Hypercalcemia in Critically Ill Surgical Patients

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Abstract
Critical surgical illness, commonly accompanied by shock, sepsis, multiple transfusions, and renal failure, is usually associated with low total calcium and/or low or normal ionized calcium. A seminal case of hypercalcemia in a surgical intensive care unit (SICU) patient prompted the review of 100 patients with longer than average SICU days (greater than 12) to determine the incidence, associated factors, and possible etiologies of this condition. Ten patients had elevated measured, and five others had elevated calculated, ionized calcium (5.9 +/- 0.25 mg%), an incidence of 15%. Compared to the 85 patients who did not develop hypercalcemia, this population had a significantly higher frequency of the following: renal failure, dialysis, total parenteral nutrition (TPN) usage greater than 21 days, bacteremic days greater than 1, transfusions greater than 24 units, shock greater than 1 day, SICU days greater than 36, and antibiotics used greater than 7. In addition, this group had significantly more days of hypocalcemia early in their hospital course. There was no difference in sex, age, mortality, or incidence of respiratory failure. Two patients studied in depth had renal failure requiring dialysis and no malignancy, milk-alkali syndrome, hyperthyroidism, or hypoadrenalism. Parathormone (PTH) concentrations were high normal or elevated (N terminal 20 and 21 pg/ml; C terminal 130 microliters Eq/ml and 1009 pg/ml) at the time of elevated calcium (total 9.2 to 14.6 mg%; ionized 4.9 to 8.2 mg%). Immobilization does not increase PTH. In renal failure, PTH elevation is a consequence of hypocalcemia rather than hypercalcemia. Moreover, five patients did not have renal failure. Shock, sepsis, and multiple transfusions containing citrate may lower total and/or ionized calcium and thus stimulate PTH secretion. Whatever the mechanism, approximately 15% of critically ill surgical patients develop hypercalcemia, which may represent a new form of hyperparathyroidism.