Elucidation of the process of delayed colonic perforation after endoscopic thermal injury in a rat model.

Abstract

Delayed perforation is a rare but serious complication following endoscopic resection of colonic lesions; however, its pathogenesis remains unclear. We hypothesized that its mechanism mirrors Jackson's burn model, where a zone of stasis progresses to a zone of coagulation, ultimately leading to perforation. In this study, thermal injury was endoscopically induced in rat colons, and histopathological changes were analyzed at 12-hour intervals. To assess the role of bacterial infection, pseudo-germ-free rats were established by administering a course of antibiotics. The incidence of delayed colonic perforation was compared between the control and pseudo-germ-free rats. Degeneration and thinning of the muscularis propria persisted for 36 hours post-injury, with destruction of this layer observed at 48 hours. Dilated vessels in the mucosa and submucosa peaked at 24 hours, forming a zone of stasis. By 36 hours, mucosal necrosis had intensified, myeloperoxidase-positive cells had increased in the submucosa, and Escherichia coli had translocated into deeper layers, coinciding with expansion of the zone of coagulation. Moreover, pseudo-germ-free rats exhibited significantly fewer perforations. These findings suggest that delayed colonic perforation follows a pathological process similar to thermal burns and that bacterial infection accelerates this progression. Therefore, local infection control may be essential for preventing this serious complication.