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Paraesophageal hiatal hernia is defined as the cephalad migration of the stomach and potentially other abdominal viscera away from their normal intraperitoneal locations into the mediastinum through an enlarged esophageal diaphragmatic hiatus. This defect occurs as a result of variable destruction of the normal attachments of the gastroesophageal junction (GEJ) and the barriers between the viscera of the abdomen and the thorax. It is estimated to occur in fewer than 1% of the population and is most likely an acquired defect given its greater frequency in the elderly population. Factors thought to contribute to the development of hiatal hernia include genetics, pregnancy, and factors that increase intraabdominal pressure, such as chronic cough, obesity, and repeated intraabdominal straining with physical activity, such as that associated with chronic constipation or childbirth.

Ninety-five percent of paraesophageal hiatal hernias are of the sliding type and are denoted type I. In type I hiatal hernia, the GEJ slides up into the lower mediastinum because of defect or deterioration of the phrenoesophageal ligament (Fig. 130-1). Type II–IV hiatal hernias account for the remaining 5%. Type II hiatal hernia involves a focal defect in the anterior aspect of the phrenoesophageal ligament and is very rare. The GEJ remains attached to the preaortic fascia and median arcuate ligament. Rather than the GEJ serving as the leading edge of the herniation, as in type I hernias, here, the gastric fundus serves as the leading edge of the herniation. As the hiatus defect enlarges, the stomach rolls into the chest along a longitudinal axis, producing organoaxial rotation.

Figure 130-1.

A. Normal paraesophageal anatomy. B. Classification of paraesophageal hernias.

Type III hiatal hernia is a combination of types I and II. Both the GEJ and the fundus herniate into the mediastinum. This is the most common form of paraesophageal hernia. Depending on the patient population and the method of determining the precise location of the GEJ, type III hiatal hernias comprise approximately 80–90% of all paraesophageal hernias. The hallmark of this disease is a foreshortened esophagus, which occurs as a result of the chronic reflux, in which inflammation, edema, and esophageal submucosal scarring cause esophageal remodeling. In addition, the adhesions associated with the hernia sac and the chronic position of the stomach and mediastinum create tension that “pulls” the distal esophagus deeper into the chest. Type IV hernias are very large. Here, other abdominal organs, such as the pancreas, spleen, omentum, and/or the small and/or large intestine, herniate with the stomach into the mediastinum.

It is difficult to determine the frequency of the complications that occur from paraesophageal hiatal hernias. According to many reports, most patients present without symptoms and have only incidental findings on radiologic examination or endoscopy performed for other reasons. However, these reports are misleading because most patients with type III hernias are revealed to be symptomatic when thoroughly ...

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