Background: Enterolithiasis refers to the formation of hard intraluminal masses within the gastrointestinal tract and may lead to obstruction. Enteroliths are categorized as primary or secondary. Primary enteroliths originate within the bowel and are classified as true or false, depending on their composition and formation. True enteroliths arise in areas of anatomical alteration and stasis, and their chemical composition depends on location—distal small bowel stones typically contain calcium phosphate or oxalate. They are most frequently associated with prior intestinal surgery or stricturing Crohn’s disease (CD). Although rare, enteroliths can cause acute large bowel obstruction.

Case presentation: A 58-year-old female presented with a four-week history of diarrhea, nausea, and acute onset of fever and chills. She had previously undergone partial large bowel resection with a caeco-sigmoid anastomosis due to obstruction caused by multiple intramucosal lipomas, followed by balloon dilatation of the anastomosis five years later for symptomatic stenosis. Clinical examination revealed fever and abdominal distension with diffuse tenderness and hyperactive bowel sounds. Abdominal X-ray showed a 6 cm colonic loop in the right lower quadrant, borderline dilated small bowel loops, and a ~40 mm calcified pelvic mass. Computed tomography (CT) confirmed cecal obstruction and identified an additional 20 mm calcified lesion, without signs of perforation. Suspecting anastomotic stenosis, colonoscopy with planned balloon dilation was performed. It revealed a stenotic anastomosis with an 8 mm lumen, successfully dilated to 12 mm. Advancement of the therapeutic gastroscope allowed visualization of a large enterolith. Ulcerations were observed at the ileocaecal valve and terminal ileum; biopsies were taken. The enterolith was identified as the likely cause of obstruction, and endoscopic lithotripsy was attempted. Fragmentation was challenging due to the stone’s hardness, resulting in multiple lithotriptor wire failures. The second calcified lesion was not detected endoscopically. Following the procedure, symptoms rapidly resolved, and the patient was discharged on day four. Stone analysis confirmed calcium phosphate composition. Histology of ileal biopsies demonstrated features consistent with CD. At three-week follow-up, the patient remained asymptomatic, and a second colonoscopy was arranged to treat the remaining stone.

Conclusion: This case illustrates a rare presentation of primary true enterolithiasis causing large bowel obstruction in a patient with a history of bowel resection and newly diagnosed CD. Endoscopic intervention successfully relieved the obstruction and avoided surgical management. Given the anatomical alteration and underlying CD, recurrence risk remains significant. Careful endoscopic follow-up is warranted. Prompt recognition of enterolithiasis, especially in post-surgical or CD patients, is essential, as timely endoscopic therapy may provide a minimally invasive and effective treatment alternative.