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Table 30 Symptoms and signs of hypothyroidism in older adults
Symptoms Signs
Fatigue Alopecia
Cold intolerance Xerosis
Constipation Hoarseness
Dysphagia Weight gain
Exertional dyspnea, atypical chest pain Bradycardia, diastolic HTN
Lack of concentration Worsened congestive heart failure
Memory loss, delusions, or psychosis Anemia
Hearing loss Hyperlipidemia, elevated CPK
Depression Myxedema
Generalized weakness or muscle cramps Neuropathy, slowed reexes
N. Pandya
Treatment ofClinical Hypothyroidism
The goal of treatment is to normalize the thyroid function test (TSH) to achieve an
euthyroid state. The dose of thyroid hormone replacement depends on the age and
weight of the resident. Synthetic thyroid hormone preparations (rather than thyroid
extracts) are preferred due to a longer half-life and a more constant serum level. The
initial replacement dose of levothyroxine is usually 25–50μg/day, but older adults
with signicant cardiac comorbidities should be started on 12.5–25μg/day and the
dose adjusted by a similar amount every 3–6weeks until the TSH has normalized,
after which, it is recommended the TSH be checked every 6–12months. In primary
hypothyroidism, the TSH alone can be used to monitor treatment, while in those
with central (secondary) hypothyroidism, a free T4 level should be used. If no residual thyroid function exists the daily replacement dose of levothyroxine is usually
1.6μg/kg body weight (typically 100–150μg). Dosage adjustments should take into
account any concomitant or worsening condition such as atrial brillation, HF, or
osteoporosis. Low normal or subnormal TSH levels should be avoided, and if
needed, thyroxine can be held for days to weeks and restarted at a lower dose once
the patient’s condition has become stable. It is important to note that linear changes
in the concentration of T4 correspond to logarithmic changes in serum TSH. If a
resident has had an inadvertent discontinuation or omission of levothyroxine therapy during a care transition, there may be a marked increase in the TSH level. When
resuming levothyroxine it should be at the prior documented dose. Measurement of
free T4 may be helpful [35].
Subclinical Hypothyroidism
This condition may also be referred as “mild thyroid failure” and is dened by an
elevated TSH with a normal free T4 level. Anti-TPO antibodies are positive in 67%
of nursing facility residents with subclinical hypothyroidism. Most elderly are
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usually asymptomatic. Prevalence of this condition in 80-year-olds ranges from 14
to 20%. The etiology of subclinical hypothyroidism is usually chronic autoimmune
thyroiditis, but poor compliance with levothyroxine therapy, suboptimal treatment,
recovery from severe illness, thyroiditis, and medications that affect thyroid function should be considered. Hence TSH should be repeated in 1–3months to conrm
this diagnosis. Subclinical hypothyroidism can progress to overt hypothyroidism in
33–55% of individuals, and be associated with elevation of lipid levels, altered
mood and cognition, impaired cardiac function, and increased mortality, especially
in those with HF. A TSH level >12 mU/L, presence of autoantibodies, goiter,
advanced age, and a history of radiation therapy are risk factors for progression to
overt hypothyroidism.
Management ofSubclinical Hypothyroidism
Current evidence does not support a benet to treating subclinical hypothyroidism
in an attempt to improve cardiac function or neuropsychiatric symptoms. The current guidelines for the management of subclinical hypothyroidism are the following [36]:
• If the TSH is 4.5–10mU/L in the absence of symptoms, repeat TSH in 6 months
and yearly thereafter if patients remain asymptomatic
• If the TSH is above the upper limit of 4.5–6.9mU/L, no treatment in those
>65–70 since TSH is age appropriate; avoid treatment in those over 80years
• If the TSH is 7.0–9.9mU/L, treat those who have symptoms of hypothyroidism;
the goal of treatment is to achieve a TSH of 3–6mU/L
• If the TSH is >10mU/L, in most circumstances administer thyroid treatment.
Hyperthyroidism
It is important to diagnose hyperthyroidism in older adults. If undiagnosed, there is
a potential for signicant morbidity, mortality, and poor quality of life. Risks include
cardiac arrhythmias, worsening osteoporosis, and increased incidence of fracture.
Primary and subclinical hyperthyroidism occur more frequently in older adults,
reported up to 2% in persons over the age of 60.
The causes of hyperthyroidism in older adults are:
Endogenous: Thyroid hyperfunction due to toxic multinodular goiter (40%),
toxic adenoma (30%), Graves’ disease (15%), and thyroiditis (5%)
Exogenous: Suppressive dosing of levothyroxine in the treatment of thyroid car-
cinoma (10%) and excessive dosing of levothyroxine in treating hypothyroidism (5%).
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N. Pandya
T3 toxicosis can occur where the TSH is low with an isolated elevation of
T3. It is usually due to excess T3 secretion from a thyroid nodule or goiter. “T4
toxicosis” is seen in patients with pre-existing primary hyperthyroidism or concurrent non- thyroidal illness, leading to low or normal T3. Amiodarone-
related thyrotoxicosis occur more frequently in older adults with atrial
fibrillation than younger patients. Prompt identification of clinical signs and
diagnostic workup is essential. Amiodarone more often causes
hypothyroidism.
Signs and Symptoms of Hyperthyroidism in the Elderly
• Atrial brillation (up to 20% of patients)/palpitations
• Unintentional weight loss
• Depression and cognitive decline, delirium, mania
• Lethargy and fatigue
• Heat intolerance
• Sweating
• Tremor
• Diarrhea, vomiting, or constipation
• Exophthalmia
• Alopecia or coarse or thinning hair
• Pretibial myxedema
• Severe osteoporosis and increased fracture risk
Signs and symptoms of hyperthyroidism such as heat intolerance, anxiety, tachy-
cardia, and tremor may be lacking in older adults. Atypical signs or symptoms
include vomiting, constipation, depression, and fatigue. Thyroid storm is less common and presents with a severe hypermetabolic state, fever, neurocognitive changes,
and possibly heart failure. The most common cause of thyroid storm in older adults
is infection, rather than due to unprepared thyroid surgery or radioiodine therapy
seen in younger patients.
Diagnosis ofHyperthyroidism
Overt, primary hyperthyroidism is diagnosed by low TSH and elevated total and
free T4 levels. Subclinical hyperthyroidism is diagnosed by the presence of low
TSH and normal levels of total or Free T4. The latter may also indicate T3 toxicosis.
Positive thyroid-stimulating immunoglobulin (TSI) or other thyroid antibodies can
help conrm a diagnosis of Graves’ disease. Review medications regimen to evaluate iatrogenic causes of hyperthyroidism.
Management of hyperthyroidism in older adults depends on its underlying
etiology, comorbidities, and the patient’s goals of care. Management is summarized
in Table31 [33, 37].
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Table 31
Causes and management of hyperthyroidism
Causes of
hyperthyroidism Management Caveats
Subacute thyroiditis
• Beta blockers for
hyperadrenergic symptoms
• Avoid in decompensated HF,
asthma, and Raynaud’s disease
• Glucocorticoids if
refractory thyroiditis
• NSAIDS for inammatory
pain (low dose)
Grave’s disease
• Antithyroid medications;
methimazole,
propylthiouracil (PTU)
• Radioiodine therapy
• Elevated risk of agranulocytosis,
during the rst 90 days with PTU
• Monitor LFT regularly
• Short course before radiodine
therapy
• Favored over long-term
medications or surgery; reduction
of mortality
Toxic multinodular
goiter or toxic
adenoma
• Antithyroid medications;
methimazole,
propylthiouracil (PTU)
• Radioiodine therapy
• Surgery for large
obstructive goiters
• Elevated risk of agranulocytosis,
during the rst 90days with PTU
• Monitor LFT regularly
• Short course before radiodine
therapy
• Favored over long-term
medications or surgery; reduction
of mortality
Amiodarone-induced
thyrotoxicosis type 1
Amiodarone-induced
thyrotoxicosis type 2
Thyroid storm • Fluid and electrolyte
• Antithyroid medications;
methimazole,
propylthiouracil (PTU)
• Long course of
glucocorticoids
stabilization
• High doses of methimazole
(40–80mg/day) or PTU
• High doses of methimazole
[40–60mg/day] or PTU [600–
800mg/day]) to block thyroid
hormone synthesis
• Glucocorticoids for relapse
• Other agents may be used to lower
thyroid hormone levels; sodium
iodate, potassium perchlorate, and
cholestyramine
(200mg q 6 h)
• Beta blocking agent
• Stress dose glucocorticoids
• Potassium iodide 1h after
antithyroid medication
Subclinical
hyperthyroidism
• Same treatment as for overt
hyperthyroidism when
TSH levels are <0.1mIU
per L
LFT liver function tests
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N. Pandya
Physical Examinaon
Thyroid smulang hormone (TSH), Thyroid ultrasound
TSH normal or elevated
Nonfunconal nodule
Ultrasound criteria for FNA met
Yes
FNA
Fig. 3 Initial approach to a patient with a thyroid nodule (adapted from American Thyroid
Association) [38]
No
Monitor
TSH below normal
Radionucleode scan
Check FT4 and T3
Funconing nodule
Ft4 and T3
normal
Subclinical
hyperthyroidism
Observe unless
treatment is
warranted
Ft4 and/or
T3 high
Overt
hyperthyroidism
Treat
Thyroid Nodules andThyroid Cancer
Thyroid nodules become more prevalent with age. Over age 65, 50% have thyroid
nodules detected by ultrasound and 5% of thyroid nodules may be malignant. The
prevalence of thyroid cancer is higher in those over 60–65years of age, history of
head and neck irradiation, family history of thyroid cancer, history of total body
irradiation for bone marrow transplantation, multiple endocrine neoplasia type 2
(MEN2), and familial adenomatous polyposis, or Cowden syndrome. The following
algorithm provides an initial approach to patients with a thyroid nodule [38] (Fig.3).
Follow-Up ofPatients withaHistory ofThyroid Cancer
It is not uncommon to assume the care a of newly established patient who has had a
history thyroid cancer. The history is usually unclear, and thus it is important to question why patients are on thyroid supplementation, to palpate the neck for thyroid
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nodules, goiter, and lymphadenopathy, and to look for neck incisional scars.
Unexplained hypocalcemia, may be due to hypoparathyroidism related to partial
parathyroidectomy during previous thyroid surgery. The presence of exophthalmos in
persons on thyroid supplementation suggests prior treatment of Grave’s disease with
radioiodine ablation or thyroidectomy. Patients who have been treated with thyroidectomy followed by radioiodine ablation or had treatment for thyroid cancer, should be
referred to an endocrinologist or oncologist [39]. Pre-referral studies to consider:
• TSH: Identify appropriate TSH goal: TSH suppression with levothyroxine may
not be necessary if the cancer was low risk and without recurrence, or the patient
has cardiac arrhythmias or a low bone density.
• Thyroglobulin: Should be undetectable with TSH stimulation.
• Anti-Tg antibodies: If present, the serum Tg level alone cannot be used as a
marker for recurrent or persistent thyroid cancer and further imaging will be
necessary.
• Neck ultrasound: Identies malignant cervical lymph nodes (common site for
recurrence of papillary thyroid cancer)
Vitamin B12 Deciency
• B12 deciency is common in older adults and can lead to hematological abnormalities (though often there is no associated anemia or macrocytosis) as well as
potentially serious and irreversible neurological consequences. Population studies show a prevalence of B12 deciency of 10–15% in older adults, with one study
of hospitalized elderly from the community and nursing facilities reporting a
prevalence of 5% with low B12 (<200pg/mL or 150pmol/L), and 20% with marginal B12 (200–349pg/mL or 150–260pmol/L). The signs and symptoms of B12
deciency are nonspecic and varied and can be misattributed to other disorders
or the neurological changes of normal aging. The elderly may have “subtle B12
deciency” with only a biochemical deciency. In a population in which the
prevalence of dementia and other neurological and neuropsychiatric abnormalities are high, early recognition and treatment of B12 deciency can be benecial
[40]. Older age and more established symptoms of B12 deciency are associated
with lower likelihood of neurologic improvement when treatment is delayed.
Vitamin B12 deciency has also been associated with low bone mineral density
and been implicated in pre-frailty.
Risk factors and causes of B12 deciency are listed Table32. Dietary cobalamin
deciency is responsible for about 40–50% of B12 deciency, and pernicious anemia
(due to decreased gastric intrinsic factor production) for about 10%. Hypochlorhydria
and atrophic gastritis are important contributing factors. Stomach acid is necessary
for the release of vitamin B-12 from food, which then binds to haptocorrin, undergoes degradation by pancreatic enzymes, then binds to intrinsic factor, and nally is
absorbed in the terminal ileum. The B-12 intrinsic factor complex then binds to
transcobalamin for transport in the blood.
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Table 32 Causes of B12 deciency [40]
• Atrophic gastritis and hypochlorhydria
• Chronic antacid use (histamine-2 blockers, proton pump inhibitors)
• Gastrectomy (total or partial), gastric by-pass surgery
• Ileal resection
• Small intestine and terminal ileum disorders (Crohn’s disease, sprue, malabsorption)
• Pancreatic insufciency
• Helicobacter pylori infection
• Bacterial overgrowth syndromes
• Strict vegetarian diet
• Pernicious anemia (positive anti-intrinsic factor antibodies)
• AIDS and AIDS treatment (zidovudine)
• Metformin
Table 33 Signs and symptoms of B12 deciency [40]
Hematologic: Macrocytosis, anemia, neutrophil hypersegmentation, pancytopenia
Neurologic: Peripheral neuropathy, paresthesias, spinal column lesions (loss of vibration,
position sense, ataxia), extensor plantars, orthostasic hypotension, limb weakness
Neuropsychiatric: Delirium, slow thinking, depression, confusion, memory loss
Other: Glossitis, pallor
N. Pandya
B12 deciency should be suspected in residents with unexplained anemia or neu-
rological symptoms, glossitis, anorexia, diarrhea, or other gastrointestinal disorders
as well as the presence of autoimmune diseases such as thyroiditis and vitiligo.
Signs and symptoms of vitamin B12 deciency are listed in Table33.
Diagnosis
• Measure vitamin B12 levels in frail older adults, those with macrocytic anemia,
hypersegmented neutrophils, gait disorders, peripheral neuropathy, or neuropsychiatric symptoms without obvious cause.
• Serum B12 levels less than 200pg/mL (150pmol/L) are consistent with a diagnosis of B12 deciency.
– Falsely low levels of B12 may be seen in AIDS, multiple myeloma, folate de-
ciency, and excessive vitamin C intake.
– Falsely normal or high levels of B12 may be seen in transcobalamin II de-
ciency, certain myeloproliferative disorders (chronic myelogenous leukemia),
liver disease, and intestinal bacterial overgrowth.
• Serum B12 levels between 200 and 350pg/mL (150–260pmol/L) indicate a borderline B12 deciency that can be treated by supplementation.
• Methylmalonic acid (MMA) by serum or urine testing is specic for B12 deciency, and should be considered in patients with borderline B12 levels if neces-
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sary to conrm clinically signicant B12 deciency. MMA levels will normalize
with treatment. Falsely elevated levels of MMA may be seen in hypovolemia and
renal insufciency.
• Consider Helicobacter pylori testing when evaluating patients with B12
deciency.
• Folate deciency can coexist, and it is prudent to check folate levels when B12
deciency is diagnosed. Failure to treat folate deciency prior to starting B12
replacement can result in spinal cord demyelination.
• No further evaluation is usually required once the diagnosis of B12 deciency is
made by a low blood B12 level. The Shilling test or other tests of gastric function
are rarely of added benet to a workup. Bone marrow biopsy is rarely needed but
should be considered in cases of pancytopenia [40, 41].
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Treatment
In symptomatic patients a common treatment is to replace B12 in the form of 1000μg
cyanocobalamin by intramuscular injection weekly for 3weeks, then monthly, or
every other month. For residents in whom B12 was discovered incidentally it may be
replaced orally. Crystalline B12 administered orally is well absorbed and at least
500–1000μg/day is required to reverse the biochemical disorder of B12 deciency.
Patients with impaired absorption of B12 may respond to higher oral doses
(1000–2000mcg daily) if there is a lack of intrinsic factor or pathology of the terminal ileum. Sublingual, transdermal, and intranasal forms of B12 are more costly
and have been less rigorously tested. There is no evidence for the use of supplemental B12 as a tonic to improve well-being.
Monitoring recommendations vary and depend on the manifestation and severity
of B12 deciency. Elderly with anemia due to B12 deciency should have a reticulocyte count checked in 1 week after starting treatment and hemoglobin level in
1–2months. Treatment of B12 deciency may unmask underlying folate and iron
deciency. Thus, as red cell production increases, folate and iron supplementation
may be required.
Skin Disorders
Scabies
Scabies is a contagious parasitic infestation of the skin caused by the human itch
mite Sarcoptes scabiei var hominis. It can cause extensive outbreaks among resi-
dents and staff unless timely treated and system-wide infection control protocols
followed. The severity of a scabies infection depends on the number of mites infesting the skin. Norwegian scabies is a severe atypical infection characterized by
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extremely pruritic crusty skin lesions with thousands to millions of live mites.
Mental retardation, dementia, immunodeciency states, renal failure, malnutrition,
HIV, insulin-treated diabetes, and administration of topical and systemic corticosteroids can increase the severity of scabies.
N. Pandya
Transmission andDiagnosis
The incubation period of scabies is 2–6weeks. Healthy individuals without prior infestation may be asymptomatic during this period. Those with previous infestation are
sensitized and often develop pruritis within 48h of reinfection as the itching originates
from an allergic reaction to the mite. This itching is often severe, particularly at night.
Skin areas typically affect the web spaces between the digits, breast folds, buttocks,
genitalia, and exor surfaces of the wrists, elbows, and axillae. Skin lesions consist of
erythematous papules and linear excoriations. The differential diagnosis will include
eczema, folliculitis, tinea, psoriasis, insect bites, or dermatitis herpetiformis.
A scabies outbreak is dened as one or more conrmed cases within a nite
period of time and in a dened facility location (e.g., a nursing unit or ward).
Norwegian scabies causes on extremely high rate of transmission. Transmission of
scabies occurs from person to person skin contact or infested clothing. Chair covers
and bed linens play a smaller role in transmission.
Skin scrapings of affected areas by microscopic exam for the presence of mites,
eggs, or fecal pellets will conrm the diagnosis of scabies. However, in recently
exposed persons, skin scrapings can be negative and the Burrows Ink Test may then
provide clues to infestation. The Burrows Ink Test is performed by running a black
or green felt tip pen over the waxy red raised burrows, and then wiping the skin off
with alcohol to reveal a black or green zigzag line under magnication [40]. An
eczematous eruption can frequently be seen covering the trunk of elderly who are
infected with scabies, but this is usually an allergic reaction to the mite and may
show little or no evidence of mite infestation. Skin biopsies are not recommended
due to low yield. Hence empiric treatment based on symptoms may be necessary.
Dermatology consultation may be needed for an indeterminate rash.
Controlling theOutbreak
Barrier precautions using gowns and gloves should be used until the diagnosis of
scabies has been eliminated as a possibility. The medical director should be notied
and treatment ordered and other practitioners notied. The infection control professional should track cases and contacts as well as implement barrier precautions. The
staff needs to treat all residents in an area if multiple cases are found. Any caregivers, exposed visitors, and volunteers should be treated as well. The local health
department or the state regulatory agency should also be notied.
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Contact precautions should be used for at least 24h after initiating treatment.
Residents with crusted scabies will require several treatments and may be contagious for several weeks. In the case of crusted scabies contact isolation in a single
room should be continued until three consecutive skin scrapings are negative.
Clothing, pillows, blankets, and wheelchair pads should be washed in hot water,
sealed in plastic for 5–7 days, or placed in a hot dryer. Environmental surfaces,
beds, assistive devices, diagnostic and therapy equipment should be cleaned with an
Environmental Protection Agency (EPA)-registered cleaning product. Furniture
with fabric upholstery will need to be removed for 5–7days, topical creams and
lotions discarded, all carpets vacuumed and the vacuum bag disposed of immediately.
Treatment ofScabies [41, 42]
• Gamma-hexachlorocyclohexane (Lindane) is no longer recommended due to
resistance of the mites and neurotoxicity concerns.
• Permethrin 5% (Elimite) cream applied head to toe and left on for 8–14h is 90%
effective after the rst application. In some patients, a second application after
7–10days may be necessary
• All symptomatic patients, and close contacts including staff should be treated
with permethrin in the same 24–48h period.
• Health care workers and their household contacts should be treated at the end of
the work shift. Leave permethrin cream on and shower after 8–12h.
• Permethrin should be applied on the entire area of skin from the hairline to the
feet, including the palms and soles, under the ngernails and toenails; the scalp
may rarely need treatment unless infested.
• Topical steroid creams or antihistamines to treat pruritis should not be applied
until the scabicide has been removed.
• Oral ivermectin (Stromectol) is an effective and cost-comparable alternative to
topical scabicides although it is not FDA approved for use in scabies. It may be
particularly useful in patients with dementia, in large outbreaks, and in the treatment of severely crusted scabies in immunocompromised residents or when topical therapy has failed. A single dose of 200μg/kg is effective or a standard dose
of 6mg for a 70kg adult.
• A second treatment is needed in 1–2weeks after the eggs mature (since therapies
are not effective against mite eggs)
Herpes Zoster
Herpes zoster (HZ) is caused by reactivation of the varicella zoster virus (VZV),
which is latent in the sensory ganglia. The prevalence of HZ in PALTC residents is
unknown, but two-thirds of cases are diagnosed in >50-year olds. Herpes zoster is
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