Sean Hersey, MD
Background
Alcohol withdrawal can significantly complicate ICU management. Trauma patients that suffer alcohol withdrawal are almost 3 times more likely to be intubated, spend twice as much time on the ventilator and are more than 5 times as likely to get pneumonia. Interestingly, this study showed that more than 14% of patients who suffered AWS had an admitting BAC of 0.
Definition, diagnostic criteria for alcohol withdrawal syndrome (AWS):
A. Cessation or decrease in alcohol use that has been heavy or prolonged
B. Two or more of the following
- autonomic hyperactivity(sweating or HR > 100 bpm)
- tremors
- insomnia
- nausea, emesis
- visual, tactile, or auditory hallucinations
- psychomotor agitation
- anxiety
- seizures
Presentation
AWS clinical presentations have a high degree of variability and is heavily influenced by each patient’s intake pattern, intake volume, comorbidities, degree of injury or surgical illness, and genetics.
AWS can begin as early as three to six hours after alcohol cessation with headache, anxiety, and diaphoresis. It can progress to visual, auditory, and tactile hallucinations occurring over the next 12 to 24 hours, and then delirium tremens(DTs), typified by fever, hypertension, tachycardia, agitation and further hallucinations which can persist for 2 -4 days post alcohol cessation. Diagnostic and Statistical Manual of Mental Disorders 5th Edition define DTs as signs of severe AWS accompanied by delirium of acute onset with disturbances of attention, awareness, and cognition without evidence of other neurocognitive disorder, coma, or substance effect. Literature reports mortality of DTs as high as 15% if left untreated. Early identification of DTs is critical with some studies reporting mortality as low as 1-2% if promptly treated.
Evaluation
Once a patient has been identified as being at risk for AWS via AUDIT-C and/or other clinical findings, we use the Clinical Institute Withdrawal Assessment for Alcohol Scale (CIWA) to assess the degree and progression of AWS. CIWA is an objective nursing driven sedation-agitation scoring scale used to rate the severity of AWS symptoms and to aid in its management. CIWA scale has been shown to be predictive for not only the development of AWS but also Delirium Tremens in the trauma population. Downsides of the CIWA scale are not insignificant and include its inherently subjective nature. Several subsets of CIWA scoring prompts require patient communication, which can be difficult to assess in the intubated, non-English speaking or neurologically compromised (TBI) patients. Patient history should also be probed to detect established AWS risk factors including: binge drinking, drug abuse, alcoholic liver disease or alcoholic neuropathy, Wernicke-Korsakoff syndrome, and the existence of prior episodes of AWS.
Consider using a RIKER or RASS scale for assessing for AWS in nonverbal critically ill patients as in a recent study from Journal of Trauma and Acute Care Surgery: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966905
Treatment
There is a high prevalence of intravascular volume depletion and significant electrolyte abnormalities in the chronic alcoholic population. Initial treatment should focus on fluid resuscitation, electrolyte correction and nutritional supplementation. We recommend administration of a “banana bag” containing Thiamine 100mg, folic acid 1mg, multivitamin, and magnesium 3g mixed in 1L NS in all patients who score positive on AUDIT-C admission screening.
Benzodiazepines (BZDs) are traditionally considered to be the first line agents in the treatment of AWS. Pharmacologic treatment typically begins with the onset of symptoms suggestive of AWS. Ultimately the goal of AWS treatment is to prevent the progression of symptoms and the development of DTs. Protocolized and symptom driven treatment has been shown to be associated with decreased ICU LOS, duration of mechanical ventilation, and BZD requirements. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966905
BZD options: lorazepam, diazepam. Advantages, disadvantages:
-Lorazepam-Shorter half life, no active metabolites so may be preferable for those with AKI. Undergoes only hepatic glucuronidation so metabolism less affected by age, liver disease. Doses usually 0.5-4 mg.
-Diazepam-Longer half life, smoother clinical course, less recurrent seizures or withdrawal in theory. Doses usually 5-10 mg.
Dexmedetomidine(DEX) is a selective alpha-2 agonist with sedative, anxiolytic and sympatholytic effects. It does not cause respiratory depression like BDZs or barbiturates. It is effective in AWS by reducing the autonomic sympathetic hyperactivity and provides significant symptomatic relief. It does not however exhibit any antiepileptic or GABA activity like BDZs. Two recent prospective single center RCTs have shown a decrease in the total BZD dose and ICU LOS when using Dexmedetomidine as an adjunct to BZDs in the treatment of AWS.
The most common side effect of DEX is bradycardia. This can be so profound that it can lead to cessation/intolerance of therapy.
Also consider beta blockers and clonidine as adjuncts for managing the hyper-sympathetic state of AWS.