Asphyxia neonatorum

How much certainty is enough?

EDITOR--The thesis set out by Little in 1862 that cerebral palsy was primarily due to perinatal cerebral injury did not meet with approval from the London Obstetrical Society--it was an obvious conflict of interests.[1] Almost 14 decades later the echoes of those opposing voices still resonate, most recently in a statement from a group calling itself the International Cerebral Palsy Task Force.[2] This statement makes some useful points, but there are aspects that need further debate.

One is the need to recognise that it is usually possible to form a view on what caused cerebral palsy only in probabilistic terms. The question then is, how much certainty is enough? In the medicolegal context the answer is clear--more than 50% certainty (that is, P [is less than] 0.5). It is irrelevant that birth asphyxia causes cerebral palsy rarely and that cerebral palsy is due to birth asphyxia rarely, as long as it is accepted that cerebral palsy is caused by birth asphyxia sometimes. In that case, when confronted with a case of cerebral palsy that could be due to birth asphyxia and in which there is evidence of birth asphyxia of potentially damaging severity, the relevant question to ask is, are these events probably causally related or are they probably coincidental? The answer is that they are more likely to be causally related, as long as no better explanation for the cerebral palsy is forthcoming.

Secondly, insisting that there is a certain severity of metabolic acidaemia before attributing cerebral palsy to birth asphyxia is unreasonable. Such evidence might be necessary to form a view that approaches certainty (for example, P [is less than] 0.05), but it is not necessary to form a view "on the balance of probabilities" For instance, if a baby is stillborn after placental abruption, responds to heroic resuscitation, experiences an acute neonatal encephalopathy, and then develops athetoid cerebral palsy with evidence of basal ganglia injury shown by a magnetic resonance imaging scan, then birth asphyxia is the probable cause of disability regardless of whether metabolic acidaemia was found.

This insistence on ascertaining metabolic acidaemia is questionable--cord blood gas analysis is not universally practised; if cord venous blood is obtained severe fetal acidaemia may be missed; bicarbonate is often used during resuscitation; and it will discourage the assessment of acid-base status at birth.

Peter Dear consultant in neonatal medicine

Simon Newell consultant in neonatal medicine St James's University Hospital, Leeds LS9 7TF

[1] Little WJ. On the influence of abnormal parturition, difficult labours, premature birth and asphyxia neonatorum on the mental and physical condition of the child, especially in relation to deformities. Trans Obstet Soc Lond 1862;3:293-344.

[2] Alastair MacLennan for the International Cerebral Palsy Task Force. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ 1999;319:1054-9. (16 October.)

There are problems with the consensus statement

EDITOR--We agree with MacLennan and Bakketeig that whenever a child presents with one of the cerebral palsy syndromes, appropriate meticulous investigation into why this has happened is needed.[1 2] We agree also that only a minority of children with cerebral palsy have sustained their brain injury as a consequence of intrapartum hypoxic ischaemic damage at term and that an even smaller number have sustained their problems as a consequence of an inappropriate standard of care. We nevertheless have multiple concerns about these papers.

Firstly, we do not accept the premise that birth asphyxia is commonly accepted either professionally or at a lay level as being a frequent cause of cerebral palsy. That view was dispelled some years ago.

Secondly, the implication in box 1 is that the International Cerebral Palsy Task Force has not attracted dissident views. Quite the opposite is true. Indeed, its signatories do not include any UK paediatric bodies or any individual paediatric neurologists.

Thirdly, we are unable to accept that unless there is documented fetal acidaemia intrapartum hypoxia can be excluded as the cause of cerebral palsy in any individual case. Retrospectively, and also frequently in practice, reliable measures of fetal acidosis have simply not been sought.

Fourthly, we are disappointed that the statement was dismissive of the role of neuroimaging and electroencephalography. We believe that the use of brain imaging and electroencephalography both prospectively and retrospectively is of particular value when attempting to determine when brain insults have occurred, especially when these data are used together with clinical information.

Furthermore, although this document undoubtedly represents consensus reached after extensive discussion among those selected to participate, in no way does it contain a meta-analysis of the kind usually required before an authoritative guideline can be produced.

Finally, we are surprised that the section on expert witnesses should have been allowed to remain in a peer reviewed journal published in Britain. Recent changes in English law subsequent to the Woolf recommendations and reforms[3] have now been instituted. These define and explain the role of the expert witness far more objectively than this consensus statement.

L Rosenbloom consultant paediatric neurologist Alder Hey Children's Hospital, Liverpool L12 2AP

J M Rennie consultant in neonatal medicine King's College Hospital, London SE5 9RS janet.rennie@kcl.ac.uk

[1] Alastair MacLennan for the International Cerebral Palsy Task Force. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ 1999;319:1054-9. (16 October.)

[2] Bakketeig LS. Only a minor part of cerebral palsy cases begin in labour. BMJ 1999;319:1016-7. (16 October.)

[3] Access to justice. Final report to the Lord Chancellor by the Right Honourable Lord Woolf, July 1999. London: Stationery Office. (www.open.gov.uk/lcd/civil/cpr/intro. htm; accessed 23 March.)

Author's reply

EDITOR--The consensus statement on cerebral palsy causation clearly challenged the views of some of those who have given expert medicolegal opinion in the past.[1]

Dear and Newell seem to support the assumption of Little in 1862 that if no antenatal cause of cerebral palsy is evident then cerebral palsy must be due to "birth asphyxia" As the antenatal causes are usually silent and difficult to detect in retrospect, the task force suggested that the expert witness seeks scientific evidence for one of the possible causes (that is, perinatal asphyxia) before presuming that this was the primary cause. The first three criteria in the template give a mechanism for identifying objectively whether asphyxia was present at birth, and the other five criteria help determine whether the hypoxia was acute or chronic. Non-specific signs such as meconium staining, non-reassuring fetal heart rate patterns, low Apgar scores, and neonatal encephalopathy can be associated with acute or chronic hypoxia, a non-hypoxic chronic cause, or no detectable abnormality and a normal outcome. Hospitals should adopt a policy to collect umbilical arterial and venous blood gases routinely from all cases where such information would be helpful--for example, caesarean section and instrumental delivery for fetal indications.

In reply to Rosenbloom and Rennie, the consensus statement was supported by several international paediatric societies and endorsed by several distinguished paediatric neurologists, of whom one was a clearly labelled author. The statement's publication enables any UK paediatric body and all international scientific groups to endorse or reject it. The task force welcomes any support or critical comment with appropriate scientific references. Like all opinions, the statement should change when convincing new evidence is available.

The task force unsuccessfully sought good evidence as to whether magnetic resonance imaging and electroencephalography could retrospectively determine the cause and precise timing of cerebral palsy. Though invited, Rosenbloom did not join the task force debates, and he and his colleagues have not supplied references in their letter to support their views. Reliable evidence would be welcome. To date, publications using magnetic resonance imaging and electroencephalography to determine asphyxial causes have used unsatisfactory criteria to determine the aetiology. It is hoped that there will be adequate validation of any association between specific neuro-imaging patterns seen in childhood and well defined acute de novo intrapartum hypoxia, chronic antenatal hypoxia, neonatal hypoxia, and non-hypoxic antenatal and infant causes of neuropathology. The sensitivity, specificity, false positive rates, and false negative rates of these diagnostic tests should be ascertained by using control groups.

Alastair MacLennan chairman, International Cerebral Palsy Task Force, Perinatal Society of Australia and New Zealand

Department of Obstetrics and Gynaecology, University of Adelaide Women's and Children's Hospital, North Adelaide, South Australia 5006, Australia

amaclenn@medicine.adelaide.edu.au

[1] Alastair MacLennan for the International Cerebral Palsy Task Force. A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement. BMJ 1999;319:1054-9. (16 October.)

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