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Chronic urinary retention in females

Chronic urinary retention in females
Literature review current through: Jan 2024.
This topic last updated: Apr 22, 2022.

INTRODUCTION — Chronic urinary retention (CUR) is the accumulation of urine in the bladder that results from incomplete or inadequate bladder emptying. Incomplete bladder emptying is most commonly described and measured as the volume of urine left in the bladder after voiding, also known as the postvoid residual. The two common causes of CUR are bladder muscle dysfunction (detrusor underactivity) and obstruction. CUR is generally a gradual process.

This topic will review the etiology, evaluation, and treatment options for females with CUR. Issues of acute urinary retention and postoperative urinary retention are discussed separately.

(See "Acute urinary retention".)

(See "Postoperative urinary retention in females".)

In this topic, when discussing study results, we will use the terms "woman/en" or "patient(s)" as they are used in the studies presented. However, we encourage the reader to consider the specific counseling and treatment needs of transgender and gender diverse individuals.

DEFINITION — Clinically relevant CUR is the accumulation of urine that results in adverse clinical outcome in the absence of intervention [1]. CUR is typically determined by measuring a postvoid residual urine volume (PVR). PVR is defined by the International Continence Society as the volume of urine left in the bladder at the completion of micturition [2]. The American Urological Association (AUA) Quality Improvement and Patient Safety committee defined CUR as "an elevated postvoid residual (PVR) of >300 mL that has persisted for at least six months documented on two or more separate occasions" [3]. However, the authors acknowledge that no single PVR value defines CUR in all individuals. Further, the AUA definition of CUR relates specifically to their proposed treatment algorithm, and the term CUR will be used in this article to more broadly encompass incomplete bladder emptying. The AUA work group defined high-risk CUR as people who are at increased risk for potential organ damage including renal failure, pyelonephritis, or urosepsis. (See 'Diagnosis' below.)

PATHOPHYSIOLOGY — Normal voiding requires coordinated urethral and pelvic floor muscle relaxation followed by bladder contraction [2]; any disruption to these actions can result in urinary retention. The voiding reflex is triggered in the pontine micturition center and leads to relaxation of the external striated urethral sphincter (via sympathetic innervation from the hypogastric nerve) and pelvic floor muscles (via somatic innervation by the pudendal nerve) (figure 1) [4]. The resultant drop in urethral pressure is followed by contraction of the bladder detrusor muscle, which is mediated by parasympathetic innervation from the pelvic plexus. Incomplete emptying can result from abnormal function anywhere along the above pathway or when there is obstruction at the outlet level.

EPIDEMIOLOGY

Prevalence — As the diagnosis of CUR requires testing such as postvoid residual (PVR) or urodynamic assessment, prevalence estimates come from the subpopulation of women referred for specialty evaluation. Estimates of CUR in women from the general population are difficult to obtain because symptoms of incomplete emptying and obstructed flow do not reliably predict CUR in women [5]. In studies that reported PVR in women presenting with a variety of lower urinary tract symptoms, 8 to 9 percent of patients were found to have PVR of ≥100 mL and up to 5 percent had PVR ≥150 mL [6,7]. (See 'Diagnosis' below.)

Risk factors — Risk factors for reduced or absent bladder contraction (ie, detrusor underactivity and detrusor acontractility) and resultant CUR include the normal aging process, neurogenic diseases such as Parkinson disease and multiple sclerosis, myogenic diseases, and iatrogenic interventions such as pelvic surgery or radiation [8]. Risk factors for obstructive causes of CUR include conditions that cause mass effect or urethral kinking, such as a urethral mass, prior incontinence surgery, or pelvic organ prolapse. These are discussed in detail below. (See 'Detrusor underactivity' below and 'Obstruction' below.)

CAUSES OF URINARY RETENTION — CUR may be caused by impaired detrusor activity, bladder outlet obstruction, or both [1].

Detrusor underactivity — The International Continence Society defines detrusor underactivity (DU) as a "contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span" [2]. DU represents an inability of the bladder to generate adequate contraction strength and is likely multifactorial [9]. The diagnosis is primarily made by urodynamic testing [8]. An extreme form of DU, acontractile detrusor, is the true absence of detrusor contraction during the voiding phase of urodynamic evaluation. Underactive bladder (UAB) is considered to be a symptom of DU; however, clinical presentation is variable, and noninvasive diagnostic criteria are lacking [10]. The International Consultation on Incontinence is developing a UAB outcomes measure; however, it is unknown whether the questionnaire will also be useful as a screening tool [11]. (See 'Urodynamic evaluation' below.)

Of note, a subset of women will have difficulty voiding in the artificial urodynamic environment, and therefore may appear to have urinary retention or obstruction, but otherwise have no signs or symptoms of incomplete bladder emptying. Caution must be made when interpreting the pressure flow data in these patients, and it is important to take symptoms and other measures such as the postvoid residual (PVR) into account when interpreting the urodynamic findings for these women.

Detrusor function may be affected by multiple factors, including bladder outlet obstruction, local neuropathy (both sensory and motor innervation), central nervous system disorders, ischemic changes, and bladder wall muscle changes. Thus, common causes of DU include aging, diabetes, neurologic diseases, and medications.

Aging — Detrusor contraction strength, urine flow rate, and bladder sensation decline significantly with age [12,13]. These age-related changes increase the risk of inadequate voiding and can ultimately result in urinary retention. Possible mechanisms of age-related decline in bladder function include decreased smooth muscle:collagen ratio [14], decreased bladder sensation [15], and diminished brain response to bladder filling [16].

Although bladder muscle function changes with increasing age, PVR urine volume does not appear to increase with normal aging. An observational study of 85 community-dwelling women reported no difference in the lowest PVR between women 20 to 39 years of age and women ≥60 years (10 mL versus 12 mL, respectively) [13]. Therefore, an elevated PVR cannot be attributed to age alone and clinical evaluation is warranted.

Diabetes mellitus — Diabetes is associated with urinary disease, including both voiding and storage disorders [17,18]. As an example, in a study of 194 women with type 2 diabetes compared with 162 nondiabetic controls, diabetic women were more likely to have a PVR urine volume >100 mL (14 percent versus 2 percent) [19]. A study of urodynamic findings in men and women with diabetes reported that 30 percent of women had impaired detrusor contractility and 13 percent had an acontractile detrusor [17].

The myogenic and neurogenic alterations in diabetes are thought to be the result of prolonged hyperglycemia and production of oxidative stress products [20-22]. Oxidative stress contributes to peripheral neuropathy and subsequently impairs bladder function. In the studies above, peripheral neuropathy was associated with acontractile detrusor [17] and decreased bladder emptying [19]. The association of peripheral neuropathy and bladder dysfunction is particularly important because the prevalence of neuropathy is estimated to be approximately 8 percent in newly diagnosed diabetes patients and greater than 50 percent in patients with long-standing disease [23,24]. (See "Diabetic autonomic neuropathy", section on 'Genitourinary autonomic neuropathy'.)

Neurologic disorders — Lower urinary tract dysfunction and subsequent CUR can result from a wide range of neurologic disorders [25]. The site of the lesion in the neurological axis, such as in spinal cord injury, determines the general pattern of lower urinary tract dysfunction, which is reflected in the patient's symptoms. (See "Chronic complications of spinal cord injury and disease", section on 'Urinary complications'.)

Progressive neurologic diseases such as multiple sclerosis are associated with DU and resultant CUR. Many (50 to 80 percent) patients with multiple sclerosis report symptoms of urinary retention, urinary incontinence, or both [26]. In a study of 170 symptomatic men and women with MS who underwent urodynamic evaluation, 63 percent of patients had an elevated PVR (≥100 mL), with a mean residual volume of 220 mL [27]. A survey study of over 9600 patients with MS (25 percent men and 75 percent women) reported that one-quarter of respondents required urinary catheterization to treat CUR, including self-catheterization or indwelling catheter [28]. Longer duration of disease and increased physical disability were associated with increased urinary catheter use.

Patients with spinal cord injury as a cause of CUR are a population with unique challenges. CUR in individuals with spinal cord injury is reviewed separately. (See "Chronic complications of spinal cord injury and disease", section on 'Bladder dysfunction'.)

In contrast with patients with progressive or permanent neurologic disease, individuals with reversible spinal disorders (eg, disc herniation or compression) can have improvement in their bladder function after correction of the spinal lesion. However, it is not known if the statistically significant reductions in PVR reported after spinal surgery are clinically relevant. As an example, in a study of patients with lumbar spinal cord compression due to either disc herniation or compression, 37 of 113 female subjects (33 percent) had bothersome lower urinary tract symptoms preoperatively [29]. While modest improvements in urinary symptom scores and urodynamic evaluation parameters were seen after decompression, it is unclear if the change in mean PVR from 48 mL to 22 mL is important clinically.

Medication — While medication use is a common cause of acute urinary retention, it is unclear how often it contributes to CUR, particularly in women. Drugs commonly associated with acute urinary retention have anticholinergic properties that can potentially affect parasympathetic-mediated detrusor contractility [30]. Such medications include antihistamines, tricyclic antidepressants, antispasmodics, antiparkinsonian medications, antipsychotics, vertigo treatments, bronchodilators, and overactive bladder drugs.

Medications can also impair other aspects of voiding function [30]. Selective serotonin/noradrenaline reuptake inhibitors have been associated with urinary retention; the mechanism appears to be increased resistance at the external sphincter that is mediated by activity at both the local and spinal neurons, though central serotonergic mechanisms may be involved as well. Benzodiazepines and opiates likely impair detrusor contractile ability and cause subsequent CUR. Finally, alpha-adrenergic agonists used for postural hypotension or nasal decongestion may lead to voiding difficulties due to increased tone at the internal urethral sphincter.

Obstruction — Bladder outlet obstruction (BOO) is defined by the International Continence Society as a "generic term for obstruction during voiding" [2]. Although BOO is one of the most common clinical complaints in adult men [31], BOO is less common in women [6,32]. The prevalence data on BOO in women range widely in part because of a lack of uniform definition and also because storage and voiding disorders can coexist [33]. When a urodynamic definition is used to diagnose BOO in women with voiding symptoms, BOO prevalence rates of 3 to 6 percent have been reported [32,34], although other studies have reported prevalence rates up to 29 percent [35]. It is important to note that BOO is a urodynamic diagnosis and not always accompanied by CUR or elevated PVR.

BOO in women is subdivided by cause into anatomic and functional subgroups.

Anatomic — Anatomic BOO represents an increased urethral pressure or resistance that prevents urine passage resulting from urethral distortion, external urethral compression, or intrinsic urethral lesions. Anatomic causes are generally more obvious than functional causes and are often suspected by the patient's history, such as a prior history of anti-incontinence surgery [36].

Urethral distortion — Pelvic organ prolapse may cause lower urinary tract anatomic distortion including urethral kinking, which can then result in impaired urine flow and an elevated PVR [37]. In a study of 636 women evaluated in a female pelvic medicine and reconstructive surgery clinic, prolapse beyond the hymen independently predicted urinary retention, defined as a PVR >150 mL [38]. In a different study, reduction of the prolapse with a pessary resolved the urinary obstruction in 17 of 18 women with prolapse beyond the hymen [39].

External urethral compression — Any process that compresses the urethra may impair urine flow and result in BOO. Biologic causes include fibroids, constipation, and malignancy. A common iatrogenic cause is a previous suburethral anti-incontinence sling.

Fibroids may cause urethral compression by displacing the cervix and subsequently compressing the urethra or bladder neck [40]. An alternate mechanism may be local pressure on the pelvic nerve plexus that causes a radiculopathy at the S1-S2 nerve roots [41]. In a retrospective review of 284 women who underwent myomectomy or hysterectomy, six women (2 percent) presented with acute urinary retention [40]. Of note, the urinary retention resolved in all women postoperatively. Similarly, a case series reported that acute urinary retention resolved in seven of eight women after surgical therapy for fibroids [42]. There does not appear to be a consistent fibroid location that is associated with urinary retention. The majority of the women in the series above had posterior-fundal fibroids, while in another small case series of four women, the fibroids were in the lower uterine segment or cervix for three of the four women [43].

While the treatment of constipation in children has been associated with a decrease in PVR [44], the role of constipation as a cause of urethral obstruction and resultant CUR in adults is unclear. A study of 44 nursing home patients with fecal impaction reported that 14 percent also had urinary retention [45]. However, bivariate analysis indicated that fecal impaction was associated with immobility and not DU or urinary retention [45]. In contrast, a study of 167 adults in a geriatric rehabilitation unit reported that the prevalence of urinary retention was 11 percent and was significantly associated with fecal impaction [46]. Although fecal impaction may contribute to CUR in certain settings, it is not known if treatment of constipation and fecal impaction will improve CUR in adults.

Intrinsic urethral lesions — Urethral lesions such as strictures, urethral diverticula, and caruncles can cause urethral blockage. Urethral strictures are typically caused by previous urethral or periurethral surgery or from previous dilation. Idiopathic urethral strictures can also occur but are less common. Strictures have been diagnosed in 4 to 13 percent of women with BOO, although the etiology of the strictures was not defined in these studies [34,35].

Urethral diverticulum and Skene's glands infrequently cause outlet obstruction, representing 1 to 3 percent of the cases of outlet obstruction in two large reviews [34,35]. Urethral cancer is rare and represents 1 percent of all malignancies, but may present with obstructive symptoms [47].

Functional — Functional obstruction is caused by abnormal contraction of the periurethral muscle (dysfunctional voiding [DV] or detrusor sphincter dyssynergia), failure of urethral relaxation (Fowler's syndrome), failure of pelvic floor muscle relaxation, or failure of bladder neck relaxation (primary bladder neck obstruction) [36]. Functional obstruction requires urodynamic evaluation for diagnosis, often with videocystourethrography or electromyography.

Dysfunctional voiding — DV is defined as "an intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the periurethral striated muscle during voiding in neurologically normal individuals" [2]. In contrast to detrusor sphincter dyssynergia, there is no neurologic cause for the findings. DV appears to be a learned behavior. In physiologic voiding, the pelvic floor muscles and external striated sphincter should relax just prior to detrusor contraction. In a retrospective review of 26 female patients diagnosed with DV, the mean age was 39 years, urgency and frequency were the most frequent presenting symptoms (82 percent), and episodes of urinary retention were reported in 19 percent [48]. One of the subjects with DV had vesicoureteral reflux and bilateral hydronephrosis, demonstrating the potential for upper tract damage with prolonged bladder outlet obstruction.

Detrusor sphincter dyssynergia — Women with neurologic disease that results in disruption between the pontine micturition center of the brain and the caudal spinal cord can develop detrusor sphincter dyssynergia [2,49]. Detrusor sphincter dyssynergia is an obstructive cause of CUR, in contrast to CUR caused by DU, which can also be seen in patients with neurologic disorders. (See 'Neurologic disorders' above.)

In detrusor sphincter dyssynergia, detrusor contraction occurs simultaneously with inappropriate contraction of the urethral striated muscle, the periurethral striated muscle, or both [50]. The end result is blockage of the bladder outlet. In a meta-analysis of five trials, the most common neurologic diseases causing detrusor sphincter dyssynergia were traumatic spinal cord injuries, multiple sclerosis, and congenital anomalies [51].

Fowler's syndrome — Another type of urethral abnormality that can result in functional BOO is Fowler’s syndrome. Fowler’s syndrome typically presents in young women (mean age 27 years old) as painless urinary retention (often in excess of 1 L) with no neurologic or anatomic etiology [52-54]. The diagnosis is made by a characteristic electromyography pattern that demonstrates failure of urethral sphincter relaxation, decrease in bladder sensation, and complex repetitive discharges are often present. It is not known if Fowler’s syndrome represents a subgroup of patients with DV or a distinct clinical entity in young women with CUR.

Primary bladder neck obstruction — In addition to abnormalities of urethral relaxation, functional BOO can be caused by primary bladder neck obstruction, which is thought to be the result of non-relaxation of the smooth muscle at the bladder neck during voiding [55]. Though the series describing diagnostic features of primary bladder neck obstruction is small, these patients tend to have significantly increased PVR (400 mL versus 125 mL) and lower flow rates compared with the dysfunctional voiding population.

CLINICAL PRESENTATION — Women with CUR often present complaining of partial or slow voiding or may be unable to void at all. In contrast to acute urinary retention, CUR is usually not painful. Additional symptoms include:

Bladder sensation abnormalities: feeling of incomplete emptying or reduced urge to void

Urine stream abnormalities: slow or intermittent stream

Voiding abnormalities: hesitancy in initiating flow of urine, straining to void, and needing to splint (reduce a vaginal bulge) to start flow of urine

Paradoxically, women with CUR from minimal or absent detrusor function can also present with overflow urinary incontinence. These women do not void but have constant urinary leakage from the overfilled bladder. Complete urinary retention with overflow incontinence is unusual in neurologically intact female patients. In one study of over 1100 women with lower urinary tract symptoms, overflow incontinence was diagnosed in 0.5 percent of women [56].

While many women with CUR will have some voiding complaints, symptoms such as sensation of incomplete bladder emptying are neither sensitive nor specific [5]. As an example, in a cohort study of 258 women with voiding symptoms, 87 percent of women had a normal postvoid residual (defined as less than 100 mL) despite voiding complaints [7]. Of the 57 women who were diagnosed with CUR by postvoid residual, the most common voiding symptom was sensation of incomplete emptying (30 percent).

POTENTIAL COMPLICATIONS — Two concerns with CUR are the potential risk of infection and elevated bladder pressures, both of which can lead to upper tract injury and impairment of renal function. However, the actual risk and clinical significance of these is not fully defined in women with CUR.

For women with CUR, urinary tract infection (UTI) is thought to be caused by retention and stagnation of urine that leads to bacteriuria and subsequent infection. However, it is unclear if CUR is truly a risk factor for bacteriuria in women, as data are mixed. In a study of postmenopausal women, women with culture-proven infections were more likely to have had any residual volume compared with women without infections (23 percent versus 2 percent) [57]. In contrast, in studies of nursing home residents, there was no association between postvoid residual (PVR) and UTI, and elevated PVR ≥100 mL did not confer a greater risk of UTI [58,59]. Similar findings have been reported in younger women as well. In a study of 213 college-aged women, there was no difference in mean PVR between women with recurrent UTIs and those without (mean PVR 43 versus 49 mL, respectively) [60].

CUR has the potential to cause renal damage, if accompanied by high-pressure storage, through the transmission of elevated bladder pressures to the upper urinary tract. The majority of literature looking at the relationship between retention, bladder pressure, and upper tract disease has been in patients with neurologic disease or in males with bladder outlet obstruction (BOO). In contrast, the majority of CUR in neurologically intact women is due to detrusor underactivity rather than BOO. Therefore, it is unlikely that women with non-neurogenic CUR are at risk for renal damage from elevated detrusor pressures. If a patient does meet the American Urological Association (AUA) definition of CUR (PVR >300 mL for at least six months documented on at least two separate occasions), a renal ultrasound and serum creatinine measurement is advised [3]. In addition, the AUA Quality Improvement and Patient Safety workgroup defined CUR patients at high risk for renal disease as those with concomitant hydronephrosis, hydroureter, bladder stones, Stage 3 chronic kidney disease, or recurrent urinary tract infections or urosepsis.

DIAGNOSIS — CUR is suspected in women who present with obstructive lower urinary tract symptoms, and the diagnosis is made by confirming an elevated postvoid residual urine volume (PVR). An abnormal test should be repeated as a single test is not highly reliable [61]. Because CUR can be associated with a range of voiding symptoms, we typically measure PVR by bladder scan on all new patients in our referral practice. The bladder scan is less invasive, has less potential to cause discomfort, and has acceptable correlation to catheterized PVR volumes. If the bladder scan is significantly elevated or if there is a high index of suspicion despite a normal PVR, we will perform a catheterized PVR to confirm. Once an elevated PVR has been established, we then proceed with a diagnostic evaluation to determine the cause.

PVR is defined as the volume of urine left in the bladder at the completion of micturition [2]. Consensus exists that a PVR of 50 mL to 100 mL is normal, PVR greater than 200 mL is abnormal, and PVR between 100 mL and 200 mL requires clinical correlation [62-64]. In the subpopulation of women with lower urinary tract symptoms, several studies support the use of 100 mL as the normal cut-off [63-66].

Assessment of PVR can be done with bladder catheterization or bladder ultrasound, commonly referred to as a bladder scan. Compared with bladder catheterization, bladder ultrasound is noninvasive, easier to perform, and preferred by patients. Standard ultrasonography may be used as well; however, multiple measurements are required to calculate an accurate bladder volume. Studies have demonstrated high correlation between bladder ultrasound PVR and catheterized PVR, in both benign gynecologic and urogynecologic populations [46,67-69]. Bladder ultrasound may be less accurate in obese patients (greater tissue depth) or in patients with ascites (adjacent fluid levels may be read as one volume). These women benefit from bladder catheterization to determine the PVR if there is clinical suspicion of incomplete emptying.

EVALUATION FOR THE UNDERLYING ETIOLOGY — We begin the evaluation of women with CUR by obtaining a complete history, including urinary, defecatory, and prolapse symptoms. While symptoms are neither sensitive nor specific for the etiology of CUR, a history can be helpful in identifying specific risk factors. For example, a sensation of incomplete emptying in a woman with a history of an anti-incontinence sling surgery is concerning for urinary obstruction at the urethra.

After obtaining the history, we perform a physical examination that includes a pelvic examination, pelvic organ prolapse quantification if appropriate, and focused neurologic testing (see "Pelvic organ prolapse in women: Diagnostic evaluation", section on 'Approach to the examination'). Either bladder ultrasound or catheterization is used to measure postvoid residual (PVR) within 10 minutes of voiding. Urinalysis and urine culture is performed to detect urinary tract infection as women with obstruction often present with both irritative and obstructive urinary symptoms.

The above examination can identify potentially reversible causes of CUR such as urinary tract infection, pelvic organ prolapse, leiomyomata, and mesh erosion. After office treatment of any suspected cause of CUR (pessary for prolapse, urinary tract infection treatment), urodynamic evaluation can help determine if the cause is detrusor underactivity (DU), bladder outlet obstruction (BOO), or a combination. Women who are diagnosed with BOO typically require additional testing to determine if the obstruction is anatomic or functional and the subtype of functional obstruction, if present. These tests can include cystourethroscopy, video urodynamic evaluation, and electromyography. Cystourethroscopy visualizes the urethra and bladder to diagnose anatomic causes of obstruction. Video urodynamic evaluation utilizes fluoroscopy at the time of voiding to correlate pressure, flow, and anatomic location of obstruction. Electromyography performed during micturition measures activity in the urethral sphincter and pelvic floor muscles. These additional tests can help distinguish subtypes of functional obstruction such as dysfunctional voiding, detrusor sphincter dyssynergia, and primary bladder neck obstruction.

Urodynamic evaluation — Urodynamic evaluation can help determine the underlying mechanism of CUR. The constellation of findings on urodynamic evaluation can help to distinguish DU from BOO.

In addition to an elevated PVR, women with CUR can demonstrate the following patterns on their urodynamic evaluation (table 1):

Women with detrusor acontractility will demonstrate absent bladder activity and no flow or possibly intermittent urine flow from straining or increasing abdominal pressure (ie, Valsalva voiding).

Women with DU will have low to normal flow rates, reduced detrusor pressure (Pdet) and/or duration [36].

Women with BOO typically have an increased detrusor pressure with reduced urine flow rates and/or prolonged urine flow time [13,36,49,70-72]. The observed changes in detrusor pressure and flow rate may be minor; a high index of suspicion and clinical correlation is required. Diagnostic nomograms of pressure and flow for men with benign prostatic hypertrophy do not apply well to pressure-flow studies in women as normal voiding detrusor pressures are significantly lower in women [72-74]. In addition, female voiding mechanisms may differ; women can use pelvic floor relaxation and abdominal straining to void.

Additional testing for women with BOO can further define the etiology. (See 'Additional tests' below.)

Women with dysfunctional voiding or detrusor sphincter dyssynergia have the typical BOO findings of increased bladder pressure and low flow rate. Additional studies demonstrate non-relaxation of the urethra (videocystourethrography) or increased urethral sphincter or pelvic floor muscle activity (electromyography [EMG]) during voiding. Of note, because detrusor sphincter dyssynergia is thought to result from neurologic dysfunction, women who are diagnosed with detrusor sphincter dyssynergia on urodynamic evaluation are evaluated for an underlying neurological disorder if one has not already been identified.

Women with primary bladder neck obstruction will have high voiding detrusor pressure and low flow rates of BOO. In addition, imaging studies obtained during voiding with videocystourethrography demonstrate the absence of bladder neck funneling [36,75,76].

Additional tests — Additional testing can be useful to further refine the diagnosis after urodynamic evaluation. Urodynamic evaluation can identify bladder outlet obstruction, but cannot determine if the obstruction is anatomic or functional. Women at risk for anatomic obstruction proceed with cystourethroscopy to evaluate the urethra, bladder neck, and bladder. Risk factors for anatomic obstruction include a history of prior anti-incontinence or prolapse surgery, pelvic mass on examination, and prior urethral surgery or procedures. Videocystourethrography is performed to rule out an anatomic or functional cause of obstruction that is only present or visible during voiding, such as increased urethral sphincter or pelvic floor activity. EMG is done for women with evidence of obstruction but no identified anatomic abnormality. EMG can assess pelvic floor muscle activity (patch EMG) or periurethral muscle activity (needle EMG), and evaluate for abnormal contraction or relaxation of the pelvic floor and urethra that results in outlet obstruction.

In addition, women at risk for upper tract disease, such as those with increased bladder pressure during filling, which indicates low compliance, can benefit from renal ultrasound to evaluate the upper urinary tract for hydronephrosis.

Cystourethroscopy — Cystourethroscopy can identify urethral anatomic causes for obstruction such as stricture, mass, or erosion of surgical material. In addition to women with known risk factors (eg, prior pelvic surgery), women with recurrent urinary tract infections and hematuria also undergo cystourethroscopy in order to evaluate for a foreign body or mass. In women with a history of a midurethral sling and symptoms of erosion, cystoscopy is performed to rule out erosion into the lower urinary tract. Careful attention must be paid to the urethroscopy portion to identify any sling material; a 0 degree lens is helpful for a circumferential view of the urethra.

Video urodynamic evaluation — Imaging during urodynamic testing, or video urodynamic evaluation, is the synchronous imaging of the bladder and urethra and measurement of bladder and abdominal pressures during filling cystometry and pressure flow study [2]. In some practices, video assessment (typically with fluoroscopy) is done during all urodynamic evaluations, while other practices utilize a more selective process. This test is also referred to as videocystourethrography.

For this technique, dual-channel cystometry is performed with the instillation of contrast media into the bladder and allows simultaneous imaging of the bladder during filling and voiding [36]. For women who have suspected BOO but no etiology evident on physical examination or cystoscopy, video urodynamic evaluation can identify functional causes of BOO such as dysfunctional voiding and primary bladder neck obstruction [35,55]. As an example, primary bladder neck obstruction is diagnosed by imaging the bladder neck during voiding and confirming a failure of the bladder neck to open during a detrusor contraction [55].

Electromyography — EMG can be done via surface patch electrode or with a needle probe. Surface patch electrode EMG is commonly done as part of the urodynamic evaluation and detects electrical potentials for a group of muscles [36]. Thus, surface patch electrodes only measure general pelvic floor muscle activity and are less reliable for assessing periurethral muscle activity [77].

For women with an unclear diagnosis but suspected functional obstruction, needle EMG can differentiate the subtypes of functional BOO. As an example, in one study of 15 women with voiding dysfunction, concentric needle EMG of the external urethra differentiated between women with normal pelvic floor activity but abnormal external urethral sphincter activity (ie, relaxed pelvic floor with abnormally contracted urethra) and women with inappropriate pubococcygeus muscle activation but normal external urethral sphincter activity (ie, abnormally contracted pelvic floor but relaxed urethra) [78]. In contrast, women with primary bladder neck obstruction will demonstrate a quiet EMG pattern in the pelvic floor and urethral muscles despite high detrusor pressure and low flow rate on urodynamic evaluation. These findings reflect a failure of relaxation at the bladder neck and not an activation of periurethral muscles [55]. The major disadvantages of needle EMG include invasiveness and limited availability.

Ultrasound — The American Urological Association Consensus paper recommends renal ultrasound for patients that meet their definition of CUR (PVR >300 mL for at least six months documented on at least two separate occasions) [3]. In addition, renal ultrasound to evaluate for hydronephrosis/ureter may be useful in women at risk for renal damage from CUR, including those with spinal cord injury or disease, Stage 3 or 4 pelvic organ prolapse, and poor bladder compliance in the setting of high storage pressure.

TREATMENT OF URINARY RETENTION — The initial intervention of CUR is aimed at resolving the urinary retention. Subsequent therapy is directed at treating the underlying etiology of CUR. (See 'Treatment of etiology' below.)

Women who are unable to void — Women with complete urinary retention are unable to void and require immediate bladder drainage. The most common methods are an indwelling bladder catheter, clean intermittent self-catheterization, or insertion of a suprapubic catheter. Options for bladder drainage are reviewed separately. (See "Placement and management of urinary bladder catheters in adults", section on 'Choice of catheter'.)

Women with incomplete emptying — In contrast to women with complete urinary retention, most women will be able to void some urine. This incomplete emptying, or partial voiding, results in urine accumulation in the bladder and the potential sequelae associated with urinary retention (see 'Potential complications' above). Depending on the degree of retention and associated symptoms, these women can be taught clean intermittent catheterization. Scheduled bladder drainage minimizes the risk of detrusor injury from overdistention and prevents transmission of high bladder pressures to the upper tract. The woman must have adequate cognitive function and mobility to perform clean intermittent catheterization herself. (See "Placement and management of urinary bladder catheters in adults", section on 'Clean intermittent catheterization'.)

A subgroup of women can be candidates for observation. Women can be safely observed if they have low filling pressures, no imaging evidence of upper tract involvement (eg, hydronephrosis), and normal renal function.

TREATMENT OF ETIOLOGY — Treatment choice for CUR in women depends on the etiology and severity of symptoms.

Women with detrusor underactivity — As there is no universally effective treatment for detrusor underactivity (DU), women with clinically significant retention from DU are typically managed with clean intermittent self-catheterization to periodically drain the bladder [79]. A 2014 systematic review based on four studies and one systematic review concluded that, while women with DU treated with sacral neuromodulation showed some improvement, there were insufficient data to determine the optimal treatment for these women [80]. Sacral neuromodulation can be trialed in women with non-neurogenic refractory DU. (See "Placement and management of urinary bladder catheters in adults", section on 'Clean intermittent catheterization'.)

Sacral neuromodulation — While the optimal treatment of women with DU is not known, sacral neuromodulation is an option to treat refractory DU that is not neurogenic. Sacral neuromodulation also appears effective for some patients with refractory obstructive CUR that is functional in nature [81]. (See 'Functional' below.)

Supporting data are limited by small sample sizes:

Trial data – In a multi-center crossover trial of women and men with idiopathic refractory CUR, 15 of the 24 patients with implants (58 percent) completely eliminated the need for catheterization [82].

Retrospective review – In a multisite retrospective review, 86 percent (243 out of 284 women with CUR) progressed to second-stage implantation, which suggests a successful first trial stage [83]. "Stable response," defined as no need for increased frequency of catheterization during follow-up, was reported in 79 percent of patients with implants at a median follow-up of two years. Older age was associated with reduced likelihood of second-stage implantation (OR 0.52, 95% CI 0.37-0.73, median interquartile range age 53 versus 67 years) and a diagnosis of detrusor underactivity was associated with stable response (odds ratio [OR] 2.82, 95% CI 1.37-5.83, p = 0.002).

Percutaneous tibial nerve stimulation – Percutaneous tibial nerve stimulation is a less invasive method of sacral modulation approved for the treatment of overactive bladder. In a 2021 systematic review of 5 studies of patients with idiopathic nonobstructive urinary retention, objective success rates (≥50 percent decrease in catheterizations per 24 hours) ranged from 25 to 41 percent, subjective success (patient request for device implantation) ranged from 47 to 59 percent, and PVR decreased a median of 76 to 83 mL over a 12-week treatment period. Longer term data were not available.

More information on sacral neuromodulation can be found separately. (See "Urgency urinary incontinence/overactive bladder (OAB) in females: Treatment", section on 'Sacral nerve stimulation'.)

Intraurethral valve-pump — An intraurethral valve-pump may be an alternate option to intermittent self-catheterization for women with DU and resultant CUR. The device does not remedy the DU itself. Women who may benefit include those with physical limitations that preclude self-catheterization or those who no longer wish to perform catheterization.

The device is comprised of a short silicone urethral catheter with an internal pump and valve mechanism that is operated by a patient-initiated external remote control unit [84]. The catheter is replaced once a month. In a multicenter crossover study of 77 women, the postvoid residual was similar between women using the valve-pump and clean intermittent catheterization techniques (16 versus 20 mL) [85]. The quality of life score improved significantly with valve-pump use compared with clean intermittent catheterization. However, 62 percent (169/273) of women withdrew from the study because of discomfort and urine leakage. A published clinician experience reported the device was successful in a small number of carefully selected patients who were reliant on indwelling catheters due to inability to perform clean intermittent catheterization [86]. However, use may be limited by lack of insurance coverage, including Medicare.

Ineffective treatments

Medication: Although a combination of bethanechol chloride (a cholinergic agonist) and prostaglandin E2 has been used to treat DU, trials have shown little clinical benefit in women with nonobstructive CUR [87-90].

Increased abdominal pressure: Maneuvers to increase abdominal pressure and force urine out of DU but are not recommended because of potential harmful effects on the pelvic floor and other complications compared with clean intermittent catheterization [91,92]. Credè's maneuver refers to applying suprapubic pressure in an effort to increase intravesical pressure and expel urine. However it appears this maneuver actually increases urethral resistance. In one study of 207 patients with lower urinary tract disorders who underwent urodynamic evaluation, the Credè maneuver resulted in a contraction of the external urethral sphincter, an increase in urethral pressure, and a closed bladder neck [93]. Only 2 percent of patients studied had appropriate synchronous relaxation of the external sphincter and bladder neck with the Credè maneuver. Therefore, we prefer clean intermittent catheterization for our patients with CUR.

Women with obstruction

Anatomic — For women with anatomic obstruction (ie, prolapse, urethral stricture, mass or tumor, foreign body), urinary retention will usually resolve with correction of the obstruction, particularly in women with adequate detrusor function. As an example, in one study of 35 women with Stage 3 or 4 pelvic organ prolapse and elevated postvoid residual (PVR >100 cc), 89 percent had normal PVRs after surgical correction of the prolapse [94]. Similarly, in a study of 24 women with pelvic organ prolapse and urinary retention, 75 percent of women demonstrated an improved PVR after pessary insertion to resolve the prolapse [95]. In women with urethral erosion from a prior anti-incontinence sling procedure, transvaginal sling excision and urethral reconstruction relieves the retention in most patients [96,97]. Urethral dilation is not used to treat obstruction unless there is a defined anatomical reason to necessitate this procedure, such as a urethral stricture. (See "Transvaginal synthetic mesh: Management of exposure and pain following pelvic surgery", section on 'Mesh exposure'.)

Functional — Treatment options for functional causes of bladder outlet obstruction (BOO) include pelvic floor muscle training with or without biofeedback, medication, sacral neuromodulation, sphincteric injections with botulinum toxin, and bladder neck incision (in select patients) [49]. The approach depends on type of functional BOO. Detailed information on pelvic floor muscle training and sacral neuromodulation is presented separately. (See "Myofascial pelvic pain syndrome in females: Pelvic floor physical therapy for management", section on 'Rehabilitation' and "Female urinary incontinence: Treatment", section on 'Initial treatment'.)

Dysfunctional voiding – For women with CUR resulting from dysfunctional voiding (DV), we typically begin with pelvic floor muscle training as it is minimally invasive and low-risk. The goal of pelvic floor muscle training and biofeedback is to "unlearn the learned behavior" of inappropriate urethral and pelvic floor muscle contraction during voiding [55]. In a trial of 86 women with DV randomly assigned to one of three biofeedback protocols or no treatment, significant similar improvements in storage and voiding symptoms were reported by all biofeedback groups compared with no improvement in the control group [98]. On urodynamic evaluation, flow rate and voided volume increased, while urethral closure pressure, detrusor pressure, and PVR all decreased significantly in the treatment groups compared with the control group.

For women with DV who do not have an adequate response to pelvic floor muscle training, we offer a trial of alpha-adrenergic blocker therapy. While small studies and trials have reported improvement in women with DV [99-101], a systematic review of 15 studies reported the treatment benefit was unclear because the studies were limited by small sample size, inconsistent study designs, and short duration of follow-up [102]. However, as DV symptoms can significantly impair quality of life and alpha-adrenergic blocker medications are generally tolerated, we offer this treatment. We use selective alpha-1a blockers, typically 0.4 mg tamsulosin taken orally once daily. Side effects are rare but can include dizziness and rhinitis.

Other medications that have been studied in women with refractory DV symptoms include benzodiazepines (vaginal valium), anticholinergics (tolterodine), tricyclic antidepressants (amitriptyline), and muscle relaxants (baclofen). The studies are too small to conclude a clear treatment benefit. However, use of these medications is reasonable for women who cannot tolerate alpha-blocker therapy or prefer to avoid an invasive procedure such as sacral neuromodulation. We discuss the limited data on treatment benefits and potential adverse effects of these medications.

Nonmedical treatment options for women with DV who do not respond adequately to pelvic floor muscle training include sacral neuromodulation and botulinum toxin injections. Success rates for sacral neuromodulation treatment in these women have been reported from 66 to 96 percent, but the number of treated women is small [103-105]. In addition, botulinum toxin injections into the urethral sphincter have been proposed for these women. In a study of 103 patients (women and men) with CUR and/or voiding dysfunction, treatment was successful in 30 to 40 percent of subjects with functional obstruction [106]. Among 45 patients with urinary retention, the indwelling catheters were removed or clean intermittent catheterization was discontinued in 39 (87 percent) patients. Approximately 10 percent of subjects developed urinary incontinence. Detailed information on sacral neuromodulation and botulinum toxin injection for women with lower urinary tract symptoms is available in other topics. (See "Female urinary incontinence: Treatment", section on 'Initial treatment' and "Botulinum toxin for treatment of lower urinary tract conditions: Indications and clinical evaluation".)

Detrusor sphincter dyssynergia – For women with detrusor sphincter dyssynergia as the cause of functional obstruction, the optimal treatment is not known. Studies of botulinum toxin injections and bladder neck incision have reported limited success in these patients, but the numbers have been small and more data are needed [51,106]. Surgical incision of the bladder neck can result in incontinence.

Primary bladder neck obstruction – For the subset of women with primary bladder neck obstruction as the cause of functional obstruction, initial therapy consists of clean intermittent catheterization and oral alpha-blocker therapy [76]. In one study of 24 women with primary bladder neck obstruction, 50 percent of patients improved with the combination of clean intermittent catheterization and alpha-blocker therapy, with the mean PVR improving from 277 mL to 28 mL [107]. For women who are unable to perform clean intermittent catheterization or tolerate medication, bladder neck incision may relieve the obstruction in carefully selected patients. In a study of 84 women followed for an average of 24 months, bladder neck incision improved symptoms in 85 percent of women, with a reduction in PVR from 115 mL to 23 mL [76]. As bladder neck incision can result in incontinence, we offer a trial of clean intermittent catheterization and medication as first-line treatment.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Urinary incontinence in adults".)

SUMMARY AND RECOMMENDATIONS

Definition – Chronic urinary retention (CUR) is the accumulation of urine in the bladder caused by incomplete bladder emptying. High-risk CUR results in adverse outcomes in the absence of intervention, while patients with asymptomatic low-risk CUR can often be observed. (See 'Definition' above.)

Diagnosis – CUR is diagnosed by confirming an elevated PVR with a bladder catheter or ultrasound. A PVR of more than 150 mL is commonly used to describe incomplete bladder emptying, while the American Urological Association Quality Improvement and Patient Safety committee defines CUR as a PVR of more than 300 mL that has persisted for at least six months. (See 'Definition' above.)

Etiologies – CUR can be caused by inadequate bladder muscle contraction (detrusor underactivity [DU]), bladder outlet obstruction (BOO), or a combination. BOO can be subdivided into anatomic and functional causes. (See 'Causes of urinary retention' above.)

Clinical sequelae – The potential risks of unrecognized CUR include recurrent infection or elevated upper urinary tract pressures, both of which can result in renal injury. However, the relationship between elevated PVR and bacteriuria in women has not been well demonstrated. (See 'Potential complications' above.)

Presenting symptoms – Women with CUR may be asymptomatic or present with a variety of lower urinary tract symptoms including inability to void, sensation of incomplete emptying, slow or intermittent urinary stream, or straining to void. (See 'Clinical presentation' above.)

Initial evaluation – The evaluation of CUR begins with a thorough history and physical examination to identify treatable causes, such as prolapse, pelvic masses, or complications of prior pelvic surgery. If clinically relevant CUR persists after treatment, further evaluation with urodynamic evaluation or cystourethroscopy can be considered in selected patients based on clinical suspicion. (See 'Evaluation for the underlying etiology' above.)

Urodynamic testing – Observations and measurements made during urodynamic evaluation can help to distinguish DU from BOO (table 1). Women with DU have decreased or absent detrusor pressure during voiding whereas women with BOO typically have increased detrusor pressures. After urodynamic evaluation, additional testing such as cystourethroscopy, video urodynamic evaluation, and electromyography can help determine the subtype of BOO. Renal ultrasound is performed for women at risk for upper tract disease, such as those with high detrusor filling pressures. (See 'Urodynamic evaluation' above and 'Additional tests' above.)

Initial treatment – The initial intervention for high-risk CUR is aimed at resolving the urinary retention. Women who are completely unable to void require bladder drainage with clean intermittent self-catheterization, an indwelling bladder catheter, or insertion of a suprapubic catheter for initial treatment, as clinically indicated. Women with partial voiding ability can elect clean intermittent catheterization if clinically indicated. Asymptomatic low-risk patients with CUR can be observed. (See 'Treatment of urinary retention' above.)

Subsequent treatments – Subsequent therapies are directed at managing the urinary retention and treating the cause in high-risk or symptomatic patients. (See 'Treatment of etiology' above.)

Clean-intermittent catheterization – Women with DU perform clean intermittent catheterization to control their symptoms as there are no established treatment options. Small studies of sacral neuromodulation have demonstrated treatment efficacy for some women with idiopathic refractory DU, but the optimal treatment is not known. (See 'Women with detrusor underactivity' above.)

Treatment of obstruction – For women with anatomic obstruction, we treat the cause of obstruction to resolve urinary retention and restore normal anatomy. (See 'Anatomic' above.)

Pelvic floor physical therapy – For women with dysfunctional voiding as the cause of functional obstruction, we suggest pelvic floor muscle rehabilitation (Grade 2C). Pelvic floor physical therapy has demonstrated some efficacy in a small trial and is low risk. (See 'Functional' above.)

For women with inadequate response to pelvic floor physical therapy, we suggest a trial of medication (Grade 2C). We typically prescribe a selective alpha-1a blocker such as tamsulosin. Women with continued refractory functional obstruction may benefit from trials of other medications, sacral neuromodulation, or botulinum toxin injections, but the supporting data are limited. Women with other types of functional obstruction, such as detrusor sphincter dyssynergia and primary bladder neck obstruction, have limited treatment options. (See 'Functional' above.)

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Topic 98554 Version 15.0

References

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