Early recognition and management of hemorrhage, damage control resuscitation, and blood product administration have optimized management of severe trauma. Recent data suggest hypocalcemia exacerbates the ensuing effects of coagulopathy in trauma.

This narrative review of available literature describes the physiology and role of calcium in trauma resuscitation. Authors did not perform a systematic review or meta-analysis.

Calcium is a divalent cation found in various physiologic forms, specifically the bound, inactive state and the unbound, physiologically active state. While calcium plays several important physiologic roles in multiple organ systems, the negative hemodynamic effects of hypocalcemia are crucial to address in trauma patients. The negative ramifications of hypocalcemia are intrinsically linked to components of the lethal triad of acidosis, coagulopathy, and hypothermia. Hypocalcemia has direct and indirect effects on each portion of the lethal triad, supporting calcium's potential position as a fourth component in this proposed lethal diamond. Trauma patients often present hypocalcemic in the setting of severe hemorrhage secondary to trauma, which can be worsened by necessary transfusion and resuscitation. The critical consequences of hypocalcemia in the trauma patient have been repeatedly demonstrated with the associated morbidity and mortality. It remains poorly defined when to administer calcium, though current data suggest that earlier administration may be advantageous.

Calcium is a key component of trauma resuscitation and the coagulation cascade. Recent data portray the intricate physiologic reverberations of hypocalcemia in the traumatically injured patient; however, future research is needed to further guide the management of these patients.