Abstract
Hiatal hernias result from a multifactorial combination of the failure of diaphragmatic integrity, degeneration of the phrenoesophageal suspensory ligament, and the normal pressure differential between the thorax and abdomen; some combination of these factors results in the cephalad migration of the gastroesophageal junction (GEJ) and the anatomic shortening of the esophagus. These changes are often combined with some degree of gastroesophageal reflux (GER). GER can lead to chronic esophageal irritation and damage, with resulting thickening of the mucosal layers, sometimes development of intestinal type columnar epithelium, and progressive fibrosis and damage of the muscularis mucosa. In especially severe and chronic cases there can even be transmural changes in the mediastinum with hypervascularity and thickening of the normally pliable areolar tissues. These factors can lead to loss of the usual elasticity of the esophagus as well as causing it to be more fixed within the mediastinum. When this process is combined with hiatal herniation (or perhaps even partially causing such migration?) it can lead to not only anatomic shortening of the esophagus but also non-reversible shortening of the esophagus, which can make it impossible to replace the GEJ into the abdominal during anti-reflux surgery or paraesophageal hernia (PEH) repair.
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Swanstrom, L.L., Goers, T.A. (2011). Lengthening Gastroplasty for Managing GERD and Giant Paraesophageal Hernia. In: Ferguson, M. (eds) Difficult Decisions in Thoracic Surgery. Springer, London. https://doi.org/10.1007/978-1-84996-492-0_33
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