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Periventricular and intraventricular hemorrhage in the neonate Cecile Osman April 9, 2010 What is PVH/IVH? Bleeding into the periventricular white matter (motor tracts) Is associated with hydrocephalus and long-term disability Where does it occur? Subependymal germinal matrix Where neuroblasts and glioblasts divide and migrate into the cerebral parenchyma Cells of the germinal matrix are rich in mitochondria so are quite sensitive to ischemia Usually regresses by term What are the subtypes: I– Subependymal region and/or germinal matrix Grade What are the subtypes: Grade II: Subependymal hemorrhage with extension into lateral ventricles without ventricular enlargement What are the subtypes: Grade III: Subependymal hemorrhage with extension into lateral ventricles with ventricular enlargement What are the subtypes: Grade IV: Intraparenchymal hemorrhage Why does it occur? GM supplied by primitive and fragile retelike capillary network Thought to be due to: 1) loss of cerebral autoregulation 2) abrupt alterations in cerebral blood flow and pressure Autoregulation Term infants and most “healthy” premature have the ability to regulate cerebral blood flow Preemie has more narrow range of perfusion pressures over which he can control regional cerebral blood flow Without autoregulation, systemic BP is what mostly controls cerebral perfusion/pressure Cerebral Blood Flow / Pressures Many things can affect CBF Asynchrony between spontaneous and mechanically delivered breaths; birth; noxious procedures of caregiving; tracheal suctioning; pneumothorax; rapid volume expansion; seizures; and changes in pH, PaCO2, and PaO2 Cerebral Blood Flow and Respiratory Pattern When mechanical breaths are not synchronized with efforts of the patient, beat-to-beat fluctuations in blood pressure occur Patients without asynchrony between mechanical ventilation and patient efforts had stable blood pressures, stable cerebral perfusion, and a lower incidence of hemorrhage Why do we care? The bleeding leads to destruction of the cerebral parenchyma necrosis Eventually causing hydrocephalus may end up needing VP shunt Depending on WHAT part of the brain is destroyed seizures / cerebral palsy / mental retardation Who gets affected? All premature infants, especially <32 weeks Can see in term infants if has trauma / asphyxia Most occur within first 72 hrs of life, 50% in the first 24 hours Can occur after 3rd day of life esp if neonate develops significant life threatening event What should we do? Initial screen usually at ~7 days of life Cranial ultrasound is tool of choice Serial ultrasounds to follow progression / evolution of the bleed What should we do? Supportive care Minimize risk factors NO NEED for serial LP may need venticulostomy VP shunt for those who have posthemorhagic hydrocephalus that need surgical intervention Eventually Medications? Indomethacin: Controversial, but possibly indicated in patients at risk for PVH-IVH, including those <32 weeks' gestation or those who weigh <1250 g at birth. Inhibits the formation of prostaglandins by decreasing the activity of cyclo-oxygenase. Thought to cause maturation of the germinal matrix microvasculature (mechanism unclear) 0.1 mg/kg/dose IV when aged 6 h, then q24h for 2 d for a total of 3 doses Prognosis Grade I and grade II hemorrhage: Neurodevelopmental prognosis is excellent (ie, perhaps slightly worse than infants of similar gestational ages without PVH-IVH). Prognosis: Grade III hemorrhage without white matter disease: Mortality is less than 10%. Of these patients, 30-40% have subsequent cognitive or motor disorders. Prognosis Grade IV (severe PVH-IVH) IVH with either periventricular hemorrhagic infarction and/or periventricular leukomalacia (PVL): Mortality approaches 80%. A 90% incidence of severe neurological sequelae including cognitive and motor disturbances is noted