Toxemia of pregnancy. Pathomorphological characteristics of organ-site damage
Toxemia of pregnancy, far more commonly known as Preeclampsia/eclampsia is the development of hypertension with proteinuria and edema in the 3rd trimester, it occurs in up to 5% of pregnant women. The term toxemia of pregnancy is a historic misnomer, there are no toxins involved. Exact etiology is unknown, but the underlying pathogenesis is insufficient maternal blood flow to the placenta, as a result of inadequate remodeling of spiral arteries. The decreased uteroplacental blood flow results in placental hypoxia, this leads to release of various antiangiogenic factors and a fall in proangiogenic factors, the consequences of which are as follows:
- Placental infarction due to chronic hypoperfusion
- Hypertension due to reduced endothelial production of vasodilators
- Hypercoagulability due to endothelial dysfunction
- End organ failure (notably kidney and liver) which occurs in full blown state
Remember: eclampsia is preeclampsia plus seizures. HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) is a severe form. The liver shows periportal fibrin deposits, haemorrhage and necrosis; the kidney shows glomerular endotheliosis (swollen endothelial cells narrowing the capillary lumens).
Morphologically, we can see placental abnormalities:
- Infarcts
- Retroplacental hemorrhage
- Premature maturation of placental villi
- Fibrinoid necrosis
H&E, placental infarct: left, crowded pale ghost villi with no nuclei (ischaemic necrosis); right, viable villi with maternal blood between them.
Image: “Placental infarct - low mag” by Nephron, CC BY-SA 3.0, via Wikimedia Commons.
Prompt therapy early in the course aborts the associated changes with all abnormalities resolving after delivery.