A Case of Postoperative Wernicke Encephalopathy Mimicking Cerebellar Infarction Complicated by Postoperative Nausea and Vomiting: A Critical Diagnostic Pitfall for Thoracic Surgeons.
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
추출되지 않음
I · Intervention 중재 / 시술
a right upper lobectomy and mediastinal lymph node dissection without intraoperative complications
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
Early recognition and empiric thiamine supplementation are crucial to prevent irreversible neurological damage. Thoracic surgeons should maintain a high index of suspicion for WE, particularly in at-risk patients, to avoid a delayed diagnosis and improve clinical outcomes.
[INTRODUCTION] Wernicke encephalopathy (WE) is a potentially life-threatening neurological disorder caused by a thiamine deficiency, most commonly associated with alcoholism or malnutrition.
APA
Oki T, Iizuka S, et al. (2025). A Case of Postoperative Wernicke Encephalopathy Mimicking Cerebellar Infarction Complicated by Postoperative Nausea and Vomiting: A Critical Diagnostic Pitfall for Thoracic Surgeons.. Surgical case reports, 11(1). https://doi.org/10.70352/scrj.cr.25-0438
MLA
Oki T, et al.. "A Case of Postoperative Wernicke Encephalopathy Mimicking Cerebellar Infarction Complicated by Postoperative Nausea and Vomiting: A Critical Diagnostic Pitfall for Thoracic Surgeons.." Surgical case reports, vol. 11, no. 1, 2025.
PMID
41281732 ↗
Abstract 한글 요약
[INTRODUCTION] Wernicke encephalopathy (WE) is a potentially life-threatening neurological disorder caused by a thiamine deficiency, most commonly associated with alcoholism or malnutrition. Although its occurrence after gastrointestinal surgery has been increasingly recognized, WE following thoracic surgery remains extremely rare and is often underrecognized by thoracic surgeons. Given that neurological symptoms of WE can mimic those of cerebral infarction, a timely diagnosis is challenging, especially when complicated by postoperative nausea and vomiting (PONV).
[CASE PRESENTATION] We report a rare case of WE following a pulmonary lobectomy in a severely malnourished 75-year-old woman with a history of recurrent thyroid cancer. A 1.6-cm pulmonary nodule was incidentally detected during routine follow-up, and a diagnosis of a primary lung adenocarcinoma was established. The patient underwent a right upper lobectomy and mediastinal lymph node dissection without intraoperative complications. Persistent PONV developed immediately postoperatively, necessitating peripheral parenteral nutrition without vitamin supplementation. On POD 3, the patient developed ataxia, dysmetria, and saccadic eye movements. Although a cerebral infarction was initially suspected, brain magnetic resonance imaging revealed hyperintense signals in the periaqueductal region, suggestive of WE. Intravenous thiamine replacement with fursultiamine led to the gradual resolution of the neurological symptoms and nausea. The patient resumed oral intake on POD 7 and was discharged on day 10 without any neurological sequelae.
[CONCLUSIONS] This case highlighted the importance of considering WE as a differential diagnosis in malnourished patients presenting with neurological symptoms and PONV after a pulmonary resection, even in the absence of alcohol use. Early recognition and empiric thiamine supplementation are crucial to prevent irreversible neurological damage. Thoracic surgeons should maintain a high index of suspicion for WE, particularly in at-risk patients, to avoid a delayed diagnosis and improve clinical outcomes.
[CASE PRESENTATION] We report a rare case of WE following a pulmonary lobectomy in a severely malnourished 75-year-old woman with a history of recurrent thyroid cancer. A 1.6-cm pulmonary nodule was incidentally detected during routine follow-up, and a diagnosis of a primary lung adenocarcinoma was established. The patient underwent a right upper lobectomy and mediastinal lymph node dissection without intraoperative complications. Persistent PONV developed immediately postoperatively, necessitating peripheral parenteral nutrition without vitamin supplementation. On POD 3, the patient developed ataxia, dysmetria, and saccadic eye movements. Although a cerebral infarction was initially suspected, brain magnetic resonance imaging revealed hyperintense signals in the periaqueductal region, suggestive of WE. Intravenous thiamine replacement with fursultiamine led to the gradual resolution of the neurological symptoms and nausea. The patient resumed oral intake on POD 7 and was discharged on day 10 without any neurological sequelae.
[CONCLUSIONS] This case highlighted the importance of considering WE as a differential diagnosis in malnourished patients presenting with neurological symptoms and PONV after a pulmonary resection, even in the absence of alcohol use. Early recognition and empiric thiamine supplementation are crucial to prevent irreversible neurological damage. Thoracic surgeons should maintain a high index of suspicion for WE, particularly in at-risk patients, to avoid a delayed diagnosis and improve clinical outcomes.
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