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Endometriosis is a disease characterized by the presence of endometrial glands and stroma outside the uterine cavity. A chronic inflammatory reaction induces scar tissue and adhesion formation that may distort a woman’s pelvic anatomy and cause disabling pelvic pain and intractable infertility. Although the cause of this disease is unknown, the most likely explanation involves the implantation of viable endometrial cells from retrograde menstruation through the fallopian tubes. Endometriosis has been estimated to affect up to 15% of all women of reproductive age. Twenty percent of women with endometriosis will have intestinal involvement, and the majority of these cases involve the rectosigmoid region. Colon and rectal surgeons most commonly become involved in the management of patients with intestinal endometriosis as a combined procedure with a gynecologist treating the other pelvic implants, or in the management of an endometrioma masquerading as a neoplastic or inflammatory lesion.
Pain, the most common symptom of endometriosis, affects up to 80% of patients who are subsequently diagnosed with the disease. Dysmenorrhea is the most common gynecologic symptom. Intestinal symptoms of patients with deep infiltrating endometriosis are pelvic pain upon defecation (which can be cyclical), dyspareunia, and rectal bleeding. In women undergoing laparoscopy for pelvic pain, endometriosis is discovered in 30% to 50% of cases. Although the total lesion volume often equates to the degree of pain, some women with extensive endometriosis experience little or no pain. Symptoms appear to be related to the depth of penetration, the type of lesion, and its location. Implants involving the uterosacral ligaments and rectovaginal septum are most often implicated in patients with pelvic pain. This pain is typically most intense just prior to the onset of menstruation. It is often associated with back pain, dyschezia, and levator muscle spasm and is more severe with advanced stages of endometriosis. The presence of dyspareunia is often seen with fixation of the pelvic organs, especially in the cul-de-sac of Douglas, the uterosacral ligaments, and the rectovaginal septum.
The exact causal relationship between endometriosis and infertility is also unclear, but the correlation is well established. In women with known endometriosis, the infertility rate is 30% to 50%, and conversely, in infertile women, the incidence of endometriosis is 25% to 50%. Fecundity in normal couples ranges from 0.15 to 0.20 per month and decreases with age, whereas women with endometriosis tend to have a lower monthly fecundity of about 0.02 to 0.1. There is little disagreement that moderate to severe disease with mechanical distortion of the fallopian tubes, ovaries, and peritoneum can potentiate infertility. Pelvic endometriosis and the resulting inflammatory response can produce dense, fibrotic adhesions that may significantly interfere with both the oocyte release from the ovary and the ability of the fallopian tube to pick up and transmit the oocyte to the uterus. In moderate or severe endometriosis, the pregnancy rates after surgical removal of the endometrial implants are 50% and 40%, respectively, compared with only 7% when expectant management is practiced. Treatment of infertile patients with mild endometriosis is more problematic. Infertile women with mild endometriosis did not have any improvement in fertility with either medical or surgical therapy compared with expectant management. Other studies have demonstrated a lower pregnancy per cycle rate in patients with mild endometriosis compared with those who are free of the disease.
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