Reply to Manno et al.

 

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We thank Manno et al. for their letter comparing their experience of single-balloon enteroscopy (SBE) with our results published in this journal [1]. We were glad to see that their findings were in line with our own.

Manno et al. performed 72 procedures in 67 patients with no serious complications, including no episodes of acute pancreatitis and no perforations. In the analysis of their own results combined with previously published findings [1] [2] [3] [4], they calculate that the perforation rate during SBE is 0.2 % by suggesting that a perforation that occurred in our cohort was the result of balloon dilation of a stricture and not due to the SBE procedure itself. We disagree with this opinion as we believe that perforations resulting from dilation procedures still have to be counted as a complication of SBE, particularly when a large, multicenter study [5] has demonstrated that the perforation rates for double-balloon enteroscopy (DBE) are notably different for diagnostic (0.1 %) and therapeutic (0.8 %) procedures. Even when our perforation is included, the overall risk during SBE remains low (2 / 484; 0.4 %) and similar to that for DBE (0.3 %) [5].

We were pleased that the authors also had no episodes of acute pancreatitis in their patients. The hypothesized mechanisms for the etiology of postenteroscopy pancreatitis include: an increased intraluminal pressure in the duodenum from balloon inflation causing reflux of duodenal fluids into the pancreatic duct; irritation of the pancreatic sphincter from inflation of the overtube balloon near the papilla; and mechanical strain on the pancreas from the repeated “push-and pull” movements that cause profound stretching of the small intestine. Manno et al. suggest that the main reason for the lowered incidence of acute pancreatitis observed with SBE is the insertion technique that delays balloon inflation until the third part of the duodenum. Therefore, they propose that the primary etiology for pancreatitis is obstruction of the pancreatic duct by inflation of the balloon near the papilla. We also agree with this theory but do not think that this is the only cause for pancreatitis. In our earlier DBE study also published in this journal [6], the occurrence of post-DBE pancreatitis was still 0.7 % despite a modified DBE insertion technique that delayed balloon inflation until after the overtube was distal to the ligament of Treitz and not near the papilla. This suggests that the mechanism for acute pancreatitis after DBE is not entirely due to balloon inflation and must be multifactorial.

Competing interests: None

References

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H. AktasMD 

Department of Gastroenterology and Hepatology
Erasmus MC – University Medical Center

Gravendijkwal 230 (room Ba 393)
Rotterdam 3015 CE
The Netherlands

Fax: +31-10-7034682

Email: h.aktas@erasmusmc.nl