Anterior compartment defect or cystocele is defined as anterior vaginal wall relaxation or prolapse with or without urethral hypermobility. It represents one of the most common types of genital organ prolapse. Cystoceles have been described by several different classification systems and were previously categorized based on the relative degree of bladder descent and anatomic defect. More recently, the International Continence Society (ICS) has accepted standardization of the terminology for prolapse of the lower urinary tract.1 To ensure consistency, examiners must note the conditions of the examination findings, such as rest, strain, or supine positioning. This chapter concentrates on repair of the high-grade cystocele that has prolapsed past the vaginal introitus—grade 3/4 in the Baden-Walker classification or stage 3/4 in the pelvic organ prolapse quantification (POPQ) terminology.

The natural history of a cystocele is a continuous progression from mild to severe prolapse, but the actual risk of progression is unknown. In some patients, the progression is rapid; in others, it can be insidious, taking many years. Most lesser degrees of prolapse (stages 1 and 2) are asymptomatic except when accompanied by urinary incontinence. Pelvic prolapse does not spontaneously regress, nor does it become symptomatic until the descent reaches the introitus.2 Cystoceles with an isolated central defect represent only 5% to 15% of all cystoceles, whereas a lateral paravaginal defect is present in 70% to 80% of patients. Stage 4 cystoceles usually manifest with both defects. Proposed risk factors for the development of a cystocele have included difficult or prolonged vaginal deliveries, elevated body mass index (BMI), parity, menopause, and previous vaginal surgery.

Cystocele may occur as an isolated defect. However, it is most commonly associated with prolapse of other genital organs, such as rectocele, enterocele, and uterine descensus. Michael and colleagues3 observed a simultaneous enterocele in 35%, rectocele in 63%, and uterine prolapse in 38% of patients with grade 4 cystoceles. Therefore, in cases of severe anterior compartment prolapse, all of the compartments must be corrected. Treatment must involve a thoughtful and thorough evaluation plus a strong knowledge of pelvic floor anatomy The goals of surgery must be to restore vaginal depth, vaginal axis, the levator hiatus, and bladder and bowel function, while also preserving sexual function.


In a well-supported woman in the standing position, the vagina forms an inverted “C” shape with two distinct vaginal angles. This can be demonstrated on a midsagittal pelvic magnetic resonance image in a patient with normal anatomy. The distal vaginal canal forms a 45-degree angle from the vertical plane, whereas the proximal vagina lies more horizontally over the posterior levator plate, forming an angle of 110 degrees. The upper vagina is held over the levator plate by the cardinal and uterosacral ligaments, and the angle is maintained by a strong levator plate and the anterior traction of the levator sling and prerectal fascia.

The bony pelvis is a scaffold from which the pelvic structures draw their support. The pelvis can be divided into posterior and anterior regions by a line traversing the ischial spines. The sacrospinous ligaments are true ligaments in that they span between bony structures, arising from the posterior aspect of the ischial spines and connecting with the anterolateral sacrum and coccyx, providing a broad support for the posterior pelvis. A linear fascial condensation arising from the obturator internus muscle, the arcus tendineus, extends from the ischial spine to the lower portion of the pubic symphysis. The arcus tendineus is also the insertion point for the semilunar-shaped levator muscles, and it provides the musculofascial support for a large portion of the anterior pelvis.

The pelvic diaphragm is the superior layer of striated muscle and fascia that provides the inferior support for the pelvic viscera. The levator ani muscle group, composed of the pubococcygeus and iliococcygeus, is a broad muscular structure that originates on each side from the arcus tendineus of the obturator fascia and the inner surface of the pubis anteriorly and sweeps medially to join its contralateral partner in the midline. The levator ani thereby forms a broad hammock upon which the bladder, proximal vagina, and intrapelvic rectum lie. The vagina, rectum, and urethra traverse the pubococcygeus through a funneled hiatus. Pubococcygeal muscle fibers entering this “U”-shaped levator hiatus form the external sphincter of the urethra. Medial fibers of the pubococcygeal portion of the levator, sometimes referred to as the puborectalis, travel posteriorly along the urethra, vagina, and rectum and fuse anterior to the rectum, forming part of the perineal support deep to the perineal body. Reflex and active contraction of the pubococcygeus elevates the urethra, vagina, and rectum, thereby helping to compress the lumens of these structures.

Like the pubococcygeus, the iliococcygeus arises from the tendinous arc, but it sweeps more posteriorly and unites with the contralateral iliococcygeus in the median raphe posterior to the rectum. The coccygeus extends from the ischial spine to the lateral aspect of the sacrum and coccyx, overlying the sacrospinous ligament. The coccygeus is a thin muscle that overlies the strong and fibrous sacrospinous ligament. These two structures are identically shaped, and when they are encountered during surgical procedures, they are approached as a single complex useful for fixation of the vaginal vault. It is important to realize that the pudendal neurovascular bundle runs in the lateral insertion of the sacrospinous ligament, near the ischial spine.

The pelvic diaphragm has investing connective tissue that is often referred to as “fascia”; it is, however, less organized and less distinct than traditional fascia (e.g., rectus abdominis fascia). This visceropelvic fascia consists of collagen, smooth muscle, and elastin. Microscopic studies suggest that it may be histologically indistinct from the deep vaginal wall and not a separate “fascia.”4 In our discussion of the musculofascial support, we will continue to refer to this tissue as “fascia” for the sake of accepted nomenclature. The pelvic fasciae have been given a confusing array of appellations by anatomists and surgeons interested in female pelvic organ prolapse. To add to the confusion, the strength of pelvic fasciae can differ significantly among individuals and races, and these differences may predispose some individuals to pelvic prolapse.5

The pelvic fascia consists of two leaves—the endopelvic fascia (abdominal side) and the perivesical fascia (vaginal side). The urethra, bladder, vagina, and uterus are all contained within these two layers of fascia. The two leaves fuse laterally to insert along the arcus tendineus. The pelvic fascia can be divided, distally to proximally, into four specialized areas; these areas play important roles in pelvic support and during surgical reconstruction of the female pelvis. They are not true ligaments; rather, they are condensations or a meshwork of connective tissue and smooth muscle that invests the visceral neurovascular pedicles.1,6 The so-called pubourethral ligaments attach to the lower portion of the pubis and insert on the proximal third of the urethra; they are analogous to the puboprostatic ligaments in the male.2 The urethropelvic ligaments provide support of the proximal urethra to the lateral pelvic sidewall.3 The vesicopelvic fascia is the region of the pelvic fascia that attaches and supports the bladder base to the arcus tendineus. Finally, the vesicopelvic ligaments are all of the structures that support the bladder to the lateral pelvic wall. Weakness in the vesicopelvic fascia results in cystocele formation.

Cystoceles are generally classified as being caused by a central defect or a lateral defect. A central defect manifests as a midline weakness. There is good lateral support, but central herniation of the bladder base into the vagina occurs through a separation or attenuation of the vesicopelvic fascia (with separation of the cardinal ligaments). A lateral defect occurs when there is weakness or disruption of the lateral (paravaginal) attachments of the vesicopelvic ligaments to the arcus tendineus fascia pelvis. High-grade cystoceles tend to involve a combination of lateral and central defects with urethral hypermobility.4 The cardinalsacrouterine ligament complex attaches to the bladder base and cervix (or vaginal vault, if reapproximated during the hysterectomy).


Pelvic organ prolapse is prevented by several mechanisms. The most important support is from the continuous contraction of the levator ani pelvic muscles. The activity of skeletal muscle is a combination of basic tone, reflex contraction or relaxation, and voluntary contraction or relaxation. The basic tone of the skeletal musculature is similar to that in other areas of the body. Muscles of the pelvic diaphragm contain type I (slow-twitch) fibers, which provide tonic support to pelvic structures, and type II (fast-twitch) fibers, for sudden increases in intra-abdominal pressure.7 The continuous contraction closes the urogenital hiatus and forms a shelf for the pelvic organs to rest upon. Patients with multiple deliveries exhibit widening and descent of the levator plate. The musculature becomes less important and the “fascial” structures become the more important elements of support as the organs cross the pelvic floor.

Innervation of the muscles is primarily derived from the ventral rami of the second, third, and fourth sacral nerve roots. These pelvic somatic efferent nerves travel on the pelvic surface of the levator ani in close association with the rectum and are separated from the pelvic autonomic plexus by the endopelvic fascia. They supply the levator ani and extend anteriorly to the striated urethral sphincter.8,9 Static support is provided by the investing connective tissue layers. Under normal conditions, the levator ani contract, and the ligaments and fasciae are under minimal stress. The fasciae stabilize the pelvic organs.

Because of the complexity of pelvic organ support, the cause of vaginal prolapse is likely to be multifactorial, including myopathic or neuropathic disorders, aging, atrophy, chronic increase in abdominal pressures, multiple deliveries, hysterectomy, and hormonal changes. Poor function of the levator ani muscles may result from direct myopathic injury or from an abnormality of innervation. Loss of tonic contraction causes the urogenital hiatus to widen, increasing the risk of organ prolapse. Pelvic relaxation decreases the angulation of the mid-vagina, so the upper vagina does not lie flat against the pelvic floor plate. Instead of an inverted “C” configuration, the vagina becomes vertically oriented and can more easily intussuscept on itself. The reason for neuropathy in a healthy woman is not clear. Childbirth has been suggested as the cause of pelvic denervation, but studies in this area have shown that uncomplicated childbirth creates only transient neurologic damage to the pelvic floor that is restored after two postpartum months.10 The pelvic floor neuropraxia related to vaginal delivery is associated with multiple births, prolonged labor, high birth weight, and traumatic deliveries. Other risk factors for neurologic damage are congenital abnormalities, aging, chronic constipation (abdominal straining), and perineal laxity.11,12 In a study of 50 women with prolapse, Sharf and associates performed electromyography of the levator ani and found evidence of denervation in half of the patients.10 Other studies have also confirmed evidence of neurologic damage to the urogenital muscles in pelvic prolapse.13,14

The connective tissue of the pelvic floor, the endopelvic fascia, can be described as a group of collagen fibers interlaced with elastin, smooth muscle cells, fibroblasts, and vascular structures. These structures may be weakened by pregnancy, parturition, lack of estrogen, aging, diet, chronic straining, and certain connective tissue disorders (e.g., Ehlers-Danlos syndrome, Marfan’s syndrome).15 However, intrinsic collagen abnormalities and other individual predisposing factors, such as genetics, differences in pelvic architecture, inherent quality of the pelvic musculature, and tissue response to injury, might explain why many patients with known risk factors do not develop prolapse and many patients without risk factors do.

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