Hypertensive Disorders in Pregnancy (Williams 22 Edition)
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Transcript of Hypertensive Disorders in Pregnancy (Williams 22 Edition)
Hypertensive Disorders in Pregnancy
Index
Diagnosis
Etiology
Pathogenesis
Pathophysiology
Prediction and Prevention
Management
Gestational Hypertension - 3.7% in 150,000 (National Center for Health Statics, 2001)
Pregnancy-related hypertension: Pregnancy-related deaths (16% of 3201 in US, 1991-1997)
Black women are 3.1 times to die as white women
Hypertensive disorders remain among the most significant and intriguing unsolved problems in obstetrics
INTRODUCTION
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Diagnosis
Etiology
Pathogenesis
Pathophysiology
Prediction and Prevention
Management
Index
Diagnosis
Gestational hypertension
Preeclamsia
Eclampsia
Superimposed preeclamsia (on chronic
hypertension)
Chronic hypertension
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Gestational hypertension
BP≥ 140/90mmHg for first time during pregnancy
No proteinuria
Blood Pressure returns to normal < 12 weeks postpartum
Final diagnosis made only postpartum
May have other signs or symptoms of preeclampsia, for example, epigastric discomfort or thrombocytopenia
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Pre-eclampsia:Pre-eclampsia:a multisystem a multisystem disorderdisorder
PreeclampsiaMinimum Criteria
BP ≥ 140/90mmHg after 20weeks gestation Proteinuria ≥ 300mg/24hrs or ≥ 1+dipstick
Increased certainty of preeclampsia BP≥ 160/110mmHg Proteinuria 2.0g / 24hrs or ≥ 2+dipstick Serum creatinine >1.2mg/dl unless known to be previously elevated Platelets < 100000/mm3 Microangiopathic hemolysis (Increased LDH) Elevated ALT or AST Persistent headache or other cerebral or visual disturbance Persistent epigastric pain
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
PreeclampsiaDiastolic hypertension ≥ 95mmHg
Increase fetal death rate (38000 prenancy in 1976)
Worsening proteinuria Increasing preterm deliveryNeonatal survival was not significantly altered.
Epigastric or RUQ painHepatocelular necrosis, ischemia, edema that stretches the Glisson capsureAST / ALT elevated signHepatic rupture: rare
ThrombocytopeniaSevere vasospasm Microangiopathic hemolysis Platelet activation, aggregation Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
PathophysiologyPreeclampsia
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Severity of Preeclampsia
Rapid increase in BP followed by convulsions is usually preceded by unrelenting severe headache or visual disturbances.
Differentiation between mild & severe preeclampsia can be misleading
because apparently mild disease may progress rapidly to severe disease
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Indications of Severity of Hypertensive Disorder during Pregnancy
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Eclampsia
Preeclampsia + convulsion
Seizures that cannot be attributed to other
causes in woman with preeclampsia
Seizures are generalized and may appear
before, during, of after labor
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Chronic hypertension
BP ≥140/90 mmHg before pregnancy or diagnosed before 20 weeks gestation (not attributable to gestational trophoblastic disease)
or
Hypertension first diagnosed after 20 weeks gestation and persistent after 12 weeks postpartum
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Underlying Causes of Chronic hypertensive Disorder
Essential familial hypertension (hypertensive vascular disease)ObesityAtrterial abnormalities
Renovascular hypertensionCoarcta tion of the aorta
EndocrinedisordersDiabetes mellitusCushing syndromePrimary aldosteronismPheochromocytomaThyrotoxicosis
Glomerulonephritis (acute and chronic)Renoprival hypertension
Chronic glomerulonephritisChronic renal insufficiencyDiabetic nephropathy
Connetive tissue diseaseLupus erythematosusSystemic sclorosisPeriarteritis nodosa
Polycystic kidney diseaseAcute renal failure
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Chronic Hypertension
Chronic Hypertension can lead: Ventricular hypertrophy, Cardiac decompensation, Cerebrovascular accidents, renal damage
That complication are more likely during pregnancy if there is superimposed preeclampsia (which 25% of these women, 1998, Sibai).
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Preeclampsia Superimposed on Chronic Hypertension
New-onset proteinuria ≥ 300mg / 24hours in hypertensive women but no proteinuria before 20 weeks gestation
A sudden increase in proteinuria or blood pressure or platelet count < 100,000/mm3 in women with hypertension and proteinuria before 20weeks gestation
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Superimposed Preeclampsia
Placental abruption, growth restriction, preterm delivery, death. These complication of Superimposed Preeclamsia.
Develops earlier than “Pure” preeclampsia, and it tends to be more severe and often accompanied by fetal growth restriction.
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Incidence and Risk Factor
Nulliparous women.Incidence: 5% (wide variation)Influence by
Parity, race, ethnicity, genetic predisposition
NulliparousTotal:7.6% and severe: 3.3% (Hauth, 2000)
Risk factorChronic hypertension, multifetal gestation, maternal old age (>35 yrs), obesity, African-American ethnicity
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Incidence and Risk FactorMaternal weight and the risk of preeclampsia is progressive.
Smoking during pregnancy reduced risk of hypertension during pregnancy (Bainbridge,2005 ; Zhang, 1999)
Placenta previa also reduced the risk of hypertension
BMI (Kg/m2) Morbidity (%)
<19.8 4.3
>35 13.3
Gestation
twin 13
single 5 (Sibai, 2000)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Incidence and Risk Factor (Eclampsia)
EclampsiaSomewhat preventable
Receive adquate prenatal care
1976 (williams Obstetrics 15th edition)1/700 deliveries (Parkland Hospitial)
1983-19861/1150 deliveries
19991/1750 deliveries
2000, National Vital Statistics Report, in US1/3250
1994, Douglas and Redman in UK1/2000
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Diagnosis
Etiology
Pathogenesis
Pathophysiology
Prediction and Prevention
Management
Index
Etiology
Basic conceptsExposed to chorionic villi for the first time
Exposed to a superabundance of chorionic villi, as with twins or hydatidiform mole
Have preexisting vascular disease
Genetically predisposed to hypertension developing during pregnancy
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Vascular endothelial damage with vasospasm, transudation of plasma, and ischemic and thrombotic sequelae.
Currently plausible potential cause (2003, Sibai)Abnormal trophoblastic invasion of Uterine vessels
Immunological intolerance between maternal and fetoplacental tissues
Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy
Diatary deficiencies
Genetic influences
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Physiology Cythotrophoblast Invasion
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Invasion Cytotrophoblast Cells
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Abnormal Trophoblastic Invasion
In normal implantation, endovascular trophoblasts invade the uterine spiral arteries
Normal placental implantation shows proliferation of extravillous trophoblasts
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
In PreeclamsiaIncomplete trophoblastic invasionThe magnitude of defective trophoblastic invasion of the spiral arteries correlated with the severity of the hypertensive disorder (2000, Madazli)
Using Electron MicorscopyEndothelial damageInsudation of plasma constituents into vessel wallsProliferation of myointimal cellsMedial necrosisLipid and macrophage accumulates in myointimal cells
Abnormal Trophoblastic Invasion
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Lipid-laden cells atherosis (Hertig, 1945)
Obstruction of the spiral arteriolar lumen by atherosis may impair placental blood flow
Placental perfusion diminished
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
ISKEMIC PLACENTA
O2
O2 radical
OH- radikal
H2O2
SEL ENDOTHEL
PROTEINMEMBRANE
NUKLEUS
Peroksida lipid
Disfunctions of Endothel
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Nutritional Factors
Dietary deficiencies and Excesses over the centuries have been blamed as the cause of eclampsia.Supplementation with various elements such as zinc, calcium, and magnesium to prevent preeclampsia (John, 2002)
Obesity, is a potent risk factor for preeclampsiaC-reactive protein, an inflammatory marker, was shown to be increase in obesity, which in turn was associated with preeclampsia (Wolf, 2001)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Genetic Factors
Hereditary hypertension is linked to preeclampsia (Ness, 2003)
Preeclampsia- eclampsia is highly heritable in sisters, daughters, granddaughters, and daughters-in-law. (Chesley and Cooper, 1986)
60% concordance in monozygotic female twin pairs (Nilsson, 2004)
HLA-DR reported an association preeclampsia and proteinuric hypertension (kilpatrick,1989)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Diagnosis
Etiology
Pathogenesis
Pathophysiology
Prediction and Prevention
Management
Index
Pathogenesis Vasospasm
Vascular constriction resistance and subsequent hypertension
Maldistribution, ischemia of the surrounding tissues caused diminished blood flow necrosis, hemorrhage, and other end-organ disturbances.
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Vasospam Spiral Arteries
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Pathophysiology VasospasmFailure of Cytotrophoblast invasion of the spiral arteries
Vasocontriction spiral arteries
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
The Complication of Vasospasm
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
PathogenesisEndothelial Cell Activation
Unknown factors (from placenta) are secreted into the maternal circulation activation and dysfunction of the vascular endothelium.
Damaged or activated endothelial cells secrete substances promote coagulation and increase the sensitivity to
vasopressors changes in glomerular capillary endothelial morphology increasd capillary permeability elevated blood concentrations
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Increased Pressor ResponsesProstaglandins
In PreeclampsiaEndothelial prostacyclin (PGI2) production is decreased
Thromboxane A2 (TXA2) secretion by platelets is increased
Increased sensitivity to infused angiotensin II
vasoconstriction
PlateletsThe Texbook’s Kidney
Disease and Hypertension in Pregnancy, 2003
Diagnosis
Etiology
Pathogenesis
Pathophysiology
Prediction and Prevention
Management
Index
Pathophysiology Vascular Changes in Pregnancy
Dewhurst's Textbook of Obstetrics and Gynaecology 7th Edition
PathophysiologyCardiovascular System
Increased cardiac afterload caused by hypertension
Cardiac preload in preeclampsiaPathologically diminished hypervolemia of pregnancy
Iatrogenically increased by iv crystalloid or oncotic solution
Extravasion into the extracellular space, especially the lung
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Cardiovascular SystemHemodynamic Changes
PreeclampsiaCardiac output elevated before hypertension developed than normal pregnancy.
With clinical onset of preeclampsiaMarked reduction in cardiac output.Increased peripheral resistance.
By contrast, Gestational hypertensionElevated cardiac outputs with development of hypertension.
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Severe Preeclamsia and Eclampsia: Associated Hemodynamic Measurements
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
(Hankin, 1984)
Ventricular Function in Severe Preeclampsia-Eclampsia
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Blood volume in termNormal pregnancy: 5000mlNot pregnancy: 3500mlEclampsia: 3500ml
Hemoconcentration in preeclampsiaVasoconstriction and Endothelial dysfunction with vascular permeability.Depending on severity, hemoconcentration is usually not as marked.Whereas, gestational hypertension have a normal blood volume (Silver, 1998)
Cardiovascular SystemBlood Volume
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Comparing nonpregnant Mean Blood Volume
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Blood and CoagulationPlatelet
Thrombocytopenia life threatening
Severe disease: < 100,000/uL
Platelet count continues to decrease indication of delivery the platelet count increases progressively after delivery (within 3 to 5 day)Platelet activation, aggregation, consumption “exhausion” thrombocytopenia (Harlow, 2002)
HELLP syndrome: hemolysis (H) , elevated liver enzymes (EL), and low platelets (LP) (Weinstein, 982)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Volume HomeostasisEndocrine changes
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Deoxycorticosterone (DOC)Another potent mineralocorticoid
Increses 3rd trimesterResult from conversion plasma progesterone rather than increased maternal adrenal secretion.
DOC is not reduced by sodium retention or hypertension
DOC may serve to explain why women with preeclamsia retain sodium.
Volume HomeostasisEndocrine changes
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
The Physiology Kidney of Pregnancy
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Pathophysiology Hipertension in Preeclampsia
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Functional Renal Alterations in Preeclampsia
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Functional Renal Alterations in Preeclampsia (Continued)
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Functional Renal Alterations in Preeclampsia (Continued)
The Texbook’s Kidney Disease and Hypertension in
Pregnancy, 2003
LiverPeriportal hemorrhagic necrosis in the periphery of the liver lobule
Serum liver enzyme is elevatedHepatic rupture (more rare), subcapsular hematoma (more common).Treatment
Surgical intervention may be life savingBlood transfusion (recombinant VIIa) to help control heptic haemorrhage. Liver transplantation.
Spontaneous hepatic rupture in 121 cases and mortality rate was 30%
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Gross Liver specimen from a woman with Preeclampsia
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Liver
HELLP syndromeHemolysis, Elevated Liver enzyme and Low Platelet
20% of severe preeclampsia and eclampsia
Adverse outcome: 40%
Other complicationEclampsia (6%), Placental abruption (10%), ARF (5%), pulmonary edema (10%), subcapsular liver hematoma (1.6%)
Steroid Theraphy - controversial
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Differential Diagnosis of Microangipathic Syndrome During Pregnancy
The Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003
Brain
Common SubjectifHeadache, visual disturbance - associated convulsion (eclampsia)
Anatomical pathologyGross hemorrhage - severe hypertension
These complications in women with underlying chronic hypertension
Postmortem cerebral lesionEdema, hyperemia, focal anemia, thrombosis, hemorrhage.
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Brain
Neuroimaging studyCT
All women with eclampsia have abnormal brain finding
Hypodense cotical area – petechial hemorrhage and infarction site (at autopsy)
MRIDescribed remarkable changes in the posterior Cerebral artery area.
25% of women with eclampsia have areas of cerebral infarction
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
MRIs performed 6 weeks after delivery complicated by eclampsia
Magnetic Resonance Imaging
Brain
Cerebral Blood FlowEclampsia loss of autoregulation of cerebral blood flow (Apollon, 2000)
Hyperperfusion similar in hypertensive encephalopathy.
Increased cerebral perfusion headache.
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
BrainBlindness
It rare with preeclampsia alone
It follow eclamptic convulsions in up 10% of women
Develop up to a week or more following delivery (Chambers and Cain, 2004)
Vasogenic edema of occipital lobe on MRI and CT
Permanent visual defect, including blindness caused by Cerebral infarction (retinal artery ischemia) (Moseman and Shelton,2002)
Retinal detachment may also altered vision
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
BrainCerebral Edema
SubjectifLetharge, confusion, blurred vision to obtundation and, coma
Mental status change correlated with brain involvement seen with CT and MRI studies
Sudden severe blood pressure elevatoinsVasogenic edema
Blood pressure control.
ElectroencephalopgraphyReported that 75% of 65 women with eclampsia had abnormal finding within 48 hours of seizure.
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Uteroplacental perfusion
Vasospasm Placental perfusion from vasospasm increases perinatal mortality and morbidity
MeasurementSpiral artery 500μm (normal), 200 μm (preeclampsia)
Placental blood flowInaccesibility, complexity, and unsuitablity
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Uteroplacental Perfusion cause Hypertension
http://hyper.ahajournals.org/cgi/content/full/38/3/718
Uteroplacental Perfusion
Doppler
Doppler measurement of blood velocity through uterine
artery estimate uteroplacental blood flow
Vascular resistance is estimated by comparing arterial
systolic and distolic velocity waveforms
Abnormal waveforms fetal indication required sectio
cesarean
HELLP syndrome 18-36% abnormal waveforms
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Fetal Velocity Waveforms
Medical Physiology Lippincott Williams & Wilkins, 2nd edition 2004
Diagnosis
Etiology
Pathogenesis
Pathophysiology
Prediction and Prevention
Management
Index
Prediction and Prevention
PredictionLots of attemption to predict preeclampsia in early pregnancy poor sensitivity, poor positive predictive value
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Roll over testHypertensive respone induce by having women at 28 to 32 weeks
Lying laterally Recumbent position supine position
Hypertension abnormal
Positive predictive value (true positive) : 33% (Dekker, 1990 ; Friedman and Lindhemier, 1999)
Prediction (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
FibronectinEndothelial cell activation elevated serum cellular fibronectin level (Brubaker, 1992)
Clinical study, Paarlberg (1998)Low sensitivity: 69%
Positive predictive value: 12%
Clinical study, Chavarria (2003)16 weeks - 20 weeks, 378 low-risk nulliparas
Positive predictive value: 29%
Negative predictive value: 98%
Prediction (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Oxidative StressLipid peroxides level increases descreases antioxidants activity preeclampsia prediction (Walsh, 1994)
MarkerLipid peroxides: malondialdehyde
Pro-oxidants: iron, transferrin, ferritin, blood lipids, Trigliseride, free fatty acid, lipoproteins, Vit C & E
HyperhomocysteinemiaAtherosclerosis risk factor (non pregnant)
Around mildpregnancy with elevated serum homocysteine had risk of preeclampsia (D’Anna, 2004; Hietala, 2001)
Prediction (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
CytokinesReleased by vascular endothelium and leukocytes
Over 50 cytokine are elevated in preeclampsia
Interleukin and TNF -
Cascade of markers (C-reactive protein) elevations in preeclampsia
Not sufficiently predictive (Savvidou, 2002)
Prediction (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Placental PeptideThe inflamatory cascade placenta producing peptide markers for prediction of Preeclampsia
Placental peptide:Corticotropin-rh, Chorionic gonadotropin, activin A and inhibin A (Aquilina, 1999; Cuckle 1998)
Activin A and Inhibin A were increased markedly in preeclampsia (keelan and colleagues, 2002)
Activin A and Inhibin A reported significant overlap in normotensive and preeclampsia (Grobman and Wang, 2002)
Prediction (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Fetal DNAIdentification of Fetal DNA in marternal serum prediction of preeclampsia (Zhong, 2001)
Endothelial activation and inflammation occur, fetal cells and cellular material maternal circulation.
Prediction (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Uterine Artery Doppler VelocimetrySecond trimester - uteroplacental vacular resistance (by doppler of uterine artery)
Basic conceptsImpaired trophoblastic invasion of the spiral arteries uteroplacental blood flow descreases
Bower (1993)Sensitivity: 78%
Positive predictive value: 28%
Prediction (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Prevention
Dietary ManipulationSalt restriction ineffective (Knuist, 1998)
Prenatal Ca supplementation significant reduction in Blood Pressure and incidence of preeclampsia (Brucher, 1996)
But, Levin, (1997) 4600 nulliparas calcium and placebo preeclampsia or gestational hypertension incidence was similar in each group.
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Low dose aspirin60 mg aspirin reduce the incidence of preeclampsia: selective TXA2, dominence of endothelial prostacyclin (Hauth, 1998, Wallenburg, 1986)
Caritis, 1998; CLASP Collaborative Group, 1994; Hauth, 1993, 1998; Rotchell, 1998; Sibai, 1993a
Low-dose aspirin was ineffective in preventing preeclampsia
Prevention (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
AntioxidantsDavidge, 1992
Markedly reduced antioxidant activity in preeclampsia women.
Chappel, 1999283 high risk women
18 - 22 weeks, Vit C and E versus placebo
Significant reduction in preeclampsia (11%-17%)
Prevention (Continued)
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
Diagnosis
Etiology
Pathogenesis
Pathophysiology
Prediction and Prevention
Management
Index
Management
Basic management objective for any pregnancy complicated by preeclamsia are:1. Termination of pregnancy with the least
possible trauma to mother and fetus.
2. Birth an infant who subsequently thrives
3. Complete restoration of health to the mother
Williams Obstetric 22 edition, Chapter 34: Hypertensive Disorders in Pregnancy
ReferensiWilliams Obstetric 22 Edition, Chapter 34: hypertension disorders in pregnancyThe Texbook’s Kidney Disease and Hypertension in Pregnancy, 2003Dewhurst's Textbook of Obstetrics and Gynaecology 7th Edition
Medical Physiology Lippincott Williams and Wilkins, 2nd edition 2004
http://hyper.ahajournals.org, 2002. Pathophysiology of Hypertension During Preeclampsia Linking Placental Ischemia With Endothelial Dysfunction.
The Journal of Clinical Endocrinology & Metabolism, 2003. Endothelial Cells and Peripheral Blood Mononuclear Cells Are a Potential Source of Extraplacental Activin A in Preeclampsia.