The syndromes of failure to thrive, pressure ulcers, and falls share features that make them particularly challenging. Their etiologies are multifactorial; they require an interdisciplinary approach to maximize care; and they often herald disability, institutionalization, and death. Small improvements in multiple domains can improve outcomes. Maintaining open communication with patients and/or caregivers is vital. Empower them to play a role in their care and keep expectations realistic. The physician can and should maintain a therapeutic relationship with the patient and the family beyond the time medical therapies are effective. Home visits enhance this relationship and often reveal opportunity for intervention.

Essentials of Diagnosis

• Weight loss of more than 5%.
  
• Functional decline.
  
• Depression.
  
• Cognitive impairment.

General Considerations

The National Institute on Aging defined failure to thrive (FTT) as “a syndrome of weight loss, decreased appetite and poor nutrition, and inactivity, often accompanied by dehydration, depressive symptoms, impaired immune function, and low cholesterol.” Two new concepts, cachexia and sarcopenia, have enhanced our understanding of the pathophysiology of FTT and should be considered in the approach to the patient. Cachexia is the catabolic state seen in illnesses such as cancer, end-stage renal disease, lung disease, and heart failure. It is progressive and characterized by weight loss, anorexia, inflammation and insulin resistance; nutrition therapy does not alter the course. Sarcopenia is loss of muscle mass that occurs with aging. It is associated with functional decline, disability, and falls; it is mitigated by exercise.

Clinical Findings

Symptoms and Signs

Weight loss is an essential feature. Functional decline contributes to falls, poor grooming, depression, and cognitive decline. As in infants, FTT can occur from organic and nonorganic causes necessitating an approach that includes medical, psychological, functional, and social domains.

History and Physical Examination

The history provided by the patient and caregiver can help identify common acute triggers: change in medication, infection, constipation, pain, loss, or grief. Undiagnosed chronic diseases: endocrine, tuberculosis, dementia, depression, substance abuse, and rarely, hypoactive delirium may trigger FTT.

Assess, do not assume, medication compliance; have the patient demonstrate how he/she is taking all prescription and over-the-counter medications. Drug effects and interactions should not be underestimated. Alendronate, antiarrhythmics, antihistamines including H2 blockers, α-antagonists, benzodiazepines, β-blockers, calcium antagonists, colchicine, digoxin even within therapeutic range, diuretics, iron or zinc, metformin, metronidazole, neuroleptics, nonsteroid anti-inflammatory drugs (NSAIDs), narcotics, steroids, SSRIs, tricyclic antidepressants, and xanthines have been associated with FTT. Levels are nonspecific; normal therapeutic levels can have adverse effects. Be aware of genetic and racial variation in drug metabolism.

A comprehensive physical examination should focus on those items noted in Table 40-1. Laboratory evaluations should include complete blood count (CBC), comprehensive metabolic panel (CMP), thyroid-stimulating hormone (TSH), erythrocyte sedimentation rate (ESR), total 25-OH vitamin D, B12 (if 200-400 pmol/L check a methylmalonic and homocysteine levels.) Additional workup could include fecal occult blood, purified protein derivative, and urinalysis.

Treatment

Assessment and Plan

Address modifiable medical conditions. Discuss risk/benefit of watchful waiting for conditions whose interventions carry high morbidity and mortality. Appetite stimulants are neither approved nor recommended and carry significant side effects. As medical interventions become more limited, palliative or hospice services should be initiated.

Team Approach

Simplify medications with help of a PharmD. Enlist the help of the Area Agency on Aging (AAA) [www.aoa.dhhs.gov or (800) 677–1116, “Elder Care Locater”]. Concerns about neglect or abuse should be discussed openly and nonjudgmentally; and should be reported. Home Health can supply short-term nursing, social worker, dietician, physical and occupational therapy and aide services.

Essentials of Diagnosis

• A skin ulcer caused by ischemia due to prolonged pressure or pressure in combination with shear and/or friction.
  
• Occur on weight bearing or bony prominences: ex: sacrum, hip, heel.
  
• Differentiate from ulcers caused by venous or arterial insufficiency.

New Considerations: Systems-Based Practice

In 2007, the Centers for Medicare and Medicaid Services (CMS) deemed pressure ulcers a “high cost, high volume” condition that was preventable. 2007 costs were estimated at $11 billion. Effective October 2008, Medicare began denying reimbursement for a stage 3 or 4 ulcer as a secondary diagnosis unless it was “present on admission (POA.)” Physician documentation is required for coders to use the POA qualifier. Hospital reimbursement is not the only arena affected by physician compliance. Pressure ulcers are projected to be a Joint Commission Quality Indicator and are one of the most highly litigated medical conditions in the United States. Physicians should be familiar with the 2007 National Pressure Ulcer Advisory Panel (NPUAP) staging system and document skin status in the daily note.

Pathogenesis

Extrinsic and intrinsic factors cause pressure ulcers. Extrinsic factors are prolonged pressure, moisture, friction, and shear. Intrinsic causes are the susceptibility of aged skin (less thickness and elasticity), loss of sensation, circulatory compromise, immobility, weight loss, dehydration, malnutrition, and cognitive impairment including sedation.

Prevention

On admission and daily, document the condition of the occiput, spinous processes, scapulae, elbows, sacrum, ischia, greater trochanters, malleoli, and heels. Extra vigilance is needed in cognitively or sensory impaired elders who wear support stockings, casts, or other orthopedic devices. These should be removed for inspection when possible. The admitting nurse will also do a complete skin assessment; the physician should review, verify, and document concurrence with the findings. Table 40-2 summarizes the AHRQ (Agency for Healthcare Research and Quality) guidelines for pressure ulcer prevention. Screening scales such as Braden and Norton help quantify risk and tailor treatment plans. The downside to these scales is the misconception that low- and moderate-risk patients are not as vulnerable: it takes them 2 hours to develop a Stage I ulcer just like the high-risk patient. Although never studied, patient repositioning every 2 hours remains a mainstay in clinical practice.

Differential Diagnosis

Among the differential diagnoses for pressure ulcers are vascular ulcers, diabetic ulcers, and cellulitis. Venous ulcers are the result of prolonged venous hypertension and are usually located over the medial malleolus. Arterial ulcers are predominantly caused by atherosclerotic vessels, and may be located between toes, over phalangeal heads, or around the lateral malleolus. Diabetic ulcers are produced by a variety of factors: micro and macrovascular injury, peripheral neuropathy, and mechanical changes in the bony architecture of the foot. These are usually located on the plantar aspect of the foot, metatarsal heads, or under the heel. Cellulitis is an acute inflammation of the dermis and subcutaneous tissue and thus blanches with palpation.

The National Pressure Ulcer Advisory Panel Classification

Stage I

Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons (a heralding sign of risk.)