Of the spectrum of pelvic floor disorders with the most profound effect on quality of life in the postpartum period, fecal and anal incontinence are arguably most disruptive. Fecal incontinence is the complaint of involuntary loss of solid or liquid feces and anal incontinence includes the complaint of involuntary loss of feces or flatus. What is often overlooked in considering these issues is fecal urgency with or without incontinence, including the sudden compelling desire to defecate that is difficult to defer [4]. The most common cause of these disorders in young women is anal sphincter injury at childbirth. The prevalence of anal incontinence reported in the literature among women with sphincter injuries ranges from 20 to 50 % reporting some sort of anal incontinence symptoms in the near postpartum period [5–7]. Anal incontinence can occur in up to one-third of women with obstetrical sphincter injuries with immediate or delayed onset of symptoms [8]. Because of occult injury, the incidence of anal sphincter damage at the time of vaginal delivery is higher than the number of observed injuries would suggest. Overt anal sphincter injury is relatively rare in women without episiotomy or operative vaginal delivery, with an incidence that ranges from 0 to 6.4 % [8–11]. The incidence of occult anal sphincter laceration identified by ultrasonography, ranges from 6.8 to 44 % in parous women [7, 12]. Additionally, data from a large US population-based study indicated that 29.3 % of postpartum women suffer from fecal incontinence (including flatus) when assessing for immediate postpartum symptoms and one in five of these women had undergone a cesarean delivery [13]. Clearly, this is a multifactorial problem that is prevalent not only with vaginal delivery but also with the cesarean delivery population.

In differentiating fecal or flatal incontinence, a systematic review of comparative studies-with short term follow up, showed that anal incontinence was increased after spontaneous vaginal delivery as compared to cesarean delivery (OR: 1.32; 95 % CI 1.04–1.68). However, the risk of severe anal incontinence was not significantly increased between these two groups, even though there was a trend towards more symptoms in the vaginal delivery group [14]. Likewise, in a longitudinal cohort study of women 5–10 years after their first delivery, there was no significant difference in anal incontinence symptoms in women who had been delivered by cesarean compared to those with spontaneous or instrumented delivery [15].

Episiotomy and operative vaginal delivery increase the incidence of severe pelvic floor trauma, yet were performed in 29 % and 9 % of vaginal births, respectively, in 2001 [16, 17] A meta- analysis of six randomized trials compared restrictive to liberal use of episiotomy in 4,850 women concluded that liberal use of episiotomies conferred no benefit and was associated with other complications [18]. Much of the incidence of OASIS depends upon the type of episiotomy performed. In these cases where mediolateral episiotomies are practiced, the rate of OASIS is 1.7 % in all comers and 2.9 % in primiparous patients [19]. Much higher rates are noted in those instances of midline episiotomy, at rates of 12 % for all comers [20] and 19 % in primiparous patients [21]. Operative vaginal delivery was similarly reviewed in 2,582 women and it was concluded that vacuum delivery was associated with a much lower risk of anal sphincter laceration than delivery with forceps (relative risk: .41; 95 % CI .33 to .50) [22]. Prevention of anal sphincter laceration and subsequent development of anal incontinence partly lies in decreasing the use of these interventions at the time of delivery.

While vaginal birth alone is not clearly a risk for fecal incontinence, OASIS increases the risk of subsequent fecal incontinence. Estimates range from 9 to 28 % [11, 23–25]. Likewise the risk of fecal incontinence is increased when there is a disruption of the internal anal sphincter, as compared to the external anal sphincter alone [26]. Although debilitating in younger life, studies of older women in their 50–60s, seem to eradicate the correlation of birth injury in explaining fecal incontinence. Most convincingly, a study of over 2600 women in their 50s demonstrated no significant difference between the prevalence of fecal incontinence between nulliparous, primiparous and multiparous women. These groups had fecal incontinence rates of 11.3 %, 9.0 %, and 10.4 % respectively. This similarity prevailed among parous women, irrespective of mode of delivery [27]. DeLeeuw et al. reported a retrospective cohort study of 125 matched pairs with median follow-up of 14 years after index delivery. Fecal incontinence was reported in 39 women with sphincter lacerations compared to 16 controls (OR: 3.1; 95 % CI 1.57–6.10) [28]. In an American cohort of sphincter injury patients followed at 6 months, the presence of fecal incontinence was associated with white race, antenatal UI, 4th- versus 3rd-degree sphincter tear, older age at time of delivery and higher BMI. There were no factors associated with fecal incontinence at the 6-month postpartum mark in the vaginal delivery group without OASIS or who had undergone a cesarean delivery [26].

The role of midline versus mediolateral episiotomy has been identified as a possible causal factor in explaining the higher rates of anal and fecal incontinence involved in an American cohort, where episiotomies, when performed are midline versus mediolateral. Careful evaluation of findings and subsequent outcomes need to assess this mechanism of OASIS versus that which occurs in the setting of mediolateral episiotomy [29].

In counseling patients for outcomes of primary repair, rates of fecal and anal incontinence vary greatly, not surprisingly, based on the variations in repair techniques, as well as the study design and the manner in which data was collected. A recent prospective study of 241 women at their first vaginal delivery, 59 of whom experienced OASIS, with subsequent repair with trained providers showed no fecal incontinence and no difference in flatal incontinence as compared to those women who had not had a sphincter disruption at 4 years postpartum [30]. What is most hopeful about this study, is that when evidence based protocols are established and implemented, not surprisingly, patient outcomes improve, and thus prognostic indicators improve as well.

In counseling women about future route of delivery, it appears that there is only a modest increase in risk for recurrent OASIS. A retrospective review of a large American cohort (n = 658) showed recurrent OASIS in only a small percentage of women at 3.2 %, with operative vaginal delivery and birth weight of ≥4000 g to be associated with recurrent OASIS [31]. This is consistent with a large Swedish cohort which although showed an increase of sixfold in incidence of sphincter rupture, the incidence was only 3 %. It was however somewhat lower than in another large studies (n = 774), which showed a rate that was still quite low at 7.5 % [21].

The role of vaginal birth as it leads to stress urinary incontinence is well established. The case for urgency incontinence is less so. Rates in the initial postpartum period vary, while 21 % of women are known to have urinary incontinence of some type within 10 weeks of delivery (Scheer). Prevalence of stress (SUI) and urgency (UUI) incontinence 5 years after first vaginal delivery has been shown to be 30 % and 15 % respectively with presence of symptoms at 3 months post-partum being predictive of more and longer lasting symptoms [32].

Most studies are short term in their follow-up, but in the observational analysis by Altman et al. women were followed 10 years out from their first delivery. They found that there were significant increases in stress as well as urgency symptoms at 10 years follow up compared with baseline compared with the 10 years preceding delivery. Most of those in the analyzed cohort experienced mild to moderate symptoms, with a five to six time increase in incidence of urinary incontinence episodes from the time of their first vaginal delivery [33]. Surrogates for perineal trauma did not correlate with the presence of incontinence 10 years after the first delivery, nor did repeat vaginal deliveries [33]. In an American cohort 5–10 years after vaginal or cesarean delivery, spontaneous vaginal birth was associated with a significantly greater odds of SUI (OR 2.9; 95 % CI 1.5–5.5) as compared to cesarean without labor [15]. These findings are not dissimilar to the large population study of Rortveit et al. which found 14.7 % of parous women having symptoms of SUI, as compared to 4.7 % of nulliparous women. In this cohort of greater than 15,000 women, a relative risk of 2.4 for developing SUI was noted, and the number of vaginal deliveries was of limited importance for the outcome as compared to that of the first vaginal delivery [34].

Predictors of postpartum urinary incontinence in several studies include leaking during pregnancy [35, 36] and predictors of incontinence at the 1 year mark, include persistent leakage 4–8 weeks postpartum [37]. Association of other factors with incontinence is worthy of investigation, with findings indicative of OASIS being associated with both pure urge and mixed incontinence. In a large American cohort of 943 women, urge incontinence alone was found in 16.2 % of women and mixed incontinence was found in 14.6 % of women. Stress symptoms were present in 21.3 % of women [38].

Assessments of persistence of urinary incontinence are difficult to obtain. In a longitudinal comparison of women undergoing spontaneous vagina delivery complicated by OASIS, vaginal delivery without OASIS and cesarean delivery without labor of all of the women reporting urinary incontinence at 6 weeks, about 40 % did not report incontinence at 6 months, and about one-third of the urinary incontinence reported at 6 months was not in women who reported incontinence at the 6 week postpartum point [26].

Understanding the significant association is only a first step in the analysis. Further understanding of the structures involved and the mechanism by which the damage occurs can be helpful in assessing pathology and prognosis. In an analysis of primiparous stress incontinent versus continent women at 9–12 months postpartum, maximal urethral closure pressure was 25 % lower in stress incontinent women. In the same analysis comparing primiparous stress continent to nulliparous women, the two groups had similar values [39]. This points to sphincter function as a key component in the continence mechanism and a potential target for therapeutic interventions.

Additionally, primparous women with SUI are twice as likely to have visible LA defects compared to content primiparas [39]. However further analysis of this relationship showed that urethral function measured as a urodynamic variable did not differ in women with and without levator ani muscle injury. This is both frustrating and hopeful. It requires a careful analysis of the continence mechanism of urethral closure pressure and levator ani support, as after birth MUCP change may not necessarily accompany LA change or other anatomical change [40] Second, birth events that injure the LA do not necessarily limit a woman’s ability to augment MUCP with a Kegel effort in the postpartum period as well as later in life [40, 41].

It is well established that vaginal delivery leads to higher rates of levator ani damage particularly involving both the pubovisceral portion of the levator ani muscle [42]. In an assessment of 160 primiparous women, 32 of the 160 were found to have levator ani defects on MRI. These women with muscle defects were more likely to have had an a difficult delivery with an odds ratio of 14.7 for forceps delivery, 8.1 for anal sphincter rupture, 3.1 for episiotomy [43]. Later in life, these levator defects are more commonly found in women with prolapse (55 %) as compared to normal controls (16 %), leading to an adjusted odds ratio of 7.3 for prolapse in those with a levator ani defect as compared to their counterparts without a muscle defect [1].

The consequences of levator ani injury in the short term are not completely clear other than those with a muscle defect were found to have weaker pelvic floor muscles in the 9–12 month postpartum period as compared to controls [39]. Birth related changes to the levator ani muscles persist in both function and structure with a significant amount of remodeling present in the course of normal postpartum healing. Analysis of the dynamic MRIs of those patients who had experience those factors putting them at risk for levator tear demonstrated that at rest diameters of the urogenital and levator hiatus were smaller on late scans (~7 months postpartum) compared with early scans (~1 month postpartum) by 7.7 and 3.2 mm respectively (p < .05) [44]. These findings were independent of the status of the levator muscles in this cohort. It was also demonstrated by Tunn et al., that the at rest locations of the perineal body, levator and urogenital hiatus locations improve greatly from the 1 day and 2 weeks postpartum mark [45]. This points to an aggressive early resolution of postpartum change in position, just in virtue of time, without any intervention. There was, however, no statistically significant difference in the ability to displace structures during Kegel and Valsalva in the comparison of 1 month and 7 month scans, showing that in this group there is little change in function of the muscles from the early to the later postpartum period [44].

In those patient who had undergone a vaginal delivery, pelvic floor muscle strength 6–11 years after vaginal delivery was similarly assessed with a significant reduction in both strength and duration of contraction in those who had undergone either spontaneous or assisted vaginal delivery. Further, among women with at least one vaginal delivery, pelvic muscle strength was lower among the women with a pelvic floor disorder as compared to those without (p = 0.12) This finding was additionally associated with the obstetric variables at delivery of macrosomia, perineal laceration, episiotomy, anal sphincter laceration, as well as the number of vaginal deliveries [46]. Further, 5–10 years after vaginal delivery an associate of prolapse to or beyond the hymen was found (OR: 5.6; 95 % CI 2.2–14.7) as compared to cesarean without labor [15].

Low back and pelvic pain (LBPP) is often reported during pregnancy and postpartum with rates of up to 70 % reported in the literature [47]. The prognosis as measured by the prevalence of LBPP in the postpartum period varies greatly. In one analysis, even at 3 years after giving birth, up to 20 % of women report that their symptoms have still persisted [48]. Another analysis also found a similar prevalence of LBPP of up to 20 % at 6 years postpartum [49], with serious pain affecting approximately 7 % of women at 18 months postpartum [50]. Clearly this is an often neglected but disabling condition facing women in pregnancy and the postpartum period.