UNDERSTANDING THE PLACENTAL AETIOLOGY OF FETAL GROWTH RESTRICTION; COULD THIS LEAD TO PERSONALIZED MANAGEMENT STRATEGIES?

Abstract

Fetal growth restriction (FGR) is defined as the failure of a fetus to attain its full genetic growth potential. It is a leading cause of stillbirth, prematurity, cerebral palsy and perinatal mortality. Small size at birth increases surviving infants’ lifelong risk of adverse health outcomes associated with the metabolic syndrome. The pathophysiology of abnormal fetal growth is extremely complex and incompletely understood, with a plethora of genetic, signalling and metabolic candidates under investigation, many of which may result in abnormal structure and function of the placenta. In contrast to, or maybe because of, the underlying complexities of FGR, the strategies clinicians have for identifying and managing this outcome are conspicuously limited. Current clinical practice is restricted to identifying pregnancies at risk of FGR, and when FGR is detected, using intensive monitoring to guide the timing of delivery to optimise fetal outcomes. Abnormal Doppler indices in the umbilical artery are strongly associated with poor perinatal outcomes and are currently the “gold standard” for clinical surveillance of the growth-restricted fetus.