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Neonatal Brain Injury:
Mechanism, Management and
Prognosis
Charlotte Patterson
4th Year Medical Student
Contents
• Why choose this SSC?
•What is Birth Asphyxia and HIE?
•Prognosis
•Treatment and Management
• Conservative & Supportive
• New therapies:
-Hypothermia
-Chemical Therapy
-Cellular Therapy
• Evidence Based Medicine?
•Disability, Disadvantage and Diversity
•Ethics, Law and Medicine
•References
What is Birth
Asphyxia and HIE?
Birth Asphyxia: The result of a critical reduction in O2 delivery
to the fetus either antenatally, during labour and/or delivery
that is sufficient to produce a lactic acidosis and render the
infant in distress at birth.
Hypoxic-Ischaemic Encephalopathy (HIE) describes the
clinical manifestation of brain injury starting immediately or
up to 48hrs post-asphyxia.
Pattern of Injury in
HIE
Miller et. al, (2005) Journal of Paediatrics
Neuro-imagery in HIE
Normal HIE
Clinical Presentation
and Prognosis
Mild:
- Irritable
- Excessive response to stimulation
- Hyperventilation
- Impaired feeding
Moderate:
- Marked abnormality: tone and movement
- Cannot feed
- Seizures
Severe:
- No normal spontaneous movements/ response to
pain.
- Limb tone fluctuation
- Seizures prolonged
- Multi-organ failure
Complete recovery
Variable Recovery
Mortality: 30-40%
Disability: 80%
Pathophysiology:
Neuronal Injury
Reduced Oxygen Supply
Cellular Hypoxia
Primary Energy Failure Primary Neuronal Death
Resuscitation
Pseudo-normal period
Secondary Energy Failure
Encephalopathy
Delayed Neuronal Death
Seizures
Management:
Supportive
• Resuscitation
• Respiratory Support
• Seizure Management
• Fluid Restriction
• Hypotension Management
• Treat and Monitor Hypoglycaemia
• Restore electrolyte Balance
- Anticonvulsants
- Continuous Amplitude
Integrated EEG (aEEG)
-Inotropes
-IV Fluids
Treatment
1. Hypothermia
2. Chemical Therapy
3. Cellular Therapy
1. Hypothermia
Reduced Oxygen Supply
Cellular Hypoxia
Primary Energy Failure Primary Neuronal Death
Resuscitation
Pseudo-normal period
Secondary Energy Failure
Encephalopathy
Delayed Neuronal Death
Seizures
1. Hypothermia
Mechanism
• Modifies cells programmed for apoptosis
• Reduces cerebral metabolic rate, therefore production of toxic NO
and Free Radicals.
Who is treated?
• Neonates with an abnormal aEEG- fairly predictive
What happens?
• Aims to lower basal ganglia temperature 32-34°c
• Whole body or Just head
Disadvantages
• Little benefit if severe brain damage
• Not yet trialled in pre-term infants
1. Hypothermia
Wachtel et. al 2011
1. Hypothermia
2. Chemical Therapy
Reduced Oxygen Supply
Cellular Hypoxia
Primary Energy Failure Primary Neuronal Death
Resuscitation
Pseudo-normal period
Secondary Energy Failure
Encephalopathy
Delayed Neuronal Death
Seizures
2. Chemical Therapy
Agents that inhibit glutamate release, uptake, or blockage of
glutamate receptors
Blockade of free radical generation or removal- free radical
inhibitor
Blockade of downstream effects and inhibitors of inflammatory
effects
Magnesium Xenon
Deferoxamine Allupurinol
Indomethacin
Erythropoetin
3. Cellular Therapy
Stem cells that may help repair ischaemic neuronal tissue
• Neural Stem cells
• Multi-potent adult progenitor stem cells
• Mesenchymal Stem cells (MSCs)
• Human Umbilical Cord Stem Cells
MSCs can differentiate into neurones and oligodendrocytes,
therefore help repair ischaemic neural tissue.
May also help with restoration of functional networks via
axonal sprouting and synaptogenesis.
3. Cellular Therapy
• 9 day old mice
• HIE artificially induced with R common carotid artery
occlusion.
• MSCs injected into mice: 1st dose 3d, 2nd dose 10d.
Velthoven et al. 2010 Journal of Neuroscience
Ethics and Law
www.topbraininjurylawyers.com
Legal Action..
Thank you- any
questions?

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Birth asphyxia and Hypoxic-Ischaemic Injury: Prognosis and Management

  • 1. Neonatal Brain Injury: Mechanism, Management and Prognosis Charlotte Patterson 4th Year Medical Student
  • 2. Contents • Why choose this SSC? •What is Birth Asphyxia and HIE? •Prognosis •Treatment and Management • Conservative & Supportive • New therapies: -Hypothermia -Chemical Therapy -Cellular Therapy • Evidence Based Medicine? •Disability, Disadvantage and Diversity •Ethics, Law and Medicine •References
  • 3. What is Birth Asphyxia and HIE? Birth Asphyxia: The result of a critical reduction in O2 delivery to the fetus either antenatally, during labour and/or delivery that is sufficient to produce a lactic acidosis and render the infant in distress at birth. Hypoxic-Ischaemic Encephalopathy (HIE) describes the clinical manifestation of brain injury starting immediately or up to 48hrs post-asphyxia.
  • 4. Pattern of Injury in HIE Miller et. al, (2005) Journal of Paediatrics
  • 6. Clinical Presentation and Prognosis Mild: - Irritable - Excessive response to stimulation - Hyperventilation - Impaired feeding Moderate: - Marked abnormality: tone and movement - Cannot feed - Seizures Severe: - No normal spontaneous movements/ response to pain. - Limb tone fluctuation - Seizures prolonged - Multi-organ failure Complete recovery Variable Recovery Mortality: 30-40% Disability: 80%
  • 7. Pathophysiology: Neuronal Injury Reduced Oxygen Supply Cellular Hypoxia Primary Energy Failure Primary Neuronal Death Resuscitation Pseudo-normal period Secondary Energy Failure Encephalopathy Delayed Neuronal Death Seizures
  • 8. Management: Supportive • Resuscitation • Respiratory Support • Seizure Management • Fluid Restriction • Hypotension Management • Treat and Monitor Hypoglycaemia • Restore electrolyte Balance - Anticonvulsants - Continuous Amplitude Integrated EEG (aEEG) -Inotropes -IV Fluids
  • 9. Treatment 1. Hypothermia 2. Chemical Therapy 3. Cellular Therapy
  • 10. 1. Hypothermia Reduced Oxygen Supply Cellular Hypoxia Primary Energy Failure Primary Neuronal Death Resuscitation Pseudo-normal period Secondary Energy Failure Encephalopathy Delayed Neuronal Death Seizures
  • 11. 1. Hypothermia Mechanism • Modifies cells programmed for apoptosis • Reduces cerebral metabolic rate, therefore production of toxic NO and Free Radicals. Who is treated? • Neonates with an abnormal aEEG- fairly predictive What happens? • Aims to lower basal ganglia temperature 32-34°c • Whole body or Just head Disadvantages • Little benefit if severe brain damage • Not yet trialled in pre-term infants
  • 14. 2. Chemical Therapy Reduced Oxygen Supply Cellular Hypoxia Primary Energy Failure Primary Neuronal Death Resuscitation Pseudo-normal period Secondary Energy Failure Encephalopathy Delayed Neuronal Death Seizures
  • 15. 2. Chemical Therapy Agents that inhibit glutamate release, uptake, or blockage of glutamate receptors Blockade of free radical generation or removal- free radical inhibitor Blockade of downstream effects and inhibitors of inflammatory effects Magnesium Xenon Deferoxamine Allupurinol Indomethacin Erythropoetin
  • 16. 3. Cellular Therapy Stem cells that may help repair ischaemic neuronal tissue • Neural Stem cells • Multi-potent adult progenitor stem cells • Mesenchymal Stem cells (MSCs) • Human Umbilical Cord Stem Cells MSCs can differentiate into neurones and oligodendrocytes, therefore help repair ischaemic neural tissue. May also help with restoration of functional networks via axonal sprouting and synaptogenesis.
  • 17. 3. Cellular Therapy • 9 day old mice • HIE artificially induced with R common carotid artery occlusion. • MSCs injected into mice: 1st dose 3d, 2nd dose 10d. Velthoven et al. 2010 Journal of Neuroscience

Notas del editor

  1. Diagnosis of HIE only made if: Evidence of hypoxia antenatally eg. Antepartum haemorrhage - during labour (eg. Cord prolapse) - Delivery (eg. Shoulder dystocia) - Resucitation needed - Fatures of encephalopathy Hypoxic damage to organs (eg. Liver, kidney, heart) No other post-natal/antenatal cause identified Characteristic neuroimigery findings Neonatal encephalopathy is a clinical syndrome of “disturbed neurological function in the earliest days of life in the term infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, subnormal level of consciousness, and often seizures.
  2. Extent of injury is dependent on severity and temporal characteristics of the insult. Final pattern of injury also depends on the gestational age of the infant when the injury occurs Severe prolonged hypoxia Diffuse neuronal injury Moderate- severe, relatively prolonged Deep cortical grey matter structures affeted eg. Basal ganglia and thalamus Severe, abrupt Deep nuclear brain-stem injuries. “watershed injury”- another common pattern of injury- parasaggital end artery regions of 3 major cerebral arteries.
  3. MRI scan of brain – term infant Left normal scan. Grey basal ganglia and white signal fro myelin in posterior limb of internal capsule. Right- HIE- abnormal signal in basal ganglia and thalami (shown by arrows)- absence of signal in the internal capsule bilaterally
  4. Picture: Brain damage from severe birth asphyxia at term following a sudden, severe antepartum haemorrhage caused this child to become microcephalic, blind and deaf and to have spastic quadriplegia. Mild: may also have ‘stary eyes’ Moderate: if they make a full clinical neurological recovery and feeding within 7 days, generally excellent prognosis. - > 10 days persistence, full recovery unlikely Severe: Poor prognosis: 80% neurodevelopmental problems.
  5. Secondary energy failure: Hyperaemia - Cytotoxic oedeme - Mitochondrial failure - Accumulatuib if excitotoxins Apoptosis No synthesis Free radical damage
  6. Resucitation: In the delivery room- oxygen- room air rather than 100% o2 due to potential deleteirous effects of oxygen during primary pahse. Correct any metaboloic acidosis. Avoid hyper or hypo capnia. RESTORE CONDITIONS THAT DELAY RECOVERY FROM PRIMARY PHASE OF BRAIN INJURY- hypoxia, hypoglycaemia, hypotension. Respiratory ensure adequate ventilation- changes in PCO2 can affect cerebral blood flow. Hypocapnia- vasoconstriction therefore compromised o2 supply Seizre: phenobarbital, phosphenytoin, lorazepam CAI EEG: Cerebral Function Monitoring – confirm early encephalopathy onitors general neurological status Monitors and records frequency and intensity of seizures to assist in the management of anticonvulsive therapy  Assists in identifying need for full EEG Assists in identifying and predicting outcome from hypoxic-ischemic encephalopathy (HIE) Hypotension: Most commonly related to LV dysfunction following hypoxic-ischaemic injury and endothelial damage therefore give inotropes such as dobutamine. May be hypovolaemic due to placental abruption therefore give fluids. Fluid restriction: Potential renal injury U&E- SIADH and cerebral oedema common. Also due to kidney injury may have derranged u&ess
  7. Secondary energy failure: Hyperaemia - Cytotoxic oedeme - Mitochondrial failure - Accumulatuib if excitotoxins Apoptosis No synthesis Free radical damage
  8. Published by group in New York- Summary of clinical trials on x- axis
  9. Baby receiving hypotherimic treatment via cooling cap.
  10. Target different steps in the cacade and pathways leading to neuronal cell death
  11. Categorised based on mechanism of action/effect Mag and Xenon- NMDA inhibitors (xenon- also an anaesthetic!) Free radical inhibitors- block reaction in production of xanthine
  12. Improved sensory motor function, and reduced lesion size- motor: time spent on rotaroad, forepaw initiation differnece- sensory function VEH- = vehicle ie. placebo. In the netherlands- applicable in clinical setting treatment in 4years...
  13. Law firm in Massachusets
  14. Asphyxia = peri-partum hypoxia