Pre-eclampsia overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Zand, M.D.[2] Ogheneochuko Ajari, MB.BS, MS [3]
Overview
Preeclampsia is one of the leading causes of maternal and perinatal mortality worldwide and is defined as new-onset hypertension after 20 weeks of gestation or near the term accompanied by proteinuria or other maternal organs involvement. Proteinuria may be negative, then other maternal organ dysfunction should be evaluated. Previous classification of preeclampsia into mild and severe is not used now due to suddenly worsening of the preeclampsia in any stages. Right upper quadrant or epigastric pain may be due to periportal and focal parenchymal liver necrosis, hepatic cell edema, or Glisson’s capsule distension. There is not always a correlation between liver pathology and laboratory tests. Headache is not a reliable symptom for preeclampsia with severe features. Other neurologic abnormalities should be evaluated. Headache,blurred vision,scotoma,hyperreflexia, temporary blindness may happen in the course of disease. If tonic-clonic seizure happens, it is defined as eclapsia.Eclampsia was first identified by Francois Mauriceau, a French obstetrician, born in 1637, following finding the correlation between convulsion in primigravidas and suppression of lochial flow or intrauterine fetal death. Preeclampsia may be the result of entering placental factors into the maternal circulation leading to endothelial dysfunction and hypertension and proteinuria. Increasing the level of an angiogenic factor named fms-like tyrosine kinase 1 in placenta correlated with endothelial dysfunction. In villous trophoblast of preeclamptic women, apoptosis was considered. Following uteroplacental ischemia, and invasion spiral arteries by trophoblasts, releasing some angiogenic factors causes other organ involvement. Incomplete penetration in recessive or dominant gene was noticed in pathogenesis of preeclampsia. Common cause of preeclampsia include uteroplacental ischemia and genetic predisposition following The formation of atheromatous plaques and fibrinoid necrosis of the spiral vessel walls, Oxidative stress in trophoblast cells, Apoptosis in trophoblast cells, Systemic inflammatory response, Vasospasm, Platelet aggregation, Thrombin formation, Deposition of the fibrin in multiple organs. In new classification proteinuria is not the main indicator for diagnosis of preeclampsia due to high percentage of false negative results. Preeclampsia may be classified according to the time of event into two groups: Early preeclampsia before 34 weeks of gestation, Late preeclampsia after delivery. Preeclampsia with severe feature includes the following characteristics:Systolic blood pressure≥ 160 mmHg, diastolic blood pressure≥ 110 mmHg, in two occasionS apart 4 hours,Thrombocytopnea (platelet count <100,000/dl0, Pulmonary edema, New-onset headache unresponsed to medications, Visual disturbances, Liver enzyme level > 2 times upper limit normal concentrations or persistent epigasteric or right upper quadrant pain, Serum creatinin >1.1 mg/dl or doubling serum creatinine level in the absent of other causes of renal insufficiency. All of the hypertensive disorder during pregnancy including chronic hypertension, white coat hypertension, mask hypertension, gestational hypertension increase the risk of preeclampsia.
Historical Perspective
Eclampsia was first identified by Francois Mauriceau, a French obstetrician, born in 1637, following finding the correlation between convulsion in primigravidas and suppression of lochial flow or intrauterine fetal death. Preeclampsia may be the result of entering placental factors into the maternal circulation leading to endothelial dysfunction and hypertension and proteinuria. Increasing the level of an angiogenic factor named fms-like tyrosine kinase 1 in placenta correlated with endothelial dysfunction. In villous trophoblast of preeclamptic women, apoptosis was considered. Following uteroplacental ischemia, and invasion spiral arteries by trophoblasts, releasing some angiogenic factors causes other organ involvement. Incomplete penetration in recessive or dominant gene was noticed in pathogenesis of preeclampsia.
Classification
Pathophysiology
Preeclampsia may be the result of entering placental factors into the maternal circulation leading to endothelial dysfunction and hypertension and proteinuria. Increasing the level of an angiogenic factor named fms-like tyrosine kinase 1 in placenta correlated with endothelial dysfunction. In villous trophoblast of preeclamptic women, apoptosis was considered. Following uteroplacental ischemia, and invasion spiral arteries by trophoblasts, releasing some angiogenic factors causes other organ involvement. Incomplete penetration in recessive or dominant gene was noticed in pathogenesis of preeclampsia.
Causes
Common cause of preeclampsia include uteroplacental ischemia and genetic predisposition following The formation of atheromatous plaques and fibrinoid necrosis of the spiral vessel walls, Oxidative stress in trophoblast cells, Apoptosis in trophoblast cells, Systemic inflammatory response, Vasospasm, Platelet aggregation, Thrombin formation, Deposition of the fibrin in multiple organs.