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Perinatal Medicine > Hypoxic Ischaemic Encephalopathy > Flashcards

Hypoxic Ischaemic Encephalopathy Flashcards

1
Q

What is HIE?

A

An acquired syndrome of acute brain injury characterized by neonatal encephalopathy and evidence of intrapartum hypoxia

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2
Q

What is the prognosis for infants with moderate or severe HIE?

A

25-90% chance of developmental delay and/or CP, depending on severity and treatment

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3
Q

What is neonatal encephalopathy?

A

Abnormal level of consciousness and abnormal tone and reflexes, often with abnormal breathing, abnormal feeding and seizures

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4
Q

What are the causes of neonatal encephalopathy? (6)

A
  • Sepsis
  • Brain malformation/damage
  • Metabolic abnormality (e.g. Hypoglycaemia)
  • Drug withdrawal (neonatal abstinence)
  • Abnormal brain perfusion (shock, cardiac failure, trauma)
  • Intrapartum hypoxia and ischaemia
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5
Q

What is birth asphyxia?

A

Failure to initiate and sustain spontaneous breathing after birth. Shown by low apgars

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6
Q

What causes birth asphyxia? (5)

A 
Sedation via maternal medication/drug abuse
Fetal infection
Fetal congenital anomaly
Trauma/ haemorrhage
Intrapartum hypoxia and ischaemia
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7
Q

What is intrapartum hypoxia?

A

Impaired gas exchange leading to progressive fetal hypoxaemia and hypercapnea with a significant metabolic acidosis

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8
Q

What is the normal base deficit at birth

A

Base excess -0.3 to -6.3 (base deficit of 0.3- 6.3)

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9
Q

What 2 parameters on cord gas/early blood gas show hypoxia/asphyxia severe enough to cause CP?

A

BE and pH. Indicate metabolic acidosis. BE >12mmol/l and art cord pH

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10
Q

What signs are suggestive of intrapartum hypoxia or fetal asphyxia severe enough to cause CP?

A 
Sentinel hypoxic event
Sudden deterioration of FHR pattern
Multisystem involvement
Imaging evidence
Apgars of 0-6 for >5 min
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11
Q

At what point is base deficit abnormal? What does this suggest?

A

Base deficit of >10mmol/l is abnormal and suggests intrapartum hypoxia

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12
Q

How does the fetus respond to hypoxia and ischaemia in utero?

A

Response: fetal bradycardia ms diving reflex (blood is diverted to the brain)

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13
Q

What occurs in prolonged hypoxia?

A

Cardiac failure

Anaerobic metabolism –> accumulation of lactic acid –> metabolic acidosis

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14
Q

What brain regions are affected by hypoxia? What is the pattern of injury!

A

Basal ganglia and subcortical white matter

Injury follows in phases

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15
Q

What ratio represents failed oxidative metabolism?

A

A decreasing PCr/Pi ratio

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16
Q

What does a decreasing PCr/Pi ratio represent?

A

Failure of oxidative metabolism

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17
Q

What are the 6 parameters used to stage HIE?

A 
Level of consciousness 
Activity
Neuromuscular control
Primitive reflexes
Autonomic function
Seizures
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18
Q

How many stages of HIE are there?

A

3

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19
Q

What are the 9 parameters used in the Thompson HIE score?

A 
Limb tone
Level of consciousness
Visible fits
Posture
Moro
Grasp
Suck
Respiratory effort
Fontanel
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20
Q

What are the Grade 3 signs according to the Thompson score?

A

Flaccid (limb tone)
Comatose or stuporose (level of consciousness)
Decerebrate (posture)
Apnoeic (respiratory effort)

21
Q

What are the 6 types of subtle neonatal seizures?

A

Ocular (tonic deviation+/- jerking, staring, fixed blinking)
Oral-Buccal-Lingual (chewing, facial wincing, cry-grimace)
Limb movements (boxing, cycling, stepping)
Autonomic (Brady/tachycardia, tachypnoea)
Apnea

22
Q

What are the 3 classes of neonatal seizures?

A

Subtle
Tonic
Clonic

23
Q

What causes neonatal seizures?

A 
Hypoglycaemia
Hypoxia
HIE
Brain damage, haemorrhage, trauma
Meningitis
Electrolyte/ metabolic abnormalities
Drug withdrawal
Abnormal brain perfusion
24
Q

How is CNS function assessed and monitored in infants with HIE?

A

Amplitude integrated EEG (aEEG)
Cerebral ultrasound
MRI

25
Q

What is the most useful prognostic tool and what is a good prognostic sign?

A

aEEG

Normal aEEG at age 6 hours correlates with normal outcome

26
Q

What is cerebral ultrasound used for and what can it show?

A

It is used to exclude congenital cerebral anomalies

It can show oedema, infarction, haemorrhage acutely and later cystic changes

27
Q

What can be seen on MRI and how is this helpful?

A

It shows cerebral injury

Can help prognosticate

28
Q

What is therapeutic hypothermia?

A

Whole body cooling to 33-34, or selective head cooling to 34-35.

29
Q

How is therapeutic hypothermia administered?

A

Consistent with clearly defined protocols
In NICU (IPPV, sats, BP monitors, inotropes available)
Started within 6 hours of birth for 72 hours
Rewarmed slowly over at least 4 hours
Monitor for adverse effects
Follow up

30
Q

What are the mechanisms of therapeutic hypothermia?

A

Metabolic depression allowing energy conservation. Specific inhibition of apoptosis
Improved protein synthesis
Inhibition of glutamate release
Decreased intracellular acidosis and free radical generation
Reduced NO production and BBB breakdown
Decreases inflammatory response

31
Q

What are the cooling criteria in HIE?

A

A. All of the following: >=35/52 and >=1.8 kg; 10; or 5min Apgar

32
Q

What is the Shankaran definition of moderate encephalopathy?

A

One or more of the following: Lethargic (level of consciousness), decreased spontaneous activity, distal flexion with complete extension (posture), hypotonia (focal/general), weak suck/ incomplete Moro, constricted pupils/ bradycardia/ periodic breathing.

33
Q

What is the Shankaran definition of severe encephalopathy?

A

One or more of the following: Stupor/coma, no spontaneous activity, decerebrate posture, flaccid (tone), absent suck/Moro, deviated/dilated/nonreactive pupils/ variable heart rate/ apnoeic.

34
Q

What else can go wrong in HIE?

A

Lungs- surfactant depletion and delayed lung fluid clearance; pulmonary hypertension
CVS- cardiac dysfunction
Renal- failure, hyponatraemia, hypokalaemia
SIADH (hyponatraemia)
Hepatic- hypoglycaemia, low albumin, coagulopathy, jaundice
GIT- ileus/’NEC
Bone marrow- thrombocytopenia

35
Q

What is the fluid management in an HIE baby with renal failure?

A 
Fluids restricted to 40ml/Ig maintenance
Avoid boluses unless hypovolaemic
Use K-free fluids
Monitor glucose (12.5-15% dextrose if low)
36
Q

What are the paO2 and paCO2 goals in an HIE baby?

A

O2- 8-10.6 kPa, 60-80mmHg

CO2- 4.4-6 kPa, 33-52.5 mmHg

37
Q

What is the primary care (systems approach) of HIE babies?

A

Brain- treat seizures: airways, breathing, glucose, phenobarbital
Lungs- monitor O2 sats, treat resp failure
CVS- monitor pulse and perfusion
Renal- monitor urine outputs, avoid too much fluid
Hepatic- monitor blood glucose
GIT- avoid feeds unless signs are mild, IV fluids preferable
Bone marrow/immunity- monitor colour and signs of bleeding

38
Q

What is the management of infants with low Apgar scores?

A

If ongoing ventilation or signs of mod/severe HIE- admit to ICU/HC, aEEG, cool
CPR or BD>10 but good response to resus, no signs mod/severe HIE-bad it to observation area, feed cautiously, routine obs, early glucose check, watch for HIE signs or seizures
Some resus (no CPR) but normal by 10mins normal blood gas and normal glucose- stay with mum

39
Q

What are the signs of stage 1 HIE?

A

Irritability, increased tone, poor sucking, exaggerated Moro with jitteriness and fisting

40
Q

What are signs of stage 2 HIE?

A

Lethargy, decreased tone and primitive reflexes, often with seizures

41
Q

What are signs of stage 3 HIE?

A

Stupor or coma, flaccid, apnoeic

42
Q

What is the aim of management of HIE babies?

A

To treat the signs and reduce further organ damage

43
Q

How is an HIE a baby managed?

A

Prevent fetal hypoxia. Prompt resus. Document and record neurological signs daily. Routine monitoring of vital signs and manage complications. Record HC at birth and daily. Document cerebral sonography during adm and at dc. Treat convulsions. Restrict fluid intake. Supplementary O2 and resp support if needed. Counsel parents.

44
Q

An abnormal Thompson score on day 7 indicates what?.

A

Poor neurological development

45
Q

What does a Thompson score of >15 indicate?

A

Increased mortality

46
Q

When is follow up performed?

A

At 20 corrected weeks

47
Q

What brain damage is commonly seen in survivors of severe HIE?

A

Microcephaly, CP and mental retardation

48
Q

What sign is seen on cranial sonography indicating persistent damage and in what regions is it prevalent?

A

Leucomalacia- densities or cystic change

Seen in the subcortex, cortex or basal ganglia

Perinatal Medicine (14 decks)

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