Child health

Andrew S Kemp Professor, Allergy Immunology and Infectious Diseases, The Children’s Hospital at Westmead, Locked Bag 4001,Westmead, NSW 2145. andrewk5ATchw.edu.au To the Editor: Publicity such as that on the recently televised “Sunday” show (Channel 9) entitled “When food can be fatal” (http://sunday.ninemsn.com.au/sunday/cover_stories/transcript_1770.asp), which contained statements that “30 in every 1000 [3%] children in Australia are at risk of a severe allergic reaction [anaphylaxis] to a food”, and a reference to a “tsunami of children” with serious allergies, provokes understandable concern and anxiety. Some perspective on this issue is required. To determine the risk, it is essential to study a population-based cohort. Allergies to peanuts or tree-nuts are the most common cause of severe childhood food anaphylaxis and death.1 What is the risk for Australian children of peanut-induced anaphylaxis that is likely to require adrenaline? Of a population-based cohort of 456 Tasmanian children aged 7–8 years, none reacted to a peanut skin-prick test.2 In the Australian Childhood Asthma Prevention Study (CAPS),3 a high-risk cohort, 4.9% of 3 year olds were prick-test positive to peanut (unpublished data) using a liberal cut-off of ≥ 2 mm (for clinical testing the usual cut-off is ≥ 3 mm). Perhaps the most helpful information comes from a population-based study of 13 971 preschool children in the United Kingdom who were followed from birth to 6 years of age. Forty-nine (0.35%) children had an allergic reaction to peanut, of whom only two (0.014%) had what was described as anaphylaxis.4 Thirty-six of the children underwent formal peanut challenge, 23 reacted and three had reactions for which adrenaline was given. Combining these three with the previous two gives a severe reaction rate requiring adrenaline of 0.036%. This suggests that, of the 49 children in the UK study who had an allergic reaction to peanut, only 10% were at risk of a severe reaction requiring adrenaline. Only a third to a half of children with a positive peanut skin test will react if exposed.5 Applying these considerations to Australian children indicates that the proportion at risk of a severe peanut reaction is only 0.25% (4.9% × 1/2 × 5/49) even in a high-risk cohort such as the CAPS. This would be substantially lower in a population-based cohort. For the cohort of 7–8-year-old Tasmanian children referred to above, the risk would be much less than 0.2%, considering none of 500 children was prick-test positive to peanut allergen. There has been a substantial increase in childhood food allergy in recent decades;5 however, sensationalist statements and inaccurate figures are unlikely to be helpful in developing appropriate responses. The Australasian Society of Clinical Immunology and Allergy recently published guidelines for the prevention of food anaphylactic reactions,6 and has other useful information for patients and medical practitioners on its website (http://www.allergy.org.au/).

Andrew S Kemp

Re: the letter “Reliability of parental reports of head lice in their children”, by Megan L Counahan, Ross M Andrews and Rick Speare, in the 7 February issue of the Journal (Med J Aust 2005; 182: 137-138). There was an error in Box 2, Sensitivity and specificity of parental report versus screening. The specificity given as 94.0% (969/1030) should have been 98.8% (1018/1030). The html and pdf versions of this article published online were corrected on 5 August 2005.

Megan L Counahan · Ross M Andrews · Rick Speare

There is growing recognition in Australia of the importance of early childhood to later health and wellbeing, with developments such as the National Agenda for Early Childhood and the National Public Health Action Plan for Children. To sustain a policy agenda for children and improve long-term outcomes, we need timely, comprehensive and accurate indicators and data on child health, development and wellbeing. Building this evidence requires a national monitoring and surveillance system that involves more than aggregating or linking existing data. Steps to building a national system are: to agree on key indicators of child health, development and wellbeing for regular reporting, to research a comprehensive set of indicators for each domain and ascertain data gaps, and to ensure development and coordination of data relevant to policy-making.

Sharon R Goldfeld FRACP, PhD · Frank Oberklaid FRACP, MD

Caroline F Finch Director, New South Wales Injury Risk Management Research Centre, University of New South Wales, Level 8, Applied Science Building, Sydney, NSW 2052. c.finchATunsw.edu.au To the Editor: I am prompted to write to you in response to a recent MJA editorial.1 It amazes me that the health sector in Australia, as I think the editorial did, continues to largely ignore the magnitude of the problem of injury in our children. This is despite clear evidence of the excess ill-health burden that injury places on our children, according to the Australian Institute of Health and Welfare (AIHW) report (the subject of the editorial)2 and other reports.3-5 Having said this, the editorial did highlight a very pleasing trend — there has been a steady decline in injury deaths in later childhood. Unfortunately, however, this was the only mention of injury in the editorial, and readers could be forgiven for thinking that this is the end of the story: the injury death rate is declining; therefore, we are doing all we can, and injuries are not a major issue. Nothing could be further from the truth. Our children continue to die from road and drowning accidents and will do so until injury prevention is recognised as paramount. The AIHW report clearly states that the single highest cause of death in children remains injury and poisoning.2 Accordingly, trauma is the single highest contributor to premature mortality and years of potential life lost of any health condition in Australia. If we don’t develop new approaches to reducing the incidence of drownings and road deaths, in particular, we will not see further declines in injury-related death rates, and injury will continue to rate highly as a killer of young people. Importantly, injuries do not only kill young people — they also hospitalise and maim them. The second most common reason for hospitalisation in Australian children is injury.2 Unlike injury deaths, there has been no trend in the rate of hospitalisation for injury. Across age groups, there appears to be a shift from fatalities to an increasing number of people with a high lifetime burden of significant disability, including brain and spinal cord damage. Imagine what this does to the quality of life and life expectancy of a child. How many of these children will be able to lead physically active lives? It is time for the health sector, particularly public health agencies, to properly recognise injury as a critical issue for the ongoing health of Australian children and to formally commit to appropriate preventive actions, commensurate with the priority ranking of childhood injuries.

Caroline F Finch

George C Patton,* Sharon R Goldfeld,† Indrani Pieris-Caldwell,‡ Meredith Bryant,§ Graham V Vimpani¶ * VicHealth Professor of Adolescent Health Research, Centre for Adolescent Health, Murdoch Childrens Research Institute, Flemington Road, Parkville, Melbourne, VIC 3052; † Paediatrician and Research Fellow, Royal Children’s Hospital, Melbourne; ‡ Senior Analyst, § Project Officer, Australian Institute of Health and Welfare, Canberra; ¶ Clinical Chair in Paediatrics, University of Newcastle, NSW. george.pattonATrch.org.au In reply: There is little to disagree with in this excellent summary of injury morbidity and mortality in Australian children. However, the principal point of our editorial1 was to highlight important problems where adequate data are currently unavailable. The Australian Institute of Health and Welfare report was able to give extensive coverage to injuries and accidents in children.2 Indeed, seven indicators specifically addressed aspects of childhood injury, with a range of others (eg, child abuse and neglect, neighbourhood safety) addressing relevant aspects of the family and social context. This emphasis reflected not only the importance of childhood injury, but the extent to which reasonably good data are available. We agree that, despite some favourable mortality trends, the burden of childhood injury remains high, as are associated health care costs. However, childhood injury is an area where advocacy has translated into action.3 One of the reasons for the success of that advocacy has been the availability of sound data, both to make the case and to ensure an appropriate focus in policy responses.4 While there is undeniably much more to do, we can learn much from injury prevention about how to tackle the newly emerging problems of childhood.

George C Patton · Sharon R Goldfeld · Indrani Pieris-Caldwell · Meredith Bryant · Graham V Vimpani

Although children in Australia generally have good health, some alarming indicators of poor health and wellbeing exist, which are related to major socioeconomic discrepancies. The pathways connecting socioeconomic disadvantage to child health outcomes are complex and poorly understood. Reducing social disadvantage requires strategies beyond the health arena, involving political, moral, cultural and economic initiatives. Developing “social capital” — cohesion in communities, a sense of belonging and involvement in community affairs — may be a key strategy in improving health indicators. Overseas studies of early intervention and home visiting programs in early childhood have shown improvements in child health and development outcomes. Similar programs have been introduced in Australia and face considerable challenges in their widespread roll-out and evaluation. Health professionals need to develop practical ways to interact with community programs and thus improve social capital.

Karen J Zwi FRACP, MRCP, MSc · Richard L Henry MD, FRACP

Peter W Holmes,* David Armstrong,† Nicholas Freezer‡ * Deputy Director, Adult Respiratory Medicine, † Director, Paediatric Cystic Fibrosis Unit, ‡ Director, Adult and Paediatric Respiratory Medicine, Department of Respiratory and Sleep Medicine, Monash Medical Centre, Locked Bag 29, Clayton, VIC 3168. peter.holmesATsouthernhealth.org.au To the Editor: We congratulate Lam et al1 for identifying the major problems in transferring adolescents from the Royal Children’s Hospital, Melbourne, to adult care. The article and the accompanying editorial2 address a difficult problem relating to the transfer of adolescent patients from a stand-alone paediatric hospital to adult services. Lam et al conclude that there needs to be a change of attitude among adult physicians, and recommend the provision of additional resources to enhance the smooth transition to adult care. As long as paediatric services remain geographically separated from their adult counterparts in stand-alone hospitals, these problems will continue, regardless of any increase in resources. In New South Wales, tertiary paediatric services have now been incorporated onto the same campus as tertiary adult hospitals in shared-site arrangements. This facilitates the transition process, as adult physicians are more closely linked to their paediatric colleagues via shared clinical and research infrastructures. Such close cooperation allows paediatric and adult physicians to share their care during transition and provides the adult physicians with full access to the patients’ medical records and radiology, microbiology, laboratory and pulmonary function data. At Monash Medical Centre, we have taken this further by totally incorporating our adult and paediatric services into one single Department of Respiratory and Sleep Medicine. This arrangement allows an integrated approach to childhood, adolescent and adult care. The combination of services generates trust between all members of staff (an issue raised in the editorial2) and gives adult physicians a greater understanding of the needs of adolescents with complex health problems. One solution to the difficult problem of transition to adult care is to phase out stand-alone paediatric services with their own costly management infrastructure. A shared campus arrangement allows greater integration of the full range of tertiary paediatric and adult services and offers many advantages in providing a seamless transition to adult care.

Peter W Holmes · David Armstrong · Nicholas Freezer

Canteens are not the main source of food for Australian school kids, but their symbolism is big There is widespread awareness of the obesity epidemic in Australian children,1 and the focus has now, quite appropriately, turned to action. In the United Kingdom, celebrity chef Jamie Oliver is trying to transform a 100-year-old school lunch service from “soggy and fried” to “crisp and fresh”. In Australia, the question is whether school canteens should be a high priority for action, because of their accessibility and visibility, or a low priority, on the grounds that canteen foods contribute little to children’s energy intake. Negative ripples from canteensOver the period of a year, children aged 5–15 years obtain only about 16% of their total energy intake from food eaten at school, and probably less than 3% comes from canteens.2 But while the energy contribution is small, the symbolism is big. Canteen users consume significantly greater amounts of foods likely to promote unhealthy weight gain, such as fast foods, confectionery and packaged snacks.2 The types of foods and beverages that predominate in school canteens not only undermine the health and nutrition curriculum, but also create the impression that foods and drinks that are high in fat, sugar and salt belong on the plate as “everyday foods”, rather than on the side as “occasional foods”. Other common practices in schools that undermine healthy eating messages include rewarding children with sweets, having soft-drink and confectionery vending machines, holding sporting events with fast-food vouchers as prizes, and using chocolate drives for fundraising. All these practices create negative ripple effects on Australian family eating practices and beliefs.3 Children are developing the food preferences that they will carry with them into adulthood, so strengthening family and school environments for enjoying healthier food choices is critical. In a 2004 survey of 18 Victorian primary schools (unpublished data), we found that, of the 17 with a food service, all sold meat pies, but only five sold fruit on a regular basis. As a rule, canteen managers provided foods that sold well and had a long shelf life. They usually had no mandate or support to do otherwise. A reliance on profits from canteens, vending machines and “junk food fundraising” also makes it hard for schools, particularly high schools, to model healthy eating. In common with a survey of 500 New Zealand schools,4 we found that schools readily recognise the rather poor job they do of providing a healthy food environment. Most schools do not see food provision as part of their core business and lack the inclination or resources to take on this “added” responsibility. Private enterprise fills this vacuum, with the result that the health of profits increasingly dominates the health of pupils. An extreme example is the “cola war” in the United States, in which the weapons of choice have been contracts with schools to sell minimum volumes of Coca Cola or Pepsi.5 Creating a new epidemic?Perhaps we should consider the task ahead of us as the creation of a new epidemic of healthy eating rather than reducing an obesity epidemic. Using the principles in Gladwell’s recent bestseller The tipping point,6 the school canteen and students themselves could be the catalyst for healthier eating among children and adolescents — turning negative ripples into positive waves. Can a “tipping point” be created from a handful of champion schools that decide to embrace the whole-of-school policies and strategies needed to get their canteens right (healthy, enjoyable, profitable and supported), hoping that others will follow their lead? This is almost certainly too much to expect to happen in 9000 schools across Australia, which tend to function semi-autonomously on these matters. Lessons from successful public health programs, such as sun protection and injury prevention, show that tipping the balance in targeted behaviours from unhealthy to healthy requires a backbone of strong central policy, ongoing social marketing, and supported and coordinated implementation of programs. Some Australian modelsVarious government-supported models influence how school canteens operate in Australia. Probably the least effective include the Victorian model of simply disseminating canteen guidelines7 and the Australian Government model from the pre-election spending spree, wherein each school could apply for $1500 to reinvent the “healthy canteen” wheel. Neither has policy, social marketing or implementation support. A third model, which has some merit, is exemplified by the Western Australian (StarCAP8) and Tasmanian (Cool CAP9) school canteen accreditation programs. Both have well developed criteria and processes for schools to work through to achieve program accreditation. StarCAP is backed by the WA government, but is managed on a shoestring budget, without policy and social marketing support, and thus has a low accreditation rate (7% of schools) and declining reach.10 Cool CAP is newer, with a higher accreditation rate (42% of schools accredited or working towards it), and so far has been successful in securing legislative and monetary support. Ultimately, however, the impact of these types of programs will probably be modest as long as the impetus to change remains with each individual school. Because they are well supported and centrally driven, the most promising models come from New South Wales and South Australia. The NSW Healthy School Canteen Strategy (“Fresh Tastes @ School”)11 grew out of the NSW Government Childhood Obesity Summit in 2002. It is now mandatory for state schools to provide food and beverage choices consistent with the Australian guide to healthy eating.12 NSW Health has also boosted support for the NSW Canteen Association so that it, in turn, can support schools to operate economically viable, nutrition-oriented school canteens. Early positive waves include support from parents, canteen managers, some food companies and, increasingly, local health and education services. A similar model released in 2004 in South Australia brings SA government backing to a set of healthy eating guidelines.13 The guidelines encourage links between the canteen, the community and teaching about nutrition food skills. Both the NSW and SA government models would now benefit from social marketing explaining the rationale, processes and support for the program. It would make sense, for example, to link these strategies with the national “Go for 2&5” (2 serves of fruit and 5 serves of vegetables) campaign.14 If we are serious about the childhood obesity epidemic, school canteens are a good place to start, because they carry a symbolism that ripples into the Australian diet far beyond their contribution to energy intake. At the moment, the ripples are a negative and undermining force. However, full implementation of the NSW or SA models for school canteens throughout the country could just tip the balance towards an outbreak of healthier eating.

A Colin Bell BSc(Hons), MSc, PhD · Boyd A Swinburn MB ChB, MD, FRACP

Brain development from late pregnancy to 3 years of age affects a child’s learning, behaviour and health throughout life. Behavioural difficulties in children are usually symptoms of underlying problems. Observing a child’s appearance and performance, and taking a detailed history (considering factors in the child, the home, the school and the wider environment) provide most of the information needed for diagnosing behavioural problems. It is important to know what is “normal” for all stages of a child’s development, but equally important not to confuse behavioural difficulties with normal variations and behaviours associated with developmental stages. Assessment and early intervention for behavioural and learning difficulties in children require a multidisciplinary team approach. As well as the recommended “multimodal” approach for managing attention deficit hyperactivity disorder, shared care with a general practitioner is available in some states, but medication is likely to be the trigger for a positive outcome.

Trevor S Parry FRACP, DCH, DPH, FRACMA

Fractures in children are common, but the plasticity of children’s bones means that they may be incomplete. If a child has deformity, swelling or bony point tenderness in a limb after a fall, it is likely to be fractured. A fractured limb that appears deformed will most probably need to be reduced. Effective splinting, using whatever means is readily available, and early, adequate analgesia, can ameliorate the severe pain associated with a fracture. In young children with open growth plates, Salter–Harris type I injuries of the distal fibula are more common than ligament injuries of the ankle. After an ankle ligament injury, functional treatment — brace or tapes, with active physiotherapy — results in a better outcome than immobilisation. A child with a head injury, who does not lose consciousness, has only one or no episodes of vomiting, and is stable, alert and interactive, and neurologically normal, is extremely unlikely to have sustained an intracranial injury.

Simon J Young MB BS, DipCrim, FACEM · Peter L J Barnett MB BS, FRACP, FACEM · Ed A Oakley MB BS, FACEM

On 14 January 2005, Western Australia lost one of its finest paediatricians. Paul Carman died suddenly of acute myocardial infarction while on holiday with his family in Capel. The loss to the medical and Catholic community is immense. In the 19 years that Paul was in Western Australia, he made significant contributions in many fields. He was Chairman of the Paediatric Clinical Care Unit at Princess Margaret Hospital for Children. He ran regular remote paediatric clinics in the Pilbara region, serving the local mining and Aboriginal communities with compassion and care — qualities that he exercised in all other aspects of his professional life. He was a foundation member of the (now disbanded) Advisory and Coordinating Committee on Child Abuse, an advisor to the Christian Brothers commission to support the needs of former child migrants who had been under their care, and an active member of St Thomas’ parish and school, which his seven children attended and where his funeral was held. However, his lasting legacy for paediatric hospitals in Perth will be his vision to establish a Child Protection Unit to provide specialised medical and forensic services to children. Paul was born in Melbourne on 17 September 1950. When he was 4 years old, his family moved to Cairns, in Queensland, and then, 8 years later, to Warrnambool, in Victoria. In Warrnambool, his father established a very successful dental practice. Paul matriculated from St Joseph’s Christian Brothers College in Warrnambool. However, his university entrance score was not sufficient to enter medicine, which was his passion (a passion sparked by the television serial “Dr Finlay’s Casebook”). The following year, Paul repeated his matriculation exams and gained entrance to the University of Melbourne Medical School in 1969. During the fifth year of his course, he met Margaret, whom he married in 1977. Paul worked for 2 years at Queen’s Medical Centre in Nottingham under the guidance of Sir David Hull. It was here that Paul developed his interest in child protection. He obtained his Fellowship of the Royal Australasian College of Physicians in 1985 and, in the following year, took up an appointment as a staff paediatrician at the Princess Margaret Hospital in Perth and as a rural paediatrician in conjunction with the legendary Dr Rex Henderson. Paul’s ability to listen, discuss and draw on his vast knowledge of Russian and European history, ethics, philosophy and common sense was a driving force in the outstanding contribution he made to children’s health in Western Australia. The love, trust and enduring friendship in his relationship with Margaret is reflected in the lives of their seven children.

Peter M Winterton BA, MB BS, FRACGP

Questions of cost-effectiveness, vaccine efficacy and feasibility are yet to be answered In the United States, routine immunisation of all healthy children aged 6–23 months against influenza has recently been introduced. The principal justification for this is the relatively high morbidity and mortality from this disease in very young children.1 The United States is also considering routine influenza immunisation of all children aged over 6 months, in view of the herd protection it would provide to the adult population. Currently, Australian guidelines recommend immunisation of children in groups considered at high risk of severe influenza.2 Should Australia introduce universal childhood immunisation? There is no doubt that children have an extremely high incidence of influenza. It is estimated that, on average, 20%–43% of children are infected during typical influenza seasons.3-5 The incidence is highest in young children less than 2 years old, who are often hospitalised.1,3-5 The mortality due to influenza in infancy is second only to that in the most elderly patients.1 In the severe 2003–04 influenza season, 143 children died from influenza in the United States, of whom 58 (41%) were less than 2 years old and 65 (45%) had no underlying condition.1 These data emphasise the importance of protecting children with annual influenza immunisation, if feasible. Another reason to consider universal childhood influenza immunisation is herd protection. In what turned out to be an illuminating natural experiment, 50%–85% of Japanese schoolchildren were immunised annually against influenza from 1962 to 1987, but there was no routine immunisation of the elderly. When mandatory immunisation of schoolchildren was relaxed in 1987 and repealed in 1994 (because of doubts about safety and effectiveness), influenza immunisation rates dropped to very low levels. A retrospective study comparing excess mortality from pneumonia and influenza in Japan and the United States concluded that the vaccination of Japanese schoolchildren prevented about 37 000 to 49 000 deaths per year, mostly of elderly people. (This represented about one death for every 420 children vaccinated.)6 In considering the feasibility of universal childhood vaccination, vaccine efficacy is one of the factors that needs to be taken into account. In healthy adults under 65 years of age, inactivated influenza vaccine is 70%–90% effective when the match between vaccine and circulating viruses is close.1 However, the same vaccine may be less immunogenic in children. Studies in children aged 6 months to 15 years show a vaccine efficacy of 31%–91% against influenza A and 45% against influenza B.7,8 However, very few of the studies have examined children aged 6–23 months,9,10 the age group currently recommended for routine influenza vaccination in the United States. An alternative form of vaccine administration is on the horizon — live attenuated influenza vaccines. A recent systematic review10 suggested that live vaccines may be more effective than inactivated vaccines in children over 2 years of age (79% versus 65%). Live attenuated influenza vaccines have been licensed in the United States, and might be more acceptable because they are given intranasally.11 However, live vaccines cost a lot more and are not licensed for use in children under 5 years in the United States (because of limited safety data). They are not yet licensed in Australia for use in any age group. The high morbidity of influenza in children and the likely benefits due to herd immunity do make annual childhood influenza immunisation appear economically attractive. However, against this must be weighed the need to immunise with a new influenza vaccine each year, because of antigenic drift in influenza strains, and the need to give two doses of vaccine to children under 9 years in the first year they are immunised.1,2 In addition, the severity of influenza seasons varies unpredictably from mild to severe, and it costs as much to immunise in a mild year as in a severe one. In the United States, indirect costs (mainly days of work lost by parents) dominate economic analyses supporting the use of influenza vaccines in children.12 In Australia, by contrast, the Pharmaceutical Benefits Advisory Committee considers only direct costs of illness, so it is unlikely that a universal, publicly funded childhood immunisation program could be justified using such cost-effectiveness criteria. There may also be practical problems with attempts to introduce routine childhood immunisation. In 2004–05, the uptake of influenza vaccine for children aged 6–23 months in the United States, when the vaccine was recommended universally, was estimated to be only 48%.13 In Ontario, Canada, where all residents aged over 6 months have been offered free annual influenza immunisation since 2000,14 the 2003 uptake in children was only 27%.15 Parents of unimmunised children were more likely to believe that immunisation resulted in a flu-like illness, caused adverse effects more severe than the disease, or weakened the immune system.15 Such immunisation myths are common, although studies have repeatedly shown inactivated influenza vaccine align="right" to be safe, with low rates of adverse events and the benefits clearly outweighing the risks.1,2,9 Another practical issue is the question of how to fit the vaccine into an already crowded childhood vaccination schedule. In general, annual immunisation against influenza is recommended in autumn at the start of the influenza season; there is no fixed age of administration of vaccine. Implementing universal influenza vaccination would place a substantial extra burden on primary care practices.16 Considering all the available information, I believe that there is currently insufficient reason for introducing universal childhood vaccination for this disease in Australia. There are too many unanswered questions about the cost-effectiveness, efficacy and feasibility of universal immunisation of healthy children, whether infants or school-aged. For the time being, we should maintain a watching brief. Future data emanating from Ontario and the United States may provide us with a clearer answer as to whether large-scale programs of routine childhood influenza immunisation are feasible and effective. Further, if the US experience with live vaccines shows consistent immunogenicity and improved ease and acceptability of administration, live vaccines may yet prove to be a cost-effective way to implement universal childhood influenza immunisation in Australia. One thing is clear: influenza vaccination is most cost-effective for children considered at high risk of severe influenza, such as those with chronic cardiopulmonary and other chronic illness. These children should clearly be vaccinated annually against influenza.1,2 Yet vaccine coverage of high-risk groups aged 2–17 years is only 35% in the United States,13 and probably lower in Australia, although we lack age-specific data. Australian immunisation providers should redouble their efforts to ensure that children at high risk are immunised annually.2 Also, it should be remembered that the Australian immunisation handbook2 does not preclude vaccinating others who are not at high risk. It states that “influenza vaccine should be administered to any person who wishes to reduce the likelihood of becoming ill”.

David Isaacs MD, FRACP, FRCPCH

Minor injuries in children (those that could reasonably be expected to heal with minimal medical intervention) are extremely common. The possibility of more serious injuries should be considered and excluded early. Successful examination requires gaining the child’s trust, relieving pain early, and using a flexible and creative examination technique. Bruising may suggest a more serious underlying injury, or the bruising pattern may indicate non-accidental injury or a bleeding disorder. Superficial abrasions and lacerations can be safely cleaned with good quality water, and all foreign material should be removed. Deeper wounds with suspected damage to nerves, tendons or circulation need formal exploration under a general anaesthetic. Good local anaesthesia can be produced by topical preparations, and many wounds can be closed with tissue adhesives with an excellent cosmetic result. Antibiotics should be prescribed for specific circumstances, such as wounds with extensive contamination or tissue damage, and all children with injuries should be checked for adequate tetanus cover for prophylaxis.

Simon J Young MB BS, DipCrim, FACEM · Peter L J Barnett MB BS, FRACP, FACEM · Ed A Oakley MB BS, FACEM

Elizabeth A Hender,* Corrine R Balit† * Scientific Officer, Hazardous Substances Section, Environmental Health Service, Department of Health, PO Box 6 Rundle Mall, Adelaide, SA 5000; † Research Pharmacist, New South Wales Poisons Information Centre, The Children’s Hospital, Westmead, NSW. elizabeth.henderAThealth.sa.gov.au To the Editor: Although there are few deaths due to poisoning in Australian children, from 1993 to 1997 there was an average of more than 2500 admissions to hospital per year for assessment of poisoning with medicines in children younger than 5 years.1 Child-resistant packaging has been effective in preventing accidental poisoning with prescription medicines and aspirin in young children in the United States.2,3 In the US, both reclosable and non-reclosable (blister or strip) packaging used for pharmaceuticals required to be in child-resistant packaging is tested to confirm its effectiveness in preventing access by children.4 In Australia, only reclosable packaging is required to be child-tested. Blister or strip packaging, which has not usually been child-tested, is accepted as an alternative to child-resistant reclosable packaging.5 We conducted a study at the New South Wales Poisons Information Centre (NSWPIC) over 9 weeks from 18 July to 17 September 2003. Our aims were to ascertain which medicines children younger than 5 years access directly from blister or strip packaging, and whether assessment at a hospital was recommended. The study was approved by the Ethics Committee of the Children’s Hospital, Westmead. Callers ringing about a suspected accidental ingestion of a solid dose medicine in a child younger than 5 years were asked whether the child accessed the medicine directly from a blister or strip pack. There were 318 accidental exposures to solid dose medicines in these children during the study period. In 186 exposures (58%), the caller said the medicine was normally in a blister or strip pack and the child obtained it directly from the pack. A wide range of medicines (40 different drugs or drug groups) were associated with the exposures; the most common were oral contraceptives (49 exposures) and paracetamol (27 exposures). Some of the exposures involved medicines that can cause severe toxicity when children ingest a small number of dose units, such as clonidine, olanzapine, narcotic analgesics, and tricyclic antidepressants. In 36 exposures where the child obtained the medicine directly from the pack, the caller was advised to take the child to hospital (Box). Many of the medicines associated with these exposures (eg, paracetamol, preparations containing narcotic analgesics, antidepressants, antihistamines, iron and clonidine) are required to be in child-resistant packaging.5 Our study shows that blister or strip packs currently in use did not prevent children accessing drugs. This finding calls into question whether blister or strip packaging that has not been child-tested presents an adequate safety barrier. No outcomes of drug ingestion are known in this study, which is a limitation. However, assessment of these children in hospital represents a financial burden to the health care system regardless of the outcome. Further studies would be required to quantify the harm associated with exposures to medications packaged in blister or strip packaging in young children and to assess the effectiveness of such packaging in the prevention of poisoning. Drugs accessed from blister or strip packs where child required referral to hospital Drug or drug group Number of exposures Paracetamol 8 Paracetamol/narcotic combination analgesics 3 Selective serotonin re-uptake inhibitors 3 Antidepressant: other/unknown 2 Antiemetics 2 Antihistamines 2 Cough/cold preparations, no paracetamol 2 Iron 2 Other (eg, clonidine, olanzapine) 12 Total 36

Elizabeth A Hender · Corrine R Balit

Graham R Wicks Medical Hypnotherapist, Department of Psychological Medicine, Women’s and Children’s Hospital, North Adelaide; 9 Collins Street, Collinswood, SA 5081. grwicksATbigpond.net.au To the Editor: I was interested to read the article about managing nocturnal enuresis in children,1 but was surprised and disappointed that there was no mention of the place of medical hypnotherapy. Hypnotherapy can be particularly valuable in the treatment of monosymptomatic nocturnal enuresis in children aged from 7 or 8 years upwards, and has the advantage of being completely non-invasive with no side effects. It focuses on empowering the children to take control of their own bodily functions.2 Hypnotherapy is also of value in the management of nocturnal enuresis associated with day-time symptoms, such as urgency with or without incontinence, and can also be used to enhance the efficacy of treatments like enuresis alarm systems. While there are few well documented comparative studies3 on the benefits of hypnosis versus other treatments for nocturnal enuresis, there are numerous anecdotal reports and studies involving a series of patients being successfully treated with hypnotherapy. Hypnosis should only be used by properly trained doctors or psychologists who have access to the full range of medical investigations. Hypnosis is of course not a panacea, but is an excellent first-choice treatment for monosymptomatic nocturnal enuresis, the commonest type seen by general practitioners. If, after three or four treatment sessions, hypnosis is not effective, other approaches can be employed. A quick search of the internet using the terms “enuresis and hypnotherapy” will reveal over 700 sites with information on the subject, and there are several highly respected professional journals that publish clinical and research papers and articles on the use of hypnosis in medicine and psychology. All of these are published by reputable professional societies whose membership is limited to registered health professionals. The Australian Society of Hypnosis (http:// www.ozhypnosis.com.au) conducts ongoing training courses in all states of Australia for graduates in medicine, psychology and dentistry. Hypnotherapy is now becoming more and more accepted worldwide as a valuable and legitimate tool that can be used, in conjunction with the more traditional approaches, in a wide variety of medical and psychological problems. It is a great pity that many clinicians are either not aware of its value or are still loathe to accept it because of negative connotations associated with its use for entertainment purposes and in the hands of non-professional therapists.

Graham R Wicks

Patrina H Y Caldwell,* Denise Edgar,† Elisabeth Hodson,‡ Jonathan C Craig§ * Staff Specialist and Lecturer, † Head, Department of Nephrology, § Associate Professor and Head of Clinical Research, NHMRC Centre of Clinical Research Excellence in Renal Medicine, The Children’s Hospital at Westmead, Locked Bag 4001, Westmead, Sydney, NSW 2145; ‡ Clinical Nurse Consultant, The Continence Foundation of Australia in NSW, Sydney, NSW. PatrinacATchw.edu.au In reply: Thank you for your interesting comments regarding hypnotherapy in the treatment of nocturnal enuresis in children. There are a number of therapies, such as hypnotherapy, electrotherapy and acupuncture, which show great promise for the management of nocturnal enuresis. We only included in our article1 treatments that were supported by evidence from well documented comparative studies. Using comprehensive search strategies, we have not found comparative studies for these complementary therapies. We would be very interested to be directed to studies that have formally evaluated other interventions. There is a huge need for randomised controlled trials comparing alternative treatment strategies with conventional therapy in this area.

Patrina H Y Caldwell · Denise Edgar · Elisabeth Hodson · Jonathan C Craig

Objective: To evaluate the role of zinc and vitamin A supplementation in the recovery of Indigenous children hospitalised for acute diarrhoea.Design: A randomised controlled 2 by 2 factorial trial of supplementation with zinc and vitamin A.Setting and participants: Aboriginal children (aged < 11 years) hospitalised for acute diarrhoea at Alice Springs Hospital, Northern Territory, April 2001–July 2002.Main outcome measures: Duration of diarrhoeal illness; re-admission for diarrhoeal illness within 120 days.Results: Our study involved 392 Aboriginal children with 436 episodes of diarrhoea. Supplementation with zinc, vitamin A, or combined zinc and vitamin A had no significant effect on duration of diarrhoea or rate of re-admission compared with placebo. Median diarrhoea duration after starting supplementation was 3.0 days for the vitamin A and zinc supplemented and placebo groups (P values 0.25 and 0.69, respectively). The number of re-admissions did not differ significantly between those receiving vitamin A or zinc and the relevant placebo groups (relative risk [95% CI], 1.2 [0.7–2.1] and 1.3 [0.8–2.1], respectively).Conclusion: Vitamin A and zinc supplementation may not be indicated for in-hospital management of acute diarrhoeal disease in Aboriginal children living in remote areas. This finding may not apply to children with malnutrition, for whom other studies suggest a benefit. Larger trials incorporating more comprehensive data on the vitamin A and zinc status as well as nutritional status of study populations might help to explain the different results in different populations.

Patricia C Valery MD, MPH, PhD · David M Purdie BSc(Hons), PhD · Paul J Torzillo MB BS, FRACP, FFICM · Peter A Stewart MB BS, FRCPA · Naomi C Boyce B Nursing · Anne B Chang MPHTM, FRACP, PhD · Andrew V White MB BS, FRACP · Gavin R Wheaton MB BS, FRACP · John Wakerman MB BS, MPH

Do we have a clear enough picture to guide rational health and social policy responses? Australia’s economic prosperity has long brought incremental health gains through better living conditions, sanitation, education, medical care and vaccination.1 The effects on child health and mortality have been striking. The latest report from the Australian Institute of Health and Welfare (AIHW), A picture of Australia’s children, documents this continuing trend. Infant and child mortality rates halved again in the past 20 years.2 The fall in deaths from sudden infant death syndrome (SIDS) to a third of 1991 rates is a tribute to outstanding Australian child health research, as well as the work of child and family health nurses and the SIDS Council of Australia.3 A steady decline in deaths from injury in later childhood has also contributed to lower childhood mortality. Judged by these indices, the present generation of Australian children is the healthiest ever. Key findings of A picture of Australia’s children The infant mortality rate in Australia halved over the past two decades, from 9.6 per 1000 livebirths in 1983 to 4.8 in 2003. The Indigenous infant mortality rate also declined by 3.3% per year, but was still 2.5 times that of other Australian infants. Rates of non-communicable health problems, such as obesity and mental disorders, appear to be rising, but lack of up-to-date national data makes it difficult to accurately assess the current rates. Rates of vaccination among children aged 1 and 2 years have increased over time, with the coverage in 2004 being over 90%. Between 1990 and 2000, children’s dental health improved, with a decrease in the mean number of decayed teeth in 6 year olds (from 2.1 to 1.7), and 12 year olds (from 1.4 to < 1). However, since 2000, tooth decay in Australian children seems to be on the increase again. The number of children on care and protection orders has risen almost 50% in the past 6 years, with the rates sixfold higher in Indigenous children. The proportion of children placed in out-of-home care also rose from 3 per 1000 children in 1997 to 5 per 1000 in 2004. Economic progress has also altered the lives of children through changing the social context of development. The transformation of Australian families has been striking. Fewer children, smaller households, older parents, working mothers, and parental separation and divorce, all affect the way in which families provide a nurturing and secure base.4 There are concerns that a greater investment in fewer children, tied with heightened parental anxieties, has produced a “bubble-wrap generation”. The effects of limiting independent exploration, risk taking and physical activity on children’s physical, cognitive and emotional development may be profound.5 Socioeconomic changes have also affected child health in other ways, such as altering material consumption and lifestyle. Industries, ranging from fashion to food and entertainment, now market to children, regarding them not only as the consumers of tomorrow but as major agents of influence on family spending.6 In this changing social context, the AIHW report attempted to capture a broad picture of the health and development of our children (Box). In preparing the report, emerging morbidities, such as childhood obesity, were to be an important focus. Obesity not only poses risks for later cardiovascular disease and diabetes, but also profoundly affects children’s quality of life and self-concept.7 However, the best available national data are 10 years old, from a time when around one in five children were overweight or obese. Moreover, national data are not available on patterns of physical activity or nutrition. Because of longer-term effects on adult health and prosperity, the socioeconomic circumstances of childhood are central in social policy considerations.8 Nowhere are these continuities between childhood circumstances and adult health clearer than in Aboriginal and Torres Strait Islanders. For this reason the report attempted to capture broader data on family functioning, local neighbourhoods, educational attainment, and the welfare of children in contact with health and social services. Some of the trends revealed by the study provide food for thought. The number of children on care and protection orders has increased almost 50% in 6 years, and rates in Indigenous children are over sixfold higher. The proportion of children in out-of-home care (ie, having to live away from their parents) has risen over 60% in the same period. Around one in ten families with children currently report that their neighbourhoods feel unsafe at least some of the time. This experience is three times commoner in poorer families. What effects these trends may be having on the mental health and emotional development of children is uncertain. Again our picture is incomplete, with the best available national data on child mental health now 7 years old.9 Data from this 7-year-old study suggested that, at any point in time, one in eight children had a diagnosable mental or behavioural disorder. These rates were twice as high in sole parent and blended families (ie, families formed by second marriages between parents with children). Thus, in attempting to paint a bigger picture of child health, development and wellbeing, the AIHW report has exposed huge gaps in the information needed for rational health and social policy responses. Perhaps the clearest gaps concern the emerging non-communicable illnesses of childhood. A need for up-to-date national data on the social and geographic distribution of childhood obesity and mental disorders stands out as a priority. What data we have suggest that these problems vary greatly according to geographic location and socioeconomic status and are worsening. If current social changes persist, the worsening trends in obesity and mental disorders seem likely to continue, and the children most affected will be those in disadvantaged and disrupted families. The federally funded Longitudinal Study of Australian Children will address some of the gaps by providing a better understanding of how current social and family contexts affect children.10 However, the study is of two cohorts separated by 4 years and will not be able to adequately capture the continuing and ongoing changes in the social context of childhood that we may expect to see in the coming years. Other gaps relate to our service systems for children and families. The aggregation of service system data to create ongoing national minimum datasets for areas such as juvenile justice, child protection and children’s services is an important first step in understanding how these systems are working. But much more is needed. The development of brief measures of development and social context in early and later childhood11,12 heralds the possibility of efficiently capturing ongoing shifts in the lifestyles, social development and health of our children. The new health problems of childhood are complex in their origins and likely to be complex in their solutions. A clearer picture of our children is needed to guide our responses — whether these be through priority research, informed government policy, better functioning of our service systems or, most importantly, the efforts of Australia’s parents, schools and local communities.

George C Patton MD, FRANZCP · Sharon R Goldfeld FRACP · Indrani Pieris-Caldwell PhD · Meredith Bryant MA · Graham V Vimpani FRACP

Objective: To report the outcome of gene therapy in an infant with X-linked severe combined immunodeficiency (SCID-X1), which typically causes a lack of T and natural killer (NK) cells.Design and setting: Ex-vivo culture and gene transfer procedures were performed at The Children’s Hospital at Westmead, Sydney, NSW, in March 2002. Follow-up to March 2005 (36 months) is available.Patient: A 9-month-old male infant with confirmed SCID-X1 (including complete absence of T cells) with an NK+ phenotype (a less common variant of SCID-X1), and no HLA-identical sibling donor available for conventional bone marrow transplantation.Procedure: CD34+ haemopoietic progenitor cells were isolated from harvested bone marrow and cultured with cytokines to stimulate cellular replication. Cells were then genetically modified by exposure to a retrovirus vector encoding human γc (the common γ chain of several interleukin receptors; mutations affecting the γc gene cause SCID-X1). Gene-modified cells (equivalent to 1.3 × 106 CD34+/γc+ cells/kg) were returned to the infant via a central line.Results: T cells were observed in peripheral blood 75 days after treatment, and levels increased rapidly to 0.46 × 109 CD3+ cells/L at 5 months. Within 2 weeks of the appearance of T cells, there was a distinct clinical improvement, with early weight gain and clearance of rotavirus from the gut. However, T-cell levels did not reach the reference range, and immune reconstitution remained incomplete. The infant failed to thrive and developed weakness, hypertonia and hyperreflexia in the legs, possibly the result of immune dysregulation. He went on to receive a bone marrow transplant from a matched unrelated donor 26 months after gene therapy.Conclusions: This is the first occasion that gene therapy has been used to treat a genetic disease in Australia. Only partial immunological reconstitution was achieved, most likely because of the relatively low dose of gene-corrected CD34+ cells re-infused, although viral infection during the early phase of T-cell reconstitution and the infant’s NK+ phenotype may also have exerted an effect.

Samantha L Ginn BSc(Hons), PhD · Julie A Curtin PhD, FRACP · Christine M Smyth MSc, PhD · Margot Latham BSc · Sharon C Cunningham BSc(Hons), PhD · Maolin Zheng BSc(Hons), MSc · Linda Hobson BPharm(Hons) · Peter B Rowe MD, FRACP · Ian E Alexander PhD, FRACP · Belinda Kramer BSc(Hons), MSc · Melanie Wong PhD, FRACP · Alyson Kakakios FRACP · Geoffrey B McCowage FRACP · Debbie Watson BSc(Hons) · Stephen I Alexander FRACP · Alain Fischer MD, PhD · Marina Cavazzana-Calvo PhD · Salima Hacein-Bey-Abina PhD

Allergic bronchopulmonary aspergillosis (ABPA) is an uncommon condition which may complicate asthma and cystic fibrosis; it is seldom considered life-threatening. We report a well 8-year-old boy with cystic fibrosis and normal lung function who progressed to respiratory failure over several days, attributable to ABPA. He recovered with non-invasive ventilation and oral corticosteroid and antifungal medications, regaining normal lung function within 2 months. To our knowledge, such an acute severe presentation of ABPA in a previously well child has not been reported before. Clinical record An 8-year-old boy with pancreatic insufficient, homozygous ΔF508 cystic fibrosis (CF) was transferred from a district hospital with a 7-day history of progressive cough, wheeze and tachypnoea, despite 4 days of broad-spectrum antibacterial therapy (intravenous flucloxacillin and cefotaxime with oral roxithromycin), frequent nebulised salbutamol, oral prednisone (2 mg/kg/day) and chest physiotherapy. There were no other systemic symptoms such as rash, myalgia, arthralgia, diarrhoea or headaches. Initial sputum cultures isolated only normal respiratory flora. The provisional diagnosis was an atypical lower respiratory tract infection, attributed to a viral infection or Mycoplasma pneumoniae. Cystic fibrosis had been diagnosed at newborn screening. His height and weight had tracked along the 10th percentile. Lung function had been normal. Previous sputum cultures had grown Staphylococcus aureus but never Pseudomonas aeruginosa or Burkholderia cepacia. He had not previously wheezed. On arrival, he was mildly dyspnoeic on supplemental mask oxygen at 6 L/minute with a blood oxygen saturation (Spo2) of 94%. He was tachypnoeic (44 breaths per minute), tachycardic (112 beats per minute), afebrile and normotensive. He had bilateral expiratory wheeze with basal crackles. Within 24 hours of transfer, our patient’s condition deteriorated, and he required more frequent nebulised salbutamol and developed signs of respiratory fatigue. At this point an arterial blood gas analysis in 12 L of mask oxygen showed: pH, 7.3; partial pressure of oxygen (Po2), 58 mmHg; partial pressure of carbon dioxide (Pco2), 62.7 mmHg; bicarbonate (Hco3) level, 30 mmol/L; and base excess, 2.7. He was transferred to the paediatric intensive care unit (PICU) for respiratory support with mask continuous positive airway pressure (CPAP). Subcutaneous emphysema developed over the chest wall and neck during the first 48 hours of his PICU admission. A full blood count showed leukocytosis (19.6 × 109/L), and his initial mycoplasma complement fixation test titre was low (< 4). The mycoplasma IgM test result was subsequently negative. Immunofluorescence and culture of nasopharyngeal secretions to isolate a viral pathogen were negative. Total serum IgE titre was 1664 IU (normal range, 0–180 IU) and the skin prick test was positive for Aspergillus fumigatus. The provisional diagnosis was changed to allergic bronchopulmonary aspergillosis (ABPA). Prednisone therapy was continued, and antifungal treatment with oral itraconazole (100 mg twice daily) was added to his therapy. His respiratory status gradually improved and he was weaned off the nasal mask CPAP after 5 days, avoiding endotracheal intubation. He had clinically apparent subcutaneous emphysema, a small pneumomediastinum, but no pneumothoraces during his PICU stay. The chest radiograph before discharge from PICU (Box 1) showed increased perihilar opacities and left lower lobe infiltrates with resolution of the pneumomediastinum and subcutaneous emphysema. His improving spirometry measurements with treatment are shown in Box 2. He was discharged on Day 13 of admission with marked improvement in symptoms and an FEV1 (forced expiratory volume in 1 second) 66% of predicted. A provisional diagnosis of ABPA was confirmed by the significantly elevated serum IgE titre, positive skinprick tests for aspergillus, positive IgG aspergillus precipitins (× 4) and clinical findings consistent with the diagnostic criteria outlined in Box 3.1-5 He received decreasing doses of oral corticosteroids over 3.5 months, as well as oral itraconazole. Within 2 months, his spirometry results had returned to normal. Predictably, he became transiently cushingoid, developed mild untreated hypertension (maximum recorded blood pressure, 116/84 mmHg), and gained 4 kg in weight, but had no glycosuria. He was weaned from corticosteroids and itraconazole, and the side effects resolved within 3 months of discontinuing corticosteroids. Ten months later, he remains well, with normal lung function. DiscussionAlllergic bronchopulmonary aspergillosis (ABPA) is an uncommon condition that can complicate asthma and cystic fibrosis (CF),6,7 and is seldom considered life-threatening.7 The rapid deterioration in the condition of our previously well patient highlights the spectrum of disease severity that can occur in ABPA, and is a reminder that not all deteriorations in respiratory function in patients with CF are attributable to Pseudomonas aeruginosa or Burkholderia cepacia.7,8 Furthermore, this patient’s prompt clinical response to systemic corticosteroids with a return to normal lung function within 2 months suggests that his prognosis will not be adversely affected.9 The presence of Aspergillus species in the sputum cultures of patients with CF has been reported in up to 57% of patients,9 yet the prevalence of ABPA is reported to be between 2% and 14%.1,6 The diagnostic criteria are listed in Box 3. ABPA is a hypersensitivity reaction to the inhalation of aspergillus spores manifesting as chronic wheeze, pulmonary infiltrates and systemic immune activation.5 This results in elevated IgE, IgG and IgA titres.9 Interestingly, although aspergillus grows in the bronchial mucus, this is not an invasive disease.3-5,9 The exact mechanism by which bronchial wall damage evolves and how this gives rise to bronchiectasis and fibrosis is poorly understood.10 Aspergillus fumigatus infection often occurs months before a clinical diagnosis of ABPA is considered. Moreover, as about 40%–50% of school-aged patients with CF have aspergillus in their sputum, comparatively few develop ABPA.3 The reasons for this are not clear, but presumably relate to genetic predisposition, host defences and environmental exposure to aspergillus. Most children with CF who develop ABPA have relatively mild symptoms, respond to treatment over weeks and can often avoid hospital admission altogether.7 Patients with ABPA complicating CF more commonly follow a course of gradually worsening lung function (because of progression of their CF related bronchiectasis) with recurring relapses of ABPA, particularly in summer and autumn, when spore levels in the environment are at their highest.9,10 Treatment of ABPA has centred on the use of systemic corticosteroids for periods of 2–6 months, reducing from doses of 1.0 mg/kg/day of prednisone.4 The adjunctive use of oral antifungals has been advocated for the treatment of ABPA complicating CF11,12 and asthma.6 The response can be dramatic, as in our patient (Box 2). Itraconazole in combination with inhaled corticosteroids was recently shown to be useful for reducing eosinophilic airway inflammation, reducing systemic immune activation and reducing severe exacerbations over a period of 16 weeks in adults with ABPA complicating asthma.13 The use of itraconazole in children is less well studied. However, a recent case series of patients aged 9 to 33 years with CF and ABPA, treated with inhaled budesonide (800–1600 μg/day) and itraconazole (400–600 mg/day), showed a high prevalence of biochemical adrenal insufficiency on adrenocorticotropin testing. This was attributed to an increased systemic budesonide concentration through a reduced or inhibited metabolism (potentially caused by itraconazole), leading to inhibited steroidogenesis.14 This reminds us to use caution when treating patients who take inhaled steroids with courses of itraconazole for exacerbations of ABPA. In conclusion, we are unable to find another case report in which a previously well child with ABPA presented with severe acute respiratory failure. This case highlights the importance of considering a diagnosis of ABPA in highly unusual presentations which may complicate cystic fibrosis. 1 Chest x-ray 3 days after admission to intensive care Shows hyperinflated lung fields, perihilar inflammatory changes, emergence of an interstitial infiltrate in the left lower lobe and a small right-sided pleural effusion. 2 Relationship between IgE levels and FEV1 (forced expiratory volume in one second) before, during and after admission Inverse relationship between IgE levels and FEV1 over time (non-linear scale), showing the drop in lung function at the peak of the disease. 3 Classic case criteria for the diagnosis of allergic bronchopulmonary aspergillosis (ABPA) in patients with cystic fibrosis1-5 Clinical deterioration (increased cough, wheezing, exercise intolerance, increased sputum, decrease in pulmonary function) Immediate cutaneous reactivity to aspergillus or presence of serum IgE from A. fumigatus Total serum IgE concentration >1000 IU/L Precipitating antibodies to A. fumigatus or serum IgG from A. fumigatus Abnormal chest x-ray (infiltrates, mucus plugging, or a change from earlier films) Adapted from the ABPA Consensus Conference of the Cystic Fibrosis Foundation4

Emma Skowronski BMedSci · Dominic A Fitzgerald PhD, FRACP

There are strong associations between childhood sleep disorders and behavioural, concentration and mood problems. Sleep disorders caused and maintained by behavioural factors (eg, sleep-onset association disorder) are common in young children, and have a significant impact on families. Evaluation should include a medical history, a physical, neurological and developmental examination, a description of any nocturnal events or daytime effects of the child’s disturbed sleep, and a good understanding of the family situation and parental management of the child. Management involves recognising the developmental age of the child and the family dynamics, and educating and supporting families in applying behavioural techniques to establish good sleep hygiene. Children with parasomnias (eg, night terrors) also benefit from good sleep hygiene, while those with respiratory or neurological causes of sleep disturbance should be referred for specialist treatment.

Helen S Heussler MB BS, FRACP

Re: MJA Practice Essentials – Paediatrics “Investigation and treatment of upper-airway obstruction: childhood sleep disorders I”, by Kennedy JD and Waters KA (Med J Aust 2005; 182: 419-423). In printed version of this article, the last two paragraphs were missing from the Case study on page 422. The complete Case study is given below. The html version of this article was correct on publication and the pdf version was corrected on 27 April 2005. Case study — a 5-year-old boy with obstructive sleep apnoea syndrome (OSAS) A mother brings her 5-year-old son to you, as she is concerned about his loud snoring. He has been snoring for 2 years, but it is gradually becoming louder. Although she is unaware of whether or not her son has obstructive apnoeas, she is anxious about his breathing during sleep. She often sits up to watch him breathe before retiring herself. The mother reports that the boy’s teacher at school says that her son has a poor concentration span and is easily distracted in class. Both the father and grandfather snore loudly but neither has sought medical advice or investigation. Management On examination, you find that the boy has relatively small tonsils and you initially reassure his mother. However, as his symptoms persist, you refer him to a paediatric respiratory physician. An overnight home oximetry study shows only mild desaturations that appear to be associated with movement. A lateral x-ray of the neck confirms adenoidal hypertrophy but a patent postnasal space. A polysomnogram shows an obstructive respiratory disturbance index of nine per hour. Based on the data from the polysomnogram, the boy undergoes adenotonsillectomy. After the operation, the boy’s snoring resolves, his behaviour and concentration improve, and his mother describes him as a “different boy”. At the 1-year follow-up, the boy’s mother reports that his snoring has returned. You resume frequent clinical monitoring, and subsequently refer him for repeat polysomnography, as his history once again suggests the presence of OSAS. If polysomnography confirms that OSAS has returned, and a lateral neck x-ray shows that his adenoids have not regrown, the use of night-time continuous positive airway pressure (CPAP) support will be considered.

J Declan Kennedy MD, FRCP, FRACP · Karen A Waters MB BS, FRACP, PhD

The most important need is for a change of attitude and approach Transition is “the purposeful, planned movement of adolescents and young adults with chronic physical and medical conditions from child-centred to adult-orientated health care systems”.1 The importance of transition of young people with chronic health conditions from paediatric to adult care is finally being recognised, but it needs to be addressed in a coordinated and integrated way. In Australia, as internationally, there are some well established and potentially effective transition programs. However, little is known about the efficacy of such programs, as there is little published evaluation.2 What is clear, both anecdotally and with some modest support in the literature, is that the journey faced by young people with chronic and disabling conditions is a complex one.3,4 The majority will face obstacles that arise from the lack of infrastructure and precedent in this specialised area of health care. Current approaches are rarely ideal, the most likely options being abrupt transfer to adult services, staying in the paediatric setting longer than is appropriate, or leaving medical supervision altogether. 5 The study at the Royal Children’s Hospital, Melbourne, reported by Lam and colleagues6 in this issue of the Journal (page 381) revealed a doubling in admissions of young adults aged 18 and over between 1992 and 2001, along with an overall increase in the numbers of adolescents admitted. In a more detailed analysis of a cohort of 247 young adults admitted during 2001, the authors also examined disease complexity and discovered a paucity of transition planning, particularly in surgical units. While some medical services (eg, Endocrinology, Respiratory Medicine) appeared to effect transition of adolescents with complex health issues efficiently, this was definitely not the norm. With increasing prevalence of some diseases and improved survival rates for previously fatal childhood conditions, pressures on all tertiary care facilities continue to rise. In paediatric hospitals, one possible outcome is pressure to improve facilities for adolescents. A psychosocial survey of Australian hospitals undertaken in 2004 by the Association for the Welfare of Child Health showed an increase in the number of “adolescent units” since the previous survey in 1994. 7 Hospitalised and ambulatory young people require developmentally appropriate health care supported by psychosocial services — needs that are usually better served in dedicated adolescent facilities. While the impact of this trend on transition practices is yet to be determined, the broader challenge is to consider transition needs in the coordinated planning of health care services. Until transition to adult care is recognised by the adult health care system as requiring a demonstrable change in attitude and resources, little real progress will be possible. Older adolescents deserve to be treated more as adults than as children. Keeping young adults in the paediatric system is working against this goal on many levels. A sense of maturity and hope for the future are implied in “moving on”, 8 but one of the prerequisites for an effective transition program is “an interested and capable adult service”. By allowing young adults to stay on in the paediatric system (which carries its own set of problems, including the inappropriate collocation of young children with “adults”), the development of such services is effectively stifled, and adult physicians and surgeons are not encouraged to develop their skills in the area. The article by Lam et al asks, “Why are they there?” It has been proposed that paediatric services may hold onto patients because of mistrust of adult services9 or through failure to promote independence and autonomy in health-care seeking. 10 Some other probable reasons are less strongly supported by the literature. One is that paediatric services are family-focused, while adult services treat patients as independent adults. This is problematic for young adults who still require family involvement because of the nature or severity of their disease or disability. Doctors and other staff in adult services may have limited knowledge and understanding of childhood chronic illnesses in young people who survive into adulthood, or of developmental issues in adolescents. Furthermore, young people are “diluted” in the adult health care system and their special needs may be largely overlooked in individual services. There are inherent difficulties in discovering, accessing and negotiating adult services for young people and their carers. The implications of “failed transition” for young people range from a lack of continuity of care and reliance on crisis services to “falling through the gap”, with significant adverse health consequences. 11 We agree with Lam and colleagues that the solution to the problems of young adults in children’s hospitals lies more in a greater focus on the infrastructure supporting transition than in admission policies per se. Unfortunately, there are no established, evaluated transition programs described in the literature on which such an infrastructure could be based. In New South Wales, the Transitional Care for Young People with Chronic Childhood Illnesses Group (part of the Greater Metropolitan Clinical Taskforce) is developing a state-wide strategy to address transition, which may serve as a blueprint for a national process (Box). Data collection, “gap” identification and the use of transition coordinators based in adult hospitals are all part of this initiative. Australia urgently needs to develop a national policy on transitional care that articulates the critical role of transition coordinators as well as the coordination of transitional care between paediatric and adult services. Success will also depend on educating health professionals and families about the value of coordinated transition; developing appropriate attitudes and expertise, particularly in adult services; comprehensively evaluating transition programs; examining health outcomes and cost–benefit issues; and involving consumer advisory groups.12,13 While additional resources may be needed, the overwhelming need is for a change of attitude and approach. Transition plan for young people and their families/carers*† * Based on a strategy being developed by the Transitional Care for Young People with Chronic Childhood Illnesses Group of the Greater Metropolitan Clinical Taskforce. †This model will require adjustment to meet the needs of special groups.

David L Bennett FRACP, FSAM · Susan J Towns FRACP · Kate S Steinbeck FRACP

Objective: To measure the pattern of admissions of young adults to a children’s hospital.Design and setting: Ten-year audit (1992–2001) of admissions of young adults aged 18 years and over to the Royal Children’s Hospital (RCH), Melbourne, with a detailed chart review of the 2001 cohort to assess disease complexity and transition planning.Outcome measures: Number of admissions, disease complexity, transition planning.Results: There was a significant increase in the number of young adults admitted over 10 years, from 308 in 1992–1993 to 659 in 2000–2001. The greatest increase was in admissions to surgical units. There was significant variation in admission practices between units over time. Many young adults required multidisciplinary care: 57% had more than three medical/surgical units involved in their care, and 34% had two or more allied health units involved. Fifty-one per cent of surgical inpatients and 28% of medical inpatients had no documented plan for transition to adult care. Only 30% of medical and 17% of surgical inpatients in 2001 had been transferred to adult services by 2002.Conclusions: Both disease complexity and failure of transition planning appear to have contributed to the increased admission of young adults to the RCH. While greater support of transition planning is needed, there are also concerns about the lack of appropriate services within the adult sector for young adults with complex, multidisciplinary healthcare needs.

Pei-Yoong Lam MB BS, FRACP · Bronwyn B Fitzgerald MB BS · Susan M Sawyer MB BS, MD, FRACP

Always take a history of snoring and sleep disturbance when reviewing children in primary care, as there is evidence that episodes of hypoxia and arousal during sleep may result in deficits in memory, attention and behaviour, in addition to the well known sequelae of growth failure, developmental delay and cor pulmonale. Check for changes in behaviour affecting school progress. To investigate for possible obstructive sleep apnoea syndrome (OSAS), clinical examination, lateral neck x-ray (adenoidal hypertrophy) and overnight oximetry (desaturation episodes) are useful screening tests, but oximetry is best used in conjunction with polysomnography. A negative oximetry test does not exclude OSAS. Polysomnography is the best method for detecting and assessing the severity of OSAS in children, and is especially helpful for prioritising treatment and evaluating the risk of perioperative complications of adenotonsillectomy. Adenotonsillectomy is thought to “cure” (ie, symptoms disappear and overnight respiratory parameters are corrected) in about 80% of children with OSAS. The remaining 20% need ongoing evaluation and treatment. Further research is needed to determine the “true” prevalence of OSAS; what degrees of severity of upper-airway obstruction lead to morbidity requiring treatment; and whether the deficits in neurocognitive function associated with sleep-disordered breathing are fully correctable.

J Declan Kennedy MD, FRCP, FRACP · Karen A Waters MB BS, FRACP, PhD