Epidemiology

Pathophysiology

Robust epidemiological studies on the natural history, incidence, and prevalence of POP are lacking. A common condition in vagi- nally parous women, the prevalence rates vary between 40% and 50% on vaginal examination.

The prevalence of POP is known to increase with age. It is pre­dicted that by 2050, the number of women suffering from symp­tomatic prolapse in the United States will increase by 46% (2). In a longitudinal study of parous women with a lifespan of 80 years in the United Kingdom, the lifetime risk of undergoing a surgical pro­cedure was 12% (3). The lifetime risk of a women undergoing sur­gery due to POP was found to be as high as 19% in Western Australia (4). Similar findings were derived from the Danish national patient registry: the lifetime risk of undergoing POP surgery for an 80- year-old woman was found to be 18.7% (5). With the increase in the ageing population across the world, the disease burden from pro­lapse is likely to grow much further.

The incidence of POP that required surgical correction following a hysterectomy is 3.6 per 1000 women-years in the United Kingdom (6). The cumulative risk rises to 5% at 15 years after a hysterectomy. The interaction between the pelvic floor muscles and the supportive ligaments was elaborated by DeLancey and Norton as the ‘boat in dry dock theory' (8). The boat is analogous to the pelvic organs, the ropes to the ligaments and fasciae, and the water to the supportive layer of the pelvic floor muscles. The connective tissue supports of the cervix and upper vagina maintain the position of the uterus/ cervix and upper vagina on the levator plate.

Three levels of support have been described by DeLancey (Box 56.1) (9).

Increases in intra-abdominal pressure compress the vagina against the levator plate rather than through the levator hiatus and prevent pelvic organ descent through the hiatus. Damage to the muscular and/or connective tissue supports of the uterus and vagina include tearing or stretching of the uterosacral and/or cardinal liga­ments and/or the levator ani muscle, or neuromuscular damage can occur at vaginal delivery.

During the second stage of labour, voluntary contractions of the abdominal wall and respiratory diaphragm muscles are initiated by

Table 56.1 Risk factors for prolapse

the mother to coincide with the peak uterine contraction to drive the fetal head through the levator hiatus. The fetal head stretches the pelvic floor muscles to a significant extent.

In a three-dimensional model on nerve stretch injury during childbirth constructed from cadaveric dissection, the inferior rectal nerve was shown to sustain the maximum strain, 15-35%, depending on the degree of perineal descent. The strain in the peri­neal nerve branch innervating the anal sphincter reached 33%, while the branches innervating the posterior labia and urethral sphincter reached values of 15% and 13%, respectively. The more proximal the nerve fixation point, the greater the nerve strain.

Thus, during the second stage, the nerves innervating the anal sphincter are stretched beyond the 15% strain threshold known to

Box 56.1 The three levels of support

Level 1 support: the upper part of the vagina adjacent to the cervix is sup­ported by Uterosacral and cardinal ligaments.

Level 2 support: this support includes pubocervical fascia anteriorly and the rectovaginal septum posteriorly and is a part of pelvic fascia. This sup­port connects vagina to the lateral pelvic wall through arcus tendinous fascia pelvis.

Level 3 support: anteriorly vagina fuses with the urethra, and is embedded in the connective tissue of the perineal membrane (urogenital dia­phragm).

Reproduced from DeLancey JO. The anatomy of the pelvic floor. Curr Opin Obstet Gynecol 1994;6(4):313-6 with permission from Wolters Kluwer. cause permanent nerve damage, and the degree of perineal descent is shown to influence pudendal nerve strain (12). Partial or complete denervation of pelvic floor musculature and sphincters following childbirth trauma may manifest many years later (following meno­pause) as pelvic organ descent and/or incontinence (13, 14).

Damage to the connective tissue and/or muscular supports re­sult in distortion of the relationship between uterus/vagina and the levator plate. An increase in intra-abdominal pressure might pos­ition the uterus and upper vagina over the levator hiatus and pre­dispose to downward displacement of pelvic organs (9). Damage to level 1 support may result in uterine descent, enterocele, or vault prolapse. Level 2 support damage results in cystocele and recto- cele. Damage to level 3 support results in widening of the hiatus and higher-stage POP.