Child health

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

The DSM-IV is more a reliable descriptive nomenclature than a valid classification of diseases The Diagnostic and statistical manual of mental disorders, third edition (DSM-III), published by the American Psychiatric Association in 1980, sought to define psychiatric syndromes in a way that increased the reliability of psychiatric terminology and diagnoses between practitioners and nations. The DSM-III’s introduction cautioned that, with regard to aetiology, it was a “generally atheoretical” document. The subsequent edition, the DSM-IV, published in 1994, went further, and cautioned specifically against diagnoses being applied in a “cookbook” fashion. Despite these warnings, conversion of the description of psychiatric disorders to discrete disease entities has not only occurred but, I believe, has also become problematic. Here, I present an allegory of a boy with “cough disorder” to illustrate. It was time for the annual post-prandial Christmas dinner nap. A niece was coughing on inhaled lemonade. Dreams are often allegorical; it had been a busy year, and I started to dream. “Cough disorder” — a dreamA mother came into my consulting room with her son. “He’s got cough disorder”, she declared. She’d read the symptoms on the internet: “a short, repetitive noise coming from the throat associated with the expulsion of air from the lungs”. This was, indeed, true. The website had quoted the DSM-IV. That is, the fourth edition of the Diagnostic and statistical manual of human noises published by the American Phoniatric Association. “He’s clearly got cough disorder, and he needs Suppressalin cough suppressant”, the lad’s mother said. Suppressalin had been advertised via a link on the “Help for Parents of Kids with Cough Disorder” website. The young chap himself broke into a succession of hacking coughs as if to emphasise the problem, at which point his mother widened her eyes and slowly and firmly nodded, to emphasise the obviousness of the diagnosis. One that, presumably, was now even more clearly in need of the advertised pharmacotherapy. I sighed. That is, I “exhaled in concert with slight laryngeal constriction, following a deep diaphragmatic inhalation”, making a “soft, rather low-pitched noise”, and this occurred “in a situation of frustration, tension, tiredness or boredom”. (I noticed my noise, recognised I was in a situation of frustration, and recalled research showing I’d just stimulated my vagus nerve to maintain autonomic nervous system equilibrium.) I coughed, but it was the “ah hem” subtype; the “short, sharp, double noise emanating mainly from the larynx without significant pulmonary air expulsion”. This is not normally considered a pathological cough, although I noted the lad’s mother raised an eyebrow. I knew my “ah hem” cough was the prelude to my well worn (and weary) noise-educative spiel to parents of coughing kids. “Well yes, he does cough; I totally agree with you there”, I said, to get mum on side, and noticed a slight easing of her wary defensiveness. “But you see ‘cough disorder’ doesn’t tell us very much. It is not really a diagnosis but a description of behaviour.” She was starting to resume the wary defensive posture; the boy uttered a quick succession of coughs. I decided to look grave and said how concerning his coughing was, and that it was very important we thoroughly investigated it. She said the parents’ help website had indicated that Suppressalin was exactly what was needed, but I noticed she was now less certain, and I made a “hmmm” sound in a particular way, to indicate understanding and empathy, but also that I knew more. I was, after all, the doctor. I sensed she seemed willing to listen to the spiel. “Cough disorder is simply a description, a starting point”, I said. “We have to find out why your young man here is coughing. Cough disorder can have many causes, and, for some children, several causes can combine.” I went on to describe inhaled objects, drinks down the wrong way, asthma, croup, bronchitis, pneumonia, pharyngitis (the tickly throat cough), postnasal discharge, and rarer, more serious causes, such as throat and lung cancer, pneumothorax, bronchiectasis, silicosis and congestive cardiac failure. It could be a reaction to dust or cold dry air; there is always an environmental context. And, it could even be something as mild as a frequent habitual “ah hem” cough to try to gain attention. I had the lad’s mother’s attention now, and the lad himself had also stopped coughing and was listening. I said that his cough may not need Suppressalin (although I acknowledged that, for some kids, Suppressalin is very beneficial, and they may need it for many years). We went on to look collaboratively for what was causing the cough. Even dad came to the next consultation. I also had an informative telephone discussion with the child’s teacher, who told me how the boy generally stopped coughing by morning recess. The problem with the DSMThe astute reader may by now have guessed that my “dream” is an allegory about attention deficit hyperactivity disorder (ADHD), and that, by corollary, the “DSM of human noises” is the Diagnostic and statistical manual of mental disorders published by the American Psychiatric Association, currently in its fourth edition.1 The DSM is sometimes referred to as psychiatry’s bible. However, like the Bible, it should be mainly read as descriptive, not literal, truth. The problem dates primarily from 1980 and the publication of the DSM-III. At the time, psychiatric terminology suffered from a different problem — psychiatrists using the same labels for different conditions; in particular, schizophrenia, which was overdiagnosed in the United States compared with Europe (and Australasia).2 The DSM-III devised “operationalised criteria” — lists of symptoms to define descriptive “disorders”, so that everyone would at least know what behaviour was being described when a term like “schizophrenia” was used. Reliability is a necessary step on the road to validity. The DSM-III brought about a more reliable nomenclature and a more robust definition of syndromes, a vital prerequisite for psychiatric nosology (the branch of medical science dealing with the classification of diseases) to advance. However, the DSM-III was not meant to be read as a valid classification of diseases, even though it aspired towards that goal. Diagnoses in other areas of medicine also vary in levels of understanding of aetiology (eg, migraine is still a syndromal diagnosis, and hypertension is a diagnosis based on deviance from normative dimensions); however, the level of scientific knowledge is more advanced in many other areas, and many disease states are well understood. Psychiatry is not so far advanced. A further complicating factor in psychiatry is the, as yet, unresolved mind–brain problem,3 and that for such a social species as Homo sapiens, the psychosocial and intersubjective domains, including narrative and meaning, are not easily accessed by symptom checklists. The DSM-III and DSM-IV attempt to address this with their multi-axial approach to a range of factors, such as personality, concomitant medical disorders, psychosocial stressors and level of functional impairment, as well as the “V-code” diagnoses — codes used to indicate problems that aren’t clinical disorders — such as “parent–child relational problem”. Further complicating nosology is the issue of multicausality and equifinality — syndromal end states may comprise a clustering of individuals with quite different aetiologies for similar presenting symptoms. This is implied in the DSM introductions, with the DSM-III purporting to take a “generally atheoretical stance” with respect to aetiology, and the advice in the DSM-IV that it is “not to be used in a cookbook fashion”. Despite these warnings, all too often, collections of symptoms classified as disorders tend, in practice, to be thought of as disease entities in their own right. This is less problematic for severe psychotic disorders such as schizophrenia and manic-depressive psychosis (now called bipolar-I disorder in the DSM-IV), which likely represent underlying brain disease. However, I do think that it is problematic with what used to be called “neuroses”, and symptoms that overlap with temperament, personality and responses to stress and trauma, where the interactions of brain, mind, body, relationships and environment are multidirectional. So the problem is not so much with the DSM itself, but with the way it is often used pre-emptively. My allegory on ADHD could apply to “conduct disorder”, “oppositional defiant disorder”, “school refusal”, “autism spectrum disorder” or, particularly in the US, the controversial “paediatric bipolar disorder”4 which, although it is not defined in DSM-IV, can be argued reflects an overly reductionist “neo-Kraepelinian” approach5 that common use of the DSM tends to foster. A similar problem occurs with anxiety, depression and adult “bipolar spectrum disorders”. The problem of seeing all depressive states as homogeneous, differing only in severity, has been raised previously.6 In his 2005 presidential address to the Royal Australian and New Zealand College of Psychiatrists (RANZCP), Boyce referred to a “dumbing down” of psychiatry by using the DSM for simplistic “cookbook” diagnoses. He also referred to the pharmaceutical industry’s pervasive influence in medical research and medical education.7,8 In psychiatry, this influence often supports a reductionist biomedical model of human emotional and behavioural problems, rather than the systemic biopsychosocial model upheld by the RANZCP. A simplistic cookbook approach to the DSM would, indeed, seem to be in industry’s interests, as behavioural symptom clusters get reified to disease states, and marketing to both the medical profession and the public can support a “pill for every ill” approach.9 Such marketing finds fertile ground — in a busy world, the siren call of such simplicity in diagnosis and treatment is appealing to both the public and the medical profession. Such misapplication of psychiatric nosology was predicted two decades ago as the rise of “biologism”,10 and eloquently expressed by Lipowski in his 1988 presidential address to the Canadian Psychiatric Association as the rise of “mindless psychiatry”.11 (Lipowski also noted the perils of the other extreme — “brainless psychiatry” — in which all psychopathology is seen in only psychosocial terms, something this essay is not advocating.) DSM-associated biomedical reductionism has been noted by many American psychiatrists.12 In contrast, an alternative approach to psychiatric nosology proposes the “four perspectives of psychiatry” (“disease, dimension, behaviour, life story”),3 which is a more radical multi-axial approach than the DSM axes and seeks to balance the neo-Kraepelinian disease approach with the “neo-Meyerian” focus on biopsychosocial case formulation.13 It was described in a course at the recent American Psychiatric Association annual meeting titled “Going from the bio-bio-bio model forward to bio-psycho-social reasoning”.14 Where disorders most likely fit the disease model, as with the psychoses, there are promising proposals to refashion the upcoming fifth incarnation of the DSM — the DSM-V — to move beyond the descriptive approach and attempt to base psychiatric classification on underlying causes.15 Further changes proposed include greater emphasis on dimensional measures (eg, to look at subsyndromal risk factors for depression and possible prodromal psychotic symptoms, like suspiciousness, that may aid early detection), rather than categorical measures (such as currently, when meeting sufficient criteria indicates disorder, and below that implies no disorder) to better reflect clinical reality. On the other hand, the head of the former DSM-IV taskforce has expressed strong concern that such moves are premature, would “flood the world with . . . false-positive patients” who “would pay a high price” in stigma and by being overmedicated and, with respect to problems like excessive Internet use, that expansion of criteria in the DSM-V would further “inappropriately medicalise behavioural problems”.16 Despite, or even because of, this problematic nosology, psychiatry remains a complex but compelling and rewarding profession that requires time, and experience, patience and wisdom acquired through clinical and life experience in helping those who come for help. There are no short cuts, DSM or no DSM. Return to our allegorical dream of cough disorderThe dream ended happily. The lad and his parents came to understand that cough disorder was not a diagnosis but a description, and that his real problem — mild asthma — required a different medication, and then no medication at all when his parents stopped smoking in his presence. We had tried Suppressalin at one point, but it gave only short-term relief. The parents and I even had a more philosophical discussion about how the third edition of the DSM of human noises focused on defining human noises descriptively, at a time when some doctors talked about “cough” when they really meant “sneeze”, “burp” or “hiccup”, and how that was a good development back in 1980. But we also discussed how, as an atheoretical descriptive system, it generally gives no information about underlying causes, and how important the search for real causes is; this is something the family now appreciates. During my last session with this family, there were several repetitions of “ah yes” and “hmmm” (shorter, higher pitched subtype, usually indicative of agreement) — all, in my opinion, completely non-pathological noises, although I understand some do think them overused and claim to have medications for them. . . . I awoke. My niece was playing happily with her Christmas presents. The cause of her coughing — inhaled lemonade — had cleared.

Peter I Parry MB BS, FRANZCP, CertChild

Objective: To describe the patterns of screening for hepatitis C virus (HCV) infection in methadone-maintained pregnant women and their infants.Design, setting and patients: Retrospective review of medical records from one rural and two metropolitan hospitals in New South Wales for pregnant women on methadone maintenance treatment and infants born to these women between 1 January 2000 and 31 December 2006, as well as records for pregnant women who were not on methadone treatment.Main outcome measures: Rates of anti-HCV antibody and HCV RNA testing for pregnant women and their infants, and ages at which infants attended follow-up appointments.Results: Of 295 pregnant women on methadone maintenance treatment, 288 were tested for anti-HCV antibodies (98%), compared with 1995 of 9987 women who were not on methadone treatment (20%) (P < 0.001). Seropositive results were obtained for 243 women in the methadone group (84%) and 54 in the non-methadone group (3%) (P < 0.001), of whom 44 (18%) and 17 (31%), respectively, were subsequently tested for HCV RNA (P = 0.03). HCV RNA test results were positive for 31 (70%) and 10 (59%) seropositive women in the methadone and non-methadone groups, respectively (P = 0.39). Of infants of HCV-seropositive methadone-maintained mothers, 27% of those for whom we had follow-up attendance data received HCV screening, and one of these infants tested positive for anti-HCV antibodies and HCV RNA.Conclusions: Screening for HCV infection in the high-risk population of pregnant women on methadone maintenance treatment and their infants is inadequate. This could lead to significant underdetection of active HCV infection in this high-risk population, and their infants. Current screening guidelines may therefore need to be revised.

Anthony J W Liu,* MB BS, FRACP, MPH · Ethan I An,* BMedSc, MB BS(Hons) · Henry G Murray MB ChB, MRCOG, FRACOG · Emma Tetstall BSc(Hons), MB BS(Hons) · Marcel J Leroi FRACP, FRCPA, MMed(ClinEpi) · Ralph K H Nanan Dr med Habil (Germany), FRACP

To the Editor: Bronchiolitis, most often associated with respiratory syncytial virus (RSV), is a major cause of hospitalisation in young children. Those with chronic lung and congenital heart disease (the latter affecting about 192 births annually in Western Australia) are at particularly high risk.2 Immunoprophylaxis with the RSV monoclonal antibody palivizumab is effective in reducing severe RSV-related hospitalisations, and monthly immunoprophylaxis is recommended in high-risk children.2,3 Monthly immunoprophylaxis is costly; therefore, the most cost-effective schedule follows the times of peak RSV activity4 — usually the winter months, May to October. Using the Western Australian Data Linkage System,5 we investigated the seasonality of bronchiolitis hospitalisations (International Classification of Diseases-10 code J21) from 1996 to 2005 as a proxy for RSV-related illness. Data specifically for RSV-related illness were considered unreliable because some children may not have been tested for RSV, test results may not have been documented on hospital discharge notes, or RSV immunofluorescence tests may have given false negative results. Furthermore, RSV codes (B97.4, J12.1, J20.5, J21.0) were not used by hospitals in WA until July 1999. We identified 11 988 hospitalisations for bronchiolitis throughout WA among 245 249 births. Most bronchiolitis admissions (81%) were in children younger than 12 months. In the Perth metropolitan region, there was a clear winter seasonal pattern, with hospitalisations peaking in July. However, in the Kimberley region in northern WA, there was a sustained bimodal seasonality, with a peak in April and second peak in August (Box). Moreover, only 51.5% (469) of bronchiolitis admissions in the Kimberley and 61.5% (444) in the Pilbara–Gascoyne (located in mid-north WA) occurred between May and October, as opposed to 84.3% (6354) in the metropolitan region. These data support an earlier implementation and longer dosing schedule with palivizumab for high-risk children in the Kimberley and Pilbara–Gascoyne than for those in Perth. Our study has some limitations. Not all bronchiolitis hospitalisations may be caused by RSV. However, when we investigated only those hospitalisations with a specific RSV code, the monthly distribution showed a similar pattern. Additionally, timing of RSV activity, and therefore bronchiolitis, may vary from year to year. Although the numbers were too small to allow separate analysis by calendar year, bronchiolitis hospitalisations in the Kimberley showed extended seasons in 8 of the 10 years. Our findings support the need for each jurisdiction to know its seasonal pattern of bronchiolitis and RSV hospitalisations, and to implement recommended palivizumab schedules accordingly. Such use of extended prophylactic regimens may well require its cost-effectiveness to be reconsidered. Our analysis highlights the relevance of population-based data linkage studies to clinical care policy. Monthly distribution of bronchiolitis hospitalisations by region of child’s birth, 1996–2005

Hannah C Moore · Anthony D Keil · Peter C Richmond · Deborah Lehmann

To the Editor: In their national analysis, Robson and colleagues found less favourable outcomes among term singleton babies born in public hospitals than in private hospitals.1 Most health services research is non-randomised, and it is unrealistic to expect studies such as this to be as internally valid as a randomised controlled trial.2 As noted by others,3,4 in the absence of randomisation, it is difficult to untangle the myriad differences between mothers, babies, and the care provided in private and public hospitals (ie, the results might be subject to confounding). Robson et al statistically accounted for the potential confounding effect of maternal smoking (although these data were only available for about half the mothers), age, Indigenous status, parity, diabetes, hypertension, rurality and method of birth. We replicated their analysis using the Queensland Perinatal Data Collection (July 2005 – December 2007), which included virtually complete data on maternal smoking. Our analysis of 124 300 term singleton babies gave an adjusted odds ratio (AOR) for perinatal mortality of 2.0 (95% CI, 1.4–2.7), which is similar to that reported by Robson et al. Using more detailed data from the Queensland dataset, we statistically adjusted for other potential confounders — including pre-existing and gestational diabetes, pre-existing and pregnancy-induced hypertension, pre-eclampsia, eclampsia, antepartum haemorrhage, anaemia, depression, urinary tract infection, low birthweight (< 2500 g), socioeconomic status (based on area of usual residence5), alcohol and drug misuse, and artificial reproductive technology — and obtained an AOR of 2.1 (95% CI, 1.5–2.9). We are not implying that adding more and more variables to a statistical model is an appropriate way to account for confounding. Our aim is simply to show that Robson et al’s result is robust to statistical adjustment using the available data; this is not the same as saying the analysis is robust to confounding. We found that the higher perinatal mortality in public hospitals was greater for neonatal deaths (AOR, 3.1; 95% CI, 1.8–5.6) than for stillbirths (AOR, 1.6; 95% CI, 1.0–2.4). Excluding lethal congenital anomalies4 did not materially change the result (AOR, 1.9; 95% CI, 1.3–2.8). We also stratified our analysis by level of hospital — tertiary referral (neonatal intensive care unit), base (special care nursery), and community — and obtained a similar twofold mortality excess in each stratum. Although perinatal mortality is uncommon among term singleton babies (1 in 1000 in private hospitals versus 2 in 1000 in public hospitals), any excess risk should be investigated and the reasons for it understood. The results from Robson et al’s article might be due to confounding, but they should not be dismissed and should be investigated with more detailed clinical data. Even if all the excess risk is due to confounding, explicit confirmation of this would be extremely useful. To this end, the Statewide Maternity and Neonatal Clinical Network in Queensland Health will undertake clinical review and classification of term singleton deaths according to national guidelines6 and collaborate with the Australian Maternity Outcomes Surveillance System (AMOSS)7 to enhance prospective monitoring of late gestation perinatal deaths nationally.

Michael D Coory · Guan T Koh · Vicki Flenady · Maarten Kamp

To the Editor: Robson and colleagues found higher crude odds of perinatal death in public hospitals — an unsurprising finding, given the maternal demographics in the public system.1 However, after taking into account known risk factors for poor perinatal outcome by “adjusting for the potentially confounding variables available in the NPDC [National Perinatal Data Collection]”, the authors found that the odds ratio actually went up — implying that the pregnancies of mothers in the private system are higher risk. This is implausible. There are a number of problems with the analysis. The possibility that potentially important maternal information was not included has been acknowledged.1,2 Of greater concern is the omission of a history of low birthweight from the regression model. Since intrauterine growth retardation is a very strong risk factor for perinatal death,3 and since the rate of low birthweight in the public hospitals was double that in the private hospitals, this omission is puzzling. Furthermore, while the authors’ stated aim was to assess the effect of the private model of obstetrician-led interventional care on perinatal outcomes, they included the method of birth and hospital type as independent explanatory variables. Since the interventional nature of obstetric care is, as acknowledged by the authors, a key component of the model of care provided in a private hospital, adjusting for this variable will lessen the usefulness of the study in assessing the impact of private hospital care on perinatal outcomes. Put another way, in deciding what is best for her baby, a mother who is considering giving birth in the private system cannot cherry-pick only the non-interventional side of the obstetrician-led model of care — she must adopt the entire package. Including method of birth as a separate explanatory variable artificially inflates the apparent “riskiness” of the pregnancies of mothers presenting to private hospitals to give birth. These mothers had a 75% increased incidence of caesarean section; however, most of these procedures would be elective rather than emergency. Since this distinction was not made, the women in private hospitals appear high risk despite having had a caesarean section for a low-risk pregnancy. This will have the effect of making perinatal outcomes in private hospitals appear more favourable than they actually are. As currently analysed, the data are of little value to prospective mums and dads in making the first, and one of the most emotive, of the many decisions they need to make as parents.

Daniel C Chambers

To the Editor: Of the many problems with the study by Robson and colleagues,1 the one that concerns us most is the outcome of perinatal death. The headline that this is twice as high in public hospitals has the potential to scare those who have no choice about where they give birth. Both the public and the medical community have a right to expect that this outcome is rigorously and accurately represented. We do not believe this to be the case. The perinatal death rate is made up of stillbirths and neonatal deaths in the first 28 days of life. Stillbirths will comprise 70% of all perinatal deaths, and more than 90% of stillbirths after 37 weeks’ gestation will occur before the onset of labour.2,3 It cannot be excluded that this relates to model of care but, because less than 10% of these stillbirths will have occurred during delivery, it is most certainly not related to the type of birth hospital or the interventions performed during labour. Most likely, it reflects differences in intrinsic risk that have not been controlled for by Robson et al.1 The neonatal death component of this statistic is probably confounded by ascertainment bias. Most neonatal deaths after 37 weeks’ gestation occur for two reasons: intrapartum hypoxia–ischaemia and severe congenital abnormalities. When the latter are diagnosed antenatally, the mothers will often be transferred to tertiary public hospitals for a second opinion and further management. Babies with undiagnosed lethal abnormalities or severe intrapartum hypoxia will invariably be transferred postnatally to a tertiary public hospital neonatal intensive care unit, where death often occurs after withdrawal of intensive care. The midwives data collection form is filled in at the birth hospital, and the baby is categorised as “discharged”, “transferred” or “died”. The 2006 national perinatal data collection report specifically cautions: Ascertainment of neonatal deaths within 28 days of birth is likely to be incomplete. In particular, deaths occurring among babies transferred to another hospital, readmitted to hospital or dying at home may not be known to midwives who collect these data or staff who compile state and territory data.2 Thus, it is unlikely that the difference in perinatal mortality described by Robson et al1 has anything to do with the birth hospital. To represent it as such in the public arena is irresponsible. Further, for the MJA to misrepresent “perinatal mortality” as “neonatal mortality” in the media release about this article defies belief.

Nick Evans · Girvan Malcolm · Adrienne Gordon