The concept of a shortened esophagus is not accepted by everyone, resulting in controversy over the years.1,2 Although an occasional patient may be seen with an esophagogastric junction clearly irreducible to its proper position under the diaphragm, there are discrepant opinions among surgeons on what constitutes a shortened esophagus and what is the real incidence of the condition in patients with gastroe-sophageal reflux disease (GERD) and hiatal hernia. There is no exact and reproducible method of measuring the length of the esophagus before and during surgery. The extent to which the esophageal surgeon has to address the problem is unknown. At present the existence of a short esophagus is based mostly on indirect and circumstantial evidences.
During the last 50 years, the natural evolution of the various anatomic hiatal hernia repairs and, subsequently, of the numerous anti-reflux operations has resulted in identifying failure patterns which were then related to the severity of the disease. How often a failed anatomic repair was the consequence of not recognizing a short esophagus remains unknown. The inadequate long-term functional results observed with a perigastric fundoplication or a slipped fundoplication, or crural disruption with mediastinal herniation of the repair, raise the hypothesis that such failures might be attributed to a shortened esophagus.3 In 1950, Norman Barrett wrongly described an intratho-racic stomach when observing a columnar-lined esophagus. He suggested the concept of progressive shortening of the esophagus with distraction of the stomach into the chest. Barrett had coined the term "reflux esophagitis" when ulcers of the esophagus were associated with reflux of gastric content.4,5 Just previously, Allison6 had associated the concept of hiatal hernia to the erosive esophagitis observed and to the occasional esophageal stricture, attributing both to gastroesophageal reflux. About the same period that Allison was proposing his anatomic repair, Belsey proposed a partial fun-doplication of the gastric fundus on the pos-terolateral wall of the esophagus. In patients treated by this operation without endoscopic
esophagitis, a reflux recurrence rate of 9.5% was observed. When esophagitis without stricture was identified before the operation, 10.3% of these patients had recurrent reflux. If a stricture was present, the operation failed in 45% of the operated population.7 The repair difficulties and imperfect results obtained when an esophagus is shortened or strictured then led Leigh Collis to propose a lengthening gastroplasty in order to provide good, healthy tissue for the repair while removing tension for its positioning under the diaphragm.8
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Gastroesophageal reflux disease is the medical term for what we know as acid reflux. Acid reflux occurs when the stomach releases its liquid back into the esophagus, causing inflammation and damage to the esophageal lining. The regurgitated acid most often consists of a few compoundsbr acid, bile, and pepsin.