|The Role of Retrograde Menstruation in Endometriosis|
The Role of Retrograde Menstruation in Endometriosis
Thomas B. Lebherz, M.D.
Endometriosis, Aspects and Proceedings of a Symposium
Patients with endometriosis almost always have patent tubes. Under certain circumstances, blood and endometrial fragments are able to pass out of the uterus by way of the tubes.
For example, Watkins operated on eight patients with retrodisplaced uteri during menstruation, and demonstrated that 10-60 cc of menstrual blood could be found in the posterior cul-de-sac in all of these women. In two instances, glandular endometrial fragments were also seen.
In discussing the problem of pelvic pain with endometriosis, Scott suggested that investigation of the cul-de-sacs of a large group of women with severe dysmenorrhea would probably disclose a large percentage with menstrual blood in the cul-de-sac. In fact, Prentice Wilson reported (at a meeting) that some 31% of women culdoscoped at the time of menstruation were found to have evidence of 5-30 cc of menstrual blood and glandular tissue in the cul-de-sac.
In a series of 450 culdoscopies we performed, ten of the cases were women somewhat late with their period, who were minimally suspect of ectopic pregnancy. We culdoscoped these latter patients and did a D&C following the culdoscopy; six of the ten were found to have menstrual blood in the cul-desac, and the D&C specimens revealed menstrual endometrium.
Endometriosis has been reported in a number of patients in whom natural outflow of menses is obstructed by cervical stenosis, vaginal atresia and similar lesions. Schiffin, Rez and Moore reported 15 cases of endometriosis in females under the age of 20. Six of these patients had congenital anomalies of the genital tract resulting in obstruction to outflow of menses. As a result, the menses went out the tubes and these six patients all had endometriosis. Clearly then, this does occur when menstrual flow is obstructed.
Grant and others have proposed that a less dramatic form of obstruction of menses will enhance tubal regurgitation-cervical stenosis, a diagnosis which many of us miss for a variety of reasons. It may also play a role in development of endometriosis in the adult, by leading to retrograde menstruation.
While the true incidence of retrograde menstruation is not known, there is certainly overwhelming evidence that it does occur. However, the mere occurrence of retrograde menstruation cannot be considered as proof of implantation theory. Sampson himself eloquently stated, "if mullerian cells carried by menstrual blood escaping into the peritoneal cavity are always dead, implantation theory as presented by me is also dead. It should be buried and forgotten." While from his perspective he was right, he was not totally correct.
Fortunately, however, other investigators have carried on with other studies. Dr. Greenblatt alluded to some of these. Heitel and Stein grew epithelium on stromal elements in tissue culture. Te Linde and Scott produced endometriosis in the Rhesus monkey.
Finally, Ridley and Edwards reported on a fascinating study with eight patients in whom the uteri were to be removed. Some endometrium was removed from those patients and injected into the area of the abdomen where they were going to make the scar for the hysterectomy three to four months later. When the hysterectomy was completed, an en-block excision of the area where the endometrial tissue had been injected was done. One patient had absolute evidence of endometriosis, which provides very strong evidence in humans to support the evidence we already have in animals. But much more recent evidence suggests a unified concept of the histogenesis of endometriosis that may well prevail.
J. Merrill has induced lesions resembling endometriosis by placing endometrium
in a millipore filter from which the cells cannot escape. He then placed
this in the peritoneum of rabbits, and demonstrated the development of
an endometroid-like lesion. Therefore, there is strong evidence that endometriosis
may be caused by something within the cell rather than by the proliferation
of endometrial cells. In short, endometrial cells, whether dead or alive,
can produce endometriosis. This work has been reproduced by Lavender and
Beck and Helwig have advanced the theory of "invitational metaplasia," which incorporates all of these findings, by suggesting that transplanted endometrial cells, no matter how they arrive, seem to stimulate metaplasia in tissue derived from celomic mesenchyme. This theory would, of course, be fully compatible with the behavior of endometriosis in virtually all of the forms that are known today. An additional benefit in advocating tuba) regurgitation as the main factor in pathogenesis is its implication for presenting a rational approach to treatment, of both therapeutic and of prophylactic value.
Therapeutic measurements would include suppression of ovulation or menstruation and conservative surgery. This theory would also allow for prophylactic treatment, with a concept predicated on the relief of obstruction of egress of menses. Therefore hymenotomy, dilatation of the cervix and correction of fixed uterine retroversions would appear to have a rational place in the prevention and treatment of endometriosis.
The keystone of prophylaxis, however, would be awareness that this problem may exist in young patients who have intestinal anomalies, because there is a very real chance of their also having a genital anomaly with obstruction to egress. In such cases, one should suspect these patients to be prime candidates for endometriosis, thus permitting further investigation by earlier conservative surgery in those patients in whom general anomalies are recognized and treated early in their infancy. Early recognition and treatment of menstrual obstruction producing retrograde menstruation may thus delay and obviate the development of endometriosis.
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