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Pediatric perinatal insult: HYPOXIC ISCHEMIC ENCEPHALOPATHY Dr. Mohit Goel, JRIII 19/5/14

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Pediatric perinatal insult: HYPOXIC ISCHEMIC

ENCEPHALOPATHY

Dr. Mohit Goel, JRIII

19/5/14

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INTRODUCTION

Hypoxic-ischemic injury (HII) to the brain is a devastating occurrence that

frequently results in death or profound long-term neurologic disability in

both children and adults.

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Imaging findings in HII are highly variable and depend on a number of

factors, including :

• Brain maturity

• Severity

• Duration of insult

• Type and timing of imaging studies

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PATHOPHYSIOLOGY

Regardless of the specific cause of injury, the common underlying

physiologic processes that result in HII are diminished cerebral blood

flow (ischemia) and reduced blood oxygenation (hypoxemia).

In general, infants and children are more likely to suffer asphyxial

events, which result in hypoxemia and brain hypoxia.

With prolonged hypoxemia, cardiac hypoxia occurs, leading to

diminished cardiac output and, ultimately, to brain ischemia.

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Hypoxic-Ischemic Brain Injury: Imaging Findings from Birth to Adulthood.

Benjamin Y. Huang, MD, MPH and Mauricio Castillo, MD. Doi: 10.1148/rg.282075066 March 2008 RadioGraphics, 28, 417-439.

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Areas of the brain with the highest concentrations of glutamate or

other excitatory amino acid receptors (primarily located in gray

matter) are more susceptible to excitotoxic injury that occurs as a

result of hypoxia-ischemia.

Areas of the brain with the greatest energy demands become

energy depleted most rapidly during hypoxia-ischemia, and are

therefore injured early on.

Because of delayed cell death from apoptosis, some injuries may

not be evident until days after the initial insult has occurred

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Patterns of brain injury in mild to

moderate hypoperfusion.

how the vascular supply changes with

maturation and affects the pattern of brain

injury in HIE.

The premature neonatal brain has a

ventriculopetal vascular pattern, and

hypoperfusion results in a periventricular

border zone of white matter injury.

Premature Term

In the term infant, a ventriculofugal vascular pattern develops as the brain

matures, and the border zone during hypoperfusion is more peripheral with

subcortical white matter and parasagittal cortical injury.

Neonatal Hypoxic-Ischemic Encephalopathy: Multimodality Imaging Findings. Christine P. Chao, MD,

Christopher G. Zaleski, MD and Alice C. Patton, MD. Doi: 10.1148/rg.26si065504 October 2006 RadioGraphics, 26, S159-S172.

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Causes of HIE.

Chao C P et al. Radiographics 2006;26:S159-S172

©2006 by Radiological Society of North America

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IMAGING MODALITIES :

Accurate identification and characterization of the severity,

extent, and location of brain injury rely on the selection of

appropriate neuroimaging modalities, including

1. Ultrasonography

2. Computed tomography

3. Magnetic resonance imaging.

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Radiation

Less sensitive

Why Not CT ??

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TERM NEONATE

Antepartum risk factors

maternal hypotension

infertility treatment

multiple gestation

prenatal infection

thyroid disease

Intrapartum factors forceps delivery

breech extraction

umbilical cord prolapse

abruptio placentae

tight nuchal cord

maternal fever

Antepartum factors in combination with intrapartum

factors.

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“1-2-3-4 sign”

Imaging Findings in Neonatal Hypoxia: A Practical Review. E. Ralph Heinz1 and James M.

Provenzale http://www.ajronline.org/doi/full/10.2214/AJR.08.1321

The four components of the 1-2-3-4 sign are :

1. Increased signal intensity in the basal ganglia on T1-weighted images

2. Increased signal intensity in the thalamus on T1-weighted images

3. Absent or decreased signal intensity in the posterior limb of the internal

capsule on T1-weighted images “absent posterior limb sign”

4. Restricted water diffusion on diffusion-weighted images.

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SEVERE ASPHYXIA IN TERM

NEONATES

Central pattern of injury involving

the deep gray matter

putamina

ventrolateral thalami

hippocampi

dorsal brainstem

lateral geniculate nuclei

occasionally perirolandic

cortex.

actively myelinating areas are

the most susceptible to

neonatal HII

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USG

Early findings - global

increase in cerebral

echogenicity and

obliteration of the CSF

containing spaces,

suggesting diffuse cerebral

edema.

1st week but more readily

apparent after 7 days.

Increased echogenicity in

the basal ganglia, thalami,

and brainstem

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USG

Late findings include prominence of the ventricles and extraaxial CSF-

containing spaces, likely due to atrophy.

The presence of diminished

resistive indexes (<60) in the

anterior and middle cerebral

arteries has been associated

with a poor clinical outcome,

even in the absence of other

US abnormalities.

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MRI Diffusion-weighted imaging

Sensitive for the detection of injury in the first 24 hours,

during which time conventional T1- and T2-weighted images

may appear normal.

Demonstrate increased signal intensity in the region of the

ventrolateral thalami and basal ganglia particularly the

posterior putamina in the perirolandic regions and along the

corticospinal tracts

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MRI - Pseudonormalization.

Although diffusion-weighted images seemingly improve and

appear relatively normal by the end of the 1st week, this

finding does not imply that there has been improvement or

reversal of underlying disease.

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MRI Day 1 ---- Conventional T1- and T2-weighted MR images are frequently

normal , therefore less useful than DWI

Day 2 ---- Injured areas may demonstrate hyperintensity on both T1- and T2-weighted images.

2 weeks --- T2 hypointensity subsequently develops in the thalami & posterior putamina.

Several months --- TI hyperintensity in thalami, basal ganglia & perirolandic cortex may persisit.

‘T1WI & T2WI ARE MOST DIAGNOSTICALLY USEFUL AT THE END OF 1st WEEK, WHEN DWI PSEUDONORMALIZE’.

Chronic stage of injury - atrophy of the injured structures

- T2 hyperintensity in the ventrolateral thalami,

posterior putamina, and corticospinal tracts.

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13 days old, male baby

Term baby with history of respiratory distress and hypotonia at birth, followed by 2

episodes of seizures.

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11 days old, male baby.

History of one episode of seizure , known case of HIE

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T1WI

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Severe neonatal HII in a 7-day-old term infant.

T1WI shows increased signal intensity in the lentiform nuclei and ventrolateral thalami.

T2WIshows decreased signal intensity in the posterior aspects of the putamina and

ventrolateral thalami.Huang B Y , and Castillo M Radiographics 2008;28:417-439

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DWI shows a relative lack of hyperintensity in the locations cited earlier, findings

that represent pseudonormalization.

Only the left globus pallidus shows high signal intensity. Corresponding ADC map

shows hypointensity

Huang B Y , and Castillo M Radiographics 2008;28:417-439

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Severe neonatal HII in a 5-day-old term infant who suffered profound birth asphyxia.

T1WI show hyperintensity in the ventrolateral thalami, basal ganglia and perirolandic

cortex.

Huang B Y , and Castillo M Radiographics 2008;28:417-439

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T2WI obtained approximately 7 months later show diffuse atrophy as well as

hyperintensity (gliosis) in the ventrolateral thalami, posterior putamina, and

perirolandic regions.

Huang B Y , and Castillo M Radiographics 2008;28:417-439

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PARTIAL ASPHYXIA TERM

NEONATES In mild to moderate hypoxic-ischemic ----

brainstem

cerebellum

deep gray matter structures

are generally spared since autoregulatory mechanisms maintain

perfusion.

Moderate insults of short duration in neonates cause little or no injury

to the brain

Prolonged insults in neonates result in injury to the intervascular

boundary (watershed) zones, which are relatively hypoperfused as a

result of this shunting.

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MRI TERM NEONATE

DWI (earliest to change)

First 24 hrs ---demonstrate cortical and subcortical WM restriction

most pronounced in the parasagittal watershed territories.

T2WI

By day 2 --- cortical swelling with loss of gray and white matter differen.

hyperintensity in the cortex and subcortical WM in the parasagittal

watershed zones occasionally involving the hemispheres diffusely.

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Partial neonatal HII in a 2-day-old term infant who experienced seizures shortly

after birth . T1WI & T2WI are normal.

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DWI and corresponding ADC map show restricted diffusion in the cortex and

subcortical white matter in a parasagittal watershed distribution.

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PRETERM NEONATE

HII is more common in preterm neonates than in term

neonates.

HII in preterm infants, particularly those of very low birth

weight is difficult to diagnose clinically early on because

signs may be lacking or mistaken to result from

developmental immaturity.

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PRETERM NEONATES

Manifest predominantly as damage to the deep gray matter

structures and brainstem.

Events of mild to moderate severity manifest as germinal

matrix–intraventricular hemorrhages or periventricular

leukomalacia.

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SEVERE ASPHYXIA IN PRETERM

Injury to the thalami, basal ganglia, hippocampi, cerebellum, and

corticospinal tracts can be seen.

The thalami, anterior vermis, dorsal brainstem are most frequently

involved.

Involvement of basal ganglia is less severe compared with

involvement of the thalami particularly among neonates born at less

than 32 weeks gestation.

Germinal matrix hemorrhages and periventricular white matter injury

also may be seen.

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USG IN PRETERM

NEONATES

May be normal particularly in the first 2 days.

OR

Demonstrate increased echogenicity in the thalami by 48–72

hours

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MRI

1st day Conventional MR may be normal or show only subtle

abnormalities.

Diffusion abnormalities are usually evident in the thalami within 24

hours .

After 2 days, T2 prolongation can be seen in the thalami and basal

ganglia.

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MRI

3rd day - T1 hyperintensity will be seen in the injured areas.

3–5 days - DW abnormalities most apparent subsequently begin

to pseudonormalize .

7 days - T2 hypointensity develops in the injured areas

T1 hyperintensity persists into the chronic stage.

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T1WI

19 days old, male baby

Preterm, AGA. History of cardiac arrest at 30 hours of life. Baby was ventilated.

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T2WI

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MILD TO MODERATE ASPHYXIA PRETERM

Weighing less than 2000 gms

Prevalence of intraventricular hemorrhage approximately

25%

Bleeding occurs within the first 24 hours of life.

Prevalence is inversely related to gestational age and weight

at birth.

Majority of intraventricular hemorrhages are associated with

germinal matrix hemorrhages.

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Sonographic grading system proposed by Burstein and Papile et.al:

Grade I

restricted to subependymal region / germinal matrix which is seen in the

caudothalamic groove

Grade II

extension into normal sized ventricles and typically filling less than 50% of the

volume of the ventricle

Grade III

extension into dilated ventricles

Grade IV

grade III with parenchymal haemorrhage

90% mortality.

It should be noted that it is now thought that grade IV bleeds are not simply

extensions of germinal matrix haemorrhage into adjacent brain, but rather

represent sequelae of venous infarction

Grading of neonatal intracranial haemorrhage

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Grade I

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Grade II

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Grade III

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Grade IV hemorrhage.

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PVL Classification

Grade I – Transient Periventricular echo densities

persisting for > 7 days

Grade II - Transient Periventricular echo density

evolving into small, localized fronto-parietal cyst

Grade III - Periventricular echo densities evolving into

extensive periventricular cystic lesions

Grade IV – Densities extending into the deep white matter

evolving into extensive cystic lesions

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Grade I PVL

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Grade III PVL

PARA SAG COR

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Grade III PVL

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MRI - PVL

Early WM injury will manifest as periventricular foci of T1

hyperintensity (without corresponding T2 hypointensity) within larger

areas of T2 hyperintensity.

These foci are usually evident by 3–4 days, subsequently giving way

to mild T2 hypointensity at 6–7 days .

In contrast, hemorrhage (reported to be present in 64% of cases of

PVL) initially manifests with much lower signal intensity on T2-

weighted images.

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1 yr male with history of right side focal seizurs with global developemental delay.

USG AF done during neonatal period revealed bilateral germinal matrix hemorrhage.

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T1WI FLAIR

1 yr male with history of hypoxic cerebral palsy with mental retardation and global

developmental delay.

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POSTNATAL INFANTS &

YOUNG CHILDREN

Hypoxic-ischemic injuries in infants and young children are

usually the result of drowning, choking, or non accidental

trauma.

As myelination nears completion by about 2 years of age,

injuries similar to the pattern seen in adults begin to appear.

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SEVERE ASPHYXIA IN POSTNATAL

INFANTS & YOUNG CHILDREN

1 and 2 years of age ---- Result in injury to the

Corpora striata

Lateral geniculate nuclei

Hippocampi

Cerebral cortex (particularly the anterior frontal and parieto-occipital cortex), with relative sparing of the thalami and perirolandic cortex.

Immediate perinatal period but before 1 year of age --- can demonstrate features of both birth asphyxia and later infantile asphyxia, with involvement of the basal ganglia (predominantly posteriorly), lateral thalami, and dorsal midbrain, as well as cortical injury.

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CT

< 24 hours of an insult --- may be negative or may demonstrate only subtle hypoattenuation of the deep gray matter structures .

Subsequent CT --- will demonstrate

diffuse basal ganglia abnormalities along with diffuse cerebral edema, manifesting as cortical hypoattenuation

loss of normal “gray-white” differentiation

cisternal and sulcal effacement.

4–6 days --- may show hemorrhagic infarctions of the basal ganglia.

Chronic phase ---- diffuse atrophy with sulcal and ventricular enlargement .

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CT

Within the first 24 hours, a small number of these patients may

demonstrate the “Reversal sign,” in which there is reversal in the

normal CT attenuation of gray matter and white matter.

“White cerebellum sign” --- diffuse edema and hypoattenuation

of the cerebral hemispheres with sparing of the cerebellum and

brainstem, resulting in apparent high attenuation of the cerebellum

and brainstem relative to the cerebral hemispheres.

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Unenhanced CT shows diffuse cortical swelling and hyperattenuation in the

white matter relative to areas of preserved cortex, i.e ‘Reversal sign’ --poor

prognosis.

A small amount of extraaxial hemorrhage adjacent to the left frontal lobe is also

seen.Huang B Y , and Castillo M Radiographics 2008;28:417-439

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Unenhanced CT demonstrates the ‘White cerebellum sign’. The cerebellar

hemispheres are hyperattenuating relative to the supratentorial structures, which

are hypoattenuating due to edema.

Huang B Y , and Castillo M Radiographics 2008;28:417-439

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Unenhanced CT scan obtained at the level of the basal ganglia after

cardiopulmonary arrest that lasted 30 minutes is essentially unremarkable.

Huang B Y , and Castillo M Radiographics 2008;28:417-439

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DWI and T2WI obtained 4 days later show high signal intensity with

corresponding T2 abnormalities in the caudate nuclei, lentiform nuclei, and

occipital lobes.

Huang B Y , and Castillo M Radiographics 2008;28:417-439

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MRI

MR imaging is frequently performed in children with HII.

Diffusion-weighted images will usually be abnormal within the first 12–24

hours, initially demonstrating bright signal intensity in the posterolateral

lentiform nuclei ; thalamic involvement (when present) will usually involve

the ventrolateral nuclei.

Over the next 48 hours, there is typically significant progression of

involvement to include the remainder of the basal ganglia and the

cortex

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MRI

Conventional T1- and T2WI obtained in the first 24 hours are

often normal and may appear so for up to 2 days.

By 48 hours, T2-weighted images will usually demonstrate

diffuse basal ganglia and cortical signal intensity abnormality

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MILD TO MODERATE ASPHYXIA IN POSTNATAL INFANTS & YOUNG

CHILDREN

As in term neonates, milder anoxic events in older infants will

generally result in watershed zone injuries involving the

cortex and subcortical white matter.

White matter lesions are more common in children under 1

year of age. Relative sparing of the periventricular white

matter will be seen.

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Unenhanced head CT scan shows bilateral cortical and subcortical

hypoattenuation in the parasagittal watershed regions

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DWI obtained at the same level shows corresponding high-signal-intensity

areas compatible with watershed infarcts.

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OLDER CHILDREN & ADULTS

HII in adults is more often a result of cardiac arrest or cerebrovascular

disease, with secondary hypoxemia.

Drowning and asphyxiation remain common causes of HII in older children.

Mild to moderate global ischemic insults to the brain usually result in

watershed zone infarcts.

Severe HII in this population primarily affects the gray matter structures: the

basal ganglia, thalami, cerebral cortex (in particular the sensorimotor and

visual cortices, although involvement is often diffuse), cerebellum, and

hippocampi

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MRI

As in younger patients, conventional T1- and T2-weighted images are

often normal or demonstrate only very subtle abnormalities.

Early subacute period (24 hours–2 weeks) --- conventional T2WI

typically become positive and demonstrate increased signal intensity

and swelling of the injured gray matter structures. DWI abnormalities

usually pseudonormalize by the end of the 1st week .

2nd week --- Gray matter signal intensity abnormalities at conventional

MR imaging may persist into the end of the.

Chronic stage --- T2WI may demonstrate some residual hyperintensity

in the basal ganglia, and T1WI may show cortical necrosis , which is

seen as areas of high signal intensity in the cortex

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Axial T2W and DWI show diffuse WM hyperintensity. On the corresponding ADC

map, the white matter is hypointense

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MR SPECTROSCOPY

MR spectroscopy is perhaps more sensitive to injury and more

indicative of the severity of injury in the first 24 hours after a

hypoxic-ischemic episode, when conventional and diffusion-

weighted MR imaging may yield false-negative findings or lead

to significant underestimation of the extent of injury.

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MR spectroscopy will demonstrate substantial lactate elevation

(appearing as a doublet centered in the deep gray nuclei, parieto-

occipital region, or white matter of the parasagittal watershed

zones by as early as 2–8 hours .

A glutamine-glutamate peak may also be detected , probably

reflecting the release of glutamate that occurs in HII.

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THANK YOU

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