Vaginal delivery and the pelvic floor: Outcomes of levator ani injury
Dr Hoyte is Professor, Fellowship and Division director, Female Pelvic Medicine and Reconstructive Surgery, University of South Florida Morsani College of Medicine, Tampa. He has no conflicts of interest to report with respect to the content of this article.
Dr Wyman is Clinical Fellow, Female Pelvic Medicine and Reconstructive Surgery, University of South Florida Morsani College of Medicine, Tampa. She has no conflicts of interest to report with respect to the content of this article.
Dr Hahn is Clinical Fellow, Female Pelvic Medicine and Reconstructive Surgery, University of South Florida Morsani College of Medicine, Tampa. She has no conflicts of interest to report with respect to the content of this article.
Levator ani injury occurs in 3 of 10 vaginal deliveries and often results in pelvic floor dysfunction including pelvic organ prolapse and incontinence. Understanding the mechanism of injury to the muscle of the levator ani is imperative to minimizing injury with delivery. It has long been recognized that the levator ani muscle group plays a key role in female pelvic floor function.1
When functioning normally, this muscle group has multiple roles, including support of the vagina and pelvic organs, and maintenance of urinary and fecal continence.2 The levator ani muscle complex is composed of 3 main muscle groups: the puborectal, the pubococcygeal, and the iliococcygeal portions with motor nerve input from the nerve to levator ani (S2,3,4), which courses over the ventral surface of the levator ani.3
The levator ani muscle complex encircles the largest potential hernia portal in the human body and compromise of this muscle complex is currently the best-defined pathogenesis for pelvic organ prolapse.1 Force vectors on the muscle during distention and passage of a fetal head result in excessive strain and stretch on the muscle, increasing the chance for injury.
During vaginal childbirth, the opening of the genital hiatus distends substantially to allow the passage of the fetus. This requires the distal-most portions of the levator ani (pubococcygeal and puborectalis) to stretch to greater than 3 times their original length, thereby putting strain on the muscles and their attachments to the pubic symphysis.4 Increased strain can result in damage or even complete disruption and detachment of the levator ani muscles from their insertion point on the pubic symphysis.
In addition, during the second stage of labor as the fetal head descends, excess stretch and distention of the iliococcygeus portion of the levator ani results in stretch and distention of the nerve to the levator ani. Prolonged stretching of this motor nerve has the potential to permanently damage the nerve, thereby disrupting the motor signaling to this normally tonic muscle, possibly leading to laxity or sagging of one or both sides of the Iliococcygeus muscle.5
The 2 childbirth-related mechanisms described above have the potential to cause significant injury to the levator ani muscle attachments and nerve supply increasing the risk of urinary and fecal incontinence and future development of pelvic organ prolapse (POP).6-8