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Effects of Ethanol in an Experimental Model of Combined Traumatic Brain Injury and Hemorrhagic Shock
Author(s) -
Zink Brian J.,
Stern Susan A.,
Wang Xu,
Chudnofsky Carl C.
Publication year - 1998
Publication title -
academic emergency medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.221
H-Index - 124
eISSN - 1553-2712
pISSN - 1069-6563
DOI - 10.1111/j.1553-2712.1998.tb02568.x
Subject(s) - medicine , anesthesia , cerebral blood flow , cerebral perfusion pressure , traumatic brain injury , hemodynamics , resuscitation , intracranial pressure , ethanol , perfusion , shock (circulatory) , mean arterial pressure , blood pressure , heart rate , chemistry , organic chemistry , psychiatry
Objectives: Given 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. Methods: A 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. Results: Ethanol 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 O 2 saturation in the postinjury period. Cerebral O 2 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. Conclusion: In this TBI/HS model, ethanol administration decreased survival time, impaired the hemodynamic response, and worsened measures of cerebral tissue perfusion.