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.
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.
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Pelvic Floor Disorders Network Members
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