Pre-eclampsia is a pregnancy-specific multisystem disorder characterised by new-onset hypertension after 20 weeks of pregnancy together with proteinuria and/or evidence of maternal organ dysfunction or uteroplacental dysfunction. It is not simply high blood pressure in pregnancy. The disorder can affect the kidneys, liver, brain, blood, cardiovascular system and placenta, and it can occur with or without substantial proteinuria. Pre-eclampsia may develop during pregnancy, during labour or after delivery, meaning that postpartum vigilance remains important.
Its underlying biology is complex and involves abnormal placental development, impaired maternal adaptation to pregnancy, endothelial dysfunction, inflammatory pathways and altered regulation of blood vessels. Severe disease can threaten both mother and fetus, while milder disease may remain stable for a period with careful monitoring. Because the condition can progress unpredictably, diagnosis is based on blood pressure, symptoms, laboratory findings and fetal assessment rather than blood pressure alone.
The placenta plays a central role in the development of Pre-eclampsia. In a normal pregnancy, placental trophoblasts remodel maternal spiral arteries so that they become wider, lower-resistance vessels capable of delivering substantial blood flow to the placenta. In pre-eclampsia, this remodelling can be incomplete or abnormal. The placenta may consequently experience relative hypoperfusion and oxidative or cellular stress, promoting release of factors into the maternal circulation that disturb endothelial function.
Antiangiogenic factors such as soluble fms-like tyrosine kinase-1 and soluble endoglin have been implicated in the pathophysiology because they interfere with signalling required for healthy vascular adaptation. The resulting endothelial dysfunction contributes to hypertension, altered kidney filtration, leakage of protein into urine, fluid shifts and abnormalities in other organs. This mechanism helps explain why Pre-eclampsia is a systemic disease rather than an isolated disorder of blood pressure.
Risk is higher in first pregnancies, multiple pregnancy, previous Pre-eclampsia, chronic hypertension, chronic kidney disease, diabetes, autoimmune conditions and certain thrombophilic or placental circumstances. Maternal age and family history can also influence risk. Prevention strategies may include low-dose aspirin for people identified as being at sufficiently high risk, but aspirin is prescribed according to specific clinical criteria and should not be started solely on the basis of general pregnancy concerns.
Calcium supplementation may be relevant in populations with low dietary calcium intake. Risk assessment at the beginning of pregnancy and again as pregnancy progresses helps determine whether enhanced surveillance is appropriate. No risk-factor checklist can predict every case because Pre-eclampsia can occur in people without obvious risk factors. The distinction between risk reduction and guaranteed prevention is therefore important.
Symptoms of Pre-eclampsia can include severe headache, visual disturbances, upper abdominal or epigastric pain, nausea or vomiting later in pregnancy, sudden swelling and feeling markedly unwell, although some people have no symptoms and are diagnosed through routine antenatal blood-pressure and urine assessment. Severe hypertension increases the risk of stroke and other acute complications. Blood tests can assess platelet count, liver enzymes and kidney function, while urine testing evaluates protein loss.
Fetal assessment can include ultrasound growth measurement, amniotic-fluid assessment and Doppler studies where indicated. Clinicians may also use placental biomarkers or angiogenic-factor testing in selected settings to help assess the likelihood of disease or its short-term development. These tests complement rather than replace clinical assessment. The condition can change rapidly, so a normal result at one assessment does not guarantee that complications cannot develop later.
Management depends on gestational age, maternal symptoms and organ function, blood-pressure severity, fetal growth and wellbeing, and the balance between risks of continuing pregnancy and risks of premature birth. Antihypertensive medication may be used to control maternal blood pressure and reduce the risk of severe hypertension. Commonly used agents include labetalol, nifedipine and methyldopa, although selection depends on clinical circumstances and local practice.
Corticosteroids may be administered when preterm birth is likely to improve fetal maturation, and magnesium sulfate may be used in selected situations to reduce the risk of seizures. Definitive resolution of Pre-eclampsia requires delivery of the placenta, so treatment can control complications but does not permanently cure the underlying placental disorder while the placenta remains in place. Some cases can therefore be monitored until a safer gestational age is reached, whereas severe disease may require earlier delivery.
Maternal complications can include eclampsia, stroke, pulmonary oedema, kidney injury, liver injury, low platelet count and placental abruption. A severe variant associated with haemolysis, elevated liver enzymes and low platelet count is commonly called HELLP syndrome. Fetal complications arise largely from placental dysfunction and can include fetal growth restriction, reduced amniotic fluid, abnormal blood-flow patterns and stillbirth. Pre-eclampsia is also an important cause of medically indicated premature birth because continuing pregnancy may become more dangerous than delivery.
The condition can occur after birth, known as postpartum Pre-eclampsia, and therefore severe headache, visual disturbance, breathlessness, chest pain or other concerning symptoms after delivery warrant urgent assessment. Long-term, people who have had Pre-eclampsia have increased risk of hypertension and cardiovascular and cerebrovascular disease later in life, making postpartum health assessment clinically important.
Pre-eclampsia is distinct from gestational hypertension. Gestational hypertension involves new hypertension after 20 weeks without the additional diagnostic features that define Pre-eclampsia, although it can subsequently progress to Pre-eclampsia. Chronic hypertension is present before pregnancy or develops early enough to suggest pre-existing disease, while chronic hypertension with new organ dysfunction later in pregnancy may represent superimposed Pre-eclampsia. These distinctions matter because prognosis, monitoring and treatment differ.
Blood pressure alone does not measure the full severity of Pre-eclampsia; someone with moderately elevated blood pressure can have significant organ involvement, while severe hypertension requires urgent treatment even if other findings are initially limited. Pre-eclampsia is therefore best understood as a syndrome reflecting abnormal placental and maternal vascular interaction rather than a single numerical threshold.
The history of Pre-eclampsia is closely connected with the development of modern antenatal surveillance. Regular blood-pressure measurement and urine assessment made it possible to detect disease before severe symptoms developed, while advances in fetal ultrasound, laboratory testing and antihypertensive therapy have improved management. Contemporary research focuses on placental biology, angiogenic biomarkers, prediction models and strategies for identifying disease earlier. Despite substantial progress, delivery remains the definitive treatment because the placenta is central to the disease process.
Clinical decisions therefore require balancing maternal safety against fetal maturity. A pregnancy affected by Pre-eclampsia may be prolonged safely under close monitoring in some circumstances, whereas rapid deterioration can necessitate urgent delivery. The condition consequently represents a major example of how maternal and fetal medicine must treat two interconnected patients whose risks can change in opposite directions as gestation advances.
