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Intraventricular Hemorrhage John Baier MD. Incidence of IVH n Late 1970’s- 80’s 39-49% n Late 1980’s –< 34 weeks19% –<1501 g16% n Still large problem.

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Presentation on theme: "Intraventricular Hemorrhage John Baier MD. Incidence of IVH n Late 1970’s- 80’s 39-49% n Late 1980’s –< 34 weeks19% –<1501 g16% n Still large problem."— Presentation transcript:

1 Intraventricular Hemorrhage John Baier MD

2 Incidence of IVH n Late 1970’s- 80’s 39-49% n Late 1980’s –< 34 weeks19% –<1501 g16% n Still large problem –1.24% of 4 million births are < 1500 g –7400 infants per year sustain IVH

3 Incidence of IVH

4 Developmental Anatomy n Bleeds originate in the subependymal germinal matrix n Site of neuronal and glial proliferation –cerebral neuroblasts weeks –after 24 weeks cerebral astrocytes and oligodendroglia n Size decreases as fetus matures –2.5 mm at weeks –1.4 mm at 32 weeks –disappears at 36 weeks

5 Developmental Anatomy n Arterial Supply –Heubner’s artery (branch of anterior cerebral artery) –deep lateral striate arteries (middle cerebral artery) –anterior choroidal artery (internal carotid)

6 Developmental Anatomy n Venous drainage –medullary veins –choroidal vein –thalamostriate vein –enters the terminal vein at head of caudate –veins change direction at internal cerebral vein making a U turn

7 Developmental Anatomy n Capillary Network –large irregular vessels –lined only with endothelium –gelatinous matrix –as term approaches these vessels develop adventia

8 Why is this region prone to bleeding ?

9 Pathogenesis of IVH n Fluctuating cerebral blood flow n Increase in cerebral blood flow n Increase in cerebral venous pressure n Decrease in cerebral blood flow and reperfusion injury n Platelet and coagulation defect n Vascular factors

10 Fluctuating cerebral blood flow n Normal –even arterial pressure wave »peak to peak systolic < 10% difference –cerebral blood flow parallels arterial wave n Fluctuating –systolic and diastolic pressure vary beat to beat –cerebral blood flow parallels arterial wave

11 Fluctuating cerebral blood flow n Fluctuations of CBF –ventilation »out of synchrony –PDA –hypercarbia –hypovolemia –high FiO 2 –restlessness n improved by neuromuscular blockade

12 Increase in cerebral blood flow n intact cerebral autoregulation in term infants n pressure passive cerebral autoregulation in sick preterm infants

13 Increased arterial BP occurs in n Hypercarbia n Stimulation n Tracheal suctioning n Pneumothorax n Rapid volume expansion n Exchange Transfusion n Ligation of PDA n Seizure n Drugs –mydriatics

14 Increased Cerebral Venous Pressure n Caused by –asphyxia –labor and delivery –respiratory »pneumothorax »high PIP »tracheal suction »respiratory mechanics

15 Decreases in Cerebral Blood Flow n Caused by asphyxia or hemorrhage –may be the required precedent for IVH –may be caused by less obvious factors »taking temperature »chest auscultation »suctioning n Ischemic changes in germinal matrix –free radical production –can be reduced by superoxide dismutase in animal models

16 Platelets and coagulation n Uncertain role in IVH n Platelet-capillary function –40% of VLBW infants have platelets < 100,000 –IVH rate is greater in thrombocytopenic infants –increased PGI may interfere with platelet function n Coagulation –common in VLBW infants –FFP may decrease IVH without changing coagulation

17 Vascular Factors n Tenuous capillary integrity –Remodeling capillary bed –Deficient vascular lining »absent muscle and collagen –Large vascular and luminal area n Vulnerability of matrix capillaries –Vascular border zone »Between striate and thalamic arteries –High metabolic activity

18 Extravascular Factors n Deficient vascular support n Increased fibrinolytic activity n Postnatal decrease tissue pressure

19 Changes in CBF with Asphyxia n Initially hypotension with decreased CBF –ischemia to germinal matrix –generation of free radicals –injury of endothelia n Resuscitation (PPV,Bicarbonate,volume etc) –loss of cerebral autoregulation –hypercarbia n Increase in blood pressure and CBF n Fluctuation of CBF

20 Ventilated Premature Infant with RDS Decreases in CBF Fluctuating CBF Increases in CBF Increases in cerebral venous pressure Capillary rupture INTRAVENTRICULAR HEMORRHAGE Vulnerable germinal matrix capillaries Extravascular: fibronolytic activity Intravascular: platelet/capillary and/or coagulation disturbances Endothelial injury (+/- prior decrease in CBF)

21 Pathogenesis of Intraparenchymal Hemorrhage n Terminal vein passes through germinal matrix n Increased pressure from germinal matrix hemorrhage obstructs venous flow n venous infarction

22 Timing of IVH Postnatal Day% infants with IVH

23 Clinical features of IVH n 3 clinical presentations –catastrophic –saltatory –silent

24 Clinical features of IVH n Catastrophic Syndrome (least common) –evolution over minutes to hours –Stupor or coma –arrhythmias, hypoventilation and apnea –Generalized seizures and “Decerebrate posturing” –Fixed Pupils, eyes fixed to vestibular stimulation –Flaccid quadriparesis

25 Clinical features of IVH n Catastrophic syndrome –falling hematocrit –bulging anterior fontanelle –hypotension and bradycardia –temperature changes –SIADH and very rarely DI –Outcome generally poor because of associated large intraparenchymal bleeds

26 Clinical features of IVH n Saltatory –more subtle –alteration in level of consciousness –change in movement (decrease) –hypotonia –minor changes in eye movements –decreased popliteal angle –outcome more favorable »depends of degree of underlying IVH

27 Clinical features of IVH n Clinically silent –symptoms may not be detected on routine exam –50% of cases of IVH –unexplained fall in hematocrit

28 Clinical Staging of IVH n Papile n Ibleeding confined to subependyma n IIintraventricular bleed without dilation n IIIintraventricular bleed with dilation n IVparenchymal bleed

29 Clinical Staging of IVH n Ibleeding confined to subependyma n IIintraventricular bleed without dilation n IIIintraventricular bleed with dilation n Periventricular Intraparenchymal Echodensity (IPE)

30 Outcome of IVH n Acute –seizures –acute hydrocephalus –intracranial hypertension –death

31 Outcome of IVH n Long Term –neurologic impairment »motor »sensory –developmental impairment »cognitive »related to sensory deficits –hydrocephalus

32 Neurologic Impairment in IVH n Incidence of impairment related to degree of IVH Incidence of Severity Neurological sequelae Mild 5% Moderate 15 % Severe 35 % Severe + IPE 90 %

33 Neurologic Impairment in IVH n Outcome is also related to extent of IPE OutcomeExtensive IPELocalized IPE Mortality 81 %37 % Major Motor abn 100 %80 % IQ < %53 % “Normal” 010 %

34 Motor Problems in IVH n Periventricular lesion affects fibres from both upper and lower extremities –Spastic hemiparesis (unilateral) –Spastic quadraparesis (bilateral)

35 Pathogenesis of Brain Injury in IVH n Preceding hypoxic-ischemic injury –PVL –pontine hemorrhage n Destruction of glial precursors in germinal matrix –effects on mylenation –cerebral organization n Destruction of periventricular white matter –infarction –intraventricular blood »potassium »glutamate »vasoactive compounds

36 Pathogenesis of Brain Injury in IVH n Arterial vasospasm with focal brain ischemia n Hydrocephalus

37 Hydrocephalus n Progressive ventricular dilation secondary to alteration in CSF dynamics n Distinguish from ventriculomegaly with normal CSF dynamics –atrophy “hydrocephalus ex evacuo” »PVL »IPE

38 Pathophysiology of Hydrocephalus n most are communicating –chronic obliterative arachnoiditis (most common) –obstruction of aqueduct by blood, clot and debris (infrequent)

39 Clinical Aspects of Hydrocephalus n onset weeks after IVH n rapidity of progression relates to degree of IVH n Head growth and signs of increased ICP follow ventricular dilation –days to weeks n Posterior horn dilate earlier and greater than anterior horns

40 Management of Hydrocephalus n Medical –acetazolamide with or with out furosemide –serial lumbar punctures –serial ventricular punctures n Surgical –ventriculostomy –Rickham reservoir –VP or subgaleal shunt

41 Prevention of Hydrocephalus n Intraventricular injection of tPA may reduce the incidence of hydrocephalus n only a single small pilot study

42 Prevention of IVH n Antenatal and Perinatal –PREVENTION OF PREMATURE BIRTHS –Maternal Transfer to high risk facility –Maternal Phenobarbital –Maternal Vitamin K –Maternal Steroids –Management of Labor and Delivery »breech delivery or prolonged labor »? CS

43 Prevention of IVH n Maternal Phenobarbital –controversial (now largely abandoned) »treated infants were more ill »lower BP required increased fluids –may decrease incidence of severe IVH –may increase need for ventilation at birth –may increase RDS

44 Prevention of IVH n Maternal Vitamin K –vitamin K administered 4 hours prior to delivery –vitamin K administered to all infants at birth –PT normal in treated (67% normal in controls) »IVH was not related to PT –incidence of IVH was decreased in two studies

45 Prevention of IVH n Antenatal glucocorticoids –currently in favor –significant reduction in IVH –reduction in degree not incidence of HMD –may relate to brain maturation »glucocorticoids mature other organ systems »gut and respiratory tract

46 Prevention of IVH n Neonatal –Resuscitation must be prompt and adequate »avoid hypercarbia and hypoxemia –Avoid rapid infusion of volume expanders and hypertonic solutions –Correction of fluctuation in cerebral blood flow velocity »paralysis »however not easy to identify which infants have this fluctuation

47 Prevention of IVH n Neonatal –Prevention and treatment of hemodynamic aberrations »apnea »acute hypercarbia (CO 2 ) > 60 mm Hg »pneumothorax »suctioning »rapid transfusions »inotrope use »exchange transfusions

48 Prevention of IVH n Neonatal –Correction of abnormal coagulation »unclear data –Phenobarbital –Indomethacin –Ethamsylate –Vitamin E

49 Prevention of IVH n Phenobarbital –not currently used –largest controlled study showed worse outcome in treated infants

50 Prevention of IVH n Indomethacin –effect first noted in studies to prevent symptomatic PDA –decreases baseline cerebral blood flow –attenuates cerebral hyperemia in asphyxia –may be deleterious if hypotension occurs »decreased oxidized cytochrome oxidase »decreased cerebral intracellular oxidation –inhibits free radical formation –may accelerate maturation of germinal matrix

51 Prevention of IVH n Ethamsylate (not available in US) –inhibits prostaglandin synthesis distal to cyclo-oxygenase »inhibits prostacyclin predominately »does not affect cerebral blood flow –polymerization of hyaluronic acid in basement membranes –promotes platelet adhesiveness –placental transfer »??? antenatal use

52 Summary n IVH remains a significant problem in the NICU despite recent improvements in care n Pathogenesis include anatomical susceptibility and pathologic changes in CBF n Incidence varies with gestational age n Prognosis depends on clinical stage n Current therapies are unsatisfactory and prevention remains the best way to reduce the incidence and impact of IVH


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