• Jennifer S Albrecht, Majid Afshar, Deborah M Stein, and Gordon S Smith.
• Department of Epidemiology and Public Health, School of Medicine, University of Maryland, Baltimore, Maryland.
• Am. J. Epidemiol. 2018 Feb 1; 187 (2): 233-241.

AbstractAlthough alcohol exposure results in reduced mortality after traumatic brain injury (TBI) in animal models, clinical trials based on proposed mechanisms have been disappointing and have reported conflicting results. Methodological issues common to many of these clinical studies may have contributed to the spurious results. Our objective was to evaluate the association between blood alcohol concentration (BAC) and in-hospital mortality after TBI, and overcome methodological problems of prior studies. We conducted a retrospective cohort study on individuals treated for isolated TBI (n = 1,084) at the R Adams Cowley Shock Trauma Center (Baltimore, Maryland) from 1997 to 2012. We excluded individuals with injury to other body regions and examined multiple cutpoints of BAC. Our primary outcome was in-hospital mortality. In adjusted logistic regression models, the upper level of each blood alcohol categorization from 0.10 g/dL (odds ratio = 0.63, 95% confidence interval: 0.40, 0.97) through 0.30 g/dL (odds ratio = 0.25, 95% confidence interval: 0.08, 0.84) was associated with reduced risk of mortality after TBI compared with individuals with undetectable BAC. In sensitivity analyses among individuals without penetrating brain injuries (95% firearm-related) (n = 899), the protective association was eliminated. This study provides evidence that the observed protective association between BAC and in-hospital mortality after TBI resulted from bias introduced by inclusion of penetrating injuries.© The Author(s) 2017. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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