SUN-624 - Large Gastric Phytobezoar and Gastric Necrosis in a Patient on Semaglutide

Background:
Bezoars are collections of indigestible material that develop in the setting of impaired gastric emptying. Diabetes and prior gastric surgery are established risk factors, and GLP-1 receptor agonists are an emerging medication-related risk because they delay gastric transit. While Semaglutide is not recommended in patients with severe gastroparesis, subclinical or unrecognized dysmotility may be present in individuals with longstanding diabetes, potentially increasing susceptibility to bezoar formation.

Clinical

Case:
A 73-year-old man with long-standing history of T2DM, treated with insulin and semaglutide for 2 years presented with sudden periumbilical abdominal pain, severe abdominal distension, and dyspnea. He reported progressive bloating and constipation over several years and had been advised to increase dietary fiber and salad intake without improvement. On presentation, he was tachypneic, tachycardic and afebrile, with leukocytosis rising from 11.8 to 15.6 and elevated lactate. CT abdomen/pelvis showed marked gastric and distal esophageal distension without bowel obstruction or free air. Repeat imaging showed gastric emphysema and perigastric fat stranding concerning for ischemic injury. He underwent emergent esophagogastroduodenoscopy with endoscopic debridement of a large phytobezoar and necrotic gastric ulcer, followed by diagnostic laparoscopy converted to open partial gastrectomy, partial omentectomy, and ventral hernia repair. Operative findings showed a large phytobezoar overlying a necrotic fundal ulcer without malignancy or frank perforation. Ogilvie syndrome with marked colonic distension was also noted. His postoperative course was complicated by acute hypoxic respiratory failure requiring mechanical ventilation, vasopressor-dependent hypotension, persistent ileus with global gastrointestinal dysmotility, ventilator-associated pneumonia, dysphagia, urinary retention, delirium, and marked deconditioning requiring rehabilitation. He was eventually discharged to post-acute rehabilitation.

Conclusion:
This case highlights severe phytobezoar formation with gastric necrosis in a patient with longstanding diabetes and prolonged semaglutide exposure. GLP-1 receptor agonist-related slowing of gastric emptying may worsen underlying diabetic dysmotility and contribute to bezoar formation, especially in patients with chronic bloating, constipation, and increased fiber intake. In patients with longstanding diabetes and upper gastrointestinal symptoms suggestive of impaired motility, careful symptom assessment and, when clinically indicated, pre-treatment gastric emptying evaluation or advanced screening tools may help identify those at higher risk before GLP-1 receptor agonist initiation.

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