HYPOXIC ISCHEMIC
ENCEPHALOPATHY DR NEHA
NUPUR JR -2
RIMS,RANCHI
DEFINITION
Hypoxic-Ischemic Encephalopathy:results when there is global rather than focal reduction in blood flow,oxygen or glucose supply .
HIE Depends on:1)Gestational age2)Duration of insult3)Collateral
ETIOLOGY MATERNAL FACTORS a) Hypotension b) Cardiac arrest c) In utero exposure to cocaine d) Infection (chorio amnionitis)
UTERO- PLACENTAL FACTORS a) uterine rupture b) Umbilical cord-entanglement/prolapse
FETAL FACTORS*
a)Anaemia
b)Cardiomyopathy
c)Severe cardiac/circulatory failure
CLINICAL FEATURES• 1- Delayed cry at birth.• 2-drowsiness/lethargic• 3-convulsions.
HEAD LAG IN AN INFANT OF CEREBRAL PALSY
PATHOLOGY
WATER SHED ZONE/BORDER ZONE:
ISCHAEMIC CHANGES IN HIE ARE CONCENTRATED PRIMARILY ALONG THE ARTERIAL BORDER ZONES BETWEEN MAJOR CEREBRAL AND CEREBELLAR ARTERY TERRITORIES
CORTICAL LAMINAR NECROSIS• INFARCTION OF GREY
MATTER OF CORTEX IN RESPONSE TO ANOXIA ,OFTEN ASSOCIATED WITH HAEMORRHAGE
AXIAL T1 IMAGE SHOWING HYPERINTENSE SIGNAL ALONG THE
GYRUS SHOWING CORTICAL LAMINAR NECROSIS
WATER-SHED ZONESBORDER OR WATER SHED ZONES ARE
THOSE AREAS BETWEEN THE TERMINAL CAPILLARY BEDS OF MAJOR TERRITORIAL ARTERIES.
a)Superficial border zone infarction: ACA and MCA MCA and PCA
b)Deep medullary zone infarction
These water shed areas occur b/w cortical branches of middle cerebral artery and lenticulostriate arteries of MCA trunck.
Border zones also exist b/w major
branches supplying the cerebellum.
..CONTD
…CONTD
AXIAL T2 WEIGHTED IMAGE SHOWING INFARCT IN WATER-SHED REGION
Cerebral ischemiaPATHOPHYSIOLOGY:Can be defined as the diminition of
cerebral blood flow to all or a portion of the brain , below the level needed to maintain normal cerebral function.
Normal regional cerebral blood flow is approx 54 ml/ 100 gm/min.
The threshold for ischemia is approx 23 ml /100g/min.
TYPES OF BRAIN EDEMA
• 1)VASOGENIC EDEMA• 2)CYTOTOXIC EDEMA • 3)INTERSTITIAL EDEMA
PATTERN OF BRAIN INJURY
• PRE-TERM (less than 37 weeks)• TERM (37 weeks or more).
PRE-TERM:MILD-TO MODERATE HYPOXIA:
The most common area to undergo
ischaemic injury in the pre-mature infant is the peri-ventricular white matter,which in the developing fetus is the vascular watershed zone and has a relatively high metabolic demand.
1 periventricular infarction(40%)2 periventricular haemorrage(15%)-bleed
may occur in the region of germinal matrix which may break through the ependymal lining resulting into intra-ventricular bleed.
…contd3) PERI-VENTRICULAR LEUKOMALACIA.4)THINNING OF CORPUS CALLOSUM5)DIALATION OF VENTRICLES6)DEVELOPMENT OF PORENCEPHALIC
CYST
GRADING OF GERMINAL MATRIX HAEMORRHAGE
• DEFINITION:it is a loose network of highly vascularised tissue with little supporting stroma containing primitive nerve cells.
• GRADE 1-haemorrhage confined to germinal matrix.• GRADE 2-haemorrhage extending into ventricle or
subependymal region.• GRADE 3-massive haemorrhage into ventricle causing
hydrocephalous.
IMAGING• USG-to exclude dialation of ventricles or
haemorrhage.• CT-to asses ventricular dilation and intra-
ventricular bleed.
• T1-intra ventricular bleed seen as hyperintense signal.
• T2-gliosis –seen as increased signal intensity in peri-ventricular white matter.
• DWI-shows restriction in peri-ventricular region with corresponding hypointense signal in ADC map
FLAIR
• Thinning of periventricular white matter.
• Thinning of corpus callosum.• Development of porencephalic cyst.• Ventriculomegaly.
USG SHOWING DIALATION OF VENTRICLES
AXIAL CT SHOWING DIALATION OF TRIGONE OF LATERAL VENTRICLE
AXIAL T1 WEIGHTED IMAGES SHOWING PERIVENTRICULAR GLIOSIS,LOSS OF WHITE MATTER
AXIAL T2 WEIGHTED IMAGE SHOWING OF PERIVENTRICULAR HAEMORRHAGE
CORONAL AND AXIAL FLAIR IMAGE SHOWING IRREGULAR CONTOUR OF VENTRICLE.
..contd
PRE-MATURE INFANTS WITH PROFOUND ASPHYXIA
• CAUSE-hypotension or cardiac arrest followed by resuscitation.
• IMAGING-infarction or bleed involving thalami,basal ganglia and brainstem.
Axial images in DWI and ADC map.
ISCHEMIC INJURY IN TERM
Less porfound asphyxia• Cause-birth asphyxia
• Injury to cortical and sub-cortical areas in a water –shed distribution with relative sparing of the peri-ventricular white matter.
Profound episodes of asphyxia• Cause-hypotension/
cardiac
• injury in the thalami and basal ganglia.
• Cystic encephalomalacia-
TERM INFANTS WITH MILD TO MODERATE HYPOXIA
• IMAGING• 1)USG-for the assement of ventricular dilation .• 2)CT-• 24 hrs-hypodensity noted in bilateral cerebral
hemisphere with sparing of cerebellum and thalamus known as reversal sign.
• 2days-early calcific changes in bilateral basal ganglia.• 5 days –ventricular dilation.• 2 weeks –coarse calcification.• 1 month-calcification resolves ,brain volume loss in
cortical and subcortical region.
…CONTD
3)T1- hypointense signal in the region of ischaemic grey matter.4)T2-hyperintense signal in the region of ischaemic grey matter .5)DWI AND ADC MAP-deep gery matter infarction showing restriction.
3)DWI AND ADC MAP-shows grey matter infarction .
AXIAL CT SHOWING REVERSAL SIGN
FEW CASES REPORTED IN DEPARTMENT OF RIMS
• . • .
IMAGING IN TERM INFANTS WITH PROFOUND ISCHEMIA
1)CT-multicystic areas of fluid collection replacing brain parenchyma.
2)T1-hypointensity primarily in grey matter.3)T2-hyperintensity primarily in the grey matter.4)DWI- high signal intensity in basal ganglia and
thalamus .5)ADC-hypointensity in basal ganglia and
thalamus.6)FLAIR- shows multicystic encephalomalacia.
AXIAL CT SHOWING MUTICYSTIC ENCEPHALOMALACIA
AXIAL FLAIR IMAGE SHOWING MULTICYSTIC ENCEPHALOMALACIA IN FRONTAL REGIONS.
DWI AND ADC MAP SHOWING INFARCT IN BASAL GANGLIA AND
DIFFERENCES BETWEEN PRE-TERM AND TERM
NEWBORN PRE-TERM• The water shed zone is
located in deep peri-ventricular matter.
• Collaterals at deep peri-ventricular matter not developed.
• Auto-regulatory mechanism not fully developed.
TERM• The water shed zone is
located in cortical and sub-cortical region.
• Collateral developed.
• Auto-regulatory mechanism developed .
VASCULAR SUPPLY CHANGES AS BRAIN
MATURES
PROGNOSIS AND TREATMENT
.. PROGNOSIS• infants with mild
encephalic changes make full recovery while 20 % of affected infants die in neonatal period ,some develop severe neurologic sequlae.the prognosis is even worse in pre-term.
TREATMENT• Maintainence of adequate ventilation
,avoidance of hypotension ,maintainence of metabolic glucose ,fluid and nutritional status ,control of seizures and control of brain edema lie the main treatment
CONCLUSION• HIE remains an important cause of
morbidity and mortality in the neonatal period and cerebral palsy is a late neurologic sequale in the post natal period .intervention remains supportive ,imaging becomes important for optimal management and rule out other causes of encephalopathy
REFERENCES1) CRANIAL MRI AND CT –LEE AND RAO.2) MRI OF BRAIN AND SPINE –SCOTT.3) DIAGNOSTIC NEURORADIOLOGY-OSBORN
THANKS
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