儿内科课件 2新生儿缺氧缺血性脑病_第1页
儿内科课件 2新生儿缺氧缺血性脑病_第2页
儿内科课件 2新生儿缺氧缺血性脑病_第3页
儿内科课件 2新生儿缺氧缺血性脑病_第4页
儿内科课件 2新生儿缺氧缺血性脑病_第5页
已阅读5页,还剩41页未读 继续免费阅读

下载本文档

版权说明:本文档由用户提供并上传,收益归属内容提供方,若内容存在侵权,请进行举报或认领

文档简介

Hypoxic-ischemicencephalopathy(HIE)新生儿缺氧缺血性脑病Children’sHospitalof

ChongqingMedicalUniversityProf.JialinYu余加林教授OutlineNeonatalasphyxia→oxygen-poor→ischemia→braininjured

inperinatalperiodCurrentlybirthtrauma↓,O2deficiency&asphyxia↑Severeconsequence:neonataldeathorchildrendisablement,oneofreasonofcerebralpalsyinchildhood.Commoninfulltermbb,alsoinprematurecauses

mothers

fetus

antepartum

intrapartum

postpartum

20%35%35%10%hypoxiaPlacenta&umbilicalcordAnte-&intrapartumCausesofHIE

alsocausesofasphyxia:

Maternalfactors:illnesses,obstetric

deseases,smokingordrugaddiction,teenagepregnancies,olderthan35yearsIntrapartumfactors:umbilicalcore,malposition,placentalinsufficiency,placentalabruptionFetalfactors:congenitalanomalies,IUGR,

hydrops

fetalisInfantfactors:apnea,HMD,MAS,PPHN,shock.EtiopathogenesisofHIECerebralbloodflow(CBF):1.failincompensation:2stepsofredistributionDivingreflexThefirsttime---skin

Adrenalgland

MaintainCBF

butleadtomultiorganicdamage,SecondaryredistributionAnteriorcerebralartery,ACAmiddlecerebralartery,MCAPosteriorcerebralartery,PCABranchofACABranchofMCABranchofPCAterminfant:parasagittaldamageincortex皮层矢状旁区受损preterminfant:periventricular

leukomalacia(PVL)

脑室周围的白质软化Consequenceof

secondaryredistribution脑室旁白质软化periventricular

leukomalacia,PVLBasalganglia

brainstem

cerebellumSuddenly&completelyasphyxia2.Non-compensation:ganglion-brainstemdamageCerebralbloodflow(CBF):3.autoregulation

↓→Pressure-passivecerebralcirculation(PPCC)Cerebralischemia,HIEBrainedemacerebralhemorrhageBPCBFPPCCCerebralbloodflow(CBF):Changeofbrainmetabolism:

1.oxygenfreeradicals→ruptureofcellmembrane

destroyBBB

(1)overproduction:

cytochrome-oxydase↓;

reperfusion:xanthine

oxidase↑

hypoxanthine----------------→urea+oxyradicals

(2)removenotenough:超氧化物歧化酶(SOD)↓Changeofbrainmetabolism:

2.imbalanceofNa&Ca:anaerobicglycolysis→lactic

acid↑,ATP↓→

pumpoutoforder→Ca++inflow→chaosofsignal

→Na++

inflow→intra-cellularedema

3.excitableneurotransmitter:

glutamicacid;

β-opioidpeptideCa++Ca++Ca++Ca++Ca++Ca++Ca++Ca++Ca++Ca++Ca++N-methyl-D-aspartate(NMDA)receptor

SynapticproductionofNeuroexcitatory

Aminoacidesp.GlutamateCa++reperfusioninjuryCa++Neuronalcelloxygenfreeradicalspumppumpexcitableneurotransmitterneuropathology:

脑细胞水肿(edema)脑细胞坏死(necrosisofbraincells)脑细胞凋亡(apoptosis)

commonlyoccurafter6-24

h,keepinseveraldaystowks

promptlyinterventioncould

decreasedamageCelldeathprimarilyneuronnecrosisdelayedneuroninjuretimeafterdamageduotohypoxiaideographofmitochondria

normalmitochondria

Clinicalmanifestation

history:asphyxia

nervoussystem:

basic:consciousdisturbance,tensionofmuscle,primitivereflex

severe:convulsions,bulgefontanel,irregularrespiration,pupilsdisorderCriteriaofSarnatgradesforHIEMild:alert,irritable,buthasnormaltoneandnoseizuresModerate:lethargic,hypotonic,oftenseizuresSevere:stuporousorcoma,flaccidorlimp,often

apneic,persistentseizuresPupilsnormalmydiasismiosisflaccidMuscletoneDecerebraterigidityAttentionsomedamageforHIEhappeninuterusbutnormalApgarscoreatbirthwithnotobviousmultiorganicdamagehowevernervoussymptomsandsignshouldbeappearedinseveralweeksorseveralmonthsafterbirth.investigationsElectroencephalogram(EEG):--maybenormalduringfirstfewday--poorprognosis:suppressedorfrequentseizureactivityinvestigationsImagingassessment:--cranialultrasound

hemorrhage,infarction,edema,cerebraarterybloodflowvelocityinvestigationsImagingassessment:

--brainCTscan

CTvalue<20hu

aslowdensity--

MRI:moredetailinformationsuchas:damageofparasagittalarea,

thalamencephalon,basalganglia,etal.--MRS(spectroscopy):

metabolin

ofhighenergyphosphatesoastojudgeoutcome

investigationsBloodbiochemistry

creatine

phosphokinase

isoenzyme(CPK-BB)

neuronspecific

enolase(NSE)bloodgasbloodsugar

diagnose:HistoryofasphyxiamanifestationofnervousdisorderinvestigationCriteriaofHIE

---onlyfortermbbAbnormalobstetrics,fetaldistress,

intrapartumasphyxiaPostpartumasphyxia:Apgarscore≤3at1min,≤5at5min,umbilicalbldgaspH≤7Nervousmanifestationsoonafterbirthandduration<24hExclude:electrolytedisorder,intracranalhemorrhage,

intrauterineinfections,hereditary&congenitaldiseases

objective

1.compensation

2.establishnewneuralnetwork

3.correctmistakesofconductionandarrangement

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----compensationgrowthHypoxic-ischemia

necrosis

neurons

damage&apoptosis

cellbody

dendron&axon

neuralnetworksynapse

gliocytestrauma(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

confidenceWithin3dof

age

(criticalperiod)4-10dAfter10dAfterneonatalperiod4stagesofHIEwithin3d:

purpose:stabilizeinternalenvionment

&controlnervoussymptom1、三项支持疗法maintenancetherapy:血气bloodgas血循环circulation血糖bloodsugarwithin3d:2、三项对症处理:symptomatictreatment

控制惊厥:phenobarbital,diazepam

降颅压:furosemide,mannitol

消除脑干症状:纳络酮naloxone指征indication:①severeHIE

②pupildisorder

③shock④frequentconvulsion3.improvemetabolismofcells:

cerebrolysin,胞二磷胆碱citicoline,复方丹参Salviamiltiorrhizahyperbaricoxygenation4-10dofage:

purpose:startimprovementin4-5doflife,obviouslyimprovementin7-9d

oflife.method:improvemetabolismofcellsAfter10d:

purpose:Consolidatetherapeuticeffect&preventsequelae

method:ifneonatalbehaviornervousassessment(NBNA)<35

1.促神经细胞代谢improvemetabolismofcells

2.新生儿期干预interventioninneonatalperiodAfterneonatalperiod:

IfNBNA<35,

developmentalquotient(DQ)<85

continuetreatmentfor3-6monthsprospectintreatment:

MagnesiumSulfate*traditionalmedicineinpregnancy-inducedhypertensionsyndrome

*↓cerebralpalsy*why?

antagonofcalciumion(Ca2+)Ca++Ca++Ca++Ca++Ca++Ca++Ca++Ca++Ca++Ca++Ca++N-methyl-D-aspartate(NMDA)receptor

Synapticproductiono

温馨提示

  • 1. 本站所有资源如无特殊说明,都需要本地电脑安装OFFICE2007和PDF阅读器。图纸软件为CAD,CAXA,PROE,UG,SolidWorks等.压缩文件请下载最新的WinRAR软件解压。
  • 2. 本站的文档不包含任何第三方提供的附件图纸等,如果需要附件,请联系上传者。文件的所有权益归上传用户所有。
  • 3. 本站RAR压缩包中若带图纸,网页内容里面会有图纸预览,若没有图纸预览就没有图纸。
  • 4. 未经权益所有人同意不得将文件中的内容挪作商业或盈利用途。
  • 5. 人人文库网仅提供信息存储空间,仅对用户上传内容的表现方式做保护处理,对用户上传分享的文档内容本身不做任何修改或编辑,并不能对任何下载内容负责。
  • 6. 下载文件中如有侵权或不适当内容,请与我们联系,我们立即纠正。
  • 7. 本站不保证下载资源的准确性、安全性和完整性, 同时也不承担用户因使用这些下载资源对自己和他人造成任何形式的伤害或损失。

评论

0/150

提交评论