Alcohol withdrawal delirium, also known as delirium tremens.
Among patients with seizures related to alcohol abuse, the risk of death is 4 times as great as the risk in the general population, but the increase risk is related to alcoholism rather than seizures.
A clinical diagnosis characterized by increased arousal, confusion, hallucinations, hypertension, fever, tachycardia, diaphoresis, and agitation following abrupt reduction in alcohol consumption or sudden abstinence from alcohol.
Symptoms vary widely among individuals, and among different withdrawal episodes in the same person.
Seizures can occur.
Typically manifests 6-8 hours after the last exposure to alcohol, and is most pronounced during the first 24 to 72 hours.
Management is directed at alleviating symptoms and identifying and correcting metabolic derangements.
Type indicator for alcohol withdrawal is a symptom-based assessment tool that guides treatment decisions and monitors clinical response.
Alcohol withdrawal is believed to be related to its affect on the central nervous system primarily by facilitating the actions of gamma-aminobutyric acid the major inhibitory neurotransmitter in the brain.
Alcohol increases the inhibitory effects of the GABAa receptor, while also suppressing the brain’s major excitatory neurotransmitter, glutamate, at the N-metyl-D-aspartate receptor (NMDA).
Chronic excess alcohol use results in changes of the GABA and glutamate neurotransmitter systems to compensate for the effects of alcohol on neural pathways to restore neurochemical equilibrium.
With the sudden cessation or significant reduction in alcohol consumption there is an acute neurotransmitter imbalance with a rapid decline in inhibitory GABA activity and increased excitatory glutamate NMDA areceptor activity, which results in increased CNS activity and the lower threshold for seizures.
Type A symptoms are characterized by CNS excitation such as anxiety and restlessness caused by gamma aminobutyric acid (GABA) withdrawal.
Type A symptoms are treated with GABA agonists, most commonly benzodiazepines.
Type B symptoms relate to fever, diaphoresis, tremor and hypertension with tachycardia caused by adrenergic access from activation of the locus ceruleus due to a hyperglutamine like-state.
Beta- blocker therapy is useful to manage type B symptoms.
Type C symptoms are caused by excess dopamine release via the mesolimbic tract and consist of confusion, hallucinations, paranoiac state and agitation.
Type C symptoms are treated with dopamine agonists.
Benzodiazepines generally first line agents for alcohol withdrawal syndromes and for the prevention of seizures related to alcohol withdrawal.
Benzodiazepines have the largest and the best evidence base in the treatment of alcohol withdrawal and are considered the gold standard of alcohol detoxification.
No best benzothiazine is indicated, but long- acting agents allow for a smoother course of withdrawal, decrease seizures, and prevention of delirium.
Benzodiazepines, with intermediate half- life have a safe profile in patients with hepatic dysfunction.
Patients may experience multifactorial delirium, which commonly occurs in patients admitted to ICUs, as part of the acute brain dysfunction.
Clinical features of alcohol dependence include tolerance and withdrawal.
With repeated doses of alcohol, neurotransmitter responses are diminished, and increase doses are required to produce the same effects.
Abrupt cessation of alcohol produces rebound effects experienced as alcohol withdrawal symptoms.