Mapping ionized calcium levels and evaluating the outcome of prehospital calcium supplementation in acute trauma and hemorrhagic shock.

BACKGROUND

Hypocalcemia is correlated with poor outcomes in trauma patients and is considered the fourth component in the "diamond of death" alongside acidosis, coagulopathy, and hypothermia.

STUDY DESIGN AND

METHODS

We characterized the kinetics of ionized calcium (iCa) at the point of injury and evaluated the efficacy of prehospital calcium supplementation in a rat model of lethal decompensated hemorrhagic shock. iCa and parathyroid hormone (PTH) were measured in models of hemorrhage-alone (H) or blunt trauma with hemorrhage (TH). Linear regression was used to analyze the correlation between iCa and key laboratory parameters.

RESULTS

Both the H and TH models demonstrated a significant decrease in iCa shortly after the onset of injury. iCa levels were negatively correlated with heart rate, lactate, and sodium. A compensatory increase in PTH was observed in both models. In the H model, a single 20 mg/kg dose of calcium gluconate (CG) alone failed to improve survival. Plasma administration improved survival; however, concurrent administration of CG failed to fully correct hypocalcemia or provide additional benefit.

CONCLUSION

This study demonstrates that while hypocalcemia occurs early and consistently in both models of trauma-hemorrhage, simple calcium repletion is insufficient to improve survival. The lack of additional benefit from calcium supplementation when combined with life-saving plasma suggests that the underlying pathophysiology is more complex than a simple calcium deficit. Future strategies must look beyond mere repletion, investigate other primary drivers of trauma-induced hypocalcemia, and optimize the dosing of calcium supplementation.