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Delirium Tremens (DT)

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Last Update: November 18, 2018.

Introduction

Alcohol abuse is a common condition that has been associated with severe impairments in social functioning and medical problems. As high as 20% of the population have been noted to exhibit alcohol abuse during their lifespan. More than 50% of those with a history of alcohol abuse can exhibit alcohol withdrawal symptoms at discontinuing or decreasing their alcohol use. However, only a few (3% to 5%) exhibit symptoms of severe alcohol withdrawal with profound confusion, autonomic hyperactivity, and cardiovascular collapse. This is defined as alcohol withdrawal delirium, more commonly known as delirium tremens (DT).

Delirium tremens was first recognized as a disorder attributed to excessive alcohol abuse in 1813. It is now commonly known to occur as early as 48 hours after abrupt cessation of alcohol in those with chronic abuse and can last up to 5 days. It has an anticipated mortality of up to 37% without appropriate treatment. It is crucial to identify early signs of withdrawal because it can become fatal.[1][2][3]

Etiology

Delirium tremens occurs in chronic alcohol abusers who abruptly discontinue alcohol use, often as early as 48 hours.[4]

Epidemiology

The 12-month and lifetime prevalence is highest in adult men, with 17.6% and 36% respectively. There is a higher prevalence in the Caucasian, younger population, and in those who were never married or previously married. The lifetime risk for developing DT in the population with alcohol abuse is approximately 5% to 10%.

Risk factors for DT include the following:

  • a history of DT
  • prior history of seizures
  • the presence of concurrent illness with associated comorbidities
  • prior history of detoxification
  • the prolonged period prior to last drink.[5][6]

Pathophysiology

Alcohol acts as central nervous system depressant. It enhances the effect of inhibitory neurotransmitters while down-regulating excitatory neurotransmitters. Alcohol interacts with GABA receptors, chloride ion receptor acting as an inhibitory neurotransmitter, via several mechanisms to enhance its activity. Over time, through prolonged alcohol exposure, there is a decrease in GABA activity and alteration in the type of GABA receptor and function. Abrupt cessation of alcohol causes a decrease in the inhibitory actions of GABA neurotransmitter resulting in overactivity of the central nervous system.

Alcohol also inhibits the action of NMDA receptor by acting as a receptor antagonist. It inhibits the action of glutamate, which is an excitatory amino acid. Prolonged alcohol abuse results in receptor up-regulation. Abrupt discontinuation of alcohol causes an increase in the action of glutamate, resulting in profound excitatory action. This may have a clinical manifestation of sympathetic overdrive, such as agitation, tremors, tachycardia, and hypertension.

Certain individuals are more vulnerable to suffer from withdrawal symptoms than others. Though the etiology remains unclear, there is a correlation between the duration of alcohol exposure and withdrawal symptoms.[7][8]

History and Physical

The initial history and physical examination are crucial to establish the diagnosis and evaluate the severity of alcohol withdrawal. Pertinent information in the medical history includes quantity and duration of alcohol abuse, duration since last drink, prior history and severity of alcohol withdrawal, and any additional drug abuse. Additional information should be identified regarding any complicating medical problems such as heart failure, coronary heart disease, chronic liver disease, among others. Some of symptoms may not be self reported, and as a result further evaluation is often needed. Physical examination and laboratory testing should be curtailed to identifying underlying medical problems and identifying potential electrolyte abnormalities, renal and liver function,  sources of infection, coronary ischemia, rhabdomyolysis, and other drug abuse.

The duration of last drink becomes critical in recognizing the severity of symptoms. The initial minor withdrawal symptoms are characterized by anxiety, insomnia, palpitations, headache, and gastrointestinal symptoms. These symptoms usually occur as early as 6 hours after cessation of alcohol use. After 12 hours, minor withdrawal symptoms can progress to alcohol hallucinosis, a condition characterized by visual hallucinations. It can typically resolve in 24 to 48 hours, and may also be associated with auditory and tactile hallucinations. Alcohol withdrawal seizure is followed by alcohol hallucinosis, though it may present as early as 6 hours before alcohol hallucinosis. It can present as the only withdrawal symptoms but typically resolves 24 to 48 hours later. Seizures can recur, though rarely lead to status epileptics. Uncharacteristic signs of seizure activity should warrant further workup. If withdrawal symptoms remain untreated, this can typically lead to DT. DT is characterized by visual hallucinations, profound confusion, tachycardia, hypertension, hyperthermia, agitation, and diaphoresis.

Evaluation

Clinicians need to evaluate the severity of alcohol withdrawal based on history and clinical presentation. The best-validated tool to assess the severity of alcohol withdrawal is the Clinical Institute Withdrawal Assessment for Alcohol, Revised (CIWA-Ar). It is a 10-item questionnaire tool to evaluate, monitor, and treat alcohol withdrawal. It includes symptoms of withdrawal such as anxiety, nausea, and sweating, among others. A score of 8 points or lower corresponds to mild withdrawal, while a score of 9 to 15 corresponds to moderate withdrawal, and a score of 15 or greater corresponds to severe withdrawal symptoms, being at risk for seizures and DT. [9][10]

Additional evaluation of a patient with DT involves identifying electrolyte, nutrition, and fluid abnormalities. Most of these patients present with severe dehydration (up to 10 L fluid deficit) and severe electrolyte abnormalities, including hypoglycemia and severe hypomagnesemia and hypophosphatemia. Multivitamins and thiamine should be supplemented before glucose is given to prevent or precipitate Wernicke’s encephalopathy.

Risk Factors

  • History of DTs
  • Concurrent illness
  • Advanced age
  • Hypokalemia
  • Prior withdrawal symptoms or detoxification

Treatment / Management

The treatment goals for alcohol withdrawal are to control agitation, decrease the risk of seizures, and decrease morbidity and mortality. The most common and validated treatment for alcohol withdrawal is benzodiazepine. There are several benzodiazepines which can be used, ranging from lorazepam (Ativan), diazepam (Valium), to chlordiazepoxide (Librium), preferably administered via an intravenous route. This can be administered either based on a symptom-triggered regimen or fixed schedule. In a symptom-triggered regimen, medications are usually given when symptoms are present, at times using CIWA score greater than 8. In a fixed schedule regimen, the benzodiazepine is administered at fixed intervals, and additional doses are given based on the withdrawal symptoms.

Based on numerous trials, symptom triggered regimens have been shown to require less medication with a smaller duration of treatment. There is no clear consensus on the dosages of benzodiazepine, and this may variably change drastically from one patient to another. Those with substantial dosing requirements warrant intensive care unit monitoring, especially if there are associated comorbid conditions. In those patients, severe DT unresponsive to benzodiazepine, barbiturates such as phenobarbital in conjunction with benzodiazepine can be effective. Another alternative is the use of propofol in conjunction with benzodiazepine; this would, however, require mechanical ventilation.

Although there are studies that demonstrate the effectiveness of central-acting, alpha-2 agonists such as clonidine and dexmedetomidine, these agents should not be used alone and as the primary treatment of alcohol withdrawal. Dexmedetomidine has been shown to work in conjunction benzodiazepine with doses up to 0.7 micrograms per kilogram per hour without requiring mechanical ventilation. It is also recommended to avoid using alcohol, antipsychotics, anticonvulsants, beta-adrenergic receptor blockers, and baclofen for the treatment of alcohol withdrawal as there are not enough studies to support the safety of these medications.[8][11][12]

Differential Diagnosis

The differential diagnosis for DT includes the following: 

  • Sepsis
  • Uremia
  • Stroke
  • Meningitis
  • Encephalitis
  • Wernicke encephalopathy
  • Neuroleptic malignant syndrome
  • Pheochromocytoma
  • Drug toxicity such as with amphetamine, hallucinogen, cocaine, heroin, and PCP
  • Electrolyte abnormalities such as hypocalcemia and hypomagnesemia
  • Thyrotoxicosis
  • Cerebral hemorrhage
  • Cerebral embolism
  • Toxic ingestion or exposures (ethylene glycol)
  • Acute liver failure
  • Diabetic ketoacidosis
  • Brain abscess
  • Hypoglycemia

Prognosis

Mortality from DT has substantially decreased with early recognition and treatment. With early treatment, the mortality rate has decreased to less than 5%. Complications from DT include severe rhabdomyolysis, arrhythmia, and associated comorbid illness. Risk factors such as pneumonia, pancreatitis, older age, history of other medical problems can lead to increased mortality.

Complications

  • Seizures
  • Disorientation
  • Hypertension
  • Hyperthermia
  • Altered mental status
  • Global confusion
  • Arrhythmias
  • Aspiration pneumonitis
  • Respiratory failure
  • Death

Postoperative and Rehabilitation Care

  • To prevent relapse, the patient should be referred to alcoholic anonymous and other support groups.
  • Cognitive behavior therapy may help some patients prevent relapse
  • A referral to a psychiatrist to assess for depression and anxiety may help abstain from alcohol.

Pearls and Other Issues

Recognizing individuals with a history of alcohol abuse can help prevent the progression of withdrawal symptoms. The US Preventative Services Task Force recommends screening individuals age of 18 or older involved with risky drinking and engaging these individuals with behavior therapy and interventions to decrease alcohol misuse. There is a lack of consensus in the prophylactic treatment of alcohol withdrawal. Variations in hospital-wide policies in treating alcohol withdrawal exist and the medications used include benzodiazepine, chlordiazepoxide (Librium), and even gabapentin (Neurontin).

Enhancing Healthcare Team Outcomes

DTs are very common in hospitalized patients and can be quite difficult to manage. DTs also prolong hospital stay and result in a high cost of healthcare. Today, the emphasis is on prevention of DTs. To prevent excessive use of alcohol, there are many screening tools available that should be performed in the emergency room or in primary care settings. The screening tools are carried out by a nurse, social worker or a pharmacist. There is good evidence showing that screening for alcohol use can result in a reduction of alcohol consumption, associated injuries and decreased rate of readmissions to the hospitals. [13][14][15](Level V) Today nurses also run computer-based programs to screen and counsel patients who have been discharged with a diagnosis of DTs. Data on short-term or acute drinkers do show that these screening protocols work, but whether they work in severe alcoholics remains debatable. Anytime a patient presents with a history of alcohol use; one should try and quantify the use.

Outcomes

DTs can be associated with a number of complications including respiratory depression, seizures, arrhythmias and aspiration pneumonitis. Even with appropriate therapy, the mortality varies from 5 to 15%. The only way to lower the mortality is aggressive resuscitation and treat any concurrent illness.  Failure to treat or delay in diagnosis always leads to high morbidity and mortality.[16][17] (Level V)

Questions

To access free multiple choice questions on this topic, click here.

References

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Bookshelf ID: NBK482134PMID: 29489272

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