Preeclampsia and Hypertensive Disorders

The hypertensive disorders of pregnancy are a spectrum of conditions defined by elevated blood pressure arising in pregnancy. Preeclampsia, the most clinically important of these, is a multisystem disorder characterized by new-onset hypertension after 20 weeks' gestation accompanied by proteinuria or other signs of maternal organ dysfunction, and it remains a leading cause of maternal and perinatal morbidity worldwide.

Definition

Preeclampsia is a pregnancy-specific multisystem disorder defined by new-onset hypertension after 20 weeks of gestation together with proteinuria or evidence of maternal end-organ dysfunction; the broader category of hypertensive disorders of pregnancy also includes chronic hypertension, gestational hypertension, and eclampsia (preeclampsia with seizures).

Scope

This entry covers the classification of hypertensive disorders of pregnancy (chronic hypertension, gestational hypertension, preeclampsia, eclampsia, and preeclampsia superimposed on chronic hypertension), the placental and endothelial mechanisms thought to underlie preeclampsia, and the warning features that make these disorders central to antenatal surveillance. It is a reference and educational overview and does not provide blood-pressure thresholds for treatment or any individualized management plan.

Core questions

• How are the hypertensive disorders of pregnancy classified?
• What distinguishes preeclampsia from gestational and chronic hypertension?
• What placental and endothelial mechanisms are thought to drive preeclampsia?
• Why does delivery of the placenta remain central to the resolution of preeclampsia?

Key concepts

• Hypertensive disorders of pregnancy spectrum
• New-onset hypertension after 20 weeks
• Proteinuria and end-organ dysfunction
• Abnormal placentation
• Endothelial dysfunction
• Eclampsia
• HELLP syndrome
• Angiogenic imbalance (sFlt-1/PlGF)

Key theories

Two-stage model of preeclampsia

Preeclampsia is conceptualized as a two-stage disorder in which abnormal placentation and reduced uteroplacental perfusion (stage one) lead to release of factors that cause the systemic maternal endothelial dysfunction and clinical syndrome (stage two).

Mechanisms

Preeclampsia is widely understood through a two-stage model. In the first stage, impaired remodeling of the spiral arteries produces inadequate placental perfusion; the resulting placental stress releases anti-angiogenic and inflammatory factors into the maternal circulation. In the second stage these factors, including an imbalance between soluble fms-like tyrosine kinase-1 (sFlt-1) and placental growth factor (PlGF), drive widespread maternal endothelial dysfunction that manifests as hypertension, proteinuria, and multiorgan involvement (Redman & Sargent, 2005; Chappell, 2021). Because the placenta is the source of the disorder, its delivery is the definitive event that allows resolution (Mol, 2016).

Clinical relevance

Hypertensive disorders of pregnancy are among the conditions most closely monitored in antenatal care, and recognizing their warning features, such as rising blood pressure, proteinuria, severe headache, visual disturbance, and right-upper-quadrant pain, is part of maternal surveillance. This entry describes how the disorders are defined and why they matter; it is not a guide to diagnosing or treating any individual patient, and clinical decisions rest with the responsible clinician following current guidelines.

Epidemiology

Preeclampsia complicates roughly 2-8% of pregnancies worldwide and, together with eclampsia, is a leading direct cause of maternal death, particularly in low- and middle-income settings (Mol, 2016; Say, see area entry). Risk is increased by nulliparity, prior preeclampsia, chronic hypertension, pre-existing diabetes, obesity, multiple gestation, and extremes of maternal age.

Evidence & guidelines

The American College of Obstetricians and Gynecologists Practice Bulletin No. 222 sets out current definitions and classification of gestational hypertension and preeclampsia (ACOG, 2020). Major narrative syntheses in The Lancet (Mol, 2016; Chappell, 2021) summarize pathophysiology, prediction, and outcomes, and the Science review by Redman and Sargent (2005) articulates the endothelial-dysfunction framework.

History

Eclampsia (from the Greek for a sudden flash) was described in antiquity as convulsions in pregnancy, and the link to hypertension and proteinuria was established with the advent of blood-pressure measurement and urinalysis in the late nineteenth and early twentieth centuries. The modern understanding shifted decisively toward a placental and endothelial model in the late twentieth century, crystallized in the two-stage framework summarized by Redman and Sargent (2005), and was extended by the discovery of angiogenic-factor imbalance as a measurable correlate of disease (Chappell, 2021).

Debates

How should preeclampsia be defined when proteinuria is absent?

Definitions have evolved to allow diagnosis of preeclampsia in the presence of new-onset hypertension with maternal end-organ dysfunction even without proteinuria, broadening the syndrome beyond its classical proteinuric form.

Key figures

• Christopher Redman
• Ian Sargent

Seminal works

• redman-sargent-2005
• mol-2016
• chappell-2021

Frequently asked questions

What is the difference between gestational hypertension and preeclampsia?

Gestational hypertension is new-onset high blood pressure after 20 weeks without proteinuria or other organ involvement, whereas preeclampsia adds proteinuria or signs of maternal end-organ dysfunction; gestational hypertension can progress to preeclampsia.

Why is delivery considered the definitive resolution of preeclampsia?

Because the placenta is the source of the factors that drive the disorder, delivering the placenta removes that source and allows the maternal syndrome to resolve, which is why preeclampsia is described as a placental disease (Mol, 2016).