TABLE 2313 Causes of Hypercalcemia

PATHOPHYSIOLOGIC EFFECTS The effects of hypercalcemia can be neuromuscular, cardiovascular, gastrointestinal, renal, and skeletal. Neuromuscular changes include decreased sensitivity, responsiveness, and strength of muscular contraction and nerve conduction. This causes increasing weakness and fatigue that may progress to ataxia and altered mental status.

In mild hypercalcemic states, the heart's conduction is slowed and automaticity is decreased with a shortening of the refractory period. There is also increased sensitivity to digitalis preparations.

Loss of renal concentrating ability, as might be expected with nephrogenic DI, is the most frequent renal effect of hypercalcemia. This is a reversible tubular defect, which results in polyuria and dehydration in spite of polydipsia. Potassium wasting results in hypokalemia in up to one-third of patients. Nephrocalcinosis and nephrolithiasis are caused by the hypercalcemia and aggravated by volume depletion. As the hypercalcemia persists, increasing microscopic calcium deposits in the kidney may result in progressive renal insufficiency.

Hypertension is seen with increased frequency in hypercalcemic patients, probably as a result of arteriolar vasoconstriction.

DIAGNOSIS Hypercalcemic patients with plasma total calcium levels below 12.0 mg/dL are usually asymptomatic, but higher levels can cause a wide variety of symptoms and signs (IabIeiiii23-14,).

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