新生儿缺氧缺血性脑病课件

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Hypoxic-ischemicencephalopathy(HIE)新生儿缺氧缺血性脑病Children’sHospitalofChongqingMedicalUniversityProf.JialinYu OutlineNeonatalasphyxia→oxygen-poor→ischemia→braininjuredinperinatalperiodCurrentlybirthtrauma↓，O2deficiency&asphyxia↑Severeconsequence：neonataldeathorchildrendisablement,oneofreasonofcerebralpalsyinchildrenhood.Commoninfulltermbb,alsoinpremature causesmothersfetusantepartumintrapartumpostpartum20％35％35％10％hypoxiaPlacenta&umbilicalcordAnte-&intrapartum CausesofHIEalsocausesofasphyxia:Maternalfactors：illnesses，obstetricdeseases，smokingordrugaddiction,teenagepregnancies,olderthan35yearsIntrapartumfactors：umbilicalcore，malposition,placentalinsufficiency,placentalabruptionFetalfactors：congenitalanomalies,IUGR，hydropsfetalis，intrauterineinfectionInfantfactors：apnea,HMD,MAS,PPHN,shock. EtiopathogenesisofHIECerebralbloodflow(CBF)：1.failincompensation：2stepsofredistribution DivingreflexThefirsttime---skinAdrenalglandMaintainCBFbutleadtomultiorganicdamage, SecondaryredistributionAnteriorcerebralartery,ACAmiddlecerebralartery,MCAPosteriorcerebralartery,PCA BranchofACABranchofMCABranchofPCA terminfant：皮层矢状旁区受损preterminfant：脑室周围的白质区受损Consequenceofsecondaryredistribution 脑室旁白质软化periventricularleukomalacia,PVL Suddenly&completelyasphyxia2.Non-compensation：ganglion-brainstemdamageCerebralbloodflow(CBF)： 3.autoregulation↓→Pressure-passivecerebralcirculation(PPCC)Cerebralischemia,HIEBrainedemacerebralhemorrhageBPCBFPPCCCerebralbloodflow(CBF)： Changeofbrainmetabolism:1.oxygenfreeradicals→ruptureofcellmembranedestroyBBB(1)overproduction：cytochrome-oxydase↓；reperfusion：xanthineoxidase↑hypoxanthine----------------→urea+oxyradicals(2)removenotenough：超氧化物歧化酶（SOD）↓ Changeofbrainmetabolism:2.imbalanceofNa&Ca：anaerobicglycolysis→lacticacid↑,ATP↓→pumpoutoforder→Ca++inflow→chaosofsignal→Na++inflow→intra-cellularedema3.excitableneurotransmitter:glutamicacid；β-opioidpeptide neuropatholgy：脑细胞水肿(edema)脑细胞坏死(necrosisofbraincells)脑细胞凋亡(apoptosis）commonlyoccurafter6-24h,keepinseveraldaystowkspromptlyinterventioncoulddecreasedamageCelldeathprimarilyneuronnecrosisdelayedneuroninjuretime Clinicalmanifestationhistory：asphyxianervoussystem：basic:consciousdisturbance,tensionofmuscle,primitivereflexsevere：convulsions,bulgefontanel,irregularrespiration,pupilsdisorder CriteriaofSarnatgradesforHIEMild：alert,irritable,buthasnormaltoneandnoseizuresModerate：lethargic,hypotonic,oftenhasseizuresSevere：stuporousorcoma,flaccidorlimp,oftenapneic,withpersistentseizures Attention:部分患儿在宫内已发生HIE,出生时Apgar评分正常,多脏器受损不明显但生后数周或数月逐渐出现神经系统受损症状。 investigationultrasound：水肿，实质病变，脑室，脑血流速度及指数等CT：CTvalue<20huaslowdensityMRI：可判断矢状旁区丘脑、基底节梗死等MRS(spectroscopy):可检测高能磷酸代谢物的相对浓度，便于判断预后 investigationsElectroencephalogram(EEG):--maybenormalduringfirstfewday--poorprognosis:suppressedorfrequentseizureactivity investigationsImagingassessment:--cranialultrasound--brainCTscan--MRIandspectroscopy HIE辅助检查脑电图：判断病情、预后及对惊厥的鉴定血生化：肌酸磷酸激酶同工酶（CPK-BB）、神经元特异性烯醇化酶(NSE)最好生后24小时内采血血气、血糖等 diagnose：Historyofasphyxiamanifestationofnervousdisorderinvestigation objective1.增强代偿性生长2.建立新的神经网络3.纠正错误的传导与支配treatment 发育中脑的可塑性Plasticityduringgrowthofbrain树突增长、增多Dendronsgrowinlengthandnumber轴突延伸Axonselongation突触增加Increasesynapse建立新的神经传导回路Rebuildloopsofnerveconduction——代偿性生长----compensationgrowth Hypoxic-ischemianecrosisneuronsdamage&apoptosiscellbodydendron&axonneuralnetworksynapsegliocytestrauma(microenvironment) 国家“九五”攻关项目简介：（治疗方案于1999.9南京全国第九届围产新生儿研究第12次会；1999.10大连第五届全国新生儿学术会上讨论并修改）治疗原则therapeuticprinciple：早治early阶段stage综合combination足程enoughcourse信心confidence Within3dofage(criticalperiod)4-10dAfter10dAfterneonatalperiod4stagesofHIE within3d：purpose：stabilizeinternalenvionment&controlnervoussymptom1、三项支持疗法：血气bloodgas血循环circulation血糖bloodsugar within3d：2、三项对症处理：控制惊厥：phenobarbital,diazepam降颅压：furosemide,mannitol消除脑干症状：纳络酮naloxone指征indication：①severeHIE②pupildisorder③shock④frequentconvulsion3．improvemetabolismofcells：cerebrolysin,胞二磷胆碱citicoline,复方丹参Salviamiltiorrhizahyperbaricoxygenation 4-10dofage：purpose:4-5d开始好转，7-9d明显好转method:improvemetabolismofcellsAfter10d：巩固疗效，防止后遗症purpose:Consolidatetherapeuticeffect&preventesequelaemethod:ifneonatalbehaviornervousassessment(NBNA)<351.促神经细胞代谢2.新生儿期干预intervention Afterneonatalperiod:NBNA<35，DQ<85,继续治疗3-6月 治疗展望:针对发病机理的药物——硫酸镁*扩血管降压治疗妊娠高血压综合征的传统药物*减少脑瘫*可能机理钙离子拮抗剂改善脑循环阻断NMDA受体 亚低温治疗*降低脑代谢率脑部温度下降1℃，脑的代谢率可降低5％*安全性头部温度降低至34℃，体部温度为34.5℃，未发现脏器损害*效果发病6小时内持续72小时 神经营养作用内源性神经营养因子（neurotrophicfactot,NF）、神经生长因子(neurogrowthfactors,NGF)鼠源性神经生长因子（商品名：恩经复)神经节苷脂(促进神经细胞可塑性) 干细胞移植干细胞：一类具有复制能力的多潜能细胞，在一定条件下可分化为多种功能的细胞。“种子”体外体内定向诱导修复取代基因修饰病变组织 谢谢您的兴趣