Pre-eclampsia part 2: prediction, prevention and management

Abstract

An antiangiogenic state might constitute a terminal pathway for the multiple aetiologies of pre-eclampsia, especially those resulting from placental abnormalities. The levels of angiogenic and antiangiogenic proteins in maternal blood change prior to a diagnosis of pre-eclampsia, correlate with disease severity and have prognostic value in identifying women who will develop maternal and/or perinatal complications. Potential interventions exist to ameliorate the imbalance of angiogenesis and, hence, might provide opportunities to improve maternal and/or perinatal outcomes in pre-eclampsia. Current strategies for managing pre-eclampsia consist of controlling hypertension, preventing seizures and timely delivery of the fetus. Prediction of pre-eclampsia in the first trimester is of great interest, as early administration of aspirin might reduce the risk of pre-eclampsia, albeit modestly. Combinations of biomarkers typically predict pre-eclampsia better than single biomarkers; however, the encouraging initial results of biomarker studies require external validation in other populations before they can be used to facilitate intervention in patients identified as at increased risk. Angiogenic and antiangiogenic factors might also be useful in triage of symptomatic patients with suspected pre-eclampsia, differentiating pre-eclampsia from exacerbations of pre-existing medical conditions and performing risk assessment in asymptomatic women. This Review article discusses the performance of predictive and prognostic biomarkers for pre-eclampsia, current strategies for preventing and managing the condition and its long-term consequences.

Conflict of interest statement

Disclosure

The authors report no conflicts of interest.

Figures

Figure 1. Uterine artery Doppler velocimetry findings in the second trimester of pregnancy

A. Normal findings. B. Abnormal findings, indicated by either the presence of bilateral uterine artery early diastolic notches (arrows) or a mean pulsatility index (calculated as [peak systolic velocity – end diastolic velocity]/time averaged velocity, averaged across both uterine arteries), above the 95th percentile for gestational age.

Figure 2. Management of pre-eclampsia

Management of pre-eclampsia depends on the severity of the disease (with or without severe features) and gestational age at diagnosis. For pre-eclampsia without severe features, delivery is recommended at term (≥37 weeks). For pre-eclampsia with severe features, delivery is recommended if gestational age is at ≥34 weeks. Before 34 weeks of gestation, the decision to deliver should be balanced between risk of maternal or fetal complications and benefit of continuing pregnancy to fetal maturity. *Patients with gestational hypertension or mild pre-eclampsia after 36 weeks who undergo induction of labour have a reduced rate of adverse maternal outcomes (especially the development of severe hypertension), lower incidence of caesarean delivery and a better quality of life than those who had expectant management.– If preterm induction of labour is contemplated, steroids are administered between 24 weeks and 34 weeks of gestation to improve fetal lung maturity. Magnesium sulfate is administered during labour and the first 24 h after delivery for seizure prophylaxis. Abbreviations: BUN, blood urea nitrogen; CBC, complete blood count; GA, gestational age; HELLP, haemolysis, elevated liver transaminases, low platelets; sCr, serum creatinine.