Wernicke Encephalopathy in Critical Illness: A Diagnostic Challenge With Evolving MRI Findings

Wernicke encephalopathy (WE) is an acute neurologic disorder caused by thiamine deficiency that can result in significant neurologic morbidity if not promptly recognized and treated.Diagnosis may be particularly challenging in critically ill patients, in whom altered mental status may be attributed to other metabolic, infectious, or neurologic processes.Magnetic resonance imaging (MRI) can support the diagnosis, although characteristic abnormalities are not always present.We present a 43-year-old woman with approximately 2 months of poor oral intake who developed progressive encephalopathy during hospitalization for multiple acute medical conditions.Initial brain MRI showed no characteristic findings of WE.Despite treatment of her underlying illnesses and correction of several metabolic abnormalities, her mental status continued to deteriorate.On hospital day eight, she experienced a cardiac arrest with return of spontaneous circulation after approximately two minutes.Repeat MRI later that day demonstrated new symmetric T2-weighted fluid-attenuated inversion recovery (T2/FLAIR) abnormalities involving the mammillary bodies, dorsomedial thalami, tectal plate, periaqueductal gray matter, region surrounding the third ventricle, and posterior frontal cortex, suggestive of WE.Collateral history subsequently revealed heavy alcohol use, and high-dose intravenous thiamine was initiated.Her neurologic examination improved over the following days, while serial MRI on hospital days 16 and 27 demonstrated marked improvement and near-resolution of the characteristic abnormalities, respectively.Although neurologic improvement followed thiamine administration, concurrent recovery from cardiac arrest and systemic illness limits attribution of this improvement to thiamine alone.This case demonstrates the diagnostic challenge of WE in the setting of critical illness and competing causes of encephalopathy.An initially nondiagnostic MRI does not rule out WE, and continued clinical suspicion with prompt empiric thiamine administration remains important when the diagnosis is suspected.