Abstract
Many
trauma patients are acutely intoxicated with alcohol. Animal studies have demonstrated that
acute alcohol
intoxication inhibits the normal release of epinephrine, norepinephrine, and vasopressin in response to
acute hemorrhage.
Ethanol also increases nitric oxide release and inhibits antidiuretic hormone secretion. This article studies the effects of alcohol
intoxication (measured by blood alcohol level, BAL) on the presentation and resuscitation of
trauma patients with blunt hepatic
injuries. A retrospective registry and chart review was conducted of all
patients who presented with blunt liver
injuries at an ACS-verified, level I
trauma center. Data collected included admission BAL, systolic blood pressure, hematocrit, International Normalized Ratio (INR), liver injury grade, Injury Severity Score (ISS), intravenous fluid and blood product requirements, base deficit, and mortality. From September 2002 to May 2008, 723
patients were admitted with blunt hepatic
injuries. Admission BAL was obtained in 569
patients, with 149 having levels >0.08%. Intoxicated
patients were more likely to be hypotensive on admission (p = 0.01) despite a lower liver injury grade and no significant difference in ISS. There was no significant difference in the percent of intoxicated
patients requiring blood transfusion. However, when blood was given, intoxicated
patients required significantly more units of packed red blood cells (PRBC) than their nonintoxicated counterparts (p = 0.01). Intoxicated
patients also required more intravenous fluid during their resuscitation (p = 0.002). Alcohol
intoxication may impair the ability of blunt
trauma patients to compensate for
acute blood loss, making them more likely to be hypotensive on admission and increasing their PRBC and intravenous fluid requirements. All
trauma patients should have BAL drawn upon admission and their resuscitation should be performed with an understanding of the physiologic alterations associated with
acute alcohol
intoxication.
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