Endometriosis

Endometriosis is a common and clinically important problem in women of childbearing age. It is classically defined as the presence of functional endometrial glands and stroma outside the uterine cavity and musculature 1. This is distinct from adenomyosis, in which endometrial tissue is confined to the uterine musculature. It may vary from microscopic endometriotic implants to large cysts (endometriomas).

Typically endometriosis presents in young women, with a mean age of diagnosis 25-29 4, although it is not uncommon among adolescents. Up to 5% of cases are diagnosed in postmenopausal women. Potential risk factors include family history and short menstrual cycles. Racial predisposition remains controversial 5,7.

It is difficult to ascertain the overall prevalence of endometriosis, but in women who underwent laparoscopy for various reasons, the prevalence is as follows: 5 

  • asymptomatic women (laparoscopy for tubal ligation): 1-7%
  • primary infertility: 17-50%
  • pelvic pain: 5-21% 
Symptoms
  • infertility: 30-50% of women with endometriosis are infertile 15
  • pelvic pain: including dyspareunia, dysmenorrhea, chronic pelvic pain
    • pain is not always cyclic 12
  • unusual symptoms
    • gastrointestinal involvement: catamenial diarrhoea, rectal bleeding and constipation
    • vesical involvement: urgency, frequency, haematuria
    • thoracic involvement: pleuritic chest pain, pneumothorax, pleural effusions or cyclic haemoptysis
  • asymptomatic: especially if the disease is isolated to the peritoneum
Examination findings
  • non-specific and stage of disease does not necessarily correlate with the severity of the symptoms 16
  • tenderness along the adnexa and uterosacral ligaments, cul-de-sac +/- thickening or nodularity
  • rectovaginal or adnexal masses

The pathogenesis of endometriosis remains unclear and is subject to much debate; potential mechanisms include:

  • metastatic theory: transplantation of endometrial cells (via retrograde menstruation, lymphatic or vascular dissemination, iatrogenic implantation) with probable immune/hormonal/inflammatory mediators 8; supporting this theory is that up to 90% of women have bloody peritoneal fluid during the perimenstrual period 9
  • metaplastic theory: retroperitoneal deep endometriosis may originate from metaplasia of Mullerian remnants located in the rectovaginal septum 10
  • induction theory: whereby shed endometrium releases substances that induce undifferentiated mesenchyma to form endometriotic tissue 2

See the illustration of theories of endometriosis.

Macroscopic

Macroscopic appearances vary depending on the duration of disease and depth of penetration:

  • superficial
    • superficial endometriosis: Sampson syndrome
    • nodules or plaques of varying size from a few millimetres to 2 cm in diameter
    • the amount of pigment appears to increase with the age of the lesion; initially they appear as white plaques, non-pigmented clear vesicles or red petechiae or flame-like areas; as they age the colour changes to bluish/brownish lesions - these are referred to as “powder burns”, representing haemolysed blood encased in fibrotic tissue 11
    • additionally, appearance not only varies with age but also with the part of the menstrual cycle
  • deep: penetrating into the retroperitoneal space or the wall of the pelvic organs to a depth of at least 5 mm, and comprises nodules, cysts and secondary scarring 3
  • endometriotic cysts (a.k.a. endometriomas or "chocolate cysts")
    • most commonly occur in the ovaries and are the result of repeated cyclic haemorrhage within a deep implant
    • often there is complete replacement of ovarian tissue
    • cyst walls may become thick and fibrotic with dense adhesions, with lining that varies in contour (smooth to shaggy) and colour (pale-to-brown)
  • adhesions and fibrosis can distort normal pelvic anatomy and lead to the obliteration of the pouch of Douglas
Location 

The most common locations for endometriotic deposits are the ovaries; then in the pelvic peritoneum. Less common locations include C-section scars (scar endometriosis), deep subperitoneal tissues, gastrointestinal tract, bladder, chest and subcutaneous tissues. Pouch of Douglas, uterosacral ligament and torus uterinus are the most common pelvic sites of involvement 13.

Deep pelvic endometriosis is divided into:

  • anterior cul-de-sac
    • endometriosis of the bladder detrusor with associated adhesion and anteflexed uterus
    • vesicovaginal septal involvement typically more caudal
  • posterior cul-de-sac
    • retroperitoneal lesions and dependent intraperitoneal locations that may result in infiltrating lesions
    • adhesions between anterior rectal wall and posterior vaginal fornix
    • rectovaginal septal involvement
  • pelvic side wall
    • including ureteral lesions said to arise from extension of pelvic foci and ovarian endometriosis
  • gastrointestinal tract
    • implantation occurs between 12-37% of patients
    • rarely proximal to the terminal ileum 1
    • rectosigmoid > appendix > caecum > distal ileum
  • urinary tract
    • involvement is typically asymptomatic except with severe pelvic disease 20
    • bladder > distal ureter  

Extra-abdominal locations include:

  • chest
    • uncommon
    • almost exclusively right sided
    • usually in the setting of long-standing (>5 years) pelvic endometriosis
  • cutaneous/disease

Although laparoscopy continues to be the gold standard for the diagnosis of endometriosis, MRI is increasingly being used, especially to evaluate deep disease, with high sensitivity (90%) and specificity (91%) 20. Ultrasound is predominantly used to evaluate the ovaries and to asses the pelvis in the work up for pelvic pain or infertility. 

Ultrasound 

Ultrasound is poor at detecting peritoneal implants (~11%) 21, and although it is unable to detect adhesions, it is able to dynamically assess mobility and fixation.

Ultrasound is better at detecting endometriomas:

  • homogenous, focal lesions with low-level echoes, reminiscent of the testicle
  • they are typically unilocular, but may be multilocular, containing thin or thick septations
  • may be multiple
  • may contain mural nodules (a finding also found in ovarian neoplasms)
    • if these mural nodules are hyperechoic, these have a high predictive value for endometrioma over non-endometrial lesions 22
  • colour Doppler: no internal vascularity
  • as opposed to many other ovarian cysts, endometriomas do not resolve

Despite repeated haemorrhage, findings of acute haemorrhage are uncommon in endometriomas (<10%), such as layering blood products or retractile thrombus 22.

MRI

Technique: pelvic MRI protocol - endometriosis.

MRI has a greater specificity for the diagnosis of endometriomas than the other non-invasive imaging techniques 1 and thus has a role to play in the evaluation of adnexal masses, as well as assessing for response to medical therapy (see below) potentially eliminating the need for follow-up laparoscopy. Typically the lesions that can be detected with MRI are those that contain blood products 23

  • haemorrhagic “powder burn”
    • lesions appear bright on T1 fat saturated sequences
  • small solid deep lesions
    • may be hyperintense on T1 and hypointense on T2
  • adhesions and fibrosis
    • isointense to pelvic muscle on both T1 and T2 weighted images
    • spiculated low signal intensity stranding that obscures organ interfaces 1
    • distortion of normal anatomy
      • posterior displacement of the uterus and ovaries
      • angulation of bowel loops
      • elevation of the posterior vaginal fornix
    • loculated fluid collections
    • hydrosalpinx
  • endometriomas
    • <5 mm: early stage disease; >15 mm: advanced disease
    • shading sign 25: may be less likely to respond to medical treatment 28
    • low T1 and T2 due to tissue and haemosiderin-laden macrophages 1
    • diagnostic criteria:
      • multiple cysts with T1 hyperintensity OR
      • one or more cysts with high T1 and shading on T2
  • uterosacral involvement 13
    • normal uterosacral ligaments are smooth and of regular contour
    • irregular margins
    • asymmetry
    • nodularity and thickening medially (>9 mm) 13
    • altered T2 signal: isointense (50%), hypointense (40%) or hyperintense (10%) cf. myometrium
    • if bilateral uterosacral involvement with additional involvement torus uterinus involvement results in an arciform abnormality
  • vaginal involvement
    • loss of hypointense signal of the posterior vaginal wall on T2WI
    • thickening, nodules and/or masses also potentially seen
  • pouch of Douglas
    • partial to complete obliteration
    • suspended or lateralised fluid collections
  • rectovaginal septum
    • nodules or masses that passed through the lower border of the posterior lip of the cervix
  • gastrointestinal tract
    • MRI has a low sensitivity (33%) for detecting rectal lesions 13 due to artefacts related to rectal content;  sensitivity may be increased with the use of  water enema, endovaginal coils and phased array coils 20
      • rectal wall thickening
      • anterior displacement of the rectum
      • abnormal angulation
    • loss of fat plane between uterus and bowel
    • inflammatory response due to repeated haemorrhage can lead to adhesions, strictures and bowel obstructions
  • urinary tract
    • bladder
      • localised or diffuse bladder wall thickening
      • signal intensity abnormality, nodules or masses usually located at the level of the vesicouterine pouch
      • involvement of bladder mucosa is rare
  • chest
  • cutaneous tissues
    • nodules
  • malignant transformation
    • solid enhancing components
Limitations of MRI

Despite all the advantages of MRI over all other imaging modalities, it nonetheless has a number of limitations, including:

  • non-pigmented lesions will not be hyperintense on T1, and thus harder to see
  • small foci may have variable signal intensity:
    • may appear similar to normal endometrium: low T1, high T2
    • hypointense on all sequences
    • hyperintense on all sequences 1
  • plaque like implants are difficult to delineate 26
  • adhesions cannot be directly identified, usually relying on distortion of normal anatomy to imply their existence 26

Treatment of endometriosis can be “expectant”, medical or surgical.

Medical treatment

Targets hormonal regulation, and includes medication with:

  • danazol (a synthetic androgen): suppresses oestrogen production
  • gonadotropin releasing hormone (GRH) analogues: control the menstrual cycle
  • oral contraceptive pill: suppress cyclical haemorrhage
Surgery
  • laparoscopic (conservative surgery)
    • adhesiolysis
    • partial cystectomy for resection of anterior cul-de-sac involvement provided ureteric re-implantation does not need to be performed
    • uterosacral ligament excision
    • used in combination with vaginal approach for vaginal disease
  • laparotomy
    • hysterectomy and oophorectomy
    • bowel involvement
Complications

Malignant transformation of an endometrioma has been documented, but is rare, occurring in <1% of cases. It is usually in the form of endometrioid carcinoma, or less commonly clear cell carcinoma. Yearly ultrasound examinations of endometriomas have been advocated by some.

Differential considerations on MRI for endometriomas include:

  • dermoid cysts
    • endometriomas have homogeneous high signal intensity on T1 which does not suppress on T1FS, unlike a dermoid which has signal drop out on fat suppression images and chemical shift artefact
  • haemorrhagic ovarian cysts: endometriomas rarely present with acute symptoms and do not resolve over time
  • mucinous lesions: e.g. ovarian mucinous tumours
    • increased signal on T1 but less intense than fat or blood
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Article Information

rID: 6699
System: Gynaecology
Section: Pathology
Synonyms or Alternate Spellings:
  • Endometriosis - general

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Cases and Figures

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    Fig 1: Endometrio...
    Figure 1: endometriosis modes of spread
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    Ax T1 Fs

the per...
    Case 1: endometrioma T1 FS
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    Fig 2 : Endometre...
    Figure 2: recto-vaginal endometreosis
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    Anterior abdomina...
    Case 2: in anterior abdominal wall
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    Fig 3 : Endometri...
    Figure 3: endometriosis distribution
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    Case 3: scar endometriosis
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    Case 6
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    Scar endometriosi...
    Case 7: scar endometriosis
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    Rectovaginal sept...
    Case 8: rectovaginal septal nodule
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    Endometeriosis
    Case 9: involving bladder
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    Scar endometriosis
    Case 10: scar endometriosis : rectus abdominis muscle
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    Endometriosis T2
    Case 11: involving right ovary
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    Case 12
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    Case 13: deep infiltration involving spinal nerves
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    Case 14: involving abdominal wall
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