ESHRE Logo ESHRE Guideline for the Diagnosis and Treatment of Endometriosis

Symptoms and clincal signs
(supporting documentation)


Establishing the diagnosis of endometriosis on the basis of symptoms alone can be difficult because the presentation is so variable and there is considerable overlap with other conditions such as irritable bowel syndrome and pelvic inflammatory disease. As a result there is often a delay of several years between symptom onset and a definitive diagnosis (Arruda et al., 2003; Hadfield et al., 1996; Husby et al., 2003).

The following symptoms can be caused by endometriosis based on clinical and patient experience:

  • severe dysmenorrhoea;
  • deep dyspareunia;
  • chronic pelvic pain;
  • ovulation pain;
  • cyclical or perimenstrual symptoms (e.g. bowel or bladder associated) with or without abnormal bleeding;
  • infertility;
  • chronic fatigue.

However, the predictive value of any one symptom or set of symptoms remains uncertain as each of these symptoms can have other causes.

A large group of women with endometriosis is completely asymptomatic. In these women endometriosis remains undiagnosed or is diagnosed at laparoscopy for another indication. A subset of women with more advanced disease, ovarian or deep invasive rectovaginal endometriosis, is asymptomatic as well. This makes the development of guidelines for the diagnosis and the therapy rather cumbersome. Endometriosis should be suspected in women with dysmenorrhea, deep dyspareunia, acyclic chronic pelvic pain and/or subfertility.


In adult women, dysmenorrhea may be especially suggestive of endometriosis if it begins after years of pain-free menses. The dysmenorrhea often starts before the onset of menstrual bleeding and continues throughout the menstrual period. In adolescents, the pain may be present without an interval of pain-free menses after menarche. The distribution of pain is variable but most often is bilateral. In addition, pain can evolve to become chronic. Depending on the type and localisation of endometriosis, pain can radiate to the upper leg (ovarian), to the perineum (rectum), or the back (uterosacral ligaments). However, deeply infiltrating subperitoneal endometriosis is associated with severe pelvic pain and dyspareunia (Chapron et al., 2003a; Koninckx et al., 1991; Porpora et al., 1999).
The types of pelvic pain are related to the anatomical location of deeply infiltrating endometriotic lesions (Fauconnier et al. 2002).
Possible mechanisms causing pain in patients with endometriosis include local peritoneal inflammation, deep infiltration with tissue damage, adhesion formation, fibrotic thickening, and collection of shed menstrual blood in endometriotic implants, resulting in painful traction with the physiological movement of tissues (Cornillie et al., 1990; Barlow and Glynn, 1993). In rectovaginal endometriotic nodules, a close histological relationship has been observed between nerves and endometriotic foci, and between nerves and the fibrotic component of the nodule (Anaf et al., 2000b).

Chronic disease

For many women, endometriosis becomes a chronic disease affecting quality of life due to incapacitating pain, emotional impact of subfertility, anger about disease recurrence, and uncertainty about the future regarding repeated surgeries or long term medical therapies and their side-effects. Therefore, there is a need to look at endometriosis, at least in a subset of highly symptomatic women, as a chronic disease. Quality of life issues should therefore be addressed (Colwell et al., 1998; Jones et al., 2001).


There is an association between the presence of endometriosis and subfertility. When endometriosis is moderate or severe (ASRM, 1997), it usually involves the ovaries and results in adnexal adhesions that by reducing tubo-ovarian motility impede pick-up function. In this situation, there is likely to be a causal relationship between endometriosis and subfertility. When endometriosis is minimal to mild, a causal relationship is controversial. An increased prevalence of endometriosis in subfertile women when compared to the prevalence in women of proven fertility has been shown (D'Hooghe et al., 2003a). A reduced monthly fecundity rate and cumulative pregnancy rate after donor as well as husband sperm insemination in women with minimal-mild endometriosis when compared to those with a normal pelvis has been shown (Hughes, 1997; Omland et al., 1998; Nuojua-Huttunen et al., 1999). An increased monthly fecundity rate and cumulative pregnancy rate after surgical removal of minimal to mild endometriosis has been shown in a multicentre randomized trial (Marcoux et al., 1997). A negative correlation between the RAFS stage of endometriosis and the cumulative pregnancy rate after surgery has also been found (Adamson et al., 1993; Guzick et al., 1997; Osuga et al., 2002).

Based on controlled prospective studies, there is no evidence that endometriosis is associated with (recurrent) pregnancy loss (Vercammen and D'Hooghe, 2000) or that medical or surgical treatment of endometriosis reduces the spontaneous miscarriage rate (Marcoux et al., 1997; Parazzini, 1999).

Other non-gynaecological symptoms

Rectal bleeding and haematuria during menstruation may occur in women with infiltrating rectosigmoidal and bladder endometriosis, respectively. Women of reproductive age with endometriosis may experience fatigue/exhaustion, abdominal bloating, diarrhoea/painful bowel movements with menstruation, pain during or after sex, heavy or irregular bleeding, nausea/stomach upsets with menstruation, dizziness/headaches with menstruation, low resistence to infection, and some allergies (Sinaii et al., 2002).

Clinical signs

Finding pelvic tenderness, a fixed retroverted uterus, tender utero-sacral ligaments or enlarged ovaries on examination is suggestive of endometriosis. The diagnosis is more certain if deeply infiltrating nodules are found on the utero-sacral ligaments or in the pouch of Douglas, and/or visible lesions are seen in the vagina or on the cervix. The findings may, however, be normal.

Deeply infiltrating nodules are most reliably detected when clinical examination is performed during menstruation (Koninckx et al., 1996).
Level 3






This guideline, which is reviewed annually, was last updated on 30 June 2007

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