The term 'birth asphyxia' has been traditionally used to describe infants who present 'flat' at delivery (eg delayed onset of breathing, bradycardia, impaired muscle tone and reflexes) where a period of foetal hypoxia is likely. However, the clinical presentation is not specific to perinatal asphyxia (see differential diagnosis) and the preferred term is 'neonatal encephalopathy' (NE), where the precise cause is not implied. Hypoxic-ischaemic encephalopathy (HIE) is reserved for the subgroup of term NE who have convincing evidence of intrapartum hypoxia; the criteria of which have been outlined by the International Cerebral Palsy Taskforce.
ESSENTIAL CRITERIA for the diagnosis of HIE, in the neonatal period
NE affects 2-9 per 1000 live births in the developed world, and carries significant mortality and morbidity. Up to 6-8% of cerebral palsy have hypoxia-ischaemia as an identifiable cause.
If the infant requires vigorous resuscitation including an endotracheal tube and positive pressure ventilation beyond five (5) minutes of age, then the infant should be admitted to the Special Care Nursery and a blood gas taken before extubation. If the pH is < 7.20 the infant should remain intubated and NETS contacted with view to transfer to a level 3 centre. If the pH is > 7.20 but the infant is still in a depressed state then there should be a discussion with NETS.
Referral to Level 3 nursery should be considered in any infant with moderate to severe encephalopathy requiring
- inotropic support
- further diagnostic workup
Ventilate if there is respiratory depression especially in the setting of
Aim for oxygen saturations = 92% in the term baby to minimise the risk of pulmonary hypertension.
Avoid hypocapnia (pCO2 <50mmHg) as this may worsen cerebral vasoconstriction and further compromise cerebral blood flow. <50mmHg) as this may worsen cerebral vasoconstriction and further compromise cerebral blood flow. </p/><50mmHg) as this may worsen cerebral vasoconstriction and further compromise cerebral blood flow.</blockquote/>
Consider crystalloid boluses (10-20 ml/kg of 0.9% saline) if
Consider blood transfusion if there has been fetal blood loss and poor perfusion and metabolic/lactic acidosis persist
Whole body hypothermia to 33 -34OC for 72 hours may be used in level3 centres for infants more than 35 weeks gestation with moderate or severe HIE who are less than 6 hours of age
The recently updated Cochrane Library systematic review 'Cooling for newborns with hypoxic ischaemic encephalopathy' included eight randomised controlled trials, comprising 638 term infants with moderate or severe encephalopathy and evidence of intrapartum asphyxia. Therapeutic hypothermia (cooling) resulted in a statistically significant and clinically important reduction in the combined outcome of mortality or major neurodevelopmental disability to 18 months of age [RR 0.76 (95% CI 0.65, 0.89), RD -0.15 (95% CI -0.24, -0.07), NNT 7 (95% CI 4, 14)] ie a relative risk reduction of 24%, absolute risk reduction of 15% and Number Needed to Treat (NNT) of 7. Cooling also resulted in statistically significant reductions in mortality [RR 0.74 (95% CI 0.58, 0.94), RD -0.09 (95% CI -0.16, -0.02), NNT 11 (95% CI 6, 50)] and in neurodevelopmental disability in survivors [RR 0.68 (95% CI 0.51, 0.92), RD -0.13 (95% CI -0.23, - 0.03), NNT 8 (95% CI 4, 33)].
Adverse effects of hypothermia included
- sinus bradycardia
- a borderline increase in the need forinotrope support
a significant increase in the incidence of thrombocytopaenia (platelet count below 150 x 109/L).
Phenobarbitone is the first line anticonvulsant. Initial loading dose of 20mg/kg/dose given IV. If seizures continue, up to 40mg/kg can be given safely. After this dose you will increase side effects with minor additional effective seizure control. It is usual to stop IV use once seizures are controlled, however if maintenance is required then 5mg/kg/day once daily should produce good levels. This is the drug of choice for maintenance monotherapy in the first 6 months of life due to its reliable absorption and long safety record.
Phenytoin is the usual second line anticonvulsant. Loading dose is 15-20mg/kg/dose IV. Phenytoin absorption orally in the newborn is highly unreliable and thus this agent is not continued after the immediate stabilisation period.
Midazolam is the third line agent and can be titrated as a continuous infusion, although some authors have stated some concerns over the continuous infusion in the preterm infant.
Clonazepam is a safe and effective alternative.
Signs of oliguria, transient haematuria, anuria and elevated serum creatinine
There is usually spontaneous recovery over 48 hours
Appropriate fluid and electrolyte management (as above)
Deranged liver enzymes and coagulation disturbances
Consider FFP, second dose of Vitamin K
Hypotension (management as above)
Elevated cardiac enzymes -difficult to interpret especially if the infant received CPR during acute resuscitation
Infection - antibiotics as per unit policy
Breast milk preferable as gut circulation may have been compromised. However it is recommended that the infant not be fed until the cardiorespiratory status has normalised
Antibiotics as per unit policy
Only prescribe one dose of Gentamicin until renal function has normalised
Full blood examination
Urea, electrolytes, creatinine
Calcium, magnesium, glucose
Liver function tests
Serum for chromosome analysis, ammonia, amino acids & Urine for amino & organic acids, ketones, reducing substances if metabolic/genetic disorders suspected
Clinical assessment (Sarnat staging)
||25% develop cerebral palsy|
||Disability or death likely|
MRI/MRS should be performed in infants with moderate to severe NE between Days 4-7.
Jacobs S, Hunt R, Tarnow-Mordi W, Inder T, Davis P. Cooling for newborns with hypoxic ischaemic encephalopathy. Cochrane Database Syst Rev 2007;(4):CD003311
MacLennan A. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement BMJ 1999;319:1054-9.
Higgins RD, Raju TN, Perlman J, et al. Hypothermia and perinatal asphyxia: executive summary of the National Institute of Child Health and Human Development workshop. J Pediatr. 2006;148(2):170-175.
Cowan F Outcome after intrapartum asphyxia in term infants. Semin Neonatol 2000;5(2):127-40.
Volpe JJ. Hypoxic-ischemic encephalopathy: clinical aspects In: Neurology of the newborn, 4th ed. Philadelphia: WB Saunders, 2002: 331-382.