One. Preeclampsia
One. Preeclampsia
Preeclampsia begins with abnormal development of the placenta during early pregnancy. Normally, the spiral arteries of the uterus widen to provide enough blood supply to the placenta. In preeclampsia, these arteries remain narrow, causing decreased placental perfusion and placental ischemia. Because the placenta is deprived of oxygen, it releases inflammatory substances into the maternal circulation that damage the endothelial lining of blood vessels.
Endothelial injury causes generalized vasospasm and increased vascular permeability. Vasospasm increases systemic vascular resistance, leading to hypertension. Increased permeability allows plasma proteins and fluid to leak into tissues, causing edema. Damage to kidney glomeruli decreases filtration and allows protein to leak into urine, resulting in proteinuria. Reduced blood flow to organs can also affect the liver, brain, and placenta, causing complications such as headache, visual disturbances, elevated liver enzymes, and fetal growth restriction.
Two. Eclampsia
Two. Eclampsia
Eclampsia is the progression of severe preeclampsia in which cerebral involvement leads to seizures. Severe vasospasm and endothelial damage decrease blood flow to the brain and increase capillary permeability. This results in cerebral edema, ischemia, and irritation of brain tissue.
As cerebral edema worsens, neurons become unstable and excessively excitable, triggering generalized tonic-clonic seizures. During seizures, oxygen delivery to both mother and fetus decreases, increasing the risk of hypoxia, placental abruption, and maternal organ failure.