Hypoxic Ischemic Encephalopathy Flashcards

1
Q

What is hypoxic-ischaemic encephalopathy (HIE)?

A

Hypoxic-ischaemic encephalopathy (HIE) is neonatal encephalopathy (NE) that occurs in the first two days of life and is caused by intrapartum hypoxia and cerebral ischemia.

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2
Q

How is neonatal encephalopathy (NE) characterized?

A

Neonatal encephalopathy is characterized by an abnormal level of consciousness, abnormal tone, and abnormal primitive reflexes.

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3
Q

What are some common manifestations of neonatal encephalopathy (NE)?

A

Seizures and feeding difficulties commonly occur in moderately or severely affected infants with neonatal encephalopathy.

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4
Q

Besides intrapartum hypoxia, what are some other causes of neonatal encephalopathy (NE)?

A

Other causes of neonatal encephalopathy include
-hypoglycemia,
-electrolyte disturbances,
-sepsis,
-drug effects,
-haemodynamic disturbances,
-brain malformations,
-inborn errors of metabolism, and
-neonatal epileptic syndromes.

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5
Q

How common are the causes of neonatal encephalopathy (NE) compared to intrapartum hypoxia?

A

While intrapartum hypoxia is the most common cause of neonatal encephalopathy, the other mentioned causes are less common but must be considered during the assessment of NE.

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6
Q

What physiological changes occur during intrapartum fetal hypoxia?

A

Initially, there is fetal bradycardia, and blood flow is shunted towards the brain. However, this shunting compromises the perfusion of other organs.

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7
Q

What happens if hypoxia continues during intrapartum fetal hypoxia?

A

If hypoxia continues, the myocardium becomes critically hypoxic, leading to a decrease in cardiac output and subsequent cerebral ischemia.

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8
Q

Which areas of the brain are most affected by cerebral ischemia during intrapartum fetal hypoxia?

A

In term infants, the basal ganglia (due to their high metabolic rate) and subcortical white matter (due to being in the “water-shed” zone) are most affected by cerebral ischemia.

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9
Q

What are the expected neurological outcomes in cases of moderate and severe intrapartum fetal hypoxia?

A

In some cases of moderate and most cases of severe intrapartum fetal hypoxia, spastic quadriplegic or dyskinetic cerebral palsy is the expected neurological outcome.

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10
Q

Why is it important to diagnose hypoxic-ischaemic encephalopathy (HIE) promptly?

A

It is crucial to diagnose HIE promptly so that appropriate supportive care can be provided and interventions such as therapeutic hypothermia can be considered for moderately or severely affected infants.

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11
Q

What is the time frame for initiating therapeutic hypothermia in infants with HIE?

A

Therapeutic hypothermia must be started within 6 hours of life in infants with hypoxic-ischaemic encephalopathy (HIE).

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12
Q

The following findings suggest that the intrapartum hypoxia and ischaemia were of
sufficient severity to potentially cause brain damage:

A
  • Metabolic acidosis with base deficit ≥ 10mmol/l in umbilical arterial blood or the
    infant’s arterial blood within the first hour of life or the ongoing need for assisted
    ventilation 10 minutes after birth.
  • Intrapartum signs or events suggesting fetal compromise or Arterial Cord pH < 7.0.
  • Severe or moderate encephalopathy during the first 48 hours of life.
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13
Q

How do the clinical signs in infants with hypoxic-ischaemic encephalopathy (HIE) typically evolve over time?

A

The clinical signs in infants with moderate or severe HIE typically become increasingly obvious or severe during the first 48 to 72 hours of life.

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14
Q

What are common manifestations of seizures in infants with HIE?

A

eizures in infants with HIE are often clinically silent, but they may also present as rhythmic clonic movements. More frequently, seizures manifest as subtle signs including buccal-lingual movements, abnormal eye movements, cycling movements of limbs, abnormal tonic posturing, or grimacing.

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15
Q

How can cycling, posturing, and myoclonus in infants with HIE be differentiated from seizures?

A

Cycling, posturing, and myoclonus may alternatively represent a lack of inhibition/control at a brainstem level. EEG confirmation is required to distinguish the etiology of these movements from seizures.

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16
Q

Stage 1 of encephalopathy

A

Irritability, increased tone, poor sucking but an exaggerated moro reflex.

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17
Q

Stage 2 of encephalopathy

A

Lethargy, decreased tone and primitive reflexes. Seizures are common.

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18
Q

Stage 3 of encephalopathy

A

Stupor or Coma, flaccid tone and seizures often clinically less apparent.

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19
Q

Why is EEG confirmation necessary in infants with hypoxic-ischaemic encephalopathy (HIE)?

A

EEG confirmation is required to distinguish the etiology of certain clinical signs, such as cycling, posturing, and myoclonus, from seizures in infants with HIE.

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20
Q

What does progression through the stages of hypoxic-ischaemic encephalopathy (HIE) represent?

A

Progression through the stages of HIE represents continuing damage occurring after birth due to reperfusion injury and oxidant damage caused by an excitotoxic cascade at a cellular level.

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21
Q

Why might some infants not manifest a typical progression through the stages of HIE?

A

Some infants are born with established damage and may not exhibit a typical progression through the stages of HIE.

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22
Q

How might the severity and prognosis of HIE be more reliably assessed?

A

The severity and prognosis of HIE may be more reliably assessed using a detailed HIE score known as the Thompson HIE Score, as there is much overlap between the signs within the stages.

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23
Q

What is aEEG and what is its significance in cerebral function monitoring?

A

aEEG is a time-compressed, processed EEG used for diagnosing subclinical seizures and providing prognostic value in cerebral function monitoring.

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24
Q

How does aEEG compare to clinical examination in assessing cerebral function?

A

aEEG is more objective than clinical examination, making it valuable for diagnosing subclinical seizures.

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25
Q

When should aEEG be applied in cerebral function monitoring?

A

aEEG should be applied as soon as possible where available for optimal diagnosis and prognosis.

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26
Q

What can cranial ultrasound reveal in cerebral function monitoring?

A

Cranial ultrasound may show established damage at birth such as oedema, infarction, ischemia, or hemorrhage, as well as evolving focal or global injury.

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27
Q

What is the primary aim of assessing and managing infants with HIE?

A

The primary aim is to minimize further organ damage.

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28
Q

What key aspects should be documented in the assessment of infants with HIE?

A

Document antenatal history, intrapartum events, and management at delivery.

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29
Q

Why is medicolegal investigation becoming more common in cases of HIE?

A

Medicolegal investigation is increasing due to the need for accountability and understanding the circumstances surrounding HIE cases.

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30
Q

How does documenting intrapartum events help in managing infants with HIE?

A

Documenting intrapartum events assists in understanding potential causes and guiding appropriate management strategies for infants with HIE.

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31
Q

What precautions should be taken during resuscitation at birth for infants with HIE?

A

Avoid over-heating and hyperoxia during resuscitation.

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32
Q

When should an arterial blood gas be obtained for infants at birth?

A

An arterial blood gas should be obtained from the umbilical cord or from the infant within the first hour of life.

33
Q

How often should the Apgar score be recorded for infants at birth?

A

The Apgar score should be recorded at 1, 5, and 10 minutes after birth.

34
Q

Where should infants with HIE be admitted after birth?

A

Infants with HIE should be admitted to a high or intensive care area for specialized monitoring and management.

35
Q

What complications can hypoxia cause in the respiratory system?

A

Hypoxia can lead to secondary surfactant deficiency and respiratory failure.

36
Q

How should oxygen saturation and blood gases be monitored in infants with HIE?

A

Monitor oxygen saturation and blood gases regularly to ensure they remain within the normal range.

37
Q

What should be the target range for CO2 and PaO2 levels in infants with HIE?

A

Aim to keep CO2 and PaO2 levels in the normal range.

38
Q

What cardiovascular complications can occur in infants with HIE?

A

Hypoxic damage to the heart,
autonomic instability, and
anaemia may be present.

39
Q

What actions should be taken if hemoglobin levels are below 10g/dl in infants with HIE?

A

Investigate the cause and consider blood transfusion if hemoglobin levels are below 10g/dl.

40
Q

How should blood pressure be managed in infants with HIE?

A

Monitor blood pressure and keep it within the normal range.

41
Q

When should fluid boluses be administered to infants with HIE?

A

Avoid multiple fluid boluses unless the infant is obviously hypovolemic, and consider inotropic support if needed.

42
Q

What are common complications related to fluid balance and electrolytes in infants with HIE?

A

Intrinsic renal failure,
SIADH, and
cerebral edema commonly occur.

43
Q

What is the initial fluid restriction recommendation for infants with HIE?

A

Initially, restrict fluids to 40 ml/kg/24 hours with potassium-free Neonatalyte.

44
Q

What parameters should be monitored regarding fluid balance and electrolytes in infants with HIE?

A

Monitor urine output,
electrolytes,
blood glucose, and
blood gases.

45
Q

What should be done if hypoglycemia occurs in infants with HIE?

A

If hypoglycemia occurs, use 12 or 15% glucose as an infusion solution.

46
Q

What complications should be anticipated and treated regarding calcium and magnesium levels in infants with HIE?

A

Anticipate and treat hypocalcemia and hypomagnesemia.

47
Q

How can multi-organ failure manifest in infants with HIE?

A

Almost all organs can be affected, with manifestations such as thrombocytopenia from bone marrow failure and coagulopathy, hypoglycemia, and hypoalbuminemia from hepatic failure.

48
Q

How does intestinal ischemia affect the management of feeds in infants with HIE?

A

Intestinal ischemia increases the risk of necrotizing enterocolitis, so feeds should be introduced slowly over the first few days, preferably with breastmilk.

49
Q

How is chorioamnionitis related to sepsis in newborns?

A

Chorioamnionitis is associated with intrapartum hypoxia and can lead to sepsis, making it difficult to distinguish from encephalopathy.

50
Q

How should sepsis be managed in newborns with suspected intrapartum hypoxia?

A

Screen for sepsis and treat empirically with antibiotics until investigations exclude sepsis. If indicated by history and investigations, perform a lumbar puncture.

51
Q

What is the importance of temperature control in newborns with encephalopathy?

A

It’s crucial to avoid overheating in newborns with encephalopathy.

52
Q

When is induced hypothermia considered for newborns with moderate or severe encephalopathy?

A

If moderate or severe encephalopathy and evidence of intrapartum hypoxia are present, induced hypothermia may improve outcomes if initiated in term or near-term newborns as soon as possible after birth and no later than 6 hours.

53
Q

What should be done if cooling therapy is considered for a newborn?

A

Cooling therapy should be discussed with a cooling center if available.

54
Q

What should be explained to parents regarding the clinical condition of their infant?

A

Explain the clinical condition of the infant without assigning a final cause to the encephalopathy if there is any doubt.

55
Q

What information should be provided regarding management and investigations?

A

Explain the management needed and the type of investigations that will be done to further understand the condition.

56
Q

How should parents be prepared regarding potential outcomes?

A

Prepare them for a potential poor outcome if investigations and signs are suggestive, while also emphasizing that definitive conclusions may not be immediate.

57
Q

What should parents be informed about regarding prognosis and follow-up?

A

Explain that early neurological examination, aEEG, and MRI can predict outcome, but they are only reliable when abnormalities are severe.

58
Q

What is the prognosis for infants with mild HIE?

A

Infants who remain at Sarnat stage 1 and are neurologically normal within 7 days usually do not develop cerebral palsy.

59
Q

What are the typical characteristics of infants with mild HIE?

A

These infants typically have a peak Thompson score of < 7 in the first six hours of life and a normal CFM.

60
Q

Why is therapeutic hypothermia not usually offered to infants with mild HIE?

A

There is no evidence of benefit from therapeutic hypothermia in this group of infants.

61
Q

What are the outcomes for non-cooled infants with moderate and severe HIE?

A

Without therapeutic hypothermia, 25-40% of infants progressing to Sarnat stage 2 develop cerebral palsy, and around 90% of those progressing to stage 3 either die or develop severe cerebral palsy.

62
Q

What predictive value does the Thompson score hold for non-cooled infants with HIE?

A

A peak Thompson score of < 10 during the first 6 days with a score of 0 by day 7 predicts a normal outcome in the majority. A peak Thompson score of 11–15 at any time or a score above 0 on day 7 predicts an abnormal outcome in 65%. A Thompson score above 15 at any time after 1 hour of life predicts an abnormal outcome.

63
Q

What is the effectiveness of therapeutic hypothermia in cooled infants with moderate or severe HIE?

A

Therapeutic hypothermia saves approximately 1 in 7 newborn infants from death and disability.

64
Q

When does the neurological state predict outcome in cooled infants with HIE?

A

Neurological state predicts outcome in cooled infants only when it is very abnormal. A Thompson score above 15 at any time after 1 hour of life predicts a severely abnormal outcome, even in cooled infants.

65
Q

What are common developmental outcomes for infants who survive severe HIE?

A

Microcephaly, cerebral palsy, and developmental delay are common outcomes.

66
Q

What type of follow-up is needed for infants affected by severe HIE?

A

Multidisciplinary specialist follow-up is required for affected infants.

67
Q

When should neurological assessment be conducted for infants with severe HIE?

A

Neurological assessment at 18–22 corrected weeks is recommended to detect motor abnormalities

68
Q

Why is longer-term follow-up necessary for infants with severe HIE?

A

Longer-term follow-up to school age is required to detect all developmental and behavioral abnormalities that may occur.

69
Q

What signs are assessed by the Thompson HIE score?

A

Limb tone, level of consciousness, visible fits, posture, Moro reflex, grasp, suck, respiration, fontanelle

70
Q

How is limb tone assessed in the Thompson HIE score?

A

It is assessed as generally hypertonic, generally hypotonic, or flaccid.

71
Q

What are the different levels of consciousness assessed in the Thompson HIE score?

A

Hyper-alert/staring/excessive irritability, lethargic, comatose or stuporose.

72
Q

How are visible fits assessed in the Thompson HIE score?

A

They are categorized as infrequent (< 3/day) or frequent (> 2/day).

73
Q

They are categorized as infrequent (< 3/day) or frequent (> 2/day).

A

Fisting and/or cycling, strong distal flexion, decerebrate.

74
Q

How is the Moro reflex assessed in the Thompson HIE score?

A

It is assessed as partial or absent.

75
Q

What is evaluated in terms of grasp and suck in the Thompson HIE score?

A

Grasp is categorized as poor or absent, while suck is assessed as poor, absent, and/or bites.

76
Q

What aspects of respiration are considered in the Thompson HIE score?

A

It evaluates hyperventilation, transient apnea, apnea requiring IPPV.

77
Q

How is the fontanelle assessed in the Thompson HIE score?

A

It is evaluated as full and tense.

78
Q

How is the total score calculated in the Thompson HIE score?

A

The maximum score in each category based on the infant’s clinical signs in the previous 24 hours is recorded and then totaled for the day.