WERNICKE ENCEPHALOPATHY AFTER GASTRIC BYPASS: A SURPRISING ETIOLOGY OF ALTERED MENTAL STATUS PROGRESSING TO CARDIAC ARREST

Abstract

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Wernicke’s Encephalopathy (WE) after bariatric surgery is more frequent than commonly understood. Doctors and patients must be aware of the risk and predisposing factors for WE to effectively prevent this potentially fatal condition. In this case, we present a patient with a late diagnosis of WE, with altered mental status resulting in eventual cardiac arrest and intubation. CASE PRESENTATION: A 63-year-old woman was brought to the ED after being found at home confused. She had no history of alcohol use. She exhibited disconjugate gaze and mental slowing, but was otherwise neurologically intact. CT brain demonstrated no acute changes and labs were normal. The patient had a sleeve gastrectomy 2 months prior, and a history of depression and anxiety. Family reported that following bariatric surgery she had poor oral intake and frequent vomiting. She was admitted for confusion and dehydration, and diagnosed with a UTI. She remained altered and on hospital day 9 the patient suffered a cardiac arrest of unclear etiology and CPR was started. She was intubated and transferred to the ICU, where she remained minimally responsive for several days. A brain MRI then demonstrated evidence of WE, specifically T2 FLAIR hyperintense signal abnormalities involving the mammillary bodies, medial thalami, periaqueductal area, and around the third ventricle. Intravenous thiamine was started immediately. Over the next few days, her mental status slowly began to recover. DISCUSSION: WE is primarily associated with malnutrition and chronic alcohol use, however hyperemesis gravidarum or bariatric surgery recovery can also produce the syndrome. Patients who undergo bariatric surgery are at risk of multiple vitamin deficiencies; B1 deficiency is common enough to have garnered the nickname “bariatric beriberi”. The classic triad for WE consists of ataxia, nystagmus, and confusion. The underlying pathophysiology is related to severe thiamine deficiency, and symptoms can be precipitated by glucose loading causing lactic acidosis in the medial thalamus resulting in neuronal damage. In a 2008 review of 84 existing cases, 94% occurred within the first 6 months post-surgery. As with our patient, MRI revealed lesions in 47% of patients. In 2007, another review found WE was most likely to occur between 4 and 12 weeks after surgery; our patient presented with symptoms at 8 weeks post-surgery. A case series from Southern Europe reported a preventive intervention after biliopancreatic diversion; no WE cases were observed after initiating administration of large doses of thiamine to patients reporting small food intakes during early postoperative weeks. CONCLUSIONS: Our patient’s altered mentation seems to have begun after diminishing PO intake for days at home. Given the risk for WE with progression to severe altered mental status, providers should consider thiamine deficiency in altered patients with recent bariatric surgeries. Reference #1: Aasheim ET. Wernicke Encephalopathy After Bariatric Surgery. Annals of Surgery. 2008;248(5):714-720. https://doi.org/10.1097/SLA.0b013e3181884308. Reference #2: Sonal S, Abhay K. Wernicke encephalopathy after obesity surgery Neurology Mar 2007, 68 (11) 807-811; https://doi.org/10.1212/01.wnl.0000256812.29648.86 DISCLOSURES: No relevant relationships by Mitchell Brown, source=Web Response No relevant relationships by Amy Wolfe, source=Web Response