Management of a placental chorioangioma with endoscopic devascularization and intrauterine transfusions

Chorioangiomas are hematomas that occur in approximately 1% of all placentas. Although most chorioangiomas are asymptomatic, they may be associated with polyhydramnios, oligohydramnios, non-immune fetal hydrops, growth restriction, microangiopathic hemolytic anemia, and intrauterine fetal death, with a perinatal loss of 30–40%1. In utero treatment of chorioangiomas has included intrauterine transfusions2, 3, ultrasound-guided intravascular thrombosis of the feeding vessels4-7, or operative fetoscopy8, 9. We describe a case of a large chorioangioma treated with combined intrauterine transfusion and endoscopic devascularization. The patient was a 24-year-old primigravida, diagnosed at 24 weeks' gestation with a large placental chorioangioma. Ultrasound showed a singleton fetus without obvious anomalies, and a large placental chorioangioma of 5.3 × 4.8 × 6.1 cm. There was polyhydramnios, with a maximum vertical pocket of 12 cm, scalp edema and ascites. Doppler studies showed tricuspid valve regurgitation of 1.2 m/s, reversed flow in the ductus venosus, pulsatile flow in the umbilical vein, normal umbilical artery resistance indices, and a peak systolic velocity of the middle cerebral artery of 56 cm/s, the latter suggestive of fetal anemia. Alternatives discussed with the patient included expectant management, intrauterine transfusions, therapeutic amniocentesis, or fetoscopic devascularization. The patient agreed to undergo invasive treatment and she signed informed consent. An intravascular transfusion was first performed for a hemoglobin of 6 g/dL, with a final fetal hemoglobin of 11 g/dL. Operative fetoscopy 5 days later disclosed three separate sets of arteries and veins, which were obliterated with 20–40 W of YAG-laser in that sequence. Color Doppler showed lack of blood flow within the mass. At the end of surgery, 2800 mL of fluid were removed, with a residual maximum vertical pocket of 4 cm. The ascites and the scalp edema resolved 7 days later, and the Doppler studies normalized as well. The patient was diagnosed with ruptured membranes 7 days later, for which she underwent an uneventful amniopatch10. A repeat fetal transfusion was performed for a fetal hemoglobin of 10 mg/dL in the same setting. No further leakage of fluid occurred; however, fetal demise was diagnosed 1 week later. Autopsy showed umbilical vein thrombosis and liver necrosis. Surgical pathology confirmed the diagnosis of a large chorioangioma, without patent vessels on air-injection studies. Our case confirms the feasibility of devascularizing large symptomatic chorioangiomas with the use of laser energy. However, it also points out the complexity of these cases, which may also involve fetal anemia, possibly from hemolysis. Although we do not know the exact cause of the fetal demise, potential explanations could include thrombosis, emboli from the thrombosed vessels, or complications from the intravascular transfusions. Based on our experience and the review of the literature, we concur with the recommendation that symptomatic chorioangiomas be managed with a combination of preoperative assessment and treatment of fetal anemia followed by endoscopic devascularization8. Further experience and a registry of cases of clinically significant choioangiomas will be required to determine the optimal management strategy of this entity. C. Bermúdez*, O. Luengas*, J. Pérez-Wulff*, U. Genatios*, V. García*, F. Guevara-Zuloaga*, R. A. Quintero†, * Unidad de Perinatología, Hospital Universitario de Caracas, Universidad Central de Venezuela, Caracas, Venezuela, † University of South Florida, Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Tampa, FL, USA