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1、Hypoxic-ischemicencephalopathy(HIE)新生儿缺氧缺血性脑病Children’sHospitalofChongqingMedicalUniversityProf.JialinYuOutlineNeonatalasphyxia→oxygen-poor→ischemia→braininjuredinperinatalperiodCurrentlybirthtrauma↓,O2deficiency&asphyxia↑Severeconsequence:neonataldeath
2、orchildrendisablement,oneofreasonofcerebralpalsyinchildrenhood.Commoninfulltermbb,alsoinprematurecausesmothersfetusantepartumintrapartumpostpartum20%35%35%10%hypoxiaPlacenta&umbilicalcordAnte-&intrapartumCausesofHIEalsocausesofasphyxia:Maternalfactors:i
3、llnesses,obstetricdeseases,smokingordrugaddiction,teenagepregnancies,olderthan35yearsIntrapartumfactors:umbilicalcore,malposition,placentalinsufficiency,placentalabruptionFetalfactors:congenitalanomalies,IUGR,hydropsfetalis,intrauterineinfectionInfantfa
4、ctors:apnea,HMD,MAS,PPHN,shock.EtiopathogenesisofHIECerebralbloodflow(CBF):1.failincompensation:2stepsofredistributionDivingreflexThefirsttime---skinAdrenalglandMaintainCBFbutleadtomultiorganicdamage,SecondaryredistributionAnteriorcerebralartery,ACAmidd
5、lecerebralartery,MCAPosteriorcerebralartery,PCABranchofACABranchofMCABranchofPCAterminfant: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,PVLSuddenly&completelyasphyxia2.Non-compensation:ganglion-b
6、rainstemdamageCerebralbloodflow(CBF):3.autoregulation↓→Pressure-passivecerebralcirculation(PPCC)Cerebralischemia,HIEBrainedemacerebralhemorrhageBPCBFPPCCCerebralbloodflow(CBF):Changeofbrainmetabolism:1.oxygenfreeradicals→ruptureofcellmembranedestroyBBB(
7、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→chaos
8、ofsignal→Na++inflow→intra-cellularedema3.excitableneurotransmitter:glutamicacid;β-opioidpeptideneuropatholgy:脑细胞水肿(edema)脑细胞坏死(necrosisofbraincells)脑细胞凋亡(apoptosis)commonlyoccurafter6-24h,keepinseveraldaystowkspromptlyinterventio