The Status of the Hiatus

Abstract

The contribution of hiatal herniae to gastroesophageal reflux disease (GERD) has been debated for over a century. Early enthusiasm for surgical repair of herniae in reflux disease was supplanted by the view of reflux esophagitis as a disorder of abnormal lower esophageal sphincter (LES) function rather than due to a mechanical defect. The subsequent development of highly effective acid suppressive therapy provided effective symptom relief and mucosal healing regardless of the underlying pathophysiology. Recent evidence from epidemiologic, clinical, and physiologic observations supports the original notion of an etiologic link between a hiatal hernia and GERD, with obesity a likely common cofactor. Determining the etiology of hiatal herniae and how they progress and contribute to excessive acid reflux has been a controversial and difficult subject. It has been complicated by variations in the methods used to diagnose herniae and investigate their pathophysiologic consequences. Current opinion suggests that in hiatal herniae the physical separation of the LES from the crural diaphragm, and the production of a trapped acidic pocket in the herniated fundus are of etiologic importance in excessive esophageal acid exposure. Furthermore, although reflux events in subjects without herniae are usually associated with transient lower esophageal relaxations, reflux episodes in those with hiatal herniae are accompanied, and probably caused by, a variety of manometric abnormalities of the LES. The precise effects of surgical correction on the abnormal mechano-physiology of the gastroesophageal junction remain largely unexplored. Given the likely etiologic role of hiatal herniae in GERD, it remains disappointing that surgical attempts to restore the anatomy of the gastroesophageal junction have not yielded outcomes superior to long-term acid suppressive therapy.