Abstract
Wernicke's encephalopathy (WE) is a prominent neurologic manifestation of thiamine (vitamin B1) deficiency. While often linked to alcoholism, it can also arise from various causes, including malabsorption, inadequate dietary intake, increased metabolic requirement, and among dialysis patients. Here, we present a case of altered mental status from acute metabolic encephalopathy attributed to sepsis, acute kidney injury (AKI), and hypoglycemia. WE was overlooked in the early hospitalization course due to the daily administration of thiamine. However, the patient's cognitive decline persisted despite the improvement of sepsis and AKI. Subsequent brain MRI revealed thalamic T2 signal intensity changes, suggesting either a past infarction or WE. Implementing an empirical regimen of high-dose thiamine resulted in the patient's rapid cognitive recovery. This therapeutic strategy was integrated into the management of her sepsis and AKI, leading to her full recovery and subsequent hospital discharge without complications.