Child health

There are many challenges in developing evidence-based physical activity guidelines for preschoolers that can ensure health benefits for children.Guidelines for the preschool years have recently been developed in several countries, but there are notable inconsistencies in the amount of physical activity regarded as sufficient for this age group.Given the currently high prevalence of childhood obesity, there is an....

Helen Skouteris PhD · Daniela Dell'Aquila BSocSci(Psych), PostGradDip(Psych) · Louise A Baur BSc(Med), PhD, FRACP · Genevieve M Dwyer MAppSc(Phty), PostgradCert (AdultEd · Marita P McCabe PhD · Lina A Ricciardelli PhD · Matthew Fuller-Tyszkiewicz PhD

Objectives: To examine the prevalence of overweight and obesity in Australian secondary school students and identify factors associated with excess adiposity....

on behalf of the NaSSDA Study Team*

Putting a team-based intervention approach to the test.

Sandy M Hopper FRACP, FACEM · Franz E Babl MD, FRACP, FACEP · Claire E Stewart PGDipENB, RN · Jia Wei Woo BSc, MB BS

Assessing health status is only the beginning. Decisions to remove children from their biological parents are never taken lightly. Such decisions are reinforced by the growing body of evidence of the adverse short- and long-term outcomes of child maltreatment,1 which are increasingly seen to be mediated through the effects of abuse on early brain development.

Graham V Vimpani PhD, FRACP, FAFPHM · Susan M Webster MPHC · Meredith J Temple-Smith BSc, MPH, DHSc

Health professionals should educate families about risk factors for accidental asphyxiation in shared-sleeping arrangements Over the past two decades, great advances have been made in identification of hazardous sleeping environments for infants and young children, with significant reductions in numbers of deaths.1 However, one issue that continues to incite heated debate is whether adult caregivers should sleep on the same surface as infants,2 referred to as “shared sleeping”. It is recognised that infants who sleep in the same room as their carers have a reduced risk of sudden infant death syndrome (SIDS),3 possibly due to an increased level of direct supervision.4 However, what of infants who sleep in the same bed as their parents or carers? First, it is important to clarify terminology. Although it is claimed that shared sleeping increases the risk of SIDS, it is perhaps more accurate to state that it is associated with an increased risk of infant death generally. An indication that shared-sleeping deaths may be different to “classical” SIDS deaths that occur among infants sleeping on their own is a finding of an almost equal sex ratio in shared-sleeping deaths, compared with the 2 : 1 male–female ratio among infants who died of SIDS.5 If some of the risk factors for shared-sleeping death (eg, parental obesity, fatigue, soft sleeping surfaces) are examined in isolation, accidental suffocation appears to be a more likely mechanism of death than subtle processes leading to SIDS.5 These apply to any shared-sleeping surface, not just to beds. It is difficult to formulate absolute recommendations on shared sleeping, as the current incidence in most communities is unknown, and the form that it takes varies greatly between families. There are also cultural issues to take into consideration — for example, shared sleeping is very common in South-East Asian communities, but with low incidences of unexpected infant deaths.6 However, a study from Avon, United Kingdom, found a disturbing percentage increase in shared-sleeping deaths among two cohorts of infants who died of “SIDS”, from 12% (17/147 in 1984–1988) to 50% (18/36 in 1999–2003) (P < 0.001).7 The authors noted that although the number of shared-sleeping deaths that were not on sofas dropped (from 16 to 14), the decrease was not as great as that among infants who were sleeping on their own, perhaps explaining the increased proportion of unexplained infant deaths found in shared-sleeping situations. This difference may be due to mechanisms of death being different in the two circumstances. A similar effect was noted in South Australia, where the proportion of shared-sleeping deaths increased from 7.5% of “SIDS” deaths (23/306 in 1983–1990) to 32.3% (21/65 in 1991–1993).8 The percentage of deaths in shared-sleeping situations in the early part of the study also showed an overrepresentation compared with the shared-sleeping rate of 1.5% in the general community in 1988.8 As some infants are particularly vulnerable to the effects of airway occlusion,9 and as there is often no clinical predictor of this vulnerability, all that can be stated is that certain infants may be inherently at increased risk in a shared-sleeping situation. It is generally agreed that in Western cultures, the safest place for an infant is in a cot that meets recommended safety features and is positioned beside the caregiver’s bed.1,2 Supporters of shared sleeping cite advantages that include an increased incidence and longer duration of breastfeeding, enhanced maternal–infant bonding and improved settling.1 However, it has been reported that 50% or more of infants who are found unexpectedly dead are sleeping with an adult.10 The suggestion of possible accidental asphyxia by a parent “overlaying” a shared-sleeping child has been criticised, because it has been assumed that a parent would always arouse. However, parents can fail to wake if they are sedated or overly fatigued. There is an increased risk of infant death when caregivers have taken illicit drugs, smoked, or consumed more than two units of alcohol.10 In addition, it is not necessary for an adult to be lying over an infant completely for respiration to be compromised, as an infant who has rolled into a trough between a parent’s much larger body and a soft mattress may also be at risk.11 This is exemplified by the dangers of shared sleeping on a sofa.7 On occasion, parents state that they successfully slept in the same bed as all of their children without any deaths occurring. While such anecdotes are undoubtedly true, few risks are absolute and so it cannot be used as definitive evidence that shared sleeping is always a safe practice. The key to assisting with this issue lies in adequately informing caregivers of potential risks. Clinicians should discuss with caregivers the risk factors for accidental asphyxiation in shared-sleeping arrangements, such as sedation, excessive fatigue and hazards predisposing to suffocation. This may help prevent infant deaths in the future.

Roger W Byard MB BS, MD

Teaching children how to behave around dogs can reduce the incidence Dogs never bite me. Just humans. Marilyn Monroe (1926–1962) Dogs have been companions of humans for over 12 000 years and have become an inseparable part of rural and urban life. Many breeds continue to do valuable work — managing livestock on farms, guiding the visually impaired, sniffing out contraband, and as guard dogs. Most of the 3.4 million dogs in Australia are family pets, with 36% of households owning a dog.1 Unfortunately, as a result of this close relationship, dog bites are common. Statistics on dog bites often seem alarming, but most bite injuries are relatively minor, not requiring hospital admission.2 In 2008 and 2009, 928 children aged 0–14 years attended accident and emergency departments in Queensland with dog bites, equating to nine bites per week (Access Information Service, Queensland Health). The Queensland Trauma Registry (QTR) contains data on 186 children (aged 0–14 years; mean age, 5.5 years) who were admitted to Queensland hospitals for more than 24 hours in 2003–2009, equating to one such hospitalisation for a dog bite injury every 2 weeks (own unpublished data). No children died from dog bites in this period. Of the dog bite injuries recorded in the QTR, 88% occurred in the home environment, and almost all (98%) required at least one operation under general anaesthetic. In 2003, the Royal Children’s Hospital conducted a telephone survey on 45 consecutive children who were admitted with serious dog bites during 1997–2002. This survey showed that the child had physically interacted with the dog immediately before the attack in 63% of cases. Most attacks (92%) occurred in a setting familiar to the child, usually the family house or garden, or that of a relative or friend. Most bites were to the head and neck region (72%) and most children (93%) were left with permanent cosmetic scarring (own unpublished data). These results are consistent with those of other Australian studies.2,3 While most dog bite reports attempt to identify the breed, this information is commonly not documented in the patient record and, when stated, relies on correct identification by the family. No one breed stands out, but breeds commonly mentioned in Australian articles include Rottweilers, German Shepherds, Cattle Dogs and the Bull Terrier group.2,3 Data on an array of other breeds and cross-breeds provide evidence that any dog is capable of biting. An American study examined 238 dog-bite-related deaths over 20 years to 1998, and identified at least 25 different breeds.4 Breed identification may not be accurate. For example, the general public might have difficulty differentiating between several breeds in the Bull Terrier group. Staffordshire Bull Terriers, American Staffordshire Terriers and American Pit Bull Terriers all appear very similar. To add further confusion, a recent Queensland Supreme Court ruling stated that there was no distinction between the American Staffordshire Terrier and the American Pit Bull Terrier. Dogs are highly regulated in Australia with mandatory registration laws. It is now prohibited to import certain breeds, including American Pit Bull Terriers, Japanese Tosa, Dogo Argentino and Fila Brasiliero. State laws on the ownership of such breeds vary, but generally require desexing (unless registered for breeding), microchipping, the use of a leash and muzzle in public places and a locked enclosure at home with a warning sign. The laws are based not so much on evidence that these breeds are inherently dangerous, but rather that they are breeds which have been traditionally used for dog fighting. Much debate continues whether this is good and fair legislation, as studies have failed to show improvement in the incidence of bites after the legislation was passed.5 Breed-specific legislation fails to take into account that any breed of dog can be dangerous in the hands of an irresponsible owner who fails to provide good and early training. Further, these restrictions may create the risk of higher numbers of unregistered animals or irresponsible owners simply turning to other breeds. It is clear that all breeds bite, and that the severity and commonality is related to the size of the dog and how many of a particular breed exist.6 In the Netherlands, where good data on breeds and bites exist, breed-specific legislation was repealed because they found no one breed more dangerous than any other. They recommended there be a focus on owners of dogs in cases where the people bitten did not interact with the dog that bit them.6 Training for dogs and education for dog owners and children can reduce the incidence of dog bites. A recent United States study reported that knowledge about dog bite prevention among young, school-aged children is poor.7 However, education programs in the primary school setting have been shown to alter a child’s interaction with dogs.8 In general, children should be taught: to ask permission from the owner before slowly approaching an unfamiliar dog; never to run from a dog or scream; to stand still if approached by a strange dog and, if knocked over, roll into a ball and lie still; to avoid eye contact with the dog by looking at their own feet; not to disturb a dog that is sleeping, eating, or caring for puppies; and not to pat a dog without supervision or without allowing it to see and sniff them first.9 Furthermore, dog owners should take their dogs to obedience classes, and dogs should be taught to obey commands from all family members. Dogs used for hunting or as guard dogs should not be allowed to mix with children.9

Roy M Kimble MD, FRCS, FRACS · Natalie Dallow · Richard Franklin PhD · Belinda Wallis BBEnv(Dist)

To the Editor: We recently reviewed the individual policies of seven Australian tertiary maternity hospitals, from across all states, regarding neonatal vitamin D supplementation. An Australian 2006 consensus statement concerning the treatment and prevention of vitamin D deficiency in children and neonates identified the need to implement vitamin D supplementation in neonates born to mothers with serum 25-hydroxyvitamin D (25-OHD) levels of ≤ 50 nmol/L.1 Despite this, we found that a number of institutions have recently adopted a policy of treating infants of mothers with an antenatal serum 25-OHD level of < 75 nmol/L. Treatment of the neonate is with oral stoss therapy (50 000 IU vitamin D as a single dose) and/or daily oral vitamin D therapy (1000 IU) until cessation of breastfeeding. It should be noted that previous research has suggested that a substantial proportion of Australian women of childbearing age have a serum 25-OHD level < 75 nmol/L.2 Vitamin D is a pleiotropic hormone that influences the expression of more than 200 human genes.3 It has a wide range of biological actions, and the full implications of vitamin D supplementation during early life are unknown. While it is clear that very low levels of vitamin D are associated with abnormal bone development and the risk of hypocalcaemic seizures, it is also possible that vitamin D supplementation may have adverse effects. For example, we and others have found that a history of vitamin D supplementation during early life may be associated with an increase in allergic outcomes such as asthma and hayfever in later life.4,5 These are observational findings, limited by potential confounding and reverse causation, but they highlight the potential concern of changes in medical practice without an accompanying updated evidence base. There is an urgent need for improved data and further debate before implementing a public health policy affecting as many as half of all Australian infants. In the interim, we would advocate treatment of neonates only if they fall within the 2006 guidelines (mother’s serum 25-OHD ≤ 50 nmol/L).

Kate M McCloskey · Natalie Wright · Anne-Louise Ponsonby · Peter J Vuillermin

To the Editor: The position statement by Jones and colleagues regarding the change of HbA1c reporting to the new Système International (SI) units — which has been recommended by the Australasian Association of Clinical Biochemists, the Australian Diabetes Educators Association, the Australian Diabetes Society and the Royal College of Pathologists of Australasia — provides a comprehensive summary of the rationale behind the proposed change and suggests a 2-year period of dual reporting.1 However, Jones et al did not specify targets for children and adolescents, and we believe that it is important to do so. The incidence of type 1 diabetes in Australian children and adolescents is among the highest in the world2 and, in New South Wales, type 2 diabetes represents at least 10% of cases of new-onset diabetes in adolescents.3 National evidence-based clinical care guidelines for type 1 diabetes in children, adolescents and adults4 include age-specific targets for HbA1c, while recognising that such targets are predominantly consensus based. HbA1c targets for young people with type 1 diabetes are higher, with a level of < 7.5% recommended for children and adolescents in the Australian guidelines4 and in those produced by the International Society for Pediatric and Adolescent Diabetes (ISPAD).5 Jones et al note that “Achievement of HbA1c targets must be balanced against risk of severe hypoglycaemia, especially among older people”;1 this is also the case for young people. For children and adolescents with type 2 diabetes, the ISPAD guidelines recommend an HbA1c target of < 7%.5 The move to SI units represents a major change in the established, widely recognised outcome measure of glycaemia; during the transition period, the specific needs of young people with diabetes must not be forgotten.

Maria E Craig · Kim C Donaghue · Fergus J Cameron · Martin Silink

In reply: We appreciate Craig and colleagues’ comments regarding the importance of reporting general HbA1c targets for children and adolescents with type 1 and type 2 diabetes. In our position statement, the headings of Box 2 and Box 3 indicated that the targets listed were for adults with type 1 diabetes and adults with type 2 diabetes, respectively.1 While it is not possible to highlight every clinical situation, we agree that providing general HbA1c targets for children and adolescents will add value to our article, and we have updated it accordingly,1 recognising the differences in these targets for type 1 diabetes (≤ 58 mmol/mol, ≤ 7.5%) and type 2 diabetes (≤ 53 mmol/mol, ≤ 7.0%).2-4 In the interests of uniformity and simplicity, the paediatric targets expressed as “<”2-4 have been adjusted to “≤”, which represents differences of less than 1.5% of the target values. Addendum p 524

Graham R D Jones · George Barker · Ian Goodall · Hans-Gerhard Schneider · Mark D S Shephard · Stephen M Twigg

Will children be “crowded out” of non-acute and preventive care visits? As a society ages, adults become a larger proportion of the population. However, in Australia, the demographic reality is that while children have become a smaller proportion of the population, their absolute number has increased modestly.1,2 Thus, solutions for the increased care requirements for older people cannot be intentionally or unintentionally associated with a diminution of the medical workforce required for children. Ensuring an adequate health care workforce is of vital importance to all countries. Much interest is being focused on the importance of caring for the increasing numbers of the aged in many developed nations.1,3 The proportion of the populations of both the United States and Australia who are aged over 65 years is increasing rapidly1,2 and the health care needs of these individuals will require additional workforce resources.1,4 In Australia, primary care is delivered by general practitioners.5 To address the growing needs of the older population, there has been a significant effort to increase the number of GPs to ensure primary care access.6 At the same time, there are unrecognised demographic trends currently taking place in the composition of GP practices nationally that parallel the demographic trends of the population as a whole. These trends have important implications for the current and future care of children in Australia. One of these demographic trends is also occurring in the US among family physicians. For example, as older people have increasing life expectancy, and family physicians have relatively static numbers of patients in their patient panels, “turnover” in general practices and the opportunity to add new (paediatric) patients is increasingly limited.7 In Australia, examination of Bettering the Evaluation and Care of Health (BEACH) data from the past decade demonstrates a significant decrease in the proportion of GP visits by patients under 15 years of age across the country. This is despite an increase in the survival of children with chronic diseases.8 Whether the absolute number of visits for children has fallen is currently unclear but must be investigated. Regardless, such findings demonstrate a change in the demography of GP practices, with a trend towards GPs providing proportionally less care to children relative to the care they provide to adults. Even with the expected increase in the overall number of GPs in Australia in the next decade, this finding raises significant issues for the health care system. As children become a smaller proportion of GP practices, it is realistic to question whether GPs will continue to devote the time and effort needed to stay up to date on paediatric issues when they will have fewer opportunities to use such knowledge. GPs will constantly be challenged with the ever-increasing complexity of caring for more adults with multiple chronic conditions in their practices. The situation also begs the question as to whether some GPs will begin to limit or discontinue providing care to children, especially in specific locations with smaller proportions of children and a more rapidly ageing population. New strategies may also emerge in which some GP practices become “adult only” or “older people only” to provide care for this population. This trend is already believed to be occurring among some family physicians in the US.7 Another related issue is whether the nature and duration of consultations that children receive in general practices are changing. Recent consumer satisfaction data in Australia demonstrate ready availability for acute paediatric problems (eg, ear infection).9 However, the increased complexity of multiple chronic conditions among the ageing population will require an increased number of longer consultations. If GPs’ patient bookings become more commonly filled with such visits for older people, questions arise as to whether children will receive fewer longer consultations for preventive care (eg, nutrition counselling, developmental assessments) and chronic illness. In other words, will children be “crowded out” of non-acute and preventive care visits? The decrease in the proportion of children in the overall population also has important implications for the future training of GPs. Already, some GP training programs are concerned about their ability to provide both inpatient and outpatient clinical settings with sufficient children having common chronic illnesses (eg, asthma) for their trainees to gain competency in their acute and longitudinal care. Such deficiencies may become more common as the ageing population trend continues. With childhood obesity, mental health problems and other antecedents of adult illness now occurring more frequently, this would be a worrisome trend. In the US, shortages in the health care workforce for children are mostly found in the paediatric subspecialties, especially in rural areas.10 There has been little research in Australia regarding the availability of paediatric subspecialty care, especially for Indigenous populations and children living in rural areas.6,8 With increasing survival of children with complex conditions and chronic diseases, the demand for paediatric subspecialty care in Australia is rising. The proportion of such care actually provided by paediatric-trained subspecialists rather than adult-trained subspecialists is currently unknown. This must be determined to assess the true need for such providers nationwide, both inside and outside major metropolitan areas. Exploration of these issues is important and urgent for medical workforce planning. Government and professional entities entrusted with assessing provision of the continuum of health care for the children of Australia, monitoring GP training, and overseeing the continuing education of GPs should investigate whether changes have been occurring that may lead to a decrease in the quality of care for this important segment of the population. Such efforts will ensure that the unique needs of children are not unintentionally lost in the current emphasis on the growing ageing population.

Gary L Freed MD, MPH · Jillian R Sewell MB BS, FRACP · Neil A Spike MB BS, FRACGP

To the Editor: The recent article by Hebden and colleagues on the frequency and content of fast-food advertising on Australian television concluded that the industry self-regulatory initiatives currently in place are ineffective in reducing children’s exposure to advertising of non-core foods.1 As the managers of these self-regulatory initiatives, we consider this conclusion to be misleading to your readers. The Australian food and beverage industry recognises the level of community concern in relation to food and beverage advertising to children. There are currently two self-regulatory initiatives in place to moderate advertising of non-core foods and beverages to children: the Responsible Children’s Marketing Initiative, that covers products found in retail outlets; and the Australian Quick Service Restaurant Industry Initiative for Responsible Advertising and Marketing to Children, that covers foods sold in quick-service restaurants. These initiatives are designed to restrict advertisements aimed at children by means of the nature of the advertisement and/or the medium by which it is delivered. Hebden et al base their conclusion on a broad definition of “advertising to children” that captures all advertisements screened between 5.30 pm and 10.30 pm on weekdays, and between 7.30 am and 11 am and 4.30 pm and 11 pm on weekends. Specific time periods are not, in fact, covered in the industry initiatives as these periods capture programs that are watched primarily by adults. If children are watching these programs, they are likely to be doing so accompanied by an adult who can provide guidance on appropriate food consumption. However, industry does recognise that times when children are watching television alone and advertisements that are designed particularly to target children are a different matter, and that it must act responsibly in these areas. The success of the initiatives should not be measured by advertising frequencies during certain time periods, as implied by Hebden and colleagues. Nevertheless, the data presented by Hebden et al actually suggest a significant reduction in the frequency of non-core-food advertisements (excluding fast food) in just the first year of operation of the initiatives, which, in terms of what the authors perceive to be “advertising to children”, should be viewed as a positive finding. The Australian Food and Grocery Council is committed to monitoring the self-regulatory initiatives and makes the results available to all stakeholders to help evaluate the effectiveness of what the initiatives set out to achieve.

Peta E Craig · Geoffrey Annison

In reply: Children’s exposure to advertising of unhealthy foods is of concern because children are exposed to a large volume of such advertisements. The World Health Organization has clearly stated that any efforts to address this issue must reduce children’s exposure to unhealthy food advertising.1 Our research article2 was based on such measures. The viewing times applied in our research were specifically those when the highest numbers of children aged 5–12 years watch commercial television, according to Australian audience data for Sydney commercial television stations, and thus are exposed to advertising. Craig and Annison refer to a decrease in the relative proportion of advertisements for unhealthy fast foods over the first year of the industry initiatives. However, readers should be aware that our research showed that the total amount of fast-food advertising increased over this period, so that the frequency of unhealthy fast-food advertisements that children were exposed to remained the same. To make meaningful changes to what advertising children see, time-based restrictions would form a more responsible approach for regulation than the current industry specifications.

Lana Hebden · Lesley King · Anne Grunseit · Bridget Kelly · Kathy Chapman

To the Editor: We published a case in the Journal in 2009 titled “Spontaneous chylothorax in a 2-year-old child”.1 Subsequently, it has come to our attention that trauma is likely to have been the cause of the chylothorax. At the time of caring for the child, and submission of our article to the Journal, we had no evidence of this. We had specifically asked for a history of trauma and looked for external signs of injury. The chest x-ray and computed tomography (CT) scan had been reviewed with our radiology staff at the time and we did not detect abnormalities of the vertebrae or paravertebral tissue, and no such abnormalities were detected during surgery. However, the child presented with serious injuries 9 months later and died on arrival at hospital. At autopsy, a CT scan showed a paravertebral haematoma and vertebral injury in the lower thoracic vertebrae where the thoracic duct traverses the diaphragm and ascends on the right side (it was a right-sided chylothorax). On further review of the original chest x-ray and CT scan, it was possible to see that some of these findings were evident at the initial presentation with chylothorax. At the time of submission of our article, we speculated that vomiting could have caused injury to the thoracic duct. We now wish to highlight that apparently spontaneous chylothorax may be due to trauma. In children, non-accidental injury must be considered as a possible cause.2

Manuel E Soto-Martinez · Vanessa Clifford · Tom Clarnette · Sarath Ranganathan · R John Massie

Clinical record A 17-year-old girl presented to her general practitioner with a 1-week history of fever, arthralgia, general malaise and dry cough. She had a history of systemic onset juvenile idiopathic arthritis (SOJIA), diagnosed at age 2 years and treated with aspirin, and had been in remission for 13 years. She was initially treated by her GP with oral roxithromycin, and admitted to hospital 3 days later with worsening of her symptoms. Her admission chest x-ray (Box 1) revealed bilateral perihilar infiltrates. A diagnosis of severe community-acquired pneumonia was made and broad spectrum antibiotics were commenced, including vancomycin, moxifloxacin, and oseltamivir. Despite this treatment, her condition deteriorated. On Day 3 of admission she required endotracheal intubation and circulatory support with noradrenaline 18–50 μg/kg/min, and was admitted to the intensive care unit (ICU). She remained hypotensive, with a mean arterial pressure of 50 mmHg, and with sinus tachycardia of 132 beats/min, and subsequently required renal replacement therapy. She remained febrile for the first 3 days after admission (temperature range 37.5°C–39°C), and her temperature settled to normal after appropriate therapy was initiated. Investigations included a computed tomography scan of her abdomen, which showed hepatosplenomegaly, and liver function tests, which showed elevated conjugated bilirubin (36 mmol/L; reference range [RR], < 4 mmol/L), γ-glutamyl transferase (84 U/L; RR, < 24 U/L), lactate dehydrogenase (3540 U/L; RR, 150–280 U/L), alanine aminotransferase (108 U/L; RR, 10–30 U/L) and aspartate transaminase (388 U/L; RR, < 30 U/L). Other abnormal parameters were her haemoglobin level (93 g/L; RR, 120–160 g/L), platelet count (65 x 109/L; RR, 150–400 109/L), white cell count (2.9 x 109/L; RR, 4.5–13 x 109/L), international normalised ratio (2.1; RR, 0.9–1.2) and fibrinogen level (0.9 g/L; RR, > 2.5 g/L). Elevated inflammatory markers included C-reactive protein (301 mg/L; RR, < 5 mg/L) and serum ferritin (50 500 μg/L; RR, 7–140 μg/L). A transthoracic echocardiogram showed a left ventricular ejection fraction of 60%, a mild reduction in right ventricular contractility, and a right ventricular systolic pressure of 48 mmHg. A full screen for sepsis was performed, including a nasopharyngeal aspirate, bronchoalveolar lavage, blood cultures and serological testing; all were unremarkable. Other immunological tests performed were for Mycoplasma pneumoniae antibodies, Streptococcus pneumoniae urinary antigen, Legionella pneumophila urinary antigen, herpes simplex virus, cytomegalovirus, Epstein–Barr virus (EBV) IgM and IgG, influenza A and B, H1N1 influenza RNA, respiratory syncytial virus, parainfluenza and adenovirus DNA, Q fever (Coxiella burnetti) IgM and IgG, and serological tests for hepatitis, dengue fever IgM and Leptospira IgM, all of which were non-reactive. Urinalysis revealed a white blood cell count of 140 x 106/L (RR, < 10 x 106) and an erythrocyte count of > 500 x 106/L (RR, < 10 x 106/L) with no microbial growth on culture. A bone marrow aspirate with trephine was performed on Day 4 (Day 2 in the ICU), and EBV DNA was detected in the resulting sample using a qualitative DNA test. The patient’s failure to improve, in combination with her past history of SOJIA, hepatosplenomegaly and a very high ferritin level led to a preliminary diagnosis of macrophage activation syndrome (MAS). Immunosuppressive treatment in the form of high-dose methylprednisolone (10 mg/kg daily) and intravenous immunoglobulin (1 g/kg daily) were commenced. Inotrope and ventilatory requirements improved within 24 hours of this treatment. On Day 9 of admission she was extubated, and was discharged home on high-dose steroids 8 days later with no complications. Her bone marrow aspirate histological examination showed haemophagocytosis which confirmed the diagnosis of MAS (Box 2). Macrophage activation syndrome (MAS) is a severe, potentially fatal condition associated with paediatric rheumatic diseases. It is a form of secondary haemophagocytic lymphohistiocytosis (HLH) with uncontrolled activation and proliferation of well differentiated macrophages and T-lymphocytes.1,2 The central pathophysiological abnormality in HLH is cytokine dysfunction, resulting in uncontrolled accumulation of activated T-lymphocytes and activated histiocytes (macrophages) in many organs. High levels of cytokines are found in these patients due to ineffective natural killer cells and T-lymphocytes (a positive feedback loop started by ineffective T-cells, triggering an unopposed release of cytokines that attracts further T-cells).3 Hyperactivated macrophages cause damage in different tissues, and this is thought to be the origin of the high serum ferritin levels characteristic of these conditions. The cause of the macrophage activation is multifactorial. Ineffective cytotoxic immunity is due to underactive natural killer cells and reduced perforin production. Secondary HLH can be precipitated by infection, drugs, malignancy and rheumatic diseases. SOJIA has been linked to polymorphisms in genes controlling production of cytokines, such as tumour necrosis factor. This could in turn be a cause for MAS, leading some authors to postulate that MAS and SOJIA could be part of the same disease.4 Clinical manifestations include fever (91%–100%), hepatomegaly (90%–92.3%), splenomegaly (77%–84%), lymphadenopathy (41%–62%), neurological symptoms (47%) and rash (43%).5,6 The central nervous system is commonly affected,7 and patients may present with agitation, seizures, coma, respiratory failure from adult respiratory distress syndrome, and multiorgan failure.7 MAS has a mortality of up to 22%.8 To our knowledge, this is the only reported case of MAS in a patient nearing adult age and with a long inactive rheumatic disease period. MAS is well described in the paediatric population with SOJIA, and has a median age of 5 years at the time of presentation.9 The mean time between initial diagnosis of SOJIA and presentation with MAS is 4 years.8 Our patient was aged 17 years at the time of presentation with MAS, and had not had symptoms of, nor required treatment for, SOJIA for 13 years. Diagnosis was described by Ravelli and colleagues,7 and is based on clinical findings such as organomegaly and laboratory findings such as hypofibrinogenaemia, thrombocytopenia and elevated serum liver enzymes. A bone marrow aspirate can aid diagnosis in uncertain cases, the pathognomonic feature being the presence of well differentiated macrophages actively phagocytosing haemopoietic cells.8 Infections, medications and malignancies have all been identified as triggers for MAS. EBV DNA was found in the patient’s bone marrow aspirate, and EBV has been identified as one of the more common triggers for MAS.5,7 It is likely that EBV was the trigger for this patient’s MAS. Treatment is based on immunosuppression using steroid therapy. Cyclosporin has been used as the first-line treatment, or used in combination with corticosteroids. Other treatment options include plasma exchanges or intravenous immunoglobulins.10 This patient presented with fever, prominent respiratory failure and cardiovascular collapse. Her initial systemic symptoms and radiological findings suggested severe sepsis, most likely respiratory in origin, her SOJIA had been in remission for over 10 years, and there was no neurological involvement. These factors made clinical suspicion of MAS difficult, but her hepatosplenomegaly and highly raised ferritin levels suggested the diagnosis, which was supported by her laboratory test results (leucopenia, thrombocytopenia, hypofibrinogenaemia and abnormal liver function test results) and bone marrow aspirate histological findings (Box 2). Despite MAS predominantly presenting in a paediatric population with active disease, this case report emphasises the need to exercise diagnostic vigilance in treating young adult patients with multiorgan failure and a distant history of rheumatic disease. Lessons from practice Multiorgan dysfunction and vasodilatory shock may not be of infectious origin. If a patient fails to improve when treated with broad spectrum antimicrobials, alternative diagnoses should be sought. Although macrophage activation syndrome (MAS) primarily affects children with active rheumatic disease close to the time of diagnosis, it may occur in adults after a prolonged disease-free period. Diagnosis of MAS is based on history, clinical examination and laboratory findings. Demonstrating haemophagocytosis in a bone marrow aspirate can aid uncertain diagnosis. 1 Chest x-ray of the 17-year-old patient, taken on admission, showing bilateral perihilar infiltrates 2 Macrophage (long arrow), containing a red blood cell (arrow head), seen in the bone marrow aspirate taken from the 17-year-old patient (May–Grünwald–Giemsa stain x 100)

David Gutierrez MD · Louis Guy MB BS · Veera S Katikireddi MB ChB(Hons), MRCP(UK) · Jason P Butler MMedSci, FRACP, FRCPA · John Gowardman FRACP, FCICM

Cause of chylothorax: In “Spontaneous chylothorax in a 2-year-old child” in the 2 March 2009 issue of the Journal (Med J Aust 2009; 190: 262-264), the cause of chylothorax was unknown, but attributed to strenuous vomiting. Additional information has become available and trauma is now thought to have been the cause. In a child, this raises the possibility of non-accidental injury. Further details are published in this issue of the Journal (See Soto-Martinez et al).

Manuel E Soto-Martinez · Vanessa Clifford · Tom Clarnette · Sarath Ranganathan · R John Massie

To the Editor: Recently, there has been an increase in the popularity and use of baby slings to transport infants. A sling is a soft fabric carrier, worn around a parent or caregiver’s neck, in which the infant is suspended. Slings are often promoted as a secure and easy way to carry an infant, that maintains close contact with the child. An issue has arisen concerning the safety of such devices, in that infants may be placed in a position where there is excessive flexion of the neck (chin-to-chest positioning) or obstruction of the mouth and nose that may cause suffocation. Warnings have recently been issued by the Australian Competition and Consumer Commission.1 Sixteen deaths attributed to the use of slings have occurred in the United States and Canada,2,3 resulting in calls for mandatory standards by the US Consumer Product Safety Commission.2 We report a South Australian case of a 2-day-old boy, born at 38 weeks’ gestation by normal vaginal delivery, who was placed into a cloth sling worn under his mother’s shirt and jumper and was subsequently noted by his mother to be cold and not breathing. At autopsy, there were no significant abnormalities identified, with no injuries visible on x-ray or physical examination. Results of toxicological, metabolic, virological and bacteriological studies were normal. In the absence of definitive pathological findings, the cause of death was undetermined, although the baby sling was considered a risk factor. It is well recognised that infants placed in certain positions, such as in car safety seats, may be at risk of significant oxygen desaturation, and even death, due to upper airway compromise. This applies particularly to preterm and low-birthweight infants.4 It appears that a similar situation occurs with certain slings, albeit rarely, as the soft and rounded sleeping surfaces may promote a potentially dangerous posture that impedes normal respiration. Certain infants may also be quite vulnerable to airway occlusion, with deaths being reported while breastfeeding, for example.5 Given the cases of infant death associated with baby slings in North America, and this Australian case, it is important that parents and carers are made aware of potential safety issues with the use of these devices, particularly in very young infants. Constant monitoring of infants in slings is advised, to ensure that the infant’s head is facing outwards, with no covering of the face.

Roger W Byard · John D Gilbert

21-Hydroxylase deficiency (21-OHD) is the most common cause of congenital adrenal hyperplasia, with an incidence of 1 : 14 000 live births and equal prevalence among males and females. Newborns with the most severe “salt-wasting” form of 21-OHD are susceptible to salt-wasting crises in the first few weeks of life. This is associated with morbidity and mortality. 21-OHD newborn screening (NBS) is currently performed in many countries. Despite several prominent medical societies recommending 21-OHD NBS, no state in Australia currently screens for this condition. We report a case that illustrates the need to reconsider including 21-OHD in NBS. 21-OHD NBS can be reliable, sensitive and effective in reducing morbidity and mortality.

Joyce Y Wu MB BS, MAACB, FRCPA · Sudeep MB BS, FRACP, DCH · David M Cowley MB ChB, FRCPA, FHGSA · Mark Harris MB BS, FRACP, MD · Ivan N McGown BSc, MIT, MHGSA · Andrew M Cotterill MB BS, FRACP, MD

Objective: To examine the association of adolescent depression and anxiety symptoms with alcohol abuse or dependence in young adulthood.Design, setting and participants: Cohort study of the health and wellbeing of adolescents and young adults in Victoria, assessed at 8 waves (periods) of data collection, from age 14 to 24 years, between 1992 and 2003. Young people who participated in the cohort study at least once during the six adolescent assessment points (conducted 6 months apart, from age 14 to 17 years), at least once during young adulthood and who were alive at Wave 8 (n = 1758).Main outcome measure: Alcohol abuse or dependence assessed using the alcohol and substance abuse modules of the Composite International Diagnostic Interview at age 24 years.Results: Adolescents with moderate to high levels of depression and anxiety symptoms (measured by the revised Clinical Interview Schedule) had an increased risk of alcohol abuse or dependence in young adulthood, compared with young adults with low levels of adolescent depression and anxiety symptoms, after adjusting for potential confounding factors. Risk was higher for those with symptoms at more than two adolescent assessment points (odds ratio [OR] 1.9; 95% CI, 1.7–2.0) and for those with symptoms at one or two assessment points (OR 1.3; 95% CI, 1.2–1.4), compared with those with no above-threshold symptoms in adolescence.Conclusions: Adolescents with depression and anxiety symptoms are at increased risk for alcohol use disorders into young adulthood. They warrant vigilance from primary care providers in relation to alcohol use well into adulthood.

Maria McKenzie BBSc(Hons) · Anthony F Jorm PhD, DSc · Helena Romaniuk BSc, MSc, PhD · Craig A Olsson PhD · George C Patton MB BS, MD

To the Editor: In their recent article on unintentional child drowning deaths, Petrass, Blivitch and Finch refer to the “limited detail within both police reports and findings” for South Australian cases of drowning.1 Since 2005, South Australia’s Child Death and Serious Injury Review Committee (CDSIRC), which I chair, has considered the circumstances and causes of all child deaths in SA. The legislation governing the CDSIRC’s work quite rightly precludes the publication of individual details of children’s deaths, but, since 2005, the CDSIRC’s annual report has given a summary of the circumstances and causes of drowning deaths for children in each year. Children drown in a variety of circumstances — in fish ponds, rivers, lakes, dams, buckets of water and in boating accidents — but the greatest number, especially among those under 4 years of age, drown in backyard swimming pools.2 In these incidents, time and again I read about failures of supervision, gate closure and adherence to pool fencing regulations and the maintenance of this fencing. Although the extent and nature of supervision may be of academic interest, the prevention of childhood drowning would best be served by the ongoing promulgation of well researched public health campaigns, such as those delivered by the Royal Life Saving Society — Australia and Kidsafe Australia, and attention to legislative changes that will ensure the regular inspection and maintenance of swimming pool fencing. The CDSIRC’s review of child drownings in SA is based on the detailed information obtained by SA police from witnesses present at the time of the event. This almost always provides a great depth of detail that enables the identification of the key risk factors present in the circumstances of the death. It is unfortunate if this information was not available to Petrass and colleagues, but it is incorrect to infer that such information is not collected in SA. The CDSIRC’s annual reports are available from its website.3 Similar reports are produced by child death review committees or teams in Queensland, New South Wales and Victoria.

Dymphna Eszenyi

In reply: Information made available by South Australia’s Child Death and Serious Injury Review Committee is similar to that in other Australian states that have a Child Death Review Committee; all produce an annual report of circumstances related to child deaths, including child drowning. While we are aware of these reports, for our study of child drowning, individual case details were required that cannot be extracted from compiled summaries in annual reports. By contrast, the National Coroners Information System (NCIS) provides access to original documents for individual drowning cases. Details for South Australian child drownings in the NCIS database were very limited, although at no point in our article did we infer that this information is not collected in SA; rather we stated that that coroners findings were only available for 38.1% of cases in the NCIS, and that autopsy and toxicology reports are not routinely uploaded.1 Further, the recently revised position paper of the National Drowning Prevention Alliance (NDPA) states that neither a single device nor a single solution can prevent child drownings, and recommended that caregivers, aquatic facility owners, managers and operators use “layers of protection” to aid in child drowning prevention.2 We certainly agree that the ongoing promulgation of well researched public health campaigns is an important layer in the prevention of child drowning, although, to date, no published studies have investigated the effectiveness or rigorously evaluated Australian aquatic death prevention campaigns (such as Keep Watch, Kids Alive — Do The Five, SafeWaters and Play it Safe by the Water). However, the NDPA did identify that supervision is the one layer that should be ever-present, regardless of what other layers are used.2

Lauren A Petrass · Jennifer D Blitvich · Caroline F Finch

No-fault compensation, based on the ethical principle of redistributive justice, should form a cornerstone of Australia’s immunisation strategy Australia has an enviable reputation for its publicly funded vaccine program — a program that has benefited Australian children and adults over many years. In 2010, the National Immunisation Program funded 12 vaccines, twice as many as a decade previously. To monitor outcomes from this program, the Australian Childhood Immunisation Register, which commenced data collection in 1996, provides a detailed record of vaccine uptake by children.1 Funding for the register and for incentives to general practitioners to improve vaccine uptake are part of the total budget for Australia’s vaccine program, estimated to exceed $400 million annually.2,3 One area for improvement in the vaccine program is monitoring of adverse events following immunisation (AEFI). Another would be the introduction of a no-fault compensation scheme for serious adverse events which can be confidently attributed to vaccination. An investigation into the unexpectedly high number of febrile convulsions in children aged less than 5 years after they had received the influenza vaccine in 2010 — in some cases, with devastating consequences4 — provided a forceful reminder that timely vaccine safety monitoring is needed in Australia.5 More active adverse event surveillance is certain to uncover more AEFI but many of these will only be coincidental, while others will be of a transient or relatively trivial nature. On rare occasions, a serious AEFI with long-term sequelae will be recognised. A decision will then need to be made on whether the vaccine was responsible for that serious event. The World Health Organization defines four categories of serious AEFI: hospital admission or prolongation of an existing hospital admission; permanent disability; any event that is life threatening; or death.6 Using these criteria, 8% (193/2396) of the AEFI reported by passive surveillance in Australia in 2009 were judged to be serious.7 However, unlike many countries where compensation schemes exist for adverse events attributed to a vaccine, Australia has no routine approach to making the assessment of attribution. Parents of children or adults who believe they deserve compensation for a serious adverse event that they attribute to a vaccine are therefore required to make their case through the adversarial legal system. This requires the demonstration that an individual or an organisation was at fault. However, fault is often difficult to demonstrate and an adverse event may be caused by vaccination through no fault of the vaccine manufacturer, the regulator or the person who administered the vaccine. We have previously argued that a Queensland child who developed transverse myelitis after receiving oral polio vaccine was an example of an adverse event following vaccination where no fault was attributable to any party.8,9 Despite detailed epidemiological evidence that was consistent in this case with the causal criteria for an AEFI promulgated by the Institute of Medicine of the National Academies in the United States,8 and despite laboratory evidence showing that the polio virus recovered from this child was similarly pathogenic to a polio virus that has been accepted as causing vaccine-associated paralytic polio,9 the polio expert committee concluded that the evidence was insufficient to support a causal relationship between the oral polio vaccine and transverse myelitis. As causality has not been accepted, this child has received no compensation. The general principles associated with this case raise a number of pertinent questions for Australia. First, should a child who may have been injured by a vaccine, which was endorsed and paid for by the community, be compensated by the community when the serious adverse event may be attributed to the vaccine? Second, what are the criteria for accepting an attributable relationship between receipt of the vaccine and a subsequent adverse event? Third, what is the best method for financing a compensation scheme? Each question may highlight a potential barrier to the implementation of a no-fault AEFI compensation scheme in Australia. By 2010, 19 countries around the world had implemented no-fault AEFI compensation, implicitly answering “yes” to the question of whether the community owes a duty of care to an individual injured by a vaccine.10 There is also a strong ethical argument for this position, based on the concept of redistributive justice. Any person who is injured while helping to protect the community — for instance, by contributing to herd immunity, such that there are sufficiently many people immunised to prevent widespread disease transmission within the community — should not bear the consequences of injury alone. In essence, the community owes a debt of gratitude to that person. Temporal association of an adverse event with receipt of a vaccine does not establish causality and the underlying notion of causation used in most compensation schemes is similar to that used in epidemiology.10 The World Health Organization has published guidelines on causality for an AEFI.11 An adverse event considered to be very likely or certainly due to a vaccine would comprise a “Clinical event with a plausible time relationship to vaccine administration, and which cannot be explained by concurrent disease or other drugs or chemicals”.11 To simplify and expedite determinations of causality in the US, a vaccine injury table is used to predetermine causality if a vaccine injury is included in the table.10 However, determining causation is a complex issue. Recognising this, most countries have a designated committee, comprising medical and legal members, which deliberates on the attributable relationship between receipt of the vaccine and subsequent adverse event.10 Concerns about funding a no-fault compensation scheme is another of the probable barriers to its implementation in Australia. Schemes are currently funded by one of four methods: a vaccine levy; compensation for AEFI as part of a much broader injury compensation scheme; specific AEFI compensation funded through general tax revenue; and funding in association with industry.10 Funding through a vaccine levy has been self-sustaining in the US. Despite compensation payments having been made to 2580 claimants since 1989, the compensation fund there has a surplus of about US$3 billion.12,13 No-fault vaccine-injury compensation programs are based on the premise that any adverse event attributable to vaccination is not due to the fault of a specific individual or organisation, but due to an unavoidable risk that is acknowledged as being associated with vaccines. Germany has been operating a no-fault AEFI compensation scheme for 50 years.10 France restricts its compensation to serious AEFI, since these are likely to have long-term implications for the injured party.10 Restricting compensation to events with long-term consequences, above a nominated clinical threshold, may be an acceptable model for Australia. We have previously argued that Australia should follow the lead of other advanced countries and implement a no-fault compensation scheme.14 We continue to argue that such a scheme, based on the ethical principle of redistributive justice, should form a cornerstone of Australia’s immunisation strategy. Disclaimer The views expressed are those of the authors and have not been endorsed by any institution or organisation with which the authors are affiliated or by any committees of which the authors are members.

Heath A Kelly BSc, MB BS, MPH · Clare Looker MB BS, MPH · David Isaacs MD, FRACP, FRCPCH

To the Editor: Young children are at increased risk of severe influenza compared with the general population. Routine vaccination of children using trivalent influenza vaccine (TIV) is recommended in the United States and Canada. The Western Australian government, with support from vaccine manufacturers, has been providing TIV free of charge to all children aged 6–59 months since 2008.1 In 2010, high fevers and an increased incidence of convulsions were observed in children aged < 5 years after administration of TIV. Most reports of adverse events were from WA, owing to higher uptake of vaccination associated with the free vaccination program. The national influenza vaccination program for children aged < 5 years was subsequently suspended,2 and high rates of fever and convulsions were confirmed.2,3 The majority of adverse events occurred after administration of Fluvax or Fluvax Junior (CSL Biotherapies). More than 50% of parents of children who were administered Fluvax or Fluvax Junior reported high fever after vaccination. The incidence of febrile convulsions after vaccination with Fluvax and Fluvax Junior was 4.4 per 1000 doses, significantly higher than expected.3,4 Fluvax and Fluvax Junior are not recommended for children aged < 5 years in the Australian 2011 influenza vaccination program.5 In response to these events, WA Health established an online registry for vaccine-associated adverse events — the Western Australian Vaccine Safety Surveillance (WAVSS). Health professionals are required and members of the public encouraged to report adverse events. In addition, a prospective safety study of the 2011 TIV in children aged < 5 years has commenced at Princess Margaret Hospital for Children and the WA Central Immunisation Clinic. From 15 March to 29 April 2011, 2227 doses of TIV were administered to children aged < 5 years in WA (2130 doses of Vaxigrip [Sanofi Pasteur]; 97 doses of Influvac [Solvay]). Adverse events in four children aged < 5 years have been reported via WAVSS: two with elevated temperature (≥38°C yet < 39.5°C) within 24 hours of vaccination, one with vomiting and diarrhoea after vaccination, and one with fever (not specified) and convulsions 4 days after vaccination (this child had a respiratory tract infection at the time of vaccination). All four children were administered other vaccines with TIV. In the safety study, 144 children were enrolled between 15 March and 29 April 2011. Adverse events after vaccination were reported in 10 children (7%), two of whom received other vaccines in addition to TIV. All 10 children had fever reported, and one child had a temperature > 39.5°C. Two children developed vomiting. No convulsions were reported and none of the children who had adverse events required assistance from a health care professional. These data demonstrate that the significant adverse events that occurred after administration of TIV in 2010 have not been observed in WA during early 2011. Ongoing surveillance is underway and will continue. Poor uptake of influenza vaccination in Australian children is likely to result in increased influenza-related hospitalisation, morbidity and mortality. Data such as those reported here are required to reassure the community of the safety of this vaccination program before the expected start of the 2011 influenza season.

Christopher C Blyth · Tracy Y Markus · Paul V Effler · Peter C Richmond

To the Editor: The Medicare item for annual child health checks (CHCs) for Aboriginal and Torres Strait Islanders involves taking a comprehensive health-related history from the antenatal period onwards, recording growth parameters, performing a medical examination, identifying new diagnoses and commencing management, which may include advice, referral, vaccinations and treatment. The CHC has had little evaluation as a primary health care tool in the urban setting; indeed, outside remote regions, it has barely been taken out of the toolbox. Although 76% of Aboriginal and Torres Strait Islander people live in urban or regional areas,1 we are unaware of any published research on CHCs outside remote areas. We therefore aimed to evaluate the role of the CHC for 0–14-year-olds at Inala Indigenous Health Service, an urban primary care service in a suburb of Brisbane. Ethics approval was obtained from the University of Queensland’s Behavioural and Social Sciences Ethical Review Committee and Metro South Health Service District Human Research Ethics Committee at the Princess Alexandra Hospital. The local Inala Elders Aboriginal and Torres Strait Islander Corporation supported the project. Descriptive statistical analysis was conducted using Stata, version 10 (StataCorp, College Station, Tex, USA). Of 867 eligible children, we completed 786 CHCs from May 2007 to December 2009. We excluded 245 “subsequent” CHCs (31%) in children who had already had a CHC in the study period, and 109 of the remaining 541 (20%) that were not accompanied by a research consent form, leaving 432 CHCs available for analysis. The children (234 male [54%]) were Aboriginal (394, 91%), Torres Strait Islander (9, 2%) or both (29, 7%). Reported health risk factors included living in households with a smoker (75%), parental unemployment (67%), exposure to domestic violence (29%), never having been breastfed (32%) and not having teeth brushed twice daily (46%), although more than half the children (57%) exercised at least 30 minutes every day. New diagnoses made at the CHC (40%) were primarily dental caries (36%) or conditions involving the skin (18%) or ears (10%). During the CHC, 63% of parents were given health advice, 24% of children were referred for follow-up and 22% were vaccinated (Box). From May 2006 (when CHCs were introduced) to June 2009, 4610 Indigenous CHCs were reported by Australia’s 54 metropolitan Divisions of General Practice, comprising just 4.3% of the eligible population.2 This contrasts with the 14 500 CHCs (89% coverage) completed in prescribed remote areas by the Northern Territory Emergency Response (NTER).3 A recent report highlights the low number of CHCs performed outside the NTER and the lack of timely follow-up within the NTER to address detected health problems. The report concluded: “It’s clearly time to reconsider this failed health policy”.4 However, a distinction should be drawn between the NTER CHCs — usually performed by “fly-in, fly-out” teams who are not in a position to provide ongoing care — and a CHC program embedded in a local clinic as a cornerstone of usual health care. In the wake of the NTER, the then National Aboriginal Community Controlled Health Organisation chairperson, Dr Mick Adams, said, “This is not to say that we do not want more child health checks [but we reject] the present way of doing them”.5 Strengths of our study include the high proportion of our clinic’s eligible population who had CHCs (541/867, 62%). Although our practice comprises only 0.8% of Australia’s urban Indigenous children, our service completed 10% of the CHCs done in Australian metropolitan areas to June 2009.2 Because the study was limited to the day of the CHC, we were unable to evaluate whether referrals resulted in attendances. Further research is required to document the success of follow-up resulting from CHCs, including referral attendance rates. We have found that the Indigenous CHC, performed within the patient’s usual primary care service, provides an important opportunity to make new diagnoses and to identify and initiate management of health risk factors. The CHC is an underused tool worth dusting off in primary care. Health risk factors (reported by parent or carer), new diagnoses and interventions from child health checks of 432 Aboriginal and Torres Strait Islander participants attending Inala Indigenous Health Service, May 2007 – December 2009* Variable No. (%) Variable No. (%) Maternal substance use during pregnancy Adolescent (12–14-year-olds) behaviour (n = 65) Tobacco (n = 432) 156 (36%) Consumes alcohol (n = 54) 5 (9%) Alcohol (n = 432) 70 (16%) Current smoker (n = 54) 4 (7%) Cannabis (n = 431) 36 (8%) Sexually active (n = 51) 3 (6%) Intravenous drugs (n = 431) 16 (4%) New diagnosis resulting from health check Household characteristics Any new diagnosis (n = 432) 174 (40%) Household with a smoker (n = 416) 312 (75%) Dental caries (n = 345) 124 (36%) Unemployed parent (n = 432) 288 (67%) Skin condition, all causes (n = 432) 77 (18%) Single parent caring for child (n = 432) 194 (45%) Ear condition‡ (n = 432) 43 (10%) Stressful event impacting on household (n = 432) 180 (42%) Overweight (n = 332) 83 (25%) Households with six or more residents (range, 6–12) (n = 408) 149 (37%) Obese (n = 332) 36 (11%) History of domestic violence exposure (past or current) (n = 432) 124 (29%) Interventions (n = 432) Perinatal characteristics Any health/lifestyle advice 270 (63%) Premature birth (gestation < 37 weeks) (n = 336) 45 (13%) Nutrition advice 119 (28%) Perinatal complication (n = 432) 170 (39%) Learning/behavioural advice 54 (13%) Never breastfed (n = 339) 110 (32%) Physical activity advice 54 (13%) Childhood health behaviour Smoking cessation advice 42 (10%) Watch electronic media ≥ 60 min/day (n = 237) 183 (77%) Alcohol consumption advice 33 (8%) Teeth not brushed twice daily (n = 360) 165 (46%) Any referral (n = 432) 103 (24%) Suboptimal physical activity† (n = 215) 92 (43%) Paediatrician referral 31 (7%) Parental/carer concerns about child’s behaviour (n = 264) 81 (31%) Dental referral 26 (6%) Parental/carer concerns about child’s learning (n = 276) 82 (30%) Audiology referral 17 (4%) Dietitian referral 13 (3%) Vaccinations given on the day of the check (n = 432) 96 (22%) * Denominators vary because of missing data. † ≤ 30 min/day for < 7 days a week. ‡ Defined as having signs (eg, perforation, bulging) or a diagnosis (eg, otitis media, otitis externa) of ear disease in at least one ear.

Justin J Coleman · Geoffrey K Spurling · Deborah A Askew · Noel E Hayman

The Thoracic Society of Australia and New Zealand has updated its guidelines on corticosteroid use in childhood asthma The understanding of childhood asthma has increased substantially since the publication of the Thoracic Society of Australia and New Zealand (TSANZ) position statement The role of corticosteroids in the management of childhood asthma in 2002.1 In particular, recognition of the need for separate asthma management guidelines for children aged 5 years or younger has increased,2 and considerably more clinical research evidence on the role of asthma medications in children has become available. The 2010 revision of the TSANZ position statement provides updated recommendations on the roles of inhaled corticosteroids, oral corticosteroids, leukotriene receptor antagonists and combination medications (inhaled corticosteroids plus long-acting β-agonists) in childhood asthma management based on recently published evidence.3 The role of leukotriene receptor antagonists in the management of childhood asthma has also been addressed in detail in a recent National Asthma Council Australia information paper.4 The National Asthma Council Australia provides a comprehensive overview of the role of preventive treatment in childhood asthma in its Asthma management handbook 2006.5 It advocates a stepwise approach to drug therapy that is based on asthma severity. If control is not achieved using initial preventer therapy, it is important to review the diagnosis of asthma — particularly in children aged 5 years or younger — as many children with recurrent cough are mislabelled as having asthma6 and different wheezing phenotypes require different treatment approaches.2 Before escalating the level of preventer therapy, it is also essential to check the child’s inhaler technique and adherence to treatment. Step-down treatment (“back titration”) is advocated once control has been achieved and sustained for at least 3 months. Two placebo-controlled studies of montelukast have established the efficacy and safety of this medication and form the basis of its current Pharmaceutical Benefits Scheme listing for children with frequent intermittent or mild persistent asthma.3,4 Compared with placebo, regular montelukast therapy produces a modest reduction in exacerbation risk in children with viral-induced wheezing.3,4 An additional benefit of montelukast therapy is its proven efficacy for protecting against exercise-induced bronchoconstriction,3,4 being more effective than long-acting β-agonists without development of the tolerance seen with long-acting β-agonists.3 This information led to the current Pharmaceutical Benefits Scheme listing of montelukast for children aged 6–14 years who have ongoing activity-related asthma despite inhaled corticosteroid treatment. The effectiveness of prophylactic inhaled corticosteroids in persistent childhood asthma is well established.3 In contrast, regular inhaled corticosteroid treatment for intermittent, viral-induced wheezing does not reduce rates of hospitalisation, use of oral corticosteroids, or frequency and duration of acute episodes.3 Systemic effects of inhaled corticosteroids in children are well documented; they include impaired linear growth, adrenal suppression, and effects on bone mineralisation.3 Although the clinical significance of these adverse effects is uncertain, factors such as individual susceptibility, severity of asthma, age, pubertal status, total dose, and dose delivery may affect risk of systemic toxicity. Although it is common to add a long-acting β-agonist to inhaled corticosteroids (as a single combination inhaler) there are few paediatric studies examining this practice, and these suggest that, while the combination improves lung function, it does not reduce exacerbation risk — in fact, it may increase it.3 These recent studies support the current National Asthma Council recommendations of reserving the addition of long-acting β-agonists for children with asthma that is not adequately controlled by 200–250 μg/day fluticasone propionate or equivalent doses of other inhaled corticosteroids,3 and highlight the potential role of montelukast as an alternative add-on therapy. The use of long-acting β-agonists is not, however, recommended for children aged 5 years or younger.2,3 Our recommendations for preventer treatment in childhood asthma are summarised in the Box. Children with infrequent intermittent asthma require no preventer therapy. Current evidence suggests that non-steroidal preventers should be trialled first in children with frequent intermittent or mild persistent asthma, while inhaled corticosteroids are indicated as first-line preventer treatment in children with moderate–severe persistent asthma. Long-acting β-agonists or montelukast are add-on options in children with persistent symptoms despite adequate inhaled corticosteroid treatment. In terms of acute asthma management, oral corticosteroids improve outcomes in children presenting to hospital with acute asthma, but the efficacy of oral corticosteroids for children aged 5 years or younger with acute, mild–moderate, viral-induced wheezing has been questioned.3 Based on current evidence, we recommend oral corticosteroids be reserved for children with moderate–severe acute asthma exacerbation and children with an incomplete response to β-agonists. However, in children aged 5 years or younger (particularly those with intermittent, viral-induced wheezing) the use of oral corticosteroids should be limited to those with severe wheeze who require hospital admission; an initial dose of 2 mg/kg prednisolone (maximum 60 mg) is recommended, followed by daily doses of 1 mg/kg if required. Although a 3-day course is generally sufficient, a more prolonged course may be indicated in severe cases. There is some evidence for the benefit of intermittent inhaled corticosteroids and leukotriene receptor antagonists in acute asthma, but oral corticosteroids remain the treatment of choice — particularly for more severe episodes, because of ease of administration, low cost and greater proven efficacy in severe acute asthma. The need for recurrent systemic corticosteroid therapy requires reassessment of the child’s interval therapy, particularly in cases of persistent asthma, and specialist referral. Preventer therapy for children who have frequent intermittent or persistent asthma symptoms* FP = fluticasone propionate. BDP–HFA = beclomethasone dipropionate – hydrofluoroalkane. BUD = budesonide. CIC = ciclesonide. * Modified from the Asthma management handbook 2006 with permission from the National Asthma Council Australia.5 † Long-acting β-agonists not recommended for children aged 5 years or younger.

Peter P Van Asperen MB BS, MD, FRACP · Craig M Mellis MPH, MD, FRACP · Peter D Sly MD, DSc, FRACP · Colin F Robertson MSc, MD, FRACP

Objective: To audit general paediatric outpatient practice in Australia, including consultation characteristics and management patterns, diagnoses, factors associated with diagnoses, and billing practices.Design, setting and participants: In October – November 2008, members of the Australian Paediatric Research Network (APRN; a national network of paediatricians established to facilitate multisite secondary care research) were invited to prospectively complete brief standardised data collection forms for 100 consecutive patients or all patients during a 2-week period, whichever came first.Main outcome measures: Length of consultation and type of diagnoses made; proportions recorded as having medications, investigations or referral; odds ratios for factors associated with diagnoses; and proportions of Medicare items billed.Results: Of 300 APRN members, 199 (66%) completed data forms for 8345 consultations in which 15 375 diagnoses were made (mean, 1.8 diagnoses per consultation); 46.0%, 30.9% and 22.8% of consultations involved 1, 2 and ≥ 3 diagnoses, respectively. New and review consultations lasted a mean of 41 (SD, 20) and 26 (SD, 15) minutes, respectively. The most common diagnoses were attention deficit hyperactivity disorder (18.3%), baby checks (9.1%), and learning difficulties (7.5%). Patients seen in 47.5% of consultations had medications (eg, prescriptions, vaccinations) recorded, and patients in 27.2% of consultations were referred elsewhere, usually to a subspecialist or psychologist (31.6% and 26.6% of referrals, respectively). Male sex of the child and owning a Health Care Card were associated with most developmental–behavioural diagnoses. Paediatricians tended to bill for single disease/non-complex consultations, even when seeing a child with multiple problems.Conclusions: Australian paediatricians see children with a range of diagnoses that are often multiple and complex. Our findings provide directions for future secondary care research, and may inform workforce planning and paediatricians’ training requirements.

Harriet Hiscock MB BS, FRACP, MD · Gehan Roberts MB BS, FRACP, PhD · Daryl Efron MB BS, FRACP, MD · Jillian R Sewell MB BS, FRACP · Hannah E Bryson BA(Hons) · Anna M H Price BA(Hons) · Frank Oberklaid MD, FRACP, DCH · Michael South FRACP, MD, FCIM · Melissa A Wake MB ChB, FRACP, MD