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Chapter: Paediatrics: Neonatology

Paediatrics: Hypoxic–ischaemic encephalopathy

Clinical syndrome of brain injury secondary to a hypoxic-ischaemic insult.

Hypoxic–ischaemic encephalopathy

 

Clinical syndrome of brain injury secondary to a hypoxic-ischaemic insult. In developed countries the incidence is 72–5/1000 live births (moderate to severe incidence is 1–2/1000 live births).

 

Causes

 

·  ‘fall’ Umbilical blood flow, e.g. cord prolapse.

·  ‘fall’ Placental gas exchange, e.g. placental abruption.

·  ‘fall’ Maternal placental perfusion.

·  Maternal hypoxia from whatever cause.

·  Inadequate postnatal cardiopulmonary circulation.

 

Presentation

 

Varies depending on severity of cerebral hypoxia. An infant may have a range of symptoms and signs affecting: level of consciousness, muscle tone, posture, tendon reflexes, suck, heart rate and central nervous system ho-meostasis.1

 

Before concluding that an infant may have HIE secondary to an intra-partum hypoxic-ischaemic event, assess for evidence of an intrapartum problem (e.g. CTG abnormality, sentinel event such as abruption or cord prolapse). There should be respiratory depression at birth and a need for resuscitation, including IPPV (Apgar score at 5min < 5). There should be moderate to severe acidosis soon after birth (pH<7.0, base excess worse than –12). The baby should develop encephalopathy within 24hr of birth. Other causes of encephalopathy should be excluded.

 

Management

 

·  Resuscitate at birth; insert IV ± arterial lines. Avoid hyperthermia.

 

·  Assess eligibility for therapeutic hypothermia (TH).

 

·  Start cerebral function analysis monitoring (CFAM).

 

·  Assess for features of dysmorphism and birth trauma.

 

·  Assess neurological features.

 

·  Exclude other causes of encephalopathy, e.g. meningitis, metabolic disturbances, maternal drugs, CNS malformation, and haemorrhage.

 

·  Expect and manage associated multi-organ failure, e.g. cardiac or renal.

 

·  Monitor and maintain homeostasis, e.g. U&E, Ca2+, Mg2+ blood glucose, Hb, blood gases, coagulation. Support BP.

 

·  Mild fluid restriction initially (e.g. 40mL/kg/day 10% dextrose) as there may be oliguria. Omit milk feeds for 1–2 days if HIE severe and then feed slowly.

 

·  Treat seizures.

 

Therapeutic hypothermia

 

This is now the standard of care for term infants with moderate/severe hy-poxic ischaemic encephalopathy.2 Cooling is achieved using a temperature controlled mattress or wrap, and eligible infants have their temperature lowered to 33–34°C within 6hr of insult. Hypothermia is maintained for 72hr before gradual re-warming.


Cerebral function analysis monitoring (CFAM)

 

Single or 2 channel machines available (2 channel = left and right hemi-spheres). Displays ‘raw’ EEG and a compressed ‘amplitude integrated’ re-cording. Pattern of a EEG is used for classification of background activity (see Figs 6.9–6.12). Normal CFAM (aEEG) recording (term infants):

Lower margin  5µV (when awake), upper margin  10µV.

 

Evidence of sleep-wake cycling, no seizures.

 



Prognosis

 

Without cooling, risk of later disability or death is: grade I <2%; grade II 24%; grade III 78%. Disabilities are likely to be one or more of the follow-ing: spastic quadriplegia, dyskinetic cerebral palsy, severely reduced IQ, cortical blindness, hearing loss, and epilepsy.

 

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Paediatrics: Neonatology


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