Download - Brain Injury in Pre-Term Infants
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Brain Injury in Pre-Term Infants
Roy Maynard, M.D.
March 24, 2011
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Objectives for Brain Injury in Pre-Term Infants
• Identify types of brain injury in pre-term infants.
• Appreciate the incidence of Grade 1-IV intraventricular hemorrhages in very low birth weight infants.
• Understand the neurodevelopmental implications of Periventricular Leukomalacia in very low birth weight infants.
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Types of Brain Injury
• Periventricular Leukomalacia (PVL)
• Severe Intraventricular/Periventricular Hemorrhage (IVH/PVH)
• Posthemorrhagic Hydrocephalus
• Other patterns of neuronal injury
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IVH/PVH of the Pre-Term Infant
• Epidemiology
• Pathogenesis
– germinal matrix anatomy
– factors: • intravascular • vascular • extravascular
– spread of IVH
• Diagnosis and Management
• Neurodevelopmental Outcomes
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What is the magnitude of brain injury in pre-term infants?
Pre-Term Infants (BW<1500g)
No. born in U.S. ………………………..55,000/yr.
Survival…………………………………..90%
Incidence of:
IVH (Grade 3&4) ………………………3-21%
PVL ……………………………………. 2-5%
Morbidity in survivors:
Spastic/motor deficits…………………10%
Cognitive/behavioral…………………..25-50%
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21
16
11
9
6
43 3
9 8
0
5
10
15
20
25
501-750 751-1000 1001-1250 1251-1500 501-1500
Incidence: Grade 3 & 4 IVH
Children’s Minneapolis
% O
ccu
rre
nce
Vermont Oxford Network
Birth Weight (501-1500 grams)
No. Patients
1994-2002
38,576 46,183 50,253 59,403 194,415 465 483 516 617 2,081
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Incidence: PVL %
Occu
rre
nce
Birth Weight (501-1500 grams)
5
3
5
1
33
2 2
4
2
0
1
2
3
4
5
6
7
8
9
10
501-750 751-1000 1001-1250 1251-1500 501-1500
1994-2002
Vermont Oxford Network Children’s Minneapolis
No. Patients 38,576 465 46,183 483 50,253 516 59,403 617 194,415 2,081
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IVH/PVH of the Pre-Term Infant
• Epidemiology
• Pathogenesis
– germinal matrix anatomy
– factors: • intravascular • vascular • extravascular
– spread of IVH
• Diagnosis and Management
• Neurodevelopmental Outcomes
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Germinal Matrix (Primary site of IVH/PVH)
GM
3rd
4th
Monro
Magendie
CP
Luschka
Arachnoid Villi
Occipital
Horn
Germinal Matrix
Choroid Plexus
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Germinal Matrix
• Primitive cellular region ventrolateral to LV
– prominent: 26-32 weeks
– involuted: term
• Contains pluripotential migrating cells – neurons, astrocytes, oligodendroglia
• Contains immature blood vessels: – thin walls (lack muscularis layer)
– immature cell junctions & basal laminae
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IVH/PVH of the Pre-Term Infant
• Epidemiology
• Pathogenesis – germinal matrix anatomy
– factors: • intravascular • vascular • extravascular
– spread of IVH
• Diagnosis and Management
• Neurodevelopmental Outcomes
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Pathogenesis of IVH/PVH
Factors
• Intravascular
– regulation of CBF, BP, Blood volume
– platelet-capillary function
– blood-clotting function
• Vascular
• Extravascular
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Intravascular Factors
• Pressure-passive cerebral circulation factors: ↑ blood pressure will increase cerebral blood flow
• Increase in central venous pressure will increase cerebral venous pressure
• Increase pressure within the brain’s blood vessels may lead to rupture of fragile blood vessel(s) and bleeding
– Tracheal suctioning
– Pneumothorax
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Vascular Factors
Intrinsic properties of GM vessels
• Immature vascular structures – Larger and lack muscle/collagen
– Incomplete basal laminae
– More susceptible to rupture
• More susceptible to hypoxic/ischemic insult – Vascular border zone in GM
– Endothelium contain ↑ mitochondria
– ↑ need for oxidative metabolism
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Spread of IVH/PVH
• 40% stays in GM (Grade 1 IVH)
• 60% enters ventricles (Grade 2 & 3 IVH)
– Large IVH → obstructs CSF flow • Aqueduct of Sylvius, Luschka, Magendie
• Rapidly progressive hydrocephalus
– Small IVH → retards CSF absorption • Obliterative arachnoiditis of basilar cisterns
• Slow evolving hydrocephalus
• PV Hemorrhagic Infarction (Grade 4 IVH)
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IVH/PVH of the Pre-Term Infant
• Epidemiology
• Pathogenesis
– germinal matrix anatomy
– factors: • intravascular • vascular • extravascular
– spread of IVH
• Diagnosis and Management
• Neurodevelopmental Outcomes
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Diagnosis and Management
Grading IVH/PVH (Papile)
• Grade 1: GM hemorrhage only
• Grade 2: GM hemorrhage extending into LV without ventriculomegaly
• Grade 3: IVH with ventriculomegaly
• Grade 4: Intraparenchymal hemorrhage vs. Periventricular hemorrhagic infarction
J Pediatr 1978; 92: 529-34
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GM
Occipital
Horn Monro
Magendie
CP
Luschka
Arachnoid Villi
Normal Anatomy
3rd
4th
Germinal Matrix
Choroid Plexus
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GM Occipital
Horn Monro
Magendie
CP
Luschka
Arachnoid Villi
Grade 1 IVH (Blood in GM only)
3rd
4th Germinal Matrix
Choroid
Plexus
Blood
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GM
Monro
Magendie
CP
Luschka
Arachnoid Villi
Grade 2 IVH (Blood in LV without ventriculomegaly)
Occipital
Horn
3rd
4th Germinal Matrix
Choroid
Plexus
Blood
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Magendie
Lateral Ventricle
CP
Luschka
OBLITERATIVE
ARACHNOIDITIS
Slowly
Evolving
Hydrocephalus
Occipital
Horn
GM
Monro
Ventriculomegaly
Blood on
Arachnoid
Villi
3rd
4th
Grade 3 IVH (Blood in LV with ventriculomegaly)
Germinal Matrix
Choroid
Plexus
Blood
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Magendie
Lateral Ventricle
CP
Luschka
Occipital
Horn
GM
Monro Obstruction
at Foramen
of Monro
Arachnoid Villi Ventriculomegaly
3rd
4th
Grade 3 IVH (Blood in LV with ventriculomegaly)
Germinal Matrix
Choroid
Plexus
Blood
Rapidly
Progressive
Hydrocephalus
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GM Occipital
Horn Monro
Magendie
CP
Luschka
Arachnoid Villi
v
PVHI
3rd
4th
Grade 4 IVH (Periventricular Hemorrhagic Infarction)
Germinal Matrix
Choroid
Plexus
Blood
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PV Hemorrhagic Infarction
Pathogenesis
Germinal Matrix/IVH ↓
PV Venous Congestion ↓
PV Ischemia ↓
PV Hemorrhagic Infarction
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Begins as Grade 1-2 IVH
IVH
in right
lateral
ventricle
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Coronal Section
May Evolve to Grade 3 IVH
Massive IVH on right
• obstruction at
foramen of Monro
• unilateral
ventricular
dilatation
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IVH IVH
Periventricular Hemorrhagic Infarction
Early
Evolving
PVHI
Coronal Section
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Diagnosis and Management
Timing of IVH/PVH
• 90% occur within first 72H
– 50%: <24H
– 25%: >24H & <48H
– 15%: >48H & <72H
• 20-40% progress further
– Maximal extension occurs 3-5 days after
initial insult
Volpe: Neurology of the Newborn: 1995 Saunders
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Conclusions
• Most intracranial pathology in sick pre-term infants is clinically silent.
• Severe lesions most often occur in tiniest of pre-term neonates.
• Shift toward a delayed presentation of the clinically significant lesions.
Arch Pediatr Adolesc Med 2000; 154: 822-826
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Cranial Imaging of IVH/PVH
Ultrasonography
• Preferred diagnostic technique
equivalent resolution
portable, practical
CT Scan
MRI Scan
PET Scan
• Subdural hemorrhage
• Posterior fossa lesions
• Complicated cerebral lesions
Diagnosis and Management
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Coronal View
Normal Cranial Ultrasound
Lateral
Ventricle 3rd
Ventricle
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Coronal View
Lateral
Ventricle
Coronal View
Normal Cranial Ultrasound
3rd
Ventricle
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Coronal View
Normal Cranial Ultrasound
Choroid
Plexus
Lateral
Ventricle
3rd
Ventricle
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GM
Monro
Magendie
CP
Luschka
Arachnoid Villi
Grade 1 Intraventricular Hemorrhage
(Blood in GM only)
3rd
4th
Occipital
Horn
Germinal Matrix
Choroid
Plexus
Blood
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parasagittal view
Grade 1 IVH
SEH
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SEH
Acute Subependymal Hemorrhage
Bilateral Grade 1 IVH
Coronal View
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Acute Subependymal Hemorrhage
Left Parasagittal View
SEH CP
Grade 1 IVH
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GM
Monro
Magendie
CP
Luschka
Arachnoid Villi
Grade 2 IVH (Blood in LV without ventriculomegaly)
Occipital
Horn
3rd
4th Germinal Matrix
Choroid
Plexus
Blood
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Grade 2 IVH
Parasagittal View
Echogenic
blood fills
< 50% of
ventricle
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Grade 2 IVH
Posterior Coronal View
Clot in posterior
right horn
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Grade II IVH
parasagittalparasagittal view view
Clot in
Posterior
Horn on R
SEHSEH
Parasagittal View
Grade 2 IVH
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Magendie
Lateral Ventricle
CP
Luschka
Occipital
Horn
GM
Monro Obstruction
at Foramen
of Monro
Arachnoid Villi Ventriculomegaly
3rd
4th
Grade 3 IVH (Blood in LV with ventriculomegaly)
Germinal Matrix
Choroid
Plexus
Blood
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Grade 3 IVH
Large blood clot filling
and distending LV
Parasagittal View
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Magendie
Lateral Ventricle
CP
Luschka
OBLITERATIVE
ARACHNOIDITIS
Slowly
Evolving
Hydrocephalus
Occipital
Horn
GM
Monro
Ventriculomegaly
Blood on
Arachnoid
Villi
3rd
4th
Grade 3 IVH (Blood in LV with ventriculomegaly)
Germinal Matrix
Choroid
Plexus
Blood
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Posthemorrhagic Hydrocephalus
LV LV
Coronal View
Extraventricular Obstruction of CSF
From Obliterative Arachnoiditis
LV LV
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Grade III IVH
Coronal viewCoronal view
Dilated,Dilated,
blood-filledblood-filled
frontal hornsfrontal horns
Grade 3 IVH
Coronal View
Dilated,
blood-filled
frontal horn
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Grade 3 IVH
Hemorrhage in
Lateral Ventricle
Dilated lateral ventricle
Parasagittal View
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body
occipital
temporal
Hemorrhage
filling lateral
ventricle
Evolution of Grade 3 IVH
Parasagittal View
Initial scan
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Evolution of Grade 3 IVH
Retraction
of IVH clot
Ventricular
Dilatation
coronal view
F/U scan weeks later
Coronal View
F/U scan weeks later
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Evolution of Grade 3 IVH
F/U scan weeks later
Coronal View
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GM Occipital
Horn Monro
Magendie
CP
Luschka
Arachnoid Villi
v
PVHI
3rd
4th
Grade 4 IVH (Periventricular Hemorrhagic Infarction)
Germinal Matrix
Choroid
Plexus
Blood
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Bulging
SEH
Evolution of Periventricular
Hemorrhagic Infarction
coronal viewcoronal view
Day 7 (scan #1)Day 7 (scan #1)
Coronal View
Day 7 (scan #1)
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Increasing size
of crescentic
PVED PVHI
BulgingBulging
SEHSEH
Evolution of Periventricular
Hemorrhagic Infarction
coronal viewcoronal view
Day 7 (scan #2)Day 7 (scan #2)
Coronal View
Day 7 (scan #2)
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coronal viewcoronal view
Increasing size
of crescentic
PVED PVHI
Day 7 (scan #3)Day 7 (scan #3)
Evolution of Periventricular
Hemorrhagic Infarction
Coronal View
Day 7 (scan #3)
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Evolution of Periventricular
Hemorrhagic Infarction
coronal viewcoronal view
Large
Porencephalic
Cyst
2 months later2 months later
Coronal View
2 Months Later
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Periventricular Hemorrhagic Infarction
Parasagittal View
(9 days)
IVH
PED
Ventricular
dilatation
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Periventricular Hemorrhagic Infarction
Parasagittal View
(3 weeks of age) Cyst Formation
• tissue necrosis
• clot retraction
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Periventricular Hemorrhagic Infarction
Parasagittal View
(2 months of age)
Porencephalic
cyst
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Periventricular Leukomalacia
Periventricular Leukomalacia (PVL)
PVL has emerged as the prinicipal form of brain injury in the
premature infant
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1. Death of white matter (WM) in the
brain’s Periventricular (PV) region
2. Caused by decrease in O2 or blood
flow to PV WM area of brain
Periventricular white matter contains nerve fibers that carry messages from the brain to the body’s muscles
What is PVL?
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3. Most common Ischemic injury in
pre-term infants
4. Occurs in Border Vascular Zone
• end of arterial distributions
5. Diagnostic hallmarks include:
• Initial: PV echodensities
• Later: PV cystic changes
What is PVL?
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Surviving pre-term infants with PVL are at risk for the following:
• Cerebral Palsy (CP),
• intellectual impairment
• visual/hearing disturbances
Importance of Diagnosis?
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1. Periventricular vascular anatomic physiologic factors
2. Cerebral Ischemia and pressure-passive cerebral circulation
3. Maturation-dependent vulnerability of cerebral white matter Oligodendroglial precursors
Periventricular Leukomalacia
Pathogenesis (3 interacting factors)
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•
Basal Penetrator Vessels
Periventricular Vascular Anatomic Physiologic Factors
Short Penetrator Vessels
Periventricular Leukomalacia
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Clinical Correlates of PVL
Spastic
diplegia
Cognitive/Behavioral
Deficits
Cranial
Ultrasound
• Focal
Necrosis
• Diffuse
Pre-Oligo Injury
Clinical Correlates Diagnostic Methods
MRI/DWI
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1. Periventricular vascular anatomic physiologic factors
2. Cerebral Ischemia and pressure-passive cerebral circulation
3. Maturation-dependent vulnerability of cerebral white matter Oligodendroglial precursors
Periventricular Leukomalacia
Pathogenesis (3 interacting factors)
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CBF Autoregulation with Maturation 180 160 140 120 100 80 60 40 20 0
0 10 20 30 40 50 60 70 80
Premature
Newborn
Child
MABP (mmHg)
CB
F (
% o
f n
orm
al)
Normal Regulatory
Control Window
Narrow Regulatory
Control Window
Periventricular Leukomalacia
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1-week-old pre-term infant without
PVL. The periventricular echo-
texture is normal.
1-week-old pre-term infant. Peri-
ventricular echotexture is increased,
consistent with early changes of PVL.
PVL: Diagnosis & Management
Coronal View Coronal View
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PVL: Diagnosis & Management
Coronal View Parasagittal View
3-week-old pre-term infant. Multiple periventricular cysts
typical of established periventricular leukomalacia.
PVL Cysts
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Postnatal Treatment
Diagnosis and Management
• Postnatal resuscitation (NICU)
• Maximize risk for fluctuation CBF & BP – avoid unnecessary BP, suctioning, rapid
infusions, pneumothorax
– avoid ventilator asynchrony
• Correct coagulation disturbances
• Indomethacin
• Antioxidants (SOD)
• Management of post-hemorrhagic hydrocephalus
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IVH/PVH of the Pre-Term Infant
• Epidemiology
• Pathogenesis
– germinal matrix anatomy
– factors: • intravascular
• vascular
• extravascular
– spread of IVH
• Diagnosis and Management
• Neurodevelopmental Outcomes
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Neurodevelopmental Outcome
Classification
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70
17
12
64
18 18
39
31 31
21
13
66
11 11
79
0
10
20
30
40
50
60
70
80
Normal U/S Grade 1&2 IVH Grade 3 IVH Grade 4 IVH PVL
Neurodevelopmental Outcome 23-26 weeks GA (552 infants: 1986-1998) -- Mean Age: 48.6 months
% O
ccurr
ence
Normal Mild-Mod. Impaired Severely Impaired
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Q&A
Thank you for attending!