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10. • To begin, normal female urinary continence is achieved when the urethra maintains a greater pressure than
the bladder during states of rest and activity.
• How stress incontinence is prevented ?
1. 1- During bladder filling and during increases in abdominal pressure, the anterior vaginal wall the female
pelvic floor, compress the urethra. Urethral closure pressures are therefore elevated relative to the
bladder pressures that are generated, and continence is maintained.
2. 2- urethral sphincter itself has an intrinsic closure mechanism that increases during exertion and further
prevents urinary leakage.
• How stress incontinence is occured ?
• Stress urinary incontinence occurs when these normal mechanisms of continence are compromised.
1. 1- Urethral hypermobility
• results when the pelvic floor musculature is unable to provide sufficient support and compress the
urethra.
• The bladder neck and proximal urethra normally maintain a high retropubic position, and increases in
intra-abdominal pressures are transmitted equally to the bladder and urethra .
• However, when pelvic floor muscle laxity occurs, the bladder neck and urethra cannot maintain their
normal anatomic position, and the bladder neck and urethra rotate posteriorly and descend caudally
which can lead to reduced urethral closing pressures and urinary incontinence.
2. 2- Intrinsic sphincteric deficiency (ISD )
• is a second mechanism that leads to female stress urinary incontinence.
• ISD is a condition in which the bladder neck and/or proximal urethra remains partially open at rest.
• Urinary incontinence in this case develops despite normal pelvic floor musculature and despite minimal or
no urethral descent during stress.
• ISD is often seen in patients due to atrophy of the sphincteric muscles from aging or in patients with
persisting SUI following urethral sling surgery.
• All patients with SUI are believed to have some degree of ISD.