Pubovisceral muscle and anal sphincter defects in women with fecal or urinary incontinence after vaginal delivery.Tech Coloproctol. 2019 Feb; 23(2):117-128.TC
Vaginal delivery is the most frequent cause of direct anal sphincter trauma as well as pelvic floor muscle defects in women with corresponding signs and symptoms. The aim of the present study was to identify anatomical and functional abnormalities of the anal canal and pelvic floor in women who had had a vaginal delivery and determine the relationship between such abnormalities and the symptoms and severity of fecal incontinence (FI).
Consecutive female patients with symptoms of fecal and/or urinary incontinence were recruited through the colorectal and gynecological outpatient clinics at two large university hospitals and were eligible if they had had at a vaginal delivery. All women were assessed for symptoms FI by means of the Cleveland Clinic Florida Incontinence Scale (CCFIS) and for urinary incontinence symptoms, including the presence of complaints of any involuntary leakage of urine, leakage on exertion, sneezing, or coughing, and/or leaking or losing urine associated with an urge to urinate. All women underwent anorectal and endovaginal three-dimensional ultrasonography and anal manometry. The extent of the anal sphincter and PVM defects identified by ultrasound was scored from 1 to 6 based on the longitudinal involvement of the external and internal anal sphincter, the radial angle of the anterior external anal sphincter defect and the longitudinal involvement of the PVM.
There were 130 women and 89 (68%) had at least one defect of the anal sphincter or the pubovisceral muscle or both (42/32% had a pubovisceral muscle defect with or without sphincter defects, 47/36% women had an intact pubovisceral muscle but sphincter defect); and 41 (32%) had intact anal sphincter and pubovisceral muscles. The mean levator hiatus area at rest in women with anal sphincter and/or pubovisceral muscle defects was 18 (± 4 SD) which was significantly greater than in women with no defects (16 ± 3 SD; p = 0.01). Women with PVM defects had significantly higher ultrasound scores (median ultrasound score = 4/range 1-10 vs Intact = 2/range 2-5), indicating more extensive defects (p = 0.001). Bivariate analysis revealed a positive association (p < 0.05) between increasing FI symptom severity (CCFIS score) and women with PVM defects (ρ = 0.6913). Within the group of women with defects mean maximum anal squeeze pressure was significantly lower in women with PVM defect (mean 73 ± 34 SD mmHg vs mean 93 ± 38 SD; p = 0.04). Women with PVM defects had significantly higher median CCFIS scores (median score, 7/range 0-16) compared to women with intact PVM (4/range 0-10) (p < 0.001). There was a significant positive correlation between the CCFIS and ultrasound scores (ρ = 0.625; p < 0.001). Bivariate analysis revealed a negative correlations between the CCFIS score and the lengths of the anterior EAS (ρ = - 0.5621, p < 0.001), IAS (ρ = - 0.40, p < 0.001) and the area of the levator hiatus (ρ = 0.5211, p = 0.001). However, no significant correlations were observed between CCFIS scores and the gap measurement (ρ = 0.101; p = 0.253) or the resting (ρ = - 0.08, p = 0.54) or squeeze pressure (ρ = - 0.12; p = 0.34) values on anal manometry. The variables associated with worsening FI symptom severity (CCFIS score) that remained significant in multiple linear regression included the shorter lengths of the anterior EAS and/or the lengths of the anterior IAS and increased area of the levator hiatus.
The study data demonstrate that half of the women had combined defects of PVM and sphincter. There were correlations between anatomical abnormalities including the anal sphincter and/or pubovisceral muscle defects with decrease in the anal pressures and increased severity of FI.