Abstract P3044: Second Trimester Severe Fetal Growth Restriction Preceding Preterm Severe Hypertensive Disorder in Pregnancy

Abstract

Background: Pregnancies complicated by hypertensive disorders are at risk of fetal growth restriction, abruption, and stillbirth. These complications are likely mediated through endothelial vascular disease of the placenta. Case: A 34 year old female G3P0111 with a history of HELLP syndrome was referred for severe fetal growth restriction at 23 weeks and 3 days. She was normotensive with normal fetal anatomic survey, low risk cell free DNA screen, negative antiphospholipid antibody panel and no evidence of TORCH infections. She returned to the clinic two weeks later with new onset hypertension, suboptimal interval fetal growth and oligohydramnios. She was admitted, and delivered at 25 weeks and 5 days for preeclampsia with severe features. Her female infant weighted 340 grams, and was intubated and admitted to the NICU. The NICU stay was complicated by respiratory distress syndrome, cholestasis, pancreatic insufficiency, dyschezia, growth failure, hydronephrosis, and vesicoureteral reflux. Today she is 12 months old and thriving. Placental pathology showed accelerated villous maturation suggestive of placenta underperfusion, consistent with clinical history of preeclampsia. Discussion: Preeclampsia is a complication of pregnancy typically characterized by elevated blood pressure and damage of other organs, most commonly the liver or kidney. While the exact mechanisms that cause preeclampsia are not known, the resultant endothelial vascular disease affecting the placenta can lead to fetal growth restriction or abruption. Second trimester fetal growth restriction can result from fetal aneuploidy, viral infections, or maternal conditions that lead to uteroplacental insufficiency such as chronic hypertension or pre-gestational diabetes. Few cases describe fetal growth restriction preceding the onset of preeclampsia, although this is not uncommon in clinical practice. Conclusion: Pregnancies complicated by severe, preterm fetal growth restriction preceding the development of hypertensive disorder appear to have a common etiologic pathway, and the absence of hypertension does not exclude the possibility of underlying preeclampsia. Increased vigilance for signs and symptoms of preeclampsia in these pregnancies is warranted.