Prenatal Ultrasound Diagnosis and Prognostic Analysis of Fetal Congenital Hepatic Hemangioma.

OBJECTIVES

This study investigates the sonographic features, treatment, and prognosis of fetal congenital hepatic hemangioma (CHH), aiming to enhance prenatal diagnostic accuracy and provide insights for standardized management during both the prenatal and postnatal periods.

METHODS

A retrospective analysis was conducted on fetuses diagnosed with CHH by prenatal ultrasound and further confirmed by MRI (magnetic resonance imaging) or CT (computed tomography) between April 2019 and April 2025 at our institution. We analyzed and summarized prenatal and postnatal diagnostic findings, clinical manifestations, management strategies, and clinical outcomes in these patients.

RESULTS

A total of 14 patients were included, with a median follow-up of 54 months. The gestational age at diagnosis was 32 ± 6 weeks, and chromosomal analysis revealed normal. Fetal CHH are predominantly solitary lesions (92.9%, 13/14), most commonly located in the right hepatic lobe (64.3%, 9/14). Sonographically, they typically present as well-defined, hypervascular mixed-echogenicity masses. In our cohort, commonly observed features included sieve-like or honeycomb anechoic areas within the lesion. Pulsed Doppler imaging frequently reveals low-to-moderate resistance flow spectra. Two fetuses presented with an enlarged cardiothoracic ratio, one with a giant hepatic hemangioma and one with a non-giant lesion. Additionally, one case of right heart enlargement was observed in a fetus with a giant hepatic hemangioma. One pregnancy was terminated due to poor prognosis secondary to rapid tumor progression in the third trimester; another termination occurred for non-medical reasons during late gestation, and the remaining 12 pregnancies progressed to live births. Among live-born infants, 10 underwent active surveillance postnatally, while 2 required interventional therapy due to oral propranolol failure or persistent tumor growth. Ultimately, complete tumor regression occurred in 8 cases (66.7%, 8/12), with a median follow-up of 24 months. Partial regression in 3 (25.0%, 3/12) and stable disease in 1 (8.3%, 1/12). Additionally, the incidence of postnatal laboratory abnormalities, including hepatic dysfunction, coagulopathy, thyroid disorders, or elevated alpha-fetoprotein (AFP), was 16.7% (2/12) in live-born infants.

CONCLUSION

While prenatal ultrasound manifestations of fetal CHH demonstrate considerable heterogeneity, features are commonly observed in our cohort. Definitive diagnosis can be achieved in most cases through multimodal imaging combining ultrasound with MRI or CT. While most fetuses with CHH have a favorable prognosis, large tumors may cause severe complications and adverse pregnancy outcomes, warranting regular surveillance. For neonates with small tumors or asymptomatic lesions, active observation is the primary management strategy; pharmacotherapy is indicated for rapidly enlarging or large tumors, with interventional or surgical interventions reserved for pharmacologically refractory cases.