Early Calcium Replacement Is Associated With Reduced Mortality in Transfusion After Injury

Hemorrhage remains a leading cause of death after trauma. Hypocalcemia is a marker of severe injury and a predictor of mortality, particularly among patients receiving blood products. Although calcium supplementation during resuscitation has been recommended, its association with outcomes remains unclear. We evaluated the association between early calcium supplementation and mortality in injured patients requiring blood transfusion.

We conducted a retrospective cohort study at a level I trauma center from 2010 to 2022. Patients were included if they received more than one unit of blood product within 6 h of injury. Early calcium supplementation was defined as administration within 4 h of the first transfused unit. Outcomes included the incidence of hypocalcemia and hypercalcemia and in-hospital mortality across initial ionized calcium levels. Multivariable logistic regression was used to assess the association between early calcium and mortality after adjustment for confounders.

A total of 547 patients met inclusion criteria, of whom 92 (17%) received early calcium. Patients receiving early calcium were more likely to experience hypocalcemia or hypercalcemia. Mortality was higher in patients with both hypocalcemia and hypercalcemia. While hypocalcemia was associated with total blood product requirements (P = 0.012), early calcium supplementation was not (P = 0.882). After risk adjustment, early calcium supplementation was associated with a 68% reduction in the odds of in-hospital mortality (adjusted OR 0.32; 95% confidence interval 0.11-0.94; P = 0.039).

Among trauma patients receiving early blood products, early calcium supplementation was associated with lower mortality. These findings provide support for the use of early calcium during trauma resuscitation and have implications for resuscitation protocols. Additional work is required to determine the optimal regimen for repleting calcium in these patients as well as the mechanism that links hypocalcemia and trauma mortality.