Specialty Neurology ICD-9-CM 291.0 MedlinePlus 000766 | ICD-10 F10.4 DiseasesDB 3543 eMedicine med/524 | |
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Delirium tremens (DTs) is a rapid onset of confusion usually caused by withdrawal from alcohol. When it occurs, it is often three days into the withdrawal symptoms and lasts for two to three days. People may also see or hear things other people do not. Physical effects may include shaking, shivering, irregular heart rate, and sweating. Occasionally, a very high body temperature or seizures may result in death. Alcohol is one of the most dangerous drugs to withdraw from.
Contents
Delirium tremens typically only occurs in people with a high intake of alcohol for more than a month. A similar syndrome may occur with benzodiazepine and barbiturate withdrawal. Withdrawal from stimulants such as cocaine do not have major medical complications. In a person with delirium tremens it is important to rule out other associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.
Prevention is by treating withdrawal symptoms. If delirium tremens occurs, aggressive treatment improves outcomes. Treatment in a quiet intensive care unit with sufficient light is often recommended. Benzodiazepines are the medication of choice with diazepam, lorazepam, chlordiazepoxide, and oxazepam all commonly used. They should be given until a person is lightly sleeping. The antipsychotic haloperidol may also be used. The vitamin thiamine is recommended. Mortality without treatment is between 15% and 40%. Currently death occurs in about 1% to 4% of cases.
About half of people with alcoholism will develop withdrawal symptoms upon reducing their use. Of these, three to five percent develop DTs or have seizures. The name delirium tremens was first used in 1813; however, the symptoms were well described since the 1700s. The word "delirium" is Latin for "going off the furrow," a plowing metaphor. It is also called shaking frenzy and Saunders-Sutton syndrome. Nicknames include the shakes, barrel-fever, blue horrors, bottleache, bats, drunken horrors, elephants, gallon distemper, quart mania, and pink spiders, among others.
Signs and symptoms
The main symptoms of delirium tremens are nightmares, agitation, global confusion, disorientation, visual and auditory hallucinations, tactile hallucinations, fever, high blood pressure, heavy sweating, and other signs of autonomic hyperactivity (fast heart rate and high blood pressure). These symptoms may appear suddenly, but typically develop two to three days after the stopping of heavy drinking, being worst on the fourth or fifth day. Also, these "symptoms are characteristically worse at night". In general, DT is considered the most severe manifestation of alcohol withdrawal and occurs 3–10 days following the last drink. Other common symptoms include intense perceptual disturbance such as visions of insects, snakes, or rats. These may be hallucinations, or illusions related to the environment, e.g., patterns on the wallpaper or in the peripheral vision that the patient falsely perceives as a resemblance to the morphology of an insect, and are also associated with tactile hallucinations such as sensations of something crawling on the subject—a phenomenon known as formication. Delirium tremens usually includes extremely intense feelings of "impending doom". Severe anxiety and feelings of imminent death are common DT symptoms.
DT can sometimes be associated with severe, uncontrollable tremors of the extremities and secondary symptoms such as anxiety, panic attacks and paranoia. Confusion is often noticeable to onlookers as those with DT will have trouble forming simple sentences or making basic logical calculations.
DT should be distinguished from alcoholic hallucinosis, the latter of which occurs in approximately 20% of hospitalized alcoholics and does not carry a significant mortality. In contrast, DT occurs in 5–10% of alcoholics and carries up to 15% 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 patients experience seizures.
Causes
Delirium tremens is mainly caused by a long period of drinking being stopped abruptly. Withdrawal leads to a biochemical regulation cascade. It may also be triggered by head injury, infection, or illness in people with a history of heavy use of alcohol.
Another cause of delirium tremens is abrupt stopping of tranquilizer drugs of the barbiturate or benzodiazepine classes in a person with a relatively strong addiction to them. Because these tranquilizers' primary pharmacological and physiological effects stem from their manipulation of the GABA chemical and transmitter somatic system, the same neurotransmitter system affected by alcohol, delirium tremens can occur upon abrupt decrease of dosage in those who are heavily dependent. These DTs are much the same as those caused by alcohol and so is the attendant withdrawal syndrome of which they are a manifestation. That is the primary reason benzodiazepines are such an effective treatment for DTs, despite also being the cause of them in many cases. Because ethanol and tranquilizers such as barbiturates and benzodiazepines function as positive allosteric modulators at GABAA receptors, the brain, in its desire to equalize an unbalanced chemical system, triggers the abrupt stopping of the production of endogenous GABA. This decrease becomes more and more marked as the addiction becomes stronger and as higher doses are needed to cause intoxication. In addition to having sedative properties, GABA is an immensely important regulatory neurotransmitter that controls the heart rate, blood pressure, and seizure threshold among myriad other important autonomic nervous subsystems.
Delirium tremens is most common in people who have a history of alcohol withdrawal, especially in those who drink the equivalent of 7 to 8 US pints (3 to 4 l) of beer or 1 US pint (0.5 l) of distilled beverage daily. Delirium tremens also commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years.
Pathophysiology
Delirium tremens is a component of alcohol withdrawal hypothesized to be the result of compensatory changes in response to chronic alcohol abuse. Alcohol positively allosterically modulates the binding of GABA, resulting in disinhibition of neurons projecting into the nucleus accumbens, as well as inhibiting NMDA receptors. This combined with desensitization of alpha-2 adrenergic receptors, results in a homeostatic up regulation of these systems in chronic alcohol use. When alcohol use ceases, the unregulated mechanisms result in hyper excitability of neurons as natural GABAergic systems are down regulated and excitatory glutaminergic systems are unregulated. This combined with increased noradrenergic activity results in the symptoms of delirium tremens.
Treatment
Delirium tremens due to alcohol withdrawal can be treated with benzodiazepines. High doses may be necessary to prevent death. Amounts given are based on the symptoms. Typically the person is kept sedated with benzodiazepines, such as diazepam, lorazepam, chlordiazepoxide, or oxazepam.
In some cases antipsychotics, such as haloperidol may also be used. Older drugs such as paraldehyde and clomethiazole were formerly the traditional treatment but have now largely been superseded by the benzodiazepines.
Acamprosate is occasionally used in addition to other treatments, and is then carried on into long term use to reduce the risk of relapse. If status epilepticus occurs it is treated in the usual way. It can also be helpful to control environmental stimuli, by providing a well-lit but relaxing environment for minimizing distress and visual hallucinations.
Alcoholic beverages can also be prescribed as a treatment for delirium tremens, but this practice is not universally supported.
High doses of thiamine often by the intravenous route is also recommended.
Society and culture
Nicknames include "the horrors", "the shakes", "the bottleache", "quart mania", "ork orks", "gallon distemper", "the zoots", "barrel fever", "the 750 itch", "pint paralysis", seeing pink elephants. Another nickname is "the Brooklyn Boys" found in Eugene O'Neill's one-act play Hughie set In 1920's Times Square.
Writer Jack Kerouac details his experiences with delirium tremens in his book Big Sur.
One of the characters in Joseph Conrad's novel Lord Jim experiences "DTs of the worst kind" with symptoms that include seeing millions of pink frogs.
In the 1945 film The Lost Weekend, Ray Milland won the Academy Award for Best Actor for his depiction of a character who experiences delirium tremens after being hospitalized, hallucinating that he saw a bat fly in and eat a mouse poking through a wall.