eMedicine Specialties > Emergency Medicine > Neurology

Delirium Tremens

Anne Yim, MD, Resident Physician, Department of Emergency Medicine, Kings County Hospital and State University of New York Downstate Medical Center
Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Updated: Oct 6, 2009

Introduction

Background

Delirium tremens (DT) is the most severe form of ethanol withdrawal manifested by altered mental status and sympathetic overdrive, which can progress to cardiovascular collapse. The syndrome was first described by Thomas Sutton in 1813, but the link to alcohol abstinence was not made until the 1950s with the work of Victor and Adams.^1,2  Delirium tremens is a medical emergency with a high mortality rate, making early recognition and treatment essential.

Pathophysiology

Ethanol interacts with GABA receptors enhancing activity. GABA receptors are a family of chloride ion channels that mediate inhibitory neurotransmission. They are pentameric complexes composed of several glycoprotein subunits. Chronic ethanol abuse seems to modify the GABA receptor via several mechanisms leading to a decrease in GABA activity. Chronic ethanol exposure has been found to alter gene expression and increase cellular internalization of certain subunits affecting the type of GABA receptors that are available at the cell surface and the synapse. Chronic ethanol exposure has also been found to alter phosphorylation of GABA receptors, which may alter receptor function. When ethanol is withdrawn, a functional decrease in the inhibitory neurotransmitter GABA is seen. This leads to a loss of the inhibitory control of excitatory neurotransmitters such as norepinephrine, glutamate, and dopamine. 

Ethanol also acts as an N -methyl D-aspartate receptor antagonist. Withdrawal of ethanol leads to increased activity of these excitatory neuroreceptors, resulting in the clinical manifestations of ethanol withdrawal: tremors, agitation, hallucinations, seizures, tachycardia, hyperthermia, and hypertension. Past episodes of withdrawal lead to increased frequency and severity of future episodes. This is the phenomenon known as kindling.

Frequency

United States

• Fewer than 50% of ethanol-dependent persons develop significant withdrawal syndrome requiring pharmacologic treatment.
• Only 5% of patients with ethanol withdrawal progress to delirium tremens (DT).

Mortality/Morbidity

• The mortality rate for delirium tremens may be as high as 35% if untreated but is less than 5% with early recognition and treatment.
• Patients at greatest risk for death are those with extreme fever, fluid and electrolyte imbalance, or intercurrent illness such as occult trauma, pneumonia, hepatitis, pancreatitis, alcoholic ketoacidosis, or Wernicke-Korsakoff syndrome.

Race

• Patients of white race have a higher risk of developing severe alcohol withdrawal.³
• Patients of black race have a lower risk of severe alcohol withdrawal.³

Sex

• Prevalence of alcohol abuse is approximately 7% in males and 3% in females.
• Incidence of withdrawal symptoms is lower in females than in males.

Age

• Prevalence of alcohol abuse is highest among young adults, but delirium tremens rarely occurs among pediatric patients because the physiological substrate for severe alcohol withdrawal takes time to develop.

Clinical

History

Alcohol withdrawal syndrome occurs when the blood alcohol level falls below a certain threshold in patients with a long history of alcohol consumption. Manifestations progress from mild withdrawal to its most severe and fatal form, delirium tremens (DT). Patients may have any manifestation of mild withdrawal independently (eg, patients may have alcohol withdrawal seizures or alcoholic hallucinosis without alcoholic tremulousness), and any form of mild withdrawal may progress to delirium tremens.

• Alcoholic tremulousness occurs 6-12 hours after cessation or decrease of alcohol intake and is characterized by autonomic hyperactivity; anxiety, tremors, hypertension, tachycardia, nausea, vomiting, or diarrhea.
• Alcohol withdrawal seizures or "rum fits" occur at 6-48 hours after last drink, most commonly within the first 24 hours. They are usually generalized tonic clonic, self-limited, and rarely progress to status epilepticus.
• Alcoholic hallucinosis (formerly known as Kraepelin's hallucinatory insanity) occurs 10-72 hours after the last drink. These hallucinations may often be visual, but they can also be auditory, tactile (formication), or olfactory. Outside of hallucinations, sensorium is intact.
• Delirium tremens usually occurs 3-7 days after the last drink. It is differentiated from the less severe forms of withdrawal by altered sensorium and autonomic instability. Confusion, obtundation, and delirium are the hallmarks of delirium tremens. Other findings include severe agitation, hyperpyrexia, tachycardia, hypertension, and diaphoresis.

Physical

• Physical examination findings in delirium tremens (DT) are generally nonspecific. A thorough physical examination should be performed to assess for level of consciousness, other serious illnesses, signs of trauma, and stigmata of chronic liver disease.
• Physical examination findings may include the following:
  • Tachycardia
  • Hyperthermia
  • Hypertension
  • Tachypnea
  • Diaphoresis
  • Tremor
  • Mydriasis
  • Altered mental status
  • Severe psychomotor agitation

Causes

Risk factors for developing delirium tremens (DT):

• Prior ethanol withdrawal seizures
• History of delirium tremens
• Concurrent illness
• Daily heavy and prolonged ethanol consumption
• Greater number of days since last drink

Differential Diagnoses

Workup

Laboratory Studies

• Serum chemistry including the following:
  • Sodium
  • Potassium
  • Chloride
  • Bicarbonate
  • BUN
  • Creatinine
  • Glucose
  • Magnesium
  • Phosphate
  • Liver function tests
  • Creatine phosphokinase (Some patients develop rhabdomyolysis.)
  • Lipase
  • Ketones
• Serum ethanol concentration – This is important because patients who exhibit withdrawal while ethanol is still present in the serum are likely to have a more severe course.
• Complete blood count with differential
• Urinalysis
• Blood cultures
• Further laboratory studies as indicated by clinical scenario

Imaging Studies

• Chest radiography
  • About 50% of patients with delirium tremens who present with fever will have an infection; pneumonia being most common.
  • A chest radiograph should be obtained in all patients suspected of having delirium tremens.
• Obtain cervical spine radiographs if any question or suspicion of trauma or head injury exists.
• CT scanning of the head is performed selectively. Indications for a head CT scan include the following:
  • New-onset seizure
  • Seizures occurring over longer than a 6-hour period
  • More than 6 seizures
  • Focal seizures
  • Evidence of head trauma
  • Focal neurologic deficits
  • A prolonged postictal state
  • Deteriorating level of consciousness or failure to improve in level of consciousness over time

Procedures

• Lumbar puncture: Consider to rule out encephalitis/meningitis.

Treatment

Emergency Department Care

Morbidity and mortality from delirium tremens (DT) are secondary to a hyperadrenergic state and other associated medical problems (eg, infections, fluid and electrolyte abnormalities). The goal is to blunt the hyperadrenergic state and treat associated medical problems.

• Secure airway appropriately
• Oxygen supplementation
• Large-bore intravenous line
• Fluid resuscitation with crystalloid solution
• Cardiac monitor
• Bedside glucose testing with supplementation if needed
• Thiamine administration (100 mg IV) to treat or prevent Wernicke encephalopathy
• Sedation with benzodiazepines
• Check electrolytes, replace as needed
• Physical restraints often needed to ensure patient and staff safety (use in conjunction with chemical restraints)

Medication

Parenteral benzodiazepines are the drugs of choice for treatment of delirium tremens (DT). Patients may require massive doses to achieve sedation. In patients refractory to benzodiazepine therapy alone, barbiturates or propofol should be added.⁴

Benzodiazepines are the medication of choice because they have a high therapeutic index and superior anticonvulsant effects. They act on the benzodiazepine-GABA-chloride receptor complex having a similar GABA potentiating effect to alcohol. No clear evidence suggests superiority of any particular benzodiazepine, but longer-acting benzodiazepines such as diazepam and chlordiazepoxide are generally preferred. Diazepam has an ideal pharmacologic profile because of its rapid onset of action and prolonged duration of effects due to active metabolites, allowing the dose to be safely and rapidly escalated until control of the patient’s symptoms is achieved.  

Benzodiazepine dose required may be highly variable and should be titrated until the patient is calm and peaceful. For some patients, several hundred milligrams of a diazepam equivalent may be required over the first few hours. Symptom-triggered therapy with intermittent boluses is superior to a fixed dose taper or infusion of benzodiazepines.^5,6 Therapy may be guided by the CIWA-A score, an assessment tool used to determine the severity of alcohol withdrawal.

Barbiturates such as phenobarbital and pentobarbital are also useful to treat delirium tremens. However, compared with benzodiazepines, they have a lower therapeutic index and can cause respiratory depression and hypotension. Barbiturates should be reserved for patients refractory to or unable to take benzodiazepines.⁷ These patients all need ICU monitoring, and many will need to be intubated and mechanically ventilated.

Propofol has been described in case series to be successful in the treatment of refractory delirium tremens in intubated patients. It has effects on NMDA and GABA receptors.

Ethanol is not recommended as there is little evidence regarding its use in withdrawal, and it has many potential adverse effects such as hepatotoxicity, hyponatremia, hypoglycemia, hypotension, and depression of level of consciousness.

Adjuvant therapies⁴

Neuroleptics have been shown to be inferior to sedative-hypnotics in reducing mortality and duration of alcohol withdrawal delirium. Drugs such as haloperidol (Haldol) should not be used, as they lower seizure threshold and can prolong QTc, while doing nothing to address the underlying pathophysiology. 

Sympatholytic agents such as clonidine and beta-blockers have been studied in mild-moderate ethanol withdrawal. There is no evidence regarding their effectiveness in delirium tremens. These drugs decrease sympathetic drive improving hypertension and tachycardia but have no GABA effects and hence are ineffective in preventing seizures. For this reason, they should not be used as sole therapies. Beta-blockers may be helpful to prevent cardiac complications in withdrawal patients with known coronary artery disease. However, use of these drugs is controversial as normalization of vitals signs may mask progression of withdrawal, leading to inadequate treatment of withdrawal. When benzodiazepines are used appropriately, with escalation of dose to clinical effect, sympatholytics are rarely necessary.

Anticonvulsants carbamazepine and valproic acid have been shown to be effective in treatment of mild-to-moderate withdrawal. No role exists for use of phenytoin in treatment of ethanol withdrawal or withdrawal seizures. However, it can be used to treat underlying primary seizure disorder.

Phenytoin is not helpful in patients with delirium tremens and seizures. Benzodiazepines or barbiturates effectively treat both seizures and other manifestations of delirium tremens.

Benzodiazepines

These agents bind to benzodiazepine receptors in the benzodiazepine-GABAa-chloride receptor complex to enhance the binding of GABA, causing enhanced chloride flux, hyperpolarization of the membrane, and neuro-inhibitory effects. First-line agents for delirium tremens.

Diazepam (Valium)

Because of rapid onset, prolonged duration of effects, and high therapeutic index, diazepam is drug of choice. Volumes of literature exist regarding usage of diazepam for ethanol withdrawal. Onset of action is within 5 min after IV administration. Has active metabolite (desmethyl-diazepam) that has longer duration of action than diazepam.

Dosing

Adult

5-10 mg IV, redose q5-15min until sedated
Large cumulative doses may be required to treat DTs

Pediatric

Not established

Interactions

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, or MAOIs

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Because of delayed peak onset of action, sedation may not peak for 20-30 min; cumulative effects of repeated bolus may cause sudden onset of oversedation or respiratory depression, especially if used intramuscularly
Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Lorazepam (Ativan)

Short onset of effect and intermediate half-life. Can be given IM in patients lacking IV access.

Dosing

Adult

1-4 mg IV, redose q5-15 min

Pediatric

Not established

Interactions

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, or MAOIs

Contraindications

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Because of delayed peak onset of action, sedation may not peak for 20-30 min; cumulative effects of repeated bolus may cause sudden onset of oversedation or respiratory depression
Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Chlordiazepoxide (Librium)

Depresses all levels of CNS including limbic and reticular formation, possibly by increasing GABA activity.

Dosing

Adult

50-100 mg IV q5-15min until sedated

Pediatric

Not established

Interactions

Coadministration with alcohols, phenothiazines, barbiturates, or MAOIs increases CNS toxicity; cisapride can increase levels significantly

Contraindications

Documented hypersensitivity; narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Cumulative effects of repeated bolus may cause sudden onset of oversedation or respiratory depression
Caution in low albumin levels or hepatic failure, as diazepam toxicity may increase

Barbiturates

These agents have direct effects on benzodiazepine-GABAa-chloride receptor complex in enhancing chloride flux. Barbiturates may be useful in patients refractory to benzodiazepines. Respiratory depression is common at large doses. Ventilatory support may be required. 

Phenobarbital (Luminal, Barbital)

Has direct effects on benzodiazepine-GABAa-chloride receptor complex in enhancing chloride flux. May be useful in patients refractory to benzodiazepines. Exhibits anticonvulsant properties in anesthetic doses. Because a barbiturate-induced respiratory depression may occur, especially after previous benzodiazepine therapy, early mechanical ventilation should be considered.

Dosing

Adult

130 mg IV over 1-2 min q5-15min until sedated

Pediatric

Not established

Interactions

Coadministration with alcohol may produce additive CNS effects and death; may decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized on anticoagulants may require dosage adjustments if added to or withdrawn from their regimen); chloramphenicol, valproic acid, and MAOIs may increase toxicity; rifampin may decrease effects

Contraindications

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

In prolonged therapy, evaluate hematopoietic, renal, hepatic, and other organ systems; caution in fever, hyperthyroidism, diabetes mellitus, and severe anemia since adverse reactions can occur; caution in myasthenia gravis and myxedema; patients with refractory alcohol withdrawal requiring barbiturates may need intubation and mechanical ventilation

Pentobarbital (Nembutal)

Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties and can produce all levels of CNS mood alteration.

Dosing

Adult

100 mg IV over 1-2 min q5-15min until sedated

Pediatric

Not established

Interactions

Concomitant use with alcohol may produce additive CNS effects and death; chloramphenicol may inhibit metabolism; may enhance chloramphenicol metabolism; MAOIs may enhance sedative effects; valproic acid appears to decrease metabolism, increasing toxicity; can decrease effects of anticoagulants (patients may require dosage adjustments if barbiturates added to or withdrawn from regimen); may decrease corticosteroid and digitoxin effects through induction of hepatic microsomal enzymes, which increase metabolism; decreases theophylline levels and may decrease effects; may decrease verapamil bioavailability

Contraindications

Documented hypersensitivity; liver failure

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Patient may become tolerant to hypnotic effects; caution in hypovolemic shock, respiratory dysfunction, renal dysfunction, previous addiction to sedative hypnotics, and CHF; patients with refractory alcohol withdrawal requiring barbiturates may need intubation and mechanical ventilation

General Anesthetic

Propofol is an anesthetic agent with action at NMDA and GABA receptors. It has advantages of rapid onset of action and rapid metabolic clearance. It is a good alternative for alcohol withdrawal resistant to benzodiazepines. Because of respiratory depression, intubation is required.

Propofol (Diprivan)

Phenolic compound that is a sedative-hypnotic agent used for induction and maintenance of anesthesia or sedation. Has also been shown to have anticonvulsant properties.

Dosing

Adult

Bolus IV injection of 0.5 mg/kg q10s to a total dose of 2-2.5 mg/kg or by continuous infusion at 25-75 mcg/kg/min

Pediatric

Not established

Interactions

Reduce propofol dose when administered concomitantly with benzodiazepines, opiates, phenothiazines, ethanol, and narcotics; propofol may potentiate neuromuscular blockade of vecuronium; theophylline may weaken effects of propofol, and dose increase may be needed

Contraindications

Documented hypersensitivity; those who are not mechanically ventilated

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Do not administer with blood or blood products using the same IV catheter; patients may develop apnea; may experience a decrease in systemic vascular resistance leading to hypotension; patients requiring propofol for control of DTs generally require intubation

Vitamins and Nutrients

These agents are used to treat the hypoglycemia, nutrient, and electrolyte deficiencies associated with DTs.

Alcoholics usually are deficient in thiamine, which functions as a cofactor for a number of important enzymes, such as pyruvate dehydrogenase, transketolase, and alpha-ketoglutarate dehydrogenase. Deficiency leads to Wernicke encephalopathy, peripheral neuropathy, cardiomyopathy, and metabolic acidosis.

Alcoholics often are magnesium deficient due to a poor nutritional status and malabsorption. Magnesium stabilizes membranes, helps in the maintenance of potassium and calcium homeostasis, and may protect against seizures and arrhythmias.

Patients suffering from alcoholism may also develop hypoglycemia due to malnutrition and poor glycogen stores. Additionally, gluconeogenesis is impaired due to a relative reduced redox state resulting from alcohol metabolism, which uses NAD⁺ as a cofactor for alcohol dehydrogenase and aldehyde dehydrogenase. The relative excess of NADH shifts the pyruvate-to-lactate ratio toward lactate, decreasing the substrate for gluconeogenesis.

Dextrose 50% (D-Glucose)

Monosaccharide absorbed from intestine and distributed, stored, and used by tissues. Parenterally injected dextrose used in patients unable to obtain adequate oral intake. Direct oral absorption results in rapid increase of blood glucose concentrations. Effective in small doses; no evidence of toxicity. Concentrated dextrose infusions provide higher amounts of glucose and increased caloric intake, with minimal fluid volume. Use 1 ampule of 50 mL of a 50% glucose solution (25 g).

Dosing

Adult

0.5-1 mg/kg IV bolus

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Caution when administering parenteral fluids to patients receiving corticosteroids or corticotropin, especially if solution contains sodium ions

Contraindications

Do not administer if blood sugar levels are extremely high, and avoid in severely dehydrated patients

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sudden onset or worsening of Wernicke encephalopathy, following glucose, may occur in thiamine-deficient patients; administer after or together with thiamine in suspected thiamine deficiency. However, dextrose administration should never be delayed pending the availability of thiamine in patients with significant hypoglycemia; instead, the dextrose should be given in this case followed as soon a possible by the thiamine once it is available. Extravasation may cause significant tissue necrosis when used IV; isolated reports of nausea, which may also occur with hypoglycemia, have been recorded; dextrose solutions administered IV can result in dilution of serum electrolyte concentrations and overhydration when fluid overload exists; caution in congested states or pulmonary edema

Thiamine (Vitamin B-1)

Used to treat thiamine deficiency, including Wernicke encephalopathy syndrome.

Dosing

Adult

100 mg IV

Pediatric

50 mg IV initially, followed by 10-25 mg/d IV/IM

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sensitivity reactions can occur (intradermal test-dose recommended in suspected sensitivity); deaths have resulted from IV use

Folic acid (Folate)

Dietary deficiency of folic acid common in alcoholics. Folic acid is an important cofactor for enzymes used in production of RBCs.

Dosing

Adult

1 mg IV

Pediatric

Administer as in adults

Interactions

Increase in seizure frequency and decrease in subtherapeutic levels of phenytoin reported when used concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Benzyl alcohol may be contained in some products as a preservative (associated with a fatal gasping syndrome in premature infants); resistance to treatment may occur in patients with alcoholism and deficiencies of other vitamins

Magnesium sulfate

Used to treat and prevent seizures. Decreases amount of acetylcholine liberated at endplate by motor nerve impulse. Blocks neuromuscular transmission associated with seizure activity. Magnesium also has CNS depressant effects by blocking the NMDA receptor. Monitor carefully; large doses may cause respiratory depression, hyporeflexia, and bradycardia. Infusion should be discontinued if reflexes are absent or if magnesium levels exceed 6-8 mEq/L. Calcium chloride, 10 mL IV of a 10% solution, can be given as antidote for clinically significant hypermagnesemia.

Dosing

Adult

2 g in 50 mL of D5W over 20 min IV

Pediatric

25-50 mg/kg/dose IV; maximum single dose of 2 g may also be administered and repeated if hypomagnesemia persists

Interactions

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, or succinylcholine; may increase CNS effects and toxicity of CNS depressants or betamethasone; may increase cardiotoxicity of ritodrine

Contraindications

Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Magnesium may alter cardiac conduction, leading to heart block in digitalized patients; respiratory rate, deep tendon reflexes, and renal function should be monitored when electrolyte is administered parenterally; caution when administering, since may produce significant hypertension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia

Follow-up

Further Inpatient Care

• Admit all patients with delirium tremens (DT) to the ICU.
• Continue pharmacological sedation in a symptom-triggered dosing regimen.
• Continue antibiotics if indicated.

Further Outpatient Care

• Outpatient management does not have a role in the treatment of delirium tremens (DT).
• Refer patients for alcohol rehabilitation upon discharge.

Deterrence/Prevention

• Upon discharge, patients should be counseled to abstain from alcohol.
• Consider referral to inpatient detoxification or alcohol rehabilitation program.
• Various types of outpatient programs are available.
  • The Substance Abuse and Mental Health Services Administration (SAMHSA) of the US Department of Health and Human Services offers an extensive listing of drug and alcohol treatment facilities by location. SAMHSA helpline: (800) 662-HELP (4357) with help in English and Spanish, or TDD at (800) 487-4889.
  • Alcoholics Anonymous
• Encourage support from family and friends.

Complications

• Oversedation
• Respiratory depression, respiratory arrest, intubation
• Aspiration pneumonitis
• Cardiac arrhythmias

Prognosis

• Mortality rate of delirium tremens (DT) is up to 35% untreated, and less than 5% with treatment.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose such conditions as hypoglycemia, trauma, pancreatitis, and infections
• Failure to administer thiamine in patients presenting with alcohol withdrawal
• Failure to use adequate chemical sedation with use of physical restraints
• Masking of withdrawal signs with sympatholytics while failing to treat the underlying withdrawal
• Failure to consider diagnosis of withdrawal in patients with abnormal vital signs, altered mental status, or single simple seizure
• Failure to admit patients with signs of major withdrawal or delirium tremens (DT)

Special Concerns

• Large amounts of sedatives may be required to achieve adequate control of symptoms. Sometimes, the airway must be controlled to permit the safe administration of adequate doses of sedatives.
• Concurrent illnesses such as pneumonia, pancreatitis, hepatitis, and trauma should be identified and treated.
• Anticonvulsant therapy is not indicated for ethanol withdrawal seizures. Treat with agents that act on the GABA receptor—benzodiazepines, barbiturates, or propofol.

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Keywords

DT, delirium tremens, delirium tremens symptoms, alcohol withdrawal delirium, alcohol withdrawal hallucinosis, ethanol abstinence, rum fits, ethanol withdrawal, ethanol alcohol withdrawal, ethanol withdrawal seizures

Contributor Information and Disclosures

Author

Anne Yim, MD, Resident Physician, Department of Emergency Medicine, Kings County Hospital and State University of New York Downstate Medical Center
Anne Yim, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD, Assistant Professor, Department of Emergency Medicine, State University of New York Downstate, Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center
Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

William K Chiang, MD, Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, William G Gossman, MD, to the development and writing of this article.

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