Establishment of an in‐vivo porcine delayed perforation model after duodenal endoscopic submucosal dissection

Abstract

Objectives Duodenal endoscopic submucosal dissection (ESD) for superficial non‐ampullary duodenal epithelial tumors has a significant incidence rate of delayed perforation. Although several methods have been proposed to prevent delayed perforation, the most appropriate methods remain unclear. Currently, there is no appropriate animal model to validate methods for preventing duodenal delayed perforation. This study aimed to establish an in‐vivo porcine delayed perforation model after duodenal submucosal dissection. Methods Two porcine models underwent either ESD or surgical submucosal dissection. In the surgical dissection model, an inverted duodenal mucosa was resected with electrosurgical energy. In the ESD model, a gauze was placed behind the duodenum with grasped transverse part to improve endoscopic maneuverability. The mucosal defects after dissection were treated with omental coverage without suture in both models. All models were euthanized 0–5 days after procedure. Body weight; resection size; procedure dissection time; presence of intraoperative perforation and delayed perforation; and adhesion score were assessed. Results There were no significant differences in body weight and adhesion score between the two models. Resection size was significantly larger in the surgical dissection models than in the ESD models (19 mm vs 14.3 mm, P < 0.01). Procedure time was significantly longer in the ESD models than in the surgical models (45.2 minutes vs 4.5 minutes, P < 0.01). Delayed perforation rates in the surgical dissection models and the ESD models were 0% (0/5) and 100% (5/5), respectively (P < 0.01). Conclusions This study indicated that our in‐vivo porcine duodenal ESD model is beneficial to evaluate a prevention strategy for delayed perforation.

The Efficacy of Autologous Myoblast Sheet Transplantation to Prevent Perforation After Duodenal Endoscopic Submucosal Dissection in Porcine Model

“…Pigs (12–20 kg) from the same farm were used for the experiments. The in vivo porcine delayed perforation model after duodenal ESD is previously described 19 . This model is known to show a 100% delayed perforation rate within several days after successful duodenal ESD.…”

Rapid and chronological expression of angiogenetic genes is a major mechanism involved in cell sheet transplantation in a rat gastric ulcer model

“…Recently, we revealed that a crucial cause of delayed perforation after duodenal ESD is ischemic changes around the mucosal defect [ 14 ], and cell sheet transplantation with omental coverage can promote tissue regeneration to prevent this lethal complication [ 24 ]. While we were unable to evaluate the gene expression profile in our porcine ESD model, the data obtained in our rats strongly suggest that revascularization at the ischemic area from the omentum and improvement of blood flow by cell sheet transplantation play a crucial role in tissue regeneration at the ESD site.…”

“…The presence of bile and pancreatic juice and duodenal wall thinness are thought to be the main causes of delayed perforation, so closure of the mucosal defect after ESD is recommended for preventing these complications in clinical practice [ [11] , [12] , [13] ]. In addition to these physiological features of the duodenum, disturbance of the intravascular flow due to extended muscularis propria with endoscopic air supply during ESD and consequent ischemia at the ESD site might be important factors contributing to delayed perforation [ 14 ]. A histological analysis of a porcine duodenal ESD model revealed atrophy of the gland and a ghost-like appearance of the surrounding mucosa at the duodenal ESD site.…”

A first-in-human clinical study of laparoscopic autologous myoblast sheet transplantation to prevent delayed perforation after duodenal endoscopic mucosal dissection

“…In addition, Hanaoka et al reported that delayed perforation after ESD occurred because of ischemic changes at the ESD site [ 19 ]. In a large animal model, we revealed that ischemia is one of the main causes of delayed perforation after duodenal ESD [ 20 ].…”