Transient hypocalcemia often occurs in critically ill pts with burns, sepsis, and acute renal failure; following transfusion with citrated blood; or with medications such as protamine and heparin. Hypoalbuminemia can reduce serum calcium below normal, although ionized calcium levels remain normal. The above-mentioned correction (see Hypercalcemia) can be used to assess whether the serum calcium concentration is abnormal when serum proteins are low. Alkalosis increases calcium binding to proteins, and in this setting direct measurements of ionized calcium should be used.
The causes of hypocalcemia can be divided into those in which PTH is absent (hereditary or acquired hypoparathyroidism, hypomagnesemia), PTH is ineffective (chronic renal failure, vitamin D deficiency, anticonvulsant therapy, intestinal malabsorption, pseudohypoparathyroidism), or PTH is overwhelmed (severe, acute hyperphosphatemia in tumor lysis, acute renal failure, or rhabdomyolysis; hungry bone syndrome following parathyroidectomy). The most common forms of chronic severe hypocalcemia are autoimmune hypoparathyroidism and postoperative hypoparathyroidism following neck surgery. Chronic renal insufficiency is associated with mild hypocalcemia compensated for by secondary hyperparathyroidism. The cause of hypocalcemia associated with acute pancreatitis is unclear.
Treatment: Hypocalcemia Symptomatic hypocalcemia may be treated with IV calcium gluconate (bolus of 1-2 g IV over 10-20 min followed by infusion of 10 ampoules of 10% calcium gluconate diluted in 1 L D5W infused at 30-100 mL/h). Management of chronic hypocalcemia requires a high oral calcium intake, usually with vitamin D supplementation. Hypoparathyroidism requires administration of calcium (1-3 g/d) and calcitriol (0.25-1 µg/d), adjusted according to serum calcium levels and urinary excretion. Restoration of magnesium stores may be required to reverse hypocalcemia in the setting of severe hypomagnesemia. |
Section 13. Endocrinology and Metabolism