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Author: Niklas Eriksson, MS4
Loyola University Chicago Stritch School of Medicine
AAEM/RSA Social Media Committee
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There are roughly eight million Americans who are alcohol-dependent, with 500,000 cases of alcohol withdrawal requiring treatment each year.[1] Being able to recognize and manage alcohol withdrawal is an essential skill for every emergency room physician. Long-term ethanol use causes downregulation of gamma-aminobutyric acid (GABA) receptors causing an increased inhibitory tone, as well as upregulation of glutamate receptors to maintain excitatory pathways. With sudden cessation of ethanol, there is decreased inhibition via GABA receptors and increased excitatory effects from glutamate receptors, causing central nervous system (CNS) excitation and the symptoms of alcohol withdrawal.[2]
As with all emergency department (ED) patients, the first step is to manage ABC’s (airway, breathing, and circulation). Aspiration can occur with withdrawal seizures. Initial symptoms of withdrawal can begin as soon as six hours after the patient’s last drink, so asking for a timeline of the patient’s last alcoholic drink is essential for determining when symptoms can be anticipated. A serum ethanol should also be obtained. Hypoglycemia is commonly associated with alcoholic abuse, so checking serum glucose remains essential. Given alcohol’s association with liver and pancreatic damage, a complete blood count (CBC), basic metabolic panel (BMP), Liver enzymes, and Lipase should be checked if there is suspicion for hepatitis or pancreatitis.[3] For the first 6 to 36 hours after the last drink, symptoms can include tremulousness, anxiety, headache, diaphoresis, palpitations, and gastrointestinal upset.[2] Benzodiazepines (often lorazepam or diazepam) are used for management, as they stimulate GABA receptors to inhibit the increased excitatory CNS effects. Withdrawal seizures can occur within 12 to 48 hours, usually occurring as singular seizures or brief flurries. Benzodiazepines are also the treatment of choice here. Examples of doses are Lorazepam IV 2-4mg every 15-20 minutes, or diazepam IV 5-10mg IV every 5-10 minutes, until symptoms resolve.[3]
CNS excitation symptoms are addressed first, then adrenergic hyperactivity and delirium. CNS excitation (tremors, seizures) is treated with benzodiazepines, while adrenergic hyperactivity such as tachycardia and hypertension are treated as they present, so beta blockers such as propranolol can be used for tachycardia, or an alpha-2 agonist such as clonidine can be used as well. [1,7]
Chronic alcohol abuse depletes thiamine through poor diet, and so initial treatment should include thiamine replacement. Thiamine depletion can cause Wernicke’s encephalopathy, where patients develop ophthalmoplegia (nystagmus), ataxia, and delirium.[5] This is especially important to consider in patients who are also hypoglycemic, as glucose needs to be given concomitantly with thiamine. Although previously taught that thiamine should always be given before glucose to prevent worsening of Wernicke’s encephalopathy, it does not necessarily hold true in the literature. In fact, glucose can safely be administered before thiamine. [5] Furthermore, thiamine replacement should not be a reason for a delay in treating hypoglycemia, so the two can be administered concomitantly.[6] Thiamine deficiency and Wernicke’s encephalopathy, interestingly, can also be found in patients who have undergone bariatric surgery (again due to reduced absorption from diet), and so patients with this surgical history should not be given glucose first when this condition is present.
Delirium tremens can affect alcohol abusers starting 48 hours after their last drink, up to 96 hours after. This condition can present with hypertension, tachycardia, fever, diaphoresis, delirium, hallucinations, and tremors or seizures. Risk factors include a history of alcohol abuse, a history of previous delirium tremens or withdrawal seizures, age above 30, concurrent medical illnesses, an elevated blood alcohol level (BAC), and burn injuries.[1,4]
Delirium tremens has a 5% mortality rate even for patients being treated in the intensive care unit (ICU), and thus chronic alcohol users going through withdrawal who exhibit these symptoms need ICU admission. Mortality without treatment is up to 35%.[4]
Overall, alcohol withdrawal and its complications will be seen commonly in every ED, and becoming familiar with identification and management is an important factor for every medical student and resident as they progress through their training.
References
1. Kosten TR, O’Connor PG. Management of drug and alcohol withdrawal. N Engl J Med. 2003; 348:1786.
2. Most D, Ferguson L, Harris RA. Molecular basis of alcoholism. HandbClin Neurol. 2014;125:89-111.
3. Hoffman, RS, and Weinhouse, GL. Management of moderate and severe alcohol withdrawal syndromes. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2014.
4. Kim DW, Kim HK, Bae EK, Park SH, Kim KK. Clinical predictors for delirium tremens in patients with alcohol withdrawal seizures. Am J Emerg Med. 2015 May;33(5):701-4.
5. Osiezagha K, MD; Ali S, MD; Freeman C, MD; et al. Thiamine Deficiency and Delirium. Innov Clin Neurosci. 2013;10(4):26–32
6. Schabelman E, Kuo D. Glucose before thiamine for Wernicke encephalopathy: a literature review. J Emerg Med. 2012 Apr;42(4):488-94.
7. Frazee EN, Personett HA, Leung JG, Nelson S, Dierkhising RA, Bauer PR. Influence of dexmedetomidine therapy on the management of severe alcohol withdrawal syndrome in critically ill patients. J Crit Care. 2014 Apr;29(2):298-302.