3.  Incidence varies from 2% to >30% in newborns
 depends on the gestational age (GA) at birth and
the type of ICH
 Diagnosis typically depends on clinical suspicion
 The presence and severity of parenchymal injury
is the best predictor of outcome

4.  Rupture of the draining veins and sinuses of the
brain
 molding, fronto-occipital elongation, and
torsional forces acting on the head during
delivery
 provoke laceration of dural leaflets of tentorium
cerebelli or falx cerebri

5.  Often results from trauma in the full-term infant
 SDH in the supratentorial space results from
rupture of the bridging veins

6.  large head size,
 rigid pelvis (e.g., in a primiparous or older
multiparous mother),
 nonvertex presentation (breech, face, etc.),
 very rapid or prolonged labor or delivery,
 difficult instrumental delivery,
 or rarely, a bleeding diathesis

7.  Large
collection especially in infratentorial
SDH results in rapid deterioration.
 Systemic signs like hypovolemia and
anemia
 Seizures
may occur in up to half of
neonates with SDH, particularly with SDH
over the cerebral convexity

8.  suspected on the basis of history and
clinical signs and confirmed with a
computed tomography (CT) scan.
 ultrasonic
imaging subdural space is
inadequate
 MRI- timing of the lesion and for detecting
other lesions
 Lumbar puncture after CT

9.  Most infants with do not require surgical
intervention
 prompt stabilization with volume
replacement
 Open surgical evacuation of the clot in case
of large SDH
 The
outcome for infants with nonsurgical
SDH is usually good

10.  Primary SAH is probably frequent but clinically
insignificant.
 normal “trauma” associated with the birth
process.
 sourceof bleeding is usually ruptured bridging
veins of the subarachnoid space or ruptured small
leptomeningeal vessels

11. Usual scenar i o i s a w l el
appear i ng t er m i nf ant
devel opi ng SAH on day 2 or
3 of l i f e

12.  Clinical presentation is similar to other forms of ICH
 Thediagnosis is best established with a CT scan or
MRI, or by LP to confirm or diagnose small SAH
 Ultrasonography is not sensitive for the detection of
small SAH
 Management of SAH usually requires only
symptomatic therapy, such as anticonvulsant therapy
for seizures

13.  Rare
 Intracerebral or intracerebellar variety
 More commonly a secondary event
 Hypoxic ischemic brain injury, venous
infarction or thrombosis, ECMO therapy, large
ICH in another compartment

14.  Presentation and management similar to SDH
 MRI – extent and age of hemorrhage and
other associated parenchymal lesions
 LP to rule out meningitis
 Symptomatic management
 Treatany coexisting pathology or predisposing
factors
 Monitoring for hydrocephalus

15.  15-20% at <32 weeks gestation
 Venous (or sinus)thrombosis and thalamic
infarction in term infants
 Relatedto birth trauma or perinatal
asphyxia
 No identifiable risk factors in 25%

16. Intravascular factors • Ischemia/Reperfusion
• Fluctuating or increase
(Pressure passive circulation) CBF
• Increase in cerebral venous
pressure
• Platelet dysfunction
• Coagulation disturbances
Vascular factors • Fragile, involuting
capillaries with large
diameter lumen
Extravascular factors • Deficient vascular support
• Excess fibrinolytic activity

17.  Usually
a clinically silent syndrome in
preterms
 Term newborns – seizures, apnea,
irritability, lethargy, vomiting, full
fontanelle
 Catastrophic presentation less likely
 Complications

18.  Routine
CUS in all infants born at <32
weeks and in older infants at risk for IVH
 Days 3,7,30 and 60 days
 Monitoring for complications
 Gradingof GMH/IVH is important for
determining management and prognosis

19. Grading Severity Description
Papile (CT) I Isolated GMH (no IVH)
II IVH without ventricular dilatation
III IVH with ventricular dilatation
IV IVH with parenchymal hemorrhage
Volpe I GMH with no or minimal IVH (<10%
(CUS) ventricular volume)
II IVH occupying 10-50% of ventricular
area on parasagittal view
III IVH occupying >50% of ventricular area,
usually distending lateral ventricle
Separate Periventricular echodensity
notation

20.  Antenatal steroids
 Slow infusion of colloid or hyperosmolar
solutions
 Avoidrapid fluctuations in CBF and
hypotension
 Sedativeor paralytic medication in
ventilated babies

21.  Supportivecare and watch for
complications
 Maintaining Normal BP electrolytes and
,
blood gases
 Transfusions as necessary
 Correctthrombocytopenia and coagulation
disturbances

22.  Supportive care and treatment of seizures
 Serial LPs and eventual VP shunts
 Prognosis relates to factors other than IVH
alone

23. Monitor OFC and fontanelle daily, Serial CUS q2-7
days to assess ventricle size, shape and RI
No PVD Slowly Progressive Rapidly progressive
Ventricular dilation ventricular dilatation
(over weeks) (over days)
No further
Close surveillance for 2-4 wk
treatment
Dilatation stops Continued dilatation
No therapy, close Serial LP Every 1-3 d,
observation for 1 yr depending on rate of
ventricular dilatation