Introduction: Wernicke’s encephalopathy is a condition most often defined clinically by a common triad of symptoms including confusion/altered mental status, ataxia, and ophthalmoplegia. However, only about 16-20% of patients present with all three of the triad. The remainder present with two or fewer symptoms, with confusion being the most prevalent of the three. In non-alcoholic Wernicke’s encephalopathy, this aforementioned percentage is even smaller, making the diagnosis of this pathology rather challenging. The differential diagnoses include sedative withdrawal, sepsis, stroke, hypoxia, normal pressure hydrocephalus, hepatic encephalopathy, and head injury. Other less common considerations include cerebral venous thrombosis, acute encephalitis due to CMV, herpes or West Nile virus, creutzfeldt-jakob disease, and CNS lymphoma.

Wernicke’s encephalopathy is caused by a deficiency of Vitamin B1 or thiamine. Thiamine is a watersoluble vitamin which is a coenzyme that is crucial in the metabolism and breakdown of glucose as well as maintaining osmotic gradients across cell membranes. The lack of thiamine then causes cell death through necrosis and apoptosis. With time and enough cell death, lesions develop in the brain which impair normal neural signaling resulting in the aforementioned symptoms.

Case Presentation: Patient is a 72 year old male with a past medical history of Type 2 diabetes, hypertension, and who was undergoing radiation treatment for a stage T2, N0 squamous cell carcinoma of the soft palate diagnosed six months prior. He was admitted to the hospital after referral by his radiation oncologist for altered mental status, hypokalemia at 2.6, hyperglycemia, and a low-normal T3 level. He had been diagnosed with and had received radiation treatments without any chemotherapy. He also reported dysphagia to solids and medications and decreased PO intake. The patient reported frequent postprandial emesis and only tolerated nutritional shakes. His wife expressed concern about his declining mental status and gradually worsening instability, confusion, and weakness.

The patient was admitted to the hospital and workup ensued. On further history, there was no significant alcohol use. Vitals were normal except for mild hypertension and on physical exam the patient had altered mentation, was disoriented, was confabulating, but did not display nystagmus or ophthalmoplegia. TSH and T4 were normal, but T3 was mildly decreased, raising suspicion for euthyroid sick syndrome. Hyperaldosteronism was ruled out and hypokalemia was corrected with potassium supplementation. The patient failed a swallow study and gastroenterology was consulted. EGD showed long-segment Barrett’s esophagus and a PEG tube was placed for long-term nutrition. The patient was found to have sepsis secondary to urinary retention and was subsequently treated with empiric antibiotics.

Final/Working Diagnosis: Non-alcoholic Wernicke’s encephalopathy

Management: As the patient continued to be altered and confabulating, a thiamine level was ordered and found to be less than 20 nmol/L. MRI brain showed: DWI restriction and T2FLAIR hyperintensities in the posteromedial thalami, periaqueductal gray matter, and the mammillary bodies (Figures 1 and 2). These findings classically suggest Wernicke’s encephalopathy. Given these findings, thiamine supplementation was started at 500 mg IV every eight hours. On follow up Brain MRI, there was resolution of the abnormal findings. Patient’s mental status significantly improved post thiamine supplementation. Palliative care was consulted and he was eventually stable for discharge to a skilled nursing facility