DOSE DEPENDENT VASOPLEGIC SHOCK ASSOCIATED WITH ETHANOL INTOXICATION: A CASE REPORT AND LITERATURE REVIEW

Abstract

SESSION TITLE: Tuesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: One in six US adults binge drinks four times a month as per the Centers for Disease Control and Prevention. Habits such as these place individuals at personal risk, as well as endanger others. Alcohol intoxication can cause physical effects including respiratory depression, hypotension, shock, coma and death. Here we present a patient who presented with respiratory depression, coma, and shock as a consequence of severe ethanol intoxication with remediation of symptoms directly correlating to metabolism and serum ethanol clearance. CASE PRESENTATION: A 43 year old male with no significant past medical history was admitted to our institute for unresponsiveness and undifferentiated shock requiring norepinephrine infusion. His history revealed that he drank 1 gallon of moonshine over the course of 20 minutes. His laboratory data were significant for a non-anion gap metabolic acidosis, osmolar gap of 40, and ethanol level of more than 700 mg/dl. No other toxic alcohols were detected including methanol and ethylene glycol. Other etiologies of shock were ruled out clinically and with lab and imaging data. Serial monitoring of his blood alcohol level was done over the course of two days, with a resolution of obtundation and shock as a direct correlate to decreasing ethanol levels. He was discharged without permanent end-organ damage. DISCUSSION: Five or more alcoholic drinks is considered binge drinking and may result in acute intoxication. Symptoms largely depend on serum ethanol level, with typical ethanol ranges of 50-400mg/dL in intoxicated patients. Exceedingly high levels may result in respiratory depression, coma, and shock, all of which may result in patient death. Focusing on the hemodynamic effects of ethanol intoxication, it has been reported in rat models by Phelan et al that ethanol may blunt hemodynamic regulatory responses to blood loss and dull response to volume resuscitation. Furthermore, it has been shown that ethanol may produce a vasodilatory effect mediated through alteration of central vasomotor control and via inhibition of vasoconstriction caused by catecholamines, angiotensins and vasopressin. Finally, it is thought that ethanol may have direct effects on vascular physiology, as described by Kudo et al. While the pathophysiology remains unclear, we posit that severe alcohol intoxication may produce hypotension and shock that appears to be concentration dependent and reversible when treated with supportive care. CONCLUSIONS: acute alcohol intoxication is a potentially lethal condition that often requires ventilatory and hemodynamic support. The presentation of shock and degree of vasoplegia appear to be dose-dependent, with high levels correlating to more profound shock. Shock is therefore an important cause of mortality in patients with ethanol intoxication, and early and aggressive supportive care is required to mediate its effect and prevent mortality. Reference #1: Severe hypotension and hypothermia caused by acute ethanol toxicity E Wilson and W S Waring Emerg Med J. 2007 Feb; 24(2): e7. https://doi.org/10.1136/emj.2006.041590 Reference #2: Impact of alcohol intoxication on hemodynamic, metabolic, and cytokine responses to hemorrhagic shock.Phelan H, Stahls P, Hunt J, Bagby GJ, Molina PE. J Trauma. 2002 Apr;52(4):675-82. PMID: 11956381 Reference #3: [Effect of alcohol on vascular function].Kudo R, Yuui K, Kasuda S, Hatake K. Nihon Arukoru Yakubutsu Igakkai Zasshi. 2015 Jun;50(3):123-34. PMID: 26502571 DISCLOSURES: No relevant relationships by Michael Bergman, source=Web Response No relevant relationships by CHINTAN RAMANI, source=Web Response