• Darrel W Hughes, Elizabeth Vanwert, Lauren Lepori, and Bruce D Adams.
• Department of Pharmacy Services, University Health System, San Antonio, TX, USA; Pharmacotherapy Division, College of Pharmacy, The University of Texas at Austin, TX, USA; Pharmacotherapy Education and Research Center, School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. Electronic address: darrel.hughes@uhs-sa.com.
• Am J Emerg Med. 2014 Jan 1; 32 (1): 112.e3-4.

AbstractLong-term alcohol use confers neurochemical changes in response to alcohol's exogenous inhibitory effects. Downregulation and decreased sensitivity of γ-aminobutyric acid receptors render benzodiazepines less effective at controlling psychomotor agitation. Propofol has been reported to have successfully relieved alcohol withdrawal syndrome (AWS) symptoms in part because of activation of γ-aminobutyric acid channels in combination with antagonism of excitatory amino acids such as N-methyl-D-aspartate. Successful use of propofol in refractory AWS in patients with endotracheal intubation and mechanical ventilation has been reported. We present a case of resolution of AWS symptoms in a benzodiazepine-refractory, nonintubated, non-mechanically ventilated alcohol withdrawal patient with low-dose, continuous-infusion propofol.

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