This presentation aims at discussion of the pathophysiology , clinical presentation and management of the different types of intracranial bleeds in a neonate. Special emphasis has been laid on intraventricular hemorrhage. The germinal matrix bleed in a preterm is discussed in depth along with the various evidence based management protocols available. Radiological diagnosis of IVH in a preterm / term baby will be discussed in the upcoming presentations.
6. Caput succedeum
Usual site of caput formation is the vertex and
marked moulding of the head is a common
accompaniment.
The edema is soft, superficial and pitting and crosses
the sites of suture lines.
The lesion steadily resolves over the first few days of
life.
No intervention is needed.
EXTRACRANIAL HEMORRHAGES
7. Caput succedeum (cont..)
This includes the hemorrhagic oedema that is
observed most commonly after vaginal deliveries.
Compression of the presenting part exerted by the
uterus or the cervix on the is the most common
pathogenesis.
Caput succedaneum occurs in approx. 20 to 40 % of
vaccum deliveries.
EXTRACRANIAL HEMORRHAGES
8. Cephalhematoma
Cephalhematoma refers to a circumscribed region of hemorrhage
overlying the skull and confined by the cranial sutures.
Incidence is approx. 1 – 2 % of live births.
Highest incidence found with use of vaccum (10.8%) followed
closely by midforcep delivery(9.5%) and less by low forceps(7.2%)
Seen commonly with Primi mothers than multipara.
The hemorrhage in cephalhematoma is subperiosteal, which
explains the confinement of the hematoma by cranial sutures.
An underlying linear skull fracture is seen in 10 – 20 % cases with
cephalhematomsa.
EXTRACRANIAL HEMORRHAGES
9. Cephalhematoma (cont..)
The lesion usually seen increasing in size after birth and
presents as a firm, tense mass that does not transilluminate.
By far, the most common location of cephalhematoma has
been parietal region and found to be unilateral.
Cephalhematoma has rarely a significance from neurological
point of view, unless complicated by underlying cerebral
bleed.
Common complications include severe hyperbilirubinemia,
anaemia, osteomyelitis.
No specific therapy is indicated. Evacuation of the lesion is
contraindicated.
EXTRACRANIAL HEMORRHAGES
10. Subgaleal Hematoma
Subgaleal hemorrhage refers to the hemorrhage
beneath the aponeurosis covering the scalp and
connecting the frontal and occipital components of
the occipitofrontalis muscle.
Also known as the Subaponeurotic hemorrhage.
Blood may spread beneath the entire scalp and may
even dissect into the subcutaneous tissues of the
neck.
Strong association with vaccum delivery.
EXTRACRANIAL HEMORRHAGES
11. Subgaleal Hematoma
The infants generally present at 1 hr of age and manifests as
a firm, fluctuant mass, increasing in size postnatally, and may
present at the subcut tissue on the posterior part of neck.
These infants have a relatively high incidence of :
1. Hypovolemic shock (10%)
2. Requirement of volume expansion or ionotropic
support (35%)
3. Need for transfusion for anaemia (35%)
4. Secondary coagulopathy (50 %)
5. Hyperbilirubinemia (35%)
After the acute phase, the lesion usualy resolves in 2 – 3 wks.
EXTRACRANIAL HEMORRHAGES
12.
13. INTRACRANIAL HEMORRHAGE
• Intracranial hemorrhage is a
collective term encompassing many
different conditions characterised by
the extravascular accumulation of
blood within different intracranial
spaces.
• In a newborn, the developing brain
injury is due to selective vulnerability
of population of cells undergoing
active metabolic change during these
periods.
14. INTRACRANIAL HEMORRHAGE
Term Infant
• Commonest are subdural,
subarachnoid or subtentorial.
• Mostly related to Birth trauma,
HIE, coagulopathies and
undetermined causes.
Preterm Infant
• Commonest is bleeding from the
subependymal germinal matrix
and may result in intraventricular
or periventricular hemorrhage.
• White matter injury due to
hypoxic ischaemia and infections.
Perinatal arterial Ischaemic stroke, sinovenous thrombosis and perinatal
hemorrhagic stroke, Trauma are responsible for hemorrhages in
TERM / PRETERM infants.
15. Epidural Hemorrhage
An Epidural hemorrhage is a collection of blood between the inner skull and the
dura.
Usually caused by injury to the middle meningeal artery, which is less
susceptible to injury as it is freely movable in the space.
Causes include TRAUMA.
Affected infants usually have a skull fracture and cephalhematoma and the
treatment is supportive with possible surgical / needle aspirations.
INTRACRANIAL HEMORRHAGES
16. Subdural Hemorrhage
Subdural hemorrhage refers to the hemorrhage in
the plane between the dura and the arachnoid
membrane and involves tears of bridging veins of the
subdural compartment.
Blood may accumulate and cause acute symptoms
of ICP or may reside as a hematoma that slowly
evolves as a chronic subdural hematoma with
increasing intracranial pressure.
Usually follows a traumatic delivery of a near term /
term infant.
INTRACRANIAL HEMORRHAGES
17. Subdural Hemorrhage (cont…)
Timing of onset of SDH and clinical findings may be
acute or delayed.
Signs may include lethargy ± irritability, asymmetric
hypotonia, impaired third cranial nervy function
ipsilateral to lesion, focal seizures, signs of raised icp.
Other clinical clues can be decreased feeding, failure to
thrive, intermittent vomiting – often related to late post
SDH neuropathic effects.
CT / MRI (esp for posterior fossa lesions) are modalities
of choice.
Management involoves a proper and repeated
neurologic followup and sos interventions.
INTRACRANIAL HEMORRHAGES
18. Subarachnoid Hemorrhage
A subarachnoid hemorrhage is an accumulation of
blood between the arachnoid mater and the pia
mater.
Infant SAH is venous , as opposed to arterial in
adults.
SAH may be primary , coming from the vessels of
the subarachnoid space, or secondary occurring
when the blood extends from existing intraventricular,
cerebral or cerebellar hemorrhages.
INTRACRANIAL HEMORRHAGES
19. Subarachnoid Hemorrhage (cont…)
Primary SAH is usually self – limited and it is the second most
common ICH seen in newborns.
Close observation and repeated neurologic assessments are
mainstay of management.
Anticonvulsant medications and IV fluid therapy are needed if
lethargy / seizures are present.
Serum electrolyte and urine output monitoring to be done for
possible SIADH , if significant SAH has been identified.
Regular sequential Head circumference assessments will
identify cases with posthemorrhagic hydrocephalus.
INTRACRANIAL HEMORRHAGES
20. Cerebral hemorrhage
An Intracerebral parenchymal hemorrhage occurs deep
within the brain tissue after venous infarction and is
commonly referred as PERIVENTRICULAR
HEMORRHAGIC INFARCTION.
The most common complications of PVHI is
Periventricular leukomalacia in preterm infants and
porencephalic cysts in term infants.
PVHI is seen most often post a perinatal hypoxic-
ischaemic event.
Clinical signs of PVHI follow those of severe neonatal
encephalopathy and overlap with clinical signs as seen
with SDH, SAH or IVH.
INTRACRANIAL HEMORRHAGES
21. Cerebral hemorrhage (cont..)
Cranial USG can also identify PVHI in form of echodense
lesion of periventricular white matter with an associated
germinal matrix hemorrhage or IVH.
CT is the most useful modality for diagnosing recent
hemorrhages
Management requires observation and supportive care. If
imaging studies show a midline shift, neurosurgical
consultation needed.
Developmental studies of preterm infants with PVHI have
shown that significant cognitive and/or motor delays
complicate the overall recovery in atleast 2/3 rd of the
survivors.
Careful follow up is therefore indicated in every case.
INTRACRANIAL HEMORRHAGES
22. Cerebellar hemorrhage
An Intracerebellar parenchymal hemorrhage is most
often seen in preterm infants with complications of labor
and delivery and in whom intense respiratory
management is required.
In term infants, ICPH is almost always associated with
birth trauma.
Incidences have been found approx 10% in preterms
<34wks, by MRI studies.
Clinically, an ICPH is unique in causing unexplained
motor agitation, in addition to respiratory compromise,
apnea and breathing irregularities. Other general
symptoms of ICH are also present.
INTRACRANIAL HEMORRHAGES
23. Cerebellar hemorrhage (cont…)
CT and MRI are preferable over Ultrasound.
Management is usually conservative.
These babies usually require longer periods of
mechanical ventilation.
They need ongoing close neurodevelopmental
assessments.
INTRACRANIAL HEMORRHAGES
24. I N T R A V E N T R I C U L A R
H E M O R R H A G E
27. INTRODUCTION
• Intraventricular hemorrhage is the most common CNS complication of a preterm birth.
• The overall incidence of IVH in preterm infants <1500gm is approx 13 – 15 %.
• Because IVH is rarely seen in term infants, their incidence rates are exceptionally low and
associated with birth related injury and / or asphyxia.
• The germinal matrix begins to involute after 34 wks postconceptional age, and thus the
peculiar vulnerability decreases, but is not totally eliminated.
• By 36 wks gestation, the germinal matrix has involuted in most infants, although sopme
residual may persists.
28. WHY PRETERMS….???
1. Lack of cerebral blood flow autoregulation.
Therefore, a PRESSURE PASSIVE state exists.
2. Highly vascularized subependymal germinal matrix, lack of supporting
basement membrane in blood vessels, and increased amount of fibrinolytic
activity in germinal matrix.
3. Pathologic increased fluctuations in the cerebral blood flow velocity.
(Eg. RDS, Pneumothorax, PDA, Hypothermia, hyperosmolarity, etc.)
4. Isolated hypertension associated with seizures, intubations and
suctionings also predisposes these babies to IVH.
29. • The occurrence of preterm IVH is greatly associated with the immaturity of the germinal
matrix of the lateral ventricles
• The cortical neuronal and glial cell precursors develop from the germinal matrix and the
adjacent ventricular germinal zone during the late 2nd and 3rd trimester.
• This ependymal germinal matrix is highly vascularized region with arterial supply from the
anterior and the middle cerebral arteries and the anterior choroidal vessels.
• Bleed in this region, thus may be confined to the germinal matrix or it may rupture into
either lateral ventricles and may thereby become a unilateral or bilateral GM / IVH.
PATHOPHYSIOLOGY
30. PATHOGENETIC FACTORS LEADING TO IVH.
Increased cerebral blood flow
Fluctuations in the cerebral blood flow.
Increased Central venous pressure.
Endothelial Injury.
Vulnerable germinal matrix capillaries.
Coagulation disturbances.
Increased Fibrinolysis.
31. CLINICAL PRESENTATION
• Asymptomatic (sometimes).
• Sudden & catastrophic deterioration in form of
neurologic signs like stupor, coma, seizures, posturing
or apneas.
• Full fontanel with sudden drop in hematocrit.
• Can be accompanied by hyperglycemia, hyperkalemia,
hypotension, bradycardia.
• SIADH may be seen.
• Sometimes, IVH can present as a gradual clinical
deterioration with altered levels of consciousness,
hypotonia, abnormal extremity or eye movements.
33. CRANIAL ULTRASOUND
• Cranial Ultrasound is the procedure of choice for Screening and Diagnosis of Intraventricular
hemorrhage.
• CT and MRI are acceptable alternatives but are more expensive and require transport to the imaging
service.
• 2 systems for classifying GM / IVH have been started for clinical use – Papille & Volpe systems.
• Papille was initially CT based system but was further adapted for the interpretation of USG. Volpe
system is ultrasound based.
• The utility of the classification schema resides in the ability of the clinicians to communicate degrees
of severity and to have a source of information for comparison of lesions as well as having means to
follow progression or regression and recovery of the initial insult of IVH.
34. CRANIAL ULTRASOUND
Grade Papille Grading system Volpe Grading syytem
1 Subependymal hemorrhage
with minimal or no /ivh
Germinal matrix hemorrhage
< 10% IVH
2 IVH without Ventricular
dilatation
IVH 10 – 50 %
3 Enlargement of ventricles
secondary to distension
with blood
IVH > 50 % with lateral
ventricle dilatation
4 Extension of hemorrhage
into the parenchyma along
with IVH and enlargement.
-
There is no Grade 4 in volpe classification. Final stage is Periventricular echodensity signifying parenchymal lesion
35. CRANIAL ULTRASOUND
SCREENING
Age USG Indication
1 day Perinatal asphyxia ,
In utero drug
exposure
3 days Unstable clinical
course
7 days All infants ≤32 wks
gestation
36 wks PMA or
before discharge
All NICU babies
• A cranial ultrasound is indicated for screening
sick preterm infants for IVH from the first day of
life , throughout hospitalization.
• Typically a Neurosonography is done between
day 1 and 7, depending on clinical presentation
and institutional protocols.
• Approx 50 % GM/IVH may occur on Day1.
• Approx 90 % GM/IVH have occurred by Day4.
• Of all GM/IVH identified by Day 4 of life, 20 – 40
% will progress to more extensive hemorrhage.
36. M A N A G E M E N T O F
I N T R A V E N T R I C U L A R
H E M O R R H A G E
37. M A N A G E M E N T O F
I N T R A V E N T R I C U L A R
H E M O R R H A G E
P R E V E N T I O N A C U T E
M A N A G E M E N T
P O S T N A T A L
P R E V E N T I O N
P R E N A T A L
P R E V E N T I O N
F O L L O W U P
38. IVH PREVENTION
Prenatal strategies
• Avoidance of Premature deliveries.
• Transportation in utero.
• Antenatal steroid therapy.
Postnatal strategies
• Avoid Birth asphyxia.
• Avoid blood pressure fluctuations
• Avoid rapid infusions of volume
expanders or hypertonic solutions.
• Prompt & cautious CVS support to
prevent hypotension.
• Correct acid –base abnormalities
• Correct coagulopathies.
• Synchronized mechanical ventilation.
39. ACUTE STAGE MANAGEMENT
• General supportive care to maintain normal blood volume.
• Maintain electrolyte and acid- base status.
• Blood transfusion to maintain hematocrit , in large bleeds.
• Thrombocytopenia or coagulation disturbances should be corrected.
• In case of Posthemorrhagic ventricular dilatation, careful monitoring of ventricular size by serial
ultrasounds and appropriate interventions ( Therapeutic lumbar punctures,VP shunts/ medical
decompressiosn) .
• Follow up serial imaging to detect progression of IVH and later progressive hydrocephalus.
40. OUTCOME
• Grade 1 & 2 IVH - Spontaneous Resolution
• Grade 3 IVH - Evolves over 1 – 3 wks.
After this it produces fibrotic reaction that
obliterates subarachnoid space & leads to
ventricular dilatation and hydrocephalus.
• Intraparenchymal Hemorrhage - Mortality / Followed in 1 – 8
wks by tissue destruction
and formation of
porencephalic cyst.
41. PROGNOSIS
• Grade 1 & 2 IVH – No significant neurologic dysfunction.
• Grade 3 IVH – neurologic abnormality in 35 % of infants.
• Grade 4 IVH – Neurologic abnormality in 55 % of infants.
• Mortality seen in approximately 50 % of neonates with hemorrhagic
infarct.
2008, Browser et al.
42. TO
CONCLUDE………. Cranial hemorrhage in infants can be 1. Extracranial 2. Intracranial
The extracranial hemorrhages include – caput, cephalhematoma & subgaleal
hematoma.
The intracranial hemorrhages can further be – Extradural, subdural, subarachnoid,
cerebral, intracerebellar, intraventricular hemorrhage.
Vaccum delivery has been implicated in etiogenesis of ICH .esp term neonates, closely
followed by high and mid forceps followed by low forceps extraction.
Intraventricular hemorrhage is the most common CNS complication of a preterm birth.
43. Germinal matrix bleed and resulting intraventricular hemorrhage is more commonly
seen with preterm babies & is greatly associated with the immaturity of the germinal
matrix.
A cranial ultrasound is indicated for screening sick preterm infants for IVH from the first
day of life throughout hospitalization.
IVH grading is performed as per the Papille & Volpe grading systems. ( Cranial ultrasound
based)
Prognosis of Grade 1 & 2 IVH has been found the best and nearly equivalent to a normal
neonate.
Strict neurologic follow up is a must in all the cases of IVH for long term morbidity
corrections.
TO
CONCLUDE……….