The effects of alcohol on coagulation in trauma patients: Interpreting thrombelastography with caution

Background: The effects of alcohol on coagulation after trauma remain unclear. In vitro studies show that alcohol may decrease clot strength and inhibit fibrinolysis. Observational data indicate that alcohol leads to altered thrombelastography (TEG) parameters indicative of impaired clot formation. Clinical studies have been inconclusive to date.

Methods: Longitudinal plasma sampleswere prospectively collected from 415 critically injured trauma patients at a single Level 1 trauma center and were matched with demographic and outcome data. Citrated kaolin TEG and standard coagulation measures were performed in parallel. Univariate and group comparisons were performed by alcohol status, with subsequent linear and logistic regression analysis.

Results: A total of 264 patients (63.6%) had detectable blood alcohol levels (EtOH, 910 mg/dL). These patients were primarily male (87% vs. 79%), were bluntly injured (77% vs. 59%), and had lower median Glasgow Coma Scale (GCS) score (9.5 vs. 14, all p < 0.05) than the EtOH-negative patients. Therewere no notable differences in pH (7.29 vs. 7.31, p = nonsignificant) or injury severity (median Injury Severity Score [ISS], 11 vs. 14; p = nonsignificant) between the groups. The alcohol-positive patients had a prolonged TEG citrated kaolin R-time (reaction time), or time to initial clot formation (5.91 minutes vs. 4.43 minutes, p = 0.013), prolonged K-time (kinetics time), or time to fixed level of clot strength (1.77 minutes vs. 1.43 minutes, p = 0.036), and decreased > angle (66.5 degrees vs. 70.2 degrees, p = 0.001). In multiple linear regression, for every 10-mg/dL increase in EtOH, R-time was prolonged by 3.84 seconds ( p = 0.015), and > angle decreased by 0.11 degrees ( p = 0.013). However, in multiple logistic regression analyses, EtOH was a negative predictor of coagulopathy by international normalized ratio (91.3) and was not predictive of transfusion requirements or early or late mortality.

Conclusion: Patients with elevated EtOH present with impaired clot formation as assayed by TEG, but this does not correlate with standard measures of coagulopathy or with outcome. Reliance on TEG for determining coagulopathy in intoxicated trauma patients may lead to a misperceived hypocoagulable state and inappropriate transfusion. TEG appears to be affected by EtOH in a previously unreported way, warranting further investigation.