End Stage Acid Reflux Disease

A 63-year-old female presented to my office with severe heartburn and food regurgitation uncontrolled with high dose antacid medications. As a teenager, she started having heartburn. Over the years, her GERD related symptoms including heartburn and food regurgitation have slowly progressed. About 10 years ago, she started feeling more bloating, maldigestion and post-prandial vomiting. Her nighttime symptoms worsened forcing her to sleep in a semi-sitting position. Her treatment consisted initially of daily Tums and Rolaids. When proton pump inhibitors were introduced in the 1990s, she was started on once daily dose and was later increased to twice daily. She has been on high dose proton pump inhibitors for many years now with poor symptom control.

The patient GERD workup showed a large hiatal hernia, distal esophagitis, undigested food in the stomach suggestive of gastroparesis, and esophageal dysmotility. Esophageal manometry showed poor peristalsis with multiple failed swallows and decreased contractile wave amplitude. Upper GI contrast study showed severe contrast reflux in the Trendelenburg position and minimal contrast emptying from the stomach into the duodenum further supporting the existence of gastroparesis. Whether her esophago-gastric motility disorder is secondary to long-term acid reflux or a contributing cause of acid reflux is hard to determine. Up to 40% of GERD patients are believed to have delayed gastric emptying. Most GERD patients presenting for Nissen surgery at Houston Heartburn and Reflux Center have esophageal abnormalities on manometry.

In my opinion, GERD is an esophago-gastro-duodenal motility disorder. The lower esophageal sphincter is controlled by this motility axis. Transient lower esophageal relaxation, TLESR, is believed to be the main cause of GERD rather than a weak lower esophageal sphincter. TLESR is however a direct result of esophago-gastro-duodenal motility disorder that is yet to be fully understood. An interesting study titled “Effect of Atropine on the frequency of Reflux and Transient Lower Esophageal Sphincter Relaxation in Normal Subjects” illustrates my point. The study was published by Mittal et Al in the journal Gastroenterology in 1995. It shows that atropine injection in the lower esophageal sphincter decreased its pressure but did not cause acid reflux in healthy volunteers. Indeed, following atropine injection, the frequency of transient lower esophageal sphincter relaxation events decreased leading to decreased reflux. One potential explanation for such a finding is that when atropine is injected in the sphincter muscle it causes gastric fundus relaxation, and inhibits esophageal longitudinal muscle fiber shortening. One may assume that increased gastric fundus tone and esophageal longitudinal muscle contractions can lead to increased acid reflux episodes. In other words, certain patterns of esophago-gastric motility that are still poorly understood may result in increased transient lower esophageal sphincter relaxation events leading to GERD. Accordingly, Nissen fundoplication can be viewed as a motility altering procedure rather than a lower esophageal sphincter reinforcement operation. Indeed, we now perform a short and floppy 360-degree fundoplication for best anti-reflux results. Rather than increasing lower esophageal sphincter pressure, Nissen fundoplication promotes stomach motility and increases gastric emptying. These altered motility patterns stop acid reflux. The same phenomenon is observed with sleeve gastrectomy. Gastric sleeve surgery when properly performed is in fact, an excellent anti-reflux procedure.

Nissen fundoplication and gastric sleeve surgery are gastric motility altering procedures. Unless motility is altered, GERD will continue to progress with time. Proton pump inhibitors, PPIs, do not alter gastric motility and one study has shown decreased gastric emptying with chronic PPI use. Patients with severe acid reflux disease maintained on PPIs are likely to end up with end stage GERD like the patient I presented in this blog. GERD is a surgical disease and early surgical intervention is more likely to be effective than medical therapy.

The surgical treatment of end stage GERD requires more than hiatal hernia repair with fundoplication. A greater curvature resection with antrum preservation must be added to promote gastric emptying and alleviate acid reflux. I therefore recommend hiatal hernia repair, Toupet fundoplication and antrum preserving longitudinal gastrectomy. I have so far obtained excellent results adopting this approach for end stage GERD.