There are various underlying causes that result in weakness of one or more of the components of the urethral sphincter mechanism (Table 7.1).

The bladder neck and proximal urethra are normally situated in an intra‐abdominal position above the pelvic floor and are supported by the pubo‐urethral ligaments. Damage to either the pelvic floor musculature (levator ani) or pubo‐urethral ligaments may result in descent of the proximal urethra such that it is no longer an intra‐abdominal organ and this results in leakage of urine per urethra during stress.

This theory has given rise to the concept of the ‘hammock hypothesis,’ which suggests that the posterior position of the vagina provides a backboard against which increasing intra‐abdominal forces compress the urethra. This is supported by the fact that continent women experience an increase in intra‐urethral closure pressure during coughing. This pressure rise is lost in women with stress incontinence, although, may be restored following successful continence surgery.

In addition to pelvic floor damage, there is also evidence to suggest that stress incontinence may be caused by primary urethral sphincter weakness or intrinsic sphincter deficiency (ISD). In order to distinguish this type of stress incontinence from that caused by descent and rotation of the bladder neck during straining, the Blaivis Classification has been described based on video‐cystourethrography observations. This proposes that Type I and Type II stress incontinence are caused principally by urethral hypermobility, whereas Type III, or ISD, is caused by a primary weakness in the urethral sphincter. Factors associated with ISD are pudendal denervation injuries, loss of integrity of the striated urethral sphincter and urethral smooth muscle, as well as the loss of urethral mucosa and submucosal urethral cushions.

The ‘mid‐urethral theory’ or ‘integral theory’ described by Petros and Ulmsten is based on earlier studies suggesting that the distal and mid‐urethra play an important role in the continence mechanism and that the maximal urethral closure pressure is at the mid urethral point. This theory proposes that damage to the pubourethral ligaments supporting the urethra, impaired support of the anterior vaginal wall to the mid urethra and weakened function of part of the pubococcygeal muscles, which insert adjacent to the urethra, are responsible for causing stress incontinence.