Endometriosis and adenomyosis

Chapter 35 Endometriosis and adenomyosis

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.

Box 35.1 Endometriosis

What is it?	Functioning endometrial tissue which is outside the uterus, most commonly found on the uterosacral ligament and ovary
Aetiology	Not understood, as retrograde menstruation (along the fallopian tubes) occurs in most women Why the endometrial lesions fail to be attacked by macrophages in some women is not understood
Prevalence	Probably occurs in 5–10% of women and can regress, remain unchanged or progress More common among women with more spontaneous menstrual cycles
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	Depends on the woman’s age, her desire for pregnancy, the severity of the symptoms and the extent of the lesions Hormonal – to prevent the cyclical ovarian production of oestrogen, and to a lesser extent progesterone Surgical – laser or diathermy ablation of the lesions, ovarian cystectomy, conservative surgery or hysterectomy with bilateral oophorectomy
Outcome	All treatments are beneficial in the short term Five years after either hormonal or surgical treatment has ceased endometriosis recurs in 20–40% of women Cystectomy is superior to drainage for endometriomata Surgery is superior to hormonal treatment for pain symptoms if bilateral oophorectomy is performed

Fig. 35.1 Common and uncommon sites of extra-uterine endometriosis. The figures given in parentheses indicate the approximate chance of the lesion affecting the organ or structure.

The incidence of endometriosis is difficult to determine, as in many instances it is only discovered at laparoscopy when the patient presents with infertility or abdominal pain. A probable estimate is that between 5 and 10% of women in their reproductive years have endometriosis. Endometriosis is found more commonly in women who have more spontaneous menstrual cycles, for example when menarche is early or childbearing delayed. The incidence is lower when women are taking oral contraception and have a history of smoking. There is emerging evidence of a genetic component to the development of endometriosis as the incidence is up to seven times greater in the relatives of affected women compared with those without a family history. It appears to be linked to chromosomes 7 and 10.

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

Only gold members can continue reading. Log In or Register to continue

Related

Stay updated, free articles. Join our Telegram channel

Tags: Llewellyn-Jones Fundamentals of Obstetrics and Gynaecology

Jun 15, 2016 | Posted by admin in OBSTETRICS | Comments Off

Full access? Get Clinical Tree

Get Clinical Tree app for offline access

Get Clinical Tree app for offline access