Female Pelvis Ultrasound

Sonography plays the primary role in imaging of the female pelvis. CT and MR are supplemental techniques used when the US examination is equivocal and in the staging of pelvic malignancy. Primary indications for female pelvic US examination are pelvic pain, abnormal vaginal bleeding, and suspicion of pelvic mass. Additional indications include evaluation of precocious puberty, infertility, and early cancer detection.

Imaging Technique

US examination of the pelvis is routinely performed both transabdominally with a full bladder and transvaginally with the bladder empty. Additional examination techniques include the translabial imaging and sonohysterography.

Examination is often begun using the transabdominal (TA) approach. The patient is asked to fill her bladder by drinking several glasses of fluid and by not urinating for at least 1 hour prior to examination. The patient lies supine on the examination table. A 3.5-5.0-MHz sector transducer is placed on the lower abdomen just above the symphysis pubis and the pelvic organs are examined through the window of the distended bladder. Bladder filling is ideal when the bladder dome is just above the uterine fundus. Overdistention compresses the normal anatomy and displaces masses and fluid out of the pelvis. Underdistention limits visualization. Images are obtained in sagittal and transverse planes. To optimally image the uterus, the transducer is aligned with the long axis of the uterus, which is often angled right or left from the midline cervix. The ovaries and adnexa are often best seen by sliding the transducer to the contralateral side and angling back toward the ovary of interest. Measurements are obtained of the uterus, ovaries, and any masses detected in three orthogonal planes. Volumes may be calculated using the formula: volume = length × width × height × 0.52. The TA technique provides the best overview of the pelvis, and is best for examining large masses, but is less comfortable for the patient because of the distended bladder.

For transvaginal (TV) examination, the patient is asked to empty her bladder and lie supine with her legs flexed. Folded sheets or pads are placed under her buttocks to elevate her pelvis above the examination table to allow room for transducer manipulation. Alternatively, the patient may be examined on a pelvic examination table with her feet in stirrups.

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A 4.0-7.0-MHz TV US probe is coated with gel and is covered with a sterile condom that is also coated with gel. The probe may be placed in the vagina by the patient, the sonographer, or the sonologist. Prudence dictates that a woman should be in the room at all times during a vaginal sonogram, either as the examiner or as a chaperone [1]. The uterus is examined for size, shape, contour, orientation, and appearance of the myometrium, endometrium, and cervix. The ovaries are documented for size, shape, contour, echogenicity, and position. Any masses or abnormalities are evaluated for origin, echotexture, size, shape, and relationship to other organs. The cul-de-sac is examined for fluid and masses. Loops of bowel in the pelvis are inspected for peristalsis and wall thickening.

The TV technique offers better tissue characterization because of the ability to use high-frequency transducers. However, the field of view is limited and large masses may be overlooked. If TV examination is performed first, the pelvis should always be examined transabdominally, even if the bladder is empty, to check for abnormalities outside the TV field of view.

The translabial approach is particularly useful for examination of the vagina and cervix, and is an effective alternative for any patient unwilling or unable to undergo TV examination [2]. A 3.5-5.0-MHz sector transducer, covered with a transducer sheath and generously coated with gel, is placed on the labia. Examination is performed in sagittal and coronal planes along the long axis of the vagina.

A transrectal approach to pelvic US may also be used especially in patients unwilling or unable to undergo TV US. The transrectal approach offers similar advantages of placing the transducer closer to the organs of interest allowing higher frequency transducers with better resolution.

Sonohysterography (SHG) is a useful technique to examine the endometrium and uterine cavity [3, 4, 5]. The examination is easiest to perform with the patient on a pelvic examination table with her feet in stirrups. A speculum is used to visualize and cleanse the cervix with antiseptic solution. A 5-F pediatric feeding tube or a balloon SHG catheter, pre-filled with sterile saline solution, is placed into the cervix. If a balloon catheter is used, the balloon is distended in the cervical canal with 3-5 mL of water, not air. The speculum is removed and a TV US transducer is placed into the vagina. Using direct US visualization, saline is injected to distend the uterine cavity, detect polypoid masses, and to assess the appearance and thickness of the endometrium.

Anatomy

The size and shape of the uterus vary with age and parity. The uterus of the neonate, stimulated by maternal hormones as a fetus, is up to 1 cm longer and 1 cm larger in diameter than the uterus of a young child. The cervix is commonly twice as long and twice as thick as the body. By the end of the first year of life the uterus has become smaller and is sausage shaped. With puberty, the uterus assumes a pear shape with the body twice as large as the cervix. The uterus enlarges with multiparity and atrophies following menopause. Normal uterine dimensions are listed in Table 5.1.

The surface of the uterus is smooth and well defined (Fig. 5.1). A slightly indented isthmus separates the body from the cervix. The cervix is fixed in the midline of the pelvis,

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but the body is often “flexed” and angled (“verted”) with respect to the cervix. The uterus is most commonly anteflexed and anteverted, lying on the bladder dome. A retroflexed uterus is bent at the isthmus with the body folded backwards on the cervix (Fig. 5.2). A retroverted uterus is straight but directed posteriorly. The body may also be angled toward the right or left pelvic sidewalls.

Table 5.1: Normal Dimensions of the Uterus

Stage of Life	Normal Dimensions (cm)
Neonate	4 × 2 × 2
Child (pre-pubertal)	3 × 1 × 1
Woman (nulliparous)	8 × 4 × 4
Woman (multiparous)	9 × 5 × 5
Woman (postmenopausal)	7 × 2 × 2

Figure 5.1 Normal Uterus–Transabdominal. Longitudinal scan through the urine-filled bladder (B) demonstrates a normal adult uterus with smooth contours, pear shape, and well-defined bright endometrial echo (open arrow). The cervix (arrow) is recognized at the junction of imaginary lines drawn through the long axis of the uterus and the long axis of the vagina (between arrowheads). This uterus is anteverted.

Figure 5.2 Normal Uterus–Retroflexed. Longitudinal transabdominal (A) and transvaginal (B) images demonstrate a normal retroflexed uterus. The uterus is flexed at the uterine isthmus (I) with the fundus (F, black arrow) directed posteriorly. The endometrium (arrowhead) is thin in the early proliferative phase. The large arrows indicate the direction of “up” when scanning transabdominally and transvaginally in longitudinal plane.

Figure 5.3 Normal Arcuate Vessels. Longitudinal transvaginal gray-scale (A) and corresponding color Doppler (B) images show prominent but normal arcuate vessels that divide the middle from the outer layer of myometrium. Visibility of these vessels varies greatly from patient to patient. This uterus is anteverted. The arrow shows the location of the fundus.

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The myometrium is medium in echogenicity and granular in echotexture. Three layers of myometrium can often be recognized. The inner junctional myometrium is thin, compressed, hypovascular, and mildly hypoechoic compared to the thick homogeneous middle layer. The arcuate vessels, which are often prominent, divide the middle layer from the slightly hypoechoic outer layer (Fig. 5.3). Calcification of the arcuate arteries occurs in older women and diabetics (Fig. 5.4).

The endometrium varies in thickness and appearance with the degree of stimulation by hormones, primarily estrogens and progesterones (Table 5.2). In the neonate, because of maternal hormones, the endometrium is brightly echogenic but thin. In the prepubertal child, the endometrium remains thin and is nearly isoechoic with the myometrium. Following puberty, the endometrial appearance varies with the menstrual cycle [6]. In the proliferative phase (Fig. 5.5A), prior to ovulation, the endometrium assumes a three-layer appearance as it thickens to 4-8 mm. The central line, which defines the endometrial cavity, is echogenic. The proliferating functional layer, which will slough with menstruation, is hypoechoic. The outer basal layer, which remains intact throughout the menstrual cycle, is echogenic and surrounded by the hypoechoic junctional zone of the myometrium. In the secretory phase, following ovulation, the functional layer continues to thicken and becomes echogenic (Fig. 5.5B). The entire double-layer thickness of the endometrium in the secretory phase is 7-14 mm. During menstruation, the functional layer is lost and the

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remaining basal endometrium appears as a thin, broken, irregular echogenic line. Following menopause, the endometrium atrophies, thins (to <4 mm), and becomes less echogenic. Hormone replacement therapy in the postmenopausal woman will stimulate the endometrium. Unopposed estrogen has the greatest effect. Sequential hormone replacement, with estrogen followed by progesterone, causes the endometrium to change to an appearance very similar to the premenopausal woman.

Figure 5.4 Calcified Arcuate Arteries. Transvaginal image of the uterus of an 85-year-old woman reveals calcification in the arcuate arteries (arrows). These calcifications occur as a result of atherosclerosis. This patient also has a small amount of fluid (f) in the uterine cavity. The thin, well-defined endometrial stripe (arrowhead) indicates the endometrium is benign and atrophic. Clinical evaluation is needed to look for evidence of cervical carcinoma.

Table 5.2: Normal Endometrial Appearance and Thickness

Phase	Normal Thickness (mm)	Appearance
Proliferative phase (pre- ovulation)	4-8	Triple layer (hyper- hypo-hyper)
Secretory phase (post-ovulation)	7-14	Uniform hyperechoic
Menstrual phase	1-2	Thin, broken echogenic line
Postmenopausal without bleeding	<8	Uniform hyperechoic
Postmenopausal with bleeding	<5 = endometrial atrophy >5 = risk of carcinoma	Uniform hyperechoic
Postmenopausal on hormone replacement therapy	Add 1–2 mm to values listed for postmenopausal women	Uniform hyperechoic
Endometrial thickness is measured perpendicular to the long axis of the uterine cavity and includes both the anterior and posterior endometrial layers. Any fluid in the endometrial cavity and the hypoechoic junctional zone myometrium is not included in the measurement.

The fallopian tubes extend laterally from the uterus in the free edge of the broad ligament. Each is 7-12 cm in length and consists of an intramural portion traversing the myometrium, a cord-like isthmus, a wider and tortuous ampullary portion, and the funnel-shaped, fimbriated infundibulum that opens into the peritoneal cavity. The fallopian tubes are not appreciated on US unless they are dilated or when peritoneal fluid defines the edge of the broad ligament.

The ovaries are elliptical in shape and lobulated in contour. Follicles project from the outer cortex, and the stroma and blood vessels occupy the inner medulla (Fig. 5.6). The ovaries are attached to the uterus by a fold of the broad ligament called the ovarian ligament, and to the pelvic sidewall by the suspensory ligament of the ovary. The fallopian tubes in the broad ligament and the mesosalpinx drape over the ovary. The ovaries are

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imaged in a shallow fossa anterior to the internal iliac vessels and medial to the external iliac vessels. The ovaries are displaced cephalad by increasing bladder distention. When the uterus is positioned toward the pelvic sidewall, the ipsilateral ovary is frequently located cephalad to the fundus. When the uterus is retroverted, the ovaries are usually ventral to the uterus at the level of the uterine body.

Figure 5.5 Physiologic Changes in the Endometrium. A. Proliferative phase endometrium (arrow) of the first half of the menstrual cycle has a triple-layer appearance. The outer (basal layer) endometrium is echogenic. The inner functional endometrium is hypoechoic, and the line demarcating the uterine cavity is echogenic. B. Secretory phase endometrium (arrow) of the second half of the menstrual cycle is uniformly echogenic and thickens to 7-14 mm.

Figure 5.6 Normal Ovary. A normal ovary (marked by calipers) is shown in this transvaginal image. Normal follicles outline the periphery of the ovary, whereas echogenic stroma is seen centrally.

The size and appearance of the ovaries change with age and with phase of the menstrual cycle (Table 5.3) [6]. In children younger than 8 years of age, the ovaries are homogeneous and solid [7]. Occasionally small follicles (<9 mm) are present. Normal follicles appear as anechoic, thin-walled cysts on the periphery of the ovary. In the follicular (proliferative) phase of the menstrual cycles, elevated levels of follicle-stimulating hormone and luteinizing hormone stimulate the development and enlargement of a variable number of follicles [6]. One follicle becomes dominant and matures as the Graafian follicle. This dominant follicle reaches a size of 20-25 mm, whereas most of the other follicles involute. Ovulation occurs when the dominant follicle ruptures, releasing the ovum and 15-25 ml of fluid into the peritoneal cavity. Mid-cycle pain, “mittelschmertz,” coincides with ovulation. The corpus luteum develops at the site of the ruptured dominant follicle. Blood clot and fibroblasts invade the collapsed follicle, which becomes intensely vascular and reforms a lymph and blood-filled cyst. The corpus luteum produces progesterone that supports the secretory endometrium to allow successful implantation if fertilization of the ovum occurs. The corpus luteum will degenerate in 14 days in the absence of an intervening pregnancy.

Size of the ovary is evaluated by measurement and calculation of volume using the standard formula (length × width × height × 0.52). Normal values are given in Table 5.3 [8, 9, 10]. The ovaries shrink with age after menopause [10].

Table 5.3: Normal Size of the Ovaries

Phase of Life	Mean Volume (cc)	Upper Limit of Normal Volume (cc)
0-3 months	1	4
3 months-2 years	1	3
Premenarchal (3-15 years)	3	9
Menstrual female	10	22
Postmenopausal	6	14
>15 years after menopause	2	4
Adapted from Cohen H, Shapiro M, Mandel F, et al. Normal ovaries in neonates and infants: a sonographic study of 77 patients 1 day to 24 months old. AJR Am J Roentgenol 1993;160:583-586; Cohen H, Tive H, Mandel F. Ovarian volumes measured by US: bigger than we think. Radiology 1990;177:189-192; and Tepper R, Zalel Y, Markov S, et al. Ovarian volume in postmenopausal women–suggestions to an ovarian size nomogram for menopausal age. Acta Obstet Gynecol Scand 1993;74:208-211.

Figure 5.7 Normal Fluid in the Cul-de-Sac. Anechoic fluid (f) is seen in the cul-de-sac posterior to the uterus (U). The fluid outlines loops of small bowel (b).

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The ovaries have a dual blood supply from the ovarian artery and from an adnexal branch of the uterine artery. Spectral Doppler shows high resistance flow in the first half of the menstrual cycle and low resistance flow in the second half after formation of the corpus luteum. The ovaries are hypovascular after menopause with flow detected only in the main ovarian artery.

The cul-de-sac frequently contains a small volume of fluid (~10 cc) that is best seen on TV US. A small volume of fluid is normal and physiologic (Fig. 5.7). The volume of fluid is increased with ovulation.

The normal vagina is a muscular tube in the midline of the pelvis extending from the vestibule of the external genitalia to the cervix. The cervix projects into the vaginal apex and is surrounded by vaginal recesses called the fornices. On sagittal images, the vagina appears as a tubular structure with hypoechoic muscular walls and a bright linear central echo caused by the apposing surfaces of the vaginal mucosa (Fig. 5.1). On transverse images (Fig. 5.8), the vagina appears as a flattened oval or flattened H-shaped structure with folds of vaginal mucosa laterally and the urethra coursing prominently in the anterior vaginal wall.

Figure 5.8 Normal Urethra and Vagina. Low transverse image shows the urethra (long arrow) in the anterior wall of the vagina. The muscular walls of the vagina appear hypoechoic compared to the echogenic line (open arrow) that marks the collapsed lumen and mucosa. The rectum (short arrow) is posterior.

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Uterus

Endometrial Abnormalities

Measuring Endometrial Thickness

Recurrence of vaginal bleeding in postmenopausal women is a common and potentially ominous complaint, with cancer as the cause of approximately 10% of cases. The majority of cases are caused by benign conditions including endometrial atrophy, hyperplasia, and polyps (Box 5.1). Conventional teaching has been that every postmenopausal woman with vaginal bleeding should undergo dilatation and curettage to sample the endometrium. US has provided a method of visualizing the endometrium and of being more selective in identifying patients for biopsy. US is used to assess the appearance and measure the thickness of the endometrium.

To properly use established criteria for basing the decision to biopsy on the thickness of the endometrium, the endometrium must be measured correctly. Endometrial thickness measurements are made “double layer” and include both the anterior and posterior endometrium (Fig. 5.9). The measurement is made perpendicular to the long axis of the uterine cavity where the endometrium is thickest and excludes any fluid in the cavity and the hypoechoic junctional myometrium. TV measurements are the most accurate. SHG aids in evaluation of the endometrium by outlining the endometrium surface and defining any polypoid protrusions [11]. A thin endometrium (<4 mm) or diffuse, smooth, regular thickening of the endometrium is the best predictor of benignancy [12]. Endometrial masses, irregular thickening, or focal thickening requires biopsy to exclude malignancy. In some patients, especially women with leiomyoma, the endometrium is distorted and is not adequately visualized for accurate measurement (~3% of patients) [13]. These women should undergo SHG or biopsy for diagnosis.

Criteria for biopsy as recommended by most authors is to biopsy patients with postmenopausal bleeding if the double-layer endometrial thickness exceeds 5 mm [13, 14]. In

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patients who are asymptomatic, that is, specifically, without vaginal bleeding, the endometrium is considered normal up to 8 mm. Endometrial thickness >15 mm in a postmenopausal patient is very high risk for malignancy.

Figure 5.9 Measuring Endometrial Thickness. Transvaginal image shows two well-defined endometrial layers separated by the dark line demarcating the endometrial cavity (arrow). Measurement (calipers, x) is made perpendicular to the long axis of the uterine cavity and includes the thickness of both layers of the endometrium. This postmenopausal patient has benign endometrial hyperplasia.

Hormone Replacement Therapy

In postmenopausal women, hormone replacement therapy is commonly prescribed to abate menopausal symptoms and to prevent osteoporosis. The supplemental hormones have a small but notable effect on the appearance of the endometrium [15].

Unopposed estrogen therapy and concurrent estrogen and progesterone therapy increase endometrial thickness by 1.0-1.5 mm.
Sequential estrogen-progesterone therapy increases stripe thickness by 3.0 mm.

Endometrial Atrophy

Atrophy of the endometrium is the most common cause of postmenopausal bleeding (~60% of cases). The endometrium becomes inactive and atrophies as estrogen stimulation diminishes with menopause.

Uniform thin endometrium (<5 mm) (Figs. 5.4, 5.10).
Cystic changes may occur and result in thickening of the endometrium.
Blood flow on Doppler US is minimal or absent.

Endometrial Hyperplasia

Endometrial hyperplasia is a proliferation of endometrial glands, which increase in size and assume an irregular shape. The hyperplasia is caused by unopposed stimulation of the endometrium by estrogen. Hormone replacement therapy with only estrogen is the most common cause of hyperplasia in postmenopausal women. In premenopausal women, causes include recurring anovulatory cycles, polycystic ovary disease, and obesity. Hyperplasia may be focal or diffuse, and is classified as adenomatous, cystic, or atypical adenomatous. Up to 25% of patients with endometrial hyperplasia with atypia will eventually develop endometrial cancer.

Diffuse or focal smooth thickening of the echogenic endometrium (Fig. 5.9).
Cystic changes are common.
Atypical hyperplasia often appears heterogeneous and irregular (Fig. 5.11).

Figure 5.10 Endometrial Atrophy and Cervical Stenosis. Echogenic fluid (f) fills and distends the uterine cavity and shows a fluid-fluid level (black arrowhead). The large white arrow indicates the direction of “up” on this transvaginal image. The endometrium (small white arrows) is thin and regular with double-layer thickness of 2 mm indicating endometrial atrophy in this 65-year-old patient. The fluid in the uterine cavity is excluded from the endometrial measurement. Further clinical evaluation confirmed cervical stenosis.

Figure 5.11 Atypical Endometrial Hyperplasia. The endometrium (e) is irregularly thickened, lobulated in contour, and has an ill-defined margin. Endometrial biopsy revealed endometrial hyperplasia with atypia. This is a transabdominal image in sagittal plane. Cursors (+) mark the extent of the uterus.

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Endometrial Polyps

Endometrial polyps are localized, pedunculated, or broad-based growths of endometrial tissue that commonly cause bleeding. Polyps peak in prevalence in the fifth decade of life, but may be a cause of infertility in younger patients. Approximately 20% present after menopause. On routine TV sonography, the polyps appear as a non-specific echogenic thickening of the endometrium. However, when fluid is naturally present in the endometrial cavity or is introduced during SHG, an oval echogenic mass of intraluminal endometrium is evident. Treatment is resection by dilatation and curettage or by hysteroscopy.

Focal polypoid thickening of the endometrium (Fig. 5.12) [16].
Polyps may be pedunculated on a narrow stalk or broad-based (Fig. 5.13).
Vascular pedicle is demonstrable on color Doppler US.
Echogenicity is uniform, hyperechoic relative to myometrium and isoechoic to endometrium.
Cystic areas are occasionally present within the polyp.
Polyps are differentiated from submucosal leiomyomas by the uniform high echogenicity of the polyp (Fig. 5.13) [17].
Multiple polyps are present in 20% of cases.

Endometrial Carcinoma

Endometrial carcinoma is the most common gynecologic malignancy, occurring in 3% of American women. Most cases (80%) occur in postmenopausal women and most present with abnormal vaginal bleeding. Endometrial carcinoma is the cause of 7-30% of postmenopausal bleeding. US shows thickening of the endometrium that is often indistinguishable from hyperplasia and polyps. Signs that suggest cancer include inhomogeneous

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echogenicity, irregular and poorly defined margins, and invasion of the myometrium [18].

Figure 5.12 Endometrial Polyp. Focal, smooth, echogenic thickening of the endometrium (long black arrow) is contrasted with a long segment of thin endometrium (short white arrow). This appearance suggests an endometrial polyp. Diagnosis can be confirmed with a sonohysterogram.

Figure 5.13 Endometrial Polyps. Two sonohysterograms (A, B) show pedunculated endometrial polyps (arrows) outlined by fluid instilled into the endometrial cavity. Note the high echogenicity of the polyp equal to that of the endometrium. Compare to the low echogenicity of the submucosal leiomyomas in Figure 5.16. Calipers (+) measure the size of the polyp in B.

Thickened endometrium is a hallmark sign. Endometrial thickening >15 mm in postmenopausal women has a high risk of malignancy.
The endometrium is usually diffusely or partially echogenic (80-90%).
The endometrium is unevenly thickened and irregular in contour in 60-70% (Fig. 5.14).
Smooth, uniform, endometrial thickening indistinguishable from endometrial hyperplasia is present in 30-40%.
Poorly defined endometrium that is difficult to visualize suggests carcinoma (Fig. 5.15).
Cystic changes are present in 24%.

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Some carcinomas are polypoid with a broad base.
Lack of distensibility of the endometrial canal may be evident on SHG [17].
Calcification is rare.

Figure 5.14 Endometrial Carcinoma. The endometrium (arrow) is thickened (to 12 mm) and is irregular in contour. Echogenicity is that of normal endometrium. Biopsy confirmed endometrial carcinoma. This transvaginal US image is in coronal plane.

Figure 5.15 Endometrial Carcinoma. This postmenopausal patient presented with new onset uterine bleeding. On transvaginal US, the endometrium (between arrows) is low in echogenicity, very poorly defined, and thickened (>15 mm). This appearance is highly predictive of endometrial carcinoma, which was confirmed at biopsy. The cursor (+) marks the fundus of the uterus.

Tamoxifen-Related Endometrial Changes

Tamoxifen is an antiestrogen chemotherapeutic agent used in patients with breast cancer [19]. Although it is used for its antiestrogen, tumor-suppressive effects, the drug has proliferative effects on the endometrium and may promote endometrial tumor growth. Histologic changes reported with tamoxifen therapy include endometrial hyperplasia, endometrial polyps, and endometrial carcinoma [20, 21]. Cystic change is characteristic. Thickness of the endometrium increases with duration of tamoxifen therapy especially after 5 years.

The endometrium is irregularly thickened (usually >8 mm in postmenopausal patients).
Multicystic changes in the thickened endometrium is characteristic.
Endometrial polyps are common (33%).

Submucosal Leiomyoma

Leiomyomas located just beneath the endometrium are prone to ulceration and bleeding. They compress the endometrium, may bulge into the endometrial cavity, and may become a polypoid mass within the endometrial cavity. SHG is used to characterize the size and intraluminal extent of the mass so that surgical resection can be optimally planned using either a TA or hysteroscopic approach.

Hypoechoic mass just beneath the endometrium (Fig. 5.16).
The mass may cause acoustic shadowing.
The mass compresses the endometrium and may project into the endometrial cavity.
Vascularity, demonstrated by color Doppler, helps to differentiate leiomyomas from blood clots.
Low and heterogeneous echogenicity differentiates leiomyomas from echogenic endometrial polyps (Fig. 5.16) [17].
Leiomyomas commonly calcify.

Intrauterine Device

Intrauterine devices (IUDs) are currently in less common use because of complications of endometritis, ectopic pregnancy, and uterine perforation. US is effectively used to document IUD location when the IUD string is lost or to confirm proper IUD placement.

IUDs are seen as brightly echogenic structures in uterine cavity. The appearance depends upon the type of IUD.
The normal location for an IUD is centered in the uterine cavity near the fundus.

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Copper-wrapped IUDs are intensely echogenic and cause comet tail artifacts (Fig. 5.17). Most are in the shape of a 7 or a T.
Lippes loops have a regular pattern of repeating echogenic foci that cast acoustic shadows.

Figure 5.16 Submucosal Leiomyomas. Sonograms on two patients (A, B) show the characteristic low echogenicity of submucosal leiomyomas (arrows) that protrude into the uterine cavity. Compare with the appearance of endometrial polyps in Figure 5.12.

Fluid in the Endometrial Canal

A small volume of anechoic fluid in the endometrial canal is common in postmenopausal women (Fig. 5.4). It usually reflects cervical stenosis, or results from hormone replacement therapy [22]. According to one study, if the single layer endometrium measures 3 mm or less (<6 mm double layer), the endometrium is atrophic and inactive, so no further evaluation of the endometrium is necessary (Figs. 5.4, 5.10) [23]. Patients should be examined clinically for evidence of cervical carcinoma.

Figure 5.17 Copper-Wrapped IUD. Longitudinal (A) and transverse (B) transabdominal images demonstrate the characteristic appearance of a copper-wire-wrapped IUD (arrows) in normal location in the uterine cavity. Note the comet tail artifacts deep to the IUD.

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Intrauterine Adhesions

Adhesions are formed by scarring that fastens the walls of the uterus together and obliterates part or all of the uterine cavity [24]. Patients with a history of repeated uterine instrumentation or uterine infections are at highest risk. Patients present with amenorrhea or repeated spontaneous abortion.

Adhesions appear as an irregular hypoechoic bridge that interrupts the endometrium and is in continuity with the myometrium. Size, shape, and extent are variable.
Adhesions are best seen when fluid is present in the endometrial cavity either naturally or during SHG.

Endometritis

Endometritis occurs within the spectrum of pelvic inflammatory disease (PID). Puerperal endometritis is most common 2-5 days after delivery.

The endometrium is thickened and edematous.
Fluid is usually found in the endometrial cavity. It is commonly echogenic and layers producing fluid-fluid levels.
Gas in the endometrial cavity is found in 15% of patients. This is not a specific finding in the postpartum patient. In women with uncomplicated vaginal deliveries, gas may be found in the endometrial cavity in 19% of women during the first 3 postpartum days and in 7% of women for 3 weeks postpartum [25].

Myometrial Abnormalities

Leiomyomas

Leiomyomas are the most common tumor of the female pelvis, occurring in up to 40% of women older than age 35 [26] years. The tumors are composed of smooth muscle with variable amount of fibrous connective tissue. Most leiomyomas cause no symptoms, but they can cause menorrhagia, dysmenorrhea, irregular uterine bleeding, pelvic pain, infertility, and the discomfort of a large pelvic mass. Tumors grow in response to estrogen and typically enlarge during pregnancy and regress after menopause. Tumor location is described as intramural, submucosal (beneath the endometrium), or subserosal (on the surface of the uterus).

Figure 5.18 Leiomyoma. Leiomyoma appears as a hypoechoic mass (between arrows) in the wall of the uterus. Fibrous areas within the leiomyoma cause streaks of acoustic shadowing. The endometrium (open arrow) is bowed around the leiomyoma.

Figure 5.19 Cystic Change in Leiomyoma. An intramural leiomyoma (between arrows) with echogenicity slightly greater than normal myometrium shows an area of cystic necrosis (curved arrow).

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A round to oval, solid, hypoechoic mass is typical. Refractory acoustic shadowing produced by fibrous elements within the tumor is highly indicative of leiomyoma (Fig. 5.18) [27].
Inhomogeneous myometrium is produced by numerous small leiomyomas.
Tumors cause a focal bulge in the uterine contour (intramural leiomyoma), or compress and distort the endometrium (submucosal leiomyoma).
Necrosis, hemorrhage, and cystic changes are common (Fig. 5.19). Irregular, coarse calcifications are characteristic (Fig. 5.20).
Isoechoic tumors may be undetectable or cause only uterine enlargement.
Subserosal fibroids may become pedunculated and present as an adnexal mass. Diagnosis is made by color flow US demonstration of a vascular pedicle continuous with the myometrium (Fig. 5.21).
Lipomatous leiomyomas contain benign fat cells. With high fat content, the tumors are intensely echogenic.
Pedunculated serosal leiomyomas on a narrow stalk may parasitize blood supply from adjacent structures and detach from the uterus [28]. These are called parasitic leiomyomas.

Figure 5.20 Calcification in Leiomyoma. A characteristic coarse calcification (arrow) is seen within an intramural leiomyoma that causes a focal bulge in the contour of the uterus.

Figure 5.21 Pedunculated Leiomyoma. A. Transvaginal US image shows a hypoechoic mass (outlined by cursors, x, +) adjacent to the uterus. B. Color Doppler image in the same location shows contiguous blood flow from the uterus into the mass, confirming a pedunculated leiomyoma (see Color Figure 5.21A, B).

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Leiomyosarcoma

Leiomyosarcoma of the uterus is a rare lesion accounting for approximately 1% of uterine malignancy. Accurate diagnosis by US or other imaging is difficult. Most patients are asymptomatic, although some present with abnormal uterine bleeding.

The most suspicious finding is documented rapid enlargement of a solid uterine mass that otherwise has the appearance of a benign leiomyoma. Local invasion, regional adenopathy, and distant metastases are signs of advanced malignancy.
Many leiomyosarcomas resemble degenerated leiomyomas in appearance with marked heterogeneity and areas of necrosis and hemorrhage. Some are indistinguishable from benign leiomyomas (Fig. 5.22).

Adenomyosis

The presence of endometrial glands and stroma within the myometrium is termed adenomyosis [29, 30, 31]. Adenomyosis is a major cause of dysmenorrhea, menorrhagia, and uterine enlargement that affects 15-20% of women, especially in their perimenopausal years.

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Dense, tightly packed, myometrial cells surround the ectopic endometrial glands. MR is the most sensitive method for imaging diagnosis. US findings are subtle and non-specific [32].

Figure 5.22 Leiomyosarcoma. Homogeneous solid mass near the uterine fundus proved to be a leiomyosarcoma. The patient presented with symptoms of partial small bowel obstruction. Computed tomography (not shown) revealed invasion of adjacent small bowel. The echotexture of this leiomyosarcoma is indistinguishable from a benign leiomyoma.

Figure 5.23 Adenomyosis. The US findings of adenomyosis are commonly subtle. This image illustrates widening and irregularity of the junctional zone myometrium (arrows). A small leiomyoma (black arrowhead) causes a focal bulge in the uterine contour.

US shows areas of decreased echogenicity or heterogeneous myometrium (~75% of cases). The foci of decreased echogenicity correspond to smooth muscle hyperplasia. The heterogeneous foci correspond to the endometrial implants (Fig. 5.23) [32].
Tiny cysts in the junctional myometrium result from dilated cystic endometrial glands or from foci of hemorrhage.
Echogenic linear striations extend from the endometrium into the myometrium.
The junction between endometrium and myometrium is poorly defined.
Diffuse uterine enlargement with normal-appearing myometrium and endometrium may be the only finding.
The hypoechoic junctional zone myometrium shows focal or diffuse thickening (Fig. 5.23).

Uterine Arteriovenous Malformations

Arteriovenous malformations (AVMs) of the uterus are a rare cause of uterine bleeding [33]. Most AVMs are isolated and congenital but some occur as a result of curettage or other uterine surgery, pelvic trauma, pregnancy, or uterine cancer. AVMs are a tangle of abnormal vessels without a capillary network.

On gray-scale US, AVMs appear as tubular spaces in the myometrium, or as an ill-defined mass in the myometrium, endometrium, or cervix [33].
Parauterine vessels may be prominent.
Color Doppler shows an intensely colorful, tangled network of vessels with prominent turbulence and aliasing.
Spectral Doppler shows high systolic velocities (>96 cm/sec) and low resistance spectra (Resistive Index [RI] = 0.25-0.55).

Arcuate Artery Calcification

Arteries that course between the intermediate and outer layers of the myometrium commonly develop atherosclerotic calcification in elderly, diabetic, or hypertensive women.

Multiple small echogenic foci in the boundary zone between intermediate and outer layer myometrium (Fig. 5.4).
Doppler confirms arterial flow if the vessels are patent.

Junctional Zone Calcification

Dystrophic calcifications in the junctional zone myometrium are caused by injury from prior instrumentation or biopsy.

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Punctate echodensities are seen in the junctional zone. Acoustic shadowing may be present.

Cervical Abnormalities

Abnormalities of the cervix are best evaluated by clinical examination. TV US demonstrates the cervix well if the transducer is withdrawn slightly and angled toward the cervix. Installation of water into the vagina improves visualization of the cervix [34].

Cervical Stump

Supracervical hysterectomy was formerly a common procedure, leaving behind a stump of cervix that may be mistaken for a mass at the apex of the vaginal vault.

Remnant of normal cervix appears as a solid tubular structure with cervical muscle appearing identical to myometrium and the endocervical mucosa forming a thin bright central linear echo.

Nabothian Cysts

Nabothian cysts are common benign inclusion cysts of the cervical mucosa. They are of no clinical significance.

Simple cysts are seen within or projecting from the cervix. They vary in size from 1-2 mm up to 4 cm and are commonly multiple (Fig. 5.24).
Internal fluid is anechoic except in rare instances when traumatic hemorrhage or infection results in internal debris.

Cervical Polyp

Polyps arise from the endocervical mucosa and are a common cause of abnormal bleeding.

Well-defined oval or round masses are seen in the endocervical canal or protruding from the cervix. Polyps are isoechoic with the endocervical mucosa [35].

Figure 5.24 Nabothian Cysts. Transabdominal longitudinal (A) and transvaginal transverse (B) images of the cervix illustrate the characteristic appearance of nabothian cysts (arrows).

Figure 5.25 Cervical Carcinoma. The cervix (between arrows) is bulbous and somewhat ill defined on this transabdominal image. A small volume of fluid (f) is present in the uterine cavity. Cervical leiomyoma may have a similar appearance. Carcinoma was confined to the cervix on pathological examination.

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Cervical Leiomyoma

Leiomyomas arising in the cervix account for 8% of uterine leiomyomas.

Solid nodules are seen within or extending from the cervix. Prolapse into the vagina is common.
Echogenicity is heterogeneous but lesions are hypoechoic compared to endocervical mucosa and usually isoechoic to cervical muscle [35].

Cervical Carcinoma

Cancers of the cervix are primarily diagnosed clinically.

Inhomogeneous enlarged cervix (Fig. 5.25). Invasion and fixation of paracervical tissues and the upper vagina are common (Fig. 5.26).
The appearance of early cervical cancer overlaps the appearance of cervical leiomyoma (Fig. 5.25).

Developmental Abnormalities

Developmental anomalies of the uterus are commonly detected with US but are more completely characterized by MR [36]. Uterine anomalies occur in 5-6% of women and are associated with an increased rate of infertility, spontaneous abortion, and other obstetric complications. The uterus, cervix, fallopian tubes, and upper vagina arise embryologically from paired müllerian ducts, which must migrate caudally and fuse with each other as well as with the distal wolffian ducts to result in normal development. Anomalies result from arrested development of the müllerian ducts, failure of fusion of the müllerian ducts, or failure

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of resorption of the midline uterine septum. Renal anomalies occur in 30% of women with müllerian defects. Unilateral renal agenesis is the most common associated anomaly. US examination must be careful, detailed, and correlated with physical examination to arrive at an accurate diagnosis. Questionable cases should be referred for MR examination.

Figure 5.26 Advanced Cervical Carcinoma. The cervix and upper vaginal region are replaced by an ill-defined soft tissue mass (M). Echogenic fluid (f) fills the uterine cavity. This cervical cancer, stage IIIB, invaded the anterior vaginal wall and extended to the pelvic side wall.

Uterine Aplasia and Uterus Unicornis Unicollis

These anomalies result from arrested development of the müllerian ducts. If both müllerian ducts are aplastic, the uterus is congenitally absent. If one müllerian duct is aplastic, the uterus develops with only one uterine horn but has a normal single cervix (uterus unicornis unicollis). Hypoplasia of one müllerian duct results in hypoplasia of one uterine horn.

Congenital absence of the uterus is exceedingly rare. The uterus, cervix, fallopian tubes, and upper four-fifths of the vagina are absent in a female of normal genotype. The vagina may be only a shallow external dimple.
Unicornate uterus may be difficult to recognize by US. The uterus appears small and is usually positioned to one side of the pelvis [37]. Hypoplasia of one horn is far more common than aplasia. The hypoplastic horn may contain fluid if endometrium is present within the horn.
The hypoplastic uterine horn may be mistaken for an adnexal mass.

Duplication Anomalies

Complete failure of fusion of the two müllerian ducts results in complete duplication (uterus didelphys). Greater degrees of müllerian duct fusion result in lesser degrees of duplication.

The key to US recognition of these anomalies is to recognize a deep external concave fundal cleft that defines the abnormal separation of the two uterine horns. The normal fundus is smoothly contoured and is convex externally.
Uterus didelphys describes the presence of two vaginas, two cervices and two separated uterine horns.
Uterus bicornis bicollis describes two separate uterine horns with two cervices and one vagina.
Uterus bicornis unicollis describes two separate uterine horns with a single cervix and vagina.

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Arcuate uterus (uterus arcuatus) describes a partial indentation of the uterine fundus with minimal alteration of the uterine cavity.
Any uterine anomaly may be associated with a transverse septum that obstructs menstrual outflow and results in hematometra and hematocolpos.
Uterine anomalies commonly are discovered in early pregnancy when fluid outlines the uterine cavity and reveals the separated uterine horns.
Careful attention to the endometrial echo, especially in transverse plane, also documents the separated uterine cavity by showing two endometrial complexes (Fig. 5.27).
Be sure to examine the kidneys for associated anomalies in all cases. Renal agenesis is most commonly associated with uterus bicornis bicollis with a partial uterine septum resulting in unilateral hematometrocolpos.

Figure 5.27 Septate Uterus. Transvaginal image shows two endometrial complexes (arrows) separated by a muscular septum. The uterine fundus was convex externally.

Figure 5.28 Hematometra. The endometrial and endocervical canals (f) are distended with bloody echogenic fluid in this patient with cervical stenosis.

Septate Uterus

A midline uterine septum may partially or completely divide the uterus into two cavities without duplication of the uterine horns [38]. This anomaly results from failure of resorption of the septum following normal fusion of the müllerian ducts.

The fundus is convex externally indicating the absence of duplicated uterine horns.
The uterine cavity is divided completely or partially by midline fibrous or muscular tissue (Fig. 5.27). Two separate endometrial complexes are visualized. Color Doppler may confirm vascularization of the septum and aid in its recognition [38].

Hematometra and Hematocolpos

Obstruction of the genital tract results in the accumulation of menstrual blood in the uterus (hematometra), the vagina (hematocolpos), or both (hematometrocolpos). Congenital obstructions are caused by imperforate hymen, vaginal septum, vaginal atresia, or obstructed, hypoplastic uterine horn. Acquired obstructions result from inflammatory conditions, tumors, radiation treatments, or cervical stenosis [39].

Echogenic fluid distends the uterus (Fig. 5.28) and/or the vagina (see Fig. 5.62). Anechoic fluid suggests non-hemorrhagic secretions (hydrometrocolpos). Pyometra is suggested by the presence of clinical signs of infection.

Ovaries and Adnexa

Follicles

Normal physiologic cysts seen on the ovaries include normal follicles, the developing dominant follicle, and the corpus luteum.

Figure 5.29 Normal Follicles. Transvaginal image shows several normal follicles (arrows) on the ovary (between calipers, +, x). Normal follicles have thin walls, are anechoic, and are <25 mm in size.

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Normal follicles are smooth, round, echo-free, thin-walled cysts on the ovary <25 mm in diameter (Fig. 5.29). As the dominant follicle enlarges (up to 25 mm) prior to ovulation, the other follicles atrophy. These follicles are normal physiologic structures and must be recognized as such.
The corpus luteum has a varying appearance [6]. It develops at the site of ovulation and is initially a solid structure with blood clot occupying the site of the collapsed dominant follicle. The corpus luteum quickly becomes cystic, enlarges to 15-25-mm size, and persists through menstruation [40]. Thus, a unilocular cyst 25 mm or less in size is normal in the second half of the menstrual cycle as well. The corpus luteum has a slightly thicker wall and more echogenic contents than a follicle. Blood flow to the corpus luteum is low resistance on spectral Doppler (RI <0.4) mimicking the blood flow pattern associated with malignancy [4].

Functioning Cysts

Follicles or the corpus luteum may fail to involute and become functioning cysts with continued hormone production. These larger cysts have a tendency to hemorrhage internally and become hemorrhagic cysts.

Smooth, round, echo-free, thin-walled ovarian cysts larger than 2.5 cm (up to 8-10 cm) (Fig. 5.30). Cysts larger than 5 cm are less likely to spontaneously regress [41].

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Doppler shows peripheral blood flow with relatively high resistance (mean RI = 0.65) in the wall of functional cysts. Doppler cannot discriminate between functional cysts and benign ovarian neoplasms [42].
Because these larger functioning cysts have an appearance identical to early ovarian carcinoma, a follow-up US examination should be performed after one or two menstrual cycles to ensure that resolution of the functioning cyst has occurred. A 6- or 10-week follow-up interval is usually recommended to ensure that the patient is examined in a different phase of her menstrual cycle.

Figure 5.30 Functioning Ovarian Cyst. A thin-walled cyst (between cursors, +) with anechoic internal fluid and size larger than 2.5 cm meets the definition of a functioning ovarian cyst.

Figure 5.31 Hemorrhagic Cyst–Homogeneous Echoes. Mass (between cursors, +, x) on the ovary shows a pattern of fine, homogeneous, low-level, internal echoes characteristic of hemorrhage within an ovarian cyst. Doppler is used to verify its cystic nature by confirming the absence of internal blood vessels.

Hemorrhagic Cysts

Hemorrhagic cysts result from bleeding into functioning cysts. Pain and expansion of the cyst may accompany bleeding. Most hemorrhagic cysts resolve in 2-8 weeks [43].

Homogeneous, low-level, internal echoes are seen in an ovarian cyst with enhanced through-transmission (Fig. 5.31). This appearance is identical to endometrioma.
A network of fine interdigitating, avascular, fibrous strands (fishnet appearance) is characteristic (Fig. 5.32).
Retracting clots and fibrous strands are evidence of acute hemorrhage (Fig. 5.33).
Fluid-fluid levels are common (Fig. 5.34).
Doppler confirms the absence of internal blood flow. Blood flow may be seen in the wall of the cyst.
Hemorrhage in a cyst is strong evidence of benignancy [44].

Postmenopausal Cysts

Benign ovarian cysts are found in 3-17% of postmenopausal women [45, 46]. Most of these cysts are serous inclusion cysts that arise on the surface of the involuting ovary. Their occurrence is independent of hormone replacement therapy or the time interval since menopause [45].

Smooth, thin-walled, unilocular, anechoic ovarian cyst in a postmenopausal woman is typical. Most cysts are <5 cm in size. With extended follow-up (2.5 years), the cysts remain stable in appearance and gradually decrease in size [47].
Normal postmenopausal ovaries are avascular. Doppler US reveals blood flow only in the ovarian artery. Increased blood flow is evidence of neoplasia [4].
Cysts >5 cm in size or with atypical features should probably be removed because the risk of tumor is increased.

Figure 5.32 Hemorrhagic Cyst–Fishnet Appearance. Cyst (between cursors, +, x) on the left ovary shows fine internal echoes with a fishnet appearance of thin, linear, fibrous strands characteristic of hemorrhage.

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Theca Lutein Cysts

Theca lutein cysts develop on ovaries that are overstimulated by human chorionic gonadotropin (hCG). These cysts occur in patients with gestational trophoblastic disease, in pregnant women with a multiple gestation, and in infertile women receiving hCG for ovulation induction.

Bilateral, multiseptated ovarian cysts with anechoic contents and thin smooth walls is a typical appearance (Fig. 5.35).
Cysts commonly persist for weeks after hCG levels return to normal.

Ovarian Hyperstimulation Syndrome

Ovulation may be induced in infertile women by treatment with clomiphene citrate, hCG, or gonadotropin releasing factor. Overstimulation of the ovaries results in induction of

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multiple follicles and multiple corpus luteum cysts following multiple ovulations [6]. Very high levels of estrogen are associated with abdominal pain, weight gain, development of ascites and pleural effusions, hemoconcentration, hypotension, and oliguria. Marked ovarian enlargement (>10 cm) is associated with risk of ovarian torsion and rupture.

Figure 5.33 Hemorrhagic Cyst–Retracting Clots. Retraction of blood clots following hemorrhage within an ovarian cyst (between cursors, +, x) forms an irregular echogenic mass. Doppler confirmed the absence of internal vessels. This appearance is characteristic of shrinking blood clots in an ovarian cyst.

Figure 5.34 Hemorrhagic Cyst–Layering Blood. Settling blood products produce a fluid-fluid layer (small arrows) within this hemorrhagic ovarian cyst shown on TV US. Large arrow indicates the direction of “up” during transvaginal scanning.

Large ovaries (>5-10 cm diameter) with multiple large thin-walled cysts.
Fluid exudes from the enlarged ovaries. Look for ascites and pleural effusions.

Polycystic Ovary Syndrome

A complex endocrine disorder of chronic anovulation, androgen excess, infertility, hirsutism, and obesity is associated with enlarged ovaries with multiple cysts. This disorder is also called the Stein-Leventhal syndrome.

Bilateral large ovaries (>15 cc) with multiple (>11) peripheral follicles (5-8 mm in diameter) (Fig. 5.36).
The normal shape of the ovary is maintained.

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The ovarian stroma is thickened and significantly increased in echogenicity [48].
Vascularity of the ovarian stroma is increased. Spectral Doppler shows a low resistance pattern [49].
The ovaries are normal in size in 30% of cases. The diagnosis is made by biochemical analysis.

Figure 5.35 Theca Lutein Cysts. Multiple thin-walled cysts enlarge the ovary in this patient with gestational trophoblastic disease.

Figure 5.36 Polycystic Ovary Syndrome. The ovary (between cursors, +) is mildly enlarged and has a large number of follicles arranged around its periphery.

Ovarian Cancer

Ovarian cancer accounts for 4% of all cancer in women and is the leading cause of death from gynecologic malignancy. Although the cancer is usually curable in its early stages, two-thirds of all patients have tumor spread beyond the pelvis when the diagnosis is made.

Epithelial tumors account for 85% of ovarian cancers. These tumors arise from the surface epithelium and the mesothelium of the outer ovarian cortex. Tumors are classified as benign (cystadenoma), borderline malignant (formally called tumors of low malignant potential), and malignant (cystadenocarcinoma) [50].

Serous neoplasms account for 60-80% of epithelial tumors and are the most common lesions in both benign and malignant categories. Approximately 50% of tumors are frankly malignant or of low malignant potential. Tumors are bilateral in 20% of benign cases and in 50% of malignant cases. Most tumors are predominantly cystic and contain anechoic fluid. The cysts may be unilocular or multilocular.
Mucinous tumors are approximately 90% benign and are less commonly bilateral (5% of benign tumors and 25% of malignant tumors). Most tumors are predominantly cystic, typically multilocular, and contain fluid of variable echogenicity caused by mucoid material, hemorrhage, and cellular debris. Tumors are often huge (up to 30 cm).
Endometrioid tumors are nearly always malignant with 25% being bilateral. Approximately 20-30% are associated with hyperplasia or carcinoma of the uterine endometrium. Most lesions are mixed cystic and solid, although some are entirely solid.
Clear cell neoplasms are nearly all invasive carcinomas, accounting for 10% of ovarian malignancies. Lesions are most commonly unilocular cysts with mural nodules.
Brenner tumors are uncommon (3% of ovarian tumors) and always benign. The tumors are homogeneously solid, usually small (1-2 cm), and commonly extensively calcified.

Germ cell tumors arise from primitive ovarian germ cells and account for 7% of ovarian malignancy. Benign cystic teratomas (dermoid cysts) are most common (30% of all primary ovarian neoplasms). Malignant lesions are of mixed histology and include immature teratomas, dysgerminomas, yolk sac and endodermal sinus tumors, and choriocarcinoma.

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Malignant tumors are usually found in girls and young women. Most tumors are large, predominantly solid, heterogeneous, and commonly contain calcifications [51]. Serum α-fetoprotein or hCG may be elevated.

Gonadal stromal (sex-cord stromal) tumors arise from the mesenchymal cells of the embryonic ovaries. Tumors include granulosa cell tumors, thecomas, fibromas, Sertoli and Leydig cell tumors, and steroid cell tumors. This group accounts for 7-8% of ovarian neoplasms. Granulosa cell tumors may produce estrogens and Sertoli-Leydig cell tumors may produce androgens resulting in conspicuous endocrine syndromes. Granulosa cell tumors are typically large and multilocular cystic with solid components. The other tumors are predominantly solid and may be homogeneous or heterogeneous with areas of fibrosis, necrosis, and hemorrhage [52].

Metastases to the ovary most commonly arise from the breast and gastrointestinal tract. Krukenberg tumors are metastatic mucin-producing adenocarcinomas with specific histologic characteristics. Lesions are bilateral, solid, and usually heterogeneous in echogenicity with poorly defined cystic areas commonly present [53].

Signs Indicative of Ovarian Malignancy

Differentiating benign from potentially malignant ovarian lesions is a primary goal of US examination. Unfortunately, no single gray-scale or Doppler US finding reliably provides this differentiation.

A solid component (Fig. 5.37) to an ovarian lesion is the most significant predictor of malignancy [44].
Irregular thick wall (Fig. 5.38) and septa (>3 mm) (Fig. 5.39).
Solid mural nodules and (Fig. 5.40) papillary projections.
Doppler demonstration of central blood flow within a solid component correlates well with malignancy (Figs. 5.39, 5.40) [44]. Color flow in septations within an ovarian cyst (Fig. 5.39) is a reliable sign of neoplasm but does not differentiate benign from malignant lesions [54, 55]. Spectral Doppler of arterial blood flow usually demonstrates a lower resistance flow pattern (RI < 0.4, pulsatility index < 1.0) in malignant lesions; however, neither RI nor pulsatility index can be used to reliably differentiate benign from malignant [54, 56]. Many benign lesions (corpus luteum, hemorrhagic cyst, tubo-ovarian abscess) will have low RI arterial signals and not all malignancies will have low RI arterial signals.

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Elevated serum CA-125 [57]. This screening blood test is elevated in only 50% of women with early ovarian cancer [58]. In addition, false-positive rate may exceed 90% in premenopausal women.
Ovarian lesions larger than 4 cm have a higher incidence of malignancy (Fig. 5.39), but the size of benign and malignant lesions overlaps greatly [59].

Figure 5.37 Ovarian Cancer–Solid Component. Solid tissue nodule (arrow) projects from the wall of this primarily cystic ovarian lesion. The diagnosis was cystadenocarcinoma.

Figure 5.38 Ovarian Cancer–Irregular Thick Wall. Cystic ovarian lesion has an irregular nodular thick wall. The diagnosis was endometrioid carcinoma.

Screening for ovarian cancer remains a popular but controversial subject. Because the prevalence of ovarian cancer is relatively low (compared to breast cancer) and the findings associated with malignancy are non-specific, it has been difficult to demonstrate cost-effectiveness or reduced cancer mortality.

Spread of Ovarian Malignancy

US documentation of tumor spread is obviously evidence of malignancy.

Figure 5.39 Ovarian Cancer– Blood Flow in Septations. Power Doppler color flow image confirms blood flow within irregularly thickened septa within this ovarian lesion. Blood flow in septations is highly indicative of the lesion being a neoplasm. In this case, the irregular thickening of the walls and septa and the large size of the tumor (>13 cm) are evidence of malignancy (see Color Figure 5.39).

Figure 5.40 Ovarian Cancer–Blood Flow in Wall. Color Doppler image reveals blood vessels within the irregular solid thickening of the wall of this cystic ovarian lesion. This finding confirms that the solid-appearing tissue is neoplasm and is not just clotted blood adherent to the cyst wall (see Color Figure 5.40).

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Local extension of tumor beyond the ovarian capsule is manifest by irregular indistinct boundaries with the uterus, localized distortion of uterine contour, encasement of small or large bowel, and displacement or invasion of blood vessels [60]. Tumors with local extension are usually large (>4-5 cm).
Intraperitoneal spread is a prominent and early feature of metastatic disease. The presence of ascites is non-specific, but is highly suspicious for peritoneal spread in the presence of an ovarian lesion. Loculation of ascites, ascites in the lesser sac, septations, fibrous strands, and echogenic fluid provides further evidence of malignancy. Peritoneal implants are typically tiny and often not visualized by US. Key areas to examine include the posterior cul-de-sac, paracolic gutters, undersurface of the diaphragm, and surfaces of the liver and spleen. Implants appear as nodules or plaque-like lesions (Fig. 5.41). Omental cake refers to tumor implantation on the greater omentum. Ill-defined, cake-like mass of cystic and solid tumor (Fig. 5.42) displaces bowel away from the anterior abdominal wall. Bowel involvement is manifest as plaque-like or nodular thickening of the bowel wall, fixation or distortion of bowel, and bowel obstruction.
Lymphatic spread of tumor occurs along the gonadal lymphatics that parallel the ovarian vein. Lymph nodes larger than 10 mm in short axis are considered involved by metastatic disease. Nodal involvement includes the hypogastric, obturator, external iliac lymph nodes, and nodes adjacent to and between the aorta and inferior vena cava.
Hydronephrosis is caused by direct tumor invasion of the ureter or by compression of retroperitoneal adenopathy.

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Hematogenous spread occurs earlier and is more common than previously believed. Intraparenchymal metastases may be seen in the liver, spleen, pancreas, and kidneys. Malignant pleural effusions are associated with lung and pleural metastases.

Figure 5.41 Peritoneal Implants. Tumor nodules (arrows) implanted on peritoneal surfaces in the cul-de-sac are well outlined by ascites (a). The uterus (U) and broad ligaments (arrowheads) are also clearly shown. The abrupt onset of ascites in a middle-aged woman without history of liver disease should stimulate a careful examination of the ovaries and a detailed search for peritoneal implants.

Figure 5.42 Omental Cake. Ovarian cancer metastatic implants on the greater omentum (between arrows) have caused “cake-like,” irregular thickening of the omentum. The omentum is suspended in ascites (a) and floats between bowel and the anterior abdominal wall.

Signs of a Benign Ovarian Mass

Purely cystic masses with no visible solid component are nearly always benign and usually represent functioning ovarian cysts (Fig. 5.30) [44, 61].
A markedly hyperechoic solid component (Fig. 5.43) is indicative of cystic teratoma and is always benign [44]. See description of cystic teratoma.
Absence of color Doppler signal in the mass is reliable evidence of benign lesion (Fig. 5.44) [55].
Hemorrhage within a unilocular cyst (Fig. 5.44) is statistically strongly associated with non-neoplastic cysts. Most are hemorrhagic functional cysts.

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Uniform thin septations are common with benign ovarian tumors such as serous or mucinous cystadenomas (Fig. 5.45). Demonstration of blood flow within septations confirms the lesion is a neoplasm but does not differentiate benign from malignant.
Mucinous tumors commonly secrete mucin, which produces fine low-level echoes within the cyst fluid (Figs. 5.45, 5.46). The presence of this echogenic material suggests a mucinous lesion but is not helpful in differentiating benign from malignant tumors.

Figure 5.43 Cystic Teratoma. A solid markedly hyperechoic mass (marked by cursors, +, x) arises from the right ovary (O). This appearance is highly indicative of benign cystic teratoma and effectively excludes malignancy.

Figure 5.44 Hemorrhagic Cyst. Color and spectral Doppler examination showed no internal flow within this complex, solid-appearing, ovarian lesion. The absence of blood vessels indicates the complex, solid-appearing tissue is blood clot within an ovarian cyst. Internal hemorrhage is rarely seen within ovarian cancers.

Cystic Teratoma

Cystic teratoma is the most common ovarian neoplasm. Most are discovered as asymptomatic adnexal masses. The risk of torsion is significant, as high as 16% in some series. Rarely, the tumor may rupture and produce acute peritonitis. Malignancy occurs in less than 2%. The tumors are cystic but may contain hair, sebum, teeth, or bone that produce a wide variety of US appearances. However, findings are often distinctive enough to provide a specific diagnosis [62, 63].

A characteristic structural feature of most cystic teratomas is the dermoid plug. The dermoid plug consists of a mixture of sebaceous material, fat, hair, and soft tissue that
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produces a highly echogenic, amorphous, nodular focus with dirty acoustic shadowing. This appearance is called the tip of the iceberg sign (Fig. 5.47) and is considered diagnostic of cystic teratoma. The plug may occupy only a small portion of the mass or may fill the entire mass.
Formation of teeth and bone fragments is another highly specific but less common feature of cystic teratoma. These structures produce discrete bright echogenic foci with dense, dark acoustic shadows (Fig. 5.48). Radiographs confirm the presence of ectopic teeth and bone.
Hair floating in fluid produces bright linear strands and punctate echoes. The hyperechoic lines and dots pattern is highly predictive of hair within a cystic teratoma [63].
Fluid-fluid levels are common and caused by sebum layering on serous fluid in cystic teratomas. This finding is seen in other conditions (such as hemorrhagic cysts and tubo-ovarian abscess) and is not specific for cystic teratoma.
Because of the heterogeneous tissues they contain, cystic teratomas commonly appear solid rather than cystic [64]. Because of their high echogenicity, they blend in with pelvic fat and other structures (Fig. 5.49).

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Approximately three-fourths of cystic teratomas show at least two of the features previously listed. If two of these features are present, the diagnosis can be made with a high degree of confidence [63].
The cyst may be well defined and anechoic (Fig. 5.50). Sebum is highly echogenic at room temperature (in a specimen bottle) but is anechoic at body temperature within the patient. In the absence of additional findings previously listed, a specific diagnosis of cystic teratoma cannot be made.
Doppler evaluation demonstrates most cystic teratomas to be devoid of blood flow. Low-to-moderate-impedance blood flow (RI = 0.42-0.72) is found in a few cystic teratomas that histologically demonstrate areas of actively dividing cells [65].

Figure 5.45 Thin Septations in Benign Neoplasm. Uniformly thin septations (long arrow) and thin wall (short arrow) are evident in this benign mucinous cystadenoma. Note the fine low-level echoes within the cyst fluid caused by mucinous fluid.

Figure 5.46 Internal Echoes Caused by Mucin. A homogeneous pattern of fine, low-level echoes suggests the presence of mucin within this cystic ovarian neoplasm (between cursors, +, x). Real-time, US observation of shifting internal echoes with patient movement and Doppler demonstration of the absence of internal vascularity confirm that this is a cystic lesion containing echogenic fluid. The diagnosis was mucinous cystadenocarcinoma.

Figure 5.47 Cystic Teratoma–“Tip of the Iceberg.” The dermoid plug is seen as a highly echogenic mass (white arrow) arising from the ovary (O). A dark acoustic shadow (black arrows) is produced by sound absorption. This appearance is characteristic of cystic teratoma.

Figure 5.48 Cystic Teratoma–Bone and Teeth Formation. A prominent dermoid plug (white arrows) within a cystic mass contains coarse echogenic foci (black arrowheads) that had the appearance of a primitive teeth and bone on plain film radiographs.

Figure 5.49 Cystic Teratoma–Easy to Overlook. A, B. Two large cystic teratomas (T) were easily palpable but difficult to define with US. u, uterus. Cursors (+) show size of the teratoma in B.

Figure 5.50 Cystic Teratoma–The Great Mimicker. This cystic teratoma contains sebum, which is near anechoic. Two small papillary projections (arrows) suggest ovarian carcinoma but were proven to be dermoid plugs.

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Adnexal Torsion

In adnexal torsion, the ovary and/or fallopian tube twist around their vascular pedicle resulting in compromised blood flow. Patients present with intense pelvic pain that is commonly intermittent and mimics many other conditions. Torsion is most common in prepubertal girls and adolescents. Differential diagnosis includes renal stone causing ureteral obstruction, appendicitis, endometriosis, inflammatory bowel disease, and urinary tract infection. Doppler evaluation is essential in the diagnosis. Doppler findings depend upon the completeness and chronicity of torsion. Prompt diagnosis and surgical intervention is required to save the ovary from necrosis. Isolated torsion of the fallopian tube is rare and usually seen in women with a history of tubal ligation.

The ovary is enlarged, sometimes massively, by edema and interstitial hemorrhage caused by venous obstruction. Central ovarian echogenicity is increased with multiple immature follicles seen in the periphery. Focal hemorrhage produces homogeneous hypoechoic zones in the ovary.
In some cases an ovarian cyst or tumor is present and is probably responsible for precipitating the torsion. Torsion is extremely rare with malignant ovarian tumors because of adherence to adjacent structures.
With partial torsion, venous flow is reduced whereas arterial flow is maintained. Spectral Doppler of arterial flow shows high resistance and occasionally reversal of flow in diastole.
Complete absence of arterial and venous flow is indicative of a non-viable torsed ovary [66].
The twisted vascular pedicle produces a “whirlpool sign” of concentric tubes in a swirling pattern [67]. Absence of flow in the vascular pedicle is predictive of necrosis of the ovary.
Isolated tubal torsion is suggested by finding a dilated tube with thickened wall and echogenic contents. Doppler shows absent or high resistance arterial flow [68].
Fluid is commonly present around the torsed structures.

Endometrioma

Endometriosis is the presence of functioning endometrial tissue outside of the uterus. It is seen most commonly in infertile women between the ages of 30 and 40. Implantation of the endometrial tissue may occur anywhere, but implantation on the ovaries is particularly common. Symptoms include pelvic pain and dysmenorrhea. The deposits induce fibrous adhesions that fixate involved structures. Most deposits of endometrial tissue are small and not detectable by US. Larger deposits form hemorrhagic cysts called endometriomas (chocolate cysts). The US appearance of endometriomas is exceptionally diverse [69].

Figure 5.51 Endometrioma–The Echogenic Cyst. A 3-cm endometrioma (between cursors, +) implanted on the right ovary (OV) has homogeneous, low internal echoes. This appearance is classic for endometrioma, but may also be seen with a hemorrhagic ovarian cyst.

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Adnexal cystic mass with diffuse, low-level internal echoes is highly characteristic of endometrioma (Fig. 5.51).
The presence of hyperechoic foci in the wall increases the likelihood of endometrioma (Fig. 5.52). These foci may represent cholesterol crystals resulting from cell breakdown in chronic hemorrhage.
Cyst wall may be thick or thin. Thickness has no diagnostic value [69].
Wall nodularity may be present and is indistinguishable from the wall nodularity of a neoplasm.
The ovary is involved in 80% of cases of endometriosis (Fig. 5.51).

Peritoneal Inclusion Cysts

Peritoneal inclusion cysts are benign collections of fluid in the peritoneal cavity confined by adhesions. Patients have a history of multiple prior surgical procedures, endometriosis, or PID. The collections are commonly mistaken for ovarian cancer. No epithelial lining is present [70, 71].

Figure 5.52 Endometrioma. This endometrioma contains blood that is higher in echogenicity and more heterogeneous in echotexture. It was initially mistaken for a solid lesion. Subsequently, Doppler demonstrated no internal blood vessels. Echogenic foci in the wall (arrows) are a subtle but characteristic sign of endometrioma.

Figure 5.53 Peritoneal Inclusion Cyst. The ovary (between cursors, +, x), recognized by its follicles (arrows), is seen within a loculated fluid collection (f). This finding is characteristic of peritoneal inclusion cyst.

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The fluid collections may be of any size but are frequently large.
Normal-appearing ovaries are frequently seen within the fluid collection. This finding confirms the diagnosis (Fig. 5.53).
The fluid collection may be septated and the fluid may contain particulate matter.
The fluid is loculated and conforms to peritoneal recesses in the pelvis.

Paraovarian Cysts

Paraovarian cysts arise between the leaves of the broad ligaments from mesothelial, wolffian duct, or müllerian duct remnants. Most are discovered incidentally in asymptomatic patients. Rare complications include hemorrhage, torsion, and malignant change (2%) [72, 73].

Cystic mass up to 28-mm size is seen in the adnexa.
Cysts are thin walled and unilocular with anechoic internal fluid (Fig. 5.54).
Mass is separate from the ovary.

Figure 5.54 Paraovarian Cyst. This extra-ovarian cyst in the broad ligament proved to be a wolffian duct remnant cyst. The appearance is non-specific. The diagnosis may be suggested by recognizing that the cyst does not arise from the ovary.

Figure 5.55 Pelvic Arteriovenous Malformation. A. Transvaginal scan shows prominent tubular structures in the right adnexa. B. Color Doppler image in the same location confirms the tubular structures are blood vessels. C. Longitudinal transvaginal scan shows high-velocity, turbulent flow within the abnormal vessels (see Color Figure 5.55).

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Pelvic Varices and Arteriovenous Malformations

Pelvic varices are associated with pelvic congestion syndrome, which is a common cause of chronic pelvic pain, dysmenorrhea, and dyspareunia [74]. Pelvic varices occur as isolated abnormalities or as a result of portal hypertension. Pelvic AVMs may also cause pelvic pain, back pain, or sciatica [74]. They occur congenitally or as a result of trauma.

Varices appear as prominent tortuous vessels in the adnexal regions. Doppler confirms venous flow within the vessels. A large varix may be mistaken for hydrosalpinx if Doppler is not utilized.
AVMs appear as pulsatile tubular structures in the adnexa (Fig. 5.55). They may be mistaken for cysts, fluid collections, or hydrosalpinx. Doppler shows high-velocity, low-resistance arterial flow and pulsatile venous flow.

Ovarian Remnants

Ovarian remnants are fragments of functioning ovarian tissue unintentionally left behind following difficult oophorectomy. Ovarian remnants occur most commonly in patients with adhesions from endometriosis, PID, or previous surgery. The retained ovarian tissue responds to systemic hormonal stimulation and may form cysts and tumors [75]. The enlarging mass may cause pelvic pain or envelop and obstruct a ureter.

Pelvic mass in a woman with history of bilateral oophorectomy.
Most ovarian remnants produce simple or hemorrhagic ovarian cysts.
Remnant ovarian tissue has the potential to produce any ovarian neoplasm.

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Focal Ovarian Calcifications

Multiple discrete echogenic foci are commonly visualized on the ovary during TV US examination [76]. Histologic data indicate these are psammomatous calcifications associated with tiny superficial epithelial inclusion cysts.

Punctate, linear, or globular calcifications in peripheral ovarian tissue appear as discrete echodensities with or without acoustic shadowing. These occur in the absence of a visible ovarian mass. These are incidental findings without documented clinical significance [76].

Fallopian Tubes

Cystic dilatation of the fallopian tubes, hydrosalpinx, hematosalpinx, and pyosalpinx commonly mimic the appearance of ovarian tumors. PID mimics metastatic pelvic tumor and endometriosis. Recognition of the characteristic findings of these conditions prevents misdiagnosis.

Pelvic Inflammatory Disease

PID is usually caused by sexually transmitted infection, most commonly chlamydia or gonorrhea. PID also occurs as a complication of appendicitis, diverticulitis, pelvic abscess, and post-abortion or post-delivery infection. Acutely, patients present with fever, pelvic tenderness, and vaginal discharge. The inflammation commonly becomes chronic and patients present with pelvic mass and dyspareunia. Most cases occur in young, sexually active women, although 1-2% of tubo-ovarian abscesses are reported in postmenopausal women [77].

Endometritis is seen on US as thickening of the endometrium (>14 mm in menstruating women) commonly with fluid in the uterine cavity and echogenic layering fluid
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(pus) in the cul-de-sac. Air produced by bacterial activity produces punctate echodensities. The margin of the inflamed uterus is ill defined [78].
Pyosalpinx is a pus-filled, dilated, fallopian tube and is recognized by the echogenic particulate matter that fills or layers within the tube (Fig. 5.56). Patients are acutely symptomatic. The wall of the dilated tube thickens as the inflammation becomes chronic.
Tubo-ovarian complex results from incorporation of the dilated fallopian tube and inflamed ovary within a mass formed by adhesions (Fig. 5.57). Pus within the mass and surrounding the ovary and tube creates a tubo-ovarian abscess (Fig. 5.58). Pus appears as layering echogenic fluid and gas within the mass. Doppler demonstrates increased vascularity with a low resistance pattern (RI <0.5) in the periphery of the abscess. As the process becomes chronic, the RI increases [79, 80]. TV US-guided aspiration confirms the diagnosis, obtains fluid for culture, and can be followed by catheter placement for TV drainage.
Chronic PID results in pelvic adhesions that can be a cause of infertility and peritoneal inclusion cysts. Walled-off regions of peritoneum may secrete fluid and may incorporate the ovary and tube in an ill-defined mass that mimics endometriosis and pelvic malignancy.

Figure 5.56 Pyosalpinx. A. Cystic adnexal mass (between cursors, +) contains layering echogenic fluid. The tube is so dilated that it shows no features that identify its etiology. B. Transvaginal image in another patient shows a characteristic appearance of a folded dilated tube containing echogenic fluid. Pyosalpinx was confirmed at surgery in both patients.

Figure 5.57 Tubo-Ovarian Complex. A markedly dilated fallopian tube (long arrows) partially envelopes the ovary (short arrow) in a patient with pelvic infection.

Tubal Obstruction/Hydrosalpinx

Distal obstruction of the fallopian tube causes infertility and may lead to hydrosalpinx, the term applied to dilatation of the tube by chronic accumulation of serous secretions. Causes of hydrosalpinx include PID (which may be subclinical), endometriosis, adhesions, surgery involving the tube, and fallopian tube carcinoma. The sensitivity of TV US for detection of a blocked tube has been reported to be as low as 34%. Sonographic diagnosis is dependent upon the blocked tube being dilated with fluid and many are not [81]. Multihormone stimulation during ovulation induction therapy for infertility may dilate a previously unrecognized blocked tube by increasing tubular secretions [82]. SHG and hysterosalpingography are more sensitive than TV US for diagnosis of tubal obstruction because the force of contrast injection dilates the blocked tube. Differential diagnosis of hydrosalpinx includes prominent pelvic blood vessels (Doppler shows blood flow), loops of bowel and dilated distal ureter (look for peristalsis), and cystic ovarian masses (arise from the ovary).

Figure 5.58 Tubo-Ovarian Abscess. A dilated tube, a distorted ovary, pus, and marked inflammation cause a complex amorphous adnexal mass in a febrile patient with severe pelvic pain. En bloc resection at surgery confirmed a tubo-ovarian abscess.

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Hydrosalpinx appears as an undulating or folded fluid-filled extraovarian tubular mass (Fig. 5.59).
Short linear echoes protrude into lumen (“cogwheel pattern”). These represent the longitudinal folds of the tubular mucosa in the ampullary portion of the tube. This finding is characteristic, when present, but is absent in approximately half the cases of hydrosalpinx.
Well-defined walls are echogenic and 1-2 mm thick.
Fluid in the tube is anechoic in uncomplicated hydrosalpinx. Echogenic fluid in the tube suggests infection or hemorrhage.
Doppler demonstrates vascularity in the walls of the dilated tube.
Hydrosalpinx is most evident during the proliferative phase of the menstrual cycle when tubular secretions are greatest. The dilated tube may empty into the uterine cavity during the secretory phase, making the blocked tube inapparent on US.

Carcinoma of the Fallopian Tube

This is the rarest (0.3%) of all gynecologic malignancies. Most patients are postmenopausal and older than age 50. A variety of US appearances of an extraovarian mass have been described [83, 84].

Figure 5.59 Hydrosalpinx. Transvaginal image shows the characteristic undulating pattern of a dilated fallopian tube. Careful examination is needed to show the tube in optimal projection. Random cross-sections may show only the non-specific appearance of an adnexal cyst.

Figure 5.60 Tampon in Vagina. An air-filled tampon in the vagina causes a bright linear echo (arrows) with acoustic shadowing. U, uterus.

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Sausage-shaped solid mass.
Dilated tube with multiple solid nodules.
Multiloculated cystic mass.

Vagina

The vagina is commonly inspected cursively or is overlooked during pelvic US examination. Because diseases of the vagina are uncommon, they may be unfamiliar or misinterpreted. Examination techniques include TA US with full bladder, translabial US with empty bladder, and TV US with attention to the vaginal wall.

Posthysterectomy, the vaginal cuff is usually bulbous at its distal end. During hysterectomy the vaginal wall is folded back on itself and closed, creating a double layer of tissue, more bulbous than the remainder of the vagina. It is important that the bulbous cuff not be mistaken for a mass and that a mass in the cul-de-sac not be mistaken for a bulbous vaginal cuff. A vaginal cuff size larger than 2 cm suggests a mass [85]. The patient should be queried as to the reason for hysterectomy. A history of malignant pelvic tumor reinforces the importance of careful examination of the vaginal cuff. A cervical remnant from a supracervical hysterectomy may be mistaken for a tumor.

Tampons in the vagina trap air and produce a bright linear echo with shadowing and ring down (Fig. 5.60). Foley catheters may be misplaced in the vagina and the vagina may

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be filled with fluid meant for the bladder (Fig. 5.61). Blood in the vagina (hematocolpos) may be congenital, caused by developmental obstruction of the genital tract, or acquired, caused by inflammatory disease that seals the vagina closed (Fig. 5.62) [39]. Copious bleeding from the uterus may fill the vagina with echogenic material and outline the cervix by blood in the fornices (Fig. 5.63).

Figure 5.61 Foley Catheter in Vagina. In a “misguided” attempt to fill the bladder with saline for pelvic US examination, a Foley catheter (arrow) was placed in the vagina and the vagina (V) was filled with fluid. U, uterus.

Figure 5.62 Acquired Hematocolpos. The vagina (V, between cursors, +, x) is markedly distended by menstrual blood. The vagina opening had been sealed shut by healing of mucosal ulcers occurring as a result of Stevens-Johnson syndrome. The patient had been amenorrheic for 3 months following her acute illness. U, uterus.

Solid Vaginal Masses

Cervical carcinoma and uterine malignancies may protrude into the vagina, appearing as heterogeneous solid masses that obliterate vaginal sonographic landmarks. Primary vaginal

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cancers, clear cell adenocarcinoma, and rhabdomyosarcoma are heterogeneous solid masses that commonly show areas of necrosis.

Figure 5.63 Blood in Vagina. Longitudinal (A) and transverse (B) US images of a patient with copious vaginal bleeding shows blood (b) in the vagina filling the fornices and outlining the cervix (C).

Figure 5.64 Gartner’s Duct Cyst. Longitudinal image shows an oblong cystic mass (arrow) in the anterolateral wall of the vagina. The bladder (b) is only slightly filled. U, uterus.

Cystic Vaginal Masses

The following cystic lesions may be characterized by US or discovered incidentally during pelvic US examination.

Gartner’s duct cysts arise from remnants of the embryologic mesonephric ducts (that form the ductus deferens and ejaculatory ducts in the male). Cysts may form anywhere along the course of the mesonephric duct in the broad ligament and along the lateral wall of the uterus and vagina as far as the hymen. Most cysts are small, but some become large enough to obstruct the vagina. Characteristic location is anterolateral (Fig. 5.64). They may be single or multiple.
Inclusion cysts are common and usually occur near the vaginal outlet. They result from tears or episiotomy incisions that heal with tags of mucosa buried beneath the mucosal surface. The cysts fill with desquamated epithelium.
Mucous cysts (retention cysts) contain mucoid material and result from obstruction of the duct of mucous glands. They may occur anywhere along the vaginal wall.
Endometriosis may occur in the vagina as a result of penetration of disease through the cul-de-sac.
Bartholin cysts present as vulvar masses. Bartholin glands (the greater vestibular glands) lie on the superficial fascia of the urogenital diaphragm on either side of the vagina. Each gland drains into the vestibule through a duct that opens just outside the hymenal ring. The glands secrete a lubricating mucus during sexual arousal. Obstruction of the duct, caused by inflammation and scarring, results in a Bartholin cyst that is a tubular dilatation of the duct to Bartholin’s gland. Infected glands or obstructed glands may enlarge to 5-6 cm and obstruct the rectum.
Nabothian cysts arising in the cervix are common and, when large, must be differentiated from a vaginal cyst. Chronic inflammation results in squamous epithelium plugging the ducts of mucous glands of the cervix. The resulting cysts are anechoic, often multiple, and vary in size from 2-3 mm up to 4 cm.

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	Core Curriculum, The: Ultrasound 1st Edition
	© 2001 Lippincott Williams & Wilkins

Core Curriculum, The: Ultrasound1st Edition

Core Curriculum, The: Ultrasound
1st Edition