Explain the etiology of preeclampsia.
Although the etiologies of preeclampsia are unknown, uteroplacental ischemia appears to be a common factor. Beer (1978) suggested that uteroplacental ischemia may result from altered immunity such as graft-versus-host reaction.
It is also possible that placental prostaglandin imbalance between thromboxane and prostacyclin leads to preeclampsia. In the normal pregnancy, prostacyclin and thromboxane are produced in equal amounts by the placenta. In the pregnancy complicated by preeclampsia, there is a relative increase in thromboxane production. Thromboxane causes increased vasoconstriction, platelet aggregation, and uterine activity as well as a simultaneous decrease in uteroplacental blood flow. These effects are observed in preeclampsia.
Uteroplacental ischemia leads to the production of substances similar to renin and thromboplastin. Renin causes release of angiotensin and aldosterone, which result in hypertension and edema. Thromboplastin can initiate coagulopathies such as disseminated intravascular coagu-lation (DIC).