Long-term results of postanal repair for neurogenic faecal incontinence.

Between 1984 and 1986, 54 patients underwent postanal repair for neurogenic faecal incontinence. Forty-two (41 women) were available for follow-up 5-8 (median 6.2) years after operation. Of these, 34 women attended for clinical and anorectal physiological assessment. Anal endosonography was also performed in 30 patients. In the 34 patients examined, continence categories (Browning and Parks' classification) of C (n = 12) and D (n = 22) before surgery became A (n = 2), B (n = 12), C (n = 16) and D (n = 1) at 6 months and A (n = 4), B (n = 5), C (n = 21) and D (n = 4) at 5-8 years. Nine patients therefore had continence for solids and liquids, five of whom were incontinent to flatus, in the long term. Assessment of outcome by patients revealed long-term improvement in 28 and no change in six. Two of the 34 patients assessed were housebound because of incontinence. Of the total of 54 patients, only one required a stoma. The length of the anal canal increased significantly from a preoperative median (range) of 2.0 (1.5-4.0) cm to 3.8 (1.8-5.5) cm 5-8 years after surgery. Perineal descent at rest decreased markedly. Progression of neuromuscular damage was demonstrated by prolongation of the pudendal nerve terminal motor latency from a median (range) 2.38 (1.80-3.35) ms to 2.80 (2.20-4.25) ms and increasing median (range) fibre density in the external sphincter, from 1.86 (1.76-2.40) to 3.63 (2.03-6.20). The pudendal nerve terminal latency was the only preoperative physiological variable that correlated significantly with long-term outcome (A and B 2.20 ms versus C and D 2.65 ms, P < 0.05). At long-term assessment, maximal anal squeeze pressure was the only physiological variable that correlated significantly with clinical outcome. Anal endosonography revealed a clinically undetected sphincter defect in 19 of 30 patients examined but the presence of a defect did not relate to clinical outcome.