Early hypocalcemia in severe trauma.

Abstract

We tested the hypothesis that colloid-induced hemodilution can induce hypocalcemia in the early phase of severe trauma resuscitation and tried to assess other potential causative factors of that hypocalcemia. Prospective cohort. Level I academic trauma center. Consecutive severe trauma patients (n = 212, mean Injury Severity Score 34) resuscitated in the prehospital phase without any blood transfusion. At admission, ionized calcium (corrected to an arterial pH = 7.40) was measured. Hypocalcemia was defined as a value <1.15 mmol/L and severe hypocalcemia as a value <0.9 mmol/L. A normal ionized calcium concentration was observed in 56 (26%) patients, a mild ionized hypocalcemia (1.05 +/- 0.06 mmol/L) in 135 (64%) patients, and a severe ionized hypocalcemia (0.77 +/- 0.10 mmol/L) in 21 (10%) patients. There were significant correlations between ionized calcium concentration with the amount of infused colloid (R = .658, p < .001) and arterial pH (R = .760, p < 0.001) but not with the amount of infused crystalloid (R = .007, not significant). Despite taking into account hemodilution, arterial pH, binding of calcium to lactates, and colloids, some patients had marked differences (>15%) between calculated and observed ionized calcium, and these patients had more severe trauma and more frequently had acidosis and/or prehospital cardiac arrest. Using the TRISS methodology, survival was not significantly different from that expected in this trauma population. Hypocalcemia frequently occurs on arrival at the hospital in severe trauma patients, and colloid-induced hemodilution and severe shock and/or ischemia-reperfusion appear to be important causative factors.