POS-216 MECHANISM OF ACUTE HYEPERCALCEMIA FOLLOWING MASSIVE TRANSFUSION DURING ORGAN TRANSPLANT

Abstract

Acute hypocalcemia is a well-recognized complication of massive transfusion but acute hypercalcemia has been described only recently.1 We have recently seen 3 patients with acute transient hypercalcemia that enabled us to elucidate the mechanism of this complication. The records of an opportunity sample of 3 patients who displayed acute hypercalcemia following organ transplantation were reviewed to identify factors possibly relevant to the genesis of the hypercalcemia. Each patient had received a major organ transplant and was transfused a total of 26-67 units of blood products. Ionized calcium rose to a peak of 1.61-2.65 mmol/l postoperatively and total calcium, albeit measured less frequently, also rose. As shown in the table, each patient had received a large amount of calcium chloride (6.25-8.25 G; 56.3-74.3 mmol) intraoperatively. Postoperatively, there was an elevation of the anion gap by 6-12 mmol/l above baseline although the infrequency with which this was measured may have obscured its true magnitude. In each case the elevation of calcium and anion gap resolved within 36 hours or less. Tabled 1PatientOperationUnits of pRBCsUnits of FFPGrams of CaCl2 infusedPeak ionized calcium (mmol/l)Peak total calcium (mg/dl)Duration of high Cai (hrs)Δ AG (mmol/l)1Liver transplant7196.251.61124.5122Heart Transplant111181.8814.434113Liver transplant31368.252.5616.517.76 Open table in a new tab Patients 1 and 2 developed anuric acute renal failure immediately postoperatively and patient 3 was in acute renal failure before the transplant and remained in renal failure Patients receiving massive transfusions are infused large amounts of calcium to prevent hypocalcemia brought about by citrate in the transfused red cells and plasma.2 Calcium infusion is now standard anesthesiologic practice to avoid critical hypocalcemia during transfusion. As a result, at the end of the operation the patient has a large excess of calcium complexed to citrate in the circulation. The presence of citrate is confirmed by the elevation of anion gap above baseline. As the citrate is metabolized, ionized hypercalcemia appears.