Secondary Logo

Journal Logo

ORIGINAL RESEARCH

Pregnancy, Labor, Delivery, and Pelvic Organ Prolapse

Sze, Eddie H. M. MD; Sherard, Gordon B. III MD; Dolezal, Jeanette M. PhD

Author Information
  • Free

Pelvic organ prolapse is a major health issue for women. A 1997 study found that women with normal life expectancy have an 11% chance of undergoing at least one operation for pelvic organ prolapse or urinary incontinence during their lifetime.1 Recently, investigators projected that over the next 30 years, the rate of women seeking care for pelvic floor disorders will double.2

Available data associate pelvic organ prolapse with reproductive tract injury sustained during vaginal delivery and its absence with cesarean delivery3–12; however, there are very few data in the literature that directly link these associations.

Race is another frequently cited risk factor for developing pelvic organ prolapse. Asian and black women are reportedly less likely to undergo surgery for genital prolapse than white women.13,14 This suggests a difference in susceptibility to developing pelvic organ prolapse.

The aims of our study were to compare the occurrence of pelvic organ prolapse after vaginal and cesarean delivery and the susceptibility of black and white women to developing prolapse during childbirth.

MATERIALS AND METHODS

In an Institutional Review Board–approved protocol, we studied 101 consecutive women at the East Carolina University School of Medicine obstetric clinic from June 2000 to June 2001. We included all nulliparous women with an uncomplicated, singleton pregnancy who presented for prenatal care in our clinic prior to 36 weeks' gestation, delivered at term, and consented to participate in the study. Each woman underwent a detailed speculum examination to evaluate pelvic organ support at the time of her 36-week visit. Pelvic support was graded using the International Continence Society staging system.15 This system divides the vagina into six segments: the proximal and distal portions of the anterior and posterior vaginal walls, cervix, and posterior fornix. The presence or absence of support defect was determined by measuring the distance (cm) between a specified point in each segment and the hymen. Each distance was measured using a cotton swab marked at 1-cm intervals while the subject performed maximal Valsalva maneuver and coughing in the supine position. Pelvic support defect was classified into five stages (0–IV). Each stage was determined by the segment that has prolapsed closest to or beyond the hymen. The International Continence Society system also designates the most severely prolapsed segment. Stages 0–II and designations “A-a” and “A-p” were used in this study. Stage 0 indicates normal support in each of the six segments. Stage I indicates a pelvic support defect in one or more segments. However, all prolapsed segments were more than 1 cm above the hymen. Stage II indicates that one or more segment had prolapsed to within 1 cm above to 1 cm beyond the hymen. A-a and A-p designate the specified point in the proximal portion of the anterior and posterior vaginal wall, respectively. A-a and A-p are located 3 cm above the external urethral meatus in the midline of the anterior and posterior vaginal wall, respectively.

At the 6-week postpartum visit, each woman was re-examined and regraded for prolapse. A change in International Continence Society stage from 36 weeks antepartum to 6 weeks postpartum was considered as a new or more severe prolapse developed during labor and delivery. A new pelvic organ prolapse was defined as the presence of prolapse in any segment at 6 weeks postpartum in a woman who had normal pelvic support at her 36-week antepartum visit. A more severe prolapse was defined as prolapse in any segment present at 36 weeks antepartum that had progressed to a higher stage at 6 weeks postpartum. Women who returned for problem visits or Papanicolaou smears after the 6-week postpartum examination were restaged for possible changes in International Continence Society stage.

Power analysis indicated that 12 women who had spontaneous vaginal delivery and 12 who had cesarean delivery would be needed to detect a 57% (57%–0%) difference between the two delivery methods, with an α value of 5% and a β value of 20%. Previous investigators reported that spontaneous vaginal delivery is associated with a 57% incidence of grade I cystocele and that emergency cesarean delivery did not increase the mobility of the anterior vaginal wall in nulliparous women.11,12 Power analysis indicated that 31 women would be needed in each racial group to detect a 33% (41.3%–8.3%) difference, with an α value of 5% and a β value of 20%. Approximately 50% of nulliparous women in our clinic had spontaneous vaginal delivery, 30% had cesarean delivery, and 20% had operative vaginal delivery. If white women in our clinic had the same incidence of pelvic organ prolapse after each type of delivery as previously described,11,12 then 41.3% ([50 × 57% = 28.5] + [20 × 64% = 12.8] + [30 × 0% = 0] = 41.3%) of women would develop prolapse postpartum. It is further assumed that black women are 80% less susceptible to develop pelvic organ prolapse than their white counterparts (41.3% × 20% = 8.3%).13

All data were entered into a computer database system for storage and analysis. Statistical analysis was performed using Epi Info 6.04b (USD Inc., Stone Mountain, GA) and Microsoft Office 1997 (Microsoft Corporation, Redmond, WA). Categorical data was analyzed for significance using the χ2 test or Fisher exact test as appropriate. Quantitative data was analyzed with analysis of variance.

RESULTS

One hundred one nulliparous women delivered at term between July 2000 and June 2001. Seven (7%) who did not return for their 6-week postpartum visit were excluded from further analysis. The remaining 94 formed the study group. Their mean age was 22.1 ± 4.6 years. At the 36-week antepartum visit, 43 (46%) of the 94 women had pelvic organ prolapse. Twenty-four (26%) had a stage II prolapse. Six weeks postpartum, 78 (83%) had pelvic organ prolapse. Fifty (52%) had a stage II prolapse. Thirty-five women (37%) developed a new pelvic organ prolapse and 14 (15%) revealed a more severe pelvic organ prolapse after childbirth. Eighteen (19%) of the 94 had a two-stage increase in the severity of their prolapse (stage 0 at 36 weeks antepartum to stage II at 6 weeks postpartum).

Forty-one (44%) of the 94 women had spontaneous vaginal delivery. The average age was 20.5 ± 3.8 years. Six weeks postpartum, 13 women (32%) developed a new pelvic organ prolapse and seven (17%) revealed a more severe pelvic organ prolapse (Table 1). Six (15%) had a two-stage increase in the severity of their prolapse.

Table 1
Table 1:
Pelvic Organ Prolapse Quantification at 36 Weeks Antepartum vs 6 Weeks After a Spontaneous Vaginal Delivery

Twenty-six women (28%) had cesarean delivery during the active phase of labor. Their cervical dilatation at the time of cesarean delivery ranged from 4 to 9 cm. Their average age was 23.5 ± 4.8 years. Six weeks postpartum, nine women (35%) developed a new pelvic organ prolapse and two (8%) revealed a more severe prolapse (Table 2). Four (15%) had a two-stage increase in the severity of their prolapse. The proportion that developed a new (13/41 [32%] versus 9/26 [35%], P = .805) and a more severe (7/41 [17%] versus 2/26 [8%], P = .237) pelvic organ prolapse and a two-stage increase in the severity of prolapse (6/41 [15%] versus 4/26 [15%], P = .598) was statistically similar between women who had spontaneous vaginal delivery and cesarean delivery during active labor (Figure 1).

Table 2
Table 2:
Pelvic Organ Prolapse Quantification at 36 Weeks Antepartum vs 6 Weeks After a Cesarean Delivery During Active Phase of Labor
Sze
Sze:
Sze. Childbirth Prolapse. Obstet Gynecol 2002.

Two women (2%) had cesarean delivery during latent phase of labor. Both had stage 0 prolapse at the 36-week antepartum visit. Six weeks postpartum, one developed a stage I and the other sustained a stage II pelvic organ prolapse.

Four women had cesarean delivery during the second stage of labor. Six weeks postpartum, one (25%) developed a new and another (25%) revealed a more severe prolapse. One (25%) had a two-stage increase in the severity of her prolapse.

Three women (3%) had elective cesarean delivery. One woman had stage 0, one had stage I, and one had stage II prolapse at the 36-week antepartum visit. Six weeks postpartum, one woman had stage 0 and two had stage I pelvic organ prolapse.

Eleven (12%) of 94 women had outlet forceps delivery. The average age was 23.1 ± 4.8 years. Six weeks postpartum, eight women (73%) developed a new pelvic organ prolapse and two (18%) revealed a more severe prolapse (Table 3). Five (45%) had a two-stage increase in the severity of their prolapse.

Table 3
Table 3:
Pelvic Organ Prolapse Quantification at 36 Weeks Antepartum vs 6 Weeks After a Forceps Delivery

Seven (7%) of 94 women had vacuum-assisted delivery. The average age was 23.1 ± 4.8 years. Six weeks postpartum, two women (29%) developed a new pelvic organ prolapse and two (29%) revealed a more severe prolapse (Table 4). One (14%) had a two-stage increase in the severity of her prolapse.

Table 4
Table 4:
Pelvic Organ Prolapse Quantification at 36 Weeks Antepartum vs 6 Weeks After a Vacuum-Assisted Delivery

At the 6-week postpartum visit, 76 (97%) of the 78 women with pelvic organ prolapse had the most severe defect in the anterior vaginal wall. The other two defects (3%) were in the posterior wall (Tables 1–4).

Fifty-four (57%) of the 94 women who completed the study were black, and 40 (43%) were white. Although the mean age of the white women was significantly higher than blacks (23.4 ± 4.7 versus 21.1 ± 4.2 years, P = .016), the proportion that had spontaneous (18/40 [45%] versus 23/54 [43%], P = .816), forceps (7/40 [18%] versus 4/54 [7%], P = .119), vacuum (2/40 [5%] versus 5/54 [9%], P = .359), and cesarean deliveries (13/40 [33%] versus 22/54 [41%], P = .283) was similar between the two groups. The proportion that developed a new (18/54 [33%] versus 17/40 [43%], P = .363) and a more severe (8/54 [15%] versus 6/40 [15%], P = .980) prolapse postpartum and a two-stage increase in severity of pelvic organ prolapse (10/54 [19%] versus 8/40 [20%], P = .857) was also similar between the two groups (Figure 2).

Sze
Sze:
Sze. Childbirth Prolapse. Obstet Gynecol 2002.

Three of the women who had cesarean delivery during active labor (Table 2), one who had elective cesarean delivery, and two who had spontaneous vaginal delivery (Table 1) experienced a spontaneous regression of their prolapse postpartum (stage II at 36 weeks antepartum to stage I at 6 weeks postpartum). The incidence of spontaneous regression was similar between women who had spontaneous vaginal delivery and cesarean delivery during active labor (2/41 [5%] versus 3/26 [12%], P = .291).

Nineteen (20%) of the 94 women returned for problem visits or Papanicolaou smears 4–7 months after their delivery. Their International Continence Society stage (stage 0 = 4, stage I = 7, stage II = 8) at their return visit did not change from that at their 6-week postpartum visit.

DISCUSSION

Available data associate pelvic organ prolapse with reproductive tract injury sustained during vaginal delivery and its absence with cesarean delivery.3–12 In 1998, one group of investigators reported that 52% of nulliparous women developed a grade I cystocele 7–11 weeks after a spontaneous vaginal delivery.11 This study seemed to directly link vaginal delivery to pelvic organ prolapse. Because the antenatal staging was done in either the first, second, or third trimester, it was difficult to determine whether this injury occurred during pregnancy, labor, or delivery. In addition, the halfway system was used to grade prolapse.16 This system classifies prolapse as descent halfway to the hymen (grade 1), to the hymen (grade 2), halfway past the hymen (grade 3), and maximum possible descent for each site (grade 4). In contrast to the International Continence Society classification, which has good inter-examiner (b 0.702, P < .001 and 0.65213, P < .001) and intra-examiner (b 0.712, P < .001 and 0.71242, P < .001) reproducibility,17 the halfway system is subjective and has not been validated with regard to its reproducibility. Consequently, there are few data that directly link pelvic organ prolapse to vaginal delivery or the absence of pelvic support defects to cesarean delivery. Nevertheless, universal elective cesarean delivery has been proposed as a solution to prevent pelvic organ prolapse.18 In a 1996 survey, 31% of female obstetricians in the London area chose elective cesarean delivery for their own delivery.19 The main reason given was fear of damaging the pelvic floor. The basis of this fear was not clear. Our study showed that elective cesarean delivery is only partially effective in preventing pelvic organ prolapse. Forty-three (46%) of the 94 nulliparous women in our study already had pelvic support defect at their 36-week antepartum visit. Twenty-four (26%) had a stage II defect. This suggests that, at best, universal elective cesarean delivery would prevent pelvic organ prolapse in 54% and a stage II pelvic support defect in 74% of nulliparous women.

Some investigators believe that cesarean delivery has a protective effect on the maternal pelvic support regardless of whether it is performed prior to the onset or during the latent or active phase of labor.20,21 Our data show that cesarean delivery performed during the active phase of labor did not have a protective effect. The proportion of women who developed a new and a more severe pelvic organ prolapse and a two-stage increase in severity of prolapse was statistically similar between women who had spontaneous vaginal delivery and cesarean delivery during active labor (Figure 1). This indicates that injuries to the maternal pelvic support occurred during the first and not the second stage of labor as previously believed.21,22

In contrast to previous findings,13,14 our data demonstrated that when their pelvic support was subjected to the stresses of labor and delivery, black women were as susceptible to developing pelvic organ prolapse as their white counterparts.

The most frequent site or the most severe pelvic support defect occurred in the anterior vaginal wall. This finding is very consistent with data from other studies and the observation that approximately 80% of the pelvic reconstructive surgeries include an anterior vaginal wall repair.1,11,12

We did not stage most of our subjects at the time of their first trimester visit because it did not occur to us that nulliparous woman in their late teens to early 30s could have pelvic organ prolapse or that prolapse could develop during pregnancy. We believe that most of the prolapse present at the 36-week antepartum visit developed during the pregnancy. During the latter half of our study, 13 women who presented for care during the first trimester of pregnancy were staged for pelvic support defect at the time of their initial prenatal visit. When examined at their 36-week antepartum visit, six (46%) of the 13 had developed a new or a more severe prolapse. In addition, O'Bovie reported at the 22nd Annual Scientific Meeting of the American Urogynecologic Society (O'Bovie AL, Woodman PJ, O'Boyle JD, et al. Pelvic organ support in nulliparous pregnant and non-pregnant women [abstract]. Presented at the 22nd Annual Scientific Meeting of the American Urogynecologic Society; October 25–27, 2001; Chicago) that 48% of their nulliparous subjects had International Continence Society stage II prolapse in the second or third trimester of pregnancy, compared with 0% in their nulliparous controls.

We do not know why the prolapse regressed spontaneously in six women. We speculate that pelvic organ prolapse present at the 36-week antepartum visit may be the maternal response to accommodate the fetus and minimize injuries to the pelvic support during parturition; however, the proportion of women who had a stage II pelvic organ prolapse 6 weeks after spontaneous vaginal delivery was significantly higher in those with antepartum prolapse than those without antepartum pelvic support defect (18/23 [75%] versus 6/18 [33%], P = .004) (Table 1).

Our study has directly linked the development of pelvic organ prolapse to childbirth. This and the previous finding that significantly more parous women have International Continence Society stage II and III pelvic support defects than nulliparous women (54% versus 15%, P < .001) demonstrate that childbirth is a major cause of pelvic organ prolapse.20

REFERENCES

1. Olsen AL, Smith VJ, Bergstrom JO, Colling JC, Clark AL. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–6.
2. Luber KM, Boero S, Choe JY. The demographics of pelvic floor disorders: Current observations and future projections. Am J Obstet Gynecol 2001;184:1496–503.
3. Sultan AH, Kamm MA, Hudson CN. Pudendal nerve damage during labour: Prospective study before and after childbirth. Br J Obstet Gynaecol 1994;101:22–8.
4. Tetzschner T, Sørensen M, Jønsson L, Lose G, Christiansen J. Delivery and pudendal nerve function. Acta Obstet Gynecol Scand 1997;76:324–31.
5. Allen RE, Hosker GL, Smith ARB, Warrell DE. Pelvic floor damage and childbirth: A neurophysiological study. Br J Obstet Gynaecol 1990;97:770–9.
6. Snooks SJ, Setchell M, Swash M, Henry MM. Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 1984;2:546–50.
7. Chiaffarino F, Chatenoud L, Dindelli M, Meschia M, Buonaguidi A, Amicarelli F, et al. Reproductive factors, family history, occupation and risk of urogenital prolapse. Eur J Obstet Gynecol Reprod Biol 1999;82:63–7.
8. Mant, J, Painter M, Vessey M. Epidemiology of genital prolapse: Observations from the Oxford Family Planning Association study. Br J Obstet Gynaecol 1997;104:579–85.
9. Tsunoda A, Shibusawa M, Kamiyama G, Kusano M, Shimizu Y, Yanaihara T. The effect of vaginal delivery on the pelvic floor. Surg Today 1999;29:1243–7.
10. Peschers U, Schaer G, Anthuber C, DeLancey JOL, Schuessler B. Changes in vesical neck mobility following vaginal delivery. Obstet Gynecol 1996;88:1001–6.
11. Meyer S, Schreyer A, De Grandi P, Hohlfeld P. The effects of birth on urinary continence mechanisms and other pelvic-floor characteristics. Obstet Gynecol 1998;92:613–8.
12. Meyer S, Hohlfeld P, Achtari C, Russolo A, De Grandi P. Birth trauma: Short and long term effects of forceps delivery compared with spontaneous delivery on various pelvic floor parameters. Br J Obstet Gynaecol 2200;107:1360–5.
13. Van Dongen L. The anatomy of genital prolapse. S Afr Med J 1981;60:357–9.
14. Nichols DH, Randall CL. Vaginal surgery. 4th ed. Baltimore: Williams & Wilkins, 1996.
15. Bump RC, Mattiasson A, Bø K, Brubaker LP, DeLancey JO, Klarskov P, et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–7.
16. Baden WF, Walker T. Surgical repair of vaginal defects. Philadelphia: JB Lippincott, 1992.
17. Hall AF, Theofrastous JP, Cundiff GW, et al. Interob-server and intraobserver reliability of the proposed International Continence Society, Society of Gynecologic Surgeons, and American Urogynecologic Society pelvic organ prolapse classification system. Am J Obstet Gynecol 1996; 175:1467–71.
18. Sultan AH, Stanton SL. Preserving the pelvic floor and perineum during childbirth—Elective caesarean section? Br J Obstet Gynaecol 1996;103:731–4.
19. Al-Mufti R, McCarthy A, Fisk NM. Obstetricians' personal choice and mode of delivery. Lancet 1996;347:544.
20. Swift SE. The distribution of pelvic organ support in a population of female subjects seen for routine gynecologic health care. Am J Obstet Gynecol 2000;183:277–85.
21. Dannecker C, Anthuber C. The effects of childbirth on the pelvic-floor. J Perinat Med 2000;28:175–84.
22. Handa VL, Harris TA, Ostergard DR. Protecting the pelvic floor: Obstetric management to prevent incontinence and pelvic organ prolapse. Obstet Gynecol 1996;88:470–8.
© 2002 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.