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Journal Article

Citation

Howard BM, Kornblith LZ, Redick BJ, Conroy AS, Nelson MF, Calfee CS, Callcut RA, Cohen MJ. J. Trauma Acute Care Surg. 2018; 84(1): 97-103.

Affiliation

From the Department of Surgery (B.M.H., L.Z.K., B.J.R., A.S.C., M.F.N., R.A.C.), San Francisco General Hospital and Division of Pulmonary and Critical Care Medicine, Departments of Medicine and Anesthesia (C.S.C.), University of California San Francisco; San Francisco, California; Denver Health Medical Center (M.J.C.), University of Colorado School of Medicine, Denver, Colorado.

Copyright

(Copyright © 2018, Lippincott Williams and Wilkins)

DOI

10.1097/TA.0000000000001716

PMID

29267182

Abstract

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 suggest that alcohol may inhibit fibrinolysis. We sought to clarify these mechanisms after 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 I 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 (58%) patients with detectable EtOH, median EtOH was 229 mg/dL. These patients were primarily bluntly injured and had lower GCS (p < 0.05) than EtOH-negative patients, but had similar admission pH and injury severity (p = NS). EtOH-positive patients had prolonged ROTEM clotting time and rate of clot formation time (CFT/α); they also had decreased fibrinolysis (max lysis %; all p < 0.05). In linear regression, for every 100 mg/dL increase in EtOH, clotting time increased by 13 seconds and fibrinolysis decreased by 1.5% (both p < 0.05). However, EtOH was not an independent predictor of transfusion requirements or mortality. In high-EtOH patients with coagulopathic ROTEM tracings, transfusion rates were significantly lower than expected, relative to EtOH-negative patients with similar ROTEM findings.

CONCLUSION: As assayed by ROTEM, alcohol appears to have a bidirectional effect on coagulation in trauma, both impairing initial clot formation and inhibiting fibrinolysis. This balancing of mechanisms may explain lack of correlation between altered ROTEM and coagulopathy-related outcomes. Viscoelastic testing should be used with caution in intoxicated trauma patients. LEVEL OF EVIDENCE: Epidemiological study, level III.


Language: en

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