Diagnostic DBE is safe with a low complication rate. The complication rate of therapeutic DBE is high compared with therapeutic colonoscopy. The reason for this is unclear. The incidence of pancreatitis after DBE is low (0.3 %), but has to be considered in patients with persistent abdominal complaints after a DBE procedure.
Capsule endoscopy and double balloon enteroscopy provide similar diagnostic yields in patients with OGIB. However, the diagnostic yield of DBE is significantly higher when performed in patients with a positive CE.
The results of this study suggest that the celiac axis compression syndrome exists and that the actual ischemia can be detected by gastric exercise tonometry and treated safely, with success.
Chronic gastrointestinal ischaemia (CGI) is generally considered to be a rare disease entity. The majority of patients with CGI are only diagnosed after a long period of slowly progressive abdominal symptoms, in some cases with impressive weight loss. These patients may have a broad range of clinical signs and quite often undergo repeated extensive evaluation of their symptoms with negative outcome. The classical triad of symptoms, also known as 'abdominal angina', is defined as the combination of postprandial pain, weight loss due to fear of pain after eating, and an abdominal bruit during physical examination. Recent studies have shed new lights on these long unchallenged concepts. These studies first showed that CGI is more prevalent than previously thought and can occur in patients with both single- and multi-vessel disease. Second, the disease presents with a much wider range in symptoms, and only a minority of patients present with the classical triad. Third, long-term positive outcomes can be achieved after endovascular or surgical revascularisation therapy in large proportion of patients. This knowledge results from a combination of clinical research by dedicated focus groups, the current widespread availability of new imaging techniques such as CT-angiography, the development of new functional tests for assessment of mucosal perfusion, and the evolution of endovascular stenting options. Clinicians diagnosing and treating patients with acute and chronic abdominal conditions have to be aware of these new developments. We therefore here review the new insights on CGI with a focus on epidemiology, pathophysiology, current diagnostics and treatment.
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 -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.
Gastric exercise tonometry proved crucial in the evaluation of possible intestinal ischaemia. Comparing patients with single- and multiple-vessel stenoses, there were significant differences in clinical presentation and mortality rates.
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