Gastric Sleeve Migration in Weight loss Surgery

Gastric Sleeve Migration in Weight loss Surgery

I read with great interest the article “Gastric Migration Crisis in Obesity Surgery” recently published in Obesity Surgery. The author, Dr. Runkel, is concerned about the increasing numbers of intra-thoracic migration of gastric sleeve leading to GERD and Barrett’s esophagus development. The mechanism behind sleeve migration into the chest remains unknown. The author points to the fact that sleeve lumen is almost as wide as the esophagus and with time and secondary to the pressure gradient between the abdomen and chest the sleeve migrates upwards. He adds that gastric pouch migration rate in gastric bypass cases is not known because most gastric bypass patients don’t develop GERD to be checked for post-op hiatal hernia development.

Dr. Runkel goes over the 2012 consensus recommendations of routinely dissecting the phreno-esophageal membrane during sleeve gastrectomy to look for a hiatal hernia. If present crural repair is recommended. He then quotes a number of studies that contradict this recommendation and show no benefit in concomitant hiatal hernia repair and sleeve gastrectomy in alleviating acid reflux or preventing de novo GERD.

The author adds there is no consensus on hiatal hernia repair technique. The crura are approximated over a calibrating tube of varying diameter. Suture placement anterior or posterior to the esophagus, mesh placement and cardia fixation vary among surgeons.

To understand sleeve migration, one need to understand hiatal hernia pathophysiology. Hiatal hernia develops and grows in response to chronic acid reflux. Acid reflux causes esophageal musculature to contract in a cephalad direction leading to progressive migration of intra-abdominal esophagus followed by cardia into the chest, thus forming a hernia. Hiatal hernia formation weakens the anti-reflux barrier and causes more reflux which in turns promotes hiatal hernia growth. This vicious circle leads to progression of disease and worsening symptoms with time. In the case of sleeve gastrectomy, both the small size of sleeve lumen and lack of attachment along the resected greater curvature lead to rapid hiatal hernia formation or growth in case of pre-existing small hiatal hernia, hence the term sleeve migration. Since most obese patients have a small hiatal hernia, it is not surprising to see a high number of sleeve migration. Post-gastric sleeve GERD occurs if the incisura angularis is narrowed, a mistake commonly committed in the early sleeve experience, or if a concomitant hiatal hernia repair is not performed. The gastric sleeve is a low compliance tube. When only a small portion of the sleeve lumen is subjected to negative intra-thoracic pressure, negative pressure is transmitted into sleeve lumen and probably across the pylorus leading to bile and acid reflux. Bile reflux is implicated in the development of Barrett’s esophagus. Indeed, a number of studies have shown increased Barrett’s esophagus incidence in gastric sleeve patients suffering from GERD.

Hiatal hernia repair is crucial in gastric sleeve surgery. Any size hernia must be repaired to avoid sleeve migration, GERD and Barrett’s esophagus leading to esophageal cancer. Sleeve migration does not happen in the absence of GERD and without the contraction of esophageal musculature.

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