Fecal incontinence is a distressing condition, recognized for its negative impact on quality of life for women of all ages. Although estimates vary widely depending on the study population and the definition of fecal incontinence, population-based studies suggest that its prevalence in community-dwelling adults is 2%1 to 12%,2 and in nursing homes, 46%.3 There are no consistent differences between men and women in the prevalence of fecal incontinence,4 although etiologies may differ.
A major cause of fecal incontinence in young healthy women is anal sphincter tear during vaginal childbirth,5 which occurs in as many as 18% of vaginal deliveries in the United States.6 Studies from other countries indicate 5–10% of women report incontinence of stool 3–6 months after sphincter tear, and 29–53% of women report incontinence of flatus, despite having the tear repaired at delivery.7–9 Studies of fecal incontinence during the first postpartum year are generally limited by their uncontrolled7,8 or retrospective10,11 designs, with small samples.9,12,13
The prevalence of urinary incontinence increases after vaginal delivery,14,15 especially with forceps or vacuum delivery. However, anal sphincter tear has not been assessed as a risk factor for urinary incontinence. Urinary incontinence affects up to 40% of women,16,17 with an estimated 6% of adults having urinary incontinence severe enough to interfere with daily activities. Women affected by moderate-to-severe fecal incontinence or urinary incontinence may suffer embarrassment, social isolation, curtailed activities, and severely impaired quality of life.2,18 The economic impact of incontinence is also a major burden; urinary incontinence impact alone has been estimated at $26 billion in the United States in 1995.19
Given that pregnancy, delivery, and delivery complicated by anal sphincter tear may all predispose women to fecal incontinence and urinary incontinence, we sought to obtain a better understanding of the impact of anal sphincter tears on the development of postpartum incontinence. The primary aim of the Childbirth and Pelvic Symptoms (CAPS) study was to prospectively compare the postpartum prevalence and incidence of fecal incontinence and urinary incontinence in primiparous women who had recognized anal sphincter tears during vaginal delivery with women who delivered vaginally without recognized anal sphincter tears. Our secondary aim was to estimate the prevalence and incidence of these conditions in women who had cesarean delivery before active labor.
MATERIALS AND METHODS
The Childbirth and Pelvic Symptoms study was performed through the Pelvic Floor Disorders Network (PFDN), a cooperative agreement network sponsored by the National Institute of Child Health and Human Development (NICHD), one of the National Institutes of Health. Each institution in the Pelvic Floor Disorders Network, including the data coordinating center at the University of Michigan, received institutional review board approval for the protocol, and all participants provided written informed consent. Subjects were enrolled from the seven Pelvic Floor Disorders Network sites: University of Alabama (Birmingham, AL), Baylor College of Medicine (Houston, TX), Johns Hopkins University (Baltimore, MD), Loyola University and Alexian Brothers Medical Center (Maywood, IL), University of Iowa (Iowa City, IA), University of North Carolina (Chapel Hill, NC), and University of Pittsburgh, at Magee-Womens Hospital and Mercy Hospital (Pittsburgh, PA). In addition, subcontracting sites at the University of Louisville (Louisville, KY) and University of Tennessee (Memphis, TN) contributed subjects.
Primiparous women (women with no prior pregnancy beyond 20 weeks), hospitalized between September 2002 and September 2004, were approached after delivery for enrollment into one of three cohorts. The first cohort included women with anal sphincter tear that was clinically recognized (ie, third- or fourth-degree perineal tear) and repaired at delivery (Sphincter Tear group). This group included women with or without episiotomy. The second cohort was a control group that included women who delivered vaginally without a clinically recognized anal sphincter tear (Vaginal Control group); these women may have had a first- or second-degree perineal tear or nonextending episiotomy. The final cohort was a second control group that included women delivered by cesarean before labor (Cesarean Control group).
Eligible women were those who delivered a single child at 37 or more weeks of gestation and were able to participate in telephone interviews. Exclusion criteria were inflammatory bowel disease (ulcerative colitis or Crohn's disease), self-reported prepregnancy fecal incontinence or anorectal surgery, and neurological conditions predisposing to urinary or fecal incontinence.
Research coordinators reviewed delivery logs daily to identify potential participants or used an alternate method approved by the local institutional review board. First, an eligible woman with an anal sphincter tear (index case) was approached for enrollment. If she declined, the next eligible woman with a sphincter tear was approached until a woman in this cohort was enrolled. Then, the next woman without an anal sphincter tear (Vaginal Control) was identified and approached for study participation. When a Vaginal Control case could not be recruited on the same day as the index case, recruitment occurred on a different day, starting at the chronological time that the index case delivered. Potential Vaginal Controls were approached until one was enrolled. This recruitment method ensured that the research coordinator did not preselect the Vaginal Controls. Because women having cesarean delivery without labor were limited in number, each woman eligible for this group was approached for enrollment. To avoid a disproportionately large representation from any one site, enrollment from a single site was limited to 25% of the sample.
While in the hospital, the clinical site research coordinator interviewed participants for ethnicity, marital and living status, and education level. During the initial interview, women were asked to recall if they experienced urinary incontinence before or during pregnancy. At 6 weeks and 6 months postpartum, participants were interviewed by telephone by the research coordinator using validated questionnaires. Research coordinators from each clinical site received training and certification in telephone interview procedures from the Central Interviewing Facility at the University of Michigan.
Fecal incontinence was assessed with the Fecal Incontinence Severity Index20 and the modified Manchester Health Questionnaire.21,22 The Fecal Incontinence Severity Index assesses the frequency of four symptoms (incontinence of gas, mucus, liquid stool, and solid stool) using the following scale: 2 or more times a day, once a day, 2 or more times a week, once a week, 1–3 times per month, or never. The Manchester Health Questionnaire is a 31-item condition-specific quality-of-life scale that was modified and validated by the Pelvic Floor Disorders Network to use American rather than British terms.22
Fecal incontinence was defined as any involuntary leakage of mucus, liquid stool, or solid stool on the Fecal Incontinence Severity Index. Incontinence of flatus was reported separately from fecal incontinence. The first question of the Manchester Health Questionnaire, “How often do you have a strong desire to move your bowels, which makes you rush to the toilet?” assesses fecal urgency and was considered affirmative if the woman gave a response of “sometimes,” “often,” or “always.” The entire Manchester Health Questionnaire was administered to women with fecal urgency or any fecal or flatal incontinence on the Fecal Incontinence Severity Index.
Urinary symptoms were measured using the Medical, Epidemiological, and Social Aspects of Aging Questionnaire,23 which includes 15 items, 9 for stress incontinence symptoms and 6 for urgency and urge incontinence. Medical, Epidemiological, and Social Aspects of Aging Questionnaire responses included 0=never, 1=rarely, 2=sometimes, and 3=often. Urinary incontinence was defined by a response of “sometimes” or “often” to any of the Medical, Epidemiological, and Social Aspects of Aging Questionnaire questions.
Sample size was determined a priori to test the primary hypothesis that women in the Sphincter Tear group would have more fecal incontinence than women in the Vaginal Control group. With 400 participants per group, power was at least 80% to identify a difference when fecal incontinence in the Vaginal Control group was less than half that of the Sphincter Tear group, provided fecal incontinence prevalence in the Sphincter Tear group was at least 11%. Urinary incontinence prevalence was not expected to differ between the two vaginal delivery groups. We included 100 women in the Cesarean Control group to assess whether fecal incontinence in the Vaginal Control group was similar to that in women delivered by cesarean. This sample size was based on the estimated number of women with cesarean deliveries without labor who could be recruited during the study. The study was not powered to identify differences between the Cesarean Control group and the Vaginal Control group.
Fecal incontinence and urinary incontinence prevalence and their 95% confidence intervals (CI) at 6 weeks and 6 months postdelivery were estimated using unadjusted estimates. Because the groups differed by demographic factors, comparisons between groups were adjusted for age, race, and clinical site.
The primary interest in the study was the estimation of prevalence at 6 weeks and 6 months after delivery. Therefore, when the outcome measure was dichotomous, the groups were compared at each time point (6 weeks and 6 months) by a Mantel-Haenszel χ2 statistic adjusted for age group (25 years or less, 25–34 years, 35 years or more), race (white, African American, other), and clinical site. Adjusted odds ratios (AOR) and their 95% CIs are presented. When the outcome measure was continuous or ordinal, the groups were compared by analysis of covariance adjusted for age as a continuous variable and race and site as categorical variables. Results are presented as mean±standard deviation (SD) or as a percentage. All tests were two-tailed using an alpha of 0.05.
A total of 921 women participated in this study; 407 in the Sphincter Tear cohort, 390 in the Vaginal Control cohort, and 124 in the Cesarean Control cohort. Of these, 837 (91%) completed interviews at 6 weeks, 759 (82%) at 6 months, and 728 (79%) provided data at both time points. Rates for completed interviews at 6 weeks and 6 months did not differ significantly between cohorts. However, in the Vaginal Control group only, women who did not complete the 6-month interview were younger (mean 23.1 versus 26.4 years old, P<.001), less likely to be married (29.4% versus 60.5%, P=.001), and less likely to have any college education (49.3% versus 67.4%, P=.004) than those who completed this interview. Differences between participants and nonparticipants in the other two cohorts were small and not statistically significant.
Descriptive characteristics of the women are presented by cohort in Table 1. The Sphincter Tear group differed significantly from the Vaginal Control group in age, race, marital status, and education. Forceps were used in 30% of the Sphincter Tear deliveries compared with 6% of the Vaginal Control deliveries (P<.001); vacuum was used in 25% and 10% of the deliveries, respectively (P<.001). Episiotomy was performed in 52% of the Sphincter Tear deliveries, compared with 26% of the Vaginal Control deliveries (P<.001). Most episiotomies (91%) were midline; the ratio of the number of midline to mediolateral episiotomies did not differ by group. Women in the Sphincter Tear group had longer second-stage labor (1.9±1.4 versus 1.4±1.1 hours, P<.001) and gave birth to larger infants (3,560±444 versus 3,358±417 g, P<.001), compared with women in the Vaginal Control group.
Prevalence of fecal incontinence after childbirth is presented for the three cohorts in Tables 2 and 3. At both 6 weeks and 6 months postpartum, women in the Sphincter Tear group were more likely to report fecal incontinence, flatal incontinence, and fecal urgency than Vaginal Controls. At both time points, women in the Sphincter Tear group also reported more severe fecal incontinence than Vaginal Controls. The attributable risk to the sphincter tear at 6 weeks was 15.4% and at 6 months was 8.8%.
Vaginal Controls did not report symptoms more often than Cesarean Controls; in fact, after adjusting for age, race, and site, Cesarean Controls were as likely as Vaginal Controls to report flatal incontinence and fecal urgency when queried 6 months postpartum.
Only 9.5% of women in the Sphincter Tear, 3.3% in the Vaginal Control, and 2.1% in the Cesarean Control cohorts reported fecal incontinence both at 6 weeks and at 6 months postpartum. Thus, more than 65% of the women who reported fecal incontinence at 6 weeks did not report fecal incontinence at 6 months postpartum (ie, they recovered fecal continence); and over 45% of the women indicating fecal incontinence at 6 months did not report fecal incontinence at 6 weeks (ie, they were new-onset cases).
At both time points, most of the women (all but two) in the Vaginal and Cesarean Control groups who reported any type of fecal incontinence indicated that it occurred at a frequency of one to three times per month. Of women in the Sphincter Tear group who reported liquid or solid stool loss, fewer than one in four reported a symptom frequency greater than one to three times per month. Flatal incontinence occurred at a much higher frequency across cohorts. Among women reporting flatal incontinence, symptoms occurred once a week or more in about one third of women, but fewer than one in five women reported symptoms daily.
In the Sphincter Tear group, 320 women (79%) had third-degree tears (ie, perineum through anal sphincter) and 87 women (21%) had fourth-degree tears (ie, perineum through anal sphincter and rectal mucosa). Compared with women with third-degree tears, those with fourth-degree tears reported higher prevalence of fecal incontinence at 6 weeks (39% versus 23%, P=.005) and at 6 months (26% versus 15%, P=.02), more fecal urgency at 6 weeks (49% versus 34%, P=.02) and at 6 months (43% versus 29%, P=.02), and a higher fecal incontinence severity score at 6 weeks (9.0±10.7 versus 5.1±7.0, P=.003) and at 6 months (6.2±8.9 versus 3.2±5.5, P=.009).
Clinical sites were compared for differences in the rate of fecal incontinence and the proportion of fourth- to third-degree tears. Differences in the rate of fecal incontinence were not statistically significantly across sites. Average rate of fecal incontinence across all sites in the Sphincter Tear group at 6 months postpartum was 17% and ranged from 5% to 28%, P=.07. The proportion of fourth-degree tears did differ statistically across sites, ranging from 9% to 42% percent, P=.02.
Only 8 women (0.9%) recalled having urinary incontinence before pregnancy (Table 1). Urinary incontinence during pregnancy was reported by 19.2% of the women in the Sphincter Tear cohort, 18.7% in the Vaginal Control cohort, and 22.6% in the Cesarean Control cohort. Urinary incontinence prevalence and severity at 6 weeks and 6 months postpartum are presented by cohort in Tables 4 and 5. Women in the Sphincter Tear and Vaginal Control cohorts had similar rates and severity of urinary incontinence at 6 weeks and 6 months postpartum (adjusted P=.76 and 0.66, respectively). Urinary incontinence was reported at both time points by 21.3%, 21.6%, and 13.5% of the women in the Sphincter Tear, Vaginal Control, and Cesarean Control cohorts. Therefore, of the women indicating urinary incontinence at 6 weeks, about 40% did not report urinary incontinence at 6 months, and conversely, about one third of the urinary incontinence reported at 6 months was in women who did not report urinary incontinence at 6 weeks.
Compared with the Cesarean Control cohort, the Vaginal Control cohort had higher urinary incontinence prevalence at 6 weeks and 6 months postpartum, but the differences were not statistically significant after controlling for age, race, and clinical site (Table 4). At 6 months postpartum, only the difference in urge urinary incontinence between the Vaginal Control and Cesarean Control attained marginal statistical significance (adjusted P=.04).
This study prospectively characterized bowel and urinary continence status in primiparous women delivered at term in the United States. The results show that women who sustained anal sphincter tears during vaginal delivery had twice the risk of fecal incontinence postpartum compared with women who delivered vaginally without observed sphincter injury. Further, the women who sustained sphincter tears reported significantly more severe fecal incontinence, and differences persisted over the 6 months postpartum. The prevalence of fecal incontinence is similar to that reported by other studies15,24–26 and is substantial, given the degree to which fecal incontinence impacts self-esteem and well-being.
Although some authors include flatal incontinence in the definition of fecal incontinence,1 thus including leakage of all bowel contents, we chose to categorize incontinence of gas separately. Leakage of gas is fairly common in both men and women,27 and indeed, a sizeable proportion of women in all three study groups (18–27%) reported flatal incontinence, which persisted at 6 months postpartum. Although we found significantly more flatal incontinence in women with sphincter tears, the differences were more modest than those of other studies, in which women with sphincter tears had twice the rate of flatal incontinence or greater, compared with those without tears.14,15 In this study, we excluded women who recalled leakage of stool before pregnancy but not those who reported leakage of gas. Therefore, it is unlikely that all cases of flatal incontinence were attributable to childbirth.
Women who sustained sphincter tears also reported more fecal urgency, another bothersome bowel symptom, compared with women who delivered vaginally without tears. However, somewhat surprisingly, 6 months postpartum, women in the Cesarean Control group were as likely to report fecal urgency as Vaginal Controls, even after adjusting for confounders. This differs from a previous study of primiparous women, in which a greater proportion reported fecal urgency after vaginal delivery than after cesarean delivery (7.3% versus 3.1%).28 Our rates are higher than those of this previous study, likely due to different definitions of fecal urgency.
When performed before labor, cesarean delivery protects against anal sphincter tear, and small studies have found that women who delivered via cesarean did not report fecal incontinence postpartum.29,30 Cesarean delivery after active labor, even in the absence of attempted vaginal delivery, can lead to pudendal nerve injury and fecal incontinence symptoms.29,31 In this study, however, women in the Cesarean Control group did not labor, and some still developed fecal incontinence. Indeed, the prevalence of fecal incontinence in women who delivered by cesarean was similar to that of women who delivered vaginally without a sphincter tear, as has been shown in other studies.24,32 Because women with prepregnancy fecal incontinence were excluded, symptoms that developed after delivery can only be attributed to physiological effects of pregnancy and the postpartum period or the mechanical effects of abdominal delivery. Based on our findings in the Cesarean Control group, it would appear that changes during pregnancy itself may be responsible for some cases of postpartum fecal incontinence. Differences between groups may become more marked with time. We know that postpartum urinary incontinence, even when transient, is a strong predictor of urinary incontinence in the future.33 Whether this is true for fecal incontinence remains to be seen. Vaginal delivery is associated with more neuromuscular damage than cesarean delivery,34 but continence may be maintained, at least in the short term, through compensatory mechanisms such as levator muscle tone. The deterioration of these compensatory mechanisms as a result of aging, menopause, or metabolic disease may result in a delayed presentation of fecal incontinence secondary to sphincter tear and in a greater prevalence of fecal incontinence later in life.
Theoretically, in addition to predisposing to fecal incontinence, anal sphincter tear could directly predispose women to urinary incontinence. Alternatively, it may be a marker for a more difficult delivery and its associated damage to surrounding nerves, connective tissue, and muscle. Some studies have shown that cesarean delivery protects women from developing urinary incontinence.35,36 However, consistent with one report,37 we did not find a statistically significant difference in symptoms of urinary incontinence between any of the three groups at 6 weeks or 6 months postpartum. This may be because the anterior compartment is protected from denervation and connective tissue disruption when the posterior portion tears into the rectum. It may also reflect a lack of power to find a statistically significant difference between the Cesarean Control and Vaginal Control groups because the study was not originally powered to detect such differences. However, given the scant data available about pelvic floor outcomes in women who delivered by cesarean without labor, our data do contribute information to this void.
One limitation of this study is that the Fecal Incontinence Severity Index,20 which was used to assess fecal incontinence symptoms, was validated originally in an older, nonobstetric population, and its validity has not yet been established in younger women with postpartum incontinence.38 Another limitation is that the short follow-up prevents us from drawing any conclusions about the long-term impact of sphincter tear or the impact of further deliveries on fecal incontinence and urinary incontinence. Although we found that these conditions resolved for many women between 6 weeks and 6 months, a sizeable number of women reported fecal incontinence for the first time at 6 months. In a previous study, the prevalence of anal incontinence in women who sustained anal sphincter tears increased from 17% at 3 months postpartum to 42% 2–4 years postpartum.39 In other studies, a second or third vaginal delivery significantly increased the risk of anal incontinence, even in women without a recognized sphincter defect.40,41 Further, transient fecal incontinence after delivery appears to be a risk factor for permanent fecal incontinence.42 These issues can only be resolved in studies with long-term follow-up.
We did not find differences between cohorts for the number of completed interviews at either time point. However, we did observe demographic differences between women in the Vaginal Control group who did and those who did not complete the 6 month interview (age, marital status, education level). Women who participated in the 6-month interview were more likely to be older, married, and have more education. This made the women in the Vaginal Control group who participated in the 6-month interview more similar demographically to the women in the Sphincter Tear group and, as such, may have reduced differences in the rates of incontinence between the groups.
We did not design this study to determine whether the occurrence of sphincter tears differed between sites. However, we did observe a wide range in the proportions of fourth-degree sphincter tears (9–42%) in the Sphincter Tear group across sites. This study was not designed to identify factors that may have contributed to the observed differences in the tear severity. In addition, although we attempted to abstract information about the actual sphincter repairs (such as suture type, number of sutures, and technique), these data were often incompletely recorded by the delivering obstetricians. We are, therefore, unable to comment on whether rates of fecal continence depend on the nature of repair. However, given the large number of obstetric providers involved in the care of our subjects, our results are likely to reflect the “real world.”
In conclusion, despite the fact that clinically observed anal sphincter tears are repaired at the time of delivery, women who sustain such tears have twice the risk of fecal incontinence as women who deliver vaginally without clinically recognized sphincter tears. It is important to note that, although the fecal incontinence may result from the sphincter tear itself, it may also be caused by other factors more common in women with a sphincter tear, such as forceps or vacuum deliveries, birth weight, and length of second stage. However, from a clinical point of view, the important message is that anal sphincter tear is a marker for increased risk of fecal incontinence, a condition that may significantly impact the lives of young women. The postpartum examination is an ideal time for physicians to target in-depth questions about bowel function to their patients who sustained an anal sphincter tear and offer appropriate interventions to those with symptoms. Such interventions include pelvic floor muscle exercises, changing dietary or fluid intake, adding bulking agents or constipating agents, and occasionally, revising the surgical repair. We have some data that suggest that antenatal pelvic floor muscle exercises may reduce postpartum urinary incontinence; further research is needed to expand on this and to determine whether postpartum fecal incontinence can similarly be prevented.43
Finally, although our study was not powered to analyze differences between urinary or fecal incontinence in women delivering by cesarean compared with those delivered vaginally, it is clear from these data that women delivering by cesarean before labor also have a substantial level of symptoms. Patients should not be counseled that cesarean delivery before labor is completely protective against pelvic floor disorders.
1. Nelson R, Norton N, Cautley E, Furner S. Community-based prevalence of anal incontinence. JAMA 1995;274:559–61.
2. Bharucha AE, Zinsmeister AR, Locke GR, Seide BM, McKeon K, Schleck CD, et al. Prevalence and burden of fecal incontinence: a population-based study in women. Gastroenterology 2005;129:42–9.
3. Dey AN. Characteristics of elderly nursing home residents: data from the 1995 National Nursing Home Survey. Advance Data from vital and health statistics; no. 289. Hyattsville (MD): National Center for Health Statistics; 1997. Available at: http://www.cdc.gov/nchs/data/ad/ad289.pdf
. Retrieved June 20, 2006.
4. Norton C, Whitehead WE, Bliss DZ, Metsola P, Tries J. Conservative and pharmacological management of faecal incontinence in adults. In: Third International Consultation on Incontinence. Bristol (UK): International Continence Society; 2005.
5. Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal-sphincter disruption during vaginal delivery. N Engl J Med 1993;329:1905–11.
6. Fenner DE, Genberg B, Brahma P, Marek L, DeLancey JO. Fecal and urinary incontinence after vaginal delivery with anal sphincter disruption in an obstetrics unit in the United States. Am J Obstet Gynecol 2003;189:1543–9.
7. Fitzpatrick M, Behan M, O'Connell PR, O'Herlihy C. A randomized clinical trial comparing primary overlap with approximation repair of third-degree obstetric tears. Am J Obstet Gynecol 2000;183:1220–4.
8. Haadem K, Dahlstrom JA, Lingman G. Anal sphincter function after delivery: a prospective study in women with sphincter rupture and controls. Eur J Obstet Gynecol Reprod Biol 1990;35:7–13.
9. Haadem K, Ohrlander S, Lingman G. Long-term ailments due to anal sphincter rupture caused by delivery-a hidden problem. Eur J Obstet Gynecol Reprod Biol 1988;27:27–32.
10. Angioli R, Gomez-Marin O, Cantuaria G, O'Sullivan MJ. Severe perineal lacerations during vaginal delivery: the University of Miami experience. Am J Obstet Gynecol. 2000;182:1083–5.
11. Signorello LB, Harlow BL, Chekos AK, Repke JT. Midline episiotomy and anal incontinence: retrospective cohort study. BMJ 2000;320:86–90.
12. Crawford LA, Quint EH, Pearl ML, DeLancey JO. Incontinence following rupture of the anal sphincter during delivery. Obstet Gynecol 1993;82:527–31.
13. Zetterstrom JP, Lopez A, Anzen B, Dolk A, Norman M, Mellgren A. Anal incontinence after vaginal delivery: a prospective study in primiparous women. Br J Obstet Gynaecol 1999;106:324–30.
14. Brown JS, Nyberg LM, Kusek JW, et al. Proceedings of the National Institute of Diabetes and Digestive and Kidney Diseases International Symposium on Epidemiologic Issues in Urinary Incontinence in Women. Am J Obstet Gynecol 2003;188:S77–S88.
15. Foldspang A, Hvidman L, Mommsen S, Nielsen JB. Risk of postpartum urinary incontinence associated with pregnancy and mode of delivery. Acta Obstet Gynecol Scand 2004;83:923–7.
16. Vandoninck V, Bemelmans BL, Mazzetta C, Robertson C, Keech M, Boyle P, et al. The prevalence of urinary incontinence in community-dwelling married women: a matter of definition. BJU Int 2004;94:1291–5.
17. Hunskaar S, Lose G, Sykes D, Voss S. The prevalence of urinary incontinence in women in four European countries. BJU Int 2004;93:324–30.
18. Andersson G, Johansson JE, Garpenholt O, Nilsson K. Urinary incontinence-prevalence, impact on daily living and desire for treatment: a population-based study. Scand J Urol Nephrol 2004;38:125–30.
19. Wagner TH, Hu TW. Economic costs of urinary incontinence in 1995. Urology 1998;51:355–61.
20. Rockwood TH, Church JM, Fleshman JW, Kane RL, Mavrantonis C, Thorson AG, et al. Patient and surgeon ranking of the severity of symptoms associated with fecal incontinence: the Fecal Incontinence Severity Index. Dis Colon Rectum 1999;42:1525–32.
21. Bug GJ, Kiff ES, Hosker G. A new condition-specific health-related quality of life questionnaire for the assessment of women with anal incontinence. BJOG 2001;108:1057–67.
22. Kwon S, Visco AG, Fitzgerald MP, Ye W, Whitehead WE. Validity and reliability of the Modified Manchester Health Questionnaire in assessing patients with fecal incontinence. Dis Colon Rectum 2005;48:323–31.
23. Herzog AR, Diokno AC, Brown MB, Normolle DP, Brock BM. Two-year incidence, remission, and change patterns of urinary incontinence in noninstitutionalized older adults. J Gerontol 1990;45:M67–74.
24. Lal M, Mann CH, Callender R, Radley S. Does cesarean delivery prevent anal incontinence? Obstet Gynecol 2003;101:305–12.
25. Donnelly V, Fynes M, Campbell D, Johnson H, O'Connell PR, O'Herlihy C. Obstetric events leading to anal sphincter damage. Obstet Gyencol 1998;92:955–61.
26. Donnelly VS, O'Herlihy C, Campbell DM, O'Connell PR. Postpartum fecal incontinence is more common in women with irritable bowel syndrome. Dis Colon Rectum 1998;41:586–9.
27. Hall W, McCracken K, Osterweil P, Guise JM. Frequency and predictors for postpartum fecal incontinence. Am J Obstet Gynecol 2003;188:1205–7.
28. Chaliha C, Kalia V, Stanton SL, Monza A, Sultan AH. Antenatal prediction of postpartum urinary and fecal incontinence. Obstet Gynecol 1999;94:689–94.
29. Fynes M, Donnelly VS, O'Connell R, Herlihy C. Cesarean delivery and anal sphincter injury. Obstet Gynecol 1998;92:496–500.
30. Abramowitz L, Sobhani I, Ganansia R, Vuagnat A, Benifla JL, Darai E, et al. Are sphincter defects the cause of anal incontinence after vaginal delivery? Results of a prospective study. Dis Colon Rectum 2000;43:590–6.
31. Schraffordt Koops SE, Vervest HAM, Oostvogel HJM. Anorectral symptoms after various modes of vaginal delivery. Int Urogynecol J 2003;14:244–9.
32. MacLennan AH, Taylor AW, Wilson DH, Wilson D. The prevalence of pelvic floor disorders and their relationship to gender age, parity and mode of delivery. BJOG 2000;107:1460–70.
33. Viktrup L, Lose G. The risk of stress incontinence 5 years after the first delivery. Am J Obstet Gynecol 2001;185:82–7.
34. Allen RE, Hosker GL, Smith AR, Warrell DW. Pelvic floor damage and childbirth: a neurophysiological study. Br J Obstet Gynaecol 1990;97:770–9.
35. Rortveit G, Daltveit AK, Hannestad YS, Hunskaar S. Urinary incontinence after vaginal delivery or Cesarean section. N Engl J Med 2003;48:900–7.
36. Chiarelli P, Brown W, McElduff P. Leaking urine: prevalence and associated factors in Australian women. Neurourol Urodyn 1999;18:567–71.
37. Wagenius J, Laurin J. Clinical symptoms after anal sphincter rupture: a retrospective study. Acta Obstet Gynecol Scand 2003;82:246–50.
38. Cockell SJ, Oates-Johnson T, Gilmon DT, Vallis TM, Turnbull GK. Postpartum flatal and fecal incontinence quality of life scale: a disease- and population-specific measure. Qual Health Res 2003;13:1132–44.
39. Tetzschner T, Sorensen M, Lose G, Christiansen J. Anal and urinary incontinence in women with obstetric anal sphincter rupture. Br J Obstet Gynaecol 1996;103:1034–40.
40. Ryhammer AM, Bek KM, Laurberg S. Multiple vaginal deliveries increase the risk of permanent incontinence of flatus and urine in normal premenopausal women. Dis Colon Rectum 1995;38:1206–9.
41. Faltin DL, Sangalli MR, Roche B, Floris L, Boulvain M, Weil A. Does a second delivery increase the risk of anal incontinence? BJOG 2001;108:684–8.
42. Bek KM, Laurberg S. Risks of anal incontinence from subsequent vaginal delivery after a complete obstetric anal sphincter tear. Br J Obstet Gynaecol 1992;99:724–6.
43. Hay-Smith J, Herbison P, Morkved S. Physical therapies for prevention of urinary and faecal incontinence in adults (Cochrane Review). In: The Cochrane Library, Issue 2, 2002. Oxford: Update Software.
Pelvic Floor Disorders Network Members
© 2006 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved.
- University of Alabama at Birmingham: Holly E. Richter, PhD, MD, Principal Investigator, Kathryn L. Burgio, PhD, Co-Principal Investigator, Patricia S. Goode, MD, Co-Investigator, R. Edward Varner, MD, Co-Investigator, Velria Willis, RN, BSN, Research Coordinator.
- Baylor College of Medicine: Paul M. Fine, MD, Principal Investigator Rodney A. Appell, MD, Co-Principal Investigator, Peter K. Thompson, MD, Co-Investigator, Peter M. Lotze, MD, Co-Investigator, Naomi Frierson, Research Coordinator.
- University of Iowa: Ingrid Nygaard, MD, Principal Investigator, Debra Brandt, RN, Research Coordinator, Denise Haury, RN Research Coordinator, Karl Kreder, MD, Co-Investigator, Catherine Bradley, MD, Co-Investigator, Satish Rao, MD, Co-Investigator.
- Johns Hopkins Medical Institutes: Geoffrey Cundiff, MD, Principal Investigato, Victoria Handa, MD, Co-Investigator, Robert Gutman, MD, Co-Investigator, Mary Elizabeth Sauter, NP, Research Coordinator, Jamie Wright, MD, Co-Investigator.
- Loyola University, Maywood: Linda Brubaker, MD, Principal Investigator, Mary Pat Fitzgerald, MD, Co-Principal Investigator, Kimberly Kenton, MD, Co-Investigator, Dorothea Koch, RN, Research Coordinator, Charity Ball, RN, Research Coordinator.
- University of North Carolina at Chapel Hill: Anthony G. Visco, MD, Principal Investigator, AnnaMarie Connolly, MD, Co-Investigator, John Lavelle, MD, Co-Investigator, Mary J. Loomis, RN, Research Coordinator, Anita K. Murphy, NP, Research Coordinator, Ellen C. Wells, MD, Co-Investigator, William E. Whitehead, PhD, Co-Investigator.
- University of Pittsburgh/Magee-Womens Hospitals: Halina Zyczynski, MD, Principal Investigator, Diane Borello-France, PhD, Co-Investigator, Judy A. Gruss, BS, MS, Research Coordinator, Wendy Leng, MD, Co-Investigator, Pamela A. Moalli, MD, PhD, Co-Investigator, Elizabeth Sagan, MD, Co-Investigator, Arnold Wald, MD, Co-Investigator.
- Data Coordinating Center, University of Michigan: Morton B. Brown, PhD, Principal Investigator, John T. Wei, MD, MS, Co-Principal Investigator, Beverley Marchant, RN, Project Manager, John O. L. DeLancey, MD, Co-Investigator, Nancy K. Janz, PhD, Co-Investigator, Dean G. Smith, PhD, Co-Investigator, Patricia A. Wren, PhD, Co-Investigator, Li Peng, M.S., Statistician, James Imus, M.S., Statistician, Yang Wang Casher, MS, Database Programmer.
- Steering Committee Chairman: Robert Park, MD.
- NICHD Project Scientist: Anne M. Weber, MD, MS