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ORIGINAL RESEARCH |
From the Departments of Obstetrics and Gynecology and Mechanical Engineering and Applied Mechanics, University of Michigan Health Systems, Ann Arbor, Michigan.
Address reprint requests to: Denise Howard, MD, MPH Department of Obstetrics and Gynecology 1500 East Medical Center Drive L4000 Women’s Hospital Box 0276 Ann Arbor, MI 48109-0276 E-mail: denhow{at}umich.edu
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Abstract |
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Methods: Eighteen black women (mean age 28.1 years) and 17 white women (mean age 31.3 years) completed this cross-sectional study. The following assessments were made: urethral function using multichannel cystometrics and urethral pressure profilometry, pelvic muscle strength using an instrumented speculum, urethral mobility using the cotton-swab test and perineal ultrasound, and pelvic muscle bulk using magnetic resonance imaging.
Results: Black women demonstrated a 29% higher average urethral closure pressure during a maximum pelvic muscle contraction (154 cm H2O versus 119 cm H2O in the white subjects; P = .008). Although not statistically significant, black women had a 14% higher maximum urethral closure and pressure at rest (108 cm H2O versus 95 cm H2O; P = .23) and a 21% larger urethral volume (4818 mm3 versus 3977 mm3; P = .06). In addition, there was a 36% greater vesical neck mobility measured with the cotton-swab test (blacks 49° versus whites 36°; P = .02) and a 42% difference in ultrasonically measured vesical neck mobility during a maximum Valsalva effort (blacks = -17 mm versus whites -12 mm; P = .08).
Conclusion: Functional and morphologic differences exist in the urethral sphincteric and support system of nulliparous black and white women.
The prevalence of genuine stress urinary incontinence (GSI) is thought to be significantly lower in black women than in white women. This is based on information from cross-sectional studies. Bump1 examined 200 consecutive patients referred to his urogynecology practice for prolapse or incontinence. Of the 54 blacks in this group, 27% were given a diagnosis of GSI compared with 61% of the white patients. He also found that the black women with GSI had a higher maximum urethral closure pressure and greater urethral mobility with stress than did the white subjects with the same diagnosis. Similarly, Peacock et al2 retrospectively reviewed 159 black women and found the prevalence of GSI to be 28%. Although these two studies suggested that the prevalence of GSI is lower in black women, additional comparative studies are needed.
Stress continence is thought to be provided by two factors: urethral sphincter function and urethral support.3–5 At present, it is not known whether racial differences exist in either one or both of these factors. Such differences, if they exist, might help explain racial differences in the prevalence of GSI and might help elucidate the pathophysiology of stress urinary incontinence. The aim of this study was to compare the structure and function of the sphincteric and urethral support mechanisms of nulliparous black and white women. Specifically, we tested the primary null hypotheses that no racial differences would be found in sphincter function as measured by passive and active urethral closure pressure, urethral mobility as measured by the cotton-swab test, levator ani muscle strength measured with the instrumented speculum, and urethral sphincter and levator ani muscle morphology as measured by the cross-sectional area. We also tested the secondary null hypotheses that no racial differences would be found in other measures of pelvic muscle morphology, such as the urethral sphincter and levator ani muscle thickness and volume, as well as urethral and levator ani functional measures such as the levator ani muscle resting tone and urethral mobility as measured by ultrasound.
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Materials and Methods |
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Eighteen black subjects and 17 white subjects completed the study. The data were collected over two separate visits. The ultrasound scans and urodynamic procedures were performed at the first visit, and magnetic resonance imaging (MRI) was performed on a second visit. Continence was determined by a standing stress test for urine leakage during a series of three hard coughs.6 After the pelvic examination was completed, an instrumented speculum, designed to quantify the force of a single pelvic muscle contraction, was placed in the vagina.7 Measurements were obtained at rest and during a maximum voluntary pelvic muscle contraction.
Post-void residual urine was obtained through urethral catheterization, and a urinalysis was performed on the specimen to ensure that none of the subjects had evidence of cystitis. Cotton-swab resting and strain angles were then obtained.8
An 8-French dual-tip Gaeltec catheter (Medical Measurements Inc., Hackensack, NJ) was inserted into the bladder and an Aquarius Urodynamic System (Laborie Medical Technologies Co, Williston, VT) was used to perform a cystometrogram and a urethral pressure profile. The bladder was filled at a rate of 100 mL/minute to a maximum of 300 mL or to maximum bladder capacity if this was less than 300 mL. A urethral pressure profile was then obtained, and the maximum urethral closure pressure at rest and the urethral pressure measured during a maximum pelvic muscle contraction (Kegel urethral closure pressure) were recorded.
Next, a midsagittal perineal ultrasound (Sonoline SI-400; Siemens AG, Erlangen, Germany) was performed in the standing position using a 5-MHz curved-array probe. The ultrasound measurements were based on the method developed by Schaer et al.9 The position of the vesical neck was measured using a rectangular coordinate system with origin at the inferior border of the symphysis. Vesical neck locations were measured at rest, during a maximum Valsalva effort, and during a maximum cough effort while intravaginal pressures were measured in the proximal vagina (Figure 1
).
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The data were analyzed using the Mann-Whitney U test for pairwise comparisons with the StatView statistical package (Abacus Concepts Inc., Berkeley, CA) and linear regression with the SPSS 9.0 statistical package (SPSS Inc., Chicago, IL).
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Results |
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Morphologically, the black subjects had a 21% greater urethral volume as measured by MRI (4818 ± 1469, range 2444–8091 mm3 versus 3977 ± 1005, range 2622–6550 mm3; P = .06). The urethral cross-sectional area comparison was not significant. The primary urethral function comparisons indicated that the mean Kegel urethral closure pressure was 29% higher in the black subjects (154 ± 29, 108–202 cm H2O versus 119 ± 37, 76–194 cm H2O; P = .008) (Figure 2). Similarly, although the difference did not reach statistical significance, the mean maximum urethral closure pressure at rest for the black subjects was 14% higher (108 ± 21, 62–148 cm H2O versus 95 ± 30, 49–147 cm H2O; P =.23).
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). Although there were no differences during cough, black women had 36% greater vesical neck excursion during a maximum Valsalva effort as measured by the cotton-swab test (blacks 49° versus whites 36°; P = .02). This finding was consistent with the 42% greater displacement of the vesical neck measured with ultrasound during the Valsalva maneuver (blacks -17 mm versus whites -12 mm; P = .08). There were no significant pressure differences between the groups during the cough or Valsalva maneuvers (Table 2). There were also no group differences in other secondary measures, such as those involving vesical neck resting location.
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Race continued to have an independent effect when linear regression was used to control for interactive and confounding effects of the dependent variables that were found to be significant in paired comparisons. When the cotton-swab strain angle was used as the dependent variable, both age (P = .02) and black race (P = .009) had an independent effect. When the Kegel urethral closure pressure was used as the dependent variable, age had no effect (P = .7), but black race continued to contribute significantly to the differences found (P = .05).
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Discussion |
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Our morphologic and functional results suggest that young nulliparous black women have greater urethral sphincter capacity than white women, as evidenced by larger urethral volume and significantly higher urethral closure pressures during a pelvic muscle contraction. A greater bulk of urethral striated muscle or a higher density of urethral striated muscle fibers could explain this difference. This is consistent with the fact that black women have a higher appendicular skeletal mass than their white counterparts.11,12 In addition, although not significant, the black subjects had a larger levator ani muscle cross-sectional area and greater levator ani strength. The variance in our data for levator ani strength is not surprising given the known difficulty that women can experience in voluntarily contracting the levator ani muscle.13
Our sphincteric function findings corroborate with those of others. They are consistent with the findings of Bump,1 as mentioned in the Introduction. Likewise, in a comparison of multiparous black and Indian South Africans, Knobel14 found that black women had a 21% higher urethral closure pressure and a 56% greater contractile power of the pelvic muscle.
Stress incontinence has been presumed to result from urethral hypermobility,15 with a lesser emphasis on sphincteric function. However, paradoxically, we found greater vesical neck mobility during a Valsalva maneuver in black women, a population thought to have a lower prevalence of stress incontinence. Because the Valsalva intra-abdominal pressures did not differ significantly in the two groups, the compliance of the vesical neck support must be greater in black women. The fact that black women were able to relax their pelvic muscles more successfully as instructed during a Valsalva maneuver might explain this finding. However, the vesical neck compliance during the hard cough was similar in both groups. Higher urethral closure pressures in black women suggest that sphincter function might play a greater role than support in maintaining continence during stress. Indeed, Fantl et al16 showed that urethral mobility was not predictive of urethral function, further emphasizing the importance of the sphincter mechanism in maintaining continence.
The present study has limitations. The black women were younger than the white subjects, although this difference was not significant. We know that maximum urethral closure pressure decreases with age; however, this decrease becomes significant only after the age of 36 years, with a 2–4% decrease in function up to age 40 years.17,18 In addition, correlation analysis of maximum urethral closure pressure on age revealed that age explained only 2.4% of the variation in the maximum urethral closure pressure. Linear regression also confirmed an independent effect of race on both the cotton-swab strain angle and the urethral closure pressure during a maximum pelvic muscle contraction. Therefore, this slight age difference between groups does not explain the differences demonstrated in sphincter function. Although the study was prospective, we cannot exclude the possibility of selection bias because the subjects were volunteers.
Other limitations include the small group sizes and lack of power. In performing power calculations, we discovered that the power of the study was limited in some areas. The power to distinguish a significant difference in the urethral volume was 47%. As far as functional measures were concerned, the power of our study to distinguish a difference in the maximum urethral closure pressure was 29%. There are likely other significant biologic differences in the structure and function of the continence mechanism between these groups that we were unable to demonstrate. This study provides the pilot data needed to estimate the adequate sample sizes required to demonstrate these suggested differences.
An advantage of this study is that the accuracy and reliability of the measurement methods have been demonstrated elsewhere.6,7,9
The insights provided by this study further emphasize the importance of understanding the biology of the continence mechanism to further define the pathogenesis of GSI. Knowledge of the factors that place individuals at increased risk allows the development of treatment strategies. Future studies might focus on further defining the prevalence of this problem in specific populations. Additionally, the influence of age and parturition in these groups deserves investigation. Histologic examination of the urethras of different populations might further clarify the role of striated muscle density and bulk. The biologic differences between the continence mechanisms noted in these women deserve further investigation.
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Footnotes |
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Received July 19, 1999. Received in revised form November 9, 1999. Accepted November 24, 1999.
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References |
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2. Peacock LM, Wiskind AK, Wall LL. Clinical features of urinary incontinence and urogenital prolapse in a black inner-city population. Am J Obstet Gynecol 1994;171:1464–71.[Medline]
3. Jeffcoate TNA, Roberts H. Observations on stress incontinence of urine. Am J Obstet Gynecol 1952;64:721–38.[Medline]
4. McGuire EJ, Lytton B, Pepe V, Kohorn EI. Stress urinary incontinence. Obstet Gynecol 1976;47:255–64.
5. Toews HA. Intraurethral and intravesical pressures in normal and stress-incontinent women. Obstet Gynecol 1967;29:613–24.
6. Miller JM, Ashton-Miller JA, DeLancey JOL. Quantification of cough-related urine loss using the paper towel test. Obstet Gynecol 1998;91:705–9.[Abstract]
7. 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;91:406–12.[Abstract]
8. Crystle CD, Charme LS, Copeland WE. Q-tip test in stress urinary incontinence. Obstet Gynecol 1971;38:313–5.[Medline]
9. Schaer GN, Koechli OR, Schuessler B, Haller U. Perineal ultrasound for evaluating the bladder neck in urinary stress incontinence. Obstet Gynecol 1995;85:220–4.[Abstract]
10. Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical measurements. Lancet 1986;I:307–10.
11. Gasperino JA, Wang J, Pierson RN, Heymsfield SB. Age-related changes in musculoskeletal mass between black and white women. Metabolism 1995;44:30–4.[Medline]
12. Cohn SH, Abesamis C, Yasumura S, Aloia JF, Zanzi I, Ellis KJ. Comparative skeletal mass and radial bone mineral content in black and white women. Metabolism 1977;26:171–8.[Medline]
13. Bump RC, Hurt WG, Fantl JA, Wyman JF. Assessment of Kegel pelvic muscle exercise performance after brief verbal instruction. Am J Obstet Gynecol 1991;165:322–9.[Medline]
14. Knobel J. Stress incontinence in the black female. S Afr Med J 1975;49:430–2.[Medline]
15. Hodgkinson CP. Recurrent stress urinary incontinence. Clin Obstet Gynecol 1978;21:787–96.[Medline]
16. Fantl JA, Hurt WG, Bump RC, Dunn LJ, Choi SC. Urethral axis and sphincteric function. Am J Obstet Gynecol 1986;155:554–8.[Medline]
17. Rud T. Urethral pressure profile in continent women from childhood to old age. Acta Obstet Gynecol Scand 1980;59:331–5.[Medline]
18. Enhorning G. Simultaneous recording of intravesical and intraurethral pressure. Acta Obstet Gynecol Scand Suppl 1961;276:1–69.
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