Delirium tremens
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: Rum fits; DT's; shaking delirium; trembling madness
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 appears after a rapid reduction in the amount of alcohol being consumed by heavy drinkers, or a rapid reduction of intake of benzodiazepines or barbiturates. If 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-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 GABAA 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
Causes of delirium tremens include
Differentiating Delirium Tremens from other Disease
Delirium tremens (DT) should be distinguished from alcoholic hallucinosis. Alcoholic hallucinosis (or alcohol-related psychosis) is a complication of alcohol withdrawal in alcoholics. This develops about 12 to 24 hours after drinking stops and involves auditory and visual hallucinations, most commonly accusatory or threatening voices. This condition is distinct from delirium tremens since it develops and resolves rapidly, involves a limited set of hallucinations and has no other physical symptoms.
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
- Alcoholism that has existed for more than 10 years
- CNS infection
- Drug abuse
- Head injury
- Malnutrition
- Sepsis
Screening
- Screening tools include the Alcohol Use Disorders Identification Test (AUDIT) and the CAGE screening test.
Natural History, Complications and Prognosis
Complications
Adrenergic storm causes a few complications which include (but are not limited to)
Diagnosis
Symptoms
The main symptoms are
Other common symptoms include
- Intense hallucinations - formication
- Tremors
- Anxiety
- Panic attacks
- Paranoia
Physical Examination
Appearance of the Patient
Patient is diaphoretic and in severe psychomotor agitation
Vital Signs
Temperature
Pulse
Blood pressure
Respiratory rate
Eye
Neurologic
Laboratory Findings
Electrolyte and Biomarker Studies
- Complete blood count, differential count
- Drug screening
- Blood lactate levels
- Osmolal gap
- Serum levels of following electrolytes[1]
- Sodium - decreased
- Potassium - decreased
- Chloride - may remain unchanged
- Bicarbonate - decrease
- Blood urea nitrogen (BUN) - may increase
- Creatinine - may increase
- Magnesium - decrease
- Liver function tests - abnormal
- Creatine phosphokinase - Some patients develop rhabdomyolysis
- Lipase -
- Ketones
- CSF examination - ruling out infections of the brain
Electrocardiogram
- To evaluate any electrolyte abnormalities causing electro physiological changes in heart muscle.
Chest X Ray
- To evaluate any associated respiratory disease
- X rays to evaluate any cervical spinal trauma .
CT Scan
- CT scan head to evaluate any intra cranial pathology.
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.
References
See also