A 3D finite element model of anterior vaginal wall support to evaluate mechanisms underlying cystocele formation

Abstract

Objectives: To develop a 3D computer model of the anterior vaginal wall and its supports, validate that model, and then use it to determine the combinations of muscle and connective tissue impairments that result in cystocele formation, as observed on dynamic magnetic resonance imaging (MRI).

Methods: A subject-specific 3D model of the anterior vaginal wall and its supports were developed based on MRI geometry from a healthy nulliparous woman. It included simplified representations of the anterior vaginal wall, levator muscle, cardinal and uterosacral ligaments, arcus tendineus fascia pelvis and levator ani, paravaginal attachments, and the posterior compartment. This model was then imported into ABAQUS and tissue properties were assigned from the literature. An iterative process was used to refine anatomical assumptions until convergence was obtained between model behavior under increases of abdominal pressure up to 168 cm H(2)O and deformations observed on dynamic MRI.

Results: Cystocele size was sensitive to abdominal pressure and impairment of connective tissue and muscle. Larger cystocele formed in the presence of impairments in muscular and apical connective tissue support compared to either support element alone. Apical impairment resulted in a larger cystocele than paravaginal impairment. Levator ani muscle impairment caused a larger urogenital hiatus size, longer length of the distal vagina exposed to a pressure differential, larger apical descent, and resulted in a larger cystocele size.

Conclusions: Development of a cystocele requires a levator muscle impairment, an increase in abdominal pressure, and apical and paravaginal support defects.

Figure 1

Model development. A: 3D volume-rendered model of anterior support system including pubic bone; B: 3D volume-rendered model without pubic bone; C: Geometrically simplified surface model; D: 3D finite element model with mesh, boundary condition (orange pin representing ligaments and muscle origin is fixed to pubic bone and pelvic sidewall), and abdominal pressure loading. PB denotes pubic bone; UT: uterus (not included in surface model); V: vagina; R: rectum; CL: cardinal ligament; US: uterosacral ligament; ATFP: arcus tendineus fascia pelvis; ICM: iliococcygeus muscle; PCM: pubococcygeus muscle; AVW: anterior vaginal wall; PC: posterior compartment; PS: paravaginal support; and IAP: abdominal pressure

Figure 2

The material properties of the vagina, ligaments and levator ani muscle used in the model simulation. Note the visceral “ligaments” in this context are mesenteric in nature thereby differing considerably from skeletal ligaments.

Figure 3

The left, three-quarter view of the model mid-sagittal configuration at maximum abdominal pressure showing the four outcome measurements: a, h, d, and length of exposed vaginal length.

Figure 4

Model validation. On the left is a model-generated simulation result showing a cystocele formed in the manner of that seen clinically in one frame of a dynamic MRI on right side of the figure.

Figure 5

Left, three-quarter, view of a mid-sagittal section of the 3D finite element model. Panel A: All support elements (levator ani muscle, cardinal uterosacral ligament, paravaginal support) have normal material properties. Panel B: The levator ani muscle was set to have a 60% reduction in its properties, and a 50% reduction in cardinal and uterosacral ligament and paravaginal support properties. LA denotes levator ani muscle, CL: cardinal ligament, AVW: arterial vaginal wall, PC: posterior compartment, and US: uterosacral ligament

Figure 6

(Left-to-right) a three-quarter, left, anterior view of the sequential development of a typical simulated cystocele during a gradually increasing load. In this simulation, the levator ani muscle had a 60% impairment, and apical and paravaginal support properties were set to having a 50% impairment. The color map shows the stress distributions in the different regions, with blue indicating a low stress region and red indicating a high stress region. The box on the up left coner shows the abdominal pressure (ordinate), increasing from zero to 100 cmH₂O, over a time course (abscissa) corresponding to the three scenarios above.

Figure 7

Relationship between cystocele size and intra-abdominal pressure in a simulated cystocele. In this simulation, the levator ani muscle had a 60% impairment, apical and paravaginal support were set to having a 50% impairment. The best fit line for non-zero cystocele size data points is plotted. The linear regression equation and coefficient of determination are shown in the illustration.

Figure 8

Simulated cystocele size for models with different impairment patterns at increasing values of maximum intra-abdominal pressure loading.

Figure 9

Effects of muscle impairment on cystocele formation. The outcome measurement was normalized to model outcome with intact levator ani muscle resistance to stretch.

Figure 10

Effects of apical and paravaginal impairments on cystocele formation. Simulations had 60% levator ani muscle impairments and were loaded with 168cmH₂O maximum intra-abdominal pressure. For apical impairment simulations, models had normal paravaginal support, but a varying degree of apical support impairment with remaining apical connective tissue stiffness ranging from 20% to 100% of the normal value. For paravaginal impairment simulations, models had normal apical support but varying degree of paravaginal support impairment with remaining paravaginal connective tissue stiffness ranging from 20% to 100% of normal values.

Figure 11

A conceptual model of the pathomechanics of cystocele. Inputs to the support system include the intensity (α) of the pubovisceral (“PV”) muscle contraction (yielding tension, T), intraabdominal pressure (p_a) and atmospheric pressure (p_o). ‘p_a’ acts on the surface of the levator ani muscle so as to increase T and help determine total hiatal area. It can also drive the uterus partially into the hiatus (dashed line), leaving the remaining hiatal aperture to be spanned by the distal anterior vaginal wall (AVW) and exposed to the pressure differential (Δp_AVW). The resulting tension (T_AVW) in the AVW then applies tension to its Apical and Paravaginal Supports helping to determine the size of the resulting cyctocele (d_AVW). Birth damage, aging, collagen/elastin disorders and hormonal effects are all postulated to affect the properties of given structures.