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The incidence of intracranial hemorrhage
(ICH) varies from 2% to >30% in new-borns,
depending on gestational age (GA) at birth and
the type of ICH. Bleeding within the skull can
occur: (i) external to the brain into the
epidural, subdural, or subarachnoid spaces; (ii)
into the parenchyma of the cerebrum or
cerebellum; or (iii) into the ventricles from the
subependymal germinal matrix or choroid
plexus.
The incidence, pathogenesis, clinical
presentation, diagnosis, management, and
prognosis of ICH varies according to the ICH
location and size, and the infants GA.
There is often a combination of two or
more types of ICH, as an ICH in one location
often extends into an adjacent compartment;
for example, extension of a parenchymal
hemorrhage into the subarachnoid space or
ventricles.
Diagnosis usually depends on clinical
suspicion when an infant presents with typical
neurologic signs, such as seizures, irritability,
depressed level of consciousness, and/or focal
neurologic deficits referable either to the
cerebrum or brain stem. Diagnosis is
confirmed with an appropriate neuroimaging
study.
The American Academy of Neurology
(AAN) states that all infants with a birth GA of
<30 weeks should undergo routine cranial
ultrasound (CUS) between 7-14 days and
optimally repeated between 36 to 40 weeks
postmenstrual age,
Management varies according to the
size and location of the ICH and the
presenting neurologic signs. In general, only
very large hemorrhages with clinical signs
require surgical intervention
More commonly, management is
focused on treating complications such as
seizures
or
the
development
of
posthemorrhagic hydrocephalus.
GMH/IVH :-
A.Aetiology and pathogenesis
A.Aetiology and pathogenesis
GMH/IVH is found principally in the preterm infant,
where the incidence is currently 15% to 20% in infants
born at <32 weeks' GA, but is uncommon in the term
newborn. The etiology and pathogenesis are different for
term and preterm infants.
GMH/IVH :-
A.Aetiology and pathogenesis
1.In the term newborn
a- IVH typically originates in the choroid plexus.
b- In association with venous (± sinus) thrombosis and
thalamic infarction,
c- IVH may also occur in the small remnant of the
subependymal germinal matrix.
GMH/IVH :-
A.Aetiology and pathogenesis
2. In the preterm infant, GMH/IVH originates from the
fragile involuting vessels of the subependymal germinal
matrix
There are numerous risk factors that have been
identified in the etiology of IVH
a- Maternal factors such as infection/inflammation and
hemorrhage, lack of antenatal steroids.
GMH/IVH :-
A.Aetiology and pathogenesis
b-External factors such as mode of delivery or neonatal
transport to another hospital, and increasingly recognized
genetic factors that predispose some newborns to IVH.
However these risk factors all contribute to the basic
pathogenesis of GMH/IVH, which relates to alterations in
blood flow and coagulation. Thus, the pathogenesis of
GMH/IVH in preterm newborns has been shown to be
largely related to intra-vascular, vascular, and extravascular
factors
GMH/IVH :-
A.Aetiology and pathogenesis
Ischemia/reperfusion (e.g., volume infusion after hypotension)
Fluctuating CBF (e.g., with mechanical ventilation)
Intravascular factors
Increase in CBF (e.g., with hypertension, anemia, hypercarbia)
Increase in cerebral venous pressure (e.g., with high
intrathoracic pressure, usually from ventilator)
Platelet dysfunction and coagulation disturbances
Vascular factors
Weak, involuting capillaries with large luminal diameter
Extra vascular factors
Deficient vascular support
GMH/IVH :-
A.Aetiology and pathogenesis
A-Intravascular factors
1- Ischemia/reperfusion:- this scenario often occurs shortly
after birth, when a premature infant may have hypovolemia
or hypotension that is treated with infusion of colloid, normal
saline, or hyperosmolar solutions such as sodium bicarbonate.
Rapid infusions of such solutions are thought to be
particularly likely to contribute to GMH/IVH.
2- Fluctuating CBF:-The large fluctuations typically occurred
in infants breathing out of synchrony with the ventilator, but
such fluctuations have also been observed in infants with
large patent ductus arteriosus or hypotension
GMH/IVH :-
A.Aetiology and pathogenesis
A-Intravascular factors
3- Increase in CBF:- Sustained increases in CBF may
contribute to GMH/IVH and can be caused by seizures,
hypercarbia, anemia, and hypoglycemia, which result in a
compensatory increase in CBF.
4-Increase in cerebral venous pressure|:- intrathoracic pressure
is high (e.g., high continuous positive airway pressure),
pneumothorax, tracheal suctioning, and both labor and delivery,
where fetal head compression likely results in significantly increased
venous pressure. Indeed, a higher incidence of GMH/IVH is found in
preterm infants with a longer duration of labor and in those delivered
vaginally compared with those delivered via caesarean section.
GMH/IVH :-
A.Aetiology and pathogenesis
A-Intravascular factors
Several studies have shown that preterm infants, particularly
asphyxiated newborns, have an impaired ability to regulate CBF in
response to blood pressure changes (hence, "pressure-passive") . Such
impaired autoregulation puts the infant at increased risk for rupture of
the fragile germinal matrix vessels in the face of significant increases in
cerebral arterial or venous pressure, and particularly when ischemia
precedes such increased pressure.
5- Platelet dysfunction and coagulation disturbances:-Finally,
impaired coagulation and platelet dysfunction are also
intravascular factors that can contribute to the pathogenesis of
GMH/IVH.
GMH/IVH :-
A.Aetiology and pathogenesis
B-Vascular factors
Vascular factors that contribute to GMH/IVH include
the fragile nature of the involuting vessels of the
germinal matrix. There is no muscularis mucosa
and little adventitia in this area of relatively large
diameter, thin-walled vessels; all of these factors
make the vessels particularly susceptible to rupture.
GMH/IVH :-
A.Aetiology and pathogenesis
C-Extra vascular factors
Extravascular risk factors for GMH/IVH
include deficient extravascular support and likely
excessive fibrinolytic activity in preterm infants.
GMH/IVH :-
B-Complications of GMH/IVH.
B-Complications of GMH/IVH.
The two major complications of GMH/IVH are:1-Periventricular hemorrhagic infarction (PVHI)
2-Posthemorrhagic ventricular dilation (PVD).
***********
1-Periventricular hemorrhagic infarction (PVHI)
 PVHI has previously been considered an extension of a large IVH
Recently,it is not accepted as an extension of the original IVH, but
is a separate lesion consisting of a venous hemorrhagic infarction.
a-Neuropathologic studies demonstrate the fan-shaped appearance of a
typical hemorrhagic venous infarction in the distribution of the
medullary veins that drain into the terminal vein, resulting from
obstruction of flow in the terminal vein by the large ipsilateral IVH.
GMH/IVH :-
B-Complications of GMH/IVH.
b-PVHI occurs on the side of the larger IVH, and Doppler US studies
show markedly decreased or absent flow in the terminal vein on the side
of the large IVH .
c-The ependymal lining of the lateral ventricle separating IVH and
PVHI has been observed to remain intact in some cases, demonstrating
that the IVH did not ""extend" into the adjacent cerebral parenchyma.
Risk factors for the development of PVHI include low birth
GA, low Apgar scores, early life acidosis, patent ductus
arteriosus, pneumothorax, pulmonary hemorrhage, and need
for significant respiratory or blood pressure support
GMH/IVH :-
B-Complications of GMH/IVH.
2-Posthemorrhagic
ventricular
dilation
(PVD).or
posthemorrhagic hydrocephalus (PHH-terminology varies),
may occur days to weeks following the onset of GMH/IVH.
Not all ventricular dilation progresses to established
hydrocephalus
The pathogenesis of progressive posthemorrhagic ventricular dilation:
a-Impaired CSF resorption and/or obstruction of the aqueduct
or the foramina of Luschka or Magendie by particulate clot
b-High levels of transforming growth factor β-1(TGFβ-1) are
found in the CSF following IVH, particularly in infants with
PVD; TGF-pl upregulates genes for extracellular matrix
proteins that elaborate a "scar," which may obstruct CSF flow
and/ or CSF reabsorption
GMH/IVH :-
B-Complications of GMH/IVH.
The pathogenesis of the brain injury resulting from PVD
is probably related in large part to :
a-Regional hypoxia-ischemia and mechanical distension of the
periventricular white matter.
b-The presence of non-protein-bound iron in the CSF of
infants with PVD may lead to the generation of reactive
oxygen species that in turn contribute to the injury of
immature oligodendrocytes in the white matter .The brain
injury associated with PVD is principally a bilateral cerebral
white matter injury.
GMH/IVH :-
C. Clinical Presentation
C. Clinical Presentation
1-GMH/IVH in the preterm newborn is usually a clinically
“Silent syndrome” and thus is recognized only when a
routine CUS is performed. The vast majority of these
hemorrhages occur within 72 hours after birth
Infants with large IVH may present with decreased
levels of consciousness and spontaneous movements,
hypotonia, abnormal eye movements. Rarely, coma,
severe hypotonia and lack of spontaneous movements,
OR generalized tonic posturing that is often thought to
be seizure, but does not have an electrographic correlate
by electroencephalogram.
GMH/IVH :-
C. Clinical Presentation
2-The term newborn with IVH typically presents with signs
such as seizures, apnea, irritability or lethargy, vomiting with
dehydration, or a full fontanel.
3-Posthemorrhagic ventricular dilation (PVD) may develop
over days to weeks following IVH, particularly in premature
infants, and may present with increasing head growth
(crossing percentiles on the growth chart), bulging fontanelle,
splitting of sutures, decreased level of consciousness,
sunsetting sign, apnea, worsening respiratory status, or feeding
difficulties. However, PVD may be relatively asymptomatic in
preterm newborns
Grading of GMH/IVH
GMH/IVH :-
Grading of GMH/IVH
Grading system
Severity of GMH/1VH
Papile
I
Isolated GMH (no IVH)
II
IVH without ventricular dilatation
III
IVH with ventricular dilatation
IV
IVH with parenchymal hemorrhage
Description of findings
GMH/IVH :-
Management and Prognosis
E. Management and Prognosis
Prevention of GMH/IVH should be the primary goal
1-Antenatal administration of glucocorticoids has clearly been
shown to decrease the incidence of GMH/IVH.
2-Aantenatal phenobarbital, vitamin K, and magnesium sulfate have
not been conclusively demonstrated to prevent GMH/IVH.
3-Minimizing risk factors as infusions of colloid or hyperosmolar
solutions should be given slowly.
4-Efforts should be directed to avoiding hypotension and large
fluctuations or sustained increases in arterial blood pressure or
cerebral venous pressure.
5-Elimination of CBF fluctuation related to mechanical ventilation
GMH/IVH :-
Management and Prognosis
Management of GMH/IVH in the premature newborn
largely consists of :
A-Supportive care and monitoring for and treatment of
complications of GMH/IVH.
1-Supportive care should be directed toward maintaining
stable cerebral perfusion by maintaining normal blood
pressure, circulating volume, electrolytes, and blood gases.
2-Transfusions of packed red blood cells may be required in
cases of large IVH to restore normal blood volume and
hematocrit.
3-Thrormbocytopenia or coagulation disturbances should be
corrected.
GMH/IVH :-
Management and Prognosis
B-Treatment of seizures during the acute phase.
C-Careful monitoring of ventricle size by serial
CUS and appropriate intervention when needed to
reduce CSF accumulation, such as serial LPs to
remove CSF, surgical interventions to divert CSF
flow, and rarely, medications to reduce CSF
production
GMH/IVH :-
Management and Prognosis
The long-term prognosis for infants with GMH/IVH
varies considerably depending on the severity of IVH,
complications of IVH or other brain lesions, the birth
weight/GA, and other significant illnesses that affect
neurologic outcome. Several recent studies suggest that
preterm infants with grades I and II IVH have an increased
risk of CP and/or cognitive impairment
GMH/IVH :-
Management and Prognosis
Infants with the two major complications of IVH, namely
PVHI and PVD, are at much higher risk of neurologic
impairments than those with IVH alone. Infants with
PVD/PHH requiring significant intervention often manifest
spastic diparesis and cognitive impairments due to bilateral
peri-ventricular WMI.
Quadriparesis and significant cognitive deficits (including
mental retardation) are more likely if the PVHI is extensive
or bilateral, or if there is also coexisting PVL
GMH/IVH :-
Management and Prognosis
Outcome in term newborns with IVH relates to factors
other than IVH alone, as uncomplicated small IVH in this
population has a favorable prognosis. Infants with a history
of trauma or prenatal asphyxia, or with neuroimaging
evidence of thalamic hemorrhagic infarction, hypoxicischemic brain injury, or other parenchymal lesions, are at
high risk for significant cognitive imparments.
INTRAPARENCHYMAL HEMORRHAGE
INTRAPARENCHYMAL HEMORRHAGE
Etiology and pathogenesis
A. Etiology and pathogenesis
1. Primary cerebral hemorrhage is uncommon in all newborns, An
intracerebral hemorrhage may occur rarely as a primary event related
to rupture of an arteriovenous malformation or aneurysm, from a
coagulation disturbance (e.g., hemophilia, thrombocytopenia), or
from an unknown cause. More commonly, cerebral intraparenchymal
hemorrhage (IPH) occurs as a secondary event, such as hemorrhage
into a region of hypoxic-ischemic brain injury
2. Intracerebellar hemorrhage occurs more commonly in preterm
than term newborns and may be missed by routine CUS.
INTRAPARENCHYMAL HEMORRHAGE
Clinical presentation
B. Clinical presentation. The presentation differs
depending on the size and location of the IPH. In the
preterm infant, IPH is often clinically silent unless the
hemorrhage is quite large. In the term infant,
intracerebral hemorrhage typically presents with focal
neurologic signs such as seizures, asymmetry of
tone/movements along with irritability or depressed
level of consciousness.
Diagnosis. MRI is the best imaging modality for IPH, but
CUS may be used in the preterm infant or when a rapid
bedside imaging study is necessary.
INTRAPARENCHYMAL HEMORRHAGE
Management
Management
1. Small hemorrhages require only symptomatic
treatment and support.
2. Large IPH with severe neurologic compromise
should prompt neurosurgical intervention. It is
important to diagnose and treat any coexisting
pathology, such as infection or sinus venous
thrombosis
INTRAPARENCHYMAL HEMORRHAGE
Prognosis
Prognosis The long term prognosis largely relates to
location and size of the IPH and GA of the infant. A small
IPH may have relatively few or no long-term neurologic
consequences. A large cerebral IPH may result in a lifelong seizure disorder, hemiparesis or other type of
cerebral palsy (CP), feeding difficulties, and cognitive
impairments ranging from learning disabilities to
significant intellectual disability, depending on the
location. Cerebellar hemorrhage in the term newborn
often has a relatively good prognosis, although it may
result in cerebellar signs of ataxia, hypotonia, tremor,
nystagmus, and mild cognitive deficits.
SUBDURAL HEMORRHAGE (SDH) AND
EPIDURAL HEMORRHAGE (EH)
SUBDURAL HEMORRHAGE
Etiology and pathogenesis
A.Etiology and pathogenesis. The pathogenesis of SDH
relates to rupture of the draining veins and sinuses of the
brain that occupy the subdural space.Vertical molding,
fronto-occipital elongation, and torsional forces acting on
the head during delivery may provoke laceration of dural
leaflets of either the tentorium cerebelli or the falx cerebri.
These lacerations can result in rupture of the vein of Galen,
inferior sagittal sinus, straight sinus and/or transverse sinus
SUBDURAL HEMORRHAGE
Clinical presentation
B. Clinical presentation.
1-When the accumulation of blood is rapid and large, as
occurs with rupture of large veins or sinuses, the
presentation follows shortly after birth as infratentorial
SDH, where compression of the brain stem may result in
nuchal rigidity or opisthotonus, obtundation or coma,
apnea, other abnormal respiratory patterns, and unreactive
pupils .With increased intracranial pressure (ICP), there
may be a bulging fontanelle arid/or widely split sutures.
SUBDURAL HEMORRHAGE
Clinical presentation
2-Seizures may occur in up to half of neonates with SDH,
3-Finally, a chronic subdural effusion may gradually develop
over months, presenting as abnormally rapid head growth,
Diagnosis. The diagnosis should be suspected on the
basis of history and clinical signs and confirmed with a
neuroimaging study. CT scan is the study of choice for
diagnosing SDH or EH for acute emergencies, if MRI
cannot be obtained quickly. US is often inadequate.
SUBDURAL HEMORRHAGE
Management
Management. Most infants with SDH do not require
surgical intervention and can be managed with
supportive care and treatment of any accompanying
seizures.
Epidural hemorrhage (EH)
Epidural hemorrhage (EH). There are approximately
20 case reports of neonatal EH in the literature. EH
appears to be correlated with trauma and a large
cephalohematoma or skull fracture was found in about
half the reported cases of EH. Removal or aspiration of
the hemorrhage was performed in the majority of
cases, and the prognosis was quite good except when
other ICH or parenchymal pathology was present.
SUBARACHNOID HEMORRHAGE
SUBARACHNOID HEMORRHAGE
Etiology and pathogenesis
A.Etiology and pathogenesis. Subarachnoid hemorrhage
(SAH) is a common form of ICH among newborns, Primary
SAH (i.e., SAH not due to extension from ICH in an adjacent
compartment) is probably frequent but clinically insignificant.
In these cases, SAH may go unrecognized because of a lack of
clinical signs. For example, hemorrhagic or xanthochromic
CSF may be the only indication of such a hemorrhage in
infants who undergo a CSF exam to rule out sepsis.
SUBARACHNOID HEMORRHAGE
Etiology and pathogenesis
SAH may also result from extension of SDH (e.g.,
particularly in the posterior fossa) or a cerebral contusion
(parenchymal hemorrhage). Finally, subpial hemorrhage may
occur, mostly in the otherwise healthy term newborn, and is
usually a focal hemorrhage likely caused by local trauma
resulting in venous compression or occlusion in the setting of
a vaginal delivery.
SUBARACHNOID HEMORRHAGE
Clinical presentation.
Clinical presentation. As with other forms of ICH,
clinical suspicion of SAH may result because of blood
loss or neurologic dysfunction. More often, neurologic
signs manifest as seizures, irritability, or other mild
alteration of mental status, particularly with SAH
The diagnosis is best established with a MRI (or CT)
scan,
SUBARACHNOID HEMORRHAGE
Management and prognosis.
Management and prognosis. Management of SAH
usually requires only symptomatic therapy, such as
anticonvulsant therapy for seizures and nasogastric
feeds or intravenous fluids if the infant is too lethargic
to feed orally. The majority of infants with small SAH
do well with no recognized sequale