Radiological approach to HIE

1. HYPOXIC ISCHEMIC
ENCEPHALOPATHY
DR NEHA NUPUR
JR -2
RIMS,RANCHI

2. 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 age
2)Duration of insult
3)Collateral

3. 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

4. FETAL FACTORS*
a)Anaemia
b)Cardiomyopathy
c)Severe cardiac/circulatory failure

5. CLINICAL FEATURES
• 1- Delayed cry at birth.
• 2-drowsiness/lethargic
• 3-convulsions.

6. HEAD LAG IN AN INFANT OF CEREBRAL PALSY

7. 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

8. AXIAL T1 IMAGE SHOWING HYPERINTENSE
SIGNAL ALONG THE GYRUS SHOWING
CORTICAL LAMINAR NECROSIS

9. WATER-SHED ZONES
BORDER 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

10. 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.

11. ..CONTD

12. …CONTD

13. AXIAL T2 WEIGHTED IMAGE SHOWING
INFARCT IN WATER-SHED REGION

14. Cerebral ischemia
PATHOPHYSIOLOGY:
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.

16. TYPES OF BRAIN EDEMA
• 1)VASOGENIC EDEMA
• 2)CYTOTOXIC EDEMA
• 3)INTERSTITIAL EDEMA

17. PATTERN OF BRAIN INJURY
• PRE-TERM (less than 37 weeks)
• TERM (37 weeks or more).

18. 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.

19. …contd
3) PERI-VENTRICULAR LEUKOMALACIA.
4)THINNING OF CORPUS CALLOSUM
5)DIALATION OF VENTRICLES
6)DEVELOPMENT OF PORENCEPHALIC CYST

20. 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.

21. 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

22. FLAIR
• Thinning of periventricular white matter.
• Thinning of corpus callosum.
• Development of porencephalic cyst.
• Ventriculomegaly.

23. USG SHOWING DIALATION OF VENTRICLES

24. AXIAL CT SHOWING DIALATION OF TRIGONE OF
LATERAL VENTRICLE

25. AXIAL T1 WEIGHTED IMAGES SHOWING
PERIVENTRICULAR GLIOSIS,LOSS OF WHITE MATTER

26. AXIAL T2 WEIGHTED IMAGE SHOWING OF
PERIVENTRICULAR HAEMORRHAGE

27. CORONAL AND AXIAL FLAIR IMAGE SHOWING IRREGULAR
CONTOUR OF VENTRICLE.

28. ..contd

29. PRE-MATURE INFANTS WITH
PROFOUND ASPHYXIA
• CAUSE-hypotension or cardiac arrest
followed by resuscitation.
• IMAGING-infarction or bleed involving
thalami,basal ganglia and brainstem.

30. Axial images in DWI and ADC
map.

31. 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-

32. 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.

33. …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.

34. AXIAL CT SHOWING REVERSAL SIGN

35. FEW CASES REPORTED IN DEPARTMENT OF RIMS
• . • .

36. 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.

37. AXIAL CT SHOWING MUTICYSTIC
ENCEPHALOMALACIA

38. AXIAL FLAIR IMAGE SHOWING MULTICYSTIC
ENCEPHALOMALACIA IN FRONTAL REGIONS.

39. DWI AND ADC MAP SHOWING INFARCT IN BASAL
GANGLIA AND

40. 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 .

41. VASCULAR SUPPLY
CHANGES AS BRAIN
MATURES

42. 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.

43. 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

44. 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

45. REFERENCES
1) CRANIAL MRI AND CT –LEE AND RAO.
2) MRI OF BRAIN AND SPINE –SCOTT.
3) DIAGNOSTIC NEURORADIOLOGY-OSBORN

46. THANKS