Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

most are mixed with other germ cell elements. The primary form has one of two origins: in association with an ovarian pregnancy and nongestationally as a primary germ cell tumor that differentiates to trophoblastic structures. Some of these tumors result in an elevated serum b-hCG level.

Imaging has a limited role in evaluating these tumors. These are solid and cystic highly vascular tumors. Larger ones become necrotic and bleed.

Metastases to Ovary

Metastases to the ovaries originate both from gynecologic and nongynecologic sites. Among nongynecologic tumors, breast and gastrointestinal tract cancers predominate. Some authors believe that a hallmark of metastases is bilateral ovarian involvement, although a multiinstitutional Radiology Diagnostic Oncology Group study of women with primary ovarian carcinoma and with a secondary ovarian neoplasm found that neither a predominately solid appearance nor bilaterality was significantly different between these two neoplasm groups (61). Some tumors metastatic to the ovary mimic a primary ovarian malignancy. At times a site of tumor origin cannot be established in the face of a widespread tumor spread.

Premenopausal ovaries appear to be more prone to developing metastases, probably because of their increased vascularity compared to postmenopausal ovaries.

Krukenberg Tumor

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oophorectomy and partial gastrectomy has led to long survival or even cure.

These tumors range from mostly solid and mostly cystic to entirely cystic. The cyst walls tend to exhibit strong CT contrast enhancement. Typically, MRI reveals a sharp tumor outline. Occasionally some of the more cystic tumors contain septations. A hypointense solid component on T2-weighted images is common with Krukenberg tumors, a nonspecific finding also seen with primary ovarian neoplasms. However, the presence of such a hypointense component, especially with bilateral ovarian tumors, should suggest a Krukenberg tumor. Some of these tumors contain fat, which is hyperintense on T1-weighted images and exhibits a decrease in signal intensity on fat-sat- urated, T1-weighted images (62).

Mesothelioma

An occasional malignant mesothelioma is confined to one or both ovaries and presumably represents an ovarian primary. More often, however, ovarian involvement occurs in a setting of widespread peritoneal seeding, and tumor origin cannot be determined. In addition, the histologic appearance of mesotheliomas varies considerably, and many of these tumors are either initially misdiagnosed by the pathologist or the diagnosis is uncertain.

These women do not have a history of asbestos exposure.

Most of these tumors are solid and of soft tissue density, with only an occasional one having a cystic component (Fig. 12.21).

The definition of a Krukenberg tumor has undergone a change since the original definition of a gastric adenocarcinoma metastasizing to either one or both ovaries; presumably this condition represents drop metastases in the peritoneal cavity.

Currently many pathologists use the term Krukenberg tumor to describe a malignant mucinous signet-ring carcinoma located in the ovaries. Tumor primaries include the gastrointestinal tract, biliary tract, pancreas, and breast. A rare androgen-secreting Krukenberg tumor is encountered. Krukenberg tumors have been reported both in young women and in a setting of pregnancy. Surprisingly, a palliative

Other Metastases

Colorectal carcinoma metastasis to the ovaries as initial presentation is uncommon. The exception is in adolescent girls, when colorectal carcinoma has an increased propensity to metastasize to the ovaries; these metastases range from solid to multilocular and mimic a primary ovarian neoplasm.

A uterine endometrial carcinoma does metastasize to the ovaries; often it is not possible to differentiate it from a primary ovarian endometrioid carcinoma.

One woman with an intraoperative diagnosis of disseminated ovarian carcinoma was found

to have a metastatic adenocarcinoid, believed to be primary in the appendix (63).

Metastatic carcinoids, and the difficulty in distinguishing a metastasis from a primary ovarian carcinoid, are discussed below (see Carcinoid).

Magnetic resonance imaging of the rare metastatic malignant melanoma reveals a hyperintense signal on T1-weighted images. This finding is not seen with the even rarer amelanotic melanoma.

Lymphoma/leukemia

Primary ovarian lymphoma is rare. Ovariectomy is curative in this setting. More often, generalized non-Hodgkin’s lymphoma involves bilateral ovaries, usually diffusely. Ascites is uncommon.

Computed tomography in women with ovarian lymphoma revealed well-marginated, often bilateral, hypodense tumors showing only mild contrast enhancement. Ultrasonography reveals solid, mostly homogeneous and hypoechoic tumors, and color Doppler US identifies mild vascularity. Magnetic resonance imaging

detects homogeneous tumors moderately hypointense on T1and slightly hyperintense on T2-weighted images, with only occasional contrast enhancement. Extensive associated lymph node enlargement should suggest the diagnosis. Little contrast enhancement, lack of a cystic or necrotic component, and no ascites argues against a primary ovarian epithelial neoplasm. An ovarian lymphoma can be associated with small peripheral cysts which represent ovarian follicles.

Leukemic infiltration of the ovaries does develop but generally systemic findings predominate.

Small Cell Carcinoma

The term ovarian small cell carcinoma is a descriptive one and includes several different tumor lineages. Some ovarian carcinomas are poorly differentiated and are difficult to categorize, and the occasional primary ovarian tumor resembling a lung small cell carcinoma falls in this category. Bilateral tumors are not uncommon. Some also contain a component of another tumor type, such as an endometrioid carci-

noma, or exhibit squamous differentiation. Some small cell carcinomas are associated with hypercalcemia; these occur mostly in girls and young women and have a poor prognosis.

Histologically, these tumors consist of diffuse sheets of small cells and a follicle-like component.

Carcinoid

Primary ovarian carcinoids are rare. Their classification is uncertain, but as mentioned earlier the current thinking is that they represent a teratoma; a worldwide registry of 329 women with ovarian carcinoids found 57% associated with a cystic teratoma or dermoid (64). Differences in carcinoid characteristics in these two groups are outlined in Table 12.6. Pathologists include strumal and mucinous varieties as subtypes of carcinoid tumor. A majority have a benign course.

Metastatic carcinoids to the ovary are more common than primary ones. At times differentiation between a metastasis and primary carcinoid is not possible; the lack of an identifiable nonovarian primary source does not exclude metastases. Some authors assume that bilateral ovarian carcinoids represent metastases rather than a primary ovarian origin, although exceptions probably occur.

Most ovarian carcinoids develop in postmenopausal women. The carcinoid syndrome is found only in a minority and appears related to tumor size.

Carcinoids are solid tumors, and their imaging appearance is similar to that of other solid ovarian neoplasms.

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Excellent survival follows resection if the tumor is confined to one ovary.

Primary Ovarian Neuroendocrine Tumors

Primary ovarian neuroendocrine tumors are sufficiently rare to be almost ignored by most authors. They are difficult to classify but probably belong in the teratoma group. Histologically they can be subdivided into differentiated, primitive and anaplastic. They range from cystic to solid, and benign to wildly malignant.

Three histologic types are identified: differentiated, primitive, and anaplastic. Some resemble a medulloepithelioma, ependymoma, neuroblastoma, or medulloblastoma. The anaplastic ones can resemble a glioblastoma. Some contain foci of a mature cystic teratoma.

Renin Secreting Tumor

The rare ovarian renin secreting tumor can result in erythropoietin production and polycythemia. An occasional one results in elevated testosterone levels and virilization. Imaging identifies a solid ovarian tumor.

Meigs’ Syndrome

Meigs’ syndrome is an association of an ovarian tumor with ascites and pleural effusion but no tumor spread. The ovarian tumors range from benign to malignant. Occasionally a nonovarian tumor, such as a fallopian adenocarcinoma, is the underlying cause. Serum CA-125 levels are elevated and often the pleural fluid CA-125 level is also markedly elevated. Pathophysiology of the pleural effusion is not clear.

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This syndrome should be suspected in a setting of an ovarian tumor, ascites and pleural effusion, elevated CA-125 level, negative fluid cytology, and if imaging detects no peritoneal implants.

Ascites and pleural effusion clear after resection of the underlying tumor.

Fallopian Tube and Broad

Ligament Neoplasms

Fallopian tube epithelial carcinomas include serous, mucinous, clear cell, endometrioid, and even a rare squamous cell carcinoma. A borderline papillary serous tumor, similar in appearance to its counterpart in the ovary, also occurs. Mesenchymal and mixed epithelialmesenchymal neoplasms are rare. The most common fallopian tube malignancy is a serous adenocarcinoma. An occasional one develops bilaterally. Still, a fallopian tube carcinoma is the least common primary malignancy of the gynecologic organs.

Fallopian tube cancers are small, solid, and lobulated tumors having a CT soft tissue density and enhancing less than myome-

trium. They tend to be hypointense on T1and homogeneously hyperintense on T2-weighted images (Fig. 12.22). Some are surrounded by fluid.

Table 12.7 lists both the FIGO and TNM staging systems for fallopian tube tumors. Published 5-year survival rates vary considerably, but range from 80% to 90% for stage I, dropping to about 20% for stages III.

Primary broad ligament neoplasms are rare. The most common one is a leiomyoma, with its malignant counterpart, leiomyosarcoma, being extremely rare. A rare granulosa cell tumor originates in the broad ligament. Broad ligament cystadenomas and carcinomas develop in a setting of von Hippel-Lindau disease; these tumors are similar in histologic appearance to the epididymal tumors found in men with von Hippel-Lindau disease.

A correct preoperative diagnosis is not common for fallopian tube and broad ligament neoplasms. Imaging simply reveals an adnexal tumor, often containing complex cystic and solid components. Some patients have an elevated CA-125 level, but the nonspecific nature of this marker precludes its use in diagnosis; it is more suitable for follow-up after surgery.

Table 12.7. TNM staging of fallopian tube tumors

Note: Both the Federation Internationale de Gynecologie et d’Obstetrique (FIGO) and TNM systems are included for comparison. Source: From the AJCC Cancer Staging Manual, 6th edition (2002), published by Springer-Verlag, New York, NY, used with permission of the American Joint Committee on Cancer (AJCC), Chicago, IL.

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The spread of fallopian tube carcinomas is primarily to the peritoneum, ovaries, and uterus. Intravascular spread via the inferior vena cava is rare.

Uterus

Endometrial Atrophy and Hyperplasia

Unopposed endometrial stimulation by estrogen leads to a greater than normal proliferation of endometrial glands and endometrial thickening. This condition develops in premenopausal women with polycystic disease, obesity, and estrogen-producing ovarian tumors. In postmenopausal women it is most often secondary to hormone therapy with unopposed estrogen.

Ultrasonography outlines the endometrium and measures its thickness, but cannot differentiate between a normal endometrium, hyperplasia, or a carcinoma. Small endometrial cysts are found both in atrophy and hyperplasia and in benign and malignant conditions. Most imaging studies have thus relied on evaluating a relationship between endometrial thickness and the presence of endometrial disease. Endometrial thickness measured by endovaginal US is greater than that obtained with a transabdominal approach, and measurements obtained with these two modalities are not directly comparable. Intraand interobserver agreement of endovaginal US endometrial thickness measurements is relatively good, but a measurement close to any cutoff value should be interpreted with caution, especially if such a measurement affects clinical management.

A thin endometrium or smooth endometrial thickening detected by endovaginal hysterosonography suggests a benign condition. The presence of any irregular endometrial thickening or an inhomogeneous nodularity suggests a malignancy.

Precontrast MR cannot differentiate endometrial thickening from uterine secretions. Both are hypointense on T1-weighted images and hyperintense on T2-weighted images. Postcontrast, however, the endometrium enhances while secretions do not. Blood in the endometrial cavity can be differentiated on precontrast images; blood is hyperintense on T1-weighted images.

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The use of oral contraceptives results in a gradual decrease in uterine size; the endometrium thins and shows little variation with menstrual cycle.

In postmenopausal women the endometrium is atrophic, and a thickened endometrium is presumptive evidence of a cancer; keep in mind that thickness measurements for hyperplasia and carcinoma overlap. Endovaginal US readily measures endometrial thickness. One problem is that the measured maximal endometrial thickness in postmenopausal women with endometrial atrophy and no abnormality varies considerably, ranging from 1.5 to 6mm in various studies. The cutoff value below which the endometrium is considered normal is somewhat arbitrary, and resultant sensitivities and specificities of detecting endometrial disease vary, depending on the assumed endometrial normal cutoff thickness. A lower assumed limit for normal thickness increases confidence in a conclusion that no cancer is present and curettage can be avoided. A higher assumed limit decreases the number of false positives and thus increases specificity, but at the expense of sensitivity. As an example, the sensitivity of endovaginal US in detecting endometrial disease is about 95% to 98% when a maximum normal endometrial thickness of 2mm is assumed, but decreases to about 80% if a 4mm cutoff is adopted. A typical study conclusion is that postmenopausal women with an endometrial thickness >4mm or some other similar limit need further study. Most cancers encountered in postmenopausal women are associated with an endovaginal US measured endometrial thickness of about 10mm or more, but it is the smaller cancers and thinner endometria that are problematic.

To place this problem in another perspective, no subsequent abnormalities are detected in postmenopausal women if the endometrial thickness is <3mm or so; an endometrial thickness of >10mm is associated with hyperplasia, polyps, and carcinoma. The difficulty is in the intermediate group, which consists of a third or more of women with bleeding. Further guidance is provided in these women if endovaginal US detects a hypoechoic signal and a central echo between symmetrical endometrial surfaces— findings associated with no significant abnor- mality—while heterogeneity and a hyperechoic signal suggests an abnormality.

Some studies suggest that endovaginal US in women with irregular bleedings is as effective as D&C in detecting endometrial abnormalities (65), although it has a low specificity in detecting endometrial abnormalities, limiting its use in this patient population. In spite of these limitations, endovaginal US has evolved into a screening test for endometrial cancer, similar to the Papanicolaou screening test for cervical cancer. One should keep in mind, however, the occasional reported malignancy with an endometrial thickness of <3mm.

Sonohysterography provides additional information. Among asymptomatic postmenopausal women evaluated with sonohysterography followed by endometrial biopsy before initiating hormone replacement therapy, hyperplasia was discovered in 23% of those with an endometrial thickness >5mm and in none with an endometrial thickness of £5mm (66); sonohysterography also detected other intrauterine abnormalities in 37% of women with an endometrial thickness of £5mm and in 64% of those with an endometrial thickness >5mm. The authors concluded that while an endometrial thickness of £5mm does exclude hyperplasia, it does not exclude other intrauterine abnormalities.

In a postmenopausal woman occasionally US identifies endometrial fluid and a thin endometrium. Although such fluid is usually benign, in rare instances it is associated with a carcinoma. Intrauterine US using a highfrequency probe potentially evaluates myometrial invasion by an endometrial carcinoma.

Magnetic resonance reveals endometrial hyperplasia as diffuse endometrial thickening, best seen with T2-weighted imaging.

Endometrial Ossification

A rare premenopausal and even rarer postmenopausal woman develops endometrial ossifications. Endovaginal US in a 62-year-old woman revealed a hyperechoic region in the uterine cavity, suggesting an intrauterine foreign body (67); histology of endometrial curettage showed mature bone and a neutrophilic infiltrate with no evidence of malignancy.

Pathologically, endometrial ossification should not be confused with a müllerian adenosarcoma.

Benign Tumors

Endometrial Polyps

While the term endometrial polyp is a descriptive one, it is generally used to describe a focus of localized intraluminal endometrial hyperplasia. It is analogous to hyperplastic polyps found in the large bowel. Clinically, these polyps range from an incidental finding, a cause for bleeding, or are associated with infertility. They range from sessile to pedunculated, single or multiple, solid or containing cysts. Most are focal, with an occasional one extending diffusely for varying lengths. Endometrial polyps are more prevalent among women with a cervical polyp compared to those without a cervical polyp.

These polyps can be detected with hysterosalpingography. Ultrasonography reveals a focal homogeneous hyperechoic tumor outlined by smooth borders; at times a stalk is seen. Endovaginal sonohysterography (i.e., uterus distended with fluid) aids in their detection and generally allows differentiation of endometrial origin polyps and more deeply placed leiomyomata, although one should keep in mind that an occasional leiomyoma is pedunculated.

T2-weighted MRI reveals endometrial polyps as hypoto isointense tumors compared to normal endometrium. They enhance postcontrast. Most authors believe that MRI is not sensitive enough to reliably distinguish a benign polyp from a malignancy. Nevertheless, T2weighted fast spin echo FSE sequences in women with surgically proved endometrial polyps or carcinomas found that a central fibrous core (suggested by a hypointense signal) and intratumoral cysts (suggested by a hyperintense signal) were more common in endometrial polyps than in carcinomas, while myometrial invasion and necrosis were signs of a carcinoma (68); overall, a mean sensitivity of 79% and specificity of 89% were achieved in diagnosing a carcinoma.

Adenomyosis

Endometrial tissue within the myometrium is adenomyosis. The etiology is unknown. Most often adenomyosis is diffuse, although it also occurs focally and is then known as an adenomyoma. It consists of a focal aggregate of endometrial tissue and smooth muscle within the myometrium and has a discrete margin.

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An occasional one extends into the cervix. It is a common condition that prior to the US and MRI era was diagnosed primarily after hysterectomy.

Presenting symptoms with adenomyosis and adenomyoma tend to be nonspecific and mimic other disorders, including leiomyomatosis. An adenomyoma is an occasional source of bleeding. Adenomyosis does not respond to hormone stimulation.

Hysterosalpingography reveals single or multiple diverticular-like outpouchings extending into the uterine wall. Not all such outpouchings represents adenomyosis; many outpouchings are due to dilated glands or have other etiologies.

The uterus enlarges in diffuse adenomyosis. Although US and MR appearances of diffuse adenomyosis are usually characteristic, an adenomyoma occasionally appears similar to a small leiomyoma. Endovaginal US, with its better resolution, does detect adenomyosis. Published endovaginal US sensitivities in diagnosing adenomyosis or adenomyomas are in the 80% range and specificity percents in the high 80s to low 90s range.

Endovaginal US criteria of adenomyomas consist of poorly defined heterogeneous, hypo-, and hyperechoic subendometrial nodules containing small anechoic lakes and an asymmetric myometrial thickness. Although small myometrial cysts are common in adenomyosis, some cysts are congenital in origin and others are found in such disorders as leiomyomas. A falsepositive diagnosis occurs secondary to vascular calcifications or muscle hypertrophy.

Endovaginal US and MRI have similar accuracies in detecting uterine adenomyosis. Magnetic resonance imaging is useful during pregnancy. Diffuse involvement typically reveals widening of the hypointense junctional zone on T2-weighted images, while cystic regions appear hyperintense. An MR junctional zone thickness of ≥12mm appears reasonable in suggesting adenomyosis. The thickened hypointense junctional zone often has an irregular appearance due to smooth muscle hypertrophy surrounding endometrial glands.

Magnetic resonance identifies focal adenomyomas as poorly marginated hypointense regions within the myometrium (Fig. 12.23). Some adenomyomas enhance with contrast, but their appearance is not specific. Polypoid ade-