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Hypoxic Ischaemic Encephalopathy Flashcards

(48 cards)

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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?

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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?

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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?

Study These Flashcards
A

Subtle
Tonic
Clonic

23
Q

What causes neonatal seizures?

Study These Flashcards
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?

Study These Flashcards
A

Amplitude integrated EEG (aEEG)
Cerebral ultrasound
MRI

25
What is the most useful prognostic tool and what is a good prognostic sign?
aEEG | Normal aEEG at age 6 hours correlates with normal outcome
26
What is cerebral ultrasound used for and what can it show?
It is used to exclude congenital cerebral anomalies | It can show oedema, infarction, haemorrhage acutely and later cystic changes
27
What can be seen on MRI and how is this helpful?
It shows cerebral injury | Can help prognosticate
28
What is therapeutic hypothermia?
Whole body cooling to 33-34*, or selective head cooling to 34-35*.
29
How is therapeutic hypothermia administered?
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
What are the mechanisms of therapeutic hypothermia?
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
What are the cooling criteria in HIE?
A. All of the following: >=35/52 and >=1.8 kg; 10; or 5min Apgar
32
What is the Shankaran definition of moderate encephalopathy?
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
What is the Shankaran definition of severe encephalopathy?
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
What else can go wrong in HIE?
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
What is the fluid management in an HIE baby with renal failure?
``` Fluids restricted to 40ml/Ig maintenance Avoid boluses unless hypovolaemic Use K-free fluids Monitor glucose (12.5-15% dextrose if low) ```
36
What are the paO2 and paCO2 goals in an HIE baby?
O2- 8-10.6 kPa, 60-80mmHg | CO2- 4.4-6 kPa, 33-52.5 mmHg
37
What is the primary care (systems approach) of HIE babies?
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
What is the management of infants with low Apgar scores?
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
What are the signs of stage 1 HIE?
Irritability, increased tone, poor sucking, exaggerated Moro with jitteriness and fisting
40
What are signs of stage 2 HIE?
Lethargy, decreased tone and primitive reflexes, often with seizures
41
What are signs of stage 3 HIE?
Stupor or coma, flaccid, apnoeic
42
What is the aim of management of HIE babies?
To treat the signs and reduce further organ damage
43
How is an HIE a baby managed?
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
An abnormal Thompson score on day 7 indicates what?.
Poor neurological development
45
What does a Thompson score of >15 indicate?
Increased mortality
46
When is follow up performed?
At 20 corrected weeks
47
What brain damage is commonly seen in survivors of severe HIE?
Microcephaly, CP and mental retardation
48
What sign is seen on cranial sonography indicating persistent damage and in what regions is it prevalent?
Leucomalacia- densities or cystic change | Seen in the subcortex, cortex or basal ganglia

Perinatal Medicine (14 decks)

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