Chorioangioma is the most common benign tumor of the placenta — originating from primitive mesenchymal capillary proliferation in chorionic villi, histologically similar to cavernous hemangioma. Incidence is ~1/100 placentas histologically but clinically significant ones (>4-5 cm) occur in ~1/3500-9000 pregnancies. Large chorioangiomas can cause fetal complications: polyhydramnios, fetal anemia, non-immune hydrops fetalis, and high-output heart failure — all developing through the tumor's arteriovenous shunt effect. On US, it appears as a well-defined, hypervascular solid mass on the placental surface or within it; shows high signal on T2-weighted MRI. Intense vascularity and feeding artery on Doppler have diagnostic value.
Age Range
18-45
Peak Age
30
Gender
Female predominant
Prevalence
Rare
Chorioangioma originates from abnormal angioblastic proliferation of primitive chorionic mesenchyme — during embryonic development, vascular progenitor cells in chorionic villi proliferate uncontrolled, forming a vascular mass. Histologically, it is a vascular structure filled with multiple capillary channels, similar to cavernous hemangioma, with three histologic variants described: angiomatous (most common, multiple capillaries), cellular (stromal cell dominant), and degenerate (fibrosis/hyalinization). Small chorioangiomas (<4 cm) are hemodynamically insignificant and do not affect placental function — most are incidentally found on postpartum histological examination. Large chorioangiomas (>4-5 cm) are hemodynamically significant: the tumor's dense vascular structure creates an arteriovenous shunt between fetal and maternal circulation — a portion of fetal blood passes through the tumor without oxygen exchange, returning to fetal circulation → effective fetal cardiac output increases → compensatory cardiac hypertrophy → high-output heart failure → non-immune hydrops fetalis. Additionally, blood pooling and turbulent flow within the tumor may cause microangiopathic hemolytic anemia (erythrocyte fragmentation) and consumptive coagulopathy (thrombocytopenia) — mechanism similar to Kasabach-Merritt syndrome. Polyhydramnios develops through two mechanisms: increased fetal cardiac output → increased renal perfusion → increased fetal urine production; and fluid transudation from the tumor surface into the amniotic cavity. The hypervascularity on US manifests as intense Doppler signal — the feeding artery, usually a chorionic artery branch, is identified at the point where the cord enters the tumor. High T2 signal reflects the long T2 relaxation time of slow-flowing blood in vascular spaces.
Well-defined solid mass on/in placenta + prominent hypervascularity and chorionic artery branch feeding artery on Doppler — pathognomonic combination for chorioangioma. Differentiates from avascular placental lesions (infarct, thrombosis, hematoma).
A well-defined, round/oval, usually homogeneously hypoechoic or mixed echogenicity solid mass is seen on the placental surface (chorionic plate) or within the parenchyma. The mass shows different echogenicity from placental parenchyma — more hypoechoic. Size can range from few mm to 20+ cm. The mass may protrude from the chorionic plate into the amniotic cavity — appearing as a mass surrounded by amniotic fluid. Internal hemorrhage, necrosis, or calcification in large lesions may cause heterogeneous appearance.
Report Sentence
A well-defined, hypoechoic solid mass measuring __ × __ mm on the placental surface is consistent with chorioangioma.
Intense vascularity is seen within the mass on color Doppler — multiple vascular channels and feeding artery are identified. The feeding artery is usually identified as a chorionic artery branch at the point where the umbilical cord enters the mass. Power Doppler better demonstrates low flow velocities and is more sensitive for detecting vascularity in small lesions. Spectral Doppler shows low-resistance arterial flow pattern in the feeding artery — hemodynamic evidence of arteriovenous shunting.
Report Sentence
The mass is markedly hypervascular on color Doppler with an identifiable feeding artery (chorionic artery branch) — supporting chorioangioma diagnosis.
On T2-weighted MRI, a well-defined mass with high signal intensity is seen — reflecting slow-flowing blood in vascular spaces. Shows brighter signal than placental parenchyma with clearly defined contours. May be isointense or mildly hyperintense on T1 — if hemorrhagic component is present, markedly hyperintense areas (methemoglobin) may be seen on T1. Progressive enhancement is seen on contrast MRI — filling from periphery to center, similar to hemangioma enhancement pattern.
Report Sentence
A well-defined mass with high T2 signal intensity measuring __ mm on the placental surface/within the placenta is consistent with chorioangioma.
Polyhydramnios may accompany large chorioangiomas (>4-5 cm) — amniotic fluid index (AFI) >24 cm or deepest pocket >8 cm. Polyhydramnios is an indirect finding of fetal high-output heart failure, developing through increased renal perfusion + transudation from tumor surface. Polyhydramnios severity correlates with tumor size and vascularity degree.
Report Sentence
Polyhydramnios (AFI: __ cm) is seen accompanying the chorioangioma — close monitoring for fetal complications is recommended.
Fetal hydrops findings are systematically assessed in large chorioangiomas: skin edema (subcutaneous hypoechoic band >5 mm), ascites (free peritoneal fluid), pleural effusion (fluid around lungs), pericardial effusion (fluid around heart), placental thickening (>40 mm). Fluid accumulation in two or more compartments meets the diagnosis of non-immune hydrops. Hydrops development is an indication for urgent intervention — intrauterine transfusion (for fetal anemia), feeding artery laser coagulation or embolization.
Report Sentence
Fetal hydrops findings (skin edema / ascites / pleural effusion / pericardial effusion) should be assessed — for large chorioangioma complication.
MCA PSV (middle cerebral artery peak systolic velocity) measurement screens for fetal anemia in large chorioangiomas. MCA PSV >1.5 MoM (multiples of median) indicates fetal anemia — reflecting microangiopathic hemolytic anemia or hemodilution from AV shunting caused by chorioangioma. Serial MCA PSV monitoring is a standard approach in chorioangioma management.
Report Sentence
MCA PSV measures __ cm/s, corresponding to __ MoM for gestational age.
Criteria
Size <4 cm, hemodynamically insignificant
Distinct Features
Asymptomatic, low fetal complication risk, serial US follow-up sufficient (every 4 weeks), no specific treatment needed, postpartum histological confirmation
Criteria
Size >4-5 cm, hemodynamically significant arteriovenous shunt potential
Distinct Features
High fetal complication risk (polyhydramnios, anemia, hydrops), close monitoring mandatory (weekly/biweekly), MCA PSV monitoring, laser coagulation or embolization may be needed, intrauterine transfusion (fetal anemia), amnioreduction (polyhydramnios)
Criteria
Degenerative changes with hemorrhage, necrosis, calcification, or fibrosis
Distinct Features
Heterogeneous appearance, calcifications cause posterior shadowing, vascularity may be decreased on Doppler — degeneration may occlude vascular structures, hemodynamic effect may diminish
Distinguishing Feature
Intervillous thrombosis is AVASCULAR on Doppler (no active flow in organized thrombus); chorioangioma is HYPERVASCULAR on Doppler (multiple capillary channels + feeding artery) — Doppler alone is differentiating
Distinguishing Feature
Subchorionic hematoma is subchorionic, crescent-shaped, and avascular; chorioangioma is within/on placental parenchyma, round, and hypervascular — localization + shape + vascularity difference
Distinguishing Feature
In molar pregnancy, entire placenta is abnormal (snowstorm pattern) with very high β-hCG; chorioangioma shows focal well-defined mass with normal remaining placenta and proportional β-hCG
Distinguishing Feature
Placental teratoma contains fat and calcification components (fat signal on MR + calcification on CT); chorioangioma has dominant vascular structure (T2 hyperintense + hypervascular) — tissue components differ
Urgency
routineManagement
surveillanceBiopsy
Not NeededFollow-up
3-monthSmall chorioangiomas (<4 cm) are clinically insignificant — serial US follow-up every 4 weeks is sufficient, no specific treatment needed, postpartum placental histology confirms diagnosis. Large chorioangiomas (>4-5 cm) require multidisciplinary close monitoring: weekly/biweekly US for fetal growth monitoring, AFI measurement (polyhydramnios tracking), MCA PSV (fetal anemia screening — >1.5 MoM anemia suspicion), fetal echocardiography (cardiac hypertrophy and heart failure assessment), hydrops screening. Treatment options if complications develop: feeding artery laser coagulation (fetoscopic — most specific treatment, closes shunt), interstitial laser ablation, alcohol sclerotherapy, feeding artery embolization, intrauterine transfusion (fetal anemia correction), amnioreduction (polyhydramnios palliation). Treatment timing is determined by fetal maturity and complication severity — early delivery may be planned for severe fetal compromise (steroid maturation + cesarean). No malignant transformation risk — chorioangioma is entirely benign.
Small chorioangiomas (<4 cm) are usually asymptomatic and require no intervention beyond follow-up. Large chorioangiomas (>4-5 cm) can develop fetal anemia, high-output heart failure, hydrops fetalis, and polyhydramnios through AV shunting. Treatment: serial US follow-up, amnioreduction (polyhydramnios), intrauterine transfusion (fetal anemia), tumor feeding artery laser coagulation or embolization (refractory cases).