Pathophysiology of Pelvic Support Disorders

Pathophysiology of Pelvic Support Disorders

Danielle Patterson

Victoria L. Handa


Pelvic organ prolapse is a prevalent condition, especially among older women. Despite our efforts to understand the genesis of this condition, its origins and its pathophysiology are still not known. This chapter reviews current theories regarding the etiology of pelvic support disorders.


The connective tissue supports of the pelvic organs are collectively referred to as the “endopelvic fascia.” This fascia is a continuous, complex web of connective tissue that envelops and supports the bladder, vagina, and rectum.1 Pelvic fascia can be divided into two types. The parietal fascia, which covers the levator ani and other skeletal muscles, is composed of a dense layer of organized collagen, mostly types I and III. In contrast, the visceral fascia, which envelops the pelvic organs, is a loose, poorly organized connective tissue layer.2 On a histologic basis, this is a loose, areolar connective tissue layer composed of smooth muscle, collagen, and elastin fibers.2 Much of the collagen and smooth muscle in the visceral fascia is perivascular.3 The contrast between parietal and visceral fascia parallels the functions of these two layers: The parietal fascia provides support for the muscles of the pelvic floor and abdominal cavity, whereas the visceral fascia envelops the organs, providing autonomic innervation to these organs and allowing for dramatic changes in their volumes (e.g., bladder filling).

Within the endopelvic fascia, there are several surgically identifiable structures, such as the arcus tendineus fascia pelvis (ATFP) and the uterosacral and cardinal ligaments. However, these “ligaments” are not discrete structures but rather consist of blood and lymphatic vessels, nerves, adipose tissue, and loose areolar connective tissue. Absent from these ligaments is any dense connective tissue composed of type I collagen like that found in skeletal ligaments.4 Nevertheless, the uterosacral and cardinal ligaments (Fig. 41.1) are thought to provide important support to the uterus and upper vagina.5 They originate along the greater sciatic foramen and lateral sacrum and insert into the lateral aspect of the vaginal apex. On magnetic resonance imaging (MRI), the deep uterosacral ligament has a band-like appearance, whereas the cardinal ligament appears as a weblike structure following the branches of the internal iliac vessels.6,7 In the standing position, the cardinal ligament provides vertical support for the uterus and vaginal apex5,8 and pulls the vaginal apex and cervix toward the sacrum (Fig. 41.2), maintaining the position of these structures over the levator plate.8 If these ligaments are deficient or lax, the vaginal apex might be positioned above the levator hiatus, thereby increasing the risk of prolapse. As these organs descend into the levator hiatus, the support of the cardinal and uterosacral ligaments becomes insufficient and fails. Norton9 likened this to a boat in dock (Fig. 41.3). In this analogy, the uterosacral and cardinal ligaments hold the ship (uterus and vagina) in position, but they are not sufficient to support the ship if the water (levator ani) is withdrawn.

Laterally, the anterior vagina is attached to the pelvic sidewall at the ATFP or “white line.”5,10 This line is a condensation of the fascia of the obturator internus muscle. Posteriorly, there is a similar attachment of the vaginal wall to the arcus tendineus fascia rectovaginalis (ATFR), which is a condensation along the fascia of the levator ani muscle.11 The ATFR fuses with the ATFP at a point 4 cm above the posterior fourchette.11 Separations in the lateral attachment of the anterior vaginal wall have been observed in women with vaginal wall prolapse.5 However, a biomechanical model developed by Chen and colleagues12 suggests that apical support and levator ani muscle function are more important to the development of cystocele than is paravaginal support.

The composition and role of the rectovaginal (Denonvilliers) fascia and pubocervical fascia are debated.2,13 In the distal rectovaginal septum, there is a dense connective tissue layer.14 However, this is limited to the lower vagina, and there is no histologic evidence of a substantial fascial layer in the upper rectovaginal septum.14,15 Histologically, there is little evidence for
pubocervical “fascia.” Cadaveric studies of the anterior vaginal wall suggest that the visceral fascia in this location is composed of a thin areolar layer that separates the vaginal wall from the bladder.14,16 Surgical repair of cystocele and rectocele has long relied on repair of the “endopelvic fascia,” but the anatomic absence of a supportive, organized fascial layer in this location casts doubt on this concept of surgical repair. The “fascia” (or “adventitia”) used in vaginal repairs is more accurately described as “vaginal submucosa” or “vaginal muscularis,”11,14,15 in recognition that this layer is part of the vaginal wall. However, others have suggested that defects in these layers result in cystocele and rectocele. This theory is the argument
for the “defect-directed” approach to the correction of cystocele and rectocele.17,18 Objective defects cannot always be demonstrated, however.2,19 Debate continues regarding the role of endopelvic connective tissue in the genesis of pelvic organ support defects and the implications for surgical repair of these defects.

There is also a role for connective tissue quality in maintaining vaginal support. Animal models show that defects in connective tissue remodeling and homeostasis contribute to prolapse. Fibulin-5 and lysyl oxidases are needed for normal elastic fiber synthesis. Mice with a genetic deficiency in fibulin-5 develop spontaneous prolapse.20 Further work with these mice has shown that vaginal fibulin-5 during development is not only crucial for baseline pelvic organ support but is also important for protection and recovery from parturition and elastase-induced prolapse.21 Lysyl oxidase like 1 gene (LOXL-1) knockout mice typically develop prolapse only after a traumatic event such as parturition.22 This suggests the mechanism may be impaired recovery and repair. These murine models suggest that interventions to improve connective tissue repair, such as regenerative medicine or stem cell transplantation, may hold promise in effective repair after pregnancy and delivery.23,24

There is also increasing evidence for genetic variation in human women with prolapse. Variants in the expression collagen type III alpha 1 chain gene (COL3A1) and bone morphogenetic protein 1 gene (BMP1) have been associated with prolapse.25,26


Levator ani muscles are important structures with respect to pelvic organ function, and there is increasing evidence of their role in pelvic organ support.1 The levator ani muscle complex is composed of the iliococcygeus, pubococcygeus, and puborectalis muscles. The pubococcygeus, which has attachments to the vagina and anus, is sometimes called the pubovisceral muscle. The urethra, vagina, and rectum pass through the levator hiatus, the space between these paired muscles. These are unique skeletal muscles because they maintain tone in the absence of voluntary contraction.3 The tone of the levator muscles keeps the levator hiatus closed27 and likely prevents chronic tension on the parietal fascia. In addition to baseline tone, the normal response of the levator ani to Valsalva effort is increased tone, thereby closing the levator hiatus.27 Laxity of the levator ani leads to a widening of the genital hiatus, and this has been suggested to be a potential initiating event for pelvic organ prolapse. We know that women with prolapse have a wider genital hiatus on MRI and three-dimensional ultrasound imaging.28,29 Similarly, on physical examination, a wider genital hiatus is associated with the development of prolapse.29,30 However, although these associations have been consistently demonstrated, they might not be causal.