Posterior gastric wall perforation and acute kidney injury after upper endoscopy with esophageal dilation: A case report

Background

Perforation is a rare but potentially fatal complication of upper gastrointestinal endoscopy, particularly when therapeutic maneuvers are performed. Posterior gastric wall perforation is particularly difficult to recognize because it may decompress into the lesser sac rather than the free peritoneal cavity and therefore produce subtle or atypical peritoneal signs. We report a 64-year-old male with a history of laryngectomy and radiotherapy for laryngeal carcinoma, advanced thoracolumbar scoliosis, atrial fibrillation, and a tracheoesophageal voice prosthesis who was found to have a posterior gastric wall perforation three days after an upper gastrointestinal endoscopy that included bougie dilation of an esophageal stricture and gastric biopsies. CASE SUMMARY On emergency department admission, the patient presented with a blood pressure of 84/50 mmHg, metabolic acidosis, and anuria, suggesting septic shock. Serum creatinine had risen from a documented baseline of 1.1 mg/dL to 4.18 mg/dL, corresponding to Kidney Disease: Improving Global Outcomes stage 3 acute kidney injury (AKI). Contrast-enhanced abdominal computed tomography demonstrated discontinuity of the posterior wall of the gastric corpus, with extravasation of contrast material into the retrogastric space and lesser sac, together with widespread free intraperitoneal air and fluid. AKI was considered predominantly sepsis-associated ischemic acute tubular injury (ATI); contrast exposure seven days earlier was regarded as a possible but unproven contributory factor. The patient underwent two surgical interventions—gastric wedge resection with feeding jejunostomy and re-laparotomy with small bowel resection, double-barrel ileostomy, and surgical gastrostomy due to a jejunostomy-related bile leak. Despite maximal intensive care unit support, the patient died on the 16th day of admission.

Conclusion

Posterior gastric perforation may present with minimal peritoneal signs in patients with altered anatomy and impaired communication, and AKI in this setting is usually multifactorial, dominated by sepsis-associated ischemic ATI.