Hypercalcemia

Calcium helps regulate neuromuscular signaling, cardiac conduction, bone turnover, and renal tubular function. When extracellular calcium rises, nerve and muscle cells become less excitable. The result is the familiar slow, weak picture: fatigue, proximal muscle weakness, diminished reflexes, constipation, and slowed thinking. The kidneys are often caught in a worsening cycle. Excess calcium impairs the kidney’s ability to concentrate urine, causing polyuria and polydipsia. Water loss produces volume depletion, which lowers glomerular filtration and reduces calcium excretion. Calcium then rises further. Cardiac conduction also slows. Hypercalcemia shortens the QT interval and can cause bradycardia, atrioventricular conduction abnormalities, and dysrhythmias. Digoxin toxicity is more likely when calcium is elevated. Primary hyperparathyroidism is the leading cause in ambulatory patients. Malignancy is the leading cause in hospitalized patients. The cause matters because urgent calcium reduction stabilizes the patient, but recurrence continues until the source is treated.