Delirium tremens (DTs) is the most severe form of ethanol withdrawal; it is manifested by altered mental status (global confusion) and sympathetic overdrive (autonomic hyperactivity), which can progress to cardiovascular collapse. DTs is a medical emergency with a high mortality rate, making early recognition and treatment essential. (See Prognosis, Clinical Presentation, Differentials, Workup, and Treatment.)
Chronic intake of alcohol affects several neurotransmitter systems in the brain. These effects include increased release of endogenous opiates; activation of the gamma-aminobutyric acid-A (GABA-A) receptor and a decrease in GABA-A receptor function, with a resultant influx of chloride ions; inhibition of the N -methyl-D-aspartate (NMDA) type of glutamate receptor (which mediates the postsynaptic excitatory effects of glutamate), with up-regulation of this receptor; and interactions with serotonin and dopamine receptors. (See Etiology.)
During withdrawal from alcohol, the loss of GABA-A receptor stimulation causes a reduction in chloride flux and is associated with tremors, diaphoresis, tachycardia, anxiety, and seizures. In addition, the lack of inhibition of the NMDA receptors may lead to seizures and delirium. Excessive nervous system excitability during periods of abstinence from alcohol is related to the effect of alcohol on the number and function of brain receptors.