Preeclampsia: Placental effects

Preeclampsia – presence of hypertension (sustained SBP ≥140 mmHg or DBP ≥90 mmHg while sitting) and proteinuria after the 20th week of gestation, present in 6-8% of pregnancies

• Pathogenesis
  • Normal trophoblastic cell invasion into spiral arteries, which occurs in the first 18 weeks of pregnancy, is incomplete or may not occur; decidual arteries are constricted with high resistance
  • Oxidative stress via increased sub-endothelial LDL accumulation which recruits monocytes that cause increased lipid peroxidation
  • Free radical and lipid peroxidases cause membrane damage, subsequent edema/proteinuria, inhibition of NO production, increased endothelin-1, increased thromboxane, and decreased prostacyclin
  • Acute atherosis via decreased prostacyclin, increased thromboxane, and endothelin-1 upsets the usual balance between these substances that leads to thrombosis and vasoconstriction of vessels in the placenta and systemically
    • Prostacyclin – decreases vasoconstriction, platelet aggregation, uterine activity, increases uteroplacental blood flow
    • NO – vasodilator, anti-aggregatory
    • Thromboxane – increases vasoconstriction, platelet aggregation, uterine activity, decreases uteroplacental blood flow
    • Endothelin-1 – potent vasoconstrictor and platelet activator
  • Plasma volume loss, hypoalbuminemia, and vasoconstriction lead to systemic hypovolemia and decreases in placental perfusion with a decrease in transplacental gas exchange
  • Antiangiogenic proteins lead to systemic endothelial damage especially in the kidney, liver and brain with associated oliguria, hypoalbuminemia, and eclamptic seizures