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14.2: Pelvic Floor Damage and Incontinence

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    Pelvic floor damage due to childbirth

    Pelvic floor disorders (PFD) include urinary incontinence (UI), anal incontinence (AI), and pelvic organ prolapse (POP). It has been shown on numerous occasions, that one of the main causes of female pelvic floor dysfunction is vaginal childbirth. The consequences can be short term or lifelong. The potential space in the female pelvis is limited and has been shown, in relative terms, to have decreased over time. Human evolution theory, postulates that the fetal head has enlarged significantly over time, and thus a larger fetal head has to pass through the female pelvis at childbirth. About 1.5 million years ago, Homo erectus had a cranial capacity of 900 cm3 while Homo sapiens now has a cranial capacity of approximately 1800 cm3. It is therefore not surprising that the structures of the pelvic floor are damaged due to pregnancy as well as childbirth. Some studies have shown that one in two parous white women will suffer pelvic floor dysfunction, to varying degrees, due to vaginal childbirth. Of these women, up to 60% of will undergo surgery. It is important to note that although vaginal birth is the most important etiological factor in pelvic floor dysfunction, other factors contribute including advancing age, vascular disease, spinal cord injury, primary bowel disease, molecular and genetic factors. This chapter shall focus on the impact of childbirth and delivery factors on the development of pelvic floor dysfunction. We shall divide the available evidence into different compartments to enable a thorough overview of this impact on the pelvic floor.

    Trauma to the nervous system

    Neuromuscular function of the pelvic floor is dependent on the integrity of the nervous system. Pelvic floor peripheral nerves, such as the nerves to the levator ani, and the pudendal nerves are at greatest risk of injury during pregnancy and childbirth. The pudendal nerve is particularly prone to damage where it curves around the ischial spine and enters the pudendal canal. Ample evidence links neurologic injury with PFD. Prolonged pudendal nerve motor latency (PNML) has been reported after delivery in 42% of women delivering vaginally, but not in those women delivered by planned caesarean section. PNTML returned to normal in 60% of these women at two months postpartum. Another study found evidence of pudendal nerve denervation in 80% of women after vaginal delivery. The mechanism of injury is most likely to be a combination of direct trauma and traction injury during delivery. Risk factors included a long second stage (> 56.7 minutes), a large baby (> 3.41 kg), and a forceps delivery. Weakness was shown in both the levator ani muscle and the external anal sphincter after vaginal delivery. This is the result of a combination of loss of total motor units as well as asynchronous activity in those that remained. Sensory nerve function is also likely to become impaired by nerve damage. This will be clinically most evident in the anal canal, with its many afferent nerve endings, resulting in anal incontinence or faecal urgency. Caesarean section has been shown to be protective, but only in women who delivered electively.

    Trauma to the pelvic floor muscles

    Anatomical and functional changes to the pelvic floor can develop secondary to pelvic floor distension during descent of the fetal head and maternal expulsive efforts during the second stage of labor. The most important muscles of the pelvic floor are the puborectalis, pubococcygeus and anal sphincter muscles. The genital hiatus in nulliparous women measures 6-36 cm2 during valsalva while the surface area of the fetal head is 70100 cm2. This clearly demonstrates the extent (± 300%) that the levator ani muscle is required to stretch during childbirth. Partial levator avulsion has been shown to occur in 15% of women during delivery (Figure 1). These women are at an increased risk for severe pelvic organ prolapse, urinary incontinence and even recurrent prolapse after surgical treatment. Studies on MRI of the pelvic floor did not identify any levator ani defects in nulliparous women, in contrast to the findings in 20% of primiparous women, who had a visible defect in the levator ani muscle. These defects were usually in the pubovisceral portion of the levator ani muscle. Reported risk factors include higher maternal age (>35 yrs), large babies, prolonged second stage, and forceps delivery. Pelvic floor muscle strength has been also been shown to decrease by 25-35% following vaginal delivery compared to caesarean section. Interestingly, 6-10 weeks postpartum there is however no significant difference from antenatal values, excepting for a lower intravaginal pressure in multiparous women.

    Injury to the anal sphincter during childbirth occurs either as a result of direct disruption of the muscles or due to injury to the pudendal nerves. The incidence of anal sphincter damage varies between 0.5 – 2.5% where mediolateral episiotomies are used, and 7% where midline episiotomies are used. The use of endoanal ultrasound has demonstrated a much higher incidence of anal sphincter injuries (Figure 2) in asymptomatic women, the socalled occult injuries with as many as 35% of primiparous and up to 44% of multiparous women having evidence of sphincter disruption. Risk factors for both the overt and occult sphincter injuries include forceps delivery, prolonged second stage, large birth weight, midline episiotomy, and occipitoposterior positions.

    Connective tissue trauma

    Pelvic organ support essentially consists of or relies on the endopelvic fascia and the condensations of this fascia that forms the ligaments (uterosacral, transverse sacral). Increased pelvic organ mobility (POM), manifesting as pelvic organ prolapse (POP), occurs as a consequence of weakness of these supports. It is far more common in parous women (50%), compared to nulliparous women (2%). During vaginal delivery, the mechanism is most likely due to mechanical trauma of these supporting structures with subsequent degrees of disruption. Spontaneous healing might also lead to weaker collagen and so predispose to incontinence and prolapse.

    This page titled 14.2: Pelvic Floor Damage and Incontinence is shared under a CC BY-NC-SA 2.5 license and was authored, remixed, and/or curated by Stephen Jeffery and Peter de Jong via source content that was edited to the style and standards of the LibreTexts platform; a detailed edit history is available upon request.