On the biomechanics of vaginal birth and common sequelae

Abstract

Approximately 11% of U.S. women undergo surgery for pelvic floor dysfunction, including genital organ prolapse and urinary and fecal incontinence. The major risk factor for developing these conditions is giving vaginal birth. Vaginal birth is a remarkable event about which little is known from a biomechanical perspective. We first review the functional anatomy of the female pelvic floor, the normal loads acting on the pelvic floor in activities of daily living, and the functional capacity of the pelvic floor muscles. Computer models show that the stretch ratio in the pelvic floor muscles can reach an extraordinary 3.26 by the end of the second stage of labor. Magnetic resonance images provide evidence that show that the pelvic floor regions experiencing the most stretch are at the greatest risk for injury, especially in forceps deliveries. A conceptual model suggests how these injuries may lead to the most common form of pelvic organ prolapse, a cystocele.

Figures

Figure 1

(a) Schematic view of the levator ani muscles from below, after the vulvar structures and perineal membrane have been removed, that shows the arcus tendineus levator ani (ATLA); the external anal sphincter (EAS); the puboanal muscle (PAM); the perineal body (PB) uniting the two ends of the puboperineal muscle (PPM); the iliococcygeal muscle (ICM); and the puborectal muscle (PRM). Note that the urethra and vagina have been transected just above the hymenal ring. (b) The levator ani muscle seen from above, looking over the sacral promontory (SAC), showing the pubovaginal muscle (PVM), sometimes called the pubococcygeal muscle. The urethra, the vagina, and the rectum have been transected just above the pelvic floor. PAM denotes the puboanal muscle. (The internal obturator muscles have been removed to clarify levator muscle origins.) From Kearney R, Sawhney R, and DeLancey JO. Levator ani muscle anatomy evaluated by origin-insertion pairs. Obstet Gynecol. 2004;104:168–73. © DeLancey 2003

Figure 2

(a) The axial proton density magnetic resonance scan shows a normal pubovisceral muscle with the muscle outlined at the level of the mid-urethra. The scan shows the pubic sympysis (PS), urethra (U), vagina (V) and rectum ( R). (b) A similar image from a woman with complete loss of the pubovisceral muscle (expected location of pubovisceral muscle shown by outline). From DeLancey JO. The hidden epidemic of pelvic floor dysfunction: achievable goals for improved prevention and treatment. Am J Obstet Gynecol. 2005;192:1488–95. © DeLancey 2005

Figure 3

(a) Simulated effect of fetal head descent on the levator ani muscles in the second stage of labor. At top left, a left lateral view shows the fetal head (as a sphere) located posteriorly and inferiorly to the pubic symphysis (PS) in front of the sacrum (S). The sequence of five images at left shows the fetal head as it descends 1.1, 2.9, 4.7, 7.9, and 9.9 cm below the ischial spines while the head passes along the curve of Carus (indicated by the transparent, light blue, curved tube). The sequence of five images at right are front-left, three-quarter views corresponding to those shown at left. (b) The upper bar graph compares, by muscle, initial and final muscle lengths corresponding to 1.1 and 9.9 cm model fetal head descent, respectively. The lower bar graph shows the maximum corresponding stretch ratio found in each levator ani muscle band. Note that the value of the stretch ratio is not simply proportional to initial or final length. For both graphs, muscles are arranged left to right, in ventral to dorsal order of origin location. (c) The relationship between fetal head descent (abscissa, icons at top) and the resulting muscle stretch ratios (ordinate) in selected levator ani muscles. The labels at right identify the pubovisceral (PC), iliococcygeus (IC), and puborectalis (PR) muscle bands. The largest stretch is induced in the medial-most pubovisceral (PC2) muscle, the last muscle to be engaged by the fetal head. The shaded region denotes the values of stretch tolerated by nongravid appendicular striated muscle without injury. From Reference . © Biomechanics Research Lab, University of Michigan, Ann Arbor 2003.

Figure 4

(a) Normal anatomy in an axial mid-urethra proton density magnetic resonance image that shows the normal pubovisceral muscle(shown by the asterisks). (b) Woman who has lost a part of the left pubovisceral muscle (displayed on the right side of the image, according to standard medical imaging convention), with lateral displacement of the vagina into the area normally occupied by the muscle. The arrow points to the expected location of the missing muscle. (c) Axial, mid-urethral section through the arch of the pubic bone (see pubic symphysis (PS), top) and the model levator ani muscles corresponding to those from the patient shown in (b). Intact muscles are shown in dark gray. The location of simulated muscle atrophy is illustrated by the light gray shading of the left-hand pubovisceral muscle. This location is shown to correspond with the location of muscle atrophy demonstrated in (b). OI: obturator internus; PB: pubic bone; U: urethra; V: vagina; R: rectum. Modified from Reference .

Figure 5

Effect of term pregnancy on the tissue properties of the rat vaginal wall. (a) Uniaxial stress-strain and (b) reduced relaxation--function relationships for pregnant and nonpregnant animals. Data are aggregated for 5 mm-long by 3.5 mm-diameter proximal, middle, and distal vaginal ring specimens excised from ten E-15 Fisher 344 rats at 20 days pregnancy and 10 age-matched nonpregnant controls. Specimens were stretched at a constant 1 mm s−1 rate to double their length, and then they were held at that length for 15 min. The quasilinear theory-of-viscoelasticity and custom software were used to identify the material constants (for example, A, B, C, τ1, and τ2), based on a nonlinear optimization algorithm. Reproduced from Reference .

Figure 6

Finite element model results for a simulated single (120 N) push delivery for a 31-year-old mother and fetus at 40 weeks gestation. (a–c) An inferior three-quarter view of the pelvic floor viscohyperelastic soft tissue deformations at three stages during the second stage of labor: (a) Station +2, (b) a middle station, and (c) delivery of the fetal head. The levator ani muscle (red), fetal head (gray), and public bone (white) are shown. (d) The maximum predicted principal strain and (e) stress distributions in the pelvic floor soft tissues at time of delivery. The largest principal strain (d) reached 259% (3.59 stretch ratio). The blue region nearest the pubic bone indicates the local region of highest stress (e), corresponding to the location of muscle defects observed on magnetic resonance scans. Reproduced from Reference .

Figure 7

Diagram showing the loading of the anterior vaginal wall and its support system. (a) Loading of the anterior vaginal wall (red) with normal muscular support. (b) Loading of the pelvic floor with defective muscular support and the distal part of the vaginal wall exposed to a pressure differential caused by intra-abdominal pressure (light gray arrows) acting on its superior surface and atmospheric pressure on its inferior surface. IAP: intra-abdominal pressure; Fpvm: reduced tensile force generated by the impaired pubovisceral muscle between the projection of its origin on the pelvic side wall and insertion on the levator plate (orange) which now has been rotated posteriorly under the action of IAP to expose the distal vaginal wall; Tc and Tu: tensile support forces generated by the cardinal and uterosacral ligaments; D: the descent of the most dependent point of the vaginal wall from the end of the perineal membrane (PM), which is used as the measurement of prolapse size in the simulation. Note the descent of the vaginal apex as well as vaginal wall protrusion. Reproduced from Chen LC, Ashton-Miller JA, Hsu Y, DeLancey JOL. Obstet. Gynecol. 108:324–332, 2006, Figure 2.