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Management of the Asphyxiated Full Term Infant

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Management of the Asphyxiated Full Term Infant 612 Archives of Disease in Childhood 1993; 68: 612-616 PERSONAL PRACTICE Arch Dis Child: first published as 10.1136/adc.68.5_Spec_No.612 on 1 May 1993. Downloaded from Management of the asphyxiated full term infant Malcolm I Levene In Britain, approximately one full term baby the effect of making paediatricians very per thousand dies or is severely disabled as the cautious in the use of intravenous glucose result of birth asphyxia. It is arguably the most during neonatal resuscitation. More recent important avoidable cause of permanent data has shown conclusively that there is a neurological injury affecting the mature fundamental difference in the way the fetus/newborn. It is generally agreed that immature and the more mature brain clinical signs of hypoxic-ischaemic encephalo- responds to glucose infusion. This is probably pathy (HIE) are the best markers for a in the main related to the impaired rate of diagnosis of intrapartum 'asphyxia'. Unfor- glucose transport across the immature tunately the severity of HIE can only be blood-brain barrier. The immature brain diagnosed retrospectively after symptoms have appears to be protected by raised glucose con- developed. Early therapeutic intervention in centrations before asphyxial insult compared the asphyxiated baby may be important to with animals that had no additional glucose.3 modify cerebral injury (see below) and there- There is conflicting data concerning the brain fore there remains a need to have early markers protective effect of high glucose concen- of asphyxia such as depressed Apgar scores, trations after asphyxia. In an immature delay in establishing respiration, or evidence of animal model, administration of glucose significant metabolic acidosis on samples of immediately after a period of hypoxic- cord blood. ischaemic insult resulted in significant reduc- Although there appears to have been a fall in tion in cerebral infarction,4 but others have both the incidence of HIE and the number of shown that in a slightly different rat pup children disabled by this condition in recent model there was significant exacerbation of years,' there is little evidence that this has been damage in the presence of hyperglycaemia due to improvement in postnatal management. after injury.5 In this paper I will consider the standard man- Hypoglycaemia must be avoided during and http://adc.bmj.com/ agement of asphyxia, potentially useful new after resuscitation of asphyxiated babies, but methods for treating the asphyxiated brain, faced with conflicting reports on the role of and consider methods of deciding when to glucose infusion after hypoxic-ischaemic injury withdraw care. The brain ofthe full term infant it is not possible at the present time to give responds to asphyxia in a very different manner practical advice concerning the role of glucose to that of a premature baby and this paper only infusion after human birth asphyxia. This considers the management of asphyxia in full question would be best answered in a double on September 24, 2021 by guest. Protected copyright. term infants. blind controlled clinical study. Rational basis of standard management PREVENTION OF CEREBRAL OEDEMA Asphyxiated infants require expert and rapid It is widespread practice to anticipate cerebral resuscitation wherever they are born. All health oedema and manage the baby so as to reduce care professionals involved in the birth of the possibility that this complication may babies must be adequately trained and develop. This is done in two ways. Firstly, a retrained in resuscitation techniques. In most cases and mask' is sufficient to maintain 'bag Summary of management ofsevere birth asphyxia. See text ventilation until someone with advanced resus- for details citation skills arrives. Appropriate cardiovascu- lar support must be available for infants born Immediate management: 1. Establish effective ventilation with poor or absent circulation. The table 2. Assist circulation if necessary summarises an approach to the management of Early management: 1. Restrict fluids by 20% for first two days the asphyxiated full term infant. 2. Monitor blood pressure and treat hypotension vigorously 3. Assess respiratory effort and Academic Unit of (a) ventilate if baby breathing spontaneously with arterial Paediatrics and Child carbon dioxide tension >7 kPa GLUCOSE (b) if baby ventilated maintain arterial carbon dioxide Health, University of tension at 4-5 kPa Leeds, D Floor, It has been shown that a raised blood glucose 4. If clinical signs of raised intracranial pressure give Clarendon Wing, The concentration before hypoxic-ischaemic mannitol 1 g/kg over 20 minutes and repeat if necessary General Infirmary at every 4-6 hours Leeds, Leeds LS2 9NS injury in adolescent animals results in more Anticonvulsants if: extensive cerebral injury than in those with 1. Frequent convulsions >3 per hour Correspondence to: 2. Prolonged convulsions lasting .3 minutes Professor Levene. normal or low blood glucose.2 This has had Management of the asphyxiatedfull term infant 613 regimen of fluid restriction is often instituted asphyxiated newborn. Babies who have Arch Dis Child: first published as 10.1136/adc.68.5_Spec_No.612 on 1 May 1993. Downloaded from and secondly corticosteroids are administered. suffered significant birth asphyxia may spon- taneously hypoventilate with resulting hyper- capnia and increased cerebral blood volume Fluid restriction which is probably undesirable. For this reason There have been no studies on the effect of all encephalopathic babies should have an fluid restriction in infants with cerebral arterial carbon dioxide tension measurement oedema. In general, measures to reduce and if this is >7 kPa (53 mm Hg) then the cerebral oedema probably have no effect on baby should be electively ventilated. The long term neurological outcome (see below) mechanical ventilator should be adjusted to and it is difficult to argue that routine fluid maintain the arterial carbon dioxide tension at restriction has any advantage in this respect. about 4-5 kPa (34 mm Hg). Fluid restriction may be important in asphyxiated infants who have complications such as inappropriate secretion of antidiuretic Osmotic agents hormone and renal compromise. Fluid reten- Osmotic agents (mannitol or glycerol) are used tion occurring as the result of these two con- to reduce cerebral oedema by increasing serum ditions may further compromise the infant and osmolality. In a neonatal animal model manni- for these reasons I recommend restricting tol significantly reduced brain water content fluids by 20% of the normal regimen for the when given immediately after an hypoxic- first two days of life or until such time as the ischaemic event,9 but it did not reduce the baby's renal function recovers. severity of distribution of brain damage in Hypotension is a relatively common compli- treated compared with untreated animals. cation of birth asphyxia and may be due to There have been no neonatal randomised con- reduction of the circulating blood volume and trolled studies of mannitol or glycerol in the therapeutic dehydration may exacerbate this management of intracranial hypertension. condition. Plasma infusion may be required in Marchal et al in an uncontrolled study gave hypotensive asphyxiated infants. Hypogly- mannitol to 225 babies with the diagnosis of caemia and overt dehydration as a result of asphyxia,1I although the precise indications for fluid restriction must be avoided. treatment were quite varied. Early treatment was defined as mannitol infusion (1 g/kg) before the baby was 2 hours of age. There were Corticosteroids significantly fewer deaths (p=0 005) and the There are no data to support the use of corti- survivors had better neurological outcome costeroids in the routine management of birth (p=0-014) in the early treatment group com- asphyxia. Studies in adults and in animal pared to those treated after 2 hours. Levene models have failed to show any benefit in and Evans showed that mannitol (1 g/kg over reducing brain swelling or improving outcome. 20 minutes) reduced ICP in a small number of In animal models of asphyxia, corticosteroids severely asphyxiated infants with intracranial http://adc.bmj.com/ have shown either a detrimental effect6 or no hypertension (>1-33 kPa or >10 mm Hg).'1 benefit at all.7 Corticosteroids are associated There was a concomitant rise in cerebral per- with a number of actual or potential side fusion pressure 60 minutes after starting the effects including hyperglycaemia, hyperten- mannitol infusion. The effect of mannitol sion, susceptibility to infection, gastrointestinal lasted for approximately four hours. haemorrhage, and restriction of later brain Providing there is adequate renal function to growth. In my view, corticosteroids should not allow excretion of mannitol, it appears to be a on September 24, 2021 by guest. Protected copyright. be used in the management of birth asphyxia. relatively safe agent in the management of cerebral oedema. Its efficacy remains in doubt, but I would recommend its use in infants MANAGEMENT OF CEREBRAL OEDEMA with a bulging fontanelle or in whom there In very severely asphyxiated infants, raised is the clinical impression of intracranial intracranial pressure (ICP, a sustained hypertension. increase to 1x33 kPa (>10 mm Hg)) lasting for There are very few studies to evaluate the 20 minutes or more occurs in 70% of cases.8 role of intracranial pressure monitoring and The management of intracranial hypertension management of intracranial hypertension. includes
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