Recurrent reflux and wrap disruption after Nissen fundoplication: detection, incidence and timingOne hundred and twenty-five patients with refractory gastrooesophageal reflux disease underwent floppy Nissen fundoplication. Median follow-up was 52 months, and included endoscopy, manometry and prolonged p H recordings in all cases in addition to clinical assessment. Using objective criteria, 12 patients (9.6 per cent) developed recurrent reflux. In nine of these patients, endoscopy had suggested that the Nissen fundoplication had disrupted; wrap disruption was confirmed in seven patients who underwent reoperation. The median time to endoscopic recognition of wrap disruption was 7 months (range 3-10 months). In contrast, of 115 patients with endoscopic evidence of an intact fundoplication, only 3 (2-6 per cent) had recurrent reflux. Endoscopy allowed reliable differentiation between those with and without reflux control after operation ( P < 0.001). These results suggest that recurrent reflux after Nissen fundoplication is due to wrap disruption. This phenomenon occurs within the first postoperative year and can be recognized by informed endoscopic assessment.
Relations between primary oesophageal peristaltic amplitude and traction force were studied in 30 normal volunteers, 12 patients with functional dysphagia, and 48 patients with gastro-oesophageal reflux disease, using a new intraluminal strain gauge device. Forces generated by swallowing in the normal oesophagus were 42 (35-60) g (median and interquartile range), a close positive correlation existing between traction force and contractile amplitude for each subject (r=0.5 (0.38-0.6). Traction force increased with increasing balloon volume from 62 (50-73) g at 2 ml to 86 (70-105) g at 4 ml (p<0.05), indicating distension related modulation of peristaltic force. Patients with oesophagitis generated lower traction forces on swallowing 30 (20-40) g compared with the normal subjects (p<0-01), the degree of impairment being greatest in those patients with the most severe mucosal damage. Patients with gastro-oesophageal reflux without endoscopic oesophagitis also showed abnormal forces (32 22-38) g p<001 v controls), which were similar to those patients with mild oesophagitis but were greater than those with severe oesophagitis (p<005). In patients with functional dysphagia, forces were also impaired (28 (10-60) g p<005 v controls) despite normal standard manometry. Our results show that measurement of the traction force generated by prunary peristalsis provides information about oesophageal neuromuscular function that is not demonstrable by manometry alone and can be abnormal in patients with oesophageal symptoms in whom standard techniques are normal. (Gut 1994; 35: 165-171) studies usually show a close relation between the amplitude of an intraluminal pressure wave and efficiency of clearance, with luminal clearance
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