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Journal Article

Citation

Albrecht JS, Afshar M, Stein DM, Smith GCS. Am. J. Epidemiol. 2018; 187(2): 233-241.

Copyright

(Copyright © 2018, Oxford University Press)

DOI

10.1093/aje/kwx254

PMID

28641392

Abstract

Alcohol exposure results in reduced mortality following traumatic brain injury (TBI) in animal models, yet clinical studies reported conflicting results and clinical trials based on proposed mechanisms have been disappointing.

METHODological issues common to many of the clinical studies may have contributed to spurious results. Our objective was to evaluate the association between blood alcohol concentration (BAC) and in-hospital mortality following TBI, overcoming methodological problems of prior studies. We conducted a retrospective cohort study on individuals treated for isolated TBI at the R Adams Cowley Shock Trauma Center between 1997-2012 (n = 1,084). We excluded individuals with injury to other body regions and examined multiple cut-points 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 following TBI compared to BAC-. In sensitivity analyses among individuals without penetrating (95% firearm) brain injuries (n = 899), the protective association was eliminated. This study provides evidence that the observed protective association between blood alcohol and in-hospital mortality following 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.


Language: en

Keywords

Traumatic brain injury; alcohol; mortality

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