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/dl), 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. The prevalence of preeclampsia is approximately 2000-8000 per 100,000 pregnancies worldwide. Between 1987 and 2004, the incidence of preeclampsia was estimated to be 25,000 per 100,000 pregnancies in the united state. Preeclampsia is more commonly observed among pregnant women aged before 20 and after 40 years old. Preeclampsia usually affects individuals of the Non-Hispanic whites and Non-Hispanic blacks and American Indians/Alaska Natives race. Common risk factors in the development of preeclampsia include: Nulliparity, Multifetal gestations, Preeclampsia in a previous pregnancy, Chronic hypertension, Pregestational diabetes, Gestational diabetes,Thrombophilia, Systemic lupus erythematosus, Body mass index greater than 30 at the beginning of prenatal care, Antiphospholipid antibody syndrome, Maternal age 35 years or older, Kidney disease, Assisted reproductive technology,Obstructive sleep apnea, African-American decent. There is insufficient evidence to recommend routine screening for preeclampsia. Preeclampsic patients are usually asymptomatic and may deteriorate rapidly without any specific signs and symptoms.Early clinical feature after 20 weeks of gestation include blood pressure ≥ 140/90 mmHg, proteinuria, evidence of maternal organ involvement. Common complications of preeclampsia include: Intrauterin growth retardation(IUGR), Uteroplacental insufficiency, Fetal asphyxia or fetal death, Maternal seizures, Maternal death. Long term complication of preeclampsia include: Chronic hypertension, Diabetes mellitus, Ischemic heart disease, Cerebrovascular disease, Kidney disease, Thromboembolism, Hypothyroidism , Impaired memory. Prognosis is generally good after delivery and controlling maternal hypertension and the 5 year mortality rate of the patients with preeclampsia is approximately 0.4%.
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.
Differentiating preeclampsia from Other Diseases
Differential diagnosis of hypertensive disorder during pregnancy including chronic hypertension, white coat hypertension, mask hypertension, gestational hypertension whether increase the risk of preeclampsia.
Epidemiology and Demographics
The prevalence of preeclampsia is approximately 2000-8000 per 100,000 pregnancies worldwide. Between 1987 and 2004, the incidence of preeclampsia was estimated to be 25,000 per 100,000 pregnancies in the united state. Preeclampsia is more commonly observed among pregnant women aged before 20 and after 40 years old. Preeclampsia usually affects individuals of the Non-Hispanic whites and Non-Hispanic blacks and American Indians/Alaska Natives race.
Risk Factors
Common risk factors in the development of preeclampsia include: Nulliparity , Multifetal gestations , Preeclampsia in a previous pregnancy , Chronic hypertension , Pregestational diabetes , Gestational diabetes , Thrombophilia , Systemic lupus erythematosus , Body mass index greater than 30 at the beginning of prenatal care , Antiphospholipid antibody syndrome , Maternal age 35 years or older , Kidney disease ,Assisted reproductive technology , Obstructive sleep apnea , African-American decent.
Screening
There is insufficient evidence to recommend routine screening for preeclampsia.