Search

Malnutrition is a common finding in elderly patients, especially at hospitalization. In those whose nutritional status is borderline, the stress of illness may bring about deficiency. Failure to correct malnutrition delays recovery and prolongs hospital stay. Inadequate intake is only one of many causes of nutritional deficiency in the elderly. Traditional height-weight tables are inexact in the elderly. To increase diagnostic accuracy in suspected malnutrition, several methods should be used (eg, calculation of weight loss over time; muscle mass-height comparisons; biochemical and hematologic measurements). After daily energy needs are determined--according to metabolic, activity, and stress expenditures--the best method of nutritional replacement must be determined. Enteral supplementation is the first choice because it sustains the integrity of the gastrointestinal tract. However, delaying implementation of parenteral nutrition when it is required is a common error that should be avoided. Continued supplementation is often needed after discharge. Depending on the health status of the patient, nutritional support can range from temporary admission to a skilled-nursing or extended-care facility to home supplementation through such programs as Meals on Wheels.

Hypercalcemia is most commonly seen in normal infants as the result of normal rapid bone growth. The most common causative diseases are malignant disease and hyperparathyroidism. A variety of pharmacologic agents, especially vitamin D and its metabolites and thiazide diuretics, can elevate serum calcium levels. Hypersensitivity to vitamin D appears to be a cause of hypercalcemia in infants and in patients with granulomatous disease, such as sarcoidosis. Ingestion of escessive amounts of calcium, especially with alkali, may also cause hypercalcemia, as may prolonged immobilization, particularly under conditions of rapid bone turnover.

Hypercalcemia calls first for supportive measures, eg, adequate hydration, movement or mobilization of the patient to the greatest amount tolerated, and reevaluation of drugs being taken. When immediate lowering of the serum calcium level is not clinically mandatory, oral administration of furosemide, corticosteroid, or phosphorus should be considered. In acute emergencies, saline loading and parenteral furosemide therapy should be tried first, except in a patient with renal failure and congestive heart failure, in whom peritoneal dialysis or hemodialysis should be used instead. Calcitonin can be given for the first 12 to 24 hours to lower serum calcium concentration until a definitive management plan is formulated. Corticosteroid, if not contraindicated, should be started as soon as possible. In severe primary hyperparathyroidism with hypophosphatemia, phosphorus can be given intravenously until oral phosphate therapy can be established. Surgery, of course, should be performed as soon as possible. In most cases of neoplasia, mithramycin given according to a recommended schedule is safe and frequently effective. In desperate cases, additional use of prostaglandin synthesis inhibitors probably now is justified by empirical observations. All of these therapeutic measures are used only to stabilize electrolyte balance so that the primary cause of the hypercalcemia can be treated.

Hemodialysis removes uremic toxins and excess fluid from the blood by diffusion dialysis and ultrafiltration. The efficiency of this process depends on the size, shape, and type of semipermeable membrane used in the hemodialyzer. Although the hollow-fiber kidney remains popular, the parallel-plate hemodialyzer is reestablishing itself, partly because it can use newer types of membranes. With newer membranes, ultrafiltration can be performed without diffusion dialysis, which appears to have important clinical advantages. The dialysate bath used in the hemodialyzer resembles plasma water in composition, with electrolytes added to compensate for abnormalities of end-stage renal disease. Although the technical problems of hemodialysis have been largely overcome, an accurate, easy-to-use method of evaluating the adequacy of the hemodialysis prescription has yet to be devised.

Nonsteroidal antiinflammatory drugs can adversely affect the kidney. They may induce sodium retention and antagonize the action of diuretics, impair free-water clearance and cause hyponatremia, and prevent aldosterone production and cause hyperkalemic hyperchloremic acidosis. If patients taking these drugs are exposed to a renal insult, acute renal failure becomes more likely. Similarly, patients with chronic renal disease who are taking them appear to be at greater risk of chronic renal failure. However, not all renal effects of nonsteroidal antiinflammatory drugs are adverse. Beneficial effects have been reported in patients with Bartter's syndrome and in those with severe orthostatic hypotension.

The number of studies in the literature on diagnostic and therapeutic uses of angiotensin antagonists has been increasing geometrically. Nearly 1,000 publishsd items deal with saralasin alone, although neither saralasin nor captopril is yet approved for general use or widely available. Reports to date represent only a fraction of the eventual situations in which these agents are likely to help the researcher and clinician. Food and Drug Administration approval of both agents is pending, and both are expected to be available soon. Consequently, the practitioner will want to become familiar with their usefulness, especially to screen for secondary forms of hypertension and to treat moderate to severe primary or secondary hypertension.