Endometriomas: Classification and surgical management

Diagnosis & Therapy

Article 6 of 10: Endometriomas

Endometriomas: Classification and surgical management

Understanding the etiology of endometriomas and implementing a more nuanced classification system can aid in the successful management of this common condition.

Rebecca C. Falik, MD, MST; Anjie Li, MD; Frances Farrimond, MD; Gity Meshkat Razavi, MD; Ceana Nezhat, MD; and Farr Nezhat, MD

Endometriosis, a disorder in which tissue resembling endometrium develops outside the uterine cavity, is a common cause of pelvic pain and infertility, affecting 6% to 10% of women.1 Although endometriosis occurs in almost all organs and anatomic locations, it most often affects the pelvic organs.2 An ovarian endometrioma, an ovarian cystic mass generally consisting of endometrial glands and stroma, is seen in 17% to 44% of women with endometriosis.3 Endometriomas are sometimes called chocolate cysts for the dark brown, thick, and tarry concentrated hemosiderin-laden fluid they contain, but histology shows that not all chocolate cysts have endometriosis within their walls.4 Understanding the etiology of endometriomas and implementing a more nuanced classification system can aid in the successful management of this common condition.

Etiology
Endometriomas are extensively described in the literature, and their origin is the subject of several theories. In 1921, Sampson noted luteal membrane and ovarian epithelial tissues within endometriomas and was the first to indicate that endometriomas may result from the invasion of functional cysts by endometrial tissue.2,4,5 In 1979, Czernobilsky and Morris6 found endometrial and oviduct-like epithelium in ovarian endometriosis and concluded that ovarian tissue may be a common histologic precursor. Several other authors subsequently have reported finding different types of tissue within ovarian endometriomas, and not all of these chocolate cysts showed histologic evidence of endometriosis.4,7,8

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Perspectives on Endometriosis Management


Disease classification
Our classification system identifies 2 types of endometriomas on the basis of their etiologies and characteristics.

Type I, which arise from endometrial tissue implanted on the ovarian surface, are also called true endometriomas.

Invagination of cortex and subsequent hemorrhage from endometrial tissue result in cyst formation. Endometrial tissue (endometrial stroma and glands) is histologically present in all type I endometriomas.1,4,9 These endometriomas usually are small (<5 cm in diameter) and have a densely adherent fibrous capsule.4 Often, there is no clear plane between cyst wall and ovarian stroma.3

Type II endometriomas arise from functional cysts involved in or invaded by cortical or pelvic side-wall endometrial implants or by type I endometriomas.

Type II endometriomas are subclassified by the extent of endometrial implant involvement in the cyst wall. Type IIA endometriomas are hemorrhagic cysts with less than 10% of endometrial tissue within the cyst wall. Similar to the functional cysts from which they originate, type IIA endometriomas have a cyst wall that is separated easily from ovarian tissue during surgery.4,7,9 Although type II endometriomas tend to be larger than their type I counterparts, in some cases they are identified at an early stage of 2 to 5 cm. Endometriomas larger than 5 cm are almost always type II.4

Type IIB and IIC endometriomas have endometrial implants and fibrosis within their cyst walls, with progressively more endometrial invasion in type IIC endometriomas (>50%) than in type IIB (10% to 50%). Consequently, type IIB cysts are relatively easy to dissect from ovarian tissue, except adjacent to an endometriotic area where the cyst densely adheres to the ovarian stroma. In type IIC, endometrial tissue more extensively penetrates the capsule, making dissection of diseased tissue from the ovarian stroma more difficult; in fact, separating type IIC cyst wall from ovarian stroma can be as challenging as excising a type I endometrioma.7 In most cases, a type IIC cyst is attached by adhesions and fibrosis to the pelvic side wall or uterus and ruptures during mobilization.

Presentation and diagnosis
Almost all patients with an endometrioma concurrently have peritoneal endometriosis, which is characterized by dysmenorrhea, dyspareunia, chronic pelvic pain, infertility, and, in some cases, gastrointestinal or genitourinary dysfunction.1 Pelvic examination may reveal an adnexal mass that is an endometrioma, or an endometrioma may appear on imaging obtained in a pelvic pain or infertility work-up.

Given its 73% sensitivity, 94% specificity, safety, and low cost, transvaginal ultrasonography is the preferred imaging modality for endometrioma.3 The characteristic ultrasonographic appearance is that of a round, homogeneous, fluid-filled mass with low-level echoes.1

Magnetic resonance imaging is appropriate when a more sensitive imaging modality is indicated, as for a patient with risk factors for malignancy. 3,10–12

SURGICAL MANAGEMENT

Clinical indications
Indications for surgical excision of endometriomas include pelvic pain, infertility, and prevention and diagnosis of malignancy. Endometriomas may be excised prior to use of assisted reproductive technology.13–15 Medical therapy, such as oral contraceptives, can be used to reduce the size of endometriomas but does not improve fertility.3 Certain ovarian cancers are more common in women with endometriosis, and ovarian tumors are thought to develop in about 1% of ovarian endometriosis cases.1,12 Therefore, endometrioma excision may reduce the risk of malignancy. As with other ovarian cysts, large endometriomas may be excised to reduce the risks of rupture and torsion.

Approach
Laparoscopy is the preferred approach for endometrioma excision. Controversy exists regarding the ideal procedure: complete excision (with stripping of the cyst capsule) or drainage and ablation of the cyst wall.

Compared with drainage and ablation, excision reduces recurrence of endometriomas; relieves dysmenorrhea, dyspareunia, pelvic pain, and other symptoms; and improves fertility.13,16

The recurrence rate may be as low as 5.8% with complete excision but is 90% with simple transvaginal aspiration.17,18 If not performed properly, however, cyst capsule stripping may damage nearby ovarian stroma and decrease the ovarian reserve.14 Some authors have advocated combining excision and ablation—performing cystectomy until there is no longer a clear plane between capsule and ovarian stroma and then ablating any remaining endometrial tissue.8

With type I and IIC endometriomas, we have seen the endometrial cyst wall infiltrating the ovarian stroma so deeply there is not always a definable plane. By contrast, type IIA and IIB endometriomas typically have a plane between the cyst wall and the ovarian cortex. In type II endometriomas, endometrial implants on the ovarian cortex infiltrate the plane of the cyst wall such that the juxtaposing lipomatous follicular cyst detaches with minimal intraoperative traction. Portions of type II endometriomas containing fibrosis and adhesions may become more difficult to peel off the cyst wall. For most endometriomas, at least 1 spot is difficult to peel off the ovary, and extra care must be taken at the hilum of ovary to avoid excising healthy ovarian cortex.4,5,7,8

Our surgical approach accounts for the described variations in type I and II endometriomas. Endometrial contents often spill as the endometrioma is dissected off neighboring structures.

When possible, endometriomas should be aspirated and irrigated prior to cystectomy to avoid seeding the pelvis and abdomen with spilled endometriotic contents.

We use hydrodissection, the injection of dilute vasopressin with a laparoscopic needle, to create a plane between cyst wall and ovarian stroma and strip the cyst capsule with laparoscopic graspers. Type I endometriomas adhere densely to the ovary. Given the presence of fibrosis and adhesions, the cyst is excised in a piecemeal fashion. Care is taken to remove any endometrial implants from the ovary while preserving as much of the ovarian tissue as possible.1

Type II endometriomas are larger cysts originating from the invasion of endometrial implants or type I endometrioma into functional cysts. The difficulty of capsule excision varies according to the extent of endometrial invasion. Type IIA endometriomas contain less than 10% endometrial tissue within the cyst capsule. Thus, the standard ovarian cystectomy stripping technique is successful in removing more than 90% of the cyst capsule. Special care is taken in stripping the residual small portion that involves the endometrial glands and stroma and adheres densely to the ovary.

The larger proportion of endometrial tissue present in type IIB and IIC endometriomas degrades the plane between the cyst capsule and the ovarian stroma, making excision more difficult. Similar to the type I excision, a piecemeal approach is often necessary. If complete stripping of the cyst capsule would result in extensive loss of healthy ovarian tissue, then electrocautery, plasma energy, or laser ablation can be selectively used to destroy focal areas of endometrial invasion. Complete ablation may be difficult, as the endometrioma wall can be up to 5 mm thick.19

For these thick-walled endometriomas, we recommend excision (vs ablation), which lowers the risk of endometrioma recurrence.

Conclusion
Endometriomas, common adnexal masses in women affected by endometriosis, may exacerbate pelvic pain and impair fertility. Gynecologists should be prepared to excise endometriomas completely and exercise care in preserving as much of the ovarian stroma as possible. We classify endometriomas into 2 types: type I, which develop from invagination of endometrial implants in the ovarian cortex, and type II, which stem from invasion of functional cysts by endometrial implants or type I endometrioma. This distinction guides surgical management.

Author affiliations and disclosures
Dr. Falik is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center, Palo Alto, California.

Dr. Li is from the Center for Special Minimally Invasive and Robotic Surgery and Stanford University Medical Center.

At the time of this writing, Dr. Farrimond was medical student, University of California–San Francisco, and is currently resident, Obstetrics and Gynecology, Kaiser Santa Clara Medical Center, Santa Clara, California.

Dr. Razavi is from the Center for Special Minimally Invasive and Robotic Surgery.

Dr. C. Nezhat is Fellowship Director, Atlanta Center for Minimally Invasive Surgery and Reproductive Medicine, Atlanta, Georgia.

Dr. F. Nezhat is Clinical Professor, Obstetrics and Gynecology, Weill Cornell Medical College, Cornell University, New York, New York, and Adjunct Professor, Obstetrics, Gynecology, and Reproductive Medicine, School of Medicine, Stony Brook University, Stony Brook, New York.

Dr. F. Nezhat reports being a speaker for Ambry Genetics. The other authors report no financial relationships relevant to this article.

References
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