Brian Christopher Misiaszek, MD, FRCPS (C)
Assistant Professor of Medicine
Michael G. DeGroote School of Medicine at McMaster University
This material is copyright to Brian Christopher Misiaszek, 2008.
The exceptions are those included materials that are copyright to their
respective owners, and no ownership if claimed or implied for them.
Please do not copy, convert to electronic form, or distribute this material in
any way without first obtaining prior written permission.
Images and illustrations used in the handbook are understood to be in the
public domain; if there are any problems with copyrighted material
mistakenly included, they will be removed on request. Cover photo
illustration of Inuksuk by Ansgar Walk from Wikipedia Commons
I would like to thank the following people for their invaluable help with their
contributions and meticulous proofreading of this manuscript:
Doctor’s Irene Turpie, Michelle Gagnon,& Nicole Didyk.
I would also like to thank the following people for their invaluable support and
enthusiasm in teaching:
Drs D.W. Molloy, Anne Braun, Alexandra Papaioannou, Mary Peat, George
Heckman, Sherri-Lynn Kane, Paula Creighton, Frank Smith, Derek Hunt, Joye
St. Onge, Cindy Hobbs, Cheryl Allaby, Lisa Huzel, Rick Paulseth, Helen
Ramsdale, David Cowan, and Chris Brymer (whose original “Red Book”
inspired this manuscript).
I would again especially like to single out and thank Dr. Christopher Patterson
for his help in providing constructive criticism, priceless feedback, and common
sense advice in the development of this; reviewing his marginalia and other
pithy comments to the manuscript was a unique, humbling and yet ultimately
invaluable and rewarding learning experience.
Forward to the Revised Edition of the
Geriatric Medicine Survival Handbook
The cover illustration for this revised edition depicts an inuksuk (sometimes
called inukshuk), a common feature of the Canadian Artic constructed by the
Inuit living there. It is a directional stone marker or cairn often in the shape of a
person (Inuk), and acts to help direct and guide lost travelers across the vastness
of the North, else indicate areas good for hunting and fishing.
This handbook has a similar aim, to help guide medical learners across the vast
topic of Geriatric Medicine. It is primarily aimed at medical students, Residents
and other learners, and can act as a portable guide for approaching common
problems encountered with older patients. It is neither fully comprehensive nor
authoritative, but will hopefully provide interested learners with a starting place
for their own journeys of self directed learning in this ever growing area of
There are many textbooks and reference materials that can be found in the
appendices for the reader who wants a more thorough review of the material
If you note any errors in this text (be it facts, spelling mistakes, grammar, etc.),
please do not hesitate to point these out so they may be corrected in any future
editions of this handbook.
Scattered inside the text are many boxed entries labeled PEARLS. These
practical clinical tips, or “pearls of wisdom” are teaching points derived from
experience and the “art” of medicine that have been backed up by evidence
Brian Christopher Misiaszek, MD, FRCPC
Geriatric and Internal Medicine
Section 1: Introduction
What is Aging?
Debunking Myths about Aging
Normal Aging & Common Disorders in the Elderly
Theories of Aging
Section 1: Geriatric Assessment
Geriatric Assessment & Introduction to the Older Patient
Getting the History
Functional Inquiry: BADLs & IADLs
Examining the older adult
Section 2: Geriatric Giants
Cognitive Impairments: Dementia, Delirium
Falls & Dizziness
Iatrogenesis & Medication Optimization
Pain in the Elderly
Failure to Thrive
Frailty [Under Construction]
Section 3: Appendices
Screening tools: CAM, MMSE, GDS, & FIM
Useful Syndromes to Know
Approach to and management of delirium and agitation.
References & Suggested Reading
Final Geriatric Pearls, & Acronyms used in the text.
What is Aging?
Aging is a multidimensional process and refers to the process of "…accruing
maturity with the passage of time." It begins with conception and continues
throughout life until death occurs. Aging is progressive, ubiquitous and
inevitable to all living things.
Normal aging and diseases associated with aging are two separate entities.
Normal aging refers to those normal deteriorative processes that all human
beings will experience if they livelong enough, such as decreased bone mass,
osteoarthritis, and lens cataracts. Diseases that are associated with aging, but
not caused by aging and does not occur in all persons (i.e. probabilistic aging)
include dementia, hypothyroidism, stroke, and congestive heart failure; while
they are common they are not inevitable to all persons, and not all seniors will
Homeostenosis is the concept where normal aging decreases the body's ability
to withstand stress and challenges as homeostatic mechanisms decline over time.
Our functional capacity and ability to respond to stress progressively declines in
a linear or exponential fashion beginning as far back as the third decade. Each
system’s decline is independent of changes in other organ systems, and is
influenced by genetics, diet, environment and personal habits. The frailty seen
in some older adults is a direct result of the attenuation of these normal reserves.
Canadian Aging Demographics
Seniors are the fastest growing population group in Canada and the
In 2000, there were about 3.8 million Canadians aged 65 and over,
up 62% from 2.4 million in 1981. The senior population has grown about
twice as fast as the overall population since the early 1980s. As a result,
more than one out of every 8 Canadians is now a senior.
In 2000, 13% of the populations were seniors, up from 10% in 1981
and 8% in 1971; this was 2.5 times the figure in 1921, when only 5% of
people living in Canada were seniors.
It is projected that by the year 2026 there will be over 7.7 million
Canadian seniors, or 21.4% of the population.
Seniors aged 85 and over represent the fastest growing segment of
the senior population (see graph below); one in ten seniors now fall into
this age category. In 2000, there were over 400,000 Canadians aged 85 and
over, up from 140,000 in 1971 and 21,000 in 1921.
PEARL: Because of these demographic trends, how seniors are served
by the health care system will become an increasingly important issue
Source: Statistics Canada
DEBUNKING MYTHS ABOUT AGING...
Myth 1: To be old is to be sick and a burden on others
Fact: In 1998, there were about 3.7 million Canadians aged 65 and older. Most
Canadian seniors living at home describe their general health as positive; in
1997, 78% said their health was either good (38%), very good (28%), or
excellent (12%), while only 16% reported their health was fair and just 6%
described it as poor. The majority of Canadian seniors also live at home; in
1996, 93% of all people aged 65 and over lived in a private household. 58% of
them lived with either their spouse or a common-law partner. Another 7% lived
with members of their extended family, such as the family of an adult child,
while 29% lived alone and 2% lived with non-relatives.
Myth 2: Older Canadians contribute nothing to society.
Fact: The majority of seniors (58% in 1997) participate in informal volunteer
activities outside their home, and a fair number continue full or part time paid
work also. In 2000, close to three-quarters of a million Canadians aged 65 and
over, 18% of the total senior population participated in some kind of formal
volunteer activities. In 1996, 37% of all seniors provided some sort of
household or personal assistance to others, 17% helped out with child care; 21%
did household maintenance; another 21% helped with shopping, transportation
or financial activities; 27% provided emotional support; and 35% checked up on
others by visiting or telephoning. They all pay taxes, and have done so for many
Myth 3: The majority of older persons are senile or demented
Fact: The prevalence estimates from the Canadian Study on Health and Aging
suggest that only 252,600 or just 8.0% of all Canadians aged 65 or over meet the
criteria for dementia; that means 92% of those over 65 do not have dementia.
Most seniors with Alzheimer's or other dementia live in a health-related
institution. In 1995, 78% of all those aged 65 and over with this condition
resided in long term care.
Sources: Health Canada: Division of Aging and Senior
Derived from Statistics Canada figures
Biological Theories of Aging
No one knows why we age, and the upper limits of the human life span, about
120 years, have not altered over the interval of recorded history despite
advances in preventative health care and medicine that have occurred over the
last few centuries. While many more persons can live longer today because of
these advances (the so-called “rectangularization” of the survival curve where
the % of individuals who live to a specific age approaches a more
rectangular form over time) there still appears to be an upper limit of ~12
decades to our maximum life span.
Using the tools of molecular and cellular biology along with modern genetics
various investigators have proposed a variety of hypotheses for why we age.
Below you can find some of these current theories of aging, and none of them
are mutually exclusive.
/ Free radicals
Various cellular mechanisms constantly repair ongoing
occurring DNA damage (i.e. caused by radiation,
mutation). The repair efficiency is positively correlated
with life span, and decreases with age.
Life span is inversely proportional to the extent of
oxidative damage caused by unstable & reactive
chemical compounds and directly proportional to
Faulty DNA/RNA transcriptional and/or RNA
translational processes produce ineffective or toxic
Cross Link Theory
Age versus Cancer
theory (Jan 2002)
Cells are programmed with a specific, finite number of
divisions, & cell death occurs when this number is
achieved (i.e. the “Hayflick limit” of ~50 doubling of
cells seen in tissue culture for fibroblasts). Telomeres
(proteins that act like plastic ends of shoelaces to seal the
ends of chromosomes, shorten with each division; once
the telomere is gone, the end begins to "fray"). This has
been suggested as the biological “clock” for aging
Programmed cell death induced by extracellular signals
or “gerontogenes” that tag a cell for removal by
Chemical bonds form between and within molecules and
affect function (e.g. cross-linking in collagen causes loss
of elasticity in blood vessels).
Ordinary insults and injuries of daily living
accommodate and decrease the organism's efficiency to
Damage to the immune-system makes the body
vulnerable to disease. B and T cells are less effective and
less numerous as we age.
Failure of cells with specific integrative functions (in the
pituitary, thyroid, adrenal, pancreas, and gonadal glands)
brings about gradual homeostatic failure
Aging may be a side effect of the natural safeguards that
protect us from cancer. Over expression of tumor
suppressor genes in transgenic mice (i.e. p53) causes
PEARL:. The oldest living person with a valid birth certificate was a 122-yearold woman named Jeanne Calment from Franc,e who was born in 1975 and who
died in 1997.
Definition: The number of years a person would be expected to live from the
day he or she was born (for life expectancy at birth) based on mortality statistics
at the time.
For a person was born in the mid 1960s (and having survived to age 20), the
average Canadian male would live to 71.5 years and the average Canadian
female would live to 76.7 years. In Canada, life expectancy has increased by an
average of seven years for men, and 13 years for women since 1920. The
reasons for this increase in the industrialized nations are mostly related to
improvements in public health (including sanitation and infection control), and
decreases in infant mortality.
Women outlive men, and twice as many women as men live to age 80. Reasons
for this include male employment hazards (job related accidents, exposure to
carcinogens), lifestyle choices (more male smokers and heavy consumers of
ETOH), and the protective effects of estrogen from cardiovascular disease (MI,
strokes). As a result of this discrepancy, many elderly women are widowed
(52%) and live alone (40%), while more older men are married (78%) and live
with a partner (85%) who is their caregiver.
Older adults are survivors. Many of them have managed to avoid or minimize
health problems that cut short others in their age cohort (i.e. MI, strokes,
cancer); ironically, the older you live, the tougher you seem to be, and you
increase your chances of living even older.
Because of this survivor effect, (and providing the person has no mortal
disease), as a rule of thumb:
At age 65, life expectancy is ~15 years (male=14.2 years, female=18.6
At age 75, life expectancy is ~10 years.
At age 85, life expectancy is ~5 years.
And if they live to age 95, they may have another 2-3 years of life
Normal Age-Related Physiologic Changes & Their
Many normal changes can lead to clear clinical consequences (i.e. arterial
stiffening leading to hypertension, absence of estrogen in post-menopausal
females accelerating bone loss).
Not all these changes with aging are necessessarily bad; for example,
autoimmune disease may “burn out” in later life. However, you should be
aware of some general themes, which may explain why disease presentation in
the elderly can be atypical (i.e. diminished perception of acute pain may alter the
presentation of pancreatitis, or myocardial infarction, etc.), and older adults are
more likely to die because of a pneumonia (decreased immune system,
decreased respiratory function and reserve)..
PEARL: Please remember that aging is heterogeneous; although these changes
occur with aging; there is much individual variation that occurs among and
between individuals. There are moribund 65 year olds, and 93 year olds who
Temperature regulation: Tendency to hypothermia:
Decreased subcutatneous fat, decreased sweating,
decreased shivering, decreased awareness to cold, less
autonomic vasoconstriction, decreased metabolic rate,
decreased heat generated in response to eating
Medical conditions: drugs (ETOH, TCA, ASA,
acetaminophen), hypothyroidism, malnutrition,
hypothalamic and Central Nervous System (CNS)
dysfunction, dementia, Parkinson’s Disease, stroke.
Extrinsic factors; poverty (unable to afford heating oil),
Fluid Homeostasis: tendency to dehydration:
Reduced Total Body Water (up to 30% more body fat)
blunted thirst sensation, less drinking response, lower
renal plasma flow, urine concentrating ability reduced
Aging Changes in Specific Organ Systems:
40% of those >65 are edentulous, mostly because of neglect rather
than any natural age related process
risk of caries increases with age as a result of gingival recession and
loss of jaw bone density
Ossification of the laryngeal cartilages causes stiffness; prevents
vocal cords coming together while speaking, resulting in a weaker,
In males, the vocal cords become thin and atrophied with age,
resulting in a higher pitched conversational voice.
In females, loss of hormonal influence leads to vocal cords becoming
more edematous after menopause, resulting in a lower pitched voice.
Presbyopia (loss of lens accommodation) due to hardening &
thickening of the lens (making it opaque) and decrease in muscle
Decreased visual acuity because of narrowed pupil, fewer rods
(cones spared) so poorer night vision; there is also the need for more
light to reach the retina (on average, an older person needs 4x more
light than a younger person); additional problems with depth and
Flattening of the corneal surface (with diminished refraction) and
clouding of lens
Presbyacusis: high sound frequencies lost and impaired speech
More prone to excess cerumen (ear wax) occlusion of ear canal,
which becomes narrower and more tortuous.
Age related changes resemble emphysema:
Loss of elastic recoil
Early airway closure (and more dead space where you are ventilating
Decreased arterial P02 (-4 mm/decade)
Decreased flow rates, FEV1, and Vital Capacity
Stiffer chest wall &weak muscles
Increased dead space
Progressive decline in carbohydrate tolerance and increasing insulin
Decreased aldosterone, renin,, calcitonin, and growth hormone.
Slightly decreased (or no change) in thyroid hormones T3 and T4,
cortisol, insulin, epinephrine, parathyroid hormone (PTH), and 25hydroxyvitamin D.
Increase in follicle-stimulating hormone (FSH), leutinizing hormone
(LH), and norepinephrine.
In women, decreased estrogen (post menopause) & prolactin
In men, decreased testosterone in some (so-called andropause)
Arterial wall stiffening (true and “pseudohypertension”)
Increased L atrial size and prevalence of S4 heart sound
Reduced LV compliance caused by: increased myocyte size,
increased LV mass, and increased posterior wall thickness
(infiltration with lipids, collagen, fat, amyloid)
Cardiac output decreases at rest/exertion; maximal HR decreases
(predicted max is 220-age in years), much less in physically active
elders with disease
Reduced Lower Esophageal Sphincter (LES) tone
Decreased acid production (leading to decreased emptying, less
calcium absorption, and differential medication absorption)
Reduced intrinsic factor
Decreased liver mass and blood flow leading to reduced oxidative
metabolism of some drugs (but not acetylation or sulfuronidation)
and protein synthesis
Increased transit time
Increased rectal resting tone, decreased contracting pressure
As a rule of thumb, "Everything slows down!"
More intense stimulation needed for erection
Erections less firm
Ejaculation takes longer, less volume, & intensity
Longer refractory period
Estrogen dependent changes [vaginal lubrication slower
atrophy (thin epithelium, honeymoon cystitis)]
Slower reaction of clitoris
prolonged refractory period
Hematologic & Immune systems
T cell: numbers decrease, delayed hypersensitivity reaction
decreased, fewer natural killer and suppressor cells
B-cell: numbers stable, but make fewer antibodies.
Smaller kidneys (cortical renal mass decreases ~20%)
Renal blood flow decreases
Glomerular Filtration Rate (GFR) progressively decreases; average
decline is 50% from age 20-80, but those 80+ show little decline.
More prone to develop SIADH
Weight decreases, body fat increases, height decreases (in women
Sarcopenia (up to 80% decrease in skeletal muscle mass and quality
in non active seniors)
Osteopenia (decrease in bone mass)
Total body calcium and potassium stores decreases
Flattening of the dermal-epidermal junction, leading to more thin and
fragile skin susceptible to tearing and sheer forces.
Dermal atrophy, and progressive loss of elastic tissue subcutaneous
fat leading to lines and wrinkling, and problems with thermal
Loss of melanocytes, and retreat of the dermal plexus leading to
pallor and increased vulnerability to sun damage and skin cancer
Hair graying and hair loss.
Decrease in brain mass and selected loss of cortical neurons (1% per
year loss after age 60)
20% decrease in cerebral blood flow from age 30 to 70
Decreased smell and taste perception
Reduced perception of acute pain
Impaired postural reflexes
Increased reaction time (up to 30% longer)
Alterations of neurotransmitter levels:
Increased MAO levels
Decreased dopamine (and binding sites), norepinephrine,
and a slight decline in GABA levels
Less sleep required, but sleep latency increased
Reduced slow-wave sleep (sleep stages 3 & 4)
Increased REM but shorter; decreased REM latency (may
compensate with am napping)
Increased night awakenings and sleep fragmentation
Disorders More Common in Older Adults
A number of disorders are more common in older adults than in younger
persons. They are not caused by aging itself, and do not occur in all older
There is insufficient space to more than list a few of the more common disorders
here (more trans-system problems can be found in the section on Geriatric
Giants), and readers are advised to consult their favourite and trusted Internal
Medicine textbook for more details on many of the items listed below.
Using WHO criteria (Hb <120 g per L in women and <130 g per L in
men), the prevalence of anemia in the elderly ranges from 8 to 44
percent, with the highest prevalence in men 85 years and older.
A cause can be found in ~ 80 percent of elderly patients.
The most common causes of anemia are anemia of chronic disease
and iron deficiency, but Vitamin B12 deficiency, folate deficiency,
GI bleeding and myelodysplastic syndrome are also common causes
Atrial Fibrillation (Afib)
The prevalence of atrial fibrillation increases with age, about 3% in
those in their early 60s, and is up to 10% in those older than 80.
Afib is associated with a higher risk of cardiovascular death,
congestive heart failure and peripheral embolic stroke in older
Cardiovascular disease is the leading cause of death in older
Canadian men and women.
Hypertension (HTN), the best predictor of coronary artery disease,
increases dramatically in prevalence with aging; isolated systolic
HTN occurs in 34% of men and 38% of women aged 65 to 74.
50% of Canadian seniors are on no treatment at all for HTN
Congestive Heart Failure (CHF) is the most common cause of
hospitalization among those aged 65+ in the US
Lung cancer is the most common cause of cancer-related deaths in
both men and women; 68% of cases occur in people over 65
>50% of breast cancer patients are older than 65 at diagnosis
Prostate cancer is the most commonly diagnosed cancer among
Canadian men (excluding non-melanoma skin cancer) over 65, and is
the second most common cause of cancer death (after lung cancer) in
this same group.
Cerebrovascular Disease (Stroke)
One Canadian study estimated 4.1% of people aged 65+ in the
community are living with the effects of stroke (CMAJ Sept. 22,
Seniors who experienced stroke more often reported their health to
be "poor" or "fair" than seniors who had not (69% v. 25%)
Chronic obstructive pulmonary disease (COPD)
COPD is the fourth-leading killer disease of the elderly in Canada.
Cigarette smoke is the underlying cause in ~80% to 90% of cases
Prevalence of COPD for those aged 65-74 years is 5.0%; and for
those over 75 years is 6.8%.
Alzheimer Disease (AD) is the leading cause of dementia in Canada
(60-70% of all), affecting about 160,000 Canadians, or 3-11% of the
general population over 60 years of age
Diabetes has a prevalence of ~13% in persons over 65.
Type II diabetes mellitus is the most common form of diabetes in the
elderly, accounting for about 92% of cases, and is the 6th leading
cause of death in men over 65.
The onset of Type II DM occurs 40% of the time after the age of 60,
and there is often a long delay before diagnosis.
Long-term studies have show that 35% of seniors with diabetes
suffer from retinopathy 18% from cardiovascular disease, 30% from
peripheral vascular disease and 12% from nephropathy
One US survey of community dwelling elders found 7% of women and 3%
of men between 60 - 89 years of age with this hormone deficiency
The Canadian Study on Health and Aging (CSHA) found 9% of their study
population had subclinical hypothyroidism.
85% of people over the age of 70 suffer from osteoarthritis
It is the number 1 cause of long-term disability in Canada
Estimates from the Osteoporosis Society of Canada suggest that 1.4
million Canadians have osteoporosis, a leading risk factor for bone
fractures and death or morbidity after a fall.
Parkinson’s Disease (PD)
Roughly 1/100 persons in North America are affected
Average age of diagnosis is 60; the rates rise in persons >70.
Dementia, a feared complication, increases in prevalence with age; it
occurs in approximately 30% of patients with advanced PD.
Influenza/pneumonia is a major contributor to deaths and hospitalization in
the elderly and is the leading cause of death from infectious disease in
Symptomatic Benign Prostatic Hypertrophy (BPH) is very common,
affecting 40 to 50% of men aged 51 to 60 years, and ~80% of men by age
US datum show that 20% of all GP visits for those 65+ are motivated by a
skin problem (i.e. rash, pruritis, photo aging, cancer)
Surveys show that 2/3 of those 65+ have at least one dermatological
Physiological changes in aging skin when combined with immobility and
incontinence predispose elderly persons to have pressure ulcers;
prevalence rate in acute care range from 3.5% to 30% and in long term
care facilities from 2.4% to 23%.
Erectile dysfunction (ED) is the most common form of sexual dysfunction
in elderly men, affecting nearly 70% of men age 70.
The prevalence of sexual dysfunction in elderly women is largely
unknown, but reduced libido, inhibited orgasm and dyspareunia are the
most common disorders, and are largely due to the decline of estrogen
Urinary Tract Infections
Prevalence of asymptomatic bacteriuria in the elderly range from 15-60%
depending on the study, with twice as many females as men affected.
The annual incidence of symptomatic bacterial UTIs is estimated to be as
high as 10% in those over 65.
Thirteen percent of Canadians over age 65 have some form of visual
Almost 8% of seniors over 65 (and 11% if over 80) have impairment
(blindness in both eyes) sufficient to meet the legal definition of blindness
(visual acuity (VA) less than 20/200)
11 % of Canadians between 65 to 74 years of age & 30% of persons over
the age of 75 have Age Related Macular Degeneration (ARMD), the most
common cause of irreversible vision loss in seniors.
Diabetic retinopathy accounts for 35% of all cases of blindness; prevalence
increases with age and the duration of the disease
The prevalence of lens cataracts sufficient to impair vision (visual acuity
less than 20/30) rises from 1% by age 50 to 100% by age 90.
Glaucoma is present in less than 1.5% of those under 65, 2-3% in those
aged 65-74, and between 2.5-7% for those over 75.
Approach to Illness in the older patient:
In older adults, the presenting problem is the “tip of the iceberg” of a
pathological process, which often takes careful diagnostic assessment to
The “iceberg” metaphor reminds us that we see only what is on the surface and
what is only immediately obvious; however, in truth 9/10ths is hidden (like the
underwater portion of the iceberg), and can only be found if you look for it.
For example, looking beyond the initial presenting problem of falls in an older
adult (“the tip of the iceberg”), may reveal not only the reason for this problem,
but also one or more diagnoses underlying this and other symptoms.
For example, a certain elderly patient is having recurrent falls. Why?
Under the Tip of the Iceberg…
After some history taking (the falls only occur after exertion), a physical
examination (hypertension, dependent crackles, an S3 heart sound, and an
elevated JVP) and some simple laboratory tests (oximetry after a short walk
shows SpO2 changes from 91% at rest to 84% with exertion), you might
discover that the falls are caused because of recurrent exercise induced
But why the hypoxia? Because of the true but hidden diagnosis of Congestive
Heart Failure (CHF) that had not been diagnosed by anyone previously and
But you can’t stop there! Where did this particular iceberg come from (i.e. why
is the person in CHF now)? And what further hazards need to be anticipated in
In Geriatric Medicine you must see not just the isolated problem, but also how
that older person’s problem fits in to the larger context of their life.
Geriatric Medicine Models
This all-inclusive way of thinking is in direct contrast to the classic medical
model of diagnostic thinking based on an ever-narrowing upside down pyramid
of taxonomy that obeys the “law of parsimony”, i.e.:
This conventional top-down “internal medicine” model does not recognize the
psychosocial and behavioral dimensions of illness, or the interactions of
multiple illnesses (i.e. there could be more than one gunman on the grassy knoll)
and is often less useful as a paradigm in Geriatric Medicine.
PEARL: You don’t just want to know one reason a person is having falls at
home, you want ALL their reasons!
Four Alternative Geriatric Medicine Models:
The Synergistic Morbidity Model (1+2=7)
The gradual accumulation of ill health events, combined with social
and environmental problems, each alone insufficient to impact
dramatically on functional performance, can eventually take its toll on
a frail older person.
For example, an older woman named Mrs. A (who has osteoarthritis gradually
getting worse) is the caregiver for her demented spouse. Mr. A is now up at
night wandering, and she cannot sleep and has become exhausted trying to
manage him. He is also hoarding things, and has hid her glasses, which she
cannot find. She has increasing OA pain, for which she begins to take Tylenol
#3, prescribed by her MD. With her continual pain and caregiver burnout, it
becomes more difficult to make meals at home, so she only prepares only soup
and sandwiches (no vegetables) for the two of them. Depressed, she starts to
drink alcohol more heavily than ever before. She is now starting to trip and fall
at home, and while at the grocery store (after having locked her husband inside
at home) she slips and breaks her wrist after falling on her outstretched hand...
The Misattribution Model (“A” not “B”)
The problem is attributed to one cause (or even normal aging)
whereas in actuality it is due to another cause.
For example, Mr. B, who lives alone and had a diagnosis of CHF (for which he
is on a diuretic and digoxin), is having frequent stomach upset, for which is MD
prescribes an H2-blocker. In actuality, he his having mild digoxin toxicity from
his too high dose of digoxin (which has not been changed in 30 years). With the
anticholinergic effects of the new
medication, in combination with his
mild digoxin toxicity he becomes acutely confused. He inadvertently stops all
his medications, and is now SOB from acute heart failure; an ambulance is
The Causal Chain Model (A->B->C>X)
A continual series of troublesome health problems in a previously
independent older person can gradually wear them down to a point of
seeming no return.
For example, Mrs. P, who has with poor balance 2o to a peripheral neuropathy,
complains of insomnia and starts taking a benzodiazapine. She then has a fall
and sustains a hip fracture, causing her admission to hospital. Immobility from
the fracture leads to deconditioning and pressure ulcers, and now Mrs. P. is in
too weak to move from her bed and becomes functionally incontinent. The
medical staff is thinking about making her Alternate Level of Care (ALC) and
discharging her to a nursing home.
The Unmasking Event (“aha!”)
A sudden stressful external event—such as an injury, acute medical
problem or a loss of a caregiver-- can reveal a previously unrecognized
and hidden medical problem.
For example, the Smiths’s had been married for 65 years when Mrs. Smith
suddenly dies of an MI. Suddenly the family notices that Mr. Smith is not
coping at home and is failing badly, more than would be accounted for by grief
alone. He doesn’t’ seem to be able to work the home security system, pay the
bills, or work the microwave to heat up food his family is bringing over. He is
burning pots in the kitchen, and mixing up his medications (if he takes them at
all). He denies being depressed, and appears to be cheerful. While he has been
somewhat vague over the last few years and poor with his memory, his wife has
always been able to jump in as his “peripheral brain”. An assessment by his MD
(whom he has not seen in 3 years) reveals signs strongly suggestive of
Please see the reference section for an article on these models
Atypical Presentations of Common diseases
Illness in old age often presents atypically, or is often masked; i.e.:
Unrecognized dementia, delirium, and/or depression
Depression w/o sadness, infection w/o fever, CHF w/o dyspnea
Silent MI or Urinary Tract Infection (UTI) presenting as confusion
Zoster-Varicella (“shingles”) presenting as chest/back pain
Dementia, depression, presenting as “failure to thrive”
Iatrogenic illness is common!
Pearl: remember that old age does itself not cause disease, and
confusion, incontinence, anemia, etc. are NOT normal parts of aging
Occam’s Razor: William of Occam (or Ockham) was a 14th century Franciscan
monk and philosopher who was famous for his use of economy in formal logic.
To paraphrase his original writings*, "when you have two competing theories
which make exactly the same predictions, the one that is simpler is the
In older patients, it is be far more likely that you will see common disorder
presenting atypically (i.e. a UTI causing confusion, sepsis without fever) than
you would find an uncommon or rare disorder.
In other words, “When you hear hoof beats, think of horses, not zebras.”
* His original saying in Latin was "Pluralitas non est ponenda sine neccesitate",
which translates into English as "Entities should not be multiplied
unnecessarily" Another version of his saying: "Entia non sunt multiplicanda
In Geriatric Medicine, it is often more practical to think of problems or
syndromes that cross several organ systems rather than starting with distinct
“Geriatric Giants” is a term coined by Bernard Isaacs, and the expression
refers to the principal chronic disabilities of old age that impact on physical,
mental and social domains of older adults. Many of these conditions, commonly
misperceived to be an unavoidable part of old age, can in fact be improved.
These “Giants” include:
Cognitive Impairments (i.e. 2’ to dementia, delirium or
Postural Instability and Falls
Caregiver Stress & burnout
Iatrogenesis & “Polypharmacy”
“Failure to Thrive” (often from the above)
See the second section of this handbook for more details on these.
Geriatric Assessment (GA)
Historically, the elderly (65 and over) accounted for a large proportion of
the total hospital days in Canada. Of the 33.9 million hospital days in
1996/97, the elderly accounted for 62% (or 20.9 million days), although
they represented only 12% of the population in that year.
To avoid entry (or re-entry) into hospital of frail older persons, or simply
to improve their quality of life by paying attention to matters that have
been neglected by others, a Comprehensive Geriatric Assessment can
prove very helpful
Comprehensive Geriatric Assessments decrease mortality, LTC placement,
readmissions to hospital, and minimize the impact of “geriatric
syndromes” such as cognitive impairment, urinary incontinence and falls.
A Geriatric Assessment differs from the conventional medical assessment
by its attention to many different functional and cognitive domains, as well
as its attention to preventative health and their current socio-environmenal
Domains covered in an assessment include:
Current living situation & social supports
BADLs & IADLs
Such assessments may be done by a Geriatrician working independently,
or as part of a interdisciplinary team that often include specially trained
nurses (RNs), Occupational therapists (OT), Physical therapists (PT),
Social workers (SW), Dieticians, Speech Language Pathologists (SLP) and
Assessments can take place in an outpatient clinic, a day hospital, or even
home hospital, and treatment goal plans can be developed, changes in
medications can be made, tests arranged, other allied health services
coordinated, and recommendations (if any) made for changes in their
PEARL: Geriatric assessments only really work if there is follow up (i.e. by a
case manager or a repeat visit) and there is medical control over the
medications and other advice (i.e. don’t just make investigations and treatment
recommendations, get your hands dirty and do them/order them yourself!). And
remember to liaise with other physicians involved in their care, especially their
How to identify elderly patients who would benefit from such an
assessment (i.e. the frail elderly)? Strongly consider if they have three or
more of the following “Red Flags”:
Needs help with ADLs/IADLs by CCAC or caregiver
>2 admissions to acute care hospital/year
“Failure to thrive”
Patients can be screened for the need of such a comprehensive assessment
when seen in the ER, a Family MD’s office, a senior’s social center, etc.
The next few pages will elaborate on just how to do a comprehensive Geriatric
Approach to the Older Patient in Geriatric
Getting the History
History taking from older patients can be difficult because of deafness, vision
impairment, dysarthria (from stroke, or lack of dentures), aphasia (from stroke
or a degenerative condition), anxiety, confusion, or language barriers (if we
don’t speak their language or vice versa). Otherwise, this is a similar process of
information capture to that used for younger patients.
Be patient, and let the patient talk at first; if after 5 minutes you aren’t getting
the information you need, change from open ended to closed ended questions.
Getting the History if the Patient has Memory Loss
If the referral is for memory loss, and there is no person with the patient to
provide a reliable collateral history, all is not lost.
First ask if the patient knows why they are there to see you. If they deny any
memory problem, ask them to tell them a little about themselves; where were
they born? Did they have any brothers and sisters? What were their names?
Did they go to school together? How much schooling did they complete? What
did they do after that? Did they ever get married? How long did they know
their spouse before they got married? When did they get married (the exact
date). How long ago was that? Did they have any children together? What are
their names? When were they born? How old are they now? Do they have any
children of their own, and what are their grandchildren’s names? Where are
they living now? Whom do they live with? How long have they lived there?
What is the address? And so on.
Keep track of their answers, and go back to verify statements (“So…your son
John’s children’s names are what again?”). Gradually, you’ll find out if the
person is struggling or not to come up with these answers. If you start to notice
this struggle, and patients are having a hard time to account for themselves, or
there are odd patches or gaps in their story, gently tell them, “I’m noticing that
you are having a little trouble with my questions and with your memory. I’d
like to test your memory, if that is okay with you.”, and then jump in with the
SMMSE and the clock drawing test (and try and check up on the facts they told
you later on with a telephone call to a caregiver or someone who knows the
patient. If there is no family member, others can act as collateral witnesses; for
example, the Family MD, their CCAC Case Manager, landlord, building
superintendent, home pharmacist, etc.) .
PEARL: Above is a picture of a highly underutilized investigative tool that is
extremely helpful in history taking (although I strongly doubt you’ll be able to
find one now with a rotary dial!).
If they admit that their memory is poor, ask them how long this has been a
problem; “ Is your memory as good as it was 5 years ago” is a good opener.
Ask if they can recall any specific examples or problems with their memory.
Then go back and use the technique above, exploring for gaps in long term and
short term memory, ending with the SMMSE and other more sophisticated
memory tests (see section on cognitive tests for Dementia).
If you are lucky enough to have a family member present, ALWAYS obtain
collateral history from that person, especially if there are questions surrounding
memory (you can do this apart from the patient, or in front of the patient; the
former technique is more efficient, while the latter is more forthright and
respectful of the patient).
Ask the caregiver if the dates and facts are accurate (with the patient’s
permission first; while they are getting ready to change for your examination
and as you step out, ask, “ Is it okay if I have a quick word with your ___ while
you are getting ready?”).
Ask the caregiver about explicit problem with memory loss (i.e. repetition,
forgetting names of family members, forgetting to pay bills), evidence of
geographic disorientation as well as safety problems because of memory
troubles (forgetting to turn off taps or kitchen burners, forgetting to lock the
door to the house, wandering)
Also ask about behavioral problems (becoming withdrawn, stopping activities,
suspiciousness, thinks people are stealing from them, hallucinations, irritability,
apathy and aggression), and how they are managing to cope through these
PEARL: ALWAYS find out if caregiver stress/burden is playing a role. You can
ask the caregivers themselves, in private. There are also a number of caregiver
burden screens and questionnaires that may be available for you to have the
caregiver fill out.
Other Hints for Easier History Taking
Use an electronic amplifier (if available; there’s a picture of one below you
can buy for about $40 Canadian at Radio Shack), or put in the patient’s
hearing aids. Ensure that hearing aids are 1) in their ears, and 2) are
Offer patients their eyeglasses if they seem hard of hearing (many
unconsciously “speech read”), and ensure they are on their nose and clean.
Stand or sit facing when you speak to an older person, and make sure they
are aware you are speaking to them (use body language, such as touch, so
that they know you are talking to them)
Offer their dentures so they can talk!
Speak in a low, deep voice (high frequency sound acuity decreases as we
age, which is why many older persons will drop off the letter S when asked
to repeat the phrase “No ifs, ands or buts” on the Standardized Mini
Make sure the room is well lit and free of other distractions
Attempt to speak to their "good" ear
PEARL: Older patients aren’t all deaf; assume they can hear you and
speak loudly only when asked to do so. Deafness by definition means
the 1’ mode of communication is not speech!
PEARL: If they are missing their hearing aids, and you have no
electronic amplifier handy, you use your stethoscope in a pinch. Place
the ear pieces in their ears, and try speaking into the bell.
Past Medical History
Much along the same lines as you would obtain any other adult. In particular,
asked about previous myocardial infarctions (when, how treated), CVA, DM
(how long, are they seeing a diabetic specialist), hip fractures (how treated),
memory troubles, or recent hospitalizations.
PEARL: Describing their current and past medical problems (diagnoses
and dates of dx) is a useful way of testing remote memory (but only if
you can verify this information by means of an accurate hospital chart or
a knowledgeable family member)!
PEARL: Past surgical history is also useful (and may be prompted by
finding unusual scars of the chest, abdomen, back or peripheries),
including joint replacements, bladder lifts, etc. which may suggest
problems such as incontinence, osteoporosis, etc.
Many patients don’t know the names or doses of their medications, and use over
–the-counter (OTC) drugs, ETOH, herbs, etc. To avoid headaches in figuring
what they are taking, use the “Brown Bag Technique” where all meds the patient
is taking placed are into a paper (or plastic these days!) bag to be brought in and
examined by the MD. Don’t forget lotions, potions, creams, eye-drops, puffers,
insulin, oxygen, ear drops, vitamins, herbals, etc.
You can also call their pharmacy for collateral information, including when
drugs were last refilled. Also find out what medications they have recently
stopped taking, and when they had their last flu shot or pneumovax inoculation.
This is also a good way to check for adherence to Rx.
PEARL: many medications prescribed to older medications are less than
ideal (ie. NSAIDS for OA, Gravol for nausea, cogentin for EPS side
effects of Haldol, etc.). Alternatively, many older adults are not on
medications that they should be on (ie. Warfarin if A-Fib,
Calcium/Vitamin D/Bisphosphonate for osteoporosis/hip fractures),
ECASA if IHD, beta-blockers post MI.
ADRs (Adverse Drug Reactions)
This includes allergies (truly nasty stuff like anaphylaxis or Stevens-Johnson
syndrome) and intolerabilities (i.e. bronchospasm with beta blockers, cough with
ACE-Inhibitors, hyponatremia while on an SSRI, etc.), or predictable side
effects (constipation on opiods, diarrhea on donepezil).
Ask what medications have caused true anaphylaxis (i.e. they had symptoms of
shortness of breath (SOB), facial swelling, tachycardia, hives, etc.), rashes, GI
discomfort (nausea, cramping, diarrhea), etc.?
Review of Systems (ROS):
Much along the same lines as what you would ask any other adult;
Headaches/Syncope/Visual blurring/ previous CVA/TIA/ sudden
weakness /vertigo/ confusion / poor memory /falls/ sensory changes
SOBOE/Chest pain or heaviness/ankle oedema /orthopnea /PND/
palpitations /previous MI or CABG or valve replacement
Cough/hemoptysis/SOB/Chest pain or tightness/using puffers more
Wheeze/ change in sputum colour
Nausea &vomiting/ Pyrosis/ Dysphagia/ dyspepsia/Melena/dyschezia
Change in bowel habit/abdominal cramps
Dysuria/ Frequency/ hematuria/ Nocturia/sexual dysfunction
Weight loss/appetite/fevers/ chills/ night sweats/pruritis/ low
energy/low mood/ ahedonia
Any disorders that run in their family? Do they smoke? Did they
Current ETOH consumption/Past abuse?
PEARL: On a Geriatric ROS always ask about under-reported disorders,
for older persons such as bladder or bowel problems, falls, pain, alcohol
use (how much and how often). Also ask about vision (when did they last
get their eyes checked?) or hearing impairments, recent and updated
vaccinations, current diet, level of exercise activity and use of mobility
aids (were they fitted for them, or where they just picked up at the
Salvation Army thrift store on a
Basic Activities of Daily Living, (aka ADLs, personal self care)
Toileting, feeding, dressing, grooming, ambulation, &
For each ask if: independent, needs assistance, supervision or
entirely dependent on others.
Instrumental Activities of Daily Living (using tools & instruments)
Shopping, meal planning & preparation, housekeeping,
laundry, transit, financial management, using a
telephone, medication management, and driving
Independent, needs assistance, supervision, or entirely dependent?
PEARL: Some of this material is captured in the FIM (see appendix for details)
Who specifically helps out at home?
Are their formal services in place?
Which ones? (i.e. Family MD who visits, CCAC, Case
Manager PT, OT, SW, Veteran Affairs, DARTS, etc.).
Where were they born and when? Are their parents alive (when did they
Siblings (and current health)?
How far did they complete their schooling (0, grade school, high school,
Their first language (English or? When did they come to Canada if not
born here? Did they work, and at what, and for how long? When and why
did they retire?
Are they a war veteran (and so eligible for extra services)?
Current Living Situation:
Type of dwelling (i.e. isolated farmhouse, apartment, 3 story walk-up?).
Is it appropriate for their needs (near a bus route if no car, close to family)?
Assess safety risks (i.e. fire, cold, appropriate clothing, falls, malnutrition,
ability to call for help, abuse <financial, physical, emotional>).
With whom do they live (alone, spouse, child, friend, or ?)
Health of spouse (if appropriate). What is the diet like now? (makes meals,
MOW, skips meals, etc.)
PEARL: for older adults, asking about the current living situation and
support network is far more useful than asking about their past family
history. Ability to do ones own shopping correlates well with
independence. Asking them how they pay for their rent, groceries and
medications is also very helpful (but only if this, and all of the above, is
Power of Attorney (POA):
A power of attorney is a legal document that allows the patient ("the principal")
to designate someone else (an "agent") to perform certain duties on your behalf.
It can also be drafted to become effective, or remain in effect, in the event they
Has this been formally given to someone? When was this done?
Who is it or are they?
For Finances, Personal Care, or both?
PEARL: This is not the same thing as a “living will” (see below); you need the
assistance of a lawyer to draw one up.
Also known as “living wills”, these are a patient’s choices on what life-saving
treatments they wish (or do not wish) to receive in the event that their life is
endangered. They are ideally decisions made previously by a capable patient
and charted and made known to others so that these wishes can be carried out if
the patient is unable to voice their wishes at that time.
Has this been discussed with the patient and their family?
What are the patient’s wishes?
Are these indicated on the chart anywhere?
Physical Examination of the older person:
Observation begins during your interview, and set-up for the physical
Features such as the patient’s dress (neat, slovenly), presence of tremor or
fidgety restlessness (? Akathesisa= restlessness secondary to neuroleptics),
condition of the skin (pallor, cyanosis, bronzing, lesions, bruising), ataxic,
antalgic (painful), or bradykinetic (slow) gait when moving, etc., can all be
Appearance: Comment if they are alert, look younger/older than chronological
age, visible stigmata,(i.e. on O2/IV/foley, visible scars), have word dyspnea
(needs to take a breath in between every few words when speaking), tremor,
BP standing/seated/lying (pick at least two; BP drop on standing?
dizzy symptoms?). Heart rate with each. Respiratory rate.
Temperature. Current weight.
PEARL: Make sure you use the appropriate size BP cuff. Not writing
these numbers down is the biggest error made in measuring BP. If BP
extremely elevated, do Osler’s maneuver*. Finally, the proper way to
auscultate is to use the bell, not diaphragm, to avoid falsely overestimate
the diastolic pressure.
*Osler’s maneuver is performed by palpating the pulseless radial or brachial
artery distal to the point of occlusion of the artery by the BP cuff. When either
of these arteries remains palpable (despite being silent in your ear pieces), the
patient is described as "Osler positive”.
Geriatric Physical Examination
Evidence of previous cataract extraction (dysmorphic pupil)
Red reflex okay (if absent, think cataracts)?
Aniscoria (unequal pupil size; if small and occurs with ptosis (eyelid
droop), think Horner’s Syndrome)
PEARL: The “100/60” rule may help assess anemia. If the Hemoglobin (Hb) is
less than 100, there will be conjunctival pallor. If lines on the hand are no
longer pink, but white, the Hb may be less than 60).
Tympanic membranes (TM) visualized? Teeth/Dentures okay (take
out the latter if they say they don’t fit right)?
Facial droop? Carotid bruits? Thyroidmegally?
Cigarette tar staining of digits? True clubbing? Accessory muscle
use? Tracheal deviation? Increased AP diameter? Egophony?
Can they use their inhalers properly (and demonstrate this)?
Kyphosis (suggestive of osteoporosis)?
PEARL: when auscultating the lungs, start from bottom, and work up!
You may only get one or two good breaths before they poop out.
Normal rhythm or irregular? Ar e they in atrial fibrillation?
JVP? Normal heart sounds? S3/S4 heart sounds?
Any Murmurs? What do they sound like? Where do they radiate??
(and what do you think it is???)
Ascites? Stigmata of liver disease? (spider angiomas, paper-money
skin, leukonychia, caput medusa, ascites, organomegally)
Rectal exam (males for prostate), for occult blood (OB) if concerned
Do they smell of urine? Why?
Is there a foley catheter in situ? If so, why? Can it come out?
Pitting oedema? Chronic stasis changes (loss of hair, hemosiderin
peppering)?Ecchymoses? Pressure ulcers? Xerosis/Dermatoses?
Dry axilla (one of the most specific signs of dehydration), +LR=2.8)
Abnormal skin lesions (possible/probably skin malignancy)
Joint examination (evidence or OA, or RA)?
Peripheral pulses all present and accounted for?
Nail changes: clubbing, pitting, splinter hemorrhages, spooning (iron
Cranial Nerves? (Don’t forget visual acuity, visual fields, and
Primitive Reflexes (suggesting frontal lobe disorder)
Muscle wasting? Muscle Tone? Strength? Deep Tendon Reflexes?
Plantars downgoing (ie. Positive Babinski)?
Vibration sense in the toes with a 128 MHz tuning fork?
Foot sensation with a 10 gauge monofilament (if diabetic)?
Involuntary movements (i.e. resting tremor, tardive dyskinesias)?
Cerebellar function tests (touching nose to finger, rapid alternating
movements, heel to shin)?
Romberg (balance with eyes open, then closed; if abnormal only with
latter, it suggests problem in proprioception)?
Stand up from seating without using hands? Shuffling? Poor turns?
“Get up and Go” Test (JAGS 1991; 39: 142-148); see FALLS
PEARL: Remember that fatigue is a big problem in older persons.
Try to be organized so that your patients do not have to be acrobats to
complete your assessment.
PEARL: Look what’s not there, and should be: gait aid, puffers, hearing
aid, Dentures, etc.
PEARL: Look at the gait aid (is the rubber worn down on their cane?
Brakes okay on rollator walker? What about shoes?
SMMSE (Standardized Mini Mental State Exam)
The Standardized MMSE is a validated and commonly used screening tool,
scored out of 30, for cognitive impairments for whatever cause.
It does NOT diagnose dementia and is insensitive to early dementia or frontal
A common cut-off is a score of 23 or less out of 30 (the caveat being the test is
dependent on language, age, education and ethnicity). Such a cut off has a
sensitivity of 69-100%, and a specificity of 78-99% (which translates into a +LR
of 9, and a –LR of 0.2
PEARL:If the attention portion of the test (i.e. WORLD spelled backwards)is
0/5, this is highly suggestive for delirium.
If recall is 3/3 (perfect), yet the history is positive for cognitive decline this
suggests a diagnosis other than Alzheimer’s dementia (such as Frontotemporal
Dementia, or even depression).
PEARL: If, for whatever reason you cannot do a full SMMSE, there are
several sub-score items you still may accomplish that may suggest a dementia
(with Likihood Ratios):
If does not know the year:
If could correctly do 3 word recall:
- LR 0.6
See appendix A for the actual test.
Clock Drawing Test (CDT)
This is another validated test for cognitive function and is particularly valuable
when used with the SMMSE (which it is not part of, but is separate test). Draw a
large circle, and ask the patient to place all the numbers in the correct position
on this empty clock face, after which you will tell them a time to put the hands
on their clock. For hand placement you must use the same time used in the
original studies; “Please set hands of the clock to 10 after 11” (remember, the 10
is a virtual 10 represented by the 2 on the clock). Rate as Normal, struggle to
complete, or abnormal)
The Positive Likelihood Ratio for cognitive impairments is 24 if their clock is
Below is an example of a “concrete” clock; persons who are concrete (i.e. only
capable of objects and concepts perceived by the senses, and incapable of
abstract or imaginary concepts) from Vad, FTD, or AD will often put the hands
at the 10 AND the 11, which is incorrect. They are “stimulus bound” by the
PEARL: If you have only limited time for a quick cognitive screen, the CDT
plus three item recall is a good compromise.
Frontal lobe testing
This is done if there is a history of personality and/or behavioral change more
striking than memory changes, or if the history suggests greater executive
functioning impairments than the SMMSE demonstrates (i.e. in vascular (VaD)
or fronto-temporal dementias (FTD).
Tests which are sensitive to frontal lobe dysfunction (dysexecutive syndrome)
Word generation (abstract thought test): Ask the patient to name as
many 4 legged animals as they can in sixty seconds (or vegetables,
words beginning with the letter F, etc.); normal is 15+/- 5.
Verbal fluency tests with word pairs (“what is the difference between
a lie and a mistake?”, river/canal?, child/midget?, etc.).
Problem solving: Ask “What would you do if you awoke in the night
and smelled smoke?” ,“What exactly would you do if you found a
flood in your kitchen at home”
Fund of knowledge testing: (“What exactly happened on September
11th, 2001?” “Who is our prime minister?” “When did WWII start?”)
PEARL: Although suggested as a test, interpretation of proverbs, is
fraught with peril because of differences in cultural upbringing. For
example, what does the following proverb mean to you: “The golden
hammer opens the door”?
PEARL: Several batteries of tests for frontal lobe syndromes have been
developed, with scoring systems. Most recently, the Frontal Assessment
Battery (FAB) was published in the December 12th 2000 edition of Neurology.
It proposes a 6 domain, scorable bedside test that takes ten minutes to
administer, and seems to distinguish patients with FTD from normal persons.
Laboratory tests & Special Investigations
Your choice of laboratory tests & investigations for older adults depends on the
clinical context, and the range of diagnostic equipment available to you.
As a rule of thumb, the abnormalities seen in most blood tests have the same
significance regardless of age (although healthy adults may have slightly
abnormal tests, because most normal values are based on 2 SD from the mean of
the local population).
PEARL: Reference ranges for most laboratory tests follow a bell curve
distribution so that 5% of tests will be abnormal even if the person is normal!
Reference ranges of laboratory tests for the elderly seldom differ from those in
the general population, the differences representing normal aging processes.
Adequate reference ranges for laboratory testing in the elderly are generally
lacking in most labs, as is specific information on persons over age 75, who,
ironically, constitute the fastest-growing segment of the population.
Some lab values change with age: i.e. WBC (slight decrease), PaO2 (slight
decrease), Creatinine Clearance (significant decrease), Alkaline Phosphatase
(30% increase), Total Cholesterol/Lipids (~30% increase)
Some lab values do not change with age: i.e. Hemoglobin (Hb), Platelet count,
Bilirubin, Liver Enzymes (ALT/AST), pH, Thyroid Stimulating Hormone
PEARL: older persons with infection or sepsis do not always mount the
same WBC response (and may not even have a fever!). If someone is
older and confused, but has a WBC is still in the “normal range,” look
closely at the absolute neutrophil levels; if you see a rise in this (e.g. a
doubling in the “band count”), they may have an occult infection despite
having a “normal” WBC.
Creatinine Clearance (CrCl) usually declines with age, and many renally
cleared medications (antibiotics like Gentamycin and Penicillin, drugs like
digoxin, lithium, NSAIDs, ACE-inhibitors and allopurinol) have to be dose
adjusted beyond the aphorism of “start low, go slow”.
To estimate a person’s CrCl, you can use the Cockcroft-Gault equation [adjusted
below to use SI units which are used in Canadian medical labs for Creatinine,
which is measured in µmol/L], which is:
ClCr (mL/second) =
(140 - age) x (weight [in kg]) x 1.23
--------------------------------------------Creatinine (in µmol/L)
The above is the ClCr for men. You need to multiply it by a “fudge factor” of
0.85 to get a more accurate ClCr for females.
Note that normal values for serum creatinine range from 70-120 µmol/L and
CrCl values range from 1.24-2.24 mL/second.
PEARL: For frail elderly patients, using their actual weight, rather than “Ideal
Body Weight” as used in the original equation is usually “good enough”.
PEARL: A creatinine of 100 in a 90 yo female who weighs 45 kg is NOT normal.
This calculates out to a CrCl of 0.39 mL/min. In contrast, a 65 kg man aged 25
with a creatinine of 100 has a CrCl of 1.53 mL/min, four times better
PEARL: many personal data assistants (PDAs) like the Palm Pilot, have
available free medical calculators to make this calculation easy. MedMath is
one I like to use.
Section 2: Geriatric Giants
Failure to Thrive & Frailty
Polyphamacy Iatrogenesis, & Optimizing Medications
Definition: A cognitive impairment is a change in how a person thinks, reacts to
emotions, or behaves.
The most common differential diagnosis in older adults of an acquired cognitive
impairment includes three major categories:
Depression (temporary and a reversible cause of
A diagnosis of dementia is made when newly acquired cognitive impairments
are sufficient to interfere with social or occupational functioning in a person
without depression or delirium. More often it is other family members, rather
than the affected person who notices the first symptoms of dementia.
There are over 70 different causes of dementia, and each has a particular pattern
of decline, impairments, and underlying neurohistopathological processes.
Alzheimer’s Dementia (AD) is the most common cause worldwide, and
accounts for about 65% of cases. Vascular Dementia (VaD), mixed vascular
and AD, Dementia Lewy Body (DLB) and Frontotemporal Dementia (FTD)
each account for about 10% of cases
PEARL: Remember that the cognitive impairments need to be acquired to meet
the criteria of a dementia; there must be a decline from a previous level.
Persons with mental retardation with impaired mental faculties are not
demented unless they start having a decline from a previous level of
In AD, memory problems usually occur first (losing items, missing
appointments), along with difficulties in the performance of complex tasks they
could normally do (i.e. complete taxes, driving in strange places, cook a
Thanksgiving meal). Other associated problems include word finding
difficulties, difficulty with names, inability to follow the plot of a film or TV
show, geographic disorientation (getting lost driving, at the mall, etc.), apathy
and disinterest in surroundings, sleep disturbance (sleeping much more in the
day time) and difficulties in inhibiting behavior (impulsivity, socially
In Canada, dementia affects 8.0% of all individuals over the age of 65, and the
prevalence increases with advancing age as per the following table (data from
the Canadian Study on Health and Aging).
Long Term Care
Criteria for Dementia (based on DSM-IV):
A. Impairment in short- and long-term memory
B. At least 1 of the following:
1.Impairment in abstract thinking
3.Other disturbances of higher cortical function (agnosia, anomia,
& visualospatial difficulties)
C. Memory impairment and intellectual impairment cause
significant social and occupational impairments
D. Absence of occurrence exclusively during the course of Delirium
E. Cannot be accounted for by any nonorganic mental disorder*
Older patients with depressive symptoms (i.e. hopelessness, excessive
guilt, inertia and suicidality may be suffering from pseudodementia (ie,
major depression). When the depression improves with treatment, the
cognitive impairments may resolve.
PEARL: Depressive symptoms are common in Dementia, and some have even
suggested that a first time depression in an older adults heralds the
transformation of dementia in some patients, a so-called “pseudodepression.”
Potentially Reversible Dementias
Dementias are usually progressive and irreversible. However, there are a
number of conditions that may rarely mimic dementia and may reverse if
identified and properly treated. These “exceptions to the rule” include:
Depression: so-called “Pseudodementia”
Electrolyte disorders (hyponatremia, hypercalcemia, etc.)
Wilson’s Disease (rare, and very rarely seen in Geriatric patients!)
Late onset Psychosis
Medication side effects (e.g. sedatives, anticonvulsants,
antihypertensives, anticholinergics, first generation neuroleptics)
Vitamin deficiencies (B-12, folate)
Obstructive Sleep Apnea
Normal Pressure Hydrocephalus (although few, if any actually
reverse with shunting)
Subdural Hematoma (SDH)
Sub-acute CNS infections (i.e. syphilis)
PEARL: More often, treatment improves but does not reverse the cognitive
In one Canadian study [Freter et al. CMAJ 1998;159:657-62], of 196 patients
seen in a tertiary care memory clinic, 45 (23.0%) were felt to have a potentially
reversible condition identified by history, physical examination, blood testing or
CT. However, in only 7 (3.6% of the total) did treatment result in improvement
or resolution of the dementia.
PEARL: Misdiagnosis of a dementia does occur, and unfortunately all too often
by physicians who only see a person in the throes of an acute delirium while sick
in hospital, and mistakenly believe that they have always been this way. If you
see a person labeled as Dementia, but there are atypical features, consider
revisiting the diagnosis and widening the differential to include the above items.
In addition, there are subtle impairments that can often be only be detected and
quantified with special neuropsychological instruments. It is thought that these
may herald the beginnings of an early dementia, a form of “pre-dementia
Mild Cognitive Impairment (MCI)
Refers to mild memory impairment alone (1.5 standard deviations
below that of age matched controls) in the absence of global
cognitive decline or functional disabilities; it can only be diagnosed
by sophisticated neuropsychiatric testing.
Approximately 30% of those with MCI will decline to dementia
within three years (the remainder have stable, mild cognitive
impairments that do not appear to progress
For these patients uncovering and management of risk factors such
as hypertensions, elevated lipids and smoking is crucial
Some clinicians recommend starting Vitamin E (400 iu po OD) and
the active extract form of Ginko Biloba (Egb 761, beginning at 40
mg po TID)
Clinical trials using COX-2 inhibitors and cholinesterase inhibitors
for patients with MCI are also underway.
PEARL: There are other closely related terms for possible “pre-dementia”
syndromes such a CIND (Cognitive Impairments Not Dementia) used by the
Canadian Study on Health and Aging (and found on population screens) and
ARCD (Age Related Cognitive Decline) used in the literature to label these
types of persons., In this very hot area of current research, each term has its
preferred champion, but MCI is emerging as the preferred designation
Approach to a Person Suspected of Having a
The history is the key. When someone is in your office with memory troubles,
find out how long there has been a problem, and how steep a decline. If it has
taken place over a period of a few years, and is very gradual, it is likely
Alzheimer’s Dementia (AD). If more steep a decline, and associated with
walking problems, it more likely a Vascular Dementia (VaD)/ mixed VaD +
AD. If behavior problems such as irritability and apathy are more prominent
than memory issues, it may be a Frontotemporal Dementia (FTD). And if they
have memory problems along with visual hallucinations and symptoms of
Parkinsonism, it is likely Lewy Body Dementia.
PEARL: Memory in a person with dementia is like an ice-cube that is starting
to melt from the top down. While old memories are frozen away and intact,
more recent memories are fleeting and melt quickly. A mildly demented person
may be able to tell you the name of their third grade teacher, but not be able to
tell you what they had for breakfast today. Most recent memories melt earliest in
the early stages of dementia, but as the dementia progresses, even those older
memories will melt..
Reliable collateral witnesses are key (i.e. it may be the caregiver who has the
dementia and is complaining about the other person’s poor memory when it is
really their own!). Review the section on History Taking in a Patient with
Memory Troubles. Ask for specific examples of memory troubles, and ask if
they are getting better or worse as time goes on. Ask about safety issues, and
find out if there is a Power of Attorney.
Ensure that you do at least an SMMSE and a Clock Drawing Test at each visit
(or regularly every 3-6 months); as important is the absolute score, see how
much of a struggle it takes on the test, and note any interval changes in the
performance of these cognitive tests.
The physical examination may be completely normal. However, it may reveal
focal signs suggestive of a stroke (i.e. up-going toe), a peripheral neuropathy
(rule out B-12 deficiency), features of hypothyroidism (slowed reflexes) or
primitive reflexes (suggestive of frontal or advanced diffuse cerebral atrophy).
Laboratory Work-Up for Dementia
You should always do screening blood work to look for the so-called “reversible
“ dementias, or factors which may aggravate or even cause the dementia
syndrome. The current Canadian Consensus Guidelines recommend only the
following screening laboratory tests in the primary care setting:
Complete blood count (CBC); measurement of thyroid stimulating
hormone (TSH), serum electrolytes, serum calcium & serum glucose.
Note that many other tests may be indicated in individual situations (e.g. liver
function tests if excess ETOH, serum B-12 if deficiency is suspected, CXR if
lung cancer is suspected, etc.)
Indications for Neuroimaging in Dementia
The 1999 Canadian Consensus Guidelines for the recognition, assessment and
management of dementia (see the reference section), only suggest order a CT
head in persons suspected of dementia only if one or more the following criteria
Age less than 60 years
Rapid (e.g., over 1 to 2 months) unexplained decline in cognition or
"Short" duration of dementia (less than 2 years)
Recent and significant head trauma
Unexplained neurological symptoms (e.g., new onset of severe
headache or seizures)
History of cancer (especially sites and types that metastasize to the
Use of anticoagulants or history of a bleeding disorder
History of urinary incontinence and gait disorder early in the course
of dementia (as may be found in normal pressure hydrocephalus)
Any new localizing sign (e.g., hemiparesis or a Babinski reflex)
10. Unusual or atypical cognitive symptoms or presentation (e.g.,
11. Gait disturbance
Diagnosis of Dementia
The diagnosis is made clinically, primarily from the history provided by the
patient and the caregiver, but also supported by memory problems demonstrated
by the patient.
PEARL: A diagnosis of dementia should not be conferred indescriminately upon
any patient, as it is a “terminal” diagnosis. Be very sure before making the
Management of Dementia: Breaking the News
Break the diagnosis gently to the patient and the family/caregiver;
Tell them “You have a memory problem that is not normal for someone
your age. We call this type of memory problem a dementia. We think this
type of dementia is (fill in the blank).”
Give them time to ask questions, offer tissues, etc.
Only if they ask, offer prognostic information given the type of dementia,
stage of the disease, (or a simple “I don’t know” if you don’t know).
Offer education and support.
Suggest they contact the local chapter of the Alzheimer’s Society (who can
also provide support for caregivers and patients; they do not limit their
activities to individuals with AD, but also deal with persons with other
types of dementia)
PEARL: You may not want to overwhelm the patient and family with all this
information on the first visit. Offer a repeat visit(s) to go over this information
again. You may wish to provide the family handouts regarding the diagnosis,
and brochures on community resources that they can link up with, because they
may not remember all the information you are giving them.
Management of Dementia Treatment and Follow-Up
If no contraindications (i.e. bradycardia, asthma, active peptic ulcer disease
or seizures), and if the person has an Alzheimer’s, Mixed, or Lewy Body
Dementia, consider starting on a cholinesterase inhibitor (if no recent
EKG, get one to ensure the patient does not have a bradycardia, or any
conduction abnormality that would prevent them from being treated).
Consider also starting Vitamin E (at least 800 iu po OD).
If mild in severity, consider aggressively treating co morbid conditions that
can accelerate the dementia (ire. treat hypertension, hypercholesterolemia,
start ECASA if previous strokes, etc.).
Arrange follow up to see the effects of treatment (if any), and the
development of any behavioral problems that need addressing. This
should be done at least every 3-6 months under treatment (and more often
if there are problems at home). Do a MMSE at least twice a year.
If there is a case manager available, have them liaise with the caregiver.
Watch out for caregiver burnout or depression, and ensure that the family
know that Dementia support services (CCAC for homemaking, respite
care) are available for them to utilize.
If there is no POA for the patient, strongly suggest the family look into
correcting this early on.
Recommend driving cessation; if this causes problems, compromise that
the patient stop driving until an on-road performance based test is
available; notify the MOTC if you have any concerns.
PEARL: Once the diagnosis is made, consider suggesting planning for eventual
relocation at a follow-up visit; this may be necessary if the patient lives along or
if caregiver shows any sign of distress or burnout.
However, filling out LTC placement papers at a first visit for a patient with mild
dementia is overkill and very threatening.
When to Suggest Long Term Care?
There are several indications that suggest that a person with dementia is no
longer able to live in the community in their current place of residence:
When the patient needs more supervision than the caregiver can provide
(usually in moderately-severe or severe dementia, when both memory and
personality is lost and the patient no longer recognizes the caregiver)
Excessive caregiver burnout, depression, or other significant co-morbidity
Safety issues at home (falls. medication noncompliance, abuse)
Behavioral issues at home (delusions, hallucinations, wandering, or
No control of bowels or bladder, and caregivers unable to manage.
When home care support services and informal help cannot manage these
and other behavioural issues.
Alzheimer's Dementia (AD)
In 1906, Alois Alzheimer first described the disease that bears his name. It is a
progressive, neurological disorder that attacks the brain and results in cognitive
problems, such as memory loss, impaired thinking, and unwanted behaviors.
Alzheimer’s is the most common form of dementia (~65%) and the fourth
leading cause of death in North American adults, after heart disease, cancer, and
Autopsies of the brains of Alzheimer’s patients reveal abnormal Beta-Amyloid
plaques, and neurofibrillary tangles. Plaques are composed of abnormally
processed amyloid precursor protein (APP) which has been converted to beta
amyloid protein. Beta amyloid Protein (BAP) is the protein deposited in
insoluble amyloid plaques sandwiched between neurons. When the beta amyloid
protein builds up, synapses become “gummed up”, unable to transmit or receive
Neurofibrillary tangles are abnormal fibres in the axons of neurons composed of
abnormally phosphoralated filaments of microtubles and a stabilizing protein
known as Tau. Normally fibres inside axons act as a form of two-directional
cable-cars to shuttle materials from and to the nucleus; the abnormal tangles
seen in Alzheimer’s appear to prevent materials from leaving the nucleus and
they accumulate in the soma, leading to cellular dysfunction, and cell death.
PEARL Which came first, nobody knows, but different investigators, dubbed
“BAP-tists” and “TAU-ists” champion their own histopathology as being the
inciting event leading to neuronal death and eventual Alzheimer’s dementia..
Risk Factors for Alzheimer’s Dementia:
Positive Family Hx
Apo E4 allele (susceptibility marker for AD; E3 is neutral, E2
Head trauma ?
Low education (<4 years; > 10 protective!)
Female sex (even after adjusting for more female seniors)
Down's syndrome (Trisomy 21
Diagnosis of AD
There is no single clinical test or unique biomarker that can be used to identify
A comprehensive patient evaluation includes a complete health history, physical
examination, neurological and mental status assessments, laboratory screening
tests, and other tests when indicated (i.e. CT of the brain).
Neuroimaging often reveal no changes, cerebral atrophy, or sometimes
leukoariosis (non-specific white matter changes seen next to the ventricles of the
In most cases the diagnosis is made by history, with other tests being done to
rule out other causes of the cognitive decline (i.e. silent strokes, metabolic
abnormalities) be they reversible or irreversible. While this type of evaluation
may provide a diagnosis of probable Alzheimer’s (clinical diagnosis is correct
80% of the time), absolute confirmation requires examination of brain tissue at
autopsy (the “gold standard”).
Prognosis of AD
At this point of time, there is no cure for AD. Available medications
(cholinesterase inhibitors) appear only to delay the need for institutionalization
by about 18 months in those who respond, but the “death date” does not change.
Adjuvant agents such as Vitamin E and Ginko Biloba are thought to be
somewhat neuroprotective, although the data is somewhat skimpy [See
Treatment Section that follows].
Depending on which study you refer to, time from diagnosis to death is about 34 or 7-10 years.
PEARL: Many persons with Alzheimer’s die from pneumonia if they have no
other co-morbid illnesses, and this is felt to be caused by the inability to prevent
recurrent aspiration due to the global neurological decline.
Treatment of Alzheimer’s Dementia
Approved treatments for treatment of AD in Canada make use of the
Cholinergic Hypothesis of AD: that loss of choline acetyltransferase &
acetylcholinesterase causes at least some of the cognitive decline that occurs in
This theory is supported by the following facts:
in early AD, there is selective cell death in subcortical cholinergic
neurons from the basal forebrain to the cerebral cortex and
hippocampus in AD pts (Whitehouse et al., 1982)
choline acetyltransferase (CAT), levels are also reduced in postmortem tissue of AD patients (Bowen et al., 1976)
decreases in acetylcholine release in AD patients (Nilsson et al., 1986
Using the building blocks of Choline and ACo-A, the enzyme Choline
Acetyltransferase (CAT), located within axon endings of neurons catalyzes the
synthesis of Acetylcholine (ACh), which is stored in pre-synaptic vesicles.
Following an action potential, ACh molecules are released by pre-synaptic
vesicles into the synaptic cleft, where they interact with post-synaptic receptors.
These post-synaptic ACh receptors (muscarinic and nicotinic) eventually opens
a post-synaptic ion “gate” (directly or via protein G), allowing cations flood in,
and start a new action potential.
ACh in turn is broken down by hydrolysis in a reaction catylized by the enzyme
acetylcholinisterase (AchE) [some is also broken down by
butyrylcholinesterase (BuChE), whose primary substrate is butyrylcholine, but it
also hydrolyzes Ach].
By blocking the breakdown of ACh by inhibiting the enzyme that chews it up it
is hoped that there will be more ACh left in the synaptic cleft to be involved in
normal cognitive processes at the cellular level.
Three acetylcholinesterase inhibitors are currently available in Canada:
donepzil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl).
These three agents are covered by under the Ontario Drug Benefits (ODB) for
dementia and only when the SMMSE score is between 10 and 26). They are all
very expensive, and cost $1875/year for those without coverage.
Each takes about 3 months before you can tell if there has been any therapeutic
effect (i.e. lack of decline, or even improvement on cognitive testing such as
SMMSE scores; improvement in function (BADL/IADL) or function).
Finally, an adjuvant agent, memantine (Ebixa) is available for patients with
moderate to severe dementia. It acts on the NMDA (N-methyl-D-aspartate)
receptor, and was recently as a treatment for AD. It’s as expensive as the above
agents, and unfortunately not covered under ODB. It’s effects are modest on
their own, but are synergestic with any one of the above.
Dosing is OD, starts at 5 mg, and increase to 10 mg after about 4 weeks.
About 30-40% of people will improve with treatment
most common side effect is GI upset, but also bronchospasm in susceptible
persons (i.e. those with asthma, COPD).
Bradycardia can also be a problem; you can’t use if any heart block other
Use Limited Use (LU) code 347 to initiate donepezil, LU code 348 to
continue it if it helps.
Acetylcholinesterase and Butyryl-cholinesterase inhibitor (found in plaque,
but significance uncertain)
Start at 1.25 mg po BID, and increase to 3 mg BID after 4 weeks, and
titrate to 4.5 mg po BID if at all possible
Not metabolized by the P450 system like donepezil or galantamine
Probably similar clinical efficacy to others, but may have more GI side
effects (nausea in up to 25%); suggest to patients take it with food)
New topical patch formulation pending approval in Canada Summer 2008
Another BID dosed drug, available in Canada as of September 2001
Start at 4 mg BID, and increase to 8 mg after 4 weeks; take preferably with
morning and evening meal.
derived from flower (Moly) alkaloid; [supposedly antidote for Circe’s
atropine; Ulysses’ men thought they were swine when poisoned by her
with it in The Odyssey]
in addition to acetylcholinesterase inhibition, there is nictotinic modulation
at both pre and post synaptic level; clinical significance is uncertain.
Levels of serotonin, glutamate, norepinephrine, and acetylcholine all
Probably similar clinical efficacy when compared to the others.
Renal excretion; made need to adjust dose if renal impairment
Not yet available for ODB
Other Possibly Helpful Medications (and will not do any
Ginko Biloba (only extract EGb 761 felt active)
A few small studies only
Felt to be helpful in MCI, rather than actual dementia
Metabolic effect, may be partial agonists to dopaminergic,
serotonergic and noradrenergic receptors; can affect
cAMP levels, and act as an anti-oxidant
Dose is 40 mg po TID of standardized extract
Suggest patients check with their pharmacist for
Vitamin B complex?
Individuals with Alzheimer's disease often have low
blood levels of vitamin B-12; the reason for the
association of low is not clear
o A recent case control study of AD patients had higher
blood homocysteine levels and lower folate and vitamin
B-12 levels; measures of nutritional status indicated that
the association was not due to dementia-related
o If normal serum levels, unknown if supplementation
useful (? Helpful role in MCI?).
Other investigational therapies for AD:
Many other agents are in development for the treatment of AD, ranging from
anti-oxidants, modulators at other receptors (GABA, 5HT), vaccines, even green
Mamba snake dendrotoxin, and brain neurogenesis via stem cells. Some of the
more promising agents for treatment of AD currently in the pipeline include:
vaccine against B-amyloid precursor protein
Human trials started in September 2001 were halted January 2002 after
several patients developed cerebral inflammation).
Talsaclidine & CI-1017
Agents acting on muscarinic and nicotinic acetylcholine receptors; when
stimulated extra stored acetylcholine is released.
cerebral inflammation seems to hasten deposition of amyloid
Three agents are being assessed in trials: celecoxib, rofecoxib, and
GW253035 after initial promise shown with indomethacin and diclofenac
in slowing loss of reasoning power (but alas, intolerable GI side effects) by
blocking this harmful inflammatory response.
Antibiotics: Doxycycline & Rifampin
A pilot randomized control study involving the above two antibiotics
showed the intriguing results of slowing down the rate of dementia
after just 6 months of therapy (D.W. Molloy et al, Journal of the
American Geriatric Society, Volume 52 Issue 3 Page 381-387,
Mechanism not likely anti-microbial; may involve secondary antiinflammatory effects, or possibly chelating away copper, needed in
processing of Beta amyloid protein.
Vascular Dementia (VaD)
Vascular dementia (VaD) differs from AD by its history of onset (often
sudden), clinical features (see below), and subsequent course (may be stepwise
or saw-tooth decline). The prevalence of VaD is thought to be about 10% in
Canada. It frequently co-exists with AD, a situation which is called Mixed
In VaD, there is a history of transient ischæmic attacks (TIAs) or strokes, with
brief impairment of consciousness, fleeting pareses, or visual loss. The dementia
may also follow a succession of acute cerebrovascular accidents or, less
commonly, a single major stroke. The pattern of cognitive impairments of the
dementia may be patchy, so that there may be memory loss, intellectual
impairment, and focal neurological signs. Insight and judgment may be normal
Associated features are gait disturbance, emotional lability with transient
depressive mood, weeping or laughter, and brief episodes of clouded
consciousness or delirium, often provoked by further infarction. Personality
changes may be present in some cases with apathy, disinhibition, or
enhancement (and coarsening) of previous traits such as egocentricity, paranoia,
or irritability. If the vascular insults occur primarily in the frontal lobes, the
features of a fronto-temporal dementia may be seen.
Different criteria have been published on dementia caused by stroke. The most
widely used is the NINDS-AIREN criteria [National Institute of Neurological
Disorders and Stroke and Association Internationale pour la Recherche et
l'Enseignement en Neurosciences; two groups working together to develop
criteria that was developed at an international workshop in 1992 involving 54
neurologists and neuroscientists]
NINDS-AIREN criteria for VaD (all the following)
2. Focal signs on exam + evidence of cerebrovascular* disease by CT or MRI
3. A relationship of the two above, with dementia within 3 months of a
recognized stroke and or abrupt deterioration in fluctuation, or fluctuating
stepwise progression of cognitive deficits.
The specificity of NINDS-AIREN criteria is high (91%) for the exclusion of AD
(Gold et al., Neurology 1997;49:690-694)
Physical Examination in VaD
May show increased tone (especially in the legs), exaggerated deep
tendon reflexes, and babinski responses (upgoing toes).
Gait apraxia (“magnetic” gait) may be seen.
Other focal signs may be detected
Treatment of Vascular Dementia (VaD)
Once VaD begins, there is no reversibility (although Mixed Dementias do
respond to cholinesterase inhibitors just like they do in AD). In fact, little is lost
in treating the same as in AD even if you are convinced it is pure VaD (the
patient has little to lose and much to gain). However, one may slow
VaD/Vad+AD progression by treating underlying comorbiditis. This includes
identification and treatment of:
Carotid Artery Disease
And finally, tobacco smoking cessation
PEARL: Needless to say, identification of stroke risk factors and treatment of
the above modifiable factors BEFORE a stroke and its sequelae occur is crucial:
Hypertension: Aim for a BP less than 140/90. Simple diuretics such as
Hydrochlorothiazide (HCTZ) starting at 12.5 to 25 mg po OD is reasonable to
begin (but watch for orthostatic hypotension). Recent guidelins ofer a choice of
beta blocker/ calcium channel blocker. Choice of drug will depend on
HTN + Angina= Rx with Beta blocker
HTN + Asthma=Rx with anything BUT Beta-blocker
HTN and DM=Rx with ACE-Inhibitor
Atrial Fibrillation: Start on warfarin (Coumadin) if there are no
contraindications, or at the very least Enteric Coated Acetylsalicylic Acid
(ECASA). Warfarin is far more effective than reducing risk of stroke than
ECASA, but its use may be problematic. Frequent falls are NOT a
contraindication as shown in a recent meta-analysis done by Man-Son-Hing
(Archives of Internal Medicine, 1999;159:677-685)
Carotid Artery Disease: Carotid endarterectomy is beneficial in preventing
stroke in selected patients and is indicated in symptomatic patients with carotidterritory transient ischemic attacks or minor strokes who have carotid artery
stenosis of 70 to 99 percent. Unfortunately, once a VaD begins, you will be
unable to find a vascular surgeon to treat this. Anti-platelet agents (ECSA,
Plavix) and risk factor modification are recommended in symptomatic patients
with less than 50 percent stenosis or those who cannot be surgically corrected.
Elevated cholesterol: Confirm Total Cholesterol levels, HLD, LDL and
Trigycerides by fasting blood analysis. While diet modification can help, most
elderly persons would benefit from starting on a ‘statin to lower their
Prognosis of VaD/Mixed VaD + AD
Highly variable; if does not succumb to a devastating stroke, may
have similar prognosis as AD patients
Lewy Body Disease (Dementia with Lewy Bodies)
A recently defined clinical entity, Lewy Body disease is a dementia where
deficits on tests of attention, and visuospatial ability are be especially
prominent. It is so named because of eosinophilic inclusion bodies (called Lewy
Bodies, found primarly in the basal ganglia of patients with Parkinson’s
Disease) are prominent histological findings in the cortices at autopsy.
For a Probable diagnosis of Lewy Body Disease you need at least two of:
Fluctuating cognition with pronounced variations in attention and alertness
Recurrent visual hallucinations which are typically well-formed and
Spontaneous motor features of parkinsonism
Features supporting the diagnosis:
Syncope or transient LOC
Neuroleptic sensitivity (i.e. new shuffling gait, tardive dyskinesia)
Hallucinations in other modalities (i.e. smell, hearing, taste)
Diagnosis of DLB is less likely in the presence of:
Cerebrovascular disease, evident as focal neurological signs or on brain
Evidence on physical examination and investigation of any physical illness
or other brain disorder sufficient to account for the clinical picture
Uncertain; overlaps between AD and Parkinson's.
Genetic studies pending
Up to 15% of all cases of dementia
Some investigators think this is the most common form of Dementia after
Investigations for DLB
There are no specific diagnostic tests for DLB.
Patients with DLB have great difficulties in not only the clock
drawing test and other simple drawing tasks
EEG typically reveals generalized slowing of background activity;
occasional patients with rapidly progressive dementia will show
periodic complexes reminiscent of CJD.
Management and Treatment for DLB:
There is no specific therapy ; general treatment limited to managing
neuropsychiatric disturbances and the associated movement
Cholinesterase inhibitors may be useful in Rx, and there is now one
open label RCT suggesting that rivastigmine may be helpful [Lancet.
2000 Dec 16;356(9247):2031-6].
Small scale studies suggest that the newer atypical neuroleptics such
as risperidone, olanzapine & quietepine may be able to treat
psychotic symptoms without causing excessive parkinsonism.
Shorter than in patients with AD
Felt to be on average 4-5 years from time of diagnosis
Frontotemporal Dementia (FTD)
A dementia characterized primarily by problems with behavior, insight and
judgment rather than memory loss; it is the “flip side” of AD in several ways:
behavioral troubles >> memory; so-called “unpleasantly demented”
anatomical deficits are 1o frontal-temporal versus bilateral parietaltemporal changes as seen in AD
Prevalence of FTD
estimates vary from between 10-25%; most agree that it is the most
common dementia after AD in the presenium (under 65s)
Core diagnostic features of FTD
Insidious onset and gradual progression
Early decline in social interpersonal conduct
Early impairment in regulation of personal conduct
Early emotional blunting
Early loss of insight
Supportive Diagnostic Features
A. Behavioural disorder
Decline in personal hygiene and grooming
Mental rigidity and inflexibility
distractibility and impersistence
Utilization behaviour Hyperorality & dietary changes
Peserevation) and stereotyped behaviour
B. Speech and language deficits
• Altered Speech Output (Aspontaneity & Economy of Speech)
• Stereotypy of speech
II. C. Physical signs
Primitive Reflexes; at least one of grasp, snout and sucking
Akinesia, rigidity and tremor (rarely)
low and labile blood pressure
II. D. Investigations
Significant impairment on frontal lobe tests in the
absence of severe amnesia, aphasia or
Normal despite clinically evident dementia
Brain Imaging (structural or functional)
predominant frontal and/or temporal abnormality
Relative diagnostic exclusion features of FTD
Typical history of chronic alcoholism/
History of vascular disease
Detection of FTD
Frontal lobe dysfunction often unrecognized in its early phases
May have normal neurologic testing when routine methods
employed (ie. MMSE.)
unfortunately, there is no good test to reliably identify a
dysexecutive function (several test batteries in use; FAB, FBI,
“Atypical” AD/ Schizophrenia/ Depression / Bipolar disorder/ OCD
/ Hypochondriasis/ Sociopathy
2o causes of FTD
Head Injury / Post lobectomy or leukotomy/ Anoxic Brain Injury/
Huntington’s Disease/ ? ETOH
Closely Related FT Dementias
1) Primary Progressive Aphasia
non-fluent agrammatic speech
2) Semantic Dementia
fluent speech, lost semantic meaning of objects/ words,
repetition is good
memory relatively good for personal, autobiographical events
Genetics of FTD
45% of pts have a family member affected
up to 18% of these have an abnormality on the short arm of
chromosome 17 localized near gene for the microtubule associated
Treatment of FTD
A: Medical Therapy of FTD
theoretically there is no cholinergic deficit and would therefore will
not benefit from cholinesterase inhibitors; however, as there is no
good way to distinguish from AD, consider doing a trial of one of the
three available agents.
As there is a serotonergic deficit it may be worth trying an SSRI
based on side effect profile (i.e. use fluoxatine if want to stimulate, if
over stimulating, use fluvoxamine or paroxetine to sedate)
B: Non-Medical Therapy
Caregiver education, respite care and emotional support; early
identification of caregiver depression
PEARL: Spatial orientation and praxis preserved (intact abilities to negotiate
the environment). Can do well on SMMSE (often 27/30) despite being unable to
perform certain tasks. Can alternatively do surprisingly well on driving tests
despite a correspondingly low SMMSE (mostly on problems not understanding
Normal Pressure Hydrocephalus (NPH)
Dementia 2o to a type of hydrocephalus which can occurs in older
NPH is an accumulation of cerebrospinal fluid (CSF), causing the
ventricles of the brain to enlarge, yet do not cause consistently
increased intracranial pressure, as is the case with obstructive
The abnormal accumulation of CSF, causing enlarged ventricles, is
thought to stretch the nerve tissue of the brain causing a triad of
Treatment of NPH:
Often disappointing; short history & a precipitating event (e.g.
meningitis or subarachnoid hemorrhage may predict better outcome
Ventriculoperitoneal shunting (shunt inserted to divert the cerebral
spinal fluid away from the brain)
About 1/3 improve [but only in terms of their gait], 1/3 no change,
and 1/3 worse (27% get complications, 7% morbidity)
Korsakoff’s Syndrome: (aka Korsakoff’s Psychosis)
Irreversible amnestic disorder caused by a deficiency of thiamine
The anterograde amnesia is commonly associated with vivid
confabulation (i.e. the patient is unaware of the memory problem,
and simply makes up false memories to fill the gap).
Most commonly seen in alcoholism (although it can be found in
severely malnourished or dialysis patients).
It is related to Wernicke's syndrome, which often precedes
Korsakoff's syndrome (and the two disorders are thought to be part of
a spectrum of a single entity) but does not respond to thiamine
Huntington’s Disease is a fatal autosomal dominant hereditary
disorder characterized clinical triad of emotional, cognitive and
Motor symptoms include chorea (dance-like involuntary
movements), clumsiness, slurred speech;
Emotional symptoms include depression, irritability and
Cognitive losses include loss of intellectual speed,
attention and short-term memory; personality changes are
As the disease progresses, movements become severe and
uncontrollable; cognitive impairments deteriorate to a dementia of
the FTD variety.
About 30% of patients with Parkinson’s Disease (PD)will develop
dementia (some studies say up to 60%)
Problems include deficits in visualspatial ability, visual
hallucinations, a and memory
May overlap with symptoms seen in Lewy Body Dementia, and
because PD and AD are both common, they may occur together by
Dementia associated with acquired immunodeficiency
syndrome (AIDS) [aka AIDS Dementia Complex].
Adults over age 50 now account for at least ten percent of reported
AIDS cases, and it is currently estimated that 8 to 16% of people
with AIDS will develop dementia as a direct effect of the AIDS virus
on the brain
The intellectual and cognitive decline in patients with AIDS
dementia is remarkably similar to those in Alzheimer’s, and
autopsies show plaques similar to those found in Alzheimer’s
Creutzfeldt-Jakob Disease (CJD)
A very rare and fatal neurological disorder caused by a prion (a
proteinaceous infectious particle) that was first described in the
Its pathophysiology is not completely understood. Although it can
occur in younger persons, peak age of onset of classic CJD is 60 to
Worldwide incidence ~0.5-1.5 cases per million per year, and most
cases are sporadic. CJD has been considered infectious since the
mid-1960s, but its transmissibility through the transfusion of blood
or blood products is controversial.
One strain, new variant Creutzfeldt-Jakob Disease (nvCJD), is linked
to bovine spongiform encephalopathy (i.e. Mad Cow Disease) in the
UK, but there have been no documented cases of human transmission
of BSE in Canada.
Classical Symptoms of CJD
a rapidly progressive presenile dementia with progressive myoclonus
and progressive motor dysfunction.
Early symptoms can include cognitive impairment, behavior
changes, visual disturbances, and lack of coordination.
Pyramidal and EPS symptoms, along with akinetic mutism develop
Diagnosis of CJD
CSF fluid analysis for the presence of 14-3-3 protein
Brain biopsies looking for spongiform changes (but don’t do it
EEG shows a typical pattern of periodic sharp-wave complexes
an autopsy is the only definitive way of diagnosing CJD. In most
cases of human prion diseases the histological features are
distinctive; spongiform change, neuronal loss, astrocytosis and
amyloid plaque formation.
Treatment of CJD
There is no treatment, and the duration of CJD from the onset of
symptoms to death is usually less than a year.
Behavioural Problems in Dementia
Up to 90% of demented patients will develop significant behavioral problems at
some point in the course of their illness
Agitation (definition=a range of purposeless verbal, motor behaviors
that put the patient or others at risk of harm) is the most commonest
problem, and is seen in up to 75% of patients with dementia.
Wandering in up to 60%
Depression in up to 50%
Repeated stories and statements in ~32%
Psychosis in up to 30%
Hoarding & Rummaging in up to 30%
Screaming in up to 25%
Aggression and violence in up to 20%
Hypersexuality in up to 10%
These problems result from the progressive inability of the demented patient to
remember, reason or solve problems. Because they are associated with frontal
involvement, they occur early in FTD and DLB, and in the later stages of AD.
They arise from the disease process and are rarely enacted to be manipulative.
PEARL: Think of dementia as a form of unwinding of learned abilities, or
retrogenesis with what was most recently learned lost first. It’s like Jean
Piaget’s stages of childhood development running in reverse, with the mind of a
demented person becoming more childlike and primitive in its logic and abilities
as the disease progresses. Remember that while a demented person’s
intellectual processes are deteriorating, their emotions and feelings may be
Behavior problems caused by dementia are often disruptive, and can lead to
social isolation, caregiver burnout, accelerate the need for LTC placement,
iatrogenesis, and the increased use of restraints (and their own problems)
Assessment of Behavioral Problems
Establish or revisit the medical diagnosis
Accurate diagnosis of type of dementia?
Is it really a dementia (consider life long personality disorder,
chronic psychiatric problems, etc.)
Assess and Reverse Aggravating Factors
Pain or discomfort that cannot be verbalized (fatigue, distended
bladder, constipation, compression ulcers, dental abscess, PND at
Anxiety or Depression?
Physical limitations, or functional disabilities?
Medical illness, delirium (from infection, drugs, etc.)?
Hearing impairment or vision loss?
Boredom, isolation, loneliness
Environmental sources (staff interaction, under stimulation, over
Document the specific behaviors
Use a behavior chart to document, using ABC analysis
A is for Antecedents (i.e. what happened just before)
Triggers for behavior (i.e. physical treatments, pain,
bathing, mealtimes, company, loneliness, noise level,
vision or hearing problems)?
B is for Behavior
Be specific! The words “Aggression” or “Agitation” are
not helpful. Were they screaming, biting, or merely
calling out because they were lonely and wanted
attention? Did they really hit someone, or were they
simply waving their hands about and someone got in the
Note the frequency, timing and location of the behavior;
related to some intervention (e.g. giving care, bathing,
meals) or spontaneous?
Note which persons or staff were involved (or just one
C is for Consequences
Events that maintain the behavior?
How did the staff handle it?
What has worked before? What has failed?
Ask yourself, is intervention really necessary?
Is this a matter of patient safety versus staff convenience?
Is the behavior distressing to the patient (i.e.
Is the behavior interfering with BADLs or socialization?
Attempt individualized Non-pharmacolgical Approaches
Behaviors are rarely random, unpredictable or meaningless events Behavior
itself is a way of communicating feelings and needs that cannot be adequately
verbalized by a patient with a dementing illness. Management of problem
behaviors can be shifted from trying to change the patient to trying to change the
triggering or exacerbating factors. Three problems and their non-drug
approaches follow below:
Check for full bladder, constipation,
infection, ulcers & clothing for
Schedule adequate rest, monitor
Assess, monitor, and reduce if
Reduce noise, pagers on vibrate, use
TV sparingly, dim lights at night.
Overstimulation (noise, overhead
paging, beepers, people, TV,
Restless, bored, no stimuli.
Provide meaningful activity (folding
towels, sorting buttons), provide safe
circular path, fenced in yards.
Reduce excessive stimulation.
Escaping from stress (noise, clutter,
crowding, activity—>“Run away!”
Lost—looking for something or
someone familiar, “There’s no place
like home, Auntie Em!”
Eloping stimuli; exit signs, people
leaving “Hey, wait for me!”
Provide familiar objects, pictures of
toilet on bathroom door, signs,
Camouflage exits, use stop signs or
barrier tape, code access doors.
Inappropriate or Impulsive Sexual Behavior
Decreased judgment and social
Misinterpreting caregivers interactions
(i.e. bathing, toileting)
No not overreact or confront; respond
calmly and firmly; distract or redirect.
Avoid mixed sexual messages,
distract while performing personal
care, bathing; be consistent.
Check room temperature. More
Model appropriate touch, offer
soothing objects (stuffed animal),
provide back massage, provide
Uncomfortable clothing; too tight or
Need for attention, affection,
General Psychotropic Approaches to the Management of
Behavioral Problems in Dementia.
Non-drug therapies work best, and should be tried first. Drugs are a last resort,
and only if the above strategies and analysis fails.
Scheduled, not prn, medications
Use monotherapy if possible
Consider and avoid drug-drug interactions
Plan duration of trial (not open ended)
“Start Low, go slow” (ie. ¼ normal starting dose), but avoid under
Chose target symptoms, and reasonable end points.
Monitor for ADRs, especially those that impact on cognitive
functioning (i.e. sedation, anticholinergic effects), movement
(sedation, EPS, orthostatic hypotension, tardive dyskinesias or
dystonia), and sexuality.
PEARL Remember that drugs work only if there is:
Psychosis and/or Aggression
PEARL: Psychotropic drugs do not help: Repetition or, Wandering
What Psychotropic Medication to Use?
Choice may be influenced by the urgency of the situation:
If requires rapid control of grossly disturbed or unsafe
situations, use neuroleptic and benzodiazepine combination
(ie. IM haloperidol + lorazapam; start with 1 mg of each for a
robust person, and 0.5 mg of each for someone frail)
If more time available, look at what psycho-behavioral “metaphors”
(not diagnoses, but what the behavior “kind of looks like”) that the
patient is exhibiting (chart below)
More and more cholinesterase inhibitors are found to be useful but
not specific Rx for behavioral problems..
Agent to try
Antidepressant (i.e. citalopram,
Anticonvulsant (i.e. carbamazepine,
(i.e. an agitated patient who is
withdrawn, apathetic, irritable,
negativistic, ruminating and/or
Anticonvulsants (i.e. divalproex,
Beta-blockers (i.e. propanolol)
(i.e. an agitated patient who is
hyperactive with pressured speech,
irritable mood, and sexual
(i.e. an agitated patient relentlessly
checking her purse for pocket money)
(i.e. a patient screaming and striking out
because she thinks that aliens are
experimenting on her)
SSRI Antidepressants (i..e.
citalopram, sertraline, paroxetine)
Anticonvulsants (i.e. divalproex)
Benzodiazepines (i.e. short term
Neuroleptics (ie. Risperidone,
Neuroleptics (i.e. low dose
Sexually Aggressive Features
Delirium, or acute confusion, is a common problem. Up to 60% of older
persons hospitalized for surgery will become delirious. 35% to 65% of elderly
patients with hip fractures will become delirious after surgery.
Why is delirium important?
Mortality is 20%/year for those >70 years (independent of all other comorbidities); Delirium is therefore a MEDICAL EMERGENCY.
DSM IV definition:
Decreased attention & disorganized thinking, with at least 2 of:
altered sleep-wake cycle
altered psychomotor activity
with acute onset and fluctuation over time (hours).
Clinical diagnose of Delirium
Method 1. Use the CAM (Confusion Assessment Method); best, see
acute onset and fluctuating course?
lack of attention?
altered Level of Consciousness?
If 1 and 2 are present, and either 3 or 4, the patient is probably delirious.
Method 2. Use the Digit Span Test
Ask the patient to repeat a sequence of numbers that you present to them at a
rate of one per second in your normal voice. Start off with a sequence of 3, then
4, then 5, etc. up to a maximum if 7 random number sequences. (i.e. 1-8-5, 6-43-7, 2-0-7-1-5, etc.) Do not use duplicate numbers or group them into obvious
patterns (ie. phone #).
Persons who are not delirious should be able to repeat 7 (+/- 2) numbers
from the sequence you initially dictate to them.
Risk Factors for Delirium
Pre-existing dementia (such brains are more vulnerable and less able
to withstand any form of insult)
Poor vision (ARMD, cataracts, no glasses)
Poor hearing (absent hearing aid, wax blocked ears, etc.)
If all 5 are present, the patient will likely become delirious if they become sick
enough to need to become hospitalized! And if they are already in hospital,
additional risks for delirium include:
Use of restraints
foley catheter in situ
>3 new medications
PEARL: Mnemonic of risk factors commonly associated with DELIRIUM:
Lungs and other organs,
Injury (pain and stress),
Unfamiliar environment, and
PEARL: Another mnemonic for causes of delirium is DEMENTIA
M etabolic, organ failure, etc.
E pilepsy (post seizure)
T rauma (head, surgery, etc.)
A poplexy or other vascular event.
Causes of Delirium:
Anything that affects the brain and its normal functioning can provoke a
delirium. A brief listing includes:
Drugs (or drug withdrawal; especially anticholinergics, sedatives, opiods)
Metabolic disturbances (hypoxia, hyponatremia, hypo & hypercalcemia,
hypovolemia, Hepatic or renal failure, Cushing's Syndrome, etc.).
Infection (obvious or occult; may include UTI, or subacute bacterial
CHF, MI, tachy- or brady-arrhythmias
ETOH (toxicity, withdrawal, or thiamin deficiency)
CNS (strokes, trauma, etc.
Pain (fecal impaction, urinary retention, recent surgery).
Management of Delirium (see also appendix):
Quiet environment; pagers on vibrate, dim lights at night, PT & OT to
attempt to mobilize the patient as early as possible
Improve vision & hearing if possible
IV boluses rather than continuous IV fluids if at all possible
Px including rectal to rule out fecal impaction, and a post-void residual to
r\o urinary retention
Lab screen: CBC, lytes, BUN\Cr\glucose, ECG, CXR, pulse oximety or
cap gases, urinalysis (also consider doing “extras” including Ca++, Mg++,
TSH, LFTs, albumin & B12
Stop medications that may be maintaining the delirium (i.e. opiods,
sedatives, anticholinergics, H2 blockers)
Keep well hydrated ; maintain fluids and nutrition.
Management of Uncontrolled Agitation with Delirium
If agitated, violent and combative, the immediate goal of treatment of treatment
is to reduce symptoms to a level where the patient is not a physical danger to
himself or others. The cessation of hallucinations and/or delusions (assumed to
be the basis of the dangerous agitated behavior), is the ultimate goal. Current
management of agitated patients involves the use of neuroleptics and
benzodiazepines either alone or in combination.
Low dose po haloperidol (Haldol) 0.25 mg po bid to 1 mg bid; may also
give IM haloperidol 0.5 mg or IM olanzapine (Zyprexa) 2.5-5 mg QHS
which should work within 30 minutes when combined with an short acting
benzodiazepine (1-2 mg lorazapam, either po or IM, can be given q 1 hour
in addition to the neuroleptics above until sedation is
Low dose Risperidone (Risperidal) 0.25 BID works well if not needed
acutely; it is less anticholinergic and has less hypotensive ADRs than seen
than in older neuroleptics.
Sublingual Olanzapine (Zyprexa Zydis) in a gelatin wafer that instantly
dissolves when placed under the tongue is now available in many Ontario
hospital formularies (one new possible ADR to watch out for is
Depression is the most common psychiatric illness in the elderly. Although
common, it is NOT a natural part of aging.
The prevalence in community dwelling elders range from 8-15%; it rises to as
much as 30% of those in long term care facilities. Depression and suicide are
common in the elderly (especially older males; those over 75, have the same risk
of suicide as 20-24 year old depressed males).
Depression is NOT present in ALL older adults, but is under recognized &
under treated. Depression is common in:
Long Term Care
Any Chronic Illness (i.e. DM, COPD,)
Chronic Pain (i.e. Cancer (Ca), RA,
To Dx a Major Depression, you need at least 5 of the below for 2+ weeks)
Anhedonia (absence of usual
Unexplained wt loss or gain
Loss of appetite
Thoughts of Suicide and hopelessness
Psychomotor changes (slow…)
Concentration and memory problems
PEARL: Mnemonic “Sig. E Caps” (Sig.=from the old Latin way to prescribe,
E=“Energy”, Caps= “Capsules”) as a check list for Depression:
S uicidal Ideation
I nterest, lack of
E nergy, none
C oncentration, poor
A ppetite(s), altered
P sychomotor changes (slowed or revved up)
Bereavement or Grief reaction is commonly misdiagnosed as depression. A
normal grief reaction after the death of a spouse or a loved one lasts about 2 months
in time, with the mourning process being complete in under 2 years. Feelings of
sadness and preoccupation with the deceased are not helped by anti-depressant
medications during this time of mourning.
However, grief can become pathological when it persists past 2 months, when the
grieving person is unable to function, and constantly expresses nihilistic thoughts of
death. Suicidal thoughts are also felt and may be verbalized, and these are never
normal, and merges into a diagnosis of true Major Depression.
Screening for Depression
Ask, "What is wrong?" Or, “Do you often feel downhearted or sad?”
15 or 30 item GDS (see below)
ROS shows up with many somatic complaints in many domains
Ask about suicidal or pessimistic thoughts
The Geriatric Depression Scale (GDS), is a screening tool for depression, and does
not itself diagnose depression. There are various forms about, including a 30
question, a 15 question short form (see Appendix) a four question, and a single
question screen (i.e. If you have time to ask only 1 question to screen, ask “Do you
feel that your life is empty?”
For short form (15 questions) GDS; >5 points are suggestive for depression, and
scores >10 points are very suggestive for depression [See the appendix for all the
For the 30 question GDS, >13 points are suggestive, and >15 very suggestive.
PEARL: The GDS has not been validated in patients with Cognitive Impairments,
and needs to be interpreted with caution.
PEARL: If positive on screen, ask about such depressive symptoms as listed above.
Also ask if they are consuming ETOH, since ~4% of older adults abuse it.
PEARL: Also, if positive for depression on both a screen and subsequent interview,
discuss treating this without delay.
Treatment of Depression in the Elderly
Psychotherapy, in particular behavioral and cognitive based therapies appear to be
Short-term psychodynamic therapy (such as cognitive behavioral therapy or
interpersonal therapy) has been reported to be effective in the treatment of
depression in elderly.
Selective serotonin reuptake inhibitors (SSRI’s) are the friendliest antidepressants to
use in older adults, because of their safety in overdose, and because they do not
interact with as many other medications as older agents.
They are also not anticholinergic as the older TCAs, and have fewer adverse
cardiovascular effects and do not cause orthostatic hypotension. They are also useful
in patients who have comorbid dementia, and this has been demonstrated in a
number of studies.
Common ADRs with SSRIs include nausea, and other GI symptoms, headaches, and
Some caution needs to be followed in using SSRIs, as there is the risk of SIADH
(hyponatremia caused by an as yet unknown mechanism). They can also cause
sexual dysfunction, which your patients may not report (and you may not remember
Good all purpose SSRIs for older adults currently available in Canada are Zoloft
(Sertraline ) and Celexa (Citalopram):
Sertraline: The initial starting dose is 25-50 mg po OD, given in the morning.
Target dose by week three is 50-100 mg/OD. By week five, the target dose is 50150. Full effective dose in those over the age of 65 after week 7 is 50-200 mg/OD
[with the upper dose range reserved for the robust older adult; for the frail elderly the
range is 100-150 mg po OD] Commonly reported side effects include tremor,
restlessness, and gastrointestinal complaints, but no more than placebo in RCTs.
Citalopram: The full effective dose is 20 mg po OD. You can start off at 5-10 mg
a day for 3-7 days, watching for tolerance and adverse side effects. If tolerated,
continue doubling the dose every week until the maximum dose of 20 mg/day is
achieved. It will take at least 6 weeks before any change of depressive symptoms
will be achieved. Citalopram appears to inhibit P450 minimally, if at all.
Effects of the SSRI to improve depression may begin by week 4-6, should be seen by
weeks 7-9. If no improvement by this point (or an adverse side effect), consider
switching to another SSRI or a Serotonin and Noradrenaline Reuptake Inhibitor
(SNRI) after first allowing the original medication to wash out. If improvement,
continue for at least 12-24 months after the remission of symptoms in older adults.
If there is a history of previous recurrent depression, consider treatment indefinitely.
Non SSRI Anti-Depressants
Other agents proven to be safe in older adults include Effexor XR (Venlafaxine)
which is a SNRI (think of it as a mixture of a TCA and an SSRI), and Bupoprion
SR. A relatively new agent now available is Mirtazapine (Remeron), which is
classed as an NASSA (noradrenaline and selective serotonin antidepressants).
Adjuvant agents include short term use of short acting benzodiazepines (i.e.
lorazapam, oxazepam) for treatment of anxiety until the antidepressant kicks in, and
mood stabilizers such as Lithium, valproic acid and carbamazepine may also be
useful. Augmentation with triiodothyroxine can be considered.
Electroconvulsive Therapy (ECT)
ECT uses electricity to cause a grand mal seizure to improve the symptoms of
major depression; the mechanism of the antidepressant effect of ECT is
unknown, but it is thought that the whole brain seizure provokes changes in
endogenous neurotransmitter systems
It is a safe, proven, yet underutilized method of treating major depression,
especially in older adults.
It is usually given 2-3 times a week for a period of several weeks, then
maintenance ECT is used
Quicker onset than conventional antidepressants, and fewer side effects.
It is often used in medication resistant depression, in patients with psychotic
features with their depression, or in patients who have previously responded to
ECT therapy, or in urgent situations where life is in danger.
Improvement of symptoms seen in ~80% of those treated with ECT.
Besides treating major depression, ECT is used in severe bipolar depression,
schizoaffective disorder and chronic psychotic disorders such as schizophrenia
and bipolar mania.
There are no absolute contraindications to ECT, only situations of increased
complications; ECT in patients with brain masses and recent stroke (less than
three months) is a concern, as is ECT in patients who have had a recent MI
(less than three months) because of the risk of further cardiac problems with
the combined actions of the anesthetic used and the increased demands on the
heart experienced during the procedure.
When to refer Depression to a Geriatric Psychiatrist?
The patient is suicidal or homicidal, and/or refusing to eat or drink
Uncertainty of the diagnosis or when the differential diagnosis of
depression and neurologic disorders overlap
Treatment resistive depression that has failed to respond to one or two
adequate trials (8 to 12 weeks at a therapeutic dose) of antidepressants
and/or gets worse during treatment
Antidepressant ADRs or drug-drug interactions that limit effective
When the patient requires maintenance of complicated treatment
When you know or suspect the patient has Bipolar Disorder (either early
or late onset)
When the patient requires evaluation for ECT
Orthostatic Hypotension (OH)
Also known as postural hypotension, orthostatic hypotension (OH) is a major
and often hidden cause of falls in the elderly!
Not a specific disease as much as it is a syndrome of abnormal postural blood
pressure response due to one or more underlying conditions that can affect the
normal autonomic reflex arc.
Definition: An excessive drop in Blood Pressure (BP) seen when changing from a
lying/sitting position to assume a standing and upright posture;
Typically the BP drop is at least 20 mmHg systolic / 10 mmHg diastolic
Warning “Red Flags” for the possibility of OH
OH symptoms (dizziness, faints and near falls/falls) that occurs early each
Symptoms of OH that occur on consecutive days
Aetiology of Orthostatic Hypotension (in order of frequency)
Hypovolemia: diarrhea, hemorrhage, salt losing nephropathy, ETOH, adrenal
Drugs: Antyhypertensives, Diuretics, Vasodilators (nitrates, hydralazine),
Alpha- and beta-blocking agents, barbiturates, opiates, Tricyclic
antidepressants, and ETOH)
CNS problems: Parkinson’s disease, Parkinson’s Plus syndromes (multisystem atrophy, Shy-Drager), Stroke.
Autonomic problems associated with Diabetes Mellitus (DM)
Deconditioning and prolonged bed rest
Post-prandial (“face down in the corn flakes!”)
2o systemic arterial hypertension
Idiopathic= Bradbury-Egglestone syndrome (this can be distinguished by
measuring supine norepinephrine levels, which are low)
Non-drug Tx of OH:
Elevate head of bed at night
Instruct the patient to first dorsiflex and plantar flexfeet before arising
slowly out of bed
Increase salt intake (ie. canned soups, vegetables)
Increase oral fluid intake (or even IV if necessary)
40 mmHg Jobst compression stockings (hard to put on, use only if they
can get them on themselves otherwise they will not be used once they are
Caffeine helpful if taken between meals!
Drug Tx of OH:
Florinef (fludrocortisone); a volume expander
Midodrine (alpha vasoconstrictor activity on resistance and capacitance
Indomethacin (but only with gastric protection; not a good idea for the
Erythropoeitin (useful only if low RBC mass)
Definition: progressive low bone mass & micro-architectural deterioration that leads
to skeletal weakness and an increased risk of bone fracture; specifically it is a Bone
Mineral Density (BMD) T-score of 2.5 or less (which is the equivalent of a bone
density lower than 648mg/cm2).
Bone is a living organ, tissue mostly made up of collagen that has been mineralized
with calcium phosphate, which provides strength and hardness to the skeleton. Bone
remodeling occurs throughout life, and osteoporosis results from an imbalance
between osteoclast resorption (“chews up bone”) and osteoblast remodeling (“builds
up bone”) activity. Normal bone has a high bone density; once it become
demineralized because of the excess action of osteoclasts, it is first becomes
osteopenic (“poverty of bone), and once it is further demineralized it becomes weak
and is at risk of fractures, a term called osteoporosis.
Osteoporosis may be primary (a combinational of post-menopasual loss of estrogen
in females, and/or related to aging losses of osteoblasts seen in both men and
women) or secondary to some other disorder (such as osteomalacia,
hyperparathyroidism, hyperthyroidism, glucocorticoid excess, renal failure, liver
PEARL: Low bone mass is the single best predictor of fracture risk
Normal cortical bone (Latin cortex=bark, and in medical use it means the outer layer
of an organ) is the dense and compact outer part of bone that imparts strength to the
skeleton, especially the long bones, and has a slower turn over; although
osteoporosis can thin cortical bone, it is less affected by post-menopausal
osteoporosis than trabecular bone. Normal trabecular bone (Latin, trabeculae= “a
little beam”) has a spongy, honey-comb appearance. It has a high turn over, and is
mostly present in the spine, distal radius. Because of its higher turn over, the
imbalance of osteoclast activity (especially in the absence of estrogen) leads it to
become progressively demineralized and osteoporotic. As these “little beams” start
to melt, they can no longer impart their normal internal structural support to bone,
making them weak.
Grim statistics for hip fractures:
40% lifetime risk if female, 13% risk for men
25% of persons will die post hip fracture, a similar % will transfer to LTC
Equally grim statistics for vertebral fractures:
Prevalence ~12% for both men and women in one European study [J Bone
Miner Res 1996 Jul;11(7):1010-8]
Mortality doubles with increasing numbers of vertebral fractures (from 0 to 5),
and is related to the risk of subsequent cancer & pulmonary death
Survival rate for a clinically significant fracture the same as for hip fractures
Chronic functional impairments also similar for hip and vertebral fractures!
PEARL most vertebral fractures occur at +/- T12 level. If you get a compression
fracture far from this location, suspect bony metastases)
Risk factors for osteoporosis
Women not on HRT 5 years after menopause
Poly Cystic Ovarian Disease (PCOD)
Hypogonadism (in men)
Hypothyroidism and hyperparathyroidism
Maternal history of fractures
Poor "get up and go" test
Any previous fracture
Prolonged corticosteroid therapy
post chemo patients (especially breast cancer or leukemia/lymphoma)
Low body mass
When to do Bone Mineral Density (BMD):
If you suspect osteoporosis (patient kyphotic, or has shrunk over the years
Falls or at risk of falling.
The purpose of doing a BMD is to
Quantify bone mass
Assess fracture risk
Follow effects of intervention
PEARL: While a BMD can determine the quantity of bone mass present, it cannot
tell the quality of the bone.
How to interpret a BMD?
The “T score” is exactly the same as the Standard Deviation
Normal is in bell curve of +1 to –1 SD;
below –1 is Osteopenia,
below –2.5 is Osteoporosis.
If osteopenia, discuss lifestyle modifications (exercise, increasing dairy
products); start Calcium/Vitamin D; monitor BMD once every two years.
If Osteoporosis, start definitive treatment (see following section), and
repeat BMD yearly for first two years.
Other lab tests:
Calcium & albumin (only the ionized calcium is biologically active;
ignoring pH effects, you can roughly calculate ionized calcium by using:
Corrected Calcium = for each fall (or rise) of albumin by 4 g/L add
(or subtract) 0.1 mmol/L to the plasma calcium.
Serum Phosphorous and Magnesium
Consider serum protein electrophoresis if you suspect multiple myeloma.
Consider serum bioavailable testosterone level in a male with a fracture
The purpose of these tests is to rule out other 2o causes of bone demineralization
Treatment of Osteoporosis:
Pearl: Purpose of Rx in Osteoporosis is to prevent fractures, maintain function and
reduce pain (if any).
A: Non drug treatment
Diet (to improve calcium rich foods, such as dairy products and green leafy
Exercise (you need not only calcium, but exercise to “pound it” into the bone)
Lifestyle modifications to minimize risk of falling (proper footwear, improved
lighting, activities that improve balance and strength like Tai Chi.
B: Drug Treatment for Osteoporosis
Calcium supplementation: 1000 mg of elemental calcium
= Calcium Carbonate 1250 mg PO BID
Vitamin D: 800 iu PO OD (aids the absorption of Calcium & Magnesium)
Estrogen: 0.625 mg po OD (or 50-100 microgram transdermal patch/day)
important for prevention & treatment in post-menopausal
woman; but cannot use if hx of Breast CA, unexplained
vaginal bleeding, active thrombosis or liver disease!
C: Specific Therapies for Osteoporosis:
Raloxifene (Evista) [Ettinger study, 50% reduction vertebral # after 1 year]
Also beneficial is the reduction in breast cancer
Good for 50-75 year old females; but can increase numbers of Deep Vein
Calcitonin [PROOF study]
Reduces incidence of verterbral #, & 40% of persons obtain analgesia
Bisphosphanates (three available)
Only one on ODB at this point in time, its cheap, but takes ~4 years to
see improvement (therefore, if life expectancy not this much, don’t start!)
Often combined in kit-form with Calcium (Didrocal), where it must be
taken cyclically 2 weeks on, 3 months off.
Need to show decline in BMD or new fracture while on etidronate before
Ontario’s Drug Benefit Program (ODB) will fun more potent
bisphosphonates (alendronate or risedronate):
More rapid acting than etidronate
Reduces vertebral fractures ~50-60%
Help build bone mass mostly in the spine; somewhat less so in the hip
Not currently covered on ODB except as limited use
Best single agent, reduces risk within 1 year by 50% and has slightly
better hip data than Fosamax; unfortunately, not covered on ODB
Can use “Pagets Disease dose” (once/week) if dosing causes intolerance.
Definition: The involuntary loss of urine in sufficient amount or frequency to
constitute a social or health problem.
Even though there are aging associated changes in the bladder and the urinary tract
which make the elderly person more prone to urinary incontinence, the problem is
not and should not be considered as part of ageing.
Normal urination (“To pee or not to pee…”)
There are three nervous-system loops for control of urination, including the cerebral
hemispheres, the spinal cord, and the local nervous system. Interruption of any of
these loops can cause urinary dysfunction.
reflex in sacral micturition center: as the bladder fills, sympathetic tone
closes bladder neck (alpha), relaxes the detrustor muscles making up the
dome of the bladder, and inhibits parasympathetic tone (via acetycholine).
With urination, sympathetic and somatic tone decreases, and
parasympathetic impulses causes the bladder to contract allowing voiding
to take place.
Cerebral cortex exerts inhibitory reflex on this process
Brainstem facilitates urination, and acts as an intermediary between the
cortex and the bladder in the spinal cord at the S2, S3 & S4 level.
Causes of Acute, Reversible cause of Urinary
restricted mobility, retention.
infection, inflammation, impaction (faecal).
Causes of Persistent Urinary Incontinence:
Stress: Involuntary loss of urine (usually small amounts) with increase in
intraabdominal pressure (e.g. cough, laugh, or exercise).
Urge: Leakage b/c of inability to delay voiding after sensation of bladder fullness is
Overflow: Leakage (small amounts) resulting from mechanical forces on an overdistended bladder or from other effects of urinary retention on bladder and sphincter
Functional: Leakage assoc. w/ inability to toilet because of impairment of cognitive
and\or physical functioning, psychological unwillingness, or environmental barriers.
Evaluation of incontinence:
Active medical conditions: CNS disease, diabetes, congestive heart failure
Medications (especially loop diuretics)
Fluid intake pattern (use a diary if necessary)
Past GU hx (childbirth, surgery, dilatations, urinary retention, radiation,
Symptoms - onset and duration, type (stress vs. urge vs. mixed vs. other),
frequency, timing and amount of incontinence and periods of continent voids.
Other urinary tract symptoms: Irritative (dysuria, frequency, urgency,
nocturia); Voiding difficulty (hesitancy, slow or interrupted stream, straining,
incomplete emptying); Other (hematuria, suprapubic discomfort).
Psychiatric symptoms (apathy, inertia, depression)
Bowel problems (constipation, stool incontinence).
Perceptions of incontinence (“Who’s problem is it?”)
Volume expanded states (liver cirrhosis, CHF, nephritic or nephrotic
Targeted Physical examination
Mobility and dexterity; gait disturbance (? NPH)?
Mental-status; cognitive function, motivation, mood and affect
Neurological: focal signs? Signs of Parkinsonism? Sacral arc reflexes?
Abdominal: bladder distension? Supra-pubic tenderness? Lower abd. Mass?
Rectal: perianal sensation? Sphincter tone? Impaction? Masses? Size+ contour
Pelvic: perineal skin condition? perineal sensation? Atrophic vaginitis?
cystourethrocele or pelvic prolapse? pelvic mass ?
Other: Lower extremity edema or signs of CHF.
Lab work-up of Urinary Incontinence
Step I: start with the following
Urinalysis & urine C&S
Blood glucose and calcium levels
Post void residuals (preferably done with bladder scan, or in-and-out
Step 2: Other tests if the diagnosis not clearly established:
Simple urodynamic tests
Complex urodynamic tests
Lab studies: renal function, urine cytology,
Radiological studies: renal U\S, voiding cystourethgraphy
urological or gynecological evaluation
If secondary to overflow incontinence, may need intermittent catheterization, in
conjunction with bethanacol (remember to stop any anticholinergic drug if this
diagnosis is made)
If 2’ to urge incontinence, try regular toileting (q2 hours when awake), and
common sense measures such as reduction of oral fluids, caffeinated beverages,
and bedside commodes/urinals within easy reach.
If 2’ to a functional incontince (ie. dementia, OA) try frequent and regular
timed toileting, and have bedside commodes/urinals nearby
If 2 to stress incontinence, try smoking cessation (and other measures to
eliminate cough), Kegel’s exercises, weight loss in obese patients.
For Anticholinergics use the minimal dose to assist preservation of cognition
Oxybutinyn (Ditropan): use pediatric syrup form (1 mg) or 2.5 BID
Detrol (Tolterodine): less dry mouth, ? crosses into brain less than Oxybutynin
Tricyclic Antidepressants (Imipramine): not used as much now
PEARL: Acetylocholine= constricts bladder detrusor muscles causing release of
urine; therefore anticholinergics may cause urinary retention (as well as contribute
to delirium!); Calcium Channel Blockers may also causes retention
Failure to Thrive (FTT)
NIA definition (National Institute of Aging): "a syndrome of weight loss,
decreased appetite, poor nutrition and inactivity, often accompanied by dehydration,
depressive symptoms, impaired immune function and low cholesterol "
Failure to thrive, a term more commonly seen in the pediatric literature, has
multifactorial causes in the elderly with a DDx that could fill a textbook of internal
medicine; you need careful and detailed Hx and a systematic approach of 4 major
Malnutrition: wt trend, BMI, lymphocytes and albumin
Depression: +/-GDS and Cornell
Cognition: CAM, SMMSE
Potential contributors to all domains:
Unrecognized illness (stroke, endocrine abnormalities, carcinoma,
Fear of Falling
Approach to Failure to Thrive
An interdisciplinary approach should be made, with involvement of the Geriatrician,
Family MD, and a Geriatric Assessment team. Depending on the acuteness of the
decline, admission to a medical ward or a Geriatric Assessment Unit is
recommended for the initial assessment.
PEARL: An excellent problem for a Comprehensive Geriatric Assessment.
Questions to ask on history:
Temporal profile of the decline; when did it start, and how fast? (if with
days or weeks, suggests an underlying medical cause)
Last weight before decline? Current weight?
Changes in medical health?
Alterations in sense of taste or smell?
Is the problem that the patient cannot (dysphagia with problems
swallowing, new stroke, cognitive impairments) , won’t eat (depressed,
anorexic, food phobic), or losing weight despite normal intake and
appetite (occult malignancy, infection, hyperthyroidism)
Who does the cooking? Has this changed?
Any medication changes (prescription or OTC) that preceded the decline?
Change in living situation, legal status or interpersonal relationships?
Alteration of finances (loss of income, loss of spouse’s income)
Is elder abuse or neglect occurring?
Are their depressive symptoms, or ETOH or other substance misuse?
Vitals, including accurate height, weight (to calculate BMI) and
Focus on ruling out malignancy, occult infection, anemia;
Check wallowing and test gag reflex
Abdominal exam; look for masses, jaundice
Thyroid exam; evidence of hyper or hypothyroidism
Pelvic and rectal exam (for masses, blood)
CNS exam; any focal deficits? , Problems with gait, or mobility?
Screening Tests for FTT
Cognitive testing with SMMSE, CDT, or more sophisticated
GDS to screen for depression
Basic Geriatric Medicine screen, including CBC, electrolytes, BUN,
Creatinine, Albumen, Calcium, TSH, folate, B-12
Liver enzymes (AST, ALT, Alk Phos, Bilibrumin, GGT)
Nutritional indices that include serum Magnesium, Phosphorus, and lipids
and cholesterol (biomarkers for malnutrition)
ESR (if suspecting occult infection)
Chest X-ray (if suspecting malignancy)
Kitchen and home safety assessments by OT
Mobility, balance and strength by PT
Adequacy of current diet and education by Dietary
Self Administered Medications (SAM) program by Pharmacy
Speech language pathology referral and video-fluoroscopy swallowing
study if suspecting dysphagia
Specific management depends on the specific clinical entities uncovered. It is
possible that one or more of the so-called “Geriatric Giants” will be discovered and
will require specialized treatment and referral to allied health services. If felt 2’ to a
Major depression, consider referral to a Geriatric Psychiatrist for consideration of
ECT. The treatment recommendations of the Dietician are very important (i.e. meal
supplements, referral to “Meals on Wheels” (MOW), placement of feeding tube if
deemed necessary, etc.)
Such follow-up and after care services should be monitored by the case manager
assigned to the patient.
Although MDsoften talk about the “frail elderly” there are unfortunately
no clear consensus on the definition of this term.
The American Geriatric Society defines it as the “…clinical expression
of cumulative biologic changes with aging which result in decreased
ability to maintain homeostasis and lead to vulnerability to stressors.”
in other words, “frail seniors” are those older adults who actively
demonstrate failure of homeostenosis.
This is an important area of health care still requiring further study for the
frailest seniors, about 3% of the total, consume ~30% of Canadian health
care resources, often in the final years of their life
Features of fraility include:
Unexplained weight loss (>5% over a year)
Poor endurance and energy (self reported)
Poor strength (in lowest 20th percentile)
Slow walking speed (Poor “Get up and Go” test).
Low physical activity (lowest 20th percentile)
Work-up for frailty is identical to that for Failure to Thrive.
Pain in the Elderly
Pain is an unpleasant subjective and personal experience associated with
actual or potential tissue damage; it is the way your body tells you to
“stop doing that!”.
Pain increases in incidence and prevalence after age 60 because of the
accumulative burden of such aging associated illnesses such as
osteoarthritis, compression fractures, diabetic neuropathy and cancer.
It is under reported by seniors, who may not tell their doctors because
they fear being labeled as bothersome, hypochondriacal, or becoming
Twenty-five percent to 50% of elderly people in the community
experience pain on a regular basis, and as many as 85% of the elderly in
residential facilities report continual pain
Unfortunately, pain is under treated in the oldest-old (>85) and in patients
with dementia who may not adequately describe their pain.
The most common causes of pain in the elderly stem from:
Osteoarthritis (prevalence is 49.5% in those 65+)
Other joint disorders (Rheumatoid arthritis, gout/pseudogout, PMR, SLE,
Osteoporosis (e.g. vertebral compression fractures)
Varicella Zoster and post herpatic neuralgia
Assessing Pain in the Elderly (OLD CART mnemonic)
Onset: When did it start
Characteristic of the Pain
Treatment’s taken or tried
Pain Control in the Elderly: Treatment Guidelines
Non Drug Rx
Icing (maximum 20 minutes/hour, over each hour)
Heat (but avoid electric heating pads, which can cause burns)
Unloader braces (knee)
Use of canes, walkers
Hylan GF 20 (Synvisc); synthetic biopolymer injected into an
osteoarthritic joint (usually knee) to restore the shock absorbing,
protecting, and lubricating properties of the synovial fluid
Acetaminophen (given regularly; maximum dose is 4 grams a day,
which translates to 2 Tylenol Extra Strength QID).
PEARL: The ”trick” to using medications for pain control is to schedule it
regularly, so that patients have the medication on board just prior to when they
experience pain. Think of the analogy of brushing your teeth; you don’t wait for a
cavity, but brush your teeth to prevent a cavity.
NSAIDS (only helps if there is an inflammatory pain component; not
recommended for OA unless flare)
Conventional NSAIDS (extreme caution given the risk of GI
bleeding if used without gastroprotection; can also cause such
renal side effectsfluid and salt retention, and provoke CHF and
COX-2 Inhibitors (newer agents, with less associated gastritis,
but still have renal side effects can occur)
Capsaicin cream (Zostrix)
Derived from red chile peppers
Depletes substance P, and works on Gate control theory of
pain by acting as a counterirritant
Useful for MSK pain (i.e. osteoarthritis) and some
PEARL: Avoid meperidine, in older patients as its metabolites can accumulate in
patients with impaired GFR.
PEARL: When starting narcotics, don’t forget to start them on a bowel regimen to
prevent constipation! And consider starting long acting dosage forms for chronic
pain (i.e. MS contin)
Adjuvant agents to Rx pain:
o SSRI Antidepressants (citalopram, sertraline)
o Tricyclic Antidepressants (nortryptyline)
o Anticonvulsants (valproic acid, cabamazapine)
o Calcitonin (for vertebral fractures)
o Gabapentin (useful for comorbid anxiety)
WHO pain ladder
Degree of Pain
Acetaminophen (max 4 grams
Or NSAID (preferably COX-2)
Codeine 30-60 mg q4h added to
Morphine 1-5 mg q4h
Or Hyrdomorphone 1-2 mg q4h
Elder Abuse (Abuse of Seniors)
Elder abuse is defined as any action or inaction that threatens the well being of an
older person. A 1990 national telephone survey of 2,000 seniors showed that up to
4% of Canadians over the age of 65 may be abused or neglected. A recent study of
31 Canadian nursing homes found that 36% of nursing home staff had witnessed the
physical abuse of an older adult in the preceding year and that 81% had witnessed
psychological abuse. A 1988 Health and Welfare Canada study found that
financial abuse accounted for over 50% of the documented cases of elder abuse.
Abuse can take many forms, but is usually grouped in five major categories:
Physical & Sexual abuse
Any act of violence or rough treatment, whether or not actual physical
i.e. slapping, punching, kicking, pinching, burning, restraints.
Emotional and psychological abuse
Any act that diminishes dignity and self worth
i.e. confinement, isolation, verbal assault, humiliation & infantilization.
Financial Abuse & material exploitation
Any improper conduct that results in monetary or personal loss for the
Abandonment & Neglect
Active Neglect - intentional (deliberate) withholding of basic necessities
and/or care for physical or mental health.
Passive Neglect - not providing basic necessities and care. There is no
conscious attempt to inflict distress.
Any medical procedure or treatment done without the permission of the
older person or their Power of Attorney or substitute decision maker.
Who are the abusers? Three categories
Domestic elder abuse (maltreatment by a caregiver in 2/3 of all cases,
financial abuse by a distant relative in 90% of cases)
Institutional elder abuse (abuse in a residential facility)
Self-neglect or self-abuse.
Reasons for abuse
Caregiver Stress/burnout & social isolation
Impairment of Dependent Elder (i.e. dementia)
Transgenerational “Cycle of Violence”
Material or other gain
Unexplained physical injuries: burns, cuts, bruises, grip marks, rope
marks, burns, cuts, head injuries pain, bruising or bleeding in the genital
Unexplained malnourishment or decubitis ulcers
Unkempt appearance (inappropriate clothing, signs of infrequent bathing
or incontinence, a lack of glasses, hearing aids or dentures when they are
Failure of a medical condition to improve or the continued presence of
pain that might indicate under medication.
Fear of certain family members, friends or caregivers
The older person is largely ignored or treated passively by caregivers or
Caregivers who are entirely ignorant of the medical problems or
treatments for the older person they are directly caring for.
Physician Legal Responsibilities
There are no specific laws against elder abuse in Canada, and no legal requirement
for physicians to report elder abuse in the province of Ontario. Many believe that
laws intended for the general public are adequate for cases of abuse of older adults,
with some of the behaviors performed by the abuser can lead to charges of criminal
offense (i.e. physical assault, sexual assault, forced confinement theft, fraud, forgery,
extortion and the wrongful use of a Power of Attorney).
PEARL: However, physicians who suspect abuse still have the moral duty to act in
the best interests of their patients.
What must you do?
An interdisciplinary team approach appears to work best. Physicians (ideally Family
Physicians, Geriatricians and Geriatric Psychiatrists) RNs, social workers, lawyers,
law enforcement officials, is essential.
If abuse is suspected, interview the patient alone. Begin with open ended questions
about , then zero in on direct questions about possible maltreatreatment and abuse. If
abuse is acknowledged, document the nature, frequency, and severity of the abuse
(and don’t forget to explore other domains of possible abuse).
Also interview the caregiver. Do not be confrontational. Sensitively enquire about
stressors they are undergoing in the performance of their role, and ask what they
understand about the medical problems of the older adult in their charge. Ask how
many hours they are involved in their care giving role, and if they are getting
supports from anyone. If they are responsible for such treatments or medications, ask
how this is done and how diligent they are following the prescription’s dosing
regimen. Also ask about the possibility of help being provided in the home via
If abuse is denied, rigorously document your reasons for abuse (physical signs such
as burn marks, rope marks, bruising). Don’t forget to do a SMMSE, as cognitive
impairments could cloud the reliability of the older person’s story.
KEY POINT: If the patient is capable of making their own health care decisions,
they should decide on their next action (pressing legal charges, changing living
arrangements) depending on the severity of the abuse, If they are not competent to
make these decisions, immediately notify law enforcement officials if obvious signs
of abuse are observed.
Management of Elder Abuse
If the patient is capable:
Educate re: options (shelter, pressing charges, support services, legal
Support their decision, even if it is one we would not make.
If the patient is incapable:
Defuse the situation if at all possible and take steps that matters do not
worsen; involve CCAC SW and, and see if a case manager can be
assigned to follow
Remove the patient if necessary on a Form 1 if you are concerned about
immediate risk or harm
Meticulously ocument your reasons for abuse (history, physical exam,
abnormalities on X-rays and blood work); consider taking photographs.
Plan relocation or alternative care with another caregiver
Involve the police
PEARL: Prevention of abuse is the key, along with early identification of seniors and
caregivers at risk, and proper support services started before the abuse begins.
PEARL: There are specific police officers with the Hamilton Regional Police
Department who are assigned to crimes involving seniors. Get them involved if you
have the patient’s permission, or they are incapable of providing this.
Falls & Poor Balance
Falls are a leading cause of morbidity and mortality in seniors. In Ontario, falls cause
600 deaths annually for those over the age of 65. Falls in the elderly are also the
leading cause of injury admissions to Ontario acute care hospitals.
It has been reported that:
30% of community dwelling elderly persons fall each year
1/2 of these have multiple falls
45% of falls occur in residents in Long Term Care facilities
Why else are falls important?
Fear of falling restricts activities
Falls are often marker for underlying disease
6th leading cause of death
5-15 % falls lead to serious injury
1-2% of falls lead to hip fractures.
Aetiology (often multifactorial)
Accidents and environmental hazards
Lower limb weakness and deconditioning
Ddizziness and\or vertigo
orthostatic hypotension (see OH section for more detail)
Past medical history
How long falling; how much, and how serious?
Exact circumstances of fall (accident, trip, “black out”, “legs just gave
Previous fractures with falling.
Medications (Meds that can contribute include diuretics,
antihypertensives, neuroleptics, antihistamines, antidepressants, long
Do they consume ETOH? How much and how often?
Collateral history can be very useful!
Look for an orthostatic drop (about 25% in patients who fall!)
Pay attention to cardiovascular system; evidence of arrythmia on taking
their pulse? Aortic stenosis murmur?
Concentrate on CNS examination; tremor and bradykinesia suggestive of
Parkinson’s disease? Focal signs of a previous stroke (weakness, upgoing
toe, asymmetrical reflexes)? Impaired vibration sense or proprioception
(suggestive of a peripheral neuropathy)
Include gait assessment; examine the speed at which they move, distance
between ankles/knees when they walk, if they shuffle when walking, or
do not swing their arms. See if they touch the wall for balance, or wobble
away from a straight line. Are their turns smooth, or do they trip over
If they use a mobility aid, examine it. Is their cane the right size for them
(and is the rubber worn down?)? Do the brakes work on their walker?
Don’t forget cognitive testing (i.e. dementia impairing judgement, leading
Specialty Testing for Falls
Timed “Get up and go” test,
This is the time it takes for a person to stand up from a straight back
chair, walk 3 m, and return and sit down.
10 seconds is normal, 11-20 is normal for a frail or disabled patient, and
>20 seconds is abnormal and warrants further assessment
Reference is JAGS 1991; 39: 142-148.
The maximal distance one can reach forward beyond arm's length, while
maintaining a fixed base of support in the standing position.
An older subject stands relaxed, extending their arm against a wall; a
mark is placed at the knuckle position; they are then asked to stretch out
and extend their arm as far as possible without losing their balance, and a
second mark is done.
Older persons with a good reach have a better chance of avoiding falls if
they can reach out 25 cm (10 inches) or greater; between 15-25 cm (6-10
inches), their odds ratio of falling is 2, if under 15 cm (6 inches), their
risk of falling is 4, and if they cannot reach out at all, their odds ratio of
falling is 8.
Laboratory investigations for falls:
CBC, electrolytes, BUN, creatinine, glucose, calcium, albumen, TSH,
serum B-12, and folate.
Do an EKG
Consider EEG if you suspect seizure activity
Consider EMG’s if you suspect a nerve conduction problem leading to a
When to order a CT Head?
Focal neurological signs
Management of Falls
Treat underlying causes (i.e. if suspect Parkinson’s Disease a trial of
levodopa/carbidopa, improve blood sugar control if DM, start on
anticoagulation for 2’ stroke prophylaxis if in atrial fibrillation, if B-12
deficient, start replacement therapy, etc.)
Review medications and consider their necessity (this may involving
contacting other physicians, such as the Family MD and other specialists)
and whether if they can be reduced or discontinued.
Taper sedatives gradually before stopping (with avoid withdrawal),
reduce neuroleptics (or change to a 2nd generation atypical neuroleptic,
etc.), stop dimenhydrate (Gravol), etc.
Management of Falls (continued)
Cut down or stop ETOH if this is playing a role (falls while inebriated,
Rehabilitation with referral to OT (home visit to examine hazards and to
see whether devices need to be installed or have the environment
modified), PT (for strengthening or balance exercises), Day Hospital or
Falls clinic referral (for complicated patients who need interdisciplinary
Enhance mobility (cane, walker, rails), improve vision, improve
Consider hip protectors (either hard plastic shell or soft foam “hockey
pants” that protect the femoral heads from a direct blow if there is a fall).
Consider getting a BMD, and starting on calcium/vitamin D; if
osteoporosis, start on a bisphosphonate.
Recommend a “Lifeline” or other device that the older person can use to
signal for help if they’ve fallen and can’t get up.
If poor balance or deconditioning, train for preventing falls, by
recommend they start Tai Chi, or joining a seniors fitness group
Often multi-factorial in aetiology:
anxiety and or depression may be playing a role
Presbystasis : minor age related changes in propioception, vestibular function,
neuromuskular function and age that can contribute to unsteadiness in gait.
Evaluation of dizziness: Questions to ask on Hx:
What do they mean by “dizzy” (light headed, room spins, unsteadiness of
feet but head okay, loss of balance or veering to one side, etc.)?
Onset + duration? Single attack or multiple?
Are the spells becoming more frequent, or lasting longer?
Any warnings it’s about to start?
Symptoms between attacks?
Is it brought on by standing, lying, rolling over in bed, neck movements,
when walking, walking in the dark.
Any fainting episodes?
Past Medical history
History of TIAs, stroke, neglect?
History of Head trauma or Falls?
Recent viral infection or ear infection? Recent hearing loss?
Recent medication change?
Any recent change in eye-glasses?
Medications that can contribute:
Diuretics (loop especially)
Antibiotics (e.g. gentamycin)
Long acting Benzodiazepiness
ECASA\NSAIDS (can also cause tinnitis)
ETOH (also ask about depression and/or anxiety]
Physical Examination for Dizziness:
Vitals: any orthostatic changes?
Neck ROM, head turning
Cranial Nerve (CN) nerve exam
LE tone, strength, power
Cerebellar function testing.
Dix-Hallpike maneuver: Starting with the patient in a sitting position on
the examination table, rapidly lie them backward with their neck extended
and their head turned to the left; repeat again, with the head turned to the
right. Each time observe if they demonstrate nystagmus or a replication
of their dizzy symptoms (see picture).
PEARL: do not do the Dix-Hallpike in elderly patients with significant carotid artery
disease; listen for bruits first, and if positive (or positive on history), do not do.
Potassium, renal function, blood glucose, B-12, CBC.
Consider EEG if suspect seizure
Consider also VDRL, digoxin and ASA levels (only if taking).
Treat underlying causes
Consider trial of antidepressant if nothing can be found
Review meds, and reduce or stop contributors
Rehabilitation with referral to OT, PT, Day Hospital
Enhance compensation mechanisms- improve vision, cane, walker
If suspect Benign Paroxysmal Positional Vertigo (BPPV) from a
(positive Dix-Hallpike) consider referral to an ENT specialist
Polypharmacy, Iatrogenesis & Medication
Although seniors represent 12% of the Canadian population, they consume 28% to
40% of all prescriptions. Unnecessary prescribing, misuse of medication and
inappropriate prescriptions can contribute to the risk of drug-related illness and result
in unwarranted costs in health care delivery.
An estimated 5% to 23% of hospital admissions are due to drug-related illness.
Physical impairments and death (estimated 200,000 per year in the US) are all too
common tragic results.
Polypharmacy literally means “Many Drugs”, and it reflects the problems that occur
when persons are taking too many (or simply too many of the wrong drugs, which is
iatrogenesis); it is an older term that is falling out of use. Previously defined as 5 or
more new drugs during a given 3 month period, it is estimated that 15% of patients
are at risk of from polypharmacy.
A more current term is Medication Optimization (since many patients truly need
the many medications for their plethora of problems), and the thinking has now
shifted from simply reducing medications, to ensuring than an older person be on the
optimum number and dose of medication for their problems.
Medications that may have been relatively benign when the patient was younger, can
accumulate risks as the person ages (and with that, changes in drug metabolism and
pharmacokinetics). The main concern in the elderly is that side effects should not
outweigh beneficial effects.
Frequent drug side effects in the elderly include:
Confusion (from sedation, anticholinergic effects)
Dehydration from diuretics
Hypotension from many cardiac medications
Digoxin toxicity (even with so-called therapeutic dig levels)
Medications causing unwanted side effects may be prescribed by different wellintended MDs (Iatrogenesis), be purchased over the counter or even “borrowed”
from another person. What can complicate matters are patients who obtain their
medications from different MDs, or from different pharmacies.
Drugs to avoid in the Elderly
Use less anticholinergic agent; change to nortriptyline (same dose), or use
an SSRI antidepressant instead.
Used to treat EPS side effects of older neuoleptics, as well as in
Parkinson’s, but itself can cause confusion and delirium itself; taper
gradually and observe.
Use a less anticholinergic H2 blocker (i.e. Ranitidine). Ask, do they need
it, and if the need is established, consider an alternative
Too anticholinergic (and a major cause of delirium in older adults); try
using Domperidone instead for nausea.
Very long half life; try newer SSRI antidepressants.
Safer agents less likely to cause NSAID gastropathy are readily available,
such as COX-2 Inhibitors (or Acetominophen if non inflammatory pain)..
Long-acting Benzodiazepines (Valium, Dalmane, Librium)
Use short-acting agents (i.e. Lorazapam, Oxazepam) as can cause excess
sedation and cognitive impairments. Avoid entirely if possible.
Safer agents available for controlling blood pressure
Safer, more effective agents available
Other beta-blockers cause fewer central CNS effects (i.e. atenolol)
Can cause nausea, vomiting, and seizures in seniors, especially if liver
impairment. Other safer asthma medications are available
* Note: These agents may be acceptable in some instances. Although they cause
CNS side effects frequently in the elderly, they have been proven to decrease
morbidity and mortality in some circumstances.
Optimizing Medications for the Elderly
A. Ask yourself, “Why they are on the following medication?”:
Haloperidol (Haldol)/ Chlorpromazine (CPZ)
Long Acting Benzodiazepines
Narcotics (ie. Tylenol #3)
NSAIDs and hypertension/renal impairment
If no good reason, titrate down and STOP.
B. Ask why yourself why they are NOT on the following medications
Bisphosphonate (if has osteoporosis or a clinical fracture)
ECASA (if previous CVA, MI or IHD)
Warfarin (if in A-fib)
Antidepressant (if depressed)
ACE Inhibitor (if has CHF or HTN with DM)
Cholinesterase Inhibitor (if diagnosed with mild-moderate AD and living
If no good reason, consider starting!
McLeod, PJ et al. Defining inappropriate practices in prescribing for elderly people:
a national consensus panel. CMAJ 1997-156:385-91.
Capacity (Competency) Assessment
Capacity Assessment is the formal assessment of a person's mental capacity
(competence) to make decisions. Medical treatment, management of property and
personal care are areas where capacity assessment is often necessary.
It is a process, not a result, and the purpose of capacity assessment to see where a
person lies on a continuum between autonomy and beneficence
In Ontario, one can be judged capable or incapable for issues surrounding
health care and finances alone
However, other domains exist for some physical tasks or functions
(driving) versus cognitive (i.e. advanced directives); most health care
decisions are cognitive; a diabetic self administering meds has both a
cognitive and functional components
PEARL: Capacity assessments are intrusive and can have extensive outcomes; one
can take away more fundamental rights given to a prisoner in jail. Making someone
incapable should be the last thing you do for a person.
In Ontario, MD’s can assess financial and personal care capacity only in a
Schedule 1 Hospital, but not outside of hospital. This is where a capacity
assessor may be needed. If a person has a signed POA and becomes
incompetent, an MD may simply write to the lawyer with their opinion whether
they believe they are capable or not (and reasons why).
How to measure capacity? 4 Step Process
Something that puts a person or others at significant risk
Have impaired decision making
A new change or shift; making choices at odds to previous personality
Only if there will be a concrete change
The person must participate in the process because it is in their best
PEARL: If they don’t consent to the assessment, you cannot assess capacity!
1. Information gathering: talk to family, lawyers, nurses, etc.
does the patient understand the following parts of each individual
Education: must not mistake ignorance from incompetence
Decision made of competent or not; if not needs POA or some form of
substitute decision maker.
There are many dilemmas and ethical questions surrounding matters of competency
and capacity. While any MD can make a determination of capacity, few are trained
in this process (or want to be involved in this medical legal process).
Formal assessors can be available (for a steep fee) to help make this determination,
and they can be arranged via the Capacity Assessment Office of the Ontario Ministry
of the Attorney General.
PEARL: If one has full understanding of the choices they have, disagreement with
the advice of their MD’s does not necessarily mean incompetence. It is the process
that counts, not the result. The analogy is that of a person living in a condemned
house: if they know that the place may fall about their head any moment, while we
may not agree with their living situation, we must abide by it. In contrast, if one is
living in a condemned house but denies that there is anything wrong with such an
unsafe living arrangement and denies that they may come to harm, in this instance
they are not capable of understanding the risks of their current situation and are
therefore not capable of making such living decisions on their own.
Capacity to Decide, D.W. Molloy, P. Darzins, D. Strang, 300 pp., 1999
Screening Tools and Instruments used in
Confusion Assessment Method (CAM)
Standardized Mini Mental State Examination (SMMSE)
15 Item Geriatric Assessment Scale (GDS)
Functional Independence Measure (FIM)
CONFUSION ASSESSMENT METHOD (CAM)
The Confusion Assessment Method (CAM) as developed by Sharon Inouye, was
designed specifically to diagnose delirium.
There are four key features to the CAM: After seeing the patient, and reviewing the
history of cognitive changes, was there
acute onset and fluctuating course?
lack of attention?
altered Level of Consciousness?
If 1 and 2 are present, and either 3 or 4, the patient is probably delirious.
Gold Standard: Geriatric Psychiatry Interview
Sensitivity: 46-94%, Specificity: 92-98%
+ Likelihood Ratio (LR) is 8.8; -LR is 0.2
PEARL: Caveats about using the CAM are in patients with dementia (chronic
confusion), or patients with primarily psychotic symptoms. The CAM was also not
validated in younger populations.
Inouye SK et al. Clarifying confusion: the confusion assessment method. “A new
method for detection of delirium”. Ann Intern Med. 1990;113(12):941-8.
STANDARDIZED MINI-MENTAL STATE EXAM (SMMSE)
Based on the copyrighted Mini-Mental State Examination (MMSE), as developed
by Folstein, Folstein, and McHugh (1975), it has undergone refinement and changes
over time to the current form. The currently used version is (scoring in parentheses):
“Now I’d like to ask you some questions to check on your memory; this is
a standard test we do on all our patients.”
ORIENTATION TO TIME
(1) What year is this?
(1) What season of the year is it?
(1) What is the month?
(1) What is the date?
(1) What day of the week is it?
ORIENTATION TO PLACE
(1) What is the name of this place?
(1) What floor are we on?
(1) What city are we in?
(1) What province are we in?
(1) What county is this?
(3) I am going to say 3 objects. After I say them, I want you to repeat them. They
are: "Car" "Ball" "Man" Now you say them. Remember what they are because I'm
going to ask you to name them again in a few minutes.
[Interviewer: Repeat until all 3 are learned]
ATTENTION (either item)
a) Subtract 7 from 100, then subtract 7 from the answer you get and keep
subtracting 7 until I tell you to stop.
Or b) Spell the word "WORLD" backwards [DLROW].
(2) Show patient wrist watch and pen and ask to name them.
(1) Repeat the following sentence exactly as I say it. "No ifs, ands, or buts."
3 STAGE COMMAND
(3) Now I want to see how well you can follow instructions. I'm going to give you a
piece of paper. Take it in your right hand, use both hands to fold it in half, and then
put it on the floor.
(1) Read the words "Close your eyes" (provided on a sheet of paper prepared
previously) silently to him/herself, and then do what it says.
On same sheet of paper, ask patient to write a complete sentence.
(1) Give patient clean sheet of paper and ask him/her to copy the design of
(1) What are the 3 words I asked you to remember earlier? (At least a 3 minute
delay, 1 point for each, score out of 3)
Total Maximum score = 30
A score of 23 or less is probably abnormal by this screening test and suggests further
cognitive testing and a search for the reason are needed; scores 24-30 may need
further evaluation based on patterns of deficits (i.e. recall 0/3), or previous
educational an intellectual achievements (e.g. a 65 year old lawyer with a SMMSE
of 26/30 is a red flag that something is wrong). If a person is blind, cannot read or
write, or has aphasia, note their deficits and provide scores out of this new
denominator (i.e. 24/27)
Geriatric Depression Scale (GDS)
This scale was developed as a basic screening measure for depression in older adults,
and is in the public domain. While there are 4 point scales and 30 point scales in
circulation, there is no advantage in having more questions asked than on the 15 item
version below (Pomeroy et al, Int J. Geriatric Psychiatry. 2001; 16:321-6).
Ask the person you are screening to choose the best answer for how they have
felt over the past week or so:
1. Are you basically satisfied with your life? YES / NO
2. Have you dropped many of your activities and interests? YES / NO
3. Do you feel that your life is empty? YES / NO
4. Do you often get bored? YES / NO
5. Are you in good spirits most of the time? YES / NO
6. Are you afraid that something bad is going to happen to you? YES / NO
7. Do you feel happy most of the time? YES / NO
8. Do you often feel helpless? YES / NO
9. Do you prefer to stay at home, rather than going out and doing new things? YES /
10. Do you feel you have more problems with memory than most? YES / NO
11. Do you think it is wonderful to be alive now? YES / NO
12. Do you feel pretty worthless the way you are now? YES / NO
13. Do you feel full of energy? YES / NO
14. Do you feel that your situation is hopeless? YES / NO
15. Do you think that most people are better off than you are? YES / NO
Items in BOLD get one point; others get no points.
Scoring: For most clinical purposes a score > 5 points is suggestive of depression
and warrant a follow-up interview. Scores > 10 are almost always depression.
Sensitivity of a score of >10 of the 15 item GDS is 82%, specificity is 60%.
Functional Independence Measure (FIM)
The FIM instrument was derived from the Barthel Index and uses seven levels of
function, two in which no human helper is required and five in which
progressive degrees of help from another person is needed . It is regarded throughout
the world as one of the most reliable and uniform methods for documenting the
severity of an inpatient’s disability and is used to evaluate functional outcomes of
adult inpatients undergoing medical rehabilitation.
Specifically, the FIM is made up of 18-item, rated on a seven level scale
(7=independent, 1= total assist), and was originally designed to track the
improvement of patients during rehabilitation.
The higher the FIM score, the more the person is able to do independently; the lower
the FIM, the greater the functional disability. The range of scores ranges from 18
(total care) to 136 (totally independent).
A FIM completed by a person trained to use this instrument at the beginning of
Rehab to document his or her level of independent functioning versus the need for
assistance from another person. Following the course of rehab treatment, the FIM
instrument is used again at discharge and for follow up.
A minimal FIM instrument score of 60 or greater increases the chances of successful
discharge in the community, and is the minimum level used by patients treated at the
Hamilton Wentworth Geriatric Assessment Unit at the Hamilton General campus..
7 Level Scale Used:
Complete Independence (timely, safely)
Modified Independence (extra time, devices)
Supervision (cuing, coaxing, prompting)
Minimal Assist (performs 75% or more of task)
Moderate Assist (performs 50%-74% of task)
Maximal Assist (performs 25% to 49% of task)
Total Assist (performs less than 25% of task)
Domains on the FIM:
SELF CARE ITEMS
Feeding/Grooming/Bathing/Dressing Upper Body/Dressing Lower Body
Bladder Management/Bowel Management
MOBILITY ITEMS (Type of Transfer)
Bed, Chair, Wheelchair/Toilet/Tub or Shower/Car Transfer*
Walking/Wheelchair (circle)/ Stairs/ Community Access*
Expression-Verbal, Non-Verbal (circle)
Reading*/ Writing*/ Speech Intelligibility*
Social Interaction/Emotional Status*/Adjustment to Limitations*
Problem Solving/Memory/Orientation*/Attention*/ Safety Judgment*
Reference: Keith RA, et al “The functional independence measure: a new tool for
rehabilitation” Adv Clin Rehabil. 1987; 1:6-18
Work-up and Rx of Delirium and Agitation
Some Curious Syndromes You May Encounter
Anton’s Syndrome: Cortical blindness, and the bizarre denial of blindness in the
blind person (i.e. not only do they not know they are blind, but they don’t know that
they don’t know, and fabricate what they think they are seeing). Occurs when
bilateral occipital strokes are combined with lesions in the parietal lobes.
Charles Bonnet Syndrome: Vivid cinematic hallucinations in older adults with
normal cognition (i.e. insight into the unreality of the visions must be full and
prompt). Felt to be 2o to vision problems (the ocular equivalent to “phantom limb
pain”). An unknown number may progress to Lewy Body Dementia.
Diogenes Syndrome: A syndrome characterized by 1) Extreme self neglect
2) domestic squalor 3) syllogomania (excessive hoarding) 4) social withdrawal
and 5) lack of concern/shame about living conditions. Not a well understood entity,
and covers a mixed bag of possible diagnoses ranging from dementia, late onset
psychosis to simple eccentricity. More of a social problem than a medical one. (aka
Senile Squalor Syndrome or better, Social Breakdown Syndrome).
Gerstmann’s Syndrome: Finger agnosia, right-left confusion, dyscalculia, and
dysgraphia. Seen in lesions of the association area of the dominant parietal lobe of
Wernickes Syndrome: Thiamine deficiency leading to an encephalopathy
characterized by a triad of confusion, ocular dyskinesias (diplopia and nystagnus),
and ataxia. It responds to thiamine therapy. It is mostly commonly seen in
alcoholism, and may proceed to Korsakoff’s Syndrome).
Work Up for Confusion/Delirium:
If an older person comes into the ER confused, and the aetiology is not immediately
clear, get a history from the family if the confusion is acute or chronic. Get as much
background info as possible (i.e. do they have an underlying dementia? Do they
consume ETOH? Recent hospitalization or medication change?).
Try to get a list of medications from the ambulance attendants). If it’s the daytime,
contact the Family MD’s office, or the patient’s pharmacy for clues for past medical
There are several screening tests that have a high diagnostic yield in sick, older
CBC with differential (may indicate occult infection, anemia, malignancy)
Electrolytes, urea, creatinine (renal failure, hyper/hypo kalemia/natremia)
Blood sugars (hyper/hypoglycemia, occult DM)
Serum albumin, Calcium, Alk-Phos, ALT (looking for liver failure,
Get a blood ETOH level if you suspect delirium tremens from withdrawal
Cardiac markers i.e. CK, Troponin (occult MI, coronary syndrome)
SpO2 (hypoxia from occult pneumonia, PE, CHF)
EKG (occult cardiac ischemia, arrythmia)
CXR (occult pneumonia, effusion, malignancy, CHF)
CT (occult CVA, SDH, intracranial bleed, tumour)
Urine for white cells, nitrite, blood and protein (occult infection, nephrotic/itic
Urine specimen for Gram stain, culture and sensitivity ie C&S (may indicate
Don’t forget PUS (Pneumonia/Urine/Skin) is the cause of 90% of infections in
Management of Delirium
Treat the underlying cause if you discover it.
Do frequent CAM to follow the progress of the delirium.
Provide supportive care (IV fluids if not drinking, O2 if hypoxic).
Move the patient to a quite, well lit room.
Have OT provide orientation measures; calendar, clock, and message board
(i.e. a placard stating “It is Tuesday February 5th, 2002, and you are in room
405 at the Hamilton General Hospital”).
If problems sleeping because of with the delirium (“up all night”), consider
starting Trazadone, beginning at 25 mg po QHS.
Minimize the use of restraints (which can both cause or maintain a pre-existing
delirium); get one-on-one care if at all possible, or at least have a family
present to soothe and console if possible.
Management of Acute Agitation in Delirium
If agitated, violent and combative, the immediate goal of treatment of treatment
is to reduce symptoms to a level where the patient is not a physical danger to
himself or others. The cessation of hallucinations and/or delusions (assumed to
be the basis of the dangerous agitated behavior), is the ultimate goal. Current
management of acutely agitated patients involves the use of neuroleptics and
benzodiazepines either alone or in combination.
Consider an oral second generation neuroleptic; Risperidone (Risperidal) 0.25
mg BID, or olanzapine (Zyprexa) 2.5 to 5 mg QHS (there is now a fast-acting
gelatin sub-lingual wafer version of olanzapine that immediately dissolves
under the tongue that will be shortly released).
If they unwilling to take medications orally, use IM haloperidol (Haldol) 0.5
mg or IM olanzapine (Zyprexa) 2.5-5 mg QHS which should work within 30
minutes if combined with an adjuvant benzodizapine.
1-2 mg lorazapam, either po or IM, can be given q 1 hour in addition to the
neuroleptics above until sedation is achieved (e.g., unresponsive to verbal
stimuli, but responsive to a noxious stimulus).
References & Recommended Reading
Final Geriatric Pearls
Abbreviations and Acronyms Used
References & Recommended Reading List
PEARL: Don’t buy these for your Geriatric Medicine clerkship experience; you can
find them in most medical & hospital libraries; the first two are the two leading
authoritative textbooks in Geriatric Medicine
Oxford Textbook of Geriatric Medicine, 2nd Edition, Evans et al
(editors), Oxford University Press, (2000)
Principles of Geriatric Medicine and Gerontology, Hazzard et al (editors),
20 common problems in Geriatrics. Adelman & Daly (editors). New
York: McGraw-Hill, 2001
Medicine in Old Age [4th edition]. S.C. Allen Churchill Livingston (1998)
Brocklehurst's Textbook of Geriatrics and Gerontology 5t h ed., Tallis,
Brocklehurst & Fillit; Churchill Livingstone, (1998)
The Challenge of Geriatric Medicine by Bernard Isaacs, Oxford
University Press, (1992)
Essentials of Clinical Geriatrics, Kane et al, 4th Edition, McGraw-Hill,
Merck Manual of Geriatrics, Abrams 3rd Edition, Beers and Berkow,
Merck and Co. (2000).
Geriatric Medicine Journals:
Age and Aging
The American Journal of Geriatric Psychiatry
Archives of Gerontology and Geriatrics
Canadian Journal of Aging
Journal of the American Geriatrics Society (JAGS)
Other Useful Books
The 36-Hour Day (3rd Edition): A Family Guide to Caring for Persons
with Alzheimer Disease, Related Dementing Illnesses, and Memory Loss
in Later Life by Nancy L. Mace, et al [Useful, detailed and
comprehensive advice for caregivers]
Parenting Your Parents (2nd edition) by Bart Mindzenthy & Michael
Gordon [ as the above, but with a Canadian & multicultural perspective]
Let Me Decide, D.W. Molloy, 1998, New Grange Press. [Living Will Kit]
Capacity to Decide, D.W. Molloy, P. Darzins, D. Strang, 300 pp., 1999
[Useful step-by-step guidelines for capacity assessment]
A Portrait of Seniors in Canada 2nd Edition. Statistics Canada. Minister
of Industry, Ottawa, 1997.
Evidence-Based Physical Diagnosis, Steven McGee, W. D. Saunders Co,
The Geriatric Medicine Model
Fried et al., “Diagnosis of Illness Presentation in the Elderly”, J Am Geriatr
Soc (JAGS), 1991; 39 (2): 117-123).
Stuck, AE et al. “Comprehensive geriatric assessment- a meta-analysis of
controlled trials”. Lancet 1993; 342:1032-1036
Counsell, SR et al. A Randomized Controlled Trial of Acute Care for
Elders (ACE) in a Community hospital. JAGS 2000;48 1572-158 1.
Creditor, MC. “Hazards of Hospitalization of the Elderly”. Ann Intern
Med 1993; 118:219-223.
Keith RA, et al “The functional independence measure: a new tool for
rehabilitation” Adv Clin Rehabil. 1987; 1:6-18.
Folstein MF, "Mini-mental state". A practical method for grading the
cognitive state of patients for the clinician. J Psychiatr Res. 1975 Nov;
Molloy DW et al. “Standardized Mini-Mental State Examination. Use and
interpretation.” Can Fam Physician 2001 Oct; 47:2018-23
Mendez MF, et al “Development of scoring criteria for the clock drawing
task in Alzheimer's disease” J Am Geriatr Soc. 1992; 40 (11): 1095-9.
Wolf-Klein GP, “Screening for Alzheimer's disease by clock drawing.”
J Am Geriatr Soc. 1989 Aug; 37 (8):730-4.
Freedman M, “Clock tests in depression, Alzheimer's disease, and elderly
controls.” Int J Psychiatry Med. 1998; 28(4):437-47.
Borson S, “The mini-cog: a cognitive 'vital signs' measure for dementia
screening in multi-lingual elderly.” Int J Geriatr Psychiatry. 2000 Nov;
Dubois et al. “The FAB: a Frontal Assessment Battery at bedside.”
Neurology 2000 Dec 12; 55(11):1621-6
Ziad S. Nasreddine et al; “The Montreal Cognitive Assessment, MoCA:
A Brief Screening Tool For Mild Cognitive Impairment”. Journal of the
American Geriatrics Society 53 (4), 695–699 doi:10.1111/j.15325415.2005.
Pre-Op Assessment in the Elderly:
Thomas & Ritchie. "Preoperative Assessment of Older Adults" J Am
Geriatr Soc. 43 (7): 811-21, 1995
Clark. "Preoperative Assessment: primary care work-up to identify
surgical risks" Geriatrics 56 (7) 36-40, July 2001
Wertheim. "Perioperative Risk: review of two guidelines for assessing
older adults" Geriatrics 55 (7) 61-66, July 2000
Nolan et al. "Surgery in the Elderly: lowering risks by understanding
special needs" Postgraduate Medicine 91 (2) 199-208, Feb 1992.
Peter H. St George-Hyslop, Piecing Together Alzheimer’s, Scientific
American, December 2000. Read it online for free at:
Canadian Study of Health and Aging: study methods and prevalence of
dementia. Canadian Medical Association Journal,1994: 150 (6).
Patterson et al. The recognition, assessment and management of
dementing disorders: conclusions from the Canadian Consensus
Conference on Dementia. Supplement to CMAJ 1999; 160(12 Supp l).
Patterson, CJS and Gauthier, S. (Editors) Canadian Consensus
Conference on Dementia. Can J Neurol Sci 2001-28 (Supplement 1) S I
-S 123 (Supplement on Dementing Disorders)
Rogers, SL et al. A 24-week double-blind, placebo-controlled trial of
donepezil in patients with Alzheimer's disease. Neurology 1998;50
Roman GC, et al, “Vascular dementia: diagnostic criteria for research
studies. Report of the NINDS-AIREN International Workshop.”
Neurology. 1993 Feb; 43(2): 250-60.
McKeith et al. Consensus Guidelines for the clinical and pathological
diagnosis of dementia with Lewy bodies (DLB). Neurology
Lund and Manchester Groups. Clinical and Neuropathological criteria for
frontotemporal dementia, consensus statement. J Neurol Neurosurg
Psychiatrv 1994; 5 7(4):416-418
Frontotemporal lobar degeneration: A consensus on clinical diagnostic
criteria Neary et al, Neurology 1998; 51: 1546-1554
Snowdon, DA et al. Brain Infarction and the Clinical Expression of
Alzheimer Disease: The Nun Study. JAMA 1997:277:813-817.
Johnson RT and Gibbs, CJ. Creutzfeldt-Jakob Disease and Related
Spongiform Encephalopathies. NEJM 1998; 339:1994-2005.
Tariot PN. Treatment of agitation in dementia. J Clin Psychiatry. 1999;60
Freter et al., Prevalence of potentially reversible dementias and actual
reversibility in a memory clinic cohort, CMAJ 1998;159:657-62
Inouye SK, et al. A Multicomponent Intervention to Prevent Delirium in
Hospitalized Older Patients. NEJM 1999-340-669-676.
Inouye SK et alClarifying confusion: the confusion assessment method. A
new method for detection of delirium. Ann Intern Med. 1990 Dec 15;
Tune LE, Anticholinergic effects of medication in elderly patients. J Clin
Psychiatry. 2001; 62 Suppl 21:11-4.
Beck, DA et al. Depression. Clinics in Geriatric Medicine 1998;
Tourigny-Rivard, M-F. Pharmacotherapy of Affective Disorders in Old
Age. Can J Psychiatry 1997; 42 (Suppl 1):10S-18S.
Brink TL, Yesavage JA, Lum O, Heersema P, Adey MB, Rose TL:
Screening tests for geriatric depression. Clinical Gerontologist 1: 37-44,
Yesavage JA, Brink TL, Rose TL, Lum O, Huang V, Adey MB, Leirer
VO: “Development and validation of a geriatric depression screening
scale: A preliminary report.” Journal of Psychiatric Research 17: 37-49,
Almeida OP, “Short versions of the geriatric depression scale: a study of
their validity for the diagnosis of a major depressive episode according to
ICD-10 and DSM-IV.” Int J Geriatr Psychiatry. 1999 Oct;14(10):858-65.
Frailty & Failure to Thrive
Sarkisian CA et al. "Failure to Thrive" in Older Adults. Ann Int Med
1996; 124 1072-1078
Winograd, CH, et al. Screening for Frailty: Criteria and Predictors of
Outcomes. JAGS 1991; 39:778-784.
Egbert AM "The dwindles". Failure to thrive in older patients.
Postgraduate Medicine 1993 Oct;94 (5):199-201, 204-6, 210
Carlson JE, “Measuring frailty in the hospitalized elderly: concept of
functional homeostasis.” Am J Phys Med Rehabil. 1998 77(3):252-7.
Falls and Risks of Falls
Tinetti, ME et al. A multifactorial intervention to reduce the risk of
falling among elderly people living in the community. NEJM
Province, MA et al. “The Effects of Exercise on Falls in Elderly Patientsa Preplanned Meta-analysis of the FICSIT Trials.” JAMA
Chapuy et al. Vitamin D3 and Calcium to prevent hip fractures in elderly
women. NEJM 1992; 327:1637-42.
Morrison, RS. et al. The Medical Consultant's Role in Caring for Patients
with Hip Fracture. Ann Intern Med. 1998;128:1010-1020.
Osteoporosis Society of Canada Scientific Advisory Board. Prevention
and Management of Osteoporosis. CMAJ 1996; 15 5
Zuckerman, JD. Hip Fracture. NEJM 1996; 334:1519-1525.
2002 clinical practice guidelines for the diagnosis and management of
osteoporosis in Canada. CMAJ November 12, 2002; 167 (90100)
Polypharmacy, Iatrogenesis & Optimizing Medications
McLeod, PJ et al. “Defining inappropriate practices in prescribing for
elderly people: a national consensus panel”. CMAJ 1997-156:385-91.
Beers MH, etc al. “Explicit criteria for determining inappropriate
medication use in nursing home residents”. Arch Intern Med
Man-Son-Hing M, Nichol G, Lau A, Laupacis A. Choosing
antithrombotic therapy for elderly persons with atrial fibrillation who are
at risk for falls. Archives of Internal Medicine 1999;159:677-685.
Papaioannou & Heckman. “Appropriate Drug Prescribing for
Cardiovascular Disease in the Elderly”. JCOM 2000;7: 47-54.
Gomberg-Maitland, M et al. Treatment of Congestive Heart Failure. Arch
Int Med 2001-161:342-52.
Stamm WE, Hooton TM. Management of urinary tract infections in
adults. N Engl J Med 1993; 329:1328
Pain & Pain Control
Gloth, FM. Pain Management in Older Adults: Prevention and Treatment,
JAGS 2001; 49:188-199.
Grobler, U. Back and Leg Pain in Older Adults. Clin Geri Med 1998;14:
Kost, RG and Straus, SE. Postherpetic Neuralgia-Pathogenesis, Treatment
and Prevention. NEJM 1996; 335:32-41.
Lachs, MS and Pillemer, K. Abuse and neglect of elderly persons. NEJM
Podnieks, E. National Survey on Abuse of the Elderly in Canada (1990).
The Ryerson Study. Ryerson Polytechnic Institute: Toronto
Frank et al. Safety and efficacy of physical restraints for the elderly. Can
Fam Physician 1996; 42:2402-2409.
Hogan, DB. Imposed Activity Restriction for the Elderly AnnaIs RCPSC
198 5; 18:410-412
Lang, AE and Lozano, AM. Parkinson's Disease (review in two parts)
NEJM 1998;339: 1044-1062 and 339:1130-1143.
Marrie, TJ. Community-Acquired Pneumonia in the Elderly. Clinical
Infectious Diseases 2000-3 1 : 1066-78 Patterson, CJS and Chambers,
LW. Preventive health care. Lancet 1995-345-1611-15.
Sloane, PD. Evaluation and Management of Dizziness in the Older
Patient. Clin Geri Med 1996:12: 785-800.
Go AS, et al. Prevalence of diagnosed atrial fibrillation in adults. JAMA
Detsky, AS et al. Is This Patient Malnourished? JAMA 1994;271:54-58.
FINAL GERIATRIC PEARLS
The longer we live, the more important basic functions are (BADLs & IADLs) in
order to maintain persons in their own homes as long as they can; a nursing home
costs $40k a year, but if you can maintain seniors at home with CCAC supports you
can save half that cost (and more importantly, improve their quality of life).
Remember, if you are taking care of an older person in an acute care hospital:
Get PT, OT & CCAC involved early for discharge planning.
Strongly consider getting SW, involved, too if discharge will likely be an issue.
Always screen for cognitive impairments (if only the year, or a clock) and
Always get a collateral history, and find out if caregiver stress is present; the
most underutilized diagnostic test is the telephone.
Anemia is never normal in an older person; work it up!
Incontinence is not part of normal aging; work it up!
Think thrice about any drug you give an older person; will it do more harm
than good? Will it interact with other medications they are on, and impact on
Older persons are more sensitive to medications; when starting new drugs, start
low, and go slow (i.e. ¼ the usually starting dose for psychotropics). Also,
look over their old meds, and see if they really need all what they are taking.
Look for the atypical presentations of typical diseases in older persons
Listen, look and touch your patients; don’t be a “foot of the bed” MD.
And finally, strongly consider doing an elective in Geriatric Medicine, to gain indepth exposure to the treatment and management of older persons in many different
settings (GAU, out-patient, Day Hospital, Outreach, Geriatric Rehab, etc). Persons
interested in Family and Internal Medicine would certainly benefit (since a good
many patients will be categorized as geriatric), but no matter what branch of
medicine you go into (even radiology or pathology!) you will have aging relatives
who would benefit for your Geriatric Medicine knowledge
Good luck on the Wards!
Brian Christopher Misiaszek, MD, FRCPC
Geriatric & Internal Medicine
Abbreviations and Acronyms Used
AD: Alzheimer’s Dementia
ADR: Adverse Drug Reaction
ALC: Alternate Level of Care
BADL: Basic Activities of Daily Living
BMI: Body Mass Index
BP: Blood Pressure
CAM: Confusional Assessment Method
CBC: Complete Blood Count
CCAC: Community Care Access Centre (previously “Home Care”)
CDT: Clock Drawing Test
CHF: Congestive Heart Failure
CJD: Creutzfeldt-Jakob Disease
CNS: Central Nervous System
CXR: Chest X-ray
CVA: Cerebrovascular Accident
DDx: Differential Diagnosis
DLB: Dementia with Lewy Bodies
DVT: Deep Vein Thrombosis
ECASA: Enteric Coated Aspirin
ETOH: Ethanol, alcohol.
FIM: Functional Independence Measure
FTD: Frontotemporal Dementia
GAU: Geriatric Assessment Unit
GARU: Geriatric Assessment and Rehab Unit
GFR: Glomerular Filtration Rate
GDS: Geriatric Depression Scale
IADL: Instrumental Activities of Daily Living
IHD: Ischemic Heart Disease
LTCF=Long Term Care Facility
MI: Myocardial Infarction
MOTC: Ministry of Transportation & Communication
MOW: Meals on Wheels
NPH: Normal Pressure Hydrocephalus
nvCJD: new variant Creutzfeldt-Jakob Disease
ODB: Ontario Drug Benefits
OT: Occupational Therapy
OTC: Over The Counter
Px: Physical Examination (aka P/E)
PD: Parkinson’s disease
PLT: Platelet count
PMHx: Past Medical History
PND: Paroxysmal Nocturnal Dyspnea
POA: Power of Attorney
PTH: Parathyroid hormone.
RN: Registered Nurse
RA: Rheumatoid Arthritis
SSME: Standardized Mini Mental State Exam
SBE: Subacute bacterial endocarditis
SOB: Shortness of Breath
SOBOE: Shortness of Breath on Exertion
SW: Social Work/Social Worker
TCA: Tricylic Antidepressant
TD: Tardive Dystonia
TIA: Transient Ischemic Attacks
UTI: Urinary Tract Infection
VaD: Vascular Dementia
VA: Visual Acuity
WBC: White Blood Cell
3MS: Modified Mini-Mental State Examination