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

Colorectal endoscopic submucosal dissection Colorectal neoplasms Electrocoagulation Gastrointestinal tract Joule heat Post-endoscopic submucosal dissection electrocoagulation syndrome

Journal

World journal of gastroenterology
ISSN: 2219-2840
Titre abrégé: World J Gastroenterol
Pays: United States
ID NLM: 100883448

Informations de publication

Date de publication:
14 Oct 2021
Historique:
received: 24 05 2021
revised: 17 07 2021
accepted: 10 09 2021
entrez: 1 11 2021
pubmed: 2 11 2021
medline: 3 11 2021
Statut: ppublish

Résumé

We hypothesized that thermal damage accumulation during endoscopic submucosal dissection (ESD) causes the pathogenesis of post-ESD electrocoagulation syndrome (PECS). To determine the association between Joule heat and the onset of PECS. We 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. We 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)]. Joule 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.

Sections du résumé

BACKGROUND BACKGROUND
We hypothesized that thermal damage accumulation during endoscopic submucosal dissection (ESD) causes the pathogenesis of post-ESD electrocoagulation syndrome (PECS).
AIM OBJECTIVE
To determine the association between Joule heat and the onset of PECS.
METHODS METHODS
We 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.
RESULTS RESULTS
We 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)].
CONCLUSION CONCLUSIONS
Joule 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.

Identifiants

pubmed: 34720533
doi: 10.3748/wjg.v27.i38.6442
pmc: PMC8517781
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

6442-6452

Informations de copyright

©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.

Déclaration de conflit d'intérêts

Conflict-of-interest statement: All the authors have no conflict of interest related to the manuscript.

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Auteurs

Masanori Ochi (M)

Department of Gastroenterology, Hitachi General Hospital, Hitachi City 317-0077, Ibaraki, Japan. maochi-tei@umin.ac.jp.

Ryosuke Kawagoe (R)

Department of Gastroenterology, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8576, Ibaraki, Japan.

Toshiro Kamoshida (T)

Department of Gastroenterology, Hitachi General Hospital, Hitachi City 317-0077, Ibaraki, Japan.

Yukako Hamano (Y)

Department of Gastroenterology, Hitachi General Hospital, Hitachi City 317-0077, Ibaraki, Japan.

Haruka Ohkawara (H)

Department of Gastroenterology, Hitachi General Hospital, Hitachi City 317-0077, Ibaraki, Japan.

Atsushi Ohkawara (A)

Department of Gastroenterology, Hitachi General Hospital, Hitachi City 317-0077, Ibaraki, Japan.

Nobushige Kakinoki (N)

Department of Gastroenterology, Hitachi General Hospital, Hitachi City 317-0077, Ibaraki, Japan.

Yuji Yamaguchi (Y)

Department of Gastroenterology, Hitachi General Hospital, Hitachi City 317-0077, Ibaraki, Japan.

Shinji Hirai (S)

Department of Gastroenterology, Hitachi General Hospital, Hitachi City 317-0077, Ibaraki, Japan.

Akinori Yanaka (A)

Department of Gastroenterology, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8576, Ibaraki, Japan.

Kiichiro Tsuchiya (K)

Department of Gastroenterology, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8576, Ibaraki, Japan.

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