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