Unique features of esophagogastric junction pressure topography in hiatus hernia patients with dysphagia

The pathophysiologic consequences of sliding hiatus hernia (HH) mainly pertain to reflux disease and compromise of the antireflux barrier.1 HH is associated with a decreased pressure at the esophagogastric junction (EGJ) and a decrease in length of the functional EGJ. These changes are attributable to axial separation of the lower esophageal sphincter (LES) and crural diaphragm (CD) and possibly to a loss of the abdominal segment of the LES.2 Furthermore, reflux disease patients with HH may exhibit dilatation of the crural aperture resulting in increased EGJ compliance and wider opening diameter during relaxation.3 In combination, these defects compromise the CD as a component of the antireflux barrier and likely increase the volume of refluxed fluid during reflux events. Although the HH defects predisposing to reflux should also reduce resistance to antegrade flow through the EGJ after swallowing, HH has also been implicated as a cause of dysphagia. Kaul et al4 used fluoroscopy and manometry to study patients with HH and dysphagia but without significant esophagitis or motility abnormalities. Fluoroscopy revealed that hiatal flow obstruction, manifest by hold-up of swallowed contrast and retrograde escape, was more common in HH patients with dysphagia than those without dysphagia. The authors speculated that this finding was due to compression of the herniated stomach within the hiatal canal, and they correlated these findings with a double-hump axial pressure profile found on pull-through manometry.4 Studies that are more recent suggest additional pathophysiologic aberrations associated with HH that could impair esophagogastric bolus transit. Using synchronized fluoroscopy and manometry through the EGJ, Lin et al5 concluded that emptying of the distal esophagus was more a function of the elastic recoil of phrenoesophageal attachments restoring resting esophageal length after peristalsis-associated shortening than it was of the peristaltic contraction per se. Both peristalsis-associated shortening and the subsequent recoil are reduced with HH, suggesting that HH might compromise this function.6 Furthermore, even in the absence of HH, the sustained CD contraction associated with a Muller maneuver can compromise esophageal emptying by outlasting the time-locked peristaltic contraction until supradiaphragmatic intrabolus pressure (IBP) exceeds esophageal (or LES) closure pressure resulting in retrograde flow.5 Although the physiologic evidence detailed above suggests mechanisms whereby HH may impede esophageal emptying, there are minimal clinical data substantiating an association between sliding HH and dysphagia. This lack of data is in part due to inconsistencies in defining sliding HH7 and in part due to the multitude of potential confounding variables, such as esophagitis, peptic stricture, peristaltic dysfunction, and Schatzki ring. Recently, high-resolution esophageal pressure topography has become available as a practical method to perform a detailed characterization of LES, CD, and IBP pressure dynamics within the EGJ after swallowing. The aim of this study was to determine whether or not the detailed characterization of these intra-EGJ pressure dynamics in well-characterized HH patients revealed a characteristic pattern associated with dysphagia.