One of the hallmarks of gastroesophageal reflux disease, GERD, is a retracted esophagus into the mediastinum in response to repeated cycles of acid reflux. Indeed, chronic acid reflux contributes to the development and worsening of a hiatal hernia. Acid reflux causes the squamo-columnar junction to retract into the mediastinum. As the mucosa retracts, the underlying submucosa and muscularis layers follow. Slowly the intra-abdominal esophagus starts moving into the chest followed by the cardia, gastric fundus and remaining stomach. This in turn leads to worsening reflux as the lower esophageal sphincter function and gastro-esophageal junction anatomy and physiology are compromised. This dynamic situation creates a vicious circle where reflux leads to hiatal hernia formation and hiatal hernia development leads to worsening reflux.
The advent of proton pump inhibitors has resulted in lower incidence of mucosal damage. Consequently, the squamo-columnar junction is less likely to retract into the chest and away from reflux. As a result, one would expect a lower incidence of short esophagus formation. Indeed, there is a striking paucity of reference to the short esophagus in the current acid reflux literature. The short esophagus is defined as the inability of the gastroesophageal junction to lie with no tension at least 3 cm below the hiatal opening. In my own personal experience of hundreds of laparoscopic hiatal hernia repair and Nissen fundoplication surgeries performed over the past few years, I have not yet encountered a short esophagus. Prior to the advent of proton pump inhibitors and laparoscopic surgery in the early 1990s, the short esophagus was an important and commonly encountered problem in anti-reflux surgery. Its incidence, however, seems to be decreasing probably secondary to widespread use of proton pump inhibitors. In 2003, Dr. DeMeester reported an incidence of 3 to 14% in his review of several published studies. In 2012, Dr. Swanstrom reported a 6.4% incidence of short esophagus among anti-reflux surgery patients during an observation period between 2001 and 2009. It would be interesting to evaluate the incidence of short esophagus in a more recent series of GERD patients. I predict that the incidence will be no more than 1%.
In conclusion, esophageal retraction into the chest is a common finding in anti-reflux surgery and is both the result and cause of acid reflux disease. Proper distal esophagus dissection and release during hiatal hernia surgery is the most important component of anti-reflux surgery. I think that proton pump inhibitor treatment of GERD has reduced the incidence of esophageal shortening over the past 20 years. More studies are needed to confirm this observation. By decreasing gastric acid, PPIs halt the migration of esophageal mucosa into the chest. PPIs, however, do not seem to reduce the incidence of esophageal cancer, the fastest growing malignancy in north America. Is it possible that by preventing the migration of the squamo-columnar junction up into the chest and the shortening of the esophagus, while not reducing bile and other digestive enzyme reflux into the esophagus, PPIs are enhancing the transformation of squamous lining to Barrett’s esophagus and esophageal adenocarcinoma?