BACKGROUND AND AIM: Colorectal endoscopic submucosal dissection (ESD) is used for the treatment of large colorectal superficial neoplasms. However, there have been no large studies on electrocoagulation syndrome developing after colorectal ESD. The aim of this study was to clarify the incidence and clinical risk factors of post-ESD electrocoagulation syndrome (PECS). METHODS: A total of 692 patients (median age: 70 years; 395 men) with 692 lesions, who underwent colorectal ESD at a tertiary cancer center between July 2010 and December 2015, were eligible. PECS was clinically diagnosed based on the presence of localized abdominal tenderness matching the ESD enforcement site and fever (> 37.5 °C) or an inflammatory response (C-reactive protein level > 0.5 mg/dL or leukocytosis > 10 000 cells/μL), without obvious findings of perforation, which developed at > 6 h post-ESD. Outcomes of the procedure, the incidence of PECS, and risk factors associated with PECS were assessed. RESULTS: The incidence of PECS was 4.8% (33 patients), and all patients improved by conservative treatment. On multivariate analysis, the female sex (odds ratio [OR] 2.6; 95% confidence interval [95% CI]: 1.2-5.7), tumor location at the cecum (OR 14.5; 95% CI: 3.7-53.7 vs rectum), and the presence of submucosal fibrosis (OR 2.8; 95% CI: 1.1-7.5) were found to be independent risk factors of PECS. CONCLUSIONS: This study identified the risk factors for PECS. Patients with high-risk factors of PECS require careful management after colorectal ESD.
BACKGROUND AND AIM: Colorectal endoscopic submucosal dissection (ESD) is used for the treatment of large colorectal superficial neoplasms. However, there have been no large studies on electrocoagulation syndrome developing after colorectal ESD. The aim of this study was to clarify the incidence and clinical risk factors of post-ESD electrocoagulation syndrome (PECS). METHODS: A total of 692 patients (median age: 70 years; 395 men) with 692 lesions, who underwent colorectal ESD at a tertiary cancer center between July 2010 and December 2015, were eligible. PECS was clinically diagnosed based on the presence of localized abdominal tenderness matching the ESD enforcement site and fever (> 37.5 °C) or an inflammatory response (C-reactive protein level > 0.5 mg/dL or leukocytosis > 10 000 cells/μL), without obvious findings of perforation, which developed at > 6 h post-ESD. Outcomes of the procedure, the incidence of PECS, and risk factors associated with PECS were assessed. RESULTS: The incidence of PECS was 4.8% (33 patients), and all patients improved by conservative treatment. On multivariate analysis, the female sex (odds ratio [OR] 2.6; 95% confidence interval [95% CI]: 1.2-5.7), tumor location at the cecum (OR 14.5; 95% CI: 3.7-53.7 vs rectum), and the presence of submucosal fibrosis (OR 2.8; 95% CI: 1.1-7.5) were found to be independent risk factors of PECS. CONCLUSIONS: This study identified the risk factors for PECS. Patients with high-risk factors of PECS require careful management after colorectal ESD.