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Thursday, August 8, 2013

Delirium tremens

Delirium tremens (Latin for "shaking frenzy", also referred to as The DTs, "the horrors", or "the shakes.") is an acute episode of delirium that is usually caused by withdrawal from alcohol, first described in 1813

Link:  http://en.wikipedia.org/wiki/Delirium_tremens

Delirium tremens

DTs is the most severe manifestation of alcohol withdrawal. It occurs 3-10 days following the last drink. 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.


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. 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. (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.


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. This is the phenomenon known as kindling.

Risk factors

Risk factors for delirium tremens are inconsistent among studies,[1] 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
Presence of structural brain lesions


About 9% of US adults meet the criteria for an alcohol-use disorder. 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 chronic alcoholics is estimated at 5-10%. Only 5% of patients with ethanol withdrawal progress to delirium tremens. White patients have a higher risk of developing severe alcohol withdrawal, while black patients have a lower risk.[2] 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.

Complications of delirium tremens (DTs) include the following:

Respiratory depression, respiratory arrest, intubation
Aspiration pneumonitis
Cardiac arrhythmias
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.

Delirium Tremens (DTs) Clinical Presentation


Link: http://emedicine.medscape.com/article/166032-overview#a0101