Child health

Objective: To determine whether changes in 24-hour average background ozone (O3), nitrogen dioxide (NO2), carbon monoxide (CO) and particulates < 10 μm (PM10) increase the risk of hospital emergency department (ED) presentations for asthma among children.Design, setting and subjects: A time-stratified case-crossover method was used to analyse data of 603 children and young adults aged 0–19 years who were resident in a south-west metropolitan area of Perth, Western Australia, and who had presented with asthma at any public ED within Perth between 1 January 2002 and 31 December 2006. Effect sizes were assessed in relation to age group, sex and season of exposure. City-wide background air pollution was estimated from air monitoring network data.Main outcome measures: ED presentation with asthma.Results: Patients 0–4 years with 1-day lagged exposure to NO2 and CO showed the most significant risk of ED presentation for asthma. An interquartile range (IQR) increase in NO2 resulted in an odds ratio (OR) of 1.70 (95% CI, 1.08–2.69). An IQR increase in CO resulted in an OR of 1.40 (95% CI, 1.06–1.84).Conclusions: The effect sizes observed in this study were higher than those of past studies, and indicated that children aged 0–4 years were the most vulnerable to the effects of air pollution. The period of exposure most clinically relevant is the day before ED presentation.

Gavin Pereira MAppStats, BCM, GCResCom · Angus Cook MB ChB, PhD · Annemarie J B M De Vos PhD, MPH, RN · C D’Arcy J Holman MB BS, MPH, PhD

Unsettled behaviour in the first few months of life is a common clinical problem, with the associated risks of postnatal depression, premature cessation of breastfeeding, long-term psychological disturbance, and child abuse. Parents of new babies complain of difficulty accessing appropriate care and receiving conflicting advice. Although organic disturbance is implicated in only 5% of cases, gastro-oesophageal reflux disease, food allergies and lactose intolerance are often mistakenly diagnosed in unsettled babies. There is no evidence that acid-suppressive medications help in treating unsettled behaviour and, until the hypothesis that proton-pump inhibitors may predispose to food allergies has been properly investigated, treatment with acid-suppressive medications should be avoided in this population. Although unsettled behaviour in infants is commonly a transient neurodevelopmental phenomenon that peaks at 6 weeks of age, failure to diagnose other correctable problems, including breastfeeding difficulty and cows milk allergy, risks entrenching anxiety and disrupted mother–infant interactions in the long term. In the current climate of health system reform, the design and evaluation of an integrated, evidence-based, multidisciplinary primary care approach to management of unsettled babies and their mothers is a priority.

Pamela S Douglas MB BS, FRACGP · Harriet Hiscock MB BS, FRACP, MD

To the Editor: Children have been seen as a key priority group for pandemic (H1N1) 2009 influenza (“swine flu”) vaccination. In Australia and New Zealand, children aged 0–4 years had the highest population rate of intensive care unit admissions for swine flu.1 From 3 December 2009, the Australian Government provided free H1N1-specific influenza vaccine for all Australians aged 6 months and older. However, it was not known how parents and other caregivers would respond to the offer of vaccination. We sought to determine caregivers’ intentions regarding whether their child would receive the pandemic vaccine. The study was approved by the human research ethics committee of the Children’s Hospital at Westmead and was conducted in November and December 2009, immediately before, and alongside, the commencement of the pandemic vaccination program for children. A paper-based questionnaire (with an alternative web-based option) was sent to caregivers of children aged 6 months to 5 years who were attending 16 long-day-care centres across metropolitan Sydney. It included questions about attitudes, behaviour, intentions and beliefs regarding swine flu, seasonal influenza and vaccines. We analysed responses using SPSS, version 17 (SPSS Inc, Chicago, Ill, USA) and conducted univariate analysis (as factors had high collinearity) to search for factors associated with caregivers’ intention for their child to receive the pandemic vaccine. The response rate was 44% (431/972). Most respondents had families of two children (47%) or one child (41%); 90% were mothers; and 48% had a postgraduate education. Caregivers were asked to report in relation to their eldest child attending the day-care centre (mean age, 38 months). Three children (out of 427 responses; 0.7%) had already received the pandemic vaccine; 23% of caregivers (92/400) said they would have their child vaccinated; 54% (217/400) were unsure; and 22% (87/400) would not. Intentions regarding seasonal influenza vaccination were similar. Factors associated with caregivers’ intention to have their child vaccinated with pandemic vaccine are shown in the Box. Those with the strongest associations included caregivers’ intention to have their child vaccinated against seasonal influenza in 2010 and belief that seasonal influenza vaccine is completely safe or only a slight risk. Factors not significantly associated with respondents’ intention to have their child vaccinated with the pandemic vaccine were the respondent’s age group, sex, education level, language spoken at home, and number of children in the household. The study indicated that at the commencement of the Australian pandemic influenza vaccination program for children, there was significant uncertainty among this sample of relatively highly educated respondents. The proportion of respondents intending to have their children vaccinated was far lower than recent Australian estimates (6% of children aged 4 years and under).2 Our findings suggest that, despite the acknowledged severity of pandemic influenza, respondents’ concerns about vaccine safety were influencing their intentions. Indeed, the program commenced in a context of public debate about the response to the influenza pandemic and the vaccination program, including concerns about the safety of using multi-dose vials for vaccine delivery.3,4 Among respondents intending for their child to have the pandemic vaccine, the association with the child having had a previous influenza vaccination suggests that, having once taken up vaccination, respondents were more likely to intend to do so again. More recent events in Australia leading to suspension of use of all three 2010 seasonal influenza vaccines for children under 5 years of age are likely to further increase safety concerns.5 While two vaccines have since been reinstated, these events present a significant challenge for future influenza vaccination programs. Providers are likely to have an important role in communicating recommendations and addressing caregivers’ concerns. Factors associated with caregivers’ intentions for their child to receive the pandemic (H1N1) 2009 influenza vaccine Survey responses Intention “yes” (n = 92) Number OR (95% CI) Would you have your child vaccinated against seasonal flu in 2010? (n = 396) No 8 1.00 Unsure 33 2.29* (1.11–5.15) Yes 51 17.49* (7.55–40.50) How safe do you think the seasonal flu vaccine is for children aged 1 to 5 years? (n = 396) Moderate/high risk 7 1.00 Don’t know 19 2.04 (0.82–5.07) Completely safe/slight risk 66 6.64* (3.00–15.22) How safe do you think the seasonal flu vaccine is for babies aged 6 to 11 months? (n = 395) Moderate/high risk 21 1.00 Don’t know 36 1.35 (0.75–2.44) Completely safe/slight risk 35 4.32* (2.27–8.22) Did your child receive seasonal flu vaccination in 2009? (n = 394) No 77 1.00 Yes 15 3.48* (1.65–7.36) How concerned do you feel about your child catching the flu? (n = 396) Not at all/ a little/ moderately 31 1.00 Very/extremely 61 2.46* (1.46–4.17) Does your child have any medical conditions requiring ongoing visits to a health care professional? (n = 396) No 76 1.00 Yes 16 2.00† (1.03–3.87) The flu vaccine can give you the flu. (n = 396) Agree 24 1.00 Don’t know 23 1.18 (0.62–2.23) Disagree 45 1.82† (1.04–3.20) OR = odds ratio. * P ≤ 0.01. † P ≤ 0.05.

Julie Leask · Maria Yui Kwan Chow · Catherine King · Robert Booy

We report a series of cases of thyroid dysfunction in adults associated with ingestion of a brand of soy milk manufactured with kombu (seaweed), and a case of hypothyroidism in a neonate whose mother had been drinking this milk. We also report two cases of neonatal hypothyroidism linked to maternal ingestion of seaweed made into soup. These products were found to contain high levels of iodine. Despite increasing awareness of iodine deficiency, the potential for iodine toxicity, particularly from sources such as seaweed, is less well recognised. Clinical recordsCases of thyroid dysfunction associated with ingestion of soy milkIn November 2008, a 36-year-old woman (Patient 1, Box 1) presented with a mildly elevated serum thyroid-stimulating hormone (TSH) level detected during screening for in vitro fertilisation. As she tested negative for thyroid antibodies, her urinary iodine level was measured to exclude iodine deficiency; this level was markedly elevated at 4445 μg/L (reference range [RR], < 200 μg/L). The source of the excess iodine was unclear until the patient did an internet search and identified that the soy milk she had been drinking (Bonsoy) contained kombu1,2 — a type of seaweed. The patient ceased drinking the soy milk, which resulted in rapid normalisation of her TSH level. Three months later, a 38-year-old man (Patient 2, Box 1) presented with florid thyrotoxicosis. Minimal uptake of technetium on a thyroid scan and absence of TSH receptor antibodies essentially excluded Graves disease. The scan result, in combination with his elevated urinary iodine level (1278 μg/L), indicated that iodine toxicity was the most likely cause of the thyrotoxicosis. He drank brands of soy milk other than Bonsoy, but also drank Bonsoy in takeaway coffee. After he ceased drinking all soy milk, his symptoms rapidly abated and his serum TSH level normalised 3 months later. No further cases of suspected iodine toxicity were seen until approximately 1 year later, when six additional patients presented to one of us (B A C) over a 6-week period (Patients 3–8, Box 1). These patients presented with thyroid conditions ranging from subclinical hyperthyroidism to florid thyrotoxicosis. Patient 3 had already been diagnosed with thyrotoxicosis due to underlying iodine toxicity (urinary iodine level, 11 427μg/L); however, the source of excess iodine was not identified until she sought a second opinion. One month after she ceased consuming Bonsoy milk (which she had been consuming for the previous 8 years), her serum TSH level normalised. An aliquot of Bonsoy milk was analysed for iodine content using a plasma mass spectrometer (Department of Biochemistry, Royal Prince Alfred Hospital, Sydney, NSW), which showed an iodine concentration of 25 000 μg/L. In comparison, the levels of iodine in other soy milks that were analysed ranged from 15 μg/L to 281 μg/L (Box 2). Two weeks later, the same laboratory received a second aliquot of Bonsoy milk for analysis, due to a case of neonatal hypothyroidism. The newborn screening program had identified a baby with an elevated TSH level (28 mIU/L; RR, < 20 mIU/L; heel-prick blood sample). Additional testing 19 days after birth showed further elevation of the baby’s serum TSH level (163 mIU/L), as well as a low level of serum free thyroxine (3.7 pmol/L; RR, 10–25 pmol/L). Exposure to exogenous iodine from a maternal source was suspected because of the marked rise in serum TSH level. Urinary iodine levels were subsequently found to be elevated in both the mother (5415 μg/L) and the baby (9797 μg/L). During the last trimester of pregnancy, the mother had been drinking about 500 mL of Bonsoy milk daily. She had been breastfeeding since delivery. The iodine concentration of the second aliquot of this soy milk (27 580 μg/L) was similar to that of the previously analysed sample. The baby was initially treated with thyroxine but, after the mother ceased ingesting the soy milk, the baby’s thyroid function normalised. Independent analysis of the soy milk (Division of Analytical Laboratories, NSW Health, Sydney, NSW) again revealed an extremely high iodine concentration (31 000 μg/L). Cases of neonatal hypothyroidism associated with maternal ingestion of seaweed soupTwo cases of neonatal hypothyroidism related to maternal ingestion of seaweed have been reported recently by two of us (P J E and M M J).3 The first case involved a Korean mother who, during pregnancy and the puerperium, consumed soup made with overseas-bought dried seaweeds. Her baby, born at 36 weeks’ gestation, had a normal TSH level at the time of newborn screening (heel-prick blood sample). However, the baby subsequently developed jaundice and, at 3 weeks of age, a repeat TSH test showed elevation of the baby’s serum TSH level (39 mIU/L; RR, 0.4–5.0 mIU/L) as well as a low level of serum free thyroxine (9.7 pmol/L; RR, 13–30 pmol/L) and an elevated urinary iodine level (690 μg/L). The baby was initially treated with thyroxine but, after the mother ceased ingesting seaweed soup, the baby’s thyroid function normalised. Dried samples of two different seaweed compounds, analysed by a commercial pathology company (Sullivan Nicolaides Pathology, Brisbane, QLD), showed iodine concentrations of 291 μg/g and 424 μg/g. The second case involved an infant born at 27 weeks’ gestation who had a normal TSH level at the time of newborn screening, and an elevated serum TSH level (24 mIU/L; RR, 0.06–7.14 mIU/L) when a routine repeat TSH test was carried out at 1 month of age. This infant’s mother had also been ingesting seaweed soup — made with Heng Fai seaweed, imported from China, to increase her breast milk supply. The baby’s urinary iodine level at the time of maternal seaweed ingestion was elevated (454 μg/L). The iodine concentration in the mother’s breast milk at the time of seaweed ingestion was elevated at 878 μg/L; 4 weeks after she ceased consuming the seaweed, the concentration dropped to 188 μg/L. NSW Health was notified and testing of the Heng Fai seaweed by the NSW Food Authority revealed high levels of iodine (4450 μg/g), which resulted in voluntary withdrawal of Heng Fai seaweed by the importers in March 2010.4 DiscussionIodine toxicity causes a spectrum of thyroid disorders, ranging from hyperthyroidism to hypothyroidism.5,6 Reasons for the variable effects are unclear, but may relate to age, pre-existing autoimmune thyroid disease, and amount and duration of iodine ingestion.5,6 The adults described here did not appear to have underlying nodular goiters or Hashimoto disease (Box 1). In iodine toxicity, thyroid technetium uptake scans usually show absent or low technetium uptake in thyrotoxicosis and increased technetium uptake in neonatal hypothyroidism. Graves disease and autonomous nodular thyroid disease are more common causes of thyrotoxicosis but can be excluded primarily by scan results, lack of a goitre and absence of TSH receptor antibodies. However, as urinary iodine levels are not routinely measured in clinical practice, iodine toxicity may be underdiagnosed. This series of cases of thyroid dysfunction led to a national recall of Bonsoy milk on 24 December 2009,7 and the distributer agreed to voluntary withdrawal of the product from sale in Australia. This brand of soy milk was fermented in seaweed, which is thought to improve the flavour, and is promoted as having wide-ranging health benefits.1 The NSW Health alert for Bonsoy milk stated that in a child, ingestion of only 5 mL, and in an adult, only 30 mL, would exceed the safe upper limit of iodine intake.8,9 It is unclear whether changes to the manufacturing process of the Bonsoy product may have increased its iodine content. However, after removal of kombu from the manufacturing process, the iodine content was reduced markedly (15 μg/L) and the product returned to the Australian market in April 2010. The World Health Organization was notified of the iodine toxicity of the Bonsoy milk, which was withdrawn from sale in a number of other countries.10 Between January and June 2010, 48 retrospective Australian cases of thyroid dysfunction associated with this brand of soy milk were also notified to local public health authorities (Katrina Knope, Coordinating Epidemiologist, OzFoodNet, Office of Health Protection, Department of Health and Ageing, June 2010, personal communication). A cluster of cases of thyrotoxicosis, linked to iodine toxicity from an unidentified soy milk, was also reported in New Zealand in 2005.11 The common practice by women from Japan and Korea of ingesting seaweed made into soup, sometimes in large quantities, to promote wellbeing in the mother and stimulate breast milk supply, does not appear to be widely known in the medical community. However, due to iodine transmission through breast milk, transient or even persistent hypothyroidism has been reported in neonates born to mothers who undertake this practice.12,13 If left undiagnosed and untreated, neonatal hypothyroidism can have devastating clinical consequences, including impaired intellectual development. Although newborn screening tests will help to identify hypothyroidism during the first week of life, there is no subsequent routine screening of thyroid function in term babies whose TSH level may not increase until after 1 week of age, as seen in one of the neonatal cases described here and in a Korean study of preterm infants.12 Our findings demonstrate the importance of: considering iodine toxicity in patients who present with thyrotoxicosis in the absence of TSH receptor antibodies and low or absent uptake on a thyroid technetium uptake scan; measuring urinary iodine level in cases where thyrotoxicosis is not explained by conditions such as autoimmune or nodular thyroid disease; and actively seeking a history of maternal seaweed consumption during pregnancy and lactation in cases of neonatal hypothyroidism. Finally, although iodine deficiency is a documented and serious concern in Australia,14,15 these cases highlight the risks of excess iodine intake from dietary sources. The food industry is not strictly regulated (eg, imported products are not usually tested to confirm their contents), and contamination of food and drink is only detected when unusual or severe clinical events ensue. There is a strong public health argument for monitoring iodine levels in imported foods and commercially available seaweed preparations. 1 Characteristics of a cluster of eight adult patients in whom thyroid dysfunction was attributed to consumption of Bonsoy, a brand of soy milk manufactured with seaweed, November 2008 to December 2009* Sex; age (years) SerumTSH level (mIU/L) Serum fT4 level (pmol/L) Serum fT3 level (pmol/L) Serum TRAb test result Serum TPO/Tg Ab test result Technetium uptake on thyroid scan Urinary iodine level (μμg/L) Thyroid ultrasound result RR 0.4–3.5 9–19 2.5–5.7 0.5%–3.5% < 200 Patient 1 F; 36 4.63 9.7 Not done Not done Negative Not done 4 445 Not done Patient 2 M; 38 < 0.02 59.4 16 Negative Negative Negligible 1 278 Normal size, single nodule (3 mm diameter), normal vascularity Patient 3 F; 46 < 0.005 50 39 Negative Negative < 0.5% 11 427 Mild enlargement, reduced vascularity Patient 4 F; 36 < 0.04 30 12 Negative Negative 0.5% 777 Normal Patient 5† F; 37 < 0.0005; 12.4 29; < 5 5.6; 3.4 Negative Negative Not done 6 208 Normal Patient 6‡ F; 29 0.04 16 4.9 Negative Negative 0.5% 48 Tiny nodules (< 3 mm diameter) Patient 7 F; 33 0.08 18 6.6 Negative Negative 1.3% 5 022 Normal Patient 8 M; 47 0.07 17 4.9 Negative Negative 0.1% 320 Single nodule (5 mm diameter) TSH = thyroid-stimulating hormone. fT4 = free thyroxine. fT3 = free triiodothyronine. TRAb = TSH receptor antibody. TPO/Tg Ab = thyroid peroxidase and thyroglobulin antibodies. RR = reference range. F = female. M = male. * Reported daily intake of Bonsoy milk ranged from < 100 mL/day to 1000 mL/day. † Patient 5 had blood tests for thyrotoxicosis performed at 5.5 months postpartum, and repeated at 7 months postpartum (when she had developed hypothyroidism). ‡ Patient 6 ceased consumption of the Bonsoy milk about 2–3 months before testing. 2 Iodine concentration in various milks, assayed in December 2009* Brand Iodine (μμg/L) Soy milks Bonsoy 25 000, 27 580 Sanitarium So Nice 27 Vitasoy 19 Coles Soy Drink 19 So Natural Original 15 Other milks Woolworths Lite (low-fat cows milk) 281 Pura Milk (full-fat cows milk) 215 So Good Rice Milk 29 * All testing was carried out at the Department of Biochemistry, Royal Prince Alfred Hospital, Sydney, NSW.

Bronwyn A Crawford PhD, MB BS, FRACP · Christopher T Cowell MB BS, FRACP · Phillip J Emder BSc(Med), MB BS, FRACP · Diana L Learoyd PhD, MB BS, FRACP · Elizabeth L Chua PhD, MB BS, FRACP · John Sinn MB BS, MMed(ClinEpi), FRACP · Michelle M Jack PhD, MB BS, FRACP

To the Editor: In their recent editorial, Bower and colleagues effectively summarised the problem of apparent governmental indifference to congenital anomalies.1 This is not unique to Australia and probably exists worldwide. National systems to collect congenital anomalies data were set up in many countries in the mid 1960s, including the National Congenital Anomaly System in the United Kingdom and the Canadian Congenital Anomalies Surveillance System. This followed the thalidomide tragedy and exemplified that it often takes an acute crisis to stimulate politicians into action. However, due to a lack of leadership, foresight and finances,2-4 these systems gradually declined to the extent that they became of very little value, lacking in accurate ascertainment and pregnancy termination data. As a result, regional registries were set up in England and Wales, and Canada was left with only two provinces (British Columbia and Alberta) collecting data. Prevention is one of the new driving forces for collecting good data, and the advent of using folic acid to effectively reduce neural tube defects brought a new urgency to the need for comprehensive useable data. Accordingly, the Canadian government set up a task force and formed a new entity in 2002, the Canadian Congenital Anomalies Surveillance Network, with a mandate to provide logistical and financial help to all 10 provinces and three territories. While progress has been slow, it has been very encouraging, with three additional provinces and one territory developing new surveillance systems this fiscal year (April 2010 – March 2011). The Network has set up guidelines and standards to enable all provinces and territories to collect data in a comparable format,5 which can then be forwarded to a central database in the national capital, Ottawa. The quality of the data should be improved because they are gathered at a local level. This model could be adapted for use in Australia because, according to Bower et al,1 a nucleus of good data from at least three states already exists.

R Brian Lowry

Consensus recommendations for managing chronic suppurative lung disease (CSLD) and bronchiectasis, based on systematic reviews, were developed for Australian and New Zealand children and adults during a multidisciplinary workshop. The diagnosis of bronchiectasis requires a high-resolution computed tomography scan of the chest. People with symptoms of bronchiectasis, but non-diagnostic scans, have CSLD, which may progress to radiological bronchiectasis. CSLD/bronchiectasis is suspected when chronic wet cough persists beyond 8 weeks. Initial assessment requires specialist expertise. Specialist referral is also required for children who have either two or more episodes of chronic (> 4 weeks) wet cough per year that respond to antibiotics, or chest radiographic abnormalities persisting for at least 6 weeks after appropriate therapy. Intensive treatment seeks to improve symptom control, reduce frequency of acute pulmonary exacerbations, preserve lung function, and maintain a good quality of life. Antibiotic selection for acute infective episodes is based on results of lower airway culture, local antibiotic susceptibility patterns, clinical severity and patient tolerance. Patients whose condition does not respond promptly or adequately to oral antibiotics are hospitalised for more intensive treatments, including intravenous antibiotics. Ongoing treatment requires regular and coordinated primary health care and specialist review, including monitoring for complications and comorbidities. Chest physiotherapy and regular exercise should be encouraged, nutrition optimised, environmental pollutants (including tobacco smoke) avoided, and vaccines administered according to national immunisation schedules. Individualised long-term use of oral or nebulised antibiotics, corticosteroids, bronchodilators and mucoactive agents may provide a benefit, but are not recommended routinely.

Anne B Chang MPHTM, PhD, FRACP · Scott C Bell MB BS, MD, FRACP · Cass A Byrnes MB ChB, MD, FRACP · Keith Grimwood MB ChB, MD, FRACP · Peter W Holmes MB BS, FCCP, FRACP · Paul T King MB BS, FRACP, PhD · John Kolbe MB BS, FRACP · Louis I Landau MB BS, MD, FRACP · Graeme P Maguire MB BS, FRACP, PhD · Malcolm I McDonald MB BS, FRCPA, PhD · David W Reid MB ChB, MRCP, FRACP · Francis C Thien MB BS, MD, FRACP · Paul J Torzillo MB BS, FRACP, FJFICM

To the Editor: The Between the Flags project of the Clinical Excellence Commission (CEC) is designed to establish a “safety net” in all New South Wales public hospitals, to enable early identification and management of deteriorating hospital inpatients.1 A paediatric advisory group within of the program is currently developing five age-group-specific paediatric observation charts to account for the changes in normal physiological parameters that occur with age in children, and these have been distributed for comment before finalisation. Each chart has specific physiological calling criteria defining when a clinical review or rapid response is required from medical staff (Box). If one or more criteria fall in the “red” zone, the patient requires an immediate, rapid response; if criteria fall in the “yellow” zone, the patient needs a clinical review within 30 minutes. A paucity of data on what represents an abnormal parameter for each age group has also led to a lack of clear triage guidelines for emergency department nurses. For example, the paediatric physiological discriminators of the Australasian Triage Scale include terms such as “mild tachycardia” as a guide for allocating patients to triage Category 3 and “moderate tachycardia” for Category 2.2 We trialled the CEC paediatric inpatient calling criteria to determine whether they could also be used for emergency department triage purposes. We carried out a retrospective review of patients presenting to triage at the emergency department of the Children’s Hospital at Westmead between 1 and 14 March 2010. We assumed that patients who met the CEC’s yellow criteria should be allocated to triage Category 3 (“urgent: review within 30 minutes”) and those who met the CEC’s red criteria should be allocated to at least triage Category 2 (“emergency: review within 10 minutes”). Patient outcomes were classified as “admitted”, “discharged” or “did not wait”. From 1968 presentations, 1885 patients had observations at triage available for review. The numbers of patients in each triage category were: Category 1 (5); 2 (41); 3 (403); 4 (422); and 5 (1014). Only 10 of the 46 patients in Category 1 and 2 would have been flagged by the CEC parameters as needing a rapid response (ie, review within 10 minutes), and none of the three patients admitted to the paediatric intensive care unit would have been identified by the CEC parameters. Of the 403 patients in Category 3 (needing review within 30 minutes), 32 would have been uptriaged to Category 2 by the CEC criteria. Twelve of these 32 patients were in fact discharged home, indicating that the CEC criteria are unsuitable for triage purposes. Of the 1436 patients in Category 4 and 5, 30 would have been uptriaged to Category 2 according to the CEC parameters and, of these, only three were admitted. A further 271 patients would have been uptriaged to Category 3 (181 of these were discharged and 54 did not wait). Of particular note is that 151 of the 271 patients met the yellow criteria because of low respiratory rates that were flagged by the charts but were normal for the patient. At present, the physiological parameters defined in the new CEC paediatric inpatient observation charts are not suitable as a triage tool in the paediatric emergency department, do not replace an experienced triage nurse, and are a poor predictor of disposition. CEC calling criteria* and physiological parameters for children, by age group Calling criteria, by age group Call Physiological parameter < 30 days 1–12 months 1–4 years 5–11 years ≥ 12 years Red† Heart rate (beats/min) Above 180 190 170 160 150 Below 80 80 70 60 40 Respiratory rate (breaths/min) Above 100 65 60 50 40 Below 20 15 15 10 5 Systolic blood pressure (mmHg) Above — — — — — Below 60 50 70 70 80 Oxygen saturation (%) Below 85 85 85 85 85 Temperature (°C) Above 38 — — — — Yellow‡ Heart rate (beats/min) Above 160 170 150 140 130 Below 90 100 80 70 50 Respiratory rate (breaths/min) Above 60 50 50 35 30 Below — 30 20 15 10 Systolic blood pressure (mmHg) Above — 120 120 130 160 Below 70 80 80 80 90 Oxygen saturation (%) Below 95 90 90 90 90 Temperature (°C) Above 37.5 — — — — CEC = Clinical Excellence Commission. * Calling criteria as of March 2010 at the time of this study (the CEC has subsequently revised some of these criteria). Only one “flag” was required to meet a calling criterion. Other calling criteria such as pain, work of breathing and level of consciousness were not measured in our study but will also generate a call. Where no values are present, there are no calling criteria for the parameter. † Red call requires immediate, rapid response. ‡ Yellow call requires review within 30 minutes.

Fenton M O’Leary · Jennifer I Major

Objectives: To examine 5-year survival from haematological malignancies in children, adolescents and young adults in Australia and determine if there has been any improvement in survival for the older age groups compared with children (the age-related “survival gap”).Design, setting and participants: Population-based study of all Australian children (aged 0–14 years), adolescents (15–19 years) and young adults (20–29 years) diagnosed with acute lymphoblastic leukaemia (ALL), acute myeloid leukaemia (AML), Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL) between 1982 and 2004, with follow-up to 2006.Main outcome measures: 5-year survival from ALL, AML, HL and NHL analysed for four periods of diagnosis (1982–1989, 1990–1994, 1995–1999 and 2000–2004).Results: During 1982–2004, 13 015 people aged ≤ 29 years were diagnosed with primary leukaemia or lymphoma in Australia. For those with ALL, 5-year survival for adolescents improved from 40% (1982–1989) to 74% (2000–2004); the improvement for young adults was smaller (31% to 47%), and both these groups still had lower survival than children, whose 5-year survival improved from 74% to 88%. There was a larger narrowing of the gap for AML: for cases diagnosed in 2000–2004, 5-year survival was similar for young adults (63%), adolescents (74%) and children (69%). For lymphoma cases diagnosed in 2000–2004, 5-year survival in all age groups was greater than 95% for HL and greater than 81% for NHL, although children fared better than adolescents and young adults.Conclusions: These Australian population-based data confirm an improvement in survival from haematological malignancies across all three age groups, but an age-related survival gap remains for adolescents and young adults compared with children, especially for young adults with ALL. Greater participation of adolescents and young adults in clinical trials and more detailed data collection are needed to provide evidence about optimal treatment regimens in these age groups.

Ross Pinkerton MD, FRACP · Rachael-Anne Wills BAppSc(Hons) · Michael D Coory FAFPHM, PhD · Christopher J Fraser MB BS, FRACP, MPH

New guidelines are timely but miss an opportunity to emphasise early intervention for all young people There are few mental health issues of greater concern to the wider community than the management of young people with depressive disorders. Consequently, the new draft clinical practice guidelines from beyondblue: the national depression initiative1 are timely. The previous National Health and Medical Research Council Clinical practice guidelines: depression in young people were produced in 1997 and rescinded in 2004, and a variety of other international perspectives are now available.2,3 Internationally, the limitations of the clinical trial database, such as small and non-representative or restricted trial samples, and exclusion of more severe cases or patients with suicidal ideation, are widely recognised. Hence, the authors rely very heavily on “good practice points” that are said to be “based on lower quality evidence, expert opinion and current good practice”. Importantly, the new draft guidelines recognise that appropriate services are still not provided to about 75% of Australian young people with depression. They suggest there is a lack of clear evidence for primary (or universal) prevention and give qualified support for pre-emptive psychological strategies for those at high risk. Recent systematic reviews of school-based prevention and early intervention programs for anxiety and depression, however, support a more optimistic view (reporting effect sizes of 0.11–1.37 for anxiety, using data from 20 programs;4 and 0.21–1.40 for indicated depression interventions, based on 28 programs5). These effect sizes were often clinically important and support the notion that school-based programs should be pursued more assertively. Other key issues covered by the guidelines include the challenges associated with engaging young people with our health care systems, the lack of focus on improving long-term outcomes, and the fact that more severe bipolar and psychotic disorders emerge against the background of earlier depressive disorders. In Australia, surveys of young people have highlighted attitudinal and knowledge barriers6 and the clinical reality that under-recognition of and lack of access to evidence-based psychological therapies are still common.7 Unfortunately, the guidelines overemphasise and reinforce stereotypes of young people who are reluctant to seek care, parents who are unaware of the nature of the disorder, the complexity of clinical assessment and lack of access to specialist mental health services. These are artefacts of the current failure to respond to youth mental health as a salient public health issue. We would encourage the authors to take full advantage of the opportunity to add depth to the emerging field of youth psychiatry and to support the development of enhanced models of empowering, collaborative and youth-focused clinical practice.8 The most novel outcome in the new draft guidelines is the Expert Working Committee’s decision to focus on the age range of 13–24 years, rather than a more restricted focus on 12–18 years. This is consistent with current understanding of the continuities in brain and social development,9 the pattern of incidence of mental disorders and the changing sociology of adolescent and early adult development.10 There is clear evidence of multiple transitions in both the genetic and environmental determinants of depressive disorders from the onset of puberty right through to the early adult period.11 The key developmental processes in the brain — synaptic pruning and maturation of the white matter tracts — are continuous throughout these years.9 However, in key areas, the guidelines fall back on the traditional divide between adolescents (13–18 years) and young people (19–24 years). While this reflects the reality that most treatment studies have used a 13–18-years age range, it ignores the fact that the division at 18 years is based on legal and educational boundaries rather than clinical, developmental, neurobiological or cultural considerations, and thus is not soundly based. What is desperately needed in both clinical research and service development12 is a shift away from this artificial divide to the more inclusive age range of 12–25 years. Short-term treatment recommendations are spelt out in the guidelines, at least for those under 18 years of age. Specific psychological therapies are the preferred first-line intervention for most patients, while new antidepressant drugs are reserved for those with more severe disorders or those who fail to respond to psychological interventions. The small risk of increased suicidal ideation in young people commencing newer antidepressant drugs (4% for active treatments versus 2% for placebo13) is appropriately re-emphasised. Previously, wide media coverage of United States Food and Drug Administration warnings about antidepressant drugs resulted in major changes in clinical practice in the US.14 Clearly, the authors expect a similar outcome in Australia, suggesting that these new guidelines may even lead to “a net saving in the area of pharmacotherapy”. This is inconsistent with the more serious emphasis that the rest of the document puts on providing evidence-based care for many more young people. Importantly, it has been suggested that the fall in antidepressant use in the US was associated with an increase in suicides in young people.14 Previous population-based data have indicated a positive relationship between exposure to antidepressants and reduction in suicides. In those under the age of 18 years, most suicide attempts occur in the month before treatment and then decline sharply once treatment has commenced.15 We need to move beyond endless debate about the appropriate threshold for providing active care — the real treatment issue is one of appropriate sequencing of treatments. Wherever possible, clinical care should start with engagement of the young person and his or her family and then be linked with active provision of relevant information and evidence-based psychological therapies. A clinical staging model16 combined with appropriate stepped care may therefore offer a useful clinical approach. In a basic stepped-care model, those presenting with early or less severe forms of illness are initially offered appropriate non-pharmacological interventions. If the condition is more severe, the clinical situation worsens or the young person fails to respond to psychological therapies, then antidepressant therapy may well have a crucial role to play. The guidelines fail to emphasise the emerging importance of early intervention services. What is really required in Australia is a fundamental commitment to increase access to evidence-based care systems for young people from 12 to 25 years of age. While various state and national planning documents and the recent Council of Australian Governments decisions on health reform point the way for future service reforms, we still lack the real investment and commitment to turn these treatment guidelines into accessible and responsive clinical services systems.

Ian B Hickie AM, MD, FRANZCP · Patrick D McGorry PhD, FRCP, FRANZCP

Objectives: To determine the extent to which children with a hospital admission related to assault or maltreatment or to a notified sexually transmitted infection (STI) have contact with the Western Australian Department for Child Protection (DCP), and to investigate injuries and conditions often associated with child maltreatment and subsequent contact with the DCP.Design, participants and setting: Retrospective cohort study using de-identified, record-linked child protection and hospital morbidity data to identify all children aged 0–17 years in Western Australia between 1 January 1990 and 31 December 2005, and a subcohort of children born in WA between these dates, admissions of these children to public and private hospitals in WA, and their contact with the Western Australian DCP.Main outcome measures: Annual trends in notifications and substantiations of child maltreatment; proportion of children with assault-related and maltreatment-related hospital admissions resulting in notifications, substantiations, or out-of-home care.Results: Most children admitted for maltreatment-related reasons (90%) had contact with the DCP, with 81% of these children being notified, 68% having maltreatment substantiated, and 50% entering out-of-home care. Specific injuries and conditions were associated with children who had greater contact with the DCP, including retinal haemorrhage, rib fractures, multiple injuries, STIs at under 14 years of age, and malnourishment.Conclusions: The health system effectively identifies and notifies real cases of maltreatment, and a high proportion of these are substantiated. Health data play an important role in improving maltreatment surveillance, providing opportunities to make valid comparisons over time and between jurisdictions, as well as to monitor conditions and injuries associated with child maltreatment.

Melissa O’Donnell GradDipEd, MPsych, PhD · Natasha Nassar BEc, MPH, PhD · Helen M Leonard MB ChB, MPH · Richard P Mathews BPsych, MA · Yvonne G Patterson BSc, MPsych, MBA · Fiona J Stanley MB BS, MSc, MD

Objective: To describe the epidemiology of acute lower respiratory infection (ALRI) and bronchiectasis in Northern Territory Indigenous infants hospitalised in the first year of life.Design: A historical cohort study constructed from the NT Hospital Discharge Dataset and the NT Immunisation Register.Participants and setting: All NT resident Indigenous infants, born 1 January 1999 to 31 December 2004, admitted to NT public hospitals and followed up to 12 months of age.Main outcome measures: Incidence of ALRI and bronchiectasis (ICD-10-AM codes) and radiologically confirmed pneumonia (World Health Organization protocol).Results: Data on 9295 infants, 8498 child-years of observation and 15 948 hospitalised episodes of care were analysed. ALRI incidence was 426.7 episodes per 1000 child-years (95% CI, 416.2–437.2). Incidence rates were two times higher (relative risk, 2.12; 95% CI, 1.98–2.27) for infants in Central Australia compared with those in the Top End. The median age at first admission for an ALRI was 4.6 months (interquartile range, 2.6–7.3). Bronchiolitis accounted for most of the disease burden, with a rate of 227 per 1000 child-years. The incidence of first diagnosis of bronchiectasis was 1.18 per 1000 child-years (95% CI, 0.60–2.16). One or more key comorbidities were present in 1445 of the 3227 (44.8%) episodes of care for ALRI.Conclusions: Rates of ALRI and bronchiectasis in NT Indigenous infants are excessive, with early onset, frequent repeat episodes, and a high prevalence of comorbidities. These high rates of disease demand urgent attention.

Kerry-Ann F O’Grady GDipPH, MAppEpid, PhD · Paul J Torzillo AM, MB BS, FRACP, FJFICM · Anne B Chang FRACP, MPHTM, PhD

Objective: To determine the burden of hospitalised, radiologically confirmed pneumonia (World Health Organization protocol) in Northern Territory Indigenous children.Design, setting and participants: Historical, observational study of all hospital admissions for any diagnosis of NT resident Indigenous children, aged between ≥ 29 days and < 5 years, 1 April 1997 to 31 March 2005.Intervention: All chest radiographs taken during these admissions, regardless of diagnosis, were assessed for pneumonia in accordance with the WHO protocol.Main outcome measure: The primary outcome was endpoint consolidation (dense fluffy consolidation [alveolar infiltrate] of a portion of a lobe or the entire lung) present on a chest radiograph within 3 days of hospitalisation.Results: We analysed data on 24 115 hospitalised episodes of care for 9492 children and 13 683 chest radiographs. The average annual cumulative incidence of endpoint consolidation was 26.6 per 1000 population per year (95% CI, 25.3–27.9); 57.5 per 1000 per year in infants aged 1–11 months, 38.3 per 1000 per year in those aged 12–23 months, and 13.3 per 1000 per year in those aged 24–59 months. In all age groups, rates of endpoint consolidation in children in the arid southern region of NT were about twice that of children in the tropical northern region.Conclusion: The rates of severe pneumonia in hospitalised NT Indigenous children are among the highest reported in the world. Reducing this unacceptable burden of disease should be a national health priority.

Kerry-Ann F O’Grady GDipPH, MAppEpid, PhD · Debbie M Taylor-Thomson BPharm · Anne B Chang FRACP, MPHTM, PhD · Paul J Torzillo AM, MB BS, FRACP, FJFICM · Peter S Morris MB BS, FRACP, PhD · Grant A Mackenzie MB BS, PhD · Gavin R Wheaton MB BS, FRACP, FCSANZ · Paul A Bauert MB BS, FRACP · Margaret P De Campo FRANZCR, MPH, GDipEpibiostats · John F De Campo FRANZCR, MHA, FRACMA · Alan R Ruben MB BS, MAppEpid

I was asked to review the article below, and found it a compelling read. Zimmet has clearly gone to central Australia with an open heart and mind, and has discovered an intriguing world previously not known to him. He ends his article with a gentle challenge to those of us who have the privilege to work in health care, to consider whether our current methods are best practice, and whether they are best suited to all who seek our help. Having read this article, I found myself with two unanswered questions. First, given that there have now been several generations of Aboriginal people advocating for improvement to the dire circumstances in Aboriginal health, how is it that our young colleagues are still so shocked when they come to our communities? What is it that we (older Aboriginal people) have failed to say to get the attention of our health care providers, and their teachers? Second, how can we see to it that we produce many more graduates of the quality of Zimmet, who see the world with fresh eyes, are not afraid to ask the obvious questions, and are bold enough to tell us all that the Emperor is indeed naked? I strongly recommend that Journal readers take the time to read this article, and spend a moment or two in reflection to examine their own souls, to see if they can rise to this young man’s challenge. Louis G Peachey, BMed, FACRRM, Foundation President, Australian Indigenous Doctors Association, Canberra, ACT. In the Alice Springs paediatric ward, the vast majority of the 20 or so children are Aboriginal. They often have unique first names with an African–American or biblical flavour and distinctive spellings. Some come from town, while others travel from hundreds of kilometres away. Parents often lie with their children on mattresses on the floor, watching Disney DVDs, drawing, and waiting for the sporadic visits of hospital staff. For families, a visit to the ward can mean a period of isolation from their community or time with relatives who live in Alice Springs or who also happen to be in the hospital. It may be an unwanted upheaval from relatively peaceful community life, or an urgent and welcome respite from upheavals at home. What distinguishes the Alice Springs ward most is the type and severity of paediatric health issues. There is a whole other spectrum of health and disease in central Australia — one that challenges the heart and the mind. Labels that don’t stickThe categorisations of disease as I knew them after several years working in Melbourne seemed to collapse when I arrived in Alice Springs. Trying to apply learnt diagnostic and management techniques proved futile in the face of the ostensibly distinct nature of “common” illnesses like gastroenteritis, pneumonia and ear infections in central Australian children, let alone their coexistence with nutritional, social, cultural and historical factors. It is not uncommon to see 4-month-old infants with perforated ear drums. In contrast to coastal city paediatrics, “pink” or “red” tympanic membranes suggesting otitis media do not show up as threats on the diagnostic radar. Ear examination in central Australia is focused on detecting the presence or absence of pus or perforation of the tympanic membrane. Anything less is considered “healthy”. A child presenting with “gastroenteritis” can mean anything from a prolonged cryptosporidium infection to multiple parasitic and worm infestations. Families often refer to these different ailments generically as “guts ache”. Treatment ranges from frequent correction of significant acidoses and hypokalaemia, to using nitazoxanide to treat cryptosporidium. This drug is only available on the special access scheme in Australia, not because it is unsafe, but because so few children need it. The evidence for its use, however, is limited to a few studies, mainly in settings somewhat different to Alice Springs. This is a recurring theme in paediatric medicine here — that evidence from either “first-world” metropolitan research centres or the “third-world” does not necessarily translate to what health workers see in central Australia, a “fourth-world” inside our country. Further, century-old pathological definitions that define disease rather than causation or environmental and social contributors often do not provide us with adequate solutions today. They help us to heal the surface of the skin or lungs, perhaps the lining of the gut, but not always the deeper tissues. The tragically prevalent conditions of chronic suppurative otitis media and chronic suppurative lung disease in children could perhaps be more accurately defined as “chronic exposure to over-crowding, tobacco smoke, inadequate nutrition and bacterial respiratory tract colonisation”. Similarly “failure to thrive” might often be described as “failures of family and community structures, supports and function”. Effects on causesAs paediatric doctors at the hospital, we work closely with families, Aboriginal liaison officers, community organisations and even traditional healers. However, I feel we see the causative cycles of the social determinants of Aboriginal child health, yet cannot always avert the outcomes. Just like someone watching the desert heat evaporate the land’s water over several days, I often feel incapable of doing more than merely waiting for the storm to arrive. Chronic ear infections cause endemic conductive hearing loss. The result for many children is developmental, learning and behavioural issues with profound ramifications for schooling, employment prospects, parenting capabilities, their own future children and their communities. We try to encourage and empower adults to mop their children’s suppurating ears regularly to facilitate healing and help antimicrobial ear drops reach the middle ear, but, often, we don’t properly explain why this is important, or there are no tissues available at home, no refrigerator to safely store the antibiotics, or more urgent daily issues arise. The daunting challenges of social disadvantage, disharmony, and physical distance can cause health practitioners to minimise our efforts. Sometimes optimum care is not provided on the basis of assumptions about what families will do when they leave. Rationalisations such as “they are not going to give the medication so why bother” or “they’ll be back with the same problem in a week” are sometimes heard. This can be a result of us not being able to see the children and families we look after in the foreground, with their own unique strengths and weaknesses, existing within and beyond these pervasive problems. Seeing difference, seeing ways through the gapsOur lack of flexibility and our inability to — accommodate difference can potentially perpetuate the health gaps. There are many situations in which the pressures of the ward have limited my time to be patient with a family, listen carefully, or negotiate a treatment plan meaningfully, in order to understand the family’s perspective better and expedite the child’s recovery. I have also found it extremely important always to look for differences between individual Aboriginal children and families to prevent comical gaffes, therapeutic disasters and the spectre of racism. Aboriginality is not homogenous. Alice Springs and central Australian people have a complexity that is at odds with the predictability of the desert heat. If we accept that a fundamental component of racism is generalisation, then we are all caught in its web more than we would like to admit. This can be as simple as me assuming that a very dark skinned Aboriginal mother could speak an Indigenous language, or that her English would be limited. Neither was true and she spent much time articulating her worries about breastfeeding. Language difficulties play a major role in paediatric health gaps in central Australia. So much still seems to be “lost in translation” in the gap between English and the multitude of local Aboriginal languages, and between differing understandings of symptom durations, rationales for treatment and discharge plans. Translators are not available after hours, when clarity is often critical. There are other dimensions. There are well known and beautiful places near and around Alice Springs called “gaps”, where the mountain ranges part to reveal waterholes and jagged red rock facades. These geographical gaps were given names like Heavitree Gap or Emily’s Gap by Anglo-European explorers. They are important dreaming sites for the local Arrernte people. Heavitree Gap is a place where the local traditional owners would formally welcome and accept visiting people onto their lands. For Arrernte people then, talk of closing “gaps”, may have very different meanings from our own. Dr Patricia Miller, a senior Arrernte woman, recalls another elder fearing that someone would literally close Heavitree Gap, thereby preventing people and transport from entering Alice Springs directly. She could not understand why there not been meetings to explain the closure of such a significant cultural place. “Closing the gap” can also have an array of ramifications for different families. For some, it may mean having to bring their children to clinics for a seemingly endless array of needles, whether for vaccinations, antibiotics or iron supplementation. For others, it is about not having to tell three or four different doctors in one day what has happened to their child after being transferred from a remote area, or not having to explain the same thing repeatedly because community and hospital information systems are in silos. For some Aboriginal people, “closing the gap” may mean doctors learning to “speak” to each other better. For one family, “closing the gap” is a hope for a larger home in which 20 people do not have to share two bedrooms, so their child can get some sleep away from noisy adults. For another family living in town, it may be that “closing the gap” means not having their child’s Aboriginal status questioned because of his or her lighter skin colour and mixed descent. Looking and listeningSome of the health gaps and misunderstandings in health care also relate to how, for many Aboriginal people, conceptions of space and time are significantly different to medical thought. The chain of cause and effect, and the ideas that illnesses have names, time courses and scientific reasons for appearing are often not the main paradigms for our patients in central Australia. A grandmother explained to me, with the assistance of an Aboriginal liaison officer, that the reason why her 18-month-old grand-daughter was not eating or growing properly was not because she was still breastfed by her mother and had trouble eating solids, but because the unborn baby her mother was carrying was playing tricks and interfering with its sibling’s eating habits. A few mothers on the ward told me about the changing winds and misplaced internal rocks that had ravaged their children’s bodies. They had taken their children to see the traditional healers before seeing a doctor. One mother, a painter and former Aboriginal liaison officer, told me she struggled with prioritising one form of healing over the other. This mother and her child are just one example of the astounding resilience of children and families in central Australia. Their ability to remain healthy, keep a sense of humour, stay positive and return to the hospital or clinic for a visit is remarkable. It is even more extraordinary considering the harsh environment and limited resources. This resilience needs to be supported and harnessed at all costs. It is critical that we strengthen Aboriginal families by using their unique structures, dynamics, hopes and needs. The challenge, then, is to balance a paediatric perspective with an Aboriginal one. The two are not mutually exclusive. We have to keep our paediatric medical gaze sharp and unprejudiced. An evidence base should be built for treating the unique conditions that are seen in central Australian children. Concurrently, ensuring that national standards of nutritional and child development health are implemented in the region is paramount, as a matter of health equity and human rights. We need to make sure that what we know as “truth” in paediatric medicine is applied equally to children living in remote areas and, at the same time, keep our eyes, ears and hearts open to the varying strengths and needs of each child, carer, family or community. We should listen to what they tell us and be comfortable with the silences. We need to find ways through the gaps from several vantage points, with Aboriginal people leading the way back to their own health.

Marcel D Zimmet MB BS/BA(Hons)

To the Editor: We report the case of a child who presented with intussusception due to heterotopic pancreas. A 10-year-old girl presented with right iliac fossa pain and nausea. She was febrile (38.4°C) and had right iliac fossa tenderness with guarding. When she started vomiting, she was taken to theatre with a provisional diagnosis of acute appendicitis. During the diagnostic laparoscopy, her appendix did not appear inflamed and she was found to have intussusception due to a 10 mm tumour in the ileum, about 80 mm from the ileocaecal valve. The tumour was resected, and microscopic examination showed the presence of ducts and lobules of exocrine acini, with occasional foci of islet cell tissue extending into the muscularis propria. These features were consistent with heterotopic pancreas. Heterotopic pancreas is defined as the presence of pancreatic tissue outside its usual location and without anatomic relation either of continuity or of vascularisation with the pancreas.1 Its overall surgical incidence has been estimated as one case in every 500 abdominal explorations at Mayo Clinic.1 During embyrogenesis, the normal pancreas arises from several evaginations originating from the wall of the primitive duodenum. If one or more evaginations remains in the wall of the bowel, it may be carried away from the rest of the gland by the developing gastrointestinal tract and give rise to heterotopic pancreas.2 In adults, the most common locations for heterotopic pancreas, in descending order of frequency, are the stomach, duodenum and jejunum.3 However, in children, the most common location is within a Meckel diverticulum.3 Heterotopic pancreas is usually asymptomatic, and most cases have been found coincidentally at laparotomy performed for other abdominal conditions.4 However, in some people, pathological changes such as inflammation, abnormal hormone secretion and cystic degeneration within the heterotopic pancreas have been reported to cause abdominal pain and discomfort.3,4 Isolated heterotopic pancreas in the ileum is very rare and usually asymptomatic. The lesion within the wall of the ileum may act as a lead point,3,5 and this is thought to be the mechanism of intussusception. It has also been postulated that intussusception arises from local disturbance in the motility of the small intestine caused by the heterotopic pancreas.3

Narotam R Jootun · Hock P Cheah · Siddath C Fernando · William S Munro · Martin Veysey

Incorrect figure: In “Early evidence for direct and indirect effects of the infant rotavirus vaccine program in Queensland” in the 3 August 2009 issue of the Journal (Med J Aust 2009; 191: 157-160), there was an error in Box 1 (Lambert et al). Under “(a) Notifications”, the values for the 5–19-years and 20–64-years age groups should have been reversed. Box 1, with the corrected figure, is reproduced here. 1 Percentage change in rotavirus notifications, tests performed* and tests positive* after introduction of a publicly funded infant rotavirus vaccination program in Queensland in July 2007 * Testing performed by Queensland Health Clinical and Statewide Services. † Percentage change in the number of rotavirus notifications in 2007 and 2008 compared with the number in 2006. ‡ Percentage change in the number of rotavirus tests performed in 2007 and 2008 compared with mean annual age group-specific values from 2000 to 2006. § Percentage change in the proportion of tests positive for rotavirus in 2007 and 2008 compared with age group-specific values from 2000 to 2006.

Stephen B Lambert · Cassandra E Faux · Lisa Hall · Frances A Birrell · Karen V Peterson · Christine E Selvey · Theo P Sloots · Michael D Nissen · Keith Grimwood

Cough is a common and distressing symptom that results in significant health care costs from medical consultations and medication use. Cough is a reflex activity with elements of voluntary control that forms part of the somatosensory system involving visceral sensation, a reflex motor response and associated behavioural responses. At the initial assessment for chronic cough, the clinician should elicit any alarm symptoms that might indicate a serious underlying disease and identify whether there is a specific disease present that is associated with chronic cough. If the examination, chest x-ray and spirometry are normal, the most common diagnoses in ADULTS are asthma, rhinitis or gastro-oesophageal reflux disease (GORD). The most common diagnoses in CHILDREN are asthma and protracted bronchitis. Management of chronic cough involves addressing the common issues of environmental exposures and patient or parental concerns, then instituting specific therapy. In ADULTS, conditions that are associated with removable causes or respond well to specific treatment include protracted bacterial bronchitis, angiotensin-converting enzyme inhibitor use, asthma, GORD, obstructive sleep apnoea and eosinophilic bronchitis. In CHILDREN, diagnoses that are associated with removable causes or respond well to treatment are exposure to environmental tobacco smoke, protracted bronchitis, asthma, motor tic, habit and psychogenic cough. In ADULTS, refractory cough that persists after therapy is managed by empirical inhaled corticosteroid therapy and speech pathology techniques.

Peter G Gibson MB BS, FRACP · Anne B Chang FRACP, MPHTM, PhD · Nicholas J Glasgow FRACGP, MD, FAChPM · Peter W Holmes MB BS, FCCP, FRACP · Peter Katelaris MB BS, MD, FRACP · Andrew S Kemp MB BS, FRACP, PhD · Louis I Landau AO, MD, FRACP · Stuart Mazzone PhD · Peter Newcombe DipT, BEd, PhD · Peter Van Asperen MB BS, MD, FRACP · Anne E Vertigan BAppSc(SpPath), MBA, PhD

Objective: To assess whether the components of the Healthy Kids Check (HKC), a preschool screening check recently added to the Australian Government’s Enhanced Primary Care Program, are supported by evidence-based guidelines or reviews.Data sources: Guideline and MEDLINE databases were searched for guidelines and systematic reviews published between 2000 and 2008 that were relevant to screening, prevention or well-child care in primary health care, and including children of preschool age. Search subjects reflected the HKC components: growth, weight, obesity, vision, hearing, oral health, enuresis, encopresis, allergic disease and food allergies.Study selection: 34 relevant guidelines or reviews were retrieved.Data extraction: For each component of the HKC, guidelines addressing the presumed rationale for screening, or the test or tool required to implement it, were reviewed. Relevant evidence-based and consensus-based guideline recommendations were assessed as either supporting or opposing components of the HKC, or stating that the evidence was insufficient to recommend screening of preschool children.Data synthesis: Guidelines were often inconsistent in their recommendations. Most of the components of the HKC (eg, screening for chronic otitis media and questioning about toilet habits) are not supported by evidence-based guidelines relevant to the primary care setting, though a number of consensus-based guidelines are supportive.Conclusions: There is currently a dearth of evidence relevant to child health surveillance in primary care. The components of the HKC could be refined to better reflect evidence-based guidelines that target health monitoring of preschool children.

Karyn E Alexander MB ChB, FRACGP, MPH · Danielle Mazza MD, FRACGP, DRANZCOG

To the Editor: We present this case to highlight the differential diagnosis of afebrile seizures in patients from many asset-poor nations. A 3-year-old Congolese girl presented with sustained loss of consciousness after a prolonged generalised seizure. She had migrated, with her family, 12 months previously after a long period in a Zambian refugee camp. She was intubated briefly and given intravenous benzodiazepines. She made an uneventful recovery; she was discharged from hospital after 2 days. This was her first seizure and there was no history of fever, trauma or poisoning. The parents declined long-term anticonvulsants. Apart from mild malaria, she had been previously well and showed normal development. HIV serology and results of blood films for malarial parasites were negative; other blood tests, including an eosinophil count, were normal. Cerebral magnetic resonance imaging (MRI), performed because the diagnosis was unclear and the patient had had a prolonged seizure, revealed a single 8 mm cyst, with an enhancing wall and surrounding oedema, in the left frontal lobe. The cyst contained a scolex, pathognomonic of neurocysticercosis (Box). There were multiple foci throughout the brain, indicating active and resolving cysts. Serology results for Taenia solium were negative at presentation and 3 months later. The child was treated with 8 days of albendazole and 3 days of dexamethasone. Repeat MRI 2 months after presentation showed significant improvement, with a residual 3 mm calcified focus. The child has remained seizure-free for 18 months. Neurocysticercosis is caused by larvae of the pork tapeworm T. solium, which may encyst in the brain, eye or spinal cord, after ingestion of ova-contaminated food or water.1 In contrast, ingestion of encysted larvae (cysticerci) in undercooked meat results in intestinal infection with the adult tapeworm.1 Neurocysticercosis is common in many asset-poor countries, including those in Asia and sub-Saharan Africa from where many people in humanitarian refugee programs originate.2 In areas where it is endemic, T. solium is a leading cause of epilepsy in children and adults.3 The diagnosis of neurocysticercosis is difficult and the diagnostic differential is broad. Cerebral imaging showing typical lesions containing a scolex is diagnostic. T. solium serology is insensitive, especially in children with few cysts. Anticercal antibodies or cysticercal antigens in the cerebral spinal fluid are helpful, but these investigations are not widely available (they are available from the Centers for Disease Control and Prevention, Atlanta, United States). Treatment with anthelmintics is controversial; parasites may die spontaneously and treatment may cause local inflammation (reduced by steroids), which potentially exacerbates seizures or causes local tissue damage.4 Ocular cysticercosis should be excluded before anthelmintic treatment as the resultant inflammation may compromise sight; surgical excision should be considered if ocular cysticercosis is present.4 Empirical anthelmintics, often given before departure or following resettlement to people at risk, may potentially precipitate seizures.5 We treated this child with albendazole as there were multiple lesions likely to contain live parasites, and because anticonvulsants were declined. This case highlights that neurocysticercosis is a possible treatable cause of afebrile seizures in patients migrating from, or with a history of visiting, endemic areas, including resettled refugees. Clinicians in affluent countries are often unfamiliar with the disease, yet are managing increasing numbers of people at risk. Misdiagnosis is of particular concern because brain imaging is not routinely performed in children presenting with their first afebrile seizure. Magnetic resonance image of brain of 3-year-old girl showing cysticercus Encysted scolex of Taenia solium, surrounded by enhancing wall and significant oedema, in left frontal cerebral lobe.

Juliette M Lucey · James McCarthy · David P Burgner

Incorrect and misleading use of tense: In the Chistmas Offerings article “Cough disorder: an allegory on DSM-IV” in the 7/21 December 2009 issue of the Journal (Med J Aust 2009; 191: 674-676), in the second paragraph under the heading, “The problem with the DSM”, “is overdiagnosed” was incorrectly used in place of “was overdiagnosed”, thus giving the impression that schizophrenia continues to be overdiagnosed in the United States. Schizophrenia is no longer overdiagnosed in the US relative to Europe and Australasia.

Peter I Parry

Objective: To examine the symptoms, level of suffering, and care of Australian children with cancer at the end of life.Design, setting and participants: In a study conducted at the Royal Children’s Hospital, Melbourne, parents of children who had died of cancer over the period 1996–2004 were interviewed between February 2004 and August 2006. Parents also completed and returned self-report questionnaires.Main outcome measures: Proportions of children suffering from and treated for various symptoms; proportion of children receiving cancer-directed therapy at the end of life; proportion of children whose treatment of symptoms was successful; location of death.Results: Of 193 eligible families, 96 (50%) were interviewed. All interviews were conducted in person, and occurred a mean of 4.5 years (SD, 2.1 years) after the child’s death. Eighty-four per cent of parents reported that their child had suffered “a lot” or “a great deal” from at least one symptom in their last month of life — most commonly pain (46%), fatigue (43%) and poor appetite (30%). Children who received cancer-directed therapy during the end-of-life period (47%) suffered from a greater number of symptoms than those who did not receive treatment (P = 0.03), but the severity of symptoms did not differ between these groups. Of the children treated for specific symptoms, treatment was successful in 47% of those with pain, 18% of those with fatigue and 17% of those with poor appetite. Of the 61 families who felt they had time to plan where their child would die, 89% preferred to have their child die at home. The majority of children (61%) died at home. Of those who died in hospital, less than a quarter died in the intensive care unit.Conclusions: Relatively high rates of death at home and low rates of unsuccessful medical interventions suggest a realistic approach at the end of life for Australian children dying of cancer. However, many suffer from unresolved symptoms, and greater attention should be paid to palliative care for these children.

John A Heath PhD, FRACP · Naomi E Clarke BMedSc(Hons) · Susan M Donath BSc(Hons), PhD · Maria McCarthy BAppSc, MAppSc · Vicki A Anderson BA, PhD · Joanne Wolfe MD, MPH

To the Editor: We write to encourage policy debate over newborn screening for congenital adrenal hyperplasia (CAH). Classical CAH is a severe, life-threatening disease affecting about one in 15 000 liveborn infants in Australia.1 An inexpensive screening test for newborns is available, but this test is not included in the current newborn screening program in Australia. Three-quarters of children with CAH have the severe salt-wasting type that typically presents with failure to thrive, and progresses to severe hyponatraemic, hyperkalaemic dehydration and shock due to an adrenal crisis within weeks of birth. CAH is the most common cause of ambiguous genitalia in neonates (due to virilisation from adrenal androgens in utero); girls with CAH may be incorrectly assigned as boys unless the diagnosis is made without delay. CAH can be easily detected in neonates before the onset of illness by an established heel-prick newborn screening test that has good specificity and sensitivity, especially when used together with second-tier testing. Screening for CAH has been available for 30 years internationally, and is used in all American states, New Zealand and many countries in Europe, Asia and Latin America. Newborn screening reduces mortality and incorrect sex assignment.2 Case reports from Australia3 and overseas4 have shown that undiagnosed CAH is a cause of apparent sudden infant death syndrome. These deaths could have been prevented if newborn screening was in place. A pilot study in New South Wales showed that newborn screening for CAH prevented salt-wasting crises and their potential long-term consequences.1 The cost-effectiveness of newborn screening is difficult to measure, and there is little published evidence on this subject. Although a recent study suggested that CAH screening is not cost-effective,5 the only outcome assessed was mortality; other benefits of early diagnosis and intervention — including reduced morbidity and psychological impact — were not assessed. Newborn screening for CAH is not expensive; the cost per test within the laboratory is about $2, and the incremental cost per infant is in line with other newborn screening tests. In a recent survey, the Australasian Paediatric Endocrine Group found that 91% of paediatric endocrinologists considered provision of newborn screening for CAH in Australia to be very important. The Newborn Screening Joint Subcommittee of the Human Genetics Society of Australasia unanimously supports the inclusion of newborn screening for CAH in all Australian states. Two Australian parent and patient advocacy organisations — the CAH Support Group Australia, and Caring and Living as Neighbours — also strongly support the proposal for adding newborn screening for CAH to the current screening program. Despite clear predicted benefits and agreement among key stakeholders and expert advisers, no state in Australia currently screens for CAH. It is the state governments — guided by the Australian Health Ministers’ Advisory Council — who decide on funding for newborn screening tests, and who should be accountable for acting against the weight of expert opinion and systematic evidence.

Garry L Warne · Katrina L Armstrong · Thomas A Faunce · Bridget M Wilcken · Avihu Boneh · Elizabeth Geelhoed · Maria E Craig

To the Editor: Our positive experience with insulin pump therapy (IPT) in children without private health insurance contrasts with that of Thong and colleagues,1 who found that IPT did not significantly reduce glycated haemoglobin (HbA1c) levels in uninsured adults. IPT improves metabolic control, reduces the risk of microvascular complications and improves quality of life in children with type 1 diabetes mellitus.2,3 Private health insurance fully rebates the cost of an insulin pump, but many uninsured Australian children with type 1 diabetes are denied access to IPT because their family cannot afford the $8000 purchase price of an insulin pump. The other major impediment to using IPT is the paucity of access to skilled local IPT teams. In November 2008, to improve access to IPT, the federal government introduced a means-tested subsidy (to a maximum of $2500 per child) to be administered through the $5.5 million Type 1 Diabetes Insulin Pump Program.4 By 30 June 2009, the program had subsidised only 31 children for insulin pump purchase (unpublished correspondence from the Hon Mark Butler MP, Parliamentary Secretary for Health, to Mr Darren Chester MP, Member for Gippsland, July 2009). The largest user of this scheme, Gippsland Paediatrics (a private practice in rural Victoria), commenced IPT in 11 of the 31 children. Through local service clubs and other charitable institutions, we raised the funds required to pay the $5500 balance for all 11 children.5 Six other financially disadvantaged Gippsland Paediatrics patients had obtained insulin pumps through grants or community fundraising before the government subsidy program was introduced. Thus we have experience of 17 children, aged between 4 and 18 years (mean, 10.8 years) who were recipients of “donor” pumps. This sample represents about a quarter of the local children with type 1 diabetes and almost two-fifths of the 46 patients we have commenced on IPT. To evaluate the metabolic outcome of IPT for these 17 children, we conducted a retrospective analysis of glycaemic control by comparing the average level of HBA1c during the 12 months before commencing IPT with the most recent HbA1c level. The pre-IPT mean HbA1c level of children using the donor pumps was 9.2% (SD, 1.45%), which fell to 7.6% (SD, 0.83%) (P < 0.001) after a mean IPT duration of 10.2 months (SD, 6.1 months). In children aged 12 years or under (10 patients), the mean HbA1c level fell from 9.0% (SD, 0.94%) to 7.6% (SD, 0.43%) (P < 0.001) after a mean IPT duration of 11.9 months (SD, 7.6 months). In the remaining seven patients, aged 13–18 years, the mean HbA1c level fell from 9.4% (SD, 2.0%) to 7.8% (SD, 1.43%) (P = 0.03) after a mean IPT duration of 7.6 months (SD, 1.4 months). Gippsland Paediatrics uses the RADICAL (Rural Australian Diabetes — Inspiring Control Activity & Lifestyle) model of care.6 The model consists of a collocated multidisciplinary team, including a general paediatrician, diabetes educator and counsellor, with the patient and family receiving proactive emotional support, consistency of personnel, and point-of-contact HbA1c testing. We individualise our approach through regular case conferences and try to match therapy with desired lifestyle. Our study demonstrated that, using this model, IPT improves glycaemic control in uninsured children targeted by government policy — at least in the short term. To improve short-term health and reduce long-term diabetic complications in families who cannot afford insulin pumps, government programs need to make IPT more accessible to those families and support local multidisciplinary IPT teams.2

Peter W Goss

To the Editor: Norovirus, previously known as the Norwalk agent, is a recognised cause of acute diarrhoeal illness in all age groups, but its significance in hospitalised children is poorly described. Noroviruses cause infection worldwide and year-round, with a distinct increase in disease occurrence in colder months.1 Rotavirus has long been recognised as the most important viral cause of gastroenteritis in young children, causing significant morbidity, as well as cost to the community of hospital admission and lost parental productivity.2 In July 2007, two new rotavirus vaccines were licensed for use in Australian infants; their use has reduced severe rotavirus disease requiring hospital admission.3 One difficulty in accurately documenting the role of norovirus in childhood acute diarrhoeal illness has been the limited availability of routine diagnostic testing. Enzyme-linked immunosorbent assay (ELISA) for noroviruses is now available commercially; it has limited sensitivity of 55%–93% but good specificity of 73%–97%. We retrospectively reviewed the frequency of detection of norovirus in the faecal samples taken from inpatients and outpatients with acute gastroenteritis at a tertiary paediatric hospital. We tested stool samples of 3962 children with episodes of acute diarrhoeal illness in a 12-month period (2007) and detected norovirus in 122 (3.1%). Ninety-one of the children infected with norovirus were admitted to hospital; 63 patients had a stay of less than 7 days with a median of 1 day, while 28 patients where in hospital for more than 7 days. The norovirus infection in 30 of the inpatients (33%) was hospital-acquired. Most hospital-acquired infections occurred in patients hospitalised for more than 7 days (19 of 28; 68%), and most of these patients had predisposing medical conditions, predominantly immunosuppression due to treatment for malignancy or other causes. Norovirus is a significant cause of viral gastroenteritis in infants and children. Our findings are comparable with those of other studies, which indicate that norovirus infection causes 20%–88% of viral gastroenteritis in children and is responsible for a significant proportion of hospital admissions of children with gastroenteritis.4,5 With the introduction of universal rotavirus vaccination for Australian infants, the importance of norovirus as a cause of gastroenteritis in infants and children is likely to increase. We recommend that hospitals which admit children consider using norovirus testing to establish the incidence and prevalence of disease, and to inform public health authorities responsible for infection control policy and practices.

Alison M Kesson · Nicola Benwell · Elizabeth J Elliott

Objective: To compare the clinical effectiveness of single-dose azithromycin treatment with 7 days of amoxycillin treatment among Aboriginal children with acute otitis media (AOM) in rural and remote communities in the Northern Territory. Design, setting and participants: Aboriginal children aged 6 months to 6 years living in 16 rural and remote communities were screened for AOM. Those diagnosed with AOM were randomly allocated to receive either azithromycin (30 mg/kg as a single dose) or amoxycillin (50mg/kg/day in two divided doses for a minimum of 7 days). We used a double-dummy method to ensure blinding. Our study was conducted from 24 March 2003 to 20 July 2005. Main outcome measures: Failure to cure AOM by the end of therapy; nasal carriage of Streptococcus pneumoniae and non-capsular Haemophilus influenzae (NCHi). Results: We followed 306 of 320 children (96%) allocated to the treatment groups. Single-dose azithromycin did not reduce (or increase) the risk of clinical failure (50% failure rate [82/165]) compared with amoxycillin (54% failure rate [83/155]) (risk difference [RD], – 4% [95% CI, – 15% to 7%]; P = 0.504). Compared with amoxycillin, azithromycin significantly reduced the proportion of children with nasal carriage of S. pneumoniae (27% v 63%; RD, – 36% [95% CI, – 47% to – 26%]; P < 0.001) and NCHi (55% v 85%; RD, – 30% [95% CI, – 40% to – 21%]; P < 0.001). Nasal carriage of S. pneumoniae with intermediate or full resistance to penicillin was lower (but not significantly so) in the azithromycin group (10% v 16%), but this group had significantly increased carriage of azithromycin-resistant S. pneumoniae (10% v 3%; RD, 7% [95% CI, 0.1% to 12%]; P = 0.001). Carriage of β-lactamase-producing NCHi was about 5% in both groups. Conclusion: Although azithromycin reduced nasal carriage of S. pneumoniae and NCHi, clinical failure was high in both treatment groups. The possibility of weekly azithromycin treatment in children with persistent AOM should be evaluated. Trial registration: Australian Clinical Trials Registry ACTRN 12609000691246.

Peter S Morris MB BS, PhD, FRACP · Gaudencio Gadil MD · Gabrielle B McCallum BNurs, MPH · Cate A Wilson EN, BPsych(Hons) · Heidi C Smith-Vaughan BAppSci, PhD · Paul Torzillo MB BS, FRACP, JFICM · Amanda J Leach BAgSc(Hons), MAgSc, PhD

Two sisters aged 6 and 11 years presented with pruritic inflammatory lesions, one on the arm and one on the shoulder (Figure). The lesions appeared 72 hours after the girls had black henna tattoos applied while they were on holiday in Egypt. On examination, each girl had eczematous eruptions that perfectly outlined the tattoo. Patch tests were positive for paraphenylenediamine, a known potent contact allergen. Black henna tattoos are a frequent source of sensitisation to paraphenylenediamine among Australian tourists to South-East Asia.1 Potential significant consequences include allergic reactions to hair dyes, textile dyes, anaesthetics, sulfonamides and sunscreens containing p-aminobenzoic acid.

Pablo J Almeida · Leopoldo Borrego