Alcohol Withdrawal in the Inpatient Setting

Kylie Lucas, PharmD, BCPS; Glenn R. Grantner, PharmD, BCPS; Jonathan Street, PharmD

Disclosures

US Pharmacist. 2019;44(11):HS-8-HS12. 

In This Article

Pathophysiology

Alcohol, a central nervous system (CNS) depressant, exerts its effect primarily by altering the neurochemical balance of the brain. This occurs through an increase in the inhibitory effects of the gamma-aminobutyric acid (GABA) pathway and suppression of the excitatory neurotransmitter glutamate, specifically through binding to the N-methyl-D-aspartate (NMDA) receptor. Chronic alcohol use can result in adaptive changes to the neurochemical balance of the brain. To recover homeostasis, a downregulation of GABA-associated receptors and an upregulation of glutamate-associated NMDA receptors occur, leading to a decrease in the CNS effects of alcohol use, which results in tolerance.[5,8–11]

These neurochemical changes may go undetected in patients with prolonged alcohol use; however, upon reduction or cessation of alcohol consumption, serious CNS effects can occur. Without the direct effect of alcohol on the neurotransmitter systems, a dramatic decrease in the inhibitory GABA pathway and increase in the excitatory glutamate-mediated pathway take place. This acute imbalance can result in the CNS effects commonly associated with AWS, including delirium, hallucinations, and decreased seizure threshold.[5,8–10]

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