From the Guidelines
Parvovirus B19 infection during pregnancy can lead to hydrops fetalis through direct viral targeting of erythroid progenitor cells in the developing fetus, resulting in severe fetal anemia and high-output cardiac failure. The virus enters these cells via the P antigen receptor, causing cell lysis and triggering compensatory mechanisms including increased cardiac output and extramedullary hematopoiesis 1. As the fetal heart struggles to maintain adequate tissue perfusion against worsening anemia, high-output cardiac failure develops, leading to increased hydrostatic pressure and decreased oncotic pressure, and ultimately, fluid accumulation in fetal tissues and body cavities, manifesting as hydrops fetalis.
The risk of developing hydrops fetalis is highest when maternal infection occurs between 13-20 weeks gestation, when fetal red blood cell production is rapidly increasing and the fetal liver is the primary site of erythropoiesis 1. The fetus is particularly vulnerable during this period because of its shorter red blood cell lifespan (45-70 days), limited erythropoietic reserve, and rapidly expanding blood volume. Additionally, the virus can directly infect myocardial cells, further compromising cardiac function. Maternal-fetal transmission occurs in approximately 30-50% of cases, with hydrops developing in about 3-5% of infected fetuses.
Key points to consider in the pathophysiology and management of parvovirus infection in pregnancy and development of hydrops fetalis include:
- The importance of prompt diagnosis through maternal serology and fetal ultrasound monitoring 1
- The role of intrauterine blood transfusions in managing severe fetal anemia and preventing hydrops fetalis 1
- The need for close monitoring of fetal condition and timely intervention to improve outcomes in cases of parvovirus infection during pregnancy. Intrauterine transfusion is recommended for nonimmune hydrops fetalis due to parvovirus infection, unless the pregnancy is at an advanced gestational age and risks associated with delivery are considered to be less than those associated with the procedure 1.
From the Research
Pathophysiology of Parvovirus Infection in Pregnancy
- Parvovirus B19 (B19V) infection can cross the placenta and result in fetal infection, leading to severe fetal anemia, hydrops fetalis, miscarriage, or intrauterine fetal death 2.
- The risk of fetal infection increases with advancing gestational age, and the risk of severe fetal anemia or hydrops is around 3-4% overall, and around 6-7% if the primary infection occurs before 20 weeks' gestation 2.
- Vertical transmission of B19V occurs in 30-50% of cases of maternal infection, and the risk of fetal infection is higher in the second trimester 3, 4.
Development of Hydrops Fetalis
- Fetal parvovirus infection can lead to marked anemia and hydrops formation, and cordocentesis allows precise assessment of fetal anemia, which can then be corrected by intravenous transfusion 5.
- Hydrops fetalis is a serious condition that can result from severe fetal anemia, and the prognosis is better if the fetal effusion regresses after transfusion 6.
- Non-anemic forms of hydrops fetalis can occur, with isolated refractory ascites or pleural effusion, and maternal mirror syndrome can reflect the intensity and persistence of the fetal anemia 6.
Diagnosis and Management
- Diagnosis of B19V infection requires a multi-method approach using mainly serology and PCR techniques, and severe fetal anemia is managed with intrauterine transfusion 4.
- Perinatal survival rates following intrauterine transfusion range from 67% to 85%, and if fetal anemia is mild, invasive therapy is not recommended, and the pregnancy can be non-invasively monitored by serial ultrasound examination and MCV-PSV measurements 4.
- Intrauterine IVIG therapy has been described as an alternative treatment for fetal hydrops, and new virus-like-particle based parvovirus B19 vaccine candidates are being developed 4.