1. Periventricular and intraventricular hemorrhage in the neonate
Cecile Osman
April 9, 2010

2. What is PVH/IVH?
Bleeding into the periventricular white matter (motor tracts)
Is associated with hydrocephalus and long-term disability

3. 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

4. What are the subtypes: Grade I – Subependymal region and/or
germinal matrix

5. What are the subtypes: Grade II: Subependymal hemorrhage with
extension into
lateral ventricles
without ventricular
enlargement

6. What are the subtypes: Grade III: Subependymal hemorrhage with
extension into
lateral ventricles
with ventricular
enlargement

7. What are the subtypes:
Grade IV:
Intraparenchymal
hemorrhage

8. 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

9. 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

10. 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

11. 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

12. 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

13. 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

14. 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

15. What should we do? Supportive care
Minimize risk factors
NO NEED for serial LP
Eventually may need venticulostomy  VP shunt for those who have post-hemorhagic hydrocephalus that need surgical intervention

16. 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

17. Prognosis Grade I and grade II hemorrhage: Neurodevelopmental
prognosis is excellent
(ie, perhaps slightly
worse than infants of
similar gestational ages
without PVH-IVH).

18. Prognosis: Grade III hemorrhage without white matter disease:
Mortality is less than 10%.
Of these patients, 30-40%
have subsequent cognitive
or motor disorders.

19. 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