: The modern surgical therapy of gastroesophageal reflux disease (GERD) is based upon the concept that the antireflux barrier has two components that form a “double-sphincter” and work synergistically to protect from reflux of gastroduodenal contents: the lower esophageal sphincter (LES) and the crural diaphragm. Factors implicated in the pathogenesis of hiatal hernia (HH) are the thoraco-abdominal pressure gradient, the esophageal shortening secondary to reflux-induced fibrosis, and the hiatal enlargement due to peri-esophageal tissue deterioration. Genetic and biologic factors can predispose to HH formation through alterations in extracellular matrix protein metabolism, and through structural changes of the muscular crura, central tendon, and phreno-esophageal ligament. This will eventually result in loss of tensile strength and/or loss of recoil ability of elastic fibers. Failure of LES or the crural diaphragm or both contribute to progression of GERD and development of complications such as Barrett’s esophagus and esophageal adenocarcinoma. Patients’ selection for antireflux surgery is critical for optimal outcomes. While laparoscopic cruroplasty and Toupet or Nissen fundoplication remain the current gold standard in antireflux surgery, the high rates of anatomical and clinical recurrence in patients with large hiatus hernia still represent a matter of concern. To reduce recurrence rates after surgical repair, it is clear that both axial and radial tension at the esophago-gastric junction (EGJ) must be minimized. This has led to an increasing interest for the use of prosthetic mesh to reinforce the esophageal hiatus. Recognition of anatomical and functional abnormalities at an early disease-stage is critical to prevent complications and to provide the most appropriate surgical therapy and the best clinical outcomes.
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