Preeclampsia
Pre-eclampsia (US: preeclampsia) is a medical condition where hypertension arises in pregnancy (pregnancy-induced hypertension) in association with significant protein in the urine. Its cause remains unclear, although the principal cause appears to be a substance or substances from the placenta causing endothelial dysfunction in the maternal blood vessels While blood pressure elevation is the most visible sign of the disease, it involves generalized damage to the maternal endothelium and kidneys and liver, with the release of vasopressive factors only secondary to the original damage.
Pre-eclampsia may develop at varying times within pregnancy and its progress differs among patients; most cases are diagnosed pre-term. It has no known cure apart from ending the pregnancy (induction of labor or abortion). It may also occur up to six weeks post-partum. It is the most common, dangerous complication of pregnancy and it may affect both the mother and the fetus
Causes
The pre-eclampsia syndrome is thought in some cases to be caused by a shallowly implanted placenta which becomes hypoxic, leading to upregulated inflammatory mediators secreted by the placenta and acting on the vascular endothelium. The shallow implantation is thought to stem from the maternal immune system's response to the placenta. But in some cases of preeclampsia, the placenta appears to have implanted normally. Possibly women with higher baseline levels of inflammation stemming from underlying conditions such as chronic hypertension may have normally implanted placentae, but less tolerance for the inflammatory burden of pregnancy.
If severe, preeclampsia progresses to fulminant pre-eclampsia, with headaches, visual disturbances, and epigastric pain, and further to HELLP syndrome and eclampsia. Placental abruption is associated with hypertensive pregnancies. These are life-threatening conditions for both the developing baby and the mother.
Many theories have attempted to explain why the preeclampsia syndrome arises in some pregnancies:
endothelial cell injury
rejection phenomenon
compromised placental perfusion
altered vascular reactivity
imbalance between prostacyclin and thromboxane
decreased glomerular filtration rate with retention of salt and water
decreased intravascular volume
increased central nervous system irritability
disseminated intravascular coagulation
uterine muscle stretch (ischemia)
dietary factors
genetic factor
The current understanding of the disease is as a two-stage process, with a variable first stage which predisposes the placenta to hypoxia, followed by the release of soluble factors which result in many of the other observed phenomena. Many of the older theories can be subsumed under this umbrella, as the soluble factors have been shown to cause, for example, endothelial cell injury, altered vascular reactivity, the classic lesion of glomerular endotheliosis, decreased intravascular volume, etc. Underlying maternal susceptibility to the damage is likely implicated as well.