Collaborative for Education on Urinary Incontinence and Women's Health (ceUIwh)

Clinical Consult

Each month, questions with a common theme will be selected and answered comprehensively by one of our Steering Committee members. Previously answered questions will be archived each month for your reference. If you wish to submit a question, click here.

This Month's Question:

What specific risk factors for stress urinary incontinence are associated with childbirth, and what are the different treatment options for women with stress urinary incontinence resulting from childbirth?

Response by Jan E. Baker, MS, APRN, CCCN, posted 1/27/2005:

Vaginal delivery may injure the pelvic floor and play a role in the development of postpartum stress urinary incontinence (SUI). Risk factors that may impact the development of SUI after childbirth include obesity, high fetal weight, increased parity, and constipation. Pushing style and the length of second-stage labor may also damage the pelvic floor. Furthermore, epidural anesthesia, episiotomy, and delivery with instruments have been implicated as risk factors for SUI. Consequently, the rate of elective cesarean section is increasing, not only because of medical necessity, fear of childbirth, or maternal request, but also to prevent pelvic floor disorders.^1-6 A cesarean section without trial of labor may protect the pelvic floor from urinary incontinence.⁷ Nearly one third of women develop SUI within 5 years after delivery of their first baby, and even those who do have a cesarean section are still at risk for an increase in urge urinary incontinence over nulliparous women.⁸ Therefore, it is important for healthcare providers to be educated in nonsurgical management and treatment options for the young mother who experiences postpartum incontinence. Evaluation of postpartum incontinence should be a standard of care.

During childbirth, forces stretch and distend the pelvic floor, altering its muscles, nerves, and connective tissue.⁹ Muscle injuries, such as damage to the perineum, may contribute to postpartum weakening of the pelvic floor. Peripheral nerves that innervate the pelvic floor muscles also may be damaged, but recovery may occur as these muscles are reinnervated by nearby intact nerves.⁹ Moreover, tearing or rupturing of the endopelvic fascia during childbirth has been linked to the development of SUI.⁹

Obesity has been shown to be a significant risk factor for the development of SUI¹ and has been associated with an increased prevalence of SUI postpartum.^6,10,11 Other factors that may play a role are high fetal weight, increased parity, and constipation. High fetal weight has been correlated with partial denervation of the pelvic floor^8,9 and subsequent incontinence surgery.¹⁰ Some studies dispute the relationship between urinary incontinence and infant birth weight, though.^12,13 Prevalence of SUI has been observed to increase with parity, or the number of births.^6,14 Constipation has been shown to increase with parity^15,16 and has been associated with lower urinary tract symptoms.^13,17 Women who chronically strain during bowel movements have been shown to have changes in pelvic floor neurologic function; such straining may lead to the development of SUI or pelvic organ prolapse.¹⁸

Pushing during second-stage labor affects the rate and intensity of stretch on pelvic soft tissues.¹⁹ Spontaneous or self-directed pushing has been reported to limit perineal tissue damage, pain, and episiotomy without significantly lengthening labor,⁵ although the influence on subsequent development of SUI requires further evaluation. Postpartum SUI also has been correlated with the length of second-stage labor,⁹ specifically in causing pelvic organ descent²⁰ and denervation injury.²¹ However, other studies indicate no relationship between the duration of second-stage labor and SUI.²²

Studies have shown that epidural anesthesia does not prevent the incidence of SUI after vaginal delivery^23,24 and may result in subsequent incontinence surgery.¹⁰ It has been suggested that episiotomy does not prevent perineal trauma²⁵ and may itself cause pelvic floor injury and SUI.^8,9 Forceps delivery has been linked to muscular and neurologic injury to the pelvic floor and long-term SUI.^9,12,22 Moreover, vacuum extraction at first delivery has been significantly associated with the onset of SUI soon after childbirth.⁸

Prevalence of SUI has been shown to be similar following spontaneous vaginal delivery and cesarean section performed after obstructed labor, possibly because damage already has been done to the pelvic floor.⁷ In contrast, elective cesarean section has been observed to yield a significantly lower rate of postpartum SUI.⁷

More women are requesting cesarean deliveries to protect their pelvic floor. It is unclear at this time if the benefits of an elective cesarean outweigh the risks of a surgical procedure. Certain risk factors may make pelvic floor injury more likely in some women who deliver vaginally so a cesarean section may be warranted. Unfortunately, these risk factors are not clearly understood at this time.

Treatment and management strategies for postpartum SUI include behavioral modifications, intravaginal support devices, or drug therapy. Behavioral modifications involve pelvic floor muscle exercises, bladder training, and lifestyle changes. Intravaginal devices, such as pessaries, provide mechanical support to the urethra. Additionally, medication may be used either alone or in conjunction with behavioral modifications or medical devices. None of the drugs currently prescribed, such as estrogen, alpha-adrenergic agonists, and imipramine, are approved specifically for SUI, and use has been limited by variable results and adverse side effects.²⁶ However, duloxetine is an investigational agent that has been shown in clinical trials to be safe and effective for the treatment of SUI.²⁷ Duloxetine, a selective serotonin and norepinephrine reuptake inhibitor, has been observed to reduce incontinence episode frequency and increase quality of life compared with the placebo.²⁸

References

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