# A Case of Postoperative Wernicke Encephalopathy Mimicking Cerebellar Infarction Complicated by Postoperative Nausea and Vomiting: A Critical Diagnostic Pitfall for Thoracic Surgeons

## TL;DR

A 75-year-old malnourished patient developed neurological symptoms after lung surgery, which were initially mistaken for a brain infarction but were later diagnosed as Wernicke encephalopathy.

## Contribution

Highlights a rare case of postoperative Wernicke encephalopathy mimicking cerebellar infarction in thoracic surgery patients.

## Key findings

- Neurological symptoms after thoracic surgery can be caused by Wernicke encephalopathy, not cerebral infarction.
- Early thiamine supplementation resolved neurological symptoms and nausea in the patient.
- Timely diagnosis of WE is crucial to prevent irreversible neurological damage.

## Abstract

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).

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.

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.