Individual differences |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |
|ICD-10||O11, O13, O14|
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 Pre-eclampsia and PIH are very serious conditions and require careful monitoring of mother and baby.
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, or renal disease, in women with a family history of pre-eclampsia, and 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".
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.
A few nontraditional theories have also been suggested as to the root cause of preeclampsia. Dr. Tom Brewer posits that protein deficiencies can lead to preeclampsia. Other research discovered low homocysteine levels in preeclamptic women, remedied in high-risk patients with folic acid and B6 supplementation.
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. Maternal response (endothelial activation, pressor response, vasospasm) to these factors eventually lead to high blood pressure and proteinuria (protein in the urine) generally after 20th weeks of gestation. The placenta, rather than the fetus, is the source of problem. This is evident as preeclampsia can occur in a molar pregnancy (Hydatidiform Mole) which does not have fetal tissue (but may be paternal). Preeclampsia can also occur in an extrauterine (eg abdominal) pregnancy which brings into question role of the maternal part (decidua) of the placenta. Although preeclampsia may worsen or even appear upon parturition (delivery) or termination of pregnancy, these are the only known means of eventually curing it as the cause, ie the placenta, is removed. The maternal response reverts back to normal within in a few months of delivery.
In normal placenta the decidual spiral arteries are invaded by extravillous trophoblasts which makes the arteries eventually open into trophoblastic cavities called lacunae (though they are initially kept plugged by the trophoblasts). The invading trophoblasts replace smooth muscles and endothelium in the wall of these arteries starting from the fetal side near the implantation site. The replacement of endothelium by these cells may continue even in the parts of spiral artery deep into myometrium. This is supposed to help the spiral arteries to become wide, thin and funnel like near their opening into the lacunae. This invasion in normal pregnancy establishes a high capacity and low resistance circulation. The maternal blood in the lacunar network bathe 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. Karumanchi et al has shown that one of the mediator of the "toxemia", ie factor released into blood from the placenta,could be a soluble splice variant isoform of the VEGF receptor 1 (sFlt 1). Intravenous injection of sFlt1 can induce a PIH like condition in rodents (preeclampsia is a disease of higher primates, not seen in any other animal in the wild).
The most successful treatment for eclampsia or advancing preeclampsia is delivery, either by induction or Caesarean section. Some forms of preeclampsia can be treated with anti-hypertensive medication. In some cases women with preeclampsia or eclampsia can be stabilized temporarily with magnesium sulfate intravenously to prevent seizures. Attempts will be made to delay delivery until the fetus has matured, but in severe cases where the mother's life is threatened, delivery must occur as soon as possible.
A few other theories on prevention of preeclampsia:
- Exercise can help reduce risk of preeclampsia
- Protein's role in prevention of preeclampsia - Dr. Tom Brewer
- Low-dose aspirin prior to bed
- Nutritional deficiencies of calcium, magnesium, folic acid, and zinc have all been suggested as contributing factors to preeclampsia, remedied by supplementation.
|This page uses Creative Commons Licensed content from Wikipedia (view authors).|