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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2939_Библиотеки_им_академика_М_И_Перельмана
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134
N. Pandya
Table 21 Standard human insulin therapy: regular and NPH insulin given twice a day
Regular NPH
Averageblood glucoseAMPMAMPM
Fasting
LOW
a
HIGH
Pre lunch
LOW
HIGH
Pre supper
b
LOW
HIGH
Bedtime
LOW
HIGH
Pre-lunch glucose levels are inuenced by both the R and NPH given in the AM
Bedtime glucose levels are inuenced by both the R and NPH given at the evening meal
a
Evaluate 3 a.m. blood glucose level to eliminate possible nocturnal hypoglycemia leading to
rebound hyperglycemia
b
Evaluate 3 p.m. BG readings for necessity of afternoon snack
Table 22 Analog insulin therapy: basal insulin with rapid acting insulin at each meal
Basal Rapid
Averageblood glucoseBreakfast LunchSupper
Fasting
LOW
b
HIGH
Pre lunch
LOW
HIGH
Pre supper
LOW
c
HIGH
Bedtime
LOW
HIGH
a
Giving rapid acting insulin up to 15min after eating may be more appropriate if a patient’s
eating is unpredictable. This allows for not giving the insulin if the patient does not eat
a
If a correction dose (sliding scale) is routinely being added to the patient’s usual rapid insulin
dose at meals due to hyperglycemia, the average correction dose used for any particular meal
can be used as the number of units to increase the rapid acting insulin dose at the pre-
ceding meal
b
Evaluate 3 a.m. BG readings to eliminate possible nocturnal hypoglycemia leading to rebound
hyperglycemia
c
Evaluate 3 p.m. BG readings for necessity of afternoon snack
Common Clinical Conditions inPost-Acute andLong-Term Care
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Goals ofTreatment
Treatment goals for diabetes should be individualized and take into account the
extent of microvascular and macrovascular disease, life expectancy, resident preferences, functional and cognitive status, presence of any psychiatric disorder, and risk
of hypoglycemia. In one study, facility physicians were noted to have managed
diabetes less aggressively in residents who were both cognitively and functionally
impaired [28]. Less stringent A1C goals (7.5–8.5%) may be appropriate for LTC
residents who have a history of hypoglycemia, limited life expectancy, or multimorbidities. Table23 reviews treatment goals for glycemic control in different PALTC
settings proposed by the American Diabetes Association and AMDA [26, 30].
Table 23 Framework for diabetes management goals
Patient
characteristics
and care status
Skilled
rehabilitation
Reasonable A1C
a
goal
– A1C
b
unreliable due
to recent acute
illness
– Follow
glucose trends
Long-term
resident
– Avoid relying
in A1C; avoid
symptomatic
hyperglycemia and
hypoglycemia
– If used,
interpret A1C
with caution
due to
conditions
that interfere
with A1C
levels
Resident at the
end of life
Source: Adapted from [26, 27]
a
Lower goals may be set for individuals if achievable without recurrent or severe hypoglycemia or
undue treatment burden
b
Community-dwelling resident receiving skilled care for short-term rehabilitation and potential
discharge to home
c
Long-term care resident with limited life expectancy and frequent changes in health condition and
potential hospitalization, affecting glucose levels
d
Resident at the end of life; avoiding symptomatic hypoglycemia and hyperglycemia as well as
d
– No role of
a
A1C
invasive diagnostic or therapeutic procedures is the priority
Fasting/premeal
glucose targets
(mg/dL) Rationale
100–200
– Optimize
glucose
control after
recent acute
illness
100–200
– Intensive
glycemic
control of
limited benet
– Focus needs to
be on quality
of life and
reducing
glucose
excursions
– Avoid
symptomatic
hyperglycemia
and
hypoglycemia
– No benet of
glycemic
control
– Avoid
symptomatic
hypo- and
hyperglycemia
Glucose
monitoring
– Monitoring
frequency
depends on
complexity of
treatment
– Monitoring
frequency
depends on
complexity of
treatment and
hypoglycemia risk
– Monitor
periodically
to avoid
symptomatic
hypo- and
hyperglycemia
136
N. Pandya
Medication Management: Focus onSafety andSimplication
As multimorbidities and diabetes-related complications also require pharmacological treatment in addition to glucose-lowering agents, patients are at risk of polypharmacy. Practitioners may have different prescribing preferences and on-call
practitioners may alter the regimen without reviewing glucose trends. Comparative
data on the effectiveness of diabetes treatments is limited in the PALTC setting. The
following treatment regimens are suggested to reduce hypoglycemia risk, simplify
treatment, be cautious in those with renal insufciency and to improve cardiovascu-
lar outcomes [24, 26, 27, 30].
• Administer basal insulin in the morning instead of at night
• The use of oral agents has been shown to achieve comparable glycemic control as
to basal insulin; e.g., linagliptin compared to basal insulin showed similar glycemic control with lower rates of hypoglycemia and not require renal dose
adjustment
• If a sulfonylurea is used, avoid glyburide; use glimepiride or glipizide, which are
primarily eliminated by the liver and monitor for hypoglycemia
• The meglitinides (nateglinide and repaglinide) are useful if meal intake is vari-
able as they can be given when a meal is taken, and help can control postprandial
hyperglycemia
• Consider linagliptin as an add-on to oral hypoglyemics and basal insulin, espe-
cially in renal insufciency.
• Consider an SGLT2 inhibitor (e.g., canagliozin or dapagliozin) as add-on if
heart failure, CKD or albuminuria is present, and the patient has adequate uid
intake, and does not have recurrent UTIs (with eGFR is >45mL/min/1.73m2 or
> 60mL/min/1.73m2, respectively).
• Consider adding a GLP1-RA if control is not achieved with oral agents, espe-
cially in those with, or at high risk for cardiovascular complications.
• If the patient is stable replace sliding scale insulin with basal insulin or a
GLP1-RA.
• Simplify the insulin regimen: titrate basal insulin dose to a BG goal of 90–150mg/
dL (5–8.3mmol/L); if mealtime dose is <10U consider, discontinuing and add
non-insulin agent; if mealtime dose is >10U, consider decreasing dose by 50%
and add non-insulin agent. If GFR is >45 ml/min/1.73m2, start metformin
500 mg/day.
• Consider use of second-generation basal insulins (degludec 200 U/mL, or
glargine 300U/mL) in those requiring a high dose of basal insulin or who have
wide uctuation in glucose levels. These provide similar glycemic control and
lower rates of severe hypoglycemia.
Common Clinical Conditions inPost-Acute andLong-Term Care
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Hypoglycemia
Hypoglycemia is dened by its symptoms and conrmed by a low blood glucose.
Hypoglycemia is classied into three levels.
Level 1—Glucose <70mg/dL (3.9mmol/L) and >54mg/dL (3.0mmol/L)
Level 2—Glucose <54mg/dL (3.0mmol/L)
Level 3—A severe event characterized by altered mental or physical status requir-
ing treatment of hypoglycemia
Recognition of hypoglycemia can be problematic. Symptoms may be atypical:
disorientation, lethargy, weakness, falls, aggression, or altered behavior.
Neuropsychologic symptoms can be mistakenly attributed to dementia or delirium.
Older adults have a lower glucose threshold at which they develop symptoms.
Hypoglycemia can increase neuropathic pain. Repeated episodes of hypoglycemia
can lead to worsening of dementia (Table24).
Insulin-induced hypoglycemia can result from delayed insulin clearance as in
renal failure, erratic absorption, and increased insulin sensitivity due to weight loss
or increased physical activity. Frequent use of SSI, improper timing of insulin relative to food intake, poor meal consumption, inappropriate tight blood glucose control, injection of the wrong type of insulin (e.g., rapid acting instead of long acting),
and unawareness of hypoglycemia can all-cause insulin-induced hypoglycemia.
Hypoglycemia may be corrected with ingestion of 15g of glucose or carbohydrate: equivalent to 1/2 cup juice or soda, 1/2 cup apple sauce, 1 cup milk, 1 table-
spoon sugar or honey, 1 mini candy bar, 1 tube of glucose 15g gel, or 4 glucose
tablets. Caregivers should wait 15min to recheck blood glucose and if still below
the target, give another 15g of glucose or carbohydrate. Elderly who are obtunded
may be treated with s.c. or i.m. glucagon (1mg or 1 unit) or 50% dextrose IV (usually 50mL, or less if hypoglycemia is not severe). Glucagon is now also available
as a nasal spray in a prelled syringe, which does not require mixing. Non-medical
personnel and caregivers should be trained in the administration of glucagon.
Table 24 Risk factors for severe hypoglycemia in older adults [31]
• Age
• Black race
• Poor nutrition or variable oral intake
• Cognitive or functional impairment
• Loss of normal counter-regulation
• Unawareness of, or previous severe hypoglycemia
• High doses of insulin or sulfonylureas
• Recent hospitalization or intercurrent illness
• Chronic liver, renal, or cardiovascular disease
• Endocrine deciency (thyroid, adrenal, or pituitary)
• Alcohol use
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N. Pandya
Monitoring
Assessment ofGlycemic Control
There is no consensus recommendation regarding the frequency of glucose checks
in LTC.The practice of routinely checking pre-meal and bedtime glucose should
only be used for those receiving multiple insulin injections or insulin pump therapy and for whom this information will be used to adjust insulin dosing. In residents who are on simpler insulin regimen (1–2 doses a day), then twice daily
glucose monitoring for at least 3–4days a week is suggested. For residents receiving oral agents or less frequent insulin injections, a reasonable approach to glucose monitoring would be twice per day for 1–2weeks after admission, then once
or twice per week, and as indicated. Postprandial monitoring may be helpful in
situations where the fasting glucose is at goal but the A1C remains elevated
[23, 26].
It is recommended that A1C should be monitored every 6months in patients who
are achieving their goals and every 3months in those who are suboptimally controlled. It is important to carefully interpret A1C results as it can be affected by
several factors.
A1C may be increased by: age, race (African American or Hispanic), hypothyroid-
ism, splenectomy, aplastic anemia, polycythemia, hemoglobin variants, iron de-
ciency anemia, metabolic acidosis/uremia.
A1C may be decreased by: hemolytic anemia, blood loss, transfusions, hemodialy-
sis and hematocrit <30%, liver disease, erythropoietin therapy.
Improving Interprofessional Communication andFacility
Care Processes
Successful implementation of a facility-wide diabetes protocols requires buy-in
from the administration, and effective education and communication with practitioners, nursing staff, and medical assistants. In an assisted living facility this may be
more difcult to accomplish due to variable clinical capabilities. In such situations,
the resident may be eligible to receive home health services to complement the care
provided by the facility staff. A “diabetes nurse” or champion can help ensure
implementation of diabetic protocols. The following are suggestions to improve the
care of patients with diabetes [24].
• Thorough evaluation on admission: Type of diabetes, its complications, function,
cognition, preferences, goals of care.
• Use a facility protocol for glucose monitoring and parameters for practitioner
notication.
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139
• Hypoglycemia: Staff education on recognition, management, and modication
of the medication regimen.
• Medication simplication and de-intensication if appropriate.
• Avoid changing the medication regimen based on an isolated hyperglycemic
episode.
• Avoid or replace SSI when possible.
• Optimize frequency of glucose monitoring: Avoid routine checks four
times a day.
• Frequent foot and skin inspections with prompt intervention for new concerns.
• Prompt evaluation of acute change of condition.
• Facility QI approach: e.g., review hypoglycemia episodes, SSI use, emergency
room visits.
Optimizing Transitions ofCare
Transitions from hospital or home to LTC, between health care settings, upon
discharge to the community, or with a change in practitioners are high risk for
patients with diabetes. Poor coordination and continuity of care without a feasible
care plan can lead to unnecessary rehospitalizations, duplicate tests, medication
errors, delays in diagnosis, and lack of follow-up on referrals. Risk factors for
rehospitalization include poor patient health literacy, inadequate social support,
black race, age >75 years, male gender, difculty managing medications, and high
comorbidity burden. The following checklist can facilitate a transition in care
(Table25).
Table 25 Suggested checklist for care transitions
From hospital to LTC From LTC to ALF or home
• History and physical exam, progress
notes, consultation reports
• Accurate diagnosis list
• Laboratory tests and imaging study reports
• Current medication list (reconciled)
• Time of last basal insulin dose
• Hypoglycemia episodes
• Approximate meal consumption
• Treatment goals and suggested BG range
• Medication reconciliation with written reason
for each medication
• How and when to take oral agents, insulin, or
GLP1-RA
• How often to monitor BG
• How to treat hypoglycemia (training
caregivers on use of glucagon)
• When to call the LTC facility and PCP (give
numbers)
• Home health services requested (agency
contacts)
• Follow-up appointment details with PCP or
specialist
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N. Pandya
Thyroid Disorders
Though thyroid disorders are common in the elderly, its presentation is often subtle
and varied and can range from subclinical disease to overt hypothyroidism or hyperthyroidism. Because of its nonspecic presentation, thyroid disease requires screening and interpretation of thyroid function tests in the context of patient signs and
symptoms, clinical scenario, comorbidities, and medication regimen. Subclinical
disease requires diligent follow-up and an evidence-based approach to its management. Nodular thyroid disease requires evaluation of thyroid function, imaging, and,
if indicated, biopsy, and be consistent with goals of care.
Pathophysiology andEpidemiology ofThyroid Disorders
inOlder Adults
Normal aging is associated with progressive brosis and atrophy of the thyroid
gland. However, the hypothalamic-pituitary-thyroid (HPT) axis, remains intact.
There is a decline in TSH levels leading to reduced thyroxine (T4) and triiodothyronine (T3) secretion, but due to reduced renal clearance, T4 levels remain normal. T3
declines in advanced old age while the inactive metabolite, reverse T3 (rT3) increases.
Acute or chronic non-thyroidal illness can lead to abnormalities of thyroid function,
as can several medications. Thyroid disease in older adults may be categorized as
functional (hypothyroidism and hyperthyroidism), inammatory (thyroiditis), and
neoplastic (thyroid nodules and malignancies). Mean TSH levels increase with age
as well as thyroid peroxidase antibodies (TPOAb), the latter associated with hypo- or
hyperthyroidism. Thyroid disorders are more prevalent in women, and lower in
blacks than in whites. Risk factors for hypothyroidism and hyperthyroidism include:
Hypothyroidism: Female, iodine deciency, autoimmune conditions, (e.g., rheumatoid arthritis), selenium deciency, medication, syndromic conditions
(e.g., Down’s)
Hyperthyroidism: Female, iodine deciency, autoimmune conditions, smoking,
selenium deciency, medication,
Screening forThyroid Dysfunction
Recommendations on screening for asymptomatic thyroid dysfunction vary, citing
the lack of evidence as to the benet in treating subclinical disease. However,
screening in older adults may be justied. In the Colorado Thyroid Disease
Prevalence Study, 16% of women and 21% of men over age 74years had elevated
TSH levels [32]. Adults over age 60 have a 2–10% prevalence of hypothyroidism.
Conditions for which screening may be reasonable are listed in Table 26. Serum
TSH is highly sensitive and is considered the rst-line test. In euthyroid persons the
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141
Table 26 Conditions
associated with
thyroid disease
• Biological agents (e.g., interferon,
tyrosine kinase inhibitors)
• Chronic kidney disease
• Cognitive impairment/psychiatric
illness
• Down’s/Turner’s syndrome
• Drug therapy (e.g., amiodarone,
lithium)
• Hyperlipidemia
• Irradiation of head/neck (recent and
remote)
• Pituitary surgery, irradiation
• Radical laryngeal/pharyngeal surgery
• Thyroid disease/surgery in the past,
goiter
• Thyroid nodule
• Type 1 diabetes
• Severe head injury
• Unexplained depression/weight loss
normal TSH reference range is 0.4–4.1mU/L.In those over 80 normal TSH levels
can be up to 7.9 mU/L. Hence values above the current upper TSH limit of
4.0–5.0mU/L may be normal and not associated with adverse clinical outcomes.
Over diagnosis of hypothyroidism can result in inappropriate treatment (i.e., iatrogenic hyperthyroidism) and other potential adverse effects.
Interpretation ofThyroid Function Tests
Measurement of serum TSH by immunoassay is ultrasensitive and able to distinguish between a normal, low, or high value. However, in the elderly with a pituitary
or hypothalamic disorder, the TSH may be misleadingly subnormal or low normal.
Thyroid dysfunction occurs with acute or chronic illness, hospitalized patients,
those with poor adherence to therapy, or treatment with drugs that alter thyroid hormone levels (see Tables 26 and 27). Measurement of free T4 and total T3 can be
useful if hyperthyroidism is suspected.
Non-thyroidal illness due to acute or chronic illness or severe malnutrition can
cause a low T3 state with normal TSH, FT4, and T4 (due to inhibition of 5′ deiodinase and decreased conversion of T4 to T3). Patients who are severely ill may have
both a low T4 and low T3. TSH can decline with severe illness, while a transient high
TSH may be seen during the recovery phase from an acute illness. Up to 32% of critically ill inpatients diagnosed with low free T3 levels. It is advisable to repeat thyroid
function once a patient is medically stable before initiating treatment with thyroid
replacement therapy. There is increasing recognition of partial hypopituitarism in
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N. Pandya
Table 27
Drugs affecting thyroid function [34]
Effect Drugs
May cause hypothyroidism Lithium, iodine (all forms, including kelp, contrast media,
topical povidone iodine), amiodarone, interferon alpha
May cause hyperthyroidism Amiodarone, iodine, interleukin-2, interferon alpha
Reduce conversion of T4 to T3 Glucocorticoids, iodine, propylthiouracil, propranolol,
amiodarone
Suppress TSH Dopamine, dobutamine, glucocorticoids, phenytoin,
bromocriptine, somatostatin analogs, metformin, mitotane
Increase clearance of T4 Carbamazepine, phenytoin, rifampin, phenobarbital
Reduce binding of T4 to
thyroid-binding globulin
Inuence absorption of
thyroxine
Table 28
Interpretation of thyroid function tests
Phenytoin, carbamazepine, salsalate, NSAIDS, furosemide,
heparin
Proton-pump inhibitors (PPIs), cholestyramine, aluminum
hydroxide, calcium carbonate, ferrous sulfate, sucralfate
TSH FT4 TT3 Tg Anti-Tg AB
Subclinical hypothyroidism ↑ NL NL
Hypothyroidism ↑ ↓ NL
Central hypothyroidism ↓ ↓
Subclinical hyperthyroidism ↓ NL NL
Hyperthyroidism ↓ ↑ ↑
TSH-producing pituitary adenoma ↑ ↑ ↑
Intermittent/poor medication adherence ↑ or NL↑ ↑
Non-thyroidal illness NL ↓ NL or
↓
Thyroiditis/thyroid injury NL or ↓NL or ↑NL or ↑↑ NL or ↑
Persistent thyroid cancer NL ↓ ↑
a
NL ↑↓
b
NL or ↑NL or ↑
TSH thyrotropin stimulating hormone, FT4 free thyroid hormone, TT3 total triiodothyronine, Tg
thyroglobulin, Tg-Ab anti-Tg antibody
a
TSH depends on degree of TSH suppression
b
FT4 depends on degree of thyroid supplementation
frail long-term care residents with cardiovascular disease. When evaluating for thyroid dysfunction a TSH and a free T4 level are the most helpful. Table28 provides a
guide for the interpretation of TSH and free T4 (FT4) levels [33, 34].
Hypothyroidism
Hypothyroidism is dened as a state of reduced thyroid hormone available to
peripheral tissues. Overt hypothyroidism is diagnosed when serum-free T4 levels
are below the normal range in the presence of hypothyroid symptoms. Mild
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143
Table 29 Causes of
hypothyroidism in the elderly
Primary hypothyroidism
Chronic autoimmune hypothyroidism
(Hashimoto’s thyroiditis)
131
Post
I treatment for hyperthyroidism
Subtotal or total thyroidectomy
Radiation therapy for head and neck cancer
Drugs
Central (secondary) hypothyroidism
Hypothalamic tumors or inltrative lesions
Pituitary tumors or inltrative lesions
Pituitary surgery
Head injury or cranial surgery
Cranial radiation
Stroke, hemorrhagic, or ischemic
thyroid failure or subclinical hypothyroidism is a condition in which the TSH
level is elevated in the presence of a normal free T4 level. An increasing TSH
level needs to be monitored and a decision made as to whether to start thyroid
replacement.
Causes ofHypothyroidism
The majority of residents with hypothyroidism have primary hypothyroidism due to
thyroid gland failure or dysfunction. Central or secondary hypothyroidism is rare
and accounts for less than 1% of cases. The latter may occur due to lesions of the
pituitary or hypothalamus or dysfunction of the hypothalamic–pituitary axis
(Table29).
Clinical Evaluation
Clinical signs and symptoms are often nonspecic. Classical signs and symptoms
are listed in Table30. Fatigue has been noted in 68 % and weakness in 53% [35].
Classical symptoms such as weight gain, cold intolerance, paresthesias, and muscle
cramps are less frequent in older adults. Neuropsychiatric symptoms (e.g., withdrawal, disorientation, delusions, or psychosis) can develop gradually and be challenging given the prevalence of dementia and the propensity for developing
delirium.
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