Perioperative Wernicke's encephalopathy associated with thiamine deficiency: Intraoperative EEG findings and...

Wernicke encephalopathy (WE) results from thiamine deficiency and frequently affects nonalcoholic surgical patients with prolonged fasting and parenteral nutrition. Perioperative WE is often misdiagnosed due to nonspecific symptoms, and its intraoperative electroencephalographic and anesthetic features remain poorly understood.

A 68-year-old male underwent hepatic surgery for malignant obstructive jaundice. Postoperative biliary anastomotic leakage and aphagia led to long-term parenteral nutrition. The patient subsequently developed confusion, somnolence, nystagmus, visual loss, and peripapillary retinal hemorrhage. He also showed abnormal cerebral reactivity to anesthetics during secondary surgery.

Clinical diagnosis: nonalcoholic WE with thiamine-deficiency retinopathy. Infectious, septic encephalopathy and cerebral infarction were excluded.

Immediate high-dose intramuscular thiamine and magnesium supplementation were initiated. During secondary surgery, anesthesia was cautiously titrated with continuous electroencephalography and patient state index monitoring, with reduced anesthetic doses. Maintenance thiamine therapy was continued postoperatively.

Neurological symptoms markedly improved within 3 days after thiamine treatment. Intraoperative electroencephalography revealed diffuse slowing and burst suppression under low anesthetic doses. The patient fully recovered without permanent neurological or ophthalmic sequelae and was discharged uneventfully.

Prolonged postoperative parenteral nutrition confers high WE risk in nonalcoholic surgical patients. Early empirical thiamine supplementation is essential. Thiamine deficiency increases neuronal sensitivity to anesthetics. Clinicians should enhance perioperative nutritional risk assessment and optimize anesthetic management to avoid severe cerebral complications.