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Delirium tremens
en.wikipedia.org/wiki/Delirium_tremens
Delirium tremens (DTs; lit. 'shaking frenzy') is a rapid onset of confusion usually caused by withdrawal from alcohol.[2] When it occurs, it is often three days into the withdrawal symptoms and lasts for two to three days.[2] Physical effects may include shaking, shivering, irregular heart rate, and sweating.[1] People may also hallucinate.[2] Occasionally, a very high body temperature or seizures (colloquially known as "rum fits")[5][6] may result in death.[2] Alcohol is one of the most dangerous drugs to withdraw from.[7]
Delirium tremens typically occurs only in people with a high intake of alcohol for more than a month.[8] A similar syndrome may occur with benzodiazepine and barbiturate withdrawal.[3] Withdrawal from stimulants, such as cocaine and amphetamines, does not have major medical complications.[9] In a person with delirium tremens it is important to rule out other associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.[2]
Prevention is by treating withdrawal symptoms using similarly acting compounds to taper off the use of the precipitating substance in a controlled fashion.[2] If delirium tremens occurs, aggressive treatment improves outcomes.[2] Treatment in a quiet intensive care unit with sufficient light is often recommended.[2] Benzodiazepines are the medication of choice with diazepam, lorazepam, chlordiazepoxide, and oxazepam all commonly used.[8] They should be given until a person is lightly sleeping.[2] Non-benzodiazepines are often used as adjuncts to manage the sleep disturbance associated with condition. The antipsychotic haloperidol may also be used,[2] as a major tranquilizer, in order to combat the overactivity and possible excitotoxicity caused by the withdrawal from a GABA-ergic sedative. The vitamin thiamine is recommended to be given intramuscularly,[2] because long term high alcohol intake and the often attendant nutritional deficit damages the small intestine, and so leads to a thiamine deficiency which sometimes cannot be rectified by supplement pills alone.
Mortality without treatment is between 15% and 40%.[4] Currently death occurs in about 1% to 4% of cases.[2]
About half of people with alcoholism will develop withdrawal symptoms upon reducing their use.[2] Of these, 3% to 5% develop DTs or have seizures.[2]
The name delirium tremens was first used in 1813; however, the symptoms were well described since the 1700s.[8] The word "delirium" is Latin for "going off the furrow," a plowing metaphor.[4] It is also called the shaking frenzy and Saunders-Sutton syndrome.[4] There are numerous nicknames for the condition, including "the DTs" and "seeing pink elephants".
Signs and symptoms
The main symptoms of delirium tremens are nightmares, agitation, global confusion, disorientation, visual and auditory hallucinations,[10] 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.[11]
These symptoms are characteristically worse at night.[12] For example, in Finnish, this nightlike condition is called "liskojen yö", "the night of the lizards", for its sweatiness, general unease, and hallucinations tending towards the unseemly and frightening.
In general, DT is considered the most severe manifestation of alcohol, or other GABA-receptor active drug, withdrawal, and occurs 2–10 days following the last drink.[10] It often overcomes the patient by surprise, because a brief period of uneventful sobriety of 1–2 days tends to precede it, it can fully manifest itself within a single hour, and unlike usual withdrawal symptoms experienced by an alcoholic, the condition will not easily go away using the typical intake amount or schedule of the drug.
Other common symptoms include intense perceptual disturbance such as visions or feelings 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 feelings of "impending doom". Anxiety and feelings of imminent death are common DT symptoms.[13]
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.[citation needed]
DT should be distinguished from alcoholic hallucinosis, the latter of which occurs in approximately 20% of hospitalized alcoholics and does not carry a risk of 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. The most common conditions leading to death in patients with DTs are respiratory failure and cardiac arrhythmias. [14]
Causes
Delirium tremens is mainly caused by a long period of drinking being stopped abruptly. Withdrawal leads to a biochemical regulation cascade.[citation needed]
Delirium tremens is most common in people who are in alcohol withdrawal, especially in those who drink 10–11 standard drinks (equivalent of 7 to 8 US pints (3 to 4 L) of beer, 4 to 5 US pints (1.9 to 2.4 L) of wine or 1 US pint (0.5 L) of distilled beverage) daily. Delirium tremens commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years.[15]
Pathophysiology
Delirium tremens is a component of alcohol withdrawal hypothesized to be the result of compensatory changes in response to chronic heavy alcohol use. Alcohol positively allosterically modulates the binding of GABA, enhancing its effect and resulting in inhibition 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 upregulation of these systems in chronic alcohol use.[16]
When alcohol use ceases, the unregulated mechanisms result in hyperexcitability of neurons as natural GABAergic systems are down-regulated and excitatory glutamatergic systems are upregulated. This combined with increased noradrenergic activity results in the symptoms of delirium tremens.[16]
Diagnosis
Diagnosis is mainly based on symptoms. In a person with delirium tremens, it is important to rule out other associated problems, such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.[2]
Treatment
Delirium tremens due to alcohol withdrawal can be treated with benzodiazepines. High doses may be necessary to prevent death.[17] 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.[18]
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.[citation needed]
It can also be helpful to provide a well lit room as people often have hallucinations.[19]
Alcoholic beverages can also be prescribed as a treatment for delirium tremens,[20] but this practice is not universally supported.[21]
High doses of thiamine often by the intravenous route is also recommended.[2]
en.wikipedia.org/wiki/Delirium_tremens
Delirium tremens (DTs; lit. 'shaking frenzy') is a rapid onset of confusion usually caused by withdrawal from alcohol.[2] When it occurs, it is often three days into the withdrawal symptoms and lasts for two to three days.[2] Physical effects may include shaking, shivering, irregular heart rate, and sweating.[1] People may also hallucinate.[2] Occasionally, a very high body temperature or seizures (colloquially known as "rum fits")[5][6] may result in death.[2] Alcohol is one of the most dangerous drugs to withdraw from.[7]
Delirium tremens typically occurs only in people with a high intake of alcohol for more than a month.[8] A similar syndrome may occur with benzodiazepine and barbiturate withdrawal.[3] Withdrawal from stimulants, such as cocaine and amphetamines, does not have major medical complications.[9] In a person with delirium tremens it is important to rule out other associated problems such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.[2]
Prevention is by treating withdrawal symptoms using similarly acting compounds to taper off the use of the precipitating substance in a controlled fashion.[2] If delirium tremens occurs, aggressive treatment improves outcomes.[2] Treatment in a quiet intensive care unit with sufficient light is often recommended.[2] Benzodiazepines are the medication of choice with diazepam, lorazepam, chlordiazepoxide, and oxazepam all commonly used.[8] They should be given until a person is lightly sleeping.[2] Non-benzodiazepines are often used as adjuncts to manage the sleep disturbance associated with condition. The antipsychotic haloperidol may also be used,[2] as a major tranquilizer, in order to combat the overactivity and possible excitotoxicity caused by the withdrawal from a GABA-ergic sedative. The vitamin thiamine is recommended to be given intramuscularly,[2] because long term high alcohol intake and the often attendant nutritional deficit damages the small intestine, and so leads to a thiamine deficiency which sometimes cannot be rectified by supplement pills alone.
Mortality without treatment is between 15% and 40%.[4] Currently death occurs in about 1% to 4% of cases.[2]
About half of people with alcoholism will develop withdrawal symptoms upon reducing their use.[2] Of these, 3% to 5% develop DTs or have seizures.[2]
The name delirium tremens was first used in 1813; however, the symptoms were well described since the 1700s.[8] The word "delirium" is Latin for "going off the furrow," a plowing metaphor.[4] It is also called the shaking frenzy and Saunders-Sutton syndrome.[4] There are numerous nicknames for the condition, including "the DTs" and "seeing pink elephants".
Signs and symptoms
The main symptoms of delirium tremens are nightmares, agitation, global confusion, disorientation, visual and auditory hallucinations,[10] 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.[11]
These symptoms are characteristically worse at night.[12] For example, in Finnish, this nightlike condition is called "liskojen yö", "the night of the lizards", for its sweatiness, general unease, and hallucinations tending towards the unseemly and frightening.
In general, DT is considered the most severe manifestation of alcohol, or other GABA-receptor active drug, withdrawal, and occurs 2–10 days following the last drink.[10] It often overcomes the patient by surprise, because a brief period of uneventful sobriety of 1–2 days tends to precede it, it can fully manifest itself within a single hour, and unlike usual withdrawal symptoms experienced by an alcoholic, the condition will not easily go away using the typical intake amount or schedule of the drug.
Other common symptoms include intense perceptual disturbance such as visions or feelings 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 feelings of "impending doom". Anxiety and feelings of imminent death are common DT symptoms.[13]
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.[citation needed]
DT should be distinguished from alcoholic hallucinosis, the latter of which occurs in approximately 20% of hospitalized alcoholics and does not carry a risk of 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. The most common conditions leading to death in patients with DTs are respiratory failure and cardiac arrhythmias. [14]
Causes
Delirium tremens is mainly caused by a long period of drinking being stopped abruptly. Withdrawal leads to a biochemical regulation cascade.[citation needed]
Delirium tremens is most common in people who are in alcohol withdrawal, especially in those who drink 10–11 standard drinks (equivalent of 7 to 8 US pints (3 to 4 L) of beer, 4 to 5 US pints (1.9 to 2.4 L) of wine or 1 US pint (0.5 L) of distilled beverage) daily. Delirium tremens commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years.[15]
Pathophysiology
Delirium tremens is a component of alcohol withdrawal hypothesized to be the result of compensatory changes in response to chronic heavy alcohol use. Alcohol positively allosterically modulates the binding of GABA, enhancing its effect and resulting in inhibition 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 upregulation of these systems in chronic alcohol use.[16]
When alcohol use ceases, the unregulated mechanisms result in hyperexcitability of neurons as natural GABAergic systems are down-regulated and excitatory glutamatergic systems are upregulated. This combined with increased noradrenergic activity results in the symptoms of delirium tremens.[16]
Diagnosis
Diagnosis is mainly based on symptoms. In a person with delirium tremens, it is important to rule out other associated problems, such as electrolyte abnormalities, pancreatitis, and alcoholic hepatitis.[2]
Treatment
Delirium tremens due to alcohol withdrawal can be treated with benzodiazepines. High doses may be necessary to prevent death.[17] 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.[18]
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.[citation needed]
It can also be helpful to provide a well lit room as people often have hallucinations.[19]
Alcoholic beverages can also be prescribed as a treatment for delirium tremens,[20] but this practice is not universally supported.[21]
High doses of thiamine often by the intravenous route is also recommended.[2]