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infants and those reported by RAWLINGS et al.2 and CALAME and PROD’HOM.5 Congenital malformations are an important cause of later handicaps and will therefore influence the prognosis of low-birth-weight infants-particularly since their frequency in these infants is thought to be increased.8 STEWARThas found that, although 16% of the infants of the sample reported by RAWLINGS et al. had birth defects (congenital malformations and genetically determined metabolic errors), only 2% of this sample had handicaps which were the consequence of the defect itself. DRILLIEN,3 however, has reported an association between major or multiple minor malformations and an increased incidence of later mental or neurological handicaps. In her view this observation indicates that the malformation and the handicaps share a common aetiology in early pregnancy, and she implies that the presence of handicaps is therefore unlikely to be influenced by perinatal care. She also notes that in the Edinburgh sample fewer of the light-for-dates infants were normal when examined at age 1-3 years than were infants of appropriate weight for their shortened period of gestation. BRANDT and SCHRODER 10 have reported similar observations. Nevertheless, DRILLIEN emphasises that the later status of both of these groups of infants may be further affected by inappropriate perinatal care. Significantly, the group who emphasise the importance of prevention and vigorous treatment of perinatal complications have found no difference in the incidence of abnormality between the light-fordates infants and those who were of appropriate weight." It will not be possible fully to assess the extent to which modern methods of perinatal care prevent brain damage among very-low-birth-weight infants until the survivors are old enough for minor degrees of cerebral dysfunction to be excluded; but all reports agree that the prognosis for serious handicap has improved. The only disagreement is on the extent of the improvement.
Edinburgh
Intensive Care and Low Birth-weight THE chance of survival for infants of low birthweight has improved considerably during the past decade. Workers in centres where this has occurred have attributed the improvement, in part at least, to the introduction of modem methods of perinatal care. 1-3 Because of the previously reported high incidence of serious physical and mental handicap among low-birth-weight survivors, the ethics of this type of care have been seriously questioned.4 Lately, two independent groups of workers, RAWLINGS et al.2 and CALAME and PROD’HOM,5 have suggested that such doubts are unjustified. They argue that methods of care designed to improve survival, by anticipating, preventing, or treating potentially lethal perinatal complications, can also be expected to improve the incidence of abnormality among the survivors. In support of this argument, both groups have reported a greater chance of immediate survival for very-lowbirth-weight infants (less than 1500 g.) and a much lower incidence of abnormality among the survivorsthan had been previously found by earlier workers.s The reports of RAWLINGS et al. and of CALAME and PROD’HOM, however, concerned young children, in whom only the more serious forms of mental and physical impairment can be diagnosed with certainty. The manifestations of lesser degrees of cerebral dysfunction such as specific learning difficulties and7 poor school performance, which FITZHARDINGE et al.’ have reported among a group of light-for-dates term infants, will not be apparent. DRILLIEN3 has now reported a reduction in the incidence of moderate or severe handicap among a new sample of Edinburgh low-birth-weight infants when compared with her original sample born in the early 1950s.6s Although the improvement in prognosis in this new Edinburgh sample is not as striking as that described by RAWLINGS et al. and CALAME and PROD’HOM,5 DRILLIEN also believes that advances in perinatal care are largely responsible. She does, however, point out that other factors, such as those causing retarded intrauterine growth or shortened period of gestation, may also influence prognosis. Thus population variations may account for some of the difference in outcome between the 1. 2. 3. 4. 5. 6. 7.
Stahlman, M. Proceedings of 59th Ross Conference on Pædiatric Research, 1969; p. 17. Rawlings, G., Reynolds, E. O. R., Stewart, A., Strang, L. B. Lancet, 1971, i, 516. Drillien, C. M. Devl Med. Chld Neurol. 1972, 14, 563. Holt, K. S. Matern. Chld Care, 1970, 6, 211. Calâme, A., Prod’hom, L. S. Schweiz. med. Wschr. 1972, 102, 65. Drillien, C. M. Hosp. Med. 1967, 1, 937. Fitzhardinge, P. M., Steven, E. M. Pediatrics, Springfield, 1972, 50, 50.
Atropine after Myocardial Infarction nodal bradycardia is a common accomof paniment acute myocardial infarction-particularly after an inferior lesion, within what is judged to be the first hour of the acute episode.12-14 It recurs as a result of vagal activity and can be corrected with intravenous atropine, which is equally effective when SINUS
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8. Yerushalmy, J., van den Berg, B. J., Erhardt, C. L., Jacobziner, H. Am. J. Dis. Child. 1965, 109, 43. 9. Stewart, A. Devl Med. Chld Neurol. 1972, 14, 585. 10. Brandt, I., Schröder, R. Mschr. Kinderheilk. 1971, 119, 275. 11. Stewart, A. Proceedings of 3rd European Congress in Perinatal 12. 13. 14.
Medicine, 1972; p. 174. Adgey, A. A. J., Geddes, J. S., Mulholland, H. C., Keegan, D. A. S., Pantridge, J. F. Lancet, 1968, ii, 1097. Stock, E. Aust. N.Z. Jl Med. 1971, 1, 315P. Webb, S. W., Adgey, A. A. J., Pantridge, J. F. Br. med. J. 1972, iii, 89.