
- •Contents
- •Preface
- •Contributors
- •1 Vessels
- •1.1 Aorta, Vena Cava, and Peripheral Vessels
- •Aorta, Arteries
- •Anomalies and Variant Positions
- •Dilatation
- •Stenosis
- •Wall Thickening
- •Intraluminal Mass
- •Perivascular Mass
- •Vena Cava, Veins
- •Anomalies
- •Dilatation
- •Intraluminal Mass
- •Compression, Infiltration
- •1.2 Portal Vein and Its Tributaries
- •Enlarged Lumen Diameter
- •Portal Hypertension
- •Intraluminal Mass
- •Thrombosis
- •Tumor
- •2 Liver
- •Enlarged Liver
- •Small Liver
- •Homogeneous Hypoechoic Texture
- •Homogeneous Hyperechoic Texture
- •Regionally Inhomogeneous Texture
- •Diffuse Inhomogeneous Texture
- •Anechoic Masses
- •Hypoechoic Masses
- •Isoechoic Masses
- •Hyperechoic Masses
- •Echogenic Masses
- •Irregular Masses
- •Differential Diagnosis of Focal Lesions
- •Diagnostic Methods
- •Suspected Diagnosis
- •3 Biliary Tree and Gallbladder
- •3.1 Biliary Tree
- •Thickening of the Bile Duct Wall
- •Localized and Diffuse
- •Bile Duct Rarefaction
- •Localized and Diffuse
- •Bile Duct Dilatation and Intraductal Pressure
- •Intrahepatic
- •Hilar and Prepancreatic
- •Intrapancreatic
- •Papillary
- •Abnormal Intraluminal Bile Duct Findings
- •Foreign Body
- •The Seven Most Important Questions
- •3.2 Gallbladder
- •Changes in Size
- •Large Gallbladder
- •Small/Missing Gallbladder
- •Wall Changes
- •General Hypoechogenicity
- •General Hyperechogenicity
- •General Tumor
- •Focal Tumor
- •Intraluminal Changes
- •Hyperechoic
- •Hypoechoic
- •Nonvisualized Gallbladder
- •Missing Gallbladder
- •Obscured Gallbladder
- •4 Pancreas
- •Diffuse Pancreatic Change
- •Large Pancreas
- •Small Pancreas
- •Hypoechoic Texture
- •Hyperechoic Texture
- •Focal Changes
- •Anechoic Lesion
- •Hypoechoic Lesion
- •Isoechoic Lesion
- •Hyperechoic Lesion
- •Irregular (Complex Structured) Lesion
- •Dilatation of the Pancreatic Duct
- •Marginal/Mild Dilatation
- •Marked Dilatation
- •5 Spleen
- •Nonfocal Changes of the Spleen
- •Diffuse Parenchymal Changes
- •Large Spleen
- •Small Spleen
- •Focal Changes of the Spleen
- •Anechoic Mass
- •Hypoechoic Mass
- •Hyperechoic Mass
- •Splenic Calcification
- •6 Lymph Nodes
- •Peripheral Lymph Nodes
- •Head/Neck
- •Extremities (Axilla, Groin)
- •Abdominal Lymph Nodes
- •Porta Hepatis
- •Splenic Hilum
- •Mesentery (Celiac, Upper and Lower Mesenteric Station)
- •Stomach
- •Focal Wall Changes
- •Extended Wall Changes
- •Dilated Lumen
- •Narrowed Lumen
- •Small/Large Intestine
- •Focal Wall Changes
- •Extended Wall Changes
- •Dilated Lumen
- •Narrowed Lumen
- •8 Peritoneal Cavity
- •Anechoic Structure
- •Hypoechoic Structure
- •Hyperechoic Structure
- •Anechoic Structure
- •Hypoechoic Structure
- •Hyperechoic Structure
- •Wall Structures
- •Smooth Margin
- •Irregular Margin
- •Intragastric Processes
- •Intraintestinal Processes
- •9 Kidneys
- •Anomalies, Malformations
- •Aplasia, Hypoplasia
- •Cystic Malformation
- •Anomalies of Number, Position, or Rotation
- •Fusion Anomaly
- •Anomalies of the Renal Calices
- •Vascular Anomaly
- •Diffuse Changes
- •Large Kidneys
- •Small Kidneys
- •Hypoechoic Structure
- •Hyperechoic Structure
- •Irregular Structure
- •Circumscribed Changes
- •Anechoic Structure
- •Hypoechoic or Isoechoic Structure
- •Complex Structure
- •Hyperechoic Structure
- •10 Adrenal Glands
- •Enlargement
- •Anechoic Structure
- •Hypoechoic Structure
- •Complex Echo Structure
- •Hyperechoic Structure
- •11 Urinary Tract
- •Malformations
- •Duplication Anomalies
- •Dilatations and Stenoses
- •Dilated Renal Pelvis and Ureter
- •Anechoic
- •Hypoechoic
- •Hypoechoic
- •Hyperechoic
- •Large Bladder
- •Small Bladder
- •Altered Bladder Shape
- •Intracavitary Mass
- •Hypoechoic
- •Hyperechoic
- •Echogenic
- •Wall Changes
- •Diffuse Wall Thickening
- •Circumscribed Wall Thickening
- •Concavities and Convexities
- •12.1 The Prostate
- •Enlarged Prostate
- •Regular
- •Irregular
- •Small Prostate
- •Regular
- •Echogenic
- •Circumscribed Lesion
- •Anechoic
- •Hypoechoic
- •Echogenic
- •12.2 Seminal Vesicles
- •Diffuse Change
- •Hypoechoic
- •Circumscribed Change
- •Anechoic
- •Echogenic
- •Irregular
- •12.3 Testis, Epididymis
- •Diffuse Change
- •Enlargement
- •Decreased Size
- •Circumscribed Lesion
- •Anechoic or Hypoechoic
- •Irregular/Echogenic
- •Epididymal Lesion
- •Anechoic
- •Hypoechoic
- •Intrascrotal Mass
- •Anechoic or Hypoechoic
- •Echogenic
- •13 Female Genital Tract
- •Masses
- •Abnormalities of Size or Shape
- •Uterus
- •Abnormalities of Size or Shape
- •Myometrial Changes
- •Intracavitary Changes
- •Endometrial Changes
- •Fallopian Tubes
- •Hypoechoic Mass
- •Anechoic Cystic Mass
- •Solid Echogenic or Nonhomogeneous Mass
- •14 Thyroid Gland
- •Diffuse Changes
- •Enlarged Thyroid Gland
- •Small Thyroid Gland
- •Hypoechoic Structure
- •Hyperechoic Structure
- •Circumscribed Changes
- •Anechoic
- •Hypoechoic
- •Isoechoic
- •Hyperechoic
- •Irregular
- •Differential Diagnosis of Hyperthyroidism
- •Types of Autonomy
- •15 Pleura and Chest Wall
- •Chest Wall
- •Masses
- •Parietal Pleura
- •Nodular Masses
- •Diffuse Pleural Thickening
- •Pleural Effusion
- •Anechoic Effusion
- •Echogenic Effusion
- •Complex Effusion
- •16 Lung
- •Masses
- •Anechoic Masses
- •Hypoechoic Masses
- •Complex Masses
- •Index

13
Female Genital Tract
Abnormalities of Size or Shape
Tract |
|
Vagina |
|
Postoperative Changes |
|||||
|
|
|
|
|
|
||||
|
|
|
|
|
|
Masses |
|
|
|
Genital |
|
|
Abnormalities of Size or Shape |
|
|
|
|||
|
|
|
|
|
|||||
|
Uterus |
|
|
||||||
|
|
|
|
|
|
|
|||
|
|
|
|
|
Fallopian Tubes |
|
|
||
|
|
|
|
|
|
|
|||
|
|
|
|
|
Ovaries |
|
|
||
Female |
|
|
|
||||||
|
|
|
|
|
|
Postoperative Changes
Hysterectomy and other operations can cause pronounced changes in the shape and position of the vagina (Fig.13.11, Fig.13.12). A knowledge of the patient’s prior history will aid interpretation of the ultrasound findings.
Fig. 13.11 Vaginal fornix after hysterectomy. |
Fig. 13.12 Bladder following resection of the uterus, vag- |
|
ina, and rectum: complete acoustic enhancement |
|
posteroinferior to the bladder. No organic structures are |
|
visualized. |
■ Uterus
Anatomy
Position
●Anteversion, anteflexion (normal finding)
●Retroversion
●Straight (especially in old age, when it is more difficult to evaluate by transvaginal scanning; the fundus should be manually flexed forward)
Uterine size and shape
●Prepubertal
–2–3.3 cm long, 1 cm wide, 0.5–1 cm thick
–Cervical diameter is greater than the corpus diameter. The cervix accounts for two-thirds of total uterine length
●Nullipara
–Pear-shaped
–5–9 cm long, transverse diameter
1.6–4 cm, 3 cm thick
●Multipara
–10 × 5 × 6 cm
–Uterine corpus comprises the upper two-thirds of the total length, the cervix the lower third
●Postmenopause
–4.5 cm long, 2 cm wide, 1.5 cm thick
–Symmetrically hyperplastic
Uterine weight
●Adolescence: 44–66 g
●Childbearing age: 50–120 g
●Pregnancy: weight increases 20-fold up to 1000 g
Blood supply. The uterus receives its blood |
tal part of the uterus bordering the bladder. |
supply (Fig.13.13, Fig.13.14) partly from the |
Venous draniage is by valveless veins of the |
uterine artery, which branches from the inter- |
uterine venous plexus. |
nal iliac artery, and partly from the ovarian |
|
artery, which branches directly from the aorta |
Histology. The uterine wall consists of a |
and supplies the upper part of the uterus with |
smooth muscle layer (myometrium) and a |
blood. The uterine artery also supplies the dis- |
very glandular mucosa (endometrium of the |
uterine corpus and cervix). Most of the uterus is covered by a layer of serosa (perimetrium).
The endometrium of the uterine corpus consists of a single row of columnar epithelium and undergoes cyclic changes in its structure and function in response to ovarian steroids. The endocervix responds to these hormones with functional but not structural changes. The cyclic structural and size changes that occur in the myometrium and endometrium can be appreciated on ultrasound. The postmenstrual uterus is small and firm. During the second half of the cycle, the uterine wall thickens due to cellular hypertrophy. The myometrium contains abundant ovarian steroids owing to its estrogen and progesterone receptors.
Endometrium. Cyclic changes in the endometrium were first described by Hirschmann and Adler in 1908. During the proliferative phase in the first half of the menstrual cycle, estrogens stimulate an increase in endometrial thickness and vascularity that continues until the LH surge. During the second half of the cycle, following ovulation, glycogen-filled vacuoles develop in response to progesterone. Mucusfilled glands develop in the later secretory phase of the cycle, and spiral arteries are
444

formed. The regression phase begins several days before menstruation, as hormone production wanes and the thickness of the mucosa decreases by approximately 50% owing to fluid loss. The hormone levels decline precipitously in the desquamation phase, and the endometrial lining is sloughed. A regenerative phase follows menstruation, reinitiating the cycle.
Uterine cervix. The cervix consists mainly of connective tissue and a few smooth muscle fibers, with the result that it undergoes minimal cyclic structural changes. The cervical canal is lined by columnar epithelium and increases its diameter at midcycle. The cervical mucus becomes more fluid in response to estrogens and then more viscous again in response to increased progesterone.
Fig. 13.13 Blood supply: the ovarian artery runs from |
Fig. 13.14 Blood supply: spiral-shaped arteries in the myo- |
cranial and lateral within the parametrium to the uterus |
metrium. |
(UT); BL = bladder. |
|
Ultrasound Morphology
Even the normal uterus is subject to certain |
postmenstrual at the time of the examination. |
cologic tumor. If a tumor is present in an ado- |
variations (Figs. 13.15, 13.16, 13.17, 13.18, |
This also has an important bearing on differ- |
lescent patient, it will tend to undergo rapid |
13.19). To interpret the findings correctly, it is |
ential diagnostic considerations. For example, |
enlargement owing to the high rate of prolifer- |
necessary to know whether the patient is pre- |
lower abdominal pain in an adolescent girl is |
ation. |
pubertal, sexually mature, premenstrual, or |
more likely due to appendicitis than to a gyne- |
|
Echogenicity
●Outer serosa: hyperechoic
●Myometrium: uniformly hypoechoic; vessels appear as anechoic areas
●Endometrium and cervical canal: hyperechoic
●Cervix: may contain anechoic areas corresponding to nabothian follicles
Fig. 13.17 Vertical position of the uterus (UT) caused by the complete filling of the bladder (BL), ballooned cervix with the portio invaginating into the vagna (arrows). R = rectum.
Fig. 13.15 Longitudinal uterine scan posterior to the bladder. Anteflexion is clearly defined. The echogenic serosa and the linear endometrium are detectable.
Fig. 13.18 Transverse scan through the uterus and rectum.
Fig. 13.16 Retroflected uterus: the uterus (UT) lies dorsally to the bladder with retroflected corpus. Small bowel loops (B) reach more caudally behind the bladder (BL). R = rectum.
Fig. 13.19 Postpartum uterus (UT PP). Uterine length is still approximately 16 cm. BL = bladder.
13
Uterus
445

13
Female Genital Tract
Abnormalities of Size or Shape
Tract |
|
Vagina |
|||
|
|
|
|
||
|
|
|
|
Uterus |
|
|
|
|
|
||
Genital |
|
|
Abnormalities of Size or Shape |
||
|
|
||||
|
|
Myometrial Changes |
|||
|
|
|
|
|
|
|
|
|
|
|
Intracavitary Changes |
Female |
|
|
Endometrial Changes |
||
|
Fallopian Tubes |
||||
|
|
|
|
||
|
|
|
|
Ovaries |
|
|
|
|
|
Uterine Prolapse
Atypical and abnormal positions of the uterus affect the shape of the uterus as displayed by ultrasound (Fig.13.20, Fig.13.21).
Uterine Prolapse
Malformations
Uterine Aplasia, Atresia
Uterine Hypoplasia, Small Uterus
Hemangioma, Lymphoma, Angiomyoma, Myoma
Fig. 13.20 Uterus descensus, longitudinal scan through |
Fig. 13.21 Uterus descensus, transverse with prolapse. |
the lower abdomen: slightly stretched uterus, reaching |
The hypoechoic uterus is descended posterior to the |
far down; echoic endometrium (E) clearly visible; M = |
bladder and prolapsed into the vagina. BL = bladder. |
myometrium; Z = cervix, BL = bladder. |
|
Malformations
●Arcuate uterus
●Subseptate uterus
●Bicornuate uterus
–Uterus bicornis unicollis
–Uterus bicornis bicolli
●Uterus septus duplex (uterus bilocularis) with a septate vagina
●Uterus didelphys with two vaginas
These malformations are caused by anomalies during the fusion and back-formation of partitioning walls of the fused müllerian duct. They are commonly associated with renal anomalies, and the kidneys should therefore be included in the ultrasound examination.2
The degree of malformation varies. The mildest anomaly resulting from the incomplete fusion of the müllerian ducts is an arcuate uterus, in which the fundus appears dented (Fig.13.22). Uterus bicornis unicollis is the most common malformation (Fig.13.23). On the posterior aspect of the bladder, the two
Fig. 13.22 Arcuate uterus; the endometrium at the midcycle demonstrates a hyperechoic transformation. The triangular form of the uterus indicates a bicornate uterus bicornis. Arrows indicate the uterine horns.
hypoechoic uterine horns curve around the floor and posterior wall of the bladder. This creates the appearance of a hypoechoic triangle in the lower abdominal transverse scan. Two separate endometrial echoes (thick prolifera-
Fig. 13.23 Bicornuate uterus. Arrows = uterine horns. Lateral: both ovaries.
tive endometrium) are seen in a transverse ultrasound scan through the uterine horns at midcycle, which is the best time for detecting this anomaly when it is suspected.
446

Uterine Aplasia, Atresia
Uterine aplasia, characterized by a rudimentary |
Fig. 13.24 Rudimentary uterus (snared) in uterine atresia. |
uterus and a vaginal aplasia, is seen in Rokitan- |
|
sky–Küstner syndrome (familial autosomal |
|
anomaly with vaginal aplasia, possible under- |
|
development of the exterior genitals, and |
|
anomalies of the uterus; incidence about 1/ |
|
5000; second most common cause of primary |
|
amenorrhea). Despite a full bladder, the uterus |
|
either is not visualized or appears only in a |
|
rudimentary form. This aplasia is asymtomatic, |
|
rare and congenital. |
|
Uterine atresia, on the other hand, is an |
|
intraor extrauterine acquired condition |
|
(Fig.13.24). |
|
Uterine Hypoplasia,Small Uterus
Uterine hypoplasia occurs in patients with incomplete vaginal aplasia (affecting only the lower third). Hematometra may develop, giving the uterus an anechoic appearance.
A small uterus (4.5 × 1.5 × 2 cm) is a normal finding in postmenopausal women (Fig.13.25,
Fig.13.26).
Fig. 13.25 Rudimentary uterus (cursors), posterior to the |
Fig. 13.26 Rudimentary uterus, transverse scan dorsally to |
bladder in an 83-year-old woman. Longitudinal scan. |
the nearly empty bladder (HB) in an 83-year-old woman. |
Hemangioma,Lymphoma, Angiomyoma, Myoma
Tumors, including benign ones, can cause significant changes in the size, shape, and location of the uterus, depending on their size and location. They can compromise the function of neighboring organs.
Myometrial Changes
Tract |
Vagina |
||||
|
|
|
|||
|
|
|
Uterus |
||
|
|
|
|||
Genital |
|
Abnormalities of Size or Shape |
|||
|
Myometrial Changes |
||||
|
|
|
|
||
|
|
|
|
Intracavitary Changes |
|
Female |
|
Endometrial Changes |
|||
Fallopian Tubes |
|||||
|
|
|
|||
|
|
|
Ovaries |
||
|
|
|
Uterine Myomas
Uterine Adenomyomatosis
Uterine Sarcoma
13
Uterus
447

13
Female Genital Tract
Uterine Myomas
Myomas (fibroids) are muscular tumors of the uterus, generally classified histologically as fibroleiomyomas.3 These benign tumors composed of smooth muscle and connective tissue are the most common type of genital tumor.
The formation and growth of uterine myomas depend on the functional status of the ovaries (relative estrogen dominance). Myomas do not occur in children or older women and tend to regress after menopause. Antiestrogens and progesterone inhibit their growth.
Myomas develop in the uterine corpus and cervix. They are rarely solitary and may have an intramural, subserous, submucous, or intraligamentous location. They lack a true capsule. The tumor nodules are initially round but may alter their shape owing to pressure effects. Myomas undergo structural changes over time.
Malacia, characterized by the following changes:
●Cavernous transformation, permeation by edema
●Rapid myxomatous growth
●Tense cystic appearance, resembling an ovarian cyst
●Fatty degeneration (especially in the puerperium)
●Necrotic foci due to vascular occlusion
Clinical Presentation
Myomas present clinically with bleeding abnormalities such as hypermenorrhea (usually only intramural myomas affect uterine wall contractility), menorrhagia, and metrorrhagia (caused by submucous myomas). Dysmenorrhea is caused by capsular tension or contractions and also depends on the tumor location.
●Suppuration due to infection ascending from the uterine cavity, spreading from the bowel, or transmitted by blood vessels or lymphatics; breakdown by putrefactive bacteria, especially in submucous myomas
Induration, consisting of the following changes:
●Progressive fibrous transformation, ranging to a pure fibroma
●Irregular or eggshell calcification. Fully calcified myomas may become dislodged, resulting in the “delivery” of uterine stones.
Sonographic features. Approximately 25% of all women over age 35 have uterine myo-
Myomas can also cause bladder complaints and constipation or hydronephrosis (intraligamentous myoma) ( 13.1 l–s). A ruptured myoma capsule can produce the signs and symptoms of an acute abdomen. Myomas can cause infertility. A necrotic myoma can lead to an elevated ESR.
mas.4 These tumors appear sharply circumscribed at ultrasound. Initially they are largely homogeneous and less echogenic than the rest of the myometrium owing to their copious blood supply.
Most myomas are subserous in location ( 13.1a,b), but 5% are submucous;5 these often cause bleeding abnormalities and are not palpable. Multiple myomas and diffuse myomatosis are found in many multiparous women, leading to uterine enlargement with no circumscribed nodularity (
13.1c,d).
Degenerating myomas may appear as hyperechoic masses. Calcified myomas cast an acoustic shadow that can obscure surrounding structures ( 13.1h–j). Central necrosis, due, for
13.1 Uterine Myomas
Solitary and multiple myomas
Di use myomatosis
a Subserous myoma. S = shadow. |
b Small subserous myoma (arrow), iden- |
c Multiple myomas (MY) in the uterus. BL |
|
tical echogenicity to the myometrium. |
= bladder. |
d Di use myomatosis with uterine en- |
e Intraligamentous myoma: hypoechoic |
f Intraligamentous myoma. The myoma |
largement. |
nonhomogeneous tumor (MY) lateral to |
(MY) is well demarcated to the uterus |
|
the uterus (UT). |
(UT) by myometrial vessels. |
g Intraligamentous myoma: large hypoechoic nonhomogeneous tumor.
448

13.1 Uterine Myomas (Continued)
Calcifications and necrosis
h Uterine myoma with di use calcification. UT = uterine sarcoma; BL = bladder; S = shadow.
k Uterine myoma with central hypoechoic necrosis.
Renal pelvic obstruction
i Uterine myoma with eggshell calcification and acoustic shadowing (S). BL = bladder.
j Uterine myoma with eggshell calcification (arrow). S = shadow.
13
Uterus
l Uterine myoma, nonhomogeneous, compressing the ureter.
o Renal pelvic obstruction (NB), right side, in a uncertain tumor of the lower abdomen. The renal cortex appears normal.
r Large non.homogeneous uterine tumor UT) compressing the bladder (HB) from posterior.
m Obstructed renal pelvis, drained with a DJ stent (arrow).
p Renal pelvic (NB) and ureter obstruction; normal size of the kidney, rarefaction of the renal cortex (NR), anechoic renal pelvis (NB), dilated ureteropelvic junction
(U).
s Complex structured ovarian tumor with solid (OV) and cystic (C) portions.
n Uterine fornix (UF) with myoma, clublike cervix (UC), bladder (B) with indwelling DJ ureteral stent.
q Hyperechoic enlarged ovary (OV) beside the uterus (UT) with accentuated endometrium. HB = bladder.
example, to tumor growth outstripping blood supply, appears as an anechoic area ( 13.1k).
Pedunculated or intraligamentous myomas ( 13.1e–g) can mimic an adnexal tumor. Unequivocal visualization of the stalk, as by color duplex examination, is required. Myomas can-
not be distinguished sonographically from other tumors with absolute confidence. Rapid enlargement is suggestive of sarcomatous transformation.
The enlargement of a myoma is normal in early pregnancy and requires surveillance.5 Large myomas can obstruct delivery.6
Degeneration. Malignant degeneration occurs in 1.3% of cases.
449

13
Female Genital Tract
Uterine Adenomyomatosis
The presence of endometrial cells in the myomas leads to the development of uterine endo- metriosis—more accurately termed adenomyo- sis—which may be associated with hyperme-
norrhea and dysmenorrhea. One-third of patients are asymptomatic.
The uterus is uniformlyenlarged and shows a number of hypoechoic zones in the myometrium 1–5 mm in size, which may grow consid-
erably larger if intramural hemorrhage occurs. The posterior uterine wall is more commonly affected than other wall regions (Figs. 13.27, 13.28, 13.29).
Fig. 13.27 Adenomyosis with hypoechoic foci in the myometrium. T = enlarged uterus; BL = bladder.
Uterine Sarcoma
Sarcomas of the uterus account for 2–4% of uterine cancers. The majority are mixed sarcomas. The most common type, leiomyosarcomas of the uterine wall (uterine wall sarcoma), can be difficult to distinguish from benign myomas. The mitotic rate is an important criterion for assessing malignancy. Sarcomas are softer than myomas, bleed easily, and show a greater degree of necrosis. There are also stromal sarcomas of the endometrium (mucosal sarcomas, see below). Carcinosarcomas are mixed mesodermal tumors that contain both sarcomatous and adenocarcinomatous elements.
Fig. 13.28 Adenomyosis: dorsally of the endometrium (arrows) hypoechoic foci (points) in the posterior wall of the uterus (UT). BL = bladder; FL = free fluid.
Most sarcomas are detected incidentally in myomas that have been surgically removed.
Sonographic features. Sarcoma appears sonographically as a nonhomogeneous hypoechoic mass with some anechoic elements and ill-de- fined margins. Rapid enlargement is noted in follow-up scans (Fig.13.30, Fig.13.31). Tumors/ sarcomas of other origin have to be considered (Fig.13.32).
Treatment consists of surgical removal of the uterus and adnexa followed by irradiation. The prognosis is poorer than for uterine carcinoma.
Fig. 13.29 Adenomyosis with nonhomogeneous hypoechoic uterus. Cursors indicate the length of the uterus.
Features Helpful in Distinguishing Uterine Carcinoma from Myoma
●Rapid uterine enlargement
●Uterine enlargement after menopause
●Change in the uterine cavity
●Secondary changes such as renal obstruction and lymph node enlargement
●Late signs such as discomfort, ascites, and cachexia
Fig. 13.30 Fast-growing uterine myoma: well-circum- scribed mass showing only slight nonhomogeneity.
Fig. 13.31 Uterine sarcoma (UT): fast-growing, nonhomogeneous mass with ascites (FL).
Fig. 13.32 Liposarcoma: hypoechoic to echogenic nonhomogeneous tumor (TU) in the lower abdomen; 62-year- old woman. Differential diagnosis: uterine sarcoma.
450