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Intraventricular Hemorrhage

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Intraventricular Hemorrhage. John Baier MD. Incidence of IVH. Late 1970’s- 80’s 39-49% Late 1980’s < 34 weeks19%

Text of Intraventricular Hemorrhage

  • Intraventricular HemorrhageJohn Baier MD

  • Incidence of IVHLate 1970s- 80s 39-49%Late 1980s< 34 weeks19%
  • Incidence of IVH

  • Developmental AnatomyBleeds originate in the subependymal germinal matrixSite of neuronal and glial proliferationcerebral neuroblasts 10-24 weeksafter 24 weeks cerebral astrocytes and oligodendrogliaSize decreases as fetus matures2.5 mm at 23-24 weeks1.4 mm at 32 weeksdisappears at 36 weeks

  • Developmental AnatomyArterial SupplyHeubners artery (branch of anterior cerebral artery)deep lateral striate arteries (middle cerebral artery)anterior choroidal artery (internal carotid)

  • Developmental AnatomyVenous drainagemedullary veinschoroidal veinthalamostriate veinenters the terminal vein at head of caudate veins change direction at internal cerebral vein making a U turn

  • Developmental AnatomyCapillary Networklarge irregular vesselslined only with endotheliumgelatinous matrixas term approaches these vessels develop adventia

  • Why is this region prone to bleeding ?

  • Pathogenesis of IVHFluctuating cerebral blood flowIncrease in cerebral blood flowIncrease in cerebral venous pressureDecrease in cerebral blood flow and reperfusion injuryPlatelet and coagulation defectVascular factors

  • Fluctuating cerebral blood flowNormaleven arterial pressure wavepeak to peak systolic < 10% differencecerebral blood flow parallels arterial waveFluctuatingsystolic and diastolic pressure vary beat to beatcerebral blood flow parallels arterial wave

  • Fluctuating cerebral blood flowFluctuations of CBFventilation out of synchronyPDAhypercarbiahypovolemiahigh FiO2restlessnessimproved by neuromuscular blockade

  • Increase in cerebral blood flow

    intact cerebral autoregulation in term infantspressure passive cerebral autoregulation in sick preterm infants

  • Increased arterial BP occurs inHypercarbiaStimulationTracheal suctioningPneumothoraxRapid volume expansionExchange TransfusionLigation of PDASeizureDrugsmydriatics

  • Increased Cerebral Venous PressureCaused byasphyxialabor and deliveryrespiratorypneumothoraxhigh PIPtracheal suctionrespiratory mechanics

  • Decreases in Cerebral Blood FlowCaused by asphyxia or hemorrhagemay be the required precedent for IVHmay be caused by less obvious factorstaking temperaturechest auscultationsuctioningIschemic changes in germinal matrixfree radical productioncan be reduced by superoxide dismutase in animal models

  • Platelets and coagulationUncertain role in IVHPlatelet-capillary function40% of VLBW infants have platelets < 100,000IVH rate is greater in thrombocytopenic infantsincreased PGI may interfere with platelet functionCoagulationcommon in VLBW infantsFFP may decrease IVH without changing coagulation

  • Vascular FactorsTenuous capillary integrityRemodeling capillary bedDeficient vascular liningabsent muscle and collagenLarge vascular and luminal areaVulnerability of matrix capillariesVascular border zoneBetween striate and thalamic arteriesHigh metabolic activity

  • Extravascular FactorsDeficient vascular supportIncreased fibrinolytic activityPostnatal decrease tissue pressure

  • Changes in CBF with AsphyxiaInitially hypotension with decreased CBFischemia to germinal matrixgeneration of free radicalsinjury of endotheliaResuscitation (PPV,Bicarbonate,volume etc)loss of cerebral autoregulationhypercarbiaIncrease in blood pressure and CBFFluctuation of CBF

  • Ventilated Premature Infant with RDSDecreases in CBFFluctuatingCBFIncreases inCBFIncreases in cerebral venouspressureCapillary ruptureINTRAVENTRICULAR HEMORRHAGEVulnerable germinalmatrix capillariesExtravascular:fibronolytic activityIntravascular:platelet/capillary and/orcoagulation disturbancesEndothelial injury(+/- prior decrease inCBF)

  • Pathogenesis of Intraparenchymal HemorrhageTerminal vein passes through germinal matrixIncreased pressure from germinal matrix hemorrhage obstructs venous flowvenous infarction

  • Timing of IVHPostnatal Day% infants with IVH1 502 253 154+ 10

  • Clinical features of IVH3 clinical presentationscatastrophicsaltatorysilent

  • Clinical features of IVHCatastrophic Syndrome (least common)evolution over minutes to hoursStupor or comaarrhythmias, hypoventilation and apneaGeneralized seizures and Decerebrate posturingFixed Pupils, eyes fixed to vestibular stimulationFlaccid quadriparesis

  • Clinical features of IVHCatastrophic syndromefalling hematocritbulging anterior fontanellehypotension and bradycardiatemperature changesSIADH and very rarely DIOutcome generally poor because of associated large intraparenchymal bleeds

  • Clinical features of IVHSaltatorymore subtlealteration in level of consciousnesschange in movement (decrease)hypotoniaminor changes in eye movementsdecreased popliteal angleoutcome more favorabledepends of degree of underlying IVH

  • Clinical features of IVHClinically silentsymptoms may not be detected on routine exam50% of cases of IVHunexplained fall in hematocrit

  • Clinical Staging of IVHPapile Ibleeding confined to subependymaIIintraventricular bleed without dilationIIIintraventricular bleed with dilationIVparenchymal bleed

  • Clinical Staging of IVHIbleeding confined to subependymaIIintraventricular bleed without dilationIIIintraventricular bleed with dilationPeriventricular Intraparenchymal Echodensity (IPE)

  • Outcome of IVHAcuteseizuresacute hydrocephalusintracranial hypertensiondeath

  • Outcome of IVHLong Term neurologic impairmentmotorsensorydevelopmental impairmentcognitiverelated to sensory deficitshydrocephalus

  • Neurologic Impairment in IVHIncidence of impairment related to degree of IVHIncidence ofSeverity Neurological sequelaeMild 5%Moderate 15 %Severe 35 %Severe + IPE 90 %

  • Neurologic Impairment in IVHOutcome is also related to extent of IPEOutcomeExtensive IPELocalized IPEMortality 81 %37 %Major Motor abn 100 %80 %IQ < 80 85 %53 %Normal 010 %

  • Motor Problems in IVHPeriventricular lesion affects fibres from both upper and lower extremities Spastic hemiparesis (unilateral)Spastic quadraparesis (bilateral)

  • Pathogenesis of Brain Injury in IVHPreceding hypoxic-ischemic injuryPVLpontine hemorrhageDestruction of glial precursors in germinal matrixeffects on mylenationcerebral organizationDestruction of periventricular white matterinfarctionintraventricular bloodpotassium glutamatevasoactive compounds

  • Pathogenesis of Brain Injury in IVHArterial vasospasm with focal brain ischemiaHydrocephalus

  • HydrocephalusProgressive ventricular dilation secondary to alteration in CSF dynamicsDistinguish from ventriculomegaly with normal CSF dynamicsatrophy hydrocephalus ex evacuoPVLIPE

  • Pathophysiology of Hydrocephalusmost are communicatingchronic obliterative arachnoiditis (most common)obstruction of aqueduct by blood, clot and debris (infrequent)

  • Clinical Aspects of Hydrocephalusonset 1 - 3 weeks after IVHrapidity of progression relates to degree of IVHHead growth and signs of increased ICP follow ventricular dilationdays to weeksPosterior horn dilate earlier and greater than anterior horns

  • Management of HydrocephalusMedicalacetazolamide with or with out furosemideserial lumbar puncturesserial ventricular puncturesSurgicalventriculostomyRickham reservoirVP or subgaleal shunt

  • Prevention of HydrocephalusIntraventricular injection of tPA may reduce the incidence of hydrocephalusonly a single small pilot study

  • Prevention of IVHAntenatal and PerinatalPREVENTION OF PREMATURE BIRTHSMaternal Transfer to high risk facilityMaternal PhenobarbitalMaternal Vitamin KMaternal SteroidsManagement of Labor and Deliverybreech delivery or prolonged labor? CS

  • Prevention of IVHMaternal Phenobarbitalcontroversial (now largely abandoned)treated infants were more illlower BP required increased fluidsmay decrease incidence of severe IVHmay increase need for ventilation at birthmay increase RDS

  • Prevention of IVHMaternal Vitamin Kvitamin K administered 4 hours prior to deliveryvitamin K administered to all infants at birthPT normal in treated (67% normal in controls)IVH was not related to PTincidence of IVH was decreased in two studies

  • Prevention of IVHAntenatal glucocorticoidscurrently in favorsignificant reduction in IVHreduction in degree not incidence of HMDmay relate to brain maturationglucocorticoids mature other organ systemsgut and respiratory tract

  • Prevention of IVHNeonatalResuscitation must be prompt and adequateavoid hypercarbia and hypoxemiaAvoid rapid infusion of volume expanders and hypertonic solutionsCorrection of fluctuation in cerebral blood flow velocityparalysishowever not easy to identify which infants have this fluctuation

  • Prevention of IVHNeonatalPrevention and treatment of hemodynamic aberrationsapneaacute hypercarbia (CO2) > 60 mm Hg pneumothoraxsuctioningrapid transfusionsinotrope useexchange transfusions

  • Prevention of IVHNeonatalCorrection of abnormal coagulationunclear dataPhenobarbitalIndomethacinEthamsylateVitamin E

  • Prevention of IVHPhenobarbitalnot currently usedlargest controlled study showed worse outcome in treated infants

  • Prevention of IVHIndomethacineffect first noted in studies to prevent symptomatic PDAdecreases baseline cerebral blood flow attenuates cerebral hyperemia in asphyxiamay be deleterious if hypotension occursdecreased oxidized cytochrome oxidasedecreased cerebral intracellular oxidationinhibits free radical formationmay accelerate mat

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