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Volume 18, Issue 1, Pages 23-29 (February 2009)


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Long-gap esophageal atresia treated by growth induction: the biological potential and early follow-up results

John E. Foker, MD, PhDaCorresponding Author Informationemail address, Tara C. Kendall Krosch, MDb, Kirsti Catton, RNFAa, Fraser Munro, MD, FRCSc, Khalid M. Khan, MBChBd

This study had two purposes. The first was to determine whether the growth procedure would allow true primary repairs of the most severe end of the esophageal atresia (EA) spectrum with the longest gaps (LG) and most rudimentary lower esophageal segments. The second goal was to provide the first short- to mid-term (3-12 years) follow-up data on the esophageal function and quality of life (QOL) data on the patients in this series. From our series of 60 LG-EA patients who underwent a growth procedure, 42 had the true primary esophageal repair completed 3 years ago. Among these, 18 had gaps over 6 cm, and for 6, only a rudimentary lower esophagus existed well below the diaphragm. No patient was turned down and all had primary repairs. These results suggest that even the most rudimentary segment has the potential to achieve normal size and that the full EA spectrum can have a primary repair. Our follow-up studies indicated that the esophageal function of these previously grown segments was very good. All contacted (40) were eating normally with only 3 receiving supplemental g-tube feeds because of other significant defects. We have actively treated significant reflux and 41/42 had fundoplication. By endoscopy (N = 15) no esophagitis was visible, but on biopsy, mild inflammation was found in 3. No conditions were found which would suggest that there would be a late deterioration or adverse consequences would arise. Based on these ongoing evaluations, the outlook seems very favorable for a good long-term QOL.

a Division of Cardiothoracic Surgery, University of Minnesota, Minneapolis, Minnesota

b Department of Surgery, University of Minnesota, Minneapolis, Minnesota

c Department of Pediatric Surgery, Royal Hospital for Sick Children, Edinburgh, United Kingdom

d Division of Pediatric Gastroenterology, University of Arizona, Tucson, Arizona

Corresponding Author InformationAddress reprint requests and correspondence: John E. Foker, MD, PhD, Division of Cardiothoracic Surgery, University of Minnesota, 420 Delaware Street SE, Mayo Mail Code 495, Minneapolis, MN 55455

PII: S1055-8586(08)00081-4

doi:10.1053/j.sempedsurg.2008.10.005


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