The aim of this study was to determine whether a detailed analysis of intra-EGJ pressure dynamics in well-characterized Type I (sliding) HH patients revealed a characteristic pattern associated with dysphagia. The major finding was that sliding HH is a heterogeneous condition such that HH patients with dysphagia and without reflux symptoms exhibit functional EGJ obstruction localized to the CD. This condition was associated with abnormally high deglutitive EGJ relaxation pressure and increased esophageal IBP of sufficient magnitude that it might be confused with achalasia in some cases. These changes were not seen in HH patients with reflux symptomatology.
Furthermore, our findings suggest that manometric indices of deglutitive EGJ relaxation in HH patients are not always indicative of LES relaxation, as the maximal residual pressure within the EGJ can be either at the CD or immediately proximal to this area in the form of an IBP or hernia sac pressure. Thus, at any 1 instant, a 6-cm value as measured with the eSleeve tool (Sierra Scientific Instruments Inc.) may be attributable to the LES, CD, IBP, or even intragastric pressure. Consequently, impaired deglutitive EGJ relaxation in HH patients has at least 2 potential causes: (1) achalasia with impaired intrinsic LES relaxation; or (2) a “tight” hiatal canal (). These entities can be discerned with high-resolution esophageal pressure topography, but only if care is taken to appropriately restrict the eSleeve analysis domain to each area of interest.
Although the mechanical obstruction associated with type II or III paraesophageal hernia is well known, there has been little scrutiny of the role of sliding HH in dysphagia. We recently analyzed 400 consecutive patients with HRM and described a subset that exhibited a pattern of EGJ obstruction associated with an abnormal EGJ relaxation pressure, intact peristalsis, and increased IBP.9
After excluding pathology at the EGJ (such as eosinophilic esophagitis, disrupted fundoplication, or stricture), we were left with a group of 14 (3.5%) with idiopathic functional EGJ obstruction. Although some of these patients may have had evolving achalasia, others had HH with normal LES relaxation and increased IBP. We hypothesized that these abnormalities could be the consequence of functional obstruction at the diaphragmatic hiatus attributable to a relatively normal-sized hiatal aperture surrounding the relatively thick-walled proximal stomach. Findings from this study support our previous hypothesis. After excluding patients with GERD symptoms, stricture, or compromised peristalsis, we concluded that sliding HH, in and of itself, can cause functional obstruction at the EGJ.
Hiatus hernia patients with dysphagia exhibited greater deglutitive CD relaxation pressure and IBP compared to HH-GERD patients or normal subjects. These data are consistent with a previous report from Kaul et al4
in which they suggested CD impingement on the herniated stomach manifests as a “double hump” axial pressure profile during a pull-through of the EGJ and a numerical difference in the amplitude of the distal (CD) hump between patients with and without dysphagia. Our results are in line with these findings; however, we were able to leverage the temporal and spatial resolution of high-resolution pressure topography plotting to analyze the pressure dynamics within the EGJ during swallowing and provide further insight into possible mechanisms. We confirmed that the distal hump of the axial pressure profiles localized at the CD and that increased IBP extended to this area in the HH-dysphagia patients, signifying that it was the site of obstruction. These findings were observed during normal LES relaxation, and they potentially represent a decrease in opening diameters of the CD in the context of intact peristalsis. This pattern is analogous to a patient with a slipped Nissen fundoplication, and studies have shown that these changes lead to retrograde escape and impaired bolus transit after the time-locked peristaltic sequence terminates.11,12
In conclusion, our results suggest that HH can result in altered pressure dynamics within the EGJ, leading to functional EGJ obstruction in a subset of HH patients. HH patients with dysphagia but without GERD symptoms exhibited a relative obstruction at the CD. This observation supports the hypothesis that sliding HH, in and of itself, could be responsible for dysphagia. Furthermore, this analysis emphasizes that not all HH patients are the same. By assessing individual pressure components within the EGJ, one can theoretically identify clinically meaningful HH subtypes that could potentially help define treatment. Patients presenting with increased EGJ relaxation pressure in the context of a small type I HH require careful analysis of the various components of the EGJ before making a diagnosis of achalasia and before surgical myotomy or dilation are considered. Although it is intriguing to further speculate that the HH-dysphagia group could benefit from surgical intervention aimed at reducing the obstruction at the CD, prospective randomized studies are still required before this approach can be supported.