Pre-eclampsia is diagnosed when a pregnant woman develops high blood pressure (two separate readings taken at least 6 hours apart of 140/90 or more) and 300 mg of protein in a 24 hour urine sample (proteinuria). Swelling or edema(especially in the hands and face)was originally considered an important sign for a diagnoses of pre-eclampsia, but in current medical practice only hypertension and proteinuria are necessary for a diagnoses.

Some women develop high blood pressure without the proteinuria, this is called Gestational Hypertension or, Pregnancy Induced Hypertension (PIH). Both Preeclampsia and PIH are very serious conditions and require careful monitoring of mother and baby.

Appearance

Pre-eclampsia is much more common in the first pregnancy (3-5% of births) and usually becomes evident in the third trimester (and virtually always after the 20th week of pregnancy). It is also more common in women who have preexisting hypertension, diabetes,renal disease, and family history of pre-eclampsia. It is also more common in women with a multiple gestation (twins, triplets and more).

Pre-eclampsia may also occur in the immediate post-partum period or up to 6-8 weeks post-partum. This is referred to as "post partum pre-eclampsia".

Causes

Pre-eclampsia is thought to be caused by inflammatory mediators secreted by the placenta and acting on the vascular endothelium. If severe, it progresses to fulminant pre-eclampsia, with headaches and visual disturbances, and further to HELLP syndrome and eclampsia. These are life-threatening conditions for both the developing fetus and the mother.

Pathogenesis

There are many theories on the pathogenesis of preeclampsia, although the exact cause is not known. Most involve abnormal development of the placenta, which leads to a distressed placenta that secretes factors into the maternal blood. These factors damage the maternal blood vessels, leading to high blood pressure and protein in the urine. In normal placenta the decidual spiral arteries are invaded by extravillous trophoblasts which makes the arteies eventually open into trophoblastic cavities called lacunae (though they are initially kept plugged by the trophoblasts). The invading trophoblasts replace some of the smooth muscles and endothelium of these arteries near the implantation site. This is supposed to help the spiral arteries to widen into thin and funnel like near their opening into the lacunae. This establishes a high capacity and low resistance circulation. The maternal blood in the lacunar network bath the chorionic villi lined by syncytiotrophoblast, supplying oxygen and nutrients to, and removing metabolic wastes from, the fetal circulation which is not in direct contact with the maternal blood. In case of preeclampsia the spiral arteries are insufficiently invaded by trophoblasts. They remain narrow and the smooth mucle layer (tunica media) around the arteries become hyperplastic. This leads to insufficient maternal perfusion of the placenta in preeclampsia. One of the factors, released into blood from the placenta, that has been speculated (by Karumanchi et al) to be a mediator of the "toxemia", is a soluble splice variant isoform of the VEGF receptor 1 (sFlt 1).