ENDOMETRIOSIS

Endometriosis denotes presence of functioning endometrial tissue in an abnormal location, in other words, outside the uterus (Box 35.1). The locations and the approximate chance of the lesion affecting the organ or structure are shown in Figure 35.1.

Diagnosis Can only be diagnosed at laparoscopy and confirmed by biopsy Symptoms Frequently symptomless, the main reasons for investigation being menstrual irregularities, premenstrual ‘dysmenorrhoea’ pain, non-cyclical pelvic pain, dyspareunia and infertility Management Outcome

Aetiology

How the endometrium reaches the ectopic locations is not entirely understood. The explanation to account for most of the endometrial lesions is retrograde passage of endometrial tissue along the Fallopian tubes during menstruation. This is supported by the observation that endometriosis only occurs in primates that menstruate and that explains the majority of sites where it is found: on the ovaries, the uterosacral ligament, or in the cul-de-sac (pouch of Douglas). It is believed that retrograde menstruation occurs in most women, but the development of other than temporary endometrial nodules (blisters) only occurs in some women. To explain the rare deposits of endometriosis in distant sites, for example the umbilicus, the lung and eye, lymphatic or haematogenous spread has been suggested. Metaplasia of mesothelial coelomic cells into endometrial cells has also been suggested.

Once viable endometriotic tissue has reached and adhered to the ectopic location, it still has to be explained why it survives and grows, instead of being eliminated by macrophages. A current theory is that there may be a defect in cell-mediated immunity which permits the endometrial tissue to survive. In order to grow in these ectopic sites, the endometrial tissue has to respond to cyclical oestrogen and, to a lesser extent, progesterone. If a constant oestrogen milieu occurs, as in pregnancy, the lesions tend to be attacked by macrophages and become fibrotic.

Why endometriosis spontaneously regresses or fails to progress in half of the cases is also not fully understood.

Pathology

Whatever the location, the ectopic endometrium, surrounded by stroma, implants and forms a miniature cyst, which responds to the cyclic secretion of oestrogen and progesterone, just as the uterine endometrium does. During menstruation, bleeding occurs in the cyst, and the blood, endometrial tissue and tissue fluid are trapped. Over the next cycle, the tissue fluid and the blood plasma are absorbed, leaving dark, thickened blood. The cycle recurs each month and slowly the cyst enlarges, containing increased amounts of tarry, chocolate-coloured inspissated blood. The maximal size of the cyst depends on its location. Small cysts may remain small, or be attacked by macrophages and become small fibrotic lesions. Ovarian cysts (endometriomata) tend to be larger than other cysts, but do not usually become larger than a medium-sized orange. As the cyst grows, internal pressure may destroy the active endometrial lining, making the cyst non-functional.

Rupture or leakage of material from even small cysts is not uncommon. The released inspissated blood is very irritating, with the result that multiple adhesions surround the cysts. The ectopic endometrium and stromal cells also tend to infiltrate adjacent tissues, leading to more pelvic adhesions and fixation (Fig. 35.2