Sunday, April 8, 2012

Pathophysiology of pelvic floor disorders (part 2)

Pathophysiology of pelvic floor disorders (part 2)


Pathophysiology and mechanisms underlying female urinary incontinence

Etiology and types of female stress urinary incontinence

A-   Genuine stress incontinence with urethral hypermobility (type I and II)

B-   Intrinsic sphincter deficiency (ISD) (type III)

      C- Coexistence of ISD with type II stress incontinence

Detrusor instability

Definition and classification of pelvic organ prolapse

Pathophysiology of pelvic organ prolapse and relaxation

Etiologies of pelvic organ prolapse
A-  Anterior vaginal wall prolapse (Descent)
B-   Posterior vaginal wall prolapse and perineal descent
C-   Vaginal apex prolapse and enterocele

Effects of pelvic floor dysfunction

Other risk factors in the development of pelvic organ prolapse, urinary incontinence and voiding dysfunction

Pelvic organ prolapse (POP)
Definition and classification
We still have not defined genital tract prolapse, determined its prevalence or provided the clinician with a simple and reliable means of testing for its presence or absence (Swift, 2002). Genital prolapse is a process in which the pelvic contents, including the reproductive organ, bladder, rectum, and/or small intestines become herniated through defects in the vaginal wall (Bai et al, 2003). Vaginal topography does not reliably predict the position of the associated viscera on pelvic floor fluoroscopy in women with primary or recurrent POP (Kenton et al, 1997). The prolapse should be described as it exists at its maximal protrusion, as noted by the patient during her daily activities. Of prime importance is the concept of describing and evaluating site-specific defects of pelvic support: anterior vaginal support, lateral vaginal support (particularly the vaginal attachments along the arcus tendineus), posterior vaginal support, support of the vaginal apex and total vaginal length (Wall and Hewitt 1994). When possible, prolapse should be described with respect to fixed anatomical points, such as plane of hymen or the ischial spines (Wall, 1996).

Pathophysiology of POP and relaxation
Normally the vaginal axis in an erect woman is nearly horizontal in the upper half of the vagina, with the uterus and upper 3 or 4 cm of the vagina lying over the levator plate in the hollow of the sacrum. The vagina is directed toward the S3 and S4 vertebrae and extends approximately 3 cm past the ischial spines in most nulliparous women. Increases in intra abdominal pressure compress the vagina anterior too posterior over the contracted levator muscles in the midline (levator plate). Diminished muscle tone may result in loss of stability of the levator plate, widening of the levator hiatus, and loss of an adequate base to support the upper vagina and uterus in the normal axis (Funt et al, 1978) (figure 17). During effort, the upper part of the vagina was stretched backwards and downwards against the perineal body. Compression of the rectovaginal fascia appeared to be related to the angle of the upper vagina to the horizontal at rest (Petros, 2001).
Figure 17 Normal vaginal axis of nulliparous woman in the standing position. The upper third of the vagina is nearly horizontal and is directed toward the S3 and S4 sacral vertebrae (Funt et al, 1978).

Pelvic organ prolapse may occur as a result of congenital or acquired factors in the bones, muscles, nerves, or connective tissues that are responsible for normal support and function. Vaginal delivery, chronic increases in intra abdominal pressure, increasing age, and decreased estrogen stimulation are important factors associated with POP (Shull and Bachofen, 1999). Connective tissue defects have been found in women with uterine prolapse and stress incontinence (Makinen et al, 1987).

Etiologies of pelvic organ prolapse
A variety of causes result in loss of anatomic support that leads to herniation of the pelvic viscera through the levator hiatus. Prolapse and UI are interrelated in their etiology and pathophysiology. Vaginal delivery with stretching and tearing or avulsion of pelvic tissues may lead to permanent changes in the integrity of pelvic support. Estrogen deficiency leads to a loss of collagen with atrophy and weakening of ligaments (Brince et al, 1983).

A-Anterior vaginal wall prolapse or descent
Most cases of anterior vaginal prolapse are due to disruption or detachment of the lateral CT attachments resulting in paravaginal defect (Richardson et al 1976).

B- Posterior vaginal wall prolapse and perineal descent
The etiology of rectocele is not completely understood and may encompass different mechanisms in different patients (Cundiff et al, 1998). Perineal descent appears associated strongly with posterior compartment symptoms in patients with posterior vaginal wall prolapse (Fialkow et al, 2002).
C- Vaginal apex prolapse and enterocele
DeLancey (1992) described the anatomy of vaginal vault eversion and divided vaginal support into levels I, II and III. In level I, the cervix (in a woman who has not had the uterus removed) or the vaginal apex (in a woman who has previously had a hysterectomy) is suspended to the cardinal and uterosacral ligaments. In level II, the area along the base of the bladder anteriorly and along the rectum posteriorly is attached to the arcus tendineus fasciae pelvis or to the fascia over levator muscle. Level III, the area along the base of the urethra or at the distal rectovaginal septum just inside the hymen, is derived from the urogenital sinus and is an area of fusion.

Enterocele is a hernia in which peritoneum is in contact with vaginal mucosa. The normal intervening endopelvic fascia is absent, and small bowel fills the hernia sac (Shull and Bachofen, 1999).

Effects of pelvic floor dysfunction
Women with SUI are capable of operating the pelvic floor muscles but do not use them adequately during cough (Wijma et al, 1991). Slightly less than half of women with urethral hypermobility and anterior vaginal wall prolapse have visibly abnormal (atrophy) levator ani muscles (DeLancey, 2002). Anorectal incontinence is associated with urinary incontinence of the stress type in 10-15% of patients (Swash, 1984).

Relationship of POP and LUTS
Symptoms of SUI and hesitancy were more frequent in the patients with anterior wall prolapse (Bai et al, 2003). It is accepted that POP impairs voiding, in particular as regards the anterior vaginal wall. The influence of central and posterior prolapse is more controversial. As regards prolapse, only enterocele had a consistently negative effect on flow (Dietz et al, 2002 II). Procidentia may occasionally imprison the ureters, leading to hydronephrosis (McGuire, 1996).

Other risk factors in the development of POP, UI and voiding dysfunctions
1- Race
Patients with GSI are more likely to be white women (Klingele et al, 2002).

2- Age
     Normal aging is characterized by decline in the reserve capacity of all organ systems. As in other muscles, volume and number of muscle cells in urethral sphincter decrease with age. Bladder capacity, ability to postpone voiding, bladder compliance and urinary flow rate decrease with age in both sexes. Uninhibited bladder contractions and elevated PVR increase with age. Maximal urethral closure pressure, functional urethral length and urethral compliance decrease with age in women (Brown et al, 1996). As with urinary function, the effect of age on anorectal function is multifactor. Fecal incontinence show increased prevalence with age (Talley et al, 1992).

3- Hormonal status
          Both estrogen and progesterone may affect the incidence of certain LUTS. The incidence of many such symptoms has been shown to increase around the fourth and fifth decades of life, which coincides with the time of the menopause, some symptoms have also been shown to be relieved or exacerbated by various forms of hormone replacement therapy (Cutner et al, 1993).

4-Lumbosacral curve
    Anatomic studies of the pelvis and spine have suggested that the normal spinal curvature protects the pelvis from direct intra-abdominal forces. Normal spinal curvature deflects forces interiorly to the anterior abdominal wall and symphysis pubis. An abnormal change in spinal curvature, specially, a loss of lumbar lordosis, appears to be a significant risk factor in the development of POP. When compared with patients with a normal curvature, patients with abnormal spinal curvature were 3.2 times more likely to have development of POP (Mattox et al, 2000).

5-Body Mass Index (BMI)
          Under weight is < 20 Kg/ m2, normal 20 to 25 Kg/ m2   and over weight > 25 Kg/ m2 (Danish Food Agency, 1987). Overweight women have increased intra-abdominal pressures, which adversely stress the pelvic floor and may contribute to the development of UI. Obesity was defined as a BMI of ≥30 Kg/ m2 (Mukherjee and Constantine, 2001).

6- Cigarette smoking
          Genuine stress incontinence develops in smokers in spite of their stronger urethral sphincter and lower risk profile than nonsmokers. More violent coughing by smokers likely promotes the earlier development of the anatomic and pressure transmission defects that allow GSI and overcomes any protective advantage of a stronger urethral sphincter (Bump and McClish, 1994).



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