Fallopian Tubes

Definitions. Sactosalpinx is a hypoechoic mass between the uterus and ovary caused by a fluid collection in the fallopian tube due to various causes (Fig.13.77).

Hematosalpinx is a collection of blood extending into the fallopian tube, e. g., due to hymenal atresia.

Pyosalpinx is a collection of pus secondary to an inflammatory stenosis.

Sonographic features. The tubal wall appears sonographically as a pair of echogenic lines. With an abscess, the wall shows echogenic thickening (Fig.13.78). The fallopian tube runs a tortuous course. When it contains a collection of clear fluid, the lumen is dilated and anechoic. With blood or pus in the tube, the lumen may appear echogenic and nonhomogeneous (Fig.13.79). An infection of the fallopian tube often encroaches on the ovaries by direct continuation. The inflamed organs (tube/ovaries) generally cannot be sufficiently differentiated.

Differentiation. Color duplex examination can differentiate a fallopian tube from varicose vessels. Bowel loops generally have a hypoechoic wall that distinguishes them from the fallopian tube. Malignant masses tend to be painless, whereas inflammatory processes cause severe pain. Tubo-ovarian cysts are not true neoplasms but residua from pelvic inflammatory disease.

is the best available imaging technique. Diseases of the ovaries are often detected at

an extremely late stage owing to the delayed onset of symptoms.

branch of the uterine artery. The left ovarian artery occasionally arises from the left renal artery. The blood vessels run to the hilum in the ovarian suspensory ligament.

Arborizing valveless veins form a network, the pampiniform plexus (ovarian venous plexus), that surrounds the organs. The right ovarian vein opens directly into the vena cava, while the left ovarian vein drains into the left renal vein.

The ovaries of the nullipara lie in a small groove (ovarian fossa) in the lateral pelvic wall on both sides of the uterus. They are located anterior to the ureter in the bifurcation of the common iliac artery (Fig.13.82).

The ovaries are attached to the pelvic wall by the ovarian suspensory ligament and to the cornual area of the uterus by the proper ovar-

ian ligament. They are attached posteriorly to the mesovarium by the broad ligament. During pregnancy, the enlarged uterus displaces the ovaries into the abdomen. After pregnancy, the ligaments are so stretched that the ovaries become mobile and can vary greatly in their position.

Ultrasound Morphology

The ovaries can usually be visualized in women of reproductive age (Fig.13.83). Both ovaries can be identified in approximately 80% of cases. The ovaries can rarely be visualized after menopause, when they are smaller and less echogenic.

On ultrasound the ovaries in fertile women measure approximately 2 × 3 × 1.5 cm,3 which corresponds closely to the anatomic dimensions of 2.5 cm long, 2 cm wide, and 1 cm thick.2 They may be slightly less echogenic than the uterus and display anechoic cystic changes during the ovarian cycle.

The ovarian cortex initially contains several rounded, anechoic masses up to 10 mm in diameter. Approximately 7 days after menstruation, one dominant follicle appears while the others regress. The dominant follicle grows to a graafian follicle by the time of ovulation, measuring approximately 2 cm in size and projecting above the organ surface. An echogenic ringlike structure, the cumulus oophorus, appears in the follicle. After ovulation, free fluid can be demonstrated in the cul-de-sac. Now the follicle is misshapen or no longer visualized. When bleeding occurs in the corpus luteum, the follicle becomes uniformly hyperechoic.

Size and shape

●2 × 3 × 1.5 cm

●Almond-shaped

Structure

●Medullary zone

●Cortical zone with follicles, corpora lutea, and corpora albicantia

●Capsule (tunica albuginea)

Landmarks

●Bladder

●Uterus

●Pelvic wall

●Iliac vessels

Anechoic Cystic Mass

Simple Follicles

Functional Cysts (Follicular and Corpus Luteum Cysts)

Theca-Lutein Cyst

Paraovarian Cyst

Polycystic Ovaries (PCO Syndrome, Stein–Leventhal Syndrome)

Cystic Ovarian Tumors

Lutein cysts develop from atretic follicles. They represent follicular cysts that have theca-lutein cells on their inner surface. Lutein cysts result from hyperstimulation by gonadotropins and therefore occur in diseases and conditions that are associated with increased α-hCG formation, i. e., in 20% of molar pregnancies, in chorioepithelioma patients, and in multiple pregnancies. For this reason they are also commonly seen in patients with polycystic ovaries and in women treated for infertility. They may contain progesterone in high doses and regress

after the cause is eliminated, although this may take several months.

Patients may become symptomatic owing to complications such as cyst torsion, intracystic hemorrhage, and rupture with hemorrhage. Ruptures and infarctions are an indication for operative treatment.

Sonographic features. Theca-lutein cysts can range from 6 to 20 cm in size.8 A single cyst is rarely larger than a lemon, but because lutein cysts tend to be multiple and bilateral, the ovaries may be substantially enlarged. The

cyst wall resembles an abscess membrane. The ovarian parenchyma is edematous. The cysts rupture easily, and pedunculated cysts often undergo torsion. Ascites may occur.

The sonographic criteria of a theca-lutein cyst are:

●Multiple

●Bilateral

●Thin-walled

●Anechoic contents

●Echogenic with intracystic hemorrhage

●Moderate to massive ovarian enlargement

Paraovarian cysts arise from fetal tissues bordering the ovaries (epoöphoron, vestiges of the caudal mesonephric duct in the mesovary). They are more accurately classified as retention cysts rather than true neoplasms. They arise in the mesovary, are invariably benign, and occur at any age. Paraovarian cysts are variable in size; they may be pedunculated, and those with long pedicles tend to undergo torsion (Fig.13.88).

Their sonographic criteria are as follows:

●Elliptical shape

●Intraligamentous

●Well delineated from the ovary, may be pedunculated

Fig. 13.88 Paraovarian cyst: near-anechoic mass (cursors) between uterus (UT) and ovary (OV); BL = bladder.

PCO syndrome develops during puberty as a result of increased androgen production by the adrenal cortex following adrenarche. It affects up to 7% of the female population. The initiating cause is poorly understood.

Stein–Leventhal syndrome develops when the hyperandrogenemia9 gives rise to a symptom complex of polycystic ovaries, hirsutism, menstrual abnormalities, and obesity.

The following are additional symptoms of PCO:

●Sterility and infertility (74%)

●Hirsutism (50–70%)

●Amenorrhea and oligomenorrhea (approximately 50%)

●Dysfunctional bleeding (approximately 30%)

●Overweight (40%)

The estrogen stimulation of the endometrium induces hyperplasia and can also lead to welldifferentiated endometrial carcinoma.

Sonographic features. The ovaries are generally larger than the uterine corpus. The smooth tunica albuginea shows echogenic thickening, and the cortex contains anechoic, usually equal-sized follicles up to 5 mm in diameter (rarely >1 cm) arranged in a circumferential pattern. Follicular maturation does not occur. Since ovulation is absent, there is no surface pitting and no corpora albicantia.

The sonographic criteria are as follows (Fig.13.89, Fig.13.90):

●Bilateral occurrence

●Enlarged ovaries

●Hyperechoic center

●Multiple cysts (anechoic follicles up to 5 mm in the cortex)

●Endometrial hyperplasia usually present

Pathogenesis of PCO Syndrome

PCO syndrome is characterized by a vicious cycle in which a stressful situation with increased ACTH secretion stimulates the formation of androstenedione in the adrenal cortex. This hormone is metabolized in the fat to estrone and sensitizes the pituitary to LHRH. The result is excessive LH secretion (FSH is unaffected), causing a nonphysiological stimulation of the ovaries and increased androgen production (androstenedione) in the theca follicles and stromal cells. The androgen is again converted to estrone in the fatty tissue, and the cycle continues.