Gastroesophageal reflux disease is the main reason for esophageal shortening. The patho-physiology of the short esophagus associated with GERD follows the sequence of erosion ulcers and inflammation associated with chronic esophageal reflux. These factors have been studied in animal experiments and in human pathological evaluation.11,12 The squa-mous epithelium of the lower esophagus has poor defense mechanisms against repeated episodes of gastric refluxes. Chronic exposure to gastroesophageal reflux episodes, particularly when acid is mixed with bile salts and/or pepsin, causes a chemical esophagitis with back diffusion through the epithelium. Edema of the lamina propria occurs initially. The inflammation can reach the muscularis mucosae at a later


stage. Most of reflux strictures are caused by fibrosis and scar contraction when damage is present at that depth of the esophageal wall. These strictures are usually easily dilatable. If prolonged exposure causes further inflammation and additional scar formation, the consequences of cyclic esophagitis reach the level of the muscularis propria and the periesophageal tissues. Progressive circumferential contraction creates a more fibrous stricture and, simultaneously, longitudinal contraction results in a shortening of the esophagus. Transmural fibrous damage is frequently seen in sclero-derma patients especially when they present with an associated complication in a columnar-lined esophagus.

Other conditions have been incriminated in the formation of a short esophagus. In such circumstances, fibrosis need not be present for the acquired esophageal shortening to occur. Type 3 and type 4 paraesophageal hernias and the periesophagitis after previous anti-reflux operations or after repairs of esophageal atresia are examples of these circumstances.

Clinical and radiological findings may immediately suggest the possibility of esophageal shortening. The presence of a reflux stricture at endoscopy or of a high stricture radiologically are known to jeopardize the success of any standard anti-reflux operation: Donnelly et al.13 and Orringer et al.14 have documented that 45-75% of patients with reflux strictures or severe esophagitis who undergo a Belsey Mark IV repair will develop a recurrent hiatal hernia or reflux disease during follow-up. The long columnar-lined esophagus, especially if a high stricture is present on radiological examination, is exposed to the same failure risk.15,16

The repair of massive hiatal hernias and redo operations are also known to result in a high failure rate.17 Long-standing type 3 and type 4 sliding and paraesophageal hernias, even if they do not reveal associated reflux esophagitis, will present some degree of circular and longitudinal esophageal muscle contracture. In many of those situations,it is not the anatomic reduction of the junction that is critical, it is the resulting tension on the repair once the esophagogastric junction has been reduced below the diaphragm.

The prevalence of a short esophagus varies significantly among observers. Ritter et al.18 reported the condition in 3-14% of patients requiring an anti-reflux operation. But in patients having redo surgery associated with an esophageal stricture, a paraesophageal hernia, or a Barrett's esophagus, a 79-fold increase in the need for an esophageal lengthening procedure has been observed.17

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