Abstracts
1999 Digestive Disease Week

# 2101 MECHANISMS OF DYSPHAGIA AFTER LAPAROSCOPIC NISSEN FUNDOPLICATION: A CASE-CONTROL STUDY
Daniel M Herron, Paul D Hansen, Legacy Hosp System, Portland, OR; Lee L Swanstrom, Legacy Minimally Invasive Surg, Portland, OR

New-onset solid food dysphagia is documented in up to 17% of patients who have a laparoscopic Nissen fundoplication antireflux procedure performed, and persists greater than 3 months in as many as 12% of patients. While technical aspects of the fundoplication such as an overly long or tight wrap have been implicated as the cause of such dysphagia, manometric measurements of the lower esophagus in these patients have not been studied in a controlled manner. We hypothesized that postoperative manometry would identify differences in lower esophageal sphincter function and esophageal body motility in dysphagia patients compared to controls. From December 1995 through April 1998 we performed 168 laparoscopic Nissen fundoplications. We identified 32 (19.0%) of these patients who complained of any postoperative solid or liquid dysphagia lasting greater than 3 months. We obtained postoperative manometry tracings on 15 (47%) of these patients. We then identified a control group of 15 Nissen fundoplication patients, matched for age and sex, without postoperative dysphagia. Postoperative esophageal manometry tracings were reviewed by blinded reviewers and evaluated for: 1) lower esophageal sphincter (LES) length, 2) LES resting pressure, 3) percent LES relaxation, 4) location of respiratory inversion point, and 5) esophageal body contraction amplitude and coordination. Pre- and post-operative 24-hr pH studies were available for all patients. Data were compared using a 2-tailed T-test and Fisher's exact test. Mean length of the LES in dysphagia patients did not differ significantly from control patients (2.7 ± 0.8 vs 2.8 ± 0.8 cm, p=0.77). Similarly, mean LES pressure did not differ between the 2 groups (20.6 ± 8.5 vs 17.8 ± 6.0 mmHg). LES relaxation was similar for the 2 groups, averaging 95.7% in dysphagia patients and 98.8% for the controls (p=0.28). The incidence of abnormal esophageal body motility in the dysphagia patients did not differ significantly from that in the control group (27% vs. 40%, p=0.70). These data suggest that dysphagia occurring after laparoscopic Nissen fundoplication is not due to abnormal esophageal body motility. Additionally, they do not support the commonly-held theory that dysphagia is caused by a wrap that is too long or too tight, or one that fails to exhibit receptive relaxation.

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