Overactive bladder syndrome
Overactive bladder (OAB) is a symptom syndrome defined as urinary urgency, with or without urgency incontinence, usually with urinary frequency and nocturia, and in the absence of urinary tract infection (UTI) or other obvious pathology ( ). Millions of Americans are affected by OAB at any given time, and the aging of the population ensures that the number of people who suffer from OAB will continue to increase over time. The symptoms of OAB can have a large negative impact on social and personal activities, which can cause significant psychological distress ( ). OAB continues to remain an underreported and undertreated condition, despite increased awareness, improved diagnosis, and increased treatment options in recent years. It is likely that the poorly understood etiology of OAB, the heterogeneity of symptom presentation and patient characteristics, and suboptimal patient-physician communication contribute to this problem.
Terminology, prevalence, epidemiology, and economic impact
The International Continence Society (ICS) is the governing body that has historically taken the lead in the standardization of terminology. The terminology used to describe OAB and associated symptoms has changed numerous times. The ICS recommends the use of symptoms, signs, and validated investigations to form workable diagnoses. In 2020, the ICS used the following terms:
• Increased daytime urinary frequency: Complaint that voiding occurs more frequently during waking hours than previously deemed normal by the individual (or caregivers) ( ).
• Nocturia:The number of times urine is passed during the main sleep period. Having woken to pass urine for the first time, each urination must be followed by sleep or the intention to sleep ( ).
• Urgency: Complaint of sudden, compelling desire to pass urine that is difficult to defer ( ).
• Overactive bladder (urgency) syndrome: Urinary urgency, usually accompanied by daytime frequency and/or nocturia, with or without urinary incontinence, in the absence of UTI or other obvious pathology ( ).
• Urgency urinary incontinence (UUI): Complaint of involuntary loss of urine associated with urgency ( ).
• Detrusor overactivity (DO): The occurrence of detrusor contraction(s) during filling cystometry. These contractions, which may be spontaneous or provoked, produce a waveform of variable duration and amplitude on the cystometrogram (CMG). The contractions may be phasic or terminal. They may be suppressed by the patient or be uncontrollable. Symptoms, for example, urgency and/or urgency incontinence or perception of the contraction, may or may not occur ( ). DO may be further qualified as neurogenic, when there is a relevant neurologic condition, or idiopathic, when the cause is unknown.
It is important to note that, although the current definition of OAB is based on symptoms, DO is a urodynamic observation. By definition, to diagnose a patient with DO, one must observe involuntary detrusor contractions during the filling phase of CMG during urodynamics testing. OAB and DO are thus not interchangeable terms, and it is important that the clinician use each term correctly.
The number of individuals affected by OAB is difficult to establish. The populations studied vary substantially from one publication to another, and the symptoms or signs used to define OAB may also vary between publications. Overall, however, the incidence of OAB is high, ranging between 7% and 27% in males and between 9% to 43% in females ( ; ).
Based on data from the EPIC study, 10.7% of the world’s population was found to be affected by OAB (i.e., almost 250 million women and over 200 million men) ( ). The Epidemiology of Lower Urinary Tract Symptoms (EpiLUTS) study, a cross-sectional, population-representative survey of men and women over 40 years old conducted via the internet in the United States, the United Kingdom, and Sweden, revealed the distribution of individual and the combination of various lower urinary tract symptoms (LUTS) within the OAB symptom complex by gender ( ; ). In this large study that included 4562 women and 2559 men with OAB, 20.2% of women and 15.6% of men reported combined urgency, UUI, nocturia, and frequency.
In the United States alone, OAB has been estimated to affect up to 33 million people. However, it is estimated that only 15% of these patients with incontinence and OAB symptoms seek medical help. The National Overactive Bladder Evaluation program ( ) contacted more than 5000 households by telephone and, among those who responded, the overall prevalence of OAB was 16.6%. Men and women had a similar overall prevalence of OAB (16.0% and 16.9%, respectively) as defined by the ICS. The prevalence of symptoms increased sharply with age in both men and women ( Fig. 31.1 ).
Men were shown to have a higher prevalence of “OAB dry,” or OAB without UUI (13.4% vs. 7.6% in women), and women had a higher prevalence of “OAB wet,” or OAB with UUI (9.3% vs. 2.6% in men) ( Fig. 31.2 ). In women, the presence of “OAB wet” rose from 2% in the youngest group (ages 18–24 years) to 19.1% in those 65 to 74 years of age ( ).
In a secondary analysis of data from the EpiLUTS survey, examined whether there were racial differences in the prevalence of OAB amongst men and women in the United States. Of the 20,000 US adults surveyed, OAB was found to be most prevalent in Black men and women. In this study, the prevalence of OAB in Black, Caucasian, Hispanic, and Asian women was 45.9%, 43.4%, 42.0%, and 26.6%, respectively.
Given that women between the ages of 60 and 80 are the most rapidly growing segment of the US population, and that up to 50% of women in this age group meet criteria for OAB syndrome, treatment of this condition clearly has a significant economic impact on our society. Using population prevalence estimates from the EpiLUTS study, estimated the total cost at $24.9 billion annually. Another study estimated the current direct (medical and nonmedical) and indirect costs of OAB in the United States ( ). In 2007, average annual per capita costs of OAB were $1925 ($1433 in direct medical, $66 in direct nonmedical, and $426 in indirect costs). When applied to 34 million people in the United States with OAB, the total national costs were $65.9 billion ($49.1 billion direct medical, $2.3 billion direct nonmedical, and $14.6 billion indirect). This study, published in 2010, also predicted annual per capita costs to rise to $1944 in 2015 and $1969 in 2020, with total annual national costs rising to $76.2 billion in 2015 and $86.2 billion in 2020.
OAB can also have a significant impact on quality of life. Both men and women with bothersome OAB were more likely to report that their bladder condition caused them at least some problems ( ). These subjects reported worse scores on health-related quality of life questionnaires, anxiety assessments, and depression assessments. Men and women with bothersome OAB also had a greater number of health care visits annually compared to those with OAB without bother and those with minimal to no symptoms ( ).
Neurophysiology of the lower urinary tract
To better understand the etiology and pharmacologic management of OAB, a brief review of the neurophysiology of the lower urinary tract is presented (see Chapter 3 for further details).
Autonomic pathways.
Sympathetic nerves, which help to control bladder relaxation, exit the spinal cord at levels T10 through L2 and synapse in paravertebral ganglions. Noradrenaline, the neurotransmitter of the sympathetic system, binds to α- and β-adrenergic receptors, and then postganglionic fibers travel to the bladder via the hypogastric nerve ( Fig. 31.3 ). When norepinephrine binds to β-receptors on the bladder, it activates adenylate cyclase, which increases levels of cyclic adenosine monophosphate (AMP), thereby relaxing the detrusor muscle of the bladder ( Fig. 31.4 ).
The parasympathetic nerves, which are important in the control of bladder contractility, exit the spinal cord at levels S2, S3, and S4. Preganglionic fibers travel to the bladder via the pelvic nerve, synapse close to the bladder, and then send short postganglionic fibers to the bladder (see Fig. 31.3 ). The parasympathetic system uses acetylcholine as its neurotransmitter and muscarinic receptors at target organs. Five subtypes of muscarinic receptors are known, with a predominance of M 2 and M 3 receptor subtypes in the bladder. Release of acetylcholine by postganglionic parasympathetic nerves activates both M 2 and M 3 receptor subtypes. M 2 receptors make up approximately 80% of the muscarinic receptors in the bladder. Activation of M 2 receptors negatively affects adenylate cyclase, thereby decreasing cyclic AMP, and ultimately inhibiting relaxation caused by the sympathetic system. M 3 subtypes, which make up the remaining 20% of muscarinic bladder receptors, activate phospholipase C, increase inositol triphosphate, and subsequently cause detrusor muscle contraction.
Somatic pathways.
The somatic pathway includes motor neurons that originate in Onuf’s nucleus in the sacral spinal cord and exit the spinal cord at level S2, S3, and S4. Their axons travel via the pudendal nerve to the external urethral sphincter, where they innervate the striated smooth muscle. Acetylcholine is the neurotransmitter for the somatic nervous system, and binds to nicotinic receptors (see Fig. 31.3 ).
Central regulation.
The central regulation of micturition is controlled by several neurotransmitters, including acetylcholine, γ-aminobutyric acid (GABA), glycine, serotonin, dopamine, and noradrenaline. The pontine micturition center (Barrington nucleus or M region) is involved in regulating voiding and incontinence by projecting directly to bladder motor neurons and indirectly to urethral motor neurons. The bladder motor neurons are preganglionic and parasympathetic (S2, S3, and S4) and located in the intramediolateral cell column of the sacral spinal cord. The urethral motor neurons are located in the sacral ventral horn (Onuf’s nucleus). When the pontine micturition center is stimulated, the urethral motor neurons are inhibited, leading to a decrease in urethral pressure, and the bladder motor neurons are stimulated, leading to an increase in intravesical pressure, thus resulting in coordinated micturition between the bladder and the outlet ( Fig. 31.5 ).
The pontine continence center projects to urethral sphincter motor neurons and, when stimulated, increases urethral sphincter tone. During the filling or storage phase, the pontine continence center sends continuous stimulation to urethral sphincter motor neurons to maintain urethral closure (see Fig. 31.5 ).
Afferent information.
Afferent sensory information is sent from the bladder via the pelvic nerve to the sacral dorsal root ganglia located within the spinal cord. These nerves are primarily made up of myelinated A and D fibers and unmyelinated C fibers. The A and D fibers respond to distension and active contraction, whereas C fibers respond to chemical irritation and pain ( Fig. 31.6 ). There are several receptors that have been identified on these nerves, such as vanilloid, tachykinin, purinergic, and prostanoid receptors, which may have a role in the development of OAB syndrome and may be potential pharmacotherapy targets ( ).
Etiology of overactive bladder
Although there are numerous neurologic diseases associated with symptoms of OAB, the majority of women who present with this syndrome are neurologically intact. There are many conditions that are associated with OAB syndrome ( Box 31.1 ) and the symptoms of this condition; however, the pathophysiology remains unknown for many patients, and the syndrome as a whole can have a heterogeneous presentation.
Congenital
Aging
Neurogenic detrusor overactivity
Multiple sclerosis
Cerebrovascular disease
Parkinson disease
Dementia
Neoplasia
Spinal cord injury
Bladder outlet obstruction and pelvic surgery
Antiincontinence surgery
Advanced pelvic organ prolapse
Psychosomatic disease
Urine in proximal urethra
Detrusor overactivity
Mixed incontinence
Neurologic diseases.
As discussed earlier, the process of bladder storage and emptying is controlled by the complex interplay of neurocircuits in the brain, spinal cord, and end-organ targets that coordinate the activity of smooth and striated muscle in the bladder and urethra. Neurologic lesions of the suprasacral spinal cord and higher centers are associated with DO because of their interruption of these circuits. Suprasacral lesions block the sacral reflex arc from the cerebral cortex and other higher centers that are crucial for both voluntary and involuntary inhibition of the bladder. Patients with suprasacral lesions typically have involuntary detrusor contractions that are usually associated with appropriate relaxation of the urethral sphincter due preservation of long tracts from the pontine region. Neurologic conditions that can result in DO include multiple sclerosis (MS), Parkinson disease (PD), dementia, and cerebrovascular disorders. (See Chapter 33 for more details.)
Multiple sclerosis.
MS is a disease of unknown etiology characterized by demyelinated white matter plaque throughout the central nervous system (CNS), typically affecting patients between 20 and 40 years of age. The various locations of plaques within the CNS (cerebral cortex, cerebellum, brainstem, spinal cord, and optic nerve) produce varied neurologic dysfunction and symptoms. Plaques in the frontal lobe of the cerebral cortex or in the lateral columns of the spinal cord are associated with producing lower urinary tract dysfunction.
It is uncommon for patients with MS to report urological symptoms at initial presentation (only 3%–10%) ( ); however, because of the progressive nature of MS, close to 100% of patients report LUTS by 10 years following diagnosis ( ). Approximately two-thirds of MS patients with lower urinary tract dysfunction show DO on cystometry ( ; ), while approximately 20% to 25% of patients have an underactive or areflexic detrusor. About 25% of patients demonstrate detrusor sphincter dyssynergia (DSD) arising from the loss of coordination between the detrusor and sphincter muscles ( ).
Cerebrovascular disease.
Based on the 2018 National Health interview surveys, the prevalence of persons in the United States who report a medical history of stroke increases with age from 3.1% for those aged 45 to 64 years to 11.8% for those over age 75 years. Overall, there has been a trend toward higher prevalence of stroke, which can result in varying degrees of chronic disability, including bladder dysfunction, over time in all age populations within the United States. Atherosclerosis, arteritis, intracranial hemorrhage, and arterial malformations may be etiologic factors. Infarction of discrete areas of the frontal lobe of the cerebral cortex, internal capsule (which sends axons between the thalamus and cerebral cortex), brainstem, or cerebellum can result in bladder dysfunction. During the initial phase following a cerebrovascular accident, urinary retention secondary to detrusor areflexia is common. However, during recovery, DO with an appropriate sphincteric response usually occurs. DSD can also rarely be seen in this patient population.
Parkinson disease.
The prevalence of PD in industrialized countries is estimated at 0.3% of the entire population and approximately 1% in adults older than 60 years of age ( ; ). The onset of disease usually occurs after 50 years of age, and the course of the disease is progressive. PD is associated with Lewy body formation and degeneration of cells within the substantia nigra of the midbrain that produce dopamine ( ). Dopaminergic mechanisms have both inhibitory effects on micturition via D1 receptors and stimulatory effects via D2 receptors. When substantia nigra pars compacta cells are depleted in PD, there is a loss in D1-mediated inhibition, which leads to DO. The coordinated stimulation of the pontine micturition center at socially acceptable times to urinate is also prevented by the decreased integration of sensory input from the bladder to the periaqueductal gray and a defective ventral tegmental area ( ). True DSD does not develop in patients with PD, because pontine micturition is spared.
The prevalence of LUTS in the presence of PD ranges from 27% to 85% ( ). A variety of storage symptoms are common, including nocturia (60% of patients), urgency (33%–54%), frequency (16%–36%), and urinary incontinence (26% of males and 28% of females) ( ). Voiding symptoms are less common than storage symptoms, but 44% to 70% of men report hesitancy and poor stream, and 28% of women report straining to void ( ). The relationship between motor symptoms in PD and bladder dysfunction is complex and nonlinear, and the effects of dopaminergic treatment on bladder control and urodynamic findings in patients with PD can be unpredictable.
Dementia.
Dementia is a diffuse loss of cognitive functioning manifested by difficulty with thinking, remembering, and reasoning, as well as impairment of behavioral abilities to such an extent that it interferes with a person’s daily life and activities. There are multiple causes of dementia, including aging, severe head injury, encephalitis, hydrocephalus, Pick disease, Alzheimer disease, Jakob–Creutzfeldt disease, and syphilis. Bladder dysfunction can occur in the presence of dementia either from direct involvement of cerebrocortical areas responsible for bladder control or from the loss or inability to control socially appropriate behavior. Depending on the cause or severity of dementia, DO or detrusor areflexia may also occur.
Neoplasia.
Neoplasias within the CNS can interrupt normal micturition, resulting in bladder dysfunction. Brain tumors in the superior medial frontal lobe can result in irritative voiding symptoms and DO. Cervical spondylosis and spinal cord tumors above the level of the conus medullaris can also produce DO.
Spinal cord injury.
Spinal cord injury is a common cause of DO. Any complete injury to the spinal cord that spares the S2, S3, and S4 segments eventually produces upper motor neuron lesions, resulting in DO. However, during the initial phase of spinal shock following a suprasacral spinal cord injury, the bladder can be areflexic, resulting in urinary retention and overflow incontinence.
Urogynecologic conditions.
Symptoms of urgency and frequency can be present with a variety of conditions, as listed in Box 31.2 . Idiopathic DO describes symptoms of urgency and frequency, with or without incontinence, that cannot be explained by the presence of other conditions.
Urogynecologic
Detrusor overactivity
Urodynamic stress incontinence
Mixed incontinence
Interstitial cystitis
Urinary tract infection
Radiation cystitis
Urogenital atrophy
Urethral syndrome
Pelvic organ prolapse
Urethral diverticulum
Pregnancy
Pelvic mass
Intravesical lesion
Medical
Neurologic disease
Congestive heart failure
Diabetes mellitus
Diabetes insipidus
Diuretics
Psychological
Habit
Anxiety
Excessive fluid intake
Cystitis.
Inflammation of the bladder epithelium, with or without associated bacteriuria, has been suggested as a cause of bladder overactivity. A historic study by performed urodynamic studies in women before and after treatment of acute UTI. These investigators found that half of patients with urodynamic evidence of DO before treatment for acute UTI had stable CMGs without DO following treatment. The symptoms of OAB syndrome and acute cystitis at onset are usually quite different because cystitis tends to cause an acute onset of dysuria, frequency, urgency, and often hematuria. It is important to distinguish the chronicity of symptoms and to obtain a urinalysis and, if indicated, urine culture to distinguish UTI as the etiology of symptoms and prevent overtreatment with antibiotics ( ).
Hypersensitive bladder disorders.
Women with OAB do not usually have accompanying pain. The presence of persistent or recurrent chronic pelvic pain, pressure, or discomfort perceived to be related to the bladder in conjunction with at least one other urinary symptom, such as urgency or frequency, suggests a hypersensitive bladder condition, such as interstitial cystitis or bladder pain syndrome ( ) – see Chapter 35 . Women who have had previous pelvic radiation and those with significant urogenital atrophy may also complain of OAB symptoms.
Urodynamic conditions.
Detrusor activity can be triggered by a rise in intraabdominal pressure (seen as P abd on CMG) if leakage of urine into the proximal urethra stimulates urethral afferents that induce involuntary voiding reflexes. If urinary incontinence occurs around the same time as an increase in intraabdominal pressure, this finding can be mistaken as stress incontinence, when in actuality the leakage occurs because of an involuntary detrusor contraction, not urethral sphincter weakness. This is called stress-induced DO and can be diagnosed on urodynamics. Stress urinary incontinence may also coexist with DO in many women, resulting in mixed urinary incontinence, and thus it is important to note if patients with stress-induced DO also have urodynamic stress urinary incontinence and/or DO independent of a stress event.
While studying urinary incontinence in the institutionalized elderly, noted a subgroup of elderly women with DO resulting in incontinence who could not effectively empty their bladders when attempting to void. Urodynamic testing revealed that impaired voluntary detrusor contraction caused ineffective emptying, while the bladder also demonstrated involuntary overactivity. They named the condition DO with impaired contractility, now known as detrusor hyperactivity with impaired contractility (DHIC) and hypothesized that this may represent the last stage of DO, in which detrusor function deteriorates.
Structural or anatomic conditions.
At the level of the urethra, urgency incontinence can occur with outlet obstruction. This is a well-known problem in men with benign prostatic hyperplasia and in younger men and women with spinal cord injuries or other neurologic impairments. In women, bladder outlet resistance from previous antiincontinence surgery can result in irritative voiding symptoms and urgency incontinence. Idiopathic bladder outlet obstruction is rare in women and requires video urodynamics to make a diagnosis of primary bladder neck obstruction ( ). Whereas abnormal voiding in women is often caused by poor detrusor function, rather than physical obstruction, obstructed voiding can be seen with advanced pelvic organ prolapse and after operations for stress incontinence.
Women who have undergone radical pelvic surgery may develop OAB postoperatively, likely because of partial denervation of the bladder during the operative process with subsequent development of detrusor dysfunction. Other conditions that can impact the lower urinary tract and result in OAB symptoms include pregnancy, pelvic mass, urethral diverticulum, and intravesical lesions including malignancy.
Orgasm.
Urinary incontinence with orgasm has been found to be associated with DO ( ). The pathogenesis is unknown, but women sometimes experience urinary urgency or urgency incontinence, with a gush of urine during sexual climax. A prospective case-control study of 132 women found that 69% of women with climacturia also had DO on urodynamics, compared to only 39% of those with incontinence with vaginal penetration ( ). Treatment is the same as for DO; sexual counseling and education are often helpful.
Mixed incontinence.
The prevalence of mixed urinary incontinence in women ranges from 14% to 61% ( ). When surgery is performed for the correction of stress urinary incontinence in women, DO postoperatively may resolve, worsen, or remain unchanged. Women may condition themselves to have urgency and frequency by becoming habitual frequent voiders. This can be seen in women with long-standing stress incontinence, because they will consciously or subconsciously void more frequently to avoid or reduce leakage. Over time, it has been proposed that functional bladder capacity is reduced, and the bladder becomes more sensitive at lower volumes of urine, thus resulting in frequency and urgency (OAB dry). This same phenomenon can occur in women with urgency incontinence, resulting in more severe frequency. This can be viewed as a cycle in which symptoms continue to worsen unless intervention is undertaken ( Fig. 31.7 ).
Idiopathic detrusor overactivity.
Idiopathic DO is defined as involuntary detrusor contractions without an identifiable underlying cause ( ). Because of the difficulty in identifying the underlying pathology for the development of OAB in most patients, their OAB is often labeled as “idiopathic.” Prior hypotheses have thought of idiopathic DO as either being of neurogenic etiology (DO arising from generalized nerve mediated excitation of the detrusor muscle) or myogenic etiology (DO resulting from a combination of an increased likelihood of spontaneous excitation within smooth muscle of the bladder and enhanced propagation and subsequent spread of contractile signals via cell-to-cell coupling). However, more recently, OAB syndrome is thought to comprise several OAB phenotypes with different underlying mechanisms and pathophysiological causes ( ). Fig. 31.8 demonstrates a new diagnostic approach to seek the underlying pathophysiological phenotypes for OAB.
Evaluation
Per the joint guidelines on the Diagnosis and Treatment of Overactive Bladder (Non-Neurogenic) in Adults from the American Urological Association (AUA) and Society of Urodynamics, Female Pelvic Medicine, and Urogenital Reconstruction (SUFU), which were amended and endorsed by the American Urogynecologic Society in 2019, the minimum requirements in evaluation for OAB of an uncomplicated, nonneurogenic patient are careful history, physical exam, and urinalysis ( ; ). One of the key elements in evaluating women with OAB is the impact of their symptoms on quality of life. Standardized quality-of-life questionnaires are available and can be administered to help with evaluation of quality of life and to track progression over time. In addition, it is important to assess concomitant pelvic organ prolapse, defecatory complaints, and sexual dysfunction. A thorough medical history should be taken, as well as a surgical history with emphasis on previous lower urinary tract or gynecologic surgery. A thorough review of all prescription medications that the patient is currently taking, and as well as previously tried OAB medications, is also vital.
Physical examination.
In the evaluation of OAB, a clinician should perform a general physical, neurologic, and pelvic examination ( ). Neurologic studies should include a brief mental status examination and evaluation of cranial nerves and deep tendon reflexes. Muscle strength can be assessed by having the patient actively move against resistance, such as shrugging her shoulders against downward pressure. Specifically testing the sacral spinal cord involves evaluating the patient’s ability to extend and flex her hip, knee, and ankle, and invert and evert her foot. Deep tendon reflexes can be checked at the biceps (C5–C6), triceps (C7), knee (L3–L4), and Achilles tendon (L5–S2).
Spinal cord segments S2, S3, and S4 contain important neurons involved in micturition. The anal sphincter and pelvic reflexes are important indicators of sacral cord integrity. Voluntary contraction of the external anal sphincter indicates a minimum level of integrity of pelvic floor innervation. Stroking the skin lateral to the anus elicits a reflex anal sphincter contraction. The bulbocavernosus reflex involves tightening of the bulbocavernosus and ischiocavernosus muscles by tapping or squeezing the clitoris. The cerebellum should also be tested because it has major functions in the control of micturition. The cerebellum can be tested by evaluating finger/nose and heel/shin coordination and examining the patient’s gait.
A pelvic examination should include a thorough inspection of the perineal area and vulva, looking for excoriation, vaginal discharge, or atrophy, suggesting estrogen deficiency. Vaginal examination should include assessment for pelvic organ prolapse, pelvic muscle function, atrophy, and anatomic abnormalities. The urethra can be palpated through the anterior vagina, checking for a mass or purulent discharge from the urethral meatus consistent with a urethral diverticulum. Pelvic floor muscle function should be described by pelvic muscle tone at rest and by the strength of voluntary contraction (see Chapter 9 ). Determining the postvoid residual, either with ultrasound or by performing straight catheterization, can help rule out occult voiding dysfunction, as well as DHIC. However, postvoid residual measurement is not necessary for patients who are receiving first-line behavioral interventions or for uncomplicated patients (those without a history of or risk factors for urinary retention) receiving antimuscarinic medications ( ). Pelvic organ prolapse should be evaluated, specifically commenting on the support of the anterior, apical, and posterior vagina. Rectal examination should also be performed to rule out fecal impaction and rectal mass while assessing sphincter tone.
Diagnostic studies
Urinalysis and urine culture.
Because the symptoms of UTI and other irritative bladder conditions commonly mimic OAB, urinalysis should be performed before further investigations or treatments are initiated. As previously mentioned, bacteriuria may cause DO, which sometimes resolves after the infection has been treated. Urinalysis and, if indicated, microscopy, should also be used to screen for microhematuria, which would warrant further investigation for urothelial neoplasm.
Voiding diary.
A voiding diary can be a useful tool for both patients and clinicians alike as a way to quantify and temporally map their urinary frequency and incontinence episodes. A completed voiding diary tracking up to 72 hours of a patient’s fluid intake and voiding habits can help to corroborate their history and symptoms. A follow-up voiding diary can also be useful to provide evidence to both patient and clinician of treatment response.
Urodynamic testing
Cystometry.
Cystometry is the critical portion of urodynamics testing for investigating bladder storage function, as it is the only method of objectively diagnosing detrusor contraction. Fig. 31.9 reviews the various cystometric patterns that may be seen in patients with DO. (See Chapter 11 for more details.) Per the AUA/SUFU guidelines, “urodynamics are not recommended in the initial diagnostic workup of the uncomplicated OAB patient” ( ). However, for complicated patients or refractory patients who have failed multiple OAB treatments, urodynamics can be performed based on the clinician’s judgment. Fig. 31.10 reviews the diagnosis and treatment algorithm from the AUA/SUFU guideline on Diagnosis and Treatment of Overactive Bladder (Non-Neurogenic) in Adults.
When performing urodynamic testing for a patient with OAB, it is important to try to replicate their bothersome symptoms during the study. Sometimes this requires clinicians to use provocative stimuli if detrusor contractions are not elicited during the filling phase. Testing should be performed with the patient in a sitting or erect position, because supine filling cystometry alone often fails to uncover a significant proportion of bladder overactivity. Other provoking factors that can be performed during the testing session include coughing, straining, heel-bouncing, jogging in place, listening to running water, and placing the patient’s hands under running water. It is also useful to ask patients what typically prompts their symptoms and try to replicate those maneuvers during urodynamic testing.
It is important to remember that DO is a diagnosis made by findings on CMG, whereas OAB is a syndrome based on clinical symptoms; therefore, the absence of DO on urodynamics does not exclude a diagnosis of OAB. found an overall incidence of DO in 76.1% of male patients and 58.7% of female patients with OAB. A higher percentage of patients (93% of men, 69.8% of women) were found to have DO when they had both symptoms of urgency and UUI. Overall, a combination of LUTS resulted in a higher likelihood of actually seeing DO on urodynamics.
explored the relationship between the presence of DO on urodynamics and the response to treatment with anticholinergics in patients with OAB. This study demonstrated that DO is not found in all subjects with OAB but that, when found, those patients respond more favorably to anticholinergic treatment. The authors suggested that anticholinergic therapy is most effective in patients with demonstrated DO and, thus, that urodynamics should be considered in all patients with OAB as a predictor for success of therapy. However, more importantly, this study sheds light on the point discussed above regarding a variety of different phenotypes of patients within the spectrum of OAB syndrome that may respond differently to various treatment options.
Overall, urodynamics testing is not necessary in a patient with uncomplicated (nonneurogenic) OAB before starting treatment and progressing through the treatment algorithm provided in the AUA/SUFU guideline (see Fig. 31.10 ). However, certain scenarios, such as refractory or complicated cases or concern for underlying neurogenic dysfunction, may warrant urodynamic testing based on the clinician’s judgment.
Urethral pressure studies.
Urethral pressure studies add little to the diagnosis of DO or to the differentiation of patients with stress incontinence from those with urgency incontinence. Detrusor contractions are almost always preceded by a drop in urethral pressure ( Fig. 31.11 ). studied urethral pressure tracings in 72 women with DO to learn whether urethral pressure changes may be the cause, rather than the effect, of bladder contractions. Patients who had urethral relaxation before detrusor contractions responded better to sympathomimetic drugs, whereas patients without urethral pressure changes responded more favorably to anticholinergic drugs.
Electromyography.
Electromyography (EMG) gives information on the activity of the external striated urethral sphincter muscles. Its potential value in patients with DO is to document voluntary control of this sphincter, as well as to demonstrate that the external sphincter and detrusor muscle function in a coordinated fashion ( Fig. 31.12 ). found that 48% of patients with idiopathic DO exhibited reflex relaxation of the sphincter at the time of a detrusor contraction. This observation is important because these patients are probably unable to voluntarily contract the external sphincter at the moment of the detrusor contraction; thus, their ability to inhibit urine loss is limited.
Endoscopy.
Similar to urodynamics, the routine use of cystourethroscopy is not indicated in the evaluation of uncomplicated OAB ( ). However, certain findings during the evaluation of a patient with OAB may warrant cystourethroscopic examination. Box 31.3 lists clinical situations in which clinicians should consider cystourethroscopy in the setting of suspected OAB. For example, a history of a midurethral sling placement with polypropylene mesh and new onset of OAB symptoms might be indicative of mesh erosion into the urethra or bladder, which could be diagnosed with cystoscopy (see Chapter 25 ). Other indications for cystourethroscopy include physical examination findings of a mass below the urethra consistent with urethral diverticulum or concern for urethral malignancy. reported an unusual case of an elderly woman with OAB and a history of lithium use for bipolar disorder. The patient was found to have suburothelial metal deposition that was felt to be related to her OAB by acting as a bladder irritant. The clinician should always pay attention to occupational exposures or medications that could potentially be bladder irritants.
| Hematuria |
| History of recurrent UTIs |
| Persistent or de novo OAB after an incontinence procedure |
| De novo OAB after pelvic surgery |
| Long-term indwelling catheter use |
| Abnormal-appearing bladder on imaging |
| Positive cytology |
| Mixed symptoms with pain |
| Prior mesh placement |
| History of bladder cancer |
| Occupational exposure |
Definitive indications for cystourethroscopy include gross or microscopic hematuria, see Chapter 40 ( ). Cystourethroscopy can also be considered if the diagnosis is in doubt or if the patient shows no response to appropriate behavioral and pharmacological therapy.
Management
There is a wide variety of treatment options available to the practitioner caring for patients with OAB. Treatments range from nonsurgical to surgical, with varying degrees of invasiveness and monetary and time investment. OAB can have a significant effect on a woman’s quality of life, and, as already discussed, before discussing management option the specific patient’s degree of bother should be assessed. The severity of the woman’s symptoms, along with the degree of invasiveness of certain treatments and associated adverse events, most likely will contribute to a woman’s perception of what will be the most reasonable therapeutic option for her to pursue. As there is no known “cure” for OAB, it is important that patients have a realistic expectation and aspiration for symptom management.
See Box 31.4 for a list of various treatment options for OAB. This chapter will specifically focus on first- and second-line treatments (see Fig. 31.10 ) for OAB. Third-line treatments are discussed in detail in Chapter 32 .
