Affiliation:
1. Saint Joseph's Hospital
Abstract
Abstract
Hypothesis: Magnetic Sphincter Augmentation device causes fibrosis at the distal esophagus which prevents reflux even after device removal
Background: Gastroesophageal reflux disease (GERD) affects over 20 million people in the United States. If left untreated, chronic reflux of gastric contents into the distal esophagus may result in benign or malignant esophageal strictures, causing varying degrees of dysphagia. We currently offer interventions which artificially create a narrowing at the distal esophagus to prevent complications of GERD. Magnetic Sphincter Augmentation device (MSA), or LINX, creates such a narrowing of the distal esophagus at the level of the LES. Individuals intolerant of this device need surgical removal which leaves scarring at the site of implantation.
Methods: There were 118 MSA devices placed at our institution between 2017 and 2021. During this time, 8 out of 118 (6.7%) patients needed to have their LINX removed due to side effects attributed to the implant. Causes for removal included esophageal perforation, dysphagia or hypersensitivity related chest pressure presumably caused by the device. Patients, who have had the LINX device removed, were followed for recurrence of reflux using Barium Swallow imaging, endoscopic findings and GERD-HRQL scores.
Results: The longer the MSA implants remained before removal, the more extensive the scar tissue encountered at site of excision. Five of eight patients (62%) experienced improvement in their GERD-HRQL scores after removal of the MSA device when compared to results before LINX implantation. The residual band of scar tissue observed after device removal appeared to control reflux by restricting the relaxation of the esophageal outlet.
Conclusions: These results indicate that fibrosis at the site of MSA device removal improves heartburn symptoms in a majority of patients. We do not recommend fundoplication at time of LINX removal as symptoms of GERD may be adequately controlled by scar tissue at the LES.
Publisher
Research Square Platform LLC