Esophageal Motility Disorder in Gastrophageal Reflux Disease

Gastroesophageal reflux disease (GERD) represents a real social problem in the western world. Brazilian consensus conference considered GERD to be “a chronic disorder related to the retrograde flow of gastro-duodenal contents into the esophagus and/or adjacent organs, resulting in a spectrum of symptoms, with or without tissue damage”. However, gastro-esophageal refluxate contains a variety of other noxious agents, including pepsin. Currently, it is recognized that this component of the refluxate (commonly called bile reflux and identified by the Bilitec bile reflux monitor using bilirubin as a marker) is composed of bile salts and pancreatic enzymes, and is also injurious to the esophageal mucosa. It causes symptoms, and could be linked to the development of Barrett’s esophagus and esophageal adenocarcinoma. A highly efficient barrier exists between the stomach and the esophagus formed by the lower esophageal sphincter, the diaphragm, the His angle, the Gubaroff valve and the phrenoesophageal membrane. The most important factors at work in preventing reflux include, well the lower esophageal sphincter, esophageal clearance mechanisms that limit contact time with noxious substances, and mucosal protective factors intrinsic to the esophageal mucosa. The most common cause of gastroesophageal reflux is an excessive exposure of the esophagus to gastric secretions during Transient Lower Esophageal Sphincter Relaxation. pH-metric studies in healthy subjects have shown that primary peristalsis is the most important mechanism of clearing after acid reflux in orthostatic position. When the subject is in supine position, however, most reflux is neutralized by means clearance produced by secondary peristalsis. Several studies have shown that oesophageal function is impaired in patients with reflux oesophagitis, especially in high grade oesophagitis. Patients with reflux oesophagitis have reduced lower oesophageal sphincter pressures, an increased incidence of failed peristalsis, reduced distal peristaltic amplitudes, slower velocity of propagation and in some studies shorter duration of contractions. In conclusion, application of the 24hour ambulatory oesophageal pressure and pH monitoring technique did not show any differences in either pH profiles or motility variables before and after healing of reflux oesophagitis. The fact that oesophageal motility does not change after healing of oesophagitis supports the hypothesis that abnormalities in motility are pre-existent rather than the consequence of the inflammation. It could be argued, however, that the inflammation has caused irreversible changes in the oesophageal wall.