Transfusion · 2026
Mapping ionized calcium levels and evaluating the outcome of prehospital calcium supplementation in acute trauma and hemorrhagic shock.
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Walsh Richard W, Meledeo Michael A, Nicolson Susannah E, Sanchez Antonio O, Orlando Hernandez Rivera, Wu Xiaowu
Аннотация
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.
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.