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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