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Emergency Medicine > NEUROLOGY
Delirium Tremens
Article Last Updated: Jul 2, 2007
AUTHOR AND EDITOR INFORMATION
Section 1 of 10  
Author: William G Gossman, MD, Associate Clinical Professor of Emergency Medicine, Creighton University School of Medicine; Consulting Staff, Department of Emergency Medicine, Creighton University Medical Center
William G Gossman is a member of the following medical societies: American Academy of Emergency Medicine
Editors: William K Chiang, MD, Associate Professor, Department of Emergency Medicine, Department of Emergency Medicine, New York University School of Medicine; Consulting Staff, Bellevue Hospital Center; John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital; J Stephen Huff, MD, Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health System; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; Barry E Brenner, MD, PhD, FACEP, Program Director, Department of Emergency Medicine, University Hospitals, Case Medical Center
Author and Editor Disclosure
Synonyms and related keywords:
DT, delirium tremens, ethanol abstinence, rum fits, ethanol withdrawal, ethanol alcohol withdrawal, benzodiazepine-GABAa-chloride receptor complex, ethanol withdrawal seizures, tremors, delusions, severe agitation, seizures, confusion, hallucinations, insomnia, irritability, status epilepticus, habitual ethanol use, alcohol withdrawal
Background
Delirium tremens (DT) is a potentially fatal form of ethanol (alcohol) withdrawal. Symptoms of ethanol withdrawal and DT have been recognized for hundreds of years, but the debate over their etiology continued into the 1950s. The work of Victor and Adams as well as Isbell finally demonstrated the symptoms related to ethanol abstinence. Symptoms may begin a few hours after the cessation of ethanol but may not peak until 48-72 hours. Emergency physicians must recognize that the presenting symptoms may not be severe and identify those at risk for developing DT. For patients in DT, early recognition and therapy are necessary to prevent significant morbidity and death.
Pathophysiology
DT is caused by the direct effect that ethanol has on the benzodiazepine-GABAa-chloride receptor complex. Persistent effects of ethanol lead to the down-regulation of the receptor complex. When ethanol is withdrawn, a functional decrease in the inhibitory neurotransmitter GABA is seen. This results in an unopposed increase in sympathetic activity with a resultant increase in plasma and urinary catecholamines. Ethanol also acts as an N-methyl D-aspartate receptor antagonist. Withdrawal of ethanol leads to increased activity of these excitatory neural receptors.
Frequency
United States
Only 5% of patients with ethanol withdrawal progress to DT.
Mortality/Morbidity
- The mortality rate 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 pneumonia, hepatitis, or pancreatitis.
Sex
Approximately 10% of males and 3-5% of females are alcoholic; 5% of each group experiences DT.
Age
Adolescence to late adulthood is typical.
History
- Delirium tremens is more common in patients with a long history of ethanol use and a prior history of significant withdrawal. Manifestations of ethanol withdrawal may start several hours to days after cessation or diminution of ethanol intake. Ethanol withdrawal seizures typically occur 6-48 hours after the last drink. DT usually begins 24-72 hours after cessation or reduction of ethanol use.
- Diagnosis is made when the course progresses beyond the usual symptoms of withdrawal to include altered mental status (eg, confusion, hallucinations, severe agitation) or generalized seizures. Symptoms may include the following:
- Tremors
- Irritability
- Insomnia
- Nausea/vomiting (frequently secondary to gastritis or pancreatitis)
- Hallucinations (auditory, visual, or olfactory)
- Confusion
- Delusions
- Severe agitation
- Seizures - Begin 6-48 hours after the last drink (Status epilepticus is uncommon in patients with ethanol withdrawal, but ethanol withdrawal is still one of more common causes of status epilepticus.)
Physical
- Examination findings may be nonspecific. Clinicians should look for stigmata of habitual ethanol use, other potential causes for altered mental status (eg, CNS trauma/infection), and any associated medical problems (eg, hepatitis, pancreatitis, pneumonia).
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- Tachycardia
- Hyperthermia
- Hypertension
- Tachypnea
- Diaphoresis
- Tremor
- Mydriasis
- Diaphoresis
- Ataxia
- Altered mental status
- Hallucination
- Cardiovascular collapse
Causes
- Risk factors for developing DT
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- Ethanol withdrawal seizures
- Prior history of DT
- Higher-than-usual quantity and frequency of ethanol consumption (So much individual variability exists that the actual answer may not be clinically relevant.)
- Associated infections or medical problems (eg, pneumonia, hepatitis, pancreatitis)
Alcoholic Ketoacidosis
Anxiety
Epidural and Subdural Infections
Herpes Simplex
Herpes Simplex Encephalitis
Hypocalcemia
Hypoglycemia
Hypomagnesemia
Meningitis
Neoplasms, Brain
Neuroleptic Malignant Syndrome
Status Epilepticus
Toxicity, Amphetamine
Toxicity, Cocaine
Toxicity, Hallucinogen
Toxicity, Monoamine Oxidase Inhibitor
Toxicity, Phencyclidine
Toxicity, Sympathomimetic
Toxicity, Thyroid Hormone
Wernicke Encephalopathy
Withdrawal Syndromes
Lab Studies
- Delirium tremens is a clinical diagnosis. Laboratory studies exclude associated medical problems or other diseases.
- Glucose level - Low levels due to chronic ethanol ingestion causing glycogen depletion
- Complete blood count (CBC) - Leukocytosis, anemia, elevated mean cell volume, low platelets
- Liver function tests (LFTs) - Elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), glutamyltransferase (GGT), and bilirubin
- Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - Elevated PT due to vitamin K deficiency and liver disease
- Arterial blood gases (ABGs) - If alcoholic ketoacidosis, diabetic ketoacidosis, or a significant metabolic acidosis is suspected
- Creatine phosphokinase (CPK) level - If myocardial infarction is suspected or the patient was unconscious for a long period of time (rhabdomyolysis)
- Ethanol level
- BUN/creatinine level
- Electrolyte levels
- Amylase/lipase level
- Blood cultures if infection is suspected
Imaging Studies
- Chest radiography: Concomitant pneumonia is common in patients with DT. Routinely obtain a chest radiograph, particularly in patients with hypoxia, tachypnea, fever, cough, or respiratory distress.
- CT scan of the head: Indications for CT scan of the head include focal seizures, status epilepticus, prolonged postictal period, or recent head injury.
- Electrocardiography
- Atrial fibrillation is the most common presenting cardiac complaint in the alcoholic patient.
- Other findings include atrial flutter, premature atrial contractions, supraventricular tachycardia, and premature ventricular beats.
Procedures
- Lumbar puncture: Consider for patients with DT since CNS infections (eg, meningitis, encephalitis) may also present with altered mental status, seizures, and fever.
Emergency Department Care
- Morbidity and mortality from 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.
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- Large-bore intravenous (IV) line, isotonic saline
- Cardiac monitor
- Oxygen, 2-4 liters per nasal cannula
- Immediate bedside glucose testing or D50 administration
- Thiamine administration (100 mg IV)
- Sedation with benzodiazepines
A large number of pharmacologic agents have been used to treat DT; however, benzodiazepines are the medication of choice because they have a high therapeutic index and interact with ethanol on the benzodiazepine-GABAa-chloride receptor complex. Benzodiazepines such as diazepam have an ideal pharmacologic profile because of their rapid onset of action and prolonged duration of effects. 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. Barbiturates such as phenobarbital and pentobarbital also are useful to treat DT despite their lower therapeutic indexes. Barbiturates may be required (rarely) for patients refractory to benzodiazepine treatment. Do not use phenothiazines because they lower the seizure threshold and do not affect the benzodiazepine-GABAa-chloride receptor complex. Ethanol is effective in blunting withdrawal symptoms, but it is no longer indicated because of associated electrolyte abnormalities, potential worsening of gastritis, hepatitis, and pancreatitis. Ethanol use may promote continued ethanol usage. Phenytoin is probably not helpful in most patients with DT and seizures. Benzodiazepines or barbiturates treat seizures and manifestations of DT.
Drug Category: 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 neural inhibitory effects.
| Drug Name | Diazepam (Valium) |
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| Description | 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 a couple of min after IV administration. Has active metabolite (desmethyl-diazepam) that has longer duration of action than diazepam. |
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| Adult Dose | 5-10 mg IV bolus q5-15min until sedated
Large cumulative doses may be required to treat DT |
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| Pediatric Dose | 0.05-0.3 mg/kg/dose IV over 2-3 min q15-30min until sedated; not to exceed 5 mg/dose |
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| Contraindications | Documented hypersensitivity; narrow-angle glaucoma |
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| Interactions | Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, or MAOIs |
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| Pregnancy | D - Unsafe in pregnancy
|
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| Precautions | Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity) |
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| Drug Name | Lorazepam (Ativan) |
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| Description | Sedative hypnotic in benzodiazepine class that has short onset of effect and relatively long half-life. Monitor patient's BP after administering dose and adjust as necessary. |
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| Adult Dose | 1-2 mg IV bolus q5-15min until sedated |
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| Pediatric Dose | 0.1 mg/kg IV slowly over 2-5 min; repeat prn in 10-15 min at a dose of 0.05 mg/kg IV administered slowly until sedated; not to exceed 4 mg/dose |
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| Contraindications | Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma |
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| Interactions | Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, or MAOIs |
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| Pregnancy | D - Unsafe in pregnancy
|
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| 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 |
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| Drug Name | Chlordiazepoxide (Librium) |
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| Description | Depresses all levels of CNS including limbic and reticular formation, possibly by increasing GABA activity. Parenteral form usually used initially. |
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| Adult Dose | 50-100 mg IV q5-15min until sedated |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; narrow-angle glaucoma |
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| Interactions | Coadministration with alcohols, phenothiazines, barbiturates, or MAOIs increases CNS toxicity; cisapride can increase levels significantly |
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| Pregnancy | D - Unsafe in pregnancy
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| 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 |
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Drug Category: 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 may be common at large doses. Ventilatory support may be required in most patients receiving high-dose barbiturates. Because of their lower therapeutic index, benzodiazepines should be considered the DOC.
| Drug Name | Phenobarbital (Luminal, Barbita) |
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| Description | Have 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 depression may occur, especially after previous benzodiazepine therapy, early mechanical ventilation should be considered. |
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| Adult Dose | 130 mg IV over 1-2 min q5-15min until sedated |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis |
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| 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; induction of microsomal enzymes may result in decreased effects of oral contraceptives in women (must use additional contraceptive methods to prevent unwanted pregnancy; menstrual irregularities may also occur) |
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| Pregnancy | D - Unsafe in pregnancy
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| 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 |
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| Drug Name | Pentobarbital (Nembutal) |
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| Description | Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties and can produce all levels of CNS mood alteration. |
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| Adult Dose | 100 mg IV over 1-2 min q5-15min until sedated |
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| Pediatric Dose | Not established |
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| Contraindications | Documented hypersensitivity; liver failure |
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| 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 oral contraceptive effect by induction of microsomal enzymes (alternate form of birth control suggested); 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 |
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| Pregnancy | D - Unsafe in pregnancy
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| Precautions | Patient may become tolerant to hypnotic effects; caution in hypovolemic shock, respiratory dysfunction, renal dysfunction, previous addiction to sedative hypnotics, and CHF |
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Drug Category: Vitamins and Nutrients
These agents are used to treat the hypoglycemia and nutrient deficiencies associated with DT.
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 usually are magnesium deficient due to a poor nutritional status and malabsorption from ethanol. Magnesium stabilizes membranes, helps in the maintenance of potassium and calcium homeostasis, and may protect against seizures and arrhythmias.
| Drug Name | Dextrose 50% (D-Glucose) |
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| Description | 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). |
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| Adult Dose | 0.5-1 mg/kg IV bolus |
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| Pediatric Dose | <12 years: Not established
>12 years: Administer as in adults |
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| Contraindications | Do not administer to a patient in diabetic coma if blood sugar levels are extremely high, and avoid in severely dehydrated patients
Do not administer concentrated solution if intraspinal or intracranial hemorrhage is present; avoid in dehydrated patients with DT, hepatic coma, or glucose-galactose malabsorption syndrome |
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| Interactions | Caution when administering parenteral fluids to patients receiving corticosteroids or corticotropin, especially if solution contains sodium ions |
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| Pregnancy | A - Safe in pregnancy
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| Precautions | 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 |
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| Drug Name | Thiamine (Vitamin B-1) |
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| Description | Used to treat thiamine deficiency, including Wernicke encephalopathy syndrome. |
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| Adult Dose | 100 mg IV |
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| Pediatric Dose | 50 mg IV initially, followed by 10-25 mg/d IV/IM |
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| Contraindications | Documented hypersensitivity |
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| Interactions | None reported |
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| Pregnancy | A - Safe in pregnancy
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| Precautions | Sensitivity reactions can occur (intradermal test-dose recommended in suspected sensitivity); deaths have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy, following glucose, may occur in thiamine-deficient patients; administer before or together with dextrose-containing fluids in suspected thiamine deficiency |
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| Drug Name | Folic acid (Folate) |
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| Description | Dietary deficiency of folic acid common in alcoholics. Folic acid is an important cofactor for enzymes used in production of RBCs. |
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| Adult Dose | 1 mg PO/IV |
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| Pediatric Dose | Administer as in adults |
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| Contraindications | Documented hypersensitivity |
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| Interactions | Increase in seizure frequency and decrease in subtherapeutic levels of phenytoin reported when used concurrently |
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| Pregnancy | A - Safe in pregnancy
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| 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 |
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| Drug Name | Magnesium sulfate |
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| Description | 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 effect. Monitor carefully; 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. |
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| Adult Dose | 2 g in 50 mL of D5W over 20 min IV |
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| Pediatric Dose | 25-50 mg/kg/dose IV; maximum single dose of 2 g may also be administered and repeated if hypomagnesemia persists |
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| Contraindications | Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis |
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| 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 |
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| Pregnancy | A - Safe in pregnancy
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| 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 |
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Further Inpatient Care
- Admit all patients with delirium tremens to the ICU.
- Continue sedation as necessary to keep patients calm. Sedation dosing may be tapered over the next 5-7 days. Because of the long duration of action of diazepam or phenobarbital, patients who are adequately sedated initially may require prolonged monitoring and treatment.
Further Outpatient Care
- Do not discharge patients with DT or those thought to be developing DT.
- Refer patients discharged after hospitalization for continued rehabilitation.
Medical/Legal Pitfalls
- Failure to diagnose such conditions as hypoglycemia, CNS trauma, and CNS infections
- Failure to use adequate chemical sedation with use of physical restraints
- Treating the patient's condition as a simple seizure case and discharging home.
Special Concerns
- Do not use neuroleptics in the treatment of withdrawal.
- Administer adequate sedation to blunt agitation and to prevent the exacerbation of hyperthermia, acidosis, and rhabdomyolysis.
- Because of the kindling phenomenon associated with ethanol withdrawal and DT, inadequate sedation initially leads to escalating drug requirement for the treatment of withdrawal.
- Anticonvulsant therapy is not indicated for ethanol withdrawal seizures; however, it is indicated for patients with underlying seizure disorders.
- Phenytoin is ineffective in preventing ethanol withdrawal seizures.
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Delirium Tremens excerpt Article Last Updated: Jul 2, 2007
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