COT DEATH

146 COT DEATH

SIR,-Your leading article (Nov. 22, p. 1024) throws a wel-

spotlight on the confused definitions which still obstruct progress in this field. You also highlight the challenging findings in Sheffield’ and in North Londonwhich support the hope that many cot deaths might be prevented by focusing additional health care on those at high risk. come

There are, however, two points which we feel need further emphasis. Firstly, we must continue to stress the major role of respiratory virus infection in deaths at this age, the evidence for which we set out last year.3 You suggest that the age-inci-

SIR,-We agree with the conclusions of your editorial on cot death, but several comments do not fit our experience. You state that about half of the babies found dead at home show macroscopic disease sufficient to account for death. In our experience, with over a thousand cot deaths, it is microscopy that reveals evidence of pathology, and naked-eye appearances can be very misleading. To carry out histology on only half of such children would lead to many errors. Complete necropsy by a psediatric pathologist with biochemistry and immunology reveals abnormalities in all but a few cases. The problem is not lesions but interpreting them. The prospective study by Carpenter and Emery1on children at increased risk of unexpected death did not involve the direct utilisation of factors found in surveys such as that of Froggatt et al. It is probably the direct use of factors from such studies that has led to much criticism of attempts to define at-risk groups. The Sheffield survey was designed to assess the numerical values of factors and evaluate factors acting together. For example, most epidemiological studies suggest an increased risk in lower social classes and in infants born to very young women. The Sheffield study showed that social class was not significant when the mother’s age was taken into

finding

account.

months

Age-distribution of R.S.V. bronchiolitis’and of Ireland" and Newcastle.

cot

death in Northern

The "classic picture" of a cherished, healthy child who is simply found dead is a myth. We showed in 1956 that a complete history revealed symptomatic evidence of recent previous disease in 49 of 50 consecutive cases referred to the coroner as having been put to bed completely fit and being found dead;’ and a study of the costochondral junction, liver, and thymus usually reveals evidence of long-standing disease.6 Unexpected deaths occur in hospital in children who have gross disease, and many of these deaths are as difficult to explain as those occurring at home. To explain cot deaths we need to know the immediate mechanism of death (and this applies to all children, wherever they die) and to find out why children with apparently the same symptoms achieve different levels of primary health care. Department of Histopathology, Children’s Hospital, Western Bank, Sheffield 10.

dence of

cot

deaths is

idiosyncratic,

but

we

I. FORREST HAY J. L. EMERY

draw attention

again to the very similar age-distribution of children with respiratory-syncytial-virus (R.s.v.) bronchiolitis (see figure). Whatever the mechanism of virus action, whether overwhelm-

ing infection, hypersensitivity,

or

is

The figure originally appeared in the British Medical Journai3 and reproduced by kind permission of the Editor.

P. S. GARDNER Royal Victoria Infirmary, Newcastle upon Tyne.

TYPE-IV HYPERLIPIDÆMIA

upper-respiratory-tract

obstruction, it seems clear that if means could be found to prevent these infections there would be a great reduction in postneonatal mortality. Secondly, controversy remains not only about the significance of necropsy findings but even about their description. This is due partly to variation in the sampling techniques of different pathologists but more importantly to the absence of agreed parameters for describing the quality and extent of histological appearances. These difficult problems are central to the further understanding and prevention of cot death, and the study being launched by the Department of Health based on five centres in which the pathologists are to standardise their techniques and descriptive parameters holds real promise of a consensus for the first time.

D. J. SCOTT

S!R,—Ithink

Dr Wetzler (Dec. 13, p. 1218) is accusing us in logic which we have not committed (Sept. 20, p, 517). It is true that weight reduction leads to a fall in serumtriglycerides. The linear correlation between A weight and5 serum-triglycerides is not good, although it is rather better if one uses log serum-triglycerides. The interrelations between weight, calorie intake, nutrients ingested, and serum-thgtycerides are complex, hence the low coefficient of determination to which he draws attention. The important point is that weight reduction works; we doubt that it is incidental. Since submitting our paper we have done a number of mu1tivariate stepwise regression analyses incorporating all the food data and weight and triglyceride changes. For all the nutrients and change in weight Rwas 0.50. Thus we could account for no more than half the observed changes in sem triglyceride. No single nutrient made a statistically significant contribution. It could be that the imprecision of the dietary calculations one had to use on outpatients obscured relation-

of

errors

M. A. P. S. DOWNHAM

1. McWeeny, P. M., Emery, J. L. Archs Dis. Childh. 1975, 50, 191. 2. Cameron, J. M., Watson, E. J. Path. 1975, 117, 55. 3. Downham, M. A. P. S., Gardner, P. S., McQuillin, J., Ferris, J. A.

J.

Br.

med. J. 1975, i, 235. 4. Public Health Laboratory Service, ibid. 1972, iii, 482. 5. Public Health Laboratory Service, ibid. 1973, ii, 788. 6. Bergman, A. B., Beckwith, J. B., Ray, C. G. (editors) Sudden Infant Death Syndrome. Seattle, 1970.

1. Lancet, 1975, ii, 1024. 2. Carpenter, R. G., Emery, J. L. in Proceedings of the Francis E. Camps Symposium on the Sudden Infant Death Syndrome; p. 91. Canadian Foundation for the Study of Infant Deaths, Toronto, 1974. 3. Carpenter, R. G., Emery, J. L. Nature, 1974, 250, 729. 4. Froggatt, P., Lynas, M. A., MacKenzie, G. Br. J. prev. soc. Med. 1971, 25, 119. 5. Emery, J. L., Crowley, E. M. Br. med. J. 1956, ii, 1518. 6. Sinclair-Smith, C., Dinsdale, F., Emery, J. L. Archs Dis. Childh. (in the

press).