Early platelet dysfunction: an unrecognized role in the acute coagulopathy of trauma.

Abstract

Our aim was to determine the prevalence of platelet dysfunction using an end point of assembly into a stable thrombus after severe injury. Although the current debate on acute traumatic coagulopathy has focused on the consumption or inhibition of coagulation factors, the question of early platelet dysfunction in this setting remains unclear. Prospective platelet function in assembly and stability of the thrombus was determined within 30 minutes of injury using whole blood samples from trauma patients at the point of care using thrombelastography-based platelet functional analysis. There were 51 patients in the study. There were significant differences in the platelet response between trauma patients and healthy volunteers, such that there was impaired aggregation to these agonists. In trauma patients, the median ADP inhibition of platelet function was 86.1% (interquartile range [IQR] 38.6% to 97.7%) compared with 4.2 % (IQR 0 to 18.2%) in healthy volunteers. After trauma, the impairment of platelet function in response to arachidonic acid was 44.9% (IQR 26.6% to 59.3%) compared with 0.5% (IQR 0 to 3.02%) in volunteers (Wilcoxon nonparametric test, p < 0.0001 for both tests). In this study, we show that platelet dysfunction is manifest after major trauma and before substantial fluid or blood administration. These data suggest a potential role for early platelet transfusion in severely injured patients at risk for postinjury coagulopathy.