Aetiology - Pre-Eclampsia and Eclampsia

The aetiology of pre-eclampsia is still unknown. However, placental delivery reverses the symptoms of pre-eclampsia, suggesting that the placenta has a central role in the condition. Additionally, women with increased placental tissue for gestational age, such as those with hydatiform moles and twin pregnancies, have an increased prevalence of pre-eclampsia. In fact, the presence of proteinuric hypertension prior to 20 weeks' gestation should initiate a search for molar pregnancy because it raises the possibility of increased placental tissue for a given gestational age, which could cause the symptoms. Other causes include drug withdrawal or a chromosomal abnormality in the fetus (eg, trisomy).

Several theories, which are not mutually exclusive, have been proposed in an attempt to explain the pathophysiology of pre-eclampsia. One theory holds that an increase of a number of active circulating mediators during pregnancy causes the symptoms. For example, increased levels of angiotensin II during pregnancy may lead to increased vasospasm. A second theory holds that improper placental development results in placental vascular endothelial dysfunction and a relative uteroplacental insufficiency. The vascular endothelial dysfunction results in increased permeability, hypercoagulability, and diffuse vasospasm. Finally, another model suggests that the increased cardiac output observed during pregnancy causes pre-eclampsia. The increased blood flow and pressure is felt to lead to capillary dilatation, which damages end organ sites, leading to hypertension, proteinuria, and edema.

Additional theories have arisen from epidemiologic research, suggesting the important role of genetic and immunologic factors. The increased prevalence observed in patients using barrier contraception, in multiparous women conceiving with a new partner, and in nulliparous women suggests an immunologic role. Also, inheritance-pattern analysis supports the hypothesis of transmission of pre-eclampsia from mother to fetus by a recessive gene.

Newer research suggests primapaternity plays a larger role than primagravidity as a risk factor for the development of pre-eclampsia. Moreover, the duration the woman is exposed to the male antigens prior to conception is inversely related to the risk of developing pre-eclampsia.

The pathophysiology of eclamptic seizures is not understood. These events are believed to arise from the same preeclamptic effects observed in other areas of the body. In the brain, cerebral vasospasm, edema, ischemia, and ionic shifts between intracellular and extracellular compartments are believed to incite eclamptic seizures.

Nearly 10% of women with severe pre-eclampsia and 30-50% of women with eclampsia are affected by the hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. The exact relationship between HELLP syndrome and pre-eclampsia is unknown. Women with pre-eclampsia and HELLP syndrome develop hepatocellular necrosis and liver dysfunction. They also have an increased mortality rate, and one third of women with pre-eclampsia develop disseminated intravascular coagulation.