Hypoxic Ischaemic Encephalopathy

Abnormal neurological behaviour in the neonatal period arising as a result of a hypoxic-ischaemic event.

  • This can present in a number of ways
    • need for resuscitation (i.e. not breathing or low respiratory rate post-delivery)
    • neurological depression (e.g. floppy)
    • seizures
  • Occurs in 1-6/1000 live births (term) in developed countries
    • ~65% have mild disease and don’t have many complications
    • ~25% have serious disease that could result in severe handicap/death
    • 5% have moderate disease that can result in cerebral palsy
    • 10% will have developmental delay (this is close to the figure for the general population though)
  • NOTE: HIE affects preterm and term infants differently
    • In preterm infants- insult affects white matter- periventricular leukomalacia
    • In term infants- insult affects mainly grey matter

Aetiology/Risk Factors

  • Maternal
    • Cardiac arrhythmia/arrest
    • Asphyxiation
    • Anaphylaxis
    • Status epilepticus
    • Hypovolaemic shock
  • Foetal
  • Uteroplacental
    • Placental Abruption
    • Cord Prolapse
    • Uterine rupture
    • Hyperstimulation with oxytocic agents

Pathophysiology

(see also Excitotoxicity)

  • Acute HIE leads to primary and secondary events:
    • Primary neuronal damage: cytotoxic changes due to failure of microcirculation → inhibition of energy-producing molecular processes → ATPase membrane pump failure → cytotoxic edema and free radical formation → compromised cellular integrity
    • Secondary neuronal damage: May extend up to 72 hours or more after the acute insult and results in an inflammatory response and cell necrosis or apoptosis (fueled by reperfusion)

Presentation

  • No specific test.  HIE is a clinical diagnosis (supported by imaging)
  • Abnormal neurological examination in the first few days of life (including reflexes and tone) may be the most useful tool
  • Essential criteria include:
    • Metabolic acidosis (cord pH<7 or base deficit of >12)
    • Early onset encephalopathy
    • Multisystem organ dysfunction
      • Acute renal failure (20%)
      • Myocardial dysfunction and hypotension (28-50%)
      • Abnormal liver function tests (80-85%)
      • Coagulation impairment

frefre

 

Investigations

  • Cerebral function monitoring (amplitude-EEG)
    • In infants who have moderate to severe HIE…
      • Marginally abnormal/normal aEEG may just reflect dysfunction and is reassuring (upper margin >10μV and lower >5μV is normal; if lower margin falls <5μV- moderately abnormal)
      • Severely abnormal aEEG suggests permanent damage and has a poor prognosis (upper margin <10μV)
  • MRI scan in the first 7-10 days should be done in Grade II-III HIE to evaluate any brain damage
    • Cranial USS can be used (hypoechoic regions) but is relatively nonspecific
  • Make sure to investigate other problems associated with HIE, usually comprising
    • FBC, LFT, U&E, Glucose
    • Urine dipstick

Management

  • Hypothermia
    • haematuria
    • Start as early as possible (within several hours of birth)
    • Aim to cool to maintain rectal temperature at 33-34°C for 72 hours
      • NB the infants observations will be dramatically abnormal at this temperature.  They require close monitoring of blood gases, glucose and other investigations regularly to prevent further complications (of disease or treatment).
    • Re-warm slowly

 

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