兒內(nèi)科課件 2新生兒缺氧缺血性腦病

Hypoxic-ischemicencephalopathy(HIE)新生兒缺氧缺血性腦病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皮層矢狀旁區(qū)受損preterminfant：periventricular

leukomalacia(PVL)

腦室周圍的白質(zhì)軟化Consequenceof

secondaryredistribution腦室旁白質(zhì)軟化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：

腦細(xì)胞水腫(edema)腦細(xì)胞壞死(necrosisofbraincells)腦細(xì)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發(fā)育中腦的可塑性Plasticityduringgrowthofbrain樹突增長、增多

Dendronsgrowinlengthandnumber軸突延伸Axonselongation突觸增加Increasesynapse

建立新的神經(jīng)傳導(dǎo)回路Rebuildloopsofnerveconduction——代償性生長----compensationgrowthHypoxic-ischemia

necrosis

neurons

damage&apoptosis

cellbody

dendron&axon

neuralnetworksynapse

gliocytestrauma(microenvironment)

國家“九五”攻關(guān)項目簡介：（治療方案于1999.9南京全國第九屆圍產(chǎn)新生兒研究第12次會；1999.10大連第五屆全國新生兒學(xué)術(shù)會上討論并修改）

治療原則therapeuticprinciple：早治early階段stage綜合combination足程enoughcourse信心

confidenceWithin3dof

age

(criticalperiod)4-10dAfter10dAfterneonatalperiod4stagesofHIEwithin3d：

purpose：stabilizeinternalenvionment

&controlnervoussymptom1、三項支持療法maintenancetherapy：血氣bloodgas血循環(huán)circulation血糖bloodsugarwithin3d：2、三項對癥處理：symptomatictreatment

控制驚厥：phenobarbital,diazepam

降顱壓：furosemide,mannitol

消除腦干癥狀：納絡(luò)酮naloxone指征indication：①severeHIE

②pupildisorder

③shock④frequentconvulsion3．improvemetabolismofcells：

cerebrolysin,胞二磷膽堿citicoline,復(fù)方丹參Salviamiltiorrhizahyperbaricoxygenation4-10dofage：

purpose:startimprovementin4-5doflife，obviouslyimprovementin7-9d

oflife.method:improvemetabolismofcellsAfter10d：

purpose:Consolidatetherapeuticeffect&preventsequelae

method:ifneonatalbehaviornervousassessment(NBNA)<35

1.促神經(jīng)細(xì)胞代謝improvemetabolismofcells

2.新生兒期干預(yù)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