Step-Up To Geriatrics

STEP-UP to
GERIATRICS
STEP-UP to
GERIATRICS
EDITORS
Mitchell S. King,
Clinical Professor
Department of Family and Community
Medicine
University of Illinois
Rockford, Illinois
Martin S. Lipsky,
Chancellor
South Jordan Campus
Roseman University of Health Sciences
South Jordan, Utah
Acquisitions Editor: Matt Hauber
Product Development Editor: Christine Fahey
Editorial Assistant: Brooks Phelps
Marketing Manager: Michael McMahon
Production Project Manager: Alicia Jackson
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Library of Congress Cataloging-in-Publication Data
Names: King, Mitchell S., author. | Lipsky, Martin S., author.

Title: Step-up to geriatrics / Mitchell King, Martin Lipsky.
Description: First edition. | Philadelphia : Wolters Kluwer Health, [2017]
Identifiers: LCCN 2016017329 | ISBN 9781496301277
Subjects: | MESH: Geriatrics | Outlines | Problems and Exercises
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.loc.gov/2016017329
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CONTRIBUTORS
MELISSA L. CANNON, PhD SEYYED ALI SAJJADI OSKOUEI, MD
Faculty Member Clinical Assistant Professor Family Medicine
Urban Studies and Planning University of Illinois
Portland State University College of Medicine
Portland, Oregon Rockford, Illinois
LINDA CHANG, PharmD, MPH PREETINDER S. PADDA, MD

Clinical Associate Professor Physician
Family/Community Medicine Rockford, Illinois
University of Illinois at Chicago
Rockford, Illinois RITA PATEL, MD
Chief Resident
PRIYANTHIE GANENTHIRAN, MD Family Medicine
Resident Physician University of Illinois
Family Medicine College of Medicine
UIC Rockford Family Medicine Program Rockford, Illinois
Rockford, Illinois
JOSEPH E. ROSS, MD
AMANDEEP KAUR, MD Clinical Assistant Professor
Clinical Assistant Professor Department of Family and Community
Clinical Family Medicine Medicine
University of Illinois at Chicago University of Illinois
Rockford, Illinois Rockford, Illinois
MOHAMMED AMIR KHAN, MD SAVNEET KAUR SONIA SARAN, MD

Resident Physician Family Medicine Resident Physician
University of Illinois Family Medicine
College of Medicine University of Illinois
Rockford, Illinois College of Medicine
Rockford, Illinois
MITCHELL S. KING, MD
Clinical Professor PATRICIA AUSTRIA SHRESTHA, MD
Department of Family and Community Clinical Assistant Professor
Medicine Clinical Family Medicine
University of Illinois Department of Family and Community
Rockford, Illinois Medicine
RONALD LEFEBVRE, MA, DC Rockford, Illinois
Professor
Clinical Education HUMERA SUBRIN TAQUI, MD
University of Western States Resident Physician
Portland, Oregon Family Medicine
MARTIN S. LIPSKY, MD College of Medicine
Chancellor Rockford, Illinois
South Jordan Campus
Roseman University of Health Sciences NATASHA VERMA, MD
South Jordan, Utah Resident Physician
Family Medicine
MAY NAWAL LUTFIYYA, PhD University of Illinois
Professor College of Medicine
Pharmacy Care and Pharmaceutical Rockford, Illinois
Sciences
University of Minnesota DARICE L. ZABAK MD
AHC Office of Education Family Physician
Minneapolis, Minnesota South Jordan, Utah
PREFACE
Over the past few decades, the United States has experienced a tremendous growth in the
number of individuals over age 65. The vast majority of these individuals have at least one
chronic condition, making the care of elderly individuals a disproportionally large part of
practice for anyone caring for adult patients. The challenge of providing successful and
cost-effective geriatric care will become even more important for clinicians currently in
training as the population continues to age.
Our goal for Step-Up to Geriatrics is to provide a comprehensive, straightforward, high-
yield review of the essentials of geriatrics. While caring for the older adult is a key element
of both family medicine and internal medicine, this book is specifically designed to supple-
ment more general texts and the Step-Up series in other subjects. We included material that
will be helpful for students taking a geriatric clerkship, residents on a geriatrics rotation,
geriatric fellows, or physicians seeking a text for overall review. Physician assistants or
advanced practice nurses with a focus on caring for older adults will also benefit greatly
from the material in this text.
The book is organized to allow someone to quickly look up a topic, prepare for an
exam, or read the entire text section by section for a more comprehensive review and to
better understand how to care for the elderly patient. The Step-Up formatwhich com-
bines numerous callouts, tables, charts, flow diagrams, Quick Hit bullet points, and sum-
mary of key facts with comprehensive paragraphs as neededallows for a quick and easy
understanding of the most important information. We have designed the text to be short
enough for a student on a 4-week rotation to master key facts and concepts, yet detailed
enough to provide a good analysis of specific elements of geriatric care when needed for a
nongeriatric rotation.
Both of us enjoy caring for older patients and hope we have instilled some of the enthu-
siasm and interest we have in geriatrics. We also encourage readers to contact us by e-mail
with any suggestions about how to make future editions better, or to correct any omissions
or inadvertent errors that we may have overlooked.
Mitchell King
msking@uic.edu
Martin Lipsky
mlipsky@uic.edu
ACKNOWLEDGMENTS
We would like to thank all those who helped make this book possible. If readers feel that
this book contributes to their understanding of geriatrics, it is largely because of the many
people who helped create this book.
First, we thank Wolters Kluwer for giving us this opportunity, and, in particular, Tari
Broderick, senior acquisitions editor, who trusted us to get this project started, Matt Hauber
and Christine Fahey, who helped guide this project along and transform our manuscript
into a final formatted product that looked like an actual book. Each of these individuals
added their expertise and insight along the way.
We also thank the reviewers who gave us critical feedback and also pointed out key
errors in earlier drafts. Their suggestions and comments, while sometimes painful and ego-
deflating, made this book so much better. In addition, we would like to acknowledge our
contributors who did so much to develop the material for this book.
Finally, and most importantly, both of us gratefully acknowledge the support of our
friends and families, especially our wives, Darice Zabak, MD, and Jacqueline King. Darice,
in particular, provided insightful review and gave us several great suggestions. Her keen
eye and attention to detail picked up several errors that we might have easily missed.
Without Darice and Jackie, this project and many others would not be possible.
CONTENTS
Contributors v
Preface vi
Acknowledgments vii
1 THEGERIATRICPATIENT
Introduction to Aging 1
Demographics and Epidemiology 5
Changes of Aging 8
Geriatric As s es s ment 19
Preventive Care for the Older Adult 22
Geriatric Pharmacotherapy 29
Preoperative Evaluation 31
Health Care Financing 37
2 GERIATRICSYNDROMES
Failure to Thrive (FTT) 49
Incontinence 52
Cons tipation 55
Falls / Gait Ins tability 58
Altered Mental S tatus / Delirium 62
3 PSYCHOSOCIAL/BEHAVIORALISSUES
Dementia 67
Depres s ion 75
Anxiety in the Elderly 84
S ubs tance Abus e and the Elderly 88
Elder Abus e 91
S exuality and the Older Adult 95
Driving 100
4 COMMONGERIATRICMEDICALCONDITIONS
Geriatric Dermatology 103
Oral Health in Geriatric Patients 112
S ens ory Dis orders 117
Neurologic Dis eas e 129
Cardiovas cular Dis eas e 144
Pulmonary Dis eas e 160
Renal Dis eas e 171
Urologic Dis eas e 190
Gynecologic Dis eas e 199
Endocrine Dis eas e 219
Rheumatologic Dis eas e 235
C O N TE N TS ix
Hematologic Dis eas e 263

Cancers 275
Chronic Pain 287
5 ENDOFLIFE
As s is ted Living and Home Care 295
Nurs ing Home Care 298
Hos pice and Palliative Care 302
Ethical Is s ues in the Elderly 308
Index 312
THE
GERIATRIC 1
PATIENT
Intro d uc tio n to A g ing

A. Geriatric patients are arbitrarily defined as patients aged 65 and older.
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1. Historically, the age of 65 as a retirement age can be traced to Otto Bismarck, Chan-
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cellor of Germany in the late 19th century, when only 2% of Germans lived past 65.
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Bismarck believed that the cost of social welfare programs starting at age 65 would
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be acceptably small for the population.
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2. Geriatric patients are frequently complex patients with multiple chronic
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conditions.
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3. Their decreased physiologic reserves place them at greater risk for complications
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from both disease and treatment than younger individuals.
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B. Gerontology and geriatrics
1. Gerontology is the study of aging and the processes and phenomena associated
with aging. Quick HIT
a. Gerontology incorporates all facets of aging, drawing upon such varied fields as Geriatric patients, who are
biology, sociology, economics, history, and medicine. defined as >65 years of age,
b. Gerontologists are scientists who study aging. have less physiologic reserve,
placing them at higher risk for
2. Geriatrics is the study of clinical practice as it relates to older individuals.
morbidity and mortality.
a. It includes the diagnosis and treatment of diseases and health problems of older
adults.
b. Physicians specializing in caring for older adults are geriatricians.
C. What is aging?
1. Aging is the inevitable chronologic changes from year to year. It can be defined
from both biologic and psychosocial perspectives.
2. Biologic aging involves changes at the molecular, cellular, and organ levels. Quick HIT
a. Starting at about age 30, aging in humans results in an internal physiologic Biologic aging is genetically
deterioration. determined and environmen-
b. Biologic aging is genetically determined and environmentally modulated. tally modulated.
3. Cellular senescence is the process by which a cell loses its ability to divide, grow,
and function, ultimately leading to cell death.
4. Aging can be characterized by the acronym CUPID, meaning that aging is Cumula-
tive, Universal, Progressive, Intrinsic, and Deleterious (see Table 1-1).
a. All humans age, making this phenomenon universal.
b. Cumulative means the effects of aging are irreversible and accumulate over time.
c. Aging is unidirectional. For example, a postmenopausal woman cannot become
ovulatory again.
d. Because even under the best environmental conditions an individual ages, aging
is intrinsic to the organism.
e. Deleterious means that aging is harmful, resulting in decreased vitality and an
increased vulnerability to disease and environmental stresses.
1
2 S T E P - U P T O G E R I AT R I C S
TABLE 1-1 Characteristics of Aging

CUPID
Cumulative
Universal
Progressive
Intrinsic
Deleterious
Quick HIT
Ageism is prejudice or dis-
crimination on the basis of
age.
5. Ageism is prejudice or discrimination on the basis of a persons age.

a. Examples include adults portrayed as being senile, hard of hearing, grumpy, set
in their ways, and as needing help.
Quick HIT b. Heterogeneity is common among older persons, and although some older adults
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do not function well, the vast majority of those over 65 live independently.
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Psychological theories of
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c. Healthcare providers are not immune to ageism and may infantilize older adults
a
aging relate to psychological
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transformations as a person and talk down to them or use derogatory terms to address or talk about them.
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d. Awareness is the first step toward addressing ageism.
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ages.
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D. Psychosocial theories of aging include the disengagement theory, activity theory, and
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social clock.
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Quick HIT 1. Disengagement theory is the process of individuals withdrawing from prior social
interactions as they age. Although popular in the 1950s, the greater health and vi-
Eriksons theory of develop- tality of older individuals today means they tend to remain more engaged in society
ment views old age as a time than in the past.
to maintain ego integrity 2. Activity theory proposes that while involvement is a human need, the meaning and
versus despair.
focus of involvement changes with age.
a. For example, when an individual retires, they may transition to volunteer work
or devote more time to a hobby.
b. In contrast, the continuity theory states that aging adults do change their inter-
Quick HIT actions with age, but still maintain many of the same activities, behaviors, per-
sonality traits, and relationships as they did earlier in life.
A key concept of aging is
3. The social clock theory proposes that behavioral expectations at different ages are
the decrease in the ability to
maintain homeostasis. dictated by norms connected to a particular age. As individuals remain healthier for
longer, societal views of older individuals will change.
4. Psychological theories of aging relate to psychological transformations that indi-
viduals experience as they age.
Quick HIT a. Eriksons theory of development views old age as a time to maintain ego integrity
versus despair, e.g., to hold on to ones sense of wholeness while avoiding the
Homeostasis is the ability of fear that there is too little time to begin a new life course.
an organism or cell to regulate b. Older age is a time to review ones life, reconcile successes and failures, and to
its internal conditions through put it all in perspective.
a system of feedback controls
that preserves function in the E. Biologic theories of aging
face of external stresses.
1. Biologic aging impairs an organisms ability to maintain homeostasis.
a. Homeostasis is the ability of an organism or cell to regulate its internal condi-
tions through a system of feedback controls that preserves function in the face of
external stresses.
Quick HIT 2. The loss of physiologic reserve, which diminishes the ability to buffer stress,
is what makes older individuals more vulnerable to disease and environmental
A common rule is that indi- stresses.
viduals lose about 1% of their
physiologic reserve (starting at 3. A common rule of thumb of aging is that individuals lose about 1% of their physi-
around age 30). ologic reserve per year, starting at around age 30. This is mostly true for the pulmo-
nary, renal, cardiovascular, and musculoskeletal systems.
T H E G E R I AT R I C P AT I E N T 3
TABLE 1-2 Major Theories of Aging

Psychological
Stochastic Nonstochastic Attempts to Explain
Evolutionary or Error or Biologic Behavior and Roles
Theories Theories Clock
Programmed death, Free radical theory Biologic clock theory Disengagement theory
mutation accumula- Somatic mutation Neuroendocrine Activity theory
tion, antagonistic Wear and Tear theory Immunologic theory Social clock theory
pleiotropy, disposable Cross-linkage
soma Rate of living
4. Heterogeneity is another key concept of aging.

a. There is an increase in variability from individual to individual and also within Quick HIT
an individuals organ systems.
Heterogeneity is a key concept
b. For example, someone might have good pulmonary function, yet have poor of aging.
renal function.
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5. Successful aging can be thought of as maintaining good health, good functional
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ability, good cognition, and remaining socially engaged.
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6. Theories of aging
Quick HIT
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a. Theories of aging fall into three broad categories: evolutionary, programed, and
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error theories (see Table 1-2). No single theory entirely
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b. No single theory entirely explains aging, and to a certain degree, aging theories explains aging, and to a cer-
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e
overlap. tain degree, aging theories
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c. Most experts believe that aging results as a combination of evolution, genetic overlap.
factors, and errors interacting in ways that are not fully understood.
d. Evolutionary theories of aging include the theories of programmed death, muta-
tion accumulation, antagonistic pleiotropy, and the disposable soma. In many
cases, programmed and error theories are consistent with genetic selection.
The theory of programmed death is one of the oldest evolutionary arguments
Quick HIT
to explain aging. Accumulated mutation occurs
(1) This theory proposes that programmed death favors the survival of a species because nature selects for
by freeing up resources for younger generations to survive and reproduce. genes with immediate survival
and reproductive value, and
The mutation accumulation theory proposes that aging is an inevitable result there is no evolutionary pres-
of the declining force of natural selection with age. sure for longevity.
(1) For example, a mutation that kills young children will be strongly se-
lected against if it prevents reproduction, while a lethal gene at an older
age may have no selection bias, because the mutation will have already
passed to offspring.
(2) Over generations, late-acting harmful mutations can accumulate.
Antagonistic pleiotropy is based on the presumption that a gene may have
multiple effects (pleiotropy).
(1) In antagonistic pleiotropy, effects are opposite, in which one effect may be
beneficial, and another detrimental.
(2) In this theory late-acting harmful genes may be favored if they have a ben-
eficial effect early in life.
(3) For example, a gene that enhances oxidative phosphorylation might in-
crease the burden of free radicals (FRs).
(4) Enhanced phosphorylation might allow an animal to be faster and stron-
ger, favoring natural selection early in life, but, over the long term, might
produce more FRs that age an organism (see free radical theory).
Quick HIT
The disposable soma theory presumes that the body has limited energy re- The disposable soma theory
sources and must budget the amount of its energy available. presumes that the body has
limited energy resources and
(1) There may be a selective advantage for organisms to adopt a strategy where must budget the amount of its
energy to accelerate development and reproduction is favored over the repair energy available.
of somatic cells with the eventual consequence of deterioration and death.
e. Programmed theories of aging propose that aging and longevity are coded into
the genome and include the neuro-endocrine, biologic clock, and autoimmune
Quick HIT theories.
Programmed theories pro- The neuro-endocrine theory proposes that aging is a part of the developmental
pose that the human body is process, that hormones control the pace of aging, and that aging is a sequence
designed to age and follows of events such as puberty and menopause coded into the genes.
an internal clock encoded into
The biologic clock theory proposes that cells of a species are programmed for
our DNA.
a certain number of divisions.
(1) Hayflick found that human fibroblasts stop dividing after about 50
divisions.
Quick HIT (2) The discovery of telomeres, areas of DNA at the end of chromosomes in-
volved in the replication and stability of DNA, supports this theory.
Neuro-endocrine theory
proposes that changes in (3) With each cellular division in a differentiated cell, the telomeres shorten
hormones control aging. until the cell becomes inactive and is no longer capable of dividing.
(4) The shortening process is associated with aging, and telomeres in cells
from older individuals are shorter than the telomeres in cells of healthy,
Quick HIT younger individuals.

(5) Telomeres in cells from individuals with chronic diseases such as cir-
The biologic clock theory pro- rhosis and congestive heart disease are shorter than healthy age matched
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poses that cells of a species controls.
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are programmed for a certain (6) Longer telomeres are found in germ cells, pluripotent stem cells, and tu-
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number of divisions.
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mor cells.
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(7) Telomerase is the enzyme that helps maintain the telomeres, and telomer-
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ase levels decrease with age. Research on aging and cancer explores ways
a
Quick HIT
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to block the enzyme as a tool to fight cancer and also ways to potentially
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restore telomere length as an antiaging tool.
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Cell senescence has been
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linked to the length of telomeres The immunologic theory of aging is based on the programmed decline of the
and to telomerase activity. immune system over time.
(1) Impaired immunity leads to an increased vulnerability to infection.
(2) Dysregulation of the immune system is also linked to diseases such as
cancer and cardiovascular disease that have an increased prevalence
Quick HIT among older adults.
The immune theory argues f. Stochastic or error theories are another major category of aging theories. Many
that the immune system is error theories overlap and share in common the idea that aging results from ac-
programmed to decline over cumulated damage to our cells over time.
time, leaving a person more
The Wear and Tear theory suggests that similar to an aging car, vital parts of
susceptible to disease.
the human body wear out with age and from the inability to continually repair
damage to crucial systems.
(1) This theory probably holds true for mechanical systems such as joints and
Quick HIT teeth.
The free radical theory is one of the most popular theories of aging.
Error theories assert that ag-
ing is caused by damages to (1) FRs are highly reactive chemical species that have an unpaired electron.
our bodys systems which ac- (2) FRs can react with and damage cellular components such as proteins,
cumulate over time. DNA, lipids, and sugars.
(3) Simply put, the free radical theory postulates that aging is caused by the
accumulation of oxidative damage.
Quick HIT (4) FRs can originate intrinsically as a byproduct of metabolism or extrinsi-
cally from exogenous sources such as ionizing radiation and sunlight.
FRs can damage cells and (a) One type of highly reactive FR is the oxygen-free radical. Mitochon-
lead to impaired function. dria generate oxygen-free radicals as a byproduct of their energy-
producing mechanisms.
(b) The body possesses natural defenses, or anti-oxidants, in the form
Quick HIT of enzymes such as superoxide dismutase and catalase peroxide that
can convert highly reactive oxygen molecules into inert molecules.
Mitochondria generate oxy-
Because not all highly reactive oxygen molecules are FRs, many prefer
gen-free radicals as a byprod-
uct of their energy-producing the oxidative stress or the oxidative theory of aging rather than the
mechanisms free radical theory.
(c) Vitamin C and E are examples of extrinsic antioxidants. Despite the

appeal of taking supplemental antioxidants to slow aging, there is no
evidence that supplemental antioxidants ameliorate aging. In fact,
giving high doses of the antioxidant -carotene to smokers increases
their risk of lung cancer, and supplemental vitamin E increases the
risk of prostate cancer.
Quick HIT
(d) Defense mechanisms prevent most oxidative damage, but small There is no evidence that tak-
ing supplemental anti-oxidants
amounts of damage accumulate over time and contribute to the
slows aging.
deterioration of tissues and organs.
(e) FRs are used as part of the bodys immunologic defenses.
The rate of living theory postulates that the faster an organisms metabolism
the shorter the life span.
(1) First proposed by Pearl in the 1920s, the theory postulates that metabolic
processes consume a vital cellular element. When this element is ex-
hausted, it leads to death.
(2) More recent arguments suggest that mitochondria generate fewer highly
reactive oxygen free species through slower metabolism, thus slowing
aging and extending life span.
(3) Caloric restriction in mice can increase life span, an argument supporting
the rate of living theory. However, when looking across the animal king-
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dom, not all animals with slow metabolisms live longer.
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(4) Caloric restriction has not been proven to extend life span in humans.
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In addition to being difficult to maintain over time, caloric restriction in
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humans have shown negative consequences, including muscle wasting,
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osteoporosis, and fatigue, as well as the difficulty of ensuring that a re-
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stricted calorie diet is nutritionally adequate.
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Somatic damage theory proposes that DNA damage occurs over time and im-
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pairs cellular function.
(1) A related theory of accumulated error proposes that aging is a conse-
quence of errors that occur during DNA replication.
(2) Although repair enzymes fix most damage, both theories attribute aging
to an imbalance between damage and repair function, which allows errors
Quick HIT
Somatic damage theories pro-
to accumulate, leading to the damage of genetic integrity, thus causing
pose that genetic mutations
aging. over time cause malfunction
Another damage theory is the cross-linkage theory, which proposes that the and aging.
accumulation of cross-linked proteins and DNA disrupts function.
D e m o g ra p hic s a nd Ep id e m io lo g y
A. Life expectancy is defined as the average number of years a population of certain age
can expect to live.
1. It is a commonly used measure to describe the overall health of a population.
2. Healthy People 2020 monitors two life expectancy measures: life expectancy at
Quick HIT
birth and at age 65. The average life expectancy
3. The average life expectancy at birth in the US in 2010 was 78.7 years, which ranks at birth in the US in 2010 was
78.7 years.
as 26th in the world. For men, the life expectancy is 76 years, and for women,
81 years.
4. The gender gap for life expectancy between men and women is present in all
developed countries, but narrows with age. By age 65, the life expectancy for men
at age 65 is 17.7 years, and for women, 20.3 years.
5. In 1900 the average life expectancy in the US was 47 years, and only 4% of Ameri- Quick HIT
cans lived to age 65.
In the US, the average life
6. There are now more Americans aged over 65 than at any other time in the US his- expectancy at birth is about
tory. Improvements in public health measures such as better sanitation, immuni- 5 years longer for woman, but
zations and advances in medicine such as antibiotics have all contributed to the decreases to about 2.5 years
increase in life expectancy. at age 65.
7. In 2010, the number of people over age 65 was 40.3 million, about 13% of the
population. By 2030, about 20% or one in five Americans will be aged over 65.
a. Individuals over 65 can be divided into the young-oldages 65 to 74, old-
oldages 75 to 84, and the oldest-oldthose aged over 85. The oldest-old
are sometimes referred to as the frail elderly.
b. Each group of elderly has different needs and services, and programs should be
tailored to the needs of each group.
c. The young-old need programs and services that reintegrate them into meaning-
ful roles and activities after retirement, whereas the older-old need supportive
and protective programs.
d. However, the aging process is so highly individualized that, although these cat-
egories help in planning for populations, chronologic age may not serve as an
accurate predictor of an individuals physical ability and health.
8. The average age of the US population is shifting as people live longer, fertility
rates decrease and immigration declines.
9. As more people are living longer, a higher proportion of deaths are being com-
pressed into a shorter age interval at the end of life. This is known as the com-
pression of mortality.
10. The shift to an aging population has important implications for work force projec-
t
tions. Although only accounting for about 13% of the population, older adults ac-
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Quick HIT count for about one-third of physician visits and one-third of hospitalizations.
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B. The maximum life span is defined as the length of life the members of a species can
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For humans the maximum
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life span is considered to be expect to live.
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120 years.
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1. For humans, the maximum life span is considered to be 120 years, and the oldest
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documented human was Jeanne Calment, who lived to an age of 122.
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2. Unlike life expectancy there has not been an increase in the maximum life span.
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a. The linear decline in organ reserve mandates a point at which function is unable
Quick HIT to support life. About 20% of physiologic reserve is the minimum needed for
basic life processes.
The maximum recorded life b. The frail elderly individual who gradually fails at home or who experiences a
span for humans has not in- catastrophic hospital course with multiple organ failure from a relatively minor
creased over the past century.
insult are examples of humans reaching their physiologic limits.
C. Causes of death and chronic disease (see Figure 1-1)

1. At the turn of the century, the leading causes of death were pneumonia, influenza,
and tuberculosis.
2. Over the past century there has been a shift in the causes of death in the US from
acute infectious diseases to chronic diseases. Now the three leading causes are heart
Quick HIT disease, cancer, and stroke, which combine to account for almost 60% of all deaths
The three leading causes among those aged 65 and older.
of death in the US are heart 3. Although there is a decline in rates of disability, about 85% of older adults can ex-
disease, cancer, and stroke, pect to have at least one chronic illness and 60% of those over 85 have two or more
which account for about 60% chronic illnesses.
of all deaths of those aged 65
and older. D. Compression of morbidity and mortality
1. As more individuals live longer, there has been a compression of mortality or a
reduction in the variability of the age at death, leading to a progressive squaring of
survival curves (Figure 1-2).
Clinical Vignette 1-1

The oldest documented life span was that of J ean Calment, a French woman who lived to
be 122 years old. She was physically active, played tennis, roller skated, swam, and enjoyed
music. She rode a bicycle until age 100. At age 110 increasing frailty forced her to move into
a nursing home and at age 115 she fell and fractured two bones. By age 120 her memory was
impaired and she was very hard of hearing. She died at 122.
Caus e o f De ath Amo ng U.S . Adults

Ag e d 65 Ye ars o r Olde r, 2007
He a rt dis e a s e 28.2
Ca nce r 22.2
S troke 6.6
Chronic lowe r re s pira tory dis e a s e s 6.2
Alzhe ime r's dis e a s e 4.2
Dia be te s 2.9
Influe nza a nd pne umonia 2.6
Uninte ntiona l injury 2.2
All othe r ca us e s 24.9
0 5 10 15 20 25 30
Pe rc e ntag e o f all de aths
FIGURE
1 -1 Leading causes of death among US adults.
(Adapted from CDC, National Center for Health Statistics. National Vital Statistics System. Atlanta, GA: CDC, 2007.)
T
100
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1980
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1960
e
75
r
g
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a
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1940
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v
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i
1920
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50
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s
a
t
1900
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e
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r
n
25
e
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0
0 10 20 30 40 50 60 70 80 90 100
Age
FIGURE
1 -2 Changes in survivorship in the United States. As more individuals live longer the curves
squares off, sometimes referred to as the squaring of mortality.
(Adapted from Fries J F, Crapo LM. Vitality and Aging. San Francisco, CA: W.H. Freeman, 1981.)
2. Fries also proposed the concept of compression of morbidity.

a. This occurs if the age of onset of infirmity can be postponed more rapidly than
the age of death, thereby compressing the burden of illness into a shorter period
of time before death.
b. Delaying the onset of aging manifestations and chronic disease shortens or
compresses the period of morbidity prior to death and allows a person to
maintain a higher quality of life into their later years.
c. The assumption of the compression of morbidity theory is that while it will be
possible to delay the onset of disease, the corresponding increases in longevity
will be more modest.
d. While compression of morbidity is generally accepted, others suggest that in the
future we will experience a failure of success as the first symptoms of aging
and chronic illness will remain the same, but life expectancy is extended.
e. In this situation, although humans will live longer, they will also experience
more years of disability and illness.
Cha ng e s o f A g ing
Quick HIT A. Aging and disease are not synonymous. Although the aging process makes individuals
more vulnerable to illness and disease, pathology is not inevitable with age.
Although the aging process
makes individuals more vul- B. Most geriatricians do not view aging as a disease, because aging is a natural process
nerable to illness and disease, and, unlike disease, aging is universal. Because the term disease carries negative
pathology is not inevitable
with age.
connotations, adopting the aging-as-disease viewpoint potentially adds to the negative
view of aging so prevalent in todays society.
C. Aging is a diverse process, in that it differs not only from individual to individual but
also among the organ systems of an individual.
1. Biologic aging and chronologic age are not the same.
2. Aging alone generally does not cause symptoms.
D. Some changes previously attributed to aging are now thought to be related to lifestyle
variables.
1. Genetic make up may only account for 25% of the variability in human longevity,
with much of our health and well-being determined by environmental factors.
2. Aging may be slowed to some extent by maintaining a healthy diet, exercising, and
t
n
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engaging in other healthy lifestyle habits. Figure 1-3 shows how lifestyle influences
i
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a
fitness.
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E. The major age-related biologic change is a diminished reserve capacity and the
t
a
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inability to maintain homeostasis in the face of stressors such as a disease or adverse
r
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environmental factors such as excessive heat.
e
1. Although physiologic aging can be viewed as the erosion of organ system reserve,
h
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most organ systems generally function adequately unless stressed.
2. Age-related changes are most pronounced in the oldest-old, e.g., those aged
Quick HIT over 85.
3. Sometimes it may be difficult to distinguish normal aging from pathology. For ex-
The major age-related biologic
change is a lessened reserve
ample, the anatomic changes of plagues and neurofibrillary tangles seen in those
capacity and the inability to with Alzheimer disease may also be seen in normal individuals, although usually
maintain homeostasis in the not to the same degree.
face of stressors such as a
disease or adverse environ- F. A diminished physiologic reserve makes older individuals more vulnerable to disease.
mental factors such as exces- 1. About 90% of older individuals have at least one chronic disease. Many may have
sive heat.
multiple chronic conditions, making management more complex and challenging
than in younger adults.
100%
Los s of function due to a ging
Ma xim
n
a l fitn e s
o
i
s
t
c
n
u
f
Amount of function within our control
n
a
g
r
o
f
o
e
g
a
t
Le
n
a
e
st
c
fit
r
e
P
0
Incre a s ing a ge
FIGURE
1 -3 How lifestyle influences fitness.
(Adapted from Rosenthal TC, Williams ME, Naughton BJ . Office Care Geriatrics. Philadelphia, PA: Lippincott Williams & Wilkins,
2006.)
2. The lack of physiologic reserve may reach a point where even minor insults can-
not be overcome, leading to significant dysfunction or even death. The reverse
is also true; minor improvements in health can lead to significant functional Quick HIT
improvement. The accumulation of disease
3. Although there is usually little or no effect on daily activity, the decline in physi- may mask disease. For ex-
ologic reserve results in greater morbidity and mortality from illnesses among ample by limiting mobility,
osteoarthritis might mask
older individuals. As organ reserve decreases to about 20% above basal rates,
cardiovascular disease.
homeostasis becomes very difficult to maintain and death may occur with trivial
events.
G. Biologic aging also affects illness in several other ways:

1. Diseases in the elderly are more likely to present atypically and nonspecifically. A
heart attack may present with dizziness rather than chest pain, a urinary tract infec-
Quick HIT
tion with confusion rather than flank pain or dysuria, depression without sadness, As organ reserve decreases
infection without fever, and congestive heart failure without shortness of breath. to about 20% above basal
rates, homeostasis becomes
2. Symptoms in one organ system may represent pathology in another. A heart attack very difficult to maintain, and
may present with nausea without chest pain, pneumonia with confusion, or a uri- death may occur even with
nary tract infection with a fall. trivial events.
3. Older individuals may underreport disease by attributing symptoms to aging.
a. A patient may attribute a symptom to aging and may not seek out a healthcare
T
h
provider. Physicians, in turn, may mistakenly attribute a symptom to aging and
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may miss a significant potentially reversible problem.
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Physiologic Changes of Aging
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Quick HIT
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Although the sequence of aging changes is similar, a fundamental principle is that the rate
a
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of physical change tends to be quite individual. The physiologic aging an individual ex-
i
e
A fundamental principle of
n
periences depends on genetics, lifestyle choices, and environmental factors. Changes from
t
aging is that the rate of physi-
disease and lifestyle choices are not considered a part of normal aging. cal change tends to be quite
individual.
A. Changes in body composition (see Table 1-3)
1. Lean body mass decreases because of muscle loss and some loss of bone. Body fat
increases relative to muscle mass up until around age 70.
CLINICAL PEARL 1-1

Diseases in the elderly are more likely to present atypically and nonspecifically. Older individuals are also
more likely to underreport disease by attributing symptoms to aging or because of denial.

Providers must be careful to evaluate complaints and not to reflexively attribute a symptom
to age. When a 90-year-old woman was told by her doctor that her left knee pain was what
she should expect at her age, the woman replied that her 90-year-old right knee did not hurt.
TABLE 1-3 Body Composition Changes with Aging

Changes in Body Composition Clinical Impact
Decreased lean body mass Changes in drug distribution

Decreased muscle and bone mass Decreased strength
Decreased total body water Greater risk of falls
Increased percent of body fat (until around 70, then decreases) Greater risk of fracture
Greater risk of dehydration
2. All individuals lose height as they age, but this varies in the age of onset and the
degree of loss.
a. On average, individuals lose about 5 cm in height by age 80.
b. A variety of factors contribute to the loss of height. These include:
Changes in posture
Vertebral compression
Compression of intervertebral discs
Increased curvature of the hips and knees
Decreased lower extremity joint spaces
Flattening of the feet
c. While it may affect how clothing fits, normal changes in height from aging usu-
ally do not cause health-related problems.
3. The percent of body water (TBW) decreases with aging.
Quick HIT a. Decreased TBW places older individuals at greater risk for dehydration.
b. Changes in body composition and body water affect drug distribution.
Aging skin is more prone to
injury and slower to heal. B. Dermatologic changes
1. Skin and hair provide the most visible clues to the aging process.
2. Epidermal cells turnover decreases by about 10% per decade, slowing the skins
healing response to injury.
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3. As individuals age, the skin thins. Thinner skin may allow more moisture to escape
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t
a
and along with a decrease in the functioning of sebaceous glands and sweat glands
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contributes to dry skin.
c
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4. The numbers of melanocytes also decrease, making older individuals more vulner-
t
a
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able to UV damage.
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a. Older individuals are at greater risk for skin cancer.
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b. The loss of melanocytes in hair causes graying.
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5. A decrease in the number of Langerhans cells reduces the skins immune response
and increases the incidence of skin tumors and infections.
6. Vitamin D production diminishes with aging.
7. Overall decrease in hair follicles thins hair along with redistribution of hair.
Quick HIT a. Men tend to lose body hair and experience hair loss around their temples. Male
pattern baldness is common with age.
The activity of the enzyme b. Conversely, in men, there may be an increase in hair growth on the eyebrows,
that synthesizes vitamin D
ears, and nose.
decreases with age.
c. Women usually do not become bald, but may experience thinning hair, a reced-
ing hairline, and a loss of body hair.
d. In women, there may be an increase in facial hair.

A 70-year-old white woman complains of scalp-hair loss. She takes no medications, and her
father became bald at a young age. On physical examination, she has diffuse, nonscarring
hair thinning with a widened part over the central portion of the scalp. How should this prob-
lem be evaluated and treated?
Although sometimes thought of as a male disorder, by age 70 about 40% of woman have
female pattern hair loss. The history should assess the duration and pattern of hair loss. Thin-
ning rather than shedding is characteristic of age-related changes. The scalp should be ex-
amined for signs of inflammation, scale, and erythema.
Female pattern hair loss is usually most prominent over the crown and typically spares
the frontal hairline. As in this case, it is gradual with a widening of the midline part without
bare patches, and there is often a family history of hair loss. In cases of nonscarring hair
loss consistent with female hair pattern loss, there is no data to support routine lab testing,
but experts often recommend testing for correctible conditions such as iron deficiency and
hypothyroidism. The only approved medical treatment for female hair loss is 2% minoxidil.
Increasingly, many women are seeking hair surgery as an option.
8. Skin cells produce less collagen.

a. Cross-linking of the collagen and elastin makes skin less elastic and prone to
wrinkling.
b. Less collagen results in thinner skin, which is more prone to injury.
c. Subcutaneous fat diminishes and increases the risk of injury.
d. With the loss of subcutaneous fat and connective tissue that support the
capillaries, even slight physical trauma can cause blood vessels to rupture and
skin capillaries become more fragile, leading to spontaneous bruising.
Seniors may develop persistent areas of ecchymosis, also known as senile
purpura.
Most often seen on the extensor surfaces of the hands and forearms, these
lesions can take days to weeks to resolve, sometimes leaving a brownish Quick HIT
discoloration that may last months or become permanent. Seniors may develop per-
9. The dermal epidermal junction flattens, making the skin more fragile and easier sistent areas of ecchymosis
to tear. This process also reduces the amount of nutrients available to the epider- without a history of trauma.
mis, impairing skin repair.
10. Toenails grow slower, become thicker and more difficult to cut with aging.
11. A loss of fat padding on the feet predisposes elders to calluses, corns, foot pain,
and ulcerations.
a. One in three people over the age of 65 have problems with foot pain, stiffness, Quick HIT
T
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or aching feet. Common foot problems in
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b. Common foot problems in geriatric patients are outlined in Table 1-4.
e
the elderly include bunions,
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calluses and corns, hammer-
a
C. Musculoskeletal system
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toes, and heel pain.
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1. Muscle strength and endurance decrease with age.
P
a
a. However, perhaps no organ system is more modifiable with age.
t
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b. Training slows muscle loss and can increase strength, even in very old age.
n
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2. Sarcopenia is the loss of muscle mass and contractile strength that occurs with age.
a. Exactly how much muscle loss is due to aging versus disuse is unclear. For ex-
ample, a highly fit 65-year-old may outperform a 30-year-old couch potato.
Quick HIT
Muscle weakness with aging
b. Sarcopenia is associated with increased fatigue, frailty, or an increased risk of
significantly increases the risk
falling and can compromise the function of an older adult. of falling and can compromise
3. The respiratory muscles and rib cage are also affected by aging, decreasing the function.
efficiency of breathing.
CLINICAL PEARL 1-2

Itching is a common complaint in the elderly and is often from dry skin. Medical conditions associated with
itching include allergic reactions, thyroid disease, uremia, and lymphomas. In institutional settings, such as a
nursing home, one needs to be careful not to overlook scabies or lice as a cause for itching.
TABLE 1-4 Common Foot Problems in the Elderly

Bunions A bony growth or misaligned bone at the base of the big toe or sometimes the small
toes. May cause the big toe to bend toward the small toe
Calluses or corns Thickened skin on the toes
Hammertoes Toe joints that curl up and under. Can result in permanently dislocated joints
Toenail problems Thickened, crumbling toenails that can be painful and hard to trim
Neuropathy Often due to diabetescan cause discomfort or lead to foot ulcers from lack of
sensation
Foot deformities May be caused by arthritis, gout
Heel pain Common at the back of the arch. Heel spurs common on x-ray
4. Alterations in muscle function in the gastrointestinal tract and urinary tract in-
crease the risk of constipation and bladder dysfunction.
5. Bone loss is a universal aspect of aging, starting in the 30s. The degree of bone loss
occurs at a highly individual rate and is influenced by diet, exercise, and lifestyle.
Quick HIT a. Aging affects the osteoblasts, which make bone, to a greater degree than the os-
teoclasts, which break down bone.
Muscle strength and endur- b. Although age-associated, osteoporosis is a disease state and is not considered a
ance decrease with age. How- normal part of aging.
ever, training slows muscle 6. With aging there is decreased water content in cartilage and more cross-linking in
loss and can also increase
strength, even in very old age. the collagen fibers, which impacts the ability of the cartilage to cushion pressure on
the bones.
a. Changes in cartilage are the underlying causes for osteoarthritis.
b. There are also similar changes in the tendons and ligament, which can contrib-
ute to decreased flexibility and mobility common to older adults.
7. There is about a 30% decrease in bone marrow cellularity. Normal hemoglobin (Hgb)
Quick HIT levels remain the same for older adults; however, because anemia is so common in
elderly individuals, there is debate about whether levels should be age adjusted.
Changes in cartilage are a. Ten to twenty percent of woman have a Hgb of <12 g/dL and 10% to 20% of men
the underlying cause for have levels <13 g/dL.
osteoarthritis.
t
b. An argument against age-adjusted norms for Hgb levels is that individuals with
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lower levels of Hgb have an increased risk of morbidity and mortality compared
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with those with higher levels.
c
c. Anemia can be linked to illness. Decisions about what investigations are merited
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in those with anemia depends on the clinical setting factoring in comorbidities,
a
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severity of anemia, rate of drop,and mean cell volumes.
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Quick HIT
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D. Respiratory system
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The respiratory system may be 1. The respiratory system may be the system at greatest risk from environmental damage.
the one most at risk systems 2. Age-related changes may be hard to distinguish from changes in the respiratory
from environmental damage. system that arise from environmental factors such as air pollution, occupational
exposures, and smoking.
3. Usually age-related changes in the respiratory system do not significantly impact
performance of normal daily activities. However, there is a diminished respiratory
reserve for tolerating high demand situations such as strenuous exercise or pulmo-
nary infection.
Quick HIT 4. Respiratory system changes include:
Weakened respiratory mus- a. The trachea and lung airways enlarge with age.
cles and a stiffer chest wall b. Weakened respiratory muscles and a stiffer chest wall reduce effective ventilation.
reduce effective ventilation in c. The number of cilia and their activity decline. Glandular cells in the large air-
the elderly.
ways secrete lesser amounts of protective mucous.
d. The cough reflex blunts with age, impairing effective coughing.
e. The nasal and pulmonary mucosa produces less IgA, impairing the ability to
neutralize viruses.
f. Although the numbers of alveoli do not change significantly with age, alveolar
Quick HIT structure and function is altered.
Alveolar walls thin, become less elastic, and enlarge.
V/Q mismatch increases with Fewer blood capillaries are available for gas exchange, reducing the surface
age. area available for gas exchange and resulting in mismatching of ventilation
and lung perfusion (V/Q mismatch).

A healthy 66-year-old with a recent drop of Hgb from 13 to 11.5 and with microcytic indices
requires investigation. In contrast, a 75-year-old woman with rheumatoid arthritis, mild renal
insufficiency, and a normocytic anemia with an Hgb of 10.5 that has been stable for years
likely needs no further investigation.
g. An increase in cross-linked collagen and fewer elastic fibers give the lungs less
elastic recoil.
h. Spirometry changes include a decrease in forced vital capacity and an increase in Quick HIT
residual volume. Before attributing shortness of
From ages 30 to 80, vital capacity decreases linearly. breath to a functional decline,
FEV1 diminishes about 30 mL per year after around age 30. consider other diseases such
as COPD, heart failure, and
Residual volume increases by about 50%.
cancer.
i. The pulmonary vasculature becomes stiffer and less elastic, thereby increasing
pulmonary artery pressure.
E. Gastrointestinal system
1. Aging of the gastrointestinal system causes fewer serious problems than most other
organ systems. Quick HIT
2. Older individuals make less saliva and more frequently complain of a dry mouth Aging of the gastrointestinal
than younger individuals. system causes fewer serious
a. Complaints of dry mouth may be related to medication or nutrition effects rather problems than most other or-
gan systems.
than aging.
b. A lack of saliva and the gradual wearing down of tooth enamel make older indi-
viduals more susceptible to caries.
3. While there may be a modest change in taste, taste and smell are linked, and the
T
Quick HIT
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loss of smell along with diminished saliva is one reason older patients may com-
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plain that food no longer tastes good.
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Although liver function is fairly
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4. Many older individuals spice and salt their food more heavily to compensate for
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well preserved with agethe
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altered taste and smell.
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liver becomes less efficient in
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5. The stomach secretes less HCl and produces less intrinsic factor, which is needed eliminating drugs.
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a
for the absorption of vitamin B12.
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6. While there is a decrease in production of gastric and pancreatic enzymes, there is
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no appreciable change in fat, protein, or carbohydrate digestion.
7. Hepatic blood flow, size, and weight decreases with age, leading to less efficient
elimination of drugs while maintaining overall function. Quick HIT
8. Decreased intestinal muscle tone results in slower peristalsis and increased transit
Slower peristalsis makes con-
time. stipation a common complaint
a. Older individuals are at greater risk of constipation. among the elderly.
b. Transit time is influenced by lifestyle, e.g., taking sufficient fluids, consuming
adequate fiber, and being physically active.
F. Urinary system
1. The kidneys become smaller with age, and there is about a 20% to 30% change in
size by age 90.
a. The change in size occurs primarily in the cortex, where the number of glom-
eruli decreases by about 30% to 50%.
b. There is gradual increase in glomerular sclerosis.
c. There is a loss of renal tubular cells and a thickening of the tubular walls, which Quick HIT
impair the kidneys ability to concentrate or dilute urine.
Aging kidneys cannot dilute
Consequently the aging kidney cannot adapt as efficiently to fluid overload or or concentrate urine as
dehydration. effectively.
2. Renal blood flow decreases with age because of a decrease in cardiac output and
changes in the renal blood vessels.
CLINICAL PEARL 1-3

Constipation is common in the elderly and often resolves with an increase in fiber, fluid, and activity. Constipa-
tion can also be a sign of a more serious illness such as colon cancer or of systemic problems such as hypothy-
roidism, hypercalcemia, and hypokalemia. Constipation can also be a side effect from many medications.
3. GFR declines at about 1% per year, starting at about age 35. By age 75, GFR may be
about 50% less than that in a young adult.
4. Several formulas can be used to calculate creatinine clearance (CrCl), which is used
to estimate glomerular filtration rate (GFR). The most commonly used formula is
the CockcroftGault formula, which is as follows:
Quick HIT (140 age) weight (kg)/serum creatinine (mg/dL)
A smaller bladder capacity 72 (0.85 for females) = CrCl (mL/min)
and a decrease in the ability to
concentrate urine are reasons 5. The bladder, ureter, and urethra are muscular structures that tend to lose tone and
why older individuals urinate elasticity with age.
more frequently.
a. The loss of muscle tone may lead to incomplete emptying of the bladder and a
greater risk of infections.
b. Prostate enlargement may contribute to incomplete bladder emptying in men.
6. Bladder capacity may decline from about 350 to 500 cc to about 200 to 300 cc in
older age.
a. This causes the need for more frequent urination as individuals age.
Quick HIT G. Cardiovascular system
After age 50, it is not uncom-
1. Anatomical changes include the following:
mon for men to have to get
a. An increase in left ventricular wall thickness and in fatty infiltration in the tis-
t
n
up at least once a night to
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urinate. sues surrounding the heart.
i
t
a
b. Decreased contractile strength of the heart muscle.
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c. The heart valves harden and thicken, making them less efficient.
c
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Soft systolic grade I to II heart murmurs are heard in about 50% of older
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adults.
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d. Pacemaker cells diminish in number, and there is increased fat and fibrous tis-
Quick HIT
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sue infiltration of the conduction system, which may result in decreased resting
T
Aging is strongly associated heart rate with increasing age.
with heart disease, but it is e. Blood vessels become thicker and less elastic, impairing their ability to expand
not certain what occurs in the and contract.
absence of disease. It is unclear whether atherosclerosis is an age-related or age-associated disease.
Lifestyle influences such as smoking, diet, and exercise are a major factor in
how well the blood vessels age.
One argument that atherosclerosis is not a normal part of aging is that in some
primitive cultures adults typically do not develop atherosclerosis.
Quick HIT 2. Functional changes may include the following:
Blood vessels become thicker a. Systolic blood pressure may increase with the loss of arterial distensibility.
and less elastic, impairing b. There is an age-related decline in the maximum heart rate that usually does not
their ability to expand and significantly affect normal activity, but it may be problematic in situations where
contract. Systolic blood pres- the heart is stressed and required to beat faster.
sure may increase with loss of
Stresses include physical exertion, emotional stress, injury, surgery, or
arterial distensability.
infection.
Several formulas exist to calculate the theoretical maximum heart rate (max
HR) based on age.
The most common simple formula to estimate max HR is (220 age), which
for a 65-year-old equates to a max HR of 155.
(1) This formula tends to underpredict the max HR in older individuals and
overpredict the max HR in younger adults.
(2) Tanaka proposed 208 (0.7 age) as being more accurate to estimate
max HR. Table 1-5 includes other formulas used for estimating max HR.
Exercise does not eliminate the decline in maximum heart rate, but may slow it.
c. Arrhythmias, such as skipped beats or extra beats are more common in older
individuals.
Quick HIT Atrial fibrillation is common in those aged over 65 (>5%) and is related to
anatomic changes in the conduction system.
Age-related anatomical
The aging heart fills more slowly, and to compensate this, elder individuals
changes make arrhythmias
more common in older adults. rely more on atrial contraction for ventricular filling, making them more vul-
nerable to cardiac decompensation from atrial fibrillation.
TABLE 1-5 Formulas Used to Predict Maximum HR

Formula Comment
Miller formula: Used for planning exercise, add 4 beats per

217 (0.85 age) minute for elite athletes
Whyte formula: Adjusts for gender:
Male: 202 (0.55 age); 65-year-old male equals 166;
Female: 206 (0.88 age) 66-year-old female equals 148
Tanaka formula:
208 (0.7 age)
220 age
TABLE 1-6 Principle Changes in the Cardiovascular System

Quick HIT
Increased stiffness of the blood vessels
The brain loses volume with
T
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Increased stiffness of the myocardium aging. Gray matter is affected
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Decreased -adrenergic response more than white matter.
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Impaired SA node function
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Impaired endothelial cell function
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Overall reduction in cardiovascular reserve
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Quick HIT
TABLE 1-7 CNS Changes Normal aging results in
plaques and tangles like those
seen in AD, although not to the
CNS Changes Clinical Impact same degree.
Decrease brain mass Atrophy on CT or MRI scans

Decreased dopamine receptors Tendency toward parkinsonismgait changes
Increase parasympathetic response Sensitivity to anticholinergic drugs
Slower reflexes Tendency to fall
Decrease in acetylcholine Diminished reflexed on exam
Poorer two-touch discrimination
d. The aging heart exhibits decreased -adrenergic response.

e. Table 1-6 lists principle changes to the cardiovascular system.
H. Nervous system (see Table 1-7)

1. The brain loses neurons with age, and about 20% of brain weight is lost by age 85.
a. Neuronal loss disproportionately affects the gray matter, e.g., the cerebral cortex
and hippocampus.
b. Gray matter atrophy with normal aging is usually mild as compared to the more
extensive loss seen in those with dementia.
2. Lipofuscin accumulates in nerves cells as individuals age. There is also some accu-
mulation of neuritic plaques and neurofibrillary tangles.
a. These anatomical changes are also characteristic of Alzheimer disease (AD), but
are present to a much greater degree in those individuals with AD.
3. From age 30 to 70 cerebral blood flow decreases by about 15% to 20%.
4. There are age-related changes in neurotransmitters.
a. Decreased dopamine and acetylcholine receptors.
b. Decrease in the amount of acetylcholine.
5. Short-term memory and the ability to learn new information may diminish with
age, but in the absence of disease, intellectual performance is usually maintained
until late in life.
6. Reaction time and performance of tasks slow with age because the nerve impulses
transmit more slowly.
7. Sleep patterns change with age with more time spent in lighter states of sleep and
less time in deeper stages.
8. As individuals age, there is a loss in the number of touch receptors in the skin and
a higher threshold to stimulate the remaining receptors.
a. The response to painful stimuli and temperature decrease with age.
b. Changes in touch may affect older individuals in subtle ways. For example,
diminished sensation in the soles of the feet increase the risk of falling, or diffi-
culty in assessing the amount of pressure to pick something up may lead to their
dropping more items such as a glass or a fork.
I. Taste and smell

1. The evidence regarding changes in taste with aging is unclear, but data suggest that
there is an increase in the threshold for detecting sweetness and salt. Table 1-8 lists
the clinical impact of these changes.
a. Changes related to taste may be caused by local factors that interfere indirectly
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with the mechanism of taste.
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b. Poor oral hygiene, dental disease, tobacco use and changes in salivary gland
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function all alter taste perception.
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c. Older adults tend to prefer more highly seasoned food as they age.
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2. Smell is more affected than taste with age and declines rapidly after age 50.
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a. Odor identification worsens and odors need to be stronger and more intense to
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be perceived and identified.
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b. By age 80, smell is about 50% worse than at peak capacity.
Smell is far more affected by c. The inability to detect a gas leak or to detect spoiled food might adversely affect
aging than taste. It may be
an older individuals health.
that much of the changes in
taste experienced by older d. Taste and smell are closely linked, and the loss of smell may dampen the enjoy-
individuals are related to ment of food.
changes in smell and local
factor such as poor dentition. J. Vision
1. The tissues around the eye atrophy, and the muscles weaken with age.
a. The upper lid may droop and the lower lid may turn either inward (entropion)
or outward (ectropion).
2. Tear production decreases and complaints of dry eye are common among older
adults.
3. The iris become more rigid and the pupils smaller.
4. Eye color may fade.
5. The cornea becomes thicker and less curved with age.
TABLE 1-8 Impact of Taste Changes

Problems Related to Changes in Taste
Loss or increased appetite

Loss because of no taste
Increased intake to achieve some taste
Complaints about how food taste
Mistaken identity of foodcannot identify spoiled food
Excessive seasoningincreasing sugar, salt
6. The cornea and lens yellow with age, making them less transparent to blue light.
a. Changes in color perception are common with aging and it may be more difficult
to distinguish between darker colors than to distinguish between brighter colors.
b. Painting doors with different bright colors might help orient older adults to
their surroundings.
7. With age the lens becomes denser, thicker, and less elastic.
8. Presbyopia is the age-related visual change in which it becomes more difficult to
focus on near objects.
a. Presbyopia results from the decrease in lens elasticity and atrophy of the ciliary Quick HIT
muscle, the muscle which changes the shape of the lens.
Glare from lights at night
b. Eyeglasses can usually correct visual problems associated with presbyopia. may be a sign of cataracts or
9. Retinal changes include a loss of rods and cones and a decline in light and dark glaucoma. A loss of central
adaption. vision suggests macular
10. Overall visual ability decreases with age due to presbyopia, a decreased ability to degeneration.
accommodate, fewer receptor cells (rods and cones) and less light reaching the
retina because of smaller pupils.
11. Glare is a common problem as the lens, cornea, and vitreous humor become less
clear, and minute particles scatter light.
a. Glare can cause problems especially at night or when driving.
b. Visual changes make it important to increase illumination, eliminate glare, and
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use strategies such as larger print material to offset the effect of age-related
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changes in visual acuity.
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K. Hearing
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1. The auditory canal atrophies with age, resulting in thinner canal walls and de-
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creased cerumen production.
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2. The tympanic membrane thickens and may appear duller and whiter when com-
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pared to younger individuals.
3. Ossicular joints can degenerate, contributing to hearing loss with aging. Presbycusis is a general term
4. There is a loss of hair cells in the organ or Corti and combined with a loss of co- used for the hearing loss in
chlear nerve cells contribute to presbycusis, a general term that describes the hear- older individuals. It typically
ing loss reported in older adults. affects higher frequencies to
a greater extent than lower
a. Both the central and peripheral parts (ocular nerve) of the auditory system are frequencies.
effected by aging.
b. Presbycusis affects the higher frequencies, e.g., 2,000 to 4,000 mHz to a greater
extent than the lower frequencies.
c. The degree that hearing loss is related to age alone versus noise exposure re-
mains uncertain.
L. Immune system
1. The efficiency of the immune system declines with age and is associated with an in-
creased susceptibility to infection, reduced efficacy of vaccination, and an increased
inflammation and level of inflammatory markers.
a. Nonspecific immune defenses diminish with age.
b. The ability to make antibodies diminishes. Quick HIT
2. The thymus gland, which is important for activating T cells, atrophies with aging. Aging diminishes the immune
a. The number of T cells decrease and peripheral T cell response slows with aging. systems response to infection.
M. Endocrine system
1. There is a progressive decline in carbohydrate tolerance and increasing insulin
resistance.
2. The levels of aldosterone, renin, calcitonin, and growth hormone decrease with age.
3. The levels of thyroid hormones (T3 and T4), cortisol, insulin, epinephrine, and
parathyroid hormone levels remain the same or only decrease slightly with age.
4. Follicle-stimulation hormone (FSH), luteinizing hormone (LH), and norepineph-
rine levels increase with age.
a. In women, estrogen and prolactin levels decrease after menopause.
b. The testosterone levels decrease with age, and there is also a blunting in the di-
urnal rhythm of testosterone levels that is noted in younger men.
N. Reproductive/sexual
1. As a general rule, everything slows down.
2. In men, the following are observed:
a. More intense stimulation is needed for erection and erections are less firm.
b. Ejaculation takes longer and occurs with less volume and intensity.
c. There is a longer refractory period.
d. The testes continue to produce sperm, but the rate of production slows and the
epididymis, seminal vesicles and prostate gland lose some of their ability to pro-
duce the fluid that carries sperm.
e. Men can father children into their 80s.
3. In women, the following are observed:
Quick HIT a. There are estrogen dependent changes such as thinning of the vaginal wall.
Older individuals are at b. A decrease in vaginal lubrication.
greater risk for both hypo- and c. There is a slower reaction of the clitoris to stimuli.
hyperthermia. d. There may be a longer refractory period.
O. General changes with aging

1. Physiologic changes make older adults more vulnerable to periods of stress such as
extremes of temperature and dehydration.
2. The reasons for the tendency to hypothermia are multifactorial and include a de-
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crease in subcutaneous fat, decreased shivering, decreased awareness of cold, less
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Quick HIT ability to vasoconstrict in order to conserve heat and a decreased metabolic rate.
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a. Conditions such as malnutrition, hypothyroidism, and stroke that are more com-
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A decreased ability to va- mon in elderly individuals also place older adults at risk for hypothermia.
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sodilate, a decline in sweat b. Extrinsic factors such as poverty, e.g., inability to afford air conditioning may be
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production, and an impaired a contributing factor.
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sense of temperature and
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3. Older adults are also at great risk for hyperthermia due to decreased ability to vasodi-
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thirst all contribute to making
older adults more vulnerable late, a decline in sweat production and an impaired sense of temperature and thirst.
to heat. 4. Aging increases the risk of dehydration.
a. The loss of fluid balance homeostasis is multifactorial and includes a lower per-
centage of total body water, a blunted thirst sensation, reduced renal blood flow
and a decrease in the ability to concentrate urine.
b. Physiologic changes in maximum cardiac output, impaired left ventricular fill-
ing and function, and a decline in maximum heart rate all contribute to making
older adults more vulnerable to developing hypotension and shock.
Quick HIT P. Clinical implications of the aging process
Biologic changes associated 1. Aging changes affect the clinical approach to the older patient, and the increased
with aging make it important biologic uniqueness seen in older patients makes it even more important to indi-
to tailor the clinical approach vidually tailor the clinical approach.
to the individual. 2. Typically, the older and frailer a patient is, the more the approach will differ from a
younger patient.
3. Aging changes make it important to evaluate the clinical setting, how the interview
is conducted, how symptoms are elicited and an awareness of how the physical
exam and testing may differ in older individuals.
4. The clinical setting should be age-friendly to foster good communication and an
Quick HIT adequate evaluation.
The older and frailer the pa- a. Sensitivity to temperature extremes means careful attention that the exam room
tient is, the more different the is neither too hot nor cold.
clinical approach will be. b. The exam room should be well lit to compensate for visual changes.
c. Many elderly have hearing deficits, and the examiner should face the speaker
with their mouth at eye level, speaking clearly, but not shouting, and keeping
extraneous noise to a minimum.
Quick HIT d. Make sure individuals bring any adaptive devices they use such as glasses, hear-
ing aids, canes, walkers, and glasses to their appointment.
Patients should be asked to e. Allow adequate time, and pace the interview to match the patient. If the patient is
bring any assistive devices easily fatigued, it may be wise to break the evaluation into multiple appointments.
they use to their appointment.
f. Providing comfortable chairs with sturdy arms and a back high enough to
provide back support and an exam table that is easy to get onto is important.
Pillows are useful to provide neck and back support.
TABLE 1-9 Examples of Common Potentially Treatable Conditions

in the Elderly
Condition
Depression
Diabetes
Foot disorders
Hearing and vision disorders
Hypothyroidism
Iron deficiency anemia
Nutritional deficiencies
Oral disorders interfering with eating
Heart failure
COPD
Basal cell carcinomas
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Falls
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Osteoporosis
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Polymyalgia rheumatica and temporal arteritis
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Parkinson disease
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g. Examination areas should be large enough to accommodate a walker or a wheel chair.
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and an emergency button.
i. It is important to remember that older patients should be treated with respect
and care, but not as children. Calmness and patience are key factors for a suc-
cessful healthcare encounter.
5. Older patients frequently have chronic conditions such as arthritis that, if effec-
tively managed, can improve their functional abilities and quality of life.
6. In approaching the elderly patients, the clinician should keep in mind those illnesses
more common among the elderly, especially those that are more potentially treatable.
Table 1-9 lists some of the more common problems to keep in mind and for which
effective management can potentially improve function and quality of life.
Ge ria tric A s s e s s m e nt
A. The comprehensive geriatric assessment (CGA) is a multidimensional,
multidisciplinary assessment designed to evaluate elderly individuals with complex Quick HIT
problems. Table 1-10 summarizes the key elements of a CGA. CGA is designed to evaluate
an older persons functional
B. The principal domains assessed are functional ability, physical health, cognition,
ability, physical health, cogni-
mental health, and the socioenvironmental situation. tion, mental health, and socio-
C. CGA differs from a typical medical evaluation by placing a greater emphasis on economic and living situation.
assessing function, quality of life, and nonmedical domains. Table 1-11 lists some
useful measures to screen for functional problems.
7. A full CGA frequently incorporates the expertise and perspective of other health
providers:
a. Dietitian
b. Social worker
c. Pharmacist
d. Occupational therapist
e. Psychologist
f. Speech therapist
g. Physical therapist
TABLE 1-10 Elements of a Comprehensive Geriatric Assessment

Detailed problem list based on history, physical, and appropriate testing
Assessment of hearing, vision, and mobility
Medication review and reconciliation
Nutrition assessment
Functional statusADLs and IADLs
Incontinence assessment
Assessment of cognition and mental health
Evaluation of support structure
Assessment of current and anticipated living environment
Legal issues, e.g., living wills, end-of-life issues
Fall risk assessment
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TABLE 1-11 Useful Screening Measures for Functional Problems
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in Older Individuals
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Condition Screen
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Hearing Ask about trouble talking on the phone or if the TVneeds to be much louder
for them. Can check pure tone audiometry or whisper test
Vision Check acuity with Snellen eye chart. Functional ability can be checked by
asking to read newspaper and inquire about difficulty driving, reading, or
watching TV
Screen for malnutrition Check for BMI <20 kg/m2. Inquire about recent weight gain or weight loss.
An involuntary weight loss of 10 pounds within the last 6 months suggests
malnutrition
Urinary incontinence In the past year, have you ever lost control of your urine and gotten wet?
Mobility and balance Inquire about falls within the last year. Ask about difficulty with walking or
risk for falls balancing. Perform timed get-up-and-go test
Medications Ask patient to bring in all current medications for review and compare with
chart medication list. Confirm the patient understands their medications and
is taking them correctly
Cognition Perform a simple initial screen such as the 3-item recall or the Mini-Cog.
More detailed evaluation for those who fail screen
Alcohol CAGE questionnaire (refer to Substance Abuse in Chapter 3)
Tobacco Inquire about use
Depression Ask: Do you often feel sad or depressed? If yes, do a more complete geriatric
depression screening.
Function Check ADLs and IADLs. Rapid screen: Do you have difficulty with shopping,
housework, walking, bathing or showering, managing finances? Inquire as to
who provides help if needed.
Social assessment Inquire about advanced directives, support system, and caregiver burnout.
Assess safety of environment, possibility of elder mistreatment
CLINICAL PEARL 1-4

In geriatrics there is a shift toward maintaining function from curative treatment.
D. The patients who typically benefit the most from a CGA are the frail elderly and those
who experience a nonspecific loss in physical, cognitive or mobility function. Some
indications are given below:
1. Older than 75
2. Those needing help with daily activities
3. Requiring a caregiver
4. Living alone
5. Having a recent fall
6. Experiencing delirium or confusion
7. Having incontinence
8. Two admissions to an acute care hospital within the past year
E. Benefits of a comprehensive assessment include the following:

1. Identifying and addressing acute problems
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5. Restoring loss of function with the goal of preserving independence
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F. A skilled CGA reduces morbidity, mortality, and NH placement and yields greater
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satisfaction with care. A focus on function is a key
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element of the CGA.
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G. A focus on function is a key element of the CGA.
1. Functional status refers to a persons ability to negotiate their environment and to
perform the tasks required for life.
2. Physical, psychological, and socioeconomic factors interact in complex ways to in-
fluence the function of the elderly.
H. There are two main categories for assessing functional capacity: ADLs and
instrumental ADLs (IADLs).
1. ADLs are self-care activities that include tasks such as bathing, dressing, eating,
grooming, toileting, and transferring.
a. The activities are usually divided into three performance levels: Quick HIT
Able to do without assistance ADLs are self-care activi-
Needing some assistance ties that include tasks such
Dependence as bathing, dressing, eat-
2. IADLs are higher-level activities that are needed to live independently. They ing, grooming, toileting, and
transferring.
include:
a. Housekeeping
b. Preparing meals
c. Using the telephone
d. Shopping
e. Managing ones transportation
f. Managing finances Quick HIT
g. Taking medications IADLs are higher level activi-
3. Observing how a patient manages a healthcare visit provides significant insight into ties such as managing money
the level of function. and shopping needed to live
independently.
a. How they complete forms
b. How well they communicate
c. How well they understand
d. How they dress
e. How they climb up and down from the exam table
I. Deficits in ADLS or IADLs suggest the need for a more detailed evaluation of the
patients setting, support systems and the need for assistance. The ultimate value of a
CGA lies in the follow-up actions.
1. An effective CGA yields solutions for hard-to-manage patients, with a focus on im-
proving/maintaining function.
2. An effective CGA establishes a plan to coordinate care among the providers caring
for the patient.
J. A functional decline may be complicated by income level, family support, and

self-esteem.
K. The traditional medical assessment should be supplemented by briefly screening for

common geriatric conditions and nonmedical issues that are particular relevance to
the health of older individuals. These include:
1. Nutrition
2. Vision
3. Hearing
4. Balance
5. Fall risk
6. Depression
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10. Social support
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12. Environmental risks
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L. Many clinicians use more extensive questionnaires to screen for conditions or to
follow up on those who fail a simple screen.
M. Outcomes of CGA
1. A CGA usually generates several recommendations.
a. Changes in medications (e.g., discontinuing unnecessary or problematic drugs)
b. The need for further testing (e.g., a work-up for cognitive impairment)
c. Referrals to specialists
d. Rehabilitation recommendations
e. Referrals to community or home care agencies
2. The wide range of CGA programs makes it difficult to evaluate their effectiveness,
but the evidence to date suggests that comprehensive assessment can improve func-
tion, satisfaction with care and quality of life.
a. Attention to making sure recommendations are implemented and followed over
time are keys for success. Clinical Vignette 1-5 provides a brief illustration of a
CGA.
P re ve ntive Ca re fo r the O ld e r A d ult

A. Background information
1. The goals of prevention are to prevent or mitigate illness, functional decline, or
premature death.
a. Prevention remains important after age 65, because men at age 65 can expect to
live 17 more years and women 20 more years.
b. Many older adults are enthusiastic about maintaining their health and seek pre-
ventive healthcare advice.
c. Disagreement about preventive care and screening recommendations among dif-
ferent organizations can make it challenging to advise older patients. Organiza-
tions making recommendations include the following:
The United States Preventive Services Task Force
The Centers for Disease Control

J .Z., an 85-year-old woman, is brought in by her daughter to the CGA clinic because of in-
creasing forgetfulness. She has a history of falling and breaking her wrist 3 years ago and two
recent noninjury falls at home. She lives alone, driving only short distances and to the store.
She is reluctant to leave home because of urinary urgency and occasional difficulty control-
ling her urine. She takes several medications including a diuretic for high blood pressure. Her
daughter reports that she has lost 15 pounds in the last 3 months. J .Z. does not have a living
will and does complain of loneliness.
On physical examination she appears gaunt with a blood pressure of 170/80 and a BMI of 20.
She is alert and oriented to person, place, and knows the year and month, but not the day. She
fails to recall any of three items after 1 minute. She finds it difficult to climb onto the exam table
and has difficulty hearing someone speak. Her daughter confirms that she can manage her own
self-care without assistance, but both she and her daughter report trouble with her IADLs, with
the exception of using the phone and light housework. Her get-up-and-go test takes 29 seconds.
The problem list generated by her CGA includes (1) cognitive impairment, (2) involuntary
weight loss, (3) possible osteoporosis, (4) impaired balance and mobility, (5) difficulty manag-
ing medications, (6) incontinence, (7) social isolation, (8) no advanced directives or surrogate
decision maker, and (9) possibly unsafe driving.
Initial recommendations by the multidisciplinary team might include the following:
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Cognitive impairmentSchedule a more comprehensive evaluation and testing to define the
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level of impairment and to rule out reversible causes. Discontinue all nonessential medica-
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tions and use a pill box and enlist the family to assist with her medication regimen.
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Weight lossJ .Z. may have lost weight because of difficulty in shopping and preparing nutri-
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tionally adequate meals. Suggest that the family help with shopping and meal preparation and
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arrange for Meals on Wheels to deliver one meal daily. If no improvement in weight over the
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next month, consider further testing for an underlying medical cause for weight loss.
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HearingReferral to audiology for testing and hearing aids if needed.
Osteoporosis and impaired mobility and balanceCheck DEXA scan, supplementary Vitamin
D and calcium. Refer to physical therapy for balance and gait training.
IncontinenceSwitch to a nondiuretic for hypertension and evaluate for other reversible
cause such as infection. If J .Z. is able, try bladder training and scheduled voiding.
Absence of advanced directivesTry to elicit goals. Assist patient and family with develop-
ing advanced directives.
Driving safetyPossibly unsafe because of impaired cognitive function and mobility. Work
with family on alternate transportation and arrange for a formal driving evaluation to assess
safety if she wants to keep driving.
Social isolationScreen for depression. Discuss participation at senior center, adult day
programs and other social settings.
The American Cancer Society

The Canadian Task Force
The American College of Physicians
The American Academy of Family Physicians
Other specialty societies
d. An additional complication is that most guidelines focus on healthier, younger
individuals, and there is little evidence evaluating prevention strategies for
adults aged over 75 or for those who have comorbid conditions.
2. Preventive services in geriatrics include both primary and secondary prevention.
a. Primary prevention interventions target preventing disease from developing in a
person who has no symptoms and no evidence of disease.
b. Common primary prevention interventions include vaccination, counseling
about behavior change, injury prevention, and chemoprophylaxis.
c. Because primary prevention avoids the suffering and burden associated with
disease, it is considered a cost-effective form of health care.
d. Secondary prevention screens for disease in order to identify and treat asymp-
tomatic individuals in which the condition is not clinically apparent and early
Quick HIT detection improves outcomes.
Secondary prevention works best for diseases with a long latency period.
Primary prevention is aimed Examples include colon cancer screening and hypertension.
at preventing disease from
developing. e. Tertiary prevention involves the care of established disease with the goals of
restoring function, minimizing the negative effects of disease and preventing
disease-related complications.
Examples include cardiac rehabilitation after a heart attack and prescribing an
ACE inhibitor to a person with CHF.
f. Depending on timeline, an intervention might be considered either primary or
Quick HIT tertiary prevention.
For example, strategies to reduce cholesterol before cardiovascular disease is
Caution should be exercised
when recommending guide- evident are primary prevention while managing hyperlipidemia in someone
lines developed for the gen- with established coronary artery disease is considered tertiary.
eral adult population to older 3. Tests such as a colonoscopy that impose a significant burden may be disproportion-
adults. ately hazardous for a frailer older adult.
a. Cancer screening typically takes years before the benefit of screening is seen and
is also unlikely to benefit individuals with limited life expectancy.
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4. Screening should be tailored to the individual taking into account risk factors, co-
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a. In older adults, screening for reversible conditions that might affect quality of
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Quick HIT
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Several preventive interven-
tions, such as influenza vacci- Clinical Vignette 1-6
nation, are beneficial and cost
effective for older adults. J .O. is an 84-year-old woman with unexplained weight loss and axillary lymphadenopathy.
Her breast examination does not reveal a distinct mass. Although a screening mammogram
in this age group is not recommended, a diagnostic mammogram is indicated to help evaluate
her for an occult breast tumor.
Quick HIT J .S. is a 70-year-old man with a history of progressive Parkinson disease. He requires help
with his ADLs and he and his wife are thinking about NH placement to manage his daily
Screening differs from diag- needs. In contrast, J .A. is a 70-year-old man with well-controlled hypertension who is other-
nostic testing. Screening is wise healthy. He walks 2 miles every day and plays golf weekly.
done in asymptomatic individ- Both J .A. and J .S. have a 63-year-old brother recently diagnosed with colon cancer and
uals while diagnostic testing neither of them have had a screening colonoscopy.
is for those with symptoms. An average life expectancy of about 10 years is needed to benefit from a colonoscopy.
J .A. would likely benefit while the burden of a screening colonoscopy for J .S. would be much
greater and also less likely to yield benefit because of a shorter life expectancy.

R.T, a 90-year-old woman with CHF, is unlikely to benefit from breast cancer screening but
might benefit from testing visual acuity and hearing. Improving vision might improve function
by allowing her to read more easily or to negotiate her environment with a reduced risk of fall-
ing. If R.T. merited a hearing aid, fitting her with one might allow her to be less socially isolated,
might improve cognition, and allow her to more easily listen to her favorite radio talk show.
B. Types of prevention
1. Primary preventionCounseling to change health behaviors
a. Tobacco
About 10% of individuals aged over 65 still smoke.
There is good evidence that smoking cessation benefits older persons.
(1) The risk of lung cancer from cigarette smoking decreases 30% to 50% by
10 years after stopping smoking.
(2) Five years after smoking cessation, the risk of a serious cardiac event is
reduced to that of a nonsmoker.
b. Physical activity
Several groups including the USPSTF recommend counseling about exercise.
Regular exercise is linked to both maintaining physical functioning and reduc-
ing the risk of chronic illnesses such as osteoporosis and coronary artery dis-
ease (see Table 1-12).
Exercise tolerance is one of the hallmarks of maintaining independence in the
elderly. The ability to perform physical activities may be the determining fac-
tor as to whether someone can live independently or needs assistance.
Exercise should be tailored to the individual. The degree of fitness varies
among older individuals and an exercise prescription that gives specific in- Quick HIT
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structions about exercise is a key element for success.
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The ability to perform physical
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The elements of an exercise program include the type of recommended exer- activities may be the deter-
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cise, the intensity, the duration, and the frequency.
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(1) Types of exercise include cardiovascular or endurance exercise, strength- someone can live indepen-
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(2) The risks of exercise include injury and cardiovascular events. If good
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judgment is used about tailoring an exercise prescription to the indi-
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vidual, the benefits of exercise outweigh risks. For example, some indi-
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viduals may require stress testing before starting an exercise program,
and someone with arthritis who finds it difficult to walk might be better
suited for swimming or water aerobics.
CLINICAL PEARL 1-5

An Exercise Prescription
A sample exercise program for an older woman who is able to easily walk 15 minutes might be to advise her
to walk 30 minutes, on average, five times per week and to do strength exercises with light weights three
times a week for 20 to 30 minutes. Since she has not used weights in the past you arrange a visit to physi-
cal therapy to develop a strengthening program. In addition you recommend 10 minutes of stretching twice a
week to maintain flexibility. If you are concerned about a risk of her falling, adding balance exercises such as
tai chi three times a week has been shown to reduce the risk of falling.
TABLE 1-12 Some Potential Benefits of Exercise

Improved aerobic capacity
Reduced mean blood pressure
Increased maximal oxygen consumption
Increased muscle mass and strength
Increased bone mass
Improved flexibility
Improved lipid profile
Reduced risk of falls
Increased sense of well being
Reduced inflammatory markers.
c. Diet
The USPSTF recommends periodically measuring BMI to identify those who
are either under- or overweight. Nutrition is such a key part of good health
that a yearly discussion about diet for older adults is prudent.
d. Injury prevention counseling
Quick HIT Injuries are the fifth most common cause of deaths for individuals aged over
65 with falls accounting for two-thirds of these deaths.
Measuring height, weight The USPSTF recommends counseling older patients and their care givers
and calculating BMI is an about environmental hazards and reducing risky behaviors.
important part of a geriatric e. Oral health
prevention visit. Daily brushing with fluoride-containing toothpaste, flossing, and regular den-
tal checkups are recommended.
f. Immunizations
Annual influenza vaccine should be given to all geriatric patients who have no
contraindications.
Influenza is one of the most effective preventive health measures. Each year
there is an excess of about 20,000 deaths from influenza epidemics and most
of these deaths occur among older adults.
Pneumococcal vaccines is recommended for all persons aged over 65. Rou-
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Quick HIT revaccinate those at higher risk (e.g., aged over 75 years and those with lung
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disease) after 5 years.
c
Annual immunization with the For individuals aged over 65 who have never been immunized against tetanus,
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influenza vaccine is one of
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a primary series should be started. The USPSTF recommends a tetanus-diph-
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the most important primary
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theria booster every 10 years.
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prevention strategies for older
adults. Herpes zoster vaccine is recommended one time after age 60 for immunocom-
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petent adults.
g. Chemoprophylaxis
Chemoprophylaxis with aspirin should be considered when the potential ben-
efits, e.g., heart attack reduction risk, outweigh the risks of GI hemorrhage.
While no routine recommendation exists for taking a multivitamin, many
geriatricians believe it prudent to prescribe a daily multivitamin especially for
individuals consuming <1,000 kcal/day.
The CDC recommends a daily calcium intake of 1,200 mg and 600 IU of
vitamin D for adults aged 51 to 70 and 800 IU for those over 70.
2. Secondary preventionDisease detection
a. Cancer screening
The USPSTF recommends a routine mammogram every 1 to 2 years for
women aged 50 to 74. For women aged 75 and older there is insufficient
evidence to recommend for or against mammogram.
(1) In healthy woman aged over 75, the prudent approach is to discuss the
lack of evidence supporting routine mammograms along with the risks
and benefits.
(2) Many physicians recommend discontinuing routine mammography at
age 75.
Both the USPSTF and ACS recommend screening for colorectal cancer in
persons aged over 50 although the optimal screening regimen is not clear.
Acceptable screening alternatives include: screening with annual high
CLINICAL PEARL 1-6
Use of Aspirin Prophylaxis

In a man aged 60 to 69 with no history of GI symptoms, GI bleeding, or ulcers and who is not taking NSAIDs,
the level at which risk of a cardiovascular event exceeds GI risks from aspirin is about 9%; and for a woman,
about 8%. The risk of GI complications from aspirin increases with age and the risk threshold for ages 70 to
79 is about 12% for men and 11% for women.
sensitivity fecal occult blood testing, sigmoidoscopy every 5 years with FOBT
every 3 years or colonoscopy every 10 years.
Because of the decrease in life expectancy, colon cancer screening is mar-
ginally beneficial in those aged 76 to 85 and in that age group screening Quick HIT
should be reserved for individuals in good health and little comorbidity The benefits of colon cancer
who wish to be screened. The USPSTF recommends against screening those screening diminish after age
aged over 85. 65 and screening among
those aged 76 to 85 should be
Prostate cancer is a leading cause of cancer death in men. However, the USP- limited to those in good health
STF recommends against routine screening for prostate cancer in average- who wish to be screened.
risk males. Although there is evidence that PSA screening detects early-stage
prostate cancer, the evidence that early diagnosis improves outcomes is
inconclusive.
(1) Most prostate cancer progresses slowly and older asymptomatic men with
prostate cancer usually die of other causes. For those who have been
screened for prostate cancer or wish to be screened, screening should be
discontinued at age 75 or if the life expectancy is <10 years.
Counseling about sun protection is prudent, especially in those with a
history of skin cancer, a family history of skin cancer, or have photosensi- Quick HIT
tive skin.
The USPSTF recommends
(1) Recommendations for skin cancer screening differ. The USPSTF states
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against routine prostate can-
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there is insufficient evidence to support screening, the ACS recom- cer screening in average-risk
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mends periodic screening and the AAFP recommends screening high-risk men.
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individuals.
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The incidence of cervical cancer increases with age and many older women
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may not have been adequately screened when they reach age 65.
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(1) If an older person has not been screened for cervical cancer recently they
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should be screened annually at least twice. If both tests are negative fur-
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ther screening can be discontinued because the risk of developing a new
cancer of the cervix is low.
(2) If someone has been screened for cervical cancer routinely and tests are
normal, screening can be discontinued after age 65.
(3) Routine pap smear screening is not required for individuals who have
Quick HIT
had a hysterectomy (removal of uterus and cervix) unless the surgery was After age 65, further screen-
done for cervical cancer or a high-grade CIN lesion. ing for cervical cancer is
Screening for ovarian cancer is not recommended at this time. unnecessary if previous
tests have been consistently
b. Screening for cardiovascular disease normal.
Hypertension is an important risk factor for cardiovascular disease. Blood
pressure should be checked at least annually after age 65.
Individuals with a BMI >28 are at greater risk for heart disease.
(1) Obese older individuals are candidates for dietary and exercise
counseling.
The associated risk of elevated cholesterol for cardiovascular disease contin-
ues up to age 75; above this age the association is less reliable. As cholesterol
levels generally do not increase above age 65, repeat screening after age 65 in
those previously screened and normal is less valuable.
Individuals aged over 65 with known cardiovascular disease, benefit from
Quick HIT
treating elevated cholesterol. Blood pressure should be
checked annually in those
Routine screening for coronary heart disease with a resting EKG or a stress
aged 65 or older.
test in not recommended. Screening may be prudent if it will influence deci-
sion making, such as an exercise recommendation, the decision to treat hyper-
lipidemia or if there are significant risk factors for CAD.
Screening for asymptomatic carotid artery stenosis is not recommended.
A one-time screening for an abdominal aortic aneurysm with an abdomi-
nal ultrasound is recommended for men aged 65 to 75 who have ever
smoked.
c. Screening for other metabolic problems.
The USPSTF does not endorse routine screening for thyroid disease in
the elderly. The American Academy of Family Physicians and American
CLINICAL PEARL 1-7

Thyroid disease is common among the elderly and if an individual is not screened then the threshold for check-
ing a TSH should be low.
Associations of Clinical Endocrinologists do recommend periodic screen-

ing in older woman. Maintaining a high suspicion of thyroid disease and a
low threshold for testing when clinically suspicious for thyroid disease is
prudent.
All women should be counseled about the risks and benefits of vitamin D
Quick HIT supplementation, calcium, and weight-bearing exercise.

The USPSTF recommends screening for diabetes every 3 years in those with a
All women aged over 65 need blood pressure >135/80 mm Hg or with hyperlipidemia.
bone mineral density testing. The USPSTF recommends screening woman after age 65 for osteoporosis at
A DEXA scan is the most com- least once with bone mineral density testing. Other groups also recommend
monly recommended screen-
screening men once after age 70.
ing test.
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d. Screening for other conditions
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Monitoring an individuals functional ability over time is considered an
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important component of geriatric care although there is little research about
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The USPSTF recommends screening for hearing impairment by periodically
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questioning patients about problems with hearing and/or screening with an
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office audiometer.
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The USPSTF does not make a recommendation about the utility of routine
visual screening. However, most geriatricians recommend asking about visual
complaints and checking visual acuity in patients with complaints.
The USPSTF recommends screening for depression in practices that have
mechanisms in place to assure accurate diagnosis, effective treatment, and
follow-up.
The USPSTF does not feel there is sufficient evidence to recommend routine
screening for dementia. However, because of the prevalence of disease and
the potential advantages of early care some geriatricians support using a brief
screen like the Mini-Cog or 3-item recall to determine who needs further
evaluation.
Alcohol remains an important problem in older individuals with approxi-
mately a 10% prevalence of persons aged 65 and older having problems with
alcohol. The USPSTF recommends routinely asking about the use of drugs
and alcohol.
There are several conditions that there are recommendations not to screen for.
The USPSTF recommends AGAINST screening for bladder cancer, pancreatic
cancer, ovarian cancer, urinalysis for asymptomatic bacteriuria and screening
for COPD using spirometry.
There are several conditions that the USPSTF states that there is INSUFFI-
CIENT evidence to make a recommendation about screening. These include
skin cancer screening, hepatitis C screening, glaucoma, screening for dementia
or domestic violence and suicide risk. Other organizations may make different
recommendations. For example, the AAFP recommends skin cancer screening
in high-risk individuals.
3. Tertiary preventionTreatment of disease to lessen its impact
a. The incidence of chronic disease rises with age and tertiary prevention involves
treatment plans aimed at preventing disability and mitigating the impact of
disease.
4. Table 1-13 summarizes common screen measures used for adults aged over 65.
TABLE 1-13 Screening Measures for Adults Aged 65 or Older

Recommendation Screening Option Comment
Tobacco use Counseling/medication Regardless of age, there are benefits

from smoking cessation
Alcohol abuse CAGE questions or other screening 5%10% prevalence among older
tool adults
Exercise Counseling FITT for exercise prescription
Diet Counseling Older adults at risk for both being
underweight or obese
Immunizations Influenza annually One of the most effective prevention
measures
Pneumococcal after age 65 Revaccinate in high-risk individuals
after 5 years
dT booster every 10 years Initiate primary series if never vaccinated
Herpes zoster once after age 60 Do not give if not immunocompetent
Depression screen Subjective questions, e.g., In the USPSTF suggests screening if good
past month, have you felt being let mechanisms available for diagnosis
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down, depressed, or sad? and treatment
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Vision screen Subjective questions and/or visual Correcting visual issue can have sig-
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acuity nificant impact on QOL
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Hearing screen Subjective questions and/or Improving hearing can have significant
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audiometry impact on QOL
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Oral health Counseling about importance of Periodic dental evaluation
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good oral hygiene
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Dementia Mini-Cog, 3-item recall USPSTF insufficient evidence to rec-
ommend for or against screening
Hypertension screen Check BP at least annually Incidence of high blood pressure in-
creases with age
Hyperlipidemia screen Lipid panel Further screening above age 65 less
important in those with good levels
Osteoporosis screen Bone mineral density Screen all woman aged over 65; some
advocate testing men over 70
Colon cancer screen FOBT, sigmoidoscopy, colonoscopy Optimal screening regimen unclear. Ben-
efits of screening diminish after age 75.
Not recommended after age 85
Breast cancer screen Mammography Every 12 years up to age 75. Uncer-
tain benefit after age 75
Cervical cancer screen Pap smear May discontinue after age 65 if previ-
ously tested normal
Skin cancer Counsel sun protection. Skin exam Skin cancer exam recommendations
vary.
Ge ria tric P ha rm a c o the ra p y

A. General overview
1. Epidemiology of older adults
a. While only 13.7% of the population, older adults account for about one third of
all prescriptions dispensed annually.
b. This translates into an average of 2 to 10 prescription and nonprescription medi-
cations daily for those residing in a community setting and 6.69 daily in the
nursing facility population.
2. Polypharmacy rates increase in the geriatric population.

a. Defined as either the concomitant use of multiple drugs or the administration
of more medications than are indicated clinically.
b. Outpatient studies found 55% to 59% of older adults and 44% patient in
the hospital at time of discharge were taking one or more unnecessary
medications.
Quick HIT c. Drug-related problems include adverse drug reactions, increased risk of cogni-
tive impairment, diminished functional status, and increased healthcare costs.
Frail older adults are excluded d. Drug-related hospitalization prevalence has been reported as high as 31% in the
from most of the clinical trials. older adult population.
B. Appropriate geriatric pharmacotherapy is challenging for the following reasons:

1. An increased number of medications increases the risk of drug interactions.
Quick HIT 2. An increasing number of drugs have switched from prescription to over the counter
status and may not be reported by the patient.
Pharmacokinetics is what the 3. An increased number of complex chronic medical conditions.
body does to a drug and phar-
4. Limited data on medication use in the elderly.
macodynamics is how the
body responds to a drug. 5. The changes in pharmacokinetic and pharmacodynamics as one ages.
C. Pharmacokinetics include four componentsabsorption, distribution, metabolism,

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and excretion.
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1. Aging changes that affect drug absorption:
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a. Decreased gastric acid secretion
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b. Decreased splanchnic blood flow
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c. Delayed gastric emptying
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d. Overall, these changes may delay peak drug concentration but usually do not
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affect the total amount of drug that is absorbed (bioavailability).
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2. Changes with aging that affect drug distribution:
In malnourished elderly pa-
tients, the amount of free drug
a. Decreased lean body mass lowers the volume of distribution for drugs that bind
is elevated out of proportion to muscle (e.g., increased risk of digoxin toxicity).
to the total serum drug level b. Decreased total body water lowers the volume of distribution for drugs that are
when compared to patients hydrophilic (e.g., increased risk of aspirin or lithium toxicity).
with normal albumin level. c. Decreased plasma protein binding raises the percentage of free or unbound drugs
One should ask for free drug
level to accurately assess
(e.g., increased the drug effects of phenytoin or warfarin).
the active drug level for this d. Increased total body fat raises the volume of distribution for drugs that are lipo-
population. philic (e.g., increased the duration of activity for diazepam or amiodarone).
e. Overall, most individuals are not affected clinically unless drug clearance is
decreased. The clinical importance of decreased protein binding is that it will
narrow safe therapeutic window levels for drugs that are highly protein bound.
Most laboratory drug measurements include both free and total drug levels, but
free drug is pharmacologically active.
3. Drug metabolism is altered in geriatric patients
Quick HIT a. Aging decreases liver mass and hepatic blood flow. For drugs metabolized by
the liver, metabolism is slower and the medication has a longer elimination
The liver is the most com-
mon organ system for drug half-life.
metabolism. b. Liver metabolism is mostly accomplished by the cytochrome P450 enzyme
system (CYP450) and it involves numerous isoenzymes. There are two pathways
for drug metabolismPhase I and Phase II pathways.
c. Phase I pathway reactions:
This pathway mainly converts a medication to a metabolite which could be
pharmacologically more, equal, or less active than the parent medication.
Quick HIT Common conversion processes are hydroxylation, oxidation, dealkylation,
or reduction.
The most common CYP450
isoenzyme for drug metabo- Phase I pathway usually slows as one agesmedication doses should be
lism is the CYP3A4. This isoen- adjusted in older adults.
zyme is responsible for many d. Phase II pathway reactions
potential clinically significant This pathway converts medication to an inactive metabolite. Aging has mini-
drugdrug interactions. mal impact on this pathway and medications metabolized by this pathway are
preferred for older adults.
4. Renal elimination of medications slows with aging:

a. Decreased renal blood flow, renal mass, GFR, filtration fraction, and tubular
secretion prolong drug half-life and increase plasma drug level. Quick HIT
b. Decreased creatinine production (due to decreased lean body mass) will cause Decreased renal drug elimi-
patients to have lower serum creatinine values and patients with a normal se- nation is the most clinically
rum creatinine may have an abnormal GFR. CrCL is used to estimate GFR and important pharmacokinetic
should always be calculated when dosing medications for the older adults. change in the older adults.
Most drugs are eliminated
c. Using a 24-hour urine collection is best to calculate patients clearance function
by the kidneys and dosage
but it is not always practical and can be expensive. The CockcroftGault formula adjustment based on a pa-
is commonly used to estimate renal function and for drug dosing and adjustment. tients renal clearance status
is crucial to minimize adverse
(140 age) weight(kg)
Estimated CrCl = (0.85 for females) events.
serum creatinine(mg / dl) 72
5. Pharmacodynamic effects are often increased in geriatric patients.
D. Pharmacodynamics is defined as the pharmacologic effect of a drug at its target site
and how the bodys response to that drug. Quick HIT
1. Cardiovascular system homeostatic mechanisms results in an increased risk of The CockcroftGault formula
orthostatic hypotension for patients taking antihypertensives. can underestimate CrCL in
2. Central nervous system (CNS)increased sensitivity to medications affecting the patients without significant
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age-related renal function
CNS. Medications such as hypnotic, anticonvulsants, benzodiazepines increase the
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changes.
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risk of cognitive impairment and/or falls in older adults.
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3. Fluids and electrolytesincreased sensitivity to medications like diuretics and
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angiotensin-converting enzyme inhibitors that affect fluid balance; patients are more
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Quick HIT
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likely to be experience dehydration and/or potassium (electrolytes) level changes.
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4. Anticoagulantsincreased sensitivity to blood thinners like warfarin, patients at
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increased risk for bleeds.
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An increased sensitivity to the
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E. Preventive measures to minimize medication-related adverse outcomes mon in an elderly patient. Use
1. Use the start Low and Go Slow strategy when prescribing medication for this lower doses or avoid drugs
population. that could potentially cause
2. Review patients medication at every clinical encounter and modify dose based on more harm than benefit for
this population.
patients renal or liver function status as needed. Make sure patients medical prob-
lem list matches with the drug listdiscontinue any unnecessary medications.
3. Monitor drug levels periodically, especially for medications with narrow therapeu-
tic window profile.
4. Assess the benefit versus risk profile of medications for every patient and consider
Quick HIT
discontinuing agents that pose more harm for patients. Age-related changes often
require adjustments in medi-
5. The American Geriatric Society in 2012 updated the BEERS list to provide clini- cations and/or dosages.
cians guidance on appropriate drug therapy for the older adults (see Appendix).
6. This BEERS list encompasses a list of medications that are potentially inappropriate for
the older adult population due to pharmacokinetic/dynamics changes or potentially
inappropriate when used in older adults with certain diseases or health conditions.
7. Always consider a medication side effect when evaluating symptoms in an elderly adult. Quick HIT
Use the start Low and Go
P re o p e ra tive Eva lua tio n Slow strategy when pre-
scribing medication for this
population. Start with a low
A. Background dose and titrate on the basis
1. Size of the geriatric population is growing and will approach 20% of the population of tolerability and clinical
response.
by 2025.
2. Overall better physical condition of this population has led to longer, more active
life spans and more surgical candidates.
3. Geriatric surgeries have increased and are now approaching 40% of all surgeries.
4. Surgical morbidity and mortality increase with age.
a. Complication rate is 7.1% in all patients versus 17% in those aged over 65.
b. Mortality is 1.2% in all patients, 2.2% in those aged 60 to 69, 6% in those aged
over 80, and 8% in those aged over 90.
5. However, age is not the only factor, and comorbidities play a major role.
6. Healthy geriatric patients have outcomes similar to healthy younger patients.
TABLE 1-14 Postoperative Complications in Geriatric Patients

Delirium
Infections
Wound
Urinary
Pneumonia
Cardiac
Infarction/ischemia
Congestive heart failure
Arrhythmia/arrest
Pulmonary
Pneumonia
Need for mechanical ventilation
DVT/PE
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TABLE 1-15 Geriatric Patients Risk Factors for Surgery
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Dementia
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Heart disease
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Coronary artery disease
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Arrhythmias
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Valvular heart disease
Peripheral vascular disease
Lung disease
Smoking
Chronic obstructive lung disease/asthma
Obesity
Renal failure/insufficiency
Diabetes mellitus
Malnutrition
Low level of physical activity
B. Clinical features
Quick HIT 1. Purpose of the evaluation is not to clear the patient for surgery but to recognize
individual risk factors for complications and to implement measures to prepare the
The purpose of the preop- patient for surgery and to lessen this risk.
erative evaluation is not to 2. Most common complications (Table 1-14) are infectious, cardiopulmonary, or neu-
clear a patient for surgery
but to manage their medical
rologic in nature.
conditions, consult with spe- 3. Patient-specific factors can increase risk (Table 1-15).
cialists, including the anes- a. Dementia can increase risk for delirium postoperatively.
thesiologist, and optimize their b. Diabetes and renal disease are associated with increased risk for cardiac
condition in preparation for complications.
anesthesiology and surgery.
c. Vascular disease is considered a coronary artery disease equivalent.
d. COPD, smoking, asthma, and obesity are associated with higher pulmonary
complications.
e. Malnutrition is associated with poor outcomes and wound healing. Table 1-16
lists some risk factors to identify those at greatest risk.
f. Low level of activity or functional capacity can be associated with increased
cardiac risk.
Less than 4 metabolic equivalents (mets) of oxygen consumption is low.
TABLE 1-16 Risk Factors for Malnutrition in Geriatric Surgical Patients

Low income status
Social isolation
Dementia
Substance abuse
Depression
Poor dentition
Weight loss
Chronic disease
NPO status >3 days related to underlying disease
Activities such as climbing a flight of stairs, mowing the lawn, and riding a
bike are >4 mets.
Patients with debilitating disease and unable to be active may need a chemical
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(adenosine or dobutamine) stress test.
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4. The nature of the procedure may also increase risk.
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a. High risk: Major vascular surgery, emergent surgeries. and those with increased
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blood loss are high-risk procedures for cardiac complications (>5%).
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b. Intermediate risk: Intra-abdominal, intrathoracic, orthopedic, and carotid endar-
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terectomy are associated with 1% to 5% incidence of cardiac complications.
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c. Low risk: Superficial surgeries, endoscopy, breast, and cataract surgeries are low
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risk and associated with <1% risk for cardiac complications.
d. Intra-abdominal and thoracic procedures increase risk for pulmonary
complications.
C. Diagnostic testing
1. Approach to diagnostic testing is based upon the history and physical examination
focusing on the elements described above.
2. Also assess for risk factors for malnutrition (Table 1-16), such as low income,
social isolation, substance abuse, mental illness, or chronic disease
CLINICAL PEARL 1-8

Anesthesiologists frequently consult with patients preoperatively in order to assess their health status and
plan the type of anesthesia and use of perioperative pain medications. The classification utilized by the an-
esthesiologists is referred to as the American Society of Anesthesiologist classification and is predictive of
complications and mortality associated with the perioperative period:
Class Mortality (%)
ASA Physical Status 1 Healthy patients 0.05

ASA Physical Status 2 Mild disease 0.4
ASA Physical Status 3 Moderate to severe disease 4.5
ASA Physical Status 4 Life-threatening disease 25
ASA Physical Status 5 Not expected to survive >24 hrs 50
ASA Physical Status 6 Organ donor
Consultation for patients with medical conditions can be actively sought by the primary care provider. For
example, a patient with obstructive sleep apnea could require an alternative form of anesthesia, use of con-
tinuous positive airway pressure, and modification of pain management postoperatively.
S implifie d Cardiac Evaluatio n fo r No nc ardiac S urg e ry

Proce e d to s urge ry with
S te p 1 : Eme rg e nc y s urg e ry me dica l ris k re duction a nd
pe riope ra tive s urve illa nce
S te p 2 : Ac tive Cardiac Co nditio ns
Uns ta ble corona ry syndrome s (uns ta ble or s eve re a ngina , re ce nt MI)
De compe ns a te d he a rt fa ilure (HF, new ons e t, NYHA cla s s TV) Pos tpone s urge ry until
S ignifica nt a rrhythmia s (Mobitz II or third de gre e he a rt block. s ta bilize d or corre cte d
s uprave ntricula r ta chyca rdia or a tria l fibrilla tion with ra pid ve ntricula r
ra te , s ymptoma tic ve ntricula r a rrhythmia ir bra dyca rdia , new ve ntricula r
ta chyca rdia )
S eve re va lvula r dis e a s e (s eve re a ortic or mitra l s te nos is )
S te p 3 : Low ris k s urg e ry (ris k <1%)

S upe rficia l or Endos copic Proce e d to s urge ry
Ca ta ra ct or Bre a s t
Ambula tory
S te p 4 : Func tio nal c apac ity

Proce e d to s urge ry
Good; >4 METs (ca n wa lk flight of
s ta irs without symptoms )
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Proce e d to s urge ry
i
No clinica l pre dictors
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S te p 5 : Clinic al Pre dic to rs
P
Is che mic he a rt dis e a s e Proce e d to s urge ry with
c
Va s cula r s urge ry
i
Compe ns a te d or prior HF HR control or cons ide r
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Ce re brova s cula r dis e a s e 12 clinica l pre dictors
a
noninva s ive te s ting if it
i
Inte rme dia te
r
(s troke , TIA) will cha nge ma na ge me nt
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Dia be te s me llitus ris k s urge ry
Re na l ins ufficie ncy
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>3 clinica l pre dictors Cons ide r te s ting if it
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Va s cula r s urge ry will cha nge ma na ge me nt
FIGURE
1 -4 Cardiac evaluation for noncardiac surgery.
(Based on Fleisher LA, Fleischmann KE, Auerbach AD, et al. ACC/AHA guidelines on perioperative cardiovascular evaluation and
management of patients undergoing noncardiac surgery: a report of the ACC/AHA task force on practice guidelines. J Am Coll
Cardiol. 2014;64:e77137.)
3. Cardiac testing (Figure 1-4)

a. Those requiring emergent surgery will need to undergo surgery with management
of complications and consultation with cardiologists and/or other specialists.
b. Those with unstable, active cardiac issues such as decompensated congestive
heart failure, arrhythmias, severe valvular disease, or recent MI/ischemia will
need cardiology consultation and delay of surgery, if possible, for assessment,
treatment, and stabilization.
c. In general, all low-risk surgical procedures can proceed without cardiac testing
unless otherwise indicated.
d. Stress testing should be considered for all high-risk surgery patients.
4. Pulmonary testing (Figure 1-5)
a. There are no definitive predictors of who with lung disease should proceed with
surgery other than lung resection.
b. Testing is directed to defining disease states and optimizing status prior to pro-
ceeding with surgery.
Consider baseline arterial blood gases and CXR.
Quick HIT Consider pulmonary function tests before and after treatment to optimize
function.
Diagnostic testing for geriat- In overweight patients suspected of obstructive sleep apnea, sleep studies may
ric surgical patients includes be warranted.
CBC and basic metabolic 5. Neurologic testing to evaluate cognition (e.g., Mini-Mental Status Examination)
profile with additional testing
determined by both the nature 6. Laboratory to screen for disease
of the procedure and the pa- a. CBC to screen for anemia and nutritional status
tients medical history. b. Metabolic profile to assess for renal disease and diabetes
c. Albumin to assess for any nutritional concerns
His to ry
V
A Ro utine pre o pe rative pre ve ntive
ke s trate g ie s
ve e
Ve ry hig h ris kCo ns ide r

Abno rmal finding s pulmo nary c o ns ult
Ye
exe
ve
As s e s s me nt, tre atme nt/s , and o the r me as ure s :

Labo rato ry evaluatio n
x- ev
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,
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i
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ve
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a
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FIGURE
1 -5 Pulmonary evaluation for surgery.
(Adapted from Sweitzer BJ . Preoperative Assessment and Management. Philadelphia, PA: Lippincott Williams & Wilkins, 2008.)
d. Urinalysis to assess for infection if prosthetic device to be implanted

e. EKG as baseline for intermediate or high-risk procedures
f. Other testing as indicated by specific associated disease or medications
D. Prophylactic therapies
1. Treat/optimize therapy for chronic underlying conditions.
2. Cardiac prophylaxis
a. Adjust medications for blood pressure stability.
b. Consider -blocker therapy, ideally 3 to 4 weeks in advance, in order to titrate
for tolerance and heart rate target of 60.
For patients with clinical indicators/risk factors
Without significant lung disease that would make -blockers a
contraindication
For intermediate and high-risk surgeries
3. Pulmonary prophylaxis
a. Initiate/adjust therapy to optimize function
b. Consider a course of steroids and inhaled steroids as adjunctive measure to
optimize treatment
c. Instruct use of incentive spirometry
d. Consider pulmonary consult depending on nature of surgery and severity of
disease
4. Delirium precautions (Table 2-13)
a. Determine level of risk
b. Appropriate environmental cues for day/night
c. Utilize eyeglasses or hearing aids as appropriate.
d. Maintain hydration and nutrition.
e. Engage patient to be as active as possible, in conversation, providing orientation.
f. Encourage time with familiar faces and use of familiar items.
g. Allow for sleep without disturbances as much as possible.

h. Monitor elimination of bowels and bladder.
i. Avoid restraints or use of foley catheters, if possible.
j. Minimize medication use.
k. Treat pain adequately.
l. Treat underlying conditions.
m. Consider low-dose antipsychotic medication in high-risk patients (Table 2-14)
5. Deep vein thrombotic prophylaxis
a. Assess for risk factors (Table 1-17)
b. Without risk factors consider:
Compression stocking
Intermittent pneumatic compression (IPC)
Heparin 5,000 units SQ every 8 hours (heparin)
c. Those with risk factors:
Low-molecular-weight heparin (LMWH)
Heparin
IPC
d. Exceptions to the above include:
Neurosurgical patients who should be provided IPC due to bleeding risk
t
Orthopedic lower extremity hip and knee surgery patients who should be anti-
n
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coagulated with LMWH or warfarin
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6. Antibiotic prophylaxis (Table 1-18)
c
a. Antibiotic varies with site of surgery
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TABLE 1-17 Risk Factors for Deep Vein Thrombosis
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Age Hypercoagulable states (protein C or S deficiency, Factor V)
Surgery Varicose veins
Orthopedic surgery History of DVT or PE
Congestive heart failure Underlying malignancy
Cerebrovascular accident Use of estrogen
Obesity
TABLE 1-18 Antibiotics and Selected Procedures for Prophylaxis

Procedure Antibiotic Alternatives
Orthopedic (spinal or Cefazolin Clindamycin, vancomycin

with implant)
Neurosurgery Cefazolin Clindamycin, vancomycin
Cardiac/vascular Cefazolin Clindamycin, vancomycin
Chest Cefazolin or Clindamycin, vancomycin
ampicillin-sulbactam
Head/neck
Clean with Cefazolin Clindamycin
prosthesis
Clean contaminated/ Cefazolin + metronidazole or Clindamycin
cancer ampicillin-sulbactam
Colorectal Cefazolin + metronidazole Clindamycin or metronidazole + aminogly-
Ampicillin-sulbactam coside or fluoroquinolone or aztreonam
Cefoxitin
b. No prophylaxis for clean procedures unless prosthetic device or higher risk/con-

sequences (e.g., cardiac or neurosurgical)
c. Often single dose or re-dosing for no more than 24 hours
d. Initial dose 60 minutes before surgery, except vancomycin and fluoroquinolones
(120 minutes) due to longer infusion times Quick HIT
7. Nutritional prophylaxis
Complications can be mini-
a. Dietitian consult and empiric nutritional supplementation mized by implementing pro-
b. If NPO, consider parenteral nutrition phylactic measures focusing
on cardiopulmonary disease,
DVT prophylaxis, delirium
He a lth Ca re Fina nc ing prevention, nutrition, and anti-
biotic use.
A. General information
1. According to the National Health Expenditure (NHE) Accounts, healthcare spend-
ing for 2012 totaled almost 3 trillion dollars, representing about 18% of the total
GDP for the US.
2. While only about 13% of the US population are aged over 65, this age group ac-
counts for about one-third of healthcare costs.
3. The US spends more on health care for older adults on a per capita basis than any Quick HIT
T
other industrialized country.
h
Healthcare costs for older
e
4. Older adults account for about one-third of all hospital admissions in the US. adults disproportionately con-
G
5. Hospital and physician/clinical services account for about half of the US NHE. The
e
tribute to the increasing cost
r
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cost of health care has been rising faster than the rate of inflation. of healthcare in the US.
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6. The prevalence of chronic conditions increases with age, and >75% of healthcare
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costs are attributed to chronic conditions.
a
t
7. The cost of caring for older individuals with a high prevalence of chronic disease
i
e
n
and the growing numbers of older adults make the healthcare costs for this popula-
t
tion an increasing public concern.
B. Government insurance programs

1. Medicare
a. Together Medicare and Medicaid account for about one-third of national health
spending.
b. Medicare spending grew to over $570 billion in 2012, or 21% of total NHE. Quick HIT
Medicare spending is projected to grow an average of 6.6% per year as the oldest
Medicare is a federal health
Baby-Boomers are expected to use more services. insurance program for older
c. Established in 1965, Medicare is a US government health insurance program adults, people with certain
administered by the Department of Health and Human Services through the disabilities, and people with
Center of Medicare and Medicaid Services. end-stage kidney disease.
Medicare provides coverage to people aged over 65, people aged under
65 with certain disabilities, and people with end-stage kidney disease requir-
ing dialysis or transplant.
More than 99% of those aged over 65 are Medicare-eligible.
d. Medicare is not means-tested. Out-of-pocket costs associated with Medicare
include premium fees, deductibles, copayments, and coinsurance.
e. Medicare has four parts: Part A which is hospital insurance, Part B which is
medical insurance, Part C which is Medicare Advantage Plans, and Part D which
is Medicares prescription drug plan. Quick HIT
f. After an individual pays a deductible, Part A covers inpatient hospital stays
Unlike Medicaid, Medicare is
including drugs, services, medical supplies, and equipment used as an inpatient.
not means-tested.
It also covers home health care, hospice, and skilled nursing home care.
Part A does not cover most physician services, personal services such as an
in-room television, and custodial care such as help with eating, bathing, or
dressing.
There are coverage limits to Part A. Medicare will pay up to 90 days of hospi-
tal or skilled care during one benefit period. A benefit period starts when you
enter a hospital or skilled nursing facility and ends when you have been out
for 60 days in a row. There are no limits on benefit periods.
There is a copay for hospital stays of 61 to 90 days ($304 per day in 2014).
For 91 days and beyond, there is a $608 coinsurance per each lifetime reserve
day for each benefit period (up to 60 days over a lifetime). Beyond the life-
time reserve days, all costs are paid by the patient.
Skilled home care or hospice care must meet certain criteria and be medically
necessary in order to be covered by Medicare.
g. Most individuals pay a monthly premium for Part B ($104.90 in 2014). After
meeting a deductible ($157 for Medicare 2014), Part B covers outpatient physician
services, outpatient care, medical supplies, and some preventive services. Part B
also covers most inpatient physician services, outpatient diagnostic testing such as
Quick HIT clinical labs, x-rays, EKGs and other diagnostic tests, ER services, outpatient men-
tal health, and a portion of medical supplies deemed medically necessary.
Assignment means that a Part B Medicare pays 80% of approved charges.
provider agrees to accept Assignment means that a doctor or Medicare service provider agrees to accept
Medicare-approved payment. the Medicare-approved payment for a covered service.
If a provider does not accept assignment, there are disadvantages to the pa-
tient. The patient may have to pay at the time of service and may also have to
pay the difference between the charge and the Medicare-approved payment.
In some instances, regulations limit charges.
Quick HIT
t
h. Services that Part B does not cover include dental services, vision or hearing care
n
e
except in very limited situations, care received outside the US, and custodial
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a
Medicare Part B pays 80% of
P
care such as help with eating, bathing, or dressing.
covered outpatient services.
c
Medicare does not pay for long-term care in a nursing home.
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While Part B helps pay for medically necessary care, it may limit coverage for
a
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a service. For example, occupational therapy and speech therapy may only be
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covered for a limited number of sessions.
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CLINICAL PEARL 1-9
Many patients and families are surprised to learn that Medicare does not pay for long-term nursing home care.

W.W. is a 78-year-old man with Part A and Part B Medicare insurance. He suffers a stroke
and is hospitalized for 11 days which leaves him with left-sided weakness and some slurred
speech. During the course of his hospitalization, he slowly improves and, while medically
stable, he is unable to care for himself. An assessment by speech and physical therapy both
indicate that he is able to attend therapy sessions and will continue to show improvement
with intensive therapy.
Arrangements are made to transfer him to a skilled facility where he will have daily ther-
apy sessions. W.W. improves, and after 25 days at the skilled care facility, he is able to walk
with a quad cane. He is able to return to his home with the help of his family. He will continue
his physical therapy three times a week at home.
Under Medicare Part A, W.W. pays a deductible of $1,216 (2014 Medicare Part A deduct-
ible) for his hospital stay. The remaining hospital costs, including his physical therapy and
speech therapy, will be covered by Part A. During his hospitalization he saw both his primary
care physician and a consulting neurologist. Both physicians agree to accept assignment or
the Medicare-approved payment for their services. Earlier in the year, W.W. met his Part B
deductible, so Part B will pay 80% of the physician services bill. W.W. does not have Medigap
insurance and will pay the remaining costs out of pocket.
His time at the skilled care facility meets Medicare eligibility requirement. For each benefit
period, days 1 to 20 of skilled care do not have a copay and his care is paid for by Medicare.
For days 21 to 100, there is $152 copay, and for his 25-day stay, W.W. incurs a cost of $760.
His cane cost $250 and Part B pays 80% for this item of durable equipment. His PT and OT
services exceed the Medicare cap, but because his therapists are able to document the con-
tinued need for these services and his improvement, Medicare continues to pays its share
for these services.
i. Medicare Advantage, also called Medicare Part C, is an alternative to original

Medicare. Medicare Advantage Plans are offered by private insurance companies
contracted by Medicare. These plans combine the benefits of Medicare Part A
with the benefits of Medicare Part B.
Patients must be enrolled in both Medicare Parts A and B to join a Medicare
Advantage Plan. They remain enrolled in Parts A and B, but receive their ben-
efits through a private insurance plan instead of through original Medicare.
Within federal guidelines, each Medicare Advantage Plan sets its own coverage
terms and limits.
Typically, the benefits of a Medicare Advantage Plan include enhanced service
coverage and less out-of-pocket costs. The disadvantage is that individuals
must use in-plan services and providers or they must pay more.
j. Part D adds prescription drug coverage to original Medicare. These plans are
offered by insurance companies and other private companies approved by
Medicare. Medicare Advantage Plans may also offer prescription drug cover-
age that follows the same rules as Medicare Prescription Drug Plans. If an
individual does not join Part D initially, he or she can enroll later by paying a
penalty.
k. While there is no premium for Part A, there may be deductibles and copays costs
to the patient. Parts B and D require that most patients pay a monthly premium
T
h
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to be enrolled.
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l. Medicare coverage falls short of meeting all the healthcare-related costs for
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r
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older adults. Three main ways older people incur costs are through premium
a
t
r
payments, cost sharing for Medicare-covered benefits and for services not cov-
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ered by Medicare. Table 1-19 illustrates the summary of benefits for individuals
P
a
on Medicare.
t
i
e
m. Medigap insurance is private insurance that can be purchased to help pay for
n
t
some of the healthcare costs that original Medicare does not cover.
Examples of gaps in Medicare coverage include copayments, deductibles,
hearing and vision services, dental care, long-term custodial care, and mental
health services that usually incur substantial copay.
About 60% of Medicare beneficiaries have Medigap coverage. These can be
employee-based plans, privately purchased insurance, and Medicaid.
2. Medicaid
a. Medicaid is a federal program administered by the state to provide health cover-
age for lower-income people, families and children, older adults, and people
with disabilities. Quick HIT
b. Medicaid is means-tested. Each state sets its own standard for Medicaid, so ben- Medicaid is means-tested.
efits and eligibility differ among states. Medicaid is available to only those low-
income individuals and families that fit into an eligibility group recognized by
both federal and state law.
c. Many older adults are dually eligible, meaning they qualify for both Medicare
and Medicaid. In some instances, Medicaid will pay the premium for Part B for
low-income individuals.
d. About one in five older adults receive Medicaid and about 65% of nursing home
residents are on Medicaid (Table 1-20).
TABLE 1-19 Summary of Medicare Benefits

Part A Hospital and skilled nursing care benefits
Part B Physician and outpatient services
Part C Medicare Advantage Plans
Part D Medication Benefits
TABLE 1-20 Chart Differences between Medicare and Medicaid

Medicare Medicaid
What is it? A federal program for individuals aged A joint federal and state program
65 and older, those with certain dis- that helps pay for health care for
abilities or end-stage renal disease individuals with limited income
Who manages it? Federal government State and federal government
What does it cover? Depends on the part the patient enrolls in. Each state sets its own program fol-
Part A, hospital services; Part B, lowing federal guidelines. Includes
physician and outpatient services; Part hospital and skilled care, physician
D prescription plan services, prescriptions and more
What does it cost? Part A is no cost. Parts B and D have a Depends on income and state re-
monthly premium quirements. Can be no cost or some
premium and deductible costs
3. PACE
t
n
a. Program for All-inclusive Care for the Elderly (PACE) is a Medicare and Medic-
e
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aid program that helps people meet their needs in the community to avoid being
a
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placed in an institutional setting such as a nursing home.
c
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b. PACE includes both comprehensive medical and support services. These services
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a
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encompass adult day primary care, dentistry, emergency services, home care,
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hospital care, diagnostic testing, nutritional counseling, OT and PT services,
e
prescription drugs, and other medically necessary support services such as
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transportation to clinic visits.
C. The Older Americans Act and Aging Network

1. Passed in 1965, the Older Americans Act (OAA) addressed a concern about a
perceived lack of community services for older adults. The OAA established the
Administration on Aging to carry out the provisions of the Act and to advocate for
older adults, to enhance service coordination, and to improve healthcare delivery
services for older adults.
2. The OAA authorizes and provides funding for a wide array of service programs
through a network of state agencies and area agencies on aging.
a. Ombudsmen program
b. Legal assistance
c. Home meals
d. Transportation
e. Adult day care
f. Health promotion and chronic disease programs
3. The National Center on Elder Abuse (NCEA) became part of the Administration on
Aging through the 1992 amendments made to Title II of the OAA. The NCEA is a
national resource center and consortium of collaborators focused on the prevention
of mistreatment, neglect, exploitation, and abuse of older adults.
A P P EN D IX
T
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FIGURE
A -1 The American Geriatrics Society 2012 BEERS Criteria.
(Adapted with permission from the 2012 American Geriatric Society BEERS List.)
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FIGURE
A -1 (continued)
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FIGURE
A -1 (continued)
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FIGURE
A -1 (continued)
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FIGURE
A -1 (continued)
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FIGURE
A -1 (continued)
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FIGURE
A -1 (continued)
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FIGURE
A -1 (continued)
GERIATRIC
SYNDROMES
2
Fa ilure to Thrive (FTT)
A. Ge n e ra l c h a ra c te ris tic s
1. Describes a state of decline in the elderly that is often multifactorial and may be
caused by concurrent processes and impairments
2. One major manifestation is weight loss 5%.
Quick HIT
3. Patients generally also exhibit decreased appetite, activity, and depression. FTT is characterized by weight
G
4. Associated with increased complications and mortality rates loss and decline in function
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r
without an identifiable primary
i
5. May have multiple chronic medical diseases, but no dominant disease or obvious
a
t
cause.
r
cause for the decline
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S
y
B. C lin ic a l fe a tu re s
n
d
1. Decline in weight
r
o
Quick HIT
m
2. Decrease in functional ability, such as walking, self-care
e
3. Apathy, inactivity, lack of engagement in prior interests
s
4. May show signs of dehydration such as decreased blood pressure, increased heart FTT evaluation should assess
rate, and dry mucous membranes the status of known chronic
5. Signs of chronic disease such as stable congestive heart failure with edema; chronic diseases and for previously
undetected diseases, such as
obstructive lung disease with diminished breath sounds; depression with decreased cancers, depression, or medi-
affect; diabetes or renal insufficiency without specific physical signs (Table 2-1) cation side effects.
C. D ia g n o s is (Figure 2-1)
1. History and physical examination to evaluate status of known conditions and to
detect previously unknown disease:
a. Ask about appetite and any difficulties eating or drinking.
b. Determine presence of diarrhea or alteration in bowel habits.
c. Inquire about any sources of blood loss, fever, shortness of breath.
d. Assess for presence of pain.
e. Determine risk status for elder abuse or neglect (see Elder Abuse, Chapter 3).
f. Perform exam to include full skin exam, signs of infection, wounds, or decubiti.
2. Assessment of activities of daily living (ADL) and instrumental activities of daily
living (IADL)
3. Use instruments to assess for depression (e.g., PHQ-9, Geriatric Depression Scale,
Chapter 3).
4. Testing to evaluate cognition (e.g., Mini Mental Status Examination, Chapter 3)
5. Laboratory to screen for disease:
a. Complete blood count (CBC) to screen for anemia or possible infection
b. Metabolic profile to assess for renal or liver disease, dehydration, and diabetes
c. Thyroid-stimulating hormone (TSH) to screen for thyroid disease
d. ESR to evaluate for polymyalgia rheumatica, temporal arteritis, or other inflam-
matory states
e. Albumin and lipids to assess nutritional status
f. Urinalysis to assess for infection, kidney disease, dehydration
49
TABLE 2-1 Medical Conditions Associated with FTT

Malignancies
Chronic respiratory conditions
Renal insufficiency
Cirrhosis
Depression/psychiatric disease
Thyroid disease
CHF
Malabsorption (e.g., infectious or celiac disease)
Oral disease
Stroke
Dementia
Parkinson disease
Rheumatologic diseases
Medications
EtOH and substance abuse
Elder abuse or neglect
s
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S
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t
a
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g. Stool for culture, ova and parasites if indicated for infectious diarrhea
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h. If malabsorption suspected, consider serology to include antiendomysial anti-
bodies and IgA tissue transglutaminase for detection of celiac disease
i. PPD or enzyme-linked immunosorbent assay blood testing (Quantiferon) to
screen for tuberculosis
j. Consider CXR or computed tomography (CT) scans to evaluate for undetected
malignancy or infection
k. HIV and rapid plasma reagin (RPR) in those individuals with risk factors
l. If no recent cancer screening, consider stool for occult blood, prostate specific
antigen (PSA), and mammography
6. Nutritional assessment:
a. Serum albumin and lipids
b. Calorie counts
c. SCALES (Table 2-2) is a tool to screen for nutritional risk in the elderly
D. Tre a tm e n t
1. Treat/optimize therapy for chronic underlying conditions.
2. Modify or stop medications suspected as causing adverse effects.
3. Initiate therapy for newly identified conditions.
4. Dietitian consult and empiric nutritional supplementation
Quick HIT 5. Empiric antidepressant therapy
In the absence of an identifi- 6. Trial of appetite stimulants such as dronabinol
able cause, nutritional assess- 7. Early and frequent communication with patient and/or family related to FTT and
ment and supplementation approach to evaluation and treatment
along with attempts to stimu- 8. Consideration of percutaneous endoscopic gastrostomy (PEG) tube placement or
late appetite can be tried as
palliative care options
empiric treatment.
9. If functionally impaired, consider occupational therapy (OT) and physical therapy
(PT) evaluation and environmental modification.
G E R I AT R I C S YN D R O M E S 51
WE IG H T LO S S
Common ca us e s :
hype rthyroidis m, dia be te s me llitus, ma la bs orption
syndrome s, ma ligna ncy, chronic illne s s, de pre s s ion,
me dica tions /drugs, s ubs ta nce a bus e, a norexia ,
HIV infe ction, TB
De cre a s e d a ppe tite

No Ye s
Dia rrhe a or loos e Me dica tions

s tools or drugs
Ye s No Ye s No
Che ck la bs : S timula nts Known chronic

TS H, glucos e, P P D Toba cco a bus e illne s s
Ye s No
Che ck s tool for ova a nd P P D+ TS H Glucos e Norma l

pa ra s ite s, fe ca l fa t, de cre a s e d e leva te d
s e rum a ntie ndomys ia l
a ntibodie s, IgA tis s ue
tra ns gluta mina s e
TB Hype rthyroidis m Type 1 Eva lua te for Ins omnia
G
dia be te s Review his tory for a nore ctic e ffe ct De cre a s e d e ne rgy
e
me llitus incre a s e d exe rcis e of chronic dis e a s e Dis torte d body
r
i
Pa ra s itic dis e a s e or its tre a tme nts ima ge
a
t
Ma la bs orption
r
i
No
c
syndrome Ye s
S
Ce lia c dis e a s e
y
n
d
P sychia tric illne s s Che ck la bs :
r
o
CBC, HIV, P P D,
m
e le ctrolyte s, glucos e,
e
TS H, cre a tinine
s
De pre s s ion
Anxie ty
Pe rs ona lity dis orde rs
Hype rka le mia TS H Cre a tinine HIV Ane mia Hype rglyce mia
de cre a s e d e leva te d infe ction, TB
Adre na l Hype rthyroidis m Re na l Chronic Type 1 dia be te s

ins ufficie ncy fa ilure dis e a s e me llitus
Eva lua te for

ma la bs orption
syndrome s
FIGURE
2 -1 Evaluation of weight loss.
(Baldor RA, Ehrlich AM. Am Fam Physician. 2002;65:640651.)
TABLE 2-2 SCALESA Tool to Identify Who is at Nutritional Risk

S Sadness (based on depression screening)
C Cholesterol (<160 mg/dL)
A Albumin (<4.0 g/dL)
L Loss of weight within the last 6 mo (e.g., 2 lb in 1 mo or 5 lb in 6 mo either unintentionally or purposely)
E Eating problems, e.g., difficulty self-feeding because of a stroke
S Shopping issues that preclude obtaining food for a well-balanced diet (economic or functional limitation)
With permission from Omran ML, Morley JE. Assessment of protein energy malnutrition in older persons, Part 1: History, ex-
amination, body composition and screening tools. Nutrition. 2000;16:5063.
CLINICAL PEARL 2-1

Instrumental Activities of Daily Living and Activities of Daily Living
Assessment of IADLand ADLcan help determine patient care needs and the appropriate living
environment/level of care needed to provide for a patient.
IADLs include using the telephone, preparing meals, managing finances, taking medications, doing laundry,
doing housework, shopping, managing transportation.
Patients that require assistance with IADLs may suffer from FTT because of an inability to care for
themselves.
Inability to provide for IADLs can be replaced with care provided by family, assisted living environments,
hired caregivers, delivery of meals, or delivery of groceries to allow a person to thrive.
ADLs include bathing, dressing, transferring, toileting, grooming, feeding, and mobility.
Patients lacking in ADLs are unable to fully care for themselves and will suffer from FTT or severe debil-
ity unless a high level of care is provided.
These are much more basic needs, and lack of these skills indicates more advanced disease.
Replacement of these needs generally requires around-the-clock care that can be provided in nursing
homes, by hired caregivers, or family.
Inc o ntine nc e
s
1. Involuntary loss of urine is severe enough to cause social and hygiene problems.
e
m
2. Although more common in the elderly, incontinence is not a normal consequence
o
r
d
of aging.
n
y
3. Incontinence can lead to social isolation, depression, skin breakdown, urinary tract
S
infection (UTI), and falls.
c
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4. One-third of community-dwelling women and one-fourth of elderly men experi-
t
a
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r
ence some degree of incontinence, which increases with age.
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5. Many have never discussed it with their physicians and believe it is part of the ag-
ing process or are embarrassed to discuss it.
6. Types of incontinence (Table 2-3)
a. Urge incontinence occurs with uninhibited bladder contractions, strong enough
to overcome urethral resistance.
b. Stress incontinence is involuntary loss of urine during coughing, sneezing, stand-
ing, or exercising, from malfunction of the urinary sphincters in the face of in-
creased intra-abdominal pressure.
c. Overflow incontinence occurs when bladder distension reaches maximum capac-
ity and urethral sphincter pressure is exceeded, resulting in overflow leakage
from the bladder. This occurs when either obstruction of urine outflow or inef-
fective bladder contractions cause urinary retention.
TABLE 2-3 Types of Incontinence

Incontinence Type Symptoms Pharm. Treatments
Urge Urgency, frequency day or night Anticholinergics: oxybutynin,

tolterodine
Stress Small volume of urine loss with Agonists, topical estrogen
coughing, sneezing
Mixed stress and urge Symptoms in both the above Treat dominant symptoms
Overflow Poor stream, incomplete emptying -Blockers: terazosin, tamsulosin
Functional Inability to get to toilet Treat underlying cause or scheduled

toileting
d. Mixed incontinence occurs when there is a combination of stress and urge

incontinence.
e. Functional incontinence occurs when there is a deficit in cognition or mobility Quick HIT
that affects voiding. Three basic pathologic mech-
anisms cause urinary inconti-
B. C lin ic a l fe a tu re s nence. These are overactivity
1. Factors associated with incontinence: of the bladder detrusor muscle
a. Leakage with coughing, sneezing, and straining suggests stress incontinence. (urge incontinence), malfunc-
b. Sudden urge to urinate with loss of control suggests urge incontinence. tion of the urinary sphincters
(stress incontinence), and
c. Constant dribbling with difficulty initiating stream suggests overflow. overflow from the bladder
d. Functional limitations due to concomitant neurologic/orthopedic disease (urinary retention).
2. Past medical history:
a. Stress incontinence associated with prior childbirth
b. Neurologic disease associated with urge or overflow incontinence
c. Prior pelvic or prostate surgeries or diseases such as diabetes associated with
incontinence
d. Medication use such as anticholinergics, diuretics, or sympathomimetics may af-
fect bladder function (Table 2-4).
3. Physical examination:
a. Palpate abdomen to detect bladder distension
b. Perineal sensory examination
c. Cystocele or rectocele on pelvic examination
d. Prostate enlargement or nodularity
G
e
e. General neurologic examination for dementia, Parkinson disease, multiple scle-
r
i
a
rosis (MS), or other disease that may contribute.
t
r
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f. Evaluate functional factors such as impaired mobility or dexterity
S
y
n
d
r
1. A urinalysis may detect infection, unsuspected diabetes, and hematuria which may
o
m
indicate presence of cystitis or bladder carcinoma.
e
s
2. Urine culture if urinalysis suggests infection.
3. Postvoid residual by either ultrasound or straight catheterization:
a. Less than 75 mL residual is considered normal.
b. 75 to 150 mL residual is borderline.
TABLE 2-4 Medications Associated with Incontinence

Class Causative Action
Diuretic (e.g., furosemide) Increased frequency and volume of urine

Anticholinergics (e.g., oxybutynin) Impaired bladder contraction, may also cause constipa-
tion, which can lead to urinary retention and overflow
incontinence
Antidepressants (e.g., amitriptyline) Anticholinergic effects and sedation, which may cause a
functional component
Antipsychotics (e.g., haloperidol) Anticholinergic effects; sedation and parkinsonism, which
may cause a functional component
Narcotic analgesics (e.g., hydrocodone) Sedation; constipation with effects
Calcium channel blockers (e.g., verapamil) Impaired bladder contraction; constipation both with
effects
-Adrenergic agonist (e.g., ephedrine) Increased contraction of the urethral sphincter, which may
exacerbate obstructive symptoms in those with benign
prostatic hyperplasia (BPH) or outlet obstruction
-Adrenergic blockers Relax the urethral sphincter and may exacerbate symptoms
in those with stress incontinence
G e r i a t r i
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c. Greater than 150 mL residual is excessive and consistent with urinary retention,
and merits urology consult.
4. Electrolytes, BUN, and creatinine to evaluate renal function.
5. Urodynamic testing is recommended if the cause of incontinence is unclear, if pri- Quick HIT
mary treatment is unsuccessful, or if surgical intervention is contemplated.
A urinalysis should be per-
formed on every patient to
PEARL
detect infection, unsuspected
CLINICAL 2-2 diabetes, and hematuria,
which may indicate pres-
Urodynamic Testing ence of cystitis or bladder
carcinoma.
Urodynamic testing can identify inadequate bladder contractions, inadequate emptying, and measure bladder
pressures during bladder filling and emptying.
Testing is done as an outpatient and does not require any anesthesia other than local anesthesia.
The most basic testing is uroflometry, which measures the amount voided over time or a postvoid residual,
where a catheter collects the residual urine after the patient empties his or her bladder. These tests can detect Quick HIT
reduced flow and emptying resulting from obstruction or inadequate bladder contractions. Postvoid residual by ei-
More technical testing involves placement of manometers along with the catheters to measure pressures ther ultrasound or straight
as the bladder is filled and empties, and to detect involuntary contractions. This testing can also elicit when catheterization:
the patient has the urge to void as well as the point at which involuntary leakage will occur. This battery of Less than 75 mL residual is
tests is termed: (1) cystometry, (2) pressure flow testing, and (3) leak point pressure testing. considered normal.
If there are concerns based upon history or examination regarding neuropathic or myopathic etiologies for 75 to 150 mL residual is consid-
the incontinence, then electromyography can be performed, assessing the bladder and perineal musculature. ered borderline.
Greater than 150 mL residual
is excessive and consis-
G
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tent with urinary retention
r
i
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D. Tre a tm e n t and the need for urology
t
r
consultation.
i
1. Treat any potentially reversible causes of incontinence.
c
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2. Patients with a significant functional component may benefit from scheduled toilet-
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ing or providing adequate access for toileting.
d
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o
3. Urge incontinence, particularly in the presence of abnormal urine findings, may re-
m
quire cystoscopy and referral to eliminate secondary causes.
e
s
4. Urge incontinence without a secondary cause is termed detrusor instability and may
be treated with anticholinergics, such as oxybutynin. These increase sphincter tone
and also reduce bladder muscle contractions.
5. Kegel exercises or -adrenergic medications, such as pseudoephedrine, may benefit
those with stress incontinence.
6. Stress incontinence unresponsive to these measures may require surgical repair of
the pelvic relaxation.
7. Nonobstructive causes of overflow incontinence may respond to cholinergic agents
to stimulate the bladder (e.g., bethanechol).
8. Benign prostatic hypertrophy may respond to -blockers, such as tamsulosin, to
relax the bladder outlet.
9. Obstructive causes, such as urethral stricture or prostate enlargement, often require
surgical repair.
10. Nonobstructive overflow that does not respond to medication requires either catheter
placement or a self-catheterization program to provide appropriate bladder drainage.
Quick HIT
Co ns tip a tio n Underlying causes of consti-
pation may include medical
conditions, medications,
A. Ge n e ra l c h a ra c te ris tic s and lifestyle factors such as
1. A common concern of the elderly sedentary activity level or
decreased oral intake of fluid
2. Less than three stools per week or hard stools associated with straining, incomplete and fiber.
evacuation, or the need for digital extraction of stool
3. Stool passage is dependent on stool, colonic motility, and patency of the lumen. Al-
teration in any of these can result in constipation.
4. Underlying causes of constipation may include medical conditions, medications,
and lifestyle factors such as sedentary activity level or decreased oral intake of fluid
and fiber.
5. Irritable bowel syndrome is an idiopathic cause associated with alternating consti-

pation and more frequent loose stools.
6. Constipation that results in a fecal impaction is a serious condition that can cause
functional deterioration, urinary or stool incontinence, and confusion.
1. History related to bowel movements, including frequency, consistency, and pas-
sage of blood
2. Dietary intake with evaluation of fluid and fiber intake
3. Inquire about laxative use. Long-term use of stimulant laxatives may lead to de-
generation of the myenteric plexus over time, causing bowel hypomotility.
a. These individuals are at risk for developing an impaction or Ogilvie syndrome
(intestinal pseudo-obstruction).
4. Past medical history:
a. Surgeries, particularly abdominal surgery
b. Medical conditions, such as hypothyroidism, scleroderma, hypercalcemia, diabetes,
and neurologic conditions such as Parkinson disease, MS, paraplegia, or dementia
c. Medications such as calcium channel blockers, anticholinergics, antidepres-
sants, antipsychotics, and narcotics
d. Ask about chronic laxative use
Quick HIT 5. Physical examination:
a. Height, weight, and general appearance
In patients with a recent onset b. Thyroid gland for enlargement
s
e
of constipation unrelated to
m
c. Abdominal exam for bowel sounds, masses, and signs of distension. Occasion-
o
a new medication, the focus
ally, excessive amounts of colonic stool can be palpated.
r
d
should be on ruling out an
n
d. Anorectal exam for masses, fissures, and hemorrhoids
y
underlying cause such as
S
malignancy, obstruction, or a e. Neurologic examination for signs of dementia, Parkinson disease, neuropathy,
c
metabolic disorder. and MS
i
r
t
a
i
r
C. D ia g n o s is (Table 2 -5 )
e
G
1. Younger patients at low risk for comorbid disease or with easily explained causes
such as medication-induced constipation that resolves may not require additional
testing.
2. Laboratory testing:
a. CBC to evaluate for anemia
b. Electrolytes to detect hypercalcemia and hypokalemia
c. TSH to assess for hypothyroidism
d. Plain abdominal x-rays are of limited value unless impaction, obstruction, or
pseudo-obstruction is suspected (Figure 2-3)
e. Stool for occult blood to screen for colon pathology
3. Patients over age 50 and those with anemia, passage of blood, stools positive for
occult blood, or weight loss require evaluation for colon cancer. Colonoscopy is
Quick HIT the diagnostic procedure of choice.
Patients with anemia, passage D. Tre a tm e n t
of blood, or weight loss require 1. Treat identifiable underlying causes, such as hypothyroidism or hypokalemia.
evaluation for colon cancer,
which is most commonly done 2. Medications that may be causing symptoms should be modified, if possible.
with colonoscopy. 3. Lifestyle factors such as low fluid, fiber, or activity levels should be addressed
through patient education to include eight glasses of water, 25 to 35 g of fiber,
and regular exercise.
a. Dietary fiber should be increased gradually to avoid gas pains and bloating.
Quick HIT 4. If these measures do not correct the symptoms, then medications (Table 2-6) may
be included in the regimen.
Lifestyle factors such as low a. Bulking agents increase fiber and water content.
fluid, fiber, or activity levels b. Osmotic agents draw fluid into the intestinal lumen.
should be addressed through c. Stimulants enhance colonic motility by increasing muscle activity and may be
patient education to include
eight glasses of water, 25 to 35 g needed in patients for whom narcotics cannot be stopped.
of fiber, and regular exercise. d. Enemas and suppositories can also be utilized and will distend and stimulate
the rectum, creating the need to evacuate.
TABLE 2-5 Differential Diagnosis for Constipation

Lifestyle factors
Inactivity
Inadequate fiber in diet
History of laxative abuse
Metabolic disease
Hypothyroidism
Diabetes mellitus
Hypokalemia
Hypercalcemia
Neurologic disease
Parkinson disease
Paraplegia
Colorectal disease
Cancer or mass
Fissure/hemorrhoids
Rectal prolapse
Medications
Narcotics
G
Calcium channel blockers
e
r
i
Anticholinergics
a
t
r
Antihistamines
i
c
S
Antidepressants
y
n
Diuretics
d
r
Antacids
o
m
Clonidine
e
s
Levodopa
FIGURE
2 -3 Intestinal pseudo-obstruction.
(Adapted from Daffner RH, Hartman M. Clinical Radiology: The Essentials. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2014.)
TABLE 2-6 Medications to Treat Constipation

Bulk Agents
Psyllium 1 tablespoon qdtid

Methylcellulose 13 tablespoons qd
Calcium polycarbophil, 1 tablet qdtid
Softeners
Docusate sodium, 12 capsules qd or split bid
Stimulants
Bisacodyl 12 tablets or suppositories qd
Senna 23 tablets qd or split bid
Casanthranol 12 tablets qd or split bid
Osmotic Agents
Lactulose 12 tablespoons qd or bid
Magnesium (milk of magnesia, magnesium citrate)
Sorbitol 70% 24 tablespoons qd
Polyethylene glycol 17 g in 8 oz water qd
Other Agents
s
e
m
Linaclotide 145 mcg qd
o
Lubiprostone 24 mcg q12 hr
r
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PEARL
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CLINICAL 2-3
a
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r
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G
Colon Obstruction
Constipation may also occur on the basis of intestinal obstruction or pseudo-obstruction. For this reason,
particularly in the inpatient setting, x-ray evaluation should be performed (Figure 2-3).
Causes of colonic obstruction and distension are intrinsic or extrinsic mechanical obstruction or loss of mo-
tility resulting from inflammatory or noninflammatory causes. An example of an intrinsic cause of mechanical
obstruction would be a tumor, whereas adhesions or an incarcerated hernia would be extrinsic causes. Toxic
megacolon can occur from inflammatory bowel disease. Noninflammatory causes of loss of motility include
a variety of major illnesses (e.g., cardiac surgery, sepsis), electrolyte disturbances, and medications such as
narcotics.
The patient with intestinal pseudo-obstruction will have constipation followed by distension, nausea,
vomiting, and then often diarrhea or loose stools may develop. Physical examination will reveal distension;
tympany to percussion; and absent, normal, or hyperactive bowel sounds that, if high-pitched, should raise
suspicion for mechanical obstruction.
Laboratory testing should include a blood count and electrolytes including calcium and magnesium. An
abdominal CT scan may be needed to rule out a mechanical obstruction.
Therapy is supportive with hydration, correction of electrolytes, and decompression of the intestines with
NG and rectal tubes. Should these measures prove unsuccessful, then neostigmine may be used with close
cardiac and respiratory monitoring. If these measures fail, then endoscopic or surgical intervention may be
warranted.
Quick HIT
Falls cause substantial mor-
bidity and mortality in geriatric
patients, accounting for up to
Fa lls / Ga it Ins ta b ility
70% of accidental deaths and
most hip fractures. One-third A. Ge n e ra l c h a ra c te ris tic s
of community-dwelling elderly 1. Falls cause substantial morbidity and mortality in geriatric patients, accounting for
patients and two-thirds of
nursing home patients will fall up to 70% of accidental deaths and most hip fractures.
each year. 2. One-third of community elderly patients and two-thirds of nursing home patients
fall each year.
3. Falls are associated with declining health and function and may be a presenting
sign of an acute illness.
4. Mortality rates following a hip fracture are as high as 25%. Another 25% of patients
who survive become dependent on others for their care.
1. Falls often occur because of an interplay of factors: those intrinsic to the patient,
such as poor balance, and those extrinsic to the patient, which are environmental
factors, such as poor lighting.
2. Intrinsic risk factors include prior history of falls, loss of ability to perform ADLs or
IADLs, need for assistive devices for ambulation, neurologic or orthopedic condi-
tions, multiple medications, altered mental status or dementia, and vision or hear- Quick HIT
ing loss. Underlying chronic diseases
a. Underlying chronic diseases such as dementia, Parkinson disease, or diabetes such as dementia, Parkinson
with neuropathy can play a role; acute illness also increases risk. disease, or diabetes with neu-
b. Medications, such as antihypertensives, psychoactive medications, anticholiner- ropathy can play a role; acute
illness and medications may
gics, and antihistamines may alter balance or cognitive function (Table 2-7). also alter balance or cognitive
3. Environmental factors, such as poor lighting, throw rugs, uneven flooring, and function.
stairs, often contribute and increase risk.
4. Patients with repetitive injuries should also be assessed for possible elder abuse and
neglect.
G
1. Gait must be assessed and can be done utilizing the Get up and go or timed Get
e
r
i
up and go testing (Table 2-8).
a
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r
2. A thorough neurologic examination including sensory, cerebellar, and mental status
i
c
testing is warranted.
S
y
3. Test extremity range of motion (ROM) and strength.
n
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r
4. Evaluate vision and hearing.
o
m
5. Check orthostatic blood pressure and pulse.
e
s
6. Cardiac examination to assess rhythm and for murmurs such as aortic stenosis
7. Labs: CBC/BMP to assess for anemia as well as dehydration
8. Other testing may be warranted in those with abnormal findings on physical exam-
ination. This may include electromyography and nerve conduction velocity testing
(EMG/NCV) to detect suspected myopathy or neuropathy, CT, or MRI of the brain
to detect suspected stroke, hemorrhage, or mass.
CLINICAL PEARL 2-4
Orthostatic Blood Pressure and Heart Rate Testing

Tilt table testing may be indicated in patients with recurrent unexplained falls. Tilt table testing can help to
detect vasovagal responses, orthostatic hypotension, and postural tachycardia syndrome.
Testing is performed by placing the patient onto a table supine, monitoring vital signs and electrocar-
diogram, and after a period of 5 to 20 minutes elevating the table so that the patient is at 60 to 70 degrees
upright. Symptoms of lightheadedness, dizziness, or frank syncope are noted and correlated with the patients
response in terms of blood pressure and heart rate.
A vasovagal response results in decreased heart rate and blood pressure. An orthostatic response will
increase heart rate and lower blood pressure. Postural tachycardia syndrome is a response with an elevated
heart rate but no drop in blood pressure. Patients with postural tachycardia syndrome develop orthostatic
symptoms despite the lack of drop in blood pressure.
Therapy for patients with vasovagal syncope includes taking precautions of lowering to the floor and
elevating their legs at the onset of warning symptoms that typically occur. Support stockings may be helpful,
and patients can also be instructed to do isometric exercises to counteract the decline in pressure. In extreme
cases, a pacemaker can be placed. There are no solid data supporting medication use as a solution.
Orthostatic hypotension is treated with hydration if needed, and with medications such as -blockers,
fludrocortisone, and midodrine. There are no definitive treatments for postural tachycardia syndrome, but simi-
lar medications have been tried with variable success.
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TABLE 2-7 Medications Associated with Falls in the Elderly

Psychoactive medications
Antidepressants
Antipsychotics
Benzodiazepines
Sedatives
Cholinesterase inhibitors
Antihypertensive medications (including diuretics)
Nonsteroidal anti-inflammatory medications
TABLE 2-8 Screening for Falls

United States Preventive Services Task Force recommends yearly screening over age 75 yrs
Number needed to screen (NNS) to prevent one fall over 1 yr is 20 (Tinetti, NEJM, 1994)
History of falls in last 12 mo
Timed Up and Go test (TUG): Rise from the chair, walk 10 feet, turn, walk back to the chair, and sit
down
G
Patient is at risk for falls if she takes more than 15 sec to complete the task
e
r
i
a
If they screen positive for falls with either of these items, then further assessment:
t
r
i
Exam for gait, orthostasis, cardiac problems, vision
c
S
Exercise program to prevent falls: Tai Chi is best
y
n
Motivational interviewing can help
d
r
Vitamin D, calcium supplementation
o
m
Evaluation of medications that may pose a risk
e
s
Environmental modifications
Eyewear, footwear, gait aids
Home safety, fear of falls
D. Tre a tm e n t
1. Home safety should be assessed and risk factors corrected (Table 2-9):
a. Floors clutter-free with no throw rugs
b. Cords and wiring clear of walkways
c. Adequate lighting
d. Handrails for stairs and tubs
TABLE 2-9 Recommended Home Safety Changes

Edges of stairs, uneven surfaces marked
No (or secured) throw rugs, mats, long electrical cords
Less clutter (easier said than done!)
Chairs, toilet at appropriate height
Furniture arranged so provides assistance, not obstacles
Night lights
Nonslip pads in shower, tub
Grab bars in shower, next to toilet (raised toilet seat)
Handrails along staircases
Even, nonglare lighting
e. Antiskid surfaces for tubs and no wax on other flooring

f. Furniture and toilets at heights easy to arise from
g. Correct vision and hearing losses.
Quick HIT h. Eliminate or change medications that may be causing imbalance.

i. Use of medications and compression stockings for orthostatic patients.
A multifaceted approach to 2. PT to strengthen muscles and improve balance
treatment should include 3. Use of assistive devices as needed for ambulation (e.g., canes and walkers)
home safety assessment,
PT, use of assistive devices,
and a review of the medical
condition(s), medications,
A lte re d Me nta l S ta tus / D e lirium
vision, and hearing.
1. Describes an acute change in mental status
2. Confusion and disorientation are central features.
3. Very poor concentration with fluctuating level of arousal
Quick HIT 4. Physiologic changes such as increases in pulse, blood pressure, and respiratory rate
may occur.
One-third of geriatric patients 5. May include hallucinations or delusions
presenting to the emergency 6. Associated with increased complications and mortality rates
room or admitted to the hospi- 7. The effects of these changes and the associated decline in condition may last
tal will experience delirium.
months.
8. Heightens risk of functional decline and nursing home placement
s
9. Exact etiology unknown, but some evidence suggests altered cerebral perfu-
e
m
sion or cholinergic deficiency may play a role; may be a multifactorial form of
o
r
encephalopathy.
d
n
y
10. Affects up to one-third of geriatric emergency room and hospitalized patients
S
Quick HIT 11. Risk factors for developing delirium include advanced age, medication use, poor
c
i
r
vision or hearing, trauma or surgery, dementia, restraint use, and serious underly-
t
a
i
Delirium is associated with ing medical conditions (Table 2-10).
r
e
G
visual hallucinations, whereas 12. Increases hospital lengths of stay and costs
auditory hallucinations are
more common with primary 13. Dementia and other acute and chronic medical conditions increase risk for devel-
psychiatric disease. oping delirium.
1. There are three types: hypoactive, hyperactive, and mixed.
2. Hypoactive patient may be difficult to arouse and keep awake for an interview or
examthis is the most common type.
3. Hyperactive patients may be agitated and physically difficult to control.
TABLE 2-10 Risk Factors for Delirium

Old age
Dementia
Hearing of vision loss
Medication use
Restraint or foley catheter use
Major trauma or surgery
Severe systemic illness
Infection
Dehydration
Malnutrition
EtOH and substance abuse
TABLE 2-11 Medications Associated with or Contributing to Delirium

Narcotics
Anxiolytics/sedatives
Anticonvulsants
Levodopa/carbidopa
Antihistamines (H1 and H2)
Anticholinergics
Psychotropics
Antihypertensives, especially centrally acting
Hypoglycemics
4. Mixed patient may be difficult to arouse during the day, but agitated and difficult to
control at nightthis is the classic sundowning that can occur with patients suf-
fering from dementia.
5. Sundowning is associated with dementia and thought to result from end-of-day fa-
tigue along with diminished sensory cues in the evening.
G
6. All types are acute in nature, affect the patients cognition, and fluctuate over time.
e
r
i
7. There may be periods of return to baseline or normalcy that can produce conflict-
a
t
r
ing assessments of the patient.
i
c
8. Disorientation and confusion are key features along with difficulty maintaining at-
S
y
tention or focus.
n
d
r
9. Memory deficits will be accentuated.
o
m
10. The sleep cycle may be totally reversed, with daytime sleeping and nighttime wake-
e
s
fulness or agitation.
11. Hallucinations, if present, are generally visual.
12. Medication use, in particular, narcotics, sedatives, and those with anticholinergic Quick HIT
effects, can precipitate or contribute to development of delirium (Table 2-11). Sundowning refers to a phe-
nomenon in dementia patients
C. D ia g n o s is (Table 2 -1 2 ) where with increasing fatigue
1. History and physical examination to evaluate status of known conditions and to and decreasing sensory cues
detect previously unknown disease. at the end of the day, the pa-
2. Medications should be reviewed. tient becomes more confused
3. History of drug and alcohol use, including recent abstention. and oftentimes agitated as a
result.
4. The condition must be differentiated from dementia and depression.
5. Testing to evaluate cognition (e.g., Mini Mental Status Examination)
6. Use instruments to assess for depression (e.g., Geriatric Depression Scale).
TABLE 2-12 Mnemonic for Causes of Delirium (DELIRIUM)

Drugs
Electrolyte disturbance
Lack of drugs (withdrawal)
Infection
Reduced sensory input
Intracranial process, e.g., stroke or bleed
Urinary/fecal (retention, constipation)
Myocardial/pulmonary
DE LIR IU M
Common ca us e s : me dica tions ,

infe ction, e le ctrolyte a bnorma lity,
toxic inge s tion, hypoxia , ne urologic
dis orde r, ps ychia tric illne s s , he pa tic
e nce pha lopa thy, ure mia
Che ck a ll me dica tions
Be nzodia ze pine s Che ck : CBC, e le ctrolyte s ,

Anticholine rgic drugs re na l function, urina lys is ,
Na rcotics TS H, fre e T4, puls e ox, CXR,
Digoxin LFTs , toxic s ubs ta nce s cre e n
Anticonvuls a nts
Dia be te s drugs
Cime tidine
Nume rous othe rs Abnorma l Norma l
Infe ction Che ck bra in CT or MI

Thyroid dys function
s
Hypona tre mia
e
m
Hype rna tre mia
o
Hypoglyce mia Norma l Abnorma l
r
d
He pa tic e nce pha lopa thy
n
(cons ide r LP )
y
Hypoxia
S
Ure mia
c
i
Toxic inge s tion
r
t
P s ychia tric illne s s S ubdura l he ma toma
a
i
r
Hype rte ns ive Bra in tumor
e
G
Concus s ion S troke
Alcohol withdra wa l
Ce re bra l infe ction
FIGURE
2 -5 Evaluation of delirium.
(Adapted from Baldor RA, Ehrlich AM. Am Fam Physician. 2003;67:10271034.)
7. Confusion Assessment Method is screening tool for delirium.

Positive screen has:
a. Acute onset with fluctuating course and
b. Attention unfocused and either
c. Altered thinking or
d. Altered consciousness
8. Laboratory/testing to screen for disease (Figure 2-5)
a. Pulse oximetry to detect hypoxia as a cause
b. CBC to screen for anemia or possible infection
c. Metabolic profile to assess for renal or liver disease, dehydration, and electrolyte
disturbances
d. TSH to evaluate for hypo- or hyperthyroidism as a cause of altered mental
status
e. Urinalysis with culture to assess for infection, kidney disease, dehydration
f. Consider electrocardiogram (EKG), cardiac markers, CXR, or CT scans to evalu-
ate for myocardial infarction, bleed/stroke, or infection, particularly in patients
who are unable to provide a reliable history.
g. Electroencephalogram may be warranted in the hypoactive form to assess for
occult seizure activity. In patients with delirium, slow wave activity would be
expected.
TABLE 2-13 Environmental/Behavioral Treatment of Delirium

Determine level of risk
Appropriate environmental cues for day/night
Utilize eyeglasses or hearing aids as appropriate
Quick HIT
Maintain hydration and nutrition Confusion Assessment
Method screening looks for
Engage patient to be as active as possible, in conversation, providing orientation the three As of Acute onset
Encourage time with familiar faces and use of familiar items of unfocused Attention and
either Altered thinking or
Allow for sleep without disturbances as much as possible consciousness.
Monitor bowel and bladder function
Avoid restraints and Foley catheters when possible
Minimize medication use
Treat pain adequately
Treat underlying conditions
D. Tre a tm e n t
1. Prevention and proactive measures can help lessen the risk of developing delirium
G
e
(Table 2-13).
r
i
a
a. Maintain hydration
t
r
i
b. Treat pain adequately
c
S
c. Prevent constipation
y
n
d. Avoid restraints
d
r
e. Minimize or avoid high-risk medications
o
m
f. Avoid urinary catheters if possible
e
s
g. Provide orientation
h. Limit sleep interruptions
i. Use sensory aids such as glasses and hearing aids
j. Involve in conversation and activities
2. Treat underlying diseases/conditions.
3. Acute therapy may involve use of medication in addition to environmental and be-
havioral methods outlined in Table 2-13.
4. Medication use (Table 2-14)
a. Antipsychotics are the preferred choice of medications.
b. Anxiolytics are second line because they can be associated with agitation or
oversedation.
TABLE 2-14 Medications Used in Treatment of Delirium

Medication Starting Dose Cautions
Antipsychotic
Haloperidol 0.51 mg po bid Sedation
Risperidone 0.5 mg po bid Parkinsonism
Olanzapine 2.5 mg po qd Tardive dyskinesia
Quetipine 25 mg po bid Neuroleptic malignant syndrome
Prolonged QT
Anxiolytic
Lorazepam 0.5 mg po q 4 hr prn Sedation, agitation
5. Prognosis is related to prompt recognition and management.

a. Improvement may occur within days.
b. Often, complete resolution takes weeks or longer.
c. Not always reversible
6. Development of delirium is associated with decline in function and worsening
dementia.
7. Mortality is increased 1.5 to 3 over the following year in those who develop
delirium.
CLINICAL PEARL 2-5

The Three Ds for Altered Mental Status
Differential diagnosis of altered mental status in the geriatric patient involves distinguishing the three Ds
Delerium, Dementia, and Depression:
Delirium Dementia Depression
Onset Abrupt Gradual Abrupt or Gradual

Course Acute, reversible Chronic, progressive Shorter course
Fluctuating Stable Reversible, may
fluctuate
s
e
m
Clinical features Disoriented early, Disorientation late, Mood disorder, prior
o
hypoactive, hyper- neurologic exam, psychiatric history,
r
d
n
active nonfocal gait and speech af- depressed mood
y
S
or mixed, may fected late precedes memory
c
have delusions/ loss
i
r
t
hallucinations
a
i
r
e
G
PSYCHOSOCIAL/
BEHAVIORAL ISSUES 3
D e m e ntia
A. General characteristics
1. Dementia is a syndrome (e.g., a group of signs and symptoms) that can be caused
by several different disorders. Dementia is a chronic acquired decline in memory
accompanied by a disturbance in at least one other cognitive function such as
language, visuospatial skills, and executive function that is sufficient to affect
daily life. Quick HIT
P
s
a. For a diagnosis of dementia, cognitive defects MUST impair social and/or
y
c
occupational function and represent a decline from a previous level of functioning. The cognitive defects in
h
o
b. Mild cognitive impairment differs from dementia and is NOT associated with dementia impair social and/
s
o
or occupational function and
impaired function, deficits in other domains, or behavioral disturbances.
c
represent a decline from the
i
a
About 10% to 12% of individuals with cognitive impairment progress to
l
persons baseline function.
/
B
dementia each year.
e
h
2. Memory impairment must be severe enough to affect function.
a
v
a. In addition to impaired memory, diagnostic criteria for dementia include at
i
o
Quick HIT
r
least one of the following:
a
l
Disturbances in language (e.g., aphasia or anomia)
I
s
s
Visuospatial deficits such as the loss of a motor skill or easily getting lost Memory impairment must
u
e
Loss of executive function characterized by the loss of the ability to plan, be present for a diagnosis of
s
dementia.
organize, sequence, and abstract. An example of executive function is
planning a social gathering.
3. Early dementia is characterized by difficulty learning and retaining new
information. Later stages of dementia are characterized by the inability to
access distant memories and impaired judgment and executive function.
Quick HIT
4. Dementia can profoundly affect a patients daily life. It can affect IADLs such as Dementia is a common
disabling condition among
planning meals, managing finances, and driving. In later stages, it can affect ADLs the elderly.
such as eating, bathing, and grooming.
5. About 5% to 15% of individuals aged over 65 suffer from dementia. The incidence
increases with age, and by age 85, > 30% of individuals have dementia.
6. Depression and dementia often overlap, and about 30% of individuals with Quick HIT
dementia have a concomitant depression.
Individuals with dementia are
7. Although delirium is a distinct syndrome, it is important to recognize that at greater risk for delirium.
individuals with dementia are at greater risk for delirium and that dementia can
coexist with treatable delirium.
B. Clinical approach Quick HIT

1. The diagnostic process has three major aims: establish the presence of dementia,
Although most cases of
determine the underlying cause, and identify treatable causes and comorbidities.
dementia are irreversible, a
2. Although < 5% of dementia cases are from reversible causes, early identification of key part of the evaluation is to
dementia can still be of value by allowing time for advanced planning when cogni- identify reversible or partially
tion is more intact, by identifying comorbidities that might influence function, and reversible causes.
by discussing the pros and cons of medical therapy.
67
3. The steps to diagnosis are patient and caregiver history, physical examination,
cognitive tests, basic laboratory testing, and neuroimaging for patients meeting
certain criteria.
4. Patient historyAsk patients and family members about onset, specific deficits,
physical symptoms, and comorbid conditions.
a. A separate interview with family and/or caregiver can be helpful because
patients may not have insight into their problems. Family members may
also be reluctant to share their concerns in front of the patient.
b. Key factors include the details of cognitive deficits, the date of onset, and the
speed of progression.
c. In early dementia, IADLs are more likely to be affected, and it is important to
assess the extent of impairment in activities such as managing money, shopping,
cooking, and transportation.
d. Review all medications, including OTC medications, for drugs that can adversely
affect cognition.
5. Physical exam
a. Physical examination should include a careful neurologic examination and
mental status testing.
Quick HIT 6. Brief cognitive tests serve to detect dementia and to evaluate the overall severity of
memory and cognitive effects.
The MMSE is the most widely
used tool to assess global a. The Mini-Mental Status Exam (MMSE) remains the most widely used
cognition. instrument with a high sensitivity and specificity for separating moderate
dementia from normal cognition.
s
b. Scores on the MMSE range from 0 to 30. Patients with mild dementia usually
e
u
score from 20 to 23; those with moderate disease score from 10 to 19; and those
s
s
I
with severe disease score < 10.
l
a
c. The MMSE tests the domains of memory, attention, construction, language, and
r
o
i
orientation.
v
a
h
d. Educational levels can affect MMSE performance, and information about literacy
e
B
and education should be obtained.
/
l
e. The clock drawing test evaluates frontal lobe function and visuospatial ability. It
a
i
c
takes about 5 to 10 minutes to administer and is widely used.
o
Quick HIT
s
o
f. The Mini-Cognitive Assessment (Mini-Cog) combines the clock drawing test
h
c
with three-item recall. The patient is asked to repeat three unrelated words,
y
Because it is quick and easy to
s
perform the clock drawing, and then recall the three words. Scores range from 0
P
administer, the Mini-Cog can
be a useful tool to screen for to 5, with 1 point for each correctly remembered word and 2 points for a normal
dementia. clock drawing. Scores from 0 to 2 suggest dementia, whereas scores from 3 to 5
make dementia unlikely.
7. Once the presence of dementia is established, a specific cause should be
determined.
a. The role of laboratory investigations and structural imaging is to rule out
reversible causes of dementia and to identify treatable comorbid conditions.
b. Recommended investigations include CBC, a complete metabolic panel, serum
B12 level, TSH, and a VDRL and HIV in those with risk factors.
c. CT and MRI can identify the < 5% cases with a structural lesion that might
otherwise be missed. Because the yield is low, recommending routine imag-
ing for all dementia patients is controversial. Criteria suggesting a greater
likelihood of detecting a structural lesion include early age of onset (< 60),
focal neurologic signs and symptoms, abrupt or rapid decline (weeks to
months), and predisposing conditions such as metastatic cancer, HIV, or
anticoagulant therapy.
d. Lumbar puncture with cerebrospinal analysis may be useful in cases of suspected
neurosyphilis, HIV, or vasculitis.
C. D ia g n o s is (Table 3 -1 )
1. The most common cause of dementia in the United States is Alzheimer disease
(AD), which accounts for about 60% of all cases of dementia. (See the section on
Alzheimer disease in The Primary Dementias.)
P S YC H O S O C I A L / B E H AV I O R A L I S S U E S 69
TABLE 3-1 Distinguishing Clinical Features among the Primary

Dementias
AD FTD LBD Vascular Dementia
(60%65%) (15%) (5%10%) (15%20%)
Memory loss, Personality change, Visual hallucinations, Abrupt onset,

language, executive function, delusions, EPS, stepwise
visual-spatial hyperorality, relative fluctuating mental deterioration,
disturbances, preservation of status, sensitivity to prominent aphasia,
indifference, visuospatial skills antipsychotics motor signs
delusions, agitation
2. Vascular dementia (See the section on Vascular dementia in The Primary

Dementias.)
3. Lewy body dementia (LBD; see the section on Lewy body dementia in The Quick HIT
Primary Dementias.) The most common cause of
4. Frontotemporal dementia (FTD; see the section on Frontotemporal dementia in dementia is AD.
The Primary Dementias.)
5. Space-occupying lesions such as a neoplasm or a chronic subdural hematoma may
cause a potentially reversible dementia.
P
6. Normal pressure hydrocephalus (NPH) is a potentially reversible cause of
Quick HIT
s
y
dementia.
c
h
a. Individuals with NPH have normal CSF pressure and dilated ventricles.
o
The somewhat unpleasant
s
b. NPH is characterized by the triad of dementia, gait disturbance, and urinary
o
phrase Wet, Wobbly, and
c
i
incontinence. The gait is typically shuffling with poor balance.
a
Wacky can be helpful for
l
/
c. Most NPH cases are idiopathic. Secondary causes of NPH include trauma, remembering the classic triad
B
e
subarachnoid hemorrhage, intracranial surgery, and meningitis. for NPH.
h
a
d. CT or MRI may suggest the diagnosis. Findings include ventricular enlargement
v
i
o
out of proportion to the degree of brain atrophy, prominent periventricular
r
a
hyperdensity, and a prominent flow void in the aqueduct and third ventricle
l
I
s
(referred to as the jet sign).
s
u
e. Treatment of NPH is with a ventricular peritoneal shunt. Because only about
e
Quick HIT
s
one-third of patients have sustained improvement after shunting, the difficulty
is in identifying which patients will benefit from shunting. Factors suggesting a
NPH is treated by ventricular
favorable outcome from shunting are recent onset of symptoms (< 6 months),
peritoneal shunting. The
onset of gait disturbance before dementia, absence of significant vascular procedure has about a 30%
disease, hydrocephalus on MRI, and a favorable response to external lumbar success rate.
drainage.
7. Other primary neurologic conditions include MS, Parkinson disease (PD),
Huntington disease, and Wilson disease.
8. Infections
a. HIV infection can cause an AIDS-related dementia.
b. Cryptococcus infection is a rare cause and is usually seen in immunosuppressed
individuals.
c. CreutzfeldtJakob (C-J) disease or spongiform encephalopathy is a rare cause
of dementia. C-J is a slow viral encephalopathy that presents with a rapidly
progressive dementia and myoclonus. C-J patients exhibit a distinctive EEG
pattern.
9. Metabolic disorders
a. Thyroid disease
b. Vitamin B12 deficiency
c. Thiamine deficiencycommon in alcoholics, which, if untreated, can lead to
Korsakoff dementia (irreversible)
10. Drugs and toxins. Chronic alcoholism may cause a dementia independent of
thiamine deficiency.
TABLE 3-2 Distinguishing Features between Dementia

and Pseudodementia
Characteristic Dementia Pseudodementia
Duration of symptoms Long Short

Rapid progression of symptoms Rare Common
Patient complains of memory loss Variable Usual
Description of memory loss Vague Detailed
Do not know answers Uncommon Common
Patient efforts in performing tasks Usually good Typically less effort
Effort to deal with dysfunction High Low
Emotional reaction to symptoms Variable Great distress
History of psychopathology Variable Common
TABLE 3-3 Potentially Reversible Causes of DementiaMnemonic

Acronym Comment
s
e
u
Drugs Anticholinergics, centrally acting drugs
s
s
I
Emotional disorders Pseudodementia from depression
l
a
r
Metabolic and endocrine disorders Thyroid disease common in elderly
o
i
v
Ear and eye impairment Usually contributes rather than causes dementia
a
h
e
B
Nutritional deficiencies B12 and folate deficiency
/
l
Trauma or tumor Subdural hematoma, space-occupying lesion
a
i
c
o
Infections Syphilis, HIV
s
o
Alcohol and drugs Can contribute to or cause dementia, easily
h
c
overlooked
y
s
P
11. Depression can cause pseudodementia, a cognitive decline that mimics AD. Unlike
an AD patient, individuals with pseudodementia do not attempt to hide their
memory loss, but often complain of poor memory. Language and motor skills
also remain intact. Table 3-2 summarizes clinical factors that help differentiate
pseudodementia from dementia.
12. It is especially important to identify potentially reversible causes of dementia.
A helpful mnemonic to remember many of the potentially reversible causes of
dementia is presented in Table 3-3.
D. Treatment and management

1. Treat reversible causes and address treatable comorbidities, which might improve
function.
a. Examples include reversing metabolic abnormalities such as hypothyroidism,
correcting nutritional deficiencies such as a B12 deficiency, or a sensory deficit
such as hearing loss.
b. Treating a concomitant depression may improve cognitive function.
c. Avoid and/or monitor doses of medications with the potential for adverse
cognitive side effects (e.g., anticholinergic drugs, centrally acting drugs such as
opiates, anxiolytics, sedative hypnotics, and steroids).
d. A multidisciplinary approach includes support groups for caregivers/families of
patients with irreversible dementia.
2. Promote brain health by exercise, a balanced diet, controlling blood pressure, blood
glucose, and lipid levels.
3. Cholinesterase inhibitors may delay the progression of dementia in Alzheimer- Quick HIT
type dementia, LBD, PD, and vascular dementia. Strategies to preserve and
protect the vasculature help
E. The primary dementias (Table 3-1) preserve cognition.
1. Alzheimer disease
a. General characteristics
AD is a slowly progressive loss of cognitive function associated with a large
number of -amyloid plaques in the cerebral cortex and neurofibrillary tangles
of tau protein.
The diagnosis requires the presence of a gradual and slowly progressive
dementia with an onset that cannot be attributed to medications or another
neurologic, physical, or psychiatric condition.
Epidemiology
(1) AD is the sixth leading cause of death in the United States (2010), fifth
for those over age 65.
(2) Prevalence increases with ageapproximately 10% to 15% of individuals Quick HIT
over age 65 and about 30% at age 80. Often those with dementia die of
Age is the greatest risk factor
other causes. for AD, and the mean age of
(3) Risk factors include age, family history (especially for early-onset onset is 81.
disease), and Down syndrome.
(4) Women are at greater risk for AD even after adjusting for a longer life
span.
P
s
(5) Heritable component may be present. Chromosomes 21, 14, and 19 have
y
c
h
been linked to AD.
o
s
(6) Chromosome 19 carries the apolipoprotein gene, and its E4 allele is a risk
o
c
factor for AD. APOE-E4 is present in 30% to 40% of patients with AD
i
a
l
over age 65, and two or more APOE-E4 increase the risk of AD by five
/
B
times. However , many normal individuals also have APOE-E4, and it
e
h
a
should not be used as a diagnostic test.
v
i
Pathologic changes consist primarily of plaques and neurofibrillary tangles.
o
r
a
(1) Plaques consist of focal collections of dilated, tortuous, neuritic
l
I
processes surrounding a central amyloid core consisting of -protein.
s
s
u
Plaques may be seen in older individuals without AD but not to as great
e
s
an extent.
(2) Neurofibrillary tangles consist of bundles of neurofilaments and tau
proteins seen in the cytoplasm of neurons. They denote neuronal
degeneration.
(3) These processes damage neurons, causing a loss of synapses and dendrites
(dendritic pruning) and a decrease in the release of neurotransmitters,
especially acetylcholine.
b. Clinical features
AD begins insidiously, but tends to progress at a steady rate (Table 3-4).
The average time from onset to death is 5 to 10 years. Table 3-4 presents the
typical but highly variable time course of AD.
c. Diagnosis
AD is a clinical diagnosis. Criteria include memory impairment plus one or Quick HIT
more of the following: disturbance of language (aphasia), impaired motor AD is a clinical diagnosis. No
ability (apraxia), inability to identify objects (anomia), and/or a disturbance in test is diagnostic for AD.
executive functions. The time course must be gradual and progressive, and the
symptoms cannot be explained by another cause.
A CT or MRI usually shows cortical atrophy with enlargement of the
ventricles. Atrophy supports the diagnosis, but is not diagnostic. Imaging is
more useful for excluding other causes than for making the diagnosis of AD.
Genetic testing and commercial Alzheimer blood tests are not currently
recommended for clinical use.
TABLE 3-4 Time Course of AD

Mild
Cognitive Mild Moderate Severe
Impairment Dementia Dementia Dementia Death
Duration 5+ yr 510 yr 510 yr 510 yr Survival can be

up to 220 yr at
each stage
MMSE score 2430 2023 1019 09
Features Subjective Functional Clear-cut Difficulty to Complications
memory loss impairment with memory loss; perform ADLs of infections,
noted by patient repetition of difficulty with altered wounds, medical
with normal questions and to perform mental status illness, and
function conversations IADLs with sleep aspiration
reversal, con-
fusion, and
agitation
Modified from Table 19-6 of Rosenthal TC, William ME, Naughton BJ. Office Care Geriatrics. Philadelphia, PA: Lippincott
Williams & Wilkins, 2009.
Autopsy findings indicate that a premortem diagnosis of AD is about 90%

s
e
u
accurate.
s
s
d. Treatment
I
l
a
The goals of treatment are to improve quality of life and executive function.
r
o
In AD, the neuronal cells that make acetylcholine are damaged, affect-
i
v
a
ing memory and thinking over time. Cholinesterase inhibitors work by
h
e
B
slowing the breakdown of acetylcholine and help compensate for the loss of
/
functioning brain cells.
l
a
i
c
Donepezil, galantamine, and rivastigmine are all cholinesterase inhibitors
o
s
approved for mild to moderate AD. Donepezil is also approved for use in
o
h
severe AD.
c
y
In about 10% to 25% of AD patients, cholinesterase inhibitors provide a
s
P
modest improvement in cognitive function, but many more show less rapid
decline. Cholinesterase inhibitors may also benefit patients with PD, LBD and
vascular dementia.
(1) Disease progression may be delayed by 6 to 18 months.
Quick HIT (2) Cholinesterase inhibitors may also improve sleep, energy levels,
and appetite, which can help delay the need for nursing home (NH)
There is a wide variation in placement.
response to cholinesterase Deciding when to stop therapy is not always clear. There is limited evidence
inhibitors. of effectiveness in severe AD, and cholinesterase inhibitors are often
discontinued in late-stage disease.
Side effects include nausea, vomiting, diarrhea, and bradycardia.
Contraindications include uncontrolled asthma, angle-closure glaucoma,
sick sinus syndrome, and cardiac conduction abnormalities.
Memantine, an N-methyl-D-aspartate receptor antagonist, is approved for the
treatment of moderate to severe AD. It is generally well tolerated and can be
combined with a cholinesterase inhibitor.
Gingko biloba and vitamin E are not recommended.
Behavioral disturbances are common, and treatment should be individualized.
Identifying whether the disturbance is distressing to the patient or potentially
harmful helps direct treatment.
Identifying and addressing environmental triggers and excluding physical
discomfort is a key principle.
(1) Exclude physical discomfort from an underlying cause such as an

infection, constipation, untreated pain, or urinary retention.
(2) Maintaining routines, avoiding unfamiliar environments, minimizing
overstimulation, relieving pain, and correcting sensory impairment are
strategies to avoid environmental triggers that cause disturbances.
(3) When confronting an agitated patient, stay calm, use a gentle approach,
use nonverbal communication such as smiling, give reassurance,
acknowledge concerns, and use distraction and redirection.
(4) Music may defuse the intensity of an uncomfortable situation.
(5) Increasing daytime activities may reduce nighttime disturbances.
Involvement in chores, such as meal preparation or caring for a pet,
is a common strategy.
(6) About 20% of AD patients experience delusions and hallucinations. If
these behaviors are not disturbing to the patient, no treatment may be
necessary. In some instances, a low-dose antipsychotic such as haloperidol
is useful.
(a) Antipsychotics have significant side effects and increase mortality.
They should be used with caution and at the lowest effective dose.
Their continued need should be reassessed periodically.
(b) Haloperidol and other high-potency phenothiazines are less sedating.
Extrapyramidal symptoms (EPS) are common with haloperidol, and
if troublesome, a trial of an atypical antipsychotic (e.g., risperidone or
quetiapine) is indicated.
P
(7) If depression is present, a trial of antidepressants is indicated.
s
y
(8) Developing a regular sleep routine and avoiding daytime naps may
c
h
help insomnia and avoid sleep/wake cycle disturbances. Trazodone is
o
s
frequently used to help restore a normal sleep/wake cycle.
o
c
i
a
l
/
B
e
h
a
v
ACASEOF AD
i
o
C.T., an 83-year-old widow who has been living alone for the last 5 years, manages her own
r
a
l
shopping, cooking, and housekeeping. Her next-door neighbor sometimes helps her with er-
I
s
s
rands and other small chores.
u
e
She was recently stopped by the police for weaving between lanes while driving. She was
s
disoriented, confused, and could not tell the police where she was going. They brought her to
the hospital, where she was admitted for further evaluation.
Her past medical conditions include hypertension and osteoarthritis. Her medications
are lisinopril and acetaminophen. She has no living relatives. When contacted, her neighbor
relates that C.T. has been gradually getting more forgetful. The neighbor also tells you that C.T.
is a former bookkeeper with at least a high school education.
C.T. is oriented to name, not to place or time. Her vital signs are 130/80, she is afebrile, and
her respiratory rate is 12. She does not appear acutely distressed and is very friendly. She
scores 20/30 on her MMSE. Her physical examination is otherwise normal.
Included in the differential diagnosis is an acute delirium, dementia, or an acute delirium
with an underlying dementia. Tests to rule out a reversible cause of her cognitive impairment
are done and her CBC, CMP, UA, TSH, B12, and RPR are all normal. A head MRI shows moder-
ate cortical atrophy. Throughout her hospitalization, she remains stable with no change in her
cognitive function.
C.T. does not appear to have delirium. Her physical examination and laboratory testing
do not show any abnormalities suggesting an acute reversible cause of her cognitive de-
fect. The two most common causes of dementia are AD and vascular dementia. Her MMSE
is consistent with dementia, and the neighbors history of C.T. getting slowly but progres-
sively more forgetful is consistent with the diagnosis of AD. Vascular dementia has a more
abrupt onset with stepwise progression and evidence of old strokes or vascular disease on
neuroimaging.
She is started on donepezil 5 mg. Her neighbor knows C.T. well and agrees to be appointed
as guardian. She and C.T. agree to C.T. being moved to an assisted living facility.
(9) Agitation is seen in up to 80% of AD patients and is a frequent cause of

NH placement. Consider a superimposed delirium when an individual
with AD becomes acutely agitated.
2. Vascular dementia is the second most common cause of dementia and accounts for
about 15% to 20% of cases in the United States.
a. Vascular dementia is characterized by a stepwise decline in cognitive function
caused by a series of small cerebral infarctions.
b. Vascular dementia can occur alone or in combination with other disorders
that cause dementia. About 10% to 30% of individuals have a mixed cause of
dementia.
c. Most individuals with vascular dementia have a history of hypertension and
other risk factors for vascular disease such as smoking, hyperlipidemia, and
diabetes.
d. It is more common in men.
e. Neurologic examination often reveals focal neurologic findings such as
weakness, a sensory defect, or a Babinski reflex.
f. Neuroimaging may show evidence of old strokes, lacunae, or damage from
small-vessel disease.
g. Treatment involves addressing risk factors, e.g., controlling blood pressure,
smoking cessation, and lipid control. Although there is no clear evidence of
benefit, many physicians prescribe daily aspirin.
h. Although not FDA-approved for treating vascular dementia, cholinesterase
inhibitors may be of modest benefit.
s
3. Lewy body dementia
e
u
a. LBD accounts for about 5% to 10% of dementia cases.
s
s
I
b. LBD has features of both AD and PD, but disease progression is typically more
l
a
rapid.
r
o
i
c. In contrast to AD, visual hallucinations are common early in the course of LBD
v
a
h
and help to clinically distinguish it from AD.
e
B
d. The EPS may be indistinguishable from PD patients, but in LBD, the cognitive
/
l
symptoms precede EPS, which is the reverse of PD.
a
i
c
e. Patients with LBD are very sensitive to the adverse effects of neuroleptic agents.
o
s
o
4. Frontotemporal dementia
h
c
a. FTD was formerly known as Pick disease. About 45% of individuals with FTD
y
s
have Pick bodies, and in those individuals, FTD is still called Pick disease.
P
ACASEOF VASCULAR DEMENTIA
S.A., an 81-year-old man, is brought into the office by his daughter for forgetfulness. S.A.
seemed to be doing well up until 4 months ago when his daughter noticed he was becoming
more forgetful, often forgetting words and names. Last month he had a fall where he sprained
his wrist, but he is unable to give you any details. He remained stable until recently when he
suddenly became a bit more confused, prompting todays visit. He has a history of hyperten-
sion and is a former smoker.
On examination, his blood pressure is 160/90, and he has some mild left leg weakness and
left-sided hyperreflexia. He scores 21/30 on his MMSE.
Lab work is normal, but a CT reveals multiple small lacunar strokes.
S.A. most likely has a mild vascular dementia. Being male, a former smoker, and hyper-
tensive places him at increased risk for vascular dementia. The CT findings of multiple lacu-
nae along with a fairly rapid onset and stepwise progression are all consistent with vascular
dementia.
His treatment consists of optimizing his blood pressure and starting a daily dose of aspirin.
The pros and cons of cholinesterase inhibitor therapy are discussed, and he wants to start
treatment with donepezil. S.A. lives with his daughter, and you initiate a discussion with her
about how to create a safe environment at home and what support services might be of
benefit to him.
b. FTD is an idiopathic neurodegenerative disease characterized by atrophy and

neuronal loss of the frontal and temporal lobes. FTD is one of the most common
forms of dementia in persons < 65 years, with an age of onset usually < 60. It
accounts for 15% to 25% of dementia cases.
c. Personality changes, inappropriate behavior, and language difficulties are
core features of FTD. Patients have relatively preserved memory, which
differs from AD.
d. Other features include a loss of insight, disinhibition, loss of language, and
apathy.
e. Neuroimaging usually shows more focal abnormalities and atrophy in the frontal
and temporal lobes that help distinguish FTD from other primary dementing
processes.
D e p re s s io n
1. Depression is defined by the Diagnostic and Statistical Manual of Mental Disorders
(DSM).
2. Diagnostic criteria include at least 2 weeks of depressed mood or loss of interest in
previously pleasurable activities, plus four other symptoms from the following:
a. Appetite/weight change Quick HIT
P
b. Change in sleep
s
y
c. Change in activity level Depression is not a normal
c
h
d. Lack of energy part of aging, nor is it a normal
o
s
response to an illness.
o
e. Feeling worthless or guilty
c
i
a
f. Inability to concentrate
l
/
g. Thoughts of death
B
e
h. Psychomotor agitation or retardation
h
a
v
3. Major depression in any age group implies that there are no manic or hypomanic
Quick HIT
i
o
features, in which case, a bipolar diagnosis would be more appropriate.
r
a
l
4. Symptoms must be significant enough to interfere with function/life.
I
Depression is three times
s
5. Symptoms must not be substance-related or caused by a medical condition.
s
more common in geriatric
u
e
6. Depression affects about 5% of the general population. patients than in the general
s
7. The incidence of depression is three times higher in geriatric patients, yet it is population.
underdiagnosed in the elderly. Depression in the elderly can occur as a single
episode or as part of a lifelong recurring history of depression.
8. Nearly one-third of residents in long-term care suffer from depression.
9. The risk of suicide increases after age 65. More women attempt suicide, but men
are more likely to complete a suicide attempt. Quick HIT
a. Older widowed white men have the highest suicide rate.
10. Risk factors for developing depression include chronic medical conditions, elevated Depression may be a side
effect of medication, and
levels of stress, social isolation, low income status, single or widowed/divorced, medications should be
history of depression, chronic pain, substance abuse, CNS disease, and use of reviewed and alternatives
certain subgroups of medication (Table 3-5). considered if depression is
considered a possible side
B. Clinical features effect.
1. Patients may present with depressed affect or very nonspecific symptoms such as
irritability, apathy, distractibility, and psychomotor retardation.
2. A common presentation in the elderly is withdrawal from activities and social
interactions (anhedonia) or decline in function.
a. Depression differs from sadness by being persistent, and unlike sadness, major
depression can be disabling, interfering with social duties, IADLs, and self-care.
Quick HIT
3. Many have symptoms consistent with dementia (see Clinical Pearl 3-2)this has Anhedonia is an inability to
derive pleasure from life and is
been termed pseudodementia. a core symptom of depression
4. Many patients complain of somatic symptoms such as abdominal pain, headaches, among the elderly.
or fatigue.
TABLE 3-5 Risk Factors for Depression

Quick HIT
Geriatric patients with depres- History of depression
sion often present with non- Lack of social support/isolation
specific somatic complaints.
Chronic medical disease
Chronic pain
Single, divorced, or widowed
Increased level of stress
Substance abuse
Female gender
Medications
Narcotics
Anxiolytics/sedatives
Anticonvulsants
Levodopa/carbidopa
Antihistamines (H1 and H2)
Anticholinergics
Psychotropics
Antihypertensives, especially centrally acting
s
e
u
Low-income status
s
s
I
l
a
r
o
i
v
a
PEARL
h
CLINICAL 3-1
e
B
/
l
Physical Symptoms of Depression
a
i
c
o
Fatigue/low energy and activity
s
o
h
Weakness
c
y
Body/joint aches
s
P
Headaches
Sleep changes
Appetite change
Memory loss
CLINICAL PEARL 3-2
Distinguishing Dementia from Pseudodementia

Dementia Pseudodementia
Onset Gradual Abrupt or gradual

Course Chronic, progressive, stable Shorter course, reversible, may
fluctuate
Clinical features Disorientation, late nonfocal Mood disorder, prior
findings on neurologic exam, psychiatric history, depressed
gait and speech affected late, mood precedes memory
answers questions wrong loss, maintains orientation,
without concern, periods of highlights own deficits, dont
increased confusion, may know answers, early morning
sundown awakening
5. Complete history should assess for medical conditions such as hypothyroidism or

anemia.
6. Patients with chronic diseases are at increased risk for depression. Quick HIT
a. Thirty percent of patients with stroke will exhibit depression. Older depressed adults are
b. Up to a third of patients with dementia suffer from concomitant depression, less likely to report sadness
which could inhibit their function. than younger adults. With-
c. More than 40% of cancer patients have depression. drawal from usual activities
and somatic symptoms are
d. Up to 40% of PD patients are also affected.
more common ways for de-
7. Maintain a high level of suspicion and screen geriatric patients with physical pression to present in older
symptoms suggestive of depression. patients.
8. Dysthymia is defined as a clinically depressed mood that occurs on most days and
persists for at least 2 years. Dysthymia also differs from major depression in the
degree of severity.
9. Always inquire about suicide.
C. Diagnosis (Figure 3-1) Quick HIT

1. DSM defines the criteria. Psychomotor agitation or
2. PHQ-9 is a questionnaire asking about these criteria and providing a score grid for retardation can be defined as
severity and follow-up response to therapy (Figure 3-2). motor and cognitive underac-
tivity or overactivity.
3. PHQ-2 is a shortened questionnaire utilizing the first two questions from the
PHQ-9if one is positive, then the full PHQ-9 can be administered to establish a
diagnosis utilizing the DSM criteria.
4. If there are questions about or symptoms suggesting mania or hypomania, then
the Mood Questionnaire can be administered to assess for possible bipolar disease
P
s
(Figure 3-3).
y
c
h
5. Signs of depression include:
o
s
a. Appearancewithdrawn appearance, stooped posture, neglected grooming
o
c
b. Behaviorspoorly cooperative with exam, angry outbursts, negative statements
i
a
l
c. Psychomotor retardationslowed speech, slowed movements, slow gait,
/
B
diminished gestures
e
h
Quick HIT
a
d. Psychomotor agitationhand wringing, pacing, inability to sit still
v
i
6. Laboratory testing to screen for disease
o
r
a
a. CBC to screen for anemia or possible infection The PHQ-2 and PHQ-9 can be
l
I
b. Vitamin B12 serum level for pernicious anemia used to screen for depression
s
s
in geriatric patients.
u
c. Metabolic profile to assess for renal or liver disease, dehydration, and electrolyte
e
s
disturbances
d. TSH to evaluate for hypo- or hyperthyroidism as a cause of depressed affect
e. Urinalysis with culture to assess for infection, kidney disease Quick HIT
D. Treatment (Figure 3-4) When considering the diagno-
sis and treatment of depres-
1. Untreated depression is associated with both psychological and physical sion in an older adult, always
dysfunction. consider whether symptoms
2. Therapy can include psychotherapy along with pharmacotherapy. are related to an illness or
a. Three-quarters of patients will respond to treatment. medication, if there is another
behavioral condition pres-
ent such as alcohol abuse or
dementia, and what conditions
CLINICAL PEARL 3-3
are present that may modify
treatment.
Distinguishing Grief from Depression

Grief typically is a reaction that may harbor feelings similar to depression but narrower in scope and in
response to a particular loss or occurrence. The person affected is generally able to function in most aspects
of life and may have sadness that comes in spurts and that is associated with remembrances or reminders of
what they are grieving for. Their basic self-worth and ability to experience pleasure is maintained. Symptoms
improve with time.
Therapy for normal grief reactions may not be necessary if the person has a support structure in place.
If they present for care to a healthcare provider, then treatment most often will include supportive
psychotherapy without the need for medications.
Have you be e n de pre s s e d or s a d ove r the pa s t 2 we e ks ?

AND
Are the re things you like to do for fun a nd have not be e n inte re s te d in doing ove r the pa s t 2 we e ks ?
If ye s to e ithe r
que s tion
How doe s your de pre s s e d mood, s a dne s s, or low inte re s t leve l a ffe ct your eve ryday life ?
Crite ria fo r Majo r De pre s s io n:

Five or more symptoms have
be e n pre s e nt for two we e ks a nd
re pre s e nt a cha nge from
previous functioning.
At le a s t one of the symptoms is
e ithe r de pre s s e d mood or
los s of inte re s t or ple a s ure
While de pre s s e d or expe rie ncing de cre a s e d inte re s t or ple a s ure :

Have you ha d a ny proble ms with your s le e p?
s
e
Have you ha d a ny cha nge s in your a ppe tite a nd have you ga ine d los t or a ny we ight?
u
Have you notice d a ny cha nge s with your e ne rgy or a bility to focus a nd conce ntra te ?
s
s
I
Have your fa mily or frie nds me ntione d tha t you have be e n moving or s pe a king s lowe r tha n us ua l?
l
a
Have you be e n having guilty thoughts running through your he a d tha t bothe r you or ke e p you up a t night?
r
o
Do you have thoughts or pla ns of hurting or killing yours e lf or a nyone e ls e ?
i
v
Do you have a ny fire a rms a t home or a t your workpla ce ?
a
h
e
B
/
l
a
S cre e n for curre nt or pa s t
i
c
o
hypoma nic/ma nic e pis ode s
s
o
h
c
y
s
P
Have you eve r fe lt the comple te oppos ite of de pre s s e d, whe re frie nds a nd fa mily we re worrie d be ca us e
you we re a bnorma lly ha ppy, a ctive, or e ne rge tic?
AND
Have you eve r ha d a high leve l of e ne rgy running through your bodys o much e ne rgy tha t, be ca us e of
tha t e ne rgy, you did not ne e d to s le e p for a t le a s t a few days s tra ight?
If ye s to e ithe r que s tion,

a s k the pa tie nt,
If no, a bipola r s pe ctrum whe n did tha t ha ppe n
dis orde r is le s s like ly. la s t a nd ca n you te ll me
exa ctly wha t wa s going on
In your life a t the time ?
Have you ha d a proble m with de pre s s ion or s a dne s s like this in the pa s t?
If no, the de pre s s ion is a s ingle

If ye s , the de pre s s ion is
e pis ode a nd will ne e d a
re curre nt a nd may ne e d
minimum of 12 months
inde finite the ra py
of tre a tme nt
FIGURE
3 -1 Screening for depression.
(McCarron RM, Xiong GL, Bourgeois J A. Lippincotts Primary Care Psychiatry. Philadelphia, PA: Wolters Kluwer Health, 2009.)
Patie nt He alth Que s tio nnaire (PHQ-9)

Nine S ymptom De pre s s ion Che cklis t
Name : ________________________________________ Date : ________________________________
Ove r the la s t 2 we e ks, how ofte n have you be e n

bothe re d by a ny of the following proble ms ?
(P le a s e circle your a nswe r.)
No t S eve ral Mo re than Ne arly
at All Days Half the Days Eve ry Day
1. Little inte re s t or ple a sure in doing things 0 1 2 3
2. Fe e ling down, de pre s s e d, or hope le s s 0 1 2 3
3. Trouble fa lling or s taying a s le e p, or

0 1 2 3
s le e ping too much
4. Fe e ling tire d or having little e ne rgy 0 1 2 3
5. Poor a ppe tite or ove re a ting 0 1 2 3
6. Fe e ling ba d a bout yourse lfor tha t you

a re a failure or have le t yourse lf or your 0 1 2 3
P
s
fa mily down
y
c
h
o
7. Trouble conce ntra ting on things, s uch
s
o
a s re a ding the news pa pe r or wa tching 0
c
1 2 3
i
a
te levis ion
l
/
B
e
8. Moving or speaking so slowly that other
h
a
people could have noticed. Or the opposite
v
0 3
i
1 2
o
being so fidgety or restless that you have
r
a
been moving around a lot more than usual
l
I
s
s
u
9. Thoughts tha t you would be be tte r off
e
0 1 2 3
s
de a d or of hurting yours e lf in s ome way
Add Co lumns ,
To tal S c o re *, *S core is for he a lthca re

provide r incorpora tion
10. If you circle d a ny proble ms, how

difficult have the s e proble ms ma de it for
you to do your work, ta ke ca re of things No t Diffic ult S o mewhat Ve ry Extre me ly
a t home , or ge t a long with othe r at All Diffic ult Diffic ult Diffic ult
pe ople ?
(P le a s e circle your a nswe r.)
A s core of: 04 is cons ide re d non-de pre s s e d; 59 mild de pre s s ion; 1014 mode ra te de pre s s ion;
1519 mode ra te ly s eve re de pre s s ion; a nd 2027 s eve re de pre s s ion.
P HQ-9 is a da pte d from P RIME ME TODAY.
P HQ Copyright 1999P four Inc. All rights re s e rve d. Re produce d with pe rmis s ion. P RIME ME TODAY is a tra de ma rk of P four Inc.
FIGURE
3 -2 PHQ-9 instrument for depression.
Instructions: Please answer each question to the best of your ability.

YES NO
1. Has there ever been a period of time when you were not your usual
self and
you felt so good or so hyper that other people thought you were not your
normal self or you were so hyper that you got into trouble?
you were so irritable that you shouted at people or started fights or
arguments?
you felt much more self-confident than usual?
you got much less sleep than usual and found you didnt really miss it?
you were much more talkative or spoke much faster than usual?
thoughts raced through your head or you couldnt slow your mind down?
you were so easily distracted by things around you that you had trouble
concentrating or staying on track?
you had much more energy than usual?
you were much more active or did many more things than usual?
you were much more social or outgoing than usual, for example, you tele-
phoned friends in the middle of the night?
s
e
u
you were much more interested in sex than usual?
s
s
I
you did things that were unusual for you or that other people might have
l
a
r
thought were excessive, foolish, or risky?
o
i
v
spending money got you or your family into trouble?
a
h
e
B
2. If you checked YES to more than one of the above, have several of these
/
ever happened during the same period of time?
l
a
i
c
3. How much of a problem did any of these cause youlike being unable to
o
s
work; having family, money, or legal troubles; getting into arguments or
o
h
fights?
c
y
s
Please circle one response only.
P
No Problem Minor Problem Moderate Problem Serious Problem
4. Have any of your blood relatives (i.e., children, siblings, parents, grand-
parents, aunts, uncles) had manic-depressive illness or bipolar disorder?
5. Has a health professional ever told you that you have manic-depressive
illness or bipolar disorder?
If the patient answers:
1. Yes to 7 or more of the 13 items in question number 1;
AND
2. Yes to question number 2;
AND
3. Moderate or Serious to question number 3;
you have a positive screen. All three of the criteria above should be met. A positive screen should be followed by a
comprehensive medical evaluation for bipolar spectrum disorder.
FIGURE
3 -3 Mood Disorder Questionnaire.
DE P R E S S IVE E P IS O DE , MAJ O R
Ma jor de pre s s ive e pis ode

(Qua ntify us ing P HQ-9 or s imila r)
PHQ 9
De pre s s e d mood
Los s of inte re s ts /ple a s ure
Cha nge in s le e p
Cha nge in a ppe tite or we ight
Cha nge in ps ychomotor a ctivity
Los s of e ne rgy
Trouble conce ntra ting
Thoughts of worthle s s ne s s or guilt
Thoughts a bout de a th or s uicide
S uicide
ris k
No Ye s
Eme rge ncy

S ubs ta nce ps ychia tric
P
Ye s No cons ulta tion
a bus e or
s
y
de pe nde nce ?
c
h
o
s
o
c
i
a
Re fe r for s ubs ta nce a bus e
l
/
tre a tme nt unde r ps ychia tric No Ma nic or Ye s
B
cons ulta tion ps ychotic
e
h
s ymptoms
a
v
i
o
r
a
l
I
1. S ta rt a ntide pre s s a nt
s
s
(S S RI a s e ffe ctive a s othe r a ge nts but with fewe r s ide e ffe cts )
u
e
2. P s ychothe ra py
s
3. Encoura ge da ily exe rcis e
Follow up eve ry 2 we e ks
until improve d a nd s ta ble,
the n eve ry 3 months
FIGURE
3 -4 Approach to diagnosis and treatment of depression.
(Domino FJ , Baldor RA, Golding J , et al. 5-Minute Clinical Consult Standard. Philadelphia, PA: Wolters Kluwer Health, 2016.)
b. The usual strategy is to start with a low dose of medication and increase the dose
over 2 to 4 weeks. It may require 2 to 6 weeks of treatment before there are signs
of improvement, and sufficient time is needed before considering a change in
treatment/medication.
c. If side effects are not tolerable or an inadequate response occurs, then a different
drug from another category should be considered.
d. Cognitive limitations may limit ability for psychotherapy.
e. Encourage physical and social activities.
3. There are several classes of medications that can be used (Figure 3-5).
a. The different classes of medications are equally effective. However, an individual
patient may fail to respond to one class of medication yet fully respond to
another class of medications.
ANTIDEPRES S ANTS
S ELECTIVE
S EROTONIN RE-UPTAKE
INHIBITORS
Cita lo p ra m
Es c ita lo p ra m
Flu o xe tin e
Flu vo xa m in e
P a ro xe tin e
S e rtra lin e
S EROTONIN/
NOREPINEPHRINE
RE-UPTAKE INHIBITORS
Ve n la fa xin e
Du loxe tin e
ATYPICAL
ANTIDEPRES S ANTS
Bu p ro p io n
Mirta za p in e
Ne fa zo d o n e
Tra zo d o n e
TRICYCLIC
ANTIDEPRES S ANTS
Am itrip tylin e
Am o xa p in e
s
Clo m ip ra m in e
e
u
De s ip ra m in e
s
Do xe p in
s
I
Im ip ra m in e
l
a
r
Ma p ro tilin e
o
i
No rtrip tylin e
v
a
P ro trip tylin e
h
e
Trim ip ra m in e
B
/
l
MONOAMINE OXIDAS E
a
i
INHIBITORS
c
o
P h e n e lzin e
s
o
Tra n ylc yp ro m in e
h
c
y
DRUGS US ED TO
s
P
TREAT MANIA
Ca rb a m a ze p in e
Lith iu m s a lts
Va lp ro ic a c id
FIGURE
3 -5 Classes of antidepressants for therapy.
(Howland RD, Mycek MJ , Harvey RA, et al. Pharmacology. Philadelphia, PA: LWW, 2005.)
b. Selection of a medication may depend on the presence of other symptoms and

other medications.
c. Prior success would favor reuse of a medication or class.
d. Selective serotonin reuptake inhibitors (SSRIs) are considered a first-line therapy
owing to tolerance and safety.
e. Tricyclic antidepressants are more cautiously used in geriatric patients because
of their sedating and anticholinergic side effects (Figure 3-6).
f. Side effects of some medications are utilized to treat coexisting symptoms.
Insomniatrazodone, tricyclic antidepressants, mirtazapine
Weight lossmirtazapine
Chronic painduloxetine, tricyclic antidepressants
Somnolence or low energySSRI or bupropion
g. For patients with a short life expectancy, methylphenidate may be an appropriate
therapy as a stimulant that can act within days.
S ELECTIVE
S e dating ; may be S EROTONIN RE-UPTAKE Gas tro -
us e ful fo r ag itatio n INHIBITORS inte s tinal
Cita lo p ra m dis tre s s
Es c ita lo p ra m
Flu o xe tin e
Flu vo xa m in e
P a ro xe tin e
S e rtra lin e
S EROTONIN/
NOREPINEPHRINE
RE-UPTAKE INHIBITORS
Ve n la fa xin e
Du loxe tin e
ATYPICAL
ANTIDEPRES S ANTS
Bu p ro p io n
Mirta za p in e
Ne fa zo d o n e
Tra zo d o n e
TRICYCLIC/POLYCYCLIC
ANTIDEPRES S ANTS
Am itrip tylin e
Am o xa p in e
P
Clo m ip ra m in e
s
y
De s ip ra m in e
c
h
Do xe p in
o
s
Im ip ra m in e
o
c
i
Ma p ro tilin e
a
l
/
No rtrip tylin e
B
e
P ro trip tylin e
h
a
Trim ip ra m in e
v
i
o
r
MONOAMINE OXIDAS E
a
Hig h po te ntial
l
INHIBITORS
I
fo r o rtho s tatic
s
P h e n e lzin e We ig ht
s
hypo te ns io n g ain
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e
Tra n ylc yp ro m in e
s
FIGURE
3 -6 Side-effect profiles of antidepressants.
(Howland RD, Mycek MJ , Harvey RA, et al. Pharmacology. Philadelphia, PA: LWW, 2005.)
4. Electroconvulsive therapy (ECT) is used more commonly in geriatric patients than

in younger adults.
a. It is indicated for severe disease or when a rapid response to therapy is needed. Quick HIT
b. Psychotic features, persistent suicidal ideation, continued weight loss, or Approach to therapy includes
worsening psychomotor retardation are reasons for considering ECT. medications and psychother-
c. ECT is refractory to therapy with two different antidepressants. apy, with choice of first-line
d. It is contraindicated in patients with congestive heart failure, recent myocardial medication determined by the
patients past history and pre-
infarction, brain tumor, or aneurysm.
vious antidepressant use. SSRI
e. Risks are primarily related to the risk of anesthesia. ECT is an effective therapy medications are as effective
that is often underused. as other classes and are well
5. Duration of therapy tolerated with a good safety
a. Following a first episode, 6 to 12 months of treatment is warranted. profile.
b. Risk of relapse increases with each successive episode.
c. With a recurrence, 2 to 3 years of therapy should be considered.
d. With additional episodes, long-term therapy is appropriate.
A nxie ty in the Eld e rly

1. Anxiety acts as a warning system to help individuals deal with real threats. Anxiety
that becomes excessive, disruptive, disabling, and disproportional to the situation
is considered pathologic.
2. Until recently, anxiety disorders were believed to decline with age partly because
older patients are less likely to report psychiatric symptoms and more likely to
emphasize their physical complaints.
3. Anxiety disorders affect about 1 in 10 persons aged 65 and older. They are more
common in elderly women than men.
4. The major types of anxiety disorders in the elderly include adjustment disorder
with anxious mood, posttraumatic stress disorder (PTSD), panic attacks, social
anxiety, generalized anxiety disorder (GAD), phobias, and obsessive compulsive
disorder (OCD).
a. Although Anxiety is a normal reaction to a stressful event but when a persons
ability to cope is overwhelmed, excessive anxiety may emerge until the patient
can adjust. This state is referred to as an adjustment disorder with anxious mood
and typically lasts < 6 months.
b. GAD is characterized by anxiety lasting > 6 months beyond a specific cause.
These feelings may wax and wane for years. Many individuals with GAD
understand they worry more than necessary.
A sudden episode of extreme anxiety may be accompanied by a flood of
s
e
u
sympathetic nervous system outflow causing sweating, palpitations, shakiness,
Quick HIT
s
s
and an impending sense of doom or fear of dying. These episodes are referred
I
l
to as panic attacks.
a
r
GAD is the most common
o
GAD is the most common anxiety disorder in older adults. Women are twice
i
v
anxiety disorder among older
a
as likely as men to be affected.
h
individuals.
e
c. Panic disorder is characterized by recurrent unexpected panic attacks.
B
/
d. Phobias are irrational concerns related to a specific experience such as fear of
l
a
i
heights or fear of flying.
c
o
e. A social phobia occurs when an individual feels overwhelmingly anxious or
s
o
h
self-conscious in everyday social situations. Some reasons older adults develop
c
y
a social phobia may be that they find it difficult to remember names or become
s
P
ashamed of their appearance because of illness.
f. OCD is characterized by recurrent intrusive thoughts (obsessions) and/or repeti-
tive behaviors performed in a stereotypical fashion (compulsions).
g. PTSD is the presence of anxiety symptoms lasting at least 1 month following a
severe traumatic episode.
Symptoms can include reexperiencing the trauma, avoidance of activities as-
sociated with the trauma, increased arousal, agitation, insomnia, and poor
concentration.
Symptoms may occur with delayed onset (> 6 months after the event).

ACASEOF PANICATTACKS
J .Z. is a 73-year-old woman who volunteers at the hospital. One day while driving, she began
to experience an overwhelming sense of dread. Her heart raced, and her hands began to
shake. She pulled over, thinking she was having a heart attack. After a few moments, the feel-
ings passed, but since then she keeps recalling the attack and is afraid to drive.
Although it is normal to experience panic in the face of true danger, people with a panic
disorder experience doom without a discernible trigger. Symptoms of a panic attack can in-
clude shortness of breath, hyperventilation, heart racing or palpitations, chest discomfort,
shakiness, sweating, dizziness, numbness, and a fear of dying.
1. Symptoms of anxiety include psychological symptoms such as worry, behavioral
manifestations such as avoidance behaviors, and the following somatic symptoms:
a. General symptomsfatigue, insomnia, and sweatiness
b. Neurologic symptomsdizziness, paresthesia, and tremulousness
c. Cardiac symptomspalpitations, chest pain, and tachycardia
d. Respiratory symptomshyperventilation, choking, and shortness of breath
e. GI symptomsdry mouth, nausea, and diarrhea
f. GU symptomsfrequency and urgency
g. Table 3-6 summarizes common manifestations of anxiety.
2. The differential diagnosis includes multiple medical conditions where there is a
stimulation of the sympathetic nervous system. These include unrecognized cardiac
disease, arrhythmias, CHF, COPD, PE, asthma, hypoxia, anemia, hypoglycemia,
endocrinopathies, movement disorders, stroke and medication reactions.
Table 3-7 lists conditions associated with anxiety.
3. Depression, dementia, and substance disorders are associated with anxiety. About
half of older patients with depression have significant anxiety.
C. Diagnosis
1. The medical causes of anxiety are too extensive to work up every possibility.
A reasonable initial approach is to focus on comorbid diseases, for conditions
suggested by the history and physical, and to eliminate important disorders
such as hyperthyroidism, dysrhythmias, and drug withdrawal that are commonly
associated with anxiety.
P
s
2. Careful history and physical
y
c
h
a. Review of all medications (OTC and prescription; see Table 3-8)
o
s
o
b. Mental state evaluation
c
i
c. Depression and alcohol screening
a
l
/
B
e
h
a
v
Manifestations of Anxiety
i
TABLE 3-6
o
r
a
l
I
s
Excessive worry or fear
s
u
Refusing to do routine activities or being overly preoccupied with routine
e
s
Avoiding social situations
Overly concerned about safety
Racing heart, shallow breathing, trembling, nausea, sweating
Poor sleep
Muscle tension, feeling weak and/or shaky
Hoarding/collecting
Depression
Self-medication with alcohol or other CNS depressants
TABLE 3-7 Conditions Associated with Anxiety

Cardiovascularcoronary artery disease, arrhythmias, congestive heart failure
Endocrinethyroid disease, parathyroid disease, hypoglycemia
Respiratoryasthma, chronic obstructive pulmonary disease, pulmonary embolus
GICrohns, ulcerative colitis
Neurologiccerebrovascular accident, multiple sclerosis, postconcussion syndrome, transient ischemic
attack, PD, essential tremor
TABLE 3-8 Medications Associated with Anxiety

Caffeine
Steroids
Nicotine
Psychotropic meds, e.g., antidepressants, stimulants, antipsychotics
-Agonists
Decongestants
Excess thyroid hormone
TABLE 3-9 General Treatment Strategies to Help Relieve Anxiety

Acknowledge worries and address any fears that can be handled
Talk with family, a friend, or spiritual leader
Consider adopting stress management techniques such as meditation, prayer, yoga, or deep breathing
Exercise
Avoid things that can aggravate the symptoms of anxiety disorders
Caffeine (coffee, tea, soda, chocolate)
s
e
u
Nicotine (smoking)
s
s
I
Overeating
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a
r
o
OTC cold medications
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v
a
Certain illegal drugs
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e
B
Certain herbal supplements
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Alcohol
a
i
c
o
Allow time for treatment to work
s
o
h
c
y
s
P
3. Lab work
a. CBC
b. TSH
c. B12/folate
d. Chemistry panel
e. Pulse oximetry
f. EKG
g. Consider drug and alcohol screening (if the index of suspicion is high)
D. Treatment
1. Anxiety disorders are very treatable, yet only about one in three individuals receive
treatment.
2. Table 3-9 summarizes general treatment strategies. Management strategies also
include psychotherapeutic and pharmacologic interventions. A combined approach
yields the best results.
3. Psychotherapy helps to alleviate symptoms through insight, education, support,
and the reconditioning of behavioral patterns. Psychotherapy requires a cognitively
intact and motivated patient.
a. Cognitive behavioral therapy (CBT) may be useful for GAD, panic disorder,
and OCD.
b. Graded desensitization using gradual exposure with strategies to manage the
resulting anxiety may be helpful for treating phobias and panic disorder.
CLINICAL PEARL 3-4

Quick HIT
CBT is viewed as an effective therapy for anxiety. It focuses on thinking patterns and behaviors that are either
triggering or sustaining anxiety. It helps an individual look at his or her fears in a more realistic light. In exposure therapy, a person
is exposed to a panic trigger in
a safe and controlled environ-
ment, giving him or her the
opportunity to learn healthier
CLINICAL PEARL 3-5 means of coping.
Regardless of medication choice, make patients aware that although treatment is likely to help, it will not
eradicate symptoms. Reviewing objective markers of improvement such as enjoying an outing with friends
is helpful for assessing therapy.

A Case of PTSD J .P. is a 78-year-old woman who was mugged in a shopping mall. In addition
to having her purse stolen, she fell and broke her arm. Several months later, she tells you that
she continually worries about the episode and finds it difficult to leave her home. She also
has difficulty sleeping.
You suspect J .P. has PTSD and prescribe an SSRI. J .P. is well educated and very motivated Quick HIT
about getting better so she can go back to enjoying outings with her friends. You also refer Supportive therapy that
J .P. for counseling. After a few weeks, you see her back in the office, and although she does
P
includes education,
s
still think about the episode, it is no longer nearly as troubling. She is sleeping better and is empathetic listening,
y
c
able to go out with her friends. reassurance, guidance, and
h
o
encouragement is strategies
s
o
for treating anxiety disorders
c
i
a
in the primary care setting.
l
/
B
c. In primary care, empathetic support and education are common strategies.
e
h
For example, reassuring patients that they are not weak and that they are
a
v
not going crazy or do not have an incurable disease can help alleviate
i
Quick HIT
o
r
symptoms.
a
l
4. Pharmacotherapy includes benzodiazepines (BZDs), antidepressants, -blockers,
I
s
Consider referring patients
s
buspirone, and anticonvulsants.
u
for psychotherapy when
e
a. SSRIs and serotonin norepinephrine reuptake inhibitors are often used as
s
symptoms are disabling or not
first-line agents in the treatment of anxiety. As with depression, it may take responding to medication. Also
several weeks for these agents to be effective. refer if there is evidence of
b. Venlafaxine is effective for social phobias and GAD. substance abuse.
c. -Blockers reduce sympathetic nervous system outflow symptoms and are useful
for panic attacks.
d. Buspirone is effective for GAD. It takes 1 to 3 weeks to see an effect. Benefits are
that it is not addictive; tolerance and CNS depression do not occur. Dizziness is
a common side effect.
Quick HIT
e. BZDs are often used for acute anxiety, GAD, panic, and OCD. In some patients, BZDs with shorter half-lives
they provide rapid symptom relief. However, the riskbenefit ratio is poorer for are safer in older patients.
older adults than for younger adults.
f. In the elderly, BZDs with long half-lives should be avoided. Side effects include
dependence, misuse, falls, MVAs, and withdrawal. BZDs have been linked to
cognitive impairment and can be fatal if taken in combination with alcohol or
other CNS drugs. Limiting BZDs to short-term use, for example, 60 to 90 days,
Quick HIT
is recommended. Advise patients of the risk of
dependence with BZDs and
g. Pregabalin is approved for treating GAD in Europe but not in the United States.
to use the medication only as
TCAs have been used for anxiety disorders, but because of their high side effect prescribed.
profile, they have been largely replaced by SSRIs.
S ub s ta nc e A b us e a nd the Eld e rly

Quick HIT 1. Substance use is defined as the problematic use of prescription drugs, alcohol,
tobacco, or illicit drugs.
Do not overlook the possibility
of alcohol or other substance 2. Traditionally, substance abuse was viewed as a problem of younger adults.
abuse in older patients. Although substance abuse occurs in a smaller percentage of the elderly, it is
still a significant problem.
a. As the baby boomer generation ages, there is an expected increase in the
numbers of older adults who may abuse substances.
3. Prescription drug abuse and misuse is a bigger problem among older adults
Quick HIT than illicit drug use. An estimated 10% to 15% of elderly intentionally misuse
prescription drugs, and about 1% use illicit drugs.
The boomers are coming, 4. The three most commonly abused classes of prescription are opioids, CNS
and the absolute number of
depressants such as BZDs, and stimulants. At least one in four older adults is
elderly with substance abuse
problems will be increasing. prescribed psychoactive medications with abuse potential.
a. The use of psychoactive drugs is more common among women.
b. Woman are more likely to become dependent if they are widowed, less educated,
poorer, in bad health, and have reduced social support.
c. The chronic use of BZDs is associated with mobility problems, disability, motor
Quick HIT vehicle accidents, falls, and problems with ADLs. Chronic use is associated with
cognitive decline.
The three most commonly d. Red flags for prescription misuse include doctor shopping, drug-seeking
s
e
abused classes of drugs are
u
behavior, poor self-care, and trouble sleeping. Table 3-10 lists some other risk
s
opioids, CNS depressants, and
s
factors for prescription misuse.
I
stimulants.
l
e. In long-term care settings, there is an associated risk of urinary retention and
a
r
o
pressure ulcers with sedative hypnotics.
i
v
a
5. Chronic pain is common in the elderly (25% to 50% in community settings), and
h
e
one in five older adults takes analgesics several times a week, often opioids.
B
Quick HIT
/
a. Candidates for opioid therapy should have a well-defined source of pain.
l
a
i
Those with ill-defined musculoskeletal pain are poor candidates for opioid use.
c
o
Opioids should be used carefully in those with a history of substance abuse.
s
Substance abuse is associ-
o
h
ated with cognitive decline. b. Patients using opioids chronically require monitoring of their pain and
c
y
functional status.
s
P
c. Nonsteroidal anti-inflammatory medications should be used cautiously for
chronic pain because of the potential for liver and kidney toxicity, GI bleeding,
and an increased risk of fluid and sodium retention.
Quick HIT
The elderly are more sensitive
to the side effects of opioids.
Their use should be monitored
TABLE 3-10 High-Risk Behaviors for Prescription Drug Misuse
carefully.
Takes multiple prescribed medications
Difficulty remembering how many or what pills to take
Gets prescriptions from two or more doctors
Taking sedatives/hypnotics or pain-relieving meds
Uses up meds too fast
Saves old medications for future use
Chooses between the cost of meds and other necessities
Needs to be reminded by a family member to take pills
Borrows someone elses medications
B. Specific substance abuse disorders

1. Alcohol Abuse
a. More than 60% of seniors drink alcohol, 13% report at-risk drinking, and 15% Quick HIT
report binge drinking. What is moderate alcohol
b. At-risk drinking for the general adult population is defined as more than seven intake for a younger adult (2
drinks per week for a woman, and 14 for a man or more than five drinks on a ounces for men per day and 1
single occasion. ounce for women) may be too
much for the older patient.
A drink is defined as one ounce of alcohol (4 ounces of wine, 12 ounces of
beer or one mixed drink).
Individuals over 65 are more sensitive to alcohol, and some authorities
recommend limiting older men to one drink per day on average and less than
one drink per day for older women. Binge drinking for older men is four or
more drinks on a single occasion or three or more drinks for women.
c. Older individuals reach higher blood alcohol levels than younger individuals
when they consume the same amount of alcohol.
Higher levels relate to a decrease in total body water, which lowers the volume
of distribution, thereby decreasing hepatic metabolism and reducing renal
excretion.
Acute alcohol consumption can interfere with drug metabolism and elevate
liver enzymes. Chronic consumption may induce drug metabolism dysfunc- Quick HIT
tion and cause fluctuating levels of drug clearance.
Alcohol abuse occurs when
d. Alcohol consumption ranges from abstinence to moderate drinking, alcohol there is continued use despite
abuse, and alcohol dependence. Abuse occurs when there is continued use negative consequences.
P
despite negative consequences (Table 3-11).
s
y
e. There is no evidence that moderate intake harms healthy older adults.
c
h
f. Alcohol abuse is a maladaptive pattern of alcohol use causing one or more of the
o
s
o
following: failure to fulfill major obligations at home or work, drinking in situ-
c
i
ations that are physically hazardous, and continued drinking despite social or
a
l
/
health problems worsened by alcohol.
B
e
g. Alcohol dependence requires three or more of the following:
h
a
Tolerancerequiring more alcohol to get high
v
i
o
Drinking in larger amounts or for a longer time than intended
r
a
l
Spending an inordinate amount of time obtaining, using alcohol, or recovering
I
s
from its effects
s
u
e
Giving up important occupational, social, or recreational activities because of
Quick HIT
s
drinking
h. There are two groups of older alcohol misusers. There are two groups of older
Early-onset (70%) drinkers are those who began drinking when younger and alcohol misusers: early-onset
who age with the medical and psychological sequelae related to drinking. drinkers (70%) and late-onset
Typically, these individuals drink more than late-onset drinkers and have more drinkers (30%).
physical, mental, and social problems.
Late-onset (30%) drinkers or those who start drinking after age 50. Late-onset
drinkers often have a stressor such as bereavement, retirement, or a decline
in health status that triggers drinking. They tend to have higher incomes, be Quick HIT
better educated, and have stronger support systems and fewer medical prob-
lems. Although they respond better to treatment, they are more likely to be Alcohol adversely affects
multiple organ systems, and
overlooked than early-onset drinkers. the elderly are more sensitive
i. Older adults are more sensitive to the adverse effects of alcohol. to its effects.
They are at greater risk from falling or delirium.
Table 3-11 WHO Definitions of Alcohol Use

Nonhazardous drinkinguse of alcohol without clear risk of complications
Hazardous drinkinguse of alcohol that increases the risk for complications (at-risk drinking)
Harmful drinkinguse of alcohol that causes complications (includes abuse and dependence)
Chronic alcoholics may develop myopathy, alcoholic hepatitis, fatty liver,

or cirrhosis. One half of elderly patients with cirrhosis die within 1 year of
diagnosis. GI bleeding from gastritis, varices, and MalloryWeiss tears and
pancreatitis are common emergency occurrences among older alcoholics.
Wernicke encephalopathy describes an acute reversible state of confusion,
ataxia, and abnormal eye movements related to thiamine deficiency. Korsakoff
syndrome refers to an isolated memory deficit often manifested by confabu-
lation. Long-term alcohol use can cause dementia, cerebellar damage, or a
peripheral neuropathy.
Alcohol may exacerbate hypertension. A binge episode may trigger an
arrhythmia (holiday heart). Chronic use may cause a cardiac myopathy.
Alcohol adversely affects the immune system and increases the risk of
infection. Aspiration pneumonia may occur with vomiting and a decreased
level of consciousness.
Nutritional deficits are common when food intake is reduced and calories are
derived from alcohol.
Cancers of the head, neck, and esophagus are associated with long-term
alcohol use. The risk is compounded in smokers.
Anemia, macrocytosis, and thrombocytopenia are common in drinkers.
Depression and disturbed sleep are common among alcohol abusers.
2. Diagnosing Alcoholism
a. The CAGE questionnaire is a frequently used screening tool for alcohol abuse
in primary care. The MAST-G (Michigan Alcohol Screening Test) is a screening
s
questionnaire specific to geriatric alcohol use disorders.
e
u
b. Two brief screening questions are: In the past year have you ever drunk or used
s
s
I
drugs more than you intended to? and Have you felt you wanted or needed to
Quick HIT
l
a
cut down on your drinking or drug use in the past year? One positive response
r
o
i
has a nearly 80% sensitivity and specificity for abuse.
v
GGT is the liver enzyme most
a
h
sensitive to alcohol intake. c. Biochemical markers such as an elevated -glutamyltranspeptidase (GGT) and/
e
B
or an elevated mean corpuscular volume suggest possible alcohol abuse.
/
l
d. Other clues to abuse include missed appointments, difficult to control blood
a
i
c
pressure, recurrent accidents or falls, unexpected delirium during a hospitaliza-
o
s
o
tion, frequent emergency department visits, and fluctuating protimes.
h
c
3. Treatment of Alcohol Abuse
y
s
a. Feedback about at-risk drinking is a simple and often effective intervention.
P
Brief interventions work best when they are nonconfrontational and supportive.
Motivational interviewing techniques may improve outcomes.
b. Older adults with alcohol dependence, especially if accompanied by heavy
denial, benefit from referral to a formal treatment program.
c. Those at risk for withdrawal should be detoxified in the hospital setting.
Table 3-12 summarizes withdrawal facts.
TABLE 3-12 Alcohol Withdrawal Facts

Features include tachycardia, sweating, anxiety, confusion, hallucinations, agitation, tremors,
and elevated BP
In older adults, confusion rather than tremor may be an early withdrawal sign
The goal is to prevent delirium tremens (DT) which has a 20% fatality rate
DT complicates about 5% of withdrawals
DT usually develops within 24 d of the last drink but may occur up to a week later
Risk factors include pancreatitis, hepatitis, or other illnessesDT is rare in healthy people
Prevention of DT is the best treatment
Early treatment with benzodiazepines is indicated if withdrawal symptoms are present
Maintaining adequate nutrition is important
d. Long-acting BZDs and supportive therapy, for example, correction of fluid imbal-
ance, vitamin supplementation, blood pressure control, and treating associated
conditions, are the cornerstones for treating withdrawal.
e. Following detoxification, patients should be immediately enrolled in an
inpatient program, day treatment, or outpatient therapy.
f. AA is a no-cost treatment option.
g. Disulfuram is not recommended in older adults because of the risk of serious
side effects.
h. Naltrexone is an opiate antagonist that reduces craving, but its role in geriatrics
is not established. Quick HIT
4. Tobacco
Older smokers are more likely
a. Smoking prevalence declines with age, and about 9% of those > 65 smoke. to suffer from smoking-related
However, those who do smoke are more likely to suffer from smoking-related illnesses.
illnesses because of a longer duration of tobacco use.
b. Regardless of age, individuals benefit from smoking cessation. Cardiovascular
benefits begin immediately.
c. Among smokers who quit at age 65, men add 1.4 to 2.0 years of life, and women
2.7 to 3.4 years.
Just cutting down on smoking instead of stopping does not reduce mortality Quick HIT
from smoking-related illnesses. Regardless of age, smoking
Treatments for smoking cessation are effective and decrease healthcare costs. cessation yields health
Effective treatments combine counseling and medications. benefits.
Nicotine replacement products improve quit rates, but are contraindicated
P
with recent myocardial infarction, unstable or severe angina, uncontrolled
s
y
hypertension, arrhythmias, and gastric ulcer.
c
h
Other agents, for example, bupropion or varenicline, can be used if nicotine
o
s
replacement is contraindicated. Can use in combination with nicotine replace-
o
c
i
ment if previous failure on nicotine replacement alone.
a
l
/
One year after quitting, the risk of heart disease is halved, and the risk of
B
e
stroke, cancer, and lung disease diminishes.
h
a
v
i
o
r
Eld e r A b us e
a
l
I
s
s
u
e
A. Background
s
1. Elder abuse is defined as a purposeful or negligent act that causes harm or a risk of
harm to a vulnerable geriatric person.
2. Being a victim of abuse is associated with increased morbidity and mortality and
decreased survival (Table 3-13).
TABLE 3-13 Health Consequences of Elder Abuse

Declining functional abilities
Increased dependency
Increased sense of helplessness
Increased stress
Worsening psychological decline
Lack of treatment/progression of medical disease
Premature mortality and morbidity
Depression and dementia
Malnutrition
Bedsores
Death
TABLE 3-14 Signs of Elder Abuse

Form of Abuse Signs
Physical abuse Bruises, scars, abrasions, scratches, sprains, broken bones, signs of restraint,
such as marks on the wrist or ankles, or broken eyeglasses
Emotional abuse Changes in the elders personality or behavior, withdrawn, depressed,
dementia-like behavior such as staring, rocking, or mumbling
Financial exploitation Significant withdrawals from accounts, belongings, or money missing from
the elders home, unpaid bills, and unmet needs of elder person despite
apparent resources
Sexual abuse Bruises, scars, scratches, abrasions, bleeding, and infections, especially
around the breasts or genital area, torn undergarments
Quick HIT Neglect Malnutrition, dehydration, poor hygiene, poor/unsafe living environment,
not receiving necessary personal or medical care
Elder abuse is underrecog-
nized and underreported.
a. Victims of abuse and neglect have a risk of mortality that is three times greater
than that for nonabused persons.
Quick HIT 3.
4.
One in ten geriatric patients is a victim of abuse.
An estimated 1.5 to 2 million older adults are abused annually, yet a maximum of
Elder abuse is associated only 5% of such cases are reported.
s
e
with increased morbidity 5. Reasons for underreporting are lack of education regarding elder abuse, attribution
u
and mortality and decreased
s
of injuries to aging, fear of causing problems, and the often vague history and
s
I
survival.
nature of the insults/injuries.
l
a
r
6. In many states it is mandatory to report suspected elder abuse.
o
i
v
7. Categories of abuse are (Table 3-14):
a
h
a. Physicalcausing physical pain or harm to a person by hitting, slapping, or use
e
Quick HIT
B
of other physical or chemical means
/
l
a
b. Sexualsexual contact that is nonconsensual
i
c
Categories of elder abuse are
o
c. Neglectlack of provision of basic needs of a vulnerable person, such as food,
s
physical, sexual, emotional,
o
medication, hygiene, housing, and safety
h
neglect, and financial.
c
d. Financial exploitationwithout permission, taking and using the property or
y
s
P
money of an elderly person for ones own benefit
e. Emotionalcausing mental pain or distress to a person through verbal or
Quick HIT 8.
nonverbal acts that result in embarrassment, humiliation, or fear
Physical disability is associated with being a victim of financial exploitation or
Neglect is the most common neglect.
type of elder abuse. 9. Low-income status, poor health, and lack of social supports are risk factors for
neglect.
10. Mental health disease, substance abuse, and being unemployed and financially
dependent are caregiver traits associated with abuse.
Quick HIT 11. Vulnerable patients in NHs include those who are physically dependent, cognitively
impaired, or who do not have regular visitors.
Any vulnerable older adult is at 12. NHs with high staff turnover or that have substandard conditions, such as over-
risk for abuse. The frail elderly crowding, are more likely to have residents who are abused.
with physical and mental 13. Facilities that have a policy regarding abuse, perform background checks on their
disability are at the greatest
risk for abuse.
employees, and that provide education and training to their staff are less likely to
have employees who are abusers.
14. Social isolation and lack of social support are common threads for risk of abuse
across different settings, both in the home and in facilities.
Quick HIT B. Clinical features

1. History
Social isolation and lack of
social supports are common
a. With suspicion of abuse, the caregiver and potential victim should be
elements in all types of abuse. interviewed separately.
b. Interactions between caregiver and patient should be noted.
c. The patients level of function will need to be determined.

Patients with dementia may not be able to be interviewed.
In these cases, caregiver attributes and assessment for signs of abuse and risk Quick HIT
factors are important. Perpetrators are usually family
d. The current living situation should be defined. members or caregivers.
e. If there are physical injuries, the history surrounding these should be assessed
and a determination should be made as to whether the story is consistent with
the observed injuries.
2. Questions to ask the patient to screen for abuse:
a. Do they feel safe and cared for at home?
b. Has anyone hurt them in any way?
c. Has anyone forced them to do anything they did not want to do?
d. Has anyone taken money or other material things from them without their
permission?
e. Have they ever felt abandoned or that their needs are not being met?
f. Has anyone treated them poorly and belittled them, called them names, or put
them down?
3. Caregiver traits to assess
a. Relationship to patient
b. Who else lives in home and helps with care?
c. Employment status
d. Sense of their socialization or isolation
e. Any obvious evidence of substance abuse or mental instability
P
4. Risk factors to note (Table 3-15)
s
y
a. Degree of disability of patient
c
h
b. Presence of dementia
o
s
c. Low-income status
Quick HIT
o
c
i
d. Amount of social support present/socialization
a
l
/
e. Relationship with caregiver
B
Red flags for the possibility
e
f. Employment and dependency of caregiver of elder abuse are delays in
h
a
g. Evidence or suspicion of substance abuse or mental health disease in caregiver seeking treatment, vague
v
i
o
5. Physical examination history of an injury, a history
r
a
inconsistent with physical
a. Cleanliness/hygiene
l
I
findings, frequent emergency
s
b. Routine physical, including weight
s
department visits, and doctor
u
c. Full skin examination for wounds/injuries, including perineum
e
shopping.
s
d. Mental status examination
TABLE 3-15 Risk Factors for Elder Abuse

Elder Caregiver
Old age Etoh and substance abuse

Dementia Shared living situation with elder
Hearing or vision loss Caregiver dependent/unemployed
Medication use Overwhelmed caregiver situation
Restraint or foley catheter use Mental illness
Major trauma or surgery Criminal history
Severe systemic illness Lack of social support/isolation
Infection
Dehydration
Malnutrition
Etoh and substance abuse
Lack of social support/isolation

ELDER ABUSE
J .S. is a 72-year-old widower who is a retired engineer. He always came to the office well
groomed and dressed. He was physically active, playing golf three times a week at a country
club where he was a member. He lived alone until he was hospitalized for a stroke that left
him with left-sided weakness, and because of this, he decided to live with his daughter. To
make it easier for her to help her father, the daughter sought and obtained power of attorney
from her father.
Over the next few months, J .S. failed to appear for three follow-up visits. The physical
therapist reported that initially J .S. was doing well, but after 2 weeks of visits, the daughter
told him there was not enough money to pay for co-pays and she stopped the visits.
After several calls, the daughter finally brought her father to the doctor. The doctor is sur-
prised to see that J .S. is disheveled, poorly dressed, and unshaven with soiled clothes. He has
lost 10 pounds since discharge. The daughter continually says there is not enough money to
pay for help and that she does not like to make the type of meals her father likes because she
is too busy. Despite recommending resuming PT and suggestions such as Meals on Wheels
or a part-time home health aide, the daughter refuses to do anything because she feels her
father is doing okay.
The doctor believes that the daughter is neglecting her father and may also be exploiting
him financially, because before his stroke J .S. appeared financially comfortable. The doctor
does not think J .S. is in immediate danger, but is sufficiently concerned that he feels both
morally and legally obligated to report the case to Adult Protective Services.
s
e
u
s
s
I
l
a
r
6. Laboratory
o
Quick HIT
i
v
a. There are no specific laboratory tests to detect or diagnose abuse.
a
h
b. If medication misuse or drugging is suspected, then serum levels of
e
B
Elder abuse should be
medications may be appropriate.
/
assessed by direct ques-
l
a
tioning of those involved, c. If urinary infection is suspected, urine culture may be necessary.
i
c
o
determination of risk factors, d. With suspected sexual abuse, examination and culture with blood samples also
s
o
and physical examination. for HIV, hepatitis, and syphilis may be appropriate.
h
c
e. If there are signs of malnutrition, then albumin, prealbumin, and CBC may be
y
s
P
warranted.
f. If physical abuse is suspected or there are injuries, then x-rays for fractures and
head CT for signs of subdural hematomas may be indicated.
C. Interventions
1. Prevention
a. Facility policies regarding abuse
b. Background checks on employees
c. Staff training surrounding the issue of neglect/abuse
d. Increase social supports/regular visits
e. Address caregiver stress and burnout
f. Provide respite care resources
g. Advanced planning
Advanced directives/living wills
Power of attorney can help manage patients finances.
2. When abuse is identified or suspected
a. Documentation of interactions, findings, and examination
b. This documentation will be discoverable as evidence in legal cases.
c. Suspected abuse must be reported to Adult Protective Services.
If safety is not an issue, tell the caregiver that you are obligated to report your
concerns.
If safety is an issue, can do the same but will need to have a social worker
assist with safe placement of patient.
If the patient is in immediate danger, contact police or 911.
CLINICAL PEARL 3-6

Adult Protective Services
Function: To ensure the safety and well-being of vulnerable elderly persons and adults with disabilities.
A vulnerable adult is defined as a person who is being mistreated or is in danger of mistreatment and
who, owing to age and/or disability, is unable to protect himself or herself.
Interventions
If patient in danger, involve emergency services and police.
If not, then case worker assesses situation and risk, and determines needed services and assists in
procuring these to lessen risk.
Ongoing monitoring for resolution.
Competent adults may refuse services.
Long-term care ombudsman programs

Advocates for long-term care residents.
Advise of their rights and help to support these rights.
Work with facilities, residents, and families to address any concerns raised.
If the patient is placed into a facility, the facility will need to be aware of
limiting visitation or provision of supervised visitation.
P
3. Reasons why physicians fail to report elder abuse include victim denial, uncertainty
Quick HIT
s
y
about reporting procedures, uncertainty about laws and reporting requirements,
c
h
and missing subtle signs of abuse.
o
An ageism bias is that sex and
s
o
sexuality are for the young.
c
i
Society may depict older men
a
S e xua lity a nd the O ld e r A d ult
l
/
exhibiting an interest in sex
B
as dirty old men, and older
e
h
women are often character-
a
v
ized as sexless old hags.
i
o
1. It is a myth that older adults are not engaged sexually. A large study found
r
a
l
Americans in the following age groups sexually active: 73% of those aged 57 to 64,
I
s
s
53% of those aged 65 to 74, and 26% of those aged 75 to 85. Many older Americans
u
e
engage in sexual activity into their nineties.
s
a. At all ages, women report less sexual activity than men.
b. Common reasons for changes in sexual activity among older women include
Quick HIT
lack of a partner, partner erectile dysfunction (ED), personal health problems, There is no age at which inter-
and vaginal dryness. est in sex and sexuality ends.
c. Individuals rating their health as good or excellent are about twice as likely to be
sexually active as those in fair or poor health.
2. Some older adults experience a decrease in sexual desire with age. Factors that may
contribute include
a. Not having a partner interested in having sex Quick HIT
b. Hormonal changes of aging, for example, menopause and age-related declines in
Older married adults are
testosterone more likely to remain sexually
active.
CLINICAL PEARL 3-7
Common Myths about Sex and the Elderly

The elderly are not interested in sex.
The elderly are not capable of having sex.
Sexual performance is impossible for those with cognitive decline.
There is no risk of STDs and/or HIV.
CLINICAL PEARL 3-8

Alex Comfort, the author of The Joy of Sex, commented that older people stop having sex for the same rea-
sons they stop riding a bicycle: general infirmity, thinking it looks ridiculous, and lack of a bicycle.
c. Fear of pain and/or discomfort

d. Relationship changes, for example, loss of spouse
3. GLBT adults may find that some healthcare facilities do not welcome same-sex
partners. Older GLBT adults may be reluctant to discuss their sexual orientation
out of fear of discrimination.
4. Sexually transmitted infections (STIs) are not limited to young people, and
providers may fail to appropriately counsel and/or screen older adults for STIs.
Many older adults do not use condoms because they do not consider themselves
Quick HIT to be at risk for STIs.
a. Almost 20% of all people with HIV/AIDS in the United States are aged > 50.
Many providers overlook the b. Thinner vaginal tissue increases the risk of tears and transmission of HIV in
fact that sexually active older
adults can acquire STIs.
older women.
c. Older adults tend to know less about HIV than younger adults.
5. Living in an institutional setting such as a NH or assisted living facility may present
barriers to individuals seeking to have relations.
s
a. Barriers in a NH setting include lack of privacy, lack of a partner, illness, and the
e
u
s
attitude of staff or family members about residents having a sexual relationship.
s
I
b. NHs are still homes, and they should allow privacy for mutually desired sexual
l
a
r
activity or for masturbation. The only true problem is coercive or aggressive
o
i
v
behavior.
a
h
e
B
/
l
1. Problems related to sexual activity and older adults can be grouped into three
a
i
c
categories: physiologic changes related to aging, medical factors, and psychological
o
s
factors. About 50% of sexually active older adults report at least one bothersome
o
h
c
problem.
y
s
a. Natural aging results in a delay in arousal with a greater need for genital
P
stimulation. Erections are less rigid, and there is a decrease in vaginal
secretions, causing more dryness.
b. Women may experience dyspareunia (painful intercourse) with age. After
Quick HIT menopause there is a thinning of the vaginal wall and reduced vaginal
lubrication in response to sexual stimulation. With age the vagina shortens, the
Sexual dysfunction in older labia atrophy, and the cervix may descend into the vagina, causing dyspareunia
women is most often caused
by vaginal dryness. with penetration. Older women are also more likely to experience a delayed or
absent orgasm.
c. Men need more intense stimulation to achieve an erection; erections are less
rigid and may soften during sexual activity; there is a decrease in intensity and
volume of ejaculation and a longer refractory period between erections.
2. The most commonly reported sexual problems by elderly women are low sexual
desire, vaginal dryness, and inability to climax.
3. For men, ED is the most common problem.
4. Men are less likely to report problems to their physician and more likely to seek
their own solutions, such as stopping medications that they think might be respon-
sible for the problem or buying medications online.
5. Past medical history may suggest medical causes of sexual dysfunction associated
with age and include
a. Prescribed medications that impair erections or reduce libido.
b. Diseases that can affect sexual function.
CLINICAL PEARL 3-9

PLISSIT
PLISSIT is an acronym for a widely used model that outlines an approach to sexual assessment and in-
tervention in older adults that includes open-ended questions about sexuality. P stands for permission to
begin the sexual assessment by asking open-ended questions to elicit concerns about sexual health. For
example, may I ask you some questions about your sexual health? LI stands for limited information, and
is the cue to provide information as needed about normal and pathologic changes that may occur with
aging or from a medical condition. Often there are misconceptions that can be dispelled, for example,
that it is unsafe to resume sexual activity after a heart attack. SS are specific suggestions tailored to the
patients needs. For example, someone with sexual dysfunction taking a diuretic for hypertension might
benefit from switching to an ACE inhibitor, or someone with arthritic pain might benefit from taking ac-
etaminophen 2 hours before engaging in sex. IT stands for intensive therapy, which may be indicated for
patients with sexual problems other than those related to normal aging, disease, or environmental factors
such as a lack of privacy. For example, someone might volunteer a history of sexual abuse and merit refer-
ral for therapy.
c. Surgery of the prostate or uterus that can affect sexual functioning.

d. Poor mobility from arthritis or previous strokes.
e. A change in body image from a surgery such as a mastectomy or amputation.
P
f. Incontinence.
s
y
g. The presence of devices such as a catheter or a pessary that can interfere with
c
h
sexual activity.
o
s
o
h. Changes in hormonal function that affect libido.
c
i
a
i. Respiratory disease, cancer, and cardiovascular disease (CVD) may all adversely
l
/
impact sexuality.
B
e
j. Cardiac disease is an UNCOMMON cause of death during or after sex. Sex
h
a
v
with a long-term partner requires the same energy as walking up two flights
i
o
of stairs.
r
a
l
k. Diabetes can cause impotence in men and also may diminish sexual sensation in
I
s
women owing to vascular and neurologic effects.
s
u
e
l. Arthritis may limit movement and impact sexual positions. Creative positions,
s
use of aids, massage, and relaxation techniques may improve sexual perfor-
mance and desire.
m. Shortness of breath from respiratory disease may hinder sexual activity. Optimiz-
ing disease management, supplemental oxygen, counseling about resting at in- Quick HIT
tervals, and limiting exertion may improve sexual function. The contributions of psycho-
n. In cancer patients, the initial focus is on survival, but with better survival times, logical factors should not be
quality-of-life issues become increasingly important, including addressing sexual overlooked when evaluating
function. an older adult with sexual
dysfunction.
6. Medications play a role in about one in four men with ED (see Table 3-16).
Although diuretics are most commonly associated with ED, all antihyperten-
sive medications can cause ED. The antidepressants least likely to cause sexual
dysfunction are bupropion and mirtazapine.
7. Psychosocial history may reveal factors such as having no partner, a lack of pri-
vacy (e.g., in assisted living or NH facilities), negative body image, or relationship Quick HIT
changes.
ED is not normal aging and
C. Diagnosis is most often associated
with neurologic or vascular
1. ED is defined as the inability to achieve a sufficient erection for intercourse. The disease.
prevalence of ED is about 20% to 25% in men 60 to 69 years old and about 30% in
those > 69.
a. Type 2 diabetes triples the risk of ED. Depression also increases the risk of ED.
TABLE 3-16 Drugs Associated with Sexual Dysfunction

SSRIs
Tricyclic antidepressants
MAOIs
Antihypertensive medications
Anticancer drugs
Anticonvulsants
Antipsychotics
Sedatives
Diuretics
Anticholinergics
Antihistamines
Cimetidine
Opiates
Steroids
Illicit drugsmarijuana, amphetamines, cocaine, heroin
s
e
u
s
s
I
b. Other risk factors include CVD, tobacco use, obesity, history of pelvic sur-
l
a
r
gery or radiation, hormonal disorders, illicit drug use, medications, Peyronie
o
i
v
disease, and neurologic conditions such as AD, multiple sclerosis (MS), and
a
h
PD.
e
B
c. Psychological risk factors include anxiety, depression, guilt, history of abuse,
/
l
a
stress, and marital or relationship problems.
i
c
Quick HIT
o
2. ED can be caused by organic causes, psychological causes, or a combination of
s
o
both.
h
c
y
ED may be a sign of
s
P
undetected CVD.
TABLE 3-17 Causes of Dyspareunia in Older Women

Vaginitis
Vaginal atrophy
Cervicitis
Gynecologic masses
Cystitis
Osteoarthritis
Sciatica
Retroverted uterus
Gastrointestinal discomfort (e.g., diverticulosis, constipation, irritable bowel)
Dermatitis
a. Organic causes can be vascular, hormonal, neurogenic, anatomic, or related to

drug/medications or systemic disease. More than 50% of ED causes are vascular.
The cause is often multifactorial.
3. Dyspareunia in women may be related to local factors such as vaginitis or vaginal
atrophy or to other diseases as outlined in Table 3-17.
4. History and physical examination
a. The history should focus on sexual interest (libido), sexual ability, sexual activ-
ity, medications, substance use, comorbid conditions, and the presence of genital
pain, vaginal discharge or dryness, and penile curvature. Loss of libido merits
testing for a testosterone deficiency.
b. Physical examination should focus on the cardiovascular, neurologic, and geni-
tourinary exams.
c. Lab testing is generally limited and may include a glucose level, lipid panel,
TSH, and morning testosterone level in males. LH and prolactin levels should be
considered in those with reduced libido.
D. Treatment
1. General strategies include planning sexual activity; being in a rested and relaxed
state; taking pain medications, if needed, 2 hours before sex; encouraging in-
timacy and communication; using aids when needed; and being affirming and
positive.
a. It is important to remember that there is more to sexuality than penile penetra-
P
tion. Intimacy through sharing, hugging, kissing, and holding each other also
s
y
offers satisfaction.
c
h
2. Strategies for older women include appropriate assessment and management of
o
s
o
urogenital symptoms.
c
i
a
a. Addressing incontinence issues
l
/
B
b. Treating vaginal dryness either with lubricants and/or local or systemic estrogen
e
h
therapy
a
v
c. Surgical intervention if required
i
o
r
3. Addressing lifestyle and modifying medications are the first line of therapy for ED.
a
l
a. Obesity doubles the risk of ED. Losing weight and increasing physical activity
I
s
s
may improve ED.
u
e
s
b. Smoking doubles the risk of ED, and smoking cessation may improve ED.
c. Reducing alcohol intake may be beneficial.
d. Optimizing the treatment of comorbidities may also improve ED.
e. Testosterone deficiency in those with abnormally low levels may improve sexual
function. Treating borderline levels is not indicated.
4. The mainstay of pharmacotherapy for ED is phosphodiesterase type 5 (PDE5)
inhibitors. Quick HIT
a. Available PDE5 inhibitors include sildenafil, tadalafil, and vardenafil. Although
there are differences in dosing, onset and duration of action, all are equally PDE5 inhibitors are contrain-
dicated in individuals taking
effective. nitrates.
b. Side effects include headache, flushing, congestion, and abnormal vision. Less
common are dizziness and nonarteritic optic neuropathy.
c. PDE5 inhibitors should NOT be taken with nitrates. The combination may lead
to a serious and sometimes fatal decrease in blood pressure.
5. Second-line therapy for those who cannot take or do not respond to PDE5 includes
intraurethral insertion of alprostadil or using a vacuum pump device. Consider re-
ferral to urology for a penile implant if other methods fail.
TABLE 3-18 Changes of Aging Contributing to MVAs

Changes in handeye coordination
Slower reflexes
Impaired visionsensitivity to glare, decreased peripheral vision, poorer night vision
Hearing impairment
Slower information processing
Changes in visual-spatial skills
Declines in physical strength
D riving
1. As the number of older Americans increases, so does the number of older drivers.
2. In 2009, there were > 33 million licensed older drivers in the United States. By
2020, about 15% of all drivers will be aged > 65.
s
e
a. About 5,500 adult drivers aged > 65 die annually from car crashes. From age 65
u
s
to 74, motor vehicle accidents (MVAs) are the leading cause of injury-related
s
I
deaths, and from age 74 to 85, MVAs are second after falls.
l
a
r
o
b. Older individuals are three times more likely to die than a younger person fol-
i
v
lowing a car crash. Age-related changes in organ systems and brittle bones make
a
h
e
older crash victims more vulnerable to injury and death.
B
3. Although age-related changes in vision, hearing, and reflexes can affect driving
/
l
a
i
ability, there is no arbitrary cut-off age as to when someone should stop driving.
c
o
The key is driving ability, not the number of birthdays.
s
o
h
4. Although many older drivers are safe drivers and do not need intensive testing,
c
y
others have cognitive impairments, medical conditions, or physiologic impairments
s
P
(see Table 3-18) that compromise their driving ability.
a. There is an increase in crash rate per mile driven for drivers aged > 65 compared
with other age groups.
b. After age 75, the number of fatal crashes increases, and there is a marked in-
crease after age 80. This is due to an increased susceptibility to injury rather
than an increased tendency to get into crashes.
c. Even mild dementia significantly increases the risk of MVAs. Individuals with
a MMSE < 24 should be assessed carefully, and a road test is recommended for
anyone with borderline or questionable impairment.
Quick HIT 5. Driving is important to preserving independence and self-esteem. The loss of the
ability to drive can lead to social isolation and depression. However, protecting a
Older individuals rely on their patients autonomy to drive must be balanced against public safety.
cars to meet their transpor-
tation demands. Although B. Driving assessment
safety should be a principal 1. Obtain a driving history including how often and how far someone drives, types of
concern, unnecessary restric-
roadways used, whether the person drives at night or during rush hour, and recent
tions can adversely impact an
older persons life and social accidents or close calls.
engagement. a. Many older individuals acknowledge a decline in their driving skills and avoid
driving at night, during inclement weather, or in heavy traffic.
TABLE 3-19 Conditions that May Affect Driving

Cardiac disease
Diabetes
PD
Visual impairment, e.g., cataracts
Hearing impairment
Dementia
Stroke
Seizure disorders
Arthritis
Sleep apnea
Neuromuscular disorders
b. Older drivers are less prone to speeding and driving while intoxicated.
c. A recent accident, close call, or getting lost in familiar areas should prompt an
evaluation.
P
s
y
d. Asking a family member if they feel safe with a driver is helpful.
c
h
2. Several conditions common in older individuals can affect driving. These include
o
s
sensory disorders, cognitive impairments, musculoskeletal disorders, stroke, and
o
c
i
sleep apnea. Illnesses such as epilepsy, cardiac disease, and diabetes, which can
a
l
/
cause an abrupt disabling change, are associated with an increased risk of crashes
B
e
(Table 3-19).
h
a
a. Key factors for safe driving are good vision, motor function, and cognition.
v
i
o
b. Visual acuity diminishes with age from physiologic changes and from age-related
Quick HIT
r
a
l
conditions such as glaucoma, cataracts, and macular degeneration.
I
s
s
c. Pain or neck stiffness may make it harder to check traffic. Reaction times slow Illnesses that can cause an
u
e
with aging and can make it more difficult to recognize and respond to an emer- abrupt disabling change need
s
gency. Leg pain and foot abnormalities can affect braking. Diminished strength to be assessed carefully.
may make it hard to turn the steering wheel quickly.
d. Driving requires cognitive skills such as memory, sensory perception, and atten-
tion. Attention deficits impair the ability to track road signs, signs, and traffic.
Drivers need to respond to stimuli such as signs, traffic, and pedestrians and Quick HIT
make appropriate driving decisions.
Sensorimotor, cognitive, and
e. Important parts of the physical exam include screening for dementia, cardiac visual functions are the key
exam, and neurologic exam including testing gait and balance, visual acuity, and factors associated with driving
checking cervical spine, hip, and knee mobility. Functional measures to assess performance.
include vision, hearing, visual-spatial skills, judgment, muscle strength, and
joint flexibility.
f. Treating conditions such as cataracts may preserve a persons ability to drive.
g. In order to keep their licenses, patients may hide impairments.
3. Older individuals are more sensitive to the effects of alcohol and should be cau-
Quick HIT
tioned about drinking any alcohol and driving. The inability to perform physi-
cal activities such as heavy
4. Activity limitation is a red flag that a persons driving ability may be compromised. housework correlates with an
For example, the inability to perform heavy housework correlates with an inability inability to drive.
to drive.
5. Many occupational therapy units offer a formal assessment of an individuals

ability to drive. This can provide an objective evaluation of someones ability to
drive.
C. Safety interventions
1. Older individuals may stop driving on their own, on the advice of a physician or
their family, on failing a driving exam, or on the loss of insurance.
Quick HIT 2. Physicians have a responsibility to express their concerns about a persons ability to
drive to the patient and/or their families.
Providers have a responsi-
bility to communicate their 3. Patients may refuse to stop driving despite advice from family and health providers.
concerns about driving Many states mandate the reporting of conditions such as AD, which may affect the
to the driver and families. ability to drive.
Many states have mandatory 4. In some instances, the family may need to remove the car keys or disable the car by
reporting laws. disconnecting a battery cable.
5. It may be helpful to point out the benefits of not driving such as reducing ex-
penses, improving health by walking more, and expanding ones social circle by
connecting with people to seek rides.
s
e
u
s
s
I
l
a
r
o
i
v
a
h
e
B
/
l
a
i
c
o
s
o
h
c
y
s
P
COMMON
GERIATRIC MEDICAL
CONDITIONS
4
Ge ria tric D e rm a to lo g y
1. Skin diseases occur more commonly with increasing age and sun exposure.
2. Normal aging is associated with increased fragility/thinning of the skin and
wrinkling.
3. Cumulative ultraviolet light exposure causes DNA injury and accentuates these
changes and predisposes to skin cancers.
C
4. Thinning of hair occurs with advancing age.
o
m
5. Loss of follicular melanocytes leads to graying of hair as one ages.
Quick HIT
m
o
n
B. Specific conditions Skin diseases occur more
G
e
1. Pruritus commonly with increasing age
r
i
a
and sun exposure. The most
a. Itching can be because of skin conditions or systemic disease such as liver or
t
r
common skin lesions in the el-
i
c
renal disease. derly are seborrheic keratosis,
M
b. Two common causes of pruritus in geriatric patients are xerosis (dry skin) and seborrheic dermatitis, actinic
e
d
neurodermatitis. keratosis, venous stasis der-
i
c
matitis, tinea pedis, and non-
a
Xerosis
l
melanoma skin cancers.
C
(1) Thinning of the skin and a diminished capacity to function as a moisture
o
n
barrier makes aging skin prone to drying.
d
i
(2) Xerosis can be exacerbated by environmental triggers such as soaps, water
t
i
o
n
exposure, and low humidity.
s
(3) Therapy involves restoring the moisture to the skin.
(a) Adequate oral fluid intake
(b) Avoiding excess contact with soaps or water
(c) Bathing in warm, not hot, water
(d) Applying emollients (e.g., Eucerin and Aquafor) after bathing
(e) For inflamed lesions, topical steroids may be beneficial.
CLINICAL PEARL 4-1
Causes of Pruritus
In addition to xerosis and neurodermatitis, the differential diagnosis of pruritus includes contact dermatitis,
reactions to food or medicines, and parasitic infections. Scabies should be suspected in patients who itch and
have contact with others who itch. Generalized pruritus in the absence of skin disease suggests the possibility
of a systemic disease such as thyroid disease, multiple myeloma, lymphoma, renal failure, or liver disease.
Psychogenic factors such as stress and depression can contribute to pruritus.
103
Neurodermatitis
(1) Occurs most commonly in geriatric patients
(2) Itching with no identifiable underlying pathology that has been associated
with anxiety or a nervous tic
(3) Repeated itchscratch cycle that causes erythema, abrasions, and licheni-
fication of the skin
(4) Therapy involves breaking the itch/scratch cycle.
(a) Topical corticosteroids
(b) Oral antihistamines
(c) Oral or topical doxepin, which is a tricyclic antidepressant with some
antihistamine effect
(d) In refractory cases, immune modulators such as topical tacrolimus or
pimecrolimus may be used.
(e) Emollients to address any component of dryness that may be
contributory
(f) Behavioral counseling
2. Wounds
a. Stasis dermatitis
Disease associated with venous insufficiency in the lower extremities
Occurs more commonly in women who have had children; obese patients;
those who have suffered trauma or surgery to the lower extremities or other
conditions that may impair venous function
Increased prevalence with age, and up to 20% of geriatric patients may be
affected
Associated with reflux of blood across malfunctioning venous valves
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(1) The increased pressure results in edema.
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(2) There is capillary leakage of leukocytes and proteins, including
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fibrinogen.
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(3) These elements are then associated with an inflammatory cascade.
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Diagnosis is clinical, and laboratory testing is not generally warranted.
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(1) Lower extremity edema with erythema and scaling at the medial ankle
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that may extend around the leg and up to the knee
(a) The lesion may develop patches of weeping open areas.
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(b) If infection develops, exudates may be present.
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(c) Erythema and warmth sometimes make stasis dermatitis difficult to
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distinguish from cellulitis.
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(d) Chronic lesions may become hyperpigmented and lichenified.
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(2) Doppler testing may reveal venous insufficiency and, more importantly,
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Quick HIT exclude deep venous thrombosis.
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(3) Biopsy may be warranted if diagnosis is uncertain.
Stasis dermatitis occurs in up Treatment
to 20% of geriatric patients. (1) Elevation and compression stockings may limit capillary leakage and
edema.
(2) Emollients and avoiding scratching/trauma to the legs are important for
preventing secondary infection.
(3) Diuretics may treat edema, but blood pressure (BP), electrolytes, and in-
Quick HIT travascular volume must be monitored.
(4) Inflammation can be treated with topical steroids.
Compression stockings, diuret-
ics, and topical corticosteroids
(5) Suspected infection should be treated with antibiotics.
are the primary treatments for (6) Appropriate topical wound care for open wounds
noninfected stasis dermatitis. (7) If incompetent perforating veins are identified on Doppler testing, referral
for consideration of ligation may be appropriate.
b. Ulcerations
Ulcerations can develop owing to trauma or secondary to a variety of skin
conditions. Ulcerations usually resolve with proper wound care.
Chronic ulcerations can occur in association with stasis dermatitis (venous
ulcers), arterial insufficiency, or as decubitus ulcers, which are also known as
pressure sores.
C O M M O N G E R I AT R I C M E D I C A L C O N D I T I O N S 105
TABLE 4-1 Wound Stages

Stage 1 Intact skin, nonblanchable, red, may be tender
Stage 2 Partial thickness loss, shallow open ulcer, or an intact or ruptured blister
Stage 3 Full-thickness loss, subcutaneous fat visible, no exposed bone, tendon, or muscle
Stage 4 Full-thickness loss with exposed bone, tendon, or muscle
Unstageable Full-thickness loss, base of the ulcer covered by slough or eschar, so the stage
cannot be determined
(1) Venous ulcers will develop in the setting of stasis dermatitis and will oc-
cur in a similar distribution as the edema and dermatitis change.
(2) Arterial insufficiency should be suspected in a nonhealing ulcer in con-
junction with risk factors and findings consistent with vascular disease.
(a) Patients may have claudication in addition to their wound.
(b) Risk factors include hypertension (HTN), smoking, diabetes, and
hyperlipidemia.
(c) Cool extremities with poor pulses, diminished hair distally, and dys-
trophic nails
(3) Decubitus ulcers develop as a result of pressure that impairs capillary flow
to the skin, resulting in necrosis of the skin and soft tissue.
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(a) Generally occur over bony prominences
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(b) Nonambulatory patients are at greatest risk, including those post-
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stroke or with paraplegia, dementia or other neurologic disease.
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(c) Other factors contributing to skin breakdown include moisture, skin
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friction, and shearing forces.
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(d) Diminished sensation is also a risk factor, which may occur with
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neuropathy.
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(e) Wound staging is performed to describe the depth of the wound
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(Table 4-1).
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Treatment
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(1) Local wound care with cleansing for more superficial wounds
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(2) Deeper wounds may require debridement of necrotic tissue.
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(a) Wound packing, special dressing, or wound vacuum may be
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beneficial.
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(b) Antibiotic therapy may be indicated if infection is suspected, as in-
dicated by surrounding skin erythema, purulence, and increased
warmth.
(c) Surgical repair with closure, grafts, or flaps in some stage III/IV ulcers
(3) For venous ulcers, include therapy directed at the underlying stasis
dermatitis.
(4) Arterial insufficiency with a nonhealing wound merits referral for possible
stenting or surgical correction.
(5) In addition to wound care for decubitus ulcers, reducing pressure to the
area (and other areas) is critical.
(a) Frequent turning of the patient with repositioning to avoid pressure
on any given area for > 2 hours
(b) Use of special mattresses designed to lessen and distribute pressure
(c) Good skin care with use of emollients, prevention of shear or friction,
and regular changing of diapers for those who are incontinent
(6) Infected wounds may benefit from systemic antibiotics.
(a) Signs of infection include an increase in necrotic tissue, foul odor, pu-
rulent discharge, increasing pain, fever, and increasing redness around
the edge of the wound.
CLINICAL PEARL 4-2

Venous versus Arterial Ulcerations
It is important to distinguish venous from arterial ulcerations. Therapy for the two types of ulcers differs, and
compression stockings may actually worsen arterial insufficiency. Venous ulcerations tend to occur medially
and in the setting of venous stasis with edema and stasis dermatitis. With arterial disease, there may not be
any edema in a cool hairless extremity with diminished pulses. Doppler testing to determine the ankle-brachial
index (ABI) can help rule out arterial insufficiency. An ABI from 0.7 to 0.9 indicates mild vascular disease, 0.4
Quick HIT to 0.7 moderate, and < 0.4 severe. In the presence of severe disease, revascularization is often needed to heal
an ulcer.
Decubitus ulcers are more
appropriately called pres-
sure ulcers, and, as the name
implies, occur over pressure
points and bony prominences
in susceptible patients. CLINICAL PEARL 4-3
Pressure Ulcers
Pressure ulcers are common, preventable, and treatable. There are four main factors that contribute to the for-
mation of a pressure sore: pressure, shearing forces, friction, and moisture. The amount of pressure required
to occlude the blood supply to the skin is small, and pressure over an area can cause skin damage in as little
as 2 hours. Shearing forces cause angulation and stretching of the subcutaneous tissues and occur when the
skin is fixed against an exterior surface while the subcutaneous tissue is subjected to lateral forces. Friction
caused by the movement of the skin across surfaces, such as sheets, increases the shearing force. These can
lead to thrombosis of small vessels, further compromising blood supply. Moisture compounds the damage.
Other risk factors include anemia and malnutrition. Ninety percent of pressure ulcers occur in the lower body,
s
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mainly in the sacrum, greater trochanter, ischial tuberosities, and heels.
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PEARL
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CLINICAL 4-4
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Principles of Wound Care
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Avoid pressure and moisture.
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Prevent further injury.
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Address risk factors such as anemia and malnutrition.
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Intensive local skin care for stage I and II ulcers
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For stage III and IVulcers,irrigate with saline or Ringers to cleanse and remove debris.
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Remove necrotic tissue with either sharp, autolytic (enzyme), or mechanical (wet to dry dressings)
debridement.
Monitor for signs of infection.
Stage III and IVulcers need special mattresses or beds for healing.
Stage III and IVulcers may require surgery to heal.
Use systemic antibiotics if there are signs of cellulitis or spreading infection.
3. Inflammatory conditions
a. Seborrheic dermatitis
Chronic condition with erythema, increased oiliness, and scales
Associated with colonization by yeast Malassezia furfur
Occurs in 5% of the population; dandruff, the mildest form is most common
More common in patients with Parkinson disease (PD) or HIV
Occurs on the face, scalp, and chest, especially the forehead and nasolabial
folds
Clinical diagnosis based on appearance and location
Treatment
(1) Antidandruff shampoos, such as selenium sulfide
(2) Tar shampoos
(3) Topical ketoconazole available as either a cream or a shampoo
(4) Topical steroids
b. Acne rosacea
Chronic erythema, telangiectasia, and acne lesions on face
Quick HIT
Onset in middle age Seborrheic dermatitis is a
common finding in patients
Associated with flushing triggered by environmental stimuli such as increased with PD.
temperature, alcohol, hot beverages, or heightened emotions
Medications such as niacin may also be a trigger.
Demadex mites may be associated with rosacea; however, this link remains
unproven.
In some cases, the skin thickens, and the nose can become bulbous, which is
termed rhinophyma.
Ocular involvement occurs in some cases with blepharitis and conjunctival
injection.
Diagnosis is made clinically.
Treatment
(1) Topical metronidazole or erythromycin
(2) Acne medications such as benzoyl peroxide
(3) Oral tetracyclines
(4) Topical azelaic acid or isotretinoin
(5) For rhinophyma or prominent telangiectasia, referral for laser or surgical
therapy may be warranted. Quick HIT
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c. Intertrigo
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Inflammation resulting from two skin surfaces being in contact and often as- Rhinophyma is a disfiguring
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complication of acne rosacea,
sociated with moisture or perspiration
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where the skin and tissues of
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Examples of areas involved include skin folds of obese people, inguinal folds,
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the nose thicken, causing it to
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undersurface of the breasts against the lower chest or upper abdomen, web become bulbous.
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spaces of toes, and axillae.
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Tends to occur predominantly in infants and the elderly owing to immobiliza-
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tion and incontinence
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Associated with heat, humidity, and obesity
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On examination, the visible skin may appear normal, but on exploration of
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the crevices of skin folds, there is maceration, inflammation, and often a mild
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odor.
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Often infected with Candida and may become secondarily infected with
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Quick HIT
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bacteria
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Treatment
(1) Drying the involved surface The presence of satellite le-
sions in intertrigo suggests
(2) Exposure to air of the affected surface a secondary infection with
(3) Cautious use of fans or hair dryers on low setting to aid drying Candida.
(4) Corn starch or other powders
(5) Use of cloth to provide a barrier between the skin folds
(6) Topical antifungal powder or cream for suspected fungal infection
(7) Absorbent diapers with frequent changing for incontinence
d. Bullous pemphigoid
Occurs most commonly in the elderly with average age of 65 years
Self-limited but chronic (1 to 5 years) autoimmune inflammatory
Quick HIT
condition Candida skin infections fre-
quently occur with intertrigo.
Antibodies to BPAg1 and BPAg2 form at the epidermal basement membrane,
leading to a local inflammatory response and formation of vesicles with clear
fluid.
The autoantibodies may be associated with or triggered by medication
use.
Symmetric and widespread but favors the trunk and flexural aspects of
extremities
Quick HIT
Bullous pemphigoid is a self-
limited autoimmune disease
frequently triggered by medi-
cation use.
FIGURE
4 -1 Seborrheic keratosis.
(Image provided by Stedmans Medical Dictionary for the Health Professions and Nursing. Illustrated 6th ed. Philadelphia,
PA: LWW, 2007.)
The vesicles resolve without scars and are associated with intense pruritus.
(1) Should be distinguished from pemphigus vulgaris, which produces wide-
spread erosion and bullae with a positive Nikolsky sign.
Diagnosis can be attained using direct and indirect immunofluorescence fol-
s
lowing biopsy
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Treatment
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(1) Oral prednisone initially
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(2) Immunosuppressive medication, such as azathioprine, as steroid-sparing
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therapy
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(3) Limited disease may respond to topical therapy, including topical steroids
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or immune modulators such as tacrolimus or pimecrolimus.
(4) Biologic therapy with rituximab may be considered for refractory disease.
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4. Benign and malignant tumors
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a. Seborrheic keratosis (Figure 4-1)
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Present in > 90% of geriatric patients and many patients have multiple
n
lesions
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Quick HIT Benign overgrowth of epidermal cells with a stuck on or waxy appear-
m
o
ance with variable pigmentation and locations excluding the mucous
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The LeserTrelat sign is an membranes
association between the rapid The sudden appearance of multiple seborrheic keratoses has been associated
appearance of numerous
with adenocarcinoma of the GI tract, leukemia, and lymphoma and is known
seborrheic keratosis and an
underlying cancer. as the LeserTrelat sign.
No diagnostic tests are warranted unless there is concern about the lesion be-
ing malignant, in which case biopsy would be indicated.
If there is a sudden appearance of many lesions, then evaluation for nonder-
matologic cancers may be warranted.
b. Actinic keratosis (Figure 4-2)
Quick HIT Present in up to 25% of the US population and increases with age and UV light
exposure. Fair-skinned individuals are at higher risk.
Seborrheic keratosis have a
stuck on appearance, are These are erythematous scaling lesions on sun-exposed areas that are consid-
usually brown or black in color, ered premalignant.
and occur most commonly on Actinic keratoses feel like areas of roughened skin and are sometimes more
the face and chest. Indications easily felt than seen.
for removal are cosmetic, if
Actinic keratoses may regress, stay the same, or progress to basal cell carci-
they cause irritation by rub-
bing against clothing, or if the noma (BCC) or squamous cell carcinoma (SCC).
diagnosis is uncertain. 30% to 60% of BCC or SCC arise from actinic keratoses, and actinic keratosis
may progress to BCC or SCC at a rate of 2% over 4 years.
FIGURE
4 -2 Actinic keratosis.
PA: LWW, 2007.)
Thick lesions or lesions with ulceration or nodularity may warrant biopsy to

differentiate from an underlying cancer.
Treatment options include:
(1) Cryotherapy
(2) Topical 5-fluorouracil
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(3) Topical imiquimod
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(4) Topical diclofenac
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(5) Photodynamic therapy with delta-aminolevulinic acid
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(6) Avoidance of sun exposure
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(7) Wear protective clothing and use sunscreen with both UV A and UV B
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protection.
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Quick HIT
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c. Squamous cell carcinoma (SCC) (Figure 4-3)
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The second most common skin cancer after BCC
e
Develops from epidermal cells Actinic keratoses are prema-
d
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lignant with < 1% per year risk
c
Risk factors are sun exposure, actinic keratoses, radiation exposure, and being
a
of transformation to a malig-
l
immunocompromised.
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nant lesion. Actinic keratoses
o
Most commonly occurs on sun-exposed areas and presents as a local indura- warrant treatment because
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d
tion, nodule, or ulceration patients frequently have nu-
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i
merous lesions, making it more
o
Is locally invasive with rare occurrence of metastasis
n
likely to develop a skin cancer.
s
Sites more likely to metastasize are those on the lips and ears and those devel-
oping in association with radiation or burn scars.
SCC developing in association with burn or radiation scars are known as Mar-
jolin ulcers.
Biopsy or excision can confirm diagnosis. Definitive therapy involves surgical
excision.
For larger lesions and to evaluate for invasion or metastasis, computed tomog-
raphy (CT) or magnetic resonance imaging (MRI) may be warranted.
For patients who are not surgical candidates or for those with metastasis, ra-
diation or chemotherapy may be indicated.
d. BCC (Figure 4-4)
The most common form of skin cancer (accounting for 70% or more of cases)
Develops from the basal cells in the lower epidermis
Risk factors are sun exposure, actinic keratoses, being immunocompromised,
having fair skin, light eye color, and red or blond hair.
Most common on sun-exposed areas and may have a variable presentation
(1) Nodular with waxy rolled up borders and telangiectasia
(2) Scar-like atrophic appearance of the skin
(3) Superficial scaly, erythematous papular or nodular lesion
FIGURE
4 -3 Squamous cell carcinoma.
PA: LWW, 2007.)
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FIGURE
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4 -4 Basal cell carcinoma.
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PA: LWW, 2007.)
Is locally invasive and rarely metastasizes

Imaging and laboratories are rarely warranted unless lesion is very large and
suspicion of invasion is of concern.
Surgical removal can confirm diagnosis and be curative.
For more advanced disease or for nonsurgical candidates, other options
include:
(1) Curettage and electrodessication
(2) Radiation therapy
(3) Topical medications
(a) 5-fluorouracil
(b) Imiquimod
Quick HIT e. Malignant melanoma (Figure 4-5)
The most common cause of skin cancer deaths despite the fact that it accounts
Both BCC and SCC are locally
invasive cancers that rarely for only 5% of skin cancers
metastasize. Risk factors include sun exposure, family or personal history of melanoma, or
dysplastic nevi.
Th e ABCDs o f Ma lig n a n t Me la n o m a
As ymme try Borde rs Color Dia me te r
6 mm
FIGURE
4 -5 Malignant melanoma.
(Anatomical Chart Company. Understanding Skin Cancer Anatomical Chart. Philadelphia, PA: LWW, 2000.)
TABLE 4-2 Malignant Melanoma Stages

Stage I Depth 1 mm No metastases or nodes involved 90% 5-yr survival
Stage II Depth 12 mm No metastases or nodes involved 40%75% 5-yr survival
Stage III Any depth Positive lymph node 25%70% 5-yr survival
Stage IV Any depth Metastases 10%20% 5-yr survival
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Characteristics to differentiate nevi from melanoma have been described.
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(1) Aasymmetry
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(2) Bborder irregularity
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(3) Ccolor variation within mole
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(4) Ddiameter > 6 mm (size of a pencil eraser)
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(5) Eevolution of the lesion over time
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Because melanoma is more aggressive and subject to metastatic disease, labo-
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ratory testing and imaging are commonly performed and may include:
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(1) Complete blood count (CBC)
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(2) Chemistry profile
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(3) Lactate dehydrogenase (LDH)
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Quick HIT
s
(4) Chest x-ray, CT scans (abdomen and chest), or positron emission tomog-
raphy (PET) scans
Despite the fact that it ac-
Malignant melanoma is staged on the basis of depth of lesion (Table 4-2). counts for only 5% of cancers,
Early disease may be cured with surgical therapy. malignant melanoma is the
Advanced disease may require the use of chemotherapy or biologic leading cause of skin cancer
medications. deaths.
Radiation therapy may be necessary for brain metastases.
CLINICAL PEARL 4-5
Types of Melanoma
There are four types of melanoma: Lentigo maligna melanoma is most often found on the areas of sun-
damaged skin, usually as a slow-growing superficial macule. Superficial spreading melanoma is an irregularly
shaped macule, papule, or plaque of variable color occurring anywhere; nodular melanoma is a rapidly grow-
ing bluish or gray nodule; and acral lentiginous melanoma is found primarily in the palms, soles, and nail beds
of dark brown or black patients.
O ra l He a lth in Ge ria tric P a tie nts

Quick HIT A. General information
Oral health is associated with 1. Oral health is a major concern for many geriatric patients.
general health in the elderly.
Poor oral health has a nega-
a. Access to dental care is limited by the lack of insurance coverage through either
tive impact on nutrition and Medicare or Medicaid.
can be a marker of systemic b. Only half of geriatric patients have had dental visits within the past year and
disease. one-quarter of patients have not seen a dentist within 5 years.
c. Pain, appearance, social function, and nutrition are all affected significantly by
the presence or absence of oral disease.
2. Oral health concerns both impact and are impacted by other diseases.
Quick HIT a. The basic risk factors for caries, periodontal disease, and poor oral health are no
different between younger and older patients.
Basic risk factors for caries, Accumulated injury and repair increase the geriatric patients vulnerability to
periodontal disease, and poor dental decay and oral disease.
oral health are similar for both Comorbid diseases magnify the risk, particularly some medications, diabetes,
younger and older patients; and vascular disease.
accumulated and comorbid
conditions along with limited Limited access to care is the third leg of the stool that leads to overall poor sta-
access to care lead to in- tus of oral health in the geriatric population.
creased incidence of dental b. Lack of diabetes control contributes to worsening caries and periodontal disease.
disease in geriatric patients. c. Dental infections and oral pain can affect nutritional status and glycemic control
in diabetic patients.
3. Dental disease is present in most geriatric patients.
a. Approximately one-third of geriatric patients are edentulous.
b. Over two-thirds of geriatric patients have < 20 teeth, which is a cutoff marker for
s
Quick HIT
n
o
diminished nutritional status.
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4. Xerostomia occurs in 25% to 30% of geriatric patients and is associated with dimin-
d
n
One-third of geriatric patients
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ished taste sensation and weight loss/failure to thrive.
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are edentulous, and two-thirds
5. Age is one of the biggest risk factors for developing oral cancers.
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have fewer than 20 teeth.
a
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a. Most oral cancer deaths occur in the elderly.
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b. 90% of oral cancers are SCCs.
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c. Unless diagnosed at an early stage, prognosis is poor.
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d. Tobacco, alcohol, and age are the biggest risk factors for oral cancer.
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Quick HIT
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1. Many patients with oral or dental disease will not present with specific complaints.
n
Age is a major risk factor for
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developing oral cancer. 2. During the history, questions related to oral health need to be included.
m
a. Problems with eating
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C
b. Pain in teeth or while chewing
c. Jaw pain
d. Fever
e. Swelling or sore gums
f. Dry mouth
g. Appetite
h. Weight loss
i. Tooth loss
j. Speech impairment
k. Receding gums
l. Nonhealing sores
m. Sore mouth
3. Past medical history should be reviewed.
a. Diabetes increases the risk of oral infections.
b. Medications should be reviewed.
Calcium channel blockers (CCBs) and phenytoin can cause gingival
hyperplasia.
Medications with anticholinergic effects may cause dry mouth.
Bisphosphonates are associated with osteonecrosis of the jaw.
c. History of cancer and treatments, such as chemotherapy or radiation.

d. Alcohol use is associated with dental disease and oral cancers
e. History of cardiac valvular disease or artificial valve may warrant antibiotic pro-
phylaxis with dental work
f. Past history of aspiration or aspiration pneumonia, which is associated with oral
disease and impaired hygiene
4. Physical examination
a. Assessment of lymph nodes in submandibular, submental, and cervical region
b. Complete oral examination
Teeth, including missing or artificial teeth
Lips
Gingival margins
Tongue
Oral mucosa to include cheeks, and roof/floor of mouth
Saliva and salivary glands
Overall oral hygiene
c. Presence of cardiovascular disease because vascular disease is a risk factor for
dental infections and periodontal disease Quick HIT
d. Neurologic examination
An oral examination should be
Motor and cranial nerve function an integral part of the physi-
Mental status cal examination for elderly
Impairment may affect ability to provide self-care. patients.
C. Diagnosis
1. Physical examination will lead to diagnosis in many cases.
a. Caries (Figure 4-6)
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o
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Major cause of tooth loss in all ages
m
Considered an infection, the primary organism being Streptococcus mutans
o
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(1) Bacteria metabolize and ferment sugars into substances that damage the
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tooth surface.
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Coronal caries occur on the surface as a discoloration and destroy the tooth; it
Quick HIT
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they occur equally in all ages.
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c
Root surface caries damage the root and is are associated with gingival reces-
M
The major factors that predis-
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sion and periodontal disease, which is more common in geriatric patients. pose older adults to high rates
d
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of dental caries and tooth loss
c
Diminished sensation in the elderly may result in significant damage and de-
a
are as follows: (1) diminished
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cay before pain is appreciated.
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sensation, (2) gingival reces-
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Nearly one-third of older adults have untreated cavities. Untreated decay usu-
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sion, (3) compromised oral
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ally gets worse, resulting in pain and potential loss of teeth.
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hygiene, and (4) xerostomia.
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b. Periodontitis (Figure 4-7)
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Inflammation of the gums and bones that surround and support the teeth
Mildest form is gingivitis with erythema and inflammation of the gums.
Like caries, an infectious process with Streptococcus but also Bacteroides, Acti-
nobacillus, and other species.
Related to plaque buildup, and with progression can damage the supporting
Quick HIT
structures of the tooth, leading to excess mobility, and possibly tooth loss Periodontal disease and tooth
decay are the most frequent
More common in older persons probably because of bone loss and gingival
causes of tooth loss.
recession
Severity of periodontal disease increases with age.
Tobacco use, poor oral hygiene, diabetes, and dry mouth increase the risk of
periodontal disease.
c. Other infections
Thrush is a fungal infection with Candida spp. that affects the mucosa.
Quick HIT
(1) Can be associated with diabetes, antibiotic use, or immunocompromised Dental caries and periodontal
state disease are infectious
(2) Also associated with denture use in geriatric patients processes associated with
Streptococcus mutans,
(3) Can also affect the corners of the mouth, in which case it is called angular Bacteroides, Actinobacillus,
cheilitis and other bacterial species.
FIGURE
4 -6 Dental caries.
(DeLong L, Burkhart N. General and Oral Pathology for the Dental Hygienist. Philadelphia, PA: LWW, 2007.)
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FIGURE
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4 -7 Periodontal disease and gingivitis.
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Quick HIT
Herpes simplex can affect the mucosal surfaces.
Sialadenitis may be indicative
of underlying stones or tumor, Sialadenitis
and if resolution does not (1) Infection/inflammation of the salivary glands
occur promptly with therapy, (2) Can be associated with stones, sialolithiasis
further evaluation is warranted (3) CT scan may be warranted to evaluate for stone or tumor.
(e.g., CT scan). d. Xerostomia (dry mouth)
Dryness and cracking of the oral surfaces may be present.
May impact speech as well as appetite and eating
May lead to increased number of caries and dental decay
Quick HIT Medications that cause dry mouth should be avoided if possible.
Although saliva production decreases with age, xerostomia should not be con-
Dry mouth in the elderly is sidered a normal change associated with aging.
more than an annoyance; it e. Oral cancers (Figure 4-8)
can have devastating effects
on the health of both the hard May appear as an ulcer, red or white patch, or nodule
and soft tissue of the elderly May be symptomatic or asymptomatic
adult. Any lesion that does not significantly improve or resolve within 2 to 3 weeks
should be referred for biopsy.
FIGURE
4 -8 Tongue cancer.
C
o
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m
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e
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FIGURE
d
i
4 -9
t
Osteonecrosis of the jaw (arrow).
i
o
n
(Koenig LJ . Diagnostic Imaging: Oral and Maxillofacial. Philadelphia, PA: Amirsys, 2011.)
s
f. Osteonecrosis of the jaw (Figure 4-9)
Avascular necrosis that causes erosion and destruction of the underlying jaw
Quick HIT
bone may lead to tooth loss. Osteonecrosis of the jaw is
Most commonly affects the mandible associated with intravenous
or prolonged use (> 4 years) of
Associated with bisphosphonate or denosumab use
bisphosphonates for cancer or
(1) Less likely with osteoporosis therapy osteoporosis.
(2) Increased risk with use for cancer treatment
(3) Intravenous therapy and prolonged use (> 4 years) are risk factors.
2. X-ray can detect the presence of caries, abscesses, and destruction of bone
(Figure 4-10).
3. Biopsy may be warranted in some cases, especially for oral lesions that are not im- Quick HIT
proved within 2 to 3 weeks.
Biopsy may be warranted for
4. Diagnostic testing for comorbid diseases that may contribute to the propensity for oral lesions that do not im-
oral or dental diseases, such as diabetes, autoimmune disease, vascular disease, or prove within 2 to 3 weeks.
thyroid disease
FIGURE
4 -1 0 Radiographs of osteonecrosis (arrows).
(Koenig LJ . Diagnostic Imaging: Oral and Maxillofacial. Philadelphia, PA: Amirsys, 2011.)
D. Treatment
s
n
o
1. Dental infections warrant antibiotic therapy, generally a penicillin, cephalosporin,
i
t
i
macrolide, or clindamycin.
d
n
o
2. Referral for suspected caries, periodontal disease, osteonecrosis, or oral cancers is
C
warranted for biopsy, debridement, and restorative therapy.
l
a
c
3. Broken or missing teeth may require removal and replacement with prostheses.
i
d
e
4. Cancer therapy may include surgery and/or radiation therapy.
M
5. Therapy for thrush includes the use of either oral nystatin or fluconazole.
c
i
6. Herpes simplex may benefit from antiviral therapy.
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t
a
7. Sialadenitis therapy includes using the same classes of antibiotics as indicated for
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dental infections, hydration, and using sialogogues, such as sugarless citrus loz-
n
enges, to increase saliva flow.
o
m
8. Xerostomia therapy should include review and cessation of possible causative med-
m
ications (Table 4-3); lubricants and sialogogues may be helpful.
o
C
9. Oral lesions or sialadenitis that do not improve with therapy warrant referral for
further evaluation for underlying cancers.
CLINICAL PEARL 4-6

Preventive Dental Measures for Geriatric Patients
a. Regular dental visits every 6 to 12 months
b. Brushing twice daily and flossing daily
c. Use of electric toothbrushes or assistive gripping devices for those with osteoarthritis or stroke who have
difficulty with their grip
d. Fluoride rinses and toothpaste, especially in those with xerostomia
e. Avoid high sugar content foods and drinks, and limit alcohol and caffeine; avoid smoking.
f. Avoid tobacco.
g. For those with dentures, cleanse with denture cleaners and not bleach or abrasives.
h. Dentures should not be worn overnight; storage should cover the dentures with water to keep them from
drying out.
i. For xerostomia, synthetic saliva, sialogogues, and lip lubricants are useful to limit drying and chapping/
cracking of lips.
TABLE 4-3 Conditions and Medications Associated with Xerostomia

Quick HIT
Medications Patients with extensive or
Anticholinergics severe dental disease war-
rant evaluation for comorbid
Antidepressants diseases, such as diabetes,
Antihistamines which may be contributing to
their propensity for poor oral
Antihypertensives
health.
Diuretics
Parkinson disease medications
Alcohol abuse
Autoimmune disease
Chemotherapy
Radiation therapy
Sialadenitis
Salivary gland tumors
S e ns o ry D is o rd e rs
C
o
Disorders of the Eye
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m
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A. Aging and vision changes
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G
1. Approximately 30% of geriatric patients have impaired vision. (Table 4-4 lists
e
r
common causes of impaired vision in the elderly.)
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a
t
2. Geriatric patients make up nearly 50% of blind persons.
r
i
c
3. The most common causes of visual impairment are cataracts, refractive error, age-
Quick HIT
M
related macular degeneration (ARMD), glaucoma, and diabetic retinopathy.
e
d
4. ARMD and glaucoma are the most common causes of irreversible vision loss.
i
c
Presbyopia, an inability to
a
5. Refractive error and diabetic retinopathy affect a wider age range than ARMD,
l
focus on near objects owing to
C
glaucoma, cataracts, and retinal detachment, which mostly occur in the elderly.
o
lens inelasticity, affects nearly
n
6. Presbyopia, an inability to focus on near objects owing to an age-related inelastic-
d
100% of the elderly.
i
t
ity of the lens, affects nearly 100% of the geriatric population. It is correctable
i
o
n
with glasses or contacts.
s
7. Adaptation to the dark is decreased because pupils are less able to dilate, allowing
less light to reach the retina.
8. Dry eye is a common problem because of an age-related decline in tear
production.
TABLE 4-4 Causes of Visual Impairment in the Elderly

Chronic Causes Acute Causes
ARMD Retinal disorders, e.g., detachment, hemorrhage

Glaucomaopen angle Temporal arteritis
Diabetic retinopathy Herpetic eye disease
Acute angle glaucoma
Corneal ulceration
Vitreous hemorrhage
9. Arcus senilis, a white ring made of lipid deposits that surrounds the cornea is
common and requires no treatment.
10. Age-related changes in elasticity may cause eyelid drooping (ptosis), which if
severe may block vision and require surgical repair.
11. Entropion, or the inward folding of the lower eyelid, may occur and can lead to a
bothersome corneal irritation. Treatment is surgery.
12. An outward drooping of the lower eyelids, known as ectropion, may cause the eyes
to water, which if bothersome can be treated surgically.
B. Specific conditions
1. ARMD
a. The leading cause of blindness in those over age 65
b. Progressive macular degeneration resulting in bilateral central vision loss but
sparing peripheral vision
c. Symptoms
Central vision loss
Blurry vision
Scotoma
Distortion
d. Ophthalmic examination may reveal yellow retinal patches (drusen) or, in
advanced stages, hemorrhage and scarring.
e. Risk factors for ARMD
Old age
Family history
HTN
s
Smoking
n
Quick HIT
o
Female sex
i
t
i
d
Caucasian race
n
o
There are two types of macu-
C
f. There are two types of ARMD: exudative, also known as wet ARMD, and atro-
lar degeneration: wet and dry.
l
phic or dry ARMD.
a
c
Exudative (wet) ARMD (10% of cases) is characterized by rapid vi-
i
d
e
M
sion loss from abnormal blood vessel formation and leakage underneath
the retina. First-line treatment includes intraocular injections of vascular
c
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r
endothelial growth factor (VEGF) inhibitors (e.g., ranibizumab) monthly
t
a
i
for up to 2 years. VEGF reduces neovascularization and helps maintain
r
e
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vision in the majority of patients and improves vision in a significant
n
minority.
o
m
(1) Complications of intraocular injections include retinal detachment,
m
o
endophthalmitis, and visual loss in 1% to 2%.
C
(2) Early intervention with laser photocoagulation may potentially reverse
the vision loss.
(3) Antioxidants may slow ARMD progression, and Ocuvite is a commercially
available combination of antioxidants containing zinc oxide, -carotene,
vitamin C, and vitamin E. It is not recommended for smokers because
-carotene supplementation is associated with an increased risk of lung
cancer.
Atrophic (dry) ARMD (90% of cases) is more common and is associated
with a slow onset of vision loss with characteristic yellowish white retinal
deposits known as drusen. This condition is caused by the degeneration of
the central retina. Antioxidants may provide some benefit for this condition
(Figure 4-11).
Patients with ARMD should be monitored using an Amsler grid to detect vi-
sual deterioration and the need for intervention.
Quick HIT 2. Glaucoma
a. Glaucoma is an optic neuropathy characterized by an acquired atrophy of the
Although wet ARMD is less
common, it causes more se- optic nerve and loss of retinal ganglion cells and their axons.
vere vision loss. b. May result in irreversible damage to the optic nerve that can lead to impaired vi-
sion and blindness
FIGURE
4 -1 1 Age-related macular degeneration in an elderly patient. Notice the drusen spots
located centrally.
(Alfaro DV, Liggett PE, Mieler WF, et al. Age-Related Macular Degeneration. Philadelphia, PA: LWW, 2005.)
C
o
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a
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C
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d
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n
s
FIGURE
4 -1 2 Optic nerve enlargement of the optic cup.
(Rhee DJ . Color Atlas and Synopsis of Clinical Ophthalmology. Philadelphia, PA: LWW, 2012.)
c. Diagnosis requires the integration of history, assessment of relevant risk factors,

measuring intraocular pressure (IOP), and a detailed ocular examination to as-
sess both structure and visual function.
d. Glaucoma is defined by its characteristic optic nerve changes and visual field
loss. IOP is no longer considered an absolute diagnostic criterion, but is an im-
portant risk factor. Individuals with an elevated IOP but without evidence of
glaucoma have intraocular HTN and usually merit treatment.
e. Pathogenesis
IOP caused by outflow obstruction and other poorly understood factors re-
sults in a progressive loss of ganglion cells in the retina, optic disc atrophy, Quick HIT
and enlargement of the optic cup. Cupping of the optic nerve is
Ophthalmic examination characterized by cupping of the optic disc and nerve pathognomonic of glaucoma.
damage characterized by a loss of peripheral vision (Figure 4-12)
CLINICAL PEARL 4-7

Glaucoma Diagnosis
Tonometry to measure IOP
Ophthalmoscopy to visualize the optic nerve
Presence of cupping, which is an increased optic cup-to-disc ratio
Gonioscopy to determine the etiology and assess the anterior chamber
f. Risk factors include:

Age > 65 years
Quick HIT HTN
Family history
Visual field testing is indicated Steroid medication
if glaucoma is suspected both Eye trauma
to establish the diagnosis and
to assess disease progression. Intraocular inflammation
More common in African Americans
g. Two forms of glaucoma are angle-closure glaucoma and open-angle glaucoma.
Primary open angle is the most common form.
Management may be challenging because patients are often asymptomatic yet
require eye medications, which can have side effects.
Quick HIT Angle-closure glaucoma
Although the primary care (1) Presents with an acutely painful red eye secondary to rapid increase in
s
IOP from impairment of aqueous humor drainage in the anterior chamber
n
physician (PCP) is usually
o
(2) It is associated with significant and distressing symptoms including:
i
not responsible for making
t
i
d
the definitive diagnosis and (a) Blurred vision
n
o
treatment of glaucoma, a PCP
C
(b) Nausea/vomiting
should be alert to risk factors
l
(c) Halos around lights
a
and recognize early changes
c
i
(d) Headaches
d
on examination in order to re-
e
M
fer to an ophthalmologist. (e) Prostration
(3) Most common among Asians and Eskimo lineage
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(4) On examination, there is an irregularly fixed, nonreactive, mid-dilated
t
a
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pupil. The eye is reddened with a congested cornea and conjunctivae. IOP
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elevation is noted on tonometry and palpation of the globe.
n
Quick HIT (5) Ophthalmologic emergency
o
m
(a) Must urgently lower the IOP with IV acetazolamide, IV mannitol, or
m
o
oral glycerin and constrict the pupil with pilocarpine drops. The IOP
C
Occasionally, nausea and
vomiting are so prominent in should be checked 30 to 60 minutes after initiating treatment.
angle-closure glaucoma that (b) Urgent referral is needed for definitive treatment with laser peripheral
eye findings are overlooked,
iridotomy. If iridotomy fails or there is difficulty in visualizing the iris,
and the patient may be misdi-
agnosed as having an acute surgical peripheral iridectomy may be performed.
abdomen or myocardial infarc- Open-angle glaucoma
tion (MI). (1) This makes up the vast majority of glaucoma cases and is caused by an
outflow obstruction at the microscopic level of the trabecular network. If
untreated, it may eventually lead to central vision loss and blindness.
(2) Often asymptomatic until significant nerve damage occurs and visual loss
is observed
(3) More prevalent among African American race and is the leading cause of
adult blindness among African Americans
(4) Early detection is possible with periodic vision tests and tonometry
(5) In its primary form, an obstructed outflow of the aqueous humor through
the trabecular meshwork causes a rise in IOP, resulting in an insidious
and painless loss of vision
(6) On examination:
(a) IOP noted with tonometry
(b) Cupping of the disc along with scotoma present on visual field testing
(7) Treatment focuses on decreasing the IOP either by increasing aqueous

outflow or by reducing aqueous production.
(8) Topical agents such as the prostaglandin analogs and -blockers are usu- Quick HIT
ally considered first-line agents. Although there is no direct
(a) Topical -blockers (e.g., Timolol) decrease aqueous production. treatment for optic nerve dam-
(b) -Agonists increase outflow and decrease aqueous production. age, lowering IOP can help
(c) Cholinergic agonists increase aqueous outflow. prevent further damage.
(d) Oral carbonic anhydrase inhibitors (e.g., acetazolamide) or topical
carbonic anhydrase inhibitors decrease aqueous production.
(e) Prostaglandin analogs increase aqueous outflow.
(9) In refractory cases, laser or surgical drainage procedures may be
performed.
(10) Avoid the use of anticholinergics because these may exacerbate the
glaucoma.
3. Cataracts
a. Slowly progressive vision loss (over months to years) caused by lens Quick HIT
opacification. When an older adult requires
b. Changes in the lens are a normal part of aging, but when lens opacification lens prescription changes,
causes functional impairment, it should be considered pathologic and treatment glaucoma should be in the dif-
considered. ferential and IOP measured.
c. Patients may have painless blurry vision with a haze or glare, making it espe-
cially difficult to drive at night.
d. Risk factors for cataracts include:
Agingoccurs in over half of Americans over age 65
Trauma
C
Steroids
o
m
Tobacco smoking
m
Diabetes mellitus (DM)
o
n
Prolonged UV radiation
G
e
e. Examination reveals clouding of the lens and a diminished red reflex. Diagnosis
r
i
a
can be made with a slit-lamp examination.
t
r
i
f. The decision to have surgery depends on the extent of functional impairment
c
M
caused by the cataracts.
e
g. Treatment
d
i
c
Lens replacement surgerywhich can restore vision to 20/40 or better in 95%
a
l
of patients.
C
o
The opacified lens containing the cataract is removed, and an artificial lens is
n
d
i
inserted in its place.
t
i
o
4. Retinal detachment
n
s
a. The sudden loss of vision caused by the separation of the retina from its blood
vessels, depriving the retinal cells of oxygen and nutrients
b. Risk factors include:
Age > 50
Trauma
Myopia
Family history
Cataract surgery
c. Patients commonly complain of:
A curtain coming down unilaterally
Blurred vision, monocular
Flashes of light
Floaters
d. A dilated retinal examination illustrates a gray cloud in which the retina is hang-
ing in the vitreous and diminished afferent pupillary reflex.
e. Treatment
Emergent ophthalmology referral
Remain NPO and avoid strenuous activity or pressure to globe of eye prior to
reaching hospital
The retina is reattached via surgery, cryotherapy, laser photocoagulation, or

Quick HIT injecting an expansible gas into the eye
If the retina does not reattach, a band may be used to bring the retina close to
The 3 Fs are the cardinal the sclera.
signs and symptoms of retinal
detachmentFlashes, Float- Disorders of the Ear
ers, and visual Field defects.
A. Hearing depends on the integration of the peripheral conductive and sensorineural
components and the central auditory system. Age-related changes include:
1. Ear wax becomes more viscous and may plug the ear canal, impairing conduction.
2. Atrophy of sebaceous glands may cause dryness and pruritus.
3. Degenerative changes of middle and inner ear affect balance and hearing. Age-
related hearing loss (presbycusis) results in high-frequency hearing loss. It is most
likely caused by cumulative damage to the cochlea over time and a defect in central
auditory processing.
4. In presbycusis, men are affected more than women, and speech discrimination is
reduced, especially with background noise.
B. General considerations
1. Hearing loss is the most common sensory impairment associated with aging, and
approximately 40% have some form of hearing impairment, defined as the inability
to identify a pure tone at 40 dB (Table 4-5).
2. Hearing impairment may be caused by an interference with sound conduction, the
conversion from electrical impulses or transmission through the nervous system to
the auditory centers in the brain.
3. Interference with the mechanical transmission of sound causes conductive hearing
s
n
loss. Conditions affecting the cochlea or nerves cause sensorineural hearing loss.
o
i
4. Hearing function should be assessed through history, physical examination, and
t
i
d
n
when indicated an audiogram.
o
C
5. An audiogram can identify the extent and type of hearing loss. Speech discrimina-
l
a
tion tests the persons ability to understand speech (Figure 4-13).
c
i
d
e
M
C. Hearing loss of the outer ear
1. Cerumen impaction is the most common cause of reversible hearing loss in the
c
i
r
elderly.
t
a
i
a. Soft wax can be flushed out with gentle irrigation using a syringe, removed
r
e
G
manually with a curette, or suction. Dry or recurrent impactions may benefit
n
o
from softening with a commercial agent, such as Debrox, Ceruminex, or Colace.
m
Prolonged use of these agents (> 4 days) may cause canal irritation.
m
o
2. Infections (otitis externa)
C
a. Infection of the external auditory canal resulting in inflammation and edema can
block the ear canal causing a conductive hearing loss.
b. Most common pathogens: Pseudomonas aeruginosa and Staphylococcus aureus.
c. Disease classification: mild disease (minor discomfort and pruritus), moder-
ate disease (intermediate pain and pruritus with partially occluded canal), and
TABLE 4-5 Common Causes of Hearing Loss in the Elderly

Conductive Sensorineural
Impacted cerumen Noise damage
Otosclerosis Injury by vascular damage and/or stroke
Tympanic membrane perforation Meniere disease
Ossicular disruption Tumors
Otitis externa and media Ototoxic medication
Cholesteatoma Presbycusis
Fre que ncy (Hz)

125 250 500 1,000 2,000 4,000 8,000
10
10 Norma l limits No s ignifica nt difficulty

with fa int s pe e ch
20
30 Mild he a ring los s Difficulty only with

fa int s pe e ch
40
Mode ra te he a ring los s Fre que nt difficultie s with
50 norma l s pe e ch
60 Mode ra te ly s e ve re Fre que nt difficultie s with

he a ring los s loud s pe e ch
70
S e ve re he a ring los s Ca n unde rs ta nd only s houte d
80
or a mplifie d s pe e ch
H
90
e
a
P rofound he a ring los s Us ua lly ca nnot unde rs ta nd

r
i
n
100
g
e ve n a mplifie d s pe e ch
l
e
v
110
e
n
i l
FIGURE
d
4 -1 3 Definitions of hearing loss.

e
c
li
b
(Humes LE, Bess FH. Audiology and Communication Disorders: An Overview. Philadelphia, PA: LWW, 2008.)
e
l
s
C
(r
o
e
m
:
A
severe disease (intense pain, complete occlusion of canal, usually periauricular

N
m
S
o
erythema, lymphadenopathy and fever).
I
n
1
9
d. Treatment: thorough cleaning of the ear and treating the infection and
G
9
e
6
inflammation.
r
)
i
a
For mild disease: use acetic acid/hydrocortisone solution; moderate disease:
t
r
i
c
use combination agents with acetic acid, topical antibiotic, antiseptic, and glu-
M
cocorticoid; for severe disease, a wick is often needed to allow penetration of
e
d
topical agents, control pain with NSAIDs, and systemic antibiotics if there is
i
c
a
evidence of cellulitis.
l
C
For all forms, avoid swimming and bathing to prevent moisture from entering
o
n
the ear canal.
d
i
t
3. Tumors (osteomas, exostosis, seborrheic keratosis, actinic keratosis, BCC, and
i
o
n
SCC)
s
a. Diagnosis confirmed by biopsy.
b. Treatment: ranges from conservative to surgical interventions depending on bi-
opsy results.
D. Hearing loss of the middle ear

1. Infections (otitis media)
a. Although more common in children, otitis media (OM) can be a cause of con-
ductive hearing loss in the elderly.
b. Fluid accumulates in the middle ear impairing normal tympanic membrane vi-
bration and sound transmission.
c. Most common pathogens: Streptococcus pneumoniae and Haemophilus influenzae.
Group A -hemolytic streptococcus, S. aureus, and Moraxella catarrhalis are less
frequent causes.
d. Diagnosis: examination of the tympanic membranes reveals erythema, bulging,
and poor mobility.
e. Treatment: First-line antibiotic amoxicillin; if allergic use macrolide; if fails to
respond or recent antibiotics use (within 1 to 2 months), use a second-line an-
tibiotic, such as amoxicillin-clavulanate or a second-generation cephalosporin,
such as cefuroxime.
FIGURE
4 -1 4 Tympanic membrane perforation (arrow).
(Anatomical Chart Company. Middle Ear Conditions Anatomical Chart. Philadelphia, PA: LWW, 2009.)
2. Tumors (most commonly SCC)

a. Rare
b. Treatment: surgical management
3. Tympanic membrane perforation (Figure 4-14)
s
Quick HIT
n
a. Perforation commonly arises from trauma or infection.
o
i
t
b. Degree of hearing loss depends on size and location of perforation.
i
d
n
Conductive hearing loss that c. Common causes: blast injury, foreign body trauma, temporal bone infection, and
o
C
may require or benefit from Q-tip or object.
l
surgery includes chronic tym-
a
d. Inspection of tympanic membrane is important to identify trapped skin, which
c
panic membrane (TM) perfora-
i
d
can result in cholesteatoma formation.
e
tion, cholesteatoma, ossicular
M
disruption, and osteosclerosis. e. Treatment: self-resolving or with aid of a paper or biogenic patch; occasionally,
c
surgical intervention required.
i
r
t
4. Otosclerosis
a
i
r
a. Bony overgrowth of the footplate of the stapes resulting in fixation
e
G
b. Autosomal dominant condition (variable penetrance)
n
o
c. Leads to conductive hearing loss
m
m
d. Treatment: hearing amplification or surgical stapedectomy
o
C
5. Cholesteatoma (Figure 4-15)
a. Growth of desquamated stratified squamous epithelial cells in the middle ear
and/or mastoid processes
b. Can become cystic with growth
c. Formation is associated with tympanic membrane trauma or impaired Eusta-
chian tube function, resulting in retraction and pocket formation.
d. Complications: hearing loss, brain abscess, vertigo, and facial nerve paralysis
e. Treatment: surgical intervention
6. Vascular
a. Jugulotympanic paragangliomas are rare benign vascular tumors that can cause
conductive hearing loss, bone erosion, and damage cranial nerves 7 to 12.
b. They often appear as a red, blanchable mass behind the tympanic membrane.
Pulsatile tinnitus raises the suspicion of glioma.
c. Treatment: surgical intervention
E. Hearing loss of the inner ear

1. Presbycusis
a. Sensorineural hearing lossassociated with aging is the most common cause of
diminished hearing in the elderly. It affects both cochlear hair cells and spiral
ganglion cells in the vestibulocochlear nerve.
FIGURE
4 -1 5 Cholesteatoma.
(Anatomical Chart Company. Middle Ear Conditions Anatomical Chart. Philadelphia, PA: LWW, 2009.)
TABLE 4-6 Hearing Aids
C
Types Advantage Disadvantage
o
m
m
Behind the ear Treats mild to severe hearing loss. Size Can be aesthetically unappealing due
o
n
allows for adequate amplification. Fits to large size. Occlusion effect
G
almost all users and hearing loss types.
e
r
i
Easy to clean and maintain
a
t
r
In the ear Effective for severe hearing loss due Feedback issues due to short distance
i
c
to larger amplification of sound. Mi- between microphone and receiver.
M
e
crophone placement enhances high Wax and moisture in the ear can lead
d
i
frequency amplification especially in a to daily cleaning
c
a
noisy environment. Improved localization
l
C
of sound stimuli with head movement.
o
n
Discretely hidden
d
i
t
i
In the canal Better high frequency amplification and Limited to individuals with mild to
o
n
sound localization with head move- moderate hearing loss. Directional
s
ment. Small size and discrete location microphones cannot be used due to
increases aesthetic appeal small size of faceplates. Feedback
issues. More susceptible to wax and
moisture
Completely in Good for high frequency hearing loss Limited to individual with moderate
the canal due to position in the ear. Appropriate hearing loss and individuals with
amplification of sound. Very aesthetically appropriate ear dimensions. Direc-
appealing as it is well hidden in the ear. tional microphones cannot be used.
More comfortable due to custom fit. Can Feedback and occlusion issues. Small
be worn several months at a time batteries result in less battery life.
Expensive
b. Hallmark of presbycusis is the progressive, symmetric loss of high-frequency

hearing over many years.
c. Diagnosis: history, physical examination, and confirmed with audiogram
d. Treatment: hearing aid, see Table 4-6 and Figure 4-16; if hearing aid fails, co-
chlear implant can be beneficial.
B
A
C D
FIGURE
4 -1 6 Types of hearing aids. (A) Behind-the-ear, (B) in-the-ear, (C) in-the-canal, and (D)
s
completely in the canal.
n
o
(Stedmans Medical Dictionary for the Health Professions and Nursing. Illustrated 6th ed. Philadelphia, PA: LWW, 2007.)
i
t
i
d
n
o
2. Noise
C
a. Noise is the second most common cause of hearing loss after presbycusis.
l
a
c
b. Mechanism of action: direct mechanical damage of cochlear structure and meta-
i
d
bolic overload (nitric oxide release, free radical generation, and low magnesium
e
M
concentration) from overstimulation
c
i
c. Audiogram characteristically shows notched pattern of sensory threshold shift.
r
t
a
d. Treatment: hearing protection (muffs and plugs) during loud noise exposure
i
r
e
G
3. Infections
n
a. Most commonly caused by viral cochleitis and bacterial meningitis
o
m
b. Sensorineural hearing loss caused by destruction of cochlear inner hair cells
m
c. Viral cochleitis commonly presents as sudden onset hearing loss.
o
C
d. Other causes of sudden onset hearing loss should be evaluated, including vascu-
lar ischemic events, acoustic neuromas, Meniere disease, multiple sclerosis, and
perilymphatic fistulas.
4. Meniere disease
a. Characterized by the triad of vertigo, hearing loss, and tinnitus. Etiology is un-
known but may be caused by an abnormally high pressure within the cochlea.
b. In contrast to presbycusis, which affects higher frequencies, Meniere usually
causes low-frequency hearing loss.
CLINICAL PEARL 4-8
Sudden Hearing Loss

Sudden hearing loss from a suspected viral infection requires immediate referral to ENT for prompt diagnosis
and treatment with steroids and/or antiviral medications either systemically or injected into the middle ear.
Eighth nerve tumors can also present with sudden hearing loss and imaging studies, such as a CT or MRI, may
be indicated.
c. Associated with episodic spells of vertigo lasting for hours, aural fullness, tinni-
tus, and sensorineural hearing loss
d. Diagnostic criteria proposed by the American Academy of Otolaryngology
and Head and Neck Surgery (AAO-HNS) requires the following: two sponta-
neous episodes of rotational vertigo lasting at least 20 minutes, audiometric
confirmation of sensorineural hearing loss, tinnitus, and/or perception of aural
fullness.
e. Over time, hearing loss can become permanent and involve other frequencies.
f. Treatment: lifestyle modification (limit intake of salt, caffeine, nicotine, and Quick HIT
alcohol); diuretics can be used if lifestyle modification alone does not provide The triad of episodic vertigo,
benefit; medically manage vertigo with antihistamines and anticholinergics; in tinnitus, and hearing loss sug-
5% to 10% of individuals, interventional techniques including both destructive gest Meniere disease.
procedures (intratympanic gentamycin, labyrinthectomy, and vestibular neurec-
tomy) and nondestructive procedures may be useful.
5. Trauma
a. Often from blunt head injury or barotrauma leading to damage of the inner and
middle ear, resulting in hearing loss
b. Blunt trauma can lead to longitudinal or transverse temporal bone fracture.
c. Longitudinal temporal bone fractures are the most common and result in con-
ductive loss with tympanic membrane perforations.
d. Transverse fractures cause fractures running through the inner ear and result in
a dead ear.
6. Endocrine, systemic, and metabolic
a. Various metabolic abnormalities can result in sensorineural hearing loss. Quick HIT
b. Diabetic small vessel disease can result in cochlear ischemia. Unilateral tinnitus should raise
C
c. Other causes include hypo/hyperthyroidism, systemic illnesses, such as syphilis, the suspicion of an acoustic
o
m
anemia, and white blood cell disorders. neuroma.
m
7. Tumors
o
n
a. Usually benign, acoustic neuroma is the most common benign tumor and origi-
G
e
nates from the vestibular portion of cranial nerve VIII.
r
i
a
b. Individuals with an acoustic neuroma are asymptomatic or complain of unilat-
Quick HIT
t
r
i
eral sensorineural hearing loss; they can also present with unilateral tinnitus,
c
M
dizziness, or headaches. Speech discrimination is much
e
c. Other tumors causing sensorineural hearing loss include meningiomas and
d
worse than predicted by pure
i
c
lipomas. tone hearing loss with an
a
l
8. Iatrogenic acoustic neuroma.
C
o
a. Inner ear injuries can result in hearing loss and can occur during surgical proce-
n
d
i
dures, following radiation therapy, or may result from medication use.
t
i
o
b. Medication with ototoxic side effects can cause hearing loss.
n
s
c. Sensorineural hearing loss from antibiotics or chemotherapeutic drugs results in
permanent hearing loss.
d. Cocaine, both intravenous and intranasal, is associated with unilateral and bilat-
Quick HIT
eral hearing loss. Aminoglycoside antibiotics
e. Heavy metals, such as lead, mercury, cadmium, and arsenic, can lead to hearing can cause ototoxicity and
loss. nephrotoxicity. Monitoring
drug levels is the best way to
9. Neurogenic avoid eighth nerve damage.
a. Strokes and transient ischemic attacks (TIAs) can result in sensorineural hearing
loss.
b. ArnoldChiari malformations can stretch the auditory vestibular nerve, causing
hearing loss and/or vestibular complaints.
c. Multiple sclerosis can present with sudden onset hearing loss and/or vertigo.
F. Vertigo (Figure 4-17)

1. Vestibular neuritis
a. Inflammation of the vestibular branch of the vestibulocochlear nerve
b. Usually a result of viral infection of the inner ear or viral infection outside of the
body (herpes, flu, measles, hepatitis, and polio)
c. Presents with vertigo, nausea, vomiting, and dizziness
VE RT IG O (S YMP T O M O F MO VE ME N T DU E
T O AC U T E VE S T IB U LAR DYS F U N C T IO N )
Common ca us e s :
be nign pos itiona l ve rtigo,
a cute la byrinthitis , M ni re
dis e a s e , me dica tions , ne uros yphilis
Nys ta gmus
S us ta ine d Brie f or none
Ce ntra l le s ion Ve rtigo is brie f or

+ DixHa llpike ma ne uve r
Ye s No
Be nign pa roxys ma l Re ce nt URI

pos itiona l ve rtigo
Ye s No
Ve s tibula r ne uronitis S troke

(a cute la byrinthitis ) M ni re dis e a s e
s
Eus ta chia n tube Ne uros yphilis
n
o
dys function Me dica tions
i
t
i
d
n
FIGURE
o
C
4 -1 7 Vertigo algorithm.
l
a
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i
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c
i
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t
a
PEARL
i
r
e
CLINICAL 4-9
G
n
o
Vertigo
m
m
Vertigo is described as a sense of abnormal motion. Terms used by patients include a spinning sensation,
o
C
weaving, feels like being on a merry-go-round, and dizziness. Dizziness is the least precise term, and an effort
should be made to distinguish vertigo from syncope or lightheadedness and imbalance. Vertigo is often divided
into peripheral vertigo and central vertigo. Central vertigo usually occurs in association with other brainstem
deficits.
d. Treatment: symptomatic measures and antiviral agents when appropriate.

Usually resolves in 3 to 6 weeks, but vestibular rehabilitation for prolonged
symptoms.
2. Labyrinthitis
a. Is an inflammation of the labyrinth affecting both branches of the vestibuloco-
chlear nerve, usually preceded by an upper respiratory infection
b. Usually viral but can be bacterial in etiology, especially if in postoperative setting
following middle or inner ear surgery
c. Presents with vertigo, nausea, vomiting, tinnitus, hearing loss, and disequilib-
rium syndrome
d. Treatment: symptomatic measures, labyrinthine sedatives (e.g., meclizine) may
be useful.
CLINICAL PEARL 4-10

Interviewing Hearing-Impaired Patients
Geriatricians often encounter hearing-impaired patients in their practice. In addition to encouraging patients to
bring their hearing aids to their office visit, other helpful strategies to improve communication include speak-
ing face to face, repeating by paraphrasing, not shouting but speaking at a normal level or slightly louder,
speaking a bit more slowly and standing within 2 to 3 feet of the patient, keeping the room quiet and free of
background noise, pausing at the end of sentences, and having the person repeat key points to make sure they
understand. Above all, remain patient and try to avoid appearing frustrated.
3. Benign paroxysmal positional vertigo (BPPV)

a. Most common form of positional vertigo resulting from dislodged otoliths in the
inner ear, producing overstimulation of the semicircular canal. Quick HIT
b. Characterized by:
Common drugs associated
Recurrent episodes of vertigo lasting 1 minute or less that are often provoked with ototoxicity include:
by specific head movements Salicylates (aspirin)
Nystagmus may be present. NSAIDs (naproxen, ibupro-
c. Diagnosis: confirmed by observing nystagmus during DixHallpike maneuver fen, and diclofenac)
d. Treatment: maneuvers designed to free otoliths: BrandtDaroff exercises, Semont Antibiotics (aminoglyco-
sides, erythromycin, and
maneuver, and Epley maneuver are effective frequent episodes; may benefit vancomycin)
from vestibular suppressants, which can also be used as premedication prior to Diuretics (furosemide and
C
o
maneuvers ethacrynic acid)
m
Chemotherapeutic agents
m
G. Tinnitus
o
(bleomycin, cisplatin, vin-
n
1. Perception of sound or noise in proximity to the head (in one or both ears, within blastine, and methotrexate)
G
e
or around the head, or outside distant noise) in the absence of an external source;
r
i
a
can be continuous or intermittent
t
r
i
2. Most commonly results from abnormalities within the auditory system, often unex-
c
M
plained in etiology
Quick HIT
e
d
3. Can be associated with sensorineural hearing loss, ototoxic medication, infection,
i
c
vascular ischemia, or acoustic neuroma
a
Ototoxicity facts
l
4. Pulsatile tinnitus is commonly vascular in nature and requires further workup.
C
Some aminoglycosides are
o
n
5. Evaluation should include thorough history, physical examination, including aus- more vestibulotoxic than
d
i
cultation for bruits and complete head and neck examination. cochleotoxic.
t
i
o
6. Treatment: aimed at treating underlying condition; cochlear implants may help Relative order of cochleo-
n
s
toxicity: gentamycin> tob
individuals with severe sensorineural hearing loss; retraining therapy, biofeed- ramycin> amikacin> neo
back, and cognitive-behavioral therapy may be useful in patients with significant mycin.
impairment.
N e uro lo g ic D is e a s e
Cerebrovascular Disease
1. Strokes are the third leading cause of death and a leading cause of hospitalization
and chronic debility. Three-quarters of strokes occur in individuals aged > 65.
Cerebrovascular accidents (CVAs) or strokes have variable presentations involv-
ing some form of neurologic deficit and neuronal damage.
2. There are two main types of stroke: ischemic and hemorrhagic; 80% are ischemic
and 20% are hemorrhagic either from an intracerebral bleed or a subarachnoid
hemorrhage (SAH).
a. Ischemic stroke
Occlusion of small vessel
Embolus of atherosclerotic material or clot from carotid, large vessel, or heart

(e.g., atrial fibrillation)
(1) Arterial to arterial (A to A) emboli, where a clot forms in an artery such
as the carotid or vertebral arteries and travels to the brain, are more
common.
(2) Strokes resulting from larger emboli from the heart usually present with a
greater neurologic deficit than an A to A embolic stroke.
(3) Embolic strokes present acutely, but may improve over time.
Less commonly, an embolism from a venous clot passes through a patent fora-
men ovale and is called a paradoxical embolus.
Ischemic strokes may be preceded by TIAs.
b. Intracerebral hemorrhage (ICH)
Bleeding into the brain from a penetrating vessel. ICH is the stroke with the
strongest association with HTN.
Hemorrhagic strokes are typically sudden events that may worsen or evolve
over time. Bleeding may occur in association with an ischemic infarction and
may present with sudden worsening in the patients condition.
Mortality rates are as high as 50%.
c. SAH
Generally caused by an aneurysm, trauma, or arteriovenous malformation
May be preceded by a sentinel bleed and worst headache of my life, then
stabilization until marked decline even up to 2 weeks later
Mortality rates are as high as 50%.
About 5% of strokes, but tends to affect younger individuals with a mean age
of about 50
s
n
d. Symptoms and neurologic signs of ischemic infarction and intracerebral bleeding
o
i
vary by location of the insult.
t
i
d
e. SAH may not show focal signs but present with more generalized signs and
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o
C
symptoms such as nausea, meningismus, and altered level of consciousness.
l
f. Over 80% of strokes are of the ischemic type.
a
c
i
g. TIAs are episodes of brief, abrupt neurologic deficits that usually last < 30 minutes
d
e
M
but not > 24 hours. A deficit lasting > 24 hours is defined as a stroke (Figure 4-18).
Equivalent of cerebrovascular angina. Symptoms of TIAs may be indistin-
c
i
r
guishable from a stroke. It is the duration of symptoms that is the determining
t
a
i
factor.
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G
Risk of stroke is 20% within 90 days of a TIA, and half of these are within
n
o
48 hours.
m
Evaluation and preventive measures can alter this outcome.
m
o
TIAs can involve either the carotid (80%) or vertebrobasilar (20%) circula-
C
tion (VBA). Signs of a TIA in the carotid distribution include loss of speech,
unilateral weakness or numbness of an extremity, difficulty speaking, or a
curtain-like loss of vision in one eye (amarousis fugax). Symptoms of a TIA in
the VBA distribution include dizziness, double vision, vertigo, dysarthria, and
dysphagia.
1. History
a. Onset of symptoms are typically abrupt and may present upon awakening.
b. Symptoms may include facial, arm or leg weakness, impaired speech, paresthe-
sias, or headache.
c. Timing the onset of symptoms is important for determining treatment, particu-
larly the use of thrombolytics.
d. Time course may suggest etiology; generally, ischemic symptoms are worse at
onset and may improve with time, whereas intracerebral bleeding may progres-
sively worsen.
e. SAH often presents with headache (often described as the worst of their life),
an altered level of consciousness, or other nonspecific symptoms.
f. Past medical history may reveal risk factors (Table 4-7).
TABLE 4-7 Risk Factors for Stroke

Heart disease
Atrial fibrillation
Valvular heart disease
Hypertension
Diabetes mellitus
Hyperlipidemia
Smoking
Obesity
Alcohol abuse
Heart disease
(1) Atrial fibrillation (AF)
(2) Congestive heart failure
(3) Valvular heart disease
HTN
DM
C
Hyperlipidemia
o
m
Obesity
m
Smoking
o
n
Alcohol abuse
G
e
r
i
a
a. Vital signs may reveal elevation of BP, which is a reflex response with neurologic
t
r
i
injury.
c
M
b. Note should be made of cardiac rhythm.
e
d
c. Mental status may be altered, making neurologic assessment more
i
c
difficult.
a
l
d. Complete neurologic examination may reveal unilateral weakness, dysarthria, or
C
o
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visual field deficits.
d
i
e. Cranial nerve or cerebellar findings of ataxia suggest involvement of the poste-
t
i
o
rior circulation.
n
s
f. A stiff neck may be present with a SAH.
C. Diagnosis (Figures 4-18 and 4-19)

1. An abrupt onset of a neurologic deficit often leads to an erectile dysfunction (ED)
visit and hospitalization for evaluation and treatment.
2. Time is brain, and the initial evaluation should focus on timing the onset of
symptoms because patients with ischemic stroke presenting within 3 hours may
benefit from thrombolytic therapy.
3. Differential diagnosis for stroke is presented in Table 4-8.
4. Immediate workup includes both labs and imaging. Tests include:
a. CBC.
b. Comprehensive metabolic profile.
c. Protime and partial thromboplastin time.
d. Urinalysis with culture.
e. Electrocardiogram.
f. CT scan without contrast of the brain.
g. Although a CT detects 90% of SAHs, cerebrospinal fluid (CSF) analysis may be
warranted in patients with suspected SAH and a negative CT scan.
h. CT detects about 95% of ICH.
T R AN S IE N T IS C H E MIC AT TAC K AN D
T R AN S IE N T N E U R O LO G IC DE F IC IT
Common ca us e s : Migra ine
( a ura ), ca rotid a rte ry dis e a s e , s troke ,
s e izure , s yncope , s uba ra chnoid he morrha ge ,
multiple s cle ros is , ALS
S troke ris k fa ctors :

HTN,
a ge >55 yr,
toba cco a bus e , hype rlipide mia ,
dia be te s me llitus
Ye s No
S ymptoms Los s of
<24 hr cons cious ne s s
Ye s No Ye s No
TIA S troke Los s of s e ns ory or Lights fla s hing,

motor function une xpla ine d odors ,
tinnitus ,
Ye s No pa re s the s ia s ,
limb move me nts
S ymptoms S e izure Ye s No
<24 hr
Ye s
s
No
n
Migra ine TIA
o
S e izure s
i
t
i
d
S troke
n
TIA
o
C
FIGURE
l
a
4 -1 8
c
Transient ischemic attack evaluation.
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c
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t
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5. Testing helps eliminate hypoglycemia, encephalopathy/delirium, anemia, infection,
n
o
and mass or bleeding within the brain as potential causes of the neurologic symp-
m
m
toms and findings.
o
C
6. If the patient presents within a window of eligibility for thrombolytics, testing
helps rule out other causes and hemorrhagic stroke.
7. Follow-up testing after the acute assessment may include:
a. Angiography in cases of SAH
b. MRI
c. Carotid imaging, most commonly ultrasound
d. Echocardiography to rule out the heart as an embolic source
e. Lipid profile
D. Treatment
1. Patients with ischemic stroke presenting within 3 hours of the onset of symptoms
may benefit from thrombolytic therapy with recombinant tissue plasminogen acti-
vator (tPA).
a. Table 4-9 summarizes the inclusion and exclusion criteria for tPA use.
b. Inclusion criteria include presentation within 3 hours of symptoms, measureable
neurologic deficit, and the absence of intracranial bleeding.
c. Exclusion criteria include minor symptoms; history of or signs of intracranial
hemorrhage; seizure at onset of stroke; recent trauma, major surgery, or lumbar
puncture; recent GI or GU bleeding; uncontrollable BP; and abnormal coagula-
tion studies.
S TROKE
Common ca us e s :
Ce re brova s cula r dis e a s e ,
e mbolic s troke , ma ligna ncy,
ce re bra l a ne urys m,
hype rte ns ive e nce pha lopa thy
He a d CT
(3-hr window from ons e t
of s ymptoms for tre a tme nt
with thrombolys is )
Evide nce of Is che mic s troke

ce re bra l ble e ding
Che ck ca rotid
duple x a nd e cho
S uba ra chnoid Intra pa re nchyma l
he morrha ge ble e ding
Thrombotic s troke Embolic s troke

AVM Ane urys m Hype rte ns ion
Ble e ding dis orde rs
Tra uma , Tumor
Ce re brova s cula r dis e a s e Va lvula r dis e a s e
Anticoa gula nts
Ca rotid a rte ry dis e a s e P ros the tic va lve
Hype rcoa gula ble s ta te Endoca rditis
Ca rotid dis s e ction P a te nt fora me n ova le
C
Ma ligna ncy Myxoma
o
m
Dila te d ca rdiomyopa thy
m
o
FIGURE
n
4 -1 9
G
Evaluation of stroke.
e
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e
TABLE 4-8 Differential Diagnosis for Stroke
d
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a
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Hypoglycemia
o
n
Seizure
d
i
t
i
Tumor
o
n
s
Migraine
Subdural hematoma
Cranial nerve or peripheral nerve palsy
Benign positional vertigo or labyrinthitis
Temporal arteritis with ocular complications
Syncope, vasovagal, or other etiologies
Multiple sclerosis
Infection
Trauma
2. Care for those not receiving tPA and general care for all stroke patients
a. Frequent neurologic checks and monitoring for complications
b. Monitoring and management of BP. Within the first 24 hours of an ischemic
stroke, BP often rises and usually should not be lowered unless > 220/120.
In most cases, BP gradually declines without pharmacologic intervention fol-
lowing the initial 24 hours.
TABLE 4-9
Criteria for Selection for Recombinant Tissue
Plasminogen Activator
Indications Measurable neurologic deficit
Symptom onset within past 3 hr
Absence of intracranial bleeding
Contraindications Minor or resolving symptoms
Current or history of intracranial hemorrhage
Quick HIT Seizure at onset of stroke
In the first 24 hours follow- History of GI or GU bleeding within past 3 wk
ing a stroke, BP elevations Trauma or surgery within past 2 wk
should not be aggressively
treated unless the BP exceeds Uncontrollable blood pressure (> 185/110 mm Hg)
220/120, in order to avoid caus-
Abnormal coagulation studies or thrombocytopenia
ing hypotension or decreases
in cerebral blood flow, which
can extend the infarction.
It is critical to avoid hypotension, which may worsen the underlying neu-

rologic condition. If BP is treated, use an agent with a short half-life such as
nitroprusside with a goal for systolic BP from 160 to 180 mm Hg and diastolic
Quick HIT > 105 mm Hg.
Long-term medical manage-
Initial BP control is important for patients with intracranial hemorrhage,
s
n
ment of stroke or TIA patients and CCBs (e.g., nimodipine) are frequently used to lessen vasospasm with
o
i
includes antiplatelet therapy SAH.
t
i
d
along with BP control, low- c. In cases of intracerebral bleeding and SAH, monitoring of and measures to
n
o
ering lipids, and lifestyle
C
lower intracranial pressure may be important, such as the use of mannitol and
changes, such as smoking
l
hyperventilation.
a
c
cessation, exercise, and
i
d. Use antiplatelet therapy with ischemic strokes, generally aspirin 81 to 325 mg
d
weight control.
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daily or clopidogrel if aspirin is contraindicated. Antiplatelet agents are contra-
indicated in hemorrhagic stroke.
c
i
r
e. IV hydration and nutritional support
t
a
i
f. Control of blood glucose
r
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g. Statin therapy to optimize lipids with a target LDL of < 70 mg/dL
Quick HIT
n
o
h. DVT prophylaxis
m
Compression stockings for those with intracranial bleeding
m
Patients with findings of > 70%
o
Low molecular weight heparin or subcutaneous unfractionated heparin for
C
stenosis on carotid imaging
may be candidates for carotid ischemic stroke patients
endarterectomy. A major con- i. Rehabilitative therapies
sideration for this surgery is Physical therapy
the experience and volume of
Occupational therapy
procedures performed by the
surgeon and the institution. Speech therapy
3. Consideration for surgical intervention
a. SAH may require aneurysmal clipping or therapy to occlude an arteriovenous
malformation.
b. Carotid endarterectomy is generally recommended for secondary prevention in
patients with carotid stenosis > 70%.
Quick HIT Important considerations for surgery are as follows: the number of cases
Patients with ICH should performed at institution, the complication rate, and the experience of the
undergo evaluation for under- surgeon.
lying causes, such as tumor Patient comorbidities must also be considered.
or aneurysm. Nonsurgical c. Carotid angioplasty and stenting has similar indications as carotid
therapy includes supportive endarterectomy.
measures, treatment directed
at lowering intracranial pres- Similar considerations related to experience and complication rates
sure, and BP control. This procedure is generally preferred for high-risk surgical patients with
significant comorbidities.
CLINICAL PEARL 4-11

Evaluating Suspected SAH
Most SAHs (75%) result from aneurysm rupture. Up to 20% have no identifiable cause, and the remainder
result from a variety of causes, including arteriovenous malformations and trauma.
Identification of subarachnoid bleeding may be suggested by history of sudden onset of the worst head-
ache in my life and confirmed by CT scan of the brain. CT scan is most sensitive if done early after onset,
best within 12 hours. The blood is progressively absorbed over time, and the sensitivity of CT scan falls off in
parallel to this.
In patients with suspected subarachnoid bleeding and normal CT scans, lumbar puncture can be performed
to assess for the presence of blood in the form of either red blood cells and xanthochromia. Xanthochromia,
which is the metabolized hemoglobin that is transformed into bilirubin and leads to yellow discoloration of the
CSF, begins to occur approximately 12 hours after red blood cells enter the CSF. So with remote bleeds where
the sensitivity of the CT scan may begin to fall off, evaluation of CSF can assist in establishing subarachnoid
bleeding as a potential diagnosis that could lead to arteriography or further study.
Parkinson disease (PD)

1. Common movement disorder with increasing prevalence with age
2. Affects 1% of people aged > 60 and 4% of those aged > 80
3. Progressive neurologic disease that leads to loss of function, debility, dependency,
C
and ultimately death
o
m
4. Although the exact cause is unknown, there is evidence of a genetic component.
m
o
5. Studies suggest that cigarette smoking and coffee intake may reduce PD risk and
n
that pesticide exposure or head trauma increases risk.
G
e
6. Results from a loss of dopamine containing neurons located in the substantia nigra
r
i
a
and locus cerulus in the midbrain, causing a dopamine deficiency
t
r
i
c
7. Cardinal features are tremor (often described as pill rolling), bradykinesia, and
M
rigidity.
e
d
8. The term Parkinsonism is often used to describe these features, even when asso-
i
c
a
ciated with other causes or disease processes, such as medication side effect.
l
C
9. ShyDrager is a syndrome of Parkinsonism with autonomic failure.
o
n
d
i
t
i
o
1. History
n
s
a. Patient may complain of fatigue, incoordination, or loss of dexterity.
b. May note an internal tremulous feeling.
c. May complain of poor balance, gait change, pain, and stiffness
d. Later in the disease process, falls and postural instability are common.
e. With advanced disease, there may also be complaints of choking, drooling, and
changes in speech.
f. Nearly all patients also develop nonmotor symptoms including:
Anxiety and depression in up to half of patients
Psychosis and hallucinations are common side effects of treatment.
Sleep disturbance
Pain
Autonomic dysfunction causing constipation, urge incontinence, or ortho-
static hypotension
Dementia is a late finding occurring in 30% to 40% of patients.
A dementia that precedes or coincides with the PD may signal a diagnosis of
Lewy body dementia.
a. Observation may reveal bradykinesia or tremor.
b. The tremor is usually an asymmetric resting tremor described as pill rolling.
c. The tremor decreases with activity, distinguishing it from other tremors; this
may require distraction of the patient to bring on the resting component.
d. Bradykinesia may be manifested by a loss of facial expression and diminished
blinking.
e. Rigidity can be tested with passive and resisted movements of the extremities
and may reveal cog-wheeling, which is a ratcheting resistance to flexion and
extension of the extremity. Cog-wheeling may be enhanced by testing while the
patient tenses the opposite extremity.
f. Micrographia, or small handwriting, is a characteristic feature of PD.
g. In more advanced disease, speech may become quieter and take on a mumbling
quality.
h. Gait instability and a stooped posture develop as the disease progresses.
i. Postural instability can be tested by standing behind the patient and pulling on
both their shoulders toward yourself.
A normal response is to not lose balance or at most to take a small step back-
ward to catch themselves.
An abnormal response is to fall onto the examiner or require more than one
step to correct the imbalance.
j. Personality change may be a late finding.
C. Diagnosis
1. The diagnosis of PD is clinically determined and should be considered with the
presence of the cardinal symptoms of bradykinesia, resting tremor, and/or rigidity.
2. Asymmetrical motor presentation is typical with PD. The side affected with tremor
tends to be the side affected with motor symptoms.
s
3. Response to levodopa therapy can help establish the diagnosis because 70% or
n
o
more of PD patients will respond to this medication, whereas non-PD patients are
i
t
i
d
unlikely to improve with levodopa.
n
o
4. Table 4-10 summarizes the differential diagnosis for PD along with some helpful
C
distinguishing features.
l
a
c
5. No laboratory testing is diagnostic for PD. MRI scanning helps eliminate other
i
d
e
causes.
M
6. Patients presenting with symmetrical findings or signs of advanced disease, such as
c
i
postural instability, dysarthria, dysphagia, or dysautonomia, should be assessed for
r
t
a
other disease processes.
i
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G
n
o
m
m
o
Differential Diagnosis of Parkinson Disease
C
TABLE 4-10
Disease Distinguishing Features
Essential tremor Action tremor, not resting, and absence of rigidity or bradykinesia
Lewy body dementia Primary dementia with concomitant bradykinesia and rigidity
Dementia usually precedes motor symptoms
Poor response to carbidopalevodopa
Corticobasal degeneration May develop bradykinesia and rigidity but not tremor
No response to carbidopalevodopa
Progressive supranuclear palsy Gaze abnormality is prominent feature along with falls and gait instabil-
ity; symmetrical motor features without tremor
No response to carbidopalevodopa
Multisystem atrophy Ataxia; symmetrical involvement; autonomic dysfunction; absence of
tremor and no response to carbidopa/levodopa
Medication induced Medications such as phenothiazine or metoclopramide; most cases
reversible with cessation of medication
TABLE 4-11 Secondary Causes of Parkinsonism

Cerebrovascular disease
Encephalitis
Hypoparathyroidism
Liver disease, including Wilson disease
Medications
Metoclopramide
Antipsychotics
Antiemetics
Normal pressure hydrocephalus
Subdural hematoma
Toxins
Trauma
Tumor
7. Table 4-11 lists secondary causes of Parkinsonism.

8. Parkinsonism from medications may be reversible.
C
D. Treatment
o
m
1. Several factors help guide therapy including:
m
a. Degree of impact on function
o
n
Dominant hand involvement has more impact.
G
e
Bradykinesia generally more bothersome than tremor alone
r
i
a
Care available at home
t
r
i
Interference with work or other activities
c
M
b. Age of patient
e
Younger patients will have longer exposure to medications.
d
i
c
More adverse effects, such as motor fluctuations, wearing off, and dyskinesias,
a
l
occur after 5 to 10 years of use.
C
o
With milder disease, especially in younger patients, may want to save
n
d
i
carbidopalevodopa, which is considered the most effective therapy.
t
i
o
c. Patient expectations and preferences
n
s
2. Categories of medications. The basal ganglia operate as a balancing system com-
prising the dopamine and cholinergic systems. In PD, the dopamine system is
compromised, and the cholinergic system is unopposed. The goal of therapy is to
enhance dopaminergic influence or inhibit the cholinergic system.
a. Levodopa is considered the most effective therapy.
Failure to respond (> 70% will) suggests the need to reevaluate the
diagnosis.
Carbidopa prevents peripheral metabolism, allowing increased
central nervous system availability at lower levodopa doses, reducing side
effects.
Most helpful for bradykinesia, rigidity, and tremor
Target dose is 300 to 600 mg of levodopa, but initiate at lower doses, titrating
up until there is a good response or adverse effects.
Immediate release medication used every 6 to 8 hours in combined
pill with carbidopa (e.g., carbidopa/levodopa 25/100 mg three times
daily).
Extended release forms are absorbed more slowly and less completely. Dosed
with one-third higher doses given q 12 hours.
Food inhibits absorption.
Adverse effects include hallucination, psychosis, and orthostatic hypotension.

Other common side effects include nausea and dizziness. Longer-term compli-
cations include dyskinesia, end-of-dose or wearing off effect, and unpredict-
able motor fluctuations (onoff phenomena).
Abrupt withdrawal may result in severe symptoms such as neuroleptic malig-
nant syndrome.
b. Dopamine agonists are medications that stimulate central dopamine
receptors.
May be preferred in younger patients as a means to save levodopa for later in
the disease course
Also adjunctive therapy in late disease
Medications include bromocriptine, pramipexole, ropinirole, rotigotine (trans-
dermal), and apomorphine (subcutaneous).
Alternative routes of therapy when swallowing difficult
Apomorphine used as rescue therapy for freezing with levodopa
Side effects include psychiatric symptoms, nausea, drowsiness, hypotension,
and edema.
Abrupt cessation can lead to withdrawal syndrome.
c. Monoamine oxidase type B inhibitors, which work by preventing dopamine
reuptake at the synapse, thus increasing dopaminergic activity
Include selegiline and rasagiline
May be used in early disease and may have neuroprotective properties
Generally not used along with levodopa
Side effects include nausea, headaches, and neuropsychiatric side effects with
Quick HIT other agents.
s
n
d. Anticholinergics
o
i
Asymmetrical motor presenta- Most effective for treating tremor, not helpful for bradykinesia
t
i
d
tion is typical with Parkinsons Most commonly used agents are trihexyphenidyl and benztropine.
n
o
along with the resting tremor.
C
The side affected with tremor
Most useful for younger patients because of side effects in older patients
l
Can impact memory, cause confusion, and other CNS effects
a
also tends to be the side af-
c
i
Also can cause urinary retention, constipation, dry mouth, blurry vision, and
d
fected with motor symptoms.
e
M
can affect glaucoma
e. Amantadine
c
i
r
Helpful with mild symptoms, including tremor
t
a
i
May be useful as adjunctive therapy in more severe disease to help with
r
e
G
dyskinesia
n
Quick HIT
o
Low side-effect profile. Side effects include edema and may exacerbate CNS ef-
m
fects of other Parkinson medications
m
o
f. Catechol-O-methyltransferase (COMT) inhibitors
C
The response to levodopa
therapy can be of diagnostic Not active alone
help because 70% or more Inhibits the metabolism of levodopa and increases the area under the curve
of Parkinsons patients will in an attempt to limit the onoff effects and dyskinesias with levodopa
respond to this medication,
whereas patients affected Used in patients with these motor complications
with other disease processes Tolcapone and entacapone are the available agents.
are unlikely to improve with Tolcapone is associated with liver toxicity, and liver function tests (LFTs) must
levodopa. be monitored.
Other side effects include diarrhea, orange discoloration of the urine, and an
intensification of any levodopa adverse effects.
g. Other measures
Physical therapy and use of assistive devices to minimize gait instability, one
Quick HIT of the most problematic manifestations
Speech therapy and dietary modification if dysphagia develops
No laboratory or x-ray testing
is diagnostic of PD, and testing Treatment of concomitant diseases, such as depression, which commonly
is largely done to eliminate affects patients with PD
other causes. For patients refractory to medication therapy, referral for consideration of
deep brain stimulation surgical therapy can be considered.
CLINICAL PEARL 4-12

Dementia and PD
Lewy body dementia is the second most common form of dementia and is often misdiagnosed as PD with de-
mentia. An important consideration is, which symptoms developed first, the dementia or the motor symptoms?
Dementia is usually a late finding with PD and occurs in up to 30% to 40% of patients. Approximately 25%
of patients have dementia at the time of diagnosis of PD, and the rest develop dementia on average 14 years
later. If the dementia develops first or concomitantly, this likely represents Lewy body dementia. The distinc-
tion may have implications regarding the success of therapy targeted toward the bradykinesia, rigidity, and
tremor. Patients with Lewy body dementia may be more sensitive to the side effects with carbidopalevodopa
leading to confusion, agitation, and hallucinations. Patients with primary PD are likely to be placed on medica-
tions for Parkinsons before the development of dementia.
TABLE 4-12 Common Seizures in Geriatric Patients

Type Features
Simple partial Auras or movements without loss of consciousness

Complex partial Stare with eyes open, not responding, movements such as lip smacking or
other repetitive movements; may then generalize
Duration typically is 13 min
Generalized tonicclonic Sudden loss of consciousness with rigidity and apnea for 3060 sec fol-
C
lowed by approximately 1 min of clonic movements. Duration typically is
o
m
13 min
m
o
n
G
e
r
i
a
t
r
i
c
Seizures
M
e
d
i
c
a
1. There is a 10% lifetime occurrence of seizures.
l
C
2. Peak ages for seizures are under age 1 and over age 65.
o
n
3. There is a linear increase in seizures for adults over age 30.
d
i
t
4. Geriatric patients are more likely to have underlying neurologic disease (> 50%)
i
o
n
and focal neurologic findings.
s
5. Simple partial, complex partial, and generalized tonicclonic seizures are most
common in geriatric patients (Table 4-12).
6. Complex partial seizures occur with greater frequency in geriatric patients than in
younger groups.
7. Generalized seizures occur with similar frequency in geriatric patients as in
younger groups.
8. Underlying causes for seizures are presented in Table 4-13.
1. History
a. Description of the symptoms noted
Level of consciousness is diminished with complex partial and generalized sei-
zures but not simple partial seizures.
Movements or symptoms with partial seizures may relate to the affected brain
area and may include auras or movements without loss of consciousness (sim-
ple) or include staring with eyes open, not responding, and movements such
as lip smacking or other repetitive movements (complex).
TABLE 4-13 Causes for Secondary Seizures

Subdural or subarachnoid hemorrhage
Cerebrovascular accident
Tumor or mass
Dementia
Parkinson disease
Trauma
Substance abuse or withdrawal
Metabolic encephalopathy, including glucose or electrolyte abnormalities
Infection
Generalized tonicclonic seizures are characterized by the sudden loss of con-

sciousness with rigidity and apnea for 30 to 60 seconds followed by approxi-
mately 1 minute of clonic movements.
Duration typically is 1 to 3 minutes.
Precipitants may include intense emotions, stress, lights, sound, fever, lack of
sleep, medications, alcohol, and drugs.
b. Postictal symptoms include:
Lethargy, sleepiness, and confusion that lasts for variable periods of time
Injuries such as tongue biting
s
n
o
Loss of bladder control
i
t
i
c. Presence of prior episodes or underlying neurologic disease
d
n
d. Presence of other disease, such as DM
o
C
e. Recent trauma or fevers
l
a
c
f. Medications and compliance with antiepileptic medications if prescribed
i
d
g. History of substance use or abuse
e
M
c
a. Evidence of trauma, such as tongue biting or contusions to extremities
i
r
t
a
b. Detailed neurologic examination looking for focal defects suspicious for stroke,
i
r
e
G
tumor, or intracranial bleeding
n
c. Assessment for tremor, bradykinesia, or rigidity for underlying PD or related disorder
o
m
d. Dementia screening with mini-mental status exam (MMSE)
m
e. Evidence of incontinence
o
C
f. Signs of alcohol abuse, such as gynecomastia, spider angiomas, testicular atro-
phy, or enlarged liver
C. Diagnosis
1. Differential diagnosis includes syncope and psychogenic seizures.
a. Syncope is often preceded by lightheadedness, diaphoresis, and palpitations and
may be triggered by noxious stimuli or emotions.
b. Psychogenic seizures are associated with underlying psychiatric disease, are
atypical in the pattern of movement and duration, and are generally not associ-
ated with injury or incontinence.
2. Evaluation
a. Laboratory testing should include blood glucose along with a metabolic profile to
evaluate liver function, electrolytes (including calcium) calcium, CBC, and urinalysis.
b. Imaging for first-time seizures using either CT scanning and/or MRI, depending
on the presenting neurologic examination
c. EEG should be performed for first-time seizure evaluation; if normal, there is a
lesser chance of recurrent seizures.
d. In patients with suspected infection or SAH (not seen on CT scan), lumbar
puncture for cerebrospinal fluid evaluation should be performed.
D. Treatment
1. Patients with no focal findings on examination and with a normal EEG and imag-
ing may not warrant therapy for first-time seizures because they are at lower risk Quick HIT
for recurrence. There is a 10% lifetime occur-
2. Patients with reversible or potentially reversible causes, such as electrolyte or glu- rence of seizures. Peak ages
cose abnormalities, are at lower risk for recurrence. for seizures are under age 1
3. Patients who may warrant therapy are those with recurrence or with a nonrevers- and over age 65.
ible cause or abnormality, such as underlying dementia, PD, or a brain tumor.
4. Older medications include phenytoin, carbamazepine, and valproic acid.
a. These medications are associated with many side effects, including confusion,
gait disturbance, dizziness/ataxia, sedation, bone loss, and liver toxicity.
b. Associated with many medication interactions
5. Newer agents include lamotrigine, levetiracetam, topiramate, and oxcarbazepine.
Quick HIT
These agents are associated with fewer interactions and adverse effects than older More than half of geriatric pa-
medications. tients with seizures will have
6. Principles of therapy are to initiate one agent and then titrate dosing either until underlying neurologic disease,
as well as focal neurologic
seizure is controlled or the agent is not tolerated. findings.
7. If not tolerated or if seizures are uncontrolled, switching to another agent is prefer-
able to adding a second medication.
8. Patients who are seizure free for 2 or more years may be considered for tapering
and cessation of therapy.
9. Patients with seizures who want to drive must be seizure free for 6 months in most
states in order to drive. Quick HIT
Complex partial seizures occur
Headaches with greater frequency in geri-
C
o
A. General characteristics atric patients than in younger
m
groups.
m
1. Primary headaches include tension, migraine, and cluster headaches.
o
2. Secondary headaches are caused by an underlying cause (Table 4-14).
n
G
3. Primary headache syndromes generally have their onset at < 45 years of age and are
e
r
uncommon as a cause of new headaches in geriatric patients.
i
a
t
4. Up to 30% of headaches in geriatric patients will be associated with an underly-
r
i
c
ing pathology, which is more than three times more likely in older adults than in
Quick HIT
M
e
younger patients.
d
i
5. Migraine headaches tend to become milder and less frequent with increasing age. Patients with no focal findings
c
a
on examination and with nor-
l
a. Atypical migraines may occur in geriatric patients with a migraine aura, such as
C
mal EEG and imaging may not
o
visual changes or paresthesias but without the headache.
n
warrant therapy for first-time
d
b. These types of symptoms mimic TIA or stroke and warrant a similar evaluation.
i
seizures because they are at
t
i
o
lower risk for recurrence.
n
s
1. History
a. Onset
Prior history of a primary headache syndrome, such as migraines, tension, or
cluster, suggests possible recurrence.
Sudden, rapid peak and worst ever suggest subarachnoid bleeding.
Morning headaches suggest tumor.
b. Associated symptoms
Fever may indicate an infectious etiology, such as sinusitis.
Visual symptoms or eye pain could indicate glaucoma as a cause.
Trauma suggests possible subdural hematoma.
Associated neurologic symptoms could indicate tumor or stroke.
Nausea and vomiting could indicate increased intracranial pressure.
Progressive worsening could indicate an intracranial process such as subdural
hematoma or tumor.
c. Past medical history
History of HTN could indicate lack of control or medication side effect.
Review of medications since polypharmacy can be a result or cause of
headache.
TABLE 4-14 Differential Diagnosis of Headaches in Geriatric Patients

Primary headaches
Migraine
Tension
Cluster
Secondary
Subdural hematoma
Subarachnoid hemorrhage
Brain tumor
Cerebrovascular accident
Temporal arteritis
Cervical spine disease
Hypertensive
Infections
Trigeminal neuralgia
Medications
Nitrates
NSAIDs
Calcium channel blockers
s
Levodopa/carbidopa
n
o
i
Alcohol
t
i
d
n
Opioids
o
C
l
a
c
i
d
e
M
c
i
r
t
a. Vital signs for uncontrolled BP or fever
a
i
r
b. Eye examination for signs of glaucoma, such as increased cupdisc ratio and for
e
G
papilledema, which indicates increased intracranial pressure.
n
o
c. Focal areas of tenderness to suggest sinusitis, temporal arteritis (temples),
m
m
or trigeminal neuralgia (trigeminal nerve distribution).
o
C
d. Muscle pain or stiffness suggests polymyalgia rheumatica. Temporal artery ten-
derness raises the possibility of temporal arteritis.
e. Neurologic examination to evaluate for deficits to suggest tumor or
stroke
C. Diagnosis
1. Patients with history of a primary headache type with an unchanged headache
pattern and normal examination may not warrant further evaluation.
2. Geriatric patients, especially those with new onset of headaches, should be evalu-
ated carefully for secondary causes of headaches.
3. History and physical examination may suggest a likely cause and help direct the
workup.
4. In general, evaluation for new onset headaches without an obvious cause warrants
laboratory and imaging evaluation.
a. CBC to evaluate for possible infection
b. Erythrocyte sedimentation rate (ESR) for possible temporal arteritis
c. CT scan or MRI of the brain to evaluate for subdural hematoma, SAH, stroke, or
brain tumor may also suggest/diagnose sinus disease.
d. Consider cervical spine films.
e. Consider ophthalmology referral for more detailed eye examination.
CLINICAL PEARL 4-13

Quick HIT
Temporal Arteritis Primary headaches include
Patients with temporal arteritis may also exhibit symptoms of polymyalgia rheumatica, a related disorder. tension, migraine, and cluster
Polymyalgia rheumatica presents with proximal muscle pain and stiffness along with an elevated ESR. Tem- headaches and are uncom-
poral arteritis should be suspected when there are concomitant headaches, temporal tenderness, and an ESR mon as a cause of new head-
in the range of 100 mm/hour or higher. Because of its association with retinal ischemia and vision loss if not aches in geriatric patients.
Headaches associated with
treated promptly, patients suspected of this diagnosis warrant immediate therapy with prednisone. Although
an underlying pathology are
definitive diagnosis involves a temporal artery biopsy, treatment should not be delayed pending biopsy results,
three times more likely in
and if the results are inconclusive, prednisone should be continued when there are clinical findings that sup- older adults than in younger
port the diagnosis. Treatment with prednisone is generally needed for 1 to 2 years with gradual tapering of the patients.
dosage as treatment is withdrawn.
5. If the ESR is elevated, consider arterial biopsy to diagnose temporal arteritis.

Quick HIT
6. Trigeminal neuralgia is a clinical diagnosis characterized by electrical shock-like Evaluation of new onset
headaches without an obvious
pains and sensitivity in the trigeminal nerve distribution. cause warrants laboratory and
imaging, including CBC, ESR,
D. Treatment and CT scan and/or MRI of
1. Depends on the cause the brain.
2. Temporal arteritis is an urgent situation because if untreated, up to 20% of patients
will experience some degree of vision loss.
a. High-dose steroids (60 to 80 mg of prednisone daily) should be promptly
C
o
initiated.
m
m
b. Biopsy should be performed as soon as possible when considering the diagnosis
Quick HIT
o
n
and within 2 weeks of starting steroids.
G
3. Tumors and SAH merit prompt neurosurgical consultation.
e
Suspected temporal arteritis
r
i
4. HTN and stroke causing headaches require hospitalization and inpatient is an urgent situation because
a
t
r
management. up to 20% of patients will
i
c
5. Cervical spine disease may respond to physical therapy, muscle relaxants, and an- experience some degree of vi-
M
sion loss if untreated; steroids
e
algesics; caution should be exercised in the use of muscle relaxants and NSAIDs in
d
should be promptly initiated
i
geriatric patients; monitor for sedative and renal or GI effects, respectively.
c
and arrangements made for a
a
l
6. Trigeminal neuralgia can be treated with anticonvulsants (e.g., carbamazepine). temporal artery biopsy.
C
o
7. Primary headache diagnoses can generally be treated with analgesics with the same
n
d
cautions as noted above.
i
t
i
a. Vasoconstrictors, such as triptans, for migraines should be used with caution in
o
n
s
geriatric patients in view of the potential for complicating underlying vascular
disease.
b. Prophylactic medications can be utilized, but tricyclic antidepressants have anti-
cholinergic side effects that may be troublesome for geriatric patients; -blockers
or CCBs may be more suitable alternatives.
Pseudobulbar Affect
1. A condition described as an emotional disinhibition syndrome associated with un-
derlying neurologic disease
2. Present in 10% to 40% of patients with stroke, PD, dementia, amyotrophic lateral
sclerosis, multiple sclerosis, and brain tumors
3. Often misdiagnosed as depression
1. Inappropriate outbursts of crying, laughing, or emotion that is incongruent with
the situation
2. May exhibit excessive emotions inconsistent with the social context
3. May or may not occur in response to stimuli; however, outbursts are not appropri-
ate in degree or content
4. Neurologic examination is consistent with the underlying neurologic disease.
5. Depression may be present in up to one-third of patients.
C. Diagnosis
1. A clinical diagnosis with no laboratory or imaging findings characteristic of the disease
2. Diagnostic criteria that support the diagnosis are as follows:
a. Change from prior emotional responses
b. Expressed emotions exaggerated or incongruent with situation
c. Unrelated to any stimulus or excessive in degree to the presented stimulus
d. Not caused by a syndrome or medication
e. Not controllable by patient
f. Causes anxiety or disruption to the patient and those around them
3. Differential diagnosis includes depression and bipolar disorder, but only a minority
of patients with this condition are depressed.
D. Treatment
1. Antidepressants
a. Selective serotonin reuptake inhibitors
b. Tricyclic antidepressants
2. Anti-Parkinsons medications
a. Levodopa
b. Amantadine
3. Dextromethorphan/quinidine
4. Dosages of these medications are lower than typical antidepressant or therapeutic
s
n
o
doses.
i
t
i
5. Onset of symptom relief occurs within days.
d
n
o
C
l
a
c
i
d
e
M
Ca rd io va s c ula r D is e a s e
c
i
r
Hypertension (HTN)
t
a
i
r
e
G
n
1. Defined as systolic BP 140 mm Hg and/or diastolic BP 90 mm Hg
o
m
2. The prevalence of HTN is 60% to 80% in individuals older than 60 years.
m
o
a. Diastolic pressure peaks in the fifties, whereas systolic pressure continues to in-
C
crease with age.
b. Despite its prevalence, HTN is not considered a normal consequence of age.
3. Systolic BP and pulse pressure are better predictors of adverse events than diastolic
pressure.
a. Isolated systolic HTN accounts for about 60% of cases in those over
age 65.
b. Adverse effects of HTN include a two- to fourfold increase in the risk
of heart attack, left ventricular hypertrophy (LVH), renal disease, stroke, and
overall cardiovascular mortality.
4. Diagnosis should be based on serial BP readings.
5. Atherosclerosis may interfere with occlusion of brachial artery by a BP cuff, leading
to erroneously elevated BP determinations or pseudohypertension.
a. It can be determined by Oslers maneuver.
The cuff pressure is raised above the systolic BP.
If the radial artery is still palpable, significant atherosclerosis is probably pres-
ent and may account for 10 to 15 mm Hg pressure error.
The only absolute way to diagnose pseudohypertension is to measure intra-
arterial pressure directly and compare it with the BP measurement taken with
a cuff. This is not practical in the office setting.
B. Risk factors for HTN

1.
2.
Obesity
High-normal BP Quick HIT
3. Hyperglycemia/diabetes The diagnosis of HTN is based
4. Hyperlipidemia on repeated elevation of BP
5. Family history readings.
6. Cigarette smoking
7. Black race
C. Clinical assessment
1. May have no symptoms, often referred to as the silent killer
2. Symptoms are usually related to target organ damage. Quick HIT
3. History should include an assessment of cardiac risk factors: smoking, dyslipid-
Although diastolic BP peaks in
emia, obesity, and diabetes.
the sixth decade, systolic BP
4. Measure BP both sitting and standing. continues to rise with age.
a. Older individuals have sluggish baroreceptors and a slowed sympathetic respon-
siveness to changes in position.
b. Orthostatic changes should alert the clinician to avoid drugs likely to cause pos-
tural hypotension, to initiate therapy at lower doses, and to titrate doses slowly
upward.
5. Physical examination should include the following:
a. BMI Quick HIT
b. Careful cardiopulmonary examination with a focus on detecting LVH, heart fail- NSAIDs may adversely af-
ure (HF), or valvular disease. fect BP control and should
c. Fundoscopy to detect hypertensive retinal disease be avoided in patients with
high BP.
C
d. Vascular examination: palpating all peripheral arteries and auscultating for ca-
o
m
rotid and femoral bruits
m
e. Abdominal examination with a focus on detecting any aneurysms, enlarged kid-
o
n
neys, or vascular bruits.
G
e
r
D. Testing
i
a
t
1. Diagnostic testing is warranted to evaluate for additional risk factors, to assess for
r
i
c
secondary causes of HTN, to evaluate target organs, and to find conditions that
M
e
may influence medication choices.
d
i
a. CBC
c
a
l
b. Urinalysis, BUN, and creatinine
C
o
c. Serum electrolytes and calcium
n
d
d. Fasting glucose
i
t
i
e. Fasting lipids
o
n
f. 12-lead EKG
s
g. Echocardiogram if there is suspicion of LVH, congestive heart failure (CHF), or
valvular disease
2. Secondary HTN is uncommon, but consider additional testing in treatment-
resistant cases (uncontrolled BP with a three-drug regimen) and if diastolic BP
remains 115 mm Hg.
CLINICAL PEARL 4-14

Evaluation of HTN
Once the diagnosis of HTN is established, the goals should be to identify secondary or contributing causes of
HTN, to detect end-organ damage, to identify other risk factors for cardiovascular disease, and to evaluate
confounding variables or comorbidities that might affect treatment. Although secondary HTN is rare in the
elderly, contributing factors such as excess alcohol intake or taking medications such as NSAIDs, which may
aggravate BP, are relatively common. Target organs include the heart, blood vessels, kidneys, and the eye.
Focusing on symptoms and signs related to these target organs is important. Because the main reason for
treating HTN is to avoid complications, it is also important to address additional risk factors such as smoking,
an elevated glucose, or hyperlipidemia.
a. Atherosclerotic renovascular HTN and primary hyperaldosteronism occur more

frequently in older adults.
b. Because primary hyperparathyroidism can increase BP, diagnose and treat
hyperparathyroidism.
c. Estrogen therapy in postmenopausal women may cause secondary HTN.
d. Renal disease (decrease in creatinine clearance).
e. Excess alcohol intake and NSAIDs may contribute to HTN.
E. Treatment
Quick HIT 1. A study of hypertensive patients aged 80 showed 30% reduction in the rate of fatal
and nonfatal stroke, 64% reduction in the rate of HF, but no significant change in
Treatment and control of HTN
lowers risk of stroke and heart overall mortality with therapy.
disease. 2. Target BP goals in elderly of < 150/90 mm Hg (instead of < 140/90 mm Hg used for
younger patients).
a. At age 60 in JNC 8 guidelines
b. At age 80 in Canadian and British guidelines
3. Lifestyle changes are not easily accomplished, but should be attempted including:
a. Losing weight if overweight or obese. Modest changes in weight, for example, 5
to 10 kg, may significantly improve BP.
b. Limiting dietary sodium
c. Eating fruits and vegetables
d. Low-fat dairy products
e. Reducing saturated and total fats
f. Aerobic exercises
g. Eating foods rich in potassium, calcium, and magnesium
s
h. Smoking cessation
n
o
4. Pharmacologic treatment
i
t
i
d
a. Reduces cardiovascular morbidity and mortality
n
o
b. Thiazide-type diuretics (hydrochlorothiazide and chlorthalidone) are generally
C
preferred as initial therapy.
l
a
c
c. CCBs
i
d
e
d. -Blockers may be ineffective as first-line therapy in > 60-year-olds.
M
e. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor
c
i
blockers (ARBs) are less likely to cause orthostatic hypotension.
r
t
a
5. Initial therapy for HTN in elderly if specific comorbidities exist.
i
r
e
G
a. Systolic HF
n
Diuretic
o
m
-Blocker
m
ACEI
o
C
ARB
Aldosterone antagonist
b. After MI
-Blocker
ACEI (or ARB)
Aldosterone antagonist
c. Coronary artery disease (CAD) or at high risk of cardiovascular disease
Thiazide diuretic
-Blocker
ACEI
CCB
d. Angina
-Blocker
CCB
e. Aortic aneurysm
-Blocker
ARB or ACEI
Thiazide diuretic
CCB
f. Diabetes
ACEI (or ARB)
CCB Quick HIT
Thiazide diuretic An ACEI or an ARB is useful
-Blocker in hypertensive patients with
g. Chronic kidney disease (CKD) CHF, LVH, CKD with protein-
ACEI or ARB uria, or a past MI.
h. Stroke or TIA
Thiazide diuretic
ACEI (or ARB)
CCB
6. -Blockers are not recommended as first-line therapy.
Quick HIT
BP medications can be tai-
CAD lored toward treating comor-
bidities, and if there are none,
A. General information thiazide diuretics are consid-
1. Pathogenesis: Atherosclerotic plaque consisting of a necrotic center and fibrous cap ered first-line therapy.
that can occlude blood flow. Rupture of a stable plaque triggers acute coronary syn-
drome (ACS), either unstable angina or MI.
2. MI occurs if a coronary artery occlusion results in cardiac muscle death.
3. Angina occurs in association with blood vessel narrowing or spasm that causes
ischemia but not necessarily tissue death. Quick HIT
B. Risk factors (Table 4-15) Most older adults will need
1. HTN more than one medication to
reach their target BP.
2. Hypercholesterolemia
C
3. Cigarette smoking
o
m
4. Diabetes
m
o
5. Obesity
n
6. Metabolic syndrome
G
Quick HIT
e
7. Family history of cardiovascular disease in first-degree relative
r
i
a
8. Peripheral vascular disease
t
r
i
Combining lower doses of
c
M
Stable Angina two medication is often more
e
effective and has less side ef-
d
i
fects than using a single drug
c
1. In stable angina, there is a fixed lesion that narrows the lumen of the coronary
a
at maximum dose.
l
arteries. Coronary ischemia occurs when there is an imbalance between the oxygen
C
o
n
demand and blood supply.
d
i
a. The key clinical feature is chest pain or pressure brought on by exertion and
t
i
o
relieved by rest.
n
s
b. In stable angina, there is a predictable pattern of exertional symptoms that lasts
< 15 minutes and is relieved by rest or nitroglycerin.
c. Angina is typically described by tightness, pressure, or a squeezing sensation.
Rarely is angina pain sharp or stabbing.
Durationangina pain typically lasts from 5 to 15 minutes.
TABLE 4-15 Cardiovascular Risk Factors

Gender Diabetes
Race Elevated cholesterol
Age Decreased HDLcholesterol
Family history Obesity
History of vascular disease Systolic hypertension
Smoking history Being treated for HTN
Risk calculator available at www.my.americanheart.org/cvriskcalculator.
d. The elderly may present with atypical symptoms such as shortness of breath
with exertion, faintness, or sweatiness. Cognitively impaired patients may be
unable to report symptoms, and the observation of exercise-induced symptoms
may be what alerts the clinician that CAD may be present.
Myocardial ischemia should be considered in any episodic difficulty.
B. Diagnosis
1. A normal EKG does not exclude CAD.
a. About 50% of individuals with CAD have a normal resting EKG. Q waves sug-
gest an old MI and the presence of CAD. Although nonspecific ST changes and
T wave suggest the presence of heart disease, they are not diagnostic.
b. An EKG obtained during an episode of angina that reveals a new ST segment
abnormality or conduction defect strongly suggests CAD. A completely normal
EKG during an episode of chest pain argues against a cardiac cause.
c. The physical examination is often unremarkable in stable angina. Clues to the
presence of CAD include HTN, vascular bruits, and poor pulses.
d. Exercise stress testing is useful for assessing patients with suspected CAD.
Many elderly may be unable to exercise sufficiently and will require pharma-
cologic agents such as dobutamine, dipyridamole, or adenosine to raise their
heart rate.
Exercise tests may be performed with or without imaging. Pharmacologic
stress testing is usually accompanied by imaging either with a nuclear scan or
echocardiography.
Coronary angiography is helpful in patients with high-risk findings on non-
invasive testing who are candidates for an interventional procedure, in those
s
whose diagnosis remains uncertain, and in those who have survived a near
n
o
fatal event or have angina and signs of HF.
i
t
i
d
n
C. Treatment of angina
o
C
1. Angina is treated with sublingual nitroglycerin, which should be taken while sitting
l
a
c
to avoid severe orthostatic hypotension.
i
d
a. Lingual solutionone to two sprays (0.4 to 0.8 mg)onto or under tongue;
e
M
repeat as needed every 3 to 5 minutes; maximum of three sprays (1.2 mg) in a
c
15-minute period
i
r
t
a
b. Sublingual tablets 0.3 to 0.6 mg; repeat as needed every 5 minutes; prompt med-
i
r
e
ical attention if pain persists after three doses in a 15-minute period
G
c. Intrabuccal tablet placed in buccal pouch and allowed to dissolve undisturbed over
n
o
m
3 to 5 hours; may place additional tablet on opposite side if additional angina attack
m
2. Do not use nitrates within 24 hours of taking a selective phosphodiesterase inhibi-
o
C
tor (sildenafil or vardenafil) or within 48 hours of tadalafil because of the risk of
severe prolonged hypotension, which can be fatal.
3. Aspirin or clopidogrel (if aspirin is contraindicated)
4. -Blockers are recommended for all patients with angina.
a. Avoid acebutolol, pindolol, carvedilol, or penbutolol owing to intrinsic sympa-
thomimetic activity.
b. If -blockers are contraindicated or fail to control symptoms, consider using a
long-acting CCB or long-acting nitrate.
5. ACEIs can help prevent MI and reduce symptoms of CAD.
6. Ranolazine may reduce angina frequency in those with continued symptoms de-
spite treatment with a -blocker, nitrates, and a CCB.
a. Indicated for those with chronic symptoms, not for acute angina
b. Is a non-nitrate alternative for treating stable angina
c. Contraindicated in those with prolonged QT interval or with hepatic impairment
7. Risk factor modification: Control HTN, weight loss if obese, smoking cessation,
diet, and lowering of lipids (Table 4-16)
a. Atorvastatin reduces frequency of angina and nitroglycerin use.
b. Dietconsider reducing saturated fat to < 7% of total calories.
c. Exercise is associated with improved BP control, decreased insulin resistance,
and an increased high density lipoprotein (HDL).
TABLE 4-16 Lipid Therapy Recommendations

Known cardiovascular disease aged > 75 Moderate intensity
Known cardiovascular disease aged < 75 High intensity
LDL> 190 mg/dL High intensity
Diabetes and LDL70189 mg/dL Moderate intensity
10-yr risk for cardiovascular disease 7.5% Moderate to high intensity
10-yr cardiovascular risk 7.5% and LDL70189 mg/dL High intensity
High intensity = rosuvastatin 2040 mg daily; or atorvastatin 4080 mg daily.
Moderate intensity = atorvastatin 1020 mg daily; or rosuvastatin 510 mg daily; or simvastatin 2040 mg daily; or pravas-
tatin 4080 mg daily.
CLINICAL PEARL 4-15 Quick HIT

A helpful mnemonic for treating CAD is Patients with chest pain
A: Aspirin or other antiplatelet therapy consistent with angina and
B: -Blockers and BP control normal laboratory testing and
C: Cigarette smoking and cholesterol EKG findings can be further
D: Diet and diabetes control evaluated with exercise stress
testing.
E: Education and exercise
C
o
m
m
o
n
8. Magnesium supplementation may increase exercise tolerance and quality of life.
Quick HIT
G
9. Coenzyme Q10 may reduce angina frequency and increase exercise time.
e
r
i
10. Invasive procedures
a
Patients with positive labora-
t
r
a. Procedure-related mortality increases with age after both coronary artery bypass
i
c
tory or EKG findings in the
grafting (CABG) and percutaneous coronary intervention (PCI).
M
evaluation of chest pain may
e
b. Early invasive therapy and medical therapy have similar outcomes at 1 year. be candidates for cardiac
d
i
c. PCI for nonacute CAD may not reduce incidence of MI, and effects on mortal- catheterization for diagnosis
c
a
and, possibly, therapy of their
l
ity are inconsistent in systematic reviews.
C
underlying disease.
o
11. Other management options
n
d
a. Nurse-led cardiac rehabilitation may improve walking performance.
i
t
i
b. Yoga lifestyle intervention may reduce angina symptoms and may be associated
o
n
s
with regression of coronary artery lesions.
c. Cognitive-behavioral self-management program reduces frequency of angina
episodes. Quick HIT
d. Enhanced external counter-pulsation might reduce frequency of angina
If -blockers are contraindi-
episodes. cated, then prescribe either
a long-acting nitrate or long-
Acute Coronary Syndrome (ACS) acting calcium blocker to
A. General information control angina.
1. Risk factors same as for CAD.
2. AF associated with increased risk of MI.
3. ACS includes unstable angina, non-ST elevation MI (NSTEMI), and ST elevation
MI (STEMI).
4. Brought on by sudden reduced blood flow that is almost always associated with the Quick HIT
rupture of an atherosclerotic plaque causing clot formation and either partial or Pain is still the most common
complete occlusion of a coronary artery presenting symptom of an
5. Although chest pain is the most common presentation, symptoms are variable and acute MI in those aged < 75.
include dyspnea, sweatiness, and nausea. The elderly are more likely to present After age 85, dyspnea is the
with atypical symptoms such as confusion or fatigue without chest pain. most common symptom fol-
lowed by chest pain.
6. Physical examination can be normal or include hypotension, signs of pulmonary
edema, an S3 or S4, heart murmur, rales, and diaphoresis.
FIGURE
4 -2 0 Acute myocardial infarction.
(Cho L, Griffin BP. Cardiology Intensive Board Review. Philadelphia, PA: LWW, 2014.)
B. Testing
1. 12-lead EKG should be evaluated within 10 minutes of patient arrival. Repeat
EKGs may be needed if the patient remains symptomatic (Figure 4-20).
2. Cardiac biomarkers (cardiac specific troponin), myoglobin, and creatine kinase MB
isoenzymes (CK-MB). If negative, remeasure at 8 to 12 hours after symptom onset.
Repeat 2 to 3 times.
3. Assess fasting lipid profile.
4. Portable CXR.
a. To assess for cardiomegaly and pulmonary edema. It also helps detect alterna-
s
n
tive causes of symptoms such as pneumonia or a thoracic aneurysm (widened
o
i
t
mediastinum).
i
d
n
5. CBC with platelet count
o
C
6. PT/INR/aPTT
l
a
7. BMP
c
i
d
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C. Diagnosis
1. Diagnosis is based on symptoms along with cardiac serum markers and EKG
c
i
r
changes. In the emergency setting, an EKG remains the most important diagnostic
t
a
i
r
test.
e
G
a. STEMI: elevated serum markers and ST-segment elevations
n
o
b. NSTEMI: elevated serum markers and depressed ST segments and/or inverted T
m
m
waves
o
c. Unstable angina; nonelevated serum markers, normal or depressed ST segments,
C
and normal or depressed T waves
d. A single enzyme measurement, particularly within 6 hours of symptoms, does
not exclude an MI.
e. An increased troponin with a normal CK-MB indicates an increased risk of an MI
within 30 days and a natural history similar to patients with a NSTEMI.
f. Troponins are not useful for detecting a reinfarction within the first week; CK-
MB is the test of choice for evaluating the possibility of an early reinfarction.
g. Both troponins and CK-MB can be falsely positive if there is subclinical ischemia
or nonischemic myocardial damage.
h. Echocardiogram may demonstrate wall-motion abnormalities and can be helpful
if the diagnosis is in question. An echo can assess the extent of an infarction and
LV function and identify complications such as an effusion, valvular disease, or
LV rupture.
D. Medical treatment
1. Aspirin 162 to 365 mg chewed as soon as possible; clopidogrel if unable to take
aspirin.
2. Nitroglycerin 0.4 mg sublingually every 5 minutes for up to three doses for ongo-
ing ischemic discomfort
CLINICAL PEARL 4-16

Patient Selection for Therapy
Despite an increasing number of elderly patients presenting with ACS, the evidence to guide treatment in
this group is limited. Subgroup analyses from some large studies suggest greater benefits for the elderly with
some therapies, but perhaps little benefit with others. Patient selection and dosing may be one explanation for
these age-related differences. Frailty, functional status, and social aspects of care in the elderly are rarely in-
cluded in clinical investigations. Bleeding and renal complications are also more likely in the elderly, and many
trials lack information on the bleeding rates associated with antithrombotic therapies and on renal failure af-
ter cardiac catheterization in the elderly. Such limitations prevent a full assessment of the risk-to-benefit ratio
for elderly patients, making this an ongoing area of research. At this time, using patients physiologic age
rather than their chronologic age is a useful principle for helping to guide therapy.
3. Bed rest and continuous EKG monitoring for all patients during early hospital phase
4. Oxygen if arterial saturation < 94%, or should be considered for all patients in
first 6 hours
5. -Blockers orally or IV within 24 hours unless contraindicated. The initial use of
short-acting -blockers is preferred in the acute setting.
6. Oral ACEI is indicated within first 24 hours if pulmonary congestion or LVEF
40%; consider for all patients.
7. IV nitroglycerin in first 48 hours if persistent ischemia, HF, or HTN
8. If persistent or recurrent ischemia symptoms after -blockers and nitrates:
a. Oral long-acting nondihydropyridine CCBs (such as verapamil or diltiazem)
C
o
b. Morphine sulfate IV if chest pain persists on nitroglycerin therapy; 2 to 4 mg
m
m
increasing to 2 to 8 mg IV and repeated as necessary every 5 to 15 minutes
o
9. Discontinue all NSAIDs but not aspirin.
n
G
10. For medical management in high-risk patients in whom an invasive procedure is
e
r
not planned, add an anticoagulant (if no contraindications), and consider a glyco-
i
a
t
protein IIb/IIIa inhibitor.
r
i
c
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E. Invasive therapy
e
d
1. Angiography with intent of revascularization is indicated if there is elevated
i
c
a
risk of clinical events, refractory angina, hemodynamic instability, and electric
l
C
instability.
o
n
2. Add anticoagulant therapy to antiplatelet therapyenoxaparin or heparin.
d
i
t
3. Start dual antiplatelet therapy in addition to aspirin before diagnostic angiography
i
o
n
with one of the following:
s
a. clopidogrel
b. IV glycoprotein IIb/IIIa inhibitor
c. prasugrel
d. ticagrelor
F. Long-term therapy
1. Dual antiplatelet therapy with aspirin and clopidogrel or prasugrel. Recommenda-
tions about dose and duration of therapy vary.
2. -Blockers
3. ACEI
a. Improves outcomes, especially if ejection fraction < 40%.
b. Elderly seem to benefit more than younger adults.
4. Statin (see Table 4-16)
5. The FDA recommends against coadministration of clopidogrel and omeprazole be-
cause of the possibility of increased adverse events.
6. Cardiac rehabilitation/secondary prevention programs are recommended, especially
if multiple modifiable risk factors present or in moderate to high-risk patients; car-
diac rehabilitation is associated with reduced total and cardiac mortality after 1 year.
7. If there is no recurrent chest pain, a stress test to stratify risk is recommended.
TABLE 4-17 ABI Values and Interpretations

Quick HIT
ABI Value Interpretation
Unless contraindicated, all
post-MI patients should be
on aspirin, a -blocker, and > 1.2 Abnormalnoncompressible arteries
an ACEI. 1.01.2 Normal range
0.91.0 Acceptableborderline
0.70.9 Mild arterial disease
0.40.7 Moderate arterial disease
< 0.4 Severe arterial disease
Peripheral Vascular Disease

A. Common in the elderly and usually caused by atherosclerosis.
1. Prevalence is 11% to 29%; can range from asymptomatic disease to mild claudica-
tion to severe rest pain, which is limb threatening
B. Risk factors similar to CAD. The association with smoking is very strong, with > 80%
of those with peripheral vascular disease (PVD) being either smokers or ex-smokers.
C. Physical examination findings include decreased pulses, cool extremities,
hairlessness, and shiny skin. More severe disease may demonstrate dependent rubor
Quick HIT with pallor on elevation.
s
n
D. An ABI can help diagnose and assess the severity of disease. Refer to Table 4-17.
o
i
Many people with intermittent
t
i
d
claudication will stabilize or E. The natural history is variable. The twin priorities of treatment are symptom relief
n
o
improve with conservative
C
and the prevention of cardiovascular events.
therapy, especially smoking
l
1. Treatment, including addressing risk factors, especially smoking, may stabilize
a
c
cessation and supervised ex-
i
symptoms, whereas others require invasive management or even amputation.
d
ercise therapy.
e
M
2. Exercise rehabilitation can increase pain-free walking time.
3. Antiplatelet therapy to reduce the risk of cardiovascular events
c
i
r
4. Medications to improve symptoms yield little benefit, but there is some evidence
t
a
i
that a statin and cilostazol are of benefit.
r
e
G
a. Cilostazol is a phosphodiesterase-3 inhibitor and may increase maximum walk-
n
o
ing distance by 40% to 50%. It should be considered in those with disabling
m
symptoms in whom an interventional procedure is not warranted.
m
o
5. Consider revascularization for disabling symptoms, ischemic rest pain, gangrene,
C
or a nonhealing ulcer.
Abdominal Aortic Aneurysm (AAA)

A. Defined as a widening of the infrarenal aorta to > 3 cm
B. Incidence increases with age, about 3% to 4% of those over age 70; more common in
men than women
C. Most expand at a rate of about 0.2 to 0.4 cm per year. As aneurysm enlarges, the risk
of rupture increases.
1. For those > 5 cm, about a 20% to 30% 5-year risk of rupture
2. Unrepaired large AAA is potentially life threatening because a ruptured aneurysm
has a very high mortality.
3. Most do not cause symptoms unless ruptured or leaking. Ultrasound is the best
way to screen for a suspected AAA.
D. The treatment of aortic aneurysm has undergone significant change with the advent of
stenting, which is far less invasive and better tolerated in the elderly than open surgery.
E. Annual risk of rupture: < 4.0 cm < 0.5%
between 4.0 and 4.9 cm = 0.5% to 5%
between 5.0 and 5.9 cm = 3% to 15%

> 8.0 cm = 30% to 50%
F. Medical management for smaller aneurysms includes monitoring, -blockers, and
modifying risk factors.
G. AAAs > 5.5 cm or those growing by > 0.5 cm in 6 months merit referral and
consideration for either endovascular or surgical repair.
Hyperlipidemia (Table 4-16)

A. An important and modifiable risk factor.
B. Lipid levels tend to modestly decrease after age 70. The risks associated with CAD
are based on younger aged adults, and there is debate over how to treat older adults.
C. Older adults have been excluded from many of the trials studying the benefit of
antihyperlipidemic agents. Limited evidence suggests that using statins in those up
to age 80 with established atherosclerotic disease appears beneficial and that using
these agents for secondary prevention in those > 80 years also seems justifiable.
1. The decision to treat should not be made solely on age but should include an assess-
ment based on both age in years and physiologic age. A cognitively impaired individ-
ual or someone with a limited life span would not be a likely candidate for treatment,
but treatment should not be withheld for a healthy older adult based solely on age.
D. Evaluate for secondary causes of hyperlipidemia such as hypothyroidism, renal
C
o
disease, diabetes, excess alcohol intake, and medications such as thiazides,
m
-blockers, and steroids.
m
o
n
E. Statins are the most powerful drug for lowering LDL cholesterol and can reduce
G
e
LDL cholesterol by 20% to 60%. They can also lower triglycerides and slightly raise
r
i
a
HDL cholesterol levels.
t
r
i
1. Side effects, which include myalgias, myositis, and elevated liver functions tests,
c
M
are more common in the elderly.
e
d
i
Atrial Fibrillation (AF)
c
a
l
C
o
n
d
1. AF occurs in 5% to 10% of asymptomatic ambulatory adults and more frequently in
i
t
i
hospitalized patients.
o
Quick HIT
n
2. Symptoms include palpitations, fatigue, dyspnea, chest pain, and an irregularly ir-
s
regular rapid pulse.
3. Causes are the same as in the younger population. An irregularly irregular rapid
heartbeat in an older adult is
a. Idiopathic usually AF.
b. Structural abnormalities
Left atrium (LA) enlargement
Rheumatic heart disease
Mitral stenosis
Mitral regurgitation
Aortic stenosis (AS)
Aortic regurgitation
Cardiomyopathy
Malignancy of atrium
c. Tachybrady syndrome
d. WolffParkinsonWhite (WPW) syndrome
e. Short QT syndrome
f. CAD
MI
Postoperative (CABG)
g. Pericarditis
h. Pulmonary embolism/hypoxemia
i. HTN
j. Electrolyte abnormalities
Hypokalemia
Hypomagnesemia
Hypercalcemia
k. Drugs
Theophylline
Albuterol
Tricyclic antidepressants
Digoxin
Ophthalmic atropine
Sympathomimetics
Adenosine
Nicotine
l. Obstructive sleep apnea
m. Hyperthyroidism
n. Alcohol abuse/withdrawal
B. Testing
1. EKG (Figure 4-21)
2. Echocardiography
a. An echocardiogram can help identify an underlying cause for AF and help direct
therapy. The size of the left atrium is inversely proportional to the likelihood of
restoring sinus rhythm.
s
3. Transesophageal echocardiography to exclude left atrial appendage thrombus and
n
o
aid cardioversion in patients not taking oral anticoagulants
i
t
i
d
4. Thyroid-stimulating hormone (TSH) to screen for hyperthyroidism
n
o
5. Electrolytes
C
6. Renal function
l
a
c
7. Liver function testing
i
d
e
8. CBC
M
c
i
r
t
a
i
r
e
G
n
o
m
m
o
C
FIGURE
4 -2 1 Atrial fibrillation.
(Baliga RR, Eagle KA, Armstrong WF, et al. Practical Cardiology. Philadelphia, PA: LWW, 2008.)
9. Coagulation profile
10. Lipid profile
11. Fasting glucose
12. Serum calcium and magnesium level
13. pO2 if hypoxia suspected
C. Treatment
1. Admit to hospital if symptomatic or having an ACS
a. Identify and treat any underlying cause or contributing factor.
2. Rate controlacute rate control with rapid ventricular rate. Goal is resting heart
rate 100 to 110 beats per minute.
a. Metoprolol 2.5 to 5 mg IV bolus over 2 minutes, up to three doses
b. Diltiazem 0.25 mg/kg IV over 2 minutes, then 5 to 15 mg IV per hour
c. Esmolol 500 mcg/kg IV over 1 minute, then 50 to 300 mcg/kg/minute IV
d. Digoxin is recommended in patients with HF and reduced EF. 0.25 mg IV with
repeat dosing up to a maximum of 1.5 mg over 24 hours.
e. Amiodarone is given if other medications are contraindicated/failed or in case of
severe LV dysfunction; 300 mg IV over 1 hour and then 10 to 50 mg/hour over
24 hours.
3. Rhythm control is recommended if patient is symptomatic. For those with minimal
Quick HIT
symptoms or in whom prolonged sinus rhythm cannot be easily achieved, rate con- The goal of rate control for
older patients with AF is a
trol plus antithrombotic therapy is the preferred treatment strategy. resting ventricular rate of 60
4. -Blocker or nonhydropyridine CCBs are considered the drugs of choice for long- to 90 that increases to < 100
term rate control. beats with modest exertion.
5. Dronedarone is not recommended for patients with permanent AF.
6. Cardioversion is recommended if there is ongoing ischemia, symptomatic hypoten-
C
o
m
sion, or HF. It is contraindicated if hypokalemia is present or if patient has digitalis
m
toxicity. It may be done with 150 to 200 J biphasic waveforms as initial energy set-
o
n
ting. 200 J is more effective than 100 J (Figure 4-22).
G
e
r
i
a
t
r
i
c
M
e
d
i
c
a
l
C
o
n
d
i
t
i
o
n
s
FIGURE
4 -2 2 Atrial fibrillation cardioversion algorithm.
(Baliga RR, Eagle KA, Armstrong WF, et al. Practical Cardiology. Philadelphia, PA: LWW, 2008.)
CLINICAL PEARL 4-17

Risk Stratification for Cardioembolic Stroke in Nonvalvular AF
CHADS2 score has been shown to be predictive of cardioembolic stroke and indicates who is at risk and
should be anticoagulated. Subsequently, refinements to this scoring index were developed and shown to add
to the sensitivitynamely the CHA2DS2-VASc. The components of each of these are presented below.
CHADS2 CHA2DS2-VASc
1 point each for: 1 point each for:

CHF CHF
HTN HTN
Age > 75 Age 6574
DM DM
Female gender
Vascular disease or MI history
2 points for: 2 points for:
Stroke or TIA history Age > 75
Stroke or TIA history
PEARL
s
CLINICAL 4-18
n
o
i
t
i
d
Risk for Bleeding
n
o
C
Anticoagulant use is associated with some risk of bleeding complications. In an effort to help predict who
l
a
might be more prone to suffering this complication, the HAS-BLED score was developed. The HAS-BLED score
c
i
d
predicts the risk of bleeding in patients with AF taking warfarin. The components of this scoring index are as
e
M
follows:
c
i
r
Prior bleeding episodes Labile PT INR
t
a
i
r
HTN Renal disease
e
G
Liver disease History of stroke
n
o
m
Age > 65 Use of other medications
m
Alcohol or illicit drug use
o
C
Number of bleeding episodes increases proportionately as the number of factors increases beyond one.
A score of 3 or more would indicate elevated risk.
a. < 48 hours of onset.

If hemodynamically unstable, then immediate cardioversion and, if possible,
start low molecular weight heparin (LMWH) or IV unfractionated heparin at
full venous thromboembolic disease (VTE) treatment dose.
b. If duration is > 48 hours or unknown:
Therapeutic vitamin K antagonist therapy (e.g. warfarin) and LMWH at full
VTE treatment doses for 3 weeks before cardioversion, and continue for
4 weeks after cardioversion.
Successful cardioversion is more likely when AF is present for < 6 months,
and left atrial size is normal or only modestly increased in size.
7. Ablation therapy is considered in patients with symptomatic persistent AF and fail-
ure of antiarrhythmic drugs.
8. Oral anticoagulation is consistently recommended for patients at high risk for
stroke compared with no therapy.
a. History of cardioembolic stroke or TIA

b. CHADS2 score 2 (Clinical Pearl 4-17)
c. Mitral stenosis Quick HIT
Rate control with AF can be
Bradycardia achieved using -blockers,
CCBs, digoxin, or a combina-
A. Common among the elderly and may be the result of conduction system aging and/ tion of these medications.
or cardiac disease
1. Deterioration of the sino-atrial node, atrio-ventricular (AV) node, and bundle of
His often leads to symptoms requiring pacemaker insertion.
B. Reversible causes of bradycardia should be identified and reversed, if possible.

1. Medications affecting the conduction system should be discontinued, if possible.
Quick HIT
Offending agents include -blockers, digoxin, clonidine, and nondihydropyridine AF increases the risk of car-
CCBs. dioembolic stroke, and antico-
agulation should be provided
C. First-degree AV block is usually not clinically significant in the elderly. on the basis of risk assess-
ment even for those with good
D. Type II second-degree AV block and third-degree block warrant pacemaker rate control.
insertion.
E. A type I second-degree AV block is not associated with significant AV nodal

disease and is usually a result of drug toxicity, myocardial ischemia, or electrolyte
imbalance. This rhythm is typically transient and usually does not require a
pacemaker.
F. Other pacemaker indications include symptomatic bradycardia, bradycardia induced
C
o
by drugs used to treat a tachyarrhythmia, post-AV node ablation, and long QT
m
m
interval.
o
n
G
Heart Failure (HF)
e
r
i
a
t
r
i
c
1. Occurs when the cardiac output is inadequate to meet the circulatory needs of the
M
body
e
d
2. About 50% of patients with HF will have a normal ejection fraction.
i
c
a
a. A cardiac output ejection fraction of < 40% indicates systolic dysfunction;
l
C
diastolic dysfunction is defined as HF with a normal or near normal ejection
o
n
fraction.
d
i
t
b. Diastolic HF is characterized by a stiff ventricle that cannot relax sufficiently to
i
o
n
allow the ventricle to fill completely during diastole, thereby reducing stroke
s
volume.
3. Over 80% of all HF patients are 65 years and older. It is the leading cause of hospi-
talization among older adults.
a. Causes
CAD (MI and ischemic cardiomyopathy)
HTN
Structural heart defects
Renal failure
Constrictive pericarditis
Cardiomyopathy
Arrhythmias
Infectious endocarditis
High-output cardiac failureanemia, thyrotoxicosis, arteriovenous fistula, Quick HIT
and Paget disease of bone
HTN and CAD are the two
Noncompliance with medicationsdigitalis, diuretics, and ACEI
most common causes of HF in
NSAIDsmay increase risk of relapse of HF older adults.
Obesity
DM
TABLE 4-18 New York Heart Association Classification of Heart Failure

I Asymptomatic
II Mild symptoms with ordinary activities and none at rest
III Severe symptoms with ordinary activities and none at rest
IV End-stage heart disease with symptoms at rest
B. Signs and symptoms (Table 4-18)

1. Dyspnea
2. Fatigue
3. Orthopnea
4. Paroxysmal nocturnal dyspnea
5. Edema
6. Atypical symptoms such as anorexia, abdominal pain, and nausea caused by he-
patic congestion
7. Cyanosis
8. Diaphoresis
9. Jugular venous distension in right HF
10. Third heart sound
11. Hepatojugular reflux
12. S4 atrial gallop
s
13. Rales
n
o
14. Ascites
i
t
Quick HIT
i
d
15. Terry nailswhite discoloration of the nail with loss of the lunula
n
o
C
16. Peripheral edema
Dyspnea and fatigue with or
l
17. Elephantiasis nostras verrucosa (cobblestone-like skin)
a
c
without peripheral edema are
18. Systolic dysfunctiontachycardia, systolic BP < 90 mm Hg
i
d
the cardinal symptoms of HF.
e
M
19. Diastolic dysfunctiondiastolic BP > 105 mm Hg
c
i
C. Testing
r
t
a
1. CBC
i
r
e
G
2. Basic metabolic panel
n
3. Blood glucose
o
m
4. Lipid profile
m
5. LFTs
o
C
6. TSH
7. Urinalysis
8. CXR
9. EKG
10. Echocardiogram is diagnostic standard
a. To assess systolic function, to detect diastolic dysfunction, and to help identify
the underlying cause.
11. Brain natriuretic peptide (BNP or NT-proBNP)
a. Helpful in evaluating HF in patients presenting with dyspnea
b. Levels increase with age; can be elevated in patients with pulmonary disease,
impaired renal function, ascites, and sepsis
c. HF unlikely if BNP < 100 pg/mL and NT-proBNP < 300 pg/mL; HF very likely if
BNP > 500 pg/mL and NT-proBNP > 1,200 pg/mL
D. Treatment
1. Measure LVEF.
2. Underlying causes should be treated when possible.
3. If LVEF is abnormal
a. Low sodium diet and diuretics as needed to maintain euvolemia
Once euvolemia is achieved, use the lowest diuretic dose needed to remain
euvolemic.
Daily weights and a sliding scale for diuretic use and dosing are useful strat- Quick HIT
egies in the elderly. BNP is useful for distinguish-
b. Consider prescribing an ACEI and a -blocker to all HF patients. ing cardiac from pulmonary
Start -blockers once volume status is stabilized. causes of dyspnea.
Metoprolol may be better tolerated in patients with a low BP.
An aldosterone antagonist such as spironolactone may be used in advanced
disease and can reduce mortality. Potassium levels should be carefully moni-
tored because it may cause hyperkalemia. Avoid if Cr > 2.5 in men and 2.0 in
women.
c. If CHF persists, add digoxin in low dose. A 125 mcg dose is usually sufficient. Quick HIT
d. If it still persists, isosorbide dinitrate plus hydralazine should be added. Systolic HF results from poor
4. Normal LVEF ejection of blood from the
a. There is no agreed-upon evidence-based therapy for patients with diastolic heart, whereas diastolic HF
results from poor filling of the
failure.
heart.
b. Use diuretics only as needed to maintain euvolemia.
c. Low sodium diet
d. -Blockers, ACEI, and/or nondihydropyridine CCB may be helpful.
e. If sinus rhythm is present, do not use digoxin.
Valvular Heart Disease Quick HIT

A. Calcific aortic stenosis (AS) Treatment protocols provide
direction, but treatment should
1. Degenerative calcification of aortic and mitral valve found at autopsy in approxi- be tailored to the individual.
C
mately one-third of those > 75 years.
o
m
2. AS is more common in men than in women until age 80, then women
m
o
predominate.
n
3. Clinically: fatigue, syncope, angina, and CHF
G
e
4. Crescendodecrescendo late systolic murmur ending before second heart sound
r
i
a
5. Echocardiography helpful in diagnosis. EKG typically shows LVH.
t
r
i
c
6. LV catheterization remains most reliable method of assessing AS in older adults,
M
but should be reserved for patients who are symptomatic and in whom surgery is
e
d
contemplated.
i
c
a
7. Surgically replace AV; good outcomes even in > 80-year-olds. Symptomatic AV as-
l
C
sociated with increased mortality if untreated
o
n
d
B. Calcified mitral annulus
i
t
i
o
1. Most frequent > 70 years
n
s
2. Incidence increases with age, particularly in women, rising from 3.2% in < 70 years
to 44% > 90 years.
3. Important for CHF and site for infective endocarditis
C. Mitral valve prolapse and regurgitation

1. Mucoid degeneration of MV
a. Other causes include infective endocarditis, ischemic papillary muscle dysfunc-
tion, or ruptured chordae.
2. MV leaflet stretches under normal intracardiac pressure with subsequent prolapse
into LA during systole.
3. Classic murmur is late systolic, but can occur anytime during systole.
4. Mucoid degeneration described in approximately 1% of autopsies
for > 65-year-olds
5. Acute muscle ruptures are usually symptomatic. Chronic disease is usually well tol-
erated, but in later stages can cause pulmonary HTN and congestion.
6. Rarely requires surgery
7. Some patients may have chest pain, or an abnormal EKG, and death has been
reported.
8. Death is likely because of rupture of chordae tendinae.
D. Mitral stenosis
1. Usually from rheumatic heart disease
2. Can cause left atrial enlargement, AF, and right-sided HF
3. Echo to diagnose and assess degree of disease
E. Aortic regurgitation
1. Many causes including myxomatous degeneration, infective endocarditis, rheu-
matic heart disease, and trauma
2. Causes left ventricular volume overload; usually well tolerated at early stages
3. Physical examination findings include widened pulse pressure, rapid carotid up-
stroke, pistol shot pulses, and a blowing diastolic murmur.
F. Idiopathic hypertrophic subaortic stenosis (IHSS)

1. Presenting symptoms can be same as CAD/AS.
2. The presence of bisferiens arterial pulse in the presence of systolic ejection murmur
and absence of AR murmur should suggest IHSS.
3. Valsalva maneuver, and moving from squatting to standing increases intensity of
murmur
4. Diagnosis: echocardiogram
5. Treatment: -blocker
6. Surgery may be indicated for those refractory to medical therapy after assessment
of coronary artery flow with cardiac catheterization.
P ulm o na ry D is e a s e
s
n
o
i
t
i
d
1. Age-related changes in lung function
n
o
a. The trachea and lung airways enlarge with age.
C
b. Changes in elastic recoil of lungs result in lower forced expiratory volume in 1
l
a
c
second (FEV1) and an increase in residual volume.
i
d
e
c. The chest wall stiffens, which offsets the tendency to increase the total lung
M
capacity.
c
i
d. Weakened respiratory muscles and a stiffer chest wall reduce effective
r
t
a
ventilation.
i
r
e
G
e. The number of cilia and their activity decline. Glandular cells in the large air-
n
ways secrete lesser amounts of protective mucous.
o
m
f. The cough reflex blunts with age, impairing effective coughing.
m
g. Although the numbers of alveoli do not change significantly with age, alveolar
o
C
structure and function are altered. Alveolar walls become less elastic and en-
large. Fewer blood capillaries are available for gas exchange, reducing the sur-
face area available for gas exchange, resulting in mismatching of ventilation and
lung perfusion (V/Q mismatch).
h. In combination, these age-related changes result in changes milder than but
similar to those of chronic obstructive pulmonary disease (COPD).
i. There is also a tendency toward increased airway sensitivity and reactivity with
aging.
j. Usually, age-related changes in the respiratory system do not significantly impact
the performance of normal daily activities. However, there is a diminished respi-
ratory reserve for tolerating high-demand situations such as strenuous exercise
or pulmonary infection.
k. Spirometry changes include a decrease in forced vital capacity and an increase in
residual volume.
From ages 30 to 80, vital capacity decreases linearly.
FEV1 diminishes about 30 mL per year after around age 30.
Residual volume increases by about 50%.
l. The pulmonary vasculature becomes stiffer and less elastic, increasing pulmo-
nary artery pressure.
2. Epidemiology
a. Lung disease is the third leading cause of death in the United States, behind
heart disease and cancer. Quick HIT
b. COPD is the fourth leading cause of death and is increasing. Age-related changes in the
Smoking is by far the most important environmental risk factor in the United respiratory system do not
States; other environmental exposures may contribute as well. significantly impact perfor-
In Third World countries, biomass fuel is an important contributing factor. mance of usual daily activities.
Most individuals with COPD are diagnosed in their sixties, and those older However, there is a diminished
respiratory reserve for tolerat-
than age 65 account for > 85% of lung-related deaths. ing high-demand situations
c. Parenchymal lung disease also affects the geriatric population, causing restrictive such as strenuous exercise or
lung disease. pulmonary infection.
d. Older age is also a risk factor for obstructive sleep apnea and pulmonary HTN.
e. Pulmonary HTN in older adults is usually secondary to underlying cardiopulmo-
nary disease.
B. Specific diseases
1. COPD Quick HIT
a. General information Lung disease is the third
Obstructive airway disease related to smoking or environmentally induced leading cause of death in the
inflammation or destruction of airways that is nonreversible or only partially United States. Most deaths are
reversible caused by COPD, which is the
fourth leading cause of death
Air trapping and obstruction to airflow occurs because of decreased elasticity and rising.
of lung tissue, inflammation, airway edema, and bronchial muscle hyperplasia/
reactivity.
Unlike asthma, COPD is progressive and not fully reversible. Asthma
and COPD share symptoms in common, such as wheezing, and asthma
C
o
m
may mimic COPD. Many asthmatics also smoke and may also have
Quick HIT
m
COPD.
o
n
Emphysema and chronic bronchitis are two variants of COPD, and although
G
Although pulmonary reserve
they may differ in their clinical presentation, there is usually significant over-
e
diminishes with age, dyspnea
r
i
lap, and most individuals with COPD have elements of both.
a
at rest is not normal and re-
t
r
(1) Emphysematous individuals have lung hyperinflation with barrel chest.
i
quires investigation.
c
(a) Emphysema is a histopathologic finding of destruction of the lung tis-
M
e
sue distal to the terminal bronchioles resulting in an increased size of
d
i
c
terminal airspaces.
a
l
(b) An inability of the chest to recoil and exhale air traps air and results
C
o
in an increase in residual volume with more dead space related to
n
d
gas exchange.
i
t
i
o
(2) Chronic bronchitis is characterized by chronic and recurrent coughing
n
s
and wheezing.
(a) Airway reactivity with increased mucous
(b) Hyperplasia of smooth muscles combined with reactivity and in-
creased mucous, cause airway obstruction
Cardinal features are cough, sputum production, and dyspnea.
Dyspnea initially occurs with exertion, but, as the disease progresses, may oc-
cur at rest.
Wheezing common
Most patients will have 2 to 3 acute exacerbations per year marked by an in-
crease in shortness of breath, worsening cough, purulent sputum, and wheez-
ing; these exacerbations may require hospitalization.
Review past history for lung disease.
Family history of early onset COPD should raise concerns about 1-
antitrypsin deficiency.
Review social history for smoking and environmental exposures.
(1) 85% to 90% of people with COPD in the US smoke.
(2) About 15% of those who smoke get COPD, suggesting that genetics and
other environmental modulators may play a role.
CLINICAL PEARL 4-19

Pink Puffers and Blue Bloaters
The two variants of COPD have been described as the pink puffer and the blue bloater. Pink puffer de-
scribes the patient with emphysema who is often thin, barrel chested, and has a prolonged expiratory phase.
The blue bloater is the patient with chronic bronchitis who may be cyanotic, wheezing, and overweight with
fluid retention. Chronic bronchitis is defined clinically as productive cough present for 3 months of the year for
two consecutive years, whereas emphysema is defined pathologically as destruction of alveoli and their walls,
including connective tissue and blood vessels. Pure emphysema or pure bronchitis is rare, and most often,
patients with COPD have elements of both.
Physical examination
(1) Barrel chest
(2) Prolonged expiration
(3) Pursed lips and use of accessory muscles
(4) Diminished heart sounds and rhonchi/wheezing on auscultation
(5) Peripheral edema as sign of right-sided HF
(6) With more advanced disease, may manifest muscle weakness and weight loss
(7) Digital clubbing may be present.
c. Diagnosis
Two clinical entities that comprise COPD are defined differently.
(1) Chronic bronchitis is defined clinically as productive cough present for
3 months of the year for two consecutive years in the absence of another
known cause.
s
n
(2) Emphysema is defined pathologically as destruction of alveoli and their
o
i
t
walls, including connective tissue and blood vessels. This results in loss of
i
d
n
elastic recoil, enlargement of terminal airspaces, air trapping, and disrup-
o
C
tion of gas exchange.
l
a
Spirometry is essential for the diagnosis and to assess the severity of the disease.
c
i
d
(1) Flow volume loop has typical appearance and is distinguished from re-
e
M
strictive disease (Figure 4-23).
c
(2) FEV1 declines with normal aging, but even more markedly with COPD.
i
r
t
a
(3) Obstructive lung disease is defined by an FEV1/FVC ratio < 0.70, or 70%
i
r
e
that is not fully reversible with bronchodilators.
G
(4) In older adults, because of age-related declines, 0.60, or 60%, is com-
n
o
m
monly used for diagnosis of obstructive lung disease.
m
o
C
8
Norma l
6
Obs truction
4 Re s triction
)
s
2
/
L
(
w
0
o
l
Volume (L)
F
2
6
FIGURE
4 -2 3 Flow volume loop for obstructive and restrictive lung disease. Examples of flowvolume
curves in obstructive and restrictive disease, compared with a normal subject. Although
it represents data from the same respiratory maneuver as the standard volumetime plot, the flow
volume loop provides a more graphic demonstration of the relationship between flow rates and lung
volumes. Although flow rates referenced to forced vital capacity are lower than normal in the patient
with restriction, when referenced to the absolute lung volumes, the flows are actually higher than in a
normal subject.
(Morris TA, Ries AL, Bordow RA. Manual of Clinical Problems in Pulmonary Medicine. Philadelphia, PA: LWW, 2014.)
(5) FEV1 determines disease severity.

(a) Mild = > 80% predicted.
(b) Moderate = 50% to 80% predicted. Quick HIT
(c) Severe = < 50% predicted. FEV1 is the amount of air that
Additional testing may be of benefit. can be forced out of the lung
(1) Chest x-ray supports the diagnosis and helps to eliminate other causes of in 1 second.
dyspnea, such as congestive HF, underlying infection, or mass.
(a) With emphysema, expect diminished lung markings, flat diaphragms
(Figure 4-24).
(b) Chronic bronchitis may appear normal or with flat diaphragms and
an increase in lung markings. Quick HIT
(c) Because smoking is a risk factor for both COPD and lung cancer, he-
moptysis raises the possibility of cancer and the need to rule it out by The diagnostic criterion for
obstructive lung disease is an
testing. FEV1/FVC value < 0.70, or 70%;
(2) With more severe disease (FEV1 < 40%), arterial blood gases are indicated disease severity is defined on
to assess for carbon dioxide retention. the basis of FEV1 values, with
(3) Echocardiogram can assess for cardiac causes for symptoms and may also mild disease defined as values
detect pulmonary HTN. > 80% predicted and severe
disease < 50% predicted.
(4) Although CT scanning has no place in a routine case, it can be helpful
when the diagnosis is uncertain and to eliminate other diagnoses.
d. Treatment (Figure 4-25)
Smoking cessation is of paramount importance.
(1) The younger the age at which smoking cessation occurs, the better.
(2) Rate of pulmonary decline in smokers is 60% faster than in nonsmokers. Quick HIT
(3) Decline reverts toward nonsmoker rates of decline after quitting smoking.
The diagnosis of COPD is made
C
(4) Overall benefit lessens as patients get older, but it is never too late to ben-
o
in the setting of a compatible
m
efit from smoking cessation. history, physical, and pulmo-
m
Immunizations
o
nary function tests (PFTS). Car-
n
(1) Pneumococcal vaccines (PSV13 and PSV23) dinal symptoms include chronic
G
e
(2) Annual influenza vaccination cough, sputum production, and
r
i
progressive wheezing.
a
Inhalation products
t
r
i
(1) Short-acting 2 agonists are first-line therapy for symptoms.
c
M
(a) Relax smooth muscles and relieve bronchospasm for 4 to 6 hours.
e
(b) Side effects include tremor and tachycardia.
d
i
c
(2) Long-acting 2 agonists used as second-line therapy
Quick HIT
a
l
C
o
n
Testing other than spirometry
d
i
in the evaluation of COPD
t
i
o
provides data to support COPD
n
s
or exclude other diagnoses;
this testing may include chest
x-rays, CT scanning of the
chest, echocardiography, and/
or arterial blood gases. None
of these tests are diagnostic
of COPD.
B
FIGURE
4 -2 4 Chest x-ray of patient with emphysema.
(West J B. Pulmonary Physiology and Pathophysiology. Philadelphia, PA: LWW, 2007.)
C H R O N IC O B S T R U C T IVE P U LMO N ARY

DIS E AS E (C O P D), DIAG N O S IS AN D T R E AT ME N T
S us pe ct COP D if:
Quick HIT
A history of dyspnea without
an identifiable cause should
lead to evaluation that may
include pulmonary function
testing, which is diagnostic for
COPD. Physical examination
alone may not be remarkable
in some cases of COPD.
FEV1
>80
5080
3080
<30
s
n
0
o
i
1
t
i
d
2
n
o
C
3
l
a
4
c
i
d
e
M
c
i
r
t
a
i
r
e
G
n
o
m
m
o
C
FIGURE
4 -2 5 Diagnosis and treatment algorithm for COPD.
(a) Effects last up to 12 hours and generally used twice daily.

(b) Maintenance medication; not to be used as rescue medication
(c) Short-acting 2 agonist can still be used as rescue medication.
(3) Anticholinergic medications are an alternative second-line option.
(a) Ipratropium can be combined with albuterol.
(b) Effects last up to 4 to 6 hours for ipratropium and 24 hours for
tiotropium.
FEV1 a nd
fre que ncy of
s ymptoms
Mild COP D Mode ra te COP D S e ve re COP D Ve ry s e ve re COP D

FEV1 30%50% FEV1 <30% pre dicte d or <50%
FEV1 >80% FEV1 50%80% Incre a s e d dys pne a , re duce d e xe rcis e plus re s pira tory fa ilure
Inte rmitte nt cough, whe e ze a nd Dys pne a with e xe rtion, ca pa city, fa tigue , a nd re pe a te d e xa ce rba tions S hort-a cting bronchodila tor P RN
minima l dys pne a on e xe rtion with/without cough a nd s putum S hort-a cting bronchodila tor P RN Long-a cting bronchodila tor a nd
initia te bronchodila tor the ra py S hort-a cting bronchodila tor P RN Long-a cting bronchodila tors a nd a nticholine rgic inha le r
S hort-a cting -a gonis t P RN Long-a cting bronchodila tors or a nticholine rgic inha le r Cons ide r low-dos e the ophylline
a nticholine rgic inha le r P ulmona ry re ha bilita tion Inha le d glucocorticos te roids
P ulmona ry re ha bilita tion Tria l of inha le d glucocorticos te roids if s ignifica nt P ulmona ry re ha bilita tion
s ymptoms , or if >1 e xa ce rba tion pe r ye a r Long-te rm oxyge n the ra py if
chronic re s pira tory fa ilure
Cons ide r s urgica l tre a tme nts
P a O 2 55 mm Hg
or S a O 2 88%
or
No
P a O 2 59 mm Hg or
S a O 2 89% a nd
s ymptoms of cor pulmona le ,
Right he a rt fa ilure or
HCT >55%
C
o
m
m
Ye s
o
n
G
Continue Cons ide r
e
curre nt tre a tme nt long-te rm s upple me nta l
r
i
oxyge n the ra py
a
t
r
i
c
FIGURE
M
4 -2 5 (continued)
e
d
Quick HIT
i
c
a
l
C
o
Maintenance therapy for
n
d
(c) Ipratropium combined with albuterol is useful for acute symptoms, COPD includes, first and
i
t
foremost, smoking cessation.
i
o
but tiotropium is a daily maintenance medication.
n
Other measures to help pre-
s
(d) Monitor for glaucoma and urinary retention as side effects. vent complications and treat
(4) Inhaled corticosteroids are useful for moderate or severe disease or in pa- symptoms include vaccina-
tients who show improvement in PFTs following a trial of therapy. tion against pneumococcus
(a) Most products in this category are used twice daily. and influenza, and inhaled 2
agonists, anticholinergics,
(b) Combination products with long-acting 2 agonists are popular. and corticosteroids. Although
(c) Thrush is a potential side effect with short-term use, and bone loss all these agents help reduce
with long-term use. symptoms, none increases
(d) Gargling and spitting after inhalation reduces the risk of thrush and longevity.
dysphonia.
Systemic medications
(1) Theophylline
(a) Not used as commonly as in the past Quick HIT
(b) Now largely used as add-on medication chronically for severe disease Systemic medications are not
when other options are maximized the first-line therapies and are
(c) Therapeutic window and levels can be followed with dose adjust- reserved for treating patients
ments to achieve therapeutic dose and avoid toxicity. who are suffering an acute
(2) Corticosteroids exacerbation of their chronic
disease or who have severe
(a) Can be used acutely for exacerbations either orally or intravenously. If disease refractory to inhala-
started, IV subsequent doses can be converted to oral equivalent. tion products.
(b) Commonly used for 10 to 14 days and often tapered

(c) Adverse effects include hyperglycemia, and with chronic or frequent
use, cataracts, osteoporosis, and myopathy.
(d) Daily steroids are indicated only for those with severe disease and are
often prescribed in consultation with a pulmonologist.
(3) Antibiotics
(a) Frequently used with acute exacerbations, defined as an increase in cough
and sputum production, increased shortness of breath, and fever. Changes
in 2 of 3 cardinal symptoms are indications to consider an antibiotic.
(b) Organisms commonly found include H. influenzae, S. pneumoniae, and
M. catarrhalis.
(c) Antibiotics commonly used include penicillins, cephalosporins, fluo-
roquinolones, macrolides, and tetracyclines.
(d) For those with severe COPD (FEV1 < 50%) and an acute exacerba-
tion, a fluoroquinolone is commonly used.
(4) Oxygen
(a) Criteria are O2 sat < 88% or pO2 < 55 mm Hg, including nocturnal
desaturation not corrected with continue positive airway pressure
(CPAP); or
(b) PaO2 55 to 59 mm/Hg and pulmonary HTN, cor pulmonale or
polycythemia
(c) For those with hypoxia, oxygen can improve symptoms and survival.
(d) Arterial blood gas testing is recommended to determine whether a pa-
Quick HIT tient has an elevated pCO2, which may impact goals of O2 therapy.
(i) pCO2 normally helps drive respiration.
s
Although medications may
n
(ii) With an increased pCO2, the drive to breathe may become de-
o
help symptoms, only oxygen
i
pendent on the oxygen level. Too much oxygen may suppress
t
therapy in hypoxic patients
i
d
respiration and lead to CO2 elevation and CO2 narcosis.
n
and smoking cessation in-
o
C
crease longevity. (iii) For CO2 retainers, O2 target levels become saturation levels of
l
88% to 92% and not higher.
a
c
i
Pulmonary rehabilitation
d
e
M
(1) Can improve efficiency of musculature and endurance
(2) May benefit quality of life, but not shown to impact survival
c
i
r
(3) In many patients, the effects can be short-lived.
t
a
i
Surgery
r
e
G
(1) In extreme cases, or for those with bullae and large amounts of dead
n
o
space and V/Q mismatch, partial resection may be beneficial.
m
Quick HIT (2) Lung transplantation is usually not an option for geriatric patients.
m
o
2. Pulmonary fibrosis
C
Pulmonary fibrosis represents a. General information
a diverse group of diseases Represents a diverse group of inflammatory/fibrotic processes that affect the
with a common denominator of lungs to variable degrees, causing restrictive lung disease and alteration in gas
decrease in lung compliance,
volumes, and gas exchange,
exchange.
all leading to dyspnea. Restrictive lung disease is characterized by reduced lung volumes, a normal or
increased FEV1, and reduced lung compliance.
The fibrosis can affect blood vessels and connective tissue, causing impaired
gas exchange, reduced pO2, and diffusion capacity (DLCO).
Pulmonary fibrosis is associated with several etiologic agents, clinical syn-
Quick HIT dromes, as well as genetic links, resulting in a wide variety of diseases linked
The underlying pathology is together by their underlying lung disease (Table 4-19).
an inflammatory process that The most common geriatric interstitial lung condition is idiopathic pulmonary
involves the alveolar wall fibrosis.
resulting in fibroelastic tissue b. Clinical features
proliferation and collagen de-
Progressive dyspnea, initially with exertion and developing into dyspnea at
position, leading to irreversible
fibroses and destruction of the rest
lung architecture, impairing Nonproductive cough, fatigue, and pleuritic chest pain may be components.
gas exchange. Other symptoms may be present secondary to an underlying related disease
such as rheumatoid arthritis, scleroderma, or other connective tissue diseases.
TABLE 4-19 Some Types of Interstitial Lung Disease

Idiopathic Systemic Diseases
Idiopathic pulmonary fibrosis Sarcoidosis
Nonspecific interstitial pneumonia Rheumatoid arthritis
Cryptogenic organizing pneumonia Wegener granulomatosis
Acute interstitial pneumonia Scleroderma
Desquamative interstitial pneumonia Systemic lupus erythematosus

ChurgStrauss syndrome
Environmental
Alveolar Filling
Farmers lung
Goodpasture syndrome
Bird breeders lung
Pulmonary alveolar proteinosis
Asbestosis
Idiopathic pulmonary hemosiderosis
Silicosis
Chronic aspiration syndrome
Coal workers pneumoconiosis Lipoid pneumonia
Medications/Therapies Genetic Causes
Nitrofurantoin NiemannPick disease
Amiodarone Gaucher disease
Bleomycin Neurofibromatosis
Radiation Tuberous sclerosis
C
Illegal drugs Familial idiopathic pulmonary fibrosis
o
m
m
o
n
G
e
r
i
a
A history related to prior respiratory problems, pneumonia, aspiration, and
t
r
i
smoking is important.
c
M
Medication exposures
e
Hobbies or work that may be a clue to potential exposures, such as asbestos,
d
i
c
coal, or other environmental agents
a
l
Family history of lung disease and ages of onset for possible hereditary dis-
C
o
eases, although these disorders tend to develop at an earlier age and are less
n
d
i
likely to first present in older individuals
t
i
o
Physical examination may be normal early in disease, progressing to the devel-
n
s
opment of bilateral crackles described as Velcro.
As disease progresses, more adventitious lung sounds with rhonchi and
wheezing may be noted.
Clubbing of digits (Figure 4-26) may be present.
With advanced disease, cor pulmonale with right-sided HF and edema may
occur.
c. Diagnosis (Figure 4-27)
The role of laboratory studies is limited and should be directed at suspected
underlying diseases supported by the history and physical examination.
(1) Rheumatoid factor, antinuclear antibodies, complement levels, and other
testing to evaluate for connective tissue disease in patients with suggestive
findings. Patients generally have signs and symptoms of their connective
tissue disease before respiratory symptoms.
(2) Antinuclear cytoplasmic antibodies (ANCA) for patients with suspected
Wegener granulomatosis
(3) Antibasement antibodies for patients with suspected Goodpasture
syndrome
Spirometry is a critical diagnostic tool to document restrictive lung disease.
Chest x-ray and a chest CT scan can assess the extent of lung disease.
FIGURE
4 -2 6 Clubbing of the nails.
(Schalock PC, Hsu J T, Arndt KA. Lippincotts Primary Care Dermatology. Philadelphia, PA: LWW, 2010.)
Eva lua tion of Inte rs titia l Lung Dis e a s e
His tory a nd phys ica l e xa m
CBC with diffe re ntia l, e le ctrolyte s , BUN, cre a tinine

(Antibodie s , pre cipitin te s ting, othe rs a s ne e de d)
P ulmona ry function te s ts
s
n
o
i
t
i
d
Che s t x-ra y a nd high re s olution che s t CT
n
o
C
l
a
c
i
Clinica l dia gnos is Clinica l dia gnos is unce rta in- Clinica l dia gnos is unce rta in-
d
e
M
ce rta in Obta ina ble by bronchos copy Not obta ina ble by
bronchos copy
c
i
r
t
Fle xible bronchos copy
a
i
with BAL^ a nd TBBx^^
r
e
G
VATS * biops y or
n
o
Dia gnos tic Non-dia gnos tic ope n lung biops y
m
m
o
C
Dia gnos is confirme d
* VATS vide o a s s is te d thora cos copic s urge ry

^ Broncho-a lve ola r la va ge
^^ Tra ns bronchia l biops y
FIGURE
4 -2 7 Diagnostic evaluation for interstitial lung disease.
(Shifren A. Washington Manual: Pulmonary Medicine Subspecialty Consult. Philadelphia, PA: LWW, 2006.)
In many patients, the diagnosis may remain uncertain, and bronchoscopy will
Quick HIT be necessary to obtain cells and tissue to establish the diagnosis.
Criteria associated with poor prognosis include low DLCO, desaturation with
Searching for an underly-
ing cause for pulmonary activity, pulmonary HTN, and honeycombing on CT scan.
fibrosis is important because d. Treatment
some etiologies respond to For those with identified etiologic agents, avoidance, if possible, is a major
therapy, and if medications step in stabilization or resolving the condition.
or environmental factors are
Patients with an underlying inflammatory condition may benefit from treat-
suspected, eliminating these
can be critical to stabilization ment with corticosteroids or other immunosuppressants.
or improvement. In cases where the diagnosis is uncertain, a trial of immunosuppressant ther-
apy may be warranted.
Geriatric patients affected with interstitial lung disease are most commonly
diagnosed with idiopathic pulmonary fibrosis, a noninflammatory condition
that typically does not respond to immunosuppressant therapy and carries a
poor prognosis.
Immunization with pneumococcal vaccine and annual influenza vaccination
are recommended.
Oxygen therapy is recommended earlier in the course to limit the develop-
ment of pulmonary HTN and cor pulmonale.
Lung transplantation is an option for younger patients with progressive
disease; however, geriatric patients are not typically considered transplant
candidates.
3. Obstructive sleep apnea
a. General information
Common sleep-related respiratory disorder
(1) Affects up to 30% of men and 15% of women
(2) Increases with increased age to peak in the sixties and seventies
Defined as apneic (lasting 10 seconds or more) or hypopneic episodes occur-
ring more than five times per hour during sleep
Associated with daytime fatigue, sleepiness, inattention, and accidents
Associated with increased cardiovascular disease, diabetes, obesity, and in-
creased surgical risk
Up to 20% will develop pulmonary HTN.
b. Clinical features Quick HIT
Patients will report snoring, daytime somnolence to the point of sleeping Patients frequently will not
while driving or at meetings. freely admit to symptoms and
C
Fatigue, poor concentration, restless sleep, or depression may also be noted. snoring, and housemates or
o
m
Many times a spouse complains about loud and irregular snoring. spouses are commonly the
m
driver for evaluation of this
Physical examination may include obesity, increased neck size, and HTN.
o
sleep disorder.
n
The oropharynx should be examined for airspace adequacy.
G
e
c. Diagnosis
r
i
a
The diagnostic test for obstructive sleep apnea is a polysomnogram often at
t
r
i
night and in a monitored laboratory setting with respirations, vital signs, and
c
M
oxygen saturations monitored.
e
EEG along with eye and body movements is also monitored.
d
i
c
The report will include sleep arousals or disruptions, apneas,
a
l
or hypopneas.
C
o
Greater than 15 apneic episodes per hour are significant or more than five per
n
d
i
hour associated with symptoms, comorbid HTN, or heart disease.
t
i
o
Other conditions to consider include gastroesophageal reflux or restless leg
n
s
syndrome.
d. Treatment
Patients should be evaluated by an otolaryngologist for any anatomical airway
impingement (adenoids, tonsils) that may be surgically remediable.
Being overweight or obese is common in patients affected with sleep apnea;
counseling and referral for dietary counseling and exercise are often war-
ranted. Weight loss may significantly improve sleep apnea. Quick HIT
Reliable use of CPAP can provide marked relief and improvement in sleep,
In addition to a detailed his-
wakefulness, and energy. tory, a thorough ENT examina-
The appropriate pressure settings for the use of CPAP are generally titrated in tion and referral are warranted
the sleep laboratory. to evaluate for reversible sur-
Some patients may feel claustrophobic from the CPAP device and drop out gical etiologies for the patients
from use. with sleep apnea.
4. Pulmonary HTN
a. General information
Pulmonary HTN is defined as mean pulmonary artery pressure exceeding 25
mm Hg.
Treated or untreated, this will lead to the development of right-sided HF.
CLINICAL PEARL 4-20

OSAand Somnolence
Patients with obstructive sleep apnea are often in a vicious cycle of disrupted sleep that causes increased
fatigue. This increased level of fatigue leads to daytime inactivity and often weight gain in patients who are
already overweight. This aggravates the airway narrowing, worsening the sleep disruption, which magnifies
the daytime somnolence and fatigue. Examples of the extreme fatigue reported have included:
1. A labor union arbitrator who would frequently engage in intense negotiations on behalf of his union clients
could not stay awake for small-group or one-on-one meetings.
2. A postman who would deliver mail house to house driving a mail delivery vehicle would fall asleep be-
tween houses.
TABLE 4-20 Types/Causes for Pulmonary Hypertension

Left-sided congestive heart failure
Ischemic
Valvular
Cardiomyopathy
Lung disease
Chronic obstructive lung disease
s
n
Pulmonary fibrosis
o
i
t
Chronic thromboembolic disease
i
d
n
Obstructive sleep apnea
o
C
Connective tissue disease
l
a
c
With secondary lung involvement/fibrosis
i
d
e
M
Associated with pulmonary hypertension
c
Primary pulmonary hypertension
i
r
t
a
i
r
e
G
n
o
m
There is a primary, idiopathic form of this disease and there are secondary
m
o
causes.
C
The exact incidence and prevalence are unknown for the various forms of pul-
monary HTN.
The idiopathic form affects two to three people per million, and the prevalence
is about 15 per million.
The number of people with secondary pulmonary HTN is believed to be much
higher, but difficult to account for because of the other related diseases and
lack of documentation of pulmonary HTN as part of their disease process.
The types of pulmonary HTN are outlined in Table 4-20.
Geriatric patients with advanced lung disease, congestive HF or thrombo-
embolic disease commonly progress to develop pulmonary HTN and subse-
quently right-sided HF.
(1) Geriatric patients with these underlying diseases make up > 60% of all ge-
riatric pulmonary HTN patients.
(2) Up to 30% of COPD patients, 50% of patients with pulmonary fibrosis
and 20% of those with obstructive sleep apnea are affected with secondary
pulmonary HTN.
May have dyspnea or fatigue to a degree greater than expected
Can precipitate chest pain or be associated with syncope
Symptoms of underlying diseases such as COPD, pulmonary fibrosis, HF, or

obstructive sleep apnea
Past history of these same diseases as well as risk factors, such as smoking, oc-
cupational exposures, prior MIs, HTN, and obesity
Prior history or risk factors for thromboembolic disease
History of connective tissue diseases that might increase the risk of pulmonary
fibrosis and restrictive lung disease
The World Health Organization (WHO) developed a functional scale graded
from 1 to 4 with those at grade 1 being asymptomatic, grade 2 with minimal
limitations with effort, grade 3 with significant limitations in activity, and
grade 4 with symptoms at rest.
Physical examination findings would be expected to be consistent with the
underlying disease process.
More advanced disease may manifest peripheral edema as a sign of right-sided
HF.
c. Diagnosis
Evaluation for underlying cardiac etiology to include an echocardiogram Quick HIT
Pulmonary function testing to evaluate for COPD and restrictive lung disease Hallmark symptoms are
Chest CT may reveal pulmonary fibrosis or pulmonary emboli. dyspnea and fatigue that are
V/Q scanning can identify perfusion defects associated with emboli. greater than expected for the
Sleep studies to evaluate for obstructive sleep apnea degree of the patients appar-
ent underlying disease.
Connective tissue evaluation may be warranted, including antinuclear anti-
body (ANA), rheumatoid factor, complement levels, ANCA, and antibasement
membrane antibodies.
If no etiology is identified, then idiopathic pulmonary HTN may be the diag-
C
nosis, but may warrant confirmation with right heart catheterization.
o
m
d. Treatment
m
Current therapies for the secondary causes of pulmonary HTN are targeted at Quick HIT
o
n
the underlying diseases.
G
e
Maintaining oxygenation is an important component of any treatment plan. In geriatric patients, pulmo-
r
i
a
Therapy for idiopathic pulmonary HTN should include referral and manage- nary HTN is most commonly
t
r
secondary to underlying heart
i
ment by a specialist.
c
or lung disease.
M
Treatment may involve the use of CCBs, phosphodiesterase-5 enzyme inhibi-
e
tors, such as sildenafil, prostacyclins, or endothelin receptor antagonists.
d
i
c
a
l
C
Re na l D is e a s e
o
n
d
i
t
i
o
n
s
1. Half of adults > 70 years have estimated glomerular filtration rate (GFR) < 60 mL/
minthe threshold to diagnose CKD.
a. Results in impairment of sodium equilibriumreducing both the conservation
and rapid excretion
b. Causes loss of the ability to both concentrate and dilute urine
c. Loss of dilutional ability increases the risk of hyponatremia, especially with di-
uretic use. The loss of ability to concentrate urine makes the elderly more prone
to dehydration.
2. There is debate over whether aging changes in the kidney are normal or disease
driven.
3. Diseases accelerate normal aging changesfor example, diabetes, HTN, nephro-
toxic drugs, nephritis, and dehydration.
B. Structural changes with aging

1. Nephrosclerosis caused by microischemic injury to glomerulus and loss of function
2. The number of functioning nephrons decreases with age.
3. Loss of kidney volume with increase in renal fatty deposits
4. Renal cysts, benign and malignant tumors, fibromuscular dysplasia, and cortical
scarring occur more frequently with age.
CLINICAL PEARL 4-21

GFR
The most common formula for estimating the GFR is the CockcroftGault equation:
(140 age) (weight in kg) (0.85 if female)
Creatinine clearance (GFR)
(72) (stable serum creatinine in mg/dL)
Many laboratories estimate the GFR with the Modified Diet in Renal Disease formula, but this has not been
Quick HIT validated for adults > 70 years and is inaccurate at high weights.
There are no proven therapies

to stop or reverse age-related C. Functional changes
declines in GFR. Prevention 1. Twenty-four-hour albumin excretion does not increase with aging. The presence of
and treatment of any underly-
ing disease or contributing
proteinuria helps to distinguish normal aging from CKD secondary to disease.
factors (e.g., HTN) are the key 2. CKD from aging does not progress to end-stage renal disease (ESRD) without an
to preserving renal function. underlying condition.
3. CKD is a CAD equivalent risk factor if ESRD is present.
4. Age-related declines in GFR have little effect on life expectancy or need for dialysis.
Acute Kidney Injury (AKI)

Quick HIT A. General characteristics
Patients with reduced GFR 1. Short-term mortality rates for older patients with AKI range from 15% to 40%.
require medication dose ad- 2. Increased risk of CKD and ESRD with AKI in the geriatric population
s
justments. Increased risks for
n
3. AKI is defined as a rapid reduction in kidney function based on increased creati-
o
potential acute kidney injury
i
nine or decreased urine output.
t
(AKI) may occur with com-
i
d
4. Acute tubular necrosis resulting from hypoperfusion or nephrotoxins and volume
n
monly used medications such
o
C
as NSAIDS and radiographic depletion are the most common causes.
contrast agents.
l
5. Classification types (Table 4-21)
a
c
i
d
e
M
Different Classification Systems and Stages for Acute
c
TABLE 4-21
i
r
Kidney Injury
t
a
i
r
Quick HIT
e
G
Rifle Classification
n
o
m
ACEIs and ARB have not been
Risk
m
shown to decrease the rate of Creatinine increase of > 50% Urine output < 0.5 mL/kg per
o
aging changes in the kidney. over 7 d hour for 6 hr
C
Injury Creatinine increase of > 100% Urine output < 0.5 mL/kg per
over 7 d hour for 12 hr
Failure Creatinine increase of > 200% Urine output < 0.3 mL/kg per
over 7 d hour for 12 hr
Loss Need for renal replacement
for > 4 wk
End-stage Need for renal replacement for
> 3 mo
Akin Classification KDIGO Classification Urine Output
Stage 1 Creatinine increase > 0.3 mg/ Creatinine increase > 0.3 mg/ As for risk above
dLor 50% over 48 hr dLin 48 hr or 50% in 7 d
Stage 2 Creatinine increase > 100% Creatinine increase > 100% As for injury
over 48 hr in 7 d above
Stage 3 Creatinine increase > 200% Creatinine increase > 200% As for failure
over 48 hr in 7 d above
a. RIFLE (acronym)based on GFR or urine output criteriauseful in critical

care patients.
Risk of renal dysfunction
Injury to kidney
Failure of kidney function
Loss of kidney function
End-stage kidney disease
b. AKINAcute Kidney Injury Network definitions based on creatinine and urine Quick HIT
output.
20% to 30% of cases of AKI are
c. KDIGOKidney Disease Improving Global Outcomes attempts to unify RIFLE preventable.
and AKIN definitions.
6. Incidence varies by clinical setting.
a. 1% of hospitalized patients on admission
b. 2% to 5% during hospitalization
c. 7% to 50% of patients in the ICU
7. Costs of treating kidney disease
Quick HIT
a. In 2011, Medicare spent $49 billion on CKD. All patients with AKI must
be evaluated for reversible
b. Estimated savings for each kidney disease patient who does not progress to
causes and complications
dialysis$250,000. of AKI.
8. Most studies have focused on causes of AKI in the hospital setting (Table 4-22).
1. History
a. Evaluation for risk factors (Table 4-23)
b. Mild to moderate AKI may have no symptoms.
c. Patients in severe cases may exhibit mental status changes, lethargy, fatigue, nau-
C
o
m
sea, or vomiting.
m
d. Search for evidence of volume depletion (vomiting, diarrhea, acute blood loss,
o
n
recent surgery, or shock).
G
e
r
i
a. Vital signs
a
t
r
BP high or low
i
c
Pulse rapid or normal
M
e
b. Rash may suggest underlying conditions
d
i
c
Fine maculopapularinterstitial nephritis
a
l
Purpuravasculitis
Quick HIT
C
o
Malar rashlupus
n
d
c. Cardiopulmonary examination may indicate congestive HF or other cardiovas-
i
t
AKI can be grouped into three
i
o
cular diseases.
n
causes: prerenal, renal, and
s
d. Abdomen examination may demonstrate a distended bladder, mass, ascites, or postrenal (Table 4-22).
CVA tenderness.
C. Diagnosis
1. Basic metabolic profileBUN, creatinine (GFR-calculated), electrolytes, calcium,
magnesium, and phosphorous
2. Urine studies
a. Urinalysis with microscopic examination for casts
b. Suggested diagnosis based on urine examination (Table 4-24)
c. Urine sodium and creatinine for fractional excretion of sodium (Table 4-25)
Helps distinguish prerenal from renal
d. Urine culture if infection suspected
3. Foley catheter to monitor urine output and to rule out obstruction
4. Renal ultrasound
a. To rule out obstruction
b. Identify chronic renal disease changes.
Kidneys affected by chronic disease are often small and shrunken with the ex-
ception of renal failure from an infiltrative process such as amyloidosis.
c. Identify mass lesions or cysts in the kidney.
TABLE 4-22 Causes of Acute Kidney Injury

Prerenal (55%60%)
Hypovolemia (e.g., dehydration and blood loss)
Hypertension
Congestive heart failure/liver failure
Medications (e.g., ACE inhibitors and NSAIDs)
Vasoconstrictive states (e.g., shock and sepsis)
Renal (35%40%)
Acute tubular necrosis (ATN)
Septic shock
Ischemia
Contrast dye
Medications
Myoglobinuria
Vascular injury
Hypertension
Diabetes
Vasculitis
Emboli
s
Glomerulonephritis
n
o
i
Interstitial nephritis
t
i
d
n
Medications
o
C
Infections
l
a
c
Sarcoidosis
i
d
e
M
Multiple myeloma
c
Postrenal (< 5%)
i
r
t
a
Urethral obstruction
i
r
e
G
Stone
n
Clot
o
m
m
Stricture
o
C
Neoplasm
External compression
Bladder outlet obstruction
Benign prostatic hypertrophy
Prostate cancer
Clot
Neurogenic bladder
Occluded Foley catheter
5. Renal biopsy
a. To assess renal causes when prerenal and postrenal causes have been excluded.
b. A tissue diagnosis is needed before immunosuppressive medications may be
used.
About half of glomerular abnormalities, for example, membranous glomeru-
lopathy and minimal change disease, are potentially treatable with steroids or
immunosuppressants.
TABLE 4-23 Risk Factors for Acute Kidney Injury
Age > 65
Hypotension
CKD
Diabetes
Hypertension
Heart failure
Sepsis
IVcontrast use
Liver disease
Neurologic impairment
Medication (NSAID, ACEI, and antipsychotics)
Recent surgery
TABLE 4-24 Urinalysis Findings in Acute Renal Failure

Finding Diagnosis
Hematuria, proteinuria, and red cell casts Renal diseaseglomerular disease or vasculitis
C
o
m
Granular or epithelial cell casts ATN
m
o
Pyuria, WBC casts, granular casts little or no casts Interstitial nephritis, vascular obstruction, and renal
n
infarction
G
e
Normal microscopic examination, no protein, high Prerenal disease, obstruction, and ATN
r
i
a
specific gravity
t
r
i
c
M
e
d
i
c
a
Laboratory Testing with Differing Etiologies of Acute
l
C
TABLE 4-25
o
Renal Failure
n
d
i
t
i
o
Test Prerenal Renal Postrenal
n
s
Urine sodium < 20 mg/L > 20 > 20
Ratio of urine:serum osmolarity > 1.2 < 1.2 < 1.2
Ratio of urine:serum creatinine > 20 < 20 < 20
Ratio BUN:creatinine > 20 ~10 ~10
D. Treatment (Table 4-26)

1. Correct fluid and electrolyte imbalance to replace volume depletion or treat
overload.
a. Monitoring weight along with intake and output is helpful.
2. Monitor BUN, creatinine, sodium, potassium, phosphorus, and magnesium levels.
3. Treat infectious causes.
4. Stop any potentially nephrotoxic medications.
5. Dose adjustments of medications
6. Nutrient support
TABLE 4-26
Treatment of Complications Associated with Acute
Kidney Injury
Diet/Fluid Management
Quick HIT Fluid overload Restrict NaCl to 2 g/d; fluids at insensible losses plus urine
output; diuretics, ultrafiltration, and dialysis if needed
Patients whose age is > 65 Dietary restrictions No magnesium; limit protein to 0.6 g/kg per day; limit K+ to
have a lower rate of recovery
40 mEq/d; limit phosphorus to < 800 mg/d
of kidney function following
AKI. Hypertension Correct fluid overload as above; antihypertensive medications
AcidBase and Electrolytes
Acidosis Bicarbonate > 16 mEq/dLrestrict dietary protein

Bicarbonate < 16 mEq/dLsodium bicarbonate orally and if pH
Quick HIT < 7.2 intravenous
Hyperkalemia < 5.5 mEq/dLdietary restrictions
Patients > 75 years are at
increased risk for contrast- 5.56.5 mEq/dLsodium polystyrene sulfonate in sorbitol orally
induced nephropathy. or rectally
> 6.5 mEq/dLintravenous insulin with 50% dextrose and so-
dium bicarbonate; consider calcium gluconate intravenously
Hypocalcemia Oral calcium carbonate and if severe or symptomatic, intrave-
nous calcium gluconate
Quick HIT Hyperphosphatemia Dietary restrictions; aluminum hydroxide orally followed by
s
n
calcium carbonate once the phosphate is normal
o
AKI is associated with an
i
t
Hyperuricemia > 15 mg/dL, allopurinol orally
i
increased risk of CKD, ESRD,
d
n
and mortality at all ages. Anemia Eliminate bleeding as etiology; transfusion and if chronic,
o
C
erythropoietin
l
a
c
i
d
e
M
c
Quick HIT
i
r
t
a
7. No diuretics are used to treat AKI except to manage volume overload. Loop diuret-
i
r
e
G
RIFLE nomenclature predicts ics do not reduce mortality or improve renal recovery.
hospital mortality in patients
n
8. Renal replacement therapy (e.g., dialysis) is indicated for life-threatening changes
o
m
> 65 years who have AKI after in fluid, electrolyte, or acidbase balance that need urgent correction.
m
major surgery.
o
C
Chronic Kidney Disease (CKD)
1. Initial evaluation consists of GFR calculation (Clinical Pearl 4-21) and a search for
Quick HIT the cause(s) of renal dysfunction.
For the treatment of AKI with 2. Nephrology referral is indicated when there is a rapid loss of kidney function, el-
associated hypotension, iso- evated urine microalbumin to creatinine ratio, or red blood cell casts in the urine.
tonic crystalloids are preferred 3. No direct relationship between the serum BUN or creatinine and signs of uremia in
for fluid resuscitation. ESRD
4. Progression from CKD to ESRD depends on the underlying cause.
5. CKD is defined as the presence of kidney damage or decreased function for 3 or
more months.
6. CKD is an independent risk factor for CAD and MI and should be considered a
CAD equivalent.
Quick HIT B. Clinical features
Postoperative hypotension 1. Symptoms depend on the degree of uremia (Table 4-27) and the underlying dis-
is primarily caused by acute
blood loss, and red cell trans-
ease. Patients with stages 1 to 3 (GFR > 30) are often asymptomatic.
fusions should be considered. 2. Physical examination findings depend on the underlying disease (e.g., Lupus and
HTN) or the presence of complications (e.g., anemia and pericarditis).
TABLE 4-27 Uremic Symptoms

Quick HIT
Anorexia Low-dose dopamine is of no
Vomiting/nausea benefit in improving renal
blood flow or renal function.
Volume overload
Peripheral neuropathy
Mental status changes
Hyperkalemia
Pericarditis Quick HIT
Peripheral neuropathy Use vasopressors with IV flu-
ids in AKI with shock.
Acidosis
Hypertension
Anemia
Bone/muscular pain
Quick HIT
The combination of a low GFR
with an associated proteinuria
increases the risk of CKD pro-
CLINICAL PEARL 4-22 gression significantly.
Evaluating for CKD
C
The differential for CKD is extensive, and, depending on the initial history and physical examination, several tests
o
Quick HIT
m
may be useful in evaluating a patient with CKD. These include a serum protein electrophoresis (SPEP) and urine
m
protein electrophoresis (UEP) in cases of suspected multiple myeloma, an ANA and double-stranded DNA anti-
o
n
body levels to screen for lupus, serum complement levels that may be depressed with some glomerulonephritides, The earlier ACEI/ARB therapy
G
C-ANCA and P-ANCA, which are helpful in suspected Wegener granulomatosis and antiglomerular basement can be instituted, the more
e
r
membrane antibodies (anti-GBM). If present, anti-GBM is highly suggestive of Goodpasture syndrome. Tests for likely progression of disease
i
a
may be slowed in patients with
t
hepatitis B and C, HIVtesting, and a venereal disease research laboratory test (VDRL) should also be considered.
r
i
CKD and proteinuria.
c
M
e
d
i
c
3. Assess for HTN, DN, vascular disease, CHF, NSAIDs, benign prostatic hypertrophy
a
l
(BPH), and hereditary kidney disease.
Quick HIT
C
o
n
4. Referral to nephrology
d
i
a. AKI or abrupt fall in GFR
t
Initial evaluation consists of
i
o
b. GFR < 30 mL/min
n
basic metabolic profile (serum
s
c. Urinary red cell casts BUN with creatinine), urinaly-
d. Persistent abnormalities of potassium sis, and renal ultrasound.
e. Microalbumin/creatinine ratio > 300 mg/g
f. Hereditary kidney disease
g. Refractory HTN
C. Treatment of CKD Quick HIT

1. General guidelines A renal US is helpful to screen
a. Search and treat reversible causes. for hydronephrosis, which is
b. Initiate strategies to prevent or slow progression of CRD. a sign of obstruction. Small,
c. Treat the underlying disease if possible. echogenic kidneys are ob-
served in advanced renal
Judicious use of ACEI/ARB therapy in CKD with proteinuria failure. In contrast, kidneys
Attaining appropriate BP goals are normal sized in advanced
Tight glycemic control (target HbA1c < 7%) diabetic nephropathy or may
Protein restriction even be enlarged in the initial
Consider statin therapy as ESRD is a CAD equivalent. stages because of hyperfiltra-
tion. Structural abnormalities
Stop smoking. such as cystic disease may
d. Review medication doses and adjust based on renal function. also be detected.
e. Avoid nephrotoxins, for example, NSAIDs, IV contrast, and aminoglycosides.
TABLE 4-28 Treatment of Chronic Kidney Disease

Quick HIT
Diet/Fluid Management
CT and MRI are helpful for
delineating masses and cysts
Fluid overload No added salt diet; fluids at insensible losses plus urine output
detected on US. CT is the most
sensitive test for detecting Dietary restrictions No magnesium; limit protein to 0.6 g/kg per day; limit phosphorus to
stones. MRI is useful for avoid- 8001,000 mg/d when GFR < 50 mL/min; calories 3550 kcal/kg per
ing IV contrast, and MRA is day
being used more frequently to
Hypertension Correct any fluid overload as above; antihypertensive medications
diagnose renal artery stenosis.
AcidBase and Electrolytes
Acidosis Bicarbonate > 16 mEq/dLrestrict dietary protein

Bicarbonate < 16 mEq/dLsodium bicarbonate orally and if pH < 7.2
intravenous
Potassium < 40 mEq/d when GFR < 25 mL/min
Calcium Oral calcium carbonate and calcitriol
Phosphate Dietary restrictions; limit aluminum hydroxide orally and use calcium
carbonate for maintenance
Anemia Erythropoietin
s
n
2. Treatment/prevention of complications of CKD (Table 4-28)
Quick HIT
o
i
a. Volume overload correction: sodium restriction to < 2 g/day; add a loop diuretic
t
i
d
if needed.
n
o
Thiazide diuretics are ineffec-
C
tive if the GFR is < 30 mL/min. b. Hyperkalemia: low potassium diet, monitor ACEI/ARB use, and avoid medica-
l
tions that retain potassium (NSAIDs, aldactone).
a
c
i
c. Metabolic acidosis: judicious use of bicarbonate also increases sodium intake.
d
e
M
d. Mineral/bone disorders: In general, need to lower high phosphorus levels,
maintain serum calcium, lower serum PTH, and, if indicated, osteoporosis
c
i
r
prophylaxis
t
a
i
r
Hyperphosphatemia is common and leads to elevation in PTH when GFR is
e
G
< 30 mL/min.
n
o
Hyperphosphatemia causes relative secondary hyperparathyroidism and renal
m
m
osteodystrophy.
o
In CKD above stage 3, measure PTH, and if above 100 pg/mL, check
C
25-hydroxy vitamin D level. If low, calcitriol or vitamin D analog to suppress
PTH.
Dietary restriction and phosphate binder if needed. Normalize serum calcium
with calcium carbonate or calcium acetate.
e. HTN
Occurs in > 80% of CKD patients.
First-line therapy is loop diuretics and cautious use of ACEI/ARB agents.
Optimal BP parameters in CKD are based on age, underlying disease, and tol-
erance to medication.
f. Anemia
Primarily caused by reduced erythropoietin production by the kidney
Incidence of anemia increases as GFR declines.
Evaluate for causes of anemia when
(1) For females, hemoglobin is < 12 g/dL
(2) For males, hemoglobin is < 13 g/dL
(3) If Hgb is low, rule out a secondary cause, for example, iron or B-12 defi-
ciency. Ferritin should be at 200 to 500 ng/mL before starting erythropoi-
etin therapy.
(a) Consider erythropoietin for hemoglobin levels below 10 g/dL.
CLINICAL PEARL 4-23

GFRand Albuminuria Stages
CKD is defined as a decrease in GFR or an increase in albumin excretion for 3 or more months. Classifying the
severity helps direct therapy. Using the KDIGO classifications, CKD can be classified as follows:
Glomerular Filtration Rate (GFR) Stages Albuminuria Stages
G1 Normal GFR > 90 mL/min/1.73 m2 A1 Normal-mild < 30 mg/day

G2 Mild decrease 6089 A2 Moderate 30300
G3a Mild to moderate decrease 4559 A3 Severe > 300
G3b Moderate-severe decrease 3044
G4 Severe decrease 1529
G5 End stage < 15
g. Hyperlipidemia
Hypertriglyceridemia is more common.
Treat as CAD equivalent for LDL goals.
Most will require statin therapy.
h. Thyroid dysfunction: abnormalities of free T3 and T4 are common with normal
TSH.
C
o
m
i. Infection prevention recommendations
m
Annual influenza vaccine
o
n
Hepatitis B immunization
G
Pneumococcal vaccine
e
r
i
a
t
End-Stage Renal Disease (ESRD)
r
i
c
M
A. General
e
d
1. GFR declines 10% per decade after 40 years of age in 70% of the population.
i
c
a
2. Adaptive hyperfiltration in the face of AKI can damage the glomeruli, causing
l
C
sclerosis and decreased glomerular density manifested by proteinuria and progres-
o
n
sive renal failure.
d
i
t
3. Prevalence of CKD in > 60-year-olds is almost 50%.
i
o
n
4. 25% of patients starting dialysis are > 75 years old.
s
5. Dialysis population > 65 years old increased from 47% (1998) to 60% (2000).
6. Medicaid costs for the first year of dialysis were $88,000 in 2011 for those > 65
years old.
7. 20% of patients stop dialysis yearly.
8. GFR decline is adversely influenced by obesity, HTN, CHF, and non-insulin de-
pendent diabetes mellitus (NIDDM).
9. Geriatric patients are the fastest growing group on dialysis.
10. Medicare costs for CKD in 2012 were almost 20% of the general medical budget.
11. Expenditures for CKD have tripled over the last 20 years.
1. History
a. Mental health disturbancescognitive impairment and depression are common
in elderly with ESRD. Screen for both as needed.
b. Falls with resultant fractures are four times more common in ESRD.
c. Multiple chronic illnesses
Reduced quality of life
High pill burden (typical ESRD patient takes 12 different medications regularly)
Increased drugdrug interactions
2. Review increased risk factors

a. BP
The onset of isolated systolic HTN in ESRD increases nephrosclerosis and kid-
ney damage.
Elderly kidney is more susceptible to acute BP changes.
The best target level is uncertain. Compared with BP ranges of 130 to 139
systolic and 60 to 79 diastolic, both higher and lower BPs worsened
outcomes.
Low diastolic BPs increase cardiovascular risk.
b. AKI superimposed on ESRD
Short-term mortality of AKI is 15% to 40%.
Independent indicator of CAD.
c. Metabolic syndrome is present in 40% of patients 60 years and above.
d. Type 2 diabetes.
The most common cause of CKD
Mortality rates are higher in the elderly who have CKD with diabetes than
without diabetes.
a. Signs of pericarditis.
b. Peripheral neuropathy may be present.
c. Mental status changes include memory impairment, lethargy, seizures, coma,
and death.
C. Diagnosis
1. No direct correlation of symptoms with BUN or creatinine levels
2. Laboratory studies are similar to those with CKD.
s
n
o
3. ESRD must exist for > 3 months to be considered permanent.
i
t
i
4. Uremic patients require renal replacement therapy to survive.
d
n
o
C
D. Treatment
l
a
1. Dialysis (Table 4-29)
c
i
d
a. Life-sustaining, prolongs life, and corrects uremia, but does not change underly-
e
M
ing disease
c
b. Reduces independence
i
r
t
c. Associated with significant morbidity, but dialysis prolongs survival by an esti-
a
i
r
mated 2 years over conservative measures
e
G
d. Low-protein diet can delay dialysis.
n
o
2. No dialysisrenal palliative care
m
m
a. Quality of life needs to be assessed.
o
C
b. If the patient is on chronic dialysis and stops, a survival time of more than
2 weeks is unusual.
TABLE 4-29 Indications for Dialysis (AEIOU Mnemonic)
Acidosis, especially if severe [(pH < 7.2) and refractory to bicarbonate (HCO3) or unable to give HCO3 due to
volume overload] or symptomatic arrhythmias
Electrolytesespecially potassium with EKG changes (calcium, D50, insulin, bicarbonate, and Kayexalate
will help temporarily)
Ingestions known to cause renal failure (e.g., salicylates, ethylene glycol, lithium, and aspirin)
Overload (volume causing pulmonary edema). Temporize with nitrates, morphine, rotating tourniquets, and
large doses Lasix (160200 mg IV)
Uremiai.e., confusion, pericarditis, seizures, platelet dysfunction with severe bleeding, intractable nau-
sea, or vomiting
TABLE 4-30 Types of Dialysis

Need Risks
Hemodialysis Vascular access Disequilibrium syndrome
Stable hemodynamics Shock
Systemic heparin Bleeding
Infection
Fluid overload
Peritoneal dialysis Intact abdomen without ileus Failure to drain
ICU care to start Impaired respirations
No heparin Shock
Continuous therapy Bleeding
Peritonitis
Bowel perforation
Hyperglycemia
Continuous renal Vascular access Bleeding
replacement therapy Heparin Clotting of filter
(CRRT) Continuous therapy Slow continuous dialysis
May have unstable
hemodynamics
Good for fluid overload
C
o
m
c. Can still treat complications (fluid status, electrolytes, HTN, pain, fatigue,
m
o
depression, and loss of weight/appetite)
Quick HIT
n
G
e
E. Renal replacement therapy options (Table 4-30)
r
i
CRRT is an extracorporeal
a
1. Hemodialysis
t
r
blood purification therapy
i
a. Advantages
c
intended to substitute for im-
M
Permanent vascular access site paired renal function over an
e
Physician/technician controlled
d
extended period of time and
i
c
Set schedule for dialysis applied for or aimed at being
a
l
b. Disadvantages applied for 24 hours a day.
C
o
Dialysis center needed
n
d
i
Time commitment: 3 to 4 hours, 3 days/week
t
i
o
Need surgical procedure for permanent vascular access
n
s
2. Peritoneal dialysis
a. Advantages
Do not need dialysis center
Can be trained to do by self or with family members help
Retains renal function and diuresis longer
More liberal diet is possible.
b. Disadvantages
Learning curve for technique
Heavier burden on family caregivers
Increased peritonitis risk
Mean survival in those > 75 years is 20 months.
3. Continuous renal replacement therapy (CRRT)
4. Renal transplant
a. Age-matched donors increase donor base.
b. Better quality of life than dialysis
c. Immunosuppressive risks, but elderly have lower acute and chronic rejection
rates
d. Higher risk of infection
e. Greater survival probability than patients staying on dialysis
Cystic Kidney Disease

Quick HIT A. General
1. Most adult renal cysts are simple cysts and diagnosed by ultrasound.
Mortality and hospitalization
a. Common in elderlyone in three aged > 50 have renal cysts.
rates are similar in hemodialy-
sis and peritoneal dialysis. 2. Autosomal dominant polycystic kidney diseases (PKD) and acquired cystic disease
in patients with ESRD are less commonly seen.
3. Small cysts, medullary sponge kidney, autosomal PKD, and medullary cystic kidney
are less common.
4. Renal cysts are considered simple or complex by the Bosniak Classification system
using CT scanning to evaluate for malignant potential.
a. Characteristics associated with increased risk of malignancy are as follows:
Septations
Enhancement
Wall thickening
Size > 3 cm
Enhancements adjacent to the cyst
b. Bosniak Classification uses grades IIV to characterize the cysts and help guide
management based on the findings.
Additional evaluation of category I and II cysts is not required.
Most category IIF cysts require additional evaluation with contrast MRI and
follow-up imaging to document stability (serial MRI at 3, 6, and 12 months).
40% to 60% of category III cysts are malignant.
95% to 100% category IV cysts are malignant.
B. Simple cysts
s
n
o
1. Most common of all renal masses: 65% to 70% of cysts identified
i
t
2. May be single, multiple, unilateral, or bilateral
i
d
n
3. More common in men and age > 50
o
C
4. Typically, do not produce signs or symptoms
l
a
5. Rarely affect renal function
c
Quick HIT
i
d
6. Rarely associated with hematuria, pain, infection, HTN, or palpable abdominal
e
M
mass
c
MRI with contrast is more
i
r
sensitive than ultrasound to di-
t
C. PKD
a
i
agnose malignancy on follow-
r
1. Positive family historyautosomal dominant
e
G
up testing when CT scanning
picks up cyst septations. 2. Gross hematuria is common.
n
o
3. Cyst infection can occur.
m
m
4. Flank pain occurs.
o
C
5. Renal function is decreased.
6. Large kidneys with multiple bilateral cysts on ultrasound or CT scanning are seen.
D. ESRDcysts
1. Multiple bilateral cysts
2. Kidneys remain small.
3. Incidence increases with duration of dialysis.
4. Most are asymptomatic, but flank pain and urinary tract infection (UTI) can occur.
5. Increased incidence of renal cell carcinoma.
6. Incidence of renal cell carcinoma is less in transplant patients with cysts.
7. Yearly screening with contrast CT scanning in patients who have been on dialysis
> 3 years.
Glomerulonephritis
A. General
1. Pattern based on urine sediment and degree of proteinuria
a. Nephrotic syndrome (Table 4-31)
Proteinuria > 3.5 g/day.
Urine with few cells or casts
TABLE 4-31 Causes of Nephrotic Syndrome

Amyloidosis
Diabetic nephropathy
Focal glomerulonephritis
IgA nephropathy
Light chain deposition disease
Membranous nephropathy
Minimal change disease
Radiation nephropathy
TABLE 4-32 Causes of Nephritic Syndrome

Fibrillary glomerulonephritis
IgA nephropathy
Mixed cryoglobulinemia
Postinfectious glomerulonephritis
Rapidly progressive glomerulonephritis
C
Vasculitis
o
m
m
o
n
G
e
r
i
a
Fatty casts with hyperlipiduria can occur.
t
r
i
Peripheral edema is common.
c
M
b. Nephritic syndrome (Table 4-32)
e
Proteinuria variable but < 3.5 g/day.
d
i
c
Urine with red and occasional white cells with and without red cell casts
a
l
Acanthocytes (dysmorphic red cells) are diagnostic of glomerular-induced
C
o
hematuria.
n
d
2. Pattern based on etiology
i
t
i
o
a. Infectious
n
s
Post group A -hemolytic streptococcal is most common.
(1) Develops 1 to 3 weeks after acute infection
(2) 5% to 10% of patients with pharyngitis
(3) 25% of patients with skin infections
Other causesrule out Streptococcus first.
(1) Diplococci, other Streptococcus, Staphylococcus, Mycobacterium, and
Salmonella
(2) Epstein Barr virus, coxsackie virus, Cytomegalovirus, hepatitis B or hepa-
titis C virus, rubella, and mumps
(3) Parasitic
(4) Fungal
(5) HIV
b. Noninfectious
Multisystem diseases
(1) Vasculitise.g., Wegener granulomatosis
(2) Collagen vascular diseasee.g., lupus
(3) Cryoglobulinemia
(4) Polyarteritis nodosa
(5) HenochSchonlein purpura
Primary renal causes (histologic)

(1) Membranoproliferative glomerulonephritis (MPGN)
(2) Ig A nephropathy
(3) Mesangial proliferative glomerulonephritis
(4) Idiopathic rapidly progressive glomerulonephritis
Miscellaneous
(1) GuillainBarre syndrome
(2) Serum sickness
(3) Diphtheriapertussistetanus vaccine
3. Pattern based on histology (Table 4-33)
a. Proliferative
b. Nonproliferative
Quick HIT B. Diagnosis

1. Routine laboratory tests
Renal biopsy is often required a. Basic metabolic profile for BUN and creatinine
for definitive diagnosis of b. Urinalysis
the cause and treatment of
glomerular disease and may
c. Twenty-four-hour urine for protein
be of value even in those > 80 d. Serum albumin
years. It is usually not helpful 2. Serologic testing
in ESRD, where the kidneys a. Serum complement levelsmay be high or low depending on disease
are small and scarred because b. ANA antibodieslupus
establishing a diagnosis is un-
likely to lead to a therapy that
c. Anti-double-stranded DNA antibodieslupus
will reverse the disease. d. Antistreptococcal antibodiespoststreptococcal
e. Antineutrophil antibodies (ANCA) titersvasculitis
s
f. Hepatitis panelhepatitis B/C
n
o
g. HIV testingHIV disease
i
t
i
d
h. Antiglomerular basement membrane antibodiesGoodpasture syndrome
n
Quick HIT
o
i. Cryoglobinscryoglobulinemia
C
j. Blood culture and sensitivityendocarditis, shunt kidney abscesses, fungal or
l
a
c
Positive serologic testing may parasitic causes
i
d
not prove the disease cause.
e
k. Urine/serum protein electrophoresisamyloidosis and MM
M
c
Kidney Stones
i
r
t
a
i
r
A. General
e
G
1. 5% to 10% lifetime risk in the United States. Identical in geriatric population com-
n
o
pared with the general adult population.
m
m
2. Risk of second stone without treatment varies15% within 1 year, 35% to 40%
o
C
within 5 years, and 50% within 10 years.
3. Multiple factors increase patients risk for renal stones (Table 4-34).
4. Treatment and prevention strategies depend on stone composition (Table 4-35).
1. History
a. Flank pain with radiation to lower abdomen or groin; varies in intensity.
b. Nausea with or without vomiting
c. Urgency and frequency for urination
d. Hematuria is present in 70% to 90%.
e. Explore risk factor identification.
2. Physical
a. Patient moving about in the room or on the hospital cart; often difficult for the
patient to get comfortable
b. Abdominal examination may demonstrate lower abdomen tenderness.
c. Back examination with possible costovertebral angle (CVA) tenderness
C. Diagnosis (Table 4-36)

1. Helical CT scan preferred over ultrasound. CT scan is more sensitive for stone iden-
tification and localization. On ultrasound, stones are hyperechoic with shadowing.
TABLE 4-33 Types of Glomerulonephritis

Proliferative
IgA nephropathy
Cirrhosis
Celiac disease
Seronegative arthritis
Tuberculosis
HIV
Membranoproliferative glomerulonephritis
Chronic lymphocytic leukemia
Neoplasm
Infections (hepatitis B or C, endocarditis, and schistosomiasis)
Systemic lupus erythematosus (SLE)
Diffuse proliferative glomerulonephritis
Poststreptococcal
Viral
Parasitic
Focal segmental glomerulonephritis
Connective tissue disease; SLE
ANCAassociated glomerulonephritis
C
o
m
Antiglomerular basement membrane disease (Goodpasture)
m
o
Systemic vasculitis (Wegener)
n
G
SLE
e
r
i
Rheumatoid disease
a
t
r
Infections (endocarditis, postinfectious glomerulonephritis)
i
c
M
Neoplasm
e
d
Lymphoma
i
c
a
Drugs (hydralazine and penicillamine)
l
C
o
Primary glomerulonephritis
n
d
Nonproliferative
i
t
i
o
Minimal change nephropathy
n
s
Drugs (e.g., NSAIDs)
Hodgkin disease
Focal segmental glomerulosclerosis
History of IVdrug use
Human immunodeficiency virus (HIV)
Neoplasm
Lithium use
Following focal glomerulonephritis
Membranous nephropathy
Drugs (gold, penicillamine, and mercury)
Neoplasm
Infections (hepatitis B, malaria, syphilis)
SLE
Sickle cell disease
TABLE 4-34 Risk Factors for Stones

Family history
Hypercalciuria
Hyperuricemia (gout)
Hypocitraturia
Low calcium intake
High oxalate intake (spinach)
High animal protein intake
High sodium intake
Low fluid intake
Excess vitamin ingestion
Medications (sulfadiazine, acyclovir, and triamterene)
Weight loss surgery
TABLE 4-35 Kidney Stones by Composition

Calcium oxalate 70%
Struvite 15%
s
n
o
Calcium phosphate 5%10%
i
t
i
d
Uric acid 5%10%
n
o
C
Cysteine 1%
l
a
Mixed 1%5%
c
i
d
e
M
c
i
r
t
a
i
r
Differential Diagnosis for Renal Stones
e
TABLE 4-36
G
n
o
m
Renal cell cancer
m
Pyelonephritis
o
C
Ovarian pathology
Abdominal aortic aneurysm (AAA)
Quick HIT Large or small bowel obstruction
Biliary colic
Acute unilateral flank pain
with hematuria and a positive Mesenteric ischemia
plain x-ray of the abdomen is Herpes zoster (before rash onset)
highly predictive of a kidney
stone (90%).
2. Laboratory studies (Figure 4-28): basic metabolic profile for electrolytes, BUN,
Quick HIT creatinine, and calcium. Consider parathyroid hormone (PTH) if calcium elevated.
Consider uric acid level if history of gout or radiolucent stone.
Radiopaque stones include: 3. CBC if hematuria or infection
calcium oxalate, struvite, and
4. Urinalysis and urine culture
calcium phosphate. Radiolu-
cent stones are uric acid and 5. Strain urine for stones.
cysteine. 6. If recurrent calcium oxalate stones, consider 24-hour urine for calcium
and oxalate.
R E N AL C ALC U LI
Common ca us e s : Idiopa thic, gout,

me dica tion e ffe ct, hype rpa ra thyroidis m,
re na l dis e a s e , colitis
S tone a na lys is if pos s ible

to de te rmine dia gnos is
No s tone ava ila ble
Me dica tion e ffe ct No me dica tion e ffe ct
Diure tics Che ck la bs : Ele ctrolyte s ,

Ca lcium a nta cids , BUN, cre a tinine , ca lcium,
Indina vir uric a cid; urine for ca lcium,
oxa la te , a nd uric a cid
S e rum ca lcium e leva te d Norma l s e rum ca lcium
P TH e leva te d Urine uric a cid
C
a nd/or s e rum uric a cid
o
m
m
Hype rpa ra thyroidis m
o
n
Eleva te d Norma l
G
e
r
i
a
t
r
Gout
i
Urina ry ca lcium le ve l
c
Acidic urine
M
e
d
i
c
Eleva te d Norma l
a
l
C
o
n
d
i
t
Idiopa thic s tone Colitis Re na l dis e a s e
i
o
forma tion Chronic dia rrhe a
n
s
P olycys tic kidne y dis e a s e
Re na l tubula r a cidos is
FIGURE
4 -2 8 Evaluation of renal stones.
D. Treatment
1. Pain control
a. NSAIDs (act as a ureteral relaxant)
b. IV morphine plus ketorolac
c. Local warming of painful site
2. Treat UTI if present.
3. Observe whether stone is < 10 mm in size, pain is controlled, no evidence of sepsis,
normal renal function, and no obstruction.
4. -Blockers and CCBs may facilitate stone movement.
5. Interventional therapyurology referral

a. Extracorporeal shock wave therapy (ESWL) if stone < 10 mm and in
proximal ureter
b. Ureteroscopy with stone retrieval and possible stenting if stone < 20 mm
and distal
c. Percutaneous nephrostomy tube if stone size > 20 mm
d. Open procedure for Staghorn calculi
6. Follow up in 7 to 14 days for stone passage, and rule out obstruction.
7. 95% of stones pass in 40 days if < 4 mm in size.
E. Prevention
1. For all stones, maintain urine volume at 2.5 L/day.
2. Calcium stones
a. Low-salt, low-protein diet
b. Thiazide diuretics reduce calcium concentration in renal tubules.
c. Moderate calcium consumption
Calcium in the intestine helps to bind oxalate in the intestine, thus lowering
the availability of this common component of renal stones.
Inadequate ingestion of calcium could increase risks for osteoporosis.
3. Oxalate stones
a. Avoid high oxalate foods.
b. Restrict fat intake.
c. Potassium citrate, pyridoxine, and allopurinol reduce recurrences.
4. Calcium phosphate stonesalkalize urine if acidic.
5. Struvite stonessurgical removal and acidify urine.
s
6. Cysteine stonesurine alkalization and potassium citrate.
n
o
7. Uric acid stones- (Clinical Pearl 4-24 and pages 240-241)
i
t
i
d
n
Renal Cell Cancer
o
C
l
a
A. General
c
i
d
1. Renal cell cancer is the most common malignant kidney tumor85% of
e
M
renal cancers
c
a. Histologic types include clear cell (70% to 80%), papillary (10% to 15%), and
i
r
t
chromophobe (3% to 5%).
a
i
r
e
G
n
PEARL
o
CLINICAL
m
4-24
m
o
C
People can help prevent kidney stones by making changes in fluid intake and, depending on the type of kidney
stone, changes in consumption of sodium, animal protein, calcium, and oxalate.
Drinking enough fluids each day is the best way to help prevent most types of kidney stones. Health care
providers recommend that a person drink 2 to 3 Lof fluid a day. People with cystine stones may need to drink
even more. Although water is best, other fluids such as citrus drinks may also help prevent kidney stones.
Recommendations based on the specific type of kidney stone include the following:
Calcium Oxalate Stones
Reducing sodium
Reducing animal protein, such as meat, eggs, and fish
Getting enough calcium from food or taking calcium supplements with food
Avoiding foods high in oxalate, such as spinach, rhubarb, nuts, and wheat bran
Calcium Phosphate Stones
Reducing sodium
Reducing animal protein
Getting enough calcium from food or taking calcium supplements with food
Uric Acid Stones
Limiting animal protein
A link describing dietary and preventive measures for renal stones is http://kidney.niddk.nih.gov/
KUDiseases/pubs/kidneystonediet/ent
b. Male-to-female ratio 2:1 and mean age of 60.

c. Estimated 209,000 new cases and 102,000 deaths yearly.
2. Transitional cell cancer less common15%
a. Curable in 90% of cases if confined to ureter or renal pelvis. With invasive
tumors, cure rates drop to 10% to 15%.
b. Treatment is total excision of kidney, ureter, and bladder cuff.
c. Incidence of bladder cancer after surgery is 30% to 50%.
1. History
a. 25% to 30% of patients are asymptomatic, and the cancer is found incidentally
on abdominal imaging.
b. Hematuria 40%, flank pain 40%, and abdominal/flank mass 25% are considered
the classic triad for renal cell cancer.
c. Other symptoms: weight loss, fever, and night sweats
d. Paraneoplastic syndromes are frequenthypercalcemia, erythrocytosis, hepatic
dysfunction, and polymyopathy
e. Risk factors are presented in Table 4-37.
2. Physical
a. Flank or abdominal mass with or without pain
C. Diagnosis
1. Usually a solid mass in kidney
2. Findings suggestive of malignant renal cysts: no calcifications, increased septations
within the cyst, nodularity surrounding the cyst, and cyst wall thickening (see re-
C
nal cyst discussion)
o
m
3. MRI with contrast
m
4. Biopsy has a limited role.
o
n
G
e
D. Treatment
r
i
a
1. Surgery
t
r
i
a. 50% cure rate with early-stage renal cell cancer
c
M
b. Surgical resection of the primary tumor in metastatic disease may prolong
e
survival.
d
i
c
c. For patients at high surgical risk or patients older than 70 years with docu-
a
l
mented slow-growing asymptomatic masses on follow-up imaging, observation
C
o
may be appropriate.
n
d
i
2. Radiation therapy
t
i
o
3. Immunotherapyspontaneous regression has been documented.
n
s
4. Molecular targeted therapyclinical trials
TABLE 4-37 Risk Factors for Renal Cell Cancer

Overweight
Smoking
Hypertension
Hysterectomy
Unopposed estrogen use
Heavy metal/asbestos exposure
Family history of renal cancer
Polycystic renal disease
Chronic dialysis
Uro lo g ic D is e a s e
A. Hematuria
1. General information
a. Up to 15% of normal individuals have evidence of hematuria.
b. Up to 20% to 30% of individuals with hematuria will have an underlying
malignancy.
c. Although most causes of hematuria are benign, the risk of malignancy increases
with advancing age.
d. Hematuria can either be microscopic or macroscopic (gross hematuria).
Microscopic hematuria is defined as greater than three RBCs per high-powered
field.
Macroscopic hematuria is visible to the naked eye.
(1) Associated with a greater risk of malignancy
(2) Must be distinguished from factitious hematuria, which is discolored
urine caused by:
(a) Beets
(b) Phenazopyridine
(c) Phenolphthalein
(d) Myoglobin or free hemoglobin
e. Timing of the hematuria can sometimes help localize the bleeding site.
At initiation of urine stream only, more likely urethral
Quick HIT Discharge into undergarments, likely urethral or external source
Terminal hematuria, classically bladder trigone
Malignancy as a cause of he-
maturia becomes more preva-
Throughout urine stream, can be anywhere, including renal, ureters, bladder,
s
n
lent with advancing age. or urethra
o
i
f. Routine screening for hematuria is not recommended in the elderly.
t
i
d
g. Urine dipsticks can detect hematuria in > 90% of cases.
n
o
C
Dipstick testing positive for blood should be followed up with microscopic
l
a
examination.
c
i
(1) Examining the urine sediment is very important in identifying possible
d
e
M
renal disease.
c
(2) If RBC casts and proteinuria are present, glomerular disease is usually the
Quick HIT
i
r
cause.
t
a
i
r
(3) If dipstick testing is positive for blood without RBCs on microscopic
e
G
Consider painless gross he-
examination, consider myoglobinuria or hemoglobinuria.
n
maturia as a sign of bladder
o
Negative dipsticks are reliably negative for blood; however, false-positives can
m
or kidney cancer until proven
m
otherwise. occur.
o
2. Differential diagnosis
C
a. Must distinguish renal source from urologic causes
Renal sources would include:
(1) IgA nephropathy
(2) Glomerular diseases
(3) Nephritis associated with medications
(4) Polycystic kidney disease
Quick HIT (5) Sickle cell disease
(6) Exercise-induced
Hematuria is present when
there are three or more red Urologic causes
blood cells visualized per high- (1) Renal calculi
power field on microscopy. (2) BPH
(3) Infection, a very common cause, is usually associated with pyuria
(4) Cancers
(a) Renal cell carcinoma
(b) Urothelial involving ureter or bladder
(5) Coagulopathies and other bleeding disorders
(6) Medications (anticoagulants and cyclophosphamide)
H E MAT U R IA, ADU LT

Mic ro s c o p ic h e m a tu ria (MH):
3 RBCs pe r HP F in 2 s pe cime ns
+ His to ry a n d p h ys ic a l to a s s e s s
Re p e a t UA/m ic ro a fte r tre a tm e n t p o s s ib le c a u s e s o f MH
o f o th e r c a u s e (s ) (UTI, tra uma , re ce nt urologic
_ proce dure , e tc.)
+
_
Re le a s e fro m c a re
Re n a l fu n c tio n te s tin g If CT u ro g ra m c o n tra in d ic a te d , le s s

Co n c u rre n t n e p h ro lo g y wo rku p (BUN, cre a tinine , e GFR) o p tim a l im a g in g :
if in d ic a te d (prote inuria , dys morphic - MR urogra m
RBCs , impa ire d re na l function, e tc.) Uppe r tra ct ima gingCT urogra m - Re trogra de pye logra ms in combina tion
with non-contra s t CT, MRI, or US
Hig h -ris k p a tie n t:
e
tre a t condition a ccordingly
C
o
m
Urina ry cytology a nd
m
dia gnos tic cys tos copy Follow-up a s indica te d by dia gnos is :
o
n
+ _
G
re s olution of condition
e
r
i
a
Tre a t condition a ccordingly 2 yr
t
r
i
c
_
M
+
e
d
Follow-up a s indica te d by
i
c
dia gnos is :
a
Re le a s e from ca re .
l
r
C
o
re s olution of condition
n
d
i
t
i
o
n
FIGURE
s
4 -2 9 Evaluation of hematuria.
(Gomella LG. The 5 Minute Urology Consult. Philadelphia, PA: LWW, 2014.)
b. Renal causes are often associated with other findings, such as proteinuria,
elevated serum creatinine, or HTN.
c. Microscopic urine examination may reveal casts or dysmorphic RBCs with renal Quick HIT
disease. The presence of proteinuria,
d. Passage of blood clots suggests an extraglomerular cause. red cell casts, elevated cre-
3. Evaluation (Figure 4-29) atinine, or HTN suggests a
a. Urine culture renal or glomerular etiology for
hematuria.
If positive, treat with antibiotic.
Recheck urine after treatment, and if negative, no further evaluation is
necessary.
If positive after treatment, further evaluation is warranted.
b. Recheck urine, and with persistent hematuria and/or risk factors, evaluate
further.
Risk factors for urologic malignancy
(1) Age > 35
(2) Smoking
(3) Chemical exposure
(4) Recurrent cystitis or inflammation
(5) Radiation exposure
(6) Treatment with cyclophosphamide
c. BUN, creatinine levels, CBC, PT, PTT, and if renal disease suspected,
serologic testing, for example, complement, ASO, antibodies to dsDNA
and ANA tests
d. Urine cytology
Low sensitivity but still used in concert with other testing
If positive, then should aggressively look for cancer because false-positive tests
are unusual.
e. Cystoscopy
Quick HIT Gold standard for diagnosing bladder cancer
Can identify in situ or invasive disease through biopsy, but not nodal involve-
Urinalysis should be repeated
and reevaluated after treat-
ment or metastases
ment for a UTI. Cannot identify upper tract disease, but can allow for the collection of urine
selectively obtained from each ureter through catheterization.
f. CT scan with and without contrast of the abdomen and pelvis to detect the ex-
tent of disease, to evaluate the kidney for anatomic abnormalities, or to detect
stones.
Quick HIT
s
n
g. With contrast sensitivity, MRI can be substituted for CT.
o
i
h. Intravenous pyelogram (IVP) and ultrasound have largely been supplanted by
t
i
d
Advanced age and smoking CT scans.
n
o
history are two major risk fac-
C
i. Patients with casts, renal insufficiency, HTN, and suspicion of a glomerular etiol-
tors for bladder cancer.
l
ogy may warrant alternative approach.
a
c
i
Ultrasound may be indicated to determine renal size because small kidneys
d
e
M
would suggest chronic disease and a long-standing process.
Renal biopsy may be warranted to determine the type of glomerular
c
i
r
disease.
t
a
Quick HIT
i
4. Treatment
r
e
G
a. Hematuria is a sign and not a disease; therapy should be directed at the underly-
n
In most cases of hematuria in
o
ing cause.
m
the elderly, the source is the
b. Surgical intervention may be needed with certain diseases, for example, renal
m
bladder, prostate, or urethra.
o
cancer.
C
In the absence of significant
proteinuria, < 10% of cases c. In about 10% of cases, a complete evaluation fails to diagnose an underlying
are of glomerular origin. cause. Patients with persistent microscopic hematuria and a negative
workup should be monitored every 6 to 12 months to detect progressive
disease.
B. Bladder carcinoma
Quick HIT 1. General information
Malignancy accounts for a. Most common cancer of the renal system. Incidence increases with age.
about one-third of cases, most b. 90% of these cancers in the United States are urothelial/transitional cell
commonly the bladder. carcinomas.
c. Recurrent disease is common with bladder cancer.
d. The risk of tumor progression and behavior are described using a grading system
and the tumor-nodes-metastases (TNM) staging system.
Grading is either low grade or high grade.
High-grade lesions are more likely to be detected in urine cytology.
The TNM descriptors are outlined in the chapter on Cancers, Table 4-47.
CLINICAL PEARL 4-25

CTUrogram
For evaluation of hematuria, a CT urogram combines the features of an IVP with that of CT scanning for thor-
ough evaluation of the upper tracts of the renal system. To complete the assessment and evaluate the lower
tract, cytology and cystoscopy are recommended.
2. Clinical features
a. Hematuria
Can be intermittent
Often gross hematuria
b. Urinary frequency and/or urgency
c. Dysuria
d. Pain can occur with more advanced disease.
Flank pain related to ureteral obstruction
Pain related to organ invasion/spread
Bone pain or headaches related to metastases
e. Symptoms of weight loss, weakness, or fatigue can occur with very advanced
disease.
f. Physical examination would be expected to be normal except in those with
Quick HIT
advanced disease who may have organomegaly or lymphadenopathy related to Bladder cancer presents clas-
spread of disease. sically with painless, gross
3. Diagnosis hematuria throughout the
C
o
urine stream.
m
a. Cystoscopy with biopsy or resection is the gold standard.
m
Sensitivity can be enhanced with instillation of a protoporphyrin into the
o
n
bladder, which is preferentially taken up by tumor cells that become fluores-
G
cent and can direct biopsy.
e
r
i
In patients with positive cytology without visible lesions, random biopsies
Quick HIT
a
t
r
should be obtained.
i
c
b. Cytology is performed routinely as part of the assessment.
M
Cystoscopy is the gold stan-
e
Overall sensitivity is about 55%; high-grade lesions are more likely to be dard for diagnosing bladder
d
i
c
positive. cancer.
a
l
Can help detect upper tract disease
C
o
Sensitivity can be enhanced with fluorescent in situ hybridization, a technique
n
d
that identifies genetic markers.
i
t
i
o
If positive, > 90% specific
n
s
c. CT urography uses contrast and studies the renal system in the various phases of
contrast excretion, combining the benefits of CT and IVP studies.
CT has largely supplanted ultrasound in the study of hematuria except in
those who cannot use contrast because of allergy or renal insufficiency.
Can detect invasive disease and metastases
In those with contrast sensitivity, MRI is another option.
4. Treatment
a. Noninvasive disease
Risk of disease progression or recurrence is determined.
(1) Based on tumor size, grade and whether recurrent or multifocal
(2) Low risk is single low-grade papillary lesion < 3 cm.
(3) Intermediate or high risk is > 3 cm, carcinoma in situ or T1 as well as re-
current or multifocal disease.
Therapy for low-risk patients is transurethral resection (TURP) of the tumor
along with a single intravesical treatment with chemotherapy at the time of
surgery.
Therapy for intermediate or high-risk noninvasive disease includes TURP

along with 6 weeks of weekly intravesical chemotherapy.
All patients need regular surveillance for recurrent disease. Removal of recur-
rent tumors is indicated.
b. Invasive disease
Radical cystectomy following a cisplatin-based neoadjuvant chemotherapy
regimen is recommended.
Chemotherapy and radiation for patients who are not surgical candidates or
Quick HIT who choose not to undergo surgery.
Metastatic disease can be treated with chemotherapy.
Long-term surveillance is re- Long-term surveillance with imaging and laboratory testing needed to detect
quired following the treatment recurrence or spread.
of bladder cancer because the
recurrence rate is very high. C. Hypogonadism/low testosterone
a. Serum testosterone decreases with age by approximately 1% per year starting at
age 35.
b. Most men never experience any symptoms or complaints related to decreased
testosterone.
c. Routine screening is not recommended. Testing is reserved for men with symp-
toms consistent with hypogonadism.
d. Testosterone production exhibits a diurnal variation with levels highest in the
morning.
a. Decline in sexual ability
s
Lower libido
n
o
Erectile dysfunction
i
t
i
d
b. Decreased energy, strength, and stamina
n
o
c. Loss of muscle mass and bone density
Quick HIT
C
d. Other symptoms include irritability, testicular atrophy, and gynecomastia.
l
a
c
3. Diagnosis (Figure 4-30)
i
d
Routine testosterone testing
e
a. Many changes associated with low testosterone overlap with normal aging and
M
in the elderly is not recom-
mended. It should be reserved may not correlate with testosterone values.
c
i
for those with symptoms. b. Whether andropause is a disease or a normal part of aging is controversial.
r
t
a
c. Also referred to as Androgen Deficiency in the Aging Male (ADAM)
i
r
e
G
d. Measurement of serum testosterone should be considered only in those with
n
symptoms consistent with hypogonadism.
o
m
e. Laboratory samples should be drawn in the AM and repeated in order to confirm
m
any abnormality.
o
C
f. If the levels are low on two samples, evaluation of pituitary function with
Quick HIT TSH, prolactin, FSH, and LH should be considered. Testosterone deficiency
can be primary from testicular failure, secondary to decreased function of the
The Saint Louis University hypothalamicpituitary axis, or a combination of both.
ADAM questionnaire is one
A low testosterone with elevated FSH and LH is consistent with testicular
available screening tool to
help identify who might ben- failure.
efit from testing testosterone Normal or low FSH and LH with low testosterone suggests secondary
levels. failure and the need to assess the hypothalamicpituitary axis with pro-
lactin levels and TSH, followed by MRI scanning if hyperprolactinemia is
present.
If prolactin, FSH, and LH are normal, reviewing medications and assessing for
systemic disease are warranted.
g. Testicular examinationsmall testes suggest primary disease. Obtain iron stud-
Quick HIT ies to rule out hemochromatosis for those with primary testicular failure.
4. Treatment
Serum testosterone should a. Testosterone replacement can be provided parenterally or transdermally. Prior to
be evaluated only in men with
treatment, a CBC and prostate-specific antigen (PSA) should be obtained. If the
signs or symptoms of andro-
gen deficiency. PSA is elevated, a prostate biopsy is recommended to rule out prostate cancer
before initiating treatment.
T E S T O S T E R O N E DE F IC IE N C Y
(H YP O G O N ADIS M)
Me ta bolic Ere ctile Clinica l

s yndrome dys function s ymptoms
or phys ica l
s igns
Clinica l s us picion of te s tos te rone de ficie ncy
Me a s ure morning tota l

te s tos te rone (711 AM)
<300 ng/dL >300 ng/dL
Re pe a t morning tota l te s tos te rone

(cons ide r fre e or bioa va ila ble T if
s us pe ct a lte re d binding globulin)
<300 ng/dL >300 ng/dL
Low te s tos te rone Norma l te s tos te rone

s e e k othe r ca us e s
for s ymptoms
Exclude re ve rs ible ca us e s :
C
Illne s s , me dica tions ,
o
m
nutritiona l de ficie ncy
m
o
n
G
e
r
Low te s tos te rone
i
Me a s ure :
a
t
FS H, LH, S HBG low or norma l
r
i
c
LH a nd FS H
M
e
d
Low te s tos te rone
i
c
high LH a nd FS H
a
P rola ctin
l
C
o
n
d
i
t
P rima ry hypogona dis m: Conge nita l Cons ide r ka ryotyping
i
o
Norma l Ele va te d
n
a norchidis m, cryptorchidis m, mumps (Kline fe lte r s yndrome , e tc.)
s
orchitis ; ge ne tic a nd de ve lopme nta l
conditions (Kline fe lte r s yndrome ,
S e rtoli ce ll only s yndrome , e tc.); S e conda ry hypogona dis m: Ge ne tic conditions Cra nia l MRI,
ra dia tion tre a tme nt che mothe ra py, (Ka llma nn s yndrome , P ra de rWilli s yndrome ), othe r te s ting
te s ticula r tra uma
P ituita ry (tumors , gra nuloma s , a bs ce s s e s ),
Hype rprola ctine mia , cra nia l tra uma or
ra dia tion, me dica tions
Mixe d (prima ry a nd s e conda ry) hypogona dis m
(ofte n include d in s e conda ry hypogona dis m):
Alcohol a bus e , norma l a ging, chronic infe ctions
(e g., HIV), corticos te roid tre a tme nt, he mochroma tos is ,
s ys te mic dis e a s e (live r fa ilure , ure mia , s ickle ce ll, e tc.)
FIGURE
4 -3 0 Evaluation of low testosterone.
b. Risks and benefits of testosterone therapy should be reviewed and include the
potential for stimulating androgen-sensitive tumors such as prostate cancer.
c. The impact on lipids and cardiovascular disease remains uncertain, but decreases
in serum HDL have been reported.
Quick HIT CLINICAL PEARL 4-26

Patients with symptoms of
hypogonadism and low testos-
Weighing the Risk/Benefit of Testosterone Therapy
terone should undergo further Evaluation and treatment of low testosterone values must be correlated with the appropriate clinical symp-
testing to evaluate pituitary toms that support a diagnosis of hypogonadism. Declining testosterone values are consistent with normal
function. aging, and the adverse effects of treatment include the risk of promoting the growth of androgen-dependent
tumors and placing the patient at risk for cardiovascular disease.
Quick HIT
During androgen therapy, d. Absolute contraindications include prostate cancer, breast cancer, and an elevated
serum testosterone, PSA, hematocrit (> 55%). Relative contraindications include severe obstructive sleep ap-
and hematocrit should be nea, severe BPH symptoms, CHF, and an hematocrit (Hct) between 52% and 55%.
monitored.
e. Within 2 to 3 months after beginning treatment, patients should be reassessed to
evaluate clinical response and to identify possible adverse effects.
f. Adverse effects include weight gain, peripheral edema, breast tenderness, symp-
Quick HIT toms of BPH, and sleep problems. Questionnaires used for the initial evaluation
of symptoms can help assess therapy.
Potential adverse effects of g. Follow-up testing includes Hgb, prostate examination, PSA, and bone density
testosterone therapy apply to monitoring. A rapid rise in PSA (1 ng/mL) within the first 3 to 6 months may
all forms of testosterone deliv- reflect a preexisting prostate cancer. Testosterone levels should be checked in 3
ery and include fluid retention,
gynecomastia, polycythemia,
to 6 months and monitored annually.
worsening of sleep apnea,
and change in cardiovascu- D. Benign prostatic hypertrophy (BPH)
s
n
lar disease risk. Alterations 1. General information
o
i
in prostate health need to a. Enlargement of the prostate gland, resulting in lower urinary tract symptoms
t
i
d
be considered both prior to (LUTS)
n
o
therapy and during treatment
C
b. Is the leading cause of acute urinary retention in older men
monitoring. Limited data are
l
c. Is present in 30% of men over age 50 and 90% of those aged 85
a
available regarding the risks
c
i
d. Enlargement of the prostate is hormonally dependent on testosterone and
d
and benefits of treatment.
e
M
dihydrotestosterone.
e. The natural history of BPH is variable.
c
i
r
f. The terms BPH and benign prostatic hyperplasia are used interchangeably. How-
t
a
Quick HIT
i
ever, the disease is a true hyperplastic process with increases in epithelial cells,
r
e
G
smooth muscle cells, and connective tissue.
n
Age is the greatest risk factor,
o
m
and BPH is nearly an inevi-
a. Weak urine stream
m
table development in males,
o
b. Urinary frequency
C
with 90% of men affected by
age 85. c. Nocturia
d. Urgency
e. Hesitancy
f. Dribbling of urine
Quick HIT g. Hematuria
h. These clinical features have been compiled into scoring systems (Figure 4-31).
The American Urologic As-
sociation Symptom Index
American Urologic Association Symptom Index (AUA symptom score)
score is a valuable tool for International Prostate Symptom Score (IPSS)
assessing and monitoring BPH 3. Diagnosis
symptoms. a. Symptom indices can help confirm the diagnosis and establish a baseline for
monitoring treatment.
b. Digital rectal examination and PSA to eliminate prostate cancer as a cause of
symptoms and to assess rectal tone.
Quick HIT c. Urinalysis to eliminate infection as a cause or contributor.
d. Hematuria should be evaluated as discussed previously in this section, eliminat-
The size of the prostate does
not always correlate with the ing other causes before attributing the hematuria to BPH. Hematuria from BPH
degree of symptoms or the is most commonly microscopic.
response to therapy. e. Focused neurologic examination to rule out conditions that might be contribut-
ing to voiding problems.
AUA S ym p to m In d e x/In te rn a tio n a l P ro s ta te S ym p to m S c o re (I-P S S )

(See also Section II: AUA (American Urologic Association) Symptom Index for BPH and International Prostate
Symptom Score (IPSS))
Am e ric a n Uro lo g ic a l As s o c ia tio n (AUA) S ym p to m In d e x fo r BP H
No t Le s s Le s s Ab o u t Mo re Alm o s t
a t a ll th a n 1 th a n h a lf h a lf th e th a n h a lf a lwa ys
tim e in 5 th e tim e tim e th e tim e
0 1 2 3 4 5
1. INCOMP LETE EMP TYING

Ove r the la s t month or s o, how ofte n ha ve you ha d a s e ns a tion of not
e mptying your bla dde r comple te ly a fte r you finis he d urina ting? 0 1 2 3 4 5
2. FREQUENCY
During the la s t month or s o, how ofte n ha ve you ha d to urina te a ga in
<2 hours a fte r you finis he d urina ting? 0 1 2 3 4 5
3. INTERMITTENCY
During the la s t month or s o, how ofte n ha ve you s toppe d a nd s ta rte d
a ga in s e ve ra l time s whe n you urina te d? 0 1 2 3 4 5
4. URGENCY
During the la s t month or s o, how ofte n ha ve you found it difficult to
pos tpone urina tion? 0 1 2 3 4 5
5. WEAK S TREAM
During the la s t month or s o, how ofte n ha ve you ha d a we a k urina ry
s tre a m? 0 1 2 3 4 5
6. S TRAINING
C
o
During the la s t month or s o, how ofte n ha ve you ha d to pus h or s tra in
m
to be gin urina tion? 0 1 2 3 4 5
m
o
7. S LEEP ING
n
During the la s t month, how ma ny time s did you mos t typica lly ge t up
G
e
to urina te from the time you we nt to be d a t night until the time you 0 1 2 3 4 5
r
i
got up in the morning?
a
(time s a t night)
t
r
i
c
M
_________________________________________________________S CORE: (0-35)
e
d
i
c
a
The In te rn a tio n a l P ro s ta te S ym p to m S c o re (IP S S ) us e s the s a me 7 que s tions a s the AUA S ymptom
l
C
Inde x, but a dds a Dis e a s e S pe cific Qua lity of Life Que s tion (s ome time s re fe rre d to a s the bothe r s core )
o
n
a nd s core d on a s ca le from 0 to 6 points (de lighte d to te rrible ).
d
i
t
i
o
If yo u we re to s p e n d th e re s t o f yo u r life with yo u r u rin a ry c o n d itio n ju s t th e wa y it is n o w, h o w
n
s
Mo s tly Mo s tly
De lig h te d P le a s e d s a tis fie d Mixe d d is a p p o in te d Un h a p p y Te rrib le
0 1 2 3 4 5 6
FIGURE
4 -3 1 Prostate symptom scores.
4. Treatment
a. Patients with obstruction causing urinary retention, recurrent UTIs, hydrone-
phrosis, or renal insufficiency warrant urologic consultation.
Patients with urinary retention may be treated with catheter placement and
subsequent voiding trial without the catheter.
In many cases, medication is started, and the catheter is left in place for 3 to
14 days before removal and a voiding trial.
CLINICAL PEARL 4-27

Quick HIT
The degree of symptoms re-
Differential Diagnosis of LUTS
mains the most common indi- BPH causes LUTS and is the most likely explanation for LUTS in an older man. However, it is important to con-
cation for medical or surgical sider other conditions that can mimic BPH. These include drugs such as diuretics that increase urine output,
intervention. or decongestants that stimulate the receptors and increase sphincter tone. Dietary factors, such as caffeine
and alcohol, may affect the bladder, and with severe constipation the colon may compress the bladder causing
irritation and symptoms that mimic BPH. Infection is a common and highly reversible cause of LUTS. Finally,
anxiety may increase adrenergic tone and lead to urinary frequency.
Quick HIT
Treatment options for BPH
consist of watchful waiting, b. Patients with less severe symptoms may obtain relief from obstructive-type
pharmacotherapy, minimally
invasive therapies, and
symptoms with initiation of an -adrenergic blocker to relax the smooth muscle
surgery. at the bladder outlet.
Selective urologic -adrenergic blockers include tamsulosin, alfuzosin, and
silodosin.
Nonselective -adrenergic blockers include doxazosin and terazosin, which,
in addition to the urologic effects, lower BP. These medications are more likely
Quick HIT to cause orthostatic symptoms than selective -adrenergic blockers.
c. 5- -Reductase inhibitors block the effects of testosterone on the prostate by in-
-Adrenergic blockers are
hibiting the conversion of testosterone to 5-dihydrotesterone (5-HT).
effective medications for pro-
viding more rapid symptomatic This effect shrinks the prostate over time; medications in this category include
relief related to obstructive finasteride and dutasteride.
s
n
urinary symptoms with BPH. A trial of 6 to 12 months may be needed to see the effects of these medications.
o
i
t
They can be prescribed with -adrenergic blockers and are synergistic.
i
d
n
PSA values diminish with these medications, and PSA levels should be moni-
o
C
tored before and during treatment. A rising PSA suggests the possibility of
l
a
prostate cancer.
Quick HIT
c
i
d
May reduce the risk of prostate cancer, but if a prostate cancer develops while
e
M
5--Reductase inhibitors can on a 5- -reductase inhibitor, it tends to be a more aggressive tumor.
c
provide long-term benefit with Side effects include impotence, loss of libido, and gynecomastia.
i
r
t
BPH but require 6 to 12 months d. Anticholinergic medications, such as oxybutynin, can be used for urgency and
a
i
r
to be effective. frequency.
e
G
Caution must be exercised to monitor for urinary retention.
n
o
May be used with -adrenergic blockers
m
m
e. Phosphodiesterase-5 inhibitors are also used to treat obstructive symptoms.
o
C
Quick HIT May be useful for patients who also have erectile dysfunction
Interact with -adrenergic blockers and can potentiate the BP- lowering effects
Treatment is driven by symp- f. Patients refractory to medical therapy or who fail a voiding trial post-urinary re-
toms, the size of the pros- tention should be referred to urology for possible surgical intervention.
tate, and the tolerability of TURP remains the most effective surgery. Those with less severe symptoms
medication. may benefit from less aggressive procedures such as transurethral needle
ablation.
Minimally invasive therapies can be done in the outpatient setting under local
anesthesia with sedation and may provide moderate-to-good relief of symp-
Quick HIT toms. Disadvantages are that although obstructive symptoms may improve,
frequency and urgency can persist, patients may temporarily need a catheter,
Indications for urology refer- and retreatment is often needed.
ral include: PSA > 4 or a PSA Complications following TURP: 5% to 10% impotence, 2% to 4% inconti-
velocity of > 0.75 in 1 year, nence, and 70% to 75% retrograde ejaculation
rising PSA on finasteride,
g. The best evidence suggests that saw palmetto is no more effective than placebo
poor response to medications,
refractory symptoms, and for treating BPH.
complications such as renal
failure, recurrent UTI, urinary E. Urinary retention
retention, and hematuria. 1. General information
a. The most common urgent problem encountered in urology
b. Most common in elderly males

c. Risk factors include age > 70, higher AUA, or IPSS, prostate enlargement, el-
evated PSA value, and reduced urinary flow rate. Quick HIT
d. Clinical presentation is an abrupt inability to void along with lower abdominal Acute urinary retention is the
discomfort. most common emergent medi-
e. Retention in patients with dementia may present with increased confusion, agi- cal condition for urologists.
tation, and restlessness.
f. Laboratory evaluation may be normal with acute presentations.
g. Elevated serum creatinine suggests more chronic obstruction, which if gradual
in onset, may be painless.
2. Differential diagnosis Quick HIT
a. BPH accounts for over half of cases. Acute urinary retention is
b. Prostate or bladder cancer largely a disease of elderly
c. Medications or postoperative stateparticularly -adrenergic agonists or anti- men, with > 50% of cases be-
cholinergic medications ing related to BPH.
d. Constipation
e. Urethral stricture
f. Phimosis or paraphimosis
g. Infectionprostate or urinary tract
h. Neuropathy related to diabetes, spinal cord injury, or stroke
3. Evaluation (Figure 4-32)
a. Physical examination
Abdominal examinationpalpate for enlarged bladder
Genitalia for phimosis, paraphimosis, cystocele, or uterine prolapse
Rectal examination for prostate enlargement or nodularity
C
Neurologic examination for neuropathy, rectal tone
o
m
b. Laboratory
m
CBC for infection
o
n
BMP for renal function
G
e
Urinalysis with culture for infection, hematuria
r
i
a
PSA may be elevated related to acute retention; recheck in 4 to 6 weeks.
t
r
i
c. Postvoid residual
c
M
After having the patient void, catheterization can measure residual volume
e
(PVR):
d
i
c
(1) If PVR < 150 mL, trial of voiding without indwelling Foley
a
l
(2) If PVR > 300 mL, leave the catheter in place for 1 to 2 weeks while begin-
C
o
ning -adrenergic blocker or addressing the underlying cause.
n
d
i
(3) Between 150 and 300 mL, individualize decision to maintain Foley
t
i
o
catheter.
n
s
If unable to void, continue catheterization.
Definitive treatment depends upon underlying cause and patients condition.
(1) For BPH -adrenergic blockers with subsequent trial of voiding
(2) Constipationinitiation of laxatives
(3) Infectionstreat with appropriate antibiotic therapy.
(4) Medicationsif possible, discontinue or modify dose of potentially caus-
ative agents.
(5) Prostate cancer, phimosis/paraphimosis, or stricture may require urologic
consultation and procedural intervention.
(6) Neurologic causes may require chronic catheter use.
Gyne c o lo g ic D is e a s e
Vaginitis
A. Definition
1. Vaginitis is the disorder of the vagina caused by inflammation, infection, or changes
in normal vaginal flora.
U R IN ARY R E T E N T IO N , MALE
His tory a nd phys ica l e xa m:

- LUTS his tory
Ne urologic findings conce rning
- Urologic s urge ry
for cord compre s s ion (ie , due to
S us pe ct a cute ba cte ria l pros ta titis : - Dia be te s , ne urologic conditions
pros ta te ca nce r or othe r CNS
- S upra pubic ca the te r pre fe rre d - Acute vs . chronic
le s ion):
if s e ptic - His tory of s tricture s , S TDs
- Fole y ca the te r pla ce me nt
- Ne urologic e xa m
- MRI or CT s ca n of s pine
- GU e xa m including DRE
- Ne uros urge ry cons ulta tion
- Me dica tion his tory
- Bla dde r s onogra m/s ca n
S us pe ct ure thra l s tricture :

Dra in bla dde r:
- Atte mpt s ma lle r ca the te r
- La rge r or coude type ca the te rs S us pe ct pros ta te ca nce r:
- Obta in ure throgra m or
ma y be ne e de d - Obta in P S A
cys tos copy to confirm
- Cys tos copy with pla ce me nt of - Bone s ca n a nd CT s ca n if
- S upra pubic tube pre fe rre d
ca the te r ove r wire indica te d
ove r re pe a te d dila tion
If a cute re na l fa ilure ,
Bla dde r dra ine d: e le ctrolyte a bnorma litie s , or
- Re cord initia l output no urina ry output for >24 hr
- S e nd urine a na lys is a nd culture cons ide r a dmis s ion for
- S e nd e le ctrolyte s , CBC monitoring of e le ctrolyte s
a nd pos tobs tructive diure s is
s
n
o
i
t
i
S top pos s ible pre cipita ting me dica tions
d
n
S ta rt -blocke r the ra py
o
C
Cons ide r s ta rting 5 -re ducta s e inhibitor
l
Cours e of a ntibiotics if s us pe ct infe ction
a
c
i
d
e
M
Voiding tria l in 12 wk
c
i
r
t
a
i
r
e
G
n
Pass: Fa il:
o
m
- Continue me dica l ma na ge me nt for - Furthe r e va lua tion options : Cys tos copy,
m
pre s ume d BP H urodyna mics , ima ging, P S A
o
C
- S urge ry if indica te d for BP H - Cons ide r pros ta te ca nce r
- Che ck P S A in 46 wk a nd cons ide r - Tre a t a s indica te d: Cle a n inte rmitte nt
pros ta te ca nce r a s ca us e ca the te riza tion, s urge ry
FIGURE
4 -3 2 Evaluation of acute urinary retention.
B. Epidemiology
1. The exact incidence of vaginitis is unknown, but most women experience at least
one episode in their lifetime.
C. Most common symptoms

1. Vaginal discharge
2. Abnormal odor
3. Pruritus
4. Vaginal discomfort
D. Etiology
1. Infectious
a. Vaginal candidiasis
b. Trichomoniasis
c. Bacterial vaginosis
2. Noninfectious causes include but are not limited to
a. Atrophic vaginitis
b. Contact dermatitis
c. Lichen simplex chronicus, lichen planus (LP), and lichen sclerosus
d. Erosive vulvar LP
Vaginal Candidiasis
A. Most common infectious cause of vaginitis in elderly women, but less common than
in younger women
B. 70% to 75% lifetime prevalence among women, with 40% to 50% recurrence rate
C. Causes
1. Candida albicans accounts for 85% to 95% of vaginal yeast strains.
2. Candida glabrata isolated in 10% to 20%
D. Pathogenesis
1. C. albicans gains access to vagina from the nearby perianal region.
2. Germination of Candida cells enhances colonization and tissue invasion.
E. Risk factors include:
C
1. Diabetes, hormone replacement therapy, HIV infection, antibiotics use, corticoste-
o
m
roids, immunosuppression, or intravaginal use of oils
m
o
n
F. Patient commonly presents with:
G
1. Vulvar pruritusthe most common symptom
e
r
i
2. White vaginal discharge
a
t
r
3. Dyspareunia
i
c
4. Vaginal irritation or soreness or burning
M
e
d
G. Pelvic examination may reveal
i
c
a
1. Thick white cottage cheese-like adherent discharge
l
C
2. Labial and vulvar erythema and swelling
o
n
d
i
H. Making the diagnosis
t
i
o
n
1. Diagnosis suspected in woman with symptoms, such as vaginal itching, vaginal dis-
s
charge, or external dysuria
a. In symptomatic woman, diagnosis confirmed with
Wet preparation or 10% KOH or Gram stain of vaginal discharge showing
yeasts, hyphae, or pseudohyphae (Figure 4-33)
Vaginal pH usually normal (< 4.5)
I. Treatment (Table 4-38)

1. Azoles (ketoconazole, itraconazole, fluconazole, etc.) are the mainstay of treatment.
a. They are antifungal and act by altering cell wall permeability.
b. Available over the counter and by prescription
c. They come in topical and oral forms.
2. Uncomplicated
a. Sporadic, infrequent episodes (3 episodes/year)
b. Mild to moderate signs/symptoms
c. Probable infection with C. albicans
d. Table 4-38 outlines treatment regimen dosages.
3. Complicated/recurrent vulvovaginal candidiasis
a. Severe signs/symptoms
b. Candida spp. other than C. albicans, particularly C. glabrata
FIGURE
4 -3 3 Microscopic exam of yeast.
(Edwards L, Lynch PJ . Genital Dermatology Atlas. Philadelphia, PA: LWW, 2010.)
TABLE 4-38 Treatment of Vaginal Candidiasis

Drug Preparation Dosage
s
n
Over the Counter
o
i
t
Clotrimazole (Gyne-Lotrimin, 1% cream
i
~5 g/d 714 d
d
n
Mycelex) 2% cream ~5 g/d 3 d
o
C
100 mg vaginal tab
l
1 tab/d 7 d or
a
c
2 tabs/d 3 d
i
d
e
M
Miconazole (Monistat) 2% cream ~5 g/d 7 d
Quick HIT 4% cream
c
~5 g/d 3 d
i
r
t
a
Vaginal candidiasis is the most 100 mg vaginal sup 1 suppository daily for 7 d
i
r
200 mg vaginal sup 1 suppository daily for 3 d
e
common cause of vaginitis in
G
geriatric women. 1,200 mg vaginal sup 1 suppository daily for 1 d
n
o
m
Tioconazole (Vagistat) 2% cream 5 g/d 3 d
m
6.5% cream 5 g in a single dose
o
C
Prescription
Butoconazole (Gynazole) 2% cream ~5 g as a single dose
Quick HIT Nystatin (Mycostatin) 100,000 unit vaginal tablet 1 tab/d 14 d
Diagnosis of candidiasis can Terconazole (Terazol) 0.4% cream ~5 g/d 7 d
be achieved with a vaginal pH 0.8% cream ~5 g/d 3 d
< 4.5 and performance of KOH
microscopic examination find- Ketoconazole (Nizoral) 400 mg oral tab 1 tab BID 5 d
ing in the presence of yeast.
Itraconazole (Sporanox) 200 mg oral tab 1 tab qd 3 d
Fluconazole (Diflucan) 150 mg oral tab Single dose
Quick HIT c. Poorly controlled diabetes, immunosuppression, and recent antibiotics use
d. History of recurrent (4/year) culture-verified vulvovaginal candidiasis
A single oral dose of fluco- e. Maintenance antifungal suppressive therapy for 6 months with either
nazole is a convenient and Ketoconazole 100 mg orally daily
effective therapy. A second
dose given 3 days later may be Itraconazole 50 to 100 mg orally daily
needed in severe cases. Clotrimazole 500 mg vaginal suppositories weekly
Fluconazole 150 mg orally weekly
TABLE 4-39 Comparison of Different Causes of Vaginitis

Atrophic Vulvovaginal Bacterial
Variable Vaginitis Candidiasis Trichomoniasis Vaginosis
Symptoms Dyspareunia, vaginal Pruritus, sore- Malodorous, Malodorous
dryness ness, dyspareu- gray-greenish whitish thin
nia, white curdy purulent discharge, discharge, no
discharge dyspareunia dyspareunia
Signs Vestibular and vagi- Vulvar ery- Purulent discharge, Adherent
nal thinning thema, edema, vulvovaginal discharge
fissure erythema
pH > 5.0 4.04.5 (normal) 5.06.0 > 4.5
Microscopic Increase cocci and Pseudohyphae Motile Clue cells
finding coliforms; parabasal trichomonads (Figure 4-34)
cells
Bacterial Vaginosis and Trichomoniasis

A. These are a rare cause of vaginitis in elderly women.
B. Table 4-39 summarizes signs and symptoms.
C
o
C. Bacterial vaginosis treatment
m
Quick HIT
m
1. Drug of choice
o
a. Metronidazole 500 mg BID 7 days or
n
G
b. Metronidazole gel 0.75% one full applicator (~5 g) intravaginally once daily 5 Trichomoniasis and bacterial
e
r
days or
i
vaginosis are unusual causes
a
t
c. Clindamycin 2% cream one full applicator (~5 g) intravaginally once daily 7 of vaginitis in geriatric women.
r
i
c
days
M
2. Alternatives
e
d
i
a. Clindamycin 300 mg orally BID 7 days or
c
a
b. Tindazole 2 g orally daily for 2 days or
l
C
c. Tindazole 1 g orally daily for 5 days
Quick HIT
o
n
d
i
t
i
o
Trichomonas can sometimes
n
be asymptomatic from months
s
to a year. So occasionally, a
trichomonas infection may be
seen in an older woman with
no history of recent sexual
activity.
FIGURE
4 -3 4 Microscopic exam of clue cells.
(Edwards L, Lynch PJ . Genital Dermatology Atlas. Philadelphia, PA: LWW, 2010.)
D. Trichomoniasis treatment
1. Treatment of choice is a single 2 g oral dose of metronidazole.
2. Alternative regimen is metronidazole 500 mg BID 7 days.
3. Treatment of all sexual partners is necessary to avoid recurrence.
Atrophic Vaginitis
A. Most common noninfectious cause of vaginitis in older women
B. It is characterized by inflammation and thinning of the epithelial lining of the
vaginal and lower urinary tract resulting from loss of estrogen.
C. Pathophysiology
1. Serum estrogen levels decline with age
2. Decline in estrogen level with the normal aging process is thought to be responsible
for many of the adverse changes seen with vaginal atrophy.
3. These changes usually develop gradually over a period of years.
Quick HIT 4. These changes include:
a. Thinning of the top layer of superficial epithelial cells
Atrophic vaginitis is the most b. Loss of elasticity of the vaginal epithelium
common noninfectious cause c. An increased subepithelial connective tissue
of vaginitis in geriatric women. d. Loss of rugae
e. Shortening and narrowing of the vaginal canal, with loss of distensability
f. Reduction in vaginal secretions and increase in vaginal pH to 5
5. Thinning of the vaginal epithelium makes it more susceptible to trauma, leading to
Quick HIT bleeding, petechiae, and ulceration. Thinning also exposes the underlying connec-
tive tissue, which is more vulnerable to inflammation or infection.
s
n
o
Decline in estrogen levels
i
D. Risk factors
t
leads to vaginal atrophy and
i
d
alteration of the vaginal pH.
n
1. Besides low estrogen levels other factors that can modulate the degree of atrophy
o
C
include the following:
l
a
a. Cigarette smoking
c
i
d
b. Cessation of coital activity
e
M
Quick HIT c. Vaginal nulliparity and vaginal surgery
c
i
r
E. Clinical presentation
t
Diagnosis is achieved on the
a
i
r
basis of clinical examination 1. Vaginal dryness, burning, or irritation
e
G
and is supported by finding an 2. Decreased vaginal lubrication during sexual activity
n
increased pH.
o
3. Dyspareunia
m
m
4. Vulvar or vaginal bleeding (e.g., postcoital bleeding)
o
5. Vaginal discharge (leukorrhea or yellow and malodorous)
C
6. Pelvic pressure or a vaginal bulge
Quick HIT 7. Urinary tract symptoms (e.g., urinary frequency, dysuria, urethral discomfort, and
hematuria)
Initial therapy is directed at
moisturizing and lubrication. F. Pelvic examination
1. The external genitalia may show scant pubic hair.
2. Decreased elasticity and turgor of the vulvar skin
3. Narrowing of introitus with decreased moisture and fusion or resorption of the la-
Quick HIT bia minora
4. Patchy erythema, petechiae, and blood vessel may be seen through thinned out
Some topical estrogen is ab- epithelium.
sorbed systemically, and these 5. Occasionally, presents with a watery white discharge.
products should be used with
caution in women with current G. Diagnosis
breast cancer, undiagnosed
vaginal bleeding, endometrial 1. The diagnosis of the urogenital atrophy is clinical and based on characteristic
cancer, and/or a history of symptoms and findings on history and physical examination.
thromboembolic disease. 2. Laboratory tests to confirm low estrogen level are available, but such testing is typi-
cally not necessary.
H. Laboratory and Imaging evaluation

1. Vaginal pH elevated to 5.0 or greater
2. Microscopic examination showing multiple WBC, few bacteria, and many exfolia-
tive cells
3. Transvaginal ultrasonography of uterine lining
a. Thin endometrial stripe, measuring < 4 to 5 mm on transvaginal ultrasound
(TVUS), suggests a hypoestrogenic state and supports the clinical diagnosis of
vaginal atrophy.
b. However, this test is expensive and routinely not performed for the sole purpose
of confirming urogenital atrophy.
I. Treatment
1. First-line treatments are vaginal moisturizers and lubricants, which acidify and coat
the vagina to minimize symptoms.
a. Many moisturizer products are available; examples include Replens, Me Again,
and Vagisil Feminine Moisturizer.
2. If these preparations do not provide adequate symptom relief, estrogen therapy may
be used for women with no contraindications to such therapy.
a. Preferred therapy is vaginal estrogen with low dose for short duration
3. In addition, sexual activity and/or use of vaginal dilators may help maintain a
healthy vaginal epithelium.
Other Noninfectious Causes of Vaginitis

A. Contact dermatitis
1. This disorder occurs when there is disturbance to the normal epidermal barrier by
C
Quick HIT
o
an irritant and leading to secondary inflammation.
m
m
2. Contact dermatitis is usually caused by common exposures used repeatedly on a
o
Contact dermatitis is caused
n
daily basis. by exposure to common ir-
G
3. Common contact irritants
e
ritants and materials encoun-
r
i
a. Urine, feces, and excessive sitting tered in everyday life.
a
t
r
b. Repetitive scratching and over washing
i
c
c. Detergents and fabric softeners
M
e
d. Toilet paper dyes
d
i
e. Hygiene pads, sprays, and douches
c
a
l
f. Lubricants
C
o
4. Irritant contact dermatitis, allergic contact dermatitis, and atopic dermatitis are dif-
n
d
ferent types of contact dermatitis and all present with:
i
t
i
a. Itching, burning, swelling, and redness
o
n
s
b. Small vesicle or bullae more likely seen with allergic contact dermatitis
5. Treatment
a. Exclude contact with possible irritants.
b. Restore skin barrier with sodium bicarbonate sitz baths.
c. After hydration, apply bland emollient.
Mineral oil and olive oil
d. Short-term mild to moderate potency steroids
Triamcinolone cream 1% BID 10 to 14 days (or Clobetasol 0.05%)
e. Cold packs: gel packs or frozen vegetable bag
f. Antihistamine like hydroxyzine (10 to 75 mg PO QHS) for itching
g. Replace local estrogen, if necessary.
h. If recurrent, refer for patch testing.
B. Lichen simplex chronicus (Figure 4-35)

1. Chronic localized pruritus skin condition caused by an irritant, which initiates a
scratchitch cycle.
2. Characterized by thickened, accentuated skin lines, also known as
lichenification
3. Classified as
a. Primarymost often idiopathic
b. SecondaryCandida vulvitis, vulvar contact dermatitis, atopic dermatitis; diabe-
tes and iron deficiency anemia
Most common causes are atopic dermatitis, contact dermatitis, or both.
4. Presentation
a. Chronic itchingmost common presentation
b. Burning
c. Vaginal pain and tenderness
a. Thickened leathery red (white if moisture) raised lesion seen commonly on labia
majora
b. Pruritus may be out of proportion to physical changes.
6. Diagnosis
a. Based on clinical findings, rarely requires biopsy
7. Treatment
a. Removal of irritants or allergens
b. Treat infectious causes.
c. Mild to moderate potency steroid cream
For example, Triamcinolone acetonide (TAC) 0.1% ointment BID 4 to 6 weeks
d. Diphenhydramine or hydroxyzine (Atarax) for relief of itching
C. Lichen sclerosus (Figure 4-35)

1. It is one of the most common chronic vulvar conditions.
2. Constitutes 40% of nonneoplastic vulvar epithelial disorders
s
3. Incidence
n
o
a. All age groups affected, including prepubertal and adolescents
i
t
i
d
b. The onset is usually postmenopausal and is most common in elderly women.
n
o
c. Is a benign, chronic progressive dermatologic disorder characterized by inflam-
C
mation and epithelial thinning
l
a
c
4. Associated disease
i
d
e
a. Prevalence of psoriasis in patients with lichen sclerosus higher than in the gen-
M
eral population
c
i
b. Autoimmune disorders may be more frequent in patients with lichen sclerosus of
r
t
a
the vulva.
i
r
e
G
n
o
m
m
o
C
A B C
FIGURE
4 -3 5 Lichen simplex (A), lichen sclerosis (B), and lichen planus (C).
(Snyder R, Dent N, Fowler W, et al. Step Up to Obstetrics and Gynecology. Philadelphia, PA: Lippincott Williams & Wilkins, 2014.)
5. Etiology
a. Disorder of epithelial growth, underlying cause unknown
b. Seems to be linked with autoimmune mechanisms
6. Clinical presentation
a. May be asymptomatic or may present with the following symptoms:
Chronic vulvar pruritus, which may be intense
Burning
Vulvar pain
Dyspareunia (in patients with cracked skin)
Bleeding
Blistering
Pain on defecation or constipation
7. Physical examination of the pelvic may reveal:
a. Very thin patchy whitish-grayish-pink homogeneous, hypopigmented epithelial
areas; occasionally white, shiny macules and papules
Affected areas often develop a parchment paper appearance.
b. Characteristic figure of eight pattern when both vulva and perianal areas involved
c. Late disease is characterized by scarring with agglutination of normal genital
structures as well as loss of labia minora and scarring over the clitoris
d. Vaginal mucosa is spared.
8. Diagnosis
a. A biopsy is indicated to confirm the diagnosis and exclude malignancy.
b. Histologic finding includes:
Blunting or loss of rete ridges, hyperkeratosis, and loss of melanocytes
9. Treatment
C
a. Educate the patient.
o
m
b. Stop irritants.
m
c. Cool, ventilated clothing
o
n
d. Topical high-potency steroids
G
e
Various regimens exist.
r
i
a
Clobetasol propionate or halobetasol 0.05% ointment qd to BID
t
r
i
For 12 weeks, then M-W-F or 1 to 2 times a week and follow-up at 6 to 12
c
M
weeks, then regularly at 6- to 12-month intervals; or
e
Clobetasol propionate 0.05% BID 1 month, then qd 2 months
d
i
c
For thick lichen sclerosus, consider intralesional steroid (triamcinolone 3.3 to
a
l
10 mg/mL).
C
o
The dose is dependent on the location and thickness of the skin that is being
n
d
i
injected.
t
i
o
Maximum dose of 40 mg of TAC per month, and do not use high steroid doses
n
s
on thin skin or in small areas because the tissue can slough off
e. Treat associated Candida or secondary bacterial infection.
f. Stop scratching.
g. Tacrolimus ointment and pimecrolimus cream have been used for the treatment
of vulvar lichen sclerosus. Burning may occur with these medications.
h. Surgery is done on occasion to improve function or for scarring. Scarring is not
reversible by any medical therapy.
10. All patients with lichen sclerosus must have a regular lifelong follow-up because
of an increased risk of developing squamous cell carcinoma (< 5% in women).
CLINICAL PEARL 4-28

Quick HIT
Vulvar Cancer in the Differential Diagnosis
Lichen sclerosis is one of the
Vulvar cancer has its peak incidence at age 85. It is curable in its early stages, but advanced disease is more most common chronic vulvar
difficult to treat. Unfortunately, its diagnosis is often delayed because physicians tend to neglect symptoms, conditions responsible for up
attributing them to common benign causes. Also, older women may be too embarrassed to discuss their gyne- to 40% of noncancer vulvar
cologic symptoms. An annual examination is a simple measure to help assure early diagnosis. skin conditions.
D. Lichen planus (LP) (Figure 4-35)

1. LP is a distinctive inflammatory eruption of the skin and mucous membranes.
2. It affects skin and mucous membranemouth, vulva, vagina, nails, scalp, esopha-
gus, nose, eye, ears, and bladder.
a. Up to 70% of women with vulvar LP have vaginal involvement.
b. May be isolated to the vulva or form part of a more generalized skin eruption
3. LP is usually categorized by site of involvement and lesion morphology, but pa-
tients may have more than one subtype and more than one site of involvement.
4. Incidence and prevalence
a. It tends to occur in women aged 30 to 60 years.
b. Oral LP affects women and men in the ratio 3:2.
c. Up to 4% prevalence of LP reported among the general population
5. Etiology
a. It is a disorder of altered cell-mediated immunity with exogenous antigens tar-
geting the epidermis.
6. Risk factors
a. Medication use
Nonsteroidal anti-inflammatory agents and ACEIs
b. Stress
c. Infectious agents, including hepatitis C virus
d. Genetic factors that influence T cellmediated immunologic response.
7. Clinical presentation based on vulvovaginal types of LP
a. Papulosquamous
Typical purple papules and plaques with a white lacy pattern on the vulvar tri-
gone and periclitoral area
s
n
It may be part of generalized LP.
o
i
Can be pruritic
t
i
d
Tends to respond to topical steroids
n
o
C
b. Hypertrophic
l
a
Least common with extensive white scarring and destruction (looks like LS)
c
i
Rough lesions affecting perineum and perianal area
d
e
M
Can be very itchy
c
Tends to be resistant to treatment
i
r
c. Erosive (vulvovaginal gingival syndrome)
t
a
i
r
Destructive LP on the mucous membranes and vulva with desquamative vagi-
e
G
nitis changes
n
o
Presents with variable erosions plus atrophy, usually pain, burning, and irrita-
m
m
tion rather than itch
o
Treatment tends to be resistant.
C
8. Diagnosis
a. Classic cases of LP may be diagnosed clinically.
b. Biopsy may be required for more atypical presentations.
Helpful for confirming diagnosis in classic cases
9. Differential diagnosis
a. Lichen sclerosus
b. Drug eruption
c. Graft versus host disease
d. Bullous mucus membrane pemphigoid
e. Pemphigus vulgaris
10. Treatment
a. Stop irritants
b. Pain control
c. High-potency steroid ointment (clobetasol) topically once to twice a day
d. Intralesional steroidtriamcinolone 10 mg/mL q 3 to 4 weeks 3
e. Intravaginal steroidhydrocortisone acetate foam 40 to 80 mg qhs or 25 to 100
mg suppository qhs
If using high-dose steroids, use for short term, then gradually taper the dose.
f. For refractory or recurrent LP, oral prednisone and other immunosuppressants
such as methotrexate and cyclosporine may be tried.
Pelvic Organ Prolapse

1. Pelvic organ prolapse is the herniation of the pelvic organs into or beyond the vagi-
nal walls.
2. This condition results in one of the most common inpatient surgeries for geriatric
women.
3. Up to 40% of women are affected, increasing with increasing age to menopause and
then with variable course of progression or regression thereafter.
4. Ten percent of those with prolapse will have symptoms, and the lifetime risk for
surgery for this condition is up to 10%.
5. The pelvic organs are supported by ligaments, fascia, and muscles.
a. Laxity in these structures can result in prolapse.
b. Prolapse is described by location or the suspected organ that is involved with the
herniation.
Locations/organ
(1) Anteriorbladder/cystocele
(2) Posteriorrectum/rectocele
(3) Apicaluterine and cervical prolapse or enterocele (may follow
hysterectomy)
Uterine procidentia is the term to describe the involvement of all three of
these locations into the vagina.
1. 90% of patients with prolapse may not report any symptoms.
2. Symptoms may include
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o
a. Feeling a bulge
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b. Visualizing a bulge or mass
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c. Vaginal spotting or discharge
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d. Urinary symptoms
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Stress incontinence
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Urgency
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Difficulty urinating or emptying bladder
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e. Rectal symptoms
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Constipation
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Incomplete emptying
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Urgency
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d
Incontinence
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3. Risk factors
o
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a. Childbirth
s
b. Increases with increased parity
c. Constipation
d. Obesity
e. Age
f. Hysterectomy
4. Diagnosis is made by clinical examination.
a. Visualization of the prolapse on pelvic examination
b. Valsalva maneuver may promote descent of the involved segment.
c. The upright posture may also provide improved assessment because the prolapse
will not be as apparent in the recumbent position.
d. A Pelvic Organ Prolapse Quantification System has been developed for staging
of disease, tracking progression and communication between clinicians, but is
beyond the scope of this chapter.
C. Treatment
1. The need for treatment depends on the presence and severity of symptoms.
a. Patients without symptoms can be observed and followed expectantly.
b. Patients with urinary or fecal obstructive symptoms should be provided
treatment.
c. Patients without obstruction but with discomfort can be offered therapy.
2. Treatment options include conservative and surgical treatments.

a. Pelvic floor exercises (Kegel exercises) may be beneficial.
Quick HIT b. Fitting the patient with a pessary, which is a device placed into the vagina, to
Pelvic organ prolapse occurs support the vaginal tissues
because of laxity of the fascia There are many different types of pessaries.
of muscles of the pelvic floor, There are also different sizes of pessaries, and they must be fitted to the indi-
resulting in herniation of ad- vidual patient.
jacent organs into the vaginal
Pessaries should be removed and cleaned every 2 weeks.
vault.
(1) Many patients do not have the dexterity to remove, clean, and replace a
pessary.
(2) Alternative options for these patients are to have office visits every 3 to 6
months to remove and clean the pessary.
Quick HIT c. Estrogen vaginal cream is of uncertain benefit, but is a form of therapy provided
as a trial in some patients.
Most women with pelvic organ d. Surgical therapy is ultimately provided to patients with more severe symptoms
prolapse are asymptomatic or or who fail conservative treatments.
experience minimal symptoms.
There are a variety of procedures and approaches, depending on the specific
defect and the preferences of the surgeon.
Complications include injury to adjacent structures, failure of the surgery and
Quick HIT new onset of incontinence, constipation, or urinary retention.

Recurrence of prolapse is common, and up to one-third of patients will require
Approximately 10% of women additional surgery.
experience significant
symptoms requiring therapy; Postmenopausal Bleeding (PMB)
generally use of a pessary or a
A. PMB refers to any uterine bleeding occurring at least 12 months after the last
s
surgical procedure.
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menstrual period.
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d
n
B. All PMB needs to be fully evaluated regardless of the amount or duration.
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Quick HIT
l
C. Epidemiology
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1. Occurring in as many as 20% of patients over the age of 65
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Although there are many 2. Approximately 10% of the PMB patient found to have either endometrial hyperpla-
causes of PMB other than sia or cancer
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cancer, malignancy must be
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ruled out because of its life-
D. Etiology
i
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threatening consequences.
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1. Hormonal
n
a. Exogenous estrogens: hormone therapy (HT)
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m
b. Endogenous estrogens: acute stress, estrogen-secreting ovarian tumor
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2. Anatomic
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a. The most common cause of bleeding in these women is atrophy of the vaginal
mucosa or endometrium. In the early menopausal years, endometrial hyperpla-
sia, polyps, and submucosal fibroids are also common causes of PMB.
b. Endometrial hypoplasia (atrophy)
Typical vaginal findings of endometrial hypoplasia include a pale, dry vaginal
epithelium that is smooth and shiny with loss of most rugae.
Diagnosis and treatment discussed in the vaginitis section.
c. Polyps
d. Endometrial hyperplasia
e. Uterine cancer: endometrial adenocarcinoma, corpus sarcoma
f. Cervical cancer: squamous, adenocarcinoma
3. Disease of bladder, urethra, and bowel should be considered and evaluated in pa-
tients in whom there is no clear genital tract etiology.
4. In women with osteoporosis, pelvic imaging should be considered to rule out frac-
ture when there is genital bleeding after trauma.
5. Medication
a. Anticoagulation
b. Post-radiation therapy
c. Herbal and dietary supplements
For example, the use of soy and phytoestrogens in large quantity
E. Diagnosis
1. The primary goal of the diagnostic workup is to exclude malignancy and identify
benign causes that can be treated.
2. It is very important to get a thorough history and physical examination in women
who present with PMB and are not on hormonal therapy.
a. Important information to be gathered from history includes:
Onset of bleeding
Precipitating factors (e.g., trauma and foreign body)
Nature of bleeding
Associated symptoms (change in bowel or bladder, fever, and pain)
Medication history (anticoagulation, hormonal therapy, and herbal/dietary
supplements)
Risk factors for endometrial hyperplasia and cancers
(1) Tamoxifen
(a) Risk of endometrial cancer increases in patient who received therapy
for > 5 years.
(2) Long-term use of hormone replacement therapy with unopposed estrogen
(3) Prolonged estrogen exposure
(a) Nulliparity
(b) Early menarche (< 12 years)
(c) Late menopause (> 52 years) Quick HIT
(d) Chronic anovulation
Postmenopausal vaginal
(4) Obesity bleeding is associated with
(5) HTN increased risk of premalignant
(6) Diabetes or malignant endometrial
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(7) Liver disease polyps.
o
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Family history of breast, colon, and endometrial cancer
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b. Physical examination
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Abdominal examination to rule out palpable masses
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Pelvic examination with speculum and bimanual
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a
(1) Examine vaginal, cervical, urethral, or rectal sites for any source of bleed-
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r
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ing or obvious visible masses.
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(2) Palpate uterine size for position and size.
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(3) Cervical cytology should be performed.
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3. After undergoing both a clinical examination and a cervical smear, per American
a
l
C
College of Obstetricians and Gynecologists (ACOG) recommendation, women with
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PMB should have an initial assessment with transvaginal ultrasound (TVUS) or en-
d
Quick HIT
i
dometrial biopsy.
t
i
o
a. TVUS examination is an acceptable initial test
n
s
If ultrasound reveals a thin, homogeneous endometrium < 4 mm in thickness, PMB women with negative
endometrial biopsy may not
then endometrial cancer can reasonably be excluded, and endometrial biopsy rule out endometrial cancer;
is not required. therefore, important to follow
Additional testing such as endometrial biopsy or hysterosonography, or hys- up with TVUS.
teroscopy is required if:
(1) The endometrial thickness is > 4 mm.
(2) The endometrium shows diffuse or focal increased echogenicity (heterogeneity).
(3) The endometrium is not adequately visualized.
(4) The woman has persistent bleeding. Quick HIT
Per SIGN 2002 recommendation, women who are on sequential HRT and Hysteroscopy is the gold stan-
present with PMB. dard test for evaluating lesions
(1) If the TVUS indicates endometrial thickness < 5 mm, no further action is within the uterine cavity and
required. assessing endometrium, but is
not the preferred initial test.
(2) If the TVUS indicates endometrial thickness > 5 mm, then tissue sam-
pling is warranted.
F. Management
1. In postmenopausal women, uterine bleeding is usually light and self-limited.
2. The main object is to rule out cancer; treatment is usually not necessary if cancer
has been excluded.
3. Reinvestigation is indicated for recurrent or persistent bleeding.

4. If lesions are found to be benign, treatment is supportive or geared toward provid-
Quick HIT ing symptomatic relief.
All PMB needs a thorough 5. Malignant lesions are evaluated and treated according to standard guidelines.
evaluation regardless of
amount or duration. Ovarian Cancer
A. Ovarian cancers are categorized into four broad categories.
1. Epithelial
a. 90% of the primary ovarian cancer
b. Divided into eight subtypes based on histologic findings
Quick HIT Serous
Endometrioid
Up to 10% of patients with Clear cell
PMB have either endometrial
hyperplasia or cancer.
Mucinous
Transitional
Mixed Epithelial
Undifferentiated
Unclassified
2. Germ cell
a. Examples of germ cell ovarian cancer
Dysgerminoma (ovarian seminoma)
Choriocarcinoma
Solid teratoma (immature teratoma)
Yolk sac tumor (endodermal sinus tumor)
3. Sex cord or Stromal
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a. Granulosa cell tumor
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b. SertoliLeydig cell tumor
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4. Metastasis to ovaries (Krukenberg tumor)
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a. Accounts for 5% of ovarian cancer
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b. Typically from breast or gastrointestinal primary sites
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B. Incidence and prevalence
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1. Highest incidence reported in women aged between 60 and 64.
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2. Lifetime risk for women being diagnosed with ovarian cancer is one in 48 to 70
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women.
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3. Ranked fifth most common cancer in women in the United States
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4. Fourth most common cause of cancer death in women in the last 10 years in the
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United States and the most common fatal gynecologic cancer
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C. Causes
1. Exact etiology unknown
2. Pathogenesis
a. Heterogeneous disease, and cancer usually follow one of two patterns.
Type I cancers
(1) Generally low-grade and indolent tumors
(2) For example, low-grade serous, mucinous, endometroid, and clear cell
(3) KRAS, BRAF, ERBB2, PTEN, PIK3CA, and ARID1A mutations have been
associated with Type I cancer.
(4) Type I cancers usually begin as slow benign precursor lesions and gradu-
ally progress to malignant lesion.
Type II cancers
(1) Tend to be high-grade and aggressive cancers
(2) For example, high-grade serous, malignant mixed mesodermal, undiffer-
entiated cancers, and high-grade endometroid
(3) Cancers of this type are frequently associated with TP53 and BRCA 1 and
2 gene mutation.
(4) There are no clear precursor lesions, but some cancers like serous and
peritoneal cancer may start in fimbria of the fallopian tube and then
spread to ovaries and peritoneal cavity.
Some research demonstrates an association with USP36 gene overexpression

in ovarian cancer.
Quick HIT
D. Risk factors
Early menarche is associated
1. Early menarche and/or late menopause
with increased risk of ovarian
2. Genetic factors cancer.
a. Family history of breast or ovarian cancer
b. BRCA1 or BRCA 2 mutation
15% to 45% lifetime risk of developing cancer with BRCA 1 mutation
10% to 20% lifetime risk of developing cancer with BRCA 2 mutation
3. Other risk factors that are associated with increased risk of ovarian cancer
a. Nulliparity
Quick HIT
b. No breastfeeding Tubal ligation, hysterectomy,
and prophylactic bilateral
c. < 1 year oral contraceptive use salpingo-oophorectomy are
d. Endometriosis associated with a decreased
e. Obesity and polycystic ovary syndrome risk of ovarian cancer.
f. Most research suggests an association between hormone replacement therapy
and ovarian cancer.
E. History and physical examination

1. History
a. In early-stage ovarian cancer, patients are usually asymptomatic.
b. May present with vague and/or persistent symptoms in early stage
Fatigue
Abdominal pain or bloating
Diarrhea and/or constipation
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Urinary urgency or frequency
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Pelvic pain and/or vaginal bleeding
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c. Patient with advanced ovarian cancer may present with symptoms such as:
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Nausea, dyspepsia
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Early satiety, decreased appetite
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Increased abdominal girth
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Abdominal mass
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Enlarged and palpable lymph nodes in the inguinal, axillary, and supraclavicu-
e
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lar regions
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Shortness of breath caused by pleural effusion
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d
a. General
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Look for any lymphadenopathy, especially inguinal lymph nodes.
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b. Lungs
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Decreased breath sounds may indicate pleural effusion.
c. Abdomen
Assess for distension, ascites, and mass.
d. Pelvic examination
Assess for any pelvic or adnexal mass.
F. Differential diagnosis
1. Peritoneal tuberculosis
2. Benign ovarian mass
3. Nonovarian malignant disease
4. Irritable bowel syndrome
G. Diagnosis
1. Making diagnosis
a. Consider ovarian cancer in women older than 50 years with
Persistent or > 12 episodes/month with the following:
(1) Abdominal distension, pain, or pelvic pain
(2) Bloating, decreased appetite, or early satiety
(3) Presenting with UTI symptoms (especially frequency and urgency) and
no evidence of infection
Patients with three or more of these symptoms has have a significant increase
in the likelihood of ovarian cancer.
b. Women > 50 years with symptoms indicative of new onset irritable bowel
syndrome within the last 1 year
> 50% of women present with irritable bowel-like symptoms.
Often at an advanced stage when first diagnosed; currently, there is no effec-
tive screening test for ovarian cancer
2. Testing
a. The best initial imaging study for women with suspected ovarian cancer is
TVUS.
TVUS can assess the ovarian size, location, texture, and presence of a mass.
Malignancy is suspected with mass > 4 cm, thickened wall > 3 mm, necrosis,
and hemorrhage.
b. Order chest x-ray, CA-125, CBC, and liver function tests as part of the initial
evaluation. It is important to consider a gastrointestinal evaluation.
CA-125 is most useful in monitoring ovarian cancer after chemotherapy;
alone, it is not an accurate diagnostic test.
c. ACOG guidelines for management of postmenopausal women with suspected
ovarian cancer include:
Performing CA-125 level
(1) Serum CA-125 35 units/mL is considered abnormal, and next step in
management is to perform an ultrasound of abdomen and pelvis.
Breast and digital rectal examination.
Mammogram, if not done within the last 12 months.
Endometrial biopsy if the TVUS finding is abnormal.
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d. CT scan of abdomen and pelvis is performed for metastatic disease and
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recurrence.
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e. A surgical or laparoscopic biopsy is required for histopathologic evaluation for
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definitive diagnosis and staging.
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H. Staging
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1. International Federation of Gynecology and Obstetrics (FIGO) staging for ovarian
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cancer.
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a. Stage Itumor limited to ovaries
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b. Stage IItumor involving one or both ovaries with extension to pelvic tissues
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c. Stage IIItumor involving one or both ovaries with regional metastases
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d. Stage IVdistant metastases excluding peritoneal metastases
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I. Treatment
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1. Treatment recommendation by stage of ovarian cancer.
2. Chemotherapy for ovarian cancer usually includes a platinum-based drug and a
taxane-based drug.
a. Stage I
Treatment is conservative surgery.
(1) Laparoscopic salpingo-oophorectomy and staging with sparing of ovarian
tissue in normal ovary.
b. Stage II to IV
Treatment is a combination of surgery plus six cycles of chemotherapy.
c. Epithelial cell cancer requires more aggressive treatment and frequent posttreat-
ment follow-up.
Usually treated with early initiation of surgical and adjuvant chemotherapy.
J. Complications
1. Most common complications reported with ovarian cancer include:
a. Ascites
b. Pleural effusion
c. Bowel obstruction
K. Prognosis
1. Ovarian cancer associated with < 50% overall survival at 5 years.
L. Prevention
1. Very limited evidence about preventing ovarian cancer.
2. Dietary recommendations that have been studied include:
a. Diets low in fat and high in fiber for > 4 years may reduce the risk of ovarian
cancer in postmenopausal women.
b. Increased vegetable consumption (but not fruit consumption) associated with
lower risk of epithelial ovarian cancer.
c. Increased consumption of onions and garlic associated with reduced incidence
of ovarian cancer.
3. Oral contraceptive use may decrease risk for ovarian cancer but not associated with
large improvement in life expectancy.
4. Society of Gynecologic Oncologists recommend considering prophylactic bilateral
salpingo-oophorectomy for postmenopausal women at high risk of ovarian cancer
based on family history and the presence of BRCA1 or BRCA2 mutation.
M. Screening
1. Ovarian cancer screening is not routinely recommended.
2. American College of Physician does not recommend screening with bimanual pel-
vic examination in asymptomatic women.
3. Routine screening is not recommended with either CA-125 or ultrasound.
Uterine Cancer
A. Uterine cancer is a malignancy involving the uterine body.
C
B. The uterine cancers are divided into two broad categories.
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1. Adenocarcinoma of the endometrium (lining of the uterus)
m
a. Adenocarcinoma of the endometrium is the most common histologic type of
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uterine cancer.
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b. It is further divided into two histologic subcategories.
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Type I endometrial adenocarcinoma
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(1) Estrogen-dependent
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(2) Accounts for 80% of the uterine cancer
e
(3) Has a favorable prognosis and typically presents at an early stage with ab-
d
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normal uterine bleeding
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Type II endometrial adenocarcinoma
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(1) Estrogen-independent
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(2) More aggressive with poor prognosis
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(3) Accounts for 10% of the uterine cancer
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s
(4) Histologically classified as serous, clear cell, mucinous, squamous, transi-
tional cell, mesonephric, or undifferentiated
2. Uterine sarcoma
a. Accounts for 10% of the uterine cancer
b. Histopathology classified as
Nonepithelial neoplasms
(1) e.g., Leiomyosarcoma
Mixed epithelialnonepithelial tumors
(1) e.g., Adenosarcoma
C. Incidence and prevalence

1. 52,000 new cases estimated in 2013
2. The mean age at diagnosis is 60 years.
3. 2.6% lifetime risk for women in the United States of developing uterine cancer
4. Fourth most common cancer in women, but eighth most common cause of cancer-
related death in women Quick HIT
5. Distribution of stage at diagnosis
Uterine cancer is the most
a. Confined to uterus (68%) common gynecologic
b. Spread to regional organs and lymph nodes (20%) malignancy.
c. Distant metastases (8%)
D. Causes and risk factors

1. Exposure to unopposed endogenous and exogenous estrogen
2. Risk factors
a. Conditions leading to elevated estrogen exposure
Polycystic ovarian syndrome
Nulliparity or history of infertility
Long-term use of tamoxifen
b. Obesity
c. Hereditary nonpolyposis colorectal cancer (HNPCC) syndrome
d. Endometrial hyperplasia
e. Prior pelvic radiation
f. First-degree relative with endometrial cancer
g. HTN and diabetes
h. Unopposed estrogen
E. History and physical examination

1. History
a. 90% of women present with abnormal vaginal bleeding.
b. Crucial to obtain history regarding prolonged exposure to unopposed estrogen
and tamoxifen use
c. Important to get information on menstruation history
Including onset, duration, childbirths, and cessation
d. Obtain family history to assess any risk of HNPCC or first-degree relative with
endometrial cancer.
2. Obesity is the most common physical finding in women with uterine cancer.
s
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F. Differential diagnosis
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1. Vaginal atrophy
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2. Polyps
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3. Endometrial hyperplasia
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a
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4. Hormonal effect
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5. Cervical cancer
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6. Uterine fibroids
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G. Diagnosis
a
i
r
e
1. Either TVUS or endometrial biopsy is appropriate initial diagnostic testing.
G
a. In postmenopausal women, the diagnosis is usually made by endometrial biopsy.
n
o
m
H. Staging
m
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1. Endometrial carcinoma is staged according to the International Federation of Gy-
C
necology and Obstetrics (FIGO) TNM classification system.
a. Stage Itumor confined to uterus
b. Stage IItumor invades cervix, but does not extend beyond uterus
c. Stage IIIlocal and/or regional spread
d. Stage IVdistant metastasis
I. Treatment
1. First-line treatment for most women is surgical.
a. Total abdominal hysterectomy with bilateral salpingo-oophorectomy
Both therapeutic and prognostic as allows staging
2. Consider adjuvant platinum-based chemotherapy in patients with stage II or higher
stage of disease.
J. Prognosis
1. Prognosis is good for most patients with an overall 5-year survival rate of > 80%.
2. Prognosis for uterine sarcoma is worse.
K. Prevention and screening

1. United States Preventive Services Task Force has no specific guidelines on screen-
ing for endometrial cancer.
2. The American Cancer Society does not recommend routine screening of asymp-
tomatic women by ultrasound or endometrial biopsy.
Quick HIT
Cervical Cancer 90% of the women with uterine
cancer will present with ab-
A. Invasive carcinoma originating in the transformation zone of cervix normal vaginal bleeding.
B. Second most common cancer in women worldwide

C. Third most common cause of female cancer mortality
D. Types
1. SCC is the most frequent type, accounting for about 70% to 80% of cervical cancers.
Quick HIT
2. Adenocarcinoma accounts for about 10% to 15% of cervical cancers. Prognosis is good for most
patients with uterine cancer
E. Incidence with an overall 5-year survival
rate of > 80%.
1. Commonly affects women aged 30 to 45.
2. Most cases are in women who have never had a Pap smear or have not participated
regularly in a routine cytology screening program.
3. Decrease in the incidence of SCC as a result of screening capacity and availability of
human papilloma virus vaccine
4. Increasing incidence of adenocarcinoma
F. Causes
1. Persistent infection with oncogenic types of human papillomavirus (HPV), primar-
ily HPV-16, HPV-18, causing metaplastic changes in the epithelium of the transfor-
mation zone of the cervix.
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o
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G. Risk factors
m
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1. Persistent HPV infectiononcogenic strains cause progressive changes in the cer-
n
vical transformation zone.
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e
2. HIV infectionimmunosuppression inhibits regression of HPV infection, increas-
r
i
a
ing the risk of developing cervical intraepithelial neoplasia (CIN) III.
t
r
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c
3. Cigarette smokingassociated with SCC and high-grade CIN.
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4. DES Diethylstilbestrol exposure in uteromay increase risk of cervical cancer
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d
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H. Diagnosis
a
l
1. Most women are diagnosed as part of an evaluation of an abnormal Pap smear
C
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2. Colposcopydirected cervical biopsy
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3. Other methods include:
t
i
o
a. Cervical biopsy of grossly visible or palpable lesion
n
s
b. Cone biopsyif microinvasion or earlystage cervical carcinoma is suspected
I. Staging
1. International Federation of Gynecology and Obstetrics (FIGO) staging for cer-
vix uteri cancer is based on primary tumor, regional lymph nodes, and distant
metastasis.
J. Treatment
1. Treatment plan is based on clinical staging, including nodal status and histologic
biopsy result.
2. Treatment includes surgery, radiation, and chemotherapy.
K. Prognosis
1. High cure rates with surgery or chemoradiation in women with early-stage disease
(International Federation of Gynecology and Obstetrics [FIGO] stages I, stage II).
L. Prevention
1. HPV vaccine
Quadrivalent HPV recombinant vaccine against HPV types 6, 11, 16, and 18 in
younger women (aged 9 to 26) to prevent cervical cancer, vaginal cancer, vulvar
cancer, anal cancer, precancerous genital lesions, and genital warts (condyloma
acuminata)
2. Cervical cancer screening
United States Preventive Service Task Force (USPSTF), ACOG, and American Can-
cer Society have the following cervical cancer screening recommendations for im-
munocompetent women without prior cervical intraepithelial neoplasia (CIN) 2 or
worse or in utero diethylstilbestrol exposure.
a. Perform cervical cancer screening at age 21 to 65.
b. Do not start cervical cancer screening before age 21.
c. Stop screening after age 65 if consecutive normal testing for prior 10 years.
d. Cervical cancer screening not recommended if hysterectomy with removal of
cervix and no prior history of CIN 2 or worse
e. For women aged 30 to 65:
Combination of cytology screening plus HPV testing every 5 years
recommended
Cytology screening alone every 3 years is an alternative.
f. HPV testing alone not recommended
Vaginal Cancer
Quick HIT A. Primary cancer of the vagina accounts for approximately 3% of all malignant cancer
of the female genital tract.
SCC is the most frequent type
of cervical cancer, account- B. Types
ing for about 70% to 80%
of cervical cancers.
1. Most of the tumors are SCCs.
2. Melanoma, sarcoma, and adenocarcinoma are other rare histologic types of cancers.
s
n
3. Primary vaginal cancer is rare.
o
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4. Metastatic disease of the vagina is common.
t
i
d
n
a. Often arising from the endometrium, cervix, vulva, ovary, breast, rectum, and
o
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kidney
Quick HIT
l
a
c
C. Incidence
i
d
Most of the cases are in
e
M
women who have never had 1. Vaginal cancer accounts for 2,140 new cases and 790 deaths per year.
2. The average patient is between 43 and 60 years of age.
c
a Pap smear or have not par-
i
r
ticipated regularly in a routine 3. Vaginal carcinoma in situ incidence peaks between ages 70 and 79.
t
a
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cytology screening program.
r
e
G
D. Risk factors
n
1. Multiple lifetime sexual partners
o
m
2. Early age at first intercourse
m
3. HPV infection
o
C
Quick HIT 4.
5.
Tobacco use
Immune compromise
Women should have Pap 6. CIN
smear screening with HPV
testing every 5 years and E. Clinical presentation
if normal, may discontinue 1. A high percentage of patients are asymptomatic at the time of diagnosis and are di-
screening at age 65.
agnosed by abnormal cytology.
2. Most common presenting symptom is postmenopausal or postcoital vaginal
bleeding.
3. Other symptoms include:
a. Watery, blood-tinged, malodorous vaginal discharge
b. Urinary symptoms with hematuria
c. GI symptoms consisting of abdominal pain, constipation, and melena
d. Occasionally, may complain of pelvic pain.
F. Diagnosis
1. A careful visual inspection of the external genitalia and vaginal wall during the
withdrawal of a speculum is the most important tool in diagnosis.
2. Cervical and vaginal Pap smear should always be obtained.
3. Definitive diagnosis is accomplished by biopsy of the suspected lesion.

a. Biopsies can be obtained with either a biopsy punch (such as Keyes) or cervical
biopsy instrument (such as Tischler or Burke).
G. Staging
1. Vaginal cancers are staged according to the International Federation of Gynecology
and Obstetrics (FIGO) and TNM classification system. Quick HIT
a. Stage Itumor confined to vagina The majority of vaginal tumors
b. Stage IItumor invades paravaginal tissue, but does not extend to pelvic wall. are SCCs.
c. Stage IIIlocal and/or regional spread, with tumor extending to pelvic wall
d. Stage IVdistant metastasis
H. Treatment
1. Once the diagnosis of invasive malignancy is determined, the patient should be re-
ferred to gynecologic oncology for appropriate treatment. Quick HIT
2. There is no consensus as to the appropriate management of vaginal carcinoma. Vaginal carcinoma in situ inci-
3. Treatment usually includes combinations of surgery, radiation, and chemotherapy, dence peaks at age 70 to 79.
with more aggressive treatment for higher-stage disease.
I. Prognosis
1. Five-year survival for vaginal cancer is 67% for stage I disease and 20% for stage IV
disease. Quick HIT
J. Prevention and screening Treatment for vaginal cancers
1. Vaginal malignancies are quite rare, so screening asymptomatic women is not cost- usually includes combinations
effective and not recommended. of surgery, radiation, and che-
motherapy, with more aggres-
C
o
sive treatment for higher-stage
m
disease.
m
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End o c rine D is e a s e
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Diabetes Mellitus (DM)
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1. General principles in older adults
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a. DM is common in older adults and is associated with increased morbidity and
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mortality, reduced functional status, and a higher rate of institutionalization.
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b. > 25% of the US population over age 65 has DM.
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c. Individuals older than 65 years tend to have a longer duration of diabetes and
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higher rates of complications.
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d. Some older adults have had DM type 1 for many years and reach 65 with signifi-
cant end-organ complications. Most develop type 2 diabetes and insulin resis-
tance in adulthood.
e. Diabetes care for active, healthy, and cognitively intact older adults with a sig-
nificant life expectancy has goals similar to those of younger adults.
f. Older, frailer individuals may be better served by less aggressive care to avoid the
risk of side effects and hypoglycemia.
2. Pathogenesis
a. Most geriatric patients with diagnosed DM have type 2 DM.
b. Type 1 DM is an autoimmune disease in which the immune system mediates the
destruction of -cells. In type 1, there is an absolute deficiency of insulin.
c. Type 2 DM results from a combination of insulin resistance and an inadequate
compensatory insulin secretory response.
Early in the course of type 2 DM, insulin levels increase as the pancreas tries
to overcome insulin resistance and maintain euglycemia. Eventually, -cells
fail, and insulin production decreases.
In type 2 DM, insulin levels can be high, normal, or low.
Risk factors include obesity, genetics, and age.
3. The American Diabetes Association (ADA) recommends screening all adults 45

Quick HIT years and older every 1 to 3 years with a FPG, A1C, or OGTT.
a. Screening in the elderly should be tempered by clinical status. Healthy individu-
Although common in the als in their sixties would likely benefit from screening, whereas those in their
elderly, DM is not a normal nineties with dementia would be unlikely to benefit.
consequence of aging, nor is it
a benign disease. It is linked to B. Diagnosis
higher mortality, reduced func- 1. Criteria for the diagnosis of diabetes
tional status, and an increased
a. A1C 6.5%; or
risk of institutionalization.
b. Fasting plasma glucose 126 mg/dL (7.0 mmol/L) on two occasions. Fasting is
defined as no caloric intake for at least 8 hours; or
c. Two-hour plasma glucose 200 mg/dL (11.1 mmol/L) during an OGTT (with 75
g anhydrous glucose dissolved in water); or
d. In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a
Quick HIT random plasma glucose 200 mg/dL (11.1 mmol/L).
2. Impaired glucose tolerance:
Type 2 DM is characterized a. A1C: 5.7% to 6.4%; or
by insulin resistance and an
inability of the pancreas to se- b. Fasting plasma glucose: 110 to 125 mg/dL; or
crete sufficient insulin to main- c. Two-hour PG: 140 to 200 mg/dL
tain normal glucose levels.
C. Clinical presentation
1. Asymptomatic patients: DM type 2 is often diagnosed by a screening urinalysis or
blood sugar measurement. Over time, DM tends to progress to overt symptoms.
2. Symptomatic patients may present with polyuria, polydipsia, polyphagia, fatigue,
blurred vision, and weight loss. Early on, symptoms can be vague and nonspecific
(Table 4-40).
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CLINICAL PEARL 4-29
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Quick HIT
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DM can be diagnosed using several different measures.
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The diagnostic criteria for DM
1. Hemoglobin A1c value > 6.5%.
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2. Fasting glucose > 126 mg/dLon more than one occasion.
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are the same for adults of all
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3. Two-hour glucose value > 200 mg/dLafter ingesting a 75 g glucose challenge as part of a Glucose Toler-
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ance Test.
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4. Random glucose > 200 mg/dLin a patient with classic symptoms of polydipsia, polyuria, or polyphagia.
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TABLE 4-40 Symptoms of Diabetes Mellitus
Asymptomatic patientsdetected by screening
Symptoms and presentation of significant hyperglycemia may include:
Polyuria
Polydipsia
Polyphagia
Blurred vision
Hyperosmolar hyperglycemic state
Diabetic ketoacidosis (DKA) (less common than in DM type 1)
Symptoms associated with chronic hyperglycemia may include:
Peripheral neuropathy
Frequent infections
Visual impairment
Sexual dysfunction
Bowel or bladder dysfunction
Cardiovascular dysfunction (e.g., chest pain)
3. Some patients present with diabetic complications such as myocardial ischemia,

stroke, intermittent claudication, impotence, peripheral neuropathy, proteinuria, or
retinopathy. Quick HIT
Early in the course of the
D. Treatment disease, type 2 DM symptoms
1. General principles develop gradually and tend
a. Control of hyperglycemia is a cornerstone of diabetes treatment. Good glycemic to be vague and nonspecific.
control both reduces the risk of developing microvascular complications and Sometimes, only after treat-
ment do patients realize they
slows progression.
were not feeling well.
b. BP control and lipid control are important in preventing end-organ complica-
tions of diabetes, particular macrovascular disease.
c. Hemoglobin A1C targets
Healthy older adults with an extended life expectancy: HbA1C < 7%.
Older patients with limited life expectancy (e.g., < 5 years) or high risk of hy-
poglycemia: HbA1C < 8%.
Tighter glycemic control in older adults has been associated with increased
rates of hypoglycemia and mortality.
d. Glycemic control targets in hospitalized patients
In noncritically ill patients, the ADA recommends a fasting (premeal) glucose
target of 90 to 140 mg/dL and a random glucose target of < 180 mg/dL.
The ADA recommends glucose levels between 140 and 180 mg/dL in both
medical and surgical ICU patients.
2. Nonpharmacologic treatments
a. Diet and exercise
Diet and exercise should be an integral component of diabetes treatment.
ADA and American Heart Association diet recommendations include:
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(1) Limiting saturated fat (< 7% of total calories)
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(2) Minimizing trans fats
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(3) Limiting cholesterol intake (< 200 mg/day)
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(4) If overweight, try to lose 5% of body weight.
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It is important to recognize that for some malnourished or ill older adults, re-
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strictive diets may be especially difficult or even harmful.
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If diet and exercise do not achieve the target A1C, then initiate drug therapy.
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3. Pharmacologic therapynoninsulin therapies
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a. Biguanides
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Most guidelines recommend metformin as first-line oral therapy for type 2
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DM.
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Decreases HbA1C approximately 1.5%
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It is contraindicated in patients with renal insufficiency (serum creatinine
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> 1.5 mg/dL or creatinine clearance < 30 mL/min).
Consider holding metformin if a patient is ill and at risk for dehydration or
undergoing a procedure with contrast.
b. Sulfonylureas (SU)
Usually well tolerated: short-acting SUs such as glipizide preferred.
Stimulate pancreas to produce more insulin
Side effects: hypoglycemia and weight gain
CLINICAL PEARL 4-30

The overall goals of diabetes management in healthy older adults are similar to those of younger adults and
include managing both hyperglycemia and risk factors. However, in older adults, the risk of hypoglycemia and
hypotension, associated comorbidities, and polypharmacy should be incorporated into management. In addi-
tion to being more prone to hypoglycemia, low blood sugars in older individuals are more likely to lead to neu-
roglycemic symptoms such as impaired cognition, weakness, and dizziness. Frail older adults are particularly
at risk for adverse events such as falls and fractures. Accepting lower levels of glucose control may be more
appropriate in these individuals.
Decrease HbA1C approximately 1% to 2%

Starting doses should be low, typically half those used for younger patients.
c. -Glucosidase inhibitors
Acarbose (Precose) and miglitol (Glyset)
Inhibits the absorption of carbohydrates in the gut and decreases postprandial
hyperglycemia.
Side effects: GI upset (diarrhea, abdominal cramping, and flatulence)
May be used with sulfonylurea, metformin, or insulin. Not typically used as
monotherapy. Do not cause hypoglycemia if used alone, but increase the risk
of hypoglycemia when used with a SU.
d. Thiazolidinediones
Rosiglitazone (Avandia) and pioglitazone (Actos)
Pioglitazone usually preferred because of the concern of an increased risk of
CVD with rosiglitazone
Act as insulin sensitizers (reduce insulin resistance)
Site of action: muscle and fat
Side effects: hepatotoxicity, fluid retention, increased risk for bladder cancer
and HF; contraindicated in class III and IV HF
e. Meglitinides
Repaglinide and nateglinide
Are short-acting insulin secretagogues that can decrease postprandial
hyperglycemia
There is limited experience with these drugs in older patients.
f. Incretin modulators
Include glucagon-like peptide-1 (GLP-1) analogs and dipeptidyl peptidase-4
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(DPP-4) inhibitors
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Exenatide and liraglutide are the GLP-1 analogs available in the United
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States.
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Sitagliptin, saxagliptin, and linagliptin are the DPP-4 inhibitors available in
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the United States.
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There is little clinical experience with these medications in older adults.
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Expensive, usually add-on drugs
4. Pharmacologic therapyinsulin
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a. Methods of administration
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Self-administered by SC injections in abdomen, buttocks, arm, and leg
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Given IV for emergency ketoacidosis
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b. Insulin is required in all patients with type 1 diabetes, and in many patients with
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moderate or severe type 2 diabetes.
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c. Different types of insulin (Table 4-41)
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Longer-acting insulins
(1) Glargine (daily) and neutral protamine Hagedorn (NPH) (1 to 2 times/
day) to provide basal insulin for control of fasting glucose levels
TABLE 4-41 Types of Insulin

Type Onset Duration Comments
Human insulin lispro 15 min 4 hr

Regular insulin 3060 min 46 hr Only type that can be given
intravenously
NPH/lente insulin 24 hr 1018 hr Most commonly used
Ultralente 610 hr 1824 hr
70/30 mixture 30 min 1016 hr 70% NPH 30% regular
Glargine 34 hr 24 hr Often given at bedtime
Short-acting insulins
(1) Lispro and regular before meals to provide bolus insulin to control post-
prandial glucose levels Quick HIT
(2) Insulin mixtures such as 70/30 (70% NPH and 30% regular) may help Therapeutic goals for geriatric
simplify insulin regimens for many patients. patients should be tempered
d. For many older patients with type 2 diabetes, once-daily long-acting insulin at by life expectancy for those in
nighttime, often in addition to metformin, may be a reasonable starting regimen. whom the risks for tight con-
5. Monitoring trol outweigh the benefits.
a. Patients with diabetes need close follow-up and monitoring including the
following:
BP and BMI measurements at each visit
Annual comprehensive foot examination, including monofilament testing
Initial screen for PVD by checking pulses and asking about claudication
A1C twice per year in patients with stable glycemic control; every 3 months in
those in poor control Quick HIT
Dilated retinal examination and visual acuity annually Tight glucose control and nor-
Lipid profiles every 1 to 2 years malization of hemoglobin A1C
Annual test for microalbuminuria and serum creatinine values are associated with
increased rates of hypoglyce-
Updated vaccinations, including annual flu vaccine
mia and mortality in geriatric
patients.
Acute Complications of DM
A. Diabetic ketoacidosis (DKA)
1. General principles
a. DKA is an acute and life-threatening medical emergency, and although more
closely associated with type 1 DM, it can occur in type 2 DM.
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2. Pathogenesis
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a. Insulin deficiency leads to decreased glucose metabolism, resulting in increased
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lipolysis, free fatty acid metabolism, and subsequent ketoacidosis.
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3. Precipitating factors
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a. Any type of stress or infection (e.g., pneumonia, MI, stroke, sepsis), inadequate
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administration of insulin
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a. Polyuria, polydipsia, polyphagia
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b. Abdominal pain, nausea, and vomiting
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c. Fatigue
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d. Dyspnea
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f. Acidosis, dehydration
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g. Mental status alteration and coma may be present.
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h. Fruity (acetone) breath odor
5. Diagnosis
a. DKA is characterized by:
Serum glucose level > 250 mg/dL (13.9 mmol/L)
Serum bicarbonate level < 18 mEq/L (18 mmol/L)
Blood pH level < 7.3
Anion gap > 10
CLINICAL PEARL 4-31

Patients may experience limited dexterity or eyesight as they advance in age, making insulin use a challenge.
Simplifying the insulin regimen can be achieved by utilizing pens that may dial in the dosage and by utilizing
regimens that limit the need for more than one insulin or mixing insulins. (e.g. 70/30 premix of NPH and regu-
lar). Although this may not be ideal for young patients who are trying to be tightly controlled to prevent long-
term complications, for the geriatric patient this may make insulin use achievable. Also, the use of a single
daily dose of a long-acting insulin can be combined with oral therapy, which may allow geriatric patients to
meet realistic goals.
Elevated serum and urine ketone levels

Dehydration
6. Treatment
a. Insulin
Give insulin immediately after diagnosis is established.
Bolus IV dose of 0.1 unit/kg of regular insulin, followed by an infusion of 0.1
unit/kg per hour.
Make sure that the patient is not hypokalemic before giving insulin.
Continue insulin until the anion gap closes and metabolic acidosis is
corrected.
b. Fluid replacement
Start fluids (normal saline) immediately.
Add 5% glucose once the blood glucose reaches 250 mg/dL to prevent
Quick HIT hypoglycemia.
DKA is far less common in
c. Replace potassium
those with type 2 DM, but can Initiate within 1 to 2 hours of starting insulin.
occur. Ensure adequate renal function (urine output) before administering potassium
Monitor K, Mg, and phosphate levels closely.
B. Hyperglycemic hyperosmolar state (HHS)

1. General principles
a. HHS occurs predominantly in older patients with type 2 DM.
b. It results in marked hyperglycemia (often glucose > 600 mg/dL), hyperosmolar-
ity, severe volume depletion, and associated AKI.
c. Patients typically have hyperglycemia and osmotic diuresis for several weeks,
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leading to marked dehydration and altered mental status.
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2. Pathogenesis
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a. Low insulin levels lead to hyperglycemia.
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b. Severe hyperglycemia causes an osmotic diuresis, leading to dehydration.
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3. Precipitating factors include serious infection, stroke, and MI.
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a. Thirst, polyuria
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b. Signs of extreme dehydration and volume depletion
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c. CNS findings and focal neurologic signs
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d. Lethargy and confusion
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5. Diagnosis (Table 4-42)
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a. Hyperglycemia > 600 mg/dL
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b. Hyperosmolarity > 320 mOsm/kg
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c. Serum pH > 7.3
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d. BUN is usually elevated.
6. Treatment
a. Fluid replacement
Intravenous fluid replacement is most important.
One liter NS in the first hour, followed by another liter in the next 2 hours
Switch to 1/2 NS once the patient stabilizes.
TABLE 4-42 Diagnostic Criteria for Hyperosmolar Hyperglycemic State

Plasma glucose > 600 mg/dL(33.3 mmol/L)
Absence of ketoacidosis pH > 7.3; bicarbonate > 18 mEq/L
Effective serum osmolality > 320 mOsm/kg
Anion gap Variable
Alteration in sensorium Stupor/coma
Dehydration Severe
When glucose levels reach 250 mg/dL, add 5% glucose as in DKA.

In patients with cardiac disease or renal insufficiency, be careful to avoid
volume overload. Quick HIT
InsulinAn initial bolus of 5 to 10 units IV, followed by a low-dose infusion HHS is associated with a
(2 to 4 units per hour) is usually sufficient. marked degree of dehydra-
tiona fluid deficit of several
Chronic Complications of DM liters. Rehydration is a key
component of therapy, along
A. Macrovascular complications with insulin use and electro-
1. These include MI, stroke, and PVD. lyte management.
2. Cardiovascular disease (CVD) is the major cause of excess mortality in older adults
with diabetes.
3. Signs and symptoms suggestive of PVD include cold feet, atrophy of the subcutane-
ous tissue, shiny shins, hair loss, and decreased or absent pulses.
a. An ABI is indicated when history and physical suggest vascular insufficiency.
4. Unless there are special circumstances that make it harmful, the ADA recommends
aspirin, 81 to 325 mg, for patients with diabetes to lower the risk of MI and stroke.
5. Diabetes should be viewed as a CAD equivalent. Lowering the LDL cholesterol
reduces the risk of stroke and heart attack. Older adults with normal or nearly nor-
mal LDL cholesterol and low HDL should be considered for medication in addition
to nutrition education.
a. If no overt CAD, statin therapy to reduce LDL < 100 mg/dL
b. If overt disease, target LDL at 70 mg/dL. Using high-dose statins is an option.
c. Triglyceride goal < 150 mg/dL.
d. Combined therapy of a statin with a fibrate or niacin is associated with an in-
creased risk of abnormal liver enzyme and myositis. There is no clinical evi-
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and so combination therapy is not generally recommended.
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6. Increased exercise and weight loss also improve cardiovascular health.
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7. BP management is also important for optimizing outcomes and reducing macrovas-
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cular complications. Because older adults may have less tolerance for BP reduction,
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medication should be started at about half the dose used for a younger adult and
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adjusted slowly upward as tolerated.
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a. Begin therapy with an ACEI or ARB.
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b. New ADA guidelines for older adults treating to < 130/70 is not recommended.
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Targeting a SBP < 130 has not been show to improve CV mortality and is associ-
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ated with increased morbidity.
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8. Regardless of age, patients benefit from smoking cessation.
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B. Microvascular complications
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1. Associated with both the duration and the severity of disease
2. Good glycemic control both reduces the risk of developing microvascular compli-
cations and slows disease progression.
3. Although macrovascular disease accounts for most of the excess mortality seen
in diabetes, microvascular disease can cause significant morbidity and functional
impairment.
4. Diabetic retinopathy
a. Diabetes is a leading cause of blindness in the United States.
b. Early detection and treatment of proliferative retinopathy with laser photocoagu-
lation decreases the risk of visual loss by > 50% at 6 years.
c. The ADA currently recommends a dilated eye exam by an ophthalmologist at
diagnosis, with regular follow-up examinations every 1 to 3 years, depending on
the individual patients risk factors and initial examination results.
5. Diabetic neuropathy
a. Diabetic neuropathy is generally classified by the types of nerves that are affected.
b. The most common type of neuropathy is sensory distal symmetric polyneuropa-
thy, or glove-and-stocking neuropathy. May also cause a mononeuropathy
such as VI nerve palsy.
c. Common symptoms include numbness and burning pain of the hands and feet.
May cause severe burning at night that is often difficult to tolerate. Treatment
Quick HIT is with gabapentin, tricyclic antidepressants, or pregabalin.
Maximizing glycemic control d. Annual screening with a 10-g monofilament at the plantar aspect of the hallux
may reduce neuropathy and metatarsal joint is recommended.
symptoms. e. Autonomic diabetic neuropathies include diabetic gastroparesis, which can cause
nausea and vomiting after eating as a result of impaired gastric emptying, as well
as erectile dysfunction and neurogenic bladder.
f. Foot ulceration is a common complication of DM and is usually caused by neu-
ropathy and vascular insufficiency. Patients should be counseled regarding foot
Quick HIT care and to examine their feet daily.
6. Diabetic nephropathy
The classic neuropathy as- a. Diabetic nephropathy is the most common cause of ESRD and is strongly associ-
sociated with diabetes is the
distal stocking-glove neu- ated with cardiovascular mortality.
ropathy that affects the feet b. Diabetic nephropathy is also more common in older diabetic patients than in
first and marches up the leg. younger patients; however, the association between severity of nephropathy and
mortality appears to be weaker in older adults.
c. Compared with other common causes of kidney disease, diabetic nephropathy
leads to more albuminuria.
This is reflected in the diagnostic criteria for diabetic nephropathy, which is
Quick HIT albuminuria > 300 mg/day in a patient with known diabetes without other po-
tential causes of albuminuria.
Annual screening for diabetic d. The ADA recommends annual screening for microalbuminuria, which can be
complications should include
monofilament sensory testing
accomplished by measuring the urinary albumin-to-creatinine ratio using a spot
of the lower extremities, urine urine specimen.
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testing for microalbuminuria, e. Limiting protein intake to < 0.8 g/kg per day may help delay progression of
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and ophthalmologic examina- CKD.
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tion for retinopathy. f. Those with microalbuminuria should be on an ACEI or ARB. These medications
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decrease the rate of disease progression. Although they can induce kidney failure
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ing therapy, with each dose increase and at least annually.
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Quick HIT
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Geriatric Syndromes in DM
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Tight blood glucose can lower Geriatric syndromes are common, serious conditions in older adults that often present
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the risk of microvascular com-
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plications. The benefit of tight similarly in different patients despite disparate causes. DM increases the risk of many ge-
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riatric syndromes, including cognitive impairment, depression, urinary incontinence, and
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control should be balanced
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against the risk and should be falls, all resulting in functional decline.
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viewed in the context of the
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patients general health and A. Cognitive impairment
functional status. 1. In epidemiologic studies, DM increases the subsequent risk of Alzheimer dementia
by 50% to 100% and vascular dementia by 100% to 200%.
B. Depression
1. Depression is associated with adverse outcomes, including poor health-related
Quick HIT quality of life, functional decline, and death.
2. Diabetes and depression commonly co-exist.
DM increases the risk of many a. 30% of older adults with diabetes report depressive symptoms, and 5% to 10% of
geriatric syndromes, including
cognitive impairment, depres-
older adults with diabetes meet the criteria for major depressive disorder.
sion, urinary incontinence, b. The American Geriatrics Society (AGS) recommends screening for depression
falls, and functional decline. with a validated instrument.
C. Urinary incontinence
1. Urinary incontinence is very common in older women with diabetes.
2. Studies suggest a strong relationship between DM and urinary incontinence, with
diabetes associated with a three-fold increase in the prevalence of urge inconti-
nence and a two-fold increase in the prevalence of stress incontinence.
3. Body mass index appears to be an important risk factor for incontinence; weight
loss reduces the incidence of new incontinence.
D. Falls and fractures

1. Falls are common in older adults and associated with increased morbidity and
mortality.
2. Insulin use, poor vision, and peripheral neuropathy increase the risk of falls.
3. The AGS recommends screening for falls risk in older adults with diabetes to iden-
tify potentially modifiable risk factors for falls and fractures.
Thyroid Disorders
Hypothyroidism
1. A common disease of older adults occurring in about 10% of females and 2% of
males > 60 years.
a. Types
Primary hypothyroidism: failure of the thyroid gland to produce sufficient thy-
roid hormone (most common type of hypothyroidism)
Secondary hypothyroidism: pituitary disease with deficiency of TSH
Tertiary hypothyroidism: hypothalamic disease with deficiency of TRH
2. Thyroid hormone deficiency can affect virtually all organ systems.
a. The onset of symptoms is often insidious, subtle, and atypical in the older adult.
A high index of suspicion and early testing is useful for detecting hypothyroid-
ism in the older adult.
b. In mild cases, the symptoms may be nonspecific and attributable to other causes
or to the aging process itself.
c. Myxedema (puffiness) of face, hands, and vocal cords caused by subcutaneous
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accumulation of mucopolysaccharide-rich material resulting in a nonpitting
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edema. It is a rare condition and usually develops only after years of untreated
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hypothyroidism.
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B. Causes
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1. Primary hypothyroidism: 95% of all cases
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a. Autoimmune thyroiditis
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b. Iatrogenic
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Surgical
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Prior hemithyroidectomy/thyroidectomy Hypothyroidism is most com-
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Radioablation: common following treatment for Graves disease monly caused by autoimmune
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disease, but can also com-
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History of prior radiation therapy to head and neck
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monly occur from surgical or
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c. Medications
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radioactive ablative therapy or
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Iodine-containing radiographic contrast agents medications.
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Lithium
Amiodarone (up to 15% of patients)
Methimazole
d. Thyroid infiltration
Sarcoidosis Quick HIT
Hemachromatosis
A low TSH and low level of
Scleroderma thyroid hormone indicates
2. Secondary hypothyroidism: caused by pituitary disease, TSH deficiency either secondary or tertiary
3. Tertiary hypothyroidism: caused by hypothalamic disease, TRH deficiency thyroid disease.
a. Both secondary and tertiary hypothyroidism are associated with a low free T4
and a low TSH.
C. Clinical presentation (Table 4-43)

1. Symptoms
a. May be asymptomatic, with diagnosis made solely on the basis of laboratory
findings
b. Fatigue and weakness: common
c. Cold intolerance
d. Muscle weakness and cramps, arthralgia
TABLE 4-43 Signs and Symptoms of Hypothyroidism

Symptoms Signs
Fatigue Dry skin

Weakness Brittle hair
Cold intolerance Edema/puffy face
Muscles aches or cramps Hypothermia
Joint pain Bradycardia
Lethargy Ascites/pleural effusion
Mental slowness Carpal tunnel syndrome
Constipation Slowed relaxation phase of reflexes
Depression Deepened voice
e. Lethargy
f. Constipation
g. Weight gain
h. Dry coarse skin (ichthyosis), hair loss
i. Depression
j. Cognitive impairment. In rare cases, a cause of reversible dementia.
2. Signs
a. General: hypothermia, hypoventilation, deepened voice
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b. Skin: dry skin, coarse brittle hair
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c. HEENT: puffiness of face and eyelids, periorbital edema, loss of lateral portion of
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eyebrow, may have palpable thyroid
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d. Heart: bradycardia, cardiomegaly, pericardial effusion
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e. Lungs: hypoventilation, pleural effusion
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f. Extremities: nonpitting edema (pretibial), carpal tunnel syndrome
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g. Neuro: increased relaxation phase of deep tendon reflexes (slow return phase),
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peripheral neuropathies, cerebellar ataxia
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D. Diagnosis (Figure 4-36)
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1. Primary hypothyroidism
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a. Elevated (TSH)
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TSH is the most sensitive test for detecting hypothyroidism.
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b. Decreased serum-free thyroxine (FT4)
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Measurement is more cost-effective than previously used measurements of to-
tal T4 and T3.
2. Subclinical hypothyroidism
a. Defined as an elevated TSH with a normal free T4
3. Secondary and tertiary hypothyroidism
a. Low serum TSH
Quick HIT b. Decreased serum FT4, or low-normal levels with symptoms
Subclinical hypothyroidism
4. Other laboratory tests
is an elevation of TSH with a. Increased antimicrosomal antibodies (Hashimoto thyroiditis)
normal T3 and T4 along with b. Elevated LDL and decreased HDL
minimal or no symptoms. c. Anemia: mild normocytic anemia
5. Euthyroid sick syndrome
a. Abnormal tests in the setting of a nonthyroidal illness
b. Typical findings are low T3, slightly reduced or normal range TSH, and a free T4
Quick HIT that is in the normal range.

c. In severe disease, findings may be low T4, low T3, reduced TSH, and a free T4 in
TSH is the most sensitive indi- the normal range or slightly low.
cator of hypothyroidism. d. General consensus is that these patients are euthyroid and that treatment is di-
rected at the underlying disease.
S e rum TS H a nd Fre e Thyroxine
TS H TS H TS H norma l TS H norma l
Fre e T4 Fre e T4 norma l Fre e T4 Fre e T4 norma l
P rima ry Mild or Ce ntra l hypothyroidis m Norma l

hypothyroidis m s ubclinica l Nonthyroida l illne s s
hypothyroidis m Drug e ffe ct
FIGURE
4 -3 6 TSH Interpretation in Hypothyroidism
E. Treatment: The most important reasons to treat hypothyroidism are to relieve

symptoms and to avoid progression to myxedema.
1. Most patients with hypothyroidism will require lifelong thyroid hormone therapy.
2. Levothyroxine is the treatment of choice.
3. Older patients and patients with CAD require a lower starting dose, generally 25 or
50 mcg daily. Quick HIT
C
4. Monitor TSH levels at 4 to 8 weeks after starting treatment, and adjust doses until
o
Levothyroxine is the medica-
m
normalization of TSH: then repeat TSH every 6 months after dose is stabilized, then
m
tion of choice for treating
o
annually. hypothyroidism and is gener-
n
5. Thyroid hormone is generally taken in the morning, 30 minutes ally continued for the life of the
G
e
before eating. patient.
r
i
a
6. Calcium and iron supplements should not be taken within 4 hours of taking levo-
t
r
i
c
thyroxine (decrease absorption).
M
e
Hyperthyroidism
d
i
c
a
l
1. Prevalence is about 2% in the elderly; about 15% of all cases occur in those age
C
o
> 60.
n
d
i
2. Because it can mimic other diseases, a high index of suspicion is needed not to
t
i
o
overlook hyperthyroidism.
n
s
a. Few present with classic features of tachycardia, palpitation, exophthalmos, heat
intolerance, and weight loss with an increased appetite.
b. Cardiac abnormalities and weight loss are common presenting symptoms.
3. May present with an apathetic form with placid facies, depression, lethargy,
weakness, weight loss, and arrhythmias in the absence of an exophthalmos and an
enlarged thyroid gland.
4. Description
a. Hyperthyroidism: increased synthesis and secretion of thyroid hormone
b. Subclinical hyperthyroidism: low serum levels of TSH, but free T4 and T3 levels
within normal range
c. Thyrotoxicosis: clinical state resulting from inappropriately high thyroid hor-
mone activity
d. Thyroid storm (thyrotoxic crisis): life-threatening thyrotoxicosis with multior-
gan dysfunction
Quick HIT
e. Isolated finding of a high T3 is known as T3 toxicosis Because the symptoms are
both variable and often atypi-
May be present in up to 10% of elderly hyperthyroid patients cal, a high index of suspicion
Usually caused by a hyperfunctioning nodule is needed so as not to overlook
Presents with low free T4 and TSH. If T3 is not measured, it can be mistaken hyperthyroidism in the elderly.
for hypothyroidism.
B. Causes
Quick HIT 1. Graves disease
a. It is the most common cause: 80%
Hyperthyroidism is most com- b. An autoimmune disorder: A thyroid-stimulating immunoglobulin (IgG) binds to
monly caused by, Graves dis- the TSH receptors.
ease, an autoimmune disease, 2. Multinodular toxic goiter: 15% of cases
where IgG is produced that a. More common in elderly patients
stimulates TSH receptors and
excess T4. b. Hyperfunctioning areas produce high T3 and T4
3. Toxic thyroid adenoma: single nodule that produces excess thyroid hormone
4. Less common causes
a. Painful subacute thyroiditis: transient hyperthyroidism
b. Iodine-induced hyperthyroidism
c. Iatrogenic or factitious excess intake of exogenous thyroid hormone
C. Clinical presentation
1. In older adults, may present with atypical instead of classic symptoms
2. Cardiac symptoms are the most frequent manifestation of hyperthyroidism in the
elderly.
a. Common cardiac findings include atrial arrhythmia, CHF, and angina.
b. Symptoms may be masked by comorbid conditions or medications.
Someone taking -blockers for hypertension may not exhibit tachycardia or
tremor.
3. Other symptoms include:
a. Fatigue
b. Weight loss
s
c. Heat intolerance, excessive sweating
n
o
d. Palpitations, shortness of breath
i
t
i
d
e. Diarrhea, frequent defecation
n
o
C
f. Hand tremor
g. Depression: more common in older adults
l
a
c
h. Nervousness, anxiety, poor concentration
i
d
e
M
i. Symptoms of Graves ophthalmopathy, such as eye irritation, pain, or eyelid
swelling
c
i
r
4. Signs
t
a
i
a. General: check for weight loss, systolic hypertension.
r
e
G
b. Skin: warm, moist skin, hair loss, hair thinning
n
c. Eyes: lid retraction, lid lag, stare
o
m
Additional findings in Graves disease: exophthalmos (proptosis), periorbital
m
edema, conjunctival erythema and edema (chemosis), incomplete eyelid clo-
o
C
sure with cornea still visible (may lead to corneal ulceration and vision loss).
Older individuals with Graves have fewer ophthalmologic findings.
d. Neck: goiter, diffusely enlarged thyroid, check for bruit
Quick HIT Older patients with Graves are less likely to have an enlarged thyroid.
AF is a common finding e. Heart: tachycardia, arrhythmia, AF, HF
in older individuals with f. Lungs: rales may suggest HF
hyperthyroidism. g. Extremities: muscle wasting
h. Neuro: tremor, muscle weakness, hyperactive DTRs
CLINICAL PEARL 4-32

When a solitary nodule is found on clinical examination, a fine needle aspirate is indicated to determine
whether the lesion is benign or malignant. If the aspirate is malignant, surgery is indicated. If benign, monitor-
ing and close follow-up is warranted.
In cases where the nodule aspirate findings are nondiagnostic, a thyroid scan should be performed to de-
termine where the nodule is hot or hyperfunctioning, or cold and hypo or nonfunctioning. Cold nodules are
more likely to be malignant and, if found, should be removed surgically. Hot nodules can be followed clini-
cally with periodic thyroid function testing to evaluate for hyperthyroidism.
Low TSH
Fre e T4
Low Norma l Hig h
S e c o ndary hypo thyro idis m Primary hype rthyro idis m
T3
Low/norma l Hig h
S ubclinic al hype rthyro idis m Primary hype rthyro idis m

or
No n-thyro idal illne s s
(in appro priate clinic al s e tting )
Thyro id s c an
FIGURE
4 -3 7 Interpretation of Low TSH
D. Diagnosis
1. Serum TSH level
a. Initial test of choice
C
b. TSH is low; if normal or high, hyperthyroidism is unlikely (Figure 4-37).
o
m
2. Serum free T4: next test
m
o
a. Free T4 should be elevated.
n
b. Normal or low serum free T4 with a suppressed serum TSH raises the possibility
G
e
of T3 toxicosis and warrants measuring serum T3 by radioimmunoassay.
r
i
a
3. Thyroid autoantibodies suggest the diagnosis of Graves disease.
t
r
i
c
4. Thyroid scan for radioiodine uptake.
M
a. Diffuse high uptake seen in Graves disease.
e
d
b. Single or multiple foci of increased uptake with remainder of gland with de-
i
c
a
creased uptake suggest toxic thyroid adenoma or toxic multinodular goiter.
l
C
c. Low or absent uptake seen with thyroiditis or a nonthyroidal source of thyroid
o
n
hormone.
d
i
t
5. Nonspecific laboratory findings
i
o
n
a. Anemia
s
b. Granulocytosis, lymphocytosis
c. Hypercalcemia
d. Transaminase and/or alkaline phosphatase elevation
E. Treatment
1. Treatment should be directed at the specific cause of the hyperthyroid state.
2. -Blockers.
a. Consider -blockers for patients with symptomatic thyrotoxicosis (strong
recommendation).
b. Use long-acting -blockers such as long-acting propranolol, metoprolol, nadolol,
or atenolol.
c. Although -blockers help with tremor, tachycardia, sweating, and palpitations,
they do not alter the natural history of the underlying disease.
3. Antithyroid medications
a. Thioamides: methimazole and propylthiouracil (PTU)
b. Side effects make these medications a less popular treatment choice.
Agranulocytosis, which occurs in < 0.5%, is a major adverse reaction that can
be fatal.
Rash, arthralgia, and myalgia are other potential side effects.
c. Because these medications act quickly they are useful when comorbid disease
warrants rapid suppression of a hyperthyroid state. After inducing a euthyroid
state, the decision can be made about definitive treatment, for example, surgery,
radioactive iodine (RAI), or continued drug therapy.
4. Treatment of hyperthyroidism usually depends on underlying cause.
a. Graves disease
Antithyroid medications
Radioactive iodine
Surgery: thyroidectomy
b. Toxic multinodular goiter
Radioactive iodine
Thyroidectomy
Less commonly, long-term low-dose methimazole
c. Toxic thyroid adenoma
Radioactive iodine
Thyroidectomy
Less commonly, long-term low-dose methimazole
d. Thyroid storm
A rare but life-threatening event usually associated with a precipitating factor
such as infection, trauma, surgery, or other stressful event
Characterized by fever, tachycardia, agitation, confusion, life-threatening car-
diac arrhythmias
Use -blockers, antithyroid medications, iodine, corticosteroids, aggressive
cooling measures, volume resuscitations, and intensive care unit monitoring.
s
Diseases of the Parathyroid Glands: Hyperparathyroidism
n
o
i
t
i
d
n
1. General principles in older adults
o
C
a. Inappropriate secretion of PTH, which results in hypercalcemia
l
a
c
b. Almost 50% of patients have no or minimal nonspecific symptoms or signs.
i
d
2. Types
e
M
a. Primary hyperparathyroidism
c
Increased excretion of parathyroid hormone (PTH) by parathyroid gland itself
i
r
t
a
The most common cause of hypercalcemia in outpatient setting
i
r
e
Adenoma (75% to 85%)
G
Hyperplasia (15% to 20%)
n
o
m
Carcinoma (~1%)
m
o
C
CLINICAL PEARL 4-33
Overall, there are three treatment strategies for hyperthyroidismmedications to suppress the gland, surgery
to remove hyperfunctioning tissue, and RAI to destroy the gland. Because of higher age-related risks of surgery
and medication side effects, RAI is usually the preferred treatment. It is generally effective, does not require
hospitalization, and has relatively few side effects. Following RAI, it may take 2 to 3 months to reverse the
thyrotoxic state, and cardiac symptoms must be managed appropriately during this time. RAI can be repeated
in 6 to 12 months if the patient is not euthyroid. In rare cases, RAI treatment may trigger a life-threatening
thyroid storm. In the long term, many patients treated with RAI may eventually become hypothyroid and need
replacement therapy. All patients receiving RAI should be monitored for hypothyroid symptoms and have their
TSH checked periodically.
CLINICAL PEARL 4-34

Secondary hyperparathyroidism is characterized by an elevated PTH level with low or normal serum calcium.
The most common cause is CKD, but secondary hyperparathyroidism is also seen with vitamin D deficiency
and renal hypercalciuria. Treatment depends on the cause. In renal disease, treat with calcitriol and oral cal-
cium supplements combined with dietary phosphorus restriction.
b. Secondary hyperparathyroidism
Result of the parathyroid glands response to hypocalcemia in an attempt to
maintain calcium homeostasis
Common causes: chronic renal failure, vitamin D insufficiency, malabsorption
syndromes
c. Tertiary hyperparathyroidism
Prolonged hypocalcemia leading to parathyroid gland hyperplasia and autono-
mous oversecretion of PTH.
B. Clinical presentation
1. Stones, Bones, and Groans
a. Stones: nephrolithiasis and nephrocalcinosis
b. Bones: bone aches and pains, osteitis fibrosa cystica (brown tumors), pathologic
fractures
c. Groans: muscle pain, pancreatitis, and constipation
2. Other symptoms
a. Depression, fatigue, sleep disorders
b. Polyuria and polydipsia
c. Weight loss
C. Diagnosis
1. Hypercalcemia (Figure 4-38)
H YP E R C ALC E MIA
C
o
Common ca us e s :
m
Hype rpa ra thyroidis m,
m
ma ligna ncy,
o
hype rthyroidis m,
n
vita min D toxicity,
G
e
milk-a lka li s yndrome ,
r
i
me dica tions
a
t
r
i
c
M
e
d
Me dica tions Che ck la bs : P TH,
i
c
phos phorus , CBC,
a
l
S P EP , TS H
C
o
n
Thia zide s
d
i
Anta cids
t
i
o
Ca lcium s upple me nts
n
P TH e le va te d P TH s uppre s s e d
s
Vita min D s upple me nts
phos phorus low/
Lithium
norma l
Milk-a lka li Hype rpa ra thyroidis m S uppre s s e d S a rcoidos is P a ge t dis e a s e Ma ligna ncy:
s yndrome TS H Me ta s ta tic or
pa ra ne opla s tic
s yndrome
P a ra thyroid a de noma Hype rthyroidis m

Ectopic P TH s e cre tion
Lithium P a ra ne opla s tic
Me ta s ta tic
s yndrome
Lung ca nce r Ova ria n

Bre a s t ca nce r Re na l
Multiple mye loma He a d a nd ne ck
Lymphoma
Le uke mia
FIGURE
4 -3 8 Evaluation of Hypercalcemia
a. Suspect hyperparathyroidism in patients with hypercalcemia.

The calcium ion is highly bound to protein, and calcium levels need to be in-
terpreted in the context of the serum albumin level. If the albumin level is low,
calculate the free ionized calcium ratio, or else measure the ionized calcium.
b. Primary hyperparathyroidism is the most common cause of hypercalcemia in the
outpatient setting.
2. PTH level (Figure 4-39)
a. Serum intact PTH: elevated relative to serum calcium level
b. In persons without hyperparathyroidism, PTH levels should be suppressed in the
presence of hypercalcemia. A normal level is abnormal because PTH should be
low if the calcium is high.
CLINICAL PEARL 4-35

The relationship between total serum calcium and albumin is defined by the following simple rule: the serum
total calcium concentration falls by 0.8 mg/dLfor every 1 g/dLfall in serum albumin concentration.
P AR AT H YR O ID H O R MO N E , E LE VAT E D S E R U M
s
Common ca us e s :
n
o
Pa ra thyroid a de noma , pa ra thyroid hype rpla s ia , e ctopic P TH,
i
t
re na l fa ilure , lithium, s ma ll bowe l dis e a s e, chronic
i
d
pa ncre a titis, low ca lcium inta ke, vita min D de ficie ncy,
n
o
fa milia l hypoca lciuric hype rca lce mia (FHH), MEN 1
C
l
a
c
i
d
Che ck la bs :
e
M
Tota l s e rum ca lcium, P O 4 ,
25 hydroxy vita min D, urina ry Ca :Cr
c
i
r
t
a
i
r
e
G
S e rum Ca on S e rum Ca on
n
o
2 occa s ions ; clinica l 2 occa s ions
m
s igns of hype rca lce mia
m
o
C
S e conda ry
hype rpa ra thyroidis m
P rima ry Te rtia ry
hype rpa ra thyroidis m hype rpa ra thyroidis m:
follows long-s ta nding
s e conda ry hype rpa ra thyroidis m
or nl urina ry urina ry
Ca :Cr Ca :Cr
Fa milia l
hypoca lciuric
hype rca lce mia
(FHH)
FIGURE
4 -3 9 Evaluation of Elevated PTH
3. Hypophosphatemia
a. A chloride-to-phosphorus ratio > 33 is diagnostic of primary
hyperparathyroidism.
4. Imaging studies
a. Bone radiography
Subperiosteal bone resorption
b. Dual-energy x-ray absorptiometry (DEXA)
Bone mineral density (BMD) measurement for both diagnosis and disease
management
D. Treatment
1. Severe hypercalcemia and symptomatic moderate hypercalcemia
a. Immediate treatment needed
b. Rehydration: with normal saline IV (may need 2 to 4 L per day)
c. Consider calcitonin 4 units/kg intramuscularly or subcutaneously.
d. Consider bisphosphonates.
2. Treatment of primary hyperparathyroidism
a. Surgery is the only definitive treatment.
b. Parathyroidectomy recommended for symptomatic patients
c. If the patient is aged > 50 years and is asymptomatic, surgery may not be
needed.
d. Surgery suggested for patients with any of the following:
Age < 50 years
Inability to participate in appropriate follow-up
Serum calcium level > 1 mg/dL above upper limit of normal
Creatinine clearance < 60 mL/minute
C
o
m
Osteoporosis
m
e. If patient is not candidate for surgery, monitor:
o
n
Serum calcium and creatinine annually
G
BMD every 1 to 2 years
e
r
i
f. Medical management of primary hyperparathyroidism
a
t
r
Maintain hydration
i
c
Bisphosphonates
M
e
Hormone replacement therapy
d
i
c
Calcimimetics (such as cinacalcet)
a
l
Minimize bone loss by staying active.
C
o
Maintain an adequate calcium intake; lower levels will stimulate PTH, whereas
n
d
higher levels may worsen calcium levels.
i
t
i
o
Consume a moderate amount of vitamin D400 to 600 IUs.
n
s
Rhe um a to lo g ic D is e a s e
Osteoarthritis (OA)
1. One of the most common chronic diseases in the geriatric population
2. Is a degenerative disease of the joint cartilage accompanied by a reactive over-
growth of periarticular bone
3. The loss of cartilage leads to bone on bone contact and loss of the shock-absorbing
and lubricating effects of the joint cartilage.
4. Prevalence likely to increase because of increased obesity and an aging population
5. Over 95% of those aged > 65 have evidence of OA. Women are more commonly af-
fected than men.
6. Commonly affects the hands, lower extremities, and spine.
a. A leading cause of disability in the elderly
7. There are primary and secondary forms of the disease (Figure 4-40).
a. Primary OA is the typical age-related form affecting the weight-bearing joints
(lower extremities, and spine) and hands.
Etio patho g e ne s is o f o s te o arthritis
Abnorma l s tre s s Norma l s tre s s

Norma l joint phys iology Abnorma l joint phys iology
Obe s ity Aging

Tra uma J oint de s truction S e ps is
Foca l de fe ct P a in Infla mma tion
Bone re mode ling Dis a bility Ge ne tic muta tion
Alte re d joint loa ding Bioma te ria l fa tigue
Ce ll/Ma trix injury

Abe rra nt re pa ir re s pons e
Enzyma tic de gra da tion
Colla ge n dis ruption a nd prote oglyca n los s
Me cha nica l fa ilure
FIGURE
4 -4 0 Mechanisms and causes for osteoarthritis.
(Moskowitz RW, Altman RD, Buckwalter J A, et al. Osteoarthritis. Philadelphia, PA: LWW, 2006.)
b. Secondary OA may occur related to trauma, infection, congenital disorders, or

deposition diseases affecting the joints, which may differ in distribution from
primary OA (e.g., elbow, wrist).
s
n
o
i
t
i
1. Classic symptoms are:
d
n
a. Pain and stiffness after activity
o
C
b. Loss of range of motion
l
a
c
c. Limited morning stiffness, < 30 minutes
i
d
d. Absence of warmth or signs of inflammation
e
M
e. Joint tenderness
c
f. Overgrowth of periarticular bone
i
r
t
a
g. Presence of crepitus on joint movement
i
r
e
2. Affects weight-bearing joints preferentially: hips, knees, feet, spine
G
3. Impact sports, exercise, or activity may aggravate OA.
n
o
m
4. OA symptoms typically increase with activity and decrease with rest.
m
5. History should address risk factors for OA (Table 4-44).
o
C
TABLE 4-44 Risk Factors for Development of Osteoarthritis
Age
Obesity
Prior joint injury/fracture
History of joint infection
Occupation
Sports participation
Female gender
Deconditioning/muscle weakness
Neuropathy
Developmental joint conditions
Metabolic disease associated with deposition
Hemochromatosis, Wilson disease, hemophilia
6. History should assess the chronology of symptoms; OA is typically insidious and

progressive. Other factors to assess include:
a. History of prior joint problems, such as infection or developmental diseases Quick HIT
(e.g., LeggCalvePerthes disease) With OA, symptoms are
b. Fracture history typically brought on by activity,
c. Other medical conditions such as diabetic neuropathy, which can predispose to and evening stiffness com-
joint problems monly occurs. OA symptoms
improve with rest, and morn-
d. Presence of metabolic medical conditions associated with substance deposition
ing stiffness is either brief or
that can affect cartilage as well as other organs not present at all.
These may be associated with atypical joint involvement.
Examples include hemochromatosis, calcium pyrophosphate dehydrate depo-
sition disease, and Wilson disease.
Hemophilia with recurrent bleeding into the joint space
7. Occupation and recreational activities that stress joints can place a patient at in-
creased risk for OA.
8. Physical examination should focus on the pattern of joint involvement, evidence of
Quick HIT
joint inflammation, and evidence of systemic disease. Other items to note include: As OA progresses, joint space
a. Obesity is associated with OA. narrowing and osteophyte
formation lead to significant
b. Range of motion may be decreased in affected joints.
decrease in range of motion.
c. The joint line may be tender.
d. Absence of warmth and erythema (presence suggests inflammatory arthritis)
e. An effusion may be present but generally minimal.
f. Crepitus may be palpable.
g. Periarticular prominence of bone; in the hands at the distal interphalangeal
(DIP) joints (Heberden nodes) and in the PIP joints (Bouchard nodes).
Quick HIT
C
h. Other joint deformities
o
m
J oint redness, increased
m
C. Diagnosis warmth, and swelling sug-
o
n
1. In most cases, the diagnosis OA can be made clinically. gest an inflammatory arthritis
G
2. Laboratory testing is not indicated in most cases and should be normal with OA. rather than OA.
e
r
i
3. Plain x-ray imaging is generally the initial test to confirm the diagnosis (Fig-
a
t
r
ures 4-41 and 4-42).
i
c
a. Joint space narrowing caused by a decrease in cartilage is an early finding.
M
e
d
i
c
a
l
C
o
n
d
i
t
i
o
n
s
FIGURE
4 -4 1 X-ray image of osteoarthritis of the hip.
FIGURE
4 -4 2 X-ray image of osteoarthritis of the knee.
PEARL
s
CLINICAL 4-36
n
o
i
t
i
d
Diagnosis of OA
n
o
C
The diagnosis of knee OA can be made without radiographic confirmation in patients > 40 years when all of
l
a
the following are present: pain with activity, brief morning stiffness, functional limitation, and more than one
c
i
typical sign on examination such as crepitus, restricted movement, and bony enlargement.
d
e
M
c
i
r
t
a
i
r
e
G
b. Periarticular bone overgrowth is often present; on radiographs, these are termed
n
Quick HIT
o
osteophytes.
m
m
c. The bone adjacent to the joint may be sclerotic as a reaction to an increased
o
Mild to moderate degenerative
C
pressure from a lack of the shock-absorbing cartilage.
changes on x-ray are common
in patients aged > 60 and may d. X-ray findings do not necessarily predict the severity of symptoms. Many pa-
be an incidental finding in an tients with radiologic evidence of OA may not report symptoms, and those with
asymptomatic individual. severe symptoms may have only modest x-ray findings.
4. Other forms of imaging, such as MRI, are not generally indicated unless additional
structures require assessment.
a. An MRI of the knee can assess ligaments and cartilage for injury or detect a sy-
Quick HIT novial cyst (Baker cyst).
b. An MRI of the spine is helpful if neurologic symptoms are present and/or to de-
Meniscal tears are common termine the presence and degree of spinal involvement.
in patients > 60 years and may
be an incidental finding.
D. Treatment
1. Therapy centers around pain relief and maintaining functional ability because the
damaged cartilage cannot be replaced.
2. Limiting ongoing factors that contribute to pain and joint damage is very
Quick HIT important.
Treatment of OA should in- a. Limit activities that stress the affected joint.
clude both pharmacologic and b. Because obesity is a major risk factor, weight loss should be part of the treatment
nonpharmacologic modalities. plan.
c. Heat or ice may provide some pain relief.
3. Strengthening the muscles surrounding the affected joint(s) can help to offload the
joint and protect it from further damage. Water-based exercise may be effective for
those with lower extremity disease.
4. Canes or walkers may assist with balance and to offload the affected joint.
5. Medicationsanalgesia is the goal of therapy.
a. Acetaminophen is the preferred choice for initial medical therapy because of its
safety profile.
Scheduled dosing may be more effective than utilizing it prn or as needed.
Total daily dosing should not exceed 3 g per day in view of potential liver
toxicity.
b. Nonsteroidal anti-inflammatory medications
Relative contraindications include CAD, CHF, and hypertension in general.
A major adverse effect of NSAIDs is gastrointestinal bleeding from gastritis
and duodenal ulcers.
Use of H1 blockers or proton pump inhibitors may lessen this risk.
COX2 inhibitors (celexicob) may also lessen risk of gastrointestinal bleeding.
(1) No class of NSAIDs is more effective than other classes.
(2) However, some classes of NSAIDS do seem to work better for some pa-
tients. The best predictor of effectiveness is a previous good response.
(3) If an individual fails to respond to a NSAID, switching to a different class
may result in better analgesia.
c. Topical therapies such as capsaicin, lidocaine, or diclofenac may be beneficial
and avoid the gastrointestinal side effects.
d. Systemic steroid medications are not recommended as therapy for OA.
e. Alternative medical therapies, such as glucosamine-chondroitin, have not been
C
shown in research trials to be beneficial, but may be helpful in select patients.
o
m
6. Procedural/surgical therapy
m
a. Intra-articular therapy
o
n
Corticosteroid injections can provide relief.
G
e
(1) Exact mechanism unclear
r
i
a
(2) May be given up to four times per year, excessive doses may damage
t
r
i
joints
c
M
(3) Primary risks are introduction of infection or bleeding.
e
Hyaluronic acid is thought to augment synovial fluid and thus provide added
d
i
c
protection against the bone on bone.
a
l
(1) Series of three injections or as single injection
C
o
(2) Adverse effects similar to corticosteroids with added cautions of allergic
n
Quick HIT
d
i
reactions (including egg allergy)
t
i
o
b. Surgery
n
Therapy for OA centers on
s
Surgical options depend upon the affected joint and the severity of the disease. pain relief and maintaining
The condition of the patient and his or her ability to withstand surgery and function; when medications
rehabilitation are important factors to consider. and physical therapy no lon-
Hip and knee replacement surgeries are, in general, effective at providing im- ger meet these goals, then
surgical options should be
proved function and pain relief. considered.
Pain relief for spine surgery is less reliable.
Patients with neurologic deficits associated with spinal disease may have im-
proved neurologic function following surgical correction.
CLINICAL PEARL 4-37
Treatment of OA
A common error is overreliance on NSAIDs to treat OA. These medications have significant risks for older
adults, and acetaminophen is equally effective, less expensive, and less toxic. Another common error is to
overlook nonpharmacologic treatments such as PT, which may not only help discomfort but may also signifi-
cantly improve function.
Osteoporosis
1. Osteoporosis is a loss of bone mass and alteration of the bone matrix that leads to
increased bone fragility and an increased vulnerability to fractures.
2. These changes can be primary and associated with aging or secondary to a variety
of lifestyle, disease, or medication factors.
3. Postmenopausal women and men aged > 70 are most susceptible to the primary
form of osteoporosis.
4. Fractures of the hip, vertebrae, and wrist are associated with osteoporosis and an
increased morbidity and mortality.
5. Mortality is increased 20% to 30% in the year following a hip fracture.
6. Osteoporosis is defined as a bone density 2.5 standard deviations below that of a
young individual; osteopenia is defined as a bone density between 1 and 2.5 stan-
dard deviations below that of a young individual.
Quick HIT 1. May first present acutely with a fracture
a. Vertebral fractures may present with back pain.
Radiographs to rule out spinal
fracture are recommended in Most commonly, compression fractures with loss of vertebral height
patients aged > 70 with sud- Over time, multiple compression fractures may lead to kyphosis (Dowagers
den nontraumatic back pain hump).
or when pain is initiated by a b. Wrist fractures
trivial event such as coughing.
Classic injury is falling on the outstretched hand.
Fracture of the distal radius is called a Colles fracture.
c. Hip fracture, either femoral neck or intertrochanteric fracture, resulting in fore-
s
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shortening and external rotation of a very painful hip
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2. Most patients will be identified as a result of screening.
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Quick HIT 3. Identify risk factors for osteoporosis (Table 4-45)
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a. Lifestyle
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a
c
Osteoporosis is generally a si- Alcohol
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lent disease, and patients be- Smoking
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come aware of the diagnosis
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when they have fractures or
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radiographs that demonstrate
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TABLE 4-45 Risk Factors for Osteoporosis
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bone loss as an incidental
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finding or a bone density test.
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Age
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Female gender
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Weight loss or low body mass index
Low level of physical activity
Smoking
Alcohol abuse
Poor dietary intake of vitamin D and calcium
Nonweight-bearing status (e.g., stroke or spinal cord injury)
Hypogonadism from any cause
Hyperparathyroidism
Renal insufficiency
Medications
Anticonvulsants
Corticosteroids
Heparin with long-term use
Overreplacement of thyroxine
Methotrexate
Lack of weight-bearing exercise

Weight loss or slender build
Poor calcium intake
Asian heritage
b. Comorbidities
Vitamin D deficiency
Hyperthyroidism
Hyperparathyroidism
Cushing disease
Multiple myeloma
Hypogonadism
Malabsorptive states
Renal failure
c. Medications
Corticosteroids
Antiseizure medications
Chronic use of heparin
Methotrexate
Cyclosporine
C. Diagnosis
1. Plain x-ray films can detect osteoporosis, but by the time changes are seen on plain
films, the disease is at an advanced stage.
2. DEXA scanning is much more sensitive and has become the standard for detecting
osteopenia and osteoporosis.
a. Recommended for women aged > 65 and for others with fractures or risk factors
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for osteoporosis/fractures
Quick HIT
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b. Testing is done at the hip and spine.
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c. Results can be compared with a normal healthy 30-year-old (T-score).
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This is the standard for defining osteoporosis, which is > 2.5 standard devia- Vertebral compression
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fractures, hip fractures, and
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tions below that of the healthy 30-year-old.
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Colles fractures are the clas-
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Osteopenia is defined as 1 to 2.5 standard deviations below the measurement
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sic fractures associated with
of a healthy 30-year-old.
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osteoporosis.
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d. Results can also be compared with a cohort of similar age and gender (Z-score).
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These results can help detect a heightened risk for secondary causes.
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3. Those diagnosed with osteoporosis should undergo laboratory screening to assess
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for secondary causes.
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Quick HIT
d
a. Complete blood count
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b. Electrolytes including calcium and phosphorus
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c. Blood urea nitrogen and creatinine USPSTF recommends screen-
d. Liver function tests ing for osteoporosis in all
women aged > 65 years.
e. TSH The National Osteoporosis
f. Vitamin D levels Foundation also recommends
screening for all men aged
D. Treatment > 70 years.
1. Lifestyle changes
a. Assess and reverse weight loss if appropriate.
b. Ensure adequate calcium (1,200 mg/day) and vitamin D (800 units) by using
supplements if needed.
c. Regular weight-bearing exercise
d. Limit alcohol use and quit smoking.
Quick HIT
2. Medications Plain radiography will not
show osteoporosis changes
a. Treat comorbid conditions.
until 30% to 80% of bone mass
b. Adjust thyroid medication to avoid overmedication. loss has occurred; dual-
c. Limit or eliminate use of corticosteroids if possible. energy x-ray absorptiometry
d. Review other potentially contributing medications for alternatives if possible. (DEXA) scanning at the hip and
e. Estrogenprogesterone therapies are no longer considered first-line treatment or spine is the current standard
tool for screening.
prevention in view of risks for breast cancer and heart disease.
f. Bisphosphonates are recommended first-line therapies and prevent bone

resorption.
Can be provided orally daily, weekly, or monthly for treatment or prevention.
For those intolerant of oral medication, an IV formulation is available dosed
every 3 to 12 months.
Oral therapies associated with esophageal/GI irritation and IV treatments with
renal failure
Duration of therapy > 4 years is associated with a risk of osteonecrosis of the
jaw and atypical femur fractures.
Some recommend drug holidays after 4 to 5 years with monitoring of bone
density.
g. Selective estrogen receptor modulators (SERMs) prevent bone resorption
through estrogen-like effects.
Available orally for daily use for prevention or treatment
May trigger menopausal symptoms such as hot flashes
May increase risk for venous thromboembolism
May lower risk for breast cancer
h. Calcitonin
Least effective agent and has more effect on the spine with less on the hip
Administered nasally daily as treatment for osteoporosis
Quick HIT May help with pain relief for compression fractures
i. PTH
Lifestyle changes must be part Anabolic except with prolonged use (> 2 years) when it may lead to bone loss
of osteoporosis therapythis
includes counseling about Administered daily subcutaneously as therapy for osteoporosis
weight-bearing exercise, After 2 years, the effects may reverse or wane, and there is some association
s
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smoking cessation, and alco- with development of osteosarcomas.
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hol use.
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Follow-up therapy with bisphosphonates appears to be beneficial.
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Because of short duration of therapy, cost, and method of administration, gen-
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erally reserved for those intolerant of bisphosphonates with severe disease
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j. Denosumab
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Monoclonal antibody that inhibits osteoclasts
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Administered every 6 months subcutaneously as treatment
Newest addition to medication options and cost and need for administration
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Quick HIT by health care personnel limit its use to more severe disease
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3. Monitoring
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Bisphosphonates are first- a. The exact frequency of DEXA scan testing for screening or monitoring therapy is
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line therapy, but should be not determined.
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combined with appropri- b. A minimum of 2 years has been a standard interval for being able to detect
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ate calcium and vitamin D
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meaningful changes in DEXA scan results.
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supplementation.
Polymyalgia Rheumatica (PMR)

1. Disease largely affects geriatric patients. The exact cause of PMR and why there is
such a high prevalence in older persons is unknown.
2. Average age of onset is 70 years.
3. Women are affected more than men.
4. Self-limited disease related to temporal arteritis; 10% to 20% will have or develop
temporal arteritis.
5. The nature and cause of the association of PMR and temporal arteritis (TA) is
unknown.
1. Pain and stiffness in the shoulders, hips, arms, and thighs
2. Morning stiffness lasting > 30 minutes
3. May be accompanied by fatigue, weight loss, and low-grade temperature
4. Physical examination reveals normal joint and strength in most patients.
5. Up to 20% may show signs of synovitis.
C. Diagnosis
1. Clinical diagnosis based upon the above features
2. An elevated erythrocyte sedimentation rate (ESR) and CRP support the diagnosis,
with an ESR value > 50 and often > 100 mm/hour. A small percentage of patients
may have a normal ESR.
3. Mild anemia may be present, but other laboratory tests are expected to be normal.
4. Imaging expected to be normal. Quick HIT
5. Patients with a diagnosis consistent with polymyalgia rheumatica who have any Polymyalgia rheumatica
symptoms of headache, visual changes, and jaw pain should be referred for tempo- should be considered in geri-
ral artery biopsy to help determine whether TA is present. Treatment should not be atric patients with nonspecific
delayed pending biopsy results if TA is suspected. complaints that include pain,
stiffness, and fatigue.
D. Treatment
1. Prednisone at 15 to 20 mg per day; higher doses of prednisone (40 to 60 mg) are
needed in cases of TA.
2. Response to prednisone occurs rapidly, and if there is no marked improvement
within a week, then the diagnosis should be questioned.
3. The dose of prednisone is continued for 4 to 6 weeks and then tapered slowly (1
mg per month) based on symptoms and sedimentation rate.
4. Patients may need months and up to 2 years of therapy before prednisone is even-
tually tapered off. Relapse occurs in 25% to 50%, and resuming or increasing ste-
Quick HIT
roid dosage may be necessary. Rapid response to corticoste-
5. Because of the prolonged expected use of steroids, glucose should be monitored, roid therapy is pathognomonic
of polymyalgia rheumatic,
osteoporosis preventive therapy initiated, and the patient skin-tested for TB. and if this does not occur, the
6. Laboratories should be reevaluated every 3 months with ESR, CBC, and glucose diagnosis of PMR should be
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values. reconsidered.
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Foot Disorders
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1. Up to 90% of geriatric patients have a foot-related problem.
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2. Foot care and comfort are important for mobility and independence.
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3. The severity of disease ranges from an inconvenience to being limb threatening.
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B. Common foot conditions
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1. Skin conditions
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a. Xerosis
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Dryness of the skin; can affect any surface of the foot.
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More common in the geriatric population because of a decreased number of
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skin glands and natural lubrication.
n
s
Leads to skin thickening, cracking, fissuring, and an increased risk for
infection.
Treatment involves use of topical urea as a keratolytic to thin the skin fol-
lowed by emollients.
Patients should maintain adequate hydration.
b. Contact dermatitis (Figure 4-43)
Eczematous rash with intense pruritus.
Generally on the dorsum of the foot and bilateral.
Materials in the shoes or socks of the patient are frequently the causative
agents.
Allergy/skin testing can be performed if necessary.
Therapy includes avoidance and use of topical corticosteroid medications.
c. Corns and calluses
Calluses are a thickening of the skin in response to repeated pressure or fric-
tion and generally are not painful.
Corns are similar but they form over pressure points on the foot or with an
abnormal gait or poorly fitting shoes; there is a central core over which the
hyperkeratosis forms.
FIGURE
4 -4 3 Contact dermatitis of the foot.
(Image provided by Stedmans Medical Dictionary for the Health Professions and Nursing. Illustrated 6th ed. Philadelphia, PA: LWW,
2007.)
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FIGURE
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4 -4 4 Tinea pedis.
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(Image provided by Stedmans Medical Dictionary for the Health Professions and Nursing. Illustrated 6th ed. Philadelphia, PA: LWW,
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2007.)
Corns often form at the metatarsal heads or between toes.

Calluses form most frequently along the margins of the feet in contact with
shoes.
Goals with either are to alleviate pressure with proper fitting shoes; may re-
quire referral and use of orthotics.
Lesions can be pared down with a scalpel and salicylic acid as a topical patch
or ointment can be applied to residual tissue to soften for further debridement
until resolution.
d. Tinea pedis (Figure 4-44)
Can occur in isolation or coincident with infection of the other foot, a hand or
toenails.
Inflammation and loss of skin barrier can predispose to superimposed bacte-
rial infections, cellulitis, and even limb- and life-threatening infections.
Can be dry and scaly, moist, and macerated or vesicular and inflammatory.
Dry and scaly is most common variant especially in geriatric patients.
Interdigital infections are often moist and irritated because of perspiration.
Therapy generally involves use of topical antifungal powders, cream or

solutions.
e. Foot wounds
Foot wounds are generally related to uncontrolled infection, poorly fitting
shoes, diabetes, vascular insufficiency or neuropathy.
Most occur over pressure points of contact with shoes, a chair or bed that oc-
cludes the capillary circulation and can cause necrosis.
Care includes debriding necrotic tissue, maintaining a clean protected wound
bed and avoiding pressure to the area.
Antibiotic therapy is warranted when signs of infection such as presence of
erythema and purulent discharge are present.
Nonhealing wounds warrant evaluation for an underlying osteomyelitis and
ruling out vascular insufficiency.
2. Nail disorders
a. Onychogryphosis
Marked overgrowth of the nails to the point where they may begin to curl.
The term rams horn has been applied to this condition because the appear-
ance, if the nail is long enough, will resemble a rams horn.
Onychomycosis may play a role in the nail thickening that can be present.
Therapy involves cutting and removal of the excess nail.
The nail thickening may also need to be treated with abrasion or chemically
with topical urea to soften and allow removal, because the thickened nail can
be painful with shoes and socks.
b. Onychomycosis (Figure 4-45)
It is common and affects up to one-third of geriatric patients.
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Fungal infection that affects the nail itself.
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May be coincident with tinea pedis.
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The nail will thicken, become discolored and accumulate debris under the
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nail.
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The nail matrix is also infected, and because of this, this type of infection usu-
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ally will not respond to topical therapies.
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r
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A small portion of the affected nail can be clipped and viewed under micros-
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copy in a KOH solution for presence of fungi.
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The affected nail can also be clipped and sent for fungal culture.
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FIGURE
4 -4 5 Onychomycosis.
PA: LWW, 2007.)
Oral therapy with fluconazole, terbinafine or itraconazole is generally neces-

sary to eradicate the fungus.
Oral therapy is required for 12 weeks and monitoring of liver enzymes is rec-
ommended during therapy.
3. Joint disorders and deformities
a. Osteoarthritis
OA can also affect the foot, most commonly the first metatarsophalangeal
joint.
In addition to pain, OA of the foot can lead to loss of motion or rigidity in the
foot and impair gait.
OA of the foot can also lead to developing bunions or hammertoes.
Abnormal joint physiology as depicted in Figure 4-40 would predispose to de-
velopment of OA.
In the foot, this abnormal physiology is often either flat feet (pes planus) or
high arch (pes cavus).
(1) Both of these conditions modify the normal alignment of the many foot
bones.
(2) Over time arthritis can develop and the foot may become more rigid and
less adaptable to the pes planus or pes cavus deformity.
Therapy for OA of the foot may include use of analgesic medications as for OA
in other areas of the body.
In addition to medications, referral for orthotics may be beneficial in changing
the foot mechanics and alleviating pain or slowing progression.
Surgical options should be considered when medical therapy is no longer pro-
viding sufficient pain relief and allowing meaningful function.
s
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b. Bunions and hammertoes are deformities that result from abnormal foot me-
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chanics and generally develop over years.
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i
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Bunions are an abduction of the digits relative to the first metatarsal, resulting
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in prominence of the medial aspect of the first MTP joint.
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(1) These are present in up to 30% of geriatric patients.
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(2) Bunions are often arthritic and can be painful.
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(3) The abnormal configuration of the foot can cause pressure, leading to
calluses or wounds to the region of the first MTP joint.
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(4) Therapy involves padding, wide shoes to accommodate the foot and in
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cases unresponsive to these measures, surgery.
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Hammertoes are flexion deformities of any of the toes that results in the toe
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curling under with prominence of the dorsum of the toe.
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(1) The flexion deformity can be at either the PIP joint, DIP joint or both.
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(2) Because of the prominence of the toe, there is often pressure on the dor-
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sum of the affected toe against the shoe, leading to calluses or wounds.
(3) Therapy involves use of padding, custom shoes, wound or callus care and,
Quick HIT c. Gout
in refractory cases, surgery.
Although an acute gout at- Gout onset occurs in men aged > 30 and after menopause in women.
tack may come on without a Gout is five times more common in patients aged > 70.
precipitating event, common
precipitating factors include:
Obesity, diabetes, diuretic use, and renal insufficiency all are associated with
alcohol, starting or stopping higher prevalence of gout.
allopurinol, binge eating, dehy- Can affect many different joints (fingers, ankles, wrist or knee), but the
dration, diuretics, fasting, and classic joint involved is the first metatarsophalangeal joint which is termed
surgery. podagra.
Gout is monoarticular in 90% of cases at onset.
Presents with a hot, warm, red, tender joint with effusion.
May require aspiration and fluid analysis to distinguish from infection.
The presence of negatively birefringent crystals (monosodium urate crystals)
confirms the diagnosis. Other typical findings include yellow to milky colored
synovial fluid with a modest elevation of the synovial fluid WBC (2,000 to
60,000 WBCs/mL) that are predominantly PMNs and the absence of bacteria
on gram staining.
Cultures of synovial fluid should be sent to rule out infection.

Serum levels of uric acid do not correlate with acute attacks and, though gen-
erally elevated, can be normal.
Therapy for the acute attack generally involves use of anti-inflammatory medi-
cations, such as NSAIDs or prednisone (20 to 40 mg until response and then
rapid taper) which may be safer alternative from a gastrointestinal and renal
perspective. Colchicine can be used 0.5 to 0.6 mg every 1 to 2 hours until
symptoms abate, GI toxicity develops or a maximum dose of 6 mg over 24
hours is reached.
Long-term therapy to prevent future attacks should be considered following a
recurrence.
(1) Therapy is directed at increasing excretion or decreasing production of
uric acid.
(2) Colchicine, probenecid or allopurinol are options for long-term therapy.
(3) They all should be adjusted for renal/hepatic dysfunction; colchicine
should not be used with liver disease; and probenecid is not effective in
patients with renal insufficiency.
Patients will be at increased risk for renal stones for which preventive therapy
may provide benefit.
d. Pseudogout
A crystalline induced arthritis associated with calcium pyrophosphate crystals.
It is called pseudogout because its symptoms resemble gout.
Most commonly affected joints are the wrists and knees.
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PEARL
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CLINICAL 4-38
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Acute Joint Pain
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It is not uncommon to overlook the possibility of a septic joint in an individual with chronic arthritic pain.
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Septic arthritis should be considered whenever there is an acute flare of joint pain. The presence of systemic
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symptoms such as malaise or fever and erythema and warmth in a single joint enhances the suspicion of
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infection. An acute flare of crystalline arthritis often mimics the clinical findings of an infected joint. Septic
d
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arthritis should always be considered if the symptoms of an exacerbation are atypical for a patient. In cases of
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uncertainty, a joint aspiration to rule out an infection should be done. Typically the fluid from an infected joint
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will be turbid with a high white count and a gram stain may reveal the presence of bacteria.
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CLINICAL PEARL 4-39
DEXAscanning
DEXA scanning reports two scores:
T-scores: compares the bone density to a healthy, normal, 30-year-old adult
Z-scores: compares the bone density to a peer cohort matched for age, body size, and gender
Osteoporosis and osteopenia are defined as follows:
Normal Within one standard deviation of the normal young adult

Osteopenia 1 to 2.5 standard deviations below the normal young adult
Osteoporosis > 2.5 standard deviations below the normal young adult
Severe osteoporosis > 2.5 standard deviations below the normal young adult along with a
fragility fracture
Z-scores are useful in young adults, men aged < 50, and premenopausal women and are abnormal when
> 2 standard deviations below their peer group bone density values. In the geriatric population, the Z-score
falling in a low range should prompt an evaluation for secondary causes of osteoporosis.
Older age is a risk factor. Other risk factors included advance OA, diabetes,
hemochromatosis, hypercalcemia, hyperparathyroidism, hypomagnesemia, hy-
pophosphatemia, and hypothyroidism.
Chondrocalcinosis or calcification of the cartilage may be seen on x-ray.
Joint fluid analysis is similar to gout except pseudogout crystals are positively
birefringent.
Management of an acute flare is similar to gout. Colchicine is less effective
and for single joint involvement aspiration and intra-articular steroids may be
effective.
Infectious Diseases
A. Cellulitis
a. Definition: acute superficial, diffuse spreading skin infection of the dermis and
subcutaneous tissue.
b. Elderly are more prone to cellulitis secondary to weakened defenses associated
with vascular disease and chronic diseases such as diabetes, cancers, and renal
disease. Aging also affects skin integrity making it less effective as a barrier to
infection.
c. Etiology and pathogenesis
May be caused by a variety of organisms but most commonly by skin flora.
Most common source is a break in the skin, but such breaks may be small and
not observed.
Lower extremity most common location, but can occur in any area.
s
Less common sources.
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(1) Spread from underlying osteomyelitis
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d
(2) Underlying abscess (e.g., colonic diverticular abscess)
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Pathogenesis varies with infecting agent and host genetic factors
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If untreated, cellulitis can spread into the bloodstream and potentially become
a
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life threatening.
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Differs from erysipelas which is bright red, edematous, and tender. Erysipelas
has a sharp border with vesicles and bullae.
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Quick HIT Folliculitis is characterized by multiple small, erythematous areas, and pus-
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tules surrounding a hair: most often affecting areas with coarse short hair,
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Erysipelas represents a such as the neck, buttocks, and thighs.
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distinct form of superficial d. Pathogens
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m
cellulitis that does not involve Streptococcal species most common cause (group A -hemolytic strep pre-
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subcutaneous tissues and oc-
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dominant type).
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curs in the dermis with sharply
demarcated borders. Staphylococcus aureus including MRSA.
Vibrio, Aeromonas, and Pseudomonas associated with marine exposure.
Immunocompromised hosts are more susceptible to gram-negative, anaerobes,
and rarely fungi.
a. History focuses on evaluation of risk factors
Past history of cellulitis
Diabetes
Vascular disease
Cancer or use of immunosuppressive medications
Liver or renal disease
Surgery
(1) Mastectomy
(2) Lymphatic disruption, such as after gynecologic surgeries involving
lymph node dissection
(3) History of radiation therapy
Any breach in skin may predispose to cellulitis, including:
(1) Skin ulcer
(2) Fissured toe webs
FIGURE
4 -4 6 Cellulitis.
PA: LWW, 2007.)
(3) Intertrigo
(4) Animal bite
(5) Venous insufficiency
History of MRSA colonization (risk for MRSA infection) Quick HIT
Other pathogens causing
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Warm, red, swollen, and tender area of skin (Figure 4-46).
o
cellulitis may include:
m
Poorly demarcated margins. Dog/cat bite: P. multo-
m
Lower legs most common location.
o
cida, Capnocytophaga
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Systemic signs usually mild, signs of more extensive infection include: fever, canimorsus
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Human bite: Eikenella
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tachycardia, confusion, hypotension.
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corrodens, anaerobes, S.
a
Severe systemic signs should raise suspicion for deeper infection such as nec-
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aureus
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rotizing fasciitis.
c
Salt water exposure by
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Assess for skin breaks which may be minor and not readily apparent including either ingesting or eating
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tinea pedis, intertrigo, scratches or bites, ulcers.
d
contaminated sea food:
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3. Diagnosis Vibrio vulnificus
a
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a. Cellulitis is a clinical diagnosis. Neutropenia: P. aeruginosa
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b. Microbiologic diagnosis is generally not needed in most cases.
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d
Blood cultures positive in < 5% cases but should be obtained in patients with
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signs of systemic illness.
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s
Blood cultures should also be considered in patients with malignancy, neutro-
penia, or animal bites.
Suspect MRSA if an infection is associated with a purulent focus such as an
Quick HIT
abscess or furuncle. Assume community-acquired MRSA until culture data Differential diagnosis of lower
proves otherwise. extremity cellulitis includes:
Hospitalized patients require antibiotic coverage for both strep and S. aureus DVT, venous stasis with skin
changes, necrotizing fasciitis,
(presume MRSA). gangrene, contact dermatitis,
c. Other routine blood tests if signs of systemic toxicity include: acute gout, thrombophlebitis.
CBC to determine degree of leukocytosis and in more severely ill patients, de-
velopment of anemia or thrombocytopenia.
C-reactive protein as a marker of inflammation.
Creatine phosphokinase to assess deeper muscle involvement.
Comprehensive metabolic profile may detect comorbid disease as well in-
volvement of other organs in a patient with systemic symptoms. Quick HIT
d. Imaging is usually reserved to evaluate complications or infections refractory to
MRI may help differentiate cel-
therapy.
lulitis from necrotizing fasciitis
Ultrasound for subcutaneous accumulation of pus or abscess. but if suspected, definitive
X-ray CT scan or MRI for osteomyelitis or deeper abscesses. diagnosis requires urgent sur-
Imaging may also be warranted to evaluate for conditions such as necrotizing gical exploration.
fasciitis and gas gangrene.
CLINICAL PEARL 4-40

Differential Diagnosis of Cellulitis
Two conditions that should be considered in the differential diagnosis of cellulitis are necrotizing fasciitis and
gas gangrene. These are limb- and life-threatening conditions that require aggressive care and often surgery
as part of the treatment.
Necrotizing fasciitis
Life-threatening rapidly progressive soft tissue infection involving the deep fasciasigns of systemic
toxicity, pain out of proportion to examination, gas in subcutaneous tissue, rapid progression despite
antibiotic therapy.
Gas gangrene (anaerobic myonecrosis)
Rapidly progressive necrotizing infection caused by clostridium spppenetrating trauma and immuno-
compromised host are predisposing factors.
4. Treatment
a. Mild cellulitis without systemic signs, a draining wound or abscess
Select agent active against streptococci
(1) Penicillin V250 to 500 mg PO q6 hours, or
(2) Amoxicillin-clavulanate500 mg PO TID, or
(3) Cephalexin500 mg PO q6 hours, or
(4) Dicloxacillin500 mg PO TID, or
(5) Clindamycin150 to 450 mg PO TID
(6) If penicillin allergic, clindamycin or a macrolide are reasonable
s
n
alternatives.
o
i
(7) In moderate cases some clinicians prefer an initial dose of a parenteral an-
t
i
Quick HIT
d
tibiotic with a long half-life such as ceftriaxone followed by oral therapy.
n
o
C
b. Patients who do not respond to initial therapy or those with MRSA risk factors
l
Most strep are sensitive to Clindamycin (dosed as above).
a
c
penicillin and clindamycin and
i
TMP-SMX (1-2 DS BID) plus amoxicillin (9500 mg q12 hours).
d
e
most community-acquired
M
MRSA are sensitive to TMP-
Doxycycline plus amoxicillin (100 mg BID) plus dosing as above for amoxicil-
lin above.
c
SMX and tetracycline. TMP-
i
r
Linezolid (600 mg PO BID).
t
SMX or tetracycline agents
a
i
do not always have adequate All but the smallest of abscesses require drainage for resolution. For a rela-
r
e
G
strep coverage and should not tively small abscess with little surrounding inflammation, drainage may be
n
be the first choice of antibiotic
o
adequate treatment.
m
unless purulence is present.
c. Cellulitis with signs of systemic infection
m
Adding a penicillin agent
o
Select IV antibiotic effective against streptococci
C
is needed to assure strep
coverage. (1) Penicillin G2 to 4 million units IV q46 hours, or
(2) Ceftriaxone1 to 2 g IV once daily, or
(3) Cefazolin1 g IV q8 hours, or
(4) Clindamycin600 mg IV q8 hours
For patients with MRSA risk factors or systemic inflammatory response syn-
drome (SIRS)
(1) Vancomycin30 mg/kg per day IV in two divided doses, or
(2) Linezolid600 mg orally BID, or
(3) Telavancin10 mg/kg IV q24 hours, or
(4) Daptomycin4 mg/kg IV q24 hours
d. Severe, deeper infection with organ dysfunction, immunocompromised
Broad-spectrum regimen
(1) Vancomycin plus either piperacillin-tazobactam 4.5 g IV q8 hours, or
Quick HIT Imipenam 500 to 750 mg IV Q6 hours, or meropenam 0.5 to 1 g q8 hours
e. Always adjust dose of medications for possible decreased renal function in
(%neutrophils elderly.
Absolute
neutrophil
%bands) 3 (WBC) f. Duration of therapy
count (100) Usually 5 to 7 days for adults, but elderly may need 10 to 14 days of treatment
If febrile neutropenia is present, then treat until ANC > 500.
g. Other management
Elevate affected area which enhances lymphatic drainage and reduces edema. Quick HIT
Deeper infections and abscesses may require surgical consultation for debride-
UTIs are the most commonly
ment and/or drainage.
diagnosed and the most com-
h. Complications monly over treated infections
Local: skin abscess, lymphedema in geriatric patients.
Systemic: bacteremia, sepsis
i. Prognosis
Most patients respond to antibiotic therapy but a minority may develop recur-
rence (8% to 20%).
B. UTIs Quick HIT

1. General information Asymptomatic bacteriuria may
a. Most common bacterial infection in adults aged > 65. occur in up to half of geriatric
b. Incidence rate approaches 10% in women, 5.3% in men aged > 80. women residing in skilled
c. Chronic catheter use is associated with much higher rates (about 85% for con- nursing facilities.
dom catheters and nearly 100% for indwelling catheters).
d. Pathogenesis
UTI begins with vaginal introitus/perineum colonization with uropathogens
from the fecal flora, followed by ascension via the urethra into the bladder.
Pyelonephritis usually develops when pathogens ascend to the kidneys via the ure- Quick HIT
ters but less commonly can be caused by seeding from bacteremia and lymphatics.
Factors determining the need
Other factors that can contribute to increased risk for infection include in-
for treating geriatric patients
dwelling catheters and poor hygiene. with bacteriuria include: the
e. Microbiology presence of symptoms such as
Uncomplicated cystitis and pyelonephritis caused mainly by Escherichia coli dysuria, fever or alteration in
C
o
(75% to 95%). behavior or mental status.
m
m
(1) Gram-negative agents such as Klebsiella pneumoniae and Proteus mira-
o
n
bilis are also common. Other pathogenic organisms include Providencia
G
spp., Citrobacter spp., and Enterobacter spp. Pseudomonas aeruginosa is
e
r
i
more common if there has been recent antibiotic exposure or known
a
Quick HIT
t
r
colonization.
i
c
Among otherwise healthy individuals, the isolation of organisms such as lactoba-
M
e
cilli, enterococci, group B streptococci, and coagulase-negative staphylococci other In most cases (75% to 95%) E.
d
coli is the causative agent for
i
than S. saprophyticus, usually represents contamination rather than infection.
c
a
UTIs and isolation of organ-
l
(1) However, it is still appropriate to consider these organisms as causative isms such as lactobacilli and
C
o
agents in symptomatic women when they are found in an uncontami- coagulase-negative staphylo-
n
d
nated voided midstream urine in high counts and with pure growth. cocci other than S. saprophyti-
i
t
i
cus, are usually contaminants.
o
(2) Asymptomatic bacteriuria occurs in 6% to 16% of community-dwelling
n
s
women and 25% to 54% of women in nursing homes; the frequency in
men is about half these numbers.
CLINICAL PEARL 4-41 Quick HIT

Asymptomatic Bacteriuria Virtually 100% of patients with
indwelling Foley catheters
Asymptomatic bacteriuria is the presence of a significant number of bacteria in the urine in the absence of have bacteriuria within 1 week
symptoms. of catheter placement.
Occurs in 6% to 16% of women in the community compared to 25% to 54% of women in nursing homes,
with a frequency in men about half those figures.
Clinical guidelines from the Infectious Diseases Society of America advise that urinalysis and urine cultures
should not be ordered in asymptomatic patients.
Diagnostic testing, including urinalysis and/or culture should be reserved for those with fever, dysuria,
gross hematuria, worsening incontinence, altered behavior or suspected bacteremia. Positive leukocyte
esterase or nitrite on dipstick does not rule in UTI.
Treatment for asymptomatic bacteriuria is not recommended, even in the presence of white blood cells in
the urine. Treatment can lead to significant side effects, expense, and the potential for selection of resis-
tant organisms.
a. Risk factors
Poor hygiene
Neurologic disorders (stroke, spinal disorders)
Diabetes
Dementia
Urinary Incontinence (neurologic or sphincter tone or pelvic floor weakening)
Coitus
Prostatitis (consider for repeated UTI in elderly males)
Female gender
Catheterization or recent instrumentation
Obstruction or urinary retention
b. Symptomatic UTI (aged > 65 years) can be defined by at least two of following
criteria (clinical and laboratory-based):
Fever (> 38C).
Frequency, urgency, dysuria, suprapubic tenderness, or costovertebral angle
pain (not explained by other diagnoses). New onset or worsening inconti-
nence may be the only symptom in the elderly.
Positive urine culture of at least 105 colony-forming units/ml with no more
than two species of microorganisms.
Pyuria (10 white blood cells/mm 3 of unspun urine).
c. Urine cultures in infected elderly patients may have lower colony counts (102 to
103) compared to 105 in younger patients.
3. Diagnosis
a. Dipstick/urinalysis
s
n
Most accurate for predicting UTI when positive for either leukocyte esterase
o
i
or nitrite:
t
i
d
(1) Leukocyte esterase: an enzyme released by leukocytes.
n
o
C
(2) Leukocyte esterase can detect > 10 leukocytes per high power field (sensi-
l
tivity of 75% to 96%; specificity of 94% to 98%).
a
c
(3) The nitrite test is fairly sensitive and specific for detecting 105 CFU of
i
d
e
M
Enterobacteriaceae per milliliter of urine.
(4) The nitrite test lacks adequate sensitivity for detecting lower colony
c
i
r
counts or other organisms, so negative results should be interpreted with
t
a
i
caution.
r
e
G
(5) False-positive nitrite tests can occur with substances that turn the urine
n
o
red, such as beets or phenazopyridine.
m
Leukocyte esterase and nitrite testing have a combined sensitivity of 75% and
m
o
a specificity of 82%.
C
Negative results for both tests do not reliably rule out infection if the history is
strongly suggestive of UTI.
b. Urine culture
Useful with increasing prevalence of antimicrobial resistance among
uropathogens.
Obtaining a urine culture and antimicrobial susceptibility testing prior to initi-
ating therapy is warranted if:
(1) Symptoms are not characteristic of UTI.
(2) If symptoms persist or recur within 3 months following prior antimicro-
bial therapy.
(3) If a complicated infection is suspected.
Quantify E. coli to at least 102 CFU/mL to improve sensitivity.
(1) E. coli should not always be considered a contaminant if it grows in mixed
flora because almost any growth of E. coli in voided urine reflects bladder
overgrowth.
c. Imaging studies (CT/Ultrasound) are not routinely required; can be helpful to
detect obstruction/abscess.
d. Depending on severity of the symptoms, a CBC, BUN, creatinine, electrolytes
and blood cultures may be warranted.
4. Treatment
a. If the diagnosis is in doubt in a clinically stable patient, a reasonable manage-
ment strategy is to withhold antibiotics for 1 week with close monitoring and
follow-up.
25% to 50% of older women with UTI symptoms improve without therapy in
this time frame.
b. If a true UTI is documented, therapy is based on the location of infection (upper
versus lower tract disease), likely causative agent and severity of symptoms.
Lower tract UTIs (cystitis): characterized by dysuria, frequency, and urgency
(not fever which indicates upper tract disease).
(1) With uncomplicated symptomatic lower UTI in elderly women 3- to
7-day courses are sufficient treatment.
(2) Shorter courses are associated with slightly higher failure and recurrence
rates.
Appropriate antimicrobials for treatment of acute uncomplicated cystitis
include:
(1) Nitrofurantoin monohydrate/macrocrystals (100 mg orally twice daily for
5 days): efficacy rate of 90% to 95%.
(a) Minimal resistance and adverse effects.
(b) Nitrofurantoin should be avoided if suspicion for early pyelonephritis.
(c) Contraindicated when creatinine clearance is < 60 mL/minute.
(2) Trimethoprim-sulfamethoxazole (TMP-SMX; one double-strength tab-
let [160/800 mg] twice daily for 3 days): clinical efficacy rate 86% to
100%.
c. Appropriate antimicrobials for treatment of acute complicated cystitis include:
C
If oral therapy is tolerated: treat with an oral fluroquinolone such as cipro-
o
m
floxacin (500 mg orally twice daily or 1,000 mg extended release once daily)
m
or levofloxacin (750 mg orally once daily) for 5 to 10 days.
o
n
(1) Appropriate with mild to moderate symptoms and rapid clinical response.
G
e
(2) Although resistance is increasing (most ESBL strains of E. coli are
r
i
a
resistant to fluroquinolones), the fluroquinolones provide a broad
t
r
i
spectrum of antimicrobial activity against most pathogens (including
c
M
P. aeruginosa).
e
(3) Achieve high levels in the urinary tract.
d
i
c
Parenteral therapy: patients who cannot tolerate oral therapy or with an infec-
a
l
tion that is suspected to be caused by resistant organisms or in cases of sus-
C
o
pected bacteremia.
n
Quick HIT
d
i
(1) Parenteral regimens that may be administered once daily include:
t
i
o
(a) Levofloxacin (500 mg)
n
s
UTIs with bacteremia can be
(b) Ceftriaxone (1 g), ertapenem (1 g)
fatal in the elderly with some
(c) Aminoglycoside (3 to 5 mg/kg of gentamicin or tobramycin) studies reporting a 28-day
(i) Monitoring of aminoglycoside levels is warranted in the setting of mortality of 5%.
unstable renal function.
(d) For suspected urosepsis, third-generation cephalosporin plus ami-
noglycoside, aztreonam, or fluoroquinolone with or without an
aminoglycoside
d. Follow-up
Follow-up urine cultures are not needed in patients with acute cystitis or py-
elonephritis whose symptoms resolve on antibiotics.
If persistent or recurrent symptoms occur within a few weeks of treatment for
acute complicated UTI:
(1) Re-evaluate for other conditions that may be causing the symptoms, such
as stones, abscess or obstruction.
(a) This may include initial or repeat imaging.
(2) Repeat urine culture.
(3) Empiric treatment with another antimicrobial agent.
(a) Treatment should then be tailored to the susceptibility profile of the
causative organism isolated.
CLINICAL PEARL 4-42

Recurrent UTIs
In older men with recurrent UTIs, chronic prostatitis should be considered. Recurrent UTIs in older women are
most often caused by reinfections. Assessment of the anatomy and bladder function is helpful, for example,
post void residual volume and/or cystoscopy. In the absence of an anatomic abnormality strategies to reduce
recurrent infection include good hydration, complete bladder emptying and low-dose antibiotics at bedtime,
for example, trimethoprim 50 to 100 mg. If recurrent infections appear to be related to coitus, have the patient
void after intercourse and consider adding low-dose antibiotic prophylaxis post coitus.
C. Pneumonia
a. Among the top 10 causes for death.
b. Incidence increases with age, three times the rate for those in their eighties com-
pared to those in their sixties.
c. Those in skilled nursing facilities are at higher risk because of an increased inci-
dence of aspiration.
d. Three mechanisms for acquiring pneumonia and each have different associated
microbial pathogens.
Aspiration most common and associated with the bacterial flora of the oro-
pharynx. These represent the classic community-acquired pneumonias.
(1) Streptococcus pneumonia most common; causing about two-third of bacte-
rial pneumonias
s
n
(2) Haemophilus influenzae next most common; about 15% of community-
o
i
acquired pneumonias
t
i
d
n
(3) Increase in gram-negative pneumonias in long term care resident (10%)
o
C
(4) Klebsiella associated with alcoholism
l
a
(5) Anaerobic infections with overt aspiration
c
i
d
Inhalation, associated with atypical pneumonia, more common in younger pa-
Quick HIT
e
M
tients or outbreaks.
c
(1) Legionellawater-associated outbreaks
i
The mechanisms for acquir-
r
t
(2) Mycoplasmawalking pneumonia
a
ing pneumonia are aspiration,
i
r
(3) Chlamydia
e
inhalation, and hematogenous
G
spread. Aspiration of normal (4) Viral pneumonias such as influenza, parainfluenza, and respiratory syncy-
n
o
colonizing flora is the most tial virus
m
common.
m
Hematogenous spreadleast common and associated with sepsis, endocardi-
o
C
tis, and bacteremia
a. Temperature elevation may be blunted in geriatric patients.
CLINICAL PEARL 4-43

Risk Factors for Pneumonia in Geriatric Patients
Advanced age Underlying cancer
Male gender Neurologic disease (Parkinsons, stroke)
Decreased functional ability Feeding tube
Smoking history History of aspiration
Chronic obstructive lung disease, recent hospitalization or
surgery
Heart disease
b. Fever, chills, dyspnea, cough with sputum production are the classic pneumonia
presenting symptoms.
Geriatric patients more likely to present with atypical symptoms such as con-
Quick HIT
fusion and fatigue. A common presentation for
c. Pleuritic chest pain may occur. pneumonia in geriatric pa-
d. Inquire about past medical history, the presence of cardiovascular or pulmonary tients is an altered mental sta-
tus in conjunction with oxygen
disease, diabetes or aspiration. desaturation and dehydration.
e. Social history: smoking history and alcohol intake.
f. Vaccination status: in particular influenza and pneumococcal.
g. Physical examination may reveal tachycardia, tachypnea > 20 breaths/minute,
fever, and lung findings such as crackles, wheezing, rhonchi, or rubs.
3. Diagnosis
a. Pneumonia severity index or CURB-65 assessment tools help determine severity Quick HIT
and the appropriate location for treatment. Risk factors that place patients
b. Chest x-ray findings (Figure 4-47) may lag behind clinical findingsin other at increased risk for death
words, the initial x-ray can be clear, but after hydration and time, x-ray findings and indicate a need for hos-
become apparent. pitalization include advanced
Patients may also get better before the chest x-ray clears. age, oxygen desaturation,
hypotension (systolic < 90),
Because of the lag in x-ray resolution, follow-up x-rays to document clearing and increased respiratory rate
after treatment should be obtained 4 to 6 weeks later after clinical resolution. (> 30/minute).
c. Oxygen status should be assessed.
d. Sputum gram stain and cultures are of variable value depending on patients abil-
ity to cooperate in providing a sputum sample.
Samples may be obtained via suction.
Samples are often contaminated with saliva and oral secretions.
C
Increased WBCs (> 25/hpf) and few epithelial cells (< 5 ppf) indicate a good
o
m
sample.
m
e. Blood cultures should be obtained for all hospitalized patients.
o
n
f. Urine antigen testing (UAT) for legionella and pneumococci can be helpful.
G
e
Specificity for pneumococcal UAT is about 95%, sensitivity about 75%.
r
i
a
Specificity for legionella is > 99%, sensitivity is around 70% to 80%.
t
r
i
c
M
e
d
i
c
a
l
C
o
n
d
i
t
i
o
n
s
FIGURE
4 -4 7 Lateral CXR of right middle lobe pneumonia.
PA: LWW, 2007.)
UAT for legionella indicated in seriously ill patients, those who are immuno-
compromised, nonresponsive to -lactam antibiotics or have features suggest-
Quick HIT ing legionella.
Chest x-ray findings often lag g. Up to 50% with pneumonia have a normal WBC, but 95% have a left shift.
behind clinical findings and an h. BUN, Cr, electrolytes, glucosehelp assess severity and comorbidities.
initial x-ray may be clear but 4. Treatment
after hydration and time, x-ray a. Outpatient with macrolide or doxycycline.
findings become apparent.
b. If patient is sick enough for inpatient care or has comorbidities of heart disease,
COPD, diabetes, or is aged > 75 use a:
Fluoroquinolone or
Cephalosporin plus macrolide
c. Facility-acquired pneumonia
Quick HIT Third-generation cephalosporin with pseudomonas coverage such as ceftazi-
dime or
Both 13-valent and 23-valent Piperacillin/tazobactam or
pneumococcal vaccines Imipenam
should be administered to ge-
riatric patients at least 6 to 12
Vancomycin can be added to any of these if the patient is sick. It adds cover-
months apart. age for staphylococcus and improved gram-positive coverage.
Duration of treatment for outpatients is 10 to 14 days.
In an inpatient setting, switch to oral antibiotics when stable, showing clinical
improvement and afebrile for 24 hours.
(1) Usually on IV antibiotics until temperature < 100, HR < 100, respiratory
rate < 25, SBP > 90, O2 sat > 90% and ability to take oral meds.
(2) Total duration of therapy 7 to 14 days depending on clinical response.
d. Other measures include:
s
n
Oxygen
o
i
Hydration
t
i
d
Nutritional support
n
o
C
When stable, preventive measures and smoking cessation
l
Good oral hygiene also has preventive value
a
c
i
If needed, update with influenza and pneumococcal vaccines
d
e
M
(1) Influenza annually
(2) Pneumococcal with 13-valent and 23-valent vaccines once each after age
c
i
r
65 spaced 6 to 12 months apart
t
a
i
(a) Preference is to administer 13-valent vaccine first.
r
e
G
(b) Spacing between administration of a first and second dose of 23-va-
n
o
lent vaccine (if given prior to age 65) should be at least 5 years.
m
m
D. Sepsis
o
C
1. General Information
a. Systemic inflammatory response syndrome (SIRS) has the following components:
Hyperthermia or hypothermia (> 38.6C or < 36C)
Tachycardia
Increased respiratory rate (> 20/minute) or decreased pCO2 (< 32)
WBC > 12,000 or < 4,000
b. SIRS is a nonspecific response and can be infectious or noninfectious.
c. A term used for the infectious form of SIRS is sepsis and includes bacteremia as a
component.
Severe sepsis is associated with organ dysfunction.
Multiple organ dysfunction syndrome is the most extreme form and may include:
(1) Hypoxia
(2) Diminished urine output/renal function
(3) Increased lactate indicating organ and muscle hypoperfusion
(4) Decreased capillary refill
(5) Elevation of liver enzymes with increases in protime and bilirubin
(6) Platelet consumption and thrombocytopenia
(7) Hypotension
Hypotension in association with sepsis has been termed septic shock.
d. Over 60% of cases of sepsis occur in those aged > 65 years.

e. Sepsis occurs more commonly in the winter months.
f. The mortality rate is as high as 50% depending on patient comorbidities and is Quick HIT
higher in the elderly. Sepsis is the presence of SIRS
g. Gram-positive organisms cause sepsis more frequently than gram-negative with an infectious etiology.
organisms.
a. Risk factors
Bacteremia
Increasing age
Immunosuppression
Quick HIT
Renal insufficiency The most severe form of
sepsis involves multiple organ
Hepatic disease dysfunction syndrome, and
DM there can be evidence of hy-
b. Physical findings poperfusion of the lungs, liver
Hyperthermia or hypothermia (> 38.6C or < 36C) kidneys, and muscles along
Tachycardia with immune destruction of
platelets.
Increased respiratory rate (> 20/minute) or decreased pCO2 (< 32)
WBC > 12,000 or < 4,000
Altered mental status
Systolic BP < 90 mm Hg
Findings related to source of infection, examples include:
(1) Suprapubic or CVA tenderness with UTI
(2) Rales, rhonchi on lung examination with pneumonia
(3) Erythema and warmth related to underlying cellulitis
C
(4) Diarrhea and abdominal discomfort with pseudomembranous colitis
o
m
(5) If no obvious source of infection, consider an intrabdominal process
m
3. Diagnosis
o
n
a. Clinical syndrome in the setting of an infection
G
e
b. Evaluation for infections
r
i
a
Urine culture
t
r
i
Blood culture
c
M
Chest x-ray
e
CBC to assess for anemia, thrombocytopenia and changes in the WBC
d
i
c
Metabolic profile to assess liver and renal function as well as hydration
a
l
Oxygen saturation and/or arterial blood gas for oxygenation and ABG to assess
C
o
acidbase status
n
d
i
Lactic acid to help assess adequacy of organ perfusion
t
i
o
4. Treatment
n
s
a. Cornerstone of therapy is supportive care and aggressive hydration combined
with early antibiotic therapy.
Repeated crystalloid boluses often needed to sustain both BP and urine
output.
May require up to 3 to 5 L of fluid in the initial 24 to 36 hours.
Anemia should be corrected with blood transfusion.
If cardiogenic insufficiency is present with pulmonary congestion/edema, then
pressor support with norepinephrine, phenylephrine, dopamine or dobuta-
mine may be necessary.
b. Antibiotic therapy
Initially broad spectrum to cover gram-positive and gram-negative
organisms.
Select based upon most likely source.
Initial therapy should include antibiotics for both gram-positive and gram-
negative coverage.
(1) Pipericillin-tazobactam
(2) Third-generation cephalosporins
(3) Fluorquinolones
(4) Aminioglycosides
(5) Imipenem
(6) Vancomycin
(7) Daptomycin
Quick HIT Considerations include:
(1) Facility acquired
As a general rule, use culture
results to identify the nar-
(2) Recent hospitalizations
rowest spectrum effective (3) Drug allergies
antibiotic. (4) Likely source of infection
Coverage for MRSA, gram-negative organisms and pseudomonas are more im-
portant with facility and hospital acquired infections.
Respiratory and skin sources as compared to a possible GI or GU sources
suggest that a gram-positive infection is more likely than gram-negative
Quick HIT bacteria.
For treatment of sepsis, the Culture results used to guide selection of ongoing antibiotics.
cornerstone of therapy in- Generally, duration of antibiotics is 7 to 10 days depending upon the specific
cludes aggressive hydration underlying infection and comorbidities.
and early antibiotic therapy. c. Supportive care
Ongoing monitoring of BP and urine output, along with volume status.
(1) May require arterial line placement
(2) May require central line placement
(3) May require Foley catheter placement
Quick HIT Target for mean arterial pressure is 65 mm Hg.
General target for urine output is > 0.5 mL/kg per hour.
Mean arterial pressure = Provide ongoing care for underlying and comorbid diseases.
(2 diastolic) + systolic/3
Nutrition must be provided and may require a feeding tube, either nasogastric
s
n
for short-term use or percutaneous gastrostomy for longer-term use.
o
i
t
i
E. Influenza
d
n
o
C
a. Annually there are flu epidemics that peak over a 2-week period and last 2 to 3
l
a
c
months.
i
d
e
b. These epidemics generally occur in the winter.
M
c. There is a 10% to 20% attack rate.
c
i
d. Disease is transmitted by close contact.
r
t
a
e. The elderly are particularly vulnerable to severe symptoms and complications.
i
r
e
G
n
a. Abrupt onset
o
m
b. Fever to 104 F
m
c. Cough and respiratory congestion
o
C
d. Sore throat
e. Myalgias
f. Headache and body aches
g. Weakness, fatigue
h. Incubation period of approximately 2 days postexposure
i. Symptoms generally last 5 to 7 days and, if not improving or resolved in
this time period, should prompt consideration of alternative diagnoses or
complications.
In the elderly adult fatigue may persist for weeks.
j. Assess for underlying heart or lung disease which increases the risk for compli-
cations (Table 4-46).
k. Hypoxia and presence of wheezing, rhonchi or rales suggest possible pneumonia.
3. Diagnosis
a. Rapid antigen nasopharyngeal swab can provide results in 15 minutes.
A positive test during an epidemic has a high predictive value.
b. More sensitive and specific tests include PCR and culture of nasopharyngeal
swabs.
PCR provides results < 6 hours.
Culture results not available for 2 to 3 days.
TABLE 4-46 Risk Factors for Complications of Influenza

Nursing home resident Immunocompromised condition
Age > 65 Diabetes mellitus
Heart disease Renal insufficiency
Lung disease Liver disease
c. Serologic testing for antibodies can be diagnostic but is impractical in the clini-
cal setting because results take 2 weeks or more. Serology is more useful for epi-
demiologic purposes.
d. Chest x-ray useful to detect viral or bacterial pneumonia.
e. Cardiac and muscle enzymes for myositis or myocarditis when suspected as
complications.
f. EKG and echocardiography if myocarditis or pericarditis is suspected. Quick HIT
g. Rarely, encephalitis or meningitis can occur and be diagnosed by lumbar Rapid antigen nasopharyngeal
puncture. swab can provide results in 15
4. Treatment minutes; PCR is more sensitive
a. Therapy is largely supportive for symptoms. and specific but results may
take up to 6 hours; Culture
b. Antiviral therapy may shorten the duration of symptoms by 1 to 2 days but must results are not available for 2
be administered < 48 hours of onset of symptoms. to 3 days and serologic testing
Neuraminidase inhibitors are preferred first line. for up to 1 to 2 weeks, mak-
C
(1) Oseltamivir can be administered orally, generally for 5 days. ing these tests less clinically
o
m
(2) Zanamivir can be administered by inhalation for 5 days. useful.
m
Amantadine and rimantidine are second-line agents because of resistance;
o
n
both are oral and best given < 48 hours of symptoms.
G
e
c. Concomitant bacterial pneumonia should be treated with supportive measures,
r
i
a
oxygen, and antibiotics to cover the potential organisms.
t
r
Quick HIT
i
Staphylococcus aureus is a classic bacterial organism that complicates influ-
c
M
enza; if giving antibiotic coverage should consider the possibility of MRSA.
e
Streptococcus pneumonia and H. influenzae are also potential pathogens that
d
Antiviral therapy may shorten
i
c
should be covered with the antibiotic selection. the duration of symptoms by 1
a
l
d. Other complications such as CNS, muscle or cardiac should be treated using an- to 2 days but must be admin-
C
o
istered < 48 hours of symptom
tiviral and supportive measures as indicated by the patients condition.
n
onset; neuraminidase in-
d
i
e. Vaccination is the best means of prevention and should be provided annually; a
t
hibitors are first-line antiviral
i
o
high-dose vaccine has been developed and proven to more effectively serocon- therapy.
n
s
vert geriatric patients.
F. Tuberculosis (TB)
a. Historically exposure rates were as high as 80%, and there were no effective
screening or treatment options. TB was the leading cause of death in the early Quick HIT
1900s.
TB in an older adult can be
b. Tuberculosis sanitariums quarantined patients to prevent additional exposure of
reactivation of old disease or a
the population. new infection caused by expo-
These were popular until the 1960s with advent of tuberculosis medications. sure to an infected individual.
Another older therapy was to collapse segments of the lung to deprive the or-
ganism of oxygen.
c. In long-term care facilities where screening is routine, up to one-fourth of patients
will test positive using the two-step PPD test, indicating prior exposure to TB.
d. Infection occurs with inhalation of the organism where it is usually contained by
the bodys defenses.
TB is aerobic, making spread via aerosol a natural means for lung infection.
Usually after a primary infection, the body defenses wall off the organism
where it lays dormant in granulomas in the lung tissue.
Up to 10% of infected individuals will develop a secondary infection or reacti-

vation of the infection in the lung.
During secondary infection, disease can also spread to other organs or dif-
fusely (miliary TB).
During secondary infection, patients are contagious, generally by aerosol
spread from the lung focus of infection.
a. Presentation
Positive screening test, asymptomatic, with or without known exposure is
considered latent infection.
Following a primary exposure, the patient will usually have nonspecific or no
symptoms.
Active infection is generally a secondary reactivation with symptoms:
(1) Fever
(2) Cough
(3) Hemoptysis
(4) Night sweats
(5) Weight loss
(6) Fatigue
(7) With meningitis, may have headache and altered mental status
(8) With urinary tract involvement may have UTI symptoms
b. Risk factors
Nursing home residence
Immigrants
Low socioeconomic status
s
n
Minority status
o
i
Immunocompromised state
t
i
d
Known exposure to active TB
n
o
C
Human immunodeficiency virus antibody positivity
l
Alcohol abuse
a
c
i
DM
d
e
M
Steroid use
Malnutrition
c
i
r
3. Diagnosis
t
a
i
a. With active infection, chest x-ray may show an upper lobe infiltrate, classically a
r
e
G
cavitary lesion with hilar adenopathy.
n
o
b. Chest x-ray findings of primary or latent disease may be granulomas and hilar
m
nodes (Ghon complex).
m
o
c. Sputum, urine or other body tissue can be obtained for acid-fast staining and culture.
C
Absence of bacteria on acid-fast staining does not exclude TB.
Cultures may take 1 to 2 months for results.
Positive cultures should include sensitivity testing because of high rates of
drug resistance with TB.
d. Screening for TB
PPD testing is most commonly performed as an intradermal injection.
(1) Results are interpreted in the context of the patient (Clinical Pearl 4-44).
(2) The diameter of induration (not redness) determines positivity/negativity.
(3) Two-step PPD testing can be performed after a first test is negativewith
the repeat test 2 weeks later.
(a) This may document true negativity if negative; or
(b) If the second dose is positive, this indicates a booster response from a
remote exposure, thus preventing future screenings from being inter-
preted as a new conversion.
Interferon- release assays (IGRA) are blood tests for Mycobacterium tuberculo-
sis antigens.
(1) These tests can be performed with one visit.
(2) No booster effect.
(3) These tests are considerably more costly.
Positive PPD or IGRA tests warrant evaluation for active TB, including chest x-ray.
Patients found to have TB should be considered for HIV testing.
4. Treatment Quick HIT
a. Therapy is generally provided to patients who are PPD- or IGRA-positive even Absence of bacteria on acid-
without evidence of active infection. fast staining does not exclude
These patients are believed to have latent infection. TB as a cause for infection.
Therapy is isoniazid (INH) for 9 months.
This therapy lowers the risk of secondary or reactivation of disease by 90%.
Patients must be monitored for neuropathy and liver toxicity.
Pyridoxine (vitamin B6) can be given orally to help prevent neuropathy.
Alternative therapies include:
(1) Rifampin daily for 4 months
(2) INH twice weekly for 6 or 9 months with direct observation of ingestion
of medication
(3) Rifapentine and INH daily for 12 weeks with direct observation of inges-
tion of medications
b. Therapy for active disease
Quick HIT
Patient must be quarantined for at least 2 weeks while under treatment and Cultures may take 1 to 2
until repeat sputum AFB smears are negative. months before growthim-
portant information from the
Therapy based upon drug sensitivity but empiric initial therapy generally in-
cultures includes antibiotic
cludes four medications. sensitivity.
(1) INH
(2) Rifampin
(3) Pyrazinamide
(4) Ethambutol or streptomycin
C
The four medication regimen is used for 2 months and, if susceptible, then a
o
m
two drug regimen (INH and rifampin) is used to complete therapy for 4 addi-
m
tional or 6 total months.
o
n
In cases of drug resistance, medications will need to be adjusted and an infec-
G
e
tious disease specialist consulted.
r
i
a
Quick HIT
t
r
G. Shingles
i
c
M
Patients with positive PPD or
e
a. Primary infection with varicella, a herpes virus, results in chickenpox.
d
IGRA have latent infection and
i
c
b. Following primary infection, which is evident in > 99% of people aged > 40, the should be treated to lessen
a
l
virus becomes dormant in a dorsal root ganglion. their chances for reactivated
C
o
disease.
n
d
i
t
i
PEARL
o
CLINICAL 4-44
n
s
PPDTesting
PPD testing is performed to screen for latent or active tuberculosis. The test is performed by intradermal in-
jection of purified tuberculin protein and assessing the bodys reaction to this material. A positive reaction is
detected by thickening of the dermal layer which is termed induration.
The amount of induration determines the significance of the reaction. The test is interpreted 48 to 72 hours
after injection. In order to be able to distinguish whether a reaction is a boosting response to a remote
exposure or a new conversion, a two-step procedure is performed in long-term residents and health care
workers. The second test of the two-step testing follows 2 weeks after the first. Any patient with a positive
test should be evaluated for active disease.
Definition of Positive PPD
Induration > 15 mm Positive for all patients Quick HIT

> 10 mm Positive in nursing home residents, immigrants, underserved, and other Patient with active TB must
high-risk groups be quarantined for at least
2 weeks while under active
> 5 mm Patients with known contact with infected person, HIVinfected person,
treatment and until negative
immunosuppressed, or with CXR findings consistent with TB infection repeat sputum AFB smears.
c. Reactivation of the varicella virus results in shingles which occurs in the skin
along the dermatomal distribution of the nerve root.
d. In shingles, the virus does not become airborne and is contagious only by direct
contact.
e. Incidence for shingles is 5/1,000 per year in the general population increasing to
> 10/1,000 per year in those aged > 60 years.
f. Up to one-third of individuals will be affected by shingles in their lifetime.
g. Over 50% suffer prolonged pain from the infection and 13% develop posther-
petic neuralgia which is dermatomal neuropathic pain > 90 days after onset of
the primary infection.
h. Postherpetic neuropathy occurs in as many as 60% of geriatric patients affected
with shingles and can be debilitating.
a. Symptoms and signs
Abrupt onset of pain in dermatomal distribution followed by an erythematous
papular rash proceeding to vesicular then scabs.
(1) Typically clears in 10 to 14 days.
(2) Patient may present with pain of uncertain etiology until characteristic
rash breaks out.
Itching
Aches and fatigue
Paresthesias
b. Complications
Patients at risk
(1) Immunocompromised (e.g., HIV, leukemia)
Quick HIT
s
n
(2) Cancer
o
i
(3) Medications, such as chemotherapy, prednisone
t
Reactivation of the dormant
i
d
Can develop secondary bacterial infection such as cellulitis or deeper infec-
n
varicella virus results in
o
C
shingles which occurs in tions such as necrotizing fasciitis
l
the skin and nerve along the Encephalitis
a
c
dermatomal distribution of the
i
Infection across multiple dermatomes or systemic spread
d
nerve root.
e
M
Myelitis
Most common complication is postherpetic neuralgia which develops more
c
i
r
commonly in geriatric patients
t
a
i
(1) Pain that persists in dermatomal distribution of infection.
r
e
G
(2) Characteristically sharp and burning.
n
o
(3) Exact definition for time not fully agreed upon but > 30 days is most
m
common and many use 90 days as definition because of initial neuritis as-
m
Quick HIT
o
sociated with primary infection.
C
3. Diagnosis
Postherpetic neuropathy is a. Generally this is a clinical diagnosis and no testing is needed.
the most common complica-
tion and has been reported to
b. For unclear cases, Tzank smear or culture of the vesicular base/fluid.
occur in as many as 60% of c. For patients with complications.
geriatric patients affected with Blood cultures for suspected systemic bacterial infections.
shingles. MRI and lumbar puncture may be warranted with CNS complications.
4. Treatment
a. Antiviral therapy within 48 hours of symptoms or rash onset
Acyclovir, famciclovir, valciclovir
Shortens the clinical course
Lessen the likelihood of postherpetic neuralgia
For complications, antiviral therapy, supportive measures and antibiotic ther-
apy if secondarily infected
Quick HIT b. Preventive measures
Vaccination recommended for all aged > 60 years; can be offered to those aged
Pain may precede the rash
leading to evaluations and > 50
testing for chest pain or ab- (1) Lessens risk for shingles by 70%.
dominal pain. (2) Is a live vaccine and contraindicated in immunocompromised patients or
those in close living/contact with immunocompromised.
Patients with no evidence of varicella immunity or who are immunocompro-

mised and are exposed to varicella can be given varicella IgG within 10 days of
exposure to prevent the varicella infection from developing. Quick HIT
c. Postherpetic neuralgia Diagnosis is clinical; however,
Most commonly treated with medications effective for neuropathy in uncertain cases, Tzanck
(1) Anticonvulsants such as gabapentin or pregabalin smear and/or culture of the ve-
(2) Tricyclic antidepressants sicular base/fluid can confirm
the diagnosis.
(3) Analgesics or anesthetics topically, such as capsaicin or lidocaine
(4) No evidence of benefit from corticosteroids
(5) Antiviral medications given during an episode of shingles decreases the
likelihood for developing postherpetic neuralgia
(6) Vaccination reduces incidence
He m a to lo g ic D is e a s e
A. Anemia
Quick HIT
1. General information Primary treatment is antiviral
therapy, best given within
a. Anemia is present when the hemoglobin is < 13 g/dL in men and 12 g/dL in women. 48 hours of symptom onset.
b. Although anemia affects up to 10% to 15% of geriatric patients, it is not a normal
part of aging.
c. May occur in up to one-third of long-term care or nursing home patients.
d. Nutritional causes account for approximately one-third of cases, including iron,
folate, and vitamin B12 deficiencies.
Iron deficiency may be related to dietary deficiency or more commonly from
blood loss.
C
o
Folate deficiency occurs from dietary deficiency or malabsorption.
Quick HIT
m
m
(1) Body stores are such that it takes 4 to 5 months to deplete.
o
(2) Food sources include vegetables and breads, with flour now being supple-
n
Anemia in geriatric patients
G
mented with folic acid in the United States. can be attributed to nutritional
e
r
Vitamin B12 stores can occur from dietary deficiency or malabsorption. causes in one-third, chronic
i
a
disease (including renal dis-
t
(1) Vitamin B12 stores may take 3 or more years to deplete.
r
i
ease) in one-third and the final
c
(2) Food sources include meats and vegans are susceptible to deficiency.
M
third has no identifiable cause.
e
(3) Atrophic gastritis is associated with absence of intrinsic factor which is
d
i
required for absorption of vitamin B12.
c
a
(4) The terminal ileum is the site of B12 absorption and diseases (e.g.,
l
C
o
Crohns) or resection of the terminal ileum can lead to deficiency.
n
d
e. Anemia of chronic disease or anemia of renal disease account for another one-
i
t
i
third of anemias in elderly patients.
o
n
f. The remaining one-third of anemia cases have no identifiable cause. Possible
s
reasons include:
Erythropoietin levels are blunted in elderly patients with anemia leading to
Quick HIT
speculation of a primary failure of the endocrine renal cells. Anemia of chronic disease and
Reduced responsiveness of stem cells. iron deficiency anemia are the
most common types of anemia
Some patients without an identified cause may have myelodysplastic syndrome. in the elderly.
a. History
Past medical history of anemia
Other chronic conditions such as renal disease, liver disease, heart disease, en-
docrine disease, cancer, or chronic infection
Medications
Symptoms
(1) Fatigue, orthostasis
(2) Dyspnea
(3) Loss of proprioceptive abilities or balance
(4) Weight loss
(5) Symptoms of malabsorption, such as steatorrhea/change in stools
(6) Bleeding from any source, including bowels or urine, tarry stools
Findings of chronic diseases
(1) Edema, rales, S3 suggestive of congestive HF
(2) Hepatomegaly, spider angioma, ascites, and jaundice or liver disease
Orthostatic hypotension, pallor or tachycardia suggesting an anemic state or
chronic blood loss
Cardiac examination for new murmurs suggestive of endocarditis
Presence of petechiae or ecchymoses
Quick HIT Lymphadenopathy or splenomegaly to suggest an underlying cancer or my-
eloid disorder
A low ferritin level almost Rectal examination
always indicates an iron Neurologic examination, including proprioception
deficiency. c. Dietary history
Determine if the patient consumes a varied diet including both meats and veg-
etables, and if they exclude any particular food group.
Picaingestion of nonfood items such as clay which may impair iron absorp-
tion or ice which may be a sign of iron deficiency.
Quick HIT Change in weight or stools to suggest an underlying disease such as cancer,
blood loss or malabsorption.
Methylmalonic acid is 3. Diagnosis (Figure 4-48)
increased in vitamin B12
deficiency but not folate defi-
a. Laboratory (Table 4-47)
ciency, whereas homocysteine Serum iron, total iron-binding capacity and ferritin
is increased in both. Combined deficiencies are common and it is reasonable to check serum B12
and RBC folate along with iron.
(1) If low, check homocysteine and methymalonic acid to help interpret
s
n
findings.
o
i
Erythropoietin levels are not routinely checked when evaluating an anemia.
t
i
d
Quick HIT Reticulocyte count can be helpful to distinguish hypoproliferative anemias
n
o
C
from acute blood loss or hemolytic states.
l
(1) Chronic disease, renal failure, B12/folate, and iron deficiency are all hypop-
a
A reticulocyte count can be
c
i
help distinguish between roliferative states and would be expected to have low reticulocyte counts.
d
e
M
hypoproliferative anemias and (2) Hemolytic or acute blood loss states would be expected to have elevated
acute blood loss or hemolytic
reticulocyte counts unless there is nutritional deficiency that impairs
c
i
states.
r
blood cell formation or a concomitant hypoproliferative bone marrow.
t
a
i
Bone marrow examination is not routinely performed but can be helpful in de-
r
e
G
tecting malignant causes, myeloma, or aplastic conditions.
n
o
b. Imaging is not routinely performed as part of an anemia evaluation but might be
m
warranted to investigate a suspected underlying or contributing conditions, such
m
Quick HIT
o
as cancer.
C
c. Other tests
An anemia should not be at-
tributed to aging and should Evaluation for renal disease and liver disease through blood tests is generally
be investigated. Although warranted, especially if there is a normochromic, normocytic anemia.
poor dietary intake may cause Evaluate for a GI and GU source if there is an iron deficiency. Gastrointestinal
iron deficiency anemia, the endoscopic testing is commonly performed with iron deficient anemias to as-
possibility of an occult GI ma- sess for GI sources of blood loss.
lignancy should be considered
and endoscopic studies done 4. Treatment
to exclude this possibility. a. Therapy for anemia depends on the underlying cause.
Transfusion may be required for severe anemia (Hgb < 8 g/dL), with signifi-
cant underlying cardiopulmonary disease or with active bleeding.
CLINICAL PEARL 4-45
Combined Anemia
Patients may have both a combined iron deficiency and an anemia of chronic disease. Clues to a combined
disorder include an anemia that is more severe than usually seen in chronic inflammation alone, a ferritin that
is low to low normal, and a low transferrin and iron saturation. The patient will usually respond to iron therapy
and demonstrate an increase in their reticulocyte count in 2 weeks.
AN E MIA
Common ca us e s : Iron de ficie ncy,

a ne mia of chronic dis e a s e,
chronic re na l fa ilure , a cute blood
los s , he molys is , B12 de ficie ncy,
mye lodys pla s ia , che mothe ra py
Low MCV Norma l MCV High MCV
Che ck la bs : Fe, Che ck la bs : Fe, Che ck la bs :

TIBC, ferritin, TIBC, ferritin, TS H, Re ticulocyte count
he moglobin BUN, cre a tinine
e le ctrophore s is
Ane mia of chronic dis e a s e Incre a s e d Norma l

Chronic re na l fa ilure re ticulocyte count re ticulocyte count
Iron de ficie ncy Hypothyroidis m
Tha la s s e mia Mixe d microcytic/
He moglobinopa thy ma crocytic a ne mia
S ide robla s tic a ne mia
Le a d pois oning
Che ck la bs : B12 de ficie ncy Me dica tions
Indire ct bilirubin Fola te de ficie ncy
Alcohol a bus e
C
o
Live r dis e a s e
m
Mye lodys pla s ia
m
o
n
Incre a s e d bilirubin No incre a s e d
G
bilirubin
S ulfona mide s
e
r
ZDV (AZT)
i
a
Che mothe ra py
t
r
i
He molys is Acute blood los s P he nytoin
c
M
e
d
i
c
a
l
G6P D de ficie ncy Me dica tions
C
Tra uma
o
P yruva te kina s e de ficie ncy Epis ta xis
n
d
He re dita ry s phe rocytos is He ma te me s is
i
t
He re dita ry e lliptocytos is
i
Dive rticulos is
o
Me cha nica l he a rt valve Me thyldopa
n
s
Vira l infe ctions Quinidine
S LE P e nicillin
FIGURE
4 -4 8 Anemia workup. MCV, mean corpuscular volume; TIBC, total iron binding capacity.
Ferrous sulfate is generally used for correcting an iron deficiency.

Dietary advice and vitamin B12 supplements in oral, intramuscular or nasal
form can treat vitamin B12 deficiency.
Folate deficiency can be treated with dietary modification or oral supplementation.
b.
c.
Mild anemia of chronic disease or renal disease do not require therapy.
More significant anemias (Hgb < 10 g/dL) may warrant erythropoietin in pa-
Quick HIT
tients with renal disease as the underlying causethe target hemoglobin range Vitamin B12 generally is
is 10 to 12 g/dL in this group. replaced parenterally with a
nasal spray or intramuscularly/
d. Patients with myelodysplastic syndrome may be treated with supportive transfu-
subcutaneously because ab-
sions as dictated by symptoms or hemoglobin < 8 g/dL. sorption is frequently impaired
e. Underlying disease states should be appropriately treated (e.g., chemotherapy for lack of intrinsic factor.
for cancers, acid suppression for gastritis or peptic ulcers).
TABLE 4-47 Laboratory Findings with Various Forms of Anemia

Iron deficiency Low MCV Decreased iron Normal or decreased
Increased TIBC reticulocyte count
Decreased ferritin
Chronic disease/ Low or normal MCV Normal iron, TIBC Normal or decreased
renal Increased ferritin reticulocyte count
B12 deficiency Increase MCV Decreased B12 level Normal or decreased

Increased homocysteine reticulocyte count
and methylmalonic acid
Folate deficiency Increase MCV Decreased RBC folate Normal or decreased

Increased homocysteine reticulocyte count
Normal methylmalonic acid

Hemolysis Normal or increased Increased bilirubin Increased reticulocyte
MCV count
Acute blood loss Normal or increased MCV Increased reticulocyte count
CLINICAL PEARL 4-46

s
n
Microcytic versus Macrocytic Anemia
o
i
t
i
Indices can be helpful in determining the cause of an anemia. Common microcyctic anemias are iron deficiency,
d
n
a previously undiagnosed congenital disorder such as thalassemia, and lead poisoning. The anemia of chronic
o
C
disease and anemias from infiltrative bone marrow diseases are usually normocytic but on occasion the ane-
l
a
mia of chronic disease is microcytic. Macrocytic anemias are associated with B12 and/or folate deficiencies,
c
i
d
bleeding or hemolysis with a brisk marrow response and on occasion myelodysplasia. Many older adults have
e
M
mixed disorders, for example, an iron deficiency and a folate deficiency which can present with a normocytic
c
anemia. Patients may also have a combined iron deficiency and an anemia of chronic disease. Clues include an
i
r
anemia that is more severe than usually seen in chronic inflammation alone, a ferritin that is low to low normal
t
a
i
and a low iron saturation. The patient will usually respond to iron therapy and demonstrate an increase in their
r
e
G
reticulocyte count in 2 weeks, whereas those with an anemia of chronic disease will not respond to iron.
n
o
m
m
o
C
f. In cases of an aplastic anemia where a bone marrow examination demonstrates
hematopoietic failure, about 50% respond to antithymocyte globulin and cyclo-
sporine or a stem cell transplant.
B. White blood cell (WBC) disorders

Quick HIT a. Aging is not associated with significant changes in the WBC counts.
b. WBC disorders occur more frequently in geriatric patients and the most com-
The most common causes for mon disorders are neoplastic diseases.
alterations of the WBC count c. Abnormalities can be either increased or decreased WBC counts; red blood cells
in geriatric patients are neo- and platelets may also be affected by the underlying cause.
plastic diseases.
d. Causes for increases and decreases in WBCs are presented in Table 4-48.
a. Infection is a common cause for abnormal WBC counts.
b. Fatigue, weight loss, weakness may occur related to underlying neoplastic dis-
ease and anemia.
c. Hemorrhage may occur if concomitant thrombocytopenia is present.
d. Medications may be an underlying cause for increases or decreases in WBC
count and must be reviewed.
TABLE 4-48 Causes for Increased or Decreased WBCs and Platelets

Increased Examples
Reactive Stress, trauma, surgery, inflammation, anemia

WBCs may be increased by corticosteroids or -agonists
Neoplastic Myelodysplastic syndrome, leukemia
Essential thrombocythemia and polycythemia vera (platelets)
Decreased Examples
Production Medications, viruses, B12 or folate deficiency, bone marrow infiltration

or failure
Destruction Connective tissue diseases, medications, or immune destruction
Sequestration Splenomegaly from any cause, commonly liver disease
e. History of other diseases

Connective tissue diseases may cause an immune destruction of WBCs.
Cirrhosis can lead to splenomegaly and splenic sequestration of WBCs, lower-
ing counts, and an associated pancytopenia.
Chronic infections can increase WBC counts.
History of prior cancers might signify recurrent disease with marrow infiltration.
C
-agonists or corticosteroid medications can cause WBCs to demarginate and
o
m
increase the number of circulating white blood cells.
m
f. Dietary history because deficiencies in folate and vitamin B12 can result in de-
o
n
creased WBC production as well as anemia as noted above.
G
e
g. Physical examination findings
r
i
a
Pallor of skin or conjunctiva
t
r
i
Stigmata of liver disease including edema/ascites, spider angioma, hepatomeg-
c
M
aly, jaundice, palmar erythema
e
d
Splenomegaly
i
c
Lymphadenopathy
a
l
Ecchymosis, petechiae
C
o
n
Evaluation of neurologic function to include proprioception
d
i
3. Diagnosis (Figure 4-49)
t
i
o
a. Laboratory testing
Quick HIT
n
s
Complete blood count, including peripheral smear
Absolute neutrophil count Bone marrow aspiration is
Liver function testing indicated when assessing pa-
Serum B12 and RBC folate in leukopenic patients tients with a pancytopenia.
b. Bone marrow examination
In patients without an easily identified cause and with sustained elevation or
decrease in WBC count, referral to a hematologist is warranted.
Often this will result in bone marrow assessment.
Besides cellularity of the bone marrow, assessment may include immunophe-
Quick HIT
notyping and cytogenetic testing. A bone marrow is often useful
c. Specific diagnoses for evaluating an altered WBC
Leukemia count, particularly when other
cell lines (RBC or platelet) are
(1) Acute myelogenous leukemia also abnormal.
(a) Over half of patients are aged > 65 years.
(b) These patients have uncontrolled production of immature myeloid
cells that interfere with effective production of normal cells.
(c) Patients will have either increased or decreased WBCs along with low
hemoglobin and platelets; presence of circulating blast forms of WBCs
is pathognomonic.
LE U K O P E N IA
Common ca us e s : Vira l
s yndrome , HIV infe ction,
me dica tions , bone ma rrow
fa ilure , S LE
Me dica tions No s us picious

me dica tions
Anticonvuls a nts Che ck la bs : CBC,

Che mothe ra py B12 , HIV
Antibiotics
Antithyroid me dica tion
P roca ina mide
Cloza pine Abnorma l la bs Norma l la bs
P e rnicious a ne mia Vira l s yndrome

Apla s tic a ne mia Be nign chronic
Mye lodys pla s ia ne utrope nia
Le uke mia Idiopa thic le ukope nia
Multiple mye loma
HIV infe ction
S LE
s
n
FIGURE
o
4 -4 9 Evaluation of leukopenia.
i
t
i
d
n
o
C
l
a
c
i
(d) Diagnosis is confirmed through identification of > 20% blasts on bone
d
e
M
marrow examination.
(e) Further classification and prognosis is achieved with immune-pheno-
c
i
r
typing and cytogenetic analysis.
t
a
i
(2) Chronic lymphocytic leukemia
r
e
G
(a) Most common leukemia and predominantly affects geriatric patients.
n
o
(b) May be present for years without symptoms and be discovered
m
incidentally.
m
o
(c) Can be subtyped into different categories; however, > 90% are B-cell type.
C
(d) Can be diagnosed with evaluation of the peripheral blood.
(i) > 10,000 lymphocytes per microliter
(ii) Characteristic immunophenotyping findings
(e) The Rai Classification is helpful to assess prognosis and utilizes the
presence of increased lymphocytes, low hemoglobin, low platelet,
lymphadenopathy, splenomegaly, and hepatomegaly in the assessment.
(3) Chronic myelogenous leukemia
(a) Also common in the geriatric population and increases in incidence
with increasing age.
(b) Can stay in chronic phase of this disease for 10 or more years with
controllable symptoms.
(c) Diagnosis is based upon peripheral blood cytogenetic analysis; the
presence of the Philadelphia chromosome confirms the diagnosis.
(d) In the chronic phase, there are < 10% blasts.
(e) The disease can progress to an accelerated phase with increasing blasts
(10% to 19%), cytopenias, increased basophils, and splenomegaly.
(f) The blast phase is basically development into an acute leukemia, with
blast counts > 20%.
(4) Acute lymphocytic leukemia
(a) Largely a disease in children but can occur in adults.
(b) The disease does not act the same way in geriatric patients as in chil-
dren, with geriatric patients being more refractory to therapy.
(c) Diagnosis is achieved the same way with cytogenetic analysis and im-
munophenotypes of the cells.
Myelodysplastic syndromes (MDS) are a group of stem cell disorders charac-
terized by a decreased production of blood elements.
(1) Disease of the elderly with two-thirds being elderly males.
(2) These patients have ineffective hematopoiesis that results in cytopenia ef-
fecting more than one cell line.
(3) Commonly these patients have low hemoglobin, platelets as well as WBCs.
(4) Peripheral blood evaluation to eliminate other causes, such as nutritional
deficiency is important.
(5) Bone marrow findings, including cytogenetic analysis are critical at arriv-
ing at the diagnosis of myelodysplastic syndrome.
(6) Classification systems have been developed to subcategorize and provide prog-
nostic information based. These schemes are beyond the scope of this book.
(7) Important prognostic factors include age, number of cell lines affected,
cytogenetics, and percentage blasts present.
(8) Treatment is largely supportive.
Iatrogenic causesmedications and treatments, such as radiation, can contrib-
ute to WBC disorders through direct toxicity and should be assessed as part of
Quick HIT
the evaluation. Myelodysplastic syndrome
Nutritional assessmentincluding vitamin B12 and RBC folate levels, serum is a premalignant condition
albumin, BMI, and inquiring about recent weight loss should be part of the with impaired production of
one or more hematologic cell
diagnostic evaluation. lines. Treatment is commonly
C
Chronic medical diseasesevaluation for liver disease, chronic infections, and
o
supportive with monitoring for
m
connective tissue diseases. malignant disease.
m
(1) Liver enzymes, albumin, and prothrombin time
o
n
(2) Antinuclear antibody (ANA), complement levels, C-reactive protein,
G
e
erythrocyte sedimentation rate (ESR), rheumatoid factor
r
i
a
4. Treatment
t
r
i
a. Supportive measures
c
M
Transfusions for anemia or thrombocytopenia based on hemoglobin level and
e
symptoms such as dyspnea, hypotension or bleeding.
d
i
c
Erythropoietin in selected patients with functional marrow.
a
l
(1) Indicated for patients with renal disease or chemotherapy-related anemia.
C
o
(2) Target hemoglobin between 10 and 12 g/dL.
n
d
i
Granulocyte colony-stimulating factor or granulocyte-macrophage colony-
t
i
o
stimulating factor in selected patients with neutropenia.
n
s
CLINICAL PEARL 4-47
Myelodysplastic Syndrome
MDS are a group of bone marrow stem cell disorders that share in common a defect in the bone marrows abil-
ity to produce healthy cells. MDS usually begins with mutation in a single blood forming stem cell but as the
disease evolves there is an increase in blast cells and cellular maturation becomes more arrested leading to
anemia, thrombocytopenia, and neutropenia. Individuals with MDS have an increased risk of developing acute
myelogenous leukemia (AML). MDS is sometimes referred to as preleukemia.
The diagnosis of MDS is first suspected by abnormalities in the CBC followed by a bone marrow aspirate
and biopsy. In patients with MDS, the marrow will show an increased number of immature or blast cells.
About 50% of patients have a detectible cytogenetic abnormality.
MDS encompasses several different bone marrow disorders and numerous factors contribute to the behav-
ior and prognosis of the disease. Several classification systems have been proposed for MDS, including the
French-American-British classification and an updated version proposed by the WHO. The goals of treatment
are to prevent and/or treat the complications of MDS, cure if possible, and prolong survival. Prognosis is di-
rectly related to the number of bone marrow blast cells, the severity of the peripheral blood cytopenias and to
certain cytogenetic abnormalities. By convention MDS is classified as AMLif bone marrow blasts exceed 20%.
CLINICAL PEARL 4-48

Myeloproliferative Disorders
Myeloproliferative disorders are a group of diseases in which the bone marrow produces an excess of cells.
These disorders are considered hematologic neoplasms and include chronic myelogenous leukemia (CML),
polycythemia vera (PV), idiopathic myelofibrosis, and essential thrombocytosis (ET), chronic neutrophilic leuke-
mia and chronic eosinophilic leukemia. All of these disorders involve dysregulation of the multipotent hemato-
poietic stem cell (CD34) and are characterized by the overproduction of one or more types of cells. They share
the following features:
Overproduction of one or several blood elements with dominance of a transformed clone.
Hypercellular marrow/marrow fibrosis
Cytogenetic abnormalities
Thrombotic and/or hemorrhagic diatheses
Extramedullary hematopoiesis (liver/spleen)
Transformation to acute leukemia
Overlapping clinical features
Bone marrow biopsy and cytogenetic analysis are needed for diagnosis and classification. Treatment for
each disorder is slightly different and is directed at controlling symptoms and at reducing excessive numbers
of blood cells.
(1) Indicated to counteract the neutropenia from chemotherapy with nonmy-

eloid cancers.
(2) Useful for patients with immune destruction as underlying cause and pos-
s
n
sibly those cases related to viral infections.
o
(3) Targeted to higher risk patients with ANC < 500 cells/mm 3 with goal of
i
t
i
d
increasing to > 1,500 cells/mm 3.
n
o
C
Aggressively treat infections because this is a leading cause of death.
l
b. Targeted to specific etiology
a
c
i
Modifying medications
d
e
M
(1) For suspected drug induced disease, medications started within past 4
weeks are most likely to be responsible.
c
i
r
(2) Stopping medications may take 2 to 4 weeks for restoration of the WBC.
t
a
i
Quick HIT (3) Steroids and -agonist medications can increase WBC. Counts will return
r
e
G
to normal after completing therapy.
n
o
(%neutrophils If indicated, supplementation to restore vitamin B12, folate, and protein/calo-
m
Absolute
rie intake.
m
%bands) 3 (WBC)
neutrophil
o
(100) Therapy for connective tissue disease (CTD) or cancer:
C
count
(1) The underlying disease can decrease WBC through immune destruction
or marrow infiltration.
(2) Treatment can affect WBC, with steroids increasing and chemotherapy
decreasing counts.
(3) With clinical remission, counts would be expected to normalize.
Therapy for stress or reactive leukocytosis should be directed toward the
underlying condition.
Specific white cell disorders
(1) Myelodysplastic syndrome
(a) These patients frequently require many transfusions and are at risk
for iron overload; chelation therapy should be considered with ferri-
tin values > 2,500 mcg/L.
(b) Chemotherapy and immunomodulators indicated for those at higher
risk for progression to leukemia.
(2) AML
(a) Chemotherapy is very toxic, especially for the frail elderly individual
or those with significant comorbidities.
(b) Chemotherapy is associated with < 50% remission and a high mortal-
ity rate.
(c) Supportive/palliative care may be most appropriate in many cases.
(3) Acute lymphoblastic leukemia

(a) Chemotherapy very successful in children but less so in adults geriat-
ric patients. Quick HIT
(b) Remission is generally short-lived with advancing age being a poor ALL is largely a disease of
prognostic variable. children whereas CML, CLL,
(c) Only about one-third are disease-free for 5 years or more. and AML are more common in
(4) Chronic lymphocytic leukemia geriatric patients.
(a) Largely asymptomatic for years and symptoms are usually related to
infections or immune destruction of red cells or platelets.
(b) Therapy is largely supportive and oriented toward treating or prevent-
ing infections (vaccines).
(c) Cytopenias by immunologic destruction of red cells or platelets may
warrant corticosteroids or intravenous immunoglobulin.
Quick HIT
(d) Chemotherapy is reserved for advanced disease. CML has become a very
(5) CML treatable form of leukemia
(a) Stem cell transplantation and standard chemotherapy has been associ- with imatinab therapy. CLL is
commonly an incidental find-
ated with significant toxicity in geriatric patients. ing and patients can remain
(b) Imatinab, a tyrosine-kinase inhibitor, is a targeted therapy resulting in asymptomatic for years. AML
decreased expression of the Philadelphia chromosome. is more difficult to treat and
(c) Imatinab can be used with any phase of the disease but is least effec- associated with shortened
tive during the blast phase. survival.
C. Multiple myeloma
a. A form of cancer where plasma cells proliferate in the bone marrow and produce
monoclonal immunoglobulin in excess.
C
Quick HIT
o
m
b. The diagnosis of multiple myeloma requires > 10% bone marrow plasma cells or
m
biopsy showing plasmacytoma along with end-organ pathology (CRAB):
o
Multiple myeloma diagnostic
n
Calciumhypercalcemia criteria require > 10% bone
G
Renal insufficiency
e
marrow plasma cells or a
r
i
Anemia biopsy showing plasmacy-
a
t
r
Bone lesions that are lytic toma along with end-organ
i
c
pathology.
c. Multiple myeloma affects bone marrow function and can cause anemia.
M
e
d. Calcium may be bound to the monoclonal proteins, causing hypercalcemia.
d
i
c
e. The myeloma protein can lead to a cast nephropathy which impairs renal
a
l
function.
C
o
f. Multiple myeloma must be distinguished from two premalignant but related
n
Quick HIT
d
conditions.
i
t
i
o
Smoldering multiple myelomahas between 10% and 60% plasma cells but
n
s
no end-organ pathology. Monoclonal gammopathy of
Monoclonal gammopathy of undetermined significance; which has < 10% undetermined significance and
smoldering multiple myeloma
plasma cells and no end-organ effects.
are related conditions with
Neither of these conditions requires therapy, whereas multiple myeloma does increased monoclonal proteins
require treatment. that are distinguished from
Both premalignant conditions can progress to active disease and require multiple myeloma by the lack
monitoring. of end-organ effects.
g. Multiple myeloma occurs almost exclusively in geriatric patients and rarely in
patients aged < 50.
a. Symptoms may be nonspecific, and laboratory findings of an increased
serum protein level with normal or low albumin may be the first clue to
diagnosis. Quick HIT
b. Bone pain may be present from the infiltration by plasmacytomas. Clinical symptoms with mul-
c. Weakness is a common symptom. tiple myeloma are nonspecific
d. Many patients will experience weight loss. and include weight loss,
e. Fever, paresthesias, lymphadenopathy, and liver or spleen enlargement are other constitutional symptoms, and
lymphadenopathy and/or
potential findings. hepatosplenomegaly.
3. Diagnosis (Table 4-49)
a. Serum protein elevation with a normal or low serum albumin.
TABLE 4-49 Clinical Features of Multiple Myeloma

Calcium elevation From increased bone resorption and binding to myeloma proteins
Renal insufficiency Can result from nephrocalcinosis or light chain cast nephropathy
Anemia From marrow infiltration with plasmacytomas
Bone lytic lesions Can be painful and are signs of the bone resorptions; can also result
in compression fractures
Plasmacytomas Can be diagnosed with bone biopsy
Plasma cells On bone aspirate/biopsy, > 10% plasma cells required for diagnosis
M-spike Monoclonal protein spike on serum protein, electrophoresis that is
pathognomonic of multiple myeloma
b. Screening for MM can be done with a serum protein electrophoresis (SPEP)

and urine protein electrophoresis (UEP) which are abnormal in 99% of cases.
A SPEP typically reveals a spike in a monoclonal protein.
c. UEP may reveal light chain spike.
d. Bone marrow aspirate and biopsy are necessary for the diagnosis.
> 10% plasma cells required for diagnosis
> 60% plasma cells associated with poorer prognosis
Cytogenetic and fluorescence in situ hybridization allow for identification of
s
n
specific genetic patterns associated with increased risk for disease progression
o
i
t
e. Metastatic plain x-ray survey to evaluate for lytic lesions support the diagnosis.
i
d
n
Lytic lesions may not show up on a nuclear bone scan.
o
Quick HIT
C
f. Other findings consistent with multiple myeloma.
l
a
Anemia
c
i
Overproduction of a monoclo-
d
Hypercalcemia
e
M
nal gamma globulin will reveal
a protein spike on serum Elevated serum creatinine
c
protein electrophoresis that is Elevated C-reactive protein and ESR
i
r
t
termed an M-spike. 4. Treatment
a
i
r
a. Chemotherapy and stem cell transplantation are the preferred treatments.
e
G
b. Not all patients are suitable for transplant due to side effects associated with
n
o
treatment.
m
m
Patients age may exclude them from treatment.
o
C
(1) Different groups have proposed various ages, for example, 65, 70, and 77
Quick HIT as exclusion criteria for transplant therapy.
Definitive therapy for multiple
(2) Some groups disregard age and use physiologic or functional age based
myeloma involves stem cell upon performance scales or comorbid diseases to determine suitability.
transplantation which can Significant heart disease, liver disease or renal disease may preclude
be quite toxic and results in transplant.
many geriatric patients being c. Those unsuitable for transplant may still be treated with chemotherapy utilizing
excluded from consideration
based upon age or comorbid
less toxic regimens
diseases.
D. Platelet disorders
a. Normal platelet count is 150,000 to 450,000 per microliter.
b. Increases (thrombocytosis) or decreases (thrombocytopenia) occur for many of
the same causes as noted above for WBC disorders.
c. Thrombocytosis may be characterized as reactive or neoplastic/autonomous.
Reactive thrombocytosis is most common (70% to 80%) and occurs as an
acute phase reactant in response to a stressor or stimulus such as:
(1) Surgery
(2) Acute blood loss
(3) Splenectomy
(4) Inflammatory condition
(5) Infection
(6) Trauma
Neoplastic thrombocytosis is a primary hematologic disorder and accounts for
a minority of cases (20% to 30%).
(1) Essential thrombocythemia refers to a primary neoplastic platelet disor-
der. Platelet counts are > 600,000 on two occasions > 1 month apart, with
normal Hgb, normal iron stores, no evidence of splenomegaly, and reac-
tive thrombocytosis is excluded.
(a) For those at high risk of thrombosis, ASA and hydroxyurea to lower
platelet count.
(2) Thrombocytosis can also be part of other underlying neoplastic or prema-
lignant processes.
(a) Myelodysplastic syndrome.
(b) CML.
(c) Polycythemia vera (PV) is a myeloproliferative disorder characterized
by over producing red blood cells creating an elevated RBC mass with
normal O2 saturation and splenomegaly.
(i) If no evidence of splenomegaly diagnosis needs two of the fol-
lowing: leukocytosis, increased leukocyte alkaline phosphatase,
or increased B12; or genetic testing showing JAK-2.
(ii) Platelets and WBC are often elevated.
(iii) Treatment is phlebotomy to achieve iron deficiency and hct
< 45%; ASA 325 mg to reduce the risk of thrombosis.
Quick HIT
C
d. Thrombocytopenia can occur because of impaired production, destruction or
o
m
consumption of platelets, or redistribution of a normal number of platelets.
m
Nonalcoholic steatohepatitis
Impaired production
o
is a common cause for cir-
n
(1) Nutritional from folate or B12 deficiency
G
rhosis and consequent sple-
e
(2) Primary toxicity from alcohol nomegaly leading to isolated
r
i
a
(3) Viral infections such as HIV, EBV, or Hepatitis C thrombocytopenia.
t
r
i
(4) Myelodysplastic syndrome
c
M
(5) Marrow infiltration with leukemia or another cancer
e
Destruction or consumption
d
i
c
(1) Immune destruction related to antiplatelet antibodies
Quick HIT
a
l
(a) Idiopathic thrombocytopenic purpura
C
o
(b) Secondary to CTD, such as lupus
n
Drug induced thrombocyto-
d
i
(c) Secondary to medications such as antibiotics, antiepileptics, quinine penia is more common in the
t
i
o
or heparin elderly.
n
s
(2) infection or disseminated intravascular coagulation (DIC)
Redistribution is generally related to splenomegaly from any cause, most
commonly cirrhosis related to nonalcoholic steatohepatitis, viral hepatitis or
alcohol-related hepatitis. Quick HIT
2. Clinical features Heparin can induce throm-
a. History of bruising, bleeding or arterial or venous thrombosis bocytopenia and patients on
b. Presence of headache, dizziness, paresthesias which may be associated with heparin should have their
platelet counts monitored.
thrombocytosis
c. Presence of constitutional symptoms of fever or weight loss.
d. Past medical history
Hematologic conditions such as polycythemia, myelodysplastic syndrome or
leukemia
Other malignant conditions
Quick HIT
History of hepatic or CTD Antibiotics and anticon-
Surgical history, including splenectomy vulsants are two of the
most common classes of
Medication use, including antibiotics medications associated with
e. Dietary history thrombocytopenia.
f. Substance use
g. Physical examination
Skin for ecchymosis, petechiae
Quick HIT Mucous membranes for similar findings
Patients with thrombocyto- Evaluation for infection and lymphadenopathy
penia or thrombocytosis can Abdominal examination for hepatic enlargement, nodularity, or splenomegaly
present with either bleeding or 3. Diagnosis
thrombotic complications. a. Evaluation for thrombocytosis
Complete blood count with peripheral smear
Nonspecific markers for reactive thrombocytosis include:
(1) Ferritin for evaluating iron stores
(2) ESR or C-reactive protein for inflammation
Quick HIT Referral for bone marrow evaluation
b. Evaluation for thrombocytopenia (Figure 4-50)
Serial blood counts may be Complete blood count with peripheral smear
necessary to evaluate patients Metabolic profile
with platelet disorders be-
cause a change from 300,000
Vitamin B12 and RBC folate
to 150,000 or from 150,000 to Viral titers (hepatitis C, EBV, HIV)
400,000 may represent an ANA and antiphospholipid antibodies
underlying disease process Consultation with hematologist; possible bone marrow evaluation if etiology
despite these falling within unclear
normal range.
4. Treatment
a. Thrombocytosis
If associated with bleeding, stop any medications that may contribute to a de-
crease in platelet function, such as aspirin or NSAIDs.
If no bleeding, then symptoms, such as headache or paresthesias may benefit
s
n
from NSAIDs or ASA.
o
i
Treat associated underlying hematologic condition (e.g., myelodysplastic syn-
t
i
d
drome or leukemia).
n
o
C
Hydroxyurea can lower platelet counts in patients with essential
l
thrombocythemia.
a
c
i
Extremely elevated counts may require apheresis followed by hydroxyurea.
d
e
M
b. Thrombocytopenia
Quick HIT Treatment of any associated underlying condition.
c
i
r
Stop medications that may be related.
t
a
Generally, surgical procedures
i
With mild decreases in counts (100 to 150,000 per microliter), no therapy
r
e
may be performed with plate-
G
let counts > 50,000 per micro- may be needed.
n
o
liter provided platelet function Spontaneous bleeding can be associated with counts < 10,000.
m
is normal. (1) Platelet transfusions can be provided.
m
o
(2) Corticosteroids and/or intravenous immunoglobulin may be helpful with
C
idiopathic thrombocytopenic purpura.
CLINICAL PEARL 4-49
Distinguishing B12 from Folate Deficiency

Elevation of methylmalonic acid aids in distinguishing vitamin B12 deficiency from folate deficiency. In addi-
tion, a clinical finding of neurologic involvement, such as neuropathy, would support a diagnosis of vitamin
B12 deficiency because this does not occur with folate deficiency.
Vitamin B12 is poorly absorbed in the setting of atrophic gastritis in geriatric patients. These patients will
not produce intrinsic factor which is required for absorption in the terminal ileum. A strict vegetarian diet can
also cause B12 deficiency. The constellation of findings of neurologic and gastric disease along with anemia
has been labeled pernicious anemia.
THROMBOCYTOP ENIA
Common ca us e s :
Idiopa thic thrombocytope nic purpura (ITP ), me dica tions , DIC,
pe rnicious a ne mia , colla ge n-va s cula r dis e a s e , hype rs ple nis m, thrombotic
thrombocytope nic purpura (TTP ), ICU pa tie nt/s e ps is
he molytic-ure mic s yndrome
P la te le t Gia nt
Che ck pe riphe ra l s me a r pla te le ts ?
clumping?
Cons ide r a rtifa ct Cons ide r he re dita ry

thrombocytope nia thrombocyope nia
Lymphocyte s , Bla s ts ,
nucle a te d Are
a typica l ce lls
RBCs or the re
or toxic
P e lge r-He ut? s chis tocyte s ?
gra nula tion?
Che ck bone ma rrow Che ck LDH, bilirubin,
C
Cons ide r infe ction a nd ha ptoglobin, coa gs ,
o
a s pira te or Bx
m
che ck ES R, CRP , CXR, D-dime r, fibrinoge n
m
virology a s de e me d
o
ne ce s s a ry
n
Cons ide r prima ry
G
BM dis orde r
e
TTP /HUS or DIC
r
i
a
t
r
i
c
M
e
d
i
Is ola te d?
c
S phe rocyte s ?
a
l
C
o
n
d
i
t
i
o
Eva lua te for he molys is Cons ide r ITP , HIV, HCV, DIC, Cons ide r drug-induce d
n
a nd continue workup ba s e d on thrombocytope nia
s
his tory
Common offe nding a ge nts : Che mothe ra py,

a nticonvuls a nts , he pa rin, P CN, s ulfona mide s , NS AIDs ,
diure tics a nd GP IIb/IIIa inhibitors
FIGURE
4 -5 0 Evaluation of thrombocytopenia. TTP, thrombocytopenic purpura; HUS, hemolytic uremic
syndrome; DIC, disseminated intravascular coagulation.
Ca nc e rs
1. Cancer is characterized by the uncontrolled growth of abnormal cells and the abil-
ity to spread or metastasize.
2. Cancer growth impairs or destroys normal tissues and is metabolically active at the
expense of normal tissues and organs.
3. Cancer cells may invade tissue locally or via the lymphatic or blood systems im-
plant in distant locations; referred to as metastases.
Quick HIT 4. The actual cause for cancer is uncertain. Several theories exist and these may
Though cancer is not a dis- alone or in concert contribute to developing cancerous tissue.
ease of exclusively geriatric 5. Cancer incidence increases with age.
patients, it disproportionately a. Several theories have been proposed to explain this association with age. Aging
affects older adults and over allows more time for environmental exposures, replication errors, and for cells
half of all new diagnoses are
in those aged > 65. Over 70%
to accumulate gene mutations that cause abnormal growth.
of cancer deaths occur in b. Normal cells can repair damage to DNA. However these repair mechanisms may
those aged > 65 years. diminish with age.
c. Age-related changes in immune function may affect the ability to destroy abnor-
mal cells.
6. Though cancer is not a disease of exclusively geriatric patients, the incidence and
prevalence are much greater in the geriatric populationover half of all new diag-
noses are in those aged > 65.
7. Cancer causes approximately 25% of all deaths.
8. Over 70% of cancer deaths are in those aged > 65.
9. The most common causes for cancer deaths vary by gender but include lung can-
cer, breast cancer, prostate cancer, and colon cancer (Figures 4-51 and 4-52).
100
s
n
o
i
Lung a nd Bronchus
t
i
d
n
90
o
C
l
a
c
80
i
d
e
M
c
70
i
r
t
a
i
r
e
G
s
e
60
l
a
n
m
o
m
0
0
m
0
,
50
0
o
C
0
1
S toma ch
r
e
P ros ta te
p
e
40
t
a
R
Colon a nd Re ctum
30
20
P a ncre a s
10
Le uke mia Live r

0
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
3
3
3
3
3
4
4
4
4
4
5
5
5
5
5
6
6
6
6
6
7
7
7
7
7
8
8
8
8
8
9
9
9
9
9
0
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
0
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
2
Ye a r of de a th
FIGURE
4 -5 1 Death rates from cancer in males.
(Feig BW, Ching DC. The M.D. Anderson Surgical Oncology Handbook. Philadelphia, PA: LWW, 2011.)
100
95
90
85
80
75
70
65
s
e
l
a
60
m
e
f
55
0
0
0
50
,
0
0
1
45 Lung a nd Bronchus
r
e
p
40
e
t
a
35 Bre a s t
R
30
25
Colon a nd Re ctum
20 Ute rus
S toma ch
15
10 Ova ry
P a ncre a s
5
0
C
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
2
4
6
8
0
3
3
3
3
3
4
4
4
4
4
5
5
5
5
5
6
6
6
6
6
7
7
7
7
7
8
8
8
8
8
9
9
9
9
9
0
o
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
9
0
m
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
2
m
Ye a r of de a th
o
n
FIGURE
4 -5 2
G
Death rates from cancers in females.
e
r
i
(Feig BW, Ching DC. The M.D. Anderson Surgical Oncology Handbook. Philadelphia, PA: LWW, 2011.)
a
t
r
i
c
M
e
PEARL
d
CLINICAL 4-50
i
c
a
l
C
Treating Geriatric Cancer Patients
o
n
d
The approach to older individuals with cancer should not be based solely on age. However, being older can
i
t
i
impact evaluation and treatment. Factors to consider include a decreasing life expectancy, comorbidities and
o
n
perhaps a concomitant illness that affects life expectancy. Appropriate clinical judgment should be used in pa-
s
tients with poor functional status, cognitive impairment, and known limited life expectancy. Altered pharmaco-
dynamics and kinetics may affect the approach to chemotherapy and frail elderly adults often do not tolerate
treatment as well as younger individuals. Finally evidence that specifically addresses how to treat older adults
with cancer is often sparse.
1. Screening for several cancers is recommended for asymptomatic adults. As people
are living healthier and longer lives, the age to discontinue screening is contro-
versial. Many experts recommend discontinuing screening at age 75 or when life
expectancy is < 10 years.
a. Recommendations include:
Lung cancerCT scan yearly between ages 55 and 80 in those with a 30 pack-
year smoking history.
Breast cancerrecommendations vary with some groups recommending
mammograms every 2 years starting at age 50, and others recommending an-
nual mammogram beginning at age 40. Several groups propose a stop date
(also controversial) of age 75.
Colon cancercolonoscopy every 10 years beginning age 50 for average-risk

patients with a stop age of 75 years.
Cervical cancerpap smear every 3 years up to age 65; women with a history
of regular and normal smears may stop after age 65.
Prostate cancer screening is controversial and should be based on a patient/
doctor discussion.
2. Clinical presentation may be asymptomatic, nonspecific or with symptoms suggest-
ing an underlying lesion.
a. Painless hematuria may signify an underlying bladder, ureteral, or renal carci-
noma, and merits investigation.
b. Painless jaundice is a classic finding for pancreatic cancer.
c. Rectal bleeding, hematochezia, or melena may be a finding with colon cancer.
d. Breast cancer may present with a painless nodule.
e. Prostate cancer may be asymptomatic or cause obstructive symptoms, such as
urinary frequency, nocturia, and weakened urinary stream that mimic BPH.
f. Lung cancer may present with hemoptysis or persistent cough.
3. Clinical symptoms may occur in the affected organ.
a. Shortness of breath with a primary lung lesion.
b. Urinary obstruction, frequency, weakened stream, nocturia, and dysuria with
prostate cancer.
c. Breast cancer with pain, erythema, tenderness, warmth, and enlargement of the
affected breast.
d. Colon cancer may cause a change in bowel habits including constipation, ribbon
like stools, and abdominal discomfort.
e. Cancer may present with pain or swelling/enlargement in the affected organ.
s
n
4. Cancer patients with significant underlying chronic medical conditions experience
o
i
a more rapid decline because of their initial weakened condition.
t
i
d
5. Although some cancers may be more or less aggressive in an older patient, most
n
o
C
cancer types follow similar courses to younger patients, barring impact from co-
l
morbid diseases and underlying physical condition.
a
c
i
6. Patients presenting with advanced disease may have symptoms related to the pres-
d
e
M
ence of metastases.
a. For example, headache or back pain in a patient with breast cancer may suggest
c
i
r
metastatic disease.
t
a
i
b. Fatigue, functional decline, weight loss, and failure to thrive suggest more ad-
r
e
G
vanced disease.
n
o
7. For patients with suspected cancer, it is important to perform a more complete
m
geriatric assessment, including functional abilities, especially because cancer treat-
m
o
ment may include invasive procedures and medications with many side effects.
C
8. Determine existing social supports.
Quick HIT 9. Introduce discussion of Health Care Power of Attorney and Advanced Directives if
not already in place.
For patients with suspected
cancer, it is important to 10. Physical examination
perform a more complete a. Focus on defining the lesion if visible or palpable.
geriatric assessment, includ- b. Evaluate for metastases.
ing functional assessment Lymph nodes
because cancer evaluation
Lung examination
and treatment may include
invasive procedures and Abdominal examination for organomegaly
medications with many side Neurologic for focal deficits
effects. Breast examination
C. Diagnosis
1. Signs and symptoms guide the initial diagnostic testing.
a. Abnormal laboratory findings may direct next steps.
For example, hematuria could lead to further testing such as urine cytology,
CT scan, ultrasound, and/or cystoscopy.
An iron deficiency anemia without an obvious source suggests the need for
endoscopic evaluation to rule out an occult malignancy.
b. Symptoms or abnormal examination findings may direct additional testing.

Pain may lead to imaging of the affected organ with ultrasound, CT scan or
MRI.
In patients with suspected cancer and headache or abnormal neurologic find-
ings, CT scanning, and/or MRI scanning is useful to rule out brain metastases.
2. Laboratory testing
a. CBC and chemistry profiles commonly performed.
b. Results may suggest the etiology, the presence of metastases and impact therapy
if renal insufficiency and/or liver disease are present.
c. Tumor markers (TMs) are available for many cancers and may be performed on
blood samples, biopsy samples, and other body fluids (Table 4-50).
TMs are most commonly proteins produced by tumor cells (e.g., CA-125,
CEA).
Quick HIT
TMs can be produced by other, noncancerous cells. TMs are not typically used as
Not all types of cancers have identifiable markers, and not all tumors produce screening tools but to assist
TMs. with prognosis, diagnosis, and
response to treatment.
TMs are not typically used as screening tools but to assist with prognosis, di-
agnosis, and response to treatment.
3. X-ray testing
a. Plain x-rays may be initial tests for suspected lung or bone/soft tissue abnormali-
ties. Abdominal films can indicate possible bowel obstruction or perforation.
TABLE 4-50 Serum Tumor Markers
C
Tumor Marker Associated Cancers
o
m
m
-Fetoprotein Liver cancer, germ cell tumors
o
n
-2-Microglobulin Multiple myeloma, chronic lymphocytic leukemia, and
G
e
lymphoma
r
i
a
-HCG Choriocarcinoma, testicular cancer
t
r
i
c
BCR-ABLfusion gene Chronic myeloid leukemia
M
e
CA 15-3 Breast cancer
d
i
c
CA 27-29 Breast cancer
a
l
C
CA 19-9 Pancreatic cancer, gallbladder/biliary cancer, and gastric
o
n
cancer
d
i
t
CA-125 Ovarian cancer
i
o
n
Calcitonin Thyroid cancer (medullary)
s
Carcinoembryonic antigen Colon cancer, breast cancer
CD20 Non-Hodgkin lymphoma
Chromogranin A Neuroendocrine tumors
Cytokeratin fragments 21-1 Lung cancer
HE4 Ovarian cancer
Immunoglobulins Multiple myeloma, Waldenstrom macroglobulinemia
Lactate dehydrogenase Germ cell tumors
Prostate-specific antigen Prostate cancer
CLINICAL PEARL 4-51

Monitoring serves to detect the reappearance or progression of cancer. Most serum tumor markers are
more useful for monitoring than for diagnosis and staging because they are generally too insensitive and
nonspecific.
b. Ultrasound or CT scan are often utilized to visualize solid tumors and assess the
gallbladder and biliary system.
c. Ultrasound is useful for evaluating prostate abnormalities.
d. A CT scan may be needed to follow up an abnormal chest x-ray or abdominal
film.
e. Mammogram is the first-line test for evaluating breast abnormalities.
f. Hollow organs, such as the gastrointestinal tract and bladder, generally require
endoscopy or cystoscopy to evaluate a suspected tumor.
4. Biopsy
a. Tissue diagnosis is the gold standard and in addition to establishing the diagno-
Quick HIT sis obtains tissue for tumor marker and hormone receptor testing.
b. Accessible lesions may warrant surgical referral for biopsy.
Tissue diagnosis is the gold
standard and obtaining tissue
c. Patients with suspected GI or GU lesions may be biopsied at the time of endo-
allows for additional testing for scopic evaluation.
TMs and hormone receptors. d. CT or ultrasound imaging is commonly used to guide biopsies of solid organs,
lung, breast, and prostate gland.
D. Therapy
1. Therapy will be directed by several factors.
a. Type of cancer
b. Stage of cancerthis represents extent of disease and is defined by the anatomic
distribution of the cancer.
Quick HIT TNM system most commonly used (Table 4-51)utilizes physical examina-
tion, laboratory, and imaging information to determine the stage
The T in the TMN system refer Leukemias, lymphomas, brain, and nervous system tumors of the spinal cord
to the primary lesion and re-
s
do not use the TMN system and have their own classifications.
n
flects the size of the tumor, N
o
Tumor staging is different from grading.
i
is the degree of nodal involve-
t
i
d
ment, and M is for the pres- (1) Grading is the degree of the histologic abnormalities of the tumor cells.
n
o
ence of metastases. (2) Well-differentiated tumors represent tumors with cells that appear close
C
to normal, whereas poorly differentiated tumors contain very abnormal
l
a
c
looking cells. Poorly differentiated tumors are associated with a poorer
i
d
e
prognosis.
M
(3) Not all tumors use the same grading system.
c
i
c. Additional risk factors such as grade of cancer, physical condition of the patient,
r
t
a
and comorbid condition such as heart disease, renal failure or liver disease
i
r
e
G
should be considered when developing treatment plans.
n
d. Cognitive function of the patient and their desires for cure vs. palliation should
o
m
be incorporated into the care plan.
m
2. Treatment options
o
C
a. Surgery
Preoperative evaluation should assess the patients comorbidities, functional sta-
tus, activity level along with the type of surgery (see Preoperative section).
TABLE 4-51 TNM Staging System

T Tumor
Tis In situ
T14 Tumor size with progressive increase from 1 to 4
N Nodes
N0 No spread to nodes apparent
N13 Increasing number and spread to lymph nodes
M Metastases
M0 No distant spread
M1 Distant spread
Assess the patients relative risk for surgery and address presurgical planning
and prophylactic therapies to minimize surgical risk.
Team approach with preoperative anesthesia evaluation can help to minimize Quick HIT
risk. Age-related changes in tissue
Neoadjuvant chemotherapy to shrink the tumor size preoperatively can some- sensitivity (pharmacodynam-
times be of potential benefit to limit the extent of surgery. ics) and pharmacokinetics
Surgery is frequently followed by radiation therapy and/or hormonal therapy should be considered when
planning chemotherapy.
in patients with breast cancer.
For lung and colon cancer patients, the best option for cure is surgery pro-
vided the patient is an acceptable surgical candidate.
One of several options for prostate cancer patients.
b. Chemotherapy
Toxic medications that preferentially destroy rapidly dividing and active can-
cer cells.
Though this happens to a large extent, chemotherapy also effects normal tis-
sues causing symptoms that range from annoying side effects to life-threaten-
ing reactions.
Bone marrow cells are commonly affected leading to cytopenias and suscepti-
bility to infection, anemia, and bleeding-related symptoms.
(1) Hematopoietic growth factors that include erythropoietin (RBCs), granu-
locyte colony-stimulating factor (WBCs), and IL-11 (platelets) can be ad-
ministered to stimulate the growth of these different populations of cells
to minimize ill effects and allow chemotherapy to continue.
Several issues specifically related to the elderly include:
(1) Age-related changes in renal and liver can alter the metabolism of
C
medications.
o
m
(2) Body and fat composition changes resulting in an altered distribution of
m
medications.
Quick HIT
o
n
(3) Age-related declines in cardiopulmonary and bone marrow reserve place
G
e
the older patient at greater risk for adverse effects. More likely to have one Two key questions to consider
r
i
a
or more chronic medical conditions that may impact treatment. when evaluating comorbidities
t
r
in an older cancer patient are
i
Patients with a limited life expectancy related to chronic underlying diseases
c
whether the patient will die
M
may be more harmed than helped by chemotherapy. from the cancer or a comor-
e
There are many different medications used in different combinations targeted
d
bidity and does another medi-
i
c
to treating different cancers.
a
cal problem limit their ability to
l
Neoadjuvant (preoperative) or adjuvant (postoperative) chemotherapy are tolerate treatment.
C
o
used to lessen the risk of surgery and the risk of postoperative recurrence.
n
d
i
Chemotherapy is also often utilized as palliative therapy in metastatic disease.
t
i
o
c. Biologics
n
s
These include monoclonal antibodies, cytokines, and Bacillus Calmette-
Guerin (BCG).
Monoclonal antibodies target different cell surface proteins or surface
receptors.
(1) Promote tumor destruction by binding to surface proteins
(2) Can inhibit cellular functions such as activation of growth factors
(3) Can deliver medications designed to destroy the cell
Cytokines are signaling proteins that include interleukins and interferon.
These proteins act by stimulating the production and activation of WBCs en-
hancing immune response.
BCG is a tuberculosis vaccine that when placed into the bladder, stimulates an
immune response against the bladder tumor cells leading to tumor destruction
and remission of the cancer in a high percentage of patients.
(1) BCG side effects generally include local reactions, such as swelling or
rash, flu-like symptoms, and allergic reactions which can vary in severity.
d. Hormonal
Use in hormonally responsive tumors such as prostate cancer and breast cancer.
Medications for breast cancer are designed to limit the effects of estrogen
either by blocking their action on the breast cancer tissue (SERMs) or by
decreasing peripheral conversion of androstenedione to estrogens (aromatase

inhibitors).
Primary side effects include an increased risk of deep venous thrombosis and
menopausal symptoms.
Hormonal therapy for prostate cancer includes castration, LHRH agonists that
prevent release of LH by suppressing production, LHRH antagonists which
block receptors that trigger LH release and antiandrogens that block the pe-
ripheral effects of androgens.
Side effects of these medications include loss of libido, erectile dysfunction,
fatigue, gynecomastia, and bone loss.
e. Radiation
Not all cancers are radiationresponsive.
Quick HIT Primary role for traditional radiation is for adjuvant therapy or palliation; ra-
dionuclide therapy for thyroid cancer can be curative.
Many factors impact therapy Cancers where radiation is commonly used include prostate, breast, bladder,
decisionsstaging of disease, cervix, esophageal, rectal, and head/neck tumors.
grade of tumor, physical con- Radionuclides can be utilized as targeted therapy, for example, I-131 to target
dition of the patient, and the
uptake by thyroid cancer cells. Radionuclide therapy has also been combined
patients desire for palliation
versus cure. with monoclonal antibodies to bind radionuclides to receptors on leukemia or
lymphoma cells.
Primary side effects of radiation therapy include both immediate and longer-
term effects.
(1) Immediate effects can include a sun burn, edema, symptoms in the
Quick HIT vicinity of the radiation for example, urinary or bowel changes if lower
abdominal sites involved, dysphagia or associated pain with upper abdo-
s
n
Therapeutic options are indi- men or chest. Localized radiation can also cause systemic symptoms such
o
vidualized with choices that in-
i
as generalized fatigue.
t
i
d
clude surgery, chemotherapy,
(2) Longer-term effects include fibrosis of normal tissues in the area of radia-
n
biologic agents, hormonal
o
C
therapy, and radiation therapy. tion, infertility, and secondary cancer development.
l
f. Specific cancers
a
c
i
Lung
d
e
M
(1) General information
(a) Not including skin cancers, lung cancer is the third most common
c
Quick HIT
i
r
newly diagnosed type of cancer after prostate and breast cancer.
t
a
i
(b) Lung cancer is the most common cause of death from cancer.
r
e
G
Not including skin cancers, (c) Disproportionately affects geriatric patients with 67% of newly diag-
n
lung cancer is the third most
o
nosed patients aged > 65.
m
common newly diagnosed type
(d) 70% of lung cancer deaths occur in those aged > 65 years.
m
of cancer behind prostate and
o
(e) Environmental exposures pose significant risk including smoking,
C
breast cancer; lung cancer
is the most common cause of passive exposure to smoke, asbestos exposure and radon.
cancer death. (2) Clinical features
(a) History may include worsening shortness of breath, cough, hemopty-
sis, weight loss, fatigue.
(b) Nonrespiratory signs and symptoms may represent tumor invasion lo-
cally or that has metastasized.
(i) Invasion and occlusion of the superior vena cava can cause su-
perior vena cava syndrome with upper extremity, neck and face
venous distention and edema.
(ii) Involvement of the laryngeal nerve will cause laryngeal nerve
palsy with resultant hoarseness.
(iii) Pancoast tumor is a local infiltration of the brachial plexus caus-
ing pain and weakness of the affected extremity; this may also
cause Horner syndrome with interruption of sympathetic inner-
vation to face and eye on the affected side causing a decrease in
pupil size, ptosis, and absence of sweating.
(c) Physical examination
(i) Lung examination may be normal or exhibit diminished breath
sounds and wheezing consistent with COPD.
(ii) May be evidence of decreased breath sounds and dullness to per-

cussion suggesting possible pleural effusion.
(iii) Supraclavicular lymphadenopathy is almost always an abnormal Quick HIT
finding and usually indicates an underlying malignancy. Invasion and occlusion of the
(iv) Other signs of lung disease or cancer include digital clubbing, superior vena cava results in
barrel chest, cyanosis, muscle wasting, and cachexia. superior vena cava syndrome
(3) Diagnosis with upper extremity neck and
face venous distention and
(a) Tissue diagnosis is needed to identify the type of lung cancer present.
edema.
(i) Sputum and/or bronchoscopy are useful for more central lesions.
(ii) Peripheral masses on imaging (CT) may be amenable to a guided
transthoracic needle biopsy.
(iii) Biopsy or cytology can identify if the tumor is a small cell car-
cinoma or nonsmall cell carcinoma which affects staging and Quick HIT
therapy. Pancoast tumor is a local infil-
(b) Imaging tration of the brachial plexus
(i) Chest x-ray may show abnormalities but is not specific; persis- causing pain and weakness
tent stable abnormalities suggest a benign lesion. of the affected extremity; this
may also cause associated
(ii) New findings, including pneumonia must be followed up (4 to 6 Horner syndrome with inter-
weeks) until resolution; CT scanning is warranted for persistent ruption of sympathetic inner-
lesions. vation to face and eye on the
(iii) CT scan with IV contrast is more sensitive and specific than a affected side with decrease in
chest x-ray and can identify adjacent organs, including lymph pupil size, drooping of lid, and
absence of sweating.
nodes.
(c) Whole body positron emission tomography imaging (PET scan) high-
lights malignant disease along with metastases.
C
(4) Treatment. At the time of diagnosis only about one in four patients have
o
m
the potential for curative therapy. Only about half of these end up being
m
potentially curable after work-up and/or surgical assessment of the re-
o
n
gional lymph nodes.
G
e
(a) Small cell carcinomaapproximately one-fourth of lung cancers.
r
i
a
(i) Staging
t
r
i
Limitedtumor confined to one hemithorax
c
M
Extensivebeyond one hemithorax
e
(ii) Therapy
d
i
c
Limitedgenerally chemotherapy +/ radiation therapy
a
l
Extensivechemotherapy
C
o
(b) Nonsmall cell carcinoma
n
d
i
(i) StagingTNM system is used.
t
i
o
(ii) Therapysurgery is the best chance for cure and adjunctive ra-
n
s
diation therapy may be used; often these types of cancers do not
respond well to chemotherapy.
(iii) At the time of diagnosis, most tumors are too advanced for the
patient to be a candidate for curative surgery.
Breast
(a) The most common nonskin cancer in women and the second leading
cause of cancer death in women.
(b) Over 40% of new cases are in patients aged > 65 years.
(c) Nearly 60% of patient deaths from breast cancer are in patients aged
> 65 years.
(d) Most breast cancers (70% to 75%) are hormone receptorpositive and
follow a less aggressive course.
(2) Clinical features
(a) History
(i) Finding on mammogram without symptoms
(ii) Painless lump or nodule noted in one of the breasts
(iii) Nipple discharge, may be bloody
(iv) Skin changes with induration, erythema, and warmth
(b) Risk factor assessment including increased risk with:

(i) Advancing age
(ii) Family history
(iii) Prolonged history of menses (e.g., early menarche, late meno-
pause, no children)
(c) Physical examination should include breast examination for charac-
teristics of the nodule
(i) Mobility
(ii) Firmness; breast cancers are typically firm and irregular
(iii) Tenderness
(iv) Skin changes
(v) Presence of nipple discharge
(vi) Presence of axillary lymphadenopathy
(3) Diagnosis
(a) Mammogram to screen and to evaluate suspicious findings.
(b) Abnormalities commonly lead to mammogram-directed biopsy or ul-
trasound imaging.
(c) If findings on examination are consistent with a suspicious lesion and
even if mammography is inconclusive or negative, consider referral
for evaluation for biopsy.
(i) Failure to diagnose breast cancer is one of the most common
causes of malpractice in the primary care setting.
(4) Treatment
(a) Utilize the TNM classification for staging.
(b) Cancers can be lobular or ductal.
s
n
(c) Grade, hormone receptor status and human epidermal growth factor
o
i
2 (HER2) status influence treatment options and choices.
t
i
Quick HIT
d
(d) In general, a geriatric patient who is in good physical condition
n
o
C
should be offered the same options as young patients.
l
Most breast cancers (70% to (e) Therapy will be individualized based upon the above noted factors.
a
c
75%) are hormone receptor
i
(i) Surgical options include breast conserving surgery or
d
positive, which has a more fa-
e
M
vorable prognosis and allows mastectomy.
(ii) Breast conserving surgery involves lumpectomy and is more
c
for use of hormonal therapy as
i
r
a treatment option. likely recommended for early-stage disease. It can be an option
t
a
i
with successful neoadjuvant chemotherapy in more advanced
r
e
G
disease.
n
o
(iii) Radiation is commonly utilized as adjuvant therapy in select
m
Quick HIT patients.
m
o
(iv) Chemotherapy is generally used as adjuvant therapy with hor-
C
Biologic adjuvant therapy mone receptor negative disease or as neoadjuvant therapy.
targeted at HER2 can be used (v) Hormonal therapy is used as adjuvant therapy in hormone recep-
in the 25% of HER2-positive torpositive patients and is an option for nonsurgical candidates,
patients along with other treat- such as a frail elderly person with advanced disease.
ment measures.
(vi) Biologic adjuvant therapy targeted at HER2 can be used in the
25% of HER2-positive breast cancer patients.
Colon
(a) Third most common cause of cancer deaths in both men and women.
(b) Over 60% of new diagnoses of colon cancer and > 70% of cancer
deaths occur in those aged > 65 years.
(a) History
(i) Finding on routine screening colonoscopy
(ii) Discovered during evaluation for incidental anemia
(iii) Abdominal pain, change in bowel habits
(iv) Melena or hematochezia
(v) Constitutional symptoms with advanced disease, such as fatigue
and weight loss
(b) Risk factors

(i) Advancing age
(ii) Family history of colon cancer: especially in a first-degree relative
(iii) History of polyps or prior colon cancer
(iv) History of inflammatory bowel disease
(c) Physical examination
(i) Pallor
(ii) Mass on rectal or abdominal examination
(iii) Organomegaly with metastatic disease
(3) Diagnosis
(a) Best accomplished by colonoscopy and biopsy.
(b) Barium enema could show characteristic applecore lesion but tissue
diagnosis still needed with surgery or colonoscopy.
(c) CT scan of abdomen and chest x-ray to evaluate for metastases and
lymphadenopathy.
(d) Lab testing to evaluate for anemia and liver involvement.
(e) CEA level in patients with high degree of suspicion or confirmed di-
agnosis as tumor marker to monitor disease status posttreatment.
(4) Treatment
(a) Surgical therapy offers the best chance for cure and to assess tumor
depth and regional lymph nodes. In advanced disease palliative sur-
gery is often recommended to avoid colonic obstruction.
(b) Chemotherapy is indicated as adjuvant therapy in selected cases.
(c) Radiation therapy utilized in cases of rectal cancer.
Prostate
C
o
m
(a) Excluding skin, most common cancer in men. About one in six men
m
are diagnosed with prostate cancer during their life time.
o
n
(b) Second leading cause of cancer death in males. About one in six diag-
G
Quick HIT
e
nosed with prostate cancer die from it, accounting for about 30,000
r
i
a
deaths annually.
t
r
i
(c) Increasing prevalence with age As many as 80% of those > 80
c
M
(i) 45% of diagnoses in patients aged > 70. years have evidence of pros-
e
tate cancer; many die with the
(ii) As many as 80% of those aged > 80 years have evidence of the
d
i
disease and not from it.
c
disease on autopsy.
a
l
(iii) Many die with the disease and not from it.
C
o
n
d
i
(a) History
t
i
o
(i) Discovered by PSA screening test.
n
s
(ii) A PSA is prostate specific but not specific for prostate cancer.
About 15% of individuals with a normal PSA (< 4 ng/mL) have
prostate cancer, whereas a PSA > 4 ng/mL has a positive predic-
tive value of about 30%.
(iii) Prostate mass felt on rectal examination.
(iv) Obstructive symptoms such as incomplete emptying, weak
stream, frequency, nocturia, dribbling.
(v) Other genitourinary symptoms such as impotence.
CLINICAL PEARL 4-52
Colon Cancer Prognosis

Prognosis depends on the extent of tumor penetration and extent of disease. Tumors limited to the colon
wall but not through the mesentery have a good prognosis and chance for cure. If regional lymph nodes are
involved the 5-year survival rate is 50% to 65%. Patients with distant metastases have only a 4% 5-year sur-
vival rate.
(vi) Symptoms related to metastases such as bone pain, edema, fa-

tigue or weight loss.
(b) Risk factors
(i) Family history
(ii) African American ethnicityassociated with both an increased
Quick HIT incidence and risk of dying
(iii) Age
Individuals with low Gleason (c) Physical examination
scores (in the range of 4 or
(i) Palpation for prostate mass
less) rarely die of prostate
cancer in the ensuing 15 (ii) Inspect for edema, lymphadenopathy
years. Those with comorbidi- (3) Diagnosis
ties or who are older often die (a) Tissue diagnosis with transrectal prostatic biopsy under ultrasound
from other causes. guidance
(b) Surgical pathology
(c) PSA to monitor disease remission, recurrence, or progression
(4) Treatment
(a) TNM staging is utilized.
Quick HIT (b) Gleason system utilized for grade determination.
(i) 1 to 5 score with 1 being well differentiated and 5 being poorly
There are four major options
for managing prostate cancer.
differentiated.
Active surveillance, radi- (ii) Two most common grades found on histologic exam are added to
cal prostatectomy, radiation determine Gleason score.
therapy, and hormone ablation. (c) Several treatment options individualized based upon staging and
Gleason score.
(i) Local disease, options include:
s
n
Active surveillance
o
i
1) Major side effect is anxiety.
t
i
d
Men with > 10-year life expectancy and/or aggressive disease
n
o
C
may benefit for a radical prostatectomy.
l
1) Side effects include erectile dysfunction in over half of pa-
a
c
i
tients and incontinence in up to 10%.
d
e
M
2) Nerve sparing surgery lowers the risk of impotence
postsurgery.
c
i
r
Radiation therapy
t
a
i
1) Side effects may include dysuria, frequency, proctitis, incon-
r
e
G
tinence, erectile dysfunction.
n
o
Brachytherapy
m
1) Side effects similar to radiation therapy.
m
o
(ii) Regional involvement
C
Radiation therapy
Hormonal therapy/androgen deprivation
1) Loss of libido, fatigue, erectile dysfunction as side effects
(iii) Metastatic disease
Surgical castration
Hormonal therapy/androgen deprivation
CLINICAL PEARL 4-53

Prostate Cancer Treatment Approaches
Formerly known as watchful waiting, active surveillance is a better term because those opting out of im-
mediate treatment need regular follow-up and repeat PSA testing, repeat DREs and ultrasounds at regular
intervals to see if the cancer is growing. Not all urologists agree on the frequency of monitoring but often the
DRE and PSA are checked every 3 to 6 months. Some urologists do transrectal ultrasound guided biopsies
annually. This approach is most suitable for asymptomatic men whose cancer is slow growing. This allows
men with less serious disease to avoid the side effects of treatment which might not allow them to live longer
anyway. Some men are uncomfortable with this approach and are willing to take the risk of treatment to try to
remove or destroy the cancer. Younger men are less likely to be select active surveillance out of concern that
the cancer will become a problem over the next 20 to 30 years.
Chro nic P a in
1. Chronic pain is defined as pain that persists beyond the expected course for a con-
dition, or persistent pain lasting > 3 to 6 months.
2. Patients with chronic pain do not usually exhibit the common autonomic manifes-
tations of acute pain (e.g., tachycardia, sweating, grimacing) but may be quiet and
withdrawn with less spontaneous movement and more irritability.
3. Chronic pain is a treatable problem affecting an estimated 25% to 50% of commu-
nity-dwelling older adults and > 75% of long-term care facility residents.
4. Chronic pain is not a normal part of aging. Failure to treat chronic pain adequately
may lead to anxiety, depression, loss of strength and mobility, poor appetite, poor
sleep, and suicidal ideation.
5. Chronic pain can cause a loss of function with a decline in IADLs, ADLs, or both.
6. Age itself does not change the quality of the pain experienced by the individual but
may change the threshold.
7. Chronic pain may be categorized as nociceptive, neuropathic, or mixed (Figure
4-53).
a. Nociceptive pain is pain associated with abnormalities in the musculoskeletal/
somatic structures or organ/visceral structures.
Somatic nociceptive pain is more localized to a structure and often sharp,
throbbing or aching.
Visceral nociceptive pain may be less localized and more vague in nature, of-
ten described as cramping, dull or aching.
b. Neuropathic pain results from abnormalities in the nerves in either the central or
C
peripheral nervous system. It is typically a described as sharp or burning pain.
o
m
c. Mixed pain is ill-defined and may result from a complex mixture of nociceptive
m
and neuropathic factors. There are often no identifiable pathologic process or
o
n
the symptoms are out of proportion to identifiable pathology. Examples include
G
e
myofascial pain syndrome and somatoform pain disorders.
r
i
a
8. Malignancies may cause visceral nociceptive pain from organ involvement or so-
t
r
i
matic nociceptive pain; especially with bone metastases.
c
M
9. Approximately 80% of older adults with cancer experience pain.
e
d
10. Common nonmalignant disorders causing somatic nociceptive pain are mus-
i
c
culoskeletal disorders, such as degenerative spine conditions, arthritis, and
a
l
C
claudication.
o
n
11. Common causes of neurologic pain in the elderly include: complications
d
i
from DM, postherpetic neuralgia, spinal disease, and trauma. Myofascial
t
i
o
n
s
Injure d tis s ue Norma l tis s ue
Norma l ne rve Injure d ne rve
Nocice ptive pa in Ne uropa thic pa in

FIGURE
4 -5 3 Nociceptive and neuropathic pain.
(Hoppenfeld J D. Fundamentals of Pain Medicine. Philadelphia, PA: LWW, 2014.)
TABLE 4-52 Conditions Commonly Associated with Chronic Pain

Malignancy
Connective tissue diseases
Polymyalgia rheumatica
Osteoarthritis
Spinal stenosis
Myofascial pain
Fibromyalgia
Neuropathy
Reflex sympathetic dystrophy
Phantom limb pain
Multiple sclerosis
Claudication
pain, generalized OA, chronic low back pain (CLBP), lumbar spinal stenosis, fi-
bromyalgia syndrome, vascular disease, and peripheral neuropathy are common
chronic nonmalignant pain conditions affecting older individuals (Table 4-52).
12. The elderly population tends to underreport pain.
Quick HIT 13. Cognitive impairment in the geriatric population may complicate the assess-
s
n
ment and treatment of pain.
o
Chronic pain is a very com-
i
14. Pain scales provide useful information to guide evaluation and treatment.
t
mon treatable problem with
i
d
n
a serious negative impact on
o
C
function and quality of life if B. Clinical features
l
left untreated. 1. History
a
c
i
a. Characterize the pain
d
e
M
Onset and location
Pain and stiffness associated with OA
c
i
r
Localized or generalized pain
t
a
i
Radiation of pain
r
e
G
Presence of numbness, tingling or weakness
Quick HIT
n
o
Claudication or pseudoclaudication
m
Presence of trigger points (Figure 4-54)
m
Assessment and management
o
Sleep disturbance
C
of chronic pain in elderly is
complex and multifactorial. b. History of diabetes, vascular disease, shingles, or malignancy
The elderly population tends c. Previous testing used to establish the diagnosis
to underreport pain. For this d. Prior treatment including current and past prescriptions and OTC drug use-their
reason, using validated pain effectiveness and adverse effects, natural remedies, and the use and effectiveness
scales can provide useful
information to guide evaluation of nondrug treatments
and treatment. e. Prior specialty care and pain management referrals
f. Functional limitations resulting from the underlying disease and pain
g. Other medical conditionsdistinguish new illness from chronic conditions
h. Impact of comorbidities and treatments on chronic condition/pain
i. Current living environment and support system
j. Psychosocial assessment including assessing for depression and anxiety, the im-
pact of the pain on the patient and family.
Quick HIT 2. Physical examination
a. General including vital signs with a focus on the pain source and the neurologic
Understanding biopsycho- and musculoskeletal examinations. Consider pain a fifth vital sign in the el-
social factors is important to derly patient, utilizing one of the pain scales described in Figure 4-55.
both the provider and patient
in understanding and manag- b. Look for signs of vascular disease such as poor peripheral pulses, diminished
ing painful conditions. hair growth, poor capillary refill or dependent rubor.
c. Skin examination for scars of shingles or wounds associated with vascular
disease.
FIGURE
4 -5 4 Trigger points.
(Hoppenfeld J D. Fundamentals of Pain Medicine. Philadelphia, PA: LWW, 2014.)
C
o
He rramie nta unive rs al para valo rac i n de l do lo r
m
Es ta he rra mie nta pa ra va lora cin de l dolor s e dis e pa ra a yuda r a los profe s iona le s de s a lud a va lora r e l dolor s e gn la s
m
ne ce s ida de s individua le s de l pa cie nte . Us a r y e xplica r la e s ca la de 0-10 pa ra la a utova lora cin de l pa cie nte . Inte rpre ta r y
o
us a r la s ca ra s u obs e rva r la conducta de l pa cie nte cua ndo s te no pue de comunica r la inte ns ida d de l dolor.
n
G
0 1 2 3 4 5 6 7 8 9 10
e
r
i
Es ca la El pe or
a
Dolor Dolor Dolor
de s criptiva S in dolor Dolor le ve dolor
t
mode ra do mode ra do inte ns o
r
ve rba l pos ible
i
c
M
e
Es ca la de ge s tos
d
fa cia le s de
i
Ale rta S in humor Ce o fruncido Na riz a rruga da P a rpa de o le nto Ojos ce rra dos
c
Wong-Ba ke r
a
S onrie nte S e rio La bios fruncidos La bio s up. e le va do Boca a bie rta Ge midos
l
P la no Agua nta la re s pira cin Re s pira r pido Lla nto
C
o
Es ca la Inte rfie re Inte rfie re con la s
P ue de Inte rfie re con Re quie re
n
de tole ra ncia S in dolor con la ne ce s ida de s
ignora rlo la s ta re a s re pos o e n ca ma
d
a la a ctivida d conce ntra cin b s ica s
i
t
i
o
n
Es pa ol
s
Ta ga lo
Chino
Core a no
P e rs a
(fa rs i)
Vie tna mita
J a pon s
FIGURE
4 -5 5 Universal pain scale.
(Barash PG, Cullen BF, Stoelting RK, et al. Clinical Anesthesia. Philadelphia, PA: LWW, 2013.)
d. Musculoskeletal examination
Range of motion of joints, including back
Signs of OA such as Heberden nodules
Joint stiffness, tenderness at joint lines, effusions

Presence of trigger points
e. Neurologic examination testing for autonomic, sensory, and motor deficits that
may suggest a neuropathic condition and nerve injury.
C. Diagnosis
1. Key aspects to the diagnostic assessment of chronic pain include:
a. Identifying the underlying disease and its severity
b. Assessing the pain severity
c. Identifying other diseases that could affect the pain or underlying disease, such
as depression or substance abuse
2. Disease assessment
a. Laboratory assessment and imaging directed by the history and physical
examination.
b. With nonspecific somatic symptoms, ESR helps screen for diseases such as poly-
myalgia rheumatica or TA.
c. Radiologic examination may identify OA or other rheumatologic disease such as
rheumatoid arthritis.
d. Patients with suspected spinal stenosis or disc herniation may warrant CT or
MRI scanning of the spine.
e. In patients with suspected vascular disease, ankle-brachial indices can be ob-
tained and followed by more invasive testing such as arteriography or MRA if
intervention is being considered.
f. Electomyographic and nerve conduction velocity testing may help define neuro-
pathic or radicular pain.
s
g. There is no specific test to confirm the clinical diagnoses of fibromyalgia or myo-
n
o
fascial pains.
i
t
i
d
3. Pain assessment
n
o
a. It is strongly recommended to use standard pain scales such as a numerical
C
scale, a pain thermometer scale, or a visual analog scale to ascertain the severity
l
a
c
of pain (Figure 4-55).
i
d
e
b. For patients with cognitive impairment, using behavioral evaluation of the pain
M
is recommended looking at the following aspects of a persons behavior.
c
i
Facial expressions
r
t
a
Verbalization/vocalization
i
r
e
G
Body movements
n
Changes in interpersonal interactions
o
m
Changes in activity patterns or routines
m
Mental status changes
o
C
c. A commonly used tool that utilizes these principles is Pain Assessment in Ad-
Quick HIT vanced Dementia (Figure 4-56).
Patient is observed for 3 to 5 minutes during an activity.
Educating the patient and They are scored on breathing, negative vocalization, facial expressions, body
caregiver on pain management
language, and consolability.
improves pain control. There
should be information given on Each is scored from 0 to 2 with total possible score of 0 to 10.
the nature of the pain, assess-
ment scales, medication use, D. Treatment
and alternative nonpharmaco- 1. Total elimination of chronic pain is usually not possible, and the goals should focus
logic therapeutic techniques on improving function and quality of life.
such as coping skills. 2. Identify the underlying cause of pain and treat if possible.
3. Nonpharmacologic approaches alone or in combination with analgesics are benefi-
cial in helping to achieve pain relief and are often overlooked. These approaches
may allow lower doses of medication, reducing the risk of adverse drug reactions.
a. Educating the patient and caregiver about pain management improves pain
Quick HIT control and includes explaining the nature of the pain, assessment scales, medi-
cation use, and the value of nonpharmacologic therapeutic techniques such as
A patients report of pain is the
most reliable way to evaluate improving coping skills.
treatment. b. Evidence supports the use cognitive-behavioral therapy as an effective chronic
pain management strategy.
Pain Assessment IN Advanced Dementia- PAINAD (Warden, Hurley, Volicer, 2003)

ITEMS 0 1 2 SCORE
Breathing Normal Occasional labored breathing. Noisy labored breathing. Long

Independent of Short period of hyperventilation period of hyperventilation.
vocalization Cheyne-stokes respirations.
Negative vocalization None Occasional moan or groan. Low- Repeated troubled calling out.
level of speech with a negative Loud moaning or groaning.
or disapproving quality Crying
Facial expression Smiling or inexpressive Sad, frightened, frown Facial grimacing
Body language Relaxed Tense. Distressed pacing. Rigid. Fists clenched. Knees
Fidgeting pulled up. Pulling or pushing
away. Striking out
Consolability No need to console Distracted or reassured by voice Unable to console, distract or
or touch reassure
TOTAL*
FIGURE
4 -5 6 PainAD (Pain Assessment IN Advanced DementiaPAINAD).
(Warden V, Hurley AC, Volicer L. Development and psychometric evaluation of the Pain Assessment in Advanced Dementia (PAINAD)
Scale. J Am Med Dir Assoc. 2003;4:915. Developed at the New England Geriatric Research Education & Clinical Center, Bedford
VAMC, MA. http://www.geriatricpain.org/Content/Assessment/Impaired/Pages/PAIDADTool.aspx.)
C
WHO 3 - S te p
o
m
An a lg e s ic La d d e r
m
o
S te p 3: Opioid for mode ra te Exa m p le s :
n
to s e ve re pa in Morphine , oxycodone ,
G
hydromorphone , me tha done ,
e
+ Nonopioid
r
tra ns de rma l fe nta nyl
i
+ Adjuva nt
a
t
r
i
P a in p e rs is tin g o r in c re a s in g
c
M
S te p 2: Opioid for mild to Exa m p le s :
e
d
mode ra te pa in Code ine , tra ma dol, oxycodone , e tc.
i
c
+ Nonopioid
a
l
+ Adjuva nt
C
o
n
P a in p e rs is tin g o r in c re a s in g
d
i
t
i
S te p 1: Exa m p le s :
o
n
NS AIDs (e .g., a s pirin, ibuprofe n),
s
Nonopioid a ce ta minophe n, a djuva nts (TCA,
Adjuva nt a ntie pile ptics )
P a in
FIGURE
4 -5 7 WHO three-step ladder for pain management.
(Urman RD, Vadivelu N. Pocket Pain Medicine. Philadelphia, PA: LWW, 2011.)
c. Complementary and alternative modes of therapy, such as physical therapy, oc-

cupational therapy, psychotherapy, acupuncture, and transcutaneous electrical
nerve stimulation are helpful in improving muscle strength, enhancing func-
tional capacity, and alleviating pain.
d. Exercise and therapies such as head, cold, relaxation, music, and distraction may
be helpful.
4. Medications (Figure 4-57 and Table 4-53)
a. Pharmacologic treatment of pain in the elderly varies and should be individual-
ized. The elderly metabolize pain medicines more slowly than younger patients.
TABLE 4-53 Medications Commonly Used for Chronic Pain

Medication Common Side Effects/Adverse Effects
OpioidImmediate Release
Morphine Constipation, nausea, sedation, and respiratory suppression; caution
Hydromorphone with use of serotonergic medications with tramadol
Oxycodone
Codeine
Hydrocodone
Tramadol
OpioidLong-Acting
Fentanyl transdermal Constipation, nausea, sedation, and with proper titration, respiratory
Morphine suppression should be much less likely
Oxycodone
NSAIDs
Acetaminophen Liver toxicity with doses over ceiling of 3 g
Ibuprofen GI and renal toxicity; may negate cardiovascular effects of aspirin
Celecoxib GI toxicity less than other NSAIDs; may negate cardiovascular ef-
fects of aspirin
Adjunctive Medications
s
Anticonvulsants
n
o
i
Carbamazepine Requires monitoring of CBC and LFTs
t
i
d
n
Monitoring for drug interactions
o
C
Pregabalin Sedation, edema and ataxia
l
a
c
Gabapentin Sedation, edema and ataxia
i
d
e
M
Antidepressants
c
Tricyclic antidepressants Sedation, anticholinergic effects of dry mouth, urinary retention,
i
r
constipation, decrease in BP
t
a
i
r
Duloxetine Hypertension and dizziness
e
G
Venlafaxine Hypertension
n
o
m
Milnacipran Hypertension, dry mouth, nausea, constipation
m
o
C
Always start patient on a low dose (e.g., 25% to 50% of the usual prescribed
Quick HIT dose) and then titrate slowly to minimize any adverse effects. Avoid using maxi-
mum doses for extended periods but instead try to use the lowest effective dose.
The adage start low and go b. When prescribing medications use the American Geriatrics Society BEERS cri-
slow is important to keep
in mind when using pain teria to avoid potentially inappropriate medication use in older adults and to
medications. improve drug safety in older adults (Chapter 1).
c. Be aware of slower drug metabolism in the presence of polypharmacy and the
increased frequency of adverse drug reactions in the elderly.
d. Nonopioids
Quick HIT Acetaminophen should be considered as initial and ongoing pharmacotherapy
in the treatment of persistent pain.
As a rule of thumb the start-
(1) Mild or moderate musculoskeletal pain often responds to acetaminophen
ing dose of a pain medication
should be 25% to 50% of the when given in scheduled doses.
usual median dose. (2) Acetaminophen is usually well tolerated if hepatic function is normal. The
daily dose of acetaminophen in elderly should not exceed 3 g.
Nonselective NSAIDs and COX-2 selective inhibitors may be considered in

patients who have failed other safer therapies. Quick HIT
(1) In view of potential adverse effects, prolonged use of NSAIDs should be
Nociceptive pain should be
avoided whenever possible. approached in a stepwise
(2) Older persons on nonselective NSAIDs or a COX-2 selective inhibitor fashion as outlined in Figure
should use a proton pump inhibitor or misoprostol for gastrointestinal 4-57.
prophylaxis.
(3) For those on long-term NSAIDs routinely assess for GI and renal toxicity,
hypertension, HF, and drug interactions.
(4) NSAIDs exhibit a low ceiling effect which means that increasing the
dose results in little or no increase in analgesia.
Quick HIT
Consider adjuvant analgesics such as the anticonvulsant gabapentin for the Neuropathic pain responds to
management of neuropathic pain. antidepressants, anticonvul-
sants, and topical agents but
(1) Anticonvulsants, steroids, topical local anesthetics, and antidepressants
conventional analgesic agent
are agents that may be used alone or in combination with nonopioid or may still be needed.
opioid analgesics.
Tricyclic antidepressants such as amitriptyline are useful for treating neuro-
pathic pain but because of their significant anticholinergic effects (dry mouth,
tachycardia, diplopia, urinary retention, delirium, etc.) may be poorly toler-
ated in older adults. Quick HIT
Lidocaine patches and capsaicin are topical analgesics that, in addition to topi- Routine dosing of pain
cal NSAIDS, may provide significant analgesia locally with minimal risk of medications for continuous
systemic effects or drug interactions. pain rather than on an as
needed basis results in better
e. Opioids
pain control and using less
Elderly patients with moderate to severe pain, pain-related functional impair- medication.
C
ment, or diminished quality of life caused by pain may benefit from opioid
o
m
therapy.
m
Addiction in the elderly is uncommon; therefore concerns about addiction
o
n
should not be used as a sole justification for withholding opiates.
Quick HIT
G
e
Use sustained-release opioids for continuous pain and short-acting prepara-
r
i
a
tions for breakthrough pain. The elderly are more sensitive
t
r
i
Doses of sustained-release medications can be determined and adjusted based to opiate drugs in part because
c
M
upon the need for use of breakthrough medications. of decreased renal clearance
e
and hepatic metabolism.
When prescribing opioids, anticipate and prevent constipation by recom-
d
i
c
mending a prophylactic bowel regimen.
a
l
Recognize and manage opioid side effects such as sedation, confusion, and
C
o
nausea.
n
Quick HIT
d
i
Avoid the use of opioids such as propoxyphene, meperidine hydrochloride,
t
i
o
and methadone hydrochloride that have a high side effect profile in the
n
When prescribing opioids
s
elderly. anticipate nausea and con-
Closely monitor patients drugdrug and drugdisease interactions be- stipation as side effects and
cause the elderly tend to be on multiple medications for multiple chronic institute prophylactic therapy
diseases. as needed.
f. Consider consultation with an anesthesiologist or pain management specialist in
cases where interventional therapy (e.g., injections, nerve block) may be of ben-
efit or when conservative approaches prove ineffective.
Quick HIT
Complementary and alterna-
tive modes of therapy, such as
physical therapy, occupational
CLINICAL PEARL 4-54 therapy, psychotherapy, acu-
puncture, and transcutaneous
electrical nerve stimulation
It is important for providers to approach an older adult with any type of chronic pain as in the context of an
are helpful in improving
the whole patient and not solely focus on the pain. For example, a patient complaining of back pain may have muscle strength, enhancing
degenerative disease of the spine, but the important treatment target may be dealing with an underlying functional capacity of elderly,
depression. and alleviating pain.

Ms. M is a 70-year-old woman with chronic diffuse aches throughout much of her body for
a couple of years. Her primary areas of discomfort are her back, neck, and shoulders. When
she talks of her condition, she calls it rheumatism. It does not limit any specific activity, but
she notes that she commonly feels fatigue and finds her sleep is not restful. She gets only
brief relief with acetaminophen or ibuprofen. She describes herself as being down because
of her symptoms but denies being suicidal.
After reviewing her record you note that multiple laboratory and x-ray examinations to
determine the cause of her symptoms have been normal.
Her physical examination reveals full ROM with normal strength in all extremities but ten-
derness with passive ROM. There are several areas of symmetrical tenderness in her neck,
shoulder, and back. The skin in these areas appears normal without any lumps or nodules.
You suspect a diagnosis of fibromyalgia because this occurs most commonly in women
and is associated with dysfunctional sleep, fatigue, and the symmetrical trigger points. Labo-
ratory testing is most often normal, and there is no diagnostic test available for fibromyalgia.
You recommend the patient begin a regular exercise regimen, keep consistent hours, includ-
ing bedtime/sleep, and you begin her on milnacipran which is a SNRI approved for treating
fibromyalgia along with scheduled doses of acetaminophen as a first step on the pain ladder.

Mr. S is a 75-year-old with long history of CLBP that recently is becoming progressively
s
n
worse. He notes significant pain when rising from sitting to standing. The pain increases in
o
i
the supine position but improves if he is able to lie on his side and bend his knees. His pain
t
i
d
worsens going down stairs but is better going up stairs. When he walks he must periodically
n
o
C
stop because of the pain but notes that if he is shopping with a shopping cart, he can walk
l
longer distances. He has no focal weakness in his legs, no urinary or bowel problems, and
a
c
i
denies numbness or tingling. Occasionally the pain radiates down into his legs. The pain limits
d
e
M
his ability to leave the home and to do his usual household chores.
He has had many plain x-rays showing arthritis but does not recall ever having a CT scan
c
i
r
or MRI of his back. He takes over-the-counter anti-inflammatories for the pain with mild relief.
t
a
i
On examination, he moves slowly because of pain, but appears to have no focal neurologic
r
e
G
findingsor significant back tenderness.
n
You refer the patient for an MRI of his lumbar spine which shows osteophyte formation
o
m
with impingement causing spinal stenosis at the L45 level. Therapy with anti-inflammatory
m
medications along with PT provides minimal relief, and although narcotic medications help,
o
C
he wants to explore other options. You refer him to a spine surgeon to discuss the options of
surgical therapy, epidural injections, or continued pain management with oral medications.
END OF LIFE
5
A s s is te d Living a nd Ho m e Ca re
A. Assisted living
1. Similarities to nursing home care
a. Several residents living under one roof and sharing resources.
b. Assistance is available to residents requiring care.
2. Differences from nursing home care
a. The range of services varies and often does not include medication
administration or, if available, incurs an extra charge.
b. It does not include physical therapy, occupational therapy, or speech therapy as a
routine type service.
c. Less regulated.
d. Patients promoted to have independence and autonomy.
e. Typically affords more privacy. Residents have their own rooms with doors that
close and lock.
f. Providers, staff, and guests are invited into their rooms.
g. May include cooking facilities.
h. May have locked units for individuals with dementia.
E
n
i. Costs much less (approximately 50%); about $3,000 per month.
d
o
j. Residential costs are not covered by Medicare or Medicaid.
f
L
3. There are approximately 1 million residents living in assisted living.
i
f
e
4. Many come to the assisted living directly from home or from a skilled nursing
facility after rehabilitative care; a minority come directly posthospitalization.
5. The average age of an assisted living resident is 86 years.
6. Besides advanced age, other qualities of assisted living residents include
(Table 5-1):
TABLE 5-1 Factors Associated with Assisted Living Care

Advanced age
Marital status single or widowed
Caregiver stress or illness
Recent hospitalization and rehabilitation
Low income status
Female sex
Dementia
Loss of one or more ADLs
295
a.Cognitive impairment in up to 80%.

b.70% are female.
Quick Hit c.Most are single or widowed.
Assisted living is generally d.Most residents are ambulatory but generally need help to perform one or more
not covered by insurance or ADLs.
governmental assistance and e. In general, residents exhibit higher levels of functioning than nursing home
must be paid for out of pocket. patients.
Home care may be covered
f. Caregiver stress or health issues contribute to the need for assisted living.
by Medicare or Medicaid,
particularly if the patient is 7. In general, diagnoses parallel the geriatric population, but there is a higher percent-
homebound or has a skilled age of individuals with dementia.
need such as nursing care or 8. Clinical care
physical therapy. a. Care may be provided on-site if the provider makes visits to the facility.
b. Many patients will be transported to their provider by family.
c. A history, physical, and orders for medication and care are required prior to
admission.
Quick Hit d. History
Circumstances leading to the decision for assisted living
Significant risk factors for
assisted living placement are Baseline level of functioning (see Clinical Pearl 2-1)
dementia and loss of social (1) Ability to perform IADLs
supports. However, these (2) Ability to perform ADLs
patients typically function at a (3) Use of assistive devices, such as hearing aids, glasses, walkers, canes,
higher level than nursing home
wheel chairs
patients but need assistance
with IADLs. Diet, including special dietary needs for diabetes or renal disease
Past medical history
(1) Surgeries, medical conditions, especially chronic diseases
(2) Medications and their indications
(3) Immunization status for pneumovax, zoster, influenza, and tetanus
Social history
(1) Social support systems
(2) Smoking
(3) Drinking
Family history becomes less relevant in older adults.
Future history/care
e
(1) Advanced directives and patient desires
f
L
i
(2) Status regarding resuscitation
f
o
(3) Healthcare power of attorney designation
d
n
e. Physical examination
E
Full-routine adult examination
Skin examination, especially if from hospital or another facility
Mental status examination
Evaluate for depression
Assessment of gait and function related to upper extremities
f. Laboratory
May include a baseline CBC, metabolic panel, TSH
Further testing determined by underlying diseases and medications the patient
is taking
PPD (two-step) or serum testing for tuberculosis
B. Home health care

1. Home health agencies
a. Regulated agencies
b. Funded by Medicare for skilled needs
c. Often provided following episodes of care that require hospitalization or a stay
in a skilled nursing facility
d. May include IV therapy, wound care, physical therapy, speech therapy, and
occupational therapy
e. Can include some personal care with assistance with ADLs and home care if
there are also skilled needs for nursing care or therapy
EN D O F LIF E 297
TABLE 5-2 Common Home Programs Available for Geriatric Patients

Home health agency
Nursing
Physical therapy
Occupational therapy
Speech therapy
Personal care
Home aid/homemaker
Meals programs
Adult day health program
Nursing, therapy, recreation, restorative care, respite
Adult day hospital
Nursing, therapy, recreation, restorative care, respite
Adult daycare
Recreation, restorative care, respite
Hospice
Nursing, certified nursing aides, dietary, music therapy, massage therapy, social work, religious
counseling
f. Must be certified as homebound by a physician

g. Physician must also certify that improvement/benefit is expected and that care is
not custodial
2. Other home health care services/programs (Table 5-2)
a. Home health programs through Medicaid may provide nursing care and
assistance with ADLs and personal care.
b. Meal programs, homemaker services, and home maintenance programs may be
E
n
available.
d
o
c. Adult day care and respite care can provide time for caregivers to attend to
f
L
personal needs.
i
f
e
d. More intense programs may include a medical component in the form of day
hospitals or adult day health center where medical care and therapy can be
incorporated.
e. Hospice (see Hospice and Palliative Care section) is a Medicare-covered
service that can be provided in the home for appropriate patients.
CLINICAL PEARL 5-1

Integrated Services
Patients may utilize different resources and living arrangements throughout the course of an illness. For
example, a patient may be admitted to the hospital for pneumonia, and although they may recover after
discharge, it should be determined whether they would benefit from ongoing physical therapy either at home
or in a skilled facility. If admitted to a skilled facility, the patient may improve sufficiently to be discharged but
still may benefit from continued therapy. After discharge from the skilled facility, home care may be ordered
for continued nursing care (e.g., wound care or IVtherapy) as well as physical therapy.
Assisted living can be an alternative to going home when patients need ongoing support for some of their
ADLs or IADLs, and there is no caregiver available to assume this role. Many patients enter assisted living
arrangements either as a step down from skilled nursing care or directly from home.
N urs ing Ho m e Ca re
DefinitionA nursing home is a long-term care institution with a minimum of three beds
that provides 24-hour nursing, medical, social, and personal services to persons in
need of long-term or restorative care.
Demographics
1. Components to the typical nursing home care
a. Rehabilitation (25%)
b. Custodial care (50%)
c. End-of-life care (25%)
2. At any given time, 5% of the geriatric population reside in a nursing home.
3. Over 40% of geriatric patients will spend some time in a nursing home during their
lifetime.
4. Most (60%) come to the nursing home directly following a hospital stay; 25% enter
from home; and the other 15% are transferred from another facility or assisted
living arrangement.
5. The average age of a nursing home resident is 79 years (Figure 5-1).
6. Besides advanced age, other characteristics of nursing home residents include
(Table 5-3):
a. Dementia in over 50%.
b. Mostly female.
c. Single or widowed
d. Loss of ADLs; 40% can no longer ambulate
85+ ye a rs 7585 ye a rs
45% 31%
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Younge r tha n 65 ye a rs 6574 ye a rs
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12% 12%
FIGURE
5 -1 Age distribution of nursing home residents.
(Carter PJ , Goldschmidt WM. Lippincotts Textbook for Long-Term Care Nursing Assistants. Philadelphia, PA: LWW, 2009.)
TABLE 5-3 Risk Factors for Requiring Nursing Home Care

Advanced age
Marital status single or widowed
Lack of family or social support
Low income status
Female sex
Dementia
Falls or wandering
Incontinence
Loss of three or more ADLs
EN D O F LIF E 299
CLINICAL PEARL 5-2

Short-Term versus Long-Term Nursing Home Care
Many health planners break nursing home residents into two groups, short-term residents (e.g., <6 months)
and long-term residents (e.g., >6 months). Those who are short stayers are usually admitted for restorative
or terminal care, whereas those who are long-term residents usually have a physical or cognitive impairment
that precludes remaining at home.
e. 75% have lost the ability to perform three or more ADLs

f. Incontinence
7. The amount of time in a facility varies, and there are different categories of nursing
home residents.
a. Approximately 10% are there for <30 days, and these are there for rehabiliatation
or end-oflife care.
Quick HIT
b. Another 10% are there for 30 to 90 days for similar reasons. The biggest risk factors for
nursing home placement are
c. Eighty percent are in the nursing home for >90 days, either to live or for a pro- dementia with loss of function
tracted rehabilitation period. and lack of social supports.
d. Approximately 10% of total patients will reside in the facility for > 3 years.
8. Common diagnoses are listed in Table 5-4 and are similar to those living in com-
munity settings except for a disproportionately high percentage of individuals with
dementia and hip fracture.
9. Financing for nursing home care is complicated and depends on insurance type,
length of stay, and personal resources (Figure 5-2).
TABLE 5-4 Common Diagnoses in Nursing Home Residents

Dementia
Cardiovascular disease
Hypertension
Osteoarthritis
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Cerebrovascular disease
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Diabetes mellitus
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Chronic obstructive pulmonary disease
Hip fracture
Depression
Me dica id P riva te pay

47% ($84.7 billion) (or out-of-pocke t)
21% ($37.2 billion)
Me dica re
17% ($30.7 billion)
Othe r Long-te rm ca re ins ura nce

5% ($8.8 billion) 10% ($18.2 billion)
FIGURE
5 -2 Financing sources for nursing home care.
a. For rehabilitation patients to be eligible for Medicare coverage, they must have
been in the hospital for at least 3 days before being admitted to a nursing home
facility.
b. Medicare covers skilled care for the first 20 days at 100%.
c. Days 20 to 100 are covered 80%.
d. Costs beyond 100 days in a calendar year are not covered.
e. Secondary insurance may help with coverage.
f. Residential care is out of pocket until the patient spends down their assets.
g. After the spend down, patients may apply for Medicaid coverage.
h. Long-term care insurance represents only a very small proportion of payments
and percentage of patients.
E. Clinical care
1. Overview
a. Nursing home care combines providing basic ADL assistance with clinical care
in the residential setting.
b. The resident loses a great deal of autonomy and often must share a room.
c. The resident no longer can come and go freely and is only able to follow their
Quick HIT own schedule to a limited degree (e.g., meals are only served at certain times).
d. A key role for a provider is to help assure that residents are treated with respect
Quality skilled nursing care
requires a team effort of clini- and are able to have privacy. Residents have the right to refuse care and should
cal and nonclinical personnel. have the freedom to pursue activities and lodge complaints.
Nonclinical staff should be e. Residents are often dependent on the staff for much of their care.
empowered to report con- f. The staff become the eyes and ears for the nurses and physicians. Staff include:
cerns or findings related to
Nonclinical: dietary, housekeeping, building maintenance, administration
patientsgood nursing home
care is an interdisciplinary Clinical: Certified nursing assistants, physical therapists, occupational thera-
team effort. pists, speech therapists, physicians, nurse practitioners, pharmacists
Care is interdisciplinary and team-based (Figure 5-3).
g. With the move to shorten hospital stays, facilities are taking patients who
require a higher acuity of care, including ventilator and dialysis patients.
h. State accreditation is mandatory and joint commission accreditation is desirable.
i. Accreditation requires performance review and quality improvement activities.
2. History
a. Circumstances leading up to and following admission to nursing home facility.
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Often there is a preceding hospitalization, fall, or other critical event that
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triggers nursing home placement.
d
b. Baseline levels of functioning and goals for functional improvement
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1. Ability to perform IADLs
2. Ability to perform ADLs
3. Use of assistive devices, such as hearing aids, glasses, walkers, canes, wheel
chairs
c. Diet, including modifications
Dysphagia diet may include thickened liquids.
Dysphagia and/or poor dentition may require soft or pureed diet.
Special dietary needs for diabetes or renal disease.
d. Past medical history
Surgeries, medical conditions, especially chronic illnesses
Medications and their indications
Review of medications prior to any hospitalization for comparison and for
eventual discharge planning, if it is to occur
Immunization status for pneumovax, zoster, influenza, and tetanus
e. Social history
Social support systems
Smoking
Drinking
Financial resources
f. Family history becomes less relevant in older adults
EN D O F LIF E 301
P hys ica l the ra pis t
La b, Hous e ke e ping
pha rma cy,
x-ra y
S ocia l Die ta ry
s e rvice s
P a tie nt or re s ide nt
P hys icia n Nurs ing

a s s is ta nt
Nurs e
FIGURE
5 -3 Team members caring for nursing home residents.
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Quick HIT
d
g. Future history/care
o
Advanced directives and patient desires. If no advance directives exist, then
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the discussion should be initiated. Determining a patients pref-
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Resuscitation status erences regarding future care
is an important element of the
Healthcare power of attorney designation history so that providers know
3. Physical examination and respect the patient/family
a. Full-routine adult examination with some added areas of focus desires for measures such as
b. Full skin examination especially if from hospital or another facility diagnostic testing, hospitaliza-
c. Mental status examination and assessment of decision-making capacity. tion, and resuscitation.
d. Evaluate for depression, because the frequency of depression is higher in medi-
cally ill patients and those with dementia.
e. Assessment of gait and upper extremity function
f. Additional elements performed by other members of the team
Nursing assessment
Physical therapy for motor and gait
Occupational therapies for function
Therapy for speech and swallowing
4. Laboratory
a. May include a CBC, metabolic panel, TSH
b. Additional testing determined by underlying diseases, medications, and
symptoms
c. Albumin warranted if there are risk factors for malnutrition
d. PPD (two-step) or serum testing for tuberculosis
CLINICAL PEARL 5-3

Preventing Hospital Readmissions from Nursing Homes
Up to 20% of patients admitted to skilled facilities following hospitalization will be readmitted within 30
days of hospital discharge. These account for a significant healthcare cost, and an estimated 50% of these
admissions are preventable. Hospital readmissions may be planned or unplanned. Examples of planned
readmissions would be for a planned surgery or chemotherapy. The focus on prevention is unplanned
readmissions, particularly those related to the original diagnosis.
Common diagnoses related to these unplanned readmissions are congestive heart failure, pneumonia or
chronic obstructive pulmonary disease, dehydration, and infections such as cellulitis, urinary tract infections,
and clostridium difficile colitis.
Efforts to prevent these unplanned readmissions are a major focus of both hospitals and nursing homes.
Improved communication of discharge information is one way to reduce preventable admissions. Other
measures relate to modifications in staffing, such as increases in registered nurse staffing, having a nurse
practitioner available to round daily on patients, and increased availability of intravenous therapies, lab, and
x-ray testing. One added measure is empowering all members of the care team as the eyes and ears and
reporting any changes they may note in a patients condition.
Preventive care
1. Prevention
a. Update immunizations (pneumovax, zoster)
b. Annual influenza vaccine
c. Calcium with vitamin D supplementation
d. Cancer and lipid screening individualized based upon age and overall condition
e. Common acute problems include pressure ulcers, infections, falls, malnutrition,
dehydration, and medication side effects. Proactively reducing the risk of these
acute conditions is important.
f. Psychotropic medications are associated with falls and an increased risk of death.
Careful monitoring of their use is mandatory. Their use should be connected
to a diagnosis and their continued need and efficacy documented in the medi-
cal record. When possible, the dose should be reduced or the medication
e
discontinued.
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g. Monitoring vital signs and weight is important to detect fluid retention,
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dehydration, or malnutrition and to intervene before a crisis occurs.
d
h. Immobile patients are at high risk for pressure sores, and prevention measures
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such as low-pressure mattresses used when appropriate. Disrobing the patient
and routinely checking for pressure sores is also part of good preventive care.
Ho s p ic e a nd P a llia tive Ca re
A. Definitions
1. Hospice
a. Philosophy of care focused on comfort, not cure
b. Patient-centered
c. Independent of patient location
d. Interdisciplinary with nursing, physicians, social work, spiritual care, bereave-
ment services, and volunteers
e. Assumes a terminal prognosis
2. Palliative care
a. Aim is to relieve suffering and improve quality of life
b. Interdisciplinary and independent of patient location
c. Continued therapy toward controlling or treating the underlying disease if
treatment improves comfort
d. Comfort care is a major focus along with other treatment measures
e. Part of the continuum of care (Figure 5-4)
EN D O F LIF E 303
Palliative
Curative c are
c are
Diag no s is Ac tive dying De ath

Pe rs on with illne s s
Dis e a s e progre s s ion
H
Curative c are o
s
p
i
Palliative c are c Be re ave me nt
e
Diag no s is Ac tive dying De ath

Pe rs on with illne s s
Dis e a s e progre s s ion
S upport s e rvice s for fa milie s a nd ca re give rs
FIGURE
5 -4 The continuum of care.
(Burggraf V, Kim KY, Knight AL. Health Aging. Philadelphia, PA: LWW, 2014.)
B. Patient selection
1. 1.5 million patients utilize hospice services.
2. Two-thirds of patients are in their homes and one-third in a facility.
E
3. Average length of time for utilizing hospice services is 70 days.
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4. Variety of diagnoses: cancer (36% of patients); other diagnoses include dementia,
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heart disease. and lung disease.
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5. Eligibility is diseasespecific.
e
6. In general, there should be a decline in status/function with estimated 6 months of
survival or less.
C. Disease-specific eligibility criteria (Table 5-5)

1. Cancer
a. Metastatic disease
b. Decline in status or progression of disease despite treatment or in cases where no
treatment being performed
2. Dementia
a. Functional Assessment Staging scale 7 or beyond
Needs assistance with dressing, bathing, toileting, or is incontinent
Progressive loss of speech, and ability to walk, sit, smile, and ultimately hold head up
b. Inability to perform ADLs
c. Infections within past year
d. Decubiti
e. Weight loss 10% or more
3. Heart disease
a. Coronary artery disease with recurrent angina despite therapy, significant
functional decline, or not eligible for interventions
b. Congestive heart failure: New York Heart Association Stage IVsymptoms at
rest or with minimal activity
TABLE 5-5 Common Medical Conditions and Their Criteria for

Hospice Eligibility
Cancer
Metastatic disease
Decline in status or progression of disease despite treatment or no treatment being performed
Dementia
Functional Assessment Staging scale 7 or beyond
Inability to perform ADLs
Infections within past year
Decubiti
Weight loss 10% or more
Heart disease
Coronary artery disease with recurrent angina despite therapy and declines or not eligible for interventions
Congestive heart failure New York Heart Association Stage IV
Lung disease
Poorly responsive to therapy
Recurrent ED visits or hospitalizations
Hypoxemia (sat < 88%) on O2 or pCO2 >50
Weight loss
Resting tachycardia (HR > 100)
Right-sided CHF/cor pulmonale
4. Lung disease
a. Poorly responsive to therapy
b. Recurrent ED visits or hospitalizations
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c. Hypoxemia (sat < 88%) on O2 or pCO2 >50
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f. Right-sided CHF/cor pulmonale
D. The hospice conversation

1. Must review patients disease and status with them
2. Avoid jargon
3. Assess what the patient knows and what they want to know
4. Determine goals and expectations
5. Try to agree on realistic goals and expectations
6. Studies on what patients want reveal these desires:
a. Pain and symptom control
b. A sense of control
c. Not prolonging the dying process
d. Not becoming a burden to their family or friends
e. Strengthening relationships with family and friends
7. Caution about language that suggests abandonment, e.g., stop treatment
E. Principles of care (Table 5-6)

1. Assessment of type and degree of pain
a. Pain scales and verbal assessment can be used (Figure 5-5).
b. Nonverbal cues, such as facial expressions, vital signs (tachycardia/tachypnea),
and behaviors (reluctance to move, agitation, restless, screaming, moaning) are
also helpful, especially in patients unable to verbalize their needs.
EN D O F LIF E 305
TABLE 5-6 Common Errors in Palliative Pain Management

Failure to use pain scales to quantitate the pain
Assume cognitively impaired patients cannot accurately report pain
Harmful use of high-dose NSAIDs to avoid narcotic use
Failure to use sufficient doses of opioids for fear of addiction
Failure to provide aggressive routine use of laxatives to avoid constipation
Failure to discontinue sedatives that might limit the dose of opioids
FIGURE
5 -5 Pain scales.
(Fishman SM, Ballantyne J C, Rathmell J P. Bonicas Management of Pain. Philadelphia, PA: LWW, 2009.)
c. Types of pain
Nociceptivetissue damage related to pain; can be visceral or somatic
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(1) Visceral related to organs such as heart, lungs, gastrointestinal tract, liver/
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gallbladder, or kidneys
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(2) Somatic is musculoskeletal or soft tissues
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(3) Visceral pain is harder to localize; typically dull or cramping
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(4) Somatic pain is easier to localize; typically sharp, aching, or throbbing
(5) Nociceptive pain usually responds to pain relievers, e.g., NSAIDs,
acetaminophen, opioids
Neuropathicresult of injury to central or peripheral nerves; radiates in
distribution of nerve and characterized as burning, shooting, or numbness/
tingling
(1) Neuropathic pain may respond better to adjuvant medications such as
tricyclic antidepressants (e.g., amitriptyline) and anticonvulsants
Quick HIT
(e.g., gabapentin) than to opioids Therapy for pain with anticon-
vulsant and antidepressant
2. Assessment for other symptoms related to disease or medications medications may be effective
a. Common symptoms at end of life that are not pain for neuropathic pain and as
Anorexia/dehydration adjunctive agents for noci-
(1) Common, especially as patients enter the dying process ceptive pain.
(2) Do not necessarily treat when end-stage
(3) Therapy may include use of steroids, dronabinol or antidepressants such
as mirtazapine to stimulate appetite
(4) No dietary restrictions in this situation
Delirium
(1) May occur as part of dying process or due to another cause
(2) Assess for underlying causes, such as infection, pain, or fecal/urinary
retention
(3) Treat underlying cause and utilize low-dose antipsychotic as needed

(4) If agitated and actively dying, consider more aggressive dosing and
sedation as goal
Dyspnea
(1) Subjective symptom with or without change in vital signs or O2
saturation
(2) Treat underlying cause if able (e.g., CHF or infection)
(3) Therapy with O2 along with narcotics for air hunger and benzodiazepines
for anxiety
b. Medication side effects
Constipation
(1) Common with narcotics
(2) Anticipatory prescribing to prevent
(3) Motility agents, such as bisacodyl or senna most helpful
(4) Can add softener, such as docusate or osmotic agent such as polyethylene
glycol or lactulose if needed
(5) Fiber/bulk agents generally not recommended
Sedation
(1) Sedation is common with anxiolytic and narcotic pain medications.
(2) Patients adapt within days; if needed, dosages may be reduced or the
medication changed.
(3) Occasionally, stimulants are added to overcome fatigue/sedation.
(4) In actively dying patients, sedation may be desirable, especially if there is
delirium and agitation.
Nausea
(1) Common at onset of treatment with narcotics but commonly resolves
within days
(2) May utilize antiemetics alone or in combination
Quick HIT (a) Metoclopramide enhances motility.
Fear of tolerance and side
(b) Prochlorperazine is a dopamine blocker.
effects do not justify providing (c) Ondansetron is a serotonergic blocker.
inadequate pain relief. Respiratory suppression
(1) Not a common issue for hospice patients.
e
(2) Pain stimulates breathing, and generally narcotic doses are titrated
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gradually upward based on pain control and tolerance.
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(3) Sedation and consciousness are generally affected before respiratory
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suppression.
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Adverse effects of narcotic (4) If needed, dosages can be reduced.
medications that require
monitoring are constipation,
(5) In extreme cases with depressed respiratory rate, naloxone can be used.
sedation, nausea, and respira-
tory depression. F. Pain management (Figure 5-6)
1. Principles are to start with non-narcotics as needed (prn) and then schedule dosing
based upon usage. The use of routine dosing rather than an as-needed basis for per-
sistent pain results in better pain management.
Quick HIT a. Acetaminophen maximum dose is 3 g. Long-term use at higher doses can lead to
kidney and/or liver damage.
There are ceilings or b. Maximum doses for NSAIDs vary with medication.
maximum doses for use of 2. Use immediate-release narcotics prn to relieve pain and to establish the daily dose
nonsteroidal anti-inflamma-
tory medications as well as
on which to base the scheduled dose needed for pain relief.
acetaminophen due to the 3. Assess narcotic usage and convert to extended-release form, either oral or
risk for renal or liver toxicity. transdermal (Table 5-7).
Opioid medications (not as a a. Utilize immediate-release forms for breakthrough pain.
combination medication) have b. Approximate breakthrough dose is 10% of total daily dose.
no ceiling and the dose can
be titrated to pain relief or
c. Adjust extended release based upon need for breakthrough medications.
onset of adverse effects. d. Narcotics do not have a ceiling and maximum dosing is based upon side
effects.
EN D O F LIF E 307
WHO 3-s te p
Analg e s ic ladde r
S te p 3: Opioid for mode ra te Example s :
to s e ve re pa in Morphine , oxycodone ,
+ Nonopioid hydromorphone , me tha done ,
+ Adjuva nt tra ns de rma l fe nta nyl
Pain pe rs is ting o r inc re as ing

S te p 2: Opioid for mild to Example s :
mode ra te pa in Code ine , tra ma dol, oxycodone , e tc.
+ Nonopioid
+ Adjuva nt
Pain pe rs is ting o r inc re as ing

S te p 1: Example s :
NS AIDs (e .g., a s pirin, ibuprofe n),
Nonopioid a ce ta minophe n, a djuva nts (TCA,
Adjuva nt a ntie pile ptics )
Pain
FIGURE
5 -6 WHO 3-step ladder for pain management.
(Urman RD, Vadivelu N. Pocket Pain Medicine. Philadelphia, PA: LWW, 2011.)
TABLE 5-7 Equianalgesic Doses for Commonly Utilized Oral or

Transdermal Narcotics
Medication Immediate-Release Extended-Release
Morphine 60 mg 60 mg
Hydromorphone 15 mg N/A
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Codeine 400 mg N/A
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Hydrocodone 60 mg N/A
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Fentanyl N/A 25 mcg/h
e. Tolerance may develop to the analgesic effects.

f. Once pain controlled, usually the dose remains stable unless disease
progresses. Quick HIT
4. If pain is not controlled or adverse effects limit use, one narcotic can be switched to Higher doses may lead to
alternative using 50% to 75% of equianalgesic dose as the starting dose. dependence and tolerance for
5. Adjuvant medications may be used at any step. pain relief but not to addiction.
a. Most commonly used for neuropathic pain
b. Most common medications are the tricyclic antidepressants (e.g., amitriptyline)
and anticonvulsants (e.g., gabapentin)
6. Meperidine or other agonist/antagonist combinations are not recommended.
7. Narcotics are metabolized by the liver and excreted in urine; adjust doses with liver
failure, renal failure, and dehydration
8. Consider nonpharmacologic interventions such as massage, acupuncture,
orthotics
CLINICAL PEARL 5-4
Patient-Controlled Analgesia
Patient-controlled analgesia (PCA) utilizes a pump to deliver medications intravenously, subcutaneously, or
epidurally. In PCA, the patient triggers administration and controls the dose. Agents used include narcotics,
such as morphine or hydromorphone. Epidural administration may also utilize anesthetic agents, such as
bupivacaine, in combination with a narcotic agent.
PCA can be useful postoperatively as well as for hospice patients. Hospice patients who may most benefit
include those with gastrointestinal obstruction, vomiting, severe pain, cancer, and sedation or diminished level
of consciousness.
Caution must be exercised in patients with liver disease or renal insufficiency because clearance of
the medication may be compromised. Dosing should be individualized based on prior use of narcotics and
conversion of oral dosing to the PCA regimen. Dosing may include:
Basal ratecontinuous hourly rate
Bolus dosespatient-triggered doses at set intervals
Lockoutlimits set so that bolus doses cannot exceed a certain amount and frequency
Ethic a l Is s ue s in the Eld e rly

A. Background
1. Ethical issues for geriatric patients will become an increasing issue in health care as
the population ages.
2. Health care has become more technological, creating scenarios for achieving
survival in situations not previously thought possible.
3. Up to 20% of the geriatric population will require hospitalization each year, and up
to 60% will require skilled nursing care at some time in their life.
4. Four guiding principles of ethics in health care (Table 5-8):
a. Autonomybelief that individuals should determine their own health care; their
decisions and choices should be respected
b. Beneficenceevery attempt should be made to do good and provide
improvement or benefit to the patient
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c. Nonmaleficencedo no harm; make every attempt to not harm or injure the
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patient while providing care
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d. Justicetreat patients in an equal and fair manner regardless of gender, race,
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religion, disability
B. Clinical issues (Table 5-8)

1. Autonomy
a. Decision-making capacity not always easy to determine.
b. Place of residence or underlying medical conditions do not necessarily alter ones
autonomy; this must be individualized.
c. Even patients with cognitive impairment may be able to make their own
decisions.
d. There are many different issues that may require determination as to who
decides (e.g., clinical, financial, living arrangements).
e. Deciding if the patient is capable of their own decisions may require cognitive
testing or neuropsychiatric evaluation.
f. Documentation of findings is extremely important to justify the outcome,
especially if a proxy is making decisions for the patient.
The proxy can be a power of attorney who is generally a person designated by
the patient to make decisions once they are unable.
A power of attorney can be for financial affairs, healthcare, or both.
A legally appointed guardian is another form of proxy who is used in
situations where the person is unable to assign a power of attorney.
In the absence of a designated power of attorney, then the spouse or next of
kin may become the proxy.
EN D O F LIF E 309
TABLE 5-8 Principles Involved in Ethical Issues

Principle Example/Important Questions
Autonomy Patient requires assistance with some ADLs and IADLs. They would benefit from
living in long-term care or assisted living, but does not want this although it might
be better from a safety perspective
Is the patient capable of making decisions for themselves?
If so, then do they understand the risks, benefits, and alternative options for care?
If not, who is the proxy who will make decisions for them?
Does the patient have advanced directives or have they previously stated their
preferences?
Does the proxy understand risks, benefits, and alternative options for care?
Beneficence A patient with terminal cancer and dysphagia has been recommended to have a
percutaneous tube for feeding and withhold oral feedings. The patient and family
decide against this and request pleasure feedings
What are the risks associated with the patient/family request?
What are the benefits?
What is the prognosis for the patients condition?
Will the decision impact long-term prognosis?
Will it enhance the quality of the patients current condition?
Nonmaleficence A patient with metastatic lung cancer who is receiving chemotherapy and has
marked weakness, nausea, vomiting, and hair loss
What are the risks with stopping therapy?
What benefits are to be achieved by continuing therapy?
What are the long-term consequences of either decision?
Which decision will most likely positively impact the patients current condition?
Justice A 90-year-old woman decides on a DNR order should she suffer cardiopulmonary
arrest. Her family disagrees and wants it changed.
Is the patient capable of making her own decisions?
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Has the patients DNR order been committed to writing and signed?
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Has she designated a power of attorney and is her family aware of her
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decision?
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What factors (financial, religious, cultural) are influencing this disagreement?
g. Elements of a decision center around the concept of informed consent. These

elements include:
An understanding of the issue/treatment/procedure
An understanding of the risks and benefits of the issue/treatment/procedure
An understanding of other options that might be available and their risks and
benefits
These elements should be well documented and, in the case of procedures,
surgeries, and code status, should be signed by the patient or their proxy
h. At times, a family or patient will want the physician to inform them but ask the
physician to be the decision makerthis has been termed informed assent and
should be well documented.
2. Beneficence/nonmaleficence
a. Providing the patient benefit and avoiding harm sounds straightforward,
but many clinical and psychosocial decisions are complicated and should be
individualized.
b. Procedures, testing, medications, and placement of the patient into a new envi-
ronment may be beneficial but can also have unintended consequences.
Exampleplacing the patient on a ventilator to resuscitate them acutely may

result in long-term ventilator dependence which may be against their wishes
Exampleperforming knee replacement in an inactive patient who suffers
major perioperative complications, leaving them totally dependent for care
Examplepositive PSA testing in an asymptomatic person with advanced
COPD who is too frail to undergo any procedural interventions
c. Questions that should be considered with regard to these aspects of ethical
issues:
What does the patient want and what are their goals for care?
What is their current prognosis?
How will the patient benefit from the planned procedure, test, medication, or
placement?
How could the patient be harmed by the planned procedure, test, medication,
or placement?
What is the real likelihood of success/achieved goal of the medication or pro-
cedure; in other words, how likely is the benefit to be achieved?
What are best case, worst case scenarios that could occur with the planned in-
terventions and how would these potential results impact the patients decision?
3. Justice
a. Several issues could result in biases regarding therapy in geriatric patients.
Clinicians opinions
Family or caregiver perspectives
Religious or cultural beliefs
Financial incentives may influence the direction of care
Quick HIT b. Dependency and the physical and mental condition of the patient may bias ag-
gressiveness of care without incorporating patient or family wishes.
The ethical principles used to
guide healthcare decisions
c. Patients residing in nursing homes or with dementia may be automatically
include patient autonomy, viewed as having a substandard quality of life.
beneficence, nonmaleficence, Geriatric persons are often treated paternalistically by their providers and fam-
and justice (Table 5-8). ily members even if they retain the abilities for decision making and self-care.
Confidentiality and autonomy must be respected.
e
f
L
i
CLINICAL PEARL 5-5
f
o
d
n
E
Patient Autonomy
A difficult principle, at times, to accept is that of patient autonomy. Patient autonomy includes the right and
ability to accept, refuse, or withdraw care. When the person making the decision is a proxy (power of attorney,
guardian, or surrogate next of kin), then these same options pertain to the proxys choices for care, provided
they are making the decision in what they believe to be the patients desires and best interests.
Examples of common ethical dilemmas that can present in geriatric care include:
1. A patient who was victim of a prior stroke and dysphagia has a percutaneous gastrostomy tube for medica-
tions and feedings. The patient suffers a second stroke and is now comatose but stable. The family no lon-
ger wants to provide feedings through the tube, fully understanding that this will lead to the patients death.
2. A patient is resuscitated and placed onto a ventilator. His condition has stabilized, but due to severe under-
lying COPD, he has become ventilator-dependent. The patient has previously developed advanced directives
indicating he did not want to live on a ventilator. The family does not want to stop the ventilator because
they know this will cause the patient to die.
3. A patient residing in long-term care who is dependent for all ADLs due to underlying dementia is currently
being treated for dementia with medications that include memantine and donepezil. He is nonverbal and
nonambulatory and does not appear to recognize family. His power of attorney wants to continue all medi-
cations despite lack of any evidence indicating benefit.
The principle of patient autonomy would dictate that the provider follow the wishes of the patient or their
proxy. The provider may not always agree with the decision, and if, as a result, they do not feel they can con-
tinue to provide care to the patient, they should arrange for another provider to assume care. If the provider is
uncomfortable with the decision for care or feels that there are ethical questions that arise, then a consulta-
tion should be requested.
EN D O F LIF E 311
C. Common interventions
1. Prevention
a. Encouraging the patient to determine and put in writing their advanced Quick HIT
directives: When patients can no longer
Desires for future care including artificial feeding, artificial respiration make their own decisions,
Wishes related to resuscitation a designated healthcare
power of attorney designates
Organ donation
an individual to make these
Powers of attorney for health care and for finances decisions on their behalf. In
If spouse and children are involved, then designating who makes what the absence of a designated
decision is helpful healthcare power of attorney
Wills and trusts, including executors and trustees or guardian, then the spouse
b. Advanced directives should be reviewed and discussed with family members or next of kin would be con-
sulted (Figure 5-7).
and those with responsibilities, such as power of attorneys, guardians, and
executors; should be aware of their roles (and be accepting)
2. Communication
a. Advanced directives should be shared with healthcare providers.
b. Copies should be placed in hospital and nursing home charts. Copies should be
maintained in an accessible location in the patients residence.
Quick HIT
3. Consultation Advanced directives should
consider many different
a. When difficult decisions present or there is disagreement, multidisciplinary
situations regarding future
ethics teams can provide review, consultation, and recommendations to assist. healthcare decisions such as
b. Often these occur in the inpatient setting, but many skilled/long-term care artificial respiration, artificial
facilities will have ad hoc teams available. feeding, and resuscitation
c. Team members may include clinicians, social work, legal, nursing, pastors, orders. In addition, designat-
ing powers of attorney, guard-
or clergy representing the appropriate religion, and community members/
ians, organ donation, and
ombudsmen. funeral arrangements may be
included.
De cis ion-ma king ca pa city?
Ye s No
Follow pa tie nts informe d choice Adva nce dire ctive ?
E
n
d
Ye s
o
f
L
i
f
e
S ta te pa tie nt wis he s ?
No
Ye s No
Follow a dva nce dire ctive De s igna te proxy?
Ye s No
P roxy de cide s with MD ba s e d on Trus tworthy s urroga te ?

s ubs titute d judgme nt or be s t inte re s ts
Ye s No
S urroga te de cide s with MD P hys icia ns de cide ba s e d

on be s t inte re s t
FIGURE
5 -7 Decision-making tree.
(Lo B. Resolving Ethical Dilemmas. Philadelphia, PA: LWW, 2013.)
INDEX
Page numbers followed by f and t indicate figures and tables respectively.
A classes of, 82f Cardiac prophylaxis, 35

Abdominal aortic aneurysm (AAA), 152153 side-effect profiles of, 83f Cardiac testing, 34
Acetaminophen, 239, 292 Anxiety, in elderly, 8487, 85t, 86t Cardioembolic stroke, risk stratification for, 156
Acetazolamide, 121 Aortic regurgitation, 160 Cardiovascular disease (CVD)
Acne rosacea, 107 Aortic stenosis (AS), calcific, 159 abdominal aortic aneurysm, 152153
Acral lentiginous melanoma, 111 APOE-E4, 71 atrial fibrillation, 153157
Actinic keratosis, 108109, 109f Aquafor, 103 bradycardia, 157
Activities of daily living (ADLs), 2122, 52 Arrhythmias, 14 chronic complications of DM, 225
Activity limitation, 101 Arterial ulcerations versus venous ulcerations, 106 coronary artery disease, 147152
Activity theory, 2 Aspirin prophylaxis, use of, 26 heart failure, 157159
Acute coronary syndrome (ACS) Assisted living care, 295296, 295t hyperlipidemia, 153
diagnosis, 149 Asymptomatic bacteriuria, 251 hypertension, 144147
general information, 149 Atrial fibrillation (AF), 14 peripheral vascular disease, 152
invasive therapy, 151 general information, 153154 screening for, 27
long-term therapy, 151 testing, 154155 valvular heart disease, 159160
medical treatment, 150151 treatment, 155157 Cardiovascular system, 1415, 15t
testing, 149 Atrophic age related macular degeneration, 118 Cardioversion, 155, 155f
Acute joint pain, 247 Atrophic vaginitis, 204205 Caries, dental, 113, 114f
Acute kidney injury (AKI), 175t Azoles, 201 Cataracts, 121
clinical features, 173 Catechol-O-methyltransferase (COMT) inhibitors,
diagnosis, 173174 B 138
general characteristics, 172173, 172t Bacillus Calmette-Guerin (BCG), 281 Cellular senescence, 1
treatment, 175176 Bacterial vaginosis, 203204 Cellulitis
Acute Kidney Injury Network (AKIN), 172t, 173 Basal cell carcinoma, 109110, 110f clinical features, 248249
Acute lymphocytic leukemia, 268269 Beers criteria for, 4148 diagnosis, 249
Acute myelogenous leukemia, 267268 Benign paroxysmal positional vertigo (BPPV), 129 differential diagnosis of, 250
Adenocarcinoma, of endometrium, 215 Benign prostatic hypertrophy (BPH), 196198 general information, 248, 249f
Adult protective services, 95 Benzodiazepines, 87 treatment, 250251
Ageism, 2 -Blockers, 87 Central nervous system (CNS), 31
Age related macular degeneration (ARMD), 118 Bethanechol, 55 Cerebrovascular disease, 129135
Aging Biguanides, 221 clinical features, 130131
changes of, 89 Biologic aging, 1 diagnosis, 131132, 132f, 133f, 133t
demographics and epidemiology, 57 Biologic clock theory, 4 general characteristics, 129130
geriatric assessment, 1922 Biologic theories, of aging, 25 treatment, 132134
introduction to, 15 Bisphosphonates, 242 Cerumen impaction, 122
physiologic changes of, 919 Bladder carcinoma, 192194 Cervical cancer, 27, 217218
preventive care for older adult, 2228, 29t Bleeding, risk for, 156 Chemoprophylaxis, 26
sensorineural hearing loss, associated with, 124 Blue bloaters, 162 Chemotherapy, 281
Alcohol abuse, 8990 Bone loss, 12 Cholesteatoma, 124, 125f
diagnosing, 90 Bradycardia, 157 Chronic bronchitis, 161
treatment of, 9091 Bradykinesia, 136 Chronic kidney disease (CKD)
-Glucosidase inhibitors, 222 Breast cancers, 283284 clinical features, 176177
Altered mental status. See also Delirium; Dementia; Bullous pemphigoid, 107108 general characteristics, 176
Depression Bunions, 246 treatment of, 177179
three Ds for, 66 Buspirone, 87 Chronic lymphocytic leukemia, 268, 271
Alzheimer disease (AD), 68, 7174 Chronic myelogenous leukemia, 268, 271
Amantadine, 138, 259 Chronic obstructive pulmonary disease (COPD)
American Diabetes Association (ADA), 220 C clinical features, 161162
Amitriptyline, 293 CA-125, 214 diagnosis, 162163, 164165f
Anemia, 178 CAGE questionnaire, 90 general information, 161
clinical features, 263264 Calcific aortic stenosis (AS), 159 treatment, 163166
diagnosis, 264, 265f, 266t Calcified mitral annulus, 159 Chronic pain
general information, 263 Calcitonin, 242 clinical features, 288290, 289f
treatment, 264266 Calcium kidney stones, 188 diagnosis, 290
Anesthesiologists, 33 Calcium oxalate kidney stones, 188 general characteristics, 287288, 288t
Angina, stable, 147149 Calcium phosphate kidney stones, 188 treatment, 290293, 291f, 292t
Angle-closure glaucoma, 120 Calluses, 243 Cilostazol, 152
Angular cheilitis, 113 Cancers CockcroftGault formula, 14
Anhedonia, 75 clinical features, 277278 Cognitive impairment, 226
Ankle-brachial index (ABI), 106 diagnosis, 278280 Colon cancers, 284285
values and interpretations, 152t general characteristics, 275276, 276f, 277f Colon obstruction, 58
Anorexia, 305 screening, 2627 Comprehensive geriatric assessment (CGA), 19, 20t
Antagonistic pleiotropy, 3 therapy, 280286 outcomes of, 22
Antibiotic prophylaxis, 3637, 36t Candida albicans, 201 Compression of morbidity, 7
Antidepressants Candida glabrata, 201 Compression of mortality, 6
312
IN D EX 313
Confusion Assessment Method, 64 Disengagement theory, 2 Extrapyramidal symptoms (EPS), 73

Constipation, 13 Disposable soma theory, 3 Exudative ARMD, 118
clinical features, 56 Donepezil, 72 Eye, disorders of
diagnosis, 56, 57t, 57f Dowagers hump, 240 aging and vision changes, 117118
general characteristics, 5556 Driving specific conditions, 118122
treatment, 56, 58t aging contributing to, 100t
Contact dermatitis, 205, 243, 244f assessment, 100102
F
Continuous renal replacement therapy (CRRT), 181t general information, 100
Failure to thrive (FTT), 50f, 50t, 51t
Corns, 243244 safety interventions, 102
clinical features, 49
Coronary artery disease (CAD), 147152 Drug metabolism, 30
diagnosis, 4950
acute coronary syndrome, 149152 Dry ARMD. See Atrophic ARMD
general characteristics, 49
general information, 147 Dry mouth. See Xerostomia
treatment, 50
risk factors, 147 Dry skin. See Xerosis
Falls
routine screening for, 27 Dyspareunia, 96
clinical features, 59
stable angina, 147149 in older women, 98t
diagnosis, 59, 60f, 61t
Corticosteroids, 165166 Dyspnea, 306
and fractures, 227
COX-2 selective inhibitors, 293 Dysthymia, 77
Creatinine clearance (CrCl), 14, 31
treatment, 6162, 61t
CreutzfeldtJakob (C-J) disease, 69
E Fasting plasma glucose, 220
Cross-linkage theory, 5
Ear, disorders of 5- -Reductase inhibitors, 198
CT urogram, 193
general considerations, 122, 122t Fluid balance homeostasis, loss of, 18
CUPID acronym, 1
hearing loss, 123f Folate deficiency, 263
Cystic kidney disease, 182
of inner ear, 124127 Foot
Cystoscopy
of middle ear, 123124 disorders
for bladder carcinoma, 193
of outer ear, 122123 common foot conditions, 243248
for hematuria, 192
tinnitus, 129 general information, 243
Cytokines, 281
vertigo, 127129 ulceration, 226
Ectropion, 16 wounds, 245
D Elder abuse, 9195 Free radical theory, 45
I
Decubitus ulcers, 105 background, 9192 Frontotemporal dementia (FTD), 7475
n
d
Deep vein thrombotic prophylaxis, 36, 36t clinical features, 9294 Functional incontinence, 53
e
x
Dehydration, risk of, 18 health consequences of, 91t
Delirium, 305306 interventions, 9495
G
clinical features, 6263 signs of, 92t
Gait instability. See Falls
diagnosis, 6364, 63t, 74f ethical issues in, 308311, 309t
Galantamine, 72
general characteristics, 62, 62t Electroconvulsive therapy (ECT), 83
Gastrointestinal system, 13
precautions for, 3536 Electroencephalogram, 64
Generalized anxiety disorder (GAD), 84
treatment, 6566, 65t Emphysema, chest x-ray of patient with, 163f
Geriatric dermatology
Dementia Emphysematous, 161
general information, 103
clinical approach, 6768 Endocrine disease
specific conditions, 103111
diagnosis, 6870, 69t, 70t diabetes mellitus, 219227
postoperative complications in, 32t
general characteristics, 67 acute complications of, 223225
preventive dental measures for, 116
primary, 69t, 7175 chronic complications of, 225226
risk factors for surgery, 32t
versus pseudodementia, 70t geriatric syndromes in, 226227
Geriatric syndromes
treatment and management, 7071 hyperparathyroidism, 232235
altered mental status/delirium, 6266
Denosumab, 242 thyroid disorders, 227232
constipation, 5558
Depression, 226 hyperthyroidism, 229232
failure to thrive, 4950, 50t, 51f, 51t
clinical features, 75, 77 hypothyroidism, 227229
falls/gait instability, 5862
diagnosis, 77, 78f Endocrine system, 17
incontinence, 5255
general characteristics, 75, 76t End of life
Germ cell ovarian cancer, 218
grief from, 77 assisted living and home care, 295297
Gerontology, 1
physical symptoms of, 76 ethical issues in elderly, 308311
Glare, 17
treatment, 77, 79f, 8183 hospice and palliative care, 302307
Glaucoma, 118121
DEXA scanning, 241, 247 nursing home care, 298302
GLBT adults, 96
Diabetes mellitus (DM), 219227 patient-controlled analgesia, 308
Glomerular filtration rate (GFR), 14, 172
acute complications of Endometrial hypoplasia, 210
Glomerulonephritis, 182184, 185t
diabetic ketoacidosis, 223224 End-stage renal disease (ESRD)
Gout, 246247
hyperglycemic hyperosmolar state, 224225 clinical features, 179180
Graves disease, 230, 232
chronic complications of diagnosis, 180
Grief, 77
macrovascular complications, 225 general, 179
Gynecologic disease
microvascular complications, 225226 renal replacement therapy options, 181
cervical cancer, 217218
clinical presentation, 220221 treatment, 180181
ovarian cancer, 212215
diagnosis, 220 Entropion, 16
pelvic organ prolapse, 209210
general characteristics, 219220, 220t Epithelial ovarian cancer, 212
postmenopausal bleeding, 210212
geriatric syndromes in Erectile dysfunction (ED), 97
uterine cancer, 215217
cognitive impairment, 226 Eriksons theory, 2
vaginal cancer, 218219
depression, 226 ESRD cysts, 182
vaginitis, 199208
falls and fractures, 227 Ethical issues in elderly, 308311, 309t
urinary incontinence, 226 Eucerin, 103
treatment, 221223 Euthyroid sick syndrome, 228 H
Diabetic ketoacidosis (DKA), 223224 Evolutionary theories of aging, 3 Haloperidol, 73
Diabetic nephropathy, 226 Exercise Hammertoes, 246
Diabetic neuropathy, 225226 elements of, 25 Headaches, 141143
Diabetic retinopathy, 225 potential benefits of, 25t clinical features, 141142
Dialysis prescription, 25 diagnosis, 142143
indications for, 180t stress testing, 148 general characteristics, 141
types of, 181t tolerance, 25 treatment, 143
314 IN D EX
Health care financing Incretin modulators, 222 Microvascular complications, in DM, 225226
general information, 37 Influenza, 26, 258259, 259t Mini-Cognitive Assessment (Mini-Cog), 68
government insurance programs, 3740 Injury prevention counseling, 26 Mini-Mental Status Exam (MMSE), 68
Older Americans Act and aging network, 40 Instrumental activities of daily living (IADL), Mitral annulus, calcified, 159
Health care, principles of ethics in, 308, 309t 2122, 52 Mitral stenosis, 160
Hearing, 17 Insulin, 222223 Mitral valve, prolapse and regurgitation, 159
Hearing aids, 125t, 126f Interferon- release assays (IGRA), 260261 Mixed incontinence, 53
Hearing loss, 123f International Federation of Gynecology and Monoamine oxidase type B inhibitors, 138
of inner ear, 124127 Obstetrics (FIGO), 214 Monoclonal antibodies, 281
of middle ear, 123124, 124f International Prostate Symptom Score (I-PSS), 197 Mood disorder questionnaire, 80f
of outer ear, 122123 Interstitial lung disease Morbidity, compression of, 7
Heart failure (HF) diagnostic evaluation for, 168f Mortality, compression of, 6
general characteristics, 157 types of, 167t Motor vehicle accidents (MVAs), 100
signs and symptoms, 158 Intertrigo, 107 Multinodular toxic goiter, 230, 232
testing, 158 Intestinal pseudo-obstruction, 56, 57f Multiple myeloma
treatment, 158159 Intra-articular therapy, 239 clinical features, 271
Heart rate testing, 59 Intracerebral hemorrhage (ICH), 130 diagnosis, 271272, 272t
Hematologic disease Ipratropium, 164 general information, 271
anemia, 263266 Iron deficiency, 263 treatment, 272
multiple myeloma, 271272 Ischemic stroke, 129130 Musculoskeletal system, 1112
platelet disorders, 272274, 275f Itching, 11 Mutation accumulation theory, 3
white blood cell disorders, 266271 Myelodysplastic syndromes (MDS), 269
Hematuria, 190192 Myeloproliferative disorders, 270
Hemodialysis, 181t
J Myocardial infarction, acute, 150f
Jugulotympanic paragangliomas, 124
Herpes simplex, 114
Heterogeneity, 3
N
Home health care, 296297, 297t K Naltrexone, 91
Hormonal therapy, for prostate cancer, 282 Kidney Disease Improving Global Outcomes
National Center on Elder Abuse (NCEA), 40
Hospice (KDIGO), 172t, 173
National Health Expenditure (NHE) Accounts, 37
definition, 302 Kidney stones, 184188, 186t
Neoplastic thrombocytosis, 273
disease-specific eligibility criteria, 303304, 304t Krukenberg tumor, 212
Nephritic syndrome, causes of, 183t
pain management, 306307
Nephrosclerosis, 171
patient selection, 303
L Nephrotic syndrome, causes of, 183t
principles of care, 304306, 305t
Labyrinthitis, 128 Nervous system, 1516, 15t
Hyaluronic acid, 239
Lentigo maligna melanoma, 111 Neuraminidase inhibitors, 259
Hypercalcemia, 233f
Leukemia, 267268 Neurodermatitis, 104
Hyperglycemia, 221
Levodopa, 137 Neuro-endocrine theory, 4
Hyperglycemic hyperosmolar state (HHS), 224225
Levothyroxine, 229 Neurologic disease
Hyperkalemia, 178
Lewy body dementia (LBD), 74, 139 cerebrovascular disease, 129135
Hyperlipidemia, 153, 179
Lichenification, 98, 199 headaches, 141143
Hyperosmolar hyperglycemic state, diagnostic
Lichen planus (LP), 206f, 208 Parkinson disease, 135139
criteria for, 224t
Lichen sclerosus, 206207, 206f pseudobulbar affect, 143144
Hyperparathyroidism
Lichen simplex chronicus, 205206, 206f seizures, 139141
clinical presentation, 233
Life expectancy, defined, 56 Neuropathic pain, 287, 287f, 305
diagnosis, 233235, 233f
Lipid therapy, recommendations for, 149t Nitrofurantoin monohydrate/macrocrystals, 253
Lipofuscin, 15 Nociceptive pain, 287, 287f, 305
treatment, 235
Liver metabolism, 30 Nodular melanoma, 111
Hypertension (HTN), 27
Longer-acting insulins, 222 Noncardiac surgery, cardiac evaluation for, 34f
clinical assessment, 145
Long-term care ombudsman programs, 95 Nonselective NSAIDs, 293
Lower urinary tract symptoms (LUTS), differential Nonsteroidal anti-inflammatory medications, 239
risk factors for, 145
diagnosis of, 198 Normal pressure hydrocephalus (NPH), 69
testing, 145146
Low testosterone. See Hypogonadism Nursing home care
treatment, 146147
Lung cancers, 282283 clinical care, 300301
Hyperthyroidism
demographics, 298f, 298300, 298t
causes, 230
preventive care, 302
clinical presentation, 230 M
short-term versus long-term, 299
diagnosis, 231, 231f Macrocytic anemia versus microcytic anemia, 266
Nutritional prophylaxis, 37
general characteristics, 229 Macroscopic hematuria, 190
treatment, 231232 Macrovascular complications, in DM, 225
Hypogonadism, 194196 Malignant melanoma, 110111, 111f, 111t O
Hypothyroidism Malnutrition, 32, 33t Obsessive compulsive disorder (OCD), 84
causes, 227 MAST-G (Michigan Alcohol Screening Test), 90 Obstructive sleep apnea, 169
clinical presentation, 227228, 228t Maximum heart rate, formulas to calculate, 14, 15t Ogilvie syndrome. See Intestinal pseudo-obstruction
diagnosis, 228, 229f Maximum life span, defined, 6 Older Americans Act (OAA), 40
general characteristics, 227 Medicaid, 39 Onychogryphosis, 245
treatment, 229 versus Medicare, 40t Onychomycosis, 245246, 245f
Medicare, 3739 Open-angle glaucoma, 120121
versus Medicaid, 40t Opioids, 293
I Medicare Advantage Plan, 39 Oral cancers, 114, 115f
Idiopathic neurodegenerative disease. See Medicare Part C. See Medicare Advantage Oral health, in geriatric patients, 112117
Frontotemporal dementia Medigap insurance, 39 clinical features, 112113
Immune system, efficiency of, 17 Meglitinides, 222 diagnosis, 113115
Immunologic theory of aging, 4 Memantine, 72 general information, 112
Incontinence Memory impairment, 67 treatment, 116
clinical features, 53, 53t Meniere disease, 126 Orthostatic blood pressure, 59
diagnosis, 5355, 54f Metronidazole, 203 Oslers maneuver, 144
general characteristics, 5253, 52t Microcytic anemia versus macrocytic anemia, 266 Osteoarthritis (OA), 246
treatment, 55 Microscopic hematuria, 190 clinical features, 236237, 236t
IN D EX 315
diagnosis, 237238, 237f, 238f Podagra, 246 Renal biopsy, 174

general information, 235236, 236f Polycystic kidney diseases, 182 Renal cell cancer, 188189, 189t
treatment, 238239 Polycythemia vera (PV), 273 Renal disease
Osteonecrosis of jaw, 115, 115f Polymyalgia rheumatic (PMR) acute kidney injury, 172176
radiographs of, 116f clinical features, 242 chronic kidney disease, 176179
Osteoporosis diagnosis, 243 cystic kidney disease, 182
clinical features, 240241, 240t general information, 242 end-stage renal disease, 179182
diagnosis, 241 treatment, 243 functional changes, 172
general information, 240 Polypharmacy, 30 general characteristics, 171
treatment, 241242 Postherpetic neuralgia, 263 glomerulonephritis, 182184
Otitis externa, 122123 Postmenopausal bleeding (PMB) kidney stones, 184188
Otitis media, 123124, 124f diagnosis, 211 renal cell cancer, 188189
Otosclerosis, 124 epidemiology, 210 structural changes with aging, 171
Ovarian cancer etiology, 210 Respiratory system, 1213
categories, 212 management, 211212 Retinal detachment, 121122
causes, 212213 Postoperative complications in, 32t Rheumatologic disease
complications, 214 Posttraumatic stress disorder (PTSD), 84, 87 foot disorders, 243248
diagnosis, 213214 Postural instability, 136 osteoarthritis, 235239
differential diagnosis, 213 Postural tachycardia syndrome, 59 osteoporosis, 240242
history and physical examination, 213 PPD testing, 260, 261 polymyalgia rheumatica, 242243
incidence and prevalence, 212 Pregabalin, 87 RIFLE, 172t, 173
prevention, 215 Preoperative evaluation, in geriatric patients Rimantidine, 259
prognosis, 214 background, 31 Rivastigmine, 72
risk factors, 213 clinical features, 3233
screening, 215 diagnostic testing, 3335
staging, 214 prophylactic therapies, 3537 S
treatment, 214 Presbycusis, 124125 Sarcopenia, 11
Overflow incontinence, 52 Presbyopia, 17 SCALES tool, 51t
Oxalate stones, 188 Prescription drug abuse, 88 Seborrheic dermatitis, 106107
Oxybutynin, 55 risk factors for, 88t Seborrheic keratosis, 108, 108f
I
n
Oxygen-free radical, 4 Pressure ulcers, 106 Secondary prevention, in geriatrics, 24
d
e
Preventive care for older adult, 2228, 29t Seizures, 139141
x
Preventive dental measures for, 116 clinical features, 139140
P Primary dementias, 69t, 7175 diagnosis, 140
Pain, types of, 305 Primary prevention interventions, in geriatrics, 23, general characteristics, 139
Palliative care 25 treatment, 141
common errors in, 305t Program for All-inclusive Care for the Elderly Selective estrogen receptor modulators (SERMs), 242
definitions, 302 (PACE), 40 Selective serotonin reuptake inhibitors (SSRIs), 82
Papulosquamous, 208 Programmed death, theory of, 3 Senile purpura, 11
Parathyroid glands, diseases of. See Programmed theories, of aging, 4 Sensorineural hearing loss, 122, 124
Hyperparathyroidism Prophylactic therapy, 3537 Sensory disorders
Parathyroid hormone (PTH), 186, 242 Prostate cancers, 27, 285286 ear, 122129
Parkinson disease (PD), 135139, 136t, 137t hormonal therapy for, 282 eye, 117122
clinical features, 135136 Pruritus, 103 Sepsis
diagnosis, 136137 causes of, 103104 clinical features, 257
general characteristics, 135 Pseudobulbar affect, 143144 diagnosis, 257
treatment, 137138 Pseudodementia versus dementia, 70t, 76 general information, 256257
Patient autonomy, 310 Pseudoephedrine, 55 treatment, 257258
Patient-controlled analgesia (PCA), 308 Pseudogout, 247248 Serum tumor marker, 279t
Pelvic organ prolapse, 209210 Pseudomonas aeruginosa, 251 Sex cord ovarian cancer, 212
Pelvic Organ Prolapse Quantification System, 209 Psychological theories, of aging, 2 Sexual dysfunction, drugs associated with, 98t
Periodontitis, 113, 114f Psychosocial/behavioral issues Sexuality and older adult
Peripheral vascular disease, 152, 152t anxiety in elderly, 8487 clinical features, 9697
Peritoneal dialysis, 181t dementia, 6775 diagnosis, 9799
Pharmacotherapy depression, 7583 general information, 9596
definition of, 31 driving, 100102 treatment, 99
general overview, 2930 elder abuse, 9195 Sexually transmitted infections (STIs), 96
pharmacokinetics components, 3031 sexuality and older adult, 95100 Shingles
preventive measures, 31 substance abuse and elderly, 8891 clinical features, 262
Phobias, 84 Pulmonary disease diagnosis, 262
Phosphodiesterase-5 inhibitors, 99, 198 general information, 160161 general information, 261262
PHQ-9 questionnaire, 77, 79f specific diseases, 161171 treatment, 262263
Pick disease. See Frontotemporal dementia Pulmonary fibrosis, 166169 Short-acting insulins, 223
Pink puffers, 162 Pulmonary hypertension, 169171 Short-term memory, 16
Pioglitazone, 222 Pulmonary prophylaxis, 35 Sialadenitis, 114
Platelet disorders, 275f Pulmonary testing, 34 Simple cysts, 182
clinical features, 273274 Skin cancer screening, 27
diagnosis, 274 Smell, 16
Q Smoking cessation, 163
Quadrivalent HPV recombinant vaccine, 217218
treatment, 274 Social clock theory, 2
PLISSIT, 97 Social phobia, 84
Pneumococcal vaccines, 26 R Somatic damage theory, 5
Pneumonia Radiation therapy, side effects of, 282 Somnolence, 170
clinical features, 254255 Ranolazine, 148 Spirometry, 13, 162163
diagnosis, 255256 Rate of living theory, 5 Spongiform encephalopathy. See CreutzfeldtJakob
general information, 254 Reactive thrombocytosis, 272273 (C-J) disease
risk factors for in geriatric patients, 254 Recombinant tissue plasminogen activator, criteria Sputum gram stain, 255
treatment, 256 for selection for, 134t Squamous cell carcinoma (SCC), 109, 110f
316 IN D EX
Stable angina Tinea pedis, 244245, 244f atrophic vaginitis, 204205

diagnosis, 148 Tinnitus, 129 bacterial vaginosis, 203204
general information, 147148 Tobacco smoking, 91 contact dermatitis, 205
treatment of, 148149 Toxic thyroid adenoma, 232 definition, 199
Staphylococcus aureus, 259 Transdermal narcotics, equianalgesic doses for, 307t epidemiology, 200
Stasis dermatitis, 104 Transvaginal ultrasound (TVUS), 211 etiology, 201
Statins, 153 of uterine lining, 205 lichen planus, 206f, 208
Streptococcus pneumonia, 259 Trichomoniasis, 203204 lichen sclerosus, 206207, 206f
Stress incontinence, 52 Tricyclic antidepressants, 82, 293 lichen simplex chronicus, 205206,
Stroke Trimethoprim-sulfamethoxazole, 253 206f
differential diagnosis for, 133t Tuberculosis (TB) symptoms of, 200
evaluation of, 133f clinical features, 260 trichomoniasis, 203204
risk factors for, 131t diagnosis, 260261 vaginal candidiasis, 201202, 202t, 203t
Stromal ovarian cancer, 212 general information, 259260 Valvular heart disease, 159160
Subarachnoid hemorrhage (SAH), 130 treatment, 261 Vascular dementia, 74
evaluating suspected, 135 Tympanic membrane perforation, 124, 124f Vasoconstrictors, 143
Substance abuse and elderly, 8891 Venlafaxine, 87
Sudden hearing loss, 126 Venous ulcerations versus arterial ulcerations,
U
Sulfonylureas, 221222 106
Ulcerations, 104105
Sundowning, 63 Vertigo, 127129, 128f
United States Preventive Service Task Force
Superficial spreading melanoma, 111 Vestibular neuritis, 127128
(USPSTF), 2528, 241
Surgery, pulmonary evaluation for, 35f Visual impairment, causes of, 117t
Urge incontinence, 52
Surgical risk factors, 32t Vitamin B12, 263
Uric acid stones, 188
Systemic inflammatory response syndrome (SIRS), Vulvar cancer, 207
Urinary incontinence, 226
256 Vulvovaginal gingival syndrome, 208
Urinary retention, 198199
Urinary system, 1314
T Urinary tract infections (UTIs) W
clinical features, 252 Wear and Tear theory, 4
Tamsulosin, 55
diagnosis, 252 Weight loss, evaluation of, 51f
Taste, 16, 16t
general information, 251 Wernicke encephalopathy, 90
Telomerase, 4
recurrent, 254 Wet ARMD. See Exudative ARMD
Telomeres, 4
treatment, 253 White blood cell (WBC) disorders
Temporal arteritis, 143
Urine antigen testing (UAT), 255256 clinical features, 266267
Tertiary prevention, in geriatrics, 24
Urodynamic testing, 55 diagnosis, 267269
Testosterone therapy, weighing risk/benefit of, 196
Uroflometry, 55 general information, 266
Theophylline, 165
Urologic disease treatment, 269271
Thiazolidinediones, 222
benign prostatic hypertrophy, 196198 Wounds, 105t
Thrombocytopenia, 273, 274, 275f
bladder carcinoma, 192194 principles of, 106
Thrombocytosis, 274
hematuria, 190192 stasis dermatitis, 104
Thrush, 113114
hypogonadism/low testosterone, 194196 ulcerations, 104105
Thymus gland, 17
urinary retention, 198199
Thyroid disorders, 227232
Uterine cancer, 215217
hyperthyroidism, 229232 X
Uterine sarcoma, 215
hypothyroidism, 227229 Xerosis, 103, 243
Thyroid dysfunction, 179 Xerostomia, 114
Thyroid storm, 229, 232 V conditions and medications associated
Thyrotoxicosis, 229 Vaginal cancer, 218219 with, 117t
Tilt table testing, 59 Vaginal candidiasis, 201202, 202t, 203t
Timolol, 121 Vaginitis

Step-Up To Geriatrics

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Step-Up To Geriatrics

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STEP-UP to

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Library of Congress Cataloging-in-Publication Data

Names: King, Mitchell S., author. | Lipsky, Martin S., author.

LINDA CHANG, PharmD, MPH PREETINDER S. PADDA, MD

MOHAMMED AMIR KHAN, MD SAVNEET KAUR SONIA SARAN, MD

Hematologic Dis eas e 263

Intro d uc tio n to A g ing

TABLE 1-1 Characteristics of Aging

5. Ageism is prejudice or discrimination on the basis of a persons age.

TABLE 1-2 Major Theories of Aging

4. Heterogeneity is another key concept of aging.

Quick HIT younger individuals.

(c) Vitamin C and E are examples of extrinsic antioxidants. Despite the

C. Causes of death and chronic disease (see Figure 1-1)

Clinical Vignette 1-1

Caus e o f De ath Amo ng U.S . Adults

2. Fries also proposed the concept of compression of morbidity.

G. Biologic aging also affects illness in several other ways:

CLINICAL PEARL 1-1

Clinical Vignette 1-2

TABLE 1-3 Body Composition Changes with Aging

Decreased lean body mass Changes in drug distribution

Clinical Vignette 1-3

8. Skin cells produce less collagen.

CLINICAL PEARL 1-2

TABLE 1-4 Common Foot Problems in the Elderly

Clinical Vignette 1-4

CLINICAL PEARL 1-3

TABLE 1-5 Formulas Used to Predict Maximum HR

Miller formula: Used for planning exercise, add 4 beats per

TABLE 1-6 Principle Changes in the Cardiovascular System

Decrease brain mass Atrophy on CT or MRI scans

d. The aging heart exhibits decreased -adrenergic response.

H. Nervous system (see Table 1-7)

I. Taste and smell

TABLE 1-8 Impact of Taste Changes

Loss or increased appetite

O. General changes with aging

TABLE 1-9 Examples of Common Potentially Treatable Conditions

TABLE 1-10 Elements of a Comprehensive Geriatric Assessment

CLINICAL PEARL 1-4

E. Benefits of a comprehensive assessment include the following:

J. A functional decline may be complicated by income level, family support, and

K. The traditional medical assessment should be supplemented by briefly screening for

P re ve ntive Ca re fo r the O ld e r A d ult

Clinical Vignette 1-5

The American Cancer Society

Clinical Vignette 1-7

Clinical Vignette 1-8

CLINICAL PEARL 1-5

TABLE 1-12 Some Potential Benefits of Exercise

CLINICAL PEARL 1-6

Use of Aspirin Prophylaxis

CLINICAL PEARL 1-7

Associations of Clinical Endocrinologists do recommend periodic screen-

Quick HIT supplementation, calcium, and weight-bearing exercise.

TABLE 1-13 Screening Measures for Adults Aged 65 or Older

Tobacco use Counseling/medication Regardless of age, there are benefits

Ge ria tric P ha rm a c o the ra p y

2. Polypharmacy rates increase in the geriatric population.

B. Appropriate geriatric pharmacotherapy is challenging for the following reasons:

C. Pharmacokinetics include four componentsabsorption, distribution, metabolism,