Delirium tremens

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Delirium tremens (colloquially, the DTs, "the horrors" or "the shakes") is a condition usually associated with complete alcohol withdrawal. However, delirium tremens can appear after a rapid reduction in the amount of alcohol being consumed by heavy drinkers, and also occurs as a complication of benzodiazepine and barbiturate withdrawal. It only occurs in individuals with a history of constant, long-term alcohol consumption. Delirium tremens typically manifests about 18 to 24 hours after discontinuation of alcohol consumption, but can appear on the second or third day of abstinence.

Five percent of acute ethanol withdrawal cases progress to delirium tremens[1]. Unlike the withdrawal syndrome associated with opiate or stimulant addiction, delirium tremens (and alcohol withdrawal in general) can be fatal. Mortality can be up to 35% if untreated, though if treated early, death rates may be as low as 5%.

1 Symptoms
2 Causes
3 Treatment
4 See also
5 External links

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Symptoms

The symptoms include severe, uncontrollable tremors of the extremities and intense hallucinations such as insects, snakes or rats. These may be related to the environment, eg drawings on wallpaper that the patient would perceive as giant spiders ready to attack her or him. Unlike hallucinations associated with schizophrenia, delirium tremens hallucinations are primarily visual, but associated with tactile hallucinations such as sensations of something crawling on the subject. Other symptoms include agitation, confusion and the associated alcohol withdrawal fits. Secondary symptoms can be anxiety, panic attacks or paranoia.

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Causes

The exact pharmacology of ethanol is not fully understood, however it is theorized that delirium tremens is caused by the effect of alcohol on the benzodiazepine-GABAa-chloride receptor complex for the inhibitory neurotransmitter GABA. Constant consumption of alcoholic beverages (and the consequent chronic sedation) causes a counterregulatory response in the brain in attempt to re-achieve homeostasis.

This causes downregulation of these receptors, as well as an up-regulation in the production of excitatory neurotransmitters such as norepinephrine, dopamine, epinephrine, and serotonin - all of which further the drinker's tolerance to alcohol and may intensify tonic-clonic seizures. When alcohol is no longer consumed, these down-regulated GABA-(A) type receptor complexes are so insensitive to GABA that the typical amount of GABA produced has little effect, compounded with the fact that GABA normally inhibits action potential formation, there are not as many receptors for GABA to bind to - meaning that sympathetic activation is unopposed. This is also known as an adrenergic storm. Effects of this "adrenergic storm" can include (but are not limited to) tachycardia, hypertension, hyperthermia, hyperreflexia, diaphoresis, heart attack, cardiac arrhythmia, stroke, anxiety, panic attacks, paranoia, and agitation.

This is all made worse by excitatory neurotransmitter upregulation, so not only is sympathetic nervous system over-activity unopposed by GABA, there is also more of the serotonin, norepinephrine, dopamine, and epinephrine. Direct measurements of central norepinephrine and it's metabolites is in direct correlation to the severity of the alcohol withdrawal syndrome.

It is possible that psychological (i.e., non-physical) factors also play a role, especially those of infections, malnutrition, or other underlying medical disorders - often related to alcoholism.

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Treatment

Pharmacotherapy is symptomatic and supportive. Typically the patient is kept sedated with benzodiazepines, such as diazepam (Valium) or oxazepam (Serax) and in extreme cases low-levels of antipsychotics, such as haloperidol until symptoms subside. If status epilepticus is present, seizures are treated accordingly. Controlling environmental stimuli can also be helpful, such as a well-lit but relaxing environment to minimise visual misinterpretations such as the spider hallucinations mentioned above.

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