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2001 Abstract: 229 The Development of Achalasia Secondary to Laparoscopic Nissen Fundoplication

2001 Digestive Disease Week

# 229 The Development of Achalasia Secondary to Laparoscopic Nissen Fundoplication
Nicholas Stylopoulos, David W. Rattner, Boston, MA

Background: We report, for the first time,the development of secondary achalasia(SA)following LNF and identify characteristics which distinguish SA from routine post-Nissen dysphagia.

Patients and Methods: 250 consecutive patients undergoing LNF were analyzed for the development of post-op dysphagia. Patients with dysphagia persisting more than 4 weeks underwent Barium esophagrams prior to consideration of esophageal dilatation. Patients who did not have radiographic evidence of obstuction were considered to have SA if they met the following criteria: 1)Normal preoperative manometry, 2)Complete disappearance of esophageal peristalsis by manometry and fluoroscopy 3)Imcomplete relaxation of the lower esophageal sphincter by manometry. Three groups of patients were identified: Group A- Development of SA following LNF; Group B- Dysphagia persistent enough to require post-op dilatation but did not have SA; and Group C- Normal post-op recovery. Groups were compared using Mann-Whitney-U and Fisher's exact test. Data are expressed as median and range.

Results: 7 patients developed SA, 12 patients had evidence of narrowing at the fundoplication that required dilatation and 231 patients had normal post-op recoveries. All pre-operative variables among patient groups were comparable except for age. Patients developing SA were older(57y range 27-66)than patients with non-SA dysphagia that required dilatation(36y range 27-63),(p<.05). The onset of severe dysphagia in patients with SA occurred later than that seen in patients requiring dilatation (median 135 days post-op(15-300 vs 20 days(9-70),(p<.01). The maximal weight loss in patients with SA was significantly greater than in patients requiring dilatation(15 lbs 2-21) vs 4 lbs(0-15), (p<.00l). Barium radiographs in patients with SA identified aperistalsis and generally did not demonstrate significant narrowing at the site of the fundoplication. In contrast, Group B patients were found consistently to have narrowing at the fundoplication site and normal motility. Dysphagia improved promptly in 9/12 Group B patients after dilatation whereas no patient in Group A improved with dilatation. Conversion of LNF to partial fundoplication failed to improve dysphagia in Group A patients.

Conclusion: LNF may cause SA. SA tends to occur in older patients and is characterized by a delayed onset of symptoms as well as failure to respond to esophageal dilatation. Mechanical obstruction by either fundoplication or crural closure does not appear to be the mechanism of SA.

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