Abstract
Background: Wernicke’s encephalopathy (WE) is an acute neuropsychiatric derangement caused by Vitamin-B1 (Thiamine) deficiency. Clinical Case: A 49-year-old Hispanic woman was admitted with abdominal pain, intractable nausea and vomiting, two weeks following a diagnosis of infectious mononucleosis. An upper endoscopy was negative. She was discharged on symptomatic treatment with pantoprazole and sucralfate. Four weeks later, she presented with worsening symptoms and a new complaint of blurry vision. Physical exam revealed decreased visual acuity with dysconjugate gaze. Brain CT and MRI were unremarkable. Outpatient ophthalmology consultation was advised. Four days later, she reported to the ophthalmologist with worsening vision, headaches, distal tingling/numbness, gait instability, mildly impaired cognition. The ocular examination revealed visual acuity restricted to counting fingers, large central scotoma, restricted abduction/adduction, and bilateral horizontal and vertical nystagmus. She was readmitted with a suspicion of Miller-Fischer variant of Guillain-Barre. She denied alcohol consumption, tobacco or recreational drug use. She reported 40lb weight loss in 5 weeks. On physical exam, strength was normal, with decreased distal vibration sensation, absent ankle reflexes and ataxic gait. Anti-GQ1b antibodies and CSF studies were unremarkable. Further testing revealed negative/normal HIV antigen/antibody, vitamin B12 level, glycohemoglobin A1c, Lyme antibodies, angiotensin converting enzyme, ANA and serum protein electrophoresis. Serial brain MRI showed FLAIR hyperintensity in both thalami, dorsal medial brainstem along the mammillary bodies, and the third periventricular white matter. Thiamine deficiency was strongly suspected. A vitamin-B1 level was sent out and she was empirically started on large dose IV thiamine. The thiamine level returned very low at 24nmol/l (70-180nmol/l) confirming WE. Her symptoms began to resolve within 12 hours of thiamine infusion. Given no preceding history of alcoholism, a workup for other causes of thiamine deficiency was pursued. Celiac serology, stool pancreatic elastase, CT chest/abdomen/pelvis, colonoscopy were unremarkable. Thiamine deficiency was attributed to her prolonged history of vomiting, decreased intake, in combination with the recently prescribed pantoprazole and sucralfate which contributed to malabsorption. Discussion: WE is typically related to alcoholism. From 1867-2014, 623 cases of WE were described in non-alcoholics. We should have a high index of suspicion for thiamine deficiency in situations of unbalanced nutrition that has lasted for 2 to 3 weeks to avoid misdiagnosis of the life-threatening WE or irreversible brain damage (Korsakoff syndrome). This should prompt immediate administration of large doses of thiamine parenterally even prior to laboratory confirmation.