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Overactive bladder (OAB) is a highly prevalent yet under-reported condition that transcends the boundaries of race, gender, and socioeconomic class. OAB is loosely defined by the International Continence Society (ICS) as a constellation of symptoms that include primarily urinary urgency usually accompanied by frequency (voiding eight or more times per 24 hours) and nocturia (awakening two or more times at night to void), with or without urge urinary incontinence (UUI). It is a symptom syndrome and not a discrete diagnosis. The most recent data suggest that OAB affects between 16% and 17% of adults in the United States, or about 34 million people. However, given the substantial underreporting and the inherent challenges in identifying sufferers of OAB, the actual prevalence is likely markedly higher. Women and men tend to be affected by OAB proportionately; however, women are more likely than men to present with the symptom of incontinence as part of their clinical picture. The incidence of OAB increases linearly with age and is predicated on a number of factors that are impacted by aging. However, OAB with or without incontinence is not considered a normal part of aging; OAB symptomatology and any instance of urgency are always considered pathologic.
OAB syndrome has extensive ramifications with respect to morbidity, mortality, and economic impact. A preponderance of literature supports the assertion that OAB is associated with increased rates of depression, decreased self-esteem, social isolation, general fragility, and falls and fracture. Upon development of OAB symptoms, patients tend to engage in avoidance behaviors in order to escape the social stigma and embarrassment associated with urinary incontinence (UI) or urinary urgency. Eventually, this translates into substantial lifestyle changes and the potential for social isolation. Total costs attributable to OAB are estimated to be $65.9 billion ($49.1 billion direct medical, $2.3 billion direct nonmedical, and $14.6 billion indirect) (Ganz et al., 2010
). A leading cause of morbidity in the elderly population and the most commonly cited reason for assisted living and long-term care facility admission, OAB needs to be assessed in the primary care setting preemptively.
The terms OAB, detrusor overactivity (DO), and UI are frequently used interchangeably erroneously. UI is a possible symptom as part of the symptomatology construct that constitutes OAB; it does not necessarily need to be present in patients diagnosed with OAB. While urgency is the cardinal symptom of OAB and must be present in order to yield a diagnosis of OAB, only about 25% to 35% of patients experience incontinence as well. DO implies an involuntary and inappropriate contraction of the bladder; however, it is considered a surrogate marker of OAB that may or may not correlate with urgency. DO is further delineated into idiopathic (absence of an identifiable cause) or neurogenic (an underlying neurological condition, deficit, or injury is the causative factor). There is considerable overlap between nonpharmacologic and pharmacologic treatments for OAB, UI, and DO; therefore, UI subtypes will be discussed. The accepted nomenclature for UI differentiates between the underlying pathophysiology and the nature of the urine loss. UUI implies a strong and sudden urge to urinate that cannot be deferred and results in involuntary loss of urine. Stress urinary incontinence (SUI) occurs when an internal or external force impacts the bladder or the musculature that supports it. Common examples of such pressures include coughing, sneezing, heavy lifting, or prolapsed pelvic organs. Mixed UI is a combination of both SUI and UUI. The historical term overflow incontinence, which suggested some level of obstruction or voiding difficulty, has been replaced with bladder outlet obstruction (BOO) and is no longer part of the classification schema.
The exact cause of the OAB symptom constellation is multifactorial and not completely elucidated. There are numerous underlying anatomic, physiologic, and comorbidity-related factors that precipitate or exacerbate OAB. The majority of cases are considered idiopathic, with the remainder being attributed to myogenic or neurogenic causation.
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