Hypoparathyroidism is usually due to deficiency of PTH following parathyroidectomy. Clinical
manifestations of hypoparathyroidism are a result of hypocalcemia ( Table 34–8), which can also be caused by kidney failure, hypomagnesemia, vitamin D deficiency, and acute pancreatitis . Hypoalbuminemia decreases total serum calcium (a 1 g/dL drop in serum albumin causes a 0.8 mg/dL decrease in total serum calcium), but ionized cal-cium, the active entity, is unaltered. The archetypi-cal presentation of hypocalcemia is tetany, classically diagnosed by Chvostek’s sign (painful twitching of the facial musculature following tapping over the facial nerve) or Trousseau’s sign (carpal spasm fol-lowing inflation of an arm tourniquet above sys-tolic blood pressure for 3 min). These signs are also occasionally present in nonhypocalcemic persons. Treatment of symptomatic hypocalcemia consists of intravenous administration of calcium salts.
Mild hypocalcemia is common following car-diopulmonary bypass or infusion of albumin solu-tions. In many adult patients this need not be treated as the response of the PTH–vitamin D axis will usu-ally be sufficient to restore ionized calcium to nor-mal values and mild hypocalcemia will usually have no hemodynamic consequences.
Serum calcium should be normalized in any patient who presents with cardiac manifestations of severe hypocalcemia. Alkalosis from hyperventilation or sodium bicarbonate therapy will further decrease ionized calcium. Although citrate-containing blood products usually do not lower serum calcium sig-nificantly, they should be administered cautiously in patients with preexisting hypocalcemia. Otherconsiderations include avoiding the use of albumin solutions (which bind and reduce ionized calcium concentrations) and being mindful of the possibility of coagulopathy.
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