Delirium tremens

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2] Zehra Malik, M.B.B.S[3]

Alcohol has a depressant effect on the brain and nervous system. If alcohol is stopped abruptly after a long period of chronic usage, the brain and nervous system struggle to recalibrate which leads to overstimulation of the brain. Delirium tremens (colloquially, the DTs, “the horrors”, “the shakes” or “rum fits”; afflicted individuals referred to as “jitterbugs” in 1930s Harlem slang; literally, “shaking delirium” or “trembling madness” in Latin) 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 minor tranquilizers).When caused by alcohol, it occurs only 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. Due to this, barbiturates are rarely used anymore, being replaced by the generally accepted less dangerous benzodiazepines, which however still cause a similar withdrawal syndrome. 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%.

There is no established system for the classification of Delirium tremens.

The most common cause of delirium tremens is abrupt alcohol cessation in chronic alcohol abusers.

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%.

Common risk factors in the development of Delirium tremens include chronic alcoholism, more days since last alcohol consumption, prior history of Delirium tremens, and extreme withdrawal symptoms.

Screening tools include the Alcohol Use Disorders Identification Test (AUDIT) and the CAGE screening test.

The symptoms of Delirium tremens usually start within 48 to 98 hours after the last drink in long term alcoholics. In some cases, it may occur up to 7 to 10 days after their last drink. Delirium tremens have a very high mortality rate if left untreated. Complications include, hypertension, hyperthermia, Heart attack, cardiac arrhythmia, stroke, seizure, respiratory failure, altered mental status, rhabdomyolysis and death. Prognosis largely depends upon early recognition and intervention. Mortality from Delirium tremens has been reduced from 35% to 5-15% due to early diagnosis and advanced ICU arrangements. Due to advanced treatment overall mortality is low, but it can vary in patient with other comorbidities including pulmonary insufficiencies, arrhythmia, pancreatitis, or if patient is older.

The hallmark of delirium tremens is tremor, confusion, disorientation, agitation, signs of severe autonomic instability (fever, tachycardia, hypertension) with a positive history of alcohol cessation 48 – 72hrs prior in a patients with history of chronic alcohol abuse.

Patients with delirium tremens usually appear diaphoretic, confused and agitated. Although there are no physical findings diagnostic of delirium tremens, patients may present with fever, tachycardia, high blood pressure, tachypnea, altered mental status, mydriasis, positional nystagmus, and tremor.

Laboratory findings consistent with the diagnosis of delirium tremens include hypoglycemia, hypomagnesemia, hypophosphatemia, and severe dehydration.

Tachyarrhythmias are common ECG findings in patients with delirium tremens. Torsade de pointes can occur as prolonged QTc interval is strongly associated with heavy alcohol consumption.

An x-ray is important in patients with suspected delirium tremens, especially if they present with a fever or trauma. A chest x-ray should be obtained in patients with fever, as fifty-percent of these patients may have an infection. Pneumonia is the most common infection.

There are no echocardiography/ultrasound findings associated with delirium tremens. Due to the stress induced by delirium tremens, few cases of Takotsubo cardiomyopathy have been reported.

A head CT scan should be performed to evaluate any intracranial pathology or to identify a head injury that may have triggered the tremors in a patient with a history of chronic alcohol abuse.

There are no MRI findings associated with delirium tremens. MRI can show signs of Wernicke’s Encephalopathy in a patient with chronic alcohol abuse.

There are no other imaging findings associated with delirium tremens.

The mainstay of delirium tremens treatment is supportive care and sedatives. Benzodiazepines are the initial choice for sedation. To establish a consistent serum level, long-acting benzodiazepines such as diazepam and chlordiazepoxide are favored over short-acting benzodiazepines.

There is no surgical intervention for delirium tremens.

There are no established measures for the primary prevention of delirium tremens other than to avoid or reduce the use of alcohol.

Effective measures for the secondary prevention of delirium tremens include early detection of symptoms, prompt treatment, CAGE assessment, and proper counseling to reduce alcohol consumption.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

• Literature
  • In Dostoyevsky‘s Crime and Punishment
  • In George Eliot‘s Middlemarch, John Raffles suffers and eventually dies from delirium tremens.
  • In Mark Twain‘s The Adventures of Huckleberry Finn, Huck’s father suffers from delirium tremens.
  • Jack Kerouac‘s Big Sur discusses his experiences with delirium tremens.
  • In Joseph Conrad‘s Lord Jim, the chief engineer of the Patna is described as having the condition which results in his being hospitalized. He suffers from DTs after a traumatizing experience, in which he hallucinated hundreds of pink toads, which represent the eight hundred people he almost killed because of his one action. The pink toads are a slight variation of the common hallucination of pink snakes related to DT.
  • Australian writer, Henry Lawson, who was himself an alcoholic, refers in numerous short stories to the “jim-jams”, a colloquialism for the “DTs”.
  • In Aleksis Kivi‘s novel Seven Brothers, Simeoni has delirium tremens and hallucinates that the devil takes him on a huge tower made of boot leather and shows him the future of the world.
  • In Charlotte Perkins Gilman‘s “The Yellow Wallpaper” the term is referenced.
  • The George Orwell book, Burmese Days features an alcoholic character known as Mr Lackersteen who suffers from delirium tremens.
  • Ignacio Solares’ Delirium tremens (1979) is a work of non-fiction that collects stories of nightmarish visions experienced by alcoholics when undergoing delirium tremens. Solares’ father had experienced delirium tremens when Solares was a boy.
  • The Brothers Karamazov, Book XI, Chapter 9: The Devil, Ivan Fyodorovich’s Nightmare, describes a delirium tremens induced hallucination.
  • In chapter 5 of Thomas Pynchon‘s The Crying of Lot 49, the dying sailor has the DTs.
  • In the S.E. Hinton novel Rumble Fish, the main character’s father is an alcoholic who is said to have suffered from delirium tremens.
  • In Jeremy Paxman‘s “The English”, he describes the life of one Jack Mytton, who “died of delirium tremens in the Kings Bench Prison on 29 March 1834”.
  • In Emile Zola‘s novel “L’Assommoir“, the alcoholic Coupeau dies of delirium tremens.
  • In Uncle Tom’s Cabin (written by Harriet Beecher Stowe), the slave Cassy drives the cruel master Simon Legree into delirium tremens with mimicking haunting, which eventually becomes fatal.^[1]

• Theater/film/television
  • In a line from the stage and movie version of West Side Story, Lieutenant Shrank asks, “How’s your old man’s DT’s Arab?”
  • Kramer and Mickey, who are both practising (Queen’s english) various diseases for a job of theirs at a medical school, briefly impersonate the DT’s in episode 172 of Seinfeld.
  • Delirium tremens is also referenced in Eugene O’Neill‘s play The Hairy Ape. Yank, the principal character in the play, cites the condition as the cause of his mother’s death when referring to his troubled childhood.
  • In the 1945 Billy Wilder film The Lost Weekend, the main character, played by Ray Milland, suffers delirium tremens after fleeing a detoxification ward following a weekend of binge drinking. In the movie, Milland’s delirium comes in the form of a bat that perches on an apartment wall and devours a mouse tucked into a crack in the plaster.
  • In Blake Edwards‘s 1965 film Days of Wine and Roses, Jack Lemmon‘s character, Joe Clay, experiences delirium tremens before detoxing and discovering Alcoholics Anonymous.
  • Another cultural reference is in Smokey and the Bandit II.
  • In the 1995 film Leaving Las Vegas, Nicolas Cage portrays a character who experiences this symptom following binge drinking and withdrawal.
  • During the filming of Monty Python and the Holy Grail, Graham Chapman suffered from DTs
  • In the television show Strangers with Candy, the main character suffers from delirium tremens due to decades of drinking.
  • In the television show “M*A*S*H“, one of “Hot Lips” Hoolihan’s nurses and best friend, Helen Whitfield, suffers from delirium tremens.
  • In the movie Fried Green Tomatoes Smokey suffers from alcoholic tremor while attempting to eat corn with a fork. He is then given a bottle of whiskey by Idgy Threadgood in order to prevent the development of delirium tremens.
  • In an episode of Coronation Street Jamie’s mother, an alcoholic is seen shaking on the sofa with DT after promising to go cold turkey
  • In Jean-Pierre Melville‘s Le Cercle Rouge, Yves Montand‘s character Jensen experiences delirium tremens.

• Music
  • Hard Rock band Aerosmith mentions it in their song “Falling in Love (Is Hard on the Knees).” “I’m Jonesin’ on love / Yeah I got the DTs.”
  • Irish folk singer Christy Moore sang a song titled “Delirium Tremens,” which appears on his Ordinary Man album. It is a comedic trawl through a protagonist’s visions; with such lines as “I dreamt Ian Paisley was sayin’ the Rosary, and Mother Teresa was takin’ the pill.” He finds the visions so scary (culminating in being in a jacuzzi with Margaret Thatcher “that oul whore in Number 10“), that he vows never to drink again.
  • “Delirium Tremens” is the title of a song contained on the disc “Enemigos Intimos,” published in 1998 by BMG España featuring Fito Paez and Joaquin Sabina
  • Musician Richard Thompson mentions this condition in his song “God Loves a Drunk,” on the album “Rumor and Sigh” (1991). “Will there be bartenders up there in heaven? / Will the bars never close, will the glass never drain? / No more DTs and no shakes and no horrors / Very next morning feel right as rain.

• Comics
  • In the comic series Preacher, the Irish vampire Cassidy swears off drinking and suffers from delirium tremens.
  • Two Asterix albums feature a perpetually drunk Roman legionnaire named Tremensdelirius.
  • In one trade paperback edition of The Sandman, one of the credits is given as “a variation of the legend says that she appears to those in the last stages of Delirium Tremens begging them to change their ways.” Also, the character Delirium is rescued by a bunch of “crazy” people, one of them an alcoholic in The Sandman:Endless Nights.

• Food and Drink
  • Huyghe Brewery in Belgium sells a blonde ale called “ Delerium Tremens“

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

There is no established system for the classification of Delirium tremens.

There is no established system for the classification of Delirium tremens.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Delirium tremens are thought to develop in chronic alcoholics who stop alcohol intake suddenly. It typically manifests within the first 48 hours of giving up alcohol.

Delirium tremens is the most severe form of alcohol withdrawal syndrome.The effects of alcohol on the brain and neurological system are depressant. When alcohol is abruptly removed after a period of chronic use, the brain and nervous system struggle to recalibrate, resulting in brain overstimulation.

It is understood that delirium tremens result from altering the activity of GABA, chloride ion, and NMDA receptors in the brain due to prolonged alcohol exposure. Abrupt cessation of alcohol causes overstimulation in these receptors.

[Disease name] is transmitted in [mode of genetic transmission] pattern.

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Genes involved in the pathogenesis of [disease name] include:

• [Gene1]
• [Gene2]
• [Gene3]

OR

The development of [disease name] is the result of multiple genetic mutations such as:

• [Mutation 1]
• [Mutation 2]
• [Mutation 3]

Conditions associated with [disease name] include:

• [Condition 1]
• [Condition 2]
• [Condition 3]

On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

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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-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”. 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, 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.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

The most common cause of delirium tremens is abrupt alcohol cessation in chronic alcohol abusers.

Common causes of delirium tremens may include:

• Alcohol withdrawal

Less common causes of delirium tremens include:

• Benzodiazepine withdrawal
• Barbiturate withdrawal

Template:WH Template:WS Causes of delirium tremens include

Delirium tremens can occur after a period of heavy alcohol drinking, especially when the person does not eat enough food. It may also be triggered by head injury, infection, or illness in people with a history of heavy use of alcohol.

It is most common in people who have a history of alcohol withdrawal, especially in those who drink the equivalent of 7 – 8 pints of beer (or 1 pint of “hard” alcohol) every day for several months. Delirium tremens also commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]

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.

Diseases	Diagnostic tests				Physical Examination					Symptoms			Past medical history	Other Findings
	Na+, K+, Ca2+	CT /MRI	CSF Findings	Gold standard test	Neck stiffness	Motor or Sensory deficit	Papilledema	Bulging fontanelle	Cranial nerves	Headache	Fever	Altered mental status
Brain tumour[1][2]		✔	Cancer cells[3]	MRI		✔	✔	✔	✔	✔		✔		Cachexia, gradual progression of symptoms
Delirium tremens		✔		Clinical diagnosis		✔	✔		✔	✔	✔	✔	Alcohol intake, sudden witdrawl or reduction in consumption	Tachycardia, diaphoresis, hypertension, tremors, mydriasis, positional nystagmus,
Subarachnoid hemorrhage[4]		✔	Xanthochromia[5]	CT scan without contrast[6][7]	✔	✔	✔	✔	✔	✔	✔	✔	Trauma/fall	Confusion, dizziness, nausea, vomiting
Stroke		✔	Normal	CT scan without contrast		✔	✔		✔	✔		✔	TIAs, hypertension, diabetes mellitus	Speech difficulty, gait abnormality
Neurosyphilis[8][9]		✔	↑ Leukocytes and protein	CSF VDRL-specifc CSF FTA-Ab -sensitive[10]	✔	✔	✔	✔		✔		✔	Unprotected sexual intercourse, STIs	Blindness, confusion, depression, Abnormal gait
Viral encephalitis		✔	Increased RBCS or xanthochromia, mononuclear lymphocytosis, high protein content, normal glucose	Clinical assesment	✔	✔	✔		✔	✔	✔	✔	Tick bite/mosquito bite/ viral prodome for several days	Extreme lethargy, rash hepatosplenomegaly, lymphadenopathy, behavioural changes
Herpes simplex encephalitis		✔		Clinical assesment			✔	✔	✔	✔	✔		History of hypertension	Delirium, cortical blindness, cerebral edema, seizure
Wernicke’s encephalopathy			Normal				✔	✔			✔		History of alcohal abuse	Ophthalmoplegia, confusion
CNS abscess		✔	↑ leukocytes >100,000/ul, ↓ glucose and ↑ protien, ↑ red blood cells, lactic acid >500mg	Contrast enhanced MRI is more sensitive and specific, Histopathological examination of brain tissue	✔	✔	✔		✔	✔	✔	✔	History of drug abuse, endocarditis, ↓ immune status	High grade fever, fatigue,nausea, vomiting
Drug toxicity											✔	✔		Lithium, Sedatives, phenytoin, carbamazepine
Conversion disorder				Diagnosis of exclusion		✔		✔		✔	✔	✔		Tremors, blindness, difficulty swallowing
Electrolyte disturbance	↓ or ↑			Depends on the cause						✔		✔		Confusion, seizures
Febrile convulsion			Not performed in first simple febrile seizures	Clinical diagnosis and EEG					✔	✔	✔	✔	Family history of febrile seizures, viral illness or gastroenteritis	Age > 1 month,
Subdural empyema		✔		Clinical assesment and MRI	✔	✔	✔	✔	✔			✔	History of relapses and remissions	Blurry vision, urinary incontinence, fatigue
Hypoglycemia	↓ or ↑			Serum blood glucose HbA1c		✔				✔		✔	History of diabetes	Palpitations, sweating, dizziness, low serum, glucose

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2] Vishnu Vardhan Serla M.B.B.S. [3]

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%.

• The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.
• In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.

• The prevalence of Delirium tremens is less than 2% in general population.^[1]
• In individuals with alcohol dependence the prevalence is approximately 2%.

• In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate/mortality rate of [number range]%.
• The case-fatality rate/mortality rate of [disease name] is approximately [number range].

• Patients of all age groups may develop [disease name].
• The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.
• [Disease name] commonly affects individuals younger than/older than [number of years] years of age.
• [Chronic disease name] is usually first diagnosed among [age group].
• [Acute disease name] commonly affects [age group].

• There is no racial predilection to [disease name].
• [Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].

• [Disease name] affects men and women equally.
• [Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.

• The majority of [disease name] cases are reported in [geographical region].

• [Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Common risk factors in the development of Delirium tremens include Chronic alcoholism, more days since last alcohol consumption, prior history of Delirium tremens, and extreme withdrawal symptoms.

Risk factors for Delirium tremens include the following:^[1][2][3][4]

• Chronic alcoholism that has existed for more than 10 years
• Prior history of Delirium tremens
• Extreme withdrawal symptoms
• Risk increases as more days go by without consuming alcohol

• History of seizures
• CNS infection
• Drug abuse
• Head injury
• Comorbidities
• Malnutrition
• Sepsis
• Hypokalemia

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Screening tools include the

• Alcohol Use Disorders Identification Test (AUDIT) is a simple ten-question test developed by the World Health Organization to determine if a person’s alcohol consumption may be harmful^[1].
  • Questions 1-3 deal with alcohol consumption
  • Questions 4-6 relate to alcohol dependence and
  • Questions 7-10 consider alcohol-related problems.
  • A score of 8 or more in men (7 in women) indicates a strong likelihood of hazardous or harmful alcohol consumption.
  • A score of 13 or more is suggestive of alcohol related harm.

• and the CAGE screening test.
• Revised Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) is the most appropriate tool to evaluate alcohol withdrawal severity^[2][3].
  • It includes a 10-item questionnaire
  • 8 points or lower indicates mild withdrawal
  • 9 to 15 points towards moderate withdrawal
  • 15 or higher means the patient suffers from severe withdrawal symptoms and is at a higher risk for seizures and Delirium tremens.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

The symptoms of Delirium tremens usually start within 48 to 98 hours after the last drink in long term alcoholics. In some cases, it may occur up to 7 to 10 days after their last drink. Delirium tremens have a very high mortality rate if left untreated. Complications include, hypertension, hyperthermia, Heart attack, cardiac arrhythmia, stroke, seizure, respiratory failure, altered mental status, rhabdomyolysis and death. Prognosis largely depends upon early recognition and intervention. Mortality from Delirium tremens has been reduced from 35% to 5-15% due to early diagnosis and advanced ICU arrangements. Due to advanced treatment overall mortality is low, but it can vary in patient with other comorbidities including pulmonary insufficiencies, arrhythmia, pancreatitis, or if patient is older.

The symptoms of Delirium tremens usually start within 48 to 98 hours after the last drink in long term alcoholics. In some cases, it may occur up to 7 to 10 days after their last drink. Delirium tremens have a very high mortality rate if left untreated^[1].

Adrenergic storm can cause following complications:^[2]

• Hypertension
• Hyperthermia
• Heart attack
• Cardiac arrhythmia
• Stroke
• Seizure
• Respiratory failure
• Altered mental status
• Rhabdomyolysis

Prognosis largely depends upon early recognition and intervention. Mortality from Delirium tremens has been reduced from 35% to 5-15% due to early diagnosis and advanced ICU arrangements^[1]. Due to advanced treatment overall mortality is low, but it can vary in patient with other comorbidities including pulmonary insufficiencies, arrhythmia, pancreatitis, or if patient is older. Some Delirium tremens symptoms may last for a year or more, including, emotional mood swings, fatigue, and/or sleeplessness.

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