Abstract
Small bowel perforation following a capsule endoscopy (CE) is a rare but dreadful complication. We report a CE induced small bowel perforation in a patient with Crohn’s disease where preoperative investigations failed to reveal any strictures.
Keywords: Capsule endoscopy, Perforation, Peritonitis
The introduction of capsule endoscopy (CE) in 20001 marked a new era in small bowel imaging. It was estimated in 2008 that more than 650,000 endocapsules (ECs) had been ingested so far2 and the procedure itself is generally considered to be safe and well tolerated with very low complication rates.3 One of the few complications of CE is retention of the capsule, defined as the EC remaining in the digestive tract for a minimum of two weeks.4 Patients with known Crohn’s disease (CD) are at a higher risk of capsule retention (8–21%) than their normal healthy counterparts (0%).5,6 A serious and rare sequela of capsule retention is bowel perforation requiring urgent surgical intervention.7
Case history
We present a 62-year-old Asian woman with a history of CD who presented with acute abdominal pain with nausea and vomiting four days after ingestion of an EC. Two days prior to presentation, her abdominal radiograph revealed an EC in the pelvic area. On examination she appeared unwell with dehydration, tachycardia and diffuse abdominal signs suggesting peritonitis. Routine blood investigations revealed a white cell count of 17.7 x 109/l with a base excess of -6. A repeat abdominal x-ray was normal apart from the EC in the pelvic area as seen on the previous radiograph (Fig 1). There was no free gas on an erect chest radiograph.
Figure 1.

Plain x-ray of the abdomen four days following ingestion of capsule endoscopy showing retained capsule in the pelvis
The patient’s past history included proven small bowel CD of ten years’ duration, which had been well maintained on methotrexate since 2003. A barium follow-through study in 2008 was reported as normal, after which her maintenance methotrexate was discontinued. Six months following this, she presented with post-prandial attacks of abdominal pain, vomiting with low albumin levels. The inflammatory markers were normal and a CE was requested to assess the disease activity.
Following her initial resuscitation, she was taken for a laparotomy. Findings revealed multiple small bowel strictures with proximal perforation and EC migration into the free peritoneal cavity. The strictures were mild in severity with minimal proximal dilatation. Presence of severe peritonitis was noted. The diseased small bowel segment, including all the strictures and the perforation site, was excised en bloc and a high-end jejunostomy with a mucous fistula was fashioned. The residual small bowel measured 80cm of proximal jejunum and 30cm of terminal ileum (non-functional). Postoperatively, she required prolonged total parenteral nutrition with a gradual introduction of enteral feeds. Six months after her resection, the stoma was reversed successfully and she is now doing well. The histology from her resected specimen failed to reveal any active CD.
Discussion
Small bowel perforation following CE is a rare complication. To the best of our knowledge only three such cases have been described in the literature.8–10 Two of these cases involved patients with known CD8,9 while the third involved obstruction/perforation at the site of surgical adhesions.10 The time interval between EC ingestion and perforation was variable with 2 of the reported perforations occurring after 2 weeks8,10 while the third case perforated within 24 hours.9 Our patient became symptomatic four days after ingestion of the EC, suggesting an unpredictable time interval between EC ingestion and perforation. With this in mind, it is imperative to investigate all patients who have not passed the EC in a timely fashion and monitor them closely until the capsule has been excreted.
Several prospective studies have shown CE to be superior to other diagnostic modalities for the diagnosis of CD11 and its role in diagnosis of CD is likely to become more significant in the future.12 The increased risk of complications with CE in patients with CD is well documented5,13 and supported by the findings of this case report. While acknowledging the risk of obstruction posed by EC ingestion, the National Institute for Clinical Excellence recommended the procedure as safe and effective for the investigation of CD patients.14 Current European Society of Gastroenterology guidelines do, however, recommend thorough imaging to exclude stricturing lesions in CD prior to CE.3
Eight months prior to ingestion of the endocapsule, our patient underwent a barium follow-through, which was reported as normal. The symptoms of pain and vomiting prior to her CE may have suggested an underlying obstructive pathology but we were misled by the reassuringly normal barium study. In retrospect, it may have been preferable to have had more recent imaging and we would recommend this for future practice.
Further innovations in the field of ‘patency capsules’, which are designed to dissolve after prolonged retention in the bowel, may help in highlighting more accurately those patients at risk of retaining the EC. Several studies have highlighted the value of these capsules in assessing functional patency of the gut lumen.15,16 Our patient did not undergo a preliminary investigation with a patency capsule and there is good evidence in the literature to suggest that such an investigation would have highlighted an underlying obstructive pathology.
We recommend that patients with CD who have a history suggestive of intermittent small bowel obstruction but normal small bowel imaging are investigated with patency capsules prior to the ingestion of a CE. In the interim it is important to have a low index of suspicion in all patients presenting with abdominal pain following ingestion of an endocapsule.
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