The impact of laparoscopic anti-reflux surgery in patients with Barrett's esophagus.

BACKGROUND: Barrett's esophagus (BE) is a major risk factor for esophageal adenocarcinoma. It is believed that BE is caused by chronic gastro-esophageal reflux disease (GERD). Laparoscopic anti-reflux surgery (LARS) restores the competency of the cardia and may thereby change the natural course of BE. We studied the impact of LARS on the histological profile of BE and on the control of GERD. METHODS: We identified all patients with BE who underwent LARS from 1994 to 2007 and contacted them to assess post-operative GERD symptoms via questionnaire. Endoscopy findings, histology, 24 hour pH monitoring, and manometry were also collected using our prospectively maintained database. Histological regression was defined as either loss of dysplasia or disappearance of BE. RESULTS: Two hundred and fifteen patients met the initial inclusion criteria; in 82 of them histology from post-operative endoscopy was available for review. Endoscopy was performed a median of 8 years (range, 1-16 years) after surgery. Regression of BE occurred in 18 (22%) patients while in 6 (7%) BE progressed to dysplasia or cancer. Thirty-six (43%) patients underwent pre- and post-operative manometry. The median lower esophageal sphincter pressure increased from 9 to 17 mmHg in these patients. Thirty-four (41%) patients underwent pre- and post-operative pH studies. The median DeMeester score decreased from 54 to 9. Sixty-seven (82%) of 82 patients completed the post-operative questionnaire; 86% of these patients reported improvement in heartburn and regurgitation. CONCLUSIONS: LARS was associated with both physiologic and symptomatic control of GERD in patients with BE. LARS resulted in regression of BE in 22% of patients and progression in 7%. Thus, continued surveillance of Barrett's is needed after LARS.

Recurrent dysphagia after Heller myotomy: is esophagectomy always the answer?

BACKGROUND: Esophagectomy has been recommended for patients when recurrent dysphagia develops after Heller myotomy for achalasia. My colleagues and I prefer to correct the specific anatomic problem with redo myotomy and preserve the esophagus. We examined the results of this approach. STUDY DESIGN: We analyzed the course of 43 patients undergoing redo Heller myotomy for achalasia between 1994 and 2011 with at least 1-year of follow-up. In 2012, a phone interview and a symptoms questionnaire were completed by 24 patients. RESULTS: Forty-three patients underwent redo Heller myotomy. All patients had dysphagia, 80% had had multiple dilations. Manometry confirmed the diagnosis, lower esophageal sphincter pressure averaged 17 mmHg; 24-hour pH monitoring was not useful because of fermentation; patients were divided into 4 groups according to findings on upper gastrointestinal series. Three patients underwent take down of previous fundoplication only, the remainder 40 had that and a redo myotomy with 3-cm gastric extension. Two mucosal perforations were repaired with primary closure and Dor fundoplication. At a median follow-up of 63 months, 19 of 24 patients reported improvement in dysphagia, with median overall satisfaction rating of 7 (range 3 to 10); 4 patients required esophagectomy for persistent dysphagia. CONCLUSIONS: The majority of failures after Heller myotomy present with dysphagia associated with esophageal narrowing. Upper gastrointestinal series is most useful to plan therapy and predicts outcomes. With few exceptions, patients improve substantially with redo myotomy, which can be accomplished laparoscopically with relatively low risk. These findings challenge the previously held concept that all myotomy failures need to be treated by an esophagectomy.