# Delayed Duodenal Ulcer Perforation Following Esophageal Endoscopic Submucosal Dissection Complicated by Perforation: A Case Report

## TL;DR

A patient developed a delayed duodenal ulcer perforation after esophageal ESD, highlighting the need for PPI therapy in high-risk cases.

## Contribution

This case report highlights the rare complication of delayed duodenal ulcer perforation following ESD and suggests prophylactic PPI use in high-risk patients.

## Key findings

- Delayed duodenal ulcer perforation occurred six days after esophageal ESD.
- Stress-related mucosal disease may have contributed to the perforation.
- Laparoscopic repair was required as endoscopic closure was unfeasible.

## Abstract

Endoscopic submucosal dissection (ESD) is an established treatment of superficial esophageal neoplasms. Common complications include bleeding, perforation, and stricture. However, delayed gastrointestinal perforation distant from the ESD site is exceptionally rare. We report the case of a woman in her 70s with a history of nonsteroidal anti‐inflammatory drug (NSAID)‐associated duodenal ulcer and Helicobacter pylori infection who underwent ESD for superficial esophageal squamous cell carcinoma. After eradication therapy and 2 months of proton pump inhibitor (PPI) use, both treatments were discontinued. Preoperative endoscopy confirmed a scarred duodenal ulcer. Intraoperative esophageal perforation occurred during ESD and was closed with clips. Postoperative computed tomography (CT) showed mediastinal emphysema without intra‐abdominal free air. The patient was treated in high care with fasting and antibiotics, but without PPI therapy. Six days postoperatively, the patient developed acute abdominal pain. CT revealed free air near the duodenal bulb, and emergency endoscopy identified a 10‐mm perforated duodenal ulcer at the scarred site. Endoscopic closure was unfeasible, and laparoscopic omental patch repair was performed. PPI therapy was resumed postoperatively, and the patient recovered uneventfully. This case suggests that stress‐related mucosal disease may have contributed to duodenal perforation. Background risks included ulcer history and scarring, whereas alleviating factors included no NSAID/steroid exposure, eradicated H. pylori, and absence of infection at the esophageal perforation. Guidelines do not endorse routine PPI use after ESD, and consensus following iatrogenic perforation is lacking. This case suggests that prophylactic PPI therapy may be considered in patients with risk factors such as recent peptic ulcer disease or intraoperative perforation.