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Evaluation of scar formation after botulinum toxin injection or Forced balloon dilation to the lower esophageal sphincter

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Abstract

Background: It has been postulated that nonsurgical treatments for achalasia cause fibrosis, increasing the risk of surgical Heller myotomy. The goal of this study was to evaluate fibrosis, muscle fracture, and esophageal inflammation after these treatments. Methods: Eighteen female swine were divided into three groups: 6 were euthanized and their lower esophageal sphincters were harvested (group 1); 6 underwent botulinum toxin injection (group 2); and 6 underwent forced balloon dilatation (group 3). Groups 2 and 3 were euthanized 30 days later and LESs harvested. LESs, were evaluated with trichrome and hematoxylin and eosin (H&E) preparations. Results: Results for both trichrome and H&E slides were the same: severe inflammation in groups 2 and 3 but only minimal inflammation in group 1 (p < 0.05) and mild fibrosis in groups 2 and 3 and none in group 1 (p < 0.05). Conclusions: Botulinum toxin injection and forced balloon dilatation caused significant inflammation in the esophagus of the swine, which would be consistent with the injury caused by reflux. Forced balloon dilatation and botulinum toxin caused fibrosis and may increase surgical risk.

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Acknowledgements

This work was funded by a SAGES research grant.

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Authors and Affiliations

  1. Department of Surgery, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121, USA

    W. S. Richardson

  2. Department of Anatomical Pathology, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121, USA

    G. W. Willis

  3. Department of Gastroenterology, Ochsner Clinic Foundation, 1514 Jefferson Highway, New Orleans, LA 70121, USA

    J. W. Smith

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  1. W. S. Richardson
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  2. G. W. Willis
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  3. J. W. Smith
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Correspondence to W. S. Richardson.

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Richardson, W., Willis, G. & Smith, J. Evaluation of scar formation after botulinum toxin injection or Forced balloon dilation to the lower esophageal sphincter . Surg Endosc 17, 696–698 (2003). https://doi.org/10.1007/s00464-002-8628-x

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  • DOI: https://doi.org/10.1007/s00464-002-8628-x

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