Laparoscopic Heller Myotomy With Toupet Fundoplication

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Abstract
Achalasia is an idiopathic primary motility disorder characterized manometrically by a poorly relaxing lower esophageal sphincter (LES) and complete loss of primary peristalsis, which leads to a compromise of the primary function of the esophagus.1 Untreated, it leads to an extremely poor quality of life because of progressive dysphagia, esophageal dilation, and stasis. All current treatments are palliative, as they are directed toward relieving dysphagia and preventing stasis-related complications, but do not restore normal esophageal motility.2-4 Surgical myotomy, endoscopic pneumatic dilation, and botulinum toxin injections of the LES are the most commonly used techniques for the treatment of achalasia at present, all of which seem to provide excellent symptomatic relief at least initially. Although most studies indicate that surgical myotomy is superior to endoscopic approaches in providing long-term relief of dysphagia,5-9 many physicians still favor endoscopic treatment because of the relatively higher morbidity associated with laparotomy or thoracotomy.10-13 Surgical myotomy, however, has regained primacy since the introduction of a minimally invasive laparoscopic approach in 1991.14 This is because of the obvious advantages associated with this approach, including less postoperative pain, a shorter hospital stay, and an earlier return to work.15 Current data suggest that, in experienced hands, results of laparoscopic Heller myotomy (LHM) are excellent and are comparable with those of open surgery.8,16-20 Even so, the symptoms of achalasia may recur in 6% to 23% of patients, and little is known, at present, about the factors that may lead to failure after myotomy. The aim of this study was to evaluate intermediate-term outcomes after LHM with a posterior 270° Toupet fundoplication and to identify patient, technical, and disease factors associated with or predictive of poor outcomes.