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Botulinum Toxin Enhanced Foker Process for Long Gap Esophageal Atresia
Shawn Izadi1, Donna C Koo1, Hester F Shieh2
1Department of Surgery, Boston Children's Hospital, Boston, MA, USA.
Journal of Pediatric Surgery
|August 3, 2024
Summary
Botulinum Toxin A (BTX) may accelerate the Foker process for long gap esophageal atresia (LGEA) repair. This enhancement reduced traction time in external traction cases, potentially lowering patient burden.
Area of Science:
- Pediatric Surgery
- Gastroenterology
- Regenerative Medicine
Background:
- The Foker process uses traction to promote esophageal growth in treating long gap esophageal atresia (LGEA).
- Botulinum Toxin A (BTX) possesses anti-fibrotic and muscle-relaxing properties that may aid esophageal growth.
Purpose of the Study:
- To investigate if BTX enhances the traction-induced esophageal growth (Foker) process for LGEA repair.
- To compare outcomes of BTX-enhanced Foker process with historical controls.
Main Methods:
- A retrospective, two-center cohort study of 20 infants with LGEA undergoing a BTX-enhanced Foker process (2021-2023).
- BTX was administered at the start of traction; outcomes were compared to historical controls (2014-2021).
- Evaluated time on traction, complications, and anastomotic outcomes.
Main Results:
- The BTX-enhanced external traction process was significantly faster (12.1 days) than controls (16.6 days) (p=0.04).
- No significant differences in time on traction were observed for the minimally invasive approach.
- Complications and anastomotic outcomes were similar between the BTX-enhanced and control groups.
Conclusions:
- BTX may accelerate esophageal growth during the Foker process for LGEA.
- Reducing traction time can decrease patient sedation and paralysis needs.
- Further research is warranted to fully understand BTX's effects on esophageal tissue.
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