ENDOMETRIOSIS I—VULVA, VAGINA, CERVIX
Endometriosis is a benign but progressive condition characterized by endometrial glands and stroma found in locations other than the endometrium. It is estimated that between 5% and 15% of women, 20% of gynecologic laparotomies, 30% of chronic pain patients, and 30% to 50% of infertility patients have endometriosis. It is most common during the third and fourth decades of life, with 5% of cases diagnosed after menopause. The occurrence of the disease in the vagina ranks ninth in order of frequency behind the ovary, uterine ligaments, rectovaginal septum, pelvic peritoneum, umbilicus, laparotomy scars, hernial sacs, and appendix. Almost invariably, vaginal endometriosis is associated with similar lesions in the ovary and rectovaginal septum. The relative frequency of implants in these areas lends support to the theory of Sampson that the etiology of the disease is from retrograde menstruation through the fallopian tubes, because gravity would tend to spread the endometrial particles in this manner. However, it is also true that these structures are covered by tissue derived from primitive coelomic epithelium, which, in response to inﬂammatory or hormonal stimuli, might undergo metaplasia, as suggested by Robert Meyer. Instances of presumed iatrogenic spread (surgical) have been reported, whereas a role for an immuno- logic defect is debated but remains to be conclusively established.
The large sagittal section shows a small area of endometriosis on the surface of the ovary and other implants on the adjacent peritoneum of the posterior cul-de-sac and lateral pelvic wall. Typical blue-domed endometrial cysts extend down the rectovaginal septum, causing agglutination of the anterior rectal wall to the posterior surface of the uterus. The thickest concentration of endometrial cysts is usually about the attachments of the uterosacral ligaments to the cervix. The presence of endometrium in the septum and its response to the cyclic inﬂuence of the ovarian hormones produce a dense, ﬁbrous reaction, which is technically difﬁcult to manage during surgery. The aberrant endometrium rarely penetrates the anterior rectal wall to involve the mucous membrane but more often invades the posterior vaginal fornix. Its presence in the rectum may cause cyclic rectal bleeding or partial obstruction and, in the vagina, dyspareunia or postcoital bleeding. Similar lesions in the anterior vaginal wall may directly involve the bladder, causing cyclic hematuria. The vaginal epithelium around involved areas is puckered and densely adherent, making attempted surgical dissection, or even biopsy, hazardous because of the possibility of damage to the rectum or bladder. Conservative operations may grossly remove the disease from the ovaries and pelvic peritoneum, but complete surgical excision of posterior cul-de-sac, uterosacral, and vaginal lesions is technically impossible, even if a total hysterectomy is performed. If annoying bleeding, dyspareunia, dyschezia, or pelvic pain develop and cannot be controlled, treatment with gonadotropin-releasing hormone (GnRH) agonists, oral contraceptives, or progestins suppresses the menstrual hormonal changes, which often controls the disease.
Although the occurrence of endometriosis is understandable in areas where coelomic metaplasia or gravitational fall of regurgitated endometrial particles may be the exciting cause, its growth in areas far removed from the pelvis is harder to explain. Occasionally, the disease is found in the vulva or perineum. In the former case, it is assumed that migration is downward through the canal of Nuck, because this tube is lined by coelomic epithelium; but in the perineum, such an explanation does not hold. Perhaps, in this instance, the spread of endometrium has been by way of the pelvic lymphatics, as suggested by Halban.
A rare case shows involvement of the Bartholin gland. In the absence of external endometriosis else-where, local excision of this lesion is indicated, if only for purposes of accurate microscopic diagnosis.