ABSTRACT
Case Report: Since the beginning of the Coronavirus Disease 2019 (COVID-19) pandemic, there has been much work to understand the negative effects of SARS-CoV-2 on tissues expressing the Angiotensin Converting Enzyme-2 (ACE2) receptor, including the placenta. However, there is limited information regarding placental pathology findings in mothers with COVID-19 and the effects of SARS-CoV-2 on the placenta. The available research reports effects on the fetus ranging from minimal to intrauterine fetal demise. Case Description: A 4680g baby boy was born at 38+1 weeks of gestation to 36y old G4P1021 female via repeat cesarian section. The pregnancy was complicated by advanced maternal age, chronic hypertension with superimposed pre-eclampsia with severe features, BMI of 80, and SARS-CoV-2 infection. The mother had mild COVID-19 symptoms and did not require hospitalization or oxygen support. Prenatal ultrasounds were limited due to body habitus. At the time of delivery, there was clear amniotic fluid. Upon delivery the infant was cyanotic and limp and was brought to the warmer immediately. Non-invasive positive pressure ventilation was initiated at 5 minutes of life with improvement in infant color and oxygen saturation. He was then admitted to the Neonatal Intensive Care Unit (NICU). APGARs were 2, 3, 5, and 7 at 1, 5, 10, and 15 minutes respectively. Cord gases showed severe metabolic acidosis. The patient was diagnosed with hypoxic-ischemic encephalopathy (HIE) and therapeutic hypothermia was initiated. Both the NICU and obstetric teams were unable to identify a clear perinatal cause of HIE in this patient. Later, the placenta pathology report revealed a large placenta for estimated gestational age corresponding to the 75th percentile, villous parenchyma with focal chorangiosis and thrombi, with unremarkable fetal membrane and three vessel umbilical cord. The cause of HIE was then thought to be due to the placental thrombi likely caused by SARS-CoV-2 infection. Discussion(s): Fetal vascular malperfusion and fetal vascular thrombus have been noted as a common finding in the placentas of pregnant women who test positive for SARS-CoV-2. There are various causes of HIE, from maternal, placental and fetal factors. This patient had no clinically evident hypoxic event, but information was limited due to the lack of monitoring of the fetus in utero. Given the mother's SARS-CoV-2 infection and the placental pathology findings, it is likely that the cause of this patient's HIE was related to the effects on the placenta from SARS-CoV-2. Conclusion(s): As more information comes to light about the effects of SARS-CoV-2 on the placenta, it is important to consider a maternal SARS-CoV-2 infection during pregnancy as a cause of HIE in a newborn.
ABSTRACT
Case Report History: Mother is a 23 year old gravida 4 para 1021, with a history of type 1 diabetes since 12 years of age. Prenatal sonogram at 20 weeks of gestation showed normal fetal anatomy with an EFW 21st percentile & 2-vessel cord. She was admitted at 23 weeks of gestation for acute hypoxic respiratory failure secondary to SARS-CoV-2 pneumonia, diabetic ketoacidosis & acute kidney failure. She refused intubation in spite of saturations in low 80s & was treated with high flow nasal cannula, non-rebreather mask, & nasal CPAP. She received convalescent plasma, Remdesivir, Tocilizumab, steroids, hydroxychloroquine, ceftriaxone & azithromycin, and was discharged home on oxygen after 29 days. Prenatal sonogram at 29 weeks of gestation demonstrated severe IUGR (abdominal & head circumference, fetal weight and femur length all < 3rd percentile), ventriculomegaly & a 2-vessel cord. Fetal MRI showed severe lateral ventriculomegaly of the brain, diffuse white matter parenchymal edema, bilateral germinal matrix & intraventricular hemorrhage & severe parenchymal volume loss. Mother was lost to follow up until time of delivery. Physical examination An infant female was born at 39 weeks of gestation via repeat cesarean-section. She was admitted to NICU for severe IUGR. The newborn's birth weight was 2126 g, head circumference 30 cm, length 43.5 cm (all <3rd percentile). Baby had mild hypertonia and tremors, rest of the exam was normal. The newborn was treated for TTN with NCPAP, hypoglycemia requiring IVF and hyperbilirubinemia requiring phototherapy and was extremely slow to feed. Diagnostic work-up CBC, BMP, LFT & CSF microscopy were normal, SARS-CoV-2 PCR was negative. SARS-CoV-2 IgM was negative in serum & CSF, but IgG was positive in serum & CSF. Baby's titers were slightly higher than mother's. US & MRI confirmed ventriculomegaly due to volume loss, a component of hydrocephalus was suspected due to presence of intraventricular hemorrhage, however there was no evidence of raised ICP. Retinal exam, hearing and BAER were normal. Chromosome analysis was normal & Zika titers were negative. The newborn was discharged home after 20 days with weighing 2580 g and head circumference of 32 cm. Placental was 222 g with <10% infarction and moderate acute chorioamnionitis. Infant has significant developmental delay at 1 year of age. Discussion There is definitive evidence of adverse neonatal outcomes in third trimester maternal SARS-CoV-2 infection, effects of earlier infections are not well reported. In our case the neurological injury can't be attributed definitively to fetal SARS-CoV-2 infection as IgM was negative, but the interval of 16 weeks between maternal infection and delivery need to be taken into account. Maternal illness likely contributed to severe acute on chronic fetal hypoxia which resulted in IUGR and in utero IVH with resultant CNS tissue loss and ventriculomegaly. (Figure Presented).