Pre-eclampsia overview

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Pre-eclampsia Microchapters
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Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Pre-eclampsia from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
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Other Imaging Findings
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Treatment
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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 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.

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%. 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.

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

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention