As is true throughout the body, both muscles and connective tissues work together and are essential for structural support. Normal pelvic organ support is provided by the interaction between the levator ani muscles (LAMs) and the connective tissues that attach the uterus and vagina to the pelvic sidewalls (cardinal and uterosacral ligaments).

There are three basic structural strategies involved in normal pelvic support (Fig. 3.1). First, connective tissues attach the uterus and vaginal walls to the inside of the pelvis and provide stability by absorbing load and limiting movement. Second, the pelvic floor muscles provide closure of the vaginal opening, which prevents prolapse from occurring. Vaginal closure within the high-pressure zone acts in the same way that, for example, the anal sphincters work. Stool does not fall out of the rectum because of the occlusive effect of the high-pressure anal canal. And third, as seen in a lateral view, these two individual biomechanical systems interact with and complement one another, thereby maintaining support even if an imbalance in one of these systems occurs.

The way in which these factors interact to provide pelvic organ support can be seen in Figure 3.2¹ and a glossary of selected biomechanical terms needed to understand pelvic organ support is provided in Table 3.1.

The LAMs hold the pelvic floor closed and provide closing forces to prevent pelvic floor descent by creating a high-pressure zone in the lower vagina.² In this situation, the closing forces in the anterior and posterior compartments are equal and opposing, creating balanced pressures (pressure is the measure of how much force is acting on an area). The LAMs maintain a balanced system—and therefore remain closed—in response to increased forces (e.g., rise in abdominal pressure during Valsalva), thereby preventing prolapse. The cardinal and uterosacral ligaments provide lifting forces that resist persistent downward descent of the pelvic organs by temporarily lengthening in response to increased force (due to their elastic properties) and absorbing any increases in force (due to their stiffness). This illustrates the principle of alignment within the biomechanical system of the pelvis, which depends on the muscles being strong enough to keep the hiatus closed and the connective tissues strong enough to resist deformation in order to hold the organs in place in response to increased load (e.g., during a cough).

When the muscles, nerves, and fascial structures involved in creating the vaginal high-pressure zone that holds the hiatus closed are damaged or weakened, the hiatus in the LAM complex can easily be pushed open. This is the principle of deformation under load. If the muscles, under the control of complex neural reflexes, fail to hold the hiatus closed, the vaginal walls descend so that one or both vaginal walls protrude below and through the levator hiatus. When the vaginal walls
descend below the hymen to the level where the levators no longer maintain proper alignment of the system, unbalanced pressures occur, creating a pressure differential between abdominal and atmospheric pressure. The force created by this pressure differential is like the one that moves a sailboat. The difference in pressure between two sides of a sail, for example, creates a force that propels the boat in a certain direction. In an anterior vaginal wall prolapse, abdominal pressure acts on the vaginal wall to create a downward force due to its misalignment. This force then places abnormal tension on the tissues that attach the uterus and vagina to the pelvic walls.

The size of the surface that is exposed to this pressure differential of exposed vagina matters. Pressure can
be expressed as force per unit area. That means that if there is 1 sq in of vagina exposed and the pressure differential is 1 lb/sq in, then there would be 1 lb of force on the ligaments and fascia resisting this downward force. The same 1 lb/sq in of pressure applied to 2 sq in results in 2 lb of force, etc. In more familiar units, 100 cm H₂O applied during Valsalva to 1 sq in results in 1.42 lb. Now, the larger the exposed area, the greater the force. As a cystocele enlarges, the force produced by the same pressure increases in a positive feedback loop. This explains why a woman can push hard with only a small descent of the anterior wall, but as the prolapse becomes a little more exposed, a greater change is seen.

The cardinal and uterosacral ligaments that attach the uterus and vagina to the pelvic walls are important to support of the pelvic organs by providing lifting forces. Their ability to maintain alignment in the pelvis is dictated by their material properties of stiffness, which is the ability to resist deformation (change in shape or length) in response to increased load, and elasticity, which is the ability to stretch (or lengthen) in response to increased force and then return to the original state when that force is removed. The cardinal and uterosacral ligaments have a normal range of lengthening, and in response, the pelvic organs have a normal range of movement. When you pull on the cervix as you would during a dilation and curettage (D&C), it lengthens the cardinal ligament somewhat like a spring. However, unlike an elastic spring, where doubling the force doubles the descent, the ligament gets stiffer the more it is elongated (Fig. 3.3). This is called a hyperelastic property. With increasing load, there is less and less elongation until an elastic limit is reached. At this point, additional load does not increase descent, as the cardinal ligament cannot stretch anymore. Any further descent would involve tearing in the short term or tissue changes in the long term.

Because the ligaments are elastic, this lengthening phenomenon is reversible and the pull on the cervix during D&C does not cause prolapse. However, Davis law states that connective tissue responds to chronic and excessive force with tissue adaptation. A skin expander is a good example of this, where it is possible to double the amount of skin present in 6 to 8 weeks by subjecting it to constant increased force. If the cardinal ligament is subjected to excessive downward force over time because the hiatus is not closed and the vaginal wall is subjected to a pressure differential, it can remodel to become longer.

The degree to which the vaginal wall moves downward in this situation has to do with the properties of the ligaments and fascial structures connecting it to the pelvic walls. Both the stiffness and length of the ligaments are involved. If the connective tissues are too lax or too long to hold the organs in alignment, the vaginal walls and uterus descend below the normal LAMs and the same imbalance in pressure can occur. Because these tissues are “stretchy,” some movement is normal, such as that seen during D&C, where the cervix can easily be drawn down to the introitus.

Another important concept concerns the principle of structural interactions. All the different anatomical elements in the pelvic floor interact with one another. The muscles that close the pelvic floor may be strong enough to support the organs under light loads. Under these conditions, increases in abdominal pressure may not cause any displacement. However, once the threshold that overcomes the ability of the muscles to resist the downward force is reached, the pelvic floor opens. This is a threshold effect.³ In some systems, if you double the load, you double the displacement. In other systems, a certain load must be reached before any change happens. The pelvic floor remains closed until enough force develops to open it. Once the hiatus is opened, the vaginal wall descends and is exposed to a pressure differential. With less than that opening force, it does not matter how much pressure there is—no opening occurs and no exposed vagina is subjected to the pressure differential. But once this threshold is exceeded, the pelvic floor opens, the structures become misaligned, and the pressure differential comes into play (Fig. 3.4). Failure of the hiatus to remain closed affects connective tissue loading.

Failure analysis is a foundational aspect of engineering. If a plane crashes or a bridge falls, the exact cause of the failure is rigorously sought and lessons learned. This type of failure analysis has now been applied to the pelvic floor to determine the causes of prolapse and, as a powerful tool, to understand why certain women have recurrence after surgery. The next section describes the evidence to support how these support systems fail. 3D stress magnetic resonance imaging (MRI) has facilitated this type of analysis, allowing the many competing hypotheses to be tested scientifically.

A brief overview of the regional differences or levels of support will help in our further consideration of how these principles affect normal and abnormal pelvic organ support (Fig. 3.5). We briefly describe the levels of
support and then provide more detail on how the attachment factors and the hiatal closure factors are each known to fail in prolapse.

In level 1, the cervix and upper third of the vagina are attached to the pelvic walls by mesenteric structures that suspend these organs (cardinal and uterosacral ligaments). In level 2, the middle third of the vagina is attached laterally to the arcus tendineus fascia pelvis (ATFP), which we refer to as the fascial arch for simplicity’s sake. This fascial arch can also be seen from the posterior compartment.⁴ It is important to remember that the cardinal and uterosacral “ligaments” have the structure of a mesentery, carrying neurovascular tissue to the organs. They do have a structural function of attachment but should never be confused with the dense regular connective tissue that comprises skeletal ligaments.

The perineal membrane (formerly known as the urogenital diaphragm) is a dense triangular membrane with a central opening through which the vagina and urethra pass.⁹,¹⁰ In its ventral aspect, the urethra, anterior vaginal wall, and perineal membrane are fused together as a single solid mass that is attached to the pubic bone laterally. This is quite different than the dorsal aspect, which is like a sheet of tissue. The LAMs attach to the cranial surface of the perineal membrane and to the perineal body, forming the perineal complex responsible for hiatal closure. Failures in the perineal membrane and perineal body are poorly understood at this time. Their structure clearly indicates their importance; yet, the exact role these structures play in maintaining hiatal closure is unclear.

Activity and integrity of the LAMs are primary factors in hiatal closure. This unusual muscle demonstrates constant tonic activity that is adjusted to offset changes in loading that occur during activities.¹¹ The LAM consists of three primary subdivisions: pubovisceral (i.e., pubococcygeal), iliococcygeal, and puborectal (Fig. 3.7). The pubovisceral muscle originates from the inner surface of the pubis and has three components: the pubovaginal, which attaches to the vagina; the puboperineal, which attaches in the perineal body; and the puboanal, which inserts between the internal and external anal sphincters.¹² We have chosen to use the term pubovisceral muscle rather than pubococcygeal because it more accurately describes the origin and insertion.¹³ The iliococcygeal muscle (ICM) is a thin sheet of muscle that spans the pelvic canal between its bilateral
origin at the arcus tendineus levator ani, we refer to as the “levator arch” for simplicity’s sake. The puborectal muscle originates on the inside of the pubic bones, near the perineal membrane, and courses laterally to the other parts of the LAMs. It forms a sling behind the rectum and is distinct from the pubovisceral muscle.

The action of pelvic floor muscles is determined by the muscle fiber direction, the muscle shape, and the points of attachment. Each muscle of the LAM complex provides action in a different vector, but they all activate at roughly the same time so that their combined actions result in one coordinated motion. If one component (muscle) of the LAM complex is lost, only that specific vector is affected. Understanding each muscle’s direction of action provides insight into how injury to a specific muscle contributes to overall failure of the system. This is particularly important given that the pubovisceral muscle is involved in obstetrical injury while others remain intact.¹⁴ Figure 3.8 shows the mean fiber directions for the pubovisceral and puborectal components¹⁵ measured in MRI images of normal women. The pubovisceral muscle fibers course 41° above the horizontal in the standing posture. By contrast, the puborectal muscles act 19° below the horizontal. Therefore, with loss of the pubovisceral muscle, both hiatal elevation and muscle constriction are affected, whereas if the puborectal were to be injured or weakened, only constriction would be affected.

There are several ways in which changes in the pelvic floor are discussed and measured. Figure 3.9 shows a conceptual model. The most familiar changes are those in the urogenital and levator hiatus that enlarge with childbirth and prolapse. In addition, the more dorsal component of the pelvic floor, in the region of the ICM, expands with age—even in the absence of childbirth.¹⁶ It is possible to see how these changes affect both the levator plate angle that is often discussed as well as the levator bowl volume—that is, the volume held within the shape of the pelvic floor.

There is strong evidence that hiatal failure is associated with prolapse.⁷ Hiatal enlargement precedes the occurrence of prolapse, indicating a causal relationship.⁸ During the first 20 years after giving birth, a quarter of women with an enlarged hiatus who were followed prospectively developed prolapse at least 1 cm below the hymenal ring.¹⁷ For a woman with
a 3-cm hiatus (distance from urethra to perineal body) on physical exam, the estimated median time to develop prolapse would be 33 years, whereas for a woman with a hiatus of 4.5 cm, it would be 6 years.¹⁷ Prolapse is also more common with reduced muscle strength (odds ratio, 0.87 per 5 cm H₂O). Prolapse was associated with levator avulsion (odds ratio, 4.2) and hiatus area and strength mediated 61% of the association is between avulsion and prolapse. This proves the first hypothesis in our model (see Fig. 3.2) indicating the essential role of hiatal closure in the development of prolapse.

Muscle tearing, often referred to as avulsion, occurs during at least 15% of vaginal deliveries¹⁸ and is strongly associated with prolapse. In women with prolapse, 55% have levator tears, whereas these injuries are seen in only 16% of women of similar age and parity who do not have prolapse, an odds ratio of greater than 7.¹⁹ The women with prolapse generated 37% less vaginal closure force during pelvic muscle contraction than controls (2.0 vs. 3.2 N), whereas those with major levator defects generated 35% less force than women without defects. In addition, the genital hiatus was 50% longer in cases than controls. Similar findings of muscle weakness with injury have been seen using a pressure-based device to compare women with and without prolapse, where pelvic floor muscle strength was associated with prolapse (odds ratio, 7.5) and endurance (odds ratio, 11.5).²⁰