Wernicke’s Encephalopathy Masquerading as Hepatic Encephalopathy in Severe Cholestatic Drug-Induced Liver Injury: A Case Report

Background Wernicke’s encephalopathy (WE) is a life-threatening neurological emergency caused by thiamine (vitamin B1) deficiency, classically associated with chronic alcohol use. However, in non-alcoholic patients, it is often precipitated by prolonged periods of malnutrition or chronic illness, where it remains frequently underdiagnosed. Case presentation: A 59-year-old lifelong non-alcoholic male presented with a three-month history of progressive cholestatic drug-induced liver injury (DILI) following a course of oral co-amoxiclav therapy. His clinical course was complicated by severe anorexia, weight loss, and severe biochemical hypothyroidism. Despite improving liver enzymes and normalisation of thyroid function following levothyroxine replacement, the patient developed acute confusion, agitation, and truncal ataxia. Initial clinical suspicion was directed toward hepatic encephalopathy (HE) due to persistent jaundice (bilirubin 230 µmol/L); however, the absence of asterixis and the presence of atypical neurological signs prompted neuroimaging. Magnetic resonance imaging (MRI) of the brain revealed symmetrical T2/FLAIR hyperintensities in the mammillary bodies, thalami, and periventricular region of the third ventricle, confirming a diagnosis of WE. Prompt administration of high-dose intravenous thiamine resulted in a full neurological recovery. Conclusions This case highlights the "diagnostic trap" of anchoring bias in hepatology, where neurological symptoms are reflexively attributed to HE in the presence of biochemical liver injury. In patients with chronic DILI and protracted anorexia, clinicians must maintain a high index of suspicion for WE to prevent permanent neurological damage.