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Ultrasonography of the Adult Male Urinary Tract for Urinary Functional Testing
Published on: August 14, 2019
Diagnosis and treatment of the overactive bladder
1Division of Urology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA. alan.wein@uphs.upenn.edu
Abstract:
Overactive bladder syndrome (OAB) is a symptomatic diagnosis based on the presence of urgency, with or without urge incontinence, and usually accompanied by frequency and nocturia, in the absence of obvious pathologic or metabolic disease. Initial management of OAB requires an integrated approach using behavioral and pharmacologic methods. Patients should be educated about the functioning of the lower urinary tract system, fluid and dietary management, timed or prophylactic voiding and bladder training regimens, the keeping of micturition charts or bladder diaries, and pelvic floor exercises. Although the effectiveness of muscarinic receptor antagonists for the treatment of OAB has been shown, adverse effects, such as dry mouth, constipation, and blurred vision have somewhat limited their usefulness. Newer agents that are more bladder selective have been and continue to be developed. The concept of clinical effectiveness-a combination of efficacy, tolerability, and compliance-can be used to evaluate not only how well a drug works, but also the side-effect profile and bothersomeness and how likely patients are to continue treatment. Patients who do not respond to antimuscarinic treatment of OAB may do so because of a variety of nonpharmacologic and pharmacologic reasons. Most cases of OAB are not cured, but rather the symptoms are reduced, with an associated improvement in the patients' quality of life. Patients who have failed behavioral and pharmacologic intervention may respond to neuromodulation and augmentation cystoplasty. Future approaches may include (1) other types of systemic pharmacologic therapy; (2) intravesical administration of drugs, including blockers of afferent input; (3) intradetrusor injection of botulinum toxin; (4) the use of tissue engineering to simplify augmentation cystoplasty; (5) genetic interventions to reverse neuroplasticity changes; and (6) combinations of these approaches.
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