Shek, Ka Lai MBBS, FRCOG; Dietz, Hans P. MD, PhD
The physiological processes of pregnancy and parturition must involve dramatic adaptations to the vagina and pelvic floor to allow marked distension at delivery and to return to a near prepregnant state after parturition. The recovery process, however, may not be complete. Vaginal parity has been identified as an important risk factor for pelvic organ prolapse.1–3 Incomplete recovery in anatomy and function may follow macroscopic trauma to the pelvic floor muscle. Recent studies using magnetic resonance imaging and ultrasonography have found levator trauma (avulsion injury) in 15–30% of parous women who delivered vaginally.4–8 Levator avulsion is a risk factor for ballooning (ie, an abnormal hiatal area on Valsalva of 25 cm2 or above)9,10 and is associated with a decrease in pelvic floor muscle strength.9,11,12 It is a risk factor for pelvic organ prolapse, especially in the anterior and central compartments, with a relative risk of 2.3 to 4.0, respectively.8,12 Alterations in levator biometry and function after avulsion also may increase the risk of prolapse recurrence after surgical repair.13,14 However, other mechanisms and factors also may play a role. The levator hiatus, defined by the puborectalis/pubococcygeus muscle and pubic bone, is the largest potential hernial portal in the human body. It is conceivable that enlargement of the hiatus, even without gross muscle trauma, may lead to pelvic organ prolapse and may be an alternative mechanism in the pathogenesis of this common gynecologic problem. In fact, significant correlations have been shown between hiatal area, a measure of the size of this potential hernial portal, and pelvic organ descent.15 Recent studies have found that the distension required for vaginal delivery varies enormously from one individual to another.16 It is therefore plausible that, apart from macroscopic avulsion injury, other forms of muscle damage (ie, microtrauma or traumatic overdistension) may lead to changes in levator hiatal biometry and ultimately pelvic organ prolapse. The aim of this study was to estimate changes in levator hiatal dimensions after childbirth in women with and without ultrasonographically visible morphological abnormalities of the levator ani and to correlate those changes with delivery mode.
MATERIALS AND METHODS
A total of 296 nulliparous women were recruited from the antenatal clinic of a tertiary care hospital from May 2005 to February 2007. The inclusion criteria were: 1) singleton pregnancy, 2) between 34 and 36 weeks of gestation, 3) at least 18 years of age, 4) no previous pregnancies of more than 20 weeks of gestation. An invitation letter was sent, and all potential participants were contacted by phone about a week later. An appointment was arranged at around 36–38 weeks of gestation for those interested in participating. All participants were contacted again by phone about 3 months after the estimated delivery date and were reinvited to attend for a second assessment.
Written consent was obtained at the first appointment. All women underwent an interview and four-dimensional translabial ultrasound examination in the supine position after bladder emptying using a GE Voluson 730 Expert system (GE Medical Systems, Zipf, Austria) with 8–4 MHz curved array volume transducer (acquisition angle 85°) as described previously.17 Volume acquisition was performed at rest, on maximum Valsalva maneuver, and on maximum pelvic floor muscle contraction. At least three Valsalva maneuvers were performed for each patient. The volume data of the best Valsalva maneuver (ie, the Valsalva resulting in the greatest degree of pelvic organ descent) was used for analysis. This assessment was repeated at the postpartum appointment, at which time the assessor was blinded to all delivery data, with the patient’s abdomen covered by a sheet. Women were asked not to divulge any information regarding their deliveries until after the assessment. Data analysis was performed on a desktop PC using the proprietary software 4D Sonoview 5.0 (GE Medical Ultrasound Kretz GmbH, Zipf, Austria) several months after the ultrasound assessment. Analysis was blinded to patient data. Hiatal diameter, circumference, and area were measured at the plane of minimal hiatal dimension as defined in the midsagittal plane,15 evident as the minimal distance between the hyperechogenic posterior aspect of the symphysis pubis and the hyperechogenic anterior border of the levator ani muscle just posterior to the anorectal muscularis (represented by the single oblique line in Fig. 1). With the GE Kretz 4D View software package used for three-dimensional analysis, this plane is defined in the midsagittal orthogonal plane, which then allows representation of exactly this cross-section of the volume in the axial plane for measurement of hiatal dimensions. Our method of obtaining hiatal dimensions has been published previously,15 and its reproducibility has been confirmed by others.18,19
To determine muscle strain, a component of elasticity, we also measured the bony arc length (the nonelastic part of the hiatal circumference). This was subtracted from the hiatal circumference to obtain the muscular component of the levator hiatus. Muscle strain on maximum Valsalva and during levator contraction was calculated as a change in muscle length relative to the resting state as previously described.20
Levator avulsion was diagnosed whenever a discontinuity was detected between the inferior pubic ramus and the puborectalis muscle on tomographic ultrasound imaging. The detection of levator defects by three-dimensional/four-dimensional pelvic floor ultrasonography has been shown previously to be highly reproducible.7
Delivery and postdelivery data were collected from the hospital database or patients’ records or both. The study was performed in the context of a larger parent study investigating predictors of delivery mode. The parent study was approved by the Sydney West Area Health Service Human Research Ethics Committee (SWAHS HREC 05/004).
Statistics were performed using Minitab 13 (Minitab, State College, PA) and SPSS 16 (SPSS, Chicago, IL) for PC. Normality was assessed visually and checked using the Kolmogorov-Smirnov method. Because this was a substudy within the above-mentioned parent project, we did not perform power calculations specific to the research question addressed in this article. All data except the length of second stage and follow-up interval were distributed normally. Paired t tests were used to compare predelivery and postdelivery changes for normally distributed data. General linear models were used to control for follow-up interval between patient-group comparisons. χ2 tests were used for categorical variables. Pearson’s correlation was used to quantify the association between change in minimal hiatal area on Valsalva with birth weight. Spearman’s correlation was used to quantify the association between change in minimal hiatal area and length of second stage. A P<.05 was considered statistically significant.
Mean maternal age at the time of first assessment was 25.8 years (range 17.7 to 40, standard deviation 5.16). Mean body mass index was 30.7 (range 19.2 to 52.3, standard deviation 5.65). Ninety-one women gave a history of a miscarriage or termination. The median maximum gestation of miscarriage or termination was 8 weeks (range 4 to 20 weeks). Of 296 women seen antepartum at a mean gestation of 37.1 weeks, 212 (71.6%) returned for a postnatal assessment (attenders). Sixty-eight of them were breastfeeding (32%). The demographics of attenders and women who did not return for the postnatal assessment (nonattenders) are shown in Table 1. Nonattenders were, on average, 2.6 years younger (P<.001) but did not differ in other demographics.
The mean follow-up interval was 5.3 months (median 4.1, interquartile range 3.7 to 5.1). Of 212 women, 101 (48%) had normal vaginal deliveries, 31 had vacuum or forceps (15%), and 80 had cesarean deliveries (38%). The postpartum data of five women (four after normal vaginal delivery, one after cesarean delivery) were excluded from analysis owing to intercurrent pregnancy. The demographics, by delivery group, of nonpregnant attenders are shown in Table 2. Three ultrasound datasets were corrupted and not available for analysis. Two women were not able to perform a Valsalva maneuver, and four failed to contract the pelvic floor muscle. One volume on pelvic floor muscle contraction could not be assessed because of inadequate acquisition, leaving 204, 202, and 199 complete sets of antepartum and postpartum data for analysis of minimal hiatal area at rest, on Valsalva, and on pelvic floor muscle contraction, respectively.
No significant relationship was found between breastfeeding and change in hiatal area (all P≥.64). Analysis of variance was used to compare delivery mode after controlling for follow-up interval. The changes in the three different measures of hiatal area were all different between patient groups (all P≤.006) (see Table 3). Minimal hiatal area on Valsalva decreased after cesarean delivery but increased after vaginal delivery. Prelabor and first-stage cesarean delivery led to a mean reduction in the minimal hiatal area on Valsalva by 1.96 and 2.22 cm2, respectively. A lesser reduction of 0.89 cm2 was noted after second-stage cesarean delivery. Vacuum and forceps delivery conferred a greater change than did normal vaginal delivery. Minimal hiatal area at rest and on pelvic floor muscle contraction showed similar trends.
Levator avulsion was diagnosed in 24 women (normal vaginal delivery 17/97, 18%; vacuum delivery 3/21, 14%; forceps 4/10, 40%). The mean age of women with and without avulsion after vaginal delivery was 25.5 years for both. No avulsion was diagnosed in the cesarean delivery group. A significant increase in the minimal hiatal area on Valsalva of approximately 6% from 21.31 to 22.61 cm2 was found in women after normal vaginal delivery (P=.035). In women diagnosed with an avulsion, there was a marked increase in the minimal hiatal area on Valsalva of approximately 28% from 19.90 to 25.46 cm2 (P=.002) (see Table 4). After cesarean delivery, there was a significant reduction in minimal hiatal area on Valsalva of about 8.5% from 20.91 to 19.13 cm2 (P=.005) (see Table 4). In cases with avulsion, hiatal area on pelvic floor muscle contraction also increased significantly by 30% from 11.63 to 15.11 cm2 (P<.001) (see Table 5), and strain on pelvic floor muscle contraction was reduced by 57% (P=.003), suggesting a decrease in contractility.
In women with vaginal birth, a significant correlation was found between an increase in the minimal hiatal area on Valsalva and length of second stage (P=.015 Spearman’s correlation, r=0.219) but not with birth weight (P=.99, Pearson’s correlation).
Figure 2 shows measurements of minimal hiatal area on Valsalva before and after a forceps delivery in a woman with left-sided avulsion.
There is a general lack of data regarding the etiology of female pelvic organ prolapse, with widespread disagreement regarding the role of a multitude of potential causative factors.21 As a result, no effective preventive strategies or treatment for genital prolapse have been devised to date, and treatment is empirical. In the United States alone, approximately 200,000 women undergo inpatient procedures for prolapse each year.22 Recent estimates suggest that the demand for prolapse surgery will increase by 45% in the next 30 years.23 There is a clear need for research into the etiology and pathophysiology of this condition. Although the pathogenesis of prolapse is likely multifactorial, its association with vaginal childbirth is well established.1–3 Current evidence suggests that avulsion injury of the levator ani muscle from the inferior pubic ramus is likely to be at least part of the missing link between childbirth and prolapse.5,7,12 Other mechanisms such as denervation/reinnervation, connective tissue remodeling, and damage to fascia may play a role in some individuals. During vaginal delivery, the pelvic floor is distended markedly by the fetal head, which potentially may lead to functional and anatomical changes in the muscles, nerves, and connective tissue of the pelvic floor.
In this study, levator avulsion was diagnosed in 19% (24/128) of parous woman who had delivered vaginally, which agrees with data in the literature.4–8 Of those with avulsion, seven women had had an operative delivery and 17 a normal vaginal delivery. The mean age of women with and without an avulsion was 25.5 years for both. Neither the mode of vaginal delivery (P=.53) nor maternal age at birth was associated significantly with avulsion (P=.85). This disagrees with findings in the literature and with our own data showing that maternal age and instrumental delivery are risk factors for avulsion.6,8,12,24 These discrepancies may be due to the small number of women with avulsion and the young population group in our series. Reduction in muscle strain on pelvic floor muscle contraction confirms findings in previous studies that avulsion is associated with a decrease in muscle function.9,11,12
Minimal hiatal area on Valsalva increased by an average of 6% and 28%, respectively, in women with and without levator avulsion after vaginal delivery. After cesarean delivery, the minimal hiatal area on Valsalva was reduced by more than 8%. This reduction may reflect reversible hormonal or mechanical effects or both of pregnancy on the pelvic floor. Comparing women who have not delivered vaginally with those who did, the actual increment in hiatal size attributable to vaginal delivery is about 18% (22.61 compared with 19.13 cm2) for women without avulsion and 33% (25.46 compared with 19.13 cm2) on average for those with avulsion.
In a study using transvaginal three-dimensional ultrasonography, Toozs-Hobson et al found that hiatal area increased at 6 weeks (15%) and 6 months postpartum (6%) after vaginal delivery compared with the third trimester, which largely agrees with our findings.25 Although it is difficult to compare results owing to different methodologies, it is remarkable that the Toosz- Hobson study also shows a reduction in hiatal area after cesarean delivery (7% at 6 weeks, 5.7% at 6 months).
The size of the levator hiatus (on imaging) or urogenital hiatus (on clinical examination) has been found to be associated with pelvic organ descent in both healthy, nulliparous individuals15 and in patients with pelvic organ prolapse.26 An increase in hiatal size may impair pelvic organ support—independent of trauma—and therefore contribute to prolapse development. It is plausible that traumatic overdistension or microtrauma of the levator ani muscle leading to a change in levator biometry may represent an alternative mechanism leading to genital prolapse. Further studies will be required to clarify the relative role of avulsion (macrotrauma) and traumatic overdistension (microtrauma) in the etiology of female pelvic organ prolapse.
The issue of pregnancy-related effects on pelvic floor function is particularly intriguing. Although we do not have prepregnancy data to allow any insight into the effect of pregnancy on hiatal size and pelvic organ support, it is interesting to note that mean hiatal area on Valsalva at 36–38 weeks of gestation in our series was 20.7 cm2 compared with 14 cm2 in studies on nonpregnant, nulliparous women.15,19 This difference may reflect an alteration in pelvic floor biomechanics attributable to pregnancy. In the rat, mean linear stiffness (ability to resist distension) of the vagina and supportive tissues decreases in pregnancy. Four weeks after vaginal delivery, all biomechanical characteristics returned to at least virgin values.27 These findings suggest maternal tissue adaptation in preparation for mammalian parturition, and such an effect could explain the discrepancy between data obtained in pregnant and nonpregnant nulliparous women. Future studies should elucidate the effect of pregnancy on the pelvic floor by assessing women before, during, and after pregnancy.
Several shortcomings of this study have to be recognized. Our follow-up return rate was only 71%, representing the particular characteristics of our study population, such as age, socioeconomic status, and mobility. However, Table 1 demonstrates that the 71% seen by us are largely representative of the study population. Furthermore, timing of follow-up varied widely, again owing to problems with recall. Also, as mentioned before, this study does not allow any insight into the role of pregnancy itself as opposed to childbirth. Despite those weaknesses, however, our study clearly had sufficient power to address the effect of childbirth on hiatal dimensions.
In summary, we found that vaginal childbirth increases levator hiatal dimensions, especially in women who suffered an avulsion injury of the levator ani muscle. Hiatal area decreased after cesarean delivery compared with data obtained in the late third trimester. Levator avulsion was associated with a more than 25% increase in hiatal area on Valsalva and on pelvic floor muscle contraction, compared with a 6–7% increase in hiatal area in women after vaginal delivery without avulsion. Hence, in addition to avulsion injury, traumatic overdistension of the levator ani muscle may be another factor in the pathogenesis of female pelvic organ prolapse.
1. Mant J, Painter R, Vessey M. Epidemiology of genital prolapse: observations from the Oxford Family Planning Association Study. Br J Obstet Gynaecol 1997;104:579–85.
2. Hendrix SL, Clark A, Nygaard I, Aragaki A, Barnabei V, McTiernan A. Pelvic organ prolapse in the Women’s Health Initiative: gravity and gravidity. Am J Obstet Gynecol 2002;186:1160–6.
3. Swift S, Woodman P, O’Boyle A, Kahn M, Valley M, Bland D, et al. Pelvic Organ Support Study (POSST): the distribution, clinical definition, and epidemiologic condition of pelvic organ support defects. Am J Obstet Gynecol 2005;192:795–806.
4. DeLancey JO, Kearney R, Chou Q, Speights S, Binno S. The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol 2003;101:46–53.
5. Dietz HP, Simpson JM. Levator trauma is associated with pelvic organ prolapse. BJOG 2008;115:979–84.
6. Dietz HP, Lanzarone V. Levator trauma after vaginal delivery. Obstet Gynecol 2005;106:707–12.
7. Dietz HP, Steensma AB. The prevalence of major abnormalities of the levator ani in urogynaecological patients. BJOG 2006;113:225–30.
8. Dietz HP, Simpson JM. Does delayed child-bearing increase the risk of levator injury in labour? Aust N Z J Obstet Gynaecol 2007;47:491–5.
9. Abdool Z, Shek C, Dietz HP. The effect of levator avulsion on hiatal dimensions and function. Am J Obstet Gynecol 2009 in press.
10. Dietz HP, Shek C, De Leon J, Steensma AB. Ballooning of the levator hiatus. Ultrasound Obstet Gynecol 2008;31:676–80.
11. Dietz HP, Shek C. Levator avulsion and grading of pelvic floor muscle strength. Int Urogynecol J Plevic Floor Dysfunct 2008;19:633–6.
12. DeLancey JO, Morgan DM, Fenner DE, Kearney R, Guire K, Miller JM, et al. Comparison of levator ani muscle defects and function in women with and without pelvic organ prolapse. Obstet Gynecol 2007;109:295–302.
13. Vakili B, Zheng YT, Loesch H, Echols KT, Franco N, Chesson RR. Levator contraction strength and genital hiatus as risk factors for recurrent pelvic organ prolapse. Am J Obstet Gynecol 2005;192:1592–8.
14. Adekanmi OA, Freeman RM, Puckett M, Jackson S. Cystoceles: does anterior repair fail because we fail to correct the fascial defects? A clinical and radiological study. Int Urogynecol J 2005;16:S73.
15. Dietz HP, Shek C, Clarke B. Biometry of the pubovisceral muscle and levator hiatus by three-dimensional pelvic floor ultrasound. Ultrasound Obstet Gynecol 2005;25:580–5.
16. Svabik K, Shek KL, Dietz HP. How much does the puborectalis muscle have to stretch during childbirth? Neurourol Urodyn 2008;27:667–8.
17. Dietz HP. Ultrasound imaging of the pelvic floor. Part II: three-dimensional or volume imaging. Ultrasound Obstet Gynecol 2004;23:615–25.
18. Yang JM, Yang SH, Huang WC. Biometry of the pubovisceral muscle and levator hiatus in nulliparous Chinese women. Ultrasound Obstet Gynecol 2006;28:710–6.
19. Kruger JA, Dietz HP, Murphy BA. Pelvic floor function in elite nulliparous athletes. Ultrasound Obstet Gynecol 2007;30:81–5.
20. Thyer I, Shek C, Dietz HP. New imaging method for assessing pelvic floor biomechanics. Ultrasound Obstet Gynecol 2008;31:201–5.
21. Dietz HP. The aetiology of prolapse. Int Urogynecol J Pelvic Floor Dysfunct 2008;19:1323–29.
22. Boyles SH, Weber AM, Meyn L. Procedures for pelvic organ prolapse in the United States, 1979–1997. Am J Obstet Gynecol 2003;188:108-15.
23. Luber KM, Boero S, Choe JY. The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol 2001;184:1496–501.
24. Krofta L, Kasikova E, Otcenasek M, Feyereisl J. Pubococcygeus-puborectalis trauma after instrumental delivery: the use of 4D ultrasound in the evaluation of levator ani muscle. Ultrasound Obstet Gynecol 2007;30:446.
25. Toozs-Hobson P, Balmforth J, Cardozo L, Khullar V, Athanasiou S. The effect of mode of delivery on pelvic floor functional anatomy. Int Urogynecol J Pelvic Floor Dysfunct 2008;19:407–16.
26. DeLancey JO, Hurd WW. Size of the urogenital hiatus in the levator ani muscles in normal women and women with pelvic organ prolapse. Obstet Gynecol 1998;91:364–8.
27. Lowder JL, Debes KM, Moon DK, Howden N, Abramowitch SD, Moalli PA. Biomechanical adaptations of the rat vagina and supportive tissues in pregnancy to accommodate delivery. Obstet Gynecol 2007;109:136–43.
© 2009 by The American College of Obstetricians and Gynecologists.