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Pre-eclampsia affects 2–8% of pregnancies worldwide. [4] [17] [12] Hypertensive disorders of pregnancy (which include pre-eclampsia) are one of the most common causes of death due to pregnancy. [6] They resulted in 46,900 deaths in 2015. [7] Pre-eclampsia usually occurs after 32 weeks; however, if it occurs earlier it is associated with worse ...
The pathogenesis of pre-eclampsia is poorly understood and may be attributed to factors related to the woman and placenta since pre-eclampsia is seen in molar pregnancies absent of a fetus or fetal tissue. [46] The placenta normally produces the potent vasodilator adrenomedullin but it is reduced in pre-eclampsia and eclampsia. [47]
Severe pre-eclampsia involves a BP over 160/110 (with additional signs). It affects 5–8% of pregnancies. [20] Eclampsia – seizures in a pre-eclamptic patient, affect around 1.4% of pregnancies. [21] Gestational hypertension can develop after 20 weeks but has no other symptoms, and later rights itself, but it can develop into pre-eclampsia. [22]
Preeclampsia superimposed on chronic hypertension occurs when a pregnant woman with chronic hypertension develops signs of pre-eclampsia, typically defined as new onset of proteinuria ≥30 mg/dL (1+ in the dipstick) in at least 2 random urine specimens that were collected ≥4 h apart (but within a 7-day interval) or 0.3 g in a 24-h period. [19]
Failure of the trophoblast to invade sufficiently is important in the development of some cases of pre-eclampsia. Invasion of the trophoblast too deeply may cause conditions such as placenta accreta, placenta increta, or placenta percreta.
[40] [41] Abdominal pregnancy has served to further clarify the disease pre-eclampsia which was previously thought (1980s) to require a uterus for it to occur, however pre-eclampsia's occurrence in abdominal pregnancy (with the conceptus outside the uterus) helped throw light on pre-eclampsia's etiology. [42]
This changes them from high-resistance low-flow vessels into large dilated vessels that provide good perfusion, and oxygenation to the developing placenta. When invasion is shallow it is inadequate, the arteries remain narrow at their openings into the intervillous space, and is the cause of pre-eclampsia, fetal growth restriction and still birth.
The genetic roots of gestational hypertension and pre-eclampsia are certain, as women with a family history of the condition are three times more likely to develop it when they are pregnant. [25] One of the potential causes of gestational hypertension and pre-eclampsia is when the trophoblast does not invade far enough into the uterine lining. [26]