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Preference: Paediatrics

792

OBITUARY

Neville Maurice Newman
9 July 1923 – 27 April 2018

Neville Newman was born in Sydney on July 9, 1923, to Horace and Ella Kate (Dids) Newman and spent his school years at Scots College, Sydney, where, in addition to this academic studies, he played rugby union and rowed for the School.

In 1941, aged 17, Neville was admitted to study Medicine at the University of Sydney and resided at St Andrew’s College, where he went on to be Treasurer and President of the student body and also Senior Student in 1945. 1941 was the first year of the war-time accelerated medical course, in which the clinical years were compressed by reducing the breaks between semesters. Neville therefore graduated in 1945 with MB BS with second class Honours, after spending his clinical years at Royal Prince Alfred Hospital (RPAH).

His preclinical years were punctuated by summer holidays spent in a Mills Bomb manufacturing facility or out in the country picking fruit. He also played rugby union for the University of Sydney, being awarded a Blue in 1943.

In 1946, Neville began his residency at RPAH. Then, after a short period as an assistant in general practice, he moved to a training position at the Royal Alexandra Hospital for Children. This was the beginning of a long career in Paediatrics.

On May 10, 1948, Neville married Peg Friend, a nurse he had met at RPAH and in 1949 they moved to London so that Neville could continue his paediatric training.  After a series of jobs in the Middlesex group of hospitals and several training courses, Neville passed the Fellowship exam of the London Royal College of Physicians in 1951. He was then able to obtain a paediatric registrar position at the Hillingdon Hospital, Uxbridge.

With one small daughter and a son on the way, Peg and Neville decided to return to Australia in October 1952, moving to Hobart in May 1953 to join the private paediatric practice of Arch and John Millar. This was a demanding job, with office consultation during the day and home visits all over Hobart and surrounds, every evening and often on unpaved suburban streets. Two more daughters were born in Hobart.

In 1962, Neville was awarded a Fulbright Fellowship to Johns Hopkins Hospital, Baltimore, Maryland, USA, where he took part in a developmental study of children from birth to five years of age, with Dr Janet Hardy. The whole family went with him from May 1962 to September 1963.

During this year in Baltimore, Neville developed his love for newborn babies.  He was able to bring back with him a specialised three-way tap which allowed efficient exchange transfusion of babies with jaundice due to Rhesus incompatibility. For these exchange transfusions, Neville perfected the cannulisation of the umbilical vein.

On his return to Hobart, Neville began to specialise in Neonatology, attending most of the caesarean sections and multiple births.

In 1964, he was appointed Senior Paediatrician at the Royal Hobart Hospital (RHH), a practice which included neonatology and paediatric oncology. However, not long after this, John Millar retired. This meant that Neville was left as the sole paediatrician in Southern Tasmania until Dr Graham Bury arrived in Hobart in 1975 to set up a second paediatric practice.

In 1975, Neville was appointed as Senior Lecturer at the University of Tasmania and began his research into Sudden Infant Death Syndrome (SIDS) together with Drs David Megirian and John Sherry.

In 1980, Neville retired from private practice to become the Inaugural Director of the Neonatal Intensive Care Unit in the Queen Alexandra Division of the RHH, a position he held until his retirement in December 1989. During this time Neville continued his research into SIDS and in 1992 was awarded an Advance Australia Award for outstanding contribution to Medical Research into Sudden Infant Death Syndrome.

In retirement, Neville continued his interest in Medicine and was made a life member of the Tasmanian Branch of the Australian Medical Association.

Neville was lovingly cared for in the later years of his life by his family and in 2015 moved into St Andrew’s Village, Hughes, ACT. He died peacefully at on April 27, 2018, aged 94.

Neville was a leader and innovator in Neonatology, a researcher and a wonderful father. His service to the community was immense. He will be sadly missed.

By Jane Twin B Med Sc, MBBS, FRCPA 
(Dr Newman’s daughter)

 

[Editorial] Solitary confinement of children and young people

Last week, in a joint statement, the British Medical Association (BMA), the Royal College of Psychiatrists, and the Royal College of Paediatrics and Child Health called for an end to the solitary confinement of children and young people held in UK detention facilities. According to a survey from the HM Inspectorate of Prisons, 38% of boys detained in the UK have spent time in solitary confinement, physically and socially isolated from others, with almost no purposeful interaction or environmental stimuli, for periods that can stretch for up to 80 days.

[Perspectives] Leo Martinez: striving to end childhood tuberculosis

Not only can Leo Martinez work opponents on the chess board—he began playing aged 8 and reached national level—he’s also a talented scientist who was awarded the 2017 Stephen Lawn TB-HIV Research Leadership Prize for his contributions to reducing the burden of tuberculosis (TB) and HIV/AIDS in Africa. “Leo has done outstanding innovative research on reducing the childhood TB burden—a much needed and underappreciated area”, says Professor Heather Zar, Chair of the Department of Paediatrics and Director of the MRC Unit on Child & Adolescent Health at the University of Cape Town in South Africa.

[Editorial] Brexit and the NHS

On March 14, the Office for National Statistics released the latest data on child mortality in England and Wales. After decades of progress, both infant and neonatal mortality rates rose for the second consecutive year. Furthermore, in an analysis of 15 similar countries done by the Nuffield Trust and the Royal College of Paediatrics and Child Health, the UK compares badly in seven of 16 indicators of child health.

My gender and my degree

BY DR DANIKA THIEMT

The first documented English-speaking female doctor was Dr James Miranda Barry, a medical officer of the British Army between 1813 and 1865.  Dr Barry devoted her life to the British Army, earning the highest medical rank available: Inspector General of military hospitals. In an era when academic professions were the sole privilege of male members of society, it was necessary for Dr Barry to conceal her gender, living and practising medicine as a man. Her sad reality was exposed only posthumously where examination revealed her secret. Even in death, she was denied her right to her true identity; her gender kept secret for a further 100 years.

In Australia, medical training was opened to women in the late 1800s, and our first female graduate was registered to practice in 1891. Female medical trainees are now thriving, with female medical graduates in Australia outnumbering men since the mid-1990s. Women currently make up more than two-fifths  of vocational  trainees, focused largely in obstetrics and gynaecology  (74.5 per cent), paediatrics  (72.8 per cent) and general practice (63.1 per cent). Contrast this to the figures from oral and maxillofacial surgery, intensive care and surgery and female trainees make up less than a third of trainees. How, when we see women making up half or more of medical graduates and provisional trainees, are we still seeing unequally representation in the ongoing workforce? What is happening along the way? How and why does a speciality that starts out gender-neutral result in a specialist workforce that is predominantly male?

Fixing gender inequity in medicine requires supporting women in leadership. Diversity in the boardroom enhances corporate performance and, to advance as a profession, we need to attract and retain female leaders. Female specialists, on average, earn 16.6 per cent less than their male counterparts. Although differences in average hours worked account for some discrepancies, other contributory factors include a lack of women in senior positions and a lack of part-time or flexible senior roles. There are already inspiring and engaged female leaders within our profession, leading the world in clinical practice, medical research and education. We should be harnessing their talent to inspire the next generation. 

The changing demographic of our workforce could, in part, be to blame. Trainees are graduating from medical school later and spending more time in vocational training. This leads to greater family and social pressures on trainees and possibly an increase in the need for breaks or flexible training options. Evidence shows that access to flexible training helps to retain female trainees and is desired by both female and male trainees regardless of parental status. We need to dispel the belief that trainees must choose between career and family and instead focus on how we enable trainees to have both.

Gender inequity extends beyond medical workforce.Many of my female colleagues report being mistaken for nursing or allied health staff, a rare occurrence among my male colleagues. Similarly, senior female doctors are often overlooked by patients who prefer to talk to the male junior by her side. How do women thrive in medicine and become leaders when public perception seems to favour male doctors? I watch senior medical staff respond to “Miss” in conversation rather than the respectful “Dr”. Although this seems petty in the scheme of everyday practice, it is easy for female doctors to believe that our degrees come second to our gender. Although the actions of some do not make a rule, it is time that we stand together as a profession to advance women in medicine. It is time to advocate for female leadership not only in the eyes of the profession but also in the eyes of the public.

Equity isn’t about creating a false forced equality. We aren’t all equal and that should be celebrated. It certainly shouldn’t hold us back. Opportunities to become leaders won’t be taken by all of our trainees, but they should be provided to all, regardless of gender.

(A version of this article first appeared in Emergency Medicine Australasia in 2016.)

[Editorial] Policy lacking to prevent adverse health for poor UK children

In the UK, 4 million children, about one in four, live in poverty, 100 000 more than in the previous year. A report launched on April 11, Poverty and Child Health—commissioned by charities, the Royal College of Paediatrics and Child Health, and the Child Poverty Action Group—illustrates paediatricians’ concern about the negative impact of child poverty on their health. The report is based on an online survey of over 250 paediatricians across the UK. Two-thirds of the respondents said that poverty and low income contribute very much to the ill health of children they work with, pointing to food insecurity and living in what is described as cold, damp, overcrowded housing, as major contributing factors to health deterioration.

Primum non nocere: rethinking our policies on out-of-home care in Australia

Are our child protection policies causing more harm to our most vulnerable children?

In Australia, there were 43 399 children in out-of-home care (OOHC) on 30 June 2015 (Box).1 Over the past 18 years, the rate at which Indigenous children have been placed in care has more than tripled and more than doubled for non-Indigenous children.1–3 This is disturbing, and particularly so for Indigenous children where one in 19 are in OOHC.1 A recent review of child maltreatment across various countries, including Australia, concluded that 40 years after contemporary child protection policies were introduced in the 1970s, there has been “no clear evidence for an overall decrease in child maltreatment”.4 Despite the call by this review for more evidence,4 there have been no studies planned to assess the effectiveness of our current OOHC policy in Australia.

OOHC refers to the care of children and young people up to 18 years of age who are unable to live with their families and who are, in turn, placed with alternate caregivers on a short or long term basis. Most children in care are in good physical health and display improvements in psychological functioning over time. Recent statistics show that 93.4% of all children in OOHC in Australia live in home-based care. Eighty-one per cent of children in OOHC are in care for more than 1 year, of whom 41% remain in OOHC for over 5 years.5

Children in care experience significantly poorer mental health outcomes than children who have never been in care, with one study recording up to 60% having a current mental health diagnosis, including attention deficit hyperactivity disorder, depression, and attachment and conduct disorders.6 Children in care are less likely than other children to continue their education beyond the age of compulsion. They are likely to attend a large number of different schools and experience substantial periods of absence from school, and many have to change school as a result of a placement change.6 Several studies have identified that children entering care have usually experienced trauma and neglect and, as a group, are at significantly increased risk of mental health problems.7,8 However, there is no evidence to indicate that OOHC reduces the prevalence of mental health problems in this population.

Community concerns about the risk of a child protection matter leading to the death of a child are out of proportion with the statistics. The homicide rate for children has remained the same at about 0.8 per 100 000 for the past two decades.9 A major concern is that there is evidence that children in OOHC in Australia may experience an increased risk of harm while in care compared with children who have never been in care. A review of child deaths in New South Wales found that there were 41 reviewable deaths due to suspected child abuse and neglect in 2012–2013; 14 of these deaths involved children who were in OOHC in NSW during the time of review.9

A South Australian study identified a significant minority of children in care (24%) with a history of placement disruption.10 This group of children experience an average of 11 placements during their time in care and have experienced five placement breakdowns in the previous 2 years. The study showed a strong coincidence of early trauma and abuse and subsequent placement instability.10 A key to mitigating the impact of the child abuse on vulnerable children is to have a stable long term placement; either reunited with their own family if possible, or in a stable alternative home as soon as practicable.11

International experience

The Australian experience of rapidly rising numbers of children in OOHC over the past two decades has not occurred in the United States or New Zealand. In the US in the 1990s, there were 570 000 children (8.9 per 1000) in OOHC,12 and there was concern that many children in OOHC languished in placements that were not permanent, leading to poor long term outcomes for those children. In response to this, in 1997 the US introduced the Adoption and Safe Families Act, which aims through legislation to compel state child protection authorities to limit the length of time children are allowed to remain in foster care. Almost two decades later in the US, there has been a 30% reduction in the number of children currently in OOHC, to 400 000 in 2014, and a 40% reduction in the rate of OOHC, from 8.9 per 1000 to 5.4 per 1000 between 1990 and 2014.12

In New Zealand, the number of children in OOHC has also been trending downwards. Between 2008 and 2012, the number reduced from 4522 to 3783.13 Based on NZ population statistics,14 this represented an almost 20% reduction in the proportion of children in OOHC, from 5.1 per 1000 in 2008 to 4.2 per 1000 in 2012. This is likely the result of the policy changes of the Ministry for Vulnerable Children, where there has been a deliberate effort to reduce the number of children entering care by having agreements to have the children placed with kin without formally placing those children under the guardianship of the court. There has been policy encouragement to have those carers seek additional guardianship and custody rights as a consequence of the Care of Children Act 2004.

Reducing the number of children in OOHC in Australia

More than 90% of the children in OOHC in Australia have been placed there after a court order. The substantiated abuse in over 70% of these cases involves neglect and emotional abuse.1 The majority of parents involved in child protection matters are from marginalised groups in society who frequently do not have access to legal representation for non-criminal matters. This means that there is frequently a great power imbalance between well resourced officers of state or territory community services departments, whose applications to the Children’s Court are mostly unchallenged by legal representatives acting on behalf of either the biological parents or the child recommended for placement in OOHC.15 In Australia, OOHC has been assumed to be the safest option for vulnerable children if there is any suggestion of risk of further harm to the child. This assumption needs to be challenged.

In 2015, a Senate committee report on OOHC was commissioned by the Australian government because of concerns about the increasing number of children in OOHC, the grossly disproportionate representation of Indigenous children in care, and the challenge of finding enough suitably trained carers and homes to cater for the increasing numbers of children. The report made 39 specific recommendations about how OOHC could be improved. The focus was on improving the quality of care and training provided to better support foster carers in Australia.16

The report noted the achievements of the US in reducing the number of children in OOHC and the need to consider similar strategies here. However, it maintained the assumption that we should expect an ever-increasing number of children in OOHC in Australia. Even if all the recommendations were to be implemented, they would not reduce Australia’s reliance on the OOHC system for vulnerable children. It is disappointing that the report did not consider the broader societal questions of why we are placing such a large number of children in foster care and whether there are ways to reduce the number of children who experience abuse and neglect and who need OOHC.

There is no one policy innovation that will change the number of children placed in OOHC in Australia. Decreasing our reliance on OOHC will require many different strategies implemented over a sustained period of time. There is little hope of achieving change if we consider OOHC in isolation from other social policies regarding welfare and increasing societal inequality evidenced by the 17.4% of our children being raised in poverty in Australia.17

We need look no further than the public health success stories in Australia of reducing cigarette smoking rates among adults from 38% in 1974 to 15% in 2013,18 and reducing the national road toll from a rate of 30 per 100 000 people in 197019 to 5 per 100 000 people in 2014.20 These successes have been achieved through multiple initiatives over decades leading to incremental and sustained improvement.

Conclusion

There are far too many children in OOHC in Australia. A child being placed in OOHC should be seen as an indicator that our society needs to do better rather than being accepted as an expected consequence of modern society. The resources to support our most vulnerable children should be directed more towards strengthening the family into which they are born as the first option. We need to ask politically charged questions, such as should we be developing policies that encourage disadvantaged families to have fewer children? We need to aggressively invest in young vulnerable mothers when they have their first child in disadvantaged circumstances, and not wait until there have been documented problems with child neglect before the child protection and social services systems react. We must incrementally reduce our reliance on OOHC as a key goal in overcoming the complex problem of child abuse, neglect and increasing inequity in Australia.

Box –
Children in out-of-home care in Australia at 30 June, 1997–20151–3

Year

Total

Indigenous children

Non-Indigenous children

Ratio of Indigenous to non-Indigenous children

No.

Rate per 1000 children

No.

Rate per 1000 children

No.

Rate per 1000 children

2015

43 399

8.1

15 455

52.5

27 817

5.5

9.5:1

2005

23 695

5.2

5450

26.5

18 245

3.9

6.8:1

1997

13 965

3.0

2785

16.3

11 180

2.5

6.5:1

Long term risk of severe retinopathy in childhood-onset type 1 diabetes: a data linkage study

The known Microvascular complications in people with type 1 diabetes mellitus are directly related to glycaemic control. 

The new This is the first study to assess the risk of complications in people with type 1 diabetes according to their glycaemic control trajectory between childhood and adulthood. Severe diabetic retinopathy (SDR) was associated with higher paediatric HbA1c levels, independent of glycaemic control during adulthood. Importantly, SDR was not documented in patients with a stable low glycaemic control trajectory. 

The implications Target-based treatment from the time of diagnosis of type 1 diabetes in childhood is required to reduce the risk of SDR during adulthood. 

Whether microvascular complications develop in people with type 1 diabetes mellitus is critically dependent on their glycaemic control.1–3 In the large Diabetes Control and Complications Trial (DCCT) and the Epidemiology of Diabetes Complications (EDIC) trial, however, mean glycated haemoglobin A1c (HbA1c) levels could only be estimated from data acquired at trial entry; consequently, the effect of the cumulative glycaemic exposure of the 195 adolescents in these studies during their 1–5 years of diabetes could not be analysed. As a result, the importance and contribution of childhood glycaemic control could not be fully assessed, which may explain some of the differences between adolescent and adult outcomes at follow-up.4 Apart from these two large scale studies, few investigations have followed individuals with childhood-onset type 1 diabetes into adult life.5,6 One longitudinal study (15 participants) found that mean HbA1c levels at diagnosis in childhood were higher for those who developed retinopathy during the 20-year follow-up, and that differences in HbA1c levels between those with and without retinopathy gradually declined with time.7 However, no study has compared the effect of optimal and poor glycaemic control across life on the risk of later complications.

The objectives of our study were to examine the impact of childhood glycaemic control on the future risk of complications in people with type 1 diabetes. Specifically, we aimed to delineate the effect of glycaemic control trajectory on risk, and to determine the relative effects of paediatric and adult metabolic control. We hypothesised that a stable low trajectory would be associated with a lower risk of microvascular complications, and that glycaemic control during childhood would modify the future risk of complications.

Methods

Study design

We undertook a retrospective cohort study of data collected from the time of diagnosis of type 1 diabetes in childhood until the time of our analysis (November 2013). Adults with a diagnosis of type 1 diabetes8 (diagnosed in childhood during 1975–2010) were included if they had attended at least one specialist adult diabetes clinic at the Royal Melbourne Hospital, and their care had been transferred from the paediatric diabetes clinic at the Royal Children’s Hospital (Melbourne) during 1992–2013. Individuals who had been lost to follow-up at the time of care transition from the paediatric diabetes clinic or who had died were therefore excluded. The choice of transition referral centre follows a discussion between the physician and young adult, and is not based on any biological or clinical criteria. Because of its proximity, the Royal Melbourne is the main adult referral centre for patients who transition from the Royal Children’s Hospital, receiving about 40% of its transitioning cohort.

We used a data linkage system, BioGrid Australia, that facilitates linkage of de-identified clinical data from member institutions. All individuals with type 1 diabetes common to both hospitals were identified. Data obtained from clinical department databases at each institution, including standardised clinical data for all routine outpatient clinic visits, were combined with mortality outcome data from the National Death Index (NDI), which has recorded all deaths in Australia since 1980. The process of sequential data linkage was performed with SAS 9.2 (SAS Institute).

Main outcomes and measures

Severe complications

The primary outcome of interest was a database record of diabetes-specific microvascular complications; in this study, only the most severe forms were considered. The date and cause of death were obtained from the NDI. Severe diabetic retinopathy (SDR) included one or more of maculopathy, proliferative retinopathy, and a need for photocoagulation surgery. Chronic kidney disease (CKD) was defined by a glomerular filtration rate of less than 60 mL/min/1.73 m2 (stage 3 CKD or worse),9 calculated from serial creatinine measurements using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation.10 Ulceration and amputation were recorded according to the clinical database files.

Glycaemic control

HbA1c levels were summarised as paediatric (mean of all pre-transition paediatric clinic measurements), adult (mean of all post-transition measurements as an adult), and life course values (mean HbA1c level from diagnosis to November 2013). The glycaemic control trajectory was defined across the life course, with 66 mmol/mol set as the upper cut-off value for good glycaemic control. This value was preferred to the standard paediatric target of 58 mmol/mol because it was anticipated that some of the cohort had commenced treatment before publication of the DCCT findings1,2 upon which the current HbA1c target values are based.8,11 The median HbA1c level in children aged 0–18 years with type 1 diabetes in Australia in 2009 was reported to be 66 mmol/mol;12 this was also the median HbA1c level for a cohort of children who had recently transitioned from care at the Royal Children’s Hospital.13

Each individual was assigned to one of four glycaemic control trajectory groups:

  • stable low (mean paediatric and adult HbA1c ≤ 66 mmol/mol);

  • improving (mean paediatric HbA1c > 66 mmol/mol, mean adult HbA1c ≤ 66 mmol/mol);

  • worsening (mean paediatric HbA1c ≤ 66 mmol/mol, mean adult HbA1c > 66 mmol/mol); or

  • stable high (paediatric and adult mean HbA1c > 66 mmol/mol).

Statistical analyses

Differences between the trajectory groups in participant characteristics, HbA1c levels, and complications were examined by one-way ANOVA (continuous variables) or in χ2 tests (categorical variables). The standardised mortality ratio was calculated as the ratio of the number of observed deaths to the number of expected deaths in the general population, based on 2012 Australian Bureau of Statistics data for Victoria. SDR was the only complication we examined in a regression analysis, as the aetiology of the other outcome measures could not be precisely defined. The relative effect of paediatric and adult glycaemic control on the risk of developing SDR was assessed by generalised estimating equation (GEE) analysis, which could allow for unmeasured variables and confounders. Statistical analyses were performed in Stata 13.0 (StataCorp); P < 0.05 was deemed statistically significant.

Ethics approval

The study received ethics approval from all participating institutions, the Royal Children’s Hospital Human Research Ethics Committee (reference, 31206), BioGrid (project reference, 201202/1), and the Australian Institute of Health and Welfare Research Ethics Committee (reference, EC2013-2-30).

Results

Participant characteristics

We identified 503 people (including 253 men) who were diagnosed with type 1 diabetes during 1975–2010 and had transitioned from paediatric to adult diabetes services over a 21-year period (1992–2013) at a mean age of 18.4 years (standard deviation [SD], 0.9 years; Box 1). The mean age at diagnosis was lower for girls (9.6 [SD, 3.9] v 10.3 [SD, 4.1] years; P < 0.05) but higher for women at the time of our analysis (28.8 [SD, 6.7] v 27.2 [SD, 5.7] years; P < 0.05); the mean duration of type 1 diabetes was therefore longer for women (19.3 [SD, 7.8] v 16.9 [SD, 7.1] years; P < 0.01). The mean number of HbA1c measurements per individual was 22.0 (SD, 13.0), 10.0 (SD, 8.1) and 29.6 (SD, 15.9) during the paediatric, adult and life course periods respectively; the corresponding mean HbA1c levels were 68 mmol/mol (SD, 13.1), 70 mmol/mol (SD, 17.5), and 68 mmol/mol (SD, 12.0) (Box 1).

Severe complications

At least one severe complication was documented for 26 participants (5.2%), including 16 with SDR (3.2%; Box 1). No severe complications were recorded in the paediatric dataset. Based on age- and sex-matched data from 2012 Victorian state data, the overall standardised mortality ratio in this cohort was 1.9 (95% CI, 0.7–4.3) (men, 1.3 [95% CI, 0.2–4.1]; women, 2.7 [95% CI, 0.7–7.4]).

Lifetime glycaemic control trajectory and risk of complications

For the stable low group (143 participants, 28%), the mean paediatric, adult and overall HbA1c levels were 57 mmol/mol (SD, 6.6), 57 mmol/mol (SD, 6.6), and 58 mmol/mol (SD, 3.3) respectively (Box 1). Only one person in this group had a documented complication (a 29-year-old man who had had an amputation).

The glycaemic profiles for the stable low, improving (82 participants, 16%), worsening (96 participants, 19%) and stable high trajectories (182 participants, 36%) are shown in Box 2. Given the low frequency of complications, further analyses were restricted to SDR, for which a causative role for hyperglycaemia could be confidently assumed. No-one in the stable low group had developed SDR, but three in the improving (4%), one in the worsening (1%), and 12 in the stable high groups (7%) had developed SDR (P = 0.004; Box 1). The overall mean age of onset of SDR was 28.8 years (SD, 4.4) years (for the improving group, 23.9 years [SD, 3.7]; worsening group, 28.5 years; stable high, 30.3 years [SD, 3.9]; P = 0.6). However, the mean interval between diagnosis with type 1 diabetes and onset of SDR was shorter for the worsening (30.5 years) and stable high groups (28.1 years; SD, 0.8) than for the improving group (31.9 years; SD, 6.2; P = 0.01).

Paediatric HbA1c level and SDR risk in adulthood

GEE analysis that included significant variables from exploratory multivariate logistic regression models (online Appendix) indicated that each 10.9 mmol/mol increase in paediatric HbA1c level was associated with an almost threefold risk of SDR (odds ratio [OR], 2.9; 95% CI, 1.9–4.3; P < 0.01); each 10.9 mmol/mol increase in adult HbA1c level was associated with a twofold risk (OR, 2.1; 95% CI, 1.4–3.1; P < 0.01). Longer duration of type 1 diabetes was also associated with an increased risk of SDR (per additional year: OR, 1.3; 95% CI, 1.2–1.5; P < 0.01).

Discussion

By incorporating all recorded HbA1c data from diagnosis onwards, this study offers a unique insight into a cohort of adults with childhood-onset type 1 diabetes who were not managed in clinical trials. None of those who maintained a mean HbA1c level of 66 mmol/mol or less from the time of diagnosis (the stable low group) developed SDR. The mean paediatric, adult and overall HbA1c levels in this group were each 58 mmol/mol or less, supporting the adoption of this target in paediatric practice.11 Each additional year of diabetes conferred a significant increase in the risk of SDR, and our data indicate that both paediatric and adult mean HbA1c levels are modifiable factors that moderate this risk. This is important for paediatric care providers, as 64.6% of participants remained in the same HbA1c level category (low or high) during the paediatric and adult periods, indicating that glycaemic control generally neither markedly deteriorates nor improves after the transition to adult services. This challenges the widely held belief that glycaemic control in young adults with type 1 diabetes improves during their mid- to late 20s following deterioration during the adolescent years,14 a premise that may not apply to every patient.

The major limitations of this study are its retrospective design and the low numbers of severe complications reported. Detailed clinical information beyond that recorded in the clinical databases was not available; as the data were de-identified, this problem could not be overcome. Assessing the potential relevance of lifetime glycaemic control for the risk of complications, with the exception of retinopathy, is therefore difficult. Further, we lacked information about outcomes for those who were lost to follow-up immediately after the transition from paediatric care, for whom we consequently have no information about glycaemic control trajectory or complication rates. This could account for the discrepancy between the standardised mortality ratio we estimated and that based on a population-based dataset in Western Australia (1.7 for men, 10.1 for women).15 Although glycaemic control for most of the participants had been suboptimal throughout their lives, the SDR rate was low, but consistent with the recent report that 3.7% of young people (14–30 years old) with type 1 diabetes in Norway required laser therapy within 20 years of the onset of diabetes.16

A number of factors contribute to a higher risk of diabetes-related complications, including genetic susceptibility and cardiovascular risk factors (such as smoking, higher body mass index, greater waist:hip ratio, hyperlipidaemia, hypertension). Data on these factors were not available, and the omission of these known confounders from our analyses is a major limitation of this study. The duration of follow-up varied between individuals, and a shorter period of follow-up during adulthood may have led to misclassification of trajectory category. Cohort studies that assess individuals from diagnosis to death could overcome this limitation, but would be possible only for population-based registries or in large, multicentre cohort studies.

As the study period was broad, we also assessed the effect of era of diagnosis on SDR outcome (data not shown). While SDR was more common among those diagnosed prior to the publication of the DCCT findings (1994), the effect was not independent of the collinear higher glycaemic control that commenced before contemporary target-based practice.

Our report describes the risk of diabetes-specific microvascular complications in a cohort of Australian adults who were diagnosed with type 1 diabetes during childhood. It is the first to assess clinical outcomes according to glycaemic control trajectory between childhood and adulthood, and is the largest to use all available metabolic data from the diagnosis of type 1 diabetes onwards, with a longer duration of follow-up than reported elsewhere. In the absence of an Australian population-based registry of individuals with type 1 diabetes, this data linkage study facilitated assessment of the effects of glycaemic control during the paediatric and adult periods. From this novel perspective, we found that, after adjusting for duration of diabetes (a non-modifiable factor), HbA1c level throughout the course of life was independently associated with the risk of retinopathy in adulthood; the predictive effects of paediatric and adult HbA1c levels were equivalent. However, as severe retinopathy commenced during the third decade of life in our cohort and most people had similar glycaemic control levels in childhood and adulthood, the contribution of metabolic memory (the concept that hyperglycaemia appears to have a chronic rather than an acute effect on the development of complications)4 from the paediatric period was integral to this risk.

Box 1 –
Participant characteristics, HbA1c levels, and complication rates for all participants and for each glycaemic control trajectory group

All participants

HbA1c trajectory group

P*

Stable low

Improving

Worsening

Stable high

Number (% of participants)

503

143 (28%)

82 (16%)

96 (19%)

182 (36%)

Sex (women)

250

58 (40%)

46 (56%)

44 (46%)

102 (56%)

0.02

Age at diagnosis (years), mean (SD)

9.9 (3.9)

10.7 (4.1)

9.1 (3.9)

10.3 (4.2)

9.5 (3.9)

0.80

Duration of paediatric observation (years), mean (SD)

8.5 (4.2)

7.8 (4.1)

9.2 (4.1)

8.1 (4.6)

8.9 (4.1)

0.02

Range (years)

0.6–19.1

1.0–19.1

3.8–19.1

1.1–18.3

0.6–18.9

Age at transition (years), mean (SD)

18.4 (0.9)

18.5 (0.8)

18.3 (0.8)

18.4 (1.1)

18.4 (1.2)

0.10

Duration of adult observation (years), mean (SD)

8.9 (5.8)

7.8 (5.3)

10.0 (6.9)

9.4 (5.5)

9.2 (5.8)

0.04

Range (years)

0.3–21.8

0.8–20.9

0.4–21.8

0.3–20.9

0.5–21.6

Age at last follow-up (years), mean (SD)

27.9 (6.3)

26.4 (5.1)

30.4 (7.7)

27.6 (5.5)

28.4 (6.3)

< 0.001

Duration of type 1 diabetes, (years), mean (SD)

18.1 (7.5)

15.5 (6.7)

21.3 (8.6)

17.5 (7.4)

18.9 (7.0)

0.07

HbA1c measurements, mean number (SD)

Paediatric

22.0 (13.0)

21.9 (12.8)

21.9 (15.5)

19.9 (12.8)

22.3 (12.8)

0.50

Adult

10.0 (8.1)

11.3 (8.9)

11.1 (9.5)

9.5 (8.0)

8.6 (8.1)

0.40

Lifetime

29.6 (15.9)

33.3 (15.4)

28.5 (18.0)

27.9 (14.3)

28.1 (15.8)

0.17

HbA1c level (mmol/mol), mean (SD)

Paediatric

68 (13.1)

57 (6.6)

74 (9.8)

60 (5.5)

78 (9.8)

< 0.001

Adult

70 (17.5)

57 (6.6)

60 (5.5)

77 (10.9)

85 (17.5)

< 0.001

Lifetime

68 (12.0)

58 (3.3)

67 (8.7)

65 (6.6)

79 (9.8)

< 0.001

Severe complications

26 (5.2%)

1 (1%)

6 (7%)

3 (3%)

16 (9%)

0.006

Severe retinopathy

16 (3.2%)

0

3 (4%)

1 (1%)

12 (7%)

0.004

Renal disease

8 (2%)

0

0

4 (5%)

2 (2%)

0.07

Ulceration/amputation

4 (1%)

1 (1%)

1 (1%)

0

4 (2%)

0.76

Death

5 (1%)

0

0

1 (1%)

4 (2%)

0.18

* Differences between trajectory groups tested in χ2 (categorical) and one-way ANOVA analyses (continuous variables).

Box 2 –
Profile of HbA1c levels over time, by glycaemic control trajectory group

Indigenous and non-Indigenous Australian children hospitalised for burn injuries: a population data linkage study

The known Rates of burn injuries are higher for Indigenous children than for non-Indigenous Australian children. 

The new Among Indigenous children admitted to hospital for burns, the proportion presenting with burns affecting more than 10% TBSA was greater than for non-Indigenous children, and their mean stay in hospital was longer. A smaller proportion of Indigenous children with burns were treated in a hospital with a paediatric tertiary burn unit. 

The implications Indigenous children with burns may require more intensive and specialised treatment and longer rehabilitation periods than non-Indigenous children because they more frequently present with burns affecting larger proportions of TBSA. 

Burns are a major cause of injury for children in Australia.1 Indigenous Australian children are disproportionally affected: they are more than twice as likely to be hospitalised for a burn injury as non-Indigenous children, and mortality is five times as high.2–4 Despite this high burden, little is known about the characteristics of burn injuries to Indigenous children or whether they differ from those to non-Indigenous children.5

A study in Western Australia4 found that a larger proportion of Indigenous than of non-Indigenous children admitted to hospital for burns presented with flame burns, and Indigenous children were more likely to sustain severe burns than their non-Indigenous counterparts.6 Similarly, a recent study in New South Wales and the Australian Capital Territory found that children from rural areas more frequently presented with flame burns and burns affecting more than 10% of total body surface area (TBSA) than children from urban areas, and that they have longer hospital stays and higher rates of re-admission after burn injury.7 However, this study did not disaggregate children by Indigenous status, and differences between urban and remote areas may reflect differences in the respective populations, as a higher proportion of Indigenous Australian children (5.1%) than of non-Indigenous children (0.5%) live in remote areas of NSW.8

Although there are differences in burn characteristics at initial presentation, a study in WA found that, once they entered the hospital system, Indigenous people with major burns (50% TBSA) experienced levels of service and had outcomes comparable with those of non-Indigenous patients.9 However, it is not known whether there are differences for patients with less severe burns, or, in particular, for children.

The aim of our study was to explore differences in the characteristics of burn injuries leading to hospitalisation, and in their treatment and outcomes, for Indigenous Australian and non-Indigenous children in NSW.

Methods

Setting

The estimated population of NSW is 6.8 million, 1.3 million of whom are aged 0–14 years.8 At the 2006 census (midpoint of our study), 2.2% of NSW residents identified as Aboriginal and/or Torres Strait Islander (Indigenous Australians), including 7.0% of children aged 0–14 years. Aboriginal people are the original inhabitants of NSW; Torres Strait Islander people comprise 0.1% of the NSW population.8

Study design and data sources

This study was a population-based cohort analysis of linked hospital and mortality data. We used hospital data from the NSW Admitted Patient Data Collection (APDC) linked with mortality data from the NSW Register of Births, Deaths and Marriages (RBDM). The APDC includes records for all separations from NSW public and private sector hospitals and day procedure centres. Patient demographic data, diagnoses and procedures are recorded for each separation and coded according to the Australian modification of the International Statistical Classification of Diseases and Related Problems, tenth revision (ICD-10-AM).10 The RBDM captures details of all deaths registered in NSW. Probabilistic linkage of the datasets was performed by the NSW Centre for Health Record Linkage (http://www.cherel.org.au); de-identified datasets of linked APDC and RBDM data from July 2000 to March 2014 were supplied to the researchers for analysis.

Participants and analysis

The linked data were used to define a cohort of children for the analysis, details of which have been described elsewhere.2 In brief, we selected all children resident in NSW and born in a NSW hospital between 1 July 2000 and 31 December 2012. We then identified children in this cohort who were admitted to a NSW hospital for a first burn injury. Based on the findings of a previous study of the impact of case selection criteria on the identification of patients hospitalised for burn injuries,11 the index burn admission was defined by a primary diagnosis of injury (ICD-10-AM codes, S00–T75, or T79) and an external cause code of exposure to smoke, fire and flames (ICD-10-AM, X00–X09) or contact with heat and hot substances (ICD-10-AM, X10–X19); or by a primary diagnosis of burns (ICD-10-AM, T20–T32). Repeat admissions for the same injury were identified as admissions with either the same primary diagnosis or the same external cause code and primary diagnosis of burn injury as the index admission.

Information about the external cause of the injury (smoke, fire and flames: ICD-10-AM, X00–X09; scalds: ICD-10-AM, X10–X14; contact burns: ICD-10-AM, X15–X19), the body part affected, %TBSA, depth of burn injury, treatment at a hospital with a paediatric tertiary referral burn unit (the Children’s Hospital at Westmead), and inhalation injury (ICD-10-AM, T27, T28.0, T58, T59) were derived from the index admission. Severe burns were defined as partial or full thickness burns affecting more than 10% TBSA.12 Length of stay (LOS) for the index admission was defined as the difference in days between the final discharge day and the date of admission for the index episode of care. Hospitalisations consisting of several continuous episodes of care for the same injury were counted as one hospital stay. The total LOS was defined as the LOS for all admissions related to the index admission. The type of care provided to the child was determined for all burn-related admissions.

Statistical analysis

The proportions of Indigenous and non-Indigenous children with specific burn characteristics were compared in χ2 tests. The influence of these characteristics on differences between Indigenous and non-Indigenous children in LOS was analysed by Cox regression analysis, adjusted for individual (Indigenous status, sex, age), burn (inhalation injury, %TBSA) and area (disadvantage, remoteness) characteristics. Geographic remoteness was defined according to the Accessibility/Remoteness Index of Australia (ARIA&plus;)13 and area-level socio-economic status according to the Australian Bureau of Statistics’ Socio-Economic Index for Areas (SEIFA) Index of Relative Social Advantage and Disadvantage.14 Indigenous status was derived from the child’s birth record in the hospital data. Data were prepared for analysis with SAS 9.3 (SAS Institute) and analysed in Stata 12 (StataCorp).

Ethics approval

Ethics approval for the study was granted by the Population Health Services Research Ethics Committee (reference, HREC/09/CIPHS/18), the Aboriginal Health and Medical Research Council Ethics Committee (reference, 684/09), and the University of Western Sydney Ethics Committee (reference, CI2009/03/141).

Results

Cohort characteristics

A total of 1 124 717 children were included in the cohort, of whom 35 749 (3.1%) were Indigenous Australians. The proportion of Indigenous children living in remote areas (9%; 3312 children) was higher than that for non-Indigenous children (1%; 7574 children). During 2000–2014, 323 Indigenous and 4246 non-Indigenous children were hospitalised for a first burn injury; including repeat admissions, these burns accounted for 5829 hospitalisations of non-Indigenous children and 464 of Indigenous children. The proportions of Indigenous children admitted for a burn injury who lived in remote (15%; 48 children) or disadvantaged areas (76%; 245 children) were higher than for non-Indigenous children (1%; 45 children, and 46%; 1955 children respectively; Box 1).

Burn injury characteristics and outcomes

Scalds were the leading cause of burn injury to both Indigenous (47%) and non-Indigenous children (62%). A larger proportion of Indigenous (18%) than non-Indigenous patients (8%) were admitted for flame burns (Box 2).

The body regions most often injured were different for the two groups of children (P = 0.005). A smaller proportion of Indigenous children presented with burns to the hand or wrist (17%) and a higher proportion with burns to the ankle or foot (12%) than non-Indigenous children (23% and 8% respectively). When stratified by area of residence, the proportion of Indigenous children with burns to the foot and ankle was greater among those living in metropolitan and inner regional areas (14%, 24 children; online Appendix).

A greater proportion of Indigenous than of non-Indigenous patients sustained full thickness burns (16% v 14%) or burns affecting more than 20% TBSA (6% v 2%; Box 2). When stratified by area of residence, the proportion of Indigenous children with burns affecting more than 10% TBSA was greater for those living in outer regional and remote areas (21%, 29 children; online Appendix).

The proportions of Indigenous children with severe burn injuries (17%) or inhalation injuries (4%) were similar to those for non-Indigenous children (12% and 3% respectively; Box 2).

A smaller proportion of Indigenous patients than of non-Indigenous patients were treated at a hospital with a paediatric tertiary burns unit (40% v 50%; P < 0.001); of children with severe burn injuries, 59% of Indigenous and 56% of non-Indigenous children were admitted to a hospital with a paediatric tertiary burns unit (P = 0.69; Box 2).

A larger proportion of Indigenous than of non-Indigenous children with severe burn injuries living in major cities and inner regional areas (63% v 58%) and a higher proportion of those living in outer regional and remote areas (56% v 43%) were treated at a hospital with a specialist burns unit (online Appendix).

Most Indigenous (85%) and non-Indigenous children (84%) were hospitalised once for their burn injury; there was no significant difference in the overall pattern of re-admissions (P = 0.19; Box 2). There were, however, differences in the care received: a lower proportion of Indigenous children underwent surgery (20% v 25% of non-Indigenous children; P = 0.025), and a higher proportion received physical and occupational therapy (13% v 9%; P = 0.015) (Box 3).

A smaller proportion of Indigenous children with burn injuries were treated as day-only patients (31% v 41% of non-Indigenous patients), and a larger proportion stayed in hospital for more than one week (32% v 17%; Box 2).

The mean LOS during the index admission (excluding day patients) for Indigenous children (6.1 days; 95% CI, 4.8–7.4 days) was almost 3 days longer than for non-Indigenous children (3.4 days; 95% CI, 3.2–3.7; P < 0.001). The median LOS for each group of children was one day (Box 4). After adjusting for sex, age, inhalation injury, %TBSA, depth of burn, geographic remoteness, and area disadvantage, LOS was still significantly longer for Indigenous than for non-Indigenous children (P = 0.002). %TBSA, depth of burn, and geographic remoteness were each significantly associated with increased LOS (Box 5).

Discussion

In this data linkage cohort study, we found that a higher of proportion of burn injuries to Indigenous than to non-Indigenous children were caused by flame burns, that their burns more often affected a larger %TBSA, and that they stayed in hospital longer.

The higher proportion of flame burns among Indigenous children admitted to hospital for burn injuries might partially be explained by the higher proportion of Indigenous children living in rural and remote areas, where the incidence of flame burns is higher,7,15 perhaps because there are more outdoor fires in rural areas or because rural children more frequently engage in risky behaviour than those in urban areas.7

A recent study similarly found that a higher proportion of children from rural areas presented to a specialist burn unit with burns affecting more than 10% TBSA;7 however, this analysis did not analyse cases by Indigenous status. Our results suggest that this difference could be partly explained by the higher proportion of Indigenous children living in remote areas.

The mean LOS for a burn injury was almost 3 days longer for Indigenous than for non-Indigenous children. This difference is similar to the reported difference in LOS between children living in remote and urban areas.7 After adjusting for burn injury characteristics, geographic remoteness, and area-level disadvantage, the difference in LOS between Indigenous and non-Indigenous children was still statistically significant, indicating that other factors also influence LOS.

A smaller proportion of Indigenous children than of non-Indigenous children were treated at a hospital with a paediatric tertiary referral burn unit. One explanation could be that a larger proportion of non-Indigenous children live near this hospital, located in western Sydney, so that it is their first point of contact. Inequities in access to medical services experienced by Indigenous Australians and people living in remote areas are recognised.16–18 In contrast, we found that a higher proportion of Indigenous than of non-Indigenous children presenting with a severe burn and living in remote areas were treated at a hospital with a tertiary burns unit. About 40% of Indigenous and non-Indigenous children with severe burns were not admitted to a hospital with a tertiary burns unit, but our data did not allow further investigation of the underlying reasons. However, separation from family and community are likely to influence decisions by physicians and families about transferring children from remote areas to specialist burn units, typically located in metropolitan areas.19 Moreover, the introduction of telehealth procedures has facilitated care of patients in remote areas, so that fewer children need to be transferred to a hospital with a specialist burn unit.20

A lower proportion of Indigenous than of non-Indigenous patients underwent surgery, but a higher proportion of Indigenous children received in-hospital physical and occupational therapy, probably because a larger proportion of their injuries were severe burns.

This is the first data linkage cohort study of the characteristics of burn injuries to Indigenous and non-Indigenous children in Australia. However, it was subject to limitations that are inherent to the use of routinely collected hospital data. Our study was restricted to injuries that resulted in a hospitalisation; hospital admission and access may vary between population groups and regions; and higher admission rates in remote areas may reflect differences in access to other health care providers and services.21 Children living in rural and remote areas are more likely to be treated as inpatients because their travelling distances to hospital are longer, making it more difficult to return as day patients.22

There is currently no source of data on injuries incurred in the community and treated in the primary care setting in Australia, and we did not capture presentations at outpatient burn clinics or to Indigenous community-controlled health services.

Inaccuracies in the coding of external cause are possible, as well as in the coding of %TBSA in hospital data.23–25 It has been reported that %TBSA is likely to be overestimated by referring hospitals when compared with assessments in specialist burn units.23,24 We may have underestimated the burden of burn injury hospitalisation in our cohort, as some repeat admissions might have been missed because of differences in external or primary diagnosis coding, and because we restricted our analysis to the first burn injury.

In view of the fact that patients admitted to hospital with a tertiary burns unit are reviewed by a physiotherapist, the proportion of children recorded as having received physical and occupational therapy was surprisingly low; the recording of such therapy in the hospital data may have been incomplete.

Anatomic location was not included as a factor in our statistical modelling of LOS because of the small numbers of cases in individual categories.

Further, underreporting of Indigenous status in routinely collected data is a recognised problem that can lead to underestimation of the number of Indigenous children hospitalised for injuries.26 We used Indigenous status as recorded in birth records to minimise the effect of differential misclassification bias, whereby the opportunity to be recorded as Indigenous rises with the number of times a child is admitted to hospital. However, applying different algorithms to identify Indigenous children on the basis of linked hospital data has been shown to increase both their identification and the sizes of differences between Indigenous and non-Indigenous children.2,27 Our estimates of differences between Indigenous and non-Indigenous children may therefore be conservative.

Conclusion

We found that the proportion of burns affecting more than 10% TBSA was higher for Indigenous than for non-Indigenous children, and that, after adjusting for the characteristics of the burn and residential location, Indigenous children spend more time in hospital.

Box 1 –
Characteristics of children admitted to hospital for a first burn injury, New South Wales, 2000–2014

All children

Non-Indigenous children

Indigenous children

P

Total number of children

1 124 717

1 088 968

35 749

Children admitted to hospital for a first burn injury (% of cohort)

4569 (0.41%)

4246 (0.39%)

323 (0.90%)

Age

0.03

< 1 year

798 (17.5%)

745 (17.5%)

53 (16%)

1–4 years

3057 (66.9%)

2854 (67.2%)

203 (63%)

4–13 years

714 (15.6%)

647 (15.2%)

67 (21%)

Sex

0.86

Girls

1902 (41.6%)

1769 (41.7%)

133 (41%)

Boys

2667 (58.4%)

2477 (58.3%)

190 (59%)

Area-level disadvantage

< 0.001

First tertile (most disadvantaged)

2200 (48.2%)

1955 (46.0%)

245 (76%)

Second tertile

1453 (31.8%)

1383 (32.6%)

70 (22%)

Third tertile (least disadvantaged)

916 (20.0%)

908 (21.4%)

8 (2%)

Geographic remoteness

< 0.001

Major cities

2716 (59.4%)

2649 (62.4%)

67 (21%)

Inner regional

1163 (25.5%)

1054 (24.8%)

109 (34%)

Outer regional

597 (13.1%)

498 (11.7%)

99 (31%)

Remote/very remote

93 (2.0%)

45 (1.1%)

48 (15%)

Number of hospitalisations

5829

6293

464

Box 2 –
Characteristics of burn injury, treatment and outcome for children admitted to hospital for a first burn injury, New South Wales, 2000–2014

All children

Non-Indigenous children

Indigenous children

P

Number of children

4569

4246

323

External cause of injury

< 0.001

Smoke, fire and flame

407 (8.9%)

348 (8.2%)

59 (18%)

Scalds

2794 (61.2%)

2641 (62.2%)

153 (47%)

Contact burns

910 (19.9%)

835 (19.7%)

75 (23%)

Other

458 (10.0%)

422 (9.9%)

36 (11%)

Anatomic location

0.005

Head/neck

874 (19.1%)

806 (19.0%)

68 (21%)

Trunk

962 (21.1%)

896 (21.1%)

66 (20%)

Shoulder/upper limb

604 (13.2%)

569 (13.4%)

35 (11%)

Wrist/hand

1027 (22.5%)

973 (22.9%)

54 (17%)

Hip/lower limb

505 (11.1%)

466 (11.0%)

39 (12%)

Ankle/foot

384 (8.4%)

347 (8.2%)

37 (12%)

Other/unspecified

213 (4.7%)

189 (4.5%)

24 (7.4%)

Total body surface area (%TBSA) injured*

0.002

< 10%

3796 (83.1%)

3546 (83.5%)

250 (77%)

10–19%

462 (10.1%)

426 (10.0%)

36 (11%)

≥ 20%

122 (2.7%)

104 (2.4%)

18 (6%)

Depth of injury†

< 0.001

Superficial

324 (7.1%)

297 (7.0%)

27 (8.4%)

Partial

3309 (72.4%)

3105 (73.1%)

204 (63%)

Full thickness

645 (14.1%)

593 (14.0%)

52 (16%)

Inhalation injury

133 (2.9%)

120 (2.8%)

13 (4.0%)

0.22

Severe burn‡,§

533 (11.7%)

487 (12.4%)

46 (17%)

0.14

Treated at hospital with tertiary referral burn unit

2260 (49.5%)

2132 (50.2%)

128 (40%)

< 0.001

Severe burn treated at hospital with tertiary referral burn unit

298 (55.9%)

271 (55.6%)

27 (59%)

0.69

Number of re-admissions

0.19

0

3825 (83.7%)

3550 (83.6%)

275 (85%)

1

608 (13.3%)

570 (13.4%)

38 (12%)

2

115 (2.5%)

109 (2.6%)

6 (2%)

> 2

21 (0.5%)

17 (0.4%)

4 (1%)

Length of stay

< 0.001

< 1 day

1841 (40.3%)

1742 (41.0%)

99 (30.7%)

1–7 days

1917 (42.0%)

1795 (42.3%)

122 (37.8%)

8–28 days

510 (11.1%)

454 (10.7%)

56 (17.3%)

> 28 days

301 (6.6%)

255 (6.0%)

46 (14.2%)

* Missing data: 170 non-Indigenous and 19 Indigenous children. † Missing data: 251 non-Indigenous and 40 Indigenous children. ‡ Missing data: 311 non-Indigenous and 45 Indigenous children. § Defined as partial or full thickness burn and > 10% TBSA.

Box 3 –
Treatment of children admitted to hospital for a first burn injury, New South Wales, 2000–2014

All children

Non-Indigenous children

Indigenous children

P

Total number of hospitalisations

6293

5829

464

Mechanical ventilation

75 (1%)

65 (1%)

10 (2%)

0.047

Surgical intervention

1547 (25%)

1453 (25%)

94 (20%)

0.025

Physical/occupational therapy

612 (10%)

552 (9%)

60 (13%)

0.015

Other allied health*

1207 (19%)

1100 (19%)

107 (23%)

0.027

* Includes nutrition and dietetics, social work, speech pathology, pharmacy, pastoral care, play therapy and social work.

Box 4 –
Length of hospital stay for children admitted to hospital for a first burn injury (excluding day patients), New South Wales, 2000–2014

Non-Indigenous children

Indigenous children

P

Number of children

2504

224

Length of stay, first admission (days)

Median (IQR)

1 (1–3)

1 (1–6)

< 0.001

Mean (95% CI)

3.4 (3.2–3.7)

6.1 (4.8–7.4)

< 0.001

Range

1–61

1–77

Length of stay, total (days)

Median (IQR)

2 (1–4)

3 (1–7)

< 0.001

Mean (95% CI)

4.1 (3.8–4.3)

7.1 (5.6–8.5)

< 0.001

Range

1–61

1–79

Box 5 –
Effects of individual and area-level characteristics on differences in hospital length of stay for Indigenous and non-Indigenous children admitted to hospital for a first burn injury, New South Wales, 2000–2014

Characteristic

Hazard ratios*(95% CI)

P

Indigenous status

Non-Indigenous

Reference

Indigenous

0.78 (0.66–0.92)

< 0.002

Sex

Girls

Reference

Boys

1.00 (0.92–1.09)

0.98

Age

0–4 years

Reference

5–13 years

0.98 (0.86–1.12)

0.82

Inhalation injury

No

Reference

Yes

0.80 (0.52–1.23)

0.30

Depth of injury

Superficial

Reference

Partial

0.72 (0.60–0.85)

< 0.001

Full thickness

0.45 (0.36–0.55)

< 0.001

Total body surface area (%TBSA) injured

< 10%

Reference

10–19%

0.53 (0.47–0.60)

< 0.001

≥ 20%

0.23 (0.17–0.29)

< 0.001

Geographic remoteness

Major cities

Reference

Inner regional

0.88 (0.80–0.97)

0.01

Outer regional

0.82 (0.72–0.94)

< 0.001

Remote/very remote

1.00 (0.75–1.33)

1.0

Area-level disadvantage

First tertile (most disadvantaged)

Reference

Second tertile

1.05 (0.95–1.16)

0.34

Third tertile (least disadvantaged)

1.05 (0.93–1.17)

0.45

* Adjusted for all other variables in table.

Reducing the incidence of burn injuries to Indigenous Australian children

Burns are a specific health burden, but understanding the detail is vital to finding solutions

It is undisputed that Aboriginal and Torres Strait Islander (Indigenous Australian) children are over-represented in statistics for injury and death caused by trauma. The incidence of each of the major mechanisms of fatal trauma in Australian children — drowning and low speed vehicle run-overs — is higher among Indigenous children.1,2 Burn injuries are also more prevalent among Indigenous children.3

In this issue of the MJA, Möller and his colleagues report a population data linkage study they undertook in New South Wales.4 Their results not only confirm that the incidence of hospitalisation of children for burn injuries is higher among Indigenous than non-Indigenous children. The authors also found that the proportion of burn injuries affecting more than 20% of total body surface area (TBSA) was greater for Indigenous than for non-Indigenous children, as was that of burns to the feet or ankles; that the incidence of being treated in a tertiary burns facility was lower and their median overall hospital stay longer for Indigenous children; and that they were less likely to undergo surgery, but more frequently received treatment from allied health professionals. This important epidemiological study not only supports the hypothesis that burn injuries constitute a significant health burden in Indigenous children, it is also the prelude to a much larger prospective study.5 Paediatric burns services throughout Australia are currently collaborating in a study funded by the National Health and Medical Research Council to examine the journey of the Indigenous child with a burn injury through the health system, including pre-hospital care and outpatient follow-up.5

The report by Möller and co-authors is initially somewhat disturbing, but more detailed analysis identifies factors that explain some of the disparities described. The proportion of Indigenous Australians living in rural and remote geographic locations, and therefore a long distance from tertiary burns facilities, is higher than for other Australians. It is consequently not surprising that many Indigenous children are treated in their local hospital, which has the advantage of keeping the family unit closer to home, with clear psychosocial and financial benefits. With the advent of telehealth services linking major burns services and local hospitals, and the application of digital photography to record wound status at each dressing change, a high standard of care can now be achieved even in remote locations.6,7

Whether a child needs to be admitted to hospital for a burn injury depends on many factors apart from the proportion of TBSA burned. One-third of children are admitted because of the impact of the injury on their family, not because immediate treatment of the burn is needed.8 It is often in the interest of the Indigenous child and family to be admitted to hospital when factors such as remoteness of the family home and socio-economic disadvantage would prevent the families traveling to outpatient appointments for dressing changes. Not only is admission to hospital more likely under these circumstances, the duration of stay will also be longer.

The region of the body affected by a burn is very much related to the mechanism of injury. For example, hot beverage scalds usually affect the face, neck and torso, whereas burns by hot embers and ash from campfires and burn-offs typically affect feet and ankles. Indigenous children have different patterns of burn injury types to other Australian children because of cultural and socio-economic differences. The higher proportion of foot and ankle burns in the report by Möller and colleagues is possibly explained by a higher incidence of campfire burns to Indigenous children.

The estimated TBSA burned is probably the greatest source of inaccuracy when documenting a burn injury.9 Areas of superficial burn (erythema only) are often erroneously included, leading to grossly overestimating the extent of the burn. Burn depth can also progress with time, but the TBSA is often not re-calculated, so that the initial estimate is the only value documented by hospital coders. Overestimation of burn extent would probably occur more frequently in non-tertiary facilities. Lund and Browder charts have traditionally been employed for calculating TBSA, but they are cumbersome to use and should therefore be replaced by mobile phone apps that accurately estimate TBSA by digitally shading on the screen the areas affected. The New South Wales Institute of Trauma has developed an app for this purpose that is free, quick and easy to use; the age and weight of the child are entered, and the degree of fluid resuscitation required (using the Parkland formula) is also calculated.10

People from populations with darker skin colour are reported to re-epithelialise burn injuries up to 25% more quickly than those from populations with lighter skin.11 However, darker skin has a higher propensity for hypertrophic scarring, explaining why the Indigenous children in this study had fewer operations for skin grafting, but significantly greater requirements for management by allied health professionals.

Preventing burns must be part of any intervention to reduce the burden of burn injuries in Indigenous children, alongside optimal first aid. Campaigns to prevent burn injuries will only be successful if they are targeted at specific populations that are at greater risk, and it is important they include collaboration between injury prevention advocates, Indigenous leaders, and health care workers.