high-output fetal heart failure characterized by excessive fluid accumulation in interstitial spaces.
| Pathogenesis | • ↑ cardiac output demand causing heart failure • ↑ fluid movement into interstitial spaces (third spacing) | | --- | --- | | Clinical features | • Pericardial effusion • Pleural effusion • Ascites • Skin edema • Placental edema and thickening (reflecting intravillous edema) • Polyhydramnios | | Etiology | • Immune ◦ Rh(D) alloimmunization • Non-immune ◦ Parvovirus B19 infection(MCC) ◦ Fetal aneuploidy ◦ Cardiovascular abnormalities ◦ Thalassemia (eg, hemoglobin Barts) |
Fetuses with hydrops fetalis are at high risk for fetal demise, this risk increases with infection acquired at earlier gestational ages.
Due to this risk, patients with fetal hydrops undergo serial ultrasounds and possible early delivery.
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.
Both fetal aneuploidy (eg, trisomy 18) and fetal alcohol spectrum disorder (ie, chronic maternal alcohol use) can have associated congenital cardiac defects (eg, atrioventricular septal defect) that can lead to heart failure and hydrops fetalis. However, these fetuses are typically growth-restricted and have limb abnormalities (eg, shortened long bones, clubfoot) or dysmorphic facial features (eg, hypoplastic midface, flattened nasal bridge). Parvovirus B19 infection is not associated with bony or facial dysmorphic features.
Rh(D) alloimmunization occurs when Rh(D)-negative mothers develop anti-D antibodies from delivering an Rh(D)-positive infant. In subsequent pregnancies, existing maternal anti-D antibodies attack Rh(D)-positive fetal erythrocytes, causing severe anemia and fetal hydrops. Although this patient is Rh(D)-negative, her antibody screen is negative, making this diagnosis unlikely.
(Choice A) Achondroplasia can present with hydrops fetalis, but affected fetuses typically have macrocephaly and shortened long bones on prenatal ultrasound.
(Choice E) Turner syndrome (45, X) can present with nuchal thickening, cystic hygroma (fluid-filled lymphatic sac), and hydrops fetalis.