BACKGROUND & AIMS: The pathophysiology of anal incontinence may be elusive using current parameters. Our aim was to establish the role of the levator ani in anal continence. METHODS: In 53 patients with anal incontinence, 30 with constipation as disease controls, and 15 healthy controls, we evaluated incontinence severity by a 0-12 scale, anorectal function by standard manometric tests, and levator ani contraction by a perineal dynamometer. RESULTS: Patients with incontinence exhibited various physiologic abnormalities (3.2 +/- 0.3 per patient), but multiple regression analysis showed that levator ani contraction was the independent variable with strongest relation to the severity of incontinence (R = -0.84; P < 0.0001), as well as a predictive factor of the response to treatment (R = 0.53; P < 0.01). Furthermore, in contrast to other physiologic parameters, clinical improvement in response to treatment (4.4 +/- 0.5 score vs. 7.9 +/- 0.5 score pre; P < 0.001) was associated with a marked and significant strengthening of levator ani contraction (448 +/- 47 g vs. 351 +/- 35 g pre; P < 0.05). CONCLUSIONS: We have shown the importance of levator ani failure in understanding the etiology of anal incontinence and in predicting response to treatment.
BACKGROUND & AIMS: The pathophysiology of anal incontinence may be elusive using current parameters. Our aim was to establish the role of the levator ani in anal continence. METHODS: In 53 patients with anal incontinence, 30 with constipation as disease controls, and 15 healthy controls, we evaluated incontinence severity by a 0-12 scale, anorectal function by standard manometric tests, and levator ani contraction by a perineal dynamometer. RESULTS:Patients with incontinence exhibited various physiologic abnormalities (3.2 +/- 0.3 per patient), but multiple regression analysis showed that levator ani contraction was the independent variable with strongest relation to the severity of incontinence (R = -0.84; P < 0.0001), as well as a predictive factor of the response to treatment (R = 0.53; P < 0.01). Furthermore, in contrast to other physiologic parameters, clinical improvement in response to treatment (4.4 +/- 0.5 score vs. 7.9 +/- 0.5 score pre; P < 0.001) was associated with a marked and significant strengthening of levator ani contraction (448 +/- 47 g vs. 351 +/- 35 g pre; P < 0.05). CONCLUSIONS: We have shown the importance of levator ani failure in understanding the etiology of anal incontinence and in predicting response to treatment.
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