.
2. a. Malignancy.
Response: Unexplained weight loss in a middle-aged man raises the
possibility of malignancy. Metastatic cancer, multiple myeloma, and
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osteosarcoma are the most common to invade the shaft of a long bone.
The physical examination is not consistent with osteoarthritis and gout,
which affect joints, or tenosynovitis, which is painful on active movement
and palpation of a tendon.
3. d. No test.
Response: Low back pain is a common primary care complaint. As many
as four out of five adults have low back pain at some time. The specific
cause of pain can be difficult to identify unless there is a neurologic
deficit; however, precise anatomical diagnosis is often not useful because
a majority of cases of low back pain resolves without specific interven-
tion. MRI scanning is the best test for herniated disc disease if there is a
neurologic deficit that may require surgery. Plain radiographs are useful if
cancer or vertebral fracture is suspected as the cause. EMG is useful in
distinguishing upper from lower motor nerve involvement and defining
the anatomical distribution of nerve injury.
Chapter 14: Dermatology in Primary Care
1. c. Basal cell carcinoma.
Response: Basal cell carcinoma is the most common skin cancer. It is also
the least aggressive. It seldom metastasizes and locally invades slowly.
2. d. Melanoma.
Response: Although melanoma has a much lower incidence than basal
cell or squamous cancer, it tends to metastasize early. Effective treatment
is largely limited to surgical cure. Depth of invasion is the most important
prognostic variable.
3. b. Acne vulgaris.
Response: Acne is almost universal at adolescence.
Chapter 15: Fatigue
1. c. Impaired cognitive performance.
Response: It is important to distinguish between fatigue and other subjec-
tive complaints such as weakness, hypersomnolence, dyspnea, or apathy.
The examining provider should pay attention to impaired cognitive
performance, which is most consistent with fatigue. Other supporting
evidence is subjective and is part of the history.
2. b. 5%.
Response: As many as half of primary care patients report fatigue when
questioned; 5% of primary care visits have fatigue as the chief complaint.
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3. b. Unremitting weariness.
Response: It is important to distinguish hypersomnolence, apathy, and
dyspnea from weariness.
Chapter 16: Erectile Dysfunction
1. b. Prevalence increases with age.
Response: Although prevalence of ED increases with age, it is not normal
or inevitable.
2. b. Depression.
Response: Depression is a common cause of ED. Men may not complain
of depression as the initial complaint, so screening for depression is
important. Colorectal cancer does not cause ED. Hypogonadism causes
ED and loss of libido, but it is not common. Occult Chlamydia infection
can cause infertility.
3. c. Peripheral vascular disease.
Response: Peripheral vascular disease is the prime arteriogenic cause
of ED. Colorectal cancer and osteoarthritis are common but do not
cause ED. Hypogonadism causes ED and loss of libido, but it is not
common.
Chapter 17: Anxiety and Depression
1. c. 1 in 5.
Response: Depression and anxiety affect 20%35% of patients in primary
care practice.
2. c. Most patients with mental illnesses are not recognized by primary
care physicians.
Response: Primary care physicians recognize only a fraction of their
patients with mental illness. Between one-fifth and one-third of primary
care patients have mental illness. The most frequent are depression and
anxiety. Most mental illness is unrecognized and not referred to psychia-
trists. Much mental illness is amenable to treatment prescribed by primary
care physicians.
3. d. Major depression.
Response: Major depression and anxiety are the most common mental
illnesses seen in primary care. Obsessive-compulsive disorder and bipolar
disorder are important not because of the prevalence but because of the
need for psychiatric specialty consultation.
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Part III: Diagnosis and Management of Common
Chronic Illnesses
Chapter 19: Congestive Heart Failure
1. a. Lethal arrhythmia.
Response: Approximately half the people who die of heart failure die as a
result of sudden cardiac death. Heart failure has increased risk of embolic
stroke. Acute pump failure can cause pulmonary edema. Chronic kidney
disease can complicate heart failure. All increase mortality but much less
than ventricular fibrillation.
2. d. Left bundle branch block.
Response: Disorganized myocardial tissue and fibrosis can disrupt the
ventricular conduction system leading to bundle branch block.
3. d. Order transthoracic echocardiogram.
Response: The entire clinical picture fits heart failure. Because her
clinical deterioration is gradual, symptomatic treatment before confirmed
diagnosis is inappropriate for three reasons: (1) although the clinical
presentation is classic for heart failure, it is not pathognomonic; (2) it is
important to distinguish between systolic and diastolic dysfunction before
treating if possible (some treatments that improve systolic dysfunction can
exacerbate symptoms from diastolic dysfunction); and (3) it is always
important to identify the cause of heart failure. The approaches to ischemic
coronary disease, valvular disease, and cardiomyopathy are very different.
Chapter 20: Hypertension
1. b. 20%30%.
Response: About 25% of adults in the United States have hypertension.
Prevalence increases with age.
2. b. Pre-hypertension.
Response: Normal blood pressure is <120/<80. Pre-hypertension is
120139/8089. Stage 1 hypertension is 140159/90109. Stage 2 hyper-
tension is <160/<100. The relative higher of systolic or diastolic pressures
define the staging.
3. c. Stage 1 hypertension.
Response: Normal blood pressure is <120/<80. Pre-hypertension is
120139/8089. Stage 1 hypertension is 140159/90109. Stage 2 hyper-
tension is >160/>100. The relative higher of systolic or diastolic pressures
define the staging.
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Chapter 21: Asthma
1. a. 510/100,000.
Response: Annual mortality in the United States is about 5.7/100,000
persons with asthma.
2. d. Over 30,000,000.
Response: Although it can be difficult to compare reported prevalence
rates reliably (because of differing definitions), GINAs data put U.S.
prevalence of asthma at 10.9%. That corresponds to over 30,000,000
Americans.
3. c. Inflammation of airways.
Response: Reversible airway obstruction describes the primary diagnostic
criterion of asthma. However, it is important to recognize that asthma is an
inflammatory disorder of the airway. Reversible airway obstruction is one
of the consequences of this inflammation. The reason this distinction is
crucial is that treatment of bronchial constriction without addressing
inflammation leads to worse outcomes.
Chapter 22: Chronic Obstructive Pulmonary Disease
1. b. Airways obstruction that is not fully reversible with albuterol.
Response: Reversible airways obstruction is characteristic of asthma.
COPD is an obstructive airway disease, not a restrictive lung disease.
Alveolar infiltration with inflammatory cells is characteristic of pneumonia.
2. c. Productive cough for at least 3 months in 2 consecutive years.
Response: To make the diagnosis of COPD, it is necessary to fulfill
requirements of both duration of productive cough and persistence in at
least 2 consecutive years.
3. d. Among cigarette smokers, 15%25% will develop COPD
(85%90% of COPD patients had been smokers).
Response: Although pipe smoking and COPD are associated, cigarette
smoking is orders of magnitude more prevalent. About 15%25% of
long-term cigarette smokers develop COPD, but among persons with
COPD 90% had been or are currently cigarette smokers.
1. b. Progressive beta-cell insulin secretory failure associated with insulin
resistance.
Response: More than 90% of Americans with diabetes have type 2
diabetes. Type 2 diabetes begins with insulin resistance, typically antedating
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diagnosis by years. Insulin hypersecretion compensates to keep
glucose normal until beta cells are unable to keep up with insulin
demands. Type 1 diabetes occurs when autoimmune destruction of beta
cells causes insulinopenia. A similar course follows pancreatectomy or
pancreatic necrosis. Glucocorticoid, whether exogenous or the result of
Cushing syndrome, interferes with glucose metabolism in a complicated
fashion.
2. a. Non-fasting plasma glucose 215 mg/dL.
Response: Random plasma glucose 200 mg/dL combined with symp-
toms establishes the diagnosis of diabetes. In the absence of symptoms,
fasting or 2-hour postprandial plasma glucose must exceed 200 mg/dL
on at least 2 separate days. Hemoglobin A
1c
is not part of the diagnostic
criteria for diabetes but is demonstrably useful in monitoring treatment.
3. d. Initiate calorie-restricted diet and vigorous exercise at least three
times weekly.
Response: Calorie-restricted diet to cause 5%10% weight loss and
3045 minutes of moderately vigorous exercise three times weekly is
initial therapy for type 2 diabetes. Other types of diabetes or severe hyper-
glycemia may require initial insulin. Use of oral antidiabetic drugs should
wait 3 months to allow assessment of therapeutic lifestyle changes.
Chapter 24: Hyperlipidemia
1. a. Subcutaneous cholesterol-filled nodules.
Response: Subcutaneous cholesterol-filled nodules, termed xanthalesma,
occur in hyperlipidemia. Retinal hemorrhage can occur in hypertension
and diabetes mellitus. Periarticular swelling of the distal phalangeal joints
of hands is typical for osteoarthritis. S3 in adults suggests decreased
myocardial compliance.
2. c. White-gray deposit around periphery of cornea.
Response: Arcus senilis is a white deposit in the periphery of corneal
tissue. It is a normal part of the aging process, but premature arcus sug-
gests hyperlipidemia. Cataracts are not the result of lipid abnormality.
Keyser-Fleisher rings are a manifestation of Wilson disease. Blue sclerae
are a manifestation of osteogenesis imperfecta. Aortic dilation and aortic
valve regurgitation occur in osteogenesis imperfecta but not in lipid disorder.
3. d. TSH.
Response: Hypothyroidism, even mild disease, can cause severe hyper-
lipidemia. Idiopathic hypothyroidism is common among women over
age 60 years. Diagnosis is critically important. It is tempting to treat with
a statin, but lipids may normalize once euthyroid state returns. Apo-B
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metabolism is abnormal in hyperlipidemia, but measurement is not useful.
Except in rare circumstances, calculate LDL rather than measure directly.
Direct LDL measurement is an expensive and complicated test. Cushings
disease is rare.
Chapter 25: Obesity
1. c. Polycystic ovarian syndrome.
Response: Polycystic ovarian syndrome is one of several chronic disorders
associated with insulin resistance. Adiposity, particular visceral adiposity, is
the most important factor in insulin resistance. Type 1 diabetes mellitus and
diabetes insipidus are unrelated to weight. Restrictive lung disease in
obesity is the result of extrinsic chest and diaphragmatic forces, not lung
parenchyma changes seen in pulmonary fibrosis.
2. d. Myocardial infarction.
Response: Obesity, particularly visceral adiposity, contributes to athero-
sclerosis. Hypertrophic cardiomyopathy is an inherited heart disease. There
is no connection between obesity and valvular heart disease.
3. a. Obesity.
Response: Along with increasing prevalence of obesity, there is an explo-
sion of nonalcoholic fatty liver disease (NAFLD). Considered benign in
the past, NAFLD is a frequent cause of liver cirrhosis, often presenting as
variceal hemorrhage. Transaminases are often normal in cirrhosis because
they represent hepatocellular injury rather than scarring. It is important to
consider alcohol or high-dose acetaminophen use despite denial, but not
to assume, especially when there is a likely alternative explanation. The
liver is not very vulnerable to atherosclerotic disease.
Part IV: Diagnosis and Management
of Age-Related Conditions
1. c. You need to observe the childs activity and socialization development.
Response: Urgent care visits are not substitutes for well-child visits.
It is important to observe childrens social development and their activ-
ity directly. Reliance on parents observations is not adequate. Many
families face financial barriers to obtaining care for their children. It is
important to recognize these obstacles and provide assistance. Although
anyone can look up immunization recommendations on the Internet, the
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reason for well-child visits is not limited to immunizations. The sched-
ule for immunizations is a convenience for organizing well-child visits.
2. a. Suffocation.
Response: Suffocation is a leading cause of death in infants. Intussuscep-
tion, volvulus, and retinoblastoma occur in this age group, but they are
uncommon.
3. c. The family lives in a 100-year-old home undergoing extensive
renovation.
Response: Lead accumulates in the body. It can cause anemia, mental
retardation, and other illnesses. Lead-containing paint was sold in the
United States until 1978. Although 30 years have passed, lead-containing
paint is still a risk because existing paint coatings did not disappear from
the walls and window frames of pre-1978 homes. Lead has also recently
appeared in foreign-manufactured toys. The greatest concern for lead
ingestion is children eating chips of old paint. Passive cigarette smoke
exposure is a risk for asthma and other chronic diseases but not for lead
toxicity. The United States outlawed lead additives in gasoline in 1976.
Smog is unhealthy but does not cause lead toxicity. Lead is not an impor-
tant groundwater contaminant.
1. b. Complication of antecedent viral upper respiratory infection.
Response: Eustachian tubes open to permit pressure equalization between
the middle ear and the ambient atmosphere. Viral upper respiratory infec-
tions can occlude eustachian tubes because of mucosal edema. Children are
more susceptible, likely the result of smaller anatomy. When the middle ear
becomes a closed chamber, oxygen depletion creates a negative pressure,
leading to transudation. The middle ear fluid is a good culture medium for
nasopharyngeal bacteria. Suppurative middle ear infections are the result of
this process. Chronic bacterial otitis media is unusual. The common process
is repeated suppurative infection of chronic middle ear effusion. The source
of bacteria is the individuals own nasopharyngeal organisms. Tympanic
membrane trauma can cause perforation, not otitis media.
2. b. Increased risk compared with breastfed infants.
Response: Bottle-fed babies have increased risk of acute otitis media.
Sterilizing bottle nipples in boiling water is an out-of-date practice.
3. b. 23 years of age.
Response: The greatest risk of acute otitis media occurs between 6 months
and 3 years of age.
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1. b. Living conditions, including stairs, floor coverings, and bathing facilities.
Response: Fall risk increases with age. Information about the home
environment is a critical part of the geriatric assessment. This includes
whether there are stairs; throw rugs, which can trip or slide; and grab
bars and slip-resistant flooring in bath or shower.
2. c. Jaeger or Snellen test.
Response: It is unnecessary to send every older person for ophthalmologic
evaluation, but checking visual acuity is important. Jaeger and Snellen
charts provide a reasonable way of determining need for referral.
Funduscopic and extraocular muscle examination do not assess acuity.
3. a. Depression.
Response: Depression often causes a decline in cognitive function. An
older term for this is pseudodementia. Antidepressant therapy often
improves cognition as depression improves.
Part V: Womens Health
Chapter 30: Benign Breast Disease
1. b. Reassurance that this is common; return for breast examination in
2 weeks.
Response: An isolated tender breast nodule in a menstruating woman is
likely to be a functional change as the result of the menstrual cycle. If the
nodule regresses in midcycle, no further evaluation is necessary. On first
inspection, it is not possible to be certain the nodule is benign. Waiting
3 months would not permit assessment of menstrual cycle change. Imag-
ing is not appropriate because it does not contribute to diagnosis; it does
pose some risk for false-positive findings.
2. b. Fine-needle aspiration of nodule.
Response: On presentation, the tender nodule might have been the result
of cyclic hormonal changes. If the nodule does not regress at a different
part of the menstrual cycle, that merits evaluation. Imaging would not
ascertain the diagnosis. Biopsy would not be necessary if the nodule is a
cyst that resolved with fine-needle aspiration.
3. d. Reassurance and observation only.
Response: Aspiration of a cyst that causes it to resolve confirms that
the cyst is benign. No further evaluation is necessary. Cytology of the
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aspirated fluid does not contribute at all. If the aspirate were to be bloody
or the cyst not resolve, benign cytology would not permit avoiding a
biopsy. Tamoxifen serves as chemoprevention for women at high risk of
developing cancer. Imaging does not aid in diagnosis. Moreover, screen-
ing implies normal disease risk rather than investigate an abnormality.
Chapter 31: Preconception Care
1. a. Ramipril.
Response: Angiotensin-converting enzyme inhibitors (ACEIs) cause fetal
birth defects. FDA classification is D. Pregnant women should not take
ACEI drugs. No antihypertensive is totally without risk; however, the
decision on treatment depends on the relative balance between risk to the
fetus and benefit to the mother. There are substantial anecdotal data to
suggest that thiazide diuretics are relatively safe. Accordingly, the FDA
rates them class B. There is similar extensive experience with beta
blockers; the FDA regards most of them (except atenolol) as class C.
Alphamethyldopa had been the antihypertensive of choice in pregnancy
for many years. Although it is a class B drug because there have been no
prospective studies, there are no confirmed reports of fetal injury. Use is
rare because side effects are more prominent than with newer drugs.
2. d. Insulin.
Response: Oral antihyperglycemic agents are class C drugs, but recom-
mendations are strong that they should not be used in pregnancy. Insulin
is the treatment of choice for diabetes in pregnancy.
3. c. Low molecular weight heparin for pregnancy duration.
Response: Warfarin causes fetal defects. Its use in pregnancy is con-
traindicated. Because pregnancy is a predisposing condition for venous
thromboembolism, treatment needs to encompass all of pregnancy and
6 weeks beyond delivery. Low molecular weight heparin is the most
convenient anticoagulant. Change to standard unfractionated heparin is
necessary at the time of delivery to permit rapid adjustment. Interrup-
tion of the IVC prevents embolization in the short term. Studies show
no advantage in long-term risk of pulmonary embolism or mortality.
It carries an increased risk of recurrent DVT. Moreover, insertion
requires significant radiation exposure for the fetus.
Chapter 32: Hormone Replacement Therapy
1. a. Osteoporosis.
Response: Estrogen replacement therapy used to be standard preventive
treatment for osteoporosis. Although it has a proven benefit, prospective
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controlled trials have demonstrated that adverse risks exceed the benefit.
Cardiac mortality and possible breast cancer are among those adverse con-
sequences. There is no evidence showing estrogen is useful at preventing
or treating depression and anxiety that can occur with menopause.
2. d. Prevention is not a use of estrogen.
Response: Estrogen replacement therapy used to be standard preventive
treatment for osteoporosis. Although it has a proven benefit, prospective
controlled trials have demonstrated that adverse risks exceed the benefit.
Therefore, it is no longer a viable approach to prevention. Estrogen without
progestin increases risk of endometrial cancer, whereas adding progestin
appears to lower the risk. Colorectal cancer has a small decrease in risk
with estrogen therapy. Adverse risk outweighs all the potential benefits.
3. d. There is no proven hormonal treatment.
Response: Depression and anxiety often complicate early menopause.
Estrogen, soy, or other hormone replacements have no effect on develop-
ment or treatment of affective disorders.
1. a. Estrogen.
Response: Estrogen causes proliferation and thickening of the endometrium.
2. b. Progesterone.
Response: Progesterone secreted by the corpus luteum after ovulation
maintains the prepared endometrium prior to implantation.
3. b. Progesterone.
Response: Progesterone secreted by the corpus luteum after ovulation
maintains the prepared endometrium prior to implantation.
Chapter 34: Female Genital Symptoms
1. d. Condyloma acuminatum.
Response: Condyloma acuminatum is the result of HPV infection.
2. d. Unknown.
Response: The cause of lichen sclerosis is unknown. Biopsy is necessary
to confirm the diagnosis. Scleroderma is not associated with vaginal
conditions. Estrogen deficiency causes atrophic changes.
3. a. Condyloma acuminatum.
Response: HPV is the most frequent female sexually transmitted disease
in the United States. It causes external warts (condyloma acuminatum)
and cervicitis. HPV does not cause ulcerations. Bacterial vaginosis and
miscarriage are associated.
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Chapter 35: Pap Smear and Cervical Cancer Screening
1. b. Squamous carcinoma.
Response: Squamous cell carcinoma is by far the most common cervical
cancer. Adenocarcinoma can arise only from the endocervix or endometrium.
Neither myosarcoma nor lymphoma is a primary cervical cancer.
2. b. Human papillomavirus (HPV).
Response: The association of HPV, most often serotypes 16 and 18, with
infection and cervical cancer risk is close to or is 100%. Co-infection and
cigarette smoking increase the risk that HPV infection will develop into
cancer.
3. b. Only some HPV serotypes are associated with high risk for cervical
cancer.
Response: Serotypes 16 and 18 have the highest rate of developing into
cervical cancer. Serotypes 6 and 11, which are responsible for genital
warts, have low risk of developing into cancer. Co-infection with a differ-
ent sexually transmitted disease increases the risk of cancer, but HPV
does not require co-infection to cause cancer.
1. d. Most cases of osteoporosis in the United States result from acceler-
ated age-related changes.
Response: Most osteoporosis occurs in postmenopausal women. Estrogen
deficiency in menopause accelerates age-related bone loss. Secondary
osteoporosis occurs in 20%30% of women who have postmenopausal
age-related osteoporosis. Calcium and vitamin D deficiency are common.
Slowing bone loss is largely ineffective unless deficiencies are corrected.
2. a. Fractures.
Response: Osteoporosis makes bones more fragile, leading to fracture.
High-output heart failure in bone disease is a complication of Paget
disease. Osteoporosis does not cause calcium depletion or precipitate
calcium in kidneys.
3. c. Aging causes osteoclasts to be relatively more active than osteoblasts.
Response: Osteoclasts resorb bone. Osteoblasts create bone matrix. The
balance between their activities determines the rate of bone growth or
loss. Osteoblast activity predominates until ages 2030 years. After that,
osteoclast activity predominates.
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505
APPENDI X
B
ABBREVIATIONS
Abbreviation Meaning
AAA abdominal aortic aneurysm
AAFP American Academy of Family Physicians
AAP American Academy of Pediatrics
ABCDs airway, breathing, circulation, disability (priorities
in emergency situations)
asymmetry, border, color, diameter (malignant
melanoma recognition)
ABG arterial blood gas
AC acromioclavicular
ACC American College of Cardiology
associated clinical conditions
ACE angiotensin-converting enzyme
ACEI angiotensin converting enzyme inhibitor
ACL anterior cruciate ligament
ACS acute coronary syndrome
American Cancer Society
ACTH adrenocorticotropic hormone
AD atopic dermatitis
ADA American Diabetes Association
ADHD attention deficithyperactivity disorder
ADP adenosine diphosphate
AGC atypical glandular cells
AGS American Geriatrics Society
AHA American Heart Association
AHI apnea/hypopnea index
AICD automated implantable cardioverter-defibrillator
AIS adenocarcinoma in situ
AK actinic keratoses
ALT alanine transaminase
AOM acute otitis media
AR absolute risk (difference)
ARB angiotension receptor blocker
ARR absolute risk reduction
ASA American Society of Anesthesiologists
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ASC atypical squamous cell
ASC-US atypical squamous cell of uncertain significance
AST aspartate transaminase
ATP adenosine triphosphate
AUB abnormal uterine bleeding
BDZ benzodiazepine
bid twice a day (bis in die)
BMD bone mineral density
BMI body mass index
BODE index body mass index, airflow obstruction, dyspnea,
and exercise capacity
BP blood pressure
benzoyl peroxide
BPH benign prostatic hyperplasia
benign prostatic hypertrophy
BPV benign positional vertigo
BRAT diet bananas, rice, apples/applesauce, toast
BUN blood urea nitrogen
CABG coronary artery bypass graft (surgery)
CAD coronary artery disease
CAM complementary and alternative medicine
CBC complete blood count
CBT cognitive behavioral therapy
CCU coronary care unit
CD contact dermatitis
CDC U.S. Centers for Disease Control and Prevention
CFS chronic fatigue syndrome
cGMP cyclic guanosine monophosphate
CHD coronary heart disease
CHF congestive heart failure
CIN cervical intraepithelial neoplasia
CKD chronic kidney disease
CNS central nervous system
CO carbon monoxide
CO
2
carbon dioxide
COPD chronic obstructive pulmonary disease
COX cyclooxygenase
CPAP continuous positive airway pressure
CPK creatine phosphokinase
CPPD calcium pyrophosphate deposition
Cr chromium
creatinine
CRF chronic renal failure
506 B ABBREVIATIONS
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CSF cerebrospinal fluid
CT computed tomography
CV cardiovascular
CVA cerebrovascular accident
costovertebral angle
CVD cardiovascular disease
CVS chorionic villus sampling
CXR chest x-ray
DASH diet Dietary Approaches to Stop Hypertension (diet
rich in fruits, vegetables, and whole grains)
DBP diastolic blood pressure
DCCT Diabetes Control and Complication Trial
DEXA dual energy x-ray absorptiometry
DHE dihydroergotamine
DHEA dehydroepiandrosterone
DIC disseminated intravascular coagulation
DIP distal interphalangeal (joints)
DLCO diffusing capacity of the lung for carbon monoxide
DM diabetes mellitus
DNA deoxyribonucleic acid
DPP-4 dipeptidyl peptidase-4
DSM-IV-TR Diagnostic and Statistical Manual of Mental
Disorders, 4th edition, text revision
DTaP diphtheria, tetanus, acellular pertussis (vaccine)
DUB dysfunctional uterine bleeding
DVT deep venous thrombosis
EBV Epstein-Barr virus
ECG electrocardiogram
ED erectile dysfunction
EDS excessive daytime sleepiness
EEG electroencephalogram
EF ejection fraction
EGD esophagogastroduodenoscopy
EMG electromyography
ERCP endoscopic retrograde cholangiopancreatography
ESR erythrocyte sedimentation rate
ETOH ethanol
FDA U.S. Food and Drug Administration
FEV
1
forced expiratory volume in 1 second
FPG fasting plasma glucose
FSH follicle-stimulating hormone
FUO fever of unknown origin
FVC forced vital capacity
B ABBREVIATIONS 507
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FWLS fever without localizing sign
GAS group A streptococcus
GBS group B streptococcus
GERD gastroesophageal reflux disease
GI gastrointestinal
GINA Global Initiative for Asthma
GIP gastric inhibitory polypeptide
GLP-1 glucagon-like peptide-1
GnRH gonadotropin-releasing hormone
GOLD Global Initiative of Obstructive Lung Disease
GU genitourinary
hCG human chorionic gonadotropin
HDL high-density lipoprotein
HEENT head, eyes, ears, nose, throat
Hgb hemoglobin
HIB Haemophilus influenzae type B (vaccine)
HLA human leukocyte antigen
HPA hypothalamic-pituitary-adrenal (axis)
HPI history of present illness
HPV human papillomavirus
HRT hormone replacement therapy
HSIL high-grade squamous intraepithelial lesion
HSV herpes simplex virus
HTN hypertension
IBD inflammatory bowel disease
IBS irritable bowel syndrome
ICS inhaled corticosteroids
ICU intensive care unit
Ig immunoglobulin
IIEF international index of erectile function
IL interleukin
IM intramuscular
INR International Normalized Ratio
IPV inactivated poliomyelitis vaccine
intimate partner violence
IUD intrauterine device
IV intravenous
IVIG intravenous immunoglobulin
JNC Joint National Committee (on Prevention,
Detection, Evaluation, and Treatment of High
Blood Pressure)
JRA juvenile rheumatoid arthritis
JVD jugular vein distention
KOH potassium hydroxide
508 B ABBREVIATIONS
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LABA long-acting beta agonist
LASGB laparoscopic adjustable silicone gastric banding
LBBB left bundle branch block
LDL low-density lipoprotein
LH luteinizing hormone
LMWH low molecular weight heparin
LR likelihood ratio
LSIL low-grade squamous intraepithelial lesion
LTOT long-term oxygen therapy
LUTS lower urinary tract symptom
LVH left ventricular hypertrophy
MAO monoamine oxidase
MAOI monoamine oxidase inhibitor
MEE middle ear effusion
MET metabolic equivalent
MI myocardial infarction
MM malignant melanoma
MMR measles, mumps, rubella (vaccine)
MRI magnetic resonance imaging
MRSA methicillin-resistant Staphylococcus aureus
MUSE medicated urethral system for erection
NAFLD nonalcoholic fatty liver disease
NAION nonarteritic anterior ischemic optic neuropathy
NCEP U.S. National Cholesterol Education Program
NCI U.S. National Cancer Institute
NCV nerve conduction velocity
NHANES U.S. National Health and Nutrition Examination
Survey
NHLBI U.S. National Heart, Lung, and Blood Institute
NIH U.S. National Institutes of Health
NIPPV noninvasive positive pressure ventilation
NNH number needed to harm
NNT number needed to treat
NO nitric oxide
NSAID nonsteroidal anti-inflammatory drug
NSVD normal spontaneous vaginal delivery
OA osteoarthritis
OR odds ratio
operating room
OCP oral contraceptive pill
OME otitis media with effusion
ONJ osteonecrosis of the jaw
OSA obstructive sleep apnea
OTC over-the-counter (drugs)
B ABBREVIATIONS 509
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PAI-1 plasminogen activator inhibitor 1
PCN penicillin
PCOS polycystic ovarian syndrome
PCR polymerase chain reaction
PDE phosphodiesterase (various types: 5, 6, 11, etc.)
PE pulmonary embolism
PEFR peak expiratory flow rate
PFT pulmonary function test
PICA posterior inferior cerebellar artery
PIP proximal interphalangeal (joint)
PLMD periodic leg movement disorder
PLMI periodic leg movement index
PMI point of maximum impulse
p.o. by mouth (per os)
PPC postoperative pulmonary complication
PPI proton pump inhibitor
prn as necessary (pro re nata)
PSA prostate specific antigen
PT prothrombin time
PTCA percutaneous transluminal coronary angioplasty
PTH parathyroid hormone
PTT partial thromboplastin time
PUD peptic ulcer disease
PUVA psoralen ultraviolet A light (treatment)
qid four times a day (quater in die)
RA rheumatoid arthritis
RAST radioallergosorbent test
RBC red blood cell
RCRI Revised Cardiac Risk Index
RCT randomized controlled trial
RICE protocol rest, ice, compression, and elevation
RLS restless legs syndrome
ROC receiver operating characteristic (curve)
ROS review of systems
RR relative risk
RRR relative risk reduction
RSV respiratory syncytial virus
RV residual volume
RYGB Roux-en-Y gastric bypass
S3 third heart sound
SBI serious bacterial infection
SBP systolic blood pressure
SCC squamous cell carcinoma
510 B ABBREVIATIONS
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SD seborrheic dermatitis
SEGUE Set the stage
Elicit information
Give information
Understand the patients perspective (and
show the patient you understand)
End the encounter
SERM selective estrogen receptor modulator
SITS (mnemonic) supraspinatus, infraspinatus, teres minor, and
subscapularis
SLE systemic lupus erythematosus
SNASI areas of guidance for parents: safety, nutrition,
activity, socialization, immunizations
SNRI serotonin-norepinephrine reuptake inhibitor
SOB shortness of breath
SQ subcutaneous
SSRI selective serotonin reuptake inhibitor
STD sexually transmitted disease
TB tuberculosis
TCA tricyclic antidepressant
TENS transcutaneous electrical nerve stimulation
TIA transient ischemic attack
tid three times a day (ter in die)
TLC total lung capacity
TM tympanic membrane
TMP-SMZ trimethoprim-sulfamethoxazole
TNF tumor necrosis factor
TOD target organ damage
TSH thyroid-stimulating hormone
tTGA tissue transglutaminase
TZD thiazolidinedione
UKPDS United Kingdom Prospective Diabetes Study
URI upper respiratory infection
USDA U.S. Department of Agriculture
USPSTF U.S. Preventive Services Task Force
UTI urinary tract infection
UV ultraviolet (light) (UVA, UVB, etc.)
VAT visceral adipose tissue
VTE venous thromboembolism
WBC white blood cell
WHI Womens Health Initiative
WHO World Health Organization
B ABBREVIATIONS 511
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512
APPENDI X
C
KEY CONTACTS AND NOTES
Physician Contacts
NAME CONTACT
Dr Home phone:
Mobile phone:
Pager:
Other:
Dr Home phone:
Mobile phone:
Pager:
Other:
Dr Home phone:
Mobile phone:
Pager:
Other:
Community Resources and Phone Numbers
NAME/PROGRAM PHONE NUMBERS
Sexual and Physical Abuse
Substance Abuse
Communicable Diseases (HIV, Hepatitis, Others)
Homeless Shelters
Child/Adolescent Hotlines
Suicide Hotlines
Hospitals (General, Veterans,
Psychiatric)
Medicare
Medicaid
Other
1389_AppC_512-516 2/5/09 6:38 PM Page 512
Facility Phone Numbers
NAME/PROGRAM PHONE NUMBERS
Main Phone:
Fax:
Laboratory Phone:
Fax:
Radiology Phone:
Fax:
Physical therapy Phone:
Fax:
ECG/EEG Phone:
Fax:
Outpatient Scheduling Phone:
Fax:
Emergency Phone:
Fax:
Operating Suite Phone:
Fax:
Admissions Phone:
Fax:
Billing Phone:
Fax:
Medical Records Phone:
Fax:
Medical Staff Office Phone:
Fax:
Other important numbers Phone:
Fax:
C KEY CONTACTS AND NOTES 513
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Formulary Notes Specific to Your Facility
514 C KEY CONTACTS AND NOTES
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Other Important Information
C KEY CONTACTS AND NOTES 515
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517
A
AAFP (American Academy of Family
Physicians), 396
AAP (Association of American
Physicians), 396
Abbreviations, 505511
Abdominal aortic aneurysm, 149t, 160
screening recommendations, 50t
Abdominal pain
approach to patient
diagnostic studies, 151, 151t154t,
153156
history, 144148, 144t
physical examination, 148151,
148t149t
chronic, 145
diagnostic clues to etiologies, 148t
differential diagnosis by location,
142t144t
emesis and, 146
gynecologic conditions, 147
introduction, 142, 142t144t
management
acute abdomen, 156
diverticulitis, 162
gastritis, 163
GERD, 157t, 162163
nonulcer dyspepsia, 158t, 164
overview, 157t160t
pancreatic pseudocysts, 161162
pancreatitis, acute, 158t, 161
pancreatitis, chronic, 161
peptic ulcer disease, 157t, 163
surgical conditions, 160161
referral or consultations, 160t, 164
referred pain, 146
resources, 165166
sudden, 145
Absolute impact, 48, 48t
Absolute risk (AR), 3739, 38f
Absolute risk difference, 31
Absolute risk reduction (ARR), 37
Abuse
domestic violence. See Intimate partner
violence (IPV)
elder abuse and neglect, 405
ACC (American College of
Cardiology), 61
ACEIs (angiotensin-converting enzyme
inhibitors). See Angiotensin-converting
enzyme inhibitors (ACEIs)
Acetaminophen
fatigue, 229
headache, 79, 83, 84t
low back pain, 193
osteoarthritis, 190
otitis media in children, 397
pharyngitis, 136
pregnancy, 421
Acne vulgaris
differential diagnosis, 202
epidemiology, 201202
grades of, 202t
history and physical examination,
202, 202t
laboratory tests, 203
pathophysiology, 201
treatment, 203205, 203t
ACS (American Cancer Society), 53
ACTH stimulation test, 72
INDEX
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Actinic keratosis, 216
Activity level, 56. See also Exercise
as factor for preventable death, 48
Acupuncture
low back pain, 194
Acute abdomen, 156
ADA (American Diabetes Association),
326
Adenocarcinoma in situ (AIS), 468
Adhesive capsulitis, 183
Advair, for asthma, 302
AGCs (atypical glandular cells), 468
Agency for Healthcare Research and
Quality, 52
Agenda, determining in an interview,
910, 14
Age-related conditions, diagnosis and
management of
fever in children. See Fever in children
geriatric conditions. See Geriatric
conditions
otitis media in children. See Otitis
media in children
well-child visit. See Well-child visit
AHA (American Heart Association), 61,
338339
AHI (Apnea/Hypopnea Index), 97
AIS (adenocarcinoma in situ), 468
Albuterol, for asthma, 301
Alcohol use
coronary artery disease, 275
factor for preventable death, 48
hypertension, 284285
osteoporosis, 477
pregnancy, 420
Aldosterone antagonists, for congestive
heart failure (CHF), 272t
Alpha-2 agonists, for perioperative
management, 66
Alpha blockers, for hypertension, 287t
Alpha-glucosidase inhibitors, for diabetes,
331332
Alprazolam, for anxiety, 255t
Ambulatory care
versus inpatient care, 12
pace of, 4
Amenorrhea
primary, 438439
secondary, 440441
American Academy of Family Physicians
(AAFP), 396
American Cancer Society (ACS), 53
American College of Cardiology
(ACC), 61
American College of Physicians, 135
American College of Radiology, 192
American Diabetes Association
(ADA), 326
American Heart Association (AHA), 61,
338339
Amitriptyline, for primary headache
prevention, 85t, 86
Amoxicillin
acute otitis media, 396
sinusitis, 129
Amsels criteria, 454, 455t
Androgens, 236, 244245
dysfunctional uterine bleeding
(DUB), 445
erectile dysfunction, 244245
Anesthesia, 59
Angina, 119, 120t
Angiotensin-converting enzyme
inhibitors (ACEIs)
antihypertensive agents for patients
with diabetes, 327328
congestive heart failure (CHF),
272273, 272t
hypertension, 285, 286t287t,
288289
Anticonvulsants, for restless leg syndrome
(RLS)/periodic leg movement disorder
(PLMD), 102
Anxiety and depression
background and epidemiology, 250
diagnostic approach, 250253
anxiety disorders, 252
biopolar disorder, 252
dysthymia, 252
generalized anxiety disorder, 252
major depressive disorder,
251252, 251t
518
I N D E X
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panic disorder, 251253, 251t252t
thyroid disorders, 253
follow-up and referral, 256257
menopause and, 429
resources, 258259
treatment
medication, 253256, 254t255t
psychotherapy, 253254
Apgar score, 360
Apnea/Hypopnea Index (AHI), 97
Appendicitis, 149t, 160
Apprehension test, 184, 185f
AR (absolute risk), 3739, 38f
ARR (absolute risk reduction), 37
Aspirin
antithrombotic therapy, 70
chemoprevention with, 51t
coronary artery disease, 122, 274
headache, 83, 84t
Association, 29
Association of American Physicians
(AAP), 396
Asthma
adult-onset, 296
cough in, 297
definition, 294
diagnosis, 297298
early-onset, 296
epidemiology and economics, 294295
management
asthma action plans, 305
controller therapy versus reliever
therapy, 299300
control of triggers, 305
monitoring, 304
overview and goals, 299
pharmacologic therapy, 299302
step therapy approach, 302,
303f, 304
natural history, 296
pathogenesis, 295296
preoperative evaluation, 68
referral to pulmonary specialist, 305
resources, 306307
Atopic dermatitis, 207208
Atorvastatin, for hyperlipidemia, 339
Atrophic vaginitis, 459
Atypical chest pain, 120t
Atypical glandular cells (AGCs), 468
Auspitz sign, 211
B
Brny test, 110
Bariatric surgery, 354355
Barium studies, for abdominal pain,
152t, 155
Barrett esophagus, 163
Basal cell carcinoma, 216
Benign positional vertigo, 108110,
109f110f
Benign prostatic hyperplasia (BPH),
erectile dysfunction and, 236237
Benzodiazepine receptor agonists, for
insomnia, 95
Benzodiazepines
anxiety, 255t, 256
restless leg syndrome (RLS)/
periodic leg movement disorder
(PLMD), 102
Benzoyl peroxide, for acne vulgaris, 203t
b
2
-adrenergic agonists, for asthma, 301
Beta blockers
congestive heart failure (CHF), 272t, 273
hypertension, 285, 286t287t, 288
perioperative management, 6566
primary headache prevention, 85t, 87
Bethesda System for Reporting
Cervical/Vaginal Cytological
Diagnoses, 466
Biest, for menopause, 433
Biguanide, for diabetes, 330
Bile sequestrant agents, for
hyperlipidemia, 342
Biphosphonates, for osteoporosis,
477478
Bipolar disorder, 250, 252
Birth history, 360
Black cohosh, for menopause, 433
Blood pressure
measurement, 281
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BMD (bone mineral density)
measurement, 475476, 479
BMI (body mass index), 350, 353354
Bouchard nodes, 190
Bowel obstruction, 148t, 160
BPH (benign prostatic hyperplasia),
Breast cancer, 54
chemoprevention, 51t
lifetime cumulative risk, 47t, 54
Breast disease, benign
breast cysts, 413
breast pain, 411413
evaluation algorithm for palpable
breast mass, 410f
fibroadenomas, 413414
fibrocystic disease, 410411, 412t
introduction, 409410, 410f
nipple discharge, 414415
relative risk (RR), 412t
resources, 416
Bronchitis, acute
chest examination, 131
epidemiology, 130
history and physical, 130131
management, 132
prevention, 130
resources, 138140
Bronchodilators, 301302
COPD, 315, 318319
Bronchoprovocation testing, 298
Bullae, 200t
Bupropion, for mood and anxiety
disorders, 254t, 255
Buspirone, for anxiety, 255t
Butorphanol, for headache, 85
C
CABG (coronary artery bypass surgery),
6465
Caffeine
pregnancy and, 420421
Calcipotriol, for psoriasis, 212t
Calcitonin, for osteoporosis, 478
Calcium
chemoprevention with, 51t
osteoporosis, 477
Calcium channel blockers
hypertension, 286t287t
primary headache prevention, 87
Cancer prevention and screening
breast cancer, 54
cervical cancer, 53
colon cancer, 5455
lung cancer, 53
prostate cancer, 5556
Candidiasis, 215, 455456
management, 458
Cardiac troponin I, 66
Carnett test (abdominal pain), 150
Carpal tunnel syndrome
epidemiology, 187
history, 187188
management, 188189
physical examination, 188
Car seats, 362
Case-control study, 29, 30f, 3233, 34f
CBC (complete blood count). See
Complete blood count (CBC)
Centers for Disease Control and
Prevention (CDC), 5253, 128
Centor criteria (pharyngitis), 135
Cervical cancer. See Pap smear and
cervical cancer screening
Cervical dermatologic conditions, 451
management, 459
Cervical dysplasia, 463
Cervical infections
chlamydia, 456457
diagnostic tests, 457
gonorrhea, 457
Cervical intraepithelial neoplasia
(CIN), 463
Cervicitis, 451
Chemoprevention, 51t, 56
Chest pain
epidemiology, 118, 118t119t
history, 119120, 120t121t
520
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management, 122123
resources, 123124
signs and symptoms, 119
Chest wall pain, 119, 123
Chest x-ray
bronchitis, 131
chest pain, 122
COPD, 312
preoperative, 60, 68
CHF (congestive heart failure). See
Congestive heart failure (CHF)
Chlamydia, 451452
management, 459
Cholecystitis, 158t, 160
Cholelithiasis, 148t
Cholesterol screening recommendations, 50t
Cholestipol, for hyperlipidemia, 342
Cholestyramine, for hyperlipidemia, 342
Chondroitin, for osteoarthritis, 190
Chronic daily headache, 79
Chronic illnesses, diagnosis and
management of
asthma. See Asthma
chronic obstructive pulmonary disease.
See Chronic obstructive pulmonary
disease (COPD)
congestive heart failure. See Congestive
heart failure
diabetes. See Diabetes
hyperlipidemia. See Hyperlipidemia
hypertension. See Hypertension
obesity. See Obesity
Chronic obstructive pulmonary disease
(COPD)
definition, 309
diagnosis, 311313
end-of-life planning, 319320
management
acute exacerbation, 318319
stable COPD, 314317
natural history, 213f, 311
preoperative evaluation, 6869
prognosis, 320321, 320f
referral to pulmonary specialist, 321
resources, 322323
risk factors, 310311
staging, 314
CIN (cervical intraepithelial
neoplasia), 463
Citalopram, for mood and anxiety
disorders, 254t
Clindamycin, for acne vulgaris, 204
Clinical epidemiology and principles of
quantitative decision making
clinical epidemiology, definition
of, 18
costs and cost-effectiveness, 4144, 43t
decision making in uncertainty:
decision analysis, 4041, 41f
diagnostic tests
receiver operating characteristic
(ROC) curve, 2829, 28f
test characteristics, 22, 23f,
2427, 25f
threshold model, 2728
treatment threshold and threshold
model, 1920, 21f, 22
frequency and prevalence, 1819
overview, 1718
prevention and screening, 39
prognosis, 3435
risk, 29, 30f, 3134, 33f34f
treatment, 3639, 38f
Clonazepam
anxiety, 255t
restless leg syndrome (RLS)/
periodic leg movement disorder
(PLMD), 102
Clonidine
hypertension, 287t
Clopidogrel, for antithrombotic
therapy, 70
Clostridium difficile infection, 174, 177
Cluster headache, 80, 81
Cognitive behavioral therapy, 9697
fatigue, 228229
low back pain, 194
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major depressive disorder, 253
obesity, 352353
Cohort study, 29, 30f, 35
Colesevelam, for hyperlipidemia, 342
College of American Pathologists, 411
Colon cancer, 5455
lifetime cumulative risk of, 47t
Colonoscopy, 5556
abdominal pain, 152t, 155
virtual, 55
Colorectal cancer screening
recommendations, 50t
Common outpatient symptoms, diagnosis
and management of
abdominal pain. See Abdominal pain
anxiety and depression. See Anxiety
and depression
bronchitis, acute. See Bronchitis, acute
chest pain. See Chest pain
dermatology. See Dermatology in
primary care
diarrhea. See Diarrhea
dizziness. See Dizziness
erectile dysfunction. See Erectile
dysfunction
fatigue. See Fatigue
headache. See Headache
musculoskeletal pain. See
Musculoskeletal pain
pharyngitis. See Pharyngitis
sinusitis. See Sinusitis
sleep disorders. See Sleep disorders
somatization. See Somatization
Communicating with patients
difficult encounters, 1314
effective strategies for communi-
cation, 13
overview, 8
resources, 15
SEGUE acronym for effective interview
Set the stage, 810
Elicit information, 1011
Give information, 1112
Understand patients perspective,
1213
End the encounter, 13
overview, 8, 9t
Complete blood count (CBC), 60
chronic COPD, 313
osteoporosis, 476
Computed tomography (CT)
chest pain, 122
chronic obstructive pulmonary disease
(COPD), 313
Condyloma acuminatum, 450, 454, 458
Congestive heart failure (CHF)
approach to patient, 270271,
270t272t
exacerbation, causes of, 271, 271t
management
disease-specific treatment, 271,
274275
general treatment, 271274
overview, 271, 272t
overview, 269270
resources, 276
underlying causes, 270, 270t
Contact dermatitis, 206207
vulvar, 450, 458
Continuous positive airway pressure
(CPAP), 100
COPD (chronic obstructive pulmonary
disease). See Chronic obstructive
pulmonary disease (COPD)
Coronary artery bypass surgery (CABG),
6465
Corticosteroids
asthma, 300
COPD, 316, 318319
fatigue, 229
preoperative evaluation of patients
taking, 72
Cost-effectiveness, 4144, 43t
erroneous uses of, 42
marginal cost-effectiveness, 4243
Cost per year of life, 49
COX-2 inhibitors, 83
CPAP (continuous positive airway
pressure), 100
Critical point, 39
Crohn disease, 171, 171t
Cromolyn sodium, for asthma, 300
522
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Cross-sectional study, 19, 22
CT (computed tomography)
chest pain, 122
chronic obstructive pulmonary disease
(COPD), 313
Cushing disease, 280, 324
Cyclosporin A, for asthma, 302
Cyproheptadine, for primary headache
prevention, 85t, 87
Cytobrush, use of, 53
D
DASH (Dietary Approach to Stop
Hypertension), 283, 284t
D-dimer test, 24, 2627
ROC curve for, 24, 2627, 28f
Decision analysis, 4041, 41f
Decision tree, 40, 41f
Defibrillator, implantable, for congestive
heart failure (CHF), 272t, 275
Dementia, 402403
Depo-Provera, for dysmenorrhea, 447
Depression. See Anxiety and
depression
Dermatology in primary care
acne vulgaris
202, 202t
treatment, 203205, 203t
eczema
atopic dermatitis, 207208
contact dermatitis, 206207
overview, 206
seborrheic dermatitis, 209210
overview, 199, 200t, 201
primary lesions, 200t
psoriasis, 210211, 212t213t, 213
resources, 219
secondary lesions, 200t
self-test questions, 219220
skin cancer, 216217
basal cell carcinoma, 216
malignant melanoma, 217
squamous cell carcinoma, 216
superficial fungal infections, 213215
Desipramine, for mood and anxiety
disorders, 254t
DHE (dihydroergotamine), for headache,
84, 84t
Diabetes
classification, 324325
complications
importance of good control, 326
macrovascular, 327
microvascular, 327329
diagnosis, 325326, 325t
epidemiology, 324
fatigue and, 224
introduction, 324
management
combination therapy, 333
diet and exercise, 329330, 329t
parenteral medications administered
subcutaneously, 332333
pharmacologic treatment with oral
agents, 330332
preoperative evaluation of patients with,
7172
resources, 335
Diagnostic and Statistical Manual of
Mental Disorders, 4th edition
(DSM-IV), 251
Diagnostic tests
receiver operating characteristic (ROC)
curve, 2829, 28f
test characteristics, 22, 23f, 2427, 25f
threshold model, 2728
treatment threshold and threshold
model, 1920, 21f, 22
Diarrhea
abdominal pain and, 146
antibiotic use and, 167
definitions and overview, 167168,
171172, 171t
evaluation
acute diarrhea, 172173, 173t
chronic diarrhea, 173175, 174t
523
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management, 175177
medications that may cause, 174t
most common causes, 168
resources, 178
viral gastroenteritis and, 168
workup of chronic diarrhea,
169f170f
Dicyclomine, for irritable bowel
syndrome, 177
Diet
children. See Well-child visit
COPD, 317
diabetes, 329, 329t
dysmenorrhea, 447
factor for preventable death, 48
hyperlipidemia, 339
hypertension, 283, 284t
obese patients, 352
Dietary Approach to Stop Hypertension
(DASH), 283, 284t
Difficult patient encounters
angry patients, 14
breaking bad news, 14
listening, importance of, 15
somatization and, 260
taking a sexual history, 14
talking to patients from different
cultures, 14
Diffusing capacity, 313
Digital rectal examination, average
increase in life expectancy with, 49t
Digoxin, for congestive heart failure
(CHF), 272
Dihydroergotamine (DHE), for headache,
84, 84t
Diphtheria immunization
Disequilibrium, 113
Diuretics
congestive heart failure (CHF), 272
hypertension, 285286, 286t287t,
288
Divalproex, for primary headache
prevention, 85t, 86
Diverticulitis, 149t, 158t159t, 162
Dix-Hallpike maneuver, 109110,
109f110f, 115f
Dizziness
approach to patient, 107108
allow patients to describe
sensations in their own words,
107108
background, 107
classification, 108
disequilibrium, 113
epidemiology, 107
presyncope, 112113
resources, 116117
treatment, 114, 115f, 116
vague lightheadedness, 114
vertigo, 108112
benign positional vertigo, 108110,
109f110f
CNS, 111112, 112t
labyrinthitis, 111
Mnire disease, 111
nystagmus, 112
vestibular neuronitis, 110111
Domestic violence. See Intimate partner
violence (IPV)
Dopaminergic agents, for restless leg
syndrome (RLS)/periodic leg movement
disorder (PLMD), 102
Doxycycline, for acne vulgaris, 204
Drop arm test, 182
DSM-IV (Diagnostic and Statistical
Manual of Mental Disorders, 4th
edition), 251
Dual energy x-ray absorption (DXA),
475, 479
Duloxetine, for neuropathies, 329
Dysfunctional uterine bleeding (DUB),
441446
Dysmenorrhea, 446447
Dysthymia, 250, 252
E
Ectopic pregnancy, 147
Eczema
atopic dermatitis, 207208
contact dermatitis, 206207
overview, 206
seborrheic dermatitis, 209210
Elder abuse and neglect, 405
Electrocardiogram (ECG)
524
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chest pain, 122
hypertension, 281
perioperative, 66
preoperative, 60
Electromyography (EMG) studies, 188
Empty can test (supraspinatus
examination), 184, 185
Epidural anesthesia, 59
Eply maneuver, 114, 115f
Erectile dysfunction
approach to patient
history, 240241
laboratory testing, 241242
epidemiology, 233
erectile physiology, 233234
indications for specialty referral, 242
management
androgen therapy, 244245
intracavernosal self-injection, 245
intraurethral treatments, 246
nonpharmacologic therapies,
242243
oral PDE-5 inhibitors, 243244
patient education, 242
penile revascularization, 246
psychosexual therapy, 243
surgery, 246
vacuum constriction devices, 246
medications associated with,
238t239t
pathophysiology
arteriogenic, 235
cavernous (venogenic), 235
chronic kidney disease (CKD), 237
diabetes, 236
diseases, 234235
endocrinologic, 236
lower urinary tract symptoms
(LUTS)/benign prostatic
hyperplasia (BPH), 236237
medication and substance-related,
238, 238t239t, 240
metabolic syndrome, 236
neurogenic, 235236
psychogenic, 237238, 238t
prostate cancer and, 56
resources, 248249
risk factors, 233, 234t
self-test questions, 249
smoking and, 240
Erythrocyte sedimentation rate
(osteoarthritis), 190
Erythromycin, for acne vulgaris, 204
Esophageal manometry (chest pain), 122
Esophageal pain, 119
Esophagogastroduodenoscopy (abdominal
pain), 152t, 155
Estrogen, 427t, 430432
Eszopiclone, for insomnia, 95
Evidence-based medicine, 18
Exercise
average increase in life expectancy,
49t
diabetes, 329330, 330t
dysmenorrhea, 447
hypertension, 285
pregnancy, 422
as treatment for fatigue, 228229
Ezetimibe, for hyperlipidemia, 342
F
Falls and gait disturbances in older
patients, 404405
Fatigue
classification, 221
clinical assessment, 226228
definition, 221
etiology, 223225
management, 228230
prognosis, 230
resources, 231
Fecal occult blood testing, 54
Female genital symptoms
differential diagnosis, 453457, 455t,
457t
management, 457459
painful versus painless genital ulcers,
451t
pathophysiology, 450451, 451t
patient history, 452
resources, 460
525
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FEV
1
, 311, 312f, 313314, 320
Fever in children
definition, 376
diagnostic evaluation
children 3 years and older, 387
neonates (028 days), 381,
382t385t
older infant or toddler (336 months),
386387
young infants (13 months), 381,
386, 386t
overview, 381
epidemiology, 376
fever of unknown origin (FUO), 376
history and physical examination, 378,
378t380t
management, 387388
resources, 390
Fibroadenomas, 413414
Fibrocystic disease, 410411, 412t
Fibromyalgia, 223
Fludrocortisone, for presyncope, 114
Fluoxetine, for mood and anxiety
disorders, 254t
Folic acid, chemoprevention with, 51t
Formoterol, for asthma, 301
Frequency and prevalence, 1819
Frozen shoulder, 183
Functional capacity, 63
Functional incontinence, 403
Fungal infections, superficial, 213215
FUO (fever of unknown origin), 376
G
Gabapentin
low back pain, 194
menopause, 434
neuropathies, 329
restless leg syndrome (RLS)/periodic
leg movement disorder (PLMD), 102
Galactorrhea, 414
Gallstones, 147
Gastritis, 148t, 163
Gastroenteritis, 148t
pediatric fever, 382t
Gastroesophageal reflux disease (GERD),
148t, 157t, 162163
General anesthesia, 59
Generalized anxiety disorder, 250, 252
Genital ulcer disease, 450
Geriatric conditions
assessment, 402405
dementia, 402403
falls and gait disturbances, 404405
iatrogenesis, 404
incontinence, 402404
elder abuse and neglect, 405
involving aid of dentists, otologists, and
ophthalmologists, 405
issues for evaluation, 400t
management strategies, 401t
nonspecific presentation of disease in
the elderly, 405
overview, 400401, 400t401t
resources, 405406
Global Initiative of Obstructive Lung
Disease (GOLD), 309, 314
Glucosamine
osteoarthritis, 190
Glycosylated hemoglobin (Hgb
A1c
), 326
Gold standard test, 22
Gonadotropic-releasing hormone
(GnRH) agonists
(DUB), 445
Gonorrhea, 451452
management, 459
Grind test, 195
Gulf War syndrome, 223
H
H. pylori (Helicobacter pylori)
testing, 153155, 153t154t
therapy, 163
Harkins test, 184, 184f
H
2
blockers, 157t158t, 162163
HDL (high-density lipoprotein), 337,
338t, 341
Headache
approach to patient, 8182
background, 7781
chronic daily headache, 79
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cluster headache, 80
migraine headache, 7879
tension-type headache, 79
brain tumor and, 82
resources, 8889
treatment, 8288, 84t85t
abortive, 83, 84t
difficulty of, 83
lifestyle, 83
Health benefits, methods of
measuring, 48
Hearing screening recommendations, 50t
Heart transplantation, 275
Heberden nodes, 190
Helicobacter pylori (H. pylori)
testing, 153155, 153t154t
therapy, 163
Hematemesis, 146
Heme-positive stools, 146
Heparin, 71
Herpes simplex in women, 454
management, 458
Hgb
A1c
(glycosylated hemoglobin), 326
High-density lipoprotein (HDL), 337,
338t, 341
High-grade squamous intraepithelial
lesion (HSIL), 466
Hip fracture for white women, lifetime
cumulative risk of, 47t
Hormone replacement therapy (HRT)
alternatives to, 432434
background, 426427, 427t
benefits, 427t, 429430
contraindications, 431
epidemiology and diagnosis of
menopause, 427428
formulations, 431432
resources, 436
risks, 427t, 430
side effects, 430431
summary, 434
symptoms of menopause, 428429
Hot flashes, 428429
HRT (hormone replacement therapy). See
Hormone replacement therapy (HRT)
HSIL (high-grade squamous
intraepithelial lesion), 466
Human papillomavirus (HPV)
cervical cancer and, 462
immunization recommendations, 51t
vaccine, 464
Hyperlipidemia
history and physical examination, 338
laboratory testing, 339
management, 339, 340t341t,
341342
pathophysiology and epidemiology,
337, 338t
resources, 343344
Hypertension
benefits of treatment, 278
blood pressure measurement, 281
coronary artery disease and, 275
definition, 279, 279t
drug treatment
general principles of, 285286,
286t287t
medications, 286, 288289
etiology
primary hypertension, 279
secondary hypertension, 279280
evaluation, 281
lifestyle modifications, 284t
nonpharmacologic treatment,
283285, 284t
overview, 278
patients to treat, 282, 282t283t
prognosis
factors influencing, 282t
risk stratification to quantify, 282t
refractory hypertension, 289290
renin and, 286
resources, 291292
Hyperthyroidism, preoperative evaluation
of patients with, 73
Hypothyroidism, preoperative evaluation
I
Iatrogenesis, in older patients, 404
IBD (inflammatory bowel disease), 148t
diarrhea and, 168, 171
527
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IBS (irritable bowel syndrome). See
Irritable bowel syndrome (IBS)
Ibuprofen
headache, 83
otitis media in children, 397
pharyngitis, 136
IIEF (International Index of Erectile
Function), 241
Imipramine, for mood and anxiety
disorders, 254t
Immunizations, 56
newborns and infants, 364
4 months, 364
6 months, 365
9 months, 366
12 months, 367
15 and 18 months, 367
2 years, 368
35 years, 370
510 years, 371
1013 years, 371
1318 years, 372
Impingement (of rotator cuff tendons),
181
Incidence, 19, 31, 36
Incontinence in older patients, 402404
Incremental cost-effectiveness, 42
Index test, 22
Inflammatory bowel disease (IBD), 148t
Inpatient versus ambulatory care, 12
Insomnia
chronic insomnia, 92
classification, 92
definition/epidemiology, 91
patient evaluation, 9294
treatment, 9497
cognitive behavioral therapy, 9697
medications, 9496
Insulin, for diabetes, 330, 333
International Index of Erectile Function
(IIEF), 241
Interstitial cystitis, 223
Interview, 3
Intimate partner violence (IPV)
assessing safety, 485
barriers to identification, 484
definition, 482
demographics, 482483
intervention strategies, 485486
lifetime cumulative risk of, 47t
medical presentation, 483484
overview, 482
relationship pattern in, 483
reporting, 486
resources, 487
screening, 484485
summary, 486
Intracavernosal self-injection, 245
Intraurethral treatments, 246
Intravenous pyelogram (abdominal pain),
152t, 155
Ipratropium, for asthma, 301
IPV (intimate partner violence). See
Irritable bowel syndrome (IBS), 148t, 223
criteria for, 171t
differentiating ulcerative colitis and
Crohn disease, 171, 171t
treatment, 176177
Isotretinoin, for acne vulgaris, 203t,
204205
J
Jaundice, abdominal pain and, 146
K
Kaopectate, for diarrhea, 176
Kidney disease, chronic, erectile
dysfunction and, 237
Koebner phenomenon, 211
L
Labyrinthitis, 111
Lactose intolerance, 168, 176
Laparoscopic adjustable silicone gastric
banding (LASGB)
obesity, 355
LDL (low-density lipoprotein). See
Low-density lipoprotein (LDL)
Leukotriene-modifying agents, for asthma,
300301
528
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Levalbuterol, for asthma, 301
Levonorgestrel-releasing intrauterine
device, for dysfunctional uterine
bleeding (DUB), 445
Lichenification, 200t
Lichen planus, 450, 453, 457
Lichen sclerosus, 450, 453, 457
Life expectancy, 48, 48t
Lifetime cumulative risk table, 47
Lightheadedness, 114
Likelihood ratio, 22, 24
Lipid therapy, for coronary artery
disease, 274
Listening skills, 9, 11, 15
Lomotil, for irritable bowel syndrome,
177
Loperamide
diarrhea, 176
irritable bowel syndrome, 177
Lorazepam, for anxiety, 255t
Lovastatin, 339
Low back pain
epidemiology, 191
imaging, 192193
treatment, 193194
Low-density lipoprotein (LDL), 339,
341342
risk factors that modify LDL goals,
340t
treatment goals based on patient risk,
340t341t
Lower urinary tract symptoms (LUTS),
Low-grade squamous intraepithelial lesion
(LSIL), 466
Lung cancer, 53
M
Macules, 200t
Magnetic resonance imaging (MRI)
chest pain, 122
low back pain, 193
shoulder, 186
Major depressive disorder, 250252, 251t
Malignant melanoma, 217
Mammography, 54, 412
average increase in life expectancy
with, 49t
Mandibular advancement devices, 100
Marginal cost-effectiveness, 4243
Massage therapy, for low back pain, 194
Mastalgia, 412
Mast cell stabilizers, for asthma, 300
Measles immunization recommendations,
51t
Meclizine, for vertigo, 114
Melatonin, for insomnia, 96
Mnire disease, 111, 114
Meninges, headache and, 77
Meningitis, pediatric fever and, 383t
Meningococcal hepatitis A and B
immunization recommendations, 51t
Menopause
diagnosis, 428
early, 427
osteoporosis and, 472
symptoms of, 428429
Menstrual cycle, normal, 438
Menstrual disorders
dysfunctional uterine bleeding (DUB),
441446
dysmenorrhea, 446447
normal menstrual cycle, 438
primary amenorrhea, 438439
resources, 448
secondary amenorrhea, 440441
Mesenteric ischemia, 149t, 151, 160
Metabolic equivalents (METs), 63, 64t
Metabolic syndrome, 337, 338t
Metformin, for diabetes, 330
Methotrexate, for asthma, 302
Methylprednisolone, for vertigo, 114
Middle ear effusion (MEE), 394
Midodrine, for presyncope, 114
Migraine headache, 7879
Minocycline, for acne vulgaris
205
Mirena IUD, for dysmenorrhea, 447
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Mirtrazapine, for mood and anxiety
Mononucleosis (EBV), 136
Montelukast, for asthma, 300
MRI (magnetic resonance imaging)
chest pain, 122
low back pain, 193
shoulder, 186
Mumps immunization recommendations,
51t
Murphy sign, 150
Musculoskeletal pain
carpal tunnel syndrome. See Carpal
tunnel syndrome
introduction, 180181
low back pain. See Low back pain
osteoarthritis (OA). See Osteoarthritis
(OA)
patellofemoral syndrome. See
Patellofemoral syndrome
resources, 197
shoulder pain. See Shoulder pain
N
Naproxen, for headache, 83
Narcotics, for headache, 84t, 85
National Cancer Institute (NCI), 464
National Heart, Lung, and Blood Institute
(NHLBI), 338
Natural history study, 35
Natural hormone therapy, for menopause,
433434
Nedocromil sodium, for asthma, 300
Neer test, 183, 183f
Nefazodone, for mood and anxiety
Neglect and abuse, elder, 405
Nephrolithiasis, 148t
Nephropathy, 328
Nerve conduction velocity (NCV)
test, 188
Neuropathy, 328329
NHLBI (National Heart, Lung, and Blood
Institute), 338
Nipple discharge, 414415
Nitrates
NNH (number needed to harm), 3133
NNT (number needed to treat), 3739,
38f
Nodules, 200t
Nonanginal chest pain, 120t
Noninvasive positive-pressure ventilation
(NIPPV), 319
Nonulcer dyspepsia, 148t, 158t, 164
Nonverbal communication, 13
Nortriptyline
mood and anxiety disorders, 254t
primary headache prevention, 85t, 86
NSAIDs (nonsteroidal anti-inflammatory
drugs)
breast pain, 412
dysfunctional uterine bleeding (DUB)
dysmenorrhea, 447
fatigue, 229
headache, 79, 83, 84t
low back pain, 193
osteoarthritis, 190
ulcers related to NSAID use, 163
Number needed to harm (NNH), 3133
Number needed to screen, 48, 48t
Number needed to treat (NNT),
3739, 38f
Nutrition. See Diet
Nystagmus, 112
O
OA (osteoarthritis). See Osteoarthritis
(OA)
Obesity
etiology, 346
history, 350
management
behavior therapy, 352353
lifestyle modification, 352
pharmacotherapy, 353354
physical activity, 352
surgical (bariatric) treatment,
354355
obesity-related comorbidities, 347
530
I N D E X
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pathology, 347348
prevention, 349
resources, 356357
Obsessive-compulsive disorder, 250
Obstructive sleep apnea
consequences, 99
definition, 97
diagnosis, 9899
pathophysiology, 98
prevalence, 97
treatment, 99100
Odds, definition of, 26
Odds-likelihood ratio, 2627
Odds ratio (OR), 33
Office management and ambulatory
patients
inpatient versus ambulatory care, 12
learn what it means to be someones
doctor, 67
principles of diagnosis and treatment
clinical presentation, 2
diagnostic and therapeutic plan, 4
management, 4
role of students, 56
OLDCARTS mnemonic, 2
Omalizumab, for asthma, 302
Onychomycosis, 215
Open-ended questions, 11
Opioid analgesics, for low back pain,
193
Opioids, for restless leg syndrome
(PLMD), 102
Oral contraceptive pills
acne vulgaris, 205
(DUB), 445
dysmenorrhea, 447
Oral PDE-5 inhibitors, for erectile
dysfunction, 243244
Orlistat, for obesity, 354
OR (odds ratio), 33
Osteoarthritis (OA)
epidemiology, 189
history, 189190
management, 190
pathogenesis, 189
prevalence, 189
Osteoporosis
definitions, 472
diagnosis, 475476
epidemiology, 473
evaluation for secondary osteoporosis,
476477
history, key components of, 473
management, 477479
monitoring, 479
physical examination findings
suggesting osteoporosis, 474
resources, 480
risk factors, 473, 474t
screening guidelines, 475
Otitis media in children
anatomy and function, 391392
diagnosis, 394395
epidemiology, 393
examining the ear, 393
infectious versus noninfectious otitis
media, 391
management
acute otitis media, 396397
otitis media with effusion, 397
microbiology, 392
pathophysiology of acute otitis media,
392
resources, 398
risk factors, 392393
Otoscope, 383
Ovarian cancer, 147, 149t
Overflow incontinence, 403
Oxycodone, for restless leg syndrome
(PLMD), 102
Oxygen therapy, for COPD, 317, 319
531
I N D E X
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P
Pancreatic disease, 325
Pancreatic pseudocysts, 161162
Pancreatitis, 148t
acute, 158t, 161
chronic, 161
Panic disorder, 250, 251253, 251t252t
Pap smear and cervical cancer screening, 53
epidemiology of cervical cancer, 463
lifetime cumulative risk of cervical
cancer, 47t
Pap smear, 464469
with, 49t
interpretation and management,
466469
pathophysiology of cervical cancer,
462463, 462f
prevention of HPV and cervical cancer,
463464
resources, 470
risk factors for cervical cancer, 462
Papules, 200t
Paradoxical insomnia, 92
Parenchymal renal disease, 280
Paroxetine
menopause, 434
Partial thromboplastin time (PTT), 60
Patellofemoral syndrome
epidemiology, 194
history, 194
treatment, 195
Peak expiratory flow rate (PEFR), 304
Penicillin
sinusitis, 129
streptococcal pharyngitis, 136
Penile revascularization, 246
Peptic ulcer disease, 148t, 157t, 163
Pepto-Bismol, for diarrhea, 176
Percutaneous coronary angioplasty
(PTCA), 6465
Pericarditis, 119
Periodic leg movement disorder
(PLMD)/restless leg syndrome
(RLS)
diagnosis, 101
prevalence, 101
treatment, 102103
Peritonitis, 148t, 161
Peritonsillar abscess, 134
Petechia, 200t
Phalen sign, 188
Pharyngitis
epidemiology, 133
management, 136
pediatric fever, 385t
prevention, 133
resources, 138140
Phentermine, for obesity, 354
Pheochromocytoma, 253, 280
pH monitoring (chest pain), 122
Physical examination, 3
Pirbuterol, for asthma, 301
Pityriasis versicolor, 215
Plaques, 200t
Pleuritic chest pain, 119
Pneumococcal influenza immunization
Pneumonia, pediatric fever and, 383t384t
Poison ivy, 206
Poison oak, 206
Polysomnography, 94
Postoperative pulmonary complications
(PPCs), 6669
Post-test probability, 22, 23f, 24, 26
calculating, 25, 25f
Prader-Willi syndrome, 346
Pramipexole, for restless leg syndrome
(PLMD), 102
Pramlintide, for diabetes, 332333
Pravastatin, for hyperlipidemia, 339
Preconception care
532
I N D E X
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evaluation, 418421
advanced maternal age, 419420
complete medical history, 418
medications, 418419, 419t
substance use, 420421
resources, 424
risk categories, 422t
specific preconception counseling,
421423, 422t
Prediction rule, 24
Pregabalin, for neuropathies, 329
Premarin, for dysfunctional uterine
bleeding (DUB), 445
Preoperative evaluation
cardiac assessment and
management, 6061, 61t, 62f,
6366, 63t64t
endocrine disorders, 7173
overview, 59
patients on antithrombotic or
anticoagulant therapy, 7071
pulmonary evaluation, risk assessment,
and risk reduction for
noncardiothoracic surgery,
6669, 68t
resources, 7475
testing, 60
Presyncope, 112113
treatment, 112114
Pre-test probability, 19, 22, 24
Prevalence, 19
Prevention and screening, 2, 3, 39
age and, 52
cancer
breast cancer, 54
cervical cancer, 53
colon cancer, 5455
lung cancer, 53
prostate cancer, 5556
chemoprevention, 56
counseling, 56
diseases to screen for, 50, 50t51t,
5253
epidemiology, 4750, 47t49t
immunizations, 56
increases in life expectancy with
screening, 49t
methods of measuring health benefits, 48t
principles of screening, 47t
resources, 5758
role of students, 5
Primary care, overview of
clinical epidemiology and principles of
quantitative decision making. See
Clinical epidemiology and principles
of quantitative decision making
communicating with patients. See
Communicating with patients
office management and ambulatory
patients. See Office management and
ambulatory patients
preoperative evaluation. See
Preoperative evaluation
prevention and screening. See
Prevention and screening
Primary headache, 78
Primary headache prevention
selective serotonin reuptake inhibitor
(SSRI) antidepressants, 87
Primary hyperaldosteronism, 280
Primary prevention, 2
Progestin
dysfunctional uterine bleeding (DUB),
427t, 431
hormone replacement therapy (HRT),
427t, 431
Prognostic factors, 35
Prognosis, 3435
Prolactin level (amenorrhea), 440441
Prostate cancer, 5556
lifetime cumulative risk of, 55
Prostate-specific antigen (PSA) test
with, 49t
Prothrombin time (PT), 60
Pseudoephedrine, pregnancy and, 421
Psoriasis, 210211, 212t213t, 213
Psychosexual therapy for erectile
dysfunction, 243
PTCA (percutaneous coronary
angioplasty), 6465
PTT (partial thromboplastin time), 60
Purpura, 200t
Pustules, 200t
533
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Q
Quality-adjusted life expectancy, 41, 43
R
Radioallergosorbent test (RAST), 208
Radiofrequency ablation, 100
Ramelteon, for insomnia, 95
Randomized controlled study design, 36
Rapid urease test, 153t, 154
Receiver operating characteristic (ROC)
curve, 28, 28f
Reflux disease, 123
Refractory hypertension
compliance, 289
diuretic changes, 290
medication interactions, 290
secondary causes, 289
Relative impact, 48t
Relative risk reduction (RRR), 36
Relative risk (RR), 31, 3639, 38f
breast disease, benign, 412t
Relaxation training, 96
Renal stones, 161
Renovascular hypertension, 280
Residual volume (RV), 313
Restless leg syndrome (RLS)/periodic leg
movement disorder (PLMD)
diagnosis, 101
prevalence, 101
treatment, 102103
Retinoids, for acne vulgaris, 203, 203t
Retropharyngeal abscess, 134
Revascularization, 6465
congestive heart failure (CHF), 272t
Review of systems (ROS), 3
Revised Cardiac Risk Index (RCRI), 60,
61t, 63
Rheumatic fever, 134, 136
Rheumatoid factor test (osteoarthritis), 190
RICE (rest, ice, compression, and
elevation) protocol, 180
Risk, 29, 30f, 3134, 33f34f
ROC (receiver operating characteristic)
curve, 28, 28f
Ropinirole, for restless leg syndrome
(PLMD), 102
ROS (review of systems), 3
Rotator cuff tear, 181
Roux-en-Y gastric bypass, for obesity, 355
RR (relative risk), 31
breast disease, benign, 412t
RRR (relative risk reduction), 36
Rubella immunization recommendations,
51t
RV (residual volume), 313
S
Salmeterol, for asthma, 301302
Screening. See Prevention and screening
Seborrheic dermatitis, 209210
Secondary headache, 78
Secondary prevention, 2
Selective estrogen receptor modulators
(SERMs), for osteoporosis, 478
Selective serotonin reuptake inhibitors
(SSRIs)
lightheadedness, treatment for, 116
menopause, 434
mood and anxiety disorders, 254256,
254t255t
Sensitivity, 22
Serial versus parallel testing, 4
SERMS (selective estrogen receptor
modulators), for osteoporosis, 478
Sertraline, for mood and anxiety
disorders, 254t
Shaken baby syndrome, 363
Shoulder pain
management, 187
physical examination, 182184,
183f186f, 186
posterior, 182
Sibutramine, for obesity, 353
sigmoidoscopy, flexible, 5455
Sildenafil, for erectile dysfunction,
243244
Simvastatin, for hyperlipidemia, 339
534
I N D E X
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Sinus headache, 80
Sinusitis
epidemiology, 127
management, 128129
prevention, 127
resources, 138140
Sitagliptin, for diabetes, 332
Skin cancer, 216217
basal cell carcinoma, 216
malignant melanoma, 217
squamous cell carcinoma, 216
Sleep apnea
hypertension and, 280
Sleep diary, 94
Sleep disorders
insomnia
chronic insomnia, 92
classification, 92
definition/epidemiology, 91
treatment, 9497
introduction, 91
obstructive sleep apnea (OSA)
consequences, 99
definition, 97
diagnosis, 9899
pathophysiology, 98
prevalence, 97
treatment, 99100
resources, 104105
restless leg syndrome (RLS)/periodic
leg movement disorder (PLMD)
diagnosis, 101
prevalence, 101
treatment, 102103
Sleep hygiene education, 96
Sleeping safety for infants, 363
Sleep restriction therapy, 96
Smoking and smoking cessation, 51t, 56
asthma, 311
with quitting, 49t
cervical cancer, 463
COPD, 310
as factor for preventable death, 48
hot flashes, 428
hypertension and, 285
osteoporosis, 477
postoperative pulmonary complications,
69
pregnancy, 420
SNASI (safety, nutrition, activity,
socialization, immunizations)
mnemonic, 361362
Somatization
differential diagnosis, 263, 264t, 265
262263, 263t
laboratory evaluations, 265
management, 265267
frequent visits, 265
patients who respond negatively to
reassurance, 266267
patients who respond positively to
reassurance, 266
pathophysiology
somatoform disorder versus
somatoform symptoms,
260261
resources, 268
signs and symptoms, 261, 262t
somatoform disorders, 261
somatoform symptoms
useful questions for patients with,
263t
verbal and nonverbal clues of, 262t
Soy, for menopause, 432433
Specificity, 22, 24
Spirometery (asthma), 304
Spirometry, 67, 298, 313
Spironolactone, 273
Squamous cell carcinoma, 216
Squamous cells, atypical (ASCs),
467468
SSRI (selective serotonin reuptake
inhibitors). See Selective serotonin
reuptake inhibitors (SSRI)
535
I N D E X
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Statins
hyperlipidemia, 339, 341
Stents, 6465, 70
Steroids, topical, for psoriasis, 212t
Stimulus control therapy, 96
Streptococcal pharyngitis, 133134
Stress incontinence, 403
Stress testing (chest pain), 122
Sulcus sign, 182
Sulfonylureas, for diabetes, 331
Support stockings, for presyncope, 114
Synovial fluid analysis (osteoarthritis), 190
T
Tadalafil, for erectile dysfunction, 243
Tazarotene, for psoriasis, 212
Teach-back technique, 3, 7
Telangiectasia, 200t
Temporomandibular joint disorder, 223
Tension-type headache, 79
Teratogenic medications, 419t
Terbinafine, for fungal infections,
214215
Teriparatide, for osteoporosis, 478479
Test characteristics, 19, 22, 23f, 2427, 25f
Tetanus-diphtheria immunization
Tetracycline, for acne vulgaris, 204
Theatre sign, 194
Theophylline, for asthma, 302
Threshold model, 2122, 21f, 2728
Thyroid disease, preoperative evaluation
Thyroid disorders, 253
Thyroid-stimulating hormone (TSH), 339
amenorrhea, 440441
osteoporosis, 477
Tilt table test, 113
Tinel sign, 188
Topiramate, for primary headache
prevention, 85t, 87
Total lung capacity (TLC), 313
Transesophageal echocardiography (chest
pain), 122
Trazodone, for mood and anxiety
disorders, 254t
Treadmill, screening
with, 49t
Treatment, 3639, 38f
Treatment threshold and threshold model,
1920, 21f, 22
Tree diagram for calculating post-test
probability, 2526, 25f
Trichomoniasis, 456, 459
Tricyclic antidepressants
low back pain, 194
mood and anxiety disorders,
254256, 254t
neuropathies, 329
primary headache prevention, 86
Triest, for menopause, 433
Triggers, asthma, 305
Triptans, for headache, 84, 84t
T score, 476
TSH (thyroid-stimulating hormone), 339
amenorrhea, 440441
osteoporosis, 477
Tympanometry, 395
acoustic reflectometry, 395
Type I diabetes, 324, 326, 333. See also
Diabetes
Type II diabetes, 324, 326327, 332333
U
Ulcerative colitis, 171, 171t
Ultrasound (abdominal pain), 152t, 155
United States Preventive Services Task
Force (USPSTF), 50, 5253, 55, 464
Upper respiratory infection (URI), 127
acute otitis media and, 392
Urea breath test, 154t, 155
Urge incontinence, 403
Urinary tract infection (UTI)
pediatric fever, 377, 385
Utilities (measure of quality of life), 41
Uvulopalatopharyngoplasty, 100
V
Vacuum constriction devices for erectile
dysfunction, 246
Vaginal dermatologic conditions, 450451
management, 458459
Vaginitis, atrophic, 456
536
I N D E X
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Vaginitis, diagnosis of, 455t
Vaginosis, 450, 454455
management, 458
Valerian, for insomnia, 96
Vardenafil, for erectile dysfunction,
243244
Varicella immunization recommen-
dations, 51t
Vascular headaches, 78
Vasovagal reaction (neurocardiogenic
presyncope), 113
VAT (visceral adipose tissue)
compartment, 348
Venlafaxine
menopause, 434
Ventilatory support, 319
Verapamil, for primary headache
prevention, 85t
Vertigo, central versus peripheral, 112, 112t
Vesicles, 200t
Vestibular neuronitis, 110111
Vestibulitis, 450, 453454, 458
Viral pharyngitis, 134135
as HIV manifestation, 134
Visceral adipose tissue (VAT)
compartment, 348
Vision screening recommendations, 50t
Vulvar dermatologic conditions, 450
management, 457458
Vulvodynia, 450, 454, 458
Vulvovaginitis, 451
W
Wallenberg syndrome, 112
Warfarin antithrombotic therapy, 7071
Weight screening recommendations, 50t
Well-child visit
age-specific examination guidelines
newborn and infant, 362
2-month examination, 362364
15- and 18-month examinations, 367
2-year examination, 367368
preschool-age (3- to 5-year-old)
examinations, 368370
elementary-age (5- to 10-year-old)
preteen or middle-school-age (10- to
13-year-old) examinations, 371
teen (13- to 18-year-old)
fundamentals, 359362
resources, 374
Wheals, 200t
Wheeze, 297
Willis, circle of, headache and, 77
Womens health
benign breast disease. See Breast
disease, benign
genital symptoms. See Female genital
symptoms
hormone replacement therapy. See
Hormone replacement therapy
intimate partner violence (IPV). See
menstrual disorders. See Menstrual
disorders
osteoporosis. See Osteoporosis
Pap smear and cervical cancer
screening. See Pap smear and
cervical cancer screening
preconception care. See Preconception
care
World Health Organization (WHO), 349,
475
Y
Yoga, for low back pain, 194
Z
Zafirlukast, for asthma, 300
Zileuton, for asthma, 300
Zolpidem, for insomnia, 95
Z score, 576
537
I N D E X
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Absolute risk = Incidence

FIGURE 3.6 Example of measuring risk in a cohort study.

FIGURE 3.8 Example of measuring benefit in a treatment study.

Family history of CHD in male first-degree

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