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Normally, several centimeters of the distal esophagus and the gastroesophageal junction (GEJ) lie below the hiatus within the abdomen. When the GEJ, the fundus of the stomach, or both migrate into the chest above the hiatus, a hiatal hernia is present. Intrinsic to the repair of a hiatal hernia is the need to bring the GEJ, stomach, and distal esophagus back into the abdomen. However, since 1950 it has been known that in some patients this can be challenging, particularly those with severe gastroesophageal reflux disease (GERD) or a large hiatal hernia. In these patients esophageal shortening can lead to loss of intraabdominal esophageal length and put tension on the repair of a hiatal hernia. Dr. John. Leigh Collis described a technique in 1957 to address acquired esophageal shortening. His technique, now referred to as a Collis gastroplasty, creates an extension to the esophagus from the high lesser curvature of the stomach. His gastroplasty was done as a transthoracic procedure. Subsequently, several techniques have been described to create a similar gastroplasty using a laparoscopic approach. However, more than 50 years after Dr. Collis described his procedure for lengthening the esophagus there is still controversy about the existence and prevalence of a foreshortened esophagus. Furthermore, the laparoscopic management of a short esophagus is challenging, and as a result there is a tendency by many surgeons to ignore esophageal length and proceed with a standard repair. Importantly, tension is the enemy of any hernia repair, and long-term successful outcomes with hiatal hernia repairs, as for all other abdominal hernias, require addressing tension when encountered.
Patients at risk for acquired esophageal shortening include those with advanced GERD with esophagitis, stricture, long-segment Barrett esophagus, a history of sarcoidosis, caustic ingestion, or scleroderma and those with a large sliding or paraesophageal hernia (PEH). In some reports patients with a PEH have the highest frequency of a short esophagus. The presence of a foreshortened esophagus in patients with severe GERD is understandable because exposure to refluxed gastric juice causes mucosal injury and can lead to transmural inflammation, fibrosis, and collagen contraction. An esophageal stricture is strongly associated with a shortened esophagus and the need for a gastroplasty. The presence of both a large hiatal hernia (>5 cm) and an esophageal stricture further increases the risk of a shortened esophagus. In addition, a history of a previous failed antireflux procedure with recurrent hiatal hernia should raise suspicion that the length of the esophagus is short. The etiology of esophageal shortening in patients with a PEH is unclear but may be related to loss of elasticity in the longitudinal esophageal muscle related to chronic loss of intraabdominal fixation of the GEJ. Although any of these histories should increase the suspicion that a patient may have a short esophagus, none are definitive. Objective studies in patients with GERD or PEH are useful to define the size, type, and reducibility of any hiatal hernia, presence of a stricture or erosive esophagitis, esophageal function, and the presence and severity of increased esophageal exposure to refluxed gastric juice. A foreshortened esophagus can effectively be ruled out when a hiatal hernia fully reduces on barium esophagram, but in any nonreducing hiatal hernia a short esophagus may be present. Therefore, although objective studies can rule out a short esophagus, none can accurately identify its presence. Instead, a foreshortened esophagus can be confirmed only by the intraoperative inability to reduce the GEJ below the hiatus by 2 to 3 cm after mediastinal esophageal mobilization and posterior crural closure.
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