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October 22, 1997

Pharmacologic Treatment of Alcohol Withdrawal

Author Affiliations

Wright State University School of Medicine Dayton, Ohio

JAMA. 1997;278(16):1317. doi:10.1001/jama.1997.03550160037026

To the Editor.  —Dr Mayo-Smith and colleagues1 eloquently present an excellent evidence-based strategy to treat patients at risk for alcohol withdrawal. They correctly note that patients who consume large amounts of alcohol are frequently thiamine deficient and, as such, should receive oral or parenteral thiamine to prevent Wernicke encephalopathy. However, they do not mention the importance of administering thiamine prior to glucose, an action that may be important in preventing this syndrome in patients with marginal thiamine reserves. Hypoglycemia may cause seizure activity; therefore, it is imperative to exclude hypoglycemia as a cause of seizures in alcohol-dependent patients before incriminating alcohol withdrawal as a cause of seizure activity. Hypoglycemia is not uncommon in alcoholic patients and is typically due to poor carbohydrate intake, vomiting, and alcohol-induced inhibition of hepatic gluconeogenesis.2 Thiamine should be administered prior to a glucose load because cases of Wernicke encephalopathy have been reported after glucose administration in