Background: Alcohol has been associated with altered viscoelastic testing in trauma, indicative of impaired coagulation. Such alterations, however, show no correlation to coagulopathy-related outcomes. Other data suggests that alcohol may inhibit fibrinolysis. We sought to clarify these mechanisms following traumatic injury using thromboelastometry (ROTEM), hypothesizing that alcohol-related clot formation impairment may be counter-balanced by inhibited fibrinolysis. Methods: Laboratory, demographic, clinical, and outcome data were prospectively collected from 406 critically-injured trauma patients at a Level 1 Trauma Center. ROTEM and standard coagulation measures were conducted in parallel. Univariate comparisons were performed by alcohol level (EtOH), with subsequent regression analysis. Results: Among 274 patients (58%) with detectable EtOH, median EtOH was 229 mg/dL. These patients were primarily bluntly injured and had lower GCS (p
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