Objective
The purpose of this study was to determine the effect of levator defects on perineal position and movement irrespective of prolapse status.
Study Design
Forty women from an ongoing study were divided into 2 groups of 20 women with and without severe levator defects. Prolapse status was matched between groups, with 50% of the women having stage III or greater anterior wall prolapse. Perineal structure locations were measured against standard axes on magnetic resonance scans at rest, maximum contraction (Kegel), and maximum Valsalva maneuver. Differences in location were calculated and compared.
Results
In women with levator defects, independently of prolapse status: (1) At rest, the perineal body was 1.3 cm, and the anal sphincter was 1.0 cm more caudal ( P ≤ .01); at maximum contraction, the perineal body and the anal sphincter were both 1.2 cm more caudal ( P ≤ .01); with maximum Valsalva maneuver, the perineal body was 1.3 cm more caudal, and the anal sphincter was 1.2 cm more caudal ( P ≤ .01). (2) At rest, the levator hiatus was 0.8 cm larger, and the urogenital hiatus was 1.0 cm larger ( P ≤ .01). (3) At rest, the bladder was 0.07 cm more posterior ( P ≤ .02); with maximum contraction, it was 1.9 cm lower ( P ≤ .02). (4) With maximum Valsalva maneuver, the bladder was 1.5 cm lower and displaced further caudally ( P ≤ .03).
Conclusion
When we controlled for prolapse, the women with levator defects had a more caudal location of their perineal structures and larger hiatuses at rest, maximum contraction, and maximum Valsalva maneuver.
Pelvic organ prolapse is a remarkably common and distressing condition that symptomatically affects 3% of the population and requires approximately 200,000 inpatient surgeries annually. Damage to the levator ani muscles is associated with pelvic organ prolapse, and has been documented on dissection and with radiography. Recent magnetic resonance (MR) and ultrasound studies have shown that levator ani muscle damage is a clinically important factor that is associated with pelvic organ prolapse. It has likewise been shown that patients with prolapse have enlarged genital hiatuses.
Biomechanical studies have long indicated the importance of levator function in the maintenance of pelvic organ support by closing the levator hiatus (LH) and reducing tension on the ligamentous support. Clinically, this is relevant because women with enlarged hiatus and reduced levator function are more likely to experience prolapse recurrence.
This enlarged hiatus could be either the cause or the result of prolapse. Evident damage and weakening of the levator ani muscle, as seen in prolapse, might result in the inability of the muscle to hold the hiatus closed. On the other hand, the presence of a prolapse that distends the hiatus might stretch tissues, making the hiatus larger. Insight into the difference between cause and effect might be gained from a comparison of hiatus size between women with and without defects, who all have similar degrees of prolapse. If the hiatal enlargement is exclusively due to levator damage, then only 1 group (those with levator ani damage) would be expected to have enlargement. If the enlargement is the result of prolapse, then both groups would have equal degrees of hiatal enlargement. This study compares measures of hiatus dimensions and perineal position while stratifying for prolapse occurrence and size to isolate the effect of levator ani muscle damage separately from the presence or absence of prolapse.
Materials and Methods
Dynamic MR imaging studies were obtained from an ongoing institutional review board–approved study of pelvic organ support. The parent study recruited women with pelvic organ prolapse in whom at least 1 vaginal wall (anterior, posterior, or apical) point or the cervix was ≥1 cm beyond the hymen. Women with normal support in whom all vaginal points were ≥1 cm above the hymen and who were of similar age, parity, and race were recruited. Patients were excluded if they had previous surgery for prolapse or pelvic floor dysfunction, had any findings that would distort pelvic anatomy (such as a pelvic mass or history of pelvic radiation), or were unable to complete the clinic examination or MR imaging study. Women who had undergone hysterectomy were eligible if the surgery had been done at least 1 year before enrollment and if the indication for surgery did not include pelvic floor dysfunction (eg, pelvic organ prolapse, urinary incontinence, or fecal incontinence).
From the parent study, we compared 20 women with severe levator ani defects (a muscle defect severity score of 5 or 6) with 20 women with normal levator ani muscles (no-defect group). Levator ani muscle damage was assessed with a scale for each side of the muscle from 0 (no defect) to 3 (complete muscle loss) that resulted in a total score from 0-6 when both sides are added, as outlined in Morgan et al. We chose scores of 5 or 6 to represent individuals with severe injury and to include sufficient numbers of women with normal support. Each case and control group for levator injury status was selected to have equal numbers of participants with and without prolapse. The limiting factor to both subject selection and study size was the number of scanned participants who had severe levator ani defects who did not have pelvic organ prolapse. There were only 10 such women available in our database who had normal pelvic organ support.
For the purposes of this analysis, cases of prolapse were defined clinically as women in whom the anterior wall of the vagina extended at least 1 cm below the hymen during straining and who previously had not had surgery for prolapse or incontinence. We have used a definition of prolapse based on findings in a population-based sample of normal women that was used to define a normal range, with a vaginal wall at the level of the hymen as the dividing line to indicate the end of the normal range. This is also the point at which women begin to have prolapse symptoms (feeling of a bulge). The pelvic organ prolapse quantitative method use of the term prolapse for stage 1 support is not based on either a normal range or the occurrence of symptoms; therefore, we have chosen not to use it. Subjects were those women who had a stage III or IV prolapse, which is clinically significant prolapse, as discussed by Trowbridge et al. Control subjects were asymptomatic women in whom no wall reached the hymen during straining and who had not had previous surgery for prolapse or incontinence.
Scans were selected in the following way: The limiting factor to both subject selection and study size was the number of women with normal support who had severe levator ani defects. Ten women were available. Scans for the other case and control groups were selected sequentially to be matched for age, prolapse type and severity, vaginal parity, body mass index, and hysterectomy status. Subjects were excluded for whom the MR scans were not of adequate quality because of motion artifact, parasagittal location of the scan plane, or the maneuvers were not performed properly such that the subject did not perform pelvic muscle contraction or Valsalva as instructed, despite extensive coaching.
MR imaging protocol and technique was completed as described by Hsu et al. In brief, imaging was performed on a 1.5 Tesla system (Signa; General Electric, Milwaukee, WI) with a 4-channel torso phased array coil with the subject in the supine position. The field of view was 30 or 36 cm, depending on subject size and weight. Subjects were coached extensively and instructed to perform a maximum contraction (C max ) and maximum Valsalva (V max ). This work deviated from the work of Hsu et al in that additional scans were analyzed with the C max variable. In this acquisition, the operator instructed the subject to hold her breath as the scan was initiated; after 5 seconds of imaging at rest, the subject was asked to contract minimally for 5 seconds, moderately for 5 seconds, maximally for 5 seconds, and then to breathe normally for 5 seconds before ending the acquisition.
All midline sagittal images were analyzed by the same expert examiner, who was blinded to levator damage and prolapse status. Analysis began with the placement of a sacrococcygeal inferior pubic point (SCIPP) line–based x and y axis to nullify for the effects of pelvic rotation in the MR scanner ( Figure 1 ). The x axis consisted of the SCIPP line, which was drawn from the inferior portion of the pubic bone to sacrococcygeal joint. A y axis was drawn perpendicularly to this line at the level of the pubic bone. Movement differences were assessed in both the y direction and the x direction with the distance in millimeters for each axis. The perineal body point was marked in the region of the perineal skin immediately anterior to the external anal sphincter. A bladder point was placed at the lowest visible point at the intersection the bladder neck and urethra. A point was also placed in the external anal sphincter muscle at the most inferomedial point ( Figure 1 ). Measures were taken at rest, with contraction (Kegel), and with Valsalva ( Figure 2 ). Point movements are noted not as vectors, but as differences in either the x or the y coordinates between different point locations. Next, a point was placed behind the anterior apex of the LH, and a line was drawn to the inferior portion of the pubic bone as a measurement of LH length. A line was also drawn from the inferior pubic point to the perineal body as a measurement of the urogenital hiatus (UGH) length. Inter- and intrarater reliability of point placement and measurement were established during data collection. Recent information has been published on the reproducibility of these measures, most notably by Hsu et al.
The locations of different anatomic landmarks were defined by establishing the (x,y) coordinate relative to the established axes. Distances between points were determined with the following formula:
d = ( x 2 − x 1 ) 2 + ( y 2 − y 1 ) 2
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