Continence or incontinence, seen from a dinamic view, depend on the balance between the strenght that tend to empty the bladder ( empty forces ) and those that try to retain urine in the bladder ( retention forces ). When the empty forces surpass the strenght of retention the result is incontinence 1,2,3.
The intravesical pressure (IVP) represent the expulsion strenght, this depends on the abdominal pressure , the pressure perfomed by the detrusor (PD) , and the tone of the smooth muscular fibre, or basal pressure (BP).
The strenght of retention result in a complex mechanism where so many factores intervene : the sphincterian (smooth and striated sphincter), length and position of the urethra, anatomic structure, hormones, and neurogenic control. The urethral closure pressure opposes to the strenght of expulsion. While the urethral closure pressure exceeds VP the continence is secured.
When IVP is superior to urethral closure pressure we will have two large groups of incontinence, the ones that occur by enlargement of IVP and the ones that occur due to diminishment of urethral closure pressure 4.
By the increase of IVP: this increase may happen in an active or passive way. The active form of incontinence is secondary to the detrusor contraction and is due to bladder instability. The passive form is a consequence of the progressive increase of volume during the bladder filling phase. An clear example of this physiopathogenic mechanism is the urinary incontinence by overflowing.
Diminishing of urethral closure pressure: are secondary to the incompetence of the sphincterian mechanism, such incompetence may be due to different factors: anatomical (urethralvesical position, weakness of the bladder neck , incompetence of the striated sphincter) in this anatomical disorders there is a multiple delivery incidence; in the hormonal alterations due the climateric period that induce mesenchyme weakness of the urethral wall; iatrogenic (post-operational urethral rigidity); neurological ( urethral denervation); inflammatory (urethral rigidity by fibrosis, bacterian endotoxins);pharmacological (beta-stimulants and alpha-blockers) and hormonal deficiency.
To finish, another component that takes an active part in continence is the external urethral sphincter to which is atributed 50% of urethral closure pressure. The weakness of the urogenital diaphragm, hysterectomies and the damage of the nervus pudendus are responsible for its incompetence.
In a separate chapter we have recurrent urinary incontinence (RUI). The RUI attempts to challenge urogynecologists difficulty to solve.