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Chronic pelvic pain is defined as constant or intermittent pain in the lower abdomen or pelvis of a woman of at least 6 months’ duration and not associated with pregnancy. The causes of chronic pelvic pain include: endometriosis and adenomyosis; ovarian cysts; scar tissue and adhesions; irritable bowel syndrome (IBS); interstitial cystitis; chronic pelvic infection; musculoskeletal and nerve entrapment. Chronic pelvic pain presents in primary care as frequently as migraine or low-back pain, and may significantly impact on a woman’s ability to function.

Endometriosis is the presence of endometrial-like tissue outside the uterus, which induces a chronic inflammatory reaction. It usually lies within the peritoneal cavity and predominantly in the pelvis, commonly on the uterosacral ligaments behind the uterus (Fig. 13.1). Rarely, it can also be found in distant sites such as the umbilicus, abdominal scars, perineal scars and even the pleural cavity and nasal mucosa. Like the true endometrium, it responds to cyclical hormonal changes and it bleeds at menstruation. Such bleeding may cause symptoms.

Adenomyosis occurs when there is endometrial tissue within the myometrium of the uterus. The uterus is enlarged and feels ‘boggy’. There is painful and heavy menstruation. Adenomyosis is difficult to diagnose clinically and is usually only apparent retrospectively, with histological examination of the uterus after hysterectomy. It is commonly considered to be a separate entity from endometriosis, occurring in a different population and having a different aetiology.


The reported incidence of endometriosis varies widely; for example among asymptomatic fertile women undergoing laparoscopic sterilization procedures, the incidence of endometriosis ranges from 4–43%. Endometriosis is more commonly identified in infertile women. Most cases of endometriosis are diagnosed in women aged 25–35 years, although the symptoms of endometriosis can present as early as the onset of puberty. As it is oestrogen dependent, it is rarely diagnosed postmenopausally, but recurrence has been associated with the use of hormone replacement therapy.


The precise aetiology of endometriosis remains unclear, with no single explanation reliably explaining all its features. Sampson’s ‘implantation’ theory (see History box) postulates that endometrial fragments flow in a retrograde manner along the fallopian tube during menstruation, ‘seeding’ themselves on the pelvic peritoneum. In support of this theory is the fact that it is sometimes possible to see blood flowing from the fimbrial end of the fallopian tube if a laparoscopy is carried out during menstruation – it is believed that retrograde menstruation occurs in 90% of menstruating women. Seeding is also observed onto scars such as after hysterectomy or caesarean section, or on perineal scars after delivery, and there is some animal research in which endometrial tissue has been surgically implanted directly onto the peritoneum. Other animal research, where retrograde menstruation has been surgically created, found that endometriosis developed in 50% of cases.


John Albertson Sampson (1873–1946), from Massachusetts, was a prolific writer, publishing 17 papers while still a resident. He proposed that endometriosis is a process produced by the retrograde escape of endometrial tissue, which leads to secondary reactions of inflammation, repair and scar formation.

This theory, however, cannot be the only mechanism of endometriosis formation, as endometriosis has been reported in women with congenitally obstructed fallopian tubes. Meyer’s ‘coelomic metaplasia’ theory (see History box) proposes that cells of the original coelomic membrane transform to endometrial cells by metaplasia, possibly as a result of hormonal stimulation or inflammatory irritation. This could explain the presence of endometriosis in nearly all the distant sites, although it is also possible that spread from the uterus to these distant sites occurs by venous or lymphatic microembolism.


Robert Meyer (1864–1947), a German-born gynaecologist and pathologist, proposed that endometriosis is the result of peritoneal metaplasia. It is acknowledged that retrograde menstruation may be a stimulus for the metaplasia.

In some instances, the presence of endometriosis may be explained by neoplasia. This is particularly so in the ovary, where a solitary ovarian endometrioma is sometimes included in the classification of ovarian neoplasia as the benign counterpart of endometrioid carcinoma.

The question remains as to why endometriosis becomes established in some, but not all, women and it is possible that there is some genetic or immunological predisposition to account for such wide variation. Endometriosis is significantly more common in first-degree relatives of women with the disease and twin studies also support a genetic basis.

Clinical presentation

In most instances, clinical presentation occurs because of pelvic disease. Endometriosis is the commonest cause of secondary dysmenorrhoea. There is usually a continuous, non-spasmodic pain, which is worse immediately before and throughout menstruation, and colicky dysmenorrhoea may also occur in association with heavy menstrual loss and the passage of clots. In addition, there may be dyspareunia, which may relate to endometriotic deposits in the pouch of Douglas or to ovarian endometriomas. Typically, this pain settles when the period ends, but some women also describe a continuous, lower abdominal pain that is not specifically related to their cycle or to sexual activity. The common presenting symptoms of endometriosis are outlined in Box 13.1.

Box 13.1

The common presenting symptoms of endometriosis

icon01.gif Severe dysmenorrhoea

icon01.gif Chronic pelvic pain

icon01.gif Deep dyspareunia

icon01.gif Ovulation pain

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