High total Joule heat increases the risk of post-endoscopic submucosal dissection electrocoagulation syndrome after colorectal endoscopic submucosal dissection

BACKGROUNDWe hypothesized that thermal damage accumulation during endoscopic submucosal dissection (ESD) causes the pathogenesis of post-ESD electrocoagulation syndrome (PECS). AIMTo determine the association between Joule heat and the onset of PECS. METHODSWe performed a retrospective cohort study...

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Published inWorld journal of gastroenterology : WJG Vol. 27; no. 38; pp. 6442 - 6452
Main Authors Ochi, Masanori, Kawagoe, Ryosuke, Kamoshida, Toshiro, Hamano, Yukako, Ohkawara, Haruka, Ohkawara, Atsushi, Kakinoki, Nobushige, Yamaguchi, Yuji, Hirai, Shinji, Yanaka, Akinori, Tsuchiya, Kiichiro
Format Journal Article
LanguageEnglish
Published Baishideng Publishing Group Inc 14.10.2021
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Summary:BACKGROUNDWe hypothesized that thermal damage accumulation during endoscopic submucosal dissection (ESD) causes the pathogenesis of post-ESD electrocoagulation syndrome (PECS). AIMTo determine the association between Joule heat and the onset of PECS. METHODSWe performed a retrospective cohort study in patients who underwent colorectal ESD from May 2013 to March 2021 in Japan. We developed a novel device that measures swift coagulation time with a sensor adjacent to the electrosurgical coagulation unit foot switch, which enabled us to calculate total Joule heat. PECS was defined as localized abdominal pain (visual analogue scale ≥ 30 mm during hospitalization or increased by ≥ 20 mm from the baseline) and fever (temperature ≥ 37.5 degrees or white blood cell count ≥ 10000 µ/L). Patients exposed to more or less than the median Joule heat value were assigned to the high and low Joule heat groups, respectively. Statistical analyses included Mann-Whitney U and chi-square tests and logistic regression and receiver operating characteristic curve (ROC) analyses. RESULTSWe evaluated 151 patients. The PECS incidence was 10.6% (16/151 cases), and all patients were followed conservatively and discharged without severe complications. In multivariate analysis, high Joule heat was an independent PECS risk factor. The area under the ROC curve showing the correlation between PECS and total Joule heat was high [0.788 (95% confidence interval: 0.666-0.909)]. CONCLUSIONJoule heat accumulation in the gastrointestinal wall is involved in the onset of PECS. ESD-related thermal damage to the peeled mucosal surface is probably a major component of the mechanism underlying PECS.
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Author contributions: Ochi M, Kawagoe R, Kamoshida T, Hamano Y, Ohkawara A, Ohkawara H, Kakinoki N, Yamaguchi Y, Hirai S, Yanaka A and Tsuchiya K contributed equally to this work; Ochi M and Kawagoe R collected and analyzed the data; Ochi M and Kawagoe R drafted the manuscript; Ochi M, Kawagoe R and Kamoshida T designed and supervised the study; Hamano Y, Ohkawara A, Ohkawara H, Kakinoki N, Yamaguchi Y, Hirai S, Yanaka A and Tsuchiya K offered technical or material support; all authors have read and approved the final version to be published.
Corresponding author: Masanori Ochi, MD, Doctor, Department of Gastroenterology, Hitachi General Hospital, 2-1-1, Jonancho, Hitachi City, Hitachi City 317-0077, Ibaraki, Japan. maochi-tei@umin.ac.jp
ISSN:1007-9327
2219-2840
DOI:10.3748/wjg.v27.i38.6442