Child health

Childhood injuries Preventing children drowning in Australia We need to take a scientific approach to drowning prevention W Robert Pitt and Danny T Cass MJA 2001; 175: 603-604

Danny T Cass

Childhood injuries Drowning and near-drowning in Northern Territory children Karen M Edmond, John R Attia, Catherine A D'Este and John T Condon MJA 2001; 175: 605-608 For editorial comment, see Pitt and Cass Abstract - Methods - Results - Discussion - Acknowledgements - Competing interests - References - Authors' details - - More articles on Paediatrics Abstract Objective: To compare incidences of drowing for children in the Northern Territory (NT) with those in Queensland and the rest of Australia. Design: Descriptive, retrospective, population-based analysis of death and hospitalisation data for drowning and near-drowning. Setting and participants: Children aged 0-14 years resident in Australia from 1983 to 1998. Main outcome measures: Age-standardised average annual incidence of drowning (1983-1998) and near-drowning (1994-1997) in children aged 0-4 and 5-14 years in the NT, Queensland and the rest of Australia. Results: The average annual incidence of drowning and near-drowning from 1994 to 1997 for children aged 0-4 years in the NT (67.82 per 100 000) was significantly higher than for Australia (24.45 per 100 000) (incident rate ratio [IRR], 2.77; 95% CI, 1.40-4.91) and for Queensland (32.55 per 100 000) (IRR, 2.13; 95% CI, 1.05-3.94). The proportion of children aged 0-4 years drowning or near-drowning in swimming pools from 1994 to 1997 was also significantly higher in the NT (83%) than Australia (64%) (difference, 0.19; 95% CI, 0.086-0.30) and Queensland (65%) (difference, 0.18; 95% CI, 0.069-0.29). From 1983 to 1998, the incidence of drowning in NT children aged 0-4 years increased by 0.4% per year (IRR, 1.004; 95% CI, 0.994-1.070), compared with a 5.0% reduction per year (IRR, 0.950; 95% CI, 0.937-0.963) in Australian children. Conclusions: The incidences of drowning and near-drowning in the NT are higher than in the rest of Australia and show no significant decrease. The NT should improve its measures for prevention of childhood drowning. In Australia, childhood drownings are second only to road trauma as a cause of injury death in children younger than 15 years.1,2 Encouragingly, the overall incidence of childhood drowning in Australia appears to be decreasing.1,3 However, drowning death rates are higher in the Northern Territory (NT) than the rest of Australia.1,4-6 There is also some evidence that rates of drowning in the NT are not decreasing as fast as those in the rest of Australia.4,5 However, there are no published studies that compare rates of near-drowning in the NT with rates in the rest of Australia. There are also no published analyses of NT drowning trends. Risk groups for drowning include children aged 0-4 years,1,3 children living in cities with high swimming pool to population ratios,7-10 children living in hot climates,3,8 children living in areas with lack of isolation pool fencing,11-14 and Indigenous children.4,5,7 However, there are no published NT data concerning these risk groups. The proportion of NT children drowning in swimming pools is also currently unknown. This study was designed to determine how incidences of childhood drowning and near-drowning in the NT compare with rates in the rest of Australia and in Queensland (another State with a similar climate and similar numbers of domestic swimming pools per capita as the NT). We aimed to stratify our analysis according to specific risk groups (children aged 0-4 years, children aged 5-14 years, children drowning in swimming pools, and Indigenous children). We also planned to compare the proportion of NT children aged 0-4 years who drowned or nearly drowned in swimming pools with Queensland and the rest of Australia. The study was designed as a descriptive, retrospective, population-based analysis of hospital morbidity and mortality data for drowning and near-drowning, identified by International classification of diseases, 9th revision, clinical modification (ICD-9-CM) codes15 in children aged 0-14 years. Methods Definitions A drowning incident was defined as a non-intentional episode in which immersion of a child in water was followed by death. A near-drowning incident was defined as a non-intentional episode in which immersion of a child in water was followed by admission into hospital and the child subsequently surviving. A case was only included as a drowning or near-drowning if it was identified by specific ICD-9-CM external (E) cause codes (830, 832, 919.0-910.9) or the ICD-9-CM disease code for near-drowning (994.1).15 E-codes classify environmental sites, events, circumstances, and conditions as the cause of injury, and include a code for swimming pool drowning.15 Data collection Mortality and hospital morbidity data for all cases of drowning and near-drowning were obtained from the Australian Institute of Health and Welfare (AIHW). Mortality data were available for 1983-1998, but hospital morbidity near-drowning data were available for 1994-1997 only, because of the introduction of casemix funding and changes in ICD-9-CM coding.16 Population denominators for the NT, Queensland and the rest of Australia were the estimated resident population data for each year published by the Australian Bureau of Statistics (ABS).17 NT Indigenous population data were the estimates of the NT Indigenous population published by the ABS.18 Data analysis Crude incidences of drowning and near-drowning for the NT, Queensland and the rest of Australia were standardised year by year within 0-4 and 5-14 years age groups using the indirect standardisation method and the Australian population as the reference population.19The annual number of cases was assumed to follow a Poisson distribution.20 Changes in annual drowning death rates from 1983 to 1998 were investigated using the Mantel test for trend and a Poisson regression model which included terms for year. NT average annual incidences of age-standardised drowning and near-drowning were compared with Queensland and the rest of Australia using incident rate ratios (IRR) and 95% confidence intervals. An IRR was defined as the ratio of two incidences. The difference between proportions of children drowning or nearly drowning in swimming pools in the NT, Queensland and the rest of Australia was compared using tests of difference between two proportions and 95% confidence intervals. Stata software was used for statistical analysis.21 Ethical approval This study was approved by the Joint Institutional Ethics Committee of the Royal Darwin Hospital and the Menzies School of Health Research. Results Drowning Forty-two NT children drowned from 1983 to 1998. There was no significant change in the incidence of drowning over this period in NT children aged 0-4 or 5-14 years (Boxes 1 and 2). In contrast, rates of drowning in Australian children reduced significantly each year in children aged 0-4 years (Boxes 1A and 2). Rates in Australian children aged 5-14 years also reduced each year, but the Poisson regression rate ratio for trend per year did not reach statistical significance (Boxes 1B and 2). The average annual incidence of drowning in NT, Australian and Queensland children from 1994 to 1997 is shown in Box 3. Near-drowning The NT incidence of near-drowning for children aged 0-4 years was higher than the Queensland rate, but not statistically significant, while the rate for children aged 5-14 years was similar to the Queensland rate (Box 3). Swimming pool drowning and near-drowning The proportion of children aged 0-4 years drowning or near-drowning in swimming pools from 1994 to 1997 in the NT (83%) was higher than in Queensland (65%) (difference, 0.18; 95% CI, 0.069-0.29) and the rest of Australia (64%) (difference, 0.19; 95% CI, 0.086-0.30) (see Box 3 for incidence). Indigenous status In the NT, non-Indigenous children aged 0-4 years had higher rates of drowning and near-drowning (73.19 per 100 000) than Indigenous children (56.63 per 100 000) (IRR, 1.29; 95% CI, 0.53-4.47), although this was not significant. Non-Indigenous children aged 5-14 years also had higher rates of drowning and near-drowning (7.27 per 100 000) than Indigenous children (5.41 per 100 000; IRR, 1.34; 95% CI, 0.81-5.42). Rates of swimming pool drowning in the NT were also higher in non-Indigenous children aged 0-4 years (24.89 per 100 000) than Indigenous children (14.04 per 100 000) but this difference was not significant (IRR, 1.77; 95% CI, 0.91-6.22). Only five of 40 children (13%) aged 0-4 years who drowned in a swimming pool in the NT from 1983 to 1998 were Indigenous. Discussion This study describes the extremely high incidence of drowning and near-drowning in children in the NT. Incidences were higher than in the rest of Australia and showed no significant decrease despite reductions in the rest of Australia. Rates in the NT are among the highest recorded worldwide.3-5Indigenous children in the NT had lower rates of drowning and near-drowning than non-Indigenous children, as well as lower rates of swimming pool drowning, although the differences were not statistically significant. Case numbers of fresh water drownings were too small to allow statistical analysis. Some studies describe rates of drowning and near-drowning in Native American children to be two to three times those of non-Native American children.7,10 However, Australian studies report rates of Indigenous child drowning mortality similar to those reported here.4,5 Reporting of Indigenous status in the NT is accurate, in contrast to other Australian States and Territories.1 Near-drowning urban and rural hospital referral patterns are similar and are unlikely to have contributed to the difference in Indigenous and non-Indigenous rates. Reduced exposure of Indigenous children to domestic swimming pools is a possible explanation. Further prospective research is required to clarify these issues. There are many reports of the high rates of drowning in children aged 0-4 years.1,2,9,11 In our study, children aged 0-4 years in the NT, Queensland and the rest of Australia had rates of drowning and near-drowning 5-10 times higher than children aged 5-14 years. Young children in the NT appeared to be at greatest risk, with rates of drowning and near-drowning nearly three times higher than the rest of Australia and Queensland. Rates of swimming pool drowning in children aged 0-4 years in the NT were more than twice the Australian and Queensland rates and among the highest in the world.2,8,9,11 The proportion of children drowning in swimming pools in the NT was also statistically higher than in Queensland and the rest of Australia. Drowning rescue and resuscitation protocols in the NT are similar to those in the rest of Australia. One possible explanation for the differences between NT and Queensland rates of swimming pool drowning is that Queensland introduced statewide pool fencing legislation in 1992, while pool fencing laws in the NT are still inadequate. All the NT swimming pool drowning deaths reported in this study occurred in pools with non-Australian Standards fencing (NT coroner, personal communication). There is no standard legislation for pool fencing in the NT. Only one jurisdiction (encompassing less than 10% of the population) requires fencing according to Australian Standards. Other reasons for the disparity between NT and Queensland rates of drowning could be differences in exposure to water, differences in exposure to swimming pools, or differences in parental supervision. Further prospective research is needed to investigate the role of these different risk factors. We may have underestimated rates of drowning and near-drowning, as retrospective data were used and case ascertainment relied on coded cause of death/hospitalisation. We may also have under-reported NT rates of near-drowning, as the ratio of near-drowning to drowning in the NT (2:1) was lower than Australia (9:1) and Queensland (9:1). Smaller numbers of NT drowning and near-drowning cases also produced considerable variation in annual NT data. However, statistical analyses, including Poisson regression, enabled analysis of trend over time. In response to this study and other reports, NT injury prevention groups are planning to expand their drowning prevention campaigns. This will include lobbying the NT government to enact isolation/four-sided pool-fencing legislation. More public awareness campaigns are also planned. These will be directed towards the need for effective pool fencing, parental supervision of young children, and cardiopulmonary resuscitation skills, and will include other measures that can assist in preventing drowning in young children. Kidsafe NT also intends to use the information from this study to develop a prospective drowning surveillance system. This system will be used to evaluate drowning prevention interventions and to further investigate NT risk factors for childhood drowning, including the role of swimming pool fencing. Acknowledgements Kidsafe, Child Accident Prevention Foundation of Australia, NT branch, provided the funding for the data extraction by the Australian Institute of Health and Welfare. Competing interests None declared. References Moon L, Rahman N, Bhatia K. Australia's children: their health and well being 1998. Canberra: AIHW, 1998. (AIHW Catalogue No. PHE 7.) Pitt WR. Increasing incidence of childhood immersion injury in Brisbane. Med J Aust 1986; 144: 683-685. Cass DT, Ross F, Lam LT. Childhood drowning in New South Wales 1990-1995: a population based study. Med J Aust 1996; 165: 610-612. Vimpani G, Doudle M, Harris R. Child accident mortality in the Northern Territory. Med J Aust 1988; 148: 392-395. Silva DT, Ruben AR, Wronski I, et al. Excessive rates of childhood mortality in the Northern Territory. J Paediatr Child Health 1998; 34: 63-68. d'Espaignet ET, Kennedy K, Paterson BA, et al. From infancy to young adulthood: health status in the Northern Territory, 1998. Darwin: Territory Health Services, 1998. Spyker DA. Submersion injury epidemiology, prevention and management. Pediatr Clin North Am 1985; 32: 113-125. Pitt WR, Balanda KP. Childhood drowning and near-drowning in Brisbane: the contribution of domestic swimming pools. Med J Aust 1991; 154: 661-665. Geddis DC. The exposure of pre school children to water hazards and the incidence of potential drowning accidents. N Z Med J 1984; 97: 223-226. O'Carrol PW, Alkon E, Weiss B. Drowning mortality in Los Angeles County 1976-1984. JAMA 1988; 260: 380-383. Fergusson DM, Horwood LJ. Risks of drowning in fenced and unfenced domestic swimming pools. N Z Med J 1984; 97: 777-779. Carey V, Chapman S, Gaffney D. Children's lives or garden aesthetics? A case study in public health advocacy. Aust J Pub Health 1994; 18: 25-32. Millner N, Pearn J. Will fenced pools save lives? A 10 year study from Mulgrave Shire, Queensland. Med J Aust 1980; ii: 510-511. Intergov-WA, Intergovernmental Working Party on Swimming Pool Safety. Preschool drowning in private swimming pools. Perth: Health Department of Western Australia, 1988. US Department of Health and Human Services. The international classification of diseases. 9th revision. Clinical modification (ICD-9-CM). 3rd ed. Bethesda, Md: DHHS, 1989. Langlois JA, Buechner JS, O'Connor EA, et al. Improving the E coding of hospitalizations for injury: do hospital records contain adequate documentation? Am J Public Health 1995; 85: 1261-1265. Australian Bureau of Statistics. Population by age and sex, Australian States and Territories. Canberra: ABS, 1997. (Catalogue no 3201.0.) Australian Bureau of Statistics. Experimental estimates of Aboriginal and Torres Strait Islander population 1991 and 1996. Canberra: ABS, 1997. (Catalogue no 3230.0.) Pagano M, Gauvreau K. Principles of biostatistics. 1st ed. California: Wadsworth, 1993. Frome EL, Checkoway H. Epidemiologic programs for computers and calculators. Use of Poisson regression models in estimating incidence rates and ratios. Am J Epidemiol 1985; 121: 309-323. Stata Statistical Software [computer program]. Version 5.0. Texas: Stata Corporation, 1997. (Received 23 Feb, accepted 30 Jul, 2001) Authors' details Territory Health Services, Casuarina, NT. Karen M Edmond, FRACP, MMedSc (ClinEpid), Community Paediatrician. Centre for Epidemiology and Biostatistics, University of Newcastle, Newcastle, NSW. John R Attia, FRCPC, PhD, Senior Lecturer; Catherine A D'Este, PhD, Senior Lecturer. Menzies School of Health Research, Casuarina, NT. John T Condon, FAFPHM, MPH, Research Scholar. Reprints will not be available from the authors. Correspondence: Dr K M Edmond, Research Fellow in Paediatric Epidemiology, London School of Hygiene and Tropical Medicine, 50 Bedford Square, London, WC1B 3DP, UK. karen.edmondATlshtm.ac.uk. Make a comment 1: Age-standardised annual incidence of drowning for the Northern Territory and the rest of Australia, 1983 to 1998 Back to text 2: Drowning trend analysis for children in the Northern Territory and the rest of Australia, 1983-1998 Poisson regression Mantel test for trend rate ratio for trend per year (95% CI) χ2 (degrees per year of freedom) P for trend per year NT children 0-4 years 5-14 years 1.004 (0.994-1.070) 0.981 (0.883-1.078) 0.02 (1) 0.15 (1) 0.895 0.696 Australian children 0-4 years 5-14 years 0.950 (0.937-0.963) 0.911 (0.889-1.067) 53.73 (1) 66.08 (1) Back to text 3: Average annual incidence of drowning and near-drowning for the rest of Australia and Queensland compared with the Northern Territory, 1994-1997 Northern Territory Australia Queensland Number Incidence* Incidence* IRR† (95% CI‡) Incidence* IRR (95% CI) Drowning 0-4 years 16 22.61 3.71 6.17 (1.60-16.68) 5.77 3.92 (0.94-12.48) 5-14 years 1 3.21 0.62 5.26 (0.12-33.48) 0.82 3.91 (0.08-39.28) Near-drowning 0-4 years 32 45.21 20.69 2.19 (1.18-4.37) 26.78 1.69 (0.70-3.52) 5-14 years 7 5.56 2.55 2.20 (1.26-8.30) 5.36 1.03 (0.12-4.14) Drowning and near-drowning 0-4 years 48 67.82 24.45 2.77 (1.40-4.91) 32.55 2.13 (1.05-3.94) 5-14 years 8 6.44 3.61 1.78 (1.21-6.58) 6.12 1.04 (0.12-4.08) Swimming pool drowning and near-drowning 0-4 years 40 56.51 15.65 3.61 (1.70-6.77) 20.69 2.74 (1.24-5.47) 5-14 years 1 3.20 1.03 3.08 (1.75-18.7) 2.63 1.22 (1.29-8.23) * Incidence per 100 000 children. † Incident rate ratio. 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Karen M Edmond · John R Attia · Catherine A D'Este · John T Condon

Childhood injuries Horse-related injuries in children Andrew J A Holland, Gerard T Roy, Valapha Goh, Frank I Ross, John P Keneally and Daniel T Cass MJA 2001; 175: 609-612 Abstract - Methods - Results - Discussion - Acknowledgements - Competing interests - References - Authors' details - - More articles on Paediatrics Abstract Objectives: To identify the frequency, spectrum and outcome of horse-related injuries in children. Design and setting: Retrospective case series of horse-related injuries in children admitted to the Children's Hospital at Westmead (CHW) from January 1988 to December 1999, the John Hunter Children's Hospital (JHCH) from January 1991 to December 1997 and deaths reported to the New South Wales Paediatric Trauma Death (NPTD) Registry from January 1988 to December 1999. Main outcome measures: Circumstances of injury; helmet use; adult supervision; type and number of injuries identified. Results: 232 children were admitted with horse-related trauma, 97 to the CHW over 12 years and 135 to JHCH over seven years, with one death at each hospital. There were six deaths reported to the NPTD Registry over 12 years. The median age was 11 years (range, 1-17). Girls accounted for 65% of those injured and 75% of children were injured while riding. Falls caused the injury in 76.3% of cases. Head and upper-limb trauma accounted for 216 of the injuries (73%). Five out of six children with severe head injuries died. In the CHW group, helmet use was documented in only 24 riders (38%) and adult supervision in 22 (22.9%). Conclusions: Horse-related trauma accounts for a considerable number of deaths and injuries in children in NSW. The use of a Standards-approved helmet for riding or horse-related activities might have decreased the severity of head injuries. In 1788, six horses — four mares and two stallions — arrived with the First Fleet at Botany Bay, New South Wales. The first paediatric equestrian death was reported in 1830.1 Both the equine and human populations in Australia have grown enormously since then, but there have been few reviews of horse-related trauma in this country.2-4 This is surprising given Australia's considerable rural population and the popularity of horse riding as a sporting and leisure activity. Trauma is the most common cause of both morbidity and mortality in children, and motor vehicle injuries are the most frequent cause of such trauma. Although horse-related injuries in children are not as common, the potential for serious injury or death in a young child is high. An adult horse may weigh over 500 kg, gallop at speeds of up to 65 km/h and kick with a force 1.8 times its weight.5 The physical differences between horses and children predispose towards severe injury and are compounded by the potential for unpredictable behaviour in both species. We reviewed the records of children admitted with horse-related injuries to two paediatric tertiary referral centres — one in Sydney receiving children predominantly from an urban and outer urban environment (the Children's Hospital at Westmead [CHW]), and the other in a more rural environment in the Hunter Valley (the John Hunter Children's Hospital [JHCH]). These two hospitals receive most NSW children admitted with horse-related injuries (except those from southern NSW, who may be admitted to Sydney Children's Hospital). These data were supplemented with cases reported to the New South Wales Paediatric Trauma Death (NPTD) Registry. We wished to establish the extent and spectrum of horse-related trauma in children to determine the most effective approach to injury prevention. Methods We performed a retrospective review of children aged under 18 years admitted to the CHW and JHCH, or reported to the NPTD Registry, with horse-related injuries. Data were collected on age, location of injury, whether the child was riding or not riding at the time of the injury, the mechanism of injury, the injuries and surgical intervention required, complications and final outcome. For children admitted to CHW and reported to the NPTD Registry, data were also collected on documented adult supervision and helmet use. In children who died, the cause of death was identified from the coronial postmortem report. CHW admissions: Data were collected from January 1988 to December 1999. Patients were identified retrospectively from the Paediatric Trauma Database compiled by the trauma research nurse at Westmead and the Royal Alexandra Hospital for Children hospitals (subsequently the CHW). In addition, a retrospective medical record search was made for children discharged with "animal-related injury external cause" code categories. JHCH admissions: Data were collected from January 1991 to December 1997. Patients were identified through a retrospective medical record search for children discharged with "animal-related injury external cause" code categories and a search of the John Hunter Hospital trauma database. NPTD Registry: This records all deaths resulting from trauma in children under 16 years of age in NSW that are reported to the coroner. Data were available from January 1988 to December 1999. The police statement and coroner's report, together with the postmortem findings, were reviewed for children who had died after horse-related trauma. Results Horse-related injuries and deaths identified The Box summarises our data on the 236 children who sustained injuries between January 1988 and December 1999. Girls accounted for 65% of those injured and 75% of children who were injured while riding a horse. Falls, or a fall followed by a further injury, was the mechanism in 76% of cases. There was no trend over time for a change in the frequency or type of injury at either hospital, or helmet use at CHW. CHW: There were 97 children with horse-related injuries, representing 6% of children admitted with all play and sporting injuries and 35% of animal-related trauma over the 12-year period. Thirty-four patients (35%) were transferred from a peripheral hospital. One child, a non-riding two-year-old boy, died in hospital. Of those children injured while riding, 24 (38%) were wearing a helmet, 21 (33%) were not, and for 18 (29%) there was no documentation. The location of the injury event was identified in 41 cases: a farm in 26, private land in seven, a riding school or competition in five, and a public highway in three. In 22, adult supervision was recorded; there was no adult supervision in 31, and this was not documented in 44. None of the children not riding were wearing a helmet at the time of the injury, even when involved in activities requiring close proximity to the horse. In four cases the children's feet were caught in the stirrup when the horse bolted and they were dragged along the ground. JHCH: There were 135 children admitted with horse-related injuries, accounting for 8% of children admitted with play and sporting injuries and 48% of animal-related trauma over the seven-year period. One child, a 13-year-old girl, died in hospital. NPTD Registry: There were six deaths from horse-related injuries (including the two mentioned above), representing 8% of the 78 play-related and sporting-related deaths recorded over the 12 years. There was only one other animal-related death reported to the registry. Five of these children were injured on a farm and one during a competition. An adult was present in three cases. Only two of the four children injured while riding were wearing helmets; one of these helmets was seen to fall off before the child struck the ground. In summary, there were significantly more children injured while riding (81% v 66%; χ2 = 6.741; P = 0.009), and more children injured through falls from a horse as opposed to being kicked or trampled (75% v 52%; χ2 = 17.3; P = 0.001), in the JHCH group compared with the CHW group. Further, there was no difference between the age of the children who survived and those who died, but boys accounted for 50% of fatalities, compared with 34% of admissions. Spectrum of injuries The Box (b) compares the injuries identified. Head and upper-limb trauma accounted for 124 and 92 of the injuries, respectively, representing a combined total of 73%. Significantly more patients had head trauma (58% v 34%; χ2 = 16.66; P = 0.001) and torso trauma (25% v 10%; χ2 = 8.588; P = 0.003) in the CHW group; limb trauma (31% v 54%; χ2 = 12.20; P = 0.001) was more frequent in the JHCH group. Major head injury was the cause of death in five of the six children who died, none of whom were wearing a helmet when their heads struck the ground. Of those children admitted to CHW who survived a head injury, 17 were wearing a helmet, 25 were not and there was no documentation for 10. Although there was no significant difference between the initial severity of head injury between children in these groups, no patient who was wearing a helmet at the time of injury, compared with five children who were not wearing helmets, had a long-term neurological deficit. Treatment and outcome One hundred and fifty patients required 174 procedures under general anaesthesia (mostly either limb fracture reduction and fixation or debridement and suturing of a laceration) and three patients had four procedures under local anaesthesia. There were significant adverse outcomes in 23 survivors (10%), eight of which involved a neurological deficit. Discussion The risk of injury while horse riding has been estimated as between 1 per 320 to 1 per 1000 hours of riding.4,6 The variation in reported population-based risk of horse-related trauma of between 18.7 injuries per 100 000 to 9.5 injuries per 1000 population per year illustrates the difficulties of accurate data collection and variable inclusion of non-riding injuries.7 Interestingly, the overall risk of injury from horse-related activity has been determined to be greater than that of car racing or riding a motorcycle, and the rate of hospitalisation from falls from a horse equivalent to that from playing rugby.8-10Our data indicate that horse-related trauma is a significant problem for children in Australia, particularly those living in rural environments. This probably reflects greater exposure to horses in rural areas, together with greater numbers of riders and riding hours compared with children living in an urban environment.11-14 The true scale of the problem is likely to be even greater than our data suggest, as children with minor injuries may not require admission to a paediatric hospital, and we may not have identified all patients.4 Girls accounted for 65% of horse-related injuries in children in this study and three-quarters of those injured while riding, but only 50% of fatalities. This overall female preponderance, a contrast to the situation for most traumatic injuries, is likely to represent the greater participation of girls in horse-related activities.4,6,13,15-17 The equal sex ratio for fatal horse-related injuries in this review resulted from the number of male preschool non-riders injured while in close proximity to a horse. Sex differences in exploratory behaviour patterns would explain this finding.18 Although the risk of injury in children involved in horse-related activities is high, of perhaps more importance is the severity of such injuries and their potential long-term consequences.2,13,15,16,19 In addition to the six deaths over 12 years in NSW, 230 children had sufficiently severe injuries to require hospital admission. While a kick from a horse may cause a lower-limb fracture or soft-tissue injury in an adult, in a child it may result in a compound skull fracture, thoracic trauma or perforated hollow viscus.2,12 Our findings indicate that the social and economic cost of horse-related trauma in children is considerable: a death every two years in NSW, over 200 children admitted with an average length of stay of three days, and 10% of survivors having complications.4 These negative outcomes must be balanced with the positive health aspects of a sporting activity that involves interaction with a companion animal. The challenge is therefore to improve the safety of horse riding. Our data suggest that some fatalities and injuries might be avoided, or their severity reduced, through a combination of increased adult supervision of preschool age children and the use of appropriate safety measures such as a Standards-approved helmet.6,18,20,21 Although the use of Standards-approved helmets is encouraged by both the Pony Club Association of NSW and the Equestrian Federation of Australia (EFA), it is not a legal requirement as it is for pedal and motor cyclists. Further, their use in place of a top hat or traditional riding helmet may even be disallowed when competing at the higher levels (national, international, Olympic, etc) of dressage competition (E Canapini, National Coaching Manager, EFA, personal communication). Compliance with helmet use in this study, although not fully documented, appeared to be poor and reflects published findings.2-4 While the number of patients in our study for whom there were complete data was small, children wearing helmets when riding appeared less likely to suffer long-term neurological sequelae compared with those who were not. We therefore propose that consideration be given to making the use of a Standards-approved helmet for horse riding mandatory. Although it would not be practical to enforce helmet use in rural areas, compulsory use in all styles of competition, in riding schools, and on public highways might have a follow-on effect on farms and in children who become occupational riders as adults.22 We see no reason why children and adults engaged in horse-related activities should not receive the benefits of helmet use that have been shown in cyclists, and which they currently enjoy by law.23 Acknowledgements Dr P Subramaniam provided assistance with the collection of data from the John Hunter Children's Hospital. Mr A J A Holland was supported by a Surgeon Scientist Scholarship from the Royal Australasian College of Surgeons. Associate Professor J Peat provided assistance with statistical analysis. Competing interests None declared. References Cone TE Jr. Playing with horses. Pediatrics 1971; 47: 784. Pounder DJ. "The grave yawns for the horseman". Equestrian deaths in South Australia. Med J Aust 1984; 141: 632-635. Williams F, Ashby K. Horse-related injuries. Edition No. 23. Melbourne: Monash University Accident Research Centre, 1995. Cripps, RA. Horse-related injury in Australia. Edition No. 24. Adelaide: Australian Injury Prevention Bulletin, Flinders University, 2000. Kriss TC, Kriss VM. Equine-related neurosurgical trauma: a prospective series of 30 patients. J Trauma 1997; 43: 97-99. Bixby-Hammett DM. Pediatric equestrian injuries. Pediatrics 1992; 89: 1173-1176. Hamilton MG, Tranmer BI. Nervous system injuries in horseback-riding accidents. J Trauma 1993; 34: 227-232. Nicholls JP. Safety of horseriding. BMJ 1990; 301: 496. Chapman MAS, Oni J. Motor racing accidents at Brands Hatch, 1988/9. Br J Sports Med 1991; 25: 121-123. Buckley SM, Chalmers DJ, Langley JD. Injuries due to falls from horses. Aust J Public Health 1993; 17: 269-271. Aronson H, Tough SC. Horse-related fatalities in the Province of Alberta. Am J Forensic Med Pathol 1993; 14: 28-30. Hobbs GD, Yealy DM, Rivas J. Equestrian injuries: a five-year review. J Emerg Med 1994; 12: 143-145. Christey GL, Nelson DE, Rivara FP, et al. Horseback riding injuries among children and young adults. J Family Pract 1994; 39: 148-152. Thompson JM, von Hollen B. Causes of horse-related injuries in a rural western community. Can Family Physician 1996; 42: 1103-1109. Barone GW, Rodgers BM. Pediatric equestrian injuries: a 14-year review. J Trauma 1989; 29: 245-247. Nelson DE, Bixby-Hammett D. Equestrian injuries in children and young adults. Am J Dis Child 1992; 146: 611-614. Campbell-Hewson GL, Robinson SM, Egleston CV. Equestrian injuries in the paediatric age group: a two centre study. Eur J Emerg Med 1999; 6: 37-40. Lam LT, Ross FI, Cass DT. Children at play: the death and injury pattern in New South Wales, Australia, July 1990-June 1994. J Paediatr Child Health 1999; 35: 572-577. Ingemarson H, Grevsten S, Thoren L. Lethal horse-riding injuries. J Trauma 1989; 29: 25-30. Finch C. Sports injury prevention. In: Ozanne-Smith J, Williams F, editors. Injury research and prevention: a text. Melbourne: Monash University Accident Research Centre, 1995. Rivara FP. Fatal and non-fatal farm injuries to children and adolescents in the United States, 1990-3. Inj Prev 1997; 3: 190-194. Condie C, Rivara FP, Bergman AB. Strategies of a successful campaign to promote the use of equestrian helmets. Public Health Rep 1993; 108: 121-126. Cameron MH, Vulcan AP, Finch CF, Newstead SV. Mandatory bicycle helmet use following a decade of helmet promotion in Victoria, Australia — an evaluation. Accid Anal Prev 1994; 26: 325-337. (Received 2 Jan, accepted 16 Aug, 2001) Authors' details The Children's Hospital at Westmead, Royal Alexandra Hospital for Children, The University of Sydney, NSW. Andrew J A Holland, FRCS, FRACS, Senior Research Fellow, and Clinical Lecturer, Department of Academic Surgery; Valapha Goh, RN, Trauma Research Nurse; Frank I Ross, BAppSc(Nurs), MPH, Clinical Nurse Consultant; Daniel T Cass, PhD, FRACS, William Dunlop Professor of Paediatric Surgery; John P Keneally, MB BS, FANZCA, Head, and Clinical Senior Lecturer, Department of Anaesthesia. The John Hunter Children's Hospital, Newcastle, NSW. Gerard T Roy, FRCS, FRACS, Paediatric Surgeon. Reprints: Mr Andrew J A Holland, Department of Academic Surgery, The Children's Hospital at Westmead, Royal Alexandra Hospital for Children, Locked Bag 4001, Westmead, NSW 2145. AndrewH3ATchw.edu.au Make a comment Children with horse-related injuries admitted to the Children's Hospital at Westmead (CHW), January 1988 to December 1999, John Hunter Children's Hospital (JHCH), January 1991 to December 1997, and horse-related deaths reported to the New South Wales Paediatric Trauma Death (NPTD) Registry, January 1988 to December 1999 (a) Demographic characteristics and manner of injury CHW survivors (n = 96) JHCH survivors (n = 6) NPTD Registry deceased (n = 134) Age (years) Median 10 11 11.5 Range 1-15 1-17 2-14 Sex Boys 33 (34%) 46 (34%) 3 (50%) Girls 63 (66%) 88 (66%) 3 (50%) Activity Riding 63 (66%) 109 (81%) 4 (67%) Not riding 33 (34%) 25 (19%) 2 (33%) Mechanism Fall 50 (52%) 101 (75%) 2 (33%) Fall plus further injury 13 (14%) 11 (8%) 3 (50%) Kick 28 (29%) 19 (14%) 1 (17%) Bite 0 2 (2%) 0 Trampled 5 (5%) 1 (1%) 0 (b) Details of injuries and number of children affected CHW survivors (n = 96) JHCH survivors (n = 134) NPTD Registry deceased (n = 6) Head injuries Concussion 19 17 0 Skull fracture 18 10 3 Intracranial haemorrhage 8 3 4 Cerebral contusion 7 1 2 Facial fracture 10 4 0 Soft tissue injury 6 10 3 Totals 68 in 56 patients 45 in 42 patients 11 in 5 patients Spinal injuries Cervical spine 1 3 1 Lumbar spine 0 1 0 Totals 1 in 1 patient 4 in 4 patients 1 in 1 patient Torso injuries Liver or spleen 11 1 1 Kidney 5 2 0 Soft tissue 5 3 1 Pulmonary contusion 3 2 0 Haemothorax/pneumothorax 2 5 0 Rib fracture 2 2 0 Pelvic fracture 2 2 0 Myocardial infarction 0 0 1 Hollow viscus perforation 1 0 0 Bladder haematoma 0 1 0 Totals 31 in 24 patients 18 in 14 patients 3 in 3 patients Limb injuries Upper limb fracture 26 58 1 Lower limb fracture 4 14 1 Upper limb soft tissue 2 4 1 Lower limb soft tissue 2 1 0 Totals 34 in 30 patients 77 in 73 patients 3 in 2 patients Back to text

Gerard T Roy · Valapha Goh · Frank I Ross · John P Keneally · Daniel T Cass

The research enterprise The Menzies Centre for Population Health Research A unique and supportive local population was a vital ingredient in the Centre's success Terence Dwyer MJA 2001; 175: 617-620 Early days: the Tasmanian Infant Health Survey and Sudden Infant Death Syndrome - The post-SIDS era: taking stock - New directions - Genomics - The future - References - Authors' details - - More articles on Psychiatry I ACCEPTED THE CHAIR IN COMMUNITY HEALTH at the University of Tasmania in 1985 with the intention of setting up a research centre that focused on epidemiological research into preventable causes of disease. While I did not know how the centre would be funded, I was certain that Tasmania would be a very competitive site for such research. Already, valuable epidemiological studies on iodine deficiency, hydatid disease and asthma had been conducted in the absence of significant research infrastructure.1 The "Island State" provided a perfect source population for unbiased selection of cases and comparison samples or controls. Further, the land area and population size (around 500 000 people) made follow-up of cohorts relatively easy. Thus, Tasmania had important advantages for the two major strategies used to search for environmental and lifestyle causes of disease — case-control and cohort studies. Funding from the Menzies Foundation came about through the input of three people — Basil Hetzel, then Chief of the Commonwealth Scientific and Industrial Research Organisation Division of Human Nutrition in Adelaide, who had a close association with the Menzies Foundation; Professor Ian Lewis, Dean of the Medical School at the University of Tasmania and a member of the Menzies Foundation Board; and Eric Wigglesworth, the Director of the Foundation. To determine the likely success of such a centre, the Foundation Board held a three-day workshop attended by representatives of State and Federal health departments and the World Health Organization, notable Australians in the field of public health, and distinguished British epidemiologist Sir Richard Doll. History of the Menzies Centre 1987 Workshop ("Towards a Centre for Population Health Research") in Hobart, Tasmania. 1988 Official opening in January. Collection of Tasmanian Infant Health Survey (TIHS) data began (prospective study on Sudden Infant Death Syndrome [SIDS]). 1990 Designated as a World Health Organisation Collaborating Centre for the Prevention of Cardiovascular Diseases. 1991 Provides prospective evidence confirming importance of prone sleeping position as a cause of SIDS (Lancet 1991; 337: 1244-1247). 1992 Evidence that SIDS death rate was falling after a national campaign on infant sleeping position. 1993 Research helps explain how prone position interacts with other factors to increase risk (N Engl J Med 1993; 329: 377-382). 1995 First follow-up of TIHS cohort searching for early life influences on childhood diseases. Shows that the major decline in SIDS deaths from 1991 onwards is the result of changes in infant sleeping position (JAMA 1995; 273: 783-789) 1997 Contract signed with AMRAD pharmaceutical company. Provides funding for Genetic Epidemiology Unit. 1997-2000 Follow-up of the Tasmanian Infant Health Survey cohort into childhood provides important evidence about early life determinants of risk for osteoporosis, blood pressure and asthma (J Clin Endocrinol Metab 1998; 83: 4274-4279; J Bone Miner Res 1999; 14: 146-151; BMJ 1999; 319: 1325-1329; Thorax 1999; 54: 664-669). 2000 Named "Tasmanian Icon" by State Premier. Core funding doubles. Key events Major scientific achievements. Subsequently, the Menzies Foundation Board decided to support the establishment of an epidemiology research centre, to be named the Menzies Centre for Population Health Research. The Foundation then met with the Tasmanian Premier and Minister for Health, who matched the Foundation's initial contribution of $100 000 per year. Early days: the Tasmanian Infant Health Survey and Sudden Infant Death Syndrome Before my departure from Sydney University, I had been reviewing the data on disease distribution in Tasmania. Sudden Infant Death Syndrome (SIDS), with an annual rate in Tasmania twice the national average, stood out. The head of neonatology at the Royal Hobart Hospital, Neville Newman, convinced me that this should be the subject of a major research effort. The cause had not been clearly identified, and epidemiological research had been limited. With helpful input from Geoffrey Berry, Professor of Biostatistics at Sydney University, we planned the first prospective cohort study on this condition. Preliminary work began just before the decision of the Menzies Foundation to support the establishment of the Centre. The epidemiology research group within the Medical School at the University of Tasmania consisted of one epidemiologist, the research fellow Trevor Beard, and limited support staff. Even with the extra $200 000 that the establishment of the new Centre brought, it would not have been realistic to work on a broad front. It was decided that we would focus most of our effort on the new SIDS research program. The next step was to build an appropriately skilled team. We advertised for another epidemiologist and a biostatistician, but it proved very difficult to attract qualified applicants. It seemed that Australian academics were either not interested in living in Tasmania, or were not confident their careers would flourish there. This problem was compensated for by a stroke of good luck when a young Tasmanian medical graduate, Anne-Louise Ponsonby, became our first postgraduate student, working on SIDS. She put an incredible amount of intelligently directed energy into the SIDS program, and together, with financial help from the Australian Rotary Health Research Fund, we were able to develop momentum in the project. In 1988, we initiated the first full data collection for the cohort study — a huge endeavour that involved measurements each year in 1500 infants and their mothers on three occasions in the first three months after birth. That we could get this work under way was pleasing, but we needed to find well-qualified biostatisticians. Given the previous lack of success with advertising in Australia, I decided to use our international network. Sir Richard Doll referred Michael Jones, a young Master of Science graduate from Oxford, who was recruited to our ranks, and then Laura Gibbons, from the University of Massachusetts, joined us. This relatively small and young team of investigators coordinated the conduct, data management and analysis of the SIDS program. They also assisted with less well resourced but developing areas in cancer and cardiovascular disease. In late 1990 evidence was accumulating from case-control studies that prone sleeping position might be a major cause of SIDS, but the research was retrospective, creating concerns that recall bias might explain the findings. We had the only prospective data in the world and were able to show that the association was equally strong prospectively, ruling out recall bias.2 A number of countries, including Australia, launched campaigns to encourage parents not to place babies on their stomachs in the cot, with astonishing results — the death rate from SIDS in Australia fell from 507 in 1990 to 139 in 1998, with similar falls in a number of other countries.3 While our work was not the only important contribution to the understanding of this major cause of SIDS, it provided an important piece of evidence needed for solving the puzzle. Later, in 1993, our team explained why prone sleeping position seemed to exert a different effect in winter than summer and a different effect across countries.4 Then, in 1995, we provided evidence that showed clearly that the fall in deaths could only be attributed to the changes in prevalence of prone sleeping position.5 This success will undoubtedly rank as one of the major contributions of the Centre in the years to come. It also established the organisation as one which, in its special location, could have a significant impact on international medical science. It was the much-needed platform that would underpin future recognition and opportunities. The post-SIDS era: taking stock The death rate from SIDS fell so rapidly after the prone sleeping position campaign that, by late 1991, it was clear there would eventually be insufficient cases occurring annually in Tasmania for epidemiological research (when we started the SIDS program, there had been an average of 27 cases a year for an extended period, and by 1998 there were only three). While this outcome was tremendously gratifying, it was clear that the research money to support our staff of now approximately 20 would dry up unless we repositioned our research program. This was confirmed by the National Health and Medical Research Council (NHMRC) Regional Grants Interview Committee's decision not to recommend refunding of our cohort study for 1992. We went from triumph to a period of considerable adversity. One of our first responses was to tell the Tasmanian public that we needed its financial and moral support. They responded generously. With a major public fundraising appeal, helped greatly by our Board and new Chairman John Tomlinson, and a timely decision by the United States National Institutes of Health, we were able to continue the study long enough to thoroughly evaluate the impact of the prone sleeping intervention campaign. In 1992, I took some time to review where we were going as an organisation and to think about where our future research opportunities might lie. I visited people like Richard Doll in Oxford, who had provided very helpful mentoring since 1987. I also had discussions with Ken Rothman (author of Modern epidemiology6), and Dimitris Trichopoulos at Harvard. These visits confirmed that, if we were to continue to conduct work of global significance, we would have to search even more thoroughly for gaps in knowledge that might be filled by an epidemiological approach. I was also convinced that we would need to develop stronger working relationships with basic scientists if we wished to use epidemiology to understand aetiology. These strategies were challenging, but all our team had learned a great deal from the SIDS research experience. While overseas, I also upgraded my skills in organisation and management by attending a management course in Salzburg, led by Peter Drucker, one of the world's most prominent management theorists. New directions The perspectives gained during my overseas visit were incorporated into planning from 1992 onwards. The major new strategy we decided on was to follow the Tasmanian Infant Health Survey (TIHS) cohort, now numbering 11 000 infants and children. The focus would be to search for links between early life exposures and later disease, using our extensive database of infant measurements that provided information on more than 450 variables measured during the first three months of life. One disease we looked at was asthma, an important disease for which preventable causes had not yet been identified and for which there was a shortage of good epidemiological data. This investigation would be coordinated by Anne-Louise Ponsonby, with help from David Couper, a biostatistician who had joined us from Seattle. We also increased our activity in research on the development in childhood of risk factors for cardiovascular disease and diabetes. Fitting into this theme was the new program started by a recent recruit from the Garvan Institute in Sydney, Graeme Jones (we were finally starting to see interest in work opportunities from well-qualified Australians outside Tasmania). He had a strong track record in osteoporosis in the elderly, and he used that background to focus on the impact of early-life factors on bone density in childhood. Fortuitously, interest in the "Barker hypothesis", which concerns the impact of fetal development on later disease, was gaining momentum. We were well placed to make an important contribution in this field, and our capacity was greatly enhanced by the addition of Ruth Morley, from the Institute of Child Health in London. Supplemented by smaller research efforts in cancer and adult cardiovascular disease, by 1994 we were able to see evidence that the research program was growing again. Between 1994 and 2000, the team was able to attract 17 new NHMRC grants from 38 applications submitted. This overall level of success was built on the tremendous preparedness of the Tasmanian public to be involved in the research. Response rates for case-control studies in this period were about 90% for cases and 80% for controls sampled from the electoral rolls, with comparable figures for cohort follow-up. In addition to our growing research effort we took on an important role in ensuring that knowledge was transferred to countries with less developed research capacity. The World Health Organization designated our institution as a Collaborating Centre for the Prevention of Cardiovascular Disease (CVD) a decade ago. That role has expanded steadily to the point where the Centre is assisting in studies on CVD in countries including Vietnam, Fiji and Samoa, where CVD and diabetes are producing an unexpectedly high disease burden. Genomics For the first seven years (1988-1995) the Centre focused solely on the environmental and lifestyle causes of disease. Meanwhile, others had been using the deep family pedigrees available in Tasmania to search for genetic causes of diseases following a Mendelian pattern of inheritance. Novel genes or linkages were discovered for several conditions, including multiple endocrine neoplasia and Huntington's disease. These successes were based on special features of Tasmania that are replicated in few other locations, namely (i) a population descended largely from identifiable founder families; (ii) comprehensive genealogical records; (iii) a modern healthcare system capable of identifying disease outcomes; (iv) a demonstrated capacity to involve the population in studies; and (v) organisational structures to facilitate the research. In 1995, David Mackey, a Tasmanian medical graduate and ophthalmologist at the Victorian Eye and Ear Hospital, approached us. He was undertaking important work in Tasmania on the more complex genetics of glaucoma. He wanted a base in Tasmania, and the Walter and Eliza Hall Institute, in Melbourne, was seeking a Tasmanian institution to manage new research and development syndicate funds to support his research. We accepted the role and our interest in the use of epidemiology to find genes for human diseases increased. Then, in 1996, the Australian pharmaceutical company AMRAD approached us about increasing its involvement in gene discovery in Tasmania through the Menzies Centre. We agreed, on the condition that the funding would be for a genetic unit that would employ people who could provide intellectual input to the work from a Tasmanian base. AMRAD signed a contract in 1997 for a five-year grant of $2.5 million, and, in 1998, we attracted Tasmanian molecular geneticist Michele Sale to coordinate the work. With financial and other help we were able to very quickly get projects under way in multiple sclerosis and osteoarthritis, and have continued to develop activity with Cerylid, a spin-off from AMRAD formed to operate its discovery arm. The genomics development has also led to an increase in postgraduate student training at the Centre, with five PhD students currently enrolled. The future During the past 12 months there have been several important developments for the Centre, driven by our very committed Board, chaired by Jean Trethewey, and strongly supported by the Dean of the Faculty of Health Science at the University of Tasmania, Allan Carmichael. The Tasmanian Government introduced an "Icons Program", which supports the Tasmanian Symphony Orchestra and our State cricket team. To this list Premier Jim Bacon added the Menzies Centre, with a commitment to provide $500 000 a year to help our organisation develop its capabilities. This, together with a large donation in 2000 from the United States-based Atlantic Philanthropies Inc, has placed us in a previously unimagined position to recruit more staff and drive our research program. To enable us to undertake these future developments with vigour, the University of Tasmania Council has established the Menzies Centre as an independent company limited by guarantee, remaining within the university structure. In 2002, the Centre will become the "Menzies Research Institute". Already, the Centre has grown to support a staff of 60. The new institute is likely to start 2002 with a budget of approximately $5 000 000 that will see staff numbers increase to more than 100, working on both environmental and genetic causes of disease. A major NHMRC grant of $2 290 000 over the next five years will enable us to study a cohort of Australians first measured as schoolchildren in 1985. They will be followed up for the emergence of adult disease, and it is anticipated this will provide the first direct evidence available on the impact of childhood lifestyle and biology on diseases such as coronary heart disease. A collaboration with similar cohorts in the US and Finland has already been established. A new director of the Cohort Studies Unit, Alison Venn, who has a strong background in this research strategy, has been recruited from the Centre for the Study of Mothers' and Children's Health at La Trobe University to coordinate developments. A large adult cohort study in Tasmania, with a focus on exposures that occur closer to the time of disease development, will also commence in 2002. Both studies will benefit from the input of a now-strong biostatistics group of three staff headed by one of our own PhD graduates, Leigh Blizzard. The level of genetic research activity will expand greatly. Tasmania presents opportunities as good as any in the world for gene discovery, and we intend to take up these opportunities. An increasing number of epidemiological studies at the Centre are focused on finding novel genes or validating candidate genes identified through animal or cell studies, or bioinformatic "data mining". This growth in activity reflects the recognition by commercial and government sources of the opportunities here, as well as the developing capacity of our genetic unit. Increasingly, our "environmental" epidemiologists and biostatisticians are developing their interests and skills in genetic research. This has not only led to the more rapid development of a critical mass for projects on gene discovery and validation, but has also opened up the possibility for in-depth investigation of gene-environment interaction. Projects with this focus are already under way in multiple sclerosis. There is great scope for us to contribute in an internationally significant way to the understanding of gene-environment interactions using Tasmania's unique population and our skill base. In the coming decade Australia will be relying more and more on its medical research institutes to maintain its competitive advantage in a knowledge-based global economy. We are confident that the new Menzies Research Institute will be making its contribution. References King H, editor. Epidemiology in Tasmania. Canberra: Brolga Press, 1987. Dwyer T, Ponsonby AL, Newman NM, Gibbons LE. Prospective cohort study of prone sleeping position and sudden infant death syndrome. Lancet 1991; 337: 1244-1247. Australian Bureau of Statistics. Deaths, Australia, 1990, 1998. Canberra: ABS, 1998. (Catalogue no. 3302.0/3303.0.) Ponsonby AL, Dwyer T, Gibbons LE, et al. Factors potentiating the risk of SIDS associated with the prone position. N Engl J Medicine 1993; 329: 377-382. Dwyer T, Ponsonby AL, Blizzard CL, et al. The contribution of changes in the prevalence of prone sleeping position to the decline in SIDS in Tasmania. JAMA 1995; 273: 783-789. Rothman K. Modern epidemiology. Boston: Little John and Co., 1986. Authors' details Menzies Centre for Population Health Research Terence Dwyer, MD, FAFPHM, Director. Reprints will not be available from the author. Correspondence: Professor T Dwyer, Menzies Centre for Population Health Research, 17 Liverpool Street, Hobart, 7000 TAS. t.dwyerATutas.edu.au Make a comment

Terence Dwyer

Editorial Chronic pain in children Despite the effects on children and their families, children's pain is often under-recognised MJA 2001; 175: 453-454 The International Association for the Study of Pain (IASP) defines pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage".1 Implicit in this definition is that pain is a subjective experience and is modulated not only by biological factors, but also by previously painful experiences, the meaning and context of the pain, fear, anxiety, depression, and a range of other factors. Chronic pain is defined as continuous or recurrent pain that persists past the normal time of healing, most commonly about three months' duration.1 If chronic pain refers simply to any pain with this predetermined duration, then all persistent pain of childhood, such as that related to chronic disease (eg, cancer, arthritis, sickle-cell disease), neuropathic pain (eg, complex regional pain syndrome, phantom limb pain) and recurrent pain syndromes (eg, migraine, recurrent abdominal pain), could be classified as causes of chronic pain in children. Little is known about the epidemiology of chronic pain in children. A recent random survey of more than 6000 children in the Netherlands aged 0-18 years indicated an overall prevalence of 25%.2 The prevalence of chronic pain increased with age, and was significantly higher for girls, particularly girls 12-14 years old. The most common types of pain were limb, abdominal pain or headache. Half of the respondents who had experienced chronic pain reported multiple sites of pain, and a third experienced pain as frequent and severe.2 Multiple sites of pain and severe pain were reported more often by girls. The combination of headache and abdominal pain was reported most frequently. These findings indicate that chronic pain is common in children and adolescents. In this issue of the Journal, Chalkiadis presents the first report on chronic pain in children in Australia.3 It is a prospective, descriptive study of the demographic and clinical characteristics of 207 children presenting to the Chronic Pain Clinic at the Royal Children's Hospital, Melbourne, over a two-year period. The study reveals that chronic pain had disturbing consequences for many children. The incidence of school absenteeism, sleep disruption and inability to play sport was high. Implied in these data is a significant psychological burden for the children and the families caring for them. Despite a relatively high prevalence of chronic pain in paediatrics and its significant physical, psychological, social and economic impact on children and their families, it is often under-recognised by clinicians. The reasons for this are multiple and include children's dependency on caregivers to be their advocate. Children with chronic pain can often be met with a dismissive attitude from their caregivers, especially if no organic cause of their pain is found. Furthermore, the advancement in our understanding of the pharmacology of analgesics in children is a relatively recent development.4 The extent to which children may suffer from inadequately managed chronic pain is not known. Recently, in the United States, a major study of children in the terminal phase of cancer painted a chilling picture of suffering, including a high incidence of problems associated with the treatment of pain.5 According to the parents surveyed, 89% of the children suffered "a lot" or "a great deal" from at least one symptom in their last month of life, most commonly pain, fatigue, or dyspnoea. Of the children who were treated for specific symptoms, treatment was successful in 27% of those with pain and 16% of those with dyspnoea.5 Given the many physical and psychological variables in children experiencing chronic pain and the different modalities of treatment now available, the assessment of a child with chronic pain needs to be comprehensive. The team approach involves: an assessment of the physical, psychological and environmental parameters; developing pain management strategies, including pharmacological and non-pharmacological approaches; and individual and family therapy as required. The long term outcomes of these strategies are not known, although Chalkiadis's report reveals at least short term benefit. There has been a long-standing recognition of the need for a comprehensive assessment of chronic pain in adults. In Australia, this has led to multidisciplinary pain centres in many of the major teaching hospitals. In addition, five medical specialist bodies recently came together to form a single physician training program and examination process for the Faculty of Pain Medicine of the Australian and New Zealand College of Anaesthetists. In contrast, it is only in recent years that a team approach to chronic pain in children has evolved in Australia and other countries. It is disturbing to read in Chalkiadis's report that only three paediatric centres in Australia and New Zealand have chronic pain management services which meet the minimum requirements for multidisciplinary staffing. Given the prevalence of chronic pain in children and the potentially serious physical and psychological consequences, a review of these services for children is required. On the basis of US data,5 strategies for the incorporation of pain management and palliative care principles into the care of children with life-threatening and life-limiting illness are a high priority. John J Collins Head, Pain and Palliative Care Service Lynette J Lane Coordinator, Chronic Pain Clinic, Pain and Palliative Care Service Susan Thompson Child and Adolescent Psychiatrist, Chronic Pain Clinic The Children's Hospital at Westmead, Sydney, NSW Merskey H, Bogduk N, editors. Classification of chronic pain: description of chronic pain syndromes and definitions of pain terms. Seattle: IASP Press, 1994. Perquin CW, Hazebroek-Kampschreur AAJM, Hunfeld JAM, et al. Pain in children and adolescents: a common experience. Pain 2000; 87: 51-58. Chalkiadis GA. Management of chronic pain in children. Med J Aust 2001; 175: 476-479. McGrath PJ, Unruh AM, Branson SM. Chronic nonmalignant pain with disability. In: Tyler DC, Krane EJ, editors. Advances in Pain Research and Therapy. Volume 15. New York: Raven Press, 1988. Wolfe J, Grier HE, Klar N, et al. Symptoms and suffering at the end of life in children with cancer. N Engl J Med 2000; 342: 326-333. Make a comment

John J Collins · Lynette J Lane · Susan Thompson

Healthcare Management of chronic pain in children George A Chalkiadis MJA 2001; 175: 476-479 For editorial comment, see Collins et al. Abstract - Methods - Results - Discussion - Reference - Authors' details - - - More articles on Paediatrics Abstract Objectives: To describe the demography, clinical characteristics, treatment, functional limitations and outcomes of patients referred to a paediatric multidisciplinary pain clinic. Design: Prospective data collection, descriptive study. Patients and setting: Tertiary referral centre pain clinic (Royal Children's Hospital, Melbourne) over two years (March 1998 - March 2000). Main outcome measures: Pain profile; functional disability (school absenteeism, sleep disturbance and inability to perform sport); treatments received; outcome. Results: 207 patients (mean age, 13.1 years; 73% females; 29% rural residents) were referred in the two years. Concomitant medical conditions were present in 106/207 (51%) patients, the commonest being cerebral palsy or spasticity (22 patients) and malignancy (18). Complex regional pain syndrome was diagnosed in 44 patients. Functional disability due to pain included school absenteeism (95% of school attenders), sleep disruption (71% of all patients) and inability to perform sport (90% of those able to participate in sport previously). Of the 105 patients who missed five or more days of school because of pain, 93 attended school regularly after treatment. Sleep disturbance improved in 129/146 (88%) patients, and 129/147 (88%) resumed sporting activity after multidisciplinary intervention. Outcome was classified as good in 134 patients (65%), moderate in 32 (15%) and poor in 16 (8%). Conclusions: Chronic pain in children and adolescents often results in considerable functional disability. Functional improvement can be achieved using a multidisciplinary approach to pain management in children. No data are available on the prevalence or incidence of paediatric chronic pain in Australia, and only limited data exist on the functional limitation that chronic and recurrent pain has on affected children, their parents and siblings.1 Specialised integrated pain management clinics that offer cognitive behavioural therapy programs are successful in the management of adults with chronic pain,2 but few programs exist for children and adolescents in Australia. As no Australian epidemiological or demographic data exist for children and adolescents with chronic pain, I performed a prospective, descriptive study to investigate the demography, clinical characteristics, treatment, functional limitations and outcomes of patients referred to a paediatric multidisciplinary pain clinic. Methods Patient population The Royal Children's Hospital is a tertiary paediatric referral centre servicing Victoria. A multidisciplinary clinic for children and adolescents with chronic pain, the Children's Pain Management Clinic, was established in March 1998. From March 1998 to March 2000, patients aged 0-18 years of age were prospectively and consecutively included in the analysis. The Statistical Local Areas defined by the Australian Bureau of Statistics3 were used to classify residential location as rural or metropolitan Victoria. Interviewers All patients were assessed by one of three paediatric anaesthetists. The initial interview involved taking a full medical and social history and physical examination of the patient in the presence of one or both parents. One or more allied health professionals (physiotherapist, occupational therapist or clinical psychologist) also assessed the children. Interview The interview followed a structured format. Responses to questions were obtained from both child and parent(s), unless the child was cognitively impaired, in which case the parent(s) or carer provided information. The questions related to diagnostic information (nature, site and intensity of the pain), functional disability (time off school, inability to partake in sporting activities) and sleep dysfunction. Definitions Chronic pain was defined as "pain persisting beyond the time of healing or pain which is persistent or near constant for three months or longer".4 Complex regional pain syndrome (CRPS) Types I and II were diagnosed according to previously published criteria.5 CRPS is a condition in which pain and disability are sustained, out of proportion to an initiating noxious event, by mechanisms that are still incompletely understood. Diagnosis is based on clinical findings, including allodynia (non-painful stimulus eliciting pain) or hyperalgesia (exaggerated sensitivity to pain) beyond the territory of a single peripheral nerve, oedema, skin blood flow abnormality (colour and/or temperature change) or abnormal sudomotor (sweating) activity. CRPS Type I is distinguished from Type II in that Type II follows nerve injury. Pain intensity was assessed by a pain assessment tool appropriate for the patient's age and cognition: Eland pain diagram; visual analogue scale; verbal numerical rating (1-10) scale; Wong-Baker faces; and parental or carer report in the case of non-verbal patients, toddlers and those with cognitive impairment. Outcomes were recorded as: Good: Marked reduction in the intensity of pain (no or minimal pain) and marked functional improvement (return to school and sport where applicable, and resumption of normal sleep pattern); Moderate: Partial reduction in pain intensity and/or some functional improvement (return to school or sport where applicable or resumption of normal sleep pattern); or Poor: No improvement in pain intensity or functional activity. Outcome was classified as unknown if there was no follow-up. The frequency and duration of follow-up were as clinically indicated. Results Over the two-year study period, 207 patients aged 1-18 years were referred to the Children's Pain Management Clinic (Box 1). Most patients (57%) were referred by orthopaedic surgeons. Medical conditions and associated disability Concomitant medical conditions (Box 2) were present in 106 (51%) patients. The disease process, its treatment, complications of the disease or side effects of the treatment accounted for the pain experienced by 93 of these 106 patients. A clear organic precipitant to the pain was identified in 39 of the 101 patients with no pre-existing medical condition. The cause of pain in these patients was neuropathic (nerve injury, nerve entrapment or neuroma) in 20 patients, soft tissue injury in 14, bone- or joint-related in four, and renal colic in one. In 62 of these 101 patients, no clear aetiology was found. The abdomen (10 patients) was the most common single site of presenting pain in this group, followed by headache or facial pain (9), multiple sites of pain (9), and pain in the foot (9), hand or forearm (8), knee (7), leg (5), back (2), shoulder (1), chest (1) and neck (1). CRPS was diagnosed in 44 of the 207 patients (Type I, 40 patients; Type II, 4 patients). Females (33 patients) and the lower limb (33 patients) were predominantly affected. Mean age was 13.7 (range, 9-17) years. CRPS was precipitated by minor trauma in 18 patients, and lower-limb surgery in six patients. No precipitant was identified in nine patients. Overall, 105 patients (95% of school attenders) missed at least five days of school because of pain (independent of medical appointments) (Box 3). There were 147 (71%) patients with impaired ability to participate in sport because of their pain. Of the remaining 60 patients, 43 were unable to participate in sport because of their concomitant condition, and 17 had no such inability on presentation. Overall, 146 patients (71%) suffered daily or almost daily sleep disruption attributable to pain. Of this group, 140 (96%) patients woke up three times or less. Parents of children with cerebral palsy, cognitive impairment or intellectual disability reported sleep disruption in 16 of 22 patients. Waking each night in these patients was more frequent and difficult to manage. Interventions Medications prescribed are listed in Box 4, and interventions are listed in Box 5. Individuals may have received one or more of these simultaneously or consecutively. No medication was prescribed in 75 of 207 (36%) patients; however, this group may have received any one or more of the interventions listed. The median duration of follow-up was four months (range, 2 weeks to 16 months). Patients diagnosed with CRPS were treated as inpatients (26 patients) or outpatients (18 patients) depending on the severity of their condition. Inpatients underwent a more intense and structured rehabilitation program tailored to their individual requirements. This involved cognitive behavioural therapy, physiotherapy (with graded return to physical activity) and re-integration into school and social activities. The median length of hospital stay was five days. Outcomes Outcome was good in 134 (65%) patients, moderate in 32 (15%), poor in 16 (8%) and unknown in 25 (12%). Box 6 shows the outcomes for patients diagnosed with CRPS. Of the 29 patients who had missed more than 40 days of school because of pain, 23 began attending school regularly once treatment for their pain syndrome commenced. Ten successfully underwent a graded return-to-school program coordinated in conjunction with the school, the Royal Children's Hospital Education Institute and the Children's Pain Management Clinic. Of the 76 patients who had missed between five and 40 days of school and who completed follow-up, 70 attended school regularly after intervention. Of the 147 patients who had impaired ability to participate in sport because of pain, 129 (88%) regained the ability after treatment. Sleep disturbance was successfully managed in 129 of 146 patients (88%). Most (122 patients or their parents) reported uninterrupted sleep as a result of either analgesic intervention or successful use of relaxation techniques. The remaining seven patients (or their parents) reported marked improvement in the frequency of waking and less troublesome return to sleep when they woke during the night. Twelve (6%) of the 207 patients died of their underlying terminal condition or its complications. There were three complications related to therapy for pain. Two were epidural-related in patients with cerebral palsy and CRPS: both developed back pain and fever. One had an epidural infection and the other paraspinous myositis with possible osteomyelitis. One patient developed paraesthesiae after lumbar sympathetic nerve block. All three patients recovered with no long-term sequelae. Discussion In my study, chronic pain in children and adolescents was associated with considerable functional limitation, most commonly school absenteeism, sleep disturbance and inability to perform sporting activities. The duration of school absenteeism was significant and could be expected to affect school performance, although this was not specifically recorded. Previous studies from other countries have reported on the incidence of functional disability in relation to specific painful sites or conditions.1 In our patients, chronic pain, irrespective of aetiology or site, commonly resulted in significant functional disability. More females than males were referred in all age brackets. CRPS, headache, fibromyalgia, recurrent abdominal pain and somatoform pain all occur more frequently in females than in males aged less than 18 years.6 More than a third of all patients referred were aged 12 years or less. Recurrent abdominal pain is commonly reported in this age group.7 However, only 11% of children in this age group referred to our clinic complained of abdominal pain, whereas half presented with limb pain. This may indicate that recurrent abdominal pain is successfully dealt with and understood by paediatricians, whereas limb pain is more likely to be referred. Patients from rural Victoria accounted for 29% of all referrals, in keeping with the population distribution in Victoria.3 This has implications regarding the provision of education of general practitioners and services to rural areas. CRPS was diagnosed in 21% of patients referred. The lower limb was more commonly involved than the upper, and females were more often affected than males. Previous studies from the United States8 and Sweden9 have shown a similar ratio of limb involvement. In these studies, females were more commonly affected than in this study (5 and 13 times more often than males, respectively). Unlike in those studies, in which a large percentage of girls with CRPS were active in sports, gymnastics, skating and dance, this was true for only 10% of our patients. Children and adolescents with cerebral palsy made up the largest single group of patients with a concomitant condition. Locating the source of pain can be difficult in this group,10 especially in those with cognitive impairment. Hip and/or back pain was the source in 55%. Spasticity itself can cause pain11 and contributes to deformity, subluxation, dislocation, capsulitis and osteoarthritis in these regions. Sleep disruption was more frequent and problematic in these children, both overall and on a nightly basis. Addressing pain resulted in most patients sleeping uninterrupted through the night. Eliminating or minimising sleep disruption is of obvious benefit to the child and carers.12 The nature and management of chronic pain in children and adolescents differs from that in adults. Bullying, sexual or physical abuse, marital disharmony and difficulties at school may all contribute to abnormal pain behaviour in children. Family therapy may be indicated, as family situations can contribute to exacerbating and maintaining pain behaviour in children. Parents as well as afflicted children often need to be taught behavioural modification and pain-coping strategies. Abolition of pain, particularly in patients with chronic conditions, is not always achievable. The diverse aetiologies which manifest as pain behaviour necessitate a coordinated, multidisciplinary approach. My results support this multidisciplinary approach and focus on regaining function and minimising pain behaviour. The lack of a psychologist (a psychologist was initially a team member, but only for three months) and psychiatrist as integral team members may have contributed to the poor outcomes observed in some patients. Poor outcome was commonest in patients from chaotic family environments or in those with moderate intellectual disability. The latter are least likely to respond to cognitive behavioural techniques. Behavioural modification is better suited to this group, but may be difficult and time consuming to implement. A recent unpublished survey of tertiary paediatric hospitals in Australia and New Zealand, conducted by the Paediatric Pain Working Party of the Faculty of Pain Medicine, Australian and New Zealand College of Anaesthetists, revealed that only three centres in Australia and New Zealand have chronic pain management services which meet their minimum requirements for multidisciplinary staffing.13 Given the magnitude of functional disability demonstrated in our population, the provision of funding for paediatric chronic pain services requires urgent attention. The socioeconomic cost of chronic pain in children and adolescents is considerable. Although not specifically addressed in this study, it was apparent that there were implications for the child (education, self-esteem, friendships), the parents (time off work caring for the child and attending appointments, cost of medication, hospitalisation and complementary therapies) and the healthcare system (medical care, including serial referrals to multiple specialists, medication and hospitalisation and allied healthcare costs). Future studies should address the prevalence and epidemiology of pain in Australian children and adolescents, the early identification of those in whom significant functional disability exists and the cost-benefits of establishing multidisciplinary paediatric pain centres. Future directions should include education programs for GPs, paediatricians, schoolteachers and counsellors and allied health professionals to recognise early warning signals such as school absenteeism, frequent sick bay attendances, failure to respond to treatment, and poor school sports participation. References Palermo TM. Impact of recurrent and chronic pain on child and family daily functioning: a critical review of the literature. J Dev Behav Pediatr 2000; 21: 58-69. Becker N, SjØgren P, Bech P, et al. Treatment outcome of chronic non-malignant pain patients managed in a Danish multidisciplinary pain centre compared with general practice: a randomised controlled trial. Pain 2000; 84: 203-211. Australian Bureau of Statistics. Melbourne. A Social Atlas. 1996. Census of Population and Housing. Canberra: Commonwealth of Australia, 1998. (Catalogue no. 2030.2.) McGrath PJ, Finley GA. Chronic and recurrent pain in children and adolescents. Progress in Pain Research and Management, Vol. 13. Seattle: IASP Press, 1999. Boas RA. Complex regional pain syndromes: symptoms, signs, and differential diagnosis. In: Janig W, Stanton-Hicks M, editors. Reflex Sympathetic Dystrophy: A Reappraisal. Progress in Pain Research and Management, Vol. 6. Seattle: IASP Press, 1999; 82. Perquin CW, Hazebroek-Kampschreur AAJM, Hunfield JAM, et al. Pain in children and adolescents: a common experience. Pain 2000; 87: 51-58. Faull C, Nicol AR. Abdominal pain in six-year-olds: an epidemiological study in a new town. J Child Psychol Psychiatr 1986; 27: 251-260. Wilder RT, Wolohan M, Masek BJ, et al. Reflex sympathetic dystrophy in children and adolescents: a follow-up of a cohort of 70 patients and development of a treatment algorithm. J Bone Joint Surg Am 1992; 6: 910-919. Olsson GL, Arnér S, Hirsch G. Reflex sympathetic dystrophy in children. In: Tyler DC and Krane EJ, editors. Advances in pain research and therapy, Vol 15. New York: Raven Press, 1990; 323-331. Nolan J, Chalkiadis GA, Low J, et al. Anaesthesia and pain management in cerebral palsy. Anaesthesia 2000; 55: 32-41. Barwood S, Ballieu C, Boyd R, et al. The analgesic effects of botulinum toxin A: a randomised, double blind, placebo controlled clinical trial. Dev Med Child Neurol 2000; 42: 116-121. Lewin DS, Dahl RE. Importance of sleep in the management of pediatric pain. J Dev Behav Pediatr 1999; 20: 244-252. Requirements for multidisciplinary pain centres offering training in pain medicine. Faculty of Pain Medicine, Australian and New Zealand College of Anaesthetists College Policy Document PM2, 2000. (Received 28 Nov 2000, accepted 18 Jun 2001) Authors' details The Royal Children's Hospital, Melbourne, VIC. George A Chalkiadis, DA, FANZCA, Anaesthetist, and Co-ordinator Pain Management. Reprints will not be available from the author. Correspondence: Dr GA Chalkiadis, Royal Children's Hospital, Flemington Road, Parkville, VIC 3052. chalkiagATcryptic.rch.unimelb.edu.au Make a comment 1: Demographic data Residential location Age* (years) Number (%) Female City Rural Other† 0-9 27 (13%) 70% 17 8 2 10-12 47 (23%) 64% 33 11 3 13-15 75 (36%) 73% 53 20 2 16-18 58 (28%) 83% 36 21 1 All 207 (100%) 73% 139 60 8 *Mean age, 13.1 years (range, 1-18 years); median age, 13 years. †These patients resided in the Australian Capital Territory, New South Wales or South Australia. Back to text 2: Concomitant medical conditions Condition Number Cerebral palsy/spasticity 22* Malignant tumours 18 Scoliosis 11* Benign tumours 7 Cystic fibrosis 6 Fibromyalgia 5 Intellectual delay 4 Talipes equinovarus or flat feet 4 Vertebral or spinal cord abnormalities 4 Others 33 *Four patients had both scoliosis and cerebral palsy, one had Duchenne muscular dystrophy and scoliosis and one had spinal muscular atrophy and scoliosis. Back to text 3: School days missed because of pain Number of school days missed * Nine children did not miss any days. †Seven children no longer attended school because of their pain. na= Not applicable; patients were unable to attend school because of a concomitant condition or because they were not of school age. Back to text 4: Medications prescribed Number of patients Tricyclic antidepressant (amitriptyline or nortriptyline) 78 Paracetamol 21 Non-steroidal anti-inflammatory drug (oral or topical, including COX-2 inhibitors) 31 Opioid: oxycodone (oral) or morphine (oral, subcutaneous or intravenous) 21 Anticonvulsants (carbamazepine, sodium valproate or gabapentin) 10 Clonidine (oral, intravenous or transdermal) 14 Benzodiazepines (diazepam, clonazepam) 7 Mexiletine 10 Capsaicin 7 Ketamine (intravenous) 5 Buscopan 2 Others (gaviscon, omeprazole, quinine, vitamin C) 1 for each medication Back to text 5: Interventions Number of patients Acupuncture 15 Relaxation techniques 98 Trigger point injection 7 Tendon, neuroma or joint injection 12 Nerve block 29* Epidural 28† Psychology/psychiatry 84 Physiotherapy 126 Iontophoresis (dexamethasone) 11 Self-administered medication 132 *62 blocks performed on 29 patients. †3 patients received 2 epidurals each. Back to text 6: Outcome in patients with complex regional pain syndrome Outcome* Upper limb Lower limb Good 8 26 Moderate 1 6 Poor 2 1 *Good: marked reduction in pain and marked functional improvement. Moderate: some reduction in pain and some functional improvement. Poor: no improvement in pain or functional ability. Back to text

George A Chalkiadis

Medicine and the Community Vitamin D deficiency in mothers of infants with rickets Josephine M Nozza and Christine P Rodda MJA 2001; 175: 253-255 For editorial comment, see Mason and Diamond; see also Grover and Morley Abstract - Methods - Clinical audit - Assay - Results - Children - Mothers - Countries of origin - Discussion - References - Authors' details - - More articles on Paediatrics Abstract Objective: To identify infants treated for vitamin D deficiency rickets, and to determine the incidence of vitamin D deficiency in their mothers and their mothers' country of origin. Design: A retrospective audit of the medical records of children diagnosed with vitamin D deficiency rickets. Inpatients were identified by discharge diagnoses of vitamin D deficiency or hypocalcaemia and outpatients by pharmacy dispensing of cholecalciferol. Setting: The Women's and Children's Health Care Network and the Southern Health Care Network (Melbourne, VIC) from June 1994 to February 1999. Patients: 55 children with vitamin D deficiency rickets. Results: Fifty-four of the 55 children were born to mothers with ethnocultural risk factors for vitamin D deficiency. Vitamin D status had been assessed in 31 of the 55 mothers (56%): 25 (81%) had 25-hydroxyvitamin D3 concentrations ≥ 25 nmol/L, consistent with osteomalacia. Conclusion: Vitamin D deficiency continues to occur in children of migrant families. When infants are diagnosed with vitamin D deficiency, vitamin D levels in their mothers and siblings should also be assessed. Vitamin D is the essential precursor of 1,25-dihydroxyvitamin D3, the steroid hormone required for calcium absorption, bone development and growth in children. Ninety per cent of the body's vitamin D is produced in the skin from the action of sunlight (ultraviolet B light), with the remaining 10% coming from dietary sources.1 Ultraviolet light acts on exposed skin only and does not penetrate clothing or glass. Moreover, there is an inverse relationship between the amount of skin pigmentation and vitamin D production. Serum levels of 25-hydroxyvitamin D3 (25OHD3) are a measure of the body's vitamin D stores and used for diagnosing vitamin D deficiency. A serum 25OHD3 level below 40 nmol/L is indicative of vitamin D deficiency, and a level below 25 nmol/L corresponds to osteomalacia or rickets.2 The recommended daily intake (RDI), if there is inadequate sun exposure, is 400 IU in children and 200 IU in adults. Pregnancy increases the RDI for vitamin D to 500-700 IU.3 In newborn infants, vitamin D stores reflect maternal stores, and human breast milk and unfortified cow's milk are poor sources of vitamin D. Vitamin D deficiency is being increasingly recognised in Melbourne.4,5 Reports have focused on infants, not their mothers, and emphasised postnatal factors (unsupplemented breast feeding, reduced sun exposure, dark skin pigmentation and dietary factors) as the cause of vitamin D deficiency. Thus, although vitamin D metabolism is considered to be well understood,6 the importance of adequate maternal sun exposure and its relationship to perinatal vitamin D deficiency appears to be poorly appreciated in clinical practice. We performed a retrospective audit of the medical records of infants diagnosed with rickets to determine the vitamin D status of their mothers and their mothers' country of origin. Methods Clinical audit We examined medical records from the Women's and Children's Health Care Network and the Southern Health Care Network (Melbourne, VIC) for the period June 1994 - February 1999. Inpatients with nutritional vitamin D deficiency were identified by a discharge diagnosis of either hypocalcaemia or vitamin D deficiency rickets. Outpatients with vitamin D deficiency were identified from records of dispensing of cholecalciferol during the study period by the Royal Children's Hospital (RCH) pharmacy. The RCH pharmacy was the sole supplier of cholecalciferol in liquid form in Victoria, so most outpatients prescribed cholecalciferol would have received it from this source. Only patients treated privately with other forms of vitamin D would not be identified this way. Children born at less than 35 weeks' gestation or who had chronic liver or renal disease, or any other underlying systemic disorder, were excluded. Assay From June 1994 to September 1996, the 25OHD3 assay was performed by an inhouse column extraction method, followed by Incstar radioimmunoassay (Incstar Corporation, Stillwater, MN, USA) (reference range, 28-165 nmol/L), and all samples were processed at the Royal Melbourne Hospital. After September 1996, samples were processed at three laboratories in Melbourne and the universal method was changed to the Incstar radioimmunoassay (reference range, 25-108 nmol/L). Results Children Fifty-five children were treated for vitamin D deficiency rickets during the study period. Thirty-six were male and 19 female, with ages ranging from 11 days to 12 years, seven months (mean age, 16 months). Twenty-four of the 55 children (44%) were aged less than 12 months and, of these, 23 were exclusively breast fed at the time of diagnosis. Twenty-three of the 55 children presented in spring (September to November). To confirm the diagnosis, biochemical analyses (serum levels of calcium, phosphate, alkaline phosphatase [ALP], parathyroid hormone [PTH] and 25OHD3 [Box 1]) and radiography of the long bones (showing widened "cupped" and frayed metaphyses and generalised osteopenia) had been performed. Box 1 shows that hypocalcaemia was more likely in children less than 9 months of age, but ALP and/or PTH levels were elevated across all age groups. The children's symptoms at presentation are given in Box 2. Mothers In only 31 (56%) of the 55 children had the 25OHD3 levels of their mothers been measured (Box 3). None of the mothers had volunteered symptoms of vitamin D deficiency at presentation of their children. Three of the children had older siblings diagnosed with rickets, but maternal vitamin D status had not been assessed when the siblings were diagnosed. Twenty-five of the 31 mothers (81%) had 25OHD3 levels of 25 nmol/L or less, consistent with osteomalacia, and 28 (90%) had 25OHD3 levels of 40 nmol/L or less. In seven mothers, further biochemical evaluation had been performed, including calcium, phosphate, ALP and PTH levels. Three women had raised PTH levels indicative of osteomalacia and, after further questioning, two of these mothers described symptoms of osteomalacia. One was a 26-year-old unveiled Ethiopian woman, who complained of back pain, tiredness and occasional hand weakness. The other was a 24-year-old fully veiled Ethiopian woman, who described a seven-month history of carpopedal spasm and musculoskeletal pain. At the time of diagnosis of her 16-month-old child, she was pregnant with her second child. Treatment of this woman not only relieved her symptoms, but prevented the appearance of vitamin D deficiency in her second child. Countries of origin The countries of origin of the 55 mothers were Africa (25; 45%), India/Pakistan (13; 24%), the Middle East (13; 24%) and Italy (3; 5%). The remaining mother was of European descent, but suffered from agoraphobia and depression. Discussion Our findings show that, of the mothers of infants with rickets whose vitamin D levels were measured, most were also vitamin D deficient, but had not complained of symptoms at presentation. Presumably, these women would not otherwise have come to medical attention. Women at particular risk of vitamin D deficiency and osteomalacia are those with dark pigmented skin, reduced sun exposure for ethnocultural reasons (including veiling) and inadequate dietary intake of both calcium and vitamin D.7-9 In children, additional risk factors include maternal vitamin D deficiency and unsupplemented breast feeding, as identified in our study and those of others.9,10 It has been shown by Hoogenboezem et al11 that total vitamin D metabolites in maternal and fetal plasma are closely correlated, indicating that vitamin D stores at birth are dependent on maternal stores. As newborn infants are generally not exposed to direct sunlight and breast milk is a poor source of vitamin D, vitamin D stores, even if normal at birth, may become depleted at eight weeks in infants exclusively breast fed.11,12 We suggest supplementing breast fed infants with 400 IU/day of vitamin D (recommended daily requirement) as the safest option for preventing vitamin D deficiency in infants of at-risk women (in Australia, infant vitamins Penta-vite [Roche] provide 0.45 mL [405 IU] per day). We recommend that when infants with vitamin D deficiency are diagnosed, vitamin D levels in their mothers and siblings should also be assessed, irrespective of whether they are symptomatic. We also recommend that 25OHD3 levels are measured in all pregnant women with dark skin pigmentation and/or limited sun exposure because of veiling. During pregnancy and lactation, these women require 500-700 IU per day of vitamin D. Their infants should also be assessed for vitamin D deficiency. Vitamin D prophylaxis in infants (400 IU per day) should be commenced at birth and continued for the period of breast feeding. References Clemens TL, Adams JS, Henderson SL, et al. Increased skin pigmentation reduces the capacity of skin to synthesize vitamin D3. Lancet 1982; 1: 74-76. Salle BL, Glorieux FH, Lapillone A. Vitamin D status in breastfed term babies. Acta Paediatr 1998; 87: 726-727. Briggs D, Wahlqvist M. Food facts. Chapter 13. Melbourne: Penguin Books, 1984: 119. Pillow JJ, Forrest PJ, Rodda CP. Vitamin D deficiency in infants and children born to migrant parents. J Paediatr Child Health 1995; 31: 180-184. Mayne V, McCredie D. Rickets in Melbourne. Med J Aust 1972; 2: 873-875. DeLuca HF. The vitamin D story: a collaborative effort of basic science and clinical medicine. FASEB J 1988; 2: 224-236. Nellen JF, Smulders YM, Frissen PH, et al. Hypovitaminosis D in immigrant women: slow to be diagnosed. BMJ 1996; 312: 570-572. Gannage-Yared MH, Chemali R, Yaacoub N, et al. Hypovitaminosis D in a sunny country: relation to lifestyle and bone markers. J Bone Miner Res 2000; 15: 1856-1862. Daaboul J, Sanderson S, Kristensen K, Kitson H. Vitamin D deficiency in pregnant and breast-feeding women and their infants. J Perinatol 1997; 17: 10-14. Ahmed I, Atiq M, Iqbal J, et al. Vitamin D deficiency rickets in breast-fed infants presenting with hypocalcaemic seizures. Acta Paediatr 1995; 84: 941-942. Hoogenboezem T, Degenhart HJ, de Muinck Keizer-Schrama SM, et al. Vitamin D metabolism in breast-fed infants and their mothers. Pediatr Res 1989; 25: 623-628. Makin HLJ, Seamark DA, Trafford DJH. Vitamin D and its metabolites in human breast milk. Arch Dis Child 1983; 58: 750-753. (Received 23 Aug 2000, accepted 2 May 2001) Authors' details Department of Paediatrics, Monash University, Monash Medical Centre, Melbourne, VIC. Josephine M Nozza, FRACP, Paediatric Emergency Fellow, Children's Program. Christine P Rodda, PhD, FRACP, Senior Lecturer, Monash University, and Head of Paediatric Endocrinology and Diabetes. Reprints will not be available from the authors. Correspondence: Dr C P Rodda, Department of Paediatrics, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168. c.roddaATsouthernhealth.org.au Make a comment 1: Serum biochemical profile at presentation in children with vitamin D deficiency rickets, by age Calcium Phosphorus Alkaline phosphatase >350U/L Parathyroid hormone >6.8pmol/L Age No. of children 16/17 8/17 16/16 13/13 Mean (95% CI) 1.53 (1.363-1.697) 1.54 (1.205-1.875) 1108 (853.5-1362.5) 40.2 (17.3-63.1) Age >9 months No. of children 14/38 19/37 35/38 21/25 Mean (95% CI) 2.08 (1.954-2.206) 1.31 (1.176-1.444) 1165 (890.8-1439.2) 29.54 (18.36-40.72) Total no. of children 30/55 27/54* 51/54* 34/38* Overall range 1.0-2.6mmol/L 0.55-3.07mmol/L 300-4042U/L 4.0-175pmol/L Reference ranges: calcium (2.1-2.6 mmol/L); phosphorus (1.3-2.3 mmol/L); alkaline phosphatase (100-350 U/L); and parathyroid hormone (1.0-6.8 pmol/L). *Some children did not have phosphorus, alkaline phosphatase, or parathyroid hormone analysed. Back to text 2: Clinical features at presentation of the 55 children* with vitamin D deficiency rickets Delayed walking 20 Leg bowing 14 Seizures 12 Failure to thrive 9 Incidental finding (detected on chest x-ray or routine biochemistry) 6 Bone pain 4 Tetany/carpopedal spasm 2 Short stature 1 Stiff hips 1 Pathological fracture 1 Sibling with rickets 1 *Some children presented with more than one symptom. Back to text 3: Age, sex, country of maternal origin, and serum 25-hydroxyvitamin D3 (25 OHD3) levels (children and mothers) of 31 children with rickets whose mothers were also assessed for vitamin D deficiency 25 OHD3 level Age of child (months) and sex Country of maternal origin Child Mother 11 days M India 24 4 F Sri Lanka 17 25 4 M Italy 19 5 M Somalia 9 9.3 6 M Somalia 6 13 6 M Turkey 7 11 8 M Sri Lanka 23 8 M Middle East 9 9* M Iraq* 6 9* F Iraq* 11 M Africa —† 5 11 M Egypt 8 11 M Ethiopia 20 12 M Africa —† 20 13 F Lebanon —† 39 14 F Sri Lanka 7 20 14 F Australia 25 16 M Ethiopia —† 16 M Somalia nd 55‡ 16 F Lebanon 12 16 M Ethiopia 15 17 17 F Turkey nd 45‡ 17 M Ethiopia 5.5 17 M Italy 36 12 17 F Lebanon 25 18 M Zaire 22 40 18 M Pakistan 9 12 18 F India 14 20 M Zaire 22 40 25 F India 22 47 27 M Sudan 17 10 30 M Kenya 26 *Twins. †Vitamin D levels measured after commencement of treatment. ‡Maternal levels measured after education regarding sun exposure/diet nd=not done. Reference range, 25-108nmol/L Back to text

Josephine M Nozza · Christine P Rodda

In 1993, a group of researchers led by Andrew Wakefield at the Royal Free Hospital, London, suggested an association between both wild and vaccine measles viruses and inflammatory bowel disease (IBD), based on a small case series of children with Crohn's disease.1 In 1998, the same researchers reported another series of 12 children, and described an apparently new syndrome of an unusual type of IBD associated with developmental disorders such as (but not limited to) autism.2 They suggested that measles-mumps-rubella (MMR) vaccine may cause IBD, resulting in decreased intestinal absorption of essential vitamins and nutrients and possibly leading to developmental disorders such as autism. Wakefield has also expressed the opinion (without any scientific evidence) that such perturbations are less likely if the components of MMR are given separately, spaced several months apart. Measles remains one of the most severe infectious childhood diseases (Box), and the current vaccine is 95% effective. Yet parents worry about sensational media reports of possible links between vaccines and a variety of medical conditions. Autism and IBD (Box) and their alleged relationship to MMR vaccine have recently been highlighted in the media. Epidemiological evidence Expert groups around the world have expressed the opinion that the suggested associations between the MMR vaccine, IBD and autism are weak and the studies flawed. The studies at the Royal Free Hospital1,2 were conducted on highly selected patients referred for gastrointestinal ailments. The studies had no controls, were unblinded and were not designed to test aetiology or harm. There were multiple potential sources of bias. For example, the association between vaccination and autism was based primarily on parental recall — parents are likely to link changes in behaviour with memorable events such as vaccination, thereby introducing "recall" bias. Such a case-series analysis is unable to determine causal links. Moreover, the onset of autism and MMR vaccination may appear to be associated in time because the average age at which parents report concerns about child development is 18-19 months and most children receive MMR vaccine before their second birthday. In contrast to Wakefield and colleagues' two small, poorly designed studies,1,2 large, well designed epidemiological studies have shown no association between MMR vaccine and autism. These include a UK population-based study of the vaccination status of 498 children with autism,6 a study of the rates of IBD and autism among 6100 French schoolchildren,7 and an examination of trends in the incidence of autism and MMR vaccine coverage over time in California3 and in UK general practices.4 Similarly, a Finnish study of 1.8 million children over 14 years that looked at adverse events after MMR vaccination did not document a single case of autism or IBD as a consequence of MMR vaccination.8 Virological evidence In their 1993 study, Wakefield and colleagues reported identification of measles virus in bowel tissue of patients with Crohn's disease.1 Other laboratory studies using similar methodology have not found measles virus in patients with IBD. In fact, one group suggested that the reported "measles virus" represented a cross-reaction with another protein structurally similar to certain measles antigens.9 More sensitive testing methods have not revealed any evidence of measles virus in the gut of patients with Crohn's disease or ulcerative colitis.10Recently, Wakefield and O'Leary presented data to the Immunisation Safety Committee of the US Institute of Medicine suggesting that measles virus has been detected by very sensitive polymerase chain reaction (PCR) methods in the gut of selected autistic children.11 These data have not been published in the peer-reviewed scientific literature. Kawashima and colleagues in Japan have published a study reporting the detection of measles virus by PCR in peripheral mononuclear cells of individuals with autism and bowel disease. However, these findings have not been replicated by other laboratories, and most studies have found no evidence for the presence of measles virus in the gut in inflammatory disease.11 Interestingly, there was no mention of detection of vaccine viruses in the bowel or brain tissues of any patients in the 1998 study of Wakefield and colleagues,2 in contrast with their 1993 report.1 Level of evidence Wakefield's studies provide very weak (National Health and Medical Research Council Level IV) evidence for harm or causation relating to the MMR vaccine.12 The "Bradford Hill" criteria for causation13 are poorly fulfilled by Wakefield's studies.1,2 Specifically, there is no estimate of the strength of association, no evidence of a dose-response relationship or temporal sequence, no consistent findings from other investigators, no coherence with established facts, and poor specificity of association.14In addition to there being no evidence to support a causal relationship between MMR and autism, Wakefield's proposal that the vaccine components of MMR be given separately is unsupported by any evidence. Indeed, giving these vaccines separately has many disadvantages. First, children will receive some components later than recommended, risking exposure and infection in the intervening time. Second, there are additional injections and some may be omitted, or viral interference may reduce vaccine effectiveness if components are given separately but too close together. Except for monovalent rubella, these vaccines are not currently available separately in Australia, and requests to give them separately should be strenuously resisted. Consensus about the safety of MMR by expert groups The World Health Organization rejects an association between MMR and autism, and "strongly endorses the use of MMR . . . vaccine on the grounds of its convincing record of safety and efficacy".15 In 1998, a meeting of the British Medical Research Council and a group of national and international experts concluded that there was "no evidence to indicate any link between MMR vaccination and bowel disease or autism".16 In April 2001, the Institute of Medicine released its report Immunization safety review: measles-mumps-rubella vaccine and autism,11which concluded that the available evidence rejects a causal association between MMR and autism, although recommending that further research into the issue be conducted because of public concern. In view of considerable epidemiological evidence on the safety of MMR vaccine, we believe that Wakefield's small, unsubstantiated case series should be seen in correct perspective, and that parents and healthcare professionals should be reassured that there is no evidence that the MMR vaccine is associated with autism or IBD. C Raina MacIntyre Senior Lecturer Peter B McIntyre Deputy Director National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases, Children's Hospital, Westmead, NSW. rainamAToptusnet.com.au Wakefield AJ, Pittilo RM, Sim R, et al. Evidence of persistent measles virus infection in Crohn's disease. J Med Virol 1993; 39: 345-353. Wakefield AJ, Murch SH, Anthony A, et al. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children. Lancet 1998; 351: 637-641. Dales L, Hammer SJ, Smith NJ. Time trends in autism and in MMR immunization coverage in California. JAMA 2001; 285: 1183-1185. Kaye JA, del Mar Melero-Montes M, Jick H. Mumps, measles, and rubella vaccine and the incidence of autism recorded by general practitioners: a time trend analysis. BMJ 2001; 322: 460-463. Fombonne E. The epidemiology of autism: a review. Psychol Med 1999; 29: 769-786. Taylor B, Miller E, Farrington CP, et al. Autism and measles, mumps, and rubella vaccine: no epidemiological evidence for a causal association. Lancet 1999; 353: 2026-2029. Fombonne E, Du Mazaubrun C, Cans C, Grandjean H. Autism and associated medical disorders in a French epidemiological survey. J Am Acad Child Adolesc Psychiatry 1997; 36: 1561-1569. Patja A, Davidkin I, Kurki T, et al. Serious adverse events after measles-mumps-rubella vaccination during a fourteen-year prospective follow-up. Pediatr Infect Dis J 2000; 19: 1127-1134. Iizuka M, Chiba M, Yukawa M, et al. Immunohistochemical analysis of the distribution of measles related antigen in the intestinal mucosa in inflammatory bowel disease. Gut 2000; 46: 163-169. Afzal MA, Armitage E, Ghosh S, et al. Further evidence of the absence of measles virus genome sequence in full thickness intestinal specimens from patients with Crohn's disease. J Med Virol 2000; 62: 377-382. Institute of Medicine. Immunization safety review: measles-mumps-rubella vaccine and autism. Washington, DC: National Academy Press, 2001. Available at: <http://books.nap.edu/html/mmr> (Accessed 4 July 2001). Levine M, Walter S, Lee H, et al. Users' guides to the medical literature. IV. How to use an article about harm. Evidence-Based Medicine Working Group. JAMA 1994; 271: 1615-1619. Wilkinson L. Sir Austin Bradford Hill: medical statistics and the quantitative approach to prevention of disease. Addiction 1997; 92: 657-666. Halsey NA, Hyman SL. Measles-mumps-rubella vaccine and autistic spectrum disorder: report from the New Challenges in Childhood Immunizations Conference convened in Oak Brook, Illinois, June 12-13, 2000. Pediatrics 2001; 107(5): 1-23. World Health Organization. Statement on the use of MMR vaccine. Available at: <http://www.who.int/vaccines-diseases/safety/hottop/mmrstatement.htm> Accessed 4 July 2001. Medical Research Council. Report from the Working Party on MMR. London: MRC, 1998. Make a comment Measles, inflammatory bowel disease and autism Measles Measles is virtually universal among unimmunised children in all countries: 99.9% of unimmunised people will contract measles, 90% before the age of 20. One in every 5000-10000 cases results in death from the acute effects of the disease. Worldwide, there were 888000 deaths due to measles in 1998, more than the number due to breast or skin cancer, homicide or violence. Inflammatory bowel disease (IBD) IBD is a group of chronic inflammatory disorders of the small and large bowel, the commonest being ulcerative colitis and Crohn's disease. The cause of IBD is not understood, but both an immune mechanism and a genetic predisposition are probably involved. IBD is relatively rare, with an incidence of 6-8 cases per 100000 population for ulcerative colitis and 2 cases per 100000 for Crohn's disease. It usually occurs in people aged between 15 and 30 years, but can occur in children. Autism Autism is a developmental disorder that is usually identified between the ages of 18 months and three years. Four times more common in boys than girls, autism occurs in all racial and social groups. Autistic children and adults typically have difficulties in verbal and non-verbal communication, social interactions and leisure or play activities. A single cause of autism has not been identified, but current research implicates neurodevelopmental, genetic and environmental factors. The sex differential suggests a strong genetic component. Many children have some features of autism but do not fulfil all the diagnostic criteria. There has been an apparent increase in the incidence of autism in recent decades. In the United States the rate increased from 44/100000 births in 1980 to 208/100000 births in 1994,3 while in the United Kingdom the rate increased from 3/100000 births in 1988 to 21/100000 births in 1999.4 This has been attributed largely to changing case definitions and classifications (which now include less severe forms of the disease) and improved recognition.5 The discrepancy between the US and UK rates may be evidence of inconsistent case definitions. It is uncertain how much, if any, of the increased incidence is independent of diagnostic practice. Back to text

Editorial Inaccurate classification of infant deaths in Australia: a persistent and pervasive problem A standardised definition of SIDS and standardised investigative protocols for unexpected infant deaths are needed MJA 2001; 175: 5-7 Australia has an excellent record internationally in the area of sudden infant death syndrome (SIDS). Australian researchers were among the first to provide data linking prone sleeping position to an increased risk of SIDS; Australia was one of the first countries to establish State and national "Reduce the risks" campaigns; and considerable local research has contributed to a greater understanding of this enigmatic disorder. Proof of the efficacy of local preventive activities has been the dramatic and continued decrease in deaths from SIDS, from over 500 in 1988 to 134 in 1999 (Ms Jan Carey, Executive Director, SIDSaustralia [ACT branch] media release, June 2001). There have also been numerous initiatives in Australia and worldwide to improve our ability to distinguish between SIDS and other causes of unexpected infant death. These initiatives include attempts to standardise the definition of SIDS and to introduce uniform guidelines for evaluation of death scenes and autopsy examinations. Unfortunately, significant problems persist. SIDS remains a diagnosis of exclusion, with no pathognomonic features at autopsy. Causes of death such as poisoning, or accidental or deliberate asphyxia, may appear to the pathologist identical to SIDS, and cardiovascular diseases, occult infections and metabolic disorders may be identified only by special dissections or investigations. The confusion that arises with individual pathologists' choosing different definitions is reflected in the recent international literature, where deaths have been accepted as SIDS in the apparent absence of recognised formal definitions. In addition, there is no consistency in the definition of SIDS being used by clinicians, researchers or pathologists in Australia. A number of different definitions of SIDS have been promulgated over the past decade, each emphasising a different aspect: for example, an association with sleep; a requirement for extensive ancillary postmortem investigations (eg, microbiological and toxicological testing); subclassifications based on the presence or absence of minor pathological findings; and specified upper and lower age limits.1-5 There is also an urgent need for a standardising of the investigation of unexpected infant deaths, including guidelines for reviewing the clinical and family history, for carefully examining the death scene and for conducting the autopsy according to established criteria. Established autopsy criteria have included full-body radiological examination and microbiological and toxicological testing. Despite the availability of standard investigative protocols for infant deaths (Box), no protocol is consistently applied in Australia. The usefulness of protocols has been clearly established: more deaths due to unsafe sleeping environments have been identified recently, and each step of the postmortem investigation has been shown to contribute potentially significant information.9,10 Failure to implement a standard approach to unexpected infant deaths may cause distress for families who subsequently discover that significant steps were missed in the autopsy evaluation of their infant. It may also have far-reaching consequences. In the United Kingdom, 42 deaths originally attributed to SIDS were found to be due to homicides.11 The initial failure to diagnose these as homicides would have interfered with police investigations and may have endangered other children in these families and allowed the perpetrators to escape punishment. Australian courts have also reached the same conclusions in similar retrospectively reviewed cases. Recent infant deaths in rural Australia have been accepted as SIDS without proper death scene examinations or autopsies.12 An investigation of autopsy practices in Queensland by a Working Group of the Queensland Council on Obstetric and Paediatric Morbidity and Mortality confirmed that major problems exist, particularly in rural areas.13 The group found that 65% of the reviewed autopsies in infants who died suddenly and unexpectedly failed to attain the minimum acceptable quality score set by the study. They concluded that these autopsies were of "poor quality" and that "a specialist pathologist with appropriate expertise" was required. Similar conclusions were reached in an inquest into a series of infant deaths in South Australia.14 Thus, we have an unacceptable situation: diagnostic guidelines are readily available but are not being used. This is partly because of isolation in rural Australia and underfunding of services. In isolated regions of Australasia infant autopsies have also been performed by non-pathologists. Infant autopsy examination is highly specialised, requiring specific dissection techniques and considerable knowledge of both paediatric and forensic pathology. Expecting non-specialists to perform infant autopsies is neither appropriate nor fair and makes the validity of some of the autopsy conclusions uncertain. It is time to undertake a national initiative to correct these deficiencies. Details of these problems were presented at a national meeting of forensic pathologists in Perth in June this year, with a proposal to convene a National Workshop of Pathologists, in association with SIDSaustralia, to choose an appropriate definition for SIDS and investigative guidelines. It is hoped that these conclusions could be evaluated and endorsed by the Forensic Committee of the Royal College of Pathologists of Australasia and appropriate national "gold standards" agreed upon. Then pathologists' concerns and consensus recommendations for change could be passed on to the respective coronial authorities to ensure proper medicolegal investigation of unexpected infant deaths. Implementing these guidelines would not be easy, requiring financial support by governments, coordinated training programs and local cooperation, and possibly legislative changes in some States. A recently established national coronial database will enable the monitoring of trends in unexpected death in Australia.15 However, idiosyncratic or inexact diagnostic practices among pathologists and failure to follow protocols will result in inaccurate statistics on infant deaths in Australia. This could lead to underdiagnosis of important diseases and conditions, and unreliability of research based on these data. Opportunities to save more lives will be lost, parents will be ill-informed, and coroners will not have a clear picture of problems within their jurisdictions. Over a decade ago, the late John Emery raised the spectre of SIDS becoming a "diagnostic dustbin"16 — unfortunately, he may well have been correct. Roger W Byard Specialist Forensic Pathologist, Forensic Science Centre, Adelaide, SA; Clinical Professor, Departments of Paediatrics and Pathology University of Adelaide, Adelaide, SA byard01ATforensic.sa.gov.au Willinger M, James LS, Catz C. Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development [review]. Pediatr Pathol 1991; 11: 677-684. Cordner SM, Willinger M. The definition of the sudden infant death syndrome. In: Rognum TO, editor. Sudden infant death syndrome. New trends in the nineties. Oslo: Scandinavian University Press, 1995: 18-20. Beckwith JB. A proposed new definition of sudden infant death syndrome. In: Walker AM, McMillen C, editors. Second SIDS International Conference. Ithaca: Perinatology Press, 1993: 418-421. Sturner WO. SIDS redux: is it or isn't it [review]? Am J Forensic Med Pathol 1998; 190: 107-108. Rambaud C, Guilleminault C, Campbell PE. Definition of the sudden infant death syndrome. BMJ 1994; 308: 1439. Cordner SM. Appendix 2: Australasian SIDS autopsy protocol. In: Byard RW, Cohle SD. Sudden death in infancy, childhood and adolescence. Cambridge: Cambridge University Press, 1994: 501-514. Krous H. An international standardised autopsy protocol for sudden unexpected infant death. In: Rognum TO, editor. Sudden infant death syndrome. New trends in the nineties. Oslo: Scandinavian University Press, 1995: 81-95. Centers for Disease Control and Prevention. Guidelines for death scene investigation of sudden unexplained infant deaths. Recommendations of the Interagency Panel on Sudden Infant Death Syndrome. MMWR Morb Mortal Wkly Rep 1996; 45(RR-10): 1-6. Mitchell E, Krous HF, Donald T, Byard RW. An analysis of the usefulness of specific stages in the pathological investigation of sudden infant death. Am J Forensic Med Pathol 2000; 21: 395-400. Mitchell E, Krous HF, Donald T, Byard RW. Changing trends in the diagnosis of sudden infant death. Am J Forensic Med Pathol 2000; 21: 311-314. Meadow R. Unnatural sudden infant death. Arch Dis Child 1999; 80: 7-14. Panaretto K. SIDS and the indigenous community. Plenary presentation at: SIDSaustralia Child and Infant Mortality Matters Conference; March 2001; Canberra. Woodgate P, Colditz P, Brookes K, et al. A review of sudden unexpected deaths in infants autopsies in Queensland 1997-1998. Report from the Sudden Unexpected Deaths in Infancy Working Group of the Queensland Council on Obstetric and Paediatric Morbidity and Mortality. Brisbane: Mater Epidemiology Unit, November 2000. Inquest into the deaths of Deane, Barnard and Nottle. Chivell W, State Coroner, South Australia, 25 August 1995. Monash University National Centre for Coronial Information. National Coroners Information System. <http://www.vifp.monash.edu.au/ncis> Emery JL. Is sudden infant death a diagnosis [editorial]? BMJ 1989; 299: 1240. Make a comment Standard investigative protocols for sudden infant deaths in Australia and overseas National Australasian SIDS autopsy protocol This was formulated in 1992 in a collaboration set up by the Victorian Institute of Forensic Medicine involving the Forensic Committee of the Royal College of Pathologists of Australasia, the ANZ Paediatric Pathology Group and the National SIDS Council of Australia.6 International standardised autopsy protocol This resulted from collaboration between SIDS International and the National Institute of Child Health and Human Development in the United States.7 It (and its instruction manual) has been endorsed by both the Society for Pediatric Pathology and the National Association of Medical Examiners in the United States. Sudden unexplained infant death investigation report form This was formulated by the US Centers for Disease Control and Prevention for the standardisation of death scene examinations.8 Back to text

Roger W Byard

CLASS="LinkBox"> Editorial Obesity: definitely a growing concern Time to implement Australia's strategy for preventing overweight and obesity MJA 2001; 174: 553-554 Obesity is increasingly recognised as a health problem by the Australian community, with frequent discussions of obesity-related issues in the media and heavy marketing of weight-loss products. There is abundant evidence to support this view, not least being the 1995 National Nutrition Survey showing that 56% of adult Australians are either overweight or obese.1A casual ...

Louise A Baur

CLASS="LinkBox"> Research Prevalence of overweight and obesity in Australian children and adolescents: reassessment of 1985 and 1995 data against new standard international definitions Anthea M Magarey, Lynne A Daniels and T John C Boulton MJA 2001; 174: 561-564 For editorial comment, see Baur; see also Eckersley Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Paediatrics Abstract Objective: To review the prevalence of overweight and ...

Anthea M Magarey · Lynne A Daniels

The Profession Job-sharing in paediatric training in Australia: availability and trainee perceptions Charlotte M Whitelaw and Margot C Nash MJA 2001; 174: 407-409 For editorial comment, see Sewell; see also Gun Abstract - Methods - Results - Discussion - References - Authors' details - - More articles on Education Abstract Objective: To examine the current availability of job-sharing in paediatric training hospitals in Australia and to evaluate job-sharing from the trainees' perspective. Design: National survey with structured telephone interviews and postal questionnaires. Setting: The eight major paediatric training hospitals in Australia. Participants: Directors of Paediatric Physician Training (DPPTs) at each hospital (or a staff member nominated by them) provided information by phone interview regarding job-sharing. All paediatric trainees who job-shared in 1998 (n = 34) were sent written questionnaires, of which 25 were returned. Results: Hospitals differed in terms of whether a trainee was required to give a reason for wishing to job-share, and what reasons were acceptable. One hospital stated that two specialty units (Intensive Care and Neonatal Intensive Care) were excluded from job-sharing, and another stated that certain units were unlikely to be allocated job-sharers. The remaining six hospitals said that all units were available for job-sharing, but the majority of their trainees disagreed. Only one hospital had a cap on the number of job-share positions available yearly. Trainees perceived benefits of job-sharing to include decreased tiredness, increased enthusiasm for work, and the ability to strike a balance between training and other aspects of life. Trainees believed job-sharing did not adversely affect the quality of service provided to patients, and that part-time training was not of lower quality than full-time training. Conclusions: Job-sharing in Australian paediatric training hospitals varies in terms of the number of positions available, eligibility criteria, and which units are available for job-sharing. In our survey, trainees' experience of job-sharing was overwhelmingly positive. In Australia there is increasing interest in developing more flexibility in the postgraduate training and work environments of medical practitioners. Much of this interest comes from women, for whom "access to flexible training and work opportunities emerges as one of the most important determinants of career choice".1 In 1999, 70% of final-year paediatric trainees were women and their average age was 35 (Gary Disher, Senior Executive Officer, RACP Medical Workforce Advisory Committee, personal communication). It is likely that a significant number of women are balancing training with family commitments. A societal shift has also seen young male doctors increasingly working part-time for family reasons,1 and doctors of both sexes seeking part-time work for a variety of other reasons. Flexible medical training is well established in the United Kingdom,2-4 but relatively new in medical training in Australia. Case reports of job-sharing (ie, two people sharing the duties, responsibilities and benefits of one full-time job) in Australia have been positive;5,6 a study by Valentine and Martin7 found broad support for job-sharing among medical staff in a Perth children's hospital. All Australian medical colleges indicate that they offer part-time training.1 The Royal Australasian College of Physicians "strongly recommends" that basic paediatric training (the first three years) be full-time, while, for advanced training (the last three years), "work sharing is acceptable" and "part-time training is available".8 We set out to determine what is currently available in terms of job-sharing in paediatric training in Australia and whether job-sharing is satisfactory from the trainees' perspective. Methods Setting The eight major paediatric training hospitals in Australia took part in our study: The New Children's Hospital, John Hunter Hospital, Sydney Children's Hospital (NSW); Royal Children's Hospital/Monash Medical Centre (VIC); Adelaide Women's and Children's Hospital/Flinders Medical Centre (SA); Princess Margaret Hospital (WA); Royal Children's Hospital and Mater Misericordiae Children's Hospital (QLD). Interviews and questionnaires We approached the Directors of Paediatric Physician Training (DPPTs) at the eight major paediatric training hospitals. They (or a staff member nominated by them) answered standard questions by phone interview about job-sharing at their hospital. We designed a trainee questionnaire (incorporating some of the statements from a UK instrument9), which we sent to all paediatric trainees who job-shared in Australia in 1998. Multiple-choice and open questions were included. Responses to statements regarding job-sharing were obtained using a five-point Likert scale: strongly agree, agree, neutral, disagree, or strongly disagree. Responses were subsequently collapsed down to a three-point scale (agree, neutral, or disagree). A pilot was performed on job-sharers at our hospital. Confidentiality was assured. Results Trainee demographics Twenty-five of the 34 trainees job-sharing in paediatrics in 1998 returned questionnaires (74% response rate). (No information is available about non-respondents.) Twenty-three respondents were female and 2 male; 11 were in basic training, 11 in advanced training, and three were FRACP qualified but included because their job was usually offered as a training position. Job-share availability and eligibility The results of the hospital survey are presented in Box 1. The DPPT survey indicated that only one of the eight hospitals restricted the number of job-share positions available per year. Only one hospital formally excluded specific units (Intensive Care and Neonatal Intensive Care) from job-sharing. At another hospital, although no units were formally excluded, trainees had to get consultant approval in advance (several consultants known to be "resistant" were unlikely to be approached). The other six hospitals indicated that all units were available for job-sharing; however, 10 of 17 trainees at these hospitals did not believe this. Five of eight hospitals indicated that trainees were not required to give a reason for wishing to job-share. Hospitals that required or preferred to be given a reason tended to regard "childcare responsibilities" as a more acceptable reason for job-sharing than "exam preparation". Reasons for job-sharing When asked to cite their main reason for job-sharing, 13 trainees nominated childcare responsibilities, nine cited exam preparation, and three gave other reasons: personal ill health, desire for more leisure time, and completion of a Master of Public Health degree. Job-share history The time trainees had spent job-sharing in paediatric training positions to the end of 1998 varied from three to 36 months (mean, 18 months). Trainees sharing because of exam preparation shared for shorter periods (mean, 11 months) than those sharing for childcare reasons (mean, 25 months). Job-sharing had taken place in a variety of non-surgical units: General Medicine, Emergency, Neurology, Neonatology, Oncology, Gastroenterology, Endocrinology, Community Medicine, Child Psychiatry, Renal Medicine, Cardiology, Intensive Care, Rehabilitation, Metabolic Diseases, Respiratory Medicine and Allergy/Immunology. Sharing methods Trainees were asked to describe the way they shared jobs in 1998 and to comment on how well it worked for them. Several had used more than one method during the year. Sharing patterns included the following (the number of trainees who had used each method is given in brackets): three weeks on / three off (2); two weeks on / two off (5); one week on / one off (11); splitting the week (13). Trainees sharing for 2-3-week blocks of time commented that there were few continuity-of-care issues and that a block of time off allowed for concentrated study or holidays (none of these trainees were sharing for childcare). All trainees who split the week were sharing for childcare reasons. Some worked the same days each week (an arrangement they felt was optimal for family routine/childcare), and some swapped days during term (allowing for equal exposure to outpatient clinics, teaching rounds, etc). Trainees' perspective Trainees' responses to statements regarding job-sharing are shown in Box 2. Perceived benefits of job-sharing included decreased tiredness, increased enthusiasm for work, and the ability to strike a balance between training and other aspects of life. Trainees did not believe job-sharing adversely affected the quality of service provided to patients, or that part-time training was of lower quality than full-time training. However, some felt that job-sharers were viewed by consultants as "less committed" than full-time trainees. Regarding attendance at educational sessions, six of the 13 trainees sharing for childcare reasons believed they often missed sessions, while only one of the nine trainees sharing for exam preparation believed they did. Discussion Successful job-sharing in a clinical training position must be of educational value to the trainee, provide quality care to patients and their families, and not have a negative impact on other staff. The experience of the job-sharers in our survey was overwhelmingly positive; however, the perceptions of trainees may be biased by the considerable personal investment most have in their positions. It should also be borne in mind that the accuracy of information provided by DPPTs may vary according to their level of involvement with job-sharing. As the total number of respondents in our survey was small, any conclusions must be somewhat tentative, but we believe some general trends are clear. The legality of requiring trainees to provide an "acceptable" reason for wishing to work part-time is questionable; as is the practice of giving trainees wishing to share for childcare reasons precedence over trainees with other reasons for sharing. Although most hospitals stated that all units were available for job-sharing, the majority of their trainees disagreed. Perhaps trainees are misinformed in some instances. An alternative and more likely explanation is that hospitals, wishing to appear progressive, claim that all units are available but do not appoint job-sharers to reluctant consultants. Trainees sharing for short periods (usually exam candidates) can compensate for restricted opportunities when they return to full-time training, but those sharing for longer periods (ie, those with childcare responsibilities) can not. Trainees in the latter group are also more likely to miss educational sessions, presumably because family commitments prevent them from attending on certain days. Demand for flexible training arrangements is likely to rise in future. Specialist medical colleges must become directly involved in the development of flexible training positions rather than simply providing reluctant permission. Hospitals must formulate clear policies regarding job-sharing and make this information available to prospective employees. Further evaluations of job-sharing are needed to ensure arrangements are satisfactory for all concerned. References Australian Medical Workforce Advisory Committee. Influences on participation in the Australian medical workforce. Sydney: AMWAC, 1998. Goldberg I. Postgraduate medical education and flexible training. Br J Hosp Med 1996; 56: 241-242. Goldberg I, Paice E. New approaches to job sharing of training posts in the North Thames region. Br J Hosp Med 1997; 58: 193-196. Montgomery S. Part time work: one year's job share in Bristol. BMJ 1984; 289: 1240-1241. York J. Job sharing — it works! Fellowship Affairs. RACP. 1993; 12(1): 33. Preston S. Job sharing — the trainee's perspective. Fellowship Affairs. RACP. 1993; 12(1): 34. Valentine J, Martin C. Job Sharing at a children's hospital. BMJ 1996; 312: 115-116. The Royal Australasian College of Physicians. Requirements for physician training guidelines. Sydney: RACP, 1998. Fiander A. Evaluation of flexible senior registrar training in obstetrics and gynaecology. Br J Obstet Gynaecol 1995; 102: 461-466. (Received 28 Aug 2000, accepted 18 Jan 2001) Authors' details Royal Children's Hospital, Melbourne, VIC. Charlotte M Whitelaw, MB BS, B MedSc, Advanced Paediatric Trainee; Margot C Nash, FRACP, MD, Director of Paediatric Physician Training. Reprints will not be available from the authors. Correspondence: Dr C M Whitelaw, Department of General Paediatrics, Royal Children's Hospital, Flemington Road, Parkville, VIC 3052. Make a comment 1: Availability of job-sharing positions for paediatric trainees in eight major Australian paediatric hospitals in 1998 Hospital No. of job- sharers in 1998 No. of job-share positions avail- able yearly Units unavailable for sharing (DPPT response) A 12 No set limit ICU and NICU B 2 No set limit None C 0 No set limit At consultants' discretion D 6 No set limit None E 4 No set limit None F 4 2 None G 4 No set limit None H 2 No set limit None No. of trainees who believe some units at their hospital unavailable (total respondents) Requirement for trainee to give reason for job- sharing (DPPT response) 3 (8) No reason required 0 (1) No reason required na No reason required 5 (6) No reason required 3 (4) No reason required 1 (2) Reason required 0 (3) Reason preferred 1 (1) Reason required DPPT = Director of Paediatric Physician Training. ICU = intensive care unit. NICU = neonatal intensive care unit. na = not applicable. Back to text 2: Paediatric trainee responses to job-share statements (n=25) Statement Agree/neutral/disagree (% of respondents) Job-sharing allowed me to strike a balance between my training and other things in my life 100 / 0 / 0 I would recommend job-sharing to other trainees 100 / 0 / 0 I found discussions with my partner during hand-over provided an opportunity to compare and contrast management decisions and share knowledge 88 / 8 / 4 I found discussions with my partner during hand-over were of benefit in solving clinical problems (two heads better than one) 80 / 12 / 8 While job-sharing I felt less tired at work than when I worked full-time 80 / 8/ 12 While job-sharing I was more likely to read up on clinical problems I encountered at work than when I worked full-time 68 / 24 / 8 Job-sharers are viewed as less committed than full-time trainees by consultants 68 / 24 / 8 While job-sharing I felt I had "more to give" to families than when I worked full-time 68 / 16 / 16 While job-sharing I felt more enthusiastic about going to work than when I worked full-time 64 / 36 / 0 While job-sharing I felt more willing to spend time teaching medical students and junior staff than when I worked full-time 52 / 24 / 24 Job-sharers have limited training opportunities compared with full-time trainees 44 / 12 / 44 While job-sharing I often missed important educational sessions during the week 28 / 50 / 22 Job-sharers are viewed as less committed than full-time trainees by their peers 24 / 24 / 52 Arranging a job-share in 1998 was difficult 16 / 12 / 72 Job-sharing has adversely affected my career prospects 16 / 8 / 76 Job-sharing is an easy option 12 / 32 / 56 The quality of job-share training is not as good as full-time training for half as long 8 / 16 / 76 I was often unable to find out what happened to my patients after I handed them over 4 / 4 / 92 The quality of service provided to patients and their families is adversely affected by job-sharing 0 / 4 / 96 Being unable to follow all patients until the end of their hospital stay adversely affected my training 0 / 0 / 100 Inadequate hand-over of information was a significant problem 0 / 0 / 100 I regret job-sharing 0 / 0 / 100 Back to text

Charlotte M Whitelaw · Margot C Nash

MJA 2001; 174: 288-292 Abstract - Recommendations 1A - Recommendations 1B - Recommendations 2 - Recommendations 3 - Recommendations 4 - References - Authors' details - - More articles on Obstetrics & gynaecology and women's health Abstract Zoster immunoglobulin (ZIG) should be offered to pregnant, varicella-seronegative women with significant exposure to varicella-zoster virus (VZV) (chickenpox) infection. Oral aciclovir prophylaxis should be considered for susceptible pregnant women exposed to VZV who did not receive ZIG or have risk factors for severe disease. Intravenous aciclovir should be given to pregnant women who develop complicated varicella at any stage of pregnancy. Counselling on the risk of congenital varicella syndrome is recommended for pregnant women who develop chickenpox. ZIG should be given to a baby whose mother develops chickenpox up to 7 days before delivery or up to 28 days after delivery. Intravenous aciclovir should be given to babies presenting unwell with chickenpox, whether or not they received ZIG. Breastfeeding of babies infected with or exposed to VZV is encouraged. A mother with chickenpox or zoster does not need to be isolated from her own baby. If siblings at home have chickenpox, a newborn baby should be given ZIG if its mother is seronegative. The newborn baby does not need to be isolated from its siblings with chickenpox, whether or not the baby was given ZIG. After significant nursery exposure to VZV, ZIG should be given to seronegative babies and to all babies born before 28 weeks' gestation. Varicella-zoster virus (VZV) (chickenpox) infection can cause severe morbidity in the pregnant woman, the fetus, and the newborn baby. 1. Management of VZV infection in pregnancy The implications of primary VZV infection in pregnancy for the mother and for the fetus vary with the period of gestation. For the mother, the risk of adverse effects is greatest in the third trimester, whereas for the fetus the risk is greatest in the first and second trimesters. A. Maternal risk In normal adults, the mortality and morbidity of primary VZV infection is greater than in children. Only about 2% of all cases occur in adulthood, but they account for 25% of all VZV-related deaths.1 Pneumonitis is 25 times more common in adults.1,2A 1995 Australian study assessed VZV seronegativity in women presenting to antenatal clinics and found 22% of women aged 14-19 years, 14% of those aged 20-24 years, 5% of those aged 25-29 years and 2% of those aged 30 years and over had not had previous exposure and were therefore susceptible to VZV infection.3 Anecdotally, chickenpox infection in pregnancy is more severe than in non-pregnant adults, but there is scant supporting evidence.4 A survey of 164 000 pregnancies in the United Kingdom described 98 women with chickenpox, of whom seven developed severe illness and two died.5 The UK confidential inquiry into maternal deaths from 1985 to 1997 reported only seven deaths associated with VZV in pregnancy, all of which occurred in the second half of pregnancy. Other reports have also suggested increased severity of illness in the second half of pregnancy.6 Zoster immunoglobulin (ZIG), given prophylactically at the time of exposure, is known to prevent or reduce the severity of chickenpox.7-9 Aciclovir, an antiviral agent, shortens the duration of illness in young adults if administered during the incubation period or within 24 hours of the onset of the rash.10,11 When administered prophylactically (7 to 9 days after family exposure) it may be up to 84% protective against infection and able to modify the illness in the remaining family members.12 Although aciclovir is not licensed for use in pregnancy (because of concerns about adverse fetal effects), there have been no reports of adverse effects among hundreds of cases over several years of monitoring.13 Management algorithms (Boxes 1 and 2) have been devised for varicella exposure in pregnancy. Recommendations 1A Zoster immunoglobulin (ZIG) (Box 3) All pregnant women who have significant exposure to VZV infection (defined as "living in the same household as a person with active chickenpox or herpes zoster or face-to-face contact with a person with chickenpox or uncovered zoster for at least 5 minutes"), who have no history of chickenpox and who are seronegative (or serological testing is not readily available), should be offered ZIG.4-6 (E3) ZIG should be administered within 72 hours of exposure for maximal effect, although it may provide some benefit up to 96 hours after exposure for immunocompromised subjects.14 (E3) ZIG is ineffective, and should not be given, once clinical illness is established.15 (E4) Aciclovir (Box 3) There is no high level evidence on the use of aciclovir in pregnancy. Based on consensus view, we recommend: Consideration should be given to using oral aciclovir prophylaxis for susceptible pregnant women with significant exposure (defined above) who have not received ZIG, or who have any underlying risk factors, such as chronic lung disease, cigarette smoking,16 systemic corticosteroid treatment,17 impaired immunity,18 or are in the second half of pregnancy (Box 3). (E4) Intravenous aciclovir should be given for varicella pneumonitis or other complications at any stage of pregnancy.4,6,19 These complications include respiratory symptoms, neurological symptoms, haemorrhagic rash and/or continued fever or appearance of new lesions after 6 days.4 (E4) Extrapolation from data in children suggests that patients receiving systemic corticosteroid therapy or those with underlying immunodeficiency should be treated with intravenous aciclovir at the earliest sign of chickenpox.18,20,21 (E4) Management of delivery of the baby There is no evidence that ending the pregnancy speeds maternal recovery. Expedited delivery should only be considered for fetal compromise or if the gravid uterus is thought to be critically impairing maternal ventilation. B. Fetal risk Chickenpox in pregnancy may result in fetal varicella which is usually benign and self-limiting.1 Occasionally, it produces a characteristic pattern of abnormalities known as "congenital varicella syndrome" (CVS).22,23 CVS very occasionally follows maternal zoster infection.5 The risk of CVS after first-trimester maternal chickenpox was estimated from prospective studies as 2.2% (range, 0-9%; 95% CI, 0-4.6%).24-26 In a large prospective European study, the incidence of CVS was 0.4% after maternal chickenpox in the first 12 weeks of pregnancy, rising to 2% between weeks 13 and 20.24 After 20 weeks the risk is far lower, although isolated cases have been reported.3 The incidence of CVS in Australia is 1 in 107 000 pregnancies.27 The congenital defects are usually severe, causing cicatricial skin lesions, limb hypoplasia or paresis, microcephaly and ophthalmic lesions.22,24,28 It is hypothesised that these lesions result from virus reactivation in utero or disseminated zoster infection.2,29 Herpes zoster (shingles) occurs in early childhood in about 1% of otherwise asymptomatic infants exposed to maternal varicella during the second or third trimester.24At present, there is no reliable marker of in-utero virus reactivation or the predicted development of CVS. Serological tests are an insensitive marker of fetal VZV infection and subsequent fetal damage.24 The polymerase chain reaction (PCR) has been used to detect VZV in amniotic fluid: a negative PCR is associated with a favourable outcome, but a positive PCR correlates poorly with the development of CVS.26 As amniocentesis carries a risk of fetal loss, amniotic fluid PCR has a limited role. While ZIG may prevent or modify the course of chickenpox in pregnancy, it may not abolish the risk of fetal infection. Therefore, close ultrasound monitoring for the development of fetal abnormalities after maternal chickenpox or administration of ZIG in pregnancy is recommended. Recommendation 1B Counselling on the risk of congenital varicella syndrome is recommended for women who develop chickenpox during pregnancy. (E4) 2. Management of babies of mothers with perinatal chickenpox Maternal chickenpox in the peripartum period poses a risk of severe neonatal varicella, with a mortality rate up to 30%.30,31 The increased peripartum severity is attributed to a large transplacental inoculum of virus in the absence of protective maternal antibody. The timing of maternal infection in relation to delivery determines the risk to the infant.31 Infection with onset more than seven days before delivery ensures adequate transplacental passage of specific anti-VZV antibody to protect the infant.32 Infection with onset 7 days or less before delivery puts the infant at risk of severe neonatal varicella. Passive immunisation of the baby by giving ZIG immediately after delivery prevents or attenuates neonatal varicella and is essential.7,33 Maternal varicella starting 1-2 days after delivery is also associated with an increased risk of severe neonatal varicella from transplacental spread of the virus.30 However, babies of seronegative mothers exposed postnatally to varicella in the first 28 days after delivery apparently have increased risk of severe illness compared with older infants.33 If the mother develops chickenpox postnatally, her baby is evidently seronegative. Therefore, ZIG is recommended for seronegative babies up to 28 days old exposed to varicella.34,35 Recommendations 2 ZIG is indicated for the baby if maternal varicella develops up to 7 days before delivery or if the mother develops chickenpox up to 28 days after delivery.7,15,31-33 (E3) ZIG should be given to the baby as early as possible after delivery or exposure, but must be within 72 hours.31,32 (E4) Maternal herpes zoster is not an indication for ZIG administration to the baby. (E4) Clinical follow-up of infants receiving ZIG is essential and they should be admitted to hospital if any rash develops, because severe varicella can still occur despite passive immunisation.35,36 (E4) Intravenous aciclovir should be administered (a) to babies presenting with chickenpox who are unwell (eg, poor feeding, tachypnoea), whether or not they received ZIG; (b) to any high risk neonate who develops chickenpox and who inadvertently did not receive ZIG prophylaxis or for whom it was delayed beyond 24 hours; and (c) to immunocompromised neonates who develop chickenpox, including those who are premature or being treated with corticosteroids.18,21 (E4) Routine aciclovir prophylaxis in conjunction with ZIG is not currently recommended in the neonatal population, due to lack of evidence. (E4) Breastfeeding of infected or exposed babies is encouraged. (E4) A mother and/or her baby with active vesicles should be isolated from other mothers and babies, but an infected mother does not need to be isolated from her own baby. (E4) 3. Management of neonates exposed to VZV infection on the postnatal wards or at home The commonest neonatal exposure to VZV is when one or more siblings develops chickenpox in the weeks after delivery. The risk of the newborn developing severe disease from postnatal exposure is considerably less than from transplacentally acquired varicella, but some babies with postnatal exposure will develop severe disease.34 The risk to the newborn baby is determined primarily by the presence or absence of transplacentally acquired maternal IgG antibody. If the mother has had chickenpox, the risk from siblings is negligible. If not, the baby should be given ZIG, which will minimise the risk.34,35 Recommendations 3 ZIG should be administered to a baby up to 28 days old exposed to VZV if the mother is seronegative, her serostatus can not be determined, or if the infant was born at or before 28 weeks' gestation.15,37 (E3) A newborn baby does not need to be isolated from its siblings with chickenpox, whether or not the baby was given ZIG. (E4) Parents should be advised that medical attention should be sought if any signs of chickenpox develop. (E4) Admit to hospital for aciclovir treatment if baby becomes unwell (eg, poor feeding, tachypnoea). (E4) The role of prophylactic aciclovir is unproven. 4. Management of VZV exposure within the neonatal unit VZV poses a particular threat in this setting, because babies born prematurely are relatively deprived of the usual third-trimester transfer of transplacental antibodies.37-39 Spread of VZV is primarily by the respiratory route, so isolation in a separate room is desirable for babies with pneumonitis, and essential if they require artificial ventilation. Staff handwashing is important in reducing spread of the virus. VZV vaccines are now available in Australia, and immunisation of susceptible staff is strongly recommended.35 A significant exposure in the neonatal unit or on the postnatal ward is defined as:10,15 patient sharing the same open ward as a person with chickenpox or zoster; face-to-face contact with a person with chickenpox or zoster for at least 5 minutes; and contact for one hour or more with person (staff or patient) with chickenpox lesions or who developed lesions up to 48 hours later. All staff who have had significant exposure to an index case (see above) and who do not have a history of previous chickenpox infection or of VZV vaccination should have serological tests. If they are VZV antibody negative, they should be removed from clinical duties from days 7-21 after exposure (days 7-28 if they receive ZIG). Recommendations 4 Infants born after 28 weeks' gestation15 should only be given ZIG if they have had significant exposure (defined above) and serological tests show the mother to be seronegative. (E4) All infants born at or before 28 weeks' gestation or born weighing under 1000 g11,37,38 with significant exposure should be given ZIG regardless of the results of serological testing of the mother. (E4) Quarantine of cases should continue until all lesions have crusted.15 (E3) Quarantine of contacts should be from days 7-21 after exposure, and from days 7-28 after exposure if they received ZIG.15 (E3) Although quarantine of cases and those considered to have significant contact is recommended, this should not compromise medical and nursing care of a sick infant. (E4) Infants with pneumonitis requiring ventilation must be isolated. Where isolation facilities are unavailable, cases should be transferred to a unit with isolation facilities. (E4) Aim to discharge all patients requiring quarantine from hospital as soon as possible. (E4) Background and evidence basis of recommendations This position statement was circulated to all members of the Australasian Subgroup in Paediatric Infectious Diseases (ASPID) for comments. The comments were analysed by the authors, discussed with colleagues, and subsequent versions incorporating the comments were re-circulated to all ASPID members. The recommendations of ASPID on the management of VZV exposure and infection in pregnancy and the neonatal period are endorsed by the Royal Australian and New Zealand College of Obstetricians and Gynaecologists. The recommendations are based on the following levels of evidence (simplified from the NHMRC's "Quality of evidence ratings")40 E1 Level I Systematic review or meta-analysis of all relevant randomised controlled trials (RCTs) E2 Level II Well-designed RCTs E3 Level III Well-designed cohort or case-control studies E4 Level IV Consensus opinion of ASPID members References Joseph CA, Noah ND. Epidemiology of chickenpox in England and Wales, 1967-85. BMJ 1988; 296: 673-676. Centers for Disease Control. Varicella-zoster immune globulin for the prevention of chickenpox. MMWR Morb Mortal Wkly Rep 1984; 33: 84-90. Chant KG, Sullivan EA, Burgess MA, et al. Varicella-zoster virus infection in Australia. Aust N Z J Public Health 1998; 22: 413-418. Gilbert GL. Chickenpox during pregnancy. BMJ 1993; 306: 1079-1080. Nathwani D, Maclean A, Conway S, Carrington D. Varicella infections in pregnancy and the newborn. A review prepared for the UK Advisory Group on Chickenpox on behalf of the British Society for the Study of Infection. J Infect 1998; 36 Suppl 1: 59-71. Smego RA Jr, Asperilla MO. Use of acyclovir for varicella pneumonia during pregnancy. Obstet Gynecol 1991; 78: 1112-1116. Brunell PA, Ross A, Miller LH, Kuo B. Prevention of varicella by zoster immune globulin. N Engl J Med 1996; 280: 1191-1194. Gershon AA. Prevention and treatment of varicella zoster virus infection. Pediatr Infect Dis J 1984; 3 (Suppl): 34-36. Bose B, Kerr M, Brookes E. Varicella zoster immunoglobulin to prevent neonatal chickenpox. Lancet 1986; 1: 449-450. Lin TY, Huang YC, Ning HC, Hsueh C. Oral acyclovir prophylaxis after intimate contact. Pediatr Infect Disease J 1997; 16: 1162-1165. Balfour HH Jr, Rotbart HA, Feldman S, et al. Aciclovir treatment of varicella in otherwise healthy adolescents. The Collaborative Aciclovir Varicella Study Group. J Pediatr 1992; 120: 627-633. Azano Y, Yoshikawa T, Suga S, et al. Postexposure prophylaxis of varicella in family contact by oral acyclovir. Pediatrics 1993; 92: 219-222. Andrews EB, Yankasksas BC, Cordero JF, et al. Aciclovir in pregnancy registry: 6 years' experience. The Acyclovir in Pregnancy Registry Advisory Committee. Obstet Gynecol 1992; 79: 7-13. US Department of Health and Human Services. Prevention of Varicella: Recommendations of the Advisory Committee on Immunisation Practices. MMWR Morb Mortal Wkly Rep 1996; 45 (RR-11): i-36. American Academy of Pediatrics. Varicella-zoster infection. In: Peter G, editor. 2000 Red Book: Report of the Committee of Infectious Diseases, 25th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2000: 624-638. Grayson ML, Newton-John H. Smoking and varicella pneumonia. J Infect 1988; 16: 312. Rice P, Simmons K, Carr R, Banatvala J. Near fatal chickenpox during prednisolone treatment. BMJ 1994; 309: 1069-1070. Balfour HH. Intravenous acyclovir therapy for varicella in immunocompromised children. J Pediatr 1984; 104: 134. Haake DA, Zakowski PC, Haake DL, Bryson YJ. Early treatment with acyclovir for varicella pneumonia in otherwise healthy adults. Rev Infect Dis 1990; 12: 788-797. Feldman S, Hughes WT, Daniels CB. Varicella in children with cancer: 77 cases. Pediatrics 1975; 56: 388-397. Reiches NA, Jones JF. Steroids and varicella. Pediatrics 1993; 92: 288-289. La Foret, Lynch LL. Multiple congenital defects following maternal varicella. N Engl J Med 1947; 236: 534-537. Scharf A, Scerr O, Enders G, Helftenbein E. Virus detection in the fetal tissue of a premature delivery with congenital varicella syndrome. A case report. J Perinat Med 1990; 18: 317-322. Enders G, Miller E, Cradock-Watson J, et al. Consequences of varicella and herpes zoster in pregnancy: prospective study of 1739 cases. Lancet 1994; 343: 1548-1551. Pastuszak A, Levy M, Schick B, et al. Outcome after maternal varicella infection in the first 20 weeks of pregnancy. N Engl J Med 1994; 330: 901-905. Mouly F, Mirlesse V, Meritet J, et al. Prenatal diagnosis of fetal varicella zoster virus infection with polymerase chain reaction of amniotic fluid in 107 cases. Am J Obstet Gynecol 1997; 177: 894-898. Forrest JM, Mego S, Burgess MA. Congenital and neonatal varicella in Australia. J Paediatr Child Health 2000; 36: 108-113. Higa K, Dan K, Manabe H. Varicella-zoster virus infections during pregnancy: hypothesis concerning the mechanisms of congenital malformations. Obstet Gynecol 1987; 69: 214-222. Birthistle K, Carrington D. Fetal varicella syndrome -- a reappraisal of the literature. A review prepared for the UK Advisory Group on Chickenpox on behalf of the British Society for the Study of Infection. J Infect 1998; 36 Suppl 1: 25-29. De Nicola LK, Hanshaw JB. Congenital and neonatal varicella. J Pediatr 1979; 94: 175-176. Erlich RM, Turner JAP, Clarke M. Neonatal varicella. J Pediatr 1958; 53: 139-147. Miller E, Cradock-Watson JE, Ridehalgh MKS. Outcome of newborn babies given anti-varicella zoster immunoglobulin after perinatal maternal infection with varicella zoster virus. Lancet 1989; 2: 371-373. Hanngren K, Grandien M, Granstrom G. Effect of zoster immunoglobulin for varicella prophylaxis in the newborn. Scand J Infect Dis 1985; 17: 343-347. Rubin L. Disseminated varicella in the neonate and implications for immunoprophylaxis in neonates exposed to varicella. Pediatr Infect Dis J 1986; 56: 100-102. Australian Technical Advisory Group on Immunisation, Commonwealth Department of Health and Aged Care. The Australian immunisation handbook. 7th edition. Canberra: NHMRC/AGPS, 2000: 231-238. Reynolds L, Struik S, Nadel S. Neonatal varicella: varicella zoster immunoglobulin (VZIG) does not prevent disease. Arch Dis Child Fetal Neonatal Ed 1999; 81: F69-F70. Linder N, Waintraub I, Smetana Z, et al. Placental transfer and decay of varicella-zoster virus antibodies in preterm infants. J Pediatr 2000; 137: 85-89. Conway SP, Dear PRF, Smith I. Immunoglobulin profile of the preterm baby. Arch Dis Child 1985; 60: 208-212. Wang E, Prober C, Arvin A. Varicella zoster virus antibody titres before and after administration of zoster immune globulin to neonates in an intensive care nursery. J Pediatr 1985; 103: 113-114. National Health and Medical Research Council. How to use the evidence: assessment and application of scientific evidence. Table 1.3. <http://www.health.gov.au/nhmrc/publicat/pdf/cp69.pdf> (accessed February 2001). Authors' details King George V Hospital, Sydney, NSW. Anne-Marie Heuchan, MB, MRCP, Fellow in Neonatal Medicine. The Children's Hospital at Westmead, Sydney, NSW. David Isaacs, MD, FRACP, FRCPCH, Paediatric Infectious Diseases Physician; and Clinical Professor, University of Sydney. Reprints will not be available from the authors. Correspondence: Professor D Isaacs, Department of Immunology and Infectious Diseases, The Children's Hospital at Westmead, PO Box 4001, Westmead, NSW 2145. davidiATchw.edu.au Make a comment 1: Management of significant exposure* to varicella zoster virus (VZV) during pregnacy (Algorithm 1) *Significant exposure is defined as living in the same household as a person with active chickenpox or herpes zoster or face-to-face contact with a person with chickenpox or zoster for at least 5 minutes. †Risk factors for severe maternal VZV infection are second half of pregnancy, underlying lung disease, immunocompromised, and smoker. See Box 3 for dosage of zoster immunoglobulin (ZIG) and aciclovir. Recommendations based on consensus view. Back to text 2: Management of chickenpox in pregnancy (Algorithm 2) *Complications: respiratory symptoms, haemorrhagic rash, persistent fever >6 days, and new lesions developing >6 days. †At high risk are those women in the second half of pregnancy with underlying lung disease, who are immunocompromised, and who smoke. See Box 3 for doses of aciclovir. Recommendations based on consensus view. Back to text 3: Administration and dosage of zoster immunoglobulin (ZIG) and aciclovir Zoster immunoglobulin High-titre ZIG is available from the Red Cross Blood Transfusion Service in Australia on a restricted basis for the prevention of VZV infection in high-risk subjects. Each vial contains 2mL (16% solution of gammaglobulin fraction of human plasma from donors with high titre of varicella antibodies + thiomersal 0.01% w/v). The recommended dose is 2mL for children 0-5 years, 4mL for children 6-12 years and 6mL for adults.32 Administration is by intramuscular injection, with few adverse effects other than local discomfort reported. This can be lessened if the ZIG is at room temperature when administered. ZIG should never be given intravenously.36 Aciclovir Aciclovir appears to be a safe and relatively well tolerated drug, although it may impair renal function if given to patients who are not adequately hydrated.17 It is not licensed for use in pregnancy but appears to be safe12 and its use is indicated in the high-risk situations outlined. The recommended intravenous dose for treating VZV infection in adults and infants is 10-20mg/kg every 8 hours. The oral dose for adults is 800mg five times daily. The use of oral aciclovir in neonates is not recommended. Back to text

on behalf of the Australasian Subgroup in Paediatric Infectious Diseases of the Australasian Society for Infectious

Defining Moments In Medicine Paediatrics MJA 2001; 174: 16-17 Australian Paediatric Association: Founded in 1950, the Association was of vital importance to the developing specialty of paediatrics in Australia. It became the Australian College of Paediatrics in 1978 and then joined with the Royal Australasian College of Physicians in 1998 to form the Division of Paediatrics and Child Health. Chemotherapy for childhood leukaemia: Melbourne paediatrician John Colebatch published the first Australian controlled trial in 1950, testing a chemotherapeutic drug in children with acute lymphatic leukaemia. This was followed by multicentre trials in Australia of treatment for leukaemia and other childhood malignancies. A majority of children with acute leukaemia can now be cured, and national and international collaborative randomised controlled trials have become the standard method for evaluating treatment. Management of premature infants: Recognition by Kate Campbell (Melbourne paediatrician) in 1951 that high concentrations of ambient oxygen caused retrolental fibroplasia in premature infants led to a major change in the management of premature infants and was an important milestone in the development of neonatology as a paediatric subspecialty. Introduction of triple antigen: Triple antigen was introduced to Australia in 1953. In 1957, the Australian Paediatric Association's recommendation to the National Health and Medical Research Council that all infants should be vaccinated routinely with triple antigen against diphtheria, pertussis and tetanus was accepted. Liberal hospital visiting times: Daily visiting by parents was introduced at the Royal Children's Hospital, Melbourne, in 1953, and two years later the Royal Alexandra Hospital for Children, Sydney, introduced extended visiting. This substantially reduced the emotional trauma of hospital admissions. Previously, visiting had been restricted in the erroneous belief that cross-infection would be increased, and the children would be upset and more difficult to care for. Vaccination for Aboriginal children: In 1954, to help reduce communicable diseases -- whooping cough, diphtheria and tetanus -- a routine vaccination program was commenced for Aboriginal children in the Northern Territory. Nasotracheal intubation: Melbourne anaesthetists Ian McDonald and John Stocks, in the British Journal of Anaesthesia in 1965, described prolonged nasotracheal intubation in infants and children, which was crucial in the development of intensive care for infants and children. It provided an alternative to tracheostomy for artificial ventilation, which had a very high complication rate. Australian Paediatric Journal: Established in 1965 by the Australian Paediatric Association, the Australian Paediatric Journal subsequently became the Journal of Paediatrics and Child Health. It publishes quality research in paediatrics from Australia and the Asia-Pacific region. Management of childhood asthma: From 1969 onwards, Howard Williams and Ken McNicol (of Melbourne's Royal Children's Hospital Research Foundation) published a series of articles clarifying the prevalence and natural history of asthma in children. These articles substantially changed the way childhood asthma was managed. They emphasised the importance of basing treatment on the pattern of symptoms, and the use of bronchodilators, rather than antibiotics, in the treatment of wheezy episodes. Preventing childhood injury: From 1969 regulations and programs were introduced in Australia to reduce morbidity and mortality of childhood injury (eg, safety standards for children's nightwear, other programs to reduce the risk of burns, compulsory child restraints in motor vehicles, and legislation to require that crash helmets be worn by bicyclists). Rotavirus in viral gastroenteritis: In 1973, Ruth Bishop, Ian Holmes, Geoff Davidson and colleagues (from the Royal Children's Hospital, Melbourne, and the Department of Microbiology, University of Melbourne) showed that rotavirus was the most important cause of viral gastroenteritis in infants and children. This was an important step in the understanding of this major worldwide cause of childhood morbidity and mortality. Vaccines are being developed in attempts to prevent this infection. Emergency transport services: The Neonatal Emergency Transport Service and the Paediatric Emergency Transport Service were established in Melbourne in 1976 and 1980, respectively. These two services have reduced morbidity and mortality from critical illness in neonates, infants and children presenting away from major tertiary centres. Fragile X syndrome: Recognition of fragile sites in chromosomes and identification in 1977 by Grant Sutherland (Adelaide Children's Hospital) of the fragile X syndrome, one of the more common causes of mental retardation, has led to an understanding of its familial nature and to in-vitro diagnosis. Adolescent Health Survey: Undertaken in Melbourne in 1992, this survey of 4000 adolescents provided essential information on risk factors for health problems and prevalence of such problems in adolescents. It was crucial in establishing adolescent health as an independent specialty with an academic base. Australian Childhood Immunisation Register: Established in 1995, the Register is an essential database of the vaccination status of Australian children and allows those whose vaccination is incomplete to be identified. There are now incentives for parents to to have their children fully vaccinated. Peter D Phelan Emeritus Professor of Paediatrics University of Melbourne, Melbourne, VIC Don M Roberton McGregor Reid Professor of Paediatrics University of Adelaide, Adelaide, SA Mike South Director, Department of General Medicine Royal Children's Hospital Melbourne, VIC and Associate Professor, Department of Paediatrics University of Melbourne, VIC Above photograph courtesy Royal Children's Hospital Archive, Victoria. Photographer: Laurie Richards. Make a comment

Peter D Phelan · Don M Roberton · Mike South

Medicine and the Community A swimming program for children with asthma Does it improve their quality of life? Colleen P Wardell and Clair Isbister MJA 2000; 173: 647-648 Methods - Results - Discussion - References - Authors' details - - More articles on Paediatrics Introduction The Asthma Foundation of NSW started the Asthma Children's Swimming Program in 1964. Previously, it was observed that many asthmatic children tended to be excluded from sport and often had difficulty learning to swim in available "learn to swim" programs. They were generally not physically fit. Many were mouth breathers, often with some chest deformity and chronic rhinitis. Even when adequately medicated, respiration was inefficient, with decreased movement of the diaphragm, and nasal obstruction and recurrent ear and throat infections. Many had low body fat, giving poor insulation against cold water pool conditions, which appeared to aggravate wheezing and exercise-induced asthma. Yet some of Australia's Olympic swimmers of the time (such as Dawn Fraser and Jon Henricks) were asthmatic, which suggested that asthma need not be a barrier to physical fitness. The value of swimming for asthmatics was supported by articles in medical journals1,2 and anecdotal evidence. It was a low weight bearing exercise, potentially life saving, easily supervised, and suited to individual tuition and practice. A swimming program also presented an educational opportunity to teach about health and asthma and efficient breathing. Logically and physiologically, swimming appeared the most suitable exercise relevant to respiratory and overall well being. The program developed by the Asthma Foundation of NSW modified the teaching methods of the day to meet the special needs of asthmatic children (Box 1). By 1994 the program had expanded from one to 36 pools throughout metropolitan and rural NSW. In those 30 years about 25 000 children were taught by 2000 volunteer instructors. This kind of growth, based on the voluntary involvement of unpaid instructors and parents of asthmatic children, is itself a measure of success. The anecdotal evidence of those involved in the program is that it improves health, reduces the frequency of asthma attacks and improves the children's quality of life. The NSW Department of Sport and Recreation had acknowledged the value of the program, and included it as an extension course for AUSTSWIM instructors. In 1994, the Asthma Foundation of NSW allocated $10 000 for an evaluation of the swimming program. That study was a retrospective survey involving a limited statistical analysis and a qualitative evaluation of the effect on the whole child.3 In this article we present the main findings of that evaluation, a full report of which is available from the Foundation.4 Methods Asthma is a multifactorial condition with many variables, including severity, seasonal incidence, and multiple trigger factors, such as allergy, climate, and infection. Medical treatment and school and home management differed, as did the geographic distribution of pools. Under these circumstances, it was not possible to assemble a suitable control group for a case-control study. After studying the relevant literature, we concluded that a quality-of-life study by means of questionnaires administered to parents and volunteer instructors was the most appropriate method. Two rural and three metropolitan swimming groups were selected for the study. Children were randomly selected from those who had attended for over one year (to avoid a seasonal influence on results). Three questionnaires were prepared: two for parents and one for instructors. The first parental questionnaire related to the child's condition on entering the program, and the second to the child's condition at the time of the study. They both asked for information about hospitalisation and doctor's visits; physical signs such as mouth breathing, snoring, and chest deformity; general health; other illnesses and allergies; peak flow readings; severity of asthma; school attendance and performance; height and weight; and participation in other swimming classes and sport. The instructor's questionnaire asked about their participation, how and why they did voluntary work, and their observations on the children and the program. Results One hundred and twenty-three sets of questionnaires were distributed to parents, and 87 sets were returned. However, it was found that one rural swimming group had not adhered strictly to the swimming instruction method and had to be excluded, leaving 73 sets for the survey. These were for 38 boys and 35 girls, with an average time of 2.4 years in the program. The main quantifiable results are shown in Box 2. Asthma medication and medication dosage were highly variable in this group of children. Parents of half the children reported a change in medication since starting the swimming program, with two-thirds showing a decrease. Almost all parents who answered the questionnaire were satisfied with the program and reported that the changes in the children had improved the quality of life of the whole family. Appreciation was expressed for the program, the value of the year-round availability, the individual tuition, and the caring attitude of the volunteers. Also valued was the opportunity to discuss common problems with other parents of asthmatic children, and the asthma education provided. Instructors had joined the program for many reasons and some had stayed over 25 years. They enjoyed their participation, and felt that they were rewarded by the children's achievements and the improvement seen in their general health and attitudes. They commented that many children were timid and anxious at first, and needed much coaxing. This made the children's eventual success and increase in confidence and self-esteem even more rewarding for the instructors. It was often noted that children who could swim before joining the program were breathing inefficiently. When this was corrected they swam longer distances with greater ease. Discussion The results of this study suggest that the program has achieved its purpose and justified its continued demand. For many people the program can improve quality of life and asthma management, and reduce medication, visits to doctors, and hospitalisations. Peak flow meter readings taken at every session have been a useful guide for the instructor regarding the child's possible need for pre-swim medication. Huang et al claim improvement in peak flow readings in a swimming program for asthmatic children conducted in the USA,5 but our study did not find significant change in this variable. Instead, the program produced more general improvements in psychological and physical wellbeing. The acquisition of a lifelong sporting skill provides a psychological boost and assists in developing self-esteem and confidence to take part in other activities. The long term commitment and enthusiasm of the volunteer instructors was most impressive and made one appreciate the special value of these people who gave their time and care. For 1999 it was calculated that, had normal hourly rates for swimming instructors been paid, the cost would have been nearly $500 000. A recent report shows that the cost of asthma to the community is $585-$728 million per year.6 Yet here is a program using volunteers, with no government support, which can improve children's health and reduce medication, hospitalisation and visits to doctors, with consequent reduction in parent absenteeism from employment, all of which should result in economic benefits. We hope that others will be encouraged to establish and evaluate programs designed to assist the overall health of people with a specific illness. References Jones RS, Buston MG, Wharton MI. The effect of exercise on ventilatory function in the child with asthma. Br J Dis Chest 1962; 56: 78-86. McEthenney RR, Petersen KH. Physical fitness for asthmatic boys. A co-operative pilot study. JAMA 1963; 185: 142-143. Meyer J. Using qualitative methods in health action research. BMJ 2000; 320: 178-181. Wardell CP, Isbister C. Report on thirty years of the Asthma Children's Swimming Program. Sydney: Asthma Foundation NSW, 1994. Huang S-W, Veiga R, Sila U, Reed E, Hines S. The effect of swimming in asthmatic children -- participants in a swimming program in the City of Baltimore. J Asthma 1989; 26: 117-121. National Asthma Campaign. Report on the cost of asthma in Australia. Canberra: National Asthma Campaign, 1992: 8. Authors' details The Asthma Foundation of New South Wales, Sydney, NSW, 2065. Colleen P Wardell, BA, Swimming Program Co-ordinator; Clair Isbister, FRACP, DCh, Medical Adviser for the Asthma Children's Swimming Program. Reprints will not be available from the authors. Correspondence: Dr C Isbister, 142 Wentworth Street, Blackheath, NSW 2785. wardelljandcATbigpond.com 1: The Asthma Children's Swimming Program A committee of three specialist clinicians, two thoracic physiotherapists, an Olympic swimmer with asthma and a professional swimming coach designed a swimming program to meet the special needs of asthmatics. The principal differences from a general "learn to swim" program were: the use of indoor heated pools to give a controlled environment, thus reducing the chance of inducing asthma symptoms weekly swimming sessions held all year a minimum admission age of four years, considered desirable for adequate coordination, concentration, and understanding eligibility for the program required parental application, supported by a medical certificate stating details of the child's asthma and current medication the presence of a responsible adult carer, to give pre-swim medication if required pre-swim breathing exercises peak flow meter readings before and after swimming individual tuition, allowing each child to learn at his/her own pace no flotation aids except kickboards strong emphasis, starting at the first lesson, on correct controlled breathing coupled with correct swimming actions An instructor's manual was prepared describing the swimming method, and including information about asthma. Volunteer swimming instructors are trained in the method and in asthma first aid. The program has been operating continuously since 1964 and has expanded to many additional locations. For information about the current swimming program or a copy of the current version of the swimming instructor's manual, contact the Asthma Foundation of New South Wales, Suite 1, 82 Pacific Highway, St Leonards, NSW 2065. Return to text2: Reported changes in children's condition after participating in the Asthma Children's Swimming ProgramNo. of repliesChangesAsthma severity7150% showed improvementNumber of trigger factors72No significant changeMouth breathing7113% showed improvementSnoring7118% showed improvementChest deformity717% showed improvementNumber of other illnesses73No significant changeChild's enjoyment of program7397% enjoyed lessonsSwimming proficiency7390% showed improvement; 63% rated good or betterContinuing swimming7389% intended to continue after leaving the programSelf confidence7277% showed improvementPeak flow readings30No significant change Number of visits to doctor7346% overall reductionNumber of hospitalisations7364% overall reductionSchool absence due to asthma (above kindergarten age)5874% reported less absenceAsthma management7367% reported improvementUnderstanding of asthma7378% reported improvementFeeling disadvantaged by asthma7381% reported improvement Return to text

Colleen P Wardell · Clair Isbister

Christmas Offerings MJA 2000; 173: 659-660

Brian J Fotheringham

Notable Cases Non-alcoholic steatohepatitis in children and adolescents Nicholas D Manton, Jill Lipsett, David J Moore, Geoffrey P Davidson Anthony J Bourne and Richard T L Couper MJA 2000; 173: 476-479 We describe 17 children with non-alcoholic steatohepatitis. All had elevated levels of serum liver enzymes and 16 were morbidly obese. Liver biopsy showed variable steatosis and fibrosis in nine patients. At follow-up, 12 of 14 patients had persistent morbid obesity and 11 had elevated liver enzyme levels. Methods - Clinical findings - Discussion - References - Authors' details - - More articles on Gastroenterology Non-alcoholic steatohepatitis (NASH) is well recognised in adults. It occurs with obesity, insulin resistance or insufficiency and associated metabolic abnormalities such as hyperlipidaemia and hyperglycaemia. NASH also occurs in childhood, but, in this group, it is not as well characterised. Obese, prepubertal children are at risk of liver disease, with liver biopsies showing fatty change, inflammation and fibrosis with progression to necrosis and cirrhosis.1-4We report here selected features of NASH in children presenting to a tertiary care child and adolescent hospital. We aimed to determine: the demographic details of these children; the presenting clinical signs and symptoms, and any associated conditions; the biochemical and radiological findings; the range of histopathological findings with liver biopsy; and the clinical and biochemical outcomes. Methods Patient identification Patients were retrospectively identified by searching a computerised database of histopathological specimens at the Women's and Children's Hospital (formerly the Adelaide Children's Hospital) for the years 1972-1999. All liver biopsies in this period were reviewed, and cases selected if the liver biopsy showed steatosis. Clinical details, investigations and disease course were determined (retrospectively) from the hospital records. The patients' weight/ideal body weight ratios were calculated using charts from the National Centre for Health Statistics Growth Curves for Children.5 Exclusion criteria Patients were excluded when a known cause of steatosis was present. These included inborn errors of metabolism, viral hepatitis, autoimmune hepatitis, total parenteral nutrition, cystic fibrosis or Wilson's disease. Liver biopsies Fatty change was described as macrovesicular or microvesicular, and the extent of steatosis was graded as mild, moderate or severe. The presence of inflammation was graded as mild, moderate or severe. Fibrosis was described (eg, portal tract fibrosis, perisinusoidal fibrosis, septal fibrosis, bridging fibrosis, cirrhosis). In all cases, tissue was submitted for electron microscopy. Clinical findings Seventeen patients were identified: 11 males and six females. Most (14 of 17) were identified in the past five years. Mean age ± SD was 11.7 ± 1.7 years (range, 9-15 years). Persisting intermittent abdominal pain (10 patients) was the commonest presenting symptom. Two patients were identified after hepatomegaly on review for known insulin dependent diabetes mellitus (IDDM) and, in two patients, abnormal liver function tests (LFTs) were detected incidentally during investigation for apparently unrelated problems (seizure and diarrhoeal illness). One patient (Patient 17) was asymptomatic and was investigated because his twin brother (Patient 13) was found to have NASH. Five patients had relevant family history: one had parents and brother with morbid obesity; one had a family history of Gilbert disease, a disorder of bilirubin conjugation; one had a father with cirrhosis; and two were twins with obesity and abnormal liver function test results. Box 1 summarises the clinical, biochemical and radiological findings for our patients. Sixteen of the 17 patients were morbidly obese (> 24% over ideal body weight [IBW]; mean, 53%; range, 25% to 118% over IBW). Eight patients had hepatomegaly either on clinical or ultrasound examination. Alanine aminotransferase (ALT) was elevated in all patients, gamma glutamyl transferase (GGT) was elevated in eight, and alkaline phosphatase (ALP) was normal in all patients. Five patients had elevated triglyceride levels and two had elevated total serum cholesterol levels. Ultrasound examination in 11 patients showed increased echogenicity (suggestive of increased liver fat) in 10. The liver biopsy changes included both macro- and microvesicular steatosis. Inflammation was present in eight patients and fibrosis was present in nine patients. The degree of fibrosis ranged from mild portal tract fibrosis to bridging fibrosis to probable cirrhosis (as identified in a repeat biopsy in one of the patients). Increased glycogen (intracellular and intranuclear) was seen in the two patients with known IDDM and a third patient in whom a subsequent diagnosis of IDDM was made. Mallory's hyalin was not seen in any of the cases on immunohistochemical staining, a noteworthy finding given that Mallory bodies are said to be seen more commonly in alcoholic steatohepatitis than in NASH.5 Box 2 shows the follow-up data. Eleven patients had continued elevation of liver enzyme levels, and persistent obesity despite counselling. Two of the obese patients had normalisation of LFTs with weight loss. None of the other obese patients lost weight, and in these patients liver enzyme levels remained elevated. One of the patients with diabetes (the only patient who was not morbidly obese) had normalisation of LFTs with improved diabetes control. Seven of the more recently identified patients were treated with ursodeoxycholic acid; one had normalisation of LFTs with weight loss. Discussion The association of abnormalities in liver function and morphological changes on liver biopsy (steatosis, inflammation and/or fibrosis) with obesity and insulin resistance/insufficiency is well established in adults and becoming increasingly recognised in children. Most cases of NASH in the paediatric age group have been described in older children and adolescents.1,2 Our series of 17 patients shows that children may be asymptomatic or present with vague, non-specific complaints, which conform to those described previously.6 One of our patients had marked acanthosis nigricans, a finding indicative of insulin resistance and reported recently in another study.2 Most of our patients were identified over the past 5-7 years, and we believe this is largely due to the increased awareness of this condition and the increasing prevalence of obesity in children in Australian society.7 Clinical findings In our series, all but one of the patients who had ultrasound of the liver showed variable enlargement and increased echogenicity, consistent with fatty change. In a study of 72 obese children,4 increased echogenicity was found in 53% of cases, and the authors proposed ultrasound as a useful tool to determine liver involvement in obese children. Certainly, our experience agrees with this. However, liver ultrasound will not detect the more subtle histopathological features of more severe liver damage, such as fibrosis. Only liver biopsy can demonstrate such abnormalities. Elevated ALT and GGT levels were the most common findings with LFTs. This is consistent with another study,4 in which ALT was the most elevated enzyme and the ALT/AST ratio was the reverse of that seen in alcoholic steatohepatitis. We found no correlation between presenting signs and symptoms, LFT abnormalities, and the morphological changes at liver biopsy, unlike those reported in adult patients with NASH.8 Liver histology We found a wide variation in biopsy findings, from steatosis alone to steatohepatitis and mild fibrosis to probable cirrhosis (with documented progression on repeat biopsy). In the patients with known glucose intolerance, increased glycogen within hepatocyte cytoplasm and nuclei was noted. In addition, in Patient 1 (where increased glycogen was noted), IDDM was subsequently diagnosed. In adults, NASH follows a relatively benign clinical course compared with alcoholic steatohepatitis.8,9 Although follow-up data in the paediatric age group are limited, the finding of evolving cirrhosis in one of our patients highlights the view that NASH may be a progressive disease.10-12 Rashid and Roberts have speculated that at least some patients with cryptogenic cirrhosis occurring in adulthood may have had NASH since childhood.2 A recent study13 found that NASH is under-recognised in many adults with so-called cryptogenic cirrhosis (with as many as 74% of such patients having a history of obesity or diabetes mellitus). Septal fibrosis occurs frequently in overweight adult patients with abnormal LFTs.14 Pathogenesis The pathogenesis of NASH is still being determined. A recent study15 based on data from the National Health and Nutrition Examination Survey concluded that reduced serum levels of fat-soluble antioxidants are present in obese children. Oxidant stress injury may be pivotal in the pathogenesis of NASH,16 resulting in adipose tissue synthesis of tumour necrosis factor (TNF). TNF antagonises insulin receptors, leading to glucose intolerance, hyperlipidaemia and steatosis. Another study17 suggests that fatty livers are vulnerable to liver ATP depletion and necrosis, indicating that altered hepatic energy homoeostasis may be involved. Increased lipid peroxidation may increase hepatic stellate cell activation.18 Activated stellate cells are matrix-producing myofibroblast-like cells which are thought to be responsible for the laying down of fibrous tissue in hepatic fibrosis.18 Intervention At this stage, therapy is limited to weight control and treatment of insulin lack or resistance. Although weight loss in adult patients has been effective in leading to regression of fatty change,19 in all but two of our obese patients weight control was not achieved and abnormalities of liver function persisted. Seven of our patients were treated with ursodeoxycholic acid, and one showed normalisation of LFTs (with weight loss). Ursodeoxycholic acid improves LFTs in patients with NASH.20 It is thought that this agent is cytoprotective and, by preventing membrane injury, may reduce liver injury in NASH.20 In our institution, treatment of NASH with ursodeoxycholic acid is largely a matter of individual preference for treating physicians, and guidelines have not been established. Recommendations Children presenting to paediatric outpatient units who are morbidly obese should have their LFTs measured, and should be counselled regarding weight loss. If the baseline LFTs are elevated, the measurements should be repeated in 3-4 months. If the LFTs are still abnormal, then other investigations (including hepatitis B and C virus serology, autoimmune antibody screen, caeruloplasmin levels, and serum triglyceride, cholesterol and blood sugar levels) should be performed and liver biopsy considered. Liver biopsy and other investigations might be performed earlier if the liver enzyme levels are grossly elevated. References Baldridge AD, Perez-Atayde AR, Graeme-Cook F, et al. Idiopathic steatohepatitis in childhood: a multicentre retrospective study. J Pediatr 1995; 127: 700-704. Rashid M, Roberts EA. Nonalcoholic steatohepatitis in children. J Pediatr Gastroenterol Nutr 2000; 30: 48-53. Ludwig J, McGill DB, Lindor KD. Review: nonalcoholic steatohepatitis. J Gastroenterol Hepatol 1997; 12: 398-403. Franzese A, Vajro P, Argenziano A, et al. Liver involvement in obese children. Ultrasonography and liver enzyme levels at diagnosis and during follow-up in an Italian population. Dig Dis Sci 1997; 42: 1428-1432. National Centre for Health Statistics Growth Curves for Children. Adapted from Hamill PVV: NHCS Growth Curves for Children. DHEW Publication (PHS) 78-1650. Neuschwander-Tetri B, Bacon B. Nonalcoholic steatohepatitis. Med Clin N Am 1996; 80: 1147-1165. Lazarus R, Wake M, Hesketh K, Waters E. Change in body mass index in Australian primary school children, 1985-1997. Int J Obes Relat Metab Disord 2000; 24: 679-684. Lee R. Nonalcoholic steatohepatitis, a study of 49 patients. Hum Pathol 1989; 20: 594-598. Mohd R, James O, Burt A, et al. The natural history of nonalcoholic fatty liver: a follow-up study. Hepatology 1995; 22: 1714-1719. Bacon B, Farakvash M, Janney C, Neuschwander-Tetri B. Nonalcoholic steatohepatitis: tightening the morphological screws on a hepatic rambler. Hepatology 1995; 21: 1742-1743. Propst A, Propst T, Judmaier G, Vogel W. Prognosis in nonalcoholic steatohepatitis [letter]. Gastroenterology 1995; 108: 1607. Kim W, Poterucha J, Porayko M, et al. Recurrence of nonalcoholic steatohepatitis following liver transplantation. Transplantation 1996; 62: 1802-1805. Caldwell S, Oelsner D, Iezzoni J, et al. Cryptogenic cirrhosis: clinical characterisation and risk factors for underlying disease. Hepatology 1999; 29: 664-669. Ratziu V, Giral P, Charlotte F, et al. Liver fibrosis in overweight patients. Gastroenterology 2000; 118: 1117-1123. Strauss R. Comparison of serum concentrations of α-tocopherol and β-carotene in a cross-sectional sample of obese and nonobese children (NHANES III). J Pediatr 1999; 134: 160-165. Lavine J. Relative antioxidant deficiency in obese children: a weighty contributor to morbidity? [editorial]. J Pediatr 1999; 134: 132-133. Cortez-Pinto H, Chatham J, Chacko VP, et al. Alterations in liver ATP homeostasis in human nonalcoholic steatohepatitis: a pilot study. JAMA 1999; 282: 1659-1664. Reeves H, Burt A, Wood S, Day C. Hepatic stellate cell activation occurs in the absence of hepatitis in alcoholic liver disease and correlates with the severity of steatosis. J Hepatol 1996; 25: 677-683. Lieverse R, Jansen J, Masclee A, Lamers C. Gastrointestinal disturbances with obesity. Scand J Gastroenterol 1993; 200: S53-S58. Laurin J, Lindnor K, Crippin J, et al. Ursodeoxycholic acid or clofibrate in the treatment of non-alcohol-induced steatohepatitis: a pilot study. Hepatology 1996; 23: 1464-1467. (Received 3 Apr, accepted 3 Aug, 2000) Authors' details Women's and Children's Hospital, Adelaide, SA. Nicholas D Manton, MB BS, Registrar, Department of Histopathology; Jill Lipsett, PhD, FRCPA, Histopathologist, Department of Histopathology; David J Moore, MB BS, FRACP, Paediatric Gastroenterologist, Department of Gastroenterology; Geoffrey P Davidson, MD, FRACP, Director, Department of Gastroenterology; Anthony J Bourne, MB BS, FRACPA, Director, Department of Histopathology; Richard T L Couper, MB ChB, FRACP, Paediatric Gastroenterologist, Department of Gastroenterology, and University of Adelaide Department of Paediatrics. Reprints will not be available from the authors. Correspondence: Dr R T L Couper, University of Adelaide Department of Paediatrics and Department of Paediatric Gastroenterology, Women's and Children's Hospital, 72 King William Road, North Adelaide, SA 5006. rcouperATmedicine.adelaide.edu.au Make a comment 1: Clinical and investigation findings Patient Examination Biochemistry* Ultrasound Liver biopsy 1 (M, 13)† 27% over IBW acanthosis nigricans ALT ratio 3.2 GGT ratio 4.4 AST ratio 1.9 Enlarged EL Severe macrovesicular steatosis with increased glycogen 2 (F, 13) 27% over IBW short stature, hepatomegaly ALT 3.2 GGT 1.1 AST 3.0 Enlarged EL Moderate macro- and microvesicular steatosis with increased glycogen and moderate inflammation 3 (F, 11) 118% over IBW ALT 1.3 GGT 5.5 Normal Severe macro- and microvesicular steatosis 4 (F, 9) 45% over IBW ALT 2.2 nd Severe macrovesicular steatosis, mild portal tract inflammation, mild portal tract fibrosis 5 (M, 12) 10% over IBW tender hepatomegaly ALT 11.3 GGT 5.1 Enlarged EL Moderate macro- and microvesicular steatosis, scattered glycogenated nuclei 6 (M, 11) 115% over IBW ALT 3.2 GGT 1.6 AST 1.6 Fatty change Severe mixed macro- and microvesicular steatosis with bridging fibrosis and evolving cirrhosis 7 (M, 13) 81% over IBW hepatomegaly ALT 1.2 nd Moderate macrovesicular steatosis, mild portal tract inflammation 8 (M, 14) 74% over IBW ALT 16.0 GGT 4.9 EL Severe macrovesicular steatosis, mild septal fibrosis 9 (M, 15) 88% over IBW ALT 2.5 AST 1.5 TG 1.8 EL Severe macrovesicular steatosis, minimal perisinusoidal fibrosis 10 (F, 10) 32% over IBW ALT 20.7 GGT 1.4 Cholesterol 1.2 nd Moderate macro- and microvesicular steatosis, mild portal tract inflammation 11 (M, 13) 60% over IBW mild abdominal tenderness ALT 1.3 GGT 1.1 TG 1.5 nd Mild macrovesicular steatosis 12 (M, 11) 55% over IBW enlarged liver ALT 1.6 TG 1.7 EL Moderate macro- and microvesicular steatosis, moderate portal tract inflammation, portal tract fibrosis with bridging 13‡ (M, 12) 37% over IBW ALT 2.2 EL Moderate macro- and microvesicular steatosis, mild perisinusoidal fibrosis 14 (F, 9) 44% over IBW palpable liver edge ALT 3.6 nd Moderate macrovesicular steatosis, focal hepatocyte necrosis, mild portal tract inflammation, mild perisinusoidal fibrosis 15 (F, 10) 26% over IBW palpable liver edge ALT 2.8 Cholesterol 1.2 EL Mild macrovesicular steatosis, mild portal tract inflammation 16 (M, 11) 25% over IBW palpable liver edge ALT 4.7 TG 1.1 EL Severe macro- and microvesicular steatosis, mild portal tract inflammation, portal tract fibrosis with early bridging 17‡ (M, 12) 37% over IBW ALT 4.8 TG 1.3 nd Severe macrovesicular steatosis, mild portal tract fibrosis with early bridging *Biochemistry results are given as a ratio of the measured value of serum liver enzyme, serum triglyeride, or serum cholesterol levels over the normal maximum for the particular method used. †Sex and age at presentation. ‡Twins. IBW=ideal body weight. ALT=alanine aminotransferase. GGT=gamma glutamyl transferase. AST=aspartate aminotransferase. TG=Serum triglycerides. EL=echogenic liver. nd=not done. Back to text 2: Outcome data at latest follow-up Patient Follow-up period Percentage over IBW Biochemistry* Remarks 1 6 years 45% ALT 1.9 GGT 5.8 Subsequently diagnosed with IDDM and Alstrom syndrome 2 Lost to follow-up 3 6 years 25% Rapid weight loss with puberty, normalisation of LFTs 4 15 months 36% ALT 3.4 5 2.5 years 8% Normalisation of LFTs with improved diabetes control 6 2.5 years 60% ALT 1.7 Persisting obesity with some improvement in LFTs. Treated with ursodeoxycholic acid. Follow-up liver biopsy showed probable cirrhosis 7 Lost to follow-up 8 2 years 78% ALT 4.1 GGT 1.9 Treated with ursodeoxycholic acid 9 1 year 51% ALT 4.0 10 4 months 30% ALT 8.0 GGT 2.0 11 1 year 56% ALT 2.3 GGT 1.4 12 1 year 57% ALT 7.9 GGT 2.2 13† 15 months 36% ALT 3.0 Treated with ursodeoxycholic acid 14 14 months 36% ALT 3.8 Treated with ursodeoxycholic acid 15 Not yet reviewed 16 1 year 15% Normalisation of LFTs with weight loss. Treated with ursodeoxycholic acid 17† 1 year 45% ALT 2.9 Treated with ursodeoxycholic acid *Biochemistry results are given as ratio of the measured value of serum liver enzyme levels and the normal maximum for the method used. †Twins. LFT=liver function test. ALT=alanine aminotransferase. GGT=gamma glutamyl transferase. Back to text

Nicholas D Manton · Jill Lipsett · David J Moore · Geoffrey P Davidson · Anthony J Bourne

Editorial SIDS: facts and controversies We need to promote the established risk-reducing behaviours, which are based on strong scientific evidence MJA 2000; 173: 173-174 Over the period 1982-1986, Australian Bureau of Statistics figures show that there were an average of 457 deaths per year from sudden infant death syndrome (SIDS) in Australia (1.89 deaths/1000 live births).1 Ten years later, over the period 1992-1996, SIDS mortality had plummeted to 210 deaths per year (0.81 deaths/1000 live births).1In spite of this dramatic decrease, SIDS still causes more deaths than traffic injuries, congenital anomalies and cancer combined in the 1-4 years age group.1 Here, I briefly discuss the established risk factors for SIDS and current areas of controversy. Sleeping position: Studies dating back to the 1960s, but mostly in the 1980s, had suggested that prone sleeping position was associated with SIDS, but it was not until SIDS prevention campaigns had been successfully run in the Netherlands and New Zealand that the potential for reducing SIDS mortality by modifying this risk factor was recognised.2 In 1991, Australia launched its "Reducing the Risk" campaign, driven by SIDS organisations and supported by Red Nose Day funds. In New Zealand, we observed a close temporal relationship between Red Nose Day education campaigns and reduction in the prevalence of placing infants in the prone sleeping position.3 This illustrates the powerful synergy that can be created when professional and voluntary/parent groups work together. The fall in SIDS mortality can be attributed almost entirely to a change in the prevalence of placing infants in the prone sleeping position,4 supporting the contention that prone sleeping is part of the causal pathway and is a cause of SIDS. Recent evidence suggests that sleeping on the side doubles the risk of SIDS compared with sleeping in a supine position, probably because of infants turning to the prone position ("secondary prone").5 Infants who usually sleep supine but are placed prone (ie, are unaccustomed to the prone position) are at very high risk of SIDS.6,7 Smoking: Maternal smoking is the other major non-controversial risk factor for SIDS.8 Since the reduction in the prevalence of prone sleeping position, there have been eight studies examining maternal smoking and SIDS. The pooled unadjusted (not adjusted for confounders) relative risk (RR) determined from these studies is 4.7, which suggests that infants of mothers who smoke are at an almost fivefold greater risk of SIDS than infants of mothers who do not smoke. Evidence for the effect of environmental tobacco smoke exposure can be obtained by examining the risk of SIDS from paternal smoking where the mother is a non-smoker. There have been six such studies. The pooled unadjusted RR for these studies was 1.4. The increased risk of SIDS with tobacco smoke is probably predominantly due to an in-utero effect of tobacco smoke rather than postnatal environmental tobacco smoke.8 Bedding and clothing: Excess bedding and clothing have been shown to increase the risk of SIDS in infants sleeping prone, but not for infants sleeping on their side or back. As few infants in Australia sleep prone,4advice on the amount of bedding and clothing could be dropped. Some 15%-20% of infants who die of SIDS are found with their head covered by bedding.9 Covering of the head might cause death by forcing an infant to rebreathe expired gases or by creating thermal stress. There have been several suggestions as to how to avoid covering of the head, including tucking bedding in firmly, removing bedding, placing infants at the foot of the cot, using the Dutch sleeping sack, and avoiding the use of duvets. The evidence to support these recommendations is limited. Bed sharing: It is well established that infants who share a bed with mothers who smoked during the pregnancy are at increased risk of SIDS.5 Whether or not there is an increased risk for infants sharing a bed with mothers who were non-smokers has not been firmly established. If there is an increased risk it is likely to be quite small (pooled unadjusted RR, 1.4). Complicating the picture is the fact that in some cultures bed sharing is an established practice. Furthermore, others have advocated bed sharing to improve breastfeeding rates.10 Breastfeeding: Most studies have shown that the incidence of SIDS is lower in breastfed infants. However, breastfeeding in most developed countries is associated with socioeconomic advantage, and, when adjustment is made for socioeconomic factors, the protective effect of breastfeeding is less apparent.11,12 Some have concluded there is no decreased risk from breastfeeding,12 whereas others have argued that breastfeeding has a protective effect.11 Use of pacifier: An unexpected finding of several studies has been that pacifiers are associated with a reduced risk of SIDS.13 However, this benefit needs to be balanced against possible detrimental effects of pacifiers, such as a reduction in breastfeeding and increased incidence of otitis media.14 Vaccinations: In the past there was concern that vaccinations might cause SIDS, as the peak age for SIDS is 2-4 months, which coincides with the age for vaccinations. However, studies have shown that vaccinations are not associated with an increased risk of SIDS -- indeed, some studies have shown a reduced risk of SIDS at the time of vaccinations.15 Despite this, the media from time to time revive this old chestnut. "Toxic gas": The "toxic gas" theory has received considerable media attention in the United Kingdom and New Zealand, but has not been substantiated.16 According to this theory, toxic gases are produced by the fungus Scopulariopsis brevicaulis as it metabolises chemicals containing arsenic, antimony and phosphorus in cot mattresses. Proponents of the theory recommend wrapping cot mattresses in polythene, but this is potentially dangerous advice in view of the evidence that plastic sheeting in a baby's sleeping environment can cause death through suffocation.17 Despite the success of the "Reducing the Risk" campaign, SIDS mortality remains unacceptably high among Indigenous Australians (mortality rates for the period 1992-1996, aggregated for South Australia, Western Australia and the Northern Territory, were 30 deaths per year among Indigenous Australians [5.29 deaths/1000 population] compared with 61 deaths/year among non-Indigenous Australians [0.81 deaths/1000 population]). The cause or causes of SIDS remain largely unknown, although the most likely mechanisms include airway obstruction, rebreathing of expired gases, thermal stress and an "arousal defect" (reduced ability to respond to hypoxia or hypercapnoea by arousing or waking up). There is now little support for the (central) apnoea hypothesis, which was the major mechanism postulated in the 1970s and 1980s. Physiologists need to show how the established risk factors might operate, and researchers need to explore the reasons for the high rate of SIDS in disadvantaged and Indigenous communities. We must also continue to promote the established risk-reducing behaviours, which are based on strong scientific evidence, and ensure that all new mothers receive this information. We need to devise and evaluate innovative methods for delivering these messages and changing behaviour among disadvantaged and Indigenous groups. New theories should be examined, and discredited ideas buried. The media have an important responsibility, as they are in a position either to create controversy and confusion about SIDS or to serve as a powerful force for producing change. Ed A Mitchell Associate Professor in Paediatrics Department of Paediatrics University of Auckland, New Zealand. e.mitchellATauckland.ac.nz Acknowledgement: I am grateful to the Australian Bureau of Statistics for supplying mortality data. Australian Bureau of Statistics website <http://www.abs.gov.au> Engelberts AC, de Jonge GA. Choice of sleeping position for infants: possible association with cot death. Arch Dis Child 1990; 65: 462-467. Mitchell EA, Tonkin S. Publicity and infants' sleeping position. BMJ 1993; 306: 858. Dwyer T, Ponsonby AL, Blizzard CL, et al. The contribution of changes in the prevalence of prone sleeping position to the decline in SIDS in Tasmania. JAMA 1995; 273: 783-789. Scragg RKR, Mitchell EA. Side sleeping position and bed sharing in the sudden infant death syndrome. Ann Med 1998; 30: 345-349. L'Hoir MP, Engelberts AC, van Well GT, et al. Risk and preventive factors for cot death in The Netherlands, a low-incidence country. Eur J Pediatr 1998; 157: 681-688. Mitchell EA, Thach BT, Thompson JMD, Williams S. Changing infants' sleep position increases risk of sudden infant death syndrome. Arch Pediatr Adolesc Med 1999; 153: 1136-1141. Mitchell EA, Milerad J. Smoking and sudden infant death syndrome. In: International consultation on environmental tobacco smoke (ETS) and child health. Geneva: World Health Organization, 1999: 105-129. Beal SM, Byard RW. Accidental death or sudden infant death syndrome? J Paediatr Child Health 1994; 30: 144-150. McKenna JJ, Mosko SS, Richard CA. Bedsharing promotes breastfeeding. Pediatrics 1997; 100: 214-219. Ford RP, Taylor BJ, Mitchell EA, et al. Breastfeeding and the risk of sudden infant death syndrome. Int J Epidemiol 1993; 22: 885-890. Fleming PJ, Blair PS, Bacon C, et al. Environment of infants during sleep and risk of the sudden infant death syndrome: results of 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. Confidential Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers. BMJ 1996; 313: 191-195. Fleming PJ, Blair PS, Pollard K, et al. Pacifier use and sudden infant death syndrome: results from the CEDI/SUDI case control study. Arch Dis Child 1999; 81: 112-116. Hunt L, Fleming P, Golding J. Does the supine sleeping position have any adverse effects on the child? I. Health in the first six months. The ALSPAC Study Team. Pediatrics 1997; 100: E11. Hoffman HJ, Hunter JC, Damus K, et al. Diphtheria-tetanus-pertussis immunization and sudden infant death: results of the National Institute of Child Health and Human Development Cooperative Epidemiological Study of sudden infant death risk factors. Pediatrics 1987; 79: 598-611. Expert Group to Investigate Cot Death Theories: toxic gas hypothesis. Chairman, Lady Limerick. Final report. London: Department of Health. May 1998. Kraus JF. Effectiveness of measures to prevent unintentional deaths of infants and children from suffocation and strangulation. Public Health Rep 1985; 100: 231-240. Make a comment

Ed A Mitchell

Public Health Driveway motor vehicle injuries in children Andrew J A Holland, Rhea W Y Liang, Shailinder J Singh, David N Schell, Frank I Ross and Daniel T Cass MJA 2000; 173: 192-195 Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Paediatrics Abstract Objectives: To describe the frequency, nature and outcome of driveway injuries in children. Design: Retrospective case series of driveway-related injuries in children under 16 years of age admitted to the New Children's Hospital (NCH), New South Wales, from November 1995 to February 2000, and deaths reported to the New South Wales Paediatric Trauma Death (NPTD) Registry from January 1988 to December 1999. Main outcome measures: Circumstances of injury; type and number of injuries identified. Results: 42 children were admitted to our institution with driveway-related injuries over four years and four months. These represent 12% of all children admitted with pedestrian motor vehicle injuries. Fourteen deaths (including one of the children admitted to NCH) were reported to the NPTD Registry over 12 years, accounting for 8% of all paediatric pedestrian motor vehicle deaths reported to the registry. Typically, the injury involved a parent or relative reversing a motor vehicle in the home driveway over a toddler or preschool-age child in the late afternoon or early evening. Four-wheel-drive or light commercial vehicles were involved in 42% of all injuries, although they accounted for just 30.4% of registered vehicles in NSW. These vehicles were associated with a 2.5-times increased risk of fatality. In 13 of the 14 deaths, the cause was a severe head injury not amenable to medical intervention. Conclusions: Driveway injuries in children account for a significant proportion of paediatric pedestrian motor vehicle injuries and deaths in NSW. Prevention represents the only effective approach to reducing deaths from this cause. Trauma is the leading cause of death and disability in children after the first year of life.1 In children with major injuries (defined as an Injury Severity Score2 greater than 15), motor vehicle accidents have consistently been the most common cause of injury.3-6 Within this group, children as pedestrians frequently suffer the most severe injuries as a consequence of their small size in relation to motor vehicles.3,4,7 As paediatric pedestrian motor vehicle injuries predominantly involve young school-age children,8,9 conventional prevention campaigns have been directed toward these age groups.3,9,10A recognised clinical scenario in children is traumatic asphyxia with associated visceral injuries resulting from low-velocity compression of the torso.11,12 Typically, a motor vehicle reverses over a toddler or older pre-school child in a driveway or car park.7,13 In these cases, the pliability of a child's skeleton and soft tissues, together with the ability of the applied force to be distributed over the short time of the impact, often allows a good outcome.7,12,13 This clinical scenario has been variously termed the driveway, back over, crush, non-traffic or low-velocity motor vehicle injury in the United States, but has not been well described in Australia.4,6,13-18 We examined the experience of the New Children's Hospital, Westmead, (NCH) with driveway injuries, together with a review of cases reported to the New South Wales Paediatric Trauma Death (NPTD) Registry. Our objectives were to ascertain the extent of this problem, the nature of injuries, and the outcomes, in order to determine the optimal intervention strategy. Methods We performed a retrospective review of records of children younger than 16 years admitted to NCH or reported to the NPTD Registry with driveway injuries. Data were collected on the age of the child; the date, time and location of the injury; the vehicle type and driver of the vehicle; how the accident occurred, including documented safety features restricting access to the driveway; and the injuries identified, together with the surgical interventions, complications, and final outcome. The ethics committee of the NCH approved the study. Admissions to NCH: Data were collected from November 1995 (when the NCH opened) to February 2000. Patients were identified prospectively from the paediatric trauma database compiled by the trauma research nurse. In addition, a retrospective search was made of the case notes of all children admitted to NCH as a result of a pedestrian motor vehicle injury to ensure no cases had been missed. Patients were either admitted directly to NCH from its catchment area of Sydney's western suburbs or transferred via the New South Wales Newborn and Paediatric Emergency Transport Service from peripheral centres. NPTD Registry: The NPTD Registry records all deaths resulting from trauma of children under 16 years of age in NSW that are reported to the coroner. Data were available from inception of the database in January 1988 to December 1999. The police statement and coroner's report, together with the postmortem findings, were reviewed for children who had died following a driveway injury. Results Driveway injuries and deaths identified Box 1 summarises data on the 55 children injured or killed and the circumstances of the injuries, and Box 2 details an illustrative case. Admissions to NCH: There were 42 children admitted with injuries sustained as a result of a driveway motor vehicle injury, representing 12% of the 354 children admitted to NCH with pedestrian motor vehicle injuries. Thirteen patients had been transferred from another hospital. One of the children died. Twenty-six (63%) of the children who survived were under three years of age. Boys accounted for 74% of the children admitted. NPTD Registry: There were 14 deaths from driveway injuries, including one of the 42 children admitted to NCH, reported over the 12-year period. These deaths represented 8% of the 174 pedestrian motor vehicle deaths reported to the registry over the same interval. Children who died were generally younger than patients admitted to NCH. Boys were again over-represented (78%). Circumstances of the injuries and deaths Although 41 (82%) injuries occurred in the afternoon or evening (most between 4:00 pm and 7:00 pm), six (43%) of the fatalities occurred in the morning. There was no marked seasonal association, although 30% of the injuries took place in the summer months, when children would be more likely to be playing outside. A relative of the child or a family friend was the driver in 39 cases, including 12 of the 14 injuries leading to death. A four-wheel-drive (4WD) or light commercial vehicle (LCV) was involved in 34% of injuries in which the child survived, compared with 64% of those with a fatal outcome. Overall, these vehicles accounted for 42% of all injuries. They were associated with a 2.5-times greater risk of fatality compared with other motor vehicles. In 42 cases, the vehicle reversed over the child; 4WDs and LCVs accounted for 19 of these cases. Documentation of access limitation to the driveway was available in only three cases; in two this involved a front door only, and in one a fence gate, all of which had been left open. Nature of injuries Box 3 summarises the injuries identified. For 13 of the children who died, the cause of death was a severe, crushing head injury that involved at least one of the wheels of the vehicle passing directly over the child's head. All but one of the children with a severe head injury died either at the scene of the injury or in the emergency department of the receiving hospital. One child without a head injury died in transit as a result of hypovolaemic shock from a near-complete transection of the right lobe of the liver. In the children who survived, there was a lower incidence and severity of head and neck injuries and a greater incidence of limb trauma compared with children who died. In the surviving children, head injury was usually a consequence of a fall to the ground or cerebral oedema from traumatic asphyxia secondary to compression of the torso. Results of treatment Fourteen patients admitted to NCH required 18 procedures; most involved skin grafting or treatment of displaced fractures. One patient with cardiac tamponade secondary to myocardial injury had a non-therapeutic laparotomy at a country hospital for hypotensive shock that subsequently responded to pericardiocentesis. Final outcome was recorded as satisfactory or good for 34 of the 41 survivors, with a full return to normal activities and no significant physical or psychological sequelae. Active clinical and social problems were identified in seven patients (Box 4). Discussion Driveway injuries in children have usually been considered a minor public health problem,13 perhaps as a result of a combination of misclassification and the failure of non-fatal injuries to be reported to the police.7,8,14,16,19 The NSW Roads and Traffic Authority, which is responsible for compiling most motor vehicle injury statistics in NSW, does not collect data on driveway injuries because they occur on private land. Our figure of a frequency of more than 1 in 10 pedestrian motor vehicle accidents involving children that require admission seems representative of more recent data, although miscoding and under-reporting may have resulted in some cases being missed.6Of great concern was the number of fatalities associated with this injury mechanism: 8% of the total number of paediatric pedestrian motor vehicle deaths. Published figures range from 10.7% in New Zealand to 20% in the US, suggesting that our figure is representative.7,18 Male predominance is a feature of most traumatic injuries,4,8,13,14,16,19 and was particularly noticeable in our series, even below the age of five years. Our data suggest a marked difference between boys and girls in their exploratory behaviour that occurs from an early age.20 A family member or person known to the child was the driver in 86% of fatalities reported to the NPTD Registry; this high incidence is a feature of other series.7,14,17,18 Clearly, the psychological consequences must be devastating to the family, friends and neighbours.18 Our results suggested a link between fatal outcome, age of the child and the size and weight of the vehicle involved.14 Both 4WDs and LCVs accounted for a much higher number of the fatalities in our study than would be expected from their prevalence on the roads. They account for less than 30.4% of registered motor vehicles in NSW (Australian Bureau of Statistics, Motor Vehicle Census 1998, personal communication), but were involved in just under two-thirds of the deaths and were associated with a 2.5-times greater risk of fatality compared with other motor vehicles. Motoring and child safety organisations and health visitors should alert parents and relatives of young children to these findings to encourage greater awareness of the risks these vehicles pose to both toddlers and preschool children. Road safety organisations need to emphasise that the risk of injury appears to be particularly great when reversing in a driveway with this type of vehicle -- the increased ride height potentially reduces visibility and makes identification of a young child much more difficult, even with the use of convex mirrors or a wide-angle lens.15,16 In some prestige vehicles, a proximity-warning device, consisting of ultrasonic transceivers located in the bumpers, at an extra cost to the customer of between $900 and $1600, allows detection of objects within 50 cm to 70 cm of the bumper and above a height of 30 cm. Although the effectiveness of such devices has not been proven in this situation, their wider introduction in high-risk vehicles may help reduce the frequency of this injury.4,16 As nearly all the deaths involved massive head injuries not amenable to medical intervention, prevention represents the only effective approach to reducing fatalities.14-16,18 We suggest that an effective form of injury prevention is urgently required, particularly in view of evidence that this injury is often associated with shared driveways.21 The frequent subdivision of redeveloped residential blocks in urban areas might be expected to lead to an increase in these injuries.22 The optimal prevention would appear to be clear separation of the driveway and garage from the children's play area by a physical barrier such as a fence, wall or self-locking gate.16,21 There are risks to the inquisitive child not only from moving vehicles but also automatic garage doors and unattended vehicles.4,23 Although the construction of circular driveways might decrease the incidence of these injuries, such an approach would be impractical in most urban situations.4 The use of reversing alarms in passenger vehicles appears unlikely to be effective given that the group most at risk of injury, toddlers and preschool children, are too young to appreciate the significance of the alarm and act with appropriate speed.4,17 We recommend that the same degree of vigilance taken with regard to swimming pool safety should be applied to the driveway, and that legislation should be introduced to limit access to this area either by design or the use of temporary fencing.18,21 As an interim measure, we advocate extreme caution be exercised by parents, relatives and neighbours of young families when reversing out of driveways, particularly in vehicles with restricted rear view vision and at greater risk of causing fatal injury, such as four-wheel-drives, vans and trucks. Acknowledgements Mr A J A Holland is supported by a Surgeon Scientist Scholarship from the Royal Australasian College of Surgeons. Dr J Peat provided assistance with statistical analysis. References Meyer AA. Death and disbility from injury: a global challenge. J Trauma Injury Infect Critical Care 1998; 44: 1-12. Baker SP, O'Neill B, Haddon W, Long WB. The Injury Severity Score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma 1974; 14: 187-196. Tanz RR, Christoffel KK. Pedestrian injury. The next motor vehicle injury challenge. Am J Dis Child 1985; 139: 1187-1190. Winn DG, Agran PF, Castillo DN. Pedestrian injuries to children younger than 5 years of age. Pediatrics 1991; 88: 776-782. Roberts I, Norton R, Hassall I. Child pedestrian injury 1978-1987. N Z J Med 1992; 105: 51-52. Agran P, Winn D, Anderson C. Differences in child pedestrian injury events by location. Pediatrics 1994; 93: 284-288. Roberts I, Kolbe A, White J. Non-traffic child pedestrian injuries. J Paediatr Child Health 1993; 29: 233-234. Lapidus G, Braddock M, Banco L, et al. Child pedestrian injury: a population-based collision and injury severity profile. J Trauma 1991; 31: 1110-1114. Dunne RG, Asher KN, Rivara FP. Behavioural and parental expectations of child pedestrians. Pediatrics 1992; 89: 486-490. Roberts I, Norton R, Dunn R, et al. Environmental factors and child pedestrian injuries. Aust J Pub Health 1994; 18: 43-46. Campbell-Hewson G, Egleston CV, Cope AR. Traumatic asphyxia in children. J Accid Emerg Med 1997; 14: 47-49. Sarihan H, Abes M, Akyazici R, et al. Traumatic asphyxia in children. J Cardiovasc Surg 1997; 38: 93-95. Bell MJ, Ternberg JL, Bower RJ. Low velocity vehicular injuries in children -- "run-over" accidents. Pediatrics 1980; 66: 628-631. Brison RJ, Wicklund K, Mueller BA. Fatal pedestrian injuries to young children: a different pattern of injury. Am J Public Health 1988; 78: 793-795. Olson LM, Sklar DP, Cobb L, et al. Analysis of childhood pedestrian deaths in New Mexico. Ann Emerg Med 1993; 22: 512-516. Robinson P, Nolan T. Paediatric slow-speed non-traffic fatalities: Victoria, Australia, 1985-1995. Accid Anal Prev 1997; 29: 731-737. Wright MS. Nonambulatory "pedestrians": infants injured by motor vehicles in driveways. Clin Pediatr 1998; 37: 515-517. Partrick DA, Bensard DD, Moore EE, et al. Driveway crush injuries in young children: a highly lethal, devastating and potentially preventable event. J Pediatr Surg 1998; 33: 1712-1715. Agran PF, Castillo DN, Winn DG. Limitations of data compiled from police reports on pediatric pedestrian and bicycle motor vehicle events. Accid Anal Prev 1990; 22: 361-370. Cass DT, Ross F, Lam LT. Childhood drowning in New South Wales 1990-1995: a population based study. Med J Aust 1996; 165: 610-612. Roberts I, Norton R, Jackson R. Driveway-related child pedestrian injuries: a case-control study. Pediatrics 1995; 95: 405-408. Australian Bureau of Statistics. Building approvals, New South Wales and Australian Capital Territory -- December 1999. Canberra: ABS, 2000. (Catalogue no. 8731.1.) Williams AF. Children killed in falls from motor vehicles. Pediatrics 1981; 68: 576-578. (Received 24 Mar, accepted 13 Jun, 2000) Authors' details New Children's Hospital, Royal Alexandra Hospital for Children, University of Sydney, NSW. Andrew J A Holland, BSc, FRCS, FRACS, Research Fellow and Clinical Lecturer, Department of Surgical Research; Frank I Ross, BAppSc(Nurs), MPH, Clinical Nurse Consultant, Department of Surgical Research; Daniel T Cass, PhD, FRACS, William Dunlop Professor of Paediatric Surgery; Rhea W Y Liang, MB, ChB, Surgical RMO, Department of Paediatric Surgery; Shailinder J Singh, FRCS (I), FRCS (Paed Surg), Clinical Fellow, Department of Paediatric Surgery; David N Schell, MB BS, FRACP, Consultant Paediatric Intensivist, Paediatric Intensive Care Unit. Reprints: Mr Andrew J A Holland, Department of Surgical Research, The New Children's Hospital, Royal Alexandra Hospital for Children, PO Box 3515, Parramatta, NSW 2124. AndrewH3ATnch.edu.au Make a comment 1: Summary of children injured and the circumstances of injuries* Survivors (n=41) Deceased (n=14) Age Median Youngest Oldest 23 m 13 m 13 y 1 m 18 m 8 m 3 y 1 m Sex Boys Girls 31 10 11 3 Time of day Morning Afternoon 8 33 6 8 Driver Parent/relative Friend/neighbour Other/unknown 30 7 4 9 3 2 Type of vehicle Car 4WD LCV Unknown 26 8 6 1 4 6 3 1 Direction of travel Forwards Reversing Both directions Unknown 9 30 1 1 2 12 0 0 *There were no statistically significant differences between survivors and deceased. 4WD=four-wheel-drive. LCV=light commercial vehicle. Back to text 2: Illustrative case of a typical driveway motor vehicle injury Unknown to his parents, a 20-month-old boy was playing in the driveway at home. The back door was open and there was no fencing restricting access to the driveway. The father was reversing his four-wheel-drive vehicle out of the garage when he felt a bump. He stopped and discovered his son underneath the vehicle between the tyres. The father pulled the child from underneath the vehicle and then called an ambulance. On arrival at the referring hospital, the child was alert but distressed and uncooperative. Clinical examination revealed bilateral conjunctival haemorrhages and facial petechiae characteristic of traumatic asphyxia (Figure). There was an abrasion of the lower chest and anterior abdominal wall, with a tyre mark on the left shin. Radiological investigations, including a computed tomography scan of the head, chest and abdomen, revealed mild cerebral oedema, pulmonary contusions of both lower lobes, a subcapsular splenic haematoma and a minimally displaced fracture of the upper third of the left tibia. The boy was transferred to the New Children's Hospital, where his injuries were treated non-operatively. He required intubation for worsening gas exchange, but was able to be extubated within 72 hours. He was discharged home 12 days after the injury and was completely well three months later. Both parents required extensive counselling by a social worker. They no longer own the vehicle. Back to text 3: Driveway motor vehicle injuries identified in children New Children's Hospital* (n=41) NPTD Registry† (n=14) Head and neck injuries Soft tissue injury Concussion Skull fracture Facial fracture Cerebral oedema/contusion Cerebral laceration Intracranial haemorrhage Avulsion cerebellum Retinal haemorrhage Cervical spine injury 18 (44%) 6 (15%) 1 (2%) 3 (7%) 1 (2%) 0 0 0 1 (2%) 0 9 (64%) 0 11 (79%) 1 (7%) 5 (36%) 6 (43%) 6 (43%) 1 (7%) 0 1 (7%) Totals 30 injuries in 24 patients 40 injuries in 13 patients Torso injuries Soft tissue injury Rib fractures Pneumothorax Pulmonary contusion/laceration Cardiac tamponade Mediastinal/retroperitoneal haematoma Splenic injury Hepatic injury Renal and pancreatic injuries Thoracic spinal injury Pelvic fracture 19 (46%) 1 (2%) 1 (2%) 2 (5%) 1 (2%) 0 1 (2%) 1 (2%) 0 1 (2%) 6 (15%) 6 (43%) 3 (21%) 0 7 (50%) 0 2 (14%) 1 (7%) 4 (29%) 2 (14%) 0 2 (14%) Totals 33 injuries in 27 patients 28 injuries in 13 patients Limb injuries Soft tissue injury: upper limb Soft tissue injury: lower limb Upper limb fractures Lower limb fractures 3 (7%) 10 (24%) 6 (15%) 8 (20%) 0 0 1 (7%) 0 Totals 27 injuries in 25 patients 1 injury in 1 patient *Injuries in children admitted to the New Children's Hospital with non-fatal injuries from November 1995 to February 2000. †Injuries in children reported to the New South Wales Paediatric Trauma Death (NPTD) Registry from January 1988 to December 1999. Back to text 4: Adverse outcomes among survivors of driveway motor vehicle accidents Incomplete spinal cord injury with lower limb weakness and neurogenic bladder Retinal haemorrhage with visual impairment Unequal leg length and gait disturbance from lower limb fracture Epiphora secondary to nasolacrimal duct injury associated with facial fracture Residual left ptosis secondary to closed head injury Significant varus deformity from upper limb fracture Prolonged social work and psychological counselling of one family Back to text

Shailinder J Singh · David N Schell · Frank I Ross · Daniel T Cass

Letter Rethinking the early childcare agenda MJA 1999; 171: 166-167 To the Editor: We are concerned that Cook's article1 lacks a balanced review of the literature on childcare, being biased in its portrayal of the possible negative effects without consideration of the likely positive ones. This could have detrimental consequences for the many children in formal childcare in Australia, their parents, and the staff and others involved in what is now an integral and vital component of Australian society. Cook's article also draws strongly on overseas studies, although childcare systems in Australia are likely to be different from those in other countries. Positive health outcomes for children attending childcare include the detection of vision and hearing problems, higher vaccination rates, appropriate nutrition, the detection of child abuse and neglect, primary health and dental care, psychosocial benefits, and opportunities for health promotion.2 The issue of socioemotional development, including attachment theory, has been debated in the literature. Cook cites Belsky, but Belsky has been noted as often citing research that did not take into account the specific characteristics and quality of care.3 It is probable that social and cognitive development are related to quality of care, and Caldwell's study suggests that childcare may provide better quality of care, at least for cognitive development, than home care.4 Thus, childcare does not appear to be consistently detrimental to cognitive and language development and may have a positive influence.4 The investigation of the influence of childcare on children's development is complex and should be considered in interpreting such research. Harvey,5 in an extensive longitudinal study, found that parental employment had "minimal effects on children's later functioning", and that increased early parental income could positively affect childhood development. We do agree with Cook that increased flexibility for working parents should be encouraged. Flexible options, such as parental leave and part-time work for parents of young children, are often advantageous. In addition to increasing work options for parents, it is important that we strive for high quality childcare, subsidised if necessary, so that all families have the choice of providing such care for their children. Linda M Slack-Smith Senior Lecturer, School of Oral Health Sciences 179 Wellington Street, Perth, WA 6000 lindasATcyllene.uwa.edu.au Anne W Read Senior Research Officer, Division of Psychosocial Research TVW Telethon Institute for Child Health Research, Perth Stephen R Zubrick Associate Professor, and Head, Division of Psychosocial Research TVW Telethon Institute for Child Health Research, Perth Cook P. Rethinking the early childcare agenda. Med J Aust 1999; 170: 29-31. Andersson B. Children's development related to day-care, type of family and other home factors. Eur Child Adolesc Psychiatry 1996; 5: 73-75. Melhuish E, Moss P. Current and future issues in policy and research. In: Melhuish E, Moss P, editors. Day care for young children. London: Tavistock/Routledge, 1991: 225. Caldwell B. Impact of day care on the child. Pediatrics 1993; 91(1 Pt 2): 225-228. Harvey E. Short-term and long-term effects of early parental employment on children of the National Longitudinal Survey of Youth. Dev Psychol 1999; 35: 445-459. In reply: A literature review was beyond my purpose, but I summarised findings of a major meta-analysis, and explained why psychological outcomes are of most concern. Benefits of childcare are often publicised, but risks, proven or probable, should not be concealed from parents and policy-makers.1 Notwithstanding the 1971 New South Wales child psychiatrists' memorandum,2 it became politically incorrect to express concerns about childcare. In social sciences, the now-discredited ideology of cultural determinism prevailed, denying the relevance of evolutionary biology to human behaviour, even mothering. A pro-childcare "spin" has pervaded research reports. Slack-Smith and colleagues' statement that "childcare does not appear to be consistently detrimental to cognitive and language development . . ." is a typical childcare-advocacy "straw man". The reply is: nobody said it was! Ochiltree's review3 seemed to me to have eight such statements within five paragraphs, and was so "unbalanced" that I wrote a book,1 to which I refer readers. It covers the points made by Slack-Smith et al, which cannot be answered in a few words. Childcare advocates seldom acknowledge that "high quality childcare" is not reliably achievable. They quote overseas studies when favourable, but, when not, they claim Australian childcare is of higher quality.3 But one carer to five infants is "nobody's definition of quality".4 I argue that the early childcare agenda is misconceived and needs rethinking. Qualitatively better outcomes should be achievable without the associated risks.1,5,6 Peter S Cook Child Psychiatrist (retired) PO Box 84, Repton, NSW 2454 Cook PS. Early child care -- infants and nations at risk. Melbourne: News Weekly Books, 1997. New South Wales Branch of the Child Psychiatry Section of the Australian and New Zealand College of Psychiatrists. Memorandum on some aspects of the welfare of children aged under three years whose mothers are in full-time employment. Med J Aust 1971; 1: 446-448. Ochiltree G. Effects of child care on young children: forty years of research. Melbourne: Australian Institute of Family Studies, 1994: 65-66. (Early Childhood Study Paper No. 5.) Hope D. Spare the non-maternal care and nurture the child. The Australian 1998; June 4. Cook PS. Home truths absent in early childcare debate: we need parent-friendly options [opinion]. The Australian 1999; March 24. Cook PS. The role of myth in childcare policy [letter]. The Australian 1999; April 14. ª 1999 Medical Journal of Australia.

Research Prevention of perinatal group B streptococcal disease: screening practice in public hospitals in Victoria Mary Connellan and Euan M Wallace MJA 2000; 172: 317-320 For editorial comment, see Oats Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Infectious diseases and parasitology Abstract Objectives: To survey clinical protocols for prevention of early-onset group B streptococcal disease (EOGBSD) of the newborn in public maternity hospitals. Design: Postal questionnaire with telephone follow-up when required. Setting: All hospitals that undertook deliveries in public patients in the State of Victoria, November 1997 to January 1998. Results: The survey was sent to 84 hospitals: 71 responded and 64 met the criteria and provided usable data (76% response rate). These 64 represented 42 784 births (68% of births in Victoria in 1996). Most hospitals (62; 97%) undertook actions that would identify and treat pregnant women at risk of EOGBSD. 48 (75%) performed bacteriological screening for maternal GBS carriage, but only 20 of these had a unified protocol. Screening was mostly by low vaginal swab (15 hospitals) and before 30 weeks' gestation (12 hospitals). Low vaginal swab plus anal swab was used in only one hospital. Bacteriological screening was significantly more common in metropolitan hospitals than in rural hospitals (100% versus 67%; P = 0.007, Fisher's exact test). Targeting of prophylaxis by recognised risk factors was reported by 59 (92%) hospitals, 45 of which also undertook screening. There was considerable variation in the specific risk factors used. Conclusions: While there was clearly widespread awareness of EOGBSD in Victorian public hospitals, prevention programs varied considerably. The development of consensus practice guidelines might improve EOGBSD prevention, reducing morbidity, mortality and costs. Introduction Since the 1970s, group B streptococci (GBS) have been recognised as a major cause of neonatal systemic infection in the first week of life -- so called early-onset group B streptococcal disease (EOGBSD). The reported incidence of this condition varies between 1 and 4 per 1000 livebirths.1 Infants acquire the infection by vertical transmission from an asymptomatic mother during delivery.2 Clinical disease manifests at birth or within 24-48 hours as pneumonia, septicaemia or, less commonly, meningitis.1In Australia, the prevalence of GBS vaginal carriage has been estimated at 12%-15%,3-5 and about 1%-2% of infants born to women carrying GBS develop EOGBSD, with about 6% of cases being fatal.2,5-7The risks of EOGBSD and death are particularly high in preterm infants.2 However, antibiotic prophylaxis given to "at risk" women during labour has been shown to significantly reduce the incidence of EOGBSD, and is an important and worthwhile public health measure.2,7-9 While the value of prophylactic antibiotic intervention in at-risk women is now widely agreed, the best means of targeting these women is perhaps less clear. Comprehensive reviews of the available evidence have been published both in Australia1,5,10 and overseas.2,11-13 There are two broad approaches to targeting prophylaxis -- identification of GBS carriers by bacteriological screening or treating by clinical risk factors. No trials have compared the efficacy of the two approaches. It is therefore perhaps not surprising that, anecdotally, GBS intervention practices differ greatly between public hospitals across the State of Victoria. However, no objective data are available to assess the extent of these differences and the appropriateness of current practice. We surveyed all public maternity hospitals in Victoria to explore what GBS intervention programs were in place and, in particular, to assess whether practice was in line with currently available evidence. Methods The Victorian Perinatal Data Collection Unit, Melbourne, provided contact details of all maternity hospitals in Victoria and identified those that undertook deliveries in public patients. Between November 1997 and January 1998, a six-page survey form containing 18 questions was sent to the Delivery Suite Nursing Unit Manager, or equivalent, in each of these hospitals. The survey was multiple-choice format with some free-text fields. Non-respondents were sent a second copy of the survey form two months later and were telephoned if necessary. Data on deliveries in 1996 were supplied by the Victorian Perinatal Data Collection Unit. Statistical analyses were performed using Statview 4.1.14 Significance was taken as P < 0.05. Results Of the 84 hospitals surveyed, 71 responded and 64 met the criteria and provided usable data, giving a final response rate of 76% (three respondents delivered only private patients, one cared for postnatal women only, and three did not provide GBS screening information). The 64 hospitals that provided usable data accounted for 42 784 births in 1996 (68% of all births and 93% of all births to public patients in Victoria) and comprised 16 hospitals in metropolitan Melbourne and 48 rural hospitals. Of the 64 hospitals, 62 (97%) reported undertaking procedures that would identify and treat at least some women with a baby at risk of EOGBSD; 48 hospitals (75%) undertook routine antenatal screening for maternal GBS carriage, including 45 which also offered antibiotic prophylaxis on the basis of risk factors. Another 14 hospitals (22%) used the latter approach alone. Screening for GBS The hospitals which undertook routine antenatal bacteriological screening accounted for 97% of all deliveries in the 64 responding hospitals. They comprised all 16 metropolitan hospitals and 32 of the 48 rural hospitals, a significant difference in proportions between metropolitan and rural hospitals (P = 0.007, Fisher's exact test). Of the 48 hospitals that undertook screening, 20 had a unified hospital screening protocol, with the remainder using individual-doctor protocols. The 20 with a unified protocol comprised nine of the 16 metropolitan hospitals and 11 of the 32 rural hospitals (P = 0.22, Fisher's exact test). Characteristics of the screening protocols among these 20 hospitals are shown in Box 1. Most protocols (65%) were less than five years old, and 40% were less than two years old. The most common approach to bacteriological screening was to perform a low vaginal swab only (15 of 20 hospitals), or, less commonly, a high vaginal swab only (four hospitals). Only one hospital performed a low vaginal swab combined with an anal swab. All but one hospital screened only once in the pregnancy, either before 30 weeks' gestation (12 hospitals) or between 30 and 34 weeks' gestation (seven). The hospital that screened more than once did not specify gestations. All hospitals that performed bacteriological screening administered intrapartum antibiotics to all women who were GBS-positive. Screening of private patients Bacteriological screening was offered to private patients by some or all obstetricians at 37 of the 64 hospitals. This was a smaller proportion of hospitals than offered screening to public patients, although the difference did not reach significance (P = 0.06, Fisher's exact test). In only 18 of these 37 hospitals did all obstetricians offer screening to their private patients. In 13 hospitals, none offered screening to private patients, and in 14 the respondent did not know if it was offered. Risk-factor-targeted prophylaxis Targeting of prophylaxis by recognised clinical risk factors was reported by 59 of the 64 hospitals (92%). Criteria used are shown in Box 2. Antibiotics were reported to be given most commonly for clinical signs of intrapartum infection (51 hospitals) and pre-labour rupture of the membranes (43 hospitals), although the time from membrane rupture to starting antibiotic administration varied considerably. Only 10 hospitals administered antibiotics to women admitted in preterm labour below a specified gestation. All were metropolitan hospitals that also performed routine bacteriological screening. Only four hospitals (6%) administered antibiotics on the basis of all five recognised criteria. Two of these also undertook screening. With regard to the antibiotic used as chemoprophylaxis, 14 of the 20 hospitals with a unified protocol used penicillin, four amoxycillin and two ampicillin. The 14 hospitals using penicillin all had different treatment regimens. Of the hospitals that lacked a unified protocol, only four reported the antibiotic regimen used -- penicillin in three and amoxycillin in one. Discussion To our knowledge, this is the first survey of GBS screening practices in pregnancy to be reported in Australia. It reveals that prenatal screening and prophylaxis for GBS infection were widely practised in public hospitals in Victoria. However, the specific strategies varied considerably, and, while this variation is understandable (given the lack of robust comparative data for the various possible approaches2,10,12,15), it translated into a less than ideal approach in many centres. Current evidence suggests that the optimum approach to reduce EOGBSD is to offer intrapartum chemoprophylaxis, using penicillin (or erythromycin in women allergic to penicillin) to at-risk mother-infant pairs. These at-risk pairs are identified by bacteriological screening, involving a low vaginal and anal swab performed at 36-38 weeks' gestation and/or by clinical risk factors (Box 3).2,10 In our survey, most hospitals reported targeting prophylaxis through bacteriological screening. However, the varied approaches to this screening revealed that current practice may not be as effective as possible. In addition, while most hospitals undertook screening, only 20 had a unified protocol, while the remaining 28 reported that protocols differed between doctors. This, together with the variable practice for private patients, suggests that it may be useful to develop more uniform Australian guidelines. Indeed, that only two hospitals (3% of respondents) reported a current protocol that would be expected to maximally prevent EOGBSD (targeting prophylaxis by bacteriological screening and by all risk factors shown in Box 3) suggests that the introduction of uniform practice guidelines would be worthwhile. The most common differences between the reported screening protocols and an approach expected to minimise EOGBSD were the maternal sites sampled and the timing of screening. GBS carriage within individuals is not constant. Consequently, bacteriological swabs taken at 28 weeks' gestation have only a 50%-70% positive predictive value for carriage at delivery, while about 5%-10% of women who are GBS-positive at delivery are negative at 28 weeks.3,13,16 Therefore, the closer to delivery that bacteriological screening is undertaken, the greater its utility, both as sensitivity and specificity are increased,2,10,16 and as the costs of screening are saved for the 5% of pregnant women who deliver preterm (and should receive prophylaxis irrespective of the screening result.2,11). Thus, bacteriological screening is probably best undertaken at 36-38 weeks' rather than at less than 30 weeks' gestation, the most popular time in our survey. Nevertheless, despite these theoretical considerations, a significant reduction in the incidence of EOGBSD was recently reported by King George V Hospital, Sydney, where screening is performed at 28 weeks' gestation.17 This result emphasises that bacteriological screening at 28 weeks' gestation is preferable to no screening at all. Detection of GBS is increased by 5%-25% if an anal swab is collected in addition to a vaginal swab.16,18,19 Only one hospital in our survey reported collecting both swabs; most took only a low vaginal swab. It has been suggested that Australian women would find collection of anal swabs unacceptable,20 but no objective evidence has been presented for this. Furthermore, most United States centres surveyed by the Centers for Disease Control took anal swabs,21 suggesting that the practice may be more acceptable than is assumed. It would certainly be worthwhile asking Australian women, and reappraising the method of screening most appropriate for our population. Collection of high vaginal swabs, reported by four hospitals in our survey, is inappropriate for GBS screening. The most cost-effective approach to preventing EOGBSD is to offer antibiotic prophylaxis to women with identified risk factors, without bacteriological screening.15 This approach has been recommended by some Australian groups (Professor James King, Mater Perinatal Epidemiology Unit, Mater Misericordiae Mothers' Hospital, Brisbane, Qld, personal communication). Most hospitals surveyed (92%) offered prophylaxis on the basis of risk factors, but only four (6%) used all recognised risk factors appropriately (Box 3). As the relative risk of EOGBSD is significantly greater in preterm neonates than in babies born at term,7 any EOGBSD prevention program should ideally include intrapartum prophylaxis for any woman labouring before 37 weeks' gestation, irrespective of whether she was screened earlier in pregnancy or of the result of that screening.2,11 It was disappointing that only a minority of the hospitals surveyed had such a policy, particularly as infection per se is a major recognised cause of preterm labour. That no rural hospital had such a policy may reflect that these hospitals transfer such women for level 3 neonatal care, and that preparation for transfer focuses more on tocolytic therapy and corticosteroid prophylaxis. If so, then an educational campaign to encourage early antibiotic treatment instituted at the referring hospital might be worthwhile. We were also surprised that only a few hospitals offered antibiotic prophylaxis to women who had had a previous baby with EOGBSD. Neonatal EOGBSD is a devastating infection, and, in our experience, parents who have had an infected child usually seek interventions to prevent infection in a future delivery. That most clinicians and hospitals do not routinely offer prophylaxis in this situation suggests a lack of awareness that this history is an important risk factor. Similarly, the variable responses to the other accepted risk factors suggest that a significant proportion of health providers are either unaware of the epidemiology of EOGBSD or do not perceive EOGBSD as an important clinical problem. Our survey of Victorian public hospitals showed that, while most are clearly aware of EOGBSD, only a minority currently have a strategy that maximises prevention of EOGBSD and represents most cost-effective practice. However, very minor changes in practice would be expected to improve EOGBSD prevention and significantly reduce costs,15 for both screening and treatment. Accordingly, our data support the case for a comprehensive, statewide, or possibly national, education program, and for the development and introduction of uniform consensus practice guidelines. Acknowledgements The authors would like to thank the participating hospitals as well as Dr Jane Halliday and Ms Sofia Mercer, from the Victorian Perinatal Data Collection Unit. EMW was partly funded by a Charles and Sylvia Viertel Clinical Investigator Fellowship. Disclosure: We are not aware of any conflict of interest arising from performing or reporting this work. References Vigneswaran R, O'Loughlin JA, McDonald HM. Group B streptococcus and pregnancy. Aust N Z J Obstet Gynaecol 1995; 35: 117-119. Prevention of perinatal group B streptococcal disease: a public health perspective. Centers for Disease Control and Prevention. MMWR Morb Mortal Wkly Rep 1996; 45 (RR-7): 1-24. McDonald H, Vigneswaran R, O'Loughlin JA. Group B streptococcal colonization and preterm labour. Aust N Z J Obstet Gynaecol 1989; 29: 291-293. Australasian Study Group for Neonatal Infections. Early-onset group B streptococcal infections in Aboriginal and non-Aboriginal infants. Med J Aust 1995; 163: 302-306. Jefferey HE, McIntosh ED. Antepartum screening and non-selective intrapartum chemoprophylaxis for group B streptococcus. Aust N Z J Obstet Gynaecol 1994; 34: 14-19. Garland SM, Fleigner JR. Group B streptococcus (GBS) and neonatal infections: the case for intrapartum chemoprophylaxis. Aust N Z J Obstet Gynaecol 1991; 31: 119-122. Zangwill KM, Schuchat A, Wenger JD. Group G streptococcal disease in the United States, 1990: report from a multistate active surveillance system. Morb Mortal Wkly Rep CDC Surveill Summ 1992; 41: 25-32. Smaill F. Intrapartum antibiotics for Group B streptococcal colonisation (Cochrane review). The Cochrane Library, 1999: 3. Oxford: Update Software. Schrag SJ, Zywicki S, Farley MM, et al. Group B streptococcal disease in the era of intrapartum antibiotic prophylaxis. N Engl J Med 2000; 342: 15-20. Gilbert GL, Isaacs D, Burgess MA, et al. Prevention of neonatal group B streptococcal sepsis: is routine antenatal screening appropriate. Aust N Z J Obstet Gynaecol 1995; 35: 120-126. Schuchat A. Group B streptococcus. Lancet 1999; 353: 51-56. Rouse DJ, Goldenberg RL, Cliver SP, et al. Strategies for the prevention of early-onset neonatal group B streptococcal sepsis: a decision analysis. Obstet Gynecol 1994; 83: 483-494. Regan JA, Klebanoff MA, Nugent RP, et al, VIP Study Group. Colonization with group B streptococci in pregnancy and adverse outcome. Am J Obstet Gynecol 1996; 174: 1354-1360. Statview 4.1. Berkeley, CA: Abacus, 1994. Garland SM, Kelly N. Early-onset group B streptococcal sepsis: economics of various prevention strategies. Med J Aust 1995; 162: 413-417. Boyer KM, Gadzala CA, Kelly PD, et al. Selective intrapartum chemoprophylaxis of neonatal group B streptococcal early-onset disease. II. Predictive value of prenatal cultures. J Infect Dis 1983; 148: 802-809. Jefferey HE, Lahra MM. Eight-year outcome of universal screening and intrapartum antibiotics for maternal group B streptococcal carriers. Pediatrics 1998; 101: E2. Badri MS, Zawaneh S, Cruz AC, et al. Rectal colonisation with group B streptococcus: relation to vaginal colonisation of pregnant women. J Infect Dis 1977; 135: 308-312. Dillon HC, Gray E, Pass MA, Gray BM. Anorectal and vaginal carriage of group B streptococci during pregnancy. J Infect Dis 1982; 145: 794-799. Prevention of neonatal group B streptococcal sepsis: is routine antenatal screening appropriate? [editorial comment]. Aust N Z J Obstet Gynaecol 1995; 35: 120. Adoption of hospital policies for prevention of perinatal group B streptococcal disease -- United States, 1997. MMWR Morb Mortal Wkly Rep 1998; 47: 665-670. (Received 10 Nov 1999, accepted 14 Feb 2000) Authors' details Monash Medical Centre, Melbourne, VIC. Mary Connellan, RM, MPH, Midwife, Women's Health Program, Southern Healthcare Network; Euan M Wallace, MD, FRACOG, Senior Lecturer, Department of Obstetrics and Gynaecology, Monash University. Reprints: Dr E M Wallace, Department of Obstetrics and Gynaecology, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168. euan.wallaceATmed.monash.edu.au Make a comment 1: Characteristics of screening for group B streptococcus in 20 hospitals with a unified screening protocol Number of hospitalsYears since screening protocol introduced < 28 (40%) 2-55 (25%) > 5-91 (5%) > 92 (10%) Not known4 (20%) Form of screening Low vaginal swab only15 (75%) High vaginal swab only4 (20%) Low vaginal swab and anal swab1 (5%) Frequency per pregnancy Once only19 (95%) More than once1 (5%)Timing < 30 weeks' gestation12 (60%) 30-34 weeks' gestation7 (35%) Unknown1 (5%)**The hospital that screened more than once did not specify gestations. Back to text 2: Criteria for intrapartum administration of antibiotics in 64 hospitals in Victoria CriteriaNumber of hospitals usingClinical signs of intrapartum infection51 (80%)Pre-labour rupture of membranes43 (67%) < 6h4 (6%) 6-12h0 > 12-18h10 (16%) > 18-24h4 (6%) > 24h21 (33%) Doctor-dependent4 (6%)Previous GBS-affected baby30 (47%)GBS-positive vaginal swab in previous pregnancy22 (34%)Preterm labour10 (16%) Gestation < 37 weeks7 (11%) Gestation < 34 weeks2 (3%) Gestation < 32 weeks1 (2%)GBS=Group B streptococcus. Back to text 3: Key risk factors for early-onset neonatal group B streptococcal disease (EOGBSD) Preterm delivery (< 37 weeks' gestation) Prolonged rupture of membranes (> 18h) Previous infant with EOGBSD GBS bacteriuria during pregnancy Intrapartum maternal pyrexia Back to text

Mary Connellan · Euan M Wallace

Editorial The health of young Australians Mental disorders account for the major burden of disease in young people MJA 2000; 172: 150-151 Community views on youth health tend to be polarised and contradictory. On the one hand, adolescents are seen as having few overt health needs: mortality is low by comparison to that in older groups, and most young people, and their parents, rate their health as good. On the other hand, the emergence in recent decades of youth suicide, drug abuse and new infectious diseases (eg, HIV) has elicited strong and sometimes conflicting opinions about moral and social threats to young people's health. Individualism, a growth in permissiveness, and a decline in religious affiliations have all attracted debate. The recent report Australia's young people: their health and well-being 1999,1 from the Australian Institute of Health and Welfare (AIHW), provides some clarity. It follows an earlier report on child health2 and gives the first comprehensive national picture of the health of young Australians (see Box for key points). In general, Australian youth remain healthy, and retain a positive view of their health. Some health trends are positive: overall mortality in young people in the 1990s was at historically low levels (mostly due to the substantial reductions in motor vehicle deaths in the previous two decades); and rates of teenage pregnancy were low compared with those of other First World countries. However, new threats to youth health have emerged: Mental and behavioural disorders are increasingly recognised as affecting youth disproportionately and account for over half their disease burden. With the changing profile of infectious disease, newer bloodborne and sexually transmitted diseases have become prominent, with threefold higher notifications of both chlamydia and hepatitis C. The prevalence of syphilis has declined further, but gonorrhoea notifications have doubled. Shifts in young people's lifestyle carry implications for health later in life. Tobacco use remains obstinately high, with 40% of young adults continuing to smoke. Physical activity declines across the teens, so that fewer than a third of women aged 20-24 years take part in regular, moderate to vigorous physical exercise. Moreover, 22% of 15-24 year olds already have a body mass index in the overweight or obese range for adults. Some groups have disproportionately high levels of health problems. Low socioeconomic status is linked to higher death and hospitalisation rates, as well as to lower self-rating of health. Recent death rates for young Aboriginal and Torres Strait Islanders are close to three times higher in males and twice as high in females compared with rates for non-Indigenous youth. High levels of mental disorders and substance abuse are major contributors at one level, but the fundamental causes are more likely to be found in social and economic conditions, the loss of cultural identity and the disaffection of youth in many of these communities. The report's findings will inevitably prompt questions about current health provision for young Australians. At present, young people's primary care attendances, for example, are mostly for relatively minor respiratory conditions, musculoskeletal problems or acne. The conditions contributing to the disease burden in young people are less common reasons for general practice presentations, suggesting scope for the development of "youth-friendly" primary-care services capable of responding to youth health problems. With training in adolescent health care, general practitioners can both learn and retain the skills for responding to youth health needs,3 and such training could be linked to health education for young people about access, availability and use of health services. Health promotion has an even greater role. Health problems cluster not only in particular groups but also in individuals. For example, the young regular tobacco user is more likely to engage in heavy alcohol consumption and illicit drug use, have poorer mental health and an overall less healthy lifestyle.4 The clustering can mostly be traced back to common determinants of health in family, community, school and developmental backgrounds. Recent North American research has emphasised the protective influence of family and school attachment on problems ranging from deliberate self-harm and emotional distress to tobacco and illicit substance use, violence and early sexual activity.5 Such findings have been mirrored in recent Australian research.6,7 More importantly, preventive intervention targeting these social risk and protective factors is feasible and can be effective.8,9 Family and school-based interventions, both in adolescence and during childhood, have been shown to reduce adolescent problems as diverse as antisocial behaviour, substance abuse and sexually risky behaviour.9 Similarly, strategies based on community mobilisation, peer support, mentoring and legislative enforcement show promise in specific areas. Many gaps in our knowledge remain. Mental health problems loom large, but available data provide an incomplete picture of current need, changes over time and effectiveness of current health provision. Health profiles of groups with the greatest needs -- the young, the homeless and the disabled -- are incomplete, as are those of Aboriginal and Torres Strait Islanders. Much remains to be learned about health interventions and their effectiveness. Most importantly, data on the psychosocial processes that underpin youth health are not available. Health promotion should be guided not only by knowledge of the health problems of young people, but also by an understanding of relevant risk and protective factors. For mental health problems, these are likely to include parental care, the experience of psychosocial adversity, trauma and violence, victimisation, school failure and underemployment. This understanding is of value, not only in selecting the focus of health promotion, but in helping to ensure its continued relevance and sustainability. A recent report from the World Health Organization noted that most investment has gone into innovation rather than continuing programs, with only one in five youth health programs extending beyond five years.10 Sustainable preventive health programs for youth necessarily depend on effective cooperation with government sectors such as education, justice and employment, as well as non-governmental organisations involved with youth, younger children and their families. As the most comprehensive available account of the health of young Australians, the AIHW report will do much to inform the intersectoral dialogue that must underpin the setting of priorities and, in turn, the development of a rational advocacy. However, implementing effective responses to these priorities will require further work to build a more complete picture of the psychosocial determinants of the major health problems of young people. George C Patton Professor of Adolescent Health, Department of Paediatrics University of Melbourne Centre for Adolescent Health, Melbourne, VIC pattonATcryptic.rch.unimelb.edu.au Lynelle J Moon Senior Analyst, Population Health Unit Australian Institute of Health and Welfare, Canberra, ACT Reprints: Professor G C Patton, Department of Paediatrics, University of Melbourne, Centre for Adolescent Health, 2 Gatehouse Street, Parkville, VIC 3052. Moon L, Meyer P, Grau J. Australia's young people: their health and well-being. PHE19. Canberra: Australian Institute of Health and Welfare, 1999. Moon L, Rahman N, Bhatia K. Australia's children: their health and well-being. PHE7. Canberra: Australian Institute of Health and Welfare, 1998. Sanci LA, Coffey C, Veit FCM, et al. Evaluation of an educational intervention for general practitioners in adolescent health care: randomised controlled study. BMJ 2000; 320: 224-230. Hibbert M, Caust J, Patton G, et al. The health of young people in Victoria. Melbourne: Centre for Adolescent Health, 1996. Resnick MD, Bearman PS, Blum RW, et al. Protecting adolescents from harm: findings from the National Longitudinal Study on Adolescent Health. JAMA 1997; 278: 823-832. Glover S, Burns JBH, Patton GC. The Gatehouse Project: the scope of school based intervention for the prevention of adolescent depression. Family Matters 1998; 49: 11-16. Silburn SR, Zubrick SR, Garton AF, et al. Western Australian Child Health Survey: Family and Community Health. Perth: Australian Bureau of Statistics, 1996. (Catalogue No. 4304.5) National Crime Strategy (Homel R, editor). Pathways to prevention. Canberra: Attorney General's Department, 1999. Toumbourou JW, Patton GC, Sawyer S, et al. Guidelines to inform planning and purchasing of evidence-based practice: interventions for promoting health in the adolescent population. Melbourne: Department of Human Services, 1999. WHO/UNFPA/UNICEF Study Group. Programming for adolescent health and development. Geneva: World Health Organization, 1999. Make a comment Key points from the report Australia's young people: their health and well-being 19991 Young Australians remain in good health... Two-thirds of young people rated their own health as "excellent" or "very good" and getting better. Overall death rates for 12-24 year olds declined by 29% over the period 1979-1992 to 60/100000 (partly due to a 60% decline in motor vehicle accident deaths, 1979-1997), and have remained stable since then. but there are areas of concern... The major burden of disease (combined effect of mortality and disability) for this age group is from mental disorders. Injury is the leading cause of death for 12-24 year olds (40/100000 per year in 1997), with two-thirds of all deaths attributed to some form of injury, including accidents and suicide. Suicide (15.1/100000 per year) and drug-related deaths (4.2/100000 per year) have not followed the declines in most other causes of death, particularly for young men. In 1998, 25% of young people aged 14-19 years and 40% of those aged 20-24 years were regular or occasional smokers. While 54% of 15-24 year olds in 1995 were of acceptable weight, 22% were overweight or obese. The proportions of young people reporting exercising at a "vigorous" or "moderate" level for sport or recreation declined with age. and some groups are worse off. Recent death rates (1995-1997) for Aboriginal and Torres Strait Islander youth were 2.8 times higher for males (278/100000 per year) and 2.0 times higher for females (70/100000 per year) than those of their non-Indigenous counterparts (males, 101/100000 per year; females, 35/100000 per year). The 20% of males in the lowest socioeconomic group were 1.7 times more likely to die and 1.4 times more likely to be hospitalised than males in the highest group; for females, these ratios were 1.4 and 1.2, respectively. Twenty per cent of unemployed youth in 1995 assessed their health status as being fair or poor, compared with 9% of employed youth and 8% of students. Back to text

George C Patton · Lynelle J Moon

Healthcare Accidental paracetamol overdosing and fulminant hepatic failure in children Fiona K Miles, Ramananda Kamath, Stuart F A Dorney, Kevin J Gaskin and Edward V O'Loughlin MJA 1999; 171: 472-475 See also Hynson Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Pathology Abstract Objective: To delineate clinical characteristics useful for identifying children with liver failure due to accidental paracetamol overdose. Design: Retrospective review of medical records of all patients admitted from 1985 to 1998 with fulminant hepatic failure. Setting: Royal Alexandra Hospital for Children, a tertiary referral centre for paediatric liver transplantation. Main outcome measures: Contribution of paracetamol to liver failure; other risk factors for liver failure; comparison of clinical features of paracetamol group and others. Results: 18 patients were identified. Eight were considered to have accidental paracetamol hepatotoxicity. In a further three, other risk factors were present but paracetamol was considered a major contributor to liver failure. The seven remaining patients had other risk factors for liver failure. Patients with paracetamol-induced liver failure usually had an acute prodromal illness with prolonged fasting and, at presentation, had encephalopathy, coagulopathy, very high transaminase levels, but disproportionately low total bilirubin levels. Five patients had hypoglycaemia. End-stage liver failure occurred in 4/11 of the paracetamol group compared with 7/7 of the others. Conclusion: Accidental paracetamol overdose is associated with fulminant hepatic failure in infants and children. Patients present with high transaminase levels and liver synthetic failure out of proportion to the level of serum bilirubin. Prompt identification of such patients is important as many recover with supportive therapy. Introduction Paracetamol is a commonly used antipyretic and analgesic medication; in 1996, it was the second most common drug used in Australia, with 4.75 million units dispensed.1 There is a large range in the preparations of doses available, and the potential for accidental overdose due to confusion over concentration and frequency of dosing is high.2Intentional paracetamol overdose is a well-recognised cause of fulminant liver failure.2 However, there are few reports of accidental overdose due to recurrent ingestion of high therapeutic doses in children.3-6 Alonso et al reported seven children with fulminant liver failure without obvious cause.5 All patients had ingested paracetamol, but serum paracetamol levels were not in the toxic range. The authors postulated that, although paracetamol may have contributed to the liver injury, it was not causative. Two other reports describe accidental multiple dosing causing liver failure in children, with many patients receiving doses in the recommended therapeutic range.3,6 Prodromal illness associated with prolonged fasting was also recognised as potentially important in the development of liver injury.4,5 Since 1985, the Royal Alexandra Hospital for Children has been a tertiary referral centre for paediatric liver transplantation. Over this period, 19 patients have presented with acute liver failure. Our aims were to review all cases of acute liver failure, to identify patients with accidental (overdose with therapeutic intent) paracetamol-induced liver failure, and to define clinical features which may be useful in identifying such cases. Methods All patients at the Royal Alexandra Hospital with fulminant hepatic failure -- severe acute liver injury with no pre-existing liver disease resulting in encephalopathy within eight weeks of onset -- are managed by members of the liver transplant service. We reviewed case records of such patients for a history of liver disease, presenting symptoms, pre-existing history of paracetamol ingestion, clinical status at presentation, laboratory investigations and outcome. Paracetamol hepatotoxicity was considered likely if patients with liver failure had: a history of paracetamol ingestion over several days, confirmed by the finding of paracetamol in the blood; and exclusion (by routine laboratory testing) of other known causes of acute liver failure, such as viral hepatitis (A, B, C, Epstein-Barr virus, cyto-megalovirus, HSV-6, varicella or adenovirus), drug- or toxin-induced hepatotoxicity, inborn errors of metabolism (Wilson's disease, α1-antitrypsin deficiency, and fatty acid oxidation abnormalities). Approval for our study was obtained from the hospital's institutional ethics committee. Results Ninteen patients were identified, aged 6-165 months. One adolescent developed liver failure from suicidal overdose (30 g), and made a complete recovery with conservative treatment; this patient was excluded from the study. Paracetamol hepatotoxicity Eleven of the remaining 18 patients had presumed paracetamol hepatotoxicity. The patient data shown in the Table represent peak levels of study parameters or stage of encephalopathy. All patients had coagulopathy, elevated transaminase levels, and abnormal total serum bilirubin. Eight patients (numbers 1-8, Table) were identified as having paracetamol overdose as the only risk factor for liver failure. All eight patients had a history of a prodromal illness for which they received paracetamol for 4-21 days prior to the identification of liver disease. Reported paracetamol intakes ranged from 20 to 200 mg/kg per day. Paracetamol was detected in the blood of all eight patients, and all were encephalopathic (stage I-III) at presentation. Patients 1, 2, 3, 5 and 7 were hypoglycaemic (blood glucose levels < 3 mmol/L) at admission. Liver failure resolved with supportive treatment in six of these patients; Patients 2 and 6 died while awaiting liver transplants. Patient 5 survived, but had severe neurological sequelae as a result of protracted hypoglycaemia and stage IV encephalopathy. Patient 4 was admitted to the intensive care unit, but was not initially recognised as having liver failure. Patients 9, 10 and 11 had probable paracetamol hepatotoxicity, but also had other risk factors for liver injury. Patient 9 had Ewing's sarcoma and had been receiving chemotherapy. Multiple doses of paracetamol had been administered in hospital before the onset of liver failure. At postmortem, hepatic centrilobular necrosis consistent with paracetamol hepatotoxicity was found. Patient 10 also had a history of paracetamol ingestion, although the quantity could not be determined from the history. However, a high level of paracetamol was detected in the blood. The patient had had one previous admission with mumps encephalitis, which resulted in epilepsy and mental retardation. He had also been taking sodium valproate for seizures for several years, with no evidence of liver abnormalities. The patient died of end-stage liver failure and post-mortem revealed severe centrilobular necrosis consistent with paracetamol- rather than valproate-induced liver injury. Patient 11 had a mild prodromal illness due to Epstein-Barr virus infection, but ingested large quantities of paracetamol and presented with the clinical picture as described for Patients 1-8. Coagulopathy precluded liver biopsy in this group of patients. Metabolic studies: Urinary metabolic studies failed to reveal abnormal metabolites indicative of fatty acid oxidation defects in Patients 1, 2, 5, 6, 7 and 8, and skin fibroblast assays for fatty acid oxidation defects were normal in Patients 3, 6, 7 and 8. For Patient 4, no metabolic studies were performed. Other causes of liver failure Seven patients presented with fulminating liver failure from other causes, including Wilson's disease (1), cytomegalovirus infection (1), hepatitis B virus infection (1), presumed viral hepatitis (3), and an adverse reaction to dapsone (1). All patients presented with evidence of severe synthetic failure (coagulopathy and hypoalbuminaemia) and hepatic encephalopathy. Distinguishing paracetamol hepatotoxicity The Figure compares the serum bilirubin levels plotted against alanine transaminase levels in both groups of patients. In contrast to patients with other causes of acute liver failure, patients with presumed paracetamol hepatotoxicity all had serum bilirubin levels less than 200 µmol/L, and most had alanine transaminase levels greater than 4000 IU/L. Hypoglycaemia was not detected in any of the patients with liver failure from causes other than paracetamol, and all patients in this group either died or received transplants. Discussion Clinical features Accidental paracetamol overdose was the likely cause of acute liver failure in most children in this series presenting to a single paediatric institution. Eight of the 18 patients had likely paracetamol-induced liver failure due to accidental overdose, and in a further three paracetamol was a major risk factor. A distinct clinical pattern emerges when the patients with definite or presumed paracetamol toxicity are compared with patients with other causes of fulminant hepatic failure. Patients with paracetamol toxicity presented with a non-specific prodromal illness, often with fasting and/or vomiting. At the time of hospitalisation they had evidence of severe synthetic failure, often with associated hypoglycaemia, coagulopathy and mild encephalopathy, but with disproportionately low bilirubin levels. Moreover, most patients recovered with supportive therapy. A history of paracetamol ingestion over several days is important in establishing the diagnosis of paracetamol toxicity. In our study, reported ingestion of as little as 20 mg/kg per day over a protracted period was associated with liver failure. Similar toxic dosage ranges have been reported in other studies of children,3,5 raising the question of whether some susceptible children could suffer acute liver failure as a result of therapeutic doses of paracetamol ingested over several days. However, it is important to emphasise that the paracetamol intake data reported in this study, as in previous published reports, rely on history alone. The dosages reported by parents could not be verified by other means. Whether therapeutic doses of paracetamol could result in liver failure in susceptible children remains unresolved owing to the poor quality of the existing paediatric data. Serum paracetamol levels Paracetamol was detected in the serum of patients with presumed paracetamol hepatotoxicity. Although other investigators have used a level of 0.04 mmol/L3,4 as indicative of toxicity, it is not clear that this is a meaningful level in an individual with repeated ingestions over several days. A level of 40 µmol/L or greater at 24 hours after the ingested dose is thought to predict the likely development of liver failure, as portrayed in the nomogram adapted by Rumack and Matthews.7 However, this nomogram was derived from adult patients presenting with liver failure from a single suicidal overdose. No studies have addressed the question of serum levels likely to predict hepatic failure after repeated doses. We observed that the possible role of paracetamol was, on occasion, discounted because paracetamol levels were lower than those predictive of the development of liver failure from the nomogram. Poor correlation between paracetamol levels and liver toxicity with accidental overdose has been observed in a large series of adult patients in whom less than 50% had peak serum levels greater than 10 µg/mL (40 µmol/L).4 Similarly, low levels were reported in a small series of children.5 Nevertheless, serum paracetamol levels should be measured routinely in the investigation of children presenting with acute liver failure as soon as possible after assessment, but should be interpreted with caution. A recent study of paracetamol toxicity in adults by Schiodt et al identified a distinct group of patients who developed liver dysfunction after accidental poisoning with therapeutic intent.4 This group of 21 patients had ingested frequent doses of paracetamol for pain relief. Toxicity may have been compounded by prior starvation.2 Mortality in that study (4/21) was similar to ours, but was substantially higher than in a group of adult patients with non-accidental overdose. Some doubts about the role of paracetamol in causing fulminant hepatic failure in the study by Schiodt et al have been raised, as a high proportion of patients had a history of concurrent alcohol abuse and dosage levels were considered by some to be too low to cause toxicity.8-11 In contrast to that study of adults, studies in children raise considerable concern that accidental paracetamol overdose causes liver failure in this age group.3,5 However, it is important to note that all the reported series in children (including our own) are anecdotal reports. No studies have included a control group or undertaken a case-control study design, although liver biopsies were performed in six of seven patients in one series.5 While one could argue that the association between accidental overdose and liver failure in children is speculative, several arguments support the likely association with paracetamol: Suicidal overdose in adults produces acute liver failure with a clinical and biochemical picture very similar to that reported in our study of overdose due to repeated ingestion. The presence of severe liver synthetic failure and encephalopathy with the pattern of liver function tests we describe (see Figure) is a very atypical presentation for most diseases which produce liver failure in children. In our study, four children had centrilobular necrosis on postmortem examination, a finding consistent with paracetamol hepatotoxicity. While some of the clinical characterisics, such as prodromal illness, hypoglycaemia, high transaminase levels and coagulopathy, would be consistent with Reye's syndrome,12 it is not likely that this diagnosis would explain the abnormalities which we attribute to paracetamol toxicity. Recent in-vitro and animal studies indicate that paracetamol or its metabolites impair mitochondrial metabolism, and this effect occurs before hepatocyte necrosis.13-15 In this regard, paracetamol hepatotoxicity demonstrates some remarkable clinical and biochemical similarities to some inborn errors of fatty acid oxidation which can present with fulminant liver failure.16 Despite several attempts to define a safe therapeutic regimen, there is still no consensus as to the appropriate dose, or even efficacy, in children. One report recommended single doses of 10-15 mg/kg four-hourly as a "safe maximum".17 However, Nahata et al demonstrated that paracetamol may accumulate substantially, with raised concentrations after therapeutic doses for two to three days, even with doses of 13 mg/kg 24-hourly.18 One study which did review the potential for chronic overdose in children was done by Penna et al,19 in which 190 of 299 paediatric inpatients received paracetamol for indications of fever and postoperative pain. Most were prescribed four-hourly doses, with potential for greater than 90 mg/kg per day. Nearly a quarter of the high doses were for children under 12 months of age. Although it can be argued that paracetamol "is commonly administered to children . . . for most febrile illnesses",5 and thus can be a frequent coincidental association, there is evidence that accidental overdose while ingesting high therapeutic doses of paracetamol for pain and fever relief may cause fulminating liver failure in children. Clinicians should be alerted to the possibility of paracetamol toxicity in an infant or child presenting with a prodromal illness associated with fasting and the regular ingestion of paracetamol over several days. Hypoglycaemia, severe synthetic failure and encephalopathy with very high transaminase levels (above 4000 IU/L) and a serum bilirubin level less than 200 µmol/L would support the diagnosis. It is important to distinguish this group of patients, as the prognosis for recovery is good with conservative therapy. If N-acetylcysteine is instituted early, liver transplantation may be avoided. References Commonwealth Department of Health and Family Services. Top 10 drugs. Australian Prescriber 1997; 20: 92. Vale JA, Proudfoot AT. Paracetamol (acetaminophen) poisoning. Lancet 1995; 346: 547-552. Heubi JE, Barbacci MB, Zimmerman HJ. Therapeutic misadventures with acetaminophen: hepatotoxicity after multiple doses in children. J Pediatr 1998; 132: 22-27. Schiodt FV, Rochling FA, Casey DL, Lee WM. Acetaminophen toxicity in an urban county hospital. N Engl J Med 1997; 337: 1112-1117. Alonso EM, Sokol RJ, Hart J, et al. Fulminant hepatitis associated with centrilobular hepatic necrosis in young children. J Pediatr 1995; 127: 888-894. Rivera-Penera T, Gugig R, Davis J, et al. Outcome of acetaminophen overdose in pediatric patients and factors contributing to hepatotoxicity. J Pediatr 1997; 130: 300-304. Rumack BH, Matthews H. Acetaminophen poisoning and toxicity. Pediatrics 1975; 55: 871-876. Walker AM. Acetaminophen toxicity in an urban county hospital [letter]. N Engl J Med 1998; 338: 543. Avorn J. Acetaminophen toxicity in an urban county hospital [letter]. N Engl J Med 1998; 338: 543-544. Rao RB, Hoffman RS. Acetaminophen toxicity in an urban county hospital [letter]. N Engl J Med 1998; 338: 544. Makin AJ, Williams R, Bernal W. Acetaminophen toxicity in an urban county hospital [letter]. N Engl J Med 1998; 338: 544. Diagnosis and treatment of Reye's syndrome. JAMA 1981; 246: 2441-2444. Burcham PC, Harman AW. Acetaminophen toxicity results in site-specific mitochondrial damage in isolated mouse hepatocytes. J Biol Chem 1991; 266: 5059-5054. Vendemiale G, Grattagliano I, Altomare E, et al. Effect of acetaminophen administration on hepatic glutathione compartmentation and mitochondrial energy metabolism in the rat. Biochem Pharmacol 1996; 52: 1147-1154. Nazareth WM, Sethi JK, McLean AE. Effect of paracetamol on mitochondrial membrane function in rat liver slices. Biochem Pharmacol 1991; 42: 931-936. Tyni T, Palotie A, Viinikka L, et al. Long chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency with the G1528C mutation: clinical presentation of thirteen patients. J Pediatr 1997; 130: 67-76. Temple AR. Pediatric dosing of acetaminophen. Pediatr Pharmacol 1983; 3: 321-327. Nahata MC, Powell DA, Durrell DE, Miller MA. Acetaminophen accumulation in pediatric patients after repeated therapeutic doses. Eur J Clin Pharmacol 1984; 27: 57-59. Penna AC, Dawson KP, Penna CM. Is prescribing paracetamol "pro re nata" acceptable? J Paediatr Child Health 1993; 29: 104-106. (Received 25 Jun, accepted 2 Sep, 1999) Authors' details The Royal Alexandra Hospital for Children, Sydney, NSW. Fiona K Miles, MB ChB, Fellow in Intensive Care; Ramananda Kamath, MD, FRACP, Associate Professor and Staff Specialist, Department of Gastroenterology; Stuart F A Dorney, MB BS, FRACP, Staff Specialist, Department of Gastroenterology; Kevin J Gaskin, MD, FRACP, Professor and Staff Specialist, Department of Gastroenterology; Edward V O'Loughlin, MD, FRACP, Staff Specialist, Department of Gastroenterology. Reprints: Dr E V O'Loughlin, Department of Gastroenterology, The Royal Alexandra Hospital for Children, PO Box 3515, Parramatta, NSW 2124. tedoATnch.edu.au Clinical characteristics of 11 patients with liver failure due to paracetamolPatient: 1Age (months): 21Paracetamol dosage (mg/kg per day): 20 (21 days) & 171 (last day)Serum:Paracetamol level (µmol/L): 10 (D2)*Bilirubin level (µmol/L): 123Alanine transaminase level (IU/L): 9618PT INR: 3.3Hepatic coma stage: IIOutcome: ResolvedPatient: 2Age (months): 63Paracetamol dosage (mg/kg per day): 100 (6 days)Serum:Paracetamol level (µmol/L): 560 (D1)*Bilirubin level (µmol/L): 87Alanine transaminase level (IU/L): > 10 000PT INR: 9.7Hepatic coma stage: IVOutcome: Died (PM: centrilobular necrosis)Patient: 3Age (months): 36Paracetamol dosage (mg/kg per day): Very frequent oral and rectal dosesSerum:Paracetamol level (µmol/L): 30 (D2)*Bilirubin level (µmol/L): 70Alanine transaminase level (IU/L): > 10 000PT INR: 4Hepatic coma stage: IIOutcome: ResolvedPatient: 4Age (months): 77Paracetamol dosage (mg/kg per day): 200 (11 days)Serum:Paracetamol level (µmol/L): 30 (D6)*Bilirubin level (µmol/L): 19Alanine transaminase level (IU/L): 1216PT INR: 1.4†Hepatic coma stage: IIIOutcome: ResolvedPatient: 5Age (months): 31Paracetamol dosage (mg/kg per day): 71 (4 days)Serum:Paracetamol level (µmol/L): 160 (D1)*Bilirubin level (µmol/L): 143Alanine transaminase level (IU/L): > 10 000PT INR: > 20Hepatic coma stage: IVOutcome: Resolved, severe brain damagePatient: 6Age (months): 129Paracetamol dosage (mg/kg per day): 20 (7 days)Serum:Paracetamol level (µmol/L): 180 (D1)*Bilirubin level (µmol/L): 82Alanine transaminase level (IU/L): > 10 000PT INR: 5Hepatic coma stage: IVOutcome: Died (PM: centrilobular necrosis)Patient: 7Age (months): 6Paracetamol dosage (mg/kg per day): UnknownSerum:Paracetamol level (µmol/L): 160 (D1)*Bilirubin level (µmol/L): 94Alanine transaminase level (IU/L): 9 170PT INR: 6.9Hepatic coma stage: IIIOutcome: ResolvedPatient: 8Age (months): 54Paracetamol dosage (mg/kg per day): 74mg/kg/day (5 days) & 150mg/kg/day (final day)Serum:Paracetamol level (µmol/L): 900 (D1)*Bilirubin level (µmol/L): 57Alanine transaminase level (IU/L): 8 300PT INR: 5.4Hepatic coma stage: IIOutcome: ResolvedPatient: 9Age (months): 79Paracetamol dosage (mg/kg per day): Unknown (frequent dosing over several days)Serum:Paracetamol level (µmol/L): 70 (D1)*Bilirubin level (µmol/L): 185Alanine transaminase level (IU/L): 4 300PT INR: 3.1Hepatic coma stage: IVOutcome: Died (PM: centrilobular necrosis)Patient: 10Age (months): 132Paracetamol dosage (mg/kg per day): UnknownSerum:Paracetamol level (µmol/L): 180 (D1)*Bilirubin level (µmol/L): 195Alanine transaminase level (IU/L): 3 620PT INR: 4.2Hepatic coma stage: IVOutcome: Died (PM: centrilobular necrosis)Patient: 11Age (months): 106Paracetamol dosage (mg/kg per day): 175 (7 days)Serum:Paracetamol level (µmol/L): 80 (D3)*Bilirubin level (µmol/L): 102Alanine transaminase level (IU/L): 6 700PT INR: 2.4Hepatic coma stage: IIIOutcome: Resolved* Days post admission to hospital. †Alanine transaminase level and INR measured on admission to hospital but not subsequently, despite deterioration of coma stage. PM = postmortem. OD = overdose. PT-INR = international normalised ratio (of prothrombin time). Normal ranges: serum bilirubin, 1-15 µmol/L; alanine transaminase, 10-50 IU/L; INR, 1-1.2. Back to textBack to text

Fiona K Miles · Ramananda Kamath · Kevin J Gaskin · Edward V O'Loughlin

Lessons from Practice Childhood hepatotoxicity with paracetamol doses less than 150 mg/kg per day MJA 1999; 171: 497 Paracetamol is widely used as an antipyretic and analgesic. Adverse effects are regarded as unlikely at doses below 150 mg/kg per day.1 However, lower doses have resulted in hepatotoxicity,2 and there is growing evidence of the potential for hepatotoxicity in children given multiple therapeutic or supratherapeutic doses of paracetamol.3-6The nomogram devised by Rumack and Matthews7 was based on data obtained from previously well adult patients who had taken a single large dose of paracetamol. The relevance of this to children given multiple doses in the context of a febrile illness is unknown, particularly as the metabolism in this population appears to be quite different.8 It has been suggested that the therapeutic index for paracetamol may be as low as 1.7,9 and that sick children under the age of two years given in excess of 90 mg/kg per day for more than one day should be regarded as being at higher risk.6 The product information recommends a maximum daily dose of 60 mg/kg, but it is not uncommon for children to receive doses in excess of 90 mg/kg per day in the hospital setting.10 Although the number of reported cases of hepatotoxicity induced by therapeutic doses of paracetamol is small, it is possible that cases have gone unrecognised. It is important to administer the drug with caution and according to current dosage guidelines. Case reports Case 1: Six days before transfer to our hospital, a previously well four-year-old, 20 kg girl had commenced a course of cefaclor for otitis media, and over 72 hours she received about 2400 mg of paracetamol in divided doses. She was admitted to her local hospital with fever (39ºC), abdominal pain, vomiting and diarrhoea. Her aspartate transaminase (AST) level was 2050 U/L (normal range, < 45 U/L). She was tachypnoeic and hypoxic, and over the next 17 hours received 2800 mg (140 mg/kg) paracetamol. Her condition deteriorated. Results of liver function tests were: AST, 4580 U/L (Figure A); alanine transaminase, 2785 U/L (normal range, < 55 U/L); and serum bilirubin, 27 µmol/L (normal range, < 15 µmol/L). The international normalised ratio of prothrombin time was 4.2, and activated partial thromboplastin time, 47 s (control, < 42 s). Left lower lobe pneumonia was diagnosed, and treatment commenced with fresh frozen plasma, vitamin K, and antibiotics. The AST level rose to 11 475 U/L. The paracetamol level 22 hours after the last documented dose of the drug was 55 µmol/L. N-acetylcysteine (150 mg/kg) was administered intravenously. After the child was transferred to our hospital, intravenous N-acetylcysteine was continued (10 mg/kg/h for 32 h). Abdominal ultrasound revealed a large homogeneous liver and a small amount of ascites. Serology for hepatitis A and B, Epstein-Barr virus, cytomegalovirus and Mycoplasma pneumoniae was negative. Respiratory syncytial virus was detected in a nasopharyngeal aspirate. Blood cultures were negative. Stool examination revealed no viral agent. The patient was discharged after seven days, with an AST level of 171 U/L. Three months later she was completely well, with normal liver function tests. Case 2: A 12-year-old, 43 kg boy with Duchenne's muscular dystrophy was admitted for posterior spinal fusion and tendon-release surgery. He was anaesthetised using propofol and nitrous oxide, and during the operation required transfusion for a one-litre blood loss. He returned to the ward on a morphine infusion (20 µg/kg/h) and cephazolin (1 g eight-hourly). Over the next 24 hours he received a total dose of 3000 mg (70 mg/kg) paracetamol rectally. Similar total doses were given over the next five days, with a maximum of 4650 mg (108 mg/kg) in any 24-hour period. Liver function tests taken the day after surgery revealed an AST level of 193 U/L (Figure B) and a gamma-glutamyl transpeptidase (GGT) level of 43 U/L (normal range, < 40 U/L). He developed paralytic ileus 48 hours after surgery; this resolved with intravenous hydration. On day seven, he became irritable and disoriented and was pale, icteric and lethargic. Results of investigations were: serum bilirubin, 120 µmol/L; GGT, 68 U/L; AST, 7377 U/L; and ammonia, 88 µmol/L (normal range, < 50 µmol/L). His serum paracetamol level was 528 µmol/L. The haemoglobin level was 68 g/L and he received two units of packed cells. Serology for hepatitis B and C was negative. The paracetamol level was 206 µmol/L 34 hours after the last dose, but, as the liver enzyme levels were falling and the child's conscious state improving, N-acetylcysteine was not administered. He was discharged 22 days after surgery with an AST level of 113 U/L. Back to text Jenny L Hynson,* Mike South** * Consultant Paediatrician ** Associate Professor, and Director Department of General Paediatrics, Royal Children's Hospital Flemington Road, Parkville, VIC 3052 Rumack BH. Acetaminophen overdose in young children. Am J Dis Child 1984; 138: 428-433. Schoidt FV, Rochling FA, Casey DL, Lee WM. Acetaminophen toxicity in an urban county hospital. N Engl J Med 1997; 337: 1112-1117. Heubi JE, Barbacci MB, Zimmerman HJ. Therapeutic misadventures with acetaminophen: hepatotoxicity after multiple doses in children. J Pediatr 1998; 132: 22-27. Alonso EM, Sokol RJ, Hart J, et al. Fulminant hepatitis associated with centrilobular hepatic necrosis in young children. J Pediatr 1995; 127: 888-894. Rivera-Penera T, Gugig R, Davis J, et al. Outcome of acetaminophen overdose in pediatric patients and factors contributing to hepatotoxicity. J Pediatr 1997; 130: 300-304. Kearns GL, Leeder JS, Wasserman GS. Acetaminophen overdose with therapeutic intent [editorial]. J Pediatr 1998; 132: 5-8. Rumack BH, Matthews H. Acetaminophen poisoning and toxicity. Pediatrics 1975; 55: 871-876. Penna A, Buchanan N. Paracetamol poisoning in children and hepatotoxicity. Br J Clin Pharmacol 1991; 32: 143-149. Heubi JE, Bien JP. Acetaminophen use in children: more is not better [editorial]. J Pediatr 1997; 130: 175-177. Penna AC, Dawson KP, Penna CM. Is prescribing paracetamol "pro re nata" acceptable? J Paediatr Child Health 1993; 29: 104-106.

Research Is sudden infant death syndrome still more common in very low birthweight infants in the 1990s? Beverley Sowter, Lex W Doyle, Colin J Morley, Anne Altmann and Jane Halliday MJA 1999; 171: 411-413 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Paediatrics Abstract Objective: To determine the rate of sudden infant death syndrome (SIDS) in very low birthweight children (VLBW) relative to children with low (LBW) and normal birthweights. Design, setting and subjects: Cohort study of consecutive live births in Victoria, 1993-1997 inclusive. Main outcome measures: All sudden unexpected deaths in early childhood over this five-year period; all deaths from SIDS (defined as a sudden unexpected death without a definite pathological explanation); and the proportion of SIDS in live births in three birthweight subgroups (VLBW, 500-1499 g; LBW, 1500-2499 g; and normal birthweight, > 2499 g). Results: There were 316 028 live births (with known birthweight) in Victoria over the five-year period; 224 (0.71 per 1000 live births) died unexpectedly. In 10 of these deaths there was a definite pathological explanation, giving a rate of SIDS of 0.68 per 1000 live births. The rate of SIDS in VLBW children was 2.52 per 1000 live births, lower than the rate reported before the 1990s. The rate of SIDS in VLBW children was not significantly different from the rate in LBW children of 1.98 per 1000 live births (difference per 1000 live births, 0.53; 95% CI, 21.45 to 2.52), but was significantly higher than the rate in normal birthweight children of 0.59 per 1000 live births (difference per 1000 live births, 1.93; 95% CI, 0.06-3.79). Conclusions: The rate of SIDS in VLBW children has fallen in the 1990s, along with the overall fall in the rate of SIDS, but remains higher than that in normal birthweight children. Introduction Most parents learn to live with the fear that their baby may die of sudden infant death syndrome (SIDS). However, the fear of SIDS can be even greater for parents of babies with low birthweight, or those with babies who have been in intensive care or who have had apnoea. Before discharge, many parents attend education sessions on reducing the risks of SIDS and on infant resuscitation. At one of these sessions the parents may ask the difficult question: "Is my baby more likely to die of SIDS because he (or she) was so tiny when born?". Before the 1990s, children with very low birthweight (VLBW, 500-1499 g) were known to have a higher rate of SIDS than those with a normal birthweight (> 2499 g).1-3 With the advent of preventive measures, the overall rate of SIDS in Australia has fallen dramatically in the 1990s (from 1.87 per 1000 live births in 1990 to 0.78 per 1000 live births in 1995).4 However, it is unclear whether the rate of SIDS has also fallen in VLBW children. We aimed to determine the rate of SIDS in the 1990s for VLBW children relative to children of other birthweights (low birthweight [LBW], 1500-2499 g; and normal birthweight, > 2499 g). Methods We studied a cohort of all consecutive live births in Victoria during the five-year period from 1993 to 1997, inclusive, and recorded all sudden deaths in early childhood (divided into the first 28 days [the neonatal period], postneonatal infancy [29-365 days], and early childhood [more than 1 year]). SIDS was defined as a sudden unexpected death without definite pathological features to explain the death. In the SIDS group, some children were considered by the pathologist to have pathological features, but these were insufficient to explain the death. Some had only a minor condition, and in the remainder no pathological features were found. All births with unknown birthweight were excluded. Data sources Data on deaths were obtained from the annual reports of the Consultative Council on Obstetric and Paediatric Mortality and Morbidity,5-9 a government-legislated surveillance body. The Council collects data on all perinatal deaths from 20 weeks' gestation, and all infant and child deaths up to 14 years of age. Death registrations are forwarded directly from the Registry of Births, Deaths and Marriages, and information on all sudden unexpected deaths is supplemented by the Victorian State Coroner. These cases are then all reviewed and classified by an expert pathologist working in the field. Data on births in Victoria were supplied by the Perinatal Data Collection Unit of the Public Health and Development Division of the Department of Human Services. The Unit collects data on all births in Victoria from 20 weeks' gestation under a legislated notification system. Statistical analysis The proportions of deaths from SIDS (and 95% confidence intervals) in each of the birthweight subgroups (VLBW, 500-1499 g; LBW, 1500-2499 g; and normal birthweight, > 2499 g) were calculated,10 and comparisons made between the groups.10 Results Over the five-year period 1993-1997, there were 316 028 live births in Victoria for which birthweight was known. (Birthweight was not known for a total of 90 live births.) Over the same period, there were 224 sudden unexpected deaths with known birthweight, of which 10 (4.5%) had a definite pathological explanation, leaving 214 deaths from SIDS (0.68 per 1000 live births). Of these 214 children with SIDS, 23 (10.7%) died in the neonatal period (including one who died during the primary hospitalisation), 171 (79.9%) died in postneonatal infancy, and 20 (9.3%) died after the age of 1 year. VLBW children made up less than 1% of all live births over this period; the rate of SIDS in VLBW children was 2.52 per 1000 live births (Table). This was not significantly higher than the rate in LBW children of 1.98 per 1000 live births (difference per 1000 live births, 0.53; 95% CI, 21.45 to 2.52), but was significantly higher than the rate in normal birthweight children of 0.59 per 1000 live births (difference per 1000 live births, 1.93; 95% CI, 0.06-3.79). LBW children had a significantly higher rate of SIDS than normal birthweight children (difference per 1000 live births, 1.39; 95% CI, 0.69-2.09). Of the seven deaths in VLBW infants, definite pathological features were found in five, but these were insufficient to explain the death; three of these infants had respiratory disease (pneumonia, bronchiolitis, or tracheobronchitis). Discussion Our study showed no significant difference in the rate of SIDS between VLBW and LBW infants; however, the rate in each of these subgroups was significantly higher than in normal birthweight children. Before recommendations for reducing the risk of SIDS were introduced in 1991, the SIDS rate was higher in VLBW infants compared with those with normal birthweight, for both hospital and regional cohorts. In a VLBW hospital cohort, 1977-1978, the rate of SIDS before 2 years of age was 30.3 per 1000 live births (7/231);1 and in a regional cohort in New Zealand (children born in 1986), the incidence of SIDS in the VLBW group was 13 per 1000 live births, more than three times the rate of 4.0 per 1000 live births for all NZ children born in 1986.2 In a Californian study of 2962 children dying of SIDS between 28 days and 1 year of age in 1978-1982, the overall incidence was found to be 1.5 per 1000 live births. The highest incidence was in the VLBW group (7.5 per 1000 live births), decreasing to 1.3 per 1000 live births for the normal birthweight group.3 Studies have not shown evidence of a fall in the rate of SIDS in VLBW infants just before the recommendations were introduced. For example, in 1985-1991, the rate of SIDS in VLBW infants in the first year of life for singleton births in the United States remained relatively constant (average, 3.66 per 1000 live births) compared with rates for normal birthweight singleton infants (average, 1.07 per 1000 livebirths).11 Studies comparing the period before and after the recommendations have shown a change in rate of SIDS in VLBW children around the beginning of the 1990s. One study cited by l'Hoir et al12 estimated the rate of SIDS in VLBW children in the Netherlands to have decreased from 10 per 1000 in 1983 to 1 per 1000 (presumably live births) in 1995-96, a change in the rate of SIDS over time similar to that comparing our results with rates in the late 1980s. A more recent US report described a smaller reduction in the rate of SIDS in VLBW children before and after the recommendations about sleeping position, and the reduction was similar across birthweight subgroups (between 1991 and 1995 reductions of 37%, 36% and 30% were found for birthweight subgroups 500-1499 g, 1500-2499 g, and > 2499 g, respectively).13 Avoidance of risk factors probably explains the fall in the rate of SIDS in VLBW infants in the 1990s, the same reason that it has fallen for infants overall. The reason SIDS remains more prevalent in VLBW infants compared with normal birthweight infants may relate to the underlying pathological features, which were more common in VLBW infants with SIDS. So, what should we be telling parents when they ask if their tiny baby is more likely to die of SIDS? Firstly, VLBW and LBW children are at increased risk of SIDS. However, 399 out of 400 VLBW children, and 499 out of 500 LBW children, do not die of SIDS. Secondly, parents can help to decrease the risk of SIDS by following the recommendations: putting their baby to sleep supine, not smoking, and not allowing the baby to become overheated or covered over by bedding.4 Thirdly, as most VLBW children who died of SIDS had a definite pathological condition at autopsy, parents should seek medical advice early if the baby appears unwell in any way. Parents often recognise that their baby is unwell, but it is not always easy for them to decide what is a minor illness and when they need to seek medical advice. A scoring system such as "Baby Check" 14 can be used both by parents and general practitioners to help them to determine whether or not a baby is seriously ill. In a recent review of 37 sudden unexpected infant deaths, 3 (8%) scored very highly for serious illness on a retrospective score with Baby Check, suggesting that such a scoring system could have identified serious illness before death and led to appropriate treatment.15 The three VLBW children with significant respiratory disease in our study probably would have shown signs of illness before they died. In conclusion, the rate of SIDS in VLBW children has fallen from over 10 per 1000 live births before the 1990s to 2.5 per 1000 live births at the end of the 1990s, but remains higher than the rate in normal birthweight children. LBW children are also at greater risk of SIDS at the end of the 1990s. References Kitchen WH, Yu VYH, Lissenden JV, Bajuk B. Collaborative study of very-low-birthweight infants: techniques of perinatal care and mortality. Lancet 1982; 1: 1454-1457. Darlow BA, Horwood LJ, Mogridge N, Clemett RS. Prospective study of New Zealand very low birthweight infants: outcome at 7-8 years. J Paediatr Child Health 1997; 33: 47-51. Grether JK, Schulman J. Sudden infant death syndrome and birth weight. J Pediatr 1989; 114: 561-567. Henderson-Smart DJ, Ponsonby AL, Murphy E. Reducing the risk of sudden infant death syndrome: a review of the scientific literature. J Paediatr Child Health 1998; 34: 213-219. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1993, incorporating the 32nd Survey of Perinatal Deaths in Victoria. Melbourne, 1994. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1994, incorporating the 33rd Survey of Perinatal Deaths in Victoria. Melbourne, 1995. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1995, incorporating the 34th Survey of Perinatal Deaths in Victoria. Melbourne, 1996. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1996, incorporating the 35th Survey of Perinatal Deaths in Victoria. Melbourne, 1997. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1997, incorporating the 36th Survey of Perinatal Deaths in Victoria. Melbourne, 1998. Gardner MJ, Altman DG. Statistics with confidence - confidence intervals and statistical guidelines. London: BMJ, 1989. Bigger HR, Silvestri JM, Shott S, Weese-Mayer DE. Influence of increased survival in very low birth weight, low birth weight, and normal birth weight infants on the incidence of sudden infant death syndrome in the United States: 1985-1991. J Pediatr 1998; 133: 73-78. l'Hoir MP, Engelberts AC, van Well GT, et al. Case-control study of current validity of previously described risk factors for SIDS in the Netherlands. Arch Dis Child 1998; 79: 386-393. Malloy MH. Birth weight and gestational age specific sudden infant death syndrome (SIDS) mortality: 1991 vs 1995. Pediatr Res 1999; 45: 249A. Morley CJ, Thornton AJ, Cole TJ, et al. Baby Check: a scoring system to grade the severity of acute systemic illness in babies under 6 months old. Arch Dis Child 1991; 66: 100-105. Cole TJ, Gilbert RE, Fleming PJ, et al. Baby Check and the Avon infant mortality study. Arch Dis Child 1991; 66: 1077-1078. (Received 21 Jun, accepted 6 Sep, 1999) Authors' details Division of Paediatrics, Royal Women's Hospital, Melbourne, VIC. Beverley Sowter, RN, Case Manager. Lex W Doyle, MD, FRACP, Paediatrician; and Associate Professor, Department of Obstetrics and Gynaecology, and Department of Paediatrics, University of Melbourne. Colin J Morley, MD, FRACP, Paediatrician. Consultative Council on Obstetric and Paediatric Mortality and Morbidity, Melbourne, VIC. Anne Altmann, MB BS(Hons), MPH, FAFPHM, Epidemiologist. Victorian Perinatal Data Collection Unit, Melbourne, VIC. Jane Halliday, PhD, Epidemiologist. Reprints will not be available from the authors. Correspondence: Associate Professor L W Doyle, Division of Paediatrics, The Royal Women's Hospital, 132 Grattan Street, Carlton, VIC 3053. l.doyleATobgyn-rwh.unimelb.edu.au Sudden unexpected deaths in early childhood in Victoria, 1993-1997Birthweight subgroup 500-1499 g1500-2499 g> 2499 gTotalLive births278115 630297 617316 028Sudden unexpected deaths (≤ 28 days)07*1623Sudden unexpected deaths (> 28 days)724170201Total sudden unexpected deaths731186224Sudden unexpected deaths explained at autopsy001010Total SIDS731176214Pathological featuresDefinite586174Minor21887107None052833Rate of SIDS (per 1000 livebirths) 2.521.98 0.590.68(95% CI)(1.04-5.19)(1.29-2.68)(0.50-0.68)(0.59-0.77)Data are numbers of infants, unless indicated otherwise. * One infant died while still in hospital after birth. SIDS = Sudden infant death syndrome (sudden unexpected deaths, excluding those explained at autopsy). Back to text

Beverley Sowter · Lex W Doyle · Colin J Morley · Anne Altmann · Jane Halliday