Location
Moultrie, GA
Start Date
17-4-2026 12:00 PM
End Date
17-4-2026 1:00 PM
Description
Introduction
Hydrops fetalis is defined as pathologic fluid accumulation in at least two fetal compartments and is associated with high perinatal morbidity and mortality. Most cases are non-immune in origin and result from cardiovascular, infectious, hematologic, genetic, thoracic, or placental etiologies due to widespread Rh immunoprophylaxis. Third-trimester hydrops is commonly associated with cardiac dysfunction and impaired venous return. We present a case of severe hydrops fetalis in a 33-week preterm neonate with confirmed maternal parvovirus infection complicated by intrauterine growth restriction (IUGR), pulmonary hypertension, placental insufficiency, and multiorgan dysfunction.
Methods
This case report describes a retrospective review of maternal prenatal history, delivery records, neonatal resuscitation, and neonatal intensive care unit course at a transfer facility. Maternal laboratory data, prenatal imaging and Doppler studies, neonatal laboratory results, imaging, and response to therapeutic interventions were analyzed to evaluate the likely etiology of hydrops and associated complications.
Results
Prenatal care began at approximately 18 weeks gestation. Aneuploidy screening was negative. Maternal blood type was A positive with a negative antibody screen. Serologies were notable for reactive rapid plasma reagin treated appropriately with penicillin prior to delivery. Maternal testing was positive for parvovirus B19 prior to transfer for higher-level care. HIV and hepatitis screening were negative. The pregnancy was complicated by progressive severe IUGR with abnormal Doppler studies, oligohydramnios, and reversed end-diastolic flow, consistent with significant placental insufficiency.
At 33 weeks gestation, emergent cesarean delivery was performed for fetal decelerations and maternal hypertension. The neonate required extensive resuscitation, including positive pressure ventilation, chest compressions, intubation, and surfactant administration. Persistent hypoxemia and hypoglycemia were noted immediately after birth, and the infant was transferred to a tertiary NICU for escalating care.
Postnatal course was significant for generalized edema, ascites on ultrasound, right ventricular dilation with pulmonary hypertension on echocardiography, hypotension requiring vasoactive support, metabolic acidosis, recurrent hypoglycemia, thrombocytopenia, coagulopathy, and acute kidney injury with oliguria. Repeat echocardiography demonstrated bidirectional shunting through a patent ductus arteriosus and foramen ovale with right-sided pressure overload. Immune-mediated hydrops was excluded by negative maternal antibody screening, and blood cultures remained negative. Despite aggressive management, including mechanical ventilation, inhaled nitric oxide, inotropic support, antimicrobial therapy, and blood transfusions, the neonate developed persistent multiorgan dysfunction consistent with severe non-immune hydrops.
Discussion
Non-immune hydrops fetalis has a broad differential, including cardiac disease, fetal arrhythmias, hematologic disorders causing anemia, chromosomal abnormalities, thoracic malformations, metabolic conditions, placental insufficiency, and infections such as parvovirus B19. Parvovirus suppresses fetal erythroid progenitor cells, leading to anemia, high-output cardiac failure, and fluid accumulation.
In this case, confirmed maternal parvovirus infection supports an infectious contribution to fetal anemia and cardiac dysfunction. Concurrent severe placental insufficiency, evidenced by progressive IUGR, oligohydramnios, and reversed end-diastolic flow, likely exacerbated fetal hypoxia and myocardial strain. The coexistence of parvovirus-related anemia and placental dysfunction likely created a synergistic effect, contributing to pulmonary hypertension, metabolic acidosis, and multiorgan compromise. This case underscores the importance of maintaining a broad differential and recognizing multifactorial contributors in the evaluation of hydrops fetalis.
Embargo Period
5-28-2026
Included in
Hydrops Fetalis in a 33-Week Preterm Neonate: A Case Report
Moultrie, GA
Introduction
Hydrops fetalis is defined as pathologic fluid accumulation in at least two fetal compartments and is associated with high perinatal morbidity and mortality. Most cases are non-immune in origin and result from cardiovascular, infectious, hematologic, genetic, thoracic, or placental etiologies due to widespread Rh immunoprophylaxis. Third-trimester hydrops is commonly associated with cardiac dysfunction and impaired venous return. We present a case of severe hydrops fetalis in a 33-week preterm neonate with confirmed maternal parvovirus infection complicated by intrauterine growth restriction (IUGR), pulmonary hypertension, placental insufficiency, and multiorgan dysfunction.
Methods
This case report describes a retrospective review of maternal prenatal history, delivery records, neonatal resuscitation, and neonatal intensive care unit course at a transfer facility. Maternal laboratory data, prenatal imaging and Doppler studies, neonatal laboratory results, imaging, and response to therapeutic interventions were analyzed to evaluate the likely etiology of hydrops and associated complications.
Results
Prenatal care began at approximately 18 weeks gestation. Aneuploidy screening was negative. Maternal blood type was A positive with a negative antibody screen. Serologies were notable for reactive rapid plasma reagin treated appropriately with penicillin prior to delivery. Maternal testing was positive for parvovirus B19 prior to transfer for higher-level care. HIV and hepatitis screening were negative. The pregnancy was complicated by progressive severe IUGR with abnormal Doppler studies, oligohydramnios, and reversed end-diastolic flow, consistent with significant placental insufficiency.
At 33 weeks gestation, emergent cesarean delivery was performed for fetal decelerations and maternal hypertension. The neonate required extensive resuscitation, including positive pressure ventilation, chest compressions, intubation, and surfactant administration. Persistent hypoxemia and hypoglycemia were noted immediately after birth, and the infant was transferred to a tertiary NICU for escalating care.
Postnatal course was significant for generalized edema, ascites on ultrasound, right ventricular dilation with pulmonary hypertension on echocardiography, hypotension requiring vasoactive support, metabolic acidosis, recurrent hypoglycemia, thrombocytopenia, coagulopathy, and acute kidney injury with oliguria. Repeat echocardiography demonstrated bidirectional shunting through a patent ductus arteriosus and foramen ovale with right-sided pressure overload. Immune-mediated hydrops was excluded by negative maternal antibody screening, and blood cultures remained negative. Despite aggressive management, including mechanical ventilation, inhaled nitric oxide, inotropic support, antimicrobial therapy, and blood transfusions, the neonate developed persistent multiorgan dysfunction consistent with severe non-immune hydrops.
Discussion
Non-immune hydrops fetalis has a broad differential, including cardiac disease, fetal arrhythmias, hematologic disorders causing anemia, chromosomal abnormalities, thoracic malformations, metabolic conditions, placental insufficiency, and infections such as parvovirus B19. Parvovirus suppresses fetal erythroid progenitor cells, leading to anemia, high-output cardiac failure, and fluid accumulation.
In this case, confirmed maternal parvovirus infection supports an infectious contribution to fetal anemia and cardiac dysfunction. Concurrent severe placental insufficiency, evidenced by progressive IUGR, oligohydramnios, and reversed end-diastolic flow, likely exacerbated fetal hypoxia and myocardial strain. The coexistence of parvovirus-related anemia and placental dysfunction likely created a synergistic effect, contributing to pulmonary hypertension, metabolic acidosis, and multiorgan compromise. This case underscores the importance of maintaining a broad differential and recognizing multifactorial contributors in the evaluation of hydrops fetalis.