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characterized by a pruritic, maculopapular vesicular rash that evolves into noninfec-
tious dried crusts over a 5- to 6-day period. It is triggered by a decline in cellmediated immunity that facilitates the reactivation of latent varicella virus.
Long-term care residents are at greater risk because of age-related decline in cellmedicated immunity, malnutrition, multimorbidity, and frailty. They also have
diminished reserves to respond to stress that can trigger an episode of HZ.
Prodromal symptoms can include hyperesthesia, localized pain, or itching. The
lesions of HZ are often described as a “dew drops on a rose petal,” which are clustered in a dermatomal distribution and not crossing the midline. Most often, HZ is
diagnosed clinically, but the laboratory diagnosis can be made by isolation of the
varicella virus from a lesion. Rapid varicella virus identication using PCR is preferred if available, but direct uorescent antibody (DFA) testing can be used to
make the diagnosis as well.
About 20% of affected older persons may develop post-herpetic neuralgia
(PHN). This can be a devastating complication requiring prolonged pharmacotherapy and pain management and lead to depression and a decline in function. Other
complications may include involvement of the ophthalmic branch of the trigeminal
branch (leading to uveitis, keratitis, blindness), the nasociliary branch (vesicles in
the pharynx and tip of the nose), and the Ramsay Hunt syndrome (vesicles in the
ear, deafness, facial palsy, vertigo).
N. Pandya
General Measures
The nursing leadership and medical staff should educate the resident and direct staff
caregivers regarding the nature of the infection and the risk of viral transmission to
individuals who have not had chickenpox. HZ is not contagious to those who have
a history of chicken pox or adequate titers of IgG to varicella. Skin lesions should
be kept clean and dry to avoid bacterial superinfection. Antibiotic ointments and
adhesive dressings should be avoided since healing and drying of the lesions will be
delayed. Shingles in immunocompromised individuals and those with ophthalmic
zoster must be treated with antiviral agents
Vaccination
Encourage Zoster vaccination for persons 50years and older, regardless of prior
history of a natural HZ infection unless a contraindication exists. It is not recommended for immunocompromised individuals [42]. Although zoster vaccine
(Zostavax) in general has been associated with 51% fewer episodes of HZ, and 66%
less PHN, these gures were only 18% and 26%, respectively, in those 80 and over.
Hence response to the vaccine in LTC residents cannot reliably be predicted and
facility immunization programs for herpes zoster are not currently recommended.
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The Shingrix vaccine released in 2019 is 97% effective in preventing HZ in those
>50years, and should be given in two doses, 2–6months apart [42, 43].
Treatment
• Topical antiviral treatment is not efcacious.
• Systemic antiviral treatment is recommended if ≥50year age, moderate to severe
pain or rash; or have non-truncal involvement within 72h of rash onset. Begin
immediately or sooner than 72h, if neurologic or ocular signs, severe pain, and/
or rash. Monitor renal function in those with renal insufciency.
– Acyclovir 800mg, ve times daily (every 4–5h) for 7–10days (less preferred
due to dosing schedule)
– Famciclovir 500mg, three times daily for 7days
– Valacyclovir 1000mg, three times daily 7days
• Adjuncts to antiviral therapy consider:
– Analgesics (acetaminophen, opioids, tramadol)
– Gabapentin (maximum 3600mg daily), pregabalin (75mg twice daily), or a
low dose tricyclic antidepressant (nortriptyline 25mg at bedtime, occasion-
ally up to 150mg daily), if no improvement in pain
• Oral corticosteroid use is common but lacks evidence in improving quality of life
or reducing the incidence of PHN.
• Referral to a pain specialist is recommended to evaluate for neural blockade if
analgesics, adjunct therapies, and corticosteroids have not been effective in
relieving post-herpetic neuralgia.
• Psychosocial evaluation if severe depression
• Attention to both nutrition and maintenance of functional status
Clostridioides difcile Infection
Clostridioides difcile (C. difcile) infections (CDI) are a serious cause of morbidity and mortality in the post-acute and long-term care setting. Nationwide 500,000
infections occur annually. One in six patients with CDI experience a recurrence in
the subsequent 2–8weeks, and one in eleven adults over 65years diagnosed with a
healthcare-associated CDI, die within 1 month [CDC website] [43, 44]. C. difcile
colonizes the gut after the normal gut ora has been altered by antibiotic treatment.
More virulent strains are emerging and the NAP1/BI/027 strain has been implicated
in CDI outbreaks, and is capable of increased production of toxins A and B.About
8–10% of PA/LTC residents are thought to be carriers. The infection is transmitted
in health care facilities from environmental surface contamination, hand carriage by
staff members, and infected patients (Table34).
156
Table 34 Risk factors for C. difcile
• Advanced age
• Frequent need for hospitalization
• Recurrent exposure to antibiotics (especially clindamycin, third-generation cephalosporins,
and uoroquinolones)
• Presence of comorbid medical conditions
• Use of proton-pump inhibitors or histamine 2 receptor antagonists for gastric acid
suppression
• Immunosuppression (organ transplant with immunosuppressive therapy, HIV/AIDS, cancer)
N. Pandya
Clinical Features
Older adults may be asymptomatic, or symptomatic with watery diarrhea, abdominal cramps, constipation or ileus, and fever, though patients may be afebrile.
Symptoms may begin during antibiotic treatment or up to 8weeks after completion
of antibiotics. In PA/LTC residents, diarrhea may not be the initial problem, but
fever, confusion, abdominal pain, anorexia, nausea, leukocytosis (often >20,000
WBC), and hypoalbuminemia. A distinctive fecal odor is also a manifestation of
CDI.The differential diagnosis of CDI includes an acute abdomen (due to ileus,
volvulus, ischemia), shock (due to sepsis or cardiogenic), infectious diarrhea (due
to antibiotics or salmonella or clostridium perfringens), or noninfectious causes
(e.g., celiac disease, Crohn’s, ulcerative colitis, collagenous colitis, IBS, fecal
impaction).
Diagnosis should be made by testing diarrheal stool. Options are:
• C. diff toxin testing by enzyme immunoassay (EIA) for toxins A and B
• PCR testing for toxins A and B is superior and can be available in 1h. Beware of
false positives.
• EIA testing for C. difcile glutamate dehydrogenase (GDH), but it cannot distinguish between toxigenic and nontoxigenic strains; results available in 1h and
may be used as a screening test.
• Repeat testing to conrm cure is not recommended!
• Discontinue the use of any potentially inciting antibiotics and avoid the use of
antiperistaltic agents!
• Consider discontinuing proton pump inhibitors (PPIs).
Management
• For mild to moderate disease (diarrhea plus other symptoms not meeting severe
or complicated criteria);
• Metronidazole 500mg p.o. TID for 10–14days
• Discontinue unnecessary antibiotics
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157
• Vancomycin 125mg p.o. QID if unable to take metronidazole or no improve-
ment in 5–7days
• For severe disease (albumin <3g/dL and one of the following: WBC >15,000,
or abdominal tenderness);
– Vancomycin 125mg p.o. QID
• For severe and complicated disease (ICU admission, hypotension, fever, ileus or
abdominal distension, confusion, WBC >35,000 or <2000), lactate >2mmol/L)
– Vancomycin 500mg p.o. QID
– Vancomycin by enema (500mg in 500mL normal saline QID and metroni-
dazole 500mg IV q 8 h if oral therapy is not tolerated
• For recurrent C. diff infection (10–20% recur within 8weeks)
– Conrm diagnosis
– Conservative treatment for mild symptoms
– Same regimen as for the initial episode
– “Pulsed vancomycin” regimen
– Fidaxomycin 200mg BID for 10days (questionable efcacy) (expensive)
– Fecal microbiota transplantation may be safe and effective in restoring nor-
mal ora
The use of private rooms will reduce transmission. Antibiotic stewardship is cru-
cial as is hand hygiene and the maintenance of contact precautions using gowns and
gloves when entering the room of a patient with CDI.Environmental surfaces should
be disinfected using an approved sporicidal agent. Proton pump inhibitors should be
used judiciously or discontinued. Moreover, there is no conclusive evidence supporting the use of probiotics though commonly prescribed during C. difcile treatment or as preventive therapy when antibiotics are prescribed for other infections.
Acute Kidney Injury
Renal function declines in many older adults, and thus are vulnerable to acute kidney injury due to age-related changes in renal functions that include:
• Decrease in glomerular ltration rate (GFR)
• Decrease in urine concentrating ability (leading to nocturia, hypernatremia, poor
compensation for hypovolemia)
• Reduced sodium conservation in the face of low sodium intake (risk of volume
depletion)
• Reduced sodium excretion in the face of high sodium intake (risk of edema and
salt-sensitive HTN)
• Decreased potassium excretion (risk of hyperkalemia)
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N. Pandya
Acute kidney injury (AKI), is dened as an acute increase in creatinine or a
decrease in urine output to <0.5mL/kg/h for at least 6h. It is increasingly common in older adults and can result in increased morbidity and even the need for
dialysis. Its incidence increases with older age, male gender, black race, chronic
inammation, and those with poor nutritional status [44, 45]. The causes of AKI
and its evaluation are reviewed in Table35 [45]. Due to low muscle mass related
to aging and frailty, serum creatinine may be normal or near normal despite severe
impairment of renal function. In evaluating for the cause of AKI, it is useful to
classify it as prerenal, intrinsic renal (glomerular, tubulointerstitial, and vascular),
and postrenal causes.
Table 35 Causes of AKI and evaluation
Category of
AKI Causes Clinical ndings Treatment
Prerenal
azotemia
Obstructive
uropathy
• Hypoperfusion due to
volume depletion
(reduced uid intake,
acute illness, GI uid
loss, diuresis)
• Low arterial volume
(decompensated HF)
• Renal hypoperfusion
(e.g., bilateral renal
artery stenosis)
• Medications (e.g.,
ACEI, ARBs, NSAIDS,
diuretics, SGLT2i)
• Bladder outlet
obstruction (e.g., BPH
in men)
• Bladder carcinoma
• Urethral stricture
• Functional outlet
obstruction (e.g.,
anticholinergic
medications, spinal
cord injury, diabetic
autonomic neuropathy)
• Ureteral obstruction
(stones, strictures, or
retroperitoneal
malignancy)
• History
• Orthostatic
hypotension
• Urinalysis: high
specic gravity,
bland urine
sediment
• Urinary hesitancy,
nocturia, overow
incontinence
• GFR maintained if
only one kidney
affected (unless
unilateral kidney
present)
• Renal ultrasound
shows
hydronephrosis,
stones
• Stop or reduce
offending
medications
• Restore
intravascular
circulating volume
with oral hydration
or intravenous
uids
• Bladder emptying
(may need to be
scheduled or
indwelling bladder
catheter)
• Specic treatment
depending on the
cause and level of
obstruction
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159
Table 35
Hyperkalemia often coexists with AKI and be aware that medications may be a contributing factor.
These include ACE inhibitors, angiotensin receptor blockers, renin inhibitors, NSAIDS, spironolactone, amiloride, cyclosporine, tacrolimus, trimethoprim-sulfamethoxazole, and pentamidine.
NSAIDS non-steroidal anti-inammatory drugs, FENa fractional excretion of sodium, SPEP serum
protein electrophoresis
(continued)
Category of
AKI Causes Clinical ndings Treatment
Intrinsic renal
disease
(selected types):
– Acute
tubular
necrosis
(ATN)
– Acute
interstitial
nephritis
– Multiple
myeloma
and other
plasma cell
dyscrasias
• Ischemia
• Sepsis
• Nephrotoxins (cisplatin,
vancomycin,
aminoglycosides,
rhabdomyolysis,
iodinated contrast
agents
• Allergic response to
medication (NSAIDS,
PPIs, and antibiotics)
• Infections
• Rheumatological
disorders
• Increased prevalence
with age
• Acute or chronic kidney
disease
• AKI caused by cast
nephropathy
• Urine sediment
includes epithelial
cells and granular
casts
• FENa >2% (usually
<1% in prerenal
azotemia
• Urine sediment
shows white cells
with or without
WBC casts, absence
of infection
• Eosinophilia on
CBC with
differential
• Low anion gap
• High globulin
• Hypercalcemia
• SPEP and
immunoxation
• Complex conditions
usually require
nephrology
consultation
• Supportive
treatment (may
include dialysis)
• Optimize volume
status
• Avoid nephrotoxins
• Stop offending
medication
• Corticosteroids may
hasten recovery
(after kidney biopsy
to conrm
diagnosis)
• Treat
dysproteinemia
• Supportive renal
care
Conclusion
The management of medical conditions in patients and residents in the long-term
care continuum is challenging due to patient complexity, multimorbidities, guarded
prognosis, individual advance directives for health care, goals of care, and the health
care setting in which care is being provided by an interprofessional team, under the
scrutiny of government and survey agencies. It is essential for practitioners to determine the risks and benets to patients in the identication, assessment, treatment,
and monitoring in the management of multiple clinical conditions. Practitioners need
not forget less common conditions that can afict residents such as cancer, Parkinson’s
disease, polymyalgia rheumatica, traumatic brain injury, and abuse and neglect.
Peals for the Practitioner
• Studies have shown that the treatment of HTN in those over age 80 can result in
a signicant reduction in fatal and nonfatal stroke and all-cause mortality within
1–2years of starting antihypertensive treatment.
• A systematic evaluation is recommended for residents with anemia, and should
be evaluated for comorbid conditions such as loss of physical function, risk for
falls, and cognitive impairment.
160
N. Pandya
• Residents with HF have a 74% or 92% 5-year mortality with either a normal or
reduced LVEF, respectively. HF is a major cause of hospital admissions and
readmissions.
• COPD, the third leading cause of US deaths, is present in one in six people
admitted to nursing facilities and yet remains either unrecognized or suboptimally treated.
• Effective management of diabetes requires an approach that is multifaceted,
protocol- driven, interdisciplinary, and individualized. If used, sliding-scale insulin is best utilized as a supplement to scheduled oral hypoglycemic agents and/or
basal insulin therapy and not as a primary means to control blood glucose.
• Subclinical hypothyroidism is both common and not associated with the classic
signs and symptoms of hypothyroidism are often seen in younger adults. It is not
uncommon in those already diagnosed with DM or vitamin B12 deciency.
• Vitamin B12 deciency in older adults is commonly not associated with anemia
or macrocytosis, so a high index of suspicion is warranted as to its possible
presence.
• For scabies, permethrin 5% cream has a 90% effective cure rate after its rst
application. A second application may be necessary 7–10days.
• Shingrix vaccine is 97% effective in preventing HZ in those 50years and older.
It is given in two doses, 2–6months apart.
Websites
• AMDA-The Society of Post-Acute and Long-Term Care Medicine. https://
paltc.org
• AHA. www.americanheart.org.
• American College of Cardiology. www.acc.org.
• The Global Initiative for Chronic Obstructive Lung Disease. www.goldcopd.com.
• American Diabetes Association. www.diabetes.org.
• American Thyroid Association Professional Guidelines. www.thyroidguide-
lines.net.
• Center for Disease Control and Prevention. www.cdc.gov.
• www.kidney.org/professionals/KDOQI/gfr_calculator.
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