Hiatal hernias (HH) are frequently encountered during routine transnasal esophagoscopy (TNE). The prevalence of hiatal hernia increases with age. Although the existence of a HH does not itself indicate the presence of gastroesophageal reflux disease, persons with a HH are prone to more severe reflux. The two mechanisms in which HH promotes reflux are through (a) a mechanically defective lower esophageal high-pressure zone and (b) the creation of a reservoir that allows for the expeditious regurgitation of gastric contents into the esophagus. Table 6.1 lists the means by which a HH contributes to a defective distal antireflux barrier. A thorough understanding of the anatomy of the distal antireflux barrier is necessary in order to accurately identify pathology in this region and to diagnose HH (1,2 and 3).

There are three primary contributors to the distal antireflux barrier. In order of decreasing importance they are: the intrinsic lower esophageal sphincter (LES), the diaphragmatic hiatus, and the valve effect created by the angle of His. The intrinsic LES is a 3- to 4-cm high-pressure zone at the gastroesophageal junction (GEJ). Although the endoscopist is unable to accurately differentiate the exact boundaries of the LES from the more proximal esophagus, the sphincter is a distinct entity that is tonically contracted at rest. The midpoint of the LES is at the approximate level of the squamocolumnar junction (SCJ). The normal anatomic relationship is such that the LES lies within the hiatus of the right diaphragmatic crura. The phrenoesophageal ligaments serve to anchor the LES at about the level of the SCJ (Fig. 6.1). These distinctions can be blurred when the gastric mucosa migrates into the more proximal esophagus, such as with Barrett’s esophagus, and when the LES migrates higher into the chest, as with HH. The diaphragmatic hiatus augments internal LES tone (4). When the hiatus is not at the level of the LES (HH), the resting LES tone is significantly lower (5). The key to evaluating the endoscopic presence of a HH is in being able to differentiate the GEJ from the crura of the diaphragm. The third contributor to the lower esophageal high-pressure zone is the valve effect created by the oblique entrance of the esophagus into the stomach at the angle of His (Fig. 6.1) (6).