Mechanism of acute pancreatitis after peroral double-balloon enteroscopy

We read with interest the article by Honda et al. [1] on hyperamylasemia and acute pancreatitis after peroral double-balloon enteroscopy (DBE). They performed peroral DBE in 13 patients, and hyperamylasemia occurred in 6 of the 13 (46.2 %). Among the 6 patients with hyperamylasemia, acute pancreatitis subsequently occurred in one patient. In the last 3 months, we performed a total of 32 DBE procedures (15 peroral and 17 peranal approaches). Whereas hyperamylasemia did not occur in the 17 patients after peranal DBE, we too saw hyperamylasemia in 7 of 15 patients treated perorally (46.7 %), and one of these suffered acute pancreatitis after the procedure. Although Honda et al. [1] suspect that the pancreatitis is mainly caused by duodenal intraluminal hypertension, we believe that another plausible mechanism should receive more attention based on the site of the pancreatitis.

Before the recent advance of DBE, our routine approach for small-bowel disease was transenterotomy panenteroscopy assisted by laparoscopy with a minilaparotomy, which can investigate the entire small bowel with a standard endoscope [2] [3]. DBE is a novel technique for visualizing the entire small bowel via either the peroral or the peranal approach, and potentially allows endoscopic therapy [4]. Although the technique is considered to be a safe procedure without major complications [1] [4] [5], five cases of acute pancreatitis after peroral DBE have been reported [1] [4] [5] [6]. In one patient the pancreatitis was located in the pancreas body and in two patients in the tail of the pancreas; for the other two patients the site of the pancreatitis site was not given. In our one recent patient with severe pancreatitis after peroral DBE the pancreatitis was in the tail. All six patients recovered from the pancreatitis with conservative therapy.

Although the mechanism of acute pancreatitis after DBE is still unclear [1] [5] [7], some possible mechanisms are currently under discussion. One mechanism is pancreatic duct obstruction by direct oppression of the papilla with the inflated balloon. Another is an increase in duodenal intraluminal pressure caused by the overtube and gastrointestinal shortening technique [5]. Groenen et al. [4] also suspected that duodenal intraluminal hypertension caused by the balloon can induce reflux of duodenal contents into the pancreatic duct, leading to the activation of pancreatic enzymes and the subsequent development of acute pancreatitis.

Because the inflation and deflation of the balloon are carried out very quickly, occlusion of the papilla caused by the balloon does not appear to be very plausible as a cause of the pancreatitis [7]. Duodenal reflux has to overcome several barriers: structural barriers of the papilla and the sphincter of Oddi, and a pressure gradient barrier with a higher pressure in the pancreatic duct and a lower pressure in the duodenum [4]. And even though high duodenal pressure may lead to duodenal reflux and the subsequent development of acute pancreatitis, we believe that the pancreatitis under these circumstances occurs in the entire pancreas with diffuse pancreas swelling, and is not localized to the body or the tail. In the reported patients and in our own patient with acute pancreatitis after peroral DBE, the pancreatitis was localized to the pancreas body or tail [1] [4] [5] [6].

Another hypothesis is that traumatic injury or ischemia may play a role when the small bowel is threaded together onto the overtube with removal of the loops, possibly exerting some torsion on parts of the mesentery [7]. During peroral DBE, the duodenum and proximal small bowel are markedly shortened, and the duodenum is sometimes found to be nearly straight from the pyloric ring to the ligament of Treitz [1]. In these conditions, the pancreas body or tail may be subjected to severe strain with traumatic injury or ischemia. We therefore believe that the pancreatitis occurring after peroral DBE probably results from prolonged mechanical strain on the pancreas body or tail by repeated stretching of the endoscope and overtube. Because DBE requires repeated stretching of the endoscope to telescope the small bowel onto the overtube in order to visualize the entire small bowel, it seems unlikely that this complication can be avoided.

Further research is necessary to clarify what factors may induce hyperamylasemia and potential pancreatitis, and then to reduce the incidence of the complications after peroral DBE.

Competing interests: None

References

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