Endometrioma: A Comprehensive Review of Its Varied Presentations, Complications, and Impact on Patient Management

Abstract

Endometriosis is a disease characterized by the presence of endometrium-like glands and/or stroma outside the uterus, usually with an associated inflammatory process. Endometrioma, a common manifestation of endometriosis, typically presents as an ovarian or adnexal cyst containing blood products at varying stages of degradation. While the typical ovarian/adnexal endometrioma is well recognized on imaging, atypical presentations and mimics can pose a diagnostic challenge. Endometriotic cysts can occur in unexpected locations, including within or on the surface of the liver, pancreas, peritoneum, and along the nerves, to name a few locations. Endometriomas can be associated with complications such as infection, rupture, and malignant transformation. An endometrioma is a marker of deep endometriosis, necessitating evaluation for the same. Endometriosis is seen in ∼50% of patients with infertility. Surgical management to improve fertility may include the excision of ovarian endometriomas with an impact on ovarian functional reserve. Finally, in pregnant patients, preexisting endometriomas may undergo decidualization and resemble ovarian malignancy, further adding to the diagnostic conundrum. This review article will describe the typical and atypical imaging features of an endometrioma, its associations, and complications, as well as its implications on patient management. Throughout this article, the term “endometriotic cyst” will be used for lesions located outside the ovary/adnexa.

Key Points

1. Endometriomas are the most commonly recognized form of endometriosis, both on ultrasound and MRI. They are cystic structures containing blood products at varying stages of degradation, lined by a thick wall containing inflammatory tissue as well as endometrium-like glands and stroma.

2. An ovarian endometrioma is a marker of the presence of deep endometriosis, a more severe form of the disease—which should be actively sought for—whenever an endometrioma is seen on imaging.

3. Any enhancing mural nodule within an endometrioma warrants further evaluation regardless of its size. Although some enhancing mural nodules can be benign, more commonly, they represent malignant degeneration and should therefore be considered for surgical management.

4. Ectopic endometrial glands/stroma within endometriomas in pregnant women respond to hormonal changes in pregnancy, similar to eutopic endometrium and undergo an increase in size and vascularity (decidualization). Decidualized endometriomas seen in pregnancy contain papillary projections that are benign; however, they can resemble and are often mistaken for malignancy.

5. Complications such as infection, rupture, torsion, and malignant transformation have been reported with endometriomas.

Keywords

ovarian endometrioma - endometriosis - transvaginal ultrasound - magnetic resonance imaging - infertility - malignant degeneration

Introduction

Endometriosis is a disease characterized by the presence of endometrium-like glands and/or stroma outside the uterus, usually with an associated inflammatory process.[1] It is a chronic multisystem disease reported to affect 10% of the general population, with more than 80% being reproductive-age women.[2] The most common presenting symptoms include chronic pelvic pain and infertility, with additional symptoms related to the specific organ of involvement.[3]

Three main morphologic subtypes of endometriosis have been described: ovarian/adnexal endometriomas (OMAs), superficial endometriosis, and deep endometriosis (DE). Endometriomas are cystic masses lined with ectopic endometrial tissue that contain degenerated blood products resulting from cyclic hemorrhage from the lining, typically located within the ovary or adnexa. They are referred to as “chocolate cysts” colloquially because of thick, dark, degenerated blood products within them resembling liquid chocolate. They occur in 17 to 44% of patients with endometriosis.[4] A typical endometrioma is the most well-recognized form of endometriosis on imaging. In this review article, in addition to the typical endometrioma, we highlight various atypical presentations of endometriotic cysts with their imaging features and management implications, including complications associated with endometriomas, such as rupture, infection, and malignant degeneration. Throughout this article, we will refer to endometriomas outside the ovary/adnexa as endometriotic cysts.

Etiology

The precise cause of endometriosis remains unclear; however, several theories have been proposed to explain its varied presentation and anatomical distribution.[5] [6] These include the retrograde menstruation theory, coelomic metaplasia theory, and vascular and lymphatic metastatic theory. Additionally, immune dysregulation is believed to contribute to disease development. Retrograde menstruation involves the reflux of menstrual debris containing viable endometrial cells through the fallopian tubes into the peritoneal cavity.[7] Endometrial stem and progenitor cells, present in the eutopic endometrium, may be shed during retrograde menstruation and contribute to the formation of endometriotic implants in the most dependent areas of the pelvis, where the disease is commonly found.[8] This theory is supported by associations with a short menstrual cycle, obstructed menstrual flow, and studies linking somatic genetic mutations in endometriotic lesions to eutopic endometrial cells.[9] [10] The coelomic metaplasia theory suggests that peritoneal mesothelium can transform into glandular endometrial tissue, which may explain cases of endometriosis in premenarchal teenagers, women who have never menstruated, and postmenopausal women.[11] The vascular and lymphatic metastatic theory proposes that endometrial cells can spread to distant extrapelvic sites through blood and lymphatic circulation, accounting for the occurrence of endometriotic implants in locations beyond the pelvis.[12]

The ovary is the most common site of ectopic endometriotic implantation.[3] Sampson proposed that endometriomas develop from ruptured functional ovarian cysts, allowing endometrial tissue to invade the ovarian cortex.[13] Another suggested mechanism involves the invagination of ovarian surface endometriosis into the ovarian stroma, with recurrent bleeding leading to the formation of thick fibrotic walls enclosing various stages of blood degradation products.[14]

Histology of Ovarian Endometriomas

The wall of an endometrioma, on histological analysis, shows endometrium-type glands and stromal elements, including scattered hemorrhage and hemosiderin-laden macrophages characteristic of endometriosis ([Fig. 1]). Another important feature is a strong positivity for estrogen and progesterone receptors on immunostaining of the stromal and epithelial cells.[15] [16] Muzii et al. found that the inner endometrium-like glandular lining of the endometrioma differs from the uterine endometrium in that it has a mean depth of only 0.6 mm. The endometriotic tissue may cover the inner aspect of the cyst from 10 to 98% of its surface.[17]

Fig. 1 Histology of an ovarian endometrioma. (A) Gross photograph and (B) low- and (C) high-power photomicrographs of an endometriotic cyst (endometrioma) of the ovary, showing endometrial stroma with arterioles, scattered foci of hemorrhage, and abundant hemosiderin-laden macrophages (white arrowheads).

Clinical Presentation

OMAs typically present in women of reproductive age. They comprise ∼27% of ovarian masses in the fourth decade of life and only 4.3% in the sixth decade. In a large prospective study of 308 adolescents presenting with severe dysmenorrhea, Millischer et al. found that 39.3% (121/308) of patients had an OMA and/or DE on magnetic resonance imaging (MRI), and 20.7% of this MRI-positive group (25/121) had isolated OMAs.[18]

OMAs are frequently associated with DE and are a marker of multifocality and severity of DE. Chapron et al. reported a direct correlation between the presence of ovarian endometriomas and an increased number of DE lesions.[19] Typical symptoms attributed to DE are dysmenorrhea, deep dyspareunia (which can be related to the menstrual cycle), noncyclic chronic pelvic pain, and infertility.[3] Fauconnier et al. found no correlation between endometriomas and any type of pelvic pain symptoms. However, they proposed that because an endometrioma was frequently associated with DE, which is implicated in causing pain, women with symptoms of pain and an endometrioma should be evaluated for DE.[20]

Diagnosis

Superficial endometriosis is difficult to diagnose on imaging, and laparoscopic visualization (with histologic confirmation) remains the gold standard.[21] Although histologic confirmation is the gold standard for diagnosing DE as well, noninvasive imaging including MRI and transvaginal ultrasound (TVUS) are now widely accepted as the initial diagnostic modalities.[22] Endometriomas are the most commonly recognized form of endometriosis on TVUS and MRI. A systematic review of diagnostic tests by Nisenblat et al. found a sensitivity of 93% and specificity of 96% for TVUS and a sensitivity of 95% and specificity of 91% for MRI in detecting OMAs.[23]

Deep Endometriosis in Patients with Endometriomas

It has been reported that one in two patients with a DE nodule presents with an associated ovarian endometrioma.[19] Chapron et al. found a direct correlation between the presence of ovarian endometriomas and an increased number of DE lesions and labeled OMAs as markers for DE multifocality and severity. For instance, in their study, the mean number of DE lesions in patients presenting with associated OMAs was statistically significantly higher than patients presenting without associated OMAs (2.51 ± 1.72 vs. 1.64 ± 1; p < 0.0001).[19] The risk of bowel and ureteral involvement by DE was multiplied in the presence of a concurrent ovarian endometrioma by ∼34 and 8 times, respectively, requiring complex surgical procedures with a nonnegligible risk of complications.[24] [25] Additionally, the presence of an ovarian endometrioma directly correlated with the development of considerable adhesions, as indicated by significantly higher rAFS (disease stage scored per the revised American Fertility Society classification) adhesion scores, requiring more complex surgeries.[19] [26]

It is therefore safe to conclude that in the context of pelvic pain, an ovarian endometrioma discovered on TVUS should prompt the radiologist to check for additional sites of deep disease.[19]

Patients with endometriomas can rarely present with massive loculated bloody ascites ([Fig. 2]). A popular proposed theory of this presentation is exudation secondary to peritoneal irritation following the rupture of endometriomas. The trans-diaphragmatic flow of ascitic fluid into the pleural space via lymphatic channels has been postulated to explain the pleural effusions—rarely seen in a subset of these patients (Meigs' syndrome).[27]

Fig. 2 A 33-year-old patient with bilateral ovarian endometriomas presenting with large-volume hemorrhagic ascites. (A) Coronal contrast-enhanced CT image of the abdomen and pelvis shows bilateral adnexal cystic lesions (white arrows) with large-volume ascites (black asterisk). (B) Axial fat-suppressed precontrast T1-weighted and (C) axial T2-weighted pelvic MR images show bilateral T1 hyperintense and T2 hypointense ovarian endometriomas (white arrows) and T1 hyperintense pelvic ascites (black asterisk). Intraoperative pictures taken during laparoscopic drainage of hemorrhagic ascites: (D) Intraoperative findings revealed 2.5 liters of dark brown, bloody ascites (white asterisk) and a 2x2 cm nodular omental soft tissue mass (not shown). E) The pelvic structures (uterus and bilateral adnexa) were not clearly visible given the extensive adhesions of the small bowel and cecum covering the pelvic organs with scattered glandular appearing deposits (black arrowheads) overlying the bowel and adhesions in the pelvis consistent with suspected endometriosis. The final surgical pathology of the omental mass denoted florid endometriosis. White star—uterus.

Imaging of a Typical Ovarian/Adnexal Endometrioma

Role of Ultrasound

Routine TVUS is the first-line imaging for the initial screening of suspected pelvic endometriosis, and transabdominal examination alone is insufficient. The ultrasound appearance of a typical OMA is a thick-walled cystic lesion within the ovary/adnexa filled with homogenous low-level internal echoes, called the “ground glass” appearance (seen in 95% of endometriomas) ([Fig. 3A]), with or without echogenic nodules along the cyst wall (36%), and no internal blood flow.[28] [29] A systematic review and meta-analysis by Kanti et al. found a sensitivity of 89% and specificity of 95% for detecting endometriomas with TVUS.[30] The echogenic mural nodules are thought to represent blood clots or nodules composed of cholesterol deposits from blood breakdown products and are avascular. If there is vascularity within the mural nodules, these should be further imaged to exclude malignant degeneration of endometriomas.

Fig. 3 (A–C) A 36-year-old patient with bilateral ovarian endometriomas. (A) Transvaginal pelvic ultrasound shows bilateral adnexal cysts with homogeneous low-level internal echoes with a typical ground-glass appearance. (B) Axial fat-suppressed precontrast T1-weighted, and (C) axial T2-weighted pelvic MR images show bilateral T1-light bulb bright ovarian endometriomas with T2 shading. (D) A 40-year-old patient with bilateral ovarian endometriomas with T2 dark spot in the right-sided endometrioma (white arrowhead). White star—uterus; yellow and white arrows—right and left ovarian endometriomas, respectively.

Role of Computed Tomography

Computed tomography (CT) is not the preferred imaging technique for evaluating a suspected endometrioma because of its nonspecific CT imaging features. OMAs are often incidentally detected on CT as complex cystic pelvic masses, usually with high-density fluid components. However, these imaging findings may be seen in other entities, such as hemorrhagic cysts or neoplasms. In general, CT plays a greater role in diagnosing various complications related to endometriomas, including torsion or rupture or in staging endometriosis-associated ovarian cancer.[28] [31]

Role of Magnetic Resonance Imaging

On MRI, OMAs are nonenhancing cystic lesions that are homogenously hyperintense on precontrast T1-weighted fat-saturated images (“T1 light bulb bright”), with signal intensity less than simple fluid and/or adjacent follicles on T2-weighted images or dependent layering with a T2 hypointense fluid level resulting from the accumulation of deoxyhemoglobin, methemoglobin, and hemosiderin due to chronic repeated intracystic bleeding (“T2-shading”) ([Fig. 3B, C]).[32] [33] The “T2 shading” sign by itself is highly sensitive (93%) but less specific (45%) for the diagnosis of endometriomas, due to overlap with a similar appearance of hemorrhage within hemorrhagic cysts and malignant lesions.[33] [34] Endometriomas may demonstrate a thickened T2 hypointense rim made of hemosiderin-laden macrophages and fibrous tissue in the wall of the endometrioma.[33] The T2 dark spot is a discrete, well-defined, markedly T2 hypointense, often linear, punctate, or oval focus adjacent to but not within the wall of an endometrioma, thought to reflect a chronic retracted blood clot ([Fig. 3D]).[34] [35] This sign has high specificity (93%) for endometriomas, and is especially useful for differentiating them from hemorrhagic cysts. Additionally, endometriomas can restrict diffusion due to the highly viscous proteinaceous and hemorrhagic content.[33]

Atypical (Extraovarian) Sites

Intraperitoneal Extraovarian Endometriotic Cyst

Peritoneal endometriotic cysts represent an uncommon presentation of endometriosis, characterized by nonspecific clinical symptoms that vary based on the mass effect on adjacent viscera or secondary to direct involvement of the serosa of specific organs. The literature documents cases of omental endometriotic cysts in both premenopausal and postmenopausal women with a notable feature in some instances being the substantial size of the lesions, reported to reach up to 26 cm.[36] Case reports of endometriotic cysts involving the rectal serosa, bladder wall, mesentery, pelvic nerves (sciatic, femoral, obturator, hypogastric plexus) have also been described.[37] [38] In our practice, we encountered a patient with multiple small extraovarian endometriotic cysts in the pelvis, some abutting the bowel serosa ([Fig. 4]).

Fig. 4 A 47-year-old patient with peritoneal endometriotic cysts. (A) Axial T2-weighted, (B) sagittal T2-weighted, (C) sagittal fat-suppressed precontrast T1-weighted, and (D) sagittal fat-suppressed postcontrast T1-weighted pelvic MR images show T1 and T2 heterogeneous cystic lesions abutting the serosal aspect of the proximal (yellow arrows) and distal (white arrows) sigmoid colon. Surgical pathology revealed peritoneal endometriotic cysts. Dotted white lines—sigmoid colon; white star—uterus.

Hepatic Endometriotic Cyst

Hepatic/perihepatic endometriotic cysts represent endometriotic cysts involving the hepatic parenchyma, the hepatic surface, and/or the perihepatic space. A case series of 30 cases of hepatic endometriosis by Mushtaq et al. revealed 25 cases of hepatic endometriotic cysts and 5 cases of DE involving the liver parenchyma.[15] Among the 25 cases, right lobe involvement was seen in 16 and left lobe in 9 cases. Intrahepatic location was found in 84% (21/25), whereas the remaining (4/25) had perihepatic cysts. Fifty-seven percent of the cases were seen in premenopausal women. Only 44% (11/25) had a prior history of pelvic endometriosis with no significant catamenial symptoms. MRI findings varied depending on the varying signal intensities of aging blood within the lesions.[15] [Figs. 5] and [6] illustrate the MRI and histological findings, respectively, of a perihepatic endometriotic cyst in a 37-year-old patient. Histology may show normal hepatic parenchyma with endometrium-type glands and stromal elements, including scattered hemorrhage, and hemosiderin-laden macrophages within the cyst wall, a finding that was also seen in our patient.[15] [16] A significant gynecological history might not be present in patients presenting with a perihepatic endometriotic cyst. In a premenopausal woman presenting with a cystic liver mass containing blood products or a spontaneous hepatic/perihepatic hematoma without an underlying cause, irrespective of a known history of endometriosis, the differential could include hepatic endometriosis.[15]

Fig. 5 A 37-year-old patient with a perihepatic endometriotic cyst. (A) Transverse transabdominal ultrasound image of the right upper quadrant shows an ovoid perihepatic collection with dependent internal debris (white arrow). (B) Axial T2-weighted, (C) axial fat-suppressed precontrast T1-weighted, and (D) axial fat-suppressed postcontrast T1-weighted abdominal MRI images confirm the presence of two ovoid loculated perihepatic cystic lesions (white and yellow arrows) adjacent to segment V/VIII of the right hepatic lobe, with inhomogeneous T1 hyperintensity, T2 shading with fluid–fluid levels and an enhancing rim, with surrounding inflammatory changes. This was surgically confirmed to represent endometriosis.

Fig. 6 Microscopic images of the perihepatic endometriotic cyst seen in the patient shown in [Fig. 5]. (A) Low- and (B) high-power photomicrographs of the perihepatic endometriotic cyst, showing hepatic parenchyma (left) with capsular adhesions involved by endometriotic glands (black arrowheads) and stroma.

Pancreatic Endometriotic Cyst

A pancreatic endometriotic cyst was first described in the literature in 1984 and is extremely rare.[39] [40] [41] [42] [43] A literature review revealed that most reported cases are described in premenopausal women.[44] Most reported cases present with symptoms such as chronic or acute epigastric pain resembling acute pancreatitis, involuntary weight loss, and digestive difficulties.[45] Only in half of the described cases does the pain have a catamenial nature, which can help make the diagnosis. Acute symptoms may also result from a spontaneous rupture.[46] Pancreatic endometriotic cysts have been commonly seen in the tail, rarely in the body. They can be either solitary or multiple. No typical imaging features have been described other than MR signal intensities correlating with varying blood degradation products. Differential diagnoses include pseudocysts with hemorrhage or solid pseudopapillary epithelial tumors of the pancreas—tumors that have a predilection for hemorrhage.

Variants of Endometrioma

Polypoid Endometriosis within an Endometrioma

Polypoid endometriosis, a histological variant of endometriosis, is an uncommon but described entity that is important to be aware of, due to its ability to mimic a malignancy on imaging or occasionally on histology.[45] It derives its name from its histological appearance of exophytic or polypoid masses that project from the serosal surface or the mucosa of the ovarian endometrioma, bowel, or bladder.[3] In an early case series reporting this entity, 60% of patients were above 50 years of age, branding this entity as seen in postmenopausal women.[47] Various case reports have described polypoid endometriosis within endometriomas as well as outside of it.[47]

Lee et al. reported a case of polypoid endometriosis of the ovary mimicking advanced ovarian carcinoma with extensive peritoneal metastases including bilateral ovarian masses, ascites, disseminated peritoneal nodules, and a highly elevated serum CA-125 level.[48]

On ultrasound, cysts with low-level internal echoes and solid, papillary echogenic nodules or masses within the cyst wall, with internal vascularity on color Doppler, may be seen ([Fig. 7A]).[49] On MRI, T2-weighted MR images demonstrate round, smooth hyperintense nodules along the wall of an endometrioma. The corresponding T1-weighted images may demonstrate T1-hypointensity with enhancement on the postcontrast sequences, mimicking endometriosis-associated ovarian cancer. In a small case series by Lee et al., no restricted diffusion was seen in the solid components of polypoid endometriosis.[48]

Fig. 7 A 41-year-old patient with polypoid endometriosis within a polyp arising from the wall of a left ovarian endometrioma. (A) Transverse transvaginal ultrasound image of the pelvis with color Doppler shows a solid mural nodule within a left ovarian endometrioma with Doppler flow within it, indicating internal vascularity. (B) Low- and (C) high-power photomicrographs of this lesion demonstrate cystically-dilated endometriotic glands (yellow arrowheads), cellular to edematous stroma, and scattered thick-walled vessels (red arrowhead) with no evidence of dysplasia or malignancy.

Though extremely rare, carcinoma can arise in polypoid endometriosis.[48] We found one prior report of the transformation of polypoid endometriosis to a malignant epithelial neoplasm.[50] In another case, Parker et al. found a small focus of grade 1 endometrioid adenocarcinoma within hyperplastic nonpolypoid endometriosis of the left ovary of a 59-year-old woman who had polypoid endometriosis within an endometrioma within the contralateral ovary.[47] Tanaka et al. investigated 49 pathologically confirmed OMAs with contrast-enhancing mural nodules on MRI. Of these, 33 exhibited malignant changes, while 7 were benign.[51] [Fig. 7 (B, C)] shows cystically dilated endometrial glands associated with changes of polypoid endometriosis within a section of a polyp arising from the wall of an ovarian endometrioma.

Decidualization within an OMA in the Pregnant and Nonpregnant Patient

During pregnancy, progesterone surge causes the uterine endometrium to thicken and transform into decidua with hypertrophy of the endometrial stromal cells, known as decidualization.[3] In a pregnant patient, similar histological changes can occur within ectopic endometrial tissue located within or outside an endometrioma. Ultrasonography is the primary method for the detection and assessment of adnexal masses in pregnancy, due to its ease of access and safety profile. On ultrasound, a decidualized endometrioma is an anechoic/hypoechoic mass demonstrating smooth or lobulated mural nodules with internal vascularity, resembling ovarian malignancy.[52]

MRI without intravenous gadolinium can also be safely performed in pregnancy and has been used to characterize adnexal masses.[52] On MR imaging, the solid nodules within decidualized endometriomas have been shown to demonstrate signal intensity characteristics similar to the decidualized endometrium of the gravid uterus. Thus, they may demonstrate high signal intensity on T2-weighted and diffusion-weighted images and ADC maps.[53] [54] [Fig. 8] shows the MRI findings in decidualized bilateral ovarian endometriomas in a pregnant patient, with increased T1 signal intensity of the intracystic fluid and “shading” on T2-weighted images. Decidualization within an endometrioma in a nonpregnant patient is a rare phenomenon described in patients on high-dose progesterone for medical management of endometriosis.[55] In our practice, we encountered a similar nonpregnant patient who presented with bilateral ovarian endometriomas containing vascular mural nodules on ultrasound and nodular enhancing soft tissue on MRI ([Fig. 9]). These were surgically excised and proven on pathology to represent changes of decidualization in the right ovarian cyst wall.

Fig. 8 A 28-year-old pregnant patient with a known history of endometriosis demonstrating bilateral decidualized endometriomas that decreased in size following delivery. Sagittal transvaginal ultrasound with color Doppler images show (A) right and (B) left ovarian cysts with low-level internal echoes and minimal internal vascularity. (C) Axial T2-weighted and (D) precontrast T1-weighted images from a noncontrast pelvic MRI study show bilateral adnexal endometriomas (white dotted lines) showing marked T1 hyperintensity and T2 shading with smooth, lobulated T1 isointense nodular soft tissue in the wall. White star—gravid uterus with fetus.

Fig. 9 A 32-year-old patient with decidualization of bilateral endometriomas in a nonpregnant patient due to the hormonal effect of high-dose progesterone. (A) Axial T2-weighted, (B) axial fat-suppressed precontrast T1-weighted, and (C) sagittal postcontrast subtraction pelvic MR images show bilateral ovarian cysts with marked T1 hyperintensity and T2-shading characteristic of bilateral ovarian endometriomas (white and yellow arrows representing the two endometriomas). Note the presence of enhancing, mildly T2 hyperintense polypoid solid components (C, white arrowheads; shown in the right endometrioma) Note the presence of enhancing polypoid nodules (white arrowheads) within the endometrioma denoted by the white arrow, on the sagittal post contrast subtraction image (C), lacking diffusion restriction (not shown). White star—uterus.

[Fig. 10] depicts changes of decidualization on histology in an ovarian endometrioma in early pregnancy characterized by plump, decidualized cells with abundant pale eosinophilic cytoplasm.

Fig. 10 Histology of a decidualized ovarian endometrioma. (A) Low- and (B) high-power histology of a decidualized endometriotic cyst (endometrioma), showing plump, decidualized cells with abundant pale eosinophilic cytoplasm (white arrowheads).

Seromucinous borderline tumors have been described to be confused with ovarian endometriomas due to the presence of low-level internal echoes on ultrasound. When these manifest in pregnancy, they may mimic decidualized endometriomas.[56] [Fig. 11] depicts a case of serous cystadenoma in a pregnant woman mimicking decidualized ovarian endometrioma.

Fig. 11 A 33-year-old pregnant patient with a serous cystadenoma of the ovary (pathologically proven) mimicking a decidualized ovarian endometrioma on ultrasound. (A) Transverse transvaginal pelvic ultrasound image shows a cystic left adnexal lesion with low-level internal echoes (yellow arrow) and small mural nodules without significant internal vascularity (white arrowheads), which was thought to be a decidualized endometrioma. (B) Axial precontrast T1-weighted, (C) axial T2-weighted, and (D) sagittal T2-weighted images from a noncontrast pelvic MR study show a T1 hypointense and T2 hyperintense cystic lesion (yellow arrows) within the left ovary situated posterior to the gravid uterus (white star). The lack of T1-bright fluid and absent T2-shading helps suspect a malignancy.

Complications

Infection

Although rare, endometriomas may get infected at the time of laparoscopic or transcutaneous (during infertility management) intervention.[57] Transvaginal oocyte retrieval is one such route that can introduce infection, resulting in a tubo-ovarian abscess.[58] Tubo-ovarian abscesses display variable T1 signal, have thickened enhancing walls, and show restricted diffusion with surrounding inflammatory changes with a clinical history corroborative of an infection ([Fig. 12]).[33]

Fig. 12 A 45-year-old patient with bilateral tubo-ovarian abscesses following oocyte retrieval in a patient with known ovarian endometriomas undergoing fertility treatment. (A) Axial fat-suppressed precontrast T1-weighted, (B) axial T2-weighted, and (C) axial fat-suppressed postcontrast T1-weighted pelvic MR images show rim-enhancing bilateral adnexal fluid collections inseparable from the ovaries, consisting of T2 heterogeneous contents and a fluid–fluid level seen on the left side. (D) Axial diffusion-weighted and (E) axial apparent diffusion coefficient (ADC) images reveal marked diffusion restriction of the contents (white arrows—right adnexal collection; yellow arrows—left adnexal collection).

Rupture

Endometriomas can grow and occasionally rupture. The leakage of hemorrhagic fluid can act as a strong irritant to peritoneal surfaces, causing severe abdominal pain and a clinical picture resembling peritonitis.[59]

These patients typically present with acute abdominal pain and tend to get imaged with a CT of the abdomen and pelvis in this acute setting. CT features of a ruptured endometrioma tend to be nonspecific and include visualization of a hyperdense/heterogeneous adnexal lesion accompanied by hemoperitoneum. The diagnosis is easier to make if the patient carries a known diagnosis of endometriosis; however, if this is not previously known, this imaging finding can mimic a ruptured ectopic gestation or a ruptured hemorrhagic cyst, or even an ovarian malignancy[59] ([Fig. 13]). Clinically, a ruptured endometrioma can lead to an increase in CA-125 levels, as well as cancer antigen 19–9 (CA 19–9) and D-dimer markers, with imaging findings falsely mimicking ascites from ovarian malignancy.

Fig. 13 A 41-year-old patient with a surgically proven ruptured right ovarian endometrioma. (A) Axial T2-weighted pelvic MR image shows a right ovarian endometrioma displaying T2 shading (white arrowhead). (B) Axial contrast-enhanced CT image through the pelvis after 2 months shows a reduction in the size of the right ovarian endometrioma with slight irregularity of its walls (white arrowhead). (C) Axial contrast-enhanced CT image through the upper abdomen (same CT study as B) shows intraperitoneal free fluid (white asterisk) with peritoneal and omental nodularity (yellow arrow). (D) Axial contrast-enhanced pelvic CT image after 2 more months shows further reduction in the size of the right ovarian endometrioma (white arrowhead) and pelvic free fluid (white asterisk); white star—uterus.

Torsion

Endometriomas incite surrounding fibrosis and are therefore thought to be less predisposed to torsion.[60] However, the risk of torsion is not negligible and the imaging findings of a torsed ovarian endometrioma may also demonstrate the same features as torsion due to other ovarian masses, except for the lead point being an endometrioma.[61]

Malignant Transformation of Endometrioma

Endometriomas predispose to malignancy with a reported incidence of 0.5 to 1% of cases. Approximately 75% of endometriosis-associated neoplasms arise in the ovary (EAOCs), with the remaining 25% being extraovarian (colon, rectovaginal septum, and rarely, small bowel, urinary tract, and abdominal wall scars).[62] [63] EAOCs affect women who are 10 to 20 years younger than those without endometriosis with a better overall survival than ovarian neoplasms in the general population; however, it is unclear if this is due to the distinct biological differences between the two cancer types or because EAOCs typically present with a higher rate of well-differentiated, early-stage tumors that are contained within the endometrioma with the opportunity for curative resection if detected early.[62] [64] Malignant transformation of endometriosis was initially described by Sampson in 1925. Sampson identified strict histologic criteria to classify a malignancy as arising from endometriosis. These include clear evidence of endometriosis in proximity to the tumor, the presence of tissue resembling endometrial stroma surrounding epithelial glands, and the exclusion of a metastatic tumor to the ovary.[65] Subsequently, Scott proposed an additional criterion: the evidence of the histological transition from endometriosis to cancer to define “ovarian cancer arising in endometriosis.”[66] Atypical endometriosis may represent an intermediate step in neoplastic progression, with some lesions demonstrating similar immunohistochemical and molecular alterations as observed in endometriosis-related tumors.

On imaging, Tanaka et al. reported that the most important imaging finding for EAOC was the presence of contrast-enhanced mural nodules; however, other benign conditions, such as polypoid endometriosis, decidualized endometriomas during pregnancy, have been reported to demonstrate enhancing nodules within endometriomas.[51] Dynamic subtraction MR imaging is a valuable tool for identifying the degree of enhancement in these nodules ([Figs. 14] and [15]). Intracystic blood clots may mimic malignant nodules by demonstrating restricted diffusion but can be distinguished by the lack of contrast enhancement. The characteristic T2 shading of cyst fluid in benign endometriomas is often lost or absent in malignant transformation because of the dilution of endometrioma content by the fluid secreted by tumors ([Fig. 16]).[33]

Fig. 14 A 46-year-old patient with malignancy arising from an ovarian endometrioma. (A) Transverse transvaginal ultrasound with color Doppler image of the pelvis shows a cystic lesion with homogeneous low-level internal echoes and polypoid solid components (white arrows). (B) Axial T2-weighted, (C) axial fat-suppressed precontrast T1-weighted, and (D) axial postcontrast subtraction pelvic MR images show enhancing T2 intermediate solid components (white arrows) within a T1 hyperintense right ovarian endometrioma. The dotted white outline shows a nonenhancing tissue posterior to the solid component, indicating a blood clot. Note the loss of T2-shading due to malignant transformation. Surgical pathology showed clear cell carcinoma arising in the right ovarian endometrioma.

Fig. 15 A 42-year-old patient with malignancy arising from an ovarian endometrioma. (A) Sagittal T2-weighted, (B) axial T2-weighted, (C) axial fat-suppressed precontrast T1-weighted, (D) axial postcontrast subtraction, (E) axial diffusion-weighted, and (F) axial ADC pelvic MR images show an enhancing and diffusion restricting solid component (white arrow) along the anterior and inferior wall of a right ovarian endometrioma. Note the loss of T2 shading within the endometrioma. White star—uterus. Surgical pathology showed endometrioid adenocarcinoma arising in the right ovarian endometrioma.

Fig. 16 A 27-year-old patient with ovarian endometrioma showing loss of T2 shading in a large endometrioma arising in the adnexa and extending into the abdomen. (A) Transabdominal ultrasound shows a cyst arising from the pelvis and extending into the abdomen, displaying homogeneous low-level internal echoes with a ground-glass appearance. (B) Sagittal T2-weighted, (C) axial T2-weighted, (D) axial fat-suppressed precontrast T1-weighted, and (E) axial postcontrast T1-weighted pelvic MRI images show a nonenhancing T2 hyperintense and markedly T1 hyperintense abdominopelvic cyst arising from the left adnexa. White star—uterus; white arrow—pathology-proven left ovarian endometrioma.

The most common types of EAOCs are endometrioid adenocarcinoma and clear cell adenocarcinoma, accounting for around 10% of all ovarian carcinomas in Western countries. While clear-cell carcinoma occurs more frequently in Asian countries, endometrioid adenocarcinoma is known to be more prevalent (75%) in Western countries.[67] A mixed clear cell-endometrioid carcinoma category has been recently introduced for tumors that displayed well-defined patterns of both subtypes with any percentage of admixture.[68] [Fig. 17] illustrates the main histological subtypes of EAOCs. The other types of neoplasms include endometrioid stromal sarcoma, mesodermal (Mullerian) adenosarcoma, and carcinosarcoma. Early detection is important for improving prognosis and preserving fertility in patients, as clear cell carcinomas generally have poor prognosis due to relative resistance to current chemotherapy regimens.

Fig. 17 Histology of malignancy arising in ovarian endometriomas. (A) Gross specimen and (D) high-power histology of ovarian clear cell carcinoma, showing atypical cells with pale to eosinophilic cytoplasm (white arrowheads), tubulocystic and papillary growth patterns, and hyalinized papillary cores (black arrowheads). (B) Gross specimen and (E) high-power histology of endometrioid adenocarcinoma, showing back-to-back, atypical endometrioid glands with areas of cribriform growth (red arrowhead). (C) Gross specimen of mixed clear cell-endometrioid adenocarcinoma, (F) high-power histology of an endometrioid carcinoma component with complex glandular growth of atypical cells with hyperchromatic nuclei (yellow arrowhead) and (G) high-power histology of a clear cell carcinoma component, showing a papillary growth pattern of atypical cells with eosinophilic to clear cytoplasm (green arrowheads).

Mimics of Ovarian Endometriomas

Few entities may be potentially confused with an endometrioma due to a certain degree of overlap in imaging features. The ultrasound appearance of an endometrioma with mobile low-level internal echoes can be seen in mucinous ovarian tumors or tubo-ovarian abscesses. To differentiate these two entities, additional imaging with MRI and a history suggestive of infection can be useful. The echogenic mural nodules within the wall of an endometrioma may be mistaken for mural nodules seen in ovarian malignancies. Nodules within a malignant mass are often more hypoechoic, larger, and with internal vascularity on color Doppler. On MRI, T1 hyperintense signal is seen in other adnexal cystic lesions such as hemorrhagic cysts, mature cystic teratoma, mucinous cystadenomas, tubo-ovarian abscesses, and struma ovarii.[34] [69] Hemorrhagic cysts are typically single and unilateral with mild, heterogeneous, or peripheral T1 hyperintense signal ([Fig. 18]). These decrease in size over time, unlike endometriomas, which typically do not resolve on short-term follow-up.[33] The T1 hyperintense signal within a mature teratoma is often heterogeneous and due to the presence of fat, which disappears on fat-suppressed images ([Fig. 19]).[33] The mucin within tumors, such as mucinous cystadenomas, can appear bright on T1-weighted images with blood clots simulating the T2 dark spot of endometriomas caused by hemorrhage and calcifications within them. However, as opposed to the homogenous T1-hyperintensity seen in an endometrioma, mucinous cystadenomas are typically multilocular with variable hyperintensity between locules due to variable mucin concentration referred to as “stained glass” appearance ([Fig. 20]).[33] Struma ovarii, also called ovarian goiter, is a highly specialized form of teratoma, entirely or predominantly composed of thyroid tissue consisting of large follicles filled with colloid material, the latter responsible for T1-hyperintense and T2-hypointense signal. They present as large multilocular cystic masses showing variable signal intensity on MRI. Intracystic areas of high T1 signal with corresponding low T2 signal may be seen ([Fig. 21]).

Fig. 18 A 39-year-old patient with an ovarian hemorrhagic cyst, mimicking an endometrioma. (A) Sagittal transvaginal pelvic ultrasound image at baseline shows a thin-walled unilocular cyst with reticular lace-like echoes. (B) Axial fat-suppressed precontrast T1-weighted, (C) axial T2-weighted, and (D) sagittal postcontrast subtraction pelvic MR images show a right ovarian hemorrhagic cyst with inhomogeneous T1 hyperintensity and a peripheral T1 hyperintense and T2 hypointense rim (white arrows). Note the smaller endometrioma immediately anterior to it (yellow arrowhead). (E) Transverse transvaginal pelvic ultrasound image shows complete resolution of the hemorrhagic cyst on 6-week follow-up.

Fig. 19 A 56-year-old patient with a mature cystic teratoma (dermoid cyst). (A) Sagittal transvaginal pelvic ultrasound image shows a complex cystic right adnexal lesion (white arrow) with an echogenic dot-and-dash appearance and mural Rokitansky nodules (yellow arrowheads). (B) Axial precontrast T1-weighted, (C) axial fat-suppressed precontrast T1-weighted, (D) sagittal T2-weighted, and (E) axial fat-suppressed postcontrast T1-weighted pelvic MR images show a nonenhancing T1 and T2 hyperintense cystic adnexal lesion with complete signal suppression on fat-suppressed images (white arrows) confirming the presence of fat, diagnostic of a mature cystic teratoma.

Fig. 20 A 53-year-old patient with an ovarian mucinous cystadenoma. (A) Transverse transabdominal ultrasound image shows a multilocular cystic adnexal lesion (white arrow) with thin septations (yellow arrowhead). (B) Axial fat-suppressed precontrast T1-weighted, (C) axial T2-weighted, and (D) axial fat-suppressed postcontrast T1-weighted pelvic MR images show a multilocular cystic adnexal lesion (white arrows) with thin enhancing wall and septations (yellow arrowheads), and variable T2 signal intensity (“stained glass” appearance) with T1 iso- to mild hyperintensity of its contents (mucin) due to varying levels of hydration.

Fig. 21 A 29-year-old patient with bilateral ovarian cysts with struma ovarii. (A) Axial T2-weighted, (B) axial precontrast T1-weighted, (C) axial fat suppressed precontrast T1-weighted, and (D) axial fat-suppressed postcontrast T1-weighted pelvic MR images show multilocular cystic adnexal masses bilaterally with few locules filled with variable T2 hypointense signal and mild T1 hyperintense signal of their contents (colloid material; right—white arrows, left—yellow arrows). Surgical pathology revealed bilateral ovarian cysts with fragments of struma ovarii.

Implications on Management

Pain

Although pain can be one of the important symptoms impacting the management of patients with endometriosis, a thorough clinical investigation is useful to determine the extent of the disease, as it does not necessarily correlate with the severity of pain.[70] [71] Other nongynecological causes of abdominopelvic pain should also be ruled out prior to medical or surgical management of endometriosis.[72] The choice of management depends on patient preferences, cost, availability, and individual efficacy of the method in use. Among these are nonsteroidal anti-inflammatory drugs (NSAIDs), hormonal treatment (combines oral contraceptives or progestins, etc.), and surgical options.[22]

Infertility

The prevalence of infertility among women affected by endometriosis has been estimated to range from 30 to 50%. Multiple theories explain endometrioma-associated infertility. Endometriomas can develop contiguously with the ovarian cortical surface, compromising clusters of primordial follicles that constitute the ovarian reserve and induce fibrosis, leading to a decrease in follicular density.[73] Additionally, these may induce significant inflammation in the surrounding tissue, thus affecting the functionality of the ovarian cortex that houses the reservoir for dormant follicles.[73] [74]

The pathophysiology involves various signaling pathways such as PI3K/PTEN/Akt/FOXO3, PI3K/Akt/mTOR, and Hippo/YAP, which contribute to elevated rates of primordial follicle activation.[75] Kitajima et al. demonstrated that this accelerated activation correlated with an increased incidence of early follicle atresia compared with the contralateral ovaries.[76]

Surgical excision of endometriomas has the potential to negatively impact ovarian reserve through the removal of healthy ovarian cortex or compromising ovarian blood flow.[73] Nonsurgical techniques, such as sclerotherapy, have been used for treatment. In a meta-analysis by Gun Ha Kim et al., the pooled technical efficacy of sclerotherapy was found to be 98.3%. In their study, the estimated rates of recurrence, pain resolution, and pregnancy were 13.8, 85.9, and 37.6%, respectively. Regardless of the impact of endometriomas on women's fertility, the surgical intervention itself was noted to negatively affect both the ovarian reserve and the levels of anti-Mullerian hormone.[77]

Conclusion

Endometriomas represent the most commonly recognized manifestation of endometriosis on imaging, yet their presentation can extend beyond the classic appearance in the ovaries or adnexa. The identification of an endometrioma should prompt a thorough evaluation for DE, a more severe form of the disease that significantly impacts patient management. Any enhancing nodule within an endometrioma should be considered malignant unless proven otherwise and sent for surgical intervention. Due to increased risk of ovarian cancer in patients with endometriosis, current recommendation using O-RADS guidelines is to follow them for 2 years and subsequently based on clinical scenario. Awareness of other complications associated with endometriomas includes rupture or torsion. A decidualized endometrioma is an important mimicker of malignancy in a pregnant patient. In nonpregnant patients, other adnexal masses can mimic a typical endometrioma and MRI can help distinguish between them.

Conflict of Interest

None declared.

Acknowledgment

We acknowledge the contributions of Priyanka Prajapati, MD, in the initial stages of manuscript preparation.

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Publication History

Article published online:
22 May 2025