A 24-year-old woman, gravida 2 para 0 aborta 1, at 26 weeks gestation comes to the office for an initial prenatal visit. Prior to this, the patient's only prenatal care was a visit to the emergency department due to 2 days of persistent vomiting. At that time, a first trimester ultrasound was performed and was consistent with gestational age. Her previous pregnancy was a spontaneous abortion at 8 weeks gestation. Blood pressure is 120/70 mm Hg and pulse is 72/min. Fundal height is 32 cm. Maternal blood type is O, Rh negative. Indirect Coombs test is negative. Transabdominal ultrasound shows a female fetus with a biparietal diameter and head circumference that are consistent with 26 weeks gestation. Abdominal circumference measures at 34 weeks gestation. Fetal heart rate is 180/min. A pericardial effusion, bilateral pleural effusions, and polyhydramnios are noted in the fetus. Which of the following factors most likely contributed to this fetal presentation?
Fetal hydrops | |
Pathogenesis |
|
Clinical features |
|
Etiology |
|
This patient's fetus has fetal hydrops (hydrops fetalis), an excessive fluid accumulation in the interstitium (eg, pericardial and pleural effusions) that is due to high-output heart failure from either immune or nonimmune etiologies. Rh(D) alloimmunization is the most common etiology of immune fetal hydrops; in contrast, maternal parvovirus B19 infection causes nonimmune fetal hydrops and is likely the reason for this patient's presentation.
Parvovirus B19 infection in adults can be asymptomatic (or associated with nonspecific flulike symptoms or arthralgias); however, in children, it typically presents with a slapped-cheek rash that follows nonspecific prodromal symptoms (corresponding with viremia). The virus is transmitted via respiratory droplets. Pregnant women should avoid infected individuals because the virus can cross the placenta and have devastating fetal consequences.
Parvovirus B19 is highly cytotoxic to fetal red blood cell precursors, which can cause severe fetal anemia and result in increased cardiac output demand (as evidenced by fetal tachycardia with a fetal heart rate >160/min). When cardiac output can no longer compensate for worsening fetal anemia and hypoxemia, fetuses develop high-output heart failure and its sequalae: effusions, ascites (eg, enlarged abdominal circumference), and polyhydramnios. Fetal hydrops has a high risk of fetal demise, and affected patients require serial ultrasounds and possible intrauterine transfusion.
(Choice B) Inadequate maternal folate supplementation increases the risk for fetal neural tube defects (eg, spina bifida, meningocele). It does not cause fetal hydrops.
(Choice C) Lack of anti-D immune globulin after delivery of an Rh(D)-positive infant can lead to Rh(D) alloimmunization in Rh(D)-negative mothers. In future pregnancies, maternal anti-D antibodies attack Rh(D)-positive fetal erythrocytes, causing immune fetal hydrops. Although this patient is Rh(D)-negative, her antibody screen is negative, making this diagnosis unlikely.
(Choice D) Maternal rubella vaccination prevents congenital rubella syndrome, which is associated with fetal growth restriction and possible microcephaly. It does not present as fetal hydrops.
(Choice E) Travel to tropical, mosquito-infested regions increases the risk of maternal Zika virus infection, which crosses the placenta and impairs fetal brain development. Affected fetuses may have microcephaly, ventriculomegaly, or intracranial calcifications on ultrasound. This patient's fetal biparietal diameter and head circumference are normal.
Educational objective:
Parvovirus B19 infection in pregnancy can cause nonimmune fetal hydrops, or excessive fluid accumulation in the interstitium (eg, pericardial or pleural effusions, ascites). Parvovirus B19 infection may be asymptomatic in adults but is commonly acquired by respiratory transmission from young children, who typically have a slapped-cheek facial rash that follows nonspecific prodromal symptoms.