All defects should be repaired at the time of pelvic floor reconstructive surgery. Any tear or defect in the area of the perineal membrane or PB should be repaired concurrently with pelvic floor reconstruction. This point was emphasized in the final step outlined in Part 2 of my series: “Repair the rectocele and perform perineorrhaphy vaginally if necessary.”
Based upon my understanding of the functional pelvic support anatomy as well as clinical observation, I maintain my position that “the perineal membrane and perineal body are not very crucial for pelvic organ support.”
The perineal membrane is a single layer of fibromuscular tissue that spans the anterior triangle of the pelvic outlet. Laterally, it attaches to the ischiopubic ramus; medially, it fuses with the sidewalls of the vagina and perineal body. The anterior portion of the perineal membrane is fused with the muscles of the distal urethra. Rather than forming a supportive sheet as it does in the male, the perineal membrane in the female—because of the large opening of the vagina—provides only lateral attachment for the PB and some support for the lower urethra.
The PB is an ill-defined, bordered mass of dense connective tissue lying between the vagina and anus. Fused anteriorly to the posterior vaginal wall and attached laterally to the perineal membrane and bulbocavernosus and superficial transverse perineal muscles, a significant portion of what is clinically called the perineal body is actually the muscle of the external anal sphincter. The strong upward traction of the levator ani muscles is much more important in maintaining vaginal outlet support than are the bulbocavernosus and superficial transverse perineal muscle.
Contrary to Dr. Grody's assertion that the PB makes a substantial contribution to pelvic support, in actuality the support is minimal. Rather, restoration of the PB is important for sexual function and anal/fecal continence. I have examined several patients with no PB as the result of chronic unrepaired fourth-degree obstetric lacerations, yet none of them had prolapse. Similarly, women who have had a radical resection of the anus and rectum for cancer, including the entire removal of the PB, suffered no significant prolapse.
Because considerable descent (up to 1 inch) of the PB is possible during voluntary straining, the perineal membrane and PB cannot be the main supportive layer of the genital outlet. The fact that the PB can move backward 3-4 cm toward the sacrum when a weighted speculum is placed in the posterior vagina likewise indicates that the position of the PB is determined by the levator ani muscle rather than by any inherent importance of its own.
Advances in technology afford greater magnification, visualization, and accuracy—leading to a level of surgical precision heretofore impossible with the relatively “blind” vaginal approach. We must train young surgeons for these state-of-the-art advances.
Although I have the utmost respect for both Dr. Grody and Dr. Liu and I believe that everyone is entitled to his or her own opinion, Dr Liu's article is certainly not worthy of such admonishment.
Dr. Liu not only correctly addresses normal vaginal anatomy, clinical assessment, and one surgeon's approach to the anatomical correction of symptomatic prolapse, he does so in a concise, informative manner.
Dr. Grody's belief that the perineal membrane and PB are crucial for pelvic organ support is indeed just that: his belief. Using the PubMed search term “perineal body surgery,” I found no scientific literature written in the past 40 years that supports the concept that either the perineal membrane or the PB is crucial in the support of any organs of the pelvis. I have yet to read or find an article that suggests that the cure rates of sacrospinous ligament suspension; sacral colpopexy; paravaginal repair; uterosacral ligament suspension; enterocele repair; or Burch, sling, or any other prolapse corrective surgery—including colpocleisis or Lefort procedures—are improved by repairing the PB.
Furthermore, there is no scientific literature that supports the concept that poor perineal support increases the incidence of prolapse. If this were a fact, patients with traumatic or congenital cloaca would also suffer a greater incidence of vaginal prolapse. I have not seen or read of any scientific literature or text that can directly show a cause-and-effect relationship between a damaged PB and vaginal prolapse.
Dr. Grody is a purist in his pursuit of vaginal anatomic correction, but this fine trait does not constitute scientific proof for his allegation. He has the right to theorize that the anatomical correction is essential to improve long-term cure rates of prolapse surgery. But a theory is belief unsupported by substantial fact, and will thus remain just a theory.