Acute Ethanol Intoxication and the Trauma Patient: Hemodynamic Pitfalls.
Summary of "Acute Ethanol Intoxication and the Trauma Patient: Hemodynamic Pitfalls."
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.
Department of Surgery, University of California San Francisco - Fresno Campus, Fresno, CA, USA, firstname.lastname@example.org.
This article was published in the following journal.
Name: World journal of surgery
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21748516
- DOI: http://dx.doi.org/10.1007/s00268-011-1191-7
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Medical and Biotech [MESH] Definitions
An acute brain syndrome which results from the excessive ingestion of ETHANOL or ALCOHOLIC BEVERAGES.
A condition where seizures occur in association with ethanol abuse (ALCOHOLISM) without other identifiable causes. Seizures usually occur within the first 6-48 hours after the cessation of alcohol intake, but may occur during periods of alcohol intoxication. Single generalized tonic-clonic motor seizures are the most common subtype, however, STATUS EPILEPTICUS may occur. (Adams et al., Principles of Neurology, 6th ed, p1174)
Acute kidney failure resulting from destruction of EPITHELIAL CELLS of the KIDNEY TUBULES. It is commonly attributed to exposure to toxic agents or renal ISCHEMIA following severe TRAUMA.
Proteins that are secreted into the blood in increased or decreased quantities by hepatocytes in response to trauma, inflammation, or disease. These proteins can serve as inhibitors or mediators of the inflammatory processes. Certain acute-phase proteins have been used to diagnose and follow the course of diseases or as tumor markers.
Acute and chronic neurologic disorders associated with the various neurologic effects of ETHANOL. Primary sites of injury include the brain and peripheral nerves.