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Hypocalcemia may be associated with a spectrum of clinical manifestations (table 1), ranging from few if any symptoms if the hypocalcemia is mild, to life-threatening seizures, refractory heart failure, or laryngospasm if it is severe. In addition to severity, the rate of development of hypocalcemia and chronicity determine the clinical manifestations.
Among the symptoms of hypocalcemia, tetany, papilledema, and seizures may occur in patients who develop hypocalcemia acutely. By comparison, ectodermal and dental changes, cataracts, basal ganglia calcification, and extrapyramidal disorders are features of chronic hypocalcemia. These last findings are most common in patients with hypoparathyroidism.
The clinical manifestations of hypocalcemia are discussed here. The etiology of, diagnostic approach to, and the treatment of hypocalcemia are discussed separately. (See "Etiology of hypocalcemia in adults" and "Diagnostic approach to hypocalcemia" and "Treatment of hypocalcemia".)
The hallmark of acute hypocalcemia is tetany, which is characterized by neuromuscular irritability. The symptoms of tetany may be mild (peri-oral numbness, paresthesias of the hands and feet, muscle cramps) or severe (carpopedal spasm, laryngospasm, and focal or generalized seizures, which must be distinguished from the generalized tonic muscle contractions that occur in severe tetany). Other patients have less specific symptoms such as fatigue, hyperirritability, anxiety, and depression, and some patients, even with severe hypocalcemia, have no neuromuscular symptoms.
Tetany — Acute hypocalcemia directly increases peripheral neuromuscular irritability [1]. As measured electromyographically, tetany consists of repetitive high-frequency discharges after a single stimulus. Hyperexcitability of peripheral neurons is probably the most important pathophysiologic effect of hypocalcemia, but hyperexcitability occurs at all levels of the nervous system, including motor end-plates, the spinal reflexes, and the central nervous system.
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