Endometriosis is extremely common among women of childbearing age. It tends to occur after the teen years and worsens during a woman’s life as more endometrial tissue builds up outside of the uterus, causing increased pelvic inflammation and increased fibrosis, which can lead to infertility. The topic of this chapter is endometriosis, including the signs and symptoms, etiology, and treatment.
Incidence and Prevalence
Endometriosis is extremely common, occurring in 7-10 percent of women of childbearing age. About four out of every one thousand females are hospitalized for various complications of this disorder every year. Because some women are asymptomatic, the true prevalence of endometriosis is unknown. The best prevalence studies come from surgical populations of women, while the best incidence studies come from women undergoing tubal ligation procedures in which endometriosis is found.
While any woman can get endometriosis, there are several risk factors for getting the disorder. Women with a first-degree relative who has endometriosis are at a greater chance of having the disease as well. Early age at menarche, short menstrual cycles, longer days of menstrual flow, nulliparity, delayed childbearing, heavy menstrual bleeding, and congenital defects in the uterus or fallopian tubes can increase the risk of developing endometriosis.
Signs and Symptoms
Only about two-thirds of women, with the disease, will have symptoms of endometriosis. The rest will have evidence of disease on laparoscopy but will have no symptoms. Common symptoms relate directly to where the endometrial tissue has landed in the pelvis. There can be dyspareunia, pelvic pain, or low back/low abdominal pain. There can be irregular, heavy menstrual bleeding with periods that are painful. Pain on defecation (dyschezia) can occur if the endometriomas are in the rectum or anal area. There can also be an inguinal pain, pain on urination, increased urinary frequency, and pain during exercise.
Common findings in the history of patients with endometriosis include being nulliparous and having short menstrual cycles with bleeding that lasts at least eight days per cycle. There is dysmenorrhea that starts before the bleeding and gets better by day three of the menstrual cycle. Pregnancy and menopause will decrease the symptoms and can cure the disease. Using HRT after menopause will bring the disease back. Providers should ask about family history as this is likely to be positive as having a first-degree relative with the disease increases the risk of endometriosis by ten-fold.
The exam can show a pelvic mass of a large endometrioma. Nonspecific abdominal or pelvic tenderness is the most common presenting finding. The classical symptoms noted above are found in most women but certainly not in all women. Some women present with acute abdominal pain when an endometrioma ruptures, leading to bleeding in the abdomen.
The exact etiology of endometriosis isn’t clear. The leading theories include the possibility that the epithelium in various pelvic structures undergo a metaplastic change so that the tissue becomes an endometrioma. There may also be a lymphatic or hematogenous spread of endometrial cells or the passage of cells through the fallopian tubes in what is called “retrograde menstruation.” In this situation, endometrial cells that are still viable will flow in a retrograde fashion through the fallopian tubes during menstruation, seeding certain areas of the pelvis. There are stem cell-like cells in the endometrium that may attach to pelvic structures. There are special properties of these cells that allow these cells to survive outside of the uterus.
The ectopic endometrial cell clusters are most commonly seen in the lower portions of the pelvis, such as the posterior cul-de-sac, the anterior cul-de-sac, the ovaries (the most common site), the fallopian tubes, and the uterosacral ligament; however, any organ system has the potential to have ectopic endometriomas on them (including the bladder and the rectum).
The ectopic areas respond to cyclic hormonal fluctuations in much the same way as the regular endometrium of the uterus, with proliferation during the first half of the menstrual cycle, secretory epithelial cell development during the second half of the menstrual cycle, and the normal sloughing of blood and dead cells at the time of menstruation. This leads to an inflammatory response, complement deposition in the area, and both neovascularization and fibrosis in the affected area.
Laparoscopy is the best way to make the diagnosis of endometriosis with a sensitivity rate of 97 percent. The areas of involvement most likely to have endometriomas (in decreasing order) include the ovaries, the posterior cul-de-sac, the broad ligament, the uterosacral ligament, the rectosigmoid colon, the bladder, and the distal ureter.
Under the microscope, cells taken from endometriomas will look like endometrial stromal cells typical of those seen in a normal endometrial biopsy. For this reason, taking a sample for pathological diagnosis will help make a correct diagnosis of endometriosis.
Treatment and Management
Because endometriosis tissue depends on the cyclical nature of female hormones in a normal menstrual cycle, hormonal interference can manage this disorder without having to do surgery in many cases. The drugs most often used for this disorder include combining oral contraceptive pills, which shrink the endometriomas, Danazol (which has androgenic properties), progestin-containing drugs (which prevent proliferation), and gonadotropin releasing hormone (GnRH) analog medications.
Surgical care may be necessary if medical treatments fail and the patient is symptomatic. Conservative surgery to remove adhesions and endometriomas only when a woman still desires to be pregnant can be successful in reducing symptoms and restoring fertility. Semiconservative surgery involves removal of the endometriomas and the uterus with retention of the ovaries. Radical surgery involves removal of the uterus, ovaries, and any endometriomas found in the pelvic cavity.
In semi-conservative surgery for endometriosis, the treatment involves also taking endometrial tissue off the ovaries—sometimes removing healthy ovarian tissue along with it. It takes only a tenth of functional ovarian tissue to have normal hormone levels in the body. Unfortunately, this procedure results in a six-fold increase in recurrent disease compared to completely removing the ovaries in a radical procedure.
As for the prognosis of endometriosis, about a third of women will have spontaneous resolution of their disease state, even without treatment. In general, however, this is considered to be a progressive and worsening disease with more and bigger clusters of endometrial cells outside of the uterus. About 95 percent of women will respond to medical treatment that suppresses ovulation, and that will decrease pelvic pain.
The downside of medical therapy is that it often doesn’t restore fertility in those women desiring to get pregnant. This is partly because many treatments suppress ovulation and therefore decrease the chances of getting pregnant. These people need surgical intervention to remove endometriomas and to remove adhesions that might be getting in the way of normal ovulation and passage of the egg to the fallopian tube and uterus.
The two biggest complications of endometriosis include chronic pelvic pain and infertility. The chronic pelvic pain is associated with monthly bleeding as the ectopic endometrium sheds, and because there are inflammation and scarring associated with this process. Infertility is mainly structural and related to the ovaries being physically unable to release an egg that will be able to travel down the fallopian tube. There can be scarring of the ovaries and endometrial tissue blocking the tubes that make pregnancy nearly impossible unless medications or surgery can decrease the size of these benign tissue masses.