A unifying theme of gastroesophageal reflux disease (GERD) is increased acid exposure on vulnerable epithelia. In most cases, the vulnerable epithelium is the esophagus, but alternatively it may be that of the supraesophageal terrain, which includes the larynx, pharynx, and airways. In 50% to 94% of patients with GERD, hiatal hernia is a significant pathophysiologic factor. The esophagogastric junction (EGJ) is anatomically and physiologically complex, making it vulnerable to dysfunction by several mechanisms, including transient relaxations of the lower esophageal sphincter (LES), hypotensive LES, and anatomic disruption. The importance of hiatal hernia is obscured by imprecise use of the term and by the misconception that it is an all-or-none, one-dimensional phenomenon. Rather, hiatal hernia can be viewed as a continuum of progressive disruption of the EGJ, with larger hernias being of greater significance and invoking several pathogenetic mechanisms. The dynamic anatomy of the EGJ highlights the difficulty of defining hiatal hernia and of elucidating the relation between hiatal hernia, the diaphragmatic hiatus, the LES, and GERD, including supraesophageal reflux.
|Original language||English (US)|
|Number of pages||5|
|Journal||American Journal of Medicine|
|Issue number||8 SUPPL. 1|
|State||Published - Dec 3 2001|
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