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妊娠期高血压疾病

2012-06-14 49页 ppt 3MB 202阅读

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妊娠期高血压疾病nullHypertensive Disorders in PregnancyHypertensive Disorders in PregnancyTeng YinCheng Shanghai Jiaotong University Affiliated Sixth People's Hospital, Dept of Obs & GynContentsContentsIncidence and Risk FactorsIncidence and Risk FactorsIncidence Commonly about 5...
妊娠期高血压疾病
nullHypertensive Disorders in PregnancyHypertensive Disorders in PregnancyTeng YinCheng Shanghai Jiaotong University Affiliated Sixth People's Hospital, Dept of Obs & GynContentsContentsIncidence and Risk FactorsIncidence and Risk FactorsIncidence Commonly about 5 percent Markedly influenced by parity Related to race and ethnicity—A genetic predisposition Main Risk Factors Nulliparous (初产妇) Multiple pregnancy History of chronic hypertension Maternal age over 35 years Obesity Lower socioeconomic status …Etiology and PathogenesisRoberts, J. M. et al. Hypertension 2005;46:1243-1249 Used with permissionTwo-stage model of the pathophysiology of preeclampsiaStage 2 develops in some, but not all women with stage 1Etiology and PathogenesisEtiology and PathogenesisEtiology and PathogenesisNormal: vessel remodeling (血管重铸) of the decidua and myometrium transforming into large-capacitance, low-resistance vesselsPreeclampsia: incomplete remodeling limited to the superficial decidua myometrial segments remain narrow Faulty Placentation (胎盘形成不良)---Stage InullnullEtiology and PathogenesisEtiology and PathogenesisOxidative distress (氧化应激) Incomplete vessel remodeling → Reduced placental perfusion → placenta ischemia(缺血) and hypoxemia(缺氧) → Oxidative distress → Endothelia dysfunction → affected production of Nitric Oxide/ Prostaglandins(前列腺素) Other factors Immune system dysfunction Genetic predisposition MalnutritionPathogenesis of preeclampsiaPathogenesis of preeclampsiaPhysiopathology ------ sgage IIPhysiopathology ------ sgage II Basic change: System Vasospasm (全身小动脉痉挛)PhysiopathologyPhysiopathologyClinical manifestationClinical manifestationHypertension Edema Proteinuria Severe cases Headache blurred vision nausea, vomit right upper quadrant pain seizure (抽搐) Usually occurs after 20 gestational weeksWHAT LINKS STAGE 1 & 2?WHAT LINKS STAGE 1 & 2?Theory exploration: Genetics/Abnormal lipid metabolism Endocrine dysfunction InflammationNot all women with reduced placental perfusion develop preeclampsia… Not all women with reduced placental perfusion develop preeclampsia… What links stages 1 and 2? Reduced placental perfusion must interact with maternal factors to result in preeclampsia.Stage 1???Stage 2Roberts, J.M., Gammill H.S. (2005)Diverse manifestations are possible: maternal and fetal/placental factors may vary in proportion.Diverse manifestations are possible: maternal and fetal/placental factors may vary in proportion. In a woman with many predisposing factors, even a minor reduction in placental perfusion is sufficient for stage 2 to develop. In a woman with few predisposing factors, a profound reduction in placental perfusion may be required for preeclampsia to develop. Roberts, J.M., Gammill H.S. (2005)Predisposing factorsReduced placental perfusionMicrosoft Office 2000Could maternal genetics play a role in the link between stage 1 & 2?Could maternal genetics play a role in the link between stage 1 & 2?Stage 1Stage 2GeneticsWhat do we know? What do we know? We know that abnormalities in lipid metabolism have a genetic basis. We have learned that preeclampsia is characterized by profound lipid abnormalities such as hypertriglyceridemia… Gratacos, E. (2000) Microsoft Office 2000Could abnormal lipid metabolism be a genetic factor linking the stages of preeclampsia? Could abnormal lipid metabolism be a genetic factor linking the stages of preeclampsia? Stage 1Stage 2Abnormal lipid metabolismPreeclampsia is characterized by metabolic abnormalities similar to those present in atherosclerosis:Preeclampsia is characterized by metabolic abnormalities similar to those present in atherosclerosis:Hypertriglyceridemia Reduced HDL cholesterol Predominance of small-dense LDL cholesterol which have an increased potential to cause endothelial cell damage as compared to larger, more buoyant LDL’s. Gratacos E., 2000. nullStage 1 Abnormal lipid metabolism Stage 2In the presence of oxidative stress and inflammation, susceptible small-dense lipoproteins may be more easily oxidized, triggering Stage 2, maternal disease. + Oxidative Stress+ InflammationGratacos E., 2000 Most of the suggested linkages could contribute to or be stimulated by oxidative stress.Most of the suggested linkages could contribute to or be stimulated by oxidative stress.Oxidative stress is proposed as relevant to many diseases. Evidence supports the presence of oxidative stress in preeclampsia: Protein products of oxidative stress present in maternal and fetal tissues Antibodies to oxidatively modified LDL’s present in maternal and fetal tissues Concentrations of certain antioxidants reduced in preeclamptic women. Roberts, J.M., Gammill H.S. (2005)In summary:In summary:Hypertriglyceridemia and predominance of small-dense LDL’s prior to pregnancy could be one predisposing factor for developing preeclampsia. Oxidative stress and inflammation may trigger the maternal disease. Gratacos E., (2000) Microsoft Office 2000Could endocrine dysfunction be a factor linking Stage 1 and Stage 2?Could endocrine dysfunction be a factor linking Stage 1 and Stage 2?Stage 1Stage 2Endocrine dysfunctionThere is growing evidence suggesting that preeclampsia may be an early manifestation of the “metabolic syndrome”: There is growing evidence suggesting that preeclampsia may be an early manifestation of the “metabolic syndrome”: elevated triglyceride levels hyperinsulinemia insulin resistance relative glucose intolerance elevated blood pressure These factors have been linked to the development of preeclampsia.Innes, K., Weitzel, L., Laudenslager, M. (2005) Studies have repeatedly demonstrated that metabolic abnormalities precede the clinical signs of preeclampsia:Studies have repeatedly demonstrated that metabolic abnormalities precede the clinical signs of preeclampsia:Insulin resistance and associated hyperinsulinemia Glucose intolerance Hypertriglyceridemia This suggests that insulin resistance and dyslipidemia may be factors involved in the development of preeclampsia.Innes, et al. (2005)Similarities between the risk factors for preeclampsia and cardiovascular disease include:Similarities between the risk factors for preeclampsia and cardiovascular disease include:Insulin resistance Dyslipidemia- decreased HDL levels and elevated triglyceride levels These risk factors are thought to play a causal role in the development of endothelial dysfunction, a characteristic feature of preeclampsia and cardiovascular disease. Innes, et al. (2005) Future implications:Future implications: Studies have demonstrated that women with a history of preeclampsia are at increased risk of developing cardiovascular disorders later in life. Women with preeclampsia who deliver preterm or with recurrent preeclampsia are at greatest risk. Women with preeclampsia have an approximate doubling of risk death from cardiovascular disease. These findings suggest that pregnancy may constitute a metabolic and vascular stress test which reveals a woman’s health in later life. Identification of maternal factors provides specific targets for prevention of preeclampsia in “at-risk” women. Innes, et al. (2005) Roberts, J.M., Gammill H.S. (2005) Could inflammation be a factor linking Stage 1 and Stage 2?Could inflammation be a factor linking Stage 1 and Stage 2?InflammationStage 1Stage 2null“Preeclampsia is associated with an excessive inflammatory response compared with normal pregnancy.” In a study done by Braekke, et.al (2005) inflammatory markers (calprotectin, CRP) were evaluated in maternal and fetal serum and amniotic fluid. Braekke, K., Holthe, Ml, Harsem, N., Fagerhol, M., Staff, A., 2005Inflammatory Markers:Inflammatory Markers:Calprotectin: Is a protein released by activated neutrophils C-reactive protein (CRP): Is a protein produced by the liver Production is stimulated by inflammatory cytokines Braekke, K. et. al. (2005)Microsoft Office 2000Calprotectin and C-reactive protein (CRP), markers of inflammation, are elevated in preeclampsia.Calprotectin and C-reactive protein (CRP), markers of inflammation, are elevated in preeclampsia.The concentration of calprotectin in the maternal plasma of preeclamptic women was higher than in the control group (normal pregnant women). No statistically significant difference in calprotectin levels was noted between women with mild and severe preeclampsia Braekke, K. et al. (2005)C-reactive protein:C-reactive protein:Has been used to evaluate low-grade inflammation as a cardiovascular risk factor Braekke et al. 2005Microsoft Office 2000CRP levels in the maternal plasma of pregnant women:CRP levels in the maternal plasma of pregnant women: Correspond to a low-grade inflammation in preeclampsia and in normal pregnancy. Braekke et al. 2005 Microsoft Office 2000No inflammatory response was noted in the fetal circulation.No inflammatory response was noted in the fetal circulation. Concentrations of calprotectin in both arterial and venous umbilical plasma, and amniotic fluid were much lower than in maternal plasma CRP levels in fetal circulation were 1/100 of maternal CRP levels. Braekke et al. 2005 Theoretically,Theoretically,“Calprotectin concentrations could play a role in the pathophysiology of preeclampsia through augmented placental cell death or reduced trophoblast invasion (stage 1)”Braekke et al. 2005What stimulates the inflammatory response (activates the neutrophils) in preeclampsia?What stimulates the inflammatory response (activates the neutrophils) in preeclampsia?Researchers have been unable to determine why or exactly where the neutrophils become activated. Maternal or placenta factors triggering maternal inflammation do not appear to be transferred into the fetal circulation. Braekke et al. 2005 Future implications:Future implications:Further research is needed to evaluate the role of calprotectin in pregnancy or pregnancy complications. Will calprotectin concentrations be used to predict preeclampsia before the onset of clinical symptoms or as a marker of the clinically established disease? Braekke et al. 2005 ClassificationClassificationGestational Hypertension BP ≥ 140/90 mmHg for first time during pregnancy No proteinuria BP return to normal < 12 weeks’ postpartum Final diagnosis made only postpartum(产后) Preeclampsia BP ≥ 140/90 mmHg after 20 weeks’ gestation Proteinuria 300 mg/24 hours or ≥ 1+ dipstick Eclampsia Seizures that cannot be attributed to other causes in a woman with preeclampsiaClassificationClassificationPreeclampsia Superimposed on Chronic Hypertension New-onset proteinuria ≥ 300 mg/24 hours in hypertensive women but no proteinuria before 20 weeks’ gestation A sudden increase in proteinuria or blood pressure or platelet count < 100×109/L Chronic Hypertension in Pregnancy BP ≥ 140/90 mmHg before pregnancy or diagnosed before 20 weeks’ gestation Or Hypertension first diagnosed after 20 weeks’ gestation and persistent after 12 weeks’ postpartumDiagnosis Diagnosis History Hypertension Proteinuria Edema Assistant examinationDiagnosis of severe preeclampsiaDiagnosis of severe preeclampsiaManagementManagementPrinciples Sedation(镇静) Antihypertension (降压) Antispasm (解痉) Diuresis (利尿) Termination of pregnancyManagementManagementGeneral management Bed rest Frequent fetal and maternal monitoring Sedation Diazepam (地西泮,安定) Hibemation (冬眠药物) pathidine派替啶, chlorpromazine氯丙嗪 promethazine异丙嗪ManagementManagementAntispasm(解痉) : To prevent seizures Magnesium sulfate (硫酸镁) Mechanism Dose regimen loading dose : 5 g, 5-10 minutes continuous infusion: 20 -25 g, 1-2 g/hour total daily dose: 25-30 g Toxicity: Mg++ Therapeutic effective concentration: 1.7~3 mmol/L Minimum toxic concentration: > 3 mmol/L Notes: knee reflex, respiratory rates, urine flowManagementManagementAntihypertension To prevent maternal cerebrovascular complications Labetalol: 拉贝洛尔 α,β -adrenaline receptor blocker Nifedipine: 硝苯地平 calcium channel blocker Hydrelazine: 肼屈嗪 ACE (angiotensin-converting enzyme inhibitors): 血管紧张素转换酶抑制剂, contraindicated (禁用)ManagementManagementDiuresis (利尿) Indication Generalized edema Acute heart failure Pulmonary edema Plasma volume expansion (扩容治疗) Indication Severe hypoproteinemia AnemiaManagementManagementDelivery– an ultimate treatment Timing maternal safety fetal safety (premature) Indications Delivery methods Vaginal delivery: induced labor Cesarean section (剖宫产)Management of eclampsia Management of eclampsia General care Control seizure: MgSO4, Diazepam (安定), mannitol (甘露醇) Supply of oxygen Anti-acidosis (纠正酸中毒) Anti-hypertension Delivery: 2 hours after seizure controlled Thank you!Thank you!
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