REVIEW

Vaginal delivery and pelvic floor dysfunction: currentevidence and implications for future research

M. A. T. Bortolini & H. P. Drutz & D. Lovatsis & M. Alarab

Received: 18 November 2009 /Accepted: 12 March 2010 /Published online: 6 May 2010# The International Urogynecological Association 2010

Abstract Vaginal delivery is the major risk factor for thedevelopment of pelvic organ prolapse and urinary and fecalincontinence, resulting from damage to the pelvic floormuscles, nerves and connective tissue. This article reviewsthe perineal trauma mechanism during vaginal delivery anddiscusses implications of current and future research projects.

Keywords Vaginal delivery . Incontinence .

Pelvic organ prolapse

Introduction

Female pelvic floor dysfunction (PFD) is a term applied toa wide variety of clinical conditions, including urinaryincontinence (UI), anal and fecal incontinence (FI), pelvicorgan prolapse (POP), sensory and emptying abnormalitiesof the lower urinary tract, defecatory dysfunction, sexualdysfunction, and several chronic pain syndromes [1].Because of its high prevalence, deleterious effects onquality of life and its impact on the health care system,PFD is an important public health issue [2]. This articleconsiders aspects of the three most common conditions:urinary incontinence, fecal incontinence and pelvic organprolapse. There is an 11.1% chance that a woman will needsurgery to correct pelvic organ prolapse or incontinenceduring her lifetime [3]. Estimates show 135,000 womenundergo surgery for UI and 225,000 have POP repair each

year in the United States [4, 5]. Statistics about proceduresfor FI have not been reported [6].

Risk factors associated with PFD include multiparity,age, chronic increase of abdominal pressure (cough,overweight, physical effort), previous pelvic surgeries,spinal cord conditions and injury, genetic conditions,ethnicity, and family history. However, most cases arerelated to vaginal childbirth trauma [7, 8].

Mant et al. [8] described relative risk of developingpelvic floor dysfunction of 10.8 during pregnancy andpuerperium. It is estimated that 425% of primiparouswomen suffer from fecal incontinence in the postpartumperiod [9], while 26% develop stress urinary incontinence[10] and 52% have some degree of anterior vaginal wallprolapse after the first vaginal birth [11].

Even under normal circumstances, vaginal delivery causesmechanical trauma to the pelvic floor that is sometimesirreversible. The integrity of muscle and ligaments composingthe endopelvic fascia is key for maintaining support, sus-pension, and anatomic position of the pelvic organs inphysiological conditions. In addition, innervation has animportant role in maintaining the support structure functionand continence mechanism integrity [1217].

This article reviews the mechanism of childbirth traumaand consequences on pelvic floor functions and then dis-cusses current and future research related to this commonand debilitating condition.

Mechanism of childbirth trauma and PFD: evidence

Pelvic floor dysfunction results from loss of support andsuspension provided by the endopelvic fascia and pelvic floormuscles, especially the components of the levator ani muscle.Many researchers had claimed that the vaginal delivery would

M. A. T. Bortolini (*) :H. P. Drutz :D. Lovatsis :M. AlarabDivision of Urogynaecology,Department of Obstetrics and Gynaecology,University of Toronto, Mount Sinai Hospital,700 University Avenue, Suite 3097,Toronto, ON, Canada M5G1Z5e-mail: maria.augusta@gmail.com

Int Urogynecol J (2010) 21:10251030DOI 10.1007/s00192-010-1146-9

cause direct damage to these structures as well as indirectdamage to the nerves of the pelvic floor [18, 19]. With nerveinjuries, pelvic muscular tonus decreases, and the weakness oflevator ani muscle overwhelms the uterosacral and parametrialligaments and endopelvic fascia implicating in secondaryinjuries of these structures [20, 21].

Pelvic floor muscle injury and PFD

During vaginal delivery, the passage of the fetal head causessignificant deformations in the pelvic floor muscles and othertissues [22, 23]. The decrease of pelvic muscle resistance aftervaginal birth can be observed using techniques of measure-ment of muscle strength, such as standardized physicalexamination, use of vaginal cones, measurements of intra-vaginal pressure and use of translabial ultrasound [12, 24, 25].Nielsen et al. [26] found that patients did not recuperatemuscle strength until 8 months postpartum, while 34% ofthem were not able to contract the pelvic muscles voluntarilyafter six weeks of puerperium [27].

The puborectalis muscle fibers and the medial portion ofthe pubococcygeous muscle stretch 3.26 more times thanother pelvic muscles during the expulsion of the fetus,exceeding by 217% the maximum point of stretching musclewithout any disruption of fibers in muscles of non-pregnantmammals [28]. Avulsion of the puborectalis muscle has amarked effect on pelvic floor muscle strength [25].

Magnetic resonance imaging studies have shown thatwomen with injury to the puborectalis muscle at 6 weekspostpartum tended to have normal images at 6 months. A 60%increase in puborectalis muscle thickness was observed in6 months compared with that seen in 6 weeks postpartum,indicating the extent of the injury. However, the total recoverywas not observed in injuries to both the puborectalis andileococcygeous muscles [29]. Image studies have shown thatup to 20% of women who have delivered vaginally havevisible levator ani defects, of which the majority is in thepubovisceral portion of the levator ani muscle [30, 31]. Thesedefects can be unilateral or bilateral and are associated withsymptomatic stress urinary incontinence (SUI).

Women with levator avulsion defects postpartum detectedby 3D ultrasound were about twice as likely to show POP ofstage II or higher than those with an intact levator muscle,especially cystocele and uterine prolapse [32].

Women with limited pelvic organ mobility antepartumhave a greater risk of developing postpartum vaginal wallprolapse [33]. Echography studies evaluated the elevationof the bladder neck in the postpartum period duringvoluntary contraction of the levator ani muscle at rest andduring effort. In the period from 3 to 8 days before birththere was a decrease in elevation of the bladder neck, lossof bladder neck support at rest, with increased mobility in

stress maneuvers. However, elevation of the bladder neckreturned to antenatal levels after 6 to 10 weeks [34, 35].

Functional magnetic resonance imaging also detectedsignificant differences in almost all the structures evaluated,such as in the pelvic position of the bladder, bladder neck,posterior vaginal fornices, anorectal junction, genital hiatusand depth of rectocele after vaginal childbirth. Urethral andbladder mobility contributed to SUI after vaginal childbirth[3638].

An increase in the size of the genital hiatus was observedafter vaginal childbirth and related to development andrecurrence of POP [39, 40]. A levator hiatal area of greaterthan 25 cm2 is considered abnormal and associated withsymptomatic prolapse [41].

Pelvic floor nerve injuries and PFD

Pudendal nerve lesions usually result in demyelination ofthe fibers; axonal break may occur in severe cases withoutrecovery of the tissues [13]. c-Fos expression (an earlyreactive nerve injury marker) in the L6 to S1 spinal cordsegments was observed in rats after simulated birth trauma,indicating acute nerve injury or irritation in spinal neurons.Also, histological studies have revealed a marked decreaseof ganglion cells in the neural plexuses posterolateral to thevagina in experimental rats after simulated birth [42].

Neuromuscular abnormal pelvic floor activation patternsmay also contribute to PFD [4345]. Electroneuromyog-raphy studies have shown that 80% of primigravidaedeveloped evidence of partial denervation with signs ofreinnervation and increase in the density of nerve fibers inthe postpartum period after vaginal delivery [46, 47]. Thelatency time of pudendal nerve motor fibers increased after2 to 3 days of vaginal delivery, but values normalized after6 months in 66% [47]. Most nerve lesions spontaneouslyrecover within a year by regenerative processes [13].However, pudendal nerve damage, even with partialreinnervation of the external anal sphincter muscle, maypersist and become more marked in the long term [48].

Neurophysiological tests revealed nerve damage in 36%of women with persistent SUI at 3 months postpartum.Compared with nulliparous control subjects, patients withSUI and POP had changes in the levator ani and externalanal sphincter consistent with either motor unit loss orfailure of central activation, or both [49].

Urethral lesion and PFD

Structural and functional alterations in the components ofthe urethra and anus after vaginal delivery will be speci-fically and separately addressed for didactic purposes.

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Some experimental studies have described the effects ofvaginal delivery in the urethra. Rocha et al. [50, 51]observed that vaginal delivery and simulation of childbirthtrauma significantly decreased the number of nerve andmuscular fibers; increased the amount of collagen andelastic fibers and the ratio collagen-muscular fibers in themid-urethra of adult female rats.

A rat model of simulated birth trauma assessed theeffects on lower urinary tract function of prolonged dilationand compression of pelvic floor tissues during vaginaldelivery. Leak point pressure was significantly decreased inboth 1- and 4-h distention groups 4 days after distension,compared to the sham-distended rats group, indicating ashort-term decrease in urethral resistance. Six weeks aftervaginal delivery, urethral resistance returned to normalvalues. However, the voided volume in sham-distendedanimals was still significantly increased at 6 weeks com-pared to the distended animals. In conclusion, this modelshows that prolonged vaginal delivery results in reducedbladder capacity and long-term urinary dysfunction [52]. Asimilar experimental model found that, four weeks aftersimulated birth injury, SUI was noted in 40% of experi-mental rats. A significant decline in urethral wall muscu-lature (both smooth and striated) and a wider genital hiatuswere noted in incontinent rats [42].

A prospective study in nulliparous women found aremarkable decrease of urethral closure pressure and thefunctional length of the urethra 8 weeks after vaginaldelivery compared with the antenatal period [53]. Lowermaximum urethral closure pressure was shown to be thefactor most associated with de novo SUI [54]. A studycollating imaging and urodynamic data showed bladderneck descent also to be a strong predictor of stress urinaryincontinence [37].

Anal lesion and PFD

Lesions of the external anal sphincter are significantlyrelated to lacerations and/or episiotomy, while internal analsphincter lesions may occur with an intact perineum [55].Wai et al. [56], in a rat model, observed that anal sphinctertransection, with or without antecedent, prolonged vaginaldistention results in severe changes of external analsphincter function immediately after injury. However, thecontractile function of the external anal sphincter was fullyrecovered by 3 months and was sustained at 6 months. Over35% of primiparous women suffer some degree of damageto the external anal sphincter, persisting until six monthspost vaginal delivery [55]. Women with recognized thirdand fourth grade perineal lacerations during vaginaldelivery have a higher rate of fecal incontinence comparedto those not injured (7.8% and 2.9%, respectively) [57].

Endoanal ultrasound findings have shown that 35% ofprimiparous women who delivered vaginally and requiredrepair of clinically evident anal sphincter third- or fourth-degree tears, still exhibited internal sphincter gaps com-pared with 3% of women with no anal sphincter tear (OR2.3, 95% CI 1.34.0). This condition is associated withfecal incontinence severity [58].

Damage to the innervation of the external anal sphincteroften co-exists with direct injury to the muscle [59, 60]. Acomputer model of vaginal delivery simulation showed thatduring the second stage of labor, the nerves innervating theanal sphincter are stretched beyond the 15% strainthreshold known to cause permanent damage in theperipheral nerve [28]. In a cohort study, 83 women withfecal incontinence underwent neurophysiologic assessment,together with anal endosonography and anal manometry, aspart of the investigative evaluation of their incontinencesymptoms postpartum. 26 women (31%) were found tohave abnormal pudendal nerve function directly attributableto past obstetric trauma [61].

Genetics, heredity, and pelvic floor dysfunction

Vaginal childbirth, despite being the major causal factor,fails to explain completely the origin and progression ofpelvic floor dysfunction. Pelvic organ prolapse and urinaryincontinence have been observed in nulliparous women; theabsence of these conditions has been confirmed in manymultiparous women [8, 55]. These findings raise thepossibility of an important individual variability in thepredisposition to pelvic floor dysfunction [62, 63].

Epidemiological studies have shown higher prevalence ofPOP and SUI in patients with a positive familial history [6369]. Family history appears to be a strong predictor of urinaryincontinence, indicated by the high degree of concordance inthe rate of incontinence between parous women and theirnulliparous sisters [32]. This was also evident in a study ofidentical twins who had identical continence status andrelaxation of pelvic support, despite parity status [69].Mushkat et al. [68] found a threefold increased prevalenceof SUI in first-degree relatives of women with this condition.

Familial incidence of POP is described to be about 60%[70]. The risk of POP among siblings of young women(fewer than 55 years) with severe prolapse is found to befive times higher than in the general population [38] and theprevalence of symptomatic prolapse was higher in womenwhose mothers or sisters had undergone surgery forprolapse compared with women without such familyhistory (OR 3.1, CI 95% 1.43.0) [63].

The evidence suggests that there is a genetic pre-disposition to PFD [62, 7173], as history of conditionssuggestive of deficient connective tissue, such as varicose

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veins, hernias, and hemorrhoids, was found significantlyand positively associated to symptomatic POP [63]. Womenwith Marfan or EhlersDanlos syndrome have higher ratesof SUI and POP. Studies have shown that women with POPand SUI have an increased incidence of joint hypermobility[71] and abdominal striae [73]. Dietz et al. [74, 75] showedthat the mobility of the bladder, bladder neck and urethra,determinants of PFD, is a heritable trait, composing 50% ofthe variability due to genetic factors in nulligravid women.In addition, bladder mobility appears to correlate to jointhyperextensibility, mostly at the elbow, composing 14% ofvariation in bladder neck mobility accounted for by genesinfluencing elbow mobility [76].

Recent animal studies have shown that female reproduc-tive organs are rich in elastic fibers that undergo massiveremodeling in the reproductive organs throughout pregnan-cy and birth [7779]. Deficiency in lysyl oxidase-like-1(LOXL1), a protein essential for the postnatal deposition ofelastic fibers, led to severe POP in mice 1 to 2 days aftervaginal birth, weakness of the vaginal wall, paraurethralpathology, and lower urinary tract dysfunction [7779].Fibulin-5 (FIB-5) is an ECM protein that acts to stabilizeand organize elastic fibers [80]. FIB-5 deficiency in vaginaltissues also resulted in prolapse in mice [81]. Vaginas ofFIB-5 knockout mice that developed prolapse exhibiteddecreased maximal stress, increased distensibility andstrain, and decreased stiffness [82], phenotypes thatresemble pelvic floor dysfunction in humans.

Based on those observations, some authors have exploredthe field of genetic basis for pelvic floor dysfunction inhumans [8386]. Most research concentrates on the analysisof extracellular matrix proteins and genes involved in thefunction of muscular and connective systems. Candidategenes have been identified that may result in alteration ofnormal metabolism of various structural proteins, which maypredispose some women to PFD, but certainly more studiesare necessary to provide a comprehensive understanding ofthe biological basis of these disorders.

Conclusion

Despite the absence of controlled studies, current literaturereaffirms vaginal delivery as the main etiological agent ofpelvic floor dysfunction. However, sparse evidence supportsthe exact participation of each element in the etiology ofpelvic floor dysfunction; this limits our ability to developeffective prevention strategies. The challenge for researchers,therefore, is to establish the role of genetic predisposition inthe genesis of pelvic organ prolapse and urinary and fecalincontinence. A full understanding of the biological basis ofthese disorders would help in planning individualizedmanagement for the obstetric patient.

Conflicts of interest None.

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1030 Int Urogynecol J (2010) 21:10251030

Vaginal delivery and pelvic floor dysfunction: current evidence and implications for future researchAbstractIntroductionMechanism of childbirth trauma and PFD: evidencePelvic floor muscle injury and PFDPelvic floor nerve injuries and PFDUrethral lesion and PFDAnal lesion and PFDGenetics, heredity, and pelvic floor dysfunctionConclusionReferences

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