Overactive Bladder and Urge Incontinence



Overactive Bladder and Urge Incontinence


Breffini Anglim

Barry A. O’Reilly



Introduction

Overactive bladder (OAB) and associated urinary incontinence (UI) affects 16.5% of the U.S. population as well as a similar percentage of European men and women and poses a significant economic burden on society through direct medical and nonmedical costs, indirect costs and intangible costs, resulting in billions of dollars of health care expenditure on a yearly basis.1,2 OAB symptoms and urge urinary incontinence (UUI) have more profound effects on quality-of-life measures when compared to symptoms of stress urinary incontinence (SUI) because nocturia can result in significant sleep disturbance and daytime fatigue.3

OAB is defined by the International Continence Society (ICS) as a symptom-based condition characterized by urinary urgency, usually with urinary frequency and nocturia, with or without UUI.4,5 Urgency is defined as the complaint of sudden, compelling desire to pass urine which is difficult to defer. Frequency is defined as the complaint that micturition occurs more frequently during waking hours than previously deemed normal by the woman. Nocturia is defined as the complaint of interruption of sleep one or more times because of the need to micturate. Each void is preceded and followed by sleep.5 Urge incontinence is defined as the involuntary loss of urine associated urgency.4 OAB is a symptom-based diagnosis and therefore does not require urodynamic testing or cystometry for confirmation. Self-reporting of UI using validated questionnaires, such as the International Consultation on Incontinence Questionnaire Short Form and International Consultation on Incontinence Questionnaire Female Lower Urinary Tract Symptoms Modules, allows for assessment of both frequency of UI, and perceived bother to the patient. It is important to establish the degree of bother of symptoms because selfreporting of severity of incontinence symptoms alone may not correlate with felt or expressed need for treatment.6

Detrusor overactivity (DO) is a urodynamic-based diagnosis characterized by involuntary detrusor contractions during filling cystometry which may be spontaneous or provoked. OAB symptoms such as urgency or urge incontinence may not always occur when DO is observed on filling cystometry, and equally, DO is not always present in women who report OAB symptoms.7 DO is only confirmed in 44% to 69% of patients with symptoms of OAB.8,9 Also, up to 50% of patients with DO visible on filling cystometry do not have associated urgency or urge incontinence symptoms.10 This confirms Jarvis and Millar11 observation that the “bladder is an unreliable witness.”

The coexistence of detrusor hyperreflexia and impaired contractility (DHIC) was first described by Resnick and Yalla12 in 1987 and was found primarily in elderly patients. This phenomenon consists of DO during the storage phase, but the emptying phase is characterized by detrusor underactivity (DU) resulting in large postvoid residuals. The contractile capabilities of the detrusor are impaired, but it is not possible to distinguish which causative factors (detrusor muscle or detrusor innervation) are compromised. The term detrusor overactivity with detrusor underactivity (DO-DU) is intended by the ICS to supersede DHIC. It is defined as urodynamic DO (on cystometry) in combination with urodynamic DU on pressure-flow studies. DU is typically seen as a low pressure, low flow, and poorly sustained detrusor contractility on urodynamic studies. In a study of urodynamics (UDS) among patients older than the age of 70 years, 6% of women were found to have DO-DU.13 DU can be seen in combination with DO or SUI in 72% of women with DU.14,15 Symptoms of underactive bladder may overlap with OAB symptoms including urgency, frequency, nocturia, and incontinence.16 Treatment of DO-DU can be problematic, and the use of anticholinergics, β3-agonist or onabotulinumtoxinA injection can pose a higher risk for urinary retention in these women due to DU during the contraction phase of emptying.17,18,19 Sacral neuromodulation is considered to be an effective treatment for this patient group because it is thought to modify the afferent pathway by increasing parasympathetic activity and also by acting on the urethral and sphincter complex by triggering the guarding reflex to relax the outlet.20,21


OAB symptoms are frequently reported in women with pelvic organ prolapse (POP) and can occur in up to 88% of women.22 Both OAB and POP prevalence increase with increasing age, which may explain their association.23,24 There is some evidence that OAB symptoms improve following repair of POP due to an improvement in voiding function; however, other studies have shown de novo OAB symptoms following pelvic floor surgery.25,26 The pathophysiology of OAB in patients with POP is poorly understood.25 A study by Frigerio et al.27 found age, body mass index (BMI), preoperative OAB (based on symptomatic diagnosis not urodynamic evidence of DO), suburethral sling insertion, and postoperative SUI to be independent risk factors for OAB after POP repair. Preoperative OAB and postoperative constipation were significantly associated with persistent OAB following POP surgery. De novo OAB was associated with age, postoperative SUI and voiding symptoms, and concomitant suburethral sling placement.27 De novo OAB following surgery for pure SUI is reported to be between 5% and 18%.28,29 It is thought that repeated surgeries at the bladder neck may disrupt the autonomic nerve supply of the bladder and cause OAB symptoms.28


PREVALENCE

Several population-based studies have reported on the prevalence and burden of OAB. The National Overactive Bladder Evaluation (NOBLE) program was a population-based, cross-sectional, computer-assisted, telephone interview survey undertaken in the United States. In this study, OAB was estimated to occur in 16.9% of women and 16.0% of men. The age related increase in urge incontinence was significantly higher in women than men and was reported in 19% of women and 9% of men older than the age of 44 years.1 The epidemiology of lower urinary tract symptoms (LUTS) study was a population-based cross-sectional Internet-based survey carried out in the United States, United Kingdom, and Sweden to update the results of the NOBLE study. ICS definitions of LUTS were also used. Specific to the United States, 20,000 participants aged older than 40 years were included. It showed a prevalence of OAB symptoms at least “sometimes” in 27.2% of men and 43.1% in women. Of this group of women 38.9% were bothered “quite a bit” by their symptoms. In both men and women, prevalence increased with age.30 The Milsom study was a population-based prevalence study carried out in France, Germany, Italy, Spain, Sweden, and the United Kingdom. A combination of telephone and direct interviews were conducted in 16,776 randomly selected men and women aged older than 40 years. They reported an overall prevalence of OAB symptoms of 16.6%, 17.4%, and 15.6% in males and females, respectively.31 The EPIC study, a computer-assisted telephone interview of more than 19,000 participants aged older than 18 years across five countries, including Canada, Germany, Italy, Sweden, and the United Kingdom, showed the prevalence of LUTS suggestive of OAB to be 10.8% in men and 12.8% in women. ICS definitions of LUTS and OAB were used to survey the population for symptoms.32 The incidence of OAB is higher in elderly women, being reported in 45% of women older than 65 years33 and higher than 80% in institutionalized women.34


EFFECT ON QUALITY OF LIFE

Patient perception of bother is important in assessing need for treatment in women with OAB. Both frequency of micturition and amount of urine lost can be used to determine OAB severity, but overall effect on quality of life is essential to determine suitable treatment options. OAB symptoms and UUI can have detrimental effects on a woman’s physical, social, and psychological well-being. Commonly used coping mechanisms to avoid incontinence episodes include fluid restriction, awareness of nearby bathroom facilities, and social isolation in order to avoid embarrassment. These factors contribute to a cycle of anxiety and psychological distress and may ultimately result in social isolation. The top 10 items affecting quality of life are listed in Table 25.1.

Health-related quality of life (HRQL) measures can be used to assess the effect of OAB on quality of life. Examples of grade A HRQL measures that exist include Bristol Female Lower Urinary Tract Symptoms Questionnaire, International Consultation on Incontinence Questionnaire Urinary Incontinence Short Form, Overactive Bladder Questionnaire Short Form, The Kings Health Questionnaire, Pelvic Floor Distress Inventory (PFDI), PFDI Short Form (PFDI-20), Pelvic
Floor Impact Questionnaire (PFIQ), PFIQ Short Form (PFIQ-7). Assessment of symptom bother and overall bother must also be carried out. The Patient Perception of Bladder Condition and the Urogenital Distress Inventory are the only Grade A validated questionnaires that exist which assess symptom bother.
















PATHOPHYSIOLOGY

Three basic functions are required for the bladder to fill and empty in a socially acceptable manner. Compliance is required so that the bladder can increase in volume without increasing intravesical pressure. The urothelium must protect the underlying neural and muscular layer from urine as the bladder expands. Finally, there must be a coordinated effort by the bladder muscle wall to contract so that the bladder empties adequately.35 An intact circuit between the brain, spinal cord, and peripheral ganglia is essential for the bladder to function, and removal of this extrinsic neural input renders the bladder nonfunctional. Switch-like patterns of activity are seen in the bladder unlike other systems, such as the cardiovascular system that are tonically contracted. Micturition is a learnt behavior and requires voluntary control. Urine storage and release are coordinated through integrated somatic and autonomic efferents in the lumbosacral spinal cord (Fig. 25.1).36

The pathophysiology of the OAB syndrome and DO is still incompletely understood and is likely to be multifactorial. The lower urinary tract function is dependent on complex central neural networks which can be altered by a variety of neurologic disorders. OAB can be triggered by discreet disease entities including infection, interstitial cystitis, urethrotrigonitis, urolithiasis, and neoplasia. Idiopathic OAB implies that a causative agent has not been identified and comprises 90% of patients with OAB.37 Pathologic causes of OAB include cerebrovascular accidents, intracranial lesions, interstitial cystitis, spinal cord injury, obstruction, Parkinson disease, multiple sclerosis, and diabetes.

Women with idiopathic OAB were compared to age-matched controls using neurophysiologic tests and subtracted cystometry. Both patients and controls had normal neurophysiologic tests, and there was no difference in testing between the two groups.38 The pathophysiology of OAB does not seem to be explained by clinical or subclinical damage of the central nervous system or motor pathways, and other causative theories have been suggested. The complex pathophysiology of OAB is likely related to a combination of four theories: outflow obstruction hypothesis, urothelium-based hypothesis, myogenic hypothesis and neurogenic hypothesis (Fig. 25.2).








Overactive Bladder Due to Outflow Obstruction

The clinical, structural, and neuropathic changes characteristic of DO are caused by bladder outflow obstruction. This can occasionally be seen in women with advanced stage POP or following midurethral sling or bladder neck surgery, leading to increased outflow resistance.37 Partial ligation of the urethra in rat models has been shown to cause muscle hypertrophy of the detrusor muscle and afferent and efferent neuronal hypertrophy.39,40 Similar observations have been shown in humans, suggesting development of new spinal circuits after obstruction of the outflow tract. Nerve growth factor which is responsible for regrowth of nerves after injury, and for maintenance of sympathetic and sensory neurons, is responsible for this plasticity.35 Speakman et al.41 hypothesized that outlet obstruction and irritative voiding symptoms are as a result of postjunctional supersensitivity, possibly as a result of partial denervation. The sensitivity to electrical stimulation of the detrusor nerve supply is reduced, but it is more sensitive to stimulation with acetylcholine.42 Brading et al.43 hypothesized that bladder instability is as a result of smooth muscle change due to a reduction in functional bladder wall innervation.


Urothelial-Based Hypothesis

The urothelium-based hypothesis postulates that enhancement of involuntary contractions is caused by alterations in urothelial receptor function and release of neurotransmitter, in addition to the sensitivity and coupling of the suburothelial interstitial cell network.44 There is increasing evidence that the response of the urothelial cells and suburothelial fibroblasts to both chemical and mechanical stimuli contributes to regulation of bladder activity through the activation of bladder afferent nerves. Nerve endings of C-fiber afferents are found in the suburothelial layer of the bladder wall and urothelium. Bladder distension has been shown to cause ATP release from the urothelium, which may lead to activation of afferent nerve terminals, resulting in bladder contraction.45 The urothelium synthesizes prostanoids and nitric oxide which are both release during distension of the bladder.46,47


Myogenic Hypothesis

The myogenic hypothesis is based on the concept that uninhibited contractions are generated by changes in the coupling and excitability of smooth muscle cells with interstitial cells or other myocytes.43,48 It has been hypothesized that partial denervation of the detrusor is a widespread feature in all cases of DO. This may lead to alteration of the smooth muscle properties, resulting in increased excitability of cells, with activity spreading more easily between cells, resulting in a coordinated myogenic detrusor contraction.43,48 This theory disputes the concept of neurogenic DO as the underlying mechanism of DO in OAB. It is hypothesized that there is a fundamental abnormality at the bladder wall level, including increased electrical cellular coupling due to altered contractile activity and variable detrusor denervation with increased sensitivity to potassium.49 Another theory is that of cellular hypertrophy. It is thought that increased elastin and collagen are produced in the muscle fascicles, and this combined with a loss of nerves, results in idiopathic and neuropathic bladders.50 Enhanced, spontaneous contractile activity of the detrusor has been noticed. In vitro studies by Kinder and Mundy51 showed that muscles from bladders with OAB, regardless of the etiology, spontaneously contract more often and with a greater amplitude than muscles from urodynamically normal bladders. Structural abnormalities have been noted in both neuropathic and nonneuropathic unstable detrusor muscles in the form of narrower junctional gaps between muscle cells as compared with the normal detrusor.52


Neurogenic Hypothesis

Central and peripheral nervous system pathways which may contribute to OAB include increase excitatory response in reflex pathways due to axonal sprouting in the spinal cord forming new synaptic connections or enforcing existing ones, reduced bulbospinal inhibition in central or peripheral nervous systems and higher afferent input from the lower urinary tract, and development of bladder reflexes which are resistant to central inhibition.36 The detrusor muscle has been shown to contract more than a normal detrusor muscle in case of idiopathic DO. These contractions are not nerve-mediated and can be inhibited by vasoactive intestinal polypeptide and activated by increased a-adrenergic activity.51,53 Cat models with central nervous system lesions noted inhibition of voiding functions by the cerebral cortex.54 In patients with Parkinson, it is postulated that the loss of dopaminergic receptors is causative of their OAB symptoms because this has been demonstrated in monkey models.55 Reorganization of reflex correction seems to occur after spinal cord injury, with facilitates C-fiber afferents and elimination of A-fiber afferents, causing OAB symptoms. These axons are sensitive to capsaicin and have been linked to upper motor neuron diseases including spinal cord injury, multiple sclerosis, and Parkinson disease.56

The pathophysiology of OAB may never be fully understood because this is likely a convergence of several pathophysiologic processes into one common clinical entity.


CLINICAL PRESENTATION

Patients with OAB present with symptoms of urgency, frequency, nocturia, and urge incontinence. A history of childhood nocturnal enuresis may exist in some patients.57 It is important to establish if there is a mixed
incontinence picture, with OAB coexisting with SUI and to accurately determine if a stressful activity may trigger a detrusor contraction causing urge incontinence. A study by Hashim and Abrams58 reported that 58.7% of female OAB patients have DO on urodynamic studies. A systematic review and meta-analysis on diagnostic predictability of UI showed that clinical history alone was found to be 0.61 (0.57 to 0.65) sensitive and 0.87 (0.85 to 0.89) specific for the diagnosis of DO.59 Because the symptoms of OAB overlap with those of other lower urinary tract conditions, a number of other diagnoses must be entertained. Differential diagnoses include urinary tract infection, severe genuine SUI, urethral diverticulum, urinary tract fistula, cystitis, foreign body, bladder tumor and urethritis.


EVALUATION OF OVERACTIVE BLADDER


History

A focused clinical history is fundamental to assessing UI.4 Some studies have shown that the type of incontinence cannot be accurately determined from history alone.60,61 However, a systematic review and meta-analyses on diagnostic assessment methods for UI showed that the clinical history alone had a sensitivity of 0.92 (95% confidence interval [CI] 0.91 to 0.93) and specificity of 0.56 (0.53 to 0.60) for diagnosis of urodynamic SUI and a sensitivity of 0.61 (0.57 to 0.65) and specificity of 0.87 (0.85 to 0.89) for diagnosis of DO.59 Reversible causes of incontinence must be ruled out using the DIAPPERS mnemonic: delirium, infection, atrophy, pharmaceuticals, psychological problems, endocrine problems, restricted mobility, and stool impaction.12

A focused history should be taken to include the following:



  • Patient demographics—age, BMI, menopausal status


  • Detailed characterization of OAB symptoms—duration, severity, voiding diary


  • Assessment of quality of life using validated questionnaires


  • Other symptoms such as SUI, POP, incomplete voiding, bowel symptoms


  • Evaluation of urinary tract—recurrent urinary tract infections, bladder calculi


  • Fluid intake including caffeine and alcohol


  • Pad usage


  • Previous treatments and their success


  • Obstetric history—number and mode of deliveries


  • Past medical history—heart failure, diabetes, disc herniation or spinal cord injury, Parkinson disease, multiple sclerosis, dementia, and psychiatric disease


  • Past surgical history—previous midurethral sling, colposuspension, or POP surgery


  • Current medications—diuretics, benzodiazepines, adrenergic blockers, angiotensin-converting enzyme inhibitors


  • Social history—living environment, mobility, falls risk


Physical Examination

The physical examination should include an observation of the patient followed by a focused examination of organ systems that may affect UI.



  • Abdominal examination for scars, masses, hernias, bladder distension


  • Neurologic screen for lower motor neuron lesions to include the bulbocavernosus and anal wink reflexes.


  • Neurologic screen for intrapelvic nerve entrapments as a cause of refractory urgency. Associated symptoms include sciatica with urinary symptoms, gluteal pain with associated perineal or vaginal pain, dysuria, or refractory pelvic and perineal pain.62


  • Neurologic screen for upper motor lesions such as Parkinson disease


  • Mental status examination


  • Pelvic examination to assess for genitourinary prolapse which may impair bladder emptying, atrophic vaginitis, vaginal masses, and a cough stress test to assess for SUI


  • A digital rectal examination will determine anal tone, the presence of fecal impaction which may compromise bladder emptying.


  • Assessment of postvoid residual by urethral catheter or bladder ultrasound


  • Urine microscopy and culture to assess for hematuria or infection


Bladder Diary

The patient is also asked to complete a daily diary, as illustrated in Table 25.2. The micturition time chart records time of voiding over a 24-hour period. Another chart used is the frequency-volume chart which captures both the amount voided and the frequency of voiding. The most comprehensive diary is a bladder diary, which may include fluid intake, UI episodes, use of pads, and the sensations and activities preceding the episode of UI. This is usually performed over 2 to 3 days. When a bladder diary is completed properly it will illustrate: day and night time input and output, urine production over 24 hours, maximum and average voided volume, median functional bladder capacity, and polyuria. These charts may not accurately predict the type of UI the patient has,63,64 and some patients may find it too complex to complete the diary accurately.65 Measuring the voided volume of urine and recording timing of voids is a minimum, and the only sure way of differentiating between polyuria with large volumes, and a hypersensitive, small-capacity bladder with small volumes.










Investigations

Advanced testing including UDS, cystoscopy, and renal tract imaging may not be part of the original workup in an uncomplicated OAB presentation. However, it should be considered in refractory patients who do not respond to multiple medication treatments and in patients with hematuria without infection.66

Uroflowmetry is a noninvasive measurement of urine flow rate. It allows the maximum flow rate, voided volume, and the flow curve to determine if the patient is emptying their bladder in a normal fashion. It may reveal obstructive voiding patterns secondary to severe genitourinary prolapse or tumor. Traditional multichannel cystometry is considered the gold standard for diagnosis. Provocation maneuvers including coughing (Fig. 25.3), positional change, and running water may help to simulate the circumstances in which OAB or incontinence usually occur.67 Multichannel cystometry may not always achieve a diagnosis, and alternative diagnostic methods should be performed in this scenario. In a subset of patients, standard urodynamic studies does not adequately verify or exclude a lower urinary tract dysfunction, particularly if the patient’s symptoms cannot be reproduced by standard examination. In this cases, ambulatory UDS may be a suitable alternative, as more physiologic conditions can be obtained with patients moving more freely during the recording, thus simulating activities that may usually provoke urinary symptoms.68 Conflicting results have been demonstrated with ambulatory UDS. One study by Salvatore et al.69 showed a low rate of DO in asymptomatic women, which was similar to findings in routine laboratory UDS. However, other studies have shown rates of up to 68% of asymptomatic women,70 and so the clinical role of this procedure is contentious. It is recommended by the ICS as a second-line diagnostic tool when standard office UDS fails to produce a diagnosis. In women with a neurologic history or in those who have had previous
pelvic surgery, videourodynamic study (VUDS) may be a more suitable test. This allows concurrent screening of the lower urinary tract during filling cystometry and voiding studies. A VUDS combines voiding pressure, urine flow, and imaging studies during the voiding phase and may aid in differentiating dysfunctional voiding from LUTS in women.71







TREATMENT OF OVERACTIVE BLADDER

Medical therapies can be commenced based on symptoms of OAB without any invasive investigations. New medical therapies are being developed which have fewer side effects and better patient compliance. Current management options are included in Table 25.3.


Conservative Management

Conservative measures are low cost, noninvasive lifestyle alterations such as altering fluid intake; weight loss; dietary changes; and reduction in caffeine, carbonated beverages, and alcohol consumption. Advice should be given to consume between 1 and 1.5 L in any
24-hour period. Caffeine and alcohol are known to irritate the bladder, and women should be advised to try to avoid caffeine-based drinks or substitute them with decaffeinated drinks. Obesity has been shown to be associated with OAB in women.72 Increased chemokines have been found in the bladders of obese women which may suggest a chronic, low-grade inflammation in the bladders of obese women.73 Weight loss programs have been shown to improve urgency UI symptoms.74 Bariatric surgery has been shown to substantially improve both urge and SUI in women who are severely obese in the first year postoperatively.75,76 In a prospective study of women undergoing bariatric surgery, 34% reported symptoms of SUI, 21% reported symptoms of OAB, and 44% reported symptoms of mixed incontinence. The cure rates at 1-year postoperatively for SUI, OAB, and mixed incontinence, were 41%, 38%, and 48%, respectively.77









Bladder Training (Timed Voiding)

Bladder retraining principles are based on the capability to suppress the urge to void and gradually extend the intervals between voids. Frequency of urination reduces the bladder capacity and leads to bladder instability. Bladder training aims to break this cycle by requiring the patient to resist urgency and delay voiding until the specified interval is reached. The patient is asked to void at strict voiding intervals and is not allowed to void in between the scheduled times, even if episodes of incontinence occur. Once she is dry, the period between intervals is lengthened. This is repeated and extended until a continence interval of 3 to 4 hours is achieved. Cure rates using conservative bladder retraining alone, without any pharmacologic therapies is 44% to 90%.11 The combination of pelvic floor exercises with bladder retraining can aid in suppressing symptomatic urinary urgency because the ability to increase pelvic floor muscle tone will increase the patient’s ability to prevent urge incontinence caused by strong, involuntary bladder contractions. The treatment is considered successful if the patient achieves a voiding interval of 2.5 to 3 hours and is free of OAB symptoms. A randomized, placebo-controlled trial of 197 women, aged between 55 and 92 years of age with either urge or mixed incontinence were randomized to pelvic floor physiotherapy, immediate release oxybutynin, or placebo. With pelvic floor rehabilitation, there was an 80.7% mean reduction in episodes of incontinence. This was statistically superior to both oxybutynin and placebo.78


Behavioral Modification in Elderly Patients

OAB incidence increases with age. The combination of OAB, reduced mobility, and cognitive deficits increase the rates of UI in this population. It is not uncommon for many elderly patients to instinctively reduce their fluid intake for better symptom control. This however can cause chronic dehydration and may cause bladder irritation with resultant highly concentrated urine, thus resulting in worsening symptoms of OAB. Dehydration is particularly common in institutionalized residents, exacerbating both constipation and OAB.79 Urinary incontinence is associated with a significant falls risk. A recent systematic review including 15 studies reported that the proportion of patients with OAB experiencing at least one fall a year ranged from 18.9%, with a significant number (10.2% to 56%) experiencing recurrent or serious falls.80 A study of 133 institutionalized women looking at the efficacy of prompted voiding by assisting them to the bathroom every hour for 14 hours a day, showed a reduction of incontinence episodes of 0.6 per day, an overall 26% reduction in episodes.


Medical Management

Medical management has an important role in the management of women with OAB symptoms and UUI; however, all current drugs that we use have systemic effects and none target the urethral and bladder alone. The extensive number or drugs available is representative of the fact that there is no perfect drug, and it is often their systemic effects which result in noncompliance and cessation of medical therapy. The pharmacology of drugs and recommendations for usage has recently been reviewed by the 6th International Consultation on Incontinence (Table 25.4).81

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May 1, 2023 | Posted by in GYNECOLOGY | Comments Off on Overactive Bladder and Urge Incontinence

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