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妊娠高血压疾病(英)

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妊娠高血压疾病(英) Hypertension Disorders Complicating Pregnancy 妊娠期高血压疾病 Hypertensive Disorders complicating Pregnancy Gestational Hypertension Preeclampsia Preeclampsia Superimposed on Chronic Hypertension Chronic Hypertension Eclampsia A Group of Related Diseases Cha...

妊娠高血压疾病(英)
Hypertension Disorders Complicating Pregnancy 妊娠期高血压疾病 Hypertensive Disorders complicating Pregnancy Gestational Hypertension Preeclampsia Preeclampsia Superimposed on Chronic Hypertension Chronic Hypertension Eclampsia A Group of Related Diseases Characteristics Systemic small arteries spasm Endothelial cell injury Hypertension Proteinuria Multiple organs dysfunction Convulsion Maternal mortality Fetal mortality Gestational Hypertension; Chronic hypertension Eclampsia Preeclampsia; Preeclampsia Superimposed on Chronic Hypertension Hypertension disorders complicating pregnancy Pathophysiology Category and clinical manifestation Diagnosis and differential diagnosis Management and prevention 病理生理 临床 关于同志近三年现实表现材料材料类招标技术评分表图表与交易pdf视力表打印pdf用图表说话 pdf 现 诊断 治疗 Epidemiology Incidence: 6-9% Preeclampsia-eclampsia: 70% Chronic Hypertension : 30% Eclampsia 0.5% - 1% China 1.0% Overseas 0.5% Reflection of medical level The second cause of maternal death (20%) Cause of premature delivery(10%) Unknown origin Pathophysiology Basic pathological changes Spasm of systemic small arteries Vascular endothelial cell injury Pathophysiology fluid protein Hypertension Edema Proteinuria Hemoconcentration Small arterial spasm Endothelial cell injury Multiple organs dysfunction Ischemia Edema malfunction Systemic Disease Brain Hydrocephalus Hyperemia/ischemia Thrombosis cerebral hemorrhage cerebral hernia headache dazzle nausea vomit Hypopsia retinal detachment Cortical blindness Dysesthesia Confusion of thinking Eclampsia convulsion coma brain: Vasospasm permeability↑ kidney renal vasospasm renal blood flow ↓ glomerular filtration rate ↓ pathology : Glomerular expansion swollen vascular endothelial cell cellulose deposition renocortical necrosis——renal irreversible damage clinical manifestation : albuminuria hypoproteinemia renal dysfunction creatinine urea nitrogen uric acid oliguria renal failure liver hepatic vasospasm; hepatic ischemia; hepatic edema liver enlargement; hepatic dysfunction elevated liver enzyme jaundice hypoproteinemia coagulation function changed severe: Periportal necrosis hepatic subcapsularhematoma hepatorrhexis HELLP symdrome: Elevated hepatic enzymes Decreased blood platelet * Cardiovascular System Blood Pressure ↑ Vasospasm Vascular Resistance ↑ Cardiac Load ↑ heart failure vasospasm Myocardial Ischemia Interstitial Edema Spotty Necrosis pulmonary vasospasm Pulmonary Hypertension Pulmonary Edema Oliguria water-sodium retention Relative Blood Volume Excess Iatrogenic Blood Volume Excess High burden Poor ability blood system Relative hypovolemia Anemia Decreased blood platelet Hypercoagulability blood clotting factor↓ placenta-fetus placenta Placental hypoperfusion Spiral arteries sclerosis Placental Infarction Placental Abruption Placental function decreases fetus IUGR fetal distress oligohydramnios fetal death Pathophysiology Brain Headache; visual blurred; coma; hernia Kidney Renal function compromised; proteinuria; renal failure Liver Persistent upper right abdominal pain; Elevated enzyme; jaundice; hematoma; rupture Systematic disease Pathophysiology Cardiovascular system Low output- high resistance; myocardial ischemia; pulmonary hypertension; edema; heart failure Blood Low volume; hypercoagulability; DIC Pathophysiology Uterus and Placenta Low perfusion; placental atherosclerosis Placental infarction; placental abruption; fetal growth retardation; fetal death High risk factors Primipara <18y or >40y Multiple pregnancy Hypertension Chronic nephritis Malnutrition Poor social status Diabetes Anti-phospholipid syndrome Angiotensin gene T235 (+) Etiology Genetic susceptibility hypothesis Immune maladaptation hypothesis Placental ischemia hypothesis Oxidative stress hypothesis Genetic susceptibility Immune maladaptation Placental ischemia Oxidative stress Abnormal placental The change of cytokine PE development Endothelium injured DIC Complications Genetic susceptibility hypothesis Hypertension Immune maladaptation hypothesis Multiple gestation Abortion and blood transfusion Ovum and sperm donation Placental ischemia hypothesis 40% total spiral artery area compared to normal pregnancy Endothelial cell injury Oxidative stress hypothesis Oxidative stress reaction Endothelial cell injury Category and clinical manifestation Gestational hypertension Preeclampsia Eclampsia Chronic hypertension Preeclampsia superimposed on chronic hypertension clinical features typical : hypertension、albuminuria、edema untypical : asymptomatic severe: nausea、vomit headache、dazzle convulsion 、coma chest distress 、palpitation Gestational Hypertension Definition Hypertension occurs 20 weeks after gestation and recovers 12 weeks postpartum SBP>=140mmHg DBP >=90mmHg Diagnosed only after delivery Preeclampsia Hypertention occurs 20 weeks after gestation BP>=140/90mmHg Proteinuria Proteinuria ≥300mg/24h Urine protein (+) Other symptoms Headache, visual blurring Upper abdominal pain Severe preeclampsia At least one of the following features: Central nervous system abnormalities Hepatic subcapsular hematoma / hepatorrhexis Hepatocyte injury :GPT Blood pressure:SBP≥160mmHg,or DBP≥110mmHg Thrombocytopenia: <100109/L Proteinuria: ≥5g/24h or (+++) 4 hours apart Oliguria: <500ml/24h Pulmonary edema Cerebrovascular accident Intravascular hemolysis : anemia, jaundice Coagulation dysfunction Fetal growth restriction / oligohydramnios Severe preeclampsia complications Hepatic subcapsularhematoma Early-onset preeclampsia : <34w HELLP syndrome HELLP syndrome Hemolysis blood smears show RBC debris Hb 60-90g/L TB>20.5μmol/L Elevated serum level of Liver enzymes AST>70u/L, or >3SD LDH>600u/L Low Platelets PLC<100*109/L HELLP Severe preeclampsia : One abnormalities 6% Two abnormalities 12% Three abnormalities 10% 20 gw seldom occur 1/3 occur after delivery 80% diagnosed prenatally HELLP——clinical diagnosis Might be asymptomatic pain in the right upper abdomen 80% weight gain or severe edema 50-60% 20% cases < 140/90 mmHg 6% cases without proteinuria Some investigatiors regard HELLP syndrome as an entirely distinct disease entity from preeclampsia Classification of HELLP By degree of thrombocytopenia: <50,000/mm3 50,000 – 100,000/mm3 >100,000/mm3 Not widely accepted Pathogenesis and epidemic characteristics of HELLP core mechanism endothelial injury——intravascular coagulation dysfunction predisposing factors the white multipara elder pregnant women HELLP--mortality Maternal 0-24% hepatorrhexis DIC Acute renal failure thrombosis cerebrovascular accidents Perinatal 7.7-60% Premature delivery IUGR placental abruption Eclampsia process: tonus convulsion sleepiness coma Occurrence prenatal intrapartum postpartum Chronic Hypertension during Pregnancy Hypertension before pregnancy or Hypertension before 20 weeks’ gestational Unrelieved 12 weeks postpartum Poor fetal outcome Perinatal mortality 3 times  Placental abruption 2 times  FGR, preterm birth  preeclampsia superimposed upon chronic hypertension Chronic Hypertension Before 20 gestational weeks Persist 12 weeks postpartum Proteinuria Before 20w After 20w; with higher BP; thrombocytopenia Differential diagnosis Chronic nephritis complicating pregnancy Renal dysfunction Seizure caused by other reasons Management Principle Sedation Anti-spasm Anti-hypertension Diuresis Terminate pregnancy timely Management Common treatment Rest Monitoring Oxygen inhalation Diet: salt restriction only for anasarca patients Management Sedation Diazepam Hibernation drugs Pethidine Chlorpromazine Promethazine Management Anti-spasm First line treatment for pre-eclampsia and eclampsia MgSO4 Mechanism Regimen ≥25-30g/d Loading dose: 25% MgSO4 10ml +10%GS 20ml iv 5-10min 25% MgSO4 60ml +5%GS 500ml ivgtt 1-2g/h 25% MgSO4 20ml +2%lidocaine 2ml im. Management MgSO4 Treatment concentration 1.7-3mmol/L Toxic concentration >3mmol/L Toxicity Muscular paralysis Prevention and treatment Before treatment Knee reflex (+); R≥16bpm; urine≥5ml/h or 600ml/24h Mg concentration monitoring If something happens… 10% calcium gluconate 10ml iv for detoxification Lower dose or stop use when renal dysfunction Management Antihypertension Indication SBP≥160mmHg, DBP ≥110mmHg, MBP ≥140mmHg Principle No feral toxicity; no lower renal and uterine perfusion Hydralazine — first line Labetalol; calcium channel blocker; methyldopa Sodium nitroprusside----only when unmanageable BP ACEI----contraindicated during pregnancy Management Volumetric dilatancy----only for severe Hypoproteinemia and anemia Diuretic agent----only for severe edema Management Terminate pregnancy Severe pre-eclampsia unrelieved after active treatment for 24-48 hours Severe pre-eclampsia, >34 w Severe pre-eclampsia, <34 w with matured fetus and placental dysfunction Severe pre-eclampsia, <34 w with unmatured fetus and placental dysfunction, terminate after dexamethasone delivery 2h after controlling eclampsia Management Terminate pregnancy Induced labor C-S Prevent postpartum eclampsia Management Eclampsia Control seizure by MgSO4 and 20% mannitol Anti-hypertension Correct acidosis and hypoxia Terminate pregnancy 2 hours after controlling seizure Nursing Management Chronic hypertension Indication SBP>150-180mmHg; DBP>100mmHg; hypertension related organ dysfunction Prevention A well organized health care system A well monitored pregnant period Appropriate diet and rest *
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