Hashiguchi Keiichi, Maruya Yasuhiro, Matsumoto Ryo, Yamaguchi Shun, Ogihara Kumi, Ohnita Ken, Kobayashi Shinichiro, Kanetaka Kengo, Nakao Kazuhiko, Eguchi Susumu
Department of Endoscopy, Nagasaki University Hospital, Nagasaki, Japan.
Departments of, Department of, Surgery, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
Dig Endosc. 2021 Mar;33(3):381-389. doi: 10.1111/den.13710. Epub 2020 Jun 22.
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.
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.
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).
This study indicated that our in-vivo porcine duodenal ESD model is beneficial to evaluate a prevention strategy for delayed perforation.
十二指肠内镜黏膜下剥离术(ESD)治疗浅表性非壶腹十二指肠上皮肿瘤时,延迟穿孔的发生率较高。尽管已提出多种预防延迟穿孔的方法,但最合适的方法仍不明确。目前,尚无合适的动物模型来验证预防十二指肠延迟穿孔的方法。本研究旨在建立猪十二指肠黏膜下剥离术后体内延迟穿孔模型。
两个猪模型分别接受ESD或手术黏膜下剥离术。在手术剥离模型中,用电外科能量切除倒置的十二指肠黏膜。在ESD模型中,在十二指肠后方放置纱布并抓住横部以提高内镜操作的灵活性。在两个模型中,剥离术后的黏膜缺损均采用网膜覆盖但不缝合的方法处理。所有模型在手术后0至5天实施安乐死。评估体重、切除尺寸、手术剥离时间、术中穿孔和延迟穿孔的情况以及粘连评分。
两个模型在体重和粘连评分方面无显著差异。手术剥离模型的切除尺寸显著大于ESD模型(19毫米对14.3毫米,P<0.01)。ESD模型的手术时间显著长于手术模型(45.2分钟对4.5分钟,P<0.01)。手术剥离模型和ESD模型的延迟穿孔率分别为0%(0/5)和100%(5/5)(P<0.01)。
本研究表明,我们建立的猪体内十二指肠ESD模型有助于评估延迟穿孔的预防策略。