Pregnancy and childbirth are major risk factors for urinary incontinence in women. This article primarily explores the potential mechanisms of injury occurring during pregnancy and the process of childbirth, aiming to improve understanding of the pathogenesis of postpartum urinary incontinence and to provide a foundation for prevention and treatment strategies.
Mechanisms of Pelvic Floor Injury: Effects of Pregnancy and Childbirth
The biological mechanisms by which pregnancy and childbirth cause injury to the pelvic floor have not yet been fully elucidated. Available evidence suggests that pregnancy and childbirth may lead to pelvic floor injury through compression, stretching, or tearing of nerves, muscles, and connective tissues. Intact neuromuscular function and adequate pelvic organ support are essential for normal pelvic visceral function.
A. Neural Injury
During labor and vaginal delivery, descent of the fetal head may stretch and compress the pelvic floor and its associated nerves, leading to demyelination and subsequent denervation. This mechanism of injury is supported by neurophysiological studies, including electromyography (EMG) and pudendal nerve motor latency testing. These studies demonstrate evidence of denervation of the pubovisceral muscles and the anal sphincter in approximately 40–80% of women following vaginal delivery.
Risk factors for denervation and pudendal nerve injury include:
1. Operative vaginal delivery
2. Prolonged second stage of labor
3. High birth weight
Cohort studies indicate that neuromuscular injury recovers within one year postpartum in most women, which may explain the spontaneous improvement of urinary incontinence during this period. However, in some cases:
1. Electrophysiological evidence of denervation persists for 5–6 years postpartum
2. Denervation injury may accumulate with increasing parity
The reasons why some women experience complete recovery of neuromuscular function while others sustain permanent injury remain unclear.
B. Injury to the Levator Ani and Coccygeus Muscles
The levator ani muscle group is a key structure in pelvic floor function, forming a U-shaped sling that supports the pelvic organs.
- At rest, levator ani tone maintains closure of the urogenital hiatus and resists downward displacement of the vagina during increases in intra-abdominal pressure.
- During active contraction, it further enhances vaginal closure forces and compresses the rectum, distal vagina, and urethra.
Loss of levator ani function—due to traumatic disruption, denervation, or muscle atrophy—may result in enlargement of the urogenital hiatus and subsequent pelvic organ descent.
Imaging Evidence: Levator Ani Avulsion
MRI and ultrasound studies demonstrate that:
- The levator ani may be avulsed from the pubic bone during vaginal delivery
- Excessive distension of the pubococcygeus muscle by the fetal head may result in detachment of the levator muscle from the pubis
Observational findings include:
- Levator avulsion occurs in approximately 20% of women after vaginal delivery
- It is rare following cesarean delivery
- Forceps delivery carries a higher risk than vacuum-assisted delivery (odds ratio increased approximately fivefold)
- Prolonged second stage of labor may result in occult levator ani injury
Biomechanical and Computational Modeling Studies
Computer simulations and biomechanical models support the hypothesis that levator ani injury contributes to pelvic organ prolapse:
- The greatest strain occurs at the bony attachments of the levator ani and pubococcygeus muscles
- The predicted degree of deformation exceeds injury thresholds, particularly in the most medial portions of the levator ani complex
Clinical Implications of Levator Ani Avulsion
Key findings include:
Mode of Delivery and Pelvic Floor Muscle Strength
- Women who undergo vaginal delivery, especially forceps delivery, exhibit lower maximal pelvic floor muscle strength and reduced contraction endurance 6–11 years postpartum
Levator Avulsion and Muscle Function
- Women with levator avulsion have weaker pelvic floor muscles and a wider levator hiatus
- Reduced muscle strength and hiatus enlargement are strongly associated with pelvic organ prolapse (POP)
Levator Avulsion and Risk of POP
- The prevalence of levator avulsion is two to three times higher in women with POP compared with those with normal pelvic anatomy
Effect on Urinary Incontinence
- Whether levator avulsion increases the risk of urinary incontinence remains unclear
- A large longitudinal study demonstrated an association between levator avulsion and prolapse beyond the hymen, but not with stress urinary incontinence
Episiotomy
- Mediolateral episiotomy typically involves incision of the levator ani and coccygeus muscles and has long been assumed to affect pelvic floor muscle function
- However, a Swedish study found no difference in pelvic floor muscle strength at six weeks postpartum following mediolateral episiotomy
Currently, no proven treatment exists to reverse levator ani avulsion caused by childbirth. A small postpartum study demonstrated similar benefits of pelvic floor muscle training in women with and without avulsion; therefore, routine postpartum screening for levator avulsion is not considered standard care.
C. Fascial Injury
Injury to other soft tissues, such as fascia, may also contribute to pelvic floor dysfunction—particularly pelvic organ prolapse—after childbirth. A paravaginal defect refers to separation of the endopelvic fascia from its lateral attachment to the pelvic sidewall and is strongly associated with:
- Urethral hypermobility
- Stress urinary incontinence
- Poor anterior vaginal wall support
D. Impaired Connective Tissue Remodeling
Collagen and elastin are the primary components of the extracellular matrix:
- Elastin contributes to tissue distensibility
- Collagen provides tensile strength
During pregnancy, synthesis of collagen and elastin increases, enhancing vaginal distensibility. Vaginal stretching stimulates fibroblasts to release collagenases, leading to increased collagen degradation. After delivery, collagen and elastin synthesis increases again, facilitating remodeling of pelvic floor and vaginal connective tissues.
Disruption of this biochemical remodeling process may result in pelvic floor dysfunction. Studies indicate that:
- Impaired elastin synthesis leads to prolapse in animal models
- Women with POP exhibit abnormal collagen composition
- Vaginal tissues of women with stress urinary incontinence show altered expression of genes related to elastin metabolism
However, in women with established prolapse, it remains unclear whether connective tissue changes represent a cause or a consequence of the disorder.
References:
https://www.uptodate.com/contents/effect-of-pregnancy-and-childbirth-on-urinary-incontinence-and-pelvic-organ-prolapse
