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Abstract
Genuine stress incontinence is the condition in which urine loss occurs when the bladder pressure exceeds the maximal urethral pressure during activities that increases abdominal pressure without an associated detrusor contraction. This may occur as a result of abnormal transmission of abdominal pressure to the urethra or an inherent loss of urethral tone. Women are particularly predisposed to the development of stress incontinence because of a relatively short urethra and trauma resulting from childbearing. Other common causes include surgery, menopause, medical conditions that increase intra-abdominal pressure, persistent heavy lifting or straining, neurologic damage, and connective tissue disorders (Robinson et al., 1998).
Urinary incontinence increases with aging (FantI et al., 1996b). Physiologic changes of the human female urethra include decreased
intraurethral pressures with aging, even among continent women (Rud,
1980). Urethral structure also changes with aging. The relative volumes of
urethra striated muscle and vasculature decrease, whereas smooth muscle
volume is preserved and connective tissue volume increases (Carlile et al.,
1988). This information suggests that intrinsic urethral function may be as
important as extrinsic support in maintaining urinary continence. Urinary
incontinence is most likely the result of a combination of urethral atrophy
and loss of support of the urethrovesical junction (Strohbehn and
DeLancey, 1997).
When UI is a problem, the patient should undergo a basic evaluation
including history, physical examination, estimation of post-voiding residual
volume and urinalysis (Fantl et al., 1996b).
Further evaluation might require urodynamics, electromyography and imaging technique (Fantl et al., 1996b).