Intracranial Hemorrhage in Neonatal

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Intracranial Hemorrhage in Neonates
By
Prof. Emad Hammad El. Daly
Head of the Neuropediatric Unit -Assiut Univeristy
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• The incidence of intracranial hemorrhage
  (ICH) varies from 2 to gt30 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.

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• 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.

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• 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.

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• The American Academy of Neurology (AAN) states
  that all infants with a birth GA of lt30 weeks
  should undergo routine cranial ultrasound (CUS)
  between 7-14 days and optimally repeated between
  36 to 40 weeks postmenstrual age,

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• 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.

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• GERMINAL MATRIX HEMORRHAGE INTRAVENTRICULAR
  HEMORRHAGE

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• Aetiology and pathogenesis

• GMH/IVH -

• Aetiology and pathogenesis
• GMH/IVH is found principally in the preterm
  infant, where the incidence is currently 15 to
  20 in infants born at lt32 weeks' GA, but is
  uncommon in the term newborn. The etiology and
  pathogenesis are different for term and preterm
  infants.

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• Aetiology and pathogenesis

• GMH/IVH -

• 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.

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• Aetiology and pathogenesis

• GMH/IVH -

• 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.

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• Aetiology and pathogenesis

• GMH/IVH -

• 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

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• Aetiology and pathogenesis

• GMH/IVH -

Ischemia/reperfusion (e.g., volume infusion after hypotension) Fluctuating CBF (e.g., with mechanical ventilation) 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 Intravascular factors
Weak, involuting capillaries with large luminal diameter Vascular factors
Deficient vascular support Extra vascular factors
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• Aetiology and pathogenesis

• GMH/IVH -

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
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• Aetiology and pathogenesis

• GMH/IVH -

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.
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• Aetiology and pathogenesis

• GMH/IVH -

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.
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• Aetiology and pathogenesis

• GMH/IVH -

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.
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• Aetiology and pathogenesis

• GMH/IVH -

C-Extra vascular factors Extravascular risk
factors for GMH/IVH include deficient
extravascular support and likely excessive
fibrinolytic activity in preterm infants.
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• B-Complications of GMH/IVH.

• 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.

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• B-Complications of GMH/IVH.

• 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

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• B-Complications of GMH/IVH.

• 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
  ß-1(TGFß-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

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• B-Complications of GMH/IVH.

• 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.

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• C. Clinical Presentation

• GMH/IVH -

• 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.

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• C. Clinical Presentation

• GMH/IVH -

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
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• Grading of GMH/IVH

• GMH/IVH -

Grading of GMH/IVH
Grading system Severity of GMH/1VH Description of findings
Papile I Isolated GMH (no IVH)
II IVH without ventricular dilatation
III IVH with ventricular dilatation
IV IVH with parenchymal hemorrhage
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• Management and Prognosis

• GMH/IVH -

• 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
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• Management and Prognosis

• GMH/IVH -

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.
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• Management and Prognosis

• GMH/IVH -

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
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• Management and Prognosis

• GMH/IVH -

• 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

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• Management and Prognosis

• GMH/IVH -

• 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

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• Management and Prognosis

• GMH/IVH -

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,
hypoxic-ischemic brain injury, or other
parenchymal lesions, are at high risk for
significant cognitive imparments.
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• INTRAPARENCHYMAL HEMORRHAGE

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Etiology and pathogenesis

• INTRAPARENCHYMAL HEMORRHAGE

• Etiology and pathogenesis
• 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
• Intracerebellar hemorrhage occurs more commonly
  in preterm than term newborns and may be missed
  by routine CUS.

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Clinical presentation

• INTRAPARENCHYMAL HEMORRHAGE

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.
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Management

• INTRAPARENCHYMAL HEMORRHAGE

• Management
• Small hemorrhages require only symptomatic
  treatment and support.
• 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

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Prognosis

• INTRAPARENCHYMAL HEMORRHAGE

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 life-long 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.
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• SUBDURAL HEMORRHAGE (SDH) AND EPIDURAL HEMORRHAGE
  (EH)

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Etiology and pathogenesis

• SUBDURAL HEMORRHAGE

• 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

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Clinical presentation

• SUBDURAL HEMORRHAGE

• 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.

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Clinical presentation

• SUBDURAL HEMORRHAGE

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.
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Management

• SUBDURAL HEMORRHAGE

Management. Most infants with SDH do not require
surgical intervention and can be managed with
supportive care and treatment of any accompanying
seizures.
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• 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.
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• SUBARACHNOID HEMORRHAGE

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Etiology and pathogenesis

• SUBARACHNOID HEMORRHAGE

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.
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Etiology and pathogenesis

• SUBARACHNOID HEMORRHAGE

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.
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• 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,
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• 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
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Thank You