• B J Zink, S A Stern, X Wang, and C C Chudnofsky.
• Department of Surgery, University of Michigan, Ann Arbor, USA. bzink@umich.edu
• Acad Emerg Med. 1998 Jan 1;5(1):9-17.

ObjectivesGiven that clinical and laboratory studies suggest that ethanol and hemorrhagic shock (HS) potentiate traumatic brain injury (TBI), the authors studied the effects of ethanol in a model of combined TBI and HS.MethodsA controlled porcine model of combined TBI and HS was evaluated for the effect of ethanol on survival time, hemodynamic function, and cerebral tissue perfusion. Anesthetized swine (17-24 kg) were instrumented, splenectomized, and subjected to fluid percussion TBI with concurrent 25-mL/kg graded hemorrhage over 30 minutes. Two groups were studied: control (n = 11) and ethanol (n = 11). Ethanol, 3.5 g/kg intragastric, was given 100 minutes prior to TBI/HS. Systemic and cerebral physiologic and metabolic parameters were monitored for 2 hours without resuscitation. Regional cerebral blood flow (rCBF) and renal blood flow were measured with dye-labeled microspheres. Data were analyzed with 2-sample t-test and repeated-measures ANOVA.ResultsEthanol levels at the time of injury were 162 +/- 68 mg/dL. Average TBI was 2.65 +/- 0.35 atm. Survival time was significantly shorter in the ethanol group (60 +/- 27 min vs 94 +/- 28 min, p = 0.011). The ethanol group had significantly lower mean arterial pressure, cerebral perfusion pressure, and cerebral venous O2 saturation in the postinjury period. Cerebral O2 extraction ratios and cerebral venous lactate levels were significantly higher in the ethanol group. A trend toward lower postinjury rCBF in all brain regions was observed in the ethanol group.ConclusionIn this TBI/HS model, ethanol administration decreased survival time, impaired the hemodynamic response, and worsened measures of cerebral tissue perfusion.

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