1、病 例,张平，女，36岁，以“停经九个月，胎动五个月，双下肢浮肿两周，头晕眼花一小时。”为主诉入院。早孕反应及胎动如期出现，两周前无明显诱因双下肢浮肿，休息后无好转。一小时前出现头晕眼花。既往无高血压，慢性肾炎病史。查体：T36.7，P78次/分，BP175/110mmHg, 心肺听诊无异常，腹膨隆，足月腹型，LOA，浮肿+。实验室检查：血常规示PL258G/L，HGB108g / L，HCT0.45。尿常规示蛋白+。辅助检查：B超示BPD9.0cm，FL7.2cm，胎盘钙化级。NST有反应型。,Hypertensive disorder complicating pregnancy,妊娠期高
2、血压疾病,Preeclampsia Preeclampsia is defined as the combination of high blood pressure (hypertension), swelling (edema), and protein in the urine (albuminuria, proteinuria) developing after the 20th week of pregnancy.,Mild preeclampsia is characterized by a systolic BP greater than 140 mm Hg or a diast
3、olic BP greater than 90 mm Hg in a pregnant patient with minimal proteinuria(300mg/d )and pathologic edema. Severe preeclampsia A systolic BP greater than 160 mm Hg or a diastolic BP greater than 110 mm Hg with significant proteinuria (5.0 g/d) and evidence of end-organ damage. Serum creatinine106mo
4、l/L, Platelet:100x109/L elevated LDH, ALT or AST,Risk factors extremes of maternal age, primigravida, multiple gestations, molar pregnancy, diabetes mellitus (DM), renal disease, connective tissue disease, vascular disease, prior history of preeclampsia or eclampsia, and family history of preeclamps
5、ia or eclampsia.,The fetus is a semi-allograft to the mother. Immune interaction between decidual leukocytes and invading cytotrophoblast cells is essential for normal trophoblast invasion and development. Immune maladaptation may cause shallow invasion of spiral arteries by endovascular cytotrophob
6、last cells and endothelial cell dysfunction mediated by an increased decidual release of cytokines, proteolytic enzymes, and free radical species.Genetic gactor Development of preeclampsia-eclampsia may be based on a single recessive gene or a dominant gene with incomplete penetrance. Penetrance may
7、 be dependent on fetal genotype. The possibility of genetic imprinting should be considered in future genetic investigations of preeclampsia.,preeclampsia is a disease of first pregnancies. The protective effect of multiparity, however, is lost with change of partner. Also, exposure to semen provide
8、s protection against developing preeclampsia. Analogous to altered paternity, artificial donor insemination and oocyte donation are reported to result in a substantial increase of preeclampsia. Thus, epidemiologic studies strongly suggest that immune maladaptation is involved in the etiology of pree
9、clampsia.,Normal placental development involves progressive loss of the musculoelastic tissue in the spiral arteries that feed the vessels of the intervillous spaces, which results in uterine blood flow increases of nearly 25% during the first trimester. In women destined to develop preeclampsia, th
10、is physiologic dilatation of the spiral arteries does not occur because the placental trophoblast cells do not invade the spiral arteries. In severe cases, other pathologic changes also occur. Accumulation of fat-laden macrophages with fibrinoid necrosis (ie, acute atherosis), disruption of the base
11、ment membranes, platelet deposition, mural thrombi, and proliferation of intimal and smooth muscle cells all decrease the luminal diameter. The narrowed and damaged spiral arteries become thrombosed, resulting in placental infarction and necrosis. Uteroplacental blood flow then is reduced by 50-75%.
12、 The anatomical reduction in blood flow may be complicated by vasospasm of the uteroplacental bed. Decreased placental perfusion is thought to lead to fetoplacental ischemia. The ischemic placenta may produce a circulating agent, which is currently unidentified but causes the widespread dysfunction
13、of the maternal vascular endothelium that leads to the systemic manifestations of preeclampsia,Pathophysiologic changes,Pathological deterioration of function I a numner of organs and systems has been identified as a consequence of Generalized vasospasm,Pathologic changes in main organs ,Brain : bli
14、ndnesscerebral edemacerebral hemmorage cardiovascular changeincreased cardiac after loadmyocardial ischemia,edemapulmonary edema,Pathologic changes in main organs ,Liver : periportal hemorrhagic necrosis（门脉周围出血坏死） kidneys :endothelial edema of glomerulus placenta : atherosclerosis low placental perf
15、usion,Blood volume: hemoconcentration Hematological changesthrombocytopenia endocrine and metabolic changes,diagnosis,History hypertensionproteinuria sign edemasymptom convulsion , comablood examination axillary liver and renal functionsexamination funduscopy of eyesothers,Differential diagnosis,Ess
16、ential hypertension and chronic nephritis convulsive disorders,the screening test : mean arterial blood pressure roll over testblood variationcalcium amount in urine,Management,Gestional hypertension A rest B diet C medication : phnobarbital （苯巴比妥） diazepam（安定）,preeclampsia,A. Hospitalization B. ant
17、ispasm medication magnesium sulfate（硫酸镁） B sedative drugs diazepam C antihypertensive drugs D expansive volume treatment albumin （白蛋白）plasma （血浆） whole blood（全血）,E Diuretics: furosemide （速尿） 20% mannitol （甘露醇） F Termination of pregnancy a indications : b methods : induction of labor （引产） cesarean section（剖宫产） G The management of eclampsia a controlling convulsion b nursing c closely monitoring,Classification of PIH syndrome,
