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{{Pre-eclampsia}}
{{Pre-eclampsia}}
Editor(s)-in-Chief: C. Michael Gibson, M.S.,M.D. [1] Phone:617-632-7753; Stacie Zelman, M.D. [2]; Associate Editor(s)-In-Chief: Ogheneochuko Ajari MB.BS, MS
{{CMG}}; {{AE}} {{Sara.Zand}}
==Overview==
==Overview==
Pre-eclampsia (US: preeclampsia) is a [[medical condition]] where [[hypertension]] arises in pregnancy ([[pregnancy-induced hypertension]]) in association with significant protein in the urine. Its cause remains unclear, although the principal cause appears to be a substance or substances from the [[placenta]] causing [[endothelial dysfunction]] in the maternal blood vessels.<ref name=DrifeMagowan>Drife JO, Magowan (eds). ''Clinical Obstetrics and Gynaecology'', chapter 39, pp 367-370. ISBN 0-7020-1775-2.</ref> While [[blood pressure]] elevation is the most visible sign of the disease, it involves generalized damage to the maternal endothelium and kidneys and liver, with the release of vasopressive factors only secondary to the original damage.


==References==
[[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 of [[spiral arteries]] by [[trophoblasts]], releasing some [[angiogenic factors]] cause other organ involvement. Incomplete penetration in recessive or dominant gene was noticed in [[pathogenesis]] of [[preeclampsia]]. Common causes 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]] unresponded to [[medications]], [[Visual disturbances]], [[Liver enzyme]] level > 2 times upper limit normal concentrations or persistent [[epigasteric]] or [[right upper quadrant pain]], [[Serum creatinine]] >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:
{{Reflist|2}}
[[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%. The diagnosis of [[preeclampsia]] is made when at least two of the following three diagnostic criteria are met: 1.[[Blood pressure]] ([[Systolic blood pressure]] of 140 mm Hg or more or [[diastolic blood pressure]] of 90 mm Hg or more) on two occasions at least 4 hours apart after 20 weeks of [[gestation]] in a woman with a previously normal [[blood pressure]], [[Systolic blood pressure]] of 160 mm Hg or more or [[diastolic blood pressure]] of 110 mm Hg or more, 2.[[Proteinuria]] (300 mg or more per [[24-hour urine collection]] or [[Protein/creatinine]] ratio of 0.3 mg/dL or more or Dipstick of 2+) , 3. Or in the absence of [[proteinuria]], new-onset [[hypertension]] with the new onset of any of the following: [[Thrombocytopenia]]: [[Platelet count]]< 100,000/dl,  [[Renal insufficiency]]: [[Serum creatinine]]>1.1 mg/dL or a doubling of the serum [[creatinine]] concentration in the absence of other [[renal disease]], Impaired [[liver function]]: Elevated blood level of [[liver transaminases]] to a twice normal level, [[Pulmonary edema]] , Intractable  [[headache]] or [[visual symptoms]].The previouse classification of  [[preeclampsia]] into mild and severe disease is not used now because [[Preeclampsia]] may deteriorate rapidly without any specific signs and symptoms. [[Preeclampsia]] may present the first time intrapartum or early postpartum. Every [[hypertensive]] [[pregnant]] woman should be investigated for the symptoms related to organ damage, even in the absence of [[proteinuria]]. Symptoms of [[preeclampsia]]  may include the following: [[Epigasteric pain]] or [[right upper quadrant pain]], [[Frontal]] or [[oxipital]] [[headache]], [[Visual scotoma]], [[Shortness of breath]], limbs [[swelling]],  [[Altered mental status]], [[Photophobia]]. Patients with [[preeclampsia]] usually appear [[edematous]] .Physical examination may be remarkable for:[[Hyperreflexia]], [[vision loss]] or [[deficit]], [[altered sensorium]], [[confusion]], [[Rale]] in [[lungs field]], [[Limbs]] [[edema]]. [[Posterior reversible encephalopathy syndrome]] should be considered in the setting of [[preeclampsia]] in patients with  [[vision loss]] or [[deficit]], [[seizure]], [[headache]], and [[altered sensorium]] or [[confusion]].Laboratory findings consistent with the diagnosis of [[preeclampsia]] include: elevated [[liver]] enzyme tests, [[thrombocytopenia]], elevated serum [[creatinine]], elevated serum [[uric acid]]. An elevated concentration of [[liver enzymes]], [[low platelets]], [[hemolysis]] is diagnostic of [[HELLP syndrome]]. There are no [[ultrasound]]  findings associated with the diagnosis of [[preeclampsia]]. However, an ultrasound may be helpful for following up on fetal complications of [[preeclampsia]], which include fetal [[growth restriction]]. There are no [[MRI]] findings associated with [[preeclampsia]]. However, a [[brian MRI]] may be helpful in the diagnosis of complications of [[preeclampsia]], which include [[Posterior reversible encephalopathy ]]. Findings on  [[brain MRI]] suggestive of [[Posterior reversible encephalopathy]] include [[vasogenic edema]], [[hyperintensities]] in the posterior aspects of the [[brain]]. The aim of therapy is starting treatment in [[blood pressure]]≥ 140/90 mmHg in office or clinic and [[blood pressure]] ≥ 135/85 mmHg at home and reaching the target [[systolic blood pressure ]] 110-140 mmHg and [[diastolic blood pressure]] less than 85 mmHg regardless the type of [[hypertension]] in [[pregnancy]]. The mainstay of therapy for [[hypertension]] in [[preeclampsia]] is [[oral methyldopa]], [[labetalol]], [[oxprenolol]], and [[nifedipine]], and second or third line agents include [[hydralazine]] and [[prazosin]]. Treatment for [[preeclampsia]] patients with  [[proteinuria]] and [[severe hypertension]] or [[hypertension ]] with [[neurologic]] signs and symptoms, is [[magnesium sulfate]] ([[MgSO4]]) for [[convulsion]] prophylaxis. Urgent therapy for [[severe hypertension]] ([[blood pressure]] >160/110) is oral [[nifedipine]] or intravenous [[labetalol]] or [[hydralazine]] or oral [[labetalol]]. [[Delivery]] is definite therapy for [[preeclampsia]] in the 37 weeks of [[gestation]] or occurrence any of the following: Repeated episodes of [[severe hypertension]]([[blood pressure]]≥ 160/110 mmHg, despite maintenance treatment with 3 classes of [[antihypertensive agents]], progressive [[thrombocytopenia]], progressively abnormal [[renal]] or [[liver]] enzyme tests, [[pulmonary edema]], abnormal [[neurological features]], [[stroke]], [[myocardial infarction]], [[HELLP syndrome]] ,[[eclampsia]], suspected acute [[placental abruption]] or [[vaginal bleeding]] in the absence of [[placenta previa]], abnormal fetal testing, [[fetal death]], fetus without expectation for survival at the time of maternal diagnosis (lethal anomaly, extreme [[prematurity]]), persistent reversed end-diastolic flow in the [[umbilical artery]]. Effective measures for the primary prevention of [[preeclampsia ]] include administration of low dose [[aspirin]] (75-162 mg/day) before the 16th week of [[pregnancy]] and [[calcium supplement]](1.2-2.5 g/day), especially in the high risk patients. Secondary prevention strategies following [[preeclampsia]] include [[blood pressure]] monitoring, repeated assessment of [[proteinuria]] if the result is negative, clinical evaluation about [[clonus]], measurement of [[blood test]] twice weekly for [[hemoglobin]], [[platelet count]], [[uric acid]], [[liver]] enzyme test, [[renal]] function test.
 
==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==
In new classification [[proteinuria]] is not the main indicator for diagnosis of [[preeclampsia]].The percentage of false-negative [[proteinuria]] especially on the dipstick is high.[[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]] unresponded to [[medications]], [[Visual disturbances]], [[Liver enzyme]] level > 2 times upper limit normal concentrations or persistent [[epigasteric]] or [[right upper quadrant pain]], [[Serum creatinine]] >1.1 mg/dl or doubling serum creatinine level in the absent of other causes of [[renal insufficiency]].
 
==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]].
 
==Natural History, Complications, and Prognosis==
[[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%.
 
==Diagnosis==
===Diagnostic Study of Choice===
The diagnosis of [[preeclampsia]] is made when at least two of the following three diagnostic criteria are met: 1.[[Blood pressure]] ([[Systolic blood pressure]] of 140 mm Hg or more or [[diastolic blood pressure]] of 90 mm Hg or more) on two occasions at least 4 hours apart after 20 weeks of [[gestation]] in a woman with a previously normal [[blood pressure]], [[Systolic blood pressure]] of 160 mm Hg or more or [[diastolic blood pressure]] of 110 mm Hg or more, 2.[[Proteinuria]] (300 mg or more per [[24-hour urine collection]] or [[Protein/creatinine]] ratio of 0.3 mg/dL or more or Dipstick of 2+) , 3. Or in the absence of [[proteinuria]], new-onset [[hypertension]] with the new onset of any of the following: [[Thrombocytopenia]]: [[Platelet count]]< 100,000/dl,  [[Renal insufficiency]]: [[Serum creatinine]]>1.1 mg/dL or a doubling of the serum [[creatinine]] concentration in the absence of other [[renal disease]], Impaired [[liver function]]: Elevated blood level of [[liver transaminases]] to a twice normal level, [[Pulmonary edema]] , Intractable  [[headache]] or [[visual symptoms]].
 
===History and Symptoms===
The previouse classification of  [[preeclampsia]] into mild and severe disease is not used now because [[Preeclampsia]] may deteriorate rapidly without any specific signs and symptoms. [[Preeclampsia]] may present the first time intrapartum or early postpartum. Every [[hypertensive]] [[pregnant]] woman should be investigated for the symptoms related to organ damage, even in the absence of [[proteinuria]]. Symptoms of [[preeclampsia]]  may include the following: [[Epigasteric pain]] or [[right upper quadrant pain]], [[Frontal]] or [[oxipital]] [[headache]], [[Visual scotoma]], [[Shortness of breath]], limbs [[swelling]],  [[Altered mental status]], [[Photophobia]].
 
===Physical Examination===
Patients with [[preeclampsia]] usually appear [[edematous]] .Physical examination may be remarkable for:[[Hyperreflexia]], [[vision loss]] or [[deficit]], [[altered sensorium]] , [[confusion]], [[Rale]] in [[lungs field]], [[Limbs]] [[edema]]. [[Posterior reversible encephalopathy syndrome]] should be considered in the setting of [[preeclampsia]] in patients with  [[vision loss]] or [[deficit]], [[seizure]], [[headache]], and [[altered sensorium]] or [[confusion]].
 
===Laboratory Findings===
Laboratory findings consistent with the diagnosis of [[preeclampsia]] include: elevated [[liver]] enzyme tests, [[thrombocytopenia]], elevated serum [[creatinine]], elevated serum [[uric acid]]. An elevated concentration of [[liver enzymes]], [[low platelets]], [[hemolysis]] is diagnostic of [[HELLP syndrome]].
 
===Ultrasound===
There are no [[ultrasound]]  findings associated with the diagnosis of [[preeclampsia]]. However, an ultrasound may be helpful for following up on fetal complications of [[preeclampsia]], which include fetal [[growth restriction]].
 
===MRI===
There are no [[MRI]] findings associated with [[preeclampsia]]. However, a [[brian MRI]] may be helpful in the diagnosis of complications of [[preeclampsia]], which include [[Posterior reversible encephalopathy ]]. Findings on  [[brain MRI]] suggestive of [[Posterior reversible encephalopathy]] include [[vasogenic edema]], [[hyperintensities]] in the posterior aspects of the [[brain]].
 
==Treatment==
===Medical Therapy===
The aim of therapy is starting treatment in [[blood pressure]]≥ 140/90 mmHg in office or clinic and [[blood pressure]] ≥ 135/85 mmHg at home and reaching the target [[systolic blood pressure ]] 110-140 mmHg and [[diastolic blood pressure]] less than 85 mmHg regardless the type of [[hypertension]] in [[pregnancy]]. The mainstay of therapy for [[hypertension]] in [[preeclampsia]] is [[oral methyldopa]], [[labetalol]], [[oxprenolol]], and [[nifedipine]], and second or third line agents include [[hydralazine]] and [[prazosin]]. The mainstay  of therapy for [[preeclampsia]], who have [[proteinuria]] with [[severe hypertension]] or [[hypertension ]] with [[neurologic]] signs and symptoms, is [[magnesium sulfate]] ([[MgSO4]]) for [[convulsion]] prophylaxis.  Urgent therapy for [[severe hypertension]] ([[blood pressure]] >160/110) is oral [[nifedipine]] or intravenous [[labetalol]] or [[hydralazine]] or oral [[labetalol]].
 
===Primary Prevention===
Effective measures for the primary prevention of [[preeclampsia ]] include administration of low dose [[aspirin]] (75-162 mg/day) before the 16th week of [[pregnancy]] and [[calcium supplement]](1.2-2.5 g/day), especially in the high risk patients .
 
===Secondary Prevention===
Secondary prevention strategies following [[preeclampsia]] include [[blood pressure]] monitoring, repeated assessment of [[proteinuria]] if the result is negative, clinical evaluation about [[clonus]], measurement of [[blood test]] twice weekly for [[hemoglobin]], [[platelet count]], [[uric acid]], [[liver]] enzyme test, [[renal]] function test.


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[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
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[[Category:Cardiology]]
 
[[Category:Up-to-date]]
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{{WS}}

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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]

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 of spiral arteries by trophoblasts, releasing some angiogenic factors cause other organ involvement. Incomplete penetration in recessive or dominant gene was noticed in pathogenesis of preeclampsia. Common causes 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 unresponded to medications, Visual disturbances, Liver enzyme level > 2 times upper limit normal concentrations or persistent epigasteric or right upper quadrant pain, Serum creatinine >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%. The diagnosis of preeclampsia is made when at least two of the following three diagnostic criteria are met: 1.Blood pressure (Systolic blood pressure of 140 mm Hg or more or diastolic blood pressure of 90 mm Hg or more) on two occasions at least 4 hours apart after 20 weeks of gestation in a woman with a previously normal blood pressure, Systolic blood pressure of 160 mm Hg or more or diastolic blood pressure of 110 mm Hg or more, 2.Proteinuria (300 mg or more per 24-hour urine collection or Protein/creatinine ratio of 0.3 mg/dL or more or Dipstick of 2+) , 3. Or in the absence of proteinuria, new-onset hypertension with the new onset of any of the following: Thrombocytopenia: Platelet count< 100,000/dl, Renal insufficiency: Serum creatinine>1.1 mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease, Impaired liver function: Elevated blood level of liver transaminases to a twice normal level, Pulmonary edema , Intractable headache or visual symptoms.The previouse classification of preeclampsia into mild and severe disease is not used now because Preeclampsia may deteriorate rapidly without any specific signs and symptoms. Preeclampsia may present the first time intrapartum or early postpartum. Every hypertensive pregnant woman should be investigated for the symptoms related to organ damage, even in the absence of proteinuria. Symptoms of preeclampsia may include the following: Epigasteric pain or right upper quadrant pain, Frontal or oxipital headache, Visual scotoma, Shortness of breath, limbs swelling, Altered mental status, Photophobia. Patients with preeclampsia usually appear edematous .Physical examination may be remarkable for:Hyperreflexia, vision loss or deficit, altered sensorium, confusion, Rale in lungs field, Limbs edema. Posterior reversible encephalopathy syndrome should be considered in the setting of preeclampsia in patients with vision loss or deficit, seizure, headache, and altered sensorium or confusion.Laboratory findings consistent with the diagnosis of preeclampsia include: elevated liver enzyme tests, thrombocytopenia, elevated serum creatinine, elevated serum uric acid. An elevated concentration of liver enzymes, low platelets, hemolysis is diagnostic of HELLP syndrome. There are no ultrasound findings associated with the diagnosis of preeclampsia. However, an ultrasound may be helpful for following up on fetal complications of preeclampsia, which include fetal growth restriction. There are no MRI findings associated with preeclampsia. However, a brian MRI may be helpful in the diagnosis of complications of preeclampsia, which include Posterior reversible encephalopathy . Findings on brain MRI suggestive of Posterior reversible encephalopathy include vasogenic edema, hyperintensities in the posterior aspects of the brain. The aim of therapy is starting treatment in blood pressure≥ 140/90 mmHg in office or clinic and blood pressure ≥ 135/85 mmHg at home and reaching the target systolic blood pressure 110-140 mmHg and diastolic blood pressure less than 85 mmHg regardless the type of hypertension in pregnancy. The mainstay of therapy for hypertension in preeclampsia is oral methyldopa, labetalol, oxprenolol, and nifedipine, and second or third line agents include hydralazine and prazosin. Treatment for preeclampsia patients with proteinuria and severe hypertension or hypertension with neurologic signs and symptoms, is magnesium sulfate (MgSO4) for convulsion prophylaxis. Urgent therapy for severe hypertension (blood pressure >160/110) is oral nifedipine or intravenous labetalol or hydralazine or oral labetalol. Delivery is definite therapy for preeclampsia in the 37 weeks of gestation or occurrence any of the following: Repeated episodes of severe hypertension(blood pressure≥ 160/110 mmHg, despite maintenance treatment with 3 classes of antihypertensive agents, progressive thrombocytopenia, progressively abnormal renal or liver enzyme tests, pulmonary edema, abnormal neurological features, stroke, myocardial infarction, HELLP syndrome ,eclampsia, suspected acute placental abruption or vaginal bleeding in the absence of placenta previa, abnormal fetal testing, fetal death, fetus without expectation for survival at the time of maternal diagnosis (lethal anomaly, extreme prematurity), persistent reversed end-diastolic flow in the umbilical artery. Effective measures for the primary prevention of preeclampsia include administration of low dose aspirin (75-162 mg/day) before the 16th week of pregnancy and calcium supplement(1.2-2.5 g/day), especially in the high risk patients. Secondary prevention strategies following preeclampsia include blood pressure monitoring, repeated assessment of proteinuria if the result is negative, clinical evaluation about clonus, measurement of blood test twice weekly for hemoglobin, platelet count, uric acid, liver enzyme test, renal function test.

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

In new classification proteinuria is not the main indicator for diagnosis of preeclampsia.The percentage of false-negative proteinuria especially on the dipstick is high.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 unresponded to medications, Visual disturbances, Liver enzyme level > 2 times upper limit normal concentrations or persistent epigasteric or right upper quadrant pain, Serum creatinine >1.1 mg/dl or doubling serum creatinine level in the absent of other causes of renal insufficiency.

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.

Natural History, Complications, and Prognosis

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%.

Diagnosis

Diagnostic Study of Choice

The diagnosis of preeclampsia is made when at least two of the following three diagnostic criteria are met: 1.Blood pressure (Systolic blood pressure of 140 mm Hg or more or diastolic blood pressure of 90 mm Hg or more) on two occasions at least 4 hours apart after 20 weeks of gestation in a woman with a previously normal blood pressure, Systolic blood pressure of 160 mm Hg or more or diastolic blood pressure of 110 mm Hg or more, 2.Proteinuria (300 mg or more per 24-hour urine collection or Protein/creatinine ratio of 0.3 mg/dL or more or Dipstick of 2+) , 3. Or in the absence of proteinuria, new-onset hypertension with the new onset of any of the following: Thrombocytopenia: Platelet count< 100,000/dl, Renal insufficiency: Serum creatinine>1.1 mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease, Impaired liver function: Elevated blood level of liver transaminases to a twice normal level, Pulmonary edema , Intractable headache or visual symptoms.

History and Symptoms

The previouse classification of preeclampsia into mild and severe disease is not used now because Preeclampsia may deteriorate rapidly without any specific signs and symptoms. Preeclampsia may present the first time intrapartum or early postpartum. Every hypertensive pregnant woman should be investigated for the symptoms related to organ damage, even in the absence of proteinuria. Symptoms of preeclampsia may include the following: Epigasteric pain or right upper quadrant pain, Frontal or oxipital headache, Visual scotoma, Shortness of breath, limbs swelling, Altered mental status, Photophobia.

Physical Examination

Patients with preeclampsia usually appear edematous .Physical examination may be remarkable for:Hyperreflexia, vision loss or deficit, altered sensorium , confusion, Rale in lungs field, Limbs edema. Posterior reversible encephalopathy syndrome should be considered in the setting of preeclampsia in patients with vision loss or deficit, seizure, headache, and altered sensorium or confusion.

Laboratory Findings

Laboratory findings consistent with the diagnosis of preeclampsia include: elevated liver enzyme tests, thrombocytopenia, elevated serum creatinine, elevated serum uric acid. An elevated concentration of liver enzymes, low platelets, hemolysis is diagnostic of HELLP syndrome.

Ultrasound

There are no ultrasound findings associated with the diagnosis of preeclampsia. However, an ultrasound may be helpful for following up on fetal complications of preeclampsia, which include fetal growth restriction.

MRI

There are no MRI findings associated with preeclampsia. However, a brian MRI may be helpful in the diagnosis of complications of preeclampsia, which include Posterior reversible encephalopathy . Findings on brain MRI suggestive of Posterior reversible encephalopathy include vasogenic edema, hyperintensities in the posterior aspects of the brain.

Treatment

Medical Therapy

The aim of therapy is starting treatment in blood pressure≥ 140/90 mmHg in office or clinic and blood pressure ≥ 135/85 mmHg at home and reaching the target systolic blood pressure 110-140 mmHg and diastolic blood pressure less than 85 mmHg regardless the type of hypertension in pregnancy. The mainstay of therapy for hypertension in preeclampsia is oral methyldopa, labetalol, oxprenolol, and nifedipine, and second or third line agents include hydralazine and prazosin. The mainstay of therapy for preeclampsia, who have proteinuria with severe hypertension or hypertension with neurologic signs and symptoms, is magnesium sulfate (MgSO4) for convulsion prophylaxis. Urgent therapy for severe hypertension (blood pressure >160/110) is oral nifedipine or intravenous labetalol or hydralazine or oral labetalol.

Primary Prevention

Effective measures for the primary prevention of preeclampsia include administration of low dose aspirin (75-162 mg/day) before the 16th week of pregnancy and calcium supplement(1.2-2.5 g/day), especially in the high risk patients .

Secondary Prevention

Secondary prevention strategies following preeclampsia include blood pressure monitoring, repeated assessment of proteinuria if the result is negative, clinical evaluation about clonus, measurement of blood test twice weekly for hemoglobin, platelet count, uric acid, liver enzyme test, renal function test.