Ovarian Endometrioma

Guidelines for Selection of Cases for Surgical Treatment or Expectant Management

Molly Carnahan; Jennifer Fedor; Ashok Agarwal; Sajal Gupta


Expert Rev of Obstet Gynecol. 2013;8(1):29-55. 

In This Article

Cause of Ovarian Endometrioma

Ovarian endometrioma, a subtype of endometriosis, affects 17–44% of women with endometriosis.[4,5] Ovarian endometriomas, also known as 'chocolate cysts', contain thick, old blood that appears as a brown fluid. The pathogenesis of ovarian endometriomas is a controversial topic, but there are three main theories: invagination of ovarian cortex secondary to bleeding of a superficial implant; invagination of ovarian cortex secondary to metaplasia of coelmic epithelium in cortical inclusion cysts; and endometriotic transformation of functional cysts. The first theory was described by Hughesdon in 1957, in which he suggested that endometrial implants, located on the surface of the ovary, are the cause of endometriomas. According to Hughesdon's theory, menstrual shedding and the endometrial implant bleeding are trapped and cause a gradual invagination of the ovarian cortex, which results in a psuedocyst.[6] Brosens et al., in agreement with Hughesdon, reported menstrual shedding and blood accumulation at the site of the implants through ovariscopy.[7] This theory is important in the treatment of ovarian endometriomas because the ovarian cortex is the internal surface of the psuedocyst wall; thus, ovarian cortex is lost during excision of the endometrioma. The second theory in the pathogenesis of ovarian endometriomas was described by Donnez et al. in 1996 and suggests that the invagination of ovarian endometriomas is not due to bleeding of the implant, but instead is caused by metaplasia of the coelomic epithelium invaginated into the ovarian cortex.[8] Donnez et al. suggest that the potential cause of recurrence after excision of endometriomas or vaporization is due to the invagination of endometriotic tissue into the ovary; thus, Donnez et al. recommend vaporization of the cyst wall.[9] The final theory postulates that the endometrioma is formed by endometriotic transformation of functional cysts and was first described by Nezhat et al. in 1992.[10]

The gold standard diagnostic technique of an ovarian endometrioma is laparoscopy. However, a transvaginal ultrasound can assist in the initial diagnosis and help differentiate endometriomas from other benign ovarian tumors with the typical endometrioma appearance of homeogenous low-level internal echoes and thick walls.[11] Van Holsbeke et al. report that the single best ultrasound variable to differentiate between endometriomas and other adnexal masses in premenopausal women is round glass echogenicity of cyst fluid, with a sensitivity of 73% and a specificity of 94%.[12] Guerriero et al. found that transvaginal ultrasounds are able to detect the presence of pelvic adhesions in patients with endometriomas, and identification of pelvic adhesions can help with determining the proper treatment.[11] Color Doppler identifies the vascularization of the mass, and endometriomas typically have peripheral blood flow. 3D ultrasounds are becoming increasingly popular in clinical practice; Alcazar et al. report that in premenopausal women, B-mode ultrasound with the use of mean gray value has a sensitivity of 80% and specificity of 91% in differentiating endometriomas from other unilocular cysts.[13] MRI can further assist in the differentiation of ovarian endometriomas and other ovarian cysts. Endometriomas are usually present as T-1 bright lesions and Froehlich et al. recommend using 'fat-saturation on pre-contrast, T1-weighted sequences instead of T2-weighted sequences' to differentiate an endometrioma from a mature teratoma.[14]

Endometriomas can occur unilaterally or bilaterally, and approximately 28% of endometrioma patients have bilateral endometriomas.[15] Women with endometriomas have many of the same symptoms as those with endometriosis, including dyspareunia and/or subfertility. One potential issue with ovarian endometrioma treatment is the presence of other pelvic endometriotic lesions. One study reported that only 19 out of 1785 patients (1.06%) had ovarian endometriomas without any other pelvic endometriosis.[5] Furthermore, Fauconnier et al. found that ovarian endometriomas did not contribute to chronic pelvic pain, but were highly associated with deep infiltrating endometriosis, which is known to cause chronic pelvic pain.[5,16] Therefore, when creating a treatment plan for women with chronic pelvic pain and endometriomas, the physician may need to consider treating the deep infiltrates as well. Ovarian endometriomas can be further complicated by the formation of adhesions that can fixate the pelvic organs. Fixation of the pelvic organs may distort the anatomical locations and reduce natural fertility.[17]