Nonalcoholic Wernicke’s Encephalopathy Associated with Unintentional Weight Loss, Cholecystectomy, and Intractable Vomiting: The Role of Dual Thiamine and Corticosteroid Therapy

A 23-year-old male with one month of intractable vomiting, subsequent cholecystitis status post cholecystectomy, and overall 40-pound weight loss over the last few months presented with altered mental status and seizures. MRI showed signal abnormalities involving the hypothalamus, periaqueductal gray matter, 4th ventricle, and bilateral thalami, indicative of Wernicke’s encephalopathy. The patient was started on empiric IV thiamine and methylprednisolone; thiamine levels were subsequently found to be low. Infectious disease workup was negative. Within a few days of this therapy, the patient’s neurological status steadily improved with increased responsiveness and communication. Repeat MRI 7 days after admission showed significant resolution of the signal abnormalities. Over the next several weeks the patient became fully conversational, cognitively intact, and increasingly ambulatory. Nonalcoholic Wernicke’s encephalopathy is rare; there have been reports relating it separately to vomiting and invasive surgery. In this case report, we associate it with both recurrent vomiting and minimally invasive cholecystectomy. We also discuss combinatorial therapy of thiamine and corticosteroids, which is poorly defined in the literature. Though there is no consensus-based optimal treatment of Wernicke’s encephalopathy, this adds to the discussion of using dual therapy and supports that the use of empiric corticosteroids does not harm the patient. 1. Introduction Wernicke’s encephalopathy manifests as a result of thiamine deficiency, causing neurological damage in multiple parts of the brain and brainstem [1]. Though most cases of this condition happen in alcoholics, a nontrivial proportion does happen in nonalcoholics. Because of the strong association with alcoholics, however, Wernicke’s encephalopathy is often not entertained as a possible differential diagnostic condition. In nonalcoholic patients, Wernicke’s encephalopathy is most commonly associated with cancer, hyperemesis gravidarum and vomiting, starvation/malnutrition, and AIDS [2]. Another major cause of this condition includes a spectrum of gastrointestinal surgeries, but the vast majority of cases are specifically associated with bariatric surgeries [3]. Hence, in nonalcoholic patients with neurological symptoms concerning for Wernicke’s encephalopathy, risk factors for nonalcoholic Wernicke’s encephalopathy must be carefully probed. In the present case, idiopathic weight loss and minimally invasive cholecystectomy along with postoperative intractable vomiting were the main risk factors for development