in benign teratomas may occur at any age group. Currently, there is no evidence of an advantage of PET/CT over MRI for ­characterization of complex adnexal masses (Lee and Catalano 2015; Iver and Lee 2010).

7.1.2\ Peritoneal Carcinomatosis

Peritoneal carcinomatosis is the typical pathway of tumor dissemination in advanced ovarian cancer (Fig. 5). It is determined by the complex anatomy of the peritoneal cavity and follows the clockwise pattern of the peritoneal fluid circulation along the paracolic gutters toward the diaphragm and downward (Lengyel 2010; Patel et al. 2011). Although all peritoneal parietal and visceral surfaces may be involved, common sites of peritoneal implants in ovarian cancer include greater omentum, paracolic gutters, the pouch of

a

Douglas, surfaces of the liver and diaphragm, and bowel surface. Less frequent sites of dissemination are the mesentery, splenic surface, along the porta hepatis, lesser sac, and the gastrosplenic ligament (Forstner et al. 2010; Nougaret et al. 2012). Peritoneal metastases are characterized by a broad spectrum of imaging findings. They may display as nodular soft tissue lesions or as more subtle findings including linear or plaquelike thickening of the parietal or visceral peritoneum (Fig. 6). Implants from serous tumors may display tiny calcifications only. Besides nodular lesions, thickening of the root of the mesentery with a stellate radiating pattern or ill-defined nodular lesions have been described in metastases of the mesentery (Fig. 7) (Nougaret et al. 2012). The majority of peritoneal lesions show moderate enhancement after IV contrast medium.

b

Fig. 5  Peritoneal implants. Findings in FIGO stage IIIC ovarian cancer are shown in an anterior (a) and posterior (b) coronal CT plane. Ascites, mild peritoneal thickening, and multiple solid peritoneal implants along the anterior abdominal wall and in the transverse

mesocolon (arrow) are demonstrated in (a). A large implant in the right paracolic gutter (arrow) resembles the morphology of the thick-walled cystic and solid adnexal tumors, which present bilateral ovarian cancer (b). U uterus

Fig. 6  Peritoneal implants. Coronal (a) and transaxial CT of the upper abdomen (b). Linear thickening of the parietal peritoneum is seen throughout the abdomen and pelvis in a patient with large amounts of ascites (a). The diffuse linear

thickening of the diaphragm is better appreciated on the transaxial plane (b). Other findings include bilateral focal diaphragmatic implants and broad band-­like tumors (arrows) adjacent to the transverse colon presenting omental cake

Fig. 7  Diffuse mesenterial involvement in high-grade serous cancer. Ill-defined mesenterial linear and nodular lesions (arrow) are seen in the root of the mesentery

Rarely, mixed solid and cystic or purely cystic lesions are found. The latter may mimic loculated ascites; however linear enhancement or tiny mural nodules may indicate the tumorous deposits. In MRI delayed enhancement at 3–10 min after gadolinium has been described to improve the detection of peritoneal metastases (Low et al. 2005). The omentum accounts for the most common site of peritoneal metastases, with the inframesocolic

omentum more often involved than the supramesocolic omentum (Fig. 8). They are typically located between the abdominal wall and bowel loops. If they coalesce they are termed omental cake. Netlike omental involvement is more difficult to evaluate. In liver surface implants, peritoneal deposits of the liver capsule should be differentiated from invasive implants, as the latter usually are not resectable (Akin et al. 2008). Bowel surface or mesenterial implants can cause tethering of bowel loops and may lead to obstruction. However, this is more likely to occur in recurrent ovarian cancer (Low et al. 2003). Depiction of peritoneal implants depends on their size and on the presence of ascites. In CT the problem of diagnosing small peritoneal implants is expressed by the sensitivity of only 25–50% for lesion size of less than 1 cm in size (Coakley et al. 2002). The performance of CT, however, improved to a sensitivity of 85–93% and a specificity of 91–96% for peritoneal disease larger than 1 cm in size (Coakley et al. 2002). Although CT has been established as primary imaging modality to assess peritoneal malignant disease, MRI has the potential to become the new standard of the reference (Rockall 2014). It seems superior to CT

Fig. 8  Omental implants. Transaxial CT (a–c) and transaxial fat-saturated T1-weighted image (d) in four different patients. Omental implants (arrows) may display a broad

spectrum of findings ranging from a netlike pattern (a) to cotton-like (b) and nodular lesions (d)

in detecting peritoneal implants (Fig. 9), particularly in the absence of ascites (Low et al. 1999, 2015). Diffusion-weighted MR imaging enables direct visualization of implants at sites that are otherwise difficult to assess throughout the peritoneal cavity and is superior in pelvic imaging to CT (Rockall 2014). In a prospective comparative study with surgery as standard of reference, whole-body MRI using DWI was superior to CT and to PET/CT in assessing bowel serosal and mesenteric disease (Michielsen et al. 2014). Another comparative study found no significant differences between CT, MRI, and PET/CT in assessing ovarian cancer. In this study PET/CT was best for assessment of supradiaphragmatic metastases (Schmidt et al. 2015). It seems that currently the role of PET/CT for staging primary ovarian cancer staging is limited (Rockall 2014). Most studies report slightly improved lesion conspicuity of PET/CT (sens. of 77–100%) over CT alone (sens. of 60–97%) (Pfanneberg et al. 2013). In one study combined PET/CT achieved a sensitivity of 88% compared to 84% for CT and 63% for PET alone in patients undergoing hyperthermic intraperitoneal chemotherapy (Pfanneberg et al. 2013). In PET/CT false negatives may occur due to small tumor size (5–10 mm) and FDGnegative tumors (Patel et al. 2011). False positives may occur in nonmalignant and inflammatory peritoneal diseases (Michielsen et al. 2014; Pfanneberg et al. 2013).

7.1.3\ Ascites

Small amounts of pelvic fluid in the cul-de-sac present a physiological finding and may be found throughout the cycle in the reproductive age. Ascites is defined as fluid outside the pouch of Douglas according to the International Ovarian Tumor Analysis (IOTA) group (Timmerman et al. 2000). In ovarian cancer, pelvic ascites may be a finding of stage I disease. Large amounts of ascites in a patient with ovarian cancer usually indicate stage III disease. In ovarian cancer the presence of ascites alone had a PPV of 72–80% for peritoneal metastases (Coakley et al. 2002).

The absence of ascites may not exclude a malignant disease, as 50% of borderline tumors and 83% of early-stage ovarian cancers are not

associated with ascites (Ozols et al. 2001). Peritoneal carcinomatosis is characterized by various amounts of ascites and diffuse or focal peritoneal thickening. Benign forms of ascites displaying the same pattern, such as postoperative inflammatory changes, bacterial peritonitis including tuberculosis, or chronic hemodialysis, often cannot be differentiated from peritoneal carcinomatosis (Diop et al. 2014; Levy et al. 2009).

7.2\ Pathways of Spread

in Ovarian Cancer

Knowledge of the pathways of tumor spread is pivotal for the interpretations of findings in CT and MRI, and they are the basis for staging of ovarian cancer. Ovarian cancer spreads primarily by direct extension to neighboring organs, by exfoliating cells into the peritoneal cavity that can implant on parietal and visceral peritoneum throughout the peritoneal cavity. It also disseminates by lymphatic pathways and less commonly metastasizes hematogenously. Locoregional spread of ovarian cancer occurs by continuous growth along the surfaces of the pelvic organs and pelvic sidewalls. Peritoneal spread and implantation outside the pelvis is caused by tumor cells that are able to slough off the ovary and enter the peritoneal circulation. Peritoneal implants are also disseminated throughout the lymphatic vessels of the peritoneum.

Tumor spread along the lymphatic pathways is found along three routes. The main pathway of lymphatic spread is along the broad ligament and parametria to the pelvic sidewall lymph nodes (external iliac and obturator chains) and along the ovarian vessels to the upper common iliac and para-aortic lymph nodes between the renal hilum and aortic bifurcation. Drainage to external and inguinal nodes via the round ligaments accounts for the rarest route of lymphatic tumor spread. In advanced ovarian cancer, the presence of nodal spread is reported in 40–60% (Ozols et al. 2001; Bachmann et al. 2016). In a series of 130 patients mostly with serous ovarian cancer, the rate of nodal metastases was 75%. In almost half of the cases, both metastases­