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Intraventricular Hemorrhage

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Presentation on theme: "Intraventricular Hemorrhage"— Presentation transcript:

1 Intraventricular Hemorrhage
John Baier MD

2 Incidence of IVH Late 1970’s- 80’s 39-49% Late 1980’s
< 34 weeks 19% <1501 g 16% 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
Bleeds originate in the subependymal germinal matrix Site of neuronal and glial proliferation cerebral neuroblasts weeks after 24 weeks cerebral astrocytes and oligodendroglia Size decreases as fetus matures 2.5 mm at weeks 1.4 mm at 32 weeks disappears at 36 weeks

5 Developmental Anatomy
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
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
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 Fluctuating cerebral blood flow
Increase in cerebral blood flow Increase in cerebral venous pressure Decrease in cerebral blood flow and reperfusion injury Platelet and coagulation defect Vascular factors

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

11 Fluctuating cerebral blood flow
Fluctuations of CBF ventilation out of synchrony PDA hypercarbia hypovolemia high FiO2 restlessness improved by neuromuscular blockade

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

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

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

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

16 Platelets and coagulation
Uncertain role in IVH 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 Coagulation common in VLBW infants FFP may decrease IVH without changing coagulation

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

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

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

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

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

22 Timing of IVH Postnatal Day % infants with IVH

23 Clinical features of IVH
3 clinical presentations catastrophic saltatory silent

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

28 Clinical Staging of IVH
Papile I bleeding confined to subependyma II intraventricular bleed without dilation III intraventricular bleed with dilation IV parenchymal bleed

29 Clinical Staging of IVH
I bleeding confined to subependyma II intraventricular bleed without dilation III intraventricular bleed with dilation Periventricular Intraparenchymal Echodensity (IPE)

30 Outcome of IVH Acute seizures acute hydrocephalus
intracranial hypertension death

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

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

33 Neurologic Impairment in IVH
Outcome is also related to extent of IPE Outcome Extensive IPE Localized IPE Mortality % 37 % Major Motor abn 100 % 80 % IQ < % 53 % “Normal” %

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

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

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

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

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

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

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

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

42 Prevention of IVH 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 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 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 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 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 Neonatal
Prevention and treatment of hemodynamic aberrations apnea acute hypercarbia (CO2) > 60 mm Hg pneumothorax suctioning rapid transfusions inotrope use exchange transfusions

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

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

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

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