Delirium Tremens (DTs)

Updated: Aug 04, 2021
  • Author: Shannon Toohey, MD, MAEd; Chief Editor: David A Kaufman, MD  more...
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Practice Essentials

Delirium tremens (DTs) is the most severe form of ethanol withdrawal, manifested by altered mental status (global confusion) and sympathetic overdrive (autonomic hyperactivity), which can progress to cardiovascular collapse. Minor alcohol withdrawal is characterized by tremor, anxiety, nausea, vomiting, and insomnia. Major alcohol withdrawal signs and symptoms include visual hallucinations and auditory hallucinations, whole body tremor, vomiting, diaphoresis, and hypertension (high blood pressure).

Signs and symptoms of delirium tremens

Signs and symptoms can include the following:

  • Minor withdrawal: Tremor, anxiety, nausea, vomiting, and insomnia

  • Major withdrawal: Visual hallucinations and auditory hallucinations, whole body tremor, vomiting, diaphoresis, and hypertension

  • Withdrawal seizures

  • Delirium tremens: Agitation, global confusion, disorientation, hallucinations, fever, hypertension, diaphoresis, autonomic hyperactivity (tachycardia and hypertension) and profound global confusion (hallmark of DTs)

See History and Physical Examination.

Treatments for delirium tremens

See the list below:

  • Supportive therapy: This important component of treatment of alcohol withdrawal syndrome and delirium tremens (DTs) includes providing a calm, quiet, well-lit environment; reassurance; ongoing reassessment; attention to fluid and electrolyte deficits; and treatment of any coexisting addictions.

  • Thiamine: Thiamine can be useful for preventing Wernicke encephalopathy (confusion, ataxia, ophthalmoplegia), an acute disorder caused by thiamine deficiency, and Korsakoff syndrome (memory impairment, amnesia), a late manifestation of thiamine deficiency.

  • Magnesium: Alcoholic individuals frequently have large total body deficits of magnesium, and symptoms and signs of magnesium deficiency include hyperactive reflexes, weakness, tremor, refractory hypokalemia, reversible hypoparathyroidism with hypocalcemia, and cardiac dysrhythmias.

  • Benzodiazepines: Based on the Clinical Institute Withdrawal Assessment Alcohol Scale Revised (CIWA-Ar) or the Richmond Agitation Sedation Scale (RASS), very–high-dose bolus therapy, with the addition of phenobarbital as needed, may help reduce the need for mechanical ventilation and the length of time in the ICU.

  • Intravenous ethanol infusions: These are not recommended for prophylaxis or treatment of alcohol withdrawal.

See Treatment.

Medications in delirium tremens

Various medications that may be used in the treatment and supportive care of delirium tremens include the following:

See Medication.



DTs is the most severe manifestation of alcohol withdrawal and clinical manifestations include agitation, global confusion, disorientation, hallucinations, fever, hypertension, diaphoresis, and autonomic hyperactivity (tachycardia and hypertension). Profound global confusion is the hallmark of delirium tremens. 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 (1) increased release of endogenous opiates; (2) activation of the inhibitory gamma-aminobutyric acid-A (GABA-A) receptor producing increased GABA inhibition, with a resultant influx of chloride ions; (3) up-regulation of the postsynaptic N-methyl-D-aspartate (NMDA) type of glutamate receptor, which mediates the postsynaptic excitatory effects of glutamate; and (4) interactions with serotonin and dopamine receptors. 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.


Etiology of Delirium Tremens

Ethanol interacts with GABA receptors, enhancing activity. GABA receptors are a family of chloride ion channels that mediate inhibitory neurotransmission. They are pentameric complexes composed of several glycoprotein subunits. Chronic ethanol abuse seems to modify the GABA receptor via several mechanisms, leading to a decrease in GABA activity. Chronic ethanol exposure has been found to alter gene expression and to increase cellular internalization of certain subunits, affecting the type of GABA receptors that are available at the cell surface and the synapse. Chronic ethanol exposure has also been found to alter phosphorylation of GABA receptors, which may alter receptor function.

When ethanol is withdrawn, a functional decrease in the inhibitory neurotransmitter GABA is seen. This leads to a loss of the inhibitory control of excitatory neurotransmitters such as norepinephrine, glutamate, and dopamine.

Ethanol also acts as an NMDA receptor antagonist. Withdrawal of ethanol leads to increased activity of these excitatory neuroreceptors, resulting in the clinical manifestations of ethanol withdrawal: tremors, agitation, hallucinations, seizures, tachycardia, hyperthermia, and hypertension. The clinical manifestations of ethanol withdrawal are due to the combination of effects on the GABA and NMDA receptors. Past episodes of withdrawal lead to increased frequency and severity of future episodes. 

Risk factors

Risk factors for DTs are inconsistent among studies [1, 2] and include the following:

  • Prior ethanol withdrawal seizures

  • History of DTs

  • Concurrent illness and more medical comorbidities

  • Daily heavy and prolonged ethanol consumption

  • Greater number of days since last drink

  • Severe withdrawal symptoms at presentation

  • Prior detoxification

  • Intense craving for alcohol

  • Older age

  • Hypokalemia

  • Thrombocytopenia

  • Elevated blood level of homocysteine

  • Presence of structural brain lesions



Using the diagnostic criteria for alcohol use disorder (AUD) listed in DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, 5th edition), the 12-month and lifetime prevalences of AUD in US noninstitutionalized civilian adults is highest in men (17.6% and 36.0%, respectively), with higher prevalences in whites, Native Americans, younger adults, and previously married and never married adults, as compared with women, African Americans, Asian Americans, and older and married adults. [3] Less than 50% of alcohol-dependent persons develop any significant withdrawal symptoms that require pharmacologic treatment upon cessation of alcohol intake. The lifetime risk for developing delirium tremens (DTs) among individuals with chronic alcohol addiction is estimated at 5-10%. Only 5% of patients with ethanol withdrawal progress to DTs. White patients have a higher risk of developing severe alcohol withdrawal, while black patients have a lower risk. [4] Whether or not sex differences exist in the rates of development of severe alcohol withdrawal is not clear. In any particular alcohol-dependent person, symptoms of withdrawal can differ widely among different withdrawal episodes.

Delirium tremens rarely occurs among pediatric patients, because the physiologic substrate for severe alcohol withdrawal takes time to develop.



Despite appropriate treatment, the current mortality for patients with DTs ranges from 5-15%, but should be closer to 5% with modern ICU management. Mortality was as high as 35% prior to the era of intensive care and advanced pharmacotherapy. The most common conditions leading to death in patients with DTs are respiratory failure and cardiac arrhythmias.

Patients at greatest risk for death are those with extreme fever, fluid and electrolyte imbalance, or an intercurrent illness, such as occult trauma, pneumonia, hepatitis, pancreatitis, alcoholic ketoacidosis, or Wernicke-Korsakoff syndrome.