COVID-19 in Pregnancy: Maternal, Placental and Fetal Implications

SARS-CoV-2 infection in pregnancy is associated with increased risk for severe COVID-19 disease including ICU admission, need for invasive ventilation, extracorporeal membrane oxygenation, and death. In addition, COVID-19 in pregnancy is associated with adverse pregnancy and neonatal outcomes. This presentation will review: (1) what is known about increased maternal and obstetric risk in the setting of SARS-CoV-2 infection;(2) how underlying comorbidities and viral strain may impact disease severity;(3) impact of COVID-19 in pregnancy on the placenta and how this may be altered by fetal sex and viral strain;(4) fetal risk and protection including vertical transmission, antibody-mediated protection, and later-life neurodevelopmental or metabolic risk in the setting of maternal immune activation.

Inter-Rater Reliability and Agreement of Fetal Echocardiography Measurements Among Investigators From Multiple Sites

Background: Single institutions specialising in fetal cardiology often have too few cases to develop robust prognostic indicators for specific conditions. The Australia and New Zealand (ANZ) Fetal Cardiology Working Group instigated a multicentre study to examine fetal risk factors for early postnatal intervention in Tetralogy of Fallot (ToF). Centralised data analysis was not possible due to COVID-19 travel restrictions and ethical constraints related to sharing of retrospectively acquired images. A study of inter-observer agreement of standardised in utero cardiac measurements was undertaken to assess the feasibility of combining data from multiple centres. Methods: Ten fetuses with ToF were randomly identified. Deidentified images were distributed securely to ten ANZ fetal cardiologists. The pulmonary valve (PV) annulus, main pulmonary artery (MPA), branch pulmonary arteries (BPA), aortic valve (AV) annulus, ascending aorta (AA), and ductus arteriosus (DA) were measured in triplicate following a defined protocol. Inter-rater reliability was assessed using a two-way random effects model to calculate the intra-class coefficient (ICC). Results: Measurements were available for seven ANZ fetal cardiologists. There was moderate inter-observer agreement for PV (ICC 0.74, 95% CI 0.49–0.91) and AV (0.71, 95% CI 0.48–0.90), and good agreement for MPA (0.81, 95% CI 0.62–0.94) and AA (0.91, 95% CI 0.80–0.97). Inadequate data were available for BPA and DA analysis. Multi-variate analysis found no patient or investigator factors that influenced measurement variability. Conclusion: Fetal cardiac structures can be measured using a defined measurement protocol by multiple investigators with at least moderate agreement. Analysis of large datasets by multiple investigators is a reasonable alternative to centralised data analysis.

PREGNANCY, VALVULAR DISEASE, AND ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS): A COLLABORATIVE APPROACH TO OUTCOMPETING COMPETING HEMODYNAMIC DEMANDS

Background: A 35-year-old G1P1 woman with a history of bioprosthetic mitral valve (MVR) and aortic valve (AVR) replacements and a tricuspid valve annuloplasty for presumed rheumatic heart disease who presented at 35 weeks gestational age with COVID-19 ARDS and shock. Case: The patient arrived with ARDS requiring intubation and distributive shock. Transthoracic echocardiogram (TTE) revealed a small left ventricular (LV) cavity with LV hypertrophy, MVR with mean gradient of 14 mmHg, and a mid-peaking transaortic gradient of 96 mmHg consistent with fixed obstruction. This gradient was likely due to LV outflow tract obstruction (LVOTO) from the combination of a small LV cavity and septal angulation of the MVR struts rather than AVR dysfunction. The patient underwent emergent cesarean section. Decision-making: The maternal and fetal risks of ARDS and distributive shock were primary considerations in undergoing cesarean section. Decisions regarding management thereafter were driven by three elements of her clinical presentation - anticipated peripartum hemodynamic shifts, multivalvular disease, and ARDS. The increased plasma volume from postpartum autotransfusion risked worsening her ARDS but also potentially benefited the LVOTO through increased preload. The effect of lower postpartum cardiac output and heart rate on valvular obstruction in series also had to be considered. To balance these hemodynamic demands, after delivery, her vasopressors were switched from norepinephrine to phenylephrine, and she was judiciously diuresed. A postpartum TTE demonstrated improved transmitral gradients (mean 5 mmHg) but ongoing LVOTO. Higher filling pressures than otherwise ideal in ARDS were tolerated given persistent gradients. She was liberated from hemodynamic and ventilator support and transferred out of ICU care. Though she died of infectious complications weeks later, close collaboration between the critical care, obstetrical, and cardiovascular teams were essential to her care. Conclusion: Care of the peripartum patient with cardiovascular disease, especially valvular disease, must take into consideration both their cardiac pathology and expected peripartum hemodynamic shifts.