Delirium tremens

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Delirium tremens
ICD-10	F10.4
ICD-9	291.0
DiseasesDB	3543
MedlinePlus	000766
MeSH	D000430

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: the horrors; rum fits; the shakes; shaking delirium; trembling madness; DT's

Overview

Delirium tremens is an acute episode of delirium that is usually caused by withdrawal or abstinence, from alcohol following habitual excessive drinking, or benzodiazepines or barbiturates (and other major tranquilizers).

Pathophysiology

Delirium tremens can also appear after a rapid reduction in the amount of alcohol being consumed by heavy drinkers, or a rapid reduction of intake of benzodiazepines or barbiturates. Caused by alcohol, it only occurs in individuals with a history of constant, long-term alcohol consumption. Occurrence due to benzodiazepine or barbiturate withdrawal does not require as long a period of consistent intake of such drugs. Prior use of both tranquilizers and alcohol can compound the symptoms, and while extremely rare, is the most dangerous especially if untreated. Barbiturates are generally accepted as being extremely dangerous, both due to overdose potential and addiction potential including the extreme withdrawal syndrome that usually is marked by delirium tremens upon discontinuation.

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-GABA_A-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 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".

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, epinephrine, and particularly glutamate. Excitory NMDA receptors are also upregulated, contributing to the delirium and neurotoxicity (by excitotoxicity) of withdrawal. Direct measurements of central norepinephrine and its metabolites is in direct correlation to the severity of the alcohol withdrawal syndrome.

Causes

• Alcohol withdrawal
• Benzodiazepine withdrawal
• Barbiturate withdrawal

Differentiating Delirium Tremens from other Disease

Delirium tremens (DT) should be distinguished from alcoholic hallucinosis, the latter occurring in approximately 20% of hospitalized alcoholics and not carrying a significant mortality. In contrast, DT occurs in 5-10% of alcohol-dependent people and carries up to 5% mortality with treatment and up to 35% mortality without treatment. DT is characterized by the presence of altered sensorium; that is, a complete hallucination without any recognition of the real world. DT has extreme autonomic hyperactivity (high pulse, blood pressure, and rate of breathing), and 35-60% of patients have a fever. Some individuals experience seizures as well..

Epidemiology and Demographics

Five percent of acute ethanol withdrawal cases progress to delirium tremens. Unlike the withdrawal syndrome associated with opiate addiction (generally), delirium tremens (and alcohol withdrawal in general) can be fatal. Mortality can be up to 35% if untreated; if treated early, death rates range from 5-15%.

Risk Factors

• Head injury
• CNS infection
• Sepsis
• Drug abuse
• Malnutrition
• Alcoholism that has existed for more than 10 years

Screening

• Screening tools include the Alcohol Use Disorders Identification Test (AUDIT), AUDIT-C, and the CAGE screening test

Natural History, Complications and Prognosis

Complications

Adrenergic storm causes a few complications which include (but are not limited to)

• Hypertension
• Hyperthermia
• Heart attack
• Cardiac arrhythmia
• Stroke

Diagnosis

Symptoms

The main symptoms are

• Confusion
• Disorientation
• Agitation

Other common symptoms include

• Intense hallucinations - formication
• Tremors
• Anxiety
• Panic attacks
• Paranoia

Physical Examination

Appearance of the Patient

Diaphoresis, severe psychomotor agitation

Vital Signs

• Temperature - Hyperthermia
• Pulse - Tachycardia
• Blood pressure - Hypertension
• Respiratory rate - Tachypnea

Neurologic

• Tremor
• Altered mental status
• Global confusion
• Disorientation

Eye

• Mydriasis
• Positional nystagmus

Laboratory Findings

Electrolyte and Biomarker Studies

• Complete blood count, differential count
• Drug screening
• Blood lactate levels
• Osmolal gap
• Serum levels of following electrolytes
  • Sodium
  • Potassium
  • Chloride
  • Bicarbonate
  • Blood urea nitrogen (BUN)
  • Creatinine
  • Magnesium
  • Phosphorous
  • Liver function tests
  • Creatine phosphokinase - Some patients develop rhabdomyolysis
  • Lipase
  • Ketones

Electrocardiogram

• To evaluate any electrolyte abnormalities causing electro physiological changes in heart muscle.

Chest X Ray

• To evaluate any associated chest infections

Treatment

Pharmacotherapy is symptomatic and supportive. Typically the patient is kept sedated with benzodiazepines, such as diazepam (Valium), lorazepam (Ativan) or oxazepam (Serax) and in extreme cases low-levels of antipsychotics, such as haloperidol until symptoms subside. Acamprosate is often used to augment treatment, and is then carried on into long term use to reduce the risk of relapse. 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 visual hallucinations mentioned above.

See also

• Alcoholism
• Withdrawal
• Cold turkey
• Delusional parasitosis