脑动静脉畸形医药类ppt课件

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CEREBRALARTERIOVENOUS MALFORMATIONSAVM:a TLA for the CNSCEREBRALAVM:a TLA for the CNSIncidencen0.52%at autopsynSlight male preponderance(1.09 to 1.94)nCongenital lesions(although rarely familial)Incidence0.52%at autopsyEmbryologynFirst half of third week of gestationepiblastic cells migrate to form mesodermmesodermal cells differentiate to arterial and venous vessels on the surface of the embryonic nervous systemEmbryologyFirst half of third EmbryologynFirst half of third week of gestationepiblastic cells migrate to form mesodermmesodermal cells differentaite to arterial and venous vessels on the surface of the embryonic nervous systemnSeventh gestational weekvessels sprout branches&penetrate developing brainreach the gray-white interface,either loop back to pial surface or traverse entire neural tube,thus epicerebral&transcerebral circneventually connect arterial and venous systems by around the twelfth week EmbryologyFirst half of third Pathology&Pathophysiologynabsence of normal capillary systemPathology&PathophysiologyabsPathology&Pathophysiologynabsence of normal capillary systemnusual function displacedPathology&PathophysiologyabsPathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthPathology&PathophysiologyabsPathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsPathology&Pathophysiologyabsparenchymal changes within and around the lesionPathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsparenchymal changes within andparenchymal changes within and around the lesionsite frequency is proportional to brain volumePathology&Pathophysiologynabsence of normal capillary systemnusual function displacednasymptomatic at birthnvessels change with timenmay develop aneurysmsparenchymal changes within andClinical presentationn95%have symptoms by age of 70 yearsClinical presentation95%have Clinical presentationn95%have symptoms by age of 70 yearsnpeak presentation second to fourth decadeClinical presentation95%have Clinical presentationn95%have symptoms by age of 70 yearsnpeak presentation second to fourth decadehigh output failure,neonate,vein of Galenhydrocephalus,first decadeheadache,hemorrhage,seizures,2nd&3rdClinical presentation95%have Clinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresClinical presentationfactors cClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentClinical presentationfactors cClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesClinical presentationfactors cClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesischaemiaClinical presentationfactors cClinical presentationnfactors contributing to symptomsvessel walls,flow and pressuresenlargement and encroachmentdural sinusesischaemiacardiac outputClinical presentationfactors cClinical presentationClinical presentationHemorrhagenAVMrupture not a function of sizenAneurysmrupture related to aneurysm sizeHemorrhageAVMAneurysmHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumanAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyHemorrhageAVMAneurysmHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severenAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyarterial,therefore more severeHemorrhageAVMAneurysmHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severemortality 6 to 13.6%nAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyarterial,therefore more severemortality 30-50%HemorrhageAVMAneurysmHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severemortality 6 to 13.6%lower rebleed mortality rate(1%)nAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyarterial,therefore more severemortality 30-50%higher rebleed mortality rate(13%)HemorrhageAVMAneurysmHemorrhagenAVMrupture not a function of sizeno marked increase with exercise,pregnancy,traumaarteriovenous,therefore less severemortality 6 to 13.6%lower rebleed mortality rate(1%)vasospasm rarenAneurysmrupture related to aneurysm sizeincrease with trauma exercise,end pregnancyarterial,therefore more severemortality 30-50%higher rebleed mortality rate(13%)vasospasm commonHemorrhageAVMAneurysmHemorrhage-AVMnNonetheless,risk of major,incapacitating,or fatal hemorrhage in untreated lesion is 40 to 50%Hemorrhage-AVMNonetheless,rHemorrhage-AVMnNonetheless,risk of major,incapacitating,or fatal hemorrhage in untreated lesion is 40 to 50%nYearly risk of initial hemorrhage 3%nRebleed in first subsequent year 6-18%,reducing to 3%again thereafternPediatric prognosis worse than adult Hemorrhage-AVMNonetheless,rSpetzler&Martin Grading SystemCriteriaScoreSize of Nidus Small(6cm)3Eloquence of Adjacent Brain No0Yes1Deep Vascular Component No0Yes1Spetzler&Martin Grading SystTreatment OptionsHSurgical ResectionTreatment OptionsSurgical ReseTreatment OptionsHSurgical ResectionHEndovascular EmbolisationTreatment OptionsSurgical ReseTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryTreatment OptionsSurgical ReseTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryHMultimodal TherapyTreatment OptionsSurgical ReseTreatment OptionsHSurgical ResectionHEndovascular EmbolisationHStereotatic RadiosurgeryHMultimodal TherapyHConservative ManagementTreatment OptionsSurgical ReseNormal Perfusion Pressure Breakthrough TheoryR.F.Spetzler et alNormal Perfusion Pressure BreaNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal perfusion pressure breaNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal hemispheric vessels are chronically maximally dilated to attempt to divert flow from the AVMNormal perfusion pressure breaNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal hemispheric vessels are chronically maximally dilated to attempt to divert flow from the AVMObliteration of the AVM diverts all flow to these maximally dilated vessels which have lost their normal control mechanismsNormal perfusion pressure breaNormal perfusion pressure breakthrough theoryLoss of autoregulation and carbon dioxide reactivity in presence of large arteriovenous malformation.Normal hemispheric vessels are chronically maximally dilated to attempt to divert flow from the AVMObliteration of the AVM diverts all flow to these maximally dilated vessels which have lost their normal control mechanismsResults in loss of protection of the capillary bed,with edema and hemorrhageNormal perfusion pressure breaArterial inflowMathematical ModelsArterial inflowMathematical MoArterial inflowNidusMathematical ModelsArterial inflowMathematical MoArterial inflowNidusVenous OutflowMathematical ModelsArterial inflowMathematical MoAnaesthesia TechniqueAnaesthesia Technique
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