Vaginal delivery and the pelvic floor: Outcomes of levator ani injury


Muscle stretch and distention during delivery lead to problems later in life.

Dr Hoyte is Professor, Fellowship and Division director, Female Pelvic Medicine and Reconstructive Surgery, University of South Florida Morsani College of Medicine, Tampa. He has no conflicts of interest to report with respect to the content of this article.


Dr Wyman is Clinical Fellow, Female Pelvic Medicine and Reconstructive Surgery, University of South Florida Morsani College of Medicine, Tampa. She has no conflicts of interest to report with respect to the content of this article.



Dr Hahn is Clinical Fellow, Female Pelvic Medicine and Reconstructive Surgery, University of South Florida Morsani College of Medicine, Tampa. She has no conflicts of interest to report with respect to the content of this article.


Levator ani injury occurs in 3 of 10 vaginal deliveries and often results in pelvic floor dysfunction including pelvic organ prolapse and incontinence. Understanding the mechanism of injury to the muscle of the levator ani is imperative to minimizing injury with delivery. It has long been recognized that the levator ani muscle group plays a key role in female pelvic floor function.1

When functioning normally, this muscle group has multiple roles, including support of the vagina and pelvic organs, and maintenance of urinary and fecal continence.2 The levator ani muscle complex is composed of 3 main muscle groups: the puborectal, the pubococcygeal, and the iliococcygeal portions with motor nerve input from the nerve to levator ani (S2,3,4), which courses over the ventral surface of the levator ani.3

The levator ani muscle complex encircles the largest potential hernia portal in the human body and compromise of this muscle complex is currently the best-defined pathogenesis for pelvic organ prolapse.1 Force vectors on the muscle during distention and passage of a fetal head result in excessive strain and stretch on the muscle, increasing the chance for injury.

During vaginal childbirth, the opening of the genital hiatus distends substantially to allow the passage of the fetus. This requires the distal-most portions of the levator ani (pubococcygeal and puborectalis) to stretch to greater than 3 times their original length, thereby putting strain on the muscles and their attachments to the pubic symphysis.4 Increased strain can result in damage or even complete disruption and detachment of the levator ani muscles from their insertion point on the pubic symphysis.

In addition, during the second stage of labor as the fetal head descends, excess stretch and distention of the iliococcygeus portion of the levator ani results in stretch and distention of the nerve to the levator ani. Prolonged stretching of this motor nerve has the potential to permanently damage the nerve, thereby disrupting the motor signaling to this normally tonic muscle, possibly leading to laxity or sagging of one or both sides of the Iliococcygeus muscle.5

The 2 childbirth-related mechanisms described above have the potential to cause significant injury to the levator ani muscle attachments and nerve supply increasing the risk of urinary and fecal incontinence and future development of pelvic organ prolapse (POP).6-8



Although the pathogenesis of POP is believed to be multifactorial, childbirth and increased vaginal parity have been identified as key risk factors.9 Furthermore, epidemiological studies have demonstrated that the first vaginal delivery is the most significant contributor to the development of pelvic floor disorders and pelvic floor dysfunction in women.10 More than 30% of all women who deliver vaginally will experience some form of direct trauma to the pelvic floor resulting in injury to their levator ani muscle,9 and it has been shown that women who are nulliparous and those who deliver exclusively by cesarean section have an extremely low rate of levator ani disruption.4 Not all women with levator ani muscle injury have symptoms, but a significant portion will have pelvic floor complaints postpartum that persist onward.11,12

Every year in the United States, an estimated 200,000 women undergo a surgical procedure and the number is expected to double within the next 30 years.13-15 Disruption of levator ani structure with detachment of muscle to the pubic symphysis has been shown to increase the risk of prolapse recurrence following surgical prolapse repair.16,17

 Reducing childbirth-related levator ani injury has the potential to reduce the occurrence of pelvic floor dysfunction including pelvic organ prolapse. Understanding the importance of the levator ani muscle during childbirth clearly is key to preventing childbirth-related injury and improving pelvic floor function in the future.


Traditionally the term “levator ani muscle complex” represents 3 separate muscles defined in clinical anatomy: the puborectal, pubococcygeal, and iliococcygeal muscles.3 With the addition of the separate coccygeus muscle, collectively the 4 muscles are termed the pelvic floor diaphragm. The levator ani morphology described by Hoyte et al in 2003 with 3D pelvic magnetic resonance imaging (MRI) images demonstrated a relationship between the size and shape of the muscle and pelvic floor dysfunction and prolapse.18 Women with worsening pelvic floor dysfunction demonstrated increased laxity and distention of the muscle resulting in a change in the shape of the muscle, as seen in Figure 1.

Hoyte et al further developed an MRI-based 3D childbirth simulation model of the female pelvic floor to study the quantity and pattern of levator ani stretch during vaginal delivery.19 Figure 2 demonstrates the axial view of the fetal head interacting with the levator ani muscle complex during simulation of childbirth.19 Figure 3 is an axial view of the levator ani muscle stretch at the different levels of the fetal head descent in the birth canal.19 The model demonstrates that during simulated childbirth, maximal levator ani stretch occurred in the anterior and inferior aspects of the levator ani muscles, specifically at the posteromedial aspects of the puborectalis at a ratio of 3.5 to 1.19 Levator ani avulsion or detachment of the insertion point of the muscle on the inferior aspect of the pubic bone has been identified in parous women in both MRI and ultrasound studies .6,8,14



Risk factors

Vaginal childbirth has been identified as a risk factor for levator ani injury. Increased vaginal parity is associated with relative lifetime risks of prolapse and incontinence of 8.0 and 2.4, respectively.2 The numbers increased to 10.7 and 2.8, respectively, for parity of 4 or more.2 Other factors such as birthweight, length of second stage, size of fetal head, and forceps delivery have also been correlated with increased risk of levator ani muscle injury.1,7,9,20

The likelihood of levator ani trauma during delivery is also strongly related to advanced maternal age at first vaginal delivery. Levator ani injury occurrence increases with increasing maternal age at first vaginal delivery.1 Studies documented a 15% probability for levator ani injury in women at age 20 compared to a 50% probability at age 40.1,21

In summary, vaginal parity, advanced maternal age, birthweight, length of second stage, size of fetal head, and forceps delivery have all been identified as risk factors for levator ani injury during childbirth which can result in pelvic floor disorders in the future.


The concept that levator ani injury leads to symptomatic pelvic floor dysfunction including pelvic organ prolapse and incontinence comes as no surprise. When the levator ani is stretched and strained by passage of a fetal head, the genital hiatus area and volume are increased, as demonstrated in the models above. Detachment of the levator ani from the insertion points on the pubic bone, in particular, is associated with future anterior and apical vaginal compartments prolapse, with relative risks of 2.3 and 4.0, respectively.9,20

A larger genital hiatus (a marker for levator ani disruption and/or laxity) reduces the inferior levator ani support for the vaginal walls during periods of increased intra-abdominal pressure, placing increased strain on the lateral and apical attachments of the anterior vaginal wall.9 Women with bilateral levator ani disruptions are at an even higher relative risk (7.1) of developing prolapse.7 Bulge symptoms are directly related to the size in width and length of the genital hiatus22 and an increased genital hiatal area is also associated with a significant decrease in pelvic floor muscle strength,7,9 which women perceive as increased vaginal laxity and reduced tone, possibly leading to perceived sexual dysfunction.23

The relationship between stress urinary incontinence (SUI) and levator ani injury is less well understood. SUI is usually associated with weakness in these muscles, and studies have shown that women with the condition are twice as likely to have had levator ani injury in their youth.6 However, some studies in older women have also shown no relationship24 or even a negative association.25,26 Dietz proposes that while this may be counterintuitive, SUI is multifactorial, and the success of pelvic floor muscle training for it may be due to strengthening of all the pelvic floor muscles, even the levator ani is detached.1

Fecal incontinence is another symptom commonly associated with levator ani injury. Women with fecal incontinence are more like to have levator ani defects than those without fecal incontinence, with an odds ratio of 14.0.27 Obstetrical observations have shown that sphincter lacerations and levator ani injuries often tend to occur concurrently, but levator ani injury effects persisted even after adjustments were made to exclude external anal sphincter defects.27



Prevention and recommendations

Numerous studies have shown how vaginal delivery affects the pelvic floor negatively yet no data exist from clinical trials on effective methods of preventing levator ani injury. During vaginal delivery, pudendal blocks and epidural anesthesia may be protective against development of levator ani injuries. In mice, a 30% stretch was sufficient to cause injury to maximally activated (tensed) muscles, whereas a stretch of 50% was necessary to produce a similar injury in passive (relaxed) muscles.28 That would support the theory that anesthesia-induced relaxation of the pelvic floor allows for passive muscle stretch and, therefore, less injury.

Factors including operative forceps delivery, length of second stage, and fetal size/head circumference should be identified and can be used when counseling patients both intrapartum and postpartum. Identifying antepartum and intrapartum factors that influence the risk of levator ani injury, such as fetal size/head circumference, length of second stage and the use of forceps, also can be useful when counseling patients and to minimize injury. Forceps should be used with caution and with appropriate anesthesia to allow the pelvic muscles adequate time to stretch with delivery.1,8

Pelvic floor education and exercises during and after pregnancy may help prevent development of pelvic floor dysfunction. In one study, women who received pelvic floor therapy from 20 weeks’ gestation were 56% less likely to report urinary incontinence in late pregnancy, 50% less likely at 12 weeks postpartum, and 30% less like to report incontinence at 6 months postpartum.29 Similar results have been shown for treatment of urinary incontinence in pregnancy. While limited studies have shown that pelvic floor exercises have no effect on pelvic organ prolapse in the immediate postpartum period, studies have shown improvement in middle-aged women, suggests that further long-term research is necessary.30,31 Routine pelvic floor education or referral to pelvic floor physical therapy during the intrapartum and postpartum period may be beneficial, especially in high-risk patients.

More practical techniques such as manual manipulation of the levator hiatus beginning in the third trimester may be beneficial and may change the biomechanical properties of the levator ani muscles.32 Manual massage or the Epi-No Birth Trainer (Starnberg Medical, Tecsana GMBH, Muenchen, Germany) can be used to stretch the perineum and vagina starting at 37 weeks’ gestation until delivery. In one randomized controlled trial, a trend toward reduction in levator ani avulsions (6% vs 13%) was found with use of the Epi-No device versus no intervention starting at 37 weeks’ gestation, but that did not achieve statistical significance.32


Numerous studies have shown that vaginal delivery affects the pelvic floor negatively. Scientific evidence is insufficient, however, to suggest that routine elective cesarean section should be advocated for levator ani risk reduction. Elective cesarean section carries substantial risks and disadvantages to both mother and baby,1 and these risks likely outweigh the risk of childbirth-related levator injury.8,9 Ways to identify women and labor scenarios that represent high risk of levator injury need to be developed and refined, such that appropriate nonsurgical risk-reducing pregnancy and labor interventions can be studied adequately.

Furthermore, new methods for identifying women at high risk for postsurgical prolapse recurrence need to be refined, such that appropriate, durable surgical interventions can be investigated and stratified by levator structural status.



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DeLancey JO, Kearney R, Chou Q, Speights S, Binno. The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol. 2003;101:46–53.

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van Delft KWM, Thakar R, Sultan AH, IntHout J, Kluivers KB. The natural history of levator avulsion one year following childbirth: a prospective study. BJOG. 2015;122:1266–1273.

DeLancey JO. Anatomy and biomechanics of genital prolapse. Clin Obstet Gynecol. 1993;36:897–909.

Shek Kl, Dietz HP. Can levator avulsion be predicted antenatally? Am J Obstet Gynecol. 2010;202:e1–6.

Luber KM, Boero S, Choe JY. The demographics of pelvic floor disorders: current observations and future projections. Am J Obstet Gynecol. 2001;184:1496–503

Deitz HP. Charntarason V, Shek KL. Levator avulsion is a risk factor for cystocele recurrence. Ultrasound Obstet Gynecol. 2010;36:76–80

Wong V, Shek KL, Goh J, Rane A, Deitz HP. Is levator avulsion a predictor of recurrence after anterior compartment mesh? Neurourol Urodyn. 2011;30:879–880.

Singh K, Jakab M, Reid W, Berger L, Hoyte L. Three-dimensional magnetic resonance imaging assessment of levator ani morphologic features in different grades of prolapse. Am J Obstet Gynecol. 2003;188:910–915.

Hoyte L, Damase MD, Warfield S, et al. Quantity and distribution of levator ani stretch during simulated vaginal childbirth. Am J Obstet Gynecol. 2008; 199:e1-e5.

DeLancey JO, Morgan DM, Fenner DE, Kearney R, Guire K, Miller JM, et al. Comparison of levator ani muscle defects and function in women with and without pelvic organ prolapse. Obstet Gynecol. 2007;109:295–302.

Dietz HP, Simpson JM. Does delayed child-bearing increase the risk of levator injury in labour?. Aust N Z J Obstet Gynaecol. 2007;47:491–495.

Thibault-Gagnon S, Yusuf S, Langer S, et al. Do women notice the impact of childbirth-related tevator trauma on pelvic floor and sexual function? Int Urogynecol J. 2012;23: S183–S185.

DeLancey JO, Trowbridge ER, Miller JM, et al. Stress urinary incontinence: relative importance of urethral support and urethral closure pressure. J Urol. 2008; 79:2286–2290.

Dietz HP, Kirby A. Modelling the likelihood of levator avulsion in a urogynaecological population. Aust N Z J Obstet Gynaecol. 2010;50:268–272.

Dietz HP, Kirby A, Shek KL, Bedwell PJ. Does avulsion of the puborectalis muscle affect bladder function? Int Urogynecol J Pelvic Floor Dysfunct 2009;20:967–972.

Lewicky-Gaupp C, Brincat C, Yousuf A, Patel DA, Delancey JO, Fenner DE. Fecal incontinence in older women: are levator ani defects a factor? Am J Obstet Gynecol. 2010;202:491.e1–6.

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