The Role of Calcium in Augmenting the Efficacy of Primary Homeostasis after Hemorrhagic Shock

Abstract

Background: Traumatic Hemorrhagic Shock (THS) causes hypocalcemia (Ca). This study assesses how low Ca affects platelet (Plt) function. Study Design: A research registry was queried for 555 studies on 341 patients (pts) with THS requiring 14.2 units RBC, 8.4 units FFP, 3.6 units Plt, and 18.9 mEq Ca by end of O.R. (7.3 hours). Factors analyzed included Plt count, Ca, Bleeding Time (BT), Plt aggregation with ADP (PAadp) and collagen (PAcol), including Max PA, T1/2 PA, and rate PA, plus platelet release factors, beta thromboglobulin (BTG) and Plt PF-4. Studies were made in O.R. (26 pts) during fluid uptake phase II at 29 hours (216 pts), during fluid mobilization phase III at 56 hours (283 pts), and as outpatients (30 pts). Results: THS caused low Plts (1x10 SD) in O.R (107 ± 43), in phase II (96 ± 35), and in phase III (105 ± 59) and low Ca in O.R. (1.6 ± 0.3), in phase II (1.8 ± 0.2), and in phase III (2.1 ± 0.2). Low Plt and Ca correlated (p=<0.05) with PAadp and PAcol in O.R., phase II, and phase III. Ca correlated directly with Plt count, aggregation, BTG and PF-4, and inversely with BT. All outpatient studies were normal. Conclusion: THS causes Ca which leads to low Plt and impaired function. Routine Ca supplementation is recommended for THS.