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Psychiatry · Chapter 21. Disorders due to use of alcohol and other psychoactive substances

Delirium tremens

*Delirium tremens*

Alcohol withdrawal delirium (delirium tremens) is a severe psychosis that occurs in patients with an established pattern of alcohol dependence. The development of delirium clearly indicates that alcoholism has progressed to stage II, which is accompanied by a pronounced withdrawal syndrome.

StageDevelops only in stage II (established) alcoholism.
CauseSevere alcohol withdrawal syndrome.
SignificanceA history of delirium is a reliable criterion for the transition of the disease to the established phase.
3 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Place of alcohol delirium in the course of the disease

Alcohol delirium (delirium tremens) does not occur out of nowhere or in the early stages of dependence. This complication is associated with stage II alcoholism (subcompensated, or addictive stage).

In stage I (when craving is still obsessive and there is no pronounced physical dependence), the conditions for psychoses do not exist. Only when the patient develops a severe alcohol withdrawal syndrome (AWS) is the groundwork laid for psychotic complications, the most well-known of which is delirium.

Features of stage II alcoholism

The development of delirium occurs against the background of profound changes in the patient's body and psyche. The stage at which delirium is possible is characterized by:

  • Compulsive craving: the patient's will is broken, the craving for alcohol is irresistible and closely linked to the withdrawal syndrome.
  • Loss of insight: the patient denies the severity of their condition, suppressing guilt using psychological defense mechanisms.
  • The presence of severe withdrawal syndrome, which is the main trigger for psychosis.
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Association with other complications

Delirium is not the only psychosis occurring in stage II. Against the background of the same severe withdrawal syndrome, the following may develop:

  • Alcoholic hallucinosis.
  • Alcoholic paranoid psychosis.
  • Korsakoff's psychosis (which is also an outcome of alcoholic polyneuropathy).

Briefly: answers to topical questions

What clinical symptoms make up the classic picture of alcohol delirium?

The classic picture of alcohol delirium includes acute psychosis with altered consciousness, true hallucinations, and somatic disorders.

Main clinical manifestations:

  • Psychopathological symptoms — scenelike true hallucinations (predominantly visual), pareidolic illusions, acute psychomotor agitation, perplexity.
  • Consciousness disturbances — disorientation in place, time, and situation while orientation to one's own identity remains characteristically intact.
  • Somatic and autonomic signs — skin hyperemia, tachycardia, dyspnea, increased blood pressure, hyperhidrosis or signs of dehydration, intractable insomnia.

Symptoms usually worsen in the evening and at night.

On which day after stopping alcohol intake does alcohol delirium typically manifest?

Alcohol delirium typically manifests on days 2–4 after complete cessation of alcohol intake or a sharp decrease in the dose.

Psychosis occurs during alcohol cessation, at the peak of the withdrawal syndrome, rather than in a state of intoxication. The development of the established stage is preceded by a prodromal phase lasting from a few hours to two days, manifesting as evening-worsening anxiety, tremor, skin hyperemia, and total insomnia.

Which groups of pharmacological agents are the drugs of choice for managing alcohol delirium?

The drugs of choice for pathogenetic therapy and management of alcohol delirium are GABAergic agents.

Main groups of drugs used:

  • Benzodiazepine tranquilizers — diazepam, bromdihydrochlorophenylbenzodiazepine (phenazepam).
  • Barbiturates — sodium thiopental, hexobarbital (hexenal).
  • GABA precursors — sodium oxybutyrate.
  • Other GABAergic agents — zopiclone, zolpidem.

In the treatment of established psychosis, the parenteral route of administration is used; due to high tolerance in patients with alcoholism, high doses are required. Antipsychotics have only a symptomatic effect and are ineffective without GABAergic drugs.

What is the neurotransmitter mechanism in the pathogenesis of alcohol delirium?

The neurotransmitter mechanism in the pathogenesis of alcohol delirium is based on a pronounced imbalance between inhibitory and excitatory systems of the brain, arising upon alcohol withdrawal.

Key links of pathogenesis:

  • Inhibition of inhibitory systems — insufficient activity of the GABAergic system and aspartate.
  • Hyperactivity of excitatory systems — excessive activity of the glutamatergic and dopaminergic systems.
  • Acetylcholine deficiency — exacerbates the neurotransmitter imbalance.

These adaptive changes develop in chronic alcoholism, and upon abrupt cessation of ethanol intake, they lead to the predominance of excitatory neurotransmitters over inhibitory ones (glutamate/GABA imbalance), which clinically manifests as psychomotor agitation and the development of psychosis.

Class and exam questions

Can alcohol delirium occur in the first stage of alcoholism?

No, in stage I the conditions for the development of psychoses are absent. Delirium occurs only in the presence of severe withdrawal syndrome, which is characteristic of stage II.

What is proven by a patient's history of alcohol delirium?

A history of delirium is reliable diagnostic evidence that alcoholism has progressed to the established (second) phase.

What other psychoses are characteristic of the stage in which delirium occurs?

In addition to delirium, hallucinosis, paranoid psychosis, and Korsakoff's psychosis may develop.

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What else to study on this topic

  • Clinical picture of alcohol withdrawal syndrome
  • Features of stage I alcoholism (development of dependence)
  • Alcoholic polyneuropathy and Korsakoff's psychosis
  • Alcoholic liver disease (hepatitis, cirrhosis) and encephalopathy
  • Marchiafava-Bignami disease and central pontine myelinolysis

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