Urinary Incontinence in the Childbearing Woman

Written By: Sam Savage

Published Date: July 23, 2008 Last Edited: July 23, 2008

By Herbruck, Lianne F

Urinary Incontinence (UI) is an often under-reported and untreated medical condition that affects the lives of women of all ages and backgrounds. Although there are six major types of UI, stress urinary incontinence (SUI) is the type most often associated with women of childbearing age. Development of SUI has also been linked to the childbirth process itself.This article will discuss the types, characteristics, and diagnosis of UI, with a focus on SUI. Precipitating factors for SUI, including the influence of pregnancy, childbirth, and aging on its development, will be reviewed. Key Words: Urinary incontinence, pelvic floor disorder, stress urinary incontinence, pelvic organ prolapse, pregnancy, aging, childbirth.

Urinary incontinence (UI) is an undiagnosed, under-reported, and often untreated medical condition that highly impacts quality of life for women of all ages (Bernier & Sims, 2009; Kelleher, 2003; Morkved, Bo, Schei, & Salvesen, 2003; Peeker & Peeker, 2003; Subak et al, 2006; Trowbridge, Wei, Fenner, Ashton- Miller, & DeLancey, 2007). Though study estimates vary widely, the estimated prevalence of UI is between 25% to 55% (Altman et al., 2006; Brolmann, 2004; Buchsbaum, Chin, Glantz, & Guzick, 2002; Culligan & Heit, 2000; Lowdermilk, 2004). As many as one-third of woman 40 years of age or older, and up to 50% of women aged 60 and older, report symptoms of UI at least once per week (Danforth et al., 2006; Huang, Brown, Thom, Fink, & Yaffe, 2007; Pantazis & Freeman, 2006; Trowbridge et al., 2007; Waetjen et al., 2003).

The number of elderly women is predicted to more than double in the United States between 2000 and 2050. Because incidence of UI increases with each decade, it is easy to predict that there will be an increased demand for services pertaining to female pelvic floor disorders (PFD) and UI (Brolmann, 2004; Trowbridge et al., 2007). However, only 20% to 25% of women with UI symptoms solicit medical advice, and many of those who do wait years before seeking care (Culligan & Heit, 2000; Kelleher, 2003; Pantazis & Freeman, 2006; Trowbridge et al., 2007; Viktrup, Rortviet, & Lose, 2006).

BACKGROUND

A woman’s biology, as well as environmental influences, contribute to and encourage the development of PFD and UI. Obesity, vaginal delivery, and multiparity are some factors that increase risk (Nygaard, 2005, 2006; Peeker & Peeker, 2003; Wesnes, Rortveit, Kari, & Hunskaar, 2007; Wilson, Herbison, & Herbison, 1996). Although primary risk factors for incontinence may differ over the course of a woman’s lifetime, damage to muscles, nerves, and connective tissue of the pelvic floor (PF) resulting from pregnancy and childbirth are believed to be major contributors to the development of disorders, such as UI, pelvic organ prolapse (POP), and fecal incontinence (Culligan, Blackwell, Murphy, Ziegler, & Heit, 2005; Danforth et al., 2006). These three conditions, either alone or in combination, make up the very definition of pelvic floor disorders (Brolmann, 2004).

The association between UI and pregnancy and childbirth is one that has been widely accepted for the last several decades. It is thought that trauma to the supportive tissue, ligaments, and pelvic floor muscles, as well as denervation of the PF during obstetric events, increases the likelihood of UI development (Altman et al., 2006; Morkved et al., 2003; Nygaard, 2005; Pantazis & Freeman, 2006; Wesnes et al., 2007). Damage to the pudendal nerve, such as that which can occur during childbirth, is associated with PFD (Peeker & Peeker, 2003; Viktrup et al., 2006). Childbirth injuries to the PF and their potential long-term sequelae are major public health concerns because the economic and psychological costs of managing UI and POP are significant (Heit, Mudd, & Culligan, 2001).

The causal association of UI with pregnancy and childbirth, particularly antenatal and prepregnancy UI, has become widely accepted over the last several decades. It is thought that childbirth-related UI results from trauma to the supportive tissue, ligaments, and pelvic floor muscles, as well as from denervation of the PF during obstetric events (Altman et al., 2006; Morkved et al., 2003; Pantazis & Freeman, 2006; Wesnes et al., 2007; Woldringh, van den Wijngaart, Albers-Heitner, Lycklama a Nijeholt, & Lagro- Janssen, 2007). Vaginal delivery may increase the risk of PFD by two to three fold, and first delivery has a greater association with longlasting SUI over first pregnancy (Viktrup et al., 2006; Wesnes et al., 2007; Nygaard, 2005; Sand et al., 1995). High parity and forceps deliveries are associated with an increased incidence of postnatal UI, which is a risk factor for long-term UI (Pantazis & Freeman, 2006; Peeker & Peeker, 2003).

Much of the literature that focuses on vaginal deliveries and their relation to PFD and UI are based on all types of vaginal deliveries. This includes instrumental deliveries as well as common second-stage interventions, including episiotomy and forced pushing. These types of interventions may increase the risk of PFD by compromising the integrity of the intact pelvic floor during birth (Leslie, 2004).

Recently, there has been a trend in primary, elective cesarean sections (CS) without medical indications. Instead of undergoing a trial of labor and subsequent vaginal delivery, women are opting for a surgical resolution to their pregnancies. Protection of the PF is one of the main arguments for this procedure (Bettes et al., 2007; Nygaard, 2006; Visco et al., 2006). However, most women who deliver vaginally do not have severe PFD (Nygaard, 2005). In addition, it is important to note that some women who never become pregnant or bear children develop PFD or UI (Buchsbaum et al., 2002).

TYPES OF URINARY INCONTINENCE

The six types of UI classifications are stress (SUI), urge (UUI), mixed (MUI), overflow, functional, and reflex (see Figure 1). The three most common types of UI are SUI, UUI, and MUI. SUI is the most common type of UI in women under age 60 and accounts for almost half of incontinence in all women (McCool & Durain, 2004; Waetjen et al., 2003).

SUI results from ineffective closure of the bladder neck and the urethral sphincter, often due to loss of integrity of the vaginal musculofascial attachments (including the pubo-urethral ligaments and endopelvic fascia) that normally support the bladder neck and urethra in a retropubic position. This loss leads to hypermobility and descent of structures, which ultimately results in impaired intra-abdominal pressure transmission to the urethra (Bernier & Sims, 2009; Culligan & Heit, 2000; Lingam, 2001; Lowdermilk, 2004; McCool & Durain, 2004; Pantazis & Freeman, 2006).

This loss of bladder neck support is often attributed to nerve, muscle, and connective tissue damage during vaginal delivery. Changes in the urethrovesical junction due to weakness of the periurethral muscles from childbirth or menopause cause general loosening of the PF, which can create a funneling effect of the bladder neck during exertion (Bernier & Sims, 2009; Culligan & Heit, 2000; McCool & Durain, 2004; Pantazis & Freeman, 2006).

Up to one-third of women experience SUI precipitated by physical activity and exertion (including laughing, coughing, and exercising) in the absence of bladder (detrusor) contraction (Culligan & Heit, 2000; Moore, 2001; Rousseau, 2004). Deficient PF support, obesity, urinary tract infection (UTI), chronic cough, or sphincter weakness (intrinsic sphincter deficiency) are contributory factors (Bernier & Sims, 2009; Culligan & Heit, 2000; McCool & Durain, 2004; Pantazis & Freeman, 2006;). Intrinsic sphincter deficiency is usually a more severe form of SUI that is associated with advanced age, estrogen loss, previous vaginal surgery, obstetric trauma, urogenital prolapse, and certain neurological conditions (Culligan & Heit, 2000). There is no urge component with SUI (Peeker & Peeker, 2003).

UUI is an involuntary loss of urine associated with a strong desire to void without delay, whether or not the bladder is full. This is accompanied by the inability to tighten the urethral sphincter to inhibit voiding. It is sometimes referred to as overactive bladder (OAB) (Bernier & Sims, 2009; Culligan & Heit, 2000; McCool & Durain, 2004; Peeker & Peeker, 2003; Pantazis & Freeman, 2006).

MUI is identified when symptoms of both SUI and UUI are present. It is diagnosed by a combination of urodynamic conditions, such as urodynamic SUI and detrusor overactivity (Bump, Norton, Zinner, & Yalcin, 2003; Culligan & Heit, 2000). Treatment of MUI is based on the predominate, or most bothersome, symptoms (Culligan & Heit, 2000; McCool & Durain, 2004; Pantazis & Freeman, 2006; Peeker & Peeker, 2003). In the clinical setting, MUI symptoms are actually more common than mixed conditions, and women whose UI is more bothersome or is perceived to be more severe tend to be diagnosed with MUI. However, upon urodynamic testing, many of these women often show conclusive results for either SUI or UUI, not both (Bump et al, 2003). In a randomized, double-blind, placebo-controlled study, Bump and coauthors (2003) found that with treatment and as the severity of UI improved, mixed symptoms resolved. This suggests that SUI that is more severe may produce mixed symptoms (Bump et al., 2003), which may indicate that UI symptoms often imprecisely predict the true pathophysiologic mechanism responsible for UI in individual patients (Bump et al., 2003; Lingam, 2001). Generally, pregnancy and childbirth are more likely to precipitate symptoms of SUI. For these reasons, this article will focus on SUI. RISK FACTORS FOR STRESS URINARY INCONTINENCE

General

Common causes of SUI include pregnancy, vaginal delivery, menopause, and surgical procedures that damage nerves leading to pelvic floor muscles (Bernier & Sims, 2009). Trauma to the supportive tissue and denervation of the PF, particularly the pudendal nerve, during obstetric events increase the likelihood of longterm UI (Altman et al., 2006; Pantazis & Freeman, 2006). The pudendal nerve innervates the anal and urethral sphincters as it travels along the pelvic sidewall, where it is particularly vulnerable to injury from the compressive forces of labor and delivery (Heit et al., 2001). High parity, operative vaginal deliveries (forceps and vacuum extraction), episiotomy, birth weight greater than 4,000 g, and second stage of labor lasting longer than 60 minutes significantly increase the risk of SUI after first delivery. This potential increase in the incidence of postnatal UI is a risk factor for long-term UI (Pantazis & Freeman, 2006; Viktrup et al., 2006). First delivery has a greater association with long- lasting SUI over first pregnancy, and women with two live births have as much as a 67% increased odds of UI compared to nulliparous women (Danforth et al.,2006; Sand et al, 1995; Viktrup et al., 2006; Wesnes et al., 2007).

Other risk factors for SUI include advanced age, ethnicity, body mass index (BMI) > 30, diabetes mellitus, smoking, hysterectomy, PF injury, spinal cord trauma, neurological disease, chronic cough, and constipation (see Figure 2) (Danforth et al., 2006; Heit et al., 2001; McFarlin, 2004; Minassian, Lovatsis, Pascali, Alarab, & Drutz, 2006; Moore, 2001; Pantazis & Freeman, 2006; Rovner & Wein, 2004; Wesnes et al., 2007).

Both former and current cigarette smoking is positively associated with frequent and severe incontinence (Danforth et al., 2006). Chronic coughing exerts significant force on the bladder; the pressure from frequent and forceful coughing may ultimately cause damage to the urethral sphincter, vaginal supports, and perineal nerves, thereby worsening symptoms of SUI (Moore, 2001; Walters, 2005). Decreases in collagen synthesis associated with smoking may weaken pelvic support structures, and smokingrelated diseases (such as chronic obstructive pulmonary disease or asthma) may have direct or indirect effects on bladder and urethral function (Danforth et al., 2006).

A study by Minassian et al. (2006) found an association between childhood nocturnal enuresis and adult detrusor overactivity. Patients with previous history of nocturnal enuresis also had a greater risk for developing bladder dysfunction as adults (Minassian et al., 2006). Further investigation of this finding would be useful to help fully assess the impact of childhood UI on UI in adulthood because it could make providers aware of women who are likely to develop UI whether or not they give birth.

Connective tissue disorders have a clear association with UI and POP (Heit et al., 2001). Although abnormalities of collagen have been implicated in pathogenesis of UI and POP, the cause or effect remains to be established (Sultan & Fernando, 2001). Vaginal deliveries do not cause, nor does CS prevent, connective tissue abnormalities. These abnormalities may occur after years of decreased pelvic support, progressive pudendal neuropathy, and hypoestrogenism (Heit et al., 2001). Primary connective tissue abnormalities occur with pregnancy, and women who present with POP may have a genetically weaker endogenous collagen type and composition (Sasso, 2006). Identifying antenatal markers of collagen weakness that can predict women who may develop UI requires further study (Sultan & Fernando, 2001).

High BMI (>30) is a significant risk factor for long-term SUI symptoms, especially during the antenatal period (Buchsbaum et al., 2002; Danforth et al., 2006; Minassian et al., 2006; Moore, 2001; Peeker & Peeker, 2003; Viktrup et al., 2006; Wesnes et al., 2007). Certain medications, including opioids, sedatives, alcohol, antihistamines, hypotensive agents, beta-adrenergic blockers, and diuretics, can contribute to SUI, as can chronic disease and caffeine intake (Carroll, 2009; Kincade et al., 2007; Moore, 2001). Family history of SUI in the mother or any UI in multiple first- degree relatives are also predictors of SUI in individual women (Heit et al., 2001). Caucasian race is associated with an increase in UI risk, and structural and functional differences in the urethra and its support systems have been demonstrated between African- American and Caucasian women. African-American women have greater levator ani (LA) strength and greater urethral sphincter closure pressure (Danforth et al., 2006; Graham & Mallett, 2001; McIntosh, 2005; Moore, 2001, Pantazis & Freeman, 2006; Waetjen et al., 2003).

Influence of Pregnancy

Physical changes during pregnancy may play a contributory role in the process of fecal and urinary incontinence, and even the most non- traumatic birth can result in loss of pelvic muscle tone from pregnancy alone (Borello-France et al., 2006; Martindale & Paisley, 2004; McCool & Durain, 2004). Pregnancy as a risk factor for UI development suggests that factors other than the delivery of a child can contribute to SUI (Nygaard, 2006; Peeker & Peeker, 2003; Wesnes et al., 2007; Wilson et al., 1996). Although UI has been reported in 34% of women at 3 months postpartum, peak incidence is during pregnancy (Sultan & Fernando, 2001).

In the first trimester, the increased weight of the uterine fundus presses directly on the bladder and can compress the ureters. The ureters, renal pelvis, and calices dilate, and increasing levels of progesterone may lead to smooth muscle relaxation. Renal blood flow increases 50% with accompanying increases in the glomerular filtration rate (Martindale & Paisley, 2004). In the second trimester, the uterus rises up and out of the pelvis to become an abdominal organ, and pressure on the bladder lessens. In the third trimester, after the presenting part of the fetus descends into the pelvis, direct pressure on the bladder, coupled with decreased room for bladder distension, increases UI symptoms again (Varney, Kriebs, & Gregor, 2004a).

Hormonal influences may also precipitate urinary changes in pregnancy leading to UI development (Viktrup et al., 2006; Woldringh et al., 2007). Though urinary frequency is often a non-pathological discomfort of pregnancy, onset of SUI during first pregnancy or the puerperal period carries the risk of long-term symptoms at 5 and 15 years post-first delivery (Dolan, Hosker, Mallett, Allen, & Smith, 2003; Varney et al., 2004a; Viktrup et al., 2006; Woldringh et al., 2007). Five years post-delivery, the risk of SUI is four times as high (Viktrup et al., 2006), and at 15 years post-delivery, it is twice as high (Dolan et al., 2003). Obesity before first pregnancy and delivery increases the risk of SUI; in this case, there is a risk that SUI will become chronic and continue up to 12 years postpartum (Viktrup et al., 2006; Wesnes et al., 2007).

Using data from the Norwegian Mother and Child Cohort Study, Wesnes et al. (2007) investigated the incidence and prevalence of UI during pregnancy and its associated risk factors. Of the 43,279 data sets examined, 26.2% of all women reported UI before pregnancy (15.4% of nulliparous women, 33% of primiparous women, and 40% of multiparous women). SUI was the most commonly reported (Wesnes et al., 2007). During pregnancy, 58.1% (25,121) of women reported UI, again with SUI the most common. Among women who were continent prior to pregnancy, incidence of any incontinence by week 30 of pregnancy was 45.6%. During pregnancy, 48% of nulliparous women and 66.6% of parous women experienced incontinence. In this study, prevalence of any UI was doubled compared with prevalence before pregnancy, with the increase most notable in the SUI component. UI both prior to and during pregnancy was found to be associated with parity, age, and BMI (Wesnes et al., 2007).

Bony Pelvis

The bony structure of the pelvis itself may indicate women at a higher risk for developing UI after pregnancy and childbirth, and may also provide further explanation for the racial differences in UI symptoms. Handa and coauthors (2003) performed a retrospective, record review, casecontrol study of women who had undergone pelvic MRI to examine differences between the bony pelvis structures of women with and without PFD. Fifty-nine subjects were in the case group (women with PFD) and 39 were in the control group (women without PFD). Of the 59 women with PFD, the most common complaints were SUI and POP. According to the demographics of the study cohort, women presenting with PFD were more likely to be white, older, and of higher parity.

Typical obstetric pelvic measurements that are adequate for vaginal delivery include a transverse inlet of 12 cm or more, an obstetrical conjugate of 10 cm or more, and an interspinous diameter of 10 cm or more (Lowdermilk, 2004; Varney, Kriebs, & Gregor, 2004b). The four common pelvic shapes are gynecoid, android, anthropoid, and platypelloid (see Table 1). Handa et al. (2003) found that women who had a wide transverse inlet (>13.9 cm) (odds ratio 3.425) and narrow obstetric conjugate (odds ratio 0.233) were more likely to have PFD. Using logistic regression to control for age and parity, PFDs were 7.2 times more likely in women with transverse inlets greater than 13.9 cm (p

Advancing Age

Before menopause, estrogen receptors are present in female urethral and bladder tissues, as well as in the PF musculature (Herbruck, 2009; Chancellor, 2000; Moore, 2001; Rovner & Wein, 2004). Depletion of estrogen at menopause is associated with diminished urethral mucosa, vascularity, and thickness, all of which can cause the urethra to loose its ability to maintain a tight seal, especially when intra-abdominal pressure increases, such as with the Valsalva maneuver, coughing, or exercise (Bernier & Sims, 2009; Moore, 2001). Reduction of estrogen with aging also leads to vaginal dryness, loss of tissue elasticity affecting support in the perineal region, devascularization and thinning of mucosal and support tissues, urogenital changes (including decreases in collagen content), and atrophic changes in tissues of the pelvic floor (McIntosh, 2005; Rousseau, 2004; Sasso, 2006). Loss of estrogen also contributes to an increased tendency for PFD development in women with pelvises damaged by the childbirth process (McIntosh, 2005).

Independent predictors of UI in older women include Caucasian race, estrogen cream use, vaginal dryness, vaginal discharge, lifetime number of UTIs (> 6), and diabetic peripheral nephropathy. History of hysterectomy is predictive of severe incontinence (Jackson, Scholes, Boyko, Abraham, & Fihn, 2006). In some women, shrinking of the uterus, vulva, and distal portion of the urethra that accompanies aging can lead to urinary frequency, dysuria, uterine prolapse, and SUI (Lowdermilk, 2004).

Pelvic Organ Prolapse

Pelvic organ prolapse (POP), a commonly occurring and distressing condition, is defined as protrusion or projection of pelvic organs into the vagina or outside the vagina that progresses over time (McIntosh, 2005; Sasso, 2006; Farkas & Radley, 2002). Vaginal anatomical models from DeLancey (1993) depict the support of pelvic structures to show that vaginal prolapse is a phenomenon of the failure of vaginal, not uterine, support (Delancey, 1999; Farkas & Radley, 2002). It is commonly thought that POP is caused by denervation of PF muscles and/or disruption of endopelvic fascia (Sasso, 2006). POP is associated with a distortion of the urethra and may cause voiding difficulties (Fernando, Thakar, Sultan, Shah, & Jones, 2006). Annual costs in the U.S. have been estimated to be around $10 billion annually for POP treatment and care (Romanzi, 2002). POP is often thought of as a silent disease because many women who suffer with the associated symptoms, including UI, rectal pressure, pain, and discomfort, often find it embarrassing to discuss it with their providers (Fernando et al., 2006; Sasso, 2006).

Risk factors for POP include age, parity, forceps delivery, neruomusclar damage of the PF, family history of prolapse, obesity, HRT use, menopause, hysterectomy, and connective tissue disorders (Bradley, Zimmerman & Nyggard, 2007; DeLancey et al., 2007; Farkas & Radley, 2002; Heit & Culligan, 2001; Sasso, 2006). Other contributing factors to POP include smoking, individual anatomy, constipation, neurological disease, long labor, instrument-assisted delivery, large birthweight babies, chronic respiratory disease, and Caucasian race (Buchsbaum et al., 2006; McIntosh, 2005; Vimplis & Hooper, 2005).

Vaginal birth confers a 4 to11-fold increase in risk for developing POP among parous women and is the single most important modifiable factor for this condition (Delancey, et al., 2007). Fiftypercent of parous women over age 50 are affected by POP (Fernando, et al, 2006); however, many parous women never develop symptoms of POP. POP can also occur in women who have never given birth because uterine prolapse occurs in 2% of nulliparous women (Buchsbaum, et al., 2006; McIntosh, 2005). Lukacz, Lawrence, Contreras, Nager, and Luber (2006) found that incidence of POP is the same in women who have had a CS after labor had begun and women who had vaginal delivery, but incidence was lower in women who had a CS without labor. This may indicate that it is the event of labor, rather than the pregnancy, that contributes more to POP development. Their study also found that women who had been pregnant but who had never delivered an infant had an increased risk in POP over nulliparous women.

Bradley et al. (2007) performed a 4-year prospective observational study on 259 postmenopausal women to examine the natural history of POP and risk factors for changes in vaginal descent. They found that prolapse progresses and regresses in older women, with rates of vaginal descent progression slightly greater than regression. DeLancey et al. (2007) studied 286 women (151 with POP and 135 without POP) using MRI to determine and compare LA defects between the groups. LA muscles are unique striated muscles that play a critical role in pelvic organ support because they provide postural and upward support to the pelvic viscera. They found that there are strong associations between POP and major LA defects (p

Although POP is a common disorder, the true incidence is not known. Some women who present with what would be considered “severe” POP have no symptoms, while some women with “mild” POP have debilitating symptoms (Sasso, 2006; Vimplis & Hooper, 2005). Patients with a major degree of POP rarely have SUI (Vimplis & Hooper, 2005; Ward, 2003).

Treatment and assessment of POP is based as much on symptomology as it is the extent of the prolapse. Symptom assessment must include the prolapse itself, as well as related PFDs, including urinary, bowel, and sexual functioning. The patient’s view of her symptoms, needs, and expectations are paramount to her treatment (Farkas & Radley, 2002). Symptoms generally relate to type and location of POP, but location and extent may not correlate well with symptom severity (Sasso, 2006). Treatment of POP strives to maintain urinary and bowel function, preserve sexual function, and decrease irritating symptoms (Farkas & Radley, 2002; Vimplis & Hooper, 2005). Symptoms generally relate to type and location of POP, but location and extent may not correlate well with symptom severity (Sasso, 2006).

Treatment of POP strives to maintain urinary and bowel function, preserve sexual function, and decrease irritating symptoms (Farkas & Radley, 2002; Vimplis & Hooper, 2005). Pessary use improves POP and associated pelvic organ dysfunction, including bladder, bowel, and sexual function. Pessaries may be an appropriate conservative treatment, and is a first-line treatment in women who are not good surgical candidates (Bernier & Sims, 2009, Fernando et al., 2006; Herbruck, 2009; Vimplis & Hooper, 2005). Sometimes pessary placement can unmask incontinence by straightening out urethral kinks that may have been causing some level of urinary retention (Walters, 2005). However, pessary placement, particularly when fitted with an incontinence ring, can help reduce symptoms of known SUI and UUI (Culligan & Heit, 2000; Fernando et al., 2006; McIntosh, 2005; Rovner & Wein, 2004).

Alternative treatment of POP may also include lifestyle changes, such as weight loss or resolution of constipation, to prevent worsening of POP (Vimplis & Hooper, 2005). Surgical treatment includes colposuspension of the anterior or posterior compartments. Newer techniques exist, including tension-free vaginal tape and other procedures that employ the use of synthetic materials. Ongoing studies aim to determine their effectiveness when compared to colposuspension (Farkas & Radley, 2002).

SUI in the Nulliparous Woman

With aging populations on the rise, greater numbers of nulliparous women are being identified with urogential prolapse and SUI (Sultan & Fernando, 2001). It is important to remember that nulliparous women experience SUI and that UI itself is not entirely related to childbirth (Lowdermilk, 2004). Additional factors other than childbirth that might contribute to UI development include heredity, menopause and the subsequent loss of estrogen, and pelvic surgeries (Altman et al., 2006; Buchsbaum et al., 2002; Nygaard, 2005).

Buschbaum and colleagues (2002) performed a study examining the prevalence of UI among a group of 149 nulliparous nuns. Individual medical history, demographic data, and symptoms of UI were examined. This study concluded that prevalence of UI among nulliparous, postmenopausal nuns was similar to UI rates reported by parous, postmenopausal women. After multivariate logistic regression, BMI (p = 0.001), multiple UTIs (p = 0.033), and depression (p = 0.022) were significant statistics that correlated with UI in the study group (Buchsbaum et al., 2002).

Since parity and pelvic trauma are considered major risk factors for SUI, one might expect the occurrence of UUI to be higher than occurrence of SUI in nulliparous postmenopausal women. However, in the Buchsbaum et al. (2002) study, they found that UI in elderly, postmenopausal, nulliparous women was associated with SUI more often than UUI, even in the absence of trauma of the pelvic floor due to pregnancy or childbirth. These results directly contradict the theories that nulliparity protects against SUI. Trowbridge and colleagues (2007) performed a cross-sectional study involving a cohort of 82 nulliparous women to evaluate the effects of aging, independent of parity, on POP, urethral support and function, and levator function. Women 20 to 71 years of age underwent a pelvic examination. Additional tests performed were POP quantification (POP- Q measured at maximal Valsalva strain), urethral angles by cotton- tipped swab, and multichannel urodynamics and uroflow. Vaginal closure was also quantified. In this study, increasing age was associated with decreasing maximal urethralclosure pressure (r = – 0.758, p

SUMMARY

The effects of UI on women are wide-reaching and life altering. Costs in both financial and emotional/social realms burden women of all ages throughout their life cycle. Though studies continue to find associations between incontinence and childbearing, it is prudent to remember that there are other genetic and environmental factors that can play a roll in the establishment of UI and PFDs in any individual woman’s health history.

Future studies may investigate which exact biological and environmental factors play roles that may place certain women at higher risk for severe PFD and UI (Nygaard, 2005). Additional studies regarding relationships between the maternal bony pelvis and obstetrical injuries may also provide further insight into PF issues. Studies that examine modifications and improvements in labor and birth procedures (including management of the second stage of labor, positional changes and perineal management during delivery, use of episiotomy, instrumental/operative vaginal deliveries, and cesarean section) to impart the least damage to the PF have the potential to benefit all childbearing women. Studies designed to evaluate the natural history of incontinence over a woman’s lifetime have the potential to provide strong scientific evidence for a cause- and-effect relationship of an etiology, as well as a better understanding of the natural occurrence and progression of UI and PF issues (Handa et al., 2003; McFarlin, 2004).

Urologic Nursing Editorial Board Statements of Disclosure

Christine Bradway, PhD, RN, disclosed that she is on the Consulting Board for Boehringer Ingelheim Pharmaceuticals, Inc.

Kaye K. Gaines, MS, ARNP, CUNP, disclosed that she is on the Speakers’ Bureau for Pfizer, Inc., and Novartis Oncology.

Susanne A. Quallich, ANP,BC, NP-C, CUNP, disclosed that she is on the Consultants’ Bureau for Coloplast.

All other Urologic Nursing Editorial Board members reported no actual or potential conflict of interest in relation to this continuing nursing education article.

Figure 1.

Major Classifications of Urinary Incontinence

Stress Urinary Incontinence

Involuntary leakage upon effort or exertion, or on sneezing or coughing; loss of urine upon increased abdomen pressure.

Causes:Urethral hypermobility due to weakened pelvic floor muscles, pregnancy, intrinsic sphincter deficiency, or aging.

Urge Urinary Incontinence (Overactive Bladder in Between Overactivity)

Involuntary leakage of urine immediately preceded or accompanied by urgency; sudden sensation of a need to urinate with inability to get to a toilet before involuntary leakage.

Causes:Overactive bladder; detrusor overactivity +/- spontaneous contraction, bladder infections, nerve damage from stroke, dementia, or multiple sclerosis.

Mixed Urinary Incontinence

Involuntary leakage associated with urgency as well as with exertion, effort, or increased abdominal pressure, causing symptoms of both conditions.

Causes:See above; usually the type causing the most bothersome symptoms will be treated first.

Overflow Incontinence

Condition where the bladder is full but not able to empty properly. This causes leaks, dribbles, and hesitancy. More common in men.

Causes:Urethral blockage hindering passage of urine from the bladder; weakened bladder contractions due to diabetes mellitus or neurologic disorder.

Functional Incontinence

Condition where the urinary system is normal, but sufferers have mental or physical conditions that preclude adequate or appropriate toileting.

Causes:Parkinson’s disease, Alzheimer’s disease, severe depression, severe arthritic conditions.

Reflex Incontinence

Involuntary loss of bladder control without warning; the bladder empties due to reflex activity with no control of urination.

Causes:Neurological impairment, such as quadriplegia or spinal cord lesions.

Figure 2.

Risk Factors for Stress Urinary Incontinence

Female gender

Pregnancy

Vaginal delivery

Advanced age

BMI > 30

Diabetes mellitus

Smoking

Hysterectomy

Spinal cord trauma

Neurological disease

Chronic cough

Constipation

Pelvic floor injury

High impact exercise

Ethnicity (Caucasian race)

Pelvic surgery

Certain medications

Pelvic prolapse

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Lianne F. Herbruck, MSN, RN, CNM, is a Certified Nurse Midwife, Cleveland, OH.

Note: Objectives and CNE Evaluation Form appear on page 172.

Note: The author reported no actual or potential conflict of interest in relation to this continuing nursing education article.

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