Effects of Ethanol in Traumatic Brain Injury

Abstract

The effects of ethanol intoxication on brain injury and cerebral blood flow (CBF) were investigated in a porcine fluid-percussion model of traumatic brain injury (TBI). Immature swine, under halothane anesthesia (1%), had a TBI delivered with a fluid-percussion device. The experimental group (n = 10) received ethanol (3.5 gm/kg) via gastric tube followed in 1 h by TBI. Two groups of control animals received normal saline and TBI (n = 10) or ethanol and no TBI (n = 5). Mean arterial blood pressure (MAP), intracranial pressure (ICP), arterial blood gases, and serum lactate were monitored for 3 h after the injury. CBF was measured with radiolabelled 15-micron diameter microspheres. Neuropathologic changes were evaluated and graded after formalin perfusion and brain removal at 3 h postinjury. The ethanol level 60 min post-head injury was 198 ± 70 (SD) mg/dL in the ethanol + TBI group. At 90 min postinjury and thereafter, ethanol + TBI animals compared with TBI only animals had significantly lower MAP (63 ± 26 mmHg vs 91 ± 15 mmHg) and lower cerebral perfusion pressure (50 ± 25 mmHg vs 78 ± 15), and at 180 min postinjury, lower CBF (87 ± 37% vs 62 ± 79% of preinjury levels). Ethanol + TBI animals had higher blood lactates (28 ± 11 mg/dL vs 13 ± 6 mg/dL) than TBI only animals. Ethanol + TBI animals also had significantly longer postinjury apneas (11 ± 8 min vs 0.6 ± 0.4 min), with three of ten ethanol-treated animals never recovering spontaneous respiration. Ethanol intoxication produced hemodynamic and respiratory changes, which may have a deleterious effect on outcome and mortality after brain injury.