Neonatal encephalopathy Flashcards

1
Q

Define neonatal encephalopathy

A

Disturbed neurological function:

  • Difficulty initiating and maintaining respiration
  • Depressed tone and reflexes
  • Subnormal level of consciousness
  • Often seizures
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2
Q

Define stage 1 mild neonatal encephalopathy

A
  • <24 hours of hyperalertness
  • Uninhibited Moro and stretch reflexes
  • Sympathetic effects
  • Normal EEG
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3
Q

Define stage 2 moderate neonatal encephalopathy

A
  • Reduced LOC
  • Hypotonia
  • Decreased spontaneous movements with or without seizures
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4
Q

Define stage 3 severe neonatal encephalopathy

A
  • Stupor
  • Flaccidity
  • Seizures
  • Suppressed brainstem and autonomic functions
  • ECC may be isopotential or have infrequent periodic discharges
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5
Q

What is the rate of moderate to severe neonatal encephalopathy in NZ?

A

1.3 per 1000 live births

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6
Q

What % of neonatal encephalopathy has risk factors?

A

○ 69% antepartum only
○ 25% both antepartum and intrapartum
○ 4% intrapartum only
○ 2% no risk factors identified

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7
Q

What is the strongest antepartum risk factor for neonatal encephalopathy?

A

IUGR

RR 38!

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8
Q

Outline the aetiology of neonatal encephalopathy

A
  • Hypoxic ischaemic injury
  • Metabolic
  • Infection
  • Drug exposure: cocaine, barbiturates, alcohol, TCAs, SSRIs
  • CNS malformations
  • Neonatal stroke (1 in 4000)
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9
Q

What markers increase the likelihood an acute peripartum or intrapartum hypoxic-ischaemic event contributed to the development of neonatal encephalopathy?

A

Neonatal signs:

  • Apgars <5 at 5 and 10 mins
  • Cord gas umbilical artery pH <7.0, base deficit >=12 or both.
  • Acute brain injury on MRI or MRS consistent with hypoxic-ischaemia
  • Multiorgan failure

Contributing factors:

  • Sentinel hypoxic or ischaemic event occurring immediately before or during labour and delivery.
  • CTG consistent with an acute peripartum or intrapartum event.
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10
Q

Discuss the utility of Apgar scoring

A
  • Apgar scoring identifies infants that need resuscitation but can be affected by maternal drugs (GA, opiates) and other causes.
  • It is a moderate level predictor of neonatal death and development of cerebral palsy.
  • Apgar <7 at 5 mins OR 27 for cerebral palsy
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11
Q

Outline the Apgar score classifications

A
  • Healthy Apgar score 7-10
  • Primary apnoea Apgar score 4-6
  • Terminal apnoea Apgar score 1-3
  • Fresh stillbirth Apgar score 0
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12
Q

What components are included in an Apgar score?

A

Assesses:

  • HR
  • Resp effort
  • Muscle tone
  • Reflex irritability
  • Colour

Each component is scored as a 0, 1 or 2.

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13
Q

What is the prognosis of neonates who have therapeutic cooling?

A
  • 50% die or have major neurodevelopmental disability at 18 months.
  • 40% have normal neuro outcome.

Seizures are associated with worse outcomes.

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14
Q

What are some permanent neurological sequelae of neonatal encephalopathy?

A

Mild:

  • Learning difficulties
  • ADD

Severe:

  • Cerebral palsy 13%
  • Epilepsy
  • Visual impairment
  • Severe cognitive and developmental disorders
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15
Q

What % of cerebral palsy cases are the result of intrapartum events?

A

10%

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16
Q

What is the effect of increasing gestational age on incidence of cerebral palsy?

A

Incidence of CP decreases significant with gestational age.

  • 14% at 22-27 weeks
  • 0.1% at term
17
Q

List some significant risk factors for cerebral palsy

A
  • Prematurity
  • Low birthweight esp <1500g
  • Placental abruption
  • Apgar <7 at 5 min
  • Neonatal infection
  • Neonatal seizures
18
Q

What is the consensus criteria for defining an acute intrapartum hypoxic event?

A

Essential:

  • Metabolic acidosis
  • Moderate or severe neonatal encephalopathy
  • Cerebral palsy (spastic quadriplegic or dyskinetic types)

Non-specific:

  • Sentinel hypoxic event immediately before or during labour
  • Sudden, rapid and sustained deterioration in FHR pattern
  • Apgar score <=6 for >5 mins
  • Multiorgan failure
  • Imaging showing acute cerebral abnormality
19
Q

What measures can help prevent cerebral palsy?

A
  • Prevention of preterm birth.
    • Magnesium sulfate for neuroprotection.
    • Delayed cord clamping for 30-60 seconds after birth of vigorous, preterm infant: reduces risk of intraventricular haemorrhage.

Postnatal:
• Maintaining adequate ventilation
• Maintaining sufficient cerebral perfusion
• Maintaining normal metabolic status
• Controlling seizures
• Treat any underlying causes for NE e.g. infection, metabolic derangements.
• Therapeutic hypothermia.