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# Preeclampsia and eclampsia

- Mechanism

A poorly built placenta releases factors that damage the mother's blood vessels; blood pressure rises and organs fail until the placenta is delivered.

Updated Nov 12, 2026

## Key points

- Normal pregnancy: invasive trophoblast replaces the muscle of the spiral arteries, turning them into wide, low-resistance channels.
- Preeclampsia: shallow invasion leaves narrow muscular arteries; the placenta is underperfused.
- The ischaemic placenta releases soluble Flt-1 (traps VEGF and PlGF) and soluble endoglin (blocks TGF-beta): endothelial dysfunction, less nitric oxide and prostacyclin, more endothelin and thromboxane.
- Clinical tests: a high sFlt-1 to PlGF ratio supports the diagnosis and predicts the course.
- Kidney: glomerular endotheliosis (swollen endothelium closing capillary lumens) with proteinuria.
- Liver: periportal fibrin, haemorrhage and necrosis, subcapsular haematoma; brain: oedema and haemorrhage (posterior reversible encephalopathy), seizures.

## What it is

Preeclampsia is a pregnancy syndrome of new hypertension after 20 weeks with proteinuria or other organ dysfunction; eclampsia adds seizures, and HELLP syndrome adds haemolysis, raised liver enzymes and low platelets. Its root is an abnormal placenta: the trophoblast fails to remodel the maternal spiral arteries, the placenta becomes ischaemic and releases antiangiogenic proteins, soluble Flt-1 and soluble endoglin, that block VEGF, PlGF and TGF-beta signalling. The result is widespread endothelial dysfunction, vasoconstriction, leaky vessels and clotting. Delivery of the placenta is the cure.

## Structure

- Placenta: small for gestational age; infarcts, retroplacental haematoma, distal villous hypoplasia, accelerated maturation and increased syncytial knots.
- Decidual arteries: fibrinoid necrosis with lipid-laden macrophages (acute atherosis) and no physiologic remodelling.
- Kidney: enlarged bloodless glomeruli with swollen endothelial cells and subendothelial fibrin.
- Liver: fibrin thrombi in periportal sinusoids with haemorrhagic necrosis.

## Step by step

- In early pregnancy, extravillous trophoblast fails to invade and remodel the spiral arteries.
- The arteries stay narrow and muscular; the placenta suffers ischaemia and oxidative stress.
- The stressed placenta releases soluble Flt-1 and soluble endoglin into the maternal blood.
- These factors neutralise VEGF, PlGF and TGF-beta, which keep the endothelium healthy.
- Systemic endothelial dysfunction causes vasoconstriction (hypertension), leaky capillaries (proteinuria, oedema) and platelet and coagulation activation.
- Organ damage follows: kidney, liver, brain, placenta; HELLP and DIC in severe cases.

## Clinical notes

- Risk factors: first pregnancy, previous preeclampsia, chronic hypertension, diabetes, kidney disease, obesity, antiphospholipid syndrome, multiple or molar pregnancy, older maternal age.
- Warning signs: severe headache, visual disturbance, epigastric or right upper quadrant pain, rising blood pressure; seizures mean eclampsia.
- Hypertensive disorders of pregnancy are a leading cause of maternal death in Colombia and Latin America; women with preeclampsia carry a higher lifelong cardiovascular risk.

## Memory aid

A shallow root makes a thirsty placenta, and the thirsty placenta poisons the mother's endothelium until it is delivered.

## Test yourself

Think of the answer, then tap the question to see it.

## What placental abnormality underlies preeclampsia?

Failure of trophoblast to remodel the spiral arteries, which stay narrow and muscular and leave the placenta ischaemic.

## How do soluble Flt-1 and soluble endoglin cause the maternal disease?

They trap VEGF and PlGF and block TGF-beta signalling, which the endothelium needs, producing systemic endothelial dysfunction.

## What is the typical kidney lesion of preeclampsia?

Glomerular endotheliosis: swollen endothelial cells occluding the capillary lumens, with proteinuria.

## What is HELLP syndrome?

A severe form with haemolysis, elevated liver enzymes and low platelets, from microangiopathy and periportal liver injury.

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## Elsewhere in DurgiPedia

- [Maternal physiological changes in pregnancy](https://durgical.com/en/physiology/maternal-physiological-changes-in-pregnancy/)
- [Placenta: structure, circulation and functions](https://durgical.com/en/embryology/placenta-structure-circulation-and-functions/)
- [The placenta and pregnancy hormones](https://durgical.com/en/physiology/the-placenta-and-pregnancy-hormones/)
- [Placenta](https://durgical.com/en/histology/placenta/)

## Connections

## Related 10

- [The placenta in late pregnancy](https://durgical.com/en/general-pathology/the-placenta-in-late-pregnancy/)
- [Placenta previa and placenta accreta spectrum](https://durgical.com/en/general-pathology/placenta-previa-and-placenta-accreta-spectrum/)
- [Hydatidiform mole: complete vs partial](https://durgical.com/en/general-pathology/hydatidiform-mole-complete-vs-partial/)
- [Liver disease in pregnancy](https://durgical.com/en/general-pathology/liver-disease-in-pregnancy/)
- [Thrombotic microangiopathy: the kidney](https://durgical.com/en/general-pathology/thrombotic-microangiopathy-the-kidney/)
- [Thrombotic microangiopathies: TTP vs HUS](https://durgical.com/en/general-pathology/thrombotic-microangiopathies-ttp-vs-hus/)
- [Tumour angiogenesis](https://durgical.com/en/general-pathology/tumour-angiogenesis/)
- [Edema and effusions: the four mechanisms](https://durgical.com/en/general-pathology/edema-and-effusions-the-four-mechanisms/)
- [Disseminated intravascular coagulation: how consumption causes both clots and bleeding](https://durgical.com/en/general-pathology/disseminated-intravascular-coagulation-how-consumption-causes-both-clots-and-ble/)
- [Infarction: red vs white, and what decides the damage](https://durgical.com/en/general-pathology/infarction-red-vs-white-and-what-decides-the-damage/)

## Related conditions 8

- [Preeclampsia](https://durgical.com/en/conditions/preeclampsia/)
- [Eclampsia](https://durgical.com/en/conditions/eclampsia/)
- [HELLP syndrome](https://durgical.com/en/conditions/hellp-syndrome/)
- [Fetal growth restriction](https://durgical.com/en/conditions/fetal-growth-restriction/)
- [Placental abruption](https://durgical.com/en/conditions/placental-abruption/)
- [Disseminated intravascular coagulation](https://durgical.com/en/conditions/disseminated-intravascular-coagulation/)
- [Arterial hypertension](https://durgical.com/en/conditions/arterial-hypertension/)
- [Stillbirth (intrauterine fetal death)](https://durgical.com/en/conditions/stillbirth/)

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: [Preeclampsia](https://www.ncbi.nlm.nih.gov/books/NBK570611/) (StatPearls (NCBI Bookshelf), 2026).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/general-pathology/preeclampsia-and-eclampsia/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/preeclampsia-and-eclampsia/
