Current Problems in Diagnostic Radiology
Volume 41, Issue 1 , Pages 1-10, January 2012

Gestatational Trophoblastic Disease: Multimodality Imaging Assessment With Special Emphasis on Spectrum of Abnormalities and Value of Imaging in Staging and Management of Disease

Department of Radiology, University of Washington, Seattle, WA

Article Outline

Gestational trophoblastic disease is a spectrum of disorders of varying malignant potential arising from trophoblastic cells and encompassing hydatidiform moles and persistent trophoblastic neoplasia. Ultrasound is the initial imaging investigation of choice when gestational trophoblastic disease is suspected. Complete hydatiform mole, the most common form of molar pregnancy, usually has a characteristic “cluster of grapes” appearance, especially on second-trimester ultrasounds. Persistent trophobastic neoplasia usually appears as a focal, hypervascular myometrial mass on pelvic ultrasound. Pelvic magnetic resonance imaging is often used as a problem-solving tool in equivocal or complicated cases of gestational trophoblastic disease to assess the degree of invasion into the myometrium and surrounding tissues. Chest x-ray, brain magnetic resonance imaging, and body computed tomography scans are primarily used for the evaluation of metastatic disease, which usually occurs in the context of choriocarcinomas. Choriocarcinoma metastases are usually hypervascular and have a tendency to bleed, features that are reflected in their imaging appearance.

 

Gestational trophoblastic disease (gestational trophoblastic neoplasia) is a spectrum of disorders of varying malignant potential arising from trophoblastic cells and encompassing hydatidiform moles and persistent trophoblastic neoplasia.1, 2, 3

Hydatidiform moles (either complete or partial) have the potential to persist as invasive moles, choriocarcinomas, or placental site trophoblastic tumors. Persistent trophoblastic neoplasia (also known as gestational trophoblastic tumors [GTT]) can also develop after term or preterm deliveries, abortions, or ectopic pregnancies.1, 2 GTT are 1 of the most curable solid tumors due to the following: (a) the possibility of early and reliable detection of primary or recurrent disease with quantitative, serum human chorionic gonadotropin assays; and (b) the exquisitely chemosensitive nature of most of these lesions.1, 2, 4

Various imaging modalities are used to evaluate gestational trophoblastic disease (GTD).3, 4 Ultrasound is the initial investigation of choice when GTD is suspected.3, 5 In addition to ruling out a normal intrauterine pregnancy, pelvic ultrasound has the potential to both diagnose the disease and determine the degree of tumoral invasion.1, 3 Pelvic magnetic resonance imaging (MRI) is often used as a problem-solving tool in equivocal or complicated cases to assess the degree of invasion into the myometrium and surrounding tissues.6 Chest x-ray, body computed tomography (CT) scan, and brain MRI are primarily used to rule out metastatic disease.3, 4

In this article, we review the types, pathology, diagnosis, and management of the various forms of gestational trophoblastic neoplasia. We specifically emphasize and illustrate the appearance of GTD and its complications on a variety of imaging modalities.

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Normal Trophoblast 

The trophoblast begins as the outer covering of the blastocyst and ultimately forms the fetal portion of the placenta. It has 3 major components: cytotrophoblast, syncytiotrophoblast, and intermediate trophoblast. The cytotrophoblast is a stem cell with high mitotic activity, while the syncytiotrophoblast synthesizes the hormone, human chorionic gonadotropin (hCG), and forms the chorionic villi.1 The intermediate trophoblast has features of the other 2 and is responsible for endometrial invasion and implantation.1 These cells variably contribute to the different forms of GTD.1

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Hydatiform Mole 

Hydatiform mole comprises 80% of cases of GTD and includes both complete (also called classic) molar pregnancies and partial moles.1 In North America molar pregnancy occurs with an incidence of 0.6-1.1 in 1000 pregnancies.6 There are wide geographic differences in the incidence of hydatidiform mole with molar pregnancy occurring in 8 per 1000 pregnancies in some Asian populations.3 The risk factors for molar pregnancy are extremes of maternal age, prior molar gestations, and history of spontaneous abortions.2 Familial clusters of biparental complete hydatiform moles associated with novel missense gene mutations have also been recognized.

Complete mole is the most common type of molar pregnancy.1, 2 The chromosomes of a complete molar pregnancy are solely paternal in origin. The most common situation is fertilization of a chromosomally empty ovum by a haploid sperm that subsequently duplicates to form a 46,XX diploid karyotype.1, 2 Unusual zygotes with a 46,XY karyotype result from fertilization of a chromosomally empty ovum by 2 different sperms (46,YY zygotes are nonviable).1, 2 Partial moles usually have a triploid karyotype (69,XXX; 69,XXY; 69,XYY) that arises from fertilization of an apparently normal ovum by 2 different sperms.1, 2 Pathologically, complete moles are composed of diffusely hyperplastic and swollen (hydropic) villi, with absent embryonal/fetal tissue.1, 2, 3 By contrast, in partial molar pregnancies focal trophoblastic changes (hyperplasia and swelling) are usually seen in association with fetal tissue.1, 2

Clinically, complete hydatiform mole usually presents with vaginal bleeding in the first or early second trimester.3 Passage of vesicles (hydropic villi) occurs in up to 80% of cases and is considered specific for this condition.7 The serum hCG level is usually considerably higher than expected for the estimated gestational age (usually more than 100,000 mIU/mL).2 However, this is variable and the level may be within the normal range of a first-trimester pregnancy.1 The other classic signs and symptoms, such as uterine enlargement greater than expected for gestational age, hyperemesis gravidarum, or early-onset pre-eclampsia, occur less frequently due to earlier diagnosis of disease because of more widespread use of ultrasonography and more accurate hCG testing.8, 9 Partial molar pregnancies usually present with vaginal bleeding and are generally misdiagnosed as missed or incomplete abortions.1, 3 Human chorionic gonadotropin levels are greater than 100,000 mIU/mL in less than 10% of patients with partial moles.

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Ultrasound Features of Molar Pregnancies 

On pelvic ultrasound, complete hydatiform mole may appear as an echogenic mass with multiple, diffusely distributed, small (1-30 mm) vesicles, in an enlarged uterus (Fig 1).1, 3, 8 This characteristic “cluster of grapes” appearance corresponds to the diffusely hyperplastic and hydropic villi described in the pathology literature. It is usually evident with transabdominal ultrasound on second-trimester ultrasound, and in some cases, in the first trimester with transvaginal ultrasound.1 A fetus or fetal parts are not seen, except in the rare event of a coexistent diploid twin pregnancy.10 The latter could be differentiated from a partial mole by identifying a separate normal placenta.11 Transvaginal ultrasound is especially valuable for evaluation of suspected first-trimester complete molar pregnancies.8, 12 During this period, the less well-developed molar tissue may appear as a homogeneously echogenic mass, a gestational-sac-like structure, or as a solid, echogenic mass within a gestational sac and has the potential to be confused with blood clots or incomplete/missed abortions.9, 13, 14 Theca lutein cysts occur in up to 40% of cases and are a reflection of the highly elevated hCG levels.1 Other causes of ovarian hyperstimulation, such as ovulation induction, twin pregnancies, fetal hydrops, and occasionally a normal pregnancy, may be associated with these types of cysts.1 On pelvic ultrasound, theca lutein cysts are seen as bilateral, multilocular ovarian cysts (Fig 2), some of which may occasionally be complicated by hemorrhage or rupture.1 These cysts usually resolve within a few months of removal of the causative factor.1

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  • FIG 1. 

    A 36-year-old woman with complete molar pregnancy. (A) Grayscale ultrasound image demonstrates a heterogenous mass (arrows) located centrally within the uterus. (B) The mass demonstrates mild internal vascularity on color Doppler ultrasound. (Color version of figure is available online.)

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  • FIG 2. 

    Theca lutein cysts in a patient with partial molar pregnancy. Ultrasound images of (A) right and (B) left ovaries show enlarged, multicystic ovaries. This appearance in a patient with partial molar pregnancy is suggestive of theca lutein cysts.

In a partial molar pregnancy, an enlarged placenta with nonuniformly distributed cystic spaces is usually associated with a deformed gestational sac or an alive or dead fetus.15, 16 The placental cysts may not be discernible on first-trimester ultrasound due to their small size (Fig 3). The fetus may be anomalous and demonstrate triploid features, such as growth restriction, hydrocephalus, cleft lip, or syndactyly.15, 17 A similar placental appearance may be caused by hydropic placental degeneration, which commonly occurs with a first-trimester demise of any cause (Fig 4).15 Therefore, when the ultrasound findings are equivocal, careful evaluation of the products of conception is recommended to avoid the possibility of missing a diagnosis of molar pregnancy.8 Theca lutein cysts occur less frequently in partial moles due to the lower hCG levels.

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  • FIG 3. 

    Evolution of placental cystic changes in partial molar pregnancy. (A) Sagittal image from a first-trimester ultrasound demonstrates an anterior placenta with a homogenous appearance. Fetus was alive, although small for gestational age (not shown). (B) Sagittal image from an ultrasound performed a month later demonstrates development of several cystic foci within the placenta (arrows) along with fetal demise (not shown). Fetal karyotype was 69,XXX.

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  • FIG 4. 

    Hydropic placental degeneration, with fetal demise (not shown). The placenta (arrows) appears thick and demonstrates cystic changes. However, pathologically this was due to hydropic changes after fetal demise and was not secondary to partial molar pregnancy.

Some cases of hydatiform moles may demonstrate abnormal vascularity on Doppler ultrasound (Fig 1B); however, this is not a specific sign.3, 8 Rarely, molar pregnancy may occur in an ectopic location.18

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Management of Molar Pregnancies 

In addition to pelvic ultrasound, the only other routine imaging study performed in molar pregnancies before the institution of definitive therapy is a chest x-ray, with pelvic MRI being reserved as a problem-solving tool in selected cases.2 The treatment of choice for hydatiform moles is suction curettage, which is successful in most cases.2 Approximately 15%-20% of complete moles and 0.5%-5% of partial moles go on to develop persistent trophoblastic disease.1, 2, 3

The likelihood of persistent disease after evacuation of a complete hydatiform mole increases in patients with evidence of marked trophoblastic growth, such as preevacuation hCG level >100,000 mIU/m, excessive uterine growth (>20 week size), and theca lutein cysts measuring more than 6 cm in diameter.2 However, since it is difficult to predict the outcome in individual cases, all cases of molar pregnancy are followed with serial quantitative serum hCG measurements as follows: every 1-2 weeks until 3 consecutive tests demonstrate normal levels, and then at 3-month intervals for 6 months. Contraception is recommended for 6 months after the first normal hCG result, as a normal pregnancy would adversely affect the specificity of rising hCG results.1, 2

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Persistent Trophoblastic Neoplasia (Gestational Trophoblastic Tumors) 

Invasive mole, choriocarcinoma, and placental site trophoblastic tumor are classified as persistent trophoblastic neoplasia (PTN). PTN may present weeks or years after molar or nonmolar pregnancies.1, 3 The components needed to diagnose postmolar GTT include at least 1 of the following: (1) hCG plateau for 4 consecutive values over 3 weeks; (2) hCG rise of ≥10% for 3 values over 2 weeks; (3) hCG persistence 6 months after molar evacuation; (4) histopathologic diagnosis of choriocarcinoma; or (5) presence of metastatic disease.19 A histologic diagnosis is not considered mandatory for the diagnosis of postmolar PTN.1, 8 The diagnosis of nonmolar gestational trophoblastic neoplasia may be less straightforward, with some cases presenting years after a pregnancy event with irregular uterine bleeding, amenorrhea, or symptoms of metastatic disease.1, 2, 3, 20

Invasive mole is the most common form of GTT.21 It almost always occurs after a complete molar pregnancy and thus usually has a diploid karyotype that is completely paternal in origin.1 On pathologic examination, hyperplastic, hydropic villi are associated with vascular and myometrial invasion.1, 4 Although usually confined to the uterus, invasive moles have the potential to spread to both adjacent structures and distant sites.1, 18

Choriocarcinoma is a rare malignancy, occurring with an incidence of 1 in 40,000 pregnancies in North America and Europe.2 Approximately one half of the cases of choriocarcinomas occur after a molar gestation, while the other half are associated with nonmolar pregnancies.22 Pathologically, nonvillous hyperplasia and anaplasia of trophoblastic cells are seen in association with extensive tissue necrosis and hemorrhage.1, 2 Distant metastases commonly occur, most commonly to the lungs, followed by the liver, brain, gastrointestinal tract, and kidneys.23

Placental site trophoblastic tumor is an extremely rare tumor that is predominately composed of intermediate cells.20 It mostly follows term delivery gestations, is usually associated with only mildly elevated hCG levels, and may demonstrate both lymphatic and vascular invasion.1, 3, 20 Epithelioid trophoblastic tumor is a rare variant of placental site trophoblastic tumor that simulates carcinoma.2 This type of tumor usually presents many years after a full-term delivery.2

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Ultrasonographic Features of Persistent Trophoblastic Neoplasia 

The various types of PTN may appear similar sonographically.1 Transvaginal ultrasound is an essential tool for the evaluation of PTN.8 The most common appearance of PTN on pelvic ultrasound is a focal myometrial mass that is best appreciated with transvaginal ultrasound (Fig 5A).15, 16, 23, 24 The myometrial mass may be uniformly echogenic or hypoechoic, or complex and multicystic.15, 16, 23, 24 Anechoic spaces within the mass may be due to hemorrhagic or necrotic tissue, cysts, or vascular spaces.3, 8 More extensive disease may appear as a lobulated and heterogeneously enlarged uterus that may be seen extending to adjacent structures, or as a large, undifferentiated pelvic mass.8 The grayscale appearance of GTT is nonspecific and has the potential to be confused with fibroids, adenomyosis, or primary and secondary pelvic malignancies.24 Accurate diagnosis depends on correlation with clinical findings and hCG levels. On Doppler ultrasound, GTT usually demonstrate extreme vascularity secondary to the contained arteriovenous shunts (Fig 5B).3, 25, 26 On color Doppler ultrasound, the lesions usually demonstrate chaotic vascularity with color aliasing and loss of vessel discreteness.8 On duplex Doppler ultrasound, trophoblastic vessels demonstrate a high-velocity, low-resistance waveform that is in contradistinction to the low-velocity, high-resistant flow usually detected in normal myometrial arteries.3, 25, 26 These Doppler features are not specific to GTT: trophoblastic tissue from other causes (missed or incomplete abortion, retained products of conception, ectopic pregnancy), rare uterine fibroids, some primary or secondary pelvic malignancies, pelvic inflammatory disease, pelvic abscesses from diverticulitis or appendicitis, or uterine arteriovenous malformations may demonstrate a similar appearance.8 Placental site trophoblastic tumors may occur in either a hypovascular or a hypervascular form. As its name implies, the former type is not associated with prominent vascularity on Doppler ultrasound.3, 27

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  • FIG 5. 

    Invasive mole presenting as rising serum hCG levels after evacuation of a complete molar pregnancy. (A) Sagittal transvaginal ultrasound image demonstrates an echogenic multicystic mass (calipers) within the posterior myometrium. Endometrium (arrow). (B) Increased vascularity is seen in the mass as color aliasing on the Color Doppler image. The anechoic cystic spaces seen on B-mode image are seen to fill in with color, confirming their vascular nature (compare this florid vascularity with the relatively scattered foci of blood flow in the complete molar pregnancy depicted in Fig 1B). (Color version of figure is available online.)

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MRI of Gestational Trophoblastic Disease 

Pelvic MRI does not have a routine role in the assessment of GTD and is usually used as a problem-solving tool in equivocal or complicated cases.27 On pelvic MRI, hydatiform mole usually appears as a heterogeneous, markedly hyperintense mass that distends the endometrial cavity on T2-weighted images (Fig 6A).5, 28 On contrast-enhanced T1-weighted images, especially during the second trimester, diffusely distributed small cystic spaces are typically noted within the mass (Fig 6B).5 The normal myometrium remains and surrounds the mass. Theca lutein cysts may be observed in some cases.28

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  • FIG 6. 

    A 23-year-old woman presenting with a third recurrent molar pregnancy. (A) Coronal-oblique SPIR shows a hyperintense mass expanding the endometrial cavity. Observe the intact junctional zone (arrows) surrounding the mass. (B) On the postcontrast THRIVE image, the multicystic nature of the mass is reflected in its lattice-like pattern of enhancement.

Invasive moles and choriocarcinomas are usually seen as a heterogeneous endometrial ± myometrial mass on T1- and T2-weighted images (FIG 7, FIG 8).29 This heterogeneous appearance may be partially due to tumor necrosis or hemorrhage. Extrauterine extension of disease into the parametrium or vagina may be noted additionally and could be better evaluated with MRI than ultrasound.3, 5 There may be a loss of normal zonal anatomy (Fig 9A) along with diffuse myometrial hyperintensity on T2-weighted images.29, 30, 31 Loss of zonal anatomy is nonspecific and may be observed in other conditions, such as missed/incomplete abortions or recent diagnostic curettage.29, 30, 31 Engorged intralesional, myometrial, parametrial, and internal iliac vasculature are a reflection of the hypervascular nature of these tumors (Fig 9B).29 Viable tumors may be seen as areas of enhancement in the early phase of contrast-enhanced, dynamic MRI.3, 30

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  • FIG 7. 

    Invasive mole occurring 3 months after an abortion. Coronal-oblique T2-weighted SPAIR image demonstrates a heterogeneous mass expanding the endometrial cavity. Areas of hemorrhage are seen as low signal intensity foci in the left aspect of the lesion. Observe the disrupted junctional zone (arrows). There is no evidence of extrauterine extension of disease.

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  • FIG 8. 

    Choriocarcinoma in a 33-year-old-female patient presenting with vaginal bleeding and markedly elevated hCG levels after an abortion. (A) Sagittal T2-weighted image depicts a heterogeneous, lower uterine segment/cervical mass. Hemorrhage is noted within the mass (white arrows). (B) The mass enhances heterogeneously as seen on the sagittal postcontrast THRIVE image. A homogeneously enhancing fibroid is noted incidentally in the anterior uterine wall (black arrow).

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  • FIG 9. 

    Invasive mole extending through Caesarean section scar. (A) Sagittal and (B) coronal-oblique T2-weighted images. Note the decreased conspicuity of the uterine zonal anatomy and extension of the signal voids both within the mass (black arrow) and as engorged arcuate (white arrow) and uterine venous plexus (arrowhead) vasculature, suggesting the hypervascular nature of the mass. There is no evidence of involvement of the adjacent wall of the urinary bladder on image (A).

The 2 types of placental site trophoblastic tumors may differ in their MRI appearance. The hypervascular type may appear as an isointense T1-weighted, and slightly hyperintense T2-weighted, avidly enhancing mass.32, 33 Numerous prominent vessels are seen surrounding the lesion.32 The hypovascular type may be hyperintense to normal myometrium on both T1- and T2-weighted images and demonstrate some enhancement after IV contrast administration.33 Signal voids due to prominent vascularity are usually absent in the latter type of lesion.33

Brain MRI may be performed to rule out metastatic disease in patients with persistent trophoblastic neoplasia. The signal characteristics of these frequently hemorrhagic metastases are widely variable and depend on the age of the hemorrhage.34

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Computed Tomography of Persistent Trophoblastic Neoplasia 

Metastatic disease has been reported in up to 19% of patients with GTT, with the vast majority of cases occurring in choriocarcinomas.3 CT is primarily performed for evaluation of metastases, although the primary tumor may be seen as a focal, low-attenuation lesion within an enlarged uterus in some cases (Fig 10).35 Except for brain and vaginal metastases that are more accurately evaluated with MRI, CT scanning is the most suitable method for evaluation of the more common sites of metastases of GTT.3 Choriocarcinoma metastases are usually hypervascular and have a tendency to bleed, features that are reflected in their CT appearances.3 The lungs are the primary sites of metastasis. Pulmonary metastases usually occur as multiple parenchymal masses (Fig 11), although solitary and miliary lesions may also occur.3 Endovascular (which may be accompanied by pulmonary infarction) or endobronchial metastases may be noted additionally.3 Hemorrhage of metastatic lesions within the lung parenchyma or pleural space may be associated with airspace consolidation or pleural effusion, respectively.3

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  • FIG 10. 

    Invasive mole occurring 2 months after a complete molar pregnancy. Consecutive axial, contrast-enhanced CT scans demonstrate a heterogeneous, hypervascular central uterine mass (white arrows). Engorged vessels both within the mass (short black arrow) and in the parametrium (long black arrows).

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  • FIG 11. 

    Pulmonary metastases in choriocarcinoma. Axial CT scan shows multiple, bilateral lung nodules, some of which are surrounded by ground-glass opacity (suggestive of hemorrhage).

Hepatic metastases are usually multiple, hemorrhagic, and hypervascular. These lesions may be amenable to selective chemoembolization.36 A variety of other hematogenous metastatic sites have been reported, including the spleen, kidneys, gastrointestinal tract, brain, and skin. Lymphatic spread (to pelvic lymph nodes) is usually seen with placental site trophoblastic tumors.4, 37, 38

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Positron Emission Tomography/Computed Tomography of Persistent Trophoblastic Neoplasia 

There are limited data on the efficacy of positron emission tomography (PET)/CT in the evaluation of patients with gestational trophoblastic neoplasia. 18F-fluorodeoxyglucose-PET has the potential to identify occult disease in patients with recurrent or metastatic GTT: it may identify sites of metabolically active disease not evident by other imaging modalities or be helpful in differentiating uterine scars from metabolically active recurrent disease.37, 38

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Management of Persistent Trophoblastic Neoplasia 

Most centers use the International Federation of Obstetrics and Gynecology (FIGO) staging and scoring system for gauging the severity and determining the appropriate type of therapy in individual cases of invasive moles and choriocarcinomas (placental site trophoblastic tumors are classified separately).4, 19 Imaging findings that affect the overall scoring in this system include largest tumor along with number and site of metastases. When a diagnosis of gestational trophoblastic tumor is suspected, a pelvic ultrasound and a chest x-ray are obtained routinely, which may be supplemented with body CT scanning or brain MRI in some cases.3, 4 Pelvic MRI is usually used as a problem-solving tool in equivocal or complicated cases.

Gestational trophoblastic tumor patients with nonmetastatic or low-risk metastatic disease that score ≤6 in the FIGO system are treated with single-agent chemotherapy, with resulting survival rates approaching 100%.3, 4 High-risk metastatic patients with scores higher than 6 are treated more aggressively with multiagent chemotherapy ± adjuvant surgery or radiation therapy, to achieve an 80%-90% cure rate.3, 19 Although the extent of uterine involvement as determined by pelvic ultrasound or MRI does not affect a patient's score in the current FIGO system, it may affect therapeutic decisions (hysterectomy may be of benefit in extensive uterine disease).1 After normalization of hCG levels and completion of chemotherapy, patients are followed up with serial quantitative serum hCG levels for 12 months (contraception should be maintained during this period).19 Placental site trophoblastic tumors are mainly managed with hysterectomy and pelvic lymph node dissection, with adjuvant chemotherapy reserved for high-risk nonmetastatic or metastatic cases.3, 19 The survival rate is approximately 100% for nonmetastatic disease and 50%-60% for metastatic disease.19

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Follow-Up Imaging After Treatment of Gestational Trophoblastic Disease 

Follow-up imaging after initiation or completion of therapy for GTD is routinely performed only when (a) complications are suspected; or (b) during the first trimester of a subsequent pregnancy (quantitative serum hCG levels at 6 weeks along with first-trimester pelvic ultrasound is recommended in subsequent pregnancies due to increased risk of GTD recurrence).19

On follow-up imaging, uterine and ovarian abnormalities usually resolve with effective therapy. On sonography, lesions usually become progressively smaller and more hypoechoic.8 However, a significant portion of patients will demonstrate persistent abnormalities, such as scar tissue or residual uterine vascular malformations, that may be difficult to distinguish from active lesions sonographically.39 Residual uterine vascular malformations may be complicated by bleeding, which is usually vaginal.40 However, life-threatening intraperitoneal hemorrhage, requiring massive transfusion, may also occur.40 Most residual uterine vascular malformations are amenable to endovascular treatment, via selective uterine artery embolization.41 Theca lutein cysts may persist for months after therapy and be a cause of mild abdominal discomfort.3

On pelvic MRI performed after effective chemotherapy for GTT, regression of vascular abnormalities, return to normal of uterine zonal anatomy, and intralesional hemorrhage may be observed in addition to a reduction of uterine volume.29 Residual vascular malformations are usually seen as tortuous vessels in a thick endometrium.3

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Conclusions 

Gestational trophoblastic disease is a spectrum of diseases with varying malignant potential, broadly categorized into hydatidiform moles and persistent trophoblastic neoplasia. Ultrasound is the main imaging modality for evaluation of complete hydatidiform moles and persistent trophoblastic neoplasia. Pelvic MRI is usually used as a problem-solving tool in equivocal or complicated GTD cases. Chest x-rays, brain MRI, and body CT scans are primarily used to rule out metastatic disease. 18F-fluorodeoxyglucose-PET has the potential to identify occult disease in patients with recurrent or metastatic GTT. Imaging is not routinely performed for follow-up of treated GTD, unless a complication is suspected or during the first trimester of a subsequent pregnancy. On follow-up imaging, uterine and ovarian abnormalities usually resolve with effective therapy. However, a significant portion of patients will demonstrate persistent abnormalities, such as scar tissue or residual uterine vascular malformations, that may be difficult to distinguish from active lesions both on sonogram and on MRI.

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PII: S0363-0188(11)00050-8

doi:10.1067/j.cpradiol.2011.06.002

Current Problems in Diagnostic Radiology
Volume 41, Issue 1 , Pages 1-10, January 2012

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