Esophagogastric junction distensibility: a factor contributing to sphincter incompetence

Abstract

Kahrilas. Esophagogastric junction distensibility: a factor contributing to sphincter incompetence. Am J Physiol Gastrointest Liver Physiol 282: G1052-G1058, 2002 10.1152/ ajpgi.00279.2001.-To quantify the effect of hiatus hernia (HH) on esophagogastric junction (EGJ) distensibility, eight normal subjects and nine gastroesophageal reflux disease (GERD) patients with HH were studied with concurrent manometry, fluoroscopy, and stepwise controlled barostatic distention of the EGJ. The minimal barostatic pressure required to open the EGJ during the interswallow period was determined. Thereafter, barium swallows were imaged in 5-mmHg increments of intrabag pressure. EGJ diameter and length were measured at each pressure during deglutitive relaxation. The EGJ opening diameter was greater in hernia patients compared with normal subjects during deglutitive relaxation at all pressures, and EGJ length was 23% shorter. EGJ opening pressure among hernia patients was lower than normal subjects during the interswallow period. In conclusion, the EGJ of GERD patients with HH was more distensible and shorter than normal subjects. These findings partially explain why HH patients are predisposed to reflux by mechanisms other than transient lower esophageal sphincter relaxations, sustain greater volumes of refluxate, and have a reduced ability to discriminate gas from liquid reflux. hiatus hernia; gastroesophageal reflux disease THE CARDINAL ABNORMALITY of gastroesophageal reflux disease (GERD) is incompetence of the esophagogastric junction (EGJ) to reflux of gastric secretions. This functional compromise can be attributable to perturbation of a number of anatomical or physiological components of the EGJ, including the intrinsic lower esophageal sphincter (LES), the extrinsic compression of the distal esophagus at the diaphragmatic hiatus, the intra-abdominal location of the LES, or the physiology of transient LES relaxations (tLESRs). Physiological investigations suggest that the net result of these perturbations is an increased number of acid reflux events by three mechanisms: 1) tLESR, 2) strain-induced reflux in the setting of a hypotensive LES, or 3) free reflux during periods of low LES pressure or deglutitive relaxation (1,12,19).Gaining acceptance as a cofactor in the pathogenesis of GERD is anatomical distortion of the EGJ inclusive of, but not limited to, hiatus hernia (7,9,13,14). When examining GERD in the context of hiatus hernia, certain distinctions become evident. Patients with more severe forms of GERD, such as erosive esophagitis and Barrett's metaplasia, almost invariably have a hiatus hernia (2, 18), and GERD patients with hiatus hernia have increased esophageal acid exposure compared with patients without hiatus hernia (8, 18). The mechanistic profile for reflux in hiatus hernia patients is also distinct. Whereas tLESRs can account for up to 90% of reflux events in normal subjects or in patients without hiatus hernia, patients with hiatus hernia have a more heterogeneous mechanistic profile with reflux episod...

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