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Original research
Predictors of anastomotic strictures following œsophageal atresia repair
  1. Madeleine Aumar1,2,
  2. Rony Sfeir1,
  3. Adeline Pierache3,
  4. Dominique Turck1,2,
  5. Frederic Gottrand1,2
  6. on behalf of CRACMO
  1. 1 Univ Lille, CHU Lille, Reference Centre for Chronic and Malformative Esophageal Diseases (CRACMO), Inserm U1286 Infinite, CHU Lille Pôle Enfant, Lille, France
  2. 2 Univ Lille, Inserm, CHU Lille, U1286 - Infinite - Institute for Translational Research in Inflammation, University of Lille, Lille, France
  3. 3 Univ Lille, CHU Lille, ULR 2694 - METRICS: évaluation des technologies de santé et des pratiques médicales, Lille University Hospital Center, Lille, France
  1. Correspondence to Dr Madeleine Aumar, Univ. Lille, CHU Lille, Reference Centre for Chronic and Malformative Esophageal Diseases (CRACMO), Inserm U1286 Infinite, F-59000 Lille, France, CHU Lille Pôle Enfant, 59037 Lille, Hauts-de-France, France; madeleine.aumar{at}chru-lille.fr

Abstract

Objectives To identify the risk factors for anastomotic, refractory and recurrent strictures and to establish whether anastomotic stricture is associated with antireflux surgery.

Design This prospective national multicentre study included all infants born with oesophageal atresia (OA) over an 8-year period. Data on OA and complications were collected at birth and at 1 year old. Univariate and multivariate analyses were conducted.

Results 1082 patients from 37 centres were included in the study. The prevalence of anastomotic stricture at 1 year old was 23.2%. Anastomosis under tension (defined by the surgeon at the time of repair) and delayed anastomosis (defined as anastomosis performed more than 15 days after birth, excluding delays due to prematurity or severe cardiac diseases) were found to be independent risk factors for anastomotic stricture (2.3 (1.42–3.74) and 4.02 (2.12–7.63), respectively). Patients with anastomotic stricture had a 2.3-fold higher rate of fundoplication compared with others (p=0.001). Anastomosis under tension and delayed anastomosis were found to be independent risk factors for recurrent stricture (1.92 (1.10–3.34) and 5.73 (2.71–12.14), respectively), while delayed anastomosis was the only risk factor for refractory stricture (8.30 (3.34–20.64)). There was a 2.39-fold (1.42–4.04) higher rate of fundoplication in the anastomotic stricture group than in the group without anastomotic stricture (p=0.001).

Conclusions Patient-related anatomical factors leading to anastomosis under tension and delayed anastomosis increase the risk of anastomotic stricture.

  • epidemiology
  • gastroenterology
  • neonatology
  • paediatrics

https://doi.org/10.1136/archdischild-2021-322577

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    Footnotes

    • Collaborators Dr Véronique Rousseau, Pr Arnaud Bonnard, Dr Audrey Nicolas, Dr Thomas Gelas, Dr Julia Boubnova, Dr Catherine Jacquier, Pr Sabine Irtan, Dr Aurélie Le Mandat, Dr Audrey Guinot, Dr Raphaël Enaud, Dr Virginie Fouquet, Dr Edouard Habonimana, Dr Isabelle Talon, Dr Frédéric Elbaz, Dr Jean-Louis Lemelle, Pr Marie-Laurence Polimerol, Dr Hossein Allal, Dr Jean-Luc Michel, Dr Philippe Buisson, Dr Thierry Petit, Pr Emmanuel Sapin, Dr Manuel Lopez, Pr Guillaume Levard, Dr Françoise Schmitt, Pr Hubert Lardy, Dr Corinne Borderon, Dr Olivier Jaby, Dr Jean-François Lecompte, Dr Cécile Pelatan, Pr Yann Chaussy, Dr Cécilia Tölg, Pr Philine De Vries, Dr Myriam Pouzac, Dr Céline Grosos, Dr Stephan Geiss and Dr Christophe Laplace

    • Contributors Every author provided substantial contribution to the conception, acquisition or design of the work (MA, RS, FG, DT), and to the analysis (AP) or interpretation (MA, FG, DT, RS) of data for the work; drafted the work or revised it critically for important intellectual content (all authors); gave final approval of the version to be published (all authors); and gave agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved (all authors). Guarantor: MA.

    • Funding This work was supported by Groupama Foundation and the national network for rare digestive diseases FIMATHO.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.