ABSTRACT
Alcohol is a psychotropic depressant of the Central Nervous System (CNS) and acts via stimulation of Gamma-Aminobutyric Acid (GABA), the main inhibitory neurotransmitter of the CNS, and the inhibition of glutamate, the main central excitatory neurotransmitter. It increases the activity of GABA, by increasing chloride channel openings at the GABA receptors. Development of alcohol withdrawal symptoms has been correlated with increased hospital stay, risk of mechanical ventilation, costs, risk of readmission with withdrawal, and mortality. As compared to a scheduled treatment regimen, a symptom-triggered therapy individualizes treatment, decreases treatment duration as well as the amount of benzodiazepine used, and is as efficacious as a standard fixed-schedule therapy for alcohol withdrawal. The most concerning of which is Wernicke's encephalopathy and Korsakoff syndrome which can be avoided with early thiamine administration. Folate and magnesium deficiency can also lead to confusion, psychosis, seizures, and QT prolongation.
