Incidence of child abuse: depends who you ask.
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Biomedical subjects
Publications and source records attributed to R Sunderland.
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During the decade January 1976 to December 1985, as a result of increased public awareness, the numbers of reported (but not proved) cases of abuse to children living in South Birmingham increased thirty-fold; the incidence of detected and proved cases of abuse increased fourfold. The increase was principally due to bruises, scalds, and neglect. The numbers of serious fractures and brain injuries did not increase. The first case of sexual abuse was reported in 1981 and this was followed by a subsequent rise in the detection rate. The combination of increased reporting, increased incidence of proved abuse, and the necessity for increased supervision of families and intervention has created a serious burden on the child health services that may necessitate a reduction in services to other children. Alternative ways of tackling the problems of child abuse may have to be introduced, but they may have unwelcome consequences.
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Accurate dating of initial mineralization in the dentition was derived from fetuses aged according to the maternal history, assessment of gestational age by obstetricians, paediatricians and pathologists, histological evaluation of their cerebellar and renal development, and accurate measurements of crown-rump length, skull circumference, brain and body weight. Serial sections of the jaws of 121 fetuses ranging from 10 to 26 weeks post-menstrual age first showed mineralized dentine in the deciduous central incisor at 15-19 weeks, in the lateral incisor at 16-21 weeks, in the canine at 19-22 weeks, in the deciduous first molar at 16-19 weeks and in the second molar at 20-22 weeks. These age ranges differ from those for initial mineralization common in textbooks, particularly for the molars.
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Postperinatal mortality rates have shown two phases of decline since 1947 which are traditionally ascribed to social and medical improvements. These factors cannot, however, explain the arrest of decline during the 1960s. There appears to be a biological effect on child mortality rates, manifesting as a generation effect. This is due partly to continuing changes in the structure of the child population, itself a consequence of social and biological changes among the parent generation when they were children. In this study national and selected urban postperinatal deaths have been divided into two categories: "probably inevitable" and "possibly preventable". The continuing prevalence of "possibly preventable" deaths gives cause for concern. If the number of these deaths is to be further reduced, reconsideration and redeployment of community child health staff may be necessary.
Agonal histories were traced for 1182 of 1782 postneonatal deaths in Sheffield between 1947 and 1979. Twenty eight per cent of these deaths were histologically inexplicable, 19% were from infections and 15% from malformations. These sudden infection and malformation deaths were explicable, yet by some definitions they would be considered as cot deaths. Varying definitions may lead to confusion, hindering the search for aetiological mechanisms.
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Factor VIII related activities and factor VIII related antigen multimeric analysis have been assessed in two sporadic and eleven epidemic cases of haemolytic uraemic syndrome. In all patients factor VIII related antigen was raised and had an abnormal multimer pattern at presentation. The return to normal of factor VIII related antigen values and multimeric analysis patterns paralleled clinical improvement and, therefore, may be useful in monitoring patients with haemolytic uraemic syndrome. We postulate that endothelial cell damage releases the abnormal high molecular weight factor VIII related antigen multimers and that this may cause platelet agglutination in vivo.
There were 469 unnatural deaths among the Sheffield child population between 1947 and 1979, 226 of which were caused by traffic accidents. The annual incidence of these fatal traffic accidents has risen steadily since the early 1960s with boys being consistently more vulnerable. Fatal accidents were disproportionately higher among socially deprived families and in poorer areas of the city. The environment rather than the child may be 'accident prone' and there is an urgent need for safer play areas in deprived areas.
Examination of small intestinal mucosa from cases of post-perinatal death in Sheffield between September 1980 and September 1981 showed mucosal changes before death in 18 of 78 cases (20%). There was no significant difference in prevalence between explained and unexplained deaths, nor was there any positive association with viral isolation from the small intestine. The lesion was much more common in males than females and showed a strong association with bottle feeding--no infant wholly breast fed showed an enteropathy. There was a low incidence of symptoms referrable to the gastrointestinal tract among affected infants, and no appreciable evidence of failure to thrive, as reflected by the postmortem body weight, was present. Mucosal changes of the small intestine in cases of sudden infant death syndrome have previously been reported and attributed to heatstroke. Although the finding of similar lesions in infants who died explicably does not appear to support this view, overheating is difficult to exclude as most of the explained deaths with a mucosal lesion occurred at home.
A steady and significant decline in the proportions of liveborn infants who died in the first week from problems associated with immaturity occurred among Sheffield babies born between 1947 and 1979. The decline occurred in all three maternity units, regardless of the availability of neonatal care facilities. The rate of decline in the best equipped and best staffed hospital, however, was significantly greater during the 1970s than would have been predicted from the trend in earlier years and in contrast to the other hospitals. This greater decline shows a closer temporal association with a reorganisation of labour wards and nurseries than with the introduction of advanced equipment but also correlates with an increasing abortion rate among women who would be expected to have premature deliveries. Factors responsible for the secular decline have not been identified, but it is postulated that Sheffield's mothers are bearing healthier children as a result of improvements in maternal health which are themselves a consequence of changes during girlhood.
In the years 1973-79, 39452 infants born to parents resident in Sheffield were scored at birth for risk of unexpected infant death. Before 1973 post-perinatal mortality in Sheffield was on average 11.5% above the rate for England and Wales. Since 1973 it has only once exceeded the rate for England and Wales. "Possibly preventable" deaths have fallen from 5.2 to 1.9 per 1000. 12% of this decline is associated with a rise in the average age of the mother and a fall in the number of pregnancies, 9% with a reduction in precipitate deliveries, 24% with an increase in breastfeeding, 18% with extra care given by health visitors to high-risk infants, and 36% with other factors. The reduction in mortality attributed directly to the effect of increased visiting of high-risk infants is numerically similar to the number of lives saved by treating cancers of children. This suggests that home visiting by health visitors is highly cost-effective.
An accumulation of granular cells associated with the enamel organ of a developing deciduous, incisor tooth was noted during light microscopy (LM) of serial sections from the right half of a mandible from a stillborn, female infant of 37 weeks gestations. There was a break in continuity of the enamel matrix associated with the focus of granular cells, which appeared to be continuous with, and arise directly from, the cells of the stratum intermedium. The granular cells were very similar histologically to those of a congenital epulis but it is impossible to say whether the lesion would have developed sufficiently to present clinically as an epulis. Less probably, the granular cells might eventually have been associated with the subsequent development of a granular cell ameloblastoma or ameloblastic fibroma. If the lesion does represent an early stage in the formation of a congenital epulis, it would support the odontogenic theory of origin of the granular cells.
Necropsy reports were traced for 3928 of the 7049 Sheffield children who died between 1947 and 1979. Comparison of these reports with the related death certificates showed important differences in the underlying cause of death in 15%, even after allowing for variation in diagnostic terms and incorrect completion of certificates. Approximately one third of certificates had the underlying cause of death entered first instead of last in Part I, and in 251 (6%), the underlying cause of death was found in Part II of the certificate. There was an overrepresentation of infectious diseases and underrepresentation of malformations, deaths associated with perinatal factors, and cot deaths in the death certificates. Discrepancies were more frequent among very young children and among hospital deaths than home deaths. There was little variation in discrepancy frequency when analysed by parental occupation. A gradual decrease in the proportion of discrepancies occurred during the period studied, but this may be a consequence of a changing pattern of referral for necropsy rather than increasingly valid certification. The historical diagnoses 'convulsions due to an unknown but natural cause' and 'teething convulsions' may be analogous to the current diagnosis 'sudden infant death syndrome'.
To test whether the seasons of birth had an effect on subsequent experience of illness, details were obtained of all Sheffield children born between 1973 and 1977 who were admitted to hospital before their second birthday with a first febrile convulsion. Analysis by date of birth in consecutive 28-day cohorts showed that the incidence of febrile convulsions ranged from 2.5 per thousand live births to 30.2 per thousand in different "month" cohorts. Statistically significant variations were noted in the incidence rates in relation to season and year of birth. The implication is that even large scale epidemiological studies which have been confined to children born in a particular week or month may not be representative of the whole child population.
Examination of the records of hospital admissions and all deaths among the 40,544 Sheffield children who were aged less than two years in the period 1975-79 revealed 475 children admitted with their first febrile convulsion and 50 children who presented as cot deaths. Rectal temperatures taken before refrigeration were traced for 24 of the latter. 10 of these 24 children had temperatures in excess of 38 degrees C and 5 were greater than 40 degrees C. There was a transition in age at presentation between the two groups, with most cot deaths occurring before six months of age and febrile convulsions after that age. No time-based clustering between the date of presentation with cot death or febrile convulsion was found to suggest a single aetiological agent. It is suggested that febrile convulsions and some inexplicable sudden infant deaths may be equivalent responses to a febrile stimulus, but with a different outcome because of the difference in age of occurrence. A common mechanism could be thermolabile syncope which, in the susceptible younger infant, leads to irreversible cerebral ischaemia. The rectal temperature should be taken as soon as possible in all cot deaths. An aberration of a vagally mediated reflex may be responsible for some cot deaths.