Magnetic sphincter augmentation surgery consists of placing a bracelet of magnetic beads around the lower esophageal sphincter. The magnetic bracelet increases resistance around the lower esophageal sphincter. LINX™ device keeps the sphincter closed at gastric pressures less than 20 mm of Hg. Acid reflux occurs at a sphincter pressure around 10 mm of Hg. Swallowing pressure is typically higher than 20 mm of Hg in a healthy esophagus. Therefore, LINX™ device allows forward food passage from esophagus into stomach while preventing backward acid reflux from stomach into esophagus. Such an approach to a complex problem like GERD is obviously very simplistic and naïve. Suffice to stay that a distal esophageal stricture creates a high-pressure area around the lower esophageal sphincter, yet it does not prevent acid reflux. Many patients presenting for acid reflux evaluation have esophageal outflow obstruction on manometry with elevated basal and relaxing lower esophageal sphincter pressure and still suffer from severe acid reflux. Decreased esophageal wall compliance around the lower esophageal sphincter has been proposed as a contributing factor to acid reflux but it is definitely not the only factor.
More interestingly, however, is the short and long-term impact of LINX™ device on esophageal motility. The lower esophageal sphincter pressure decreases in response to a swallow to facilitate food bolus passage into stomach. In the presence of LINX™, esophagus must overcome a pressure barrier of around 25 mm of Hg, with each swallow, to push a food bolus across LINX™ device into the stomach. Swallowing pressures are typically strong enough to do the job, but what happens in the long run? Does LINX™ device weaken esophageal motility leading to achalasia like symptom development?
Food impaction, difficulty swallowing food, chest and epigastric pain and pooling of solid food and liquids above the lower esophageal sphincter are well described LINX™ complications. A poorly sized LINX™, weak esophageal motility, and scar tissue formation are obvious causes for such symptoms to develop shortly after LINX™ implantation. However, a number of patients present one or two years after LINX™ surgery with contrast pooling on barium swallow necessitating LINX™ device removal. Such patients raise the concern of slow esophageal motility deterioration over time. Future studies are needed to better understand this issue.
The gastro-esophageal junction, GEJ, area is a complex physiologic and anatomic structure that constitutes the anti-reflux barrier. Competency of the GEJ depends on a complex interplay of myogenic, neurogenic and mechanical properties of that area. Nissen fundoplication surgery remains the most effective solution for a weak anti-reflux barrier. Its mechanism of action remains unknown. However, Nissen fundoplication does not work by creating a high pressure or increased resistance area around the Lower esophageal sphincter. Indeed, the most effective Nissen fundoplication is a short and floppy fundoplication that does not cause any stricture or LINX™ like effect around the GEJ. Failed LINX™ device is best revised to a fundoplication procedure to best help your GERD patient.