Delirium Tremens (DTs) Treatment & Management

Special concerns in the treatment of alcohol withdrawal include the following:

• Failure to consider the diagnosis of alcohol withdrawal syndrome in patients with altered mental status, abnormal vital signs, or single simple seizure
• Failure to treat patients with severe alcohol withdrawal syndrome with adequate doses of benzodiazepines, because these patients may require extremely large doses of parenteral benzodiazepines.
• Making the assumption that all seizures in people with alcoholism are due to alcohol withdrawal without considering other causes of seizures, such as infection, hemorrhage, or trauma.
• Failure to exclude other etiologies of altered mental status in patients with suspected alcohol withdrawal
• Failure to admit patients to the hospital with signs and symptoms of major withdrawal or delirium tremens (DTs)
• Failure to diagnose such conditions as hypoglycemia and pancreatitis
• Failure to administer thiamine in patients presenting with alcohol withdrawal
• Failure to use adequate chemical sedation with use of physical restraints

The administration of a sympatholytic drug (ie, clonidine, atenolol), either alone or with inadequate doses of benzodiazepines, can potentially cause problems, because the use of these drugs provides a false sense of security by correcting some of the autonomic manifestations of withdrawal in a patient who may be progressing to DTs. Sympatholytic drugs should not be administered unless adequate doses of benzodiazepines also are administered.

Phenytoin is not effective in preventing or treating alcohol withdrawal seizures. Seizures due to alcohol withdrawal are best prevented and treated with benzodiazepines. A Cochrane systematic review concluded that clinical trials have not shown a benefit for anticonvulsant therapy in treatment of alcohol withdrawal syndrome, but because of the heterogeneity of the trials in interventions and in the assessment of outcomes, definite conclusions about their safety and effectiveness cannot be made.

The use of neuroleptic drugs (phenothiazines, butyrophenones) alone to treat agitation or hallucinations caused by alcohol withdrawal potentially can cause problems, because these drugs are not effective in preventing or treating DTs and may increase the risk of seizures. The administration of a small dose of a butyrophenone, such as haloperidol, may be useful as adjunctive therapy to treat agitation and hallucinations, as long as adequate doses of benzodiazepines have been administered.

The use of alcohol to prevent or treat alcohol withdrawal and DTs is not recommended. Alcohol has multiple toxicities, including pancreatitis, hepatitis, cardiomyopathy, gastritis, and bone marrow suppression. It also has a short half-life and requires monitoring of blood levels when used intravenously, and its use may make it appear to the patient with alcoholism who is beginning recovery that alcohol intake is being condoned. Alcohol treatment has not been shown in controlled trials to be effective in preventing seizures or DTs.

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.

Indications for hospital admission of a patient with alcohol withdrawal syndrome include DTs; severe symptoms, such as hallucinations, disorientation, confusion, autonomic hyperactivity, or extreme agitation; the presence of a medical or surgical condition requiring treatment; a recent history of head injury with loss of consciousness; recurrent seizures; partial seizures; or focal neurologic findings upon examination.

Supportive therapy is an important component of the treatment of alcohol withdrawal syndrome and delirium tremens (DTs). Such therapy includes providing a calm, quiet, well-lit environment; reassurance; ongoing reassessment; attention to fluid and electrolyte deficits; and treatment of any coexisting addictions. Commonly, patients with alcohol withdrawal syndrome have coexisting medical, surgical, and psychiatric conditions that need careful diagnosis and treatment. Multivitamins and folate are frequently administered to these patients, but no evidence exists that vitamins other than thiamine have any benefit in the acute setting.^[3]

Administer intravenous (IV) fluids for rehydration, as necessary. Most patients with severe alcohol withdrawal are significantly dehydrated, and their fluid requirements range from 4-10 L in the first 24 hours. Because hypoglycemia is common in these patients due to depleted glycogen stores, a 5% dextrose solution (in 0.90% or 0.45% saline) should be used to prevent hypoglycemia.

Aspiration precautions are often necessary. This may include placing the patient in the left lateral decubitus position or intubating the patient, depending on the patient's level of consciousness. Also, the patient should not be administered any oral medications or fluids.

Monitor and replace electrolytes as necessary, because people with alcoholism often have low calcium, magnesium, phosphorous, and potassium.

Thiamine is useful in preventing Wernicke encephalopathy (confusion, ataxia, ophthalmoplegia) and Wernicke-Korsakoff syndrome. Thiamine has no effect on the symptoms or signs of alcohol withdrawal or on the incidence of seizures or DTs. Routine use of thiamine is recommended because the development of Wernicke encephalopathy or Wernicke-Korsakoff syndrome is disastrous in these patients and can remain unrecognized. Because orally administered thiamine may have poor enteral absorption in alcoholic patients, high-risk patients should receive parenteral thiamine at 100-250 mg once daily for several days.

People with alcoholism frequently have large total body deficits of magnesium. Symptoms and signs of magnesium deficiency include hyperactive reflexes, weakness, tremor, refractory hypokalemia, reversible hypoparathyroidism with hypocalcemia, and cardiac dysrhythmias. Serum magnesium levels are often normal in spite of a total body magnesium deficit with significant intracellular magnesium deficiency. Magnesium levels that are initially low may return to normal even though a total body deficiency persists. In animal studies, magnesium deficiency has exacerbated hepatic damage caused by alcohol.

Randomized trials have not demonstrated any effect of parenteral magnesium administration on withdrawal symptoms, but because the administration of magnesium is safe in the absence of renal insufficiency, consider routine administration of magnesium in patients with alcohol withdrawal. In severe deficiency, the deficit is about 1-2 mEq/kg of body weight.

When magnesium is administered intravenously to patients without renal insufficiency, about 50% of the dose is excreted into the urine and not retained by the body. About half of the deficit should be replaced in the first 24 hours. For a 70-kg person with normal renal function, 4-6 g of magnesium sulfate (32-48 mEq of magnesium) is administered by continuous IV infusion on the first day, followed by half that amount daily for 4 days. Alternatively, the same daily dose of magnesium can be administered intramuscularly at 6- to 8-hour intervals. Oral administration of magnesium-containing antacids can be effective but is limited by the development of diarrhea.

In critically ill patients in intensive care units (ICUs), symptom-triggered benzodiazepine treatment using very-high-dose bolus therapy has been associated with a reduction in the need for mechanical ventilation. Fixed-dose regimens often result in excessive sedation.

A guideline was instituted for ICU patients thought to have benzodiazepine-refractory alcohol withdrawal that maximized the bolus dose of benzodiazepine, with the addition of phenobarbital if necessary, and with doses determined by the score on the Riker Sedation Analgesia Scale.^[4] This led to a reduction in mechanical ventilation, with a trend toward reduction in length of stay and nosocomial infection. Single IV bolus doses of diazepam of 100-200 mg may be required.

Intravenous ethanol infusions have been used in the past, especially in surgical ICUs, as prophylaxis against alcohol withdrawal among patients with suspected or proven alcohol dependence. Retrospective, uncontrolled, noncomparative case series have reported the successful and unsuccessful use of IV ethanol in trauma and burn patients.

Comparative or randomized studies have not demonstrated efficacy for this treatment, and this therapy was inferior to diazepam in a prospective, randomized trial.^[5] As IV ethanol has a short duration of action; a narrow margin of safety; and toxic effects on the gastric mucosa, pancreas, liver, and bone marrow and on other organs, and requires considerable volumes of fluids for administration, this treatment cannot be recommended.

Using the Revised Clinical Institute for Withdrawal Assessment for Alcohol (CIWA-Ar) scale may not be appropriate for guiding symptom-triggered therapy in patients who have complex medical problems or who are postsurgical, critically ill, or in an ICU. Studies demonstrating the effectiveness of the CIWA-Ar scale in safely managing alcohol withdrawal were performed in medically stable ward patients. Patients with complex medical issues, postsurgical patients, ICU patients, and critically ill patients were generally excluded from these trials. The CIWA-Ar scale has not been validated in these patients.

Moreover, the CIWA-Ar protocol and symptom-triggered therapy have been applied inappropriately to patients who had not been drinking for many weeks and who were not able to communicate, resulting in misdiagnosis and delayed diagnosis of other causes of delirium, as well as severe benzodiazepine intoxication due to inappropriate medication use. Postoperative delirium, for which there are many etiologies, has been misdiagnosed as alcohol withdrawal and the CIWA-Ar applied inappropriately with subsequent mistreatment. Patients with complicated medical and surgical comorbidities are not appropriate candidates for symptom-triggered therapy guided by the CIWA-Ar scale.

The issue of alcohol dependence should be addressed prior to hospital discharge, because detoxification from alcohol in the hospital is not sufficient to prevent a patient’s return to hazardous alcohol use. Treatment to prevent relapse frequently requires extended management over long periods of time. Alcohol cessation programs and support groups, such as Alcoholics Anonymous, should be recommended.

Pharmacologic aids to alcohol cessation should be considered, because they may prevent relapse in patients who have been treated for alcohol dependence. Disulfiram, naltrexone, acamprosate, and topiramate have been used in the long-term treatment of alcohol dependence and are initiated after detoxification to alcohol has been completed.

Cognitive behavioral therapy and motivational enhancement therapy (which are sometimes combined with pharmacologic therapy) have been used successfully to prevent relapse.

To prevent hazardous alcohol use, routine screening for alcohol use should be performed in primary care settings. The employment of the AUDIT or CAGE questionnaire is helpful in screening. Protocols for screening persons at risk for hazardous alcohol use, followed by a brief intervention (5-10 min) carried out by a clinician, nurse, or social worker, have been shown to result in a reduction in alcohol consumption and alcohol-related injuries and decreased readmissions to the emergency department. Computer-based screening and counseling programs may be useful when clinicians do not have time to perform screening and face-to-face intervention.