高血压英文ppt精品课件pregnancyinduced

Pregnancy Induced Hypertension Dr. H. Mansouri FRCS Canada Significance : Hypertensive disease in pregnancy: 12- 22% Preeclampsia: 5-8% Chronic hypertension: 5% Directly responsible for 17.6% of maternal deaths in the United States Classification o The National High Blood Pressure Education Program Working Group: 1. gestational hypertension replace PIH 2. Preeclampsia 3. Eclampsia 4. Preeclampsia superimposed on chronic hypertension 5. Chronic hypertension Definitions Gestational hypertension: oBP 140/90 for first time during pregnancy oNo proteinuria oBP return to normal =140 mmHg Diastolic blood pressure =90 mmHg o Severe: Systolic blood pressure =180 mmHg Diastolic blood pressure =110 mmHg o Use of antihypertensive medications before pregnancy o Onset of hypertension before 20th week of gestation o Persistence of hypertension beyond the usual postpartum period Severe PET Preeclampsia is considered severe if one or more of the following criteria is present: o Blood pressure of 160 mm Hg systolic or higher or 110 mm Hg diastolic or higher on two occasions at least 6 hours apart while the patient is on bed rest o Proteinuria of 5 g or higher in a 24-hour urine specimen or 3+ or greater on two random urine samples collected at least 4 hours apart o Oliguria of less than 500 mL in 24 hours o Cerebral or visual disturbances o Pulmonary edema or cyanosis o Epigastric or right upper-quadrant pain o Impaired liver function o Thrombocytopenia o Fetal growth restriction Risk factors o First pregnancy o Multifetal gestations o PET in previous pregnancy o chronic hypertension o Pregestational diabetes o Vascular &connective tissue disease o Nephropathy o Antiphospholipid syndrome o Age 35 y or older o Role of genetics &environmental factors Etiology Endothelial activation: o m vascular disease o Faulty placentation: genetic, immunologic or inflammatory factors o Excessive trophoblast All these lead to reduced uteroplacental perfusion which can lead to endothelial activation Endothelial activation: will lead to: vasospasm capillary leak activation of coagulation Pathophysiology oAbnormal trophoblastic invasion of uterine vessels oImmunological intolerance between maternal & fetoplacental tissues. oMaternal maladaptation to cardiovascular or inflammatoy changes of normal pregnancy. oDietary deficiencies oGenetic influences. Pathogenesis o Vasospasm o Endothelial cell activation: center-piece in pathogenesis. unknown factors provoke activation & dysfunction of vascular endothelium. Damaged or activated endothelial cells secrete substances that promote coagulation &increase sensitivity to vassopressors : prostaglandins, nitric oxide, endothelins, angiogenic factors-vascular endothelial growth factor (VEGF),& placental growth factors (PIGF). Pathophysiology o Vascular changes : 1. intense vasospasm due to interaction of various vasoactive agents: prostacyclin, thromboxane A2,nitric oxide, & endothelins. 2. Hypervolemia of normal pregnancy not develop 3. Contraction of intravascular space 4. Capillary leak 5. hemoconcentration continued o Hematologic changes: 1. thrombocytopenia 2. hemolysis 3. HELLP syndrome 4. hemoconcentration 5. Elevated LDH continued Hepatic changes: 1. elevated liver enzymes 2. hyperbilirubinemia 3. hepatic hemorrhage. 4. subcapsular hematoma 5. hepatic rupture 6. abdominal pain 7. high mortality continued HELLP syndrome: in 20% of women with severe PET increased risk of adverse outcome Neurologic & cerebral manifestations oEclampsia oIntracranial hemorrhage oTemporary blindness oHeadache blurred vision oScotomata ohyperreflexia Continued o Renal changes: 1. the normal expected increase in GFR & renal blood flow not occur 2. oliguria 3. acute tubular necrosis 4. acute renal failure Continued Fetal changes: impaired uteroplacental blood flow or placental infarction: o intrauterine growth restriction o oligohydramnios o placental abruption o nonreassuring fetal status Prediction & Prevention o Uric acid:33% positive predictive value o Roll-over test: positive predictive value :33% o Fibronectin: low sensitivity69% &positive predictive value 12% o Coagulation activation:platelets,PAI-1and2 increased- decreased fibrinolytic activity o Oxidative stress: increased lipid peroxides, decreased antioxidants. Marker of oxidative stress-malondialdehyde. homocysteine o Cytokines o Placental peptides o Fetal DNA o Uterine artery Doppler velocimetry Prevention oDietary manipulation: salt restriction: ineffective calcium supplementation: no difference fish oil capsules: modify abnormal prostaglandin balance - ineffective oLow-dose Aspirin: ineffective oAntioxidants: vitamin C,E Management o Early prenatal detection o Newly diagnosed: admit to evaluate severity o BP q 4h, daily weight. o Detailed examination ,observe for new symptoms. o Investigation: CBC, U&Es, LFT. Frequency according to severity o Evaluation of fetal size & AFV o Bed rest Further management depends on: oSeverity oGestational age oCondition of cervix Continued Delivery is the CURE of preeclampsia Continued oMild: conservative until term, spontaneous or induce if cervix is favorable oSevere: anticonvulsants, antihypertensives