Cranial hemorrhage in newborns can be extracranial (e.g. cephalhematoma) or intracranial (e.g. subdural hemorrhage). Intracerebral hemorrhage, especially germinal matrix and intraventricular hemorrhage, is the most common type seen in preterm infants. Risk factors include prematurity, fluctuations in blood pressure, and hypoxic events. Intraventricular hemorrhage is graded based on its extent using cranial ultrasound or CT scan. Most hemorrhages occur within 3 days of birth and management involves supportive care though progressive ventricular dilation may require ventricular shunting. Outcomes depend on the grade of hemorrhage

1. Cranial Hemorrhage
of
The Newborn

2. Contents
 Introduction
 Classification
 Etiology
 Risk factors
 Pathophysiology
 Clinical feather
 Approach of diagnosis
 Spread of hemorrhage
 Timing of hemorrhage
 Management of IVH
 prognosis

3. Central Nervous System Disorders are
important cause of neonatal mortality & both
short & long term morbidity. The CNS can be
damaged as a result of asphyxia, hemorrhage,
trauma, hypoglycemia or direct toxicity.
Traumatic hemorrhage may involve any layer of
the scalp as well as intracranial contents.

4. Classification
Cranial Hemorrhage
Intracranial
Hemorrhage
Extra cranial
Hemorrhage
• Cephalhaematoma
• Caput succedaneum
• Subgaleal haemorrhage
• Retinal & sub conjunctival
haemorrhage
• GM hemorrhage
• Subdural hemorrhage
• Epidural hemorrhage
• Subarachnoid hemorrhage
• Intracerebral hemorrhage
• Intracecrebellar
hemorrhage

5. Extra Cranial Hemorrhage

6. Caput Succedaneum
Subcutaneous fluid collection in
the soft tissue of the scalp that
is presented during vertex
delivery.

7. Cephalhaematoma
• Sub periosteal collection of
blood which does not cross
the suture line.
• Presents as a soft , fluctuant
mass usually over the parital
bone.

8. Sub Galeal Hemorrhage
• Hemorrhage between galea
aponeurotica of scalp & the
periosteal.
• It appears as a fluctuant mass
within few hours after birth &
can extend from the orbital
ridge to the nape of neck &
laterally to the ears crossing the
suture line.

9. Sub Conjunctival & Retinal Hemorrhage
• These are frequent ;
petechiae of the skin of the
head & neck are also
common.
• These hemorrhages are
temporary & the result of the
normal vaginal delivery.
• These lesion resolves rapidly
within the 1st two weeks of
life.

10. Intracranial Hemorrhages

11. Intra Cranial Hemorrhages
• Traumatic epidural, subdural or subarachnoid
hemorrhage is specially likely when the fetal head is
large in proportion to the size of the mothers pelvic
outlet, with prolong labor, in breach presentation or
as a result of mechanical assistance with delivery.
• The majority of subdural & subarachnoid
hemorrhages resolves without intervention.

12. Subdural Hemorrhage
• A sub dural haemorrhage (SDH)is an accmulation of
blood between the dura & arachnoid mater.
• SDH is very common after birth : upto 50% of term
asymptomatic infants may have SDH.only on rare
ocassions does SDH become serious.
• Symptomatic subdural hemorrhage in large term infants
should be treated by removal of the subdural fluid
collection with a needle placed through the lateral
margin of the anterior fontanel.
• Asymptomatic subdural hemorrhage following labour
should resolve by 4 weeks of age.

13. Epidural Hemorrhage
Blood between the inner skull & dura mater. It is
extremely rare in newborn infants.
In case of epidural hemorrhage, removal or aspiration
of the hemorrhage was performed in the majority of
the cases, and the prognosis was quite good except
when other Intracerebral or parenchymal pathology
was absent.

14. Subarachnoid Hemorrhage
• Subarachnoid hemorrhage(SAH) is an accumulation of
blood between the arachnoid mater & pia mater.
• Subarachnoid hemorrhage is rare & typically silent.
• Some infants experience seizure on the 2nd day of life.
• Rarely infants has a life threatening catastrophic
hemorrhage & dies.
• There are usually no neurologic abnormalities during
the acute episode or on follow-up.

15. Intracerebral Intraparenchymal
Hemorrhage
• It occurs deep within the brain tissue after
venous infarction & is commonly referred to
as periventricular hemorrhagic
infarction(PVHI).
• Occurrence of PHHI may be as much as 10 -
15% among infants with ICH.

16. Intracerebellar Parenchymal
Hemorrhage(ICPH)
• ICPH is most often seen in preterm infants
with complications of labor & delivery.
• Using cranial USG
2.8% <1500gms
8.7% <750gms
• Using MRI
infants <34 weeks of gestation it is 10%.

17. Germinal Matrix & Intraventricular
Hemorrhage(IVH)
IVH is the most common CNS complications of a
preterm birth. the occurrence is greatly
associated with the immaturity of the germinal
matrix of the lateral ventricles.

18. Etiology
• The over all incidence has decreased over the past
decades as a result of improved perinatal care.
• Incidence & severity is inversely proportional to the
gestational age & birth weight.

19. Etiology
• 30% premature infants < 1500 grams may
develop IVH.
• 7% of 1 kg to 1.5 kg( grade 3 or 4)
• 14% of 751 to 1000gms
• 24% of < 750 grams may develop severe
IVH(grade 3 or 4)
• 3% of infants <1000gms develop
periventricular leukomalacia.

20. 1) Prematurity is the most important risk factor for IVH.
2) Rapid volume expansion
3) Hypertension
4) Coagulopathies
5) Hypoxic-ischemic insults
6) Respiratory disturbances
7) Acidosis
8) Infusions of hypertonic solutions
9) Anemia
10) Vacuum-assisted delivery
11) Frequent handling
12) Tracheal suctioning
Risk Factors

21. Germinal Matrix
• Primitive cellular region ventrolateral to LV
prominent : 26-34
involute : term
• Contains pluripotential migrating cells
neurons, astrocytes, oligodendroglia
• Contains immature blood vessels
thin walls(lack muscularis layer)
immature cell junction & basal lamina

22. Pathogenesis
• IVH in preterm occurs in sub ependymal germinal
matrix.
• This is located between caudate nucleus and the
ependymal lining of the lateral ventricle.
• This area is site of origin of embryonal neurons and fetal
glial cells.
• This area is highly vascularized and weakly supported.
• The blood vessels in this area are immature and are prone
to hypoxic ischemic injury.

23. Pathogenesis
• Fluctuation in cerebral blood flow play an important role in
developing IVH.
• A sudden rise in systemic blood pressure may result in an
increase in cerebral circulation with subsequent rupture of
the germinal matrix vessels.
• Decreases in cerebral blood flow can result in ischemic injury
to germinal matrix vessels, which rupture on reperfusion.

24. Clinical Feature
Three types of presentations
1. Catastrophic Deterioration –
least common, evolution over minutes to hours.
marked detorioration of sensorium, aponea, seizures, pupil
fixed to light, eye fixed to vestibular stimulation, decrebration
& flacid quadriparesis.
2. Saltatory detorioration –
evolution over hours to days. alteration in
sensorium, hypotonia, decreased spontaneous
movement, abnormal eye position or movement, bulging
fonanelle.

25. Clinical Feature
3. Clinically Silent –
most common. usually occur with
smaller lesion. there can be associated signs of
blood loss such as pallor, shock, decreased
haematochrit, metabolic acidosis, jaundice.

26. Approach of Diagnosis
History
Clinical
Manifestations
CT scanCranial
Ultrasonography

27. • The clinical signs of IVH are non specific, so
therefore, it is recommended that cranial ultrasound
should be done in premature infants <32 week of
gestation .
• Infants <1000g are at highest risk and should
undergo cranial ultrasonography within, first 3-7 days
of age after birth.
Approach of Diagnosis

28. Volpe’s grading(CUS)
Severity Description
1 GMH with no or minimal IHV(<10% of
ventricular volume)
2 IVH occupying 10-50% of ventricular area
3 IVH occupying >50% of ventricular area
4 Periventricular echodensity

29. Papile’s grading(CT)
Severity Description
1 Isolated GMH
2 IVH without ventricular dilatation
3 IVH with ventricular dilatation
4 IVH with parenchymal hemorrhage

37. Spread of Hemorrhage
• 40% stays in GM( grade1)
• 60% enters ventricles (grade 2& grade 3)
large IVH obstructs CSF flow
rapidly progressive hydrocephalus
small IVH retards CSF absorption
slow evolving hydrocephalus
• PV hemorrhagic infarction (grade 4)

38. Timing of IVH
• 90% occurs within first 72 hours
50% : < 24 hours
25% : >24 & <48hours
15% : >48 & < 72 hours
• 20% - 40% progress further
maximal extension occurs 3 – 5 days after
initial insult.

39. Management of
Intraventricular hemorrhage
Prevention Acute
Management
Follow up
Post natal
prevention
Antenatal
prevention

40. • Avoid preterm delivery
• Antenatal phenobarbital, vit K, & magnesium
sulfate have not been conclusively demonstrated to
prevent IVH.
• C section of high risk deliveries.
• A single course of antenatal corticosteroids is
recommended in pregnancies 24-34 weeks of
gestation that are at risk for preterm delivery.
Antenatal Prevention

41. • Avoid birth asphyxia.
• Avoid large fluctuation in blood pressure.
• Avoid excessive handling.
• Avoid rapid infusion of volume expander or hypertonic
solutions.
• Correct acid base balance.
• Correct coagulation abnormalities.
• Prophylactic administration of low dose indomethacin
(0.1mglkglday) for 3 days, reduces the incidences of severe
IVH.
Postnatal Prevention

42. Management of IVH
• No specific management is available for IVH, it
may be associated with other complications
that require therapy.
• ABC management.
• Seizures are treated aggressively with
anticonvulsant drugs.

43. Management of IVH
• Anemia & coagulopathies requires transfusion
with packed red blood cells or fresh frozen
plasma.
• Shock & acidosis are treated with slow
administration of sodium bicarbonate & fluid
resuscitation.

44. Management of IVH
• Insertion of VP shunt is the preferred method
to treat progressive & symptomatic PPH.
• Serial lumber punctures, ventricular taps or
reservoirs & externalized ventricular drains are
potential temporizing interventions.

45. No further
treatment
No therapy, close
observation for 1 yrs
VP shunt or VSG
shunt
No further
treatment, observe
for 1 yr
Slowly progressive
ventricular dilation
Close surveillance for 2-4 weeks
Continued dilation
Serial LP or placement of ventricular
drainage device,+/- medication
Continued dilation
Stop dilation
No PVD Rapidly progressive
ventricular dilation
Monitor OFC & fontanelle daily, serial
CUS(2-7) days to asses ventricle
size,shape & RI
Serial LP every 1-3 days ,
depending on rate of
ventricular dilation
Continued dilation
Dilation stops

46. Prognosis
Grade of GM-
IVH
Mortality
rate(%)
Progressive
ventricular
dilatation(% of
survivors)
Incidence of
definitive
neurological
sequlae(% of
survivors)
1 5 5 15
2 10 20 25
3 20 55 50
4 50 80 75

47. References
• Nelson Textbook of Pediatrics
• Neonatology
(Tricia Lacy Gomella)
• Manual of Neonatal Care
(John P. cloherty, Eric C .Eichenwald , Ann R
Stark)