Environmental health

Australia faces a federally instigated migration drive aimed at increasing its population to 35 million by 2049. Immigration is welcomed by politicians, economists and businesspeople, who credit it with helping Australia fare better than other developed countries during the recent global financial crisis. Australia’s capital cities will have to expand considerably to house the new migrants. Increased urbanisation, when not accompanied by appropriate town planning, is associated with higher rates of chronic disease. Despite the migration drive, Australia’s population will continue to age, and by 2056 one in four Australians will be over the age of 65 years. Australian health services are already heavily burdened. Health professionals must engage with governments to ensure that appropriate plans are put in place to accommodate the increased burden of disease that will accompany a more populous Australia. Failure to do so will compromise the health of our nation.

Deborah Pelser BSc, MB BCh

Obesity, ill health and global warming are linked. The risks to health of climate change have been well articulated but have not been accompanied by clear policy and effective action. Four areas where doctors can and should act, and where changes will benefit both the environment and human health in the short-to-medium term are: reduction in the adverse environmental impact of the health care industry; development of a nationwide comprehensive food and nutrition policy that takes account of the entire food production cycle; urban redesign to encourage active transport; and more support for sexual and reproductive health services in developing countries. Finally, climate change policies should be assessed for their impact on global health and equity.

Robyn A McDermott MPH, FAFPHM, PhD

To the Editor: In their recent article, Beaman and Leung raised a number of important and pertinent issues about what we can learn from the influenza pandemic of 2009.1 However, we would like to correct a number of misconceptions on their part, including claims that Western Australia’s central public reference laboratory, PathWest Laboratory Medicine WA, (i) unreasonably favoured polymerase chain reaction (PCR) testing over antigen testing; (ii) rationed and prioritised testing primarily because of inability to cope with the high demand; (iii) rarely achieved the benchmark turnaround time of 48 hours; and (iv) spent excessive time processing a large number of specimens, of which 96% were reported as negative. State reference laboratories had to provide tests that would best guide individual patient management and the most effective use of hospital beds, as well as informing the public health response. The decision to avoid antigen detection tests was supported by the World Health Organization from the beginning of the pandemic2 and confirmed by subsequent published data showing that PCR testing was more reliable than antigen testing.3,4 Inaccurate test results hinder rather than help the pandemic response,5 especially in the early stages. From very early in the pandemic, we prioritised samples from hospitalised patients, health care workers, people at higher risk of severe disease and cases of special public health importance. For these urgent samples we aimed for, and largely achieved, a 48-hour turnaround time. Beaman and Leung did not allow for the substantial delays in transport and processing of samples before testing, which contributed 2–3 days to the turnaround time. A similar experience was reported in Victoria.6 This has highlighted the need to improve the way in which samples are handled at all stages between collection and testing. Rationing of services was a decision made in consultation with our public health colleagues, to ensure sustainable testing capacity for essential clinical and public health needs. In the end, PathWest tested 24 310 samples, representing 92.8% of the samples received, which included all of the high-priority and/or critical samples. It is misleading to suggest that a 96% negative rate was inefficient, and is a misunderstanding of the purpose of testing in the different phases of the pandemic. In the early phases, the yield of positive test results was expected to be low, as there was active case-finding at a time when no or very little virus was present in Australia. Across the course of the pandemic, the positive rate at our laboratory was 23% overall and 40% during the peak week. The response of public and private laboratories to the pandemic throughout Australia was impressive, and has now been the subject of state and national debriefings to identify potential improvements and the highest priorities for action. As part of that, we should all look at how we could improve our own laboratory’s performance and how we could make the best contribution to dealing with future pandemics and other emerging infectious diseases, both as individuals and as members of organisations. We would like to take this opportunity to acknowledge all the people within and outside laboratories who made a huge effort to save lives and reduce the impact of the pandemic.

David W Smith · David J Speers · Rodney A Bowman

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

Older road users. Myths and realities, a guide for medical and legal professionals. Morris S Odell, Editor. Tucson, Ariz: Lawyers & Judges Publishing Company, Inc, 2009 (xvi + 302 pp). ISBN 978 1 933264 70 7. Traffic medicine is an emerging discipline, so not many resources are available on the subject. The fact that the editor of this book, Morris Odell — a Forensic Physician at the Victorian Institute of Forensic Medicine in Melbourne — is also my former teacher for whom I have great respect, made me read it with added interest. The proportion of elderly drivers is expected to rise significantly in the next 50 years and the role of medical practitioners in assessing their medical fitness to drive will increase. At present, there are no strict guidelines for assessing elderly drivers’ medical fitness to drive since, in many instances, the evidence available is contradictory. This book acknowledges the limitations of the assessment process, but provides abundant information to help readers form their own opinions. I found this approach to be unbiased, unintrusive and fair. The book was commissioned by VicRoads, in response to the 2003 Inquiry into Road Safety for Older Road Users by the Victorian Parliament Road Safety Committee. It addresses the main factors that affect driving skills — vision, cognition and motor function, with particularly interesting chapters on the effects of prescription drugs, and respiratory and sleep disorders. In addition, it examines different patterns of road injuries and the distinct crash epidemiology of elderly drivers. Odell has assembled a stellar team of contributing authors and the information provided is contemporary, easy to understand and backed up by evidence. The assessment options and principles of the assessment process of elderly drivers are explored in detail but the book stops short of recommending a particular assessment tool. Furthermore, it does not take a preferred position or make recommendations for when the elderly should not drive. This omission could be compensated by grabbing a copy of Austroad’s Assessing fitness to drive 2003, which gives strict recommendations for when people should not be driving. Apart from these small omissions, this is a great reference that gave me a lot of answers to questions that I haven’t been able to find for years. It will benefit medical and legal professionals whose work involves elderly drivers, as well as students and young doctors who would like to learn more about the relationship between different medical conditions and their impact on driving safety.

Ilian Kamenoff

Publication deadlines for reporting causes of deaths not yet finalised by coroners and different methods employed by different jurisdictions may have disguised Australia’s true suicide rate Suicide is a topic of public health, public policy and general community interest. Accurate and timely suicide statistics are needed to measure and monitor this cause of death, to guide the development of prevention programs, and to enable evaluation and research.1 The main source of suicide data in Australia is the national mortality database of the Australian Bureau of Statistics (ABS).2 Recently, the ABS data have been used to report reductions in the annual rates and overall numbers of completed suicides since 1997;3,4 another such report, by Large and Nielssen, appears in this issue of the Journal.5 Surely a decline in suicide rates is good news? It is good news if the reported declines have really occurred. However, there are reasons to think that part of the apparent recent decline in suicide, as estimated using ABS data, is the result of changes in the data collection system.1,6-8 The ABS has published cautionary notes concerning suicide statistics in recent years,9,10 and has changed its process for coding deaths registered after 2006, prompted by awareness of the problem of slow finalisation of some cases.1,11 The system underlying cause-of-death statistics is quite complex, and suicide is a particularly challenging cause to record and classify. If a death is suspected to be the result of suicide, an obligation arises to refer it to a coroner. Police, forensic pathologists and staff at the coroner’s office are involved in obtaining and preparing information for the coroner. Sometimes the coroner decides that a formal inquest is warranted, but most cases are dealt with by a simpler administrative process. Details differ between jurisdictions, but the process always results in a conclusion on the cause of death. Coroners are alert to the sensitivity of a finding of “suicide”. Accordingly, they require positive evidence before making a finding of suicide. Findings normally state the means of death (eg, “ligature asphyxiation”), but often remain silent on intent. Coroners’ records are used by ABS officers to guide their selection of a cause of death code. Historically, this information was mainly obtained by ABS officers visiting coroners’ offices and inspecting records. In 2000, an electronic register of coroner cases, the National Coroners Information System (NCIS), commenced operation. ABS officers began to use information in the NCIS, from about 2003, to supplement visits to coroners’ offices; then, from 2006, to replace these visits.11 NCIS records are entered by coroners’ staff. Some information can be entered soon after a death is referred to a coroner, but the record cannot be finished and the finding cannot be entered until the case has been closed by the coroner, sometimes years after the death has occurred. The ABS has operated a system in which all of the deaths registered in a particular year were processed by a deadline, and then reported as final data. For this system to work well, the information that is necessary for coding the causes of all of the deaths registered in that year must be available to the ABS before its deadline. It turned out that the NCIS did not provide complete information on some deaths, including many suicides, in time to meet the ABS deadline.1,9 Often, the mechanism of injury was known by the deadline (eg, gunshot) but the final conclusion on intent was not. Following advice about the use of the International Classification of Diseases codes in this situation, ABS officers assigned to such cases the same codes that are used for unintentional injury deaths.7 Hence, suicide was under-enumerated. The ABS has changed its system for coroner-certified deaths registered after 2006.11 A death registered in 2007 and incomplete in the NCIS at the former ABS deadline (early in 2009) will have been reported in the first release of ABS data on deaths registered in 2007, probably with a code in a range being used as a “holding bay” for incomplete cases (eg, “Hanging, strangulation and suffocation, undetermined intent”), or as unknown cause of death. If the NCIS record for that death closed during 2009, then the ABS reviewed and, if necessary, recoded it for the second release of 2007 deaths data, issued in March 2010.2 Many of the deaths that were initially assigned “holding bay” codes have characteristics suggesting that they will be recoded as suicides when final information is available. As expected, a rise in the number of suicide deaths was observed between the first and second releases of 2007 deaths data, and further rises are likely in subsequent releases. The first estimate of suicides for 2008, based on a further modification of the ABS system, is 2191, which is higher than the first (1881) and second (2054) estimates for 2007. We don’t yet know final ABS suicide numbers for 2007 or 2008. We do know that ABS suicide counts for the several years before that are low. It is likely that this problem reflects the increasing reliance placed on the NCIS by the ABS in the period 2003–2006. Accordingly, a great deal of caution must be employed when interpreting trends in suicide in Australia during the past decade, particularly when making comparisons between jurisdictions (as these have been found to be differentially affected, as a result of differences in coronial processing times1). Unfortunately, it is likely that at least part of the apparent decline since about 2002 shown by ABS statistics and reported by various authors, including Large and Nielssen,5 is an artefact of increased misclassification of suicide deaths. Changes that have been put in place, chiefly by the ABS, are likely to result in materially more reliable suicide statistics in future, providing a better (though still imperfect) basis for efforts to analyse and interpret changes in this important cause of death.

Clare E Bradley PhD · James E Harrison MB BS, MPH · Amr Abou Elnour MB BCh, GradDipPHC

Objective: To evaluate the changes in the understanding of the manner and cause of death occurring during the course of coronial investigations.Design: Retrospective analysis of deaths reported to coroners in Australia between 1 July 2000 and 31 December 2007, using the National Coroners Information System.Main outcome measures: (i) Manner of death (natural, external, unknown); (ii) intent classification (eg, unintentional injury, suicide, assault) among deaths with external causes; and, (iii) changes in the manner of death and intent classification between the presumption made at case notification and the coroner’s final determination.Results: The coronial investigation changed the presumption about manner of death or intent classification in 5.2% (6222/120 452) of cases in which a presumption was made. Among deaths with a change in attribution from natural causes to external causes, unintentional falls (442/1891) and pharmaceutical poisoning (427/1891) each accounted for 23%. Among deaths with attribution changing from external causes to natural causes, the leading medical causes of death were cardiovascular compromise (551/842; 65%) and infection (124/842; 15%). Of deaths understood correctly at notification to be due to external causes, but the wrong external cause, 34% (206/600) were ultimately judged to be unintentional injuries, and 22% (133/600) were judged to be suicides.Conclusions: Coronial investigations transform basic understanding of cause of death in only a small minority of cases. However, the benefits to families and society of accurate cause-of-death determinations in these difficult cases may be considerable.

David M Studdert LLB, ScD, MPH · Stephen M Cordner MB BS, BMedSc, DipCrim

Suicide and intentional self-harm are issues of major importance in public health and public policy, with rates widely used as progress indicators in these areas. Accurate statistics are vital for appropriately targeted prevention strategies and research, costing of suicide and to combat associated stigma. Underreporting of Australian suicide rates probably grew from 2002 to 2006; Australian Bureau of Statistics (ABS) suicide data were at least 11% or 16% undercounted (depending on case definitions) in 2004. In coronial cases with undetermined intent for 2005 to 2007, intentional self-harm was found in 39%. Systemic reasons for undercounting include: (i) absence of a central authority for producing mortality data; (ii) inconsistent coronial processes for determining intent, as a result of inadequate information inputs, suicide stigma, and high standards of proof; (iii) collection and coding methods that are problematic for data stakeholders; and (iv) lack of systemic resourcing, training and shared expertise. Revision of data after coronial case closure, beginning with ABS deaths registered in 2007, is planned and will reduce undercounting. Other reasons for undercounting, such as missing or ambiguous information (eg, single-vehicle road crashes, drowning), differential ascertainment (eg, between jurisdictions), or lack of recorded information on groups such as Indigenous people and gay, lesbian, bisexual and transgender people require separate responses. A systemic coordinated program should address current inaccuracies, and social stigma about suicide and self-harm must be tackled if widespread underreporting is to stop.

Diego De Leo MD, PhD, FRANZCP · Michael J Dudley MB BS, FRANZCP · Caroline J Aebersold BA(Hons) · John A Mendoza DipTeaching, BEd, GradDipHealthSci · Michael A Barnes BA, LLB, LLM · James E Harrison MB BS, MPH, FAFPHM · David L Ranson BM BS, LLB FRCPA

Recent research has confirmed that Australian children and pregnant women are mildly iodine deficient. A considerable proportion of the pregnant population is moderately to severely iodine deficient. Even subclinical hypothyroidism in the mother, occurring as a consequence of iodine deficiency, can cause irreversible brain damage in the fetus, making it essential to avoid iodine deficiency in pregnancy. The proposal of Food Standards Australia and New Zealand (FSANZ) — Mandatory Iodine Fortification for Australia (P1003) — has been implemented. FSANZ openly admits P1003 is inadequate for covering the needs of pregnant women. Therefore, health professionals and the public must be properly informed about the limitations of this proposal. Views differ about the most effective measures to prevent iodine deficiency in Australia. We propose that women planning a pregnancy, and pregnant and lactating women should be advised to take an iodine supplement. Women with pre-existing thyroid disease should exercise caution and seek medical advice before taking a supplement.

Gisselle Gallego BPharm, PhD · Stephen Goodall BSc, MSc(Health Econ), PhD · Creswell J Eastman MD, FRACP, FAFPHM

In the United States, policy experiments over a 20-year period have demonstrated that road crash deaths among young adults can be substantially reduced by raising the minimum legal drinking age to 21 years. A recent evaluation of the cost-effectiveness of policies for reducing alcohol-related harm in Australia found that, if the US experience were to be replicated in Australia, raising the minimum legal drinking age would be more cost-effective than random breath testing and drink-driving campaigns. Given the major political obstacles to increasing the minimum legal drinking age, we propose another policy that could achieve a similar reduction in road crash deaths — requiring licensed drivers to maintain a blood alcohol concentration (BAC) of zero until at least the age of 21 years (close to the current policy of zero BAC until age 22 years in Victoria), and preferably until 25 years. This would allow young Australians to drink or drive but not to combine these activities for at least the first several years of driving. If all Australian jurisdictions had adopted this policy in 2003, 17 deaths could have been be averted among young Australians as they aged from 18 to 21 years and many more serious injuries could have been prevented each year. If we had enforced a zero BAC until age 25, the number of deaths averted until age 25 years could have been as high as 50.

Wayne D Hall PhD · Angela L Wallace BSc, MPH · Linda J Cobiac BEng, MEngSc, MPhil · Christopher M Doran PhD · Theo Vos MSc, PhD

To the Editor: In April 2009, a registered nurse at the Sydney Medically Supervised Injecting Centre (MSIC) overheard two clients warning others about the effects of injecting from a particular glass vial, believing it had given them a “dirty shot” (bacterially contaminated injection). Seeing an unlabelled, discarded vial containing cloudy fluid, the nurse was concerned that it may have contained insulin, and assessed all four clients who reported injecting from similar vials. Three clients were sweaty, nauseated, and looked unwell, while only two (who had subsequently injected heroin) showed the pin-point pupils and hypoventilation typical of opioid use. Blood glucose levels confirmed likely insulin use, with the lowest reading being 1.5 mmol/L. MSIC staff made sweet drinks available, but one client became unconscious and required intramuscular glucagon and hospital admission. She was subsequently discharged without complications. Staff were concerned that insulin from an unknown source and of unknown concentraion was for sale in the local area, and immediately informed the local police and health and social welfare agencies. Thankfully, no further cases were noted, and no permanent harm resulted from this incident. The vial found at the injecting centre was later identified as Humulin 30/70 (Eli Lilly Australia, Sydney, NSW). Insulin-induced hypoglycaemia may result in brain damage and death.1 To our knowledge, this is the first case of inadvertent insulin injection in an injecting facility reported in the scientific literature. Given the unlikely nature of the substance, and that two clients showed physical signs consistent with opioid use because of subsequent heroin injection, their presentation in another setting could well have been confused with opioid overdose. We believe the MSIC was able to avert serious morbidity and possible death because of the presence of experienced staff able to provide immediate medical attention. The MSIC opened in 2001 in Kings Cross, Sydney, the first of its kind in the English-speaking world. The centre reduces morbidity and mortality from drug overdose, enhances access to health and social welfare services, reduces transmission of blood-borne viruses and reduces the incidence of drug injecting in public places.2 The main drugs injected at the MSIC include heroin, other opioids, cocaine and methamphetamines. There are now 70 such facilities around the world; these are legally sanctioned sites where people may inject previously obtained drugs under the supervision of qualified personnel. There is growing scientific evidence internationally to show that supervised injecting facilities reduce the harms associated with illicit drug injection.3-5 This case highlights their role in preventing harm associated with more unexpected drug injections.

Marianne E Jauncey · Anita P Trevan · Richard P Sulovsky

To the Editor: The comments about health literacy by Adams and colleagues1 and Nutbeam2 are timely, given findings that 60% of Australians lack basic health literacy skills.2 Despite attention given to health literacy by the National Health and Hospitals Reform Commission, current discussions remain worryingly limited. In the 1990s, Nutbeam was prominent among those who recognised both the individual and the larger environmental settings of health literacy, as well as its relevance to prevention. “Health literacy and health skills” was included as a category in a landmark health goals and targets framework, as “personal health knowledge and positive attitudes towards changing behaviour demonstrably influence people’s ability to adopt healthy lifestyles”.3 Significantly, the goals of improving health literacy were expressed as enabling people to make more informed choices about their health and to take an active role in bringing about changes in environments that influence health. Since then, surprisingly scant attention has been given to health literacy in the context of coping with everyday life, including new situations4 — surprisingly, given that “nearly every choice we make throughout the day is relevant to health in some way — what we eat, how much we move, what products we buy”.5 Most discussions focus on the skills and knowledge individuals need to navigate the health system. Studies of health literacy in broader health contexts remain comparatively rare and frustratingly dispersed throughout numerous disciplines.6 It is time for greater recognition of health literacy as both a consumer issue and a public health issue relevant to disease prevention. (It is perhaps no coincidence that the Newest Vital Sign test for health literacy involves the comprehension of nutrition information about ice cream.) Nutbeam’s suggestions for building health literacy and consumer engagement in health services could easily be expanded. Why not, for example, develop a national plan with specific objectives and approaches, and definitions and indicators to measure health literacy progress? There are obvious tie-ins with the “prevention agenda” and with Australia’s new national policies on men’s and women’s health, and just bringing together the scattered articles on health literacy and gender would be a major task.7 Australian health initiatives aimed at reducing the burden of chronic and preventable disease should consider the role and challenges of health literacy beyond its application to health services use. Our growing understanding of the complex behavioural, social, systemic, and ecological forces that influence health and wellbeing should help guide these efforts.

Margo H Saunders · Anita Peerson

To the Editor: A recent editorial about health literacy and a research article on the prevalence of low health literacy in a South Australian population sample2 highlight the potential negative impact of low health literacy on treatment outcomes. Adams and colleagues also suggest a need to assess health literacy in clinical practice.2 Although calls for the introduction of screening to identify patients with low health literacy appear frequently in such articles, we urge caution in taking such a step at this time, because of a lack of sound evidence to support such a recommendation. High-level evidence related to health literacy screening is scarce. One randomised controlled trial found that making physicians aware of patients’ health literacy status led to greater use of recommended strategies, but did not translate to expected improvements in patient self-efficacy.3 An unanticipated outcome was that physicians who received advice about their patients’ health literacy status reported significantly lower satisfaction with the consultation and felt marginally less effective than those not given such information. The authors caution against health literacy screening in clinical practice unless system-wide training and support for both health practitioners and patients is in place. A fundamental principle of screening is that it should not be introduced without an effective intervention — to do so offers no advantage to patients and may be harmful.4,5 Health literacy screening raises the potential for harm due to high levels of stigma and shame that may be experienced by those with poor literacy. In Australia at this time, it is uncertain whether effective intervention strategies suitable for use in clinical settings are readily available. Moreover, we do not have reliable information about the skill levels of practitioners to address low health literacy. Published studies consistently show that 40%–60% of clinical and population samples have low or marginal levels of health literacy. This means that one of every two people attending a medical consultation can be expected to have suboptimal health literacy. Therefore, a universal approach to the assurance of comprehension in every consultation, supported by practitioner training in health literacy communication and evidence-based tools to enhance patients’ encounters with health services, may offer a more effective and efficient alternative to screening.

Robert A Bush · Frances M Boyle · Remo Ostini

What did we do well in the first year of pandemic (H1N1) 2009, and what can we do better? In Mexico in April 2009, a new H1N1 influenza strain appeared to be associated with a high mortality rate. This fuelled fears that a highly virulent virus would quickly spread internationally and cause millions of deaths. Appropriately heightened surveillance and controls were put in place, and Australia activated its “well-rehearsed plan for response to pandemic influenza”.1 Across the country by mid May, we had in place accurate polymerase chain reaction (PCR) testing for “swine flu”, improved public awareness of infection control and good public health surveillance. By September, Australia was among the first countries with a vaccine available. Now, a year after the virus first emerged, what have we learnt and how could our pandemic response be improved in the future? Swine flu did spread rapidly internationally. However, by late May, data from the United States spring showed that case-fatality rates were lower than those from seasonal influenza (< 0.1%).2 But what would happen in the Australian winter? By mid June, we knew that case-fatality rates here were also low.3 Despite this knowledge, many costly interventions continued, including border control, widespread use of antivirals, school closures and contact tracing, but with little evidence that these made much difference to the overall rate or spread of the virus. Appropriately, when it became obvious that the spread of the virus could not be controlled, the national pandemic plan was modified. A new phase, “Protect”, was adopted on 17 June,1,4 with a greater focus on treating and caring for those patients who were more vulnerable to severe outcomes. The word “pandemic” can evoke needless fear and panic. This term would be best used when a virus not only spreads widely but also has increased virulence — this latter aspect is currently not considered in the World Health Organization definition.5 Virulence needs to be measured quickly and accurately. Pandemic plans seem to assume a case-fatality rate of 1% or more. However, a different approach could be better for a virus such as swine flu with a mortality of 0.01% or less — predetermined responses that take into account different levels of virulence, not just the spread of a virus. The US has such a grading system (similar to that used for hurricane severity),6 but it was not used to guide this public health response. “Real-time” viral spread and activity can be followed with remarkable accuracy using Google Flu Trends.7 In the Australian community, the effects of the pandemic (H1N1) 2009 influenza virus were “at most like influenza circulation in a season of moderate seasonal activity”.8 Rates of absenteeism from work and school were similar to those seen in the winter of 2007.1 The 191 associated deaths were substantially fewer than the 3000 estimated yearly deaths from seasonal influenza in Australia.1,4,9 Although there may have been additional influenza-associated deaths that were not diagnosed by laboratory testing, [a] broader measure of all Australian deaths resulting from influenza or pneumonia currently indicates that there have been fewer such deaths than in other influenza or winter seasons.1 Some groups, such as Indigenous peoples and pregnant women, were more vulnerable. Pregnant women had a tenfold higher rate of severe complications than others of the same age.8 Astute clinicians in Melbourne found that pregnant women with complications were often IgG2-deficient. Thus, we now potentially have a marker that identifies those at much greater risk from influenza and also new, related therapeutic options (using gamma globulin).10 Intensive care units (ICUs) in Australia managed to cope with the larger numbers of generally younger influenza patients, but had major problems and were, worryingly, very stretched.1,4 This demonstrated the lack of spare capacity in our hospitals and ICUs — a problem most apparent every winter. Australia’s population mortality rate from swine flu was 0.9 per 100 000.1,4 If a more virulent virus with a 1% case-fatality rate infected 30% of the population, our hospitals and ICUs could not cope, and we would have to find other ways of managing the problem. Despite the widespread use of costly oseltamivir stockpiles in Australia and elsewhere, there were no obvious effects in terms of slowing or altering the overall epidemic. Antivirals probably benefit individuals who are at high risk of complications, but in the general population the benefits may be marginal.11 In addition, the recommendations for who should receive antivirals changed with the different declared phases of the pandemic (eg, from “Contain” to “Protect” phases). This led to confusion for both clinicians and the general public — were antivirals to be used to reduce transmission by ill patients, limit disease severity by stopping sick patients getting sicker, or for prophylaxis? Testing for swine flu was problematic. Most of those infected had only mild disease, but demand for testing was high. Rapid influenza tests had poor sensitivity, and no specific serological tests were available. PCR was the only reliable form of testing, but it is relatively expensive and labour-intensive. Thus, testing was often not available. Testing was also commonly centralised, which meant results were not readily available in a timely fashion, even for ill patients in many hospitals. Vaccines were also problematic. Australia was one of the first countries to manufacture and distribute a vaccine for pandemic (H1N1) 2009. However, it only became available after the epidemic finished around the end of September, in multidose vials containing thiomersal, and when a large proportion of the population may have been already immune (from recent infection or prior immunity). In vaccine trials, Australian participants had higher-than-expected levels of pre-vaccination cross-reactive antibodies.1 Thirty per cent of children aged > 3 years and 27% of adults aged 18–65 years had protective antibody levels, with 62% of adults having detectable antibodies.12,13 Older people are likely to have even higher pre-existing immunity, given their relatively lower rate of pandemic (H1N1) 2009 infection last winter. In the future, it could be worthwhile to consider another approach to vaccination. Currently, effective vaccines are usually only available “after the horse has bolted”. Because of poor matching, seasonal influenza vaccine efficacy varies from 50% to 80%.14 New vaccines that are safe and more effective, but that only have to be given once every 5–10 years and protect against a variety of influenza strains, could be a useful development. Large amounts of public money and resources were spent on antivirals and vaccines in Australia during the pandemic (H1N1) 2009 outbreak. Pandemic vaccines cost over $120 million here, widely reported and mass immunisation delivery costs for 20 million doses would likely be another $500 million. We also saw that infections spread easily. If people are sick, they should not be at work, school or travelling on public transport. Disproportionate fear generated by media reports resulted in many people presenting to emergency departments or medical practices when they had mild illness and should have stayed at home to recover on their own. However, we do need the ability to quickly assess those in risk groups or those whose condition deteriorates. This may require a phone triage system. Health care workers would then only need to directly assess the much smaller numbers of patients who may need antimicrobials or hospital admission or who are severely ill. Front-line general practitioners and other clinicians faced extreme difficulties because of deficiencies in implementing parts of the pandemic plan.15 This involved resource supply failures, time-consuming administrative burdens, delays in receiving laboratory test results and approval for provision of oseltamivir to patients, and a lack of clear communication about policy changes as the situation progressed.15 We could learn to adapt better as circumstances change and improve consultation with front-line clinicians in any future planning. The core components of current pandemic planning are influenza vaccination and antivirals. This may not be the best approach. Simple infection control measures such as hand hygiene and barrier methods (gloves, masks, isolation) reduce the spread of respiratory viruses.16 In the 1918–1919 pandemic, the vast majority of deaths were probably from bacterial complications rather than the influenza virus itself.17 Effective prevention, treatment and vaccines against bacteria are therefore potentially more effective in preventing deaths. The swine flu outbreak has provided lessons for all of us in the community — clinicians, health officials, politicians and patients. Despite our efforts to contain this virus with pandemic plans, the pandemic (H1N1) 2009 strain behaved like seasonal influenza and spread rapidly throughout the population, and then stopped just as rapidly. We need to devise better ways to decrease the spread of viruses and to identify and treat the small proportion of people infected with influenza who are likely to develop serious disease or complications. Most importantly, we need to establish better trigger points that take virulence as well as virus spread into account before we roll out pandemic plans.

Peter J Collignon FASM, FRACP, FRCPA

Because of the complex aetiology of modern obesity patterns, isolated therapeutic or public health measures will not solve the obesity problem. Consumers must be made aware of the ways in which the food industry influences their food purchases. Government needs to prioritise health ahead of industrial productivity and increased consumption. An obesity intervention wish list is presented as a suggested reform package: prohibit all forms of marketing of energy-dense, nutrient-poor foods; introduce measures such as kilojoule caps, prohibition of bundling, and greater uniformity in packaging design to make energy-dense, nutrient-poor foods less enticing and less amenable to bulk purchase; redesign supermarkets to promote fresh rather than energy-dense, nutrient-poor foods; cease provision of government subsidies to food processing industries; tax energy-dense, nutrient-poor foods to create a disincentive to purchasing of these foods; and regulate the location and number of fast-food outlets by enacting urban planning laws

Bebe Loff LLB, MA(Lond), PhD · Brad R Crammond MA(Hons), LLM

A 19-year-old Sudanese woman, who had lived for about a decade in Ugandan refugee camps, was referred for investigation of a 12-month history of a generalised rash. Two months later, her condition had deteriorated to include cachexia and drowsiness. Despite initial negative findings on investigation, human African trypanosomiasis (HAT) was suspected, and parasites were found in a double-centrifuged sample of cerebrospinal fluid. Eflornithine, the appropriate drug for treatment of late-stage disease, was obtained through the World Health Organization. This case highlights the diagnostic and therapeutic difficulties in managing late-stage HAT in a non-endemic country. Clinical recordIn January 2008, a 19-year-old Sudanese woman was referred from the community to a tertiary hospital for investigation of a 12-month history of generalised pruritus. There were no obvious precipitants or triggers for the itch. She was born in southern Sudan, but had lived in refugee camps in north-western Uganda for about a decade before migrating to Australia in November 2006. Her past medical history was non-contributory. Initial examination showed generalised hyperpigmented papules and nodules with excoriations. Prurigo was diagnosed, and treatment with topical corticosteroids was trialled. By March 2008, her condition had deteriorated, and she experienced lethargy, apathy, fevers, night sweats, weight loss, reduced rousability, abulia (impairment or loss of willpower) and seizures. The pruritus was pervasive and the scratching automatic. A past family history of human African trypanosomiasis (HAT) in her mother, which was diagnosed and treated in Uganda, was elicited. On examination, she had cachexia, and was drowsy, but rousable, and oriented to person, but not place or time. She had generalised itch with hyperpigmented, lichenified papules and excoriated nodules (Figure 1). Neurological examination showed symmetrical brisk reflexes, bilateral upper-limb cogwheeling, and myoclonic jerks involving her limbs, mouth and periocular muscles. She had palpable posterior cervical lymph nodes of less than 1 cm in diameter. Late-stage HAT was suspected, and she was admitted to hospital for further investigation. Differential diagnoses included other infective encephalitides (tuberculous and viral), vascular events and malignancies (lymphoma). Investigations showed that the patient had microcytic anaemia (haemoglobin concentration, 96 g/L; reference range [RR], 115–145 g/L), which was attributed to a known α-thalassemia trait: her renal function and hepatic function were normal. Her erythrocyte sedimentation rate was 42 mm/h (RR, < 20 mm/h). Elevated concentrations of total serum protein (104 g/L; RR, 60–80 g/L), gammaglobulin (32 g/L; RR, 8–16 g/L), IgG (24.3 g/L; RR, 5.8–13.7 g/L) and IgM (7.8 g/L; RR, 0.3–1.7 g/L) were detected. A skin biopsy suggested lichen simplex chronicus. Initial peripheral blood smears, lymph node and bone marrow aspirates all tested negative for parasites. Examination of the cerebrospinal fluid (CSF) revealed a mononuclear pleocytosis of 100 × 106 cells/L (RR, < 5 × 106 cells/L), an elevated protein level (0.9 g/L; RR, 0.15–0.45 g/L), markedly elevated level of IgM (0.36 g/L; RR, undetectable) and a low level of glucose (2.1 mmol/L; RR, 2.4–4.6 mmol/L); micro-organisms were not seen on examination of the centrifuged deposit. Gadolinium-enhanced magnetic resonance imaging (MRI) showed bilateral, symmetrical, widespread high-signal white matter change on T2-weighted imaging (Figure 2). Simultaneous T2-weighted images demonstrated high signal changes in the splenium, the brainstem and the cerebellar white matter (images not shown), and post-gadolinium images showed minimal leptomeningeal enhancement (images not shown). An electroencephalogram (EEG) showed diffuse delta-wave slowing consistent with a metabolic encephalopathy, with no evidence of ictal activity. Despite initial negative results on CSF testing, HAT was suspected on clinical grounds. Thus, repeat large-volume CSF examination was performed. Direct examination of CSF was again negative, but double-centrifuged CSF microscopy showed trypanomastigotes (Figure 3), confirming the diagnosis of late-stage HAT. Both subspecies of Trypanosoma brucei can be acquired in Uganda.1 We considered Trypanosoma brucei gambiense infection to be more likely in this patient as it is hyper-endemic in north-western Uganda and because of the subacute clinical presentation. However, as Trypanosoma brucei rhodesiense infection remained plausible, given the patient’s past travel to southern Uganda, subspecies testing was indicated. Lacking an Australian medical reference laboratory for this, we referred specimens to the Institute of Tropical Medicine (Antwerp, Belgium) for serological testing, and to a local reference laboratory for nucleic acid amplification testing.2 While awaiting results, the patient became uncommunicative, bed-bound and increasingly cachectic, making empiric trypanocidal therapy imperative. Treatment for late stage T. b. gambiense infection was commenced 19 days after admission, with intravenous eflornithine (obtained through the World Health Organization [WHO]) at a dose of 100 mg/kg every 6 hours for 2 weeks. This was tolerated without significant toxicity. At discharge on Day 39, the patient was orientated, communicative and walking independently despite persistence of slight limb hypertonia. Subsequently, subspecies serology showed elevated titres to T. b. gambiense on a serum immunofluorescent antibody test (IFAT; titre, 1:1600; RR, negative) and a card agglutination antibody test (CAAT; titre, 1:32; RR, negative). The CSF IFAT titre to T. b. gambiense was 1: 8 (RR, negative). The local nucleic acid amplification test suggested T. b. rhodesiense (data not shown), but this was felt to be clinically discordant. Three months after discharge, the patient was lucid, conversant in both English and her native tongue, neurologically intact and free from itch. Examination of her CSF showed improving pleocytosis with normal biochemical findings. MRI verified improvement; the post-contrast enhancement had resolved, but mild, diffuse cerebral atrophy was evident. She has resumed her studies and normal social activities and was relapse free at 16-month follow-up. DiscussionHuman African trypanosomiasis or sleeping sickness is caused by two subspecies of the haemoflagellate parasite Trypanosoma brucei — T. b. rhodesiense (east-African HAT) and T. b. gambiense (west-African HAT).1,3 The parasite is transmitted by the bite of tsetse flies (Glossina spp.).1 HAT is endemic only in sub-Saharan Africa, where the WHO estimates that between 300 000–500 000 people are currently infected, with 100 000 deaths directly attributed to this disease annually.3 Uganda is currently the only country where infection with both subspecies occurs. While the two foci of trypanosomiasis within Uganda appear separate, as a result of civil unrest, population displacement and the northward spread of wild and domestic animals from central and south-east Uganda, it is likely that these foci will soon converge.4-6 HAT is rarely diagnosed outside Africa. When T. b. gambiense infection is diagnosed, it is usually in the late (secondary) stage.1,7 To our knowledge, this is the first case of T. b. gambiense infection diagnosed in Australia. HAT is a biphasic disease. Early-stage disease (Stage I) denotes the post-inoculation period followed by haemo-lymphatic spread.1 An inflammatory nodule or ulcer (chancriform) may be seen at the site of inoculation, more commonly with T. b. rhodesiense infection.1 Lymphatic spread results in lymphadenopathy, with posterior cervical lymphadenopathy (Winterbottom’s sign) typical in T. b. gambiense disease.1,3 Haematogenous spread produces fluctuating fevers, hepatosplenomegaly, serositis and myocarditis, which occur in both forms of the infection, but are more common in T. b. rhodesiense disease.1 In late-stage disease (Stage II), the parasite passes through the blood–brain barrier into the central nervous system, resulting in meningoencephalitis, which is invariably fatal if not treated.1,3 Headache, ataxia, itching, speech disturbance, behavioural change, extrapyramidal signs and mental state changes may manifest.1,3 Pineal and thalamic invasion leads to hypersomnolence and circadian rhythm disruption.3 The natural history of the diseases caused by the two subspecies varies significantly; T. b. gambiense infection is insidious (over months to years), whereas T. b. rhodesiense infection usually progresses over days to weeks.1 Dermatological manifestations of HAT are non-specific. Pruritus is a pervasive symptom, present in over 50% of cases, and is a feature of disease chronicity.8 Pruritus generally correlates with greater CSF pleocytosis.8 Parasternal and generalised pruritus are common, as is peripheral oedema. Transient urticarial and macular eruptions have also been described.1,9 In very chronic disease (of more than 24 months’ duration), pruritus may decrease, heralding a pre-terminal phase of illness.8 Definitive diagnosis of HAT requires direct visualisation of the parasites in blood, CSF or tissue. Detection of trypanosomes in the CSF confirms late-stage disease. False negative results are common because of the low number of parasites in T. b. gambiense infection.1 As in the case we present here, concentration techniques such as double-centrifugation of CSF increase the sensitivity of microscopy.10 Non-diagnostic CSF changes include: lymphocyte counts of > 5/μL, increased CSF protein and IgM concentrations, and morula (Mott) cells.9,11 Identifying the subspecies of trypanosomes is difficult because both subspecies are morphologically identical. The serological tests CAAT and IFAT are available for the detection of T. b. gambiense antibodies, and this is useful in screening high-prevalence populations.9 The use of nucleic acid tests for the subspeciation of T. b. rhodesiense and T. b. gambiense is an emerging technique, and has been used successfully in the research setting.5,6,9 However, these assays are not widely available.9 Obtaining a detailed travel history from patients and recording the timing of symptoms and signs over the course of the illness remain important for differentiating the two forms of the disease. Treatment of HAT depends on the subspecies of infecting trypanosome and disease stage. Patients with early-stage disease should have CSF examination to exclude subclinical neurological involvement.9 In Australia, treatment is challenging because we have limited access to targeted therapies for HAT. The necessary drugs are accessible through the WHO. Treatments for early-stage HAT infections are parenteral pentamidine for T. b. gambiense disease and suramin for T. b. rhodesiense disease.1,6 For late-stage HAT, melarsoprol was formerly the treatment of choice.1 However, 3%–10% of patients treated with melarsoprol develop encephalopathy, which is fatal in 10%–70% of cases. Survivors of encephalopathy frequently have residual brain damage.12,13 Eflornithine is equally efficacious and less toxic than melarsoprol12,13 for late-stage T. b. gambiense infection, with lower treatment-related mortality (about 0.8%).13 Adverse effects of eflornithine include seizures, gastrointestinal upset and neutropenia, but treatment interruption is generally not required.1 Recently, one week of combination therapy with nifurtimox and eflornithine was shown to be equally effective, less toxic and easier to administer than eflornithine monotherapy for late-stage T. b. gambiense infection,14 and is now considered the treatment of choice for this infection.15 Recommended follow-up after treatment for late-stage HAT includes 3–6-monthly CSF examinations for 2 years.4 This case highlights the diagnostic and therapeutic difficulties in managing late-stage HAT in a non-endemic country. Clinicians need to be aware of infections that are non-endemic to Australia that can occur in recently arrived travellers and migrants. Appropriate treatment of HAT is life-saving and associated with good clinical outcomes. Figure 1 The patient’s rash on presentation in March 2008, showing hyperpigmented, lichenified papules and nodules with excoriation involving the trunk. Figure 2 Axial T2-weighted magnetic resonance image showing high signal in both basal ganglia (white arrow) and symmetrical high signal in the white matter, including the internal and external capsules (black arrows). Figure 3 Double centrifuged sample of the patient’s cerebrospinal fluid shown on direct microscopy showing a trypanomastigote typical of Trypanosoma brucei, the pathogen of human African trypanosomiasis (Giemsa stain; original magnification, × 800).

Paul Cherian MB BS · Ralph K Junckerstorff MB BS · David Rosen MB BS, FRACP, PhD · Prasad Kumarasinghe MD, FACD · Alan Morling BSc · Philip Tuch MB ChB, FRACP · Sonja Raven MB ChB, FRANCR · Ronan J Murray MB BS, FRACP, FRCPA · Christopher H Heath MB BS, FRACP, FRCPA

To the Editor: Sweet and Simons are right to raise concerns about the quality and reliability of the health information available on the internet in this new digital age.1 Similar to the “old media” paradigm, the driving pressure is to maximise readership, thereby maximising advertising revenue. The task of providing content of sufficient volume and quality to meet the needs of readers permanently connected to the internet appears overwhelming. As an example of the way such pressure damages the quality of health reporting, we need look no further than the way Sweet’s health blog, Croakey, and its parent publication, Crikey, dealt with the 2009 H1N1 influenza pandemic. After initially calling for a rational discussion about the merits of the population-based vaccination program,2 Croakey and Crikey published a series of articles that either trivialised the severity of the H1N1 outbreak or focused on perceived problems of the vaccine or the program. There was no corresponding focus on possible benefits of vaccination or solutions implemented to minimise perceived problems with the program. Former Minister for Health Michael Wooldridge had a piece supportive of vaccination published,3 but this was immediately followed by a response from Sweet suggesting, without supporting evidence, that he was acting as an agent of CSL.4 So effective at rallying anti-vaccination supporters has Crikey’s campaign been that members of the anti-vaccine Australian Vaccination Network now copy in Sweet and Crikey on correspondence to the federal Minister for Health denouncing H1N1 vaccines.5 Although it is unlikely this negative reporting will have a major impact on H1N1 vaccine coverage, it adds a veneer of credibility to vaccine conspiracy material widely available on the internet. Sweet and Crikey would do well to consider the wider public health implications, beyond improving readership and advertising profit, of pushing their controversial and strident anti-H1N1 vaccine message.

Stephen B Lambert

In reply: Lambert has previously raised similar concerns in comments published by Crikey and its health blog Croakey.1-3 Leading public health and medical experts contribute to Crikey and Croakey’s coverage of pandemic influenza. As has been noted in this Journal, there are many questions and controversies surrounding the pandemic and the policy response.4 It is a misrepresentation to describe Crikey and Croakey coverage as being stridently anti-H1N1 vaccination or a “campaign”. Indeed, I recently received a note of thanks from the Australian Government Department of Health and Ageing Media Unit for a “very fair report” in Crikey regarding an influenza vaccination safety issue (Department of Health and Ageing Media Unit, personal communication, 8 Dec 2009). Michael Wooldridge and CSL’s Director of Public Affairs, Rachel David, are scheduled to speak at a conference in Sydney on 24 March 2010 about their use of online media to promote pandemic vaccination.5 It cannot be controversial, in these times of heightened concern about conflicts of interest and their consequences, to suggest that if Wooldridge is publishing related comment, as in his Crikey article, any association with CSL should be declared.6 Additionally, I am regularly copied on emails or correspondence by a variety of individuals and organisations. This does not mean I am involved with these groups or necessarily support their work. Lambert is entitled to his views about the forces driving the media; my own is that an open, transparent debate about public policy, whether it relates to vaccines or other interventions, is important for the health of populations and of societies more broadly.

Melissa A Sweet

Objective: To test the effectiveness of using a full-time project nurse to assist residential aged care facilities in using evidence-based approaches to falls injury prevention.Design, setting and participants: Cluster randomised controlled trial involving 5391 residents in 88 aged care facilities in the Hunter and Lower Mid North Coast areas of New South Wales. Residents were followed for 545 days or until death or discharge. Data were collected from July 2005 to June 2007.Intervention: Employment of a project nurse to encourage best-practice falls injury prevention strategies during the 17-month intervention period.Main outcome measures: Monthly data about falls, falls injury and falls injury prevention programs; audit of hospitalisation for fractured neck of femur.Results: Despite significant increases in the provision of hip protectors and use of vitamin D supplementation in both intervention and control facilities, there was no difference in the number of falls or falls injuries between the intervention and control groups, nor a reduction in falls overall. There was also no difference between the 7-month pre-intervention period and the intervention period in the number of falls or falls injuries. Factors related to residents having an increased risk of falls with fractured neck of femur included being ambulant, having dementia, increasing age, and having a high falls risk assessment score.Conclusion: It is difficult to change falls risk among high-risk populations, including people with dementia. The use of important strategies such as hip protectors and vitamin D and calcium supplementation increased during the study, probably with contamination of control facilities. Longer follow-up may be required to measure the impact on falls outcomes of the strategy of using a facilitating nurse.Trial registration: Australian New Zealand Clinical Trials Registry ACTRN12605000540617.

John A Ward MB BS, FRACP MSc(CommHealth) · Mandy Harden BA, GradDipEd · Richard E Gibson BSc, DipEd, DipMedStats · Julie E Byles BMed, PhD

To the Editor: As health professionals, we urge Australian politicians (and the public) to recognise the overlap in the underlying cause of two great health threats that our population now faces: the rise of obesity and its life-threatening disease consequences, and the great threats to health from global climate change.1-3 Big health gains have been made since the onset of industrialisation. However, we are now seeing the emergence of health risks caused by excesses in market-driven consumerism (including the consumption of energy-dense processed foods), energy-subsidised exertion-free living, an over-arching preoccupation with gross domestic product and (particularly relevant to climate change) population growth.4,5 In light of our profession’s long experience with the smoking–disease debate, we recognise the serious threat posed to population health by the well financed, doubt-fostering opposition of vested interests. In the case of smoking, it took 50 years and several million deaths to progress from acknowledgement of the health hazard to application of effective interventions. With climate change, we lack the luxury of time — and the stakes are much higher.6 Hence, a prudent, precautionary strategy to tackle the big issues is essential. We propose two initiatives: Convene a high-level, ongoing forum to discuss post-growth alternatives to unsustainable, consumption-based growth as the economic norm. This should involve health and social scientists, among others, and economists prepared to objectively take into account the real environmental costs of our actions; and Convene a multidisciplinary taskforce to develop an Australian population policy. Population is a key driver of energy use, greenhouse pollution and resultant ill-health.7 Despite the apparently widespread bias against public discussion of population issues, the topic is now attracting renewed attention and the debate should be facilitated. The irony of adopting a “no change” approach to these two issues is that, if this happens, involuntary change to everyone’s lifestyle will become unavoidable. We must seek a sustainable economic system and stable population size that ensures prosperity without endangering both health and environmental quality.8 For the moment, our actions are seriously damaging our planet and our children’s health. One in three children born today will become obese and/or diabetic in their lifetime, and the population at large will face increasing health risks from climate change.

Garry J Egger · Boyd Swinburn · Fiona Stanley · Kerryn Phelps

Registries can provide sound data needed by clinicians and organisations to improve patient safety and quality of care In June 2009, the National Health and Hospitals Reform Commission released its report proposing an agenda to transform the Australian health system.1 A critical element of this agenda is improved monitoring of service delivery and outcomes of care. Clinical-quality registries are an important development in monitoring and benchmarking quality of clinical care. Registries systematically and uniformly collect information from people who undergo a procedure, are diagnosed with a disease or use a health care resource. They are particularly appropriate for monitoring and benchmarking processes and outcomes of care where there is known variation and where poor performance results in high additional cost (eg, renal transplantation) or poor quality of life. Before outcomes are benchmarked, data must be statistically adjusted to isolate quality of care from prognostic factors that are beyond the influence of clinicians. Variables such as age and clinical comorbidities are typically included in risk-adjustment models. Registries are ongoing data-collection exercises, and the validity of their results relies on near-complete inclusion of all eligible patients. To achieve this goal, use of an “opt-out” consent process is recommended. Where registries have used “opt-in” consent, recruitment rates have been as low as one in six of those eligible, making data unreliable for benchmarking, and rendering the registry ineffective.2 Where an opt-out approach has been used in the United States, recruitment rates as high as 97% have been achieved,3 with even higher rates in Australia (< 1% opt-out in the Australian Orthopaedic Association [AOA] National Joint Replacement Registry and Victorian State Trauma Registry). Clinical-quality registries aim to improve quality of care through benchmarking clinical outcomes and stimulating competition in achieving best practice. The registry set up by the Danish Lung Cancer Group exemplifies what can be achieved. Feedback of indicators of high-quality care derived from registry data to those delivering care has been largely responsible for improvement in 30-day, 1-year and 2-year survival rates for people with lung cancer of 1.6%, 8% and 10%, respectively.4 In addition to providing information on safety and efficacy of treatment, data from registries can also be used to determine whether patients have timely access to care,5 and whether care is delivered in line with best practice and evidence-based guidelines.4,6 Process measures are frequently built into clinical-quality registries to detect variations in clinical approach and explore differences in outcomes. For example, stroke registries established in Canada routinely collect data to assess speed and appropriateness of thrombolytic treatment.7 Collection and feedback of data must be underpinned by an effective central governance structure for the registry, with strong clinical leadership, and a regulatory framework providing incentives for quality improvement and proactive approaches for managing poor performance. There must also be strong local clinical leaders who are accountable for ensuring that registry outcomes drive quality improvement. The impact of poor registry governance was highlighted in an inquiry into cardiac surgery at the Bristol Royal Infirmary in the United Kingdom.8 Since the inquiry, improvements have been made to ensure that findings from the Central Cardiac Audit Database are provided to surgeons and are also publicly reported. Clinical-quality registries can improve safety and reduce costs. Findings of the AOA National Joint Replacement Registry show a decline in the rate of hip and knee revision surgery over a 4-year period from 14.8% to 11.1% and from 10.4% to 7.9%, respectively, with an associated annual cost saving of $44.6 million.9 Since its inception in 2001, the Victorian State Trauma Registry has shown a 30% reduction in mortality among trauma victims.10 These improvements may be attributed at least in part to a monitoring system that provides ongoing feedback to contributing sites, detailing their risk-adjusted outcomes relative to those of peer organisations, and to the institution of remedial processes to manage outliers. International momentum is gathering to develop new clinical registries as quality-improvement measures. For example, Sweden has established a network of more than 70 quality registries and has made available resources to assist in establishing new registries.11 In the UK, a national directory of registries has been established to enhance the usefulness of registries in monitoring quality of care.12,13 The US Agency for Healthcare Research and Quality has produced a guide to the design, operation, analysis and evaluation of patient registries.14 In Australia, the document Operating principles and technical standards for Australian clinical quality registries has been developed under the auspices of the Australian Commission on Safety and Quality in Health Care and is now being evaluated.15 Australia has 28 clinical registries, which continuously collect patient-level health-related data, including outcomes, and operate across many health care sites.16 In Australia, new registries are required in a range of areas where improved quality of care is likely to lead to significant improvements in safety and outcomes. A national registry of cardiac procedures and devices has been widely advocated.17 New registries should be established in strong clinical research environments with access to people skilled in clinical epidemiology, biostatistics and clinical data management. Registry custodians must ensure that their registries collect complete data from as many eligible patients as possible; give accurate and timely feedback to clinicians and organisations; and have well-functioning governance structures. They must ensure that lessons are shared among contributors and that data are continuously used to drive improvement in practice. With high-quality data from clinical registries, there is a strong potential to engage clinicians more intensely in quality improvement activities.

John J McNeil FRACP, MSc, PhD · Sue M Evans PhD · Niall P Johnson PhD · Peter A Cameron MB BS, FACEM, MD

Objective: To assess and compare health care costs for normal-weight, overweight and obese Australians.Design, setting and participants: Analysis of 5-year follow-up data from the Australian Diabetes, Obesity and Lifestyle study, collected in 2004–2005. Data were available for 6140 participants aged ≥ 25 years at baseline.Main outcome measures: Direct health care cost, direct non-health care cost and government subsidies associated with overweight and obesity, defined by both body mass index (BMI) and waist circumference (WC).Results: The annual total direct cost (health care and non-health care) per person increased from $1472 (95% CI, $1204–$1740) for those of normal weight to $2788 (95% CI, $2542–$3035) for the obese, however defined (by BMI, WC or both). In 2005, the total direct cost for Australians aged ≥ 30 years was $6.5 billion (95% CI, $5.8–$7.3 billion) for overweight and $14.5 billion (95% CI, $13.2–$15.7 billion) for obesity. The total excess annual direct cost due to overweight and obesity (above the cost for normal-weight individuals) was $10.7 billion. Overweight and obese individuals also received $35.6 billion (95% CI, $33.4–$38.0 billion) in government subsidies. Comparing costs by weight change since 1999–2000, those who remained obese in 2004–2005 had the highest annual total direct cost. Cost was lower in overweight or obese people who lost weight or reduced WC compared with those who progressed to becoming, or remained, obese.Conclusion: The total annual direct cost of overweight and obesity in Australia in 2005 was $21 billion, substantially higher than previous estimates. There is financial incentive at both individual and societal levels for overweight and obese people to lose weight and/or reduce WC.

Stephen Colagiuri MB BS, FRACP · Crystal M Y Lee BMedSc(Hons), MIPH, PhD · Ruth Colagiuri BEd, GradCertHlthPol · Dianna Magliano BAppSci(Hons), MPH, PhD · Jonathan E Shaw MD, MRCP, FRACP · Paul Z Zimmet AO, MD, PhD, FRACP · Ian D Caterson MB BS, PhD, FRACP

Researchers have longstanding concerns about the logistical and administrative burdens posed by ethics review of multisite studies involving human participants. Centralised ethics review, in which approval by one committee has authority across multiple sites, is widely touted as a strategy for streamlining the process. The Harmonisation of Multi-centre Ethical Review (HoMER) project is currently developing such a system for Australia. It is unclear how centralised review will work for multisite Indigenous health research, where the views of local stakeholders are important and community consultation is mandatory. Our recent experience in conducting the National Indigenous Eye Health Survey (NIEHS) shows how elaborate the current ethics approval and community consultation processes can be, and points to several lessons and ideas to guide pending reforms.

David M Studdert LLB, ScD, MPH · Tamara M Vu LLB · Sarah S Fox BA · Ian P Anderson MB BS, PhD · Jill E Keeffe PhD · Hugh R Taylor MB BS, MD

Incorrect internet address. In “AUSDRISK: an Australian Type 2 Diabetes Risk Assessment Tool based on demographic, lifestyle and simple anthropometric measures” in the 15 February 2010 issue of the Journal (Med J Aust 2010; 192: 197-202), there was an error in the second-last paragraph of the Discussion (page 201). The internet address for the AUSDRISK patient-friendly questionnaire should have been <http://www.bakeridi.edu.au/aus_diabetes_risk>.

Lei Chen · Dianna J Magliano · Beverley Balkau · Stephen Colagiuri · Paul Z Zimmet · Andrew M Tonkin · Paul Mitchell · Patrick J Phillips · Jonathan E Shaw

Objective: To develop and validate a diabetes risk assessment tool for Australia based on demographic, lifestyle and simple anthropometric measures.Design and setting: 5-year follow-up (2004–2005) of the Australian Diabetes, Obesity and Lifestyle study (AusDiab, 1999–2000).Participants: 6060 AusDiab participants aged 25 years or older who did not have diagnosed diabetes at baseline.Main outcome measures: Incident diabetes at follow-up was defined by treatment with insulin or oral hypoglycaemic agents or by fasting plasma glucose level ≥ 7.0 mmol/L or 2-hour plasma glucose level in an oral glucose tolerance test ≥ 11.1 mmol/L. The risk prediction model was developed using logistic regression and converted to a simple score, which was then validated in two independent Australian cohorts (the Blue Mountains Eye Study and the North West Adelaide Health Study) using the area under the receiver operating characteristic curve (AROC) and the Hosmer–Lemeshow (HL) χ2 statistic.Results: 362 people developed diabetes. Age, sex, ethnicity, parental history of diabetes, history of high blood glucose level, use of antihypertensive medications, smoking, physical inactivity and waist circumference were included in the final prediction model. The AROC of the diabetes risk tool was 0.78 (95% CI, 0.76–0.81) and HL χ2 statistic was 4.1 (P = 0.85). Using a score ≥ 12 (maximum, 35), the sensitivity, specificity and positive predictive value for identifying incident diabetes were 74.0%, 67.7% and 12.7%, respectively. The AROC and HL χ2 statistic in the two independent validation cohorts were 0.66 (95% CI, 0.60–0.71) and 9.2 (P = 0.32), and 0.79 (95% CI, 0.72–0.86) and 29.4 (P < 0.001), respectively.Conclusions: This diabetes risk assessment tool provides a simple, non-invasive method to identify Australian adults at high risk of type 2 diabetes who might benefit from interventions to prevent or delay its onset.

Lei Chen MD, MMed · Dianna J Magliano BAppSci(Hons), MPH, PhD · Beverley Balkau PhD · Stephen Colagiuri MD, FRACP · Paul Z Zimmet MD, PhD, FRACP · Andrew M Tonkin MB BS, MD, FRACP · Paul Mitchell MD, PhD, FRANZCO · Patrick J Phillips MB BS, MA, FRACP · Jonathan E Shaw MD, MRCP, FRACP