A 70-year-old man previously being treated for stable alcoholic liver disease presented with gradually progressive diffuse abdominal pain associated with vomiting and constipation for 7 days. Physical examination revealed gaseous abdominal distention without tenderness or mass. He had a history of 2 laparotomies in the past both for small bowel obstruction secondary to enterolith impaction that had failed to resolve with conservative measures. The finding on first operation 3 years ago was that of a 3 × 5 cm obstructing enterolith in the ileum 20 cm proximal to the ileocaecal junction. This was removed through an enterotomy and the affected segment of ileum was resected with primary end to end anastomosis. There were no diverticula or any other inciting factors identified. The histopathology of the resected small bowel was reported to have no specific findings. Following this, he presented 2 years later with similar symptoms. On second operation the findings were again similar to that of the first operation with an impacted enterolith in the mid ileum along with minimal adhesions. He underwent enterotomy and removal of the enterolith. Following the second operation he was asymptomatic till this presentation. At the current presentation, his hematological and biochemical workup was normal and abdominal radiographs were inconclusive. USG revealed a normal study. He was initially managed conservatively in lines of adhesive bowel obstruction. In view of patient's general condition and lack of facilities, CT scan and endoscopy could not be done. After a mild initial symptomatic improvement, he developed gradual and progressive abdominal distention with pain and obstipation. Suspecting adhesive obstruction and keeping in mind the possibility of a recurrent enterolith bowel obstruction, he was taken for an exploratory laparotomy. On table findings were those of a recurrent enterolith 5 × 5 cm in size impacted in the mid ileum with multiple dense serosal adhesions and bands as shown in Figures and. Apart from this no other abnormal findings were identified. The enterolith was disimpacted through an ileal enterotomy followed by primary closure of the enterotomy. The enterolith was not sent for biochemical analysis considering that it may not contribute to additional information from management point of view. His subsequent postoperative course was stormy and developed burst abdomen on 8th postoperative day that required mass closure. But following this he showed gradual and steady improvement. After a total stay of 6 weeks, he was discharged in a stable state and had improved on follow-up visit at 3 months. At follow-up he was advised to avoid high roughage diet and consume stool softeners on PRN basis thinking that this would help him avoid another similar episode.