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Intracardiac Fetal Transfusion for Parvovirus‐Induced Hydrops Fetalis: A Salvage Procedure

Parvovirus is the most common cause of nonimmune fetal hydrops in the United States, with a fetal death rate of 2% to 6%.1 Historically, hydrops has a 30% fetal mortality rate; however, newer data demonstrate resolution of 90% of cases within 6 to 12 weeks and mortality of less than 10% if the fetus can be supported by transfusion.1 A 32-year-old woman was referred to our institution at 17 weeks’ gestation for baseline cervical length in view of a bicornuate uterus and a history of multiple abortions. On sonography, the cervical length measured 4 cm, and the fetus showed gross hydrops fetalis with ascites, pleural effusion, pericardial effusion, and subcutaneous edema (Figure 1). The fetus appeared moribund with markedly reduced fetal movements, and imminent fetal death was anticipated. The middle cerebral artery peak systolic velocity (PSV) was 45.44 cm/s (1.95 multiples of the median), consistent with severe fetal anemia. The amniotic fluid was normal in volume, and no other fetal anatomic abnormalities were detected. Limited fetal echocardiography was performed because of the early gestational age and pericardial effusion and showed a normal cardiac structure with no evidence of fetal tachyarrhythmia. There was cardiomegaly with poor cardiac contractility. Doppler echocardiography showed tricuspid regurgitation. Absent end-diastolic flow in the umbilical artery and reversed flow in the ductus venosus were visualized before transfusion. On inquiry, the mother gave a history of exposure to fifth disease at 7 weeks’ gestation with a documented maternal nonimmune status at that time. The patient was counseled about the fetal condition, complications, and the management options. Amniocentesis subsequently confirmed parvovirus infection by polymerase chain reaction. Due to the diminutive fetal blood volume circulating at this very early gestational age, we opted not to check the initial fetal hematocrit to avoid further deterioration of the already compromised fetal condition. Therefore, given the profound fetal anemia, we predicted the initial opening hematocrit at 10%, and on the basis of an estimated fetal weight of 213 g, we calculated that 9 mL of donor blood (80% hematocrit) would be required to achieve a target fetal hematocrit value of 40%. Under direct sonographic guidance, a 22-gauge needle was used to perform a fetal cordocentesis. However, the umbilical vein near the placental cord insertion was extremely thin because of the early gestational age and proved difficult to manipulate. Thus, we resorted to other