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13

Female Genital Tract

Solid Echogenic or Nonhomogeneous Mass

Female Genital Tract

Vagina

Uterus Fallopian Tubes Ovaries

Anechoic Cystic Mass

Solid Echogenic or Nonhomogeneous Mass

Endometriotic Cysts

Thecomatosis

Inflammatory Adnexal Mass

Ovarian Carcinoma

Metastases

Pseudomyxoma Peritonei

Ovarian Tumors (by Histological Criteria)

EndometrioticCysts

Fifty-five percent of patients with endometriosis have ovarian involvement. The endometriotic cysts are usually located on the ovarian surface, initially have a uniformly hypoechoic cystic appearance, and later become nonhomogeneous owing to recurrent bleeding. In this case the endometriosis is no longer distin-

Table 13.2 Differential diagnosis of endometriotic cysts

Hemorrhagic functional cyst

Cystadenoma

Ovarian carcinoma (endometrioid carcinoma)

Intraligamentous myomas

Inflammatory processes

guishable from carcinoma. The full differential diagnosis is shown in Table 13.2.

The sonographic criteria are as follows (Figs. 13.96, 13.97, 13.98):

Anechoic mass on the cortex, 1–5 mm in diameter

Ovarian Endometriosis

Pathogenesis. The cyst wall is lined with endometrioid epithelium. This can result from the dissemination of endometrium from the uterus, but a more likely cause is the primary formation of cysts composed of celomic epithelium. This would better explain the primary occurrence of ovarian adenocarcinoma (approximately 5% of ovarian tumors are endometrioid tumors, mostly carcinomas).

With intracystic bleeding, the mass enlarges and may show homogeneous internal echoes

Thick, echogenic wall

Difficult to localize to a specific organ

With recurrence, a nonhomogeneous echo pattern may be seen

Management. Histological confirmation is always required. Ultrasound follow-ups should be scheduled at 6-month intervals. Response should be monitored in cases that have been treated with GnRH analogues.

Fig. 13.96 Endometriotic cysts of the ovary. Multiple hy-

Fig. 13.97 Large, solitary histological endometriotic cyst

poechoic foci in the ovary.

(surgery and histology; first sonographic diagnosis: ab-

 

scess). The clinical and sonographic diagnosis was ab-

 

scess. The absence of vascularity is not consistent with

 

ovarian carcinoma. BL = bladder; UT = uterus.

Thecomatosis

Thecomatosis is a pure stromal hyperplasia causing moderate enlargement of the ovary, which undergoes nodular changes. Histologically, the cortex is hyperplastic and shows intracellular fat deposits. Stromal hyperplasia occurs only in menopause.

Fig. 13.98 Endometriosis with bleeding: hypoechoic mass, hematomas (H) due to bleeding in foci of endometriosis. UT = uterus.

464

Inflammatory Adnexal Mass

Enlargements of the ovaries due to inflamma-

Tubo-ovarian abscess or infections originat-

densely matted (making them difficult to

tion fall under the heading of adnexal masses.

 

ing from the fallopian tube (Fig.13.100,

distinguish from carcinoma)

They include the following entities:

 

Fig.13.101; see also Fig.13.79)

 

Ovarian abscess (Fig.13.99)

Hematogenous tuberculosis. Conglomerate

 

 

 

masses are formed, usually bilateral and

 

13

Ovaries

Fig. 13.99 Ovarian abscess: The ovary (OV) is enlarged

Fig. 13.100 Adnexitis: nonhomogeneous enlarged ovary

and hyperechoic; it appears in the center anechoic to

(cursors) causing pain under palpation.

hypoechoic as a sign for an abscess.

 

Ovarian Carcinoma

Sonographically ovarian tumors of uncertain importance can only be assessed by morphological criteria such as solid or cystic portions, size of cysts, wall thickness, and septation. A central vascularization is a sign of malignancy in tumors of the adnexa. Biopsies to establish a diagnosis are contraindicated due to the risk of spreading along the injection canal. To date, non-invasive diagnostic measures cannot replace surgical staging and give reliable assessments of the operability of ovarian cancer.

Any kind of tissue can give rise to a malignant tumor, but only tumors derived from the germinal epithelium are classified as ovarian carcinoma. Theca-like transformation in ovarian tumors leads to small amounts of estrogen production in 15–20% of all epithelial cancers.

Tumors in postmenopausal women who are not on hormone replacement therapy are always suspicious. If findings are equivocal, diagnostic laparoscopy is always advised, although a diagnosis can not always be made. Surgical

exploration and extirpation is needed to make a definitive diagnosis.

Some 10% of ovarian cancers are determined by genetic factors. Characteristics of familial ovarian cancer are clustering of cases within the family, often associated with increased cases of breast cancer (hereditary breast and ovarian cancer), less often associated with bowl and uterine cancer (HNPCC) or other tumors (Li–Fraumeni syndrome). An uncharacteristically early age of onset is noticeable. Ovarian cancer is mainly diagnosed in late stages of the disease, but screening will not improve early detection. This is why general screening for ovarian cancer was not recommended in the latest guidelines (2007).

Sonographic features. Carcinoma can have almost any sonomorphological appearance: cystic, hyperechoic, hypoechoic, and nonhomogeneous (Figs. 13.102, 13.103, 13.104). Large tumors contain nonhomogeneous solid com-

Fig. 13.101 Adnexitis: nonhomogeneous hypoechoic fallopian tube (T), nonhomogeneous hyperechoic ovary (OV), surrounded by a fluid collection (E).

ponents, may show central anechoic necrosis, and tend to invade neighboring structures, producing ill-defined margins. It is common for ovarian carcinoma to coexist with uterine or tubal cancers. Primary malignant tumors of the ovary are indistinguishable from metastases arising from other primary malignancies.

Endometrioid adenocarcinomas are more heavily permeated by cysts and papillomas. They account for approximately 5% of ovarian tumors (Fig.13.105).

Ovarian cancers secreting hormones can cause hyperplasia of the endometrium (Fig.13.106, Fig.13.107).

Peritoneal carcinomatosis. Serous or mucinous carcinomas usually become disseminated throughout the abdominal cavity while the primary tumor itself is still relatively small. The peritoneum in these cases is studded with small tumor nodules and shows irregular hyperechoic thickening. Metastases are seeded

Fig. 13.102 Ovarian carcinoma: nonhomogeneous hypoechoic/hyperechoic mass (cursors) in the lower abdomen.

Fig. 13.103 Ovarian carcinoma, transvaginal ultrasonography; same patient as in Fig. 13.101.

Fig. 13.104 Ovarian carcinoma: hypoechoic tumor (cursors) combined with metastasis and intensive hypoechoic peritoneal carcinomatosis (PC).

465

Cancer cells are only in the inner lining of the fallopian tube. They have not grown into deeper layers. Also called carcinoma in situ
The cancer is in the fallopian tube(s), but has not grown outside of them
The cancer is only inside one fallopian tube—it has not grown through to the outside of the tube. It has not grown through the capsule and is not in fluid taken from the pelvis
The cancer is growing in both fallopian tubes—it has not grown through to the outside of the tube. It has not grown through the capsule and is not in fluid taken from the pelvis (like T1a but with tumor in both tubes)
The tumor is in one or both fallopian tubes and has either grown through the outer wall of the tube or cancer cells are found in fluid taken from the pelvis
The tumor has grown from one or both fallopian tubes into the pelvis
The cancer is growing into the uterus and/or the ovaries The cancer is growing into other parts of the pelvis
The cancer has spread from the fallopian tubes into other parts of the pelvis and cancer cells are found in fluid taken from the pelvis (either from ascites or from washings obtained at surgery
The tumor has spread outside the pelvis to the lining of the abdomen
The areas of cancer spread outside the pelvis can be found only when the area is biopsied and looked at under the microscope
The areas of spread can be seen with the naked eye but are 2 cm or less in size (less than an inch)
No description of the tumor's extent is possible because information is incomplete

13

Female Genital Tract

T and FIGO Categories for Ovarian Cancer (after WHO 201312)

TNM

FIGO

 

Description

T1

I

 

The cancer is confined to one or both ovaries

T1a

 

IA

The cancer is only inside one ovary; it does not penetrate the capsule

T1b

 

IB

The cancer is inside both ovaries but does not penetrate to the outside and is not in fluid taken from the

 

 

 

pelvis

T1c

 

IC

The cancer is in one or both ovaries and is either on the outside of an ovary or grown through the

 

 

 

capsule of an ovary or is in fluid taken from the pelvis

T2

II

 

The cancer is in one or both ovaries and is extending into pelvic tissues

T2a

 

IIA

The cancer has metastasized (spread) to the uterus and/or the fallopian tubes

T2b

 

IIB

The cancer has spread to pelvic tissues besides the uterus and fallopian tubes

T2c

 

IIC

The cancer has spread to the uterus and/or fallopian tubes and/or other pelvic tissues (like T2a or T2b)

 

 

 

and is also in fluid taken from the pelvis

T3

III

 

The cancer is in one or both ovaries and has spread to the peritoneum outside the pelvis

T3a

 

IIIA

The cancer metastases are so small that they cannot be seen except under a microscope

T3b

 

IIIB

The cancer metastases can be seen but no tumor is bigger than 2 cm (0.8 inches)

T3c

 

IIIC

The cancer metastases are larger than 2 cm (0.8 inches)

N categories

 

 

 

NX

IV

 

No description of lymph node involvement is possible because information is incomplete

N0

 

 

No lymph node involvement

N1

 

 

Cancer cells are found in the lymph nodes close to tumor

M categories

 

 

 

M0

 

 

No distant spread

M1

 

 

Cancer has spread to the inside of the liver, to the lungs, or to other organs

T categories for fallopian tube cancer

Tx

Tis

T1

T1a

T1b

T1c

T2

T2a

T2b

T2c

T3

T3a

T3b

466

13

Ovaries

Fig. 13.105 Endometrioid ovarian carcinoma (TU), complex hyperechoic/cystic mass. UT = uterus; BL = bladder.

Fig. 13.108 Peritoneal carcinomatosis (cursors) in a nonovarian carcinoma of the ovary; 59-year-old woman: peritoneal carcinomatosis without a detectable ovarian carcinoma.

Fig. 13.106 Cystadenocarcinoma: hyperechoic polypoid masses (TU) of the cystic epithelium; C = cyst.

Fig. 13.109 Malignant ascites caused by a peritoneal carcinomatosis; nonhomogeneous fluid suspension with deposits of echogenic spots.

Fig. 13.107 Endometrial hyperplasia (transvaginal scan) in ovarian carcinoma: uterus with endometrial hyperplasia (16.3 mm).

early to the greater omentum (Fig.13.108). A large, flat, confluent, hypoechoic tumor may be formed ( 8.3a,d, 8.6f, Fig. 8.34). Hypoechoic masses also form on the diaphragm and along the umbilical vein. With the associated obstruction of lymphatic drainage, the serous fluid produced by the tumor cells usually leads to a copious ascites that is often bloodtinged on percutaneous aspiration (Fig.13.109). Cytological analysis of the ascites has a diagnostic accuracy of 80%.

Metastasis. Lymph node metastases (paraaortic, inguinal, lesser pelvis) are of minor importance. Ovarian carcinoma spreads hematogenously to the pleura, lung, and liver and less commonly to the brain and bone.

Differential diagnosis. Differentiation from intestinal carcinoma can be difficult. Bowel cancers are frequently associated with hepatic and lymph node metastases, but they rarely show omental involvement or peritoneal carcinomatosis with ascites.

In differentiating ovarian cancer from uterine myomas, a short, firm pedicle not attached to the cornual region suggests a subserous myoma, whereas a soft, mobile pedicle connected to the cornual region suggests an ovarian tumor (Fig.13.110, Fig.13.111). The full differential diagnosis is listed in Table 13.3.

Table 13.3 Differential diagnosis of ovarian masses

Gallbladder hydrops

Splenic tumor

Pelvic kidney, renal tumor, hydronephrosis

Pancreatic cysts

Mesenteric cysts

Bowel tumors, diverticulosis

Tuberculous conglomerate masses

Nodal packages in the mesentery

Distended bladder

Uterine myomas

Tumors of the pelvic connective tissue (lipoma, sarcoma, endothelioma, retroperitoneal liposarcoma, retroperitoneal pseudomyxoma, osteoma, enchondroma)

Tumors of the bony pelvis (may invade the connective tissue)

The sonographic criteria for carcinoma are as follows:

Larger than 5 cm

Nonhomogeneous, cystic-solid

Ill-defined margins

Lobulated or nodulated

Echogenic

Borderline Criteria

Borderline tumors are tumors that have a low malignant potential:2

Epithelial tumors

Confined to the organ

No stromal invasion

Amenable to curative surgery

Five-year survival rate 80–90%, even with peritoneal seeding

Occurrence in premenopausal women: two-thirds of malignant tumors in women under age 40 are borderline tumors, as opposed to only 10% in women over age 40.

Broad septa

Bilateral

Papillary deposits

Free fluid

On palpation: fixed, matted, firm (Table 13.4)

467

13

Female Genital Tract

Fig. 13.110 Tumor in the lower abdomen (abdominal pain): nonhomogeneous cystic mass with suspicion for ovarian tumor.

f Fig. 13.111 Peritoneal duplication; surgical specimen.

Table 13.4 TNM and FIGO classifications for ovarian cancer11

Primary tumor (T)

TNM

FIGO

 

T1

I

Tumor limited to the ovaries (one or both)

T1a

IA

Tumor limited to one ovary; capsule intact, no tumor on ovarian surface; no malignant cells in ascites or peritoneal washings

T1b

IB

Tumor limited to both ovaries; capsules intact, no tumor on ovarian surface; no malignant cells in ascites or peritoneal

 

 

washings

T1c

IC

Tumor limited to one or both ovaries with any of the following: capsule ruptured, tumor on ovarian surface, malignant cells in

 

 

ascites or peritoneal washings

T2

II

Tumor involves one or both ovaries with pelvic extension

T2a

IIA

Extension and/or implants on the uterus and/or tube(s); no malignant cells in ascites or peritoneal washings

T2b

IIB

Extension to other pelvic tissues

T2c

IIC

Pelvic extension (T2a or T2b) with malignant cells in ascites or peritoneal washings

T3

III

Tumor involves one or both ovaries with microscopically confirmed peritoneal metastasis outside the pelvis and/or regional

 

 

lymph node metastasis

T3a

IIIA

Microscopic peritoneal metastasis beyond the pelvis (no macroscopic tumor)

T3b

IIIB

Macroscopic peritoneal metastasis beyond the pelvis, ≤ 2 cm in greatest dimension

T3c

IIIC

Macroscopic peritoneal metastasis beyond the pelvis, > 2 cm in greatest dimension, and/or regional lymph node metastasis

Regional lymph nodes (N)

TNM

FIGO

 

NX

 

Regional lymph nodes cannot be assessed

N0

 

No regional lymph node metastasis

N1

IIIC

Regional lymph node metastasis

Distant metastasis (M)

TNM

FIGO

 

M0

 

No distant mestastasis

M1

IV

Distant metastasis (excludes peritoneal metastasis)

468

Metastases

Ovarian metastases are very rare and originate

Krukenberg tumor is the term applied to

metastasize chiefly by the lymphogenous route

from cancers of the bronchial system, gastro-

enlarged ovaries (generally both) that are dif-

and less commonly via the bloodstream.

intestinal tract, breast, and gallbladder. Ap-

fusely permeated by epithelial signet-ring cells,

 

proximately 3% of malignant ovarian tumors

usually from gastric carcinoma and occasion-

 

are metastases.

ally from colon carcinoma. The tumor cells

 

PseudomyxomaPeritonei

In pseudomyxoma peritonei, the peritoneal

carcinoma of the appendix. Pseudomyxoma

As there is no effective treatment, the dis-

cavity is filled with a large quantity of mucin.

peritonei can also arise secondarily from the

ease runs a malignant course marked by intes-

Ultrasound demonstrates anechoic fluid in the

rupture of a mucinous cystoma (usually at op-

tinal adhesions and obstructions, with patients

peritoneal cavity (see Fig. 8.33).

eration) or possibly as a primary epithelial dis-

dying from cachexia.

The cause may be tumor cells seeded from a

ease based on peritoneal metaplasia.

 

mucinous ovarian tumor or a mucinous adeno-

 

 

Ovarian Tumors (byHistological Criteria)

Because many different cell types exist in the ovaries, a large number of different neoplasms can arise. As a result, the ovaries are subject to a greater diversity of tumor types than any other organ in the human body.

Incidence data.

Epithelial tumors:

66% of all ovarian tumors are epithelial tumors

Of the malignant tumors, 85% are epithelial tumors

Serous tumors:

50% of all ovarian tumors are serous tumors

70% of serous tumors are benign, and 20–25% of serous tumors are true invasive carcinomas

40% of ovarian carcinomas are serous carcinomas, making this the most common type

Sex cord–stromal tumors:

7% of all true ovarian tumors are sex cord–stromal tumors

Germ cell tumors:

15–20% of all ovarian tumors are germ cell tumors

95% of germ cell tumors are benign cystic teratomas

2–3% of germ cell tumors are malignant

Approximately 65% of malignant ovarian tumors up to age 20 are germ cell tumors

Bilateral occurrence:

20–30% of benign tumors

30–40% of borderline tumors

65–75% of carcinomas

Epithelial tumors. Epithelial tumors arise from inclusion cysts in the germinal epithelium. The ovary contains numerous germinal epithelial cysts whose origin is still unexplained. Mixed epithelial tumors occur. Epithelial tumors can vary considerably in size. They may be cystic, cystic/solid, or solid. Most solid tumors are malignant.

Sex cord–stromal tumors. These tumors arise from sexually differentiated mesenchyma.

Classification of Ovarian Tumors5,10

Superficial epithelial–stromal tumors

Serous tumors

Mucinous tumors

Endometrioid tumors

Clear cell tumors

Transitional cell tumors (Brenner tumor)

Squamous cell tumors

Epithelial mixed tumors

Undifferentiated carcinoma

Sex cord–stromal tumors

Granulosa–stromal cell tumors

Sertoli–stromal cell tumors, androblastoma

Sex cord tumors with annular tubules

Gynandroblastoma

Unclassifiable

Steroid (lipid) cell tumors

Germ cell tumors

Dysgerminoma

Yolk sac tumor

Embryonic carcinoma

Choriocarcinoma

Teratoma

Mixed types

Gonadoblastoma

Germ cell–sex cord–stromal tumors

They are palpable, hormone-producing ovarian tumors that are composed of one or more cell types. They produce estrogen or androgens.

Germ cell tumors. Germ cell tumors are more prevalent in Africa and Asia than in Europe (5–15% of malignant ovarian tumors), whereas epithelial tumors are less common. Germ cell tumors occur predominantly in childhood and from 20 to 30 years of age; they are rare after menopause. Approximately two-thirds of malignant ovarian tumors in patients under age 20 are germ cell tumors. They are derived from primordial germ cells (direct: dysgerminoma; indirect embryonic: teratoma; extraembryonic tumors: choriocarcinoma, yolk sac tumor). Germ cell tumors grow rapidly, are unilateral,

Tumors of the rete ovarii

Mesothelial tumors

Tumors of uncertain histogenesis

Gestational trophoblastic diseases

Soft-tissue tumors, not ovary-specific

Malignant lymphoma

Unclassifiable tumors

Metastases

Tumorlike lesions

Solitary follicular cyst

Multiple follicular cysts

Luteinized cyst in pregnancy

Hyperreaction luteinalis (multiple lutein cysts)

Corpus luteum cyst

Gestational luteoma

Ectopic pregnancy

Stromal hyperplasia

Stromal hyperthecosis

Massive edema

Fibromatosis

Endometriosis

Nonclassifiable cyst

Inflammatory lesions

and metastasize by hematogenous and lymphogenous spread. They are very sensitive to chemotherapy and have a favorable prognosis overall. Consistent therapy and follow-ups can provide a cure rate of up to 90%.

Morphological and sonomorphological criteria. Tables 13.5, 13.6, and 13.7 summarize the principal morphological and sonomorphological criteria for the three main groups of superficial stromal tumors, sex cord–stromal tumors, and germ cell tumors. The following box, p. 473, then reviews the essential aspects of the clinical manifestations, diagnosis, and treatment of ovarian tumors.

13

Ovaries

469

13

Female Genital Tract

Table 13.5 Features of epithelial tumors

 

 

Tumor

Tumor behavior, frequency, Histology, morphology

Sonographic criteria

Special features

 

bilateral occurrence

 

 

Serous tumors

Cystadenoma

Most common benign

Thin cyst wall, lined with

 

ovarian tumor

epithelium

 

Generally unilateral

Serous contents

 

 

Usually large cysts

Cystadeno-

Most common malignant

Predominantly cystic with

carcinoma

ovarian tumor (1/3 of all

solid elements

 

ovarian cancers)

Circumscribed thickening

 

 

of cyst wall

 

 

Polypoid structures, intra-

 

 

tumoral hemorrhage, and

 

 

necrosis may occur

 

 

Stromal infiltration

Mucinous tumors

 

 

Mucinous

25% of all ovarian tumors

Multifocal

cystoma

Initially benign, eventually

Often septated

 

degenerates

Thin-walled

 

5–20% bilateral (depend-

 

 

ing on malignancy)

 

Mucinous

10% of ovarian carcinomas

Mixed cystic and solid

cystadeno-

20% bilateral

Intratumoral hemorrhage

carcinoma

 

and necrosis may occur

Endometrioid

20% of ovarian carcinomas

Mixed cystic and solid

tumor

30–40% bilateral

Cyst contents serous or

 

 

bloody

 

 

Foci of bleeding and ne-

 

 

crosis

Anechoic mass

See “Cystic ovarian

Smooth surface

masses”

Thin echogenic wall

Thin septa, possibly multilocular

Mixed anechoic (cystic ele-

See “Cystic ovarian

ments) to hyperechoic

masses”

(cyst wall)

 

Nonhomogeneous echo-

 

genic areas (bleeding and

 

necrosis)

 

Often with ascites in

 

metastases/peritoneal

 

metastases

 

Variable echogenicity

See “Cystic ovarian

Fine to coarse internal

masses”

echoes in the septated

 

spaces

 

Anechoic (cystic) to echo-

Often associated with

genic (solid) with hypo-

pseudo-myxoma peritonei

echoic areas (bleeding and

 

necrosis)

 

Cyst contents hypoechoic

Coexists with endometrial

to echogenic

carcinoma in 15–30% of

 

cases

Clear cell tumor

5–10% of ovarian carcino-

Mixed cystic and solid

Mixed anechoic and hyper-

 

 

mas

 

echoic

 

 

40% bilateral

 

Indistinguishable from oth-

 

 

 

 

er tumors by ultrasound

 

Transitional cell

1–2% of all ovarian tumors

Smooth margins

With calcifications: high-

Patients are approximately

tumor (Brenner

Usually benign

Not visible or up to 2–3 cm

level internal echoes with

50 years old

tumor)

Unilateral

large

acoustic shadows

 

 

 

Calcifications may occur

 

 

470

Table 13.6 Features of sex cord–stromal tumors

 

 

 

Tumor

Tumor behavior, frequency,

Histology, morphology

Sonographic criteria

Special features

 

bilateral occurrence

 

 

 

Granulosa-stromal cell tumors

 

 

 

Granulosa cell

Most common estrogen-

Solid structure

Hypoechoic

Estrogen production can lead to

tumor

producing ovarian tumor

Up to 30 cm in diameter

Possible cysts

precocious pseudopuberty in ado-

 

Usually unilateral

 

 

lescents, to uterine and breast

 

Frequent malignant

 

 

enlargement in sexually mature

 

growth without correla-

 

 

women, and to endometrial hyper-

 

tive histology

 

 

plasia or carcinoma in postmeno-

 

 

 

 

pausal women

 

 

 

 

Can recur after 10–20 years

Thecoma

Less common than gran-

5–10 cm in diameter

Smooth margins

Estrogen production

(theca cell

ulosa cell tumor

Consists of fat-rich stro-

Hypoechoic with echo-

Rare in puberty, common around

tumor)

Unilateral

mal cells, collagen-pro-

genic strands

menopause

 

Generally benign

ducing cells, and nests of

 

Causes menstrual abnormalities and

 

 

granulosa cells

 

breast enlargement; endometrial

 

 

 

 

hypertrophy and carcinoma may

 

 

 

 

occur

 

 

 

 

Often confused with fibroma

Ovarian fibro-

Most common ovarian

Arises from sexually un-

Smooth margins, oval,

40% of fibromas > 6 cm associated

ma

stromal tumor

di erentiated mesenchy-

uniformly hypoechoic

with ascites

 

4% of all ovarian tumors

ma

Occasional cystic de-

Rare development of fibrosarcoma

 

Usually unilateral

Firm due to collagen

generation

Meigs syndrome: benign ovarian tu-

 

Usually benign

production

Often heavily calcified

mor (fibroma) with ascites and

 

 

“Adenofibroma”: also

 

pleural e usion (usually on the right

 

 

contains glands and cysts

 

side), caused by lymphatic obstruc-

 

 

 

 

tion?

Differentiation required from Krukenberg tumor: metastases from bowel or breast tumors

Sarcoma

Highly malignant

Solid, less firm than fi-

Solid, predominantly

 

Pure sarcomas are rare,

bromas

hypoechoic (less hypo-

 

mostly mixed forms: fi-

Histological structure re-

echoic than fibroma)

 

brosarcoma, leiomyosar-

sembles “fish flesh”

 

 

coma, adenosarcoma

 

 

Sertoli stromal

0.2% of all ovarian

Solid, up to 10 cm in

Smooth margins, non-

cell tumors, an-

tumors

diameter

homogeneous hypo-

droblastomas

Usually benign

Cells resemble Sertoli

echoic/hyperechoic

 

Unilateral

and Leydig cells

texture

In young women and children

In young women (ca. 25 years)

80% produce androgens, causing hirsutism with beard growth, deep voice, secondary amenorrhea, clitoral hypertrophy, breast and uterine atrophy, alopecia, increased libido

Androblastomas: incomplete development of a testis from stroma of embryonic gonads; special form composed of ovarian hilar cells (hilar-Leydig cell tumor) may produce estrogen

Steroid (lipid)

Usually benign

Resemble a hyperneph-

Urinary 17-ketosteroids sometimes

cell tumors

 

 

roma, may arise from

 

elevated

 

 

 

heterotopic adrenal

Obesity, virilization, abdominal

 

 

 

tissues

 

striae

 

 

Soft, slightly necrotic

 

 

13

Ovaries

471

13

Female Genital Tract

Table 13.7 Features of germ cell tumors

 

 

 

Tumor

Tumor behavior, fre-

Histology, morphology

Sonographic criteria

Special features

 

quency, bilateral occur-

 

 

 

 

rence

 

 

 

Dysgerminoma

5–10% of all ovarian tu-

Very fast-growing, solid

 

Very radiosensitive

(gonocytoma, round

mors, ca. 2% of malig-

tumor up to about 30 cm

 

Good prognosis

cell sarcoma, semi-

nant ovarian tumors up

 

 

Occult tumors on the opposite

noma)

to age 20

 

 

side

 

Most common malignant

 

 

 

 

germ cell tumor (50%)

 

 

 

 

Most common malignant

 

 

 

 

tumor in pregnancy and

 

 

 

 

intersexuality

 

 

 

 

10% bilateral (large tu-

 

 

 

 

mors)

 

 

 

Yolk sac tumor

20% of immature germ

Reticular epithelial cells

 

Produces AFP (used as tumor

(entodermal sinus

cell tumors of the ovary

Papillary structure

 

marker)

tumor)

Malignant

 

 

Better prognosis today with

 

 

 

 

cytostatics

Teratomas

 

 

 

 

Dermoid (benign

15% of all ovarian tumors

Composed of embryonic

Ill-defined margins

In younger women

teratoma,

One-third of all benign

germ cells

Solid with high non-

Strictly speaking, a retention

dermoid cyst)

ovarian tumors

Grows very slowly

homogeneous echo-

cyst; enlarges when skin secre-

 

80% of all germ cell

Rarely larger than fist-

genicity, occasionally

tions expand the cyst sac

 

tumors

size

with calcium

Prone to torsion, suppuration;

 

Benign, but the squa-

Surface smooth but ir-

Cyst with layered in-

may penetrate into the rectum

 

mous portion may show

regular

ternal structure; path-

 

 

malignant change (1%)

 

ognomonic, especially

 

 

Usually unilateral

 

when echogenic part

 

 

 

 

is anterior (floating se-

 

 

 

 

bum, liquid at body

 

 

 

 

temperature)

 

 

 

 

May contain tooth bud

 

 

 

 

and bone with acous-

 

 

 

 

tic shadowing

 

Malignant solid

Highly malignant

Dermoid with disordered

 

Destructive spread

teratomas

 

cell pattern and glial

 

Metastases

 

 

proliferation

 

 

 

 

Rapid growth

 

 

Struma ovarii

 

Monodermal neoplasm,

Requires di erentia-

Hormone production can cause

 

 

predominates in thyroid

tion from hemorrhagic

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tissue

cyst, cystadenoma, fi-

 

 

 

 

broma

 

472

Clinical Aspects, Diagnosis, and Treatment of Ovarian Tumors

Symptoms

There are no early symptoms.

Ovarian tumors cause few if any complaints and have ample room to expand from the lesser to the greater pelvis. Often they are detected only after the abdominal girth increases. Many of these tumors are detected incidentally.

Uterine bleeding (7%) occurs when there is a coexisting uterine tumor or when the ovarian cancer has penetrated the vaginal wall.

Estrogen production and its associated symptoms occur in 18% of all ovarian tumors and 25% of ovarian carcinomas.

In 70% of cases, metastases are already present at operation.

Typical complications

Torsion of a pedunculated uterine tumor (10–20%) may be caused by an external force acting on the tumor (sudden deceleration), especially if the mass contains fluid. A gradual occlusion of the blood supply causes a gradual increase in complaints, while sudden occlusion produces a shocklike condition with peritonitis. Torsion can lead to necrosis.

Infections occur in 2% of ovarian tumors, usually owing to the migration of infectious microorganisms from the bowel. They can lead to suppuration (pyogenic organisms) and putrefaction (putrefactive bacteria). The results are high intermittent fever and life-threatening peritonitis.

Incarceration occurs if the tumor cannot move upward out of the lesser pelvis.

Rupture occurs in 3% of all ovarian cysts, usually spontaneously and often as a result of torsion. Life-threatening internal bleeding can develop. The draining cystic fluid and spillage of cells lead to chronic ascites.

Complaints relating to the complications are low back pain, a bloated feeling, difficulties in passing urine and stool, varices, and leg edema.

Diagnosis

Gynecological examination and ultrasonography by an experienced examiner using modern equipment should ensure that no malignant tumors are discovered incidentally at operation.

Tumor locations:

Large ovarian tumors can exert traction on the uterus, causing it to assume a transverse position in the lesser pelvis.

Small ovarian tumors are located in the lesser pelvis adjacent to the uterus, which they may displace.

Dermoid cysts are often located anterior to the uterus.

Tumors of the pelvic connective tissue are difficult to define.

Rule:

The attachment of a tumor is located opposite the site of greatest mobility. Testing this mobility sign will usually help in distinguishing between an abdominal tumor and a tumor of genital origin.

Suspicious signs during palpation:

Palpable nodule on the uterine attachment of the sacrouterine ligaments, in the cul-de-sac, or on the epiploic appendages of the rectum.

Ovaries palpable after menopause.

Imaging and invasive studies

The patient may be examined by ultrasound, laparoscopy, CT (in exceptional cases; see below), or laparotomy with extirpation and histological evaluation.

Ultrasound with a well-distended bladder:

Criteria for malignancy: solid, irregular, mixed solid/cystic elements, ascites.

Criteria for benignancy: smooth, unilocular or multilocular cysts.

Cysts should not be aspirated:

Danger of rupture and possible cell spillage.

Needle aspiration cannot exclude intracystic carcinoma.

Cyst aspiration is never curative.

Aspiration of ascites:

The ascites in early ovarian carcinoma is free of tumor cells.

Laparoscopy:

Laparoscopy is unsafe owing to the risk of cell spillage and uncertain because a wedge excision may be nondiagnostic. Because every ovarian tumor ultimately should be removed, laparoscopy merely wastes time.

CT:

Whenever possible, CT should be performed only after menopause because of radiation exposure to the ovaries.

Treatment

Wait for menstruation to occur before performing surgery, as functional cysts will regress spontaneously.

With malignant ovarian tumors, both ovaries and fallopian tubes should almost always be removed along with the uterus and greater omentum because of the likelihood of metastases.

A cure is possible if the largest tumor remnant left behind is no larger than 1–2 cm.

Ovarian tumors are responsive to chemotherapy. If tumors recur, they do so quickly after the therapy is discontinued.

Even during pregnancy, every true ovarian tumor should be surgically removed because of the risk of torsion, rupture, and suppuration in the puerperium (10%).

Prognosis

The prognosis depends critically on the timing of the first operation and the corresponding tumor stage, the histological type (serous tumors have a poorer prognosis than mucinous or endometrioid lesions), the degree of tumor differentiation (grading), the postoperative residual tumor mass, the age and the overall health of the patient.

The 5-year survival rates (after surgery and chemotherapy) are as follows:

Stage I–IIA

65–90%

Stage II

approx. 50%

Stage III

approx. 10–12%

Stage IV

approx. 1–2%

Today, 70% of ovarian carcinomas are diagnosed in stage III or IV; the 5-year survival rate is 30%.

13

Ovaries

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13

Female Genital Tract

Tips, tricks, and pitfalls

In general

Uterus, cervix, vagina, and ovary need to be examined routinely and systematically, even by the examiner not belonging to the group of “specialists.” History and clinical findings ought to be integrated.

Complexity in anatomy in the region examined must be considered.

Color-coded sonography and contrast-en- hanced ultrasonography (CEUS) must be used carefully.

Further imaging techniques must be available, such as transvaginal endosonography (TVS) and MRI. In uterine adenomyomatosis especially, MRI shows better specificity; otherwise TVS and MRI are equally useful in classifying myometrium and layers of endometrium.

The occurrence of sarcoma in patients with myoma is only about 0.27%. There are no good ultrasound criteria for it.

Special

Before menopause:

Routinely, ovaries are detected in lower abdominal sections by following parametria from ovary in the direction of iliacal vessels (color-coded sonography), taking the obturator muscle as another landmark.

Ovaries are detected by their (small, cystic) follicles, showing different degrees of maturity, and their oval shape; in midcycle liquid masses in the minor pelvis are normal as a result of ruptured graafian follicles.

Fig. 13.112 a and b Unevenly thickened endometrium (arrows and distance bars) exceeding 12.4 mm—highly suspicious of carcinoma of endometrium (no hormonal therapy); lower abdominal sections.

After menopause:

Endometrium thickness less than 4–5 mm presents no risk.

If the endometrial thickness is greater than this, histology is needed, especially if it is 20 mm or more.

In asymptomatic patients, an endometrial diameter of more than 1 mm is regarded as a cancer risk situation (Fig. 13.112).

In cystic lesions, the same tumor entity may show different sonographic features, and vice versa: the same sonographic tumor appearance may represent different histologic entities.

Signs of malignity:

Uneven texture

Ascites

More than four papillary structures

Multilocular cysts

Strong vascularization

Signs of benignity:

– Cystoid structure solitary and less than 7 mm in diameter

Acoustic shadowing

Smooth contour

No vascularization

Experienced examiners can distinguish the harmless from the harmful in TVS.

References

[1]Kaiser R, Pfleiderer A. Keimzelltumoren. In: Lehrbuch der Gynäkologie. Stuttgart: Thieme, 1985

[2]Frank K, Goldhofer W. Uterus und Adnexe. In: Rettenmaier G, Seitz K (eds.). Sonographische Differentialdiagnostik. Stuttgart: Thieme, 1999

[3]Kozlowski P, Böhmer S. Gynäkologische Fragestellung in der Ultraschalldiagnostik. Landshut: ecomed, 1991

[4]Schmidt-Gollwitzer M. Abnorme vaginale Blutungen. In: Martius G, Schmidt-Gollwitzer M (eds.). Differentialdiagnose in Geburtshilfe und Gynäkologie. Stuttgart: Thieme, 1984; p.16

[5]Sohn C, Krapfl-Gast AS, Schiesser M. Checkliste Sonographie in Gynäkologie und Geburtshilfe. Stuttgart: Thieme, 1998

[6]Kaiser R, Pfleiderer A. Geschwülste. In: Lehrbuch der Gynäkologie. Stuttgart: Thieme, 1985

[7]Schmidt-Gollwitzer K, Schmidt-Gollwitzer M. Der palpable Unterbauchtumor. In: Martius G, Schmidt-Gollwitzer M (eds.). Differ-

entialdiagnose in Geburtshilfe und Gynäkologie. Stuttgart: Thieme, 1984

[8]Moltz L. Androgenisierungserscheinungen. In: Differentialdiagnose in Geburtshilfe und Gynäkologie. Stuttgart: Thieme, 1984; p. 46

[9]Merz E. Anatomie des weiblichen Beckens. In: Sonographische Diagnostik in Gynäkologie und Geburtshilfe. Vol1, 2nd ed. Stuttgart: Thieme, 1997

[10]Scully RE. Histological typing of ovarian tumours, 2nd ed. Berlin: Springer, 2000

[11]Tavassoli FA, Deville P, Eds. Pathology and Genetics of Tumours of the Breast and Female Genital Organs (IARC/World Health Organization Classification of Tumours). Lyon: IARC, 2003

[12]National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Ovarian Cancer: Including Fallopian Tube Cancer and Primary Peritoneal Cancer V1.2013

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