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TAS Neonatal Medicine ✅ > Hypoxic-Ischaemic Encephalopathy ✅ > Flashcards

Hypoxic-Ischaemic Encephalopathy ✅ Flashcards

1
Q

What is the incidence of HIE?

A

1-1.5 per 1000 live births

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2
Q

What % of cases of cerebral palsy are caused by HIE?

A

30%

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3
Q

How much higher is the incidence of HIE in low-income countries?

A

Up to 10x

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4
Q

What does perinatal hypoxia mean?

A

Lack of oxygen to the fetus and newborn

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5
Q

What does perinatal ischaemia mean?

A

Lack of blood flow to the fetus and newborn

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6
Q

What does perinatal asphyxia mean?

A

Lack of gas exchange to the fetus and newborn

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7
Q

What is more damaging, ischaemia or hypoxia?

A

Ischaemia

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8
Q

Why is ischaemia more damaging than hypoxia?

A

It also leads to glucose depletion, which is important in the causation of neuronal injury

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9
Q

What results from impaired respiratory gas exchange in asphyxia?

A

Hypoxia and hypercarbia

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10
Q

What is the result of hypercarbia produced from asphyxia?

A
  • Acidosis

- Reduced cerebral blood flow

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11
Q

What is HIE?

A

A specific type of encephalopathy due to low oxygen and blood delivery to the brain

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12
Q

What are the categories of causes of neonatal encephalopathy?

A
  • Hypoxic-ischaemic
  • Infection
  • Trauma and haemorrhage
  • Metabolic
  • Neuronal migration defects
  • Congenital myotonia
  • Neonatal stroke
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13
Q

What are the haemorrhagic cases of neonatal encephalopathy?

A
  • Subgaleal
  • Extradural
  • Subdural
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14
Q

What are the metabolic causes of neonatal encephalopathy?

A
  • Non-ketotic hyperglycinaemia
  • Mitochondrial myopathies
  • Aminoacidaemias
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15
Q

Give a neuronal migration defect that can cause neonatal encephalopathy

A

Lissencephaly

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16
Q

Give 3 congenital myotonias that can cause neonatal encephalopathy?

A
  • Myasthenia gravis
  • Peroxisomal disorders
  • Prader-Willi syndrome
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17
Q

What are the infectious causes of neonatal encephalopathy?

A
  • Neonatal sepsis
  • Meningitis
  • Herpes meningoencephalitis
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18
Q

When should a clinical diagnosis of HIE be made?

A

In the presence of all criteria;

  • Evidence of intrapartum asphyxia, such as a sentinel event
  • Respiratory depression at delivery
  • Encephalopathy in the immediate postnatal period
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19
Q

Give 7 sentinel events during labour and delivery which may cause an acute brain injury

A
  • Cord prolapse
  • Uterine rupture
  • Abruption of placenta
  • Amniotic fluid embolism
  • Acute maternal haemorrhage
  • Maternal circulatory failure
  • Acute neonatal haemorrhage
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20
Q

Give 3 causes of acute neonatal haemorrhage

A
  • Vasa praevia
  • Acute loss from cord
  • Feto-maternal haemorrhage
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21
Q

What features might indicate intrapartum asphyxia and respiratory depression at birth?

A
  • Apgar score ≤5 at 10 minutes after birth
  • Continued need for resuscitation, including endotracheal or mask ventilation, at 10 minutes after birth
  • Acidosis within 60 minutes of birth
  • Base deficit ≥16mmol/L within 60 minutes of birth
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22
Q

What is acidosis within 60 minutes of birth defined as?

A

Umbilical cord, arterial, or capillary pH of <7.0

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23
Q

What samples can base deficit be measured in to detect intrapartum asphyxia?

A

Umbilical cord or any blood sample

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24
Q

What might indicate moderate to severe neonatal encephalopathy?

A
  • Early onset seizures
  • Altered sensorium
  • Abnormal tone
  • Abnormal primitive reflexes
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25
Q

What is meant by altered sensorium?

A

Reduced or absent response to stimulation

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26
Q

How might tone be abnormal in moderate to severe neonatal encephalopathy?

A

Hypotonia or flaccidity

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27
Q

What primitive reflexes might be abnormal in moderate to severe neonatal encephalopathy?

A

Weak or absent suck or Moro reflex

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28
Q

What is used to determine which cases require treatment/intervention for HIE?

A
  • Clinical assessment

- Cerebral function monitoring (aEEG)

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29
Q

What finding on aEEG might indicate a need to intervene in HIE?

A

Moderate or severe abnormalities in the background electrical activity

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30
Q

What are the indicators for intrapartum asphyxia?

A
  • Abnormal CTG
  • Reduced fetal movements
  • Cord pH ≤7.0
  • Base deficit ≥16mmol/L
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31
Q

Is the presence of indicators for intrapartum asphyxia without moderate to severe encephalopathy an indication for intervention?

A

NO

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32
Q

Why is the adherence to criteria for intervention in HIE important medico-legally?

A

Has potential consequences in relation to maternal care during labour and delivery

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33
Q

In how many phases does hypoxic-ischaemic injury lead to neuronal death?

A

Two

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34
Q

What are the phases in which hypoxic-ischaemic injury leads to neuronal death?

A
  • Primary neuronal necrosis

- Delayed neuronal death

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35
Q

What causes primary neuronal necrosis in HIE?

A

Cellular hypoxia and primary energy failure following depletion of cellular high-energy compounds

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36
Q

How long after the insult does primary neuronal necrosis occur in HIE?

A

May occur immediately

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37
Q

How can primary neuronal necrosis in HIE be treated?

A

It can’t - it is not amenable to nay treatment or intervention

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38
Q

When does delayed neuronal death occur in HIE?

A

Usually following a latent period of at least 6 hours

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39
Q

What causes delayed neuronal death in HIE?

A
  • Repercussion and hyperaemia
  • Cytotoxic oedema
  • Programmed apoptotic cell death
  • Mitochondrial failure
  • Free radical damage
  • Accumulation of excitotoxins
  • Nitric oxide synthesis
  • Cytotoxic actions of microganglia
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40
Q

What is the delayed neuronal death in HIE associated with?

A
  • Seizures

- Encephalopathy

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41
Q

What is the clinical significance of the delayed phase of neuronal damage in HIE?

A

The latent period before secondary neuronal necrosis offers a ‘therapeutic window of opportunity’

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42
Q

Why does the latent period before delayed neuronal damage in HIE offer a therapeutic window?

A

Because delayed neuronal damage leads to large proportion of the neuronal necrosis following a severe and global insult, so is an opportunity to prevent this

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43
Q

What intervention can be useful before the delayed phase of neuronal damage?

A

Cooling (moderate hypothermia)

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44
Q

How does moderate hypothermia have its neuroprotective actions?

A
  • Decreased number of apoptotic but not necrotic cells
  • Reduction in cerebral metabolic rate and oxygen consumption
  • Attenuation of excitatory amine release such as glutamate
  • Improving update of glutamates in neuronal cells
  • Reduction in the synthesis of toxic nitric oxide and free radicals
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45
Q

What are the main patterns of brain injury in HIE?

A
  • Basal ganglia and thalamus (BGT)
  • Watershed pattern
  • Global pattern
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46
Q

What is a BGT brain injury associated with?

A

A sentinel event

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47
Q

Why are the basal ganglia and thalamus often differentially affected when there is a sentinel event causing HIE?

A

These structures are more susceptible to hypoxic-ischaemic type injury

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48
Q

Why are the basal ganglia and thalamus more susceptible to a hypoxic-ischaemic type injury?

A

Because of their high metabolic rate and high concentration of NMDA receptors

49
Q

What is a BGT HIE often accompanied by?

A
  • Brainstem injury

- Involvement of posterior limb of internal capsule

50
Q

Where are lesions found in brainstem injuries associated with a BGT HIE?

A
  • Midbrain
  • Pons
  • Cerebellar vermis
51
Q

How severe are BGT HIE injuries?

A

Vary, from mild-focal to involving the whole of the BGT area

52
Q

What is the prognosis of BGT HIE injury?

A
  • 50% die in 2-3 years

- Range of impairments in survivors

53
Q

What impairments might be present in survivors of BGT HIE injuries?

A
  • Cerebral palsy
  • Speech and language difficulty
  • Visual and hearing impairment
54
Q

What % of survivors of BGT HIE injuries develop cerebral palsy?

A

75%

55
Q

What is the best predictor of motor problems in HIE?

A

BGT lesions

56
Q

What is the best predictor for an inability to walk at 2 years in HIE?

A

Posterior limb of internal capsule (PLIC) involvement

57
Q

What is the watershed pattern of HIE also known as?

A

Parasagittal cerebral injury

58
Q

What causes a watershed pattern HIE?

A

Mainly chronic partial hypoxia

59
Q

What can produce similar lesions to watershed HIE?

A
  • Hypertension
  • Infection
  • Hypoglycaemia
60
Q

Where are the areas of necrosis found in watershed HIE?

A

Border zones between major cerebral arteries

61
Q

What impairment might watershed HIE lead to?

A

Communication problems

62
Q

What part of the pain is affected in global pattern HIE?

A

Subcortical white matter and cortex

63
Q

When is global pattern HIE seen?

A

In severe neonatal encephalopathy

64
Q

What is the prognosis of global pattern HIE?

A

Usually fatal

65
Q

What scoring systems can be used in HIE?

A
  • Sarnat stages

- Thompson scoring system

66
Q

What is the advantage of Sarnat stages?

A
  • Brief
  • Objective
  • Good correlation with outcomes
67
Q

What is Sarnat stage 1 characterised by?

A
  • Irritability
  • Lethargy or hyperalertness
  • Hyper-reflexia
  • Tachycardia
  • Dilated pupils
  • Abnormal tone

Improves with 24-48 hours

68
Q

What is the prognosis of Sarnat stage 1 HIE?

A

Mild encephalopathy with no risk of death or significant disability

69
Q

What is Sarnat stage 2 characterised by?

A
  • Seizures
  • EEG abnormaliites
  • Abnormal tone
  • Proximal weakness
  • Loss of consciousness
70
Q

What is the mortality of Sarnat stage 2 HIE?

A

5%

71
Q

What is the chance of neurodisability in Sarnat stage 2 HIE?

A

25%

72
Q

What is Sarnat stage 3 HIE characterised by?

A
  • Deep coma and unresponsiveness
  • Flaccid tone
  • Areflexia
  • Abnormal EEG
73
Q

What is found on EEG in Sarnat stage 3 HIE?

A

Discontinuous background electrical activity or burst suppression pattern

74
Q

What is the mortality of Sarnat 3 HIE?

A

80%

75
Q

What is the chance of neurodisability in survivors of Sarnat 3 HIE?

A

Most survivors have severe disability

76
Q

What are the advantages of the Thompson scoring system for HIE?

A
  • Objective
  • Can be used for monitoring
  • Simpler to use
77
Q

What is scored in the Thompson HIE score?

A
  • Tone
  • LOC
  • Seizures
  • Posture
  • Moro
  • Grasp
  • Suck
  • Respiration
  • Fontanelle
78
Q

How is tone scored in the Thompson HIE score?

A

0 - Normal
1 - Hyper
2 - Hypo
3 - Flaccid

79
Q

How is LOC scored in the Thompson HIE score?

A

0 - Normal
1 - Hyper alert, stare
2 - Lethargic
3 - Comatose

80
Q

How is seizures scored in the Thompson HIE score?

A

0 - None
1 - Infrequent, <3/day
2 - Frequent, >2/day

81
Q

How is posture scored in the Thompson HIE score?

A

0 - Normal
1 - Fisting, cycling
2 - Strong distal flexion
3 - Decerebrate

82
Q

How is Moro scored in the Thompson HIE score

A

0 - Normal
1 - Partial
2 - Absent

83
Q

How is grasp scored in the Thompson HIE score?

A

0 - Normal
1 - Poor
2 - Absent

84
Q

How is suck scored in the Thompson HIE score?

A

0 - Normal
1 - Poor
2 - Absent/bites

85
Q

How is respiration scored in the Thompson HIE score?

A

1 - Normal
2 - Hyperventilation
3 - Brief apnoea
4 - Apnoea

86
Q

How is fontanelle scored in the Thompson HIE score?

A

0 - Normal
1 - Full, not tense
2 - Tense

87
Q

What is the limitation of scoring systems in HIE?

A
  • Difficult to measure some clinical parameters
  • Many infants have intermediate signs between stages
  • Assessment is complicated by interventions
88
Q

In what situations might it be more difficult to measure some clinical parameters when scoring HIE?

A
  • Soon after birth

- Sedated or ventilated infants

89
Q

What therapies might make it more difficult to score an infant with HIE?

A
  • Anti-convulsant therapies
  • Paralytic agents
  • Co-morbidities
90
Q

What investigations may be useful in HIE?

A
  • Amplitude modulated EEG (aEEG) or cerebral function monitor
  • Cranial ultrasound
  • Magnetic resonance imaging
91
Q

What is aEEG/cerebral functioning monitoring useful for?

A
  • Clinical assessment at the bedside
  • Grading the severity of encephalopathy
  • Seizure detection
  • Identifying patients suitable for therapeutic hypothermia
92
Q

What are the advantages of aEEG/cerebral function monitoring?

A
  • Easy to obtain a trace and interpret
  • Robust and objective
  • Excellent correlation with neurodevelopment abnormality
93
Q

What findings on aEEG/cerebral function monitoring are associated with poor neurodevelopment outcome?

A

Severely abnormal patterns persisting for more than about 48 hours after birth

94
Q

What % of infants with severely abnormal patterns on aEEG/cerebral function monitoring will have a poor neurodevelopmental outcome?

A

70%

95
Q

What is a normal aEEG within 6 hours of birth a good predictor of?

A

Normal outcome

96
Q

What is cranial ultrasound useful for?

A
  • Exclude other causes of encephalopathy
  • Detecting calcification and cysts
  • Detecting atrophy
  • Detecting cerebral haemorrhage
97
Q

Give 2 other causes of encephalopathy that can be excluded with cranial ultrasound?

A
  • Metabolic causes

- Structural malformations

98
Q

What are calcification and cysts on cranial ultrasound suggestive of?

A

Viral infection

99
Q

What is atrophy on cerebral ultrasound suggestive of?

A

Longstanding damage

100
Q

What are Doppler cerebral flow velocity indices used for?

A
  • Markers of cerebral perfusion

- Assessing severity of HIE and predicting long-term outcome

101
Q

What is the preferred imaging modality in HIE?

A

MRI

102
Q

Why is MRI the preferred imaging method in HIE?

A
  • It’s sensitivity for detecting HIE
  • Can provide information about the timing of the injury
  • Can identify other causes
103
Q

When is the optimal time to do a MRI in HIE?

A

Between 5-14 days

104
Q

Why should MRI ideally not be done before 5 days in HIE?

A

Injury may be underestimated if performed during the first few days after birth

105
Q

What form of imaging can provide useful prognostic data about HIE in the first week?

A

MRS (magnetic resonance spectroscopy)

106
Q

What findings on MRS correlate with later neurological problems?

A

Reduction in N-acetylaspartate (NAA)

107
Q

What does a reduction of NAA on MRS reflect?

A

Neuronal injury and elevation of lactate (indicating tissue ischaemia and hypoxia)

108
Q

What does supportive treatment in HIE include?

A
  • Maintaining cardiorespiratory stability
  • Maintaining biochemical parameters
  • Management of renal failure
  • Management of deranged clotting
  • Seizure control
  • Initial fluid restriction
109
Q

What biochemical parameters should be maintained in supportive management for HIE?

A
  • Glucose
  • Electrolytes
  • Blood gases
110
Q

Why are fluids initially restricted in HIE?

A

To prevent cerebral oedema

111
Q

What ethical concerns arose when conducting RCTs into the benefit of therapeutic hypothermia in infants with HIE?

A
  • Concerns about ethics of significant early intervention in a newborn infant with a severe, unexpected condition
  • Concern that intervention reduced death at expense of worsening neurodisability
112
Q

What infants with HIE were excluded from studies looking at the benefits of therapeutic hypothermia?

A
  • Infants with mild HIE

- Infants with the most extensive brain injuries that needed palliative care

113
Q

Why do infants with HIE not need therapeutic hypothermia?

A

They have excellent prognosis without it

114
Q

What ‘dose’ of therapeutic hypothermia has been shown to be effective in reducing death and neurodisability at 18 months in patients with HIE?

A

Mild hypothermia (33-34 degrees C) started within 6 hours and continued for 72 hours

115
Q

What is the number needed to treat for therapeutic hypothermia in HIE?

A

7

116
Q

What proportion of infants with moderate/severe HIE have a normal outcome at 2 years of age with cooling?

A

6 out of 10

117
Q

What did the UK TOBY study show regarding therapeutic hypothermia for HIE?

A
  • Significant reduction in risk of cerebral palsy and moderate-severe disability at 7 years with cooling
  • Significantly improved survival
118
Q

What is the rate of death or moderate-severe disability in infants with moderate to severe HIE?

A

46%

119
Q

What drugs are being researched to see if they can produce an improvement in HIE?

A
  • Magnesium sulphate
  • Melatonin
  • N-acetylcysteine
  • Erythropoietic
  • Xenon inhalation

TAS Neonatal Medicine ✅ (35 decks)

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