Imaging of hypoxic ischemic encephalopathy in neonates .role of early diagnosis and imaging manifestations

1. HYPOXIC ISCHEMIC
ENCEPHALOPATHY
DR. JAISA RAM
JR 2

2. DEFINITION
Hypoxic-Ischemic Encephalopathy:
Insufficient cerebral blood flow(ischemia)
and decreased blood oxygenation(hypoxia)
leads to loss of normal cerebral auto-
regulation. This results in diffuse brain
injury that known as HIE.
HIE Depends on:
1) Gestational age(Brain maturity) at time of insult.
2) Duration and Severity of insult.

3. ETIOLOGY
1. INTRAUTERINE ASPHYXIA
 Inadequate placental perfusion
a) Maternal Hypotension
a) Preeclampsia
a) Abruptio placentae
b) Infection (chorio amnionitis)
• Impaired maternal oxygenation
a) Asthma
b) Pulmonary embolism
c) CO poisioning
 Disrupted umbilical circulation
a) Tight nuchal cord
b) Umbilical cord-entanglement/prolapse

4. FETAL FACTORS*
a) Anaemia
b) Fetal thrombosis, FM hemorhage
c)circulatory failure( bradycardia)
2. POSTNATAL ASPHYXIA
a) Severe hyaline membrane disease
b) Meconium aspiration

5. CLINICAL DIAGNOSIS OF HIE
• 1- Low umbilical cord pH<7.1
• 2-Poor Apgar score (0-3) at 5min
• 3-necessity for resuscitation
• 4-convulsions, hypotonia, coma.
• 5-Multiorgan dysfunction

6. PATHOPHYSIOLOGY

7. VULNERABLE AREA FOR HIE
• Areas with greatest demand of energy
• Areas with highest concentration of
glutamate or other excitatory amino acid
receptor
BORDER ZONE
Preterm neonate – Periventricular
Term neonate- para-saggital in location

8. VASCULAR SUPPLY CHANGES AS
BRAIN MATURES
TERM
PRETERM
PARASAGGITAL BORDER ZONE DIST.

9. PRE-TERM:
MILD-TO MODERATE HYPOXIA
Most common site of insult –border zone
(periventricular region)
1 periventricular infarction(40%)
2 periventricular haemorrage(15%)

10. IMAGING
• USG-to exclude dialation of ventricles or
haemorrhage, periventricular
leukomalacia.
• CT-to asses ventricular dilation and intra-ventricular
bleed. Less sensitive modality.
• MRI- common sequence are done T1 ,T2, DWI , ADC
SWI if hemorrhage is suspected . MRS is done when
DWI findings are normal,but clinical suspicion for
HII still remain High.
• 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

11. FLAIR
Useful in demonstrating following feature.
• Thinningof periventricular white matter.
• Thinningof corpus callosum.
• Development of porencephaliccyst.
• Ventriculomegaly.
ROLE OF MRS--
. MR spectroscopy provides gross biochemical analysis of the
“compromised anaerobic” cerebral tissues, as it reveals changes in
the concentrations of lactate, choline, creatine, N-acetylaspartate
(NAA), and glutamine
USEFUL WHEN DWI IS NORMAL BUT HIGH
CLINICAL SUSPICION OF HIE
Elevated lactate and diminished NAA concentrations are common
findings in infants with HIE.

13. g
GRADE – I GMH
GRADE –II GMH
GRADE-II GMH
GRADE-III GMH

15. WHITE MATTER INJURY OF PREMATURITY

16. Doppler interrogation and the assessment of
resistive index (RI) provide additional information on
cerebral perfusion. Normally, the RI decreases with
increasing gestational age, and thus correlation with
gestational age is necessary for accurate
interpretation of RI results.
Decreased RI is noted to be an abnormal finding
and is postulated to be caused by impairment in
cerebral auto-regulation and subsequent decreased
cerebrovascular resistence and increase in end-
diastolic flow. However, Sustained asphyxia with
subsequent development of intracanial hemorrhage
or diffuse cerebral edema and loss of forward
diastolic flow result in increased RI and is indicative
of a poor outcome
ROLE OF COLOR DOPPLER IN HIE

18. PVL-I
T1 W – PVL-1
(SHOW
HEMMORHAGE)
T2W HIGH SI

19. END STAGE OR CHRONIC PVL
T2 FLAIR
T1 W

20. PROFOUND HYPOXIC-ISCHEAMIC INJURY IN
PRETERM NEONATE
• SEVER HYPOXIC INJURY AFFECT PREDOMINANTLY DEEP GRAY
MATTER STRUCTURES AND BRAINSTEM I.E. thalami, dorsal brainstem,
anterior vermis.
• With relative low involvement of basal ganglia hippocampus,
periolandic cortex, and corticospinal tracts.
• why? Because early myelination of thalamus and globus pallidus at
25weeks of GA. Late myelination of caudate nucleus and putamen ,
perirolandic cortex at 35weeks of GA.
• May be associated with GMS OR PVL.
• MRI FINDING- earliest MRI finding is diffusion abnormality in thalami
which usually evident within the first 24hrs. Increased T2 SI is seen by
the 3rd day and T1 SI by 4th day.

21. T1WI AXIAL

22. Acute profound asphyxia -results in lesions in high-oxygen-
demand areas(deep gray matter), sometimes called the basal ganglia-
thalamus pattern
ventrolateral thalamus
posterior putamen, hippocampi, dorsal brainstem
corticospinal tract from perirolandic cortex to posterior limb of internal
capsule (including absent posterior limb sign)
Prolonged partial asphyxia- results in hemispheric cortical-
subcortical lesions in a watershed (border zone or watershed zonel)
distribution (parasaggital white matter and when severe extending to
overlying cortex).
Auto-regulatory mechanism maintain perfusion to highly metabolically
active area(deep gray matter and brain stem ).
PATTERN OF HIE IN TERM NEONATE

23. MRI FINDINGS IN MILD TO MODERATE HIE
DWI is earliest to change and show cortical and
Subcortical white matter restriction.
By 2nd day T2 WI show cortical swelling , loss of gray white
Matter differentiation and hyperintensity in cortex and
Subcortical white matter.
T1WI show abnormal cortical high SI beginning from the 3rd
Day of insult, reach max. during 2nd week, last for several for
Weeks this is referred to cortical highlightning.
T1WI and T2WI may show punctuate T1 high SI and
corresponding T2WI low SI, representing Astrogliosis in the
Parasagittal subcortical white matter. No blooming on SWI will
Rule out hemorrhage.
ULEGYRIA – shrunken cortex with flattened mushroom
shaped gyri and diminished white matter
Predominantly in P-O region is seen in the chronic stage

24. FT WITH LESS SEVERE HIE
T2WI AXIAL SCAN SHOW
PARASAGITAL PATTERN
T1WI AND T2WI
ULEGYRIA- MUSHROOM
SHAPE MORPHOLOGY

25. FT WITH SEVERE HIE
T1WI SHOW BGT PATTERN
FLAIR AND T2WI

26. DWI SHOW PP AND INTERNAL CAPSULE INJURY
PERIOLANDIC CORTEX

27. DWI AND ADC SHOWS CORPUS
CALLOSUM INJURY
AXIAL T1 WI SHOWS CORTICAL
HIGHLIGHTING IN PERIOLANDIC
REGION

28. HIE IN YOUNG CHILD AND ADULT
Corpora striata lateral geniculate nuclei, hippocampi ,cerebral cortex are affected with
Relatives sparing of thalami and perirolandic cortex.
Results from drowning ,cardiac arrest .
Cranial USG- not useful once the AF has closed
CT becomes the initial imaging study of choice.
Early CT performed within 24hrs of an insult may be negative.
Within the first 24hrs
REVERSAL SIGN
WHITE CEREBELLUM SIGN
Pseudosubarachnoid hemorrhage
SUBSEQUENT CT SHOWS
Diffuse basal ganglia abnormalities
Diffuse cerebral edema with loss of G-M junction
Cisternal and sulcal effacement
Relatives sparing of periolandic cortex and thalami.
Cortical laminar necrosis/pseudolaminar necrosis become evident as early as 3-4days.
Hemorhgic infarction of basal ganglia may be evident by 4-6 days
CHRONIC PHASE- diffuse atrophy with sulcal and ventricular enlargement.
MRI IMAGING – DWI is abnormal within 24hrs , T1 AND T2 WI are normal in first 24hrs.
By 48hrs T2WI will show diffuse basal ganglia and cortical SI abnormality representing edema
With/without sparing of perirolandic cortex and thalami.

29. AXIAL CT SHOWING REVERSAL SIGN and WHITE
CEREBELLUM SIGN

30. PSEUDOSUBARACHNOID
HEMORHAAGE ON NCCT
HEAD

31. 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

32. THANKS