Chapter 16 - Progression of GERD From the Perspective of LES Damage

Abstract

The new method of assessment of abdominal lower esophageal sphincter (LES) damage by pathology provides a new way to assess cellular changes in the esophagus. It also permits correlation of cellular damage with the measured amount of abdominal LES damage. Like any new method, there are no data whatsoever that are directed at this endeavor. Data exist from previous studies that have correlated manometric LES length with cellular damage. These provide a theoretical basis for extrapolating abdominal LES damage (which is inversely related to manometric abdominal LES length) with cellular changes. I have created a theoretical construct of what happens when the abdominal LES undergoes damage in increments of 5mm. The available evidence suggests that there is a phase of LES damage in which the LES exhausts its reserve capacity. In this phase of compensated LES damage, the abdominal LES is damaged but retains functional competence. This is abdominal LES damage from 0 to 15mm. There is no LES failure or reflux. Recognition of this phase allows diagnosing changes causing gastroesophageal reflux disease (GERD) even before reflux and symptoms of GERD occur. With abdominal LES damage>15mm, the LES fails when it is subjected to the stress of gastric overdistension, where dynamic shortening causes the residual abdominal LES to become <10mm at which point LES failure occurs leading to reflux. From this onset of clinical GERD, the severity of reflux and cellular changes in the thoracic esophagus increases as LES damage progresses to complete destruction of the 35mm of the abdominal LES. The new method permits measurement of LES damage to an accuracy of micrometers. In this chapter, I will develop clinicopathologic correlations for various levels of abdominal LES damage at 5mm increments, recognizing that the test will provide much more accurate measurements.