Clinical Review

Pelvic-support defects: a guide to anatomy and physiology

OBG Manag. 2002 November;14(11):71-81

References

1. Baden WF, Walker T. Surgical Repair of Vaginal Defects. Philadelphia: Lippincott; 1992.

2. Richardson AC, Lyons JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol. 1976;126:568-573.

3. Julian TM. The efficacy of Marlex mesh in the repair of severe, recurrent vaginal prolapse of the anterior midvaginal wall. Am J Obstet Gynecol. 1996;175(6):1472-1475.

4. Julian T. Physical examination and pretreatment testing of incontinent women. Clin Obstet Gynecol. 1998;41(3):663-671.

5. Julian T. Pelvic support defects. In: Precis: An Update in Obstetrics and Gynecology. 2nd ed. Washington, DC: American College of Obstetricians and Gynecologists; 2001:42-54.

6. Berglas B, Rubin IC. Histologic study of pelvic connective tissue. Surg Gynecol Obstet. 1953;97:222-232.

7. Uhlenhuth E, Nolley GW. Vaginal fascia, a myth? Obstet Gynecol. 1957;10:349-358.

8. Ricci JV, Thom CH. The myth of a surgically useful fascia in vaginal plastic reconstruction. Q Rev Surg. 1954;(Dec):253-260.

9. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol. 1992;166:1717-1728.

10. Porges RF, Porges JC, Blinick G. Mechanism of uterine support. Obstet Gynecol. 1960;15:711-726.

11. Allen RE, Hosker GL, Smith ARB, Warrell DW. Pelvic floor damage and childbirth: a neurophysiologic study. Br J Obstet Gynaecol. 1990;97:770-779.

12. Smith ARB, Hosker GL, Warrell DW. The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine: a neurophysiologic study. Br J Obstet Gynaecol. 1989;96:24-28.

13. Snooks SJ, Badenoch DF, Tiptaft RC, Swash M. Perineal nerve damage in genuine stress urinary incontinence: an electrophysiologic study. Br J Urol. 1985;57:422-426.

14. Koelbl H, Strassegger H, Riss P, Gruber H. Perineal nerve damage in genuine stress urinary incontinence: an electrophysiologic study. Obstet Gynecol. 1989;74:789-795.

15. Makinen J. Collagen synthesis in the vaginal connective tissue of patients with and without uterine prolapse. Eur J Obstet Gynecol Repro Biol. 1987;24:319-325.

16. Norton P, Boyd CD, Deak S. Collagen synthesis in women with genital prolapse or stress urinary incontinence. Neurourol Urodyn. 1992;11:300-311.

17. Theofrastus JP, Addison WA, Timmons MC. Voiding function following prolapse surgery. Impact of estrogen replacement. J Reprod Med. 1996;41:881-884.

18. Schellart RP, Schouten WR, Huikeshoven FJ. Anorectal manometry before, during and after estrogen replacement therapy. Int Urogynecol J Pelvic Floor Dysfunct. 1996;7:77-80.

19. Mikkelsen AL, Felding C, Clausen HV. Clinical effects of preoperative oestradiol treatment before vaginal repair operation. A double-blind, randomized trial. Gynecol Obstet Invest. 1995;40:125-128.

20. Bump RC, Copeland WE Jr, Hurt WG, Fantl JA. Dynamic urethral pressure/profileometry pressure transmission ratio determination in stress-incontinent and stress-continent subjects. Am J Obstet Gynecol. 1988;159:749-755.

21. DeLancey JO. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol. 1994;170:1713-1720.

22. Bradley WE, Rockswold GL, Timm GW, Scott FB. Neurology of micturation. J Urol. 1976;115:481-486.

23. American College of Obstetricians and Gynecologists. Urinary and fecal incontinence. In: Precis: An Update in Obstetrics and Gynecology. 2nd ed. Washington, DC: ACOG; 2001;54-73.

24. Gilpin S, Gosling J, Smith ARO, Warrell D. The pathogenesis of genitourinary prolapse and stress incontinence of urine. A histological and histochemical study. Br J Obstet Gynaecol. 1989;96:15-23.

25. Snooks SJ, Swash M, Mathers SE, Henry MM. Effect of vaginal delivery on the pelvic floor: a 5-year follow up. Br J Surg. 1990;77:1358-1360.

26. Richardson AC. The anatomic defects in rectocele and enterocele. J Pelvic Surg. 1995;1:214-221.

The connective-tissue attachment of the urethra to the pubic bone and laterally to the levator muscle supports the distal vagina (DeLancey Level III). The midvagina is supported by the connective-tissue sheath that surrounds it and its lateral connective-tissue attachments to the levator muscle (DeLancey Level II). The vaginal apex and cervix (DeLancey Level I) are held by the surrounding endopelvic connective tissue—mainly the thickened lateral and posterior portions referred to as the cardinal and uterosacral ligaments (FIGURE 3).⁹

FIGURE 1 The pelvic musculature

These are transabdominal (A) and lateral (B) views of the pelvic floor demonstrating the pelvic musculature.

Reprinted with permission from American College of Obstetricians and Gynecologists. Precis: Gynecology, Second Edition. Washington, DC, ©ACOG, 2001.

FIGURE 2 Pelvic connective-tissue network

The heavy black lines in these lateral (A) and coronal (B) views represent the pelvic connective-tissue network known as endopelvic fascia. It demonstrates the continuity of the pelvic connective tissue as it surrounds the pelvic organs and ultimately attaches to the pelvic sidewall.

Reprinted with permission from American College of Obstetricians and Gynecologists. Precis: Gynecology, Second Edition. Washington, DC, ©ACOG, 2001.

FIGURE 3 Anatomic and physiologic support mechanisms

This demonstrates the levels of support described by DeLancey. Level I shows connective-tissue fibers extending both cephalad and dorsally toward the sacrum. Level II shows the lateral attachment to the arcus tendineus fascia of the pelvis. Level III shows the lateral attachment and anterior attachment of connective tissue to the lateral arcus tendineus fascia and posterior pubic symphysis.

Reprinted with permission from DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol. 1992;166:1717-1728.

Physiologic support mechanisms

In addition to the anatomic components of female pelvic-organ support, there are physiologic mechanisms that help maintain the positioning and functioning of pelvic organs. The muscles, vessels, and nerves of the pelvic floor function interactively as a compression mechanism in a manner similar to a valve, maintaining positioning of the viscera. The resting tone of the pelvic floor provides a valvelike closure surrounding the urethra, vagina, and rectum. This mechanism helps to close the genital hiatus, thereby preventing descent of the uterus, vagina, and adjacent structures.¹⁰

The pelvic axis. The connective-tissue supports of the vagina anchor it to the pelvic skeleton and hold the vagina in the previously described semihorizontal axis. When this axis is maintained, increased abdominal pressure pushes the vaginal tube into the hollow of the sacrum, maintaining an intra-abdominal position (FIGURE 4).^5,10

When the connective-tissue supports of the vagina and uterus are broken, the pelvic organs align in a more vertical axis. Increased intra-abdominal pressure causes the pelvic organs to descend through the natural openings in the pelvic floor (genital hiatus). The resulting descent of the uterus and vagina is what we refer to as pelvic organ prolapse. The genital hiatus also may be widened secondary to the trauma of childbirth.^5,9,10

FIGURE 4 Connective-tissue supports

This figure demonstrates how the uterus is held over the levator plate. In this position, increases in intra-abdominal pressure push the uterus caudally into the levator plate rather than through the genital hiatus.

Reprinted with permission from the American College of Obstetricians and Gynecologists (Obstetrics and Gynecology, 1960, Volume 15, pages 711-726)

Causes of pelvic-support defects

Childbirth. Damage to the levator muscle during childbirth has been associated with the beginning of pelvicorgan dysfunction, either as noticeable descent of the pelvic viscera, or bladder or bowel incontinence. Studies have shown damage to the muscle bundles of the levator and to nerves of the pelvic floor after childbirth, including atrophic and degenerative muscle changes and slowed nerve-conduction velocities.^10,11 While there is some evidence of muscle and nerve recovery, these postnatal findings of injury have been generalized to populations at increased risk for pelvic-organ prolapse and fecal and urinary incontinence,^12,13 especially multigravid patients and patients with disruption of the anal sphincter.

Age. Aging also has been shown to decrease the functioning of the pelvic-floor muscles. The microscopic findings here are similar to those after childbirth, demonstrating both a loss of muscle substance and degeneration of the nerve supply. In addition, there appears to be atrophy of the remaining musculature.¹⁴

Collagen in the pelvis. In addition to an age-related loss of the endopelvic fascia, there also may be inherited differences in the ratio of collagen types and in the quality of the collagen ground substance. This is best exemplified by nulliparous patients who demonstrate pelvic-organ prolapse or joint hypermobility and by patients with hereditary hyperelastosis syndromes.^15,16

Estrogen and pelvic-floor dysfunction. The theory that estrogen helps maintain the quality of connective tissue stems from the observation that urinary incontinence and pelvicorgan prolapse seem to begin around the time of menopause. While estrogen may indeed play a role, no prospective study has shown that estrogen replacement has a significant effect on urinary or fecal incontinence.^17-19 Nor have any parallels been found in young women who have experienced surgical castration, chemotherapy, or premature ovarian failure.