If both pre-assessment probability and imaging studies demonstrate low probability of malignancy, additional tests can be avoided [3].

The most challenging decision-making cases are the ones with intermediate risk for malignancy. A large proportion of intermediate-risk adnexal masses represent benign entities. Tests with greater specificity allow point-of-care triage that may obviate the need for surgery that would otherwise be purely for diagnostic purposes. However, in case of malignancy they would potentially offer a more timely diagnosis than a “watch and wait” strategy with interval ultrasound reassessment [3]. Tumor markers such as CA125 may be selectively performed, particularly in the postmenopausal population in which specificity is higher. Alternatively, surgical evaluation can be considered if the perceived risk for malignancy justifies this intervention [3].

If there is sufficiently high risk, then additional diagnostic studies may not be necessary, and clinicians may wish to proceed with studies most relevant to surgical planning and gyne-oncology referral [3].

Cystic masses may include nonneoplastic cysts, benign neoplasms, and borderline neoplasms. Functional cysts, para-ovarian cysts, hydrosalpinx, endometriotic cysts, serous cystadenomas, mucinous cystadenomas, and mucinous cystic tumors of borderline malignancy are the ovarian cystic lesions most frequently found.

In general, a combined cystic and solid mass strongly supports the diagnosis of ovarian malignancy. Primary epithelial carcinomas and metastatic tumors often show a cystic and solid appearance. Mature cystic teratoma is the important exception to this appearance.

Predominantly solid ovarian masses include benign, borderline, and malignant tumors. The main entities are fibrothecomas, Brenner tumors, granulosa cell tumors, dysgerminomas, epithelial ovarian carcinomas, and metastatic carcinomas.

Ovarian cysts below 3 cm are generally considered physiological. These entities can be divided into functional (associated with hormone production) or nonfunctional [32]. Functional cysts comprise follicular cysts, corpus luteum cysts, and uncommon cysts such as the theca–lutein cysts [33] (Fig. 6.1). Simple cysts are thin-walled (<3 mm), unilocular, and below 3 cm in diameter, but can occasionally grow larger. They usually develop during reproductive age, but may also be found in postmenopausal age and are almost always asymptomatic. The majority are follicular cysts and result from failure of rupture or of regression of the Graafian follicle. They are usually self-limiting and usually regress spontaneously within 2 months. Sometimes they are complicated by rupture and may cause abdominal pain and hemoperitoneum [7]. Most functional cysts appear as unilocular small cystic lesions with high signal intensity on T2-weighted images and intermediate to low signal intensity on T1-weighted images, reflecting simple fluid content. Hemorrhagic cysts usually present high signal on T1-weighted images [10, 34]. The thin wall of functional cysts is best depicted on T2-weighted images as a hypointense structure and on contrast-enhanced images as hypervascular in respect to ovarian stroma [11, 35, 36]. When below 3 cm of diameter, they cannot be differentiated from mature follicles. Unilocular cystadenomas may mimic functional cysts, but a follow-up that shows regression over 2–3 ovarian cycles allow the diagnosis of functional cyst. Corpus luteum cysts may get bigger in size because of internal hemorrhage [2, 37, 38]. Hemorrhagic and corpus luteum cysts usually have thicker walls with relatively higher signal intensity on T1-weighted images and intermediate to high signal intensity on T2-weighted images [11]. Among nonpregnant women, corpus luteum cysts derive from failure of regression or hemorrhage into the corpus luteum [2]. Theca–lutein cysts develop when choriogonadotropin levels are abnormally increased – e.g., in the gestational trophoblastic disease or in the ovarian hyperstimulation syndrome [31, 39]. Progesterone production may persist in corpus luteum cysts, therefore resulting in dysmenorrhea. When these cysts are large in size, they can cause abdominal pain because of rupture, hemorrhage, or torsion. Corpus luteum cysts often require indeed up to 3 months to regress [2, 7]. Both corpus luteum cysts and endometriomas may show hemorrhagic content; however, a prominent T2 shading can be observed only in endometriomas, while corpus luteum cysts contain less concentrated hemoglobin, so the T2 shading is less common [32, 40]. Internal debris and fibrin clots can be differentiated from papillary projections of epithelial tumors by their lack of enhancement [32].

External endometriosis is defined as the condition in which endometrial tissue is found in extrauterine sites [40, 41]. Endometrioid cysts, or endometriomas, are benign entities that can reach fairly large dimensions [40]. Malignant transformation is a rare complication (less than 1 %), and the most common histological subtypes include endometrioid and clear cell carcinoma [42].

External endometriosis mainly affects ovaries [41] and bilateral ovarian involvement occurs in 30–50 % of patients [43]. Endometriomas contain an obliterated loculus, lined by endometrial glands [44, 45]. These lesions range from cystic to solid appearance, depending on cyclic modifications under hormonal stimulation – likewise the normal endometrium. As a result, endometriomas may enlarge [7] and their walls can become fibrotic and thickened and may present an irregular external border [46]. These aspects have been explained with the attitude of endometrial loculi to perforate, producing a severe fibrosis as a result of the irritating effect of blood, with subsequent adhesion to the surrounding structures. Another hypothesis is that endometrial cysts have a free exit to the peritoneal cavity and are necessarily sealed off by organized blood or adhesions to surrounding organs [7]. Malignant transformation is a rare complication (less than 1 %); the most common histological subtypes include endometrioid and clear cell carcinoma [42, 47].

On MRI endometriomas usually present as multiple hemorrhagic cysts [34, 48–50]. They have an iron concentration many times higher than even the whole blood [51–53], and this characteristic gives them their typical very high signal intensity on T1-weighted fat-suppressed images and low signal intensity on T2-weighted images [54]. Homogeneous T2 shading, defined as signal loss on T2-weighted images [55], is a characteristic feature of endometriomas, and it mainly depends on their age and the amount of hemosiderin [56]. Other MRI findings include: adhesion to surrounding organs, a distinct low-intensity zone surrounding a cyst loculus on both T1- and T2-weighted images (thick fibrous capsule), loculus content with short T1 and T2 values (recent hemorrhagic content), dependent layering and a T2-hypointense fluid level representing different-aged blood products, and a hypointense peripheral ring caused by hemosiderin staining in chronic lesions [7, 34]. Non-cystic endometriomas may be difficult to identify due to their small size. Nevertheless, these implants are obviously more evident on fat-saturated T1-weighted images and show low signal intensity on T2-weighted images due to fibrosis surrounding glandular islands [57–60]. DW imaging may aid in differentiation between clots and clear cell cancer development within almost-solid endometriomas [48, 60, 61].

Cystadenomas are common epithelial ovarian tumors. Two main histological cystadenomas subtypes have been identified: serous and mucinous [33]. Although an overlap exists, imaging features may aid in the differentiation of serous from mucinous cystadenomas [5].

They account for 40–50 % of benign ovarian tumors in the reproductive age, with an increasing frequency with age, so that after menopause cystadenomas account for up to 80 % of the benign ovarian tumors [5, 32]. Cystadenomas are thin-walled unilocular or multilocular cystic lesions filled with serous or mucinous content, sometimes showing hemorrhagic content [22]. Papillary projections within cystic walls are rarely found; therefore, these findings should raise the suspicion of malignancy [22, 62, 63]. Serous and mucinous cystadenomas differ in pathology and prognosis. Serous cystadenomas account for 20–40 % of all benign ovarian neoplasms, with a peak incidence in the 4th to 5th decade of life, and up to 20 % of them are bilateral. They are often unilocular and the inner lining may be smooth or have gross papillary projections [5, 33, 64] (Fig. 6.2). Mucinous cystadenomas account for 20–25 % of benign ovarian neoplasms. They are more common during the 3rd to 5th decade of life and are bilateral in only 2–5 % of cases. They tend to be larger at the time of presentation and are more frequently multilocular, with different contents of the loculi. Mucinous cystadenomas are lined by a single layer of tall, columnar epithelial cells and contain a sticky gelatinous fluid; rupture of a mucinous cystadenoma can result in pseudomyxoma peritonei [5, 22, 25]. At MRI serous cystadenomas have simple fluid signal and hypointense on T1- and hyperintense on T2-weighted images. In contrast, mucinous cystadenomas have often various signal intensities depending on the content of different loculi, varying from simple fluid to proteinaceous to hemorrhagic. Mucin has lower intensity than serum on T2-weighted images. Rarely, mucinous cystadenoma can present as a simple cyst [5].

Adenofibromas and cystadenofibromas are classified as surface epithelial–stromal tumors. They represent about half of all benign ovarian cystic serous tumors and are usually found in women aged 15–65 years [65]. Imaging features are nonspecific and may be similar to malignant or borderline tumors [66]. In fact, the variable amount of fibrous stroma determines various aspects, from oligocystic to complex cystic with solid components or even totally solid, that can mimic ovarian cancer [22, 67]. Almost half of the patients with cystadenofibroma have an abnormal contralateral ovary [68]. Adenofibromas and cystadenofibromas are histologically characterized by fibrous tissue components with epithelial elements, similar to those of ovarian cystadenomas. They can also be completely cystic, with microscopic stromal foci, and their margins are usually well defined and smooth [22, 59, 69]. A black spongelike appearance on T2-weighted images is characteristic of these tumors, consisting of tiny high T2 signal intensity foci within very hypointense solid components, reflecting small cystic glandular structures within a dense fibrous stroma [60]. The majority of solid components shows very low T2 signal intensity and minimal enhancement [5, 6, 33, 60, 70]. Low signal intensity and diffusely or partially thickened cystic wall on T2-weighted images are features suggestive of cystadenofibroma [62] (Fig. 6.3). On DW images, the majority of fibromas and fibrothecomas show both low signal intensity on high-b-value images and low corresponding ADC values (mean 1.156 × 10⁻³ mm²/s) owing to collagen-producing fibroblasts and a dense network of collagen fibers and also to the T2 blackout effect [24, 25, 60]. Fibrothecomas with degeneration may display intermediate to high signal intensity on high-b-value images [33, 64, 65, 71]. The presence of prominent solid components with high T2 signal intensity and strong enhancement are typical for cystadenocarcinofibroma [62].

Brenner tumors are rare (1–3 %), mostly benign and incidentally found solid tumors, belonging to the epithelial surface derived tumors. They are composed of transitional cells with dense stroma, and a malignant component is rare [54]. They represent about 2–3 % of ovarian tumors and usually occur at a mean age of 50 years. They are usually small (<2 cm), solid, and unilateral [54]. Cystic components can be found in Brenner tumors, and in 20–30 % of cases they are associated with mucinous cystadenomas or other epithelial neoplasm [32, 54, 72, 73]. Brenner tumors may rarely produce estrogen; therefore, they can be associated with endometrial thickening [67]. On T2-weighted MR imaging, the dense fibrous stroma presents low signal intensity, similar to that of a fibroma. Extensive amorphous calcification is often present within the solid component [62, 67, 68]. On DW images, Brenner tumors show both low signal intensity on high-b-value images and low corresponding ADC values (mean 1.156 × 10⁻³ mm²/s) owing to collagen-producing fibroblasts, to a dense network of collagen fibers, and also to the T2 blackout effect [64, 65]. The combination of a multi-septated ovarian tumor with a solid part with extensive calcifications may suggest the presence of a collision tumor consisting of a Brenner tumor and a cystic ovarian neoplasm, like cystadenoma [54].

These are relatively common benign ovarian lesions, containing structures derived from the three germ cell layers. At imaging, the presence of fat within a cystic ovarian mass is pathognomonic for a mature cystic teratoma [74]. They are the most common ovarian neoplasms below 45 years of age, accounting for up to 70 % of tumors in women below 19 years of age [75]. They are usually unilateral, with only 10–15 % of dermoids found bilaterally [54]. They can be divided into three categories, among which mature cystic teratomas account for 99 %; less common types are the monodermal, which include struma ovarii and carcinoid tumors [54]. Although all three germ cell layers are present, ectodermal components predominate [63]. In the vast majority (88 %), dermoids are unilocular cystic lesions; a protuberance, called Rokitansky nodule or dermoid plug, projects into the cavity and is the hallmark of dermoids. Mature teratomas typically have a lipid content (90 %), consisting of sebaceous fluid, or adipose tissue within the cystic wall or the dermoid plug [73]. The Rokitansky nodule contains a variety of tissues, often including fat and calcifications, which represent teeth (31 %) or abortive bone [54, 74, 76]. A minority (8 %) of dermoid cysts do not demonstrate fat [74]. Dermoids are usually asymptomatic, incidentally discovered, and tend to grow slowly [77, 78]. Malignant degeneration, torsion and rupture, which can cause acute abdomen due to granulomatous peritonitis caused by leakage of the fatty content, can be present [79]; in particular, malignant degeneration, mainly arising from the dermoid plug, occurs in up to 2 % and is usually found in the 6th to 7th decades of life. The risk of malignancy is associated with larger size (>10 cm) and postmenopausal age [80]. Capsule perforation is a sign for malignant transformation of a mature teratoma [81]. At MRI mature teratomas are usually round or oval and sharply delineated; the lipid-laden cyst fluid shows high signal intensity on T1-weighted images and intermediate signal intensity on T2-weighted images (Fig. 6.4). Fat has a high signal intensity on T1- and T2-weighted fast spin-echo images and loss of signal on fat-saturated T1-weighted images. Chemical shift artifacts can be observed, differentiating fat from hemorrhage. There are some typical internal patterns, such as palm tree-like protrusions or dermoid nipples [40, 82, 83]. Calcifications can be missed on MRI due to the low signal intensity on both T1- and T2-weighted images. The presence of sebaceous fluid floating in the peritoneal cavity can suggest rupture [72]. Low ADC values caused by keratin may be useful in differentiation of mature teratomas with little fat from other cystic tumors; despite this, chemical shift imaging seems a better alternative [22, 35, 51]. MR fat-suppressed or chemical shift images are reliable for the differentiation of fat from hemorrhage [84]. In particular, when no or small amounts of fat are present, dermoids cannot be distinguishable from benign cystic ovarian tumors or ovarian cancer [79]. Monodermal teratomas are solid lesions, mainly or exclusively composed of one tissue type. They include struma ovarii, ovarian carcinoid tumors, and tumors with neural differentiation. Monodermal teratomas are typically solid lesions [22]. Struma ovarii is the most common type (3 %); it consists of mature thyroid tissue, but a mixed morphology with acini filled with thyroid colloid, hemorrhage, fibrosis, and necrosis can be found. Rarely, struma ovarii may produce thyrotoxicosis. They present as cystic or multilocular lesions with loculi displaying high signal intensity on T1- and T2-weighted images, without fat [85].

They are sex cord–stromal tumors, composed of spindle cells forming a variable amount of fibrosis and other cells [33] and can occur in both pre- and postmenopausal women. They are solid tumors accounting for 3–4 % of all ovarian tumors, typically unilateral (90 %), occurring in middle-aged and peri- and postmenopausal women. Fibromas are composed of whorled bundles of spindle-shaped fibroblasts with abundant collagen [18, 22, 86]. Fibromas are important from an imaging standpoint because they mimic malignant neoplasms. They can also be associated with ascites and rarely with pleural effusion [87, 88]. The association of an ovarian fibroma, ascites, and pleural effusion is known as Meigs syndrome. Thecomas and fibrothecomas can have estrogenic activity [63]. Bilateral fibromas are also present in basal cell nevus syndrome, along with basal cell carcinomas, bony, ocular, and brain abnormalities as well as other tumors [63].

Fibrothecomas are composed of thecal cells with abundant fibrosis. Unlike fibromas, they can have estrogenic activity and may present with uterine bleeding. In more than 20 %, endometrial carcinomas may be present concomitantly [63]. Because of their abundant collagen content, small fibromas and fibrothecomas have imaging features similar to uterine leiomyomas, with intermediate to low signal intensity on T1-weighted images and hypointensity on T2-weighted images. Larger lesions may have an inhomogenous structure with high signal intensity foci within the low signal intensity lesion, representing edema or cystic degeneration [22, 83, 89] (Fig. 6.5). In larger lesions, dense amorphous calcifications are present but not well appreciated because of their low signal intensity on T2-weighted images. Fibromas and fibrothecomas tend to show mild or delayed gadolinium enhancement [22, 83]. Differential diagnosis should be made with ovarian lesions with fibrous components other than fibroma and fibrothecomas that are cystadenofibroma and Brenner tumor [35, 82]. Pedunculated uterine leiomyomas and broad-ligament leiomyomas can appear as ovarian masses and have the same signal intensity features of fibromas and fibrothecomas. The recognition of the interface vessels between the uterus and adnexal mass is a useful tool in differentiating leiomyomas from ovarian fibromas [90, 91].

Sclerosing stromal tumors are rare benign ovarian tumors occurring in young women [92]. They present as large masses with cystic and solid components. On MRI, they show a mixed hyper- and hypointense appearance on T2-weighted images. On dynamic images, the tumors show early peripheral enhancement with centripetal progression. A central area of prolonged enhancement of the mass represents fibrous hypocellular areas. The appearance after contrast medium administration is useful to differentiate sclerosing stromal tumors from fibromas [85, 93, 94].

Worldwide, ovarian cancer accounts for 4 % of all female cancers and is the most frequent cause of death from gynecological malignancy with 239 new cases/year. In the majority of cases, it is a sporadic tumor and presents over the age of 30 years. There is a correlation between age distribution and tumor histology. Epithelial ovarian carcinomas usually present in postmenopausal women, whereas sex cord–stromal tumors and germ cell tumors are prevalent in young women around the age of 20–30 years. Several risk factors for ovarian cancer have been identified: increasing age, nulliparity, early menarche, late menopause, and long-term hormone replacement therapy. There are three recognized hereditary forms of ovarian cancer: breast–ovarian familial cancer syndrome (related to BRCA1 gene mutation), multiple site cancer family syndrome (Lynch II syndrome) and site-specific ovarian cancer. These tumors account for 5–10 % of the total cases; they tend to present mostly in premenopausal women and cause an increased –around 50 % – lifetime risk of developing ovarian carcinoma [95].

The most frequent clinical presentation of all ovarian malignancies consists of abdominal pain and swelling due to the fact that the tumor tends to manifest itself only when it has reached a large size. Functional ovarian neoplasms may present with specific endocrine and non-endocrine syndromes [96]. CA125 is currently the most commonly used serum marker for ovarian cancer, particularly in monitoring treated patients. Its role for initial diagnosis and staging is limited due to low sensitivity and specificity, particularly for stage I ovarian carcinoma. It also has a high false-positive rate in premenopausal women [97].

The gold standard for staging ovarian cancer remains surgery according to the International Federation of Gynaecology and Obstetrics (FIGO) guidelines. Those are based on the concept that ovarian cancer spreads centrifugally from the pelvis into the peritoneal cavity metastasizing outside the peritoneum only in advanced disease (National Comprehensive Cancer Network – NCCN guidelines for ovarian cancer). A TNM classification has also been defined [98] (Table 6.2).