U rinary incontinence is a common problem, affecting up to two-thirds of all women. Its prevalence is easily underestimated in the clinical setting, since patients will often fail to bring the condition to the attention of their physician; it is estimated that only 1 in 4 symptomatic women seek help for this problem.1 By recent estimate, the total annual cost of urinary incontinence in the United States is about US$19.5 billion.2 In addition to affecting quality of life, complications of urinary incontinence include urinary retention, chronic lower urinary tract infection and vesicoureteral reflux, all of which affect health greatly. The aim of this review is to give primary care practitioners an overview of the current understanding of the taxonomy, pathophysiology, evaluation and treatment of female urinary incontinence.
PathophysiologyPatients present with symptoms rather than diagnoses -an important distinction in the discussion of female urinary incontinence. Most patients with any degree of urinary incontinence will have symptoms that point to stress incontinence, urge incontinence or mixed incontinence. The symptom of stress urinary incontinence is the involuntary loss of urine accompanying sudden increases in intra-abdominal pressure (i.e., "stress"); this loss is sudden, coincident with the stressor and usually without warning. Urge incontinence occurs when an overwhelming urge to void results in leakage of urine; about half of all patients with overactive bladder syndrome experience urge incontinence.3 Mixed incontinence is the concurrence of stress and urge incontinence symptoms.As the bladder fills, sensory afferent signals are carried via the pelvic and hypogastric nerves to the spinal cord ( Fig. 1), where they are relayed to the pontine micturition centre via the lateral spinothalamic tracts and dorsal columns. Sympathetic tonus via the hypogastric nerve maintains smooth musclebased activity of the urethral sphincter and aids in detrusor relaxation, which thus promotes urine storage. Somatic efferent signals to the striated muscle of the pelvic floor via the pudendal nerve provide voluntary urethral sphincter activity, as well as momentary augmentation of urethral resistance in response to sudden increases in bladder pressure. As afferent signaling increases in intensity with bladder filling, a threshold of consciousness is reached, at which point a socially appropriate opportunity to void is sought. With permission to void, pontine signaling to the sacral cord via reticulospinal and corticospinal tracts results in parasympathetic cholinergic activation of the detrusor and reflex relaxation of the striated muscle of the pelvic floor, which allows pressurized urine flow.
4Neurologic insults commonly cause involuntary detrusor contractions and urinary incontinence by interrupting the pathways that control and coordinate the micturition reflex. Although lesions and conditions may vary in their effect on voiding dysfunction and incontinence, central nervous system lesions at or above the thoracic spin...