International journal of surgery case reports · 2026
Non-alcoholic Wernicke encephalopathy following pancreaticoduodenectomy (Whipple procedure): a case report and review of the literature.
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Hanada-Angulo Ricardo Mitsuru, Young-Tabusso Frank
Аннотация
INTRODUCTION AND IMPORTANCE: Wernicke encephalopathy (WE) is an acute neurological emergency caused by thiamine deficiency. It is uncommon after pancreaticoduodenectomy and may be overlooked when postoperative metabolic disturbances coexist.
PRESENTATION OF CASE: A 66-year-old woman underwent pancreaticoduodenectomy for a duodenal neoplasm. Her postoperative course was complicated by pancreatic fistula, extended-spectrum beta-lactamase-producing Escherichia coli infection, impaired oral intake, and prolonged nutritional support. During the third to fourth postoperative weeks, she developed fluctuating encephalopathy, bradylalia, and horizontal nystagmus. Serum thiamine was 1.2 µg/dL (reference range: 2.8-8.5 µg/dL), and magnetic resonance imaging showed periaqueductal T2/fluid-attenuated inversion recovery hyperintensity. Hypoosmolar hyponatremia with clinical euvolemia and preserved thyroid and adrenal function was considered compatible with probable postoperative syndrome of inappropriate antidiuretic hormone secretion, although urinary biochemical confirmation was unavailable. Intravenous thiamine 500 mg every 8 hours for 3 days, followed by 250 mg daily for 5 days, produced partial improvement within 24-72 hours. At 3-month follow-up, the neurological manifestations had resolved.
CLINICAL DISCUSSION: Pancreaticoduodenectomy and its complications can accelerate thiamine depletion within a broader spectrum of postoperative nutritional and metabolic disturbances. The oculomotor findings, low serum thiamine, characteristic imaging findings, and treatment response supported a diagnosis of WE. Hyponatremia probably contributed to the altered mental status but did not explain the ocular signs or periaqueductal lesions.
CONCLUSION: WE should be considered in postoperative patients with nutritional compromise and new neurological or oculomotor findings. Parenteral thiamine should not be delayed while awaiting confirmation, and coexisting electrolyte disorders should be corrected cautiously.
PRESENTATION OF CASE: A 66-year-old woman underwent pancreaticoduodenectomy for a duodenal neoplasm. Her postoperative course was complicated by pancreatic fistula, extended-spectrum beta-lactamase-producing Escherichia coli infection, impaired oral intake, and prolonged nutritional support. During the third to fourth postoperative weeks, she developed fluctuating encephalopathy, bradylalia, and horizontal nystagmus. Serum thiamine was 1.2 µg/dL (reference range: 2.8-8.5 µg/dL), and magnetic resonance imaging showed periaqueductal T2/fluid-attenuated inversion recovery hyperintensity. Hypoosmolar hyponatremia with clinical euvolemia and preserved thyroid and adrenal function was considered compatible with probable postoperative syndrome of inappropriate antidiuretic hormone secretion, although urinary biochemical confirmation was unavailable. Intravenous thiamine 500 mg every 8 hours for 3 days, followed by 250 mg daily for 5 days, produced partial improvement within 24-72 hours. At 3-month follow-up, the neurological manifestations had resolved.
CLINICAL DISCUSSION: Pancreaticoduodenectomy and its complications can accelerate thiamine depletion within a broader spectrum of postoperative nutritional and metabolic disturbances. The oculomotor findings, low serum thiamine, characteristic imaging findings, and treatment response supported a diagnosis of WE. Hyponatremia probably contributed to the altered mental status but did not explain the ocular signs or periaqueductal lesions.
CONCLUSION: WE should be considered in postoperative patients with nutritional compromise and new neurological or oculomotor findings. Parenteral thiamine should not be delayed while awaiting confirmation, and coexisting electrolyte disorders should be corrected cautiously.