Abstract

Background: Achalasia is a primary motility disorder of the esophagus characterized by poor mid-esophageal motility and failure of the lower esophageal sphincter to properly relax. The optimal treatment of the disease would improve esophageal peristalsis and promote lower esophageal sphincter relaxation. Currently, such therapy is not possible, so treatment of the disorder is aimed at relief of symptoms by disruption of the lower esophageal sphincter.

Methods: Data were collected prospectively on all patients undergoing laparoscopic myotomy and Toupet fundoplication during a 6-year period.

Results: Fifty-nine patients with a mean age of 44 years were treated during a 6-year period. Fifty-three patients underwent laparoscopic myotomy with Toupet fundoplication (91%), and four had laparoscopic myotomy without a fundoplication (6%). Fundoplication was not performed in two patients who had a megaesophagus. Two patients required conversion to an open operation. Sixty percent of patients were discharged the day after surgery; the average length of stay for all patients was 2.1 days. Ten percent of patients had minor complications; none required reoperation. Mortality was 0%, and 96% of patients rated their postoperative swallowing ability as excellent or good.

Conclusion: Surgical myotomy is becoming first-line therapy for all patients with achalasia. A strong working relationship between surgeon and gastroenterologist helps to optimize patient care.

Achalasia is a primary motility disorder of the esophagus that is characterized by poor mid-esophageal motility and failure of the lower esophageal sphincter (LES) to properly relax. The term achalasia is of Greek origin and means “failure to relax.” The disorder has been recognized since the late 1600s and was given the name achalasia by Lendrum in 1937. ¹Clinically, patients most often present with progressive dysphagia and frequently have the concomitant symptoms of regurgitation, chest pain, or weight loss. Men and women are equally affected. Symptoms typically appear between the third and fifth decades, but achalasia can be seen in children and the elderly.

Physiologic changes in achalasia include failure of LES relaxation, esophageal aperistalsis, and eventual esophageal dilation. Pathology reveals selective loss of the postinhibitory neurons of Auerbach’s plexus. These neurons inhibit smooth muscle contraction of the LES, and their loss results in unopposed stimulation of contraction by acetylcholine. ² A decrease in the amount of nitric oxide released from the postganglionic cells, which normally mediates the relaxation of the LES, also occurs. The actual cause of achalasia is unknown, but viral and autoimmune mechanisms have been proposed. The optimal treatment of the disease would improve esophageal peristalsis and promote LES relaxation. Currently, such therapy is not possible, so treatment of the disorder is aimed at relief of symptoms by disruption of the LES.

Key Points

* Physiologic changes in achalasia include failure of lower esophageal sphincter relaxation, esophageal aperistalsis, and eventual esophageal dilation.

* The dysphagia associated with achalasia must be differentiated from dysphagia caused by stricture, spasm, or obstruction from a benign or malignant mass.

* Treatment of achalasia can be divided into pharmacologic, endoscopic, and surgical management.

* Endoscopic treatment includes forceful dilation of the lower esophageal sphincter to disrupt the muscle fibers of the lower esophagus or injection of botulinum toxin at the gastroesophageal junction to paralyze the muscle.

* Surgical myotomy has been used to successfully treat achalasia since the early 1900s. Relief of dysphagia is achieved in 90 to 95% of patients, and symptoms are relieved long term.