Blood Vessels

The common iliac bifurcation is located approximately at the level of the third to fourth lumbar vertebrae. The common iliac arteries run anterior to the common iliac veins. The common iliac arteries are divided into internal and external iliac arteries at the level of the fifth lumbar to first sacral vertebrae. Two branches of the external iliac artery that can be identified on imaging are the inferior epigastric artery and the deep circumflex iliac artery. The internal iliac arteries course posteroinferiorly and at the lower margin of the sacroiliac joints divide into anterior and posterior trunks.¹

Pelvic Lymph Nodes

Lymphatics from pelvic organs drain to pelvic nodal chains bilaterally and to the retroperitoneum. Familiarity with the lymphatic drainage pathways is of great importance for staging pelvic tumors. Fig. 20-2 illustrates pelvic lymph node groups on axial CT images.

FIGURE 20-2 • A-D, Axial contrast-enhanced computed tomography images depicting pelvic lymphadenopathy. 1, Common iliac lymphadenopathy; 2, internal iliac lymphadenopathy; 3, external iliac lymphadenopathy; 4, obturator lymphadenopathy; 5, inguinal lymphadenopathy.

The most peripheral lymph nodes draining the pelvis are the inguinal nodes (see Fig. 20-2D). The inguinal lymph nodes are divided into superficial and deep groups. The superficial inguinal nodes drain the anus, the perianal skin, and the round ligament of the uterus. The lymph from the gluteal region and the anterior abdominal wall below the level of the umbilicus also drain to lateral nodes in this group. The medial group of superficial lymph nodes receives lymphatics from the perineal genitalia. The lower group of superficial inguinal lymph nodes receives superficial lymphatics from the lower extremity. The deep inguinal lymph nodes are located on the medial side of the femoral vein. They receive efferents from the deep lymphatics of the lower extremity, a small number of efferents from the superficial inguinal nodes, and lymphatic drainage from the glans penis or clitoris. The superficial and deep inguinal nodes drain to the external iliac lymph nodes.¹

The external iliac lymph nodes accompany the external iliac vessels and are divided into medial, posterior, and lateral groups (see Fig. 20-2B and C). The medial group of the external iliac lymph nodes drains the urinary bladder, prostate, membranous part of the urethra, cervix, and upper part of the vagina. The posterior group receives lymphatics from the internal iliac nodes via the obturator lymph nodes. The lateral group drains lymph from the superficial and deep inguinal nodes. The external iliac lymph nodes drain to the posterior and lateral common iliac nodes.¹

The internal iliac nodes accompany the internal iliac vessels and drain lymph from all of the pelvic viscera such as the body of the uterus, the prostate gland, the upper part of the vagina, the seminal vesicles, the vas deferens, the lower part of the ureters, and the bladder (see Fig. 20-2B). They also receive lymphatic drainage from the deeper parts of the perineum, the buttock muscles, and the posterior aspect of the thigh. They send efferents to the external iliac and common iliac chains. The sacral lymph nodes, which drain directly into lumbar lymphatics, and the anatomic obturator lymph nodes, which are occasionally present in the obturator canal, are members of the internal iliac group.¹

The common iliac lymph nodes accompany the common iliac vessels and are divided into lateral, medial, and posterior groups (see Fig. 20-2A). The lateral group directly drains the external iliac lymph nodes. The posterior group receives efferents from both the internal and external iliac lymph nodes. The medial common iliac group receives lymph from the internal iliac nodes. The common iliac nodes drain into the left and right lateral aortic nodal chains, which are part of the lumbar nodes.¹

The lumbar lymph nodes are divided into right lateral aortic, left lateral aortic, and preaortic lymph node groups. The right lateral aortic chain includes paracaval and retrocaval lymph nodes. The preaortic chain also includes precaval lymph nodes.¹

Bones and Muscles

The pelvic skeleton is composed of two paired innominate bones, the sacrum, and the coccyx. The innominate bones are formed by three separate bones: the ilium, ischium, and pubis. The acetabulum, which is a socket for the head of the femur, is formed by the fusion of these three bones on each side laterally. The two innominate bones unite anteriorly at the symphysis pubis and posteriorly at the sacrum.¹

The psoas muscles originate from the vertebral bodies and transverse processes of the 12th thoracic to 4th lumbar vertebrae. At the level of the first sacral vertebra, the psoas muscle unites with the iliacus muscle, which originates from the upper two thirds of the iliac fossa and sacral ala. Then, the iliopsoas muscle inserts on the lesser trochanter of the femur.¹

The levator ani and coccygeus muscles are the main muscles of the pelvic diaphragm. The levator ani muscle originates from the pubis, ischium, and the fascia of the obturator internus muscle and inserts on the coccyx and the anococcygeal raphe. The coccygeus muscle arises from the ischial spine and attaches to the coccyx posterior to the levator ani. The other pelvic floor muscles are the deep and superficial transversalis perinei muscles, the ischiocavernosus and bulbocavernosus muscles, and the external anal sphincter muscle.¹

The obturator internus muscle arising from the anterolateral wall of the true pelvis and the piriformis muscle arising from the lateral aspect of the sacrum insert on the greater trochanter of the femur and form part of the pelvis sidewall.¹

Endometrial Cancer

Endometrial carcinoma is the fourth most common cancer in females and the most common invasive gynecologic malignancy in the United States.⁶ Up to 90% of endometrial cancers are adenocarcinomas. Although the exact causal factors of endometrial cancer are still unknown, two distinct mechanisms may play a role in its origin: (1) unopposed estrogen stimulation, causing endometrial hyperplasia, which then progresses to carcinoma; and (2) spontaneous carcinoma arising from atrophic or inert endometrium.⁷

The most important prognostic factors in endometrial cancer include the histologic grade of the tumor, the stage of the tumor, depth of myometrial invasion, and the lymph node status.⁸ Because of the inability of clinical staging to assess the depth of myometrial invasion or the presence of lymphadenopathy, the International Federation of Gynecology and Obstetrics (FIGO) revised the staging of endometrial cancer to incorporate surgical findings. Surgical staging, however, is not suitable for elderly and obese patients and those with additional medical problems that make them poor candidates for surgery. Noninvasive cross-sectional imaging is particularly helpful in such cases to depict the depth of myometrial invasion, tumor extent, and presence of lymphadenopathy. Pretreatment imaging improves patient care by affecting the type and extent of surgery or radiation treatment or both.³

Ultrasound is a simple technique that can depict endometrial tumors (Fig. 20-4). The use of transabdominal ultrasonography in staging of endometrial cancer is not advocated. However, transvaginal ultrasonography is helpful in the evaluation of myometrial invasion, with accuracy rates varying between 68% and 99%.³ Myometrial invasion is suggested when the tumor disrupts the subendometrial halo and extends asymmetrically into myometrium.⁹ The limitations of ultrasound include: (1) poor soft-tissue contrast resolution, which hampers delineation between tumor, adjacent myometrium, and coexisting pathologic conditions such as uterine leiomyomas; (2) a relatively small field of view, which precludes assessment of the cervix, parametrium, and the lymph nodes, especially in patients with large tumors or large body habitus or both.³

FIGURE 20-4 • Transvaginal ultrasound depicts large heterogeneous mass containing cystic areas within the endometrial cavity.

CT is widely used for the preoperative evaluation of endometrial carcinoma to assess the extent of disease and lymph node status.³ The accuracy of preoperative staging with conventional CT for endometrial cancer varies between 84% and 88%.^10,11 However, even when helical CT was used, magnetic resonance imaging (MRI) was reported to be more sensitive and specific than CT for preoperative staging of endometrial cancer.¹²

At present, magnetic resonance is the most accurate imaging modality for the pretreatment evaluation of endometrial cancer. The reported staging accuracy of MRI for endometrial cancer is between 83% and 92%.^13–15 A suggested MRI protocol includes orthogonal T2-weighted; transverse T1-weighted; and sagittal, dynamic, contrast-enhanced, T1-weighted sequences.³ This protocol is optimal for detection of primary tumor, myometrial and cervical involvement, local spread, and lymphadenopathy.³ Current National Comprehensive Cancer Network (NCCN) guidelines do not suggest a role for fluorodeoxyglucose (FDG)-PET in the management of endometrial cancer.¹⁶ Yet FDG-PET appears highly-sensitive for the detection of metastatic endometrial cancer.¹⁷ When added to MRI or CT, FDG-PET may improve detection of malignant lymphadenopathy^18,19 and visceral²⁰ metastases, changing clinical management in approximately one third to one half of patients.^19,21 FDG-PET combined with CT appears to be more reliable than FDG-PET alone for detecting adenopathy.^18,20,22,23 Evaluation of the primary tumor by FDG-PET is limited, as FDG-PET cannot precisely determine the extent of tumor invasion, and MRI is clearly superior for that purpose. Endometrial tumors are isointense to myometrium on T1-weighted sequences and demonstrate a variable appearance on T2-weighted sequences (Fig. 20-5). Following dynamic administration of contrast, they enhance less than the normal myometrium, which is more marked on early phases.³ Stage 0 (carcinoma in situ) tumors appear as normal or widened endometrium. Stage I endometrial cancers are confined to the uterine corpus. In stage IA, the tumor is limited to endometrium and may demonstrate normal, diffuse, or focal abnormal signal intensity with a smooth endometrial-myometrial interface. Stage IB tumors penetrate into myometrium less than 50% of myometrial thickness with partial or full-thickness disruption of the junctional zone and an irregular endometrial-myometrial interface. In stage IC, the tumor extends into more than 50% of the myometrial thickness; however, the outer stripe of myometrium is intact. Stage II endometrial cancers extend beyond the uterine corpus into the cervix. In stage IIA, the internal os and endocervical canal are widened; however, the low-signal-intensity, fibrous cervical stroma is intact. In stage IIB, fibrocervical stroma is disrupted. Stage III endometrial cancers extend beyond the uterus but not to the true pelvis. In stage IIIA, the outer myometrium is irregular and disrupted. The ovaries may be involved by direct extension or as metastases. Parametrial involvement is seen as disruption of the serosa and direct tumor extension into parametrial fat. Stage IIIB tumors involve the upper vagina. Tumor involvement of the vagina is seen as disruption of the low-signal-intensity vaginal wall. In stage IIIC disease, there is lymph node involvement, which can be diagnosed when the short axis of lymph nodes exceeds 1 cm. Unfortunately, metastatic and hyperplastic lymphadenopathy cannot be distinguished based on signal intensity characteristics. Stage IV tumors extend beyond the true pelvis. In stage IVA there is disruption of tissue planes with loss of the low-signal-intensity of the bladder wall or the rectal wall, or both, indicating invasion of these organs. In stage IVB, there is distant organ metastasis.³

FIGURE 20-5 • Sagittal (A) and axial (B) T2-weighted magnetic resonance images depict endometrial cancer. Note that the low-signal-intensity junctional zone is disrupted, indicating myometrial invasion.

Cervical Cancer

Cervical cancer occurs more commonly in young women with low socioeconomic status. Risk factors include early age at first intercourse, several sexual partners, nulliparity, smoking, and a history of sexually transmitted diseases. There is strong evidence that the human papilloma virus is a main cause of cervical cancer. Cervical cancer arises at the squamocolumnar junction. The two main histologic types are squamous cell carcinoma, which accounts for 80% to 90% of cases, and adenocarcinoma, which has a worse prognosis. Tumor prognostic factors include the histologic grade of the tumor, the location of the tumor (exocervix versus endocervix), tumor volume, depth of stromal invasion, adjacent organ invasion, and lymph node status.⁵

The FIGO staging system includes findings obtained from physical examination, examination under anesthesia, cystoscopy, rectosigmoidoscopy, barium enema, biopsy, intravenous pyelography, and chest radiography. There is a discrepancy between clinical staging and intraoperative or pathologic findings in 20% to 35% of cases depending on the stage of the tumor.^5,24–26 In addition, lymph node metastases and extension into adjacent organs are difficult to detect clinically.

The diagnosis of cervical cancer is made by cytologic examination or biopsy. Imaging is warranted when the tumor diameter is greater than 2 cm, when the clinical examination to determine tumor size is difficult, or when the tumor is primarily endocervical in location. The role of imaging in the pretreatment evaluation of cervical cancer is to define the extent of tumor to decide on a suitable treatment modality.

Ultrasound has a low diagnostic value in cervical cancer staging. The patient’s habitus, lack of soft-tissue contrast, and operator dependence are limitations of ultrasound in the staging of pelvic malignancies.⁵ CT cannot differentiate normal cervical tissue from tumor and is therefore also limited for evaluating tumor size and stromal invasion⁵ (Fig. 20-6). In the staging of cervical carcinoma, CT was found to be 65% accurate and MRI was found to be 90% accurate. In evaluating lymph node metastasis, both modalities had an accuracy of 86%.²⁷ For detection of metastatic adenopathy, FDG-PET has been found more sensitive than CT²⁸ or MRI,^29,30 with equivalent or superior specificity (approximately 95% in all stages).^31,32 FDG-PET is recognized as superior to CT for the detection of abdominal paraaortic lymph node metastases in either early-stage or advanced cervical cancer.^28,31 Paraaortic lymph node metastases carry an adverse prognostic implication, necessitating detection of these sites of disease.^33,34 The superiority of FDG-PET for evaluation of paraaortic lymph node metastases has led to its use in the planning of IMRT for cervical cancer,^35,36 and FDG-PET has been used in planning doses to the primary tumor as well.^37,38 The initial clinical experience suggests that FDG-PET–guided radiotherapy improves and increases tumor irradiation without increasing doses to adjacent organs.³⁸ No large studies of FDG-PET/CT have been reported in presurgical staging of cervical cancer—only FDG-PET has been studied; FDG-PET/CT is expected to be more sensitive and specific than FDG-PET alone, as it has proven in other types of cancer.²³ Possibly, PET/CT findings may be able to limit the extent of surgical lymph node sampling, although the assay is unlikely to be sufficiently sensitive to obviate surgical lymph node staging altogether.²⁹ In a retrospective study, Grigsby and colleagues³⁹ found that patients with pretreatment FDG-PET who showed no evidence of metastases received no benefit from adjuvant chemotherapy as compared with pelvic radiotherapy alone. Whether pretreatment FDG-PET findings are a reliable basis for omitting adjuvant chemotherapy remains to be validated prospectively, in a randomized trial. FDG-PET appears very sensitive for detection of distant metastases, providing a potentially useful means of excluding patients from futile surgery.⁴⁰ The NCCN recommends FDG-PET as part of the pretreatment assessment for patients with cervical cancer of clinical stage IB2 or higher.⁴¹ In disease of a lesser stage and as part of tumor surveillance, the NCCN recommends use of FDG-PET “as clinically-indicated”⁴¹ (Fig. 20-7). In the setting of initial staging or suspected recurrence, FDG-PET (or PET/CT) changes clinical management of cervical cancer patients in approximately 21% to 55% of cases.^42–44

FIGURE 20-6 • Contrast-enhanced axial computed tomography image demonstrates large cervical mass.

FIGURE 20-7 • Fluorodeoxyglucose–positron emission tomography/computed tomography (FDG-PET/CT) of 69-year-old female with cervical cancer. Top row: Pretreatment images, including a maximum-intensity-projection image, anterior view (left); axial fusion PET/CT (middle); and axial CT (right). The pretreatment scan reveals metastatic abdominopelvic retroperitoneal adenopathy (arrowheads) and FDG uptake in the cervical lesion (white arrows). Bladder: grey arrow. Bottom row: 2 months after completion of chemoradiation (4 months after prior PET) tumor activity is no longer evident.

MRI is accepted as the most accurate imaging modality in the staging of cervical cancer and provides important information in selecting patients for surgery or radiation therapy.

Cervical cancer appears as a relatively high-signal-intensity mass within low-signal-intensity cervical stroma on T2-weighted sequences (Fig. 20-8). The contrast enhancement of cervical cancer varies considerably. Because contrast enhancement makes the tumor isointense with the surrounding cervical and parametrial tissue on T1-weighted images, it does not increase the ability of MRI to depict the tumor or stromal or parametrial invasion.^45–49 Contrast enhancement may help in the evaluation of tumor extension into the pelvic wall or adjacent organs.⁴⁵

FIGURE 20-8 • Sagittal (A) and axial (B) T2-weighted magnetic resonance images demonstrate a large cervical mass growing into the uterus.

Stage 0 (carcinoma in situ) tumors are not visible on MRI. Stage I tumors are confined to the cervix. Depending on their size, these tumors may be identified by the high signal intensity they display within a low-signal-intensity cervical ring on T2-weighted images. The depth of stromal invasion can be determined easily. Preservation of a low-signal-intensity cervical stripe is a good indicator for the exclusion of parametrial invasion. Complete disruption of the cervical ring, indicating full-thickness stromal involvement, may hamper exclusion of parametrial involvement. Stage II tumors extend beyond the cervix. In stage IIA tumors, less than two thirds of the upper vagina is involved, which is seen as loss of normal low signal intensity and thickening of the vagina. The tumor is classified as stage IIB when there is parametrial invasion. The tumor extends directly through low-signal-intensity cervical stroma into the parametrium. Stage IIIA tumors extend into the lower third of the vagina, as indicated by the loss of low signal intensity and thickening of the lower part of the vagina. In stage IIIB tumors, there is pelvic side-wall invasion, and hydronephrosis can be seen if there is ureteral involvement. Stage IV tumors invade the bladder or rectum, as indicated by the loss of normal low signal intensity and thickening of the walls of these adjacent structures.^45–49

Signal intensity characteristics are not helpful in differentiating between malignant and hyperplastic lymph nodes. MRI has a sensitivity of 62%, a specificity of 98%, and an accuracy of 93% in detecting metastatic lymphadenopathy in cervical cancer if the upper limit of normal lymph nodes is accepted as 1 cm in the short axis.⁵⁰ MRI and CT are not significantly different in the detection of metastatic lymphadenopathy in cervical cancer.⁵¹ Schwarz and colleagues⁵² prospectively studied 92 cervical cancer patients, with stages ranging from IB1 to IVA, correlating clinical outcomes (progression-free and cause-specific survival) to FDG-PET/CT findings obtained 8 to 16 weeks after completion of treatment (brachytherapy, external beam radiotherapy, and chemotherapy). The post-treatment FDG-PET/CT findings were more predictive of outcomes during the 3- to 5-year follow-up period than was the pretreatment lymph node status. At the 8- to 16-week post-therapy point, patients with a complete response by FDG-PET (i.e., a resolution of all PET evidence of metastatic disease) had a 5-year cause-specific survival rate of 84%. Patients with progressive disease detected by FDG-PET (i.e., new metastatic sites) had a survival rate of 10%. Patients with a partial PET response (i.e., no new disease, with no resolution or partial resolution of the old disease) had a survival rate of 33%. These specific results cannot be generalized to other therapeutic regimens, of course, but they highlight the fact that in patients with cervical cancer (as in patients with numerous other types of cancer), FDG-PET is effective in predicting long-term response to therapy.^53–58 The sensitivity and specificity of FDG-PET for the detection of recurrent cervical cancer appears to be similar in asymptomatic and symptomatic patients.⁵⁹ Data from more than 600 patients, cumulatively, have been reported regarding FDG-PET and the detection of recurrent cervical cancer.^{42–44,59–61} In studies with 40 or more patients,^43,44,59,61 FDG-PET has overall sensitivity ranging from 80% to100% and overall specificity ranging from 76% to 100% for the detection of recurrent cervical cancer.

Cancer of the Vagina

Most of the primary vaginal malignancies are squamous cell carcinomas. Adenocarcinomas are only 5% to 10% of primary vaginal malignancies. Clear cell adenocarcinoma of the vagina is a subtype of adenocarcinoma associated with maternal ingestion of diethylstilbestrol during pregnancy. Vaginal melanomas and vaginal sarcomas are other rare primary vaginal malignancies. In children younger than 6 years of age, the most common primary vaginal malignancy is embryonal rhabdomyosarcoma (sarcoma botryoides). Metastases to the vagina are more common than primary vaginal tumors and usually occur by direct extension from adjacent organs such as the endometrium, cervix, rectum, or bladder.⁶²

The most important prognostic factors in vaginal malignancies are tumor stage and tumor size. Staging of vaginal cancer according to FIGO includes clinical examination, chest x-ray examination, complete blood count, and the biochemical profile. Often cystoscopy, sigmoidoscopy, barium enema, and intravenous pyelography are also included in FIGO staging.⁶²

Cross-sectional imaging has been increasingly used in the evaluation of patients with vaginal cancers. Ultrasound is limited in the evaluation of the cervix and vagina. Both ultrasound and CT have low soft-tissue contrast and are therefore not good enough in depicting early vaginal cancer. CT is useful in the evaluation of advanced disease and in the assessment of lymph node status. MRI has excellent soft tissue resolution and is therefore very useful in evaluating the tumor size, location, and extent of disease.⁶²

On T2-weighted magnetic resonance images, vaginal carcinomas appear as intermediate- to high-signal-intensity masses. When the tumor is confined to the vaginal wall (stage I), the normal low-signal-intensity vaginal wall is intact on T2-weighted sequences. Stage II lesions invade paravaginal tissues but do not extend to the pelvic side wall. On T2-weighted sequences, the interface between fat and tumor is not well defined and there is medium to high signal intensity similar to tumor intensity within paravaginal tissues. In stage III tumors there is increased signal intensity within pelvic floor muscles on T2-weighted images, indicating extension into the pelvic wall. Stage IVA tumors invade the bladder or rectum or extend beyond the true pelvis. Direct tumor extension into the bladder or rectum can be seen as disruption of soft-tissue planes and increased signal intensity within the bladder or rectal wall.⁶²

Little has been written about the use of FDG-PET in vaginal cancer. Vaginal cancer is an FDG-avid disease.⁶³ FDG-PET appears to be more sensitive than conventional CT for detection of metastatic adenopathy.⁶³ In a small study⁴⁰ combining vaginal and cervical cancer patients, FDG-PET was found 100% sensitive for detection of extrapelvic metastases, thus posing FDG-PET as an attractive means for excluding patients from treatments futile in that setting (e.g., pelvic exenteration). One potential false-positive result worth noting is the presence of excreted FDG often found in the vaginal vault; small spots of contamination can mimic soft-tissue disease.

Cancer of the Vulva

Vulvar cancer is a rare malignancy occurring most commonly in women older than age 60. The most common histologic type is squamous cell carcinoma. The other vulvar cancers consist of melanoma, Bartholin gland cancer, Paget’s disease, sarcomas, basal cell carcinoma, and adenocarcinoma.⁶²

Prognosis of vulvar carcinoma depends on tumor size, depth of tumor invasion, and lymph node metastases. CT is useful in the evaluation of advanced disease and lymph node status. MRI is superior to both ultrasound and CT in evaluating local extension of the tumor.⁶²

Stage I vulvar cancers are less than 2 cm in size and can be seen as high-signal-intensity lesions on T2-weighted sequences. Stage II tumors are larger than 2 cm but confined to the vulva. In stage III tumors, there is invasion of the lower urethra with or without involvement of the vagina and anus. A high-signal-intensity mass extending into these structures can be seen on T2-weighted magnetic resonance images. In stage IVA, tumor extension to the upper urethra, bladder, rectal mucosa, or pelvic bones can be seen as areas of intermediate- to high-signal-intensity within these structures.⁶²

Although, to date, no large studies have examined the usefulness of FDG-PET in cancer of the vulva, FDG-PET can provide useful information for treatment planning and post-treatment follow-up in patients with vulvar cancer (Fig. 20-9).

FIGURE 20-9 • Fluorodeoxyglucose–positron emission tomography/computed tomography (FDG-PET/CT) of a 68-year-old woman with recurrent vulvar cancer. Top row: maximum-intensity-projection PET images, showing pretreatment staging scan (left) and follow-up scan (right), 2 months after completion of chemoradiotherapy. Although pelvic adenopathy (arrowheads, left image) resolves, after treatment the vulvar recurrence (arrow) persists and new pulmonary metastases (arrowhead, right image) developed. Axial images of the vulvar recurrence are shown before (middle row) and after (bottom row) treatment; marked metabolic activity persists in this multiple recurrent tumor.

Ovarian Cancer

Ovarian cancer is the fifth most common cause of cancer-related deaths in women and the most common cause of death from gynecologic malignancy.⁶ Approximately 90% of ovarian cancers are of epithelial origin, with subtypes such as serous, mucinous, endometrioid, clear cell, and undifferentiated. Nonepithelial cancers of the ovary include malignant granulosa cell tumor, dysgerminoma, immature teratoma, endodermal sinus tumor, and metastases.^65,66

The FIGO staging system of ovarian cancer reflects the three primary mechanisms of ovarian cancer spread: local, peritoneal, and lymphatic. Stage I ovarian cancer refers to tumor confined to one or both ovaries. Stage II indicates ovarian cancer with peritoneal metastases confined to the true pelvis. Stage III refers to ovarian cancer with extrapelvic peritoneal metastases or nodal disease. Stage IIIA indicates that there are microscopic implants. Stage IIIB refers to implants smaller than 2 cm and stage IIIC indicates that the implants are larger than 2 cm. Stage IV consists of ovarian cancer with distant metastases such as malignant pleural effusion and intrahepatic metastases. The management of ovarian cancer is closely related to stage. The standard of care for FIGO stage I, II, IIIA, and IIIB ovarian cancer is an exploratory staging laparotomy. The standard of care for resectable FIGO stage IIIC ovarian cancer is primary surgical cytoreduction (i.e., debulking) followed by adjuvant chemotherapy. Optimal debulking refers to the reduction of all tumor sites to a maximal diameter of less than 1 cm. The management of FIGO stage IV disease is primary chemo and cytoreduction. Considering different management options, the importance of imaging is in the distinction among FIGO stages IIIA, IIIB, and stage IIIC disease. Furthermore, in the category of FIGO stage IIIC disease, the importance of imaging is in the detection of nonresectable disease. The assignment of FIGO stage IV disease is also important for patient management. There are two potential pitfalls in assigning FIGO stage IV disease. On imaging, the presence of pleural effusion can be benign or malignant. The findings of pleural thickening or nodularity in addition to the presence of pleural effusion indicate the malignant nature of effusion. In the absence of those findings, thoracentesis is essential. The other important distinction is to differentiate liver surface implants (peritoneal spread and therefore stage III disease) from true intraparenchymal metastases (as a result of hematogenous spread and therefore stage IV disease).^65,67 Current NCCN guidelines suggest use of FDG-PET “as clinically-indicated” for monitoring of patients with epithelial ovarian cancer (at any stage) that has demonstrated a complete response to treatment.⁶⁸ Ovarian cancer is composed of several histologic subtypes, possibly with differing levels of FDG-avidity; however, in general, ovarian cancer is FDG-avid.^69–71 FDG-PET and FDG-PET/CT appear superior to conventional CT for staging of newly-diagnosed ovarian cancer.^69,72 For detection of recurrent disease, FDG-PET/CT and MRI appear to be grossly equivalent, overall, in sensitivity and specificity,^73,74 although MRI is superior for detection of peritoneal recurrence after cytoreductive surgery.⁷³ FDG-PET appears to be superior to CT^75–77 for the detection of recurrent disease. These generalities remain to be confirmed by well-controlled prospective trials comparing the modalities. Recurrent disease is best detected by FDG-PET in the setting of a rising cancer antigen (CA)125 value (PET sensitivities reported are approximately 85%, whereas reported PET/CT sensitivities are approximately 95%).^78–80 Only lesions smaller than 6 mm are regularly missed.^81,82 Hence, FDG-PET/CT is capable of detecting “macroscopic” disease amenable to cytoreductive surgery.⁸¹ Rising tumor marker serum levels cannot distinguish local recurrence from spreading disease, so a clear rationale for tumor localization is present in that setting. The lesion-based accuracy of FDG-PET/CT in recurrent ovarian cancer seems superior to that of PET alone.⁸³ Direct comparisons of FDG-PET/CT with CT or MRI in the setting of recurrent ovarian cancer have suffered from patient selection bias (for example, in some studies FDG-PET/CT was performed only in cases in which MRI or CT had already provided negative or equivocal results^74,78,81,84) or have used PET techniques that are no longer state-of-the-art.⁸⁵ Nevertheless, it appears that the addition of FDG-PET/CT to conventional imaging modalities frequently alters therapeutic management (>50% of cases, in some series) in patients with persistent disease or suspected recurrence, usually by detecting unresectable disease or unsuspected distant metastases.^75,78,83,86

In patients with an adnexal mass, ultrasound is very accurate in the assessment of tumor location (e.g., differentiation of uterine from adnexal masses), as well as distinguishing between a benign and a malignant adnexal lesion (Fig. 20-10). In addition to the morphologic features of the mass depicted on gray-scale ultrasound, Doppler ultrasound findings are also very helpful.^87,88 If ultrasound findings are inconclusive, MRI is recommended for further evaluation.⁸⁹ The use of contrast media in MRI allows better characterization of solid nodules within a cystic lesion or the presence of necrosis within a solid lesion. In the characterization of adnexal masses, MRI also demonstrates high inter- and intraobserver agreement.^90,91 CT is not commonly used in the characterization of adnexal masses. Characterization of an adnexal mass on CT relies on the depiction of morphologic features such as enhancing mural nodularity or heterogeneity and necrosis within the solid lesion (Fig. 20-11). The presence of ancillary findings such as ascites and peritoneal carcinomatosis are strong indicators of a malignant adnexal mass on ultrasound, CT, or MRI. For characterizing ovarian tumors, FDG-PET/CT appears at least equivalent to other modalities in sensitivity^69,71 and possibly superior to them in specificity.⁶⁹ The University of Ulm group found FDG-PET (not PET/CT) inferior.^89,92,93 Yet the Ulm reports must be reviewed critically: no reference is made to patients’ menstrual cycles. and PET/CT is generally superior to PET alone in both sensitivity and specificity, especially in the pelvis.^23,76,84 Normal ovaries can demonstrate prominent FDG uptake that is physiologic and variable,⁹⁴ related to the menstrual cycle;^94,95 hence, premenopausal patients with an adnexal mass must be scheduled for FDG-PET at an appropriate day in the cycle to avoid false-positive results; in general, the week before and after midcycle ought to be avoided.

FIGURE 20-10 • Ovarian serous adenocarcinoma. Transvaginal ultrasound depicts a cystic ovarian mass with nodular solid components.

FIGURE 20-11 • Contrast-enhanced axial computed tomography reveals a left ovarian cystic mass with thick nodular wall.

Ovarian cancer can spread by local continuity to the opposite ovary; uterus; and adjacent structures such as the sigmoid colon, urinary bladder, and pelvic sidewall. Imaging criteria for rectosigmoid and urinary bladder invasion include focal obliteration of the fat plane between the tumor and these organs.

Peritoneal spread is the most common route of ovarian cancer spread. Peritoneal nodules are commonly seen in the pouch of Douglas, right paracolic gutter, right subphrenic space, and left paracolic gutter. Peritoneal metastases appear as nodular or plaquelike enhancing soft-tissue masses of varying sizes. Ascites in a patient with ovarian tumor usually indicates its malignant nature. Ascitic fluid often outlines small peritoneal implants, facilitating their detection.

Ovarian cancer can also spread to lymph nodes. Most commonly, nodal disease is seen along the aortocaval and paraortic retroperitoneal sites. Second, nodal spread along the broad ligament can reach the internal iliac, obturator, and external iliac vessels. Third, lymph node involvement can occur via the round ligament to the external iliac and inguinal nodes. Superior diaphragmatic lymphadenopathy is considered distant nodal disease and indicates advanced ovarian cancer. Extra-abdominal lymph node metastases, at presentation, have traditionally been thought to be rare in ovarian cancer based on clinical examination. Yet using FDG-PET/CT, Risum and colleagues⁹⁶ found extra-abdominal nodal metastases in 37% of patients with newly diagnosed ovarian cancer.

Hematogeneous spread from ovarian cancer commonly occurs to sites such as the liver, lung, pleura, adrenal gland, and spleen. Bone and brain metastases are rare.

FDG-PET has demonstrated a considerable ability to predict and monitor the response of ovarian cancer to therapy. For example, detection of large-bowel mesenteric implants by pretreatment FDG-PET/CT was an independent predictor of incomplete cytoreduction in a multivariate analysis (primarily of patients with stage IIIC disease).⁹⁶ In a study of patients with stage IIIC and IV disease, reductions in tumor FDG uptake, induced by presurgical carboplatin-based chemotherapy, were predictive of significantly prolonged survival, whereas clinical response data (including CA125 response) and histopathologic tumor response data were not.⁹⁷