Management of Acute Alcohol Withdrawal Syndrome in Critically Ill Patients

Abstract

Approximately 16-31% of patients in the intensive care unit (ICU) have an alcohol use disorder and are at risk for developing alcohol withdrawal syndrome (AWS). Patients admitted to the ICU with AWS have an increased hospital and ICU length of stay, longer duration of mechanical ventilation, higher costs, and increased mortality compared with those admitted without an alcohol-related disorder. Despite the high prevalence of AWS among ICU patients, no guidelines for the recognition or management of AWS or delirium tremens in the critically ill currently exist, leading to tremendous variability in clinical practice. Goals of care should include immediate management of dehydration, nutritional deficits, and electrolyte derangements; relief of withdrawal symptoms; prevention of progression of symptoms; and treatment of comorbid illnesses. Symptom-triggered treatment of AWS with γ-aminobutyric acid receptor agonists is the cornerstone of therapy. Benzodiazepines (BZDs) are most studied and are often the preferred first-line agents due to their efficacy and safety profile. However, controversy still exists as to who should receive treatment, how to administer BZDs, and which BZD to use. Although most patients with AWS respond to usual doses of BZDs, ICU clinicians are challenged with managing BZD-resistant patients. Recent literature has shown that using an early multimodal approach to managing BZD-resistant patients appears beneficial in rapidly improving symptoms. This review highlights the results of recent promising studies published between 2011 and 2015 evaluating adjunctive therapies for BZD-resistant alcohol withdrawal such as antiepileptics, baclofen, dexmedetomidine, ethanol, ketamine, phenobarbital, propofol, and ketamine. We provide guidance on the places in therapy for select agents for management of critically ill patients in the presence of AWS.

Use of Phenobarbital in Delirium Tremens

“…Currently, the standard of care for alcohol withdrawal centers on benzodiazepine therapy until cessation of alcohol withdrawal symptoms occurs or additional pharmacological therapy is needed. 1 , 2 The choice of additional therapy, however, is not standardized nor are there well-established regimens in place. 1 This is particularly important for high-risk patients such as those who have a personal or family history of alcohol withdrawal or DT.…”

Analysis of BMSCs-intervened viscoelasticity of sciatic nerve in rats with chronic alcoholic intoxication

“…bFGF can promote the regeneration of peripheral nerves. However, previous studies [5][6][7][8][9][10][11] did not analyze the viscoelastic reduction, dull/drowsy body, significantly increased sleep time, body weight growth, and less eating than group CON, proving the successful establishment of the CAI rat model. Electrophysiological test: Alcoholism in humans or animals always resulted in damage to the peripheral nerves.…”

“…Chronic alcohol intoxication (CAI)-induced peripheral neuropathy was discovered earlier, but caught people's attention only towards the end of the 19th century 4 . Many scholars have conducted research on drug therapies against CAI 5,6 . Monforte et al 7 showed that long-term intake of ethanol can cause changes in the cytoskeletal structure of peripheral nerves, and affect the transportation among the axons, thus affecting the functional integration of neurons.…”

<p>Management of Alcohol Withdrawal in the Emergency Department: Current Perspectives</p>

“…[69][70][71][72] Other studies, however, have demonstrated that propofol is associated with longer hospital stays, and the significant risks of hypotension and respiratory depression associated with this medication necessitate mechanical ventilation and close monitoring in the ICU. 71,73,74 Ketamine is another NMDA-antagonist with less potential for respiratory depression. Two small retrospective studies found that the use of ketamine as an adjunct reduced benzodiazepine requirements in patients with RAW.…”