The relationship between hiatal hernia and GERD remains controversial. Mainstream opinion has shifted widely from one that virtually equated hiatal hernia with GERD to one that denied it a causal role. Currently, both epidemiologic and physiological data confirm the importance of the hiatal hernia in patients with more severe esophagitis, peptic stricture, or Barrett esophagus. Hiatal hernias, identified endoscopically or radiologically, are reported in 54% to 94% of patients with reflux esophagitis; a rate strikingly higher than in the healthy population.
The functional impact of the hiatal hernia has been clarified by elegant combined manometry and videofluoroscopic studies that show that hiatal hernia impairs LES function through several mechanisms as well as impairing esophageal clearance. Reflux is worse in patients who have a nonreducible as opposed to a reducible hiatal hernia. Nonreducing hernias are those in which the gastric rugal folds remain above the diaphragm between swallows. Furthermore, statistical modeling has revealed a significant interaction between hiatal hernia and LES pressure, such that the likelihood of GER is increased as basal LES pressure decreases, an effect that is substantially amplified by the presence of a hiatal hernia and as hernia size increases.
Displacement of the LES from the crural diaphragm into the chest reduces basal LES pressure and shortens the length of the high-pressure zone primarily because of the loss of the intra-abdominal LES segment. Both these effects are caused by the loss of the extrinsic support of the diaphragmatic crura resulting in increased GER. Hiatal hernia virtually eliminates the increase of LES pressure that occurs during straining and may increase the triggering of transient LESRs during gastric insufflation with gas. , Large, nonreducible hernias also impair esophageal acid clearance because of increased tendency for reflux to occur from the hernia sac during swallow-induced LESRs.
The origin of hiatal hernia remains unclear. Familial clustering of GERD suggests the possibilities of inherited muscle weakness in this area. Animal studies propose that reflux itself causes esophageal shortening promoting the development of a hiatal hernia. Other studies find an association with obesity and lifting of heavy weights, raising the possibilities that over time, chronic intra-abdominal stressors may weaken the esophageal hiatus and may cause the development of a hiatal hernia. This theory is attractive because it helps to reconcile the increased prevalence of hiatal hernias as the population ages.

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