Endometriosis is an enigmatic disease affecting about 7% of reproductive-aged women -approximately 5 million Americans. Although they may suffer significant symptoms ranging from pelvic pain to infertility, most of these women do not know that they have endometriosis,. Physicians' understanding of (1) the clinical presentation of endometriosis, (2) its proper diagnosis and staging, and (3) the management of its sequele have improved dramatically over the past few years. The result has been better, more cost-effective patient care.

Endometriosis is the presence of endometrial tissue (normally found only on the inside of the uterus) in locations outside the uterus. This tissue reacts to estrogen and progesterone. The usual location is in the pelvis (on the ovaries, fallopian tubes, uterus, or bladder), but endometriosis has also been found in sites outside the pelvis (including omentum, small intestine, appendix, anterior abdominal wall, surgical scars, diaphragm, lung, urinary tract, and musculoskeletal and neural systems). This endometrial tissue reacts to hormonal changes during the menstrual cycle, just as endometrial tissue lining the inside of the uterus reacts during the normal ovulatory cycle.

Prevalence and Incidence
The prevalence and incidence of endometriosis depends on the population of women being studied, ranging from 1 to 50%. It has been reported to occur in 10 - 15% of women undergoing diagnostic laparoscopy, 2 - 5% of women undergoing tubal sterilization, 30 -40% of infertile women having laparoscopy, and 14 - 53% of women with pelvic pain.

There are several theories that attempt to explain how endometriosis develops. The most popular theory describes retrograde menstruation through the fallopian tubes, with subsequent implantation and growth of endometrial cells contained in the menstrual blood. Other theories involve metaplasia (normal tissue in the abdominal cavity spontaneously changing to endometriosis), direct implantation of endometrial cells into the abdomen during surgery, and spread of endometrial cells from the inside of the uterus to other locations via blood vessels or lymphatics. Each of these may contribute to endometriosis in different patients. Altered immunity may also play a role.

Numerous factors seem to affect whether a woman will have this condition, the severity of the disease in any particular woman, her symptoms, and her response to treatment. These include:

  • genetics (an affected sister or mother doubles the risk)
  • hormonal status (higher estrogen levels and prolonged heavy menses increases risk)
  • lifestyle (low body weight and cigarette smoking reduce risk by decreasing estrogen levels)
  • contraceptive use (oral contraceptives possibly reduces progression of disease)
  • obstetric history (pregnancy and lactation reduce risk)
  • anatomic factors (cervical stenosis increases risk)
  • treatment history (prior medical or surgical treatment reduces risk)
  • race (caucasions are at higher risk than african-americans)
  • and possibly exposure to environmental toxins, especially those which are estrogenic

Endometriosis is thought to cause infertility by distorting anatomy, creating hormonal abnormalities, altering the pelvic biochemical enviornment, influencing the immune system, interfering with sperm function, and (possibly) altering the process of embryo implantation.

Clinical Presentation
Endometriosis primarily presents with pelvic pain (about 80% of patients). About 20% of patients presenting with endometriosis are also infertile, and 5% present with a "tumor" of endometriosis in one or both ovaries (these are called endometriomas). Anywhere from 1 to 40% of patients with endometriosis will have no symptoms. Endometriosis may occur anytime after puberty, including adolescence.

The extent of a patient's pain often does not correlate with severity of her endometriosis. Pain may occur as a result any or all of the following:

  • endometrial implants secreting irritating factors (e.g., histamine)
  • scar tissue (adhesions)
  • leaking endometriomas
  • compression of other abdominal structures (e.g., bowel, ureter)
  • compression of endometriotic nodules deep in the pelvis
  • invasion of the urinary tract (bladder or ureters)
  • invasion of the gastrointestinal tract (small bowel or colon)

Even in patients with minimal and mild disease (AFS stage I or II), endometriosis is probably associated with infertility. A cause-effect relationship most certainly exists for moderate and severe disease (AFS stage III or IV). These patients usually have adhesions, deep invasive lesions, and endometriomas. Endometriosis may also be associated with structural abnormalies and damage to the fallopian tubes. Studies overall do not, however, support an association between endometriosis and increased spontaneous abortion rates.

Endometriosis lesions occur throughout the pelvis. They tend to be more frequently in the posterior cul-de-sac and the ovary, and less frequently on the fallopian tubes. Endometriosis is almost certainly a progressive disease, but the rate of progression and nature of lesions varies from patient to patient.

Adhesions develop as a result of the inflammatory process caused by long standing endometriosis, with more extensive and dense adhesions developing over time. The worst adhesions in the most advanced cases usually involve the uterus, ovaries, and lower colon (near the rectum). Laparoscopic surgical treatment of these cases is always preferable, but demands skill, extensive experience, and patience on the part of the operating surgeon.