Intended for healthcare professionals

Letters

Birth events and cerebral palsy: facts were not presented clearly

BMJ 2001; 322 doi: https://doi.org/10.1136/bmj.322.7277.50 (Published 06 January 2001) Cite this as: BMJ 2001;322:50
  1. Fiona Stanley, professor of paediatrics,
  2. Eve Blair, senior research officer,
  3. Eva Alberman, professor emeritus (e.d.alberman{at}mds.qmw.ac.uk)
  1. TVW Telethon Institute for Child Health Research, University of Western Australia, PO Box 855, Subiaco, Western Australia 6008, Australia
  2. Department of Environmental and Preventive Medicine, Wolfson Institute of Preventive Medicine, St Bartholomew's and the Royal London School of Medicine and Dentistry, London EC1M 6BQ

    EDITOR—It is regrettable that a report of a conference in a scientific journal should have a headline such as the article by Silvert.1 Its tone belongs to the counterproductive adversarial approach of lawyers concerned with litigation. It is common ground that causes of the heterogeneous group that comprises the cerebral palsies include antenatal, intrapartum, and postnatal events. The precise proportions contributed by each remain uncertain.

    The consensus statement reportedly attacked at the conference, far from denying the importance of intrapartum causes, was entitled: A template for defining a causal relation between acute intrapartum events and cerebral palsy.2 This well describes its aims, which were to recognise those cases in whom acute intrapartum hypoxia was most likely to have caused cerebral palsy and consider their preventability. There was wide consultation before this consensus was agreed and published.

    Certain facts are largely consistent and undisputed. In developed countries the prevalence quoted in the report of 2-2.5 per1000 births includes about 10% cases with a postneonatal cause. About 25% are very preterm births, in which there is often a causal chain spanning both the antenatal and the postnatal period, and they include a proportion of those in whom infective and genetic causes can be firmly established. The identification of these is constantly increasing with developments in medical technology.

    A history of the cluster of characteristics suggesting that adverse intrapartum events have contributed to the causal pathway has been reported in about 16%, but in only 10% is there no additional evidence of antenatal damage.3 Not all cases in these 10% are necessarily the result of medical accidents. Some might not have been preventable even with the best obstetric care, both because there may have been unrecognised antenatal damage and because the professionals in charge are neither omniscient nor omnipotent, and there are often problems in the systems under which they work. Among these 10%, however, are the cases the most likely to have been preventable by better intrapartum medical care, and it is important that they be recognised, not simply for the purposes of litigation, but to prevent recurrence. In an issue as sensitive as this it is a disservice to both parents and the health professions not to present the facts clearly, or to reiterate views for which there is no substantive evidence.

    References

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