W. M. Brigode1, C. Cohan1, G. Beattie1, G. Victorino1 1University of California – San Francisco – East Bay,Department Of Surgery,Oakland, CA, USA
Introduction: Alcohol (EtOH) poses a diagnostic and therapeutic challenge in traumatic brain injuries (TBI) given its impact metabolically and neurologically. Studies on the interaction of EtOH and TBI have had conflicting results. Most suggest increased complications secondary to elevated EtOH, however, the correlation with mortality in TBI remains controversial. We sought to elucidate the patient factors that explain the mixed results and supply further insight into EtOH physiology in TBI. We hypothesized that trauma mechanism, brain injury severity, and blood alcohol concentration (BAC) would influence the impact of EtOH on mortality in TBI.
Methods: We performed a single-institution retrospective review from January 1, 2016 to June 30, 2018 of adult trauma patients admitted to our urban Level I Trauma Center with any measured BAC and a diagnosis of TBI. Exclusion criterion included patients in whom BAC was not assessed. The primary outcome assessed was mortality comparing EtOH positive and negative patients, and at different threshold values of BAC. Secondary outcomes included discharge Glasgow Coma Scale (GCS), Abbreviated Injury Score (AIS) of the head and neck, ventilator days, ICU and total length of stay (LOS), and mechanism subtypes.
Results: Admission EtOH was assessed in 583 patients with TBI, with 256 testing positive for EtOH and 327 testing negative. Overall, intoxicated patients had lower mortality when compared with sober patients (4.7% vs 8.9% respectively, p=0.05). The absence or presence of EtOH showed a two-fold mortality difference, while raising the threshold of BAC to 0.15% improved the benefit to three-fold (mortality 3.1% with BAC<0.15, 9.0% with BAC>0.15, p=0.01). EtOH was also associated with significantly higher discharge GCS (14.2 vs 13.4, p=0.01), reduced likelihood of mechanical ventilation (20.3% vs 30.0%, p=0.008), fewer ventilator days (1.3 vs 2.4, p=0.01), and decreased hospital LOS (7.4 vs 9.4, p=0.02). There was no effect of EtOH on mortality when patients were stratified by AIS-head/neck or admission GCS (p>0.05). When grouped into blunt (n=558) and penetrating trauma (n=25) the mortality benefit remained two-fold for blunt (3.7% intoxicated vs 7.6% sober, p=0.049) but was absent in penetrating trauma. In the blunt trauma sub-group, when trauma associated with automobiles was excluded, the mortality of positive EtOH was increased three-fold from the mortality of sober patients (2.8% intoxicated vs 9.0% sober, p=0.01).
Conclusion: Alcohol appears to be protective against mortality in brain-injured trauma patients. This appears to be most significant in blunt traumatic mechanisms that do not involve motor vehicles. There may be a dose related effect, as we found a three-fold difference in mortality when using a higher BAC threshold of 0.15%. Further research should be done to unravel ongoing controversies in the influence of EtOH on TBI.