Several theories have been proposed to explain the histogenesis of endometriosis. The implantation theory proposes that endometrial tissue desquamated during menstruation passes through the fallopian tubes, where it gains access to and implants on pelvic structures. The incidence of retrograde menstruation is similar in women with and without endometriosis. Thus, the development of endometriosis could depend on the quantity of endometrial tissue reaching the peritoneal cavity, specific factors enhancing attachment of endometrial cells to the peritoneum and ovary, or the capacity of a woman’s innate immune system to remove the refluxed menstrual debris.

The direct transplantation theory is the probable explanation for endometriosis that develops in episiotomy, cesarean section, and other scars following surgery. Endometriosis in locations outside the pelvis likely develops from dissemination of endometrial cells or tissue through lymphatic channels or blood vessels. The coelomic metaplasia theory proposes that the coelomic (peritoneal) cavity contains undifferentiated cells or cells capable of dedifferentiating into endometrial tissue. This theory is based on embryologic studies demonstrating that all pelvic organs, including the endometrium, are derived from the cells lining the coelomic cavity. The induction theory, an extension of the coelomic metaplasia theory, postulates that the refluxed endometrial debris releases a product that activates undifferentiated peritoneal cells to undergo metaplasia. There is no conclusive proof that the peritoneum can undergo spontaneous or induced metaplasia.

Anatomic alternations of the pelvis that increase tubal reflux of menstrual endometrium increase a woman’s chance of developing endometriosis. The incidence of endometriosis is increased in young women with genital tract obstructions that prevent expulsion of menses into the vagina and increase the likelihood of tubal reflux. Studies have suggested that deficient cellular immunity results in an inability to recognize the presence of endometrial tissue in abnormal locations. Decreased natural killer cell activity resulting in decreased cytotoxicity to autologous endometrium has been reported in women with endometriosis. The presence of increased concentrations of leukocytes and their cytokine products in peritoneal fluid of women with endometriosis may play a role in the initiation and growth of the ectopic implants. The immune system clearly has an important, albeit unclear, role in the pathogenesis of endometriosis. Other studies indicate that there are abnormalities of the eutopic endometrium in patients with endometriosis, including aberrant production of cytokines and growth factors. These characteristics may contribute to the establishment and maintenance of this disease.

The possibility of a familial tendency for endometriosis has been recognized for several decades. If a patient has endometriosis, a first-degree female relative has a 7% likelihood of being affected similarly. Studies are ongoing to determine the major susceptibility gene(s) involved.

The true prevalence of endometriosis in the general population is unknown. Estimates of its prevalence are based on visualization of the pelvic organs. Pelvic endometriosis
is present in approximately 1% of women undergoing major surgery for all gynecologic indications, 6% to 43% of women undergoing sterilization, 12% to 32% when laparoscopy is performed to determine the cause of pelvic pain in reproductive-age women, and 21% to 48% of women undergoing laparoscopy for infertility. Endometriosis is found in 50% of teenagers undergoing laparoscopy for evaluation of chronic pelvic pain or dysmenorrhea.

The influence of age, socioeconomic status, and race on the prevalence of endometriosis remains controversial. The age at time of diagnosis is commonly 25 to 35 years, and endometriosis rarely is diagnosed in postmenopausal women. Many believe that endometriosis is more common in women of upper economic classes because they delay pregnancy, which is postulated to increase the risk of developing endometriosis. It is unknown whether this reflects a true increased incidence or results from greater access to medical care. Evidence indicates that blacks have a prevalence of endometriosis similar to that in whites when controlled for socioeconomic status.

The most common sites of endometriosis, in decreasing order of frequency, are the ovaries, anterior and posterior cul-de-sac, posterior broad ligaments, uterosacral ligaments, uterus, fallopian tubes, sigmoid colon, appendix, and round ligaments. Other sites less commonly involved include the vagina, cervix, and rectovaginal septum. These latter lesions usually result from extension and invasion of posterior cul-de-sac implants. Uncommon locations include the inguinal canal, abdominal or perineal scars, ureters, urinary bladder, umbilicus, kidney, lung, liver, diaphragm, vertebrae, and extremities.

The common signs and symptoms of endometriosis are pelvic pain, dysmenorrhea, dyspareunia, abnormal uterine
bleeding, and infertility. The type and severity of symptoms are dependent on the extent of disease, the location, and the organs involved. Even limited amounts of disease may cause significant symptomatology.

Endometriosis is present in approximately one third of patients with chronic pelvic pain. The pain may be described as crampy, dull, or sharp and usually increases around menses. The discomfort may be unilateral or bilateral, and many patients complain of rectal pressure or low backache. Acute abdominal pain may result from hemorrhage secondary to a ruptured endometrioma.

Dysmenorrhea is a more frequent complaint than dyspareunia. There is some correlation between the extent of disease and the severity of pain. The morphologic appearance of an endometriotic implant appears to be unrelated to pain symptomatology. Dyspareunia is more common in women with invasive endometriotic nodules in the cul-de-sac, uterosacral ligaments, rectovaginal septum, and vagina.

Abnormal uterine bleeding occurs in up to one third of women with endometriosis with symptoms of oligomenorrhea, polymenorrhea, and midcycle or premenstrual spotting. The abnormal bleeding likely results from conditions associated with endometriosis: oligoanovulatory luteinized unruptured follicles, luteal phase defects, and other pathology such as uterine fibroids.

Endometriosis involving the gastrointestinal or urinary tracts and extrapelvic sites causes symptoms characteristic of the location of disease. Bladder involvement is associated with frequency and urgency. Invasion of the mucosa results in hematuria. Ureteral and rare cases of renal endometriosis occasionally cause flank pain or gross hematuria. Symptoms suggestive of gastrointestinal involvement include, in decreasing order of frequency, diarrhea, rectal bleeding, constipation, and dyschezia. All symptoms usually are exacerbated catamenially.

There are numerous case reports of extrapelvic endometriosis. Pulmonary endometriosis causes catamenial hemoptysis and dyspnea. Cutaneous lesions are associated with catamenial bleeding, tenderness, and swelling.

It is estimated that 25% to 50% of infertile women have endometriosis and that 30% to 50% of women with endometriosis are infertile. Although the association of endometriosis and infertility is well recognized, the pathophysiologic mechanisms are poorly understood. Endometriomas and endometriosis with adhesions distort pelvic anatomy and impair tubal ovum pickup, which is an acceptable explanation for infertility. In less severe cases, there are several theories to explain the observed subfecundity (Table 41.1).

Research to explain the subfertility has focused on peritoneal fluid leukocytes and their cytokine products. Studies have suggested that constituents in the peritoneal fluid inhibit sperm function, fertilization, embryonic development, and implantation. The clinical significance of these findings has not been established.

Endometriosis usually is diagnosed during the third and fourth decades of life. It has not been found in prepubertal girls and rarely is diagnosed in postmenopausal women unless they are taking replacement hormones. Endometriosis should be suspected in any woman having the classic symptoms of pelvic pain, dysmenorrhea, dyspareunia, abnormal menstrual bleeding, and infertility. These symptoms are present in other gynecologic disorders. No one constellation of signs or symptoms is pathognomonic of endometriosis. Many women with endometriosis are completely asymptomatic, and endometriosis should be considered in all reproductive-age women with infertility or an adnexal mass.

Physical findings in women with endometriosis are variable and dependent on the location and severity of disease (Table 41.2

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