The Gastroesophageal Junction

The focus of perendoscopic treatments to prevent gastric reflux is directed towards the gastroesophageal junction (GEJ). Both the physiologic and anatomic components to the acid reflux barrier occupy this zone (Figure 13-1). Primary factors enhancing gastroesophageal reflux are a hypotensive lower esophageal sphincter (LES) pressure and transient LES relaxations (tLESrs). Structural alterations at the anatomic hiatus enhance the opportunity for orad escape of gastric contents into the esophagus.

FIGURE 13-1. Schema of gastroesophageal junction (GEJ).

The zone of the LES is approximately 4 cm in length. The proximal 2 cm of the LES is surrounded by the crural diaphragm; the distal portion of the sphincter is intraabdominal in position. Sling or oblique fibers of the gastric fundus located beneath the LES contribute to the overall antireflux barrier. The sling fibers anatomically form a "C" configuration. (The open side of the "C" is oriented to the lesser curvature of the stomach) (Boyle et al, 1985). A "flap valve" results from this design. Pressure within the gastric fundus accentuates the "flap valve" mechanism, which embraces the distal portion of the esophagus and enhances the LES pressure (Mittal et al, 1995).

tLESr events are a vagovagal reflex and are triggered by gastric distention. The afferent receptive field is located in the gastric cardia and fundus where vagal fibers with specialized terminal endings called intraganglionic laminar endings (IGLEs) exist (Zagorodnyuk et al, 2001). These IGLEs are deformity sensitive neural transducers arranged within the proximal stomach and appear to be responsible for receptive relaxation and tLESr initiation.

The majority of patients with severe esophagitis have an axial hiatus hernia (Jones et al, 1991). Thinning and elongation of the phrenoesophageal membrane leads to herni-ation of the stomach into the posterior mediastinum. Hiatal hernias may range in size from a type I or "sliding" variety to a type IV that is associated with a large enough hiatal defect to allow other organs to enter the sac (Kahrilas and Pandolfino, 2004). A hiatal hernia may add complicating features to the GERD algorithm by several mechanisms. A hernia may impair acid clearance from the esophagus, or crural contractions can force compartmentalized acid upwards into the distal esophagus. A large hiatal hernia is associated with widening of the esophageal hiatus that impairs the ability of the crural diaphragm to function as a sphincter (Sloan et al, 1992). Finally, hiatal hernias are associated with loss of the flap valve mechanism and the intra-abdominal portion of the esophagus obviating important factors in the prevention of gastroesophageal reflux (Mittal and Balaban, 1997).

Thus, gastroesophageal reflux is multifactorial offering a number of target choices for proponents of peren-doscopic therapies.

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