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INTRODUCTION

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Pre-eclampsia and eclampsia are hypertensive disorders of pregnancy associated with maternal mortality and fetal complications. Pre-eclampsia is defined as new onset of maternal hypertension after 20 weeks gestation and proteinuria. The term eclampsia is used when the central nervous system (CNS) is involved, which surfaces as new onset of seizures in the setting of pre-eclampsia. Pre-eclampsia occurs in 3%–4% of pregnancies with an increasing incidence in the United States. Women with chronic conditions associated with endothelial dysfunction (chronic hypertension, diabetes mellitus, and renal disease) are at an increased risk for developing pre-eclampsia during pregnancy. Advanced maternal age, nulliparity, obesity, and African American race are also considered to be risk factors.

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PRE-ECLAMPSIA

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Pathogenesis

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Although the initiating pathogenic mechanism is unknown, abnormal placentation is the focus of the current two-stage hypothesis. This widely accepted hypothesis is supported by studies that show increased levels of biomarkers (e.g., endothelin-1, fibronectin, von Willebrand factor, and thrombomodulin) indicating endothelial activation or endothelial injury in women with pre-eclampsia.

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  • Stage One—The asymptomatic first stage occurs early in pregnancy when the spiral arteries that supply the placenta undergo remodeling. The embryo-derived cytotrophoblasts fail to invade the myometrial layer of the uterus and only the spiral arteries within the decidual segments remodel. This results in small constricted spiral arteries within the myometrium that may cause hypoperfusion of the placenta and placental ischemia.

  • Stage Two—Pregnancies with abnormal placentation do not always progress to the second symptomatic stage of pre-eclampsia. However, when placental ischemia results in release of antiangiogenic factors into maternal circulation, it can trigger a systemic inflammatory response leading to widespread endothelial dysfunction.

  • Maternal Systemic Disease—Maternal systemic disease from pre-eclampsia is a result of the endothelium to losing its ability to properly respond to vasopressors, regulate fluid balance, and prevent platelet activation. Placental dysfunction and ischemia lead to release of antiangiogenic factors like soluble fms-like tyrosine kinase (sFLT-1) and soluble endoglin (sEng). Studies have demonstrated that an increase in sFLT-1 levels during a pre-eclamptic pregnancy reduces circulating levels vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) which are required for normal vascular endothelial function. This widespread vascular endothelial dysfunction results in maternal hypertension, glomerular dysfunction leading to proteinuria, brain edema, liver edema, and coagulopathies.

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Prophylaxis

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The American College of Obstetrics and Gynecology (ACOG) currently recommends low-dose aspirin beginning late in the first semester for certain women at high risk of developing pre-eclampsia. Specifically, those who have a past history of developing pre-eclampsia prior to 34 weeks gestation, or those who have had pre-eclampsia in one or more prior pregnancies. Calcium supplementation and antioxidant supplementation have not been shown to prevent or benefit pre-eclampsia.

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Clinical Presentation

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Pre-eclampsia most commonly presents near term in pregnancy during the third trimester. Women who have onset earlier than 34 weeks gestation often have severe ...

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