Vaginal Birth and Pelvic Floor Disorder

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ISSN 1745-505710.2217/WHE.13.17 © 2013 Future Medicine Ltd Women's Health (2013) 9 (3), 265–277

Vaginal childbirth and pelvicfloor disorders

Hafsa U Memon*1

& Victoria L Handa1

Childbirth is an important event in a woman’s life. Vaginal childbirth is the most common mode

of delivery and it has been associated with increased incidence of pelvic floor disorders later in

life. In this article, the authors review and summarize current literature associating pelvic floor

disorders with vaginal childbirth. Stress urinary incontinence and pelvic organ prolapse are strongly

associated with vaginal childbirth and parity. The exact mechanism of injury associating vaginal

delivery with pelvic floor disorders is not known, but is likely multifactorial, potentially including

mechanical and neurovascular injury to the pelvic floor. Observational studies have identified

certain obstetrical exposures as risk factors for pelvic floor disorders. These factors often coexist

in clusters; hence, the isolated effect of these variables on the pelvic floor is difficult to study.

1Department of Gynecology& Obstetrics, Johns Hopkins School ofMedicine, MD, USA*Author for correspondence:

Tel.: +1 410 550 2787Fax: +1 410 550 [email protected]

Keywords

• levator ani muscle injury

• prolapse • urinary incontinence

• vaginal childbirth

REVIEW

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Release date: 3 May 2013; Expiration date: 3 May 2014

Learning objectives

Upon completion of this activity, participants should be able to:

•Describe risk factors for pelvic floor disorders following vaginal childbirth, based on a review

•Describe mechanisms of injury underlying pelvic floor disorders following vaginal childbirth, based

on a review

•Describe strategies for minimizing risk of pelvic floor disorders following vaginal childbirth, and

directions for future research, based on a review

Financial & competing interests disclosure

CME Author

Laurie Barclay, MD, Freelance writer and reviewer, Medscape, LLC

Disclosure: Laurie Barclay has disclosed no relevant financial relationships.

Hafsa U Memon, MD, Department of Gynecology & Obstetrics, Johns Hopkins School of Medicine, MD, USA

Disclosure: Hafsa Memon has disclosed no relevant financial relationships.

Victoria L Handa, MD, MHS, Department of Gynecology & Obstetrics, Johns Hopkins School of Medicine, MD, USA

Disclosure: Victoria L Handa has received support from the Eunice Kennedy Shriver National Institute of Child Health

and Human Development (R01HD056275).

Editor

Elisa Manzotti, Publisher, Future Science Group

Disclosure: Elisa Manzotti has disclosed no relevant financial relationships.

CME

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The term ‘pelvic floor disorders’ (PFDs) refersto stress urinary incontinence, overactive blad-der syndrome, pelvic organ prolapse and fecalincontinence. These disorders are prevalent inadult women. For example, in the USA, 24%of women are affected by one of these disorders,

with 16% of women experiencing urinary incon-tinence, 3% of women experiencing pelvic organprolapse and 9% of women experiencing fecalincontinence [1]. The prevalence of these condi-tions increases significantly with age: 10% ofwomen aged 20–39 years compared with 50%of women aged 80 years or older suffer from atleast one of these disorders [1]. The number of American women with at least one PFD is esti-mated to increase from 28.1 million in 2010 to43.8 million in 2050 [2]. The lifetime risk ofundergoing a single operation for prolapse or

incontinence by the age of 80 years in the USAis 11% [3], with a reoperation rate of 30%. Over225,000 women underwent prolapse operationsin the USA in 1997, making this one of the mostcommon indications for surgery in women [4].The financial burden of these disorders includesboth direct (routine care, medical visits and med-ical treatments) and indirect (loss of productiv-ity) costs. The cost of ambulatory care relatedto female PFDs is significant and is increasing.Using Medicare reimbursement to estimate med-ical care costs, the direct annual costs associatedwith ambulatory care for PFDs was estimated tobe US$412 million in 2006 [4]. This was almostdouble the direct annual cost of US$262 mil-lion in 1997. Due to the increasing prevalence ofPFDs, it is anticipated that these expenditures willcontinue to increase in the future. The estimatednational annual direct cost for surgical manage-ment of pelvic organ prolapse operations was overUS$1 billion in 1997 [5], while the annual directcost of surgical treatment of urinary incontinencewas US$1032 million in 1995 [6]. The annualdirect cost of surgical treatment for female fecalincontinence was US$24.5 million in 2003 [7].

Although severe morbidity from PFDs is rare,these patients score significantly worse on theprolapse, urinary and colorectal sca les and over-all score of pelvic floor distress inventory [8]. Inaddition, pelvic organ prolapse negatively affectswomen’s self-perception of their body image [9].Thus, PFDs are common and have significantpublic health impact.

Risk factors for PFDs

Various studies have identified age [1,10,11], vaginalchildbirth [12,13] and obesity [14,15] as risk factors

for PFDs. Other studies suggest that some PFDs

are associated with diabetes [16], connective tis-sue disorders [17] and neurological diseases [18–20].Some women have a genetic predisposition to thedevelopment of PFDs [21,22].

Given that the biological causes of PFDsremain uncertain, the study of the associa-

tion between childbirth and PFDs may offerimportant insights into the pathophysiologyof these disorders and may lead to the devel-opment of prevention strategies. In this review,the authors focus on the accumulating evidencelinking obstetrical events and the incidence ofPFDs later in life. Since stress urinary inconti-nence, fecal incontinence and prolapse are themore common PFDs, this review focuses on theassociation between these disorders and variousobstetrical variables.

It is important to note that, although vagi-

nal delivery appears to be the most importantpredisposing factor for PFDs, the evidence tosupport this finding is derived from observa-tional studies because randomized controlledtrials comparing different modes of deliveryand the number of deliveries are not feasiblefor various reasons (e.g., patient’s preferenceand the unpredictability of the labor course,among others).

Parity & PFDs

Several studies have shown that PFDs are morecommon in parous women compared with nul-liparous women of the same age, irrespectiveof the mode of delivery. Hansen et al . reportedthat urinary incontinence was three-times morecommon in primiparous women comparedwith their aged-matched nulliparous counter-parts [23]. The effect of parity is most notablein young women between the ages of 20 and34 years and disappears in women older than65 years [24]. Similarly, in a study of 4000 Turk-ish women, the prevalence of various PFDs wassignificantly higher in parous women comparedwith nulliparous women [25]. In one study, pri-

miparous women were at a twofold higher riskof pelvic organ prolapse compared with nullipa-rous women [26]. Parity is also associated withan increased risk of anal incontinence. In theNorthwestern twin-sister study, the risk of analincontinence was threefold higher in parouswomen compared with nulliparous women [27].

Among parous women, an increasing num-ber of childbirths further increases the risk ofPFDs. Kepenekci et al . reported an increase inthe risk of urinary incontinence and other pel-vic floor symptoms with increasing parity [25].

Increasing parity also leads to a linear increase

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in the probability of developing prolapse [26]. Ina British study, women with one child were four-times more likely, and those with two childrenwere 8.4-times more likely, to develop pelvicorgan prolapse when compared with nulliparouswomen [28]. Similarly, prevalence of fecal incon-

tinence increases with an increase in the numberof childbirths [1].

Mode of delivery & PFDs

Several studies support that the incidence ofPFDs varies with the mode of delivery. MacLen-nan et al. reported pelvic floor dysfunction in58% of women who had spontaneous vaginaldelivery, compared with 43% of those whounderwent cesarean section [12]. Increased prev-alence of PFDs have been noted in vaginallyparous women in the immediate postpartum

periods and at several years postpartum.In a recent study of parous women, history ofa vaginal childbirth was associated with twicethe risk of developing bothersome symptomsof stress incontinence compared with womendelivered exclusively via cesarean section [13].In contrast to this finding, the follow-up studyof the randomized, multicentered Term Breechtrial, which compared maternal outcomes2-years after planned cesarean section withplanned vaginal birth for breech presentationat term, showed no differences in the incidenceof urinary incontinence between the two deliv-ery groups (17.8% in the planned cesarean sec-tion group and 21.8% in the planned vaginalbirth group). In addition, there was no differ-ence in the degree of bother caused by urinaryincontinence between the two groups [29].

Vaginal childbirth that is complicated by analsphincter trauma has been linked to postpar-tum fecal incontinence. A history of third- andfourth-degree obstetric lacerations was identifiedas the only obstetrical risk factor for postpartumfecal incontinence in a recent systemic review[30]. However, in the absence of anal sphincter

trauma, vaginal delivery does not appear toincrease the risk of anal incontinence [31].

Several studies have linked vaginal childbirthto pelvic organ prolapse [13]. In one study, his-tory of a single vaginal delivery was associatedwith a tenfold increased likelihood of developingprolapse [32].

Compared with other PFDs, the associationbetween mode of delivery and overactive bladdersyndrome is not well established. For example, thelikelihood of overactive bladder syndrome doesnot differ significantly in women who underwent

vaginal or cesarean birth 5–10 years ago [13].

Other obstetrical events & interventions

Among vaginally parous women, observationalstudies have identified certain obstetrical fac-tors that may increase the risk of PFDs. Thesefactors include operative vaginal delivery,prolonged second stage of labor, fetal mac-

rosomia and perineal lacerations. These riskfactors often occur in clusters (F IGURE 1), andmay impact pelvic floor outcomes synergisti-cally. Urinary incontinence is common in theimmediate postpartum period and is morelikely to occur in women who had prolongedlabor in combination with operative vaginalbirth [33]. In addition, these variables may act asconfounders or effect modifiers for each other.For example, Brown et al . reported that mater-nal age and infant birth weight had a minimaleffect on incontinence rates after adjusting for

mode of delivery and duration of second-stagelabor [34].In summary, due to the clustering of some

putative risk factors for PFDs, it is impossible toattribute the risk to a single variable. Acknowl-edging this limitation, the sections that followreview the available evidence for the impact thatobstetrical factors have on the development ofPFDs among parous women.

Vaginal childbirth & pelvic floor disorders – REVIEW

6% (27)

5% (22)

6% (27)

2% (9)

12% (49)

7% (31)

7% (28)

ASLAC

20% (85)

OVD26% (108)

Prolonged secondstage 27% (113)

Figure 1. Clustering of obstetrical exposures in a population of418 primiparous women who delivered vaginally. There is substantial overlapin the occurrence of these characteristics, each of which may be associated withthe later development of pelvic floor disorders.ASLAC: Anal sphincter laceration; OVD: Operative vaginal delivery.Data taken from [13].© Johns Hopkins University, 2013.


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Operative vaginal delivery

‘Operative vaginal delivery’ or the ‘instrumen-tal vaginal delivery’ refers to the use of trac-tion devices to assist uterine contractions andmaternal expulsive efforts during the secondstage of labor to achieve delivery of the fetus.

Forceps and vacuums are the most commonlyused instruments for this purpose. Indicationsfor operative delivery include a prolonged secondstage of labor or the need to shorten the secondstage of labor due to nonreassuring fetal statusor maternal comorbidity [35], hence operativevaginal delivery can be a surrogate marker fordifficult labor.

Operative vaginal delivery significantlyincreases the risk of PFDs. In a cohort of par-ous women 5–10 years after delivery, history ofoperative vaginal delivery was associated with a

fourfold increase in the adjusted odds for stressurinary incontinence and overactive bladdersyndrome, while adjusted odds for prolapseincreased eightfold [36]. Risk of surgical interven-tion for stress urinary incontinence and prolapseis also higher after operative vaginal delivery. Forexample, the odds of surgical intervention forstress urinary incontinence is 20-times higherfor those who have experienced forceps-assisteddelivery compared with women who gave birthexclusively via cesarean [25,37]. Operative vaginaldelivery is also a risk factor for anal sphincterinjury, which is an independent risk factor forthe development of anal incontinence.

In a randomized controlled trial comparingmaternal outcomes after forceps versus vacuumdelivery, no difference was noted between for-ceps and vacuum delivery groups in terms ofvarious urinary and bowel symptoms at 5 yearspostpartum [38]. However, more recent studieshave shown that forceps-assisted vaginal deliveryis more likely to be associated with overactivebladder syndrome, prolapse [39], subclinicalsphincter defects and altered continence [40,41] compared with vacuum-assisted delivery.

Episiotomy & perineal laceration

Episiotomy is an incision on the female perineumthat is performed just prior to crowning of thefetal head to increase the diameter of pelvic out-let, thus expediting delivery of the fetus. It isone of the most common surgical proceduresexperienced by women [42]. A total of 30–35%of vagina l births include episiotomy in the USA[43], while 46% of low-risk nulliparous womenin the UK experience episiotomy [44].

Historically, episiotomy was introduced as a

strategy to prevent fetal trauma and maternal

perineal injury and its routine use gained popu-larity as it was endorsed by prominent obstetri-cians in the early 1900s [45,46]. However, researchon the relative benefits and harms of routine epi-siotomy has led to conflicting results. Early advo-cates of routine episiotomy argued that it protects

the mother’s perineum, resulting in better post-partum pelvic organ support [47,48]. However,high-quality evidence to support the practiceof routine episiotomy is lacking. In a systemicreview of 28 prospective studies looking at pelvicfloor outcomes after episiotomy, no differencewas found in symptoms of urinary incontinencebetween spontaneous laceration and episiotomygroups. In addition, episiotomy was not found tobe protective against fecal incontinence, prolapseor decreased pelvic floor muscle strength [49].

The use of routine episiotomy also started to

gain criticism with the appearance of literaturesuggesting a possible association between episi-otomy and third- and fourth-degree lacerations[50]. Helwig et al. showed that midline episiot-omy doubled the risk of third- and fourth-degreelacerations after controlling for neonatal birthweight and primiparity [51]. Handa et al . alsofound an association between episiotomy andfourth-degree laceration [52].

Anal sphincter laceration is an independentrisk factor for fecal incontinence. The prospectivemulticenter CAPS study showed that comparedwith women who underwent vaginal childbirthwithout observed injury to anal sphincter, womenwho had anal sphincter lacerations during vaginalchildbirth were twice as likely to develop postpar-tum fecal incontinence [13]. In addition, womenwith a sphincter laceration had greater severity offecal incontinence. More recently, in a prospectivecohort study of women who underwent vaginalchildbirth without injury to the anal sphincter,women who sustained an observed injury to theanal sphincter during childbirth are twice aslikely to develop postpartum fecal incontinence[13]. More than 90% of the episiotomies in this

population were midline.Mediolateral episiotomy has not been found

to increase the incidence of prolapse and urinaryand fecal incontinence compared with first- andsecond-degree spontaneous perineal lacerationsand intact perineum [53]. There is also evidencesuggesting a protective role of mediolateralepisiotomy against the development of central-support defects of the anterior vaginal wall [54].Hence the role of episiotomy as a risk factor ver-sus a protective factor for the development ofPFDs remains unknown, as was concluded by a

2005 systematic review [49].



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Another interesting and relevant subject isthe role of spontaneous lacerations in the devel-opment of PFDs and whether lacerations com-pared with episiotomy are less traumatic to theperinium. A retrospective cross-sectional surveyof women 12 months after vaginal childbirth

found no statistically significant differences inthe reported levels of urinary incontinence andother pelvic floor symptoms between womenwith an episiotomy and women with first- orsecond-degree perineal trauma. This study con-cluded that women with an episiotomy have sim-ilar perineal morbidity to those with a spontane-ously occurring laceration [55]. Milsom et al ., ina cohort study of singleton primiparous women20 years after childbirth, reported that neitherepisiotomy nor second-degree laceration wereassociated with an increased risk of symptomatic

pelvic organ prolapse[56]

. This is in contrast toa recent study that suggested a potential asso-ciation between spontaneous perineal lacerationand prolapse in vaginally parous women [13].

In summary, episiotomy and severe perineallacerations are both markers of a difficult child-birth, and they are often associated with clini-cal scenarios confounded with operative vaginalbirth, fetal macrosomia and a prolonged secondstage of labor. Most of the evidence is derivedfrom observational studies. It has been difficultto conduct a randomized controlled trial com-paring liberal use of episiotomy with restric-tive use of episiotomy and perineal lacerationsbecause of high rates of crossover in interven-tions between the groups [57]. Hence the role ofepisiotomy and spontaneous perineal lacerationwith respect to PFDs remains debatable andrequires further investigation.

Prolonged second stage of labor

The second stage of labor is characterized byprogressive descent of the fetal head through thecompletely dilated cervix. This is achieved by theexpulsive forces generated by uterine contrac-

tions. During these contractions, intrauterinepressure can be as high as 8 kPa. Maternal push-ing can further increase intrauterine pressure toas high as 19 kPa [58]. Ischemic necrosis of thepelvic tissues (including nerves and muscles) andstretch injuries, leading to permanent denerva-tion of the tissues, can occur if this pressurecontinues for an extended duration [59]. Thus,a prolonged second stage may increase soft tis-sue injury and neuromuscular damage to thepelvic floor. Both of these mechanisms may becentral to the pathophysiology of PFDs. This

finding is further supported by the suggestion

that prolonged pushing for more than 1 h dur-ing the second stage of labor is associated withdenervation injuries to the pelvis in primiparouswomen, whereas a passive second stage of labordoes not increase the risk for denervation injury[60]. Kearney et al . reported the increased prob-

ability of levator ani muscle defects with longerduration of the second stage of labor in primipa-rous women; these levator defects may be a riskfactor for later development of PFDs. However,in this study, the authors were unable to excludethe confounding effects of other obstetricalvariables because this study did not allow for amultivariate analysis [61].

Prolonged second stage of labor has beenidentified as a risk factor for postpartum urinaryincontinence in primiparous women [62]. A small Japanese study identified duration of the second

stage of labor of more than 30 min as a riskfactor for pelvic organ descent in primiparouswomen [63].

Prolonged second stage of labor has not beendirectly associated with fecal incontinence, butsome studies have shown an increase in inci-dence of third- and fourth-degree lacerationswith prolonged duration of second stage of labor[64]. As discussed above, these severe perineal lac-erations are risk factors for anal incontinence.This increase in severe perineal lacerations ismost likely a result of obstetric interventions,such as operative vaginal delivery, to manage theprolonged second stage of labor. Adjustment forthese factors has been shown to eliminate theassociation between prolonged second stage andanal sphincter injuries [65].

It is critical to understand that a prolongedsecond stage of labor is often associated withfetal macrosomia, occiput posterior position,operative vaginal delivery and the use of episi-otomy. Hence the observed association betweenPFDs and prolonged second stage of labor mayrepresent a combined effect of the above factors.

Fetus-related factorsSeveral studies have reported an associationbetween higher birth weights and postpartumurinary incontinence [66,67]. Viktrup et al . notedthat primiparous women who developed post-partum urinary incontinence had neonates witha greater head circumference; however, theseresults were not statistically significant [62].Computer simulations of vaginal delivery alsoreport a positive association between fetal headdiameter and stretch on the pubovisceral muscleof the levator ani muscle complex [68]. Larger

neonatal size and occiputposterior positions



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often coexist and synergistically increase therisk of perineal injury [60].

Maternal age

Delayed childbearing has been identified asa risk factor for PFDs in several studies. Kuh

et al . found a strong association between thesymptoms of stress urinary incontinence and amaternal age of 30 years or older at first vaginaldelivery among British women [69]. Foldspanget al . found increased risks of urinary inconti-nence with increasing age at the time of the lastchildbirth for women aged 30–44 years [70].Pregazzi et al . reported an association betweenurinary frequency and advanced maternal age[71]. The risk of requiring surgery for stress uri-nary incontinence and pelvic organ prolapse alsoappears to increase with increasing age at first

childbirth, irrespective of the mode of delivery.For example, in one study, 14% of the women30 years or older at first vaginal birth requiredsurgery for pelvic organ prolapse comparedwith 6% of women younger than 30 years [72].Rortveit and Hunskaar also noted an associa-tion between increased prevalence and severityof urinary incontinence in women with delayedchildbearing [73]. The trend toward delayedchildbearing in developed countries may resultin an increased prevalence of PFDs in comingdecades.

In summary, several obstetrical and non-obstetrical factors contribute to the associationbetween vaginal childbirth and PFDs. Thesefactors often coexist and the individual con-tribution of these variables may be difficult toassess. Our knowledge on this subject is basedon observational studies because randomizedtrials cannot control for some of the risk factorsdiscussed above.

Mechanism of obstetrical injury

Preservation of the function of pelvic visceradepends upon the interaction between the ana-

tomical as well as neurological integrity of theorgans and their support systems. For example,the maintenance of urinary continence dependson the anatomical and functional competence ofthe urethral sphincter and integrity of the ure-thral coaptation mechanism, as well as structur-ally and neurologically intact urethral supportsystem (levator muscles and endopelvic fascia,among others). Loss of any of these componentscan lead to incontinence. The trauma to thepelvic floor during childbirth that predisposeswomen to develop PFDs appears to be multifac-

torial, as shown in FIGURE 2. For example, vaginal

childbirth has been associated with an increasein urethral mobility, decreased leak point pres-sures [74] and injury to pelvic floor muscles [75].Mechanical injury to the pelvic floor supportsystem, denervation, ischemia and reperfusioninjury and defective soft tissue remodeling are

some of the underlying mechanisms of injury fordevelopment of PFDs.

Mechanical injury to the pelvic floor

Mechanical support to the pelvis is provided bythe muscles of the pelvic diaphragm, endopelvicfascia and its lateral condensations (arcus ten-dentious fascia pelvis and pelvic ligaments), andtheir bony attachments. The levator ani musclecomplex, which consists of the pubococcygeus,puborectalis and iliococcygeus muscles, is thelargest muscle of the pelvic floor and a critical

component of the pelvic floor support system.This muscle complex forms a U-shaped slingaround the urethra, distal vagina and rectum,thus providing support to these structures. Thenormal baseline activity of the levator ani musclekeeps the urogenital hiatus closed against theopening action of intra-abdominal pressure. Amaximum voluntary contraction of the levatorani muscles further increases the vaginal closureforce by 46%, leading to further compression ofthe rectum, distal vagina and urethra behind thepubic bone [76]. Damage to levator ani musclesmay lead to the widening of the urogenital hia-tus and downward descent of the pelvic organs.Several MRI [77] and ultrasound studies haveshown increased odds of levator ani muscleinjury in women with pelvic organ prolapse[78]. Increased prevalence of levator ani muscleinjury has also been shown in women with stressurinary incontinence [79].

Vaginal childbirth has been identified as arisk factor for levator injury. Overstretching anddamage to the levator muscle, particularly to thepubococcygeal muscle, which is the shortest andmost medial component of levator ani complex,

has been linked to vaginal delivery [68]. Opera-tive vaginal delivery further increases the risk oflevator ani injury [80].

. Increase in the incidence

of levator ani muscle injury has been listed as oneof the potential explanations for the observedassociation between older age at first birth andhigher incidence of PFDs. Dietz and Simpsonperformed 3D ultrasounds on vaginally parouswomen who presented with symptoms of PFDs. Women with evidence of levator muscle traumaon 3D ultrasounds were older than women with-out evidence of levator trauma (mean age: 25.5

vs 23.5 years) [81].



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Denervation injury

The pudendal nerve innervates the external

urethral and external anal sphincter, and henceplays an important role in maintaining conti-nence. Due to its relative superficial anatomi-cal location in the female pelvis, the pudendalnerve is at risk of injury during vaginal injury.Stretching and compression injury to the puden-dal nerve has been reported with 38–42% ofvaginal deliveries [82]. Concentric needle electro-myography in women with a history of vaginaldelivery has shown evidence of transient dener-vation of the pelvic floor [60]. The majority ofpelvic floor injuries are reversible and reinnerva-tion, as indicated by increased density of neuro-filaments, leads to the return of continence inthe postpartum period [83]. However, if there isa complete transaction or a severe crush injury tothe pudendal nerve, return of function may bedelayed [84]. Several studies (animal and human)have implicated childbirth injury to the puden-dal nerve as an etiology for postpartum urinaryand fecal incontinence. Kerns et al . developeda rat model to examine the effect of pudendalnerve crush injury on the structure and functionof the external urethral sphincter and noted thatthe crush lesion of the pudendal nerve induces

mild urinary incontinence [85]. Childbirth injuryto the pudendal nerve is also associated with sub-sequent fecal incontinence in women. In a studyof primiparous women who were undergoingevaluation for postpartum fecal incontinence,31% of the women had neurophysiologic evi-dence of pudendal nerve injury [82]. Tetzschneret al . reported that patients with pudendal nerveterminal motor latencies >2.0 ms had an 18%increased risk of having fecal incontinencecompared with patients with pudendal nerveterminal motor latencies ≤2.0 ms at 3 months

postpartum [86]. There is also some evidence that

increased pelvic pressure during the second stageof labor may lead to combined neurovascular

injury[87]

.Connective tissue remodeling

Defects in the endopelvic fascia have beenreported in patients with anterior vaginal wallprolapse and stress urinary incontinence. Rich-ardson et al . noted that separation of the endo-pelvic fascia from its lateral attachment to thepelvic side wall (i.e., paravaginal defect) resultsin urethral hypermobility, stress urinary incon-tinence and anterior vaginal wall descent [88].They reported excellent anatomic and functionaloutcomes when surgical repair was directedtowards closure of these defects [89]. DeLanceyalso noted the presence of paravaginal defectsin 91% of the patients undergoing retropubicsurgery for urinary incontinence or prolapse. Healso found that detachment of the arcus teten-dinous fascia pelvis from the ischial spine wasassociated with anterior vaginal wall descent [90].These studies highlight the important contribu-tion of the pelvic floor connective tissue in main-taining the structural and functional integrity ofthe pelvic floor.

The endopelvic fascia and other connective

tissue elements of the pelvic floor are at risk ofstretch and detachment from their bony attach-ments during childbirth. During pregnancy, thepelvic floor undergoes hormone-mediated physio-logical changes in its biomechanical properties,resulting in increased distensiblity of the vagina. Animal models have shown that the vaginal walland its supportive tissue complex is more disten-sible and less stiff during pregnancy [91]. This pro-cess is mediated by increased synthesis of collagenand elastin by fibroblasts. Collagen and elastin aretwo main components of the extracellular matrix

of the connective tissue. Collagen determines


Childbirth

Vaginal

deliveryOther risk factors(operative delivery and prolonged

second stage, among others)

Levatorinjury

Pelvic floor disorders

Pudendalnerve injury

Defects in softtissue remodeling

Othermechanisms

Figure 2. Multifactorial nature of obstetrical trauma leading to pelvic floor disorders.


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the tensile strength while elastin contributes totissues’ ability to stretch. Fibroblasts are sensi-tive to mechanical stretch and connective tissuesynthesis is proportional to the degree of stretch.Excessive stretching of the vaginal wall initiates adegradative response mediated by release of colla-

genases from activated fibroblasts. This results inincreased degradation of collagen, as well as otherconstituents of the vaginal wall. Thus, difficult orprolonged labor may exceed the stretch limits ofthe soft tissue, causing imbalance in the reparativeand degradative processes and increasing suscepti-bility of pelvic floor supportive structures to birthtrauma [92].

After delivery, there is substantial remodel-ing of the connective tissue components. This isaccomplished by an increase in collagen and elas-tin synthesis; however, the new tissue that results

from healing after childbirth is not as strong asthe original tissue that it replaces. Defects in theprocess of remodeling of the vaginal wall afterchildbirth have been investigated as a possiblemechanism for the development of PFDs. In ani-mal models, impaired elastin synthesis has beenshown to be associated with development of pro-lapse [93]. Differential expression of genes involvedin elastin metabolism was noted in vaginal tissueof women with stress urinary incontinence [94].Similarly, changes in the composition of collagenhave been reported in women with prolapse [95].

It is unclear whether these observed differencesin the connective tissue of women with PFDs arethe cause or the result of these disorders. Thusthe clinical relevance of ‘knockout’ mice models(e.g., those with impaired elastin metabolism) isuncertain.

Conclusion & future perspective

PFDs are common conditions and are responsiblefor significant financial and emotional burden topatients and the healthcare system. Current litera-ture suggests a strong association between vaginaldelivery and both stress urinary incontinence andprolapse. Observational studies have identifiedcertain obstetrical exposures, which appear to bemore traumatic to the pelvic floor, particularlyforceps delivery, prolonged second stage of laborand sphincter lacerations. Randomized controlled

trials to study the effect of individual variablesare not practical. Some potential risk factors suchas maternal age, occiput posterior position andfetal weight, are nonmodifiable. However, in thelight of currently available data, efforts shouldbe directed toward avoiding exposure to modifi-able risk factors, such as minimizing the use offorceps, shortening duration of active pushing inthe second stage of labor and increased vigilancefor anal sphincter injuries. Whether these effortswill result in a reduction in the incidence of PFDsis an interesting area for future research.

ReferencesPapers of special note have been highlighted as:• of interest

•• of considerable interest

1. Nygaard I, Barber MD, Burgio KL et al. Prevalence of symptomatic pelvic floor disordersin US women. JAMA 300, 1311–1316 (2008).

2. Shamliyan T, Wyman J, Bliss DZ, Kane RL , Wilt TJ. Prevention of urinary and feca l

incontinence in adults. Evid. Rep. Technol. Assess . 161, 1–379 (2007).

3. Olsen AL, Smith VJ, Bergstrom JO, Colling JC, Clark AL. Epidemiology of surgicallymanaged pelvic organ prolapse and urinaryincontinence. Obstet. Gynecol. 89(4), 501–506(1997 ).

4. Sung VW, Washington B, Raker CA. Costsof ambulatory care related to female pelvic

floor disorders in the United States. Am. J. Obstet. Gynecol . 202(5), 483 (2010).

5. Subak LL, Waetjen LE, van den Eeden S,Thom DH, Vittinghoff E, Brown JS. Cost ofpelvic organ prolapse surgery in the UnitedStates. Obstet. Gynecol. 98, 646–651 (2001).

6. Wilson L, Brown JS, Shin GP, Luc KO, SubakLL. Annual direct cost of urinary incontinence.Obstet. Gynecol. 98, 398–406 (2001).


Executive summary

Risk factors for pelvic floor disorders

• Vaginal childbirth and parity appear to be important risk factors for the development of pelvic floor disorders (PFDs), such as stress

urinary incontinence and pelvic organ prolapse.

• Obstetrical exposures, such as operative vaginal delivery, prolonged second stage of labor, fetal macrosomia and perineal lacerations,

often coexist. Hence, the isolated effect of these variables on the pelvic floor is difficult to study.

Mechanisms of obstetrical injury

• Trauma to the pelvic support system, denervation injury, ischemia, combined neurovascular injury and defective soft-tissue remodeling

are some of the mechanisms that may explain the association between vaginal delivery and PFDs.

Future directions

• Studies are needed to understand the relative contribution of episiotomy and perineal lacerations with respect to prolapse.

• Pathophysiologic mechanisms underlying the association between PFDs and childbirth need further investigation. For example, whetherthe observed differences in connective tissue components of women with and without PFDs are a consequence or the cause of these

disorders is an interesting area of research.


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7. Sung VW, Rogers ML, Myers DL, AkbariHM, Clark MA. National trends and costs ofsurgical treatment for female fecalincontinence. Am. J. Obst et. Gynecol. 197,652.e1–652.e5 (2007).

8. Segedi LM, Ilić KP, Curcić A, Visnjevac N.Quality of life in women with pelvic floor

dysfunction. Vojnosanit. Pregl. 68(11),940–947 (2011).

9. Jelovsek JE , Barber MD. Women seekingtreatment for advanced pelvic organ prolapsehave decreased body image and quality of life. Am. J. Obstet. Gynecol. 194(5), 1455–1461(2006).

10. Teunissen TA, van den Bosch WJ, van denHoogen HJ, Lagro-Janssen AL. Prevalence ofurinary, fecal and double incontinence in theelderly living at home. Int. Urogynecol. J. Pelvic Floor Dysfunct. 15(1), 10–13 (2004).

11. Progetto, Menopausa Italia Study Group.

Risk factors for genital prolapse in non-hysterectomized women around menopause:results from a large cross-sectional study inmenopausal clinics in Italy. Eur. J. Obstet.Gynecol. Reprod. Biol. 93(2), 135–140(2000).

12. MacLennan AH, Taylor AW, Wilson DH, Wilson D. The prevalence of pelvic floordisorders and their relationship to gender, age,parity and mode of delivery. Br. J. Obstet.Gynaecol. 107, 1460–1470 (2000).

13. Handa VL, Blomquist JL, Knoepp LR,Hoskey KA, McDermott KC, Muñoz A.Pelvic floor disorders 5–10 years after vagina lor cesarean childbirth. Obstet. Gynecol. 118,777–784 (2011).

14. Uustal FE, Wingren G, Kjolhede P. Factorsassociated with pelvic floor dysfunction withemphasis on urinary and fecal incontinenceand genital prolapse: an epidemiologicalstudy. Acta Obstet . Gynecol . Scand. 83,383–389 (2004).

15. Melville JH, Katon W, Delaney K et al. Urinary incontinence in US women:a population-based study. Arch. Intern . Med.165(5), 537–542 (2005) .

16. Lawrence JM, Lukacz ES, Liu IL, Nager CW,Luber KM. Pelvic floor disorders, diabetes,and obesity in women: findings from theKaiser Permanente Continence AssociatedRisk Epidemiology Study. Diabetes Care 30(10), 2536–2541 (2007).

17. Chen B, Yeh J. Alterations in connectivetissue metabolism in stress incontinence andprolapse. J. Urol. 186(5), 1768–1772 (2011).

18. Busacchi P, Perri T, Paradisi R et al. Abnormal ities of somatic peptide-containingnerves supplying the pelvic floor of womenwith genitourinary prolapse and stress urinaryincontinence. Urology 63(3), 591–595 (2004).

19. Burakgazi AZ, Alsowaity B, Burakgazi ZA,Unal D, Kelly JJ. Bladder dysfunction inperipheral neuropathies. Muscle Nerve 45(1),2–8 (2012).

20. Sakakibara R, Panicker J, Fowler CJ et al. Vascular incontinence: incontinence in theelderly due to ischemic white matter changes.

Neurol. Int. 4(2), e13 (2012).21. Altman D, Forsman M, Fa lconer C,

Lichtenstein P. Genetic influence on stressurinary incontinence and pelvic organprolapse. Eur. Urol. 54(4), 918–922 (2008).

22. Skorupski P, Miotła P, Jankiewicz K,Rechberger T. Polymorphism of the geneencoding alpha-1 chain of collagen type I anda risk of pelvic organ prolapse – a preliminarystudy. Ginekol. Pol. 78(11), 852–855 (2007).

23. Hansen BB, Svare J, Viktrup L, Jørgensen T,Lose G. Urinary incontinence duringpregnancy and 1 year after delivery in

primiparous women compared with a controlgroup of nulliparous women. Neurourol.Urodyn. 31(4), 475–480 (2012).

24. Rortveit G, Hannestad YS, Daltveit AK,Hunskaar S. Age- and type-dependent effectsof parity on urinary incontinence: theNorwegian EPINCONT Study. Obstet.Gynecol. 98(6), 1004–1010 (2001).

25. Kepenekci I, Keskinkilic B, Akinsu F et al. Prevalence of pelvic floor disorders in thefemale population and the impact of age,mode of delivery, and parity. Dis. ColonRectum 54, 85–94 (2011).

26. Kudish BI, Iglesia CB, Gutman RE, Sokol AI,Rodgers AK, Gass M. Risk factors forprolapse development in white, black, andHispanic women. Female Pelvic Med. Reconstr.Surg. 17(2), 80–90 (2011).

27. Abramov Y, Sand PK, Botros SM et al. Riskfactors for female anal incontinence: newinsight through the Evanston–Northwesterntwin sister’s study. Obstet. Gynecol. 106(4),726–732(2005).

28. Mant J, Painter R, Vessey M. Epidemiologyof genital prolapse: observations from theOxford Family Planning A ssociation Study.Br. J. Obstet. Gynaecol. 104, 579–585 (1997).

29. Whyte H, Hannah ME, Saig al S et al. Outcomes of children at 2 years afterplanned cesarean birth vs planned vaginalbirth for breech presentation at term: theinternational randomized Term Breech Trial. Am. J. Obstet . Gynecol. 191, 864– 871 (2004).

30. Bols EM, Hendriks EJ, Berghmans BC,Baeten CG, Nijhuis JG, de Bie RA. A systematic review of etiologica l factor s forpostpartum fecal incontinence. Acta Obst et.Gynecol. Scand. 89, 302–314 (2010).

• Provides evidence that history of third- or

fourth-degree laceration is the only

obstetrical variable that is strongly

associated with fecal incontinence.

31. Borello-France D, Burgio KL, Richter HE et al. Fecal and urinar y incontinence inprimiparous women. Obstet. Gynecol. 108,863–872 (2006).

32. Quiroz LH, Muñoz A, Shippey SH, GutmanRE, Handa VL. Vaginal parity and pelvicorgan prolapse. J. Reprod . Med. 55(3–4),93–98 (2010).

33. Gartland D, Donath S, MacArthur C, BrownSJ. The onset, recurrence and associatedobstetric risk factors for urinary incontinencein the first 18 months after a first birth :an Austra lian nulliparous cohort study.Br. J. Obstet. Gynaecol. 119(11), 1361–1369(2012).

34. Brown S, Gartland D, Donath S, MacArthurC. Effects of prolonged second stage, methodof birth, timing of caesarean section and other

obstetric risk factors on postnatal urinaryincontinence: an Australian nulliparouscohort study. Br. J. Obstet. Gynaecol. 118,991–1000 (2011).

35. Cunningham FG, Leveno KJ, Bloom SL,Hauth JC, Rouse DJ, Spong CY. Forcepsdelivery and vacuum extraction. In: WilliamsObstetrics (23rd Edition). McGraw HillCompanies, Inc., NY, USA, 511–526 (2010).

36. Handa VL, Blomquist JL, McDermott KC,Friedman S, Muñoz A. Pelvic floor disordersafter vagina l birth: effect of episiotomy,perineal laceration, and operative birth.

Obstet. Gynecol. 119, 233–239 (2012).• Provides interesting evidence that

spontaneous perineal lacerations might be

more traumatic to pelvic oor disorders

than episiotomy.

37. Leijonhufvud A, Lundholm C, Cnattingius S,Granath F, Andolf E, Altman D. Risks ofstress urinary incontinence and pelvic organprolapse surgery in relation to mode ofchildbirth. Am. J. Obstet. Gynecol. 204(1), 70(2011).

38. Johanson R B, Heycock E , Carter J, Sultan AH, Walk late K, Jones PW. Maternal and

child health after assisted vaginal delivery:five-year follow up of a randomised controlledstudy comparing forceps and ventouse.Br. J. Obstet. Gynaecol. 106(6), 544 (1999).

39. Martin JA, Hamilton BE, Ventura SJ et al. Births: fina l data for 2009. Natl Vital Stat.Rep. 60(1), 1–70 (2009).

40. Sultan AH, Kamm MA, Bartram CI, HudsonCN. Anal sphincter trauma duringinstrumental delivery. Int. J. Gynecol. Obstet. 43, 263–270 (1993).

41. Fitzpatrick M, Behan M, O’Connell PR,O’Herlihy C. Randomized clinical trial toassess anal sphincter function following



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forceps or vacuum assisted vaginal delivery.Br. J. Obstet. Gynaecol. 110, 424–429 (2003).

42. Weber AM, Meyn L. Episiotomy use in theUnited States, 1979–1997. Obstet. Gynecol. 100, 1177–1182 (2002).

43. Kozak LJ, Owings MF, Hall MJ. NationalHospital Discharge Survey: 2001 annualsummary with detailed diagnosis andprocedure data. Vital Health Stat . 13, 1–198(2004).

44. Will iams FL , du V Florey C, Mires GJ,Ogston SA. Episiotomy and perineal tea rs inlow-risk UK primigravidae. J. Public Heal th Med. 20(4), 422–427 (1998).

45. Gabbe SG, DeLee JB. The prophylacticforceps operation. Am. J. Obst et. Gynecol. 1,34–44 (1920).

46. Pomeroy RH. Shall we cut and reconstructthe perineum for every primipara? Am. J. Obstet. Dis. Women Child. 78, 211–220

(1918).

47. Nugent FB. The primiparous perineum afterforceps delivery. Am. J. Obst et. Gynecol. 30,249–256 (1935).

48. Aldridge AH, Watson P. Analysis of end-results of labor in primiparas after spontaneousversus prophylactic methods of delivery. J. Obstet. Gynecol . 30, 554–565 (1935).

49. Hartmann K, Viswanathan M, Palmieri R,Gartlehner G, Thorp J Jr, Lohr KN.Outcomes of routine episiotomy: a systematicreview. JAMA 293(17), 2141–2148 (2005).

•• Reviews the evidence regarding long-term

sequelae of episiotomy and concludes that

the current literature does not support a

role of episiotomy in the prevention of

fecal and urina ry incontinence or pelvic

organ prolapse.

50. Thorp JM Jr, Bowes WA Jr. Episiotomy: canits routine use be defended? Am. J. Obstet.Gynecol. 160, 1027–1030 (1989).

51. Helwig JT, Thorp JM, Bowes WA. Doesmidline episiotomy increase the risk ofthird- and fourth-degree lacerations inoperative vaginal deliveries? Obstet. Gynecol .82(2), 276–279 (1993).

52. Handa VL, Danielsen BH, Gilbert WM.Obstetric anal sphincter lacerations. Obstet.Gynecol. 98, 225–230 (2001).

53. Sartore A, De Seta F, Maso G, Pregazzi R,Grimaldi E, Guaschino S. The effects ofmediolateral episiotomy on pelvic floorfunction after vaginal delivery. Obstet.Gynecol . 103(4), 669–673 (2004).

54. Cam C, Asoglu MR, Selcuk S, Aran T, TugN, Karateke A. Does mediolateral episiotomydecrease central defects of the anterior vaginalwall? Arch. Gynecol. Obst et. 285, 411–415(2012).

•• Provides evidence for the protective effect

of mediolateral episiotomy against central

defects of the anterior vaginal wall.

55. Will iams A, Herron-Marx S, Carolyn H.The prevalence of enduring postnatal perinealmorbidity and its relationship to perinealtrauma. Midwifery 23(4), 392–403 (2007).

56. Gyhagen M, Bullarbo M, Nielsen TF,Milsom I. Prevalence and risk factors forpelvic organ prolapse 20 years afterchildbirth: a national cohort study insingleton primiparae after vaginal orcaesarean delivery. Br. J. Obstet. Gynaecol. 120(2) , 152–160 (2013).

57. Sleep J, Grant A, Garcia J, Elbourne D,Spencer J, Chalmers I. West Berkshireperineal management trial. Br. Med. J. (Clin.Res. Ed.) 289(6445), 587–590 (1984).

58. Rempen A, Kraus M. Pressures on the fetalhead during normal labor. J. Perinat. Med. 19,

199–206 (1991).59. Lien KC, Morgan DM, Delancey JO,

Ashton-Mil ler JA. Pudendal nerve st retchduring vaginal birth: a 3D computersimulation. Am. J. Obste t. Gyneco l. 192,1669–1676 (2005) .

60. Allen RE, Hosker GL, Smith AR, WarrellDW. Pelvic floor damage and childbirth:a neurophysiological study. Br. J. Obstet.Gynaecol. 97(9), 770–779 (1990).

61. Kearney R, Miller JM, Ashton-Miller JA,Delancey JO. Obstetric factors associatedwith levator ani muscle injury after vaginal

birth. Obstet. Gynecol. 107, 144–149 (2006).62. Viktrup L, Lose G, Rolff M, Bar foed K.

The symptom of stress incontinence causedby pregnancy or delivery in primiparas.Obstet. Gynecol. 79(6), 945–949 (1992).

63. Tsunoda A, Shibusawa M, Kamiyama G,Kusano M, Shimizu Y, Yanaihara T.The effect of vaginal delivery on the pelvicfloor. Surg. Today 29(12), 1243–1247 (1999).

64. Cheng YW, Hopkins LM, Caughey AB.How long is too long: does a prolongedsecond stage of labor in nulliparous womenaffect maternal and neonatal outcomes?

Am. J. Obstet. Gynecol . 191(3), 933–938(2004).

65. Christianson LM, Bovbjerg VE, McDavittEC, Hullfish KL. R isk factors for perinealinjury during delivery. Am. J. Obstet. Gynecol. 189(1), 255–260 (2003).

66. Eftekhar T, Hajibaratali B, Ramezanzadeh F,Shariat M. Postpartum eva luation of stressurinary incontinence among primiparas. Int. J. Gynaecol. Obst et. 94(2), 114–118 (2006).

67. Baracho SM, Barbosa da Silva L, Baracho E,Lopes da Silva Filho A, Sampaio RF, Mello deFigueiredo E. Pelvic floor muscle strength

predicts stress urinary incontinence in

primiparous women after vaginal delivery.Int. Urogynecol. J. 23(7), 899–906 (2012).

68. Lien KC, Mooney B, Delancey JO, Ashton-Miller JA. Levator ani muscle stretch inducedby simulated vaginal birth. Obstet. Gynecol. 103(1), 31–40 (2004).

69. Kuh D, Cardozo L, Hardy R. Urinaryincontinence in middle-aged women:childhood enuresis and other lifetime riskfactors in a British prospective cohort. J. Epidemiol . Community Health 53, 453–458(1999).

70. Foldspang A, Mommsen S, Lam GW, ElvingL. Parity as a correlate of adult female urinaryincontinence prevalence. Epidemiol.Community Health 46(6), 595–600 (1992).

71. Pregazzi R, Sar tore A, Troiano L et al .Postpartum urinary symptoms: prevalenceand risk factors. Eur. J. Obstet. Gynecol.Reprod. Biol. 103(2), 179–182 (2002).

72. Leijonhufvud Å, Lundholm C, Cnattingius S,Granath F, Andolf E, A ltman D. Risk ofsurgically managed pelvic floor dysfunction inrelation to age at first delivery. Am. J. Obstet.Gynecol. 207(4), 303 (2012).

73. Rortveit G, Hunskaar S. Urinary incontinenceand age at the first and last delivery: theNorwegian HUNT/EPINCONT study. Am. J. Obstet. Gynecol. 195(2), 433–438 (2006).

74. DeLancey JO, Miller JM, Kearney R et al. Vaginal birth and de novo stress incontinence:relative contributions of urethra l dysfunctionand mobility. Obstet. Gynecol. 110(2 Pt 1),

354–362 (2007).75. Albrich SB, Laterza RM, Skala C , Salvatore S,

Koelbl H, Naumann G. Impact of mode ofdelivery on levator morphology: a prospectiveobservational study with three-dimensionalultrasound early in the postpartum period.Br. J. Obstet. Gynaecol. 119(1), 51–60 (2012).

76. Ashton-Mil ler JA, DeLancey JO. On thebiomechanics of vagina l birth and commonsequelae. Annu. Rev. Biomed. Eng. 11,163–176 (2009).

77. Delancey JO, Morgan DM, Fenner DE et al. Comparison of levator ani muscle defects and

function in women with and without pelvicorgan prolapse. Obstet. Gynecol. 109, 295–302(2007).

78. Dietz HP, Simpson JM. Levator trauma isassociated with pelvic organ prolapse.Br. J. Obstet. Gynaecol. 115, 979–984 (2008).

79. DeLancey JO, Kearney R, Chou Q, SpeightsS, Binno S. The appearance of levator animuscle abnormalities in magnetic resonanceimages after vaginal delivery. Obstet. Gynecol. 101(1), 46–53 (2003).

80. Shek KL, Dietz HP. Intrapartum r isk factorsfor levator trauma. Br. J. Obstet. Gynaecol. 117, 1485–1492 (2010).



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Vaginal childbirth and pelvic floor disorders

1. Your patient is a 32-year-old woman pregnant with her second child. Her first childwas delivered vaginally. Based on the review by Drs. Memon and Handa, which ofthe following statements about risk factors for pelvic floor disorders is most likely correct?

£ A Randomized controlled trials have proven that forceps delivery increases risk for pelvicfloor disorders

£ B None of the known risk factors are modifiable

£ C Studies have determined the effect of each risk factor in isolation

£ D Risk factors include maternal age, occiput posterior position, and fetal weight

2. Based on the review by Drs. Memon and Handa, which of the following statementsabout mechanisms of injury underlying pelvic floor disorders following vaginalchildbirth is most likely correct?

£ A The exact mechanism of injury associating vaginal delivery and pelvic floor disorders hasbeen clearly demonstrated

£ B Mechanical injury to the pelvic floor is the only known mechanism

£ C Trauma to the pelvic support system, denervation injury, ischemia, and combinedneurovascular injury may all be involved

£ D Defective soft tissue remodeling has not been proposed as a potential mechanism



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CME

3. Based on the review by Drs. Memon and Handa, which of the following statementsabout strategies for minimizing risk of pelvic floor disorders following vaginal

childbirth and directions for future research would most likely be correct?

£ A Shortening the duration of active pushing has been proven to reduce the incidence ofpelvic floor disorders

£ B Increased vigilance for anal sphincter injuries has been proven to reduce the incidence ofpelvic floor disorders

£ C Studies are needed to understand the relative contribution to prolapse of episiotomy andperineal lacerations

£ D Observed differences in connective tissue components of women with and without pelvicfloor disorders are proven to cause these disorders


Documents

Vaginal Birth and Pelvic Floor Disorder