OAB comprises a constellation of symptoms including urinary frequency, urgency with or without urinary incontinence in the absence of definable pathology such as urinary tract infection, bladder outlet obstruction, bladder cancer, or disorder of the neurologic system (i.e., SCI, MS, cerebrovascular accident, spina bifida, Parkinson’s disease, etc.) which can result in a similar clinical presentation. The prevalence of OAB in the United States ranges from 7–27 % in men and 9–43 % in women (Gormley et al. 2012). It also disproportionately affects the elderly population and can heighten the risks of falls potentially resulting in hip fractures and skull injuries with their concomitant comorbidities (deep vein thrombosis, pulmonary embolus, intracranial hemorrhage etc.). Despite not having direct impact on duration of life, OAB can have tremendous negative effects on the quality of life. Many find that their ability to perform and/or enjoy daily activities and ability to obtain satisfactory sleep is encumbered by the frequent and urgent need to void. Furthermore, management of the often associated urinary (urgency type) incontinence can often be a costly venture requiring the use of various types of protective devices such as sanitary pads and diapers. In severe cases, chronic urethral catheterization may be chosen as the most pragmatic method of management, exposing the patient to some of the long-term consequences previously mentioned when used in the neurogenic population.

Evaluation of the patient with OAB revolves around diagnostic tests able to detect causative and potentially treatable etiologies. Simple urinalysis can detect evidence of urinary tract infection, glucosuria which may be causing an osmotic diuresis, and hematuria (microscopic or gross), a potential indicator of urinary tract pathology such as neoplasia or urolithiasis. Urine cytology while not highly sensitive does have good specificity (low false positives) and can be utilized when social data (tobacco use or exposure to chemicals) suggest predisposition to urothelial malignancy. Measurement of post-void residual urine can assist in the detection of bladder outlet obstruction and neurogenic vesicourethral dysfunction when elevated. Direct inspection of the bladder and urethra with cystourethroscopy may be indicated when there are reasons to suspect bladder neoplasm (primarily hematuria or suspicious urine cytology). Urodynamics, although not required for diagnosis, can be helpful in determining if bladder outlet obstruction or neurogenic bladder is the underlying pathophysiological process. Typical findings in patients with OAB are the presence of involuntary detrusor contractions of varying magnitudes during the filling phase, sometimes accompanied by the loss of urine. The absence of this pattern, however, is not sufficient to eliminate the diagnosis of OAB as the study can be normal in up to 50 % of affected patients.

Management and treatment of OAB is dictated primarily by the severity of the symptoms and the level of impact it has on the patient’s quality of life (Table 13.2). Oftentimes behavioral modification by the moderation in fluid intake, reduction in the use of caffeinated products and others with diuretic properties (i.e. alcohol), and elimination of food stuffs with high spice content can be sufficient at satisfactorily ameliorating the symptoms of OAB. In most instances, however, this is not adequate and pharmacological or surgical options must be considered. The goal of these therapies is either reduction in the frequency or amplitude of the associated involuntary detrusor contraction or their elimination altogether. As with NGB, pharmacotherapy for OAB generally involves the use of agents with antimuscarinic properties that interfere with detrusor contractions. Many are commercially available with no significant differences in their efficacy. Oral preparations are most commonly used; however, agents that can be topically administered (transdermal patch, gel) exist. Recently, another agent with beta-3 agonist properties (mirabegron) has become commercially available that has similar efficacy to the antimuscarinics but without the typical side effects of dry mouth and constipation (Herschorn et al. 2013). Studies to investigate the potential benefit of combination therapy with the antimuscarinics and beta-3 agonists are currently in development and may provide an additional option for treatment. When pharmacotherapy fails to achieve significant clinical benefit, surgical options include intravesical injections of botulinum toxin or sacral neuromodulation utilizing the Interstim device made by Medtronic. Both have demonstrated acceptable results in patients in whom medical therapy is inadequate or side effects are intolerable. The advantages of botulinum toxin are its simplicity of administration and low side effect profile. Repeat injections (every 6–9 months), however, are necessary to maintain efficacy and there is the potential for transient urinary retention requiring catheterization (indwelling or intermittent) until resolution. Sacral neuromodulation typically requires two phases, one of which is a testing period with a stimulating lead in place to establish efficacy followed by surgical implantation of the generator when successful. Complications can include infection, pain, and lead displacement.