I read with great interest the recent study “Esophagogastric junction function and gastric pressure profile after minigastric bypass compared with Billroth II” published in SOARD journal. The authors compared two small group of patients each containing around twenty patients. First group consisted of obese individuals who underwent mini-gastric bypass for weight loss. Second group underwent distal gastrectomy and Billroth II reconstruction for refractory ulcers. All patients did not have evidence of clinical acid reflux or hiatal hernia prior to surgery. Weight loss patients were evaluated prior to mini gastric bypass surgery and at one and five year follow up, with GERD questionnaire, upper endoscopy, esophageal manometry and 24-hour pH-impedance study. Billroth II patients underwent upper endoscopy, manometry and impedance studies after surgery.
Results showed increased acid and alkaline reflux, and distal esophagitis in Billroth II patients only. Manometry showed decreased lower esophageal sphincter in Billroth II patients only favoring GERD. Furthermore, gastric pressure in Billroth II patients significantly dropped compared to mini-gastric bypass patients favoring bile reflux across the gastro-jejunostomy. The authors observe that bile stasis in the gastric remnant leads to deterioration of the anti-reflux barrier and increased incidence of GERD in the setting of classical Billroth II reconstruction. In a classic Billroth II reconstruction gastric fundus and part of the gastric body are preserved. This is in sharp contrast to the sleeve like gastric pouch created in the setting of mini-gastric bypass surgery. There is no doubt in my mind that gastric fundus resection, similar to plication, alters the anti-reflux barrier. Studies have shown increased lower esophageal sphincter pressure following gastric sleeve surgery as well as increased gastric emptying. Therefore, it is no surprise to me that a Billroth II reconstruction in the setting of mini-gastric bypass is associated with lower GERD and bile stasis incidence when compared to a classic Billroth II. Unfortunately, the current study has a number of limitations that significantly weakens its results. It does point however, to an important concept in GERD pathophysiology: the stomach and in particular the gastric fundus plays an important role in the acid reflux barrier and pathogenesis of acid reflux disease. Gastric fundus surgery in the form of Nissen fundoplication or sleeve gastrectomy accelerates gastric emptying and moves the gastric acid bubble away from the gastro-esophageal junction. These physiologic changes contribute to heartburn control independent of lower esophageal sphincter pressure increase. The purpose of fundus plication is neither to create a mechanical valve around the distal esophagus nor to create a high-pressure area. Nissen fundoplication mechanism of action is much more complicated than LINX™ device for acid reflux management. For this reason, a floppy and short fundoplication is as effective as a bulky and tight fundoplication in terms of acid reflux control. The advantage of a floppy fundoplication is the lack of postoperative dysphagia.