Does vaginal closure force differ in the supine
and standing positions?
Daniel M. Morgan, MD,a,
* Gurpreet Kaur, BS,a
Yvonne Hsu, MD,a
Dee E. Fenner, MD,a
Kenneth Guire, MS,a
Janis Miller, PhD,b
James A. Ashton-Miller, PhD,c
John O. L. Delancey, MDa
Department of Obstetrics and Gynecology, Pelvic Floor Research Group,aSchool of Nursing,bDepartments of Mechanical Engineering and Biomechanical Engineering, and Institute of Gerontology,cUniversity of Michigan Medical School, Ann Arbor, Mich
Pelvic floor Posture Levator ani
Vaginal closure force
Objective: This study was undertaken to quantify resting vaginal closure force (VCFREST), maximum vaginal closure force (VCFMAX), and augmentation of vaginal closure force augmentation (VCFAUG) when supine and standing and to determine whether the change in intra-abdominal pressure associated with change in posture accounts for differences in VCF.
Study design: Thirty-nine asymptomatic, continent women were recruited to determine, when supine and standing, the vaginal closure force (eg, the force closing the vagina in the mid-sagittal plane) and bladder pressures at rest and at maximal voluntary contraction. VCF was measured with an instrumented vaginal speculum and bladder pressure was determined with a microtip catheter. VCFRESTwas the resting pelvic floor tone, and VCFMAXwas the peak pelvic floor force during a maximal voluntary contraction. VCFAUG was the difference between VCFMAX and VCFREST.Ttests and Pearson correlation coefficients were used for analysis.
Results: VCFRESTwhen supine was 3.6G0.8 N and when standing was 6.9G1.5 Nda 92%
difference (P!.001). The VCFMAXwhen supine was 7.5
G2.9 N and when standing was 10.1G
2.4 Nda 35% difference (P!.001). Bladder pressure when supine (10.5G4.7 cm H2O) was
significantly less (P!.001) than when standing (31.0G6.4 cm H2O). The differences in bladder
pressure when either supine or standing did not correlate with the corresponding differences in VCF at rest or at maximal voluntary contraction. The supine VCFAUG of 3.9 G 2.7 N, was
significantly greater than the standing VCFAUGof 3.3G1.9 N.
Conclusion: With change in posture, vaginal closure force increases because of higher intra-abdominal pressure and greater resistance in the pelvic floor muscles.
Ó2005 Elsevier Inc. All rights reserved.
Stress urinary incontinence and pelvic organ prolapse can be highly morbid conditions with a signiﬁcant impact on quality of life. The pathophysiology of symptomatic disease is not well understood, but the upright posture of humans is generally considered a contributing factor. The pelvic ﬂoor soft tissues close the genital hiatus (GH), support the pelvic viscera, and play an important role in bladder and bowel continence.
Support by the National Institutes of Health grant NICHD R01 HD 38665, P50 HD44406, R01HD38665-05.
Presented at the Joint Scientiﬁc Meeting of the Society of Gynecologic Surgeons and the American Urogynecologic Society, San Diego, Calif, July 29-31, 2004.
* Reprint requests: Daniel M Morgan, MD, University of Mich-igan, Department of Obstetrics and Gynecology, Women’s Hospital L4000, 1500 East Medical Center Dr, Ann Arbor, MI 48109.
0002-9378/$ - see front matterÓ2005 Elsevier Inc. All rights reserved. doi:10.1016/j.ajog.2004.11.050
The levator ani muscles, which are an important com-ponent of this soft tissue, exhibit constant activity1,2and have evolved to meet the increased support needed with upright posture. To visualize the perineum and vagina optimally, examinations are usually performed with patients in lithotomy position. Although this approach is understandable, it may not adequately reﬂect the physiologic function of the pelvic ﬂoor soft tissues.
Vaginal closure force (VCF), which is that force exerted by the pelvic ﬂoor soft tissues to close the vaginal opening, can be quantiﬁed using an instru-mented speculum.3-5 In previous work, our research group has shown that the VCF is correlated with levator ani muscle damage seen on magnetic resonance imaging scans.6 The relationship between posture and vaginal closure pressures has been studied by other investigators who used a balloon device,7,8 but with this methodol-ogy, it has not been possible to diﬀerentiate intra-abdominal from vaginal pressure. The objectives of this study were to determine posture-related diﬀerences in resting vaginal closure force (VCFREST), maximum vaginal closure force (VCFMAX), and augmentation of vaginal closure force (VCFAUG)and to explore whether the change in intra-abdominal pressure is related to diﬀerences in VCF.
Recruitment and protocol
A convenience sample of 39 asymptomatic, continent women was recruited through 3 Institutional Review Board–approved projects. Information on age, body mass index (BMI), and obstetric history were collected. A pelvic examination, a cystometrogram, and a full bladder stress test were performed. GH was measured from the mid-urethra to perineal body. Women were excluded if the vaginal wall descended below the hymen with valsalva or if they experienced inconti-nence caused by a detrusor contraction, a cough, or a valsalva eﬀort.
An 8F micro-tip dual sensor (Gaeltec Ltd, Isle of Skye, Scotland) was placed in the bladder to monitor pressure during ﬁlling with 300 mL of normal saline solution and was used throughout testing as a surrogate for intra-abdominal pressure. The subject was instructed in pelvic ﬂoor muscle contraction until satisfactory performance of a contraction was demonstrable. The upward motion of the perineum and vaginal palpation of the levator ani muscle were used by the examiner to conﬁrm proper technique. If pelvic ﬂoor muscle con-traction caused the bladder pressure to rise above its baseline, patients were reinstructed on technique and advised to avoid use of the abdominal and gluteal muscles.
An instrumented vaginal speculum (Figure 1) was used to measure VCF in newtons. Similar to a stan-dard speculum with respect to size and shape, the 2-billed instrumented vaginal speculum is equipped at the handle with a strain gauge that sums the forces on the anterior and posterior bills. VCF was measured at rest (VCFREST) and during maximum voluntary con-traction (VCFMAX). Augmentation of VCF (VCFAUG) was the diﬀerence of VCFMAX and VCFREST (Figure 2). The subject voluntarily contracted the pelvic ﬂoor muscles 3 times when supine and when standing. A trial was repeated if intravesical pressure increased and if it seemed that an improvement in technique was possible. Values are expressed as the mean and SD.
Two-sided pairedttests were performed to compare the means of VCF and bladder pressure when supine and standing. Pearson correlation coeﬃcients were used to evaluate the relationship of age, BMI, parity, most dependent point of vaginal wall support, and GH with VCFREST, VCFMAX, and VCFAUG when supine and standing. A level ofP!.05 was considered signiﬁcant.
Mean age (GSD) was 45.8G9.5 years, BMI 28.7G4.9
kg/m2, and parity 2.2G1.3. Mean GH was 2.7 G0.8
cm. Thirty-two women had delivered by vaginal delivery only, 3 women had delivered by cesarean section only, and 3 women had delivered by both vaginal and cesarean delivery. One woman was nulliparous. There Figure 1 Photograph of speculums. The instrumented vagi-nal speculum (top) and a standard vaginal speculum are shown. The depth of insertion was 7 cm, similar to a standard speculum, and the cross-sectional area of the anterior bill was 18.8 cm2.
was a trend, which was not statistically signiﬁcant, between increasing parity and GH.
VCFs and bladder pressures
Standing VCFREST was 92% greater than supine VCFREST and standing VCFMAX was 35% greater than supine VCFMAX (Table and Figure 3). Bladder pressure when standing (31.0 G 6.4 cm H2O) was signiﬁcantly greater (P! .001) than when supine (10.5
G 4.7 cm H2O). The diﬀerence in resting bladder pressure when standing and supine did not correlate with the corresponding diﬀerence in VCF (r= 0.1, P= .58, Figure 4). The diﬀerence in bladder pressure at maximal voluntary contraction when supine and standing also did not correlate with the corresponding diﬀerence in VCF (r= 0.01, P= 0.93). The mean diﬀerence in bladder pressure during a voluntary pelvic ﬂoor muscle contraction was 1.7G 2.5 cm H2O when supine and 7.5G5.1 cm H2O when standing.Figure 5 illustrates that almost all subjects when standing had more diﬃculty contracting the pelvic ﬂoor muscles without a concomitant increase in intra-abdominal
pressure. VCFAUG when supine was 18% greater (P= .009) than when standing (Table).
Factors possibly influencing VCF
Factors that could inﬂuence VCF were evaluated. Supine VCFREST was inversely correlated with genital hiatus (r= –0.36, P= .02) but not with age, BMI, parity, or most dependent point of vaginal wall support. Standing VCFRESTwas positively correlated with BMI (r= 0.36, P= .02) but not with age, parity, most dependent point of vaginal wall support, or GH. There were no statistically signiﬁcant correlations between supine VCFMAX, standing VCFMAX, supine VCFAUG, or standing VCFAUG and age, BMI, parity, most dependent point of vaginal wall support, or GH. Figure 2 Example of a vaginal closure force tracing. A trial in the supine and standing position is shown to illustrate how a tracing is analyzed to determine VCFREST, VCFMAX, and VCFAUG.Bolded vertical linesbefore pelvic muscle contraction indicate when the computer is available for data capture and do not indicate the latency between instruction to contract and time of contraction.
Table Mean VCF when supine and standing
VCFREST VCFMAX VCFAUG Supine 3.6G0.8 7.5G2.9 3.9G2.7 Standing 6.9G1.5 10.1G2.4 3.3G1.9 Arithmetic difference (N) 3.3 2.6 0.6 Percent difference (%) 92 35 18 Statistical significance P!.0001 P!.0001 P = .009
Figure 3 Mean VCFRESTand mean VCFMAXin the supine and standing positions. There was a 92% diﬀerence (P!.001) between supine and standing VCFRESTand a 35% diﬀerence (P!.001) between supine and standing VCFMAX.
This study revealed a 92% increase in VCFREST when a woman moves from the supine to the standing position. What might have caused this? An increase in intra-abdominal pressure or greater resistance from the pelvic ﬂoor muscles are 2 potential factors. The simul-taneous measurement of these 2 measures allows the relative contribution of increased intra-abdominal pres-sure on VCF to be explored. The lack of a signiﬁcant correlation between the diﬀerences of them when supine and standing suggests that an increase in intra-abdom-inal pressure does not entirely account for the increase in VCF.
The design of the instrumented vaginal specula and the deﬁnition of the term VCF have implications regarding what is measured. VCF is an assessment of the resultant force acting normal to the vaginal axis in
the midsagittal plane. VCFREST consists of 3 compo-nents:
1. The passive force on both the anterior and posterior bills from the circumferential stretch of the ﬁbro-muscular tissue of the vagina and pelvic ﬂoor muscles on insertion of the speculum;
2. The superiorly directed force on the posterior bill of the levator ani muscle resisting intra-abdominal pressure; and
3. The inferiorly directed force on the anterior bill from the intra-abdominal pressure acting perpen-dicular to the speculum’s longitudinal axis on the cross-sectional area and from the presence of the pubic symphysis.
The force related to intra-abdominal pressure on the anterior bill results from the hydrostatic pressure caused Figure 4 Diﬀerence in bladder pressure and VCF associated with change in the supine and standing position. The slope of the regression line demonstrates that there is a weak correlation between these 2 factors.
by the weight of the superincumbent intra-abdominal contents and intra-abdominal pressurization caused by abdominal muscle contraction. Unlike the balloon pressure devices, the speculum is insensitive to pressures acting in the mediolateral direction or craniocaudally along the axis of the vagina.
Our ﬁndings of increased intra-abdominal pressure with change in posture are consistent with previous studies. The mean resting intra-abdominal pressure we reported was 31 cm H2O, which is similar to the ﬁndings of Henriksson et al9 and Iosif et al.10 When standing, higher intravesical pressures occur for 2 reasons: (1) the height of the superincumbent intra-abdominal contents (eg, the height of the column of water) above the bladder is increased and (2) in comparison to supine positioning, abdominal muscle tone increases,11 leading to additional intra-abdominal pressurization.
It is instructive to estimate the contributions to VCF when supine and standing. The force that is due to supine intra-abdominal pressure can be calculated by converting the measured intravesical pressure to units of N/cm2 and then multiplying the result by the cross-sectional area of the anterior bill of the speculum:
10 cm H2O = (0.1 N/cm2)(18.8 cm2) = 1.9 N This suggests that 1.9 N of the 3.6 N of supine VCFRESTis an inferiorly directed force on the anterior bill caused by intra-abdominal pressure and the remain-ing 1.7 N is due to the passive tissue stretch and the presence of the pubic symphysis. Because the speculum is in equilibrium, the sum of the forces on the 2 bills must be equal. Therefore, the pelvic ﬂoor muscles provide a supe-riorly directed force on the posterior bill of 3.6 N as they hold the speculum against the pubic symphysis and resist the action of intra-abdominal pressure. Now, what happens when standing? We can again estimate the Figure 5 Change in bladder pressure with maximal voluntary contraction when (A) supine and (B) standing. When supine, subjects were able to isolate the pelvic ﬂoor muscles and avoid increasing intra-abdominal pressure. When standing, they had diﬃculty contracting the pelvic ﬂoor muscles without increasing intra-abdominal pressure.
contribution of intra-abdominal pressure to the standing VCFRESTif we multiply the intra-abdominal pressure by the area of the anterior blade:
31 cm H2O = (0.31 N/cm2)(18.8 cm2) = 5.6 N This means that 5.6 N of the 6.9 N of average standing VCFREST is the inferiorly directed force of intra-abdominal pressure on the anterior blade. The remaining 1.3 N is due to the passive forces of tissue stretch and the presence of the pubic symphysis. The superiorly directly force from the pelvic ﬂoor muscles is now 6.9 N. The weak correlation between the diﬀerence in supine and standing VCFREST and bladder pressure can be explained by interindividual variability in the recruitment and tone of the abdominal and pelvic ﬂoor muscles. However, the fact that VCFAUGwas 3 to 4 N in the supine and standing positions suggests that the maximal volitional increase in the pelvic muscle force elevating the speculum is independent of body orienta-tion and that the instrumented speculum captures the increase of VCF in the sagittal plane.
The closure of the vagina with change in posture has been evaluated by previous investigators. By using vaginal pressure transducers, both Bo¨ and Finkenhagen7 and Miller8 found diﬀerences between resting supine and standing measures. However, their ﬁndings at maximum voluntary contraction with respect to vaginal closure pressure were not consistent. With change in posture, Bo¨ and Finkenhagen7 found a diﬀerence in intravaginal pressure at maximum voluntary contrac-tion but Miller8did not. It is not clear if this discrepancy could be due to the methodology used or diﬀerences in the population of women studied (eg, Bo¨ and Finken-hagen7only studied women who were stress incontinent and Miller8 studied both asymptomatic and stress incontinent women).
The associations of clinical factors with standing VCFREST and supine VCFREST deserve further investi-gation. It was not possible to determine how parity and route of delivery aﬀected VCF with this sample size and the distribution of obstetric events. The importance of the correlation between higher BMI and standing VCFREST is interesting given the known inﬂuence of obesity on symptoms of urinary incontinence. The clinical signiﬁcance of each of these ﬁndings will need further examination.
This study has certain limitations. The number of neuromuscular units recruited, the presence/absence of neurologic damage, and the role of muscle fatigue cannot be quantiﬁed with this technique. Supplemental studies with electromyography may help clarify these issues but this technique too has limitations. Electro-myography can only be used to study intact muscle and it has been shown that pelvic ﬂoor muscle can be missing.12,13 Multiple techniques of examination may be needed to better understand pelvic ﬂoor structure and function. Second, the most eﬀective technique of pelvic
ﬂoor contraction may involve coactivation of the abdominal muscles.14 When standing, women tended to tighten their abdominal muscles during contraction, even if they had demonstrated excellent technique when supine. Third, the sample of subjects should be consid-ered. Although this cohort was asymptomatic and continent, they were also parous and may have some underlying, subclinical neuromuscular damage.15 The BMI is also high and may not be generalized to all populations.
The levator ani muscles close the urogenital hiatus and supports the abdominopelvic organs. Injury to them can result in increased risk for pelvic organ prolapse and stress urinary incontinence.16,17 Physiologic diﬀerences in levator ani function may have broad implications for patients. They may explain diﬀerences in symptom control and account for many of the successes and failures of both conservative and surgical treatments. Although it will always be more convenient to study pelvic ﬂoor muscle action when supine, data taken in the upright posture captures the natural action of the muscle in the position in which it must function daily. Investigations of pelvic ﬂoor muscle in upright postures may bring new insights to pelvic ﬂoor function.
1. Shaﬁk A, Doss S, Asaad S. Etiology of the resting myoelectric activity of the levator ani muscle: physioanatomic study with a new theory. World J Surg 2003;27:309-14.
2. Taverner D. An electromyographic study of the normal function of the external anal sphincter and pelvic diaphragm. Dis Col Rect 1959;2:153-60.
3. Sampselle CM, Miller JM, Mims BL, DeLancey JOL, Ashton-Miller JA, Antonakos CL. Eﬀect of pelvic muscle exercise on transient incontinence during pregnancy and after birth. Obstet Gynecol 1998;91:406-11.
4. Ashton-Miller JA, DeLancey JOL, Warwick DN. Method and apparatus for measuring properties of the pelvic ﬂoor muscles. US patent 6,468,232 B1. October 2002.
5. Dumoulin C, Bourbonnais D, Lemieux MC. Development of a dynamometer for measuring the isometric force of the pelvic ﬂoor musculature. Neurourol Urodyn 2003;22:648-53.
6. DeLancey J, Kearney R, Umek W, Ashton-Miller JA. Levator ani muscle structure and function in women with prolapse compared to women with normal support. Neurourol Urodynam 2003;22:542-3. 7. Bo¨ K, Finckenhagen HB. Is there any diﬀerence in measurement of pelvic ﬂoor muscle strength in supine and standing position? Acta Obstet Gynecol Scand 2003;82:1120-4.
8. Miller JM. Eﬀect of standing and lying postures on the distal intravaginal pressure measured in activities that relate to stress urinary incontinence. Doctoral Dissertation, Chapter V, School of Nursing, University of Michigan, 1996.
9. Henriksson L, Ulmsten U, Andersson K. The eﬀect of changes of posture on the urethral closure pressure in stress-incontinent women. Scand J Urol Nephrol 1977;11:207-10.
10. Iosif S, Ulmsten U, Andersson K. The eﬀect of changes of posture on the urethral closure pressure in healthy women. Scand J Urol Nephrol 1977;11:201-6.
11. De Troyer A. Mechanical role of the abdominal muscles in relation to posture. Resp Physiol 1983;53:341-538.
12. Hoyte L, Schierlitz L, Zou K, Flesh G, Fielding JR. Two- and 3-dimensional MRI comparison of levator ani structure, volume, and integrity in women with stress incontinence and prolapse. Am J Obstet Gynecol 2001;185:11-9.
13. Singh K, Jakab M, Reid WM, Berger LA, Hoyte L. Three-dimensional magnetic resonance imaging assessment of levator ani morphologic features in diﬀerent grades of prolapse. Am J Obstet Gynecol 2003;188:910-5.
14. Sapsford RR, Hodges PW, Richardson CA, Cooper DH, Markwell SJ, Jull GA. Co-activation of the abdominal and pelvic ﬂoor muscles during voluntary exercises. Neurourol Urodyn 2001;20:31-42.
15. Snooks SJ, Swash M, Setchell M, Henry MM. Injury to in-nervation of pelvic ﬂoor sphincter musculature in childbirth. Lancet 1984;2:546-50.
16. DeLancey JOL, 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.
17. Tunn R, Paris S, Fischer W, Hamm B, Kuchinke J. Static magnetic resonance imaging of the pelvic ﬂoor muscle morphology in women with stress urinary incontinence and pelvic prolapse. Neurourol Urodyn 1998;17:579-89.