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Neonatal shaken baby syndrome—lessons to be learned
  1. D B Knight1
  1. 1Neonatal Paediatrician National Women’s Hospital, Auckland, New Zealand davidk{at}adhb.govt.nz
    1. R Sunderland2,
    2. A N Williams3
    1. 2Birmingham Children's Hospital; rs.sunderland{at}bch.nhs.uk
    2. 3Northampton General Hospital; anw{at}doctors.org.uk

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      Williams and Sunderland,1 and the accompanying commentary from Rosenbloom and Ryan,2 discuss a severe cystic brain lesion associated with chest physiotherapy in very preterm infants. Rosenbloom is correct that the topic lacks topicality, but mainly because neonatal chest physiotherapy is now used very little if at all. I disagree that there is an abundant literature detailing appropriate treatment and the absence of brain damage associated with neonatal chest physiotherapy. Older data suggested benefit,3–5 but more recent publications demonstrate none.6–8 The reported benefits were transient improvements in oxygenation and slight increased removal of secretions. The older studies are all too small to adequately address safety. Chest physiotherapy, by whatever method, has little or no place in neonatal intensive care.

      There are several lessons to be learned from the experience of the units who found these brain lesions. Firstly, a treatment generally recognised as being beneficial may not be so, especially with other changes in care over the passage of time. Continued reassessment of the usefulness of treatment is needed. Secondly, side effects can appear, even when a treatment has supposedly passed the test of time. Ongoing audit is needed. Thirdly, there is a dilemma that clinicians face in reporting complications. The first hospital to find this lesion did not further investigate the cause, report its suspicions, or inform the parents of the affected babies.9 The second hospital did all of these.10 That hospital has been subject to a long official public inquiry and law suites, and had 20 medical, nursing, and physiotherapy staff investigated by registration authorities, lasting 8 years. All this happened in the supposedly non-litigious medicolegal environment of New Zealand. There needs to be the ability to be open about complications and side effects and have an atmosphere of learning from, rather than blame for, them.

      I would like to correct one statement by Williams and Sunderland. In our nursery there was no change in the vigour of chest physiotherapy from the introduction of the technique in 1985 until we stopped all chest physiotherapy at the end of 1994. The cerebral lesions appeared 1992–94. From 1985, the same physiotherapist was teaching and supervising the technique. During those 3 years, babies who developed the brain lesion had more chest physiotherapy than matched concurrent controls, but considerably less than many infants in previous years. Why the brain lesion began to appear remains a mystery.

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      Authors’ reply

      We are grateful to colleagues for their comments on our annotation.1 We would stress that we merely abstracted the views of others, so any criticisms (apart from our brevity) will be of the lawyers, doctors, nurses, physiotherapists, and parents who contributed to the Royal Commission Report. We found it to be systematic, rational, and objective.

      We strongly refute any suggestion that any of the New Zealand professionals should be criticised let alone made scapegoats (witness our final paragraph). We are puzzled that Drs Rosenbloom and Ryan discount the quoted witness statements of the parents and involved clinicians.1 The lawyers and doctors are clear that the physiotherapy and nursing practices did occur and that the levels of head shaking were not monitored.

      We are concerned with infant brain injuries not lung disease and consider this to be topical. We share colleagues’ concern at the need to base opinions on speculative presumption extrapolated from animal or accident research and are aware of the limited evidence that identifies the minimal forces needed to cause shaken brain damage in neonates or older infants. We found the reported experiences to be a helpful insight.

      We are delighted that Dr Rushton has taken this opportunity to state he thought vigorous chest physiotherapy without supporting the head was responsible for the porencephalic lesions and to inform of his pivotal involvement in advising New Zealand colleagues.2 We understand there were earlier concerns that publishing the speculation about physiotherapy would open liability to litigation. Lawyers might consider the inference that fear of litigation led to suppression of information that might have prevented the New Zealand deaths and the dilemma facing clinicians who reported the cerebral implications of vigorous physiotherapy. Dr Knight reports their unit has been ‘subject to a long official public inquiry, law suits and had 20 medical, nursing, and physiotherapy staff investigated by registration authorities, lasting 8 years.’3

      We do not accept criticisms of inaccurate references. The Cochrane review we both cited was last updated in 1997. There has been an updated review this year (dealing with lung not brain disease), which was unavailable to the editors or us at the time of submission. Dr Knight states3 there was no change in the vigour of chest physiotherapy from 1985 until the end of 1994 but he co-authored the paper4 we cited that states that there was no policy to support the head during chest physiotherapy and no data on the extent the head moved during physiotherapy, whether given by nurses or physiotherapists. The Royal Commission Report found no record of the vigour of chest percussion and understood there was considerable variation with no standardisation of training.

      We recommend interested colleagues to read this report and the publications of Knight et al4 before dismissing the possibility that vigorous chest physiotherapy without supporting the head may cause brain injuries in certain circumstances.

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