Case of non-alcoholic Wernicke’s encephalopathy

Abstract

A 61-year-old obese man presented with 8-week history of nausea and occasional vomiting. He reported poor appetite and unintentional weight loss of more than 20 kg of his body mass. A week after admission, he developed double vision and unsteady gait. Neurological examination revealed isolated sixth cranial nerve palsy on the left side with horizontal nystagmus that progressed to bilateral lateral gaze palsy with normal vertical gaze. Brain MR revealed T2/fluid attenuation inversion recovery (FLAIR) high signal in mammillary bodies, tectum of the midbrain and the periaqueductal grey matter. He was diagnosed with Wernicke’s encephalopathy (WE). WE is a medical emergency that carries high mortality yet can be often under-diagnosed in the non-alcoholic patient. Varied presentation and absence of alcohol dependence lowers the degree of suspicion and this was true in this case. The patient was given intravenous thiamine and made a rapid and dramatic recovery.

Development of Wernicke’s Encephalopathy during Total Parenteral Nutrition Therapy without Additional Multivitamin Supplementation in a Patient with Intestinal Obstruction: A Case Report

“…The daily requirement of thiamine is 5 mg [3], and 0.5 mg thiamine per 1,000 kcal meal should be supplied to maintain thiamine-related functions [1]. Because the thiamine body reserves are approximately 30 mg, depletion of the body's stores can develop within two to three weeks in patients receiving a strict thiamine-free diet [2,3,7].…”

“…WE is frequently reported in patients with hyperemesis gravidarum and dialysis-related loss of thiamine, in those who undergo chemotherapy or bariatric surgery and in people with long-term alcohol abuse [1,[7][8][9][10]. However, longterm total parenteral nutrition (TPN) therapy with insufficient multivitamin support can also cause WE iatrogenically [1,3,[7][8][9][10].…”

“…WE is frequently reported in patients with hyperemesis gravidarum and dialysis-related loss of thiamine, in those who undergo chemotherapy or bariatric surgery and in people with long-term alcohol abuse [1,[7][8][9][10]. However, longterm total parenteral nutrition (TPN) therapy with insufficient multivitamin support can also cause WE iatrogenically [1,3,[7][8][9][10]. Parenteral nutrition (PN) is often given to increase or ensure nutrient intake in malnourished patients, but it is a complex therapy that requires a robust system to ensure its safety and efficacy [11].…”

A Case of Wernicke Encephalopathy Secondary to Anorexia Nervosa Complicated by Refeeding Syndrome and Takotsubo Cardiomyopathy

“…Once ventilatory support was provided, she was supplemented with thiamine and slowly fed to avoid worsening of her refeeding syndrome. Thiamine is known to play an important role in glucose metabolism, which is aggravated by hypomagnesemia, as magnesium is a cofactor for thia-mine-dependent enzymes [ 16 ]. Thiamine is recommended for patients with a diagnosis consistent with WE; however, the optimum dose, frequency, and duration have not been supported by substantial evidence.…”

Wernicke Encephalopathy as the First Presentation of Neuromyelitis Optica Spectrum Disorder With Horizontal Nerve Palsy

“…Females with low body weight are believed to have a higher risk of WE (2). The most common cause of nonalcoholic WE include persistent vomiting, poor nutritional intake, and chronic diarrhea (3). WE cannot be diagnosed based on thiamine level measurement alone, as there is no exact critical level at which patients may develop the symptoms (3).…”